xxix. The Hippocratic and Galenical belief has been transmitted with

but little alteration through Stoll, Andrie, Abernethy, and Copland to the writers of to-day on biliousness.]

8. Certain vegetable and mineral substances taken either intentionally or by accident constipate the bowels. Chief among these stand opium and its preparations. All opium-eaters are constipated. Lead which is accidentally taken into the system by workers in metals, painters, etc. invariably produces obstinate constipation. The use of tobacco in excess has the effect of deranging digestion and causing constipation in many persons, but this result is occasional only.

9. Chronic diseases of the lungs and heart, by enfeebling the muscular movements which take part in defecation, as well as by the general feebleness and the chronic intestinal catarrh and indigestion which they create, are causes of constipation. Chronic diseases of the liver, especially cirrhosis, are also causes. Constipation accompanies obesity, for in very fat persons the abdominal walls have but little power of contraction; the {642} muscle-layer is thin and flaccid. There is also in such persons in advanced life an accumulation of fat in the mesentery and around the colon. The muscle of the bowel is in a state of fatty degeneration, and atony and dilatation of the gut follow.

10. Painful affections about the rectum and anus deter persons from yielding to the desire for defecation. Fissure of the anus is the principal one of these, but fistula, hemorrhoids, and local eczema have a similar influence. A simple rigidity or spasmodic stricture of the anal sphincter creates constipation.[4]

[Footnote 4: Kunemann, _De la Constipation compliqués de Contraction du Sphincter anal, et de son Traitement par la Dilatation de l'Anus_, Paris, 1851.]

11. Constipation is a symptom in chronic cachexiæ and wasting diseases, in the convalescence of acute exhausting illness, as typhoid fever and pneumonia, or in persons bedridden from any cause. Defective nutrition and degeneration of the muscle-fibre of the intestine explain these cases. In some of them, with improved nutrition, regeneration takes place with a return of contractility.

12. Disorders of the digestive system have constipation as a consequence and a symptom. The reflex sympathy between the movements of the stomach and of the intestines brings this about in gastric diseases.[5] It occurs in gastric cancer and ulcer, in acute and chronic gastritis, in dilatation of the stomach, and in pyloric stricture. The small amount of ingesta entering the duodenum in these diseases diminishes the bulk of fecal matter. In acute intestinal catarrh diarrhoea is the rule, but the bowels may be constipated in intense inflammation and ulceration of the mucous membrane, as is often the case in typhoid fever. In chronic intestinal catarrh constipation is more common in the mild forms than diarrhoea. The thickening and irritation of the mucous membrane lead to a diminution of reflex excitability and loss of elasticity and contractility in the muscular coat. Hence, except in cases where the inflammation is low down or where ulcers have formed, constipation is a more frequent symptom than diarrhoea. The alteration in the quantity and character of the intestinal secretions in chronic catarrh is stated to be an important element. This is to some extent true. Mucus, which is the chief product of this condition, leads to indigestion and fermentation of the intestinal contents and to increased irritation of the mucous membrane. The evolved gas distends the bowel and weakens its contractile power. The fecal mass when it reaches the rectum has an excess of mucus within it or around it which makes its expulsion more difficult. But the diminution or absence of bile does not constipate. In simple jaundice diarrhoea is not uncommon, and an excess of bile does not of necessity cause diarrhoea.[6]

[Footnote 5: Leube, in _Ziemssen's Cyclopædia_, vol. vii. p. 211.]

[Footnote 6: Legg, _op. cit._, p. 271.]

The effects of the modifications of the pancreatic secretion are not well known. Pancreatitis is attended by constipation. Fatty diarrhoea is believed to follow occlusion of the pancreatic duct by pancreatic calculi and chronic catarrh of the duct. Peristalsis is lost in peritonitis from the muscular coat being infiltrated with serum and paralyzed, but tuberculous peritonitis is frequently accompanied by diarrhoea.

13. Loss of fluids by abundant perspiration, by diuresis, diabetes and lactation, increases the dryness of the bowel contents and hinders free {643} evacuations. This is observed as a result of the arrival in a tropical climate and in very hot weather in any climate. The profuse sweats accompanying phthisis, acute rheumatism, intermittent fever, and unusual exercise cause constipation. Another explanation which applies to this has been offered by Good and Eberle, who ascribe constipation to the excessive action of the absorbents in the small intestine, by which the fluid portion is too rapidly and too thoroughly removed.[7] Exercise by promoting activity of the functions in general may induce constipation in this way. In spermatorrhoea the stools are infrequent. An insufficient amount of water taken with food is another cause.

[Footnote 7: Dick, _Braithwaite's Retrospect_, xvii. p. 152.]

14. Food which has but little waste to be got rid of--as milk or beef--leaves a small residuum to be propelled along the intestine, and therefore in one sense is constipating. Insufficient food acts in the same way. An indigestible diet in excess, especially vegetable food, a large part of which is insoluble, constipates by filling the bowel with matter which cannot be got rid of, and chronic catarrh results. The stones and seeds of fruits, as cherry- and plum-stones, raspberry- and currant-seeds, husks of corn and oats, produce acute or chronic constipation with serious symptoms. Intestinal worms (generally lumbricoids) when in large numbers cause obstruction of the bowel;[8] and various foreign substances taken by caprice or to take the place of food have produced the same result: among these stick cinnamon,[9] sawdust,[10] and clay (among the clay-eaters of the South) have been mentioned. Magnesia, insoluble pills, and other medicines sometimes form concretions in the bowel. Enteroliths and accidental concretions form in the intestinal canal and are sources of obstruction. Any foreign body is a nucleus around which concentric layers of phosphate of lime are deposited, and thus a hard calculus is formed. Gall-stones may pass into the canal and there accumulate in such numbers as to interfere with the passage of the fecal matter.

[Footnote 8: Copland, _Medical Repository_, vol. xvii. p. 243.]

[Footnote 9: Ware, _Boston Med. and Surgical Journal_, 1858, vol. lviii. p. 501.]

[Footnote 10: Bonney, _ibid._, 1859, vol. lix. p. 39.]

PATHOLOGICAL ANATOMY.--In cases where constipation has lasted many years no alteration of the parts involved may be found. When lesions do occur the pathological anatomy includes changes in the position,[11] calibre, and in the walls and contents of the intestines. The most common displacement is that of the transverse colon, which is depressed in its centre; the acute angle of the descending part may reach as far down as the hypogastrium. The cæcum sometimes lies in the centre of the abdomen. Dislocations of the intestines are congenital, due to anomalies of intra-uterine development, in which case they become causes of death in newly-born children from obstruction, or if insufficient to cause death they establish habitual and incurable constipation; or constipation may bring about displacement by the greater weight of a portion of the bowel constantly loaded with fecal matter.

[Footnote 11: Vötsch, _Koprostase_, Erlangen, 1874.]

The sigmoid flexure is usually the seat of the greatest dilatation; its expansion may be a cause or a consequence of constipation.[12] It may reach a maximum of distension when it fills the entire abdominal cavity, compressing all the abdominal organs and pushing the stomach, liver, {644} and intestines into the thorax. In a case of this kind the circumference of the dilated part was twenty-seven inches.[13] The descending colon may be distended with the sigmoid flexure, or the whole colon may be dilated from the upper part of the rectum to the cæcum;[14] the same thing happens rarely in the small intestine. In one case, in which there was an accumulation of feces in the sigmoid flexure, the large intestine presented itself as two immense cylinders lying side by side, extending from the epigastrium to the pelvis.[15] Each was about five and a half inches in diameter, and together they filled the abdominal cavity. The circumference of the stretched colon varies from ten to thirty inches. Pouches forming little rounded tumors are seen on the outer surface of the colon; they are sometimes hernial protrusions of the mucous membrane through the muscular coat (Wilks and Moxon), or if large they are dilatations of the pouches of the colon.[16]

[Footnote 12: Trastour, "De la Dilatation passive de l'Iliaque, et de ses conséquences," _Journal de Méd. de l'Ouest_, 1878-79, tome xii. p. 165.]

[Footnote 13: Dupleix, _Le Progrès médicale_, Paris, 1877, tome v. p. 953.]

[Footnote 14: Peacock, "Fatal Constipation, with Excessive Dilatation of the Colon," _Tr. Path. Soc. London_, vol. xxiii. p. 104.]

[Footnote 15: Lewitt, _Chicago Med. Journ._, vol. xxiv., 1867, p. 359.]

[Footnote 16: Gay, "Sacculated Colon, Prolonged Constipation," _Tr. Path. Soc. London_, vol. v. p. 174.]

The colon is sometimes much lengthened. But little weight can be attached to this anomaly, as there is a difference in the length of the colon in different nations and individuals, depending upon the character of the food, being longer in those who eat largely of vegetable food.[17]

[Footnote 17: _Ziemssen's Cyclopædia_, vol. vii. p. 606.]

The mucous membrane is normal or hyperæmic, or is in various stages of chronic catarrh. Proctitis may exist with follicular ulcers; ulcers form in the cæcum, sigmoid flexure, and in the bends of the colon; perforations and peritonitis rarely occur. Chronic peritonitis has resulted from the stretching of the bowel from retained and hardened feces; adhesions may form which ultimately cause death by obstructing the canal. The walls of the intestines are in long-standing cases much thinned. There are many reasons to believe that fatty degeneration of the smooth muscular fibre takes place, in consequence of which it loses its contractile power and atrophies. This lesion is most common in advanced life, and accompanies fatty accumulation and degeneration elsewhere. Its results would be constipation, distension of the bowel with gas, and sometimes symptoms of intestinal obstruction.[18] A thinned and dilated bowel may easily be lacerated under unusual stimulation, as from a purgative. In a case recently seen by the writer such an accident, rupture of the colon and death from peritonitis, occurred from the effects of an active purge taken to bring on abortion. Hypertrophy of the wall, especially of the muscular coat, coexists with dilatation, and is most common in the upper part of the rectum and sigmoid flexure. It is caused by overwork in expelling fecal accumulations. The walls never become as much thickened as in constipation from organic stricture.

[Footnote 18: Cases are recorded of death with symptoms of intestinal obstruction in which no lesion was found beyond a dilated colon; as, for example, in _British Medical Journal_, April, 1879, p. 621.]

Collections of fecal matter may be found in any portion of the colon, but more frequently in the rectum, sigmoid flexure, descending or {645} transverse colon, or cæcum. They lie within the intestinal tube, partly or wholly occluding it, or within lateral pouches, forming tumors which are sometimes quite large. In this last form there is no obstacle to the free passage of feces along the canal. Fecal accumulations occur as small round, oval, or irregularly-shaped lumps (scybalæ), and are often covered with layers of transparent semi-fluid mucus, puriform mucus, or mucus in filaments. The small concretions vary in density; they may be so hard as to resist the knife, and may be mistaken for gall-stones; larger masses, semi-solid or solid, are most commonly seen in the rectum and sigmoid flexure. Here the collection may reach an immense size. In one case fifteen quarts of semi-solid, greenish-colored fecal matter were removed at the autopsy.[19] In two other cases the weight of the feces found in the bowel was thirteen and a half[20] and twenty-six pounds[21] respectively. The whole colon from the anus to the cæcum may be filled with such a mass, as in a case mentioned by Bristowe, where the colon "was completely full of semi-solid olive-green colored feces. The small intestines were also considerably distended, ... and were filled throughout with semi-fluid olive-green contents."[22]

[Footnote 19: Peacock, _Tr. Path. Soc. London_, vol. xxiii. p. 104.]

[Footnote 20: Lamazurier, _Archives générales_, Paris, 1824, t. iv. p. 410.]

[Footnote 21: Chelius, _Heidelberg Med. Ann._, 1838, vol. iv. p. 55.]

[Footnote 22: Bristowe, "Diseases of Intestines and Peritoneum," _Wood's Library_, New York, 1879, p. 21.]

The color of these collections is black, reddish, deep green, or yellow. In composition the scybalæ, concretions, and larger masses consist of fecal matter, with unaltered vegetable fibre; they may be composed partly of skins of grapes, cherry-stones, biliary calculi, hair, woody fibre, magnesia, or other foreign substances. Where fecal concretions long remain in the intestine they acquire a hardness like stone, and can with the microscope only be distinguished from mineral matter.[23] Hemorrhoidal tumors, anal fissures, perirectal abscesses, fistulæ communicating externally or with the gut, are found in connection with constipation. Abscess of the iliac fossa has been observed in the same relationship.[24]

[Footnote 23: A remarkable case is recorded (_Dictionnaire de Médecine_, Paris, 1834, t. viii. p. 435) in which an ulcerating cancer of the fundus of the uterus had opened communication and formed adhesions with the small intestine, from whence the feces passed into the uterus and out through the vagina. The large intestine, totally occluded, contained petrified fecal matter.]

[Footnote 24: Richet, "Abscess of Iliac Fossa," _Revue de Thérapeutique médico-chirurgicale_, 1876, p. 563.]

SYMPTOMS.--In persons who have a daily movement an occasional interruption of two to four days may take place without local or general signs of inconvenience. It is often asserted by patients that one day's omission induces suffering, and recourse is immediately had to laxatives. This may be justified sometimes, but in the majority of cases no actual suffering follows a very rare and short constipation.[25] If, however, symptoms do occur after a constipation of one to three days, there is a sense of fulness and heat about the rectum which is greater after stool; when the bowels are moved, it is with effort (provided that no enema or purgative has been taken), and the bulk of the expelled mass is much greater {646} than usual, being moulded and hardened from its longer retention in the rectum. The margins of the anus are tender, and the unsatisfied feeling after stool is due to distension of the hemorrhoidal veins and oedema of the tissues around them--a condition which ends in painful or bleeding hemorrhoids. There are signs of impaired digestion, loss of appetite, a coated tongue, oppression after eating and flatulence, and distension of the abdomen. Headache is apt to be present, with flushing of the face and general discomfort or irritability of temper. These phenomena may all disappear within two or three days by a spontaneous stool or by the use of a purgative.

[Footnote 25: Some interesting remarks in connection with the idea that constipation is not necessarily hurtful, and is in some cases beneficial, may be found in a pamphlet by C. I. Harris, _Is our Physiology of the Large Intestine correct, and is Constipation in certain cases as Injurious as is supposed?_ London, 1878.]

Acute symptoms of a violent nature are sometimes developed in persons who have been constipated a long or short time, in consequence of attempts at purgation or from the accumulation of indigestible food. Violent paroxysmal pains in the abdomen and efforts at stool are soon followed by symptoms of intestinal obstruction and serious collapse. Quick relief follows a free movement from the bowels obtained by an enema, or if not so relieved the case may terminate fatally.

A frequent recurrence of fecal retention from the causes mentioned will in time develop the constipated habit. Distension of the rectum increases its capacity and destroys its sensibility and expulsive power. The colon above the point of stoppage is distended with gas and weakened. The bowels are rarely moved spontaneously, and finally are never emptied without artificial aid. The literature of medicine contains many extraordinary records of prolonged fecal retention, ranging from a few weeks to many months.[26]

[Footnote 26: _Am. Journ. Med. Sci._, Philada., 1846, p. 260 (three months and twenty-two days); Renaudin, _Dict. des Sci. méd._, t. vi. p. 257 (four months); Strong, _Am. Journ. Med. Sci._, Oct., 1874, p. 440 (eight months and sixteen days); Valentin, _Bull. des Sci. méd._, t. x. p. 74 (nine months); Staniland, _London Med. Gaz._, vol. xi. p. 245 (seven months); _Dublin Hosp. Reports_, vol. iv. p. 303 (eight months); Inman, _Half-Yearly Abst. Med. Sci._, vol. xxxi. p. 275 (two years); Devilliers, _Journ. de Méd._, 1756, t. iv. p. 257 (two years); J. Chalmers, _Med. Gaz._, London, 1843, vol. xxi. p. 20 (three years); _Philada. Med. Museum_, 1805, vol. i. p. 304 (fourteen years).]

The evacuations in chronic constipation are harder and more dry than they should be; they are passed in masses of various sizes, and in color are brown, black, dark-green, or yellow. Sometimes a coating of mucus is on the outside, and sometimes streaks of blood, or there is an intimate admixture of mucus, giving a slimy, gelatinous appearance to the mass. Semi-digested food, as partly-altered milk, meat, or vegetable matter, is seen, and quite frequently there is an intercurrent diarrhoea which alternates with costiveness.

The local symptoms about the pelvis and anal opening and in the lower extremities come from the pressure of accumulations of feces. Thus, compression of the iliac veins delays circulation in the lower extremities; cold feet or oedema of the feet and ankles and varicose veins follow. If the pressure is on the ilio-hypogastric and ilio-inguinal nerves, there are neuralgic pains in the groin and over the crest of the ilium. The sciatic and crural nerves may be the seats of pain. Varicocele is the effect of weight upon the spermatic veins. Erections and seminal emissions in men follow pressure on the pubic veins and prostatic portion of the urethra. Retention of urine also may come from the latter cause. If the kidneys and ureters are compressed by fecal tumors in the descending or transverse {647} colon, nephritic pain, albuminuria, or retraction of the testicle, with delay in the escape of urine, may happen. Icterus and its consequences are owing to pressure on the common bile-duct; the liver and other organs may be displaced and the aortic circulation obstructed by fecal compression. In women the retention of fecal matter in the rectum is the source of special symptoms; it contributes largely to the occurrence of cervical anti-flexion in the soft, pliable, growing uterus of girlhood (Thomas), and unites with retroversion in women who have borne children to produce great suffering.

An unnatural state of the digestive system, as a cause or result, is the invariable accompaniment of chronic constipation. The appetite is wanting; the tongue is coated, and may be pale, soft, and indented by the teeth. Distress follows eating; the abdomen is distended with gas and is hard; all the evidences of gastric or intestinal indigestion may be found. Nutrition is imperfect, as is shown in loss of flesh and in the signs of functional disorder to be next described.

The nervous system is soon deranged; sleep is unrefreshing, restless, and disturbed by dreams. There are headache and mental and physical indolence. The patient speaks of being giddy, faint, and nervous. Disturbance of vision (muscæ volitantes), of hearing (tinnitus aurium), and alarming attacks of dyspnoea and cardialgia may occur.[27] Heart-palpitations and profuse perspirations are the effect of excitement or effort of any kind. Chilliness or violent chills can be traced to this cause also. In women hysteria, disturbed menses, anæmia, and chlorosis accompany constipation.

[Footnote 27: C. C. Melhose, _Hufeland's Journal_, 1841, xcii., Stuch iv. p. 105.]

Nervous symptoms are very common in the young, and it is doubtful whether they are consequences of constipation or whether they form a part of a general state of malnutrition and anæmia. Hypochondria is undoubtedly closely connected with the constipated habit, and the failure to secure a daily movement becomes the subject of unceasing thought and anxiety. Hallucinations and sudden loss of consciousness, aphasia,[28] and delirium, have been found to depend upon fecal accumulation.[29] The absorption of fluids and gases from too-long-retained and decomposing feces may explain such cases. The nerve-centres soon show the effect of the supply of altered or contaminated blood.[30] It is probable that the marked nervous symptoms are more due to this cause than to reflex influences.

[Footnote 28: Mattei, "Aphasia cured by relieving Constipation," _Bull. de l'Acad. de Méd._, Paris, t. xxx., 1864-65, p. 870.]

[Footnote 29: Pulitzer, _Wien. med. Presse_, 1866, x. p. 439. Case.--A man æt. 42, with sleeplessness, hypochondriasis, hallucinations, and one attack of sudden loss of consciousness; symptoms relieved by removing a large quantity of fetid fecal matter from bowels. Also Dujardin-Beaumetz, serious nervous symptoms due to constipation (_Bullétin de Thérap._, Paris, t. 89, 1875, p. 179).]

[Footnote 30: Bell, _Lancet_, London, 1880, i. 243-283.]

A coincidence exists between dislocation of the colon and various states of mental disturbance. Ten cases of suicide were seen by Vötsch in which there were displacements of the colon. Laudenberger of Stuttgart found that in ninety-four autopsies of insane persons there were anomalies of position of the transverse colon in one-seventh of the number (Vötsch).

Fever is not infrequently due to constipation. During the course of typhoid and other fevers an unusual elevation of temperature is often {648} traced to a neglect to have the bowels emptied. But very high temperature sometimes depends upon constipation alone, and is at once reduced by removing the cause. This may occur in the course of chronic diseases or in health, especially in children.[31] The temperature rises from normal to 104° F., and even higher, and immediately drops to normal when the bowels are moved. When a sudden rise in temperature comes with acute constipation, the influence must be a reflected one from the mucous surface to the heat-centre.

[Footnote 31: F. Barnes, "On the Pyrexial Effects of Constipation," _Med. Press and Circular_, 1879, N. S. xxviii. p. 477. Also, C. H. Jones, _Lancet_, London, 1879, ii. p. 229--a case in which there was a temperature of 104.1°, pulse 180, and delirium due to scybalæ in bowel; Cabot and Warren, "High Temperature from Constipation," _Boston Med. and Surg. Journ._, 1880, ciii. p. 1571.]

The urine is dark-colored and scanty, loaded often with urates, or it may be limpid and of a very low specific gravity. The escape from the bladder and through the ureters may be obstructed by compression, as already mentioned. Suppression of urine has occurred, and been relieved by removing large fecal collections.[32] In women catamenial irregularity and dysuria are generally associated with constipation. Disturbances in pelvic circulation and local pressure of a distended rectum explain these conditions.

[Footnote 32: Barnwell, _Cincin. Med. News_, 1875, vol. viii. p. 353--female æt. 45. Had no movement for five days; suffered with tympanites; severe pain in right iliac region, with persistent vomiting; tumor in same region; complete suppression of urine. At the end fifth day passed large quantity of apple-peelings and fecal matter. Return of flow of urine; passed two gallons in ten hours.]

The skin is often parched, sallow, and is sometimes covered with eruptions, as acne, psoriasis, eczema, erythema, or prurigo. Injuries, wounds, and cracks of the skin heal slowly.

RESULTS AND COMPLICATIONS.--The lateral pouches of the colon, most commonly at the sigmoid flexure, become distended, and deeper pouches are formed, where fecal matter is retained.[33] This need not interfere with the regular daily movements. Fecal tumors are thus formed, the nature of which is often not recognized. The colon may be distended so as to fill a large part of the abdomen. The pressure of hardened feces brings about ulceration of the mucous membrane, perforation and extravasation of the contents into the abdominal cavity, with fatal peritonitis. Abscesses in the perirectal tissues, with fistulæ,[34] anal fissures, hemorrhoids, prolapse of the rectum, varices of the prostate gland and bladder, owe their origin to fecal collections, especially in advanced life.

[Footnote 33: Long, _Med. Times and Gazette_, 1856, vol. ii. p. 286.]

[Footnote 34: Bannerot, C., _Du Phlegmon pelvi-rectal inférieure et de la Fistule de l'Anus consécutive causées par la Constipation_, Paris, 1880.]

Intussusception has been attributed to the weight of a mass of feces. Typhlitis and perityphlitis may come from retention in the cæcum. Pressure upon the viscera brings about derangements in their functions, many of which have already been described. From straining at stool a hernia, hæmoptysis, or cerebral hemorrhage may happen. Cases have been reported of death from rupture of an aneurism of the aorta while at stool, and J. F. Hartigan met with a case of spontaneous rupture of the aorta, where the vessel was apparently but little diseased, occurring in a man aged sixty during the act of defecation.[35]

[Footnote 35: Hartigan, _Tr. Med. Soc. District of Columbia_, vol. i. No. 3, 1874, p. 55. See also same number for a valuable paper on spontaneous rupture of aorta, by J. J. Woodward.]

{649} The effects upon the general system are those connected with malnutrition. The health may be profoundly altered and death occur from secondary diseases. Many general symptoms are due to the retention in the blood of excrementitious matters or to their reabsorption.[36]

[Footnote 36: Sterk, "Ueber den schudlichen einfluss der chronischen Stuhlverhatten auf den Gesamur organismus," _Wien. med. Presse_, xxii., 1881, p. 330 _et seq._]

DIAGNOSIS.--The diagnosis of constipation is not difficult except in hysterical women, who select this as one of their subjects of deception. Primary must be distinguished from secondary constipation, the last being a symptom of some general or local disease. The history of the case and the predominating symptoms will be guides to a decision, but constipation should be regarded as a symptom until it is proved to be otherwise. The tendency is to look upon it and to treat it as a distinct malady; important organic changes elsewhere may thus be overlooked. Simple habitual constipation may be mistaken for constipation due to lesions in the wall of the intestine or to closure from the external pressure of tumors.

Slowly-developed symptoms of obstruction may come from polypoid growths or benign tumors in the rectum, colon, cæcum, duodenum, and ileum. They are usually found in the rectum. The diagnosis can only be made when the growth is in the rectum or when the tumor is expelled from the bowel. Cancerous obstruction is accompanied by cachectic changes, by the presence of an abdominal or rectal tumor, the passage of blood and mucus, and violent rectal or abdominal pain. Primary cancer in the small intestine appears in the form of lymphoma; it readily ulcerates, and rather widens than narrows the channel of the bowel.[37]

[Footnote 37: Wilks and Moxon, _Path. Anat._, Philada., 1875, p. 417.]

Stricture of the bowel is most commonly found low down in the rectum or sigmoid flexure, within reach of the finger or exploring bougie. If high up, it can only be diagnosed by exclusion and by its slow progression from bad to worse. Syphilis or dysentery has nearly always preceded the development of stricture.

Tumors in the abdomen or pelvis compress the colon, and while they are small they may be overlooked; sooner or later they grow so as to be recognized.

The presence of gall-stones as obstructions may not be detected until they are passed. The previous occurrence of attacks of hepatic colic, followed by jaundice, gives rise to the suspicion that gall-stones are in the intestine if they have been carefully looked for in the stool but never found.[38] Enteroliths give no indication by which they could be known to be in the bowel.

[Footnote 38: In a case seen by the author three separate attacks of typhlitis occurred in a young woman suffering from chronic constipation. After the last attack she passed from the bowel several dark, irregularly-shaped concretions. The largest of these was a gall-stone covered with fecal matter. Since this time--two years ago--there has been no recurrence of inflammation and the constipation is much better.]

All forms of constipation from organic modification of the walls grow worse and have no remissions; some rapidly progress toward a fatal termination. Simple constipation is subject to improvement and relapses due to the character of the food, climate, exercise, etc. The etiology is an important guide.

Stercoral tumors may be known by their position and character as {650} ascertained by physical examinations and by their history. They are found in the iliac, lumbar, or hypochondric regions, and sometimes in other parts of the abdomen. The most common seat is in the sigmoid flexure and descending colon. They are nodulated, movable, painless, can be made to change shape or are indented by pressure, and have a doughy feel. Exploration of the rectum, by detecting impaction, will make the diagnosis clear when the obstruction is low down. The distension of the abdomen above the point of obstruction is limited at first to the region of the colon; but if the colon is much dilated with gas or is displaced, the enlargement becomes more central and more general. On percussion the sound is of a dull tympanitic quality, and never absolutely dull even in cases of great fecal accumulation.[39]

[Footnote 39: Case referred to by Guttmann (_Physical Diagnosis_, Sydenham ed., p. 360), in which the sound was dull tympanitic over two large fecal tumors which weighed when removed at the post-mortem six kilogrammes (sixteen pounds).]

Fecal tumors[40] are preceded by habitual constipation, and are most common in elderly people; they are changed in position and size or made to disappear by cathartics or rectal injections. Persistent treatment will bring away scybalæ which by their color and consistence show that they have long been in the canal. But the free movement of the bowels and the non-disappearance of the tumors are no proof that they are not fecal.

[Footnote 40: _Tumeurs stercorales_, Paris, Thèsis No. 240, 1878.]

Fecal accumulations have been mistaken for ovarian tumors,[41] cancerous tumors of the mesentery, uterine fibroids, and retro-uterine hæmatocele. Fecal tumors in the transverse colon have been taken for enlargement of the liver and spleen. In one instance obstruction of the bowel from fecal impaction was supposed to be a strangulated gut in a patient suffering from hernia: an operation was performed, the patient dying in sixteen hours afterward.[42] Ovarian tumors in their early stages are sometimes thought to be fecal.[43]

[Footnote 41: Jas. Y. Simpson, _Med. Times and Gazette_, London, 1859, vol. ii. p. 549.]

[Footnote 42: Thomas Bryant, _Med. Times and Gazette_, London, vol. i., 1872, p. 303.]

[Footnote 43: J. B. Brown, _Lancet_, London, 1850, vol. ii. p. 48.]

Fecal impaction in the rectum, with ulceration and bloody and mucous stools, may for a time be called cancerous ulceration. Sacculated scybalæ cannot be distinguished from submucous tumors even by the hand pressing on them in the rectum.[44]

[Footnote 44: H. R. Storer, _Gynæcological Journ._, 1869, vol. i. p. 80.]

The history of each individual case, a full knowledge of etiological factors, and a careful physical examination will in most instances lead to a proper diagnosis.

PROGNOSIS.--The result of treatment depends upon the age. Although in infancy constipation is very common, cure is the usual result where a mixed diet begins to be taken in childhood. At from one to fourteen years of age regular movements can usually be secured, unless there is a radical defect in the organization of the child. In young girls at puberty and after, if constipation once is established it is apt to become inveterate, associated as it is with imperfect development and with uterine displacements. In middle life in men the result depends upon the cause and upon attention to the physician's counsel. If intestinal catarrh or atony is the cause, a persistent subordination of the life of the individual to the object in view will generally end in cure. In women who have borne {651} children the hope of relief depends upon the duration of the malady before treatment. It is a dispiriting task to attack a constipation of many years' standing in women with relaxed abdomens, uterine prolapsus or retroversion, and general debility. In old age the causes are generally such as cannot be removed. The bowels can be moved when the occasions demand, but there is very little expectation of establishing a spontaneous habit of regular fecal movements.

At every age and from whatever cause perseverance and hope on the part of the patient and doctor are the chief elements of success. In neglected cases the worst results may happen: dilatation of the colon, ulceration, fecal impaction and obstruction, perforation; or in milder cases chronic indigestion, hypochondria, etc.

TREATMENT.--The physician can render great service by giving to parents advice which will prevent constipation in children. He should insist upon the importance of habits of regularity in defecation. At the period of puberty in young girls this is of even greater moment, and no opportunity should be lost for pointing out the danger of neglect. As a prophylactic measure in adults counsel should be given suited to the occupation. To persons leading sedentary lives the necessity of exercise ought to be made clear. In the trades little can be done, but in the case of literary men and those who read or write for many hours prevention is easier than cure. Daily exercise, walking or riding, frequent bathing with active sponging and friction of the surface, especially over the abdomen, will be of much service. Avoiding constrained positions where pressure is brought to bear upon the abdomen, as in bending forward to write, is quite an important item. Among ignorant people advice of this kind is rarely attended to, but even here the doctrine of regularity should never cease to be preached. Active business-men, especially young men, need emphatic teaching. They cannot plead ignorance for the habitual and persistent neglect of the simplest rules of health of which they are in this country so often guilty. The symptoms of indigestion which are precursors of constipation should receive due attention, and a mode of life and dietary suited to a complete digestion of the food will favor the timely and proper expulsion of waste matter.

Acute constipation in a previously healthy person, lasting for one to three days, does better without interference. No harm attends temporary inaction of the bowel, and if a spontaneous stool takes place at the end of this time it is a sign of a healthful and vigorous condition. After this the normal regularity is restored. The habitual clearing out of the bowel by a purgative pill or dose of mineral water whenever such a state of matters occurs creates the necessity for the interference. The man who never lets himself go over a day without an action is miserable if he misses his purgative and its effects.

In the onset of acute diseases the custom of giving a preliminary purgative is generally unnecessary, often injurious. It disturbs the rest which such cases need; it produces exhaustion in some diseases, as pneumonia, pleurisy, and rheumatism; it irritates the mucous membrane when irritation involves danger, as in intestinal catarrh and typhoid fever.

When it is desirable to empty the bowel in acute constipation a warm-water enema for adults and children is the best means. When a laxative is necessary in case of a failure of the enema, one mild in its operation {652} should be chosen--a compound rhubarb pill, one to five grains of calomel, a teaspoonful of Rochelle salts, or half a bottle to a bottle of the solution of the citrate of magnesia or the tartro-citrate of sodium. For children calomel, in doses of one-third of a grain to one grain, is one of the most certain and least objectionable. One grain of powdered rhubarb can be added to this for a more active effect.

Under such circumstances as a blocking up of the bowel with a mass of partially digested or undigested food, fruit-stones, skins, or other foreign bodies, where the symptoms are violent pain, tympanites, and vomiting, the best method is to give large enemata of warm water through a long rectal tube passed as high up as possible, and to administer calomel in doses of one to three grains, repeated every two to three hours until the bowels are moved. Cold can be applied to the abdomen to diminish tympanites and prevent inflammation. Should the constipation not yield and the pain, vomiting, and tympanites augment, the case will then be considered one of intestinal obstruction, and be treated as such.

When called upon to treat chronic constipation, the physician should remember that it is not the symptom, but its causes, to which he should direct attention. Constipation is so often a symptom, a complication, of other diseased states that its management is a matter of secondary importance. Moreover, its causes are so peculiar to the individual and depend upon so many variable habits of life that each case asks for special study. The cure is only to be found by learning the particular cause--the habit of neglect, hurried eating, the use of aperients, uterine displacement, or any of the many causes enumerated.

The digestion and all that concerns it is of primary importance, and to it attention should be at once directed. The stomach and intestinal digestion should be examined separately, and the relative power to digest different articles of food determined. A diet, then, should be selected, not with a view to correcting the constipation, but as to its suitability to the digestive capacity of the patient. No system of diet can be fixed upon as suited to every case: the aim is to secure normal digestion and absorption and normal peristalsis. Many trials may have to be made before a proper dietary can be chosen. When there is indigestion of fats and malnutrition, with pale offensive stools containing much mucus, an exclusive nitrogenous and easily digestible diet--such as is advised in the article on INTESTINAL INDIGESTION--should be prescribed. In constipation connected with membranous enteritis a similar system of diet is proper. The drugs given should be those which aid intestinal digestion, and reference must be made again to this subject, already treated of. Many cases of constipation can only be cured by this treatment; the routine treatment by purgatives and a diet of vegetables and fruits would aggravate and not relieve. A course of exclusive milk or skim-milk diet, if persevered in for some weeks, will cure cases of constipation of this kind without the use of laxatives. Of course a purgative must sometimes be given if enemata fail, but the least irritating one should be selected.

The mineral waters best suited to constipation depending upon intestinal catarrh are in this country those of the Rockbridge Alum Springs and Capon Springs (Va.), the California Seltzer Springs, and the milder {653} waters of Saratoga. The most suitable from Europe are the waters of Apollinaris, Vichy, Buda, Vals, Ems, Salzbrunn, Selters, Mt. Doré, and Kissengen. The warm baths of Virginia (Warm Springs, Hot Springs) are useful in increasing the activity of the skin and in giving relief to the catarrhal state. A month spent at the Warm Springs, with a daily bath the natural heat of which is 98°, will work a complete transformation in the abdominal circulation. This should be conjoined, of course, with a properly-regulated diet and exercise. Another month spent at the Rockbridge Alum Springs will complete the restoration of the bowel to a normal state. It is much to be regretted that the really valuable mineral springs of Virginia lack so many of the comforts which the invalid requires. In cases where it is more convenient a stay at the Arkansas Hot Springs is to be suggested, and for obstinate cases of intestinal catarrh with sluggish circulation, obesity, and gouty tendencies these springs are to be preferred. A season at some of the mineral baths of Europe, as Aix-la-Chapelle, followed by the strict regimen of the grape cure (as at Bingen, Durkheim, Vevay, Montreux, or Meran), is a rational mode of treatment which offers an almost certain prospect of cure.

If the case is one of atony of the colon due to impaction of the rectum and dilatation of the rectum and colon, without gastric or intestinal indigestion, a quite different regimen is required. The constitution and mode of life are the guides to the general plan to be followed. Sedentary pursuits are to be given up as far as possible. Long vacations and travel must be insisted on, with active exercise by walking and riding; also cold bathing or sponging, with brisk friction of the whole body. Sea-bathing is useful both as an exercise and for the effect upon the sluggish peripheral circulation, but the slothful life at the seashore, with over-indulgence in eating and drinking, is a source of more harm than good. Warm baths, and cold douches to the abdomen, compresses of cold water or of alcohol, the cold douche to the spine while in the hot bath, are all beneficial. Massage for women, children, and feeble persons takes the place of exercise. The kneading of the muscles over the abdomen can be combined advantageously with an effort to accelerate the passage of the contents of the colon by manipulation in the direction of movement.

The interrupted electrical current, used for the purpose of developing the feeble abdominal muscles, is a source of much advantage.[45] But to be of service it should be persevered in for months, the patient himself making the application under the direction of the physician. In addition, the introduction of one insulated electrode into the rectum, while the other is in contact with the abdominal muscles or along the line of the large intestine, has been advised. The Swedish movement cure may be a useful aid in some cases. The movements exercise the muscles of expulsion. These are deep inspiration, flexion and extension of thighs or trunk, twisting the trunk, pressure on the abdomen and colon, stroking in the direction of fecal movement.

[Footnote 45: S. T. Stern, "Die faradische Behandlung der Obstipation und der nervosen Enteropathie," _Centralblatt für Newenheil_, 5 Jahrg., Mai, 1882, p. 201; also, I. Althaus, "Treatment of Obstinate Constipation by Faradization of the Bowel," _Lancet_, London, 1867, ii. 606.]

In the relaxed condition of the abdomen in women who have borne {654} children or in old persons the wearing of an abdominal support sometimes gives help and comfort.

The best diet for cases of atony of the colon and rectum is one which is easily digested and has a moderate amount of waste, as a full colon will stimulate muscular action. Various articles are suggested with a view to excite peristalsis by irritation of the mucous surface, but as such substances are in themselves insoluble and innutritious, it is unwise to resort to them. The following list includes the foods suitable to such cases: Fresh vegetables, as spinach, raw or stewed tomatoes, lettuce, kale, salsify, peas, asparagus, kohlrabi, and other summer vegetables; in winter canned vegetables, if well prepared, take their place. Among fruits, fresh fruit in general, especially grapes, peaches, and oranges; dried fruit, as figs, raisins in small quantity, stewed prunes, and baked or stewed apples, can be tried.

Too much vegetable matter is harmful, as the bowel is filled with an excess of waste, much of which is undigested food; the quantity must be regulated by the appearance of the stools and by the success of the regimen. If the blockade continues obstinately, the vegetable diet should be reduced. The microscope in many cases can alone decide the amount of undigested vegetable matter. Meats are all advisable in moderation. The least digestible, as ham and veal, are to be avoided. Graham-flour bread, brown bread, or bran bread are better than bread made of the best bolted flour. The first is more digestible, and bran bread[46] is thought to increase peristalsis, but this is a doubtful effect. Oatmeal well boiled, fine hominy, corn meal, or cracked wheat with milk are pleasant and digestible. A cup of café au lait at breakfast or before breakfast is the best morning drink;[47] it has a laxative influence. Tea is thought to have the opposite effect. Milk at breakfast answers well for those who take it with relish. An orange on rising in the morning is a pleasant remedy.

[Footnote 46: "The Efficacy of Bran Bread in relieving Despondency ... dependent on an Irregular and Constipated State of the Bowels," _Journ. Ment. Sci._, London, 1858-59, v. 408-411.]

[Footnote 47: "Treatment by Café au Lait," _Gaz. des Médecins prat._, 1840, No. 4, p. 13.]

Certain drugs are called for to aid these measures in giving tone directly or indirectly to the weakened bowel muscles. Strychnia stands first, but it woefully disappoints one who trusts much in the theoretical arguments for its use. In fact, it may be said of all drugs given for constipation that they stand in a very subordinate rank to the measures already discussed. They should be thought of last, not first, and but little confidence should be put in the vaunted value of new drugs. Strychnia can be combined in anæmia and debility with the dried sulphate or carbonate of iron, and with quinia or arsenic,[48] or in feeble digestion with dilute hydrochloric acid and pepsin. Belladonna was advised by Trousseau as a stimulant to unstriped muscular fibre, and it can well be given with strychnia; ipecacuanha and atropia are approved of in conjunction.[49] A pill of ergot, belladonna, and strychnia would answer the indication of a feeble peristalsis. DaCosta has suggested giving one drop {655} of the fluid extract of belladonna with compound tincture of gentian or cinchona three times daily after meals. The sulphate or valerianate of zinc, oxide of zinc, extract of valerian or gentian, capsicum, or black pepper can be tried in pill form with belladonna and strychnia.

[Footnote 48: Bartholow thinks arsenic overcomes constipation when due to deficient secretion and dryness of the feces (_Mat. Med._, New York, 1879, p. 129).]

[Footnote 49: Legros and Onimus, _Journal de l'Anat. et de la Phys._, t. vi. pp. 37 et 163. Ringer says one grain of ipecacuanha taken while fasting each morning will relieve constipation from torpor (_Therapeutics_, New York, 1882, p. 438).]

These remedies are slow-acting, and in the mean while the bowels must be moved artificially, methodically, and taught to act at stated hours. For this purpose a small enema of cool or cold water at the same hour every day after breakfast does well. It is irrational to distend the bowel, already weakened by distension, with large enemata of warm water. Recourse should not be had to this until all hopes of effecting a cure are gone, or only as an occasional remedy in impacted accumulations where the mass must be softened before it can be removed. If the enema does not in time empty the colon sufficiently, laxatives will have to be taken with some regularity until the habit is created. A tumblerful of water with or without a teaspoonful of salt, or a tumblerful of any alkaline water charged with carbonic acid, taken on rising in the morning, may prove effective. A tablespoonful of sweet oil at night acts well as a lubricator and softens the feces. If these more simple means fail, it becomes unfortunately necessary to give a purgative drug: any one of this class can be combined with strychnia, belladonna, vegetable tonics, and iron. Those to be preferred are aloes, colocynth,[50] and podophyllin. The compound podophyllin pill or a pill of one-sixth of a grain of belladonna and podophyllin at night or three times daily, the pill of aloes and myrrh, or the Lady Webster pill, are well-approved forms of administration. A compound rhubarb pill acts well if taken after dinner.

[Footnote 50: A few drops of the Prussian tincture of colocynth several times daily is advised by Ringer (_Therapeutics_, New York, 1882, p. 642).]

If one desires to select a purgative which will probably increase the outflow of bile, selection can be made from the following drugs: podophyllin, aloes, rhubarb, colchicum, euonymin, colocynth, calomel, jalap, sodium sulphate, potassium sulphate, cream of tartar; and among the rarer alkaloids iridin, sanguinarin, physostigma, and juglandin. These, according to Rutherford, Vignal, and Dodds, increase the secretion of bile in fasting animals. Ox-gall and pig-gall are laxatives only; they have no effect on the liver, but can be added to other purgatives in pill forms.

Salines largely diluted may be given to strong adults: Epsom or Rochelle salts quite early in the morning, a solution of sulphate of magnesia with dilute sulphuric acid, to which dried sulphate of iron may be added, are quite popular; and of the bitter waters, Hunyadi Jânos, Friedrichshall, or Pullna water serves the purpose. One grain of sulphate of quinia added to a saline will increase its effect. The milder laxative waters are to be preferred to the bitter waters. The Saratoga waters, Congress, Geyser, Hathorn, answer the purpose taken early in the morning, or among the European springs those of Kissengen, Plombières, Marienbad, Homburg, Seltzer, or Leamington in England, are not too active in their effects. In atonic constipation, the form now under consideration, the laxative chalybeate waters are indicated where there is anæmia or debility. These are represented by the Columbian, Pavilion, Eureka, and Excelsior Rock among the Saratoga waters, and by the Bedford Springs water.

{656} It is well to administer a number of drugs in rotation in habitual constipation, as the susceptibility to a particular drug is lost after continued use. Increase of the dose is the usual method to offset this result, but it is irrational to meet exhaustion by over-stimulation. Rest of the part stimulated by using a remedy which brings about the result in a different way is the wiser course. The dose should be gradually reduced, tempting the bowel to act more and more without aid. Among the laxatives which can be borne in mind in alternating treatment the following list includes some which can be used with advantage: the fluid extracts of rhamnus (buckthorn) and cascara sagrada; alum, which is called for in certain forms of atony; sulphur in the form of confection or sulphur with guaiacum[51] (half a drachm of each in powder at night); the wine of colchicum (five drops or more three times daily), advantageously used in gouty or rheumatic persons; the infusion or tincture of euonymus; the tincture of benzoin; senna in fluid extract and in the compound powder of liquorice.

[Footnote 51: Fuller, _Lancet_, London, April 23, 1864, p. 459.]

Infants and children should be cured of constipation without purgatives if possible. Attention to the diet of the infant, and close inspection of the stools to see the effect of the food given, will guide to a proper system of feeding. Breast-milk is the best remedy; next, a food which most nearly resembles mother's milk--cow's milk properly diluted with barley-water, oatmeal-water, or rice-water--stands first. Condensed milk, given in barley- or oatmeal-water, is a second and excellent substitute in cities. Antacids prevent a too rapid coagulation of the casein and the formation of curdy lumps. Lime-water with milk or bicarbonate of potassium or of sodium may be administered with the food or before it. The quantity of food must be lessened until the child can digest all it takes.

The infant should be taught to empty the bowel at the same hour daily by always placing it at this hour in a position favorable to and suggestive of defecation. Dilating the sphincter at the same time with the soap suppository or the small end of a Davidson's syringe, or just touching the margins of the anus, will excite the necessary reflex movement. If defecation is painful, examine the inner edge of the anus for small cracks or for eczema ani.[52] Over-stretching the sphincter with the finger in cases of rigid or spasmodic contractions will sometimes produce permanent relief.

[Footnote 52: Betz, "Eczematous Proctitis," _Memorabilien_, iv., Dec. 28, 1859, S. 190.]

In children the question of diet is equally important. Most cases of constipation in them originate in intestinal catarrh from improper diet and over-feeding. Strict rules of diet should be rigidly enforced, and each case receive special study in order to determine upon the best dietary. The minutest details of the child's life, its habits and surroundings, are to be controlled so as to secure the best possible influences for health. Feeble development and muscular inertia must be remedied by change of climate and tonics--iron, strychnia, and cod-liver oil. When other methods fail to give early relief, a purgative may be needed. Rhubarb, magnesia, calomel, Friedrichshall or Hunyadi water, given in milk, the compound liquorice powder, the compound anise {657} powder, are better than the more active cathartics.[53] Habitual administration of laxatives to children ought to be regarded as a confession that the case is incurable; it is a last resort, for which necessity is the only argument.

[Footnote 53: The compound anise powder, a non-officinal preparation in use in Washington, is a convenient form of administration: heavy calcined magnesia, 360 grs.; rhubarb powdered, 180 grs.; oil of anise, 40 minims; stronger alcohol, one fluidrachm. The bicarbonate or fluid magnesia is also a good preparation. Ringer knows nothing so effectual in bringing back the proper consistence and yellow color to the motions of children as podophyllin. Dissolve one grain of the resin in one drachm of alcohol, and of this give one or two drops on a lump of sugar twice or three times a day (_op. cit._, p. 458). Bouchut suggests the same solution, with simple syrup as a menstruum.]

In old persons tonics should be combined with the laxatives, as strychnia, iron, quinia, gentian with aloes, colocynth, rhubarb, or podophyllin. The rectum should always be examined, as impacted fecal masses will often be found there.

{658}

ENTERALGIA (INTESTINAL COLIC).

BY W. W. JOHNSTON, M.D.

SYNONYMS.--Enterodynia, Tormina, Colicodynia, Colalgia, Dolor colicus, Passio colica, Spasmus intestinorum, Ileus spasmodicus, Spasmus ventriculi, Neuralgia mesenterica; Spasm of the bowels, Cholick or Cholick Colic, and Pain in the Belly; _Ger._, Das Banchgrimmem, Die Kolik; _Fr._, La colique.

HISTORY.--Colic is described by Hippocrates.[1] He recommended the use of emetics and gave other sound advice regarding the treatment of the affection. Galen[2] administered sedatives, as opium and henbane, and he advised them to be combined with carminatives. Aretæus[3] speaks of the pain of colic extending to the back, limbs, and testicles, and also states that when affecting the sides of the body it may be confounded with pleurisy, hepatitis, or splenitis. Alexander[4] points out the differential diagnosis of the disease and directs a proper course of treatment. Cupping, friction of the extremities, and dry fomentations were recommended by Celsus;[5] and internally he advocated a mixture of poppy, anise, pepper, etc. Aëtius[6] describes the affection. Serapion[7] and Avicenna[8] treated of colic more clearly than any previous writers had done, and advised narcotics administered by the mouth and rectum. Atony of the bowels is given as a cause of the disease by Haly Abbas,[9] and Alsaharavius adds[10] to the etiology a hot intemperament, indurated feces, and poisonous medicines. Rhazes[11] directs the administration of emetics when the colic is due to indigestion.

[Footnote 1: _De Affect._, xv.]

[Footnote 2: _De Med. Sec._, loc. ix.; iv., de loc. _Affect._, vi. 2.]

[Footnote 3: _Morb. Acut._, ii. 6; _Chron._, ii. 8.]

[Footnote 4: Lib. x. 1.]

[Footnote 5: _Medicina_, Libri octo, iv. 14.]

[Footnote 6: Lib. iii. 1, 29.]

[Footnote 7: iii. 32.]

[Footnote 8: iii. 16, 4.]

[Footnote 9: _Pract._, vii. 28.]

[Footnote 10: _Ibid._, xvii. 2, 12.]

[Footnote 11: Divis. 69.]

NATURE AND DEFINITION.--Enteralgia is the name given to intestinal pain which is independent of indigestion and of inflammation or other organic change in the wall of the bowel, and corresponds to gastralgia and other visceral neuralgias. It involves the nerves which pass to the intestine along the line of attachment of the mesentery, and which are derived from the superior mesenteric plexus, with a prolongation from the junction of the right pneumogastric nerve with the coeliac plexus.[12]

[Footnote 12: The very extensive distribution of terminal nerve-filaments in the intestine is an explanation of the frequency and severity of attacks of intestinal pain. "We may form some estimate of the extent to which the nervous system of the intestines is developed from the fact that about one hundred ganglia belonging to the submucous and over two thousand to the myenteric plexus are to be found in one square inch of the intestine of the rabbit" (Frey, _Histology_, New York, 1875, p. 493).]

{659} The pain of enteralgia is not spasmodic, and is not accompanied by flatulence, borborygmi, or other signs of indigestion and gaseous distension of the bowels.

Colic, on the other hand, applies to intestinal pain accompanied by indigestion, distension of the bowel with gas, or the contact of irritating ingesta. The pain is spasmodic, and is relieved by the passage of gas and other contents from the bowel. The pain is due to the local irritation of the richly-gangliated plexus of nerves seated in the submucous layer and which extends from the pylorus to the anus.

At present enteralgia must be considered from its symptoms and from post-mortem examinations as a pure neurosis of the sympathetic system. Opportunities are rarely offered for studying the post-mortem appearances of the disease, from the fact that when idiopathic it seldom ends fatally. Out of forty-nine autopsies on patients who had suffered from colic due to lead-poisoning, only one was found with any change of the abdominal ganglia of the sympathetic. Ségoud found the ganglia and some of the fibres of the sympathetic hypertrophied and indurated,[13] and "in recent times Kussmaul and Maier have published an example of sclerosis of the coeliac and superior cervical ganglia."[14]

[Footnote 13: Ségoud, _Essai sur la Névralgie du Grand Sympathique_, Paris, 1837.]

[Footnote 14: M. Rosenthal, "Diseases of the Nervous System," _Wood's Library_, New York, 1879, vol. ii. p. 265.]

The pathology of enteralgia due to a vitiated state of the system, a morbid condition of the tissues of the intestines, the presence of irritating ingesta, or to reflexion from other organs, differs in no wise from a neuralgia of other parts arising from constitutional, local, or reflex causes. Pain will likewise manifest itself here in consequence of deleterious substances circulating in the blood, as in Bright's disease, rheumatism, gout, or lead-poisoning. The terminal nerve-fibres of the intestines are irritated in attacks of colic by substances or food within the alimentary canal; gases are generated from the decomposition of the ingesta. The consequent dilatation of the gut produces loss of tone and abolition of the contractile power of the muscular coat. Constipation and pain from pressure exercised on the neighboring nerves will be the result.

Obstinate constipation, and even symptoms resembling ileus, may arise from a portion of the intestine thus distended becoming bent upon itself, the sharp angular flexure interrupting or completely obstructing the passage of the feces.[15]

[Footnote 15: F. H. Hamilton, _Med. Gaz._, New York, 1880, vii. p. 3.]

ETIOLOGY.--Enteralgia may be either idiopathic or symptomatic. The causes can best be considered by dividing them into general and reflex.

Under the head of general causes may be mentioned an inherited neurotic temperament, particularly in individuals of a hypochondriacal tendency. Females are far more apt to suffer from this affection than males, on account of their more impressionable nature and greater liability to nervous diseases in general. Hereditary tendencies, overtaxing the mental powers during the developmental period of youth, and later in life excessive mental labor and anxiety of business affairs, are causes. It may occur in the cachexia developed during the course of many chronic diseases, as diarrhoea, rheumatism, gout, phthisis, cancer, Bright's disease, etc. Various morbid conditions of the blood are followed by {660} enteralgia, as anæmia arising from prolonged lactation, masturbation, or venereal excesses, and the presence of various blood-poisons, as syphilis, malaria, lead, copper, and arsenic. Other causes are living in cold, damp climates, with sudden changes of temperature and chilling of the body. Persons addicted to the use of tobacco or alcohol and to dissipations of various kinds may become predisposed to enteralgia. Idiosyncrasy is a predisposing cause.

Enteralgia is often secondary to ovarian, uterine, or other distant disease. Also, owing to intimate sympathetic relations, pain is often felt in the bowels as a result of disease situated in some of the solid abdominal viscera, as the liver, spleen, and pancreas. In the same way, organic affections of the brain and spinal cord, especially acute myelitis and spinal sclerosis and lesions of the vertebral bones, excite intestinal pain. Emotion may also bring it about. The application of cold to the feet or catching cold in general is followed by pain which is due to reflex influence.

There may be a predisposition to colic from hereditary influence and the neurotic temperament. A feeble digestion is a source of constant risk. Much of the pain occurring in the course of dysentery, catarrh of the bowel, invagination, fecal impaction, and other structural affections is of the nature of colic. The most frequent by far of the local causes is the direct irritation of the terminal nerve-fibrils by substances within the alimentary canal and by over-distension of the bowel with contained gas. Some of these irritants are partly-digested and indigestible articles of food; food taken cold or in excessive quantity; the decomposition of food and consequent distension of the bowel by gas. Acid drinks and alcohol have the same effect. Constipation with scybalæ may produce colic in an otherwise healthy person. A morbid state of the intestinal secretions, either as regards quantity or quality, is said to have a like result, but this is a doubtful cause. Foreign bodies within the canal, as fruit-stones, various concretions, worms, and gall-stones if of large size, may produce pain during their passage through the bowel. Cathartic medicines may be enumerated as among the local causes, and also various poisonous drugs. Lesions of any sort seated in the intestinal wall, as ulcers and neoplasms, induce paroxysmal pains.

SYMPTOMS.--The pain of enteralgia occurs in attacks which come on slowly and continue for a variable time--some hours or days. The pain is situated about the umbilicus, and is relieved by deep pressure, although at the same time there may be hyperæsthesia of the skin. The intensity of suffering ranges from a dull heavy pain to one which is acute and lancinating. Retraction of the abdomen is common, but there may be tympanites. No signs of indigestion may appear, but eructations of tasteless gas, or even borborygmi, may be complained of.

The duration of an attack of enteralgia is variable and depends to a great extent upon the cause. Usually, when the symptoms are severe, the duration is short. It may pass off in less than an hour, or a succession of paroxysms continue to recur, and the attack will be kept up for several days, weeks, or even a month. One seizure predisposes to another, and each is liable to be more severe than its predecessor.

The malady may end gradually or as rapidly as it was ushered in. Attacks are often mitigated, or even terminated, by the occurrence of some other morbid condition--by a profuse sweat, the discharge of lochia, {661} the menses, or some secretion which has been checked. The development of rheumatism or gout may relieve it. Attacks often terminate with vomiting, belching, and more especially with movements of the bowels and discharge of flatus. A free emission of pale, colorless urine is sometimes followed by relief. This occurs in hysterical cases, and the disease is generally accompanied with some uterine disorder and with tenderness along the spine.

The attack of intestinal colic may be developed suddenly and with full intensity, or it may be preceded a short time, usually a few hours, and rarely much longer, by prodromic symptoms. These are nausea, a sensation of weight in the epigastrium, anorexia, eructations, tympanites, rumbling, and slight griping pains. The patient is irritable and restless, his bowels are usually confined, and urination is often rendered painful by the distended bowels pressing upon the bladder.

These symptoms, which are in truth but a part of the attack, being only of a lower grade, increase in severity and the pain becomes more acute and distinctly paroxysmal. It is of a sharp cutting, twisting, or most frequently griping character, and is in the earlier part of the attack usually referred to the umbilicus or to one of the iliac fossæ, and sometimes radiating thence in different directions. Generally it becomes concentrated about the umbilicus. The exacerbations of pain vary in degree of severity, in duration, and in frequency of recurrence, while the intervals may afford complete relief or merely a remission of the acute suffering. The sufferer either lies quietly upon his abdomen or upon one side or the other, with his body bent forward and thighs flexed, or he is restless and writhes in pain, groaning and crying out from the intensity of suffering. He may seek relief by trying a variety of positions and by pressure applied with the hands or some solid object against the abdomen. Anxiety and pain are depicted in his features. His face and extremities are cool and covered with a clammy sweat. The pulse is small, hard, and generally slower than normal. Breathing is sometimes oppressed, as a result of spasmodic contraction of the abdominal and thoracic muscles. Often the muscles of the hands, calves of the legs, and the feet are similarly affected. The tongue is moist and as a rule clean. The bowels are constipated--at times so much so as to amount to obstruction--or, again, diarrhoea and tenesmus may be present.

Other abdominal symptoms are nausea or vomiting, eructation of gas, and borborygmi. Micturition is at times urgent and painful, and the testicles are frequently retracted.

The abdomen is occasionally tender, but pressure generally affords relief. It is distended with gas, especially over the large bowel. Palpation often reveals lumps or knots situated within the abdominal walls and due to spasmodic contraction of its muscles, particularly of the recti. In thin persons the constricted and dilated coils of the intestines can also be distinguished as nodular masses which rapidly alter in shape and position.

The severity of attacks of colic varies from a few slight griping pains felt at intervals to a seizure of such intensity that the patient suffers agony and presents symptoms of an alarming nature. Fortunately, these grave cases are comparatively seldom observed. In them the local and general symptoms are aggravated. Pain is more intense and {662} constant, having less marked intervals of relief, and the patient may pass into collapse, with a small, rapid, and wavering pulse, restricted respiration, shivering and chilliness, and a cool, clammy skin. The abdomen is greatly distended; hiccough comes on, also stercoraceous vomiting, tenesmus, and in the worst cases involuntary stools and suppression of urine. Nervous symptoms have been observed, as dizziness or fainting, and finally delirium and convulsions may end the scene.

VARIETIES.--Attention has been called to a distinct form of enteralgia due to the effects of alcohol.[16] It affects steady drinkers, and is, as a rule, met with only during the hot months. The presence of undigested food within the alimentary canal or exposure to cold may act as exciting causes of the disease. The development is usually gradual. Dull pains, felt at first over the abdomen, become later more continuous and fixed about the epigastrium or umbilicus. Sometimes they are complained of more over the bladder. Bilious vomiting and hiccough are prominent symptoms; the patient is thirsty, and the liquids taken only promote vomiting; and the bowels are constipated. There is restlessness, and sleep is obtained with difficulty. Paralysis at times supervenes, and affects the lower as well as upper extremities. In the worst cases delirium and even convulsions occur. The disease nearly always ends in recovery in from three to ten days. Severe intestinal and gastric pain occurs in opium-eaters, but especially in women who use morphia in excess. The suffering is always greater when the opiate is reduced, but can only be cured by breaking up the bad habit.

[Footnote 16: Colica bacchanalium, J. H. Claiborne, _Med. Monthly_, New York, 1855, p. 227.]

A variety of colic which occurs epidemically[17] in some of the inter-tropical countries has been studied and described by different observers. It is known by various names, such as colique sèche; colique végétale; rachialgie végétal; colic of Poitou, of Devonshire, of Madrid, of Java, of Surinam; colique nérveuse; endémique des Pays Chauds (Fonssagrives); endemic colic, dry colic, bilious colic, nervous colic; girafy; dandy, etc. Ségoud called it a neurosis of the great sympathetic, and attributed the disease to the effect of cold.[18] The symptoms resemble, in many respects, those of lead colic, and at one time they were erroneously considered identical with it.[19] Thompson and Chisholm,[20] after an {663} experience with the disease in the West Indies, assert that such is not the case. Epidemics which occurred in Madrid and several of the Spanish provinces, and many hundred cases witnessed among the French soldiers by other observers, were ascertained not to be due to lead-poisoning.

[Footnote 17: Colique végétale, or endemic and epidemic colic, did not escape the notice of the older writers. It is mentioned by Aretæus; Paulus Ægineta describes an epidemic of the disease which extended through Italy and a large part of the Roman empire, and he states that attacks were often followed by paralysis. François Citois gives an account of an epidemic which raged at Poitou in 1616. Monson Smith described the disease in 1717. In 1724 it appeared in Devonshire, England, and presented the characteristic symptoms and sequelæ. In more recent times epidemics of the disease have occurred in nearly all the countries of Europe. It prevailed in the northern part of France and in Belgium from 1853 to 1859, inclusive. It has likewise visited the Caribbee Isles, Cayenne, Guadaloupe, Madagascar, India, the West Indies, some of the provinces of Spain, Java, the west coast of Africa, the Antilles, Senegal, New Zealand, Brazil, and various other localities. The disease occurs in all seasons, but is more prevalent in summer and in the commencement of autumn.]

[Footnote 18: Ségoud, _Essai sur la Névralgie du Grand Sympathique_, Paris, 1837.]

[Footnote 19: The disease frequently appeared on board of French war-vessels, and was regarded by Lefèvre (_Recherches sur les Causes de la Colique sèche_) as due to lead-poisoning. He asserts that lead is more used in French ships than in those of other nations, and accounts for its being epidemic in tropical countries because a warm climate aids in developing the affection, and because there men drink more freely of water. (See also Dutrouleau, _Arch. gén._, 1855, "Mal des Européens dans les Pays Chauds.")]

[Footnote 20: Quoted by Oppolzer, _Wien. med. Woch._, Bd. xvi., 1867, p. 724.]

The affection is not accompanied with any constant lesion. Pascal[21] made post-mortem examinations in six cases and found the mucous membrane of the duodenum a little reddened: the gall-bladder contained thick bile, and in a few cases there was congestion of the sympathetic ganglia. The attack is usually marked by certain prodromic symptoms. The patient complains of malaise, loss of appetite, a load in the epigastrium, embarras gastrique, dull pains in the colon, borborygmi, and cramps or tingling in the limbs. For the first few days the bowels generally move several times daily. The stools are difficult, painful, and of a black or dark-green color, offensive odor, and accompanied with the discharge of flatus. As the disease progresses the bowels become constipated and the discharge of gas ceases. After a few days the pain is more severe and radiates to the lumbar region, the testicles, or the thighs. It is seated principally in the epigastrium, in the line of the transverse colon, or it may involve the whole abdomen. Movement aggravates the pain, while pressure often relieves it. The tongue is large, trembling, and coated white or yellow; the breath is fetid, the saliva viscid, and mouth sticky. Anorexia is complete; there are hiccough, nausea, vomiting of undigested food and mucous or bilious matters, and constipation with hard black stools. The patient is restless and sleepless. The abdomen may be distended or retracted, and micturition is often painful and the urine high-colored. The pulse is generally slower than in health, but becomes accelerated when the attack is over. The skin is pale, the conjunctiva often stained with bile, and in the later stages oedema of the lids and emaciation come on. The effect upon the nervous system may manifest itself by amaurosis, deafness, delirium, mania, coma, epileptiform convulsions, or paralysis. The paralysis affects the extensors of the hand, arm, and leg, or it may become general and end in death.

[Footnote 21: "Recherches anatomico-pathologique sur la Colique dite de Madrid," _Rec. de Mém. de Méd. mil._, Paris, 1826, xix. pp. 98-113.]

The duration of the disease is from eight to fifteen days, but in some cases it becomes chronic. Relapses frequently occur. At times intermittent or remittent symptoms develop, and occasionally the affection is complicated with enteritis or peritonitis. The prognosis depends very much upon the character of the epidemic, and the most serious cases are those accompanied with either cerebral symptoms or peritonitis.

The paralysis sometimes passes off in a few days, but oftener lasts indefinitely. Emetics, purgatives, and anodynes are recommended in the treatment of the disease, and frequently a change of climate is necessary in order to recover fully from the affection.

DIAGNOSIS.--The diagnosis of enteralgia usually presents some difficulty even when the symptoms are well marked. That the disease is a true neuralgia is apparent from the periodical recurrence of the pain, its sharp and darting character, from the sudden cessation followed by complete relief, and from the absence of symptoms of indigestion. Affections bearing a certain resemblance to enteralgia are to be excluded.

In lumbo-abdominal neuralgia the pain is unilateral and extends around {664} to the back. Tender spots can usually be detected by pressure on the umbilical or hypogastric regions or on the spinous processes of the vertebræ. In dermalgia the soreness is superficial, and light pressure gives more pain than deep compression, while nervous and hysterical symptoms are constantly associated with this form. Gastralgia is more frequent than enteralgia, and the pain is located about the ensiform cartilage. In myalgia of the abdominal parietes pressure causes pain, as do also movements of the body, coughing, sneezing, etc. Rheumatic pains would likely be felt in other muscles. In ileus the pain is more continuous, the tenderness localized; there is constipation of a most obstinate character, and vomiting of stercoraceous matter. The patient has an anxious expression and a rapid, feeble pulse. In renal calculus the pain is situated in the course of the ureter and shoots down to the pubes and thighs. There is frequent desire to urinate, accompanied by a scanty discharge of urine, and a copious flow of urine is followed by cessation of pain. The maximum of pain in hepatic colic is situated in the right hypochondrium, and is often reflected into the shoulder of the same side. Icterus may also be expected. Colic arising from lead-poisoning is usually associated with sufficiently characteristic symptoms to render the diagnosis easy. When syphilitic the pain is apt to be most severe at night.

In catarrh of the bowel the skin is hot and dry, the pulse accelerated, and other indications of a symptomatic fever are presented. The pain is more constant, more localized, and pressure causes it to be increased. Tenderness on pressure is not invariably met with, but the rule holds good that when deep pressure increases the pain inflammation rather than enteralgia is indicated.

If colic is due to indigestible food, a sensation of weight will be complained of at the epigastrium, griping pains occur at short intervals, with flatulence, vomiting, and later diarrhoea. If the attack be wind colic, the abdomen is enlarged by tympanitic distension; borborygmi and belching occur. If it is the result of accumulation of feces, there would be a previous history of constipation, and the lump of feculent matter can be located by palpation and percussion.

PROGNOSIS.--The prognosis of idiopathic enteralgia is favorable, the disease generally terminating after a variable period. Attacks are very apt to recur, and each one will, in all probability, prove more severe than the preceding. In symptomatic enteralgia the prognosis will depend upon the nature of the fundamental disease.

Colic terminates favorably in nearly every case. Death has rarely occurred from complications, as convulsions, and rupture of the bowel has been observed from great distension.

TREATMENT.--If attacks of enteralgia are associated with hysterical symptoms, it would be proper to employ antispasmodic sedatives. The compound spirit of ether is very useful in these cases, especially if they are accompanied with flatulence. Rubbing the spine with stimulating or anodyne liniments frequently promises well. The hypodermic dose of morphia gives relief more quickly than can be got in any other way, but in pure enteralgia with frequently recurring paroxysms care must be taken not to create the demand for the remedy by giving it often. The radical cure of the disease is a more important matter than the treatment of the acute attacks.

{665} If the cause of enteralgia be located in some of the solid viscera or in the nervous system, remedies should be addressed to these parts, and the reflex nervous impressions allayed by the bromides or other nervous sedatives. The valerianate of zinc in doses of one grain three or four times a day is extremely useful in neuralgia from reflex irritation of the female pelvic organs. Constitutional remedies are indicated in the cases due to a morbid condition of the blood--iodide of potassium and mercury if a syphilitic poison or if of a rheumatic or plumbic origin; colchicum if gouty; quinia if malarial; and iron when an anæmic state is presented. H. C. Wood states that alum is used with success; being of service when there is no lead in the primæ viæ, it must act in some other way than as a chemical antidote. Arsenic is very highly recommended in idiopathic enteralgia. Excellent results have been reported from the use of nitrate of silver,[22] hydrocyanic acid, belladonna,[23] and iodoform. Change of climate and travel may have to be resorted to in obstinate cases.

[Footnote 22: Nauman, _Deutsche Klinik_, Bd. iii., 1851, p. 388.]

[Footnote 23: _Lancet_, vol. i., 1867, p. 81.]

The objects of treatment in colic are to relieve suffering and terminate the attack as soon as possible. For this purpose the various anodyne and antispasmodic remedies, as opium, hyoscyamus, chloral, ether, chloroform, Indian hemp, and camphor, may be employed. Carminatives are most useful, alone or combined with anodynes and cathartics. Oleum cajuputi often affords immediate relief. Warm teas of chamomile, ginger, valerian, or peppermint sometimes do good. When the suffering is very acute nothing acts so promptly as a hypodermic injection of morphia, either alone or combined with atropia.

The surface of the body should be kept warm, and hot applications to the abdomen assist in relieving pain. The heat may be conveniently applied by means of poultices, hot salt- or sand-bags, or rubber bottles filled with hot water. Cold,[24] used externally, is more grateful in some cases, and is preferable if there be much tympanites. Sinapisms, turpentine stupes, and stimulating and rubefacient liniments answer well in some cases, and should be tried. Anodyne applications to the spine occasionally do good, and cold, applied by means of the spinal ice-bag, is recommended by Ringer.

[Footnote 24: Roux, _Journal de Médecine_, Paris, 1765, p. 48.]

In order to treat the disease successfully and bring the attack to an end, its cause should be ascertained if possible, and remedies directed to its removal. If it be the result of indigestion, the contents of the stomach should be removed by emetics. Drastic or powerful cathartics will only tend to aggravate the disease, and on that account mild laxatives are to be preferred in all cases. Castor oil, calomel, pil. rhei comp., senna, etc. may very properly be prescribed.

In flatulent colic means should be directed to expel the gas. Anodynes--preferably chloroform--and carminatives should be administered by the mouth, and enemata containing turpentine or asafoetida injected into the rectum. In severe cases a clyster with ten or fifteen drops of liquor ammoniæ is said to do good. If distension of the bowel be so great as to threaten rupture, it may with propriety and safety be relieved by puncturing the colon with an exploring-needle or a fine trocar. In cases of flatulent colic where the gas arises from the decomposition of food {666} remedies to check fermentation, such as alkalies, creasote, carbolic acid, or the sulphites, would be indicated. Good sometimes results from pressure and massage of the abdomen. Rubbing with etherized oils and electricity have also been used successfully. If the attack be from fecal impaction, it may be possible to liquefy and remove the mass by using saline cathartics, as sulphate of magnesium, aided by large oily or mucilaginous clysters, which in obstinate cases should be injected through a flexible rubber tube passed up the rectum as far as possible. Injections of an infusion of tobacco are now seldom used for this purpose, on account of the dangerous symptoms which often supervene. If pain or tenderness be present at the seat of impaction, cathartics should be used very cautiously or not at all, and opium given instead. The administration of this drug, by relieving pain and allaying spasmodic action, is often followed by free catharsis.

Persons subject to attacks of colic may diminish the intensity, or even prevent the recurrence, of the disease by employing during the intervals such remedies as would be indicated in their individual cases. Phosphate of sodium has been highly recommended for preventing the recurrence of attacks of colic. R. N. Taylor states[25] that his experience with the use of the drug is quite extensive, and he found the treatment uniformly successful. Thirty grains dissolved in a glassful of water may be taken three times a day--preferably before meals--and this quantity should be reduced if it causes any irritation of the stomach. The bowels should be regulated and strict attention given to diet. A milk diet is of course best in obstinate cases. Any article of food known to disagree must be excluded, and tea, coffee, and alcoholic drinks should also be prohibited.

[Footnote 25: _Med. Herald_, Louisville, 1880-81, ii. p. 348.]

{667}

ACUTE INTESTINAL CATARRH (DUODENITIS, JEJUNITIS, ILEITIS, COLITIS, PROCTITIS).

BY W. W. JOHNSTON, M.D.

SYNONYMS.--Enteritis, Catarrhal enteritis, Mucous enteritis, Endo-enteritis, Ileo-colitis, Entero-colitis, Diarrhoea. Older synonyms: Chordapsus, Cauma enteritis, Enterophlogia, Enterophlogosis, Colica acuta seu inflammatoria, Ileus inflammatorius, Enteralgia inflammatoria, Febris intestinorum seu Iliaca inflammatoria, Colique inflammatoire.

HISTORY.--It is interesting to start at the fountain-head of the two streams of inquiry--the clinical and the anatomical--and to follow each in its widely-diverging wanderings until they unite to give to the phenomena of intestinal inflammation a just interpretation.

The symptom diarrhoea was fully described by the earliest writers in medicine.[1] The symptomatic differences between diarrhoea, dysentery, and lientery and the different forms of diarrhoea (bilious, watery, etc.) were given in detail by the Greek and Roman physicians. The Arabians had a much more elaborate classification of the fluxes. Avicenna made seven varieties of simple diarrhoea. European writers followed closely in these footsteps. Sennert made twelve and Sauvages twenty-one varieties of diarrhoea, depending upon as many different causes, as undigested food, worms, the bile, etc. Many recent writers have adhered closely to the older authors in their method of treating of diarrhoea, regarding it as a disease and dividing it into varieties based on the causes or on the appearances of the stools. Among them may be mentioned Cullen (1789), Good (1825), Tweedie (1841), G. B. Wood (1852), Trousseau (1865), and Habershon (1879).

[Footnote 1: J. J. Woodward, _Med. and Surg. Hist. of the War_, Part 2, Medical Volume, foot-note, p. 273 _et seq._]

It was only after many years of laborious investigation that the appropriate lesion was affixed to a symptom so well understood and described in its clinical aspects. The first conception of abdominal and intestinal inflammation had no relation to diarrhoea. Under the name [Greek: eileos], Hippocrates described abdominal symptoms of intestinal obstruction and inflammation. For Sennert (1641) inflammation of the intestines meant peritonitis. Bonet (1679), Hoffman (1710), and Boerhaave (1758) included under this head peritonitis, ileus, and all febrile and painful abdominal affections. Sauvages (1763) and Morgagni (1779) gave in detail the symptoms of peritonitis and called the disease intestinal inflammation--enteritis. In 1784, Cullen made an advance in subdividing {668} enteritis into e. phlegmonodoea and e. erythematica--the one involving the entire wall of the intestine and the peritoneum, the other the mucous membrane lining the intestine. John Hunter (1794) first fixed the place of peritonitis as a distinct affection from inflammation of the mucous membrane of the intestines.[2]

[Footnote 2: J. Hunter, _A Treatise on the Blood, Inflammation, and Gun-shot Wounds_, London, 1794, p. 284.]

Up to this time constipation was the chief symptom of enteritis. The meeting of the streams, the affixing the symptom diarrhoea to its appropriate lesion, was brought about hypothetically at first by J. Carmichael Smith in these words: "I think it is probable (for we can have no positive evidence of the fact) that in diarrhoeas from catching cold the villous or interior coat of the stomach is sometimes slightly inflamed."[3]

[Footnote 3: Paper read Jan. 8, 1788, _Med. Communications_, London, vol. ii., 1790, p. 168.]

On the Continent enteritis soon after this was limited in its meaning by Pinel (1798) to inflammation of the mucous membrane of any part of the intestines. He gave the name catarrhal diarrhoea to the same condition. A still further restriction of its meaning was made by Broussais (1821), who defined enteritis to be an inflammation of the mucous membrane of the small intestine; he gave the name colitis to the same disease in the colon. This distinction was adopted by Rostan (1826), Andral (1836), C. H. Fuchs (1846), G. B. Wood (1852), Wunderlich (1856), Grisolle (1865), Flint (1866), and Aitkin (1868). According to the views of some authors, chiefly English, as Copland (1844), Bristowe (1871), Roberts (1874), Habershon (1879), enteritis includes inflammation of the serous as well as of the mucous coat of the intestines.

Niemeyer (1864), Jaccoud (1869), Leube (1875), Bartholow (1880), and most German and French authors prefer the name intestinal catarrh as applied to inflammation of the mucous coat; inflammation of the serous coat is peritonitis; the word enteritis is abandoned as involving a pathological error.

NATURE AND CLASSIFICATION.--Catarrh of the intestines is an inflammation of the mucous membrane of the intestinal tract. There are various peculiarities of the catarrhal process due to the anatomical structure of the parts involved, the presence of open glands, lymphatic follicles, etc. This disease is to be distinguished from inflammation of the serous coat of the intestine (peritonitis). The two are quite distinct in their etiology, pathological anatomy, and symptomatology, although they have been often confounded under the same name, enteritis.[4] As so much confusion prevails as to the proper meaning of enteritis, it is best to abandon the word altogether.

[Footnote 4: For cases called enteritis in which the lesions of peritonitis were found, see Hamilton, _Edin. Med. Journ._, vol. ii., 1857, p. 304; also Breed, _Chicago Med. Examiner_, Oct., 1869, p. 579.]

Diarrhoea is still regarded by some authors (J. J. Woodward) as synonymous with intestinal catarrh; by others it is considered separately as a disease distinct from catarrh. Habershon describes the lesions of catarrhal diarrhoea and mucous enteritis almost in the same words.[5] It is an unscientific method to take one symptom of a pathological state, to {669} erect it into a disease, subdividing it into varieties which are but differences in the intensity of its manifestation, and to assign to it no fixed lesion. Diarrhoea is in reality but a sequence and symptom of hyperæmia or inflammation of the intestinal mucous membrane.

[Footnote 5: Such a method of treating the subject involves a repetition, with an inversion, of the same description. Thus, catarrhal diarrhoea has as its lesion mucous enteritis; mucous enteritis has for its symptom (catarrhal) diarrhoea.]

ETIOLOGY.--Intestinal inflammation is more prevalent in the Northern, Middle, and Western than in the Southern States. There is no relation between the distribution of malarial and intestinal diseases: in some regions where malarial disease is rife there is very little disease of the intestines. Limited areas in Lower Mississippi, Eastern Kentucky, Eastern North Carolina, etc. have a special predisposition to diseases of this class.[6]

[Footnote 6: F. A. Walker, _Statistical Atlas_, 1874, table v. p. 3; also plates xlii. and xlv.]

During the Civil War diarrhoea and dysentery were more frequent and fatal in the central region than in the Atlantic and Pacific regions.

It is difficult to compare the relative liabilibity of the native and foreign-born populations in the United States to intestinal disease. Inasmuch as children, among whom the bulk of such cases occur, bear such a small proportion to the adult foreign population, allowing for differences due to this cause, statistics show that the foreign-born race has a very distinct predisposition to these forms of disease.[7] The Swedes, Norwegians, and Danes have a marked susceptibility to intestinal diseases; the English and Welsh have the same tendency; but the Irish have a comparative immunity. The colored race is more prone to intestinal than to malarial diseases in the Middle States, but there is the reverse susceptibility in the Northern and Southern States.

[Footnote 7: The number of children under ten to 1000 native population is 306; number of children under ten in 1000 foreign population, 47 (F. A. Walker, "Relations of Race and Nationality to Mortality in the United States," _Statistical Atlas_, 1874, p. 213).]

Under ten years more males than females have enteritis, in the proportion represented by the figures 362 and 299. After ten the predisposition of the two sexes is about the same.

The summer is the season when diarrhoea is most prevalent and most fatal. June, July, and August are the months in which the greatest number of cases occur and in which there is the highest mortality. The extraordinary death-rate in these months in cities is of course due to the influence of summer heat on children, and the death-rate from diarrhoea and entero-colitis is chiefly among infants under one year. But among adults the same rule holds. The highest monthly mortality from acute diarrhoea among the U.S. troops (white) between 1861 and 1866 was 147, in July, 1862; the next highest was 114, in August, 1862. June and September were after these the most fatal months. According to the census of 1870, the most fatal month is August.

Elevation of temperature in the summer months is the cause of the prevalence of intestinal catarrh and of its great mortality among infants and children. The number of deaths bears a direct ratio to the degree of heat, the highest death-rate occurring in seasons of unusual high temperature.[8] The effect of excessive or prolonged heat is to arrest or weaken the digestive processes; undigested masses in the stomach or the intestines act as foreign bodies and produce inflammation.

[Footnote 8: Among the numerous publications bearing on this subject, those contained in _The Sanitary Care and Treatment of Children and their Diseases_ (Boston, 1881) are of especial value. S. C. Busey's article contains much valuable matter on the relation of summer heat to illness and mortality among children.]

{670} Sudden changes of temperature from cold to heat or from heat to cold develop diarrhoea. If the air is at the same time saturated with moisture, the effect of a change in temperature is greatly intensified. In the first hot days of June there is on the Atlantic coast, especially in cities, a rapid increase in the number of cases of gastro-intestinal disturbance. A larger number of children are taken ill in June than in August. The child in time becomes habituated to heat, and if not attacked early runs less risk of illness in the later months. A sudden or unusual exposure to low temperature, as in lying on damp ground, leads to the same result. The check to perspiration after violent exercise is especially provocative of diarrhoea. In these instances the congestion and consequent inflammation of the mucous membrane are brought about through the effect of heat or cold upon the peripheral nervous system. Cold may act more directly by the driving of suddenly-cooled blood from the surface of the body to the interior. External burns belong to the same category, as they lead to extensive inflammation, sometimes to ulceration, of the duodenal mucous membrane through reflex influence. A case is reported of a boy aged twelve years who after an external superficial burn of the left thigh was taken with profuse diarrhoea which ended fatally in three hours (Ziemssen).

Contamination of the atmosphere with emanations the result of the overcrowding of many human beings together, as in prisons, camps, or asylums, especially where decomposition of organic matter is going on, is of great influence in causing diarrhoea. Persons living in badly-ventilated houses, or in houses improperly drained where the air is vitiated by escaping gas from sewer-pipes, are especially prone to be attacked. But sewer-gas, per se, does not cause diarrhoea any more than it causes diphtheria or scarlatina.[9] It is a step backward to hang upon this ready explanation all our doubts and our ignorance of the origin of disease. The specific germ of the zymotic diseases may be conveyed in the gases from sewers, but there are other and more direct modes of communication which should receive equal attention.

[Footnote 9: Longstaff (_Brit. Med. Journ._, London, 1880, vol. i. p. 519) believes that summer diarrhoea has a specific poison which is intimately connected with the process of putrefaction, and that the infective material has its source in the public sewers.]

Children are much more liable to intestinal inflammation than adults. This is due to the greater susceptibility of the mucous membrane in them to congestion and catarrh from external influences and from direct irritation. In infants fed upon an unsuitable diet--cow's milk or other substitutes for mother's milk--this susceptibility is much increased. The age most liable to attack is under one year, or from the first to the second year, when, in consequence of dentition, weaning, and a change from a diet chiefly or almost wholly liquid to one of solids, there is a great liability to a disturbance of the normal equilibrium. Intestinal catarrh forms almost one-third of the total number of the affections of childhood. According to the census of 1870, 761 out of every 1000 deaths from diarrhoea, dysentery, and enteritis occurred under the tenth year. In old age a similar predisposition exists, and a mild attack will in old persons induce more serious symptoms than in middle life. Epidemics of diarrhoea among the aged in asylums and hospitals are not uncommon.

{671} Temperament and idiosyncrasy are causes of differences in predisposition. Many persons in consequence of taking cold invariably have diarrhoea, while others as invariably have nasal catarrh or bronchitis. Certain articles of food, as oysters and eggs, lead always in some persons to intestinal disturbance. An exaggerated sensibility of the mucous membrane to particular impressions is the cause of this peculiarity.

Previous attacks of intestinal inflammation render the individual liable to recurrences from very slight causes. The suppression of the menses and of hemorrhoidal discharges and the healing of eruptions are said to be followed by serious diarrhoea, but such an occurrence is probably more often a coincidence than a result.

Sedentary life, by enfeebling muscular movement and by inducing indigestion and constipation, brings on diarrhoea. Constipation impairs the muscular tone of the bowel, and hardened fecal accumulations act as irritants which sometimes provoke acute catarrhal processes--diarrhoea and dysentery. Insufficient clothing in children and in adults makes the skin more susceptible to changes of temperature and conduces to intestinal congestion. Smoking in excess and the use of narcotics and stimulants are mentioned as debilitating causes which pave the way for disease in the intestine; the habitual use of the stronger liquors, by keeping up chronic engorgement of the mucous membrane, is undoubtedly a potent cause. Occupations which involve deprivation of fresh air and sunlight, and all trades which enfeeble the individual, make him liable to all digestive disorders. A feeble constitution, debility from disease, from over-fatigue, or from loss of sleep, or any perturbing influence, puts the body in a state favorable to indigestion and diarrhoea.

The eruptive fevers are accompanied more or less by gastro-enteric catarrh. In scarlet fever, measles, and variola there is a state of equilibrium between the skin and the intestinal mucous membrane. When the morbid manifestation does not normally appear upon the skin there is a transference of irritation to the intestine. The administration of purgatives in the early periods of scarlet fever and measles delays, sometimes prevents, the outburst of the eruption on the skin. The intestinal catarrh of the eruptive fevers has sometimes the significance of an exanthem and sometimes of a secondary complication. In measles it is more frequently the former; in scarlatina and variola it comes later as a complication.

Uræmia, malarial infection, chronic suppuration, pyæmia and septicæmia, cancerous and strumous disease of the mesenteric glands, scurvy, tuberculosis, Bright's disease, and chronic wasting diseases in general, are conditions in which diarrhoea appears as a result of the defective nutrition of the vessels of the intestinal wall and their liability to dilatation and hyperæmia, or from the presence in the blood of septic matter.[10]

[Footnote 10: For experiments relating to the production of intestinal catarrh by injections of irritating or putrid matter into the blood consult _Traité clinique et expérimentelle des Fièvres dites essentielles_, Gaspard et Bouillaud; also, _Path. anat._, Lebert, tome ii., Texte, Paris, 1861, p. 205.]

The ingestion of a larger quantity of food than the stomach and intestines are able to soften, and the taking of food essentially indigestible or improperly prepared by cooking, are causes of the passage of masses of food more or less unaltered along the intestinal tract. Hyperæmia {672} follows the mechanical irritation of the mucous surface. When articles of food are in a partial state of putrefaction, so that the antiseptic properties of the gastric juice cannot be quickly enough brought into play, there is a rapid fermentation in the stomach, with the development of symptoms of gastric and subsequently of intestinal catarrh. Unripe fruit, vegetables composed of hard tissue, as early potatoes, cucumbers, pineapples, and cherries, by their indigestible nature, are frequent causes. Oysters, crabs, fish, and lobsters often occasion acute diarrhoea in consequence of being in an unfit condition for food. Cheese has been known to produce violent illness with symptoms of intense intestinal irritation; these effects are due to some poisonous substance, hitherto undiscovered, developed in the course of putrefaction. New coffee causes diarrhoea; six months is usually the time before coffee grown in Ceylon reaches the European and American markets; by this time it does not have this effect.[11]

[Footnote 11: J. Stevenson, "Medical Notes from Ceylon," _Edin. Med. Journ._, Feb., 1862, p. 693.]

The irritant and caustic poisons, as mineral acids, caustic alkalies, corrosive sublimate, arsenic, oxalic acid, tartar emetic, and carbolic acid, kindle an intense inflammation of the mucous membrane of the stomach, duodenum, and of the lower portion of the intestinal canal. Softening of the coats of the intestines from corrosion, with perforation, is not an infrequent result.

Drastic purgatives act as irritant poisons in producing acute hyperæmia of the mucous coat with excessive transudation of serum; or, in other words, an acute catarrh. A discharge of vitiated bile or an excess of bile is given by recent[12] as well as by older writers as a provoking cause of diarrhoea. The proper relationship is the reverse of this: an intestinal catarrh the result of irritant action upon the mucous surface entails a more active outflow of bile, just as some cathartics by irritating the duodenum excite the gall-bladder to empty itself.[13] Impacted fecal masses are direct irritants, exciting inflammation (typhlitis, dysentery); putrefactive changes in long-retained fecal collections have an additional power of irritation. Foreign bodies accidentally or purposely swallowed, intestinal parasites, the pus from an abscess which bursts into the intestine, likewise are excitants of disease. Tubercle nodules, typhoid ulcers, cancer, or other neoplasms in the wall are surrounded by areas of inflammation.

[Footnote 12: Roberts, _Th. and Pract. Medicine_, Am. ed., Philada., 1880, p. 160.]

[Footnote 13: "The propositions which are the foundation of the whole theory that bile can cause diarrhoea, and that its absence leads to costiveness, cannot be looked upon as proved" (J. Wickham Legg, _On the Bile, Jaundice, and Bilious Diseases_, New York, 1880, p. 661).]

Alcohol taken in excess, as in a debauch, leads to acute gastro-intestinal catarrh. The stomach symptoms are the earliest to develop and are the most prominent. Habitual alcoholic indulgence is a more common source of chronic than of acute intestinal catarrh.

The influence of unwholesome drinking-water as a cause of diarrhoea has been carefully examined by Woodward.[14] Turbid or muddy water holding inorganic matters in suspension, he concludes from the evidence, is not a source of disease, and the injurious effects of such waters have been grossly exaggerated. Water containing inorganic substances in solution produce diarrhoea, and are purgative if the dissolved matters have purgative properties. Limestone-water may produce {673} temporary disturbance of the bowels, but is wholesome. Carbonate and sulphate of lime and magnesium in solution are more cathartic, but not as much so as selenitic waters which contain an excess of sulphate of lime. The salts of sodium and potassium in the waters of Colorado, New Mexico, and Utah are still more liable to produce diarrhoea.

[Footnote 14: _Med. and Surg. History of the War_, Part 2, Medical Volume, p. 599 _et seq._]

Water contaminated with organic matters of vegetable origin, which are found in states of decomposition in marshes and stagnant pools, does not, in the opinion of Woodward and Parkes, have very great influence in the production of diarrhoea or dysentery. Impurities from decomposition of animal matters are unhealthful. This is especially true of water impregnated with soakage from privies and sewers; and yet epidemics of diarrhoea cannot as often be clearly traced to this source as can outbreaks of typhoid fever. Parkes says water contaminated with three to ten grains per gallon of putrescent animal matter may be hurtful.

Contusions and injuries of the bowel by sudden pressure or shock to the abdominal wall may lead to intestinal inflammation. The large intestine is more exposed from its size and position to such injuries. Pressure upon the bowel by a tumor, as an enlarged or retroverted uterus, may cause diarrhoea, the source of which may be overlooked. Early-morning diarrhoea from a displaced womb is of frequent occurrence.

Emotional influence, as sudden fright or grief, will produce sudden diarrhoea. Lesions of nerve-centres--corona radiata, optic thalamus, or corpus callosum--induce hyperæmia, softening, and ulceration of the mucous membrane of the small intestine.[15]

[Footnote 15: Rosenthal, "Diseases of the Nervous System," _Wood's Library_, New York, 1879, vol. ii. p. 266.]

Minute organisms (bacteria) are thought by some observers to be the cause of diarrhoea, especially of a zymotic form, which prevails in the summer months. In accordance with this theory, the dejecta from infected persons are the vehicle of the contagious poison which by air- and water-contamination infects others.[16]

[Footnote 16: Wm. Johnston, _Lancet_, London, 1878, vol. ii. p. 397; also, _Brit. Med. Journ._, London, 1879, p. 81; also, G. E. Paget, "On the Etiology of Zymotic Diarrhoea," _Brit. Med. Journ._, Nov. 19, 1881, p. 819.]

PATHOLOGICAL ANATOMY.--A description of the morbid anatomy of acute intestinal catarrh includes the changes which are observed (1) in the exterior appearances of the intestines, (2) in their contents, and (3) in the condition of their mucous lining.

1. The external appearances of the intestines depend upon the degree of distension of the tube, the character of the contents, and the presence or absence of inflammation of the serous coat. Great distension of the colon, of the cæcum, and of the small intestines is met with in acute intestinal catarrh of some duration, and is due to relaxation of the muscular coat. The colon usually presents the greatest distension. The calibre of the tube may be lessened by strong contraction of the muscular layer in acute intestinal inflammation of great intensity with early and fatal termination. The color of the exterior varies with the tension of the wall, the color of the contents, and the amount of vascular injection. If the bowel is much distended with gas, the color is pale; the mingling of bile with the feces causes a yellowish or brownish color; if blood is in the tube a dull red hue is given to the walls. If the intestine is congested or inflamed, the vessels are outlined distinctly and can be seen in {674} different layers. The areas of external redness generally correspond to internal hyperæmic patches. The serous membrane shows arborescent congestion at the mesenteric attachment or is inflamed from perforation; the signs of peritonitis are most marked in the neighborhood of the irregularly-shaped, round, oval, or pin-point openings in the gut. The abdominal cavity may contain fecal matter, food, medicines, or worms which have passed through the perforation.

2. The intestinal contents, instead of being homogeneous, of pale-yellow color, and pea-soup-like appearance in the small intestine, brown and more condensed in the lower part of the large intestine, may present various changes. The fluid is usually increased in quantity, and is thinner than normal in the colon: the color is greenish from the bile, very pale from the closure of the bile-duct, red or black from blood. The odor is absent from excess of serum, or very offensive from decomposition due sometimes to the closure of the common bile-duct and the want of bile. Shreds or masses of mucus may float in the liquid. Undissolved pills or drugs, as bismuth, accumulated seeds, skins of fruits or vegetables, parasites, or foreign bodies are seen. Epithelial cells, the débris of digestion, micrococci, and bacteria are visible under the microscope.

3. Inflammation involving the mucous membrane of the whole intestinal canal is rarely or never met with. The nearest approach to generalized catarrh of the bowel is found in eruptive fevers, especially measles. Inflammation extending throughout the whole length of either the small or large intestine alone, and affecting all parts equally, is also rare. The ileum is the part of the small intestine most frequently the seat of disease, but the ileum is rarely affected alone. Inflammation is more frequently limited to the colon than to the small intestine. The most common form of intestinal inflammation is ileo-colitis, where the lower part of the ileum and a part of the colon, sometimes of considerable extent, are inflamed. The duodenum is sometimes the seat of a local inflammation, but this rarely happens except in the case of external burns; duodenitis is most frequently an extension of catarrh from the stomach, but the pathological anatomy of the duodenum presents some peculiarities which will be described hereafter.

(_a_) Hyperæmia of the intestinal mucous membrane may exist without inflammation. The engorgement of the veins by mechanical retardation in disease of the liver, heart, or lungs does not constitute catarrh, although it is sooner or later followed by catarrhal processes, usually of a chronic nature. Gravitation of blood to the most dependent parts in cases of long illness distends the vessels, and post-mortem hypostasis leads to the passage of serum and coloring matter into the meshes of the mucous and submucous tissue. In fatal cases of acute diarrhoea sometimes no lesion has been observed. The hyperæmic membrane pales after death, as does the skin in scarlatina and erysipelas.[17] The presence or absence of hyperæmia is therefore no positive proof of the previous existence or non-existence of inflammation. To constitute inflammation there must be other changes besides hyperæmia, as oedema, softening, and infiltration with cell-elements.

[Footnote 17: It is difficult to recognize post-mortem hyperæmia in the mucous membrane of the mouth or throat where intense inflammation has been seen in life.]

{675} A degree of vascular turgescence visible to the naked eye is nearly always present in the mucous and submucous tissues which have been the seat of catarrh. It is usually found in the lower part of the ileum, the cæcum, sigmoid flexure, and other parts of the colon. The redness is diffused over a surface of several feet in length or is circumscribed in patches of varying size. When vessels of small size are distended with blood, red branching lines are seen (arborescent or ramiform injection) which have their starting-point in the insertion of the mesentery. When the capillary system is engorged a fine interlacing network can be discovered, which gives to the membrane a more uniform red color. Parallel lines or bands of redness extend in a transverse direction across the axis of the canal corresponding to the folds of mucous membrane in the small and large intestine.

The shades of color depend upon the intensity and duration of the congestion. In acute mild forms the color is light red; in more intense grades the membrane is more vivid or purplish. Brown and slate-colored tints show a passage into the chronic stage. A black hue occurs in gangrenous inflammation. Minute dots (speckled redness) are due to minute extravasations, and ecchymotic irregular patches are sometimes seen.

Bile-staining of the mucous surface is met with; this cannot be removed by washing. In metallic poisoning the redness is more vivid and the mucous membrane is eroded.[18]

[Footnote 18: For colored plates illustrating hyperæmia and inflammation of the intestines see Carswell, _Path. Anat._, London, 1838, plate ii. figs. 1 and 2. These are beautiful representations of (1) ramiform vascular injection passing into (2) capilliform injection, which becomes (3) uniformly red, or from its intensity (4) ecchymotic or hemorrhagic. See also Annesley, _Morbid Anatomy_, London, 1828, plates x. (Fig. 2), xiii., xxii., xxiv., and xxv. Many of these are illustrations of peritonitis as a complication of enteritis. See also Kupferlafelnzer, Lesser, _Ueber die entzundung und Verschwarung der Schleimhaut des Verdauungskals_, Berlin, 1830, tab. iv. fr. 3; also J. Hope, _Illustrations of Morbid Anatomy_, London, 1834, figs. 116, 118, 124, and 125. These plates are wonderful in their truthfulness and execution.]

(_b_) Acute oedema and increase in the cell-elements in the inflamed parts give rise to swelling and to softening, so that the mucous membrane seems to be easily scraped off. This is not always the case, as no loss of firmness of the reddened tissue is often found. In the small intestine the villi, which in health are not seen, become enlarged, giving a "plush-like" or velvety appearance to the mucous membrane; they are sometimes club-shaped from epithelial accumulations on their free extremities.

(_c_) When the small intestine is examined the solitary glands, which in the normal state are barely visible, are so enlarged that they appear as rounded prominences. They are described as looking like grains of mustard-seed on a red ground, and are the size of pinheads. When they are distinctly seen it may be concluded that they are enlarged. In children the glands are enlarged when there has been slight or no diarrhoea.

Peyer's patches are also tumefied, and are more distinct from being elevated above the surface, but they have not in intestinal catarrh as great a relative enlargement when compared with the solitary glands as in typhoid fever. The interfollicular substance of the patch may hypertrophy without any increase in the size of the follicles; a reticulated {676} appearance is then given to the gland. The color of the swollen follicles in recent inflammation is translucent from oedema; later they are gray and opaque. These changes are more marked at the lower end of the ileum, because the isolated follicles and Peyer's patches are more numerous there.

(_d_) Catarrhal ulcers--erosions--are produced by the loss of epithelium or from a process of vesicle-forming and rupture, as in stomatitis. They may enlarge, undermine, and coalesce, thus reaching quite a large size. They may deepen and perforate the wall of the bowel, causing peritonitis, or they may heal, forming cicatrices which in contracting may narrow the canal.

Small follicular ulcers are found on the mucous surface. They result from the breaking down of the exposed wall of the closed follicle from over-distension. The ulcer is either on the apex of the dome of an isolated follicle or is within the area of a Peyer's patch. Sometimes several ulcers may be seen on the surface of the swollen patch.[19] The ulcerative process is sometimes very rapid. In the case of a child aged eight years, with no previous intestinal disease, who died in the Children's Hospital, Washington, in June, 1882, after a two days' illness with watery discharges and rapid prostration, the solitary glands throughout the ileum were many of them enlarged. As many as a dozen small ulcers were seen at the apices of the enlarged follicles.

[Footnote 19: See photograph facing page 302 of _Med. and Surg. History of the War_.]

In the large intestine the same lesions are found, but in a more advanced stage, especially in the cæcum and descending colon. Enlarged solitary glands of the size of a pinhead or small bird-shot are scattered along the canal.

Follicular ulcers[20] are found in the large intestine, occupying the summit of the enlarged follicles and involving a large extent of mucous surface. Pigment-deposits are seen which give rise to the appearances described as occurring in chronic intestinal catarrh.

[Footnote 20: For description of the mode of formation and growth of follicular ulcers see article on CHRONIC INTESTINAL CATARRH.]

(_e_) The mucous surface is covered, especially in the areas of redness, with an adhesive, opaque mucus of neutral or alkaline reaction and of yellow, red, or brown hue, depending upon the relative amount of bile or blood. It is composed of mucus-corpuscles, epithelium-cells of cylindrical and prismatic form, pus-cells, and sometimes blood-corpuscles. Vibrios and bacteria also are seen.

The chief distinction between the lesions of acute intestinal catarrh and typhoid fever are these: In typhoid fever the number of Peyer's patches involved is larger; there will be a chain of enlarged glands from the ileo-cæcal valve throughout the ileum, those nearest the ileum being the most altered. Near the valve there is usually some ulceration, so that the gland acquires a ragged appearance. In catarrh of the bowel there is a more irregular distribution of enlarged glands; they project less above the surface, and if ulcerated have one or two spots of erosion. In typhoid fever the Peyer's patch has the most prominence. In catarrh of the bowel the solitary glands are the most enlarged. In catarrh the large intestine may be the seat of the most advanced lesion; in typhoid fever, except with rare exceptions, the lesions in the ileum are most advanced.

{677} (_f_) The mesenteric glands are enlarged, but not so uniformly so or to the same extent as in typhoid fever. The stomach is sometimes found inflamed, the mucous membrane being reddened, thickened, or softened. The liver, spleen, and kidneys are normal or present accidental conditions of disease. In the respiratory organs pulmonary congestion, pleurisy, and pneumonia are found. The heart contains clots which are fibrinous or soft and red; they are found on both sides, but when one cavity alone is filled the right is the common seat. The brain is usually normal; fluid may be in the subarachnoid space, and thrombi in the cerebral sinuses.

PATHOLOGICAL HISTOLOGY.--In the genesis of catarrh of the intestinal mucous membrane the first effect of the exciting cause is an over-distension of the capillaries and small vessels; this congestion is most marked in the meshwork of vessels around the closed follicles. A transudation of serum takes place into the mucous layer, and in more marked congestion into the submucous layer also; these tissues become more or less oedematous and swollen. Transudation of serum into the intestinal tube follows. From over-stretching the walls of minute vessels may rupture and small extravasations take place, staining the tissue red. These subsequently become black pigment-spots. Post-mortem extravasations are due to decomposition of the wall of the vessel. Rupture of vessels on the surface leads to escape of blood into the bowel, which is mixed with the transuded serum. The proper secretion, intestinal juice, is diminished as a result of these changes, but an excess of the mucus with which the mucous membrane is always coated immediately follows. The origin of the mucus is not to be sought for in the activity of the glands alone, but in the transformation of the protoplasm of the epithelial cells.[21] The varying proportions of serum, mucus, and blood cause the stools to be serous, mucous, slimy, or bloody, hence the terms serous, mucous, and bloody diarrhoea.

[Footnote 21: Rindfleisch, _Path. Histology_, Sydenham ed., vol. i. p. 412.]

Hypernutrition, swift life of the mucous membrane, the result of continued excess of blood, entails the increase of the cell-elements. Lymphoid cells accumulate in the submucous layer, especially where these cells are normally most numerous. There is a saturation of the membrane with an excess of plasma. Cells also appear in increasing numbers in the interfibrillary spaces of the mucous membrane, which increase its bulk, and the follicles of Lieberkühn appear as if pushed apart. Lymph-corpuscles accumulate in the meshes of the closed follicles, which are distended and project above the surface as described. Multiplication of the cells within the follicle (follicular suppuration) causes over-stretching and the wall bursts, forming the first stage of the follicular ulcer. The appearance upon the epithelial surface of an increased number of loosened cells, which are sometimes epithelial in character and at other times resembling pus-cells (epithelial and purulent catarrh), is believed to be due to a rapid manufacture and exfoliation of epithelial elements, and to constitute one of the essential features of catarrh. Desquamation of the epithelium in catarrh of the bowel, even in that of Asiatic cholera, has been called in question by Woodward, who thinks that the stripping off of epithelium is cadaveric.

SYMPTOMS.--Owing to the difference in the intensity and extent of {678} the catarrhal process there is every possible variation in the symptoms of intestinal inflammation. No one symptomatic picture will properly represent all cases, and with a view to greater convenience and exactitude of illustration a division may be made into mild and severer forms.

Under the head of mild forms can be included all cases of intestinal catarrh which by their short duration and benignant character point to a mild degree of inflammation. They correspond to the following anatomical states: hyperæmia of the mucous membrane of parts of the small or large intestine, or of parts of both simultaneously; slight or moderate swelling of the membrane from serous saturation; transudation of serum into the canal; increase of lymphoid cells in the mucous and submucous tissues; and increased manufacture of epithelial cells, but without any marked tumefaction or ulceration of the closed follicles. The termination is by resolution, which is reached in a few days usually, and the membrane is rapidly and entirely restored to the normal state. Between the normal condition of the mucous membrane, with its recurring periods of physiological hyperæmia, and the hyperæmia with exaggerated secretion and peristalsis which leads to diarrhoea, there is no well-defined border-line. Diarrhoea may be regarded as the most certain sign of the catarrhal process. Whenever the frequency and fluidity of the stools are such as to be regarded as pathological, some stage or other of catarrhal inflammation may be assumed to exist.

In a large number of mild forms the onset is sudden. After a meal of indigestible food or an unusual excess pain will be felt in the abdomen, recurring in paroxysms, which start in the neighborhood of the umbilicus and radiate throughout the abdomen. The pain is accompanied by borborygmi, and is succeeded sooner or later by a desire to go to stool. The first one or two movements, which follow each other in quick succession, are more or less consistent or moulded, but in a short time diarrhoea is established by frequent discharges of watery fluid, containing perhaps some undigested fragments of food, which may have been the exciting cause of the illness by mechanical irritation. Each stool is preceded by colics, griping pains in the abdomen, which are relieved by the evacuation. An attack beginning in this way and from such causes may cease in a few hours, and be unattended by any general symptoms if proper precautions are taken. A slight dryness and coating of the tongue, with loss of appetite and occasional griping pains or a tendency to looseness of the stools, may continue for a day or two. Indiscretions in diet or other imprudences, as fatigue, may prolong the mildest attack during one or more weeks, but the character of the illness is here due not to the nature of the disease, but to the addition of fresh causes which delay the natural progress toward recovery.

Severer forms either begin suddenly, as in the milder forms just described, or are preceded for a time by symptoms of gastric or intestinal indigestion. The patient may have complained of distress after eating, flatulence, colicky pains, distension of the abdomen and tenderness on pressure, loss of appetite, with a general feeling of ill-health--symptoms which point to the existence of a condition of the mucous membrane of the gastro-intestinal canal favorable to the action of an exciting cause.

A feeling of chilliness ushers in the attack. This is accompanied by fever, which at first, and sometimes throughout, is of a marked remittent type. {679} The griping pains, colics, which at first are infrequent and dull, now recur at short intervals and become sharper. They are sometimes attended with vomiting of food or of a greenish fluid. The intensity of suffering may be so great as to cause pallor of the countenance, a feeling of faintness, and coldness of the surface with sweating. The paroxysm usually precedes a movement. The more severe pains extend to the lower extremities and the scrotum.

Movement of gas in the intestines produces rumbling, gurgling, or splashing sounds, called borborygmi. They are paroxysmal, lasting a few moments, or are coincident with pain, and frequently are the immediate precursors of an evacuation. The cause for their production is the quick propulsion of the fluids by strong peristaltic action from one part of the bowel to the other or the rapid movement of gas within the bowel. Relief is obtained both from the pain and from the sense of distension by expulsion of flatus.

Tympanites is closely connected with the symptoms just described. An excess of gases within the bowel is not primarily a result of the inflammation of the mucous membrane, but is an early phenomenon due to the decomposition of indigestible food in its transit through the intestine. Later, the gases are developed very readily by the decomposition of even the most digestible articles of food, the mucus, which is the product of the catarrh, acting as a ferment.

The distension of the intestinal canal produces an intumescence of the abdomen which is commonly uniform, but may be greater in some portions of the tract than in others. Thus the transverse and descending colon are more projecting and more distinctly outlined than other portions of the canal.

Sensibility of the abdomen to pressure exists along the line of the colon or over a considerable area. But no defined limitation of the affected part can usually be made by the location of pain to the touch. If there is any local tenderness, it is over the descending colon. In one form of enteritis--typhlitis--the localization of the inflammation in the cæcum produces subjective pain and pain on pressure in a restricted region--a peculiarity which results no doubt from the early intensity of the inflammation and the implication of the connective tissue behind the bowel. But this is not true of inflammation of any other part of the intestinal canal.

A sensation of soreness on movement, as in turning in bed, standing, or walking, is not uncommon, even when the attack is of no great gravity. The patient on standing bends forward to relieve tension, and he may feel nervous when the bed is shaken.

Diarrhoea is the most important symptom, as it is directly related to catarrh. The number of evacuations varies from one or two to twenty or more in the day. In cases of medium intensity there are from six to ten in twenty-four hours, the interval between the movements being two to three hours during the day and somewhat longer at night. The matters passed in quantity range from two ounces to a pint; the average is about four fluidounces. This, however, is subject to great variations, depending upon the intensity of the disease; the more choleriform the attack the greater the amount of fluid passed. The weight of the evacuations varies from five ounces to forty pounds in twenty-four hours; this increase does not depend upon the greater quantity of water only, but the solid constituents are in greater amount.

{680} The normal brown color, which is due to hydrobilirubin, changes as the movements become thinner to yellowish-brown or pale yellow from dilution of the fecal matter with water. An excess of serum or mucus renders them colorless. A greenish-brown, greenish-yellow, or green hue is due to the presence of bile. The rapid descent of the contents of the bowel delays or prevents the reabsorption of bile,[22] or the fluid is expelled before the usual transformations in color take place.[23] The bile-pigment is also absent in duodenal catarrh from closure of the opening of the ductus choledochus.

[Footnote 22: L. Brunton, "On the Action of Purgative Medicines," _The Practitioner_, London, June, 1874, p. 403.]

[Footnote 23: The reaction of bile-pigment with nitric acid, which does not take place in the contents of the colon or in normal feces, is seen in the green stools of acute intestinal catarrh, especially in children.]

The coloration of the stools further depends upon the character of the food and drink and upon the drugs given. From an exclusive milk diet the discharges are pale or contain undigested whitish lumps of casein. The preparations of bismuth and iron give a black color and the sulphate of copper a dark-green hue. A green or greenish-brown tint is observed after the use of calomel, and while the experiments of the Edinburgh committee demonstrated that no increase of bile follows its administration in dogs, yet the opinion is still general that the green stools contain an excess of bile.

Blood appears in three forms in the stools: as a coffee-ground or black powder from hemorrhage in the stomach or upper bowel; as a reddish fluid with small coagula in flakes, which come from intense congestion or ulceration of the intestine; or an abundant hemorrhage may result from deep ulceration in the duodenum or elsewhere.

The characteristic odor of the feces is altered in several ways. As the movements become less solid they acquire a nauseous or sour smell, due essentially to the volatile products formed in connection with the decomposition of fatty matters.[24] When very thin and containing little or no feculent matter the discharges lose odor, as in cholera, or they become excessively offensive--cadaveric--in intense and fatal inflammation and in ulceration of the bowels. After exposure to the air the stools of diarrhoea undergo decomposition and develop offensive smells more rapidly than in health. The absence of bile, whether there is diarrhoea or not, gives rise to a peculiar and unpleasant odor, showing that this secretion is to some extent an antiseptic. The escape of fetid gas from the anus is rarely an accompaniment of a decomposed state of the rectal contents. In children the stools are more variable in quantity, color, and odor than in adults, and are more readily affected by the ingesta.

[Footnote 24: Guttmann, _Physical Diagnosis_, Sydenham Soc. ed., p. 404. The odor of normal feces is due to a substance isolated by Briequer, called scatol, which is a final product of the putrefaction of albumen (Ewald, _Lectures on Digestion_, New York, 1881, p. 106).]

In the diarrhoea of old persons the discharges are thin, yellow, offensive, and often frothy.

The disorder of the digestive apparatus is attended with other symptoms. The tongue is normal in some cases; in others red at the point and edges with a central whitish coat, or the surface is red, polished, and dry. Marked change in the appearance of the tongue is due to a complicating gastric catarrh. There is thirst, with loss of appetite, and a tendency to {681} nausea and vomiting in children and feeble persons. The breath has a peculiarly offensive odor (spoken of as fecal) in some instances.

Fever is not always present. In cases of moderate severity it occurs in the beginning of the illness, but declines rapidly under treatment by rest and diet. The course of fever does not conform to any type even in severe cases, although it so nearly resembles that of typhoid fever in its first week as to lead to mistakes in diagnosis. The height of the fever and its duration are measures of the extent of the lesions and their gravity. Sudden outbursts of fever point to some complication. In catarrh of the bowel due to cold the fever is higher than when indigestion is the cause. In very feeble persons, in children, and in any case from neglect and improper feeding the body-heat may be very high.

The urine is diminished and high-colored. Very little disturbance of the nervous system is seen except in young and old patients; some headache and restlessness are all that may be observed. Moderate delirium at night accompanies very acute attacks. In children convulsions are not unusual in the onset and at the end of the attack. In the aged exhaustion from the illness soon lapses into stupor or coma.

Paraplegia and contraction of the muscles of the extremities are referred by some observers to gastro-intestinal inflammation.[25]

[Footnote 25: Potain, _Le Praticien_, Paris, 1879-80, p. 88.]

In uncomplicated mild cases of intestinal catarrh there is a movement toward recovery after a few days' illness. The stools become less frequent, smaller, and more consistent. In a week to ten days the tongue cleans, the thirst ceases, the appetite returns, the tympanites and pain diminish. The fever declines, and ceases before the diarrhoea is completely arrested. There are always more or less emaciation and loss of strength from the fever and arrest of nutrition. The liability to relapse is great, and the patient by indiscretions reproduces the same symptoms, thus prolonging the attack for several weeks. Acute intestinal catarrh may pass into the chronic form by a disappearance of fever and amelioration of all the abdominal symptoms. The patient begins to take solid food, gains strength and flesh, but complete recovery does not come. The diarrhoea recurs at variable intervals as the result of indulgences in a mixed diet, over-exercise, or exposure to cold, and in time we have some degree of chronic catarrh permanently established.

Very mild cases may be prolonged by the neglect of the patient to consider his painless diarrhoea of sufficient moment to need attention.

In inflammation of the more intense kind the picture is somewhat different. The prodromes are longer and the general symptoms more severe. Restlessness, a sense of prostration, delirium, and high fever mark the early stages and continue for a longer time. The patient loses flesh and strength quickly. The features express anxiety and illness, the skin is hot and dry, and the thirst great. Vomiting is repeated. Borborygmi, the tension of the abdomen, pain, and sensibility to pressure are all intensified. The stools are at first yellow and thin, but change much from day to day. They may be green or very thin and dark or grayish, and are sometimes very offensive in odor. Blood and mucus may be seen in them, being slimy or grumous and bloody. When the patient is very weak the discharges are involuntary; the tongue is coated white, with bright red tip and edges, and is often dry.

{682} The severer forms last from three to six weeks. After a tedious period of alternate improvement and relapse the illness becomes chronic or the patient dies from asthenia, perforation and peritonitis, or some other complication.

In the most intense varieties which find examples among Europeans and Americans in intertropical countries, or result from acute mineral poisoning and from rapidly-progressing cases of acute ulceration of the intestinal wall, especially in children, there is a sharper and more violent invasion. The strength is reduced in a very short time, and there is rapid emaciation; the features assume an anxious expression; the complexion is leaden or livid; the skin is cold and clammy; the pulse is small, weak, and rapid; the breath comes quick and short, and is frequently complicated with hiccough. In the early stages vomiting occurs, due to a concurrent gastritis; in cases of poisoning vomiting is incessant.

The pain in the abdomen is intense, and less paroxysmal than in other forms. The abdomen is tympanitic and excessively tender to the touch, and the knees are drawn up to relieve the tension of the abdominal muscles. Thin, black, or reddish stools are passed every few moments. As the attack progresses the urine is suppressed, the voice becomes whispering, and collapse is developed. This is marked by cold extremities, dyspnoea, feeble and finally imperceptible pulse. Death may end the scene in a few hours or the patient may rally and recover slowly.

Choleriform diarrhoea occurs chiefly in children during hot weather.

VARIETIES DUE TO SEAT.--The symptoms and progress of acute catarrh of the intestines present numerous differences depending upon the seat of the inflammation. The symptomatology already given is that of the most common form (ileo-colitis), in which the lower part of the ileum and a considerable portion of the colon are simultaneously involved. Many cases no doubt occur in which the disease is limited and in which early recovery is the rule. The pathological anatomy of cases of generalized catarrh is better known, as they form the bulk of the fatal cases.

I. Acute Duodenitis.--The most common form of duodenitis is that in which the inflammation spreads by continuity of tissue from the stomach to the duodenum, as in acute gastric catarrh after a debauch. The prominence of the gastric symptoms disguises the intestinal lesion, unless the catarrh, as is frequently the case, extends into and obstructs the common bile-duct and its branches, and suddenly develops icterus with clayey stools and altered urine. Besides icterus, a careful isolation of symptoms will show that some cannot be attributed to the stomach: there is a dull pain seated in the right hypochondrium, extending to the right shoulder or shoulder-blade, which is increased by pressure upon the region of the duodenum. As the gastric symptoms improve there is no change in the icterus, which continues for some days or weeks longer. The connection between burns of the integument and ulcer of the duodenum is well known. Symptoms of perforation, with death, may be the first sign of this lesion, but vomiting of blood, icterus, purging of blood, indigestion, and cardialgia occur from duodenal ulcers.

The typical acute duodenitis described by authors as an independent {683} affection is of rare occurrence. An epidemic of duodenitis[26] has been reported where many persons were simultaneously attacked, all the cases having had the same traits--headache, pain in the line of the duodenum at the left edge of the right hypochondrium, pain in the first and second lumbar vertebræ, constipation, jaundice, slow pulse, and mental depression. Gangrenous inflammation of the duodenum[27] has been once seen, and produced a chill, a severe sense of weight and pain in the epigastrium, retching and eructations of gas, tenderness on pressure, frequent pulse, and high temperature. There was obstinate constipation, with dyspnoea, death ensuing in a few days. At the autopsy gangrenous inflammation of the duodenum was found, which ended abruptly twelve inches from the pylorus. There was a large gall-stone in the gall-bladder.

[Footnote 26: McGaughey, _Philada. Med. Times_, Aug. 1, 1872, ii. p. 407; also, T. N. Reynolds, _Detroit Clinic_, June 7, 1882, p. 181.]

[Footnote 27: Eskridge, _Philada. Med. Times_, Feb. 15, 1879, ix. p. 239.]

A fatal case of duodenitis is recorded[28] in which the following symptoms were observed: sudden and severe pain in the right hypochondrium, increased by pressure; rigors, vomiting and purging of a green flocculent fluid, and later of blood; jaundice, fever, delirium, collapse, and death. The pylorus and two-thirds of the duodenal mucous membrane were much inflamed and the orifice of the bile-duct closed.

[Footnote 28: _Die Krankheiten des Duodenums_, Mayer, quoted by Leube in _Ziemssen's Cyclopædia_, Am. ed., vol. vii. p. 373.]

II. Acute Ileitis, Acute Jejunitis.--When the ileum, with or without the jejunum, is the seat of catarrh, diarrhoea may not be present, provided the inflammation is slight and there is no increase of colon peristalsis. The symptoms then are borborygmi, pain and fulness about and below the umbilicus or between it and the right ileum, especially after eating, and the general symptoms arising from indigestion and malnutrition. Fever is slight or absent; there are malaise and loss of strength. The feces give important indications. They contain unaltered bile and fragments of muscular fibre and starch-granules in excess of the quantity found in health. An increased quantity of mucus, diffused evenly in a fluid evacuation, or globules of mucus stained with bile, or bile-stained epithelium, denote inflammation confined to the small intestine. A larger amount of indican in the urine than is normally present is a sign of the same lesion.[29]

[Footnote 29: These conclusions are based upon the results of one thousand examinations of feces made by H. Nothnägel, and reported in _Zur Klinik der Darmkrankheiten; Zeitschrift für klin. Medicin_, iv., 1882, p. 223.]

Intense inflammation of the small intestine may exist without diarrhoea or other symptoms betokening the real nature of the attack. Flint[30] mentions having met with three such instances, and Goodhart[31] records thirteen cases of enteritis with marked lesions in which no diagnosis had been made before death. Rilliet and Barthez report twenty-four autopsies in children with intestinal lesions in which no symptoms had been observed.[32]

[Footnote 30: _Clinical Medicine_, Philada., 1879, p. 280.]

[Footnote 31: _Guy's Hospital Gazette_, Sept., 1878, p. 98 _et seq._]

[Footnote 32: _Maladies des Enfants_, Paris, 1861, tome i. p. 748.]

III. Acute Colitis.--Fifty years ago colitis was synonymous with enteritis, and not with dysentery, as at a more recent date.[33] The older {684} signification expressed the fact that inflammation in the colon is essential to diarrhoea. Later the term was used synonymously with dysentery.[34]

[Footnote 33: _Journal général de Médecine_, Paris, 1825, t. xci. p. 18.]

[Footnote 34: Tweedie, _System of the Practice of Medicine_, 1841.]

The colon is a conducting tube; the contents are composed of matters unabsorbed in the small intestines. At first the mass entering the colon is fluid, but by the gradual absorption of its watery part it approaches solidity. The discharge from the rectum of a fluid shows that the propulsion through the large intestine is so rapid that the process of drying does not take place, or that from inflammation of the colon there is an excess of fluid transudation from the intestinal wall. The superficial position of the colon, its great size and length, expose it to the action of external cold, to blows, etc.

In catarrh limited to the colon there are essentially the same symptoms as in ileo-colitis, inasmuch as the inflammation of the colon gives to that form its characteristic features--borborygmi, diarrhoea, and tympanites. When the disease in the colon preponderates or exists alone, the pain and tenderness are more superficial and confined to the line of the large intestine. The distended colon projects and the abdominal swelling is not so uniform. If the attack is subacute or mild, the stools contain normal feces mixed with a great deal of mucus; when the inflammation is in the sigmoid flexure, pure mucus is passed. Blood mixed with mucus and tenesmus accompany inflammation low down. Blood may, however, come from intense inflammation of the ascending and transverse colon without disease of the lower bowel.[35]

[Footnote 35: In a case seen by the writer of colitis terminating fatally from perforation of the transverse colon this point was illustrated. A woman aged fifty was taken with diarrhoea in August, 1873. In November the symptoms became worse: tongue dry and red; abdominal pain; tympanites; frequent stools, ten to seventeen in twenty-four hours; quantity large, of a yellow or brownish-red color with floating flakes. General symptoms grew worse; blood in stools from time to time. November 24, sudden cessation of discharges from the bowels, and the following day sudden collapse and death. Autopsy: Descending colon and sigmoid flexure comparatively healthy. Transverse colon adherent to stomach; deposits of lymph on colon and small intestines; fluid and feces in the peritoneal cavity. The mucous membrane of the ascending and transverse colon in a state of black pulpy disintegration. In the transverse colon the walls were thinned by ulceration and easily torn; gangrenous appearance of mucous coat; perforation of the colon wall below greater curvature of the stomach.]

IV. Proctitis.--The rectum may be the seat of simple catarrh, which differs in its symptoms from catarrh of other portions of the canal. By many this form is called simple, non-infective dysentery. But as it is a form of intestinal catarrh, it is right that it should be considered in connection with colitis. The first indication of its onset is a frequent desire to go to stool, with an unsatisfied feeling after each effort. Normal fecal matter is first expelled in solid form, coated with mucus which may be streaked with blood. Soon, however, the discharges consist of jelly-like mucus, alone or mixed with blood. A small quantity of this is passed with tenesmus at short intervals. The patient complains of a burning feeling in the rectum and a constant and irresistible desire to strain. The same spasmodic contraction may involve the bladder.

This affection rarely assumes a serious form. It usually ends in recovery spontaneously or under treatment by the cessation of the mucus and blood and the discharge of normal fecal matter.

DIAGNOSIS.--A combination of the symptoms described as belonging to inflammation of the small and large intestine gives the most common {685} form of intestinal catarrh, ileo-colitis. This union is diagnosed by the following symptoms: fever; general distension of the abdomen; paroxysmal pains starting from the umbilicus, but having a general distribution; noisy movements of gas; diarrhoea, the stools being large, thin, stained more or less with bile, containing more or less mucus intimately mixed with fluid matter and with particles of partially-digested or unaltered food. It is possible in many cases to recognize the part of the intestinal canal which is the seat of disease from differences in symptoms which have already been described. But great care in observation is needed, combined with a minute inspection and microscopical examination of the stools, to arrive at accurate and well-founded conclusions.

Acute follicular ulceration may be thought to have begun if after a week or more of illness thin and sometimes putrescent stools are passed containing small blood-coagula, with mucus and pus.[36] This opinion would be confirmed by an increase in abdominal tenderness and the persistence of the diarrhoea or tendency to relapse notwithstanding careful treatment and diet. The transition of the disease into the chronic form would give additional support to this view of the nature of the lesion.[37]

[Footnote 36: "The intestinal mucous membrane, especially that of the small intestine, scarcely ever produces pus without ulceration" (Virchow's _Cellular Pathology_, Philada., 1863, p. 492).]

[Footnote 37: For a more detailed account of the symptoms and diagnosis of follicular ulceration see article on CHRONIC INTESTINAL CATARRH.]

Some or all of the symptoms of acute intestinal catarrh are, however, found in other diseases. It is well, therefore, to devote some attention to differential diagnosis, giving a résumé of the salient points of distinction.

Typhoid fever in many of its features resembles intestinal catarrh, and in many cases is confounded with it. Until within quite recent times the symptoms of typhoid fever were grouped under the names gastro-enteritis and follicular enteritis. In the first week of the illness there is reasonable ground for delay in making a positive diagnosis. Etiological data are here of great help. The occurrence of the symptoms in children under two years and in adults beyond fifty years points strongly to intestinal catarrh. Spring and early summer are the seasons for diarrhoea; typhoid belongs to late summer and to autumn. A sudden onset after errors in diet or exposure to cold, with the early development of pain in the bowels, rumbling of gas, diarrhoea, would be easily recognized as a local disorder. In typhoid fever there is a less sudden onset, with prodromal debility, anæmia, indigestion, and nocturnal fever. To these symptoms the diarrhoea, which is attended with little or no pain, plays a very subordinate part. In many cases of mild typhoid the development is sudden, with rigors. A week's study of the temperature, if no rose-spots appear, will be needed before the diagnosis can be made. There is not much difficulty in making the distinction when the attack has reached its second week. At this period in catarrh of the bowel the high fever, with regular morning remissions and evening exacerbations, is not constant, as in typhoid fever; there is tenderness on pressure over the abdomen and gurgling, but no great meteorism; sibilant râles are not heard in the chest; there are no rose-spots; rarely cerebral symptoms except insomnia; and delirium is uncommon. The spleen is not enlarged. The prostration is proportioned to the diarrhoea, and is by no means as {686} great as at the same period in enteric fever. The colicky pains preceding and accompanying the stools are a more marked feature of intestinal catarrh; they are absent in enteric fever or have a feeble intensity.

In children between the ages of two and seven years there are certain peculiarities which augment the difficulties of diagnosis. Intestinal catarrh in them is accompanied by an abundant, frequently painless diarrhoea, by tympanites, cerebral disturbances, a dry and coated tongue, with sordes on the lips and gums, and by a rapidly-developed anæmia, emaciation, and exhaustion. Typhoid fever in children of this age is generally benignant; vomiting is more common than in adults; high grades of meteorism are infrequent; tenderness of the cæcal region is determined with greater difficulty; and severe nervous phenomena and fatal intestinal complications rarely occur.[38] In other words, in young children intestinal catarrh by its severity and enteric fever by its benignity more nearly approach each other than in adults; in many instances the diagnosis must be undecided until late in the attack.

[Footnote 38: Consult "Diseases of Children," Henoch, _Wood's Library_, New York, 1882, p. 300.]

Typhoid fever can of course be known if rose-spots, a splenic tumor, or the characteristic delirium are manifested, or if the fever-curve conforms to the type; but in children all these symptoms may be negative; even the fever has great variability. If fever is continued beyond ten days, and is accompanied by progressive anæmia and emaciation and debility, the attack is enteric fever if all local causes of fever can be excluded. There is no minimum limit to the temperature in typhoid fever, and no matter how low the maxima of the fastigium may be, typhoid fever cannot be excluded.[39]

[Footnote 39: Johnston, "On the Diagnosis of Mild Cases of Typhoid Fever," _Am. Journ. Med. Sci._, Oct., 1875, p. 372; also, "On the Mild Forms of Continued Fever in Washington," _Am. Journ. Med. Sci._, Oct., 1882, p. 387.]

The large watery stools and the absence of tenesmus mark the difference between diarrhoea and dysentery. Blood may be present in colitis, owing to a high grade of inflammation and to ulceration. Simple catarrh of the rectum, proctitis, is not readily distinguished from infective dysentery. Small mucous and bloody stools may be catarrhal. In the present state of our knowledge dysentery would be known by marked tenesmus, by the grave general symptoms, the reddish fluid stools with flocculi, and by its occurrence in epidemic form.

Enteralgia presents the following features which distinguish it from intestinal catarrh: The tongue in enteralgia is clean or coated white, but with no red tip and edges; the appetite is capricious, but not lost; the bowels are constipated; the pain bears no relation to the ingestion of food or drink, as in enteritis. Fever is accidental, and there are other nervous phenomena. In lead colic there is no fever, tympanites, nor diarrhoea. In rheumatism of the abdominal walls the pain is superficial and sharp, not griping, and is increased by movements of the trunk. The digestive system is in no way disordered. From peritonitis intestinal catarrh is distinguished by a less degree of illness and by its usually favorable result, by diarrhoea, a greater freedom in movement, and by a less degree of suffering on palpating the abdomen. Tympanites, constipation, great tenderness on pressure over the abdomen, and a small, quick pulse, point to peritonitis.

{687} PROGNOSIS.--A simple intestinal catarrh of the form first described involves no danger, and if treated by rest and diet soon recovers. The more severe form, beginning as a primary disease, when rationally treated ends in recovery in most instances.

Unfavorable predisposing causes are--a hot climate (India, the West Indies, and intertropical climates in general); very hot weather of the summer and autumn months; a very early or very advanced age; the contaminated atmosphere of prisons, camps, etc.; all bad hygienic influences; and previous or coexisting illness. When diarrhoea occurs as a complication of the acute infectious diseases it has a special gravity. In typhoid fever, scarlatina, measles, acute tuberculosis, etc. it adds another element of illness and danger. During the progress of chronic general diseases (malaria, scurvy, tuberculosis) it becomes an obstinate and sometimes a fatal complication. Among the exciting causes mineral poisons induce the most dangerous form of intestinal catarrh. Unfavorable symptoms occurring during the course of acute diarrhoea are the early development of high temperature, cerebral disturbance, great sensibility to pressure over the abdomen, thin and bloody or highly offensive stools, involuntary discharges, and very rapid emaciation and loss of strength.

TREATMENT.--There have been many fluctuations of opinion as to the relative value of modes of treatment in this disease. Various therapeutic measures have been suggested which, after enjoying favor for a time, have been abandoned, and revived after long periods of disfavor. Venesection was alternately recommended and forbidden. Emetics and evacuants, mercurials, diuretics, diaphoretics, have been in turn warmly supported and vigorously opposed. Opium, belladonna, the various astringents, and cinchona-bark have run through many changes of favor. Individual drugs give curious evidence of inconstancy. Oxide of zinc, suggested by James Adair in 1785 and by Hendy in 1784, after a hundred years of weak approval is commended highly by Penrose (1863), Brakenridge, and Mackey (1873),[40] and by more recent writers. Acetate of lead, which dates back to Paracelsus, had varying fortunes of repute and disrepute. In the end of the seventeenth century it had a name for curing diarrhoea, but in the following century it was spoken of by Boerhaave as a deceitful and destructive poison, and Cullen in 1789 said that hardly any one then thought of using lead internally.[41] In 1799 it had warm advocates in this country; among them, Thomas Ewall of Washington, who wrote in 1808. Since then it has come into very general use and favor, which it still holds.

[Footnote 40: J. J. Woodward, _op. cit._, p. 776.]

[Footnote 41: Ibid., _op. cit._, p. 780 _et seq._]

In view of the many changes of faith in systems of treatment and in drugs, we have no right to assume that we have as yet reached the perfection of treatment. In fact, experience brings the conviction that our systems are quite imperfect and that drugs fail in our hands when they are most needed.

The prophylactic treatment is of importance, especially in children, delicate persons, and in those suffering from disease or predisposed by idiosyncrasy to intestinal catarrh. Directions must be given by the physician as to the food for children appropriate to their age and digestive capacity. Summer heat and city life being so fatal to them, they should {688} be sent to the cool climate of the seashore or mountains during the first and second years of life. In warm weather laxatives should not be given to children, except with precautions against their acting too freely; the same rule applies to the aged. Too great care in diet in older children predisposes to indigestion and diarrhoea. Variety in food is of service, therefore. It is not well to give children food prepared so as to do away with the necessity for mastication and for active gastric movements. The stomach gains strength by exercise. All reasonable care should be used not to take food in excess of the individual's power of digestion. Unripe fruit, stale vegetables or fruits, cheese, pork, shellfish which are not absolutely fresh, are among the aliments which may produce diarrhoea, and are to be avoided. Many people have to be told what food is unsuited to them, and certain articles of food in individual cases invariably excite diarrhoea. Alcohol is often to be blamed for diarrhoeas which are attributed to indigestible food, and frequent recurrences of intestinal catarrh can only be prevented by abandoning stimulants altogether. The bad effects of sudden changes in temperature are warded off by wearing flannel next to the body. This is an important rule for adults as for children. Even in summer thin flannel or gauze gives protection. Well-ventilated rooms, good house-drainage, personal cleanliness, with all other hygienic aids, are means of prevention. Persistent disinfection of sources of air- and water-contamination should be practised, especially in hot weather. In the country the open privies and wells need frequent clearing out. Cases of fatal diarrhoea are met with in elevated regions where the continued low temperature renders it improbable that heat could have anything to do with their causation.[42] Water should not be used which could in any way be tainted with soakage from privies, barnyards, or other places where animal decomposition is going on.[43] Avoiding the use of cathartics in the onset of acute illness, the nature of which is not known, is a useful prophylactic measure. A fatal diarrhoea may result from injudicious purging in such cases. Care in the use of laxatives should be observed in the chronic wasting diseases--tuberculosis, rachitis, cancer, etc.

[Footnote 42: The yearly occurrence of typhoid fever and diarrhoea at seashore hotels shows that there is great danger in crowding persons together and saturating the soil with the excreta. In the summer of 1882 in a boarding-house in the mountains of Maryland, where the temperature was never above 75°, there were three fatal cases of diarrhoea in children, and several others of diarrhoea and dysentery which recovered.]

[Footnote 43: The drinking-water supplying a country boarding-house visited by the writer passed through iron pipes imbedded in the manure-heap of a barnyard.]

The selection of a plan of treatment for intestinal catarrh will depend upon the nature and cause of the symptoms. The diagnosis of the case is incomplete and the treatment irrational until the indications furnished by etiology have been obtained.

If cold has been the exciting cause, the patient should be confined to bed. In the beginning a full dose of pilocarpin, hypodermically,[44] or of the fluid extract of jaborandi by the mouth, may cause a powerful diversion from the bowel to the skin. A hot-water or vapor bath has the same object in view. Hot fomentations or mustard poultices can be next applied to the abdomen. This should be succeeded by a febrifuge {689} mixture containing the tincture of aconite-root, to which an opiate (the deodorized tincture of opium or morphia) is to be added if there is much pain or diarrhoea. A hypodermic injection of morphia given on the first day of the attack immediately after a hot bath will give a quiet night and diminish the intensity of the illness. The subsequent treatment is that common to all the acute forms.

[Footnote 44: Atropia can be given with pilocarpin to diminish its effect on the heart; atropia is the antidote for pilocarpin. (See Schuk, _Centralb. f. d. med. Wissen._, Bd. 20, 1882, p. 357; also, Frohnmüller, _Med.-Chir. Centralb._, July 14, 1882.)]

If summer heat has been the cause in adults or children, artificial cooling of the temperature of the room by the evaporation of ice-water or by one of the refrigerating machines yet to be perfected meet the indication. If there is much body-heat (thermic fever), cold sponging, the application of cold to the head, or the giving of pounded ice to satisfy the intense thirst, are all advisable. Such cases are benefited by a change of climate when the acute symptoms subside. The form of diarrhoea due to malaria is to be treated by quinia and change of air to a more healthful climate. Iron, with quinia or arsenic, is needed in obstinate cases.

Intestinal catarrh which proceeds from the presence of undigested food or hard fecal lumps in the bowel is benefited by early removal of the irritating cause. It is not often that substances of this kind are retained when the stools are large and frequent. The peristalsis is here as active as it need be, and no good, but only harm, can come from over-stimulating the contractile muscles. In those instances where there is a distinct history of the taking of indigestible food, especially fruit with seeds or skins, and where the efforts at stool are frequent, ineffectual, and accompanied by colic and borborygmi, or where scybalæ are found floating in the fluid passed, a large enema of warm water given slowly will excite the bowel to successful expulsive efforts. If this does not give a certain amount of prompt relief, a moderate dose of castor oil, calomel, Rochelle or Epsom salts ought to be prescribed, and repeated after some hours until a free fluid or semi-fluid stool results; one or two doses will usually suffice. If the inflammation is localized in the cæcum (typhlitis), as indicated by local pain, tenderness on pressure in the right iliac or right lumbar regions, constipation, flexing of the right thigh on the trunk, and vomiting, a purgative should not be given, nor should prolonged efforts be made to empty the bowel by injection through long rectal tubes. If there is doubt as to whether typhlitis or undigested food and fecal impaction is the cause of the local pain, it is better to err on the safe side, and not to give a purgative unless the case is seen in the onset before the more pronounced symptoms appear; then calomel or castor oil may be tried once, but not repeated in case of failure.

As the diarrhoea of Bright's disease is salutary, no effort should be made to arrest it. Its periodical recurrence prolongs life. In tuberculosis the special character of the diarrhoea must be considered, and every effort must be made to control it. In the eruptive fevers an early diarrhoea, as in scarlet fever, does harm; it delays or prevents the normal development of the eruption. In the later stages it is of service sometimes, as in measles, when it leads to a rapid fall of temperature. The course of action depends upon the nature of the specific disease and upon the time of the appearance of diarrhoea.

There are certain principles, founded on the knowledge derived from pathological study and from the experience of the past in the treatment {690} of intestinal catarrh, which guide us to a treatment which is more or less rational in all cases.

Rest is essential to the cure of the inflamed intestine, but absolute inertia of the bowel is undesirable, even injurious. The retention of fluids, transuded serum, bile, intestinal juices, and partly-altered food is hurtful. Decomposition sets in and gas is developed, which by distending the bowel causes great suffering and increases the inflammation. The movements of the intestine are not entirely under control; the patient must be fed; digestion and assimilation involve the activity of inflamed parts. The stomach can be made to do most of the work, but the sympathy of action is so close between the stomach and intestines that one cannot function without the other being excited into activity.

The first rule of treatment is to put the patient to bed and to keep him in a horizontal position. Even in mild cases time will be saved by resorting to absolute rest at once. If the attack is at all severe, the bed-pan should be used; the effort to rise and the straining at stool exaggerate peristaltic movement, increasing the frequency of the evacuations. Additional rest can be given to the intestines by applying a flannel binder around the trunk, compressing the abdomen; broad strips of adhesive plaster could be used for the same purpose. In cases where the diarrhoea, tympanites, and griping pain are not relieved by other measures this suggestion may be of service.

In order to lessen intestinal hyperæmia and allay suffering, counter-irritants and soothing external applications are employed. Local blood-letting, although in vogue during more than two centuries, has fallen into disuse. Recent authors still continue to advise the application of leeches to the anus in order to deplete the portal circulation,[45] but it is a decided objection to this remedy that the fluid stools irritate the leech-bites and cause much discomfort. Sinapisms or turpentine stupes may be of some service apart from the relief which they give to pain. Blisters might be more generally used than they are when the tenderness on pressure is confined to the colon. In intense inflammation they should always be tried. Hot poultices of flaxseed meal or hot fomentations of any sort applied over the entire abdomen have a soothing and beneficial effect. A flannel compress saturated with alcohol and covered with gutta-percha cloth makes a most agreeable application.

[Footnote 45: Niemeyer, _Practice of Medicine, Intestinal Catarrh_.]

The directions for diet should be carefully and explicitly given. In the onset of the attack entire deprivation of all food for twenty-four or forty-eight hours is expedient. To relieve thirst, cracked ice, carbonic-acid water, Apollinaris, Seltzer, or Deep Rock water can be ordered; barley- or rice-water is slightly nourishing and relieves thirst, but all liquids should be given in moderation. When it becomes necessary to give food, the stomach must be made to do the work of digestion, and, as far as possible, of absorption also. Such substances are to be chosen as are converted in the stomach into peptones, and which do not require contact with the intestinal juices for their absorption.

The peptones transformed in the stomach from nitrogenous alimentary principles are highly soluble and diffusible. Milk is better suited to the conditions of intestinal catarrh than any other nitrogenous food. It is palatable, relieves the thirst, and can be taken for a long time without {691} aversion. By removing the cream, the fat, which would require intestinal digestion, is partly got rid of. Skimmed milk does not produce a feeling of distaste and what is called biliousness, as does milk unskimmed. In cases where there is gastric catarrh the milk can be made more digestible by adding an equal quantity of barley-water or rice-water. The casein is then more slowly acted on by the gastric juice and more thoroughly digested. Milk should be given in small quantities at short intervals, as in this way the stomach performs the entire work more thoroughly. If a large quantity is given, a portion of it passes into the intestine unaltered. Buttermilk contains less fatty matter than skimmed milk, and is a pleasant substitute for it. Koumiss, if it could be properly prepared, would be an excellent food for diarrhoea. Even the imperfect imitations are retained and digested when other aliments fail. The whey of milk contains lactin, salts, a little casein, and fatty matter. It may be made by adding to milk rennet, sherry or other wine, cream of tartar, tamarind-juice, or alum. Milk-whey is slightly nourishing, and is said to be sudorific; when prepared with wine it is a mild stimulant well suited to the cases of children.

Where it is desired to give as little work to the digestive organs as is possible, milk and other foods can be given already partly digested, as peptonized milk prepared according to the formulæ of Roberts and Fothergill.[46] Eggs are changed quickly in the stomach. Egg albumen is more easily digested by artificial gastric juice than by pancreatic extract (Roberts). A solution of egg albumen boiled in the water-bath is swiftly and entirely transformed by pepsin and hydrochloric acid. Raw eggs have been thought to be the most digestible, but Roberts found that a solution of egg albumen when raw was very slowly acted on by pepsin and acid, but after being cooked it was rapidly and entirely digested. Eggs are best given, therefore, boiled slightly at a slow heat; when an egg is plunged in boiling water the white sets hard, leaving the yelk soft. The albumen of the white and the yelk should be equally cooked throughout.

[Footnote 46: J. M. Fothergill, _Indigestion and Biliousness_, New York, 1881, p. 63 _et seq._ See also quote to article on CHRONIC INTESTINAL CATARRH.]

Beef-tea is said by the chemist to possess little nutritive value; practical experience convinces the physician that it supports life. Peptonized beef-tea may be substituted when thought best. Animal broths thickened with rice, barley, or with peptonized gruel, as advised by Fothergill, or with the addition of vermicelli, are valuable aids when the palate is capricious. Raw beef is not as digestible as when the tendinous and aponeurotic structures of the muscular fibre have been softened, disintegrated, and converted into the soluble and easily-digested form of gelatin by cooking.[47] Scraped raw beef, when the pulp is removed from much of the connective tissue, is easily digested by children as well as by adults.

[Footnote 47: Ibid., _op. cit._, p. 47.]

In most cases of acute intestinal catarrh the patient can be well sustained by a diet consisting of one or other of the aliments described. For the largest number milk alone--that is, skimmed milk or milk diluted with barley-water, rice-water, or Seltzer water--is all that is necessary to support strength during the attack. Although starch after deglutition is {692} acted on in the intestine only, it becomes desirable sometimes to give farinaceous food in some form or other; milk may be undigested and animal broths may become distasteful; the palate craves some change. In this case a blanc mange made after the formula of Meigs and Pepper is as well suited to adults as to children,[48] the proportion of cream and arrowroot being made larger for adults. Sago[49] and tapioca[50] can be tried to tempt the palate. The flour of the Egyptian lentil[51] is made into a gruel also. Most of the patent foods for infants and invalids contain starch in some form or other. Racahout is one of the pleasantest and best of these. Nestle's food contains baked biscuits of wheat flour ground to a powder. Liebig's food is made of wheat flour, malt flour, and a little bicarbonate of potassium. Revalenta Arabica is an attractive name for the flour of Arabian lentil with barley flour. Any of these may be advantageously employed in cases of some duration and in the later stages of convalescence.

[Footnote 48: Meigs and Pepper, _Diseases of Children_, Philada., 1870, p. 304.]

[Footnote 49: Put half an ounce of sago into an enamelled saucepan with three-quarters of a pint of cold water, and boil gently for an hour and a quarter. Skim when it comes to the boil, and stir frequently. Sweeten with a dessertspoonful of sifted loaf sugar. If wine be ordered, two dessertspoonfuls; and if brandy, one dessertspoonful.]

[Footnote 50: Half an ounce of the best tapioca to a pint and a quarter of new milk. Simmer gently for two hours and a quarter, stirring frequently; sweeten with a dessertspoonful of sifted sugar.]

[Footnote 51: Take three tablespoonfuls of lentil flour, a salt-spoonful of salt, and one pint of water. Mix the flour and salt into a paste with the water and boil ten minutes, stirring (_Food for the Invalid_, Fothergill and Wood, New York, 1880).]

The diet for convalescence should be controlled by the physician until the patient has been well for at least two weeks. Liquid preparations give place to fine hominy, corn meal or oatmeal porridge, with milk. Then bread or crackers may be given, the intervals between the meals increasing to three or four hours. Raw oysters, sweetbreads, tender rare steak or mutton finely divided and well masticated, rice, and ripe peaches, succeed the simpler diet. Much saccharine, starchy, or fatty food is to be avoided for at least two weeks after entire recovery.

When the indications derived from the study of the cause have been acted on, and the patient has been placed under a rigid discipline of rest and diet, the treatment of symptoms comes next in order.

In mild cases, where the cause has been irritating ingesta, diet may relieve the symptoms in a short time without medicine. If diarrhoea with slight colicky pains and flatulence continue after a few hours, a mixture holding in suspension subnitrate of bismuth, with five drops of the deodorized tincture of opium in each dose, or a pill of lead and opium, will suffice in a short time to give relief. In severer attacks the fever heat may mount to a high point, giving great distress to the patient. If a temperature of 103° to 104° F. is reached--which is not unusual in children--a warm bath is a sedative and antipyretic remedy, or a bath of 95° can be gradually cooled down to 75° or 65° F.--a procedure which will bring down the body-heat two or three degrees. A substitution for the bath is sponging with cool or cold water, to which vinegar or bay rum may be added; or towels wrung out of cold water can be applied to the trunk and extremities (Ringer) with a very happy effect.

Quinia can be used antipyretically in full doses, dissolved in dilute hydrochloric acid. Pills, especially the sugar- or gelatin-coated pills, {693} should not be given, as they irritate the mucous membrane whether they are dissolved or not. In diarrhoea quinia pills often pass unaltered.

Flatulence, eructations of gas, and borborygmi are controlled by strict diet according to the rules given. Bismuth subnitrate or subcarbonate unites with sulphuretted hydrogen and absorbs it. The alkalies, sodium and potassium bicarbonate, sodium hyposulphite, the aromatic spirits of ammonia, either relieve acidity or prevent fermentation and the development of gas. A satisfactory formula for the early stages of intestinal catarrh is one containing bismuth subcarbonate, sodium bicarbonate, aromatic spirits of ammonia in water or cinnamon-water. When the abdominal distension is great enough to be a cause of distress, external cold--dry cold--is the best, applied with a rubber bag filled with cracked ice or ice-water; it causes absorption of gas. Abdominal compression with a bandage may be of some service also. Mineral acids, especially the dilute hydrochloric acid, by affording aid to the digestion prevent acid fermentation.

Diarrhoea is the central symptom and the best standard by which to measure the intensity of the catarrh and its progress. But it is only a symptom, and the mind ought to be directed to the lesion and not to it. Having the cause in view, the object in all cases is to allay the inflammation. This done, the diarrhoea decreases, then ceases. Shall the effort be made to check the discharges, or shall they be allowed to continue? The evacuant plan of treatment has been advocated, on the ground that the purgative, by increasing intestinal secretion, relieves the congestion of the intestinal blood-vessels and leaves the membrane in a better state than before.[52] But inasmuch as a purgative only acts by bringing about an intestinal hyperæmia and catarrh, there is no good reason for, and many reasons against, treatment by evacuation.

[Footnote 52: Woodward, _op. cit._, pp. 727, 728.]

A preliminary purgative, as has already been stated, is necessary to expel undigested food and scybalæ, but for the purpose of increasing intestinal or biliary secretion and diminishing engorgement of the vessels this method is unsuccessful and unnecessary. When irritating substances have been removed (and this is done usually without the physician's aid by the spontaneous expulsive movements of the bowel) the effort to check the discharge and to give rest is one and the same. Opium is the one invaluable remedy which we cannot do without.[53] As little of it should be given as is necessary to relieve the intensity of the symptoms. The aim should not be to stop the pain and check diarrhoea, but to take the edge off the sharp agony and to lengthen the interval between the stools. Thus gradually the spasms of peristalsis cease, and there is a diminution, and finally cessation, of the fluid accumulation in the bowel. The diarrhoea is relieved entirely in a period ranging from an hour after the giving of the first dose to one week, according to the severity of the attack. Opium is given in pill form, in the deodorized tincture, Dover's powder, or one of the salts of morphia may be preferred. Any of these may be combined with antacid and antifermentative mixtures, relieving the colic, gaseous distension, and diarrhoea. If opium is combined with, {694} or followed by, evacuants, its effects are thwarted, and it might as well not be given at all.

[Footnote 53: The objections urged against opium, that it increases thirst and nervousness, causes a retention of fermenting products, produces opium intoxication, and that it is a routine practice to give it, and does not cure the inflammation, may be valid, but we cannot do without opium, nevertheless.]

It is the custom to combine astringents with opium, but in acute cases of short duration it is a question whether astringents do not do more harm than good. When good does come from the combination, it is the opium which acts promptly and decidedly. The astringent lags behind, and in cases of some duration and severity supplements the work of the active partner. Bismuth is classed under this head, although it is not an astringent. Its action is mechanical; much that is taken is passed from the bowel as the black sulphide, which appears as a black granular powder in the fluid stool. This is no proof that it may not have been of service in its transit.[54] After death, when large doses have been given, it has been found lining the whole intestinal canal.[55] The subnitrate or subcarbonate can be given in powder on an empty stomach in doses of five to twenty grains alone or in combination with opium, or it can be dispensed with alkalies in water. The enormous doses (one hundred and fifty to nine hundred grains daily), as given by Monneret, are useless or hurtful. The value of bismuth is based on empirical grounds only, but it is irrational to load the bowel with an insoluble powder which if retained must cause irritation. As the discoloration of the stools is an objection to bismuth when it is desired to study their character for diagnosis, oxide of zinc may be substituted for it, as the latter is an absorbent of acids and gases.[56] Gubler has insisted upon combining it with bicarbonate of sodium to prevent the formation of the irritating chloride of zinc in the stomach.[57] One of the oldest and most popular remedies tor diarrhoea is lime in the form of the carbonate or lime-water. The officinal mistura cretæ is perhaps more generally used for children than any other remedy. Lime-water is added with advantage to milk when given to adults as well as children. Carrara-water, made by dissolving the bicarbonate of lime with an excess of carbonic acid, is less nauseous than liquor calcis, and may be mixed with an equal part of milk.[58] Chalk and its preparations are less beneficial than bismuth as astringents, but may be used merely for their antacid effect.

[Footnote 54: Headland asserted that bismuth was insoluble, but it has been detected in the liver, in milk, in urine, and in the serum of dropsy by Orfila, Sewald, Bergeret, and Mayençon (_Materia Med._, Phillips, vol. ii. p. 81).]

[Footnote 55: Levick, _Am. Journ. Med. Sci._, July, 1858, p. 101.]

[Footnote 56: Bonamy, "Du Traitement des Diarrhées rébelles par l'Oxyde de Zinc," _Bull. gén. de Thér._, t. xcii., 1877, p. 251; also, J. Jacquier, _De l'Emploi de l'Oxyde de Zinc dans la Diarrhée_, Paris, Thèsis, 1878, No. 118.]

[Footnote 57: Gubler, _Principles of Therapeutics_, Philada., 1881, p. 25.]

[Footnote 58: Phillips, _Materia Medica_, vol. ii. p. 105.]

The sugar of lead is a valuable astringent, because unirritating and sedative to the mucous membrane. With opium in pill form, in doses of one to three grains, it checks diarrhoea if the inflammation has not lasted long and is not extensive. If there are cases where the bile is passed in quantity, it is especially called for, as it is the only astringent which diminishes the flow of bile.

The mineral acids--dilute hydrochloric, nitric, and sulphuric acids--are given with some success. The first aids gastric digestion, and in small doses with pepsin can be directed after food irrespective of other treatment. The great repute which it has enjoyed in the diarrhoea of typhoid is no doubt due to the improved digestion and assimilation {695} which follow its use. The acid principle is what is lacking in the gastric juice in fever and debility.[59] In all cases of intestinal catarrh rapidity of gastric digestion should be sought for. Nitric acid is of doubtful utility. Without an opiate in combination there is little reason to hope for any result from its use; all the suggested formulæ contain opiates.[60] Dilute sulphuric acid is thought to be more astringent than the others. If it has any efficacy, it is due to the local astringent or alterative effect by contact with the inflamed surface. Much testimony is to be found in its support in cases tending to become chronic and where astringents combined with opiates have failed after some days' trial. It should be administered in doses of five to twenty drops in the form of mixture with mucilage or some aromatic, as lavender and cardamom. An opiate should not be combined with it if it is desired to test it fairly. It would be called for when the stools are pale, abundant, watery, and alkaline.

[Footnote 59: Manassein, _Virchow's Archiv_, lv., 1872, p. 451.]

[Footnote 60: The favor in which nitric acid is held is due to the advocacy of nitrous acid by Hope ("Observations on the Powerful Effects of a Mixture containing Nitrous Acid and Opium in curing Dysentery, Cholera, and Diarrhoea," _Edin. Med. and Surg. Journ._, vol. xxvi., 1826, p. 35). Nitrous acid, the same as the fuming nitric acid of the shops, is a reddish-yellow fluid highly charged with nitrogen trioxide. Hope said that ordinary nitric acid did not produce the same effects, and yet nitric acid is now given with the belief that it is of service.]

Calomel is of ancient repute as a remedy in the early stages of diarrhoea. According to recent views, it acts as a sedative to the gastro-intestinal mucous membrane and checks fermentation. It should be given in small doses (one-twelfth to one-eighth of a grain to children, one-fourth to one-half of a grain to adults); it should not be continued for more than two or three days. In combination with Dover's powder it acts well, but it is doubtful which of the two remedies should receive the greater praise for the resulting improvement. A very small dose of the bichloride of mercury has been found beneficial by Ringer for clayey, pasty stools or straining stools containing slime and blood. His formula is--Hydrarg. bichloridi gr. j; Aquæ fluidounce x; a teaspoonful frequently during the day. The gray powder is not as much thought of now as formerly; it is not so good for the early stages of diarrhoea as calomel, but may be tried as an alterative when the stools are green and offensive.

In the vegetable materia medica there are many and ancient remedies. Tannin represents a large class, and there is nothing more than fancy in preferring to it kino, catechu, hæmatoxylon, or blackberry-root. Tannin is precipitated in the stomach as an inert tannate; gallic acid is to be preferred for this reason, and also for its pleasant taste and less irritating effect on the mucous membrane. It is well borne by children, even in large doses, when given with water and syrup. It is to be hoped that the unsightly and unsavory combinations of the astringent tinctures with chalk mixture will be soon given up. They are given chiefly to children, who are repelled by the sight, and still more by the taste, of such compounds. The syrup of krameria is the least objectionable, and catechu and krameria are made into troches which are sometimes available.

Ipecacuanha is said by Bartholow to be extremely serviceable in the diarrhoea of teething children with greenish stools containing mucus or blood. He prescribes it with bismuth and pepsin.

{696} Recently some favor has been paid to coto-bark and its active principle, cotoin. The latter is advised to be given in the following formula:

Rx. Cotoinæ, gr. j; Aquæ distillat. fluidounce iv; Alcohol, gtt. x; Syrupi, fluidounce j.

A tablespoonful every hour. Five to eight drops of the fluid extract of coto are given. It is said to have a speedy and certain effect in acute diarrhoea.[61]

[Footnote 61: Coto-bark was imported into Europe from Bolivia in 1873, and was called quinquina coto. Wittstein of Munich and Julius Jobst of Stuttgart made the first analyses (_Neues Repertorium für Pharmacie_, xxiv. and xxv.). Von Gietl (_idem_, xxv.) first concluded from experiments that it was of use in diarrhoea. Cotoin and paracotoin were separated by Jobst. It has been found successful in the treatment of diarrhoea in Germany and of cholera in Japan (Baelz, _Centralb. f. d. med. Wissen._, 1878, xvi. p. 482). Cotoin sometimes disturbs the digestion to a marked degree. Paracotoin may be used hypodermically.]

Salicin,[62] ergot, guarana, have all been spoken of by enthusiasts as possessing valuable properties in diarrhoea.

[Footnote 62: Lawson, "Diarrhoea and its Treatment at the London Hospitals," _Med. Times and Gaz._, vol. ii., 1868, p. 122; Bishop, "Salicin in Diarrhoea and Dysentery," _Southern Med. Rec._, vol. iv., 1874, p. 585; "Comparative Value of Opium and Salicin in Diarrhoea and Dysentery," _Detroit Review of Med. and Pharm._, vol. x., 1875, p. 387.]

Alum is not often prescribed. Sulphate of copper is fitted for cases in danger of passing into the chronic stage. Sulphate of zinc might be more generally ordered than is the case. The sulphate of iron and the fluid preparations of iron--tincture of the chloride, solution of the pernitrite, and persulphate--are astringents, and could be tried if other remedies fail. The effect of nitrate of silver is to constrict vessels, to coagulate and disinfect excretions, and to form an adherent protecting membrane (Phillips). It occupies the next place to lead, and is suited to a subacute stage when acute symptoms have subsided. It is warmly recommended by William Pepper and others.[63] The oxide of silver has been preferred by some writers.[64] For the protracted diarrhoea of children, in whom follicular ulcers form so rapidly, the nitrate of silver is of special value. To adults it is administered in a pill freshly made in doses of one-eighth to one grain. A solution in distilled water with syrup answers well for children, the dose varying from one-twentieth to one-fourth of a grain.

[Footnote 63: J. Maggregor, "On the Internal Use of Nitrate of Silver in Inflammation of the Intestines," _Lancet_, 1841, vol. ii. p. 937.]

[Footnote 64: Lane, _Med.-Chir. Rev._, July, 1840, p. 289 _et seq._; Eyre, _The Stomach and its Difficulties_, London, 1852.]

The theory of the germ origin of diarrhoea has naturally brought into notice antiseptic remedies. Carbolic acid,[65] creasote,[66] naphtha,[67] sulpho-carbolate of calcium,[68] salicylic acid,[69] and chlorine-water have each been advocated. Practice does not support their claim to be considered remedies for intestinal inflammation.

[Footnote 65: Habershon, _Lancet_, London, 1868, vol. i. p. 7; C. G. Rothe, _Berliner klin. Wochenschrift_, 1871, p. 527.]

[Footnote 66: _Southern Med. and Surg. Journ._, vol. ii., 1846, p. 583; _ibid._, vol. iii., 1847, p. 147; _London Med. Gaz._, vol. ix., 1849, p. 254; _ibid._, vol. xii., 1851, p. 235.]

[Footnote 67: _Gaz. des Hôpitaux_, 1849, p. 46.]

[Footnote 68: _Tr. Obstet. Soc. Lond._, vol. xii., 1870, p. 12.]

[Footnote 69: W. Wagner, _Kolbe's Journ. für prakt. Chemie_, Bd. xi., 1875, S. 60.]

{697} Treatment by the rectum may be employed when medicines are rejected by the stomach or when it is desired to bring the drugs into more direct contact with the inflamed colon. Opiates, astringents, and alteratives are employed in this way. Laudanum in two to four ounces of warm water or in warm milk or starch-water can be thrown into the rectum, the fluid being allowed to remain. The injections are to be given often enough to relieve pain and lessen the number of discharges. With the laudanum, or without it, the mineral astringents can be used by enema. Acetate of lead or sulphate of zinc is to be preferred. The objection that but a small portion of the inflamed surface is reached by the fluid is a valid one, and therefore those cases are most benefited where the catarrh is in the lower colon and rectum. Ringer[70] says that it is not at all necessary for the fluid to reach that part of the intestine which is the seat of the catarrh; the impression made on one part is communicated to the other by sympathy. It was the practice with O'Beirne,[71] Hare,[72] and others to inject fluid by a long flexible tube passed beyond the sigmoid flexure. This method is advocated and employed in Europe by Mosler, Winterinz, and Monti. Quite recently Dulles has drawn attention to irrigation of the large intestine as a means of treating inflammation of the colon, according to the plan of Alois Monti of Vienna.[73] Henoch has tried with partial success in children the throwing into the rectum of a large quantity of water holding in solution acetate of lead, alum, or tannin. His method contemplates medication above the sigmoid flexure; a part of the fluid escapes, while the rest remains five or ten minutes in the bowel.[74] Monti says as much as two pints can be injected into the bowel of a nursing child--for older children twice this quantity.

[Footnote 70: _Therapeutics_, New York, 1882, p. 99.]

[Footnote 71: _New Views of the Process of Defecation_, Washington, 1834, p. 85.]

[Footnote 72: E. Hare, "On the Treatment of Tropical Dysentery by means of Enemata of Tepid Water," _Edin. Med. and Surg. Journ._, vol. lxxii., 1849, p. 40.]

[Footnote 73: Dulles, "Irrigation of the Colon," _Philada. Med. News_, Aug. 19, 1882, p. 199. The patient is placed on the side, back, or on belly, with the hips elevated. A large flexible catheter if a child, a stomach-tube if an adult, is inserted into the rectum. The tube is connected with a reservoir of water elevated above the patient. The rectum is first distended with water, and the tube is gradually made to follow the course of the bowel until it finds its way into the descending colon. Thus the water may be made to distend the whole of the colon to the cæcum. The fluid remains from a few minutes to half an hour.]

[Footnote 74: Henoch, _Diseases of Children_, Am. ed., New York, 1882, p. 206.]

Messemer[75] reported three cases (one child and two adults) treated in this way with the most striking success. His object at first was to cleanse the rectum, but warm water did not check the diarrhoea. Cold water was tried, and (probably by reflex influences) diminished rapidly the number of the discharges. And Ewald[76] has imitated Messemer's method with results which are surprisingly good. He injected 200 and 300 cc. of cold water, which was expelled by pressure on the abdomen; 50 cc. were then thrown in and allowed to remain. He has used the treatment in a large number of cases in children. The question as to the ability to force water thrown into the rectum through the sigmoid flexure and distend the colon has been settled by the experiment of Mosler in a case where there was a cæcal fistula. Water injected into the {698} rectum traversed the colon and escaped through the fistula in two minutes.[77]

[Footnote 75: J. B. Messemer, "Cold-Water Enemata as a Therapeutic Agent in Chronic Diarrhoea," _American Journal of the Med. Sci._, vol. lxxvi., 1878, p. 133.]

[Footnote 76: _Lectures on Digestion_, New York, 1881, p. 149.]

[Footnote 77: _Berlin. klin. Woch._, No. 45, 1873, p. 533. Woodward, in discussing the claims of Battey of Georgia to priority in the discovery of the permeability of the entire alimentary canal by enema (see paper by Battey in _Virginia Med. Monthly_, vol. v., 1878, p. 551), quotes from A. Guaynerius, who lived in the fifteenth century, from J. M. de Gradibus (1502), Sennertus (1626), and from others among the older writers to show that it was well known that suppositories and enemata introduced into the rectum are sometimes thrown up by the mouth. He mentions experiments by Alfred Hall (1845), G. Simon (1873), and F. Köster (1874) which demonstrated that large quantities of water may be forced from the rectum into the stomach. (See Woodward, _op. cit._, foot-note, p. 836.)]

When ulcers are thought to be present, the remedies of particular value are nitrate of silver, bismuth or turpentine, and the mineral acids, given in conjunction with a rigid system of diet.

In hemorrhagic diarrhoea ice externally or ice-water injections, opium, acetate of lead in large doses (ten to fifteen grains), gallic or tannic acid, and ergot are the appropriate remedies.

Some modifications of treatment are required for the choleraic form (in children, cholera infantum); the danger here is imminent from the drain of water and collapse. For the vomiting of the early stages, pounded ice eaten freely, potassium or sodium bromide in ice-water, and counter-irritants over the abdomen, with cold sponging or cold baths and ice to the head if there is much body-heat. Brandy, whiskey, or coffee in full doses is called for early. Iced coffee can be given to children. Spirit of camphor in five-drop doses every ten minutes aids in averting collapse. Small doses of calomel every hour or two may benefit nausea and vomiting. Arsenic is said to do well for vomiting and profuse watery diarrhoea. For adults, morphia hypodermically is perhaps the best remedy for the vomiting and purging; even for children, minute doses given in this way are best for alarming illness. Hypodermic injections of ether have also been suggested.

For the relief of duodenitis means are used to relieve the digestion of the want of the biliary and pancreatic secretions. Nitrogenous food is to be taken, but no fats or starch. Counter-irritation over the epigastrium and right hypochondrium by a blister or iodine is of direct service. If icterus accompany duodenitis and catarrh of the bile-ducts, all treatment must be directed to the duodenum. For ileo-colitis and colitis the rules already given apply.

{699}

CHRONIC INTESTINAL CATARRH.

BY W. W. JOHNSTON, M.D.

ETIOLOGY.--Chronic intestinal catarrh has many of the same causes as the acute form; it is the expression of a large number of different pathological states and complicates many general and local diseases.

It is very common in children under two years of age, and is associated with change in diet in weaning and with the irritability of all the tissues during dentition. It is also a frequent disease in old persons, being due to imperfect mastication, the weakness of digestion, portal congestion, the gouty diathesis, and other causes.[1] Men have the disease more frequently than women. Hereditary influence and idiosyncrasy predispose to chronic catarrh of the bowel as to catarrh of the bronchi. Bad hygiene, want of cleanliness with an unhealthy condition of the skin, constant breathing of foul air due to want of proper ventilation, animal decomposition, or overcrowding predisposes to chronic diarrhoea. The chronic diarrhoeas among soldiers in camps,[2] among the inmates of prisons, workhouses, and asylums, are examples of these influences. Overwork, especially mental overwork with anxiety, and privation of sleep act in the same direction. In the chronic constitutional diseases and in many chronic diseases of organs diarrhoea sooner or later appears, and very generally is the immediate cause of death. In phthisis pulmonum, whether tubercular or not, simple catarrh of the bowel is nearly always present.

[Footnote 1: _La Diarrhée chez les Viellards_, Paris, Thèsis, 1865, No. 112. See also works of Durand-Fardel and Charcot and Loomis.]

[Footnote 2: According to the statistics prepared in 1871 by T. B. Hood of the U.S. Pension Office, chronic diarrhoea was the disease for which a pension was granted in 20 per cent. of all cases of disability from disease and in 75 per cent. of all the diseases of the digestive system (_Report of Commissioner of Pensions_, 1871).]

During the course of chronic Bright's disease, more frequently in the cirrhotic form, lesions are developed in the intestine which cause obstinate diarrhoea. The discharge of urea into the intestine, and its conversion into carbonate of ammonium, which acts as an irritant to the mucous membrane, is the reason of the diarrhoea in this disease, according to Luton and Treitz;[3] and in so far as the discharge represents the escape of urea by the bowel, it may be regarded as salutary. In gout, especially in old persons, periodical diarrhoea gives relief. Chronic gouty subjects assert that they are not benefited by colchicum until it has purged them. The {700} lithic-acid diathesis, pyæmia, septicæmia, scurvy,[4] diabetes, leucocythæmia, Addison's disease, and syphilis[5] have diarrhoea during some part of their progress. The malarial cachexia is often attended with a diarrhoea which quinia alone will relieve; this symptom may occur periodically or be constant.

[Footnote 3: A. Luton, _Des Séries morbides, Affections urémiques de l'Intestin_, Paris, Thèsis, 1859, No. 38, p. 45; also, Treitz, "Ueber urämische Darmaffectionen," _Prager Vierteljahrschrift_, Bd. 64, 1859, S. 143.]

[Footnote 4: See testimony as to the influence of scurvy in promoting diarrhoea (Woodward, _Med. and Surg. History of the War_, Part 2, Medical Volume, p. 638).]

[Footnote 5: A. Trousseau, "Comments on a Case of Syphilitic Diarrhoea cured by Mercury," _Clinique méd._, Paris, 1868, t. iii. p. 123.]

Disease of the liver, heart, or lungs, by retarding the circulation in the portal system, causes venous stasis and catarrh in the gastro-intestinal mucous membrane. The chief conditions which bring this about are tumors compressing the mesenteric veins, cirrhosis of the liver, tumors pressing on the ascending vena cava, valvular disease of the right and left heart, fatty degeneration or dilatation of the heart, cardiac debility from chronic exhausting diseases, fibroid phthisis, chronic pneumonic phthisis, chronic pleurisy, and pulmonary emphysema.

An unsuitable diet may not set up an acute catarrh, but may slowly induce changes of a chronic nature in the mucous membrane. This is the case in infants fed upon artificial food instead of breast-milk, or when the digestion is overtaxed after weaning. In adults food difficult of digestion and over-eating bring about the same result. Alcohol, spices, and condiments, if taken in excess, and the habitual use of purgatives, lead to chronic inflammation of the intestine.

Foreign bodies, such as fecal concretions, gall-stones, stones of fruit, bones, coins, and pins, by remaining in contact with the mucous membrane for a length of time, determine inflammation and ulceration.[6]

[Footnote 6: Lothrop, "Case of a Child in whom seventeen plum-stones, three cherry-stones, and seven small bones were impacted In the cæcum and ileum for a year. Inflammation, ulceration, and perforation of the bowel resulted" (_Buffalo Med. and Surg. Journ._, March, 1882, p. 346).]

Neglect in the treatment of acute catarrh, the prolongation of an acute attack, from its intensity and the incurability of the lesions, establish chronic disease.

All chronic lesions of the bowel are complicated with chronic catarrh, as chronic tubercular ulcer, neoplasms in the wall, pressure of a tumor from without, etc.

PATHOLOGICAL ANATOMY.--The alterations in the intestines in chronic catarrh involve the walls to a much greater extent than in the acute form.

The intestinal tube is dilated, contracted, or irregularly dilated and contracted. When the calibre is increased the walls are thinned. Hypertrophy and hardening of the tunics, chiefly of the muscular and submucous tissue, are accompanied by a narrowing of the canal, and this change, most common in the rectum and sigmoid flexure, sometimes involves a very considerable extent of the colon. Lebert records the case of a woman who had diarrhoea for six weeks; constipation and vomiting with abdominal tenderness ensued. There was hypertrophy of all the coats of the stomach and of the ascending colon and rectum. The rectum was so narrowed by the thickening of its wall that a female catheter could not be passed through it.[7] In chronic catarrh the mucous membrane {701} of the colon and of the lower part of the ileum is the seat of the most characteristic lesions. The colon was alone the seat of disease in 9 out of 99 cases analyzed by Woodward; in the remaining 90 the two were involved together. In these the lesions in the colon (especially in the rectum and sigmoid flexure) were always more advanced and more serious than in the small intestine.

[Footnote 7: Lebert, _Path. Anat._, t. ii. pp. 247, 248; another case, Laboulbène, _Anat. path._, Paris, 1879, p. 194.]

Gastric catarrh may by extension become duodenal catarrh, and from the duodenum the disease may extend into the common bile-duct and its branches. The duodenitis and catarrh of the ducts may persist, and become chronic after the stomach lesion is gone.

The mucous lining of the intestine is changed in color, form, thickness, consistence, and in the appearance of its glandular structures. The shades of color in chronic inflammation are dark red, livid, brown, drab, or slate-color, light blue, and greenish. The coloration is not uniform. Dark-red and gray spots are seen on a pale and uniform red ground; grayish streaks and patches are mingled with red or whitish areas, giving rise to a mottled or marbled appearance.[8] In some cases red predominates, in others the slate-color.[9] Dark-brown, almost black, patches are also seen. These different tints depend upon the intensity and character of the inflammation and the stage which it has reached. Diffused bright-red discolorations belong to acute inflammation, and are rarely seen in the chronic form. Acute hyperæmic patches appearing in the midst of a slate-colored membrane indicate intercurrent acute attacks. Dark-red streaks or spots are caused by extravasations. Brown and slate-colored areas represent the changes in old extravasations or pigment-deposits where inflammation or ulceration has existed. Where the inflammation is progressing toward the destruction of tissue the membrane is dark-purplish or black in color, mottled with patches of dull reddish hue and minute spots of bright red. Black dots are seen in the small and large intestine isolated or in close proximity. They are due to minute specks of black pigment deposited in the apices of the villi, in the centres of solitary glands, in rings around them, or in the glands of a Peyer's patch. The juxtaposition of pinhead black points gives rise to the shaven-beard appearance[10] of the mucous membrane. Dark streaks or wavy lines of pigment are also seen.[11]

[Footnote 8: For illustration of color of mucous membrane in chronic inflammation see the following illustrations in color: _Med. and Surg. Hist. of the War_, Part 2, Medical Volume--plates facing pp. 308, 518, and 520; also, _Illustrations of Morbid Anatomy_, J. Hope, London, 1834, figs. 128, 129.]

[Footnote 9: For an excellent illustration of slate-color of chronic inflammation, with supervening acute inflammation and hemorrhagic patches, see Carswell, _Path. Anat._, Plate ii. fig. 4; also, Lebert, _Path. Anat._, t. ii. Pl. cxiv. fig. 7.]

[Footnote 10: For an excellent illustration of this change see _Med. and Surg. Hist. of the War_, volume cited, plates facing pp. 298, 304; also, _Atlas d'Anatomie path._, Lancereaux, Paris, 1871, Pl. iii. figs. 3 and 4.]

[Footnote 11: See colored plates _Med. and Surg. History of the War_, volume cited, facing p. 308.]

In the ileum the mucous folds are obliterated or swollen and thickened. Obliteration of the folds occurs in connection with a dilated intestine; when the intestine is contracted they are elevated, tortuous, and close together. The villi are hypertrophied, looking often like minute polypi. The mucous coat is usually thickened, measuring from one-fifth to one-fourth of an inch. It is softened, and more easily scraped off,[12] but quite {702} frequently there is induration instead of softening. The solitary glands of the ileum are hypertrophied and appear scattered over the mucous surface as small rounded elevations. They are quite numerous or a few only may be seen. A ring of vascular injection usually surrounds each enlarged follicle. Peyer's patches may be unchanged or from swelling of the follicles are more prominent than is normal, but relatively the enlargement of the solitary glands is greater. In chronic catarrh the follicles acquire greater size than in the acute form. The apices of the solitary glands in the small intestine may be broken down, leaving small follicular ulcers, with swollen rings around them formed of the undestroyed and hypertrophied gland-structure. Here and there one or two of the follicles in the Peyer's patch may have its centre indented by ulceration. These changes are usually in the lower part of the ileum near the cæcum.

[Footnote 12: The mucous membrane is often tumefied and softened in cases where there are thickening and contraction of the intestine with great reduction of its calibre (Elliot Coues, _Med. and Surg. Rep._, Philada., 1863, vol. x. p. 207).]

In the colon the enlarged solitary glands are in greater number, and are dotted about more closely in the descending colon and sigmoid flexure.[13] When there is ulceration the large intestine has many more ulcers than the ileum, and they are more numerous in the lower part of the colon. They appear as sharply-punched openings, and give to the mucous surface a honeycombed look; their diameter varies from one-tenth to one-fourth of an inch. Large ulcers formed by the confluence of smaller ones measure from one-fourth to one inch in diameter; they may be so deep as to have the muscular tunic for their base, and quite often the bottom of the ulcers is black. A ragged or uneven appearance is given to the surface by the ulcers being close together. Such extensive destruction sometimes takes place that no normal mucous membrane seems to be left. Perforating ulcers are occasionally seen in the large intestine or ileum. Perforation occurred in two of Woodward's ninety-nine cases. Healing ulcers[14] are found by the side of others which are growing. Healed follicular ulcers are known by a puckered, stellated appearance[15] of the mucous membrane, which is pigmented and of a slate-gray or marbled-brown color[16] if the process has been long completed. Larger dense cicatrices, pigmented also, mark the site of more extensive ulcerations.

[Footnote 13: Illustration, _Kupfertafeln zu_ DR. LESSER _über die Entzündung und Verschwärung du Schleimhaut des Verdauungskanales_, Berlin, 1830, Bei Enslin, Tab. ii. fig. 4.]

[Footnote 14: Illustration, J. Hope, _Illustrations of Morbid Anatomy_, figs. 168, 169.]

[Footnote 15: Illustration, _Med. and Surg. Hist. of the War_, _tom. cit._, p. 528.]

[Footnote 16: Illustration, Cruveilhier, _Anat. path._, xxx. livraison, Pl. iii.; also, J. Hope, _Illustrations of Morbid Anatomy_, figs. 128, 129.]

Besides follicular ulcers the mucous membrane is disorganized by ulcers which have their origin in a loss of epithelium and superficial erosion. These deepen and may attain considerable size.

In addition to the lesions already described, the inflamed and ulcerated surface is sometimes covered with a pseudo-membranous layer of greenish-yellow color.

Chronic catarrh of the duodenum is the cause of dilatation of the vessels and thickening of the coats. A varicose condition of the veins may give rise to hemorrhage without ulceration.[17] The orifice of the common bile-duct and the ducts for some distance are narrowed by swelling of their lining membrane.[18] Ulcer of the upper part of the duodenum {703} is found rarely in connection with external burns and chronic Bright's disease. It is more common in men between thirty and forty years of age. An embolized artery is the starting-point of the lesion. The mucous layer, deprived of its nutrition in a limited area, dies or is destroyed by the acid gastric juice; a round ulcer with terraced edges is left, its base being the muscular or serous coat. Adhesions may form between the peritoneum near the ulcer and the liver, gall-bladder, or pancreas, or an opening may take place posteriorly in the right seventh intercostal space or into the peritoneal cavity. Cicatrization of the ulcer may lead to narrowing of the canal of the bowel or of the pancreatic and common bile-ducts.[19]

[Footnote 17: G. Coulon, _Bull. de la Soc. Anat. de Paris_, 1879, p. 690.]

[Footnote 18: Duodenitis was made much of by Broussais and his followers, and a great deal has been written about it. (See Boudin, Paris, Thèsis, 1837, No. 76, _Essai sur la Duodenite chronique_.)]

[Footnote 19: _Ziemssen's Cyclopædia_, Amer. ed., vol. vii. p. 404.]

Suppuration in the wall of the duodenum is still rarer. One case only is on record of pus being found in the intestinal wall.[20]

[Footnote 20: Picard, _Bull. de la Soc. Anat. Paris_, t. xv., 1840-41, p. 393. See also microscopic view of suppuration in wall of duodenum, Thierfelder, _Atlas d. path. Histologie_, 2 lief., Tab. x. fig. 6.]

Chronic proctitis or inflammation of the rectum may exist by itself. The mucous membrane is swollen, hyperæmic, and the walls may be indurated and thickened so as to reduce the calibre of the tube. Superficial erosions or deep ulcers and perforation are due to the retention of hard fecal matter in the distended pouches of the rectum. Inflammation in the tissue around the rectum (periproctitis) is excited by inflammation of the wall without perforation; abscesses form and burst externally or into the bowel, thus establishing fistulæ.

PATHOLOGICAL HISTOLOGY.--The essential primary feature of chronic catarrh is the increase and persistence of cell-accumulation in the reticular connective tissue of the mucous and submucous layer. After an acute or subacute attack some time elapses before the large number of cell-elements are disintegrated or absorbed. By remaining they offer a constant invitation to causes of irritation, hence the necessity for prolonged care in diet after acute attacks. Fresh causes--imprudence in eating, etc.--induce additions to the number of cells, and the tissue becomes overcharged with active elements of growth. Hypertrophy of tissues results, the mucous and submucous tissues thicken, and the glandular structures are stimulated to a condition of morbid activity. The glands of Lieberkühn elongate, the number of acini increases, and the contained cells multiply. Accidental closure of the gland-openings from outside pressure or over-accumulation of the contents leads to cyst-formations. The lymph-cells in the reticular tissue of the closed follicles undergo rapid increase; the follicle is over-distended, projects above the surface, bursts, and a small ulcerating cavity is left. This is now enlarged by the breaking down of the remaining tissue of the follicle, then of the submucosa. The overhanging roof of mucous membrane, deprived of its nutrition, sloughs off at the edges and the exposed ulcerated surface is increased. By the confluence of two or more burrowing ulcers more extensive destruction of the mucous and submucous layers is brought about. The large deepened ulcers have the mucous layer for their base. Cicatrization of the ulcers takes place by the formation of cicatricial tissue at their base; the excavation is filled up partially, by contraction the edges are brought together, and the tissue solidifies. No villi or epithelium covers these cicatrices.

{704} There are rarer pathological changes. In catarrh of long duration cysts are found, especially in the large intestine. They are about the size of a small pea, projecting above the mucous surface. They have a yellow or amber color, and contain a jelly-like yellow fluid which can be pressed out. They originate in the distension of the dilating glands of Lieberkühn; according to Woodward, they find a favorable nidus for their growth in the softening tissue of the solitary glands; hence the cystic forms are seen occupying the interior of follicles undergoing disintegration.[21] The presence of the glands of Lieberkühn in the interior of the closed follicles has been observed by other pathologists, some of whom are unable to explain so remarkable a lesion.[22] Around the edges or in the midst of healing ulcers in the intestine granulation-like excrescences or polypoid growths are observed as a rare lesion. These seem to be projections from undestroyed islands of mucous membrane, being surrounded by the ulcerated surface. The minute polypi originate in a process of growth of the undestroyed mucous tissue. Cicatricial contractions around their bases give them peculiar forms; they are club-shaped, simple, or branched. This lesion has been described by Johann Wagner,[23] Carl Rokitansky,[24] and J. J. Woodward[25] from original specimens. According to Woodward, the growths (pseudo-polypi he calls them) are composed of a central portion of connective tissue continuous with the submucous connective tissue of the intestine and a peripheral portion of diseased mucous membrane. The central connective tissue was filled with large and numerous cells, and the glands of Lieberkühn in the mucous covering were elongated and branched and showed evidences of an active hyperplasia.

[Footnote 21: J. J. Woodward, _op. cit._, pp. 570, 571.]

[Footnote 22: A. Laboulbène, _Anat. path._, Paris, 1879, p. 186.]

[Footnote 23: "Einige Formen von Darmgeschwüren; iii., die Dysenterische Darmverschwärung," _Med. Jahrb. des k. k. öst. Staates_, Bd. xi., 1832, S. 274.]

[Footnote 24: "Der dysenterische Prozess auf dem Dickdarme und der ihm gleiche am Uterus, vom anatomischen Gesichtspuncte, beleuchtet," _ibid._, Bd. xxix., 1839, S. 88.]

[Footnote 25: "Pseudo-polypi of the Colon," _Am. Journ. Med. Sci._, Jan., 1881, p. 142.]

Polypi of the colon have been seen and figured by other pathologists, but they were not connected with ulceration and cicatrization of ulcers. Luschka[26] saw the mucous membrane from the ileo-cæcal valve to the end of the rectum covered with polypi, club-shaped, the size of a hempseed or bean, and made up of glandular tubes simple or branched. Other cases have been described by Lebert, Heuriet, and others,[27] in which polypi were distributed in the rectum, colon, cæcum, or about the ileo-cæcal valve. This is the condition described by Virchow as colitis polyposa.

[Footnote 26: _Virchow's Archiv_, vol. xx. p. 133.]

[Footnote 27: Heuriet, _Bull. de la Soc. Anat. Paris_, t. xlviii., 1873, p. 250; _Tr. N.Y. Path. Soc._, vol. ii., 1877, p. 172. For illustration of multiple polypi of colon and rectum, Lebert, _Path. Anat._, tome ii., Pl. cxxii. figs. 1 and 2; granular elevations in ileum, _idem_, Pl. cxxi. fig. 1. Also, mucous polypi of rectum, Thierfelder, Tab. xiii. figs. 3, 3_a_, 3_c_; also, intestinal polypi of rectum, Lancereaux, _Atlas Path. anat._, 1871, Paris, Pl. iv. fig. 4. Polypi are rarely seen in the small intestine; see Böttcher, "Polypöses Myom des Ileums," _Archiv der Heilkunde_, xi. Jahrgang, 1870, p. 125.]

Atrophy of the wall of the intestine, chiefly of the mucous layer, supervenes upon catarrh. It is confined to certain areas, the rest being normal or in a state of chronic catarrh. It is found in 80 per cent. of the cases examined either in the large or small intestine. The cæcum is the most frequent seat; next in the order of frequency it is seen in the ascending {705} colon, the lower part of the ileum, the other parts of the colon, and is least common in the upper part of the ileum. In children the lesion is more common in the small intestine than in adults. The changes in the mucous membrane of the colon are a diminution in its thickness and disappearance of the glands of Lieberkühn. The mucous layer is reduced to one-fifth of its normal size, and no trace of the glands may be left; a layer of connective tissue with imbedded round cells is all that remains. The surface of the membrane is irregular and colored with yellowish pigment. In the ileum the villi are shrunken, with few cells; in some cases they disappear altogether. The muscular tunic may share in the atrophy.[28]

[Footnote 28: Nothnägel, "Zur Klinik der Darmkrankheiten," iii. Abtheilung, Darmatrophie, _Zeitschr. f. klin. Med._, Berlin, 1882, iv. p. 422; Virchow, "Ueber den Gang der amyloiden Degenerationen," _Virchow's Archiv_, Bd. viii. S. 364; E. Neumann, "Neue Beobachtungen über amyloide Degeneration," _Deutsche Klinik_, Bd. xii., 1860, S. 337, 353, and 373; Lambl, "Ueber amyloide und colloide Degeneration im Allgemeinen und die des Darmsinsbesondere," _Beob. und Studien_ (_aus dem Prager Kinder-Spitale_), Prag., 1860, S. 319; Frerichs, "Diseases of the Liver," New York, 1879 (_Wood's Library_), vol. ii. p. 180; M. G. Hayem, "Note sur la Dégénérescence amyloide du Tube digestif," _Compte Rend. des Séances de la Soc. de Biologie_, Nov., 1865, 4me Série, t. ii. p. 191; also, _Gaz. méd. de Paris_, t. xxi. p. 99.]

Lardaceous (amyloid or waxy) degeneration of the intestinal mucous membrane is met with in chronic catarrh. The small arteries of the villi and submucous layer, the muscular and other tissues, are infiltrated with a new material allied to fibrin. The membrane to the eye is paler than normal. When iodine is applied, a characteristic red staining of the infiltrated parts is noticed. This lesion is a cause of diarrhoea and of hemorrhage,[29] from the greater permeability and greater fragility of the arteries. It is also associated with follicular ulceration, and is probably a cause of disintegration of the mucous membrane.[30]

[Footnote 29: T. Grainger Stewart, "On Hemorrhage from Waxy or Amyloid Degeneration," _Br. and Foreign Med.-Chir. Rev._, vol. xli. p. 201.]

[Footnote 30: Frerichs, "Diseases of the Liver," New York, 1859 (_Wood's Library_), vol. ii. p. 180; also, E. Aufrecht, _Berl. klin. Woch._, 1869, p. 315.]

The abdominal organs present other lesions in chronic intestinal catarrh, few of which have any distinctive character. The peritoneum shows signs of old or recent inflammation. The former is subacute or chronic, and is recognized by the adhesions of opposed surfaces in a limited area, frequently corresponding to the seat of intense intestinal inflammation. Fatal perforations are delayed or prevented by these adhesions. General peritonitis with soft lymph or sero-purulent effusion is found with perforation. The mesenteric glands may be enlarged. The liver is larger or sometimes smaller than normal, and its tissue is softened and may be fatty. Abscess of the liver[31] is a very rare result of chronic intestinal catarrh, with ulceration. The gall-bladder is usually filled with bile. The spleen is small and firm in texture; less commonly it is soft and friable. The pancreas is healthy. The kidneys are large and pale; the cortical substance is relatively increased and the tubules contain granular epithelium.

[Footnote 31: It occurred in 4 per cent. of Woodward's cases of chronic follicular ulceration. See case reported by the writer in which the ulcers healed before the death of the patient from hepatic abscess (_Maryland Med. Journ._, March 15, 1883, p. 562).]

In the thorax the heart is flabby, pale, and small; clots are found in the right and left side extending into the pulmonary artery and aorta. Sudden death has been attributed to cardiac thrombosis. That coagula {706} do form in the heart during life is shown by the sudden occurrence of cerebral embolism with aphasia.[32]

[Footnote 32: The writer has seen one case of this kind occurring during the effort at stool in a patient who was very feeble and very anæmic from chronic intestinal inflammation with ulceration.]

Pneumonia is the most frequent pulmonary lesion; it may be single or double. It was found in 18 of the 99 cases of Woodward, and in 21 out of H. A. Allen's 41 cases. Inflammation of the pleura is not infrequent. The brain and its membranes may be congested, and fluid is found in the subarachnoid space, in some instances in cases which have had a sudden termination. The cornea is ulcerated, and the eye destroyed by opening of the anterior chamber in a small proportion of cases. The sloughing process begins in the lower part of the cornea and in the sclerotic.

SYMPTOMS.--When chronic intestinal catarrh succeeds the acute form, the transition is marked by the disappearance of fever and an amelioration of all the symptoms, with apparent recovery. The patient begins to go about, but diarrhoea returns whenever there is any unusual fatigue or excess in eating. In some cases there is no improvement in the diarrhoea, but in the general symptoms only. When the malady is chronic from the beginning, the onset is characterized by symptoms of indigestion and occasional diarrhoea, which become more and more pronounced according to the severity of the illness.

Mild forms of catarrh have constipation, or diarrhoea alternates with a normal or constipated state of the bowels. The form in which constipation is continuous is associated with mechanical stasis from liver and heart lesions and with the gouty and uric-acid diathesis. The mucous membrane is in a state of passive hyperæmia, an excess of mucus being the product of the inflammatory process. Mucus coats the lining tunic, lessens its irritability, interferes with digestion and absorption, and acts as a ferment, exciting decomposition in the food. The bowel is atonic and is distended with contained gas; there is great feebleness of peristaltic contractions.

Intestinal indigestion and constipation are therefore the symptoms of this form. The signs of indigestion occur one to three hours after eating, according to the location of the maximum of catarrh and the time taken by the food to reach this point. They are a sense of fulness or distress in the abdomen from gaseous distension, slight colicky pains, and a rumbling of gas, which may be prolonged during several hours after a meal. The constipation is indicated by the spontaneous passage of dry masses or scybalæ coated with layers of mucus which are clear or cloudy, or the mucus may be intimately mixed with solid matter. Pure mucus is also expelled without fecal matter. There may be no stool without a purgative, and then softened matter with scybalæ and mucus is passed. Altered mucus in the form of membraniform shreds or cylinders occasionally pass in the so-called membranous enteritis.

The abdomen is full and not sensitive to pressure. The tongue is coated and usually pale and flabby. In appearance the patient exhibits a general want of tone; the skin is white or muddy, the muscles are soft, and the expression indicates the depression of spirits, the lassitude, and the inertia which he feels. Hemorrhoids are very likely to {707} exist. Such a condition may last for months or years without much change. Under proper treatment recovery may take place, but if entirely neglected or improperly treated the disease inevitably becomes worse.

In a second mild form there is no permanent disease, only an impressionability of the mucous membrane of the bowel to causes which induce hyperæmia and excessive secretion ending in diarrhoea. Exposure to cold, fatigue, or slight indiscretions in diet may bring it on; even an emotional cause may do it. The attacks last one or several days, and may at times assume some gravity. This predisposition to diarrhoea lasting through a lifetime is analogous to the tendency to inflammation of the nasal and other mucous membranes.

In severer and typical forms the symptoms point to permanent lesions. The tongue is smooth, shining, or glazed, sometimes with a central brown streak, but it may be also pale and covered with a white coat. The appetite is diminished or lost, or it is capricious, craving unsuitable food. If there is no gastric catarrh, the chief distress does not come until some hours after eating, but the taking of food sometimes excites pain and brings on an evacuation of the bowels through reflex influence.

There may be slight tympanites or a retracted abdomen. The imperfect digestion of food and the fermentation of the intestinal contents develop gas which keeps the abdomen distended and causes slight pains and borborygmi. Pain may, however, be entirely absent. A feeling of abdominal soreness is not unusual; it is increased by coughing, sneezing, or any sudden movement. Sensibility to pressure is usually wanting; when it exists it is found along the line of the colon in most cases.

The diarrhoea is the characteristic symptom. The number of the stools varies from one to eight in twenty-four hours; four is about the average number. They occur usually in the early morning hours, from two to six o'clock, but food may at any time bring on peristaltic contraction, so that a motion after every meal is not uncommon. In quantity there is much variability; two to four ounces of fluid matter is the rule perhaps, but a very much larger amount than this is often passed with each evacuation. As a rule, the larger the quantity of fluid the more extensive is the catarrh and the more advanced are the lesions. The matters passed are composed chiefly of fecal matter varying in consistence from a solid or semi-solid mass to a watery fluid. In the soft stool, like thickened gruel, the consistence is due to the presence of mucus; in the thinner evacuation water is the chief element. Liquid stools are sometimes frothy. In color the dejecta are brown, yellow, red, green, slate-color, or white. They may be colored dark by medicines, as iron or bismuth, or by blood. The presence of blood gives a pinkish, bright-red, dark-brown, or black color, depending upon the amount of blood and the changes it has undergone in the bowel from a longer or shorter retention. Blood, when it comes from the rectum, is in bright-red streaks or small coagula. When its source is higher up, it is much altered, being dark and granular. Coffee-ground sediment in a fluid stool is blood from the upper part of the intestine or stomach. The spreading of an ulcer may open a vessel of some size, and a fatal hemorrhage follow. A yellow tint like that of a child's movement may arise from a mixture of pus and fecal matter. Pus, as a milky or creamy fluid which may be {708} streaked with blood, is a frequent appearance in disease of the rectum and sigmoid flexure. The odor of the stools is fecal, sour, or sickening from fermentation or offensive from decomposition. In bad forms of chronic diarrhoea in children the black watery stools have a most offensive odor.

Mucus is the most constant ingredient of the diarrhoeal stool, and is in itself a sufficient evidence of catarrh, as it is not seen in normal stools except as a temporary phenomenon. It is present in flakes in watery evacuations, giving a jelly-like character to the fluid if it is in excess, or it is mixed with semi-solid feces. Pure mucus may be passed, if the catarrh is low down, in clear, glairy, or opaque masses. The frog's-egg or boiled-sago particles supposed by Niemeyer and others to point to follicular ulceration, and by Traube to be the swallowed bronchial secretion, are said by Virchow to be partly-digested starch, and also by Nothnägel to be of vegetable nature.[33] The stools may contain small yellow or brownish masses which are mucoid in nature, being yellow from bile-staining. Pavement epithelial cells are found in the coating of mucus around a hard fecal lump. Cylindrical epithelium is passed uncolored or stained with bile. These cells are separated, and are deformed and shrunken, with a granular protoplasm and indistinct nucleus. Goblet-cells are also seen. Round cells in the form of mucus-corpuscles or giant-cells are mixed with shreds of mucus or float in the thin stools. Crystals of triple phosphate, of neutral phosphate, oxalate of lime, and other lime salts, and of cholesterin, are also seen.

[Footnote 33: _Virchow's Archiv_, v. S. 329; Nothnägel, "Zur Klinik der Darmkrankheiten," _Zeitschrift für klin. Med._, iii., 1881, p. 241.]

Micrococci and bacteria have no pathological importance; they are seen in different diseases and in health.

Unaltered food may be expelled (lientery) by rapid peristaltic movements. But the microscope will detect what cannot be seen by the eye--unaltered starch-granules, filaments of meat-fibre, or fat in drops or in needle-shaped or feathery crystals.

The nervous system is disturbed after a certain time. There is languor, with depression of spirits, mental weariness, and inaptitude for work of any kind. The patient is querulous, morose; his sleep is restless, but sometimes profound until disturbed by the demand to empty the bowel. Melancholia is attributed to this as to other diseases of the abdomen, but their influence in producing insanity is doubtful.[34]

[Footnote 34: Griesinger, _Mental Path. and Therap._, Am. ed., New York, 1882, pp. 137, 138.]

No decided symptoms are exhibited in the respiratory and circulatory systems. Even slight exertion will cause shortness of breath and increased frequency or palpitation of the heart. This irritability of the heart is a marked feature of the disease.[35]

[Footnote 35: DaCosta found that of 200 cases of irritable heart, 61 were in patients who had suffered from or still had diarrhoea (_Am. Journ. Med. Sci._, vol. lxi., 1871, p. 37).]

The appearance of the urine is normal; it may be abundant, with phosphatic deposit, or it is scanty and high-colored. In bad cases albumen and casts have been found.[36]

[Footnote 36: Alonzo Clark, "Proc. of New York Path. Soc.," _Med. and Surg. Reports_, vol. ix., 1862-63, p. 312.]

The symptom indicative of atrophy of the mucous membrane is believed by Nothnägel to be the persistent passage of one soft, unformed stool daily. Mucus and fat, which diminish the consistence of the stool, are {709} excluded by microscopical examination. One stool daily shows that there is no exaggerated peristalsis which hurries the food along so rapidly that water cannot be absorbed.[37]

[Footnote 37: Nothnägel, "Zur Klinik der Darmkrankheiten," _Zeitschrift für klin. Med._, iv., 1882, p. 422.]

PROGRESS AND TERMINATION.--As the disease advances it is marked by progressive emaciation and debility. The skin gradually acquires great pallor, indicating profound anæmia. The loss of flesh is very rapid. An exacerbation of the disease will in a few days cause the cheeks to grow hollow, the eyes to appear sunken with dark rings around them. In all cases of long duration the progress is intermittent; frequent relapses occur from which the patient may rally and regain a moderate degree of flesh. Recovery may take place in weeks or months--eighteen months is the average duration[38]--but in most instances a tendency to a recurrence of the diarrhoea from cold, fatigue, or indiscretions in diet will continue throughout life. An incomplete recovery may take place by the cessation of the diarrhoea and formation of a stricture from the healing of an intestinal ulcer. In the worst cases there is no rule as to the rapidity or regularity of the march of the disease.

[Footnote 38: C. H. Ralfe, Seamen's Hospital, London: see Aitken's _Handbook of Treatment_, New York, 1882, p. 116.]

When the advance is toward a fatal issue the emaciation progresses until it becomes extreme; nothing but skin and bone are left. The cuticle is hard and dry, pale or brownish in color. The muscular strength is so reduced that the patient is unable to move from bed. The voice may sink to a whisper. The nervous depression and moroseness assumes a more marked character. Among the soldiers during the Civil War who had undergone great privations with insufficient or improper diet the mental phenomena were those of dementia.[39] In them the disease was modified also by the symptoms of scurvy and malarial poisoning.

[Footnote 39: W. Kempler, "Entero-Colitis," _Am. Journ. of Med. Sci._, vol. lii., 1866, p. 337.]

Fever is seen in the late stages; it is nocturnal at first, and later assumes the features of hectic. The pulse grows more frequent and thready; aphthous deposits appear on the inside of the mouth and pharynx. Toward the end the discharges may become more frequent and very abundant; they are more fluid, lighter colored or black, with floating particles of blood and mucus. There may be a loss of odor or they may have a cadaveric smell.

Death takes place in a few weeks or after years of alternate suffering and relief. The immediate causes of death are exhaustion, marasmus from starvation, collapse from perforation of an intestinal ulcer and consecutive peritonitis, syncope from sudden exertion, pneumonia, or acute pulmonary congestion, pleurisy, or subarachnoid effusion in the brain, with coma and convulsions.

COMPLICATIONS.--General dropsy results from the hydræmia and languid circulation of the late period of the disease. Other causes of this symptom are coincident diseases of the liver, kidney, or the malarial cachexia. Oedema of one extremity follows a thrombus in the crural vein. Chronic bronchitis and pulmonary phthisis are sometimes met with. Acute pneumonia[40] and acute pulmonary congestion are occasional {710} causes of death. Peritonitis may occur with and without perforation. The latter variety begins as a local inflammation of subacute or chronic nature, and spreads slowly until it becomes general. Extensive adhesions and abundant accumulations of serous, sero-purulent, or purulent fluid in the abdominal cavity result.

[Footnote 40: Pneumonia (8 double and 12 single) occurred in 20 out of 41 fatal cases reported by Harrison Allen, _Tr. Path. Soc. Philada._, 1867, vol. ii. p. 161.]

The causal conditions which have been enumerated may be considered as complications. They are tuberculosis, Bright's disease, cirrhosis of the liver, abdominal tumors, scurvy, tubercular and other neoplasms in the wall of the intestine; attacks of intercurrent, intermittent, or remittent fever arise from the malarial influence to which the intestinal catarrh is due. These fevers and rheumatism and pseudo-rheumatism are complications in soldiers from the exposure to malarial influences and to cold and dampness.[41]

[Footnote 41: Woodward, _op. cit._, p. 495.]

Ulceration of the cornea, escape of the aqueous humor, and collapse of the eye were observed in quite a number of cases occurring among soldiers.[42]

[Footnote 42: Elliot Coues, _Med. and Surg. Reporter_, Philada., 1863, vol. x. p. 207, and H. Allen, _Tr. Path. Soc. Philada._, 1867, vol. ii. p. 161.]

SEQUELÆ.--The alteration of structure from long-standing inflammation leaves the mucous membrane prone to recurrence of inflammation. Chronic intestinal indigestion and permanent malnutrition come from the same cause. The glandular and lymphatic structures of the intestine and the mesenteric glands are so changed by disease that they imperfectly perform their function. Tabes mesenterica is the ultimate phase of this change. Constipation succeeds chronic diarrhoea, and is due to atony of the muscular wall from long-continued distension, and probably from degeneration of the muscular structure. A more serious cause of constipation, and sometimes of intestinal obstruction, is found in stenosis of the bowel from the healing of the ulcers of long-standing chronic catarrh. Stricture is more common in the colon, sigmoid flexure, and rectum. How frequently such a result follows the cicatrization of intestinal ulcers is not definitely known. Woodward concludes from a careful search of books and pathological museums that stenosis from this cause is very rare.[43] Syphilis is the most common cause of ulcer. Local or general peritonitis leads to the formation of adhesions or fibrous bands uniting neighboring links of intestine. By the contracting of these narrowing of the intestinal canal may result. Paralysis, hemiplegia, paraplegia, etc. have been found to follow upon diarrhoea of long standing.[44]

[Footnote 43: Woodward, _op. cit._, p. 504.]

[Footnote 44: Potain, "Parésie des Membres inférieurs ayant succedé à un Catarrhe gastro-intestinal," _Rev. de thérap. Med.-Chir._, Paris, 1880, xlvii. p. 562; "Paralysis spinale sécondaire à une Diarrhée chronique," _Journ. des Conn. méd. Prat._, Paris, 1880, 3, S. ii. p. 57.]

DIAGNOSIS.--The mild form of chronic catarrh of the intestines associated with constipation has been confounded with hepatic disorders, and the obscure symptoms attending it have been attributed to excess or diminution of bile, and medicines to regulate the liver have been given accordingly. In the absence of lesions in the liver, in cases where symptoms such as have been described have preceded death, the opinion is not justified that disease of this organ has existed. On the contrary, alteration in the mucous membrane is almost always found, which points to the true nature of the disease. The diagnosis is based upon the accompanying {711} gastric catarrh and upon the symptoms of intestinal indigestion and malnutrition. Greater sensibility to pressure over the right hypochondrium and along the line of the colon, pain one to two hours after eating, with distension of the abdomen, the passage of well-formed and somewhat indurated feces mixed or coated with mucus, are symptoms peculiar to these mild forms.

The tendency to diarrhoea from cold, indigestible food, etc. which marks the second form of mild catarrh is easily recognized.

The characteristic symptom of the severe form is the persistent diarrhoea. Paroxysmal pains, tympanites and rumbling of gas, tenderness on pressure over the colon, the alternate periods of improvement and relapse, with the constitutional signs of impaired nutrition and progressive anæmia and debility, point out the nature and the seat of the lesion with sufficient clearness. It is futile to attempt to distinguish chronic intestinal diarrhoea from chronic dysentery. The lesions of the two conditions are essentially the same; it depends upon the fancy as to which name is given to the lesions described here under the title chronic intestinal catarrh. A greater amount of blood and mucus in the stool with tenesmus would more properly be called dysenteric, but the same case may present at one time diarrhoeal, at another dysenteric, symptoms.

Primary must be distinguished from secondary diarrhoea. Therefore the liver, heart, and lungs must be examined to discover diseases which might cause portal congestion. Any constitutional malady may be a cause and an explanation: tuberculosis or pulmonary phthisis stands first in its influence; next, chronic Bright's disease, septicæmia, scurvy, syphilis, and gout are attended by intercurrent diarrhoea. If all general disease can be excluded and the morbid process be located in the intestine alone, its cause may be known by studying the habits, occupation, and diet of the patient. Foreign bodies--hardened feces, gall-stones, fruit-stones, etc.--are possible causes which the history of the case may point to.

Having located the disease in the intestine and decided upon its primary or secondary nature, it remains to determine more precisely (_a_) the locality of the lesion, and (_b_) the stage of the inflammatory process.

(_a_) In what part of the intestinal canal is the disease located? It must be remembered that in typical and fatal cases the large intestine is the home par excellence of the lesions of chronic catarrh, and that the lower part of the ileum is often associated in the morbid processes, but limited areas of the small or large intestine are affected in mild forms which yield readily to treatment.

Icterus, clay-colored stools, and bile in the urine show that the catarrh is in the duodenum and involves the opening of the common bile-duct. The absence of diarrhoea, with flatulence and colics, limits the area of inflammation to the duodenum. Symptoms of duodenal indigestion accompany this form of catarrh; the failure of bile to neutralize the acid chyme impairs the effect of the pancreatic secretion. Fats are not digested and there is fatty diarrhoea. To this may be added tenderness in the right hypochondrium, and pain and oppression in the epigastrium and to the right one hour after eating. There may be wasting and hypochondriasis.

{712} The lower part of the duodenum below the opening of the bile-duct, the jejunum, and the ileum can be taken together as forming the small intestine. Chronic catarrh of the small intestine is attended with pain about the umbilicus, which comes on immediately or in one hour after taking food. Tympanitic distension gives a full, rounded prominence to the abdomen, which is more central than lateral, and greater below the umbilicus than above it. It is accompanied by a sense of oppression, which is greater after eating. Inability to digest food consisting largely of starch or sugar, as well as tardiness in the digestion of all foods, with resulting loss of flesh, are signs of intestinal indigestion. There may be no diarrhoea; if there is, important help to diagnosis can be gained by examining the stools. They contain undigested or partly-altered meat-fibre and starch-granules, discoverable only by the microscope. The discharges are soft and pulpy from an intimate admixture of mucus. To the naked eye no mucus is visible, but a thin layer under the microscope shows clear islets of pure mucus, or mucus may only be detected by the adhesion of the covering-glass to the slide. Bile-stained epithelium and globules of stained mucus are seen in the liquid stools from catarrh of the small intestine and of the ascending colon. There is the characteristic reaction and play of color on testing for bile-pigment. These are evidences that the stool with the bile has been hurried along the ileum and colon, and expelled before the transformation in the coloring matter has had time to take place.[45]

[Footnote 45: "II. Abtheilung, Diagnostische Bemerkungen zur Localisation der Catarrhe," _Zeitschrift für klinische Medicin_, Berlin, 1882, iv. p. 223.]

In catarrh of the large intestine there is sensitiveness to pressure along the line of the colon; the distension of the abdomen is not uniform, depending upon the prominence of the transverse or descending colon. The pains are more severe and precede the stools, which are more frequent and larger than in catarrh of the ileum. The discharges are pulpy or watery. Globules of mucus are visible to the naked eye, and mucus is intimately mixed with fecal matter.

If the lower half of the colon is chiefly the seat of the disease, pure mucus coats the more solid stool and is in its substance. With catarrh limited to the descending colon scybalæ are imbedded in mucus. From the sigmoid flexure and rectum larger masses of mucus, without fecal matter or with it, are expelled. Pure lumps of mucus, mixed or stained with red blood and without fecal matter, indicate catarrh of the rectum--proctitis.

(_b_) The stage of the process of inflammation is diagnosed by the condition of the patient, the course of the disease, and the character of the stools. As long as there is a pulpy fecal diarrhoea, with no blood, pus, or fragments of tissue and no marked emaciation or fever, and with a tendency to improvement under favorable conditions, there is every reason to believe that there is no ulceration.

In follicular ulceration the course of the disease is essentially chronic, and is marked by periods of improvement under careful treatment, with exacerbations and relapses from slight causes of irritation. There is progressive emaciation and debility, with fever of hectic character, which is worse in the later stages. The abdomen may be retracted. The movements are frequent and liquid, and are without odor or fetid. They {713} contain mucus, glassy-gray or green, pus-cells imbedded in masses of mucus, blood in small amount, but sometimes abundant, and shreds of the tissue of the mucous membrane. This last is an important aid to diagnosis.

The higher the ulcer the less marked is the diarrhoea. The lower its situation the greater is the frequency of the stools and the more liable are they to be accompanied by tenesmus and to contain blood and pus. Toward the last, ulceration is accompanied by rapid emaciation, fever, sweats, a feeble circulation, a dry tongue, great thirst, and oedema of the feet and ankles. Death takes place by gradual exhaustion, more rarely from perforation and peritonitis or from intestinal hemorrhage.[46]

[Footnote 46: Nothnägel, "Die Symptomatologie der Darmgeschwüre," _Klinische Vorträge Volkmann_, No. 200, Aug. 24, 1881.]

Duodenal ulcer is with difficulty recognized during life.[47] The following are the symptoms which have preceded death from this lesion: Profuse hemorrhage from the bowel, vomiting of food as well as blood, icterus, dysphagia, hiccough, oppression in the epigastrium after eating, attacks of cardialgia with tenderness on pressure in the right hypochondrium, and sudden death with symptoms of collapse. If these symptoms follow an extensive burn of the skin, they are easily referred to a duodenal ulcer.

[Footnote 47: W. L. Loomis, "Perforating Ulcer of Duodenum and Sudden Death." For two years the patient had suffered with dyspepsia and epigastric pain after eating, was gouty, and had lost flesh. Autopsy: atheroma of arteries, beginning cirrhosis of kidneys, walls of stomach thickened, perforated ulcer one inch below pylorus (_Med. Record New York_, 1879, vol. xv. p. 188; also _Boston City Hospital Report_, 1882, p. 374).]

Tuberculous ulcers are distinguished from follicular ulcers by the history of hereditary predisposition, the existence of pulmonary tuberculosis, higher fever, and more rapid emaciation and debility.

A cancerous ulcer may be the cause of bloody stools; it is usually within reach of the finger in the rectum; the mass exercises pressure upon the prostate, and at times occludes the bowel, causing obstruction. The cachexia and rapid decline are not seen in catarrhal ulceration.

PROGNOSIS.--Chronic catarrh of the intestine is most fatal in children. Among infants artificially fed, when the illness develops and continues during hot weather, the mortality is very great. Recovery in the young is rendered less probable if chronic diarrhoea is associated with rickets, scrofula, or tuberculosis.

If the catarrh in adults is a complication of some previously existing constitutional disease, as Bright's disease or scurvy, or is connected with lesions of the liver, spleen, heart, or lungs, there is less hope of cure. In old persons this disease has a special gravity.

The longer the disease has lasted before treatment is begun, and the longer it continues without being influenced by treatment, the more unfavorable will be the prognosis. Discouraging symptoms are an uninterrupted loss of flesh and strength, lientery, hectic fever, relapses notwithstanding care in diet, and the signs of ulceration--blood, pus, and tissue-shreds in the stools, with an odor of decomposition.

Favorable promises may be based upon a hearty willingness of the patient to submit to the strictest regimen and to subordinate his life to the plans of treatment, the absence of other diseases, early improvement in his general condition and local symptoms under rest and diet. A {714} complete cure cannot be assumed to exist unless the patient has passed one or more years without a relapse.

TREATMENT.--As chronic intestinal catarrh is a complication of so many conditions, the prevention of it becomes a matter of great importance and of very general application. All rules for preserving health--temperance in eating and drinking, bathing, exercise, good ventilation, the avoidance of overwork, both mental and physical--are so many means for escaping an intestinal catarrh which may present itself as an indigestion with constipation or as a diarrhoea.

The special liability of infants and children, and to a less extent of very old persons, and the greater dangers they run, call for the most careful selection of appropriate diet at these periods of life.

Where there is hereditary predisposition, idiosyncrasy, chronic diseases of organs, or constitutional diseases, an easily-digested dietary should be supplemented by precautions against chilling of the surface by the wearing of flannel underclothing and woollen socks.

The etiology of each case may at once suggest a line of treatment. Among the causes which point to appropriate measures are--the continued presence in the bowel of indigestible or undigested food, constant exposure to cold or to changes of temperature, chronic cardiac disease and portal congestion from any cause, chronic cachexiæ, as syphilis, malaria, tuberculosis, or Bright's disease, the crowding together of individuals in prisons, asylums, etc.

1. The mildest form of intestinal catarrh characterized by intestinal indigestion and constipation or by the passage of fecal matter more or less solid, mixed or coated with mucus, is best treated by a diet such as is advised for intestinal indigestion, bathing with friction, outdoor life, exercise on horseback or by walking, pleasurable occupations, and travel. Iron if there is anæmia, and strychnia if there is a sluggish capillary circulation, with cold hands and feet, are available and useful in many cases. Massage and the Swedish movement treatment find useful application in feeble men and in women who are not strong enough for outdoor exercise. To aid the digestion the liquor pancreaticus as advised by Roberts, a teaspoonful one hour and a half to two hours after each meal, with ten to twenty grains of the bicarbonate of sodium, is, theoretically at least, to be warmly recommended. The Rockbridge alum water, a small glass three times daily between meals, has astringency enough for the hyperæmic membrane and is of good service without increasing constipation.

Purgatives should be avoided as much as possible. An enema of cool water, not more than a tumblerful, taken each morning after breakfast if persevered in, may do all that is needed in this direction. If it fails to empty the bowel completely, a larger enema of warm water--one pint--holding in solution sulphate of zinc or alum in the strength of one grain to three or four ounces, can be thrown high up with a rubber tube once daily. This acts upon the mucous surface, constringes mildly the congested vessels, and when expelled brings away the retained fecal matter. These astringent rectal injections offer promise of cure in many obstinate cases where the colon is chiefly the seat of disease. Belladonna is advised for cases of this kind in combination with strychnia for the constipation. Mild laxatives are often necessary. Bedford mineral water, Hunyadi water, or other salines and the less active vegetable {715} cathartics, can be given alternately. Ipecacuanha has had quite a reputation in combination with purgatives in intestinal catarrh. Aloin pills empty the bowel without much attendant irritation.

2. The form of catarrh which shows itself in a tendency to diarrhoea from indiscretions in diet or from exposure to cold must receive prophylactic treatment. Especially in this form is it important to improve the activity of the skin by bathing and friction, and to lead a temperate life in all things, regulating the diet according to the rules already stated. Tonics are called for in such cases. Fowler's solution of arsenic (one drop before each meal, Ringer), the potassio-tartrate or the tincture of the chloride of iron, dilute sulphuric acid, nitro-muriatic or hydrochloric acid, are efficient in improving digestive activity or in opposing the anæmia which is nearly always present. Quinia is indicated in malarial anæmia with a disposition to loose bowels. Quassia or other vegetable bitters can be given if the appetite is languid; the bitters are, as a rule, of little benefit, and may do harm if diarrhoea exists. Strychnia with quassia or columbo stimulates the appetite and the gastric digestion. When intercurrent attacks of diarrhoea come on with coated tongue, flatulence, distress about the umbilicus after eating, bismuth given on an empty stomach in full doses is serviceable. Small doses of morphia or of opium in some form can be added to the bismuth if there is much pain or when the stools are frequent.

In this and in other forms of intestinal catarrh mineral waters are profitably employed. They are best taken at their sources; and here, as in the case of sea-bathing, the benefit is largely due to the change of air and scene and to the more simple mode of life. Any of the watering-places where alkaline-saline waters or ferruginous waters are found may be of benefit. A trip to Europe and a stay at Carlsbad will break up many an obstinate case of chronic abdominal disorder; but other beneficial waters in Europe are Tarosp, Rohitsch, Marienbad, Kissengen, and Plombières.

In this country the comfort and conveniences of the summer hotels and climate are as much to be considered as the chemical composition of the waters. For milder forms of catarrh with constipation a season at Saratoga, with a life of temperance there, is a wise procedure. Bedford Springs, Pa., offer the same advantages in part, but the waters are best suited to catarrh with constipation. Many of the Virginia springs benefit health-seekers who do not place too much reliance upon the virtues of the waters, and who trust to the value of pure air, exercise, diversion, and rest.

3. All plans of treatment for the more severe form of catarrh with chronic diarrhoea (follicular enteritis) must be based upon a knowledge of the lesions. Bearing in mind the alterations in the mucous and submucous tissues, it is clear that no treatment can be successful which is not carried out with the most careful attention to details, and which is not continued for some time after all the symptoms of the disease have ceased. The complete resolution of hypertrophied glandular tissue, the scattering of cell-accumulations, and the healing of ulcers can only be secured in this way. It is best to present the whole case before the patient, so as to enlist in the task his intelligent co-operation.

Directions for the guidance of cases of this kind must include every {716} detail of the patient's life. The question of residence is of importance to begin with. A cool and dry climate is better than a wet and warm one, and where other means fail change of climate is sometimes the only cure. A sea-voyage, a residence in a mountain-region, will oftentimes promptly and effectually cure an obstinate diarrhoea. House-drainage and ventilation should be examined into and improved. The occupation may have developed the disease; in overwork may lie the origin and the cause of its continuance. Rest from work is therefore in some instances the one thing needed. In all cases the energies and the brain should not be overtaxed. The bath to keep the skin active can be combined with friction. The hot bath, as hot as can be borne, is the best. It is a stimulant, not a depressant, as is the tepid bath, and it is safer than the cold bath.

The cold sitz bath or the application of cold compresses diminishes abdominal plethora, and is wisely advised in strong persons who are not depressed or chilled by external cold. Sea-bathing is another hydro-therapeutic measure which is of unquestioned advantage in all forms of intestinal catarrh.

Permanent baths have been found very serviceable in many chronic diseases, and there are many reasons for advising them in obstinate diarrhoeas. There can be no better means for bringing to bear a strong and continued influence upon the intestinal mucous membrane. The patient should be kept in the warm bath for one, two, or three weeks, according to his strength and the effect upon the disease. Systematic hot bathing under the direction of a physician at Richfield, Sharon, the Hot Springs of Virginia or Arkansas, is an invaluable aid.

Rest in the recumbent position for cases where the symptoms indicate marked tissue-alteration is very often the most important part of the treatment. Rest and diet are alone necessary to cure many cases, and without these combined means relief is often impossible. The rest should be absolute, the patient using a bed-pan and lying down all the time. The contraindications for this method are a slight diarrhoea which yields to other treatment, and loss of strength and appetite from the deprivation of air and exercise.

If rest is not advisable, or does no good after a fair trial of two to four weeks, outdoor life in fair weather by driving or walking slowly can be suggested. A long drive will bring back a diarrhoea which has taken many weeks to relieve.

The rules for diet must be clearly given and strictly enforced. An exclusive milk diet should have a trial in every case. Skimmed milk can be taken in larger quantities and with less repulsion, and is therefore to be preferred. The exclusive milk diet can be varied with buttermilk, koumiss, or wine-whey; and fruit-juices, as orange-juice, lime-juice, or tamarind-water, please the patient without doing harm. In the case of adults as well as children the milk is made more digestible by diluting it with barley- or rice-water or by adding transformed farinaceous food to milk in the form of Mellin's food and other foods of this class.

Animal broths, as chicken-soup and beef-tea, are well digested if properly made and given in small quantities. Raw meat scraped, beef or mutton rare and thoroughly masticated, the breast of poultry, game, broiled fish, raw oysters, raw or very slightly boiled eggs, or sweetbread, are foods from which selection can be made to add variety to the dietary. {717} Saccharine, starchy, and fatty foods are to be given as little as possible. Vegetables may be added to the list as the condition improves. Rice and fine hominy (grits) are to be thought of first, as being easily digested and nourishing. Good wine in moderation is not hurtful; the red wines diluted with water are the best, but good port, tokay, and whiskey well diluted find application in particular cases.

Whatever food be given, it should be taken in the quantities and at hours prescribed by the physician, who by careful inspection of the stools judges of the necessity of changes in his regulations and of the success of his treatment.

The further treatment of chronic diarrhoea has for its object by the aid of drugs to change the anatomical state of the mucous membrane. Manifestly, the choice depends upon the state of this tissue. In the earlier stages the increased vascularity and hypersecretion call for mild astringents or for medicines which are believed empirically to oppose these conditions. When drugs can be dispensed with, it is better to do so; they should always be made subordinate to the careful regimen already described.

Bismuth in large doses (ten to thirty grains) is a safe and efficacious remedy in this stage. Nitrate of silver in pill form (one-sixth to one-fourth of a grain) has the endorsement of Wm. Pepper and many other practitioners. It should be continued for two or three weeks at least, but it may be given in small doses during several months, with intermissions, without danger of silver staining.[48]

[Footnote 48: A case is recorded of silver staining of the skin after four weeks' administration (Woodward, _op. cit._, p. 780).]

A routine administration of any drug or class of drugs is reprehensible, and from the numerous remedies which are advocated in chronic diarrhoea selection can be made for trial in the course of intractable cases. The list would include sulphate of copper (one-fourth to one-half a grain), the liquid preparations of iron (liquor ferri nitratis, tinct. ferri chloridi), dilute nitric and sulphuric acids, gallic acid and other vegetable astringents, oxide or sulphate of zinc, alum, precipitated phosphate of calcium, salicin, corrosive sublimate (1/100 gr. every hour), the Indian bael-fruit, etc. No remedy should be abandoned until it has been continuously given for one or more weeks.

The Rockbridge (Va.) alum water is markedly astringent, is not unpleasant, and may be used as a substitute for water with advantage. In fact, there is no better way of introducing in quantity a mild astringent into the intestine than by the drinking of this water.

Cold-water rectal irrigation has a sedative and astringent influence, and when properly used is of great advantage to both children and adults.[49] The patient should be placed in the proper position, and the water made to enter the rectum as high up as possible. The number of stools lessens almost immediately after this treatment, peristalsis being inhibited thereby.

[Footnote 49: A long rectal rubber tube, such as advised by Surgeon-General Wales, U.S.N., serves this purpose well.]

To the water used in irrigation astringents may be added in small doses. Sulphate of zinc, sugar of lead, or alum may be given in this way in the strength of one grain to four or six ounces of water. This {718} method of treatment promises more and is more rational than the internal administration of drugs.

Opium and its preparations should be avoided except to control frequent or watery discharges or to relieve pain, but it is not often that this is called for if wiser measures are first employed. Any of the remedies spoken of may be given in the form of suppositories with greater advantage often than by the mouth.

In that more severe class of cases called follicular ulceration, in which the follicles are known to be ulcerated from a prolongation of the illness, the obstinacy of the diarrhoea, the character of the discharges, and the effect upon the general health, other measures are to be adopted. The diet should be most strictly regulated and the digestive power of the patient carefully studied. Cod-liver oil is added with advantage to other foods if there is a lack of nutrition. Aids to gastric digestion are called for.

The intestinal lesion is to be reached through the stomach or the rectum. Nitrate of silver in small doses is more especially applicable, and is to be preferred to all other drugs in this stage. It is to be given in small doses and for several weeks.

Turpentine and copaiba have something in their favor in ulceration. Ergot has been suggested, and where there is much hemorrhage from the bowel may be prescribed.

Irrigations with solutions of nitrate of silver seem to be a direct and certain remedy in cases where ulceration has existed for a long time. Two and a half to three pints of distilled water, holding in solution five grains of nitrate of silver, should be thrown up the rectum as high as possible with a rubber tube; the effort should be made to secure immediate exit to the fluid. This procedure is to be repeated after the bowels are moved--once every day or every other day if the rectum becomes irritable.[50]

[Footnote 50: See case reported by the writer to the Medical Society of the District of Columbia, and published in the _Maryland Medical Journal_, March 15, 1883, p. 562.]

{719}

CHOLERA MORBUS.

BY W. W. JOHNSTON, M.D.

SYNONYMS.--Cholera nostras, Sporadic cholera, European or English cholera, Spasmodic cholera, Cholera biliosa, Passio cholerica, Cholerhagia, Trousse-galant, Die Gallenruhr, Brechruhr.

DEFINITION.--An affection of the gastro-intestinal mucous membrane characterized by violent abdominal pain, nausea, and sudden, violent, and incessant vomiting, and by purging of a watery fluid containing little albumen and bile; attended with spasms of the muscles of the abdomen and extremities, a pinched and sunken countenance, pallor, cyanosis, and coldness of the surface of the body; a feeble and rapid pulse, oppressed respiration, and great restlessness; dryness of the tongue, great thirst, and diminished or suppressed urinary secretion and a state approaching collapse, which may rarely prove fatal, but is, as a rule, followed by reaction.

HISTORY.--The term cholera has been in use since the time of Hippocrates, but he confounded with it every disease which seemed to him to come from acridity or corruption of humors, as colics and meteorism with constipation.[1] He well described cholera morbus in saying that "it is a disease which appears in summer, due to imprudence in eating, at the same time as intermittent fever."[2] If Celsus be correct in deriving the name from [Greek: cholê] "bile," and [Greek: reô] "I flow," it is more applicable to the disease now under consideration than to the Asiatic disease, as it is the bile which is absent in the colorless rice-water discharges of Asiatic cholera. Trallian and Ruysch, however, ascribe it to [Greek: cholêra] the rain-gutter of a house.

[Footnote 1: _Append. au Traité du reg. les Maladies aigues_, 19, ii. p. 495, ed. Littré.]

[Footnote 2: _Epidémies_, lib. v., ed. Littré, 71, p. 247.]

In the Old Testament mention is made of a disease resembling cholera morbus.[3] Its true pathogeny was known to Galen, and it was accurately described by Celsus,[4] and Aretæus[5] mentions the nature of the discharges and its frequency among young people and children.

[Footnote 3: _Hist. Méd. des Maladies epidémiques_, Paris, 1825.]

[Footnote 4: Lib. iv. cap. 2.]

[Footnote 5: Lib. ii. cap. 5.]

The first mention of epidemics was in the sixteenth century. Various epidemics in 1695, 1717, and 1718 in Germany were probably cholera morbus. Forestus[6] reports seven observations from 1559 to 1565 of attacks due to indigestible food or drastic medicines. F. Hoffman,[7] {720} J. Frank,[8] and L. Rivière speak of the benignity of the disease as contrasting it with its apparently dangerous symptoms.

[Footnote 6: _Opera Omnia_, Rothomagi, 1633, "De stomachi affectibus," lib. xxviii.]

[Footnote 7: _Medicina rationalis systemica_, t. iv. pt. 3, 1734.]

[Footnote 8: _Praxeos medicæ universæ præcepta_, Leipzig, 1826, p. 43.]

Sydenham's[9] description of the epidemics in England in 1669-72 is the earliest account of the disease in modern literature, and it was he who gave it the name cholera morbus.

[Footnote 9: Sydenham Soc. edition, vol. i. p. 163.]

NATURE.--There prevails at the present time a great diversity of opinion in regard to its nature; the want of uniformity in the appearances presented by post-mortem examinations may in some measure account for this. The present state of our knowledge, derived both from pathological anatomy and a study of the symptoms, will not warrant a positive opinion in regard to it.

Niemeyer,[10] in common with most German and some French authors, considers cholera morbus to be a variety of gastro-intestinal catarrh. Leube[11] thinks it a variety of gastric catarrh with simultaneous inflammation of the intestines and running a peculiar course. It is certainly not identical with the specific Asiatic disease, although in some cases the symptoms and morbid anatomy are exactly similar, and any differentiation is impossible. By some it is believed that cholera morbus is due to surviving germs implanted by previous epidemics of Asiatic cholera.

[Footnote 10: _Pract. Med._, 1879, vol. i. p. 480.]

[Footnote 11: _Ziemssen's Cyclopædia_, New York, 1876, vol. vii. p. 146.]

The slight changes found in some fatal cases would lead to the belief that the effect of the exciting cause is something more than a mechanical irritation of the gastro-intestinal mucous membrane.

The sudden onset, rapid development of symptoms, and dangerous collapse justify the theory that there must be some previous change in the individual or some peculiar result of food-decomposition. The nervous system may be so enfeebled by prolonged heat that an irritant quickly destroys its equilibrium and brings about vaso-motor paralysis of the intestinal vessels and abundant serum transudation. Or the irritation may be specific, depending upon the development of poison germs in food which has been subjected to heat influences. There is a close relationship between cholera morbus and cholera infantum in their etiology, symptoms, and pathology.

ETIOLOGY.--Predisposing Causes.--The disease is more common in the tropics, but is not confined to any climate. In temperate latitudes it is more likely to occur in July and August, when the variation of temperature between day and night is great, although the other months of summer and autumn are not entirely exempt. It is said to be more frequent and fatal in Southern Europe than in the northern and temperate climates. In periods immediately preceding and following epidemics of Asiatic cholera many persons are attacked, although there is great liability to errors in diagnosis at these times.

It occurs more frequently in youth and adolescence than in advanced life, and males seem to be more liable to attacks than females, but difference in occupation may assist in this predisposition. Persons endowed with an extreme sensibility of the nervous system and who are subject to frequent attacks of intestinal catarrh are much more liable to the disease. The exhaustion of the nervous system by heat, which is the {721} probable explanation of the phenomena of cholera infantum, has no doubt much to do with the development of cholera morbus. Mental anxiety or overwork in summer increases this nerve-exhaustion and renders the termini of nerves and the centres very susceptible to peculiar irritation.

Exciting Causes.--It is probable that the cause of most attacks is a septic material generated in the fermentation and decomposition of food. This poison acts as an irritant upon the gastric and intestinal nerves and gives rise to excessive peristaltic movements and vomiting. Hence the quality of the food is an element of more importance in the causation than the mere quantity ingested; and herein may reside the chief difference between cholera morbus and Asiatic cholera, the latter being due to a specific, imported, or acclimated poison which invariably produces the same specific form in those exposed to its action.[12] Unripe fruits, partially cooked or decaying meats and vegetables, shellfish and fish some time from the water, may produce the disease in those predisposed to it. The intemperate use of ice-water and other cold drinks after a full meal or when the body is exhausted by heat and fatigue, exposure to showers at the close of a hot day, or passing from a heated room into damp cellars and outbuildings, are frequent exciting causes.

[Footnote 12: "Bias the pugilist, naturally a great eater, had a sudden choleraic attack after having eaten of succulent food" (Hippocrates, lib. v. p. 247, ed. Littré).]

At times there exists a certain condition of inactivity of the digestive organs when the gastric juice is not secreted in sufficient quantity, and perfectly sound food may undergo fermentation and set up an attack.

The offensive exhalation from a filthy alley which had been recently cleaned was the exciting cause of a fatal epidemic in a London school,[13] and Levier recounts an epidemic caused by the drinking-water during the winter in Berne.[14]

[Footnote 13: _Lond. Med. and Surg. Gaz._, 1829, iv. p. 375.]

[Footnote 14: _Schweiz. Zeitschr. f. Heilk._, iii., 1864, p. 140.]

Nervous disturbance from other diseases may act as a cause. Leube reports a case of intermittent fever which was followed by an annual attack of cholera morbus preceded by febrile symptoms.[15]

[Footnote 15: Leube, _Ziemssen_, 1876, vol. vii. p. 148.]

Malaria, sewer-gas, and sudden and powerful mental emotions are credited with the causation of some attacks.

PATHOLOGICAL ANATOMY.--In a few cases an examination of the body has revealed no phenomena sufficient to account for the symptoms, even when they have been the most severe during life. In these cases either the inflammation has not passed the first stage of development and the resulting hyperæmia has disappeared after death, or the irritation of the gastro-intestinal nerves has been sufficiently intense to cause death before the alimentary tract has undergone any consequent structural change.

Usually, however, there are evidences of a general gastro-intestinal catarrh: the mucous membrane is congested throughout and denuded of epithelium. The solitary glands are enlarged and Peyer's patches swollen and prominent. The blood is thickened and dark in color, and the serous membranes dry, sticky, and covered with desquamated epithelium. Indeed, the appearances may be identical with those observed in true Asiatic {722} cholera. The kidneys are congested, sometimes enlarged, and the tubules devoid of epithelium. In protracted cases the general muscular system shows a beginning of granular degeneration.

In no case, however, can a positive diagnosis between Asiatic cholera and cholera morbus be made from post-mortem appearances.

SYMPTOMS.--The attack is usually sudden in its onset, but in some cases is preceded by nausea, thirst, loss of appetite, and slight general distress for some hours, or it may come on in the course of some gastro-intestinal disturbance. Frequently it is developed during sleep, particularly after midnight, the patient being aroused by a feeling of pressure at the pit of the stomach, which is followed by nausea and violent and incessant vomiting with intense pain, the contents of the stomach being ejected with great force.

The matters first vomited consist mainly of the food last eaten, little altered or mixed with gastric mucus and tinged with bile. In a certain proportion of cases the amount of bile is increased, although it is difficult to judge of the relative proportion by the color and taste of the vomited liquid. The general belief that the liver is implicated and the bile secreted in morbid quantity rests upon conjecture alone, and has no solid basis. After a time only yellow, brown, or greenish mucus, with more or less bile, is ejected, and in protracted cases hiccough is most distressing.

Following the vomiting or at the same time with it purging comes on, and it is usually preceded by borborygmi. In rare cases there is no vomiting, but only intense pain in the bowels and copious alvine discharges from the beginning to the end of the attack. The stools in the beginning are normal in color, but soon become pulpy or semi-fluid. As they increase in quantity they become watery, consisting of blood-serum with mucus, cast-off epithelium and pus-cells, and are nearly odorless, and sometimes resemble very closely the discharges of Asiatic cholera, but almost invariably retain the yellow or green color of the bile. Colorless rice-water discharges are observed in undoubted cases of cholera morbus outside of any epidemic influence. The discharges are acrid and irritating, and the neighboring parts become red and excoriated.

At the same time there is intense burning or tearing pain in the abdomen, generally centring at the umbilicus, great thirst and painful contractions of the muscles of the abdomen and extremities, particularly in the calves of the legs, and of the flexors of the thighs, forearms, fingers, and toes. In the beginning there may be tympanites, but this soon disappears, and the abdomen becomes retracted and the muscles drawn up into knots. The cramps usually come on after each act of vomiting and purging, but they may appear spontaneously. Abdominal tenderness is either wanting or slight. As the transudation continues the thirst becomes intense, the tongue cold, dry, and coated, and the tissues shrivelled from loss of water. The skin is cold, clammy, or covered with a viscid sweat, and the surface of the body is cyanosed, violet, or in the extremities it may have a marbled appearance. The nose is pointed, the eyes dark and sunken, and there is a general appearance of collapse.

The mind may be clear throughout, but in protracted cases there is great nervous prostration. The patient becomes dull and lethargic, passing into stupor after great restlessness and jactitation. The voice is faint {723} or whispering, the breath cold, and the respiration sighing. The pulse in the beginning may be depressed, but soon becomes rapid and often imperceptible, and there is great præcordial anxiety.

As the blood becomes thickened the urine is highly colored, small in quantity, and it may be suppressed. An examination shows traces of albumen, casts and desquamated epithelium, and a decrease in the amount of urea and salts. In the last stages there may be a slight rise in temperature, but it has no definite course and it is usually absent. In collapse the temperature of the surface of the body sinks below normal, but the temperature of the interior may rise as high as 101° or 102° F., as shown by the thermometer in the rectum or vagina.[16]

[Footnote 16: _London Hosp. Reports_, 1856, vol. iii. p. 457.]

PROGRESS AND TERMINATION.--But, fortunately, the course of the disease tends toward recovery in the large majority of cases. The discharges gradually decrease in quantity, the intervals are longer, the appearance becomes more natural, and a profuse perspiration is followed by a refreshing sleep. The surface becomes warmer, the pulse slower and more full, and the skin regains its normal color.

If the case has been a severe one or if it occurs in a person much enfeebled by disease, it pursues a different course. The discharges become almost uninterrupted, and at last are passed involuntarily. The cramps are almost continuous or are convulsive, the pulse grows rapidly weaker and is finally lost, coma succeeds stupor, and death follows in collapse.

The duration of the disease varies from a few hours to two or three days; death has occurred within twelve hours.

Recovery is generally complete after a few hours; and this rapid return to the normal condition shows that there have been no textural change of organs. Sometimes great emaciation, irritability of the stomach, and slight diarrhoea persist for a few days, or symptoms of a general gastro-enteritis may supervene.

DIAGNOSIS.--In making the diagnosis of cholera morbus it is necessary to carefully differentiate it from epidemic cholera and the effects produced by irritant poisons, such as the metallic salts, poisonous fungi, etc.

Occurring during an epidemic of Asiatic cholera, it is not possible to make a diagnosis, as the symptoms of cholera morbus and of mild cases of the Asiatic disease are identical. From severe cases it is to be distinguished by the absence of antecedent diarrhoea, by the presence of bile in the vomited matters, and by the color and fecal odor of the stools. The nausea and abdominal pain are more marked, while the dyspnoea, cyanosis, and shrunken condition of the skin are less marked. The mortality of cholera morbus is slight, whilst about one-half of those attacked with epidemic cholera die.

In irritant poisoning the vomiting follows quickly after the ingestion of a meal or poisonous matter; it continues for some time before purging begins, and is out of all proportion to the diarrhoea. The vomited matters contain blood and mucus and are never serous in character. Corrosive poisons may cause redness, charring, or ulceration of the mouth and throat and a burning sensation in the stomach. The pain over the stomach is more constant and severe, particularly in the intervals of {724} vomiting, and there may be abdominal tenderness and bloody discharges. The expression is more anxious and the pulse rapid and weak.

Elaterium and tartar emetic will bring on vomiting and purging which resemble the symptoms of cholera morbus. Choleriform attacks due to uræmia simulate cholera morbus. The distinction is to be made by the previous history--pain and purging being relatively less prominent in uræmia--by the presence of albumen and casts in the urine, and by the early tendency to coma.

Acute peritonitis, attended by copious vomiting and purging, has been mistaken for cholera morbus, and the true nature of the affection only revealed by the autopsy.

PROGNOSIS.--As a rule, cholera morbus occurring in persons otherwise healthy ends favorably in a few hours. Cases of secondary fever, with gastro-intestinal catarrh, may prolong the attack from a few days to two weeks. Should treatment have no effect in lessening the vomiting and purging, and should the evidences of heart-failure become apparent, a fatal result may be feared. Death has occurred within twelve hours, and the mortality is 3 per cent. of uncomplicated cases.[17]

[Footnote 17: Bartholow, _Pract. Med._, New York, 1880, p. 58.]

Cases occurring in the course of other diseases possess a special gravity.

TREATMENT.--During the summer months, and particularly in August and September, when the hot days are succeeded by cool nights, iced drinks should be used in moderate quantities; the diet should be light, nutritious, and easy of digestion. Unripe fruits and articles of food liable to fermentative changes should not be indulged in.

Exposure to the night air, particularly after a full meal, should be especially avoided, and the clothing ought to be so arranged that additions may be made as night approaches. Slight attacks of indigestion should not be neglected, and any irregularity of the bowels must receive immediate attention.

The period when the physician is called upon to prescribe for an attack of cholera morbus is usually when the stomach has been emptied of food and the patient is vomiting incessantly, purging, and writhing in pain. If vomiting has not occurred and violent epigastric pain is the only symptom, the stomach should be emptied by an emetic of hot water and mustard repeated until the overcharged organ is completely emptied. Partially-digested food in a state of acid fermentation will thus be got rid of, and the sufferings may be immediately but not wholly relieved.

If spontaneous vomiting has expelled the food, and the matters vomited are green and watery, while pain and frequent stools with muscular cramps, heart feebleness, and threatening collapse are the symptoms presented, the remedy par excellence is a hypodermic injection of sulphate of morphia (gr. 1/8 to 1/3) with sulphate of atropia (gr. 1/120 to 1/100). If one dose is not followed by decided mitigation of suffering, the injection is to be repeated in a half hour or an hour, not giving above one grain of morphia in divided doses. At the same time, and while waiting for the full effect of the narcotic, efforts can be directed to giving ease to the muscular spasms and pain by brisk friction with stimulating lotions or by mustard poultices to the abdomen and extremities. The morphia will be the best and quickest stimulant which can be used; it will therefore be useless in most cases to administer brandy, camphor, chloroform, {725} or other remedies of that sort. Waiting and giving nothing by the mouth is the wiser course. In twenty minutes to half an hour the most perfect bien être succeeds to the previous agony and exhaustion. In some cases the vomiting, purging, and cramps cease more gradually, and six hours will pass before the patient is at ease. The intense thirst is best treated by the giving of cracked ice sparingly at first, more freely later.

Nothing substitutes morphia hypodermically with success, but in some instances or when the stomach is not very irritable it may be necessary to give medicine by the mouth. In this case chloroform (xv to xxx drops), chlorodyne (x to xx drops), or spirits of camphor (v to x drops) every quarter or half hour in ice-water may be directed. Chloroform and camphor can be combined with the deodorized tincture of opium in ten- to twenty-drop doses. Time is wasted in expecting relief from remedies which are inevitably rejected as soon as taken; it is only when the stomach is very tolerant that it is judicious to begin with them.

The weakness of the heart's action must be combated by brandy or whiskey, given by the mouth with pounded ice or administered hypodermically. A considerable quantity of brandy or diluted alcohol may be introduced by repeated injections beneath the skin. Iced champagne may be tried with good effect. H. C. Wood quotes Hall[18] as recommending hypodermic injections of chloral in the cold stage of cholera. Five to eight grains in twenty minims of distilled water can be thus given, and repeated at intervals of fifteen to twenty minutes until some effect is perceived.

[Footnote 18: _Lancet_, May 2, 1874.]

If vomiting persists after the other symptoms--pain and muscular spasms--are relieved, it is due to the intense gastric hyperæmia; giving nothing which is not necessary is the wiser plan. Carbolic acid, hydrocyanic acid, bismuth, bromide of sodium, or small doses of calomel are remedies which meet the indication. Food should be withheld as long as possible; then iced barley-water, followed by milk and lime-water in very small quantities at short intervals, will test the power of the stomach to retain and digest food.

{726}

INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER.

BY J. LEWIS SMITH, M.D.

Entero-Colitis.

The summer affections of the intestines in children are chiefly of a diarrhoeal character. Diarrhoeal attacks, as is well known, are much more frequent and severe in the summer months than in other portions of the year. Moreover, the diarrhoea of the summer season occurs chiefly among children under the age of two and a half years, and is much more common and fatal in the cities than in the country. In the large cities this malady has heretofore been the annually-recurring scourge of infancy, but of late years its prevalence has been in some degree diminished and its severity controlled by the establishment of health boards and the enforcement of sanitary regulations. Still, it remains an important disease in all our cities, and one that largely increases the aggregate mortality. The truth of this statement is shown by the statistics of deaths taken at random from the mortuary records of any large city. Thus, in New York City during 1882 the deaths from diarrhoea reported to the Health Board, tabulated in months, were as follows:

Jan. Feb. Mar. Apr. May. June. July. Aug. Sept. Oct. Nov. Dec. Under five 34 32 50 50 72 231 1533 817 362 195 68 35 years. Over five 14 15 14 20 15 19 131 149 84 55 31 24 years.

Therefore, in 1882--and the statistics of other years correspond in this particular--it is seen that nine times as many deaths of children under the age of five years occurred from diarrhoea during the five months from June 1st to October 31st as in the remaining seven months of the year. It is also seen, in corroboration of the statement that diarrhoea due to hot weather is chiefly a disease of infancy and early childhood, that during these same five months, which embrace the summer season, the number of deaths from diarrhoea under the age of five years was seven and a half times greater than the number over that age. These statistics agree with the general experience of physicians in city practice. The summer diarrhoea would indeed be comparatively unimportant were its death-rate as low in the first five years of life as subsequently.

The following statistics show how great a destruction of life this malady causes even under the surveillance of an energetic health board; and before this board was established it was much greater, as I had abundant opportunities to observe. The last annual report of the New York Board of Health was made in 1875, since which time weekly bulletins have been {727} issued. The deaths from diarrhoea at all ages in the three last years in which annual reports were issued were as follows:

1873. 1874. 1875. January 94 43 46 February 84 34 52 March 97 40 58 April 114 47 45 May 95 61 89 June 220 144 157 July 1514 1205 1387 August 967 1007 1012 September 424 587 608 October 213 255 185 November 87 105 57 December 53 56 50

Thus, in these three years the aggregate deaths from diarrhoea during the months from June to October inclusive, in which months the summer diarrhoea prevails, were 9885, while in the remaining seven months the number was only 1407. How large a proportion of these deaths in the warm season occurred in children we may infer from remarks made by the Health Board in regard to another year. In their annual report for 1870 the board state: "The mortality from the diarrhoeal affections amounted to 2789, or 33 per cent. of the total deaths; and of these deaths 95 per cent. occurred in children less than five years old, 92 per cent. in children less than two years old, and 67 per cent. in those less than a year old." Every year the reports of the Health Board furnish similar statistics, but enough have been given to show how great a sacrifice of life the summer complaint produces annually in this city.

What we observe in New York in reference to this disease is true also, to a greater or less extent, in other cities of this country and Europe, so far as we have reports. Not in every city is there the same proportionate mortality from this cause as in New York, but the frequency of the summer diarrhoea and the mortality which attends it render it an important disease in, I believe, most cities of both continents. In country towns, whether in villages or farm-houses, this disease is comparatively unimportant, inasmuch as few cases occur in them, and the few that do occur are of mild type, and consequently much less fatal than in the cities.

The comparative immunity of the rural districts has an important relation, as we will see, to the hygienic management of these cases.

ETIOLOGY.--In the causation of this disease two distinct factors are recognized--the one atmospheric, the other dietetic.

The prevalence and severity of the summer diarrhoea correspond closely with the degree of atmospheric heat, as may be inferred from the foregoing statistics. In New York this disease begins in the month of May--earlier in some years than in others--in a few scattered cases, commonly of a mild type. Cases become more and more numerous and severe as the weather grows warmer until July and August, when the diarrhoea attains its maximum prevalence and severity. In these two months it is by far the most frequent and fatal of all the diseases in cities. In the middle of September new patients begin to be less common, and in the latter part of this month and subsequently new cases do not occur, unless under unusual circumstances which favor the development of this malady. In New York a considerable number of deaths {728} of infants occur from the diarrhoea in October. October is not a hot month in our latitude--its average temperature is lower than that of May--and yet the mortality from this disease is considerably larger in the former than in the latter month. This fact, which seems to show that the prevalence of the summer diarrhoea does not correspond with the degree of atmospheric heat, is readily explained. The mortality in October, and indeed in the latter part of September, is not that of new cases, but is mainly of infants, as I have observed every year, who contract the disease in July or August or earlier, and linger in a state of emaciation and increasing weakness till they finally succumb, some even in cool weather.

The fact is therefore undisputed, and is universally admitted, that the summer season, stated in a general way, is the cause of this annually-recurring diarrhoeal epidemic, but it is not so easy to determine what are the exact causative conditions or agents which the summer weather brings into activity. That atmospheric heat does not in itself cause the diarrhoea is evident from the fact that in the rural districts there is the same intensity of heat as in the cities, and yet the summer complaint does not occur. The cause must be looked for in that state of the atmosphere engendered by heat where unsanitary conditions exist, as in large cities. Moreover, observations show that the noxious effluvia with which the air becomes polluted under such circumstances constitute or contain the morbific agent. Thus, in one of the institutions of this city a few years since, on May 10, which happened to be an unusually warm day for this month, an offensive odor was noticed in the wards, which was traced to a large manure-heap that was being upturned in an adjacent garden. On this day four young children were severely attacked by diarrhoea, and one died. Many other examples might be cited showing how the foul air of the city during the hot months, when animal and vegetable decomposition is most active, causes diarrhoea. Several years since, while serving as sanitary inspector for the Citizens' Association in one of the city districts, my attention was particularly called to one of the streets, in which a house-to-house visitation disclosed the fact that nearly every infant between two avenues had the diarrhoea, and usually in a severe form, not a few dying. This street was compactly built with wooden tenement-houses on each side, and contained a dense population, mainly foreign, poor, ignorant, and filthy in their habits. It had no sewer, and the refuse of the kitchens and bed-chambers was thrown into the street, where it accumulated in heaps. Water trickled down over the sidewalks from the houses into the gutters or was thrown out as slops, so that it kept up a constant moisture of the refuse matter which covered the street, and promoted the decay of the animal and vegetable substances which it contained. The air in the domicils and street under such conditions of impurity was necessarily foul in the extreme, and stifling during the hot days and nights of July and August; and it was evidently the important factor in producing the numerous and severe diarrhoeal cases which were in these domicils.

In another locality, occupied by tripe-dealers and a low class of butchers who carried on fat- and bone-boiling at night, the air was so foul after dark that the peculiar impurity which tainted it could be distinctly noticed in the mouth for a considerable time after a night visit. In the street where {729} these nuisances existed and in adjacent streets the summer diarrhoea was very prevalent and destructive to human life. Murchison states that twenty out of twenty-five boys were affected with purging and vomiting from inhaling the effluvia from the contents of an old drain near their school-room. Physicians are familiar with a similar fact showing this purgative effect of impure air--that the atmosphere of a dissecting-room often causes diarrhoea in those otherwise healthy.

The exact nature of the deleterious agent or agents in foul air which cause the diarrhoea, whether they be gases or organisms, has not been fully determined; but at a recent meeting of the Berliner Med. Gesellschaft, A. Baginsky made a report on the bacilli of cholera infantum, which he states he has found both in the dejections and in the intestinal mucous membrane in the bodies of those who have perished with this disease. In the stools, along with numerous other organisms, Baginsky states that he found masses of zoögloea, and the same organisms he detected on the surface of the small intestines, and could trace their wanderings as far as the submucous tissue.[1] But it is evidently very difficult to determine whether such organisms sustain a causative relation to diarrhoea or spring into existence in consequence of the foul secretions and decomposing fecal matters which are present.

[Footnote 1: _Allegem. Wien. Mediz. Zeitung_, Nov. 6, 1883.]

The impurities in the air of a large city are very numerous. Among those of a gaseous nature are sulphurous acid, sulphuric acid, sulphuretted hydrogen; various gases of the carbon group, as carbonic acid, carburetted hydrogen, and carbonic oxide; gases of the nitrogen group, as the acetate, sulphide, and carbonate of ammonium, nitrous and nitric acids; and at times compounds of phosphorus and chlorine (Parkes). A theory deserving consideration is that certain gaseous impurities found in the air form purgative combinations. D. F. Lincoln, in his interesting paper on the atmosphere in the _Cyclopædia of Medicine_, writes in regard to sulphuretted hydrogen: "When in the air, freely exposed to the contact of oxygen, it becomes sulphuric acid. Sulphide of ammonium in the same circumstances becomes a sulphate, which, encountering common salt (chloride of sodium), produces sulphate of sodium and chloride of ammonium. The sulphates form a characteristic ingredient of the air in manufacturing districts." The sulphates, we know, are for the most part purgatives, but whether they or other chemical agents exist in the respired air in sufficient quantity to disturb the action of the intestines, even where atmospheric impurities are most abundant, is problematical and uncertain.

Again, the solid impurities in the air of a large city are very numerous, as any one may observe by viewing a sunbeam in a darkened room, which is made visible by the numerous particles floating in it. These particles consist largely of organic matter, which sometimes has been carried a long distance by the wind. The remarkable statement has been made that in the air of Berlin organic forms have been found of African production. Ehrenberg discovered fragments of insects of various kinds--rhizopods, tardigrades, polygastrica, etc.--which, existing in considerable quantity and inhaled in hot weather, when decomposition and fermentation are most active, may be deleterious to the system. Monads, bacteria, vibriones, amorphous dust containing spores which {730} retain their vitality for months, are among the substances found in the air of cities. The well-known hazy appearance of the atmosphere resting over a large city like New York when viewed from a distance is due to the gaseous and solid impurities with which the air is so abundantly supplied--impurities which assume importance in pathological studies, since minute organisms are now believed to cause so many diseases the etiology of which has heretofore been obscure. With our present knowledge we must be content with the general statement that impure air is one of the two important factors which cause summer diarrhoea, without being able to state positively which of the elements in the air are most instrumental in causing this result. But the theory is plausible that minute organisms rather than chemical products are the chief cause. Henoch of Berlin, writing upon this subject, calls attention to the disease known as intestinal mycosis, its prominent symptom being a severe diarrhoea produced by eating diseased meat containing a fungus. He believes that "a portion of the fungus not destroyed by the gastric juice settles upon different parts of the intestine, and there produces its effects;" and he adds, "At present, however, we can regard the mykotic theory of cholera infantum only as a very probable hypothesis. There is no doubt that high atmospheric temperature increases the tendency to fermentation dyspepsias which is present in imperfectly-nourished children at all seasons, and causes them to appear not only epidemically, but also in an extremely acute form which is not frequent under ordinary circumstances. This would lead to the conclusion that, in addition to the heat, infectious germs are present, which, being developed in great masses by the former, enter the stomach with the food." The fungus theory of the causative relation of atmospheric heat to the diarrhoea of the summer season as thus explained by Henoch commands the readier assent since it comports with the well-known facts relating to the etiology of the summer complaint. This disease, as we have seen, is most prevalent and fatal under precisely those conditions of dense population, filthy domicils and streets, and atmospheric heat which are favorable for the development of low organisms.

In those portions of our cities which are occupied by the poor, more than anywhere else, those conditions prevail which render the atmosphere deleterious. One accustomed to the pure air of the country would scarcely believe how stifling and poisonous the atmosphere becomes during the hot summer days and close summer nights in and around the domicils in the poor quarters of the city. Among the causes of this foul air may be mentioned too dense a population, the occupancy of small rooms by large families, rigid economy and ceaseless endeavor to make ends meet, so that in the absorbing interest sanitary requirements are sadly neglected. Adults of such families, and children of both sexes as soon as they are old enough, engage in laborious and often filthy occupations. Many of them seldom bathe, and they often wear for days the same undergarments, foul with perspiration and dirt. The intemperate, vicious, and indolent, who always abound in the quarters of the city poor, are notoriously filthy in their habits and add to the insalubrity by their presence. Children old enough to be in the streets and adults away at their occupations escape to a great extent the evil effects of impure air, but the infantile population always suffer severely.

Every physician who has witnessed the summer diarrhoea of infants is {731} aware of the fact that the mode of feeding has much to do with its occurrence. A large proportion of those who each summer fall victims to it would doubtless escape if the feeding were exactly proper. In New York City facts like the following are of common occurrence in the practice of all physicians: Infants under the age of eight months, if bottle-fed, nearly always contract diarrhoea, and usually of an obstinate character, during the summer months. The younger the infant, the less able is it to digest any other food than breast-milk, and the more liable is it therefore to suffer from diarrhoea if bottle-fed. In the institutions nearly every bottle-fed infant under the age of four or even six months dies in the hot months with symptoms of indigestion and intestinal catarrh, while the wet-nursed of the same ages remain well. Sudden weaning, the sudden substitution of cow's milk or any artificially-prepared food in place of breast-milk in hot weather, almost always produces diarrhoea, often of a severe and fatal nature. Feeding an infant in the hot months with indigestible and improper food, as fruits with seeds or the ordinary table-food prepared in such a way that it overtaxes the digestive function of the infant, causes diarrhoea, and not infrequently that severe form of it which will be described under the term cholera infantum. Many obstinate cases of the summer complaint begin to improve under change of diet, as by the substitution of one kind of milk for another or the return of the infant to the breast after it has been temporarily withdrawn from it. It is a common remark in the families of the city poor that the second summer is the period of greatest danger to infants. This increased liability of infants to contract diarrhoea in the second summer is due to the fact that most infants in their second year are table-fed, while in the first year they are wet-nursed. Such facts, with which all physicians are familiar, show how important the diet is as a factor in causing the summer complaint.

Occasionally, from continued ill-health, the milk of the mother or wet-nurse does not agree with the nursling. Examined with the microscope, it is found to contain colostrum. Under such circumstances if a healthy wet-nurse be employed the diarrhoea ceases. It is very important that any woman furnishing breast-milk to an infant should lead a quiet and regular life, with regular meals and sleep. In the _Louisville Med. Journal_, Aug. 19, 1882, R. B. Gilbert relates striking cases in which venereal excesses on the part of wet-nurses were immediately followed by fatal diarrhoea in the infants which they suckled.

One not a resident would scarcely be able to appreciate the difficulty which is experienced in a large city in obtaining proper diet for young children, especially those of such an age that they require milk as the basis of their food. Milk from cows stabled in the city or having a limited pasturage near the city, and fed upon a mixture of hay with garden and distillery products, the latter often largely predominating, is unsuitable. It is deficient in nutritive properties, prone to fermentation, and from microscopical and chemical examinations which have been made it appears that it often contains deleterious ingredients. If milk be obtained from distant farms where pasturage is fresh and abundant--and in New York City this is the usual source of the supply--considerable time elapses before it is served to customers, so that, particularly in the hot months of July and August, it frequently has begun to undergo {732} lactic-acid fermentation when the infants receive it. That dispensed to families in the morning is the milking of the previous morning and evening. The common result of the use of this milk in midsummer by infants under the age of ten months is more or less diarrhoea.

The ill-success of feeding with cow's milk has led to the preparation of various kinds of food which the shops contain, but no dietetic preparation has yet appeared which agrees so well with the digestive function of the infant as breast-milk, and is at the same time sufficiently nutritive.

In New York City improper diet, unaided by the conditions which hot weather produces, is a common cause of diarrhoea in young infants, for we meet with this diarrhoea in infants who are bottle-fed at all seasons; but when the atmospheric conditions of hot weather and the use of food unsuitable for the age of the infant are both present and operative, this diarrhoea so increases in frequency and severity that it is proper to designate it the summer epidemic of the cities. Several years since, before the New York Foundling Asylum was established, the foundlings of New York, more than a thousand annually, were taken to the almshouse on Blackwell's Island and consigned to the care of the pauper-women, who were mostly old, infirm, and filthy in their habits and apparel. Their beds, in which the foundlings were also placed alongside of them, were seldom clean, not properly aired and washed, and under the beds were various garments and utensils which these pauper-women had brought with them as their sole property from their miserable abodes in the city. With such surroundings, the air which these infants breathed day and night manifestly contained poisonous emanations; while their diet was equally improper, for it was prepared by these women from such milk and farinaceous food as were furnished the almshouse. When assigned to duty in the almshouse, this service being at that time a branch of Charity Hospital, I was informed that all the foundlings died before the age of two months; one only was pointed out as a curiosity which had been an exception to the rule. The disease of which they perished was diarrhoea, and this malady in the summer months was especially severe and rapidly fatal. The unpleasant experiences in this institution furnished additional evidence, were any wanting, that foul air and improper diet are the two important factors in causing the summer diarrhoea of infants. Since that beneficial charity, the New York Foundling Asylum, in East Sixty-eighth street, came into existence, providing pure air and, for a considerable proportion of the foundlings, breast-milk, many of these waifs have been rescued from death.

I have already stated that this disease occurs, with an occasional exception, under the age of two and a half years. The following table embraces all the cases that came to one of the city dispensaries during my service between the months of May and October, inclusive:

Age. Cases. 5 months or under 58 5 months to 12 months 212 12 months to 18 months 174 18 months to 24 months 93 24 months to 36 months 36 --- Total 573

After the third year the liability to the summer complaint so rapidly {733} diminishes that comparatively few are affected by it. It is seen from the above statistics that by far the largest number of cases occur during the period of first dentition; hence the prevalent opinion among families that dentition causes the diarrhoea. It is the common belief among the poor of New York that diarrhoea occurring during dentition is conservative, and should not be checked. They believe that an infant cutting its teeth suffers less, and may be saved from serious illness, if it have frequent stools. Every summer I see infants reduced to a state of imminent danger through the continuance of diarrhoea during several weeks, nothing having been done to check it in consequence of this absurd belief. The progressive loss of flesh and strength and wasting of the features do not excite alarm, under the blinding influence of this theory, till the diarrhoea has continued so long and become so severe that it is with difficulty controlled, and the patient is in a state of real danger when the physician is first summoned. The following statistics, which comprise cases occurring during my service in one of the city dispensaries, show the preponderance of cases during the age when dental evolution is occurring:

Cases. No teeth and no marked turgescence of gums 47 Cutting incisors 106 " anterior molars 41 " canines 40 " last molars 20 All the teeth cut 28 --- Total 282

It so happens that the period of dental evolution corresponds with that of the most rapid development and the greatest functional activity of the gastric and intestinal follicles, and the predisposition which exists to diarrhoeal maladies at this age must be attributed to this cause rather than to dentition.

SYMPTOMS.--The summer diarrhoea of infants commonly begins gradually with languor, fretfulness, and slight febrile movement. The diarrhoea at first usually attracts little attention from its mildness. The stools, while they are thinner than natural, vary in appearance, being yellow, brown, or green. Infants with milk diet are apt to pass green and acid stools containing particles of undigested casein. The tongue in the commencement of the attack is moist and covered with a slight fur. At a more advanced stage it may be moist, but is often dry, and in dangerous forms of the malady, accompanied by prostration, the buccal surface is red and the gums more or less swollen and sometimes ulcerated. Vomiting is common. It may commence simultaneously with the diarrhoea, especially when food that is unusually indigestible and irritating to the stomach has been given, but more frequently this symptom does not appear until the diarrhoea has continued a few days. I preserved memoranda of the date when vomiting began in the cases treated in two consecutive summers, and found that ordinarily it was toward the close of the first week. When it is an early and prominent symptom it appears to be due to the presence in the stomach of imperfectly digested or fermented and acid food, which, when ejected, gives a decidedly acid reaction with appropriate tests. It contains coagulated casein and undigested particles of whatever food has been given. In many patients the progressive loss of flesh and {734} strength is largely due to the indigestion and vomiting by which the food, which is so much required for proper nourishment, is lost.

Emesis occurring at a late stage of the summer complaint is often due to commencing spurious hydrocephalus, which is not an infrequent complication, as we will see, of protracted cases. Perhaps when a late symptom it may sometimes have an uræmic origin, for the urine is usually quite scanty in advanced cases. It seems probable, however, that deleterious effects from non-elimination of urea are to a considerable extent prevented by the diarrhoea.

The fecal evacuations may remain nearly uniform in appearance during the disease, but in many patients they vary in color and consistence at different periods. In the same case they may be brown and offensive at one time, green at another, and again they may contain masses of a putty-like appearance, the partly-digested casein or altered epithelial cells. The stools sometimes consist largely of mucus, with or without occasional streaks of blood, indicating the predominance of inflammation in the colon. This is the mucous diarrhoea of Barrier. The stools are sometimes yellow when passed, but become green on exposure to the air from chemical reaction due to admixture with the urine.

The character of the alvine discharges is interesting. In addition to undigested casein I have found epithelial cells, single or in clusters (sometimes regularly arranged as if detached in mass from the villi), fibres of meat, crystalline formations, mucus, and occasionally blood, as stated above. In one instance I observed an appearance resembling three or four crypts of Lieberkühn united, probably thrown off by ulceration. If the stools are green, colored masses of various sizes, but mostly small, are also seen under the microscope.

The pulse is accelerated according to the severity of the attack. The heat of the surface is at first apt to be increased, though but slightly in ordinary cases; but when the vital powers begin to fail from the continuance of the diarrhoea the warmth of the surface diminishes. In advanced cases approaching a fatal termination the face and extremities are pallid and cool, and the pulse gradually becomes more frequent and feeble. The skin is usually dry, and, as already stated, the urinary secretion diminished. In severe cases attended by frequent alvine discharges the infant does not pass urine oftener than once or twice daily. The imperfect action of the skin and kidneys is noteworthy.

Protracted cases of the summer complaint are apt to be complicated by two cutaneous eruptions--erythema extending over the perineum and frequently as far as the thighs and lower part of the abdomen, due to the acid and irritating character of the stools; and boils upon the forehead and scalp. The latter sometimes extend to the pericranium, and in case of recovery leave permanent cicatrices. This furuncular affection of the scalp has seemed to me useful in consequence of the external irritation which it causes, since it occurs at a time when, on account of the feeble heart's action and languid circulation, passive congestion of the vessels of the brain and meninges is liable to be present.

Patients who are weak and wasted in consequence of protracted diarrhoea, remaining almost constantly in the recumbent position, often have an occasional dry cough which continues till the close of life. It is due to hypostatic congestion in the lungs, usually limited to the posterior and {735} inferior portions of the lobes, extending but a little way into the lungs. It is the result of prolonged recumbency with feeble heart's action and feeble pulmonary circulation. Infants reduced by chronic diseases, lying day after day in their cribs with little movement of their bodies, are very liable to this passive congestion of depending portions of their lungs, toward which the blood gravitates, and into which but little air enters in consequence of their distance and position and the feeble respirations. The hyperæmia which results is of a passive character, a venous congestion, and the affected lobules have a dusky-red color. This congestion, continuing, soon results in pneumonitis of the catarrhal form, subacute and of a low grade, for pulmonary lobules in which the blood remains stagnant soon exhibit augmented cell-proliferation, perhaps from the irritating effects of the elements of the blood now withdrawn from the circulation.

I have made or procured a considerable number of microscopic examinations in these cases of hypostatic pneumonia, and the solidification of the pulmonary lobules has been found to be due to the exaggerated development of the epithelial cells in the alveoli, together with venous congestion. The affected lobules, whether in the stage of hypostatic congestion or the more advanced stage of hypostatic pneumonitis, when examined at the autopsy, were somewhat softer than in health, of dark color, and many of the lobules could be inflated by strong force of the breath; but in protracted cases the alveoli in central parts of the inflamed area resisted insufflation. The lung in hypostatic pneumonia, even when it is inflated, still feels firmer between the fingers than normal lung.

Hypostatic pneumonia is so common in hospitals for infants that some physicians whose observations have been chiefly in such institutions have almost ignored other forms of pulmonary inflammation. Billard, many years ago, wrote: "... The pneumonia of young children is evidently the result of stagnation of blood in their lungs. Under these circumstances the blood may be regarded as a kind of foreign body." Of all the chronic and exhausting diseases of infancy, no one has, according to my observations, been so frequently complicated by hypostatic pneumonia as the disease which we are considering, although it does not usually give rise to any more prominent symptom than an occasional cough. Limited to a small and almost immovable part of the lung, it does not ordinarily accelerate respiration or render it painful, and the cough is also apparently painless.

When progressive loss of flesh and strength has continued several weeks, and the patient is much exhausted, another complication is apt to occur, known as spurious hydrocephalus or the hydrocephaloid disease, the anatomical characters of which will be described in the proper place. The commencement of spurious hydrocephalus is announced by gradually increasing drowsiness, perhaps preceded by a period of unusual fretfulness. Vomiting and rolling the head are occasional early symptoms of this complication. As the drowsiness increases the pupils become less sensitive to light than in their normal state, and are usually contracted. When the drowsiness becomes profound and constant, the pupils remain contracted as in sound sleep or in opium narcotism. The functional activity of the organs is now also diminished, the vomiting ceases, the stools become less frequent, the buccal surface dry, and the urine more {736} scanty, while the pulse is more frequent and feeble. Spurious hydrocephalus either continues till death, or by stimulation the patient may emerge from it. When profound the usual result is death.

Although the summer complaint in its commencement may be promptly arrested by proper hygienic and medicinal treatment, if it continue a few weeks the anatomical changes which occur are such that recovery, if it take place, is necessarily slow and gradual. Improvement is shown by better digestion, fewer stools and of better appearance, less frequent vomiting, a more cheerful countenance, and the absence of symptoms which indicate a complication. Many recover after days of anxious watching and perhaps after many fluctuations.

Death may occur early from a sudden aggravation of symptoms and rapid sinking, or the attack may be so violent from the first that the infant quickly succumbs; but more frequently death takes place after a prolonged sickness. Little by little the patient loses flesh and strength, till a state of marked emaciation is reached. The eyes and cheeks are sunken, the bony projections of the face, trunk, and limbs become prominent, and the skin lies in wrinkles from the wasting. The altered expression of the face makes the patient look older than the actual age. The joints in contrast with the wasted extremities seem enlarged and the fingers and toes elongated. The stools diminish in frequency from diminished peristaltic and vermicular action, and vomiting, if previously present, now ceases. A feeble, quick, and scarcely appreciable pulse, slow respiration, and diminished inflation of the lungs, sightless and contracted pupils, over which the eyelids no longer close, announce the near approach of death. The drowsiness increases and the limbs become cool, while perhaps the head is hot. The infant no longer has the ability to nurse, or if bottle-fed the food placed in the mouth flows back or is swallowed with apparent indifference. So low is its vitality that it lies pallid and almost motionless for hours or even days before death, and death occurs so quietly that the moment of its occurrence is scarcely appreciable.

ANATOMICAL CHARACTERS.--Since the prominent and essential symptoms of the disease which we are considering pertain to the digestive apparatus, it is evident that the lesions which attend and characterize it are to be found in this part of the system. Lesions elsewhere, so far as they are appreciable to us, are secondary and not essential. I have witnessed a large number of autopsies of infants who have perished from the summer complaint, chiefly in institutions, and they have been sufficiently marked and uniform to enable us to designate it an entero-colitis. Several years since I preserved records of the autopsical appearances in the intestinal catarrh of infants, most of the cases being of summer diarrhoea. The number aggregated eighty-two. Since then I have each summer witnessed autopsies in the institutions in cases of this disease, and the lesions observed were the same as in the eighty-two cases.

The question may properly be asked: Can inflammatory hyperæmia of the intestinal mucous membrane be distinguished from simple congestion if there be no ulceration and no appreciable thickening of the intestine? It is possible that occasionally I have recorded as inflammatory what was simply a congestive lesion, but I do not think I have incorporated a {737} sufficient number of such cases to vitiate the statistics. In a large proportion of the cases there was evident thickening of the intestinal mucous membrane or other unequivocal evidence of inflammation. The following is an analysis of the eighty-two cases:

The duodenum and jejunum presented the appearance of inflammatory hyperæmia in 12 cases. The hyperæmia was usually in patches of variable extent or of that form described by the term arborescent. In 51 cases the duodenal and jejunal mucous membrane was pale and without any other appearance characteristic of catarrh or inflammation. In the remaining 19 cases the appearance of the duodenum and jejunum was not recorded, so that it was probably normal. On the other hand, in the ileum inflammatory lesions were present as a rule. In 49 cases I found the surface of the ileum distinctly hyperæmic, and in that portion of it nearest the ileo-cæcal valve, including the valve itself, the inflammation had evidently been the most intense, since in this portion the hyperæmia and thickening of the mucous membrane were most marked. In 16 cases the surface of the ileum appeared nearly or quite normal; in 14 hyperæmia in the small intestines in patches, streaks, or arborescence was recorded, but the records do not state in which division of the intestines they were observed.

Billard, with other observers, has noticed the frequency and intensity of the inflammatory lesions in entero-colitis in the terminal portion of the small intestines, and the thickening in many cases of the ileo-cæcal valve, and he asks whether the vomiting which is so common and often obstinate in this disease may not be sometimes due to obstruction to the passage of fecal matter at the valve in consequence of the hyperæmia and swelling, but has not observed any retained fecal matter above it, such as we find in any part of the colon, or any other appearance which indicated sufficient obstruction to cause symptoms. Still, it seems not improbable that the reason why the inflammatory lesions are more pronounced at and immediately above the valve than in other parts of the small intestine is that the fecal matter, so commonly acid and irritating in this disease, is somewhat delayed in its passage downward at this point.

Small superficial circular or oval ulcers were observed in the ileum in 4 cases, in 2 of which they were found also in the lower part of the jejunum. In 1 case the records state that ulcers were in the jejunum, but do not mention whether they were also in the ileum. In 1 case, in which there was much thickening of the ileum next to the ileo-cæcal valve, many small granulations had sprouted up from the submucous connective tissue, so that the mucous surface appeared as if studded with small warts.

Softening of the mucous membrane was also apparent in certain cases. The firmness of its attachment to the parts underneath varied considerably in different specimens. I was able in cases in which there was considerable softening to detach readily the mucous membrane with the nail or handle of the scalpel within so short a period after death that it was probable that the change of consistence was not cadaveric. In some cases the vessels of the submucous tissue were injected and this tissue infiltrated.

In all the cases except one lesions were present indicating inflammation {738} of the mucous membrane of the colon. In 39 hyperæmia, thickening, and other signs of inflammation extended over nearly or quite the entire colon; in 14 the colitis was confined to the descending portion entirely or almost entirely; in 28 cases the records state that inflammatory lesions were found in the colon, but their exact location is not mentioned. In 18 of the autopsies the mucous membrane of the colon was found ulcerated.

Therefore, according to these statistics--and autopsies which I have witnessed that are not embraced in them disclosed similar lesions--colitis is present, almost without exception, in cases of summer diarrhoea, associated with more or less ileitis. The portion of the colon which presents the most marked inflammatory lesions is that in and immediately above the sigmoid flexure--that portion, therefore, in which any fermenting fecal matter has reached its greatest degree of fermentation, and consequently contains the most irritating elements, and where, next to the caput coli, it is longest delayed in its passage downward.

The solitary glands of both the large and small intestines and Peyer's patches undergo hyperplasia. In cases of short duration, and in parts of the intestine where the inflammatory action has been mild, the solitary glands present a vascular appearance, like the surrounding membrane, and are slightly enlarged. The enlargement is most apparent if the intestine be viewed by transmitted light, when not only are the glands seen to be swollen, but their central dark points are distinct. If a higher grade of intestinal catarrh or a catarrh more protracted have occurred, the volume of these follicles is so increased that they rise above the common level and present a papillary appearance. Peyer's patches are also distinct and punctate. The enlargement of Peyer's patches, like that of the solitary glands, is due to hyperplasia, the elementary cells being largely increased in number.

The small ulcers which, as we have seen from the above statistics, are present in a certain proportion of cases in the mucous membrane of the colon, and more rarely in that of the small intestine when the inflammation has been protracted and of a severe type, appear to occur in the solitary glands and in the mucous membrane surrounding them. While some of these glands in a specimen are simply tumefied, others are slightly ulcerated, and others still nearly or quite destroyed. The ulcers are usually from one to three lines in diameter, circular or oval, with edges slightly raised from infiltration. Rarely, I have seen minute coagula of blood in one or more ulcers, and I have also observed ulcers which have evidently been larger and have partially healed. The ulcers are more frequently found in the descending colon than in other portions of the intestines. When ulcers are present they commonly occur in the descending colon, or if occurring elsewhere they are most abundant in this situation.

According to my observations, these ulcers are found chiefly in infants over the age of six months--during the time, therefore, when there is greatest functional activity and most rapid development of the solitary glands. Peyer's patches, though frequently prominent and distinct, have not been ulcerated in any of the cases observed by me.

The appendix vermiformis participates in the catarrh when it occurs in the caput coli, its mucous membrane being hyperæmic and thickened. In {739} certain rare cases the inflammation is so intense that a thin film of fibrin is exuded in places upon the surface of the colon. It is apt to be overlooked or to be washed away in the examination. The rectum usually presents no inflammatory lesions, or but slight lesions in comparison with those in the colon. It usually remains of the normal pale color, or but slightly vascular even when there is almost general colitis. Hence the infrequency of tenesmus.

As might be expected from the nature of the disease, the secretion of mucus from the intestinal surface is augmented. It is often seen forming a layer upon the intestinal surface, and it appears in the stools mixed with epithelial cells and sometimes with blood and pus.

The mesenteric glands in cases which have run the most protracted course and end fatally are found more or less enlarged from hyperplasia. They are frequently as large as a pea or larger, and of a light color, the color being due not only to the hyperplasia, but in part to the anæmia. Occasionally, when patients have been much reduced from the long continuance of the diarrhoea, and are in a state of marked cachexia at death, we find certain of these glands caseous.

The condition of the stomach is interesting, since indigestion and vomiting are so commonly present. I have records of its appearance in 59 cases, in 42 of which it seemed normal, having the usual pale color and exhibiting only such changes as occur in the cadaver. In the remaining 17 cases the stomach was more or less hyperæmic, and in 3 of them points of ulceration were observed in the mucous membrane.

All physicians familiar with this disease have remarked the frequency of stomatitis. In protracted and grave cases it is a common complication. The buccal surface in these cases is more vascular than natural, and if the vital powers are much reduced superficial ulcerations are not infrequent, oftener upon the gums than elsewhere. The gums are apt to be spongy, more or less swollen, bleeding readily when rubbed or pressed upon. Thrush is a common complication of the summer complaint in infants under the age of three or four months, but is infrequent in older infants. Occurring in those over the age of six or eight months, it has an unfavorable prognostic significance, indicating a form of summer diarrhoea which commonly eventuates in death.

The belief has long been prevalent in the past that the liver is also in fault. The green color of the stools was supposed to be due to vitiated bile. But usually in the post-mortem examinations which I have made I have found that the green coloration of the fecal matter did not appear at the point where the bile enters the intestines, but at some point below the ductus communis choledochus in the jejunum or ileum. The green tinge, at first slight, becomes more and more distinct on tracing it downward in the intestine. It appears to be due to admixture of the intestinal secretions with the fecal matter.

I have notes of the appearance and state of the liver in 32 fatal cases. Nothing could be seen in these examinations which indicated any anatomical change in this organ that could be attributed to the diarrhoeal malady. The size and weight of the liver varied considerably in infants of the same age, but probably there was no greater difference than usually obtains among glandular organs in a state of health. The following was the weight of this organ in 20 cases: {740}

Age. Weight. | Age. Weight. 4 weeks 5 ounces. | 10 months 6¾ ounces. 2 months 3½ " | 13 " 6 " 2 " 3½ " | 14 " 9 " 4 " 5 " | 15 " 6 " 5 " 6½ " | 15 " 7½ " 5 " 9 " | 15 " 9½ " 7 " 4½ " | 16 " 6 " 7 " 6 " | 19 " 4½ " 7 " 6¼ " | 20 " 9¼ " 9 " 8 " | 23 " 15 "

In none of these cases did the size, weight, or appearance of this organ seem to be different from that in health or in other diseases, except in one in which fatty degeneration had occurred, but this was probably due to tuberculosis, which was also present. In most of these cases the liver was examined microscopically, and the only noteworthy appearance observed was the variable amount of oil-globules in the hepatic cells. In some specimens the oil-globules were in excess, in others deficient, and in others still they were more abundant in one part of the organ than in another. Little importance was attached to these differences in the quantity of oily matter.

Hypostatic congestion of the posterior portions of the lungs, ending if it continue in a form of subacute catarrhal pneumonia and giving rise to an occasional painless cough, has been described in the preceding pages. The character of the cough in connection with the wasting might excite suspicions of the presence of tubercles in the lungs; but tubercles are rare in this disease, and when present I should suspect a strong hereditary predisposition. They occurred in only 1 of the 82 cases.

The state of the encephalon in those patients in whom spurious hydrocephalus occurs is interesting. In protracted cases of the diarrhoea the brain wastes like the body and limbs. In the young infant, in whom the cranial bones are still ununited, the occipital and sometimes the frontal bones become depressed and overlapped by the parietal, the depression being of course proportionate to the diminution in size of the encephalon. The cranium becomes quite uneven. In older children, with the cranial bones consolidated, serous effusion occurs according to the degree of waste, thus preserving the size of the encephalon. The effusion is chiefly external to the brain, lying over the convolutions from the base to the vertex. Its quantity varies from one or two drachms to an ounce or more. Along with this serous effusion, and antedating it, passive congestion of the cerebral veins and sinuses is also present. This congestion is the obvious and necessary result of the feebleness of the heart's action and the loss of brain substance.

DIAGNOSIS.--The occurrence and continuance of diarrhoea in the warm months, without any apparent cause except the agencies which hot weather produces, indicate this disease. The exciting cause of the attack may be the use of some indigestible and irritating substance, dietetic or medicinal, as fruits with their seeds or a purgative medicine; but if it continue after the immediate effects of the agent have passed off, it is proper to attribute the diarrhoea to the summer season.

In the adult abdominal tenderness is an important diagnostic symptom of intestinal catarrh, but in the infant this symptom is lacking or is not in general appreciable, so that it does not aid in diagnosis. When the {741} diagnosis of the disease is established, the symptoms do not usually indicate what part of the intestinal surface is chiefly involved, but it may be assumed that it is the lower part of the ileum and the colon. The presence of mucus or of mucus tinged with blood in the stools shows the predominance of colitis.

PROGNOSIS.--Although this disease every summer largely increases the death-rate of young children, most cases can be cured if the proper hygienic and medicinal measures be early applied. It is obvious, from what has been stated in the foregoing pages, that cholera infantum is the form of this malady which involves greatest danger. Except in such cases there is sufficient forewarning of a fatal result, for if death occur it is after a lingering sickness, with fluctuations and gradual loss of flesh and strength. Patients often recover from a state of great prostration and emaciation, provided that no fatal complications arise. The eyes may be sunken, the skin lie in folds from the wasting, the strength may be so exhausted that any other than the recumbent position is impossible, and yet the patient may recover by removal to the country, by change of weather, or by the use of better diet and remedies. Therefore an absolutely unfavorable prognosis should not be made except in cases that are complicated or that border on collapse. The most dangerous symptoms, except those which indicate commencing or actual collapse, arise from the state of the brain. Rolling the head, squinting, feeble action or permanent contraction of the pupils, spasmodic or irregular movements of the limbs, indicate the near approach of death, as do also coldness of face and extremities and inability to swallow. It is obvious also that in making the prognosis in ordinary cases we should consider the age of the patient, the state of the weather, the time in the summer, whether in the beginning or near its close, and the surroundings, especially in reference to the impurity of the air, as well as the patient's condition.

Cholera Infantum, or Choleriform Diarrhoea.

This is the most severe form of the summer complaint. It receives the name which designates it from the violence of its symptoms, which closely resemble those of Asiatic cholera. It is, however, quite distinct from that disease. It is characterized by frequent stools, vomiting, great elevation of temperature, and rapid and great emaciation and loss of strength. It commonly occurs under the age of two years. It sometimes begins abruptly, the previous health having been good; in other cases it is preceded by the ordinary form of summer diarrhoea. The stools have been thinner than natural and somewhat more frequent, but not such as to excite alarm, when suddenly they become more frequent and watery, and the parents are surprised and frightened by the rapid sinking and real danger of the infant.

The first evacuations, unless there have been previous diarrhoea, may contain fecal matter, but subsequently they are so thin that they soak into the diaper like urine, and in some cases they scarcely produce more of a stain than does this secretion. Their odor is peculiar--not fecal, but musty and offensive, and occasionally almost odorless. Commencing simultaneously with the watery evacuations or soon after is another {742} symptom, irritability of the stomach, which increases greatly the prostration and danger. Whatever drinks are swallowed by the infant are rejected immediately or after a few moments, or retching may occur without vomiting. The appetite is lost and the thirst is intense. Cold water is taken with avidity, and if the infant nurse it eagerly seizes the breast in order to relieve the thirst. The tongue is moist at first, and clean or covered with a light fur, pulse accelerated, respiration either natural or somewhat increased in frequency, and the surface warm, but the temperature is speedily reduced in severe cases. The internal temperature or that of the blood is always very high. In ordinary cases of cholera infantum the thermometer introduced into the rectum rises to or above 105°, and I have seen it indicate 107°. Although the infant may be restless at first, it does not appear to have any abdominal pain or tenderness. The restlessness is apparently due to thirst or to that unpleasant sensation which the sick feel when the vital powers are rapidly reduced. The urine is scanty in proportion to the gravity of the attack, as it ordinarily is when the stools are frequent and watery.

The emaciation and loss of strength are more rapid than in any other disease which I can recall to mind, unless in Asiatic cholera. In a few hours the parents scarcely recognize in the changed and melancholy aspect of the infant any resemblance to the features which it exhibited a day or two before. The eyes are sunken, the eyelids and lips are permanently open from the feeble contractile power of the muscles which close them, while the loss of the fluids from the tissues and the emaciation are such that the bony angles become more prominent and the skin in places lies in folds.

As the disease approaches a fatal termination, which often occurs in two or three days, the infant remains quiet, not disturbed even by the flies which alight upon its face. The limbs and face become cool, the eyes bleared, pupils contracted, and the urine scanty or suppressed. In some instances, when the patient is near death, the respiration becomes accelerated, either from the effect of the disease upon the respiratory centres or from pulmonary congestion resulting from the feeble circulation. As the vital powers fail the pulse becomes progressively more feeble, the surface has a clammy coldness, the contracted pupils no longer respond to light, and the stupor deepens, from which it is impossible to arouse the infant.

In the most favorable cases cholera infantum is checked before the occurrence of these grave symptoms, and often in cases which are ultimately fatal there is not such a speedy termination of the malady as is indicated in the above description. The choleriform diarrhoea abates and the case becomes one of ordinary summer complaint.

ANATOMICAL CHARACTERS.--Rilliet and Barthez, who of foreign writers treat of cholera infantum at greatest length, describe it under the name of gastro-intestinal choleriform catarrh. "The perusal," they remark, "of anatomico-pathological descriptions, and especially the study of the facts, show that the gastro-intestinal tube in subjects who succumb to this disease may be in four different states: (_a_) either the stomach is softened without any lesion of the digestive tube; (_b_) or the stomach is softened at the same time that the mucous membrane of the intestine, and especially its follicular apparatus, is diseased; (_c_) or the stomach is healthy, {743} while the follicular apparatus or the mucous membrane is diseased; (_d_) or, finally, the gastro-intestinal tube is not the seat of any lesion appreciable to our senses in the present state of our knowledge, or it presents lesions so insignificant that they are not sufficient to explain the gravity of the symptoms.

"So far, the disease resembles all the catarrhs, but what is special is the abundance of serous secretion and the disturbance of the great sympathetic nerve.

"The serous secretion, which appears to be produced by a perspiration (analogous to that of the respiratory passages and of the skin) rather than by a follicular secretion, shows, perhaps, that the elimination of substances is effected by other organs than the follicles; perhaps, also, we ought to see a proof that the materials to eliminate are not the same as in simple catarrh. Upon all these points we are constrained to remain in doubt. We content ourselves with pointing out the fact."[2]

[Footnote 2: _Maladies des Enfants_.]

On the 1st of August, 1861, I made the autopsy of an infant sixteen months old who died of cholera infantum with a sickness of less than one day. The examination was made thirty hours after death. Nothing unusual was observed in the brain, unless perhaps a little more than the ordinary injection of vessels at the vertex. No marked anatomical change was observed in the stomach and intestines, except enlargement of the patches of Peyer as well as of the solitary and mesenteric glands. Mucous membrane pale. In this and the following cases there was apparently slight softening of the intestinal mucous membrane, but whether it was pathological or cadaveric was uncertain, as the weather was very warm. The liver seemed healthy. Examined by the microscope, it was found to contain about the normal number of oil-globules.

The second case was that of an infant seven months old, wet-nursed, who died July 26, 1862, after a sickness also of about one day. He was previously emaciated, but without any marked ailment. The post-mortem examination was made on the 28th. The brain was somewhat softer than natural, but otherwise healthy. There was no abnormal vascularity of the membranes of the brain, and no serous effusion within the cranium. The mucous membrane of the intestines had nearly the normal color throughout, but it seemed somewhat thickened and softened; the solitary glands of the colon were prominent. The patches of Peyer were not distinct.

In the New York Protestant Episcopal Orphan Asylum an infant twenty months old, previously healthy, was seized with cholera infantum on the 25th of June, 1864. The alvine evacuations, as is usual with this disease, were frequent and watery, and attended by obstinate vomiting. Death occurred in slight spasms in thirty-six hours. The exciting cause was probably the use of a few currants which were eaten in a cake the day before, some of which fruit was contained in the first evacuations. The brain was not examined. The only pathological changes which were observed in the stomach and intestines were slightly vascular patches in the small intestines and an unusual prominence of the solitary glands in the colon. The glands resembled small beads imbedded in the mucous membrane. The lungs in the above cases were healthy, excepting hypostatic congestion.

{744} Since the date of these autopsies I have made others in cases which terminated fatally after a brief duration, and have uniformly found similar lesions--namely, the gastro-intestinal surface either without vascularity or scantily vascular in streaks or patches, sometimes presenting a whitish or soggy appearance and somewhat softened, while the solitary glands were enlarged so as to be prominent upon the surface. In cases which continue longer evident inflammatory lesions soon appear which are identical with those which have already been described in our remarks on the ordinary form of the summer diarrhoea.

During my term of service in the New York Foundling Asylum in the summer of 1884, an infant died after a brief illness with all the symptoms of cholera infantum, and the intestines were sent to William H. Welch, now of Johns Hopkins Hospital, for microscopic examination. His report was as follows: "I found undoubted evidence of acute inflammation. There was an increased number of small, round cells (leucocytes) in the mucous and submucous coats. This accumulation of new cells was most abundant in and around the solitary follicles, which were greatly swollen. Clumps of lymphoid cells were found extending even a little into the muscular coat. The epithelial lining of the intestine was not demonstrable, but this is usually the case with post-mortem specimens of human intestine, and justifies no inferences as to pathological changes. The glands of Lieberkühn were rich in the so-called goblet-cells, and some of the glands were distended with mucus and desquamated epithelium, so as to present sometimes the appearance of little cysts. This was observed especially in the neighborhood of the solitary follicles. The blood-vessels, especially the veins of the submucous coat, were abnormally distended with blood. I searched for micro-organisms, and found them in abundance upon the free surface of the intestine in the mucous accumulations there, and also in the mouths of the glands of Lieberkühn. Both rod-shaped and small round bacteria were found. I attach no especial importance to finding bacteria upon the surface of the intestine. The general result of the examination is to confirm the view that cholera infantum is characterized by an acute intestinal inflammation."

NATURE.--Cholera infantum appears from its symptoms and lesions to be the most severe form of intestinal catarrh to which infants are liable. The alvine discharges, to which the rapid prostration is largely due, probably consist in part of intestinal secretions and in part of serum which has transuded from the capillaries of the intestines. That the intestinal mucous membrane sometimes presents a pale appearance at the autopsy of an infant who, previously well, has died of cholera infantum after a sickness of twenty-four or forty-eight hours, is perhaps due to the great amount of liquid secretion and transudation in which the inflamed surface is bathed. Moreover, it is, I believe, a recognized fact that the hyperæmia of an acutely-inflamed surface when of short duration frequently disappears in the cadaver, as that of scarlet fever and erysipelas. The early hyperplasia of the solitary and mesenteric glands, and the hyperæmia and thickening of the surface of the ileum and colon in those who have survived a few days, indicate the inflammatory character of the malady.

The opinion has been expressed by certain observers that cholera {745} infantum is identical with thermic fever or sunstroke. There is indeed a resemblance to thermic fever as regards certain important symptoms. In cholera infantum the temperature is from 105° to 108°; in sunstroke it is also very high, often running above 108°. Great heat of head, contracted pupils, thin fecal evacuations, embarrassed respiration, scanty urine, and cerebral symptoms are common toward the close of cholera infantum, and they are the prominent symptoms in sunstroke. Nevertheless, I cannot accept the theory which regards these maladies as identical, and which removes cholera infantum from the list of intestinal diseases. In cholera infantum the gastro-intestinal symptoms always take the precedence, and are, except in advanced cases, always more prominent than other symptoms. It does not commence as by a stroke like coup de soleil, but it comes on more gradually, though rapidly, and it often supervenes upon a diarrhoea or some error of diet. In the commencement of cholera infantum the infant is not apt to be drowsy, and it is often wide awake and restless from the thirst. Contrast this with the alarming stupor of sunstroke. Sunstroke only occurs during the hours of excessive heat, but cholera infantum may occur at any hour or in any day during the hot weather, provided that there be sufficient dietetic cause. Again, intestinal inflammation is not common in sunstroke, while it is the common or, as I believe, the essential lesion of cholera infantum. These facts show, in my opinion, that the two maladies are essentially and entirely distinct. Nevertheless, cases of apparent sunstroke sometimes occur in the infant, and if the bowels are at the same time relaxed the disease is apt to be regarded as cholera infantum, and if fatal is usually reported as such to the health authorities. Cases of this kind I have occasionally observed or they have been reported to me, although they are not common.

With the exception of the organs of digestion no uniform lesions are observed in any of the viscera in cholera infantum, except such as are due to change in the quantity and fluidity of the blood and its circulation. Writers describe an anæmic appearance of the thoracic and abdominal viscera, and occasionally passive congestion of the cerebral vessels. The cerebral symptoms often present toward the close of life in unfavorable cases of cholera infantum are often due to spurious hydrocephalus, which we have described above; but as the urinary secretion is scanty or suppressed, cerebral symptoms may in certain cases be due to uræmia.

DIAGNOSIS.--This form of the summer diarrhoea is diagnosticated by the symptoms, and especially by the frequency and character of the stools. The stools have already been described as frequent, often passed with considerable force, deficient in fecal matter, and thin, so as to soak into the diaper almost like urine. The vomiting, thirst, rapid sinking, and emaciation serve to distinguish cholera infantum from other diarrhoeal maladies.

When Asiatic cholera is prevalent the differential diagnosis between the two is difficult if not impossible.

PROGNOSIS.--Cholera infantum is one of those diseases in regard to which physicians often injure their reputation by not giving sufficient notice of the danger, or even by expressing a favorable opinion when the case soon after ends fatally. A favorable prognosis should seldom be expressed without qualification. If the urgent symptoms be relieved, {746} still the disease may continue as an ordinary intestinal inflammation, which in hot weather is formidable and often fatal. If the stools become more consistent and less frequent without the occurrence of cerebral symptoms, while the limbs are warm and the pulse good, we may confidently express the opinion that there is no present danger.

The duration of true cholera infantum is short. It either ends fatally, or it begins soon to abate and ceases, or it continues, and is not to be distinguished in its subsequent course from an attack of summer diarrhoea beginning in the ordinary manner.

TREATMENT.--Preventive Measures.--Obviously, efficient preventive measures consist in the removal of infants so far as practicable from the operation of the causes which produce the disease. Weaning just before or in the hot weather should, if possible, be avoided, and removal to the country should be recommended, especially for those who are deprived of the breast-milk during the age when such nutriment is required. If for any reason it is necessary to employ artificial feeding for infants under the age of ten months, that food should obviously be used which most closely resembles human milk in digestibility and in nutritive properties. Care should be taken to prevent fermentation in the food before its use, since much harm is done by the employment of milk or other food in which fermentative changes have occurred and which occur quickly in dietetic mixtures in the hot months.

It is also very important that the infant receive its food in proper quantity and at proper intervals, for if the mother or nurse in her anxiety to have it thrive feed it too often or in too large quantity, the surplus food which it cannot digest if not vomited undergoes fermentation, and consequently becomes irritating to the gastro-intestinal surface. The physician should be able to give advice not only in reference to the frequency of feeding, but also in regard to the quantity of food which the infant requires at each feeding. Correct knowledge and advice in this matter aid in the prevention and cure of the dyspeptic and diarrhoeal maladies of infancy.

Chadbourne of this city and myself made some observations in order to ascertain how much food well-nourished infants receive daily. We selected infants that had an abundance of breast-milk, and weighed them before and after each nursing, so as to determine how much each infant took during twenty-four hours. The avoirdupois ounce contains 437.5 grains, and we ascertained by careful weight and measurement, employing the metric system for its greater accuracy, that one fluidounce of human milk, with a specific gravity of 1.031, weighed 451.9 grains. With these data it was easy to determine the quantity of milk in fluidounces from its weight. Our first observations related to 12 infants under the age of five weeks, 8 of which nursed twelve times, and the remaining 4 eight, nine, nine, and eleven times respectively, in the twenty-four hours. The quantity of milk received by them in twenty-four hours varied considerably in the different cases, but the average was 12.41 fluidounces. Therefore if a baby in the first five weeks nurse every two hours, it receives only a little more than one fluidounce at each nursing.

The next observations were made upon 15 infants between the ages of five weeks and ten months: 8 of the 15 were under the age of six {747} months, and the remaining 7 were between the ages of six months and ten months. The weighing showed that the younger took nearly the same quantity per day, on the average, as the older infants in this group. The average quantity received by each was twenty-four and six-tenths fluidounces. Hence if the nursings were eight in the twenty-four hours, three ounces were taken at each nursing; if the nursings were twelve, the quantity each time was two ounces.

Biedert of Germany has also made similar observations in order to determine the amount of nutriment required by infants. The results of his weight-studies, as he designates them, were published in the _Jahrbuch für Kinderheilkunde_, xix. B., 3 H. His weighing showed that infants during their first month, if fed on cow's milk, required from 160 to 200 grammes of milk daily, and in the third month 300 grammes. These quantities in fluid measure are 5.44 to 6.83 ounces, the quantity required each day in the first month, and 10.22 ounces, the quantity required daily the second month. Therefore, both my weights and Biedert's show that infants under the age of two months assimilate a smaller quantity of milk than is usually supposed. For infants older than two months he estimates the quantity of milk required by infants by their weight. He believes that the greater the weight the greater is the amount of food which the infant needs. The method pursued by Chadbourne and myself is more simple, and it seems to indicate with sufficient exactness the amount of food required.

Some infants, like adults, need more food than others, so that there can be no exact schedule of the quantity which they require at each feeding; but while in the first and second months they do not need more than from one to one and a half fluidounces at each feeding, whether of breast-milk, or of cow's milk prepared so as to resemble as closely as possible human milk, infants as they grow older and their stomachs enlarge can take food in larger quantity, and therefore require less frequent feeding. Under the age of two months the stomach is so small that it cannot receive much more than one or one and a half fluidounces without undue distension. At the age of six months it can probably receive and digest without discomfort three ounces, and in the last half of the first year even four ounces. Infants nourished at the breast should be allowed to nurse every two hours in the daytime, whatever the age, after the second month, but less frequently at night, for frequent nursing promotes the secretion of milk, and the milk is of better quality than when it is long retained in the breast. If by the fifth or sixth month mothers or wet-nurses find, as is frequently the case, that they do not have sufficient milk, other food should be given in addition, perhaps after each second nursing or every fourth hour. The kind of food which it is best to employ to supplement the nursing will be mentioned under the head of curative measures. By knowledge on the part of the mother and nurse of the dietetic needs of the infant, and by consequent judicious alimentation, and by measures also to procure the utmost purity of the air, there can be no doubt that the summer diarrhoea may to a great extent be prevented.

Curative Treatment.--The indications for treatment are--1st, to provide the best possible food; 2d, to procure pure air; 3d, to aid the digestive function of the infant; 4th, to employ such medicinal agents as can be safely given to check the diarrhoea and cure the intestinal catarrh.

{748} The infant with this disease is thirsty, and is therefore apt to take more nutriment in the liquid form than it requires for its sustenance. If nursing, it craves the breast, or if weaned, craves the bottle, at short intervals to relieve the thirst. No more nutriment should be allowed than is required for nutrition, for the reason stated above, and the thirst may best be relieved by a little cold water, gum-water, or barley-water, to which a few drops of brandy or whiskey are added.

Since one of the two important factors in producing the summer diarrhoea is the use of improper food, it is obviously very important for the successful treatment of this disease that the food should be of the right kind, properly prepared, and given in proper quantity. I need not repeat that for infants under the age of one year no food is so suitable as breast-milk, and one affected with the diarrhoea and remaining in the city should, if possible, at least if under the age of ten months, be provided with breast-milk. It can be more satisfactorily treated and the chances of its recovery are much greater if it be nourished with human milk than by any other kind of diet. If, however, the mother's milk fail or become unsuitable from ill-health or pregnancy, and on account of family circumstances a wet-nurse cannot be procured, the important and difficult duty devolves upon the physician of deciding how the infant should be fed. In order to solve this problem it will be well to recall to mind the part performed in the digestive function by the different secretions which digest food:

1st. The saliva is alkaline in health. It converts starch into glucose or grape-sugar. It has no effect upon fat or the protein group. It is the secretion of the parotid, submaxillary, and sublingual glands, which in infants under the age of three months are very small, almost rudimentary. The two parotid glands at the age of one month weigh only thirty-four grains. The power to convert starch into sugar possessed by saliva is due to a ferment which it contains called ptyalin.

2d. The gastric juice is a thin, nearly transparent, and colorless fluid, acid from the presence of a little hydrochloric acid. It produces no change in starch, grape-sugar, or the fats, except that it dissolves the covering of the fat-cells. Its function is to convert the proteids into peptone, which is effected by its active principle, termed pepsin.

3d. The bile is alkaline and neutralizes the acid product of gastric digestion. It has no effect on the proteids. It forms soaps with the fatty acids and has a slight emulsifying action on fat. The soaps are said to promote the emulsion of fat. Their emulsifying power is believed to be increased by admixture with the pancreatic secretion. Moreover, the absorption of oil is facilitated by the presence of bile upon the surface through which it passes.

4th. The pancreatic juice appears to have the function of digesting whatever alimentary substance has escaped digestion by the saliva, gastric juice, and bile. It is a clear, viscid liquid of alkaline reaction. It rapidly changes starch into glucose. It converts proteids into peptones and emulsifies fats. While the gastric juice requires an acid medium for the performance of its digestive function, the pancreatic juice requires one that is alkaline. This important fact should be borne in mind, that such a mistake as presenting pepsin with chalk mixture, or the extractum pancreatis with dilute muriatic acid, may be avoided.

{749} 5th. The intestinal secretions are mainly from the crypts of Lieberkühn, and their action in the digestive process is probably comparatively unimportant, but in some animals they have been found to digest starch. It will be observed that of all these secretions that which digests the largest number of nutritive principles is the pancreatic. It digests all those which are essential to the maintenance of life except fat, and it aids the bile in emulsifying fat.

One of the most important conferences in pædiatrics ever held convened at Salzburg in 1881 for the purpose of considering the diet of infants. Among those who participated in the discussion were men known throughout the world as authorities in children's diseases, such as Demme, Biedert, Gerhardt, Henoch, Steffen, Thomas, and Soltmann. None of the physicians present dissented from the following proposition of the chairman: That "all the advances made in physiology in respect to the digestive organs of children only go to prove that the mother's milk is the only true material which is quantitatively and qualitatively suited to the development of the child, which preserves the physiological functions of the organs of digestion, and under favorable circumstances of growth unfolds the whole organism in its completeness." All agreed that when the breast-milk fails animal milk is the best substitute. Henoch, who was one of the conference, expresses the same opinion in his well-known treatise on diseases of children, as follows: "Cow's milk is the best substitute for mother's milk during the entire period of infancy. I consider the administration of other substances advisable only when good cow's milk cannot be obtained or when it gives rise to constant vomiting and diarrhoea."

The many infants' foods contained in the shops were considered by the conference, and, in the words of the chairman, "Now and evermore it is unanimously agreed that these preparations can in no way be substituted for mother's milk, and as exclusive food during the first year are to be entirely and completely rejected." But, unfortunately, we soon learn by experience that animal milk, although it is the best of the substitutes for human milk, is, especially as dispensed in the cities, faulty. It is digested with difficulty by young infants, and is apt to cause in them diarrhoea and intestinal catarrh. Therefore in the hot months its use is very apt to act as one of the dietetic causes of the summer diarrhoea in infants exclusively fed upon it, unless it be specially prepared so as to more closely resemble human milk. The frequent unsatisfactory results of its use have led to the preparation of the many proprietary substitutes for human milk which the shops contain, and which have been so summarily discarded by the German conference.

Woman's milk in health is always alkaline. It has a specific gravity of 1.0317; cow's milk has a specific gravity of 1.029. That of cows stabled and fed upon other fodder than hay or grass is usually decidedly acid. That from cows in the country with good pasturage is said to be alkaline, but in two dairies in Central New York a hundred miles apart, in midsummer, with an abundant pasturage, two competent persons whom I requested to make the examinations found the milk slightly acid immediately after the milking in all the cows.

The following results of a large number of analyses of woman's and cow's milk, made by König and quoted by Leeds, and of several of the {750} best known and most used preparations designed by their inventors to be substitutes for human milk, show how far these substitutes resemble the natural aliment in their chemical characters:

-------------+-----------------------+-----------------------+ | Woman's Milk. | Cow's Milk. | +-------+-------+-------+-------+-------+-------+ | | Mini- | Maxi- | | Mini- | Maxi- | | Mean. | mum. | mum. | Mean. | mum. | mum. | ---------------------+-------+-------+-------+-------+-------+ Water | 87.09 | 83.69 | 90.90 | 87.41 | 80.32 | 91.50 | Total solids | 12.91 | 9.10 | 16.31 | 12.59 | 8.50 | 19.68 | Fat | 3.90 | 1.71 | 7.60 | 3.66 | 1.15 | 7.09 | Milk-sugar | 6.04 | 4.11 | 7.80 | 4.92 | 3.20 | 5.67 | Casein | 0.63 | 0.18 | 1.90 | 3.01 | 1.17 | 7.40 | Albumen | 1.31 | 0.39 | 2.35 | 0.75 | 0.21 | 5.04 | Albuminoids | 1.94 | 0.57 | 4.25 | 3.76 | 1.38 | 12.44 | Ash | 0.49 | 0.14 | ... | 0.70 | 0.50 | 0.87 | -------------+-------+-------+-------+-------+-------+-------+

The following analyses of the foods for infants found in the shops, and which are in common use, were made by Leeds of Stevens's Institute:

_Farinaceous Foods_. ----------------+-------+-------+-------+-------+--------+-------+ | 1. | 2. | 3. | 4. | 5. | 6. | | | Hubb- |Imper- | | |Robin- | |Blair's| ell's | ial |Ridge's|"A.B.C."| son's | | Wheat | Wheat |Granum.| Food. | Cereal |Patent | | Food. | Food. | | | Milk. |Barley.| ----------------+-------+-------+-------+-------+--------+-------+ Water | 9.85 | 7.78 | 5.49 | 9.23 | 9.33 | 10.10 | Fat | 1.56 | 0.41 | 1.01 | 0.63 | 1.01 | 0.97 | Grape-sugar | 1.75 | 7.56 | Trace.| 2.40 | 4.60 | 3.08 | Cane-sugar | 1.71 | 4.87 | Trace.| 2.20 | 15.40 | 0.90 | Starch | 64.80 | 67.60 | 78.93 | 77.96 | 58.42 | 77.76 | Soluble | | | | | | | carbohydrates | 13.69 | 14.29 | 3.56 | 5.19 | 20.00 | 4.11 | Albuminoids | 7.16 | 10.13 | 10.51 | 9.24 | 11.08 | 5.13 | Gum, cellulose, | |Undet- | | | | | etc. | 2.94 |erm'd. | 0.50 | ... | 1.16 | 1.93 | Ash | 1.06 | 1.00 | 1.16 | 0.60 | ... | 1.93 | ----------------+-------+-------+-------+-------+--------+-------+

_Liebig's Foods_. ----------------+------+------+-------+-------+------+------+------+ | | | | Keas- |Savory| | | | Mel- | Haw- | Hor- |bey and| and | Baby | Baby | |lin's.|ley's.|lick's.| Matti-|Moor- | Sup | Sup | | | | | son's.| e's. |No. 1.|No. 2.| ----------------+------+------+-------+-------+------+------+------| Water | 5.00| 6.60| 3.39 | 27.95 | 8.34| 5.54| 11.48| Fat | 0.15| 0.61| 0.08 | None. | 0.40| 1.28| 0.62| Grape-sugar | 44.69| 40.57| 34.99 | 36.75 | 20.41| 2.20| 2.44| Cane-sugar | 3.51| 3.44| 12.45 | 7.58 | 9.08| 11.70| 2.48| Starch | None.| 10.97| None. | None. | 36.36| 61.99| 51.95| Soluble | | | | | | | | carbohydrates | 85.44| 76.54| 87.20 | 71.50 | 44.83| 14.35| 22.79| Albuminoids | 5.95| 5.38| 6.71 | None. | 9.63| 9.75| 7.92| Gum, cellulose, | | | | | | | | etc. | ... | ... | ... | ... | 0.44| 7.09| 5.24| | | | | | |Undet-| | Ash | 1.89| 1.50| 1.28 | 0.93 | 0.89|erm'd.| 1.59| ----------------+------+------+-------+-------+------+------+------+

{751} _Milk Foods_. ----------------+-----------+-----------+-----------+-----------+ | | Anglo- | | American- | | Nestle's. | Swiss. | Gerber's. | Swiss. | ----------------+-----------+-----------+-----------+-----------+ Water | 4.72 | 6.54 | 6.78 | 5.68 | Fat | 1.91 | 2.72 | 2.21 | 6.81 | Grape-sugar and | | | | | milk-sugar | 6.92 | 23.29 | 6.06 | 5.78 | Cane-sugar | 32.93 | 21.40 | 30.50 | 36.43 | Starch | 40.10 | 34.55 | 38.48 | 30.85 | Soluble | | | | | carbohydrates | 44.88 | 46.43 | 44.76 | 45.35 | Albuminoids | 8.23 | 10.26 | 9.56 | 10.54 | Ash | 1.59 | 1.20 | 1.21 | 1.21 | ----------------+-----------+-----------+-----------+-----------+

It is seen by examination of the analyses of the above foods that all except such as consist largely or wholly of cow's milk differ widely from human milk in their composition, and although some of them--as the Liebig preparations, in which starch is converted into glucose by the action of the diastase of malt--may aid in the nutrition and be useful as adjuncts to milk, physicians of experience and close observation will, I think, agree with the German conference that when breast-milk fails or is insufficient our main reliance for the successful nutrition of the infant must be on animal milk. Nestle's Food, which consists of wheat flour, the yelk of egg, condensed milk, and sugar, and which has been so largely used in this country and in Europe, is probably beneficial mainly from the large amount of Swiss condensed milk which it contains.

Although the preference is to be given to animal milk over any other kind of food as a substitute for human milk, yet even when obtained fresh and from the best dairies and properly diluted it is very apt to disagree with infants under the age of one year, producing indigestion and diarrhoea. The close resemblance in chemical character of cow's, ass's, and goat's milk to human milk would lead us to expect that either would be a good substitute for the latter. The fact that the milk of these animals is apt to cause indigestion and intestinal catarrh, especially in the hot months, when the digestive function of the infant is enfeebled from the heat, must be due to the quality rather than quantity of its constituents. The difference in quality of the casein of human and animal milk is well known, since that of human milk coagulates in the stomach in flakes, and that of animal milk in firm and large masses. The German conference saw at once the importance of the problem which confronted them--_i.e._ how to modify cow's milk so that it bears the closest possible resemblance to human milk. They even discussed the difference of the milk of different breeds of cows, and the proper feeding and care of cows, but the most important suggestion made--and one which has already produced good results in this country and in Europe, and promises to be instrumental in saving the lives of many infants who by the old method of feeding would inevitably perish--was made by Pfeiffer of Wiesbaden. I allude to the peptonizing of milk. The pancreatic secretion digests milk that is rendered alkaline at a temperature between 100° and 150° F. Milk thus treated becomes in from twenty minutes to one hour thinner, resembling human milk in appearance, and if the peptonizing be continued beyond a certain point, and is more complete, its taste is decidedly {752} bitter. The process should be watched and the peptonizing suspended as soon as the bitterness becomes appreciable, for, although more advanced peptonizing so changes the milk that it is more easily digested by the infant than when the peptonizing is partial, yet the bitterness which is imparted to it renders it very disagreeable as a dietetic preparation. Milk thus prepared closely resembles human milk in appearance, and its casein is so digested that it is either not precipitated by acids or is precipitated, like that of human milk, in flakes. By this process a digested or an easily-digested casein is produced, instead of the casein of ordinary cow's milk, which produces large and firm masses in the stomach--masses that the digestive ferments penetrate with such difficulty that they cause indigestion, and occur in the stools in coagula of greater or less size. Pfeiffer pointed out that when peptonized milk is employed "the feces showed absolutely no trace of the white cheesiness." Milk thus prepared quickly spoils, and it is necessary to peptonize it in small quantity and often during the twenty-four hours.

In New York City during the last year peptonized milk has been employed largely as recommended by Pfeiffer, and with such results as to encourage its further use. It is now used in the New York Infant Asylum and New York Foundling Asylum. Five grains of extractum pancreatis (Fairchild & Co.'s) and ten grains of sodium bicarbonate are added to one gill of warm water. This is mixed with one pint of warm milk, and the mixture, in some convenient vessel, is placed in water kept at a temperature of 100° F. for one hour, when it is placed upon ice to prevent further digestion. It should be tasted frequently during the peptonizing process, and if the least bitterness be observed the process should be suspended before the expiration of the hour. With some specimens of milk, especially at a temperature of 115° to 120°, a half hour or even less is sufficient. This artificial digestion is arrested either by boiling the peptonized milk, which destroys the ferment, or by reducing its temperature to near the freezing-point, which renders it latent and inactive, but does not destroy it. I need not add that placing the peptonized milk on ice is preferable to boiling it, since we wish the ferment to continue to act in the stomach of the infant. In the present state of our knowledge of infant feeding, therefore, we can recommend no better substitute for human milk than peptonized cow's milk.

Leeds recommended the following formula for peptonizing milk in his very instructive remarks made before the New York County Medical Association, July 16, 1884. In order that no mistake might be made, I wrote to him for his formula, which he kindly sent me. The following is an extract from his letter: "The formula which I ventured to suggest for the preparation of humanized cow's milk was as follows: 1 gill of cow's milk, fresh and unskimmed; 1 gill of water; 2 tablespoonfuls of rich cream; 200 grains of milk-sugar; 1½ grains of extractum pancreatis; 4 grains of sodium bicarbonate. Put this in a nursing-bottle; place the bottle in water made so warm that the whole hand cannot be held in it without pain longer than one minute. Keep the milk at this temperature for exactly twenty minutes. The milk should be prepared just before using."

The object is of course to provide from cow's milk a food which will be the nearest possible approximation to healthy human milk; and this {753} appears to be achieved by the peptonizing process. Certainly, what physicians have long been desiring--namely, some mode of preparing cow's milk so that its casein will coagulate in flakes like that of human milk--has been obtained by peptonizing.

It is a common error to expect too much of a new remedy which has a real value, and we must not expect that all patients not in an utterly hopeless state will begin to improve as soon as peptonized milk is prepared for them, or that it is a full and exact substitute for human milk, so that wet-nurses may be dispensed with. Healthy human milk is the best of all food for infants under the age of twelve months, and should always be preferred when it can be obtained, but we claim that peptonized milk is a most useful addition to the dietetic preparations for infants, probably surpassing in value the best of those in the shops. We employ it in the belief that it affords important aid in curing the dyspeptic and diarrhoeal maladies of infancy. Who first formulated and recommended the process of peptonizing milk I am not able to state, but I am informed that Roberts of Great Britain called attention to it as a means of improving milk at a time antedating the German conference.

Milk from healthy, properly-fed cows may be prepared without peptonizing, so as to agree with many infants except in the warmest weather, but is obviously less easily digested than peptonized milk. It should be diluted as follows with water boiled so as to free it from germs: In the first week after birth one-fourth milk with the addition of a little sugar. The milk should be gradually increased, so that it is one-third by the end of the fourth week, one-half by the end of the third month, and two-thirds to three-fourths by the end of the sixth month. After the sixth month it is still proper to add one-fourth water, but pure milk may be given. Water increases the urination.

Before peptonizing--which, as we have seen, digests the casein to a great extent, and changes that which is not digested so that it coagulates in flakes in the stomach like breast-milk--was resorted to, it was customary to use a thin barley- or oat-water in place of the water used for diluting the milk. One heaped teaspoonful of barley flour to two tablespoonfuls of water make a gruel of proper consistence. A little farinaceous substance added to the milk by mechanically separating the particles of casein tends to prevent their coagulation in large and firm masses. This was the theory which explained the beneficial action of the admixture. If for any reason peptonized milk be not employed, milk prepared in the way I have mentioned, by admixture with a farinaceous substance, is probably the next best substitute for human milk.

It is very important to determine when and how farinaceous foods shall be given in this disease. It is well known that infants under the age of three months digest starch with difficulty and only in small quantity, since the salivary and pancreatic glands which secrete the ferments which digest starch are almost rudimentary at that age. The artificial digestion of starch is, however, easily accomplished. Among the last labors of the renowned chemist Baron Liebig was the preparation of a food for infants in which the starch is digested and transformed into grape-sugar, and thus infants at any age who are fed with it are relieved of the burden of digesting it. The baron led the way which has been so successfully followed since in the artificial digestion of foods. A considerable part of the starch {754} in wheat flour is converted into grape-sugar by the prolonged action of heat. I frequently recommend that from three to five pounds of wheat flour be packed dry in a firm muslin bag, so as to form a ball, and be placed in water sufficient to cover it constantly and the bag kept over the fire three or four days. During the nights the fire may go out for a few hours. At the expiration of this time the external part, which is wet, being peeled off, the remainder resembles a lump of yellowish chalk. The flour grated from it gives a decided reaction of sugar by Fehling's test. Starch is also quickly transformed into glucose by the action of the diastase of malt, which indeed Liebig employed. If to a gruel of barley flour, oatmeal, or other farinaceous substance, when hot, a little of a good preparation of extract of malt, such as that prepared by Trommer & Co. at Fremont, Ohio, which acts promptly, or by Reed & Carnrick, be added, it becomes thinner. It is claimed that the starch is thus quickly converted into glucose; which seems doubtful. It is, however, so modified that it is apparently more readily digested and assimilated. Farinaceous substances thus prepared may be employed with peptonized or other milk. Infants frequently do better with this admixture than when either the milk or gruel is used separately.

Of the foods contained in the shops which have been most prescribed, and which have apparently been useful in certain cases, I may mention those which have been prepared according to Liebig's formula, of which there are several, the analyses of which I have given, and Nestle's farina. In the use of those foods which contain no milk, as Ridge's food, Imperial granum, etc., it is recommended that milk be added, while for such as contain condensed milk, as Nestle's and the Anglo-Swiss food, only water should be employed. The Anglo-Swiss food contains about 60 per cent. condensed milk and about 20 per cent. each of oatmeal and Russian wheat flour. It gives an acid reaction, unlike Nestle's, which is alkaline. When Biedert's cream conserve was announced great expectations were awakened from the fact that the inventor is an authority in pædiatrics, but, unfortunately, they have not been realized in this country. Much of Biedert's conserve when it reaches us is spoiled, and the directions for its use are too complicated for ordinary family use, since a different mixture is required for each month of the infant's age. I have employed this food, but, with Henoch, "could not convince myself that it is more efficacious than cow's milk." I am informed that the sale of it in this country has ceased.

Condensed milk is largely used in the feeding of infants. The milk is condensed in vacuo to one-third or one-fifth its volume, heated to 100° C. (212° F.) to kill any fungus which it contains, and 38 to 40 per cent. of cane-sugar is added to preserve it. In the first month one part of milk should be added to sixteen of water, and the proportion of water should be gradually reduced as the infant becomes older. The large amount of sugar which condensed milk, preserved in cans, contains renders it unsuitable in the dietetic rôle of the summer diarrhoea of infants. The sugar is apt to produce acid fermentation and diarrhoea in hot weather. Borden's condensed milk, freshly prepared, as dispensed from the wagons, contains, I am informed by the agent, no cane-sugar or other foreign substance, and on this account is to be preferred to that in the cans. It is cow's milk of good quality, from which 75 to 79 per cent. of the water {755} has been removed under vacuum. The sole advantage which it possesses--and it is an important one--is that it resists fermentation longer than the ordinary milk.

To select the best food for the infant from this considerable number of dietetic preparations is one of the most important duties of the physician. If called to an infant unfortunately deprived of wholesome breast-milk, and suffering in consequence from indigestion and diarrhoea, what diet shall we recommend? My recommendation would be as follows: Use cow's milk of the best possible quality and peptonized in the manner stated above, and peptonized in small quantity at a time, such as a pint, or, better, half a pint. This may be the sole food till the age of five or six months. Unfortunately, in the cities the milk that is delivered in the morning is the milking of the preceding evening, mixed with that of the preceding morning, brought often many miles from the farms where it is produced. Milk twelve and twenty-four hours old, notwithstanding the use of ice around the milk-cans, is apt to undergo some fermentative change before it reaches the nursery. This prevents the preparation of the best quality of peptonized milk, so that in some instances during the heated term I have found that the peptonized milk did not agree as well as the condensed milks, like Borden's or Nestle's food. Not a few infants suffering from diarrhoeal maladies seem to do better if some farinaceous food properly prepared be added to the peptonized milk than when the milk is used alone. It is better, I think, that the starch, or a considerable part of the starch, be converted into glucose before the admixture. This can be done if a few pounds of wheat flour be pressed dry in a bag, so as to form a ball, and boiled three or four days, as I have elsewhere recommended. The flour grated from the mass gives a decided sugar reaction to Fehling's test. For infants under the age of six months one tablespoonful of the flour thus prepared should be mixed with twelve tablespoonfuls of water and boiled. When it has been removed from the fire and become tepid, a small quantity of a good extract of malt, as Trommer's or Reed & Carnrick's, may advantageously be added to the gruel to increase the transformation of starch and render it more digestible. To avoid the time and trouble of preparing the food in this manner, one of the foods contained in the shops, in which the starch has been transformed into glucose by the employment of Baron Liebig's formula, may be used, as Mellin's or Horlick's, instead of the wheat flour prepared by long boiling. The older the child, the thicker should be the gruel.

Beef-, mutton-, or chicken-tea should not be employed, at least as it is ordinarily made, since it is too laxative. Occasionally, for the older infants, we may allow the expressed juice of beef, raw scraped beef, or beef-tea prepared by adding half a pound of lean beef, finely minced, to one pint of cold water, and after allowing it to stand for half an hour warming it to a temperature not exceeding 110° for another half hour. By this process the albumen is preserved. Salt should be added to it, and I am in the habit of adding to it also about seven drops of dilute muriatic acid to facilitate its digestion. It is chiefly for infants over the age of ten months that the meat-juices are proper. A concentrated nutriment, prepared, it is stated, from beef, mutton, and fruits, has lately been introduced in the shops under the name Murdoch's Liquid Food. Young {756} infants with dyspeptic and diarrhoeal symptoms can take it, and it appears to be readily assimilated, as the quantity given at each feeding is small. It has its advocates, and it appears to be of some service in cases of weak and irritable stomach.

But since one of the two important factors in producing the summer diarrhoea of infants is foul air, it is obvious that measures should be employed to render the atmosphere in which the infant lives as free as possible from noxious effluvia. Cleanliness of the person, of the bedding, and of the house in which the patient resides, the prompt removal of all refuse animal or vegetable matter, whether within or around the premises, and allowing the infant to remain a considerable part of the day in shaded localities where the air is pure, as in the parks or suburbs of the city, are important measures. In New York great benefit has resulted from the floating hospital which every second day during the heated term carries a thousand sick children from the stifling air of the tenement-houses down the bay and out to the fresh air of the ocean.

But it is difficult to obtain an atmosphere that is entirely pure in a large city with its many sources of insalubrity; and all physicians of experience agree in the propriety of sending infants affected with the summer diarrhoea to localities in the country which are free from malaria and sparsely inhabited, in order that they may obtain the benefits of a purer air. Many are the instances each summer in New York City of infants removed to the country with intestinal inflammation, with features haggard and shrunken, with limbs shrivelled and the skin lying in folds, too weak to raise, or at least hold, their heads from the pillow, vomiting nearly all the nutriment taken, stools frequent and thin, resulting in great part from molecular disintegration of the tissues--presenting, indeed, an appearance seldom observed in any other disease except in the last stages of phthisis--and returning in late autumn with the cheerfulness, vigor, and rotundity of health. The localities usually preferred by the physicians of this city are the elevated portions of New Jersey and Northern Pennsylvania, the Highlands of the Hudson, the central and northern parts of New York State, and Northern New England. Taken to a salubrious locality and properly fed, the infant soon begins to improve if the disease be still recent, unless it be exceptionally severe. If the disease have continued several weeks at the time of the removal, little benefit may be observed from the country residence until two or more weeks have elapsed.

An infant weakened and wasted by the summer diarrhoea, removed to a cool locality in the country, should be warmly dressed and kept indoor when the heavy night dew is falling. Patients sometimes become worse from injudicious exposure of this kind, the intestinal catarrh from which they are suffering being aggravated by taking cold, and perhaps rendered dysenteric.

Sometimes parents, not noticing the immediate improvement which they have been led to expect, return to the city without giving the country fair trial, and the life of the infant is then, as a rule, sacrificed. Returned to the foul air of the city while the weather is still warm, it sinks rapidly from an aggravation of the malady. Occasionally, the change from one rural locality to another, like the change from one wet-nurse to another, has a salutary effect. The infant, although it {757} has recovered, should not be brought back while the weather is still warm. One attack of the disease does not diminish, but increases, the liability to a second seizure.

Medicinal Treatment.--The summer diarrhoea of infants requires, to some extent, different treatment in its early and later stages. We have seen that acids, especially the lactic and butyric, the results of faulty digestion, are produced abundantly, causing acid stools. In a few days the inflammatory irritation of the mucous follicles causes such an exaggerated secretion of mucus which is alkaline that the acid is nearly or quite neutralized. In the commencement of the attack these acid and irritating products should be as quickly as possible neutralized, while we endeavor to prevent their production by improving the diet and assisting the digestion. In the second stage, when the fecal matter is less acid and irritating from the large admixture of mucus, medicines are required to improve digestion and check the diarrhoea, while the indication for antacids is less urgent. Therefore it is convenient to consider separately the treatment which is proper in the commencement or first stage, and that which is required in the subsequent course of the disease.

First stage, or during the first three or four days, perhaps the first week.--Occasionally, it is proper to commence the treatment by the employment of some gentle purgative, especially when the disease begins abruptly after the use of indigestible and irritating food. A single dose of castor oil or syrup of rhubarb, or the two mixed, will remove the irritating substance, and afterward opiates or the remedies designed to control the disease can be more successfully employed. Ordinarily, such preliminary treatment is not required. Diarrhoea has generally continued a few days when the physician is summoned, and no irritating substance remains save the acid which is so abundantly generated in the intestines in this disease, and which we have the means of removing without purgation.

The same general plan of medicinal treatment is appropriate for the summer diarrhoea of infants as for diarrhoea from other causes; but the acid fermentation commonly present indicates the need of antacids, which should be employed in most of the mixtures used in the first stage as long as the stools have a decidedly acid reaction.

Those who accept the theory that this disease is produced by micro-organisms which lodge on the gastro-intestinal surface and produce diarrhoea by their irritating effect are naturally led to employ antiseptic remedies. Guaita administered for this purpose sodium benzoate. One drachm or a drachm and a half dissolved in three ounces of water were administered in twenty-four hours with, it is stated, good results.[3] I have no experience in the use of antiseptic remedies.

[Footnote 3: _N.Y. Med. Rec._, May 31, 1884.]

If by the appearance of the stools or the substance ejected from the stomach, or by the usual test of litmus-paper, the presence of an acid in an irritating quantity be ascertained or suspected, lime-water or a little sodium bicarbonate may be added to the food. The creta præparata of the Pharmacopoeia administered every two hours, or, which is more convenient, the mistura cretæ, is a useful antacid for such a case. The chalk should be finely triturated. By the alkalies alone, aided by the judicious use of stimulants, the disease is sometimes arrested, but, unless {758} circumstances are favorable and the case be mild, other remedies are required.

Opium has long been used, and it retains its place as one of the important remedies in this disease. For the treatment of a young infant paregoric is a convenient opiate preparation. For the age of one to two months the dose is from three to five drops; for the age of six months, twelve drops, repeated every three hours or at longer intervals according to the state of the patient. After the age of six months the stronger preparations of opium are more commonly used. The tinctura opii deodorata or Squibb's liquor opii compositus may be given in doses of one drop at the age of one year. Dover's powder in doses of three-fourths of a grain, or the pulvis cretæ comp. cum opio in three-grain doses every third hour, may be given to an infant of one year.

Opium is, however, in general best given in mixtures which will be mentioned hereafter. It quiets the action of the intestines and diminishes the number of the evacuations. It is contraindicated or should be used with caution if cerebral symptoms are present. Sometimes in the commencement of the disease, when it begins abruptly from some error in diet, with high temperature, drowsiness, twitching of the limbs--symptoms which threaten eclampsia--opiates should be given cautiously before free evacuations occur from the bowels and the offending substance is expelled. Under such circumstances a few doses of the bromide of potassium are preferable. In the advanced stage of the disease also, when symptoms of spurious hydrocephalus occur, opium should be withheld or cautiously administered, since it might tend to increase the fatal stupor in which severe cases are apt to terminate.

The vegetable astringents, although they have been largely employed in the treatment of this as well as other forms of infantile diarrhoea, are, I think, much less frequently prescribed than formerly. I have entirely discarded them, since they are apt to be vomited and have not proved efficient in my practice. As a substitute for them the subnitrate of bismuth has come into use, and in much larger doses than were formerly employed. While it aids in checking the diarrhoea, it is an efficient antiemetic and antiseptic. It should be prescribed in ten or twelve grains for an infant of twelve months; larger doses produce no ill effect, for its action is almost entirely local and soothing to the inflamed surface with which it comes in contact. It undergoes a chemical change in the stomach and intestines, becoming black, being converted into the bismuth sulphide, and it causes dark stools. Rarely it gives rise in the infant to the well-known garlicky odor, like that occasionally observed in adult patients, and which Squibb thinks may be due to tellurium accidentally associated with the bismuth in its natural state. For those cases in which the symptoms are chiefly due to colitis, and the stools contain blood with a large proportion of mucus, it has been customary to prescribe laudanum or some other form of opium with castor oil. I prefer, however, the bismuth and opium for such cases as are more decidedly dysenteric, as well as for cases of the usual form of intestinal catarrh. In ordering bismuth in these large doses it is important that a pure article be dispensed.

The following are convenient and useful formulæ for a child of one year: {759}

Rx. Tinct. opii deodorat. minim xvj; Bismuth. subnitrat. drachm ij; Syrupi, fluidrachm ij; Misturæ cretæ, fluidrachm xiv. Misce.

Shake thoroughly and give one teaspoonful every two to four hours.

Rx. Tinct. opii deodorat. minim xvj; Bismuth. subnitrat. drachm ij; Syrupi, fluidounce ss; Aq. cinnamomi, fluidounce iss. Misce.

Shake bottle; give one teaspoonful every two to four hours.

Rx. Bismuth. subnitrat. drachm ij; Pulv. cret. comp. c. opio, drachm ss. Misce.

Divid in Chart No. X. Dose, one powder every three hours.

Rx. Bismuth. subnitrat. drachm ij; Pulv. ipecac. comp. gr. ix. Misce.

Divid in Chart No. XII. Dose, one powder every three hours.

Cholera infantum requires similar treatment to that which is proper for the ordinary form of the summer diarrhoea, but there is no disease, unless it is pseudo-membranous croup, in which early and appropriate treatment is more urgently required, since the tendency is to rapid sinking and death. As early as possible, therefore, proper instructions should be given in regard to the feeding, and for an infant between the ages of eight and twelve months either one of the above prescriptions should be given or the following:

Rx. Tinct. opii deodorat. minim xvj; Spts. ammon. aromat. fluidrachm j; Bismuth. subnitrat. drachm ij; Syrupi, fluidounce ss; Misturæ cretæ, fluidounce iss. Misce.

Shake bottle. Give one teaspoonful every two or three hours.

An infant of six months can take one-half the dose, and one of three or four months one-third or one-fourth the dose, of either of the above mixtures.

If cerebral symptoms appear, as rolling the head, drowsiness, etc., I usually write the prescription without the opiate; and with this omission it may be given more frequently if the case require it, while the opiate prescribed alone or with bromide of potassium is given guardedly and at longer intervals. Although every day during the summer months I have written the above prescriptions, it has been several years since any case has occurred in my practice which led me to regret the use of the opiate; but it must not be forgotten that there is danger in the summer complaint, and especially in cholera infantum, of the sudden supervention of stupor, amounting even to coma, and ending fatally. A few instances have come to my knowledge in which, when death occurred in this way, the friends believed that the melancholy result was hastened by the medicine. But injury to the patient in this respect can only occur, in my opinion, through carelessness in not giving proper attention to his condition. It is chiefly in advanced cases, when the vital powers are beginning to fail, when the innervation is deficient, and the cerebral circulation sluggish, that the use of opiates may involve danger. Explicit and positive directions should {760} be given to omit the opiate or give it less frequently whenever the evacuations are checked wholly or partially and signs of stupor appear.

Second Stage.--The summer complaint in a large proportion of cases begins in such a gradual way that the treatment which we are about to recommend is proper in many instances at the first visit of the physician, who is frequently not summoned till the attack has continued one or two weeks. The alkaline treatment recommended above for the diarrhoea in its commencement does not aid digestion sufficiently to justify its continuance as the main remedy after the first few days. In a large number of instances, however, one of the above alkaline mixtures may be given with advantage midway between the nursings or feedings, while those remedies, presently to be mentioned, which facilitate digestion and assimilation are given at the time of the reception of food.

Some physicians of large experience, as Henoch of Berlin, recommend small doses of calomel, as the twelfth or twentieth of a grain, three or four times daily for infants with faulty digestion and diarrhoea. To me, this seems an uncertain remedy, without sufficient indications for its use, and I have therefore no experience with it. The following are formulæ which I employ in my own practice, and which have been employed with apparent good results in the institutions of New York:

Rx. Acid. muriat. dilut. minim xvj; Pepsinæ saccharat. (Hawley's or other good pepsin), drachm j; Bismuth. subnitrat. drachm ij; Syrupi, fluidrachm ij; Aquæ, fluidrachm xiv. M.

Shake bottle; give one teaspoonful before each feeding or nursing to an infant of one year; half a teaspoonful to one of six months.

Rx. Tinct. opii deodorat. minim xvj; Acid. muriat. dilut. minim xvj; Pepsinæ saccharat. drachm j; Bismuth. subnitrat. drachm ij; Syrupi, fluidrachm ij; Aquæ, fluidrachm xiv. Misce.

Shake bottle; give one teaspoonful every three hours to a child of one year; half a teaspoonful to one of six months.

Rx. Pepsinæ saccharat. drachm j-ij; Bismuth. subnitrat. drachm ij. Misce.

Divid in Chart No. XII. One powder every three hours to a child of one year; half a powder to one of six months.

I have also obtained apparent benefit from lactopeptin, given as a substitute for one of the above mixtures before each feeding or nursing. In several instances which I recall to mind I have ordered as much as could be placed on a ten-cent piece to be given every second or third hour, while midway between the feedings in some instances of considerable diarrhoea one of the mixtures of bismuth and chalk recommended above was employed, and the result has been good.

Enemata.--It will be recollected, from our remarks on the anatomical characters, that inflammatory lesions are commonly present in the entire length of the colon, and that at the sigmoid flexure, where acid and irritating fecal matter is probably longest delayed in its passage downward, the colitis is usually most severe. Aware of this fact, I was {761} led to prescribe at my first visit a large clyster of warm water, given with the fountain or Davidson's rubber syringe, especially in cases in which the stools showed mucus or mucus tinged with blood. This, given with the lower part of the body raised a little above the level of the shoulders, washes out the large intestine and has a soothing effect upon its surface. The benzoate of sodium may be added to the water for its antiseptic effect, as in the following formula:

Rx. Sodii benzoat. drachm j; Aquæ, pint j. Misce.

In occasional cases in which the stomach is very irritable, so that medicines given by the mouth are in great part rejected, our reliance must be largely on rectal medication, and especially on clysters containing an opiate. Laudanum may be given in this manner with marked benefit. It may be given mixed with a little starch-water, and the best instrument for administering it is a small glass or gutta-percha syringe, the nurse retaining the enema for a time by means of a compress. Beck in his _Infant Therapeutics_ advises to give by the clyster twice as much of the opiate as would be required by the mouth. A somewhat larger proportion may, however, be safely employed. The following formula for a clyster has given me more satisfaction than any other medicated enema which I have employed:

Rx. Argent. nitrat. gr. iv; Bismuth. subnitrat. oz. ss; Mucilag. acaciæ, Aquæ, _aa_ fluidounce ij. Misce.

One-quarter to one half of this should be given at a time, with the addition of as much laudanum as is thought proper; and it should be retained by the compress. It is especially useful when from the large amount of mucus or mucus tinged with blood it is probable that the descending colon is chiefly involved.

Alcoholic stimulants are required almost from the commencement of the disease, and they should be employed in all protracted cases. Whiskey or brandy is the best of these stimulants, and it should be given in small doses at intervals of two hours. I usually order three or four drops for an infant of one month, and an additional drop or two drops for each additional month. The stimulant is not only useful in sustaining the vital powers, but it also aids in relieving the irritability of the stomach and in preventing hypostasis in depending portions of the lung and brain, which, as we have seen, is so frequent in advanced cases.

The vomiting which is so common a symptom in many cases greatly increases the prostration, and should be immediately relieved if possible. The following formulæ will be found useful for it:

Rx. Bismuth. subnitrat. drachm ij; Spts. ammon. aromat. fluidrachm ss-fluidrachm j; Syrupi, Aquæ, _aa_ fluidounce j. Misce.

Shake bottle. Dose, one teaspoonful half-hourly or hourly if required, made cold by a piece of ice.

Rx. Acid. carbolic. gtt. ij; Liquor. calcis, fluidounce ij. Misce.

Dose, one teaspoonful, with a teaspoonful of milk (breast-milk if the baby nurse), to be repeated according to the nausea.

{762} Lime-water with an equal quantity of milk often relieves the nausea when it is due to acids in the stomach, but it is rendered more effectual in certain cases by the addition of carbolic acid, which tends to check any fermentative process. Perhaps also some of the recent antiseptic medicines introduced into our Pharmacopoeia, as the benzoate of sodium, may be found useful for the vomiting. A minute dose of tincture of ipecacuanha, as one-eighth of a drop in a teaspoonful of ice-water, frequently repeated, has also been employed with alleged benefit.

Of these various antiemetics, my preference is for the bismuth in large doses, with the aromatic spirits of ammonia, properly diluted, that the ammonia do not irritate the stomach. Nevertheless, in certain patients the nausea is very obstinate, and all these remedies fail. In such cases absolute quiet of the infant on its back, the administration of but little nutriment at a time, mustard over the epigastrium, and the use of an occasional small piece of ice or the use of carbonic acid water with ice in it, may relieve this symptom.

In protracted cases, when the vital powers begin to fail, as indicated by pallor, more or less emaciation, and loss of strength, the following is the best tonic mixture with which I am acquainted. It aids in restraining the diarrhoea, while it increases the appetite and strength. It should not be prescribed until the inflammation has assumed a subacute or chronic character:

Rx. Tinct. calumbæ, fluidrachm iij; Liq. ferri nitratis, minim xxvij; Syrupi, fluidounce iij. Misce.

Dose, one teaspoonful every three or four hours to an infant of one year.

{763}

PSEUDO-MEMBRANOUS ENTERITIS.

BY PHILIP S. WALES, M.D.

SYNONYMS.--Membranous enteritis; Infarctus (Kaempf); Diarrhoea tubularis, Tubular looseness (Good); Follicular colonic dyspepsia, Follicular duodenal dyspepsia (Todd); Pellicular enteritis (Simpson); Pseudo-membranous enteritis (Cruveilhier); Pseudo-membraneuse entérite (Laboulbène); Painful affection of the intestinal canal (Powell); Mucous disease (Whitehead); Hypochondriasis pituitosa (Fracassini); Fibrinous diarrhoea (Grantham); Mucous disease of the colon (Clark); Chronic, catarrhal, or mucous diarrhoea; Colique glaireuse (of the French); Chronic exudative enteritis (Hutchinson); Diarrhoea febrilis (Van Swieten); Paraplexia rheumatica, Chlorosis pituitosis, Diarrhoea pituitosa (Sauvages); Arthritis chlorotica (Musgrave); Colica pituitosa (Sennertus); Scelotyrbe pituitosa (Perywinger); Mucositas intestinalis colloides, Concretiones gelatiniformes intestinales (Laboulbène); Tubular exudation-casts of the intestines (Hutchinson).

DEFINITION.--The disease is a non-febrile affection, consisting in a peculiar, and usually persistent, morbid condition of the intestinal mucous membrane, marked by the periodical formation of viscous, shreddy, or tubular exudates composed chiefly of mucin, on the discharge of which temporary amelioration of the accompanying acute digestive and nervous symptoms occurs.

HISTORY.--Although no distinct and separate accounts of pseudo-membranous enteritis occur in the medical writings of the ancients, nor even in those dating up to the eighteenth century, yet there may occasionally be detected in some of the descriptions of certain pathological conditions grouped under such titles as colic, passage of gall-stones, tenesmus, coeliac and pituitous affections, diarrhoea, dysentery, etc., the peculiar features of the disease under consideration. This confusion ruled up to a comparatively recent time. J. Mason Good,[1] writing in the first quarter of the nineteenth century, groups the disease as a species of diarrhoea--diarrhoea tubularis--and remarks that he had "never hitherto seen this species classified, and not often described, although it occurred frequently in practice."

[Footnote 1: _Study of Medicine_, 1822.]

Aretæus,[2] in the second century, in discussing the subject of dysentery, speaks of alvine discharges sometimes occurring of a substance of considerable length, in many respects not to be distinguished from a sound piece of intestine, which he regarded as the inner coating of the bowel. {764} This false interpretation of a fact arose from the circumstance that the membranous exudate occasionally assumes a tubular form, bearing the impress of the inner surface of the bowel upon which it is formed, and was perpetuated up to a comparatively recent period by successive authors. This error befell Simpson,[3] Morgagni,[4] Lancisi, and Spindler;[5] the last of whom describes the material discharged as worked up into a "materia alba, longa, compacta."

[Footnote 2: Lib. ii. cap. ix.]

[Footnote 3: _Ed. Med. Essays_, vol. v. p. 153, 1752.]

[Footnote 4: 31st Epistle.]

[Footnote 5: _Actis Nat. Cur._, vol. v. p. 483.]

Bauer[6] under the title of "intestinal moles" describes in Haller's _Disputations_ the discharges of this disease as "concreta fibrosa quædam pro parte pinguedine rara abducta, membranacea molarum ex utero muliebri rejectarum formam accurate sistentia."

[Footnote 6: "De Moles Intestinorum," _Disputationes ad Morborum_, Dresdæ, 1747, p. 463.]

In the same volume Kaempf[7] discourses on this subject under the title of "infarction of the intestinal vessels," and also in a separate treatise[8] published somewhat later. In the latter he groups the disease with others of a far different nature, their only point of convergence being preternatural alvine discharges.

[Footnote 7: _De Infarctu Vasorum Ventriculi_, Basiliæ, 1751.]

[Footnote 8: _Abhandlungen von einer neuer methode der hartnackigsten Krankheiten die ihren Sitz im unterleibe haben, zu heilen_, Leipzig, 1784.]

Subsequent authors, as a rule, fell into the same error, and it was not until 1818 that membranous enteritis was discriminated by Powell[9] from that condition in which we recognize the presence of gall-stones. Since then more correct views have prevailed, and the disease has now a recognized place in nosology.

[Footnote 9: _Trans. of Col. of Phys. London_, vol. vi. p. 106.]

ETIOLOGY.--As in other diseases of obscure nature, so in this, there has been much divergence of opinion as to its cause.

The influence of age is striking, as it is rarely seen in childhood or in persons who have passed the forty-fifth year. Of my own cases, the youngest was forty, and the oldest fifty-four. Rilliet and Barthez[10] state that membranous formations in the intestinal canal of children are very rare; that they always occupy the summits of the folds, rarely the intervals, of the mucous membrane; and that they are detached in layers of greater or less extent. They are not diphtheritic. Heyfelder[11] has described similar exudations under the name of enteritis exudatoria.

[Footnote 10: _Traité clinique pratique des Maladies des Enfants_, t. i. p. 677, 1853.]

[Footnote 11: _Studien in Gabiete der Heilwissenschaft_, p. 173.]

Sex exerts as marked an influence as age, as the immense preponderance of cases occurs in females. In an analysis of 100 cases, 4 only occurred in males, 2 of which were children. All of my cases were women; with the exception of two cases occurring in males, the same experience is reported by Powell and by Copeland.

In regard to temperament, it is undoubted that the disease invades nervous and hypochondriacal subjects oftener than others, but all temperaments are liable in the presence of those enervative influences that degrade physical health and impair nerve-power. All of my patients belonged to the nervous type. Whitehead says that those of a phlegmatic temperament, not easily excited into action, or persons deficient in elasticity of fibre, compose all but a very small percentage of the sufferers from this {765} complaint, and he had particularly noticed that a large proportion of the women have light flaxen hair, fair complexions, and white skins.

The determinative causes, whatever they may be, occasion perversion of nutrition and innervation of the gastro-intestinal canal, principally, I believe, by their action upon the ganglionic nerves presiding over those functions originating the peculiar exudatory phenomena of this disease. This condition of the nervous system once established, local irritation of any sort may precipitate an attack, and hence the multitudinous influences that have been assigned as exercising a causative agency, as exposure to wet and cold, coarse, bad food, fecal impaction, and the abuse of cathartic medicines, as alleged by Grantham,[12] who asserts that the use of mercury, conjoined with a too frequent use of aperient agents, is the cause of the disease in every case.

[Footnote 12: _Facts and Observations in Med. and Surg._, 1849, p. 205.]

Farr considered the irritation of the intestinal canal owing to a parasitic growth of a confervoid type (oscillatoria). This view is supported by no other authority than that of himself and Bennett, as nothing of this sort is recorded as occurring in the discharges of patients of other observers; certainly in mine there was no parasitic development. The presence of it in their cases may then be fairly regarded as accidental, or at least unessential.

Habershon regarded ovarian diseases and painful menstruation in the female, and prostatic diseases in the male, as exciting causes.

SYMPTOMS.--The most characteristic symptoms disclosing the presence of pseudo-membranous enteritis are those arising from derangements of the digestive organs. They are, in the beginning, vague and irregular in occurrence, or so over-veiled by associated disorders of the genito-urinary and nervous systems that their nature and import often escape recognition until, weeks, and even months, of fruitless medication addressed to these secondary phenomena having been expended, the disease assumes such severity and presents such a complex of peculiar symptoms that it no longer eludes identification.

The disease rarely starts as an acute affection; sometimes it is subacute, but in the great majority of cases its course is chronic. Its initiation is marked with symptoms of gastro-intestinal disturbances--irregularity of the bowels, constipation and diarrhoea alternately; and dyspeptic annoyance of one sort or another--capricious appetite, nausea or vomiting, and pyrosis, usually increased by liquid diet. In Dunhill's case there was almost daily vomiting of mucus and pus streaked with blood, and occasionally pure blood. This prominence of gastric derangement supplies an explanation why Todd conferred upon the disease the title of follicular dyspepsia.

There is a sense of discomfort, soreness, or rawness of the abdomen, especially along the line of the colon, and in two of my cases the rectum was tender and raw, which augmented to decided pain in sitting or riding, and the abdominal muscles were tense; a feeling of heat or burning in the bowels often occurs, and almost always more or less lassitude and mental depression. These symptoms aggravate, especially upon indiscretions in diet, exposure to wet, or indeed under any sort of enervative influences, at irregular intervals. Their persistence finally induces grave disorders of nutrition, marked by the blood becoming poor and thin, by sluggish {766} circulation and local congestions in the pelvic and abdominal viscera, and loss of strength and flesh. Yet certain patients seem to retain their flesh for a long time, as I have seen, after suffering several years from the disease. The depression of vital powers is still further manifested in a small, slow, soft pulse and a temperature running below the normal standard. The tongue is usually moist, pale, and flabby, and coated with a pearl-white or yellowish-white coating; sometimes, however, it is raw, red, tender, and fissured, or patchy from exfoliation of the mucous coating. The gums and cheeks are usually pale and bloodless, and often the seat of small roundish painful ulcers, which occasionally invade the palate and throat. Grantham[13] says that ulceration of a phagedænic kind sometimes forms on the tonsils. The complexion usually assumes a muddy or flavescent tint, which during the attack may deepen to a jaundiced hue. At other times it presents a transparent or waxy appearance.

[Footnote 13: _Op. cit._, p. 204.]

The skin is dry and furfy, sometimes cold and clammy, or, from over-action of the sebaceous glands, greasy. There is a disposition, especially on the chest, neck, and face, to papular eruptions or even phlegmonous or carbuncular inflammation.

The urine is high-colored and loaded with abundant phosphates, which in cooling precipitate as a heavy deposit. The bladder is often irritable, and discharges more or less mucus. According to Grantham,[14] patients occasionally pass urine with evident traces of albumen, and seldom containing a normal quantity of phosphates. On an increase in fever or mental excitement a larger quantity than natural of the lithate of ammonium is found; frequently the mucous membrane of the bladder is found thickened in these cases.

[Footnote 14: _Op. cit._, p. 204.]

The characteristic symptom, however, of this disease is the periodical formation and discharge of mucous exudates varying in physical appearances and frequency. The discharge may occur daily, with every stool, or at irregular intervals--a week, month, or longer--but usually in from twelve to fifteen days. The recurrence may be precipitated by irregularity in diet, exposure to wet and cold, or by excesses of any sort. The paroxysm is marked by tormina or severe pain, which may resemble that of colic or that of the passage of a biliary calculus, extending down the thighs or to the bladder, in the latter case sometimes causing retention, requiring the use of the catheter. The pain is usually referred to some part of the large intestine. In certain cases the paroxysm is announced by chills radiating from some point in the abdomen or even from other parts of the body.

After the paroxysm has endured two, three, or more days--usually a week--membranous exudates, either with a spontaneous or with an artificial movement of the bowels, are voided; after which there is a gradual assuagement of the local and general symptoms, but the patient experiences a sense of exhaustion or lassitude, and the tenderness of the abdomen and the irregularity of the bowels usually persist.

During the attack there is anorexia, but in the intervals the appetite remains fairly good, and the alvine discharges may assume quite a natural condition.

In the course of the disease there is more or less disturbance in the functions of the nervous system. During the paroxysm, when the {767} sufferings are severe, the cast of symptoms running through the case is of a decidedly hypochondriacal type. At times, with the expulsion of the exudates and succeeding respite from suffering, there often occurs a mental rebound which lifts the patient from the slough of despair to the most hopeful anticipations of future health and happiness. In one of my cases this transition was remarkable. This hysterical type is common enough, and the irritability of the nervous system is still further manifested in the occurrence of irregular contractions of various groups of the voluntary muscles, as shown in hysterical tetanus, general convulsions, or chorea in children, or by paralyses of motion.

Copeland[15] reports a case of a lady in whom this disease was complicated with the severest symptoms of hysteria, occasionally amounting to catalepsy. The paroxysms of pain recurred at intervals between four and six weeks, followed or attended by the discharge of large quantities of false membrane in pieces, and sometimes in perfect tubes. The menstrual flow was painful and irregular, accompanied with shreds of false membrane--not, however, contemporaneous with those of the intestine. The sensory nerves are often deranged, for in some cases there is paræsthesia--anæsthesia or hyperæsthesia--in limited areas of the skin. There is more or less headache, neuralgic pains in this or that nerve, or in several at the same time.

[Footnote 15: _Dictionary of Medicine_, vol. ii. p. 669.]

The special senses do not escape; they manifest various forms of functional derangement. In one of my cases there were constant buzzing in the ears and perversion of the sense of smell, and in another the vision was thought impaired and the services of an oculist sought.

The uterine functions are always involved in greater or less degree. The menstruation is difficult and painful, and occasionally accompanied with membranous discharges. In one of my cases there was a uterine exudate, though the menopause had occurred several years before. Leucorrhoea and cervical inflammation are common.

PATHOLOGY.--Despite the fact that the disease in question, without being very frequent, is far from rare, little light has been shed upon its pathology. Indeed, even its individuality as an independent and distinct affection has been contested, although it is marked by a complex of symptoms as peculiar and characteristic as those of any other disease in the nosology.

There are those who maintain that the disease consists essentially in an inflammatory condition of the intestinal mucous membrane, either of the ordinary or of some specific type, croupous or diphtheritic. Copeland says the formation of the membranes depends upon a latent and prolonged state of inflammation extending along a very large portion, sometimes the greater part, of the intestinal canal, as is evinced by the quantity thrown off. Valleix[16] dismisses the subject summarily with the delivery of the oracular judgment that the greater number of cases of this disease are dysenteric, and the remainder diphtheritic. Habershon is in full accord with this view, having, as he says, seen these membranous exudates "follow severe disease of the intestines of a dysenteric character, and sometimes associated with a state of chronic congestion of the liver, and often perpetuated by the presence of hemorrhoids, polypoid {768} growths, etc." Wilks and Clark,[17] after a full examination of the enteric exudates submitted to them, concluded that they are true casts of the large intestines produced by chronic inflammatory action of the mucous membrane and subsequent exudation. Conjectures have been ventured as to the exact anatomical structure in which the process occurs. Thus, Todd[18] says that the proximate cause of the disease is dependent upon a morbid condition of the intestinal mucous follicles. Golding-Bird[19] holds similar language. He says: "It is probable that the follicles are the principal seat of the disease, for we know that they sometimes secrete a dense mucus differing little in physical qualities from coagulated albumen or even fibrin." Livedey[20] attributed the process to a morbid secretion into the mucous crypts.

[Footnote 16: _Guide du Médecine practicien_, vol. iii. p. 10.]

[Footnote 17: _Trans. Path. Society_, vol. ix. p. 230.]

[Footnote 18: _Cyclopædia of Practical Medicine_, vol. ii. p. 279.]

[Footnote 19: _Guy's Hospital Reports_.]

[Footnote 20: _L'Union médicale_, 1868.]

Among those believing in its croupous nature was Powell, who assumed the character of the inflammation to be specific, and the exudate of the same nature and formed in the same manner as that of ordinary croup. This was the view entertained by Cruveilhier and Trousseau and other French authors. Good was misled in a similar manner, as shown by his statement that the exudation bears a striking resemblance to the fibrous exudation thrown forth from the trachea in croup. He says, however, that it is discharged in longer, firmer, and more compact tubes. Serres,[21] in a dissertation upon pseudo-membranous colitis, confounds the exudate with that of thrush, muguet, and infective dysentery. Laboulbène,[22] a later writer, also remarks that there are found in many treatises and in periodical literature a great number of occurrences of false membranes in the dejecta. Most of these cases are referable to dysentery, to muguet, hydatids, etc., but there remain a certain number which are owing to different inflammatory and non-diphtheritic affections of the digestive tube.

[Footnote 21: _Thèse de Paris_, No. 39, 1836.]

[Footnote 22: _Recherches cliniques et anatomiques sur les Affections pseudo-membraneuse_, Paris, 1861.]

Whitehead, in summing up his conclusions respecting the nature of the disease, compares it with dermic inflammation. He says: "The mucous membrane (intestinal), like the skin (and is not the one looked upon as an inversion of the other?), is prone under certain conditions in certain constitutions to develop products unnatural to its functions. It is not natural for the skin to produce eczema, neither is it natural for mucous surfaces to produce mucus in a concrete form; that the proximate cause of the symptoms referable to this disease is the hypersecretion and accumulation of mucus on the free surface of mucous membranes; such accumulations sheathe and prevent the healthy performance of the functions natural to the part, and thus induce immediate and remote results, the effect of such suppressed functions; that this hypersecretion indicates a want of balance between nerve-force and germinal matter, and that the nerve-force is perverted by irritation."

Simpson held similar views, and regarded the disease as a chronic pellicular or eruptive inflammation of the mucous lining of the bowels.[23] Other observers have been inclined to ignore the inflammatory nature of the disease, at least as a primary condition, and have sought the proximate cause in some as yet undefined derangement of the nervous {769} system. Thus, Clark does not regard the membranous exudates as the products of inflammation, properly so called--that is, of capillary blood-stasis which has preceded their formation--as the characteristic of such exudates is that they contain fibrin. He says the abnormal cell-forms present arise in some other way than by free cell-development out of an exuded blastema. Good[24] asserts its dependence upon what he calls a "peculiar irritability of the villous membranes of the large intestines, which in consequence secrete an effusion of coagulating fibrin--fibrin mixed with albumen--instead of secreting mucus, occasionally accompanied with some degree of chronic inflammation."

[Footnote 23: _Obstet. Works_, Am. ed., p. 279.]

[Footnote 24: _Study of Medicine_, _op. cit._]

Also, DaCosta doubts whether the disease is originally inflammatory at all. "Where inflammation," he says, "occurs, is it not secondary rather than primary, the result rather than the cause?" "Is not the true trouble in the nervous system, in the nerves presiding over secretion and nutrition in the abdominal viscera?"

Bennett and Byford represent the opinions of a very small minority who regard the disease as simply an expression of uterine derangement.

MORBID ANATOMY.--As none of the cases coming under my observation terminated fatally, no opportunity was offered to me of making personal investigation into the anatomical changes occurring in membranous enteritis. Such opportunities have been so rarely met with that, indeed, it may be said that the nature of these changes is wholly unknown.

Simpson alludes to a case of phthisis in which the patient had passed large quantities of "membranous crusts or tubes," and in which the mucous membrane of the colon was covered with an immense number of small spots of a clear white color, or vesicles, which, when punctured, discharged a small quantity of clear fluid; and also refers to the case of Wright, in which the mucous membrane of the colon and of the lower portion of the small intestine was studded everywhere with a thickly-set papular eruption.

My endoscopic examinations revealed, in the living subject, the intestinal mucous membrane of a red, verging into a scarlet color, thickened, and denuded of epithelium in patches of varying extent. This condition does not always invade the ampulla of the rectum, but with the long tube I am in the habit of using it was possible in all my cases to reach a point where it existed. The extent of diseased surface can only be conjectured by an inspection of the exudates and by abdominal palpation.

In most cases the exudate is restricted to the large intestines--colon and rectum--and often to a circumscribed portion of them; but in rare cases its length and quantity would seem to indicate that extensive portions of the surface are covered. One of the most remarkable cases recorded is that of a woman forty years old who had been sick for five years with gastro-intestinal derangement. Suddenly the case became acute, and after much suffering she passed membranous exudates three millimeters in thickness and many centimeters long, weighing in all three kilograms.[25]

[Footnote 25: _Recueil de Mémoires de Médecine, de Chirurgie, et de Pharmacie militaires_, tome xxxvii. p. 297, 1855.]

Kaempf[26] gives another case, in which the length of the membranes {770} discharged was sevenfold greater than the stature of the patient. In Dunhill's[27] case the patient had suffered from this disease for a long period, and during two years passed many yards of perfect cylindrical shape, many of them several feet in length, and sufficiently coherent to permit of their being handled, held up, etc. In one of my cases a perfect cylinder three-quarters of a yard long was voided.

[Footnote 26: _Op. cit._, p. 232.]

[Footnote 27: _Trans. of Path. Society of London_, vol. ix. p. 188.]

Laboulbène[28] describes the gastro-intestinal false membrane as thin, soft, and granular, of a more or less yellow color, slightly adherent to the mucous membrane, and when stripped off forming a yellow pultaceous mass. He says it is first deposited in small, irregular, sparsely-scattered patches, located on the summits of the intestinal folds; afterward these patches increase, and cover the folds entirely and almost the whole calibre of the intestinal canal. The mucous membrane, he remarks, beneath the deposit is greatly inflamed.

[Footnote 28: _Op. cit._, p. 105.]

Powell believes that at times the deposit extends as high as the duodenum, his opinion being solely based upon the clinical features of the disease. In the first of his cases the membrane was found in perfect tubes, some of them full half a yard in length, and certainly sufficient in quantity, he says, to have lined the whole intestinal canal.

In examining the membranes it is always best to float them from the fecal or other foreign material by passing the discharges in a clean vessel containing water. Their physical characters can then be readily studied. They are best preserved in a 10 per cent. solution of alcohol. The exudate consists usually of a single lamina, but at various points in certain cases several superposed laminæ may be observed, enclosing between them particles of undigested food of various kinds. In most cases the superficial layers are more opaque, drier, less elastic, and friable than the deeper.

The configuration of the exudate varies greatly. The more common variety is that occurring in loose, transparent, jelly-like masses, like the white of an egg or glue, tinged often with various hues of yellow. In three of my cases I noticed also the frequent occurrence of a thin, serous, yellow discharge. In some cases the discharge resembles pieces of macaroni, tallow, or wax; in others it assumes a shreddy or ribbon-like form; and in a still rarer class it is tubular, being an exact reprint of the surfaces from which detached. These tubular pieces are, however, more or less torn and broken into smaller fragments of an inch or two in length when discharged.

Its thickness also varies: sometimes it does not exceed that of the thinnest film, and at others it is a quarter of an inch or more.

Its consistence ranges from that degree of loose aggregation that permits elongation into stringy, breaking masses when fished up from the water in which it floats, to a firmness and tenacity that will enable it to be handled without fear of breakage.

The color differs in different cases. It is usually yellowish-white, but this is often modified by tints dependent upon admixture with extraneous matters from the intestinal canal--biliary coloring, blood from the rupture of the vessels beneath the exudate, or with blood and pus. It exhales a feculent odor.

The surfaces of the membranes are ordinarily smooth and uniform, but sometimes reticulated. Certain observers have described the outer {771} surface of the tubular exudate as uniformly smooth, and the inner as broken and flaky at some points, at others ragged and flocculent, and in many places thrown into shallow folds, lying in some situations across, but chiefly along, the axis of the gut.

The microscopic characters of the exudate are pretty uniform. Wilks and Clark[29] describe the surface of the tubes, examined with a linear magnifying power of forty diameters, as exhibiting the appearance of a gelatinous membraniform matrix traversed by a coarse network of opaque yellow lines, studded at their points of intersection by similarly colored rounded masses. From the larger network proceeds a smaller secondary network, and in the recesses of this were found, at close and regular intervals, well-defined round or oval openings, with elevated margins, resembling in size and appearance the mouths of the follicles of the great gut. With higher powers the exudate was found in many cases to consist of a structureless basement membrane, which in certain points showed a fibrous appearance, owing doubtless to the presence of filaments of mucin. Numerous irregular granular cells, as well as granules from the breaking up of these cells, thickly studded the surface of the membrane. In the specimens of Wilks and Clark the surface, besides being marked by the opaque yellow lines and dots, presented various foreign matters, such as bile-pigment, earthy and fatty granules, portions of husks of seed, gritty tissues of a pear, a peculiar form of elastic tissue, stellate vegetable hairs, and a mucedinous fungus. Clark, in describing the fibres found between the layers of the exudates, says that they exhibited a very distinct and regular transverse striation, approaching in character that found in the ligamentum nuchæ of the giraffe. Quekett and Brooke have met with the same fibres in the feces. The transverse division depends probably upon beginning decay. The division is sometimes so distinct and complete as to lead, according to Beale,[30] to their confounding with confervoid growths. Farre[31] actually describes the formation as of a confervoid character.

[Footnote 29: _Op. cit._, p. 232.]

[Footnote 30: _The Microscope in Medicine_, p. 194.]

[Footnote 31: _Trans. Microscopical Society_.]

Here and there, in my specimens, were observed scattered epithelial cells which were occasionally gathered in patches. Small colored masses of irregular shape, doubtless of fecal origin, were also noticed. The cells imbedded in the matrix, according to the above-quoted observers, consisted of two kinds--one more or less spherical, the other more or less cylindrical. In size the spherical cells varied from 1/2000 to 1/800 of an inch in diameter. The smaller cells had no distinct cell-walls. Some of the larger cells were filled with fat-granules, and represented granular cells; others had a single or double vesicular nucleus; a few were acuminated at two opposite points and somewhat compressed. All the other cells possessed demonstrable cell-walls. The cylindrical cells resembled in their general characters those which normally coat the mucous membrane of the larger gut, but they were much more elongated, compressed, and firmly matted together. Many of the more elongated cells were constricted in the middle, and exhibited a nucleus on each side of the constriction. The more or less spherical cells occupied the attached, and the cylindrical cells the free, surface of the membranous tubes.

The perforations in the matrix were of uniform size and appearance, {772} surrounded by elevated margins formed of closely-grouped cylindrical cells, and led to two kinds of pits--one short and flask-shaped, the other long and uniformly cylindrical. The flask-shaped pits were about one-tenth of an inch in diameter and distinctly hollow. The wall of each pit was made up of one or two layers of subspheroidal cells, held together by an amorphous stroma. A few of these follicles contained a deposit which was opaque in situ, and which when broken up was found to consist of large flattened nuclear cells, analogous to those met with in epithelial growths.

The cylindrical pits were also for the most part hollow, about one-sixteenth of a line in length and one-thirty-first of a line in breadth. These walls, devoid of membrane, were composed of small, more or less spherical cells in various stages of development, imbedded in a gelatinous matrix.

In examining the chemical characters of the specimens obtained in my cases the membranes were thoroughly washed, when they were nearly as colorless as the water in which they floated. They were drained on a sieve, and presented a gelatinous appearance, much like the white of an egg. Their specific gravity was about that of distilled water. When treated with strong alcohol, the membranes shrank and assumed a striated appearance. Chemical tests of tincture of guaiacum, peroxide of hydrogen, and others failed to show the presence of fibrin or albumen. Treated with ether, globules of fatty matter were obtained, which were identified by their microscopical characters and by their reaction with osmic acid. By boiling the liquid in which the membranes had been soaked it became faintly hazy, indicating a trace only of albumen. Faint evidence of the presence of this body was also presented by picric acid and Mehu's test. Treated with a weak solution of caustic potassa and heat, the membrane dissolved, leaving a little haziness. The liquid was then filtered, and exactly neutralized with acetic acid, and plumbic acetate added, when a copious precipitate was formed. Mercuric chloride and potassic ferrocyanide failed to produce this effect. From these and other tests used the conclusion was reached that these membranes were composed essentially of mucin.

Both the microscopical and chemical characters of the exudates of the disease under consideration show that they are widely different in nature from those of other diseases. They are evidently a production of the muciparous glands (follicles of Lieberkühn) of the intestinal canal, and consist essentially of mucin. Perroud[32] concluded from his analysis that they contain a small quantity of albumen, but are principally formed of the same substance as that which enters into the composition of the epidermis. The exudates of other diseases of the alimentary mucous membrane contain albumen and fibrin, as well as molecular or homogeneous filaments. The ordinary croupous exudate, according to Cornil and Ranvier, always contains filaments of fibrin, sometimes mucin and pus-corpuscles mingled with the cellular constituents, which vary in character with the locality of the inflammation. The filaments form a reticulum in the meshes of which are contained the other elements.

[Footnote 32: _Journal de Médecine de Lyon_, 1864.]

Diphtheritic exudates, as shown by Lehmann,[33] consist of fibrin, a large {773} quantity of fatty matter, and 4 per cent. of earthy phosphates, while its structure is made up of epithelial cells united together, which, becoming infiltrated with an albuminous substance and gradually losing their nuclei and walls, are finally converted into homogeneous branching masses. The cells of these masses are liable to undergo fibrinous degeneration. The inflammation determining the exudate is not confined to the conglomerate glands, but involves all the textural elements of the part affected, and the material of the membrane originates from the capillary disturbance in them.

[Footnote 33: _Lehrbuch der Physiolog. Chemie_, Leipzig, 1855.]

Andrew Clark[34] states that he has observed in his studies of exuded blastema, the product of diseased action in mucous membranes, three varieties. The first is clear, jelly-like, and imperfectly membranous. The second is yellowish, semi-opaque, flaky, and usually membranous. The third is yellowish-white, dense, opaque, distinctly membranous, tough, and rather firmly adherent to the subjacent surface. The first contains only the merest trace of albumen, and no fibrin; the second contains an abundance of albumen, and no fibrin; the third contains both albumen and fibrin in abundance, the latter in a fibrillated form. They all contain the same cell-forms. Yet it is to be noticed that in the first variety there is no evidence of transudation or exudation; in the second, no evidence of a true exudation; and that in the third, in which the existence of a true inflammatory exudation is undeniable, the only additional structural element present is fibre.

[Footnote 34: _Op. cit._, p. 133.]

DIAGNOSIS.--The diagnosis of membranous enteritis can never in its advance, and rarely in its early stages, present much difficulty. Its chronic course, irregular exacerbations, lack of febrile excitement, the persistent derangement of the intestinal canal, the mental depression, the gradual impairment of health, the various visceral complications, and, lastly and chiefly, the peculiar character of the alvine discharges,--stamp the disease with an individuality entirely its own.

The mucous discharges of certain forms of chronic diarrhoea and the membranous discharges of infective dysentery are all so different in physical character, and are associated with such a different complex of general symptoms, that they cannot be confounded with those of the diseases in question. The peculiar irritative quickness of the pulse of ordinary enteritis, according to Powell and Good, suffices to differentiate this disease from membranous enteritis. The peculiarities of the physical and chemical properties of these exudates, already fully dwelt upon, not only distinguish them from those of the above diseases, but also from such dejecta as may contain fragments of undigested connective tissue, of hydatids, or of worms. The flakes of mucus discharged from the bowels in protracted constipation, fissura ani, and in the later stages of cirrhosis of the liver are composed of mucus in which are found imbedded epithelial cells from the colon and mucus-corpuscles. The microscope will also reveal the character of the fatty discharges that may be associated with diseases of the pancreas, liver, and duodenum. The mucous flakes of cholera stools are composed of masses of intestinal epithelium mixed with amorphous and granular matter, crystals of different substances, and, according to Davaine, of parasitic forms, particularly the Circomonas hominis.

{774} Membranous casts from the upper part of the digestive track are, in rare cases, passed by the bowels. One of the most curious instances of this sort is reported by Villermé:[35] A woman swallowed a tablespoonful of nitric acid, and seventy days afterward a long membranous exudate, one or two lines thick and of a brown color, was discharged, which corresponded in form with the oesophagus and stomach. The patient died a few days later.

[Footnote 35: _Dictionnaire des Sciences médicales_, tome xxxii. p. 264.]

PROGNOSIS.--The prognosis of the disease as regards life is not unfavorable, but as regards permanent restoration to health and strength the case is entirely different. Theden[36] and Hoffman[37] have, however, stated that the disease is not an unfrequent cause of sudden death.

[Footnote 36: _Remarques et Experiences_, tome ii.]

[Footnote 37: _Med. Ration._, vol. v.]

Abercrombie[38] records a case of death from phthisis complicated with this disease, and Wright another case in which the patient died in an extreme state of marasmus. The acute and subacute forms are more amenable to treatment, and the chances are correspondingly greater of permanent recovery, though in all cases there is a strong tendency to relapse. The chronic forms may almost be enrolled among the opprobria medicorum when once they have made deep inroads upon nutrition and the vital powers, and produced that condition named by Todd the pituitous cachexia (cachexia pituitosa). These cases may, however, be alleviated by judicious treatment, diet, and climatic changes, but repeated relapses may be expected as the rule under slight exciting causes or even without apparent cause. Patients under these circumstances drag out a life of valetudinarianism, but it may be cut short at any time by the supervention of some intercurrent disease, as phthisis, renal degeneration, etc., or, according to Grantham, atrophy of the intestines. Broca[39] records two cases of this disease, one of which lasted ten and the other fifteen years. Three of my cases have endured over six years.

[Footnote 38: _Inflamm. Affec. of Mucous Memb. of Intestines_, pp. 213, 279.]

[Footnote 39: _Bullétin de la Société Anat. de Paris_, 1854.]

TREATMENT.--The treatment of membranous enteritis embraces medical and hygienic measures. The medical means have for their object, first, the removal of the membranous exudation when it has once formed; and, second, to correct the conditions upon which its formation depends by improving nutrition and invigorating the nervous system. The severe sufferings of the paroxysms are greatly alleviated and the duration of this stage cut short by freely emptying the bowels. The best means to do this is by the injection of hot water with the long elastic bougie three or four times a day, and to assist this with laxatives. Instead of water, solutions of potassa, soda, and lime-water are preferred by some practitioners. As a rule, the enemata cause considerable discomfort, but in the end are followed by improvement in the condition of the bowels. The best laxative is emulsion of castor oil, but occasionally a mercurial, guarded by the extract of belladonna, will furnish more marked relief. Powell and Copeland say that they have employed with decided advantage a purgative consisting of the compound infusion of gentian and infusion of senna, to which were added ten or twenty minims of liquor potassæ. This was repeated, so that four stools in the twenty-four hours were obtained. Clark preferred to regulate the bowels, when needed, with rhubarb, soda, and {775} ipecac, conjoined or not, as required, with mercury and chalk. Good recommends four grains of Plummer's pill every night, and the bowels kept open by two drachms of sublimed sulphur daily. It should always be borne in mind that all active or irritating purgatives are harmful. The bowels by this treatment will not only be disembarrassed of the membranous exudates, but also of any fecal collection the retention of which would surely cause irritation, as occasionally happens even when there is an apparent diarrhoea. This condition may be easily determined by abdominal palpation. The relief from pain procured by free evacuation of the intestine will be enhanced by the employment of hot fomentations to the abdomen. Despite these means, its severity may, however, demand the administration of narcotics. The best form will be a hypodermic injection of a sixth or a quarter of a grain of morphia; enemata of starch and laudanum are also beneficial. Burrows mentions a case in which he succeeded in allaying nervous irritation by the nightly use of thirty drops of laudanum. The patient noticed that the habitual constipation was increased when the accustomed narcotic was omitted. Bromide of potassium in large doses long continued will also be found useful for the same purpose.

During the intervals of the paroxysms local medication of the bowels and medical and hygienic measures should be had recourse to to prevent the re-formation of the exudates by modifying the vital activities of the intestinal mucous membrane and by restoring the general tone of the constitutional powers. For local treatment the nitrate of silver, sulphate of zinc, the sulphate of copper dissolved in glycerin, the tincture of iodine, and carbolic acid cannot be over-prized. From five to ten grains of the metallic salts, fifteen drops of tincture of iodine, ten of the acid, administered through the long rubber tube, are suitable doses to begin with. I am also in the habit of using stronger solutions by mopping it on to the bowel through the endoscopic tube. Kaempf made frequent and large injections of decoctions of various plants--saponaria, taraxacum, etc.--which he imagined possessed dissolvent and resolvent virtues. Cumming[40] speaks highly of the efficacy of electricity.

[Footnote 40: _Lond. Med. Gazette_, 3d Series, vol. ix.]

For the purpose of improving the general health the preparations of iron are advisable, of which the best are the tincture of the chloride, pernitrate, pyrophosphate, lactate, and potassio-tartrate. Habershon advises infusions of the bitter tonics with hydrocyanic and nitro-muriatic acid. I have found a combination of these acids with henbane and infusion of serpentaria useful. I also employ hot solutions of the latter acid as a local bath over the abdominal region, applied with a large sponge. Clark speaks favorably of the extract of nux vomica and astringent remedies. Simpson praises the oleo-resins under the form of pitch pills and tar, while Clark and others laud copaiba and turpentine. Good advises the copaiba to be given by enema when it cannot be borne by the stomach. Brodie used cubebs in small doses.

The alterative effects of small doses of arsenic, corrosive sublimate, sulphate of copper, etc. may be tried in obstinate cases. Grantham in the early stages of the complaint advises the use of ten grains of iodide of potassium combined with one-quarter of a grain of morphia at bed-time. He {776} also strongly urges the use of cod-liver oil, which, he says, improves the strength and increases the flesh, lessens the spasmodic pains, but does not check the discharges.

Counter-irritation of the abdominal region with tincture of iodine, fly blisters, mustard, etc. has afforded little if any advantage. Dunhill kept a blister open for six months without any good results.

The mineral waters of Pyrmont, Harrogate, and Carlsbad have been found serviceable; the latter, Henoch[41] says, should be preferred before all.

[Footnote 41: _Klinik der Unterleub. Krankheiten_, p. 668.]

The case will amend more speedily and surely by the adoption of those sanitary measures, as regards clothing, diet, bathing, exercise, and change of climate, which have such important influences upon health. The healthy performance of the functions of the skin is of such paramount necessity in maintaining that of the intestinal canal that the patient should endeavor to avoid any exposure likely to lead to checked perspiration, and should use flannel underwear and stimulate the skin by friction with the hand or the flesh-brush. The diet should be graded to the ability of the stomach to digest and the body to assimilate. Our chief reliance will be upon milk, plain or peptonized, eggs, and beef given in the various forms of acceptable preparations, so as not to impair the tone of the stomach nor clog the appetite by sameness. Such vegetables and fruits as agree with the patient may be allowed. I have tried exclusive diets of milk, farinacea, and meat without marked benefit. All stimulants, tea, and coffee should as a rule be interdicted.

Systematic exercise in the open air and change of climate to a cool, dry, bracing atmosphere will contribute to comfortable existence, if not lead to recovery.

{777}

DYSENTERY.

BY JAMES T. WHITTAKER, M.D.

DEFINITION.--Dysentery is the clinical expression of a disease of the large intestine, of specific and non-specific (catarrhal) origin and form; characterized by hyperæmia, infiltration, and necrosis (ulceration) of its mucous membrane; distinguished by discharges of mucus, blood, pus, and tissue-débris; and attended with griping and expulsive pains (tormina and tenesmus).

ETYMOLOGY.--The name is compounded of the two Greek words [Greek: dys enteron], which, though untranslatable literally into English, have long since received the exact Latin equivalent, difficultas intestinorum. With appropriate alteration the same name is still employed in every civilized language in the common as well as the classical description of the disease. The French synonym, colite, locates the anatomical seat of the disease, while the German Ruhr and the English flux express one of its cardinal symptoms, the frequency (flow) of the evacuations.

HISTORY.--Ancient.--In its clinical history dysentery is one of the oldest known diseases, the name being found in common use before the time of Hippocrates, as in the often-quoted passage from Herodotus (443 B.C.), who relates that it and the plague reduced the army of Xerxes on the desert plains of Thessaly.

Fayrer informs us that in the ancient system of Hindoo medicine of the Ayur Veda, and in the commentaries of Dhanwantari, Charaka, and Sussutra, which carry us back nearly three thousand years, and in later Sanskrit writers, dysentery is described by the name of atisar, under two forms--amapake, or acute, and pakistar, or chronic; these again are subdivided into six varieties, ascribed by those ancient sages to changes in air, bile, phlegm, food, or to perturbations of the emotions and passions.

Hippocrates (430 B.C.) makes frequent reference to the disease, the nature of which he regards as a descent of the humors from the brain. "Men of a phlegmatic temperament are liable to have dysenteries," he says, "and women also, from the humidity of their bodies, the phlegm descending downward from the brain."

"The disease is caused," he says more exactly in another place, "by the overflow of phlegm and bile to the veins of the belly, producing ulceration and erosion of the intestine." In his country, at least, it seemed most to prevail in spring, but it was clearly connected with the heat and moisture of this season in Greece--prime factors everywhere in the genesis of the disease: "For when suffocating heat sets in all of a {778} sudden while the earth is moistened by the vernal showers and by the south wind, the heat is necessarily doubled from the earth, which is thus soaked by the rain and heated by a burning sun, while at the same time men's bellies are not in an orderly state, nor is the brain properly dried." Of the prognosis he observes with great acumen, "Dysenteries when they set in with fever ... or with inflammation of the liver and hypochondrium or of the stomach, ... all these are bad. But such dysenteries as are of a beneficial nature and are attended with blood and scrapings of the bowels cease on the seventh or thirtieth day, or within that period. In such cases even a pregnant woman may recover and not suffer abortion;" whereas, "dysentery if it commence with black bile is mortal." Galen comments upon this statement that such a discharge is as incurable as cancer. The practitioner of our day will interpret this assertion, which was repeated with singular unanimity by all the writers of antiquity, with the belief that the black bile was blood, and that such cases really were cancers. Indeed, Paulus Ægineta distinctly says, "Dysentery arising from black bile is necessarily fatal, as indicating an ulcerated cancer."

Thus, although dysentery is among the oldest of the known maladies, and was recognized then as now by the same symptoms, the disease was by no means closely defined or differentiated in ancient times. As Ackermann long ago pointed out, many other affections were included under the term dysentery, and some of the symptoms of true dysentery, notably the tenesmus, were raised to the dignity of distinct diseases.

The gravity of the so-called lotura carnea, the fleshy stools, was fully appreciated by Hippocrates, as is evidenced by the remark that "if in a person ill of dysentery substances resembling flesh be discharged from the bowels, it is a mortal symptom." Fleshy masses, [Greek: xysmata], scrapings of the guts (originally epidermic exfoliations from the bodies of gladiators, used in pills as a tonic), were frequently alluded to by the older writers, more especially by Aretæus, in description of the discharges of dysentery. Hippocrates was also aware of the fact that dysentery may be a secondary as well as a primary malady. "One may expect," he says in speaking of the victims of gangrene, "that such patients will be attacked with dysentery; for dysentery usually supervenes in cases of mortification and of hemorrhage from wounds." Finally, Hippocrates recognized the effects of emesis in relief of the disease with the remark in one of his aphorisms that a spontaneous vomiting cures dysentery.

Celsus (25 B.C.-45 A.D.), the great encyclopædist, whose works "constitute the greatest literary monument since the days of Hippocrates," compiles all the information obtained up to his time; but it is plain as regards dysentery, though he defines it in terms that might stand in a modern text-book, that he has nothing new to add to the knowledge of the Hippocratic school. He named the disease from one of its most prominent symptoms, tormina (tenesmus he considered a separate affection), speaks of the stools as being mixed with mucus and fleshy masses, and in its treatment especially enjoins rest, "as all motion proves injurious to the ulcer."

Aretæus (50 A.D.), of all the authors of antiquity, wrote the most perfect and at the same time the most picturesque account of the morbid anatomy and symptomatology of this disease. The gross appearance of the ulcers in the intestine and the common character of the discharges he {779} describes with the accuracy of the modern pathologist and the ardor of the true clinician. He speaks of the superficial, the deep-seated, the irritable, and the callous ulcer. There is, he says, "another larger species of ulcers, with thick edges, rough, unequal, callous, as we would call a knot of wood; these are difficult to cure, for they do not readily cicatrize, and the cicatrices are easily dissolved." Their tendency to arrest and renewal and their general and local effects he notices at length. "There may be a postponement of their spreading for a long time," he says, "various changes taking place in the ulcers, some subsiding and others swelling up like waves in the sea. Such is the course of the ulcers; but if nature stand out and the physician co-operate, the spreading may indeed be stopped, and a fatal termination is not apprehended, but the intestines remain hard and callous, and the recovery of such cases is protracted." Vivid descriptions he gives of the stools: "Sometimes they are like chopped tallow, sometimes merely mucus, prurient, small, round, pungent, causing frequent dejections and a desire not without a pleasurable sensation, but with very scanty evacuations." Again, they are "fetid like a mortification;" composed of "food now undigested, as if only masticated by voracious teeth, ... the dejection being discharged with much flatulence and noise; it has the appearance of being larger than its actual amount."

Galen (164 A.D.) attempted to correct the pathology of his contemporaries, who considered all bloody discharges dysenteric. There are four distinct varieties of bloody stools, he claims, only one of which, that due to ulceration of the intestine, deserves to be called dysentery. The bilious stool he derived from melancholy, and the fleshy stool from disease of the liver. But, though Galen regarded the presence of blood as a necessity, he was well aware of the fact that the stools contained ingredients other than blood. It was Galen who first used the word scybala ([Greek: schybala], feces) to express the small, solid masses of excrementitious matter often voided with the stools. In his treatment of the disease he made much use of the various drying earths, the Samian, Lemnian, Armenian, the sources of which he made long journeys to visit in order to become better acquainted with their properties, and which are better substituted in our day by bismuth, chalk, magnesia, and the carbonate of iron. It is the distinguished merit of Galen to have called special attention to the anatomical seat of the disease. Ulceration of the intestine he claimed as the very essence of the disease, and all the physicians of his day, he maintained, regarded as dysenteric only such cases as are attended with ulceration.

Galen was the exponent of the flower of Grecian, we might say of ancient, medicine. With very few exceptions, the later writers, if they do not obscure the original text with their speculations, are content to simply paraphrase the observations of their predecessors, and the subsequent contributions to the ancient history of dysentery may be briefly summed up in a few additional notes.

Coelius Aurelianus (400 A.D.) adopted the humoralistic doctrine of Hippocrates and regarded dysentery as an intestinal rheumatism (catarrh) with ulceration. He seems to have been the first author to recognize the cardinal fact that dysentery, notwithstanding the number of its stools, should be classed with the diseases which constipate the bowels, or, as it {780} was centuries later aptly put by Stoll, "ut hanc morbis adnumeres alvum potius occludentibus," and he blames Erasistratus for using nothing but astringents, whereas many cases of dysentery require laxatives. It is worthy of note that Coelius Aurelianus ascribes the first use of opium in the treatment of dysentery to Diocles of Carystus (300 B.C.), who administered the juice of poppies combined with galls. By the time of Galen opium was so freely used in the treatment of the fluxes as to call for protest against its abuse.

Alexander of Tralles (575 A.D.) is often credited as having been the first to locate the disease in the large intestine. The truth is, he suggested various rules by which the seat of the disease, whether in the small or large intestine, might be definitely determined. But none of these rules--the seat of the pain, for instance, whether above or below the umbilicus, and the interval of time between the pain and discharges, whether long or short--possess the least diagnostic value or add to the attempts in this direction of previous writers--Aretæus, Archigenes, and Galen. Like these, his predecessors, he recognized an hepatic dysentery with discharges of bloody serum, which he attributed with them to atony of the liver, but more boldly than they, and with characteristic independence, he ventured to treat his patients with fresh vegetables and fruits, damsons and grapes.

Paul of Ægina (660 A.D.) locates the disease in the rectum, and gives a graphic account of its symptomatology. He made the mistake of many later practitioners in regarding as a separate disease a symptom, tenesmus, which he describes as an irresistible desire of evacuation, "discharging nothing but some bloody humor, which is the cause of the whole complaint, being an oedematous inflammation of the rectum which creates the impression of feces lodged in the intestine and a desire of evacuation." "Dysentery," he continues, "is an ulceration of the intestines, sometimes arising from the translation of tenesmus, and sometimes being of itself the primary affection; and is attended with evacuations at first bilious and of various colors, then accordingly bloody, and at last ichorous, like that which runs from dead bodies."

In curious contrast to these accurate observations is the absurd suggestion of an obsolete therapy (Galen), that the dried dung of dogs who had eaten bones, when drank in milk which has been curdled by having heated pebbles put into it, is of great service; but as an offset to this freak of fantasy is the renewed advocacy of warm milk, fallen somewhat into disuse since the days of Hippocrates and Galen: "And milk itself moderately boiled is an excellent thing"--a recommendation of the milk diet which now plays such an important rôle in the treatment of so many diseases of the alimentary canal.

Modern.--From this brief survey it is seen that the writers of antiquity left nothing in the symptomatology of dysentery for subsequent authors to describe. All further advance in our knowledge of this, as of all diseases, was now rendered impossible by the extinction of the light of science in the long night of the Middle Ages, whose gloom deepens with succeeding centuries and whose shadows fall close up to our own times.

The modern history of dysentery may be said to begin with Daniel Sennertus, whose first _Tractatus de Dysenteria_ was published at {781} Wittenberg in 1626. Sennert gave the deathblow to tenesmus as a distinct disease, or as even a pathognomonic sign of dysentery, showing that it is often present in purely local troubles, ulcers, fissures, hemorrhoids, etc., or is due to disease of other organs--stone in the bladder, tumors in the womb, etc. He recognized sporadic and epidemic attacks of the disease, and described under the terms fiens and facta forms which coarsely correspond to the catarrhal and diphtheritic varieties of modern pathologists. Improper food, unripe fruits, at least, cannot be the cause of dysentery, because, he shrewdly observes, the epidemic of 1624 began in May, before the fruits were ripe, and ceased in autumn, when they were ripe and in daily use. Moreover, sucklings at the breast suffered with the disease. Nor could moisture alone account for the disease, as this epidemic occurred after an unusually hot and dry spring and early summer. Some other cause must be invoked, and this other cause is perhaps the occult influence of the constellations and planets--an explanation which he afterward admits to be only an asylum of ignorance. In the treatment of the disease the indication should be to heal the abraded or ulcerated intestine; but since this cannot be done unless the cause is first removed, "the abrading, eroding humor should be evacuated and absterged, at the same time its acrimony mitigated and corrected; then the flux should be checked by astringents, and the pain, if vehement, lenified and removed." Purgatives should be repeated until all vicious humors are discharged.

Sydenham colored his descriptions of the epidemic which he witnessed in London in 1669-72 with the artistic touches of the master's hand. "The disease sets in," he says, "with chills and shivers. After these come the heat of the fever, then gripings of the belly, and lastly stools. Occasionally there is no fever; in which case the gripes lead the way, and the purging follows soon after. Great torment of the belly and sinking of the intestines whenever motions are passed are constant; and these motions are frequent as well as distressing, the bowels coming down as they take place. They are always more slimy than stercoraceous, feces being rarely present, and when present causing but little pain. With these slimy motions appear streaks of blood, though not always. Sometimes, indeed, there is no passage of any blood whatever from first to last. Notwithstanding, provided that the motions be frequent, slimy, and attended with griping, the disease is a true bloody flux or dysentery." The efficacy of opium in its treatment causes him to break out in praises of the great God who has vouchsafed us a remedy of so much power. But Sydenham was too good a practitioner not to know that all treatment must be prefaced with laxatives. For "after I had diligently and maturely weighed in my mind," he says, "the various symptoms which occur during this disease, I discovered that it was a fever--a fever, indeed, of a kind of its own--turned inwardly upon the bowels. By means of this fever the hot and acrid humors contained in the mass of the blood, and irritating it accordingly, are deposited in the aforesaid parts through the meseraic arteries." The indications then were plain--viz. "after revulsion by venesection to draw off the acrid humors by purging." It was the frequent and successful practice of Sydenham also to drench the patient with liquids, per os et per rectum--a mode of treatment which both he and the learned Butler, who accompanied the {782} English ambassador to Morocco, where dysentery was always epidemic, hit upon, "neither of us borrowing our practice of the other." Butler declared that the method of deluging the dysentery by liquids was the best. But many attacks are cured almost on the expectant plan alone. This was the case with the excellent and learned Daniel Coxe, Doctor of Physic, in whom "the gripes and bloody motions ceased after the fourth clyster. He was kept to his bed, limited to milk diet; and this was all that was necessary in order to restore him to perfect health."

Zimmermann (1767) did not believe that improper food could be a cause of dysentery, as in the epidemic of 1765 fresh grapes were plentifully supplied to patients and proved an excellent remedy. He also noticed the muscular pains (rheumatism) which had been mentioned by Sydenham before him, and the paralyses first noticed by Fabricius in 1720, as occurring in the course of, or as sequelæ to, the disease. It was only contagious, he thought, in bad cases, when the stools have a cadaveric odor. But his main and most useful contributions were in the field of therapy. He discarded venesection entirely, was among the first to recognize the value of ipecacuanha, and objected strenuously to opium until the cause of the evil was expelled. Hence he was vehemently opposed to all astringents, to the use of which he ascribes the rheumatisms and dropsies which sometimes occur. Wines and spices were likewise put under ban; whey he permitted, but not milk, and water freely, but always warm. Barley-water and cream of tartar were sufficient food and medicine for ordinary cases, while camphor and cinchona best sustain the strength in bad cases.

Pringle (1772) observed the frequent occurrence of dysentery coincidently with malarial fever, and was a firm believer in the contagion of the disease. He claimed that the foul straw upon which the soldiers slept became infectious, but maintained that the chief source of infection were the privies "after they had received the dysenteric excrements of those who first sicken." It is spread in tents and in hospitals, and may be carried by bedding and clothing, as in the plague, small-pox, and measles. Neither food nor drink propagates the disease, he thinks, for, so far as the fruits are concerned, he too had seen it prevail before the fruits were ripe. The first cause of the disease is "a stoppage of the pores, checking the perspiration and turning inward of the humors upon the bowels." Antimony was his specific in its treatment. He was also fond of Dover's powder in its relief, and preferred fomentations to opium, which "only palliates and augments the cause." The best drink for patients with dysentery was lime-water (one-third) and milk.

This period of time is made memorable in the history of dysentery, as of nearly all internal diseases, by the contributions from direct observation upon the dead body by the father of pathological anatomy, John Baptist Morgagni (1779). From the days of Hippocrates down, the seat of the disease had been, as has been shown, pretty accurately determined, and the same acumen which enabled the clinicians to localize the affection had inspired them, as we have seen, to define and describe its nature. But any descriptions from actual post-mortem examinations were not put upon record until the beginning of the sixteenth century, when were published the posthumous contributions of Benivieni (1506-07). In his description of the lesions of the disease he says that "the viscera displayed {783} internal erosion from which sanies was continually discharged." Nearly three centuries elapsed before Morgagni made his anatomical studies--an interval of time void of any contributions from pathological anatomy; and so little attention was paid to this branch of medical science that the descriptions of Morgagni and of his more immediate successors failed to excite any general interest or make any permanent impression. Morgagni himself, while he fully recognized their significance, did not consider the ulcerations of dysentery as absolutely essential to the disease, as many cases, even fatal ones, did not exhibit them at all. They were not liable to be mistaken for the lesions of typhoid fever, the ulceration of Peyer's glands, because, though they may, they only rarely, coexist in the same subject. As to the membranous fragments sometimes evacuated with the discharges of dysentery, Morgagni showed that they are occasionally true fragments or shreds of the intestinal coats, as has been maintained by the older writers, Tulpius and Laucisius, but are far more frequently nothing else than inspissated mucus--conceptions which subsequent studies with the microscope have fully confirmed.

In view of the general disregard of direct observations, it is therefore not surprising to learn that the nature of the intestinal lesions gradually fell into oblivion or at least became underrated in its import. But it is a matter of surprise that Stoll (1780) was able to declare as the result of autopsies made by himself that, although the colon is thickened and inflamed, ulcerations in dysenteries are very rare. This distinguished author did not at all believe in the contagion of the disease, as he had never seen it attack physicians or nurses. It developed, he thought with the older writers, as the result of exposure to cold during a perspiration. He emphatically insisted upon the frequency of rheumatism as complicating the disease, and describes in proof a number of cases of painful swollen joints during and subsequent to the attack. It was his especial merit to have succeeded in dispensing with the acrid bile as a cause of the disease, maintaining that hepatic derangements were only accidental complications, and thus disposed, but only for a time, of bilious dysentery in so far as it was supposed to depend upon defective or abnormal action of the liver.

But Annesley (1828) soon reinstated the liver in the pathology of dysentery, with the exhibition of colored plates displaying abscess of the liver in connection with the disease, as well as illustrating the displacements and constrictions of the colon which sometimes occur in its course.

The fourth decade of our century now brought in the anatomical contributions of Cruveilhier and Rokitansky, to be followed later by those of Virchow, upon which the modern morbid anatomy of the disease is based; while the labors of the Indian physicians and of Copeland, Parkes, and Vaidy put us in possession of the facts pertaining to its general pathology. Fayrer has quite recently published the results of his vast experience with dysentery in India, an important contribution to the practical study of the disease, and Hirsch has treated exhaustively of its medical geography. But the merit of publication of the most complete chapter or work upon dysentery that has ever been written anywhere belongs to, and is the especial pride of, our own country. It constitutes the bulk of the second volume of the _Medical and Surgical History of the War of the Rebellion_. It is a veritable encyclopædia of knowledge, not {784} only upon the subject of which it treats, but upon all subjects immediately or even remotely collateral to it, and is a lasting monument to the labor and the learning of its author, Joseph J. Woodward, Surgeon of the United States Army.

GENERAL REMARKS.--Dysentery may be a primary or a secondary disease. As a primary disease it occurs in sporadic, endemic (often closely, sometimes curiously, circumscribed), or epidemic form, and is either acute or chronic, according to the nature of its symptoms and lesions. The ancient types of sthenic and asthenic or adynamic, typhoid, bilious, and malarial dysenteries belong rather to history than to modern medicine. The classification of cases in general use at present--viz. the catarrhal and croupous or diphtheritic forms--has reference rather exclusively to the nature of the lesion, and is hence extremely defective. Nor are the divisions (as in cholera) into sporadic and epidemic forms much more satisfactory, in that they indicate simply the range or extent of the disease, and by no means define a separate array of symptoms or lesions; precisely the same symptoms or lesions being encountered in individual cases of either form. None of these divisions clearly indicate differences in etiology, upon which factor alone can any acceptable division of cases be based. Perhaps less objection may be urged against the assumption of catarrhal and specific forms, including under the provisional term catarrhal all the cases which cannot as yet be accounted for by the action of a special or specific cause.

It will become apparent in the study of the etiology of dysentery that while any of the factors invoked may suffice to produce the catarrhal (sporadic) form, none will explain the specific (epidemic) form of the disease; both forms may be alike in their lesion and signs, but they differ widely in their cause. In other words, dysentery is only a clinical, and is in no way an etiological, expression of a disease. In this respect dysentery finds its analogue in a much grosser lesion of the bowels--namely, occlusion, acute or chronic, which, while it presents pretty much the same train of symptoms, may depend upon a great variety of causes, as impaction, strangulation, intussusception, etc. While any of the causes cited may be sufficient to excite the catarrhal form of the disease, the same causes may stand to the specific form only in the relation of predisposing agents. Or, as Maclean has better put it, "It appears that many of the so-called causes of dysentery must be regarded more as acute agents of propagation than of causation."

As a secondary disease dysentery occurs in the course of, or as a sequel to (not infrequently as the terminal affection of), pyæmia and septicæmia (puerperal fever), typhus and typhoid fevers, pneumonia, Bright's disease, variola, scarlatina, abscess of the liver (though the order of sequence is here oftener reversed), scorbutus, marasmus from any cause, tuberculosis, and cancer. It must not be forgotten, however, of these latter affections that each produces its own lesions in the large intestine, which are not to be confounded with those of genuine dysentery.

The view that dysentery shows a periodicity of recurrence at certain distinct intervals or cycles--three, five, or ten years--is entirely without foundation in fact; but there is strong ground for believing that the disease is gradually abating both in frequency and virulence with improvements in sanitation and hygiene. Thus, Heberden shows that the {785} number of deaths set down in the seventeenth century under the titles of bloody flux and gripings of the guts was never less than 1000 annually, and in some years exceeded 4000, whereas during the last century the number gradually dwindled down to 20 (Watson)--a number which is certainly a misprint for 200; and Aitken states that as a cause of death it has been decreasing since 1852. Geissler also remarks[1] that the variation in epidemics is nowhere so well illustrated as in the case of dysentery. A noticeable reduction in the number of cases in England began about 1850, and has continued almost without interruption to the present time, so that now (1880) six to eight times less cases occur than in the forties. The same diminution has been noticed in Bavaria and Sweden. In Sweden the cases treated by physicians in 1857 numbered no less than 37,000, with over 10,000 deaths; whereas now the number is reduced to 400-500 a year, and the mortality has experienced a corresponding reduction from 20-30 to 6-8 per cent.

[Footnote 1: _Periodische Schwanderungen der wichtigsten Krankheiten_.]

At the same time, it is known of dysentery that it sometimes shows an almost freakish recurrence after long intervals of time, appearing in a place for many decades free from the disease, to establish itself there for years as a regular endemic malady, not to disappear again for a long series of years; in which respect, Hirsch remarks, it much resembles malaria.

Allusion has been already made to the occasional curious circumscription of the disease in definite localities. In fact, dysentery, even when late to assume the proportions of a widespread epidemic, begins, as a rule, and is confined for a time, in individual enclosed regions--prisons, barracks, hospitals, etc.; and in the process of dissemination it is rather characteristic of the disease to leap over or to spare intervening territory and appear in new foci at some distance from its original seat. A direct irradiation or linear transmission of the disease is the exception, and not the rule. The significance of this fact will become evident in the study of the etiology of the disease.

Dysentery is pre-eminently a disease of army life, its victims among soldiers numbering more than all other diseases together. Sir James MacGrigor, Medical Superintendent of the British army, called it the scourge of armies and the most fatal of all their diseases. Aitken says that "it has followed the tracks of all the great armies which have traversed Europe during the continental wars of the past two hundred years." It decimated the French, Prussian, and Austrian armies in 1792. In Cape Colony in 1804 every fourth man among the soldiers was attacked with the disease, and of those attacked every fifth man died. In Napoleon's campaign in Egypt dysentery numbered one-half more victims than the plague; Kinglake says that 5000 men died of dysentery alone in the war of the Crimea; and in our own country during our Civil War from 1861-65 chronic camp dysentery was the cause of more than one-fourth of all the diseases reported, the mortality being at the rate of 12.36 per 1000.

Woodward relates that the dysenteries, acute and chronic, with diarrhoeas, made their appearance in the new regiments at the beginning of the war, and, though mild at first, quickly assumed a formidable character. "Soon no army could move without leaving behind it a host of the victims. They crowded the ambulance-trains, the railroad-cars, the {786} steamboats. In the general hospitals they were often more numerous than the sick from all other diseases, and rivalled the wounded in multitude. They abounded in the convalescent camps, and formed a large proportion of those discharged for disability." Most of the prisoners died of this disease, and great numbers succumbed to it on retirement to their homes after the cessation of the war. It is the story of many a campaign, Eichhorst says, that dysentery kills more men than the enemy's guns.

The fact that it sometimes shows itself in periodic form or with periodic exacerbation, that it is sometimes successfully treated with quinia, and that, as has been noticed from the days of Hippocrates down, it prevails in greatest intensity in malarial regions, has given rise to the view that dysentery is a malarial disease. This view, which was strongly advocated by many of the older writers, Senac, Fournier, Annesley, met with renewed support at the hands of many of the surgeons in our Civil War. But wider observation has shown the fallacy of such a view; for not only may the diseases prevail entirely independently of each other in malarial regions, but there are regions where one does and the other does not exist. Thus Huebner quotes from Rollo concerning St. Lucie (West Indies), a town situated on a mountain in the midst of a swampy country in which both dysentery and malaria abound, while the town itself is almost free from dysentery; and Dutrolan cites Réunion as a place where marsh fevers do not occur, while dysentery is very common. Bérenger-Féraud[2] scouts the idea of any such connection. "Let us mention only St. Pierre de la Martinique," he says, "where there is not a piece of marsh as big as a hand, but where dysentery has made great ravage more than once. We might cite also Mauritius, Gibraltar, Malta, New Caledonia--places exempt, or almost exempt, from malaria, but often visited by dysentery."

[Footnote 2: _Traité théorique et clinique de la Dysenterie, etc._, Paris, 1883.]

The view that dysentery is a form of typhus or typhoid fever (Eisenmann) or scurvy needs no refutation in the light of existing knowledge regarding the pathogenesis and pathology of these affections. These diseases may often complicate, but can never cause, dysentery.

Dysentery is a disease which spares no age, sex, or social condition, the seeming greater suffering of the poorer classes being due to the filth, food, darkness, dampness--in short, to the bad sanitation--of poverty.

Though the disease is often confined exclusively to soldiers in the midst of a civil population, examples are not wanting of an exclusive selection of civilians or of an indiscriminate attack in every direction. Lastly, dysentery is a disease which may recur repeatedly in the same individual, one attack rather predisposing to than preventing another.

ETIOLOGY.--Dysentery is an omnipresent disease. "Wherever man is," Ayres observed of it nearly a quarter of a century ago, "there will some of its forms appear." But the character of the form, and more especially the extent and severity of the disease, vary in extreme degree with the conditions surrounding the abode of man. No one of these conditions affects the disease so markedly as the climate. It is the testimony of Hirsch, based upon the study of seven hundred epidemics of the disease, that no other disease is so dependent upon the influence of the climate. The home of dysentery is the tropical zone. It prevails in greatest frequency {787} and virulence in the tropics, and in those regions of the tropics where the characteristics of this zone are more pronounced, diminishes in intensity in the temperate regions, and occurs only in sporadic form farther north. At 40° latitude the line may be pretty sharply drawn; beyond it dysentery as an epidemic is almost unknown.[3]

[Footnote 3: Shakespeare (_Troilus and Cressida_) cites "griping of the guts" among the "rotten diseases of the south."]

India has been from time immemorial the hotbed of this disease. Henderson says it is perhaps more fatal to natives than all other diseases put together, and Hutchinson, Hunter, and Tytler observe that it causes three-fourths of the deaths among the natives of Hindostan. In Egypt the disease is indigenous, and is, according to Frank, post pestem maxime timendus. Greisinger reports that one-half of all the autopsies made by him in Egypt showed dysentery as a primary or secondary affection. It is epidemic here at all times, Roser says, and all fatal cases of acute or chronic disease finally perish with it.

Similar testimony might be adduced from a large part of Africa, much of Asia, the Indian Archipelago, and the West Indies. It rages "murderously" in Peru, causing a mortality in some epidemics of 60 to 80 per cent., and occurs in this country not only in the valleys, but in cities and provinces at the lofty elevation of 8000 to 13,000 feet.

Heat, moisture, vegetable decomposition, and sudden atmospheric change are the distinguishing characteristics of southern climes, and the study of the etiology of a disease incident or indigenous to these conditions calls for an investigation of these various factors.

It is well established of dysentery that it occurs for the most part in the hottest season of the year. Of 546 epidemics tabulated by Hirsch, 404 prevailed in summer and fall, 113 in fall and winter, 16 in spring and summer, and only 13 in winter. Fourteen-fifteenths of the whole number of epidemics occurred in the months of June to September. And it is corroborative of these conclusions that of 1500 deaths from dysentery in the cities of Boston, New York, Philadelphia, and Baltimore from 1816 to 1827, 1100 occurred in the months of July, August, and September. In fact, the Census Reports (1860-70) of our country show the maximum mortality in August and September, and the minimum in January and February.

The prevalence of unusual heat may also call out an epidemic in places where the disease usually shows itself only in endemic or sporadic form. Thus, the severe epidemic of 1540 in England was preceded by a heat so intense as to dry up the wells and small streams, in consequence of which many cattle died of thirst; and the epidemics of 1583 in Germany, of 1758 in France, and of 1847 in our own country, were characterized in the same way. Interesting in this connection is the statement of Frick concerning the epidemic in Baltimore in 1849, who found the cases to increase and decrease almost in proportion to the elevation and depression of temperature. The epidemic of Weimar in 1868, where 12,000 people fell ill with the disease, illustrated the rule when it ceased suddenly on the approach of cool weather at the end of August.

But that heat alone is not sufficient to account for the genesis of the disease is apparent from the occasional occurrence of it in the tropics in the colder seasons of the year; in the colder climates, Russia, Sweden, {788} and Canada; and in temperate regions during exceptionally cool seasons, as in Plymouth in 1769, London in 1808, Massachusetts in 1817. Moreover, the temperate zone is often characterized by seasons of unusual heat, during the prevalence of which dysentery may be almost unknown. Thus, during the summer of 1881, in Cincinnati, the thermometer scarcely fell below 95° F. for weeks at a time, and was often nearly 100° during the entire night, but the records at the Health Office show that while cases of heatstroke were alarmingly frequent, dysentery was unusually rare during the entire season.

That moisture cannot act more, at most, than as an occasional predisposing cause of dysentery is sufficiently clear from the statement of Hirsch, that of 119 epidemics, 62 commenced or were preceded by wet and 57 by dry weather. In truth, dryness long continued and excessive heat have already been invoked as remote causes of the disease. But moisture, as contributing to, or being a necessary element of, vegetable decomposition, the third characteristic of tropical regions, is entitled to further consideration. Annesley observed that among troops stationed in the vicinity of rivers, canals, and places abounding with emanations from the decay of animal and vegetable matters dysentery became extremely prevalent and assumed a more or less malignant nature; and Baly, who studied the disease in its famous outbreak in the Milbank Penitentiary, remarks that "it is greatest at those seasons and in those states of the atmosphere which most favor decomposition of organic matter in the soil."

In Africa it has been noticed that dysentery appears with the rainy season, to disappear only at its close; and the same observation has been made of Bengal, while in Lower Egypt the disease follows the inundations of the Nile. Burkhardt says of 10,000 cases that one-half occur in wet hot seasons, two-fifths in dry hot seasons, and but one-tenth in cold seasons. Moreover, the removal of camping-grounds to dry localities has often arrested the disease or checked its further dissemination. Thus, Mursinna states that the removal of the army of Prince Henry of Hesse from Nîmes, where the disease raged fearfully, to Leitmeritz was attended by its immediate cessation, notwithstanding the fact that the soldiers ate large quantities of fruit. A statement of Dillenius, quoted by Heubner, is in this connection exceedingly instructive: "Dillenius had to march with a dysentery hospital of more than 500 patients from July 26 to August 3, 1812, and it required four whole days to accomplish an ordinary nine or ten hours' march. The patients, extremely exhausted, were finally put into a sheep-shed. Here, in the fresh air and lying on hay, they all improved very quickly. By advice of the physician they ate for medicine the fresh whortleberries which they themselves had picked." Werneck attributes the exemption of the city of Halle since the end of the last century to the draining and drying of the neighboring marshes.

On the other hand, numerous observations go to prove that dysentery is likewise prevalent in dry sandy soils where the factors so necessary to the production of malaria are entirely unknown. Thus, Hirsch quotes from Harthill to the effect that dysentery never occurred among the English troops in Afghanistan until they entered upon its thoroughly dry and sandy plains; and from Lidell, who declared that the disease prevailed most in Panama in March, the dry season at this place. Again, a striking confirmation of exemption from dysentery in a marshy region {789} is offered in the Antilles at Grande-Terre, "a wet, marshy plain severely visited by malaria, but used by patients attacked with chronic dysentery at Basse-Terre as the safest place of refuge and recovery."

The rôle of moisture and vegetable decomposition may be, then, summed up in the words of Annesley, that "all situations which furnish exhalations from the decay of animal or vegetable productions under the operation of a moist and hot state of the atmosphere will always occasion dysentery in the predisposed subject--_circumstances which, with other causes_ [italics ours], combine to generate the disease."

Atmospheric vicissitudes, checking of perspiration, catching cold, are synonyms in the present popular as in the ancient professional conception of the genesis of dysentery. "Of the remote causes of dysentery," Johnson says, "I need say little; they are the same in all parts of the world--atmospheric vicissitudes." And in making this statement the author expresses the almost universal testimony of the Indian physicians. "Sudden change of temperature," observes Kaputschinsky of the Trans-Caucasus, where dysentery is rife, "is in this region no rarity. The sultry heat of noon often alternates with a cutting cold wind, and vice versâ. In the same place is now a warm, now a cold, now a glowing hot breeze, and such changes most predispose to dysentery." And McMullin says of the Barbadoes that "it is a curious fact that this disease is most prevalent where from the immediate contiguity of mountains sudden vicissitudes of temperature are experienced." Didelot says also of South France, "It is not the fruits, as people still believe to-day, which act as causes of dysentery, but the sudden variations of the air." Ruthay remarks of the dysentery of China that the most common cause is a chill caught by sleeping in a draught uncovered or in the open air. Metzler attributes the exemption of Stuttgart (since 1811) from any great epidemic to the fact that the city lies in a valley open only to the east, which permits no contrast of hot days and cold nights; and Seeger, in speaking of the epidemic which occurred in Ludwigsberg in 1872 (a city of twelve thousand population, where no epidemic of any kind had appeared since 1834, and where 870 were suddenly attacked with dysentery) that it first broke out in Kaffeeburg in two streets exposed to the wind, and thence spread to different parts of the city. Exposure of the body, especially the abdomen, during sleep or when perspiring, the sudden laying aside of flannel body-clothes, are proceedings, Fayrer says, pregnant with danger in dysenteric regions. A lamentable dysentery appeared, according to Trotter, on board H.M.S. Berwick Oct., 1780, "in consequence of the hurricane on the fifth of the month, by which the clothes and bedding of the seamen, and indeed all parts of the ship, were soaked in water, and many of the men slept for nights together on the wet decks overcome with fatigue and debilitated from want of food." Fayrer also quotes from Moseley the observation that "it often happens that hundreds of men in a camp have been seized with the dysentery almost at the same time after one shower of rain or from lying one night in the wet and cold."

As illustrating the conjoined operation of all these various causes, together with filth and foul effluvia, more especially exposure to cold, the story of dysentery was never better told than by Sir James MacGrigor, who, in speaking of the Peninsular campaign, remarks that "the army during June as well as July was traversing Castile, where it was {790} exposed to the direct influence of a burning sun darting its rays through a sky without a single cloud, the troops marching and fighting during the day, and bivouacking during the night on arid, unsheltered plains. They felt at times every vicissitude of heat and cold. In the rapid advance they could not be regularly supplied with food or had not time to cook it, and not unfrequently indulged in bad wine and unripe fruit." ... The thousands of sick (chiefly from diarrhoea, dysentery, and remittent fever) were hurried off to Ciudad Rodrigo, the nearest hospital-station to the frontier of Portugal, a town "composed chiefly of ruins with very narrow streets," ... and from having been "so much the object of contest, and alternately the site of the hospitals of all the contending armies, nearly twenty thousand bodies were calculated to have been put into the earth either in the town or under its walls in the course of a few months." ... "It may easily be conceived," the author adds, "in what state cases of dysentery must have arrived after having sustained a journey in extent from four to twenty days, conveyed chiefly in bullock-carts or on the backs of mules, sometimes under incessant rain for several days together."

It is really quite superfluous to cite further opinions or examples in illustration of a fact which is so universally conceded as to be exaggerated in its general significance. Taking cold is the common idea of the cause of dysentery, and is always a satisfactory explanation in a case of obscure origin in this or any disease, even though the patient may be able to recall no possible exposure. The physician himself contents himself only too easily with resort to this refuge, and with further appeal to the locus minoris resistentiæ, as the explanation of the seat of the disease, which he hopes to cure with the aid of the vis medicatrix naturæ. But taking cold is only a popular paraphrase for contracting a disease, and will bear no scientific analysis of its meaning. Mere reduction of temperature will certainly not produce a disease whose habitat is the hottest zone, nor will a sudden chill of the surface be accepted as a sufficient cause so long as men daily remain exempt after a sudden plunge into cold water. Some other factor must be invoked to account for the outbreak of specific (epidemic) dysentery.

The influence of the nervous system, the mechanical and chemical or specific action of the ingesta and dejecta, remain to be especially considered in the etiology of the disease.

The influence of the nervous system is more directly seen in the production of diarrhoeas than dysenteries, but that sustained disturbances of the emotions play an important part in the production of dysentery is shown by the greater frequency of the disease among prisoners of war. In the Franco-Prussian war the French prisoners suffered more than the Germans, and the records of prison-life in our own war, at Andersonville, Libby, and Salisbury, furnish ghastly chapters in the history of this disease. Many other factors contribute to the development of the disease under such circumstances--in fact, all the cruelties of man's inhumanity to man--but the influence of the nervous system is too plain to be mistaken. The communication between the cervical ganglia and the sympathetic nerve-fibres which preside over the cerebral circulation and regulate intestinal peristalsis has been invoked (Glax) in explanation of the direct action of the brain upon the intestinal canal. Curious in this {791} connection is the claim of Savignac, who considered dysentery a disease of the nervous system because in two cases he found spots of softening in the spinal cord.

The noxious action of irritating articles of diet has been recognized in the production of dysentery from the earliest times. Aretæus mentions acrid foods, and Aëtius crudities, as directly causing the disease; and unripe fruits have been especially stigmatized from the days of Galen down. Decomposing, fermenting food and drink cause diarrhoea much more frequently than dysentery, but if the irritation be severe or prolonged, or be superimposed upon a catarrhal state, a diarrhoea, it is claimed, may pass over into dysentery. Impurities in drinking-water were charged with causing dysentery by Hippocrates himself, with whom Avicenna fully coincided; and the view that epidemics of the disease are caused in this way has been abundantly advocated ever since. So far as running water is concerned, the researches of Pettenkofer have shown that all impurities are speedily destroyed, for even at the distance of a few rods from the reception of sewage the water is perfectly safe. Nor does standing water lack the means of purification, provided it be sufficiently exposed to the air. The observations of Roth and Lex have shown that the water of the wells of fifteen churchyards in Berlin contained nitrates in less quantity than the average wells in the city; and Fleck made a similar statement with regard to the wells of Dresden. But no one in our day would rely upon a mere chemical analysis in the detection of the organic poisons or particles of disease. It is the physiological test which remains the most conclusive, and the evidence in favor of the production of dysentery by the ingestion of drinking-water poisoned by the reception of excrementitious matter, especially the dejecta of disease, is as positive as in the case of typhoid fever. Thus, De Renzy found that the number of cases of dysentery "immediately decreased at Sibsagor (India) so soon as better drinking-water was obtained from wells deeply sunk and lined with earthenware glazed pipes;" and Payne found that the cases of dysentery (as well as diarrhoea and lumbrici) almost disappeared from the asylum at Calcutta as soon as the habit of drinking water from the latrines was stopped. In face of such facts, which might be infinitely multiplied, one would hesitate to subscribe to the statement of Fergusson that "true dysentery is the offspring of heat and moisture, of moist cold in any shape after excessive heat; but nothing that a man could put into him would ever give him a true dysentery."

The relation of the action of the dejecta must be studied from the double standpoint of the development and the dissemination of the disease, as originating the catarrhal form by mechanical or chemical irritation of the intestinal mucosa, and as spreading the specific form by direct or indirect infection.

By the time the contents of the alimentary canal have reached the colon they have become, through absorption of their fluids, more or less inspissated, and hence as hard, globular masses fill the sacculi of the large intestine. Mechanical irritations by crude, indigestible residue of any kind of food, more especially of vegetable food, or chemical irritations, as by fermenting food, accumulate in this region, fret the mucous membrane into a state of inflammation, even ulceration, and produce the anatomical picture and the clinical signs of dysentery. If there be a superadded or {792} pre-existent catarrhal condition of the mucosa or a defective peristalsis of the muscular coat, which is sluggish enough at best, the development of a pathological state is much facilitated. And there is no doubt that the dysentery of the tropics is increased by the bulky, indigestible, feces-producing character of the food.

The anatomical construction of the colon may also favor these processes by its mere abnormal length or size or by duplicatures in its course. The protracted constipation of the insane, in whom the transverse colon is often found elongated or displaced--to assume the well-known M-form, for instance--may partially account for the frequency of dysentery in these cases (Virchow), though the neglect which comes of preoccupation of the mind, with the general inhibition of peristalsis, is a more frequent cause of the constipation.

Wernich (1879) sums up the action of the feces, independently of a specific cause, in attributing the dysentery of the tropics, aside from the great changes of temperature, to (1) bad aborts, the dejecta being deposited in all parts of the towns or into an opening made in the floor of the hut, with which is associated total lack of personal cleanliness; (2) to the diet, which causes a large amount of feces; and (3) to the relaxation of the intestine in general, permitting accumulations of infecting matter.

Upon the question of the propagation of the disease by the dejecta rest in great measure the all-important problems of a specific virus and of the contagiousness of the disease.

It is the almost universal opinion of those who have had the opportunity of widest observation that epidemic dysentery arises from, or is due to, a specific cause, a miasm, a malaria (in its wide etymologic sense, bad air), which emanates from the soil. The simultaneous sudden attack of great numbers under the most diverse surroundings admits of explanation in no other way. But the precise nature of the morbific agent is still unknown. The similarity of epidemic dysentery to malaria would indicate the existence of a low form of vegetable life, a schizomycete, as the direct cause of the disease. But the proof of the presence of a specific parasite or germ is still lacking, and though its speedy disclosure by means of the solid-culture soils may be confidently predicted, it cannot, in the light of existing knowledge, be declared as yet.

Especial difficulty is encountered in the study of micro-organisms in diseases of the alimentary canal because of the myriad variety in enormous numbers found in healthy stools. Decomposition and fermentation both begin in the large intestine, so that the feces swarm with the bacteria and torulæ productive of these processes. Woodward declares that his own observations have satisfied him that "a large part of the substance of the normal human feces is made up of these low forms in numbers which must be estimated by hundreds of millions in the feces of each day," bacteria, micrococci, and torulæ being found "floating in countless multitudes along with fragments of partly-digested muscular fibres and other débris from the food;" but while the torulæ are increased, the other micro-organisms, bacteria, etc., do not appear to be more numerous in the stools of dysentery than in healthy feces.

The doctrine that dysentery depends upon parasites is very old in medicine, and included animal as well as vegetable growths. Langius (1659) declared that swarms of worms could be found in dysenteric stools, and {793} Nyander (1760) went so far as to call dysentery a scabies intestinorum interna; which extravagant conception would have speedily met with merited oblivion had not his preceptor, the great Linnæus, incorporated the Acarus dysenteriæ into his _Systema Naturæ_. Sydenham about this time (1670) expressed a much clearer conviction of the cause of the disease when he spoke of "particles mixed with the atmosphere which war against health and which determine epidemic constitutions."

Baly (1849) first proclaimed the idea of a vegetable fungus, similar to that described by Brittan and Swayne in cholera, as the parasite of the disease; and Salisbury (1865) described algoid cells and species of confervæ as occurring abundantly in all well-marked cases. Klebs (1867) found spore-heaps and rod-like bacteria in the stools of dysentery as in cholera, but maintained that those of dysentery were larger and thinner than those of cholera. Hallier (1869) maintained that although there was no morphological difference in the micro-organisms of the stools of dysentery, typhoid fever, and cholera, he was able by culture-experiments to develop the micrococcus of dysentery into a special fungus, which he called Leïosporium dysentericum. Busch (1868) demonstrated nests and colonies of micrococci, as well as mycelium, in the villi and among the glands of the mucous and submucous tissues in the cases of dysentery from Mexico which he examined, but Heubner (1870) was able to disclose them in equal numbers in preserved preparations or fresh contents of healthy intestines. Dyer[4] (1870) believes that the parasites constituting the mildew or sweat which forms a viscous pellicle upon fruit is the agent which directly produces and propagates the disease. Mere immaturity of fruit gives rise only to diarrhoea. This parasite occurs in some years more than others, which accounts for the irregularity of occurrence of the disease. He avers that it is only necessary to clean fruit, more especially plums, to prevent the disease. This suggestion merits place only as a curiosity in the history of the mycology of dysentery.

[Footnote 4: _Journal f. Kinderkrankheiten_, No. 317.]

More important are the results of the experiments of Rajewski (1875), who found the lymph-spaces filled with bacteria, and who was able to produce a diphtheritic exudation upon the surface and in the substance of the mucous membrane of the colon by the injection of fluids impregnated with bacteria into the bowels or blood of rabbits; but this result was only obtained when the mucous membrane had been previously irritated or brought into a catarrhal state by the introduction of dilute solutions of ammonia. It remains for subsequent investigation to confirm these highly significant conclusions, which, when properly interpreted, may explain the action of the predisposing and exciting causes of the disease. Rajewski's bacteria, it is needless to state, were simply the bacteria of common putrefaction. Lastly, Prior (1883) describes a micrococcus as the special micro-organism of dysentery, and Koch (1883), in prosecuting his studies of cholera in Egypt, remarks incidentally upon a special bacillus which he encountered in the intestinal canal in dysentery, though he is as yet by no means prepared to ascribe to it pathogenetic properties.

The question of contagion hinges upon the specificness of the disease, and cannot be definitely determined until this problem is finally solved. The old writers believed in the contagion of dysentery. Helidæus {794} declared that he "had often seen it communicated by the use of clyster-pipes previously used in the treatment of those suffering with the disease, and not properly cleaned;" and Horstius and Hildanus speak of the communicability of the disease from the latrines contaminated by dysenteric excreta. Van Swieten maintained that washerwomen contract it, and that physicians and nurses might be affected. Degner saw the disease spread from street to street in Nimeguen, while every one who came in contact with the disease became affected. Pringle observed it spread from tent to tent in the same way; and Tissot went so far as to declare, "Sil ya une maladie veritablement contagieuse c'est celle ci." Ziemssen believed that the disease is only contagious when the element of crowd-poisoning is superadded; and Heubner states that trustworthy army surgeons in the Franco-Prussian War frequently saw infection occur when many severe cases were heaped together in a small space. Under these circumstances thorough disinfection of the privies checked the spread of the disease. But it was the universal testimony of these surgeons, as also of our own surgeons of the Civil War, that the disease was never transported to the civil population by any of the tens of thousands of cases on their return to their homes.

By most modern writers dysentery is given a place, in respect to contagion, between the exanthematous maladies, typhus and scarlatina, which are without doubt contagious, and the purely miasmatic diseases, malarial and yellow fevers, which are without doubt not contagious. Dysentery is ranked with typhoid fever, which is contagious, not by contact with the body, but with the discharges. It is not a question in dysentery of epithelial drift or pulmonary exhalations, but of ingestion or reception of the dejecta of the disease. By this observation it is intended to convey the impression that dysentery, like typhoid fever, is mostly spread in this way, but the reverse may be true; it may be spread, like yellow fever and malaria, by poisons in the air. But dysentery, as has been repeatedly remarked, is only a clinical expression of a disease which may be caused in many ways; and among these causes, least potent perhaps, but present nevertheless, is contagion. For, not to mention the epidemics which were undoubtedly spread in this way, as among the Allies at Valmy in 1792, among the French in Poland in 1807, and in the hospital at Metz in 1870, dysentery has been directly communicated by the use of clysters, bed-pans, and privies in a most unmistakable way.

According to Eichhorst, the poison of dysentery is endowed with extraordinary persistence of duration or tenacity of life in the stools; for "observations are recorded where dysenteric stools have been emptied into privies, and individuals employed to clean them out after the lapse of ten years have been infected with the disease. These observations go to prove, of this as of other similar affections (typhoid fever), that the virus or microbe of the disease finds its most favorable nidus in vaults, cesspools, sewers, etc. When the poison is exposed to the air it is much more speedily destroyed, but is in the mean time of course a possible conveyer of the disease." Fayrer quotes from an anonymous writer, "whose views are as remarkable for their force as for their originality," the rather extravagant assertion that "if human excrement be not exposed to the air there can be no dysentery."

{795} Knoewenagel has recently[5] opened up a new series of reflections in his suggestion of a possible direct infection of the large intestine per rectum, where the disease usually begins and is mostly best expressed. He calls attention to the fact that people who suffer with constipation indulge in longer sessions at stools and induce in straining efforts a degree of relaxation of the rectal mucosa. The mucous membrane at its orifice may become at the same time abraded by hardened fecal masses, to leave open surfaces or crevices upon which germs may lodge. Moreover, aspiration follows the efforts at expulsion, and the air with its particles is drawn directly into the rectum, thus affording all the conditions for immediate or direct infection.

[Footnote 5: _Schmidt's Jahrbucher_, Sept. 25, 1882.]

At any rate, it must be admitted that the evidence in favor of contagion is in some cases too strong to be ignored. A single instance may suffice for illustration: Flügel reports that the towns of Nordhaben and Reichenbach, containing together twenty-two hundred inhabitants, were visited by dysentery in 1873, when nearly four hundred people were attacked. The visit of a relative carried the disease from Reichenbach to the daughter of an innkeeper at Tauchnitz, and from this house the disease spread over the whole place, so that in a short time more than one hundred people fell ill. Four to six, sometimes as many as eleven, members of one family were successively or simultaneously affected. The use of the same bed was the surest means of contagion.

The duration of the poison was proven in an exquisite case, which is, however, not entirely free from objection: Two children of an officer were severely affected in September and October, 1872. In January, 1873, the house was vacated and occupied by a successor in office, whereupon in April, six months after dysentery had disappeared from the place, the wife and child of the second officer were affected with the disease.

To sum up the etiology of dysentery in a few words, it may be said that few chapters in medicine are so thoroughly unsatisfactory, as the prospect of reconciling the accumulated discordant facts is very discouraging. Because of the singular uniformity in the symptoms and lesions the temptation is strong to look for a common cause, and to ascribe all cases to this cause, explaining differences by degree rather than by kind. Such a view would find solid support in the assumption of a specific germ, and would ally dysentery with typhoid fever, a disease which has likewise, in all cases, uniform symptoms and lesions, and which prevails in both sporadic and epidemic form. The advocates of this view would fix the poison of the disease in the air and alimentary canal (but not in the blood), and explain the existence of individual cases, as well as the prevalence of epidemics, by meteorological conditions as affecting the growth or dissemination of specific germs. Nor would the adoption of this view exclude the possibility of producing the catarrhal (sporadic) cases by many kinds of noxious germs, including those of common putrefaction. Hot air and wet air are notorious bearers and breeders of germs, and the law of gravity keeps them near the surface of the earth--conditions which coincide with the prevalence of the disease in the tropics and among individuals (soldiers) who sleep upon the ground. If the contagion of the disease be admitted, the existence of a {796} contagium animatum is implied at once, for no chemical poison has the power of propagation.

But the germ of dysentery has not been found as yet, and until it has been found, cultivated in suitable soil, and inoculated to produce the disease, the evidence of its existence remains merely presumptive.

So that at the present time dysentery must be regarded as a malady which stands in closer relation to, or finds a better analogue in, cholera than typhoid fever; for cholera is a disease which has the same geography, has likewise nearly uniform symptoms and lesions, so far as it leaves any, and certainly has two distinct forms of origin--one clearly specific, cholera Asiatica, and the other catarrhal, cholera morbus.

PATHOLOGY.--Dysentery is a local malady, but, like every local malady if sufficiently severe, it may show constitutional effects. It is usually gradually ushered in from a lighter form of gastro-intestinal catarrh. After a stage of incubation which lasts from a few hours to a few days symptoms of dyspepsia and diarrhoea set in or increase, attended with anorexia, heartburn, nausea, eructation or borborygmi, pain in the abdomen, and copious fluid discharges. Hereupon ensue the pains and the discharges characteristic of the disease. Violent griping and colicky pains (tormina) traverse the abdomen, with sickening sensations of depression. The desire of evacuation of the bowels (tenesmus) becomes intense and more or less constant, and the discharge itself is attended with little or no relief. At the same time the region of the rectum, intensely inflamed, is the seat of intolerable burning pain, which becomes excruciating with the introduction of a speculum or the finger.

The discharges may be copious, dark-brown, thin, and highly offensive (bilious dysentery), may contain occasional hard round fecal casts of intestinal sacculi (scybalæ), or may become more and more scant, until with the most violent efforts only the minutest quantity is extruded of mucus, generally streaked or tinged with blood (rose mucus) like the rusty sputum of pneumonia. Later, all effort at emptying the alimentary canal may be futile (dysenteria sicca), or the mucus may be pure or commingled with pus to remain perfectly colorless (dysenteria alba), or with blood in larger quantity (dysenteria rubra). In other cases, or at other periods in the same case, the discharges consist of fleshy masses composed of inspissated mucus or pus, blood, and tissue-débris (lotura carnea). Sometimes, though rarely, the discharges consist of pure blood, but oftener of a copious turbid fluid, which on standing separates into a clear upper layer of serum and a sediment of disintegrated lotura carnea. Or, lastly, the sediment is composed of small round vitreous masses, evidently swollen by maceration to look like sago-grains, which have been erroneously supposed to represent the liberated contents of the intestinal follicles.

The general condition of the patient suffers correspondingly. There may be fever or there may be none throughout the whole course of the disease, but the pain and discharges quickly exhaust the strength of the patient, and in severe or long-continued cases lead to emaciation and profound prostration.

The skin is hot and dry; the tongue is heavily coated; the face wears an anxious expression. The abdomen is tumid with gases, or in more advanced cases sunken, discolored, and tender, especially in the course {797} of the colon, whose thickened walls may often be felt beneath the emaciated surface. The anus is spasmodically constricted, or in the worst cases paralyzed, patulous, and livid or blue. Prolapse of the rectum is common in children, and excoriation of the perineum by the acrid discharges is not infrequent.

Finally, a typhoid state may set in or a pyæmia occur, when the discharges may become involuntary or unconscious, and brain symptoms--insomnia, stupor, delirium, and coma--supervene; or the patient may linger long enough to perish by simple exhaustion or marasmus.

Under favorable hygiene the great majority of cases of catarrhal dysentery recover without special treatment in the course of from three to ten days, but specific dysentery has no definite duration and but little tendency to spontaneous cure. The worst cases are often quickly controlled by appropriate interference, and the most surprising results may be sometimes obtained in cases of even years' duration. On the other hand, a certain percentage of cases is characterized by a defiance to every kind of treatment, including the last resort, a change of climate.

An acute case of catarrhal dysentery generally subsides without lesions, and the natural duration of the attack may be much abbreviated by proper treatment. Specific or epidemic dysentery lasts from two to four weeks, or, becoming chronic, continues for years or for life, with exacerbations and remissions.

Various complications are liable to occur in the course of the disease. Three deserve especial mention--viz. affection of the joints (rheumatism), paralysis, and abscess of the liver. Perforation and peritonitis, always possibilities, and deformities of the colon, thickenings, and constrictions, are not infrequently left.

MORBID ANATOMY.--The lesions of dysentery are the ordinary signs of inflammation of a mucous membrane and its subjacent structures. They do not differ in any essential way from those of any mucous surface in a state of inflammation, the minor variations being due to differences in the anatomy and physiology of the part affected. Thus, a description of the pathological process in inflammation of the pharynx, bronchi, or uterus would answer upon the post-mortem table for the same process in the large intestine, and the finer microscopic lesions could be differentiated in any case only by the histology of the part affected.

A slight lesion of any mucous membrane constitutes what is known as a catarrhal process; a more grave affection, a diphtheritic process; a more chronic inflammation, a hypertrophic or hyperplastic process. Hence an easy distinction between sporadic and epidemic cases might be based upon the character of the lesion found. But, as has been stated already, it is impossible to draw a line between catarrhal and specific cases, the same lesions being found in either form. The difference, so far as the morbid anatomy is concerned, is wholly in degree or stage, and not at all in kind, the specific (epidemic) form presenting the graver lesion as a rule. So most cases of sporadic dysentery show only catarrhal lesions, while most cases of epidemic dysentery show diphtheritic lesions.

Catarrhal dysentery shows as its first obvious alteration a hyperæmia of the mucous surface. It is limited exclusively to the large intestine in the vast majority of cases, and only in rare exceptions affects the small intestine, though cases have been mentioned as curiosities in which the {798} process has reached the stomach in its upmost prolongation. The hyperæmia is most marked, as a rule, in the lowest parts of the large intestine, the rectum and descending colon, but there is, as Virchow has pointed out, a peculiar predisposition to affection at the seat of all the flexures, the iliac, hepatic, splenic, sigmoid, where the additional element of fecal arrest or impaction is superadded to the cause of the disease.

The catarrhal process occurs first in detached spots or streaks upon the projecting folds or duplicatures of the mucous membrane; which spots coalesce to form extensive surfaces. Examined by transmitted light, these surfaces show a distinct arborescence of the vessels. Or the disease may commence in the follicles in distinct areas of the large intestine, and may remain confined to these structures to constitute the variety known as follicular dysentery.

The hyperæmia of inflammation is attended with dilatation and paresis of the vessel-walls and retardation of the circulation. The whole process may be arrested at this stage, so that there escapes from the vessels, at most, only serum to develop the oedema which, with the defective nutrition from arrest of the circulation, gives rise to the softening of the epithelial cells. These cells may be thus lifted from their bed to constitute the process of desquamation, the fundamental anatomical characteristic of acute dysentery, by which process the submucous connective tissue is laid bare and the so-called catarrhal ulcer results. Or the epithelium, but partially detached, may remain upon the surface, "either raised in the shape of small vesicles which contain clear serum, or it forms a grayish-white layer resembling the mealy scurf of the epidermis--an appearance which probably induced Linnæus to term dysentery scabies intestinorum interna" (Rokitansky).

Kelsch maintains that the inflammatory process in dysentery commences in the delicate connective tissue between the follicles, the network of small spindle-shaped cells with multiple nuclei becoming speedily penetrated by a number of very small, newly-formed vessels. Where the epithelium is desquamated the surface is covered with granulations as after a wound. The disposition of the follicles is soon deranged, for, instead of standing in rows like gun-barrels, they are pushed asunder and uplifted, so as to remain at different heights. Their interior becomes blocked with mucus or their orifices occluded, so that retention-cysts are formed to give rise to the appearance of the bead necklace. Soon the walls of neighboring follicles coalesce, dissolve away, and communication is established between them. The interior of these communicating tubes or canals is filled with vitreous mucus; the walls are stripped of their lining cells, but their "blind extremities contain still adherent colossal epithelial cells." Moreover, the follicles break into each other under the proliferative budding process, so that the end of a distorted tube may be found in the interior of another. Where follicles are destroyed the mucous membrane above them or in their vicinity collapses--a condition observed and described by Colin as effrondement. The mucosa in these regions may appear perfectly uninjured, but by "blowing upon it with a tube it is lifted up like an ampulla to show an opening in its centre," though more frequently the mucous membrane collapses or sinks in at the region of destruction. The inner surface of the mucosa is rendered additionally uneven by the elevations or protuberances caused by the {799} proliferations in the submucous connective tissue. The older writers (Pringle, Hewson) regarded these projections as tumors of the mucosa, and Rokitansky, who describes their true nature, speaks of them as warty, tubercular (nodular) swellings or fungoid excrescences--constituting a condition, he says, which Gély has termed hypertrophie mamelonné. The alternate elevations and depressions thus produced have been likened to the representations of bird's-eye views of mountain-chains.

As a rule, occasional red blood-corpuscles are also permitted to escape through the vessel walls in the process of diapedesis to give to the surface mucus its characteristic tinge, and punctate submucous hemorrhage is very frequently seen.

The pressure of the swollen, softened mucosa upon the sensitive nerves, and the irritation of the acrid intestinal contents, are often invoked to account for the constant desire of defecation (tenesmus) which constitutes such an essential symptom of the disease; but both the tenesmus and the colicky pains (tormina) precede the anatomical changes, and are much more rationally explained by the direct action upon the nerves of the cause of the disease, or by the derangement of innervation effected through changes in the circulation.

An acute case of catarrhal dysentery may exhibit no further lesions, and in the lightest cases even these may have entirely disappeared post-mortem, so that no change at all may be observed at the autopsy.

In a more severe or protracted case the other alterations which constitute the more complete cycle of the inflammatory process follow the stage of hyperæmia. The arrest of circulation becomes more or less complete, and the white corpuscles emigrate from the vessels to form the pus-cells. Fibrin, or the elements which compose it, also escapes to infiltrate the mucous membrane and remain upon its surface. The pseudo-membranous or diphtheritic process is now developed, and may vary in intensity from a mere frosting of the surface to dense infiltration of the entire thickness. The false membrane, as well as the mucous membrane, next suffers necrosis to form more or less extensive sloughs. These sloughs are grayish-white when fresh, dark-brown when stained by the intestinal contents, or greenish or black when undergoing gangrene. They may cover patches of the mucosa or the whole mucosa from the ileo-cæcal valve to the rectum. They soon become soft and pultaceous, hang in flaps or festoons in the interior of the intestinal tube, or, detached, are voided in fragments or shreds. One such fragment nine inches long is recorded in Woodward's exhaustive description of the pathology of this disease. Examined under the microscope, they are seen to consist of coagulated fibrin, red and white blood-corpuscles, epithelial cells and débris, necrotic pieces of mucosa, and myriads of micrococci and other micro-organisms.

The fall of the sloughs leaves the dysenteric ulcer. Its edges are irregular and ragged, its base uneven like a crater, and its surface is more or less covered with pultaceous débris. The submucous connective tissue may form its base, or, this structure having been also destroyed, the muscularis may be exposed, or in more extensive necrobiosis the peritoneum itself may be laid bare. Occasionally this last barrier is broken down, and perforation occurs. Or an acute peritonitis may be developed, in dysentery as in typhoid fever, by simple extension of the inflammatory {800} process without perforation. Perforation is very rare in cases of follicular ulceration, and is by no means frequent in the diphtheritic process, but it is the most frequent cause of peritonitis in chronic dysentery. It may occur in any part of the colon, but does occur most frequently in the cæcum. The resulting peritonitis is fatal as a rule, but the danger is obviated sometimes, as in typhoid fever, by agglutination of the gut to a contiguous structure or viscus. Perforation usually occurs late in the disease, but it may occur very early. Thus Nägele reports from the Franco-Prussian War a case in which perforation took place on the fourth day, the diagnosis having been confirmed by an autopsy. In rare cases a perityphlitis may ensue, with its natural consequences, or periproctitis may be developed with perineal abscess, or, finally, fistulæ may form to burrow about and discharge themselves anywhere in or upon the surface of the abdomen, the lumbar region, or the thigh. Bamberger describes cases of perityphlitis attending dysentery, in some of which resorption occurred, while in others pus was discharged upon the surface of the abdomen; and the writer of this article once saw, in consultation with T. A. Reamy, a case of fistula which extended from the descending colon to the vagina. Through the opening made to discharge the pus from a fluctuating abscess pointing in the vaginal vault an india-rubber tube could be passed for six to eight inches. The patient finally died from marasmus.

Chronic dysentery is distinguished by the alterations which occur in inflammation developing more gradually and extending over a longer period of time. Under the irritative changes resulting from an altered circulation the connective tissue undergoes marked hyperplasia, so that the wall of the intestine becomes at times enormously thickened, and its calibre is often correspondingly diminished. Cornil observes that acute or subacute dysentery is characterized by infiltration of the submucous connective tissue, followed by destruction, while in chronic dysentery the predominant lesion is essentially a proliferation and thickening of the connective tissue of the large intestine. The muscular tissue also undergoes hypertrophy, and the peritoneum becomes thickened and opaque. Sometimes the peritoneum is covered with patches of false membrane, or agglutination occurs with other portions of the intestine to give rise to contortions or occlusions.

Ulceration shows itself in chronic dysentery in every grade and stage of the process, from the first denudations to old cicatrizations. In bad cases the whole course of the colon from the ileo-cæcal valve to the rectum may constitute one vast tract of suppuration. Blood-vessels may be opened by the necrotic process, and copious, even fatal, hemorrhage may ensue. When pure blood is discharged, the hemorrhage usually occurs in this way per rhexem, but the quantities of blood evacuated with other elements usually escape per diapedesem.

The cicatrization which results puckers the edges of the ulcers, and may in cases of extensive or circular ulceration lead to more or less stenosis of the intestinal tube. According to Rindfleisch, the scars of dysenteric ulcers are very prone to contract, so that "the liability of a subsequent stricture is directly proportionate to the extent of the previous ulceration." The danger in these cases may be immediate from entire, or more remote from partial, occlusion. Thus, Bamberger records a case of {801} typhlitis due to impaction of feces above a stenosis gradually developed from a dysenteric ulcer.

Although dysentery is a disease of the large intestine, its lesions are not exclusively limited to this structure. It is always a purely local disease at first, and, strictly speaking, continues so throughout its course, yet it produces in severe or chronic cases widespread and general effects. Rapid emaciation sets in, and anæmia is soon pronounced in all the internal organs. The mesenteric glands show signs of irritation or of absorption of specific products in hyperæmic pigmentation and hyperplasia. The kidneys in acute cases exhibit venous stasis, and in chronic cases may undergo parenchymatous change. The joints are peculiarly liable to suffer in certain cases, and the nervous system may exhibit lesions--points to be described in the symptomatology of the disease. Should pyæmia occur, it superimposes its own particular lesions in the serous membranes and internal organs. All of these affections are to be regarded, however, rather as complications than essential effects.

But the liver is found affected so frequently in dysentery as to constitute more than a mere coincidence. Schneider has recently (1873) reported of the results of his observations on 1400 cases of tropical dysentery that in the 395 post-mortem examinations the liver was found normal in but 10 cases. The abnormalities were as follows: hyperæmia of various grades, 160; fatty degeneration, 62; abscess, 57; nutmeg liver, 47; perihepatitis, 25; granular atrophy, 19; syphilitic atrophy, 8; cicatrices, 6; excavation with helminth, 1. Bérenger-Féraud (1883) reports of 411 fatal cases of dysentery observed at Senegal that the liver appeared sound to the naked eye 98 times (23 per cent.) and diseased "undeniably" 313 times (77 per cent.). Of the 313 cases of hepatic affection there were found--hypertrophy, softening, or hyperæmia, 123 times (39 per cent.); abscess, 143 times (46 per cent.); simple discoloration, 29 times (9 per cent.); atrophy or cirrhosis, 18 times (6 per cent.). Annesley found abscess of the liver 21 times in 29 cases of dysentery; Hospel, 13 times in 25 cases; and Budd found ulceration of the large intestine 10 times in 17 cases of hepatic abscess. Gluck had the opportunity of making 28 post-mortem examinations in 151 cases of dysentery in Bucharest, finding abscess of the liver 16 times. All these authors adopt the explanation first offered by Budd of direct transfer of diseased products through the mesenteric and portal veins.

But more extensive observation has developed the fact that the frequency of abscess of the liver in connection with dysentery is a peculiarity of tropical climates. In the temperate and colder regions of the North this complication is not by any means so frequent. Frerichs declares that of 16 observations collected by Louis and Andral, "ulcers were present in only 3, and in 2 of these cases the ulcers were tubercular; of his own 8 cases, there was intestinal affection in none." Gluck believes that the liver is more prone to show suppuration when already predisposed to it by a preceding amyloid or cirrhotic change of malarial origin. Eichhorst calls attention to the well-known fact that abscess of the liver is especially a disease of the tropics independently of dysentery, and the frequency of its occurrence here may be a mere coincidence. But it must be remembered that opportunity for post-mortem examination, upon the {802} results of which these statistics are based, does not occur in the great majority of cases of dysentery, and abscess of the liver is very often overlooked. Thus, Schneider cites cases where persons with abscess of the liver of the size of the head were considered simulants up to twenty-four hours before death. Since the diagnosis of hepatic abscess has been made so easy by aspiration, cases begin to multiply; and it is doubtless the experience of most practitioners, in the temperate zone at least, that the decided majority of cases of hepatic abscess acknowledge an existing or previous attack of dysentery. Certainly, few authors would now venture to subscribe to the view of Annesley, that the abscess of the liver was the primary malady and was the cause of the dysentery.

SYMPTOMATOLOGY.--Dysentery, as stated, begins, as a rule, with the general signs of a gastro-intestinal catarrh. So frequent is this mode of inception, and so few are the exceptions, that it is impossible to resist the conclusion that the disease is caused by the introduction of a noxious element into the alimentary canal. The irritation thus induced begins at the stomach, and is rapidly propagated throughout the whole tract of the intestine. In the course of a few days the cause of the disease becomes strictly localized to the large intestine, whose greater capacity and more sluggish movement fit it for the easier reception and longer retention of noxious matter.

But specific dysentery and the more intense forms of catarrhal dysentery occasionally exhibit distinctive symptoms from the start, and in rarer cases the disease is suddenly announced with such tempestuous signs as to excite the suspicion of poisoning. Thus, a case (one of five lighter cases) is reported from the Rudolfstiftung in Vienna (1878) where the disease closely simulated Asiatic cholera, and where it rapidly ran a fatal course, in spite of laudanum, soda-water, ice pills, mustard plasters, injections of amyl nitrite, camphor, and ether, and faradization of the phrenic nerve to stimulate the failing respiration. Finger reports similar cases from the hospital at Prague.

Ordinarily, the peculiar pains of dysentery first proclaim the character of the disease. The severe grinding, twisting pains, tormina, are more or less localized in the course of the colon, and hence surround or traverse the entire abdomen, the pains at the epigastrium being due to spasmodic contractions of the transverse colon. The patient in vain adopts various postures in relief or sits with his hands firmly compressing the abdominal walls. The tormina are more or less intermittent or remittent, and are usually experienced in greatest severity toward evening. During their acme the face wears the aspect of the intense suffering, which is expressed in outcries and groans. At the same time there is upon pressure over the whole abdomen more or less tenderness, which soon comes to be especially localized at the cæcum or sigmoid flexure.

The tenesmus (cupiditas egerendi) is a more distressing, and certainly more distinctive, sign of dysentery. It is the feeling of heavy weight or oppression, of the presence of a foreign body in the rectum, which demands instant relief. At the same time intense heat is felt in the rectum, which the patient likens sometimes to the passage of a red-hot iron. The desire of evacuation becomes as frequent as urgent. In well-marked cases the patient sits at stool half an hour or an hour at a time, straining until faint {803} and exhausted, leaving the commode with reluctance, only immediately or very soon to use it again.

Great depression is felt at the stomach at the same time, with nausea, occasionally with vomiting; and strangury, with the discharge of only a few drops of scalding urine or blood from the bladder, adds additional suffering to the disease. Retraction of the testicle and prolapsus ani, especially in children, are prone to occur in severe cases.

But neither the pain nor the prostration is so characteristic of dysentery as the stools, which, though of very varied nature, are nevertheless distinctive. After the discharge of the intestinal contents the first evacuations consist of mucus in the form of glairy, stringy matter, like the white of an egg, expressed as the result of the violent efforts at straining. The mucus may be pure or tinged with blood, but it is usually very scant in quantity, and stands in this regard in marked contrast with the violence of the efforts to secure its extrusion. It is the frequency of its discharge which constitutes an especial distress. Twenty to forty, even two hundred, times in the twenty-four hours the patient must go to stool. In the worst cases the patient sits at stool or lies upon the bed-pan the most of the day.

The mucus is sooner or later mingled with pus or stained with blood. The presence of pus by no means necessarily implies the existence of ulceration, as the apparently pure mucus always shows occasional white blood-corpuscles under the microscope, and even extensive suppurations occur without apparent solutions of continuity.

The presence of blood is equally characteristic of dysenteric stools. Usually it is intimately commingled with the mucus or pus or forms the chief element of the copious so-called bilious discharge. The evacuation of pure blood indicates erosion of vessels low in the colon, often in the rectum itself, though enormous quantities of blood are sometimes voided from unbroken surfaces. Thus Lécard reports the case of a soldier who "while sitting restless at stool lost one and a half quarts of blood." The patient died on the fifth day of the disease, and at the autopsy there was found "apoplectiform congestion from the ileo-cæcal valve to the anus, but no ulcers anywhere, nor any broken vessels."

Besides the mucus, pus, and blood, the dysenteric stools contain the sloughs which have been torn off by violent peristalsis in cases of the diphtheritic form. Usually they are separated in shreds and fragments, but occasionally large sheets, even casts of a section of the colon, are voided en masse. These were the cases considered by the older authors to be detachments of the mucous membrane itself. As already observed, these fragments consist for the most part of inspissated mucus, pus, blood, and tissue-débris; but there is no doubt that in some cases partially necrosed mucosa also enters into their construction. One enormous tubular cast fourteen inches long, preserved in our Army Medical Museum, was found to be "composed of pseudo-membranous lymph in which no traces of the structure of the mucous membrane could be detected" (Woodward).

There still remains to be mentioned the boiled-sago or frogs'-spawn matter whose origin has given rise to such a curious mistake. Not infrequently these vitreous-looking bodies compose the bulk of the sediment in the stools of dysentery, and even some of our modern authors, {804} unacquainted with the more searching investigations of Virchow, have regarded them as expressed contents of intestinal follicles. Virchow found that under the application of iodine they always assumed a blue color, whereupon he ironically remarks that the sago-like mucus is really mucus-like sago. They are simply granules of starch ingested as food, to remain partially or wholly undigested.

The scybalæ, the composite matter known as the lotura carnea, and the micro-organisms found in the stools have already received mention elsewhere.

Although the stools of dysentery are scant, as a rule, they are so frequent as to discharge during the entire twenty-four hours a very large quantity of albuminous matter. Oesterlen has made the curious calculation to show that the mean daily loss of albuminates in dysentery of moderate intensity is from 50 to 60 grammes during the first fourteen days, and on an average about 20 grammes during the next eight days. The total loss experienced in an attack of three weeks' duration thus amounts to about 1000 grammes--in rough figures, two pounds avoirdupois. The rapidity with which emaciation, hydrops, and marasmus occur in severe cases is thus easily accounted for. Nägele speaks of cases where patients were reduced to skeletons in eight to fourteen days, so that the convalescence extended over six weeks to eight months.

The alteration in the character of the secretion in dysentery is not confined to the mucous membrane of the large intestine. On the contrary, all the digestive juices are changed, in some cases entirely checked. In the graver cases the saliva takes on an acid reaction and loses its glycogenic properties; the gastric juice in the same cases becomes alkaline and loses its peptonizing properties; while the secretion of the bile is wholly arrested. Uffelmann, who had the rare opportunity of studying the secretion of bile in a case of biliary fistula, relates that during an attack of dysentery the bile ceased entirely to flow, and only began to show itself again, at first greenish, then greenish-brown, finally brown, during the process of resolution on the ninth day of the disease. The anorexia, nausea, and vomiting which so often mark the access or attend the course of dysentery find thus easy explanation.

Should the disease continue, the general strength of the patient becomes so profoundly reduced as to resemble the status typhosus. The tongue, which has been hitherto thickly coated, now becomes black, shows fissures, and bleeds, while the gums are covered with sordes. The pulse becomes feeble, thready, or barely perceptible. The skin is dry and harsh or scaly. The abdomen is tumid or collapsed, the anus paralyzed, and the discharges continuously ooze out to excoriate the perineum. While the brain is usually clear throughout the disease, insomnia, stupor, or coma develop in the gravest cases from absorption of disease-products (Senator), or death suddenly ensues from heart-clot or from thrombus of the venous sinuses of the dura mater (Busey).

Pyæmia announces itself with a series of chills, followed by irregular temperature, by the speedy occurrence of multiple abscesses in distant organs, venous thromboses, affections of the serous membranes, pleuritis, pericarditis, and embolic pneumonia. Gangrene of the intestine, which may occur as early as the third day of the disease (Nägele), is evidenced by the signs of general collapse.

{805} COMPLICATIONS AND SEQUELÆ.--The lighter cases of dysentery, as well as most of the grave cases, run their entire course without complication, and often without sequelæ. But a certain percentage of cases is attended with complications on the part of the joints (rheumatism), of the nervous system (paralysis), and on the part of the liver and the kidneys.

Arthritis, when it occurs, shows itself, as a rule, in the second week of the disease (Eichhorst), or after the disease has run its course, during the period of convalescence (Huelte). That it is not a mere coincidence is evidenced by the fact that it is present in a large number of cases in certain epidemics, while it is not present independently of dysentery. Thus, Braun of Stannenheim saw in the two epidemics of 1833-34 more than forty cases of rheumatism, and Huelte reports ten cases observed by himself in the epidemic at Montargis in 1854. Certain epidemics are distinguished by the rarity of this complication, while most are marked by its absence altogether. In the epidemic at Rahden (1872), 400 cases among 3800 inhabitants, Rapmund saw inflammation of the joints set in only six times; and the entire absence or extreme rarity of it in later epidemics have led most physicians to deny any connection between the diseases, or to regard the joint affection as incident to a complicating scorbutus or neuralgia. All authors who admit it describe the knee-joint as being the most frequent seat of the affection, but acknowledge that it is mostly polyarticular; while there is much difference of opinion whether it ever presents the general signs of true rheumatism--pyrexia, diaphoresis, or its complications on the part of the heart. Huelte maintains that it does not, and that it is allied to gonorrhoeal rheumatism in this respect, while Eichhorst states that it may not only show all these signs, but may be followed in exceptional cases by suppuration and ankylosis. It usually lasts four to six weeks, but neither its occurrence nor its severity stands in any relation to the intensity of the attack of dysentery. It is probably to be regarded as a manifestation of a light pyæmia or septicæmia, as it is a frequent manifestation of this condition in or after scarlatina, puerperal fever, and the septic fevers of surgery.

Paralysis has been observed to occur after dysentery ever since the days of Galen, and, disregarding the observations of ancient and of the older periods of modern times, we find occasional records of cases in our own days. Leyden,[6] in reporting a case of paresis and rheumatic pains following an attack of dysentery, says that although post-dysenteric paralysis is now rarely mentioned, it was frequent in the older reports, and claims it as an admitted fact that it occurs not at all infrequently now. Joseph Frank quotes some observations of this kind, and refers especially to the dissertation of Fabricius.[7] These paralyses, Fabricius observes, have been seen after the premature suppression of malignant epidemics of dysentery by opiates and astringents. Observations were afterward recorded by Graves in which paralysis occurred after colics and inflammation of the intestines; and English veterinary surgeons mention the fact that paralytic weakness of the posterior extremities of horses and cattle follow attacks of intestinal inflammation. The paralysis, when it occurs, is usually confined to the lower extremities, but may extend to {806} and involve the upper extremities, by preference in the form of paralysis transversa (opposite arm and leg). Brown-Séquard attributes it to reflex contraction of the blood-vessels; Jaccoud, to exhaustion of the nerve-centres; and Röser, to the contact of the inflamed transverse colon with the solar plexus. Remak first suggested the idea of an ascending neuritis--a view which would seem to be corroborated by the paralysis observed after the experiments, by Lewisson, of crushing the uterus, kidneys, bladder, or loop of intestine, and which finds additional support, as Leyden remarks, in the length of time which lapses before it appears. Landouzy[8] says that Finger found diffuse myelitis in a patient affected with paralysis supervening upon cancer of the intestine, and that Delioux and Savignac saw spots of softening in the cervical and lumbar region of the cord in the case of a man affected with post-dysenteric paralysis. Weir Mitchell suggests the possibility of other factors--long marches, malaria, bad diet, and injuries to the spine--in the genesis of the cases, mostly paraplegias, observed by him; and Woodward calls attention to lead-poisoning (as by treatment) in explanation of a certain number of cases.

[Footnote 6: "On Reflex Paralysis," _Volkmann's Sammlungen_.]

[Footnote 7: _Paralysis seu hemiplegia transversa resolutionem brachii unius et pedis alterius exhibet_, Helmstedt, 1750.]

[Footnote 8: _Des Paralysies dans les Maladies aigues_.]

Abscess of the liver gives rise to few distinctive symptoms, and is mostly recognized or suspected, in the absence of positive signs, by the persistence or obstinacy of the dysentery. The ease and impunity with which aspiration may be performed in its recognition justifies the use of it in every doubtful case.

Regarding complications on the part of the kidneys, Zimmerman recognizes four classes of cases: (1) mild cases, showing no albumen and no casts; (2) severe, long-continued cases, with putrid stools, status nervosus, and collapse, showing albumen; (3) cases commencing with nervous symptoms, paralysis, scanty urine, showing kidneys filled with exudation-cells and detritus; and (4) cases of speedy renal complication and death. To these may be added the cases of protracted chronic dysentery with long-continued suppuration, entailing the possibility, of really rare actual occurrence, of amyloid degeneration and chronic parenchymatous change (Bartels).

Dysentery may be further complicated by parotitis; by venous thrombosis (phlegmasia dolens); by diphtheritic deposits on other mucous surfaces, which Virchow declares to be exceedingly rare; and by hydrops, which is oftener a concomitant of the period of convalescence.

Besides the deformities of the colon, which may ensue as a consequence of ulceration or peritonitis, a long attack of dysentery is apt to leave a hyperæsthetic or non-resistant state of the mucous surface, so that every imprudence in exposure or in diet begets an intestinal catarrh or a relapse of the disease.

DIAGNOSIS.--When dysentery presents itself with its whole train of symptoms the recognition of the disease is very easy. The tormina and tenesmus, the peculiar discharges, the rapid reduction of strength, leave no doubt as to the nature of the affection. The prevalence of an epidemic of the disease will often establish the character of a case even when all the signs are not present or when anomalies occur. Embarrassment in diagnosis only attends the recognition of catarrhal or isolated cases, and in these cases there may be a doubt as between dysentery and {807} diarrhoea--if such a symptom can be called a disease--or typhoid fever, cholera, or some purely local affection of the rectum, cancer, hemorrhoids, etc. In children difficulty of diagnosis may arise as between dysentery and intussusception.

Dysentery is differentiated from that lighter form of intestinal catarrh whose main symptom is diarrhoea by the presence of tenesmus in dysentery, as well as by its mucous, muco-purulent, diphtheritic, and bloody discharges. Dysentery lasts longer than diarrhoea as a rule, and does not yield so readily to treatment.

Typhoid fever shows from the start brain symptoms, which are absent from dysentery; has a typical temperature-curve, whereas there may be no fever in dysentery, or, if any, of irregular remittent type; is often prefaced by epistaxis and attended with bronchitis, both of which are absent in dysentery; and exhibits ochre-colored pea-soup stools, altogether different from those of dysentery.

Cholera morbus distinguishes itself from dysentery by its sudden onset, its profuse vomiting and discharges, its violent cramps, and the speedy collapse.

Cancer of the rectum can be usually felt, and hemorrhoids can be always seen, so that no difficulty should be experienced in the recognition of these cases.

Intussusception occurs mostly in children, and has, in common with dysentery, vomiting, mucous or bloody stools, colic, tenesmus, nervous unrest, and prostration, so that a differential diagnosis may be impossible for a few days. The more strict localization of an intussusception, which may sometimes be felt as a sausage-like mass, most frequently in the right ileum and hypochondrium, the greater frequency and persistency of the vomiting and pain, the presence visibly or palpably of the invaginated gut at the anus or rectum, soon enable the careful examiner to recognize the case.

PROGNOSIS.--The prognosis of dysentery varies between extremes. Some cases are so mild as to merit the remark of Sydenham concerning certain cases of scarlet fever: "Vix nomen morbi merebantur." They terminate of themselves under favorable hygiene without especial treatment. On the other hand, no known disease has a more frightful mortality than dysentery in some of its epidemics, especially in army-life. It was this class of cases which Trousseau had in mind when he called dysentery the most murderous of all diseases. Sixty to eighty may be the appalling percentage of death in these cases.

Under favorable surroundings the average mortality of dysentery amounts to 5-10 per cent., but is much influenced by the age and the general condition of the patient, as well as by the complications which occur in its course. Thus, Sydenham said of it over two hundred years ago, "It is not infrequently fatal to adults, and still more so to old men, but is nevertheless exceedingly harmless to infants, who will bear it for months together without suffering, provided only Nature be left to herself." But dysentery is by no means always harmless to infants, for in some epidemics this period of life has been visited with the greatest severity. Thus, Pfeilstücker reports of Würtemberg (1873-74) that the greatest mortality, 39 per cent., occurred at the age of one to seven years, and the least, 4 per cent., at the age of thirty-one to fifty years; {808} and Oesterlen says of England that dysentery causes 20 per cent. of deaths from all causes in the first year of life.

Nor does the prevalence of a greater number of cases necessarily imply a heavier mortality. For Bianchi reports of Rome that cases of dysentery constituted but 2.28 per cent. of all the admissions into the Ospedale di San Spirito in 1873, while in 1874 the percentage increased to 3.68; yet the mortality of 1873 was 17.02 per cent., while that of 1874 was but 9.09 per cent.

Complications on the part of the nervous system, the status typhosus, pyæmia, and great prostration, necessarily render the prognosis grave, yet even these cases are not necessarily fatal. Thus, Jules Aron reports from the epidemic at Joigny (1876) a case of recovery after complete paralysis of the sphincter ani. The recognition and discharge of an hepatic abscess relieves the patient from the dangers of this complication. Peritonitis alarmingly aggravates the prognosis, and perforation is almost of necessity fatal.

PROPHYLAXIS.--The improved sanitation of modern times has already diminished the frequency and mitigated the severity of epidemics of dysentery; and this fact, which is only an accidental observation as it were, gives the clue to the means of its further prevention.

The selection of proper sites for camping-grounds, barracks, and hospitals, the prevention of overcrowding in tenement-houses, ships, and jails, the regulation of sewage, the care for the food and drink, the observation of the strictest cleanliness by authoritative control,--all these are general measures which suggest themselves in the prophylaxis of this or any disease.

In the management of individual cases the first precaution is to prevent the dissemination of the disease. Whether it be really contagious or not, every case should be managed, as Bamberger suggests, as though it were contagious; and this protection of others secures for the individual patient the most favorable hygiene.

The bedding must be frequently changed; the windows kept open to secure free ventilation, which, in the light of existing knowledge, is the only true disinfectant; and all the furniture of the sick-room, especially including the receptacles for the discharges, must be kept perfectly clean. For this purpose the best purifier is very hot water. The temperature of the sick-chamber, if it be subject to regulation, should never be allowed to sink below or rise above 65-70° F.

The drinking-water should be secured, during an epidemic, from the purest possible source, and if good drinking-water cannot be had, what there is should be thoroughly boiled.

The discharges should properly be mixed with sawdust or some combustible substance and burned, or if this be impracticable should be buried in the soil a few feet below the surface, and not emptied into water-closets or privy-vaults used by others.

Such articles of food should be abjured as have a tendency to produce intestinal catarrh. So unripe fruits, vegetables which readily undergo fermentation--in short, all indigestible substances--should stand under ban. But no prohibition should be put upon ripe fruits or simple nutritious food of any kind.

Lastly, individuals should protect themselves from catching cold. The {809} researches of Pasteur have disclosed the fact that certain germs of disease will grow and multiply in the body of an animal whose temperature is reduced, when they would not increase without it.

TREATMENT.--The first requisite in the treatment of an individual case is perfect rest. Patients with even the lighter forms of catarrhal dysentery should observe the recumbent posture, and cases of more serious illness should be put to bed. Rest in bed, an exclusive diet of milk--which should always have been boiled--and the time of a few days is sufficient treatment for the mildest cases. Where there is objection to milk, meat-soups, with or without farinaceous matters, rice, barley, etc., may take its place.

A case which is somewhat more severe will require perhaps a light saline laxative--a Seidlitz powder, a dose of Rochelle salts or Epsom salts in broken doses--or a tablespoonful of castor oil or five to ten grains of calomel, to effect a cure. For the relief of the pain of the lighter cases nothing is equal to tincture of opium, of which five to ten drops every three or four hours in a tablespoonful of camphor-water acidulated with a few drops of nitric acid will generally suffice; or Dover's powder in broken doses, one to three grains, with five to fifteen grains of bismuth or soda, or both, is a good substitute for a change.

The successful treatment of dysentery in any form depends upon a recognition of the fact that the disease is local as to its seat, and is probably specific as to its cause. The anodynes relieve the effects, but the laxatives remove the cause. Consequently, the most rational treatment of the severer cases is the irrigation of the large intestine and the thorough flushing out of its contents. The use of clysters in the treatment of dysentery dates from the most ancient times, with the object, however, rather of medicating than washing out the bowel. O'Beirne (1834) and Hare (1849) were the authors of the irrigation treatment, which they executed by means of a long tube introduced into and beyond the sigmoid flexure. Since Hegar has recently shown how the whole tract of the large intestine can be thoroughly inundated and flushed with a common funnel and rectal tube, the practice has continually gained ground, until it is now admitted as the most valuable method of treatment. H. C. Wood of Philadelphia, and later Stephen Mackenzie of London, have reported a number of cases in which irrigation of the bowel with large injections medicated with nitrate of silver, drachm j-pint j, was attended with the most surprising results--sometimes but a single injection effecting a cure; and the writer of this article has reported one case almost in articulo mortis where complete cure followed the irrigation of the bowel--on three occasions with three pints of water containing three drachms of common alum. This case was all the more instructive from the fact that a relapse had occurred after very striking but only temporary relief had been obtained with the nitrate of silver, the alum having been substituted simply on the ground of expense.

Salicylic acid has also been extensively employed in this way with the best effects, but carbolic acid has been discarded since the reports of several cases of poisoning have been published. Should it become a question of the necessity of a parasiticide, the bichloride of mercury in extremely dilute solution, 1 to 1000, would be the agent par excellence; but it is probable that the simple flushing of the bowel is the chief {810} curative agent. The use of alum is not attended with the dangers which have ensued from the absorption of carbolic acid, and which might ensue from the bichloride of mercury. The water used in the injections should always be cold. Ice-water injections alone give at times the greatest relief. Wenzel uses injections of ice-water in all recent and acute cases, whether slight or severe--in bad cases every two hours. He seldom finds it necessary to use opium. The object is to introduce as much water as possible without producing too much pain. The large intestine of an adult holds, on an average, six imperial pints, but in the author's experience not more than three or four pints can be safely introduced. The patient should lie upon the back or the left side with the hips elevated and the head low, while the injection is slowly introduced from a funnel, fountain, or a bulb syringe whose nozzle is thoroughly anointed with vaseline. In the absence of a thoroughly competent assistant the operation should be performed by the physician himself, for the proper use of an irrigating enema is a practice which requires both judgment and skill. When pain is experienced, the further influx of the fluid should cease for a few minutes, when it may be resumed again and again until the largest possible quantity is introduced. It is impossible to over-estimate the value of this treatment in cleansing, disinfecting, and constringing the foul and flabby surface of the whole seat of the disease. As was said by Hare, "It changes a huge internal into an external abscess, and enables us to cleanse the bowel of its putrid contents."

Of all the remedies which have been recommended in the relief of dysentery besides the irrigation method, but one, ipecacuanha, deserves the name of a specific. This remedy was first introduced into practice in 1648 by the botanist Piso, who was led to adopt it from the popular praise he had heard of it while travelling in Brazil. He considered it the most exquisite gift of nature, and administered it in infusion according to the Brazilian (subsequently known as the French) method. Légros made three successive voyages to South America to import supplies of the drug to France, but neither he nor the French merchant Grènier, who had brought over more than one hundred and fifty pounds of it, could secure its general use. Thereupon, Grènier acquainted Adrian Helvetius, a Dutch physician practising in Paris at the time, with the wonderful virtues of the Radix dysenterica, who, having experimented with it first upon patients of the lower classes, was later successful in curing the Dauphin of France. The further use of it, by permission of the king, at the Hôtel Dieu, enabled him to secure a monopoly of its sale and secured for him a grant of a thousand pounds. Grènier hereupon put in his claim for a division of the profits, and upon the refusal of Helvetius instituted suit to obtain his rights. Justly indignant at the loss of his suit, he revealed the secret, and ipecacuanha became common property at once. Extravagant ideas were now entertained of its value, but in the extreme reaction which followed every virtue of it was disavowed, so that the drug came to be almost forgotten. From this temporary oblivion the remedy was rescued by an English army surgeon, E. Scott Docker, in 1858, who administered it, in combination with laudanum, in his regiment, on the island of Mauritius, in all cases and stages of the disease with such success that out of fifty cases he lost but one. Although such indiscriminate use and such almost unvaried success has not attended, and from the nature {811} of different cases could not attend, its universal employment, there is no doubt of the inestimable value of the service rendered in the restoration of the remedy in the treatment of dysentery. Yet over twenty years elapsed before its author received from his country, at the urgent solicitation of the Director-General, in recognition of this service, a grant of four hundred pounds.

Remarkable testimony as to its efficiency soon began to appear. Ewart[9] recommends ipecacuanha in every form and type of acute dysentery, as well as in the acute attacks supervening upon chronic cases. Its advantages are simplicity, safety, comparative certainty, promptitude of action, decrease of chronic cases and of complications, especially abscess of the liver, and great reduction of mortality. "It produces all the benefits that have been ascribed to bloodletting, without robbing the system of one drop of blood; all the advantages of mercurial and other purgatives, without their irritating action; all the good results of antimony and other sudorifics, without their uncertainty; all the benefits ascribed to opium, without irritating, if not aggravating or masking, the disease." To the objections urged against it he replies that the nausea is only temporary and evanescent--that vomiting is exceptional and of but short duration; moreover, it permits nourishment and assimilation and produces sleep. If uncontrollable sickness and vomiting occur, they are probably due to abscess of the liver, malaria, some other cachexia, Bright's disease, strumous mesenteric glands, hypertrophy of the spleen, peritonitis, or extensive sloughing.

[Footnote 9: _Indian Annals Med. Science_, April, 1863.]

Cunningham prefaces the treatment by a sinapism to the epigastrium and half a drachm of the tincture of opium. Then from one to one and a half drachms of ipecacuanha are administered in powder. It causes considerable nausea, and vomiting occurs in one to two hours. During the nausea copious perspiration breaks out, the pulse becomes fuller, softer, and less frequent, the tenesmus and abdominal pains cease, and the patient has no more stools for twelve to twenty-four hours. The next evacuation is easy, fluid, but free from blood or mucus. Sometimes the dose of ipecacuanha may require to be repeated.

Malun reports the results of treatment of 436 cases occurring in twenty-one months. There were only 6 deaths, and in only 1 of these could the remedy be fairly said to have failed. Under all other plans of treatment the mortality has varied from 12 to 22.3 per cent.

Mr. Docker says that the mortality of dysentery in the British army during the ten years that followed the adoption of the ipecacuanha treatment fell from 11 to 5 per cent.

The remedy is best administered in large doses, 20 to 40 grains, and should be repeated every four to twelve hours until permanent good effects are secured. A dose of 15 to 30 drops of tincture of opium, or morphia, one-fourth grain hypodermically, will best protect the patient from too great exhaustion. The beneficial results are mostly obtained in the acute cases, though surprising results sometimes follow in cases of very long standing. Thus, Gayton records a case of severe chronic dysentery of eighteen months' duration which was entirely cured by ipecacuanha, and probably most physicians of large practice can recall cases where the continual relapses of the dysenteric habit have been completely broken up by {812} one course of active treatment. Should the remedy fail to be of service in the course of forty-eight hours, it should be discontinued.

Batiator, the bark of the root of the Ailanthus glandulosa; mudar, the bark of the root of the Calotropis gigantea; and bael-fruit, more especially in chronic cases,--have been proposed by Roberts, Duval, Chuckerbutty, and others as substitutes for ipecacuanha, but are not likely to soon supplant it.

Materia medica is rich in drugs whose virtues have been vaunted in dysentery, and cases occur where the judicious physician will make his selection according to the indications in a given case. Turpentine internally, as well as externally in the form of a stupe (Copland), has had advocates from ancient times; astringents, tannic acid or the substances which contain it, kino, catechu, krameria; the acetate of lead, nitrate of silver, etc.; antiseptics, carbolic acid, salicylic acid, boracic acid; anodynes, opium and its preparations; and quinia,--are among the agents most frequently employed.

Bonjean (1870) had occasion to laud the efficacy of ergotin in checking hemorrhage and controlling the discharges in a report which substantiates the claim of Rilliet and Lombard in the epidemic at Geneva in 1853. Massolez had the same good results in the war of the Crimea, as had also Andrea in the Spanish hospitals of Ceuta and Tetuan.

Clysters of nitrate of silver, 4 grains to 5 ounces of water (Duchs), or with a few drops of tincture of opium (Berger); of ipecacuanha (Begbie and Duckworth); of laudanum and starch (Sydenham, Abercrombie); of the various astringents,--may be tried in obstinate, more especially chronic, cases.

Local inspection of the rectum by means of the speculum may possibly reveal an ulcer, which is the chief or sole cause of the tenesmus and bloody discharge. Maury reports such a case in which the ulcer was deep enough to hide a small sponge. In such cases topical treatment may effect a cure.

Dilatation may suffice to overcome a stricture in the rectum, the result of cicatricial contraction, or colotomy may be necessary in cases more refractory or situated higher in the bowel. Post[10] reported a successful colotomy, with the formation of an artificial anus in the left lumbar region, in such a case.

[Footnote 10: _New York Med. Record_, 1879, xvi. 24, p. 260.]

The food should be fluid, but nutritious, and milk best fulfils both these requisites. Where milk cannot be tolerated it may be substituted by soups, beef-tea, mutton-broths, chicken-soup, etc. But it should be known of these substitutes that they contain little or no nutritious matter on account of the insolubility of the albuminoids, and are really only stimulants. Soft-boiled egg, thin custards, sweetbreads, scraped or chopped raw beef--albumen thus in substance--constitute the best food. But during the intensity of an attack the patient should almost altogether abstain from food, both from lack of inclination for it and from lack of ability to digest it. During convalescence the food should be on the basis of animal diet, though ripe fruits and fresh succulent vegetables should not be altogether withheld.

In all cases of pronounced prostration stimulants are to be freely used, and of all stimulants alcohol is the best, as it has also nutritive and {813} antiseptic properties. Alcohol is thus triply indicated in the treatment of dysentery, but the choice of the form and strength will be a matter of judgment in the individual case.

Where life is imperilled by hemorrhage or anæmia from any cause, a forlorn hope is offered in transfusion, which in the hands of C. Schmidt (1874) has proved successful in two cases.

Abscess of the liver is best treated by aspiration or hepatotomy; rheumatism, by the salicylates; and paralysis, by the constant current of electricity.

Obstinate cases of chronic or continually recurring dysentery are thoroughly cured only by a sea-voyage, a sojourn at the seashore, a mountain-excursion, or a permanent change of climate.

{814}

TYPHLITIS, PERITYPHLITIS, PARATYPHLITIS.

BY JAMES T. WHITTAKER, M.D.

HISTORY.--Typhlitis ([Greek: typhlos], blind), inflammation of or about the head of the colon, more especially the vermiform process, is a disease of modern recognition. Individual cases had been reported as curiosities where foreign bodies or fecal accumulations had excited inflammation in this part of the intestine, but it is undoubtedly to Dupuytren[1] that the credit is due of having first individualized this disease as a separate affection. About the same time (1827) Longer Villermay published his communications in the _Archives gén._, t. v. 246, on the diseases of the vermiform process, to be followed in the same year by Mêlier[2] and Hussar and Dance with observations on inflammation of the connective tissue in the region of the cæcum. These affections, which had been hitherto described as inflammatory tumors in the right iliac region, now received from Puchelt[3] the distinct name perityphlitis.

[Footnote 1: _Leçons oral de Cliniq. chirurg._, t. iii. art. xii.]

[Footnote 2: _Arch, gén._, Sept., 1827.]

[Footnote 3: _Heidelberg klin. Annal._, i. 571 and viii. 524.]

Perhaps the most remarkable events in the history of these affections since this time are the contributions of Stokes and Petrequin (1837) on the value of opium in the treatment of perforation of the vermiform appendix, of Albers,[4] who first distinguished the special form of typhlitis stercoralis, and of Oppolzer (1858-64), who set apart, perhaps as an unnecessary refinement in differential diagnosis, a paratyphlitis, an inflammation of the post-cæcal connective tissue. Matterstock[5] (1880) deserves especial mention for having given such prominence to anomalies of the vermiform appendix in the etiology of the affection; and Kraussold[6] (1881) has connected his name with the therapy of the disease by the boldness with which he expresses his convictions regarding the necessity of early evacuation, by incision, of inflammatory products, as first practised by Willard Parker in 1843.

[Footnote 4: _Beobacht. aus dem Gebiete der Pathologie_, ii. 1.]

[Footnote 5: _Handbuch d. Kinderkrank._, Bd. iv. p. 893.]

[Footnote 6: _Volkmann's Sammlung._, No. 191.]

GENERAL REMARKS.--Typhlitis, strictly speaking, is limited to affections of the cæcum and its appendix vermiformis; perityphlitis is mostly due to extension of the inflammation to the peritoneal envelope of these organs; while paratyphlitis signifies an involvement of the extra-peritoneal and post-cæcal connective tissues. Both perityphlitis and paratyphlitis are therefore secondary processes, though they may, in exceptional cases, arise from affections of organs other than the cæcum, as from {815} perinephritis, psoitis, vertebral caries, or as an expression of metastatic processes in pyæmia, septicæmia (puerperal fever), typhoid fever, etc.

ETIOLOGY.--Typhlitis and its allied affections or complications show especial predilection for the male sex and the period of adolescence. Nearly three-fourths (733) of the whole number (1030) of cases of perityphlitis collected from the literature by Matterstock were males, and this proportion holds good in infancy and early youth as well as in adolescence. The greatest number of cases, 33 per cent., occurred at the ages of 21-30; next, 30 per cent., at 11-20; while the ratio gradually decreases toward both extremes of life. So the opinion is expressed with singular unanimity by all authors that these diseases pre-eminently affect the bloom of life.

The observation that typhlitis has so often been found to arise from disease of the vermiform process has led to a closer study of its anatomical relations, and developed the fact that this organ is subject to great variation in size, shape, and situation.

Normally, the appendix vermiformis arises from the posterior interior aspect of the cæcum as a tube of the diameter of a goosequill and a length of three to six inches, with a general direction upward and inward behind the cæcum. It is commonly provided with a small mesentery, which retains it in its place. Its cavity communicates with the cavity of the cæcum by a small orifice which is at times guarded by a valvular fold of mucous membrane, while its free closed end terminates abruptly in a blunt point. It is commonly found filled with mucus throughout its entire length. The existence of this superfluous structure, which is found only in man and certain of the higher apes, has given rise to much speculation among the anatomists and physiologists, especially of the teleological school, as to its possible use. It is now, however, the generally acknowledged opinion that the appendix vermiformis is a relic or rudiment of a subsidiary stomach in lower forms of life. The head of the large intestine, which forms almost an additional stomach in the Gramnivora, and is three times the length of the whole body in the marsupial koala, is very much reduced in the Carnivora, whose food contains but little indigestible matter, and is greatly reduced in the Omnivora, as in man. The vermiform appendix is the shrivelled remnant of the great cæcal receptaculum of the lower animals. In the orang it is still a long convoluted tube, but in man it is reduced, as stated, to the size of a quill three or four inches in length, and is often entirely absent.

Kraussold, who complains that the vermiform process has hitherto received only step-motherly treatment at the hands of anatomists and clinicians, undertook a series of investigations which went to show how often and what extreme anomalies do occur. In some cases the appendix was disposed in an exactly opposite to the normal direction, its blind end being turned upward along the ascending colon. In one case it was found wound about the ileum; in another, spirally turned at its end and lightly adherent to a hernial sac. Sometimes it was abnormally long or short, open or closed with a valve, cylindrical, saccular, or bulbed, fixed or free, curved or bent upon itself at a sharp angle, provided with a short mesentery, and sometimes, as stated, it was entirely absent.

But by far the most interesting point connected with this organ was the frequency with which it was found the seat of ulceration or stricture {816} from cicatrization somewhere in its course, the result of dysentery, typhoid fever, syphilis, and more especially of tuberculosis. Clinicians who have been struck with the frequency with which typhlitis has occurred in tuberculous subjects find in this discovery a satisfactory explanation of this very remarkable coincidence.

Normally, the vermiform appendix is found filled, as stated, with a tough vitreous mucus, but not infrequently masses of feces, foreign bodies, intestinal worms, etc. find their way into it, where they may remain innocuous or may excite a dangerous inflammation. This fact, in connection with the general uselessness or superfluousness of this structure, has led pathologists to characterize the vermiform process with the significant appellation of a death-trap.

Two anatomical factors deserve especial emphasis in explanation of the frequent origin of disease in the vermiform appendix. One is the existence of the valvular fold of mucous membrane, already mentioned, at or near the orifice of the tube in the cæcum, the clinical importance of which was first pointed out by Gerlach. This fold is most marked between the ages of three and twelve, and when pronounced narrows the orifice to one-half or one-third of the whole calibre of the tube. As a rule, this fold, and the consequent diminution in the size of the orifice, are but little marked in the first years of life and in old age, which accounts for the relative infrequency of typhlitis at these periods of life.

The second mechanical factor is the deformity caused by the abnormal anatomical position of the organ, either as a congenital defect or as a pathological change. Matterstock quotes from Züngel, who observed in 59 cases in the Hamburg hospital whole or partial obliteration 30 times, catarrh and old fecal concretions 43 times, abnormal adhesions 12 times, and tubercular ulceration (without perforation) 11 times. Toft claims as the result of 300 personal investigations that every third person between the ages of twenty and seventy showed the traces of present or past inflammation, and that actual ulceration existed in 5 per cent. of all bodies examined. Kraussold declares that this percentage is rather too low than too high, and adds that among his patients--who were, it should be stated, mostly phthisical--it was remarkable how extraordinarily often the whole vermiform appendix was the seat of an encroaching ulcer. In a number of cases cicatrices or cicatricial alterations were found where typhoid fever or dysentery had existed in the previous history.

Attention should at least be called to a last anatomical factor in explanation of the frequency of ulceration and inflammation of this structure, in that its walls are so sparsely endowed with muscular tissue as to render it unable to empty itself of the virus or germs of disease which enter it from the comparatively stagnant reservoir, the cæcum.

Constipation is usually invoked as a cardinal factor in the genesis of typhlitis (typhlitis stercoralis). Speck calls attention to the frequency of the disease in East Siberia, where the food, mostly vegetable, contains a large amount of indigestible residue. But that this condition cannot sufficiently account for the disease in most cases is proved by the fact that constipation is more frequent in advanced life and among females, in whom typhlitis with its associate lesions is more infrequent. For the same reason a sedentary mode of life loses force as an argument in its production. Perhaps the most efficient cause of the condition is a local {817} paresis of the muscular tissue of the cæcum produced by the irritation of intestinal catarrh, of disease virus, of a fecal concretion or a foreign body--an irritation which may induce first a spasmodic action, and subsequently, as a result, a partial paralysis or a paresis. The same condition may be brought about more directly by the presence of a centre of irritation--viz. by reflex inhibition of innervation. Accumulation and impaction of feces must then necessarily ensue, and it is highly probable that this accumulation occurs in this way as a result more frequently than as a cause of the condition. For the symptoms of a simple accumulation of feces (coprostasis) are never so severe, at least at the start, as to mark the onset of a genuine typhlitis. Nor is there anything in healthy feces to induce the signs of a severe blood-poisoning which so commonly announces the advent or course of typhlitis.

Room is here open for the surmise that most cases of typhlitis pur et simple are due to the presence in the cæcum of the germs or virus of disease taken with the food or drink, and traversing innocuously the whole length of the alimentary tract, to finally bring up in this most stagnant part of the intestinal canal.

The rôle of pure mechanical causes cannot be ignored or underrated in perityphlitis, understanding by this division processes which commence in the vermiform appendix. For it is the rule to discover in the vermiform appendix in these cases either fecal concretions or foreign bodies. Haeckel and Buhl found concretions of meconium in a new-born child, and fecal concretions, intestinal stones, are far more frequently encountered than foreign bodies. In 146 accurately observed adult cases recorded by Matterstock, fecal concretions were met with 63 times, foreign bodies 9 times, while in the other cases nothing could be discovered; and in 49 cases among children, fecal concretions were discovered 27 times, foreign bodies 3 times, and nothing abnormal in the remaining cases. Not infrequently a small foreign body acts as a centre of crystallization for feces which become superimposed in successive layers. Hairs, as of the beard, sometimes officiate in this way. Among other foreign bodies met with in fatal cases of perforation, independently of feces, may be mentioned round-worms (Faber), cherry-stones (Paterson), needles (Payne), fish-bones (Züngel), gall-stones (Hallete), a mass of ascarides (Klebs), buttons (Gerhardt), etc., etc. As already intimated, supposed foreign bodies are often found on examination to be nothing else than intestinal concretions. As to cherry-stones, which are so often accused of producing typhlitis, Biermer and Bossard found it difficult or impossible to force them into the vermiform process.

MORBID ANATOMY.--The lesions revealed upon the post-mortem table show for the most part the ordinary picture of perforative peritonitis, which is by far the most frequent cause of death. The peritoneum in the vicinity of the perforation is found hyperæmic, swollen, necrosed, covered with flakes of soft fibrin, or partially agglutinated to contiguous structures. The wall of the bowel is very much thickened by catarrhal swelling of its mucosa, proliferation of its submucous tissue in more chronic cases, oedema of all its coats, or suppurative processes. Not infrequently the mucous tissue is the seat of extensive ulceration which may involve other structures of the gut or form an abscess, even as large as a man's head, in its immediate vicinity. The abscess may remain strictly localized or {818} may wander to discharge itself into the ileum, cæcum, duodenum, and diaphragm (Bamberger) with resultant empyema (Duddenhausen), colon (Prudhomme), bladder (Bossard), in which case the fecal concretion became the nucleus for a vesical stone; acetabulum (Aubry), inferior vena cava (Demaux), or peritoneal cavity, the most frequent eventuality. Duddenhausen saw in one case a pylephlebitis result, Von Buhl a pylephlebitis and metastatic liver abscess, which condition, Matterstock says, is noted 11 times in 146 autopsies; and older writers speak of discharges into the pleural sac, into the lungs, pericardium, uterus, vagina, etc. A curious case was observed by Eichhorst in Frerichs' clinic, where pus found escape through the umbilicus. So cases of burrowing sinuses with abscesses at distant seats, as in the groin or lumbar region, fistulæ with continuous discharge, and other curiosities, may be found among the records by the curious.

In cases of more acute course the lesions are often found centred about the vermiform appendix. The most various contortions, adhesions, or erosions are observed in this structure. Occasionally a constriction occludes the course of the tube, while the distal end is dilated into a condition of hydrops. It may be found perforated in one or in several places. The cicatrices or agglutinations of old attacks may be encountered; it may be cut in two or three pieces (Matterstock), or have been entirely absorbed. Kraussold records a case of this kind in a colleague who died of typhlitis. Upon the post-mortem table no trace of the vermiform appendix could be encountered except a dimple on the mucous surface of the cæcum, indicating the site of its former orifice.

SYMPTOMATOLOGY.--Typhlitis announces itself in two ways--suddenly and insidiously. In adults the disease begins as a rule with violent signs; in children there is often a prodromatous stage which may last for days or for months before a positive diagnosis can be established. There are in these cases anorexia and vomiting, constipation and diarrhoea, colicky pains, mostly concentrated about the ileo-cæcal region. There are at this time a disinclination to stand or walk, a stooped posture or gait, occasionally a light icterus, a feeling of formication or paresis in the right leg, and lastly an increased resistance or a palpable tumor in the right ileum.

In the adult the disease is wont to begin with more tempestuous signs. Not infrequently it is ushered in with a well-marked chill, upon which immediately supervenes a sharp pain at the affected region. A general collapse of strength soon follows, with fever, thirst, a husky voice, a coated tongue, vomiting, singultus, and an expression of anxiety. The impression of serious illness becomes apparent at once. The case early bears the aspect of a grave infectious disease. A constant, dull, boring, gnawing, or lancinating pain in the right iliac region first excites the suspicion of the physician as to the real nature of the disease. In children the pain is sometimes felt first in the epigastrium; in three cases mentioned by Büchner, Herzfelder, and Traube it was first experienced in the left ileum. There may be at this time no tumor, but there is increased resistance to pressure and exquisite tenderness to touch in the neighborhood of the cæcum. The whole abdomen is more or less tender, and often tumid. If there should be also gurgling from displacement of gas, doubt is excited as to the possible existence of typhoid fever.

{819} In the course of a few days the tumor takes shape. A typhlitis stercoralis shows a distension of the whole ascending colon, a sausage-shaped tumor, smooth or nodulated, along the entire right side of the abdomen, with increased resistance also in the transverse colon. More frequently in typhlitis--and, as a rule, in peri- and paratyphlitis--the tumor or tumefaction is more localized about the head of the colon. Frequently the swelling is so great as to be visible as a protrusion or bulging of the affected region. Percussion shows dulness, tanquam femoris, in cases of pure typhlitis, whereas in peri-, and more especially in paratyphlitis, there is tympanites on light and dulness only on deep percussion. Palpation or palpatory auscultation occasionally, though very rarely, reveals a peritoneal friction sound (Gerhardt).

The third cardinal symptom of the disease is the disturbance of digestion, which, as stated, often precedes or attends the first manifestation of the pain and the tumor. Anorexia, nausea, and vomiting--which is in the last stage of the disease often substituted by singultus--present themselves as occasional or constant signs of the disease. Constipation remains as a rule throughout the whole course of the disease with an obstinacy which sometimes excites apprehension of an intestinal occlusion; or the constipation may alternate with diarrhoea or dysenteric phenomena, more especially in the earlier stages. The tongue is, as a rule, heavily coated, or in typhoid states is dry, glazed, or fissured, and sordes covers the teeth and gums.

Fever is not a necessary factor in typhlitis, but when present distinguishes itself by its irregular range. The pulse is usually accelerated, full, and hard; the skin is dry and harsh; the urine is scanty and high-colored, and contains "almost without exception unusually large quantities of indican" (Eichhorst).

Perforation, when it occurs, is usually recognized at once by the signs of more or less immediate collapse, which quickly results in death.

The abdomen becomes suddenly distended, meteoric over its entire surface, the normal hepatic dulness giving place to a tympanitic resonance.

Not infrequently perforation occurs as the result of an accident, as after a push or blow upon the abdomen (Volz), heavy lifting (Volperling), riding in a wagon (Marsh), after dancing (Cless), mere turning of the body in bed (Langdon Downs), after emesis (Urban), purgation (Stokes), enema (Mêlier), etc., etc. That the slightest agitation may suffice at times to break down the last barrier of serous tissue separating the intestinal and peritoneal cavity is shown in the case recorded by With, where fatal perforative peritonitis occurred after a fit of immoderate laughter.

Paratyphlitis distinguishes itself from the other forms of the disease by its more insidious character. There is also in paratyphlitis, as a rule, less disturbance in the alimentary canal. The cæcum in paratyphlitis is mostly empty or is filled with gas, whose presence is recognized by tympanitic resonance on lighter percussion. On the other hand, paratyphlitis is characterized by the greater frequency of pressure signs in the right lower extremity. If the subjacent iliac and psoas muscles be implicated, the thigh is flexed upon the leg in decubitus. Various paræsthesiæ, formication, numbness, pain, and veritable paresis are experienced in the right leg. Dysuria, retraction of the testicle, and priapism may also occur in this form of the disease. Or pressure upon the iliac vein {820} induces thrombosis, with oedema, milk leg. The long-continued process of suppuration in paratyphlitis leads also at times to hectic fever or pyæmia, with slow marasmus.

In all cases relapses are very frequent, as repeated occurrences of the disease constitute the rule. Eichhorst records the case of a court-officer who suffered five attacks of paratyphlitis in the short space of one and a half years.

DIAGNOSIS.--The recognition of the disease is mostly simple. The pain, the tumor, and the disturbances of digestion sufficiently, and for the most part sufficiently early, distinguish the affection.

Simple impaction of feces is differentiated by the history of constipation; by the feel of the hardened feces, which form an elongated, nodulated, sausage-shaped tumor along the entire ascending colon, and later in shifting along the transverse colon; by the comparatively slight tenderness; and by the entire relief which follows thorough irrigation of the bowel.

Cancer may be eliminated by regard of the age of the patient, the slow development and course of the symptoms, and the gradual manifestation of its cachexia.

Invagination is an affection for the most part of early childhood--is marked by the sudden appearance of violent symptoms of disturbance of digestion, vomiting, often stercoraceous, occlusion, diarrhoea, or dysentery, with straining and discharges of blood.

DURATION.--Typhlitis and its complications have no definite duration. A case may terminate fatally in the course of a few days or may extend itself over months, or with its effects over years or for life. The disease is, as a rule, much shorter in childhood than in adult life. According to Matterstock, nearly one-half (44 per cent.) of children succumb to the disease within the first three days. Wood records the case of a girl aged ten who died in nine hours. The average duration of cases of typhlitis without suppuration ranges from fourteen to twenty-one days. The early evacuation of inflammatory products by aspiration or incision may cut the disease short at any time, or exacerbations and remissions may manifest themselves for months or years--a condition especially liable to occur when burrowing sinuses or fistulæ develop, or when passive encapsulated abscesses are aroused into activity by some accident or indiscretion on the part of the patient.

PROGNOSIS.--A case of typhlitis stercoralis has no gravity, and should terminate or be terminated within twenty-four to forty-eight hours after its recognition. Neglected or unrecognized cases, however, are not infrequently fatal from the circumscribed or more especially diffuse peritonitis which may ensue.

Typhlitis independent of fecal impaction is always a grave affection, requiring in every instance a very guarded prognosis.

Every form of typhlitis is more fatal in childhood than in adult life, and any case of the disease may present grave complications or assume a dangerous form at any time. The greater danger of childhood lies in the greater liability to peritonitis. Most subsequent writers confirm this statement, first made by Willard Parker, who also remarked that suppurative processes, abscess formation, is more common in the adult. The mortality of perityphlitis alone in childhood is 70 per cent., in adult life 30 per {821} cent., so that the proportion of recoveries is exactly the reverse of these figures at the different periods of life.

The general adoption of the opium treatment has, however, rendered the prognosis of typhlitis far more favorable--has, in fact, reduced the mortality in adult life from 80 per cent., the appalling figures of the older statistics (Volz), to 30 per cent., the ratio of modern times.

The means of earlier detection and readier relief of accumulated pus have also contributed much to reduce the mortality of typhlitis. In 1872, Bull of New York had to report of 67 cases of perityphlitic abscess collected by him, mostly treated without operation, a mortality of 47½ per cent., while ten years later (1882) Noyes of Providence was able to report of 100 cases treated by operation a mortality of only 15 percent. (Pepper[7]).

[Footnote 7: "Contribution to the Clinical Study of Typhlitis, etc.," _Trans. Med. Soc. Penna._, 1883.]

The development of fistulæ or wandering abscess, the occurrence of pyæmia and peritonitis, necessarily aggravate the prognosis of a simple case. Perforation is fatal of necessity, yet cases are not wanting where recovery has occurred even after this gravest of all the accidents of the disease. Thus, Patschkrowski reports, from Frerichs' clinic, a case of recovery after perforation, and Pepper mentions the results of an autopsy made upon an old man who died of vesical hemorrhage, in whom he "found that there had, at some unknown previous time, been perforation of the appendix."

PROPHYLAXIS.--The prevention of typhlitis has reference more especially to cases of habitual recurrence of the disease in adults, or to the earliest, prodromatous, stage in childhood. The slightest manifestation of pain in the right iliac region should be looked upon with suspicion in these cases, and absolute rest enjoined at once. Since in childhood perforation has occurred in insidious cases after so slight an irritation as a laxative or an enema, or even after a bath, every provocation of this kind should be avoided. Injunction is to be put upon all solid food in all cases in the inception as well as throughout the course of the affection, that the element of coprostasis be not superadded to the irritation of the disease. Adults subject to frequent recurrences or relapses will thus avoid also the development or aggravation of an intestinal catarrh, which in other cases of trivial import may become dangerous to them. Many cases of typhlitis are doubtless aborted at the start by the observance of absolute rest and abstinence from food or rigid diet at the start.

TREATMENT.--Perhaps no disease requires such careful consideration of its cause or form, inasmuch as the different varieties call for entirely different treatment. A typhlitis stercoralis, for instance, requires an exclusive evacuant treatment, whereas a peri- or paratyphlitis demands a treatment that shall put the bowels at rest.

The safest and most effective method of emptying the cæcum of impacted feces is by irrigation of the bowels by means of the funnel syringe devised by Hegar. The patient is put in the knee, elbow, or chest posture, and warm water--which is the best solvent for hardened feces--is allowed to slowly inundate the whole tract of the colon, after the manner and with the precautions already pointed out in the article on dysentery. Feeble or reduced patients should be supported in this posture until as much water as possible is slowly introduced. As a rule, a single thorough irrigation will suffice, or one or several additional operations may be required {822} to secure the desired effect. At the same time, broken doses, twenty grains, of sulphate of magnesia may be administered every hour or two, not so much for the purpose of exciting additional peristalsis as of turning water into the intestinal canal from above.

The other varieties of the affection call for opium at the start, with the double view of preventing the irregular, spasmodic, or tetanic contraction of the muscular coat and of obviating the danger of peritonitis. Opium is not contraindicated in these cases, even if the element of fecal impaction be superadded, as all clinicians are familiar with the fact that the bowels will move of themselves at times even under its full narcotic effects.

The remedy is best given in fluid form, as in the tincture, that the dose may be graduated in its repetition to secure its full effect without danger. When a quick action is required, morphia hypodermically may be preferred; yet it is to be remembered that opium with all its active principles is of more value in the relief of peritonitis than morphia alone. A careful watch should be kept upon all patients treated with large or frequently-repeated doses of opium, that its toxic effects be avoided. Not infrequently symptoms of poisoning have supervened after a sudden relief of pain, necessitating the use of means to keep the patient awake for a number of hours.

Hot embrocations, or poultices applied over large surfaces of the abdomen, give great comfort to the patient, though the very opposite treatment of an ice-bag, occasionally shifted or suspended, is more agreeable in some cases in the inception of the disease.

So soon as a distinct doughy sensation or a more marked fluctuation indicates the development of pus, steps should be undertaken at once to secure its evacuation. In cases of doubt it is best to make a tentative exploration with the needle of the aspirator, a large-sized needle being preferred on account of the liability of occlusion with tissue-shreds or other débris. It is quite surprising how rapidly a case clears up at times after the evacuation of even only a drachm or two of oedematous fluid. More frequently, however, the aspiration must be repeated until a quantity of pus is secured and the abscess completely discharged.

An abscess of more superficial situation, of larger size, or of continuous formation is best relieved by free incision. As to the time of the operation, the old rule, ubi pus ibi incisio, holds good here as elsewhere. An early evacuation of the products of inflammation prevents the supreme danger of perforative peritonitis or the formation of burrowing sinuses, fistulæ, amyloid degeneration, and marasmus.

Indurated tumors are sometimes made to soften under the long-continued use of cataplasms, and chronic thickenings of the walls of the intestine are relieved by general tonics, mild laxatives, mineral waters, and gentle frictions with iodine or mercurial ointments.

Perforative peritonitis calls for opium in maximum doses as a means of facilitating possible agglutinations or encapsulations, and a forlorn hope is offered in an early laparotomy, which the bolder surgeons are now undertaking in the equally desperate cases of perforation by gall- or kidney-stones, etc.

Under no circumstances should a patient affected with typhlitis leave the bed until the last trace of inflammation has subsided, as in no disease is there greater liability to recurrence or relapse.

{823}

INTESTINAL ULCER.

BY JAMES T. WHITTAKER, M.D.

Intestinal ulcer, Ulcus intestinorum entero-helcosis ([Greek: helchôsis], ulcer), represents a solution of continuity in the wall of the intestine, affecting first, as a rule, its mucous coat. Ulcer of the intestine, like ulcer of the stomach, its occasional congener and not infrequent associate, is the expression of an insult or injury offered to the intestinal coat in its inner exposed surface, or of a necrobiosis the result of a local occlusion in the general blood-supply. Hence, ulcer of the intestine may be a purely local disease, or be the local expression of a general, so-called constitutional, disease. While in many cases the lines differentiating these conditions may not be distinctly drawn, as many so-called constitutional conditions (tuberculosis, typhoid fever, etc.) are discovered to be--at first, at least--local processes, the toxic ulcer (arsenic, mineral acids) may be taken as a type of the local process, acting from within, and the syphilitic ulcer as the type of the general process, acting from without. At the same time, it must be recognized of syphilis that an ulcer may result from the dissolution or breaking down of a gummatous mass anywhere in the course of the intestine, or may be the effect of infection by extension into the rectum of syphilitic processes about the genital organs, or, lastly, of direct introduction of the disease in perverted intercourse (pederasty, coitus heterotopicus).

Ulcer of the intestine is occasionally, though comparatively very rarely, observed also as the result of pressure from within or without. Such an ulcer is properly considered of traumatic or mechanical origin, as it is induced as the direct effect of mechanical irritation or arrest of blood-supply. Thus, dense masses of inspissated feces, foreign bodies, indigestible residue of food, may fret the mucous surface into a condition of hyperæmia, and, later, absolute ulceration. Undue retention, as behind a cicatricial contraction, or an occlusion from whatever cause at places where the intestinal tube normally offers resistance (at the ileo-cæcal valve, sigmoid flexure, etc.), may lead to ulceration in the same way. Schönlein has called attention to the paralytic condition of the intestinal muscularis in age as a predisposing cause of mechanical intestinal ulcer; and Virchow has noticed the same condition among the insane, whose intense preoccupation leads to neglect of evacuation of the bowels. Certain intestinal parasites, more especially ascarides, are admitted as occasional causes of ulceration, and more superficial solutions of continuity in the rectum have been noticed as the result of too frequent or too careless use of enemata.

{824} Curling was the first to call attention to the fact that extensive burns of the skin are sometimes followed by ulceration of the intestines. The ulcerative process is almost exclusively confined to the duodenum. Various attempts have been made to explain the intestinal ulcer consequent upon burning of the skin, but a satisfactory explanation is lacking as yet. Leube suggests an inhibition in the force of the circulation by reason of accumulation of waste products in the blood, while Billroth believes the ulcer to be the result of an embolic process. Whatever the cause, the frequency of its occurrence makes it more than a mere coincidence. According to Meyer, it is observed most frequently in women, and shows its first symptoms in seven to fourteen days after the initial burn.

Aside from toxic and traumatic causes, ulcer of the intestine occurs as the result of dysentery, typhoid fever, and tuberculosis--diseases mentioned in the order of frequency in the production of intestinal ulcer. The ulcers of dysentery in the large intestine, and of typhoid fever in the small intestine, assume such prominence in these affections--having even been erroneously considered at one time as the cause of these maladies--that their study belongs to the history of these diseases. The ulcer of tuberculosis is rather an accident in the course of this affection, and is now recognized as the occasional result of direct infection by the ingestion of tuberculous flesh, or, far more frequently, of the deglutition of tuberculous sputum. As a rule, the tuberculous ulcer shows itself late in the course of pulmonary phthisis, and is the cause of the obstinate and colliquative diarrhoea which speedily exhausts the patient. Yet cases are occasionally met in which numerous or extensive ulcers occur in the intestinal canal early in the history of phthisis, before any serious damage has been inflicted upon the lungs. The tuberculous ulcer affects, and for the most part is confined to, the same structures which form the seat of disease in typhoid fever--viz. the solitary and agminated glands of the ileum. When the bacilli tuberculosis are conveyed to the intestine by means of the lymph- and blood-supply through the mesenteric vessels, the resulting ulcer takes the shape of the vascular arrangement; that is, the long axis of the ulcer is at right angles to the course of the tube. Thus, if sufficiently extensive, the ulcer may be circular or form a girdle or ring entirely around the tube. With the tubercular ulcer or ulcers are usually found tubercular nodules or plaques in the serous coat, which are visible to the naked eye as opacities or milky deposits beneath the peritoneal coat. The glands of the mesentery may be at the same time so much increased in size as to form visible or palpable tumors in the abdomen.

The frequency with which tuberculosis affects the vermiform appendix has already been noticed in detail in the etiology of perityphlitis.

The ulcer of the intestine which is the result of a catarrhal process, so called, belongs to the history of chronic diarrhoea and dysentery.

The true intestinal ulcer, per se, which has its analogue in the stomach as the gastric ulcer, ulcus rotundum, is due to the same cause as in the stomach--viz. to arrest of circulation and erosion by the gastric juice. It is a well-established fact in physiology that gastric digestion is continued--is, indeed, mainly effected--in the small intestine; hence it is not surprising to learn that an arrest of circulation in the small intestine {825} is attended by the same result. The fact that this so-called peptic ulcer is found almost exclusively in the duodenum speaks most emphatically for this origin of the disease. Arrest of the circulation in the intestinal wall may be due to embolus, which, according to the observations of Nothnägel and Parènski, is not infrequently found in the branches of the duodenal artery; to infarction, the condition so commonly encountered in pyæmia and septicæmia; or to thrombotic occlusion, as seen in amyloid degeneration--a disease process which selects by preference the vessels of the alimentary canal, along with those of the kidney and spleen.

The duodenal resembles the gastric ulcer in form as well as origin. It has the same appearance, in its recent stage at least, of having been cut out with a punch, shows no inflammation, induration, or thickening about its borders, and presents the same funnel-shape with terraced walls, its apex below eccentrically situated, as a rule corresponding to the situation of the artery. It is most frequently found in the upper horizontal portion of the duodenum, but is occasionally, though rarely, seen in the descending portion. In the further course of the duodenum the gastric juice becomes gradually neutralized, so that ulcers situated below the orifice of the gall-ducts are very great exceptions. In Krauss' collection of 47 cases but 2 were found in the lower sections of the duodenum. The intestinal like the gastric ulcer is usually found single or alone, but occasionally two, three, or even four ulcers are encountered. According to the tables of Morot, a single ulcer is found in 81.8 per cent. of cases, two in 9.2 per cent., and three and four in 4.5 per cent. each.

Duodenal like gastric ulcers are attended with the liability to hemorrhage and perforation in equal if not greater degree. There is also the same tendency to implication of contiguous structures. Stich records a case of perforation of the aorta; Eichenhorst mentions the formation of abnormal communication with the gall-bladder; and Frerichs, a thrombosis of the vena porta in consequence of duodenal ulcer. Lastly, the process of cicatrization may be followed by the same disasters as occur in pyloric ulcers in consequence of contraction and constriction. Thus, the orifices of the pancreatic or choledochus ducts may be narrowed or completely closed, or the whole lumen of the duodenum obliterated, with consecutive dilatation of the stomach and oesophagus, as in the case narrated by Biermer. A very nice question in differential diagnosis as between pyloric carcinoma and pyloric or duodenal ulcer is sometimes raised in this way. In the vast majority of cases it is safe, even in the absence of a palpable tumor and without regard to the age of the patient, to decide this question in favor of carcinoma. Cases of complete occlusion constitute the rule in carcinoma, and the very great exception in ulcer.

It remains to be said that duodenal is much more rare than gastric ulcer, in the ratio of 1 to 30, and that, unlike gastric ulcer, it chiefly affects males. According to the statistics of Krauss, already cited, the ratio of males to females is 9 to 1, and according to Trier the ratio is 5 to 1. It occurs in greatest frequency between the ages of thirty to forty, diminishing in frequency with advancing age.

SYMPTOMATOLOGY.--Ulcer of the intestines announces itself by symptoms which are, as a rule, much more vague and indefinite than the same process in the stomach. In a certain percentage of cases the symptoms {826} may be entirely latent, and the cause of a sudden death be revealed only on the post-mortem table. In less severe cases the entire symptomatology of intestinal ulcer is grouped under the term dyspepsia, no characteristic phenomena being manifest throughout the course of the disease.

On the other hand, a very small ulcer may give rise to the most dangerous symptoms--hemorrhage and perforative peritonitis, which may be even fatal in the course of a few days or hours.

Among the symptoms that appear with prominence in the course of the disease is pain. Although cases are abundantly on record marked by the entire absence of pain, and although pain is by no means so universally present as in gastric ulcer, it occurs in the great majority of cases of ulcer of the intestine. The pain of intestinal ulcer distinguishes itself from gastric ulcer by being more independent of the character of the food or the time of taking it. For the most part, it occurs in attacks of colic, which are characterized at times by their extreme severity, long duration, and obstinacy to every means of relief. These attacks occur in paroxysms with complete or only incomplete remissions, and are ascribed, as in gastric ulcer, to the erosive action of the gastric juice upon exposed nerve-fibres, the intervals of relief corresponding to the periods of exhaustion of the nerve-centres. At the same time, in exceptional cases, a long-continued localized tenderness to pressure may indicate the seat of the disease.

Palpation may elicit, besides tenderness, points or regions of induration or intumescence. Such a condition is more especially encountered in cases of tuberculous disease, the so-called scrofula of the intestine or the tabes mesenterica of childhood. More localized enlargements are occasionally to be felt in the vicinity of the duodenal or other intestinal ulcer in consequence of circumscribed peritonitis, with its resultant agglutinations and adhesions. In this connection caution must be exercised not to confound masses of impacted feces with tumefactions. The history of constipation or the administration of a light laxative will generally suffice to remove this source of error.

Anorexia is a symptom of intestinal ulcer as a rule. The loss of appetite may amount to a complete aversion to all food or only to the more fatty articles of diet. A curious exception to this rule is not infrequently seen in the unappeasable hunger of children the victims of tuberculous ulceration. The contrast offered in the extreme emaciation of these patients has been made the subject of frequent comment.

With this loss or perversion of appetite and defective digestion of the food, the general condition soon begins to fail. Though cases are occasionally met in which a bien-être has been maintained for years, or a condition of obesity has been retained, these cases form the exception in the history of intestinal ulcer. More or less emaciation gradually develops as a rule, and a reduction of the general strength that is out of all proportion in its degree to the loss of flesh. At the same time the mental condition of the patient suffers a degradation to the level of the sufferer with chronic dyspepsia.

The disturbances of digestion which occur in intestinal ulcer present many varieties in degree and kind. Some patients show none or but few of the signs, while others run the gamut, so to speak, in the semeiology of dyspepsia. Heartburn, eructations, pyrosis, borborygmi, flatulence, gastralgias, pseudo-anginas, nausea, and vomiting, the familiar {827} phenomena of gastric or intestinal catarrh, attend at some time or other in the course of the disease most of the cases of intestinal ulcer.

The condition of the discharges demands notice in detail, more especially as abnormalities in the evacuations belong among the few of the more constant symptoms of the disease.

Diarrhoea is the rule in intestinal ulcer. The discharges consist at first of the undigested food and the digestive juices, which have been hurried along the alimentary canal and prematurely evacuated on account of the increase of peristalsis caused by the irritation in the upper part of its tract. The arrest of the digestive process leads to early decomposition of the ingested matters, and thus imparts to the discharges an exceedingly offensive odor. While, in exceptional cases, constipation may be present, or even obstipation of the bowels, the discharges are usually so abundant as to constitute a diarrhoea, which in some cases is so frequent or profuse as to become colliquative and speedily exhaust the strength of the patient.

An ulceration situated in the colon or rectum would furnish the discharges characteristic of dysentery, already described in detail, while the same process in the ileum would show the evacuations characteristic of typhoid fever or tuberculosis.

The most characteristic ingredient of the true duodenal ulcer is blood. As stated in the article on HEMORRHAGE OF THE BOWELS, ulcer of the intestine constitutes the most frequent source of this accident, which is sometimes so grave as to destroy life in the course of a few days or hours. The blood from an intestinal ulcer may be evacuated both by the mouth and the anus, or may be retained in the alimentary canal and not appear at all. Such cases constitute the condition known and described under the heading of occult or concealed hemorrhage, which is recognized by the rapid general collapse of the patient. When the blood issues from a duodenal ulcer, it is intimately commingled with the contents of the alimentary canal. The discharges in such cases are usually black, tarry, and more or less fluid; whereas blood from the colon or rectum still preserves its fresh red color and is discharged separate from the feces or simply coats its exterior. Occasionally cases are met where the blood coagulates in the interior of the intestinal canal, to form a cast of its lumen or to accumulate in great mass in the sigmoid flexure or rectum. In one case in the experience of the author such an accumulation was the cause of a very severe tenesmus, which was only relieved by the digital evacuation of large masses of inspissated, coagulated blood.

The presence of pus would indicate lesion of the colon, as typically shown in dysentery, as suppuration, at least with any visible products, does not occur in ulcer of the duodenum.

DURATION.--Ulcer of the intestine has no definite duration. As in the case of its prototype, gastric ulcer, it may speedily be covered with cicatricial tissue and never appear again in the course of a long life. But such a course is as unusual as in gastric ulcer. Frequent recurrence constitutes the rule in intestinal ulcer, or a partial recovery with frequent relapses, as in the course of ulcer of the stomach. So ulcer of the intestine is not infrequently a lifetime malady, with exacerbations and remissions dependent largely upon the prudence or imprudence of the patient with regard to diet. It need hardly be stated that ulcer of the intestine {828} may terminate fatally even in the course of a few days from hemorrhage, circumscribed and later diffuse peritonitis, or may drag out a slow length of years, to finally destroy the patient with the general symptoms of inanition, hydrops, and marasmus.

DIAGNOSIS.--From what has been already stated, it is seen that ulcer of the intestine is often entirely overlooked or may be readily confounded with other maladies of the digestive tract. Cases of traumatic or toxic origin are generally readily recognized by the history of the patient, and tuberculosis reveals itself by the youth of the individual, the existence of the disease elsewhere, the gradual emaciation, the premature senescence--in short, the general signs of the phthisical habitus, the meteorism, and perhaps the presence of nodular enlargements of the mesenteric glands.

The most characteristic symptom of the peptic ulcer is, as has been stated, hemorrhage. But hemorrhage is present in only the minority of cases, is, as a rule, occasional and transitory, and is at all times difficult of differentiation as to its source. Blood from a gastric ulcer may also be voided per rectum as well as per os, and the blood from a duodenal ulcer after regurgitation may be wholly discharged by vomiting. The absence of vomiting and the presence--more especially the persistence--of tarry evacuations from the bowels would speak for ulcer of the intestine. Dilatation of the duodenum, a condition of ectasia, closure of the bile-duct with consecutive jaundice, or the presence of fatty stools from occlusion of the pancreatic duct (a sign not now regarded of the same value as in the days of Bright), would also declare in favor of ulcer in the duodenum.

As between intestinal ulcer and catarrh or intestinal ulcer and carcinoma, precisely the same rules would hold as in the case of the stomach. A simple enteralgia would be recognized by its more frequent occurrence among females or individuals of neurotic temperament; by its connection with faults of diet, malaria, or exposure to cold; by the absence of hemorrhage, diarrhoea, or peritonitis.

PROGNOSIS.--Too much caution cannot be exercised in the prognosis of ulcer of the intestine; for even in the cases which run a perfectly mild course the gravest, even fatal, accidents are liable to occur. The danger of perforation in cases of typhoid fever from a single or from one of the few ulcers that may be present imparts one of the chief elements of gravity to this disease; and the same catastrophe may occur at any time in dysentery or tuberculosis. The duodenal ulcer may likewise have a sudden gravity imparted to a mild case by a copious hemorrhage or a peritonitis, and, even though the patient escape all possible complications, to recover with the surface of the ulcer healed so that the loss of substance is filled in with firm cicatricial tissue, the danger of contraction or stenosis still remains. The ulcers of dysentery in the colon and of syphilis in the rectum are especially liable to be followed by deformities of this kind, while the tuberculous ulcer in the ileum not infrequently results in a more or less complete stenosis. The ulcer of typhoid fever in its cicatrization almost never reduces the size of the intestinal canal.

TREATMENT.--The most valuable therapeutic means of relieving the pain and obviating the dangers of ulcer of the intestine consist in the {829} regulation of the diet. The food should be light, easily digestible, and during the acute stage of the disease as nearly fluid in its consistency as may be. Milk would be the staple article of diet in all cases were it not for the fact that in some cases constipation attends its too exclusive use. The various soups, without solids, broths, preparations of starch (sago, arrowroot, tapioca, etc.), may sufficiently nourish the patient until the healing process shall have commenced. Raw beef, chopped up and made into an emulsion, is perhaps the most nutritious and least injurious of any kind of food. Bread, potatoes and other vegetables should be ruled out altogether, because of their liability to produce masses of feces whose inspissation may do mechanical damage to ulcers in process of cicatrization.

Where there is failure in the general strength early resort should be had to alcohol, which may be administered in the form of red wine (in preference to white, because of the tannin it contains), wine-whey, or, in more serious prostration, of sherry wine, milk punch, egg-nog made with good whiskey or brandy.

In the worst cases, where all food irritates, feeding by the mouth may be abandoned altogether for a time, and the strength of the patient sustained by nutritive enemata of beef or pancreatic emulsion.

The diarrhoea should be controlled rather than entirely checked, for fear of the greater evil of constipation. A little bismuth with bicarbonate of sodium or oxide of zinc may suffice for the milder cases, while in the more aggravated cases resort must be had sooner or later to opium.

Constipation is best relieved by careful injections of warm water or by the administration of the lighter laxatives--mineral waters, Seidlitz powders, citrate of magnesia, castor oil, etc.

Vomiting is combated by ice, soda-water, champagne, cherry-laurel water, and in graver cases morphia hypodermically.

Pain may be relieved by applications of hot water, cataplasms, injections of hot water, and, when necessary, by morphia with or without belladonna.

Hemorrhage is checked by ice internally and externally, turpentine, ergot or preferably ergotin by hypodermic injection, and opium.

Peritonitis, more especially perforative peritonitis, calls imperatively for the liberal use of opium.

Patients the victims of intestinal ulcer must maintain a guarded diet for months, often for years, after all signs of the disease have disappeared as the best prophylaxis against recurrence. Constant vigilance is also required to avoid constipation, and the greatest temperance exercised with regard to the use of alcohol. The author has at the present time a patient under treatment who presents all the symptoms of duodenal ulcer, including hemorrhage, with every indulgence in strong drink, and in whom all symptoms disappear under entire abstention. Sometimes a course of mineral waters, a sea-voyage, or other change of life or scene constitutes the best means of avoiding frequent relapse.

It need hardly be said that an ulcer in the rectum, which is readily recognized by its attending tenesmus, calls for local treatment; and it is equally plain that tuberculosis or syphilis requires appropriate internal means of relief.

{830}

HEMORRHAGE OF THE BOWELS.

BY JAMES T. WHITTAKER, M.D.

GENERAL REMARKS.--Hemorrhage of the bowels occurs in both sexes, though more frequently in the male, and at all ages, though more frequently at the middle period of life. In the infant a form of it is sometimes considered as a distinct affection under the head of melæna neonatorum, and in age it sometimes shows itself as a distinct sign of a disease characteristic of age--namely, cancer. According to the tables of Bamberger, it is caused in the order of frequency by dysentery, typhus fever, cancer (of the colon), mechanical injury, poisons and foreign bodies, ulceration (tubercular, follicular), the round ulcer of the duodenum, and aneurism; last and least frequent is the so-called vicarious hemorrhage.

ETIOLOGY.--Hemorrhage from the intestinal canal arises from (1) anomalies in the contents of the bowel; (2) disease of the wall of the bowel; and (3) from general diseases.

(1) The inspissation of the natural contents of the bowel during long-standing or habitual constipation may convert the feces into dense masses which irritate and scratch the mucous membrane, and thus induce hemorrhage directly by simple solution of continuity, or indirectly as the result of extreme hyperæmia. Such hemorrhage is nearly always slight, streaking or coating the surface of the scybalous mass or being extruded from the anus as a small deposit of blood during the last act of defecation; in which latter case it is found mostly associated with hemorrhoids or fissure of the anus--conditions which require separate description. Independent of these conditions, the hemorrhage nearly always has its origin in the lowest regions of the large intestine, where condensation of the feces is naturally greatest.

Foreign bodies in the intestinal canal descended from the stomach may also be the cause of hemorrhage in the same way. Thus, stones of fruits, bones of fish, fragments of oyster-shell, or other substances in no way connected with aliments (false teeth, buttons, pins and needles, etc.), may be swallowed accidentally or purposely (as by children or the insane) to produce intestinal hemorrhage. Drastic cathartics (podophyllin, gamboge, etc.) and poisons (arsenic, mineral acids) occasionally act in the same way. Thus, Tardieu reports[1] the case of a servant to whom was administered by a homoeopath veratrin with coffee, with fatal effect in six days. At the autopsy, made by Amussat and Reymond, the stomach and small {831} intestine were found filled with a dark-brown or black bloody fluid, but there was no trace of perforation, ulceration, or organic disease.

[Footnote 1: _Annales d'Hygiène_, July, 1854.]

Under this head mention should be made also of certain parasites whose habitat is the intestinal canal, the walls of which they perforate. Two varieties, the Anchylostoma duodenale and the Distoma hepaticum, are frequent causes of hemorrhage, the former from the duodenum and jejunum, the latter from the rectum, in hot climates, more especially in India and Egypt.

(2) Anomalies in the intestinal walls produce hemorrhage as the result of intense hyperæmia (per diapedesin) or of actual loss of substance (per rhexin). Copious, even fatal, hemorrhage has thus ensued from dysenteric and typhoid processes (and even without discoverable cause) where no ulceration or loss of substance could be discovered on autopsy; and this accident is so frequent as the result of ulceration in the diseases mentioned as to constitute a characteristic sign or complication. It must be said, however, that cases of alarming or fatal hemorrhage without apparent cause during life or lesion after death were more frequently reported in the literature of the times preceding our more accurate knowledge of pathology and pathogeny. Few clinicians or pathologists would now be content with reports made without full knowledge of the history of the case or microscopic examination of the intestinal walls. Thus, the report to the Société Médicale d'Emulation, April 2, 1834, by Dubois of a young man who quickly died of intestinal hemorrhage five days after a severe headache, and on the same occasion by Guillemot of several similar cases, would awaken the suspicion of masked typhoid fever; and the case of an old man aged seventy-four who died of intestinal hemorrhage after four days' diarrhoea, reported by Husson,[2] would call for a close examination of the vessels in the intestinal walls. In fact, Bricheteau, who reported a case from the Hôpital Neckar, was able on autopsy to discover a rupture in a small artery of the intestines.

[Footnote 2: _Proceedings of the Anatomical Society at Paris_, 1835.]

Embolic processes leading to the formation of ulceration (by predilection in the duodenum) are often attended with intestinal hemorrhage, which would be more constantly present were it not for the fact that, as in the stomach, the speedy establishment of collateral circulation prevents the consequences of complete infarction.

Besides dysentery and typhoid fever, tuberculosis and syphilis are occasional causes of ulceration and necrosis of the intestinal walls which may be attended with hemorrhage. Cancer of the intestine most frequently affects the rectum, but wherever situated may show hemorrhage as one of its signs.

The local hyperplasia of the mucous tissue which constitutes a polypus--and which in children, in whom it most frequently occurs, is mostly situated in the rectum--is suspected to exist or is recognized by the frequent discharge of blood from the bowels. A far more grave affection of the intestinal walls, likewise most frequent in childhood, is the peculiar dislocation known as intussusception or invagination. This condition is so commonly attended with distressing evacuations of blood and mucus as to simulate dysentery. The strangulation of the intussuscepted mesentery with its vessels easily accounts for the hemorrhage in such cases.

A more extensive compression is exercised at times by tumors in the {832} abdominal cavity, as by pregnancy, ovarian growths, etc., occlusions in the course of the portal system (cirrhosis hepatis), interference with the general circulation, as in diseases of the heart or lungs, with intestinal hemorrhage as a consequence.

Diseases of the blood-vessels themselves, as amyloid degeneration, aneurism, should not be omitted from the list of factors possibly productive of this result.

(3) The general diseases attended with hemorrhage from the bowel are characterized for the most part by more or less general disintegration or dissolution of the blood, with the manifestation of hemorrhage in various parts of the body--kidneys, uterus, subcutaneous tissue, etc.; the enterorrhagia being an accidental localization, so to speak, of the effusion. The most prolific causes of this disorganization are the micro-organisms which "touch the life of the blood corruptibly;" and hence the various acute infectious diseases may show in the severer forms hemorrhage from the bowels. Under this head may be ranged variola, which boasts even of a hemorrhagic form; typhus, yellow, and malarial fevers; the forms of nephritis marked by uræmia, cholera, icterus gravis, erysipelas, etc. Disintegration of the blood or partial dissolution of its corpuscular elements occurs also in those obscure affections which constitute the group, or are included in the description, of the hemorrhagic diatheses, as hæmophilia, leuchæmia, pernicious anæmia, scurvy; of any of which enterorrhagia may be a distinct or dangerous sign.

Melæna neonatorum is the distinct name given to a hemorrhage from the bowels which occurs a few hours or days after birth, and which is often so profuse as to cause death at once or in a short time. In most cases no anatomical lesions can be discovered after death, save an intense hyperæmia of the intestinal mucosa, so that the etiology of this affection is involved in obscurity. The various causes assigned in its production--ulceration of the stomach or duodenum (Bohn), embolism (Landau), fatty degeneration (Steiner), premature ligature of the umbilical cord (Kiwisch)--answer only for individual cases. Betz reported a case in a family subject to hæmophilia, and Trousseau once saw twins thus affected; but that heredity cannot account for all cases is shown by the fact that it occurs mostly in healthy children from healthy parentage. Klebs is inclined to attribute the affection to the action of micro-organisms, introduced perhaps as the result of puerperal infection, but this cause can be assumed in only a small minority of cases; at least, but a small percentage of cases coincide with puerperal disease on the part of the mother.

The affection is fortunately rare. Eichhorst states that Hecker observed it but once in 500 births, and Gemich but once in 1000 births. According to Rilliet, the hemorrhage is oftener (8/14) intestinal, rarer (4/14) gastric, and rarest (2/14) both. It is almost always abundant and quickly repeated, the blood being mostly pure, in clots or masses and fluid, though it is sometimes commingled with meconium. It usually ceases within twenty-four hours, though it may continue for three, five, or more days. Of 23 cases reported by this author, 12 recovered and 11 died.

MORBID ANATOMY.--Hemorrhage from the bowels, being only a symptom of very many different conditions, is marked by lesions characteristic of the condition in an individual case. These lesions are more appropriately described in connection with the various diseases. Not {833} infrequently in these cases the intestine is distinguished by the absence of any lesion at all; but, from whatever cause, hemorrhage from the bowels, like hemorrhage from any other source, shows a more or less profound anæmia of all the internal organs, and in more chronic and protracted cases leads to fatty degeneration, more especially of the heart.

SYMPTOMATOLOGY.--Hemorrhage from the bowels is usually readily recognized by the discharge of blood, either pure or mixed with the natural contents of the alimentary canal. The actual seat of the hemorrhage may, however, only rarely be recognized by the rectal speculum. The colicky pains, borborygmi, or sensations of fluids in the abdomen which are occasionally experienced may not be relied upon in fixing the seat of the effusion. Should the hemorrhage occur in quantity, or, more especially, should the seat of the effusion be low in the intestinal canal, the blood which escapes is more or less pure. When the hemorrhage is higher, or when the stay of the blood in the bowel is longer, it becomes more or less incorporated with the contents of the bowels or altered by the intestinal juices to present a discharge of mushy or semi-fluid consistence, of dark-brown or black color. So-called tarry stools are thus largely composed of blood.

But serious, even fatal, hemorrhage sometimes occurs without the escape of any blood at all. Such are the so-called cases of concealed, occult, or internal hemorrhage, in which the nature of the malady is only suspected or recognized by the general symptoms attending the profuse loss of blood. Should the hemorrhage be gradual, anæmia slowly supervenes, with hydræmia and subcutaneous dropsy. Traube reports a fatal case of oedema of the glottis from such a cause. Sudden hemorrhage announces itself by pallor and prostration, dyspnoea, vertigo, and syncope. Amaurosis, tinnitus aurium, formication, emesis, and, if the disease be high up in the intestinal canal, hæmatemesis, are the common attendants of serious hemorrhage. In the worst cases of sudden effusion the patient may present the appearance of complete collapse, and the intestinal canal be found on autopsy distended with blood throughout a great part of its course, while no blood whatever has escaped from the rectum. In such cases, or with more gradual loss of blood, the patient experiences a sense of increasing weakness, the skin becomes cold and bedewed with a clammy sweat, the pulse grows feebler, the temperature falls, and death from exhaustion more or less speedily ensues.

DIAGNOSIS.--The presence of blood in any quantity in the stools is readily recognized by its coarser characteristics. Ridiculous errors have been made by mistaking the coloration produced by bismuth, iron, logwood, etc. administered internally, or by coloring matters introduced into the discharges for purposes of deception. The microscope, Zeichmann's test for blood-crystals, and in extremely doubtful or medico-legal cases the spectroscope, furnish easy means of detecting blood in whatever quantity or character.

It is the cause and seat, rather than the existence, of the hemorrhage that mostly cause embarrassment in differential diagnosis. Hemorrhage from the lungs, nose, or stomach is usually readily excluded by the absence of any evidence of disease of these organs, and the presence of the other symptoms of any general disease attended with enterorrhagia makes a diagnosis in most cases easy enough. Alterations in the contents of the {834} bowel, the presence of foreign bodies, are recognized by the history of the case and by careful local examination, while a diagnosis of anomalies in the walls of the bowel is usually reached by exclusion. In no doubtful case should local inspection or digital examination of the anus and rectum be omitted.

TREATMENT.--As in all cases of hemorrhage, the first requisite is absolute rest. The patient should be at once put to bed and kept perfectly quiet. Many a case of hemorrhage in typhoid fever is produced by arising from bed to go to stool. The bed-pan is an absolute necessity in the management of a case of typhoid fever after the second week of the disease. Rest is the chief agent in prophylaxis as well as therapy.

The most effective styptic in enterorrhagia is cold. An ice-bladder should be laid upon or suspended immediately above the abdomen during the whole duration of the flow. The injection of ice-water into the bowel should be practised only in cases where the hemorrhage is believed to come from the colon. Otherwise, the peristalsis it awakens may only aggravate the danger. Should rest and cold fail to quickly check the hemorrhage, resort should be had at once to ergot. This remedy, in the form of ergotin, is most effective when introduced beneath the skin. In cases of less imminent danger the practitioner may be content to give the remedy by the mouth.

Small doses of the simple or camphorated tincture of opium frequently repeated speedily arrest contractions of the bowel, and at the same time feed the brain in threatening syncope. The astringents proper--tannic acid or its preparations, acetate of lead, alum, the perchloride of iron--are seldom necessary or advisable, but may be called for in obstinate or protracted cases.

To turpentine has been ascribed, from time immemorial, specific virtues in relief of hemorrhage of the bowels, and its administration is still a routine system with many older practitioners. It is most effective in large doses--one drachm, with milk or in emulsion, every hour or two until the hemorrhage ceases.

In relief of collapse, alcohol, ether, and musk are imperatively indicated, with the external application of heat; and in the treatment of the anæmia and hydræmia the preparations of iron, including, later, the mineral waters which contain it. In the worst cases of sudden alarming hemorrhage the physician should not fail to practise the transfusion of blood or solutions of salt or soda.

Milk is the best food and drink during the attack, and after it for some days or weeks. Chopped or scraped raw beef may substitute it later, while all farinaceous foods are to be strictly avoided for some time.

{835}

INTESTINAL OBSTRUCTION.

BY HUNTER MCGUIRE, M.D.

When a mechanical impediment to the passage of the contents of the bowel along the intestinal canal exists, the condition is known as intestinal obstruction. The causes of this occurrence are numerous, the symptoms urgent, the diagnosis difficult, the treatment uncertain, and the termination, unless relieved by nature or art, speedily fatal. There is no class of cases to which the practitioner is called more important, or which demands on his part greater skill and judgment.

It is customary to divide the causes of obstruction of the bowels into two great classes--acute and chronic.

In acute cases the attack is sudden, the symptoms violent, and, unless the cause is speedily removed, life ends in a few hours or at most in a few days. In chronic cases the causes act comparatively more slowly, the symptoms are chronic and less urgent, and danger of death less imminent. In this class the cause is not uncommonly spontaneously relieved, and the individual restored to perfect health without the aid of medicine or the surgeon's art. This result may happen in apparently the most desperate cases.

This classification of acute and chronic obstruction is necessary for a proper clinical study of the subject, but it should be remembered that in practice there will be found some cases which partake of many of the symptoms of both acute and chronic obstruction, making it difficult to determine to which division the cases properly belong. It will also be seen that some, at first, well-marked acute cases subside and become chronic in character, and that (old) chronic cases of obstruction sometimes suddenly change their nature and become acute. Again, some of the causes mentioned as giving rise to acute obstruction of the bowel in rare instances produce symptoms of chronic obstruction, and some of the causes referred to as giving rise to symptoms of chronic obstruction in rare instances provoke signs of acute obstruction. These cases are exceptional. As a rule, the following list embraces conditions which produce symptoms of acute obstruction:

1. Congenital malformations.

2. Impaction of foreign bodies, gall-stones, enteroliths, etc.

3. Twisting of the bowel--volvulus.

4. Internal strangulation by loops, bands, false membranes, diverticula, mesenteric pouches, slipping of a portion of bowel into natural or unnatural openings, diaphragmatic hernia, etc.

{836} 5. Invagination.

As a rule, the following causes produce symptoms of chronic intestinal obstruction:

1. Constipation and fecal accumulation.

2. Stricture of the bowel, sometimes cancerous.

3. Compression of the bowel from abdominal tumors.

4. Contraction of the bowel from inflammatory changes, often tuberculous.

A consideration of external hernia is, of course, not included in this paper, but the possibility of the symptoms of intestinal obstruction being due to this cause should never be overlooked.

Congenital Strictures and Malformations.

Cases of congenital strictures and malformations are confined almost wholly to the rectum and anus, and come more properly under the province of the surgeon. Some of the cases, however, belong to the physician, the obstruction being so slight as not to require surgical assistance. With all of them, however, the physician should be familiar, that he may be able to distinguish between congenital malformation giving rise to immediate obstruction and other forms of intestinal occlusion. He should know, too, when to seek the aid of the surgeon. For these reasons, as well as to make the history of the causes of intestinal obstruction as complete as possible, it has been thought proper to include in the list congenital occlusion and malformation of the intestine. They will be treated, however, in the briefest possible way, and the reader is referred to works on surgery for a more detailed account of the pathology, symptoms, and treatment.

When congenital occlusion of the colon occurs, it is almost invariably found in the sigmoid flexure, and is due, as most congenital atresia of the intestine, to foetal peritonitis. Congenital occlusion may be found in any portion of the small bowel, but a frequent site is the lower part of the ileum and the ileo-cæcal opening. The following case[1] gives an example of a form of stricture of the duodenum in infants, with the symptoms and pathological changes. The septum is supposed to be an unnaturally developed valve, or two valvulæ conniventes united: "A child when born presented no unusual symptoms for the first twenty-four hours. Vomiting then came on, and continued with short intermissions until death, which took place some thirty-eight hours after birth. The bowels were never relieved during life. The only disease found was stricture of the duodenum close to the entrance of the gall-duct, so that a probe passed down the latter entered the duodenum immediately below the constriction. There was nothing to indicate in what manner the constriction had occurred. On the gastric side of the latter the duodenum was immensely distended--so much so that at first sight it appeared like the pyloric end of the stomach itself, and only by a more careful examination was the distinction between the stomach and intestine detected by a ridge running around their place of junction."

[Footnote 1: Quoted by Mr. Pollock in Holmes's _System of Surgery_, from _Pathological Transactions_, vol. xii. p. 101.]

{837} Cases like this, a number of which are on record, are instructive and of pathological interest; when, however, congenital occlusion exists in the small intestines, no treatment can be suggested. If the sigmoid flexure is the part involved and diagnosis can be made, opening the intestine in the right groin and establishing an artificial anus should be attempted.

In the development of the foetus the anal part of the bowel, beginning below, develops upward, and the intestinal portion, commencing above, grows downward; both portions, advancing, finally unite, making one continuous tube. When, however, there is some interruption in the foetal development of the intestine, and the two portions of bowel fail to unite, we have malformation of the rectum and anus and intestinal obstruction; or the two portions of bowel may have been united and continuity of the intestinal track established, and subsequent intra-uterine inflammation may obliterate the canal. Under these circumstances a ligamentous cord represents the original tube. The cord descends from the cul-de-sac in which the upper part of the bowel ends to the skin about the anus, or is lost in the tissues about the neck of the bladder. In congenital malformations the following conditions may be found: 1st. The anal orifice may be so minute as not to allow the feces to escape; or the aperture may be occluded by a membrane, through which the meconium may be seen; or the anus may be entirely absent. 2d. The rectum may be occluded by a membranous septum, the presence of which is not suspected until symptoms of intestinal obstruction arise, and then it is discovered by introducing the finger or a probe; or the rectum may be entirely absent, the colon terminating in the iliac fossa in a dilated pouch, or ending at the top of the sacrum or stopping at any point between this and the normal anus, the place being determined by the period of arrest of foetal development; or, the anus being absent, the rectum may open into the vagina, bladder, urethra, and other places. These cases belong exclusively to the surgeon.

Impaction of Foreign Bodies.

Intestinal obstruction may arise from the introduction, accidental or otherwise, of foreign bodies into the stomach and bowels. Coins, marbles, bullets, fruit-seeds, etc. are often swallowed by children, sometimes intentionally, and if the object is round and small it rarely gives rise to any serious trouble. The foreign body, however, if small, may drop into the appendix vermiformis or some other diverticulum and end in serious mischief, or if the individual has stricture of the bowel the foreign body may be arrested by it.

Foreign bodies which are pointed or irregular in shape, swallowed by accident or design, may give rise to dangerous and fatal symptoms, but not unfrequently they escape per vias naturales. Thus, pins, needles, pieces of bone, artificial plate and teeth, small pen-knives, and other pointed or irregular-shaped bodies, have passed in this way. Sharp-pointed bodies, as needles, sometimes make their way through the walls of the stomach and present themselves at other and more distant parts of the body. I have removed a needle from the calf of the leg which {838} the patient had a month before accidentally swallowed. Jugglers accidentally, in practising their calling, and insane people, not unfrequently intentionally, introduce into the stomach all sorts of foreign bodies, such as buckles, forks, spoons, knives, pieces of wood, iron, bone, etc. Gross[2] records the case of a juggler who let a bar of lead ten inches long and weighing a pound slip into his stomach. Bell of Iowa removed it by gastrotomy, and the man recovered. Agnew[3] reports a post-mortem of an insane woman in whose intestinal canal he found three spools of cotton, two roller bandages, a number of skeins of thread, and a pair of suspenders.

[Footnote 2: _System of Surgery_, by S. D. Gross, 6th ed., vol. ii. p. 616.]

[Footnote 3: _Agnew's Surgery_, vol. i. p. 393.]

The morbid appetite of some people, particularly girls and pregnant women, sometimes induces them to swallow powdered chalk, magnesia, and other substances, and when this practice is continued for a long time the insoluble powder is deposited in the bowel and forms hard masses which more or less completely obstruct the intestines.

Stony concretions or enteroliths are found generally in the cæcum or in the sacculi of the colon, very rarely in the small intestines. They are round or oval, and when two or more are found together they have facets. They consist usually of carbonate of lime or magnesia or sesquioxide of iron. Other concretions are sometimes seen composed of starch or the felted husks of oats, called oat-stones (avenoliths), found particularly among the poorer classes of people in Scotland. Other vegetable remains of husks, fibres, etc. may produce the same thing. Young and middle-aged people more frequently suffer with these concretions than the old. Foreign bodies made up by the gradual accumulation of hair, string, and other substances are not unfrequently found in the stomach and intestines. The mass produced in this way is often very large. Sometimes the foreign body is arrested in the oesophagus. In a post-mortem reported to the writer by Fairfax a large copper coin, accidentally swallowed a few days before, was found lodged in the gullet. Ulceration followed, a neighboring artery was opened, and the patient died from hemorrhage.

Impaction of the bowel by gall-stones escaping from the gall-bladder into the bowel is by no means an unfrequent cause of fatal obstruction. Small gall-stones, after giving rise to intense pain and often grave symptoms during their passage through the bile-ducts, may escape into the duodenum and be discharged through the rectum, as any other small foreign body. If, however, there is constriction or stricture of the bowel at any point, the small gall-stone may lodge there, and if other stones follow and lodge, the collection may soon be great enough to produce obstruction. A very large single stone or a number of stones forming a coherent mass may collect in the gall-bladder, slowly distend the dilatable biliary passages, and escape into the bowel; or--and this is more common--an opening made by ulceration between the distended gall-bladder and the duodenum allows the concretion to escape into the small intestine. These stones or aggregation of stones are sometimes three, four, or five inches in circumference and from one to four inches long. They occur, as a rule, in people over fifty years of age, and more commonly in women. Brinton, in his excellent book on _Intestinal Obstruction_, makes the average age in these cases fifty-three and a half {839} years, and from the statistics he has gathered it will be seen that their occurrence is four times as often in females as in males. In 41 cases collected by Leichtenstern, 32 were women and 9 men. The site of the impaction is always in the small intestines. In 32 cases observed by Leichtenstern, 17 were found in the lower part of the ileum, 10 occupied the duodenum and jejunum, and 5 the middle part of the ileum.

SYMPTOMS.--Foreign substances introduced into the stomach do not always immediately give rise to serious symptoms. It is wonderful sometimes to see how tolerant the stomach is of their presence. Many instances are recorded of foreign bodies remaining in the stomach for months without producing dangerous symptoms. The mass may be discharged by vomiting, or it may escape through the pyloric opening into the intestine, and ultimately be discharged through the rectum, or, lodging in the bowel, give rise to symptoms of inflammation and obstruction. If, however, the foreign mass remains in the stomach, and is not removed by the surgeon's art or spontaneously discharged by ulceration, as in several rare instances has been the case, it uniformly proves fatal.

Before the foreign body is discharged by ulceration through the walls of the abdomen, adhesive inflammation unites that portion of the alimentary canal, gastric or intestinal, in which the mass is lodged with some part of the abdominal wall. By this union the cavity of the peritoneum is protected, just as we see the peritoneal sac protected by an effusion of lymph in hepatic abscess opening into the small intestine. If the adhesion between the canal and abdominal wall is imperfect, or by an undue amount of inflammation is disunited, the foreign body or inflammatory products which surround it may escape into the peritoneal sac and produce fatal peritonitis. Instead of passing through the abdominal wall, the foreign substance may escape into the bladder or vagina, or from the small intestine into the colon or rectum. Dangerous peritonitis may follow the simple presence of the foreign body in the alimentary canal from the obstruction it produces when no attempt at discharge by ulceration has been made. If the size and shape of the body permit its passage into the small intestine, it makes its way very slowly along this tube, giving rise to occasional attacks of colicky pains and symptoms of partial impermeability of the bowel.

At any moment the foreign body may lodge, become impacted in the canal, and all the grave symptoms of enteritis and general peritonitis present themselves. Symptoms of inflammation may appear, and after a longer or shorter time suddenly disappear, as if the foreign body had glided over some point of obstruction and again begun its descent through the tube. Its course is always irregular, passing quite rapidly over a portion of the intestine, then going more slowly, then lodging for a time at some point where it is obstructed by a fold or the contents of the bowel or by spasmodic contraction of the muscular coat of the intestines. As the calibre of the small intestine gradually diminishes as it approaches the cæcum, the passage of the foreign body becomes more and more difficult as it is propelled onward toward the ileo-cæcal valve. After a time it may reach the cæcum, where, of all places, it is most apt to lodge; but it may continue its course to the rectum, where it gives rise to tenesmus and a constant desire to go to stool. Finally, spontaneously or aided by the finger of the physician or some instrument, it is {840} evacuated per anum. Not unfrequently, the foreign body can be felt through the abdominal walls, and its course traced day after day as it makes its way along the canal.

It is a common practice with uninformed persons to give castor oil or some purgative medicine when a pin, needle, coin, or other foreign substance has accidentally passed from the mouth into the stomach. Such practice is irrational and hurtful. Experience has shown that the larger and more solid the alvine discharges, the more likely the foreign body is to escape by the natural outlet; and the physician should order such a regimen and diet as will probably secure this condition of the contents of the bowel.

Long residence of a foreign mass at any point in the intestinal canal is certain to produce some chronic enteritis and effusion of lymph and subsequent stricture of the bowel, or the presence of the foreign body may produce an ulcer; and when this is healed the resulting cicatrix may end in serious obstruction from the natural tendency of the new material to contract. Signs of constriction of the bowel may not be noticed for some time after the escape of the foreign body.

Obstruction from the presence of intestinal stones and concretions is almost invariably preceded by impaired health, emaciation, or cachectic appearance, signs of partial impermeability of the bowels, and repeated attacks of inflammation, especially in the region of the cæcum. It terminates sometimes by the concretion becoming encysted, by its spontaneous evacuation, or by ulceration and perforation, or sometimes by complete occlusion of the bowel, and death.

As occlusion of the bowel by the presence of gall-stones always occurs in the small intestines, the symptoms are at once of the most urgent and violent character. The signs are those of internal strangulation, and the termination is often rapid in the extreme. Colicky, griping pains are soon succeeded by violent agony; vomiting begins at once, and is constant; at first bile is thrown up, and afterward feculent matter; the pulse is small, wiry, and frequent; the belly is retracted; the features are pinched, the extremities cold, and prostration soon comes on, succeeded by collapse.

Evidences of disorder of the liver, symptoms of inflammation of the peritoneum in that region, or attacks of hepatic colic sometimes precede obstruction of the bowel by gall-stones; unfortunately, however, for the purposes of diagnosis, these premonitory symptoms are not invariably present.

Acute Internal Strangulation, Twisting, etc.

When a portion of bowel within the abdomen is constricted, its circulation interfered with, and the passage of the contents of the bowel interrupted, it gives rise to acute internal strangulation. This condition is very similar to that of external strangulated hernia. The difference is, that one is inside and the other outside of the cavity of the abdomen.

Twisting of the gut upon its mesenteric axis, the passage of the bowel through some natural or unnatural opening, the encircling of one portion of bowel by another or by bands, false membranes, etc., may cause {841} internal strangulation. It may happen at any age, and involves generally the small intestine or the more movable parts of the large bowel--viz. the sigmoid flexure and cæcum.

Twisting, or torsion, is not an unfrequent cause of intestinal obstruction, and may involve almost any portion of the intestinal tube. Its most common site is the sigmoid flexure, and next in point of frequency the cæcum. It sometimes, but rarely, involves the small intestines, and may occur as a simple twisting of one loop of intestines upon another. Several conditions are necessary for its production. First, the mesentery must be elongated. This change in the mesenteric root may have been caused by the dragging of an old and large hernia, or the mesentery may have been lengthened by relaxation of the abdominal walls from childbearing or by the disappearance of fat. However caused, before torsion of the gut takes place the mesentery is elongated, so that the two ends are approximated and something like a pedicle formed. Second, the portion of bowel attached to the lengthened mesentery may become filled with an enormous quantity of fecal matter and paralyzed by the great distension. In this paretic condition it may be displaced by the living, moving parts around it, and become bent and twisted, or the length of bowel belonging to the elongated portion of the mesentery may be the seat of inflammation, and, paralysis following, it becomes without resistance subject to the pressure and movements of the active vital parts surrounding it. A portion of bowel with its accumulated contents having a redundant mesentery and paralyzed by enormous distension or by inflammation, or by both, may readily be twisted more or less completely, and in some cases several times upon itself.

The weight of the bowel and its contents, along with the rapid distension of the intestine above, fixes the gut in this state of torsion and effectually prevents it from untwisting. A semi-rotation of the paretic and distended bowel about the mesenteric axis is sufficient to interfere with the supply and return of blood and provoke enteritis. Indeed, the rotation is rarely sufficiently great to produce complete obstruction, and the symptoms are frequently rather those of inflammation than of internal strangulation. For weeks before the final attack the patient usually has symptoms of intestinal disorder, such as flatulence, constipation, and spells of colic, due no doubt to the changes provoked by the elongated mesentery and bent or curved intestine. When torsion takes place the attack is sudden and the symptoms violent and urgent. Vomiting, meteorism, insuperable constipation, and frequently tenesmus, are soon followed by collapse and speedy death. The patient may die in twenty-four hours; he rarely lives beyond the fourth day. In some cases excessive tenesmus and bloody stools are seen in the early stages of torsion of the bowel. The condition may be mistaken for intussusception, but can usually be distinguished by the premonitory symptoms of twisting and by the more rapid course, the sudden meteorism, and quick collapse of the latter.

Still another way by which displacement of intestine may occasion obstruction to the passage of its contents is when a portion of the intestine has a long and narrow mesentery, and around this mesentery, which is like a pedicle, another portion of the bowel is thrown, encircling and compressing it. The accompanying figure, taken from _Ziemssen's Cyclopædia_, gives a good idea of this condition (Fig. 23). It represents a {842} loop of the small intestine placed around the mesenteric pedicle of the sigmoid flexure. Leichtenstern calls this "intertwining or knotting of two intestinal loops."

In consequence of inflammation of the peritoneum and effusion of lymph, peritoneal surfaces are joined together, and before the lymph is fully organized these surfaces are separated by the constant movements of the organs and the change in the relationship of the parts, and strings and bands of various shapes and sizes are formed in which a portion of the intestine may become entangled and constricted. Sometimes the bowel accidentally becomes engaged in a loop or noose of false membrane, or becomes bound down under a band of fibrin; or, the peritoneal surfaces of some of the organs having been joined together or to the wall of the abdomen or pelvis, a loop of bowel may escape into a slit or opening and become incarcerated; or a fold of bowel may fall into a fissure in the omentum or mesentery or broad ligament of the uterus or suspensory ligament of the liver, and become constricted; or the appendix vermiformis may be twisted around the intestine in such a way as to cause ligation of the tube, or, by becoming attached to some neighboring part, it may form a loop through which the intestine may pass and become obstructed. In the same way the bowel may be constricted by a diverticulum. (This is well shown in Figs. 23, 24, and 25.) Bands entangling the bowel and causing strangulation may be attached to the fimbriated process of the Fallopian tube or the ovary or uterus. Indeed, it is impossible to describe in a limited space the almost infinite ways in which these bands and strings may engage and incarcerate the intestinal tube (Figs. 24, 25).

{843} [Illustration: FIG. 25. An appearance of the natural relations of the diverticulum to the intestine. _a_, gastric extremity; _b_, rectal extremity.]

Internal strangulated hernia may result from the bowel falling into a pouch of the peritoneum and becoming ligated by the orifice of the pouch, or passing into the foramen of Winslow, of which there are three cases of strangulation recorded; or a retro-peritoneal hernia may be formed; or, more common still, a hernia of the intestine through the diaphragm.

In diaphragmatic hernia an opening is more frequently found in the posterior part of this muscle. Two hundred and fifty-two cases of this form of internal hernia have been collected by Leichtenstern, in which the diagnosis was made in only five cases. He found the oesophageal opening, a spot just behind the sternum, and a gap between the lumbar and costal parts of the muscle, the weakest points in the diaphragm.

Diaphragmatic and other forms of internal hernia may exist and not produce symptoms of strangulation either at the time of formation or subsequently, just as we so commonly see in cases of external hernia. When the bowel is constricted, however, and its circulation interfered with, symptoms of internal strangulation come on, and are exactly like the symptoms of external strangulated hernia. The attack is sudden, the symptoms acute and urgent, and the course and termination very rapid. Unless the constriction is relieved death may take place in twenty-four hours; life is rarely protracted beyond three or four days.

The patient has first eructations, soon succeeded by nausea and vomiting. The matter vomited consists of the contents of the stomach, then of gastric fluid, bile, and the contents of the intestines. When the last is ejected the vomiting is called fecal or stercoraceous. The patient complains of a sense of constriction about the abdomen, griping pains about the umbilicus, flatulence, tenesmus, and insuperable constipation. One or two free stools from the large intestine below the site of strangulation may be passed, but this should not deceive the practitioner. As a rule, peritonitis soon follows strangulation. The belly becomes tympanitic and tender, the pulse small and wiry, and the face anxious. When gangrene supervenes the pain subsides, the pulse becomes weak and intermittent, the surface cold and clammy, and the patient soon dies in a state of collapse. Slight delirium may precede death, or the mind remain unimpaired to the end. Very often, when gangrene sets in and pain disappears, the patient has a grateful sense of relief and is hopeful of recovery.

{844} Intussusception, Invagination.

One of the most frequent and important causes of intestinal obstruction is intussusception or invagination of the bowel; by which term is meant the protrusion or slipping of one portion of bowel into a portion immediately adjoining.

This condition is sometimes found after death in persons old or young, but particularly the latter, in whom during life there were no symptoms of intestinal obstruction or intestinal trouble of any kind. The displaced intestine in these subjects is easily reduced, is unattended by any signs of inflammation, and is evidently the result of spasmodic contraction of the transverse muscular fibres of the bowel at one part, with distension and relaxation at another part, by which, just before death, one piece of the bowel is pushed into an adjacent piece. Not unfrequently two or more invaginations are seen in the same subject. Flint[4] counted as many as fifteen in a child who died of typhoid fever. This invagination of the death-struggle almost invariably involves the small intestine, and may be the protrusion of a piece of the bowel above into a piece immediately below, or the reverse, a portion of bowel below being pushed into a portion above. It has been suggested that this slight and temporary intussusception may occur during life and give rise to temporary symptoms of intestinal obstruction, which disappear when reduction of the displacement spontaneously takes place.

[Footnote 4: _Practice of Medicine_.]

It will be seen by the diagrams that three successive portions of intestine enter into the formation of an intussusception--an entering, returning, and receiving portion. Two mucous surfaces and two serous surfaces are thus brought into apposition. The mesentery attached to the included lengths of bowel--viz. the entering and returning lengths--is necessarily pulled down with the bowel in its descent, and is also embraced by the receiving portion of the intestinal tube. The traction excited by this portion of mesentery, thus wedged in between the middle and inner layers of the bowel, materially alters what would otherwise be the relationship of the parts. Fig. 26 shows simple invagination of the ileum like the finger of a glove, in consequence of the traction exerted. The entering or invaginated portion does not always lie in the axis of the enveloping tube, but is more or less curved, until very often its lower orifice is in contact with the wall of the outer layer. The concavity of this curve looks {845} toward the mesenteric edge of the invaginated portion of bowel, and the convexity toward the opposite side of the receiving portion. The convex side of the middle cylinder is often thrown into transverse folds or convolutions. Intussusception, which gives rise to symptoms characteristic of intestinal obstruction during life, is invariably from above downward. It is doubtful whether there is on record a single well-authenticated case of inflammatory invagination where the lower segment of bowel protruded into the upper.

Reference to the diagrams will show that the lumen of the bowel is diminished, and that more or less intestinal obstruction must follow invagination. This obstruction is increased by the inflammation which necessarily follows this condition. The large and numerous blood-vessels of that portion of the mesentery involved in the invagination are compressed and stretched; arterial supply, and especially venous return, are interfered with; congestion quickly follows, with copious inflammatory exudation; the layers of intestine become swollen, and blood, sometimes in abundance, is poured out from the mucous membrane. Peritonitis, limited sometimes to the invaginated part, more often spreading to the peritoneum covering neighboring structures, soon begins, and the contiguous serous surfaces are agglutinated and the intussusception rendered irreducible. Lymph and other inflammatory products are poured out freely; the coats of the intestine become distended and thicker, and the inner and middle layers of the invagination are separated by the deposit; the invaginated part becomes more and more curved toward the mesenteric border of the outer layer; and occlusion of the bowel, begun by the invagination, is made more or less complete by the changes wrought by inflammation (Fig. 27). That intestinal obstruction is not always complete in intussusception is shown by the fact that fecal matter, often in considerable quantity, is passed through the bent and narrowed tube, the intestine retaining, at least for a time, its contractile power. The changes produced by inflammation are chiefly seen in the inner and middle layers of intestine, the receiving or outer layer of the invagination often escaping any serious damage. These changes vary with the character and duration of the inflammation. Sometimes they are limited to an agglutination of the opposed serous membranes, an effusion of blood and serum from the mucous surfaces, and an enormous distension and swelling of all the invaginated parts; or the inflammation may end in mortification of the middle or both the inner and middle cylinders, the dead part coming away in shreds or in large fragments, or, if the patient lives long enough, the entire invaginated tube being discharged through the anus. If the inflammation involves the invaginated parts unequally, strips and shreds of the bowel are detached by ulceration and sloughing, and may escape in the discharge from the bowels in pieces so small as to be unnoticed; but if the intussuscepted part dies en masse, a circular line of demarcation is formed by ulceration, and the dead segment is detached and drops into the cavity of the bowel below, and escapes through the rectum. It is often so complete that the inner and middle cylinders can be recognized, and the part of the intestinal tube to which the expelled bowel belonged can be determined. In favorable cases the blood-vessels of the healthy bowel above and below the dead segment pour out a circular mass of coagulable lymph, which, becoming organized, closes the breach and {846} completes the intestinal tube. To accomplish this it is necessary that the ends of the two portions of bowel should be accurately coaptated: if they are not, some opening may be left through which the contents of the gut may escape into the peritoneal cavity, producing fatal peritonitis; or the new formation may be imperfectly organized, and burst during some peristaltic movement of the bowel or from the pressure of gas accumulating in the gut; or the supply of lymph may be so redundant as to obstruct the calibre of the bowel, or end in cicatricial contraction, stricture, and obstruction. Aitken[5] records four instances where the curved end of the invaginated portion of bowel by prolonged pressure caused ulceration and perforation of the coats of the enclosing bowel, the invaginated portion passing through the side of the enclosing segment and projecting into the cavity of the peritoneum.

[Footnote 5: _Science and Practice of Medicine_.]

Gangrene and ulceration, however, do not always follow intussusception. The mesenteric injuries may be sufficient to produce congestion and exudation, and the patient survive the invagination for weeks, and death eventually occur without sloughing or ulceration; or spontaneous reduction of the invagination may take place and recovery of the patient follow. The last termination must be rare, and impossible when firm adhesion between the serous surfaces has taken place; but that it does exceptionally occur is proved by cases where the diagnosis of intussusception was undoubted, the invagination being felt in the rectum or seen prolapsed through the anus. The most common termination, if the patient survives, is mortification of the invaginated part and separation in mass or by shreds or fragments.

Intussusception may occur in any portion of the intestinal canal, but some points are more liable to it than others. 56 per cent. of the cases collected by Brinton were ileo-cæcal; in 32 per cent. the small intestine alone was involved; 28 iliac and 4 jejunal; in 12 per cent. the colon, including its sigmoid flexure, was the part implicated.

When the rectum is involved, it usually forms the outer layer of the invagination, the middle and inner layers being formed by the bowel which has passed from above into it; when prolapse of the rectum itself occurs, the mucous membrane is generally alone involved, but along with this the muscular coat may also descend and a true invagination of the rectum be found.

The most common variety of intussusception is the ileo-cæcal. It is in this form that we find the greatest length of bowel involved. This invagination begins generally at the ileo-cæcal valve, the lips of which at first turn toward, and descend into, the cavity of the cæcum, drawing with them the end of the ileum; in this case the valve forms the lowest point of the invagination. If the invagination continues, the end of the cæcum is next inverted; and if the process still goes on, more and more of the colon is invaginated, until in some rare cases it traverses the whole of the large intestine, appearing just above or even protruding through the anus. In this variety the vermiform appendix lies between the middle and inner layers of the intussusception, and its opening, usually stretched and enlarged by the inverted cæcum and inflammatory effusion, is found close to the ileo-cæcal orifice. In this intussusception the cæcum and colon are large and roomy, and the invaginated portion not so liable, {847} as it is when the small intestine is alone implicated, to strangulation and sloughing; nor is there seen in ileo-cæcal intussusception, unless the portion of bowel involved is very short, the marked curvature of the invaginated portion so commonly found in the small intestine. In the ileo-cæcal form it is twisted or much convoluted rather than bent.

Another variety of ileo-cæcal invagination--very rare, however--is where the ileo-cæcal orifice does not descend into the cavity of the cæcum, but the lower end of the ileum passes through the valve into the large intestine. In this instance the invaginated portion is tightly compressed by the valve, and strangulation is speedy and complete. An invagination may occur in the lower part of the ileum, and the inner and middle layers pass on to the ileo-cæcal valve, and be arrested at that point, and afterward, in consequence of violent peristaltic action, the whole intussusception, inner, middle, and outer layers, be invaginated into the colon. In this way the invagination becomes doubled.

While intussusception may occur in either sex and at all periods of life, it happens nearly twice as often in males as in females, and is most frequently seen in childhood. Leichtenstern[6] found in his statistics of 473 cases that one-half were seen in children under ten years old, and one-fourth of all intussusceptions occurred in children from four to twelve months old. Invagination of the small intestine is found almost exclusively in adults. Brinton from his records gives the mean age of its occurrence 34.6 years. According to the same author, the average age of ileo-cæcal invaginations is 18.57 years, and one-half of all cases of this form of intussusception observed by him were in children under seven years of age. Leichtenstern states that the lower part of the ileum is the most frequent site of invagination in the small intestine, and the descending colon and sigmoid flexure the most common portion involved in intussusception occurring in the large intestine.

[Footnote 6: _Op. cit._]

The mechanism of intussusception is probably not always the same. The following is thought to be the most frequent process: A segment of bowel becomes paralyzed by local peritonitis, some injury, diarrhoea, or colic, and while in this state a segment of bowel above is subjected to violent peristaltic action, and is forced into the unresisting portion below. In this case the paretic segment forms the outer or receiving layer of the intussusception. Leichtenstern believes that the paretic portion is turned in and invaginated into the normal bowel below, and that the clinical course of intussusception and post-mortem appearance correspond with this explanation. If such is the case, the paralyzed portion forms the inner layer, and the active bowel below the receiving layer. Another theory, which applies with much force to the most common of all invaginations--viz. the ileo-cæcal--is, that as violent anal tenesmus produces prolapse of the rectum, so prolonged and powerful tenesmus at the ileo-cæcal opening may cause prolapse of the lips of this orifice, and, eventually, invagination of the ileum, or of both this and the cæcum, into the colon. When we remember that the ileo-cæcal valve is furnished with a sphincter muscle, the analogy is complete. The idea so long entertained that intestinal worms may occasion invagination of the bowel has generally been abandoned. A polypoid tumor, by dragging down the portion of bowel to which it is attached, may produce invagination; and {848} Brinton's statistics give 5 per cent. of cases of intussusception from this source. An examination of a larger number of cases would probably show a much smaller percentage due to this cause.

A majority of cases of intussusception, however, take place suddenly, without previous diarrhoea, colic, traumatism, or ill-health of any kind, and probably occur without any tenesmus or paresis of a portion of bowel. It may be that the longitudinal fibres of a segment of gut contract, dilating and shortening a portion of the bowel; while this part is distended a portion immediately above may be lengthened and narrowed by contraction of the circular fibres, and violent peristalsis going on at this moment, aided, possibly, by contraction of the muscular wall of the abdomen, forces the upper and narrow segment into the lower and dilated one.

At first the invagination involves a small portion of the bowel, but, active peristaltic action continuing, it rapidly increases in size. This increase is made at the expense of the sheath or outer layer, which turns in to form the middle layer. The length of the invagination varies from two or three inches to three, four, or five feet.

The symptoms of intussusception generally come on suddenly, and indicate both intestinal obstruction and inflammation. Pain resembling violent colic, and referred to the site of the invagination, is a prominent symptom. The pain is intense, paroxysmal in character, but after a time it becomes continuous. At first pressure gives relief, but in a few hours tenderness, denoting peritonitis, appears, limited to the invagination or spreading gradually over the whole abdomen. Vomiting soon follows, and, with rare exceptions, is persistent. After two or three days occasionally blood and sometimes fecal matter are ejected from the stomach. Diarrhoea, with bloody, mucoid stools, is rarely ever absent, and is characteristic of invagination. The patient has from fifteen to twenty passages a day. If the large intestine is involved, the diarrhoea is accompanied with tenesmus. Above the obstruction gas and ingesta accumulate, and produce abdominal distension, sometimes well marked. Generally the tumor formed by the invagination can be felt through the abdominal wall, and is a symptom of great importance. Meteorism and peritonitis may render the existence of the tumor obscure or altogether prevent its recognition, but in intussusception of the colon and at the ileo-cæcal valve the solid cylindrical mass can usually be found, and frequently, when the small bowel alone is implicated, a very careful and patient examination will enable the observer to detect it. Sometimes it changes its site, size, and shape; occasionally it can be felt in the rectum or is seen protruding through the anus.

The urgency of the symptoms of invagination depends upon the portion of bowel involved and the degree of constriction of the gut and its attached mesentery. When the bowel is tightly constricted the symptoms are acute, and the patient may die in a day or two; when the bowel is not constricted the symptoms are chronic in character, and in the early stages not urgent. The difference here is like that between strangulated and incarcerated hernia.

In acute cases the attack is sudden, obstruction complete, and the symptoms those of internal strangulation of the bowel, often followed by collapse, which may destroy life in a few hours. These cases are {849} chiefly jejunal and iliac invaginations, and the higher up in the small intestine the seat of obstruction the more violent and urgent the symptoms. Constriction, being great, is followed by engorgement and inflammation of the invaginated bowel, and if the patient lives long enough gangrene ensues, by which the obstructing mass is separated and discharged en masse or in fragments through the anus. Not unfrequently life is saved in this way. That gangrene has taken place and separation of the invaginated segments is in progress are often known by the very fetid character of the evacuations and by their admixture with blood and shreds of necrosed bowel. When the sequestrum has been detached entire, it is often passed with difficulty. Frequently it lodges at some point in the bowel, producing temporary obstruction and giving rise to tenesmus and pain as it passes along the large intestine. There is no doubt that the continuity of the intestine above and below the neck of the invagination has been established, and complete cures effected in the way already mentioned. Usually, however, the patient dies from collapse, peritonitis, or perforation of the bowel before the obstructing mass can be removed by gangrene. Children almost invariably die before this can take place, and adults live from the seventh to the fourteenth day, according to the greater or less violence and acuteness of the symptoms. When the slough has been discharged and the continuity of intestine established, recovery is still uncertain, and death very often happens for reasons referred to in speaking of the separation of the sequestrum.

Separation of the invaginated portion and its expulsion, according to Leichtenstern, in the majority of cases takes place from the eleventh to the twenty-first day, but in chronic cases it is often delayed for months. According to Brinton, separation of the sequestrum occurs between the eighth and fifteenth in intussuscepted small intestine, and between the fifteenth and twenty-second days in acute cases of ileo-cæcal and colic invaginations.

In chronic cases of intussusception, which usually embrace the ileo-cæcal and colic varieties, strangulation is not common and the course of the disease is protracted. These cases often last for several months, and the symptoms are not always well defined. At first the pain is paroxysmal, with long intervals of ease. Vomiting succeeds, but is not persistent; discharge of the contents of the bowel below the seat of lesion takes place and afterward fecal matter from above this point, because the permeability of the bowel is not usually lost in chronic cases. Eventually the alvine discharges become bloody, mucoid, and characteristic of intussusception; the severity of the symptoms may gradually increase, the pain becoming greater, more constant, the vomiting more incessant, the discharges from the bowels more frequent, and in one, two, or three months the patient dies from asthenia. Several authentic cases are related where the disease lasted one or two years before terminating fatally. Very often some days before death the pain and tenderness cease, and the operations become free from blood and normal in character.

{850} Constipation.

Constipation is a prominent symptom in all of the conditions which give rise to intestinal obstruction, and habitual constipation or loss of the powers provided for the advance of the contents of the intestines not unfrequently leads to permanent occlusion of the canal. It is impossible to fix any definite rule as a standard of health for the number and quantity of alvine evacuations. Some individuals have a passage from the bowels once every day; others, in the enjoyment of as good general health, suffer from the ordinary inconveniences of constipation if they have less than two or three daily fecal discharges; others, again, apparently equally as well, have a movement from their bowels once in two or three days or once a week, or even once in two weeks. Habershon[7] records the case of a "woman sixty years old who from youth upward had had a passage from the bowels only every six or eight days, and whose health had been perfect." A lady under my own observation, for twenty years never had an alvine discharge oftener than once in two weeks, and three times in her life had passed two months without a movement of her bowels. This lady was the mother of several children, and, although not in perfect health, was able to attend to her ordinary household duties. Such cases are not very uncommon, and occur, as far as I have been able to ascertain, more frequently in women than in men.

[Footnote 7: _On Diseases of the Abdomen_, quoted by Leichtenstern in _Ziemssen's Cyc. P. of Med._, vol. vii. p. 588.]

The number of fecal evacuations and the quantity discharged have been shown by Bischoff and Voit to depend, to some extent, upon the character of the food ingested, vegetable diet producing abundant, and animal diet scanty, stools. Doubtless, the quality of the food partly explains the quantity of the alvine evacuation, although, to some extent, this must depend upon the time that the feces remain in the colon, a long residence there taking away a greater part of the watery constituents and making the fecal mass thicker and harder; but the variations in the number of stools in persons living on the same diet can only be explained by the variations in the activity of the peristaltic action in different individuals, or in the same individual at different periods and under different surroundings.

The causes of habitual constipation are of the most varied and diversified character, and it is not always possible in an individual case to point out the original or primary one. Not unfrequently several causes are in operation at the same time to produce sluggishness of the intestinal canal and constipation. Very often it begins with change of scene and habits, by which the daily visit to the water-closet is interfered with, or after confinement to bed with some temporary indisposition. It is more likely to occur in men and women whose habits are sedentary and who are constitutionally lazy and indolent. The feces are allowed to remain in the rectum and colon, and every hour after the ordinary time for going to stool diminishes the watery parts of the fecal mass and makes it harder and more consistent. Many cases of chronic constipation, begun in this way, have ended in dilatation and thickening of the intestine, ulceration of the mucous membrane, and, eventually, perforation of the coats and escape of the contents of the gut into the peritoneal cavity. Rapid {851} excretion of water by the kidneys, lungs, and skin produces constipation by withdrawing a large proportion of the water from the fecal mass, rendering it unnaturally dry and of diminished bulk. In diabetes, constipation arises from this cause unless the patient makes up the loss by drinking an unusually large quantity of water. Constipation in nursing-women is explained by the loss of water in the secretion of milk. The profuse sweating which attends malarial fever, phthisis, and other diseases readily accounts for the constipation which often accompanies these disorders.

Certain articles of food not necessary to mention here produce constipation. They fail to excite peristaltic action; or articles of diet which at first act as a stimulus to the bowels, and even provoke temporary diarrhoea, lose their power if kept up too long--just as certain purgative medicines lose their force if continued for too long a period. Gradually they cease to increase the peristaltic action, and rather add than otherwise to the inactivity of the intestines. Eating the same kind of food day after day is very apt, sooner or later, to result in diminished sensibility of the intestinal canal, a reduction of the peristaltic force, and deficiency in the secretion of the digestive juices, which in itself is a common cause of constipation. Frequent change of diet is generally needed to supply the stimulus necessary for that intestinal motion which relieves the bowels.

Bile is looked upon as one of the most powerful agents in stimulating peristaltic action, and when, from any cause, mechanical or otherwise, it is not poured into the bowel, constipation ensues. Unnatural flexures, congenital or acquired, of the large intestine are not unfrequently the source of chronic constipation. These flexures, normal or factitious, favor accumulation of feces, especially in subjects who have diminished sensibility of the bowel and a paretic state of the muscular coat. Certain injuries and diseases of the brain and spinal cord reduce, and sometimes altogether prevent, intestinal activity. Hysteria, if it exist for any length of time, is generally attended by sluggishness of the bowels, and great mental depression (melancholia) is sometimes preceded and sometimes followed by habitual constipation. In treating such a case it is important to make the distinction.

Temporary paralysis of the muscular coat of the bowel, followed by symptoms of intestinal constriction, with insuperable constipation, sometimes attends violent contusion of the abdomen. In some cases prolonged functional weakness of the muscular coat follows the injury. Many chronic diseases leave the bowel in a sluggish condition by the pathological changes produced in the intestine. The function of the muscular coat is frequently injured by the infiltration which accompanies peritonitis. The fibres are separated by the serous effusion which attends this inflammation; they become overstretched, and, losing their contractility, end in paralysis and obstinate constipation. Occlusion of the canal from this cause may last for days, and be accompanied with tympanitis, stercoraceous vomiting, and all the signs of internal strangulation, ending in death. Post-mortem examinations in such cases show no stricture or unnatural diminution in the size of the canal, but that the fatal occlusion was due to paralysis of the muscular coat of the bowel and arrest of its power.

The normal advance of the contents of the bowel is interfered with by any cause which lessens the contractility of the muscular coat. Chronic {852} diseases which debilitate the general muscular system affect at the same time the contractile power of the muscular coat of the canal, and the debility and degeneration of old age are felt here, and sometimes occasion the constipation which often accompanies this period of life. Leichtenstern[8] says that chronic intestinal catarrh is a common factor of constipation--that when this catarrh is of long standing it produces relaxation of the muscular coat and diminishes the elasticity of the intestinal walls. He believes that this pathological condition exists in a large proportion of the cases of habitual constipation attended with mental depression, that the hypochondriasis makes its appearance after the constipation has become chronic, and that it is a secondary symptom. This affection is located chiefly in the small intestine, and does not usually involve the colon.

[Footnote 8: _Op. cit._]

Probably the most common form of chronic constipation is that which accompanies loss of sensibility and muscular inactivity of the colon and rectum. The large bowel becomes sometimes so distended by the accumulated fecal masses that it has been found after death to measure ten or fifteen inches in circumference and to contain an astonishing quantity of feces. Any part of the canal, except the last two inches of the rectum, which is kept empty by the contraction of the sphincters, may be occupied by the mass, but the accumulation is greatest in the rectum, cæcum, and sigmoid flexure. At the last-named location the distension is so great that the mass can be readily felt through the abdominal walls. The tumor may be as large as a foetal head, and may be mistaken for a simple or malignant tumor of the omentum, stomach, or other organ, or for pregnancy or ovarian growth. The dilatation may be so enormous as to push the small intestines into the back part of the abdominal cavity and to interfere with the function of any organ upon which it encroaches. It may press upon the concave surface of the liver, and, arresting the flow of bile, produce jaundice or mechanically interfere with some portion of the track of the urinary organs and cripple their functions. When situated in a portion of the canal not tightly attached to the abdominal walls it is slightly movable, more or less hard and consistent, according to its duration, for it remains often for months unchanged, sometimes giving to the fingers the impression of a rather soft, easily-indented swelling with a uniform smooth surface--more often feeling like a hard, irregular, elongated, and corrugated mass of fecal balls. Contraction here and there of bundles of the circular muscular fibres of the gut produces the irregular, corrugated impression imparted to the fingers. Their shape and position may sometimes be changed by pressure through the abdominal wall. If the accumulation occurs in the rectum, the introduction of a tube or bougie is prevented by the impacted mass, which can be gotten away only by the fingers or by some instrument. The colon and rectum may be dilated to their utmost capacity with an enormous amount of feces, enough to fill a common-sized pail, and both the patient and medical attendant be deceived as to the sufferer's condition by the fact that he has his daily number of stools. The semi-fluid contents of the small intestines find their way through this mass by some irregular and uncertain track, undermining and breaking down sometimes a lump of the old fecal accumulation, which, if small in size or broken up, may pass on and {853} escape by the anus, but if large and hard may drop into the irregular and uncertain passage and permanently close it; then sudden and complete intestinal occlusion takes place, with all of its fearful consequences. If this, however, should not occur, and the accumulation is not recognized and removed, the enormous dilatation may go on until complete paralysis of the muscular coat is produced, and entire stoppage of the current of feces, with permanent occlusion of the bowel; or before this takes place ulceration may set in, partly because of the great pressure of the fecal mass upon the mucous membrane, and partly from the irritating character of the contents of the bowel. Ulceration begins, most likely, at some point where resistance is greatest, and perforation of the bowel may ensue.

SYMPTOMS.--If the accumulation occupies only a portion of the colon, as the cæcum or sigmoid flexure, the distended part may become displaced and twisted on its long axis. This condition scarcely ever happens in the large intestines except at the parts mentioned. Torsion of the cæcum rarely takes place except in persons of from forty-five to sixty years of age, while twisting of the sigmoid flexure may happen at any period of life. When distended and very heavy from the weight of feces, with probably some congenital defect about its mesenteric attachment, the sigmoid flexure may become twisted and drop into the pelvis, producing at once symptoms of internal strangulation.

Individuals accustomed to having one or more alvine evacuations a day are made uncomfortable by two or three days of constipation. A feeling of distension about the abdomen, with flatulence and heat, follows this condition, and soon afterward headache, loss of appetite, and symptoms of indigestion supervene. If this state of the bowels continues unrelieved, pressure upon the hemorrhoidal veins takes place and interference with venous return, producing congestion in the lower end of the rectum. This is attended by straining, diarrhoea, evolution of gaseous matter, colicky pains, and possibly sympathetic disturbance of the genito-urinary organs. When at last the hardened and enlarged mass is discharged, it produces some pain and burning about the anus, with possibly rupture of the mucous membrane in that region. Fissure of the anus may thus originate. In the case of a lad aged about nine years under my care fissure of the anus began in this way, and after its formation the pain of defecation was so intense that he resisted for ten days every attempt of his bowels to move. After this time he passed every day or two one or more hardened fecal balls, but always with such atrocious pain that he looked forward to the next attempt with terror. This case ended in fecal impaction, which nearly proved fatal.

Not unfrequently persons who habitually go two or three days without having a passage from the bowels are not apparently inconvenienced, and after a time any of the discomforts ordinarily felt from constipation are not noticed, if indeed any exist.

Generally, however, chronic constipation leads to a host of troubles of the most varied character. There is not an organ in the body that is not more or less influenced by it. The generation of gas in the intestines produces a sense of fulness of the abdomen and elevation of the diaphragm which interferes with the action of the lungs and heart. The sufferer is oppressed, sighs, and has difficult respiration and attacks of {854} palpitation of the heart. The influence of the abdominal pressure is conducted by the sympathetic nerves to the brain, and the patient frequently has vertigo, headache, ringing in the ears, faintness, etc., and in consequence of the pressure upon other nerves or of hyperæmia of the spinal cord and its membranes he has dull aching pains in his back, groins, genitals, or extremities. I have seen in several instances pain in the legs, coming on after the patient has retired and lasting until morning, violent enough to prevent sleep, at once permanently relieved by an active cathartic after antiperiodics, alteratives, and anodynes had failed to do any good.

A patient suffering from habitual constipation usually obtains temporary relief by the bowels acting either spontaneously or after a dose of medicine; but, the causes of constipation continuing, the physical discomforts and suffering continue, varied in every conceivable way. His digestion being disturbed, appetite poor, and assimilation imperfect, he gradually loses flesh and his complexion becomes sallow and unhealthy. In addition to this, he soon grows irritable and fretful, trifling affairs trouble him, he has fits of great mental depression, and soon settles down into hypochondriasis, his life becoming a burden to himself and a nuisance to his friends.

If the constipation ends in fecal accumulation, the worst symptoms of mechanical obstruction may present themselves at any time, and death of the individual follow. The practitioner should always keep this fact in mind in treating every case of intestinal obstruction, and search for fecal impaction by examining the rectum and the whole length of the large intestine through the anterior abdominal wall. Very often symptoms of impaction come on gradually in one who has been ailing for some weeks or months, but sometimes the onset is as sudden as in a case of acute occlusion of the intestines. The patient is seized with pain like that of colic and an urgent desire to empty his bowels, but all attempts to do this are futile, and the straining is followed by great exhaustion; borborygmus, nausea, vomiting, and possibly hiccough, soon come on, with tympanitic distension of the belly. If the impaction is not overcome, death by collapse or from peritonitis follows. Post-mortem examination shows enormous fecal accumulation, peritonitis as a consequence of the obstruction, perforating ulcer in some part of the large bowel, more often the sigmoid flexure, or, in some cases, absolute rupture of the cæcum itself, and escape of its contents into the peritoneal cavity.

Stricture of the Bowel.

In a report by George Pollock[9] of 127 cases of intestinal obstruction, 77 belonged to the above class; and Brinton, in his analysis of the whole group of cases collected by him, says stricture constitutes about 73 per cent. In 124 cases of intestinal obstruction reported by Mr. Bryant[10] from the post-mortem records of Guy's Hospital, 47 were found to be stricture of the bowel. The above statements show that stricture, or diminution of the calibre of the bowel, is the most frequent cause of {855} intestinal obstruction, and the subject is worthy of our earnest consideration.

[Footnote 9: _Medico-Chirurgical Review_, 1853.]

[Footnote 10: _Practice of Surgery_.]

While stricture of the bowel may be found in any portion of the intestinal canal, it occurs most frequently in the sigmoid flexure and rectum. Brinton found in 100 fatal cases of stricture 30 in the rectum and 30 in the sigmoid flexure; only 8 cases in 100 were in the small intestine. Brinton's statistics correspond very nearly with those of other writers. The affection is more common in men than women, and the average age at death is about forty-four years.

The most common cause of stricture is contraction following cicatrization of ulcers of the mucous and submucous coats of the intestine. The ulcer may involve the circumference of the bowel, and the resulting cicatrix terminate in uniform constriction of its lumen, or the ulceration may extend several inches along the side of the intestine, ultimately causing contraction in the direction of its longitudinal axis, marked stenosis, and kinking of the gut. When ulceration, continuous or in patches, involves a large extent of bowel, it may reduce the gut to a mass of indistinguishable cicatricial tissue. Bristowe[11] says he has seen the whole cæcum thus contracted "into a channel barely capable of admitting a goose's quill."

[Footnote 11: Reynolds's _System of Medicine_.]

Stricture of the intestine often follows dysentery or tubercular and syphilitic ulceration of the bowel. Follicular or hemorrhoidal ulceration is sometimes the beginning of a stenosis which ends in stricture of the rectum. Stercoral ulcers of the colon are not unfrequently the starting-point of cicatricial contraction of the calibre of the bowel. Sometimes, but rarely, ulcers of typhoid fever end in constriction of the intestinal tube. The diameter of the gut is also contracted by the effects of caustic substances, by ulceration following the lodgment of foreign bodies, and by effusion of lymph or thickening attendant upon long-standing hernia. Very often after death it is impossible to determine what particular kind of inflammation and ulceration caused the stricture. Generally, the cause which provokes the ulceration sets up chronic peritonitis, which materially aids in producing the obstruction. Spasm of the circular muscular fibres usually accompanies these lesions, and materially contributes in many cases to fatal intestinal obstruction. Some authors assert that spasm without organic change can produce acute obstruction: such an occurrence, except possibly in the rectum, must be very rare, if indeed it ever happens.

The most common cause of stricture is cancer. This disease may originate in the bowel itself, or, beginning in some neighboring organ or tissue, gradually spreads and involves the gut. It may extend around the bowel or be infiltrated along the sides of the canal for several inches, and may be scirrhous, medullary, or epithelial in character. Eighty per cent. of the cases of cancer of the bowel are situated in the rectum. Usually, but not invariably, cancerous deposits are found in persons who have passed middle age.

An impediment to the passage of fecal matter is invariably produced in constriction of the intestine from the above causes, and it frequently continues until fatal occlusion occurs. The contents of the bowel accumulate above the block, producing distension of the gut and thickening of the muscular coats above the stricture, with contraction and atrophy {856} of the portion of intestine below. Dilatation of the bowel above the seat of lesion is sometimes great enough to cause rupture and peritoneal extravasation, or distension and stretching of the coats of the canal may be sufficient to interfere with its circulation, and ulceration ensue.

Occasionally cases of stricture or well-marked circumscribed contraction of the bowel are seen which give rise to no marked symptoms of constriction during life. Such was the case in the instance related by Bristowe and referred to above. These instances are, however, exceptional in the large intestine.

Symptoms of stricture vary according to the site, cause, and extent of the lesion. They are gradually developed, and in this respect are unlike the symptoms of internal strangulation or of intussusception, which are generally acute and rapid in their course. When the obstruction in stricture is complete, progress toward death is comparatively slow. If the stricture is seated in the small intestine, the symptoms are often so obscure that for a long time the presence of the contraction may not be suspected; the contents of the small bowel are usually fluid, and in this state readily pass through the constricted part. The more solid the contents of the bowel, the greater the difficulty in passing a contracted and narrow orifice, and the more conclusive and characteristic the assemblage of symptoms of obstruction from stricture.

The history of a case of intestinal obstruction from stricture is often instructive. For weeks or months there have been colicky pains and intestinal disorder; possibly, in the early stages, diarrhoea, but later marked constipation, and probably previous attacks where constipation was for a time insuperable and death from obstruction imminent. Hemorrhage, except in cancer or when complicated with piles, is rare. The attack may come on suddenly, or constipation become more and more difficult to overcome; violent peristalsis presents itself, accompanied by pain and abdominal distension, and followed by nausea and vomiting, the latter often being stercoraceous. During the throes of pain--for it is paroxysmal--the outline of the distended gut can be felt and seen through the abdominal walls if they are thin and free from fat. Unless the stricture is relieved the patient gradually dies from asthenia. Inflammation is often absent throughout, but enteritis or peritonitis may come on, or perforation and peritoneal extravasation ensue and hasten the fatal termination.

When the obstruction is in the rectum it can be felt with the finger; if in the sigmoid flexure, it may be felt with a gum bougie or probe, but the use of the former is unreliable, and the latter, unless carefully employed, dangerous. Obstruction at this point, however, is attended with marked distension of the descending and transverse colon. If seated in the small bowel, the large intestine is flaccid and collapsed. Careful manual exploration often enables the practitioner to determine the site of the contraction. Weight, pain, dulness, and fulness are usually found about the stricture, but these signs may be of little value when the abdominal wall is thick and unyielding, or peritonitis or tumor is present, or the contracted portion of bowel is compressed or drawn out of its proper site. Brinton suggests that the site of stricture may be determined by the quantity of water which can be injected through the anus into the bowel. Such an estimation must often be erroneous, as stricture {857} is rarely ever complete and fluid may be forced through the constricted part. Indeed, Battey of Georgia has demonstrated upon dead and living subjects that fluid may be made to pass through the entire canal from the anus to the stomach.

Obstruction due to cancer of the rectum can be determined by digital examination. When seated in the small intestine or higher up in the large bowel, the presence of a painful tumor, preceded for weeks by evidences of impaired nutrition, emaciation, and followed by lancinating pain, cancerous cachexia, etc., will indicate the character of the trouble.

Compression and Contraction of the Bowel.

Obstruction of the bowel is sometimes occasioned by compression or traction exerted on the intestine by abdominal tumors or cysts. Fibrous tumors of the uterus, ovarian cysts, hydatid growths, or indeed any form of abdominal tumor, may by pressure on some part of the intestinal track produce fatal obstruction. Several inches of bowel may thus be compressed and rendered impervious, or if traction is exerted by the tumor, which is often adherent to the bowel, the tube may be sharply bent or twisted and its action interfered with. A case is reported of compression of the bowel from a great accumulation of fat about the colon. Adhesions of intestinal coils from chronic peritoneal inflammatory changes constitute a large and important class of cases of intestinal obstruction. This condition is known as contraction of the bowels: 23 of the 124 cases reported by Bryant were of this character.

The usual site of stricture is the large bowel: contraction is far more frequently seen in the small intestine, and is caused by an effusion of lymph following simple peritonitis or the inflammation attending the formation of cancer or tubercle of the peritoneum. Coils of intestine are matted together or to neighboring parts in this way by bands of lymph or false membranes, and the action of the bowel interfered with or obstructed. Constriction of a length of bowel may be found after death, or a sharp, angular bend by which complete obstruction has been produced.

Circumscribed peritonitis may produce adhesion of a portion of bowel by bands of lymph to the uterus or its appendages, or to some part of the large intestine, or to the abdominal wall, and the action of the bowel become embarrassed by traction, constriction, or bending. In consequence of the irritation following this condition, spasmodic contraction may follow and add to the difficulty, or enteritis may ensue; and this will especially be the case if the circulation of the part is interfered with, and render complete what before was a partial obstruction. Distension and fulness of the bowel above the obstruction, with contraction and emptiness of the portion of the gut below, are found after death in cases of contraction, just as we see in fatal cases of stricture. The history of the case and presence of a tumor will generally enable the practitioner to determine when obstruction is due to the presence of some adventitious growth. When contraction is complicated with the presence of tubercle or cancer, symptoms attending these conditions will be present.

Obstruction of the intestines from contraction generally comes on {858} insidiously. The patient may date the beginning of his trouble from an old attack of circumscribed peritonitis which probably took place weeks or months before. He has attacks of colicky pains, indigestion, and constipation. The last is difficult to overcome, continuing for hours before it is relieved by medicine or the efforts of nature. During the attack of almost insurmountable constipation violent peristaltic movement of the bowel above the impediment may be noticed. The patient may gradually become more and more feeble from suffering and interference with nutrition, and die from exhaustion, or fits of obstinate constipation may continue to recur, until finally one of them becomes insuperable and fatal.

The symptoms of contraction closely resemble those of stricture, but it is important to distinguish one from the other, as the treatment, especially if surgical interference is demanded, is very different. A rigid analysis of all of the signs will usually, but not invariably, enable the practitioner to make the distinction.

There is an important difference between the constipation of stricture and that of contraction. In the former the difficulty is in defecation, emptying the large bowel, the usual site of stricture; in the latter the difficulty is in the passage of the contents of the gut along the narrowed and contracted small intestine, the common site of contraction. In stricture the calibre of the bowel is diminished by some sharply-defined mechanical impediment seated in the cavity or in the walls of the tube; in contraction the bowel is bent or kinked by adhesions, or coils of intestine are matted and glued together and peristalsis interfered with. In stricture defecation is difficult and painful; in contraction the alvine discharges are painless. In the former blood and mucus are not unfrequently seen in the feces; in the latter the motions are healthy. In stricture constipation alternates with diarrhoea; in contraction looseness of the bowels is rarely seen. In stricture distension of the abdomen is lumbar and epigastric; in contraction the distension is less and is central and hypogastric. In both conditions violent distinct peristaltic action is seen during a fit of constipation, and in both the bowel above the constriction is distended and hypertrophied. In contraction the powerful, writhing peristalsis involves the small intestine above the impediment, and in stricture the large bowel above the obstruction. In both stricture and contraction inflammation of the bowel and peritoneum may supervene. In contraction, when inflammation sets in or when enteritis and peritonitis are absent and the attack of constipation is insurmountable, I have noticed that the symptoms are more urgent and rapid in their course, and danger of death from collapse greater, than when these conditions exist in stricture.

DIFFERENTIAL DIAGNOSIS.--In every case of intestinal obstruction a careful examination should be made for external strangulated hernia. All of the regions of the abdomen in which hernia may occur should be thoroughly inspected, as the symptoms of the two conditions are identical. A small or incomplete external strangulated hernia may easily be overlooked. An individual with an old hernia may suddenly have symptoms of intestinal obstruction, and it may be doubtful whether the obstruction is due to internal constriction or to the external hernia. Diagnosis is especially difficult when the chronic hernia is irreducible in character. If the cause {859} of the impermeability is internal and below the external hernia, that portion of intestine in the hernial tumor becomes swollen, tense, and hard, and closely resembles the local symptoms of strangulated hernia. If the external hernia is reducible, reduction en masse may take place and a retro-peritoneal hernia be formed. When the case is doubtful and urgent, an operation for strangulated hernia should be performed.

Functional obstruction of the bowel is sometimes seen, closely simulating obstruction from one of the structural changes mentioned. Cases of functional obstruction are seen usually in hysterical or nervous women, and are generally recognized by the history, course, and termination of the malady. The fact that local enteritis, peritonitis, or typhlitis, by paralyzing a portion of the bowel, may produce all the signs of acute and complete obstruction, should not be lost sight of.

In cases of congenital stricture or malformation, or the presence of foreign bodies in the intestine, or acute internal strangulation, or twisting of a length of bowel, and generally in intussusception, symptoms of acute obstruction are present. The individual may have been in perfect health, and suddenly symptoms of the gravest character set in. Intense pain, referred to some special part of the belly, is the first sign of trouble. Nausea soon follows, and with it great prostration; the depression of vital power approaches, and sometimes reaches, syncope; the patient rolls and tosses in agony; his mental distress is equally great, and if old enough he is conscious of his danger and is anxious and despondent. Vomiting succeeds the nausea: at first the contents of the stomach, and then those of the small intestines, are thrown up; after a time the vomiting is stercoraceous. The belly becomes swollen, tympanitic, and exquisitely tender; the weight of the bed-clothes or the slightest touch of the finger upon his abdomen is intolerable; he keeps his head and shoulders raised and his lower limbs retracted to avoid pressure of the abdominal muscles. Constipation is complete and insuperable. If the abdominal wall is thin, the violent motion of the intestines can be seen and felt through it. These painful peristaltic movements of the bowel are paroxysmal and attended by loud rumbling or gurgling noises. The pain gradually increases; the patient is very restless and complains of great thirst; his pulse is small, hard, and frequent, his extremities cool and features pinched. If not soon relieved, exhaustion comes on; he has muttering delirium, cold clammy perspiration, hiccough, twitching of the tendons, and death soon follows from collapse or from peritonitis or gangrene, or from both. The average period of death is from six to eight days. It may occur in thirty-six or forty-eight hours, or the patient may last for two weeks.

In congenital occlusion and malformation the history of the case, the age of the patient, and the fact that the deformity in such cases is almost always confined to the anus and rectum, usually render the diagnosis sufficiently easy.

Obstruction caused by foreign bodies impacted in the intestines can generally be diagnosed. The history of the case may show that foreign bodies have been swallowed or that the patient has been subjected to some of the conditions which cause the formation of enteroliths. These stony concretions are usually found in the cæcum or colon, and frequently give rise for days and weeks to symptoms of indigestion, emaciation, {860} constipation, and other evidences of bad health before complete occlusion of the intestine takes place. Not unfrequently, before the sudden attack of impermeability of the bowel the patient has had repeated attacks of typhlitis, and has been conscious for a long time of the presence of a tumor in the region of the cæcum or colon. Possibly he has passed on some former occasion pieces of the stony concretion.

Diagnosis of obstruction by gall-stones is often aided by the fact that the patient has recently suffered characteristic pains of hepatic colic and by the icterous condition of the skin. Possibly the individual has suffered repeated attacks of hepatic trouble and has previously passed a gall-stone. Obstruction from this cause is seen four times as often in women as in men, and always after the middle period of life.

In obstruction occasioned by internal hernia or the presence of membranous bands, loops, mesenteric pouches, the symptoms are often such as to baffle all attempts at accurate and certain diagnosis. The onset of the symptoms is sudden and the course of the disease rapid; prostration of vital power is extreme, sometimes amounting to syncope; vomiting incessant and persistent; pain constant and fixed. The most characteristic symptom of internal strangulation is the very great and prolonged depression of vital power; it occurs generally in early adult life.

Erichsen states that in twisting of the bowel the abdomen is unevenly distended, it being tympanitic on one side and flattened on the other. This condition of the bowel is usually seen after middle age. In intussusception the principal signs are, usually, the early age of the patient--obstruction from other causes in children being rare--the suddenness of the onset of symptoms, the frequent desire to go to stool, the tenesmus, and the characteristic bloody mucus discharges. By abdominal palpation frequently the sausage-like tumor can be recognized, and very often the intussuscepted part can be felt in the rectum or seen protruding through the anus. When invagination involves the upper part of the small intestine, diagnosis of the cause of occlusion is almost impracticable.

In obstruction of the bowel from fecal accumulation, inflamed and thickened intestine, stricture, compression and traction, and contraction of the gut from cancerous deposit, the symptoms are gradually presented and chronic in character. They are unlike the signs of acute obstruction, which occur in persons apparently in perfect health and are sudden and violent from the beginning. In chronic obstruction of the intestine the patient has probably been complaining for some time, with symptoms of abdominal trouble. He has been unwell for weeks, his appetite poor, digestion disordered, strength diminished, and bowels constipated. The last symptom is the most distressing of all. Purgatives do not give the relief ordinarily obtained, but add to the griping, colicky pains, nausea, and general depression. When his bowels do act, the stool is sometimes liquid, sometimes very hard (scybalous), or the form of the matter passed is tape-like or pipe-like. Sometimes, in his frequent attempts at stool, the only discharge is blood and mucus or pus. Attacks of eructation and vomiting often take place during the progress of the disease. Stercoraceous vomiting is, however, rare, and only seen in the later period of the attack. Abdominal distension is slow in making its appearance, but after a time is well marked, and due more to tympanitis than to {861} constipation; the tympanitic distension is accompanied by loud rumbling and gurgling noises in the bowels. After a period which varies much in different cases, inflammation, suddenly or gradually, is set up, and all the symptoms of acute obstruction are presented, grafted on signs of chronic occlusion. We have pain, nausea, vomiting, great distension and tenderness of the abdomen, peristalsis plainly seen and felt if the abdominal wall is thin, the small, frequent, wiry pulse, clammy perspiration, prostration with hiccough, tendinous twitchings, and death, very like that following a case of external strangulated hernia.

Obstruction due to fecal accumulation generally happens in persons who have passed middle age, and can often be diagnosed by digital rectal examination and palpation of the abdomen, by the presence of fecal tumors, and the history of long-existing constipation with its manifold consequences; previous attacks of impermeability, and relief by discharge of enormous masses of feces.

Obstruction caused by the presence of some abdominal tumor is generally known by the history of the case, the fact of the existence of the tumor being known to the patient or discovered by the physician by an examination through the abdominal walls or through the vagina or rectum. The progress of such cases is essentially chronic, but acute symptoms may at any time come on. Diagnosis of obstruction due to stricture is frequently made by examination of the rectum and sigmoid flexure, the usual sites of constriction from this cause. Complete occlusion from stricture is almost always preceded by well-marked premonitory symptoms.

When the obstruction is situated in the lower part of the colon and rectum, its precise seat can be determined by digital or manual examination or the use of a bougie or tube. When the site of obstruction is above the sigmoid flexure, it is difficult, and occasionally impossible, to determine its exact locality. As a rule, when the constriction is in the small intestine the symptoms are acute and urgent; pain is intense, vomiting comes on soon, and prostration is early and extreme. When the large intestine is involved, except in volvulus, the symptoms are generally chronic. In twisting of the gut the symptoms are rapid and uncommonly severe. The higher up the obstruction, the earlier stercoraceous vomiting begins. Above the constriction the bowel is distended and tympanitic; below the constriction it is generally collapsed. In obstruction of the large intestine the outline of the tympanitic and distended gut may be traced with the eye and hand. In constriction of the small intestine the secretion of urine, as has been shown by Hilton, G. Bird, and Barlow, is less than where obstruction is seated in the large bowel. Besides rectal and vaginal examinations, which should never be neglected in any case of intestinal obstruction, abdominal palpation may also aid in determining the site of constriction. It should not be forgotten, however, when a tumor is found--as, for instance, in invagination--that the bowel may be displaced; a distended cæcum may be pushed into and occupy the left side of the belly. Cases are not uncommon where the symptoms are so combined and uncertain as to render accurate diagnosis of the site of obstruction impracticable.

Very little light is thrown upon the diagnosis by pain, constipation, or vomiting when these symptoms are considered separately. Pain is common to many diseases of the abdomen; obstinate constipation, lasting for {862} days and weeks, is often seen where there is no mechanical obstruction; and vomiting attends many morbid conditions of the body. But when these symptoms are combined and examined along with the history of the case and mode of invasion, they are often characteristic of constriction of the intestine. Pain in acute obstruction is fixed, umbilical, and intermittent; in chronic cases it is more diffused and increases with the distension. In acute cases constipation is complete and insuperable; in chronic cases this symptom gradually increases; in intussusception we have frequent discharges of a dysenteric character, and hemorrhage, sometimes copious, when the small bowel is involved. The bowel below the seat of complete constriction may be full of fecal matter, and the discharge of this spontaneously or by the aid of enemata may induce the attendant not to regard the case as one of occlusion. Stercoraceous vomiting, as a rule, comes on early in acute and late in chronic cases of complete occlusion of the gut; in spasmodic ileus or impermeability not due to mechanical occlusion feculent vomiting is only occasionally seen.

The duration of life in acute intestinal obstruction varies very much in different cases: death may ensue in a few hours or not for ten or twelve days; the average period is six days. The duration depends upon the site of the constriction and the mechanical injury to the bowel; the nearer to the pylorus the constriction, the more rapid the progress. In volvulus involving the sigmoid flexure, when injury to the bowel is great, the symptoms are acute in the extreme. After peritonitis or enteritis begins, progress toward a fatal issue is very rapid, the patient rarely living more than three or four days. In occlusion from stricture, compression, fecal impaction, and chronic intussusception the patient may live for weeks or even months.

The statistics of Leichtenstern show that from 5 to 10 fatal cases of intestinal obstruction occur every year among every 100,000 inhabitants; and according to the mortuary records of England an average of 1 death from this cause is seen in every 260 deaths. Brinton reports 1 death from intestinal obstruction in every 280 deaths; his statement is based upon 12,000 promiscuous autopsies. The first author states that the statistical reports of the general hospital of Vienna inform us that out of 60 cases of ileus, 6 or 10 per cent. recovered. This report, however, is too meagre to be of much value. From Brinton's statistics of 500 deaths from obstruction we find that out of 100 cases, 43 are intussusception, 17 stricture, 4.8 impaction of gall-stones, 27.2 internal strangulation, and 8 torsion.

TREATMENT.--There are few conditions of the body which cause the practitioner more anxiety and embarrassment than cases of intestinal obstruction, and when the precise seat and nature of the occlusion are not known the treatment is almost entirely empirical. The distinction, however, between acute and chronic cases of obstruction of the bowels, or of acute supervening upon chronic symptoms, can almost always be made, and a patient investigation of the history of the case, the mode of invasion, and a rigid analysis of all the symptoms presented will generally enable the attendant to come to some positive conclusion as to the cause and site of the occlusion. One fact in the treatment which cannot be too strongly impressed upon the mind, especially of the young practitioner, is not to use purgatives and irritating enemata, formerly so much in vogue, {863} in the hope of forcing a passage through the occluded bowel. The patient is urgently solicitous for medicine which will open his bowels, but the use of purgatives to overcome internal strangulation is as senseless and hurtful as when used to overcome the constipation of external strangulated hernia. These agents only add to the nausea, vomiting, pain, and peristalsis. The latter is violent enough already to render coils of intestine visible, and with every paroxysm is adding to the entanglement and impermeability. It is said that cathartics in some instances have unlocked the bowel in intestinal obstruction: these cases are exceptional, and many of them were probably functional and not structural in character. The only exception to the rule of avoiding purgatives is as stated by Jonathan Hutchinson: "In certain cases when impaction of feces is suspected, and in cases of stricture when fluidity of feces is desirable."

Formerly, some of the best practitioners resorted to the exhibition of one or two pounds of quicksilver, in the hope of overcoming intestinal obstruction by the weight of the metal. This plan has properly been almost if not quite abandoned. Crude mercury is very slow to reach the obstruction, is divided into small portions by the peristalsis, which its presence increases, and if it should finally arrive at the point of constriction in any considerable quantity, it is more liable to add to than overcome the difficulty.

The great remedy in intestinal constriction is opium, in large or small and repeated doses. Its use arrests the vomiting, stops the pain, and quiets the violent movements of the bowel. Very often by it the intestine is preserved and the life of the individual saved. No special dose can be prescribed: it should be administered until slight narcosis is obtained and pain and vomiting cease. Small doses of morphine, given hypodermically and quickly repeated, is the best plan of exhibiting it. It may be given by the stomach, but under such circumstances it is apt to be rejected, or if retained absorption goes on slowly, or possibly not at all. If for any reason its hypodermic use is impracticable, it had better be given by the rectum. Opium lessens the danger of death from collapse: it gives nature an opportunity to untwist the gut in volvulus, or to unroll it in intussusception, or to cut off the invaginated part by gangrene; and in internal hernia, morbid adhesions, strangulation by bands of lymph, stricture, and other forms of obstruction, it diminishes violent peristaltic action, postpones inflammatory infiltration, fixation of the strangulated portion, and keeps the parts in better condition for operative interference, which in many cases offers the only hope of relief. To carry it farther than slight narcosis and arrest of the most painful symptoms of obstruction is an abuse of the remedy. By such abuse the symptoms will be masked and both patient and practitioner deceived.

When obstruction is due to fecal impaction or spasm, the opium treatment is still often indicated. Not unfrequently, after pain and vomiting are relieved and slight narcosis kept up for some hours, the bowels relax and spontaneous evacuation takes place. If not, discharge of the contents of the bowel should be assisted by the administration of castor oil, calomel, or repeated enemata of warm water. These agents should not be used, however, as long as there is pain, tenderness of the belly, or any evidence of peritonitis, but the opium treatment continued until all signs of inflammation have disappeared. It has been proposed to give {864} belladonna in place of opium; in small doses and carefully watched it may be added to the opium, but should not be substituted for it.

The local application of ice-water or pounded ice to the abdomen has been recommended; and it is asserted that the danger of general peritonitis is lessened, and that the strangulation itself has disappeared, under the influence of cold. If, however, cold increases pain and peristalsis, it should be abandoned. The local application of moist heat or fomentations will more probably do good and give a grateful sense of relief to the sufferer. General bleeding should never be resorted to, and the use of leeches, except to ward off or subdue some local inflammation, is of doubtful expediency. Blisters, ointments, and cups are useless in such an emergency. Cracked ice, strong coffee, and carbonated water in small quantities are valuable in allaying thirst and nausea.

Cases are reported where obstruction of the bowels has been overcome by the use of electricity; both the continuous and induced currents, but chiefly the former, have been used; its value in such cases is improbable.

Abdominal taxis or massage has been earnestly recommended and frequently practised in cases of constriction. Successful results from this procedure have been reported. It has been attempted while the patient was in a warm bath or under chloroform or while taking large enemata of warm water. Abdominal traction by the use of large cups to the belly has also been advised. We can only hope for success from these measures in the early stages of obstruction, before inflammatory action or fixation of the strangulation has taken place, and any attempt of this kind should be made with tact and gentleness. Inversion of the body has also been suggested.

The injection of large quantities of warm water into the bowels to overcome obstruction should never be omitted before resorting to operative interference. The author has seen this plan in five or six instances succeed after all other means had failed. Simple warm water should be used, introduced by means of the common Davidson or a fountain syringe. The injection should be made slowly, with occasional intervals of rest, to allow the fluid time to pass through the intestinal coils. During the operation the patient should be in the knee-elbow or Sims's left lateral position, and under the influence of an anæsthetic. One or two gallons of water may be used. In place of water, the bowel may be inflated with air, introduced by a pair of common bellows to the nozzle of which a piece of India-rubber tubing is attached. The addition of castor oil, turpentine, carbonic acid gas, and other irritants will more likely detract from than add to the efficacy of these measures. In chronic intussusception, or in acute cases when fixation of invagination is believed to have taken place, and especially when inflammation is great, gangrene threatening or in existence, injections of air or water should not, of course, be attempted.

In invagination, when the intussuscepted part is low down in the rectum or protruding from the anus, replacement by fingers or sound should be tried; reduction begun in this way may be completed by injections of air or water. The propriety of introducing the whole hand into the rectum is very questionable. In occlusion of the gut by compression and traction the cause should be found, and, if possible, removed. An abdominal or pelvic tumor may be pushed out of the way of the compressed bowel, a cyst punctured, a displaced womb replaced.

{865} Great care should be taken to support the strength of the patient by concentrated and nutritious food, and in the later stages by stimulants. When the bowels are distended by gas an injection into the rectum of ten grains of sulphate of quinia will often give marked relief.

It has been proposed to tap the distended gut with a fine trocar when accumulation of gas is enormous, causing dyspnoea and great general distress; temporary relief is often obtained by this plan, which is an imitation of a common practice among veterinary surgeons. Something more than temporary relief may, however, follow the tapping. In twisting of the bowel, in internal strangulation by band or loop or ring, and in some cases of invagination, the constriction is kept up by the enormous gaseous distension. The obstruction is continued as much by causes within as without the intestine. When tapped and the gas drawn off, the bowel collapses, and may escape from its constriction and return to its natural condition. Tapping is not always certain or safe. The trocar or aspirating tube may pass between the convolutions and no escape of gas take place, or it may be followed by fecal extravasation into the peritoneal cavity. Notwithstanding the risk, the plan is a valuable one, and in suitable cases should be resorted to.

SURGICAL TREATMENT.--In cases of acute obstruction of the bowel from bands of lymph, diverticula, internal hernia, slipping of a portion of gut into some opening, or twisting, when the treatment suggested has been tried and fails, laparotomy should be performed; that is, the abdomen should be laid open, the cause of the obstruction searched for, and, if possible, removed. In acute cases a few hours, at most one day, may be spent in trying the medical means recommended. After that time, if the patient is not relieved, the sooner laparotomy is resorted to the better the chance to save life. Acute internal strangulation of the bowel from these causes has the same symptoms, course, and termination that acute external strangulated hernia has. It demands the same treatment--removal of the cause of the constriction. Delay in performing the operation in the former is as certain to be followed by peritonitis, gangrene, and death as it is in the latter; and the surgeon who hesitates to open the abdomen and attempt to remove the constriction in a case of acute obstruction after a fair trial and failure of medical measures, is as culpable as the one who delays the operation of herniotomy for unrelieved strangulated hernia.

In rare instances spontaneous self-reduction of external strangulated hernia takes place; the cases are exceptional, and the fact is no apology for postponing herniotomy. So in occasional instances acute internal strangulation is spontaneously relieved; here too the cases are exceptional, and the occurrence should be no excuse for delay in laparotomy. To justify the operation it is not necessary that the precise site and nature of the mechanical impediment should be determined, although this can usually be done. It is only necessary to know that the cause of the acute obstruction is not enteritis or peritonitis, but a constriction mechanical in character, which no medicine or manipulation or expectant treatment can relieve. When diagnosis is clear and laparotomy is indicated to save or prolong life in intestinal obstruction, the aid of the surgeon should at once be invoked. Delay is fatal. Peritonitis beginning or in actual existence makes abdominal section more dangerous and {866} lessens materially the chances of recovery. To make the operation absolutely the last resort when the bowel is injured beyond repair, when peritonitis is in full progress, gangrene threatening, or the patient on the verge of collapse, is a useless cruelty to the sufferer and his friends, and only serves to bring surgery into disrepute. If the truth were known, many of the cases of death following laparotomy should be ascribed not to the fact that the knife was used, but to the fact that it was used too late.

In intussusception not relieved by medical means the propriety of abdominal section is questionable. The subjects of this condition are usually children. Dislodging the invaginated bowel is not always practicable, and the opium or expectant treatment may end in spontaneous cure by the bowel righting itself or by sloughing of the intussuscepted part. It is doubtless true that many of the so-called cures from the latter process subsequently die from contraction of the cicatrix at the site of the separation of the slough. In 43 cases collected by Ashhurst of laparotomy for invagination, 13 recovered and 30 died. The record is bad, and to some extent the heavy mortality is due to the fact that the operation was put off too long--delayed in acute cases until sloughing had taken place, and in chronic cases until adhesion of the invaginated parts had occurred. Indeed, some of the cases reported were moribund when the operation was undertaken. Recently many successful cases have been reported, and it is fair to presume that the percentage of recoveries in the future will be greater than they have been in the past.

In acute intestinal obstruction due to bands, internal hernia, volvulus, or the presence of foreign bodies, as gall-stones, there is no question that laparotomy should be performed after other measures for relief have been employed and failed. Death in such cases is inevitable and imminent, and operative interference should not be postponed until peritonitis has set in. After the abdominal cavity has been opened the distended gut can easily be found and the fingers of the operator carried on down until the site of the constriction is reached and the cause of the obstruction discovered. If the constriction is due to the presence of bands or adhesions, they should be cut or broken up and the gut relieved. If an internal hernia is found or a portion of bowel has slipped into some fissure or pocket, it should be withdrawn and the parts restored to their natural position. If the cause of the obstruction is a volvulus, the bowel should be untwisted. If a foreign body is felt impacted in the bowel and closing it, unless it can be readily and without danger of lacerating the coats of the gut pushed on by the fingers of the operator until it has passed the ileo-cæcal valve, the foreign body should be removed from the bowel by an incision and the wound in the bowel afterward closed by sutures. If the case is one of intussusception, the invaginated parts should be pulled out: this is practicable where adhesions are absent or slight, but if the adhesions are very firm, and it is impossible to restore the parts to their natural position, the gut should be laid open above the occlusion, the edges of the opening should be attached to the margin of the external wound, and a fecal fistula established. If the case of acute obstruction be due to stricture of the small intestine, which is exceedingly rare, the gut may be laid open, and the patient recover with fecal fistula, or entorectomy or resection of the diseased part of the gut be resorted to. The operation of entorectomy has been recommended by many {867} surgeons, and a large proportion of the cases reported recovered. In one case by Koeberle six and a half feet of the gut were successfully excised.

The following table by Ashhurst[12] shows the results of laparotomy. It will be seen that in 230 cases 68 recovered:

| | Result | | | | not | | | | ascer- | Recov- | | Cases. | tained. | ered. | Died. ---------------------------------+--------+---------+--------+------ Operations for-- | | | | Volvulus | 14 | 1 | 4 | 9 Strangulation continuing after | | | | herniotomy or taxis | 18 | ... | 6 | 12 Invagination | 43 | ... | 13 | 30 Foreign bodies, impacted | | | | feces, gall-stones, etc. | 18 | 1 | 7 | 10 Strangulation by bands, | | | | adhesions, or diverticula | 76 | 1 | 20 | 55 Obstructions from tumors, | | | | strictures, ulcers, etc. | 28 | 2 | 7 | 19 Internal hernia and ileus | 20 | 1 | 7 | 12 Obstructions from other causes | 4 | ... | 1 | 3 Causes of obstruction not | | | | ascertained | 9 | 1 | 3 | 5 ---------------------------------+--------+---------+--------+------ Aggregate | 230 | 7 | 68 | 155 ---------------------------------+--------+---------+--------+------

[Footnote 12: _Surgery_, p. 835.]

Enterotomy is an operation originally performed by Nélaton. It is done by making an incision, preferably in the right groin, above the crest of the ileum and parallel with Poupart's ligament. When the abdomen is opened a coil of intestine is found and carefully stitched to the walls of the incision. A very small opening is then made into the bowel, and a fecal fistula established. Enterotomy is less dangerous than laparotomy, as by it there is less interference with the peritoneum; but no relief could be afforded by this procedure in cases of intussusception or acute obstruction from bands, hernia, or volvulus. It is applicable to cases of intestinal constriction when the obstruction is about the lower part of the small or upper part of the large intestine. It may be resorted to as a palliative measure when exact diagnosis as to the character and site of the obstruction is not clear, the case being otherwise hopeless, or in cases of obstruction where severe symptoms persist and death is near, and yet for any reason laparotomy or colotomy is inapplicable; or it may be performed in cases of contractions after failure of patient and persistent medical treatment. Many successful cases of enterotomy have lately been reported, and the operation has been earnestly advocated by Trousseau, Maunders, Wagstaffe, Bryant, and others. In chronic constriction due to stricture or other mechanical obstructions, malignant or otherwise, not remediable by any medical measures, colotomy should be performed. By this operation the colon is opened and an artificial anus established. The sigmoid flexure in the left lumbar region is the part selected for the colotomy if the obstruction is situated in the gut below that point. When the obstruction is higher up in the colon or its exact site cannot be determined, the cæcum in the right lumbar region is the part chosen. In cases of obstruction from the mechanical pressure of tumors, the possibility of relieving the compressed bowel by treating the tumors should of course be considered before resorting to colotomy.

{868}

CANCER AND LARDACEOUS DEGENERATION OF THE INTESTINES.

BY I. E. ATKINSON, M.D.

The term cancer of the intestines is used here in a clinical sense to designate new formations in the intestinal tract the tendency of which is to destroy life, and has no reference to the histological characters of the tumors, inasmuch as these are, during life, for the most part, concealed from the eye of the pathologist. It so happens, however, that in a histological as well as in a clinical sense the term is appropriately applied to all but a very few of the malignant new growths that develop in the parts under consideration, if we adopt, as seems proper, the opinion of most modern pathologists, that cancer or carcinoma should only include those tumors "consisting of cells of an epithelial type, without any intercellular substance, grouped together irregularly without the alveoli of a more or less dense fibroid stroma."

Carcinoma of the intestines appears either as cylindrical-cell cancer, as scirrhus, or as gelatinous or colloid cancer. Scirrhous cancer of the intestines may resemble in appearance and texture the ordinary medullary cancer, degrees of hardness or of softness depending upon the predominance of the stroma or of the cellular elements in the constitution of the tumor. Rarely, and in a purely clinical sense, cancer of the bowels may exist as a lympho-sarcoma in the small intestine, and then through progression from the glands of the mesentery or elsewhere. Primary intestinal sarcoma has, however, been observed. Similarly, melano-sarcoma has been detected in the intestine as secondary to this form of sarcoma, originating in the skin or in the eye.

Of the forms of carcinoma, cylinder-cell cancer is the most frequent. Carcinoma gelatinosum or colloid cancer is of great relative frequency, but it is altogether probable that here, as elsewhere, this represents a degenerative form of ordinary carcinoma. At all events, it is certain that it may be detected in many cases where the essential changes reveal the ordinary glandular or cylinder-cell variety. These forms of cancer may affect the bowel primarily or secondarily by extension from adjacent organs and textures, or by metastasis. Primary cancer occurs most frequently, metastatic cancer with great rarity. The relative frequency of the different forms of cancer is not definitely known. In the article on carcinoma in the _Dictionnaire Encyclopédique des Sciences médicales_ (xii. pp. 576, 577) cancer of the bowels is said to constitute about 8 per centum of all carcinomatous new growths. Sibley[1] found that primary {869} carcinoma occurred in the alimentary canal (exclusive of the mouth, tongue, and the annexed organs) in 6 per centum of the cases collated by him. Tauchou's compilations of nine thousand fatal cases of carcinoma show that intestinal cancer was present in 4 per centum.[2] These computations include cancer of the rectum. If statistics of cancer of the bowels exclusive of rectal cancer were available, they would show, doubtless, a much smaller proportion.

[Footnote 1: _Medico-Chir. Transact._, xlii., 1859.]

[Footnote 2: Leube, _Ziemssen's Cyclop._, vii. p. 432.]

Any portion of the intestinal tract is liable to be attacked by cancer, though undoubtedly some parts of it with much greater frequency than others. Köhler[3] reported that in thirty-four cases the cancer was situated twenty-two times in the large intestine (the rectum excluded) and twelve times in the small intestine (nine times in the duodenum). It is not unlikely that in the cases of duodenal cancer the new growth extended from the pylorus. At all events, primary cancer is seated with far greater frequency in the large intestine, and, not including the rectum, usually in either the sigmoid flexure or the cæcum. Grisolle[4] declares the large intestine to be four times more often affected with cancer than the small intestine; that the sigmoid flexure is attacked as often as all the rest of the colon taken together; and that the cæcum is still more often affected. Where the intestinal new growth is secondary to carcinoma elsewhere, it is usually so by extension from neighboring parts; thus, the ileum may become implicated by contact with uterine cancer, etc., and cancer of the stomach, liver, kidney, etc. may invade the colon.

[Footnote 3: _Ibid._, vii. p. 431.]

[Footnote 4: _Pathologie int._, 1865, ii.]

Cancer of the intestines usually begins after the middle period of life, and apparently irrespective of sex. Nevertheless, young persons are occasionally affected, and children sometimes develop malignant new growths of the bowels (usually sarcomatous), either primarily, which is rare, or secondarily, by extension from other parts. The influence of heredity seems not to be well established. There can be no doubt that chronic irritation may act as an exciting cause of cancer of the bowels, as it may in cancer of other parts. It has been impossible to recognize any specific influence from especial forms of irritation, and it is not likely that such exist. Indeed, the etiological relations of intestinal cancer remain exceedingly obscure.

SYMPTOMATOLOGY.--Up to a certain period of development cancer of the bowels will give no sign of its presence; indeed, cases have been observed where, death having occurred from other causes, the existence of the malady became apparent only at the necropsy. In all cases the symptoms are, at first, of an indefinite character and very inconstant. Vague abdominal pains are experienced; these gradually tend to become referable to a certain locality and to become associated with irregular action of the bowels. Constipation, alternating with short intervals of diarrhoea, supervenes, and a varying amount of meteorism is developed. These symptoms may be attended by the signs of failing nutrition. The body gradually shows the effects of chronic imperfect assimilation, and becomes emaciated. The complexion slowly assumes the peculiar hue of chloasma cachecticorum. Long before this occurs, however, the cancerous new formation usually becomes perceptible as a more or less distinct abdominal tumor, movable or fixed, as the part affected permits of free movement {870} or is bound down to the neighboring parts either by normal attachments or by adhesions resulting from inflammatory processes or from the extension of the cancerous growth. When the tumor is movable, it is generally situated in the small intestine or transverse colon or sigmoid flexure, the other portions of the intestinal canal being comparatively fixed. It should be mentioned, however, that portions of the intestines normally freely movable may become adherent to contiguous parts, as the transverse colon, with the gall-bladder, liver, stomach, spleen, etc. etc.; the transverse colon and small intestine, drawn down by the weight of the new growth, with the pelvic organs, the bladder, uterus, uterine appendages, etc.; and that, finally, different portions of the bowels may become involved in one mass.

When the duodenum is the portion implicated the tumor may escape observation or may be indistinguishable from cancer of the pylorus. It occasionally happens that no tumor can be discovered until the malady is far advanced whatever part of the bowel is affected. In nearly all cases, however, before very long the tumor will be detected wherever situated, but it will often remain difficult, owing to its situation, to arrive at exact conclusions as to its precise character. Usually, it offers considerable resistance to the touch, but its features may readily be obscured by the fecal accumulation that forms above the constricted portion of the gut and by the gaseous distension of the bowel. This tumor will be slightly painful to pressure, and the patient will refer to it a spontaneous pain, usually of a dull aching, sometimes of a stabbing, character. Percussion yields a sound of muffled resonance, due to the tubular nature of the tumor. Cancerous neoplasms of the bowel, and of the duodenum especially, are apt to be associated with a distinct pulsation caused by the subjacent abdominal aorta. This may readily be distinguished from aneurismal pulsation by the absence of an expansile character, by the disappearance of the impulse that may sometimes be observed when the patient is made to kneel upon all fours, and by the occasional mobility of the cancerous tumor. By extension and by inflammatory infiltration the tumor frequently becomes converted into a conglomerate mass where all determination of locality becomes conjectural. The tumor is, with very rare exceptions, single.

The symptoms that accompany the development of these growths depend mostly upon their position in the alimentary tract. Pain alone seems independent of this, but is at best a most uncertain concomitant. When the duodenum is the part affected by extension from the pylorus, the symptoms are indistinguishable from ordinary pyloric cancer. Even primary cancer of this part may exactly simulate pyloric cancer. The localized pain and tumor, the vomiting after meals, the frequent presence of blood in the vomited matters, the progressive emaciation from starvation, the absence of abdominal distension (a result of the constriction of the gut at its upper extremity), the gastric dilatation,--all combine to make the diagnosis difficult.

Cancer of the duodenum in its descending part may be suspected when signs of hepatic and pancreatic obstructive difficulties point to implication of the ducts, through which are produced jaundice upon the one hand, and evidences of imperfect pancreatic digestion, in the presence of undigested fat in the stools, upon the other. In the lower portions of the {871} intestines the cancer becomes more and more associated with meteorism and fecal accumulations. Constipation becomes steadily more obstinate, but there are occasional fluid evacuations containing blood, pus, and mucus, often stinking abominably. When the tumor is toward the end of the large intestine--in the sigmoid flexure, for example--fluid discharges occur with very great frequency at times; but these are scanty in amount and but slightly fecal in character. In these cases one does not usually observe the compressed, ribbon-like stools that are seen in rectal cancer. These symptoms may precede the appearance of the tumor, when the diagnosis will be less readily made. The constipation will at first be more amenable to the use of purgatives. (It is said to be due more to a loss of contractility of the bowel than to the narrowing of its lumen.) Gradually these will lose their efficacy, and finally complete obstruction of the lumen of the gut is effected; in which event the symptoms of ileus will develop, with cramps and vomiting, finally of a fecal character, and the fatal issue quickly follow. Not unfrequently peritonitis is developed, and may be of a chronic character or may destroy life within a day or two, or the patient may die from exhaustion before the obstruction becomes complete.

It may happen that the integument will become involved in the malignant process, or may become continuous with the tumor by adhesive inflammation. In such cases an opening may be formed by suppuration, or the lancet may secure the passage of feces through an artificial anus, and temporary respite be obtained. Sometimes a sudden disappearance of the symptoms of obstruction--a result due to the softening and breaking down of the cancerous mass, restoring temporarily the integrity of the intestinal tube--may give an unjustifiable hope to the patient; or the same effect may follow the establishment of a communication, by ulceration, between the bowel above the tumor and some portion nearer to the anal orifice. The progress of the new growth soon annuls the benefits thus gained.

Not uncommonly, particles of the cancerous mass may become detached, and, if diligently searched for, may be discovered in the feces. Microscopic examination may then definitely determine the nature of the disease. It has been claimed that colloid cancer may be diagnosticated in this manner even before the appearance of other symptoms.[5] Death may be hastened by the occurrence of metastatic deposits in other and vital organs. Oedema of the lower extremities (of the left extremity in cancer of the sigmoid flexure) will often be observed as a result of the interference of the cancerous mass with the return of blood from the extremities by pressure upon the large veins. The combination of pain, tumor, constipation, tympanitis, progressive wasting, and the cachexia that sooner or later supervenes, stamps eventually most cases with unmistakable characters.

[Footnote 5: Charon and Ledegank, _Journ. de Med.-Chir. et de Pharm._, v. lxviii., 1879, p. 493.]

The duration of intestinal cancer may extend from several months to one, rarely two, years, the latter age sometimes being attained by colloid cancer, the most chronic and least malignant form.

MORBID ANATOMY.--By far the most frequently encountered malignant new growth of the bowel is carcinoma, in one or another of its forms. The cylinder-cell epithelioma is probably the most common of {872} these, and, as seen in the intestine, offers many naked-eye points of resemblance with ordinary encephaloid carcinoma. It is soft, filled with a milky juice, and may attain considerable size. The tumors appear as discoid prominences of varying size and number. Later, these may become fungoid and ulceration ensue. The growths early involve the whole intestinal wall, and by their increase tend to obstruct the passage of the intestinal contents. When ulcerated they present a nodular, uneven surface, situated upon a thickened base consisting of the infiltrated coats of the bowel. Villous prolongations (villous cancer; the undestroyed connective-tissue stroma) may project into the lumen of the bowel and give a peculiar tufted appearance to the part implicated. One or more points may be invaded by cancerous growth, and above each will be developed a dilatation of the gut (the result of distension) containing uncertain quantities of fecal matter, upon the removal of which the tumor will appear much smaller than it appeared during life.

Scirrhus usually implicates the gut in its entire circumference, so that a high degree of constriction may result from a small amount of cancerous infiltration. It begins as small nodules or plates upon the mucous membrane. As commonly observed, the lumen of the intestine is narrowed by an annular band of gristly hardness. All the coats of the bowel, with the peritoneum, become involved, and frequently the contiguous parts are included in the cancerous infiltration, forming an undefinable mass through which the contracted channel of the bowel may be traced, though often impervious to any but the smallest articles (a crow-quill, for example). The surface of the gut is generally ulcerated, irregular, and nodular. The walls of the ulcer are irregular and infiltrated. It will sometimes happen that the autopsy reveals permeability of the bowel where total obstruction prevailed during the latter days of life. This may be probably accounted for by the disappearance of the hyperæmia that doubtless existed during life and caused more or less turgidness of the growth. Sometimes the connective-tissue element is less predominant, and gives place to a more or less luxuriant cell-development; in a word, scirrhous carcinoma is replaced by soft or encephaloid cancer. This difference is simply one of degree, but is associated with greater rapidity and extent of growth. Ulceration is extensive, and one may here also often discover the villous, tufted appearance of villous cancer, caused by the fringe-like shreds of stroma entangling cellular elements not yet detached from the mass.

Colloid cancer, or carcinoma gelatinosum, may be associated with either of the above-described forms as a degenerative form, or may, apparently, develop as such from the beginning. It is a very frequent variety of the malady. In 27 cases of intestinal cancer, colloid cancer was present in 5, as reported by Lebert. It is most often observed in the sigmoid flexure and cæcum, as are the other forms of carcinoma. It is composed of a considerable mass extending around the bowel. Ulceration is less often found here than in the other forms, nor is there the same tendency to secondary infiltrations. By the unaided eye an alveolar structure may be detected, and when the mass is extensive a soft, jelly-like consistency is presented, together with "a bright, honey-yellow color." Small deposits of the colloid matter may be seen upon the surface. These have been described as resembling wheals of urticaria or herpetic or eczematous {873} vesicles (Bristowe). The glairy fluid of colloid carcinoma oozes from the cut surface of the tumor, bathes it, and is to be found in the intestine.

These different forms of cancer sooner or later invade neighboring parts, as the peritoneum, mesenteric and retro-peritoneal glands, and adjacent organs. On the other hand, the intestines may become invaded by cancer of the peritoneum and other parts. It has even been observed, reversing the usual order of things, as secondary to cancer of the liver (Wilks and Moxon). Under these conditions the symptoms of intestinal cancer will have been associated with those due to the primary affection. Lympho-sarcoma will rarely be found as an extension from the lymphatic glands and involving the small intestine. Melanotic sarcoma may occur as metastatic from an original melano-sarcomatous tumor of the skin or eyeball.

DIAGNOSIS.--In its earlier stages it is impossible to recognize cancer of the intestines. After its symptoms have become established they may resemble those of several disorders. Cancer of the duodenum cannot be distinguished from that of the pylorus unless evidences of pancreatic or biliary disturbances indicate obstruction to the passage of the bile and pancreatic secretions. Previous to the appearance of a tumor one must often remain in doubt. The alternations of constipation and diarrhoea, the signs of partial obstruction, the localized pain usually present, the gradual wasting, will arouse suspicions of cancer, though chronic inflammatory affections of the bowels may induce symptoms not altogether unlike these. The presence of a tumor will supply the additional evidence necessary for a definite diagnosis. It will be necessary to exclude fecal enlargements of the bowels. The cancerous tumor will be somewhat painful, hard, nodulated. A tumor due to fecal accumulation may closely simulate it, and is, indeed, usually associated with it. By manipulation the fecal mass may be moulded, and even displaced, and by appropriate purgative treatment may be caused to entirely disappear. Foreign bodies, mesenteric tumors, and other abdominal enlargements may offer physical resemblances to intestinal cancer, but their symptomatology is usually so different that doubt may be easily dispelled. Syphilitic gummy infiltration, with resulting stricture, is more apt to occur in the rectum than in other parts of the alimentary tract.

The presence of fragments of the new growths may sometimes be detected in the stools, when microscopic examination will determine their nature. With cylinder-cell epithelioma and glandular cancer this is not common, but with colloid cancer much information may be gained by examining the evacuations. According to Charon and Ledegank,[6] colloid cancer of the intestine may be detected before symptoms develop, by the presence of colloid matter in the feces. In the later stages, however, the gelatinous change of all the histological elements may occasion embarrassment, as at this stage the peculiarities of the cellular structure will have been destroyed.

[Footnote 6: _Journ. de Med.-Chir. et de Pharm._, lxviii., 1879.]

PROGNOSIS.--Intestinal cancer always proves fatal. Death may result from the debility resulting from the cancerous cachexia or from intestinal occlusion or from peritonitis. The duration of the malady is usually not long. It runs its course in from several months to one, rarely to two, years.

{874} TREATMENT.--Treatment must be directed to the alleviation of the distress caused by the disease. No curative treatment is known. When the cancer is situated in the colon, especially in the sigmoid flexure, the operation for artificial anus often affords great though temporary relief. The diet should consist of such articles in the digestion of which a large residue is not formed. Milk, eggs, soups, etc. should compose the principal articles of food. Mild laxatives will be required to secure the proper evacuation of the bowels, and to relieve pain and discomfort opium is invaluable and should be freely used. When obstruction is imminent nutrient enemata afford the most efficient means of administering nourishment.

Lardaceous Degeneration of the Intestines.

SYNONYMS.--Albuminoid degeneration, Waxy degeneration, Amyloid degeneration, etc.

Lardaceous degeneration of the intestines is an affection of quite frequent occurrence in those persons who are the subjects of a like change elsewhere; for although it has been asserted that it may be present as a primary affection, it almost always succeeds the same form of degeneration in other organs. Since, for the most part, it only makes itself manifest at an advanced stage of the disease, its importance is usually masked by the grave constitutional condition of the patient, whose vital forces are wellnigh exhausted by the already advanced degenerations present elsewhere. The extensive implication of other organs and tissues in the same degenerative process also creates great obscurity in the symptomatology of intestinal lardaceous disease, and is doubtless the cause of the existing dearth of definite knowledge upon the subject.

That the intestines are comparatively frequently involved in lardaceous disease is shown by dead-house statistics. Thus, Charlewood Turner[7] reported from the London Hospital that in 58 cases of lardaceous disease the intestines were affected 10 times; and Goodhart[8] in 150 consecutive necropsies of lardaceous disease at Guy's Hospital reported implication of the intestines 63 times.

[Footnote 7: _Transactions Path. Soc. London_, 1879, p. 517.]

[Footnote 8: _Ibid._, p. 533.]

Although the bowels do not become affected as early as several other parts, they will almost certainly become involved should the patient's life be prolonged; and in those cases where death is a direct result of the degeneration the intestines share with the kidneys the chief responsibility. It is not, however, until an advanced stage of lardaceous degeneration that its presence in the alimentary canal is revealed by symptoms; indeed, many cases do not, throughout life, betray evidences of the pronounced alterations that are to be discovered after death. Even in extreme cases there are no symptoms that would, even with probability, be referred to lardaceous disease of the bowels in the absence of the same degeneration in other organs and parts. There are, then, no specific symptoms following lardaceous degeneration of the bowels.

Where the normal functions of the intestines can no longer be properly performed in consequences of the changes that have taken place in them, there results a moderate diarrhoea. At first the number of movements {875} may not be increased; the evacuated matters are fluid and of a greenish or pale color. Usually, little or no pain is experienced, though at times and in certain individuals this may be severe and colicky. The diarrhoea is not always steadily progressive, but may from time to time disappear. With the progress of the disease it may become more free and persistent, and in the later stages hemorrhage from the bowels may be superadded. This may vary in amount, and where, as is often the case, the stomach participates in the degeneration, hæmatemesis may also appear. These hemorrhages may be insignificant, or may at once assume alarming proportions, and even bring to an unexpected termination the life of the individual. Already, at the outset of the intestinal symptoms, the general health will have shown evidences of profound alteration, but upon the supervention of the diarrhoea more rapid progress will be observed, consequent upon the increased nutritive disturbance. The use of remedies in temporarily controlling this diarrhoea may prolong for months the life they are powerless to save.

So far as concerns the intestinal affection, there is no special tendency toward febrile excitement. It must not be forgotten, however, that acute inflammatory attacks of various tissues and organs frequently arise in the course of lardaceous disease.

Though there seems to be reason to believe that mild degrees of lardaceous degeneration may sometimes be cured, especially when dependent on syphilis, there is but little hope of arresting its progress at the late stage when the bowels become implicated. Indeed, when pronounced degeneration of the bowels takes place the disease is usually nearing the end of its course; for it is a well-settled fact that in this degeneration extensive implications of organs may occur without markedly reducing the patient's general condition, so long as the kidneys and intestines remain unaffected. The cause of death is usually to be traced to these organs. Dickinson[9] found that in 35 cases where death was apparently due to renal lardaceous disorder, the immediate result was brought about by diarrhoea in 13 cases. Presumably, in a large proportion of these lardaceous disease of the bowel was present.

[Footnote 9: _Diseases of Kidney_, Part ii., 1877, p. 496.]

The degeneration usually affects the lower portion of the small and the upper part of the large intestine. Occasionally it will be found to have invaded the whole alimentary tract. As in lardaceous degeneration generally, the process begins in the small arteries and capillaries and veins, affecting primarily the arterial and venous muscular coats--not, however, according to the latest authorities, the muscular fibres themselves, but their perimysium and the cement substance, the degeneration being one limited to the connective tissues.[10] In the mildest cases only some of the small vessels of the mucous membrane are involved, and no naked-eye changes can be detected. In more advanced stages the mucous membrane is pale and shows evidence of catarrh. Thickening occurs, and as the process advances a peculiar appearance is revealed which has been compared to that of wet wash-leather (Wilks). The iodine test now gives the mahogany-colored reaction of lardaceous matter, with the tissues affected, or, if the methyl-aniline-violet test of Cornil be employed, the lardaceous material will display a red-violet color, while {876} normal structures will be tinged blue-violet. It is said to be better to make the test near a Peyer's patch, since the latter is seldom affected by the degeneration, and brings out, by contrast, the surrounding lardaceous material.[11] This distribution of the material cannot be considered as constant, however, since Hayem found the patches of Peyer most frequently affected.

[Footnote 10: Cohnheim, _Allgem. Path._, 1882, p. 667.]

[Footnote 11: Wilks and Moxon, _Path. Anat._, p. 404; Kyber, _Virchow's Archiv_, Bd. 81, H. 1 and 2.]

In more advanced stages the surface may become irregular from glandular enlargement, and ulceration may occur. Microscopic examination shows the lardaceous material in the vessels, and also in the stroma of the mucous membrane and villi.[12] The epithelium is not involved. The degeneration, at first confined to the mucous membrane, extends to the submucous tissue, the proper muscular coat of the intestines being often implicated--so far, at least, as concerns its connective tissue. In the more severe cases Hayem found the agminated and solitary glands extensively involved. Fine branches from affected vessels penetrate to the interior of the glands. In such cases the mesenteric glands will be found implicated. The degeneration of the vessels running through the gland structure causes disappearance of this substance by fatty degeneration, and occasions a reticulated arrangement of the lardaceous material, and, secondarily, ulceration. In a similar manner ulcers may arise in any part of the affected tract. Finally, the lardaceous material may involve the whole thickness of the gut.

[Footnote 12: Eberth, _Virchow's Archiv_, 80, S. 138.]

The diagnosis of lardaceous disease of the bowels can only be made with certainty in the presence of pronounced albuminoid disease of other parts in association with the symptoms of intestinal disorder. It possesses no characteristic symptoms.

Inasmuch as the disorder invades the bowels only at a late stage of its existence, the prognosis acquires additional gravity. It is probable that advanced albuminoid disease is never cured; so much the more hopeless is it when affecting this tract. If unchecked, the diarrhoea rapidly saps the powers of life; if temporarily alleviated, the approach of death is more gradual.

Whatever attempts are to be made to cure the disease, they must be through the general system, and are identical with those directed toward the cure of lardaceous disease generally. Treatment directed to the intestines must be palliative. The diarrhoea must be combated by appropriate diet and the administration of such remedies as protect the surface of the mucous membrane and control the intestinal movement. Bismuth subnitrate in large doses is therefore indicated. Various astringents may be employed, while the use of opium often secures most gratifying relief. It should be given in generous doses. Preparations of the crude drug seem to answer better than its salts. The necessity of keeping the gut free from undigestible matters that may irritate the already badly-damaged mucous membrane is apparent. Patients with this form of lardaceous degeneration usually show the cachexia resulting from profound modifications of nutrition, and their intestinal symptoms can only be regarded as links in a long pathological chain. Hemorrhage will call for remedies that under ordinary circumstances are employed to control bleeding from the bowels.

{877}

DISEASES OF THE RECTUM AND ANUS.

BY THOMAS G. MORTON, M.D., AND HENRY M. WETHERILL, M.D., PH.G.

Diseases of the inferior and terminal portion of the large intestine may be divided into primary and secondary--the former when the morbid cause is local and independent of disease elsewhere, the latter when it is consequent upon or incident to some other bodily affection. Among the primary lesions may be classed congenital malformations, prolapse of the rectum, hemorrhoids, and some varieties of new growths; also diseases caused by local irritations, infection, or traumatism, such as proctitis, ulceration, fissure, non-malignant stricture, chancroidal invasion and primary syphilis, including obstruction of the bowel by impacted feces and foreign bodies. Thread-worms and various cutaneous eruptions about the anus may also be included among the causes of the primary diseases of this portion of the alimentary canal.

The secondary affections are quite numerous, and may be caused by direct extension of disease from the colon, as in the dysentery following typhoid fever, and follicular enteritis, or entero-colitis of children; by contiguity, from diseases in neighboring organs--_e.g._ ischio-rectal abscess causing fistula--or by changes in the nervous or vascular supply, such as is seen in spasmodic contraction, paralysis, epidemic dysentery, cholera, and the action of certain remedies.

The rectum, the third or terminal portion of the large intestine, has no sharply-defined upper limits: it is usually understood to begin at the sigmoid flexure, opposite the left sacro-iliac symphysis; it is from six to eight inches in length and terminates in the anus. As the sigmoid flexure is the narrowest portion of the colon, so the calibre of the first part of the rectum is narrower than the portion below, where it gradually becomes more commodious, and near the anus presents a peculiar condition of the walls which gives it a capacity for remarkable distension. The rectum, which is somewhat cone-shaped, in its anatomical and pathological characters retains those of the large intestine with slight variation. Upon the upper or first part of the rectum the duplicature of the peritoneum is continued, forming the meso-rectum, which invests the bowel, attaching it to the sacrum. Below this the middle portion of the rectum (extending to the tip of the coccyx) is attached to the sacrum by connective tissue only, but also has a peritoneal investment on the upper portion of its anterior surface.

{878} The third or terminal part of the rectum, which is only an inch and a half in length, and is entirely without peritoneal covering, terminates at the anus. The circular and transverse muscular fibres, mucous crypts, and appendages throughout the rectum are identical with those above, except that the general muscular tunic is thicker; but the longitudinal fibres are less distinctly aggregated into bands than in the colon, being disposed in a more uniform manner, except that, like the circular fibres, they are especially aggregated between the sacculi. The fact that the meso-rectum limits the mobility of the upper and more narrow part of the rectum has led some to locate a third sphincter at this point, but the existence of such an organ has not been generally admitted. Van Buren characterizes it as an organ which "anatomy and physiology had been equally unsuccessful in assigning either certainty of location or certainty of function."[1]

[Footnote 1: Kelsey, _Diseases of the Rectum and Anus_, New York, 1882, p. 20.]

The anus guards the outlet of the bowel by its double sphincter muscle, which under normal circumstances affords voluntary control, within certain limits, over defecation. The well-known peculiarity of the vascular supply, a sort of erectile tissue being formed by the inferior hemorrhoidal plexus and the passage of some of the efferent veins through the sphincter muscle, by which they are subjected to pressure, is very favorable to the development of certain forms of disease which will be considered among the local disorders. As embryology has thrown considerable light upon the pathology of morbid growths by demonstrating relationships that were previously unsuspected, so a consideration of the development of the lower portion of the intestinal canal may lead to a better understanding of some of its diseases, especially those which are symptomatic or secondary. In early foetal life the third division of the primitive intestine, the pelvic portion, terminates in a cloaca in common with the urachus; subsequently, about the eighth week, a partition (the perineum) is formed which divides the cavity into two portions, the uro-genital sinus and the anal cavity. In the mean time, at an early period a depression occurs on the cutaneous surface at the site of the anus, which deepens progressively until it encounters the primitive intestine, with which it unites at the end of the fourth week, and the continuity of the tube becomes established. It therefore is seen that the rectum in its upper and middle portions is derived from the internal and middle layers of the blastodermic membrane, while its lower third, with the anus, like the buccal cavity, is formed by the external and middle layers.

In its diseases, then, the greater part of the rectum would seem to naturally participate in those of the large intestine, to which it structurally belongs, while its inferior portion and the anus would partake more in the disorders of the general cutaneous system. This peculiarity of development also explains the difference noticed in the vascular supply. The rectal veins are usually divided, like the rectal arteries, into three sets--superior, middle, and inferior. They are arranged so as to form two distinct venous systems, the rectal returning its blood through the inferior mesenteric veins into the portal system, the anal terminating in the internal iliac. The first system is made up of the superior hemorrhoidal, the second of the remaining veins.

The superior hemorrhoidal forms a venous plexus which surrounds the {879} internal sphincter muscle; the inferior hemorrhoidal vein also forms a plexus, but it is subcutaneous and principally below the inferior border of the external sphincter.

There are, however, a number of communicating branches passing along the walls of the rectum from one plexus to the other. The internal hemorrhoidal veins also communicate freely with the branches of the internal iliac around the trigone of the urinary bladder by means of small vessels, which pass through the prostate gland and seminal vesicles. By this method of anastomosis some relief is afforded when there is an obstruction in the portal circulation, which is such a common cause of turgescence of these veins, often resulting in permanent dilatation or hemorrhoids.

At the lower part, or at the junction of the middle and lower third of the rectum, the internal circular fibres of the muscular coat of the intestine become quite numerous, forming what is called the internal sphincter muscle; it is nearly an inch in breadth, and completely surrounds the lowest part of the rectum. It is about an inch above the margin of the anus; its muscular fibres are of the involuntary or unstriped variety; in function it assists the external sphincter in closing the anus and preventing the involuntary escape of the contents of the bowel.

The external sphincter lies directly under the skin and upon the internal sphincter and the levator ani muscle; its fibres encircle the anus: arising from the coccyx, they are inserted into the tendinous centre of the perineum, joining the transversus perinæi, the levator ani, and accelerator urinæ muscles. The sphincter ani is constantly in a state of tonic contraction, but the force of its contraction may be voluntarily increased. In the skin and superficial fascia are found minute branches of the pudic and small sciatic nerves; in the ischio-rectal space the internal pudic nerve; crossing about the centre are the inferior hemorrhoidal nerves, which are distributed to the anus and the lower portion of the rectum; the perineal nerve is especially distributed to the anterior part of the anus.

Thus it is seen that the rectum and anus have vascular and nervous supplies of considerable diversity and importance.

Congenital Malformations.

The simplest form of congenital malformation in this region consists in an anus of insufficient size for the natural demands of the system, but in no other manner abnormal. The most frequent variety of imperforate anus is where complete occlusion is effected by the common integument or by two cutaneo-mucous flaps, which owing to defective development remain united without forming a raphé or perceptible line of union. The rectum is not involved, and when the child strains the contained meconium causes bulging of the part, which disappears under slight pressure, but reappears when again free. In other cases the occluding tissue is very firm, dense, with a disposition to pucker or form rugæ. The sphincter muscle is rarely perfect, and though an artificial anus may be made, years may elapse before the child can control the evacuation. In conjunction with an imperforate anus the colon may terminate in a cul-de-sac, or it may communicate with the urethra, the bladder, or the vagina.

{880} An imperforate rectum has been known to discharge at the umbilicus, upon the face, under the scapula, upon the penis or the anterior part of the scrotum. Sometimes, though very rarely, a common cloaca has been found, as in fowls, common to the rectum and to the genito-urinary organs; and still more rarely the rectum has opened in abnormal sites upon the perineum and upon the buttocks.

The anus may be entirely absent. The rectum may be entirely absent or it may be incomplete, terminating at various distances from the anus. These malformations of the bowel may be associated with a perfect anus, or with any of its imperforate forms, or with a fecal fistula. In occlusion of the rectum the offending structure is in some cases a hymen-like fold of mucous membrane, which, during straining, can be recognized by the finger as a fluctuating protrusion; while in others it consists of a mass of dense fibrous tissue which extends upward from an inch to an inch and a half: in the former there is always found a normal anus; in the latter there is either no trace of anus or one in a more or less rudimentary state. In those cases where the rectum is entirely absent the intestine terminates either in a cul-de-sac or a fecal fistula; very rarely the rectum is replaced by a fibro-ligamentous cord or band which springs from the colon, and, descending toward the bladder, blends with the connective tissue of the part. In the latter the pelvis is always in an imperfect state of development, being much contracted in its lower diameters, and the anus is absent; and Rokitansky and Curling lay stress upon the non-development of the pelvis as a diagnostic guide in determining the absence of the rectum. The passage of a sound into the bladder or vagina is a procedure of some diagnostic value, as if its point impinges directly against the sacrum it may be presumed that no rectum exists. If the malformation is of such a character that the fecal matter can find no exit, a train of symptoms ensues analogous to those seen in the adult affected with intestinal obstruction: the infant cries and is constantly restless, refuses food, vomits, the abdomen distends, and death speedily ensues. A remarkable exception to this rule was the case mentioned by Bodenhamer of a child with absence of the rectum who was not operated on until three months after birth, and who was apparently in perfect health. At the operation the intestine was found three inches from the surface, and the child made a good recovery.

Although the statistics of this class of malformations are somewhat contradictory and confusing, it is safe to state that more male than female children are so afflicted.

The prognosis in the large majority of these cases is grave, for unless the operator can see or feel the fluctuating protrusion, or can recognize it after a very slight exploratory incision, he is working totally in the dark and in close proximity to the peritoneum. Hemorrhage, peritonitis, pelvic cellulitis, and septicæmia diminish the chances for recovery. Indeed, the majority of these cases are scarcely amenable to surgical treatment.

{881} PRIMARY DISEASES OF THE RECTUM AND ANUS.

Prolapse and Procidentia of Rectum and Anus.

These conditions obtain most frequently at the two extremes of life, infancy and senility, but have a very different causation in each. Prolapse of the bowel may be partial or complete--partial when a portion of the mucous membrane is extruded, and complete when the entire rectum appears outside the anal orifice. A predisposing cause in infants is found in the mobility of the bowel--in the fact that it and the sacrum are much less curved than in the adult, and the abdominal viscera are more voluminous: this, associated with the undeveloped state of the muscular system, causes the weight and strain to act directly and forcibly upon the sphincters, and the extrusion takes place. It is often excited by allowing children to sit for a length of time upon the chamber-vessel. It is frequently caused among children by the presence of vesical calculi, by Oxyuris vermicularis, diarrhoea, constipation, dysentery, polypi, and by the long-continued acts of coughing and crying.

In adults and the aged it may be caused by loss of tone of the anus and rectum in chronic diarrhoea and dysentery, or from the energetic action of drastic cathartics, by urinary calculi, the long-continued use of enemata, chronic cough, diarrhoea alternating with constipation, stricture of the urethra, prostatic hypertrophy, tenesmus due to the presence of polypi, and by the pressure of a pelvic tumor. It may accompany procidentia uteri and hemorrhoids. An incomplete, reducible prolapse consists of two or more overlapping plications of normal-looking mucous membrane, sensitive but painless. In these cases there is provoked a hyperplasia of much-elongated connective tissue in the submucous space which undergoes serous infiltration and causes an oedematous condition of the part. In a complete prolapse the entire rectum--all of its component layers--is protruded through the anus. In a recent case the folds of the gut are well marked, but in one where the bowel has remained in this abnormal condition for some time the submucous tissue becomes charged with inflammatory deposit which effaces the plications and causes the bowel to become pale, hard, dry, and tough; and finally pigmentation occurs and the part assumes somewhat the character of true skin. These vary greatly in size, from the slightest protrusion of mucous membrane to a tumor the size of a melon. Usually they are reduced with ease, but their reappearance is occasioned by the slightest tenesmus.

In old age the soft parts of the floor of the pelvis and the anal sphincters lose to a great extent their tone and contractile vigor, and the rectum, also participating in this change, is often unable to withstand the increased thrust of the diaphragm and the compression of the abdominal muscles during defecation; which act frequently demands more exertion on account of a tendency to constipation in advanced life.

In these long-standing cases of senile procidentia it is a matter of experience, verified by post-mortem dissection, that the fibres of the sphincters and of the levatores ani muscles are flattened, pale, and stretched beyond the possibility of contraction, while the entire perineum is in a state of atrophy.

{882} Polypi of the Rectum.

There are two varieties of these--the gelatinoid or soft, and the fibroid or firm. The latter is of rare, the former of common, occurrence, especially in children under the age of twelve years. The fibroid polypus is only found in adults, and is composed of dense connective-tissue elements and blood-vessels. The gelatinoid or soft polypi are also partly composed of connective tissue and vessels, but much finer than in the other: they contain hypertrophied follicles and are covered with spherical epithelium. They resemble nasal polypi, but are more dense. These growths are not malignant in character, but are very troublesome, as they are almost always pedunculated, the stem being from half an inch to four inches in length, which admits of the descent of the tumor within the grasp of the sphincters during defecation, and frequently admits of its escape from the anus. Their presence is not free from danger, as they are very vascular, bleed readily, and are sometimes detached by the breaking of the pedicle during defecation. They frequently bleed spontaneously. The presence of these abnormal growths teases the rectum and brings on tenesmus and frequent desire to go to stool; the feces are flattened, and with them escapes a quantity of glairy red mucus which has been compared to thin currant-jelly. When caught in the grasp of the sphincters they often bleed profusely, and especially is this the case with children so affected. The presence of these bodies is accompanied with a sense of weight and uneasiness in the bowel. They may be single or multiple; they may be round, reniform, oval, fusiform, or irregular; they may be smooth or villous. In size they vary from that of a marble or cherry to that of a small hen's egg, and they are usually found about three inches above the anus, but they vary in position from a point just within the sphincter to one six inches up the rectum. Their presence is usually diagnosticated without difficulty, or, if any is experienced, a digital exploration will reveal them. A child with functional disturbances of the bowels accompanied with frequent hemorrhages should be examined for polypus. One of these growths sometimes unpleasantly complicates a case of hemorrhoids.

A rectal polypus is an adenoma, consisting of dilated glands of Lieberkühn imbedded in connective tissue, also containing nerves and blood-vessels, and is covered with the epithelium of the bowel.

Hemorrhoids, or Piles.

These are usually fibrous when situated below, or vascular when situated above, the sphincter ani muscle. They are conveniently known as external and internal piles, but in some instances it is impossible to say whether these tumors are external or internal. In either variety they are due to an abnormal state of the blood-vessels, and especially of the plexus of superior, middle, and inferior hemorrhoidal veins disposed around the lower extremity of the rectum immediately above the internal sphincter muscle. The inferior mesenteric and internal iliac veins receive a large portion of the blood from this plexus, so that a very free intercommunication exists, around the lower portion of the rectum, between the general {883} venous system and that of the liver. It should be borne in mind that these veins are destitute of valves, and are situated in a very dependent part, which is normally in a high degree of functional activity.

External hemorrhoids are found at the very verge of the anus, and, when not irritated or inflamed, appear like movable, dependent plications of hypertrophied skin. They appear either singly or in groups, but it is nothing unusual to find five or six of them together, and they are not infrequently associated with the internal variety. These pendulous tabs of integument are very prone to inflammation, and they then become exquisitely tender, painful tumors, which vary in size from that of a small pea to that of a pigeon's egg. That portion of the tumor presenting toward the anus is covered with mucous membrane; the other is covered with integument; the former is dark-colored, due to engorgement of its vessels. These, being composed internally of tortuous, dilated veins which have totally lost their normal resiliency, bleed freely on section, but after a time they undergo the following changes: the over-distended vein, of which each is mainly composed, either becomes obliterated by the encroachment of inflammatory deposit or its walls give way and the contained blood escapes; its serum is absorbed, and the tumor now consists of a blood-clot, the remains of a vessel, inflammatory lymph, a hyperplasia of connective tissue, mucous membrane, and integument. It undergoes a still further change by absorption, and remains a permanent pendulous teat of cutaneous and connective tissue, bearing no trace of vascular channels.

On account of the extremely sensitive nature of the mucous membrane and skin of the anus, an inflamed condition of these tumors entails an amount of suffering very disproportionate to their size: there is torture in the act of defecation, constant tenesmus, spasm of the sphincters, a sense of weight and heat in the perineum, and sometimes a swollen, very painful, condition of the raphé, which stands out like a cord.

Occasionally there is a total inability to urinate, combined with a frequent desire to do so. When an attack such as this ends in suppuration of the tumor a radical cure is effected, but a marginal ulcer of the anus sometimes follows. An unclean and neglectful habit provoking constipation, sexual incontinence, over-indulgence in highly-seasoned food or in stimulating beverages, exposure to cold and wet, and the straining attendant upon dysuria, will provoke an attack. No age or sex is exempt from this affection (Gross). It is claimed that before puberty females are more subject to it than males; after that age the reverse obtains, except during pregnancy.

Internal hemorrhoids are round, oval, or sometimes cylindroid-shaped tumors covered by mucous membrane; they are smooth, granular, or rough to the touch, much less sensitive and painful than the inflamed external variety, and are situated within the rectum it may be an inch or two above the internal sphincter muscle. They occur in groups or scattered over the surface of the bowel. In structure they are soft, spongy, vascular tumors composed of dilated and tortuous blood-vessels, the veins predominating over the arteries, their interstices scantily supplied with connective tissue, and their covering is of mucous membrane. In color they are dark red, but when compressed and strangulated by the sphincters they assume a dusky purple hue. After long exposure they take on a pseudo-cutaneous appearance.

{884} The columns of the rectum are the seat of the cylindroid pile, which is brighter in color and much more arterial in its structure than the ordinary variety, and bleeds very freely. Anything which causes stasis and accumulation of blood in the hemorrhoidal plexus of veins predisposes to this very common affection. Constipation is the usual cause; and among others may be named diseases of the liver which cause portal obstruction, pelvic tumors causing engorgement from pressure, the gravid uterus, labor, prostatic hypertrophy, urinary calculi, stricture of the urethra, stricture of the rectum, and rectal tumors. Among other causes are horseback-riding, the erect posture, violent cathartics, seat-worms, dysentery, diarrhoea, dyspepsia, and a sedentary life, with a diet of rich, stimulating food.

These piles do not usually cause much suffering; they vary in size from that of a pea to that of a pigeon's egg, and cause a sense of weight and stuffing in the bowel; but when they are large and numerous they cause severe pain, tenesmus, difficult defecation, spasm of the sphincters, and prolapse of the anus. When the patient is at stool the tumors are forced down and protrude in a bunch, surrounded and constricted by a collar of prolapsed mucous membrane: under these circumstances the tortuous and dilated vessels of which they are composed give way and free arterio-venous hemorrhage takes place. In some cases this happens at every stool, the patient losing from a few ounces to a half pint of blood almost daily until alarmingly depleted. Usually, the protruded piles are easily restored after a motion of the bowels, and so remain until the next one occurs; but in other cases of longer standing and of more gravity the sphincter loses all tone and the piles remain constantly prolapsed. This affection is very chronic, and the subject of it has to regulate his life with the greatest care, as the least unusual effort or excess may provoke an exacerbation. Excepting in the worst cases the general health is not materially impaired. They occasionally become so strangulated as to slough off, which effects a cure, but this is accompanied by grave constitutional disturbance. The disease is rather rare before the age of puberty, but is very common in both sexes in adult life, and is frequently associated with fistula, polypus, fissure, or carcinoma of this region. In females suffering with piles a free hemorrhage from them sometimes takes the place of the menstrual flow. The presence of internal piles causes a sense of weight and fulness and the sensation of a foreign body or of feces remaining in the rectum, with troublesome and obstinate itching about the anus. These symptoms, with the occurrence of hemorrhage from the rupture, erosion, ulceration, or abrasion of the dilated vessels, render the diagnosis easy. Should the piles not protrude, they can readily be made to do so by directing the patient to sit and strain over a vessel containing hot water. If the piles do not appear, a digital examination should be made. Indeed, it would be better to make one in every case of this kind.

About the margin of the anus the superficial veins are prone to great dilatation, and when presenting form masses of a bluish color, often very dark, covered partly by mucous membrane, partly by integument. These are also commonly known as piles.

{885} Dilatation of the Rectal Pouches, or Physick's Encysted Rectum.

This is an uncommon disease, generally occurring in those advanced in years, and consists of an hypertrophy, and sometimes of an inflammation, of the natural rectal sacs. These pouches are quite small in early life, and enlarge gradually as age advances, this condition being favored by the lodgment in them of extraneous substances, such as indurated fecal matter, inspissated mucus, the seeds of fruit, and other undigested masses. Constipation, so usual with the old, predisposes to this affection, as it keeps the bowel distended with hardened feces. The pouches vary much in size, the largest of them admitting the end of a finger. The disease is insidious and slow, but is capable of producing intense suffering should inflammation, suppuration, or ulceration attack them. Sometimes as many as a dozen are involved.

The symptoms, which are rather misleading than suggestive of the disorder, are a sensation of weight and uneasiness just within the anus and uneasy sensations in the rectum, distressing itching, and, after a time, pain following defecation and lasting often for hours. The pain, which is aching and burning in character, is not confined to the parts affected, but radiates down the thighs, toward the back, and into the perineum. An increased secretion of mucus always exists in these cases, but the discharge of purulent matter is uncommon, and its presence indicates the existence of very active inflammation.

It is said that even in the worst cases no spasm of the sphincters occurs. An exploration of the bowel with a blunt-pointed hook affords the only reliable guide to correct diagnosis: this, as it is moved about in the rectum, engages the rim of a sac, which may thus be drawn down through the anus and examined.

Non-malignant Stricture of the Rectum.

In the absence of ulceration or syphilitic infection this is an uncommon disease, and very many of the cases of so-called stricture of the rectum are caused by spasm which always disappears during anæsthesia.

The affection may be described as a narrowing of the lumen of the rectum, more or less circumscribed, by the deposition of inflammatory lymph or fibrous tissue in the mucous, submucous, or muscular tunic of the bowel. It may be due to traumatic causes, such as the introduction of foreign bodies, the frequent and careless use of enema-pipes, or the presence of sharp or irritating substances swallowed, as pieces of shell or bone. It is said to have been caused by indurated feces, but no cases have been published in which this causation is clearly shown. This condition has also been brought about by various operations upon the mucous coat of the bowel, such as the application of nitric acid and other escharotics and the removal of portions of mucous membrane and of hemorrhoids.

Stricture may be secondary and a result of extension of an inflammation outside the bowel, as pelvic cellulitis; and it is frequently caused by syphilitic deposition and by chancroidal invasion--in the former by {886} infiltration, ulceration, and cicatrization, in the latter by unnatural sexual connection, or by infecting vaginal discharge running into the bowel.

When the stricture involves only the mucous tunic, it imparts to the finger the sensation of a ring-like elevation or a valve-like projection, into which the finger enters or beyond which it passes usually without much difficulty; but when it involves the submucous and muscular layers, as after the cicatrization of a large rectal ulcer, the finger encounters a dense fibrous mass which in some cases appears to have no lumen, but in others will admit only the end of the finger. In these grave cases of long standing there occurs considerable dilatation of the rectum above the stricture due to fecal detention and impaction at this point, and hypertrophy of the muscular coat of the bowel produced by long-continued straining and expulsive efforts.

Allingham[2] speaks of chronic constipation as a cause, and says, "Straining to evacuate the contents of the bowel forces down the upper part of the rectum into the lower, causing an intussusception; it gets within the grasp of the sphincter muscles, and this may be the starting-point of the irritation." Stricture does not usually follow proctitis, even when the latter is very chronic. The long-continued pressure of the child's head in cases of delayed labor is said to have caused stricture of the rectum.

[Footnote 2: _Diseases of the Rectum_, p. 195.]

This affection is a disease of adult life, and more cases of it occur among women than among men. "If stricture of the rectum is found in a young woman, it is probably due to chancre cicatrices; if it is met with in old women and men, the inference should be that it is either caused by cancer or by syphilitic infiltration and its consequences. Only in those cases in which no cicatricial tissue has been formed--that is, when the contraction is due to the infiltration alone--will the results of the antisyphilitic treatment contribute anything toward rendering the diagnosis more certain."

Stricture of the bowel may exist for months and years without being recognized and without causing the patient much uneasiness; more frequently, however, there is marked uneasiness, with an increased desire to go to stool and a sense of weight or of a foreign body in the bowel. Violent straining accompanies the act. It is given usually as one of the most common and reliable symptoms of this condition that the feces are flattened, ribbon-shaped, or triangular or wire-drawn: in true stricture, according to Allingham, this is not the case, but the characteristic stool consists of small, irregular, broken fecal fragments. When the contents of the bowel happen to be watery, the loose stool is spurted out with great force. In this disease diarrhoea alternates with constipation; the intestines become distended with quantities of gas and feces, which provoke frequent and severe attacks of colic; the appetite and digestion fail; the complexion becomes sallow; the patient emaciates; ulceration sets in, and the patient slowly sinks from exhaustion. Usually, these cases do not give rise to much pain, and what there is, is usually referred to the back, thighs, penis, or perineum. A discharge of mucus resembling white of egg immediately precedes each action of the bowels. Usually, these strictures are within two and a half or three inches of the anus, but sometimes they have been found high up in the sigmoid flexure, and rarely at a greater distance. A syphilitic stricture by direct inoculation {887} is found just within the sphincter muscle, and consists of an infiltration of inflammatory lymph in a circumscribed portion of the submucous tissue. It is tight, highly sensitive, thickened, inflamed, and bathed in pus; there are also constitutional symptoms, as fever, anorexia, and mental irritability. The subjects of this variety are usually women. The tissues composing strictures of the rectum of a very chronic character are found to be gray or bluish-white in color, of very dense fibrous structure, and creaking under the knife when cut, as a piece of cork would do.

Besides the before-mentioned stricture, due to the contraction of a chancroidal ulcer, is another caused by submucous gummata of the ano-rectal region, which is very rare; and yet another, the diffuse gumma, or ano-syphiloma of Fournier, which is the most frequent of all causes of stricture of the rectum. The diffuse gumma is one of the later manifestations of syphilis, and consists in "an infiltration of the ano-rectal walls by a neoplasm of as yet undetermined structure originally, but susceptible of degenerating into a retractile fibrous tissue, and thus giving rise to narrowing of the intestinal calibre to a greater or less extent."

Proctitis, or Inflammation of the Rectum.

Inflammation and suppuration in the lower part of the rectum are even more common than the corresponding affections of the cæcum, and their causes are quite as various. In many cases, no doubt, this affection is traceable to ulceration (perforative or otherwise) of the mucous membrane; in others it probably originates in the connective tissue which surrounds the rectum (periproctitis). The rectum, still more frequently than the cæcum, becomes involved in inflammation and suppuration originating in the various pelvic, and even in distant, organs. Abscesses arising in the abdominal cavity or its parietes are peculiarly apt to gravitate into the pelvis and to communicate with the rectum.

Proctitis in its acute form has some symptoms in common with dysentery, but it differs from it by the absence of abdominal pain, tenderness, and severe constitutional symptoms. The pain in proctitis is usually referred to the sacrum and perineum, and there is frequently dysuria from sympathetic affection of the bladder. This disease may be acute or chronic; the latter form occurs in those advanced in life. Frequent attempts to evacuate the bowels, with great tenesmus, heat, weight, and fulness in the bowel, and a mucous and bloody discharge in the absence of impaction of the rectum, characterize the attack. Should it be protracted and severe, the discharge will become purulent. A digital exploration should always be made to ascertain if any foreign or irritating substance is exciting the inflammation.

The presence in large numbers of Oxyuris vermicularis may excite irritation and inflammation of the rectal mucous membrane, which is sometimes very intense.[3]

[Footnote 3: Curschmann, _Ziem. Encyclop._, Am. ed., vol. viii. p. 848.]

Inflammation of the anus and buttocks, caused by the application of the leaves of Rhus toxicodendron after defecation, has extended into the {888} rectum and produced proctitis and peritonitis.[4] "In some cases of dysentery the pathological lesions are limited to the rectum, which would produce an apparently local inflammation very similar to proctitis. The irritation of unnatural sexual intercourse and the contact of gonorrhoeal poison have been known to excite intense inflammation of the mucous membrane of the rectum, with a copious discharge of pure pus, and accompanied by intense burning pain and great heat of the parts involved."[5]

[Footnote 4: Case of Dunmire, _Philada. Med. Times_, vol. xii.]

[Footnote 5: Heubner, _Ziemssen's Cyclopæd._, vol. i. p. 552.]

Fissure of the Anus and Rectum.

The painful ulcer of Allingham is quite a common affection, attacking women more frequently than men, and no age is exempt from it. Of 4000 consecutive cases of rectal and anal disease observed by Allingham, 446 presented fissure of the rectum. They are rarely multiple. Their usual position is dorsal, although they may be found at any part of the circumference of the anus, and just within the verge of the anus at the junction of the skin and mucous membrane, extending upward toward the rectum usually not more than half an inch, and appearing as a crack or fissure, often very trifling in appearance, or a club-shaped ulceration, the floor of which will be very red and inflamed if it is recent, but if chronic the floor will be grayish, with hard, well-defined margins. Sometimes there will be found at the external extremity of the fissure a small club-shaped papilla or muco-cutaneous polypoid growth; but this is not to be confounded with the ordinary polypus, nor is it the cause of the fissure, but the result of irritation caused by the latter. In other cases the external site of the fissure is indicated by a very tender and swollen flap of integument, which often becomes the seat of a small but very painful fistula. The club-shaped papilla is said to indicate invariably the existence of fissure.

Fissure of the rectum is often associated with anteversion and retroflexion of the womb. In many of these cases the fissure will heal spontaneously when the malposition is rectified. However treated, the result will not be satisfactory while the uterine trouble remains uncorrected.

Fissure is not infrequently caused by and accompanied with polypi: it may be caused by any accident whereby the verge of the anus is torn or superficially lacerated--by chronic diarrhoea, by violent expulsive, straining efforts, as in labor, by the passage of very hard, dry stools--and very frequently it is syphilitic in origin. The most prominent symptom of this disease is pain, and this is very severe and peculiar in character, coming on in most cases not during the act of defecation, but twenty minutes to half an hour afterward, and is preceded by a hot, burning, throbbing sensation at the anus: then comes on spasmodic contraction of the sphincters, and the patient endures agonizing pain, often for several hours, when relief is gradually experienced, and no pain is felt until defecation again becomes necessary. Now, it has been observed that in some cases where the local lesion is very trifling the pain and spasm are intense and long-continued; in other cases, where spasm and agonizing {889} pain followed every act of defecation, no lesion of the anus or rectum could be found. This led Dolbeau to consider the essence of fissure of the anus neuralgic, and to define it as "a spasmodic neuralgia of the anus with or without fissure." The mental depression is so much out of proportion to the local disease that this may come within Curling's observation, that "mental causes may produce local disease in the rectum."

Rodent, or Lupoid, Ulcer of the Rectum.

This is, fortunately, a rare disease, and is peculiar and distinct from any other form of ulceration in this region. It is not cancerous, although bearing some resemblance to epithelioma. As it first appears it is very like a syphilitic sore, and its situation and the character of the pain might lead to the supposition that fissure existed. Rodent ulcer is usually situated upon the mucous membrane, although it occasionally invades the integument about the anus; its shape is irregular, its edges sharp and well defined, and it does not undermine the neighboring tissues. There is no induration about this sore, as nature does not seem to attempt to limit it or to set up any reparative action, and its surface is red and dry. The surrounding tissues seem quite normal. It is very destructive, and seems to prefer mucous membrane, although sometimes it destroys deeply. It does not cause infiltration; it does not spread by the lymphatic system, forms no secondary deposits, nor does it produce stricture. It may remain in a quiescent state for some time, and a certain amount of cicatricial tissue may form; but it never heals spontaneously, and an exacerbation comes on which destroys in a very few hours the repair which may have been the work of many days. This form of ulceration of the rectum is usually considered incurable; the pain is intense, being compared to that produced by hot iron, and of course being much aggravated by the acts of defecation. Patients so affected die from exhaustion and pain, although recovery may take place, I have known one case entirely cured by complete excision. Spasm of the sphincters is a usual accompaniment, and greatly augments the suffering of the patient. Of the four thousand consecutive cases of rectal disease tabulated by Allingham, only two were cases of rodent ulcer.

Obstruction of the Rectum.

This condition may be caused by foreign bodies introduced into the anus, by indigestible substances swallowed, by impaction of feces, by pressure of tumors external to the rectum, and by intestinal concretions. Any condition which causes loss of muscular and nervous tone in the large intestine favors its obstruction; thus, it is not uncommon in the aged of both sexes, but especially is this the case in women, and in them it often follows parturition. Hysterical, nervous, and debilitated persons are particularly prone to it. The insane, if not carefully watched and regulated, will become the subjects of it. Impaction of feces is a very common cause of obstruction of the rectum, and atony of this organ is usually the primary cause, the feces in these cases being {890} either very hard and dry or clayey and tenacious. These masses are of a more or less globular shape, and, as they irritate the bowel and produce diarrhoea, the practitioner sometimes falls into the error of prescribing doses of opium and the astringents, misled by the appearance of feculent fluid which oozes around the impacting mass. The impaction occurs just above the internal sphincter. Habitual constipation soon stretches the rectum and robs it of expulsive force, and an accumulation of months of fecal matter is sometimes found. The appearance of persons so affected suggests malignant disease: they are cachectic, sallow, dyspeptic, irritable, and nervous. Vomiting, anorexia, thirst, cough, hectic, irregular and profuse sweating, are also among its symptoms. Cases of melancholia and of hypochondriasis have been cured simply by the discovery and removal of rectal impactions. This condition has been mistaken for cancer, phthisis, intermittent fever, and enlarged mesenteric glands. Accompanying impaction, and as a result, is spasmodic contraction of the sphincter ani, which causes the anus to protrude in a nipple shape and to firmly resist the introduction of the finger. Usually, there is no discharge from the anus in these cases. Tenesmus, a sense of weight and of a body present in the bowel, are experienced. Young people are not often subjects of impaction.

Concretions also cause obstruction of the rectum: these are more frequently cylindroid in shape, and sometimes have a nucleus consisting of some firm foreign body. Wetherill reports a case of a young adult, who had been accustomed to the daily ingestion of a substance known as hygienic bread (this substance is made from the husks of grain, and is very coarse: it is used to excite peristaltic action), from whose rectum he removed a very hard ball of this substance which was covered with mucus, but which contained no nucleus. He reports another case in which the offending substance was a globular mass of casein, stained with bile and covered with mucus, and which had for a nucleus a small mass of hardened fecal matter.

Guéneau de Mussy[6] reports a case in which there was an occlusion of the rectum by a mass of magnesia, which was so firmly impacted that it had to be removed by a mallet and chisel. A similar case occurred in the practice of Dunlap of Norristown. Fendick[7] relates an instance of impaction by a fish-bone near the anus, causing obstruction requiring surgical interference; which illustrates the importance of examining carefully all cases of acute piles and threatened abscess.

[Footnote 6: _Medical Times and Gazette_, 1879, vol. ii. p. 214.]

[Footnote 7: _Lancet_, 1880, vol. ii. p. 239.]

These concretions often consist of animal and vegetable fibres matted together about a nucleus, the latter consisting of the seeds of fruit, fragments of bone or gristle, hair, small coins, or pins. "Enteroliths may lodge in the rectal ampullæ" and cause obstruction. Indigestible substances swallowed with the food may be arrested in the rectum, such as grape-skins, fruit-pits, husks, and fibres, and where there already exists stenosis of the bowel a dangerous form of obstruction may be produced. Jones[8] reports a case of chronic impaction of the rectum by plum-stones, which gave rise to trouble in defecation, and at the end of eighteen months produced symptoms of piles; at the end of two years impaction occurred, and the mass was removed by the surgeon. Hazelhurst relates {891} a case of impaction in a negro where two hundred and eighty plum-stones were removed from the rectum after having been there for a week. The records of the Pennsylvania Hospital furnish the following interesting case of obstruction:[9] "The patient (a male) stated that twenty years before he swallowed a peach-stone. Two years afterward he had symptoms of rectal irritation, tenesmus, constipation alternating with diarrhoea, and liquid stools, etc. These symptoms had continued ever since. His health had been markedly impaired. A digital examination revealed a hard, stony mass two and a half inches above the anus. Under ether Morton divided the external sphincter, and with a pair of bone-forceps removed, with considerable difficulty, a good-sized peach-stone which was lodged in the rectal tissues. The stone was very sharp at the ends, and had evidently lodged crosswise and become imbedded. The patient was discharged quite well and free from all symptoms."

[Footnote 8: _Lancet_, 1856, vol. ii. p. 278.]

[Footnote 9: _Surgery in the Pennsylvania Hospital_, Phila., 1880, p. 335.]

Gall-stones may cause impaction or they may form the nuclei of concretions. A case of impaction is related by Walker,[10] who removed a gall-stone from the rectum which measured three and a half inches in its longest and one and a quarter inches in its shortest diameter; also one by Roberts,[11] in which he removed a gall-stone measuring five inches in circumference from the rectum of a woman two weeks after confinement. Mischievous, revengeful, insane, or intoxicated persons sometimes force very curious foreign bodies into the rectum, among which may be mentioned hot iron, bottles, cups, bougies, pieces of wood, stones, a champagne flask, a goblet, slate-pencils, and the tail of a pig with the bristles cut short. Some foreign bodies introduced from below find their way through the sigmoid flexure and lodge in the colon, or they may remain for a long time in the rectum. The cæcum is the favorite resting-place of foreign bodies. Turgis[12] removed by linear rectotomy a cup which had been forced into the bowel. These foreign substances, if not promptly removed, set up violent inflammation. Obstruction of the rectum may be caused by vast numbers of round- or thread-worms twining themselves together in a mass; and when this happens in children or in adults of very nervous organization a curious train of reflex symptoms may be developed, among which may be mentioned choreic movements, convulsions, pruritus ani, insomnia, irritability, melancholia, and hypochondriasis. Finally, the rectum may be obstructed mechanically by pressure exerted from without. Such an effect might be produced by morbid growths from the sacrum or ileum; by deposits in Douglas' cul-de-sac; by ovarian disease; by pelvic cellulitis causing stricture of the rectum; by vesical trouble; by ascites with hepatic disease; and by various abnormalities of the uterus, such as inflammation, morbid growths within or upon, simple retroversion or retroflexion, or retroflexion of this organ in a gravid state.

[Footnote 10: Flint, _Prac. Phys._, 460.]

[Footnote 11: _Bost. Med. Journ._, 1879, vol. ii. p. 116.]

[Footnote 12: _Société de Chirug._, 1878.]

Impaction of feces under some circumstances may give rise to extensive sphacelus of the rectum and the contiguous parts from pressure. This is well illustrated in the following case of a woman aged sixty-five, who was found to have an immense distension of the abdomen from ascites, incident to a large omental scirrhus. The patient suffered greatly from the pressure caused by the accumulation of water, and she was tapped. Soon after this an impaction of feces was observed, which probably had been forming {892} for some time prior to her coming under observation. A week or ten days after the tapping the impaction was detected, but not soon enough to prevent the formation of a large slough of the posterior and inferior part of the rectum immediately above the anus. The submucous tissues and the skin, owing to the greatly enfeebled condition of the patient, soon gave way, leaving a large opening which communicated with the bowel. The tissues adjacent were oedematous, red, and painful. The finger carried into the bowel through the anus discovered the slough to have involved a region of at least two and a half inches in diameter.

Cutaneous Eruptions and Parasitic Conditions of the Anus.

These are quite numerous, and they almost invariably produce much distress and excite painful pruritus, which is augmented rather than relieved by scratching or friction of any sort. The application of the leaves of Rhus toxicodendron after defecation is capable of exciting considerable inflammation upon and around the anus, accompanied by small pearly vesicles, which, when ruptured by scratching, seem to spread the disease wherever the contained serum flows. Eczema, when found in the anal region, is usually due to parasitic growth. Erythema intertrigo is caused by the friction of moist opposing surfaces, as between the nates of stout persons, who perspire freely, and infants. The abraded derma exudes a sero-purulent fluid which excites troublesome pruritus. When this condition exists about the anus it causes painful defecation and spasm of the sphincters. Erythema chronicum occurring in this locality is frequently a sequel to chronic eczema and chronic lichen: the skin cracks, is moist, thickens, and the epidermis exfoliates. The proximate cause in both of these conditions is congestion of the vascular rete of the derma. In prurigo podicis papules appear which itch intensely, and when scratched bleed, the summit of each papule bearing a small black scab. If not cured, in time a true psoriasis may develop. Herpes of the anus occurs similar to herpes at the other mucous outlets of the body, and is usually symptomatic of slight disorder of digestion. Wetherill has seen a case of herpes zoster, (var. proserpens,) in which the vesicles extended from the side of the scrotum along the perineum to the verge of the anus. This condition was accompanied with neuralgia of the rectum, painful defecation, and spasm of the sphincters. Furunculi sometimes form at the verge of the anus, causing spasm, pain at stool, and occasionally marginal fistulæ. Various syphilodermata also appear in this region. Gross was the first to describe a condition of trichiasis of the anus--a very irritating complication to fissure--due to a perverted recurvation of the hairs usually found in the anal region. Villermé states that hairs have been found growing from the mucous membrane of the rectum. The colonization of pediculus pubis about the anus occasions a certain amount of irritation. Sarcoptes hominis is sometimes found in this region, having been carried there by hands infested with this parasite. The result is very distressing. The peculiar tracks or burrows made by this little animal, and the use of the microscope, make the diagnosis certain. The Acarus autumnalis, or mower's mite, has been found in the skin of this part, and it is capable of causing great distress. These do not furrow the {893} integument longitudinally, but burrow vertically, and may be picked out of the summits of the wheals, where they appear as small red points.

Ulceration of the Rectum and Anus.

This is a condition very different from fissure or the painful ulcer of Allingham--much more grave, difficult to treat, and, in chronic cases, much less hopeful of cure. It is not an uncommon affection, Allingham's table of 4000 consecutive cases of diseases of the rectum and anus furnishing 190 of the disease under consideration. An ulcer of the rectum may be partly within, partly without, the internal sphincter, but in most instances is found above that muscle, from an inch and a half to two inches from the anus, situated dorsally.

The symptoms are unfortunately obscure and insidious, misleading not only the patient, but also too frequently his medical adviser, and gaining grave headway before a correct diagnosis is reached. Often the very first symptom is a slight diarrhoea every morning as soon as the patient rises, accompanied with a little discharge resembling coffee-grounds; or, again, the discharge is like the white of an egg; in some rare instances pus is formed. At this stage there is little or no pain, but the patient suffers from tenesmus--which is not followed by relief--and a sense of uneasiness in the part. Several stools of this nature or streaked with blood may be passed during the earlier part of the day, after which the patient feels partly relieved, and no more evacuations occur until the following morning, when he again experiences the same train of symptoms; and this repeats itself daily for a long time. Finally, these discharges occur in the evening as well as in the morning, then at various times during the day: his general health begins to give way; the discharge becomes augmented in amount and contains more blood and pus; and he suffers occasional pain from flatulent distension. Local pain in the rectum is now felt, which is not acute, but is very wearying, is augmented by much walking or by long standing, and which has been described as similar to a dull toothache. These ulcers may be multiple, and not infrequently lead to stricture of the rectum, which condition is indicated by the alternation of attacks of diarrhoea and constipation. As the ulcerative process proceeds, nature makes efforts to limit the process, which causes infiltration and thickening of the submucous and muscular tissues, and produces narrowing of the lumen of the intestine, which in time loses its tone and contractile power and becomes a passive tube, utterly unfit to perform its normal duties. The sphincters give way and the patient loses control over his evacuations. Finally, abscesses form, which, burrowing toward the surface, form fistulæ, and may perforate the bladder, the vagina, or the peritoneal cavity. If one of these ulcers be examined while yet in the acute stage, it will be found to be oval in shape, with well-defined edges: the base will be either grayish or very red and inflamed, the surrounding mucous membrane appearing normal. The rectal glands will be found to be enlarged. Should the ulcer be examined at a later stage, it will be found to be much deeper and more extensive, with great thickening and nodulation of the mucous membrane, and looking in places as though the latter {894} had been torn off. At this stage the ulceration may be partial or may involve the entire lower portion of the rectum. The suffering is now intense, and a constant discharge of fetid pus and mucus takes place. The appearance of the anus at this time suggests malignant disease: it is covered with swollen, shiny, tender, club-shaped flaps of integument constantly bathed in an ichorous discharge. The entire rectum and sigmoid flexure have been involved in some cases, while in others necrosis of the sacrum has occurred. Patients suffering from ulceration and stricture are very liable to a low form of peritonitis, attended by intense abdominal pain.

The causation of these ulcers of the rectum is frequently very obscure: some are of syphilitic, others of strumous, origin. Some are of traumatic origin, but more often the patient was in apparent health up to the time of the appearance of the disease. The experience of Allingham would indicate that neither chronic constipation nor dysentery is a frequent forerunner of this malady. T. Claye Shaw,[13] in an article entitled "On Some Intestinal Lesions of the Insane," says: "After death are found patches of ulceration sometimes so extensive as to resemble a honeycomb network. The edges are usually slightly raised, and perhaps hardened; but the ulcers are at other times mere local punchings out of the mucous membrane, and there is often a little loose gelatinous material." It is claimed that such disorders are not infrequent among the insane.

[Footnote 13: _St. Bartholomew's Hospital Reports_, 1880.]

It is also claimed that the chronic mechanical irritation from foreign bodies, impacted feces, and the like exert a causative influence in the formation of ulcer of the rectum. Like typhlitis, this affection leads to chronic inflammatory changes in the immediate neighborhood (periproctitis), with the formation of fistulæ and crater-shaped ulcerations, and to the extensive destruction of the mucous membrane, followed by wasting and contraction of the rectum. The healing of these ulcers is much delayed by the fact that the ulcerated and undermined mucous membrane is irritated by the fecal masses which are especially apt to accumulate in the lower part of the bowel and around the anus. We find also hemorrhoidal swelling and ulcerations, which may be regarded as partly a cause, partly a result, of the ulcerative proctitis.

Follicular Ulcerations.

In this condition the most extensive ravages are found in the rectum and sigmoid flexure. The causes are identical with those of catarrh of the large intestine, if we except the follicular disease produced by dysenteric infection. In this form of the disease, at least in its earlier stage, the form of these ulcers is always round and funnel-shaped, with distinct thickening of the edges of the mucous membrane around the ulcers. These appearances may be explained by the mode in which the follicular ulcerations originate: "The solitary follicles become swollen, a result of catarrhal irritation, and the cellular elements accumulate in the reticulum, giving rise at first to nodules which project above the level of the mucous membrane: then the newly-formed tissue-elements become necrosed in consequence of the mutual pressure of the cells upon {895} each other; finally, the apices of the follicular nodules give way and the ulcers are formed. The surrounding mucous membrane bends over downward toward the base of the ulcer, so that the orifices of the crypts look down into the same."[14] As the suppurative process extends, particularly in the submucosa, and the tissue surrounding the follicles becomes destroyed, these small ulcers coalesce to form larger ones, and the undermined edges of the mucous membrane project over the base of the ulcers, bleed, and become necrosed. Healing is possible by cicatrization, the borders of mucous membrane becoming applied to the base of the ulcer and gradually drawn together by the cicatricial tissue. Still, this result is extremely rare if the ulcerative process has gained much headway. When, however, a follicular ulcer of some size does heal, cicatricial stenosis may result, followed by chronic constipation, just as in the case of simple catarrhal ulceration. The situation of follicular ulcerations is almost always in the large intestine, and they vary considerably in number: sometimes only a few follicles are thus affected, while in other cases the bowel is crowded with them.

[Footnote 14: Rokitansky, _Path. Anat._, iii. 1861, S. 226.]

The anus and rectum may become the seat of chancroidal invasion. An ulcer of this character fairly within the rectum is very rarely met with, especially in this country, and could scarcely be produced except by unnatural intercourse. They are of not uncommon occurrence in the anal region, and are met with in this situation more frequently among females than among males. Occurring among the former, they no doubt often arise from accidental contact during normal sexual intercourse. When this condition is found in males, it rather indicates at least an attempt at unnatural intercourse. Of 1271 males affected with chancroids, only 3 were found with the disease in the anal region. Out of 388 females similarly affected, 33 were found with chancroid of the verge of the anus. The table of Debauge gives 23 cases among 206 females having chancroid in various other situations. The destruction of tissue in these cases may be very serious should the nature of the ulcer not be recognized, and stricture of the rectum or cicatricial stenosis of the anus might result. Ulceration of the rectum may occur during chronic proctitis; it may accompany advanced states of prolapse and procidentia of the bowel; it may attack a stricture of the rectum and cause peritonitis by erosion. Ulceration may accompany hemorrhoids, or it may attack them and cause dangerous hemorrhage. Finally, a very intractable form of ulceration may follow the clamp-and-cautery operation upon piles. When this untoward result is seen, it is usually due to the fact that the patient has been allowed to move about too soon. Allingham claims to have seen these ulcerated stumps of piles even ten days after operation.

Peri-anal and Peri-rectal Abscess.

The ischio-rectal fossa is peculiarly liable to attacks of inflammation resulting in abscess, as it is filled with much loose connective tissue which supports a considerable amount of fat, and is situated in a region which is constantly exposed to injury both from within and without. It is a very vascular part, being freely supplied by branches of the inferior {896} hemorrhoidal arteries and veins; the latter, being large and destitute of valves, empty into the portal circulation. Abscess in this region is of very common occurrence, and may attack any one at any period of life. It occurs more frequently among men than among women, and usually during middle life.

Abscesses in this situation may be acute or chronic. The former variety may be caused by injury to the anus or to the surrounding parts; by exposure to cold and wet, and particularly by sitting upon damp seats while the body is overheated; by impaction of feces, constipation, and straining at stool. Irritating substances swallowed with the food, such as small pieces of bone, oyster-shell, or the stones of fruit, may excite abscess by their presence in the rectum. Among other causes are general debility, an impoverished state of the blood, the scrofulous and tuberculous diatheses. The disease sometimes occurs in quite young infants. Wetherill reports the case of an infant attacked by an enormous ischio-rectal abscess while nursing from the mother, who was at the time suffering from a succession of boils. Many cases have been traced to sitting upon the outside of damp omnibuses. Hepatic disorders, causing engorgement and stasis of the blood in the hemorrhoidal plexus, have frequently occasioned this condition. These abscesses are not always situated in the ischio-rectal fossa; frequently they are subcutaneous and just outside the anus: in other cases the starting-point may be ulceration of the mucous membrane of the rectum, with escape of fecal matter into the areolar tissue; they also originate in the submucous connective tissue of the rectum. The acute abscess is sudden and very severe in its onset; the pain is continuous, throbbing, and augmented during defecation; dysuria is almost always present, and in some cases there is total inability to pass water. There is local tenderness, dusky redness, and fluctuating prominence, and, if not interfered with, a rupture of the integument will take place and the pus will escape externally. Sometimes their formation is accompanied with a chill or with a succession of rigors: there is always considerable constitutional disturbance, febrile movement, loss of appetite, and malaise. This form of abscess is usually circumscribed and does not burrow irregularly, and sudden relief of pain and distress is coincident with their evacuation.

Chronic rectal abscess corresponds to the cold or chronic abscess in other situations: it is apt to occur among those who are much debilitated or among those of the scrofulous diathesis. These abscesses have little disposition to open spontaneously upon the surface, but they burrow extensively in all other directions--high up along the outside of the rectum, laterally into the tissues of the buttock, or downward and forward into the perineum. The process of formation may occupy many months, and sad havoc may be occasioned before their existence is suspected. They occasion no pain nor distress nor acute febrile movement, but may be accompanied with a hectic condition, erratic sweatings, and rapid loss of strength. Upon examination of the anal region in these cases a painless flat, boggy, crepitating enlargement is the only surface-indication of the probably extensive damage sustained by the deeper structures.

This form of abscess may be of traumatic origin, but more frequently the inflammatory process arises in the cellular tissue of the ischio-rectal fossa; in some cases the morbid action is due to ulceration of the rectum. {897} In either case peri-rectal or peri-anal cellulitis will be induced. When these abscesses are of strumous origin the pus is thin, curdy, and offensive.

Both the acute and the chronic abscesses of this region are often difficult to heal, the external opening remaining permanently patulous, communication with the bowel resulting from internal burrowing and erosion, with the formation of extensive sinuses in all directions, resulting in fistulæ in ano.

Fistula in Ano.

This condition occurs more frequently than any other of the abnormalities of this region, Mr. Allingham finding 1208 out of his table of 4000 consecutive cases of diseases of the rectum and anus. He found also that fistulæ followed rectal abscess in 151 out of 196 cases, the abscesses which healed kindly and gave no further trouble being only 45 in number. A fistula in ano is a linear ulceration with a patulous orifice which discharges pus: it may or may not communicate with the bowel, and it may have more than one external opening. The great majority of fistulæ in this region are caused by abscess, either arising in the submucous areolar tissue of the bowel, or in the subcutaneous connective tissue in the immediate neighborhood of the anus, or in the ischio-rectal fossa, or in an ulcerated state of the mucous membrane of the rectum: in other cases it is congenital, or it may result from the presence of foreign bodies or worms in the bowel, or from puncture of the rectum by pins, scales of shell, fragments of bone, or other sharp substances swallowed with the food. Abscesses leading to fistulæ have followed kicks, blows, or wounds of the anal region: in short, anything which induces an abscess here may result in a fistula, and as in the former more cases occur in males than females, and more during middle age than at any other period, the same is true as to the latter. Fistula is quite common among the phthisical as a result of malnutrition and septicæmia, aided by the constant succussion of the perineum produced by efforts at coughing. Of the 4000 cases previously referred to, 1208 were cases of fistula; "of these, 172 presented more or less marked symptoms of lung trouble, hæmoptysis, cough, or impaired resonance in some portion of the chest."

A fistula may be complete or incomplete. To be complete, it must have two openings (it may have more)--one in the anus or rectum, and one upon the surface. There are two forms of the incomplete or blind fistula--one in which there exists an internal but no external opening, and the other in which there is an external but no internal opening. In complete fistula there may be more than one external opening, and this is in the majority of cases not far from the anus, but it may open in the perineum or upon any part of the gluteal region. When the openings are multiple they usually converge to form a common tract or sinus. The external opening presents nothing to the untutored eye to lead to the suspicion of grave internal trouble: frequently the vent is so minute and valvular or shielded by a thin pellicle as to be entirely overlooked; in other cases a little teat formed of superabundant granulations guards the entrance: there may or may not be discoloration, elevation, or depression of the surrounding integument, and erythema resulting from the {898} irritating nature of the discharge. Inflamed and suppurating follicles in the integument about the anus are not to be mistaken for the orifices of fistulous tracts.

The internal opening in anal fistula is situated between the sphincter muscles, sometimes just within the anus, but oftener about half an inch above; in rectal fistula the internal opening or openings may be at any point above the internal sphincter. These sinuses may be very tortuous, with pockets, blind passages, or diverticulæ, and are known as horseshoe fistulæ when they commence at one side of the bowel and ulcerate around it to a point opposite before making an opening.

Of the two varieties of incomplete fistulæ, by far the least frequent is that where no internal opening exists, but where there are one or more external orifices: these do not invariably even run toward the bowel, but may extend off through the tissues in any direction. In the other variety, where there exists no external evidence of disease, considerable damage may be done before its recognition. Fistula may coexist with hemorrhoids, stricture, ulcer, or malignant growth: it may be a very trivial affair, with the internal but a fraction of an inch from the external opening, or it may be long, deep, and tortuous, with sinuses running in all directions through the buttock.

Usually, fistulæ become worse when not operated upon, but there are cases which have healed without surgical interference--others in which this condition has gone on for many years without getting any worse or without the discharge increasing in amount. The fluid discharged from a chronic fistula loses after a time much of its purulent character and becomes serous and watery; but fresh abscess and inflammation is apt to take place in these cases from feculent matter lodging in the sinus. Those which burrow most readily are the internal fistulæ with large openings, into which the feces are pushed, with the sinus running toward the anus, because of their funnel-shape.

The presence of fistula may be suspected if there are in the anal region abscesses which have not completely healed, or which, having apparently done so, break out from time to time and discharge pus; or from the existence of a circumscribed hardness or swelling unaccompanied by an opening which varies in size and is at times painful; or if there exist any ulcerated moist openings. To make a positive diagnosis the tract must be explored by a probe: enter the oiled, blunt-pointed probe gently into the external opening and let it find its way along without force, bending the probe if necessary, until it has traversed the sinus as far as it will go; then pass the finger into the rectum and feel about for an internal opening or for the point of the probe. If the finger be introduced first, the relations of the parts are interfered with and the internal opening, should one exist, might not readily be found. Sometimes the bottom of the tract does not correspond in situation to the internal opening, but extends beyond it. In those cases where no external opening exists, the rectal speculum, aided by judicious pressure, will discover an issue of pus from a sinus upon the mucous membrane of the rectum.

In order to illustrate the amount of damage which a small foreign body may cause when lodged in the rectum, Wetherill relates the following case, which occurred in his practice at the Pennsylvania Hospital for the Insane: The patient was a middle-aged man, intelligent, and an {899} employé of the hospital. "Upon examination of the anal region I found a small, tender, firm swelling, which did not fluctuate, about an inch to the left of the anus: this had been forming for about a week, and there was no history of painful defecation, of exposure to damp and cold, nor of a blow or injury of the part. Without waiting for the development of fluctuation, I made a free and deep incision into the ischio-rectal space, and a large quantity of very fetid pus escaped: upon introducing a large probe I found that it passed up into the fossa to a depth of four and a quarter inches and turned but slightly toward the bowel. Remembering the experience of Allingham, that when the pus in these cases was very offensive there existed an opening in the bowel, I questioned the patient again as to pain in the bowel or painful defecation, which was answered in the negative. No communication could be found with the finger in the bowel and a probe in the wound, and poultices were applied, liquid diet ordered, and the man kept in bed. The cavity was loosely filled with absorbent cotton and the entire wound (apparently) healed slowly, but kindly, and in about ten days after operation the patient left the house to all appearance sound. About a week after the patient returned with the report that he felt uneasy throbbing in the part, and that there was a very slight discharge. Upon inspection I found in the surface-line of the cicatrix a pinhole opening which yielded upon pressure a drop or two of pus; upon entering a very fine probe it passed into a narrow sinus to a depth of three and a quarter inches, but no communication could be made with it with the finger in the bowel. Upon withdrawing the probe it grated over something which felt like dead bone, about two inches from the surface. I enlarged the opening, introduced a pair of fine dressing-forceps, and withdrew a piece of the rib of a chicken about half an inch in length and sharpened at one extremity to a fine point. Upon making inquiry I found that he had not eaten any chicken since the development of the abscess. He then suddenly remembered that while he was at stool a few days prior to the formation of the abscess he experienced a sudden pang of very acute pain in the rectum, which, however, soon passed off. This was no doubt the moment when the piece of chicken-bone pierced the rectum."

Hemorrhage from the Rectum.

Hemorrhage from the rectum may be accidental, primary, or secondary--accidental when it follows the ulceration of internal piles or the erosion of large arterial or venous trunks during the progress of malignant disease, or when it occurs from the rupture of a rectum during defecation--a very rare and curious occurrence reported by M. E. Quénu;[15] primary when it occurs during, and secondary when it occurs after, a surgical operation upon these parts.

[Footnote 15: _Révue de Chirurg.; Practitioner_, p. 29, Oct., 1882.]

Hemorrhage from the rectum without any structural lesions is quite unusual, but occasionally copious losses of blood are seen in vicarious menstruation, and several instances have been reported.

When ligatures separate after operations upon those of broken-down constitution very copious and dangerous bleeding may occur without any symptoms save a "sensation of something trickling in the bowel," {900} a feeling of weight and fulness in the part, with increasing weakness and syncope of the patient, until he expresses a desire to go to stool, when suddenly a large quantity of blood escapes.

SECONDARY DISEASES OF THE RECTUM AND ANUS.

This class of affections depends upon constitutional infection, direct extension of disease by contiguity, by contiguity from disease in neighboring organs, or by abnormal conditions excited by disease of remote origin; and are frequently due to changes in the nervous and vascular supply.

Syphilis of the Rectum and Anus.

True primary syphilitic chancre of the rectum must be an extremely rare lesion, and could have been acquired only by unnatural intercourse. There are syphilographers who deny that the hard chancre has ever been found within the sphincter muscles; but it certainly is not uncommonly found in the anal region, and oftener among women than men. The table of Jullien gives 12 instances of this lesion in males, and 1 instance of chancre of the buttock, out of 77 cases, while among 82 cases occurring in the opposite sex, 21 were of the anus and perineum and 4 of the buttocks. The French authorities give the frequency of this condition in men as 1 case in every 119; in women, 1 case in every 12.

Anal chancres are easily overlooked, as they occupy the puckered folds of the anus, which when not opened out to the fullest extent afford perfect concealment: they may be either in the form of cracks or slight fissures, elongated ulcerations, or firm papules. It has been claimed that the initial lesion has provoked stricture of the rectum, but this is not probable.

The secondary manifestations of this disease which show themselves in the anal region are some of the syphilodermata, moist papules, mucous patches, and moist papillomatous excrescences or condylomata. The statistical tables of Davasse and Deville[16] in regard to the occurrence of moist papules and mucous patches in women show that out of 186 cases they appeared about the anus in 59 and on the perineum in 40. Bassereau's[17] statistics show that in men these lesions occurred in the anal region 110 times out of 130 cases. These are, of course, very contagious. Besides true syphilitic warts, which sometimes occur in this region, it is quite usual to see the anus surrounded and the entire gluteal cleft filled up with moist, offensive, papillomatous excrescences, which remain obstinately so long as these surfaces are permitted to rest in moist contact. Syphilitic stricture of the rectum is one of the results of a later stage of infection, and occurs oftener among women than men. It is stated by Jullien that of 60 cases only 7 were men, the remaining 53 women. They are invariably formed as follows: A gummatous deposit in the {901} submucosa undergoes ulceration, and the subsequent cicatricial contraction gives rise to the stricture. Whether the stricture will be valvular or annular depends upon the extent of rectal mucous membrane involved in the ulcerative process. The diffuse gummatous infiltration of the ano-rectal tissues and the subsequent deposition of contractile tissue are the most usual causes of these specific strictures. The lower portion of the rectum is commonly the situation of specific ulcerations, usually of the secondary or tertiary stage, which lead to the formation of stricture: this occurs more frequently among women than men, and between the ages of seventeen and thirty years. Gosselin and Mason regard strictures as the result of chancres, and not as the result of constitutional infection; but it is known that ulcerations of secondary syphilis may extend upward from affections about the anus, and also that gummata do commonly give origin to this condition. Gummata, and strictures following them, may be distinguished from other affections on account of the greater distance from the anus at which they occur, chancres or chancroid ulcers being usually within four or five centimeters of the anal orifice. Strictures due to gummata are more apt to occur late in life, but may therefore be easily confounded with cancer. Condylomata at the anus are often associated with syphilitic disease of the rectum.

[Footnote 16: _Internat. Encyclop. of Surgery_, vol. ii. p. 508.]

[Footnote 17: _Loc. cit._]

Scrofulous and Tuberculous Affections.

There are cases which yield abundant evidence of struma in the form of enlarged glands, chronic abscess in the neck, swelling and abscess in the vicinity of the articulations, and the like, in which ulceration of the mucous membrane of the rectum has been found: this condition may result in fistula in ano by erosion, permitting escape of flatus and excrementitious products into the cellular tissue. A similar result may follow by erosion of the bowel from a strumous abscess in the connective tissue around the rectum; both these forms tend to the production of that class of fistula which has no outlet at the surface, but which has one or more openings upon the mucous membrane of the rectum. Thus concealed (for often there is no marked surface indication of either abscess or fistula), they may remain for a long time unsuspected and acting as a serious drain upon the already impaired constitution. The pus in these cases is watery, curdy, and offensive. These chronic conditions are subject to intercurrent attacks of acute inflammation, due to the lodgment in the abscess cavity or the fistulous tract of fecal matter or indigestible solid substances. Any or all of the abnormalities of this region may be complicated by the existence of tubercular or scrofulous conditions of the system. Tubercular ulceration of the rectum is now a well-recognized condition. Rectal ulceration and tubercular disease of the lungs have not been found to coexist in any marked preponderating number of tabulated cases. The frequent association of fistula in ano and tubercular disease of the lungs has long been recognized, Allingham having found 172 such cases among 1208 cases of fistula in ano.

The pathology of tubercular ulceration of the rectum is graphically described in _Ziemssen's Encyclopædia_ as follows: "These [ulcerations] begin in the follicular apparatus with swelling of the individual {902} follicles and their vicinity from tuberculous deposit. The newly-formed cells become caseous, the superficial layer of the tubercle breaks down, and thus ulcerations arise of a round funnel shape. The enlargement of these ulcerations is probably produced by the constant formation in the base and edges of the ulcers of new nodules, which themselves caseate and ulcerate. This process of extension, to which these tuberculous ulcerations of the intestines exhibit a marked tendency, takes place chiefly in a transverse direction (girdle-shape), following the direction of the blood-vessels. The infiltration and necrosis may advance longitudinally, and, finally, the individual ulcerations coalesce with each other: in this way may be explained in part the dentate appearance of the edges of these ulcerations. The ulceration extends also in depth, although usually the muscular coat appears to be covered by a thick layer of connective tissue: the destruction advances slowly in the muscularis, but in the lymphatic vessels which pierce the muscularis less opposition is presented to the progress of the tuberculosis; and thus it is not uncommon to find tubercles ranged one after the other, like links in a chain, from the base of the ulcer directly down to the serosa. Healing is extremely rare. The most frequent situation is the lower end of the ileum, but the process may extend upward to the stomach, or downward, involving the rectum. There is almost invariably unmistakable signs of tuberculosis in other organs. It is possibly never primary, but this is a still-disputed point. It usually occurs with tuberculosis of the lungs, and when so occurring it is always secondary. The clinical symptoms of this state are by no means characteristic."

Dwelling upon the subject of intestinal tubercle, it has been suggested by Klebs[18] that the intestinal disease is produced by swallowing morbid products derived from phthisical lungs--an hypothesis supported also by the fact that tubercle in the intestines tends so strongly to spread downward. "The seat of the deposit is the submucous tissue or the corium of the mucous membrane: it is certainly subjacent to the basement membrane, and not contained in the follicles, as Creswell taught."

[Footnote 18: Jones and Sieveking, London, pp. 593-595.]

Woodward, in his article upon diarrhoea,[19] says: "The lesions, whether mild or severe, are most generally seated in the cæcum and colon, but more or less extensive tracts of the small intestine, especially of the ileum, are often involved also." He continues: "Tubercular disease of the lung was noted in nearly one-sixth of the autopsies of fatal cases of forms of flux heretofore described. Possibly the frequency in chronic cases may be explained by the fact that protracted intestinal flux forms the development of lung phthisis in the predisposed."

[Footnote 19: _Med. and Surg. History of the War of the Rebellion_, p. 266.]

The rectal fissure or painful ulcer may be connected with diathetic causes, as struma or scrofula: it is doubtful if syphilis should be included among its causes.

Cancer, Malignant Stricture, and Malignant Ulceration.

The forms of cancer met with in these regions are epitheliomatous, scirrhous, encephaloid, and colloid. Considerable diversity of opinion has {903} existed as to which variety occurs most frequently; but it is now probably a matter of absolute knowledge that the epithelial form is the one most commonly observed, and next to that in frequency the scirrhous form. Encephaloid and colloid are of quite infrequent occurrence. Again, as to the sex in which this affection appears the most often, there is much disparity existing between surgical writers: it is usually thought to be much more prevalent among women than among men. This is not the experience of many of the authorities upon this subject, yet the statistics of the Hôtel Dieu, Paris, furnish overwhelming evidence in favor of its preponderance in women. Carcinoma of the rectum, occurring as a primary infiltration in the rectum, probably occurs oftener in men, but there are among females so many contiguous structures prone to cancerous degenerations, as the uterus, the vagina, the ovaries, the Fallopian tubes, tumors and cancerous masses occupying Douglas's cul-de-sac, that it would seem likely that they would be more frequently the victims of secondary cancerous deposit in the bowel or of erosion and extension of disease by contiguity or continuity. Epithelioma in other situations attacks men much more frequently than women. This form of disease usually occurs in middle life and in old age, but to this general rule there have been many exceptions; it has been seen in children. Allingham quotes its occurrence in a lad of seventeen, and Gowland in one of thirteen. It very rarely occurs as a secondary deposit of cancer in a remote region or organ. In the table of 4000 cases of rectal and anal disease, before referred to, cancer existed in 105. This disease is usually within easy reach of the finger, except when the growth is in the sigmoid flexure, being within an inch or two of the anus or from two and a half to three inches above it. The epithelial form, when it commences at the anus, is closely analogous to epithelioma of the lip: from the anal outlet it spreads upward into the bowel, or it may be primarily seated there. When occupying the junction of skin with mucous membrane it is sometimes sluggish, and a long time may elapse before it takes on aggressive action: induration, nodulation, obstinate fissure, or fungous growth marks its inception; as the condition proceeds, infiltration of surrounding structures takes place and large, hard, irregular masses form, which ulcerate, split, and form cauliflower excrescences. The rectum becomes blocked with fungoid growths: both these and the cancer proper are very vascular, and frequent hemorrhages occur, and an offensive muco-purulent discharge constantly oozes from the bowel.

Scirrhus of the rectum commences as an infiltration of the submucosa, which rapidly involves the other elements of the bowel, pushing hard nodules upward into the lumen of the intestinal tube: these break down and form ragged ulcers with indurated margins, and bleed profusely. Its situation is usually not higher than three inches above the anus. It has a tendency to invade all the neighboring organs and soft structures, to bind them to itself in a firm, dense mass, and to form communications with the vagina, bladder, uterus, perineum, and penis. Abscesses and fistulæ are common complications.

These neoplasms are insidious in their onset, and when seated at some little distance from the anus do not excite much pain at first. In the epithelial form the anus presents an abnormal appearance: it is inflamed and is covered with irritated, hypertrophied tags of integument bathed in {904} a sanious, offensive fluid. Difficult defecation, of which the natural form is absent, with inordinate tenesmus, a sense of weight and fulness in the bowel, and an irritable condition of the bladder, are among the symptoms. The feces are passed in little, irregular lumps or broken fragments, or this state is accompanied by or alternates with small, liquid, offensive stools. As the diseased action proceeds, very severe local and general pain is endured: this is of a dull, lancinating character, and affects not only the diseased bowel, but involves the entire contents of the pelvis, shoots down the thighs, up the back, and into the penis: frequent and exhausting hemorrhages take place; the patient exhales a peculiar sickening odor; his complexion becomes cachectic; his strength fails; and death ensues, after a variable period of intense suffering, from a few months to two or three years after the first symptoms appeared. The modes of termination of life in these cases are--exhaustion, secondary deposition, septicæmia, peritonitis, and hemorrhage. Stricture of the bowel and very extensive ulceration attend all of these advanced cases of malignant rectal disease.

The encephaloid variety is prone to very sudden and rapid breaking down, and may destroy life within a few months. If the finger be passed into the bowel in a case of encephaloid degeneration, it will encounter a large soft tumor occluding the gut: this is a very different sensation from that imparted to the finger in a case of epithelioma or scirrhus. In the former there will be felt a crepitating, as though due to the giving way of a moist, friable substance; in the latter the touch will perceive dense, irregular nodulations and ragged ulcerations having very firm margins.

The rectum may also be involved and destroyed by any of these neoplasms in neighboring organs. A middle-aged woman who was admitted to the Pennsylvania Hospital in a very advanced stage of epithelioma of the cervix uteri died from hemorrhage from the rectum and uterus in eight minutes. At the autopsy it was found that the disease had almost separated the cervix from the body of the uterus, had involved the cul-de-sac of Douglas, and had eroded a large opening into the rectum. Numerous ends of large vessels were observed which had undergone erosion.

Carcinoma of distant organs does not seem to frequently involve the rectum by secondary deposition. "In 160 cases of gastric cancer examined at the Pathological Institution in Prague, Dittrich found secondary cancer of the rectum only twice."[20]

[Footnote 20: Leube, _Ziemssen's Cyclopæd._, vol. vii. p. 235.]

In these cases of carcinomatous disease originating in the bowel the neighboring lymphatic glands are indurated and enlarged, and secondary deposition in neighboring and distant organs is the rule.

The lower portion of the intestinal tract may become involved in disease by direct extension from the colon, as in dysentery following enteritis or entero-colitis. Habersham says that diarrhoea arises generally from an irritated condition of the large intestine, catarrhal and mucous diarrhoea from slight inflammatory disease closely allied to ordinary coryza affecting the mucous membrane of the large intestine. "In the diarrhoea of soldiers the lesions of the large intestine have been either those of congestion with varying degree of extravasation or of ulceration more or less extensive. The colon in the former cases has invariably presented {905} patches of intense congestion, and in numerous instances extravasation, the amount and intensity varying in different subjects, in a few the whole mucous surface of the intestine having a livid red color; in others tracts of more or less intense congestion at irregular intervals, as in the small intestines, would be noticed. The ileo-cæcal valve almost invariably presented intense congestion. The rectum has uniformly presented intense congestion, with more or less fibrinous exudation. Frequently the presence of fibrinous exudation was a question of doubt."[21] The entero-colitis or ordinary summer complaint of infants not infrequently causes a very troublesome form of proctitis. Besides the ordinary causes of dysentery, Feyrer[22] states that it is caused by irritation of the solar plexus of nerves, also by the inhalation of sewer emanations and by the ingestion of impure water.

[Footnote 21: _Med. and Surg. History of the War of the Rebellion_, vol. ii. p. 102.]

[Footnote 22: _Times and Gazette_, 1881, p. 87.]

"In dysentery the anus becomes bluish-red, and is even marked with cracks and rents; it is painful to the touch and tightly contracted. In the later stages of severe cases it becomes large and gaping; then the stools are generally discharged unconsciously, and the pain is slight, paralysis of the sphincter ani having occurred. These symptoms indicate generally that death is to be expected. In some of these cases the pathological lesions are limited to the rectum. Dysentery may succeed typhoid fever."[23]

[Footnote 23: Heubner, _Ziemssen_, vol. i. p. 552.]

"Pigmentation is common after dysentery, and also after typhoid fever when dysentery has existed. Pigment-deposits are encountered in the large intestine in those who have suffered from repeated attacks of acute diarrhoea or from protracted flux. They may be seated as diffuse patches on the general surface of the mucous membrane or may be more especially localized in the closed glands. The diffuse form of these deposits is more frequently encountered in the large than in the small intestine, and is apt to be more intense in the former, producing darker and more extensive discoloration; hence the ash- and slate-colored, greenish, and blackish tracts which are so frequently observed in the cæcum, colon, and rectum."[24] Follicular ulceration of the rectum sometimes follows chronic dysentery and typhoid fever. Woodward has observed that a catarrhal condition of the rectum commonly occurs in typhoid fever cases. Referring to typhoid fever lesions of the large intestine, Rokitansky[25] says: "The ulcerative process is by no means confined to the small intestine; we have seen the mucous membrane of the large intestine riddled with ulcers. They were many of them of large size, and had clean-cut, non-thickened margins. This condition, indicating the absence of reparative action, is not nearly so frequent as that of thickening and induration, which generally took place to some extent in the edges of the ulcers. The bottoms of the ulcers are commonly formed by the submucous tissue. Sometimes the muscular fibres are completely exposed: this, however, is generally the result of secondary advance subsequent to the reception of the morbid action."

[Footnote 24: _Med. and Surg. History of War of Rebellion_, vol. ii. p. 308.]

[Footnote 25: Jones and Sieveking, p. 590.]

John Harley[26] calls attention to the intestinal lesions of scarlatina as follows: "I know of no disease in which the morbid effects are more {906} uniform. Scarlatina is essentially a disease of the lymphatic system. It is attended with inflammatory action of this system of glands, in which are included the agminated glands of the intestine. In 28 cases examined, 8 had the solitary glands of the large intestine enlarged and inflamed; in 1 there was acute desquamation of the mucous membrane of nearly the whole of the large intestine. In about half the cases the large intestine was found healthy."

[Footnote 26: _Med.-Chir. Trans._, vol. iv. p. 102.]

The rectum and anus are frequently subject to attacks, by contiguity, from diseases in neighboring organs. The most frequent of these is doubtless that form of ischio-rectal abscess which invades the bowel, causing fistula in ano. Various neoplasms having their seat in the tissues or organs near the bowel may obstruct it by simple mechanical pressure, or may cause inflammation, infiltration, and ulcerative erosion. Mechanical encroachment by the pressure of a foreign body in the vagina may cause grave interference with the normal functions of the lower bowel. At the out-patient department of the Pennsylvania Hospital in 1880, Arthur V. Meigs, assisted by Wetherill, removed a large, hollow, glass ball-pessary from the upper end of the vagina of an aged woman, who declared the pessary had been so placed by a physician sixteen years before, and had remained ever since, despite her repeated efforts to remove it with an ordinary table-fork. Upon its extraction, which was accomplished with difficulty, a small portion of its surface was found covered with scratches. Its presence had caused constipation, impaction of feces, and atony of the rectum.

Interference with the rectal functions often follows tedious cases of labor where the child's head remains long in the perineum.

The Effect of Abnormal Conditions of the Spinal Cord and its Membranes upon the Rectum and Anus.

"In diseases of the spinal cord and its envelopes there is a great tendency to constipation, owing to impairment of the secretion of the intestinal juices. The intestinal movements are usually much affected, either in the way of increase or diminution, in the former of which the symptom is a frequent, watery, slimy diarrhoea; as a less common condition it is even capable of being produced reflexly. Thus in a patient with chronic myelitis I observed the regular evacuation of a mucous fluid mass from the intestine as often as his bed-sores were cleansed; and the like has been seen in dogs after division of the lumbar cord. Much more commonly there is habitual, even excessively obstinate, constipation, of which almost all chronic spinal patients complain. The stool is slowly discharged, dry and hard, and the evacuation occurs only at considerable intervals and after the application of energetic remedies. Several causes doubtless contribute to this: diminution of intestinal secretion and peristaltic contraction, and probably also weakness of the abdominal muscles of compression, which is often present. If there is an extreme degree of weakness, meteorism and accumulation of feces are other consequences. We do not know exactly from what portions of the cord these disturbances proceed."[27]

[Footnote 27: Erb, _Ziemssen's Encyc._, xiii. p. 138.]

{907} "There are also in many diseases of the cord disturbances of evacuation caused by paresis or paralysis of the sphincter ani. In mild cases simple difficulty in retaining stool for any length of time exists. There may be also great disturbance of sensibility, so that the patient does not feel the call, and even if he possess some voluntary control, he is surprised by the discharge, of which he feels nothing."[28]

[Footnote 28: Erb, _loc. cit._, p. 139.]

The sphincter ani is affected in cases of myelitis, the usual symptoms being those of paralysis; the same is true in softening of the cord or myelo-malacia, and there is also diminished reflex excitability of the anus.

Paralysis of the bladder and rectum is often delayed in cases of slow compression of the cord; but if the compression exists to any considerable extent, involuntary discharges of urine and feces will be sure to occur. A pressure-myelitis of the lumbar portion of the cord causes paralysis of the bowel, and in the later stage of some cases of bulbar paralysis it also occurs.

Early in the course of spinal meningitis there exists a spasmodic condition of the sphincters: these muscles are also paralyzed in spinal and in meningeal hemorrhage, and from the pressure of tumors upon the cord giving rise to paraplegia. "In acute ascending paralysis the bladder and rectum are generally quite undisturbed in their functions. In hemiplegia and in hemi-paraplegia specialis disturbances in the evacuation of the bladder and bowels are almost always present, and in the acute traumatic cases it is especially common to find severe paralytic symptoms at the beginning of the attack (complete retention or complete incontinence, involuntary stools, etc.), which, however, generally soon recede and give place to lighter, more permanent trouble, as weakness of the sphincters. Sometimes these disturbances are very significant."[29]

[Footnote 29: Ibid., _loc. cit._, p. 740.]

The following is an extract from Gower's _Diagnosis and Diseases of the Spinal Cord_:[30] "The spinal cord possesses centres, situated in the lumbar enlargement, which preside over the action of the bladder and rectum. They are probably complex reflex centres: that for the sphincter ani is the more simple.... But if the volitional path in the cord is damaged above the lumbar centres, the will can no longer influence the reflex processes: as soon as the feces irritate the rectum they are expelled by the reflex mechanism.... If the damage to the cord involves also the sensory tract, the patient is unconscious of this process; if the sensory tract is unaffected, the patient is aware of the action of the bladder or bowel, but cannot control it. It is often said that there is permanent relaxation of the sphincters, but this is true only when the lumbar centres are inactive or destroyed. In this condition evacuation occurs as soon as feces or urine enter; the urine escapes continuously instead of being expelled at intervals.... We may, however, distinguish between the two states of the rectum by the introduction of the finger: if the lumbar centre is inactive, there is a momentary contraction due to local stimulation of the sphincter, and then permanent relaxation. If, however, the reflex centre and motor nerves from it are intact, the introduction of the finger is followed first by relaxation, and then by gentle, firm, tonic contraction."

[Footnote 30: London, 1880, p. 37.]

{908} Morton has at this time in his wards at the Pennsylvania Hospital two cases of rectal paresis following fracture of the vertebræ. The first, a lad aged nineteen years, while crossing the Atlantic was struck during a gale by a spar upon the back about the region of the lower dorsal vertebræ. From the deformity and from other symptoms there was undoubtedly a fracture destructive to the normal functions of the cord. Upon the arrival of the steamer, some ten days after the accident, the lad was brought to the hospital, where he has remained for the past eighteen months. Total palsy of sensation and motion has continued from the time of the accident to the present day, and extends from the navel downward: the sphincter ani is constantly but feebly contracted; the finger, when pressed into the anus, encounters slight resistance, which continues during and after the simple passage of the finger; very slight pressure, however, against the sphincter causes a very marked relaxation, which continues so long as this is kept up. With the removal of the finger the sphincter slowly and fairly contracts. The second case is also one of vertebral fracture which has been in the hospital about ten months. In this instance the sphincter is always found contracted, but it readily yields under finger pressure, and contracts quickly and regularly in the absence of this pressure. Constipation and rectal impaction readily occur, and the bowel requires to be regularly emptied. In another case, at the Episcopal Hospital, under the care of W. B. Hopkins, there is fracture of the spine, with total palsy below the seat of injury. The margins of the anus were found in apposition, but in no firm contraction: mere contact of the finger appeared to have little or no effect, but slight pressure upon the sphincter caused a contraction, and very moderate pressure upon the anus after the introduction of the finger produced excessive dilatation. The action of the sphincter was in all respects very tardy.

Two recent cases (August, 1883) of fracture of the dorsal vertebræ have been admitted into the Pennsylvania Hospital. One, a lad aged ten years, was struck by a bale of cotton which fell upon him; the other, a man aged thirty years, fell from a second-story window. In both cases total palsy occurred at once upon the receipt of injury, and in each the same conditions of the anus have obtained as before described.

In the convulsive attacks incident to epilepsy the sphincters of the bowel and urinary bladder are relaxed and the discharges are involuntary; probably, also, one of the first symptoms indicative of tumor of the base of the brain is recognized in involuntary rectal evacuations. Rectal incontinence may be also due to tabes, while atony and constipation are sometimes noticed as a result of excessive intellectual exertion (DaCosta). The same may be said of chronic lesions of the brain and spinal cord. Paresis of the rectum has been noticed as a result of chronic congestions of the heart and in hepatic disease. Allingham has observed failing nerve-power as a cause of rectal atony: the latter, with constipation, is one of the commonest troubles attendant upon melancholia and the chronic forms of insanity. Seeley of Ovid, New York, related to Morton a case of paraplegia with rectal paresis and dysenteric symptoms from malarial poisoning in a married lady aged thirty years. An examination revealed an immense rectal impaction. A free administration of quinia was followed by complete recovery in a few weeks.

{909} Spasm or Spasmodic Contraction of the Rectum and Anus.

Apart from those cases in which spasm is induced by the irritating stools of diarrhoea and dysentery, or by local ulcerations, fissures of the anus, and intestinal worms, there are those in which painful spasm occurs, due to the presence of a vesical calculus: it is also caused by urethral stricture, impaction of feces, irritations and inflammations involving the bladder or the adjacent organs. Spasm is also seen in nervous females, without constipation; also in the varied irritations of the female genito-urinary apparatus. In cases where spasm is due to rectal impaction retraction of the anus is frequently seen.

Pruritus Ani.

This most painful, distressing, and obstinate affection belongs to the class of neuroses, and is simply functional in character, without the least structural change in the skin or mucous membrane of the anus or rectum: the itching may be confined to the former or it may extend into the latter. It may be brought about by a constipated state of the bowels, but it is more often due to derangements of the digestive apparatus.

Sufferers from pruritus ani are generally dyspeptics, although the malady is observed in persons who are otherwise in most robust health. Overwork, mental and physical exhaustion, have been charged with producing pruritus, and in some instances spinal irritation seems to have been unquestionably the exciting cause: now and again, pruritus ani has been produced by the pregnant condition, and in some cases this malady has persisted during the entire period of utero-gestation. Intestinal worms, uterine maladies, rheumatism, and especially gout, have unquestionably been exciting causes. Some years since a gentleman having the most intense pruritus, which defied all treatment, was suddenly relieved of all former distressing symptoms by the passage of a small vesical calculus, the presence of which had never been suspected, as no vesical symptoms had at any time existed. Some of the most aggravated instances of anal pruritus are found in those far advanced in diabetes mellitus. The nerves of the lumbar plexus in rare instances have suffered from compression, more or less severe, from fecal accumulations; in one case of spinal curvature detailed by Portal[31] the rectum at its upper part was so narrowed by the encroachment of the false ribs that excessive fecal accumulation occurred which gave rise to remote pain in the great toe.

[Footnote 31: _Cours d'Anatomie médicale_, tome iv. p. 276.]

Neuralgia of the Rectum.

It seems to be unquestionable that there are instances of pure neuralgia of the rectum, for in such cases the most carefully conducted explorations have failed in demonstrating any evidences of disease. The pain is doubtless reflex, due to depressing causes, to atmospheric conditions, or to exposure to cold and wet. Neuralgia of the rectum has also been noticed in malarial {910} poisoning, and especially in those who have long been victims of intermittent fever. Neuralgia in this region of the body is also due to general causes, as witnessed in cases of rheumatism and of the gouty diathesis. Patients now and again complain of "violent and painful pressure in the rectum, conjoined with active pains in the perineum and anus and in the sexual parts: these symptoms probably have a neuralgic character."[32] In many nervous disorders, but especially in spinal irritations or inflammation, the rectum is invaded by pains of a neuralgic nature more or less severe, which are undoubtedly only functional in character. But 12 cases of neuralgia were observed out of 4000 cases of rectal disease. Anstie[33] says: "It needs some very powerful irritant to set up neuralgia in any portion of the alimentary canal: ... this condition has been described by Ashton.... In one case the patient complained of acute, paroxysmal, cutting pain extending about an inch within the rectum.... The cause of this attack was his getting chilled from sitting in his wet clothes." Curling says that constantly directing the mind to this part of the body will excite congestion and disease, possibly by producing abnormal sensations, itching, and superficial inflammation.

[Footnote 32: Erb, _Ziemssen's Cyclop._, vol. xiii. p. 139.]

[Footnote 33: _Neuralgia and its Counterfeits_, p. 130.]

"In patients with piles hyperæmia of the spinal cord may become habitual, returning regularly and frequently, and this may lead by degrees to severer disturbance by the development of chronic inflammation and proliferation."[34] Among some of the reflex troubles arising from rectal disease are--sterility in women, simulation of uterine disease, pruritus ani, pseudo-sciatica, pains in the legs and feet, and impairment of co-ordination in the muscles of defecation. There is a case reported[35] of a curious pain in the sole of a foot caused by rectal disease; and another[36] in which irritation of the eyes was caused by hemorrhoids.

[Footnote 34: _Ziemssen's Cyclop._, vol. xiii. p. 138.]

[Footnote 35: _Med. Times and Gazette_, 1868, vol. ii. p. 175.]

[Footnote 36: Cooper, _Lancet_, 1862, i. p. 625.]

There are some cases occasionally met with of so-called irritable rectum. Now, a rectum may be irritable because irritated, but in some of these instances there is no apparent cause. There occur frequent, small stools expelled with force, but without pain: there must be abnormal peristaltic action to cause this condition.

The Effects of Cholera and of Certain Poisons and Remedies upon the Rectum.

After death from cholera there is found congestion and a swollen state of the mucous membrane of the rectum: in some cases the epithelium of the entire alimentary canal is almost absent. In slow poisoning by arsenic the bowels show ulceration, but more particularly the rectum. After phosphorus-poisoning the large intestine has been found inflamed and contracted to the calibre of a quill. Among the effects of copper have been seen ulceration and a peculiar green staining of the rectum; of lead, no marked change of the mucous membrane except, in some instances, hardening, but the muscularis was in an advanced state of hardening and contraction. The action of croton oil is to render the mucosa very soft and friable. Extensive destruction of the mucous membrane of the rectum has resulted {911} from poisoning by bichromate of potassium. The mineral acids and the caustic alkalies, when not immediately fatal, cause corrosive ulceration of the rectum; the soluble salts of zinc, tin, bismuth, and antimony produce a like effect. Corrosive sublimate in its action upon the large intestine produces a dysenteric condition; similar in their effects are colocynth, jalap, elaterium, and cantharides. Strychnia causes a deep violet congestion; alcohol, congestion and thickening; and tobacco, redness of the mucous membrane with great engorgement of the vessels of the rectum. One of the results of the long-continued abuse of morphia is a catarrhal condition of the large intestine, accompanied with exfoliation of the intestinal epithelium. Some persons are very susceptible to the action of jaborandi, and in such its exhibition is followed by hyperæsthesia and dull pain in the rectum and the urethra.

It is interesting to note that an abnormal condition in the rectum may cause extensive disease in a remote organ; thus, a stricture of the rectum may cause abscess in the liver. Wilkes[37] exhibited at the Pathological Society a specimen in which an abscess, a diffuse, purulent infiltration of the liver, and a gall-bladder filled with purulent bile were distinctly traceable to the suppuration arising from an ulcerating stricture of the rectum consisting of dense fibrous tissue situated about four inches from the anus of a man aged thirty-seven years. "Any form of suppurative intestinal disease seems capable of producing hepatic abscesses of a metastatic or pyæmic character."[38] It has not been found, however, that tubercular ulceration of the intestines has ever given rise to hepatic abscess.

[Footnote 37: _Soc. Trans._, vol. ii.]

[Footnote 38: Darley, _On the Liver_, 1883, p. 536.]

Examinations and explorations of the abdominal viscera by the hand introduced into the rectum, having for their object the detection of tumors or morbid growths, are procedures which have fallen into merited disrepute, and are mentioned here in condemnation. However, some years since, Morton, in consultation with (J. Forsythe) Meigs, satisfactorily demonstrated the absence of a suspected renal calculus by this method.

The distension of the rectum with water, either free or contained in a rubber bag, in order to facilitate operations upon the pelvic viscera, has been lately brought into notice by Garson at a meeting of the British Medical Association. The most significant point brought out at the meeting was that the water-distended rectum displaced the distended urinary bladder upward and forward until it occupied a position quite outside of the pelvic cavity, carrying along with it the peritoneum both in front and behind. By this method of distension it was found possible so to raise the peritoneum in front of the bladder as to leave a clear working space of four centimeters between the upper border of the symphysis pubis and the edge of the peritoneum: this may prove useful in suprapubic lithotomy, as well as in operations upon the uterus and its appendages during laparotomy.

RÉSUMÉ OF THE THERAPEUTICAL AND SURGICAL TREATMENT.

FISSURE OF THE ANUS, in its true sense, is not to be confounded with ulcerations either slight and superficial in extent, or with more grave ulcerations involving not only the anus, but the mucous membrane of the {912} rectum also. The true fissure is a mere linear crack or abrasion or superficial ulceration. The pain accompanying this condition is out of proportion to the length and depth of the fissure, varying from slight uneasiness to as severe suffering as that caused by a deep and extensive ulceration.

The treatment to be adopted in such cases is first to regulate the bowels and to insist upon a scrupulous cleansing of the part after each evacuation. Much sitting is to be avoided and a sedentary mode of life is to be discouraged. Sometimes a few light topical applications of the solid nitrate of silver will bring about a cure, or a lotion of the same of the strength of from two to ten grains to the ounce of water should be applied with a camel's-hair brush every other morning. The ointment of the oxide of zinc, combined with any of the local anæsthetics, will be found useful. As a dernier ressort in obstinate cases an incision should be made through the fissure, together with a thorough dilatation of the anal sphincter.

ULCER OF THE RECTUM, OR THE GRAVER FORM OF FISSURE OF THE ANUS.--In the milder forms of this very common and painful affection the treatment consists in thorough cleanliness of the part; the ulcerated surface may be cauterized with nitrate of silver, and subsequently the application of the red precipitate ointment or the lotio nigra. Should a vaginal discharge exist, treatment should be instituted with a view to its arrest, as the irritating fluid coming in contact with the ulcer would prevent its healing. The treatment of that variety of ulceration where the disease is situated partly without the anus and partly within the rectum, besides the use of the means enumerated above, embraces the daily introduction of a full-sized bougie made of wax or of yellow soap. Henry Hartshorne says: "Experience leads me to have especial confidence in collodion, to which one-fiftieth of glycerin has been added to lessen its constricting effect." Glycerite of tannin and tinct. benzoin. comp. have been useful. J. C. Peters[39] recommends the use of iodoform suppositories. Tarnier[40] dusts the part with the same drug in fine powder. Créquy[41] has had success with a dressing of charpie saturated in a solution of hydrate of chloral. For the more extensive and obstinate forms of ulceration the three methods of treatment mainly relied on are--by cauterization, by dilatation, and by incision. The caustics usually relied upon are the fuming nitric acid and the acid nitrate of mercury, one application of either of these often exciting healthy granulation. This application is to be followed by the use of an ointment consisting of thirty grains of calomel and three grains of morphia to one ounce of lard. If there is much spasm of the sphincters, extract of belladonna may be added.[42] During this treatment the bowels should be kept rather loose by the use of compound licorice powder, and if much pain is experienced an opium suppository should be used. Dilatation, first practised by Récamier, consists of the introduction of the thumbs of the operator into the rectum, placing them back to back, and then forcibly separating them from each other until the sides of the bowel can be stretched out as far as the tuberosities of the ischia. On account of the fact that both cauterization and dilatation are not infrequently followed by relapse, the method of operation which includes both incision and dilatation can usually be relied {913} upon. The bowels should be thoroughly emptied by a laxative, and an enema should be given three hours before the operation.

[Footnote 39: _Philada. Med. Times_, Nov. 8, 1879.]

[Footnote 40: _Bull. gén. de Thérap._, Sept. 30, 1875.]

[Footnote 41: Ashton, _On the Rectum_, p. 157.]

[Footnote 42: Agnew's _Surgery_, vol. i. p. 418.]

After full anæsthesia the ulcer may be readily exposed. The left index finger of the operator is then carried into the rectum, and a sharp-pointed curved bistoury is entered, three-quarters of an inch or more from the side of the anus, to the depth of an inch or less, and carried on toward the bowel until the point is felt by the finger within, when it is made to puncture the mucous membrane, and then to cut out to the surface. In some cases of deep fissure, before dividing the sphincter the ulcer may be scraped freely or the entire ulcer may be removed. The anus should now be well dilated with the fingers, after which an opium suppository should be introduced and a fragment of lint or linen well oiled be placed in the wound. The subsequent treatment consists in keeping the patient in a recumbent position and confining the bowels with opium. After three or four days a laxative may be given. No dressing is necessary save attention to cleanliness.

The subcutaneous division of the sphincter has been proposed, but is objected to on account of the liability of the extravasated blood retained in the very loose cellular tissue of the part to form abscess. In one case which Morton operated upon in this manner many years ago a large abscess formed very rapidly, with serious constitutional symptoms, which were relieved only after the freest opening and division of the sphincter.

Should any polypi be found, their removal by ligation or by the knife is an essential element of success in the operation; retention of urine is not infrequent after operations upon fissure. When fissure or ulceration makes its appearance in a syphilitic subject, it will usually disappear under appropriate constitutional treatment.

TUBERCULOUS ULCER OF THE ANUS is best treated by the topical use of a weak solution of chloral hydrate.

CHRONIC ULCER OF THE RECTUM.--In this condition the treatment should include the use of anodyne and astringent lotions, suppositories or enemata, and the internal administration of Ward's paste--_i.e._ confection of black pepper.

RODENT ULCER OF RECTUM.--In this rather rare, exceeding painful, and generally incurable malady the patient sometimes dies merely from the exhaustion of pain. Another mode of death is by diarrhoea; another by hemorrhage. To quote Allingham:[43] "I have really nothing to offer as regards treatment; all the various sedatives will be required in their turn, and in the earlier stage I should recommend excision--not that I have much hope that you will eradicate the malady, but you will remove the pain, and for some time the sufferer will be comparatively comfortable. I think also the application of fuming nitric acid should be tried with the same object; one of my patients was fairly easy for three months after I had destroyed the ulcer with the acid." Morton accomplished the permanent healing of an undoubted rodent ulcer of the rectum by the complete divulsion of all the involved tissues.

[Footnote 43: Page 30.]

CANCER OF THE RECTUM.--The medical treatment of this affection is necessarily restricted to efforts to alleviate suffering and to obtain sleep--anodynes in the form of suppositories of pil. saponis comp. or of morphine mixed with ext. hyoscyamus in the proportion of a half grain of the {914} salt to ten grains of the extract. Enemata of warm water are useful. D'Arpene of Elba has suggested enemata of gastric juice. The profuse discharge of sanious pus must be met by weak injection of sulphate of copper and opium or a very dilute solution of chloride of zinc. Now, as to the use of bougies in these cases, it may be laid down as a general rule that their employment may be mischievous, yet in certain cases justifiable--indeed, absolutely necessary. When the disease is met with in its early stage, has not ulcerated, is within reach of the finger, and is producing much contraction of the calibre of the gut, a gum-elastic bougie, thoroughly lubricated, may be introduced through the contraction. In case this produces much suffering, the attempt must be abandoned; if not, once or twice a week is often enough. Where no extensive ulceration exists the patient can be much helped by this procedure. F. N. Otis[44] has reported a case of malignant stricture in which he completely divided the recto-vaginal septum, sphincter ani, and perineum with great temporary relief to his patient. When large portions of a malignant mass protrude from the anus, they may be removed by the application of a paste of arsenite of copper or by the elastic ligature, the destruction being safe and rapid. The injection of acetic acid into these growths has been practised, but is useless and harmful.

[Footnote 44: _Arch. Clin. Surg._, 1877.]

As to operative procedure, when the morbid growth is an epithelioma situated within a short distance of the anal opening an excision is not only justifiable, but may be recommended. The results show that its removal from this situation is as frequently successful as is its removal from the lip. When a cancer completely fills the lumen of the gut and plugs it so that the act of defecation becomes impossible, excision of the rectum and the establishment of an artificial anus are the two operative procedures open to the choice of the surgeon. A decided reaction of opinion has lately taken place among members of the profession relative to the latter of these; the few surgeons who did practise excision of the rectum in cases of cancer were looked upon as being rather unscientific and unsurgical. Billroth has excised the rectum 16 times, with 4 fatal cases; Dieffenbach performed it 30 times; Lisfranc had recourse to this operation as early as 1826; while the operation has been performed very frequently in this country, and with success.

Morton says: "In the spring of 1882, I was consulted in the case of a lady aged fifty-six who had suffered for two years from what were supposed to be internal hemorrhoids. An examination revealed the existence of a large scirrhous mass encircling about two-thirds of the gut, on the anterior part especially, and extending upward three inches. The patient was worn down by long suffering, but was otherwise in fair condition of health. With the assistance of Gross and Agnew, I excised the mass, which included the entire lower part of the rectum. The wound healed kindly, without an untoward symptom, and the patient was very soon enabled to leave her home for the seaside, where she passed the summer. The disease, however, resumed, but without any of the severe pains which she had had prior to the operation. Death occurred from gradual exhaustion seven months afterward."

He also relates the following case of excision of the rectum: The patient, a female aged thirty-five years, first noticed some rectal {915} irritation about four years ago. This was followed by distressing pain during defecation and by hemorrhages; finally a tumor, which was described by her medical attendant as being like an opened umbrella, protruded, partly at first, then fully, through the anus. The growth seemed to be spongy in character, and was very vascular. It was removed by carrying a double-threaded needle through the mass, and thus ligating it. Upon the seventh day after the operation a hemorrhage occurred, which was controlled by plugging the rectum. Although the growth was removed, the patient did not make a good recovery; symptoms of rectal irritation continued. In September, 1884, the patient presented herself in a wretched condition, with bearing-down pains and frequent hemorrhages. Upon digital examination an elevated mass was readily detected upon the sacral aspect of the bowel. By carrying the fingers beyond this mass and making traction, it was brought down within working distance, and was excised along with the entire lower portion of the rectum. The freshly-cut edges of the gut were then drawn down and stitched to the mucous membrane just above the anus. The patient made a good recovery and has a serviceable anus.

R. J. Levis[45] has operated upon two cases of cancerous growth in the rectum, removing the lower part of the bowel. The first case was that of a man aged sixty, who made a very good recovery from the successful operation, although three inches of the gut were removed. The second case was that of a man aged fifty-two, who had a carcinomatous tumor the size of a hen's egg at the right side of the rectum. The section of gut excised was about one and a half inches in length. The patient died of peritonitis upon the fourth day after operation. At the autopsy there was no wound found in the peritoneum, the lowest point of which was one inch above the end of the excised bowel.

[Footnote 45: _Surgery in the Pennsylvania Hospital_, pp. 81-83.]

The etherized patient, his bladder having been emptied, should be placed in the lithotomy position. If a male, a sound should be passed into the bladder. An incision is then carried from the centre of the perineum along the raphé to the anterior margin of the anus, encircling the latter by two semicircular cuts and continuing the division directly back to the coccyx. In the female the incision should begin just posterior to the vagina. If the anus is not included in the diseased mass, the external sphincter may be spared by raising the skin and the muscle together and turning them on each side. When the lower end of the rectum is reached the dissection should be made entirely by the fingers or by the handle of the knife, tying vessels as they spring. Double ligatures should be introduced through the gut from its mucous surface outward, and, when possible, then stitched to the skin at the margins of the wound. The bowels should be controlled by opium for the following eight or ten days.

The other operative procedure is lumbar colotomy. This was first advocated by Amussat in 1839, when he appeared in a treatise upon the subject entitled _On the Possibility of Establishing an Artificial Anus in the Lumbar Region_. It is denied that he ever performed this operation. It has happened to sound surgeons and skilful operators, when the patient has been very muscular or very fat or when the colon has been collapsed, that they have been at length compelled to abandon the search for the gut {916} and to stitch up the external wound. Allingham states that the cause of failure often is that the colon is searched for too far from the spine, resulting, in the opening of the peritoneum, in the starting up into the wound of a mass of small intestine which baffles the operator very seriously. He, having made more than fifty dissections, has come to this conclusion: "that the descending colon is always normally situated half an inch posterior to the centre of the crest of the ileum (the centre being the point midway between the anterior, superior, and posterior-superior spinous processes)." An incision four inches in length should be made midway between the last rib and the crest of the ileum. The incision may be made transverse, or, better, obliquely downward and forward, as suggested by Bryant. Allingham says that care should be taken to preserve the original length of the incision down through all structures, lest when the operator approaches the gut he finds himself working in the apex of a triangle the base of which is the line of the wound. If the surgeon has reason to expect the gut to be collapsed, an attempt should be made to distend it with some fluid. The intestine should be drawn well out through the wound, and a longitudinal opening an inch in length made in it. The edges of this are to be stitched to the edges of the skin. Fecal matter is much less likely to flow into the wound if the sutures are passed through the intestine previous to opening it. A weak carbolated wash is all that is required as a dressing. In one case of stricture of the rectum from a scirrhous mass, in which Morton performed colotomy, an immense cyst of the kidney, which was somewhat puzzling for a moment, protruded in the wound. After emptying the cyst the gut was readily discovered and opened.

DILATATION AND INFLAMMATION OF THE RECTAL POUCHES.--This is a comparatively rare condition of the rectum, called by Physick encysted rectum, which is treated by bending the end of a probe into a hook, passing it up into the bowel, and then withdrawing it with its extremity resting against the surface, so as to engage and draw down the pouches, the straining or bearing down of the patient assisting in their extrusion; they may then be incised or cut off with a pair of curved scissors.

LOSS OF CO-ORDINATION IN THE MUSCLES OF DEFECATION.--In those cases where it can be ascertained that this curious trouble is not symptomatic, sympathetic, nor reflex, the treatment must be directed to the building up of the general health, such as electricity, baths, asafoetida, and iron. Regular outdoor exercise should be enforced.

SPHINCTERISMUS.--This condition, though frequently attendant upon, may exist in the absence of, any fissure, crack, or ulcer of the anus. It is usually associated with constipation. In its treatment magnesia and rhubarb are to be used, and the diet must be simple, unstimulating, and taken at regular intervals. A hot hip-bath at night, with the use of a belladonna suppository, often proves effective. In more obstinate cases a bougie covered with ointment of belladonna should be used daily. In still more intractable cases the muscle must be forcibly stretched with the fingers. In the more obstinate cases which now and then occur it becomes necessary to completely divide the fibres of the sphincter muscle, followed by a thorough stretching of the parts.

{917} PRURITUS ANI.--This distressing and vexatious complaint proceeds frequently from hemorrhoids. When caused by the presence of seat-worms, they must be dislodged by purgatives and enemata of quassia or of one composed of one part of carbolic acid to six parts of sweet oil, or of turpentine and flaxseed tea. An enema of milk of asafoetida answers a good purpose. If the pruritus is a result of the burrowing of the itch insect, any wash, ointment, or dressing that evolves sulphuretted hydrogen will rapidly bring relief. If caused by other parasites, an application of ung. hydrarg. or red precipitate ointment, followed by a warm bath, will be all that is necessary. In some it is a symptom of dyspepsia, in others of a disordered state of the nerves of the anus independent of local cause: in this case iron, quinia, and arsenic should be given, and the patient should live an outdoor life as much as possible. The remedies that have in turn been extolled and abandoned during the treatment of this distressing condition it would require too much space to even mention. The following are among the best: Sulphate of zinc and alum, equal parts, are to be placed in an earthen vessel and heated until a glassy mass is left, which is to be dissolved in a little water and thrown into the bowel; palm soap pressed into the anus, ointments of carbolic acid and morphia or of bromide of potassium and cosmoline, citrine and other mercurial ointments, and suppositories containing iodoform. Allingham uses a bone or a metallic plug of peculiar construction, so as to keep the anus upon the stretch at night without slipping into the bowel. The pressure which this exerts upon the nerves and vessels prevents the itching. Hot (not warm) water pressed against the anus with a sponge, or ten-drop doses internally of tincture of gelsemium, or washes of dilute hydrocyanic acid or of chloroform, or ointments of balsam of Peru or of veratria and aconitia, or the corrosive chloride of mercury in solution applied locally, are a few of the more reliable among this host.

STRICTURE OF THE RECTUM (NON-MALIGNANT).--The main modes of treatment of non-malignant stricture of the rectum are two--by dilatation or by linear incision (rectotomy). Dilatation may be practised by the finger alone or by the finger covered with hollow rubber covers of various sizes. These are open at the end, so that the guiding and recognizing sense of touch may be left to the end of the finger. When the stricture is out of reach of this method, either gum or metallic bougies must be used, beginning with the smaller sizes and deliberately and carefully adding sizes. When the lumen of a stricture is tortuous it is best to use a long rather flexible rubber bougie having an olive-shaped extremity. It is not necessary to leave these bougies standing for hours in a stricture, according to the practice of some; this merely excites inflammation. Should the stricture be irritable, every second or third day would be sufficiently often to attempt dilatation. In constrictions which are firm, but not sensitive, a good plan is to insert a Molesworth elastic tube and gradually distend it by hydrostatic pressure; Barnes's dilators have also been successfully used. When the stricture is elastic and re-forms itself at once after dilatation, incision should be practised. In those strictures which are low down, the constriction may be nicked in several places by a hernia knife, the blade of which is guided along a finger in the bowel; when high up, a long double-bladed knife must be employed. In syphilitic strictures, in addition to dilatation, proper alterative treatment is {918} indispensable. As dilatation has often to be kept up for a long time, the patient may be taught to practise this for himself.

PERI-ANAL AND PERI-RECTAL ABSCESS.--When acute, and when the surgeon is called in time, the prompt application of leeches may abort the abscess, but usually, by the time the surgeon sees it, it is necessary to apply hot flaxseed poultices as fast as they become cool, keeping the patient in bed upon light diet. The rule is to open deeply and freely so soon as the least softening under the poultices indicates that pus is within reach. After lancing, the poultices should be continued for a few days: then the deep wound should be packed with a strip of oiled lint and allowed to granulate from the bottom. As the fetor of these abscesses is horrible, they should be injected with a solution of permanganate of potash or liq. sodii chlorinata. When the chronic variety of this abscess is discovered, it, with all its sinuses, diverticula, and pockets, should be laid freely open upon a director and packed with carbolized lint. It is often very necessary in these chronic cases to use tonic and alterative treatment, such as cod-liver oil and iodide of iron.

GONORRHOEA OF THE RECTUM.--Undoubted cases of gonorrhoea of the rectum in the persons of prostitutes have been observed. Burning heat and great pain are usually felt, with a free discharge of pure pus: the mucous membrane is always intensely inflamed. The treatment is simple; an injection of lead-water and laudanum or of sulphate of zinc answers a good purpose. Primary syphilitic disease of the anus and rectum is rarely seen, but of course the treatment indicated would be similar to that laid down for primary syphilis in its usual localities.

IMPACTION OF FECES.--This condition usually occurs among the aged and in women after parturition and in cases of paralysis. Those persons of sedentary habits who do not pay sufficient attention to the necessity of a daily alvine evacuation sometimes find themselves in this condition. Impaction occurs not infrequently among the insane, and more frequently among women than men. Allingham states that he has never seen a case of impaction in a young person; but Wetherill now has under his care a most obstinate case of this disorder in a young man whose system has been completely broken down by intemperance in drink.

In paralysis of the rectum of traumatic origin impaction is almost certain to take place unless great care is taken to prevent it. Diarrhoea is a very misleading element in these cases, and is a symptom which frequently deceives those who are not on their guard. The clayey mass of feculent matter forms a hard ball in the distended bowel, around which the small loose passages flow. Spasm of the sphincter ani is the usual accompaniment of impaction, and the muscle should be gently but thoroughly dilated before means can be used to free the canal. The finger or the handle of a tablespoon is best to use in the dislodgment of these masses, and should be oiled before introduction, the accumulation broken up, and then washed out by an enema of soap, turpentine, and warm water. Purgatives and hydragogue cathartics usually fail to give relief, and add much to the patient's discomfort. The bowel once freed, care must be taken to prevent a reaccumulation, which very readily takes place, as the bowel in these cases is distended and has lost tone. To this end frequent enemata of cold water should be used, and the patient should {919} take a pill of dried sulphate of iron, sulphate of quinia, extract of nux vomica, extract of aloes, as recommended by Allingham. The diet should be restricted. An excellent adjunct to this treatment is the local use of the faradic galvanic current daily after breakfast. Let the patient lie upon a bed and apply one pole or electrode to the anus, while the other one is passed with pressure along the course of the large intestine. Not infrequently it happens after this has been continued for a few minutes that a very urgent desire is felt to go to stool. In the case mentioned of the young man affected with impaction this treatment answered admirably well, but before its use he had to take a small dose of croton oil daily to cause an action of the bowels, all milder measures having proved ineffectual. It is important in these cases to interdict a sedentary mode of life.

IRRITABLE RECTUM.--A rectum is said to be irritable when it shows an intolerance of the presence of feces or flatus, causing frequent desire to go to stool. From such abnormal activity of the part there arise a burning, uncomfortable impression of fulness and a soreness of the anus. If after examination it is found that there is no local exciting cause, a starch enema containing forty drops of laudanum should be given and retained. This plan of treatment will usually afford relief. Should the irritability prove to be obstinate, examine the rectum, and if a spot of redness or increased vascularity be found, touch the spot with strong nitric acid.

CONCRETIONS IN THE RECTUM.--These occur less frequently than do impactions, and differ from them in being cylindrical and nucleated, the nuclei being such bodies as balls or tangled masses of hair, or coins, buttons, biliary calculi, or the like. Covering these are matted animal or vegetable fibres or hardened fecal matter. They are not so readily dislodged as are impactions, and it is necessary to dilate the sphincter thoroughly and remove them with a scoop. Not infrequently these bodies are bathed in pus and are very fetid.

PROCTITIS, OR INFLAMMATION OF THE RECTUM.--This may be either acute or chronic, the latter being a disease of the aged. Allingham recommends in this variety small doses of Barbadoes aloes to stimulate the bowel, also such drugs as copaiba, turpentine, and black pepper. As an injection in the acute form starch and laudanum, or bismuth suspended in a mucilaginous vehicle, should be used. Probably the use of small, smooth fragments of ice in the rectum would allay the tenesmus and help to subdue the inflammation.

PROLAPSUS ANI AND PROCIDENTIA.--Prolapsus occurs much more frequently in children than in adults, making its appearance at every movement of the bowels. The child thus affected should not be allowed to sit upon the chamber-vessel and strain, but should lie upon the side or stand, while the nurse should be instructed to draw to one side one of the buttocks so as to tighten the anal orifice. After the motion the protruded part should be well washed in cold water, and afterward with some astringent solution of oak-bark, matico, or a weak solution of carbolic acid applied with a soft sponge. The bowel should then be gently returned and the child be allowed to lie at rest for a while. If there exists intestinal irritation, small doses of mercury with chalk, with rhubarb at night, with wine of iron three times daily, would be indicated. {920} The application of an anal pad and a T-bandage will give sufficient support. If this treatment be carried out a cure usually results in a few weeks. Some cases do not yield to this mode, and then the surgeon has to make trial of ergotin given hypodermically, each injection representing a grain of ergot, which is to be thrown into the submucous tissue of the rectum every second day for two weeks. Should relief not follow its use, cauterization is to be tried. The cauterants usually applied are nitrate of silver, acid nitrate of mercury, and nitric acid. Of these, nitric acid is the best. After anæsthesia is complete every portion of the extrusion should be touched with the acid, care being taken not to bring it into contact with the skin; afterward the bowel is to be freely oiled and returned. To prevent its extrusion the bowel should be filled with soft cotton wool, a compress placed over the anus, and the buttocks strapped tightly together with adhesive plaster. For a general quieting effect the child should be given paregoric. About the fourth day the adhesive plaster may be removed and a dose of castor oil administered, which will bring away the cotton plug with the dejection.

Prolapsus and procidentia in the adult are much less manageable; indeed, these conditions are usually very obstinate. There may exist causes extraneous to the bowel, such as urethral stricture or enlarged prostate or an impacted renal calculus or a calculus of the prostate. The bowel should be searched for polypi or hemorrhoids, and the prolapse may be cured by the removal of the irritating cause. Failing to find any such cause, the surgeon has at his command either cauterization or a removal of redundancy. The former may be by nitrate of silver or acid nitrate of mercury or the actual cautery. It is well not to apply these strong acids to the aged or those who are broken down in health, as very destructive sloughing has followed their use in these cases. When these are used, the same plan as that mentioned in case of prolapse in children should be pursued. Strong carbolic acid may be used in these cases with much less risk of sloughing than when the acid is employed, and it may be applied oftener--indeed, daily if desirable. Van Buren has recommended linear cauterization with the hot iron to the mucous membrane, the bowel contracting as a result of cicatrization. In adults generally, and especially in the aged, all the forms of cauterization are less satisfactory as a means of relief than either of the various modifications of Copeland's operation, which consists in removing by ligation elliptical portions of the mucous and submucous tissues of the prolapsed bowel. The most satisfactory of these is either to excise two or three oval portions of the mucous membrane with flat-curved scissors and bring the edges together with interrupted suture, or to pinch up in several places the redundancy in a Smith's clamp and cut off the folds in advance of the instrument, applying to the stumps the hot iron. Allingham prefers ligatures of horsehair in these operations, and mentions the carbolized catgut in preference to silk. He cautions the operator not to carry his knife into the submucous tissue, as free hemorrhage would inevitably occur.

In old cases of prolapsus or of procidentia that are not amenable to operative treatment much can be done to render them comfortable: the air-dilated gum pessary will sometimes afford relief, or a pad and T-bandage will prevent the parts becoming ulcerated by friction. Neither gallic {921} nor tannic acid answers the purpose so well as acorn flour. The frequent use of cold water to the part is always attended with comfort, and sometimes with relief. In these old cases of great relaxation Nélaton has used strychnia by the mouth, and Weber (of New York) hypodermically, with fair result. Vidal has cured three cases by the repeated use of ergotin locally, hypodermically. In order to bring about a radical cure in these very chronic cases, very decided means sometimes are justifiable. The late Mr. Hey of Leeds was the first to propose a plan by which, through cicatricial contraction and inflammatory gluing together of the various tissues composing the bowel, the anus and sphincter muscle might be strengthened and improved in tone; to which end he proposed to cut away the pendulous flaps of skin around the anus. In cases where these flaps are very redundant a cure is sometimes effected by this procedure alone. Other cases will be benefited by the operation proposed by Dupuytren, which consists in the removal of radiating folds of the skin and mucous membrane at the edge of the anus. To quote from Holmes's _System of Surgery_: "This operation is effected by laying hold of the fold of skin on each side of the anus with forceps, then with a sharp curved pair of scissors removing both skin and mucous membrane. In very severe cases four or six applications of the scissors may be necessary."

POLYPUS OF THE RECTUM.--The polypi of the rectum are the gelatinoid and the fibroid, but as a very rare occurrence a villous or warty polypus has been found. Polypoid growths are very different bodies, but they are too frequently confounded with true polypi. The only treatment is their removal, and the safest method is by ligation of the pedicle, and either cutting off the growth in advance of the knot or returning it into the bowel. The patient should remain quiet until the sloughing is complete, and his bowels must be confined, otherwise profuse and very troublesome hemorrhage might ensue. Their removal by the clamp and cautery is equally safe. Their removal by torsion or by the scissors is unsafe.

The peculiar villous polypus causes great and exhausting hemorrhage. A case was successfully treated by the application of fuming nitric acid.

FISTULA IN ANO.--In the palliative treatment of this very common malady no great amount of relief can be afforded. Those who are aged and feeble or those who are much broken down will find comfort to attend the free local use of warm water, and the sinuses should be injected with dilute solutions of one of the mineral astringents, the strength of these not exceeding two grains to the fluidounce of water. Cosmoline, simple cerate, ointment of the oxide of zinc, and even fresh lard, make the patient easier, as they prevent friction of the buttocks. One of the forms of the radical treatment consists in the division of all the structures between the fistulous tract and the surface. This may be accomplished either by the use of the knife or by seton. Stimulating injections or cauterization has been known occasionally to permanently close fistulæ in ano; but such plans of treatment are unreliable, and usually unjustifiable. When the fistula is not so high up in the bowel as to render the use of the knife unsafe, this plan of treatment should be adopted. As an invariable preliminary to all operations upon the rectum the bowels should be thoroughly emptied and the patient should be placed under the influence of {922} an anæsthetic. A flexible grooved director should then be carried through the opening of the tract upon the surface and along the tract to its opening in the bowel, should such exist. The forefinger within the rectum will meet the point of the director as it emerges from the internal opening, and the director should be pushed onward and its extremity guided outward until it rests fairly upon the sound integument outside, and all the included structures should be divided along the groove of the director with a sharp-pointed curved bistoury. Should the fore finger in the rectum not discover an internal opening, one should be forced at the very bottom of the tract by rotating the point of the director while making counter-pressure with the end of the finger. Should several fistulæ be found, they should be treated in like manner. Sometimes it will be found that the incision is overlapped by the dusky-red flaps composing its margins, in which case they should be trimmed off with scissors. When the tract extends deeper than its internal opening, the latter should be ignored and the sinus laid open to its very bottom. When no external opening exists, one should be made, and the guide for this incision will be a point of induration felt by the finger at some point not far from the surface. The director entering at this point will find the tract, and should be pushed forward as described above. These opened sinuses should be packed with lint soaked in carbolized oil and confined by a pad and a T-bandage. It is the practice at the Pennsylvania Hospital to apply after division a stick of caustic potassa, allowing it to remain in contact with the cut surfaces for several seconds, after which the wounds are to be packed. This procedure ensures their healing from the bottom. The bowels should be confined for a few days, after which a dose of oil may be given. Besides attention to cleanliness and a daily renewing of the packing no further treatment will be demanded. The hemorrhage attending these operations is usually trifling. Should a vessel spring, a ligature may be thrown around it. When an abundant general oozing occurs, the rectum must be packed and a compress and bandage firmly applied. Should the surgeon prefer the seton operation, he should carry several threads of stout silk or a piece of rubber cord on an eyed probe into the fistula and out of its internal opening, and by tying their ends firmly down upon the enclosed tissues slowly effect the same result as in the cutting operation. When the seton used is silk, the ends should be carried through holes in a round leaden plate or through those of an ordinary button, and tied. These setons are to be drawn tighter every three or four days until the division of the enclosed tissues is complete. The subsequent treatment is the same as in the other operation.

A difference of opinion exists among surgeons as to the propriety of operating for fistula in ano in persons afflicted with tubercular disease of the lungs. The practice of the present day is decidedly in favor of operating, without reference to the condition of the lungs, provided the patient is not too much reduced in strength.

An operation for fistula in ano has been proposed and practised by Reeves, which is a compromise between cutting and ligation. He says: "It consisted in passing a strong and well-waxed silk ligature along the track of the fistula into the bowel. An ordinary surgical probe with an eye in its end carried this thread into the rectum. My bivalve expanding speculum was previously introduced, and by its use there was no difficulty {923} in seeing and seizing the ligature and bringing it out through the anus. The probe was then withdrawn, and the ends of the silk were wound round two strong pieces of wood which were held between the fingers of each hand. An assistant passed a finger on either side of the track of the fistula to steady the tissues and to resist the traction which was put on the silk thread. The two pieces of wood were then drawn toward me with a rapid sawing motion, and the fistula was quickly divided, with the loss of scarcely any blood. Some oiled lint and a pad and bandage were applied in the usual way; and the wound healed well. No anæsthetic was administered, and although the patient did not relish the operation, still it was quite bearable, and what she felt most was a burning sensation, due, doubtless, to the friction of the silk."

HEMORRHOIDS.--The treatment of this form of rectal and anal disease is either medical or surgical according to the gravity of the case and according to the obstinacy with which it resists local and general therapeutic agents. An ordinary acute attack of external piles, such as is often produced by neglect of the bowels, causing constipation, may be treated in the following manner: The patient should rest and avoid stimulating food and beverages. He should employ cold bathing to the part frequently: indeed, great comfort and relief often follow this treatment alone. An ointment of tannic acid, glycerin, and simple cerate, or one containing calomel and extract of opium, will be found useful. Fresh lard, cosmoline, vaseline, cold cream, ointment of the oxide of zinc (benzoated) or an ointment containing extract of opium, extract of galls, and extract of belladonna or stramonium, are some among many agents that have been extolled for their relief. H. C. Wood[46] recommends enemata of solution of chlorate of potassium and laudanum. Enemata of lime-water and linseed oil are recommended by Agnew: "One of the very best formulas for allaying the irritation incident to hemorrhoidal affections consists of the following combination: Acetate of lead and tannin, of each fifteen grains; carbonate of lead and extract of stramonium, of each thirty grains; creasote, five drops. With a sufficient quantity of cocoa-butter mould this into fifty suppositories."[47] The internal exhibition of the balsam of copaiba, twenty drops in capsules taken four or five times daily, or the use of fifteen drops of liquor potassa rubbed up with half a drachm of the balsam into emulsion, taken three times a day, has been much extolled, as has also the confection of black pepper. Sometimes these various means will cure a chronic or long-standing case of piles, either internal or external. Wetherill has found that the topical application of rectified oil of amber has cured long-standing cases of piles. This oil should not be applied in cases where much inflammation exists, and where the piles are internal the best mode of bringing it in contact with them is to incorporate from three to five minims of the oil with sufficient cocoa-butter to make a suppository. One of these, pushed into the bowel night and morning for a week, will not infrequently cause the piles to shrink up and finally to disappear. The bowels should be kept open with the compound powder of licorice. It should be remembered that magnesia irritates hemorrhoids. Success has followed the internal use of ergotin, of the fluid extract of hamamelis virginica, of the corn blast (ustilago maidis), and of small doses of aloes combined with hyoscyamus. {924} D. Young has had good results follow the internal use of glycerin. Chronic cases of piles have been cured by the application of ointments containing carbonate of lead, creasote, carbolic acid, or iodoform. Ergotin used hypodermically in the vicinity of the anus or injected into the piles has frequently resulted in a complete cure, and the same may be said of the injection of carbolic acid directly into the tumors. In the application of cold water to inflamed piles it should be borne in mind that its forcible impingement upon them in a fine stream acts far more efficiently than the mere bathing them. Some cases do better under the use of warm water or warm sedative and astringent lotions. A warm flaxseed poultice mixed with laudanum is a very comfortable application. In obstinate cases of prolapse Agnew[48] recommends the use of a rectal obturator or the use of a hemorrhoidal truss.

[Footnote 46: _Philada. Med. Times_, Dec. 6, 1879.]

[Footnote 47: _Surgery in the Pennsylvania Hospital_, p. 210.]

[Footnote 48: Agnew's _Surgery_, vol. i. p. 445.]

Those who suffer from prolapse of piles should avoid the habitual use of cushioned seats. They should assume a semi-erect posture during defecation, or, when this is attended with difficulty or inconvenience, they should contrive a portable water-closet seat by boring a hole an inch and a half in diameter through a piece of planed board, bevelling it so as to fit the person. These means will often prevent the extrusion of the tumors. After defecation the patient should rest for a little while in the recumbent attitude.

The careful touching of external piles with strong nitric acid is a mode of treatment that has been quite successful in the hands of some surgeons. The intolerable itching of these bodies can be allayed by touching them with tincture of aconite-root or with a concentrated tincture of prickly-ash bark. Freezing them with the ether spray allays the pain and itching for the time being, but these symptoms return with redoubled energy after the effect has subsided.

Should an attack of the external variety of piles not result in absorption, but leave an excrescence, painless but inconvenient, and liable at any time to become inflamed, excision would be in order. Divide the integument by an incision radiating from the anus, separate the skin from the tumor down to its base, and after seizing it with toothed forceps cut it off with scissors curved on the flat. Little flaps or tabs of skin remaining after piles may be snipped off with scissors. It is not well to operate upon external piles unless they obstinately resist all milder treatment. There are frequently venous enlargements containing blood-clot, and when this condition exists proceed as follows: Pinch up the little tumor between the thumb and finger of the left hand; transfix its base with a curved bistoury, and cut out; at the same time, by pressure with the thumb and finger, extrude the clot. Fill the bottom of the little sac with cotton wool, and the operation is complete. It is not necessary in these cases to wait until the inflammation subsides before operating.

The operative treatment of the internal variety may be by strangulation, by the cautery, by the écraseur, and by the use of caustics. The former of these is the safest and most convenient method, and the one usually employed in the Pennsylvania Hospital, and should be performed in the following manner: The lower bowel having been thoroughly evacuated and the patient etherized, the operator should gently but firmly stretch the sphincter. The patient should be placed upon the side, with {925} the upper part of the body prone, the hips elevated, and the thighs flexed upon the abdomen. Transfix the largest tumor with a strong, long-handled tenaculum, cut through the skin at the base with a knife or scissors around its external half, and hand the hook to an assistant, instructing him to make gentle traction. Then encircle the mass with a stout cord if the mass is not too large, or pass a stout needle threaded with a double silk ligature, from without inward, deeply through the base of the pile, drawing it through the mucous membrane on the opposite side; cut loose the needle and tie tightly, so as to completely strangulate the included tissues on either side and leave the ends of the ligature long. Treat all the remaining tumors in a similar manner seriatim, and then with scissors cut away the strangulated bodies to within a safe distance of the ligatures, the ends of which are now to be cut off close. Place an opium suppository in the bowel, and the operation is complete.

When for any sufficiently good reason the patient will not bear the ordinary anæsthetics, it will become necessary to modify the operation as follows: The tumors having been well extruded by enema of warm water or by the efforts of the patient, bend him forward over a chair and direct an assistant to draw aside the buttocks. Then pass the double ligatures as before indicated, but refrain from tying until all the tumors are thus secured, as the operator will find it convenient to draw upon the ligatures to keep the mass of piles within view and working-distance. Then draw down each tumor, cut around its base, and tie as before; cut off the ends of the ligatures and the greater portion of each strangulated tumor, and return everything within the bowel, and follow with an opium suppository. In many cases Morton has used the nitrous oxide gas with the best results. The hook should then be withdrawn, and each knot should be drawn more firmly down prior to its reduplication. Following this procedure, if properly carried out, the tumors will change color, becoming blue, thus indicating complete strangulation.

The operation by the clamp and cautery is a good method when the hemorrhoidal tumors are small. The operation is that of Mr. Cusack of Dublin, and the clamp employed is that invented by Mr. H. Smith of London. This instrument is so well known that a detailed description of it would be unnecessary. In operating with it the tumor is to be drawn well out and the clamp applied close up to its attachment with the bowel. Strangulation is effected by means of the screw which runs through the shafts of the handles. This accomplished, the strangulated portion is cut off with scissors, which should leave a stump three-eighths of an inch long. To this stump apply the actual cautery at a dull red heat, touching its every portion, after which unscrew and remove the clamp and look for hemorrhage. Should any occur, touch the bleeding point with the hot iron. Confine the patient to bed for five or six days and give sufficient opium to confine the bowels. After this time has elapsed administer a dose of oil. Remember that but one pile should be clamped at one time. "The taking two piles into the clamp at once is sure to result in hemorrhage." Do not allow the cautery-iron to touch the clamp. After the operation return the parts within the sphincter and cut off any tabs of redundant integument with scissors.

The removal of internal piles by means of the écraseur was the favorite operation of Chassaignac, but it is a mode of procedure which is now {926} regarded with disfavor by the best surgeons on account of the liability to hemorrhage, and from the fact that troublesome and injurious contractions of the anus have not infrequently followed its use. The employment of iron or copper wire instead of the usual chain has been recommended by those who prefer this mode of operation. The plan adopted by Chassaignac was to pedunculate the piles by tying a ligature around the base and drawing them down. The chain being then applied, the strangulation and crushing off was slowly accomplished by means of the lever of the instrument. It should take from twenty to twenty-five minutes' crushing to accomplish this object.

For the treatment of internal piles by caustics Houston of Dublin used strong nitric acid. A fenestrated speculum should be employed, and the acid should be applied with a piece of wood or with a glass brush, care being taken to limit its action to the tumors, the redundant liquid being mopped up with a swab of lint or prepared absorbent cotton. The entire surface should afterward be bathed in oil. The acid is relied upon to produce a granulating surface, by the healing of which and by the subsequent contraction a cure is sometimes achieved. At best, this plan of treatment has proved tedious and unsatisfactory.

Chloride of zinc and caustic potassa are even more unsatisfactory agents for this purpose than the acid, as they are very violent in local destruction and their action is very difficult to limit. The use of caustic potassa was last revived by Amussat, but failed to find favor from his contemporaries, and soon fell into merited disuse. Van Buren says: "From recent experience with the thermo-cautery of Paquelin, I am disposed to regard it as more manageable than nitric acid, and at least equally efficient." Allingham mentions favorably the strong carbolic acid as a substitute for the nitric as an application to vascular and granular surfaces. The reckless method employed by the older surgeons of cutting off internal piles with the knife or with scissors, without any precautions against bleeding, is merely mentioned in condemnation. Usually no serious symptoms are to be expected after operations for hemorrhoids, but to this general rule there are exceptions. Morton knows of two consecutive cases of tetanus after this operation performed in a hospital in this city, and both terminated fatally. One of the most common occurrences after the ligation of piles is retention of urine, generally lasting for a day or two and requiring the use of the catheter.

HEMORRHAGE FROM THE RECTUM.--Bleeding from these parts is more usually of a venous than an arterial character, but in some cases of hemorrhoids the bleeding is either arterial or arterio-venous. The latter occurs upon the detachment of a polypus, but not necessarily of a polypoid growth. Arterial or mixed bleeding occurs in carcinoma and in rodent ulcer, and also from the stumps of badly-occluded piles. In cases of vicarious menstruation from the rectum the venous blood simply oozes from the surface of the over-congested mucous membrane. This condition should be readily diagnosed by the physical properties of the blood and from the history of the patient. In almost all cases of bleeding near the anus it will be possible to pick up the vessel or the bleeding point on a tenaculum and ligate with silk, which is the most satisfactory method to the surgeon. The rectum has been dragged down with volsella forceps to apply a ligature to a point high up, but in some of these cases the acupressure pin {927} with the twisted suture will be found more convenient. Should hemorrhage occur after the ligation of piles which cannot be checked by ligature, such as a general oozing, pass all the ligatures through a hole made in the centre of a small round sponge, then tie them across a piece of stick (thus constructing a sort of tourniquet), and twist this around. Van Buren cites a case in which a sudden laceration of the integument and sphincter occurred during forcible dilatation in a case of hemorrhoids in a very broken-down subject, with very copious hemorrhage. He passed a sponge armed with a double ligature into the bowel, and, directing an assistant to make traction upon the threads, the bleeding was checked. Injecting ice-water and perchloride of iron into the rectum will often check hemorrhage. Allingham prefers the persulphate of iron to any other styptic for this purpose. Passing fragments of ice into the bowel while holding a lump of ice upon the sacrum sometimes answers a good purpose. In many cases of secondary hemorrhage from large venous sinuses in a state of ulceration it will be impossible to ligate, and the use of the ordinary styptics will be but the waste of valuable time: the bowel must be tamponed as follows: Thread a strong silk ligature through near the apex of a cone-shaped sponge, and bring it back again, so that the apex of the sponge is held in a loop of thread. Wet the sponge, squeeze it dry, and fill its meshes with ferric alum or with persulphate of iron. Pass the left fore finger into the bowel, and upon it push up the sponge, apex first, by means of a metal rod or any other convenient body, fully five inches into the rectum. Now fill the rectum below this with cotton-wool filled with the styptic. The bowel having been completely filled, make traction upon the ligatures (thus spreading out the bell-shaped sponge), while with the other hand push up the packing. If this is carefully done no fear of bleeding need be apprehended. In these cases the patient often suffers from collections of flatus, which may be obviated at the time of packing by placing a flexible catheter in the bowel and packing around it. These plugs should remain for at least five or six days, and frequently eight or ten days are none too long. The packing must then be picked carefully away from the sponge. Agnew's rectal chemise answers the same purpose. In describing its application he says: "Through the openings at the end of the largest-sized gum catheter pass a strong silk thread; take three square pieces of the material usually known as mosquito-netting, placing them one on top of the other; at the centre of these squares or pieces make an opening, and pass the catheter through it, securing the two together by the threads. In applying the instrument the different layers of the chemise must be moistened with water, and afterward well filled with the persulphate of iron. It is then conducted some distance into the rectum on a finger previously inserted; after which it is expanded like a parachute by packing between the catheter and its hood with long strips of lint thrust up on the end of a bougie until the bowel is distended on every side. The catheter will serve to conduct away the flatus, and when, after eight or ten days, its removal becomes necessary, this is very easily effected by drawing out the ribbon-like pieces of lint which were used as packing." Another method is to stuff the bowel with fragments of sponge to which threads are tied, the ends of which, protruding from the anus, facilitate their withdrawal. In conjunction with these procedures the patient's pelvis should be elevated. {928} After excision of portions of the mucous membrane the risk of hemorrhage will be lessened by the surgeon introducing through the edges of each incision a few fine sutures.

Enormous quantities of blood may escape into the bowel after operations without any external symptom being apparent until the patient becomes pallid and weak. In other cases the patient will complain of tenesmus and desire to go to stool, or of a sensation of something trickling into the bowel. Upon the recognition of these symptoms search should at once be made for internal hemorrhage.

Rectal Alimentation.

Before taking leave of this very interesting class of diseases and of their modes of treatment, it seems proper to introduce a few remarks upon the subject of rectal alimentation, as it is now a well-recognized and much-practised means of sustaining those whose stomachs are unequal to the work which in health is so easily and unconsciously performed. In the use of the lower bowel as an absorbent surface of alimentary substances many failures have been reported, a fair proportion of which, it is safe to infer, are due to the methods employed, to the nutritive matters employed, and to the condition of the rectum at the time. Firstly, as to the state of the rectum, it must be empty. Wait a reasonable time, say an hour, after stool, so that the gut may be more passive; have the patient in the recumbent posture; direct him to resist tenesmus and to exert both the will and the muscular power to retain the aliment. The syringe must be of hard rubber, must be rectal-ended, and of the capacity of two fluidounces, and perfect in action.

The preparation to be introduced, after being warmed to a temperature of 98° or 99° F., should be very slowly injected with the syringe, which should be also warmed and oiled. The enema must never exceed in amount two fluidounces. If this be rejected, wait a reasonable time and try again, using a less amount. If tenesmus proves an insurmountable barrier to ordinary means, an opium suppository is to be introduced three hours prior to another attempt. It has been suggested, inasmuch as tenesmus is often relieved by the application of cold to the rectum, to introduce the aliment in that state; but this method is open to the objection that rectal digestion would be much less likely to take place under this condition, as the bowel would then have thrown upon it the additional work of warming up the substance prior to absorbing it.

The usual errors made in applying this means of sustaining the patient are, that the injections are too large, are too rapidly introduced, and are not of the proper temperature. Allowing an interval of eight hours between the enemata would afford three in the twenty-four hours, which method has been found to offer the best results. This must be persevered in at regular daily intervals for the patient to derive its full benefit, and there is reason to suppose that the nervous system gets expectant of these daily hours of support, as it does in the case of our ordinary meal-times. An examination of the well-formed daily stools of patients thus sustained will prove how close the analogy is between this and digestion proper.

{929} Next, as to the substances to be employed. The best of these are milk, eggs, concentrated beef-extracts or beef or chicken peptones, and brandy or whiskey of good quality. These substances may be combined in various proportions to suit the individual requirements of the case. A very good mixture for this purpose is two tablespoonfuls of milk, one tablespoonful of whiskey, and an egg, using both the yelk and the albumen. To this add a little salt. This should be well beaten up and properly warmed.

It is well to persevere in the use of these enemata even though at first most of them appear to be rejected, as after a time, the rectum becoming accustomed to their presence, absorption or so-called rectal digestion may take place. This form of alimentation should be kept in reserve in a case of chronic illness until all other methods of sustaining the patient prove insufficient to support life. It is not contraindicated even in some cases of chronic diarrhoea with persistent vomiting and loss of peptic function, advantage being taken of the intervals between the evacuations to introduce a small and very concentrated nutrient enema. In ordinary cases not complicated by diarrhoea the most convenient times will be found to be about seven o'clock in the morning, three in the afternoon, and eleven at night. Wetherill suggests the possibility of forming with solid extract of beef, pepsin, and pure suet a nutrient suppository which might be retained and absorbed in some cases in which it has been found impossible to retain the enemata. A very small addition of white wax, he thinks, would keep these solid during warm weather; if not, the suet might be replaced by ol. theobroma (as in ordinary suppositories), which is probably as likely to be absorbed as the suet.

{930}

INTESTINAL WORMS.

BY JOSEPH LEIDY, M.D.

All animals, except in general the simple cell-forms constituting the sub-kingdom of protozoa, under ordinary circumstances are more or less liable to be infested with others, called parasites, which commonly live at the expense of their hosts, frequently with little or no inconvenience, but often causing discomfort and suffering even unto death. Parasites are distinguished as external and internal, the two being mostly of a widely different character. The former chiefly pertain to the division of arthropoda, or animals with jointed limbs, as exemplified by lice, fleas, and flies of the class of insects, mites of the class of arachnides, and epizoans and isopods of the class of crustaceans.

Internal parasites, from their usual habitation named entozoa, are commonly observed in the intestines of animals, and hence their distinction as intestinal worms. The name has proved to be appropriate, for investigations have shown that most entozoa, observed from time to time in other parts of the bodies of animals, pass part of their life in the intestinal canal of the same or of some other animal.

By far the greater number of entozoa are peculiar animals, constituting the chief part of the scolecides, an extensive group of the sub-kingdom of vermes or worms. Of this group they comprise the orders of CESTODES, or tape-worms; the ACANTHOCEPHALI, or thorn-headed worms; the TREMATODES, or fluke-worms; and the greater portion of the NEMATODES, or thread-worms. Many entozoa also belong to the protozoa, but these, so far as relates to man in a medical point of view, appear unimportant, and will therefore not here enter into consideration.

In the course of their life entozoa undergo changes of form and condition, and pass these in different organs of the same or of different animals, and it may be for a brief period externally or in a non-parasitic state. In many instances, as in the tape-worms and the fluke-worms, the transformations accompanying the changes are of so extraordinary a character that until their life-history was investigated the successive metamorphoses were viewed as distinct animals. Mostly, the entozoa pass one stage of existence within the intestine of some animal, and another stage in different organs of other animals. Many, perhaps most species, in each stage are peculiar to one or a few nearly-related animals, but others of the same kind infest a number of different animals. The animals infested by the same parasite may be remotely as well as nearly related. Thus the Tænia saginata, or beef tape-worm, in the mature state lives in the small intestine of man {931} only, but in its juvenile or larval condition in the flesh meat of the ox. The Tænia elliptica, the common tape-worm of the intestine of the dog, in the larval condition lives in the louse of this animal. The liver-fluke, Distomum hepaticum, occasionally found in the liver of man, but of common occurrence in the sheep, to which it proves so destructive in the affection known as rot, in the juvenile condition lives in a little fresh-water snail of the genus Lymneus. The guinea-worm, Filaria medinensis, which in the mature state is found beneath the skin of man, in the larval condition inhabits the minute crustacean cyclops of stagnant waters.

As would be reasonably supposed, entozoa commonly gain access to their hosts through the food and drink, though in the case of aquatic animals they also obtain entrance directly through the integument from the surrounding medium. So long as they remain in the intestinal canal they may occasion little trouble or inconvenience. When they are numerous in this position or proportionately large, according to their peculiar nature they may produce more or less suffering and even the most serious consequences. Generally, however, it is when they occupy other positions, to which they have migrated from the intestine, that they induce aggravated symptoms proportioned to their numbers and the nature of the organs they infest.

Many species of entozoa have been discovered in man, and most of them are peculiar in kind. Many are common, and, while some are widely extended, others are more or less restricted to certain localities. They are variable in their frequency, largely proportioned to the prevalence of habits which are favorable to their transmission, and which, though under control, are more or less disregarded. Some species are so rare in their occurrence that they seem to be accidental, and therefore of comparatively little interest to the physician.

In general, the frequency of occurrence of intestinal worms is proportioned to the extent of use of uncooked or insufficiently cooked meats, the drinking of unfiltered standing waters, uncleanly habits, and the intimacy of association with domestic animals. It therefore follows that important prophylactics against infection by parasites are properly-cooked food, the use of spring or freely-running water or filtered standing water, cleanly habits, and the avoidance of intimacy with domestic animals.

The Cestodes, or Tape-worms.

Tape-worms in the mature condition inhabit the intestines of vertebrate animals, and are usually conspicuous for their long, tape-like appearance and jointed character. In the juvenile or larval state they infest the various organs, except the interior of the intestinal canal, of both vertebrates and invertebrates, and in this condition are so diminutive and inconspicuous that until a comparatively recent period they for the most part remained unnoticed, and when known their relationship with the mature forms was not recognized.

The mature tape-worm, as ordinarily observed, is a long, soft, flat, white worm, which from its resemblance has received its familiar name. {932} It has a small head, succeeded by a short, more slender neck gradually widening into the body, which is divided transversely into segments. These, which are usually called joints or links, and also named proglottides, are so many individuals, and finally become separated to hold an independent existence. The tape-worm clings to the mucous membrane of the intestine by its head, which is provided for the purpose with suckers, and in many cases also with circlets of hooks. The segments of the body are incessantly produced by gradual growth and successive division of the neck, and as they enlarge they become more distinct and develop within a bisexual generative apparatus for each. The worm has neither mouth nor intestine, but is nourished by imbibition from the surrounding liquid in which it lies constantly bathed. A pair of longitudinal vessels commences in the head and extends throughout the body, one on each side, and in some genera is joined by a transverse vessel at the fore and back part of every segment. The mature segments have no body-cavity, but are occupied with a complex bisexual generative apparatus, which is self-impregnating. Finally the uterus, usually much ramified, becomes especially conspicuous through distension with eggs, and the rest of the organs for the most part become atrophied. The ripe segments successively detach themselves from those in advance, often singly and not infrequently several linked together. In this condition, often in lively movement, they are discharged with the feces, and thus commonly render themselves obvious to their host. Subsequently they may continue to live a brief period externally in a non-parasitic condition. Ordinarily, in moist excrement, or in water or similar materials, they will remain alive for several days.

After the discharge of the tape-worm segments, together with the eggs which had been previously laid by the latter and those still contained within them, any or all may be swallowed by animals feeding in places where the infected excrement has been deposited. When the proglottides and eggs are taken into the stomach they are digested and the embryos or proscolices are liberated.

The embryo or proscolex of the tape-worm is a microscopic spherical or oval body, provided at one pole with three pairs of divergent spicules, by which it is enabled to penetrate the walls of the stomach or intestine of its host. From these positions the embryo migrates either directly or through the blood-vessels to some other organ, most frequently the liver or the muscles. Having reached its destination, it becomes fixed in position, and for a time remains comparatively quiescent, but undergoes further development. The embryo loses its spicules and is transformed into the larval form or scolex. In most species of tape-worms the scolex is simple or individual in character, and consists of a head like that of the parent or mature worm, with a neck ending in a capacious cyst, within which the head and neck are inverted. In this form the scolex is contained in a sac of connective tissue induced by the presence of the parasite. Such sacs, frequently observed imbedded in the flesh, liver, lungs, and other organs of animals, are familiarly known as measles. In this condition the scolices of certain tape-worms have long been known, but as their relationship was not recognized, they were viewed as distinct species of parasites and described as cysticerci. In other species of tape-worms the scolex is of compound character; that is to say, the embryo {933} in its further development gives rise to the production of one or more groups of individuals in conjunction. The compound scolex thus forms a sac or a group of sacs, the basis of hydatid tumors. These occur of various sizes, even up to that of a child's head, and may occupy any organ of the body. They consist of a spherical sac or group of sacs, simple in character or containing others, ranging in size from that of a mustard-seed to that of a marble, or larger to that of a walnut, enclosed in an envelope of connective tissue induced by the presence of the parasite. The sacs are filled with liquid, and have, attached within or free and floating, or less frequently attached without, variable numbers of little white grains, which on examination with the microscope exhibit the same constitution as the simple scolex above described. As in the case of the cysticerci of measles, the scolices of hydatids have long been known, but as their relationship with the mature forms was unrecognized until lately, they were regarded as distinct parasites and described as echinococci and coenuri. Sometimes the compound scolex fails in development further than the production of the sacs, which then constitute the so-called acephalocysts.

Measles with their occupants, when retained in the muscles or other organs, ordinarily undergo no further development, but ultimately, after some months to a year or two, undergo degradation. The larva or scolex dies and atrophies; the measle degenerates, and often becomes the focus of calcareous deposit, shrinks to a little cicatrix, and may finally disappear. Of a more serious nature is the tape-worm embryo which produces the hydatid tumor. With the increase of this, proportioned to the production of sacs and scolices, it may become so large as greatly to interfere with the function of the organ it occupies, and according to the nature of this organ will be the gravity of the affection.

When, however, the flesh or other parts of animals affected with measles or hydatids containing active scolices are used as food in a raw or insufficiently cooked state, the meats are digested in the stomach and the scolices liberated to pursue their further development. Passing into the small intestine, the active scolex everts its head from its caudal sac, which atrophies and disappears, and the parasite attaches itself to the mucous membrane, and rapidly develops and grows into the conspicuous and familiar form of the adult tape-worm. The duration of life of the latter while maintaining its position in the intestine is uncertain, but under favorable circumstances it commonly continues for years, and thus, with the incessant production of ripe segments charged with eggs, it becomes a constant focus of infection.

* * * * *

Three species of tape-worm in the mature condition are common parasites of man, living in the small intestine. They are the Tænia saginata, Tænia solium, and Bothriocephalus latus.

* * * * *

TÆNIA SAGINATA.--SYNONYMS: Tænia mediocanellata; Beef tape-worm; Unarmed tape-worm; Fat tape-worm.

Larval condition: Cysticercus saginata; Beef measle-worm.

This, which is now regarded as the most common tape-worm of man, is named the beef tape-worm because it is derived from the beef used as food. In the mature condition it lives only in the small intestine of {934} man, and in the juvenile condition it lives in the ox. Its frequency is proportioned to the prevalence of the custom of eating beef in a raw or insufficiently cooked state, conjoined with the careless habit of leaving human excrement in pastures where it is accessible to cattle.

The mature beef tape-worm is commonly observed as a soft, yellowish-white, thickish, band-like worm, ranging from six to twenty feet or more in length. The head, about the size of a yellow mustard-seed, is rounded quadrate and provided with four equidistant hemispherical suckers. Succeeding the head is a short, slightly narrower, flattened neck, which merges into the gradually widening and segmented body. The segments, at first narrow fore and aft and several times wider than the length, become successively larger, proportionately longer, more distinct, and quadrate in outline; and finally the length may exceed the breadth two or three times. A full-grown tape-worm may possess twelve hundred segments and more, and specimens are recorded as reaching a length of thirty feet. The larger segments measure from a quarter of an inch to an inch long and from three to four lines wide. The larger or riper segments exhibit on one border, irregularly alternating on the two sides, at or near the middle, a papilla in which is the external aperture of the genital apparatus. In the fully-ripe segments the uterus, distended with eggs, may be obscurely seen through the wall of the body, but is rendered more visible by drying the segments, moderately compressed, between two pieces of glass. It appears as a long, narrow, white or brownish median line or tube, giving off laterally numerous short, transverse, more or less branching tubes.

The worm in its usual position lies along the course of the intestine in loose coils, and exhibits lively movements, alternately shortening and elongating, expanding and contracting the head, and protruding and retracting the suckers. The ripe segments spontaneously detach themselves, and may be found scattered along the large intestine ready to be discharged with the excrement, or, as is sometimes the case, they may spontaneously creep from the anus. Rarely more than a single worm infests a person at the time. The species is of rapid growth. According to Perroncito, quoted by Cobbold, a mature worm was reared from a beef measle, swallowed by a student, in fifty-four days.

It is estimated that the number of eggs in the mature segments of the beef tape-worm amounts to about 35,000. As the full-grown worm may consist of 1200 segments, and there is reason to believe these are renewed several times annually, we learn that the whole number of eggs produced by a single individual is enormous. The ripe segments, attached to the parent or becoming spontaneously detached, lay their eggs in the intestine to be discharged with the feces. When more or less emptied they shrink and appear reduced in size, and in this condition are expelled or spontaneously creep from the anus. If the ripe segments are forcibly expelled and are alive, they will lay their eggs in the feces externally. The ripe eggs are brown, oval, about 0.03 mm. long, and have a thick shell, with an outer vertically striated envelope.

As previously intimated, the common source of the beef tape-worm in man is the use of raw or insufficiently cooked beef affected with measles. The ox becomes infested by swallowing the eggs, or, it may be, even the entire segment, of a tape-worm deposited with feces in the {935} pastures of cattle. The measles usually occur in the muscles, including the heart, though they have also been noticed in the liver and lungs. They appear, in beef, as oval, whitish bodies from the size of a mustard-seed to that of a pea. They consist of a sac of connective tissue containing the larval tape-worm or cysticercus. Measles under ordinary circumstances are seldom noticed in beef, and when they occur are commonly few in number.

According to the latest authorities--Leuckart, Cobbold, Stein, and others--the beef tape-worm is the most common of the cestodes which infest man. Until within about thirty years it was generally not distinguished from the pork tape-worm, and this was accordingly regarded as the most common human species. Since the writer distinctly recognized the beef tape-worm within the last twenty years, all the specimens of Tæniæ, from people of Philadelphia and its vicinity, that have been submitted to him for examination--perhaps in all about fifty--have appeared to belong solely to Tænia saginata. The prevalence of this species with us is no doubt due to the common custom of eating underdone or too rare beef, while the pork tape-worm is comparatively rare, as with us pork is only used in a well-cooked condition.

* * * * *

TÆNIA SOLIUM.--SYNONYMS: The Pork tape-worm; Solitary tape-worm; Armed tape-worm.

Larval condition: Cysticercus cellulosæ; Pork measle-worm.

Until a recent period this species was generally regarded as the most common tape-worm of man--a view which in great measure was due to the circumstance that the beef tape-worm was not distinguished from it. It was called the solitary tape-worm, still expressed by the specific name, from the impression that it rarely occurred otherwise than single at a time in a person. This has also proved to be incorrect, likewise due to the two kinds of tape-worms having been confounded together; for while the beef tape-worm most commonly occurs solitary, the pork tape-worm not unfrequently occurs with several together.

The species is now appropriately named the pork tape-worm, as indicating its common source--pork used as food. The frequency of the parasite is proportioned to the prevalence of the custom of using pork in a raw or imperfectly cooked state, conjoined with that of depositing excrement where it may be accessible to hogs. In the mature condition the pork tape-worm is peculiar to man and lives in the small intestine, but in the larval condition, though especially infesting the hog, it also occasionally infests man, and lives in any organs of the body, but mostly the muscles, liver, and lungs.

The mature pork tape-worm, as commonly seen, is a soft white, thin, band-like worm, from five to ten feet long and about four lines where widest. The head is spheroid, about the size of that of an ordinary pin, and smaller than that of the beef tape-worm. It is furnished with four hemispherical cup-like suckers, and the summit forms a blunt papilla armed with a double circle of twenty-five or twenty-six hooks. The neck is narrow, thread-like, about an inch long, and merges into the segmented body, which gradually widens to the extent mentioned. The segments, at first much wider than long, as they successively enlarge also become more distinct and proportionately longer, so that the more {936} posterior ripe ones are as long as they are wide, and often longer, though not to the same degree as in the beef tape-worm. The genital papilla, with its external aperture, is marginal as in the latter. The fully-developed uterus is quite distinctive in character from that of the beef tape-worm. The median tube is coarser, and the lateral branches are likewise coarser, much fewer--half the number or fewer--less branched, and less crowded. The ripe and often spontaneously detached segments are commonly longer than broad, more or less elliptical in outline, with truncated ends, and usually measure about half an inch in length by about a third in breadth. The ripe eggs resemble those of the beef tape-worm, but are usually spheroid in shape.

The common source of the pork tape-worm is pork affected with measles eaten in the raw or insufficiently cooked state. The hog becomes affected with measles when it has access to human excrement containing eggs and ripe segments of the tape-worm, which it eats with avidity. The eggs, with their already developed embryos, when swallowed, undergo the same series of transformations and course as those indicated in the account of the beef tape-worm. Pork affected with measles is much more common than beef affected in the same way, and is frequently a subject of ordinary observation. From the difference in habit of the hog and ox this is what might have been suspected; and the fact that the beef tape-worm is more common than the pork tape-worm is to be explained from the circumstance that fresh beef is in more general use than pork, and is usually employed less thoroughly cooked.

The pork measles are commonly seen as round or oval, hard, whitish bodies, from the size of a hempseed to that of a pea, imbedded in the connective tissue of the muscles or flesh. The measle consists of a sac of connective tissue enclosing the scolex or larval tape-worm, which resembles that of the beef tape-worm, but differs especially in the possession of a double circlet of hooks to the head, as in the adult worm. The scolex has long been known, and was regarded as a distinct parasite, with the name of Cysticercus cellulosæ. When fresh pork measles are swallowed by man they are digested in the stomach, and the cysticercus or scolex is released and passes into the small intestine. Here, attaching itself to the mucous membrane by means of its suckers and crown of hooks, it rapidly develops and grows into the adult tape-worm. In this condition it lies in loose folds along the intestine, to which it clings so tenaciously that commonly the neck gives way when the greater part of the worm is forcibly detached by the use of medicines. Fragments, consisting of the more mature segments, frequently appear detached from the posterior part of the worm, and the fully-ripe segments may be seen scattered singly in the course of the large intestine. The isolated segments are thinner and more translucent than those of the beef tape-worm, and in this condition are discharged with the feces, but may also spontaneously creep from the anus, though seldom as compared with the other species.

Experiments repeatedly made by swallowing pork measles prove that the mature tape-worm may be developed in the course of three months. The length of life attained by it under favorable circumstances is uncertain, but it probably continues a dozen years or more.

The scolex of the pork tape-worm, or the cysticercus, so common in the hog, is also less frequently a parasite of man, and in this condition is a {937} more potent agent of danger than in its ordinary or mature state. The infection is due to the introduction of eggs or mature segments of the tape-worm into the stomach--a circumstance which may readily occur through handling these objects and transferring them to the mouth, or more rarely perhaps by their transference from the intestine into the stomach through vomiting.

In the measle form the parasite may occur in any organ of the body, but is mostly found in the muscles and subcutaneous tissue. Its pathological significance depends on its number and position. Located in the nerve-centres, it may occasion the most serious consequences. Usually it occurs in small numbers and gives rise to no obvious inconvenience, and is only accidentally detected in dissection after death. It appears to maintain its vitality for some years, but finally dies, and undergoes degradation. Only when it can be detected in such position as the interior of the eye or beneath the conjunctiva can the patient be relieved by surgical aid. Elsewhere, even if its presence is suspected, it is ordinarily beyond the reach of medical treatment. The writer a few years since, in dissecting the body of a colored man to illustrate his lectures on the muscles, found two living measles, of which one was in the diaphragm and the other in the transversalis muscle of the abdomen, but none were detected elsewhere. The parasite unquestionably gave no inconvenience to its host during life.

* * * * *

Other species of Tænia which have been observed as parasitic in the human intestine are mostly of rare occurrence.

* * * * *

TÆNIA CUCUMERINA, the common tape-worm of the dog, and TÆNIA ELLIPTICA, the common tape-worm of the cat, are very much alike in appearance, and are regarded by many authorities as the same species. They occur frequently in considerable numbers in these animals, living in the small intestine. They have also been occasionally found in man, especially children.

It is a comparatively delicate worm, chain-like in appearance, ranging from four inches to a foot in length. The head is provided with four suckers and a prominent rostellum armed with about sixty hooks. The neck and anterior part of the body are thread-like. The mature segments are elliptical in outline or like a melon-seed, whence the name. There is a double set of sexual organs, and a genital orifice occupies the middle of both lateral margins of the segments. The ripe segments become readily detached and creep actively in the intestine, and are either expelled with the feces or they spontaneously creep from the anus. The eggs are comparatively few and measure 0.05 mm.

Late researches appear to show that the eggs adhering to the hair about the anus or elsewhere are eaten by lice of the same animals, and within these insects undergo further development. The dog and cat, subsequently swallowing the lice, infect themselves with the mature worms. Thus also persons, especially children, from too great familiarity with these animals, directly or through their food, may likewise become infected.

* * * * *

TÆNIA NANA, the Dwarf tape-worm, has been observed but once. It was discovered by Bilharz, in Egypt, in a boy who died of meningitis. It {938} is a little worm, about half an inch in length, and occurred in large numbers in the duodenum.

* * * * *

TÆNIA TENELLA.--This is another small species, which has been but once observed. It is described by Cobbold, who suspects it to be derived from measles of the sheep.

* * * * *

TÆNIA FLAVOPUNCTATA is also a small species, from eight to ten inches long, with ripe joints about one millimeter long and from one and a half to two millimeters broad. It is described by Weinland, and has also been but once observed. A half-dozen specimens were discharged from a healthy child, of nineteen months, in Boston, Mass.

Since the above was written the author has had the opportunity of examining some little tape-worms which he suspects to be of the same kind as the former. They occurred in the practice of T. V. Crandall in Philadelphia, and were expelled from a child of three years of age after the use of santonin. About a dozen fragments appear to have pertained to three worms, from twelve to fifteen inches in length. The head in all was lost. The anterior part of the body is thread-like, the posterior part about two and a quarter millimeters wide. The width of the joints is more than twice the length. The ripe joints are pale brown, and are remarkable for the comparative simplicity of the uterus, which is distended with brown eggs. A peculiarity of the worm is the repeated but irregular alternation of fertile with sterile joints.[1]

[Footnote 1: _Amer. Journ. of Medical Sciences_, 1884, p. 110.]

The species is probably more common than might be supposed, and from its small size, and perhaps harmless character, has generally escaped notice.

* * * * *

TÆNIA MADAGASCARIENSIS.--This species, described by Davaine, is imperfectly known. Fragments of the worm have been twice observed in the Comoro Islands.

* * * * *

BOTHRIOCEPHALUS LATUS.--SYNONYMS: Dibothrium latum; Tænia lata; Broad tape-worm.

This tape-worm, of another genus than the preceding, is a common parasite of man in certain localities of Europe, but has not been found as an indigenous product elsewhere. It occurs especially in Sweden and Russia, East Prussia, Poland, and West Switzerland. In the latter country it prevails to such an extent that it is reported that about one-fourth of the inhabitants of Geneva are thus infested. Among the tape-worms submitted to the writer from time to time for identification a few years ago was a large specimen of Bothriocephalus latus, but it proved to have been derived from a Swede who had arrived in this country only a few months previously.

There are many species of Bothriocephalus, which in the adult condition mainly live in fishes. The genus is distinguished from Tænia by many points, chiefly in the form and construction of the head, the form of the joints and uterus, and the position of the genital aperture, which is situated centrally on one of the broad surfaces instead of the lateral margin.

{939} The broad tape-worm is the largest of the tape-worms infesting man, a full-grown specimen reaching to twenty-five feet in length with a breadth of three-fourths of an inch, and consisting of upward of four thousand segments. It is a soft, grayish, flat, band-like worm, with head, neck, and segmented body holding the same proportions as in the other tape-worms. The head is elongated, clavate, and is provided with a long, narrow, elliptical sucker on each side. The narrower neck is short and merges into the segmented body, which gradually widens to half an inch or more. As the segments successively enlarge, they increase proportionately to a greater extent in breadth, so that their width for the most part measures from two to four times their length. A few toward the end of the series become narrower and longer than those in advance. In the ripe segments the uterus, distended with brownish eggs, forms a central rosette-like group of pouches. The genital aperture is central in the broad surface of the segments, and is always on the same or ventral side.

The broad tape-worm inhabits the small intestine, and is usually found single, but occasionally several together, and sometimes also in association with one or both the other common tape-worms. The species is also reported to be not infrequent in the dog.

Ripe portions of the broad tape-worm become detached in fragments of variable length, to be discharged with the feces. The partially-emptied appearance of the uteri in these fragments indicates the laying of the eggs previous to the expulsion of the latter. The eggs are oval, of a light-brown color, and measure about 0.07 mm. long. The shell at one pole is furnished with an operculum or lid for the escape of the embryo. This is developed subsequently to the discharge of the eggs from the intestine. If the eggs are placed in water, in the course of some months the embryos are developed and escape from the shell. The embryo is a round or oval body furnished with three pairs of spicules, as in that of the Tæniæ, but differs in possessing a ciliated envelope, by means of which it freely swims about in the water. After some days the embryo discards its envelope and creeps about in an amoeboid manner. Further than this, until recently, the fate of the embryo was unknown. Braun of St. Petersburg, after determining the presence of scolices of Bothriocephalus in the muscles, liver, and organs of generation of the pike, trout, and eel-pout, by feeding these to cats and dogs succeeded in rearing worms which differed in no respect, except in being smaller, from the Bothriocephalus latus of man. Such being the case, it becomes evident that man may ordinarily become infested with the parasite by eating raw or insufficiently cooked fishes of the kind mentioned.

* * * * *

BOTHRIOCEPHALUS CORDATUS, described by Leuckart as a common species infesting the dog in Greenland, has been reported as having once been found in a woman. Böttger regards it as not distinct from Bothriocephalus latus.

* * * * *

BOTHRIOCEPHALUS CRISTATUS.--This species, but once observed, is described by Davaine. It was passed by a child in Paris, and the worm was upward of nine feet in length.

* * * * *

SYMPTOMS OF TAPE-WORMS.--Whichever may be the species of {940} tape-worm infesting the human intestine, the symptoms to which it gives rise are mainly of the same character, modified of course in degree by the size and number of the parasites and the susceptibilities of the patient. Clinging by means of the head to the mucous membrane of the intestine, and involved among the valvulæ conniventes and villi, the worm may extend in loose folds along the greater part of the course of the intestine or lie coiled in an elongate mass. Besides being rendered evident from time to time by the discharge of segments or fragments, the beef tape-worm especially sometimes introduces itself to the notice of its host through the segments creeping from the anus. Sometimes segments of tape-worms are vomited, especially in women; and the exhibition in this way, especially of the pork tape-worm, is to be deplored, for should segments be retained in the stomach the patient becomes further liable to be affected with measles or cysticerci.

Some persons continue infested with a tape-worm a long time without suspecting its existence and with little or no inconvenience, and perhaps first become aware of its presence by the accidental discovery of segments discharged from the bowels. Usually, however, the parasite creates more or less disturbance, and not unfrequently occasions great discomfort. The symptoms are both local and of a general nature. Itching at the extremities of the alimentary canal and various dyspeptic symptoms are common; uncomfortable sensations in the abdomen, uneasiness, fulness or emptiness, feeling of movement attributed to the worm, and colicky pains; disordered appetite, sometimes deficient, oftener craving; paleness, discoloration around the eyes, furred tongue, fetid breath, and sometimes emaciation; fulness of the forehead, dull headache, buzzing in the ears, twitching of the face, and dizziness; often uncomfortable feelings in the abdomen increased by fasting, which are temporarily relieved by taking a full meal. Certain kinds of food also at times appear to produce greater uneasiness, apparently due to more than usual disturbance of the parasite. Symptoms of a more grave character are sensations of fainting, chorea, and epileptic fits. Others of a chlorotic and hysterical character are not unfrequent, especially in women, who also may suffer more or less from uterine disorder.

All the ordinary symptoms are quickly relieved by the expulsion of the tape-worm--permanently if it is entirely removed, but temporarily, as is frequently the case, when only the greater bulk of the parasite is discharged and the head continues to remain securely attached to the intestine and ready to renew its many-segmented body. The tape-worms are capable of a wonderful amount of extension from traction without detachment; and from the delicacy of the neck and the anterior part of the body, and the action of medicine on the peristaltic motion of the intestine, the posterior part of the worm, including its great bulk, is most apt to be torn away and discharged, while the head remains. So long as this is the case, and the worm has not been poisoned or killed, the anterior portion grows, and thus the parasite is renewed and accompanied by a return of all the former symptoms. Under the appropriate treatment the evacuations of the patient should be carefully inspected, so as to satisfy both physician and patient that the parasite has been completely expelled. To properly examine the evacuations, they should be repeatedly drenched with clear water, and the sediment, after the settling {941} of the washings, must be inspected. It is only when the physician has seen the head of the parasite that he can reasonably ensure his patient a permanent cure.

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TREATMENT.--To get rid of tape-worms many remedies have been employed, though comparatively few retain a reputation for positive success. Some act by powerfully operating on both bowels and worms, producing the detachment and discharge of the latter without killing them, as is often indicated in the lively movements they exhibit after their expulsion. Others poison and kill the worms, and also cause their detachment and expulsion from the bowel.

Before the administration of the appropriate medicine for tape-worms, with the object of rendering it more effective it is advisable to bring the alimentary canal into a condition which will render the parasites most vulnerable. For this purpose fasting is to be recommended for several days previously, and when food is used it should be in moderate quantity, and of such a character as to leave little residue to accumulate in the intestine. Wheat bread, the ordinary meats, milk and coffee, are best, while the usual vegetables should be avoided.

One of the most effective remedies is the oil of turpentine in the dose of one or two fluidounces, made into an emulsion with white of egg and sugar; children require about half the quantity. The large dose is less apt to produce the usual objectionable effects of that medicine than small ones. The only inconvenience caused by it is the heat of the stomach, some febrile excitement, and fulness of the head or headache lasting for one or two days. The effects are more apt to occur when the medicine does not act as a cathartic. The oil usually operates quickly, killing the worm and producing its discharge. If it does not act in the course of two or three hours, a full dose of castor oil may be given, and, if necessary to aid the action of this, enemata may be employed. To ensure the purgative action of the oil of turpentine it may be advantageously associated with the castor oil, of each a fluidounce made into an emulsion.

Another and effective remedy is the root of the male fern, Aspidium filix-mas, used in decoction or electuary. Stein of Frankfort recommends the ethereal extract as the best preparation, and prescribes it in doses of from seven to ten grammes, enclosed in half the number of gelatin capsules and administered at short intervals within half an hour. It should be taken in the morning fasting, after taking a cup of coffee, swallowing the capsules with the aid of a second cup. Half an hour after the capsules are taken a mixture of castor oil, brandy, and ginger syrup, of each fifteen grammes, should be administered. The treatment has proved all that could be desired, and the worm, including the head, is discharged altogether, rolled into a ball.

The bark of the pomegranate-root, Punica granatum, is also a powerful and efficient remedy, but often proves very disagreeable from its producing violent pains in the abdomen, with nausea and vomiting. It also generally purges, occasioning the discharge of the worm. Küchenmeister prefers it to any other medicine, given in the form of decoction prepared by macerating three ounces of the fresh bark in twelve fluidounces of water for twelve hours, and concentrating the infusion by gentle heat to one-half. He recommends it to be taken after fasting a day and the {942} administration at night of two fluidounces of castor oil. It is to be given in three or four doses within an hour. Should the medicine not purge, it should be followed by another dose of castor oil.

Recently, Feraud has recommended the tannate of pelletierin, the alkaloid of which is derived from the pomegranate-root, as the most powerful of remedies for tape-worm, the dose for an adult being one-half to three-fourths of a grain. The patient should fast a day on bread and milk, and the following morning, before rising, take an infusion of one-third of an ounce of senna. This should be followed an hour later by half the medicine diffused in a little water, and the patient should remain quiet in bed to avoid nausea and vomiting. Half an hour later the rest of the medicine is to be given, followed in another half hour by a dose of castor oil. Should there be no stool after an hour, purgative enemata may be used. In one case twelve beef tape-worms were discharged together measuring, collectively, fifty meters.

Kousso, the flower of Brayera anthelmintica, an Abyssinian herb, has been of late much employed as a remedy for tape-worms, but with many physicians of experience it has lost favor. Heller speaks of it highly, and recommends it to be taken in the morning, an hour after the patient has taken coffee. The dose is from half an ounce to an ounce, and is conveniently taken in compressed balls or disks, coated with gelatin, and swallowed at intervals in the course of an hour, aided by mouthfuls of coffee. Any disposition to vomit should be repressed, which is rendered easier by taking small mouthfuls of strong coffee or pieces of ice.

Koussin, an alcoholic preparation of kousso, is also efficient, and has the advantage over the latter that it does not occasion nausea. It has been used in the medical clinic of Munich in the dose of 30 grains, and it has been a very rare occurrence that the result was not all that could be desired.

The seeds of the common pumpkin, Cucurbita pepo, are extolled by many physicians as a remedy for tape-worms; and the writer has twice had the opportunity of observing large specimens of the beef tape-worm which were expelled after the administration of this medicine. The dose is an ounce of the seeds bruised into a paste and made into an emulsion. It should be taken in the morning, fasting, and followed in an hour or two with a full dose of castor oil.

Santonin, a principle derived from santonica, Artemisia maritima, is reported as a remedy for tape-worms, but its efficacy has also been denied. The dose is from two to four grains for an adult, and from one-quarter to one-half a grain for children over two years. It is best administered in lozenges prepared with sugar and tragacanth.

The quinia sulphate has also been recommended as an effectual remedy both in tape- and seat-worms.

As regards the prophylaxis of tape-worms, there are some important points to which we direct attention.

The evacuations of patients containing tape-worms, their segments and eggs, should not be carelessly thrown away, at least in places accessible to animals which may become infected. They should be treated with boiling water, the heat of which is sufficient to kill all animal parasites. The handling of living tape-worms and segments should be avoided, as eggs {943} which may adhere to the hands, if transferred to the mouth and swallowed, will produce infection.

Meats visibly infested with measles are not fit and should not be used as food. Raw meat should altogether be discarded as food, both for the sick and well, and all meats should be thoroughly cooked. As a rule, meat should not be used so long as it appears red or on cutting emits a bloody liquid. A large piece of meat requires long boiling or roasting for sufficient heat to penetrate to the interior to destroy any parasites that may be present. Even salted meats and hams should be cooked to ensure against parasitic infection. It is important also to avoid food prepared by uncleanly persons who may be infested with tape-worms.

As regards our domestic animals, which are the common source of the infection of man with tape-worms, they should also be protected from infection as far as possible. This is to be done by preventing them from having access to human excrement. As Heller remarks, with this object the barbarous custom of defecating in every place promiscuously should be put down with a high hand.[2]

[Footnote 2: Several years since a physician of Texas sent to the writer a piece of pork, making inquiry as to its condition, and stating that all the pigs of his vicinity were diseased and their flesh similarly affected. It contained a number of measles or larval tape-worms. On giving the information and the probable cause of the affection of the pigs, the doctor reported in return that there was not a privy in his village. Until our people are more careful with the raising of pigs, European governments will have reason for prohibiting the importation of our pork.]

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TÆNIA ECHINOCOCCUS.--SYNONYM: Hydatid tape-worm.

Larval condition: Echinococcus; E. hominis; E. veterinorum; E. granulosis; E. scolicipariens; E. altricipariens; E. hydatidosus; E. multilocularis; E. cyst; Hydatid; Hydatid cyst; Acephalocyst.

This tape-worm, in its mature state the most insignificant looking of its kind, though not strictly an intestinal worm of man, in the juvenile condition is one of his most dangerous parasites, as being the source of hydatid tumors. The adult tape-worm lives in the small intestine of the dog and wolf, in some localities often existing in these animals in thousands together. From its diminutive size it may be readily overlooked, concealed or obscured by the villi among which it is suspended to the mucous membrane. It is about a fourth of an inch in length, and consists of but four segments, of which the last alone exhibits the ripe condition. The head resembles in construction that of the pork tape-worm, being provided with four suckers and a prominent crown, with from thirty to fifty hooks arranged in a double circle. The terminal ripe segment exceeds in size all the preceding together, and before it separates from the series another is ready to take its place. The ripe eggs contain the usual six-spined embryo as in other tape-worms.

The mature worm is remarkable for the comparative shortness of its life, which, according to Siebold, is about seven weeks. Apparently to compensate for the small number of its segments, the larval form is endowed with the power of multiplying itself to a wonderful degree.

It is only in the larval condition that the hydatid tape-worm infests man, and in this state also it infests the ape, the ox and sheep and other ruminants, also the horse, hog, and indeed many other animals of the same class.

{944} If the eggs of the tape-worm are swallowed, which may readily happen by too free intimacy or association with infested dogs, the liberated embryos obtain access to the intestine. Penetrating the mucous membrane, the embryos thence may migrate to any part of the body. From the comparative frequency of hydatid tumors in the liver we may suspect they mostly enter the portal venous system and take the course of the blood-current. It is, however, probable that they migrate directly to their destination, for hydatid tumors are also frequently seated in the neighboring organs and the abdominal walls. The embryo tape-worm, once fixed in position, becomes the starting-point of a hydatid tumor.

When dogs are fed on the liver, or other parts affected with hydatid tumors, from the sheep or other animals, the scolices are liberated, and, passing into the small intestine, are there developed into the mature tape-worms.

Hydatid tumors occur in any of the organs of the body, but are more frequent in the liver than in all others together. They are common in the lungs, kidneys, spleen, omentum, and subperitoneal tissue of the abdominal walls. They are less common in the heart, brain, spinal canal, the pelvic viscera, and the bones. Mostly but a single tumor is found in the same person, but occasionally several occur together in the same or in different organs.

There are several varieties of the hydatid tumor. In man the more common form consists of a cyst or a group of cysts enclosed in a connective-tissue envelope induced by the presence of the parasite. The simple cyst is produced through the transformation of the echinococcus embryo, and the group of cysts is derived from the former by proliferation; and hence the first has been called the parent cyst, and the others the daughter cysts. These also in the same manner may produce a third series, called granddaughter cysts. The parent cyst, at first spherical, becomes modified in shape according to the space it occupies and the resistance to which it is subjected, thus assuming an oval, lobulated, or other form. It may increase in size to that of a cocoanut or larger, and may remain simple, but usually is compounded by proliferation in the production of daughter cysts. These may be few or many up to hundreds, and range from a minute size up to that of a walnut, and are spherical or modified in shape by mutual pressure or other cause. The cysts are filled with a clear watery liquid of saline taste, but without albumen.

The hydatid cysts are usually composed of an outer thick, translucent, homogeneous, laminated, glistening, highly elastic membrane, the ectocyst, and an inner thin, granular, and cellular layer, the endocyst. From the endocyst originate minute buds, which become the brood-capsules of the larval worms or scolices. These form little groups of a few to a dozen individuals suspended within the brood-capsules, but capable of eversion from them. The individual scolices, which appear to the naked eye as mere white points, have the form and construction of the head-segment of the mature Tænia echinococcus. After death or by violence they become easily detached, and then float free in the liquid containing them. In some cases the echinococcus cysts develop no scolices, in which condition they constitute acephalocysts. Occasionally the echinococcus embryo undergoes imperfect development, constituting the multilocular hydatid tumor, rarely found elsewhere than in the liver.

{945} Echinococcal tumors, especially those which have many daughter cysts, when accessible are remarkable for exhibiting a tremulous movement when grasped by the hand and quickly tapped with the finger.

Infection through the embryonic form of the Tænia echinococcus, as the source of hydatid tumors, is productive of the most disastrous consequences, and has ended in the destruction of many lives both of men and domestic animals. The parasite is not directly productive of suffering, but its effects and dangers are proportioned to the size of the tumor it occasions and the character and importance to life of the organ in which the latter is situated. With the increase of the hydatid tumor, usually of very slow growth, it encroaches upon the surrounding parts, and if these are not displaced they become disorganized and atrophied.

The liability and frequency of infection with the hydatid disease appear to be proportioned to the prevalence of intimate association with the dog. In Iceland, in which it is said every peasant owns half a dozen dogs, which share his dwelling with him, it is also reported that one-sixth of all the deaths are due to the hydatid parasite.

Ordinarily, the hydatid disease is beyond the reach of medical treatment. The mercurials and potassium iodide have been recommended, but the results are very doubtful. Apparently as an indication how little hydatid parasites may be influenced by medicine, the following incident will show: The writer once received for dissection the body of an English sailor which had been injected with zinc chloride for preservation. In the abdominal wall in the right iliac region there was a hydatid tumor the size of a fist. On examination of the tumor it was found full of daughter cysts, and these contained living scolices, though the man had been dead several days and the tissues were bleached by the zinc solution.

Favorable results in the treatment of hydatid tumors are only to be expected through surgical means when they are accessible.

As a prophylactic measure against infection the avoidance of too intimate association with dogs is especially to be recommended.

In concluding the chapter on Tænia echinococcus, as a prophylactic against this and other parasites Cobbold gives the advice that "all entozoa which are not preserved for scientific investigation or experiment should be destroyed by fire when practicable, and under no circumstances whatever should they be thrown aside as harmless refuse."

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TÆNIA ACANTHOTRIAS.

Larval condition: Cysticercus acanthotrias.

This species has been but once observed, and only in the larval condition or that of the scolex, which was first described by Weinland. About a dozen specimens were found by Jefferies Wyman of Boston in the body of a woman of Virginia who died of phthisis. They were situated in the connective tissue beneath the skin and in the muscles, except one, which was attached to the dura mater. The scolex is distinguishable from that of the other human tape-worms in possessing a triple circle of hooks. The mature form of the worm remains unknown.

{946} The Trematodes, or Fluke-worms.

The trematodes or fluke-worms, though allied to the tape-worms, differ in many important characters. In the mature condition, like the latter, they are solid worms or are devoid of a body cavity or coelum, and are with rare exceptions hermaphroditic. They are, however, never compound, but simple or consist of single individuals, and are provided with a mouth and alimentary canal, but this is closed or is without an anal aperture. They have a water vascular system, communicating with the exterior by a pore at the posterior extremity of the body. They are commonly of flat, elliptical shape, with a sucker-like mouth at the fore end, and with a second sucker situated ventrally near the middle.

The fluke-worms are remarkable for their successive transformations and course of life, and, like the tape-worms, they pass the different stages of their existence in different animals. A number of species have been described as infesting man, but most of them are, fortunately, of rare occurrence.

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DISTOMUM HEPATICUM.--SYNONYMS: Fasciola hepatica; Liver-fluke.

This species, the common liver-fluke, occasionally occurs in the human body, but is especially frequent in the sheep and other ruminating animals, as the ox, goat, and deer, and it likewise occurs in the horse, hog, and some other animals. It usually inhabits the liver, occupying the bile-ducts, but is also sometimes found in the portal and other veins and in the intestine, and more rarely in abscesses beneath the skin. It is the cause of the affection in sheep called rot, of which many thousands die annually.

The liver-fluke is a flat, tongue-shaped, brownish worm about an inch long and about half as wide. It is invested with minute scale-like spines. The head end is somewhat prolonged, and terminates in a small oral sucker, a short distance behind which is a small ventral sucker. The intestine is forked and much branched. The genital aperture is situated between the oral and ventral suckers. The commonly yellowish eggs are numerous and large, oval, and measure about 0.135 mm. long.

The common liver-fluke frequently occurs in large numbers, even hundreds, in the liver of the sheep, obstructing the bile-ducts and occasioning more or less destruction of the organ. The eggs pass off with the bile into the intestine, and are discharged with the excrement. In water the eggs are hatched, and deliver a ciliated and freely-swimming embryo. This in favorable positions, such as marshy pastures, obtains access to small fresh-water snails and penetrates to the interior of their body. Here the embryo sheds its ciliated integument and is transformed into a sporocyst. This is an elliptical pouch containing reproductive bodies, which become developed into individuals of more elongated form than the sporocyst, provided with a mouth and stomach, and named redias, or nurses. The nurse penetrates to the liver of the snail, and there develops within itself new forms called cercarias, which resemble the parent fluke-worm, but are provided with a long, powerful tail and have no apparent generative apparatus. The cercaria escapes through an aperture of the nurse, and makes its way out of the snail into the water, where it swims about actively by means of the tail, much in the manner of a tadpole. {947} The cercaria after a time fixes itself to a submerged plant, becomes encysted, shakes off its tail, and remains in a quiescent state. If in this condition, in the feeding of sheep or other animals, the tailless cercaria or incipient fluke-worm is transferred to the stomach, it makes its way to the liver, and there grows and is developed into the sexually mature worm.

Recently it has been ascertained both in England and Germany that the juvenile state of the fluke-worm is passed especially in the little fresh-water snail Lymneus truncatulus. As, however, the common liver-fluke occurs in America, while the last-named species of Lymneus does not, it is rendered probable that the juvenile condition of the parasite also occurs in other species of snails. Incidentally, the writer may here mention that he has found certain of our smallest fresh-water snails, such as Planorbis parvus, frequenting meadows in the vicinity of our rivers and creeks, swarming with nurses of several different species of fluke-worms.

Notwithstanding the frequency of the common liver-fluke in the sheep and other domestic animals, its occurrence has been rare in man, and in all the cases reported it has been few in number, either single or from two to half a dozen. In man it has been found to occupy the bile-ducts, the portal vein, and abscesses beneath the skin.

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DISTOMUM LANCEOLATUM.--SYNONYM: Smaller Liver-fluke.

This species, much smaller than the preceding, is of lanceolate form, acute behind, smooth, and about a third of an inch long. Its suckers are moderately large, and the bifurcate intestine is unbranched. It infests the liver of the sheep and ox and some other animals, and not unfrequently is found in association with the former species. It usually does not occur in such great numbers together as in the latter; from which and other circumstances, as the smaller size and smooth investment, it does not produce the same serious results. Its continuous history remains unknown, though it is probable that its course is similar to that of the common liver-fluke. Several cases are reported of its occurrence as a parasite in man.

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DISTOMUM SINENSE.--Under this head Cobbold has recently described a species somewhat larger than the D. lanceolatum. It occurs in the liver of Chinese.

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DISTOMUM CONJUNCTUM.--Another species described by Cobbold under this name, originally found in the liver of an American fox, has also been detected in man. The worm is about one-fourth of an inch long.

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SYMPTOMS.--Cases of fluke-worms in the human liver have occurred so rarely that we are not prepared to indicate with certainty what may be the nature of the peculiar symptoms. If the parasites were numerous, they would give rise to more or less obstruction of the bile-ducts, with accumulation of bile, accompanied with jaundice and other symptoms usually attendant on functional disturbance of the liver. As in sheep, they would occasion dilatation of the bile-ducts, catarrhal inflammation, incrustation with biliary matters, hyperplasia of the surrounding {948} tissues, and more or less disorganization and atrophy of the secretory structure.

TREATMENT.--As regards the treatment, we can say almost nothing. In the destructive disease of rot in sheep there are no known means to expel the parasites from the liver. If present in man, as they occur but few in number, we may hope for their spontaneous expulsion in due time without leaving any serious result. As a means of prophylaxis persons should carefully avoid salads prepared from subaquatic vegetables, like cress, which may harbor little fresh-water snails.

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DISTOMUM HETEROPHYES.--This is a small species, about half a line long, with the fore part of the body covered with minute spines, and having a large, nearly central, ventral disk. It has been but once observed, and was reported by Bilharz, in Cairo, as having been found, in the post-mortem examination of a boy, in the small intestine, in which it existed in hundreds.

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DISTOMUM CRASSUM.--This is the largest of the fluke-worms infesting man, and measures from one to three inches in length. It is elliptical, comparatively thick, and smooth. The two suckers have nearly the same relative size and position as in the D. hepaticum. It inhabits the duodenum, and has been observed a number of times infesting inhabitants of China and India.

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DISTOMUM RINGERI.--A species by this name, about half an inch long, has recently been described by Cobbold as infesting the lungs of people in Formosa and China.

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DISTOMUM OPHTHALMOBIUM.--A minute species, described under this name, has been detected several times in the human eye.

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BILHARZIA HÆMATOBIA.--SYNONYM: Distomum hæmatobium.

As a human parasite this is the most important of the fluke-worms, being the most common and dangerous. It is apparently restricted to Africa and Arabia, and is especially frequent in Egypt, Abyssinia, the Cape of Good Hope, and Natal. So far as known, it is peculiar to man and monkeys, and inhabits the veins, especially those of the portal system, and it lives on the blood.

The blood fluke-worm is remarkable among its kind in having the sexes distinct. The female is slender, cylindrical, and tapering toward the ends, looking more like an ordinary thread-worm than a fluke-worm, and is about three-fourths of an inch long. The male is about half an inch long, but wider than the female, which it partially embraces at maturity by doubling upon it laterally.

This parasite, of the same essential nature as the more ordinary fluke-worms, is most probably introduced in the juvenile condition into the stomach by drinking unfiltered standing waters, and perhaps also by eating vegetables which grow in wet places and upon which the young fluke-worms may be encysted. From the stomach the worms gain access to the portal venous system, within which they undergo development to sexual maturity. The worms, proportioned to their number, {949} occasion more or less sudden and dangerous hæmaturia. According to Bilharz, who first discovered the parasite, it also induces inflammation of the ureters, bladder, and rectum, accompanied with ulceration and incrustations and concretions in the same, due to the abundant deposit of eggs in the mucous membrane. The symptoms in the hæmaturia are obvious; all treatment fails, but the prophylaxis is evident.

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AMPHISTOMUM HOMINIS.--The genus Amphistomum is distinguished from Distomum in having the ventral disk placed at the posterior extremity of the body.

A species has been recently described by Cobbold under the above name, and is reported as having been observed several times in natives of India. It is a red worm, about the fourth of an inch long, and inhabits the cæcum and ascending colon, in which it was found in hundreds together. The mucous membrane exhibited venous congestion and was marked with numerous red spots resembling leech-bites, produced by the parasites. One of the patients died of cholera.

We have too little information as to the symptoms induced by this parasite, and of its treatment, to say anything. It is probable that calomel, turpentine, and castor oil would be appropriate remedies.

Several other fluke-worms which have been reported as having been found in the human body are generally viewed with doubt as to their genuineness. Such are the Hexathyridium pinguicola, from a tumor of the ovary; the H. venarum, said to have been found in the blood and in the sputum of hæmoptysis; and the Tetrastomum renale, said to have been found in the urine.

The Acanthocephali, or Thorn-head Worms.

The thorn-head worms in the mature condition are comparatively robust cylindrical worms, with a body-cavity or coelum, but devoid of mouth and alimentary canal. They are provided with a protrusile and retractile proboscis-like head armed with circular rows of recurved hooks, by which they firmly cling to the wall of the intestine of their host. The sexes are distinct. There are many species, which mostly in the mature state live in fishes. In the juvenile or larval condition they live in other animals, mostly crustaceans and insects. It is doubtful whether any species naturally infests man.

* * * * *

ECHINORHYNCHUS GIGAS.--The great thorn-head worm is a common parasite of the hog, living in the small intestine. It is a large white worm, the female of which reaches a foot in length, while the male is about one-third the size. It is doubtful whether it occurs as a human parasite, though a worm less than the fourth of an inch found in a man in Prague has been attributed to this species.

The Nematodes, or Thread-worms.

The nematodes, or thread-worms, are slender, cylindrical, and inarticulate, and usually more or less tapering toward one or both extremities. {950} They have a distinct coelum or body-cavity, with thick muscular walls limited by a transparent elastic, chitinous integument, which is sometimes more or less distinctly and regularly transversely wrinkled. The alimentary canal extends the length of the coelum, with the mouth at the anterior extremity, and usually an anus at or near the posterior extremity. In some forms in the mature condition the intestine is atrophied and the anus absent. The sexes are distinct, and commonly the male is very much smaller than the female. The organs of generation occupy the coelum along the sides of the intestine. The female aperture is commonly situated ventrally near or in advance of the middle of the body, while the male aperture is at or in the vicinity of the anus. Mostly, the worms are oviparous, but many are viviparous. The development is direct, and usually the transformations are inconspicuous, so that the embryos mostly differ but little from the parent, except in the absence of the generative apparatus.

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OXYURIS VERMICULARIS.--SYNONYMS: Ascaris vermicularis; Seat-worm; Pin-worm; Maw-worm; Maggot-worm; Thread-worm; Ascarides.

The seat-worm is the most common intestinal parasite of man, prevails everywhere, and is peculiar to him. It is a lively, wriggling creature which inhabits the small and large intestines and feeds on their contents. It frequently occurs in large numbers together, and in such cases incessantly makes its appearance, associated with multitudes of eggs, in the evacuations.

The female, which is ordinarily seen alone in the greatest abundance, is a white cylindrical worm tapering toward both extremities. The head end is thickened, and is provided with three prominent labial papillæ enclosing the mouth. The posterior end extends from the anal aperture in a long and straight, narrow, conical, sharp-pointed tail. The double uterine tube, distended with eggs, terminates in a vagina, the external aperture of which is situated ventrally near the anterior third of the body. The smaller male hardly tapers behind, but is incurved and ends in a short, blunt, conical tail. The penis is a single chitinous spicule, the end of which is usually seen projecting from the cloacal aperture.

The young seat-worms, in various degrees of growth and development, and the mature males are chiefly to be met in the lower portion of the small intestine, while the pregnant and mature females chiefly occupy the cæcum.

The seat-worm is exceedingly prolific, it being estimated that a single ripe female contains from 10,000 to 12,000 eggs, and these, it is suspected, may be renewed several times before her functions become exhausted. From time to time the ripe females proceed along the large intestine to the rectum, in which position they lay most of their eggs. These are discharged, together with many of the worms, in the feces.

The eggs are ovoid in shape and about 0.05 mm. long. After they are laid under favorable conditions the embryos are rapidly developed. Left in water, they soon die.

The investigations of the helminthologists of the day make it appear that it is necessary that the eggs of the seat-worm should be swallowed {951} and pass through the stomach, in which the embryos are freed, before they can undergo development to sexual maturity. Moreover, observations go to show that infection may, and probably ordinarily does, occur from eggs scratched from the anus and conveyed to the mouth directly or by being applied to food from uncleanly hands. It is evident that itching of the anus, induced by the presence of the parasites in the rectum, often accompanied by itching of the nose and lips, may lead to alternate scratching of the parts and the transference of eggs from one to the other. Thus, too, uncleanly nurses who may be infested with seat-worms after scratching may handle food and infest children under their charge. Children are commonly more liable to the parasites than others, no doubt from the circumstance that they are less capable of avoiding the conditions favorable to infection. Seat-worms prevail in all conditions of society, but their prevalence is largely proportioned to the more or less uncleanly habits. Persons sleeping with others infested are liable to infection, especially if they are uncleanly and in the habit of eating in bed. Obvious hints to avoid the parasites are obtained by regarding the statements thus given.

SYMPTOMS.--The presence of a few seat-worms is usually attended with no obvious inconvenience, and they may remain unnoticed unless accidentally observed in the evacuations. The symptoms occasioned by them are in great measure proportioned to their quantity and the susceptibility of the patient. The most prominent symptom is excessive itching of the anus; often trifling or even absent during the day, it becomes very annoying and distressing in the evening or during the night. This periodic change appears to be due to the movement of the worms to the rectum, apparently induced by the position and repose of the patient and the increased warmth of the body in bed. Under these circumstances the patient attempts to relieve the incessant itching by scratching, and often by boring with the finger in the anus. In this way eggs become adherent to the finger-nails, under which they have been repeatedly detected, and may thus be inadvertently transferred to the mouth. Occasionally, some of the worms wander from the anus, and in women may thence penetrate into the vulva. The itching of the anus may induce more or less sexual irritation, which in the young may further lead to onanism and its attendant evils. Other symptoms of the presence of the parasites are itching of the nose and lips, restlessness in sleep, grinding of the teeth, startings, twitchings, and general nervous disturbance. When the worms are very numerous they may produce intestinal catarrh, with discharges of mucus, pain, and diarrhoea. In children especially they may give rise to more serious nervous symptoms, as epileptic fits and chorea.

TREATMENT.--Generally, persons are readily relieved of seat-worms. Epsom salt alone or with senna as a purgative, repeated once or twice, often answers to completely expel them. Castor oil, also alone or with a few drops of the oil of turpentine or of wormseed, is also an effectual remedy. The tincture of aloes, in the dose of from half a fluidounce to two fluidounces, once or twice repeated, the writer has found to fully answer the purpose. Besides the purgatives, medicated suppositories, in obstinate cases injections of olive oil, and enemata of a solution of castile soap introduced by means of an elastic tube, so as to wash out the entire length of the large intestine, may be employed.

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{952} ASCARIS LUMBRICOIDES.--SYNONYMS: Round-worm; Long round-worm; Maw-worm; Lumbricus.

The round-worm is the largest of the nematodes which ordinarily infest man, and is second only in frequency to the seat-worm. It is a well-known parasite, and prevails everywhere in all conditions of society. It is less lively in its movements than the seat-worm, and is remarkable for possessing a peculiar disagreeable odor, which is independent of the medium in which it lives. It inhabits the small intestine and feeds on the contents. It also infests the hog and the ox.

The round-worm is cylindrical, reddish or brownish, and tapering toward both extremities. The head end terminates in three prominent labial papillæ surrounding the mouth, and the tail end is short and conical. The female, as commonly seen, ranges from six inches to a foot in length, and is about a fourth of an inch in thickness. The ovarian tubes are long, thread-like, and tortuous, and, with the shorter, nearly straight, and wider uterine tubes, contain many millions of eggs. The genital aperture is situated ventrally near the anterior third of the body. The male is about half the size of the female, but is capable of considerable extension, and the tail end is incurved. The penis consists of a pair of slender, clavate, chitinous spicules, the ends of which protrude from the cloacal aperture at the root of the tail.

The round-worm is exceedingly prolific, it being estimated that the genital tubes of a large mature female contain the enormous number of 60,000,000 of eggs. The ripe eggs are laid in the intestine, and are discharged with the evacuations in great numbers, and often in considerable masses together. They are oval, about 0.05 mm. in length, and are provided with a thick shell and an additional tuberculate albuminoid envelope, usually colored by the intestinal contents.

The eggs of the round-worm after being expelled from the body are very tenacious of life, and under ordinary favorable circumstances they may remain in a condition capable of development for several years. Experiments have shown that they have great power in resisting the destructive influences of heat and cold, dryness, and the agencies of decomposition. In water and moist earth they have been retained alive for a year or two. When ripe eggs are placed in water the development of the embryo is observed to proceed very slowly, and is only completed after five or six months. The embryo while still contained within the egg sheds its skin and becomes provided with a tooth-like spine to the head end. The smallest examples of reputed round-worms found in the human intestine measured only about a line in length.

The further history of the round-worm is unknown, nor has it yet been positively ascertained in what manner man becomes infected with the parasite. Repeated experiments, not only on the hog and other animals, but on man himself, go to show that he is not directly infected by swallowing the recently-laid ripe eggs. It is rendered probable that the eggs are swallowed by some common but yet unknown minute aquatic animal, within which the embryo may undergo further development, and in this condition may be swallowed by man in drinking-water. In confirmation of the view that man becomes infected in the latter way, Davaine remarks that the "people of Paris, who drink only filtered {953} water, are rarely infected with the round-worm, which is otherwise the case in the rural districts of France."

The round-worm is most prevalent in warm climates, and especially among the less-civilized peoples. The better classes among the more enlightened nations suffer comparatively little from the parasite, and it is the lower classes, especially the ill-fed and uncleanly, who are most afflicted. It is exceedingly frequent in the Orient, in Africa, the West Indies, and Brazil.

Most commonly, only a few round-worms--one, two, three, up to a dozen--occur together in the same person, but they often occur in considerable number, even to several hundreds. Not unfrequently they are found in association with seat-worms. They are more frequent and usually occur in greater abundance in children, perhaps in a measure due to the circumstance that they are less able to discriminate the conditions favorable to infection and avoided on other grounds by adults.

The natural and ordinary habitation of the round-worm is the small intestine, especially the jejunum, and it commonly only occurs in the large intestine, mostly dead, on the way to be discharged with the evacuations. Under disturbing circumstances, as the character of certain irritating food, the parasite is disposed to become restless and wander from its usual position. Not unfrequently it enters the stomach, and thence may ascend to the mouth or nose, and perhaps the first intimation of the presence of such an unwelcome guest is in its expulsion from the mouth. From the pharynx the worm may enter the larynx and trachea, or advance farther into the air-passages, giving rise to the usual symptoms of foreign bodies in these parts. Occasionally the parasite forces its way through the bile-ducts into the liver and gall-bladder, creating disturbance in those organs proportioned to the number and size of the worms and the extent of their progress. In the liver it may occasion inflammation and the formation of an abscess attended with all the usual symptoms of hepatitis. It has been reported that it may penetrate the intestinal wall and enter the peritoneal cavity, but it is generally regarded as doubtful whether the worm can do so in a healthy state of the intestine, but only where there may be ulceration or other similar condition.

SYMPTOMS.--The symptoms indicating the presence of the round-worm in the intestine vary with its numbers and with the age and susceptibility of the patient. In general, the presence of one or two worms is unattended with any marked disturbance, and is mostly unsuspected until the parasite is accidentally seen in the discharges. The ordinary symptoms are disordered appetite (usually increased), flatulence, hiccough, foul breath, dyspepsia, abdominal pains, itching at the extremities of the alimentary canal, furred tongue, darkening of the eyelids, and emaciation. The nervous symptoms are restlessness in sleep, unpleasant dreams, starting in fright, grating of the teeth, and muscular twitchings. In more aggravated cases, especially in children, epileptic fits may occur. If the parasites are numerous, they produce diarrhoea with copious mucus discharges, and may induce enteritis with all its attendant symptoms. When the worms wander into the stomach, they induce colic, nausea, retching, and vomiting, all of which disappear with the expulsion of the parasites.

TREATMENT.--The remedies employed for seat-worms often serve to {954} expel the round-worm, and not unfrequently the two are discharged together. Wormseed, or the seed of Chenopodium anthelminticum, has been a favorite remedy for the round-worm, especially in children. The dose in these cases is one or two scruples of the powdered seeds in electuary with syrup or molasses, administered in the morning before breakfast and at bedtime for three or four days. It should be followed by calomel or other brisk cathartic. The volatile oil, in the dose of from five to ten drops in emulsion, may be used in the same manner.

A much-extolled remedy to destroy and get rid of the round-worm is santonin, given in doses of from one-third to one and a half grains three or four times a day, the larger dose being used only for adults. It should be followed by a purgative, for which a dose of castor oil answers a good purpose.

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ASCARIS MYSTAX, the common round-worm of the cat and dog, has been reported as occasionally infesting man. It resembles the former species, but is much smaller, commonly from one to four inches in length, and has the head end furnished with a pair of lateral narrow, wing-like expansions of the integument. It inhabits the small intestine, and when present in man would no doubt induce symptoms like those of the ordinary round-worms which infest him.

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TRIOCEPHALUS DISPAR.--SYNONYMS: Long thread-worm; Whip-worm.

The long thread-worm is a not unfrequent intestinal parasite of man, though rarely observed unless specially sought, as it ordinarily gives rise to little or no disturbance. It is common in England, Southern Europe, and the Orient. Davaine reports that half the cases of persons investigated in Paris were infested with it; it also occurs in this country. It inhabits the lower end of the ileum, the cæcum, and vermiform appendix, and feeds on the intestinal contents. It commonly occurs in small numbers, two or three to a dozen, occasions no evident inconvenience, and is rarely discharged with the evacuations.

The long thread-worm is yellowish-white and cylindrical, with the anterior half or more of the body attenuated in a hair-like manner. The female reaches about two inches in length, has the tail end conical, and the anus subterminal. The male is about two-thirds the length of the former, has the thicker portion of the body enrolled, and the tail end blunt. The eggs are laid in the intestine and discharged with the feces. The subsequent history of the parasite and its mode of infecting man remain unknown.

Only in cases where long thread-worms are numerous do they give rise to trouble. According to Leuckart, Pascal gives as constant symptoms of the presence of large numbers of the parasite, headache, redness of the face, prominence of the eyes, small, irregular, and intermittent pulse, and pains in the lower part of the abdomen.

The usual remedies addressed to the seat-worm and round-worm will most probably be equally applicable to the long thread-worm.

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LEPTODERA STERCORALIS.--SYNONYMS: Anguillula stercoralis; Rhabditis stercoralis.

{955} This is a minute nematode worm recently observed infesting French soldiers in Cochin China. It is about half a line in length, and inhabits the small and large intestine, and also penetrates into the biliary and pancreatic ducts. It occurs in myriads and occasions diarrhoea and dysentery. Another species, Leptodera intestinalis, nearly three times as large, has been noticed in smaller number associated with the former. The eggs of these worms are laid in the intestines, and both together are discharged in multitudes with the feces. They are probably introduced into man by drinking stagnant water, and undergo complete development after passing through the stomach.

It is probable that the remedies employed in the treatment of the familiar seat-worms and round-worms would be equally efficacious in the expulsion of these parasites.

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ANCHYLOSTOMUM DUODENALE.--SYNONYMS: Strongylus duodenalis; Dochmius duodenalis; Sclerostoma duodenale.

This intestinal parasite, first noticed in Milan by Dubini in 1838, is of more dangerous character than any of the nematode worms previously described. In Europe, besides Italy, it was frequently observed among the workmen of the St. Gothard tunnel. It is exceedingly common in Egypt, and Bilharz found it in nearly all his post-mortem examinations of bodies. It probably prevails to a considerable extent in most tropical countries, including the East and West Indies and Brazil. There is also reason to suspect, from the nature of the affection it induces, that it may exist in the Southern States.

The Anchylostomum is a red, cylindrical worm, with the anterior extremity tapering and recurved. The head end, somewhat enlarged, encloses a capacious oral capsule armed with strong hook-like teeth. The caudal extremity of the female ends in a conical point, and the genital aperture is situated behind the middle of the body. The caudal extremity of the male ends in a trilobate pouch, within which projects the bispiculate penis. The female is from five lines to three-fourths of an inch long; the male is about half the size. The eggs are oval and measure 0.05 mm. long.

The worm inhabits the small intestine, especially the duodenum and jejunum, clinging tenaciously to the lining membrane by means of the armed mouth. It penetrates the mucous membrane to the submucous coat, from which it sucks the blood that forms its food. In the position of its attachment it gives rise to little ecchymoses. It often occurs in large numbers, even to hundreds and thousands. The eggs are laid in the intestine and are discharged with the evacuations. Externally, in water, the embryo undergoes development within the egg, and then escapes to lead for some time an independent existence. Subsequently, it is most probable that the worm obtains access to the human stomach by drinking standing water, and completes its development in the intestine.

The Anchylostomum proves to be a prolific source of wasting diseases in tropical countries, and is pernicious to an extent proportioned to the numbers infesting the intestine. By depriving the body of blood it produces a greater or less degree of anæmia. The affection begins very insidiously, and the general nutrition of the body may not be visibly disturbed {956} until a late period. In moderate cases the disease is indicated by general paleness of the skin and mucous membranes, fatigue on slight exertion, and a tendency to palpitations and quickened pulse. In more severe cases there is constantly increasing debility, with increase of paleness, indisposition to exertion, excessive sleepiness, and feeling of coldness. Dyspeptic symptoms sometimes appear, and loss of appetite may alternate with ravenous hunger. Accompanying this there is often a disposition to eat innutritious articles, as coal, clay, wool, etc. Feeling of weight and oppression in the epigastrium and abdominal pains are frequent. In the advance of the affection shortness of breath appears, increased on exertion to violent dyspnoea. Emaciation becomes obvious in the later stage of the disease. In the worst cases the symptoms increase in severity, the patient becomes dropsical, is attacked with profuse diarrhoea and vomiting, and finally dies.

The severity of the affection is proportioned to the number of parasites present and the quantity of blood they consume and cause to be lost. Bad cases may end fatally in a few weeks, but generally the disease lasts for months, and where the patient is provided with abundance of good food it may continue for years.

The prognosis of the disease is rather unfavorable; if, however, the nature of the affection is ascertained before it has greatly exhausted the patient, and the parasites can be expelled, the result should be favorable.

We have thus far obtained but little information as to the best treatment for Anchylostomum. Calomel and turpentine have been recommended, and, as these are most powerful vermicides, we have reason to believe they would prove most effectual remedies.

In regard to the prophylaxis for Anchylostomum--and we may add in general for all parasites which gain entrance to man through drinking-water--all stagnant or standing waters should be filtered, so as to remove any source of infection, whether by eggs or free embryos of parasites or of larval forms existing within minute aquatic animals which serve as intermediate hosts to parasites. Standing waters, such as those of puddles, ditches, marshes, and ponds, more or less swarm with minute animals, all of which may be entirely removed by filtration. Even the water of cisterns and wells, if supplied from the free surface of the country, may not be free from minute animals, and especially eggs, and therefore requires filtration to be safe. Only spring and freely-running water of rivers and creeks and of lakes is commonly free from microscopic animals and their eggs, and therefore devoid of all danger in these respects.

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STRONGYLUS LONGEVAGINATUS; S. bronchialis.--This nematode has been only once satisfactorily observed. Many occurred in the lungs of a boy in Germany, but the real cause of his death was not stated. The female worm is about an inch long, the male about five-eighths of an inch.

Certain worms previously discovered in the bronchial glands of a case of phthisis, and described under the name of Hamularia lymphatica, are regarded by Cobbold as the same with the former; but the descriptions of the two render this improbable. Treutler's drawing of Hamularia, as copied by Leuckart, looks like an Ascaris upside down.

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{957} EUSTRONGYLUS GIGAS; Strongylus gigas; Palisade-worm; Kidney-worm.--This worm, recorded in the catalogue of human parasites, is doubtful as such. Pertaining to the same family as Anchylostomum, as the common name indicates its usual habitation is the kidney. It is the largest of the nematodes, and is a long, cylindrical red worm, slightly tapering, and blunt at the ends. The mouth is enclosed by six rounded labial papillæ. The caudal extremity of the male ends in an inverted cup-like pouch, from which the penal spiculum protrudes. The female commonly ranges from one to three feet in length and from a fourth to nearly half an inch in thickness. The male ranges from six inches to a foot in length and from one to three lines in thickness.

The mature parasite is common in many fish-eating mammals, from which it is inferred that fishes are the intermediate host for the juvenile condition of the worm. It is frequent in the wolf, dog, mink, weasel, raccoon, otter, and seal. It also occurs in the hog, and is reported to have occurred in the horse, ox, and man. Usually it is solitary, and occupies one of the kidneys coiled upon itself. Under its influence the kidney is atrophied and reduced to the condition of a capsule of connective tissue, often containing bony spicules. It feeds on blood and on the purulent matter resulting from the inflammation it produces. The worm is occasionally found in other positions, as the mesentery, the abdominal cavity, the intestine, liver, urinary bladder, and lungs, but perhaps in most of these cases has been derived from its usual habitation. In this country the writer has repeatedly observed the kidney-worm in the mink, the dog, and the wolf. In one instance in the former animal he found a female and a male associated together in one kidney, which was reduced to the condition of a fibrous capsule containing in its wall a large radiated plate of bone.

The cases on record of the occurrence of this formidable parasite in man are of very early date, and are mostly doubtful as to the authentic nature of the worm, and are all unsatisfactory as to the attendant phenomena.

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TRICHINA SPIRALIS.--The trichina, or flesh-worm, a minute nematode, is a common parasite of man, and from its wide prevalence and results may be regarded as the most dangerous of all. Perhaps from the earliest ages it has been dealing death freely and indiscriminately to our kind without its existence having been suspected until within the last half-century. Frequently, the affection, now named trichinosis, produced by its presence has been so prevalent in communities as to appear epidemic. The parasite was first discovered, and is commonly observed, as a little worm coiled up and imbedded in the flesh of man. In the same manner it is frequently seen in the flesh of the hog. In the adult or mature state it lives in the small intestine of both man and the hog, but its duration of life in this position is comparatively brief.

Trichinosis, or the disease induced by the introduction of trichinæ into the intestinal canal and the migration thence into the voluntary muscles, varies in symptoms and gravity with the number, condition, and position of the parasites and the susceptibility of the patient. The presence of trichinæ in the alimentary canal, though often accompanied by violent symptoms, is comparatively free from danger, whereas in the muscular {958} system they not only produce the greatest suffering, but often the most disastrous results.

Man is ordinarily infected with the trichina by eating the raw or insufficiently cooked meat of the hog, or pork in any of its varieties of food. Infected meat often contains immense numbers of the parasite, a single ounce at times being estimated to contain from 50,000 to 100,000 worms.

The trichina was first distinctly noticed in the muscles of the human body by Paget in 1835, and was described by Owen with the name it now bears. It was subsequently observed under the same circumstances by other investigators. In 1846 the parasite was found by the writer in the muscles of the hog, but neither he nor others for some time afterward suspected the significance of the discovery. In 1860, Zenker of Dresden treated a supposed case of typhus complicated with excessive muscular pain and oedema. On post-mortem examination the muscles were found swarming with trichinæ, and to these the affection altogether was attributed. Nearly at the same time the investigations of Leuckart confirmed the relationship of the parasites as the cause of the disease. In 1862, Friederich first diagnosticated the affection and experimentally determined the presence of the worms in the living patient.

The trichina is also found infesting other animals of the same class besides man and the hog, especially the rat, mouse, rabbit, cat, and fox. Experiments further prove that mammals are generally more or less susceptible to infection with the parasite, though some appear to resist its extension to the muscular system, as in the case of the dog. The horse, ox, and sheep exhibit little disposition to artificial infection of the muscles, and hence from this circumstance and the nature of the food of these animals they are rarely found to be infested with trichinæ. In experiments on birds and lower classes of animals, though trichinæ were ascertained to advance in development in the intestine, they failed to invade the muscular system.

Ordinarily, it appears that while man is infected with trichinæ through the hog, this animal becomes infected by eating infested rats, mice, and cats, fragments of waste pork, and perhaps occasionally by feeding on the excrements of infested animals.

The trichinæ occupying the muscles are immature, and it is only after they are swallowed and the parasites are freed by digestion of the envelopes and pass into the intestine that they undergo development to sexual maturity. In this state the female is viviparous and gives birth to a multitude of active embryos, which immediately commence to migrate to the muscular system. As it is estimated that each female may give birth to upward of a thousand embryos, it is readily conceived to what an extent the body may become infested from eating a few ounces of trichinous pork.

The immature or larval trichinæ are also distinguished as muscular, and the sexually mature ones as intestinal, trichinæ, in accordance with their position in the two principal conditions.

Muscular trichinæ vary in condition from the embryo, which works its way among the muscular fibres or has obtained entrance into these, to the coiled-up worm lying quiescent in a capsule imbedded among the muscular fibres.

Infected flesh in the early state is scarcely distinguishable as such with {959} the naked eye, but in old cases the trichina capsules become imbued with calcareous matter, and are thus rendered visible as minute white or grayish specks scattered through the red meat.

In the recent state of invasion the worms are found free among the muscular fibres or within these. Later, they appear mostly solitary and at rest, coiled within a fusiform mass of semi-liquid granular matter resulting from the degradation of the muscular substance. Subsequently, they become enclosed in an elliptical capsule, apparently derived from the myolemma of the muscular fibre they had entered. The capsules, situated among the bundles of sound muscular fibres, are arranged with their long diameter parallel with the latter. The trichina capsules commonly measure about one-fifth of a line long, and the coiled worm within is scarcely a half-line long.

If muscular trichinæ remain with their host, after a year or more they exhibit signs of decay. Commonly, little fat-globules appear at the poles of the capsules, and these become the seat of calcareous deposit. Finally, the worms die and undergo degeneration.

When meat with living trichina capsules is swallowed, the freed worms pass into the intestine, and here in the course of four or five days reach maturity.

The adult intestinal trichina is a minute, filiform white worm, thicker behind and tapering forward. The female is about an eighth of an inch long, and has the genital aperture at the anterior fourth of the body. The male is little more than half the length of the former, and has the caudal end provided with a pair of conical processes, between which is the genital aperture.

The ripe female trichinæ give birth to living embryos, and continue the function for about a month, after which they appear exhausted, ordinarily die, and disappear from the intestinal canal. The new-born embryos, about 1/200 of a line long, quickly leave the intestine to be disseminated throughout the body. Penetrating the mucous membrane, they probably enter the blood-vessels to be carried onward by the blood-currents, and perhaps also, in part, directly migrate to their destination in the muscles. The latter mode of progress is rendered the more probable from the circumstance that the muscles contiguous to the intestinal canal, as the diaphragm and those of the abdominal walls, are commonly most abundantly infested with the parasites. In the muscles of the limbs they are sometimes noticed to predominate toward the extremities of the former, as if retarded in their course by the tendinous connections.

It would appear that muscular trichinæ, to be capable of producing infection--that is to say, of further development--must have reached a certain stage, corresponding with the encapsulated condition, before they are swallowed. In this stage they may remain within their host probably for a year or two.

Children seem to suffer less in proportion to the quantity of trichinous meat they eat than adults, and they appear less susceptible to muscular invasion of the parasites. The difference is probably in a measure due to the greater susceptibility of the intestinal canal and the consequent production of more copious diarrhoea in children, with more complete expulsion of the worms.

SYMPTOMS.--In general, the effect produced by eating trichinous meat {960} is proportioned to the number and condition of the trichinæ ingested and to the susceptibility of the patient. A few of the parasites may pursue their entire career and die within their host without ever exhibiting any obvious evidence of their presence. Sometimes the symptoms of trichinosis are obscure or trifling, sometimes sufficiently well marked, but moderate, and often they are more or less striking and violent. The period of incubation of the affection varies from a few hours to a week or more, and the duration of the disease also varies--both in a measure proportioned to the number and condition of the parasites.

In mild cases of trichinosis the patient may pass through the course of the disease without being confined to bed, and in a few weeks may be regarded as convalescent. The majority of cases pursue a slow course of from six or seven weeks to three or four months. A fatal termination is frequent, and is most common from the fourth to the sixth week, and appears mainly to be due to the loss of respiratory power. Fatal cases rarely happen after the seventh week.

From a few hours to a few days after eating trichinous meat the patient may be seized with dyspeptic symptoms--nausea, cardialgia, flatulence, eructations, and vomiting. These may be accompanied with complete loss of appetite, excessive thirst, bad taste, and fetid breath. There is also commonly a feeling of general uneasiness, with fulness of the forehead or headache, and feeling of weakness and fatigue to exhaustion or complete prostration. Neuralgic pains are felt in the abdomen and limbs, and the muscles generally are more or less relaxed and flabby.

Violent disturbance of the alimentary canal occurs only when large quantities of active trichinæ are taken with the food. The subsequent symptoms, due to invasion of the muscular system, may, but do not necessarily, accord in degree with the former.

Diarrhoea usually comes on early, and the evacuations, at first more consistent, become thin and clay-colored, like those of typhus or like the rice-water stools of cholera. In the severest cases the patient may die in this stage from extreme exhaustion and with all the appearance of cholera. Sometimes the diarrhoea subsides and gives place to obstinate constipation.

The muscular symptoms induced by the invasion of the trichinæ may be trifling or moderate, varying to a most violent character. They commonly appear after a week, and later up to the sixth week. The muscles become more or less swollen, hard and tender to the touch, or highly painful under pressure. Motion is extremely painful, and the patient usually lies in a helpless state with the limbs flexed--adults on the back, children on the side. Difficulty, with pain, in chewing and swallowing ensues, and even complete trismus, due to the presence of the parasites in the muscles of mastication and deglutition. Difficulty of breathing also arises from the presence of the trichinæ in the respiratory muscles, especially the diaphragm and those of the larynx. Even movement of the eyes is painful, due to the parasites in the orbital muscles. Bronchial catarrh comes on early, attended with hoarseness and asthmatic cough.

Fever may be absent in mild cases of trichinosis, but is considerable in the severer forms, though not in the first few days. The pulse accords with the increase of temperature.

Profuse sweating is a common symptom of the affection, commencing {961} early and continuing throughout. Generally there is considerable decrease in the quantity of urine, which is highly colored.

Adults suffer with insomnia, while the reverse state prevails in children, who commonly lie in a soporose condition. Formication and dilatation of the pupils are frequent symptoms.

Oedema is a characteristic and pathognomonic symptom of trichinosis, and is seldom so slight as to escape attention. It commonly appears in the eyelids and face about the end of the first week, and may disappear after several days, to recur after several weeks. It usually commences in the limbs in the second week, and is more marked and persistent, and increases, especially in severe cases.

Peritoneal and pleuritic irritation and inflammation, with bronchitis and pneumonia, are not unfrequent complications in the more aggravated form of trichinosis.

Most cases of the disease reaching the seventh week advance in convalescence, while those of mild character by this time have recovered, except from the weakness and emaciation, which remain as evidences of serious illness.

Trichinosis in children is distinguished by greater mildness, less danger, abundant oedema, less muscular pain, a dormant condition, and more rapid convalescence.

The distinct recognition of trichinosis is difficult in isolated cases, but becomes more evident where it occurs in numbers, as in an entire family or in large portions of a community. The proof that the patient has partaken of trichinous pork helps to establish the diagnosis.

In the beginning of severe cases of the affection symptoms of a more or less violent gastro-intestinal catarrh are commonly present, often associated with slight fever and almost invariably excessive perspiration. Muscular lameness, both in mild and severe cases, is an early symptom. The disease is distinguished from cholera by the profuse perspiration and the peculiar muscular symptoms; from ordinary rheumatism by the gastro-intestinal catarrh and general exhaustion. With the appearance of oedema of the eyelids and face at the end of a week the diagnosis becomes more certain. The further progress of the affection is so characteristic that its distinction can scarcely remain in doubt. The general prostration, the violent muscular symptoms, the bronchial catarrh, the hoarseness and dyspnoea, the profuse sweating, and the sleeplessness, render the case pretty clear.

In the prognosis of the disease no positive conclusion can be derived from the severity or early appearance of the initial symptoms. Commonly, the more speedily they occur and the more violent they are, the less favorable will be the prognosis, while the later they appear, the more propitious it is. Long-continued diarrhoea is especially unfavorable, while a profuse diarrhoea at the beginning is to be viewed as a fortunate event. The prognosis is more favorable in cases in which sleep and the appetite are maintained, and in those in which the disturbance of the respiratory organs is slight. A favorable termination of the affection is the rule with children.

TREATMENT.--The treatment of trichinosis is not generally promising in favorable results. No means have yet been discovered to destroy or remove trichinæ which have migrated from the intestinal canal. While {962} the parasites continue within the latter we may have reasonable hope of expelling them from the body by means of the usual remedies for intestinal worms. Experience, however, with these remedies has not been in accordance with expectations. In the mean time, until some more potent vermicide is discovered applicable to the destruction and removal of trichinæ from the intestine, we are disposed to place most reliance on such purgatives as oil of turpentine and castor oil and calomel and jalap. Subsequently, a good nutritive diet with wine is recommended to preserve the life of the patient until the affection has reached that period when the parasites become capsulated and there is no longer danger from them as irritants.

As a preventive of trichinosis, besides the avoidance of pork or its varied preparations of ham, sausages, etc. when it is known or suspected they may be infested, thorough cooking of meats is a certain means. A boiling temperature surely kills all animal parasites, but care is requisite that large pieces of meat should be cooked sufficiently long that the desired heat may extend to the interior throughout. The writer may add that it was in a slice of boiled ham, from which he had partly made his dinner, that he first discovered trichina in the hog.

* * * * *

Of the nematode worms there are many species of comparatively long, slender proportions, which constitute the family of Filaridæ. As parasites they rarely occupy the interior of the intestinal canal, except by way of transit, and live in most other organs and tissues of the body of both vertebrate and invertebrate animals.

* * * * *

FILARIA MEDINENSIS.--SYNONYMS: Dracunculus; D. medinensis; Medina-worm; Guinea-worm.

The Medina-worm has long been recognized as a parasite of man, and by competent authorities has been regarded as the fiery serpent which afflicted the children of Israel in the wilderness of Judea. It prevails in the tropical regions of Africa and Asia, and thence has been introduced into tropical America. It is ordinarily observed as a long, white, cord-like worm, situated beneath the skin in any part of the body, but mostly in the lower limbs, and especially in the vicinity of the ankle. Though a frequent parasite, only the female is known. In the mature condition it is nearly uniformly cylindrical, and ranges from eighteen inches to three or four feet in length and less than a line in thickness. The head end is rounded and furnished with a little papillate plate, in the centre of which is situated a minute oral aperture. The caudal end is conical and incurved. The intestinal canal is atrophied and without an anal aperture. The coelum is mainly occupied by a capacious uterus filled with free embryos. A generative aperture appears also to be absent, and the young can only escape by rupture of the parent.

Experiments made about a dozen years since in Turkestan by Fedschenko, at the suggestion of Leuckart, have shown that when the embryos of the Medina-worm are introduced into water containing the familiar little crustacean cyclops, they penetrate into this, and within it undergo transformation into the larval stage. The subsequent history of the larval worms remains unknown, but from what we have learned of the history of many parasitic worms it is reasonable to suppose that if {963} the infested cyclops is swallowed in drinking-water, it may explain the presence of the mature worm in the human body. The young worms, liberated from their crustacean host by digestion in the stomach, probably enter the intestine, and thence migrate to their destination. In the young condition, advancing to maturity, the worms have been found in all parts of the body except within the cranium and eyeball. They appear to migrate in the course of the least-resisting connective tissues, along the route of the principal blood-vessels, until they reach the surface of the body.

Usually, a single worm is found in a person, though cases occur where several, to a dozen or more, are present. Commonly, the parasite is solitary, though two or three may be associated together. When deeply seated the Medina-worm ordinarily produces but little discomfort, though in some cases its movements are accompanied with more or less severe pain. It also gives rise to inflammation and the formation of an abscess, in the purulent matter of which the worm lies bathed. The removal of the worm, when accessible, by the proper surgical aid is followed by complete relief.

It is evident that filtration of the drinking-water would be a certain prophylaxis for the Medina-worm.

* * * * *

FILARIA SANGUINIS.--SYNONYMS: Filaria sanguinis hominis, Lewis; F. sanguinolenta; F. Bancrofti, Cobbold.

Another species of Filaria, a more dangerous parasite of man and indigenous to the tropics, is of frequent occurrence, though of comparatively recent discovery. It has been observed in India, Africa, Brazil, and the West Indies. It is commonly seen in the embryonic condition, living in the blood of patients affected with elephantiasis and certain other diseases, and is also found in the urine. In this early condition it is a minute worm, scarcely more than the 1/100 of an inch in length, and occurs together in immense numbers.

In the sexually mature condition the female filaria is a white hair-like worm three or four inches in length, living in the lymphatic vessels distally to the glands, especially in those of the lower limbs and scrotum. The embryos after leaving the parent pass into the lymphatic stream, and thence into the circulating blood. According to recent observations of Manson, they enter the blood in the evening and increase in number until midnight, after which they decrease and disappear by morning, from which time during the day they remain absent from the circulation. The investigations of the same authority have shown that when the blood of infected persons is sucked by mosquitoes these insects also imbibe the embryos, which subsequently undergo transformation in the mosquitoes into the larval state. In this condition the filariæ may be transferred to water, by drinking which man may become infected with the parasites. The larvæ introduced into the stomach appear thence to make their way to the lymphatics, within which they undergo further development to maturity, and thus remain a long time.

The presence of the worms in the lymphatics, with their numerous brood in the circulating blood, gives rise to hæmaturia and chyluria. As results of the obstruction of the lymphatic currents, the parasites induce inflammation, suppuration, lymphatic abscesses, buboes, lymphangiectasis, {964} oedema, ascites, chylous hydrocele, elephantiasis,[3] and certain cutaneous affections.

[Footnote 3: Several years since, with the view of ascertaining the presence of parasitic worms, the writer examined the blood of a case of elephantiasis under the charge of T. G. Morton, but none were detected. From what we have since been informed of the habits of Filaria sanguinis, the absence of the parasites may have its explanation in the circumstance that the blood examined was withdrawn in the daytime.]

TREATMENT.--While the treatment of the affection induced by the Filaria sanguinis is varied and uncertain, the prophylactic measures are obvious and certain. Under favorable conditions of bright light, high temperature, and abundant food the stagnant waters of tropical countries are especially prolific of the minute forms of animals which harbor parasites. It hence becomes evident that all such waters, whether obtained from puddles, ponds, tanks, or cisterns, should be filtered before being used for drinking. Boiling is also effectual in destroying all the animal life of waters, and thus rendering them innocuous so far as parasites are concerned.

* * * * *

Several other species of Filaria have been found in the human body, but are little known and very rare in their occurrence.

* * * * *

FILARIA LOA.--This species occurs in Western Africa, on the Gaboon River, and is perhaps more frequent than now commonly supposed. It is an active worm, little more than an inch in length, and is usually found beneath the conjunctiva of the eye. It probably also occupies other positions, and a missionary on the Gaboon informed the writer that he had extracted one from the back of one of his own fingers. Its presence produced an intense burning pain. The negroes are reported to extract the worm by means of a thorn. The worm has also been observed in Brazil and the West Indies.

* * * * *

FILARIA RESTIFORMIS.--Under this name the writer recently described a large Filaria reported to have been withdrawn from the urethra of a man in West Virginia. It was obtained by C. L. Garnett, and sent, together with an account of the case, to the Army Medical Museum of Washington, where it is now preserved. It was a red cylindrical worm, twenty-six inches in length, tapering at the head, and thick, incurved, and obtusely rounded at the tail end.[4]

[Footnote 4: _Proceedings of the Academy of Natural Sciences_, Philada., 1880, p. 130.]

* * * * *

FILARIA OCULI HUMANI; FILARIA LENTIS.--A few cases are on record of the occurrence of little worms in the aqueous humor and crystalline lens of the human eye, to which the accompanying names have been applied.

* * * * *

FILARIA TRACHEALIS.--Recently some minute worms found by Rainey in the trachea and lungs have been described under this name.

* * * * *

In conclusion, the writer acknowledges his indebtedness for much of the information of this article to the articles on "Intestinal Parasites" and "Diseases from Migratory Parasites" in _Ziemssen's Cyclopædia of the Practice of Medicine_, and to Glazier's _Report on Trichina and Trichinosis_.

{965}

DISEASES OF THE LIVER.

BY ROBERTS BARTHOLOW, A.M., M.D., LL.D.

I. FUNCTIONAL DISORDERS.

Biliousness.

DEFINITION.--The term biliousness is used to signify a disturbance of the gastro-intestinal digestion, with coincident excess in the production of bile. According to the popular conception, both lay and medical, the excess of bile is the cause of the symptoms; but when the whole subject is carefully examined it will be found that biliousness is made up of several factors, and that the hepatic disorder, if it exist at all, is a mere incident.

PATHOGENY.--From the time of Galen biliousness has been regarded as a morbid entity and the liver as the organ affected. Stoll, amongst moderns, first revived the Galenical doctrines. Abernethy[1] was amongst English physicians the most conspicuous advocate of the condition called biliousness, and was the apostle of blue pill and black draught. Copland in his great dictionary[2] more distinctly formulated the views of the English school--especially that portion of it influenced by the results of Indian practice--than had been previously attempted, and hence his work best represents the opinions and practice of the time amongst the English-speaking peoples. In this country the great Rush first promulgated the notions of biliousness which have since so dominated the medical opinion of this continent. A large part of the United States has proved a fruitful soil for the cultivation of theories of biliousness, since the condition known under this name is a frequent accompaniment of malarial poisoning. To this fact must be attributed the preponderating importance of biliary derangements in the practice of the physicians of India also.

[Footnote 1: _Surgical Works_, London, 1811, vol. i. p. 36.]

[Footnote 2: _A Dictionary of Practical Medicine_, vol. ii. p. 723.]

It is a fact which will be hereafter more fully developed that malarial infection may, and often does, derange the hepatic functions without producing fever. The malarial poison irritates the liver, and thus more bile is produced, but the quality deteriorates with the increase in quantity. The functions of the liver are more disturbed during an access of intermittent fever: the organ is swollen, the skin is muddy, the eyes yellow, the tongue coated with a thick yellow fur, and the urine is deeply tinged with bile-pigment.

Many of the metals employed as medicines and as poisons, as gold, {966} silver, antimony, arsenic, phosphorus, etc., irritate the liver both in their entrance and in their exit from the organism, and cause biliousness; and the same fact is true of some vegetable alkaloids and animal poisons. The liver excretes many of these substances, and in their passage out from the blood the hepatic cells are irritated and an increased production of bile is a result. Improper food, indulgence in fats, sweets, condiments, and all kinds of fermented and alcoholic liquors, intestinal indigestion arising from any cause, and gastro-duodenal catarrh, are the most usual and obvious pathogenic factors. In respect to food and indigestion as etiological factors there are several points requiring more explicit statement. When nitrogenous elements (albuminoids) are in excess in quantity or as respects the power to digest and convert them, immature products, of which uric acid is the chief, accumulate in the blood. When the fats, sugars, and starches are in excess of the requirements of the organism or are imperfectly disposed of in the small intestines, a local irritation of the mucous membrane is produced, and various complicated, immature products enter the blood. With these troubles and faults of intestinal digestion a gastro-duodenal catarrh is usually associated. Without the production of catarrhal jaundice, gastro-duodenal catarrh, with the forms of indigestion accompanying it, keeps up a reflex irritation of the liver. Just as the presence of normal chyme induces the flow of bile, so the unhealthy products of intestinal indigestion excite an irritation of the liver. The continued operation of this cause maintains an abnormal activity of the liver, and more bile is produced than is easily disposed of.

SYMPTOMS.--The condition of biliousness, as now understood, is made up of derangement of the gastro-duodenal mucous membrane, with bile-production in excess and bile-absorption probably delayed. The symptoms are the product of these complicated conditions. The complexion is muddy; the conjunctivæ are yellow; the tongue is heavily coated with a yellowish-white fur; a bitter taste persists in the mouth; the breath is heavy in odor, even fetid; the appetite may be keen or there may be complete anorexia; a sensation of nausea, of heaviness, and fulness of the stomach is experienced, especially after eating; the bowels are confined usually, but occasionally the movements are relaxed, bilious in appearance, and cause heat and irritation about the anus; headache is constantly present to some extent, and there is a sense of fulness with more or less dizziness, and singing in the ears; vision is rather blurred, and there is a hebetude of mind; the urine is high-colored, high in specific gravity, and deposits lithates abundantly on cooling. When these symptoms are conjoined with hemicrania, nausea, and vomiting, the case is called bilious sick headache, and when diarrhoea supervenes, the discharges apparently containing much bile, it is bilious diarrhoea. The symptoms which above all others give the character to the morbid complexus are the muddy (bilious) complexion, the yellow-coated tongue, the yellow conjunctivæ, and the high-colored urine. The first departure from the normal may be scarcely observed. Gradually, owing chiefly to errors of diet, to climatic changes, or to malarial influences, or to these several factors combined, the affected person drifts into the condition of biliousness above described. Besides the general malaise, he experiences no little despondency, inaptitude for exertion, and indeed actual weakness. Finally, he is unable to apply himself to business, relinquishes the effort, and seeks advice.

{967} COURSE, DURATION, AND TERMINATION.--Those who are accustomed to experience attacks of biliousness suffer from them at certain intervals which may be tolerably regular--at intervals of a few days, two, three, or four weeks--when the cause is uniform; but they may happen very irregularly when the conditions producing them are variable. The duration of an attack is from two days to a week or more, according to the severity of the symptoms and to the character of the measures instituted for relief. The termination is in a return to the normal state. If the conditions which produced it continue, when one attack is ended the preparations for another begin at once, and at length sufficient derangement of the organs concerned arises to constitute the morbid complexus of biliousness.

TREATMENT.--Prophylaxis has great importance, since the causes of the malady are to a considerable extent, at least, preventable. Errors of diet in respect to the use of condiments, fats, meat, pastry, etc. must be corrected. When there is pronounced gastro-duodenal catarrh and acid fermentation in the duodenum, the saccharine, fatty, and starchy elements of the food must rather be excluded and lean meats allowed. Abundant exercise, bathing, and an open-air life in general should be directed. Whenever a malarial infection is causative a change of climate becomes imperative. Heredity cannot, of course, be excluded, but the tendency to hepatic derangement can be rendered inoperative by an abstemious life.

The remedial management includes the dietetic as well as the medicinal treatment. When the distress has reached sufficient proportions to justify such an extreme measure, the patient should be restricted to a diet exclusively of skimmed milk, of which he is directed to take a gill or more every three hours. This serves a double purpose, as aliment and as a depurative agent, for this considerable quantity of fluid promotes the urinary excretion and the elimination of waste products. If the case is not severe enough to allow of such an expedient, the diet should in any event be restricted to skimmed milk hot, milk and hot water, hot lemonade, a little chicken or mutton broth, a bit of dry toast, etc. As a rule, although not so palatable, hot drinks are more beneficial than cold, but if the preference is decidedly for cold, they may be allowed. After the more severe symptoms have subsided a little lean meat broiled may be added, and as the cure proceeds the succulent vegetables and acid fruits may be permitted. Abstinence from potatoes, hominy, cracked wheat, and oatmeal should be enjoined during the convalescence of those who suffer from habitual attacks.

Medicines may not be necessary to those who have the resolution to adhere to skimmed milk for several days or who can abstain from food altogether for a day. Many experienced sufferers, especially through the South and West and in England, procure rather prompt relief from a blue pill of ten to fifteen grains or from one to five grains of calomel at night, followed by a Seidlitz powder, Rochelle or Epsom salts, or phosphate of soda on the following morning. Such patients find that no other treatment is as serviceable. They get relief from other measures, it is true, but neither as promptly nor as satisfactorily. It is held by the advocates of this practice that the mercurial acts on the liver--that the surplus bile is carried off; and they point to the peculiar stools and to {968} the relief experienced in evidence of the truth of this theory. Without entering on the argument, which would occupy too much space, it must suffice here to state that calomel and blue pill do not increase bile-production,[3] but they do stimulate the intestinal glands and increase excretion from them. The peculiar greenish stools produced by these mercurials do not owe their characteristic appearance to the presence of bile, but rather to the chemical transformations of the mercury itself and to the waste products excreted by the intestinal glands. Since the researches of Rutherford have been published, euonymin has been much prescribed in cases of biliousness. From three to five grains are taken at the bed-hour, and a mild laxative in the morning. In the same group of cholagogues are ipecac, iridin, sanguinarin, and especially podophyllin; but the serious objection to their use is that they stimulate the liver when this organ is in an irritable state. As calomel and blue pill have a sedative rather than a stimulant action on the liver, they are more useful in biliousness than are the true cholagogues. It should be borne in mind that one-half of a grain of calomel will have a distinct purgative action on many persons, and that one grain will rarely need to be exceeded.

[Footnote 3: That calomel, the type of a mercurial purgative, does not increase the discharge of bile has been demonstrated on dogs by Röhrig and Rutherford, and confirmed by observation of the effects of 20 grains on Westphalen's case of biliary fistula in man--a case in which, for a time, all the bile escaped externally, and none apparently entered the intestine (_Deutsch. Archiv f. klin. Med._, 1873, Band xi. pp. 598 and 600).]

In general, notwithstanding the unquestionable utility of the mercurial, it is better to relieve cases of biliousness by less objectionable measures. A saline which acts at the same time on the intestines and kidneys, as Rochelle salts, is usually effective in bringing relief. A bottle of solution of magnesia citrate, of Saratoga water (Congress, Hathorn, or High Rock), and of Blue Lick, the famous sulphurous laxative of Kentucky, may remove the disorder in mild cases if at the same time a suitable diet is enjoined. Phosphate of soda in laxative doses, with or without Vichy water, is also a good remedy, if somewhat slow. The warm purgatives, rhubarb, colocynth, aloes, etc., are useful when there is pronounced constipation.

Lithæmia.

DEFINITION.--By the term lithæmia is meant a condition of the system in which uric (lithic) acid is produced in excess, and in which certain derangements occur in consequence of the accumulation of this material in the blood. Uricæmia was the term first suggested by Flint, Sr.,[4] to express this state, and subsequently lithæmia was employed by Murchison.[5] The latter has been more generally accepted. In one of the most recent and valuable contributions to this subject by DaCosta[6] lithæmia is the term used to designate the complex of symptoms produced by uric acid in excess.

[Footnote 4: _The Principles and Practice of Medicine_, Philada., 1882.]

[Footnote 5: _Clinical Lectures on Diseases of the Liver_, 2d ed., p. 565.]

[Footnote 6: _The Medical News_, vol. ii., 1883.]

PATHOGENY.--The ultimate product of albuminoid substances in the organism prepared for final excretion is urea. That this substance is {969} finally formed in the liver, to be excreted by the kidneys, seems now well established.[7] In acute yellow atrophy of the liver, with the disappearance of the proper structure of the organs urea ceases to be produced, and instead leucin and tyrosin are excreted. In certain states of the system characterized by deficient oxidation urea is not sufficiently formed, and instead uric acid, a lower grade of oxidation and a product of the disintegration of albuminoid substances, results. An excess of urates is not always pathological. Their excretion seems to be in a certain sense a safety-valve function. When albuminoid matters are taken in excess of the power of the system to convert them, or when the supply of oxygen to the blood is deficient from any cause, urea is not formed, but uric acid and urates are abundantly excreted by the urine.[8] Imperfect digestion of the albuminoids when they are not taken in relatively too large an amount, and limitation below the normal of the oxidation process when the supply of oxygen is not insufficient, will have the same effect: in place of urea, uric acid and urates will be formed and excreted. One of the early results of the persistent presence of an excess of uric acid is the production of lithæmia, the morbid complexus of which this excess is at once the cause and the proof.

[Footnote 7: This proposition is not universally accepted. Valmont (Thèse de Paris, _Étude sur les Causes des Variations de l'Urée dans quelques Maladies du Foie_, 1879) has carefully studied the excretion of urea in several diseases in which the proper structure of the liver is damaged--in atrophic cirrhosis and in cancer. As in these maladies not all the secreting portion of the organ is destroyed, the argument is so far weakened. His conclusions are as follows: "1. Patients with cirrhosis or cancer of the liver who eat little excrete but little urea. If they eat and do not absorb, or vomit or have diarrhoea, the result is the same. When they partake largely of nitrogenous aliment the proportion of urea rapidly increases. 2. In a cachectic or simply anæmic patient the urea falls, apparently in proportion to the state of the general nutrition and of the work done by the organic functions. 3. Absolute immobility of the patient seems to have an influence on the amount of urea excreted. 4. In sclerosis or cancer the quantity of urea falls rapidly on the occurrence of ascites or oedema, when a notable quantity of urea is found in the fluid. 5. The digitalis often used in the treatment also contributed to the loss of urea." If these conclusions are verified, the formation of urea must depend on some other function.]

[Footnote 8: Genevoix, _Essai sur les Variations de l'Urée et de l'Acide urique dans les Maladies du Foie_, Paris, 1876.]

The persons who suffer from lithæmia are usually those who indulge in the pleasures of the table and habitually consume much meat, pastry, and highly-seasoned and rich food of all kinds. The idle, luxurious, and indolent, literary men of sedentary habits, men who have led active lives, but on retiring from business have continued to indulge in a full diet, are apt to suffer from this malady. Women are less disposed to it, but if subjected to the same conditions may also be similarly affected. Especially do those suffer from lithæmia who indulge in malt liquors or in alcoholic drinks of any kind. These substances act by deranging digestion, and thus preventing the proper conversion of the albuminoids, by inducing congestion of the liver, and also by interfering with the process of oxidation.

SYMPTOMS.--The symptoms of lithæmia include derangements of the digestive organs and of the liver, of the circulation, and of the nervous system. As these subjects suffer from gastric and gastro-duodenal catarrh, they present the usual symptomatology of these affections, as a sense of weight and oppression at the epigastrium, acidity, pyrosis, a capricious--sometimes voracious, sometimes good--appetite, a coated {970} tongue, a bitter taste, etc. The bowels are irregular, sometimes constipated, occasionally relaxed, with scybalæ. The stools may be liquid, almost black or light-yellow and grayish. The motions are apt to be offensive, and a good deal of offensive gas is discharged with them. Hemorrhoids are often present, and there may be heat and irritation about the anus, and not unfrequently intolerable itching. After meals there is much depression, and often an insupportable drowsiness. Irregularity in the rhythm, even intermissions, of the pulse are not infrequent.

The nervous symptoms, as DaCosta has lately insisted on, are the most important and pronounced. The connection between oxaluria and mental despondency has long been known, but the nature of the relation remains undetermined. Headache, frontal and occipital, especially the former, dizziness, tinnitus aurium, suffusion of the eyes, ecchymoses of the conjunctiva, are usually present. Not unfrequently the subjects of this affection experience sudden attacks of vertigo, accompanied by dimness of vision and intense headache, and are supposed to have some organic lesion of the brain. They are irritable, despondent, and often intensely hypochondriacal, almost suicidal--are subject to neuralgic attacks, and have aching in the limbs, a sense of weariness, and more or less burning in the palms and soles.

The skin is rather dry and the complexion muddy. Urticaria is of frequent occurrence, and sudden attacks of nausea, vomiting, and intestinal pain coincide with the appearance of the eruption on the skin.

The urine is usually rather increased in amount, its color heightened, its acidity above normal, and floating in it, usually visible to the naked eye, are reddish masses composed of uric acid. More or less pain in the back, referable to the situation of the kidneys, and sometimes extending along the course of the ureters, is common. The bladder is rather irritable, and the passage of the urine produces heat and scalding. The testicles are apt to feel sore and are somewhat retracted. On standing, the urine may deposit uric acid and the urates copiously, or the acid may be seen to form a cloud which slowly subsides.

COURSE, DURATION, AND TERMINATION.--The course and duration of lithæmia are much influenced by the habits of life of the person affected. When unopposed by treatment and no change is made in the conditions producing it, a gradual increase in the various disturbances takes place. After a time structural changes occur in the liver; the organs of circulation early undergo atheromatous degeneration; various cerebral disorders due to degenerative changes arise; and acute intercurrent affections may terminate life. Amongst the secondary maladies due to lithæmia are gout, diabetes, renal calculi, and nephritic colic. If the cases are subjected to appropriate treatment, curative results may be certainly obtained. The prognosis, then, will be influenced materially by the moral strength of the patient. If he is one who can surrender his appetites and live abstemiously, a cure may be promised. The case is far different with those who will continue the use of malt, vinous, or alcoholic drinks, and will persist in indulging in the pleasures of the table.

DIAGNOSIS.--The differentiation of lithæmia from other affections offers no special difficulties. From gastro-duodenal catarrh it is separated by the {971} excess of uric acid in the urine only, the other symptoms being for the most part the same. The cerebral symptoms--the vertigo, headache, etc.--are to be distinguished from the same due to actual disease of the brain by the previous history, by the absence of changes seen on ophthalmoscopic examination and of other signs of brain disease, and by the subsequent behavior. Cases of cerebral mischief producing such effects would rapidly develop into serious states, whereas in lithæmia there are great fluctuations, but no apparent progress in many months. In lithæmia also there are no changes in the fundus oculi, whereas in brain diseases choked disk, hemorrhage into the retina, white atrophy, etc. are often discovered. Further, in lithæmia there are no disorders of sensibility, of motility, or of intellection, whilst these are ordinary evidences of cerebral mischief.

TREATMENT.--Attention to diet is of the first importance. As uric acid is an intermediate product in the metamorphosis of albumen, it might be supposed that to diminish the quantity of this constituent of the food would be sufficient. In some cases this suffices, but usually attention must be given to the peculiarities of digestion characteristic of each patient. More frequently trouble arises from indulgence in the starchy and saccharine constituents of the diet; in some a very considerable gastro-duodenal catarrh exists, and the mucus, acting as a ferment, sets up an acetic fermentation in the starchy and saccharine substances, with the necessary production of much carbonic acid gas. If the fats disagree, the butyric fermentation also takes place, and very irritating fat acids result. In these cases there is usually much gas formed in the stomach and intestine, and an immediate ratio appears to exist between the degree of mental despondency and the quantity of gas in the intestinal canal. It follows, then, that in cases of lithæmia the saccharine, starchy, and fatty constituents of an ordinary diet should be omitted from the food of such subjects. Bread should be partaken of very sparingly, and the foods containing starch, sugar, and oil ought not to be partaken of at all. The succulent vegetables, as lettuce, spinach, celery, cole-slaw, tomatoes, etc., ought to be substituted. Lean fresh meats, poultry, game (plainly cooked), fresh fish, oysters, eggs, etc. should constitute the basis of the diet. On the other hand, there may be those who do better on a diet of vegetables and fruit, excluding meat. In such we may suppose the fault lies in the stomach digestion, where the albuminoids are converted into peptones, the intestinal digestion being active and normal. All kinds of wine and malt liquors should be prohibited. Coffee and tea must also be relinquished. Without the carefully-regulated diet medicines can accomplish but little; hence he who would obtain curative results must give careful attention to every dietetic detail.

As deficient oxidation is an important factor in developing lithæmia, active exercise must be enjoined. The amount of exercise must be determined by the condition of the individual and the time, regulated as far as may be by the period after meals. As when the food prepared for assimilation is entering the circulation oxygen is needed to perfect the final changes, it seems clear that exercise should be taken three or four hours after the process of digestion has begun. Walking exercise is better than any other for this purpose, but it should not be carried to the point of exhaustion from fatigue. Sea-air and sea-bathing are oxidizing agents of considerable value, and are especially useful to the {972} subjects of lithæmia suffering at the same time from malarial infection.

Medicines are administered with the view to accomplish two purposes: to correct the disorders of digestion, to promote oxidation. One of the most useful remedies is nitric acid, five to ten minims of the official diluted acid being given before meals. It is more especially effective when there is an excessive production of acid. The fermentation which produces acid and the diffusion of acid-forming materials from the blood are alike prevented by it. The injunction to administer it before meals must be borne in mind when these purposes are to be subserved. Nitric acid, as well as the other mineral acids, but in a greater degree, promotes the flow of bile. This well-known clinical fact has been confirmed by experiments. Under the use of nitric acid, as above advised, uric acid and the urates disappear from the urine, being excreted as urea, and hence this remedy accomplishes both of the objects for which medicines are administered in this disorder. No other mineral acid can fill its place in this connection.

Alkalies possess very decidedly the power to promote oxidation. The soda salts are objectionable, for, combining with uric acid, they form the insoluble urate of soda. The salts of potash and lithium, on the other hand, form soluble combinations, and they also increase elimination. Much depends on the time at which they are administered, as Bence Jones,[9] and since Ralfe[10] especially, has shown. To increase the alkalinity of the blood and urine, they must be taken after meals, for then the acid materials of digestion are pouring into the blood. For the same reason, if alkalies are administered to neutralize the acidity of the intestinal canal, they must be given after meals. The most useful alkaline remedies are liquor potassæ, bicarbonate of potash, Rochelle salts, citrate of lithium, etc. The effervescing preparations of potash and of lithium are elegant and palatable forms in which to administer these remedies. They may also be taken dissolved in Vichy water, in our Saratoga Vichy, or in Carlsbad or Bethesda. When the use of mineral waters is not contraindicated in the state of the digestive organs, great good is accomplished by the persistent use of Vichy, foreign or domestic, of Carlsbad, and the alkaline waters of Wisconsin.

[Footnote 9: _Lectures on Pathology and Therapeutics_, by H. Bence Jones, London, pp. 90, 280.]

[Footnote 10: _Physiological Chemistry_, by Charles Henry Ralfe, London, 1883.]

The so-called cholagogues are unquestionably useful, but they become less and less necessary according to the success achieved in the dietetic course. Phosphate of soda is one of the most effective of this group of medicines. As it acts as a compound, and not as a salt of soda merely, it does not come within the prohibition against the use of soda salts. It promotes the flow of bile and appears to remove the catarrhal state of the mucous membrane. A teaspoonful three times a day is the quantity usually required. Under some circumstances it may be advantageously combined with arseniate of soda. Mercurials were formerly almost universally used, but they have been largely supplanted by podophyllin, euonymin, baptisin, etc., and by the phosphate of soda above mentioned. Podophyllin is indicated when constipation is a symptom. An efficient mode of giving it is in the form of granules, but it must be continued without intermission for some time or during the existence of {973} the lithæmia. The quantity given should be sufficient to maintain the evacuations in a soluble state. Good results are obtained from a combination of podophyllin with extracts of physostigma, nux vomica, and belladonna. When distinct torpor of the liver without constipation exists, euonymin, combined with physostigma, may be advantageously used. For the vertigo and hypochondriasis no remedy is more beneficial than arsenic (Fowler's solution) in small doses kept up for some time, and it is also distinctly curative of the catarrhal state of the mucous membrane. When malarial infection is the cause of lithæmia, quinine becomes indispensable.

Topical agents in some cases render important aid to the other curative measures. A daily sponge-bath, the water made more stimulating by the addition of sea-salt, is very useful in the absence of sea-bathing. Friction of the hepatic region with the official ointment of the red iodide of mercury unquestionably stimulates the hepatic functions. General faradization and faradic and galvanic excitation of the chylopoietic system promotes activity of the digestive apparatus and of the organic functions in general.

Hepatic Glycosuria (Temporary).

DEFINITION.--By the term hepatic glycosuria in this connection is meant a temporary glycosuria due to excessive formation of glycogen. The liver, unduly stimulated, produces more glycogen than can be disposed of, and hence it is excreted by the kidneys as grape-sugar.

PATHOGENY.--In the normal condition it is supposed that the glycogen produced by the liver is converted into grape-sugar, and soon oxidized and thus consumed. One theory of diabetes maintained that in some way the conversion of glycogen into grape-sugar was excessive and beyond the oxidizing power of the blood, and hence this substance was discharged in the urine. The recent discovery by Pavy[11] of glycogen in considerable amount in the blood of all parts of the body renders it certain that there are peculiar conditions necessary to the formation of grape-sugar in sufficient quantity to constitute diabetes. It is tolerably certain that an excess of acid in the intestinal canal, diminishing thus the alkalinity of the blood, will have as a symptom sugar in the urine. Persons disposed to the accumulation of fat, and eating freely of sugar and starchy food, are apt to have intestinal indigestion, and the acid produced by the fermentation of these substances will, after its absorption, hinder the conversion of any food-sugar. In such subjects also there may be an increased conversion of the glycogen of the blood into sugar under the same conditions. Such a glycosuria must necessarily be temporary and a purely functional disorder.

[Footnote 11: _The Lancet_, vol. ii., 1883.]

SYMPTOMS.--The subjects of the malady under consideration are of full habit, even obese. They habitually consume considerable quantities of malt liquors and a diet composed largely of the starchy and saccharine foods. If not in malt liquors, they at least indulge freely in bread, potatoes, pastry, cakes--in all forms of farinaceous food, fats, and sweets. They have a keen appetite, eat largely, and drink freely of fluids. As {974} a rule, these subjects are but little disposed to physical exercise and lead rather sedentary lives. Indulgence in such a mode of life tends to increase the accumulation of fat, weakens the muscles, and with them the heart-muscle, and slowly induces a gastro-intestinal catarrh accompanied by stomachal and intestinal indigestion. At first, heaviness, oppression, and drowsiness after meals are experienced; then acidity, pyrosis, and eructations follow; and ultimately the evidences of intestinal indigestion--flatulence, pain, irregular and unhealthy evacuations, etc.--come on. Meanwhile, the appetite is not usually impaired, and the disposition to drink fluids increases; the amount of urine voided is greater, and to rise during the night for the purpose of emptying the bladder comes to be a fixed habit. The urine under these circumstances is copious, high-colored, acid, and deposits on cooling abundantly of uric acid and urates. The amount passed in twenty-four hours will reach sixty, eighty, or more ounces, and the specific gravity will range from 1025 to 1035. On testing in the usual way, traces of sugar, more or less distinct, will appear,[12] but not constantly, and hence repeated examinations are necessary to determine the quantity. As a rule, the evidence of the presence of sugar in small amount is satisfactory.

[Footnote 12: In testing for sugar, when the urine contains the urates in such abundance there is danger of error. In using Trommer's, Fehling's, or Moore's test, on heating, the urates will effect a reduction of the copper or bismuth. It is necessary, therefore, to separate them before applying the test. This is accomplished as follows: The urine is evaporated to dryness on a water-bath; the sugar in the evaporated residue is dissolved out by absolute alcohol, and then an aqueous solution is prepared, to which the test is applied. An experienced operator will not need to take such precautions, for, familiar with the reactions, he can readily judge of the results.]

Various affections of the skin appear in the subjects of this malady, and urticaria, prurigo, eczema, and boils are the forms most usual.

COURSE, DURATION, AND TERMINATION.--Slow in developing, this temporary glycosuria is also slow in its course. It remains nearly stationary for months, even years. Meanwhile the degenerative changes associated with it slowly develop on all sides. The quantity of sugar does not greatly increase, for its amount, being apparently dependent on the quantity of acid entering the blood from the intestinal canal, must continue nearly at the same standard. It is comparatively rare for true diabetes to develop out of this state, although such a termination must be regarded as a natural outcome. One reason, it may be, why such a conclusion is not often reached is because of intercurrent maladies. It is an important fact that acute serous--less often parenchymatous--inflammations are very apt to occur during the existence of even temporary glycosuria. Under appropriate management this disorder is readily amenable to treatment. Hence the prognosis will be favorable or not according to the skill exhibited in its treatment.

DIAGNOSIS.--This malady offers no special difficulty in diagnosis. From gastro-duodenal catarrh and from lithæmia it is distinguished by the saccharine condition of the urine. From diabetes it is separated by the rate of progress, by the protracted duration of the case without any distinct advance, and by the temporary and fugitive character of the glycosuria.

TREATMENT.--To carefully regulate the diet is the first consideration. The traces of sugar and the excess of urates rapidly disappear when the {975} starches, sugar, and fats are withdrawn from the diet. Indeed, the rule as to alimentation must be as rigidly enforced as in true diabetes, but after the gastro-intestinal catarrh has subsided the ordinary mixed diet--that before the disturbance began--may be returned to gradually. Active exercise must be enjoined under the same conditions and for the same purpose as in the treatment of lithæmia. In these obese subjects, unaccustomed to movement, exercise must be cautiously undertaken; beginning with short excursions, it must be gradually increased. Horseback riding is an excellent expedient, but should not take the place of walking.

The merely medical measures have a twofold direction: to remove the gastro-duodenal catarrh; to promote oxidation of the sugar in the blood or prevent the conversion of glycogen into grape-sugar. Vichy water, the potash salts, and alkalies generally serve to accomplish the latter, and phosphate and arseniate of soda, tinctures of nux vomica, and of physostigma, bismuth, and carbolic acid, relieve the former. Small doses of Fowler's solution (two drops ter in die), and a minim three times a day of a mixture in equal parts of tincture of iodine and carbolic acid, are effective remedies in gastro-duodenal catarrh.

Jaundice (Icterus).

DEFINITION.--The term jaundice has its origin in the French word jaune, yellow. Icterus, which has come to be a more technical word, is of uncertain Greek origin, and is much employed by French writers as ictère. The common German name is Gelbsucht, a highly expressive designation. Jaundice signifies a yellow discoloration of the skin caused by the presence of bile. It is a symptom rather than a disease. As a symptom it will receive much consideration in the pages to follow, but there is also a functional disorder--a jaundice due to a disturbance in the biliary functions, without evidences of structural change--which must be discussed here. This preliminary statement of our present knowledge of jaundice will facilitate the comprehension of it as a symptom, and will render unnecessary explanations that will be merely a repetition of previous ones.

CAUSES.--The theories of the causation of jaundice may be reduced to three: 1, that it is due to a disorganization of the blood in which the coloring matter is set free, and hence is known as hæmatogenous; 2, that the materials of the bile, which it is the office of the liver to remove from the blood, are not so disposed of; 3, that the bile, after being formed by the liver, is absorbed into the blood because of an obstacle to its escape, and hence this is called hepatogenous jaundice.

The modern view of hæmatogenous jaundice had its origin in the supposed discovery of the identity of hæmatoidin with bilirubin. If the pigment of the blood has the same composition as the pigment of the bile, hæmatogenous jaundice will be produced whenever hæmatoidin is set free in the blood. Virchow[13] was the first investigator to show the close resemblance between these two pigments. Since his observation was made an identity of hæmatoidin and bilirubin has been maintained by Zenker, Valentiner, Kühne, and others, and as strenuously denied by {976} Städeler, Preyer, Young, and others. At the present time it appears to be established that although the blood- and bile-pigments are closely related, they are not identical.[14] Nevertheless, a hæmatogenous jaundice is still admitted to exist by Leyden,[15] Immermann,[16] Gubler,[17] Ponfick,[18] and some others. The existence or non-existence of this form of jaundice is, however, of little importance in this connection, since, if it ever occur, the malady of which it is a symptom is not an affection of the liver, but of the blood, as phosphorus-poisoning, pyæmia, etc.

[Footnote 13: _Archiv für path. Anat., etc._, Band i. p. 370, 1847.]

[Footnote 14: Legg, J. Wickham, _On the Bile, Jaundice, and Bilious Diseases_, p. 243.]

[Footnote 15: _Beiträge zur Pathologie des Icterus_, Berlin, 1866, p. 6.]

[Footnote 16: _Deutsch. Archiv für klin. Med._, Band xii. p. 502.]

[Footnote 17: _Union médicale_, 1857, p. 503.]

[Footnote 18: _Ziemssen's Cyclopædia_, vol. ix. p. 24.]

The second theory, that the bile is preformed in the blood and separated by the liver, and that jaundice results because of the failure of the liver to perform this office, is no longer entertained, although largely held down to within a very recent period. As the bile acids and bile-pigments are not to be found in the blood, chemistry lends no support to the theory of jaundice by suppression of the hepatic function. As they do not exist in the blood and are found in the secretion of the liver, there can be no other view held than that they are formed by this organ.[19]

[Footnote 19: The old doctrine of jaundice by suppression, which has always been maintained by Harley (_On Jaundice_, London, 1863, p. 20 _et seq._), has been again restated and strongly advocated by him in his treatise on _The Diseases of the Liver_, p. 83, which was issued in 1883. In the two following postulates he formulates his view:

"1. The biliary secretion can be actually retarded, and even totally arrested, without alteration of hepatic tissue.

"2. When the liver strikes work and secretes no bile, the animal body becomes jaundiced as a direct consequence thereof."

This view, he affirms, "can be made comparatively easy of absolute proof."

The evidence on which he chiefly relies is exceedingly fallacious. It rests on two facts: the existence of a case of jaundice in which the ducts and gall-bladder contain no bile, but only ordinary mucus; the appearances presented by a liver in a case of jaundice due to obstruction of the common duct. The evidence afforded by the former is entirely fallacious, because in an old case of jaundice with catarrh of the bile-ducts such changes take place in the bile that it loses all of its distinctive characteristics. This may be seen in an ancient example of obstruction of the cystic duct, where the bile which the gall-bladder contained is ultimately transformed into a whitish or colorless mucus. The changes which occur in the so-called cysts of the arachnoid are comparable, and exhibit the entire transformation of blood-pigment, which is closely allied to bile-pigment.]

The third theory of jaundice--that which refers the disease to an absorption of the bile into the blood after it has been formed by the liver--is the one now most generally held, and, indeed, as one of the causes is universally held. The bile is absorbed into the blood because an obstacle to its passage by the bile-ducts exists at some point in their course. This is the principal, but not the only, cause of absorption. When the pressure in the vessels falls below that in the ducts, bile will pass toward and into the vessels. Again, it sometimes happens that a considerable part of the bile discharged into the intestines is reabsorbed unchanged, and enters the portal vein and the general circulation, thus causing jaundice.

The disturbances of the liver causing jaundice are various. It sometimes occurs without cause, and the first intimation of it is the peculiar tint of the skin. It is certainly true that powerful emotions are causative; thus, a violent anger has brought on an attack. In such a case we must suppose a depression of the vaso-motor system, and such a lowering of the blood-pressure as to favor the passage of bile into the {977} veins rather than into the bile-ducts. Thus, it has been abundantly shown that a slight difference in pressure will divert the bile in either direction. Heidenhain[20] has demonstrated that the bile passes in the direction of least resistance, and in the case of the considerable vaso-motor depression caused by extreme emotion the least resistance is in the direction of the vessels. More frequently than moral emotion is catarrh of the bile-ducts. It is not necessary for the catarrhal swelling of the mucous membrane to close the ducts to have the bile pass into the veins; such a degree of swelling as to make the passage of the bile somewhat difficult suffices. A simple hyperæmia of the mucous membrane may cause sufficient obstruction of the bile-ducts to give rise to jaundice. Gastro-intestinal catarrh plays an important part in the production of simple jaundice. Frerichs[21] ascertained that of 41 cases, gastro-duodenal catarrh existed in 34. Ponfick[22] considers catarrh of the ducts the principal factor. In fact, at the present time there is but one dissenting voice on this point.[23]

[Footnote 20: Quoted by Legg, _supra_, p. 253.]

[Footnote 21: _Diseases of the Liver_, Syd. Soc. ed., by Murchison.]

[Footnote 22: _Ziemssen's Cyclopædia_, vol. ix., _supra_.]

[Footnote 23: Harley, _Diseases of the Liver_, 1883, p. 440 _et seq._]

Gastro-duodenal catarrh extends by contiguity of tissue to the mucous lining of the bile-ducts. The catarrhal state of the mucous membrane is produced by errors of diet, acid indigestion, indulgence in condiments, wines, and rich foods in general. Climatic changes, malarial infection, exposure to cold and dampness, etc. are indirectly causative of jaundice through the intermediation of gastro-duodenal catarrh.

Formerly, obstruction of the gall-ducts was supposed to be caused sometimes by a spasmodic contraction of the organic muscular fibre assumed to exist in the walls of the ducts. Although the presence of these muscular elements has been denied, Heidenhain has lately, apparently, demonstrated them. Audigé has made observations confirmatory of those of Heidenhain, and Dujardin-Beaumetz[24] has verified the statements of Audigé. It seems, therefore, in a high degree probable that organic muscular elements exist in the walls of the hepatic ducts, and that spasmodic icterus may therefore occur.

[Footnote 24: _Bull. gén. de Thérapeutique_, vol. lxxxv. p. 385, 1873.]

SYMPTOMS.--Simple icterus may exist without any other obvious symptoms than the yellow discoloration of the skin. In most cases, however, the yellowness is preceded for a week or more by the symptoms of a gastro-intestinal catarrh, or these symptoms accompany the jaundice. There is much mental depression and a general malaise is experienced. Headache, mental hebetude, a total loss of appetite, a furred tongue, and a bitter taste, nausea and sometimes vomiting, constipation or diarrhoea, precede or accompany the jaundice. When these symptoms precede for some time the appearance of yellowness, it is probable that the biliary derangement is secondary to the gastro-duodenal catarrh, but when they occur with the jaundice it is probable that they are due to the absence of bile from the intestine.

The yellowness first appears in the conjunctiva for a day or two before the skin is tinted, and within forty-eight hours after the flow of bile into the intestine has ceased. The face next becomes yellow, then the body, {978} and afterward the limbs, but in some cases the limbs remain free from discoloration. The lips do not exhibit any change of color, but the roof of the mouth, the palate, and the mucous membrane under the tongue are yellow. The saliva does not, as a rule, contain bile-pigment or exhibit any changes of color unless mercurial salivation is caused, when it becomes greenish in color and has a bitter taste.[25] A yellow tint of the sweat, especially under the arm-pits, is common. The milk very often contains bile-pigment or is changed in color in some way.

[Footnote 25: Legg, _On the Bile, etc._, _supra_.]

The feces are colorless or have a grayish or clay-colored tint, and are semi-solid, although sometimes hard and dry. In simple jaundice diarrhoea is very often present. There may be considerable flatulence, and more or less pain in consequence about the umbilicus, and the gas when discharged is very offensive. The stools also, in some cases, have an odor of decomposition, and if carefully examined particles of food, undigested and decomposing, will be found. The feces may have a parti-colored appearance--part whitish or grayish or clay-colored, and part of a normal color. This condition is not difficult of explanation. The obstruction to the flow of bile may be in a part, and indeed in a small part comparatively, of the liver, and hence there may be sufficient bile flow down to color the feces to a greater or less extent. But a small amount of bile-pigment in the blood suffices to tint the whole surface of the body.

The urine may exhibit changes in appearance before the conjunctiva becomes yellow. It is colored in all possible degrees, from a merely high normal hue to a deep brownish almost black tint. It may be deep red and clear like dark brandy or brown like porter, and thick with urates. Usually, the urine of jaundice deposits abundantly of urates, but this fact is more especially true of those patients retaining appetite or having a voracious appetite and indulging in a full diet without restraint. The reaction of the urine is acid, and the specific gravity does not often descend below 1010, and may be 1030. The amount passed in twenty-four hours varies, but does not differ materially from the normal. Toward the termination of some fatal cases the quantity of urine has greatly diminished, and in a few instances was suppressed, but in such examples other factors than hepatic disease were concerned. More or less albumen is nearly constantly present in the urine of jaundice, but the detection of a trace is very difficult when the urine, as is so often the case, is cloudy. The urine should be carefully filtered before applying the test, and a specimen for comparison should be placed alongside of that being examined. If on boiling no haze appears, it may be developed by dropping in some nitric acid. The nitric-acid test, so often employed by allowing some drops of urine to trickle down the test-tube and observing the reaction at the point of contact, is, in the writer's experience, very fallacious. The source of the albumen in jaundiced urine is obviously the blood-globules. As Von Dusch first demonstrated, and Kühne[26] afterward clearly confirmed, the bile acids dissolve the red corpuscles. As the quantity of albumen in the urine is small, it is reasonable to conclude, as suggested by Legg, that the bile acids are not present in the blood in any considerable amount.

[Footnote 26: _Archiv für path. Anat._, Band xiv. p. 333.]

When any large quantity of bile is contained in the urine, its detection is not difficult. A strip of muslin dipped in the urine will be stained, and the underclothing of the patient will have the yellowish spots {979} caused by bile. Gmelin's test is the most convenient. This is applied as follows: Some nitric acid containing nitrous--which is the case of the ordinary commercial article--is put into a test-tube, and some of the suspected urine is allowed to trickle down the side of the tube to come in contact, but not mix, with the acid. At the point of contact, when the urine contains bile-pigment, first a zone of green, then blue, violet, and finally red color, develops. As this play of colors takes place on the instant, the attention must be sharply fixed to see the changes. Rosenbach[27] suggests this test be applied by filtering some urine containing bile through filtering-paper and touching the paper with a drop of nitric acid. The result is, a green circle forms at the point of contact. The usual mode of applying Gmelin's test is to place on the bottom of a common white plate or on a porcelain dish a thin film of the urine, and carefully bring in contact with it a thin film of nitric acid. The color reaction mentioned above takes place at the margin of contact.

[Footnote 27: _Centralblatt für die medicin Wissenschaft_, 1876, p. 5.]

Besides the presence of bile and albumen, and some fatty epithelium from the tubules, there is no material change in the composition of the urine. At one time it was supposed that the amount of urea was greatly lessened, but later and more accurate investigations have shown that this excretion is in greater or less quantity according to the food taken, and bears no relation to the jaundice. On the other hand, Genevoix[28] maintains that the quantity of urea is increased in spasmodic icterus, and in the same ratio the uric acid declines. As regards the chlorides and other salts, there seems to be a tolerably constant ratio in their variations with the changes of quantity of urea and uric acid--are therefore nearly related to the amount of food taken.

[Footnote 28: _Essai sur les Variations de l'Urée et de l'Acide urique dans les Maladies du Foie_, Paris, 1876, p. 59 _et seq._]

As regards the condition of the liver, there is no apparent change. In topography, in the area of hepatic dulness, and in the dimensions of the right hypochondrium the local condition does not deviate from the normal in simple jaundice. There may be more or less tenderness over the epigastrium and along the inferior margin of the liver, but there is rarely any actual pain.

The circulation of bile in the blood and the action of the bile acids on the red corpuscles must have an influence on the functions of various organs. In some cases of jaundice, but by no means in all, the pulse is slow, in a few instances descending as low as 40 per minute, and, according to Frerichs,[29] as low as 21 per minute. Usually, the pulse-rate is not lower than 60. To observe the slowing of the heart the patient must be recumbent, for the pulse rises to the normal or above on assuming the erect posture and moving about. The occurrence of fever also prevents the depression of the circulation. The slowing of the heart is found to be due to the action of the bile acids on the cardiac ganglia. The other elements of the bile were ascertained to have no influence on the circulation. As the heart may be slowed by an increase of inhibition through stimulation of the vagi or by a paralyzing action on the cardiac muscle, it was necessary to eliminate these effects to establish the influence of the bile acids on the ganglia. By exclusion, and by ascertaining the effects {980} of the bile acids on a properly prepared Stannius heart, Steiner and Legg have succeeded in demonstrating this important point.[30]

[Footnote 29: _Diseases of the Liver_, Syd. Soc. ed., _supra_.]

[Footnote 30: _Archiv f. Anat. u. Physiol._, 1874, p. 474; Legg, _On the Bile, etc._, _loc. cit._]

The temperature of jaundice is normal usually, sometimes below. When a febrile affection occurs during the course of jaundice, the rise of temperature belonging to it is prevented in considerable part, sometimes entirely. The depression of temperature is referred by Legg to the lessened activity of the hepatic functions; but it seems to the writer more satisfactory to refer it to the action of the bile acids on the red corpuscles, the conveyors of oxygen. Röhrig[31] has shown experimentally that the injection of bile acids has this effect on the temperature of animals.

[Footnote 31: _Archiv der Heilkunde_, 1863, p. 418.]

The nutrition of the body early suffers in jaundice; more or less loss of flesh soon occurs, and debility and languor are experienced. There are several factors concerned in this result. The diversion of the bile from the intestine interferes in the digestion of certain materials; when jaundice occurs, glycogen ceases to be formed--and this substance has an important office in nutrition and force-evolution--and the injury done to the red blood-globules interferes with oxidation processes.

The functions of the nervous system are variously disturbed in jaundice. Headache, frontal, occipital, or general, is present in most cases to a greater or less extent. Hebetude of mind and despondency are nearly if not quite invariable, although it is not unusual to see men with jaundice engaged in their ordinary avocations. Drowsiness is a common symptom. More or less wakefulness at night, or sleep with disturbing dreams, not unfrequently coincide with drowsiness during the waking moments. In severe cases of icterus dependent on structural changes the cholæmia may produce stupor, delirium, convulsions, etc., but such formidable symptoms do not belong to the simple and merely functional jaundice.

Vision is sometimes colored yellow, or, rather, white objects appear yellow, but this must be a rare symptom, since Frerichs never met with an example. Murchison[32] narrates a case, and the writer has seen one. It is a fugitive symptom, rarely continuing longer than two or three days. The term xanthopsy has been applied to it.

[Footnote 32: _Clinical Lectures on Diseases of the Liver_, New York, 1877, p. 321.]

A nervous symptom of common occurrence is pruritus of the skin. This may be so severe as to prevent sleep, and in any case is a disagreeable and persistent affection, always worse at night. It may appear before the jaundice so long a period as ten days, as in a case mentioned by Graves,[33] and two months in a case narrated by Flint.[34] It is most severe at the beginning of the jaundice, and usually disappears before the jaundice ceases, but it may continue to the end. It is not limited to any particular part of the body. Pruritus is sometimes accompanied by urticaria, and the irritation caused by the friction of the skin may set up an eczema. Occasionally boils, and more rarely carbuncles, appear during the course of jaundice. Another curious affection of the skin which occurs during chronic jaundice is xanthelasma or vitiligoidea. First mentioned by Rayer, this disease was afterward well described by Addison and Gull[35] under the name vitiligoidea, and they recognized two varieties, v. plana and v. tuberosa. The plane variety is found on the {981} mucous membrane of the mouth, the eyelids, the palms of the hands, and the flexures of the joints, and consists of a yellowish-white soft eruption slightly raised above the surrounding skin and varying in size from a pin's point to a dime in size. The color is described as like that of a dead leaf or chamois-skin. The tuberose variety consists of small tubercles from a millet-seed to a pea in size. They have a yellowish color, are tense and shining, and are placed on the ears, neck, knuckles, elbows, knees, and other parts. Whilst the plane variety gives little if any uneasiness, the tuberose is apt to become irritated and painful. From the pathological point of view this eruption consists of proliferating connective-tissue corpuscles, some of which have undergone fatty degeneration.[36] The morbid process tends to occur symmetrically, as on the eyelids, to which it may be confined, but it usually develops in patches, and may indeed extend over the whole body, when it is called xanthelasma multiplex.

[Footnote 33: _Clinical Lectures on the Practice of Medicine_, 2d ed., by Neligan, p. 637.]

[Footnote 34: _Philada. Med. Times_, 1878, p. 507.]

[Footnote 35: _Guy's Hospital Reports_, 1851, p. 265.]

[Footnote 36: Waldeyer, _Archiv für path. Anatomie, etc._, vol. lii. p. 318.]

The disorganization of the blood caused by jaundice sets up a hemorrhagic diathesis. This result, however, is not usual in simple jaundice, but belongs rather to acute yellow atrophy, sclerosis, and other chronic affections of the liver. It will therefore be more appropriately considered in connection with those maladies.

COURSE, DURATION, AND TERMINATION.--When jaundice is a symptom merely, it pursues a course determined by the peculiarities of the disease. The duration of simple jaundice varies from one to four weeks, the average being about three weeks. If it continues longer than two months, suspicions may well be entertained that the case is of a more formidable character than simple jaundice. The termination of this form of the disease is always in health. A favorable prognosis can be given only in the case of an accurate diagnosis. Those cases may terminate more speedily which, being of malarial origin, are treated by efficient doses of quinine. If delirium and coma come on, the apparently mild case means, probably, acute yellow atrophy, which cannot at the onset be distinguished from simple jaundice. If any nervous symptoms occur or if hemorrhage appears, the case will prove to be serious. A rise of temperature usually indicates mischief. When the stools begin to exhibit the normal appearance from the presence of bile, a satisfactory termination of the case may be soon expected. The yellowness of the skin disappears slowly after the natural route of the bile has been restored, and the urine is the last to lose the pigment, as it was the first to exhibit its presence.

DIAGNOSIS.--The diagnosis of jaundice as a symptom is usually easy. It should be remembered that jaundice cannot be detected at night by any ordinary light, and when it is disappearing the tint varies, now being distinct, again absent. Mental emotion when the color is fading develops it. Browning by the sun's rays causes an appearance which might be mistaken by a superficial observer for jaundice, but it is only necessary to look at the parts protected and at the urine to discover the true state of the case. The detection of bile in the urine and the ocular evidence of its absence from the stools will be conclusive. In some cases of jaundice the stools are golden yellow, and in many instances they are offensive.

{982} It is important to mark out the limits of the gall-bladder, if it is of sufficient size to do so, for any accumulation of bile in this sac signifies an obstruction of the ductus communis choledochus. If the jaundice has come on after the symptoms of gastro-duodenal catarrh, is recent, continues but two or three weeks, and then subsides without any nervous symptoms or hemorrhage, it is a case of simple jaundice, probably due to catarrh or spasm of the bile-ducts. If the jaundice be preceded by attacks of severe pain, nausea, and vomiting, and disappears after a week or two, the case is one of hepatic calculi. If the jaundice persists months after such an attack of acute pain, and does not disappear after a year or more, it is probably due to an impacted calculus. The other diagnostic relations of jaundice are more properly considered in connection with the malady of which jaundice is a symptom.

TREATMENT.--For jaundice the symptom the treatment is included in that of the disease. Here the treatment of simple jaundice, the functional disorder, is to be discussed. If there is much nausea, the tongue is heavily coated, and, especially if the seizure has followed dietetic excesses, an emetic of ipecac may be highly serviceable. Recent experiments have proved the accuracy of the clinical observations which recognized the cholagogue property of ipecac, and hence the emetic effect of this remedy is aided by its power to promote the discharge of bile. Emetics are of course contraindicated when jaundice is due to an impacted calculus, to malignant disease, to echinococci or other kinds of tumor. If there is much irritability of the gastro-intestinal mucous membrane, as shown in vomiting and diarrhoea, small doses of calomel (1/12 to 1/4 grain) three or four times a day are highly useful. If calomel possessed the property ascribed to it of stimulating the liver, it would be injurious; it is beneficial here because it has a sedative effect at first, followed, when a sufficient amount has accumulated, by an eliminant action. Such hepatic stimulants as euonymin, sanguinarin, podophyllin, jalap, colocynth, rhubarb, etc. have long been used in cases of jaundice with the view that the liver is torpid and needs stimulating. It may be inquired, however, If the bile already formed has no outlet by the proper route, what utility can there be in making the organ produce more? The true reason for the administration of such remedies in any case of obstructive jaundice is to cause such downward pressure as to force out of the duct an obstructing plug of mucus. The writer has known this result to be accomplished by a dose of compound jalap powder when a great variety of remedies had been employed in vain. One of the most efficient remedies--in the writer's considerable experience the most efficient--is phosphate of sodium, of which a drachm or more is administered three times a day. This remedy liquefies mucous plugs and promotes the flow of bile without harshly and rudely forcing the biliary secretion, and it also has a marked curative effect in gastro-duodenal catarrh. It may be given advantageously with arseniate of soda--the latter in dose of 1/20 grain--and dissolved in a tumblerful of Vichy water or Saratoga Vichy water, or preferably in a wineglassful of hot water. Free use of alkaline and laxative mineral waters is desirable, for a double purpose--to act on the liver and on intestinal digestion, and to promote the excretion of biliary matters by the kidneys. In this country we have a number to select from--the Saratoga, Bethesda, Michigan, and others. Certain sulphurous waters, {983} as the Blue Lick of Kentucky, are highly useful in the more chronic cases. Sulphur baths may be conjoined to the internal administration of the waters.

Nitric and nitro-muriatic acids have long been celebrated for their good effects in jaundice. It is the presence of the acid chyme in the duodenum which excites the normal flow of bile, and Bernard found that applying acid to the orifice of the common duct in the intestine has the same effect. There is then a rational reason for the administration of this remedy. A nitro-muriatic bath, both local and general, was formerly more used than now. Its utility is questionable, and the difficulties in the way of applying it great.

Recently, Gerhardt[37] has proposed to faradize the gall-bladder, and by compression with the fingers to empty it, forcing the bile into the intestine, and thus clearing out obstructions. This seems to be very questionable if not dangerous practice, but repeated successes will justify it.

[Footnote 37: _Sammlung klinische Vorträge_, Volkmann, p. 112.]

Regulation of the diet is of the first importance. Fats, starches, and sweets cannot be well digested when no bile enters the small intestine, where they undergo conversion. These substances fermenting, much acid results, and hence if a catarrh exist it is increased. An exclusive diet of skimmed milk, kept up for two weeks or as long as possible, is the best mode of alimentation for this part of the treatment. Afterward, the diet should be composed of milk, meat-broth, lemonade, and subsequently of the succulent vegetables, acid fruits, and fresh meat. Indulgence in malt liquors, wines, and spirits should be strictly prohibited.

A new method of treating jaundice has been lately proposed by Krull,[38] which has the merit that no injury is done by it if no good is accomplished. It consists in injecting into the rectum from two to four pints of water at 60° F., which is retained as long as possible. Each time the injection is repeated the temperature is raised a little. Krull reports that he has uniformly succeeded, and has never found it necessary to repeat the injection more than seven times. It may be given twice or thrice a day.

[Footnote 38: _Berliner klinische Wochenschrift_, 1877, p. 159.]

II. STRUCTURAL DISEASES OF THE LIVER.

Hyperæmia of the Liver.

DEFINITION.--An abnormal quantity of blood in the liver, constantly present, constitutes hyperæmia or congestion. During the period of repose there is less, but during the period of activity more, blood circulating in the liver, but the physiological hyperæmia is not, nor does it contribute to, a diseased state unless abnormal conditions continue it beyond the proper limits. The term hyperæmia, here used, applies to a pathological state in which various structural alterations grow out of the continual congestion of the blood-vessels of the organ.

CAUSES.--A physiological congestion of the liver ensues when the {984} process of digestion is going on. The afferent vessels dilate, and not only more blood, but various materials taken up from the foods and products of digestion, many of them having directly stimulating effects, also pass to the organ. Frequent and large indulgence in food, especially if rich in quality and highly seasoned with spices, mustard, etc., the consumption of malt liquors, wines, and alcoholic fluids in general, the habitual use of strong coffee and tea, gradually induce a state of hyperæmia. If to the consumption of a large quantity of highly-stimulating food there is added the mischief of insufficient waste, the danger of congestion of the liver is the greater. Persons addicted to the pleasures of the table are apt to pursue sedentary lives, and hence, besides the inappropriation of the material digested, the process of oxidation is insufficient to burn off the surplus. A sedentary life further tends to make the circulation in the hepatic veins sluggish by lessening the number and depth of the respirations, and with the obesity developed under these conditions the propelling power of the heart is diminished by fatty degeneration or fatty substitution of the cardiac muscle. Disease of the semilunar ganglion, the solar plexus, and of the splanchnics under circumstances and of a nature not now well understood may cause dilatation of the hepatic vessels.

Suppression of a long-existing hemorrhage from piles and from the uterine system has caused hyperæmia of the liver. Evidences of hepatic congestion are comparatively common about the menstrual period in consequence of the tardy appearance of the flow, of its insufficiency, or of its sudden suppression. There is a form of jaundice known as icterus menstrualis, and attacks of hepatic congestion are not uncommon at the climacteric period.

The most important causes of hyperæmia of the liver are mechanical, and consist in obstruction to the circulation in the ascending vena cava from disease of the heart or lungs. Dilatation of the right cavities, incompetence of the tricuspid, and stenosis of the mitral orifice are the usual cardiac changes leading to congestion of the liver. The same effect, to a much less extent, however, is produced by any cause which weakens the propelling power of the heart, as myocarditis, pericarditis, etc. Amongst the pulmonary lesions obstructing the venous circulation are emphysema, interstitial and croupous pneumonia, effusions into the pleura, intrathoracic aneurisms or tumors, etc. It should not be forgotten that effusions into the left pleura, as was demonstrated by Bartels[39] and confirmed by Roser,[40] so push over the mediastinum toward the right and bend the vena cava in the same direction, just as it emerges from the opening in the diaphragm, that the circulation in this vessel is impeded, and consequently congestion of the liver induced.

[Footnote 39: _Deutsches Archiv für klin. Medicin_, Band iv. p. 265.]

[Footnote 40: _Archiv der Heilkunde_, Band vi. p. 40.]

The influence of climate, especially of long-continued high temperature, has been warmly disputed. On the whole, it seems probable that in warm climates congestion of the liver is much more common. Malarial infection is an unquestionable cause. In the section on Jaundice it was stated that this symptom may occur without the phenomena of fever, and, indeed, without any other disturbance of the system. In a large proportion of cases of intermittent fever, probably in all, more or less congestion of the liver occurs.

{985} PATHOLOGICAL ANATOMY.--Congestion may take place in the portal system, and be due to conditions of the gastro-intestinal mucous membrane, or in the hepatic vein and radicles, due to obstructive troubles in the heart or lungs. The appearances vary accordingly. Restricting the observations to the hyperæmia, and not including subsequent lesions, it suffices to say that the liver is somewhat enlarged, rather darker in color than the normal, and uniformly so; the radicles and branches of the portal vein in the liver, the trunk of the vein itself, and the veins of the spleen, stomach, intestines, mesentery, etc. are distended with black blood, and the tissue of the liver rather wet, inclined to soften, and here and there marked by minute hemorrhages from rupture of small vessels. The extravasations of blood accompany the hepatic congestion of hot climates, and probably are the preludes to suppurative inflammation. The portal system the more readily suffers from a passive congestion because of the provision for the alternate expansion and contraction of the tunics of the vessel, scantily supplied with contractile elements. An acute congestion of the liver produced by sudden dilatation of the capillaries of the hepatic artery has not been described, but it would appear to be possible.

The most important form of hepatic congestion is the mechanical, arising from obstruction of the circulation in the heart or lungs. In consequence of this obstruction the blood accumulates on the venous side, and there is in consequence an ischæmia of the arterial side. The hepatic vein becomes distended, and its terminal radicle in the centre of each acinus--the central vein--enlarges with the increased pressure. It follows that the minute capillaries emptying into the central vein are also distended with blood, and finally the portal vein and its radicles throughout are similarly affected. The same condition of the hepatic circulation was long ago observed by Virchow[41] as a result of weakness of the muscular tissue of the heart, and consequently diminished propelling power of the organ. On section of the liver much black blood flows out; each central vein is a distinct dark object in the centre of each acinus, and contrasts strongly with the surrounding paler substance, whence the common term for this appearance is nutmeg liver. The long-continued distension of the central vein leads to sclerosis of its walls,[42] and the neighboring hepatic cells undergo atrophy in consequence of the greater pressure. A relatively increased quantity of connective tissue seems to result, but whether hyperplasia occurs is disputed. By Talamon[43] such increase of the connective tissue is denied, but Thierfelder[44] admits that there is an apparent and also in some cases a real increase. The atrophy of the cells induces more or less shrinking and consolidation of the liver; it is therefore smaller in size and firmer in texture, and presents a brownish-red color. The atrophic change in the hepatic cells is represented finally by some brownish or black pigment, but it is rare, indeed, for all the cells of an acinus to disappear. To this change has been applied the term cyanotic atrophy. In some instances Liebermeister[45] {986} has found an increase of the connective tissue of the liver; and this opinion is confirmed by Legg.[46] When this multiplication of the connective tissue occurs, the condition of the liver is entitled cyanotic induration. The sclerosis originating in this way is distinguished from true cirrhosis by its less extent, irregularity, situation, and the marked degree of hepatic congestion.

[Footnote 41: _Archiv für path. Anat., etc._, Band v. p. 289.]

[Footnote 42: Talamon, _Recherches anatomo-pathologiques et cliniques sur le Foie cardiaque_, Paris, 1881 (pamphlet).]

[Footnote 43: _Ibid._]

[Footnote 44: _Atlas_.]

[Footnote 45: _Beiträge zur path. Anat. u. Klinik der Leberkrankheiten_, Tubingen, 1864, p. 209 _et seq._]

[Footnote 46: _Medico-Chirurgical Transactions_, vol. lviii. p. 345.]

SYMPTOMS.--Hyperæmia of the liver is usually one of the complex conditions of a morbid state, and hence is associated in its symptomatology with the connected maladies. On the one hand associated with gastro-intestinal disorders, on the other with cardiac and pulmonary diseases, the symptoms must be varied accordingly. It is necessary, however, to indicate as clearly as may be those belonging to the hepatic circulation.

Congestion of the portal circulation is a condition to which frequent references are made, but which is rarely clearly defined. As seen in the West and South, it signifies a gastro-intestinal catarrh more or less acute, with an obvious condition of biliousness, as manifested in a faint jaundiced tint of the skin and of the conjunctivæ, uneasiness in the right hypochondrium, with enlargement of the area of hepatic dulness, the evacuations from the bowels being either grayish or clay-colored, or more frequently bilious, acrid, and offensive.

The gastro-intestinal disorder which initiates the hepatic disturbance should not be confounded with that which succeeds to congestion of the hepatic veins. The latter invariably comes on after the obstruction at the heart or lungs has continued for some time. There occurs in this state very extensive hyperæmia of the gastro-intestinal mucous membrane, and consequent disorders of stomachal and intestinal digestion. The former is a reflex cause of disturbance, probably through the intermediation of the solar plexus. The gastro-intestinal irritation, by depressing the functions of the hepatic through the solar plexus, induces a paresis of the muscular layer of the portal system, and thus congestion ensues. Such a result is aided by high temperature, but especially by the constitutional tendencies of some subjects to hepatic disturbances. In such examples of hyperæmia the symptoms consist of those belonging to gastro-intestinal catarrh, succeeded by those referable to the liver, consisting in uneasiness, heaviness, and fulness of the right hypochondrium, increase in the area of hepatic dulness, soreness on pressure along the inferior margin of the ribs and over the epigastric region, yellowness of the conjunctivæ, a fawn color of the skin generally, and high-colored rather scanty urine, depositing abundantly uric acid and urates. A liver considerably enlarged and projecting one or two fingers' breadths below the ribs may be quickly relieved and return to the normal size on the occurrence of hemorrhage from piles or after free watery evacuations produced by a hydragogue cathartic.

The form of hepatic congestion most usually observed is that of the hepatic vein, caused by obstructive troubles of the heart or lungs, and known as the nutmeg liver. The increase of size of the liver under these circumstances may be very considerable. To determine an increase in the area of hepatic dulness the position of the organ must be ascertained with reference to the position of the body, whether recumbent or erect. In the former position the liver gravitates toward the thorax; in the {987} latter, downward into the abdomen. If palpation only were employed to detect an increase in the size of the organ, an error might readily be committed in this respect. Some congestion may doubtless exist without an actual increase of size recognizable by our means of investigation; there may be merely some distension manifested by a sense of increased resistance; the liver may project a hand's breadth below the ribs; and between these extremes there may be all possible degrees of enlargement. When the liver, in consequence of hyperæmia, projects below the ribs, it offers to the sense of touch the impression of a smooth, elastic, rather rounded surface, and not the hardness and nodular character of sclerosis, and not the sharpness of border and hardness of texture belonging to amyloid disease. The enlargement of the liver due to hyperæmia is further distinguished by the fact that it varies much in size at different times, and may be much reduced by hemorrhage from the portal system, and increased suddenly by an attack of dyspnoea.

When the liver is enlarged by hyperæmia the patient usually has a distinct appreciation of the fact, feels a sense of weight, tenderness, and oppression in the right hypochondrium, and experiences a painful dragging from the right toward the left when turned on the left side. In some cases pain is felt in the shoulder, or, if not pain, a feeling of weight. A slight icteroid hue of the conjunctiva, face, upper extremities, and trunk is often present, but the stools are not wanting in bile and the urine contains but little pigment--facts indicating that the obstruction is limited to a small number of ducts. If the jaundice is decided, the stools clay-colored, and the urine loaded with pigment, a catarrhal swelling of the common or hepatic duct exists.

As nutmeg liver is an incident in the course of the venous stasis from cardiac or pulmonary obstructive disease, it is not unusual to find ascites and general dropsy occur. When ascites precedes the other manifestations of dropsy, and is relatively more important, the hepatic congestion has led to atrophy of the cells and contraction of the organ, or to cyanotic induration, as it has been designated in contradistinction to cirrhotic induration.

The subjects of hepatic congestion, especially of that form of the malady due to gastro-intestinal irritation, are apt to experience no little mental depression, even hypochondriasis, as, indeed, is usual in most cases of hepatic disease.

COURSE, DURATION, AND TERMINATION.--The behavior of any case of hyperæmia of the liver is determined, first, by the character of the cause, and, secondly, by the extension of the mischief and the atrophic changes which ensue. The congestion arising from gastro-intestinal irritation is comparatively short-lived, since the causal conditions may usually be promptly removed. It is far different in the cases due to pulmonary or cardiac disease. If caused by a left pleuritic exudation, the congestion will disappear as soon as the bend in the ascending vena cava is removed by paracentesis. If, however, produced by a permanent pulmonary obstruction, the course of the hepatic disease is toward cyanotic induration. The same is true of obstructive cardiac lesions. If compensation--as, for example, of a mitral regurgitation--is not effected, the continual congestion must lead to the ultimate lesions of the liver; but if compensation can be brought about, the liver will be saved the irremediable {988} changes. The prognosis, therapeutical and pathological, must necessarily be dependent on the lesions of which the hyperæmia of the liver is merely a symptom.

DIAGNOSIS.--The decision in any case of hyperæmia of the liver must rest on the determination of the gastro-intestinal, pulmonary, or cardiac diseases causative. When, for example, to the gastro-intestinal disturbance or cardiac disease there are added heaviness, uneasiness, increased area of dulness of the right hypochondrium, a hyperæmia of the liver may be concluded to exist. The extent to which the organ is damaged may be judged from its size, the duration of the congestion, and the character of the determining cause. If the area of hepatic dulness declines steadily after having been increased, the causative conditions continuing, the shrinking is due to atrophy. This view is confirmed if ascites has appeared and increased out of proportion to the general dropsy.

TREATMENT.--Those cases of hyperæmia dependent on excesses in eating and drinking require the substitution of a diet composed of lean meat, skimmed milk, acid fruits, and such succulent vegetables as lettuce, tomatoes, celery, etc. When there is a high degree of gastro-intestinal catarrh, an absolute milk diet may be enforced with great advantage. The diet, exercise, bathing, etc. enjoined in the section devoted to lithæmia are equally applicable here. Amongst the special plans of diet sometimes advocated in the condition of abdominal plethora or portal congestion are the grape cure, the whey cure, etc. Great good is accomplished by a simple diet and a course of the Saratoga saline laxative waters--the Congress, Hathorn, Geyser, etc. The alkaline waters of Wisconsin and Michigan, the White Sulphur of Virginia, and others having similar properties in this country may be employed for the same purpose. The saline laxatives, Pullna, Friedrichshall, and other purgative salines, may be used in robust, plethoric subjects with much portal congestion, hemorrhoids, etc. Phosphate of soda, given in sufficient quantity to maintain a soluble state of the bowels, is also a useful remedy. The resinous cathartics, podophyllin, jalap, rhubarb, aloes, euonymin, iridin, baptisin, etc., are all useful when the indication is to unload the portal circulation. The mercurials, formerly so much used, are now discredited to an unwarranted degree. In an irritable state of the gastro-intestinal mucous membrane calomel in small doses is remarkably useful.

The treatment of congestion of the hepatic vein is included in that of the lesion causing it. In some rather exceptional cases the liver enlarges considerably in consequence of incompetence of the mitral, without there being any other conspicuous evidence of the lesion. Remarkable relief is afforded to the hepatic symptoms by the administration of digitalis. The important point in all cases due to cardiac disease is to bring about compensation, and thus obviate the consequences of the lesion. Remediable pulmonary affections should be cured as promptly as possible, and the evil results of incurable affections lessened by efforts to remove the hepatic hyperæmia. Careful alimentation, saline laxatives, and diuretics are the most efficient measures. It would be encroaching on the subjects of pulmonary and of cardiac diseases to enter more minutely into the therapeutical questions connected with a symptom of these affections.

{989} Perihepatitis.

DEFINITION.--By the term perihepatitis is meant an acute inflammation of the serous envelope of the liver. It may be acute or chronic, very rarely the latter, and it is usually a secondary affection, although primary cases are not uncommon.

PATHOGENY.--Inflammation of the hepatic portion of the peritoneum may arise by an extension of the morbid process from neighboring parts, as in perforation of the stomach or duodenum, pleuritis of that part of the membrane reflected from the diaphragm, etc. More frequently it arises by contiguity from some disease of the liver itself, as chronic interstitial hepatitis, abscess, echinococci cysts, cancer, etc. The author has frequently (comparatively) seen perihepatitis follow the passage of gall-stones. It is usual to find considerable organized exudation at the hilus of the liver in the case of those who have had several attacks of hepatic colic, and attachments to various neighboring parts also. In those instances of secondary hepatitis there may be more or less extensive connective-tissue formation and compression of the hepatic substance (Budd).[47]

[Footnote 47: _Diseases of the Liver_; also, Bamberger, _Krankheiten des Chlylopoietic Systems_, p. 495, 2d ed.]

Direct perihepatitis arises from traumatic causes--from contusions of the right hypochondrium by spent balls, blows and falls, etc. Tight-lacing and wearing a strap to support the trousers are supposed to excite a slow, chronic hepatitis, but the latter is more certain to bring about such a result than the former.

SYMPTOMS.--Acute perihepatitis, if of sufficient extent, causes more or less fever; pain is felt in the right hypochondrium, and is increased by pressure and by deep inspirations, and in some rare instances a friction murmur is audible synchronous with the respiratory movements. These symptoms succeed to attacks of hepatic colic, perforation of the stomach or intestine, and contusions of the abdominal wall. The chronic form is not febrile; there is a feeling of soreness instead of acute pain; pressure, the movements of the body, respiration, etc. increase the distress, and on turning on the left side a painful dragging is experienced. A slight degree of icterus may be present in both acute and chronic cases.

COURSE, DURATION, AND TERMINATION.--The course of the acute cases is toward recovery. In two or three days the inflammation reaches the maximum, adhesions form, and then the morbid process declines. The whole course of an acute perihepatitis caused by external injury or by the passage of gall-stones is terminated in a week or ten days. The mischief done may not be limited to the adhesions formed. The large quantity of newly-organized connective tissue may, in its subsequent contraction, compress the common, cystic, or hepatic duct, or the portal, or both ducts and vein. The course of the chronic cases is determined by the causative lesion. The contraction of the new-formed connective tissue may compress the organ and lead to sclerotic changes which cannot be distinguished from cirrhosis. In some instances contusions set up suppurative inflammation, and an abscess forms between the parietal and glandular layer of the peritoneum. Such a case will then present the phenomena of hepatic abscess.

DIAGNOSIS.--The determination of the character of the case will be {990} largely influenced by the history. If the attack has followed a blow on the side or a paroxysm of hepatic colic or the symptoms of perforation, there will be no difficulty in determining its seat and character. In the absence of the history the differentiation must be made between perihepatitis and pleuritis. The distinction consists in the fact that in the former the pain and soreness are below the line of respiratory sounds, although synchronous with them. In chronic perihepatitis the symptoms come on in the course of the hepatic disorder, or are consequent on a local injury, as the pressure of stays or a band.

TREATMENT.--If the symptoms are acute and the subject robust, the local abstraction of blood by leeches affords relief and diminishes the violence of the disease. A bandage should be tightly applied around the body at the level of the hypochondrium to restrain the movements of the affected organ. A turpentine stupe may be confined in this way, or a compress of water may be utilized to serve the same purpose. If the pain is acute and the peritonitis due to perforation or to the passage of calculi, the hypodermatic injection of morphia is the most important resource.

Interstitial Hepatitis; Sclerosis of the Liver; Cirrhosis.

DEFINITION.--The terms interstitial hepatitis and sclerosis of the liver express the nature of the malady: they signify an inflammation of the intervening connective tissue, resulting in a sclerosis--an induration of the organ. The term cirrhosis, now so largely in use, was originally proposed by Laennec[48] because of the yellowish tint of the granulations, from the Greek word, [Greek: chirros], yellow. As Laennec's theory of cirrhosis was erroneous, having regarded these granulations as new formations, the word is a very faulty one, and hence it would be preferable to use the term sclerosis, since a similar change in other organs is thus designated, as sclerosis of the kidney, sclerosis of the lungs, etc. It is also called in England gin-drinker's liver, hobnail liver. Carswell[49] first described the anatomical changes with accuracy, and illustrated them with correct drawings. The following year Hallmann[50] confirmed the truth of Carswell's descriptions, and contributed a good account of the morbid anatomy; and subsequently French, German, and English authorities added new facts, which will be set forth in the further discussion of the subject.

[Footnote 48: _Traité de l'Auscultatlon médiate_, tome ii. p. 501.]

[Footnote 49: _Illustrations of the Elementary Form of Diseases_, fasciculus 10, plate 2.]

[Footnote 50: _De Cirrhosi hep._, Diss. Inaug., Berolini, 1839, quoted by Thierfelder.]

CAUSES.--Sclerosis of the liver is, conspicuously, a disease of adult life and onward. Except the congenital example mentioned below, the earliest age at which the disease has occurred, so far as I am able to ascertain, is four years--a case reported by Wettergreen[51] of hypertrophic sclerosis, in which neither a syphilitic nor paludal cause could be ascertained. Cayley[52] reports a case in a child of six; Murchison,[53] Frerichs,[54] Griffith,[55] one each at ten. After this period the increase relatively to age is rapid. The majority of cases occur between thirty {991} and fifty years. Yet Virchow[56] has given the details of a congenital example. According to Förster, of 31 cases of cirrhosis, 16 were between forty and sixty years. The preponderance of cases in the male sex is very decided. Of Bamberger's 51 cases, 39 were men, 12 were women; of Frerichs' 36 cases, 20 occurred in men and 16 in women--a larger proportion of women than any other author records; of 12 cases observed by myself, only 1 was a woman. Nationality does not affect the production of cirrhosis, except as regards the personal habits of the people. This disease is comparatively uncommon in wine- and beer-drinking countries, and frequent amongst a spirit-drinking people.[57] The great etiological factor is the abuse, the habitual use, of spirits, and hence the number of cases observed in North Germany, England, Scotland, and the United States. Murchison affirms that he has never seen a case produced in any other way. Even in children of tender years the abuse of spirits can usually be traced. Nevertheless, there are instances of the disease the origin of which cannot be referred to alcoholic excess. The congenital cases, as that narrated by Virchow, and the instances occurring in children and adults not given to spirits in any form, indicate that there are other pathogenetic influences which may bring about a sclerosis of the liver. Virchow[58] was one of the first to illuminate the subject of visceral syphilis and to demonstrate the occurrence of sclerosis of the liver from syphilitic infection. Very often the syphilitic cachexia coincides with alcoholic excess. There can be no doubt that chronic malarial poisoning causes, or powerfully predisposes to, cirrhosis. I have submitted elsewhere pathological evidence on this point,[59] and the Italian physicians, who have the opportunity to obtain accurate data, maintain that malarial toxæmia does bring about this state. It is probable that the overgrowth of connective tissue is induced by the repeated congestions of the malarial attacks, and by the obstruction due to catarrh of the bile-ducts which so often occurs in the febrile paroxysms.

[Footnote 51: _Hygeia_, 1880, quoted by _London Medical Record_, March 15, 1881.]

[Footnote 52: _Transactions of the Path. Society of London_, vol. xxvii., 1876, pp. 186, 194.]

[Footnote 53: _Clinical Lectures_, _loc. cit._]

[Footnote 54: _Clinical Treatise, etc._, Syd. Soc. ed., by Murchison.]

[Footnote 55: _Clinical Lectures_, _loc. cit._]

[Footnote 56: _Archiv f. path. Anat._, Band xxii. p. 426.]

[Footnote 57: Baer, _Der Alcoholismus_, Berlin, 1878, p. 62 _et seq._]

[Footnote 58: _Virchow's Archiv_, vol. xv. p. 281; also, Lancereaux, _A Treatise on Syphilis_, Syd. Soc. ed.]

[Footnote 59: _Memoirs of the Sanitary Commission_, medical volume.]

J. Wickham Legg[60] and Charcot[61] nearly simultaneously discovered that obstruction of the bile-ducts, if continued a sufficient length of time, sets up a hyperplasia of the connective tissue of the liver. The evidence is pathological and experimental. Thus, Legg has seen a liver markedly cirrhotic in a case where a small cancer of the duodenum completely obstructed the flow of bile into the intestine.[62] By tying the common duct in dogs it was found that a hyperplasia of the connective tissue very soon occurred, and this was followed, of course, by contraction of the new tissue and atrophy of the hepatic cells. Closure of the hepatic vein has the same effect, and also, as Solowieff[63] has asserted, closure of the portal vein; on the other hand, by Frerichs and others the closure of the portal is attributed to the sclerosis.

[Footnote 60: _On the Bile, Jaundice, etc._, _loc. cit._, p. 351 _et seq._]

[Footnote 61: _Leçons sur les Maladies du Foie, etc._, p. 231 _et seq._]

[Footnote 62: _On the Bile, Jaundice, etc._, _loc. cit._, p. 355.]

[Footnote 63: _Arch. f. path. Anat., etc._, Band lxii. p. 195.]

Certain poisons, as antimony, arsenic, notably phosphorus, have the power to set up an irritative hyperplasia of the connective tissue of the {992} liver. These metals accumulate in the liver in preparation for excretion. Wegner,[64] in the study of the action of phosphorus on dogs, rabbits, and other animals, has induced a marked degree of sclerosis, but such results have not been observed in cases of poisoning by phosphorus in man, except in an instance reported by Küssner.

[Footnote 64: _Virchow's Archiv_, Band lv. p. 18.]

Finally, a condition of the liver corresponding in all respects to cirrhosis has been induced by perihepatitis, by the organization of the exudation and its subsequent contraction, and by the extension of the morbid process from the capsule to the interlobular connective tissue (Poulin[65]).

[Footnote 65: _Étude sur les Atrophies viscérales consécutives aux Inflammations chroniques du Sereuses, etc._, Thèse de Paris, 1880.]

PATHOLOGICAL ANATOMY.--Several forms of cirrhosis are recognized by the modern French school of pathologists. According to Sabourin,[66] there is an annular, a monolobular, and a multilobular form. These differ merely in regard to the arrangement of the new connective tissue. At the outset of the disease the liver is increased in size and hyperæmic. Its consistence is also greater than normal. The outer surface is at this period smooth, but on section the islets of the parenchymatous tissue, yellowish in color, are distinctly visible between the grayish or pale-rose tint of the intervening or proliferating tissue. This reddish-gray material consists of fine connective-tissue elements containing spindle-shaped cells.[67] The development of this material is such as to even exceed in quantity the proper glandular structure. The bands of newly-formed connective tissue extend between individual lobules (monolobular cirrhosis) or between groups of lobules (multilobular cirrhosis). A portion of the spindle-shaped cells form new vessels communicating with the branches of the hepatic artery.[68] Coincidently with the formation of the new connective tissue ensues its contraction. The enlarged organ diminishes in size from a slight degree to one-half its original volume; especially in the left lobe is the diminution of size most marked. On the surface it exhibits a knobbed or nodular aspect (hobnail liver), and these knobs present through the capsule a yellow appearance. The granulations, so called, consist of small prominences corresponding to lobules or groups of lobules, and hence vary in size from that of a pinhead to that of a pea.[69] Between these are the sharply-defined masses of connective tissue. On section the organ is found to be of firm almost cartilaginous hardness, and between the interlacing bundles of connective tissue are the small islands of parenchymatous tissue projecting above the cut surface and having a yellowish or brownish-yellow color. As the terminal branches of the portal are compressed in the process of shrinking undergone by the new connective tissue, they are destroyed. The result of this obliteration of the portal radicles is the impaired nutrition of the lobules and atrophy of the cells. Formerly it was held that the atrophy of the hepatic cells was due to the compression exercised by the contracting connective tissue, and Beale[70] even maintained that the change began in {993} the cells, the connective tissue contracting as the cells receded before them. This view has been reaffirmed by Ackermann in a paper read last year before the Congress of German Naturalists and Physicians, but without any acknowledgment, so far as I can ascertain, of Beale's long-before expressed opinions. In the discussion which followed the reading of Ackermann's paper the position of its author was supported by Aufrecht, Küssner, and others, but controverted by Rindfleisch. It has been demonstrated by Cohnheim and Litten[71] that the lobule is nourished not only by the portal radicles, but by the branches of the hepatic artery, which enter, by the interlobular vein, the capillaries of the lobule, and hence the nutrition of the cells suffers in consequence of the lessened blood-supply; but it is probable also that more or less compression is exercised. When the cells are destroyed, their remains may be discerned in the mass of connective tissue as fine fat-granules or masses of pigment yellowish or brownish in color. The peculiar appearance to which the name cirrhosis is applied is due to the lobules or groups of lobules which project on section above the divided surface, and are colored yellowish by the bile-pigment, which here exists in an exaggerated quantity. The cells themselves are not normal: they are enlarged by compensatory hypertrophy, and they contain much bile-pigment and a considerable quantity of fat. The compression of the capillaries, especially their obliteration, leads to stasis of the blood and its consequences in the whole chylopoietic system.

[Footnote 66: Ch. Sabourin, "Du Rôle que joue le Système veineux sus-hépatique dans la topog. de la cirrhose du foie," _Revue de Médecine_, June, 1882.]

[Footnote 67: Förster, _Lehrbuch der pathologischen Anatomie_, Jena, 1873, p. 264.]

[Footnote 68: Cornil, "Note sur l'État anatomique des Canaux biliaires et des Vaisseaux sanguins dans la cirrhose du foie," _Gaz. méd. de Paris_, 1883.]

[Footnote 69: Charcot, _Leçons sur les Maladies du Foie, etc._, p. 226.]

[Footnote 70: _Archives of Medicine_, vol. ii. p. 82.]

[Footnote 71: _Archiv für path. Anat._ (Virchow), Band lxvii. p. 153 _et seq._]

SYMPTOMS.--The development of sclerosis is usually very insidious. After some years' indulgence in spirit-drinking or affected for a length of time with the other causes of the malady, a gradual decline of vigor occurs. The complexion takes on a fawn color, stigmata slowly form on the face, there is more or less yellowness of the conjunctiva, and attacks of headache, giddiness, and even severe vertigo, are experienced. An increasing indisposition to mental effort, some hebetude of mind, and a gradually deepening despondency are felt. The appetite gradually fails, becomes capricious, and only highly-seasoned, rather odd, or unusual articles of food can be taken. Such subjects acquire a taste for condiments, for such uncooked vegetables as onions, celery, raw cabbage, etc., for fruits, and get a distaste for plainly-cooked meats and vegetables, for sweets, etc. The digestion is as capricious as the appetite: at first there are times of appetite, again of indifference, then of disgust; some heaviness is felt after meals; gaseous eructations, acidity, pyrosis, nausea, occur day after day as the case advances; and ultimately morning vomiting is regularly experienced. Nausea is felt on rising; then with much straining and distress a little glairy mucus and a teaspoonful of bile are brought up; after which, it may be, a little food can be taken. It is only after the case is fully declared that these troubles of stomach digestion become constant; previously they occur now and then in a paroxysmal way, whilst between there is only labored digestion.

As the compression of the portal radicles maintains, by reason of the obstruction, a constant hyperæmia of the intestinal mucous membrane, a catarrhal state, with fermentation of the fatty, starchy, and saccharine constituents of the food, and hence complicated products of an irritating kind, must result therefrom. Hemorrhoids, varying in size according to {994} the degree of obstruction, form, sometimes bleeding more or less profusely, again being merely troublesome or painful. Fissures of the anus and fistula in ano not unfrequently complicate the case. The bowels are necessarily rather relaxed than confined, but at the onset of the malady they may be confined, afterward assuming more or less of the characteristics of diarrhoea. The stools may be offensive with the products of decomposition, rather clay-colored or golden, or brownish and almost black from the presence of blood. In some cases the stools are parti-colored--clay-colored in part, brownish in part--and in exceptional examples continue normal or nearly so until near the end. As the transudations from the portal vessels increase, the mucous membrane of the intestinal canal becomes oedematous, and, the normal secretions being arrested, the discharges finally consist of a watery fluid, whitish or grayish, dark-brown or blackish, and very offensive. The decomposition of foods instead of their proper digestion and solution, and especially the fermentation of the starchy and saccharine constituents of the aliment taken, produce a great quantity of gas; hence meteorism comes to be an ordinary symptom. The accumulation of gas is greatly promoted by the paretic state of the muscular layer and by the relaxation of the abdominal walls consequent on the oedema of the muscular tissue. A high degree of distress is sometimes caused by the great accumulation of flatus; the abdomen is greatly distended and the diaphragm is pushed up against the heart and lungs, compelling the patient at length to sit up to breathe with ease. Of course the accumulation of fluid may be greater, and the gas only add to the discomfort.

A very common symptom is hemorrhage. Sometimes it happens, indeed, that this is the only evidence of the portal obstruction at first observed. Hæmatemesis is more common than intestinal hemorrhage. Now the blood may be large in quantity, appear little changed from its usual coagulated state, and be brought up promptly with slight effort of vomiting; now it is passed by stool, is in coffee-colored, granular masses or in a tar-like, semifluid state; and again it appears in coffee-grounds mixed with the contents of the stomach. These variations are due to the character, seat, and extent of the hemorrhage and to the condition of the mucous membrane. Merely-distended capillaries, yielding, may furnish a little blood, which, acted on by the gastric juice, forms coffee-grounds, or, if not acted on in consequence of the failure of the gastric glands to functionate, appears as bloody streaks mixed with mucus. Enlarged veins, giving way, may furnish a large quantity of partly-coagulated venous blood, charred or not as the state of the juices will determine. In some cases hemorrhages into the submucous tissue or thromboses of the submucous veins lead to solution of the membrane thus deprived of its nutritional supply, and ulcers form. Two admirable examples of this kind have been seen by the writer in which large hæmatemesis occurred from ulcers near the pylorus. They were round, smooth ulcers, containing coagula, and the eroded vessels (veins) were readily seen opening into the cavity of each.

The obstruction to the portal circulation results also in an enlargement of the spleen. There may be a simple enlargement due to the hyperæmia merely; there may be an enlargement due to the hyperæmia and to a resulting hyperplasia of the connective tissue; there may be also, in {995} addition to the second form of enlargement, amyloid degeneration, syphilitic hyperplasia, etc. The increased dimensions of the spleen are by no means always made out, and authorities differ greatly as to the proportion of cases in which the enlargement can be detected. The organ may indeed be considerably enlarged whilst pushed upward into the left hypochondrium by the effusion, and yet the attempt to measure and define its dimensions may be fruitless. From a slight increase due to the hyperæmia up to the enormous dimensions acquired by the added amyloid material there are all possible variations in size.

Partly in consequence of the increased blood-pressure in the vessels of the peritoneum, and partly in consequence of the watery condition of the blood itself, effusion takes place into the sac of the peritoneum. Such an accumulation is known as ascites, or dropsy of the abdomen. The time at which the effusion begins, the amount of it, and the degree of contraction of the liver necessary to produce it, vary in each case. Ascites may be the first symptom to announce the onset of cirrhosis; it is more frequently amongst the later symptoms, and is the evidence of much interference in the portal circulation. However, it is not due wholly to hepatic disease. The blood in cirrhosis is much reduced and watery, hence slight causes suffice to induce an outward diffusion. Given a certain obstacle to the passage of the blood through the liver, transudation will be the more prompt to appear the greater the anæmia. In some cases an enormous quantity of fluid collects: from ten to thirty pounds may be regarded as usual, and forty to sixty pounds as exceptional, although the highest amount just given is not rare. The fluid of ascites nearly represents the serum of the blood. It has a straw color and is clear, but it may have a reddish tint from the presence of blood, a greenish-yellow or brown from bile-pigment. The solids of the serum are in the proportion of from 1 to 3 per cent., and consist of albumen chiefly and salts, of which sodium chloride is the principal. Hoppe's[72] analysis gives this result: 1.55 to 1.75 solids, of which 0.62 to 0.77 is albumen. According to Frerichs, the amounts of solids ranges from 2.04 to 2.48, and of these albumen constitutes 1.01 to 1.34.

[Footnote 72: _Virchow's Archiv für path. Anat., etc._, Band ix.]

Oedema of the inferior extremities comes on after, usually--rarely with--the ascites. If the mechanism of this oedematous swelling be as supposed, the effusion into the areolar tissue necessarily succeeds to the abdominal effusion. The pressure of the fluid in the cavity on the ascending vena cava and iliac veins seems to be the principal factor; but to this must also be added the intestinal gas, which in some instances exerts a powerful force. The ankles have in rather rare cases appeared swollen before the abdomen, but the detection of fluid in the peritoneal cavity when in small quantity is not always easy. Obese women, with much accumulation of fat in the omentum and flatus in the intestines, have swollen feet and legs if erect for some time, the effusion being due to pressure on the vena cava. The legs may become enormously distended. The scrotum and penis in the male, the vulva in the female, the buttocks and the abdominal wall, also become oedematous, sometimes immensely. Walking grows increasingly difficult. Warmth and moisture and the friction of the sensitive surfaces excite vesicular and pustular eruptions where the {996} scrotum and labiæ come in contact with the thighs. Urination may be impeded by the oedema of the prepuce.

An attempt at compensation for these evils growing out of the obstruction in the portal system is made by the natural powers. Anastomoses of veins through minute branches are made use of to convey the blood of the obstructed portal circulation into the general venous system, and to this end become greatly enlarged. The interlobular veins being obliterated by the contracting connective tissue, the pressure in the branches and trunk of the portal vein is much increased. Hence an outlet is sought for in the veins which communicate between the portal and the ascending vena cava. One of the most important of these is a vein in the round ligament, at one time supposed to be the closed umbilical vein, but proved by Sappey to be an accessory portal vein. Bamberger,[73] however, has found the umbilical vein pervious, and since, Hoffmann[74] has demonstrated the same fact. It is probable, indeed, that Sappey's observation is correct for some cases. In either event, the veins of the abdominal wall about the umbilicus communicating with the epigastric become enormously distended, and in some advanced cases of cirrhosis form a circle known as the caput Medusæ. Further communication between the portal and the veins of the diaphragm takes place by means of the veins in the coronary and suspensory ligaments. In some instances a new route is established between the veins of the diaphragm and the portal by means of new vessels formed in the organized connective tissue resulting from perihepatitis. Still another channel of communication exists between the inferior oesophageal veins, the azygos, and the coronary, and finally between the inferior hemorrhoidal and the hypogastric. The more completely can communication be established between these anastomosing veins the less severe the results of portal obstruction.

[Footnote 73: _Krankheiten des Chylopoiet. Syst._, _loc. cit._]

[Footnote 74: Quoted by Thierfelder, _op. cit._]

Besides these indirect evidences of portal obstruction and a contracting organ, there are direct means of ascertaining the condition of the liver. By the methods of physical diagnosis we may acquire much information. On auscultation, as our Jackson[75] was the first to show, a grating or creaking like leather, or friction sound, is audible over the right hypochondrium synchronously with the respiratory movements or when produced by moving with the fingers the abdominal wall on the liver. This sound is caused by the bands of false membrane which extend between the two surfaces, and hence indicates a secondary perihepatitis.

[Footnote 75: _The American Journal of the Medical Sciences_, July, 1850.]

To ascertain the dimensions of the liver--to mark out the area of hepatic dulness--with accuracy is a most necessary procedure. The period of the disease is an important element in the problem. When the new material is deposited and the congestion of the portal system first occurs, an increase in the dimensions of the organ is observed. This enlargement, of brief duration, must not be confounded with the hypertrophic sclerosis, another form of the malady. So considerable is the increase in the size of the liver that there is an evident enlargement of the right hypochondrium, and the whole abdomen seems fuller. The organ may be felt, on palpation, projecting one, two, or even three fingers' breadths below the margin of the ribs, and the left lobe extends well across the epigastrium, increasing the sense of resistance and the area {997} of dulness in this direction. The enlarged liver, as felt below the ribs, appears firmer than is natural, is yet smooth, and the margin is sharply defined. The duration of this period of enlargement is indefinite, but it is rather brief, and is followed by the contracting and atrophic stage. It is not often, indeed, that the patient presents himself during the period of enlargement. Sometimes a perihepatitis or an unwonted tenderness in the right side compels attention during this stage, but more frequently it escapes notice. If perihepatitis occur, there will be fever, pain, and tenderness, a slight icterode hue of the skin, and possibly Jackson's[76] friction sound. These symptoms, taken in conjunction with the history of the case and the obvious enlargement of the organ, will indicate the existence of the first stage of sclerosis.

[Footnote 76: _The American Journal of the Medical Sciences_, July, 1850, _supra_.]

The contraction of the liver, or, as it may be expressed, the atrophy of the hepatic cells and the consequent shrinking of the interlobular connective tissue, goes on slowly. Several months may be occupied in an amount of atrophy distinct enough to be recognized by the narrowing of the area of hepatic dulness. Especially difficult is the recognition of the contraction when ascites has fully distended the abdomen. It may be necessary under such circumstances to postpone a decision until tapping has removed the fluid. If the organ can be felt by depressing the walls of the abdomen, more or less unevenness of surface may be detected, and the inferior margin may give the impression of hardness and sharpness of outline. At the same time, the increased dulness of the epigastric region observed during the hypertrophic stage will have gradually ceased because of the shrinking of the left lobe. The liver may be undergoing the atrophic degeneration to a marked extent and yet remain large--larger even than normal. Such a state of things may be due to conjoint amyloid or fatty degeneration of the organ, and, indeed, more or less fatty change occurs in all cases of cirrhosis. The shrinking of the liver persists until the area of dulness is not greater in area than two or three ribs.

The disturbances of function in sclerosis of the liver are not limited to the chylopoietic system. As the secreting structure of the liver is continually lessened in extent by the atrophy, symptoms result from the necessary interference in the hepatic functions. These symptoms are concerned with the liver, with the nutrition of the tissues of the body, and with the kidneys. As regards the biliary function of the liver, the quantity of bile acids and pigment is reduced below the normal in proportion to the damage done to the organ. As a rule, there is little jaundice in sclerosis, and very little bile-pigment present in the urine. Hence there must be little produced. Instead of a jaundiced hue of the skin, it has a fawn color--an earthy, sallow tint eminently characteristic of a chronic affection in which the power to produce bile is much impaired. Occasionally it happens, particularly in the early stages of cirrhosis, that a well-marked jaundice appears in the face and body, but this probably is due to a catarrh of the bile-ducts. In most cases the integument presents the earthy and sallow hue above mentioned. Graves[77] appears to have been the first to interpret aright the greater significance of this appearance of the skin than the purely jaundiced tint. The glycogenic {998} function of the liver must be impaired in the same ratio as the biliary. The nutrition of the body suffers; the skin becomes dry and harsh; the fat disappears; the temperature of the body, unless the conditions for producing fever are present, is barely up to normal, if not somewhat below; a marked degree of anæmia supervenes; and the action of the heart becomes feeble and rapid after a period of slowness. The blood is altered in quality, and hence hemorrhages--epistaxis especially--occur, petechiæ and ecchymoses appear in the skin, and stigmata are numerous about the face and nose.

[Footnote 77: _Clinical Medicine_, _op. cit._]

The urine in cirrhosis is high-colored because of the abundance of pigment, and in the early stages of the disease is increased in amount, although of lower specific gravity. When much effusion takes place into the peritoneal sac, the compression of the renal veins by the fluid lessens the activity of the kidneys and diminishes the urinary flow. Much discussion has taken place over the quantity of urea present in the urine in cases of cirrhosis, but it has been established that the relative quantity of urea lessens in proportion to the damage suffered by the liver.[78] The urates are in excess.

[Footnote 78: Charcot, _Leçons sur les Maladies du Foie_, _loc. cit._, p. 252; also, _Essai sur les Variations de l'Urée dans les Maladies du Foie_, par F. Genevoix, Paris, 1876; _Des Rapports de l'Urée avec le Foie_, par A. Martin, Paris, 1877; _Sur l'Urée et ces Variations dans la Cirrhose_, Thèse de Paris, Audiguier; _Contribution à l'Étude du Rôle du Foie dans la Product. de l'Urée_, Reufflet.]

COURSE, DURATION, AND TERMINATION.--There are enormous variations in the course of the disease as respects the rate of its progress. In general, it may be said that the whole duration is from three months to six years. The onset is often insidious, and little distress is occasioned until effusion begins in the abdomen. In other cases there is considerable pain in the right hypochondrium, severe disorders of digestion and intestinal derangements, rapid emaciation, ascites, and some intercurrent malady which terminates them, often quite unexpectedly. The usual course is as follows: After the protracted use of alcoholic stimulants the symptoms of gastro-intestinal catarrh appear; there occur acidity, pyrosis, morning vomiting, and distress after meals; the bowels are irregular, the stools rather dark and offensive; the bodily vigor declines and the mental condition is depressed and hypochondriacal; emaciation progresses; the skin becomes dry, harsh, and fawn-colored; stigmata appear on the face; some uneasiness is felt in the abdomen, through the right hypochondrium, and about the umbilicus; presently the abdomen enlarges and the feet and legs swell; after a time the abdominal enlargement is extreme and the walls become thin, the genitals and thighs are greatly distended, and the prepuce is so swollen that urination grows more and more difficult, the penis almost disappearing in the surrounding oedema; notwithstanding the immense size of the abdomen and lower extremities, the chest, face, and upper extremities are wasted away; to lie down is impossible, and only snatches of disturbed sleep are procured in the upright sitting posture; breathing grows more and more difficult, and a sense of suffocation is imminent; and, thus worn out by suffering and want of sleep, the patient at last sinks into a soporose state and dies comatose, if not cut off before by some acute serous inflammation--pleuritis, peritonitis, peri- or endocarditis, pneumonia, etc.

{999} The course of any case of cirrhosis is much influenced by the amount of damage to the hepatic cells and by the extent of the compensatory changes in the circulation. Ulcers of the stomach or intestine, opening vessels, or hemorrhages from the mucous membranes may have a pronounced effect on the progress of any case. A fatal result was determined in a case under the writer's charge by hemorrhage from ulcers near the pylorus, which were caused by thromboses of the stomach veins at that point. Occasionally, the occurrence of thrombosis of the portal vein adds an embarrassing and dangerous complication. The liver, besides the change due to cirrhosis, may be affected by amyloid or fatty degeneration, or by both combined. It should not be forgotten that more or less fatty change takes place in the hepatic cells undergoing atrophy, whence the appearance called cirrhosis. Sclerosis may be a general condition in which several organs participate, the kidneys notably. These organs are changed by a hyperplasia of the connective tissue, and especially by fatty degeneration of the epithelium. In the brain the sclerosis consists in chronic pachymeningitis, adhesions of the dura, etc., and with these connective-tissue changes are often associated extravasations of blood. These lesions are probably due to chronic alcoholism rather than to the cirrhosis--are simultaneous lesions, instead of consecutive.

The duration of cirrhosis must necessarily depend largely on the occurrence of the complications above mentioned and on the appearance of intercurrent diseases. The most usual intercurrent maladies are peritonitis, pleuritis, and other serous inflammations. An attack of cerebral (meningeal) hemorrhage may occur. Failure of the heart may be due to fatty degeneration of its muscular tissue. Stupor, coma, and insensibility may come on toward the close in consequence of the retention of excrementitious matters. By Flint, Jr., these cerebral symptoms were referred to the retained cholesterin, and hence he designated this state cholesteræmia. Numerous experimentalists (Pagès,[79] Chomjakow,[80] Von Krusenstern,[81] Koloman Müller[82]) have studied this question, and only Müller has been able to confirm Flint's theory. The condition is more suitably designated cholæmia, which signifies blood-poisoning from the excrementitious biliary matters retained in the system.

[Footnote 79: Quoted by Legg, p. 233.]

[Footnote 80: Quoted by Krusenstern.]

[Footnote 81: _Virchow's Archiv_, Band lxv. p. 412.]

[Footnote 82: _Archiv für experimentelle Pathologie und Pharmakologie_, Band i. p. 213.]

Any fully-developed case of cirrhosis can only terminate in one way, for we possess no means of restoring the hepatic cells when once destroyed. At the outset of the disease, before any serious changes have taken place, it is probable it may be arrested. Proceeding to its natural termination without complications or intercurrent affections, death finally occurs from exhaustion. The emaciation becomes extreme, the stomach gets to be excessively irritable, and an exhausting diarrhoea consumes the last remains of strength. Then an oedema of the lungs or failure of the heart or a deep coma ends the scene.

DIAGNOSIS.--Cirrhosis in its first stage is to be distinguished from diseases which cause enlargement of the liver, and in its second or contracting stage from diseases that induce contraction of the organ. The history of alcoholic excess is an important means of differentiating this {1000} from other affections. The enlargement belonging to alcoholism is distinguished from that due to amyloid disease by the permanent character of the latter and by its history of chronic suppuration, in addition to, it may be, alcoholic excess; from cancer, by the character of the enlargement, by its permanence, by the secondary deposits in the mesentery and elsewhere, by the severe and persistent pain; from hydatids or echinococci cysts by the painless enlargement of the latter, by the absence, usually, of any interference with the hepatic functions, by the purring thrill, and by the presence of the characteristic hooklets in the fluid withdrawn. From the maladies characterized by the contraction of the organ it is distinguished by the rapidity with which the case is developed in acute yellow atrophy, and by the profound constitutional disturbance characteristic of this form of contraction. When the liver is lessened in size in consequence of the compression exercised by the contracting exudation of a local peritonitis, there is a history of pain and soreness of the right hypochondrium, followed by the symptoms of contraction--a very different history from that of cirrhosis, in which the local attacks of pain and distress succeed to or accompany the symptoms of contraction. Occlusion of the gall-ducts by a calculus may set up a slow atrophy having some points of resemblance to cirrhosis; but in this malady attacks of hepatic colic precede the signs of obstruction, the jaundice, and gray evacuations, and the evidences of contraction succeed to these very characteristic symptoms; whereas in cirrhosis paroxysms of pain followed by jaundice are not known. Occlusion of the portal vein may also be followed by atrophy, but this is usually due to some other affection of the abdominal organs, and the change in the condition of the liver occurs very promptly, there being neither the history nor the course of symptoms belonging to cirrhosis.

TREATMENT.--As the abuse of alcoholic liquors--even their habitual use in moderation--is the chief pathogenetic factor, they should be entirely given up. Condiments, coffee and tea, highly-seasoned animal foods, are of less importance as causes, but are sufficiently injurious to require them to be discontinued. The food of such subjects should not contain fat, because the bile is necessary to its right assimilation, and should have but a small proportion relatively of starch and sugar, since these articles readily ferment in the presence of an excess of mucus and in the absence of the bile. The succulent vegetables, as lettuce, celery, spinach, etc., should be substituted for the starchy and saccharine. A diet largely composed of skimmed milk renders an important service both as a nutrient and a diuretic and depurant. Lean meats, acid fruits, and the weak alkaline mineral waters should be the basis of a proper system of alimentation.

As malarial intoxication is a cause now distinctly recognized, patients should be removed from such influences. If this be impracticable, the effects of the poison should, as far as possible, be removed, especially the glandular complications. To this end, such remedies should be employed as will affect the overgrowth of the connective tissue, as the compound solution of iodine, the bichloride of mercury, and the chloride of gold (or gold and sodium). Quinine will be necessary, according to circumstances.

Do we possess any means to check the overgrowth of connective tissue {1001} in cases of sclerosis? The writer believes that those remedies have this power to a less or greater extent which are separated by the liver from the blood. These are chiefly the salts of gold, silver, copper, arsenic, and mercury (chloride), and phosphorus. The most useful of these are the chloride of gold and sodium and the chloride of mercury, and some phosphates. The writer has had, he thinks, curative results in the commencement of the disease from the chloride of gold and sodium and the phosphate of sodium. German practitioners believe that the chloride of ammonium is a powerful alterant and deobstruent, and prescribe it in this affection to stop the overgrowth of connective tissue. That it does have this effect can hardly be disputed, but the daily quantity necessary is large, the taste very disagreeable, and the stomachal effect that of an irritant. Hence it is by no means so effective as the chlorides above mentioned. The chloride of gold and sodium (1/10 grain) can be given at the same time with chloride of mercury (1/20 grain) if it is desirable to combine their effects. The writer has seen what appeared to be cases of cirrhosis in the first stage yield to the persistent administration of phosphate of sodium--drachm j ter in die--and the chloride of gold and sodium.

When contraction of the liver has ensued, and hemorrhages, effusion into the cavity of the peritoneum, and a high degree of gastro-intestinal catarrh have occurred, the relief of the secondary symptoms takes the first place in importance. There are but three modes by which an effusion into the abdomen can be removed: by the skin, by the kidneys, by the intestinal canal. Each of these may be employed in turn. By the skin warm baths, vapor baths, digitalis stupes, and especially the subcutaneous injection of pilocarpin, may be employed. These alone may be sufficient in some cases--rather rarely, however. They may all be used simultaneously or in turn to effect the purpose. A digitalis stupe may be made to have the effect of a vapor bath: a large one is placed on the abdomen and the body is covered with blankets, which results in the production of abundant sweating. The vapor bath is applied in the ordinary way, so that no explanation is needed. If there be no contraindication in the state of the heart, pilocarpin salts can be injected in sufficient quantity to induce active diaphoresis. These measures proving inadequate, an attempt should be made to dispose of the fluid by acting on the kidneys and promoting diuresis. Amongst the diuretics in ascites, Wilks places the resin of copaiba first. The dose ranges from two to five grains, and it may be given in combination with gold or mercury chloride. When this remedy increases the flow of urine, it does good, but if the quantity of urine remains unchanged, it does no good, and should be discontinued.

As the effusion of fluid is due to the portal obstruction, it follows that depletion of the terminal radicles of this system will act most directly on the origin of the troubles. Hydragogue cathartics have, therefore, an important place in the treatment of ascites of hepatic origin. One of the most generally efficient of these remedies is the compound jalap powder, for whilst it produces free watery evacuations, it also stimulates the kidneys somewhat. It is generally better to give a full dose--one or two teaspoonfuls--in the early morning, so that the disturbance caused by it will subside before the time for taking food. Several free watery evacuations should be produced by it. Sometimes the resin or extract of podophyllin is added to the compound jalap powder to increase its activity. {1002} Purgative combinations of colocynth, gamboge, and resin of podophyllin are also occasionally employed, but the most efficient hydragogue is elaterium. The last-mentioned may act very efficiently without causing any considerable depression, but the results obtained by it are usually fleeting. After even a very free discharge of fluid the effusion quickly increases, and further purgation is required. Tapping is a palliative expedient which must sometimes be considered. With the present improved aspirator and the antiseptic method the fluid may be withdrawn with ease and safety. It is not necessary in any case to remove all the fluid--merely that quantity which will relieve the pressure on the diaphragm and on the renal vessels. The author has seen general peritonitis result from tapping. As such a complication will increase all the difficulties of a case, it is very desirable to prevent it by careful application of the antiseptic method and sealing of the punctured orifice to prevent the entrance of germs.

In the protracted cases of cirrhosis there ensues, finally, a highly catarrhal state of the mucous membrane, the bowels become very irritable, and frequent offensive and watery discharges occur. If under these circumstances the abdominal effusion increases, the remedies must consist of diuretics and diaphoretics rather than purgatives. Indeed, an exhaustive colliquative diarrhoea may require bismuth, copper, and other astringents, combined with opium, to prevent the patient passing into the condition of collapse. Hemorrhage by vomiting or by stool will demand ice, subsulphate of iron, ipecac, ergotin in the form of subcutaneous injection especially, and other remedies which have been found useful in gastric or intestinal hemorrhage.

Topical remedies are not without utility if used early. When the changes in the liver are secondary to peritonitis of the hepatic portion, the application of leeches and cups renders an important service. At any time during the course of cirrhosis wet or dry cups may be used with advantage whenever local pain, tenderness, and a catching respiration indicate the extension of mischief to the peritoneum. The tincture of iodine or flying blisters, or both in turn, may be applied over the right hypochondrium after cups and leeches, or at any time when local distress indicates the need of counter-irritants. Probably the most efficient topical application during the hypertrophic stage of cirrhosis is the official ung. hydrarg. iodidi rubri. A piece the size of a large pea should be thoroughly rubbed in over the hepatic region daily until some irritation of the skin is produced. When this irritation has subsided the applications should be renewed.

Suppurative Hepatitis; Abscess of the Liver.

DEFINITION.--Suppurative hepatitis is an acute inflammation of the hepatic parenchyma, terminating in suppuration. The inflammation may be primary or due to local conditions entirely, or it may arise from morbid processes occurring in parts or organs in anatomical relation to the liver.

CAUSES.--Climate exercises an unquestionable influence in the production of hepatic abscess. Those warm countries visited by dysentery, {1003} says Lombard,[83] are almost exclusively affected by this disease. Hirsch,[84] whilst recognizing the influence of climate, shows that the natives are not affected to the same extent as are Europeans. Both writers maintain that hepatic abscess does not occur frequently in the corresponding parallels of latitude in the United States; which is true of the Atlantic border, but is not correct for the interior continent, the valley of the Mississippi, and its tributaries. In this vast region the conditions for the production of hepatitis exist abundantly. The mean annual temperature, the malaria-breeding soil, the social and personal habits of the people (males), combine to favor the production of hepatic abscess. As the native population and females in tropical countries are not affected, there must be other influences to the action of which the high temperature contributes. The rich and highly-seasoned food in which Europeans indulge and the large consumption of alcoholic drinks are doubtless responsible in a large measure for the occurrence of this malady in such excessive proportions amongst them.

[Footnote 83: _Traité de Climatologie médicale_, tome iv. p. 386.]

[Footnote 84: _Handbuch der historisch-geographischen Pathologie_, Band ii. p. 300.]

Sex has a remarkable influence in securing immunity against hepatic abscess. According to the statistics of Rouis,[85] of 258 cases of hepatic abscess, only 8 were in women. He rightly enough attributes this exemption rather to the difference in habits of the two sexes than to any merely sexual peculiarity. In 12 cases observed by the writer, only 1 was in a woman. In Waring's[86] collection of 300 fatal cases of tropical dysentery, only 9 occurred in women. These facts are most conclusive regarding the relatively greater frequency of the affection in men. As might be expected, the age at which this disease occurs is the period of adult life, when exposure to the conditions developing it is most likely to happen. In general, then, hepatic abscess may be referred to the period mentioned by Rouis--from twelve to seventy-five years of age. In my own cases the youngest was eleven years and the oldest fifty-four years of age. It is not the broken-down subject of mature age or the weakling of youth who is attacked by hepatic abscess, but the more vigorous and able-bodied, who have, because of their strength and activity, been exposed to the manifold conditions producing it.

[Footnote 85: _Recherches sur les Suppurations endémiques du Foie d'apres des Observations recueilles dans le Nord de l'Afrique_, par J. L. Rouis, Paris, 1860, p. 189.]

[Footnote 86: _An Inquiry into the Statistics and Pathology of Some Points connected with Abscess of the Liver_, by Ed. John Waring, Resident Surgeon of Travancore, 1854, p. iii.]

Rouis finds that a combination of the lymphatic and nervous temperaments seems most favorable to the production of this malady. It is certain that those who have the bodily conditions influential in the formation of gall-stones are not unfrequently attacked by abscess. The passage of the calculi may induce a local peritonitis of considerable severity; their arrest in the duct, with the result of ulcerating through, producing peritonitis and adhesions, are conditions eventuating in the formation of an abscess always large and sometimes of enormous size. Under such circumstances the element of temperament has a secondary place in the aggregate of causes.

Not very often hepatic abscess results from external blows, contusions, and from penetrating wounds. The liver is so placed as to glide aside when a blow is inflicted on the right hypochondrium, and thus escapes {1004} direct compression. An injury which elsewhere would have but little effect may excite suppurative inflammation in the tropical--or, as it may be entitled, the hepatic--abscess zone. Climatic conditions, or the changed habits of Europeans in tropical and subtropical regions, exert a distinct influence in traumatic cases.

The most important causes of hepatic abscess exist in the state of the portal vein, hepatic artery, and the hepatic veins. In the valley of the Mississippi and its tributaries, where abscess of the liver is a comparatively common disease, it has been found that in a large proportion of the cases the initial stage is an affection of the rectum--a form of dysentery properly entitled proctitis. So far as this vast region is concerned, the intestinal disease which precedes abscess of the liver, and stands in a causative relation to it, is an affection of the mucous membrane from which the inferior hemorrhoidal veins arise. This disease, although having a dysenteric form, is not ordinary dysentery. The onset of the disease and its symptomatic expression are those of a mild affection of the mucous membrane of the rectum--so insignificant in some cases as to be recalled with difficulty. In tropical countries abscess of the liver may be associated with dysenteric ulcerations. This relation has been frequently observed, but is far from constant. In Waring's[87] cases, which occurred in India, 31 per cent. of the fatal cases of hepatic abscess arose during the course of acute or chronic dysentery. De Castro of Alexandria[88] finds that dysentery is the most frequent cause of abscess in that region, especially in the Greek hospital. Murchison[89] considers tropical abscess of the liver as secondary to dysentery in a considerable proportion of the cases, but by no means in all. In non-tropical countries abscess of the liver is found to succeed to ulcerations of the stomach, the intestines, the bile-ducts, etc. In the case of ulceration of any part of the mucous membrane from which the portal vein receives branches a morbific material may be conveyed to the liver. This morbific material may be some unknown septic principle the presence of which in the liver will excite suppurative inflammation; it may consist of an embolus having septic power or a merely mechanical irritant; it may be micrococci or some other living organisms, which, arrested in the portal radicles, set up inflammatory foci, etc. There are many examples of hepatic abscess connected with dysenteric ulcerations of the intestine in which no embolus can be found. Admitting the presence of the embolus originally, its disappearance is readily understood by reference to the changes induced by suppuration. Excepting these cases there must be many in which no embolus can be found, because none existed; an unknown septic substance has excited the suppurative inflammation. Emboli may be lodged in the liver from thrombi formed in the peripheral distribution of the portal vein, or from distant parts of the systemic circulation, as in bone diseases. There has been no satisfactory explanation of the manner in which such emboli pass the pulmonary capillaries to be lodged in the liver. At one time there was supposed to be a special relation between injuries of the bones of the head and hepatic abscess, but it is now known {1005} that these cases are not more numerous than those due to osteo-myelitis in any situation. Abscesses in the lungs are greatly more frequent than in the liver in cases of this kind. According to Waldeyer,[90] whilst in two-thirds of the cases of death from surgical diseases and injuries there were abscesses in the lungs, in only 6 per cent. were there abscesses of the liver. It is evident that the emboli entering the systemic circulation are usually arrested in the pulmonary capillaries. Klebs maintains that such emboli consist of parasitic organisms.

[Footnote 87: _On Abscess of the Liver_, _supra_.]

[Footnote 88: _Des Abcès du Foie des Pays chauds, et de leur Traitement chirurgical_, par le Dr. S. V. Castro (d'Alexandrie d'Egypte).]

[Footnote 89: _Clinical Lectures_, _loc. cit._, p. 178.]

[Footnote 90: _Virchow's Archiv für path. Anat., etc._, Band xl. pp. 380, 408.]

Dilatation and ulceration of the bile-ducts were the principal causes of hepatic abscess, as ascertained by Von Baerensprung, in the Berlin Pathological Institute. Duodenal catarrh involving the orifice of the common duct, catarrh of the biliary passages leading to obstruction, and plugging with a gall-stone have resulted in abscess, the initial lesion being probably rupture of one or more of the finer tubes or inflammation leading to suppuration.[91]

[Footnote 91: Grainger Stewart, _The Edinburgh Medical Journal_, January, 1873.]

Finally, a considerable proportion of cases of hepatic abscess arise under unknown conditions. In such cases, however, it is usually found that there has been more or less indulgence in alcoholic drinks, or the liver has been taxed by excesses in the use of rich foods and condiments, or exposure to extreme degrees of temperature has occurred. In the interior valley of this continent, where hepatic abscess is comparatively common, the causes are to be found in malarial influences, in alcoholic indulgence, in dysenteric attacks the product of climatic variations and improper alimentation, and in the formation and arrest in transitu of hepatic calculi also the result of long-continued gastro-duodenal and biliary catarrh.

PATHOLOGICAL ANATOMY.--Great differences of opinion have been expressed as to the initial lesions in hepatic abscess. It is probable, however, that these differences are due to the character of the abscess. Some have their origin in the hepatic cells, others in the connective tissue, and others still in the vessels. There may be a number of points at which the suppurative process begins, or it may be limited to one. Virchow[92] describes the initial lesion as beginning in the cells, which first become coarsely granular, then opaque, and finally soften, and pus appears. Klebs, who maintains the constant agency of septic micrococci, affirms that the changes in the cells are due to compression exerted by the mass of these organisms distending the neighboring vessels, and then suppuration begins on the portal side of the lobules. Liebermeister originally held that the initial lesion is in the connective tissue; and this view is also supported by Köster, who brings to bear experimental data. In the walls of the vessels of the connective tissue and about them, between the hepatic cells, great numbers of lymphoid cells accumulate. The intercellular spaces are also distended with plasma and round cells, and in the vicinity of the central vein the swollen hepatic cells are pressed together; soon pus-corpuscles appear, and the proper anatomical elements are broken up into a diffluent mass composed of fat-granules, pus-corpuscles, and disintegrating hepatic cells.

[Footnote 92: _Archiv für path. Anat., etc._, Band iv. p. 314.]

When suppurative hepatitis arises from an embolus, or emboli, the {1006} first step is the change in the appearance of the acini, which are enlarged and grow softer by disintegration of their cells; then at the centre a yellowish spot appears, and is made up of the detritus, granules of fat, and pus. Surrounding such softening portions of the hepatic tissue is a zone of congestion. When the morbid processes are excited by emboli, there will be as many centres of pus-formation as there are particles distributed by the vessels--from two or three to fifty or more. They may be uniformly distributed through the organ or be collected in one part. Emboli conveyed by the portal vein will be arranged with a certain regularity and through the substance of the liver, whilst those coming from some part of the systemic circulation tend to form at the periphery under the capsule. Small abscesses in close proximity unite ultimately by the softening and disintegration of the intervening tissue.

In the so-called tropical abscess, which is the variety so frequently met with in the interior of this country, the mode of development is different from the embolic, above described. Owing to the deposit of some morbific matter whose nature is now unknown, the vessels dilate and hyperæmia of the part to become the seat of suppuration ensues. The cells become cloudy, granular, and opaque from the deposit of an albuminous matter in them. Within the area of congestion a yellowish spot soon appears, surrounded by a translucent, pale-gray ring, and here suppuration begins; the neighboring cells disintegrate and a purulent collection is formed, which enlarges by the destruction in succession of the adjacent portions of hepatic tissue. Whilst this process is going on there is a border of deep congestion about the abscess, fading off gradually into the normal tint of the hepatic parenchyma; the walls of the abscess are rough and irregular from projections of tissue just beginning to disintegrate, and the pus burrows in various directions more or less deeply into the softening parts. The size to which such purulent collections attain is largely determined by the condition of the liver as a whole. If the organ attacked is healthy otherwise and the general health is not deteriorated, the area of the abscess may be limited by a well-defined membrane and continue inactive for a long time. This limiting membrane is of inflammatory origin, developed from the connective tissue, and varies in thickness from a mere line to several. It was formerly called a pyogenic membrane, because the pus discharged was supposed to be formed by it. When such a limiting inflammation cannot take place, the abscess continually enlarges by the softening and destruction of the adjacent hepatic tissue, and may finally attain to enormous proportions. The embolic abscesses vary in size from that of a pea to that of an orange. The so-called tropical abscesses are usually single--in three-fourths of the cases, according to Rouis;[93] in 62.1 per cent., according to Waring.[94] Of the fatal cases collected by the latter author, 285 in number, a single abscess existed in 177, and multiple abscesses in 108. In 11 per cent. there were two abscesses; in 3.6 per cent., three; and in 5.6 per cent. there were four abscesses. As regards the part of the liver in which abscess occurs, the statistics show a great preponderance in favor of the right lobe. In Waring's collection of 300 cases the right lobe was the {1007} seat of the abscess in 163, or 67.3 per cent.; the left lobe was affected in 16, or 6.6 per cent.; and both lobes in 35, or 14.4 per cent. The preponderance of cases affecting the right lobe is the more striking when it is understood that, other parts being invaded, the right is included with them in the morbid process. In my own cases the right lobe was the seat of the abscess in 70 per cent.

[Footnote 93: _Recherches sur les Suppurations endémiques du Foie_, _loc. cit._, p. 146.]

[Footnote 94: _An Inquiry into the Statistics and Pathology, etc. connected with Abscess of the Liver_, _loc. cit._, p. 125.]

The contents of the abscesses are affected in character by the form of the disease, whether embolic or tropical, by its rate of development, by the condition of the hepatic parenchyma, by the formation of a limiting membrane, etc. In the more chronic cases, surrounded by a dense membrane, the pus is usually laudable or dry and cheesy; in the acute embolic cases the pus is dark brown, ichorous or grumous, and contains a good deal of detritus of the hepatic parenchyma; and in the tropical cases it is of a sanguinolent, dark color, or more frequently of a grayish purulent fluid; and in the acute forms contains much broken-down tissue, whilst in the chronic cases, in direct ratio to their duration, the pus approaches the laudable character. The source of an abscess discharging from the neighborhood of the liver may be ascertained by a microscopical examination and the discovery of the hepatic elements (the cells) in the fluid. Bile may also be present in the pus.

The abscesses not confined by a limiting membrane constantly enlarge by the softening and disintegration of the adjacent liver substance, and those enclosed or encysted after a period of quiescence of variable duration begin active efforts to establish communication outwardly. The point to which a purulent collection in the liver tends becomes an important element in diagnosis and in treatment. As the abscess approaches the surface of the liver the capsule inflames, and if adhesions are not formed more or less sloughing occurs, and the contents are discharged into the abdominal cavity. Adhesions may form to the parietes, an external swelling appear, and after a time discharge take place in the right hypochondrium at some point. Pus may escape at the umbilicus, in the right inguinal region, posteriorly at the sacro-iliac junction, and in other situations. Adhesions may form to the stomach, duodenum, the ascending vena cava, to the diaphragm opening the thoracic cavity, the pericardium, or the mediastinum; and the accumulated pus may thus find a vent. According to Waring,[95] the termination of hepatic abscess is as follows: Of 300 cases, 169, or 56.3 per cent., remained intact--that is, had not advanced beyond the liver; 48 were evacuated by operation, or 16 per cent.; 14, or 4.6 per cent., entered the thoracic cavity; 28, or 9.3 per cent., opened into the right lung; 15, or 5 per cent., entered the abdominal cavity; 7, or 2.3 per cent., opened into the colon; 1 entered the stomach; 3 entered the hepatic vein near the vena cava; 1 communicated with the hepatic ducts, 2 with the right kidney, etc. The termination of 162 fatal cases, according to Rouis,[96] was as follows: 125 proved fatal in consequence of the extent of the abscess or of the severity of the accompanying dysentery; 3 terminated by gangrene of the walls of the abscess; 3 by peritonitis; 12 by opening of the abscess; 2 by rupture of adhesions; 11 by opening of the abscess into the pleura; 2 by intercurrent and 3 by secondary pneumonia. Notwithstanding the differences {1008} in the mode of expressing the conditions, the general results are the same.

[Footnote 95: _An Inquiry into the Statistics and Pathology, etc. of Abscess in the Liver_, _loc. cit._]

[Footnote 96: _Recherches sur les Suppurations endémiques, etc._, p. 149.]

An abscess of the liver having discharged in a favorable way, healing may take place. There may be such an extent of injury--the whole secreting structure of the liver being destroyed--that repair is beyond the power of the organism. The best results are attained when discharge occurs by the most direct route externally; the next, by way of the right lung; the third, by the stomach or intestine. Repair cannot be hoped for when a large part of the normal hepatic structure is destroyed. When the pus escapes the walls of the abscess approximate, and union takes place by connective tissue, leaving a radiated or a merely linear cicatrix to mark the site of the purulent collection. So perfectly does repair take place in suitable subjects that no trace of the lesion may remain.

Those portions of the liver outside the borders of the abscess, and beyond the vascular derangements produced by it, may be entirely healthy. In the cases terminating in recovery the portion of the liver unaffected by abscess continues to functionate normally. More or less of the liver may be destroyed; hence it follows that recovery may be partial. According to the damage done to the proper secreting structure of the organ will the recovery be partial, limited, or complete.

SYMPTOMS.--The existence of an abscess of the liver is determined by systemic or general and by local symptoms, and they may be acute or chronic.

Systemic.--In acute cases the beginning of mischief may be announced by a rigor, but more frequently this indicates the onset of suppuration, and is one of the phenomena of the chronic form. As the disease occurs in this country, a chill takes place suddenly in a case which presents the usual symptoms of proctitis (dysentery) during the course of this affection or soon after its apparent cure; then a febrile movement occurs, and subsequently an irregular intermittent, the rise of temperature being preceded by rigors or mere transient chilliness. With these febrile symptoms there may be associated uneasiness in the right hypochondrium, acute pain, or a feeling of weight and pressure, with jaundice, etc. The fever is septicæmic, intermittent, or remittent if it have any special type. In the septicæmic form the rigors are severe, occur irregularly, sometimes daily, sometimes twice a day, and at intervals of two or three days or longer; the fever rises to a high point--104°, 105°, or higher--and the sweats are profuse. In the intermittent form the fever usually has the quotidian type; some slight chilliness is experienced in the early morning as a rule, and the exacerbation occurs in the afternoon and evening, the sweating being slight toward the morning. More frequently, in the writer's observation, the type of fever has been remittent, with periodical, but not regularly so, exacerbations. In such cases the morning temperature has been at 99° or 100°, and the evening 102° or 103°. Such a range of temperature may be present during three or four weeks or even longer, the abscess gradually making its way outwardly. Conclusions may be drawn from the behavior of the febrile movement as to the character of the local affection, with the limitations imposed by the necessary uncertainty of the data. If the chills are decided rigors, the fever {1009} high, and the sweats profuse, either pyæmic abscesses or large tropical abscesses implicating neighboring organs exist. The simple intermittent, especially the remittent, form of fever suggests abscesses of medium size making their way outwardly, with only partial injury to the parts traversed. In a certain portion of the cases the type of fever changes when a large accumulation of pus takes place; after several weeks of a mild remittent the fever becomes irregularly intermittent with rigors, strong exacerbations, and profuse sweats. In protracted cases the fever assumes the typhoid aspect; there is profound adynamia, dry tongue, sordes, diarrhoea, and the usual symptoms of this state. When the secreting structure of the liver is destroyed to a large extent, the condition of acholia is superadded to the typhoid state.

The pulse is irritable and quick from the beginning of the symptoms. In a few instances a slow pulse, such as occurs in jaundice, has been observed, but generally the number of cardiac contractions is in a direct ratio with the body temperature. When typhoid symptoms supervene in advanced cases the pulse becomes weak and dicrotic.

Not every case presents the symptom sweating. The chronic cases with mild remittent fever have little more than slight moisture of the surface, whilst the acute and pyæmic cases are characterized by profuse sweats. If to an irregular febrile movement, preceded by chills and followed by sweats, there is added the tendency to sweat on all occasions--on slight exertion, on sleeping, under any excitement--suppuration may be suspected.

General malaise, a sense of fatigue and exhaustion, and progressive decline in flesh and strength occur. It is remarkable, however, how some obese subjects preserve their roundness and apparent fulness of habit. Usually, however, emaciation advances pari passu with the progress of the suppuration. The more acute the symptoms, the more rapid the wasting. When an encysted abscess develops in the course of a chronic dysentery, there may be no appreciable change in the condition of the patient properly attributable to the additional lesion. The loss of appetite, the frequent vomiting, and often the dysenteric troubles, contribute materially to the exhaustion and the wasting of the tissues. The stomachal derangements may be present with the initial symptoms, but they are usually more pronounced when the abscess attains to considerable size.

A peculiar tint of the skin, especially of the face, is observed in those cases without jaundice. There is an earthy or sallow hue, which to the practised eye signifies suppuration. Jaundice is present in a less proportion of cases. In 13 of Waring's cases the skin is said to be sallow. In Rouis's collection icterus was present in 17 per cent., or 26 times in 155 patients. According to Waring, jaundice is rarely present. In the 12 cases in my own hands actual jaundice was not present in one, but 9 had an earthy hue or presented some yellowness of the conjunctiva. In fact, jaundice does not have the importance as a symptom which might, a priori, have been expected.

The mental condition of these subjects is that of depression. They sleep poorly, are disturbed by vivid dreams of a horrifying character, and the nocturnal sweats increase the tendency to wakefulness. Hypochondria, or at least marked symptoms of mental depression, as {1010} Hammond[97] has shown, are present in many cases. So frequent, indeed, seems to be the association of a depressed mental state with hepatic abscess that in every case of the former the liver should be carefully explored. Hammond goes so far as to say that in every case of hypochondriasis puncture of the liver with the aspirator needle should be practised when any symptom, however indefinite, indicates the existence of an abscess. Besides the condition of hypochondriasis in many cases, there may be stupor, hebetude of mind, confusion due to acholia, cholæmia (Flint's cholesteræmia), when a large part of the liver structure is destroyed.

[Footnote 97: _Neurological Contributions_, vol. i. No. 3, p. 68: "On Obscure Abscesses of the Liver, their association with Hypochondria and other Forms of Mental Derangement, and their Treatment."]

Sweating has already been referred to as a phenomenon connected with the febrile movement. It is necessary to state further that this may vary in amount from a mere moisture of the surface connected with sleep, or it may be a profuse diaphoresis with which the febrile paroxysm terminates. As a systemic symptom, sweating is strongly suggestive of suppuration, and may therefore be extremely significant, in this connection, of suppuration in the liver. According to Waring, of 75 cases specifically interrogated on this point, 72 presented this symptom. Rouis refers (p. 123) to it as very constantly present, coming on chiefly at night--sometimes generally over the body, sometimes limited to the head, and always accompanied by an accelerated pulse.

The urine in cases of hepatic abscess varies; it is never normal. There may be merely an excess of urates--a symptom common enough in all febrile affections and in suppuration. It is usually high-colored, deficient in urea, and contains leucin and tyrosin, and not often bile-pigment, except when jaundice is present, which, as we have seen, is rather uncommon.

It should be borne in mind that whilst the above-described mental and cerebral and other symptoms are often present, they are by no means invariably so. There are cases, usually of encysted abscess, in which no functional disturbance of any kind exists. But the systemic symptoms are by no means so important as the local. To these we must now direct attention.

Local.--The position, size, and shape of the liver are not without significance, but it is strictly correct to say that an abscess of the liver may exist without any change in the size of the organ or in its relations to the surrounding organs. In 2 of 12 cases in the hands of the writer there was no evidence of enlargement of the right hypochondrium, but a difference in circumference of half an inch was ascertained in favor of the left side. In 4 cases there was no appreciable change in the size of the hepatic region; in one-half there was an increase in the area of hepatic dulness. In one of the cases in which the left side was the larger the abscess was of enormous extent, and discharged by the stomach and intestine. The enlargement of the liver may be very great. In one instance observed by the author the abscess reached to the upper border of the third rib. Rarely does the dulness extend more than two fingers' breadth below the inferior margin of the ribs, although cases are reported in which the enlarged organ reached to the crest of the ileum. As a rule, the diaphragm is pushed up and the lung displaced, rather than the dulness is extended downward. When the first tumefaction {1011} due to the initial congestion takes place, the organ may be much larger than subsequently, the pus becoming encysted and the normal state outside of the area of suppuration being restored. The purulent collection in a large proportion of the cases taking place in the right lobe, the extension of dulness is in the same lines as the normal. When, however, the right lobe is the seat of abscess, or a purulent collection forms around an impacted calculus, the swelling may appear in the outer border of the epigastrium next the ribs, and the increased area of dulness will be across the epigastrium and occupying the superior portion of this region. The general experience on these points corresponds to my own. Thus, according to Waring, there was an evident enlargement of the liver in 90 cases, and no enlargement in 11. In most cases the increase in size gives the impression of a fulness or hardness of the liver or of a diffused swelling or tumor of the epigastrium. In some instances the right hypochondrium is bulged out, the intercostal spaces widened, and the side appears to be or is actually elevated, and occasionally enlarged veins form, as in cases of the obstructed portal circulation of cirrhosis. In a case recently presented at Jefferson College Hospital clinic by the author, a globular swelling formed in the walls of the abdomen just below the inferior margin of the ribs near the site of the gall-bladder, and was held by an eminent surgeon to be a tumor of this locality; but it had the history of an hepatic abscess, and ultimately proved to be one. Rouis furnishes statistical evidence of the time when the increase in size of the liver occurs with respect to the other symptoms. He has noted an enlargement of the organ 73 times in 122 cases. Of 51 cases, the liver was enlarged in 12 before suppuration, in 22 at the onset of suppuration, and in 17 after suppuration was established. In 49 examples the liver was enlarged in 2 before any other symptom was manifest, in 8 at the onset of symptoms, and in 39 after the symptoms were well declared.

Fluctuation is not referred to by the writers in general, and there are no statistical data on this symptom, so far as our observation extends. No symptom could be more uncertain in all doubtful cases. When a large accumulation has taken place and the parietes of the sac are thin, fluctuation may be detected, but it cannot then be regarded as decisive. When an abscess in the interior of the right lobe is encysted, no fluctuation can be effected. The best mode of eliciting fluctuation, according to Hammond, is to place the extremities of the fingers of the left hand in the depression between the ribs over the most prominent part of the right hypochondrium, and gently tap with the fingers of the right hand the right border of the epigastrium. In 3 out of 12 cases this method has apparently elicited fluctuation in my own experience. The elasticity of the hepatic structure is such that the method of palpation, however practised, must return a sensation nearly allied to that of fluctuation in a purulent accumulation. It is certain, therefore, that errors of observation are liable to occur, and hence conclusions based on an apparent fluctuation should be accepted with caution; under any circumstances it should be very distinct, and even then should not be acted on unless supported by other suggestive evidence.

The uneasiness or pain felt in the right hypochondrium varies greatly according to the position of the abscess, the degree and kind of pressure exerted on neighboring organs, and the period of its development. When {1012} the peritoneal layer of the liver is involved, there will usually be acute pain, and this happens at two periods--when the abscess first forms from an impacted calculus or from any cause which includes the peritoneum, and subsequently when the pus, making its way from the liver, excites inflammation in the peritoneal investment of the liver, of the diaphragm, or affects ultimately the pleural membrane. In the so-called pyæmic abscesses there is very little pain, and in the case of the large single abscess in the interior of the right lobe there is rather a sensation of weight or of heaviness, of dragging than of acute pain. When the capsule of the liver is put on the stretch or the peritoneal investment is inflamed, then acute pain may be felt. More or less pain or local distress is, on the whole, a usual symptom. According to Rouis,[98] local pain is present in 141 out of 177 cases, or in 85 per cent. The statistics of Waring[99] closely correspond, for of 173 patients affected with this malady, in 153 there was more or less pain referable to the affected organ. The position of the pain has some influence in determining the seat of the malady, and often indicates the position of the abscess. As respects the character of the pain, there is little uniformity; in general it is a tensive, heavy, throbbing sensation, but under the circumstances above mentioned this may have an acute or lancinating character, as when the capsule or the peritoneal investment of the organ becomes involved.

[Footnote 98: _Recherches, etc._, _loc. cit._]

[Footnote 99: _An Inquiry, etc. into Abscess of the Liver_, _loc. cit._]

Besides the pain directly referable to the liver there are painful sensations felt in the neighboring parts, of very considerable significance. These are often described as sympathetic pains, and are referred to the shoulder--to the right shoulder when the right lobe is the seat of mischief, and to the left shoulder when the abscess forms in the left lobe of the liver. Although this statement has many limitations, it is not without diagnostic importance. Rouis ascertained the existence of the shoulder pain in 17 per cent. of the cases, or in 28 in a total of 163. Waring reports that this symptom was observed in 52 in a total of 76 cases. The right shoulder seems to be affected in about the same ratio as the right lobe of the liver in 25 times out of 26 cases, according to Rouis. The shoulder pain appears at the same time, in a majority of cases, as the hepatic pain, but it is very capricious. It is most frequently at the top of the shoulder, but it may be at the end of the clavicle, in the scapula, or extend down the arm. Its duration is very irregular, appearing occasionally during the existence of the disease, coming on at the outset, and lasting weeks or months, or only felt on pressure over the liver, on coughing, or on taking a full inspiration. The character of the pain is equally uncertain. It is usually heavy, tensive, stinging, or may be merely a sensation of soreness or of uneasiness or of weariness. The behavior of the shoulder pain is partly explicable by reference to the path by which the reflex is conveyed. As Luschka[100] has shown, the filaments of the phrenic nerve supplied to the suspensory ligament and capsule of the liver, put on the stretch or irritated, convey the impression to the cord, and it is reflected over the sensory fibres of the fourth cervical distributed to the shoulder. Rouis reports an instance in which the deltoid was wasted.

[Footnote 100: Quoted by Thierfelder, _op. cit._]

The decubitus of patients affected with hepatic abscess is often {1013} extremely characteristic. To obviate the pressure on the swollen and inflamed organ the position assumed is right lateral-dorsal, the body inclined to the right, the right thigh flexed on the pelvis, and the spinal column so curved as to relax the abdominal muscles of the right side. When the pain and tenderness are not great there may be frequent changes of position, but in repose the lateral-dorsal decubitus is assumed. When the suppuration is well advanced and the accumulation large, the patient keeps in that position nearly constantly. If pressure interferes with the normal play of the lungs, and dyspnoea is produced on assuming the recumbent posture, the attitude taken expresses this state also: then the decubitus is lateral and partly dorsal, but the body is raised to a half-upright. There are many exceptions to these rules. Some lie easiest on the back, some on the left side; but it is quite certain that much the largest number, when uninfluenced by special circumstances, naturally place themselves as above described.

Jaundice is amongst the rarer symptoms. Rouis finds it to be present in 17 per cent. of the cases, Thierfelder in 16 per cent., and Waring in somewhat less than 6 per cent. Referring to my own observation, jaundice has rarely been present, but some yellowness of the conjunctivæ and a faint yellow tint of the skin generally have been evident. The peculiar aspect of the countenance connected with suppuration has rarely been wanting. When jaundice does occur, it is referable to two conditions--to a catarrhal swelling of the bile-ducts, which may be coincident with the onset of the suppurative inflammation; to the pressure of the abscess on the hepatic or common duct, which must happen at a late period.

As an abscess of the liver forms and enlarges, pressure is exerted on neighboring organs, producing very decided disturbances. Nausea and vomiting, anorexia, a coated or glazed tongue, diarrhoea or dysentery, are amongst the disorders of this kind involving the digestive apparatus. Each of these symptoms will require examination.

There is nothing characteristic in the condition of the tongue which does not belong to suppuration in any situation. Nevertheless, there are some appearances that have a certain value in conjunction with other diagnostic signs. At the onset of the suppurative inflammation the tongue is more or less heavily coated, but as the case proceeds it becomes dry and glazed in parts, whilst covered with a well-defined membrane-like crust at the base and margins. This appearance is very characteristic of the cases of suppuration, the abscess enlarging. In a very important case observed by me lately there was a well-marked diphtheritic-like exudation of the tongue and fauces toward the termination of the case, the membrane forming as the pus accumulated. This appearance was coincident with a typhoid state.

Nausea and vomiting appear with the beginning of symptoms, are associated with the general signs of systemic disturbance, and are especially prominent when an accumulation of pus takes place, being due under these circumstances to pressure on the hepatic and solar plexuses or to direct encroachment on the stomach--probably to both causes. The frequency and persistence of the vomiting are points of much diagnostic importance, according to Maclean[101] and Fayrer,[102] which I {1014} am able to fully confirm from my own experience. The matters ejected by vomiting consist of the contents of the stomach--glairy mucus, the accumulation in the gall-bladder, altered blood (coffee-grounds)--and the contents of the abscess if it discharge by the stomach. The vomiting is most apt to occur during the febrile exacerbation or at the time of sweating. The statistics are conclusive as to the frequency of vomiting as a symptom. Of 84 cases in which special reference was made to this point, in 74 nausea or vomiting existed. In my own experience this symptom has never been wanting.

[Footnote 101: "The Diagnostic Value of Uncontrollable Vomiting," by W. C. Maclean, _Brit. Med. Journ._, August 1, 1873.]

[Footnote 102: _Ibid._, September 26, 1873.]

The relation between abscess of the liver and dysentery has been much discussed. Under the head of Causes the influence of dysentery as a pathogenetic factor has already been examined. We have now to study its symptomatic relations. A considerable proportion of the cases occurring in this country have been preceded by proctitis--simple, sporadic dysentery affecting the rectum. In India a close relationship has been traced between ulcerations of the intestinal canal and abscess. According to Waring, 75 per cent. of the cases have occurred in those who were actually suffering from dysentery or recent or old ulcerations. As observed by Rouis in Algiers, out of 143 cases there were 128 with dysentery, or 90 per cent. Budd[103] long ago maintained that a peculiar poison generated at an open ulceration in the intestine was the true cause. Moxon,[104] Dickinson, and others have lately reaffirmed this explanation. A case by the latter[105] casts a strong light on this question: A patient had extensive dysenteric ulceration of the intestine and an abscess of the liver, without any symptoms indicating their existence. Such a case teaches the instructive lesson that dysenteric ulcerations may escape detection, and hence the connection between abscess and the intestinal lesion remains unknown. In a small proportion of cases--about 5 per cent.--dysentery is a result, apparently, of hepatic abscess. Whether the relation is admitted to exist or not, it is a curious fact that in so many cases ulcerative disease of the intestinal canal accompanies the hepatic affection. Hemorrhoids, prolapse of the rectum, gastro-intestinal catarrh, etc. are produced by the pressure of an enlarging abscess on the portal vein.

[Footnote 103: _Diseases of the Liver_, 3d ed., p. 82.]

[Footnote 104: _Pathological Transactions_, 1862 and subsequently. Numerous cases are recorded in the various volumes up to 1880.]

[Footnote 105: _Ibid._, vol. xiii. p. 120.]

The urine contains bile-pigment when jaundice is present, is usually loaded with urates, and the amount of urea may be deficient when much of the hepatic tissue is destroyed.

From the beginning of symptoms some cough is experienced: it is short and dry, but after a time in many cases the cough is catching and painful, and finally may be accompanied by profuse purulent expectoration. The breathing is short and catching when by the upward extension of the mischief the diaphragm is encroached on, and may become very painful when the pleura is inflamed. Ulceration of an abscess into the lungs is announced by the signs of a local pleuro-pneumonia--by the catching inspiration, the friction sound, the crepitant râle, the bronchophony and bronchial breathing, and bloody sputa usually, etc. Some time before the abscess really reaches the diaphragm, preparation is made in the lung for the discharge through a bronchus. The author has seen {1015} many examples of this, and a very striking illustration of the same fact is afforded in a case by Dickinson,[106] in which an abscess holding about four ounces was contained in the upper part of the right lobe; its walls were irregular and not lined by a limiting membrane. It is further stated that the "right pleura was coated with flocculent lymph, and the cavity contained serous fluid," etc. Here, in advance of the abscess, preparation was made for its discharge through the lung. The tendency of an abscess of the abdomen to external discharge is manifested in two directions: those of the upper part tend to discharge through the lungs, those of the lower part through the natural openings below. Abscesses of the liver come within the former rule, but it is not of invariable application, since some discharge by the stomach or intestine, some externally; yet a large proportion make their way through the lungs. Another symptom referable to the pulmonary organs in cases of hepatic abscess is singultus, or hiccough. This is a symptom of the period of discharge rather, and is often extremely protracted and exhausting. Pericarditis occurs in those cases in which discharge takes place in this direction, and it may develop, as does pleuritis, in advance of any change in the diaphragm. This preparation of the thoracic organs for external discharge seems almost like a conscious purpose, as if an intelligent supervision of these processes were exercised.

[Footnote 106: _Transactions of the Pathological Society_, vol. xxxii. p. 127.]

COURSE, DURATION, AND TERMINATION.--As the facts already given have sufficiently shown, the course of abscess of the liver is extremely uncertain. From the beginning to the end there may not be a single indication of its presence. On the other hand, a well-marked case is perfectly characteristic. Abscesses of the liver are acute and chronic--the former of short duration, accompanying pyæmia, portal phlebitis, and similar conditions; the latter, arising in the course of chronic dysentery or from unknown causes, especially if encysted, remaining latent for weeks or months. The course of an abscess is much influenced by the direction taken by the pus in the attempt at discharge. This portion of the subject requires careful statement and thorough treatment, and we therefore present it somewhat in detail. Beginning with his individual observations, the abscess in the author's 12 cases discharged--3 externally, 5 by the lungs, and 4 by the stomach or intestines. In Waring's[107] collection of 300 fatal cases, 169 remained intact at death, 48 were operated on; consequently, only 83 are left for the purpose of this comparison. Of 83 cases of hepatic abscess discharging spontaneously in some direction, 42 escaped into the thoracic cavity or by the right lung (in 28); into the abdominal cavity (15) or stomach (1) or intestine (7), 23; externally 2, besides in special directions to be hereafter referred to. Rouis[108] has tabulated the results in 30 cases of abscess fatal without an operative influence. Of these, 2 discharged externally, 17 by the thorax (15 by the lung), 5 by the stomach, 4 by the intestine, and 2 by the biliary canals.

[Footnote 107: _An Inquiry, etc. into Abscess of the Liver_, _loc. cit._, p. 131.]

[Footnote 108: _Recherches sur les Suppurations endémiques du Foie, etc._, _loc. cit._, p. 148.]

The appearances presented when the discharge takes place through the external parts are by no means uniform. When the epigastric or umbilical region is the point of discharge, a globular tumor forms, which may {1016} be mistaken for a fibroid or fatty growth; softening in the centre of the mass occurs, and ultimately the pus is discharged. If the pus makes its way outwardly through the right hypochondrium, the tumor formed is furrowed by the attachment to the ribs, and several openings usually occur. The pus may burrow under the skin for some distance and point in the axilla, or, making its way along the suspensory ligament, emerge at the navel, or, descending, appear in the lumbar region or under Poupart's ligament.

As the statistics prove, the most usual route for discharge to take place is by the thoracic cavity, especially the right lung. Some time in advance of an opening in the diaphragm a localized pleuro-pneumonia occurs, adhesions form between the pulmonary and costal pleura, and a channel is tunnelled out for the passage of the pus to a bronchus. The discharge of pus suddenly occurs after some days of cough and bloody expectoration. Even in favorable cases the amount is so large that the patient has extreme difficulty in disposing of it, and in unfavorable cases, the quantity being large, the patient's life is ended by apnoea. In still other cases an extensive purulent accumulation may form in the pleural cavity, the lung is compressed, and all the phenomena of an empyema superadded to those of a hepatic abscess. In a case reported by Westphalen[109] all the bile secreted by the patient came out by an opening in the fifth intercostal space. The empyema thus induced may indeed be the principal lesion, as in the case of the late Gen. Breckenridge, on whom thoracentesis was performed by Sayre of New York, and in a case reported by Löwer.[110] So far from this being uncommon, as asserted by Thierfelder, when an abscess of the liver approaches the diaphragm inflammatory symptoms begin on the pleural side, and thus pyothorax may occur in advance of the perforation of this septum.

[Footnote 109: _Deutsches Archiv für klin. Med._, 1873, Band xi. p. 588.]

[Footnote 110: _Berliner klinische Wochenschrift_, 1864, p. 461.]

The opening of an hepatic abscess into the pericardium is rare, since in Waring's collection of 300 fatal cases there was not one. When it does occur, pain is experienced about the heart; the action of the organ becomes irregular; præcordial anxiety and oppression are felt; suffocative attacks occur; and very soon the symptoms of pericarditis arise. Perforation of the ascending vena cava or of the hepatic vein happens in about 2 per cent. of the cases. When a quantity of pus is thus turned into the circulation, disastrous results follow, not so much from the infective nature of the pus as from the sudden increased pressure within the vascular system and the labor imposed on the heart, already failing.

The escape of the pus into the peritoneal cavity occurs in about 11 per cent. of the cases of spontaneous evacuation, according to Waring. Of the 162 fatal cases collected by Rouis, 14 opened into the peritoneum--about the same proportion as Waring gives. When discharge takes place into the peritoneum, the patient passes into a condition of collapse, or peritonitis is excited and rapidly proves fatal. In rare instances the inflammatory reaction is restricted to a small area, ulceration takes place through the abdominal parietes, and thus discharge is effected.

An opening may be made into the intestine or into the pelvis of the kidney. In the former case pus is discharged by stool or by vomit, and often in enormous quantity; in the latter by the urine, frequent and {1017} painful micturition, with much pus, being the evidence of the accident. In either case communication may be kept up with the abscess, and the patient be worn out with the exhausting discharge maintained by the intercommunication between the abscess and the canal through which discharge takes place.

Cases of hepatic abscess prove fatal without perforation. In Waring's collection of 300 cases, 169 remained intact, in the words of the author--that is, did not extend beyond the boundaries of the liver. Of 203 cases collected by Rouis, 96 did not extend beyond the liver. According to Thierfelder, about one-half of the cases of hepatic abscess perforate the liver. These statistics therefore closely correspond, and the general conclusion is very nearly expressed in the formulated statement of Thierfelder.

The duration of hepatic abscess cannot readily be expressed in figures. The acute cases terminate early by reason of the various complicating conditions. The chronic cases are much influenced in their duration by the presence of a limiting membrane, for if this be formed the duration will be protracted over weeks or months; and those cases not thus confined are necessarily of shorter duration. A period of latency may result when the extension of the morbid process is thus hindered. Forming a conclusion from the general conduct of the cases, it may be said that the duration of hepatic abscess is from two weeks to six months. Of 220 cases collected by Waring, the average duration was 39 days. Rouis fixes the average duration in 179 cases at 60 days. Of Waring's cases, the largest number (59) terminated in from 10 to 20 days; whilst Rouis places the maximum number (104) at from 11 to 60 days, the shortest duration of any case being 10 days, and the longest 480 days.

The termination may be accelerated by the manner of discharge, as when the abscess opens into the ascending vena cava, into the sac of the pericardium, or into the peritoneal cavity. In my own cases, carefully selected for these observations, death occurred in one during discharge by the right lung, one within twelve hours after discharge by the intestine, and one within ten days after discharge by the stomach and intestine, the mortality of the whole being 75 per cent. In Waring's collection of 300 fatal cases, 169 died whilst the abscess was still intact--that is, in the liver.

The mortality from abscess of the liver is very large. In Rouis's collection of 203 cases, 162 died, 39 recovered entirely, and 2 improved; 80 per cent., therefore, proved fatal. According to De Castro,[111] whose observations were made at Alexandria, Egypt, 93 in 208 cases died, this being 72.5 per cent. According to Ramirez,[112] of 11 cases of which an account is given in his memoir, 10 died and 1 recovered--a mortality of 90 per cent. De Castro (p. 40) also gives the results arrived at by the Medico-chirurgical Society of Alexandria, who collected 72 cases of abscess, of which 58 died, making the percentage of deaths 80.5. Various circumstances besides the abscess affect the result. An early successful operation, the mode of discharge, the amount of hepatic tissue destroyed by the {1018} suppuration, the extent of pre-existing lesions--especially ulcerations of the intestinal canal--are important factors in the result. In respect to some of these we have valuable statistical data. The discharge through the lungs is the most favorable route, next by the parietes of the abdomen, and lastly by the intestinal canal. One-half of those cases in which discharge is effected by the right lung get well. This is my own experience, and it accords with the observations of Rouis, of De Castro, and others. Rouis gives the result in 30 cases of hepatic abscess discharging by the right lung; of these 15 recovered. Of 25 cases observed by De Castro, discharging by the lungs, 19 recovered. Next to the discharge by the bronchi, the most favorable mode of exit is externally, through the parietes of the abdomen; much less favorable is by the stomach or intestine; but still more fatal is the discharge into the cavity of the peritoneum. When the abscesses are multiple and due to pyæmia, the termination is always in death. The numerous lesions besides the hepatic accelerate the fatal issue. In the case of large single abscesses the result is in a great measure due to exhaustion from protracted suppuration. When in addition to the formation of a great quantity of pus there is frequent vomiting and rejection of aliment, the failure of strength is proportionally rapid. In favorable cases, after an abscess is evacuated through the right lung, recovery takes place promptly. When the discharge occurs through the abdominal wall, the process is much slower, and often fistulous passages with several orifices, very slow to heal, are formed. Complete recovery may ultimately take place. The recovery will be incomplete in those cases with large loss of hepatic substance, especially when this coincides, as it usually does, with catarrh, ulceration, and other lesions of the intestinal tube. Again, the recovery will be incomplete in those cases where there are imperfect healing of the abscess site and a fistulous communication with the exterior.

[Footnote 111: _Des Abcès du Foie des Pays chauds, et de leur Traitement chirurgical_, _loc. cit._, p. 40, Paris, 1870.]

[Footnote 112: _Du Traitement des Abcès du Foie, Observations receuilles à Mexico et en Espagne_, par Lino Ramirez, M.D., Paris, 1867, _loc. cit._]

It is possible for the arrest and healing of a suppurative inflammation of the liver to take place without discharge. Under such circumstances the watery part of the pus is absorbed, the solid constituents undergo a fatty metamorphosis, are emulsionized, and thus absorbed, and gradually closure of the damaged area is effected by a connective-tissue formation. We must, however, accept with caution those examples of this process which are supposed to have occurred because radiating cicatrices are discovered on the surface of the liver. In a case of hepatic abscess discharging through the lung, known to the writer, after death, which occurred fifteen years subsequently, there was no trace of the mischief, so perfectly had repair been effected. Radiating cicatrices are so often of syphilitic origin that they cannot be accepted as proof of the former existence of an abscess.

DIAGNOSIS.--He who finds the diagnosis of abscess of the liver easy under all circumstances can have had but little experience with the numerous difficulties in the way of a correct opinion. There are cases so plain that the most casual inspection suffices to form a conclusion; there are cases so difficult that the most elaborate study fails to unravel the mystery. The maladies with which hepatic abscess may be confounded are echinococcus of the liver, dropsy of the gall-bladder, cancer, abscess of the abdominal wall, empyema, or hydrothorax, etc. As regards echinococcus, the difference consists in the slow and painless enlargement characteristic of echinococcus, and the absence of any symptoms other than those {1019} due to the mere pressure of the enlarging mass. In abscess there may be no apparent enlargement, or the increase in the area of dulness may be very great, or after a period of increase of size there may be contraction due to the formation of pus, and hence limitation of the inflammation; finally, the accumulation of fluid may be sufficient to cause dulness up to the inferior margin of the second rib. There are no corresponding changes of size in the echinococcus cyst. Furthermore, abscess of the liver large enough to be recognized by the increased dimensions of the organ will be accompanied by more or less pain in the right hypochondrium and by a septicæmic fever. On the other hand, an echinococcus tumor is not accompanied by fever, pain, or tenderness, and it has that peculiar elastic trembling known as the purring tremor. The most certain means of differential diagnosis is the use of an aspiration-needle and the withdrawal of a portion of the fluid. The presence of pus with hepatic cells will be conclusive of abscess, whilst a serous fluid with echinococci hooklets will prove the existence of the echinococcus cyst.

In cases of dropsy of the gall-bladder there are no febrile symptoms, no chills, and the tenderness when present is limited to the pyriform body, the seat of the accumulation of fluid, and no general enlargement of the liver can be made out. At the point of swelling fluctuation may be detected, or if the gall-bladder is filled with calculi the sensation imparted to the touch is that of a hard, nodular body of an area and position corresponding to that of the gall-bladder. Tapping the gall-bladder, an easy and safe procedure, will resolve all doubts. When an impaction of a gall-stone is the cause of abscess, the clinical history is eminently characteristic: there are attacks of hepatic colic, after one of which the chills, fever, and sweats belonging to hepatic abscess occur.

The differentiation of cancer of the liver from abscess rests on the following considerations: In cancer there is slow enlargement, with pain; a more or less nodular state of the organ without fluctuation; usually ascites; no rigors; no fever and sweats. In abscess the liver may or may not be enlarged; there are rigors, fever, and sweating, and the surface of the organ, so far as it can be reached, is smooth and elastic, and it may be fluctuating. Cancer happens in persons after middle life, develops very slowly, and is accompanied by a peculiar cachexia; abscess occurs at any period, very often succeeds to or is accompanied by dysentery and by the usual phenomena of suppuration.

It is extremely difficult to separate an abscess in the abdominal wall, in the right hypochondrium, or a tumor in this region, from an abscess of the liver. The history of the case, the existence of a dysentery or of an apparent intermittent or remittent fever before the appearance of a purulent collection, will indicate the liver as the probable source of the trouble. Attention has already been called to a case in which an abscess of the liver was supposed by an eminent surgeon to be a tumor of the abdominal wall. The history in this case of an obstinate remittent fever, followed by the appearance of a tumor of the hypochondrium and by a preliminary discharge at the umbilicus, clearly indicated the nature of the trouble. In the absence of any history of the case it is extremely difficult to fix the origin of a suppurating tumor originating, apparently, in the depth of the right hypochondrium.

Mistakes are frequently made in the case of an abscess developing in {1020} the convexity of the right lobe of the liver and pushing the diaphragm up to the third, even to the second, rib, and thus producing conditions identical with empyema of the right thorax. Such instances of hepatic abscess are peculiarly difficult of recognition, because, the physical signs being the same as those of empyema, the differentiation must rest on the clinical history. In cases of empyema proper the effusion in the chest is preceded by pain and accompanied by an increasing difficulty of breathing; in hepatic abscess there are, as a rule, symptoms of disturbance in the hepatic functions, fluctuation in the hepatic region, dysentery, etc., long anterior to any disturbance in the thoracic organs. Again, empyema may be a latent affection, without any symptom except some obscure pain and a progressive increase in the difficulty of breathing; on the other hand, abscess of the liver is preceded by symptoms of liver disease and of associated maladies. A dry, purposeless cough is present in many cases of abscess; a painful cough with bloody expectoration occurs when preparation is making for discharge through the lungs.

Errors of diagnosis are liable to occur in the consideration of symptoms unquestionably hepatic in origin. Thus, the intermittent fever accompanying some cases of hepatic colic, like the shivering fits and fever which occur in cases of nephro-lithiasis, may be confounded with the septicæmic fever of hepatic abscess. An attentive examination of the attendant circumstances, especially a careful survey of the right hypochondrium, can alone determine the nature of the symptoms. In all doubtful cases the experimentum crucis of puncture with the exploring-needle becomes a measure of necessity. When all diagnostic indications are at fault, the needle of the aspirator may decide the issue. An abundant experience has shown that a needle of suitable size may be introduced into the right lobe without any ill result--often, indeed, with distinctly good effects when there is no suppuration or when pus cannot be detected. In the present state of our knowledge it cannot be determined why puncture of the organ should be beneficial in cases having the symptomatic type of hepatic abscess when none exists; but of this fact there is no doubt.

TREATMENT.--As the formation of pus is coincident with or causative of the first symptoms, it is obvious that treatment directed to prevent an abscess can rarely succeed. Yet it is probable that now and then an abscess just forming has been arrested and healing effected. At the onset of symptoms some large doses of quinine, with a little morphine (scruple j of the former and 1/8 gr. of the latter), every four or six hours, may have a decided curative effect. During the course of the septicæmic fever, with its chills and febrile exacerbations, quinine in full doses and alcohol according to the conditions present are necessary remedies. As the symptoms develop saline laxatives are useful until the formation of pus becomes evident, when all perturbating treatment of the intestinal canal should cease. If dysentery be present when the hepatic symptoms arise, it should be cured as promptly as possible; and of all remedies for this purpose, ipecac given in the usual antidysenteric quantity offers the best prospect of relief. For the dysentery which succeeds to abscess, and is probably, in part at least, dependent on portal obstruction, the mineral astringents, as copper sulphate, are the most effective remedies. As far as practicable, after an abscess has formed the intestinal canal should be kept quiet, for any considerable disturbance will {1021} endanger the escape of pus into the peritoneal cavity. Persistent vomiting is very significant of pressure by an enlarging abscess in the stomach, and usually signifies an abscess associated with impacted calculus. It is important in such cases to maintain, as far as can be done, a quiescent condition of the stomach, for the purpose of preventing rupture into the peritoneal cavity and to favor the nutrition which is seriously endangered by the repeated vomiting. Effervescent soda powders are very useful; carbolic acid in solution, or creasote-water with or without bismuth, is beneficial; champagne, very dry and highly effervescent, has been, in the writer's hands, remarkably efficient. As food becomes a most important need in such cases, milk and lime-water, wine-whey, egg-nog, and similar aliments must be given in small doses and frequently. Nutrient enemata, prepared from eggs, milk, and beef-juice, with the materials for digestion--acid and pepsin--may be made to supplement the stomach, but such efforts have a very limited utility, owing to the state of the hepatic functions and to the obstruction of the portal circuit. In all cases it is necessary to maintain the strength by suitable aliment and the judicious use of stimulants. The long-continued and profuse suppuration makes an enormous demand on the vital resources of the patient, and this must be compensated by suitable food-supplies.

As the formation of pus has taken place in most cases when symptoms have begun, the question of highest importance is, Shall the pus be evacuated? The statistical evidence relating to this question becomes then an extremely valuable guide. As in almost all cases of puncture of the liver for the evacuation of an abscess some part of the liver substance must be passed through, it is necessary to note how far this can be done without inflicting permanent injury on the organ. Hammond has punctured the liver in eight cases without the presence of an abscess, and of these not one has presented any unfavorable symptom. The author has punctured the liver, penetrating well into the interior, in two cases in which no abscess was discovered, but the symptoms of hepatitis existed, with the effect to improve the symptoms. In Condon's[113] collection of 11 cases there were 8 of abscess evacuated by the trocar, and 3 of acute hepatitis in which abscess had not formed, but in which the puncture procured the most decided amelioration of the symptoms. We have heretofore referred to Hammond's experience in the puncture of the liver in cases of hypochondriasis, this condition appearing to depend in some instances on the presence of abscess. In a number of instances abscesses did exist, but in many others there was no apparent lesion of the liver, but in these cases the puncture of the organ was without any ill result. Testimony to the same effect is given by Ramirez,[114] who asserts that he had not known a single instance in which any ill result followed puncture of the liver. It may therefore be regarded as certain that exploratory puncture of the organ for the purpose of diagnosis as well as for treatment can at any time be performed with suitable precautions in respect to the size, condition, and character of the instrument.

[Footnote 113: "On the Use of the Aspirator in Hepatic Abscess," Dr. E. H. Condon, _The Lancet_ (London), August, 1877.]

[Footnote 114: _Du Traitement des Abcès du Foie, Observations recueilles à Mexico et en Espagne_, par Lino Ramirez, M.D., Paris, 1867, p. 65.]

The authorities of most experience are agreed that, provided with the {1022} aspirator, the abscess may be punctured as soon as a purulent collection can be ascertained to exist. The obvious reason for tapping the abscess is its tendency to extend in various directions, destroying the hepatic substance. In those examples confined by a limiting membrane, after a time of inactivity ulceration begins, and the pus seeks an outlet in some direction. The early evacuation by a suitable aspirator becomes then a measure of the highest necessity. The good effects of puncture with even such a crude instrument as the trocar is well exhibited in the statistics collected by Waring.[115] In a collection of 81 cases opened by the knife or trocar there were 66 deaths, making the percentage of recoveries 18.5. In these cases the operative procedure was a final measure, and the mischief had been done almost if not quite in its entirety. The statistics of Waring are concerned with a period anterior to 1850. Although they demonstrate the value of the trocar and evacuation of the abscess, as compared with the results of the natural course of the disease, the far greater success of the treatment by the aspirator is shown by the statistics of recent times. Thus in McConnell's[116] 14 cases, also of India, in which the aspirator was used to empty the sac, 8 recovered and 6 died. The statistics of Waring may also be profitably compared with those of Condon,[117] in which, of 8 cases of abscess evacuated by the aspirator, 4 recovered, or 50 per cent. They may also be compared with Sach's[118] cases, 21 in number, of which 8 recovered, or 38 per cent., and with the cases of De Castro[119] of Alexandria, who reports 22 large abscesses operated on, the proportion of cures being 31.8 per 100, and 10 small abscesses, the proportion of cures being 70 per 100. In a case seen in consultation with Collins, in this city, last year, the aspirator was used by us about three months after the symptoms of abscess declared themselves. About a quart of bloody pus was drawn off at once, the opening sealed, and no subsequent accumulation occurred, the patient entirely recovering, for after a year he was seen (December, 1884) in complete health. From these data we draw the important conclusion that early operation is desirable. This fact may be formulated in the expression: In all cases of hepatic abscess use the aspirator whenever the presence of pus is made out. When the abscess is large, and especially when communication is established with the parietes of the abdomen, a free opening, followed by the insertion of a drainage-tube, is the proper method to pursue. If the pus reaccumulates, it is good practice to inject the cavity with tincture or compound solution of iodine after the pus is drawn off, provided the dimensions of the abscess are not too great.

[Footnote 115: _An Inquiry into the Statistics of Abscess of the Liver_, _loc. cit._]

[Footnote 116: "Remarks on Pneumatic Aspiration, with Cases of Abscess of the Liver treated by this Method," _Indian Annals of Medical Science_, July, 1872, quoted.]

[Footnote 117: _Lancet_, _supra_.]

[Footnote 118: _Ueber die Hepatitis der heissen Länder, etc._, von Dr. Sachs in Cairo.]

[Footnote 119: _Des Abcès du Foie des Pays chauds, et de leur Traitement chirurgical_, par le Docteur S. V. de Castro (d'Alexandrie d'Egypte), Paris, 1870, p. 59.]

As regards the mode of proceeding, the following are useful rules: Ascertain, if possible, the existence of fluctuation; locate the point where the walls of the abscess are thinnest; insert an exploring-needle, and if the dépôt of pus is reached substitute a trocar having a sufficient calibre to evacuate the contents of the abscess; observe antiseptic precautions in respect to each detail of the operative procedure, and after the removal of the canula or needle, if a drainage-tube is not necessary, close the {1023} wound antiseptically. If drainage is necessary, keep the cavity empty and use proper solutions to prevent septic decomposition. When an abscess of the liver is pointing, the best place to puncture is where the abscess is most prominent and it walls thinnest, but if the accumulation of pus is encysted and there is no attempt at effecting an exit, the exploring-needle should be passed into the interior of the right lobe, the most usual site of suppuration. If pus be reached, a larger trocar may be inserted to evacuate the cavity thoroughly. Repeated insertion of the needle-trocar is preferable when the abscess is small, but when the accumulation is large and sufficiently firm attachments to the abdominal parietes exist, a drainage-tube will be necessary.

In what direction soever discharge of an abscess may take place, the general indications are to support the powers of life by food and stimulants. The utmost quietude should be maintained. It is useful, by the application of a firm flannel bandage, to keep the liver in its proper position and maintain it there. When pointing of an abscess occurs, a large flaxseed poultice is a soothing and a mechanically supporting application.

Acute Yellow Atrophy.

DEFINITION.--By the term acute yellow atrophy is meant an acute affection of the liver, characterized by rapid wasting or degeneration of the organ, accompanied by the systemic symptoms belonging to an acute acholia or cholæmia. It is an acute, diffused inflammation, with atrophy of the proper gland-elements. It has been called icterus gravis, malignant icterus, hemorrhagic icterus, malignant jaundice, etc.

HISTORY.--Cases having a more or less exact resemblance to acute yellow atrophy have been occasionally reported from the earliest period. Amongst English physicians, Bright[120] was one of the first to give an accurate account of the clinical history of some well-defined cases. Rokitansky[121] was really the first to define the disease from the pathological standpoint, and it was he who designated it acute yellow atrophy, this term being intended to signify the nature of the objective changes. The first treatise ever published on the disease as a distinct morbid entity was the monograph of Horaezek,[122] which appeared in 1843. Amongst the French, Ozonam in 1847 was the first to recognize and describe the disease as a distinct affection, although Andral[123] had several years before mentioned an affection of the liver which corresponded in some of its features to this affection. In 1862, Wagner[124] asserted that many of the cases of acute yellow atrophy were only examples of acute phosphorus-poisoning, and that no real distinction exists between the two affections. This statement has been warmly disputed by various German observers, but there is no doubt a close resemblance between the two affections.

[Footnote 120: _Guy's Hospital Reports_, 1836, vol. i. p. 621.]

[Footnote 121: _Handbook of Pathological Anatomy_, Am. ed.]

[Footnote 122: Quoted by Legg, _On the Bile, Jaundice, and Bilious Diseases_, _loc. cit._]

[Footnote 123: _Clinique médicale_, 1839, tome ii. p. 363.]

[Footnote 124: _Archiv der Heilkunde_, 1862, p. 364.]

CAUSES.--There can be no doubt that acute yellow atrophy is a very rare disease, since so few examples are found post-mortem. In the course of a very large experience in autopsical examinations I have met with but {1024} one characteristic example.[125] According to Legg, it is "one of the rarest diseases known to man."

[Footnote 125: _General Field Hospital_, December, 1863.]

Several theories have been proposed to explain the occurrence of this affection, but without success. It has been ascribed to an excess in the production of bile, to stasis in the bile, and to a sudden saturation of the hepatic cells with biliary matters contained in the portal vein. That these supposed causes are really influential in producing the malady can hardly be entertained. That there is a peculiar poison which has a causative relation to the disease is rendered probable by the fact that a condition closely allied to this disease is produced by phosphorus, antimony, arsenic, and other poisons. Is it not a ptomaine generated under unknown conditions in the intestine? Especially does the morbid anatomy of phosphorus-poisoning nearly agree in all its details with icterus gravis--so nearly that by many German authorities they are held to be identical.

Age has a certain influence in the causation of this disease. It is rarely seen in early life, Lebert in a collection of 63 cases having found only 2 before ten years of age, yet there has been a well-marked case at three, and Hilton Fagge reports one at two and a half years of age. Nevertheless, much the largest number occur between fifteen and twenty-five years of age, and the maximum age may be fixed at sixty.

The influence of sex in the pathogeny is most remarkable. It is true in Lebert's collection of 72 cases there were 44 men and 28 women, but it is now known that he did not properly discriminate in his selection of supposed examples of the disease. The statistics of all other observers are opposed to those of Lebert. Thus, in Frerichs' collection of 31 cases, carefully sifted to eliminate error, there were 22 women and 9 men. Legg has also collected 100 cases of acute yellow atrophy, and of these 69 were women or girls. The most active period of life--from twenty to thirty years of age--is the usual period for the appearance of this disease. More than one-half of Lebert's cases occurred between fifteen and twenty-five; and of Frerichs', two-thirds happened between twenty and thirty years of age. In Legg's collection of 100 cases, 76 were between fifteen and thirty-five years of age. What is the condition of women at this period in life which renders them so susceptible to this malady? There can be no doubt that pregnancy is the great factor. Of 69 cases especially interrogated on this point, examined into by Legg, in 25 pregnancy was ascertained to exist. In Frerichs' collection one-half were women in the condition of pregnancy. The period of pregnancy at which the disease appears varies from the fourth to the ninth month, the greatest number occurring at the sixth month. So long ago as 1848, Virchow drew attention to the remarkable changes in the liver due to pregnancy. Sinety[126] has studied the effect of lactation on the liver, and has ascertained the existence of fatty degeneration. There is a form of jaundice which accompanies menstruation, as shown by Senator,[127] Hirschberg, and others. These facts indicate a certain relationship between the sexual system of the female and the liver, but they do not indicate the nature of the connection, if any exist, between this condition and acute yellow atrophy.

[Footnote 126: _De l'État du Foie chez les Femelles en Lactation_, Paris, 1873 (pamphlet).]

[Footnote 127: _Berliner klinische Wochenschrift_, 1872, p. 615, "Ueber Menstruelle Gelbsucht."]

The influence of depressing emotions has been supposed to be effective {1025} in producing this disease, but it is more than doubtful if such a relationship exists. Lebert, however, refers 13 of his cases to this cause, but Legg, who bases his statements on the study of 100 carefully-recorded cases, is sceptical regarding the effect of such influences. Syphilis has in some instances appeared to be the principal, if not the only, pathogenetic factor, and Legg[128] compares the action of the virus of syphilis to the effect of phosphorus, mercury, etc.

[Footnote 128: _On the Bile, Jaundice, and Bilious Diseases_, _loc. cit._]

PATHOLOGICAL ANATOMY.--The anatomical changes occurring in this disease indicate the existence of a systemic condition: the lesions are not limited to the liver, but involve various other organs. The changes in the liver should be first described, since the name of the disease is derived from the alterations in this organ. As the name indicates, the lesions are atrophic, but not all examples show this. In some cases there is little change in the size of the organ; in others the wasting is extreme; certainly in all typical examples the liver is reduced in size. The variations in size observed are probably due to the stage at which the inspection is made: if early, the organ may not be reduced in size, may be even somewhat enlarged by the deposition of new material; if later, the atrophic changes will be more or less pronounced. When the atrophy has taken place, the size of the liver is reduced to one-half, even to one-third, of its original dimensions; it is then soft, almost like pulp, and cannot maintain its shape, but flattens out on the table. The capsule is much wrinkled and the color of the organ is yellowish, variegated by islets of reddish or brownish-red color, these spots being somewhat depressed below the general surface and having a firm texture. On section the boundaries of the lobules are either lost or have become very indistinct, the line of section being bloodless. The knife with which the sections are made becomes greasy. In some instances ecchymoses are discovered under the capsule, and rarely hemorrhagic extravasations in the substance of the liver. The bile-ducts are found intact, as a rule. The greatest change in the size of the liver is observed in the left lobe. The duration of the disease, as has been indicated above, has a marked influence over the size and condition of the liver. The atrophic shrinking of the liver occurs more decidedly after the ninth day. In general, the tissue of the liver is soft and pulpy in consistence. On microscopic examination the most important alterations are seen to have occurred in the hepatic cells; ultimately, these cells disappear, being replaced by fatty and connective-tissue detritus; but before this stage is reached important alterations have taken place in the form and structure of these bodies: the cells become granular and fatty, and lose their sharpness and regularity of contour, especially at the periphery of the lobule, but ultimately all the cells within the lobule undergo atrophic degeneration. In this atrophic degeneration of the hepatic cells, in their fatty degeneration, and ultimately entire disappearance, consist the real proofs of the disease. The red islets of tissue already alluded to consist of the fatty detritus mixed with crystals of hæmatoidin.

More or less increase of the connective tissue is noted in many of the cases--increase of connective tissue with numerous young cells formed around the vessels and the bile-ducts (Waldeyer[129]). The changes in the {1026} liver would surely be incomplete without some references to the minute organisms which play so important a part in modern pathology. Waldeyer was the first to demonstrate the presence of bacteria in the pigment-remains of the hepatic cells. Other observers have been unable to detect them, so that at present the parasitic origin of this affection remains sub judice.

[Footnote 129: _Arch. für path. Anat._, 1868, p. 536, Band xliii.]

Important changes also take place in the spleen, but the opinions on this point are somewhat contradictory. Frerichs found the spleen enlarged in most of his cases; Liebermeister, on the other hand, and Legg,[130] find that the spleen is enlarged in about one-third of the cases. When the atrophic changes occur in the liver, more or less swelling of the splenic veins must occur in consequence of portal obstruction. The peritoneum, especially the omental part, is the seat of multiple ecchymoses, and the endothelium is fatty. The mesenteric glands are usually swollen. More or less blackish or brownish fluid, consisting of altered blood, is usually found in the stomach, and the same, assuming a tar-like consistence, in the large intestine. Ecchymoses of rather small size are distributed over the stomach and intestines. The epithelium of the stomach-glands is found granular and disintegrating, and a catarrhal state of the gastro-intestinal mucous membrane exists throughout. The secretions are never normal, and the stools are wanting in bile or present a tarry appearance, due to the presence of blood.

[Footnote 130: _On the Bile, Jaundice, and Bilious Diseases_, _supra_.]

Important changes take place in the kidneys. They consist essentially in a granular and fatty degeneration of the tubular epithelium, whence the altered appearance of the cortex. Multitudes of bacteria crowd the pyramids. Ecchymoses also are found in the mucous membrane of the pelvis of the kidney, in the bladder, and indeed all along the genito-urinary tract.

The muscular tissue of the heart is in a state of acute fatty degeneration, beginning with a granular change which may at the outset be of very limited extent and involve but few fibres. The endo- and pericardium are studded with ecchymoses or marked by hemorrhagic extravasations, and the pleura presents similar appearances, but not to the same extent.

The brain does not always show evidences of change, but in many instances there are ecchymoses of the meninges; the walls of the vessels are affected by fatty degeneration.

The tissues of the body are more or less deeply stained with bile. The pathological change on which the jaundice depends has been variously stated, but the most probable explanation is that which refers it to mechanical obstruction of the bile-ducts, either by catarrhal swelling or fatty degeneration of the epithelium. Notwithstanding the prominence of the hepatic symptoms, acute atrophy of the liver is probably only one element in a constitutional morbid complexus.

SYMPTOMS.--Acute yellow atrophy begins in two modes--the grave symptoms preceded by mild prodromes, or the most serious symptoms appear at the onset. The former mode is the more common. The usual prodromes are referable to the gastro-intestinal canal, and consist of loss of appetite, nausea, vomiting, a bitter taste in the mouth, headache, and general malaise. Indeed, the opening attack may be much like an {1027} ordinary bilious seizure or acute gastro-duodenal catarrh or a sick headache. In some cases the initial symptoms--nausea and diarrhoea--appear to be induced by an indigestible article of food. Jaundice never fails to be present at some period, but is usually one of the prodromic symptoms. It has no special characteristics by which the gravity of the approaching seizure may be measured. It is usually rather deep, and all parts are deeply stained, but the coloration may be limited to the body and upper extremities. No change in pulse or temperature, except the usual depression of both functions, is to be observed; the urine is deeply stained with pigment, and the feces are grayish, colorless, or parti-colored.

The period of time elapsing before the serious symptoms come on is not constant; from one week to several months have been the variations observed. In a minority of the cases no prodromes have occurred, but the grave symptoms have declared themselves at once. From the appearance of the jaundice up to the onset of severe symptoms the time has varied from two weeks to several months, but has rarely exceeded three months. During this time there may be nothing to indicate the gravity of the approaching symptoms; in fact, the case then, as at the onset, seems to be one of simple gastro-duodenal catarrh associated with catarrhal jaundice. The onset of serious symptoms is most usually announced by dilatation of the pupil. If, therefore, in a case of apparently simple catarrhal jaundice, especially in a pregnant female, there should occur without apparent reason a marked and persistent dilatation of the pupil, the possibility of the case being one of acute atrophy should be apprehended. This symptom is not, alone, of sufficient value to decide the character of the case, but then an obstinate insomnia comes on, violent headache is experienced, there is more or less confusion of mind, and jactitations or an extreme restlessness occurs. When such pronounced nervous symptoms appear the character of the attack is explained.

Various divisions have been proposed to mark the type of the symptoms: thus, the icteric period embraces the prodromal symptoms with jaundice; the toxæmic period is that stage characterized by profound nervous disturbances. Ozonam has divided the symptoms into those of the prodromal period and those of the serious stage, the latter being subdivided into the symptoms of excitation and those of collapse. There may be no prodromal period, however; without any preliminary symptoms the patient is suddenly seized with delirium and passes into a condition of coma and insensibility, or the first evidence of serious illness may be convulsions. It is probable, however, that in even the most sudden cases mild prodromal symptoms had occurred, but were overlooked. There is much variability in the symptoms of the toxæmic period. There are three symptoms: excitement with delirium, sometimes delirium ferox; coma, less or more profound; and convulsions. Legg has numerically expressed the relative frequency of these symptoms thus: Of 100 cases of unquestionable acute atrophy, 76 had become comatose, 59 were delirious, and 32 had suffered convulsions.[131] According to the same authority, delirium and coma were associated together in about one-half of the cases, but in pregnant women coma often occurs alone (Legg). Usually, when convulsions happen there has been either coma or delirium. With these cerebral symptoms there are often present various {1028} disturbances of motility and sensibility, such as local convulsions, jactitations, hiccough, extreme restlessness, paralysis of the sphincters, and incontinence of urine and feces or retention, grinding of the teeth, exalted sensibility of the skin, or it may be complete anæsthesia, severe itching of the surface, etc.

[Footnote 131: _On the Bile, Jaundice, and Bilious Diseases_, _loc. cit._]

During the toxæmic period, and directly dependent on the retention of excrementitious matters in the blood, hemorrhages occur from the mucous surfaces, from wounds, and into the various serous membranes. A changed state of the blood being present in all cases of this disease, the proportion in which extravasations take place is high--in about 71.3 per cent. according to Liebermeister, and 80 per cent. according to Legg. The latter author regards these estimates as rather low. When hemorrhage occurs in the stomach in small amount, it presents itself as coffee-grounds or as black vomit, and in the intestine in the form of black, tarry stools or melæna. Hemorrhage may also occur from the surface of an ulcer, from a fresh wound, a leech-bite, etc.; but the most usual form of extravasation of blood after the gastro-intestinal is epistaxis or bleeding from the nose. Women who abort, as they are very apt to do when this disease comes on, may suffer from frightful hemorrhage, and deaths have been thus caused. Various opinions have been expressed as to the cause of the hemorrhagic condition--by some attributed to the changes in the composition of the blood; by others to the alterations of the vessel walls; both factors are doubtless concerned.

During the prodromic period the temperature of the body, as in the case of ordinary uncomplicated jaundice, is rather depressed below normal, sometimes as much as two degrees; but when the toxæmic stage comes on the body-heat rises to a variable extent, but usually over 100° F. In some cases no febrile movement can be detected; in others a very considerable elevation of temperature occurs, but very rarely attains to 105° or 106° F. The pulse becomes very rapid, in some instances rising to 140; but without any apparent cause it may fall suddenly to 70 or 80, and these fluctuations may take place several times a day. The rise of temperature and a very rapid pulse may come on in the final coma only; and immediately after death, as Legg points out, the body-heat may attain the maximum elevation.

As the toxæmic period develops the tongue becomes dry, glazed, fissured, sordes form on the teeth and lips, the breath becomes fetid, and the breathing may assume the Cheyne-Stokes type. The nausea and vomiting of the prodromal period persist, and the ominous coffee-grounds appear in the rejected matters, or grumous masses--clots acted on by the gastric juice--are brought up. Black, pitch-like, or tarry stools, the result of hemorrhage, are passed toward the end--involuntarily when liquid. When no blood is present the stools are grayish and without bile. Constipation may be the condition instead of diarrhoea in about one-third of the cases.

Various eruptions have been observed on the skin, such as petechiæ, roseola, eczema, etc., but their very variety, as their occasional appearance, indicates their accidental relationship to the disease.

The urine is much altered in character, but it is usually acid in reaction, although it has been observed neutral or alkaline. The specific gravity is at or nearly normal, and it has a deep-brownish or bilious hue {1029} due to the presence of bile-pigment. The most important change in the composition of the urine is the diminished quantity of urea or its entire disappearance; the phosphates, and especially the chlorides, are also usually diminished in amount; and albumen and leucin and tyrosin appear to a lesser or greater extent, together with hyaline, fatty, and granular casts.

Although the observations are somewhat contradictory, it seems pretty definitely established that the blood is more or less altered in composition, morphological and chemical. The red corpuscles are diminished in amount, and often deformed; the white corpuscles are increased; and excrementitious products--urea, leucin, tyrosin, and cholesterin--are found in greater or less quantity.

COURSE, DURATION, AND TERMINATION.--Although, as a rule, the course of acute atrophy is rapid, it is not invariably so. In some instances the prodromic symptoms have continued through several months, but, according to Thierfelder, one-half of the cases terminate in from three to five weeks, and in only 10 per cent. is the duration continued into eight weeks. The course of the disease is extremely rapid in pregnant females, rarely extending beyond the second week. An extended course of the disease is due to delay in the prodromic stage, the toxæmic period being always absolutely and relatively shorter. In the condition of pregnancy the danger is increased by the hemorrhages, and the early termination is due chiefly to this factor. When the duration of the disease is protracted and its evolution normal, the accumulation of hepatic excrementitious matters sets up cerebral disturbance, which becomes a pronounced feature of the case.

The termination cannot probably be otherwise than fatal. As in the course of the disease the hepatic cells undergo solution and disintegration, their restoration can hardly be regarded as possible, certainly not probable. Any curative result must, then, be wrought in the prodromic period, when the diagnosis must be viewed with some mistrust.

DIAGNOSIS.--George Harley[132] maintains the singular doctrine that acute yellow atrophy is only the "sporadic form of the contagious jaundice of the tropics," or yellow fever. He bases his opinion on the identity of their symptoms, pathological anatomy, mortality, and contagious character; for he affirms that acute yellow atrophy may exhibit contagious power in temperate climates.

[Footnote 132: _Diseases of the Liver_, Amer. ed., 1882, p. 255.]

As acute yellow atrophy comes on as an ordinary catarrhal jaundice, it is impossible to distinguish it from the latter affection during the prodromal period. When cerebral symptoms, black vomit, and tarry stools appear, the area of hepatic dulness very decidedly diminishes, and leucin and tyrosin replace urea in the urine, acute atrophy may be suspected.

Acute phosphorus-poisoning, as regards its symptomatology and morbid anatomy, does not differ from acute yellow atrophy, and many cases of the latter have been mistaken, it is supposed, for the former. To distinguish between them the history of the case must be carefully ascertained.

When, after the prodromal symptoms, which may not be accurately diagnosticated, there occurs a rapid decline in the area of hepatic dulness, hemorrhages take place from the mucous surfaces, stupor and delirium {1030} supervene, and urea disappears from the urine, being replaced by leucin and tyrosin, there can be no difficulty in coming to a conclusion: the case must be one of acute yellow atrophy.

TREATMENT.--It was formerly supposed that a case of acute yellow atrophy must necessarily prove fatal, but this opinion must now be modified, since examples of cure of supposed cases have been reported from Oppolzer's clinic,[133] by Lebert,[134] by Harley,[135] and others. As at the onset the symptoms cannot be distinguished from a bilious attack or from catarrhal jaundice, the treatment must be appropriate to these states. When the serious symptoms begin, a large dose (scruple j) of quinine should be at once administered, and half the quantity at regular intervals to keep up the cinchonism. Phosphate of soda, with some arseniate and such mild hepatic stimulants as euonymin, iridin, etc., should be given to maintain a gentle aperient action. Experience has proved that active or drastic cathartics do harm rather than good; on the other hand, mild laxatives, especially those having cholagogue action, seem to do good.

[Footnote 133: Thierfelder, _op. cit._]

[Footnote 134: _Ibid._]

[Footnote 135: _Diseases of the Liver_, Amer. ed., _supra_.]

Important symptoms arising during the toxæmic period require remedies to combat them. Nausea and vomiting, and also diarrhoea, are best relieved by carbolic acid and bismuth in combination. Hemorrhage requires, when intestinal, the chloride and perchloride of iron; when from other mucous surfaces, ergotin, gallic acid, and other hæmostatics. The depression of the vital forces should be treated by small and frequently-repeated doses of alcohol, by quinine, by iron, and, under some conditions, by digitalis. After the disintegration of the hepatic cells has been produced no remedies can be of any service. Until this occurs, however, it seems to the author well worth while to attempt to stay the destruction by the administration of those remedies which, by their accumulation in that organ, indicate a special affinity for its tissue. These drugs are phosphorus, antimony, gold, silver, and mercuric chloride. By the timely administration of one or more of these would it not be possible to stay the progress of the atrophic degeneration?

The Liver in Phosphorus-Poisoning.

DEFINITION.--Poisoning by phosphorus may seem to be a toxicological question rather than a merely hepatic disease, but as the morbid complexus thus induced is so similar to acute yellow atrophy that the conditions are regarded as identical by many of our German colleagues, it is necessary to enter into some details regarding it.

PATHOGENY.--Phosphorus-poisoning occurs at any period from youth to old age, but is most common from twenty to thirty years of age. Women seem more inclined to effect self-destruction in this way than are men, probably because phosphorus matches are so readily obtained. Children may munch match-heads in a spirit of mischief. That form of chronic poisoning seen in workmen in match-factories, and consisting in necrosis of bone, etc., does not come within the scope of the present inquiry.

A body poisoned by phosphorus does not exhibit a tendency to putrefactive decomposition within the usual period. The tissues are more or less {1031} deeply stained by bile-pigment, and this coloration extends to pathological fluids as well. The serous and mucous membranes contain points of blood-extravasation, but they are especially numerous in the serous membranes. Hemorrhages of this kind are due to two causes--to the disorganization of the blood, and to fatty degeneration of the arterioles. The heart is also more or less advanced in fatty degeneration, the muscles granular, the striations obscure or obliterated, and the whole soft and easily torn. The spleen is usually enlarged--often, indeed, to twice its natural size. The liver presents highly-characteristic alterations. When death occurs early the organ is generally enlarged, infiltrated with fat, the connective tissue undergoing hyperplasia; but in more advanced cases atrophy has taken place, the cells have disappeared and are replaced by fat-granules, crystals of leucin and tyrosin, connective tissue, etc.--in fact, the changes characteristic of acute yellow atrophy. The jaundice has been variously interpreted. As the bile-ducts in advanced cases are found to contain no bile, but only a colorless mucus, the advocates of a hæmatogenic jaundice hold that the jaundice is due to a failure of the liver to excrete the biliary principles in the blood; whilst the opponents of this view maintain the existence of an obstruction in the ultimate ducts. Harley[136] has recently brought forward some strong facts and arguments--which we believe can be successfully controverted--maintaining the former view. The jaundice of phosphorus-poisoning, if Harley's opinion prove to be correct, must be regarded as a hæmatogenic jaundice.

[Footnote 136: _Diseases of the Liver_, _loc. cit._]

The mucous membrane of the stomach, as might be supposed, is more or less ulcerated or in an advanced state of catarrh, and the gastric glands are affected by fatty degeneration.

The kidneys are affected in a similar manner to the liver; the epithelium is fatty and sometimes detached, and the same process is found to occur in the vessels and epithelium of the cortex.

SYMPTOMS.--Not only in the morbid anatomy, but in the symptoms, do we find that a very remarkable resemblance exists between acute yellow atrophy and phosphorus-poisoning. As phosphorus is usually swallowed in bulk, some hours may elapse before the local symptoms begin, for the contents of the stomach and the tough mucus lining the mucous membrane may, and usually do, prevent immediate contact of the poison with the mucous membrane. When the stomach is entirely empty the symptoms may begin in an hour or two. The symptoms produced may be arranged in two groups--those due to the local irritation excited by the poison; those due to its systemic impression. In the first group belong burning in the gullet, pain, nausea, and vomiting. According to Lewin,[137] who has collected a number of cases for analysis, vomiting occurs in 26 out of 32 instances of poisoning. Some hours--often, indeed, three or four days--then elapse before the systemic symptoms begin. Vomiting, which was for the time being suspended, occurs again, and instead of the mere contents of the stomach, containing more or less phosphorus, blood, somewhat changed by the gastric juice--chocolate-colored or as coffee-grounds--appears in the vomited matters. The evacuations from the bowels may at first, as the contents of the stomach, appear phosphorescent, and afterward exhibit the appearances due to the presence in them {1032} of altered blood. At this time, if the liver be examined it will be found somewhat enlarged and tender to pressure, and on or about the third day jaundice appears; but it should not be overlooked that jaundice, as Bamberger[138] has shown, may be postponed to the second or third week after the phosphorus has been taken.

[Footnote 137: _Virchow's Archiv für path. Anat., etc._, Band xxi. p. 514 _et seq._]

[Footnote 138: Legg, _On the Bile, Jaundice, and Bilious Diseases_, _loc. cit._]

In favorable cases the area of hepatic dulness decreases and the jaundice declines. In the fatal cases certain nervous phenomena become prominent. There occur drowsiness, developing into coma, with intercurrent attacks of delirium which may be of a maniacal character; convulsions, spasmodic attacks, dilated pupils, and involuntary evacuations. The disorganization of the blood and the fatty change in the vessels are exhibited in the hemorrhages from the gastro-intestinal mucous membrane. The nervous phenomena are due chiefly to the retention in the blood of various excrementitious matters which it is the function of the liver to separate from the blood. Flint's theory of cholesteræmia has been so abundantly disproved that no one upholds it at the present time, but the cerebral symptoms are properly referred to the retention of all hepatic excrement.

The temperature in phosphorus-poisoning rises from 99° to 102° F., but it may reach in severe cases to 103° to 105° F., and at death or immediately afterward to 105°, even to 107° F. The same fact is true of acute yellow atrophy. With the jaundice the pulse declines, but in the further progress of the case, especially toward the close, the pulse becomes rapid and small.

The changes occurring in the urine are highly significant. The amount of urea decreases as the symptoms increase in severity, and leucin and tyrosin take its place. If the case tends to recovery the urea again increases in amount, but if the tendency is in the opposite direction the quantity of urea steadily diminishes. Bile acids and bile-pigment are found in quantity, and albumen is present in small amount.

COURSE, DURATION, AND TERMINATION.--Phosphorus-poisoning is necessarily an acute affection, but the duration of cases is much influenced by the form in which the poison is taken. If in a liquid and diffusible form, as oleum phosphoratum, the local and systemic symptoms will develop in a few hours, but if in solid masses, as particles of match-heads, many hours (six to ten) may elapse before the local irritation begins. The proportion of cures in phosphorus-poisoning varies from one-fourth to one-half of the cases. Much depends, however, on the promptness and efficiency of the treatment. The prognosis is the more favorable the earlier proper measures of relief have been instituted. If the case has proceeded to jaundice, hemorrhages, black vomit, etc. without the administration of suitable antidotes, little can be expected from any kind of treatment.

DIAGNOSIS.--The history of any case involved in doubt is indispensable to a correct conclusion. The phosphorescent appearance of the matters vomited or passed by stool may make the differentiation comparatively easy; but if the case has passed beyond this stage, phosphorus-poisoning can be separated from acute yellow atrophy only by the history of the case. If the fact of the administration of phosphorus is successfully concealed, no differentiation can be made, since {1033} even the best authorities hold to the identity of the toxic symptoms produced by this poison and of the morbid anatomy, with the symptoms and lesions of acute yellow atrophy.

TREATMENT.--The poison should be evacuated as quickly as possible by emetics and proper diluents. The best emetics are sulphate of copper, apomorphia, and ipecacuanha, the antimonial and mercurial emetics being unsuited, since their effects are similar to those of phosphorus. Oleaginous protectives do not prevent, but really favor, the absorption of phosphorus. Decoctions of flaxseed, slippery elm, acacia, etc. are suitable demulcents and protectives. The fatty matter in food, eggs, etc. will have an injurious effect by promoting the solution and absorption of the phosphorus, and should hence be excluded from the diet. The most effective antidote is oleum terebinthinæ, and the most suitable preparation is the French acid oil. Freshly-distilled turpentine appears to be almost if not entirely useless. It is probable that the American oil which is old and has been exposed to the air for many months will answer the purpose, but it cannot be too strongly insisted on that the turpentine which has proved to be efficient in phosphorus-poisoning is the French acid oil. Turpentine when exposed to the air absorbs oxygen as ozone, and to this principle are probably due the curative effects of old turpentine. Phosphorus when acted on by this agent is converted into a spermaceti-like substance entirely devoid of toxic power. As rapidly as possible the poison should be acted on by the antidote, and then the stomach should be evacuated, using, cæteris paribus, the sulphate of copper, since this forms an insoluble phosphide with any portion of free phosphorus, whilst at the same time it empties the stomach of its contents. Although the immediate results of the poison may be thus removed, the damage to the red corpuscles and to the whole mass of the blood requires special management. The success of transfusion, as practised by Jürgensen,[139] proves that the substitution of fresh blood may save life when the existing blood-supply is inadequate to the performance of its proper functions. It follows that if the toxic effects of phosphorus have continued for several days, blood-transfusion will be necessary in those cases characterized by an inability to recuperate notwithstanding the successful removal of the poison.

[Footnote 139: _Berliner klinische Wochenschrift_, No. 21, 1871.]

For the inflammatory symptoms produced by the local action of phosphorus, opium in some form is indispensable. This remedy is equally valuable as a means of maintaining the vital resources and to prevent the evil results of shock and inflammation.

Carcinoma of the Liver.

DEFINITION.--Under the term carcinoma of the liver are included primary and secondary cancer of the liver. The malady with which we are now concerned is the primary affection, occurring in the organ proper or in some pathological new formation connected with it.

ETIOLOGY.--Heredity is the most important factor. A careful investigation of the reported examples demonstrates that from 15 to 20 per cent. owe their origin to hereditary influence clearly, and probably {1034} considerably more are indirectly derived in this way when the immediate connection may not be demonstrable. Next to heredity, age must be regarded as the most important pathogenetic influence, much the largest number occurring at from forty to sixty years of age. It is a malady of advanced life, therefore, rather than of youth or middle age. Excluding the female organs from consideration, it is quite certain that sex has little special influence, and that males and females are affected about equally.

Primary cancer of the liver is comparatively infrequent, occurring in not more than one-fourth of the cases. Frerichs collected 91 cases, and of these 46 were secondary to cancer in organs having vascular communication with the liver.

PATHOLOGICAL ANATOMY.--Under the term cancer of the liver are included several distinct forms of morbid growth, but united in the characteristic of malignancy. From the merely clinical standpoint this characteristic is the most decisive bond of union between them, and serves as the point of departure in the study of this affection. Primary cancer of the liver is divisible into two forms: 1, as a single, defined tumor; 2, as an infiltration through the whole mass of the organ.[140] Secondary cancer occurs in nodular masses, and with extreme rarity as an infiltration. The form of cancer is really the same; the differences in structure are only apparent, the variations being due to the relative proportion of cells, fibres, and vessels. If the fibrous stroma is abundant and the cells small in quantity, the form of structure approaches scirrhus; on the other hand, if the cells largely preponderate, the type is encephaloid; if vessels predominate, it is called telangiectatic. The usual form in cancer of the liver is the soft, cellular variety, encephaloid or medullary. When the cancerous new formation is nodular, the masses vary in size from a pea to a child's head,[141] and are numerous inversely as their size. When the cancer occurs as a solitary tumor, it may attain to enormous dimensions. It has a spherical shape usually, protrudes from the surface of the organ somewhat irregularly, and the overlying peritoneum is thickened, cloudy, and adherent from a local inflammation. The central portion, whether there be one, several, or many nodules, is depressed, giving an umbilicated appearance to the tumor; and this central depression is found to be soft, almost diffluent, and full of juice. The fibrous stroma which extends through this central soft material has a reticulated arrangement and a shining, fibrous appearance. The cancerous masses are not confined to these nodules, but extend into the surrounding hepatic structure, push their way into the portal (especially the hepatic) veins, block the ducts, and invade the lymphatic glands in the fissure of the liver.

[Footnote 140: Virchow, _Krankhaften Geschwülste_, _loc. cit._; Perls, _Virchow's Archiv für path. Anat., etc._, Band lvi. p. 448 _et seq._; Frerichs, _A Clinical Treatise, etc._, Syd. Soc. ed., _loc. cit._, vol. ii. p. 281 _et seq._]

[Footnote 141: Förster, _Lehrbuch der Pathologischen Anatomie_, by Seibert, Jena, 1873.]

When the cancerous new formation takes the form of an infiltration of the organ instead of distinct nodules, the liver is usually uniformly enlarged and its outlines preserved.[142] The peritoneum is opaque, thickened, and adherent. The organ is traversed by fibrous bands, and the {1035} intervening portion is a soft, juicy pulp, stained by the imbibition of bile. In extreme cases hardly any portion of the proper hepatic tissue remains, but is replaced by a cancerous new formation having the same shape.

[Footnote 142: Perls, _Virchow's Archiv_, Band lvi. p. 448 _et seq._]

As regards the minute structure of cancer of the liver, it may be regarded as a degeneration (cancerous) of the proper gland-cells and of the epithelium of the bile-ducts. As cancer develops in the liver it is to be noted that the cellular elements preponderate over the fibrous or the stroma, and hence the new formation presents the characteristics of softness, rapid growth, and a multitudinous cellular hyperplasia. As regards the form of the new cells, it cannot now be doubted that they are descendants of the secretory gland-cells and of the epithelial lining of the ducts. According to some observers, it is to the proliferation of the proper gland-cells that the new formations owe their origin; according to others, to the hyperplasia of the cells lining the ducts. As the growth of the new formation can take place only through an adequate blood-supply, it becomes very important to ascertain its source. There can be little doubt that primary cancer of the liver receives its nutrient supply through the hepatic artery, in connection with which new capillaries form in the pathological tissue.

Secondary cancer of the liver is the usual form of the specific manifestation. From the merely clinical standpoint the primary affection is the more important. From the pathological point of view the secondary implication of the liver may be a true metastasis or a mere communication by contiguity of tissue. The most usual metastasis occurs from epithelial cancer of the face (Schüppel), but the ordinary communication of the new formation is from primary cancer of the stomach, intestine, pancreas, mesentery, etc. The cancer elements, as the author has several times verified, crowd the lymphatics and veins, and through these channels reach the liver and other parts. As the cancer elements in the case of secondary implication of the liver are distributed chiefly by the portal vein, it follows that there must be numerous secondary foci and multiple nodes. Cancerous infiltration under these circumstances is the rarest possible form for the new growth to take. The size and number of nodes forming in these cases of secondary implication of the organ vary greatly--from two or three to twenty, or a hundred, or even more. As regards the form, structure, and ultimate behavior of the secondary formation, they do not differ from the primary. As respects the relative proportion of stroma and cellular elements--fibres and cells--they vary greatly, some presenting the firm texture of a predominating fibrous stroma, others the softness and ready diffluence of the excessive cellular production. The latter is undoubtedly the usual condition, and when the nodular masses are incised an abundant creamy juice exudes. With the development of these nodules an increase in the size of the liver takes place and the organ has an uneven and indurated feel. As the cancerous masses develop the proper hepatic structure undergoes atrophy, and finally little is left of the organ but the cancerous new formation. The blood-vessels, lymphatics, and peritoneal investment are invaded, the first mentioned most decidedly; and especially are organized exudations the favorite seats of cancer new formations, those, for example, about the gall-bladder and cystic duct resulting from repeated attacks of passage of calculi.

{1036} Secondary changes take place in the cancerous nodes. As the cells develop pressure is brought to bear on the vessels supplying them and on each other, with the result of fatty degeneration of the central portion, which effects the change in the form of the nodules and in their consistence, already mentioned. The blood-supply to the cancerous nodes in the liver is derived from the hepatic artery, as Frerichs has determined by carefully-made injections; they also are new formations of exceedingly delicate structure, and form a network about the periphery of each mass or node. By reference to these anatomical considerations it is easy to understand the failure of nutrition of the central portions of the nodes.

Pigment cancers of the liver are rare as secondary formations, and excessively infrequent as primary formations. They are, properly speaking, melano-sarcomas (Schüppel). They are more often metastatic than merely secondary--that is, transferred from different parts, as in the case of melanotic sarcoma of the choroid--than due to neighboring disease transferred by contiguity of tissue. This variety of cancer, so called, takes the form of multiple nodes or of diffused infiltration, the former more frequently; but both modes of development may go on at the same time. The nodes vary in size from a pea to a child's head, have a grayish, brownish, or blackish tint, and exude on section a fluid not creamy like true cancer-juice, but rather watery and containing black particles floating in it. In the case of diffuse infiltration the pigment masses are thoroughly distributed through the original hepatic tissue. In both forms the size and weight of the organ are enormously increased. In the case of the melanotic infiltration the whole organ is uniformly enlarged, reaching in a few months the enormous size of twelve to twenty pounds.

Sarcomas also occur very rarely as primary growths in the liver, but secondary sarcomas are more frequent. There are fibro-sarcoma, lympho-sarcoma, and osteo-sarcoma as secondary deposits, the first being very firm in consistence, the second soft and medullary, and the last of hard, bony consistence.

SYMPTOMS.--We are especially concerned here with primary cancer of the liver. The secondary disease is so obscured by the main and primary lesion that a diagnosis may be impossible. Furthermore, the progress of the original disease is that which demands immediate consideration. As, therefore, the secondary implication of the liver is of relatively trifling importance, and only an incident in the course of the main disease, the matter for consideration now is primary cancer of the liver.

It is the fact that in some, even a considerable proportion, of the cases the onset and progress of cancer of the liver are very obscure. For some time the symptoms may be of the vaguest description. The usual history is this: A person of forty to sixty years begins to fail in flesh and strength, becomes sallow, has disorders of digestion, pain and uneasiness in the right hypochondrium, and the bowels are now confined, now relaxed. The abdomen, notwithstanding the general loss of flesh, increases in size, and the superficial veins are enlarged; very considerable pain is experienced in the right hypochondrium, and often extreme tenderness to pressure is a pronounced symptom. The pains are not limited to the hepatic region, out extend widely from this point in all directions. On palpation the {1037} liver is found to be enlarged, its texture indurated, and its outline irregular and nodular, and pain--often, indeed, quite severe--is developed by pressure.

The condition of the liver on palpation is best ascertained by suddenly depressing the abdominal wall with the tips of the fingers arranged in a line. Displacing thus the movable bodies in the cavity, the liver is quickly reached, and nodules, if they exist, are readily felt. If the new formation has developed from exudations about the gall-bladder and cystic duct, it may be felt by suddenly depressing the walls of the abdomen over this organ in the usual position of the fissure.

In the case of general cancerous infiltration of the organ, with the remarkable enlargement which occurs in such cases, there will be present an obvious distension of the right hypochondrium; the intercostal spaces will be forced outward and the arches of the ribs rendered more prominent; the area of hepatic dulness, both vertical and transverse, will be increased; and the limits of dulness will move with a full inspiration downward, and with a full expiration upward. This mobility of cancer-nodules of the liver with the inspiratory and expiratory changes serves to distinguish them from tumors of the abdominal walls. Seen early, the changes in the size of a nodule or of the liver itself may be noted from week to week,[143] especially in cases of rapidly-growing cancer.

[Footnote 143: Murchison, _Clinical Lectures_, p. 187.]

As the cancerous new formations extend into the portal system within the liver, obstruction to the portal circulation results from the blocking of the blood-current. Also, interference in the portal circulation arises by compression of the vessels from without, either through the accumulation of cancer-products in the liver or by the enlargement of the lymphatics in the fissure of the organ. In what way soever it may be produced, the practical fact remains that ascites is a frequent symptom, occurring in somewhat more than one-half of the cases. The character of the fluid varies. It may be a clear serum containing a small proportion of albumen; it may be colored by bile or be of a deeper greenish or reddish hue; it may contain flocculi of lymph and numerous leucocytes floating in it; and the ordinary serum may be rendered cloudy and be filled with shreds of exudation in consequence of peritonitis, or bloody because of hemorrhage from a softening nodule. When the fluid is considerable in amount the difficulty of ascertaining the condition of the liver is greatly enhanced, and symptoms due to the interference of the fluid with the action of various organs are introduced into the complexus of morbid signs. Especially is the upward pressure of the ascitic fluid, and the consequent interference in the movements of the lungs and heart, a source of considerable distress. First, a local and afterward a general peritonitis ensues as a consequence of the extension outwardly of the new formations to the peritoneal layer, and its implication by contiguity of tissue or the rupture of a spreading fungous growth and hemorrhagic extravasation into the cavity. The peritoneal complication is not only a serious addition to the sufferings experienced by the patient, but it adds to the difficulties of a diagnosis. In the case of a celebrated savant who died of cancer of the liver (seen by the writer) there was such a pronounced peritonitis that the diagnosis made by the attending physician was chronic peritonitis. When this complication occurs, there takes place {1038} a decided increase in the local tenderness, and this increased sensibility to pressure quickly extends over the abdomen, causing a general exquisite tenderness. Besides this tenderness characteristic of most cases of peritonitis, distension of the abdomen and the decubitus peculiar to this state are obvious symptoms. It is therefore clear that the occurrence of peritonitis not only contributes to the severity and painfulness of the case, but seriously complicates the diagnosis.

It has been already stated that pain in the right hypochondrium is a nearly constant symptom in cancer of the liver. With the initial symptoms, uneasiness, heaviness, a sense of pressure in the hepatic region are experienced, and as the case progresses more or less acute pain develops as a rule. But there are exceptions. In cases of cancer involving the deeper portion of the liver there may be little pain, and in some rare cases of cancer involving the external part of the liver--the capsule and peritoneum--but little pain is experienced. In much the largest proportion of cases the pain is severe, and the production of any considerable pain means the implication of the hepatic plexus of nerves or the hepatic peritoneum. It follows, then, that the pain in the former case is not limited to the locality of the disease, but is more or less widely distributed through the anatomical relations of the hepatic plexus, being felt in the epigastrium, the walls of the chest, the shoulders, etc.

In secondary cancer of the liver, following cancer of the stomach, vomiting is a constant symptom, but also in those cases of primary disease in which the left lobe is especially enlarged, relatively, are nausea and vomiting pronounced symptoms. At the onset of the malady the appetite fails and a gastro-intestinal catarrh is set up. More or less catarrh of the bile-ducts also ensues. The interference with nutrition thus occasioned is enhanced in those cases in which the obstruction of the ducts is sufficient to prevent the escape of bile into the intestine. Jaundice is not a constant symptom, occurring in little more than one-third of the cases. When it occurs, the peculiar stools are present and the intestinal digestion is deranged, as in cases of ordinary obstruction to the ducts. In two cases of cancer of the liver occurring in the writer's practice, and examined by post-mortem, there were calculi present in the gall-bladder; in one case the principal calculus was egg-shaped and the size of a pullet's egg.

The nutrition rapidly fails from the beginning of cancer of the liver. The downward pace is accelerated when the gastro-intestinal digestion fails and vomiting occurs after taking food. The skin becomes dry and wrinkled, and if not jaundiced has a peculiar tint, varying in depth of color from an earthy or fawn-like hue to a deep bronze. Failure of strength is a pronounced symptom from the beginning, and is out of proportion to the loss of flesh. As the wasting advances the decline of strength is accounted for, but the feeling of weakness and the distaste for exertion which occur so early are very significant signs of internal cancer, although they do not indicate the position of the neoplasm. Emaciation finally becomes extreme.

The urine declines in amount as the case progresses. It is usually very high-colored, contains bile-pigment when jaundice is present, and other forms of pigment produced by conditions not at present known. Sometimes albumen is present, and leucin and tyrosin rarely.

{1039} COURSE, DURATION, AND TERMINATION.--As has been already set forth, cancer of the liver may present so few really distinctive symptoms as to escape recognition. Under favorable circumstances the diagnosis may be comparatively easy. In forming an opinion it is useful to review the whole course of the malady and draw conclusions not only from the characteristic signs, but from the development of the symptoms as a whole.

A case of cancer of the liver occurs usually after the middle period of life. The person so affected begins to decline in flesh and strength, has uneasiness in the right hypochondrium, disorders of digestion, and begins to have a pallid or earthy hue of the countenance. Presently, much pain is felt in the hepatic region, the organ distinctly enlarges, and some effusion of fluid and much flatus increase the dimensions of the abdomen. Much tenderness, often exquisite sensibility, is produced by pressure over the liver, and often over the whole abdomen. By careful palpation nodules can be made out and their growth noted in those cases free from peritoneal inflammation. The abdominal swelling and tenderness incommodes the lungs, and a semi-erect decubitus is assumed to relieve the pressure on them; the breathing becomes short, catching, hurried, and painful, and sometimes a most distressing hiccough is superadded to the other sufferings. Great wasting and weakness ensue. Jaundice appears, or the earthy hue of the skin deepens into a bronze discoloration. The case may be terminated by some intercurrent disease--by an attack of pleuritis, pneumonia, by peritonitis from rupture or perforation, by intra-peritoneal hemorrhage, by an exhausting diarrhoea. The natural termination is by gradual failure of the powers, by marasmus, the immediate cause of death being due to cerebral anæmia, to failure of the heart from fatty degeneration of the cardiac muscle, from thrombosis of the portal vein, from the development of a hemorrhagic state, and hemorrhages from the various mucous surfaces, etc. The duration is much influenced also by the character of the cancer, whether scirrhous or medullary. The latter are not only more rapidly growing, more destructive of the hepatic tissue, and more rapidly distributed to neighboring organs, but more quickly perforate the capsule and excite a fatal result by hemorrhage or by peritonitis. The average duration of cancer of the liver is variously stated. Having reference to my own personal observation, controlled by the experience of other observers, the duration is from three to nine months, one year being exceptional. There are cases in which the symptoms are very acute, the progress rapid, the whole course from the initial symptoms to the termination being completed in from two to three months. It need hardly be observed that no case of cancer of the liver has been cured. The invariable termination is in death. If any case has seemed to be cured, it may be asserted with confidence that cancer of the liver did not exist.

DIAGNOSIS.--The differential diagnosis is concerned, first, with the existence of cancer; second, with its form. As cancer causes enlargement of the liver in two textural conditions--namely, uniformly smooth, and nodular--it must be differentiated from other diseases producing similar results. Amyloid disease and echinococcus cysts present us types of the former; cirrhosis and syphilis, of the latter. The history of the amyloid disease and of the echinococcus cyst is very different, and both {1040} develop much more slowly. Amyloid disease of the liver arises simultaneously with the same form of degeneration in other organs, and is connected with suppurative disease of some kind, with syphilis, with chronic malarial poisoning, etc., and may occur at any age. Echinococcus cysts enlarge painlessly and do not impair the vital forces; the liver is elastic, and under favorable circumstances presents by palpation the purring-tremor symptom. Cirrhosis may have to be differentiated at two periods--during the time of enlargement, which, however, is rather brief; and during the stage of contraction and nodulation. The history in cancer and in cirrhosis is different: the age, the habits of life, the rate of hepatic change, are opposed in the two diseases; the diminution in size with nodulation is characteristic of cirrhosis; enlargement with nodulation belongs to cancer. The rapid progress of cancer, the wasting, the debility, the cachexia, serve to distinguish it from all other affections of the liver except acute yellow atrophy and phosphorus-poisoning; both, however, are so different in history and development as not to require differentiation. It may be quite impossible in latent cases to distinguish primary cancer of the liver from secondary, but in those examples of the disease occurring in the stomach, intestines, and pancreas there is usually an antecedent history of the primary malady which distinctly separates it in point of time and the character of the symptoms from the secondary implication of the liver. Cancer of the gall-bladder, and especially of the organized exudation about it, may not be readily separated from cancer of the pancreas or of the duodenum. In doubtful cases the history of attacks of hepatic colic becomes an important element in making the differentiation.

TREATMENT.--As we are not in possession of a cure for cancer, the treatment of cancer of the liver must be palliative. Anodynes to relieve pain, paracentesis of the abdomen to remove accumulation of fluid which causes distress, carbolic acid to check nausea and vomiting, and the usual hæmostatics for hemorrhage, are the measures most necessary. In fact, the treatment must be throughout symptomatic--for the relief of symptoms as they arise.

Amyloid Liver.

DEFINITION.--By amyloid liver is meant a deposit in the cells of the organ, in its vessels and interstitial tissue, of a peculiar albuminoid matter called amyloid because of a superficial resemblance to starch-granules. Various designations have been applied to this condition of the organ; thus it has been entitled waxy liver and lardaceous liver, because of the apparent resemblance to wax and lard respectively.

CAUSES.--There exists in the blood a peculiar material, albuminoid in form, applied in the normal state to the structure of tissue--dystropodextrin, as it is called by Seegen--which, when precipitated under certain conditions not now known, assumes the peculiar appearance with which we are now familiar under the term amyloid. The character of the amyloid matter was first distinctly set forth in 1858 by Virchow, who also discovered the characteristic reaction by which it can always be detected. The reaction to iodine gave to the material the designation amyloid, or starch-like, by which it is chiefly known. The {1041} circumstances inducing the deposit of this material are by no means clearly understood. It has long been known that suppuration, especially in connection with bone, has had a distinct influence. Syphilis, especially the tertiary lesions accompanied by pus-formation, has an evident causative relation. Chronic malarial infection has a more distant and doubtful, but still recognized, power to develop this morbid state. Of the various causes above mentioned, the most frequent is the suppuration of pulmonary cavities. In regard to the influence of this, however, it must be remembered that no form of suppurative disease is so common. The relative frequency of the association between suppurating cavities and amyloid disease is not greater than long-standing necrosis with an extensive sequestrum is with the same state; but the actual number of the former is greater. Amyloid disease of the liver is most frequent between the ages of ten and thirty, but it may occur at any age, the period in life being determined by the operation of the causes. Thus, Frerichs' statistics are: under ten there were 3 cases, from ten to twenty there were 19, and from twenty to fifty there were 37 cases. Men are, relatively to sex, more frequently attacked, and in the proportion of three-fourths, but this difference means, of course, the character of men's occupations and their greater liability thereby to the accidents and diseases incident to such employments.

Besides the pathogenetic factors above mentioned, it may be well to refer in this connection to the effect of long-standing neoplasms. It has been found that amyloid disease is produced in some subjects by the cachexia resulting from the slow development and persistence of such a new formation. The special character of the neoplasm is of less importance in respect to this condition than the constitutional condition--the cachexia--induced by its slow growth and interference with nutrition. Although long-standing disease, especially of a suppurative kind, is known to be necessary to cause amyloid disease, Cohnheim[144] has lately published some facts which seem to prove that the degeneration may occur more speedily than has been heretofore supposed. He has shown, contrary to the previously-accepted view, that amyloid degeneration may follow in three months after the reception of a gunshot wound. He records three cases in which the amyloid deposits ensued in six, five, and three months, respectively.

[Footnote 144: _Virchow's Archiv_, vol. liv. p. 271 _et seq._, "Zur Kentniss der Amyloidentartung."]

According to the author's observation, a peculiar somatic type is either necessary to, or at least is greatly promotive of, the amyloid degeneration. If, for example, the same suppurative process occurs in a person of a blond and lymphatic type and in another of brunette and nervo-muscular type, the former will be much more likely to suffer from amyloid change than the latter. "The gelatinous progeny of albuminous parents" is the mode of expression used to designate this particular type.

PATHOLOGICAL ANATOMY.--To use the term amyloid liver is rather misleading, since this indicates the restriction of the morbid process to the liver, whereas it is perfectly well known to be rather widely distributed through various organs and tissues of the body. The term amyloid is itself confusing, since the albuminoid material so designated is not really starch-like. The corpora amylacea, so called, differ materially from starch-granules, and still more from the amyloid matter. According to {1042} Wagner,[145] these substances "have nothing in common." In the study of the amyloid deposit it has not been possible to separate it from the tissue in which it is imbedded; hence the published analyses of this peculiar material are probably far from correct. However, it has been rendered probable that the amyloid deposit has close affinities with fibrin. One of the theories--that of Dickinson of London--assumes that this material is fibrin deprived of the potash associated intimately with it. According to Seegen, dystropodextrin, a material existing in normal blood, agrees with amyloid matter in its most essential characteristics. Although Dickinson's theory is not tenable, it has served a useful purpose in showing the close affinity of fibrin with this pathological product. What view soever may be entertained of its nature, it is certain that the material to which we apply the term amyloid is of albuminous origin. Under circumstances with which we are now unacquainted this material is deposited from the vessels, and, instead of undergoing organization and contributing to the structure of tissues, remains unorganized and unappropriated. It is known that this deposition of the amyloid material is related to the process of suppuration and to certain cachexiæ, but the intermediate steps remain unknown and inexplicable.

[Footnote 145: _A Manual of General Pathology_, by Prof. Dr. E. Wagner, p. 325 _et seq._]

The amyloid matter is first exuded into the coats of the finest ramifications of the hepatic artery, and therefore the first appearance of the disease is in the middle zone of the lobules. In this respect pathologists are agreed: that the amyloid deposits first appear in the walls of the vessels. Wagner maintained, in opposition to Virchow, that the exudation is limited to the vessels and does not extend to the hepatic cells, which perish by pressure and consequent atrophy. This point has not yet been decided. It seems most probable, however, that the ramifications of the hepatic artery and all the capillaries of the lobule are affected, and that the deposits in them lead to atrophic degeneration of the cells.

In consequence of this extensive implication of the vascular system of the liver important changes occur in the size, density, and appearance of the liver. The organ is greatly enlarged in all its diameters. When felt through the walls of the abdomen its outline is distinct, it is firm, even hard, to the sense of touch, and it projects from a finger's breadth to a hand's breadth below the margin of the ribs. The increase of size of the amyloid liver is very great, attaining in weight, on the average, twice that of the normal organ; but this size may be largely exceeded in exceptional instances. In respect to shape and outline the amyloid liver does not differ from the normal organ; for although its dimensions are increased, its relations to the parts adjacent are not altered. The weight of the amyloid liver may reach ten, twelve, even sixteen pounds avoirdupois. The color of the amyloid liver is very different from that of the normal organ: instead of having the reddish-brown tint, it becomes grayish, yellowish, or reddish-gray. In consistence the amyloid liver is firm and rather elastic and doughy, and on section the margins of the incision are well defined, even sharp. A very characteristic feature of the cut surface is its paleness, anæmia, or bloodlessness, and scarcely any blood is exuded, even from the large vessels. The appearance of the incised surface of the liver has been described by comparison with various substances: according to one, it is waxy; according to another, it is lardaceous. A thin {1043} section of a part of the liver far advanced in the amyloid change is distinctly translucent, almost transparent; but a marked difference is observable between the amyloid matter and the lobules proper, even in the cases of extreme deposit. The lobules are separated by an opaque yellow border, and the centre of each is marked by a spot of a similar yellow color.

The amyloid material is remarkable for its power to resist the action of chemical agents and putrefactive decomposition. The test originally proposed by Virchow--iodine--continues to be the most characteristic. Orth[146] suggests a method of applying it which is very excellent in respect to the clearness with which the reaction is shown: A large, thin section of the affected liver is placed in a saucer of water containing some iodine, and after the reaction has taken place is laid on a white plate. Iodine tincture, diluted or the compound solution, is brushed over the affected region, when the amyloid matter assumes a deep mahogany tint and the normal tissues a merely yellowish hue. The distinctness of the reaction may be increased by brushing over the iodized surface some dilute sulphuric acid, when the amyloid matter takes a deep violet, almost black, color.

[Footnote 146: _Diagnosis in Pathological Anatomy_, Riverside Press, 1878, p. 321.]

Only a part of the organ--namely, the smaller vessels--may be involved in the degeneration, and this may be restricted to patches or parts of the organ. With the amyloid change there may be associated syphilitic gummata, or the liver may be more or less advanced in fatty degeneration or in cirrhosis. Those parts of the organ not invaded by the disease are not often entirely normal; they are more or less darkened in color by venous congestion, distinctly softer, etc. The amyloid change is not limited to the liver, but extends to the kidneys, lymphatic glands, the intestinal mucous membrane, etc.

SYMPTOMS.--As the amyloid change in the liver is usually coincident with a simultaneous alteration of other organs, and as the deposits characteristic of the affection are dependent on long-previous disease of an exhausting kind, it is not surprising that the subjects of this affection present the evidences of a cachexia. To the effects of a chronic malady we have added the complications growing out of the amyloid change in the liver, associated, as it usually is, with amyloid degeneration of other important organs.

The symptomatic expression of amyloid liver is therefore mixed up with various derangements that occur simultaneously, but especially with the causes inducing the existing cachexia, with chronic suppuration of pulmonary cavities, or in connection with diseased bone, with the syphilitic cachexia, or with chronic malarial toxæmia. With what cause soever the cachexia may be associated, the symptomatology of amyloid liver is secondary to, or ingrafted on, the conditions produced by the cachexia. The liver is enlarged in all well-marked cases from a finger's breadth to a hand's breadth or more below the inferior margin of the ribs; it is also firm to the touch, well defined, elastic, and its margin rounded, but yet well defined. There is usually no tenderness nor pain, and, without any uneasy sensations to indicate the change taking place, the organ is found to have slowly enlarged, sometimes to an extraordinary extent. Careful palpation may also demonstrate an enlargement of the spleen. When the abdominal muscles are relaxed and there is no swelling of the abdomen by flatus or peritoneal effusion, the very considerable enlargement of {1044} the liver can be readily ascertained. If the effusion is not so great as to distend the abdomen unduly, the increased consistence and dimensions of the liver can still be made out with comparative ease. The hepatic functions are not always sufficiently disturbed to produce characteristic symptoms. In a small proportion--scarcely one-tenth--of the cases does jaundice appear, and when present it is due, usually, to enlargement of the lymphatics in the hilus of the organ, and thus directly compressing the hepatic duct. In the writer's experience, although jaundice has not occurred, there was present a peculiar dark earthy or bronzed tint of the skin, significant of chronic hepatic troubles. Obstruction of the portal circulation is rather unusual, and the explanation is to be found in the fact that the amyloid degeneration occurs first in the radicles of the hepatic artery. In about one-fourth of the cases ascites is present, but in a somewhat larger proportion hemorrhoids, blackish, tarry stools, and other evidences of portal congestion. When the intestinal arterioles are attacked, an intractable colliquative diarrhoea comes on; the stools are offensive, sometimes light from the absence of bile, sometimes dark from decomposition or the presence of blood. When the stomach arterioles are also involved, which is usual under these circumstances, the blandest and simplest articles of diet will pass unchanged or simply decomposed. Blood may be vomited sometimes in large quantity from thrombic ulcers, but the matter ejected from the stomach when the case is well advanced is a thin, watery fluid, faintly acid or neutral, and greenish or brownish in color.

An enlarged spleen is often present, produced by the same conditions--by amyloid degeneration. The same change taking place in the kidney, the urine becomes pale, abundant, of low specific gravity, and albuminous. General dropsy supervenes in a majority of the cases finally, due largely to the hydræmia; and of this condition ascites is a part. In some cases enlargement of the abdomen is the first step in the dropsical effusion, and may throughout be the most prominent, as the author has seen. In other cases oedema of the feet and legs is the first evidence of dropsy; in still others the dropsy is general from the beginning.

Amyloid liver may coexist with a fairly good state of the bodily nutrition, but if digestion and assimilation be interfered with by any of the causes above mentioned, the strength rapidly declines and emaciation reaches an extreme degree.

COURSE, DURATION, AND TERMINATION.--As amyloid liver is never a substantive affection, but secondary to some constitutional malady or to long-continued suppuration, its course must be considered in relation to the agency producing it. It is very silent in its origin and progress, and causes no pronounced symptoms until it attains considerable size and its functions are interfered with by the extent of the deposits. The history of the affection to which it is secondary therefore precedes the onset of the amyloid change and accompanies it throughout. The enlarged organ, with the results of its enlargement in altered functions of the abdominal organs, is a symptom superadded to existing disturbances. The period elapsing in the course of a chronic suppurative disease before the amyloid change occurs differs greatly in different cases, and may be stated as from three months (Cohnheim's case) to many years. Many of the cases terminate by an intercurrent disease; others by uræmic {1045} convulsions; a very few by hemorrhage from the stomach or intestines; and those pursuing their course uninterruptedly, by exhaustion.

The prognosis is very unfavorable. By some a cure at the beginning of the morbid deposits is regarded as possible, and examples of cures have been reported. The writer has seen supposed cases of amyloid liver terminate in recovery. There must always remain an impression that in such instances an error of diagnosis was committed. Those of syphilitic origin are probably more curable, but syphiloma of the liver may be confounded with amyloid disease, and hence the cure may be referred to the latter.

DIAGNOSIS.--Amyloid degeneration of the liver may be confounded with the various non-febrile enlargements of the organ. An important element in making the differentiation is the history of suppuration in connection with bone, with lung cavities, with constitutional syphilis, with chronic malarial toxæmia, etc. From fatty liver, amyloid degeneration is distinguished by the history as just sketched; by the fatty tendencies of the body in the former, emaciation in the latter; by the concomitant changes in the spleen, kidneys, and elsewhere; and by the subsequent history, fatty liver terminating by a weak heart usually, whilst the amyloid disease ends in the modes described in the preceding paragraph. From hydatid disease, amyloid liver is differentiated by the history, by the difference in the physical characteristics of the enlargement, by the presence of the purring tremor in the one, its absence in the other, and especially by the subsequent course. In all doubtful cases the use of an aspirator-needle and the withdrawal of some fluid containing the characteristic hooklets of the echinococcus will serve to determine the nature of the growth. From cancer, amyloid liver is separated by the previous history, by the nodular character of the enlargement, by the pain, and by the cachexia and associated derangements. Whilst amyloid liver is secondary to suppurative diseases, cancer is usually secondary to cancer of the stomach or other organ within the limits of the portal circulation.

TREATMENT.--As amyloid disease owes its origin to syphilis, to chronic malarial toxæmia, to suppuration, these, so far as they are remediable conditions, should be cured as speedily as may be, to prevent the development of the amyloid disease or to arrest it if begun. Unfortunately, the condition of the liver is not recognized until the morbid change is effected, and therefore practically irremediable.

The treatment necessarily involves that of the morbid state to which the amyloid deposits are owing. The syphilitic disease requires iodine and mercury; the malarial, quinine, iodine and the iodides, eucalyptus, iron, etc., according to the state of each case; and surgical diseases, especially necrosis of bone, should be effectively treated by suitable surgical expedients. The cause being removed if possible, what means, if any, can be resorted to to cause the absorption of the amyloid matter? The only specific plan of treatment hitherto proposed is that of Dickinson,[147] based on his theory of the constitution of amyloid matter; according to which the amyloid deposits consist of fibrin altered by the separation of the potash and soda salts, which have been eliminated in the pus. If this theory be admitted, the obvious indication is to supply the alkaline materials. The cases reported by Dickinson in which this theory was {1046} practically demonstrated were not sufficiently improved to lend any empirical support to this method.

[Footnote 147: _The Pathology and Treatment of Albuminuria_, p. 214 _et seq._]

The medicinal remedies which do any good are the iodides--notably the iodides of ammonium, of iron, of manganese, etc., the compound solution of iodine, and the double iodide of iron and manganese. As the officinal ointment of the red iodide of mercury, rubbed in over the splenic region, does so much good in chronic enlargement of the spleen, it is probable that it will prove effective in this form of enlargement of the liver. The writer has observed results from it in such cases that justify him in strongly urging its employment. The method of its application consists in rubbing perseveringly a piece of the ointment, a large pea in size, over the whole hepatic area, and repeating it daily until some irritation and desquamation of the skin is produced, when it should be suspended until the parts will bear renewed applications. Besides the topical application of the red iodide, this remedy may be given internally with advantage without reference to syphilitic infection. It seems to the writer probable that bichloride of mercury may be as useful, as it is certainly more manageable. The chloride of gold and sodium, arsenic in small doses, and the metallic tonics, so called, may be useful carefully administered, especially the first mentioned, which the writer believes has some real power over the disease.

Dietetic rules are of great importance. As the hepatic functions are much disturbed, if not entirely suspended, it is necessary to give those foods which are converted into peptones in the stomach. As a rule, fats, starches, and sweets are mischievous, and milk, meats, oysters, and the nitrogenous foods best adapted to nourish the patient. If the diarrhoea should prove exhausting, the mineral acids, with opium, are the best remedies. Nausea and vomiting are best relieved by carbolic acid mixture, and hemorrhages by the solution of the chloride or subsulphate of iron.

Fatty Liver; Fatty Degeneration of the Liver (Hepar Adiposum).

DEFINITION.--By the term fatty liver is meant a change in the organ characterized by the excessive quantity of fat- or oil-globules contained in the cells of the parenchyma.

CAUSES.--The liver acts, under normal conditions, as a reservoir for the surplus fat, which it gives out as the demand is made. It is not only the fat brought to the liver by the blood which accumulates in the organ, but it apparently possesses the power to transform certain substances--albumen, for example--into fat. An important causative element, therefore, is the quantity of fat present in the food habitually consumed. This has been proved by the investigations of Radziejewsky[148] and others, who have shown that the fat in the food is stored up in the normal places of deposit, one of which, of course, is the liver. Another causative element is the formation of fat from the albumen of the hepatic cells in consequence of diminished oxidation. In respect to both causes the consumption of oxygen is an important factor. The insufficient supply of oxygen {1047} which is a necessary result of a sedentary life leads thus, directly, to the accumulation of fat in the liver-cells. A constitutional predisposition is also an important factor. There are those who under certain conditions of daily life store up large supplies of fat, and others who under the same conditions continue lean. Women more than men are subject to such inherited predispositions.

[Footnote 148: _Virchow's Archiv für path. Anat., etc._, Band lvi. p. 211.]

Again, fatty liver occurs in the course of certain cachexiæ, notably phthisis. In this case the obstructive pulmonary lesions interfere with the process of oxidation, and also maintain a constant hyperæmia of the portal system. This condition of the liver also occurs in the cancerous cachexia, in anæmia and chlorosis of long standing, in chronic suppurative diseases, etc. The dyscrasia of chronic alcoholism is a very common cause of fatty liver. At the same time that hyperplasia of the connective tissue is taking place the fat is accumulating in the hepatic cells. So great is the accumulation of fat in the blood that the serum presents a milky appearance. This excess in the quantity of fat is rather due to diminished oxidation, to lessened combustion, than to increased production. Another causative element of the fat-production in cases of alcoholism is the interference of alcohol with the process of digestion and assimilation.

Poisoning by phosphorus, antimony, arsenic, and other metals sets up an acute fatty degeneration of the liver. Pregnancy, lactation, and suppuration also have the same effect, but to a slighter and less permanent extent.

PATHOLOGICAL ANATOMY.--Fatty liver agrees with amyloid liver in that the fatty deposits increase the size and weight of the organ. The surface is smooth, the peritoneal investment unaltered, and the margins rounded. Sometimes the organ is merely increased in thickness, sometimes in diameter. It has a greasy feel and cuts like a mass of fatty tissue. Examined at a low temperature--below freezing--it seems like a mass of suet, the proper structure being almost extinguished in the fatty metamorphosis. The outline of the lobules remains distinct even in cases far advanced in the fatty degeneration, but in the extreme cases it is obliterated, the cut surface presenting a uniformly yellowish or grayish-yellow tint. The fatty liver is also wanting in blood; it is dry, and on section only the largest vessels contain any blood. When cardiac disease of a kind to produce congestion of the venous system exists--for example, mitral or tricuspid lesions--the same relative decrease in the quantity of blood in the liver is observable after death, although during the life of the subject the opposite condition may have been present. The cause of this bloodlessness of the fatty liver is to be sought in the pressure exerted by the growing fat-cells.

Not all cases of fatty liver are advanced to the degree indicated in the above description. From the normal size up to the maximum attained by the most advanced fatty liver there are numerous gradations in the quantity of fat and in the dimensions of the organ. Fatty degeneration may accompany cirrhosis, in which the liver is contracted. The deposits of fat may take place in particular areas. In cases of fatty liver per se the deposit occurs within the liver-cells, as may be demonstrated on microscopic examination, the initial change consisting in the formation of granules in the protoplasm which ultimately coalesce, thus producing {1048} fat-globules or cells. The fatty change in the hepatic cells proceeds in a certain methodical manner from the cells at the periphery of each lobule to the centre. The quantity of fat deposited in the liver in cases of fatty change is very great. In the normal condition of the organ fat exists, according to Perls,[149] in the proportion of 3 per cent. of the weight of the liver. When the condition of fatty liver exists the quantity of fat rises to 40, even 45, per cent.--almost one-half. It is important to note, as was pointed out by Frerichs, that in an inverse ratio with the increase of fat was the quantity of water.

[Footnote 149: _Virchow's Archiv_, _supra_.]

That more or less fatty change in the liver is not incompatible with a normal functional activity is quite certain, but the boundary between health and disease is by no means well defined in respect to the quantity of fatty change in the liver-cells. The liver, within certain limits, is a mere reservoir of the surplus fat of the body, and hence a variable, but not excessive, amount of accumulation of fat is not incompatible with a normal functional performance of the organ. The limits of a merely functional state and of a diseased state are not, therefore, very clearly defined. In certain inferior animals, as Frerichs has shown, a fatty condition of the liver is normal.

SYMPTOMS.--The signs and symptoms of fatty liver are by no means well defined. This state of the organ, as a rule, accompanies the general tendency to fatty metamorphosis and deposit in the body. It is a symptom in the course of phthisis, of chronic alcoholism, and of various forms of metallic poisoning, but under these circumstances there is no material change in the course of the symptoms produced by this complication. As an independent affection it rarely, if ever, exists alone. So far as its symptoms can be defined, they are referable to the organs of digestion and assimilation and to the liver itself.

The appetite is generally good, but distress after eating, acidity and heartburn, eructations of acid liquid and of certain articles of diet, are experienced. The stools are usually rather soft or liquid, wanting in color, whitish or pasty, and occasionally dark, almost black, owing to the presence of blood. Hemorrhoids are usually present. The discharges are often offensive from the decomposition of certain constituents of the food, acid and burning because of the presence of acetic, butyric, and other fat acids, or merely offensive because of the formation of hydrogen compounds with sulphur and phosphorus. Notwithstanding the derangement of the stomachal and intestinal digestion, the deposition of fat continues in an abnormal ratio. With the increase in body-weight a decline in muscular power takes place. The respiration is hurried on the slightest exertion, and dyspnoea is produced by any prolonged muscular effort. The circulation is feeble and the pulse slow in the state of repose, but on active exertion the pulse becomes rapid and at the same time feeble. The sleep is disturbed by horrifying dreams, and only on assuming a nearly sitting posture can the patient sleep with any degree of quietude.

In these cases of fatty liver a very considerable mental inquietude, despondency, even hypochondria and melancholia, result. The relation of insufficient hepatic excretion to the mental state is yet sub judice, but there can be no doubt that some connection exists. From the earliest {1049} period hepatic derangements--as the term hypochondria denotes--have been associated with certain disorders of the mind. This relation certainly holds good in respect to the mental perturbation occurring in cases of fatty liver. With a rotund countenance and a well-nourished body there is associated very considerable mental despondency.

Without distinct jaundice the skin has an earthen or tallow-like hue, the conjunctiva is muddy or distinctly yellow, and now and then well-defined jaundice appears.

The urine is rather scanty, high-colored because of the presence of bile-pigments, and deposits urates abundantly. When jaundice accompanies fatty liver the urine will be very dark, muddy, thick, and will react to the usual tests for bile, urates, etc.

The area of hepatic dulness is, as a rule, enlarged in cases of fatty liver. The deposition of fat in the cells adds to the gross size of the organ, and hence the inferior margin extends below the border of the ribs to a degree determined by the amount of increase in its substance. If the liver can be felt, it is smooth, not hard and resisting, and is free from nodules. Usually, however, owing to deposits of fat in the omentum and in the abdominal walls, the outlines and condition of the liver cannot be ascertained, and must remain merely conjectural. Rather, therefore, by implication than by direct examination can the condition of the liver be ascertained.

COURSE, DURATION, AND TERMINATION.--The course of fatty liver, as an element in a general change not of a toxic character, is essentially of a chronic character. The fatty liver of acute phosphorus, antimonial, and other forms of poisoning is acute and fatal, but it is not these forms with which we are here concerned. Acting the part of a reservoir of the surplus fat stored up in the body, which may be disposed of under normal and physiological conditions, the fatty liver becomes by careful management a normal organ again. The course, duration, and termination will therefore largely depend on the nature of the management pursued. A fatty liver cannot, then, be regarded as fatal, or even as dangerous to life per se. The course and termination will therefore be those of the associated condition.

DIAGNOSIS.--The determination of the existence of fatty liver will not be difficult in all those cases in which this condition may properly be suspected; for example, in phthisis, in chronic alcoholismus, in obesity, and in cases of habitual indulgence in eating and drinking. If in these cases the organ is distinctly enlarged, is smooth, and is flabby in outline; if at the same time the digestion is deranged, the stools are light in color, there are hemorrhoids, flatulence, acid indigestion, and torpid bowels,--a fatty liver may be reasonably suspected. The subjects of fatty liver are usually obese, and present the characteristics typical of that condition, or they are the victims of alcoholismus or present the evidence of habitual indulgence in the pleasures of the table. The differentiation of fatty liver from amyloid degeneration, from cystic disease, and from other maladies causing enlargement of the organ is made by reference to these points in the etiological history--by a careful study of the condition of the organ itself and of the organs associated with it in function. As the amyloid liver is more likely to be confounded with the fatty liver, it should be noted that the former is an outgrowth of the process of suppuration, that the organ {1050} is hard in texture, and that amyloid change occurs at the same time in other organs--conditions opposed to those characteristic of the fatty liver. Cancer of the liver is accompanied by a peculiar cachexia; the body wastes, and the enlarged liver is hard and nodular instead of being smooth and flabby.

TREATMENT.--When fatty liver is a symptom merely, its treatment is merged into that of the primary condition. Thus, in phthisis and in the various forms of metallic and phosphorus-poisoning the condition of the liver is quite secondary. There are cases of obesity, however, in which the fatty change in the liver is a part of the general morbid process, and must be treated accordingly. There are still other cases in which, without a decided tendency to obesity, the food habitually consumed is of a fatty or fat-forming nature. The first requisite in the treatment of fatty liver is to amend the diet. From the time of Hippocrates down to Mr. Banting it has been recognized that the starchy and saccharine constituents of the food, as well as the fatty, contribute to the formation of fat. In arranging a dietary in cases of fatty liver this fact should be regarded. Besides excluding the fats, saccharine and starchy substances should be cut off. The diet should be composed of fresh animal foods, game, fish, oysters, and such succulent vegetables as lettuce, celery, spinach, raw cabbage (cole-slaw), etc. Amongst the articles excluded should be bread, but the greatest difficulty is experienced in its withdrawal, many patients declaring themselves unable to live without it. In such instances a small biscuit (water-cracker) may be allowed, but, as far as may be accomplished, bread should be cut off from the diet.

If there are acidity, heartburn, pyrosis, and regurgitation of acid liquid, much good may be expected from the administration of diluted nitric acid before meals, especially if there be considerable uric acid in the urine. The simultaneous administration of tincture of nux vomica will prove useful if the appetite is poor and the digestion feeble. When the complexion is muddy, the conjunctivæ yellow, and the tongue coated, excellent results are had from the persistent use of phosphate of sodium. Under these circumstances also arsenic is very beneficial. Even better results may be had from a combination of the two agents, a teaspoonful of the pulverized phosphate being given with one-fortieth of a grain of the arseniate of sodium. Alkalies, as lithium citrate, solution of potassa, etc., are unquestionably useful as remedies for obesity and fatty liver, but they must be administered with a proper caution. Also, the permanganate of potassium has seemed to the author to be especially valuable as a remedy for these states.

Remedies to increase the activity of the portal circulation and diminish congestion of the hepatic vessels are useful at the outset, but the anæmia which succeeds renders their use improper at a later period. Amongst the hepatic stimulants of great use in those cases characterized by whitish, pasty stools, yellow conjunctivæ, etc., are resin of podophyllin, euonymin, baptisin, and others having the same powers. Saline laxatives are also useful, but to a less extent. It must be remembered, however, that these subjects are wanting in bodily vigor, often suffer from weak heart, and always have flabby muscles, so that they bear all depleting measures badly. The hepatic stimulant of greatest utility in these cases is sulphate of manganese. The writer has had excellent results from a {1051} combination of quinine and manganese. For the general state, which denotes insufficient oxidation according to the chemical pathologists, permanganate of potassium is a remedy of value, as above mentioned. The best form in which to administer this is the compressed tablet, and the dose usually is two grains. As chalybeate tonics are indicated, the oxidizing power of the succinate of the ferric peroxide, the remedy so warmly advocated by Buckler, may be utilized with advantage. The combination of quinine, iron, and manganese in pill form, or the syrup of the iodides of iron and manganese, or the phosphate of iron, quinine, and strychnine, are tonics adapted to the relief of the depression accompanying this malady.

III. AFFECTIONS OF THE BILIARY PASSAGES.

Catarrh of the Bile-Ducts.

HISTORY AND DEFINITION.--Although catarrh of the bile-ducts had been incidentally referred to by some previous writers, notably by Stokes of Dublin, Virchow[150] was the first to treat of this condition systematically. Amongst recent writers, Harley[151] appears to be the only one disposed to question the importance of catarrh of the bile-ducts as a factor in the production of jaundice. Even in phosphorus-poisoning the appearance of jaundice, at one time supposed to be hæmatogenic in source, has been referred to a catarrh of the bile-ducts.[152] It seems probable that opinions have too decidedly veered toward the importance of this condition as a factor in the production of jaundice.

[Footnote 150: _Archiv für path. Anat._, Band xxxii. p. 117 _et seq._]

[Footnote 151: _Diseases of the Liver_, _supra_.]

[Footnote 152: Wyss, _Archiv der Heilkunde_, 1867, p. 469 (Legg).]

CAUSES.--Catarrh of the bile-ducts has been referred to all those causes which can excite a catarrhal process in any situation. These are systemic and local. Amongst the systemic may be placed peculiarities of constitution or idiosyncrasy. A tendency to hepatic disorders is a feature in certain types of constitution, and, as such types are transmitted, the hepatic disorders seem to be inherited. In such persons, possessing the so-called bilious nature, catarrh of the biliary passages is not uncommon, and a special susceptibility to it apparently exists. The atmospherical and other causes which in some subjects will set up a catarrh of the bronchi will in the bilious type induce a catarrh of the duodenum and bile-ducts. The malady is not inherited; only the character of bodily structure which favors it under the necessary conditions.

Climatic changes and certain seasons, especially the autumn, are influential causes. Exposure to cold and dampness, the body warm and perspiring, will set up a catarrhal process in the bile-ducts and intestine, especially in those having the special susceptibility which belongs to certain bodily types. Malarial miasm is an especially active cause in malarial regions. The writer has seen many examples in various parts of the United States within the malaria-breeding zone. Other miasmatic agencies are not without importance. The exhalations from the {1052} freshly-upturned soil of some cities, the gases from cesspools and sewers, and illuminating gas exert a causative influence. The bad air thus made up has been happily called civic malaria.

The most influential causes of catarrh of the biliary passages are local in origin and in action: they are the agencies which induce catarrh of the duodenum. Disturbances of the portal circulation should be first named. Whenever obstructive lesions of the cardiac orifices exist, whenever the pulmonary circulation is impeded by disease of the lungs, the portal vein is kept abnormally full, and as a necessary result of the stasis a catarrh of the mucous membrane follows. Congestion of the portal system may be a result of vaso-motor paresis. The abdominal sympathetic may be the seat of various reflex disturbances: those of a depressing kind induce stasis in the portal system. Certain medicinal agents have this effect, and prolonged and severe cutaneous irritation, it is probable, may act on the portal circulation in the same way. The action of cold on the peripheral nerves may be similarly explained.

Catarrh by contiguity of tissue is the most frequent factor. Catarrh of the duodenal mucous membrane is the initial condition, and from thence the process extends to the bile-ducts. Although the duodenum may be alone affected, the usual state of things is a gastro-intestinal catarrh, the stomach and the whole length of the small intestine being simultaneously diseased. When the catarrhal process is thus diffused the duodenal mucous membrane is most deranged, probably because the acid and fermenting chyme is first received here, and what acridity soever it may possess attacks this part in its greatest strength. It must be remembered that the secretion of the duodenal glands and of the pancreas and liver must also have an abnormal character; hence those foods which in the healthy condition of things are digested in this part of the canal undergo ordinary putrefactive decomposition and furnish very irritating products. This observation is especially true of the fats: the fat acids are in the highest degree irritating. The digestive fluid of the duodenum has a more or less pathological character, because the catarrhal process not only interferes with the habitually easy flow of the gland secretions, but, extending to the gland elements themselves, gradually alter their structure.

Gastro-intestinal catarrh results from the misuse of foods and the abuse of certain condiments and of spirits. Excess in the quantity of starchy, saccharine, and fatty foods which undergo conversion and absorption in the intestine, habitually consumed, decomposition of such portions as escape proper digestion ensues, and the products of this decomposition exercise an irritant influence on the mucous membrane. The daily consumption of sauces and condiments and of highly-seasoned foods has a constant irritating action; but more influential than any other causative agency is the abuse of malt liquors and spirit. Whilst the latter acts more on the stomach and the liver proper, the former affect more the duodenal mucous membrane and the bile-ducts.

To these causative agencies must be added a pathological state of the bile itself. Under conditions not now known the bile seems to acquire acrid properties and set up a catarrh in passing along the ducts.

PATHOLOGICAL ANATOMY.--The area affected by the catarrhal process varies greatly. The termination of the common duct for a short space may be the only part affected, but with this there is always more or less, {1053} sometimes most extensive and severe, duodenal catarrh, followed by jaundice. The extent to which the common duct is affected may be exactly indicated by the staining with bile, which extends down to the point of obstruction. The catarrhal process may invade the whole extent of the common duct, the cystic duct, gall-bladder, and the ramifications of the tube throughout the organ. The resulting appearances will vary accordingly.

The first change observable is a more or less considerable hyperæmia of the mucous membrane; but this is rarely seen, because the examination cannot be made at the time when this condition is present. The epithelial layer is swollen, sodden, the cells cloudy, undergoing rapid multiplication and desquamating. The cast-off cylindrical epithelium, mucous cells, and serum make up a turbid mixture, which, with bile, fills the smaller ducts, and may in places, especially at the orifice of the common duct, form an obstruction sufficient to prevent the passage of the bile; which may, however, be readily pressed out with a little force. Especially near the end of the common duct the mucus is apt to accumulate, and a plug of it, often tenacious and somewhat consistent, obstructs the orifice. It is probable that whilst catarrh is the chief cause of jaundice, it may also, by a merely intermittent activity, cause the condition of biliousness--now so far relieved as to permit the bile to descend into the intestine, now so much obstruction as to prevent the escape of any considerable part of that formed. When the common duct is the seat of the catarrhal process, and the outflow of bile thus prevented, it accumulates in the gall-bladder, which may be so far distended as to present a recognizable tumor of pyriform shape through the abdominal parietes.

When the catarrhal process invades the finer ducts the appearances are somewhat different. There are no bile-stains along the course of the common and cystic ducts, and the gall-bladder is empty, or at most contains only some mucus, with altered bile. The tubes at or near their ultimate ramifications contain a turbid mucus composed of cylindrical epithelium and lymphoid cells, and tenacious enough to close them firmly. More or less hyperæmia of the liver-structures proper, and consequent increased dimensions of the organ, a more or less active catarrhal condition of the duodenal mucous membrane, accompany the changes in the finer ducts.

SYMPTOMS.--There are marked differences in the behavior of the more acute cases of catarrh of the bile-ducts and the chronic examples of the same disorder. The former is held to be the most frequent cause of jaundice, whilst the latter is an important element in the so-called bilious state, in lithæmia, and as a secondary condition in some cardiac and pulmonary diseases. Also, the morbid complexus of catarrh of the bile-ducts includes the symptoms of duodenal and gastro-duodenal catarrh.

The acute form of this disease sets in with the symptoms of gastro-duodenal catarrh. Usually, after indulgence in too highly stimulating food or in some article having a specially irritating character, an attack of acute indigestion supervenes. The tongue is more or less heavily coated, the breath heavy, the taste bitter, pasty, or sourish, the appetite poor or actual repugnance to food, especially to the offending articles, is experienced, and nausea, not unfrequently vomiting, ensues. The epigastrium and the hypochondriac regions have a heavy, overloaded, distressed, {1054} and sore feeling; there is some tenderness to pressure; sometimes the gall-bladder, abnormally full, may be detected by careful palpation; and the area of hepatic dulness will usually be increased. The abdomen is more or less distended by gases, and eructations of offensive gases (hydrogen and sulphur compounds, volatile fat acids, etc.) occur. Constipation exists when the catarrhal process is limited to the duodenum, and the stools consist of hard lumps having a light yellow, clay-colored, or whitish appearance. When the whole extent of the small intestine is affected, the stools will be soft, liquid, or watery, and will vary in color from yellow to gray or white. In some cases the fecal matters will have an offensive odor--the odor of decomposition--and considerable discharges of very foul-smelling gas will attend the evacuations. This symptom will occur when the intestinal digestion is suspended and the contents of the bowel in consequence undergo putrefactive decomposition.

During the initial period of the disorder the urine will simply be high-colored and loaded with urates and uric acid, but when jaundice supervenes the pigment will convert the urine into a dark, coffee-colored, and somewhat thick liquid.

With the onset of the malady symptoms referable to the nervous system appear. Headache, dizziness, and hebetude of mind are present, and now and then an attack of catarrh of the bile-ducts will have the objective signs of an ordinary migraine or sick headache. Usually, however, as the intestinal and hepatic troubles develop, headache and some mental hebetude come on, but when jaundice supervenes the headache becomes more severe, and very considerable mental depression, irritability of temper, and moroseness are experienced. Chilly sensations, with flashes of heat, are felt at the outset, but with the appearance of jaundice the sensation of coldness predominates. In some cases, the intestinal catarrh being extensive, there will be, after some preliminary chilliness, a febrile movement, but this is never of a pronounced character, and in the slighter cases of the disease or when the catarrhal process is limited to the bile-ducts, there is no elevation of temperature. With the first symptoms the pulse is somewhat quickened, but as the bile acids accumulate in the blood they effect a decided slowing of the heart's action, the pulse falling as low, it may be, as 50 per minute. This lessened activity of the circulation is accompanied by corresponding reduction of temperature, the body-heat falling a degree or more.

The most distinctive symptom of catarrh of the bile-ducts is jaundice. In the acute or quickly-developing form above described of catarrhal icterus the symptoms of gastro-intestinal disturbance precede the first indication of jaundice from five to eight days. Yellowness of the conjunctiva and of those parts of the body exposed to the air is the first manifestation; afterward the jaundice hue becomes general. The tint varies in depth from a faint gamboge-yellow, only discernible in a favorable light, to a deep greenish- or brownish-yellow.

In the more chronic cases of catarrh of the bile-ducts the symptoms are simply those of a gastro-duodenal catarrh, to which some hepatic disturbances are superadded. Some abdominal uneasiness felt in the epigastrium and in the right hypochondrium, especially in two to three hours after meals; flatulence, sometimes accompanied by colic; {1055} constipation, persistent or alternating with diarrhoea--in the one case in hard lumps with more or less mucus adherent, in the other soft or liquid, and in both cases having a rather golden-yellow color, grayish or black and tar-like appearance,--such are the symptoms referable to the intestinal canal. The disturbances in the hepatic functions produced by the catarrhal swelling of the mucous membrane of the ducts are further exhibited in a somewhat sallow, earthy, or muddy complexion, yellowish tint of the conjunctiva, high-colored, acid urine loaded with urates and phosphates. Such subjects, although having, it may be, a keen appetite, rather lose than gain in weight: they experience lassitude, headache, much depression of spirits, and the mental symptoms are most pronounced during the time intestinal digestion is going on. In fact, the morbid complexus is rather that of intestinal catarrh; nevertheless, the slight degree of obstruction to the outflow of bile occurring in these cases has an influence both in the intestinal digestion and in the nutritive functions. Any degree of obstruction, as has already been pointed out, leads to serious structural change of the liver, and this in turn produces well-defined symptoms.

Disturbances of the hepatic functions, even jaundice, accompany the paroxysms of malarial fever. Without the occurrence of fever, catarrhal jaundice may come on during the course of chronic malarial poisoning. Catarrh of the bile-ducts is the pathogenetic factor in these cases. More especially in malarial regions, but also in temperate and warm climates, paroxysmal attacks, with or without jaundice, are comparatively frequent. These acute seizures occur in those having the chronic form of the malady, and are excited by sudden climatic changes, by excesses in eating, especially by the use of improper articles of diet. Considerable nausea, flatulence, and constipation or diarrhoea, weight, tension, and soreness in the right hypochondrium and sometimes in the shoulder, chilliness, general malaise, headache, and an increasing icterode tint of the skin, constitute the complexus of symptoms belonging to these cases.

COURSE, DURATION, AND TERMINATION.--Acute catarrh of the bile-ducts with jaundice has a well-defined course--in its mildest form, with little gastric or gastro-intestinal disturbance--lasting ten days or two weeks; in the ordinary form, with the accompanying gastro-duodenal catarrh, running its course in a month to six weeks. In the chronic form, with acute exacerbations due to indiscretions in diet or to climatic influences, the course of the disease is chequered by vicissitudes, the result of the causes just mentioned, and its duration must therefore be indefinite and, as a rule, protracted. Catarrh of the bile-ducts, or catarrhal jaundice, usually terminates in health after a period of functional derangement of the intestines and liver. Without exhibiting any features of a special character, some cases do not pass through this benign course: the intestinal catarrh sets up an ulcerative process at one or more points in the duodenum; but more especially the obstruction to the free course of the bile caused by the catarrhal swelling of the mucous lining of the ducts induces structural changes in the liver--an hypertrophy of the connective-tissue elements, a sclerosis.

DIAGNOSIS.--There are but two signs which indicate the nature of the disorder, and only one that is really distinctive. Intestinal indigestion with slight coincident biliary derangement is one, and jaundice is the {1056} other. When, after the signs and symptoms of gastro-duodenal catarrh have declared themselves, jaundice appears, there can be no question as to the nature of the case. The diagnosis is more difficult in the chronic cases with exacerbations due to the exciting causes above mentioned, for the persistence of the jaundice will suggest the occurrence of some permanent organic lesion. The differentiation of the various kinds of jaundice has already been made.

TREATMENT.--Regulation of the diet is of the first importance. Those foods requiring the intestinal juices for their solution and absorption, and which cannot be properly digested when a duodenal catarrh exists or when bile is absent, should of course be excluded from the diet. These articles are the fats, starches, and sweets. The mucus playing the part of a ferment, these substances are converted into various secondary products of an irritating character. Flatulence is caused by the evolution of carbonic acid gas and the hydrogen compounds of sulphur and phosphorus; and acetic, butyric, and other acids not only change the reaction of the intestinal juices, but are directly irritating to the mucous membrane. In the acute cases a diet of skimmed milk, taken hot and at three hours' interval, and after the acute symptoms have subsided, in conjunction with some other aliment, is the most appropriate mode of alimentation. Meats, fish, eggs, and oysters are the chief articles of diet, besides the milk, during the whole course of the more chronic cases; and to these may be added the succulent vegetables, as lettuce, spinach, celery, raw cabbage, and tomatoes. If, in consequence of irritability of the mucous membrane or of idiosyncrasy, any article occasions distress, it should be omitted from the diet.

The medicinal management includes the administration of remedies for gastro-intestinal catarrh. The treatment of catarrhal jaundice has been discussed. When constipation exists, saline laxatives, especially phosphate of sodium and Rochelle salt, are useful. If there be diarrhoea, the most appropriate remedies are bismuth, with or without carbolic acid, Hope's mixture, oxides of zinc and silver, and other mineral tonic astringents.

The propriety of the administration of special hepatic stimulants--cholagogues--has been much disputed. When the disorder consists merely in an obstruction to the outflow of bile, the utility of stimulating the production of this secretion seems more than doubtful. Much harm has been done by the indiscriminate use of mercury. Its power to increase the production of bile having been assumed, and the quantity of bile present in the feces being manifestly less in cases of catarrhal jaundice, it followed that mercury should be employed in this disorder. Modern experience has quite demonstrated its inutility in the mode and for the purpose to which it was formerly devoted. Nevertheless, good effects are had from calomel in small doses as a sedative to the mucous membrane. When there are nausea, headache, vertigo, and constipation present, excellent results may be had from the 1/20 gr. to 1/10 gr. of calomel, exhibited at short intervals until the bowels are moved. If calomel possessed the property formerly ascribed to it, of stimulating the hepatic functions, it would be contraindicated in catarrh of the bile-ducts. This contraindication exists in respect to all hepatic stimulants.

If there be decided irritability of the stomach and constipation, {1057} Seidlitz powders may be given at regular intervals. Phosphate of sodium in drachm doses is highly useful for the double purpose of a laxative effect and to prevent the tendency to inspissation of the bile, which is one of the most important results of catarrh of the bile-ducts and gall-bladder. In the more chronic cases the persistent use of sodium phosphate is to be highly commended.

In this disease, especially as it occurs in gouty subjects, sulphate of manganese is often decidedly serviceable. If anæmia and debility coexist, this remedy can be combined with sulphate of iron and sulphate of quinine--a combination which the writer has found peculiarly effective under such circumstances. When oxidation is deficient and the urates are present in the urine in excessive quantity, good effects are had from the permanganate of potassium, a tablet containing two grains being given four times a day. In the more chronic cases the salts of silver, copper, and zinc are really very useful, especially the oxides of silver and zinc; and of these the former is more efficient. Better than any of those mentioned is arsenic, as arseniate of sodium or as Fowler's solution, but the best results are had from small or medium doses persistently used. If there be much intestinal catarrh and consequent diarrhoea, bismuth and aromatic powder, oxide of silver, Fowler's solution with a little opium, Hope's mixture, etc. are appropriate remedies.

It is in catarrh of the bile-ducts that nitric and nitro-muriatic acids have proved useful, rather than in cirrhosis and other diseases of the liver-tissues. They prevent fermentation, promote oxidation, and increase the activity of the assimilative functions. When there occurs active fermentation of certain foods, and consequently considerable flatulence, excellent results are obtained from the members of the antiseptic group--from creasote or carbolic acid, salicylic acid, biborate of sodium, the benzoates, etc. To these may be added quinine, the dose of which will be determined by the purpose for which it is prescribed. So often is catarrhal jaundice of malarial origin that quinine becomes a remedy of high importance in the cases occurring in the malarial-forming zone.

Certain special plans of treatment have been proposed for the cure of catarrhal jaundice. One of the most effective of these is enemata of cold water. By means of an irrigating apparatus the large intestine is well distended with water once a day for several days. The first enema has a temperature of 60° F., and subsequent injections are a little warmer. The increased peristalsis of the bowels and the reflex contractions of the gall-bladder dislodge the mucus lining and obstructing the gall-ducts. When the bile flows into the intestine, digestion is resumed and the catarrhal inflammation subsides. But with the irrigation method may be employed other remedies, as above indicated.

Faradization of the gall-bladder has been used successfully for the expulsion of the stored-up bile and the removal of the mucus obstructing the ducts. It is applied by means of one moistened sponge electrode placed directly over the gall-bladder, and the other on the opposite side of the body and posteriorly. A slowly-interrupted faradic current is then passed. This expedient is not suitable when the case is acute in character.

{1058} Biliary Concretions; Gall-Stones; Hepatic Calculi; Hepatic Colic.

DEFINITION.--There are two classes of concretions which may occasion symptoms: inspissated bile and regularly-formed gall-stones. Slowly-developing symptoms of jaundice from obstruction may arise from the deposit of particles of inspissated bile in the hepatic ducts, or sudden attacks of hepatic colic be due to the passage of concretions. When biliary calculi reach the intestines, certain kinds of disturbance may be caused by their presence there. Under the term biliary concretions must be considered, therefore, the mechanism of their production, their composition, the symptoms caused by their passage through the ducts (hepatic colic), and the intestinal disturbance due to their retention in the bowel.

Formation: Inspissated Bile.--Those concretions consisting of inspissated bile are irregularly-shaped masses of a brownish, greenish-brown, or reddish-brown color, friable and crumbling into a gritty dust with slight pressure of the fingers. When recent and before drying, they are softer, almost pultaceous, and may take the form of the canal through which pressed. But as seen after drying they present the appearance of a dark vegetable extract, dried and partly pulverized. When examined as found in the gall-bladder or lodged in the larger hepatic ducts or distributed in irregular fragments (gall-sand) in the various hepatic passages, they present the shape, color, and general characteristics of a partly-dried vegetable extract roughly broken up, but still soft enough to take any shape from pressure. The writer has seen them thus in situ accompanying regularly-formed gall-stones in a case of gunshot wound of the liver. These masses of inspissated bile differ from gall-stones in composition; they consist of bile, but with a preponderance of the coloring matter. According to Harley,[153] who has given a more correct account of these bodies than any other systematic writer, their composition is as follows:

Water 5.4 Solids 94.6

The contents of the solids are--

Bile-pigment 84.2 Cholesterin 0.6 Salts (iron, potash, soda) 15.2

[Footnote 153: _The Diseases of the Liver, with and without Jaundice, etc._, by George Harley, M.D., F.R.S., Philada., 1883, p. 349.]

Some years ago, before I was aware of the nature of such concretions. I detected a number in examining the stools of a patient who had in quick succession many attacks of hepatic colic, but as the usual form of concretion was looked for and not found, the relation of these bodies to the symptoms in the case was not understood. I now recognize the value of Harley's observations on these bodies.

The biliary concretion which is properly a gall-stone has a definite form and a more or less well-defined crystalline structure. The forms taken are various. The most usual form is octagonal or hexagonal or polyangular, with smooth facets, corresponding to points of contact of other calculi. Instead of smooth facets and sharp angles, the concretion may be studded with irregularly-shaped masses. When there are numerous {1059} calculi present, they have smooth surfaces and rather sharp angles, made, not by attrition, as has been supposed, but by deposition of the new material under pressure. When they have this form there are many present, but the number of facets does not indicate the number of calculi, and the absence of facets is not proof of the absence of other calculi. The smooth opposing surfaces are not always plane, but may be convex or concave to fit the shape of the adjacent bodies.

Calculi may be globular, ovoid, cylindrical, and truncated cones. The largest in my collection is egg-shaped, and nearly filled the gall-bladder which contained it, a little mucus free from bile-elements only being present. If a concretion forms in a duct or a single one is present in the gall-bladder, the shape is determined by the pressure of the walls of the duct or of the gall-bladder, respectively. As found in the stools, and still somewhat soft, the shape will represent the form of the common duct through which it has been pressed. Such a soft, recently-formed gall-stone will have the crystalline structure and chemical constitution of these bodies, and will therefore differ from, apparently, similar masses of inspissated bile. Although a round, ovoid, or cylindrical calculus indicates the absence of others because there are no evidences of mutual pressure and adaptation, a positive conclusion cannot be reached in that way, for the gall-bladder may contain numerous calculi of long-standing, and a recent concretion formed in a duct be discharged with the usual symptoms.

The number of calculi which may be present at any time or be produced in the course of years ranges from one to several thousand. The number is in inverse ratio to the size. One case[154] is reported in which 7802 calculi were found in the gall-bladder, but they must have been very minute in size. Of the specimens now in my collection, there are 230 obtained from one gall-bladder, which they entirely filled; they are nearly uniform in size, have an average weight of two grains, and contain four, five, and six smooth facets. Another collection of calculi removed from a closed gall-bladder contains 45, of large size, distending the organ and forming a tumor which projected beyond the margin of the liver. Hepatic calculi are rarely solitary; hence if one attack of hepatic colic occur, others may be expected.

[Footnote 154: Frerichs, _op. cit._, vol. ii. p. 499.]

In color gall-stones vary from a clear white to a dark-brown, almost black, tint. The most usual tint of the mature calculi in the gall-bladder is that of the ripe chestnut. Long stay in the intestines increases the depth of the color, until it becomes almost black; on the other hand, detention in the gall-bladder has a slightly bleaching action; but the real cause of difference of color is the presence or absence of pigment. If composed of pure cholesterin, the color will be whitish, opaque, or glistening and almost translucent.

In size gall-stones vary from the smallest pea up to a hen's egg. When several hundreds are contained in the gall-bladder, they will usually be of the dimension of a medium-sized pea. Two large solitary concretions in my possession are respectively 2 inches and 1½ inches in long diameter, and 1 inch and ¾ of an inch transversely. Very much larger calculi have, however, been recorded; thus, one mentioned by Frerichs is 5 inches in length and 4 inches in circumference. The most frequently {1060} encountered calculus, at least in this country, is polyangular in shape and of the size of a large pea. Globular or ovoid seems to be the prevailing form, and the dimensions that of a small pea, in Germany, according to Frerichs and Von Schüppel, but this statement must refer to the initial shape of these bodies.

Not all hepatic calculi have defined mathematical forms, but may consist of branching cylinders composed of irregular nodular masses, not unlike the concretions of inspissated bile. As a rule, in each case where the calculi are multiple there is uniformity of color, shape, and composition. This feature is well exhibited in my collection. The calculi obtained from each subject are in one case white, polyangular, rather unctuous, and nearly equal in size; in another, chestnut-brown in color, polyangular in shape, and varying slightly in size, but uniformly characteristic in shape; and in a third, singular in number, ovoid in shape, dark-brown in color.

In composition gall-stones vary somewhat. When fresh they contain considerable water, and at all times are hygroscopic. Dried in the air, they are composed of--

Water 4 Solids 96 --- 100

The solids consist of--

Cholesterin 98 Pigment 1 Inorganic or mineral matter 1 --- 100

Such are the constituents, according to Harley, of the usual concretion, the cholesterin calculus. But as other varieties are encountered occasionally, it may be well to give the composition of these. The following table by Ritter, to be found in _Robin's Journal_ for 1872 (p. 60), is a correct representation of the contents of different specimens:

+------+------+------+------+------+------+------+----- Composition | | | | | | | | of Different | | | | | | | | Kinds. | 1st. | 2d. | 3d. | 4th. | 5th. | 6th. | 7th. | 8th. ---------------+------+------+------+------+------+------+------+----- Cholesterin | 98.1 | 97.4 | 70.6 | 64.2 | 81.4 | 84.3 |trace.| 0 Organic | | | | | | | | matter | 1.5 | 2.1 | 22.9 | 27.4 | 15.4 | 12.4 | 75.2 | 18.1 Inorganic | | | | | | | | matter | 0.4 | 0.5 | 6.5 | 8.4 | 3.2 | 3.3 | 24.8 | 91.9 Number of | | | | | | | | specimens | 28 | 16 | 580 | 94 | 220 | 16 | 3 | 1 ---------------+------+------+------+------+------+------+------+-----

The above may be regarded as the average composition, expressed in round numbers. The variations from these figures will be comprehended in two parts.

A calculus consists of three several parts: the nucleus, the body, the rind. A calculus of small or medium size may be a nucleus for the formation of a large one. Usually the nucleus consists of a bit of mucus, casts of the biliary ducts (Thudicum), inspissated bile, a blood-clot, a liver-fluke or other parasite, as a desiccated round-worm, or some foreign body, as a seed, or, as in one reported example, a globule of mercury.[155] {1061} The central mass of mucus may contain a large proportion of pigment or crystals of cholesterin or lime-salts, giving it special characteristics.[156] There may be several nuclei. Fauconneau-Dufresne reports an instance in which a pyramidal concretion contained four, and Guilbert a globular stone with five, distinct nuclei. Such examples of calculi having multiple nuclei are produced by the adhesion whilst in a soft state of two or more, and the subsequent addition of material to the conjoint mass, welding it into a single stone. A few calculi are homogeneous throughout, composed of nearly pure cholesterin, mixed intimately with a little coloring matter and lime salts. The cholesterin calculus will have a somewhat translucent appearance, will be a dead white or a yellowish-white, or present a greenish- or brownish-yellow tint through the white. Even the white calculus, apparently composed of nearly pure cholesterin, will be found on section to contain traces of a nucleus. By long detention in a gall-bladder whose duct is permanently occluded, and is therefore free of fluid, the mucus nucleus may so shrivel as to leave a cavity which is merely stained. One of my specimens--a solitary calculus of large size--exhibits this peculiarity.

[Footnote 155: Thudicum, J. L., _On Gall-stones_, London, 1863; also Frerichs, _op. cit._, vol. ii. p. 503.]

[Footnote 156: Cyr, Jules, _Traité de l'Affection calculeuse du Foie_, Paris, 1884, p. 11 _et seq._]

The body consists of cholesterin, nacreous or darkened by pigment, deposited in radiating lines or in concentric layers, or in both together. Pigment may be intimately incorporated with the cholesterin or deposited between the layers of this substance, pure or nearly pure, forming an alternating arrangement.

The crust or rind usually is smooth, unctuous to the touch, firm, but when broken with the finger-nail readily crumbles. When composed of lime salts, or when the cholesterin is mixed with varying proportions of these salts and of pigment, the surface is still smooth, but thicker, firmer, and darker in color. The rind may not be smooth, but studded with wart-like projections, or it may consist of several layers of earthy matter separated by pigment. These layers may be very friable, and readily crumble and fall off. In some instances the crust, several lines in thickness, is the body of the calculus, and the cavity contains only a light honeycomb of mucus and pigment.

The specific gravity of gall-stones composed of crystallized cholesterin is nearly that of water. Air-dried calculi will float on water, but the recent ones, full of moisture, sink. The relation of the weight of the calculus to that of the bile is more important. As the specific gravity of bile ranges from 1020 to 1026, it is obvious that on this fluid air-dried calculi will float, but, holding in the recent state much water, ordinary gall-stones will sink. Those containing much mineral matter will have a correspondingly high specific gravity--much higher than bile.

ORIGIN AND FORMATION OF HEPATIC CALCULI.--Certain conditions are necessary to the formation of these bodies on the part of the bile and on the part of the gall-bladder and ducts. Constituted for the most part of cholesterin, which exists in such small quantity in normal bile, there must be some change in the composition of this fluid to increase the quantity or to diminish the solubility of that constituent. It will conduce to a better understanding of the subject to premise the composition of the bile: {1062}

Bile contains, in 1000 parts, Water 860 Solids 140

The solids of bile are, Glycocholate and Taurocholate of soda 90.8 Fat 9.2 Cholesterin 2.6 Mucus 1.4 Pigment and extractive 28. Salts 8. ----- 140.

Normal bile is neutral or slightly alkaline in reaction. If the reaction become acid from any cause, the constituent cholesterin is precipitated; and this occurs the more readily the larger the proportion of this substance held in solution. Cholesterin is an excrementitious material found in the blood and excreted by the liver. It represents in part, probably, the waste of nervous matter, but more certainly of the fatty tissues in general. Conditions of the system in which the metamorphosis of the fatty elements occurs more freely--as obesity, advancing life, etc.--are accompanied by an increased production and excretion of cholesterin.

So long as the neutral state or the alkalinity of the bile is maintained, the cholesterin will be kept in solution, although its relative proportion may be in excess of the normal. A lack of the soda constituent of the system is one factor, but the most important is a catarrhal state of the mucous membrane of the bile-ducts and gall-bladder. The mucus formed plays a double rôle: it furnishes a nucleus about which cholesterin crystallizes; it acts as a ferment and inaugurates a process of acid fermentation which results in the precipitation of cholesterin. When all the conditions favorable to the separation and crystallization of cholesterin are present, any foreign body may serve the purpose of a nucleus. The articles which have thus served have been enumerated.

A by no means infrequent combination is that of bilirubin with calcium; and this may constitute the nucleus or form a part of the body or the crust of a calculus. The mechanism of its formation is not unlike that of the cholesterin concretion. Bilirubin is soluble in alkalies, and is precipitated from its solution by acids. It follows that when acid fermentation takes places under the influence of mucus, bilirubin may be precipitated in combination with calcium. The salts of sodium and potassium are much more abundant in bile than those of lime, but the latter much more often enter into the formation of calculi because of their slighter solubility. Other combinations of bile-pigments, mucus, and the salts of the bile take place, but they are relatively less frequent. The principal lime salt is the carbonate, and this combines in varying proportions with the bile acids, the fat acids, and bile-pigment.

Certain physical conditions are not less important than the chemical in the production of hepatic calculi. Accumulation of bile in the gall-bladder, stasis, and concentration are essential conditions. If bile remains long in the gall-bladder, it becomes darker in color and more viscid, its specific gravity rises, and the relative proportion of solids increases, doubtless because of the absorption of a part of the water. The reaction--which, as has been stated, is in the fresh state neutral or {1063} alkaline--becomes acid in consequence of a fermentative change (Von Gorup-Besanez) set up by the mucus. If a catarrhal state of the mucous membrane exist, the mucus, epithelium, and lymphoid cells cast off play the part of a ferment. The lime which is so important a constituent of biliary concretions is not present even in concentrated bile in sufficient amount to account for its agency in the formation of these bodies, is furnished by the diseased mucous membrane (Frerichs). Indeed, numerous crystals of carbonate of lime have been seen in situ in contact with the mucous membrane in cases of chronic catarrh. It follows, then, that catarrh of the biliary passages has an important causative relation to that pathological condition of the bile which precedes the formation of calculi. In this connection we must not lose sight of the researches made by Ord[157] on the action exerted by colloids on the formation of concretions. The mucus is the colloid; cholesterin, lime, and soda salts are the crystalloids. These latter diffusing through the colloid medium, the resulting combinations assume spheroidal forms. The union of bilirubin and lime salts illustrates the same principle.

[Footnote 157: _On the Influence of Colloids upon Crystalline Forms and Cohesion, with Observations on the Structure and Mode of Formation of Urinary and other Calculi_, by W. Miller Ord, M.D., F.R.C.P. Lond., etc., London, 1879.]

CAUSES.--We have here to consider the external conditions and the general somatic influences which lead to the formation of biliary concretions. Age has an important causative action. Besides other agencies due to advancing life, the increase of cholesterin is an influential factor. The less active state of the functions in general, diminished oxidation, loss of water, and concentration of the bile are influential factors in determining the formation of hepatic calculi in advancing life, as the opposite conditions oppose their production in early life. Although not unknown in infancy, at this period in life and until twenty years of age they occur but rarely. Fauconneau-Dufresne,[158] of 91 cases, had 4 in infants; Wolff[159] had 1 in a collection of 45 cases; and Cyr,[160] 2 cases under ten in a group of 558 cases. The following table illustrates the influence of age on the productivity of gall-stones:

AUTHORS.

HEIN. Whole No. 395 From infancy to 30 18 From 30-70 377

FAUCONNEAU-DUFRESNE. Whole No. 91 Before 20 10 From 20-40 13 From 40-90 68

WOLFF. Whole No. 45 Before 20 3 From 30-60 42

DURAND-FARDEL. Whole No. 230 Before 20 2 From 20-30 28 From 30-60 162 From 60-90 38

CYR. Whole No. 558 Before 20 20 From 21-30 208 From 31-40 185 From 41-50 91 From 51-60 48 Above 60 6

[Footnote 158: _Traité de l'Affection calculeuse du Foie_, Paris, 1851.]

[Footnote 159: _Virchow's Archiv f. path. Anat., etc._, Band xx., 1861, p. 1.]

[Footnote 160: _Traité de l'Affection calculeuse du Foie_, Paris, 1884, p. 53.]

Although there is a general correspondence in the results of the observations on the age most liable, there are differences. Thus, Cyr, whose figures represent the experiences at Vichy, makes the age of maximum liability from twenty to forty years--distinctly earlier than any other observer; and hence it is necessary to bear in mind the extreme latitude of his diagnosis. Of my own collection, 30 in number, all doubtful cases {1064} excluded, there were 20 between thirty and fifty years, and 10 between fifty and seventy. Of these, 22 occurred in subjects between forty and sixty. The period of maximum liability is about fifty years of age. Cyr refers the difference of his statistics from those of other observers to the character of the patients. The preponderance in the number of cases of hepatic calculi at or about the fiftieth year is referable to the lessened activity of the nutritive functions at this period, and to the increase in the relative proportion of cholesterin in the blood in advanced life (Luton[161]). Charcot[162] maintains that after sixty biliary calculi are more frequent, but owing to the physiological conditions then existing the migration of these bodies is effected without notable inconvenience.

[Footnote 161: Jaccoud's _Dictionnaire encyclopéd._, art. "Voies Biliaires;" _idem._, _Bull. gén. de Thérap._, March 15, 1866.]

[Footnote 162: _Leçons sur les Maladies du Foie, etc._, p. 145.]

According to most authorities, females are more liable to the formation of gall-stones than are men. Thudicum, after an analysis of the statistics given by the most experienced and celebrated authorities, places the proportion at 3 to 2. Von Schüppel gives the same figures. Cyr, whilst recognizing this estimate as true of the great mass of observations on this point, finds that in his own cases the preponderance of females over males was even greater, being 4 to 1--inversely to the liability of the sexes to gout; but this excess is to be explained by the character of the subjects falling under his observation. Women are subjected to influences which favor the formation of these concretions, such as pregnancy, sedentary habits, diet of a restricted character, the use of corsets, and the somatic changes at the climacteric period.

The social state, by reason of the conditions associated with a good position in life, has an influence in the production of calculi. Luxurious habits and indulgence in the pleasures of the table are important factors, and hence this malady is encountered amongst the better class of patients in private practice rather than amongst laboring people in the hospitals.

As the somatic conditions which exert a predisposing action, and the social circumstances also favoring the formation of hepatic calculi, are transmitted, heredity is by some classed among the etiological factors, but it can only be regarded as indirect.

Malarial influences unquestionably exert a very powerful influence as this malady occurs in this country. Paroxysms of intermittent either induce or accompany the seizures of hepatic colic, and chronic malarial poisoning exerts a direct causative influence through the hepatic disturbances and the gastro-duodenal catarrh which are associated with it. Attacks of hepatic colic are extremely frequent in the malarial regions of the West and South. It may be, however, that this malady is frequent rather in consequence of the diet of pork than of climatic causes, for it is probable that indulgence in such food plays an important part in the formation of biliary concretions (Harley). Due allowance made for diet, climate is yet, no doubt, an influential factor. In warm, especially in malarial, regions the functions of the liver are taxed to compensate for the increased action of the skin and lungs; but this organ is, besides, affected by the poison of malaria, and to the congestion caused by it is superadded a catarrhal state of the bile-ducts and of the duodenum. A {1065} pathological condition of the bile itself is first induced; then the fermentative changes set up by the mucus cause the separation and crystallization of pigment and cholesterin.

Certain seasons favor the formation of biliary concretions, because then the special influences which operate at all times are more active and persistent. These seasons are fall, winter, and early spring, and gall-stones are more numerous then in consequence of the activity of the malarial poison, the character of the diet then employed, and the lessened oxidation due to the more sedentary life. Climate is a factor of some consequence, but not in the direction that might have been supposed. Gall-stones are more common in temperate than in tropical climates--a statement confirmed by the observation of the physicians of India. They are, according to Harley, quite common in Russia, where also they attain to extraordinary dimensions; but these circumstances are not due to the climatic peculiarities of that country, so much as to the diet habitually consumed, consisting so largely of fatty substances.

Of all the conditions which favor the production of gall-stones, none are so influential as the bodily state and the associated dietetic peculiarities. Those troubled with these concretions, as they have occurred under my observation, have been either obese or have had a manifest tendency in that direction. They have had a strong inclination for the fat-forming foods, also for starchy, saccharine, and fatty articles, such as bread and butter, potatoes, beans and peas, pork, bacon, and fat poultry, etc. Harley thinks indulgence in bacon (p. 367) is a prime factor. Thudicum rejects this notion on chemical grounds, for obesity and the free consumption of fat cannot be concerned in the production of these bodies, because cholesterin is an alcohol.[163] The agency of a fatty diet has been so strongly indicated in clinical observations, and the relation of cholesterin to the fats so obvious, that it can hardly be doubted the free consumption of fat in food contributes directly to the formation of calculi. An indirect relation may also be traced. A catarrhal state of the duodenal mucous membrane existing, and the bile excluded by swelling and obstruction of the bile-ducts, fats are decomposed, and the fat acids, absorbed into the portal blood, contribute to those chemical changes in the bile which result in the precipitation of cholesterin. Beneke[164] traces a connection between atheromatous degeneration of the vessels and the formation of biliary concretions. A general increase in the amount of fat in the body is usually coincident with the atheromatous change, and at the same time the relative proportion of cholesterin in the bile becomes greater.

[Footnote 163: _A Treatise on Gall-stones_, p. 214.]

[Footnote 164: _Deut. Archiv für klin. Med._, Band xviii.]

Indulgence in the starchy and saccharine foods plays a part in the formation of gall-stones not less, if not more, important than the consumption of fats. A diet of such materials is highly fattening, and if the necessary local conditions exist they readily undergo fermentation, and thus cause or keep up a catarrh of the mucous membrane.

Too long intervals between meals, Frerichs[165] thinks, is more influential than errors of diet in causing concretions. The bile accumulates in the gall-bladder, and the condition of repose favors the occurrence of those changes which induce the separation and crystallization of cholesterin. {1066} Obstacles to outflow of every kind have the same effect. The largest calculus in my possession was obtained from a case of cancer of the gall-bladder which compressed, and finally closed, the cystic duct. Sedentary habits have the same mechanical effect, but, as already pointed out, insufficient air and exercise act by lessening oxidation. Corpulent persons indulging in rich food and avoiding all physical exertion, those of such habits confined to bed by illness or injury, the literary, the well-to-do, self-indulgent, lazy, are usual subjects of this malady. Any condition of things which causes a considerable retardation in the outflow of bile will have a pathogenetic importance, especially if the causes of chemical change, the lessened quantity of taurocholic and glycocholic acid, and an increased quantity of cholesterin, coexist. Moral causes, as fear, anxiety, chagrin, anger, etc., have seemed to exercise a causative influence in some instances (Cyr).

[Footnote 165: _A Clinical Treatise on Disease of the Liver_, Syd. Soc. ed., vol. ii. p. 511.]

To the causes of retardation of the bile-flow mentioned above must be added catarrh of the bile-ducts. This acts in a twofold way--as an obstruction; a plug of mucus forming the nucleus. It has already been shown that fermentative changes may be set up by the mucus, which plays the part of a ferment, an acid state of the bile resulting.

Situation of Gall-stones, and their Destiny.--The gall-bladder is, of course, the chief site for these bodies, but biliary concretions and masses of inspissated bile may be found at any point in the course of the ducts. Single stones may be impacted at any point in the cystic, hepatic, or common duct, or masses composed of numerous small calculi may take the form of a duct and branches, making a branching calculus of the shape and size of the mould in which it is cast. Such casts may be hollow, thus permitting an outlet to the bile, or they may completely close the tube, and a cyst form, the walls of which grow thicker with connective-tissue deposits. Stones of very large size may be thus enclosed, Frerichs having seen one the size of a hen's egg formed about a plum-seed, which was the nucleus. In some rare instances the major part of the larger tubes have been filled with inspissated bile, through which the fluid bile could only be slowly filtered.

Calculi are not often found in the hepatic duct, since they can only lodge there in descending from the smaller tubes, and hence are too small to become wedged in. The usual site, as has been sufficiently explained, is the gall-bladder. At the entrance to the cystic duct and at the terminus of the common duct in the duodenum are the points where migrating calculi are most apt to be arrested.

Spontaneous disintegration of gall-stones sometimes occurs. Cholesterin being dissolved off of the corners and edges, the cohesion of the mass is impaired and it falls apart in several fragments. By very slight mechanical injury air-dried calculi will be broken up. In the gall-bladder two factors are in operation to effect the disintegration of the contained calculi: the movements of the body, by which the corners and the borders are crumbled; the solvent action of the alkaline bile on the cholesterin. When, however, these concretions are made up of lime and pigment, their integrity can be impaired only by the process of cleavage; no solvent action can take place.

Various changes occur in the ducts or in the gall-bladder in consequence of the presence of these concretions. Whilst a catarrhal state of the mucous {1067} membrane of the ducts is an element of much importance in the process by which concretions are formed, on the other hand the presence of these bodies excites catarrh, ulceration, perforation, and, it may be, abscess of the liver. When concretions form or are deposited in the ducts, they cause inflammatory reaction, the walls yield, and the neighboring hepatic structures may also be affected by contiguity. The dilatation of the tube is usually cylindrical, much more rarely sacciform. The neighboring connective tissue may undergo hyperplasia and a more or less extensive sclerosis occur. More frequently the calculus ulcerates through, and an abscess is produced which will take the usual course of that malady. Very rarely a calculus is found enclosed in a separate sac and surrounded by healthy hepatic tissue (Roller).[166]

[Footnote 166: _Berliner klin. Wochensch._, No. 42, 1879; _ibid._, Nos. 16, 17, and 19 for 1877, Fargstein.]

As the gall-bladder is the usual place for the formation and storage of gall-stones, the changes in connection with this organ are the most important. The calculi may be so numerous or so large as to distend the gall-bladder and cause it to project from under the inferior border of the liver, so as to be felt by palpation of the abdominal wall. The stones may be few in number and float in healthy bile, or they may fill the bladder to the exclusion of fluid, the cystic duct being closed permanently; or there may be, with one or more concretions, a fluid composed of mucus, muco-pus, serum, and bilious matter. The mucous membrane may be in a normal state, but this is rare; usually it is affected by the catarrhal process, and atrophic degeneration has taken place to a less or greater extent; the rugæ are obliterated, the muscular layer hypertrophied. When attacks of hepatic colic have occurred, more or less inflammation of the peritoneal layer of the gall-bladder and cystic duct is lighted up, and organized exudations form, changing the shape and position of the organs concerned. It is usual in old cases of hepatic colic to find the gall-bladder bound down by strong adhesions, the cavity much contracted or even obliterated, the cystic duct closed, and the neighboring portion of the liver the seat of sclerosis. Such inflammatory exudations about the gall-bladder may become the seat of malignant disease--of scirrhus. Several examples of this have been reported, and one has occurred in my own practice.

The contact of a gall-stone, especially of a polyangular stone, may cause ulceration of the mucous membrane. This is the more apt to occur if the muscular layer of the gall-bladder is hypertrophied, especially if certain fasciculi are thickened and overacting, leaving intervening parts weak and yielding to the pressure of the stone forced in by the spasmodically contracting muscles. Finally yielding, the stone and other contents of the gall-bladder escape into the cavity of the abdomen. Adhesions to neighboring parts may prevent rupture. Such adhesions are contracted with the colon, the duodenum, the stomach, and other organs. In some rare instances the closed gall-bladder has undergone a gradual process of calcification, the mucous membrane losing its proper structure, the muscular layer degenerating, and a slow deposit of lime salts taking place, the ultimate result being that the biliary concretions are enclosed in a permanent shell.

As above indicated, biliary concretions may remain where deposited for an indefinite period. Very often they migrate from the point of formation, the gall-bladder, into the duodenum, producing characteristic {1068} symptoms called hepatic colic. As the size of the ducts increases from above downward, obviously but little vis a tergo is needed to propel the concretions onward. The chief agency in the migration of these bodies is the discharge of bile. Common observation shows that the symptoms of hepatic colic usually declare themselves in two or three hours after a meal--at that time when the presence of the chyme in the duodenum solicits the flow of bile. The gall-bladder contracts on its contents with an energy in direct ratio to the amount of bile present, and with the gush of fluid the concretion is whirled into the duct. Once there, the cystic duct being unprovided with muscular fibres, the onward progress of the stone must depend on the flow of bile; and, as the canal is devious, this may not always carry the concretion into the common duct. Just behind the neck of the gall-bladder the duct makes an angle somewhat abrupt, and here also its folds project into the canal, so that at this point the stone is apt to lodge; but much depends on the size and shape of the calculus. If it pass through the cystic duct, the inflammation resulting may close the canal, several instances of which have fallen under my observation. The next point where stoppage of the migrating calculus may, and frequently does, occur is the orifice of the common duct in the duodenum. This orifice has a funnel shape, the smaller extremity toward the intestine, the object of this being to prevent the entrance into the duct of foreign bodies from the intestine. A diverticulum is thereby made (Vater's) in which a concretion may lodge, partly or wholly preventing the escape of bile into the bowel. The various forces concerned in the propulsion of the concretion onward from the common duct into the intestine are the discharges of bile, the contraction of the few muscular fibres in the walls of the duct, the respiratory movements, especially forced expiration, coughing, sneezing, vomiting, defecation--in fact, all of those acts in which the abdominal muscles, the diaphragm, and the sphincters are simultaneously brought into strong contraction. The symptoms produced by the migration and stoppage of a concretion will vary according to the size and shape of the stone, and the consequent diminution in the amount of bile discharged or its complete arrest. In other words, the stone may be firmly wedged in, completely closing the canal against the passage of bile, or it may lie loosely in the diverticulum Vateri, acting as a sort of ball valve, now permitting a gush of bile, and now stopping the passage-way more or less tightly.

The migration of calculi may take place by ulcerating through into neighboring hollow organs. Usually the first step consists in stoppage of the bile. To the accumulating bile mucus is added, and the gall-bladder or the duct--usually the common or cystic duct--dilates, often to a considerable extent, and, adhesions forming, discharge ultimately takes place through some neighboring hollow organ. The routes pursued by such fistulous communications are various. The organs most frequently penetrated are the stomach, duodenum, and colon, less often the urinary passages, and very rarely the portal vein. Numerous examples of external discharge of calculi have been reported. The most usual, as it is the most direct, is the fistulous connection of the gall-bladder or common duct with the duodenum. Solitary stones of immense size have been thus discharged. Murchison[167] gives references to many interesting {1069} examples, and the various volumes of _Transactions of the Pathological Society_ are rich in illustrative cases. The symptoms produced by the migration of calculi by the natural route and by ulceration into other organs will be hereafter considered.

[Footnote 167: _Clinical Lectures on the Diseases of the Liver_, 2d ed., p. 487 _et seq._]

SYMPTOMS DUE TO THE PRESENCE OF GALL-STONES AT THEIR ORIGINAL SITE.--Very large calculi or numerous small ones may be present in the biliary passages without causing any recognizable symptoms. The migration of these bodies by the natural channel and by ulceration into the duodenum may also be accomplished without any local or systemic disturbance.[168] That the retention of calculi may not induce any characteristic reaction by which they may be recognized is probably due to the fact that the gall-bladder, in which they chiefly form, possesses but slight sensibility, and as it is in a constantly changing state of distension or emptiness according to the amount of bile present, it is obvious that a foreign body made up of the biliary constituents, and having nearly the same specific gravity as the bile, is not likely to cause any uneasiness or recognizable functional disturbances. Furthermore, the slowness with which biliary concretions form enables the organ to accommodate itself to the new conditions. The lack of sensibility which is a feature of the gall-bladder, and which I have had the opportunity to ascertain by actual puncture in an individual not anæsthetized, is in some instances supported by a general state of lowered acuteness of perception. There are great differences in respect to readiness of appreciation and promptness of response to all kinds of excitation in different individuals. To what cause soever we may ascribe the lack of sensibility, the fact remains that in not a few cases of gall-stones in the gall-bladder there are no symptoms to indicate their presence. On the other hand, there are some disturbances that have a certain significance.

[Footnote 168: Amongst the numerous examples of this kind to be found recorded may be mentioned the case reported by M. L. Garnier, Agrégé à la Faculté de Médecine de Nancy (_Archives de Physiologie normale et pathologique_, No. 6, 1884, p. 176): An hepatic calculus, weighing 24.5 grammes, was discharged without any symptoms or even consciousness on the part of the patient, a man of sixty years. He had had colic and jaundice, but these subsided entirely, and there was no further disturbance. As has happened in so many instances, this stone must have ulcerated through into the bowel without causing any recognizable symptoms.]

The subjective signs are uneasiness--a deep-seated sensation of soreness--felt in the right hypochondrium, increased by taking a full inspiration and by decubitus on the left side. Pain or soreness, sometimes an acute pain, is experienced under the scapula near the angle, at or about the acromion process, and sometimes at the nape of the neck. In one case under my observation within the past year a patient who had had several attacks of hepatic colic, the usual polyangular stones having been recovered, had from time to time severe pain over the right side of the neck, shoulder, and scapula, accompanied by a severe herpes zoster in the district affected by the pain. This is of course an extreme example, but it is very suggestive of the relation which may exist between hepatic disturbances and shingles. Attacks of gastric pain coming on some time after food, and not soon after, as is the case in true gastralgia, are usual in the early stage of the disease--are constant, according to Cyr,[169] who quotes approvingly an observation of Leared on this point. Migraine {1070} or sick headache and vertigo occur in many cases, but it may well be doubted whether these symptoms are not due to the accompanying gastro-duodenal catarrh, which is a nearly constant symptom. Acidity, flatulence, epigastric oppression, a bitter taste, a muddy rather bilious complexion, and constipation are symptoms belonging to catarrh of the gastro-duodenal mucous membrane. Most of these symptoms are rather indefinite. Some additional information may be supplied by palpation. When the gall-bladder is distended with gall-stones, or is in the enlarged state which occurs when the common duct is obstructed, it may project beneath the inferior border of the liver far enough to be felt. In thin persons a grating sound, produced by the friction of the calculi, may be heard, the stethoscope being applied as palpation is made over the hypochondrium. It is rare that these symptoms can be elicited, since the calculous affection of the liver occurs for the most part in persons of full habit, in whom the abdominal walls are too thick to allow of the necessary manipulation. There may be also some tenderness on pressure along the inferior margin of the ribs, especially in the region of the gall-bladder.

[Footnote 169: _Traité de l'Affection calculeuse du Foie_, p. 71.]

SYMPTOMS DUE TO THE MIGRATION OF GALL-STONES BY THE NATURAL CHANNELS.--A calculus passing into the cystic duct from the gall-bladder causes the disturbance known as hepatic colic or bilious colic, because of the jaundice which accompanies the major part of these seizures. But jaundice is not a necessary element in these cases; it is not until the concretion reaches the common duct that the passage of bile into the intestine is interfered with. The gall-bladder has a function rather conservative than essential, for its duct may be permanently closed without apparently affecting the health.

The time when an attack of hepatic colic is most likely to occur would seem to be determined by the flow of bile; for this, as has been stated, is the chief factor in moving calculi along the ducts. As, no doubt, the presence of the chyme in the duodenum is the stimulus for the production of bile and also for the contractions of the gall-bladder, it follows that a few hours after meals is the time when the attacks of hepatic colic would a priori be expected. This is in accord with experience, but there are exceptions. In one of the most formidable cases with which the writer has had to deal--the diagnosis confirmed by the recovery of the calculi--the most severe attacks occurred in the early morning. According to Harley,[170] colic from the passage of inspissated bile occurs when the stomach and duodenum are most nearly empty--from ten at night until ten in the morning--and this he relies on as a means of diagnosis, but the exceptions are too numerous to assign much importance to this circumstance.

[Footnote 170: _On Diseases of the Liver_, p. 354.]

The onset of pain is usually sudden, but it may develop slowly from a vague uneasiness in the region of the gall-bladder; or after some pain and soreness at this point, accompanied by nausea, even vomiting, the paroxysm will begin with very acute pain. The situation of the pain is by no means constant, and usually varies in position in the same case. The point of maximum intensity is near the ensiform cartilage, outward and downward two or three inches, about the point of junction of the cystic and common duct. From or about this region the pain radiates through the epigastrium, the right hypochondrium, upward into the chest, {1071} backward under the scapula, and downward and inward toward the umbilicus. In some instances under my observation the most acute suffering was located in the right iliac region, in others in the lumbar region, and in still others in the epigastrium. The position of the pain may be such as to draw attention from the liver, and thus greatly confuse the diagnosis. In a well-defined attack the pain is intense, shooting, and boring, irregularly paroxysmal; the patient writhes in agony, screams and groans, rolls from side to side, or walks partly bent, holding the part with a gentle pressure or rubbing with an agonized tension of feeling. Meanwhile the countenance is expressive of the intensest suffering, is pallid and drawn, and the body is covered with a cold sweat. Nausea presently supervenes, and with the efforts to vomit a keen thrust of pain and a sense of cramp dart through the epigastrium and side. Very considerable depression of the vital powers occurs; the pulse becomes small, feeble, and slow, or very rapid and feeble. The patient may pass into a condition of collapse, and, indeed, the pain of hepatic colic may cause death by sudden arrest of the heart's action. The cases which prove fatal in this way are doubtless examples of fatty heart, the degeneration of the cardiac muscle being a result of the action of the same factors as those which cause gall-stones to form, if the relation of general steatosis to these bodies which I have set forth prove to be true. The pain is not continuously so violent as above expressed: it remits from time to time, and seems about to cease altogether when a sudden access of anguish is experienced and the former suffering is renewed, and, it may be, more savagely than before. The pain of an attack of hepatic colic has no fixed duration. It will depend on the size of the calculus, on the point where impacted, and on the impressionability of the subject. The severity of the seizures varies within very wide limits. The attack may consist in a transient colic-like pain, in a mere sense of soreness, in epigastric uneasiness with nausea, or it may be an agony sufficient to cause profound depression of the powers of life--to destroy life, indeed. The usual attack of hepatic colic is one in which severe suffering is experienced until relief is obtained by the exhibition of anodynes. Under these circumstances the subsidence of the pain may be rather gradual or it may be sudden: in the former case, as the effects of the anodyne are produced, we may suppose that the spasm subsides and the stone moves onward, at last dropping into the intestine: an enchanting sense of relief is at once experienced. Very serious nervous disturbances may accompany the pain. Paroxysms of hysteria may be excited in the hysterical; convulsions occur in those having the predisposition to them from any cause, and in the epileptic.

The onset of a severe seizure is announced by chilliness, sometimes by a severe chill. Now and then the paroxysms commence with the chill, and the pain follows. It occasionally happens that the attacks in respect to the order in which the symptoms occur, and in their regularity as to time, behave like an ordinary ague. In fact, there appear to be two modes or manifestations of the attacks of hepatic colic in malarious localities: those in which the phenomena are merely an outcome of the passage of the calculi; those in which an attack of intermittent fever is excited by the pain and disturbance of hepatic colic. To the first Charcot[171] {1072} has applied the phrase fièvre intermittente hépatique. It is supposed to correspond pathogenetically to urethral fever produced by the passage of a catheter. On the other hand, the second form of intermittent can occur only under the conditions producing ague. A calculus passing in a subject affected with chronic malarial poisoning, the latent malarial influence is aroused into full activity, and the resulting seizure is compounded of the two factors. The truly malarial form of calculus fever differs from the traumatic in its regular periodicity and the methodical sequence of the attacks, which occur in the order of an intermittent quotidian or tertian. During the attacks of hepatic colic, when protracted and severe, a sense of chilliness or distinct chills occur, sometimes with the regularity of an intermittent; but these differ from the seizures which the chill inaugurates at distinct times, the intervening period being free from disturbance.

[Footnote 171: _Leçons sur la Maladies du Foie_, p. 178.]

The fever which accompanies some severe paroxysms of hepatic colic has a distinctly intermittent character, hence the name applied to it by Charcot. There are two forms of this calculus fever as it occurs in malarious localities: one intermittent, coming on during a protracted case, and immediately connected with and dependent on the passage of the stone; the other a regular intermittent quotidian or tertian, which determines and accompanies the paroxysm of colic. A case occurring under my observation very recently, in which these phenomena were exhibited and the calculi recovered, proves the existence of such a form of the malady. In this case with the onset of the pain a severe chill occurred; then the fever rose, followed by the sweat, during which the pain ceased, but much soreness and tenderness about the region of the gall-bladder, and jaundice, followed in the usual way. At the so-called septenary periods also attacks come on in accordance with the usual laws of recurrence of malarial fevers.

Not all cases are accompanied by fever. In many instances, probably a majority, the pulse is not accelerated, rather slowed, and the temperature does not rise above normal. The inflammation which follows an attack of hepatic colic will be accompanied by some elevation of the body-heat, and fever will occur when ulceration of the duct and perforation cause a local peritonitis; but these conditions are quite apart from those which obtain in the migration of calculi by the natural channel.

Nausea and vomiting are invariable symptoms of hepatic colic. First the contents of the stomach are brought up, then some glairy mucus only, with repeated and exhausting straining efforts; and with the sudden cessation of the pain there may appear in the vomit a quantity of bilious matter, the contents of the gall-bladder liberated by the passage of the stone into the intestine. If bile is present in the vomit from the beginning, it may be concluded that the obstruction is not complete.

Constipation is the rule. The abdomen may be distended with gas--is usually, indeed, when constipation exists. Free purgation gives great relief. The stools are composed of scybalæ chiefly at first, afterward of a brownish offensive liquid, and when jaundice supervenes they become whitish in color, pasty, and semi-solid. Now and then it happens that a copious movement of the bowels takes place as the attack is impending, but during the paroxysm no action occurs.

Jaundice is an important, but not an invariable, symptom. It comes on within the first twenty-four hours succeeding the paroxysm, and appears {1073} first in the conjunctiva, thence spreading over the body generally. The intensity of the jaundice depends on the amount of the obstruction: if complete, the body is intensely yellow; and if partial, the tint may be very light. The very slight degree of obstruction which suffices to determine the flow of bile backward has been already stated. There may be no jaundice, although all the other symptoms of the passage of gall-stones may be present. Such is the state of the case when a calculus enters and is arrested in the cystic duct. Under these circumstances the natural history differs from that which obtains when the obstruction is in the common duct and ends abruptly by the discharge of the calculus into the intestine. After the persistence of the symptoms of hepatic colic for a variable period without jaundice, this sign of obstruction may appear, indicating the removal of the stone from the cystic into the common duct. The symptoms accompanying the jaundice--the hebetude of mind, the slow pulse, the itching of the skin, the dark-colored urine--have been sufficiently detailed in the section on that topic in another part of this article.

The duration of the jaundice is different in different cases, and is influenced by the degree and persistence of the obstruction. When the obstruction is partial and the stone is soon removed, the jaundice will be slight and will disappear in a day or two; on the other hand, when the stone completely blocks the passage and is slowly dislodged, the jaundice will be intense and will persist for ten days to two weeks.

After the paroxysm has passed, if severe, the liver will be swollen, more or less tenderness will be developed by pressure, and in some instances, a local peritonitis coming on, there will occur the usual symptoms of that condition.

Although all the symptoms produced by the passage of biliary calculi may be present, some uncertainty will always be felt unless the body causing the disturbance is recovered from the feces. A properly-conducted search is therefore necessary. As this is so often done inefficiently and the calculus not found, an error of diagnosis may seem to have occurred. Every stool should be examined in the mode hereinafter described for a number of days after the attack until the calculus is found. It should be remembered that only air-dried calculi float on water. The stool, as soon as passed, should be slowly stirred up in water sufficient to make a thin mixture, and all solid particles removed for further examination, the thinner portion poured off, and more water added from time to time until only solids remain at last. It should not be forgotten that masses of inspissated bile, biliary sand, may produce symptoms not unlike those due to gall-stones proper, and hence all particles having the appearance of this material should be examined chemically. Place some of the supposed bile on a white plate and pour over it some drops of strong sulphuric acid, when the biliverdin will take on a brilliant scarlet color.

The discharge of particles of inspissated bile causes symptoms not unlike those due to the migration of biliary calculi, but there are points of difference. A strongly-marked case diagnosticated biliary calculi, and in which masses of inspissated bile were discharged in great quantity, will furnish the symptomatology to be now described. The onset of the paroxysms of pain is less abrupt than is the case with gall-stones, and the attacks may occur at any time; the pain also subsides more gradually, and hardly {1074} ceases at any time, but revives every now and then, so that several days, even weeks, may be occupied with one seizure. Jaundice is less apt to follow, and indeed well-defined jaundice rarely occurs in this affection. There is much swelling of the liver, also considerable tenderness, and relief is most certainly afforded by free purgation, anodynes seeming rather to keep up the disturbance, probably by checking the hepatic secretions.

Attacks of hepatic colic may be expected to recur when a calculus with multiple facets migrates, but the time when its associates may be expected to move cannot be predicated on any data now available. Single attacks may happen at intervals of weeks, months, or years. The migration of one large stone may so dilate the ducts as to facilitate the passage of those that remain behind, thus ensuring a recurrence of the seizures at an early period.

IMPACTION OF CALCULI AND MIGRATION BY ARTIFICIAL ROUTES.--The point at which impaction takes place is an element of great importance. The size of the calculus is far from being decisive as to the certainty of impaction or as to the untoward results. A not unfrequent accident is the blocking of the cystic duct at its opening, thus preventing the influx or outgo of bile from the gall-bladder. If the stone does not ulcerate through, in this position it does no damage, for the gall-bladder, as has been stated, may be closed without any apparent detriment. Just at the bend of the cystic duct, near its origin, is the point where arrest of a calculus is most likely to take place. The next most likely point is the duodenal end of the common duct. When impaction occurs a local inflammation comes on, an exudation is poured out, ulceration begins, and presently the peritoneum is reached. Adhesions usually form with the neighboring organs, but now and then perforation takes place, and bile, pus, and the calculus are precipitated into the peritoneal cavity. A fatal peritonitis follows, as a rule; but rarely the inflammation is localized, and an abscess forms which pursues the usual course of such accumulations; or adhesions may take place about the site of the perforation and prevent a general inflammation of the peritoneum. In this way a very large sac may be produced, with the ultimate result of rupture into the general cavity, although a fistulous communication may be established with some neighboring organ, permitting safe discharge in this direction.

A gall-stone impacted in one of the hepatic ducts or in the main duct, ulcerating through, may form an abscess not distinguishable from other solitary hepatic abscesses except by the presence of the concretion causing the mischief and the absence of the usual conditions giving rise to these accumulations of pus. It is probable that fatal abscesses of the liver not infrequently are caused in this way in extra-tropical countries. Adhesions forming to neighboring hollow organs or to the external integument, such abscesses discharge, carrying out the calculus with them. In this way may be explained the discharge by the intestine of calculi much too large to have passed by the natural route and unattended by the usual symptoms of hepatic colic. These gastro-intestinal biliary fistulæ extend from the gall-bladder and the larger ducts to the stomach, to the duodenum, and to the transverse colon; but of these the communication with the stomach is the least common. The adhesion of the gall-bladder or common duct to the duodenum or colon may be direct, exudations uniting {1075} the two parts without the intervention of an abscess cavity, or such a sac or cavity may be interposed. In some cases the discharge of biliary calculi is effected through these routes with so little disturbance as to escape notice, or the symptoms may be only vague indications of a local inflammation in the neighborhood of the liver.

Biliary fistulæ communicating externally, caused by the migration of calculi, are comparatively common. They have the clinical history, and are usually treated as cases, of hepatic abscess. Sometimes hundreds of calculi are thus discharged. In such instances it may be assumed that communication has been established with the gall-bladder. Hepatic abscess thus due to the migration of calculi may discharge into the pelvis of the kidney, into the ascending vena cava, or through the lung, but these places of outlet are comparatively uncommon.

COURSES AND COMPLICATIONS.--Although symptoms cease for the time being when the calculus passes into the duodenum, and although in most instances no after unpleasant effects are experienced, there are cases in which the presence of the concretion in the intestine proves to be fruitful of mischief. Calculi of very large size--from a pigeon's to a hen's egg--are also found in the intestine, without the occurrence of symptoms indicative of their migration. It has been shown that this silent migration of calculi from the liver-passages to the intestinal is not uncommon. Hepatic concretions are distinguishable from the intestinal by their crystalline form and by their composition. The former are usually polyangular, and are composed of cholesterin crystallized about a nucleus of bile-pigment, inspissated bile, or mucus. After entrance into the intestine, lime salts and mucus are deposited in successive layers, so that the form of the calculus is modified and its size increased. The solitary ovoid concretion is most frequently found in the intestine, without previous symptoms of hepatic source, and, although increased in size in the intestine, it retains its original shape. A specimen of this kind now in my possession illustrates these points. It is composed of cholesterin crystallized in radiating lines and concentric rings about a central nucleus of inspissated bile. Around the hepatic concretion there have formed layers of lime and mucus since it has reached the intestine, and after drying this rind became brittle and was readily detached. The polyangular calculus is apt to form the nucleus of a scybala-like mass of feces; hence in the search for these bodies every such mass should be broken up. An example of this has recently come under my own observation. Concretions of all sizes, having reached the intestines, as a rule pass down without creating any commotion, and are silently discharged. But various disturbances occur in some instances. Obstruction of the bowels is one of the results. A great may cases have been collected by Murchison,[172] as many more by Leichtenstern,[173] of impaction of the intestine produced by an accumulation of feces about a biliary concretion. A calculus may be retained in a fold or diverticulum of the small intestine, and may indeed cause a loop to be formed which in turn readily twists, becoming an immovable obstruction. This mode of obstructing the bowels is less common than the simple impaction. It is affirmed by some authorities, especially by Von Schüppel, that obstruction of the bowels--impaction--is more often caused by stones that have ulcerated through into the {1076} intestines than by those that have descended by the common duct; and this conclusion must be reached if jaundice has not been present. It is not only the size of the calculus which determines impaction, as has been stated: several may be agglutinated in one mass, and reflex spasm of the muscular layer may be induced by their presence in the bowel. Nevertheless, some enormous concretions have been found in the canal, and others have been discharged without special trouble. Hilton Fagge exhibited to the Pathological Society[174] of London two gall-stones passed with the stools, measuring 2½ by 1-1/5 inches in long and short diameter, and Fauconneau-Dufresne[175] refers to concretions of the size of a hen's egg. Mention has been made of one in the writer's possession of the size of a pullet's egg, which, until its discharge, caused a train of characteristic symptoms. These immense bodies may have ulcerated through from the gall-bladder or may have grown by successive deposits of carbonate and phosphate of lime after reaching the intestine.

[Footnote 172: _Lectures on Diseases of the Liver_, p. 573.]

[Footnote 173: _Ziemssen's Cyclopædia_, vol. vii.]

[Footnote 174: _Transactions of the London Pathological Society_, vol. xix. p. 254.]

[Footnote 175: _Op. cit._]

The symptoms caused by the presence of concretions in the intestines are, when pronounced, sufficiently characteristic. At a variable period after an attack or attacks of hepatic colic the disturbance begins. The condition of impaction above referred to does not differ from ordinary fecal accumulation. It is true that occasionally the intestinal irritation due to the presence of these bodies in some instances preceded the symptoms of impaction, but usually there is no evidence to indicate that the stoppage of the bowel is due to anything else than feces. The irritability manifested by the intestinal mucous membrane when gall-stones are present varies remarkably. There may be only some ill-defined pain which, as a rule, indicates the position of the calculus, or it may be pain with a feeling of soreness, or it may take the form of violent colic, with nausea, vomiting, and depression. In my own cases pain was experienced at or near the ileo-cæcal valve, where one was lodged, and along the descending colon, where the others were; the pain and soreness ceased when these bodies were discharged.

In a few instances gall-stones are brought up by vomiting. The most remarkable example of this is a case to be found in the _Transactions of the Pathological Society_ (vol. xii. p. 129): A woman ninety-four years of age vomited a stone the size of a nutmeg. In the reported examples violent pain, nausea, and much vomiting preceded the discharge of the calculus.

Like other foreign bodies, a gall-stone may ulcerate through the intestine, producing fatal peritonitis.

Many conditions due to the presence of biliary concretions, and which arise during their migrations, may be viewed as complications. Many of those produced directly have been described as a part of the proper course of the malady; others are local and reflex, and these may with propriety be considered as complications. First in importance are those due to obstruction and the local inflammation.

The passage of a calculus along the duct excites an inflammation of the mucous membrane, which by contiguity of tissue invades the peritoneal layer if the stone is retained for a sufficient time, and especially if it is immovably lodged. The stoppage in the flow of bile leads to dilatation of the ducts, and a change takes place in the character of that fluid, {1077} owing to the admixture of mucus with the bile and to the pouring out of a pathological secretion: it loses the bilious appearance and becomes a merely sero-purulent fluid. Serious changes ensue in the structure of the liver, as was first suggested by O. Wyss and Leyden, and afterward more especially by Wickham Legg[176] and Charcot.[177] A ligature to the common duct in animals is followed in so short a time as two weeks by hyperplasia of the connective tissue and atrophy of the gland-elements. It has been ascertained that similar changes ensue in man from the impaction of a calculus in the common duct. Under these circumstances the size of the liver, as indicated by the area of hepatic dulness, at first enlarges, and subsequently more or less contraction, coincident with the atrophy, ensues. When the cystic duct is obstructed the contents of the gall-bladder increase, and become ultimately sero-purulent (dropsy). In some instances, the walls of the abdomen being thin, a globular elastic tumor may be felt projecting from beneath the liver.

[Footnote 176: _St. Bartholomew's Hospital Reports for 1873_. See also _Treatise on Diseases of the Liver_, by the same author, _loc. cit._]

[Footnote 177: _Leçons_.]

Angiocholitis, or inflammation of the duct, is caused by the passage, especially by the impaction, of a calculus. The inflammation may extend by contiguity of tissue and involve the surrounding parts. Several cases have been examined by the writer in which the gall-bladder and the cystic and common duct were imbedded in a mass of organized exudation. An extension of inflammation may take place, and be confined to the hepatic peritoneum. Heavy organized exudations will form, adhesions be contracted to the diaphragm, to the parietal peritoneum, and to the neighboring organs, and the capsule, thickened and contracting, will ultimately induce changes in the structure of the adjacent part of the liver. When the inflammation extends to the peritoneum there are the usual systemic symptoms, and locally acute pain, increased by the respiratory movements and by pressure, and assuming a constrictive character; nausea and frequent vomiting, and often a very troublesome hiccough, caused, doubtless, by implication of some branches of the phrenic nerve; constipation, etc.

The relation of biliary colic to cancer of the biliary passages was first noted by Frerichs, who ascertained the occurrence of gall-stones in 9 out of 11 cases of cancer of these parts. Hilton Fagge[178] reports a case of the kind, and the writer can add another from his own observations.

[Footnote 178: _Guy's Hosp. Rep._, 1875.]

The most important of the reflex symptoms are those pertaining to the circulatory system. The action of the heart becomes irregular in rhythm and diminishes in force. The circulation of the bile acids in the blood causes slowing of the heart's action, as has been set forth in the section on jaundice; but that is a direct consequence, and is not a reflex impression. Potain was the first to show that the structure of the heart is affected. A mitral murmur is a recognized symptom in the icterus of gall-stones, but Potain[179] has shown that the real seat of this murmur is the tricuspid, and that the affection of the heart is a dilatation of the right cavities. The physiological reason for this condition of the heart is the rise of tension in the pulmonary artery, which is secondary to irritation of the splanchnic nerves; and to this factor is also due the reduplication of the first sound and the accentuation of the second sound--characteristic signs of the cardiac change in these cases.

[Footnote 179: Cyr, _Traité de l'Affec. calc. de Foie_, _loc. cit._]

{1078} There are certain reflex nervous troubles in cases of hepatic colic, some of them of great importance. One of the lesser troubles is herpes zoster. A very violent attack in the course of the distribution of the first, second, and third cervical nerves has happened in a case under the writer's observation. There have been reported from time to time cases of sudden death during the paroxysms of hepatic colic, in which a calculus lodged in Vater's diverticulum, at the intestinal extremity of the common duct, was the cause of the accident. An explanation of this result is to be found in the intimate nervous communications between the liver and the heart through the solar plexus and the large number of ganglia contained in Vater's diverticulum. The most severe pain is felt as the calculus is passing through the orifice of the common duct into the intestine, and here also the spasm of the muscular fibre is most tense. The so-called crushing-blow experiment of Goltz illustrates how intense suffering, such as the passage of a gall-stone, can paralyze the heart through the solar plexus. The depression of the heart's action does not always occur on the instant, but it may be gradual--several hours, even a day or two, being occupied in the suspension of activity. Leigh of Liverpool[180] has reported an example of death in six hours in a female of thirty, previously in good health; Cornillon,[181] another in a female of fifty-three, who died in twelve hours from the beginning of the paroxysm; Williamson,[182] a female of fifty-one years, who expired on the fourth day; Habershon,[183] two, who died during the paroxysms at a period not stated; and Brouardel, one which was the subject of a medico-legal investigation. In the first case the calculus was yet in the gall-bladder, the appearances indicating that persistent spasms had occurred to force the calculus into the cystic duct; in the others in which the position of the stone is mentioned, it was engaged in the orifice of the common duct or had reached the intestine.

[Footnote 180: _Medical Times and Gazette_, 1867, vol. i. p. 248.]

[Footnote 181: Cyr, _op. cit._, p. 185.]

[Footnote 182: _The Lancet_ (London), vol. ii. p. 780.]

[Footnote 183: _Lectures on the Pneumogastric_, 3d Lecture.]

In several instances sudden death has resulted from uncontrollable vomiting induced by the paroxysms of hepatic colic. Trousseau[184] mentions a case in which strangulated hernia and death ensued in consequence of the violent vomiting brought on by the passage of a calculus.

[Footnote 184: _Clinique médicale_.]

DIAGNOSIS.--Unless the distension of the gall-bladder is sufficient to cause a recognizable tumor, gall-stones in that organ do not produce symptoms by which they can be diagnosticated. If sudden attacks of violent pain in the right hypochondrium, accompanied by nausea and vomiting and followed by jaundice, have occurred from time to time, then the presence of biliary concretions may be suspected if the symptoms belonging to them are present in the intervals between the seizures. The migrations of calculi produce symptoms so characteristic that error is hardly possible. The only disorders with which an attack of hepatic colic may be confounded are gastralgia and hepatalgia. As regards the first, the distinction is made by the seat of pain, by the absence of after jaundice, and by the lack of a concretion passed by stool. As the diagnosis may depend on the finding a concretion, the writer must again affirm the importance of a properly-conducted search of all the stools passed for several days after the paroxysm.

{1079} Hepatalgia is diagnosticated with great difficulty, for the pain has the same seat, the same character, but as a rule it does not terminate so abruptly, is not accompanied by such severe vomiting and depression, jaundice is absent, and no stone can be found in the evacuations. Both gastralgia and hepatalgia occur in the subjects of neurotic disturbances--in the pale, delicate, and hysterical--whereas, as a rule, hepatic colic happens to the obese, to the persons of active digestion addicted to the pleasures of the table.

The passage of calculi may be confounded with flatulent colic, with the pain caused by lead and other mineral poisons, with impaction, internal strangulation, local peritonitis, and similar causes of sudden and violent pain. The differentiation is made by attention to the seat and character of the pain, by the previous history, and especially by the absence of jaundice and of a concretion. From renal colic the hepatic is separated by the position of the pain, by the direction taken by it, and by the retraction of the testicle, the irritability of the bladder, and the appearance of blood in the urine--all characteristic symptoms of the renal affection.

TREATMENT.--The treatment of biliary concretions includes the remedial management for the calculi in position, for the paroxysms of hepatic colic caused by the migration of these bodies, and for the results and complications.

Treatment of the Calculus State: Of Inspissated Bile.--As the particles of inspissated bile are deposited along the larger hepatic ducts, and form in consequence of a deficiency in the amount of glycocholate and taurocholate of soda, two methods of treatment are to be carried out: free purgation by an active cholagogue to wash out the offending substance, and the exhibition of a soda salt to promote the alkalinity of the bile and the consequent solution of the bile-pigment. Harley's method, which he strongly urges, consists in the administration of "one or two drachms of sulphate of soda in a bitter infusion every morning before breakfast, or from twenty to thirty grains of bicarbonate of soda, along with a drachm of taraxacum-juice in a bitter infusion, every night at bedtime at regulated intervals for a month or so, according to the constitution of the patient and the severity of the symptoms."

As persons who suffer from inspissation of the bile are naturally bilious, it is of the first importance in the prophylactic treatment to regulate the diet. Indulgence in malt liquors, in fatty and saccharine articles of food, must be forbidden. Acid fermentation in the course of duodenal digestion should be prevented by withholding the starches and sugars. Peptonized foods, given with an alkali, are highly useful. Milk, fresh meat, and the succulent vegetables are the proper constituents of a diet for these subjects. Bread is one of the most offending articles, and should be restricted in amount as much as possible.

Next to a suitable diet, systematic exercise is a measure of the highest utility in these cases. A daily morning sponge bath of a weak alkaline water not only maintains the skin in a healthy state, but also promotes the oxidation processes of the body. The alkaline mineral waters of Wisconsin, Michigan, Virginia, and other States, especially of the Bethesda Spring of Wisconsin, may be drunk with great advantage to accomplish the same purpose.

{1080} We possess direct means for preventing inspissation of the bile--remedies which act in the physiological way by increasing the proportion of glycocholate and taurocholate of soda. Harley prefers the sulphate and bicarbonate for this purpose, but my experience is in favor of the cholate and phosphate of sodium, especially the latter; for, whilst it plays the part of a soda salt, it exerts a decided cholagogue action, thus effecting the results achieved by the combined use of sulphate of soda and taraxacum. A cure may be confidently looked for in this malady by the persistent use of sodium phosphate--drachm j ter in die. It seems to act more efficiently when given dissolved in hot water.

The paroxysms of hepatic colic due to the passage of inspissated bile are to be treated in the same way as when this condition of things is caused by the migration of formed calculi. The action of cholagogue purgatives is more decidedly beneficial in the attacks due to the passage of inspissated bile.

Biliary Calculi in Situ.--Notwithstanding their crystalline form and firmness of texture, it is possible to effect the gradual solution of biliary calculi. Outside of the body it is easy to dissolve a calculus in chloroform, in Durande's remedy, etc., if time enough be given, but the problem is a far more difficult one when the calculus is in position in the gall-bladder or in a hepatic duct. As Trousseau[185] has wisely observed, it is not safe to apply to conditions within the body conclusions reached by experiments in the laboratory. Nevertheless, facts are known which justify the belief that an impression may be made on concretions in the gall-bladder. The motion of respiration and the voluntary actions of the abdominal muscles cause more or less attrition and breaking off of the angles and margins of the crystals, thus permitting the solvent action of the bile. If, however, the bile continues in the state in which it was at the time of the crystallization of the cholesterin, it will make no impression on this substance. We have now the means of restoring its power to dissolve crystallized cholesterin. As a necessary preliminary, fracture of the crystals must be effected. This may be accomplished, when the natural forces have failed to effect it, by manipulation of the gall-bladder through the walls of the abdomen, but especially by faradization. Excellent results have been achieved by this last-mentioned expedient, but no satisfactory explanation has been made of its methodus medendi, unless we accept the mechanical effect of the muscular movements. In applying the faradic current an electrode is introduced into the rectum, and the other, a sponge well moistened, is placed over the gall-bladder. An interrupted galvanic current is indicated, the electrodes in the position just mentioned, when a migrating calculus is stopped on its way. Such an application has rendered important service in a few cases.

[Footnote 185: _Clinique médicale de l'Hôtel Dieu de Paris_.]

Except that calculi have been found in a state of decay, their angles and edges broken, divided by cleavage, there is no evidence that they have undergone solution when in situ, except the clinical evidence which consists in a disappearance of the symptoms. The remedy of Durande, which consists in a mixture of ether and turpentine--three parts of the former and two of the latter--has been celebrated since the close of the last century, and is yet much employed in France, notably at Vichy. It {1081} is preferred by Cyr,[186] who advises its administration in capsules taken immediately before meals. Chloroform readily dissolves calculi out of the body, and hence it has been proposed, and indeed much used, for the purpose of effecting their solution in the gall-bladder; but, as Trousseau urges, there is no warrant for the belief. Corlieu,[187] who first proposed its use, and afterward Bouchut,[188] maintained that chloroform does exert this solvent action, and reported cases in confirmation; but there are so many sources of fallacy that such evidence must be viewed with suspicion. It has usually been administered in small doses (five minims) three times a day for a long period. That it is beneficial by stimulating the flow of pancreatic secretion and by allaying spasms is probably true, but that any quantity which can be administered in safety will act as a solvent of cholesterin concretions cannot be believed.

[Footnote 186: _Traité de l'Affection calculeuse du Foie_, p. 287.]

[Footnote 187: _Gazette des Hôpitaux_, 1856, June 19.]

[Footnote 188: _Bullétin gén. de Thérap._, vol. lxi. p. 49.]

If solution of hepatic calculi is possible under any circumstances, the most rational mode of effecting it would seem to be to restore that condition of the bile which in the normal state maintains cholesterin in the state of solution. Cholesterin is precipitated and crystallizes about a nucleus when the glycocholate and taurocholate of soda are deficient in amount. The agents most effective in restoring the solvent power of the bile are the salts of soda, of which the sulphate is preferred by Harley. In 1873 the cholate of soda was brought forward by Schiff, who prescribed it in doses of 50 centigrammes (8 grains nearly) three times a day, to be gradually increased until digestive or circulatory troubles arose. This remedy, which is eminently rational from the point of view above indicated, has apparently been of decided service in many published cases and in the writer's experience. It will be found, however, that five grains three times a day is as large a quantity as can be easily borne.

Another soda salt which in my own hands has proved in a high degree effective is the phosphate. As has been explained when referring to its use in cases of disorders due to inspissated bile, it has a distinct cholagogue action, but the chief sources of its utility in this affection are its chemical and resolvent powers. The usual quantity is one drachm three times a day, dissolved in sufficient warm water.

Bile itself, in the form of inspissated ox-gall, was formerly much used, a scruple to a drachm being given three times a day, and not without good results. It was also prescribed with chloride of ammonium. For the gastro-duodenal catarrh and the accompanying catarrh of the bile-ducts this combination is sometimes useful.

I have recently proposed a new expedient for effecting the solution of hepatic calculi. This method consists in puncture of the gall-bladder with a fine exploring-trocar, and the injection through the canula, after withdrawing the stylet, of a suitable solvent. Durande's remedy, chloroform, and other solvents can be introduced in this way without injury to the parts. I have punctured the gall-bladder, removed its contents, and explored its interior without damaging the organ in any way and without leaving after traces. The measure proposed offers no special difficulties in its execution.

The Paroxysms of Hepatic Colic.--The pain of hepatic colic being {1082} the most acute suffering known to man--in its severest form at least--the most powerful anodynes are required. The measures employed for relief of pain happen to be the most efficient for promoting the expulsion of the calculus and for limiting, if not preventing, the subsequent inflammation. As soon as the character of the seizure is manifest a hypodermatic injection of morphine and atropine--1/8 to 1/2 grain of the former and 1/200 to 1/80 grain of the latter--should be given; ether administered by inhalation if necessary; and by the stomach chloroform, chlorodyne, or chloral. As the stomach is usually exceedingly irritable, the subcutaneous injection of remedies is a precious resource: this failing or contraindicated, relief may be given by the rectal injection of laudanum or chlorodyne. As relief is often afforded by the act of vomiting, the attempts to empty the stomach should be encouraged, and to this end large draughts of warm water should be given. Hot fomentations and mustard plaster should be applied over the right hypochondrium, and an entire warm bath may be used if available.

Great relief is usually afforded by the action of purgatives. The irritability of the stomach forbids the employment of drastic purgatives, yet podophyllin resin is warmly commended by Dobell. It must be given in small doses, and preferably dissolved in spirit. Calomel in one-grain doses, every four hours until it purges, allays nausea and lessens the after-uneasiness in the right hypochondrium, but mercurial treatment given with a view to a supposed cholagogue effect only does evil by prolonged administration, especially if ptyalism is induced. If evidences of portal congestion are present, such remedies as euonymin, iridin, baptisin, and others of the cholagogue group give good results. The most effective of the remedies of this kind is ipecacuanha, given in purgative doses: the emesis induced by it favors the extrusion of the stone, and the powerful cholagogue effect relieves the portal congestion. Twenty grains at once, and repeated if need be in three hours, is a suitable quantity.

The various complications which may occur, and the results which follow the migration of the calculus, require treatment adapted to the conditions existing, and will be mentioned in the sections devoted to these topics.

Occlusion of the Biliary Passages; Stenosis of the Ductus Communis Choledochus.

DEFINITION.--By occlusion of the biliary passages is meant an obstruction, internal or external, of the hepatic, cystic, or common duct. The causes of the obstruction are various, but the results are quite uniform; hence the term includes a complexus of symptoms of a very distinctive type. Occlusion may be congenital or acquired: it is the latter with which we have especially to deal.

Stenosis signifies a narrowing which in its extremest form produces a nearly complete obstruction; when the canal is entirely closed the term occlusion is applied. Stenosis also may be congenital or acquired.

PATHOGENY.--The conditions producing narrowing of a hepatic duct or its complete obstruction are numerous, and some of them complex in their relations. As regards the ducts themselves, the interference may {1083} be entirely within the canal, or it may affect the walls, or it may be wholly extraneous; as, for example, when a cancer of the pancreas encroaches on the common duct. It will be convenient to consider the causes of stenosis and obstruction from these points of view: 1, internal; 2, of the duct walls; 3, extraneous.

The most usual situations for the occurrence of those changes that lead to occlusion by inflammatory adhesions are the beginning of the cystic duct, obstruction of which is of little moment, and the end of the common duct, which finally proves fatal.

The passage of a large polyangular calculus may cause such irritation, abrasion of the epithelium, and subsequent inflammatory exudation as to effect a direct union of the opposing sides of the canal. This takes place at the beginning of the cystic duct especially, since, owing to the spasm of the gall-bladder and the absence of muscular fibres in the walls of the duct, the stone crushes into, without passing through, the canal. The inflammatory exudation thus excited may close the duct. Not unfrequently the gall-bladder, full of calculi, is thus shut off from the liver permanently. In one instance the writer has seen a calculus wedged into the orifice of the cystic duct, whilst just beyond the lumen was permanently obstructed by an organized exudation. Permanent closure of the cystic duct is of far less consequence than of the common duct, and may, indeed, be a conservative condition, as in the case above mentioned, where numerous polyangular calculi may have migrated, except the closure of the passage.

The most usual point of obstruction in the course of the common duct is the intestinal end, but various processes are employed to effect it. The first in importance is catarrhal inflammation. This seems the more credible when it is remembered that to a simple catarrh of the mucous membrane is due the temporary stoppage of the duct, producing jaundice in much the largest proportion of cases. When the epithelium is detached and granulations spring up from the basement membrane, adhesions of the surfaces will readily take place, and the union may be so complete as that all traces of the duct will disappear. It is probable that in many, if not in most, of these cases the initial condition of the canal is that of simple catarrh, the more positive changes in the mucous membrane arising from peculiarities in the tissues of the individual affected, or from local injury caused by the passage of a concretion or irritation of pathological secretions of the duodenum.

Stenosis, and finally occlusion, of the common duct may arise from the cicatrization of an ulcer. Such ulcers may occur in several modes. They may result from catarrhal inflammation of a chronic type, much new connective-tissue material forming, and in the process of cicatrization, with the contraction belonging to it, the lumen of the canal is so far filled up that the passage of bile is effectually prevented. They may be produced in that state of the tissues which accompanies certain cachectic and profoundly adynamic conditions, as in severe typhoid fever. Such ulcers may also be due to the mechanical injury effected by the migration of a gall-stone. In cicatrizing, a tight stricture, impermeable to the passage of bile, may result, or the lumen of the canal be entirely obliterated. In the latter case the duct itself may disappear and leave no trace. An ulcer situated at the duodenal end of the common duct and extending into the {1084} duodenum may also in the process of healing so contract as to render the orifice impermeable to bile. The same effect may follow the cicatrization of an ulcer of the duodenum in the immediate vicinity of the orifice of the common duct.

Without the intervention of an ulcer as a means of explaining closure of the common duct, this accident may be caused by a catarrhal inflammation which effects denudation of the basement membrane, and thence union may be produced by the mere contact of the freshly-granulating surfaces. Congenital occlusion of the bile-ducts or obstruction occurring in a few days after birth, it is probable, is effected in this way, but no direct evidence of the process has thus far been offered. During intra-uterine life, as at any period in after-life, it seems necessary to the production of such changes that a peculiar constitutional state must exist; otherwise, such a result might happen to every case of catarrhal inflammation of the bile-ducts. The extent of the changes is further evidence in the same direction; for not only are the walls of the duct in permanent apposition and adhesion, but the duct degenerates into a mere fibrous cord, and in some instances is nearly, even entirely, obliterated.[189]

[Footnote 189: _Ziemssen's Cyclopædia_, p. 589.]

The cystic or common duct--the latter to be chiefly considered--may be occluded by the retention in its lumen of some foreign body. The impaction of a biliary calculus has already been repeatedly referred to, but there are some additional points demanding consideration. The larger concretions may be stopped in the neck of the gall-bladder; those small enough to enter the canal may be arrested at its bend behind the neck, and the very entrance of the cystic duct may be blocked, as in a case examined by the writer.

The hepatic duct is very rarely permanently occluded. As the calibre of this canal continuously enlarges downward, there is no point at which a stone is likely to be arrested; nevertheless, it occasionally happens that such an obstruction does occur. An example has occurred under the observation of the writer, but the cause was a gunshot wound of the liver.

The most usual, and for very obvious reasons the most important, of the sites where occlusion occurs is the common duct and at the termination of the duct in the small intestine, the intestinal orifice. Just behind and to the right of its orifice the duct is dilated into a fossa--the diverticulum Vateri; and here concretions of a size to pass along the common duct are stopped. It is not essential that the stone fit the canal: it may do so and prevent any bile passing into the duodenum; it may be a polyangular body, and, though wedged in, leave spaces through which more or less can slowly trickle. The symptoms will be modified accordingly. Again, the diverticulum may contain numerous concretions, which distend the canal greatly, but through the interstices of which some bile can flow.

Other foreign bodies very rarely close the intestinal end of the ductus communis; thus, for example, a cherry-seed, a plum-seed, a mass of raisin-seeds, may slip into the orifice after the passage of a gall-stone has stretched it sufficiently. A much more common cause of occlusion is an intestinal parasite, which crawls in and is fastened. The common round-worm is the most frequent offender, and much less often liver-flukes find a lodgment there.

{1085} The ductus communis choledochus may be closed by agencies acting from without. They are various, but the most common are the carcinomata. Primary cancer of the gall-bladder and gall-ducts, although not of frequent occurrence, is by no means rare. It develops in connection with the connective-tissue new formations produced by the inflammation following the migration of large calculi. A very instructive example has been examined by the writer. The patient, a woman aged forty-eight, had had numerous paroxysms of hepatic colic, and after death, which followed a protracted stage of jaundice by obstruction, a large ovoid calculus, filling the gall-bladder, was found, and an extensive organized exudation of inflammatory origin was the seat of carcinomatous disease involving the cystic and common ducts and closing the lumen of both. Cancer of the pylorus, of the duodenum, of the pancreas, of the right kidney, and of the liver itself, not unfrequently by exterior pressure permanently occlude the common duct. To this category of obstructing causes must be added enlarged lymphatic glands of the transverse fissure, large fecal accumulations, tumors of the ovaries and uterus, aneurisms of the abdominal aorta, and especially aneurism of the hepatic artery, several examples of which have been reported, and one has occurred in a case seen by the writer.

The effects of obstruction are much less important when the cystic duct is closed. The contents of the gall-bladder accumulate, constituting the condition known as dropsy of the gall-bladder. A catarrhal state of the mucous membrane is set up; the muco-pus formed mixes with the bile, and the mixture undergoes fermentative changes which further alter its character and impart to it irritating qualities, in consequence of which the mucous membrane becomes more decidedly inflamed, and a still more purulent fluid forms, so that ultimately the contents of the gall-bladder are entirely purulent, and that organ may attain to enormous size. Instead of a catarrhal inflammation leading to suppuration, the mucous membrane may pour out serum abundantly, the biliary contents and mucus disappear by absorption, and finally the gall-bladder will be moderately distended by a serous-like fluid. No further disturbance ensues, and the gall-bladder, thus shut off from participation in the hepatic functions, ceases to give trouble.

The results are far different when the obstruction occurs in the hepatic or common duct, for then the bile can no longer perform its double function of secretion and excretion--of contributing materials necessary to digestion and assimilation, and excreting substances whose removal is necessary to health. The liver continuing to functionate after closure of the duct is effected, obviously the secretion of bile continues to accumulate, and the irritation of the mucous membrane causes a catarrhal state; mucus is poured out, and serum escapes from the distended vessels. If the hepatic duct only is obstructed, the dilatation will not involve the cystic duct and gall-bladder, but as the common duct at its termination is occluded, usually the whole system of tubes will be affected by the ensuing changes. The alterations already described as occurring in the gall-bladder take place in all the hepatic ducts. The bile-elements are absorbed, and the fluid distending the whole system of hepatic tubes becomes finally a semi-transparent serum or a very thin sero-mucus, having in bulk a pale sea-green color. Although an intense jaundice {1086} coexists with the obstruction, no portion of the bile escapes into the ducts. At the beginning of the obstruction more or less bile is in the tubes, and then the fluid will have a distinct biliary character; but as it accumulates, first the bile-constituents disappear, then the mucus--which at the outset was formed freely--is absorbed, and at last only a colorless serum remains. This fluid, which has been examined chemically by Frerichs, is found to be slightly alkaline, to have only 2 per cent. of solids, and to present no trace of any biliary constituent. As the fluid accumulates the gall-bladder and ducts dilate, sometimes to an enormous extent, the fluid they contain amounting to several pints. The walls of the ducts grow thinner, and may finally give way with the pressure or from external violence, the fluid exciting an intense and quickly-fatal peritonitis. Important changes occur in the structure of the liver also. With the first retention of bile the liver conspicuously enlarges, and may indeed attain to twice its normal size, but it subsequently contracts, and may lessen in as great a degree as it had enlarged. Changes begin in the glandular structure as pressure is brought to bear on the cells by the enlarging ducts. The liver-cells become anæmic and the protoplasm cloudy, but granular and fatty degeneration does not take place. Even more important as an agency affecting the condition of the hepatic cells is the hyperplasia of the connective tissue, which ensues very promptly when an obstruction to the flow of bile arises from any cause, as has been shown by Legg[190] and Charcot.[191] The liver on section has a rather dark olive-green color, and is firmer in texture, owing to the increased development of the connective tissue; the cells are bile-stained and contain granules of coloring matter and crystals of bilirubin, and although they are at first not altered in outline, subsequently more or less atrophy is produced by the contraction of the newly-formed connective tissue and the pressure made by the dilated hepatic ducts.

[Footnote 190: _On the Bile, Jaundice, and Bilious Diseases_, p. 352 _et seq._]

[Footnote 191: _Leçons sur les Maladies du Foie, etc._, p. 205 _et seq._]

SYMPTOMS.--The symptoms produced by occlusion of the cystic duct are not sufficiently characteristic to be diagnosticated with any certainty. When an attack of hepatic colic has slowly subsided without jaundice, and an elastic tumor, globular or pyriform in shape, has appeared from under the inferior margin of the liver in the position of the gall-bladder, dropsy of that organ may then be suspected. As paracentesis of the gall-bladder may be performed with ease, safety, and little pain, the diagnosis may be rendered more certain by the use of the exploring-trocar.

Obstruction of the hepatic or common duct is accompanied by symptoms of a very pronounced and distinctly diagnostic character. Without referring now to the antecedent symptoms or to those belonging to the obstructing cause, the complexus of disturbances following the obstruction is the subject to which our attention must be directed. The great fact dominating all other considerations is the stoppage of the bile, whether this has occurred suddenly or slowly. Jaundice begins in a few hours after the canal is blocked. At first there is yellowness of the conjunctiva, then diffused jaundice, deepening into the intensest color in two or three weeks, or, when the obstruction is sudden and complete, in a few hours. At first the color is the vivid jaundice tint, a citron or salmon or yellow-saffron hue, but this gradually loses its bright appearance, grows darker, and passes successively into a brownish, bronze-like, and ultimately a {1087} dark olive-green, which becomes the permanent color. Under some moral emotional influences there may be a sudden change to a brighter tint, lasting a few minutes, but otherwise the general dark olive-green hue persists throughout. In a few instances, after some weeks of jaundice, the abnormal coloration entirely disappears, signifying that the liver is too much damaged in its proper glandular structure to be in a condition to produce bile. Such a cessation of the jaundice is therefore of evil omen.

Pruritus, sometimes of a very intense character, accompanies the jaundice, in most cases appears with it, and in the supposed curable cases it has persisted after the cessation of the discoloration. The irritation may become intolerable, destroying all comfort, rendering sleep impossible, and so aggravating as to induce a highly nervous, hysterical state. The scratching sets up an inflammation of the skin, and presently a troublesome eczema is superadded. In some of the cases a peculiar eruption occurs on the skin and mucous membranes, entitled by Wilson[192] xanthelasma. It has been carefully studied by Wickham Legg,[193] who has ascertained the character of the changes occurring in the affected tissues, and also by Mr. Hutchinson.[194] As a rule, this eruption appears after several months of jaundice, and manifests itself first on the eyelids, then on the palms of the hands, where it makes the most characteristic exhibit, and after a time on the lips and tongue. It occurs in irregular plaques of a yellowish tint slightly elevated above the general surface, and rarely assumes a tubercular form. As was shown by Hilton Fagge, xanthelasma occurs more especially in the milder cases of catarrhal icterus that had been protracted in duration, but it is also occasionally seen in the jaundice of obstruction.

[Footnote 192: _Diseases of the Skin_, 6th ed., Lond., p. 773.]

[Footnote 193: _On the Bile, Jaundice, and Bilious Diseases_, p. 317 _et seq._]

[Footnote 194: _Medico-Chirurgical Transactions_, vol. liv. p. 171.]

According to the stage of the disease during which the examination is made the liver will be enlarged or contracted; more or less tenderness may be developed by pressure in the area occupied by the ducts, and a tumor in a position to effect compression may possibly be detected. The area of hepatic dulness will be increased in the beginning of all the cases in which the obstruction is complete, but will remain normal so long as the flow of bile persists despite the obstruction. When enlarged, the liver can be felt projecting below the inferior margin of the ribs, and with it, in most cases, the elastic globular body, the gall-bladder. The state of the hepatic secretion, and in consequence the duration of the obstruction, may be ascertained by puncture of the gall-bladder and withdrawal of some of its contents for examination. The presence of unaltered bile will indicate recent obstruction; of serum, will prove long-standing interruption of bile-production. The presence of concretions in the gall-bladder will indicate the character of the obstructing cause, and an increased amount of bile of a normal or nearly normal kind will be conclusive evidence that the obstruction is in the course of the common duct. In a fatal case of permanent occlusion examined by myself the cystic duct was closed by inflammatory adhesions and the common duct was stopped up by a calculus.

The enlarged area of hepatic dulness will, in a protracted case, not continue. The proper secreting structure, the hepatic cells, undergo atrophy, {1088} and the increased connective tissue--to the development of which enlargement of the organ is mainly due--contracts. The ultimate result is that the liver becomes sclerosed, and is distinctly smaller, the area of hepatic dulness diminishing to a greater relative extent than the area of dulness due to hypertrophic enlargement. The contraction of the liver goes on at the rate that several months are required to make the result evident on percussion and palpation. Not unfrequently, the contraction is too slight to affect the percussion note of the right hypochondrium, and then, to realize the condition of the organ, the history and rational signs must be closely studied.

Whilst the liver thus varies in size, the gall-bladder remains enlarged and projects from the under surface of the organ, elastic, globular, and distinctive. The shrinking of the liver from around it makes the impression of growing size; it may be increasing, indeed, but more frequently the enlargement is merely apparent.

Whether the liver be enlarging or diminishing in size, its functions are impaired, or indeed entirely suspended. As the digestive canal receives the bile immediately on its production, it will be best to begin with the gastro-intestinal disorders which accompany occlusion of the bile-ducts. The appetite is either wanting entirely and food is loathed, or an excessive or canine appetite is experienced. The latter belongs rather to an early stage of the disorder, and comes on after the first disturbance of the stomach belonging to the immediate effects of the occlusion. The former is the result of long-standing interference with the primary assimilation. The tongue is coated with a thick yellowish fur, which, drying, is detached in flakes, leaving the mucous membrane beneath red, raw, fissured, and easily bleeding. The taste is bitter, and the mouth has a pasty, greasy, and unclean feeling. There is much thirst, and as a rule the patient experiences a keen desire for acid drinks and for fresh fruits. The stomach is rather intolerant of food, and nausea comes on as soon as it enters the stomach. The mucus and stomach-juice accumulating over night, in the morning there is much retching and nausea until the acid and rather foul contents of the organ come up. When food is retained it causes much distress, gases of decomposition accumulate, distending the stomach and giving prominence to the epigastrium, and eructations of offensive gas, with some acid liquid, occur from time to time. Similarly, in the intestines the foods undergo decomposition instead of normal digestion; gases of putrefaction are evolved, the abdomen generally is swollen, and flatulent colic results. Very irritating fat acids are liberated by the decomposition of the fatty constituents of the food, which, with the acid products of the fermentation occurring in the starch and sugar of the diet, cause a sensation of heat and distress through the abdomen. Usually, the bowels are torpid, but in some cases the stools are relaxed, having the consistence and presenting somewhat the appearance of oatmeal porridge. They may be firm, moulded, even hard. The gas discharged and the stools are offensive, with a carrion-like odor. Sometimes decomposing articles of food can be detected in the stools by very casual inspection--always, indeed, when the examination is intimate. An excess of fat is also a characteristic of the condition induced by occlusion of the ducts, especially when the pancreatic duct is closed, as does happen in cancer of the head of the pancreas.

{1089} A significant change in the color of the stools takes place. They lose their normal brownish-red tint and become yellowish or clay-colored or white, pasty, or grayish. Sometimes the stools are very dark, tar-like in color and consistence, or more thin like prune-juice, or in black scybalæ. The most usual appearance of the stools in occlusion is grayish, mush-like, and coarsely granular. The very dark hue assumed at times or in some cases signifies the presence of blood. A dark tint of the evacuations may be caused by articles of food, as a greenish hue may be due to the use of spinach; a clay-colored tint to the almost exclusive use of milk; a grayish tint to the action of bismuth; a bilious appearance to the action of rhubarb; and many others. When the occlusion is partial, although it be permanent, sufficient bile may descend into the duodenum to color the stools to the normal tint, and yet all the other signs of obstruction be present.

The bile-pigment, not having an outlet by the natural route, by the intestine, passes into the blood; all the tissues of the body and the various secretions and excretions, notably the urine, are stained by it, constituting the appearance known as jaundice or icterus. This malady has been described (see anté), but it is necessary now to give a more specialized account of those conditions due more especially to the prolonged obstruction of the biliary flow. These are a morbid state of the blood; changes in the kidneys and in the composition of the urine; a peculiar form of fever known as hepatic intermittent fever; and a group of nervous symptoms to which has been applied the term cholæmia.

It has already been shown that but little pressure is required to divert the flow of bile from the ducts backward into the blood. Changes consequently ensue in the constitution of the blood and in the action of the heart and of the vessels. The bile acids lower the heart's movements and lessen the arterial tension; hence the pulse is slower, softer, and feebler than the normal. Should fever arise, this depressing action of the bile acids is maintained; and hence, although the temperature becomes elevated, the pulse-rate does not increase correspondingly. There are exceptions to this, however, in so far that the heart and arteries are in some instances little affected, but it is probable under these circumstances that there are conditions present which induce decomposition of the bile acids.

The most important result of the action of the bile on the constitution of the blood is the hemorrhagic diathesis. Soon after the occlusion occurs in very young subjects--at a later period in adults--the occlusion having existed for many months, in some cases only near the end, the disposition to hemorrhagic extravasations and to hemorrhages manifests itself. From the surface of the mucous membranes, under the serous, in the substance of muscles, the hemorrhages occur. Epistaxis, or nasal hemorrhage, is usually the first to appear, and may be the most difficult to arrest. The gums transude blood, and wherever pressure is brought to bear on the integument ecchymoses follow. The conjunctiva may be disfigured and the eyelids swollen and blackened by extravasations, and the skin of the cheeks and nose marked by stigmata. Hæmatemesis sometimes occurs, but the extravasations into the intestinal canal more frequently--indeed, very constantly--take place in a gradual manner, and impart to the stools a dark, almost black, tar-like appearance. In the same way the urine may contain fluid blood and coagula, or it may have a merely smoky {1090} appearance from intimate admixture with the blood at the moment of secretion.

Both the bile-pigment and bile acids exert an injurious action on the kidneys. In cases of prolonged obstruction not only are the tissues of the organ stained by pigment in common with the tissues of the body, but the epithelium of the tubules, of the straight and convoluted tubes, are, according to Moebius,[195] infiltrated with pigment. In consequence of the size and number of the masses of pigment, the tubes may become obstructed and the secretion of urine much diminished. Other changes occur, due chiefly to the action of the bile acids, according to the same authority. These alterations consist in parenchymatous degeneration. The urine contains traces of albumen in most cases, and, according to Nothnägel,[196] always casts of the hyaline and granular varieties stained with pigment. As the alterations in the structure of the kidneys progress, fatty epithelium is cast off, and thus the tubules come finally to be much obstructed and the function of the organ seriously impaired. To cholæmia then are superadded the peculiar disturbances belonging to retention of the urinary constituents.

[Footnote 195: _Archiv der Heilkunde_, vol. xviii. p. 83.]

[Footnote 196: _Deutsches Archiv für klin. Med._, vol. xii. p. 326; also, Harley, _op. cit._, p. 503.]

One of the most interesting complications which arises during the existence of obstruction of the bile-ducts is the form of fever entitled by Charcot[197] intermittent hepatic fever. Although its character was first indicated by Monneret,[198] we owe the present conception of its nature and its more accurate clinical history to Charcot. It does not occur in all cases. As has already been pointed out, the passage of a gall-stone may develop a latent malarial infection or a febrile movement comparable to that caused by the passage of a catheter, and known as urethral fever. Charcot supposes that true intermittent hepatic fever is septicæmic in character, and can therefore arise only in those cases accompanied by an angiocholitis of the suppurative variety--such, for example, as that which follows the passage of calculi. Illustrative cases of this fever, one of them confirmed by an autopsy, have been recently reported by E. Wagner,[199] who is rather inclined to accept Charcot's view of the pathogeny. A remarkable case has been published by Regnard,[200] in which the angiocholitis was induced by the extension of echinococcus cysts into the common duct. Whilst there are some objections to Charcot's theory, on the whole it is probably true that this intermittent hepatic fever is produced by the absorption from the inflamed surface of the ducts of a noxious material there produced. It may be likened to the fever which can be caused by the injection of putrid pus into the veins of animals.

[Footnote 197: _Leçons sur les Maladies du Foie, etc._, p. 178 _et seq._]

[Footnote 198: Cyr, _Traité de l'Affection calculeuse du Foie_, p. 193.]

[Footnote 199: _Deutsches Archiv für klin. Medicin_, vol. xxxiv. p. 529.]

[Footnote 200: _Gazette méd. de Paris_, No. 49, 1873, quoted by Wagner, _supra_.]

Intermittent hepatic fever, as its name implies, is a paroxysmal fever, having a striking resemblance to malarial fever, but differs from it in less regularity of recurrence, in the fact that urea is below the normal amount instead of increased, and in the effect of quinine, which in the case of malarial fever is curative, but not curative in hepatic fever. The paroxysms are sometimes quotidian, rarely double quotidian, tertian, quartan, and even longer, and in the same case all of these varieties may occur; on {1091} the other hand, there may be entire regularity of the seizures. The severity of the chill, the maximum temperature, and the amount of sweating vary within considerable limits; there may be merely a slight sense of chilliness or a severe rigor; the temperature may rise to 101° or to 104° F., and there may be a gentle moisture or a profuse sweat. There does not seem to be any relation between the extent and severity of the local mischief and the systemic condition.

The period of onset of intermittent hepatic fever, and its duration and mode of termination, are by no means readily determined. Cyr fixes on the paroxysms of colic as the beginning, but he obviously confounds the chill and fever caused by the passage of a calculus with the true intermittent hepatic fever. In a carefully-observed case, the facts confirmed by an autopsy, E. Wagner[201] gives the clinical history of a typical example of this malady: Gall-stones were found in the duodenum, in the common and cystic ducts, but the most important one was a polyangular stone obstructing the hepatic duct. There was an ulcer with thickened margin at the entrance to the gall-bladder, and the mucous membrane of the common duct near the intestinal orifice had a smooth, cicatricial aspect of recent origin, indicating inflammatory ulceration. The conditions favorable to the production of a morbid material of a kind to induce septicæmic fever were therefore present. The onset of fever occurred ten days after the last seizure, time being thus afforded for the local changes necessary. The duration of the fever in this case was five months, but the existence of pulmonary phthisis with cavities will explain this apparently protracted hepatic intermittent fever. The duration of the disease in its usual form is uncertain, and ranges between a week and two months, or even three months, according to Charcot.[202]

[Footnote 201: _Deutsches Archiv für klinische Medicin_, Band xxxiv. p. 531, 1884.]

[Footnote 202: _Leçons sur les Maladies du Foie_, p. 180.]

Suspension of work by the liver necessarily involves retention in the blood of various excrementitious matters. The attempt of Flint[203] to establish the doctrine of cholesteræmia has not been supported by the evidence of contemporary or subsequent physiologists. This theory denies to the other constituents of the bile any morbific action, and concentrates those disturbances known as cholæmia on the effects of cholesterin. As uræmia signifies not merely the presence of urea in the blood, but of all of the toxic substances excreted by the kidneys, so the word cholæmia comprehends all the constituents of bile having power to derange the organism by their presence in the blood.

[Footnote 203: _The American Journal of the Medical Sciences_, 1862, p. 349 _et seq._]

By cholæmia is meant those disturbances, chiefly nervous, which are due to the presence of biliary excrementitious matters in the blood, and not less to the effect on nutrition of the absence of bile from the process of digestion in the intestine. As the atrophic changes proceed in the liver, the quantity of urea and uric acid in the urine diminishes, and presently leucin and tyrosin appear. Amongst the means of differential diagnosis of hepatic intermittent fever from malarial fever Charcot mentions the quantity of urea present--in the former greatly lessened, in the latter much increased. There is, however, a source of fallacy here not mentioned by Charcot: that is, the variations in the amount of urea due to destruction of the hepatic secreting structure. It follows that as changes {1092} occur in the kidneys, to the condition of cholæmia is superadded the derangements belonging to uræmia.

When the occlusion has existed for some time--a variable period, partly due to peculiarities of individual structure--there come on certain characteristic symptoms of nervous origin: headache, hebetude of mind, dull hearing, obscure or hazy vision, xanthopsia; somnolence and greatly increasing stupor, leading into coma; rambling and incoherence of mind, passing into delirium; muscular twitching, subsultus; muscular weakness, deepening into paralysis; and finally, it may be, general convulsions. As these derangements of the nervous system develop, a light febrile movement supervenes, so that the whole complexus has the typhoid type, or, as it can be more definitely expressed, the patient thus affected lapses into the typhoid state.

COURSE, DURATION, AND TERMINATION.--Occlusion of the gall-ducts is an essentially chronic malady in the greatest number of cases. As a rule, the causes of obstruction operate slowly, but to this rule there are exceptions. Permanent occlusion may take place suddenly, as when a gall-stone is impacted immovably in the common duct, or when a round-worm makes its way into the duct and is firmly fixed there, incapable of further movement.

When occlusion is once effected the gradual changes occurring in the liver lead to slow decline of the nutrition; the bile-elements circulating in the blood poison it and set up alterations in the structure of the kidney, and ultimately, the brain becoming affected, the end is reached by convulsions and coma. Although permanent occlusion, if unrelieved, terminates in death, a small proportion of cases get well, either in consequence of giving way of the obstructing cause or from the opening of a new route to the intestine. Thus, a calculus lodged in the fossa of Vater may suffer such injury to its outer shell as to yield to the action of solvents, or, suppuration occurring around it, the stone may be loosened and forced onward, or ulceration may open a channel into the bowel. An incurable malady causing the occlusion, the termination in death is only a question of time. The duration of any case must be indefinite. There are several factors, however, whose value can be approximately estimated. When the obstructing cause is merely local--as, for example, a gall-stone or the cicatrix of a simple ulcer--the duration of the case is determined by the mere effect of the suspension of the hepatic functions. As the eliminating action of the liver and the part played by the bile in the intestinal digestion are necessary to life, it follows that the complete cessation of these functions must lead to death. The rate at which decline takes place under these circumstances varies somewhat in different subjects. Probably two years may be regarded as the maximum, and three months the minimum, period at which death ensues when no other pathogenetic factor intervenes.

DIAGNOSIS.--To determine the fact of occlusion is by no means difficult: the persistent jaundice, the absence of bile in the stools, and the appearance of the bile-elements in the urine are sufficient. It is far different when the cause of the occlusion is to be ascertained.

The ease and safety with which the exploring-trocar can be used in cases of supposed obstruction of the cystic duct enable the physician to decide with confidence points which before could only be matters of mere {1093} conjecture. The writer of these lines was the first to puncture the gall-bladder and to explore, by means of a flexible probe passed through the canula, the course of the duct.[204] It is possible in this way to ascertain the existence of gall-stones in the gall-bladder, to find an obstruction at the entrance of the cystic duct, to demonstrate the presence of echinococci cysts, and to remove for microscopical examination pathological fluids of various kinds. More recently, Whittaker and Ransohoff[205] of Cincinnati have attempted the detection of a gall-stone impacted at any point by the introduction of an exploring-needle; and this practice has been imitated by Harley[206] of London, but without any reference to the pioneer and prior investigation of his American colleagues. The case of Whittaker and Ransohoff survived the exploratory puncture, but Harley's case proved fatal from traumatic peritonitis. Notwithstanding this untoward result, Harley persists in the advocacy of this method. It must appear to any one familiar with the intricate arrangement of the parts composing the anatomy of this region a most hazardous proceeding, and hardly to be justified in view of the superior safety and certainty of my method. To explore the interior of the gall-bladder an aspirator-trocar is introduced; any fluid intended for microscopical examination is then withdrawn, and through the canula a flexible whalebone bougie is passed.

[Footnote 204: _The Cincinnati Lancet and Clinic_ for 1878-79; also, W. W. Keen, M.D., "On Cholecystotomy," _The Medical News_, Sept., 1884.]

[Footnote 205: _Lancet and Clinic_, 1884.]

[Footnote 206: _Lancet_ (London), July, 1884.]

When icterus comes on in a few days after birth and persists until death ensues by convulsions and coma, there can be no doubt regarding congenital absence or impermeability of the common duct. Permanent retention-jaundice, accompanied by the characteristic symptoms of that condition immediately succeeding an attack of hepatic colic, is probably due to impaction by a calculus. When, at or after middle life, in a patient with a history of former attacks due to gall-stones, there begins a fixed pain in the right hypochondrium, and subsequently retention-jaundice, the existence of a malignant growth in connection with the cicatricial tissue and ancient organized exudation should be suspected; and this suspicion will be confirmed if subsequently a tumor can be felt. If with a localized pain slowly-developing jaundice, intestinal indigestion, fats and oils appearing unchanged in the stools, and a condition of prostration more than is properly referable to the derangement of the hepatic functions, come on in a man or woman after thirty-five, cancer of the head of the pancreas should be suspected; and this suspicion will be confirmed if a tumor can be detected in that situation. It should not be forgotten, however, that in emaciated subjects the head of the pancreas may be so prominent as to be mistaken for a scirrhous growth.

A pulsating tumor of the right hypochondrium, accompanied by jaundice, may be an aneurism of the hepatic artery. Pulsation may be communicated to a bunch of enlarged portal lymphatic glands, which will compress the common duct, but in this case, as the increase in the size of the glands is due to caseous, amyloid, or cancerous deposits, there will be found a source whence these morbid products are derived, and will explain the nature of a tumor thus constituted.

The differentiation of hypertrophic cirrhosis from occlusion of a slowly-forming character is by no means easy. In both jaundice {1094} gradually appears; in both the liver is enlarged, but in hypertrophic cirrhosis much more than in occlusion; and in the latter the gall-bladder is full--may indeed be distended--whilst in the former it is empty or contains but little bile. The history of the case may indicate the nature of the symptoms. Previous attacks of hepatic colic, and the symptoms of occlusion supervening on the last, are highly significant of calculous occlusion.

TREATMENT.--To ascertain the nature of the occlusion is a necessary preliminary to any exact treatment. In many cases this must remain a mere conjecture, when, of course, the treatment is only symptomatic. When it is probable or certain that the duct is obstructed by a calculus, two methods may be resorted to for its removal: one method is to break up the calculus by mechanical means; the other is to effect its solution by chemical agents.

Fracture of an impacted calculus is not a merely fanciful expedient. If the site of the obstruction is ascertained, an attempt may be made to penetrate the calculus by an aspirator-needle passed through the abdominal walls, according to the method of Whittaker and Ransohoff. The dangers attendant on this mere puncture are great, and a fatal result has occurred in one of the very few cases in which it has been done. Less severe and dangerous methods for attempting the disintegration of a calculus should be first tried, as follows: Make firm friction with the fingers along the inferior margin of the ribs and toward the epigastrium and umbilicus, whilst the opposite side posteriorly is supported by the hand spread out and applied firmly. A strong faradic current sent through the region of the gall-bladder and ducts has in several instances seemed to do good--indeed, to remove obstructions. A calculus impacted may be dislodged either by the fracture of its surfaces or by the strong muscular contractions of the abdominal walls and of the muscular layer of the duct. Most calculi are easily broken, and when the smallest breach is made in the external crust disintegration follows; and some calculi are so friable as to yield to slight pressure. Furthermore, the slightest solution in the continuity of the rind disposes the whole mass to dissolve in suitable menstrua. Mechanical rupture is so important a step in the process of disintegration of an impacted calculus that so serious an operation as section of the abdomen as a preliminary to it should be considered. The cavity exposed, the obstructed duct is found, and its retained calculus is mashed without section of the duct. I find one instance[207] in which this was done as a subordinate part of a cholecystotomy, and the breaking up of the stone proved to be easy of accomplishment. It is also the method of Tait, who proposes to mash the calculus by means of suitable forceps fitted with padded blades.

[Footnote 207: Harley's case, _op. cit._]

I have suggested a means of effecting solution of an impacted calculus which seems, on further reflection, well worthy of consideration. The proposal is to inject, through a canula introduced into the gall-bladder, one of the solvents of the cholesterin calculus before mentioned. I have already used the canula as a duct for the passage of an exploring-sound, and have by means of it explored the interior of the gall-bladder. It is quite as feasible to inject through the canula a solvent, successive charges of which can be thrown in and withdrawn by the aspirator.

{1095} That the usual solvents introduced by the stomach can effect the solution of impacted calculi has been declared impossible by Trousseau;[208] and with this conclusion I unhesitatingly agree. I have already discussed this part of the subject, and need now only refer the reader to that section.

[Footnote 208: _Clinique médicale_, _loc. cit._]

The various causes of obstruction besides calculi do not offer an inviting field for the exercise of therapeutical skill. Each case must be treated according to the nature of the obstructing cause; hence to make an accurate diagnosis is an essential preliminary to suitable treatment.

IV. DISEASES OF THE PORTAL VEIN.

Thrombosis and Embolism of the Portal Vein; Stenosis; Pylephlebitis.

DEFINITION.--By the terms at the head of this section are meant the various pathological processes which induce coagulation of the blood in some part of the portal system. As the portal vein is made up of many branches coming from the various organs of the abdominal cavity except the kidneys, and as it empties, so to speak, into the liver, it is obvious that various and complex derangements will ensue on the formation of thrombi.

CAUSES.--Thrombosis of the portal vein occurs under three general conditions: the blood is in a readily coagulable state; the action of the heart is weak and the blood-current sluggish; the circulation through the vein is impeded by external pressure. The coagulability of the blood is increased in diseases characterized by an excess of its fibrin-producing constituents, of which cirrhosis of the liver may be mentioned as one having this peculiarity. In chronic maladies of a depressing kind there may be simply a weak action of the heart, or the muscular tissue of the organ may be affected by a fatty and atrophic degeneration. The external pressure by which the blood-current through the vein is impeded may be caused by the newly-formed connective tissue of Glisson's capsule, by enlarged lymphatics in the hilus of the liver, or by tumors of various kinds. The first named of these causes of compression--atrophic cirrhosis--is most frequently acting. Very rarely, organized exudations of the peritoneum may be so situated as to compress the portal vein. This result can only happen when the hepatic portion of the peritoneum is involved.

Pylephlebitis exists in two forms: the adhesive and suppurative. The former results in changes not unlike those of simple thrombosis. The blood coagulates in the affected part of the vessel, the clot is organized, and the vessel ultimately forms a solid rounded cord which is permanently occluded. The suppurative variety is so different in its origin and in its results that it requires separate treatment, and I therefore postpone the consideration of it to the next section.

{1096} SYMPTOMS OF THROMBOSIS AND ADHESIVE PYLEPHLEBITIS.--It is a remarkable fact that the biliary function of the liver is not necessarily affected in cases of occlusion of the portal vein. It is true, in advanced cases of cirrhosis, when the interlobular veins are obliterated by the pressure of the contracting newly-formed connective tissue, the functions of the liver are arrested in so far as the damage thus caused extends. Notwithstanding the blocking of the portal, sufficient blood reaches the hepatic cells by the anastomosis between the hepatic artery and the interlobular veins--an anatomical connection demonstrated by Cohnheim and Litten.[209] So long as this anastomosis continues bile will be formed, although the portal vein is occluded.

[Footnote 209: _Virchow's Archiv_, Band lxvii. p. 153, "Ueber Circulationsstörungen in der Leber."]

The most significant symptoms of thrombosis of the portal vein are the sudden formation of ascites, which quickly assumes a very high grade, and equally sudden passive congestion of the gastro-intestinal mucous membrane, enlargement of the spleen, and distension of the superficial veins of the abdominal parietes. When these symptoms succeed to cirrhosis of the liver, or appear after the formation of a tumor in the hepatic region, or come on in the course of phthisis or chronic inflammation of the hepatic peritoneum, the existence of thrombus of the portal vein may be reasonably suspected.

Coincidently with the occlusion of the portal vein the gastro-intestinal mucous membrane becomes the seat of a catarrhal process, and to the fluid thus produced is added a much more abundant transudation from the distended capillaries. Nausea, vomiting, and diarrhoea result, the rejected matters being serous, watery, and in many cases tinged with blood. Now and then quite a severe hemorrhage takes place, and the blood is brought up by vomiting (hæmatemesis) or is discharged by stool. Hemorrhoids form, and, in large masses protruding, much pain is experienced, and free bleeding may result from rupture of a distended vein.

The veins of the abdominal parietes, which in the normal state are invisible or at least not prominent, and which form anastomoses with the portal, when the obstruction occurs dilate, sometimes to a remarkable extent. The most important anastomosis is that between the femoral and saphena and internal mammary and epigastric veins. When the hepatic branches of the portal are closed, but the trunk remains pervious, the parumbilical vein enlarges greatly, and, communicating with the superficial veins of the anterior part of the abdominal walls, forms a radiating network of tortuous veins to which is given the striking title of caput Medusæ.

The most significant symptom of portal thrombosis is a quickly-forming ascites. It is true, ascites is a common symptom in advanced cirrhosis, but the rapid accumulation of fluid and the prompt filling of the cavity after tapping distinguish that which arises from portal thrombosis from all others. Besides its excessive extent, the ascites presents the usual symptoms.

Due to the same cause as the enlargement of the superficial veins, the hemorrhages, the ascites, etc., there occurs considerable hypertrophy of the spleen in many of the cases. It sometimes happens that the new compensatory circulation and the hemorrhages from some part in the {1097} usual route of the portal so dispose of the blood that the spleen does not enlarge sufficiently to be readily made out.

COURSE AND TERMINATION.--It is obvious that a condition such as that induced by thrombosis of the portal must be comparatively quickly fatal; but the cases vary in duration as the compensatory circulation is more or less complete. Whilst the majority of cases terminate within two weeks, instances of several months' duration are not unknown, but a fatal termination, sooner or later, is inevitable in all cases.

Coming on in the course of some chronic affection of the liver or some obstructing cause exterior to the organ, there soon follow ascites, nausea and vomiting, hæmatemesis, bloody stools of a liquid character, enlargement of the spleen, distension of the abdominal veins, and the distressing symptoms produced by an excessive accumulation of fluid in the peritoneal cavity.

DIAGNOSIS.--As there is no symptom of thrombosis of the portal which may not be caused by advanced cirrhosis, the diagnosis rests on the rapid production of the attendant phenomena and their conjoint appearance.

TREATMENT.--A symptomatic treatment is alone possible. The highly irritable and congested intestinal mucous membrane precludes the employment of hydragogue cathartics. Salines which cause outward diffusion from the vessels are the only cathartics which can be used with propriety. Action of the kidneys and of the skin must be maintained. To this end the resin of copaiba in pilular form and pilocarpine subcutaneously may be used. If the strength of the patient will permit, leeches around the anus can be applied, and much relief may be expected from free bleeding. It is probable that opening a swollen hemorrhoid would give the same kind of relief as that caused by a free hemorrhage. In any case the benefit derived from treatment must be merely palliative and temporary.

Suppurative Pylephlebitis.

PATHOGENY.--Primary pylephlebitis rarely if ever occurs. On the other hand, the secondary form is by no means uncommon; it succeeds to ulcerative or purulent inflammation at some point in the circuit of origin of the portal radicles. The most frequently-occurring cause is ulceration and suppuration of some part of the intestinal tube, and hence the most common result is multiple abscess of the liver. Pylephlebitis has often resulted from typhlitis; from ulcers of the large intestine, as in dysentery; from such traumatic injuries as tying hemorrhoids; from proctitis; from ulcers of the stomach and similar morbid processes elsewhere within the range of origin of the portal system. The pathogeny is clear. The inflammatory or ulcerative action extends to and involves the walls of the veins, or some morbid material diffuses through the vein walls. In either case coagulation of the blood in the vessel ensues, and the clot undergoes a series of changes resulting in the formation of emboli, which, carried into the main current, are subsequently lodged in the hepatic capillaries.

There are three steps in the morbid process: the changes in the vein wall; the production and transformation of the thrombus; and the formation of secondary suppurating foci in the liver.

{1098} The appearance of the tunics of the inflamed vessels varies with the stage at which they are examined. At first the walls of the vessels are reddish from congestion, succulent, and swollen, infiltrated by leucocytes and inflammatory exudation and the cellular elements undergoing proliferation. The intima especially is much altered in its appearance and structure, becoming thick, opaque, grayish or yellowish in color, and having adherent to it a thrombus passing through its characteristic changes. Ulceration of the intima then occurs, and the purulent elements, with shreds of tissue, mingle with the degenerating blood-clot, and ultimately there remains a purulent dépôt lined with sloughing, even gangrenous, contents. Emboli detached from such decomposing thrombus are arrested in the vessels of the liver, and there set up a suppurating phlebitis, ending in an abscess formation, or a quantity of pus from the original point of ulcerative phlebitis passes into the portal vein, and is generally distributed through the hepatic branches, here and there foci of suppuration being established by the deposit of decomposing emboli. There may be numerous small abscesses irregularly distributed through the liver, or there may be one or two larger collections of pus. Very often the vessel whose occlusion by a suppurating embolus has caused the mischief is destroyed, and hence no communication with the abscess-cavity can then be traced. These abscesses are not limited by a line of inflammatory demarcation or by a limiting membrane, but the hepatic tissue adjacent is congested and infiltrated with pus.

Ulceration, abscesses, or purulent inflammation occurring at any point within the area of origin of the radicles of the portal vein may induce pylephlebitis and consequent hepatic abscess. There are two points at which, suppuration established, secondary pylephlebitis is most apt to occur: the cæcum; the rectum. As respects the former, the symptoms of typhlitis precede the hepatic disturbance; and as respects the latter, usually dysentery, or rather proctitis, is the initial disease. In both sources of the hepatic trouble the inferior hemorrhoidal veins are chiefly concerned--a fact explicable by reference to the sluggishness of the circulation and the distended condition of these veins, whence it is that thrombus is very readily induced. Numerous instances of pylephlebitis following suppurative lesions of the cæcum have been reported. One of the most recent, and at the same time typical, examples of such conditions is that published by Bradbury[210] of Cambridge, England. The initial lesion was "an ulcer the size of a split pea" situated near "the junction of the vermiform appendix and cæcum." "The hemorrhoidal veins and the inferior mesenteric above were filled with breaking-down clot and pus," and "the liver contained many abscesses of various sizes, the largest about the size of a lemon, which had burst through the diaphragm." As is so often the case, the ulcer of the cæcum produced no recognizable disturbance, and important symptoms were manifest only when the emboli lodged in the liver set up suppuration, when there occurred the usual signs of hepatic abscess. In the West and South hepatic abscess due to pylephlebitis, induced by proctitis, with ulceration of the rectum, is a common incident. Various examples of this kind have fallen under my own observation. The relatively greater frequency of this form of pylephlebitis is due to the fact above {1099} stated, that the inferior hemorrhoidal veins are voluminous, have a sluggish current, and are liable to over-distension by pressure of feces and by external abdominal bands and clothing. Cases of a corresponding character arise from suppuration and ulceration elsewhere within the portal circuit. Thus, Bristowe[211] reports a case in which pylephlebitis resulted from an ulcer of the stomach, the neighboring veins becoming implicated and the usual results following.

[Footnote 210: _The Medical Times and Gazette_, Sept. 27, 1884, p. 450, "Proceedings of the Cambridge Medical Society."]

[Footnote 211: _Transactions of the Pathological Society of London_, vol. ix. p. 278.]

When inflammation has begun in a radicle of the portal vein, it may proceed to the liver by contiguity of tissue, the whole intervening portion of the vessel being affected. Probably more frequently the intra-hepatic portion of the portal is inflamed by emboli, and the adjacent hepatic tissue then undergoes suppuration, as has been already set forth.

SYMPTOMS.--There being two points of disease--the primary lesion of the peripheral vessel and the secondary results in the hepatic portion of the portal--the symptomatology must have a corresponding expression. The stomach, the cæcum, or the rectum, or some other organ or tissue, being occupied by a morbid process, there will be a characteristic complex of symptoms. Taking up the most usual primary disturbance, a typhlitis or an ulcer of the cæcum, there will be pain, tenderness, and possibly fever, occupying in point of time the period proper to such a malady and an amount of disturbance of function determined by the extent of the lesion. The symptoms caused by a single small ulcer of the cæcum, as in the example narrated by Bradbury, may present no characteristic features and may have little apparent importance, and yet the lesion is productive of very grave consequences.

When from any of the causes mentioned above a thrombus forms in a vein of the portal system in consequence of the extension of the inflammation about it, the case, what importance soever it previously had, now takes on new characters. The onset of the inflammation of the vein walls and the puriform degeneration of the thrombus is announced by a chill--a severe rigor, or chilly sensations at least. At the time of the chill, and sometimes before it, pain is felt, significant of the lesion in the vein. When proctitis or typhlitis precedes the pylephlebitis, pain appropriate to the malady is a significant symptom; but the pain which comes on with the beginning of the inflammation in the liver is a new sign. The most frequent sites of the pain are the right hypochondrium and the epigastrium, but it may also be felt in the left hypochondrium or in either iliac fossa. Unless there be diffuse peritonitis the pain is accompanied by a strictly-localized tenderness to pressure. The situation of the pain may afford an indication of the vein attacked, and when there are two points at which pain is experienced, one may originate at the first situation of the morbid action; the other will be due to pylephlebitis.

The fever succeeding the chill is decided, and in some cases may attain to extraordinary height--a manifestation indicative of the pyæmic character of the affection. The fever intermits or remits, with a more or less profuse perspiration. The febrile phenomena are similar in their objective expression to malarial fever, but there is an important difference in respect to the periods of recurrence of the chills. The paroxysms are very irregular as to time: there may a daily seizure at different hours, or there may be several chills on the same day. In other words, the {1100} paroxysms have the pyæmic characteristics rather than the malarial. After a time the intermittent phenomenon ceases, and there occurs a remission merely, the exacerbation being preceded by chilliness and succeeded by sweating. The sweats are characteristically profuse and exhausting. During the sweating the temperature begins to decline, and reaches its lowest point just before the chilly sensations during the early morning announce the onset of the daily exacerbation of the afternoon and evening. The thermal line exhibits many irregularities until the febrile movement assumes the remittent type, when there occur the morning remission and nocturnal exacerbation. The maxima may be from 103° F. to 105°, even to 106°.

When the pain and chill come on, disturbances of the digestive organs ensue. When a large vein of the portal system is occluded, the remaining veins must be over-distended, and congestion of a part or of all of the digestive tract will be a result. An acute gastric catarrh is set up. The appetite is lost, the stomach becomes irritable, and vomiting is a usual incident. Sometimes the disgust for food is extreme, and the nausea and vomiting are almost incessant. The vomited matters consist of a watery mucus mixed with thin bile after a time, and now and then of a bloody mucus. Thrombosis of a stomach vein may occur, to be followed by an acute ulcer, and from this considerable hemorrhage may proceed, when the vomit will consist of blood. Such an accident, happening to the mucous membrane of the intestine, will be indicated by bloody stools if the ulceration is low down, or by brownish, blackish, or chocolate-colored stools if higher up in the small bowel.

The tongue has usually a characteristic coating in these cases. Large patches of a rather heavy and darkish fur form, and, cast off from time to time, leave a glazed and somewhat raw surface. Sometimes there is a profuse salivary flow, but more frequently the mouth is dry. The lips are fissured or contain patches of herpes, and the buccal cavity may be more or less completely lined by patches of aphthæ.

Diarrhoea is a usual symptom, the stools being dark when mixed with blood, or grayish and pasty or clay-colored when there is jaundice.

Three-fourths of the cases of pylephlebitis are free from jaundice. This symptom may occur at the onset when the common duct is obstructed by a calculus, but in other cases it appears when the formation of pus in the liver exerts sufficient compression of the hepatic ducts to prevent the passage of the bile.

When jaundice occurs, it is accompanied by the usual symptoms. The urine, previously unchanged, is now colored by bile-pigment, and the alterations in the renal structure and function belonging to jaundice also take place.

It sometimes happens that the obstruction of the portal vein is sufficient to cause enlargement of the superficial veins of the abdomen, but the duration of the disease is usually too brief to permit much deviation from the normal, except rarely. In the cases characterized by the occurrence of diffuse peritonitis the abdomen will present a swollen and tense appearance, and there will be acute tenderness to pressure. The area of hepatic and splenic dulness is not increased from the outset, but is evident, as respects the spleen, soon after the obstruction at the liver, and as respects the liver when the formation of abscesses occurs.

{1101} COURSE, DURATION, AND TERMINATION.--The course of pylephlebitis is compounded of the disturbance at the original point of disease, and of the secondary inflammation at the several points in the liver where emboli set up purulent inflammation. There are, therefore, two distinct symptom-groups, and a short intervening period in which the first is being merged into the second. The duration is variable, but the extreme limits are not remote from each other, the condition of pylephlebitis terminating in from two weeks to three months, the shorter being the more usual. The termination is death, doubtless invariably; for, as in true pyæmia arising from other causes, the septic changes in the blood are such as to preclude the possibility of a return to the normal condition.

DIAGNOSIS.--The main point in the diagnosis consists in the occurrence of an evident local inflammation, followed by the signs of suppuration in the hepatic region coming on subsequent to ulceration and suppuration at some point in the peripheral expansion of the portal system. Thus, when a proctitis with ulceration of the rectum has been in existence for some time, there occur pain and tenderness in the hepatic region, accompanied by an irregularly intermittent fever and by profuse sweating, it can be assumed with considerable certainty that emboli have been deposited in some one or more of the terminal branches of the portal. The evidences of hepatic trouble--swelling of the organ, jaundice, etc.--and of portal obstruction, which then supervene, indicate with some precision the nature of the case.

TREATMENT.--Although pylephlebitis wears a most unfavorable aspect, the possibility of a favorable result should always be entertained by the therapeutist.

As absorption of medicaments must be slow--indeed, uncertain--by the gastro-intestinal mucous membrane when there is portal occlusion, it is well to attempt treatment by the skin and subcutaneous connective tissue. Gastro-intestinal disturbance--nausea, vomiting, and diarrhoea--should be treated by a combination of bismuth, creasote, and glycerin--remedies acting locally chiefly. Ammonia--the carbonate and solution of the acetate--is indicated, and should be given for the purpose of dissolving thrombi and emboli. Corrosive sublimate, carbolic acid, and quinine can be administered by the subcutaneous areolar tissue. Quinine may also be introduced by friction with lard, and in considerable quantity.

V. PARASITES OF THE LIVER.

Echinococcus of the Liver; Hydatids of the Liver.

DEFINITION.--The echinococcus is the intermediate or larval stage in the development of the Tænia echinococcus--the completed parasite--whose chief habitat is the intestine of the dog. As the natural and clinical history of parasites is elsewhere treated of, the subject is here confined to the development of echinococci cysts in the liver, its ducts, and vessels.

CAUSES.--The presence of echinococcus vesicles in the liver is due to {1102} the migration of the embryo from the intestinal canal. As Davaine[212] has ascertained by analysis of all the recorded examples previous to the publication of his treatise, echinococci are found in as large a proportion in the liver as in all the other organs combined. This statement is repeated with approval by Cobbold[213] and by Heller.[214] The embryo, set free in the intestine from the food or drink containing the ova, starts on its migration. There are several reasons why the liver is selected for its habitat: it is the largest accessible organ; the common duct and the portal vein offer the most convenient roadway for reaching and penetrating its substance. The exact route or routes of which the parasite avails itself in migrating have not been definitely settled, although Friedreich has shown that the portal vein is the medium of transmission of the Echinococcus multilocularis. The comparative frequency with which the liver is entered indicates that the portal vein is the favorite route of migration.

[Footnote 212: _Traité des Entozoaires et des Maladies vermineuses, etc._, par C. Davaine, Paris, 1877, p. 383.]

[Footnote 213: _Entozoa_, by T. Spencer Cobbold, M.D., F.R.S., London, 1874, p. 275.]

[Footnote 214: In vol. iii of _Ziemssen's Cyclopædia_, p. 561.]

PATHOLOGY AND SYMPTOMS.--The number of echinococci reaching the liver varies from one to ten or twelve or more. They increase in size from the time of their deposit in the organ, and ultimately attain to large proportions. The rapidity of growth depends somewhat on the character of the tissue in which imbedded, and the amount of disturbance of function is determined by the position of the parasite in the organ. Echinococci may be deposited in any part of the liver--in the substance of the organ, in the ducts, or in the vessels--but the most usual site is near the capsule, and, developing outwardly in the direction of least resistance, impart to the outline of the organ an irregular contour. As the echinococci develop, the adjacent parts of the liver pressed upon undergo atrophy, but the connective tissue of the organ contributes to the formation of the dense capsule which envelops them. But as the increase in size is not rapid, although continuous, if the cysts are situated at the periphery and adjacent to the capsule, they may be present for many months without causing any distinct symptoms. In a case occurring under my own observation last year the only symptom which attracted attention was an enlargement of the hepatic region, and on examination a characteristic elastic, irregular, and painless tumor could be readily detected by sight and touch occupying the right hypochondrium and extending into the epigastric and umbilical regions. When the echinococci cysts impinge on the portal vein or on the hepatic duct, there will be caused the usual results of such pressure--ascites or jaundice, or both conditions may occur simultaneously, with obstruction of both vein and duct. When the cysts develop downwardly, the stomach and intestines will be displaced, and nausea and vomiting, diarrhoea or constipation, and, it may be, considerable pain of a colic-like character, will be caused. An upward development of the cysts gives rise to more pronounced disturbances. The diaphragm is pushed upward, the heart displaced, and the lungs, especially the right, compressed. Occasionally the diaphragm is softened and perforated by the pressure of the enlarging cysts, and the lungs are ultimately tunnelled, the parasites being discharged by the bronchi.

{1103} The growth of an echinococcus tumor may spontaneously cease, and then retrograde changes take place, leading to its final disappearance. This arrest of development may occur without any obvious cause, but now and then such a change from the ordinary course of tumors may be effected by an external injury, as a blow on the abdomen, but more frequently the death of the parasite is caused by ulceration into a bile-duct, and the entrance of bile, which is a poison to these hydatids. It sometimes happens that, opening into a duct of large size, the daughter and granddaughter vesicles are slowly discharged through it into the intestine, and thus a cure is effected. Inflammatory action occurring in the cysts, adhesions may form and rupture into a neighboring cavity take place. Direct communication may be established with the intestine, or the cavity of the pleura or peritoneum be entered, with results entirely disastrous.

A necessarily fatal termination must also ensue when the hydatids penetrate the ascending vena cava, but this accident is, fortunately, very rare.

The passage outward through the abdominal wall is an exceedingly uncommon but fortunate issue of echinococcus of the liver, for in this mode the hydatids may be discharged without much difficulty.

The echinococcus vesicle is enveloped in a dense, resisting, and elastic capsule, constructed out of the connective tissue of the part in which it is deposited. The innermost layer of the vesicle is the germinative (endocyst), and from its granular surface are developed the brood-capsules and their scolices--_i.e._ the head with its suckers and crown of hooklets.[215] Each vesicle may contain not only daughter, but also granddaughter, progeny, numbering from a dozen up to many thousands, and they will vary in size from the head of a pin to a pullet's egg. It follows that the mother vesicles must also greatly vary in size: they range from a large pin's head to a child's head. The vesicles or sacs contain a clear, faintly yellowish, or opalescent fluid, neutral or slightly alkaline in reaction, and holding in solution a large per cent. of sodium chloride, but free from albumen. The specific gravity of the fluid ranges from 1007 to 1015, according to the quantity of sodium chloride present. Succinic acid and also hæmatoidin are usual constituents, besides the ingredients already mentioned.

[Footnote 215: _Entozoa_, Cobbold, p. 273 _et seq._, chapter viii.]

Although the form of hydatid or echinococcus cyst above described is the usual one, there is occasionally produced an anomalous development of the parasite, which from its resemblance to colloid cancer was supposed to have this character until Virchow[216] unravelled the mystery by demonstrating its true structure. This form of the parasite is designated Echinococcus multilocularis. Its resemblance to colloid cancer is the more striking because of the tendency of the interior of the mass to undergo degeneration, to disintegrate, and to break up into pus-sacs with greenish, cheesy, and bilious contents. An Echinococcus multilocularis tumor is of almost stony hardness; it has a very dense fibrous structure, intersected by cavities with thick gelatinous contents. These minor cavities[217] are sacs of echinococci, but they depart widely from the typical form, well-defined scolices being seldom encountered.

[Footnote 216: _Archiv für Anat._, Virchow, vol. xi. p. 80.]

[Footnote 217: Carrière, quoted by Davaine, _op. cit._, p. 961.]

{1104} Echinococci of the liver develop very slowly, and it is characteristic of them to attain to very large proportions in most cases without causing any very pronounced symptoms. There are certain signs common to hydatids in any situation; there are others which are due to particular circumstances.

A hydatid tumor of the liver is smooth but somewhat irregular in outline, and elastic, when it develops downward, extending below the margin of the ribs. If, however, it grows upward, the area of hepatic dulness extends in that direction beyond the usual limits; the diaphragm is pushed up, the lungs forced upward to the left and compressed, and the heart also displaced upward toward the left. The extension of the tumor downward, in the direction of least resistance, is more usual. If the walls of the abdomen are sufficiently thin, the tumor large enough, and if made up of many daughter vesicles, there may be evoked by palpation the very characteristic sign known as hydatid purring. To produce this effect an oscillation must be caused by a sudden impulse communicated to the tumor on one side, the hand resting against the other side. This sensation is likened to the impression on the eye of the vibration of a bowl of jelly. Even when there is a well-defined tumor this symptom is comparatively infrequent, but if present it is pathognomonic, since no other kind of tumor possesses the property of oscillation and elastic collision of its several constituents.

When the tumor is so situated as to occlude the hepatic or common duct, jaundice will be a symptom, and when the stomach is pressed upon there will be epigastric oppression and nausea. If the vena cava is impinged on or the portal vein, the usual results--ascites and oedema of the lower extremities and of the scrotum--will be manifest. There is, of course, nothing distinctive in these results.

The Echinococcus multilocularis, situated in the substance of the liver, causes the usual disturbances of a new formation in such a position. Much of the hepatic tissue is destroyed by its growth, and many of the minor ducts closed. Jaundice is an early symptom--the first, indeed, in many cases--and is also one of the most persistent. It is present, according to Griesinger, in 10 out of 13 cases. The usual gastro-intestinal disorders belonging to jaundice occur under these circumstances; also the nervous disturbances of cholæmia.[218]

[Footnote 218: Davaine, _op. cit._, p. 962.]

Enlargement of the spleen is a very frequent symptom, being present, according to Davaine, in 11 out of 13 cases, and, according to Heller, in 25 out of 29 cases, in which this fact was made the subject of direct inquiry.

Pressure on the vena cava causes oedema of the inferior extremities in a small number of cases; and on the vena porta, ascites. There may occur thrombosis of the portal, in which event the ascites will form very quickly, and return as quickly after tapping.

The usually placid course pursued by echinococcus of the liver may be much modified by inflammation and suppuration. Some external injury may develop the inflammation. Having occurred, the clinical history corresponds to other cases of hepatic abscess, and the reader is therefore referred to the section on that topic for fuller information.

DIAGNOSIS.--At the outset of echinococcus of the liver the {1105} differentiation of the tumor from other tumors, and of the disturbances produced by it as contrasted with the effects of other morbid growths, becomes exceedingly difficult, if not impossible. The size, painlessness, elasticity, the purring tremor of the echinococcus tumor, afford a sure basis for constructing a diagnosis, and as ultimately developed they become the means of accurate differentiation from other morbid growths of that locality. All doubt as to the nature of a given hydatid tumor of the liver may be set at rest by the use of the aspirator. The discovery of the characteristic hooklets of the scolex in the fluid withdrawn from the tumor will be conclusive as to the presence of echinococci. The hooklets may be absent, as in the case of acephalocysts, but the fluid is characteristic in other respects: it contains a large quantity of chloride of sodium and is free from albumen.

Very great difficulty is experienced in diagnosticating an echinococcus tumor developing from the upper surface of the liver, pushing the diaphragm and lungs upward and displacing the heart to the left. Whilst the physical signs may be, and are, usually alike when the condition calling for diagnosis has existed for some time, there are means of differentiating in the history of the cases and in the initial symptoms.

The origin and growth of the echinococcus tumor are obscure and free from constitutional disturbance; the onset of a pleuritic exudation is marked by pain, fever, and hurried respiration and by physical signs of a characteristic kind. It is true there are cases of so-called latent pleurisy in which a hydrothorax forms without any well-marked indications, but it will usually be found that some local pain, hurried breathing, or other symptoms existed from the beginning. Those cases of hydrothorax accompanying renal and cardiac diseases are readily enough associated with their original cause.

Echinococcus of the liver may be confounded with abscess of the liver, but a differentiation can be readily made by attention to a few considerations, except in the rare condition of the Echinococcus multilocularis which has proceeded to suppuration. In this latter condition there are no means of differentiation, since an abscess-formation has already occurred, nor is there any need to attempt a distinction without the occasion of a difference. Echinococcus differs from abscess in history, in the character of the swelling, and in progress. Abscess of the liver is preceded by paroxysms of hepatic colic, by inflammatory ulceration of some part of the intestinal tract, or by local injury--traumatism. The onset of a hydatid tumor is silent and painless. The swelling of the liver when an abscess forms is not considerable at any time, and appears to be a uniform enlargement of the organ, except when the pus tends to make its way through the walls of the abdomen externally. An enlarging echinococcus tumor is an obvious projection from the surface of the liver at some point, and it does not have the characteristic tenderness, the fluctuation of an abscess matured and ready to discharge, and the constitutional disturbance; but it does have a peculiar elasticity, and now and then may present that eminently characteristic sign, the purring tremor. The use of the exploring-trocar will usually suffice to clear up all doubts by the withdrawal of the characteristic fluid of the hydatid cyst or of pus.

DURATION AND TERMINATION.--The progress of an echinococcus {1106} tumor is exceedingly slow, and the development of symptoms produced by its extension is early or late according to its position and to the nature of the parts impinged on. A spontaneous cure may take place under the rather rare circumstances of an opening into the hepatic duct or one of its principal divisions, and the gradual discharge of the cysts by this outlet into the intestine. Next to this mode of termination, the most fortunate direction taken by the enlarging cysts is through the walls of the abdomen externally. When the growth is upward through the lungs, the symptoms belonging to empyema or hydrothorax, with pulmonary abscess, ensue, and the termination is fatal after a protracted course. Rupture into the peritoneal cavity is a fatal event. Ulceration into the intestine, and the discharge of the cysts through the route thus made, may effect a cure, but more frequently the fistulous communication becomes a means of forming a fecal abscess.

The result in any case of hydatids of the liver is much influenced by the mode of treatment adopted and the period at which it is undertaken. As these parasites can be readily reached and destroyed by safe means, obviously the more early the diagnosis is made and the treatment carried out, the less the injury done to the hepatic structures and neighboring parts.

TREATMENT.--Prophylactic.--As the intestine of the dog is the natural habitat of the Tænia echinococcus, and as the hydatid is the first stage in the development of the ovum and the second in the life-history of the parasite, the means of prophylaxis consist in preventing contamination of human food and water with the dog's excrement, which contains the ova of the parasite. In Iceland, where hydatid disease is very prevalent, dogs and human beings living in the same huts and obtaining their water-supply by melting the snow just about them, contamination of food and drink must readily occur. In this country such conditions cannot exist; nevertheless, cases of hydatids are not infrequent. The chief, if not the only, source of contamination is through the consumption of such uncooked vegetables as lettuce, celery, cabbage, etc., in the folds of which the ova may be retained, and from which an ordinary washing does not suffice to detach them. It follows that such articles of food should be minutely inspected and cleansed before being placed on the table.

Boiling and filtration are the means of removing impurities of this kind from potable waters.

Therapeutical.--The remedial management of cases of Tænia echinococcus is necessarily restricted to that stage in their development when by increasing size the functions of organs begin to be affected. Internal medicines given with the view to arrest the growth of the parasite are useless. Formerly, such attempts were made and successes were claimed, but it is now known that no medicine can act on organisms enclosed as these are in a dense capsule. It is needless to occupy space with therapeutical details of this kind, but mention may be made of the agents that were supposed to be effective. Laennec held that baths of a solution of common salt had a distinct curative effect. The internal use of iodide of potassium and the local application of iodine paint were believed to cure a case in St. George's Hospital, London, in the practice of Mr. Cæsar Hawkins. Kameela was, in Iceland, supposed to have a curative effect, but notwithstanding this the physicians of that island resort to very heroical surgical methods in the treatment of this affection.

{1107} The one means of relief consists in the removal of the vesicles, either by suitable incisions or by compassing the death of the parasite, after which the power of nature may be adequate to the cure. In Iceland large incisions are made into the tumor at its most prominent part, and, although accidents are not uncommon, the results in many cases are eminently satisfactory. The accidents are shock, hemorrhage, and especially peritonitis. Under favorable circumstances now no procedure is more satisfactory in its results than free incision and drainage. The tumor should be prominent, adherent all round to the peritoneum, and the walls of the abdomen thin to ensure complete success without accident. At the present time, so great have been the advances in abdominal surgery, this operative procedure may be preferable in some few cases presenting the favoring conditions above mentioned.

Very simple expedients, however, suffice in most cases. The most simple is puncture. This is now much practised in Iceland, and, as the statistics show, with considerable success. Thus, Hjaltelin[219] reports 100 cases cured in this way, and in his own hands this expedient proved successful in 41 out of 50 cases operated on. In Australia, where hydatid disease is also quite common, simple puncture has effected a large proportion of cures,[220] and is the method of treatment usually pursued. In England puncture has the approval of some of the best authorities.[221]

[Footnote 219: Davaine, _op. cit._, p. 605.]

[Footnote 220: _The Medical Times and Gazette_, August, 1873, p. 164.]

[Footnote 221: _Transactions of the Clinical Society_ for 1872: discussion participated in by Gull, Bryant, Greenhow, etc.]

The mode of performing this operation consists in the introduction of an exploring-trocar into the most prominent part of the tumor. It may be withdrawn at once or be permitted to remain for a few minutes to several hours. The dangers are suppuration in the sac and peritonitis; but the former, although sometimes accompanied by severe constitutional symptoms, is not likely to endanger life, and even formidable disturbances due to the latter are usually recovered from. The facts show that puncture very rarely indeed causes dangerous, especially fatal, symptoms. An eruption of urticaria has been observed to follow puncture with the trocar, and also aspiration, in a considerable proportion of the cases, but it has no special significance.

Since the introduction of the aspirateur, puncture and withdrawal of the fluid by means of this instrument has been practised more frequently, and this appears to be a more effective procedure, than simple puncture with an exploring-trocar, although in most cases the escape of the contained fluids suffices to destroy the parasite. The aspirateur is less likely to permit the escape of fluid into the peritoneal cavity or the entrance of air into a vein punctured by accident. If puncture with the trocar or aspiration be practised, shall all the fluid be withdrawn at once? The answer to this question may be decided by the character of the sac. Does it contain daughter and granddaughter vesicles? If so, one puncture may not permit the escape of much fluid; but in any event it is the practice of the most judicious and experienced authorities[222] to withdraw as much as possible of the contents of the cysts at the first operation. Formerly, a method practised by some French surgeons consisted in successive tappings, a small quantity of fluid being drawn off each time.[223] {1108} There is no good reason for this method of treatment now, and it seems to have been discontinued.

[Footnote 222: _Transactions of the Clinical Society_, _loc. cit._]

[Footnote 223: Davaine, _supra_.]

Yet another method of treatment, but less effective than puncture or aspiration, consists in injecting into the sac, after the removal of its contained fluid, certain agents toxic to hydatids. A solution of the extract of fern, alcohol, solution or tincture of iodine, and bile, are the chief remedies thus employed. It has long been known that bile is destructive of these parasites, and cases have occurred of spontaneous cure in which the opening of the growing cysts into a bile-duct has secured the entrance of bile and consequent arrest of growth and atrophy of the hydatids. Several successful cases have been reported in which the injection of aspidium (male fern) was the effective agent, but the threatening symptoms produced by it, and the comparative freedom of other methods of treatment from such disturbances, do not recommend the injections of fern. In the case reported by Pavy[224] the extract of fern was mixed with a solution of potassa.

[Footnote 224: _Lancet_ (London), July, 1865.]

Injections of iodine in solution or in the form of tincture have been more frequently practised than of any other material. Davaine,[225] who finds it less successful than simple puncture and aspiration, recommends, as affording the best results, a dilute aqueous solution of iodine. Alcohol, a solution of permanganate of potassium, and various antiseptic agents have been used to some extent, but none of them possess any advantages over more simple measures.

[Footnote 225: _Op. cit._, p. 650.]

The latest proposal for the treatment of hydatid cysts, and probably the most effective consistent with entire safety, is electrolysis. Originally suggested by Althaus[226] to those who first employed the measure on any considerable scale, it had been mentioned thirty years before by Budd, and appears to have been first practised in Iceland on a single case. The first elaborate attempt to establish electrolysis on a sound basis as a regular procedure was made by C. Hilton Fagge and Mr. Arthur E. Durham.[227] They operated on eight cases, and all were successful. The method consists in the introduction of two needles connected with the negative pole, and the application of the positive--a moistened sponge--on the exterior in the neighborhood of the hepatic region. The strength of current employed by Fagge and Durham was that furnished by a battery of ten cells, and which by previous trial was found to decompose a saline solution. The two electrolytic needles, connected with wires attached to the negative pole, were introduced into the most prominent part of the tumor about two inches apart. The current was allowed to pass about ten minutes usually, sometimes a little longer, the sponge on the exterior--the positive pole--being shifted occasionally. The immediate effects are not considerable. The tumor may be rendered somewhat more tense and appear to be enlarged, but more frequently it becomes softer and is lessened in size, the increase of size being due to the disengagement of hydrogen gas, and the diminution caused by the escape of more or less fluid. The immediate effects of the operation varied. In one case no symptom followed, and in this the result was regarded as doubtful, although a cure was considered probable. In the others more or less {1109} constitutional disturbance followed, the symptoms being pain and fever, the temperature ranging between 100° and 103° F. The duration of the fever was from two to nineteen days, the latter in one case only. As has been observed in some of the cases treated by puncture or by aspiration, a rash appeared on the skin--in some instances scarlatinous, in others of urticaria. It is a curious circumstance that an eruption of urticaria is reported to have appeared in one subject in whom a rupture of the sac into the peritoneal cavity is supposed to have occurred.

[Footnote 226: _On the Electrolytic Treatment of Tumors, etc._, London, 1867.]

[Footnote 227: _Medico-Chirurgical Transactions_, 1871, p. 1 _et seq._]

Although so little change in the tumor occurs immediately after the operation, yet it undergoes slow absorption, and ultimately disappears. The time occupied in the disappearance of the tumor varies from a few weeks to many months, the difference being due probably to the situation of the growth, those occupying the substance of the liver requiring a longer time to fill up.

Fagge and Durham report a case in which simple acupuncture was followed by a result apparently as good as obtained by electrolysis, and other similar experiences have been published. If the simple introduction of a needle suffices to arrest the growth of a hydatid cyst and induce its atrophy, of course the more complex procedures will be abandoned.

The tendency of the treatment of hydatid cysts has constantly been toward simplicity, and the success occurs in a direct ratio thereto. In forming an estimate of the relative value of the methods of treatment, the average of mortality of each plan becomes the most important factor. Simple tapping and paracentesis, the most frequently adopted mode of treatment, is not without immediate and remote danger. Of 46 cases carefully tabulated by Murchison,[228] there were 3 deaths properly attributable to the operation; but the after results--suppuration of the cyst and its consequences, peritonitis, etc.--cannot be measured so accurately. About two-thirds of the cases thus treated result in cure, and in a majority of these a single operation suffices. The injection of the various substances which have been employed for that purpose does not seem to increase the proportion of cures, and their use distinctly enhances the dangers of the treatment. At present, the decision as to the method of treatment to be employed in any case should be made between simple tapping, electrolysis, and acupuncture. Of these, the last mentioned, it can hardly be doubted, is the method which is most desirable, for although it has not been employed so largely as the others, thus far the results have been better: the percentage of recoveries without accident has been higher relatively than by other methods of treatment. As acupuncture presents no special difficulties or dangers, and is but little painful, it may be tried first, reserving more formidable measures for the failures by this simple expedient.

[Footnote 228: _Clinical Lectures on Diseases of the Liver_, _loc. cit._]

Distoma hepaticum and Distoma lanceolatum (Liver-Flukes).

The Distoma hepaticum, entitled by Linnæus Fasciola hepatica, occurs very frequently in herbivorous animals and occasionally in the biliary {1110} passages of man.[229] It is, however, less important than the Distoma lanceolatum, which, although much smaller than the former, occurs in much larger numbers.

[Footnote 229: Davaine, _Traité des Entozoaires_, Paris, 1877, p. 240 _et seq._; also, Cobbold, _Entozoa_, p. 148.]

Distoma hepaticum is a leech-like parasite from 25 to 30 mm. in length, of a brownish color, smooth to the naked eye, but thickly covered with minute spikes or spines to be seen with a low power, and provided with a cephalic (entrance to oral cavity) and an abdominal sucking disk, which are also organs of locomotion. The Distoma lanceolatum owes its name to its lancet shape; it is smaller than D. hepaticum, measuring about 8 mm. in length and half this or less in width; it is unprovided with spines, but contains two suckers at the side. Both parasites are hermaphrodite; the ova, according to Cobbold (p. 166), have "an average longitudinal diameter of 1/180, whilst their greatest transversal measurement is about 1/270." These ova are capable of some movement, provided as they are with a ciliated envelope.

The disease known as the rot in sheep, and a peculiar cachexia entitled by Davaine la cachexie aqueuse, are caused by the presence of distoma. The ova gain access to man through the use of unwashed cress, lettuce, and similar vegetables eaten in the raw state, and in drinking-water. Fortunately, this accident is rare. The number of reported examples collected from all sources by the indefatigable Davaine is twelve.[230]

[Footnote 230: _Ibid._, p. 253 _et seq._]

The larger distoma passes into the common and hepatic duct and gall-bladder, whilst the smaller (lanceolatum) enters the finer ramifications, and, there multiplying, several consequences may ensue. The irritation caused by their presence and development will excite a more or less severe cholangitis, or, accumulating in sufficient numbers, an actual obstruction will be induced, and jaundice and structural alterations of the liver will in turn be brought on.

The DIAGNOSIS of such a malady is, in the very nature of the case, uncertain at best, and in most cases impossible. Nevertheless, it may be made in rare instances. The existence of the rot may cast suspicion on the mutton and kitchen vegetables so situated as to suggest the possibility of contamination with the ova of distoma. Definite and conclusive information will be afforded by the presence of the ova, still more of the more or less fully-developed parasite, in the feces of a patient effected by the symptoms of catarrhal jaundice or occlusion of the biliary passages. By tapping the gall-bladder parasites may be withdrawn.

The SYMPTOMS are those common to cases of catarrh of the bile-ducts (cholangitis), catarrhal jaundice, or occlusion of the passages, as may be. As these have been detailed under their respective heads, it is not necessary to repeat the observations already made.

As regards the TREATMENT, in addition to the methods of management recommended in such cases it may be stated that the use of certain parasiticides offers a reasonable prospect of good results. Creasote, bichloride of mercury, thymol, eucalyptol, oil of wintergreen (gaultheria), and similar agents are rational remedies and should be fairly tried.

{1111} Parasites in the Portal Vein.

The entozoön which by its presence in the blood causes the disease chyluria also inhabits the portal vein. In some parts of the world--Brazil more especially--this disease is exceedingly common. It has occurred also in two or three instances in England, and the writer has had a case within the past year (1884) in Philadelphia. The parasites in this case were found in immense numbers in the urine.

The blood of the portal vein sometimes is actually filled, and the liver substance itself is penetrated, by them, but nothing is known of the alterations they induce in these organs. When cases of hæmaturia or chylous urine due to the Filaria sanguinis hominis occur, the changes are not confined to the urinary organs, but often, doubtless, involve the liver. There are no signs in the present state of our knowledge by which the existence of these parasites in the portal vein and liver can be determined.

{1112}

DISEASES OF THE PANCREAS.

BY LOUIS STARR, M.D.

Until the middle of the seventeenth century the prevalent views upon the functions and diseases of the pancreas were vague in the extreme. By some the organ was regarded simply as a cushion provided for the protection of the neighboring blood-vessels and nerves; by others it was looked upon as the seat of lesion in many very diverse diseases, as ague, hypochondriasis, melancholia, and so on.

In 1642, Wirsung's discovery of an excretory duct demonstrated the fact that the pancreas was a special organ, and initiated the successful investigation of the physiology and pathology of the gland. For many years after this, however, little progress was made, and it is only comparatively recent investigations that have furnished definite and reliable information upon the subject. Even now our knowledge of the clinical and pathological features of diseases of the pancreas is far behind that of many of the other viscera of the body, the chief reasons for this being the uncertainty in regard to the physiology of the gland and the rarity with which its lesions are primary and uncomplicated.

ANATOMY AND PHYSIOLOGY.--The pancreas is a long, somewhat flattened, narrow, acinous gland, pinkish-white in color, and of looser texture than the salivary glands, which it otherwise closely resembles in structure. It is hammer-shaped, measures from six to eight inches in length, one and a half inches in breadth, and about three-fourths of an inch in thickness, and varies in weight from three to five ounces. The gland is situated in the upper part of the abdominal cavity; the expanded portion, or head, lies in the concavity of the duodenum; thence it extends transversely across the epigastric and both hypochondriac regions on a level with the first lumbar vertebra and in contact with the posterior abdominal wall. As it passes toward the left it gradually decreases in size, and the narrowest part, or tail, rests against the spleen. Behind the organ are the crura of the diaphragm, the aorta, the inferior cava, the superior mesenteric vessels, and the solar plexus; in front of it, the stomach and the left lobe of the liver. Its anterior surface alone is invested with peritoneum, being covered by the posterior layer of the lesser omentum. The ascending portion of the head is intimately connected with the duodenum by dense connective tissue, and at times the descending portion, by extending backward and outward, forms an almost complete ring around the gut; the body is loosely attached by connective tissue to the posterior abdominal wall, and the {1113} left extremity and tail are joined to the left kidney and suprarenal capsule and to the spleen by loose areolar tissue. The gland is supplied with arterial blood by branches springing from the pancreatico-duodenal and splenic vessels; its veins join the splenic and superior mesenteric veins; its lymphatics communicate with the lumbar glands; and its nerves are branches from the solar plexus. The principal excretory duct, the canal of Wirsung, has at its widest part the calibre of a goose-quill. It begins by the union of five small branches at the tail, and extends transversely through the substance of the gland from left to right, nearer the lower than the upper border, and the anterior than the posterior surface; it is joined throughout its course by numerous small branches from the acini, which enter it at acute angles. In the head the duct curves slightly downward, and as a rule opens with the ductus choledochus into the ampulla of Vater in the second portion of the duodenum; sometimes, however, it has a separate opening into the intestine. A second, smaller, duct runs from the ascending portion of the head, and usually joins the main duct, but may also open independently.

The acini of the gland are from .045 mm. to .090 mm. in diameter, and are composed of a very thin membrane lined with pavement cells. The thin walls of the excretory ducts are formed of connective tissue and elastic fibres, and are lined by a single layer of small cylindrical epithelial cells. The terminal extremities of the ducts form a complete network around the glandular cells, resembling the intralobular biliary canaliculi. The acini are imbedded in a mass of adipose tissue which contains the vessels and nerves.

The topographical relation of the head of the pancreas to the ductus choledochus is of clinical importance. As a rule (fifteen times in twenty-two, Wyss), the bile-duct descends near the head, toward the duodenum; frequently it runs through this part of the organ, being either partially or entirely surrounded by the gland substance. Now, when the bile-duct merely passes over the pancreas, any enlargement, unless excessive, would simply push it aside, but when it passes through the head, a comparatively slight amount of disease is sufficient to close it entirely and cause jaundice.

It is only since the observations of Bernard in 1848 that the prominence of the pancreatic juice as a digestive fluid has been recognized. It fulfils several important purposes: in the first place, it emulsifies the fatty articles of food; secondly, it converts starch and cane-sugar into glucose; and, finally, it supplements the action of the gastric juice upon nitrogenous materials and completes their digestion. Each of these changes is probably brought about through the agency of a special ferment (Danilewsky). The pancreatic juice is not secreted continuously. According to the observations of Bernstein, there are two separate secretory flows following each ingestion of food--one occurring shortly after the food enters the stomach; the other a few hours later, corresponding in time to the passage of the food from the stomach into the intestine, the latter being followed by a period of rest until the next meal. Both the condition of nausea and the act of vomiting arrest the secretion. When the vagus is divided and the central extremity of the cut nerve is irritated, the secretion is also arrested, and remains checked {1114} for a long time. The arrest in each instance is attributed to reflex action of the spinal cord and sympathetic nerve. At the same time, irritation of the mucous membrane of the stomach caused by the presence of food increases the flow of pancreatic juice, and so too does simple section of the nerves which accompany the arteries. It would seem, therefore, that the gland is under the influence of two sets of nerves from the vagus--one inhibiting, the other exciting, its secretion.

GENERAL ETIOLOGY.--Pancreatic disease occurs more frequently in men than in women. No period of life is exempt from it, but it is most commonly met with in the aged. The predisposing causes are constitutional syphilis, pregnancy, and hereditary tendency. Among the apparent exciting causes may be mentioned the habitual over-use of alcoholic drinks, gluttony, the excessive use of tobacco, suppression of the menstrual flux, the abuse of purgatives, excessive and prolonged mercurial medication, and mechanical injuries, either prolonged pressure or blows upon the epigastrium. As a secondary affection, disease of the pancreas is associated with chronic diseases of the heart, lungs, liver, alimentary canal, and abdominal glands, and the organ may be the seat of metastatic abscesses and tumors.

GENERAL SYMPTOMATOLOGY.--The objective symptoms are--rapid and extreme emaciation of the entire body; sialorrhoea; obstinate diarrhoea with viscid stools; fatty stools; lipuria; and the presence of masses of undigested striped muscular fibres in the stools.

The well-established fat-absorbing and peptonizing properties of the pancreatic juice furnish a ready explanation of the wasting of the body which occurs when this secretion is arrested, diminished in quantity, or altered in quality by disease. Emaciation is not a constant symptom of pancreatic disease. A number of cases are mentioned by Abercrombie, Claessen, and Schiff in which, notwithstanding disease of the gland and complete closure of the duct, revealed by post-mortem examination, the patients during life were not only well nourished, but even moderately corpulent. In such instances it is probable that the digestive functions of the absent pancreatic juice are more or less adequately performed by the bile and succus entericus. When present, emaciation is an early symptom; it is at the same time progressive, and is usually very intense in degree, being most marked in those cases where there is associated hepatic disease or obstruction to the passage of bile into the intestine, where the disease of the pancreas interferes mechanically with the processes of nutrition by pressing upon the pyloric extremity of the stomach or upon the duodenum, and when the organ is the seat of carcinomatous growths. In the last-named condition, in addition to the perversion or arrest of the secretion, the loss of flesh is attributable to the general causes of malnutrition attendant upon carcinoma wherever situated.

Sialorrhoea, or an excessive secretion from the salivary glands, is noticeable as a symptom of disease of the pancreas only when there is an associated lesion of the stomach, either of a catarrhal or cancerous nature. Under these circumstances a quantity--six or eight fluidounces--of a colorless, slightly opalescent, and adhesive and alkaline fluid may be expelled from the mouth at once as an early morning pyrosis; or by frequent and repeated acts of expectoration, following a sudden filling of the mouth with fluid, a large bulk of thin saliva may be expelled {1115} during the day. This hypersecretion must not be looked upon as any indication of an especial sympathy existing between the salivary glands and the pancreas, neither can it be regarded as a pancreatic flux with a regurgitation of the fluid from the duodenum into the stomach and thence through the oesophagus into the mouth, since during the nausea that must always attend the passage of the intestinal contents into the stomach the pancreatic secretion is arrested, and since the liquid contains salivary, and not pancreatic, elements.

The diarrhoea pancreatica is the least constant of all the objective symptoms; in fact, constipation is present in many pancreatic affections, notably carcinoma. The fecal evacuations in this condition are frequent, thin, viscid, and contain an abundance of leucin. Under the microscope the leucin appears either in the form of concentrically sheathed globules, or as small crystalline rods and scales collected together in the form of wheels or aggregated in clusters. This form of diarrhoea may be attributed to a hypersecretion from the pancreas.

That the presence of fat in the stools is an important diagnostic symptom of pancreatic disease is proved both by clinical and experimental observations. The characters of these stools vary considerably. The fat may appear mixed with the feces in small lumps, ranging in size from a pea to a hazelnut, yellowish-white in color, soluble in æther, and easily melted and burned. Again, after the evacuation has become cool fat may be seen covering the fecal masses, collected into a thick cake around the edges of the containing vessel, or, when the feces are liquid, floating as free oil on the surface. Finally, the fat may be in a crystalline form, the crystals being needle-shaped and aggregated into sheaves and tufts. The quantity of fat also varies. It may be present only in small quantities, or may even be entirely absent from the evacuations in those cases in which the secretion from the pancreas is simply diminished, and the amount is greatest in those instances where there is a simultaneous arrest of the pancreatic and hepatic secretions. It must be remembered, too, that even in health the stools may contain fat; this occurs when an excess of oleaginous food is consumed and after the administration of castor oil or cod-liver oil. These conditions must be eliminated, therefore, in estimating the value of fatty stools as a diagnostic symptom; if, then, at the same time, coincident disease of the liver can be excluded, the symptom becomes almost pathognomonic. The appearance of fat in the stools may be due not only to an arrest of the pancreatic secretion, but also to pressure upon the large lymphatic trunks, interfering with the circulation of the chyle and checking the absorption of fat from the intestine.

Usually, the amount of fat expelled is in direct proportion to the quantity consumed, but occasionally the former greatly exceeds the latter. In such cases there must be some other source for the evacuated fat than the food; and it is probable that fat from the adipose tissue passes into the blood, and thence through the mesenteric vessels into the intestine. This theory would likewise account in part for the rapid and extreme wasting, and for another less frequently observed symptom--namely, lipuria. A case is recorded by Clark of medullary cancer of the pancreas with nutmeg liver, and another by Bowditch of cancer of the pancreas and liver in which lipuria was noted. The fat was observed, after the urine had cooled, floating about on the surface in masses or globules; differing, {1116} therefore, from chyluria, for in this condition the fat is present in the form of an emulsion, and gives the urine either a uniform milk-like appearance, or, after it has been allowed to stand, rests upon the surface in a creamy layer.

When the pancreatic secretion is arrested, most of the animal food which has escaped gastric digestion will pass unchanged through the intestine and give rise to another characteristic condition of the evacuations--namely, the presence in the feces of undigested striped muscular fibres. The amount of these fibres, and indeed their appearance at all in any given case, will depend directly upon the nature of the food consumed.

SUBJECTIVE SYMPTOMS.--The subjective symptoms of disease of the pancreas are abnormal sensations in the epigastrium, and pain.

The abnormal sensations in the epigastrium are weight and pressure, attended at times by præcordial oppression and discomfort. The feeling of weight is usually deep-seated, may be intermittent or constant, and is generally increased or developed by pressure. It is often influenced by position, the assumption of the erect posture or turning from side to side giving rise to a stretching or dragging sensation, as if a heavy body were falling downward or moving about in the upper abdomen.

The pain may be due either to an inflammation of the peritoneum covering the gland or to pressure upon the solar plexus, and consequently varies in character. When it depends upon localized peritonitis, it is constant, circumscribed, and deeply seated in the epigastrium at a point midway between the tip of the ensiform cartilage and the umbilicus; it is rather acute, and is greatly augmented by pressure. The second variety occurs in paroxysms, and is neuralgic in character, the sharp, excessively severe lancinating pains extending from the epigastrium through to the back, upward into the thorax, and downward into the abdomen. These paroxysms--in reality attacks of coeliac neuralgia--are attended by great anxiety, restlessness, and oppression and a tendency to syncope. That calculi in the duct of Wirsung, tightly grasped at the position of arrest, may give rise to paroxysms of pain analogous to biliary colic, cannot be doubted, though there are no positive facts in support of this view.

PRESSURE SYMPTOMS.--When the pancreas becomes enlarged it encroaches upon the neighboring blood-vessels and viscera, interferes with their functions, and thus produces prominent symptoms.

The ductus choledochus from its close relation to the head of the gland is especially liable to become obstructed, with the consequent production of chronic jaundice and the general effects of the absence of bile from the intestinal canal. Pressure upon the portal vein gives rise to enlargement of the spleen; on the inferior cava, to oedema of the feet and legs; and on the aorta, occasionally, to aneurismal dilatation of the vessel above the point of obstruction and to subsequent alteration in the size of the heart. By encroaching on the stomach an enlarged pancreas may cause either displacement of the viscus or stenosis at its pyloric extremity, attended with occasional vomiting of large quantities of grumous, fermenting liquid, pain, constipation, general failure of health, and the distinctive physical signs of dilatation of the stomach. The duodenum may also be pressed upon and more or less occluded, and pain and vomiting occur several hours after food is taken. Occasionally hydronephrosis is {1117} produced, the accumulation being usually in the right kidney and due to obstruction of the corresponding ureter.

A sufficient number of cases have been collected to show that there is an intimate connection between disease of the pancreas and diabetes mellitus. One or other condition may take the precedence, melituria occurring during the progress of pancreatic disease, demonstrating the onset of diabetes, and the appearance of fatty stools in diabetes a secondary involvement of the pancreas. Various theories have been advanced to account for this association, but the true explanation seems to be based upon the experiments of Munk and Klebs. By experimenting upon dogs these observers found that extirpation of the solar plexus produced either permanent or temporary diabetes, whereas section of the hepatic and splanchnic nerves, removal of the pancreas, or ligature of the duct of Wirsung was without effect. From the intimate anatomical relation of the pancreas to the solar plexus it is easy to understand how disease of the gland may give rise to alterations in the nerve-structure, either by direct pressure or by the extension of inflammation along the nerve-fibres connecting the gland with the ganglia; and these alterations in time produce diabetes. In the instances in which diabetes is the primary affection the condition of the pancreas, as proved by post-mortem section, is usually one of simple or fatty atrophy; and it may be assumed that a lesion of the solar plexus is the cause of both diseases, the changes in the pancreas being produced in a similar way to the atrophy of the submaxillary gland after section of the vaso-motor nerves in Bernard's experiments.

The same nerve-lesion may give rise to bronzing of the skin, and two cases are recorded in which disease of the pancreas (cheesy infiltration, cancer) was attended by this symptom.

PHYSICAL SIGNS.--To make a successful exploration of the pancreas the stomach and colon should be as far as possible empty, and the patient placed in a position, with the head and shoulders slightly elevated and the thighs drawn up toward the belly, to relax the abdominal muscles; or if necessary this relaxation must be brought about by the administration of æther. The knee-elbow position is often preferable to the dorsal position in practising palpation.

The condition of the gland giving rise to physical signs is one of enlargement, affecting chiefly and primarily its head, and due generally to the presence of some morbid growth.

Inspection reveals either a diffuse bulging of the upper third of the abdomen to the right of the median line, or a well-defined tumor situated beneath the right costal border, about the line of junction of the right hypochondriac and epigastric regions. Often the pancreatic tumor does not come in direct contact with the abdominal wall, but presses against and thrusts forward the left lobe of the liver, producing simply a prominence in the epigastrium. In the first condition palpation elicits an ill-defined sense of resistance; in the second, the fingers readily outline a tumor, which is slightly movable, rounded in shape, firm or fluctuating, with a smooth or nodulated surface, usually tender to the touch, and often giving a false impulse transmitted from the aorta lying beneath; and in the third, the smooth surface and the sharp edge of the left lobe of the liver are easily distinguishable.

{1118} Percussion over a pancreatic tumor is commonly dully-tympanitic, absolute flatness occurring only when it is very large and comes directly in contact with the abdominal wall, pushing aside the stomach and intestines.

On auscultation a blowing murmur may, in some instances, be heard over the tumor. These murmurs are due to pressure upon the aorta, and must be distinguished from the sound produced in aneurism of this vessel.

The various complications of pancreatic disease, such as dilatation of the stomach, ascites, and secondary lesions of the liver, greatly modify the physical signs, and sometimes entirely prevent an exploration of the gland.

INFLAMMATORY AFFECTIONS OF THE PANCREAS.

Acute Idiopathic Pancreatitis.

This is a rare disease. It occurs most frequently in males during and after adult life, and the strumous diathesis appears to predispose to it. Intemperance, the suppression of normal or morbid discharges, and traumatism act as exciting causes.

ANATOMICAL APPEARANCES.--The pathological changes may be divided into two stages. In the first the gland is deep red in color, intensely injected with blood, greatly increased in consistence, enlarged to the extent of two or three times its normal size, and when an incision is made the divided lobules feel firm and crisp. The interlobular tissue is sometimes dotted with bloody points, and the same hemorrhagic changes may occur in the connective tissue surrounding the gland. In this stage resolution may occur or the inflammation may pass into suppuration. At the beginning of the second, or suppurative, stage numerous minute collections of pus are seen scattered throughout the gland in the interacinous tissue; these gradually collect into a single large abscess, and at times the whole gland is converted into a mere pus-sac, the capsule being much thickened. In other instances the formation of pus is entirely peripancreatic. The pus is usually inodorous and creamy, but is sometimes grayish-white or greenish in color; it then has a faint disagreeable odor, and occasionally is very fetid. When mixed with pancreatic juice it becomes clear and yellowish in color, and contains numerous minute curd-like masses.

In the first stage secondary peritonitis may arise from a simple extension of the inflammatory process, and bands of lymph are formed, gluing the pancreas to the neighboring organs. In the second, fatal acute peritonitis may result from the bursting of an abscess into the peritoneal cavity. These abscesses also occasionally open into the duodenum or stomach. Gangrene and peripancreatic sloughing occur very exceptionally, and are probably due to extensive hemorrhagic changes.

SYMPTOMS AND COURSE.--The disease may be preceded for an indefinite period by symptoms of impaired gastric or intestinal digestion, but its onset is usually sudden. The attack begins with colic or continuous {1119} deep-seated pain, starting in the epigastrium and extending toward the right shoulder or the back, and quickly becoming very intense. The pain is attended by pallor of the face, great restlessness, præcordial anxiety, dyspnoea, and faintness. The tongue is furred or dry and red; thirst is increased; the appetite is lost; there are frequent eructations, nausea, and constant vomiting of a clear, greenish, viscid fluid; the vomiting produces no sense of relief, and even increases the epigastric pain. The bowels are obstinately constipated. The epigastric region is tense, tumid, and excessively tender, so that it is usually impossible to elicit the physical signs of enlargement of the gland. There is moderate pyrexia, with evening exacerbations, and the pulse is increased in frequency. Jaundice does not occur.

These symptoms progressively increase in severity, and reach their maximum intensity in from three to five days. The pulse then becomes small, compressible, and irregular, the extremities cold, the face hippocratic, and death takes place in a state of collapse. The fatal termination is preceded by the symptoms of acute peritonitis in the cases which are complicated by an extension of inflammation or the rupture of an abscess into the peritoneal cavity.

Recovery is quite possible in the early stage of the disease. On the other hand, the course may be greatly protracted by a change in the type of the inflammation, resulting in induration and enlargement of the gland or in the formation of chronic abscesses. Again, when peritonitis from extension has been confined solely to the portion of the peritoneum that covers the gland, and has resulted in the formation of fibrinous bands binding the pancreas to the adjacent viscera, the symptoms of pancreatitis will on subsiding give place to those of obstruction of the stomach, duodenum, or bile-duct.

DIAGNOSIS.--The diseases most likely to be confounded with acute pancreatitis are biliary colic and the catarrhal form of acute gastritis.

From biliary colic it is distinguished by the absence of rigors, jaundice, enlargement of the liver, and a tender pyriform tumor corresponding in situation to the gall-bladder and due to its distension with accumulated bile. The pain in both affections is sudden in its onset, and very similar in character and distribution; but when caused by the passage of a gall-stone it usually begins either after a heavy meal or after some severe muscular exertion or shaking of the body--circumstances inoperative in the production of the pain of pancreatitis. The pain, too, in the former condition is less severe at first, increases gradually in severity, is more paroxysmal, is at the outset lessened by pressure, and is often temporarily relieved by the act of vomiting. The attacks at the same time are rarely isolated, and all doubt is removed when the pain ceases suddenly and a calculus is discovered in the feces.

Acute gastric catarrh is almost always traceable to the ingestion of some irritant substance, usually alcohol or food of bad quality. This history, together with the liability of the attack to occur during the course of chronic dyspepsia, the comparatively trifling severity of the pain, the headache, the irregularity of the bowels, the condition of the urine, which is either high-colored or deposits lithates abundantly, and the tendency of the affection to become chronic, are the points of distinction between this and the pancreatic disease.

{1120} Acute inflammation of the stomach, or gastritis proper, resulting from corrosive poisons, presents a train of symptoms entirely different from those of acute pancreatitis.

TREATMENT.--Absolute rest is essential. The diet should consist of milk guarded by lime-water and of meat-broths, this food being administered in small quantities--one to two or three fluidounces of the milk and lime-water or half as much broth--at proper intervals. In the early stage an effort must be made to reduce the inflammation by the application of ice to the epigastrium or of leeches to the same region, or preferably to the anus. The excessive pain demands the free use of opium. The nausea and vomiting may be relieved to some extent by directing the patient to swallow small lumps of ice, and by the employment of iced carbonic-acid water and the effervescing draught; and the tendency to constipation may be overcome by enemata. Later in the course of the disease, if the epigastric tenderness permits of it, light linseed poultices should be placed over the upper abdomen. During the stage of collapse alcoholic stimulants and the application of heat to the extremities are necessary. The occurrence of acute peritonitis or other complications and sequelæ demand appropriate treatment.

Acute Secondary Pancreatitis.

In this condition the pancreas may be the seat of either acute parenchymatous inflammation or of metastatic abscesses.

Acute parenchymatous degeneration of the muscles, kidneys, liver, and so on is recognized as a frequent lesion in the acute infectious diseases, particularly typhoid fever; and it is under these circumstances, and in association always with similar changes in some of the organs mentioned, that parenchymatous degeneration of the pancreas takes place.

Metastatic suppurative inflammation is very rare: it has been observed in cases of disease of the testicles after the operation of extirpation of these organs, and occasionally in puerperal peritonitis.

ANATOMICAL APPEARANCES.--In parenchymatous inflammation the gland at first is hardened, swollen, and reddened, and on section presents a reddish-gray surface, with indistinctness of the glandular structure, due to the amount of swelling of the acini. Under the microscope the gland-cells are found to be enlarged; they contain several nuclei, their protoplasm is infiltrated with fatty granules, obscuring the nuclei to a certain extent, and their outline is well defined. These alterations are most marked in the head of the gland. After a time the hypertrophy of the cells, by pressing upon the blood-vessels, produces an anæmic condition and the organ becomes pale; in the advanced stages softening occurs.

Metastatic suppurative inflammation leads to the formation of a single large abscess or to multiple minute purulent collections.

SYMPTOMS AND COURSE.--Parenchymatous degeneration gives rise to no distinctive symptoms. Its occurrence in typhoid fever or other infectious disease may be suspected when after prolonged hyperpyrexia there are enlargement of the liver and spleen and albuminuria. The appearance of jaundice (from pressure) increases the probability of involvement of the pancreas in the general gland-change.

{1121} The development of rigors, alternating with flushing, during the course of one of the lesions liable to be attended with metastatic abscesses in the pancreas might suggest the formation of pus in the gland, but an absolute diagnosis is impossible.

Several cases are on record pointing to the possibility of a metastasis of mumps from the parotid gland to the pancreas. In these the disappearance of the parotiditis was followed by symptoms resembling those of idiopathic pancreatitis--namely, thirst, fever, loss of appetite, anxiety, and burning in the epigastrium, with deep-seated pain extending toward the right side; in addition there was diarrhoea, with numerous, yellowish, watery stools. In one case that resulted fatally the secondary diarrhoea suddenly ceased and the parotid swelling reappeared. At the autopsy the pancreas was found to be swollen, reddened, engorged with blood, and indurated. Such a metastasis, however, must be very infrequent, and more extended observations are necessary to establish its course and clinical features.

The first form of acute secondary pancreatitis may be a comparatively unimportant complication of the acute infectious diseases, or, together with the parenchymatous degeneration of other organs, may form a distinct element in the fatal issue of these diseases.

Metastatic abscesses are prone to be followed by ulceration and the formation of fistulous communications with the neighboring viscera.

TREATMENT.--The management of secondary inflammation of the pancreas is regulated solely by the indications derived from the originating disease.

Chronic Interstitial Pancreatitis.

Inflammation of the connective tissue of the gland usually occurs after adult life, and depends upon a variety of causes.

The secondary form, due to long-continued venous engorgement resulting from lesions of the cardiac valves and from chronic disease of the lungs or liver, is the most frequently observed.

Other causes are closure of the duct of Wirsung, the retained secretion producing pressure upon the glandular tissue; the extension of inflammation from adjacent organs, as the bile-duct when there is an impacted gall-stone, or the stomach and duodenum, especially in cancer and perforating ulcer, where the floor of the ulcer is formed by the pancreas; the pressure of tumors, as aneurisms of the abdominal aorta and coeliac axis; chronic alcoholism; and syphilis.

ANATOMICAL APPEARANCES.--The lesion may be limited to the head or to isolated portions of the gland, or be uniformly distributed. The general changes are a hyperplasia of the interacinous connective tissue, with subsequent contraction and atrophy, or, in extreme instances, entire destruction of the glandular elements proper, the organ becoming granular and firmer and tougher than normal. A section shows a pale surface, studded at intervals with white spots, from which little cheese-like and fatty masses may be squeezed, and, when there has been intense hyperæmia, with minute collections of reddish pigment and small hemorrhagic cysts, indicating previous interstitial hemorrhages.

{1122} When the contraction causes closure of the small excretory ducts or of the duct of Wirsung itself, the section shows secondary cysts and beaded canals.

In exceptional instances of acquired syphilis the pancreas is the seat of gummata or sclerosis, but in congenital syphilis hyperplasia of the glandular connective tissue frequently occurs, being usually associated with specific lesions of the lungs, liver, kidneys, and general glandular system.

SYMPTOMS AND COURSE.--As chronic pancreatitis rarely attains a sufficient degree of development to interfere seriously with the function of the organ, the disease is usually latent, or masked by the symptoms of the originating lesion in secondary hyperplasia, or by the associated diseases of the abdominal viscera in alcoholism and acquired syphilis.

When due to hereditary syphilis, the foetus is stillborn or death takes place soon after birth, and there are no characteristic symptoms.

Occasionally, however, especially when it depends upon a complete obstruction of the duct of Wirsung, a diagnosis may be made from the presence of emaciation, fatty stools, and melituria, with epigastric pain of a neuralgic character, and the discovery of a deep-seated, dense tumor extending transversely across the epigastrium.

The duration is indefinite, and varies greatly with the cause. While a return to the healthy condition is possible during the early stage of the lesion, the usual course is similar to that of chronic interstitial inflammation in other organs.

TREATMENT.--The management, when a diagnosis can be made, must be guided mainly by the etiological indications. The restoration of the functions of the heart, lungs, or liver when these organs are at fault, the abstinence from alcohol in the drunkard, and an energetic use of mercurials or iodide of potassium in syphilis, are of the first importance in arresting the disease. A persistent course of mild purgatives and of cathartic mineral waters is serviceable. Pain should be relieved by belladonna or opium. The diet must be simple and digestible, and if an arrest of the pancreatic secretion be indicated by the appearance of fat in the stools, an effort should be made to supply the deficiency. For this purpose pancreatin, prepared by precipitation by alcohol from a watery extract of a calf's or pig's pancreas, may be used.[1] The pancreatin may be given in doses of from five to fifteen grains, in the form of a pill or in capsules, and at an interval of two hours after food is taken, or the same quantity of pancreatin may be added to the food a few moments before it is eaten. Probably the best substitute is a watery infusion of the gland containing all its soluble principles. To prepare an active infusion the pancreas must be taken from the animal during the act of digestion. It is then freed from its surrounding fat, and macerated for two hours in four times its weight of water at a temperature ranging between 25° and 30° C. (58.3° and 61.1° F.). Another plan is to beat a calf's pancreas in a mortar with six fluidounces of water until a milk-like fluid is obtained, and strain. One-third of the infusion obtained by either method is administered after each meal, an entire pancreas being thus used every twenty-four hours.

[Footnote 1: One gramme of pancreatin is sufficient to emulsify fifteen grammes of fatty substances, to convert eight grammes of starch into glucose, to digest fifty grammes of fibrin, twenty grammes of syntonine, and thirty-three grammes of boiled albumen (Raymond).]

{1123} The extractum pancreatis,[2] as it is now furnished to the profession, is a very useful preparation. It may be employed to peptonize milk, milk-gruel, and broth, or be given in combination with bicarbonate of sodium at a fixed interval after each meal, as in the following formula:

Rx. Ext. pancreatis, drachm j; Sodii bicarbonatis, drachm ij; M. et. ft. Chart No. XII.

S. One powder to be taken two hours after each meal.

[Footnote 2: That prepared by Fairchild Brothers & Foster of New York has proved the best in my hands.]

Peptonized milk is prepared by putting into a clean quart bottle 5 grains of extractum pancreatis, 15 grains of bicarbonate of sodium, and a gill of cool water; shake, and add a pint of fresh cool milk. Place the bottle in water not so hot but that the whole hand can be held in it without discomfort for a minute, and keep the bottle there for exactly thirty minutes. At the end of that time put the bottle on ice to check further digestion and keep the milk from spoiling.

Peptonized milk-gruel is made of equal parts of any farinaceous gruel and fresh cold milk. To a pint of this combination 5 grains of extractum pancreatis and 15 grains of bicarbonate of sodium are added, and the whole allowed to stand in a warm place for thirty minutes, when the process of digestion must be arrested by placing on ice.

Peptonized broth is made in the following way: Take one-fourth of a pound of finely-minced raw lean beef or mutton or chicken, and one-half pint of cold water; cook over a slow fire, stirring constantly, until it has boiled a few minutes. Then pour off the liquor, beat the meat to a paste, and put both into a bottle with a half pint of cold water. Add 30 grains of extractum pancreatis and 20 grains of bicarbonate of sodium; shake well, and set in a warm place (110-115°) for three hours, shaking occasionally; then boil quickly. Finally, strain or clarify in the usual way and season to taste.

MORBID GROWTHS OF THE PANCREAS.

Carcinoma.

Cancer is probably the most common of the chronic affections of the pancreas. It is usually secondary, being due to an extension of carcinoma of the stomach, duodenum, liver, or abdominal lymphatic glands, but there are enough cases on record to show that it may be primary. It has been discovered in the foetus at birth, but the vast majority of cases occur after the age of forty. Men are more frequently affected than women. Nothing is known as to the influence of inherited tendency in the production of the disease, and as little of the exciting causes, though some authors attach much importance to prolonged pressure upon the epigastrium and to blows and contusions on the upper part of the abdomen.

ANATOMICAL APPEARANCES.--Primary carcinoma may be either {1124} scirrhous, encephaloid, or colloid, the first being the variety most frequently observed.

The lesion begins in the head of the gland in the form of several small nodules which gradually coalesce. Sometimes the whole gland becomes involved in the new formation; again, isolated nodules may be scattered throughout its substance, and exceptionally the growth is limited to the tail or middle portion. When the head alone is involved, the remainder of the gland either remains healthy, undergoes fatty degeneration, or becomes indurated. The tumor is rounded in outline and nodular, and varies in size, density, and color according to the form of carcinoma present. The duct of Wirsung is ordinarily obstructed, large retention cysts, containing a yellowish-red liquid, are formed, and the changes already described under the head of Chronic Interstitial Pancreatitis take place in those portions of the gland which are free from carcinoma. The disease is very prone to extend to the surrounding organs, particularly the neighboring lymphatic glands, the duodenum, and the liver, rarely to the stomach. When the contiguous organs are not directly implicated in the carcinomatous changes, they are subjected to pressure by the tumor, and in the case of the stomach and duodenum adhesions often form, and are followed by perforation. There seems to be a tendency also to infiltration of the adjacent subperitoneal connective tissue and to hyperplasia of the fibrous tissue of the viscera, even when they are not secondarily involved in the morbid growth, leading to narrowing of the aorta, thickening of the walls of the stomach and duodenum, and a sclerosis of the liver. Obstruction of the common bile-duct, with dilatation of the gall-bladder from retention of bile, is a frequent result of the disease.

Secondary carcinoma of the pancreas usually first appears in, and is limited to, the head of the gland. It seldom occurs in isolated nodules, but the growth is generally continuous with the primary cancerous mass. The form is either scirrhous or encephaloid. Wagner records a case of cylindrical-celled epithelioma following a simple epithelioma of the mucous membrane of the duodenum; and a similar instance has come under the author's own observation;[3] but this variety of morbid growth is rare. The primary growth is almost uniformly situated in the stomach, duodenum, liver, or gall-bladder, though occasionally it may be seated in some distant organ; in such cases the pancreatic tumor appears as an isolated nodular mass.

[Footnote 3: _Transactions of the Pathological Society of Philadelphia_, vol. ix. 13.]

SYMPTOMS AND COURSE.--The symptoms may be divided into two classes--namely, first, those which arise from the lesion of the gland itself; and, secondly, those which depend upon the effect of this lesion on the neighboring viscera.

The features belonging to the first class are general marasmus, pain, the appearance of fat and perhaps undigested muscular fibres in the fecal evacuations and of fat in the urine, and the physical signs of an abdominal tumor.

Loss of flesh is one of the earliest symptoms: it is generally progressive, and is at times so great that the spine can be distinctly traced through the abdominal walls. Together with this emaciation there is debility, often extreme, but sometimes not so marked as might be expected from the degree of wasting. The skin is commonly pale and dry, and before jaundice is {1125} developed has the ordinary sallow hue of cancerous cachexia. The features are pinched, and the face wears an expression of anxiety and suffering. In cases uncomplicated by peritoneal inflammation the temperature remains about normal, or it may be lowered as the general exhaustion increases. The pulse is feeble and slightly increased in frequency.

Pain is the most uniformly present and the earliest symptom. It is always situated deep in the epigastrium, and from thence extends to the back, to the right or left side, downward to the umbilicus or lower part of the abdomen, and upward into the chest. It is generally continuous, but is subject to remissions and paroxysmal exacerbations. During the remissions sensations of distress, of burning, or of dull pain are experienced at the pit of the stomach; during the exacerbations, which may last several days, the pain becomes extremely acute and lancinating and extended in distribution. The ingestion of food and pressure upon the epigastrium have no constant effect upon the pain. Quick movements of the body from side to side often increase it and excite exacerbations. The suffering is greatest in the erect posture, and on this account the patient bends his body forward so as to relax the abdominal muscles. The paroxysmal and neuralgic character of the pain indicates implication of the coeliac plexus.

The appearance of fat in the stools is an important symptom, unless there be at the same time an obstruction to the passage of bile into the duodenum, indicated by jaundice. Lipuria has been noticed in a few cases only.

In many instances (nearly one-half of the number of recorded cases) physical exploration reveals the signs of enlargement of the organ. At times there is merely a sense of fulness and resistance to the touch, and a modified tympanitic percussion note in one of the three regions of the upper segment of the abdomen. But usually when a tumor is present it is readily mapped out by palpation. The tumor is seated in the epigastrium, and may extend into the right or left hypochondrium or downward into the umbilical region. It varies much in size, is rounded, nodulated, firm, slightly movable or fixed, and tender, though sometimes painless, to the touch. Percussion yields dulness or a dull-tympanitic sound. On auscultation a blowing murmur may be heard when the tumor presses upon the aorta; and when this murmur is present there is usually also transmitted pulsation.

The symptoms belonging to the second class arise when the adjacent viscera become involved in the cancerous disease, or when their functional activity is disturbed by the encroachment and pressure of the enlarged pancreas.

From the association of a catarrhal condition of the mucous membrane of the stomach, particularly when the pyloric orifice is obstructed, several prominent symptoms of gastric catarrh are frequently observed--namely, sialorrhoea, pyrosis, acid eructations, flatulence, abnormal sensations, such as burning, weight and oppression in the epigastrium after taking food, and increased thirst. The tongue varies in appearance: it may be dry and covered with a brown or yellow fur, but when the flow of saliva is increased it is peculiarly clean and moist; and this condition is rather characteristic. The appetite is also variable; sometimes it remains good {1126} until the end, and occasionally it is perverted. Hiccough in some cases is an obstinate and annoying symptom.

Nausea and vomiting are late but moderately constant features. Their relation to the ingestion of food is not fixed. The vomited matter may consist of food, of glairy mucus more or less tinged with bile, of colorless liquid, or of a fluid resembling a mixture of bran and water. If there is marked pyloric obstruction with dilatation of the stomach, large quantities of frothy and fermenting material containing sarcina ventriculi are rejected at intervals. In the rare cases in which secondary sarcoma of the viscus is developed the ejecta are bloody or have the coffee-ground appearance, and the vomiting occurs several hours after eating, as the new growth is generally situated at the pylorus. When there is adhesion of the pancreatic tumor to the stomach, with perforation, both blood and pus are vomited. Dilatation of the stomach is attended by prominence of the epigastrium and an extended area of gastric tympany, and in cancer of the pylorus a tumor is often appreciable on palpation. The bowels are usually constipated. The fecal evacuations are hard, and when the biliary secretion is absent from the intestine they are clay-colored, and often contain fat. When there is ulceration of the mucous membrane of the duodenum following secondary cancer or adhesion, the stools become black and tar-like from the presence of altered blood. Complete obstipation occurs in mechanical obstruction of the gut from direct pressure or from bands of lymph. Occasionally, just before death there is diarrhoea, and there may be an alternation of vomiting and diarrhoea.

The symptoms and signs of secondary carcinoma or sclerosis of the liver may be present, but the most commonly observed indications of impaired hepatic function depend upon pressure-obstruction of the common bile-duct. These are jaundice, fatty and clay-colored stools, and the appearance of a tumor in the region of the gall-bladder. Jaundice is a very common symptom. It occurs late in the disease as a rule, is progressive and persistent, resisting all treatment, and is extreme in degree, the skin becoming deep-yellow or greenish in color. The tumor of the distended gall-bladder is pyriform in shape, firm and elastic to the touch, yields a dull percussion sound, and occupies a position opposite the extremity of the tenth rib on the right side of the abdomen.

Dropsy occurs in a large proportion of cases (nearly one-half) during the advanced stages of the disease. It is due to vascular obstruction occasioned by the pressure of the enlarged pancreas itself or of the secondarily degenerated coeliac glands, and finally by secondary lesions of the liver. The dropsy appears either in the form of ascites or anasarca, is not often extreme in degree, and is subject to variations, disappearing and reappearing at intervals. Ascites is the more common form, but both conditions may exist in the same patient.

It is impossible in the majority of instances to definitely fix the date of onset of a pancreatic cancer, but the average duration of the disease may be stated to be about one year. The uniformly fatal termination usually takes place slowly from gradual exhaustion or with the symptoms of an adynamic fever, but death may occur suddenly from hemorrhage.

DIAGNOSIS.--The principal features of carcinoma of the pancreas are extreme emaciation, loss of strength, dyspepsia, pain of a neuralgic {1127} character in the epigastrium, constipation, obstinate jaundice, moderate ascites or anasarca, the appearance of fat in the stools, lipuria, occasional vomiting, and the physical signs of an epigastric tumor.

These symptoms are not pathognomonic, however, and the diagnosis can be certainly established only when it is possible to exclude primary disease of the surrounding organs, especially of the stomach and liver.

Cancer of the stomach may be excluded by the less-marked character of the functional disturbances of the viscus; by the absence of frequent vomiting, hæmatemesis, and the rejection of coffee-ground material; by the somewhat different situation and greater immobility of the tumor, by the seat, distribution, and constancy of the pain; and by the presence of jaundice and of fat in the stools and urine.

Diseases of the liver attended with alterations in the size of the organ, as cancer, abscess, albuminoid and fatty degeneration, sclerosis and hydatid tumor, have sufficiently characteristic physical signs and symptoms to be readily distinguished from cancer of the pancreas. On the other hand, the tumor of an enlarged gall-bladder is often confusing. The situation of this tumor opposite the tenth rib and its pyriform shape are important; other distinguishing points depend upon the cause of the enlargement. In enlargement from accumulated bile the tumor is elastic and fluctuating; from accumulation of gall-stones, hard and nodulated, movable, painless on palpation, and often the seat of crackling fremitus, produced by manipulation and due to the rubbing together of several calculi; from cancer, hard, nodular, the size of an orange, tender on pressure, rapid in growth, preceded by attacks of biliary colic, and attended by fistulous communications with the intestines and the passage of gall-stones per anum.

In aneurism of the aorta or coeliac axis the tumor may present in the epigastrium and produce analogous pressure symptoms. But the pain is more of the character described as wearing, and is usually augmented at night: on grasping the tumor a uniform expanding pulsation is felt in place of the to-and-fro movement appreciable in a tumor resting upon a healthy blood-vessel and receiving a transmitted impulse, while the constitutional symptoms and course are quite different.

The tumor of malignant disease of the omentum, although it appears in the epigastrium or upper part of the umbilical region, is much more movable, and is accompanied by ill-defined symptoms very dissimilar to those of pancreatic cancer.

In cancer of the transverse colon the mass may occupy nearly the same position as a pancreatic growth, but the pain occurs several hours after food is taken; vomiting is absent, and there is frequently hemorrhage from the bowels.

Chronic pancreatitis is accompanied by symptoms simulating those of cancer; the enlargement of the gland, however, is not so great, nor are the indications of pressure upon adjacent organs so prominent. The pain is less severe, the general failure in health more gradual, the progress slower, and constipation less common.

TREATMENT.--The indications are to maintain the strength of the patient, to provide a diet that is nutritious and at the same time easily digested, to allay pain by the employment of narcotics, and to relieve as far as possible the various symptoms as they arise. The plan of {1128} administering a calf's pancreas or extractum pancreatis will prove serviceable when the fecal evacuations contain fat. Nutritious and peptonized enemata may be of service in some cases.

Sarcoma and Tubercle of the Pancreas.

Sarcoma of the pancreas occurs with extreme rarity. It is impossible during life to distinguish it from carcinoma.

Tubercle of the gland is infrequently met with. Some pathologists deny its occurrence, and believe that the cases recorded as such are merely instances of caseous degeneration of the neighboring glands. When it does occur, it is always secondary, the primary disease being situated in the lungs or intestines. The alterations in the gland consist in the development of cheesy masses or of miliary granulations in the connective tissue between the acini. The condition gives rise to no definite symptoms, and its diagnosis during life is impossible.

DEGENERATIONS OF THE PANCREAS.

Fatty Disease of the Pancreas.

Two forms of fatty degeneration occur, either separately or combined--namely, fatty infiltration and fatty metamorphosis.

Fatty infiltration consists of a true hypertrophy of the fat-tissue normally existing in the gland, or of an increase and extension into the gland of the peripancreatic adipose tissue. Yellow bands and masses of fat-tissue appear between the acini, and by constantly increasing in size lead gradually to a total atrophy of the cells of the acini. The canal of Wirsung contains a fatty liquid. These changes are found associated with fatty liver, heart, and omentum, in drunkards especially.

Fatty metamorphosis of the gland consists of a change analogous to fatty metamorphosis of other organs. When hyperplasia of the interstitial connective tissue is absent, the organ is flaccid, soft, and diminished in size; the acinous structure remains distinct, though the acini and ducts are filled with a fatty emulsion: after this is discharged or absorbed the gland appears as a flaccid band, and finally becomes entirely atrophied. Fatty metamorphosis occurs in drunkards, in diabetes, in advanced age, in cancer, phthisis, and other wasting diseases.

Neither form of fatty disease gives rise to symptoms by which it can be recognized during life.

Albuminoid Degeneration of the Pancreas.

This is only found in combination with amyloid change in other organs of the body, and a diagnosis cannot be made.

{1129} Hemorrhages into the Pancreas.

Hemorrhages into the pancreas may be divided into three classes.

The most common form depends upon passive hyperæmia, the result of chronic diseases of the heart, lungs, or liver. In this condition the effusion of blood coexists with chronic inflammatory changes in the interstitial connective tissue. The appearance at first is of minute bloody points scattered throughout the areolar tissue; later, these change into round or oval pigment masses, or spaces containing reddish serum and surrounded by thickened, rust-colored, irregular walls.

The second class includes the rare cases of hemorrhage resulting from the rupture of one of the large blood-vessels of the gland, and due to some pre-existing change in the vessel walls. In these the pancreas is enlarged, may be converted into a sac containing blood, either fluid or coagulated or partially crystallized according to the duration of life after the hemorrhage has taken place, and a ruptured blood-vessel may be readily discovered on dissection.

The condition in which, without any evidence of passive hyperæmia or gross vascular lesion, the entire pancreas become hemorrhagic, constitutes the third class. The gland is then dark-red or violet in color, the meshes of the interstitial tissue are filled with recent or altered blood, and the acini are stained of a dull-gray hue. The hemorrhage may extend to the connective tissue surrounding the gland. Finally, the organ becomes soft, the peritoneal covering sloughs, and fragments of broken-down gland-tissue escape into the peritoneal cavity. These lesions are so analogous to those which attend thrombosis occurring in other organs that their dependence upon the same cause seems probable.

The first form of hemorrhage is unattended by special symptoms. In the second a pulsating tumor may suddenly appear in the epigastrium, and the ordinary indications of hemorrhage--vomiting, fainting fits, cold extremities, feeble pulse, and general exhaustion--are present. Death may occur suddenly or the patient may linger on for months. In the third condition death usually occurs very suddenly, probably from pressure upon the sympathetic ganglia. There are no symptoms, and the rapid termination prevents the development of general peritonitis, which would otherwise occur from the sloughing of the peritoneum.

There are no indications for treatment.

OBSTRUCTION OF THE PANCREATIC DUCT.

Obstruction of the excretory duct is a frequent occurrence in pancreatic disease, and is due to two classes of causes--namely, 1st, pressure from without; and, 2d, closure of the canal by catarrhal swelling of its mucous membrane or by calculi.

In the first class may be placed obstruction depending upon contraction occurring in sclerosis of the gland, upon carcinoma of the head of the gland, upon peripancreatic adhesions and indurations, upon the {1130} presence of large gall-stones in the ductus choledochus, and upon carcinoma of the pylorus and duodenum and enlargement of the neighboring lymphatic glands.

In catarrh of the canal of Wirsung the obstruction results either from simple swelling of the mucous membrane or from the presence of a plug of tough mucus.

The formation of pancreatic concretions is by no means a rare event, though these calculi are met with far less frequently than either gall-stones or salivary concretions. They result from precipitation of the inorganic ingredients of the pancreatic juice, and are usually seated in the main duct, although they may be situated in the smaller branches. They may be single or multiple, as many as twenty having been counted in one gland. In shape they are spherical, oval, or branched, with sometimes a smooth, at others a spiculated, surface; their size varies from that of a minute granule to a small walnut; they are usually white or grayish-white in color, but may be black; and are composed of the carbonate of lime or of a combination of the carbonate and phosphate with oxalate of lime. Coincidently with these calculi it is common to find concretions in the kidneys and gall-bladder.

Concretions composed of insoluble protein substances have also been found in the pancreatic ducts (Virchow).

The most probable causes of the formation of pancreatic calculi seem to be catarrhal conditions of the mucous membrane of the ducts and an alteration in the chemical composition of the secretion.

Whatever the cause, the obstruction, when complete, leads to retention of the secretion and the formation of retention cysts.

When the obstruction is situated at the duodenal extremity of the duct, the canal and its secondary branches are either uniformly dilated or sacculi are formed. These sacculi are round or oval, vary greatly in size, sometimes reaching the dimensions of the fist or of a child's head; they may be single, or several of them may be present, differing in size and causing irregular projections of the outer surface of the gland. When the obstruction occurs at some point in the course of the duct, the dilatations and sacculi are found only behind the point of occlusion. The small cysts contain a fluid resembling the pancreatic juice; the larger, a whitish, chalky fluid, which in old cases may contain white friable concretions composed of carbonate and phosphate of lime, and become purulent, or be stained bright red or chocolate-colored from the occurrence of hemorrhage. In such instances hæmatoidin crystals can be discovered by the microscope. The interior of the dilated ducts and of the retention cysts is lined by a single layer of thin flat cells, with irregular edges and with oval flat nuclei. The walls are thickened, and composed of superimposed layers of laminated connective tissue separated from one another by flat nucleated cells. The secreting structure of the gland undergoes atrophy from pressure, or fatty metamorphosis takes place, and, although the gland is increased in size from the presence of the cysts, its functional power is lost.

In addition to causing obstruction of the duct of Wirsung and the changes mentioned, pancreatic calculi may produce induration, atrophy, acute inflammation, or even suppuration of the surrounding glandular tissue.

{1131} SYMPTOMS AND COURSE.--The main feature is the presence in the epigastrium of a rounded, smooth, fluctuating, painless tumor. There are also indications of the absence of the pancreatic secretion from the digestive tract--notably, emaciation, general debility, and the appearance of fat in the stools. Jaundice resulting from a coincident obstruction of the bile-duct is a frequent symptom, and melituria has been noted in some cases. It is probable, too, that the passage of a calculus along the duct may give rise to pain resembling in character and distribution the pain of hepatic colic.

The duration is indefinite. Sometimes the termination is sudden from the rupture of a cyst into the peritoneal cavity or into the stomach or duodenum, with hemorrhage.

DIAGNOSIS.--The absence of pain, of tenderness, and of cachexia, together with the physical characters of the tumor, distinguishes it from carcinoma of the gland.

Though not likely to be confounded with this disease, both hydatid tumor of the liver and distension of the gall-bladder must be borne in mind in making the diagnosis of a fluctuating tumor situated in the upper third of the abdomen.

TREATMENT must be entirely symptomatic. Attention to the general health, proper regulation of the diet, and the employment of pancreatin or an infusion of calf's pancreas to supply the place of the deficient pancreatic juice, are the important steps. Attacks of pancreatic colic indicate the use of anodynes.

In two reported cases in which the cysts were very large paracentesis for the removal of the fluid contents was resorted to, and there are two cases on record in which the cysts were extirpated after abdominal section. Kulenhampff of Bremen records a case of a man, thirty-nine years of age, in whom, after a succession of severe blows upon the abdomen, a tumor appeared in the epigastrium. An exploratory incision was made, and a few ounces of pancreatic fluid evacuated by aspiration. Six days afterward the abdomen was opened, the peritoneum united to the incision, and antiseptic gauze inserted to produce adhesive inflammation between the sac and the abdominal wall. Adhesion taking place after four days, the cyst was opened, a liter of fluid evacuated, a tent inserted, and an antiseptic dressing applied. For sixteen days fluid constantly escaped in slowly diminishing quantities, and the tumor disappeared, a fistulous tract remaining. This completely closed under the use of tincture of iodine and nitrate of silver at the end of the seventh week. Thiersch opened a pancreatic cyst and evacuated three liters of chocolate-colored fluid; recovery with a fistula followed.

From a patient supposed to be suffering from ovarian dropsy Rokitansky partially extirpated a cyst connected with the tail of the pancreas; death from suppurative peritonitis occurred on the tenth day.

N. Bozeman[4] on December 2, 1880, successfully removed from a woman forty-one years old a pancreatic cyst weighing, with its contents, twenty and a half pounds. In this instance also the operation was undertaken for the removal of a supposed ovarian tumor, the diagnosis not being established until after the abdomen was opened.

[Footnote 4: _New York Medical Record_, Jan. 14, 1882.]

{1132}

PERITONITIS.

BY ALONZO CLARK, M.D., LL.D.

Italian physicians in the later years of the seventeenth century and in the early ones of the eighteenth had acquired some knowledge of the symptoms of the disease we now call peritonitis, but known to them as inflammation of the intestines. Indeed, it is claimed by some of the admirers of Hippocrates that there are passages in his writings that indicate some knowledge of the disease. But this claim will probably be always received with many doubts as to its validity.

In confirmation of the first statement I will transcribe certain passages from Morgagni's thirty-fifth letter: In inflammation of the intestines "Albertini had observed the pulse to be low and rather weak, such as you will find it to have been in general in the foregoing letter under Nos. 9, 11, 18, and 25." He also observed the abdomen to be tense and hard, the face and eyes to have something unusual in their appearance. "Medical writers, indeed, agree in the tension of the abdomen, but they add many other symptoms, which prove beyond a doubt the intestines to be inflamed; yet they mean that evident inflammation which all may easily ascertain, and not that obscure disorder which we now speak of, and which few suspect" (gangrene of the intestines). "By the same writers it is also supposed that there is an obstinate costiveness and continual vomiting."

Morgagni refers to the assistance rendered by Albertini, Valsala, Van Swieten, Rosa, and others in elucidating this subject. It is singular, considering the clearness of his perception of the symptoms of inflammation of the intestines, that he should be so greatly confused regarding gangrene and sphacelus of the same parts. He looks on these as the result of inflammation, and when the two classes of cases are considered and compared, the result is a contrast and not a resemblance. Yet he supposes that the differences are to be accounted for by the different modes in which the same disease may be developed in different persons.

Another thing obtrudes itself on the attention in these letters: that while a number of post-mortem examinations are reported of those who had died of inflammation of the intestines, of gangrene and sphacelus of the intestines, of hepatic abscess opening into the peritoneal cavity, there is no record of finding in the abdomen anything corresponding to what is now known as the inflammatory effusions from serous membranes.

Sydenham died in 1689. I have searched his works, not for {1133} peritonitis, for the word was not in use in his day, but for some account of inflammation of the intestines or of some disease in the description of which symptoms are named that distinguish or belong to peritonitis, and with the single exception of pain the search has been fruitless.

Cullen in 1775 mentions the disease, but says that so little is known about it that he will not attempt a description of it.

Bichat died in 1802 in the thirty-eighth year of his age. I am not able at present to lay my hand on his _Pathological Anatomy_; I therefore quote from Chomel's article on peritonitis in the _Dictionnaire de Médecine_ to show his claim to important studies regarding that disease: "For a long time peritonitis was confounded under the name of inflammation du bas ventre with inflammations of the abdominal viscera; and it is to Bichat belongs the merit of having proved that inflammation of the peritoneum is a disease distinct, and that it ought to be separated from enteritis, gastritis, etc., as pleurisy is separate from pneumonia. The studies of Gasc and of Laennec soon confirmed the opinion of Bichat, and assured to peritonitis the important place which it ought to occupy in all nosological tables. It has become since then a subject of numerous observations and of interesting researches regarding the causes de sa marche and the lesions it causes."

The references are not given by Chomel, but they are probably these: Laennec, _Histoire des Inflammations du Peritoine_, 1804; and Gasc, _Dictionnaire des Sciences Méd._, p. 490, 1809.

Gasc says that the twenty years next preceding his publication witnessed the first stage of the true history of peritonitis. Walther in 1786 had contributed some facts, and S. G. Vogel in 1795, but the rounding off and completing their work was left for Bichat.

Acute Diffuse Peritonitis.

MORBID ANATOMY.--The first thing that strikes the observer in the post-mortem examination of a person who has died of this disease is the tendency of the intestines to protrude through the cut made in the abdominal wall. This is produced by their dilatation generally, both small and large, by gas. No gas, under these circumstances, ever escapes from the peritoneal cavity unless there has been perforation of the alimentary canal somewhere. While the intestines are in this manner dilated, the stomach is small and usually empty.

On the surface of the intestines there will be found a layer of coagulated fibrin, often very thin and delicate, requiring a scraping of the surface of the peritoneum to demonstrate it, but commonly obvious enough, and sometimes quite abundant. This same false membrane can be found on the viscera covered by the peritoneal membrane, on its anterior extension, and most at the point of contact of one coil of the intestine with another. Incorporated with this new membrane or lying under it will often be seen blood-spots, thin, translucent, diffused, and having ill-defined boundaries.

The blood-vessels themselves are not remarkably congested. Here and there may be spots where some redness remains, and the vessels are larger than natural. But the congestion and redness, which analogy leads us to {1134} believe belong to the active stages of the disease, have in great degree disappeared after death.

The peritoneal membrane itself has hardly become thickened, certainly not in marked degree, but it has lost its lustrous surface, is, at least in parts, of an opaline color, as if it had absorbed diluted milk, and there is an effusion of serum or slight oedema on its attached surface. Whatever may be the popular opinion regarding the termination of inflammation of the bowels in mortification, whatever the opinion of the older physicians, it is safe to say that gangrene of the peritoneum has never been the result of uncomplicated, diffuse, acute peritonitis. Peritonitis from strangulation of the intestine or analogous causes is of course excepted. But in puerperal peritonitis I have noticed a fact to which I have nowhere seen an allusion. The parietal peritoneum is at two points in the abdomen but loosely attached to the wall. One of these is on the anterior wall, anterior to and a little above the iliac fossa; the other is above and below the kidney on each side of the body. In these parts I have seen the membrane forced off from its attachment to the walls, which with it made a sac containing pus. Such an abscess, if the patient live long enough, would doubtless cause the death of the membrane.

There is in almost every case of peritonitis more or less of serous effusion, commonly not seen at first on opening the abdomen, for it has sunk into the pelvis. It is transparent, of a yellowish hue, and sometimes flocculi of lymph are found in it.

Whether the inflammation of the peritoneum extends to organs covered by it is a question that has been much discussed; but it is admitted that these organs, to a shallow depth on their surface, have an unnatural color; and when it is remembered that the peritoneum is nourished by vessels not exclusively its own, but running along its attached surface, and distributed as well to the surface of the organs it covers, it is easy to admit that to a very limited depth the organs partake of the inflammatory disease. This supposition gives an easy explanation of the constipation which is so prominent a feature among the symptoms of the disease.

The manner in which the false membrane is disposed of in those who recover is an interesting question. Forty or more years ago Vogel described the process by which the new effusion became a living tissue, and the manner in which blood-corpuscles and blood-vessels were formed in it; and another author had found that the time needed to complete this vascularization was twenty days. But now Bauer and most of the German writers inform us that the coagulated fibrin is converted into fatty matter and is absorbed, and that when adhesions occur they result from the coalescence of a new formation of the connective-tissue elements built up into granules. The question, then, arises, Will the chemical constitution of fibrin permit its conversion into oil? If it will, then the further question presents itself, By what chemical action is the change effected within the body? I do not intend to discuss these questions, but propose them by way of expressing some doubt regarding the accuracy of this statement.

I have always supposed that the epithelial layer of the peritoneum was pushed off by the first of the effusions in peritonitis, and that this was one of the causes of the lustreless appearance of the membrane. This {1135} opinion I have never attempted to confirm or correct by the microscope. Bauer confounds this idea. He says: "The deposition of fibrin occurs before the endothelium presents any changes. This fibrinous effusion encloses, primarily, hardly any cellular elements, and only a few cast-off endothelial cells are to be found in it. The endothelium itself is swollen and turbid; the cell-body is increased in size; the contents are granular; multiplication of the nuclei is apparent; the cells are, in fact, in active division. In the tissue of the serous membrane itself, soon after the deposition on its surface, an accumulation of indifferent (?) cells takes place, especially around the vessels, so that the spaces between the vessels are thus completely filled up. The fixed connective-tissue corpuscles take part in the inflammatory process."

Delafield says: "If the autopsy is made within a few hours after death, we find the entire peritoneum of a bright-red color from congestion of the blood-vessels; but that is all: there is no fibrin, no serum, no pus; epithelial cells are increased in size and number." For this kind of peritonitis he proposes the term cellular. He finds it in cases of local abscess of the abdominal cavity in which inflammatory action has extended over the whole membrane, and particularly on the omentum also, in the first two days of puerperal peritonitis. "The ordinary form of acute peritonitis is attended with changes in the endothelium and fixed connective tissue, and with the production of serum, fibrin, and pus." He describes the migration of white corpuscles of the blood through the walls of capillaries to become pus-cells, and then says: "Minute examination shows that two distinct sets of changes are going on at the same time: first, a production of fibrin, serum, and pus; second, swelling and multiplication of the endothelial cells. If the inflammation is very intense, the pus and fibrin are most abundant; if milder, the changes in the endothelium are more marked."

I have said above that the epithelium is early washed off by the inflammatory effusions. In opposition--or, perhaps better, in correction--of this idea, Delafield says: "There may be a considerable amount of pus produced, and yet the layer of endothelium remains in place." "If, however, the pus and fibrin are produced in large amounts, the endothelium falls off and leaves the surface of the peritoneum bare." The connective-tissue cells of peritoneum, he says, undergo but little change in the first three days of the inflammation, "but by the seventh day these cells are marked by increase in size and number in all parts of the peritoneum."

Two or three times in my life I have met with a peculiar arrangement of the false membrane and serum of peritoneal inflammation, of which I do not remember to have seen a description. It is this: the serum is enclosed or encysted in bladders, the walls of which are the false membrane. There may be two or three layers of these bladders, one upon another, all more or less flattened, and each holding from two to six ounces of fluid. It would seem that in these cases the inflammatory activity rose and fell in its progress, early reaching the point at which coagulable lymph was effused, then falling to the stage in which serum alone escaped. This serum lifted the false membrane irregularly, so that several pools were formed. After this the inflammation returns to the fibrous exudation stage, and gives to these bladders a floor which blends with the {1136} roof at the edges, and thus makes a complete sac. Once more the inflammatory action is changed in its intensity, so that the only effusion is serum; and this serum again raises the new layer of false membrane into bladders--not always or generally in the exact position of the first series. Still again, the inflammation may be so changed as to make a fibrinous flow to this second series of bladders. I am not certain that I have seen a third series of these rare productions. They have doubtless been seen by other persons, and may have been described. I have not been an exhaustive reader on the subject, but I can well understand how they may have been called hydatids on examination of the sacs without looking at the contents. The fluid in the cysts is simply serum, with no echinococcus sacs, and then the number of these inflammatory sacs greatly exceeds the probable number of the fibrous sacs of hydatids.

Pus in large quantity is not often a product of simple acute diffusive peritonitis, although it is frequently found in that form of the disease that attends puerperal fever, septicæmia, or erysipelas. Yet I have seen it a few times. The pus is not generally pure, but is mixed with serum in different proportions, and there will be seen at the same time deposits of lymph attached to the peritoneum or scales of it floating in the fluid effusion, or both. There is reason to believe that in the cases of this class a very large proportion are fatal in the acute stages, but in the cases that live for a few weeks the pus is disposed to collect in pools and become abscesses by adhesions around them at their borders. These abscesses are disposed to find an exit from the body. In one case four abscesses that were found in this way in different parts of the abdominal cavity had each burrowed toward the umbilicus, and were actually discharging their contents at this point when I saw the case. In another case one abscess only was formed, and in four weeks it had perforated the colon. The opening was nearly an inch in diameter.

Kalantarians says, in eight examinations of the solar and hypogastric plexus in persons who had died of acute peritonitis changes which he regards as inflammatory had occurred, with subsequent opaque swelling of the nerve-cells, ultimate fatty degeneration, brown pigmentation, and atrophy. In chronic peritonitis the cells are often converted into amorphous pigment matter, with increase and sclerosis of the ganglionic connective tissue. Still, it is worthy of notice that these changes do not express themselves in symptoms in those that recover.

ETIOLOGY.--Numerous writers have expressed a doubt whether a spontaneous acute peritonitis ever occurs, or if it is ever primary its occurrence in this way is very rare. Habershon[1] has presented the case with more apparent force than any other writer. He studied the record of five hundred autopsies of peritonitis made at Guy's Hospital during twenty-five years, but he "cannot find a single case thoroughly detailed where the disease could be correctly regarded as existing solely in the peritoneal serous membrane."

[Footnote 1: _Medico-Chirurgical Trans._, vol. xliii. p. 5.]

This statement must be received with some caution. In twenty-five years the records were probably made by a number of different persons, and persons of varying views and varying capacity and judgment. It is possible that the quotation may embrace some of the changes already referred to as the consequences of peritonitis. It does embrace the cases {1137} "when inflammation of the serous membrane occurs in the course of albuminuria, pyæmia, puerperal fever, erysipelas, etc." It also includes "peritonitis caused by general nutritive changes in the system," as seen "in struma, cancer, etc.," "comprising also those cases in which the circulation of the peritoneum has been so altered by continued hyperæmia (modifying its state of growth) that very slight existing causes suffice to excite mischief, as in peritonitis with cirrhosis, disease of the heart, etc."

With these explanations the statement differs widely from what it would seem to mean without them. It is far from saying that peritonitis always follows some abdominal lesion and is caused by that lesion.

Habershon's paper was published twenty-three years ago, and during all these years the curative treatment of peritonitis, to which the paper itself gave currency, has enabled us to study our cases after recovery as well as before the sickness, and it can hardly be doubted that a much larger proportion of the cases are primary and idiopathic than either Louis or Habershon found reason to admit. That a large number are produced by preceding lesions and constitutional conditions no one will be likely to doubt.

Among the 500 post-mortem examinations of peritonitis reported by Habershon, he found preceding disease or injury recognizable in the abdominal cavity in 261. The following is his table, viz.:

From hernia, of which 19 were internal obstruction . . . . . . . 102 From injuries or operations . . . . . . . . . . . . . . . . . . 35 From perforation of the stomach, ileum, cæcum and appendix, colon, etc. (other 13 mentioned with hernia, or with cæcal disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 And leading to fecal abscess (2 otherwise mentioned) . . . . . . 17 From typhoid ulceration without perforation . . . . . . . . . . 5 From disease or operation on bladder and pelvis, viscera, etc. . 42 From disease of the liver and gall-bladder . . . . . . . . . . . 11 From acute disease of the colon (3 others enumerated with perforation) . . . . . . . . . . . . . . . . . . . . . . . . . 3 From disease of the cæcum or appendix (9 others previously mentioned) . . . . . . . . . . . . . . . . . . . . . . . . . . 3 --- 261

Habershon says that in the (his) second and third divisions of the cases the causes were as follows:

From Bright's disease . . . . . . . . . . . . . . . . . . . . . 63 From pyæmia, 13; erysipelas, 5; puerperal fever, 10; with pneumonia, 3 . . . . . . . . . . . . . . . . . . . . . . . . . 31 From strumous disease . . . . . . . . . . . . . . . . . . . . . 70 From cancerous disease . . . . . . . . . . . . . . . . . . . . . 40 From hepatic disease . . . . . . . . . . . . . . . . . . . . . . 27 From heart disease . . . . . . . . . . . . . . . . . . . . . . . 9 --- 240

I have drawn thus liberally from Habershon's paper because it is the only paper that I know, in any language, founded on the analysis of a large number of cases (for five hundred post-mortem examinations is a large number for a disease no more frequent than peritonitis), in the belief that he dealt with facts and that his conclusions must be of great value. He may differ with other physicians regarding what constitutes strumous disease and in the agency of heart disease. He may have mistaken coincidence for consequence, but the paper bears the marks of honesty and good faith from the beginning to the end.

In Habershon's second division, under which he ranks the cases of {1138} peritonitis caused by "a changed condition of the blood," he ascribes 63 to albuminuria. Every physician knows how often meningitis or pericarditis or pleurisy may occur under these circumstances, especially in young persons; but, for myself, I cannot but express surprise at these figures. In one capacity or another I have been connected with large hospitals for forty-eight years, and have seen many cases of albuminuria in private practice, and can recall but few instances in which kidney disease, excepting cancer and other tumors, has terminated in peritonitis. In modification of this statement, however, it is proper to add that the hospital physician cannot know how half the diseases he treats terminate, on account of the American plan of interrupted service, and even less can he know of the mode of death in cases which he sees in consultation. Even with this admission, from my standpoint it is not easy to believe that one-eighth of the cases of peritonitis are caused by albuminuria.

The word pyæmia used by Habershon, it seems to me, ought to be replaced by septicæmia, and it has been by many of the profession. Sédillot many years ago proved that laudable pus injected into the blood-vessels of the dog produced no signs of disease, but that septic pus, so used, was followed by grave symptoms, even death. Among the author's cases thirteen were associated with the septic poison. He also found five which he thinks were independent of erysipelas. One in one hundred is a proportion hardly large enough to establish the relation of cause and effect against the chances of concurrence.

I can make a remark with reference to the inquiry by C. Dubacy in the October number (1881) of the _American Journal of Medical Sciences_, whether diphtheria produces peritonitis. When diphtheria became epidemic among us in 1860 or 1861 for several years, I saw a great deal of it, but did not recognize any relation between it and peritonitis.

The relations of hernia, injuries, and operations to peritonitis need no commentary.

Perforations of the alimentary canal may require some illustrative statements. These occur most frequently in the vermiform appendix of the cæcum, and are almost invariably caused by some irritating substance imprisoned in its tube. In some cases it is a seed of some fruit, as the orange or lemon; in others, a cherry-pit; in one that I remember it was a small stone, such as is sometimes found in rice; in others, a hard fecal concretion; in one, a child, a singular formation: a strawberry-seed was the centre; around this a layer of fecal matter, around the fecal matter a calcareous layer, on this, again, a fecal layer, and so on to the number of six layers, the external one being calcareous. This body was about one-fourth of an inch in diameter, and may have been years in forming. In this connection I may state, per contra, that I am informed that in a pathological museum in Boston is preserved an appendix that contains, and did contain, a large number of bird-shot, which did no mischief except to enlarge the appendix. This was from the body of a man who had shot and eaten many birds. My observation has led me to the belief that a large proportion of the cases of peritonitis occurring in children are due to perforation of the appendix.

Of the diseases of the liver producing acute diffuse peritonitis, the foremost, I think, is abscess, single or multiple. The different modes in which gall-stones may produce it may be illustrated by the following {1139} cases: (1) A lady died of acute peritonitis. At post-mortem examination a large abscess was found, bounded above by the liver, in other directions by adherent intestines; it contained nearly a quart of pus: at the bottom of the sac was a single gall-stone, very large and very black; the gall-bladder was perforated and very much shrunken. The gall-stone had caused an ulceration of the gall-bladder, but none of the intestines, in this respect differing from the process known as painless transit of a gall-stone. So the calculus caused the abscess, and the abscess caused the general peritonitis. (2) A lady between fifty and sixty years of age had an attack of gall-stone pains; she had had them before. In a few hours symptoms of peritonitis were manifest, and she died. The post-mortem examination showed the ductus cysticus was ulcerated and perforated. Two gall-stones of large size had been formed in the gall-bladder, and had been pushed forward into the duct about halfway to the common duct, leaving it enlarged as they advanced. The foremost one had caused an ulcer on the anterior or lower side of the duct, and bile had escaped, staining all the right half of the abdominal cavity, and throughout this half only the parts were covered with false membrane and stained with bile.

These cases are not so very uncommon. John Freeland of Antigua had a patient, a colored woman sixty-five years of age, who had been suffering from intermittent fever, gastric disorder, and retching. In one of the vomiting spells she experienced great pain, which, being relieved by an opiate, soon returned and was attended by tympanitic and tender abdomen. Death occurred in collapse about eight hours later. The cavity of the abdomen was found filled with blood and bile, the intestines inflamed and gangrenous in spots, and there was general peritonitis. The gall-bladder was empty; the hepatic duct was lacerated, and contained pouches in which gall-stones were encysted. One of these bags was lacerated. This laceration was surrounded by evidences of recent inflammation, and caused the general peritonitis.[2]

[Footnote 2: The _Medical Record_, Dec. 9, 1882.]

The perforations of the stomach which I have seen have been attended by little inflammation of the peritoneum. Death has followed this accident in twenty to thirty-six hours. There has been little pain, little tumefaction of the bowels, little tenderness, but a sense of sinking and a peculiar feeling at the stomach which the patient finds it difficult to describe.

The ulcers of dysentery do at times perforate all the coats of the colon, and yet do not with any uniformity cause general peritonitis; but as the destructive process approaches the outer covering the latter becomes inflamed, and lymph enough is effused to close the opening and prevent the escape of the contents of the intestine; so that, while perforation is not uncommon, I have rarely seen diffuse peritonitis accompanying dysentery.

Habershon reports 5 cases in which incomplete typhoid ulcers of the intestines caused peritonitis, and 15 from the complete perforation. I believe that the physicians of this country and those of France have found the complete perforation much the most common.

I do not remember to have seen fecal accumulation in the intestines produce peritonitis at all general. I did see, years ago, a man of middle {1140} age in whom fecal impaction in the ascending colon had caused destruction of all the layers of the abdominal wall on the right side, so that the contents of the intestine were exposed to view in a space of three inches by two. This implies that there had been peritoneal inflammation enough to seal the intestine to the abdominal wall on all the borders of this extraordinary ulcer. The man recovered in about six months, and returned to his business.

The inconsiderable operation of tapping for abdominal and ovarian dropsy has sometimes been followed by acute peritonitis. In the early part of my professional life I met with several such cases, and have witnessed the same from time to time since. These were mostly cases of dropsy from cirrhosis of the liver. Habershon found 5 such cases, and 7 in the tapping of ovarian cysts.

The rupture of ovarian cysts has produced peritonitis, but in a larger number of cases such rupture, even when the result of violence, has not led to inflammation; but the kidney secretion has been greatly augmented and the fluid absorbed, so that the rupture has been beneficial rather than harmful.

Tumors, particularly those of a malignant character, are apt to grow to the surrounding structures by adhesions the result of chronic inflammation, but now and then they provoke an acute attack which becomes general. Benign tumors may, in rare instances, do this. In one case a man died of acute peritonitis, and the examination showed that a tumor noticed before death, a very large serous cyst standing out of the left kidney, downward-forward, was the only lesion that antedated the inflammation.

Infiltration of urine, in any of the several ways in which it can reach the peritoneum, is a cause of peritonitis. Pelvic cellulitis may also be a cause, though twenty or thirty cases in succession may run a favorable course with no secondary lesions; it is still recognized as one of the occasional causes of peritonitis.

Among the rare causes of diffusive peritonitis is perforation of the intestine by lumbricoid worms. In such cases the product of the inflammatory action is apt to be sero-purulent, with but a limited amount of fibrin. E. Marcus reports such a perforation, and it was called by Peris ascaridophagie. The worms were apparently not found in the peritoneal cavity, but in the intestines. The perforation had bloodless edges, which lay quite close upon one another, as if they had been separated by a piercing action of the attenuated extremity of the parasite not eaten through.[3]

[Footnote 3: _N.Y. Med. Journal_, Jan. 27, 1883.]

Lusk finds that certain vaginal injections excite a local peritonitis. Sentey gives the details of a case in which a midwife undertook to procure an abortion by the douche. She used a tube that was large with a spreading mouth or opening, which probably received the neck of the uterus in such a way as to prevent the return of the water. It was, in consequence, forced into the uterus and through one of the Fallopian tubes into the peritoneal cavity. By this a rapidly-fatal peritonitis was developed. He refers to two other similar cases. It would seem that this mode of procuring abortion can be frightfully misused, however safe it may be in skilful hands.

There is a word still to be said regarding the difference between peritonitis produced by wounds, operations, violence, and internal growths, or {1141} what, with a little liberty, may be called traumatic causes, and that which arises spontaneously or without recognizable cause. The first shows a tendency to limit itself to the immediate neighborhood of the injury, and more frequently does not become general; while the latter spreads pretty quickly over the whole extent of the peritoneum.

SYMPTOMS.--There is, perhaps, no grave disease whose symptomatology is more easily interpreted, in which the diagnosis is more easily made, than the average case of acute diffuse peritonitis. Yet there are obscure cases which it is difficult to recognize.

In a well-marked case the first symptom is pain. Chomel and even some later writers believe that chill precedes the pain, but to the best of my recollection it has not generally so occurred to me; and the question arises, Have they kept the symptoms of puerperal peritonitis separated from those of simple peritonitis?

The pain is first felt in a somewhat limited space in the abdomen, and pretty rapidly spreads, so that it is soon felt in every part of the bowels. It may remain greatest in the part where it first began, but there are many exceptions to this statement. As the disease advances the pain and tenderness become more marked, and the patient will try to diminish the tension of the abdominal walls by lying on his back and by bending the hip- and knee-joints, often also for the additional purpose of lifting the bedclothes from his abdomen. Often the patient will resist the physician's movement to examine his bowel with the hand. In the last few hours of life the pain ceases.

The pulse in its frequency follows the advances in the disease. At the onset it is not much accelerated, but in two or three hours it may reach 100 to 120 in the minute. Besides becoming more frequent, it becomes smaller in volume and more tense. Toward the end of a fatal case it may reach 140 to 160 in the minute and be very small.

In the early hours of peritonitis the bowels begin to swell, and percussion shows that the swelling is caused by gaseous accumulation. This increases as the disease goes on, so that in some the bowels become greatly distended--so much, indeed, as to diminish the thoracic space and interfere with the respiration. As the disease advances the tympanitic resonance may give place to dulness on percussion on the sides and lower part of the abdomen. This is due to fluid effusion.

Before the introduction of opium in the treatment of peritonitis the green vomit was a marked feature of the disease. It occurs in other conditions, but rarely, and its occurrence in this disease was so common that it was regarded as almost diagnostic. The fluid vomited is of a spinach-green color, and the color is probably derived from the bile; at least, I have examined it repeatedly for the blood-elements, and have not found them. In these days this symptom of peritonitis is not often observed.

Constipation is absolute in uncomplicated peritonitis of ordinary severity, and I believe is caused by a temporary paralysis of the muscular layer of the intestine. It has already been stated that the blood-supply of the peritoneum is through vessels whose capillaries are shared by that membrane and the tissues which it covers. Inflammatory action in the peritoneum of average severity would naturally extend to this muscular layer and render it inactive. When the inflammation abates it recovers its contractile power. Thus, the intestines become entirely insensitive to {1142} cathartic medicines. This fact is not observed in puerperal peritonitis, probably because the large share which the uterus takes of the disease may act, in some degree, as a derivative; and then, so far as I know, the muscular layer of the intestines does not undergo the change of color and appearance in the latter disease that has been observed in the former. This obstinate constipation has been noticed from the first discovery of the disease, and during forty years in the first part of this century many physicians believed that if they could overcome it their patients would recover. The present interpretation of this conviction is that if catharsis, which was very rarely effected, did precede recovery, the disease was not of a grave type--if, indeed, it was peritonitis at all.

Sometimes peritonitis occurs in the course of a diarrhoea; then the constipation is not at once established, but the symptoms of the two diseases concur for one or two days, when the diarrhoea ceases.

Abdominal respiration ceases when peritonitis is established, either because the movements of the diaphragm produce pain or because the diaphragm is partly paralyzed, as is the muscle of the intestines. Then the gaseous distension of the bowels obstructs the action of this muscle. As a clinical fact it is important, and has often helped me in a diagnosis. Another kindred fact is that all the indications of peristaltic action cease. I have a great many times placed my hand on the abdomen and patiently waited for a sensation that would be evidence of intestinal movements, but did not discover any--have placed my ear on the surface of the abdomen, and have long listened for the gurgling which is so constant in healthy bowels, and have listened in vain. In this respect my observations differ from those of Battey, who reports that he has heard the friction of the newly-made false membrane in respiration, while I concur with him in the statement that the sensation of friction can be felt by pressure of the ends of the fingers into the abdominal wall so as to produce indentation. It should be said regarding the friction sound in respiration that Battey has the support of Chomel, and he in his turn quotes Barth and Roger; so that there may be in this sign more than I have thus far found. (See case hereafter related.)

The temperature of the body is not, considering the extent of membrane involved, remarkably high. I have recently attended a most carefully-observed case in which the temperature never rose above 104° F. It falls below the temperature of health as the disease approaches a fatal termination.

From the time this disease was recognized as a separate and distinct affection the countenance has fixed the attention of writers. The face is pale and bloodless and the features pinched, and the general expression is one of anxiety and suffering. I do not remember to have seen a flushed face in peritonitis, although the degree of paleness differs in different patients.

The mind is almost always clear, unless disturbed by the medicines used in the treatment. Yet cases are recorded in which a mild, and still more rarely a violent, delirium has been noticed. Subsultus tendinum, and even convulsions, have been witnessed, but whether these symptoms belong to the peritonitis or to an accompanying uræmia has not received the attention of those who have witnessed them.

The urine is usually scanty and high-colored, but it does not often {1143} contain either albumen or casts. This statement is presumably untrue of the cases in which Bright's disease preceded the peritonitis and is supposed to be the cause of it--a variety of the disease with which I have already declared my scanty acquaintance. The urine is often voided with difficulty, and sometimes retained, so that resort to a catheter becomes necessary.

The symptoms of this disease are not invariable. In one case the inflation of the bowels is only enough to be perceptible; in another, as I have said, it becomes a distressing symptom, while in most the bowels are obstinately constipated. A case may now and then occur in which evacuations can be procured by cathartics. Pain is regarded by all physicians as the most constant symptom, and it has existed in every case that I have seen, or at least tenderness; but the late Griscom stated to me that a man once came to his office for advice in whom he suspected peritonitis; but the man asserted that he had no pain, and the doctor placed his fist on the abdominal wall and pushed backward till he was resisted by the spinal column, the man asserting that the pressure did not hurt him; yet he died the next day, the doctor declared, of peritonitis. This may be credible in view of the fact that absence of pain in puerperal peritonitis is not very uncommon. The green vomit, which was expected in all cases forty years ago, for the most part, as I have intimated, disappears under the opium treatment. There are persons in whom peritonitis does not accelerate the pulse beyond 100 beats in the minute. The pain, in rare cases, remits and recurs with some degree of regularity, in this respect resembling intestinal colic. Andral reports such a case; I have also witnessed it.

MORTALITY.--Up to the time when the opium treatment was adopted, peritonitis was a fearful word; a large proportion of those attacked by it died of it. In 1832, I began to visit hospitals as a medical student, and for eight years, at home or abroad, was almost a daily attendant. The number of recoveries of those that I saw in that time can be counted on the fingers of one hand. This may be regarded as its natural mortality, for the treatment of that day seemed to exercise little or no control over it. (Farther on this matter will be referred to again.)

DURATION.--Chomel believed that the disease might prove fatal in eighteen hours, while he regards its average duration as seven or eight days. I very much doubt whether peritonitis, not caused by perforation, violence, or surgical operation, was ever fatal in eighteen hours. I do not remember any case of shorter duration than two or three days. Then, on the other hand, the period of seven or eight days in the fatal cases appears to me too long. In the early part of my professional life I remember to have looked for death in three or four days. At present, in the fatal cases, life is prolonged to double or more than double that time. In the majority of those that recover at present the duration of the symptoms is from two days to a week; in a few they have continued fourteen days; and lately I have assisted in the treatment of a case in which there was little amelioration for forty days, and yet the peritonitis was cured.

DIAGNOSIS.--When the symptoms are fully developed there are few diseases that are more easily recognized. It is when these symptoms are slowly or irregularly manifested, or when some other disease which may account for many of the symptoms occurs with it or precedes it, that there {1144} should be any real difficulty. It is customary to regard the danger of confounding the transit of a renal or hepatic calculus with peritonitis as worthy of comment. But if the reader will turn to the articles in this work which relate to these topics, he will find the symptoms so widely different from those enumerated in this article as belonging to peritonitis that he will be surprised that this item in the diagnosis should have occupied so much room.

In a case already referred to, in which peritonitis followed gall-stone pains, the transition was so marked by the rapid acceleration of the pulse and swelling of the abdomen that each of the three physicians in attendance at once appreciated the significance of the change. A physician who resided in the country called on me to report his own case. He had a little before had a very painful affection of the abdomen which continued for three days. The pain was paroxysmal, confined to the region of the liver, back and front, for one day; after that there was some tenderness over most of the abdomen, but no tympanitis. His pulse became frequent and his temperature advanced to 103°. His physicians believed that these symptoms justified them in treating him for peritonitis. Yet his position in bed was constantly changed, and no one attitude long continued--a restlessness which never occurs in peritonitis, but is common in calculus transits. Add to this the absence of gaseous distension and of the green vomit, the paroxysmal character of the pain (though I remember one case in which peritoneal pain increased and diminished somewhat regularly, but only one), and, finally, the sudden cessation of the pain, such as often happens in calculus transit when the calculus passes into the intestine,--it is plain that his sufferings were caused by a gall-stone. The elevation of temperature was the result of a long-continued worry of the nervous system, and the abdominal tenderness came from the many times repeated contraction of the abdominal muscles which occurs in hepatic colic. And then, to make the diagnosis more complete, this gentleman, after twelve or fourteen hours of pain, became jaundiced--in the end very much so. There was no absolute constipation, and the stools were of the color of clay from the absence of bile.

The points of difference between renal colic and peritonitis are even better defined and easier recognized than those between it and hepatic colic.

In intestinal colic there may be some inflation of the bowels, and if it continues a day or two there may be some tenderness; but it is for the most part distinguished from peritonitis by the intermittent or remittent character of the pain, by its greater severity while it lasts, by its courting, rather than repulsing, pressure, by the moderate acceleration of the pulse, by no or only slight elevation of temperature (exception being made for long continuance), by the absence of the green vomit, by the absence of the fixed position of peritonitis, etc.

There does not seem to me any need of spending time to distinguish gastritis or enteritis or neuralgia from peritonitis, their symptoms are so wholly different; and if, as is said, the mucous inflammation can penetrate all the coats of the stomach or intestine, and so cause inflammation of the peritoneal layer, that is peritonitis, and will be distinguished by the proper symptoms of peritonitis.

TREATMENT.--Chomel[4] says: "If general peritonitis is intense, it {1145} should be attacked by the most powerful therapeutic agents. One should immediately prescribe a large bleeding from the arm--from 500 to 600 grammes, for example--and repeat according to the need once or even twice in the first twenty-four hours; apply to the abdomen, and particularly to the part of it where the pain was first felt, leeches in large number--fifty, even a hundred--as the violence of the disease may demand and the strength of the patient will permit." He recommends baths, presumably tepid, and describes an apparatus by which the patient can be put into the bath and lifted out of it without pain; prescribes a fixed posture, gentle laxatives, mercurial frictions, blisters; conditionally and doubtfully, paracentesis, emetics under certain circumstances--musk, etc. under others. In the treatment of general peritonitis there is no reference to opium. The word does not occur, but it does in the treatment of peritonitis following perforation. In this condition he would, among other things, give opium à haute dose, but he does not prescribe any repetition or give any details. It is probable that the idea was obtained from Graves, whose first use of opium in this accident was in 1821, although its first publication appears to have been by Stokes in 1832.

[Footnote 4: _Dictionnaire de Médecine_, 1841.]

Wardell,[5] who has written the latest treatise on the disease we are considering, relies greatly on bloodletting, but falls short of Chomel in the quantity of blood he would take--would bleed, not to withdraw a certain number of ounces, but to produce certain effects. The venesection is to be followed by the application of leeches--twenty, thirty, or forty--to the abdomen; after this turpentine applications to the bowels. After depletion, he says, opium should be given at once: "two or three grains may be given in urgent cases." Vesication he calls "another of our aids." He disapproves of cathartics, but when there is accumulation in the colon would use injections. "Opium in the asthenic form is the chief agent, and Graves and Stokes were among the first physicians who gave it very largely." "Two or three grains may at first be prescribed, and a grain every four or three, or even two, hours afterward." "In perforation there is sometimes great toleration of the drug. Murchison has known so large a quantity as sixty grains to be given in three days with impunity." Mercurials, he thinks, are of doubtful efficacy. In the paragraph devoted to the treatment of puerperal peritonitis the word opium does not occur, and it is only by a very doubtful inference that we can assume that he would ever use it. Chomel makes no allusion to the use of opium in the same disease.

[Footnote 5: _Reynolds's System of Medicine_.]

For two years (1834-36) I was connected with the New York Hospital as house-physician or in positions by which that office is reached. The treatment of acute diffuse peritonitis then and there was formulated as follows: First, a full bleeding from the arm, commonly sixteen ounces, then a dozen or more leeches to the abdomen; following this, another bleeding or not, in the discretion of the physician. Meantime, the patient would take half a grain to a grain of calomel every two hours, with a little opium "to prevent the calomel acting on the bowels," of which there was no danger, in truth. Mercurial inunction was used at the same time. The belief was that after depletion the most important thing was "to establish mercurial action in the system;" in other words, {1146} "to diminish the plasticity of the blood." Under this plan I saw one recovery in these two years.

In 1840, I went to Vermont to give a course of lectures in the Vermont Medical College, and while there was called by the physicians to see with them several cases of peritonitis. I found that they were treating the disease on the Armstrong plan; that is, bleeding freely, and then administering a full dose of opium, as they said, "to prolong the effects of the bleeding." In most cases there was a second bleeding and a second administration of opium. Leeches were also used, and irritating applications to the abdomen, and in some cases purges. I found they were getting better results than we were in New York, and I studied their cases as closely as I could, and reached the conclusion that opium was the curative agent, and that it would be safe to omit the abstraction of blood. This conviction grew in strength with every new case, and I saw, with different physicians, several cases, the disease being more prevalent among the mountains there than in the city--at least that year. The idea then formed was that to establish the narcotic effects of opium within safe limits, and continue them by repeated administration of the drug, would cure uncomplicated peritonitis--that a kind of saturation of the system with opium would be inconsistent with the progress of the inflammation, and would subdue it. There was no theory to build the treatment on, and no explanation of the action of the drug in my mind. What I saw of the action of two full doses of opium was the only foundation for the idea. I had in the course of two years after those observations in Vermont 9 cases of general acute peritonitis, 8 of which were cured. All these were reported in succession, as they occurred, to the medical societies and in my college lectures. The plan was adopted by many members of these societies and by others with whom I had opportunity of conversing on the subject, so that soon there were several--I may say many--workers in the field; and in all instances where the practitioner had the courage to carry out the treatment favorable reports were returned. Not that every case of peritonitis was cured, but the recoveries generally exceeded those that followed any other plan ever before used. No physician tried it with a proper understanding of its details, and with courage to execute them, who if living does not practise it to-day.

The treatment of puerperal peritonitis is not allotted to me, and I am very reluctent to encroach in any degree on the province of the very competent and highly-esteemed gentleman to whom that disease was assigned. But the history of the opium treatment is very incomplete without the statement I am about to make, and I trust to his generosity to forgive this encroachment; and all the more confidently because he was not at the time acquainted with the manner in which opium was first introduced into the treatment of puerperal fever.

After the curative action of the drug was demonstrated in general peritonitis, I was anxious to try it in puerperal fever, of which peritonitis forms a part. But I had no hospital and no obstetrical practice. In 1847, I was appointed one of the physicians to Bellevue Hospital, to which an obstetrical department was attached. After one or two years a single case occurred and was sent to my division. I gave her 100 grains of opium in four days, with more or less of calomel--I have {1147} forgotten how much. She recovered, but after the symptoms of puerperal fever passed away she had secondary abscesses of the lungs. These kept her ill for several weeks. At length her recovery was complete.

In 1840 there was a very fatal visitation of puerperal fever in this hospital, and on invitation of Vaché, who then had charge of the whole institution, I was a daily visitor and took notes of all the cases. It was from these notes that Vaché compiled his report of the epidemic published in the _Medical and Surgical Journal_. The disease was fearfully fatal, although every known mode of treatment was tried in different cases, including Brenan's plan by turpentine, but all, with one or two exceptions, with the same result. At this time the opium plan was on its trial, and I had not acquired a confidence in it that authorized me to try it in these cases. The time for it came in 1851. Then a sudden, vigorous attack occurred. One woman was sent to me in whom the disease was well advanced. I instructed my house-physician not how much opium to give, but what effects to produce by it. I found this woman dying the next day, and that she had taken only three grains of opium in three doses. In three or four days seven cases were sent me from the lying-in wards. One was returned for error in diagnosis, and six put under treatment. Having found that prudence in my house-physician was so much more conspicuous than courage, another house-officer, who combined them both, was selected to be in almost constant attendance. The instruction I gave him was in these words: "I want you to narcotize those women to within an inch of their lives." He did it, and saved every one of them. This gentleman is now known over the whole land as a learned and distinguished surgeon. I feel called upon to give his name in this connection, that he may be a witness to the facts I state, and for the admiration with which his nerve and prudence impressed me. One of these patients took first two grains, then three grains, then four, and so on till she took twelve grains of opium at a dose, the intervals being two hours. The state into which the patient was to be brought I have denominated a state of semi-narcotism. The quantity of the drug necessary to produce this state varied surprisingly in different persons. One of these women was pretty fully narcotized by four grains every two hours. She was watched with anxiety; restoratives were kept in readiness, but nothing was done but to suspend the administration of the medicine and to wait. In seven hours the consciousness was fully restored, and the improvement in her condition was wonderful. The disease seemed to be cured. But in a few hours more the symptoms recurred, and the same medicine was again given in three-grain doses, and again narcotism was produced. Taught by the experience of the day before, we waited, and when she recovered from this second narcotism her disease was completely cured. She took no more medicine of any sort. This case was very instructive, as it taught me that over certain cases of puerperal fever opium has absolute control.

From the time here referred to, so long as the obstetrical service was maintained at Bellevue Hospital, a large proportion of cases of this fever, as they occurred, were sent to my wards, and in all these years I have not lost faith in opium. This statement, however, requires an explanation. Puerperal fever is a compound disease. Its great inflammatory lesions are found in the uterus and its appendages and in the peritoneum. {1148} When the inflammation of the uterus is the dominant lesion, and is purulent, opium has little or perhaps no control over its fatality; but in the cases in which peritonitis is the ruling lesion, if begun early, it will show its power. In this connection I will only add that in private practice the drug has been perhaps more curative than in the hospital. I have seen many cases in consultation, and a decided majority have recovered. In some instances the patient has fallen into a pleasant sleep, only broken by some administration, and ending with her recovery. In one instance a very eminent physician had undertaken to treat a case by the opium plan, but he had administered the drug so timidly that for fourteen days he had done no more than hold the disease in check. After trial, I found that I could not induce him to give the drug in my way, and I asked him to give me sole charge of the patient for twenty-four hours. To this he assented, remarking, "If you cure her, doctor, I will have it announced to the profession that she was the sickest person I ever saw get well." In half the time allowed me I was able to establish the opium symptoms as given farther on, and the lady slowly recovered.

The treatment of any form of peritonitis by opium permits the use of the drug itself, or of any extract or preparation of it which contains its narcotic qualities, but it is wise to persevere with that one first chosen unless there is strong reason for a change. This caution is based on the fact that we cannot change from one to another and be certain to obtain the same drug activity. For example, we begin with laudanum, and find what it will do. We cannot take in its place the sulphate of morphia with the certainty that we can so graduate it as to get precisely the same effects. Then the quantity which will be effectual in one case may be quite inadequate for the next. The tolerance of opium in different persons varies remarkably, and probably the disease itself increases the tolerance in all. This will be illustrated by some of the details of this paper.

The drug symptoms to be produced are as follows: Subsidence or marked diminution of the pain; some or considerable tendency to sleep; contraction of the pupils; reduction of the breathing to twelve respirations in the minute; in the favorable cases a considerable reduction in the frequency of the pulse; a gentle perspiration; an itchy state of skin, or oftener of the nose; absolute inactivity of the bowels, and after a time a subsidence of the tumor and tenderness in them; some suffusion of the eyes.

Of these several signs of opiumism there is none more easily observed and none more valuable than the frequency of the respiration; and while the physician aims to reduce it to twelve in a minute, there are chances that he will see it fall to something below that. I have often counted it at seven, and in perhaps two cases it fell to seven in two minutes; and yet these cases of marked oppression from opium all recovered. In the cases in which the respiration has fallen so low there has been considerable obtuseness of the mind; but in no case except in the hospital patient already referred to have I seen unconsciousness. Then the sleepiness, so long as the patient is easily awakened, is wholly within the limits of safety.

As to the quantity of opium to be given, I have known two grains every two hours do the work, and in other cases many times this {1149} quantity was necessary to produce this condition of semi-narcotism. The plan is to begin with a dose that is safe--say two or three grains of opium or its equivalent of sulphate of morphia--and in two hours notice its effects. If any of the opium symptoms have appeared, repeat the dose; if none, increase by one grain, and so on at intervals of two hours till the degree of tolerance in the patient is ascertained. After that the case can be treated by a diminished occupation of the physician's time--two or three visits a day. The dose is to be increased if the opium symptoms diminish before the disease yields, but always to be diminished or discontinued if narcotism is approaching. The duration of the treatment will be sometimes no more than two or three days; it may be a week, or even a fortnight, and in one case already mentioned the symptoms persisted mildly for forty days, and then yielded. In this case the medicine used was the sulphate of morphia, and the enormous dose reached by steady and graduated increase was one grain and a quarter every forty minutes in a boy ten years old.

In some puerperal cases the doses have been so large as to require witnesses to make the statement of them credible, and the administration of them criminal had not the effect of each dose been carefully studied and the amount of each measured by the action or inadequate action of the next preceding one.

Here are the doses given a woman who fell sick October 13, 1857; the record was made by C. H. Rawson during the treatment, and was kindly given me two or three years ago: On the first appearance of her disease, while the diagnosis was uncertain, 10 grains of Dover's powder gave her a quiet night. The next day the disease was more manifest, and she took of Magendie's solution (2 grains of sulphate of morphine to a drachm of water) x minims every hour; growing worse, at night she took xxx minims every hour; the next day, xl minims every hour, and no change of symptoms. She took in twenty-four hours 32 grains of sulphate of morphia; slept, but was awakened by the slightest noise. On the fourth day 3-1/3 drachms of the solution, and opium as follows: at 4 P.M., 3 gr.; at 5 P.M., 4 gr.; at 6 P.M., 5 gr.; at 7 P.M., 6 gr., and 6 gr. hourly after 7 P.M. Sleep light. Fifth day, in twenty-six hours took in opium and morphine the equivalent of 208 gr. of opium. The sixth day, 212 gr. of opium; on the seventh day, 221 gr. of opium; on the eighth, 224 gr.; on the ninth, the same quantity; on the tenth, the same; on the eleventh, 247 gr., pulse subsiding; on the twelfth, 261 gr., other symptoms better; on the thirteenth, 144 gr.; fourteenth day, 4 gr. hourly; slept for the first time heavily, all other symptoms improving, bowels moved freely, ate well, tympanites subsiding; fifteenth day, 1 gr. of opium every two hours, and at night the last dose. Recovery was complete. The woman denied the opium habit, and the medicines were tested by the apothecary. Such doses can only find their justification in the demonstrated fact that smaller doses will not produce the degree of narcotism desired.

In Keating's edition of Ramsbotham's _Midwifery_ a case is reported by myself in which a woman, by pretty rapidly increasing doses, reached forty-eight grain doses of opium, with the effect of curing her disease and substituting a temporary active delirium.

A word of caution is probably necessary regarding the use of opium in high doses when peritonitis and Bright's disease coexist. I have {1150} already said that I have but scanty personal knowledge of such a concurrence, but in Bright's disease alone I have known a large, non-heroic dose of an opiate fatal. For example: A young man had a felon on his finger, and did not sleep, so great was his pain. His physician prescribed 40 drops of laudanum at bedtime. Not sleeping on this, he took another portion of 40 drops, and in the morning he was found in a comatose condition, and in the course of the day he died. A post-mortem examination revealed Bright's disease, which was not before suspected. A woman took half a grain of the sulphate of morphine--for what reason I do not know. I was called to see her when she was in a semi-comatose state. The time between my seeing her and that of taking the morphine was fourteen or fifteen hours; its removal from the body was therefore hopeless. Her limbs were swollen with oedema, and the urine contained albumen and casts. Although the usual means of opposing the poisonous effects of opium were resorted to, they were of little use, and the patient died in the course of the day. These are selected from a considerable number of similar cases that show a similarity in their action on the brain of opium and urea. It seems that opium precipitates the uræmic coma, yet the coma produced by these agents combined is not so profound as that produced by opium alone. There is in it some movement of the limbs or body or some imperfect utterances, yet it seems to be more fatal than the coma of opium unaided. Notwithstanding all this, I have met with several cases of cardiac disease combined with Bright's--perhaps I should say many--in which half a grain of morphia sulphate has been taken every night to procure sleep with only beneficial results. This has been observed several times when physicians have been the patients.

These facts are stated to show the hesitation and prudence that should control the administration of opium when there is urea in the blood, whether there is peritonitis or not; but a case in which one form of Bright's disease preceded, and perhaps caused, peritonitis will be more instructive: A gentleman sixty-eight years of age was attacked by peritonitis on Thursday evening. There was a moderate chill at the onset (this being one of the few cases in which I have witnessed this occurrence). The diagnosis was then uncertain, and he took quieting doses of Dover's powder, which gave him sleep. The next day the diagnosis was easily made. The urine was examined for albumen, and none found. It was, however, scanty. He took only six-eighths of a grain of sulphate of morphine in the first twenty hours. It was then increased, so that in the next twenty-four hours he took two grains of the sulphate in divided doses--a quantity which has been greatly exceeded in hundreds of cases with the best results; but in this case coma was the result. At 10 A.M. on Sunday he was comatose, but not profoundly; he could be aroused. The breaths were five in the minute, the pulse increasing in frequency; secretion of urine next to none. The galvanic battery was used. After seven hours, while the respiration was growing more natural, the pulse grew more frequent and the stupor increased. At 8.30 P.M. the breathing was fifteen in the minute, and full and perfectly easy, but the pulse was running at 140, and the coma unbroken, and the pupils of good size. The effects of the opiate had passed off, but those of uræmia were profound. He died at 11 P.M. After the alarming symptoms occurred we tried to procure another specimen of the urine for fuller examination, but {1151} could not. It was only after his death that we procured the evidences that he had shown symptoms of contracted kidney for months. The urine contained no albumen at the time of our examination, as very often happens in that disease.

Regarding other points in the opium treatment there is little to be said. Purgatives are entirely inadmissible. The bowels should be left entirely at rest till they recover their muscular tone; then they will expel first the gas, and then the feces; or if, after the inflammation is subdued, they do not move of their own accord, injections are admissible. I have often left the bowels absolutely inactive for fourteen days without any recognizable consequences. If I meet a physician who believes that leeches are essential, I yield him his point, but never advise them. I do this because a moderate bloodletting will do no harm, and little if any good. The same rule I apply to irritating applications to the surface of the abdomen. Mercurials, I think, are harmful, and therefore I object to them. As to food, it should be milk, fresh eggs beaten up with water and pleasantly flavored, peptones, etc. selected from among those that leave no refuse.

The testimony of physicians who have adopted this plan within my own circle is unanimously in favor of it. B. R. Palmer of Woodstock, Vt., afterward of Louisville, Ky., who was the first to test it, told me after a few years' trial that he used to dread peritonitis as he would dread the plague, but with opium in his pocket he met it cheerfully and hopefully, as he did a pneumonia. Chalmers of New York, who is known by many readers of this article, has a very extensive practice, and he told me lately that he had not had a fatal case of peritonitis in twenty-two years. He embraced the plan early.

Now, how did this treatment originate? From whom did the profession adopt it? In 1836-37, I visited daily the hospitals of London, Edinburgh, and Paris, was in frequent intercourse with the physicians of those cities, and never saw a patient anywhere treated by opium, and never heard the least allusion to it. I can safely appeal to any physician who was familiar with the history of the profession before the year 1840, or for two or three years later perhaps, to inquire whether anything was generally known regarding this treatment of peritonitis, or whether he himself ever heard of it. Let the inquiry be made of Willard Parker of New York or Alfred Stillé of Philadelphia--men of a degree of intelligence and learning that has made them leaders in the profession--and of all the profession at that time. I venture to assume that they were as ignorant as I was of what Graves and Stokes had done.

The following fact is significant: In 1843, Graves published _A System of Clinical Medicine_, the preface of which is dated January, 1843. In this he says he had previously published essays, lectures, and articles in several medical journals. In this volume he intends, he says, "to revise what I have written, and to compress the whole within the limits of a single volume." There is nothing in the table of contents or explanatory headings of the several chapters of this volume which alludes to treating peritonitis by opium. It is fair to infer that the cases treated in 1823 had made little impression on his mind, and that he did not think his treatment could take rank as a discovery; and yet Stokes had made favorable mention of it eleven years before this publication. Graves, then, did not {1152} publish his cases, and the first knowledge which the profession could have of them was through Stokes's paper, published in the _Dublin Journal of Medical and Chemical Science_, No. 1, in 1832. Perhaps the reason why Stokes's paper produced so little impression on the profession may be found in the fact that first numbers of journals of every sort have few readers. Anyway, it was not till after the opium treatment had attracted much attention in this country that anybody here knew that Graves or Stokes had ever had anything to do with it. Besides, Graves and Stokes had only used opium in cases of perforation, and they had no plan or symptomatic guide in the use of the drug.

There is something new and strange in the following case copied from the _Medical Record_ of May 12, 1883, under the heading, "Operative Measures in Acute Peritonitis:" "Dr. Reibel relates the case of a child, eight years old, suffering from acute idiopathic peritonitis. The disease had resisted all treatment, and the child being, apparently, about to die, it was determined to open the abdomen with a view to removing the fluid and washing out the peritoneal cavity with a solution of carbolic acid. The meteorism was intense. No fluid was found in the abdominal cavity. In prolonging the incision a loop of the intestine was punctured, as evidenced by the escape of gas and intestinal fluid. The wound was washed with carbolic acid and covered with a layer of antiseptic cotton. The following day the little patient was nearly free from pain, and was able to retain a little milk. The temperature had fallen from 104° to 101°, and the tympanitis was almost entirely gone. The (wounded) loop of intestine was adherent to the abdominal wall, and there had been no escape of fluid into the peritoneal cavity. The patient made an excellent recovery."

If the statements of this abstract are true, and the future supports the practice pursued in this case, acute peritonitis is likely to become a surgical rather than a medical disease. Reibel thinks that opening the intestine in the way he did is a better plan than the punctures with the exploring-needle to relieve the patient of the tympanitis. But it will require more facts than one to persuade the profession that this mishap of the scalpel can grow into a rule of practice. (The _Record_ finds this report in the _Journal de Médecine de Paris_.)

I cannot say that I see the value of a distinction made in 1877 by Gubler between peritonitis and peritonism. By the latter term is meant the total of nervous and other symptoms that arise in the course of peritonitis. Trasour has lately revived this distinction, and thinks it important, and that a light peritonitis may be attended by a grave peritonism. He holds that the distinction is important, because "the treatment of peritonism consists in the administration of alcohol, chloral, and especially of opium in large doses. Of the latter fifteen grains may be given in twenty-four hours." "The symptoms [of peritonism] are produced through the agency of the great sympathetic."[6]

[Footnote 6: _Med. Record_, Aug. 28, 1883.]

I cannot say that I have seen great effects follow small causes, but think that, in general, the effects of peritonitis on the pulse, strength, nervous tone, etc. are, to some extent at least, a measure of its severity.

CONSEQUENCES OF PERITONITIS.--These are usually nothing. When recovery takes place it is commonly complete, but cases have been known {1153} in which the intestines have been left bound to the abdominal wall and to each other, and so made incapable of their natural action. The results of this are a swollen, tympanitic abdomen and impaction of the bowels, but the general health may be very good. A woman at Bellevue was left in this condition, yet she performed the duties of nurse in one of the wards for some years, and finally disappeared from the institution, and I do not know how it ended with her--probably by the breaking up of the adhesions and a return of the bowels to their natural condition.

In some few cases there remains new tissue, which in time is partly broken up and remains partly attached. In this manner strings and bands of considerable strength can be formed, and into these loops the intestine may pass, so as to form an internal hernia of a very dangerous character. In some bands are formed across the intestine, which by contraction flatten the tube and obstruct the fecal movement. There is reason to believe that such bands and bridles are formed by local inflammation of such imperfect manifestation by symptoms that the patient knows nothing about it. A very striking case illustrating the possible sequence of this inflammation came under my observation early in my professional life: A colored woman about twenty-five years of age gave a very clear history of a peritonitis from the consequences of which she had suffered two years before I saw her. About six months after recovery she began to have constipation and to suffer from small and frequent discharges of urine. The latter gradually grew milky and to have a bad odor; the constipation grew more and more, and at length came to be absolute for many days; then would come a diarrhoea of some hours' continuance, after which she would have a feeling of relief. This was her state when I saw her. She was emaciated, and so feeble as hardly able to leave her bed. She vomited occasionally, and her appetite for food was all gone. The urine was heavily loaded with pus, and was ammoniacal. She died after a few weeks. At post-mortem examination a firm membrane was found strained across the upper strait of the pelvis, wholly separating the abdominal cavity from the pelvic. It looked like a drum-head. The left posterior border was drawn very tensely over the colon where it passed into the pelvic cavity, flattening it down completely and making stricture. To the under or lower surface the fundus of the uterus and the base of the bladder were firmly adherent, and in this way both were suspended. The effect of this unnatural suspension of the inactive uterus did not seem to be noticeable, but with the bladder it was very different: it contained three to four ounces of water, ammoniacal and full of pus, and it could never have emptied itself. The explanation is very simple. During the peritonitis a false membrane was effused on the pelvic viscera in situ. When the period of contraction which is common to all such structures came, the new membrane was separated from the greater part of these two organs, but not from their bases. The firm attachment to the brim of the pelvis did the rest. So unusual a sequel of peritonitis I think deserves a record. I should add there were no adhesions above the pelvis. Such a structure as this, found long after the active symptoms of peritonitis have passed, as also the bands and cords before spoken of, does not give support to the doctrine that the false membranes are broken down into fatty matter, and in this condition absorbed.

{1154} The possible remote effects of peritonitis are shown in a case reported by E. A. Mearns to the _Medical Record_, published Sept. 15, 1883: A young man, aged nineteen, four years after he had had acute general peritonitis was attacked with constipation, which was absolute. He had had before occasional attacks of pain in the bowels and constipation, which were overcome. But this was invincible. He had the train of symptoms usual in intestinal obstruction. There was no fever or tympanitis, and this time but little pain. He lived eight days. There was a tangle and a constriction of the intestines at the middle of the ileum, caused by the contraction and hardening of the effusion of the old peritonitis, and the intestine was very much softened.

H. B. Sands reports in another number of the same journal: "The patient was a man about thirty who had suffered from acute obstruction for a week. No exact diagnosis was made. When the abdomen was opened the intestinal coils were found extremely adherent one to another in consequence of a former peritonitis. A careful search failed to discover the nature or seat of the obstruction. The abdominal wound was closed, and the patient died soon after."

Peritonitis from Perforation.

There is no part of the gastro-intestinal canal that may not, from one cause or another, become the seat of ulceration. The jejunum is the part of the tube long supposed to be an exception to this rule, but even in it one or two observers have found ulcers. These ulcers often exist without distinctive symptoms, and may go on to cicatrization without announcing themselves. In the stomach, however, there are commonly indications which will admit a conjecture of their existence, and perhaps a diagnosis. Sometimes these ulcers penetrate all the tissues of the tube and allow the contents of the intestine to escape into the peritoneal cavity, or they may have destroyed all but the external layer, and some succussion, as in coughing, sneezing, laughing, or perhaps straining at stool, may make the opening complete, with the same results. In these cases it seems to be inevitable that inflammation should follow, unless it has preceded, the complete opening and sealed it up by adhesions. The tendency of such an inflammation is to be local and limited, but when the contents of intestines escape into the peritoneal cavity it usually becomes general. These accidents are usually attended by the sudden development of local pain, by rapid increase in the frequency of the pulse, paleness, and prostration. The perforation of the vermiform appendix is often a partial exception to this statement, for, while the local symptoms are marked, the sympathy of the general system is not so quickly awakened. The same can be said of perityphlitis. The symptoms are often local for some time--a day or more; sometimes subside, as if the disease were cured, and then return in full form. This is produced by the tendency of the inflammation to limit itself to the immediate neighborhood of its cause. Lymph is effused at a short distance from the point of irritation, and seals the parts together, so as to shut in the offending substance; and though this substance may produce pus in contact with intestine or appendix, that {1155} fluid is held for a time, as in abscess. It may be permanently held in its new-made sac till it burrows into some near part, as the intestine or bladder, or remain an abscess till opened by Willard Parker's puncture. On the other hand, the contents of this sac may be increased till it breaks bounds and causes extension of the peritoneal inflammation or general peritonitis. In one particular case this process of setting limits and breaking through them occurred in a young lady four times at intervals of from one to two days. When the limiting adhesions were established symptoms would subside, so as to encourage in her physicians the hope, even the expectation, of recovery; but again and again the fire was rekindled, and she died eight days after the first attack. In the greater number of cases the first breaking of the adhesions is followed by full peritonitis, and this often by death.

The perforations of the stomach which I have seen have not been attended by the severe pain described by most authors, but by a sudden prostration of strength and a feeling of disquiet and sinking at the stomach; more of collapse than of inflammation in the symptoms; no tumefaction of the bowels; almost nothing to indicate the nature of the accident, but a sudden new sensation in the bowels, a rapid increase in the frequency of the pulse, it growing small as it increases in rapidity, and a pale and shrunken countenance, and death in from twelve to thirty hours. Then, on inspection, hardly any signs of peritonitis are found. The peritoneal vessels are fuller and the membrane redder than in health, and its surface covered with the thinnest possible film of lymphy exudation, and some serum in the deeper parts of the cavity.

These ulcerations of the stomach are not always fatal by peritonitis. A few instances are recorded in which adhesions of the outer surface of the organ to adjoining organs have taken place, so as to protect the peritoneum almost wholly from the fatal contact with the gastric fluids, and death has occurred in some other way. I have a remarkable specimen illustrating this fact. It was taken from the body of a woman of about middle age who had long had symptoms of dyspepsia, and had from time to time vomited a little blood. It was not difficult to recognize ulcer, but the extent and peculiarities of it could be learned only by inspection. She died suddenly of copious hæmatemesis. On examination an ulcer two and a half to three inches in its several diameters was found, beginning near the pylorus and extending toward the left, which in this large space had destroyed all the coats of the stomach and exposed an inch and more of the right extremity of the pancreas and about the same extent of the liver. The liver and pancreas were both perceptibly eroded when exposed, and in the latter an artery that would admit the head of a large pin was opened. The stomach, outside of this extraordinary ulcer, was strongly attached to the adjacent organs.

The ulcerations of typhoid fever penetrate the intestine about three times in a hundred cases of the fever. This result is reached by the study of a large number of cases, and appears to be pretty generally admitted. The point where this perforation occurs is in the ileum, near the ileo-cæcal valve--within a foot or eighteen inches of it in the great majority of cases, although it has been known to occur seventy-two inches above the valve, and it has been seen very rarely in the cæcum. The fever itself may be either severe or mild. Suddenly severe pain {1156} sets in, oftenest in the lower part of the abdomen, and spreads rapidly; the pulse is quickly accelerated and becomes small; and it has been lately stated that in this and other intestinal perforations the gases of the bowels, escaping into the peritoneal cavity, will give resonance to percussion over the lower part of the liver. Fetid gas found in this cavity after death is not without importance; for example, a distinguished Senator at Washington died not long ago of a very painful abdominal disease which his physicians declined to relieve with opium, though the patient pleaded for it. His family physician at home was summoned. Although the distance he had to travel was many hundred miles, he found the patient alive and still suffering. He at once gave morphine for the relief of the pain, but the patient died. Now, this gentleman had diabetes a year or more before his death, recognized by his physician at home and also by myself. While under my observation the urine ceased to contain sugar and its quantity became normal, but soon after this albumen was occasionally found in it. The quantity was generally small, and casts were only found now and then. This new disease was mild, and seemed to be, within certain limits, manageable. He went to Washington under injunction that he was not to let official and professional labors bear with any weight upon him. This last sickness and the death would naturally enough be supposed to be some new phase or consequence of the previous illness. But, while a post-mortem examination was not permitted, the family wished to have the body embalmed. The family physician accompanied the embalmer, and as the latter made a cut through the abdominal walls there was a gush of air laden with fecal odor, and he through this opening saw the intestines covered with false membrane. He satisfied himself that the intestine was not opened. This fetid gas came from the peritoneal cavity. An ulcer had perforated the intestine somewhere, and caused the death. The final disease could be only remotely dependent on the patient's previous illness, if at all. His impaired health may have made the ulcer possible.

All kinds of perforations in the bowels, except those of the stomach, cæcum, and appendix, even the cancerous, have one history and the same symptoms; and if treatment is ever successful in such occurrences it must all be based on one set of rules--absolute rest, no pressure on the bowels, and no movements of the muscles that will aggravate it; food that will be wholly digested and absorbed by the stomach; complete abstinence from cathartic and laxative medicines, and the free administration of opium or morphine. By these means, I fully believe, numbers have already been saved from the fatal consequences of peritonitis caused by perityphlitis and perforation of the vermiform appendix--some under my own observation and others under that of my friends. A boy fourteen years of age was brought to bed by a pain in the right iliac fossa. After a few hours his father, a physician, desired me to see him. There was already a perceptible fulness, with dulness on percussion, in the fossa, and some febrile excitement. I gave a portion of morphine, and promised to call the next morning. In the morning a message came from the father stating that the boy was better and there was no need of further attendance. In the evening I was recalled. The pain had returned, and had spread over most of the bowels. He had general peritonitis. He took tincture of opium, of which I believe the largest dose was 100 {1157} drops, reached after three or four days of gradual but steady increase of dose. From that point the patient got better, and the quantity of the medicine was correspondingly reduced. There were a relapse and a repetition of the treatment, and again the disease yielded. During convalescence, about fourteen days from the attack, the boy, after emptying his bladder, was suddenly pressed to continue the discharge. Now he voided what appeared to be blood, two or three tablespoonfuls. It was, however, pus with blood enough to color it. This purulent discharge from the bladder continued for about three weeks, the boy steadily recovering his health. This occurred twenty or more years ago, and that boy is now a well-known physician. Similar cases could be recited.

In 1850, or thereabout, I attended a physician through an attack of typhoid fever. In the third week there was a sudden outbreak of peritonitis. The opium treatment was resorted to, and he recovered, and had good health for twenty years after. Peritonitis occurs rarely in typhoid fever from any other cause than perforation, and its occurrence in this case at this time, when perforation is more likely to occur, renders it probable, at least, that this attack was produced by that cause.

March 3, 1883, autopsy of Wm. Fletcher, age 59, iron-worker. On Friday last, Feb. 23d, he was attacked with pain in the region of the right iliac fossa; it was severe. There was no chill, but little fever, and only slight acceleration of the pulse. His stomach was a good deal disturbed, and the bowels were soon distended with flatus. I saw him on the Tuesday following, with James D. Elliott. The bowels were a good deal swollen and very resonant on percussion; pulse 84. His stomach was still greatly disturbed, so that he retained no food, yet there was no green vomit, but much flatulency. The movements in respiration were particularly noticeable, being nearly or quite as much abdominal as in health. There was a short friction sound in inspiration, but an entire absence of the sound produced by peristaltic action. There was no dulness on percussing over the iliac fossa, and no pain on pressure over any part of the abdomen. I was careful in examining the right fossa, for the first pain was there, and it was severe; but there was no physical sign by which the perforation could be ascertained. Still, my mind dwelt on the probability of perforation, and I expressed my fears to Elliott regarding it. The respiration was of natural frequency. The bowels had not moved for two or three days.

The next day Flint was added to the consultation. The symptoms had changed but little; the pulse was 102; no pain, no tenderness, no peristaltic action; slight friction at one point only; the abdominal respiration was as marked as before. Frequency of respiration, 18; patient sleepy; pupils only slightly contracted. When we were in consultation I again expressed my fear of perforation, but Flint expressed the most decided opinion as to its absence, because there was dulness to percussion over the liver. I had read his paper on the intrusion of gas between the ribs and liver in cases of intestinal perforation, and felt as if I were almost reproved for entertaining the thought without this physical corroboration.

Thursday, March 1st, the stomach had become much more retentive; there were no pain and no tenderness on pressure; pulse 109; no friction sound, no sound of peristaltic action, no dulness on percussion over right iliac fossa, but resonance over the whole abdomen, excepting over the {1158} pubes; there the resonance was not clear; over a small space there was dulness; this was ascribed to moderate fulness of the bladder, and, as there had been no difficulty in emptying it, nothing was said of it. The abdominal respiratory movements were the same as before.

Friday morning, at 3 A.M., no marked change had occurred in the symptoms, but from this time onward there was a steady sinking of the vital powers. The pulse grew small and frequent, the hands became cool, the breathing more frequent, and without any sudden change or new symptom he died early in the morning. At the last visit there was no resonance on percussion over the liver.

Autopsy, Saturday, March 3d, 2 P.M. The bowels were distended, as they mostly are in peritonitis, but not extraordinarily. There was now pretty free resonance over the liver. The section to open the abdominal cavity was carefully made, with the aim of ascertaining whether there was air or gas in the peritoneal cavity. When a half-inch opening was made through the peritoneum, gas was forced out through it for some seconds with an unmistakable noise. The bowels were not opened by this cut. The bowels exposed, a very thin film of false membrane was found on all the middle and upper portions of the intestines, with a fringe of injection where the folds came in contact. But two or three inches above the symphysis pubis the section opened a collection of pus which extended downward into the pelvis. Somewhere hereabout--neither of us could say exactly where--was found a lump of fecal matter, not indurated, as large as a marrowfat pea, the intestine still unopened. Search was made for the vermiform appendix. At first it was not recognized on account of its remarkable shortness. It was found, however, pointing directly toward the median line of the body, and was short because a part had been separated from the rest by slough. The end of what remained was marked by a border, one-eighth of an inch deep, of a very dark-green gangrenous color. We did not attempt to measure the quantity of pus. It was six ounces or more. It was completely bounded and shut in by adhesions.

At no time during life was there resonance over the liver, but there was some at the time of post-mortem examination before the bowels were opened, due perhaps to the fact that at death the relaxation of the muscles allowed the gas to rise higher than it did during life. The unusual median position of the abscess is important in accounting for absence of dulness, when it is usually found in slough or ulcer of the vermiform appendix.

"A Fatal Case of Typhlitis without Recognizable Symptoms." Under this title José M. Fisser published a case of inflammation of the vermiform appendix causing general peritonitis in a young woman nineteen years of age. The peculiarities of the case were that the appendix was not perforated, and consequently there was no tumor in the right iliac fossa--that the symptoms were all referred to the epigastrium, without even tenderness in the fossa. She walked the floor and tossed about in bed; the highest temperature was 103°, and the most frequent pulse was 120, and these continued but a short time. Of tympanitis there was none till near death, and then but little. The obscurity in diagnosis led to the publication of the case. The cause of this disease was fecal matter, not very hard, in the appendix.[7]

[Footnote 7: _Med. Record_, Sept. 1, 1883.]

{1159} As much has been said in this article on the diagnosis of peritonitis, it may be well to introduce a case where that diagnosis was conjectural, and yet quite another state existed. I visited Mrs. H----, when her disease was advanced, twice. My impression was that she had peritonitis, but this opinion was held with grave doubt. After her death, Smith sent me the following record of the autopsy: "Mrs. H---- died Friday evening at ten o'clock; next day, at three in the afternoon, we made an autopsy. No gas or fluid in the peritoneal cavity; the small intestines inflated almost to bursting, with injection of the capillaries. In the left iliac region we at once discovered a portion of the intestine almost black, and on examination found a firm white band encircling and constricting that portion. Upon liberating the gas the intestines collapsed, and the constricted portion was released and easily removed. A further examination showed that two of the epiploic appendages, coming off from the colon above the sigmoid flexure, had united at their extreme points and formed a loop two and a half to three inches long, and through this loop or ring a portion of the ileum had passed, and was there constricted. The constricted intestine was about four feet in length. This examination has been gratifying to me. There was a small quantity of bloody serum in the peritoneal cavity low down in the pelvis. The dark grumous blood that passed the bowels on the second and third days can now be accounted for, and corroborates your remark that the hemorrhage looked like strangulation. This was at your first visit. This must be a new cause of strangulation, and one that we could not anticipate."

There was, before I saw her, a single vomit of a suspicious fluid, but the evidence was not strong enough to enable us to pronounce it stercoraceous. Some of the observers noticed bloody serum in the peritoneal cavity, and perhaps some shreds of lymph, but that was in consequence of the strangulation.

Local Peritonitis.

This may occur anywhere in the broad extent of the peritoneum, and will be more or less limited in different cases, or may be limited for a time, and then become general. It is either acute or chronic. The product of the diseased action may be serum or lymph or pus, or all of them. The cause of this local inflammation is sometimes very obvious, in other cases wholly unknown. The consequences vary all the way from harmlessness to death; the symptoms are as variable as the consequences, making the diagnosis easy in some cases, in others impossible. Some cases in which it was not difficult to recognize it have already been recorded--those caused by perityphlitis and perforation of the vermiform appendix, for example. In such cases the local pain, the swelling, the dulness or resonance on percussion, depending on whether the tumor is made by inflammatory exudation or gas, together with the general symptoms and the history, leave but little ground for doubt regarding the character of the disease. Perhaps one-half the local abscesses which form between the folds of the peritoneum are recognizable during life by the local, associated with the general, symptoms. When situated in the posterior and upper part of the abdominal cavity, the hand gives little, {1160} perhaps no, assistance, as in the most widely-known case of abscess that has been recorded in all time. While the physicians were giving to the country hopeful reports day by day, thousands of medical men shook their heads and spoke sadly of the prospects. The illustrious patient was losing rather than gaining strength and flesh, his appetite poor, his digestion poor--a strong man growing helpless--and, above all, a pulse that for months never fell below 100. With an adequate cause of abscess, whether there were chills or not, what else could it be? Thus, in peritoneal abscesses that cannot be felt the general symptoms are of great importance to the diagnosis. When abscesses tend to discharge their contents soon or late--sometimes into the intestine, sometimes into the bladder, sometimes externally: in such cases there is a fair chance. Sometimes they burst into the peritoneum: such cases are almost inevitably fatal; even opium will not cure them. The pus of these abscesses often has the fecal odor, which it acquires by the transmission of the intestinal gases through the intestinal walls. I was attending, with the late James R. Wood, a young lady in whom peritoneal abscess had been recognized. It was anterior to the intestines. In the consultation, while we were discussing the propriety of using the trocar, the mother became alarmed at the odor and appearance of the urine just passed, and summoned the doctors back to the chamber. The abscess had opened into the bladder. The urine contained pus which gave off the fecal odor strongly. This patient recovered. It should be added that these abscesses, as well as those of the convex surface of the liver and those that are post-peritoneal, sometimes pierce the diaphragm and produce empyema, or by previous adhesion of the lung to its upper surface find a way into a bronchial tube, and so the pus is expectorated.

The history of local fibrinous exudations is not as easily told as that of the purulent. We find from time to time, on the peritoneum, bands, patches, or cords of false membrane, which were produced in so quiet a way that we can get no information regarding the time when they were formed, and perhaps the subject of them was not aware that anything was wrong with the bowels till he began to have the symptoms of obstruction. These unnatural structures are formed in great variety. The omentum is found thickened and contracted. The mesentery and mesocolon are seen in a similar condition, causing wrinkling and shortening of the bowels. The spleen has on its surface patches or even plates, or one great plate, of firm fibrinous deposit, often cartilaginous in density, sometimes calcareous; and we can rarely fix the time of these occurrences by any symptoms. It is not always so with the liver. We are acquainted with a perihepatitis which is acute, attended by pain in the right side, a febrile movement, and, if the inflammation reaches the under surface of the organ, by jaundice, and have learned to combat this with cups and opiates, the latter in rather free but not heroic doses, and to expect recovery in a few days. This may leave the liver wholly or partly invested with a layer of false membrane which may have a sequel of importance. Then, again, we find the organ invested with a thick contractile membrane, but cannot learn that the symptoms of perihepatitis have ever occurred. The diseased action which produced this bad investment appears to be analogous to that which not only covers the organ with a thinner coat of similar new tissue, but inlays it everywhere with the same material in cirrhosis. This also is {1161} unattended by local pain. The effects that may result from this encasing of the liver in a strong contractile capsule may be illustrated by the following case (the late Buck was the physician): The patient was an unmarried lady of middle age who had consecrated her life to charitable works. In searching for the suffering poor she often had to ascend several flights of stairs. The time came when she found this fatiguing and a tax on her respiration. She observed at the same time that the bowels were enlarged. She called Buck, and he had no difficulty in discovering ascitic fluid. He was surprised, as he knew that her habits were perfectly good, and she had very little the appearance of an invalid. Notwithstanding the proper use of the usual remedies for dropsy, the fluid slowly increased, and at length he was obliged to draw it off. He found it to be a clear, yellowish serum. In the course of about two years she was tapped four times. I saw her, with Buck, after these tappings, when the fluid had again been effused in quantity that half filled the peritoneal cavity. The emaciation was not considerable; there was nothing of the semi-bronzed color of the skin so common in cirrhosis of similar duration; her appetite and digestion were not materially impaired; the temperature was natural; the pulse was increased in frequency only a few beats. The skin over the abdomen was in a soft, natural state, and there was nothing that suggested a hyperæmic or inflammatory dropsy. The liver on percussion appeared to be reduced in size. Taking all things into account, and especially the patient's habits and the absence cancerous cachexia, it seemed probable that the dropsy arose from atrophy of the liver, and that the atrophy was caused by an adventitious capsule of the organ, although the patient had never had symptoms of perihepatitis. From this point the fluid did not increase or diminish, but remained stationary till she died, perhaps two years after, of some other disease. Meanwhile, the lady resumed her favorite charity-work to a limited extent. At the post-mortem examination the capsule was found investing nearly the whole liver, but not materially obstructing the gall-duct. The new membrane was thick and strong, having a thickness of at least one-twentieth of an inch. The remaining liver structure was of natural appearance. The organ was reduced to one-half its natural size. No other cause of dropsy was found.

Chronic Peritonitis.

I have doubted whether any disease deserving this name really exists independent of such low inflammatory action as may arise from the irritations of tumors or heterologous deposits. This statement refers to general not local peritonitis. I have never seen anything that would lead me to believe that acute diffuse peritonitis can be deprived of its acute character and still continue an inflammation. With me it has always been death or cure. I have already referred to a case in which after recovery the bowels were greatly disturbed by tympanitis for years. But this came from adhesions: her general health was good. I have at long intervals met with cases of ascites in which the peritoneal membrane was redder than natural, and in which no obstruction to the portal {1162} circulation was discovered. This, however, I have regarded as hyperæmia rather than inflammation.

Bauer,[8] however, gives to these cases the title latent general peritonitis, especially when after death an abnormal adhesion is found here and there. In the cases that I have seen there was a peculiar state of the surface of the abdomen. The skin there was more or less scaly and dry, but I do not remember whether there were internal adhesions. Bauer regards the diagnosis of this form of disease as difficult, but refers to the constantly present meteorism as well as serous fluid. I have met with three or four instances in which at the time of puberty an abdominal dropsy has rather suddenly occurred, lasting one to three months, and disappearing on the use of diuretics. I have had no reason to attribute this effusion to inflammatory action, except in one case. A lady of extraordinary symmetry and beauty of form, in excellent health, whom I had treated for this disorder twelve years before, applied to know whether there was anything in that disease that would prevent her having children. She had been married seven or eight years, and had not been pregnant. The question then occurred to me, At the time of the dropsy could there have been lymphy exudation that has since confined the ovaries in an unnatural position? The question I could not answer. The treatment which Bauer prefers for his latent peritonitis consists in "painting with iodine, the use of diuretics, and the regulation of diaphoresis by means of Turkish baths."

[Footnote 8: _Cyclopædia of the Practice, etc._, vol. viii. pp. 297-302.]

Another form of general chronic peritonitis is, according to Bauer, that which follows acute peritonitis. He quotes several authorities in support of his views. I must draw on him for a description of it, for, as I have said, practically I know nothing about it.

The symptoms of acute peritonitis are all toned down, but do not all disappear. Vomiting occurs occasionally; tenderness is diminished, but is quite perceptible; meteorism diminishes, but fluctuates greatly; appetite is poor or variable; constipation alternates with diarrhoea or is followed by dysentery; now there is a febrile heat, and then the temperature is normal--this fever is most likely to come in the evening; the pulse is frequent and varying; ultimately extreme emaciation and anæmia. The most striking feature of this condition appears to be sacculation of the fluid in the abdomen, wholly or partially; this fluid then is not freely movable, but will give dulness on percussion, which may contrast well with intestinal resonance in its immediate neighborhood. When the tension of the abdominal wall is diminished these sacs can be felt by the hand as uneven tumors. Colicky pains occur, and in a case cited it was at one time very severe, at another only slight. The majority of the cases terminate, after a protracted course, fatally. Recovery may occur by absorption or external evacuation of the fluid. He gives no special treatment.

Bauer makes still another class of cases of chronic peritonitis--those arising in the course of old ascites; he, however, does not make much out of it. He thinks the cases of this kind occur with cardiac and hepatic disease, and particularly with the nutmeg liver. The symptoms, he admits, are neither well defined nor severe, and the anatomical changes consist "in thickening of the serous membrane by a slight deposit of fibrin, {1163} slight turbidity of the ascitic fluid, and a few flakes of fibrin suspended in it." He then, strangely, gives, as if they were illustrations of such a disease, two cases in which death by acute peritonitis followed the last of many tappings, in one of which a pool of pus was found encysted in front of the intestines. Both are borrowed.

Probably most practitioners who are in the habit of making post-mortem examinations have seen the flakes of lymph in the ascitic fluid, etc., but the German physicians have been the first, I believe, to regard such cases as belonging to separate forms of disease.

William Pepper has published[9] a case observed by himself and G. A. Rex which shows non-malignant chronic peritonitis better than any I can recall to mind. The report forms the sequel to the case of the young woman on whom he successfully performed paracentesis of the pericardium.

[Footnote 9: _Am. Journ. of Med. Sci._, April, 1874.]

This young woman began to have double pleuritic effusion, and this was soon followed by ascites three and a half months after the operation. From that time the ascites was better or worse, but did not wholly leave her, and became considerable before her death. This was sudden, she having some convulsive movements in extremis. Lesions were found in the thoracic cavity like those discovered in the abdominal, showing, it was believed, a special tendency in this person to plastic exudation on the serous membranes. "The lower part of the abdomen was found occupied by an extensive effusion. The intestines were floated upward. There were few if any signs of inflammation of the intestinal peritoneum, but marked changes were observed in the parietal peritoneum and in the capsules of the liver and spleen. The peritonitis was most marked in the upper segment of the abdomen, while the parietal membrane presented large patches of irregular thickening. No tubercles were found on any part of the peritoneum. The capsules of the liver and spleen were greatly thickened, whitish, opaque, and densely fibrous. The liver was enlarged and heavy, and so tightly bound by its thickened capsule that its shape was somewhat altered.

"The diaphragm, especially that part of it underlying the pericardial sacs, had undergone marked fibroid degeneration. The muscular tissue was much atrophied; many fasciculi had evidently disappeared, while many others were markedly narrowed, some of them shading off to a width of less than 1/3000 of an inch, and finally disappearing altogether. They retained, however, even in their narrowest dimensions, their transverse striæ."

(It may be remarked, in passing, that this substitution of fibrous for muscular tissue follows the same law that it does in the heart when that organ is the seat of fibrosis or fibrous degeneration. Here it was supposed to be the consequence of a low grade of inflammatory action. Is it when it occurs in the heart?)

In the abdomen these observers found nothing which suggested the possibility of tubercles or any obscure form of cancer. In the pericardium, on the heart side, were found numerous small nodular roughnesses. Irregularities of the pericardial false membrane are so common that nothing but the close and universal adhesions would raise any question of these relations. But tubercles would hardly be here and nowhere else.

{1164} Delafield says that one form of the chronic disease is the continuance of his cellular peritonitis. In this, he says, the surface of the omentum is covered with cells which look as if they were derived from the endothelium and connective-tissue cells, although they differ from the normal shape of these. The new cells are for the most part polygonal, of different size, with one or several nuclei, and giant-cells--large granular masses filled with nuclei. Although these new cells are produced over the entire surface of the peritoneum, yet, as a rule, they are more numerous in little patches here and there. These little patches may be heaped together in such numbers as to form nodules visible to the naked eye. There is never any stroma between these cells.

This form of peritonitis occurs most frequently with organic heart disease, with cirrhosis of the liver, with chronic pulmonary phthisis, and with acute general tuberculosis. In the two latter diseases he thinks they have been improperly called tubercles.

He describes a form of chronic adhesion of peritoneal surfaces that occurs without the intervention of fibrin, but, as he supposes, by coalescence of the branching cells and a production from them of a fibrillated basement substance, the fibrils crossing in all directions. In the midst of these fibrils he finds the nuclei of these cells. He finds also in the immediate neighborhood of these adhesions thousands of branching cells that are attached one to another and float free in the water, the fixed end being attached to the peritoneum. He regards such a peritonitis with adhesions as a more advanced stage of the forms of cellular peritonitis already described, and the new cells are changed into membrane.

Sayre has published an extraordinary case in the _Transactions of the Pathological Society_. He calls it chronic proliferative peritonitis; it might be called more aptly the consequence of peritonitis.

A large, strong man fell from a hammock, the rope breaking, upon his shoulders, and felt a severe pain in his stomach, and soon developed symptoms of peritonitis. This pain never entirely subsided. The peritonitis was recognized. About one month after he was tapped, and 240 ounces of serum were drawn. He was tapped one hundred and eighty-seven times, and 1203-5/16 pounds of fluid were taken from him during the remainder of his life. At post-mortem examination 3000 cc. of yellow serum were found. The liver and spleen were covered by a thick layer of false membrane, intestines were glued together in the upper part of the abdomen, and the stomach was adherent to the lower surface of the liver. The portal vein was contracted by this membranous coating. There were numerous other lesions in the heart and pleura, but these will account for the dropsy.

This man was unusually strong and hearty until 1876, when he had an attack of double pleuro-pneumonia, and in 1878 he slipped on the front steps and fell, but seemed to recover from the effects of this. The fall from the swing occurred in July, 1879. He died in February, 1884.[10]

[Footnote 10: _Med. Record_, April 19, 1884.]

{1165} Tubercular Peritonitis.

This form of disease is by no means uniform in its first symptoms or in its progress. The only things uniformly attending it are tubercles on the peritoneum and more or less of inflammatory effusion, chiefly lymph and serum; tumor and hardness of the bowels, general or local; deranged function of the stomach and intestines; emaciation; and extreme fatality.

In some cases the invasion is acute and marked--a chill followed by fever, vomiting, early development of meteorism, and in a few days a point or points of resistance to pressure, but not necessarily dulness on percussion. In a few days the febrile action and the meteorism may subside, leaving the symptoms of local peritonitis. But we have not long to wait for a renewal of them and an evident extension of the inflammatory action. Remission and relapse alternate at varying intervals, until the whole extent of the peritoneal surface seems to be involved in inflammation. With this mode of development meteorism may not be renewed in the most common way. The lymphy product of inflammation may so bind the intestines to the posterior walls of the abdomen that they cannot extend forward, but are pushed upward against the liver and diaphragm, and so encroach on the thoracic space. But then the anterior parietes are tense and hard, and do not move in respiration. The febrile heat may not continue more than two or three months, but the pulse will be frequent to the end. There will be a thinning of bowel walls, and here and there a knuckle of adherent intestines may cause some prominence and give some resonance on percussion. There will be also occasional vomiting, and the dejections will be irregular--maybe only deficient or thin; there may be an alternation of constipation and diarrhoea.

Tuberculous ulcerations of the mucous layer of the bowels is not uncommon in tubercular peritonitis, and these ulcers have in rare cases perforated and allowed the fecal matter to accumulate in considerable quantity in a sac limited by previous adhesions. In all forms of tubercular peritonitis death is caused as often by grave complications as by what appears to be the primary disease. The affection occurs in probably every instance in those who had at the beginning, or had acquired in its progress, what we call the tubercular diathesis. We are not surprised, therefore, to find on inspection a wide diffusion of tubercles in the body, particularly on other serous membranes, and in the lungs. Death may occur, then, from phthisis pulmonalis or from pleurisy or meningitis, as well as from the exhaustion and accidents of the peritoneal disease. The effusion serum or turbid serum is very common in tubercular peritonitis, and can be recognized by the dulness it produces in part of the cavity, and sometimes by fluctuation. It is often sacculated, but it is not constantly found after death, it having been absorbed before, and perhaps long before, that event.

In other cases the invasion of the disease is stealthy and deceiving. It comes so quietly that the patient is not conscious of any local disorder beyond a dyspepsia and irregular action of the bowels. He has a pulse of growing frequency, but if he knows it he ascribes it to his dyspepsia. He is slowly losing flesh and strength; this he accounts for in the same way. At length a perceptible swelling of the bowels attracts his attention. At this stage the physician finds that the swollen bowels are tympanitic everywhere or only in the upper, while there is evidence of fluid {1166} effusion in the more depending, parts. He discovers some, it may be little, tenderness on pressure, and a pulse of 85, or maybe 90, increasing in frequency toward evening. The appetite is poor, the digestion slow, and occasionally there is vomiting; the complexion is pale and a little dingy; the skin of the abdomen may be dry and rough or may be natural; some colicky pains have been or soon will be felt. From this point the disease gradually advances. The distension of the bowels slowly increases or they are firmly retracted; the emaciation increases; the strength diminishes; there is often cough, which is generally dry; the bowels are slow or diarrhoea alternates with constipation; with the distended bowels there is always more than natural resonance on percussion, except when there is fluid effusion, though not often the full tympanitic sound observed in acute diffuse peritonitis. This resonance is not equal, always, in different parts of the abdomen; the respiration is embarrassed and almost wholly thoracic. The abdomen is often as large as that of a female at full term of pregnancy, and indeed the condition has been mistaken for pregnancy. This is an inexcusable blunder in a case like that which I have in mind--a young unmarried woman. She had no dulness on percussion in the space that would be occupied by the gravid uterus, but rather resonance. The case might have been a little less clear if there had been fluid effusion in the abdominal cavity, but if this were not encysted it would flow from one side of the abdomen to the other when the patient turned correspondingly in bed; if it was encysted, there would be small chances that it would have the shape and position of the gravid uterus; if it had, there would be no chance of hearing in it the foetal heart or feeling the foetal movements; and after all this there remains the experimentum crucis--a vaginal examination.

At first the diagnosis is unavoidably uncertain. Some aid is found, possibly, in the medical history of the family, in tuberculous antecedents, yet I remember cases in which no phthisis could be found in any living or dead member of the family on the paternal or maternal side as far back as it could be traced. Some aid is found if the patient himself has any of the physical or rational indications of pulmonary phthisis, and yet there are recorded cases in which the abdominal symptoms were the first to appear. The prominent German physicians attach great importance to the pre-existence of a cheesy mass or degeneration somewhere in the body as the real parent of tubercles wherever they appear. The truth of this doctrine, I do not think, has received anything like universal recognition; and if it had, as this cheesy degeneration is often, perhaps commonly, only discoverable after death, it could rarely give any assistance in diagnosis, so that the early diagnosis is always difficult, and a very early one often impossible. But as time goes on, and the symptoms are better defined and show themselves one after another as they are above described, it seems as if a careful observer could not confound it with anything except perhaps one of the other forms of chronic peritonitis or cancerous peritonitis. As to the latter, the cough which exists in most cases of tubercular peritonitis will assist in the distinction, but a physical examination much more; for a cough does not always attend phthisis when this disease exists; for example, I visited a daughter of one of the distinguished gentlemen of Vermont. She had had the bowel symptoms that indicated tubercular peritonitis for eight or ten months, and the diagnosis was not {1167} difficult. Remembering Louis's opinion that if tubercles invade any other part of the body, they are likely to be found at the same time in the lungs and in a more advanced condition, I examined the lungs, and found in the upper part of the right a cavity so large that it could have received a fist. I was only surprised by the fact that she did not cough, and had not coughed. She herself assured me of that (she was twenty-one years old); her physician, who was present at the visit, had never heard her cough, and had no suspicion of any pulmonary complication; but, more than all, her mother, who had walked with her, slept with her, eaten with her, travelled with her, and from the beginning of the illness had not been out of her company more than twenty minutes in any twenty-four hours since the disease began, had never heard her cough. Here, then, the nervous deviation to the abdomen, or whatever else it may have been, had so benumbed the sensibility of the pulmonary nerves that the alarm-bell of phthisis had never been sounded; but the cavity, had there been any doubt whether the bowel disease was cancerous or tuberculous, would have almost fully settled the question. But more of the peculiarities of cancerous peritonitis a little farther on.

The lesions of this disease (or its pathological anatomy) differ considerably, but the differences are in the amount of tuberculous deposit and the secondary results, not in the real nature of the disease. Lebert has published among his plates of pathological anatomy one which shows the peritoneum thickly sprinkled over with small tuberculous grains, and represents each particular grain surrounded by a little zone of inflammatory injection. There is yet no exudation, but that would soon follow. A fibrinous exudation will soon come over this primary deposit, and undergo a kind of organization, or at least get blood-vessels, which in their turn can furnish the material for a new crop of tubercles. These again provoke a new layer of fibrous tissue, which also becomes studded with tubercles, and so on, till a thick covering is formed over the intestines. But the same material is interposed between their folds, separating one from another and compressing them and diminishing their calibre; at the same time this agglomerated mass is firmly adherent to the abdominal walls everywhere. The new material may have a thickness of half an inch or even more. I remember how surprised and confused I was when I made my first inspection of such a case. The abdominal walls were cut through, but they could not be lifted from the intestines, but were firmly adherent to something. They were carefully dissected off and the bowel cavity (?) exposed; there was apparently an immense tumor filling the whole space: no intestines, no viscera, could be seen. A section was made through this mass from above downward, and another parallel with it and an inch distant from it, and this part removed. It appeared like a large, hard tumor, through which the intestine made several perforations. The new material appeared to be fibrous, with grayish-white tubercles sprinkled in through it everywhere, and pretty abundantly. In another case this fibro-tubercular material may occupy one part of the abdomen, and a large serous cyst or serous cysts another. The tuberculo-fibrous material may be found in markedly less quantity than is so far described, till there will be no more than in a case from Ziemssen's clinique, quoted by Bauer: "In the peritoneal cavity about four liters of yellowish-brown, slightly turbid fluid. Omentum {1168} thickened, stretched, adherent to the anterior wall of the abdomen and beset with hemorrhages; the same was true of the parietal peritoneum; between the hemorrhages whitish-yellow and entirely white tubercles occur, varying in size from the head of a pin to a lentil. The intestinal serous membrane was similarly invaded. The intestines intensely inflated; a number of ulcers on the mucous membrane, one approaching perforation. Covering of the liver thickened by fibrinous deposition."

The lungs and serous membranes generally will, in all probability, show more or less of tubercular deposit, the pericardium less frequently than the others.

The result in this affection, after it is fully established, is believed to be uniformly fatal, and at its commencement the difficulty of diagnosis may lead one to doubt whether his apparent success is anything better than apparent. Still, a plan which I have relied on is, I believe, worth announcing. As soon as the disease is recognized the patient is put upon the use of the iodide of potassium and the iodide of iron, in full average doses, and a solution of iodine in olive oil is applied to the whole surface of the abdomen by such gentle friction as will produce no pain; and after a minute or two of such friction the oil is brushed thinly over the surface and the whole covered with oiled silk. This dressing is repeated twice a day. The quantity of iodine to an ounce of oil will vary considerably in different persons; for some, seven to ten grains will be enough; for others, thirty will be needed. The iron is to make the application moderately irritating, and if it produce pinhead blisters or blisters a little larger, all the better. When the application becomes painful the oil is washed off, and the application is not renewed for two or three days. In this manner it may be continued for two or three months. Meantime, the patient is put upon the diet and regimen of the consumptive, the appetite encouraged; he takes sustaining food, with plenty of milk and cream, or cod-liver oil, as much fresh air as possible, and friction is applied to other parts of the body with dry flannel.

Cancerous Peritonitis.

Benign tumors of the abdomen are not frequently the cause of general peritonitis, and when they are, the grade of the disease is acute rather than chronic. They very often provoke local inflammation and become adherent to the neighboring structures. The same is true of malignant growths in the abdominal cavity, except that the adhesions are earlier formed and more likely to occur. Localized cancer, of whatever variety, is not very prone to produce general peritonitis, even though there be multiple developments of it. But when the disease takes the disseminated form, and is sprinkled over the whole extent of the peritoneum, then inflammation is almost certain to occur--not of high grade, and yet deserving the name subacute rather than chronic. A case which illustrates this statement has come under my observation within the last year. I will recite it with sufficient detail to make it intelligible.

A lady about forty years of age had, up to the summer of 1881, enjoyed very good health, though she was never robust. At that time she felt her strength abating and her stomach disordered. She sought {1169} health in various places, and took professional advice in September. It availed her little; the bowels were gradually swelling and fluctuation could be felt. She was losing strength and flesh. There was not a cachectic countenance, but the features were growing sharp. She had suffered but little from pain till October. At that time she was at the family country home. Then she began to suffer from a severe pain in the left thigh; and this, it was noticed, increased as the accumulation in the bowels increased, and at length her physician felt compelled to tap her--not so much on account of great distension of the bowel as in the hope of relieving the pain. He drew off nine quarts of gluey, viscid fluid, and her pain was wholly relieved. Twelve or fifteen days after this she was brought to her city home, and her city physician, seeing that her case was a grave one, sought the aid of a distinguished gynæcologist. She was then again tapped to give him a more satisfactory examination. He found the ovaries considerably enlarged and hard. They could not, however, be felt by pressing the fingers into the pelvis from above--only by the vagina. I saw her on the 10th of November. The fluid had again made considerable tumefaction of the bowels, and she was again suffering great pain in the region of the right kidney and in the leg of the same side, together with cramps. The relief given by the first tapping induced us to propose its repetition. It was, however, delayed till the 14th, that the physician who had tapped her before might be present and assist. The quantity of water drawn was again nine quarts, and again the pains and spasms were quieted. The examination of the abdominal fluid was interesting. It was nearly clear, reddish, of syrupy flow and consistence, and so viscid that while a portion of it had remained on the slide of the microscope long enough for the examination of its constituents the thin cover became so firmly attached to the slide that it could not be removed without breaking or long maceration. The albumen was so abundant that the fluid was completely consolidated on boiling. Fibrinous threads were running through it in great numbers, and here and there was a cell of large size, round, granular, but not plumped up with granules, with a nucleus barely less in size than the cell itself; its outer border within, but only just within, the boundary or wall of the cell. It was the nucleus that was granular, for there was little room for granules between the nucleus and the cell wall. The vial containing the fluid had been standing three or four hours for a sediment. This in a vial four inches high occupied the lower half, and gave nothing to the dropping-tube till the sedimentary matter was drawn into it by suction. This matter consisted of fibrillated fibrin in large quantity; a great number of the cells just described, some grouped, but most separate or single. There were pus-cells in moderate quantity, each having the amoeboid movements, and a considerable number of red blood-corpuscles, some of natural form, some crenate.

Immediately after the tapping the flaccid condition of the abdominal walls admitted an examination. A solid, hard mass was found running across the upper part of the bowels, a nodule of which was lying on the stomach at the point of the ensiform cartilage. A harder mass of irregular shape was also found just above the pelvis on the right side, extending upward and to the right. This was in extent two by three inches. The ovary, however, could not be detected by pressure from above {1170} downward. The diagnosis up to this time was hardly doubtful, but these revelations made it complete, and crushed any lingering hope of the patient's recovery.

While the pain and spasm ceased after the tapping, the oedema of the left leg, which came on some time before the last tapping, did not diminish. The hard spot near the right iliac fossa was tender on pressure, but otherwise hardly painful. While the fluid did not exceed six quarts or so, she had little pain anywhere. There were no external glandular swellings. Her appetite was poor, and she took but little food. She vomited very little till the end was approaching. The urine contained a few globules of pus, some pigment matter, two or three hyaline casts, but no trace of albumen. For sixteen days following November 14th the patient was comfortable, but the fluid was slowly filling the bowels again. At that time the pains already referred to began to return. On December 5th they required another tapping, and preparations were made for it, but vomiting, rather severe, led to its postponement to the next day. The quantity of fluid drawn was nine and a half quarts. It was of the same syrupy consistence as that previously drawn, and under the microscope showed exactly the same constituents and gave the same quantity of albumen. The next day stercoraceous vomiting commenced, with no movement of the bowels, except what was produced by 10 grains of calomel given on the second day of this vomiting. That acted well and produced a temporary relief. She after this took no food by the mouth, but milk and beef-tea were injected into the rectum. Still, the fecal vomiting returned, and she died on the 15th.

The post-mortem examination was made on the 17th by William H. Welch. I could not attend it. His report is complete as to the main features of the case, though it does not furnish an explanation of the spasms and the oedema of the left leg, regarding which Welch was not informed. The pain and spasm were doubtless due to backward pressure of a diseased part on a nerve or nerves, and the oedema to a narrowing of the iliac vein by pressure or constriction by fibro-cancerous matter on its outer sides. "The peritoneal cavity," he says, "contained somewhat over a gallon of clear, yellow serum. Both the visceral and parietal layers of the peritoneum were thickened, in some places more than in others; this was especially marked on the anterior of the stomach and on the lower part of the ileum and in the left iliac region. The omentum was greatly thickened and retracted into a firm mass (or roll), which extended somewhat obliquely across the body, more to the left than to the right. The mesentery was much thickened and contracted, drawing the intestines backward. In a few places only was the peritoneal surface coated with fibrin, and the intestines were mostly free from adhesions. The coils of the lower part of the ileum, however, were firmly matted together by organized connective tissue in such a way that they were twisted, often at a sharp angle, so as greatly to constrict the calibre of the gut. The serous and muscular layers of the intestine at this point were greatly thickened. By these causes there appeared to be a complete obstruction at a point about six inches above the ileo-cæcal valve. By careful dissection these coils were straightened out, so as to remove the main cause of obstruction. The peritoneal covering of the liver was adherent to the parietal layer.

{1171} "The surface of both the visceral and parietal peritoneum was studded over with hundreds of small, firm, whitish nodules, generally not larger than a pea, and often not larger than a pin's head. In some places they had coalesced and made firm patches an inch in extent. This same material was found in the contracted omentum in considerable quantity. In a few places, particularly on the uterus, a blackish pigmented deposit appeared.

"The ovaries were not adherent, but both were enlarged to the size of a hen's egg. The outer surface of each was rough and corrugated. The new growth was deposited on the exterior and penetrated each a quarter to half an inch. It was of uniform white color and of firm consistence.

"The stomach wall was thickened nearly throughout its extent, but particularly in the anterior part, where it amounted to thrice the normal thickness. This consisted wholly of hypertrophy of the muscular coat and increase of fibrous tissue in the peritoneal layer. This new growth was traced, in the interlacing bands, from the surface into the muscular coat. In the outer layer of the stomach were found three small white nodules. The mucous membrane of the organ was healthy or a little pale.

"The retro-peritoneal glands along the aorta were enlarged, soft, and of a reddish-gray color. A nodule was found in the wall of the duodenum outside the mucous membrane, and one in the Fallopian tube."

Every organ in the abdomen and chest was examined, but nothing important found except what is here recorded. Welch concludes his record with the following diagnosis: "Primary scirrhous carcinoma of the ovaries. Secondary deposits in the peritoneum, in the outer layer of the right Fallopian tube, of the stomach and duodenum, and in the retro-peritoneal glands. Chronic peritonitis, intestinal obstruction."

This case presents to the reader so accurately the usual course of cancerous peritonitis, and the inspection its lesions, that a treatise on the subject is hardly called for. It often happens that cancerous antecedents in the patient or his relatives will lend an aid to the diagnosis, which this case did not present. To distinguish this disease from tubercular peritonitis no question can arise except in its dropsical form, and then the lungs in every case of the latter that I have met with have the physical signs of tubercles, though not always the rational indications. The pulse is much more accelerated in the tuberculous variety. I omitted to state that the temperature of this patient was often taken, and till the closing scene was never found more than one or two degrees above the healthy standard, and the morning and evening heat did not materially vary; the opposite of both, then, would be expected in a tuberculous case. The existence of meteorism is much more common in the tubercular disease; indeed, in the cancerous case recited there was none of it. The duration of the two is different--that of the cancerous kind is recorded in months, while the tuberculous variety may continue two years. The cancerous is more likely to be attended by alarming accidents, like the complete obstruction of the bowels, large hemorrhages, and a sudden lighting up of acute peritonitis. Finally, in the light of the case here recorded, it seems probable that the examination of the abdominal fluid will become of great importance. I have never carefully examined the fluid of tubercular dropsy, but it does not seem probable that it will have the syrupy {1172} appearance, the large amount of albumen, the abundance of fibrin-fibres, and the granular large cells with nuclei only perceptibly less in size than the cells themselves, that were repeatedly found in this case--found by two observers, and at every tapping after the first.

TREATMENT cannot be curative; it therefore consists of such administrations as will relieve pain, give sleep, improve the appetite, increase the flow of urine if it be scanty, and relieve the bowels if there is a tendency to constipation. It is as much the duty of the physician to put off the fatal day, when he can, in incurable affections as it is to cure those that will yield to his prescription and advice. In the case just narrated opium or an opiate alone produced such unpleasant after-effects that she was unwilling to take it, but when the extract of belladonna was given with it she slept pleasantly, and could take her food the next day.

Infantile Peritonitis, or Peritonitis of Childhood.

Bauer, in _Ziemssen's Cyclopædia of Practice of Medicine_, and Wardell, in _Reynolds's System of Medicine_, have each devoted a chapter to this form of disease. They refer to the fact that the foetus may have peritonitis before birth or be born with it, or may have it when a few days old. They say that this form of the disease occurs most frequently in lying-in asylums or foundling hospitals, and that it has been supposed to depend on a syphilitic taint. They say, too, that it follows erysipelas, scarlet fever, measles, etc. I do not perceive that the description of either of these authors makes any marked distinction between this and the same disease in adults, except what may arise from the inability of the infant to describe its sensations, and the more rapid course of the disease to a fatal result--in some cases twenty-four hours. Having myself had no obstetrical practice, or next to none, I have nothing to add to their statements, and can from my own knowledge abate nothing. I therefore refer the reader to these chapters, and to the references given by the first of these authors, for a fuller knowledge of the matter.

Regarding the comparative exemption of children, after the first few weeks of life, from spontaneous peritonitis, referred to by one of these authors, I can fully confirm his statement. Though I have assisted in the treatment of many children suffering from peritonitis, I have difficulty in recalling to mind a single case in which the disease was not caused by perforation of the intestine or vermiform appendix of the cæcum, and in much the greatest frequency perforation of the appendix.

B. F. Dawson,[11] after reciting a case in which the liver had undergone a peculiar degeneration and was attended by peritonitis before birth, states that Sir J. Y. Simpson observed nine cases in his own practice "and notes more than a dozen from different sources." These cases seemed to have been caused by the ill-health of the mother during gestation, or excessive labor, injuries, venereal disease, and were mostly attended by grave disease; the viscera often, the liver; but sometimes the mother was perfectly healthy, and the peritonitis was the primary disease. Death almost always occurred in utero or shortly after birth. In one instance the child recovered.

[Footnote 11: _N.Y. Med. Journ._, Dec., 1882.]

{1173} The _Med. Record_ takes the following from _Schmidt's Jahrbucher_ for Jan. 7, 1883: "Dr. Oscar Silbermann recognizes two varieties of peritonitis in the new-born. The non-septic or chronic is developed usually in the first third of foetal life, and is generally syphilitic in origin. If the peritoneum covering the intestines be involved, as well as that over the liver and spleen, various forms of intestinal obstruction may result. Most frequently there is occlusion of the anus, less often stenosis or complete stricture of the small intestine. Of a number of cases of congenital occlusion of the intestine collected by the author, all ended fatally, only one living beyond twelve days.

"The second, acute or septic, form of peritonitis in the new-born the author divides into two varieties, according as the peritonitis is only a part of general infection or is the sole manifestation of the septic poison. In either case the point of entrance of the poison is always the navel wound. The symptoms, which need not all be present in a given case, are vomiting, watery stools, meteorism, ascites, abdominal tenderness, icterus, etc. The pulse and temperature may vary in degree in different cases. A cure of the septic form is possible; therefore the treatment should be carefully considered. The navel wound should be cleansed, and the child is to be isolated from its mother. To control the fever quinine may be given. Priessnitz's sheet is of value; vomiting may be checked by chloral (one-half to one grain in water). The strength should of course be maintained by stimulants if necessary."

Ascites.

The accumulation of fluid indicated by this name has already been referred to in its relations to several causes. There are, however, conditions producing it which have not been considered or only considered partially.

The most prolific source of abdominal dropsy is obstruction of the portal circulation on its way to or through the liver. Condensation of the liver structure in cirrhosis, with destruction of many of the portal capillaries and compression of many more, is prominent in this connection. The compression of the liver caused by an adventitious external covering, referred to under the head of Local Peritonitis, acts similarly, whether it compresses the vein at its entrance into the liver or not, although it is not known to produce any destruction of the portal capillaries. Some enlargements of the organ are attended by the same result, but they are always associated with a hardening of its structure. The disease lately called waxy liver, now often denominated lardaceous, belongs to this class, as does that condition in which the organ is enlarged, hardened, and fissured, regarded as syphilitic liver. That both these diseases may have a syphilitic and mercurial origin is not a point now under consideration. They both harden the hepatic structure and obstruct the portal circulation, while they may not in equal degree hinder the progress of arterial blood. This is explained when we remember the diminished force that propels the portal blood. Neither of these diseases produces dropsy early in its progress, but, as I have seen it, always before it reaches its fatal termination. Fatty liver has not, in my observation, produced dropsy, {1174} although I have seen livers made very large by that disease, and the absence of dropsy when the liver has been large has aided me in distinguishing it from the waxy disease. Cancer of the liver in some instances does, and in others does not, produce dropsy of the bowels. It is only certain to have this result when a tumor is in position to press upon and obstruct the portal. Hypertrophy of the liver, caused by mitral regurgitation or other disease of the heart, does not generally produce dropsy, but, aided by anæmia or watery condition of the blood, such a result is possible. In children, however, it is not very rare to see the bowels distended by dropsy, and to discover that the liver is enlarged at the same time. It is common in such cases that the dropsy and the hypertrophy disappear after a few weeks of treatment. This may occur in a child that is anæmic, but without any disease of the heart. Such a case was brought to me two or three months ago, and after four weeks of treatment by tonics and diuretics the health was re-established. There is one point in these cases of some importance. When the child lies on his back, if the abdomen is much distended, the liver cannot be felt. It has sunk away into the fluid, and in this position ordinary percussion cannot ascertain its dimensions. In the July number (1840) of a quarterly journal edited by Swett and Watson, I published an article in which I reported the conjoined labors of the late Camman and myself on a new method of combining auscultation and percussion, with its results, under the heading "Auscultatory Percussion." By the method described in that article--viz. by placing a solid stethoscope, or for that Laennec's first stethoscope, a rolled-up pamphlet, on the chest at a point where the liver has not fallen away from its walls, and percussing on the abdomen from below upward--a point is reached whence the percussion sound is brought sharply to the ear, while half an inch below the sound is dull and distant. The lower edge of the liver is thus easily recognized, and its upper boundary is found in a similar manner or by ordinary percussion, so the difficulty of measurement disappears.

In such case, when the dropsy disappears and the liver recovers its natural dimensions at the same time, the inference is that the hypertrophy caused the dropsy, and that the hypertrophy was of the kind called simple. The nutmeg liver is thought to have an agency in producing dropsy, but as it is for the most part associated with diseases that have been called dropsy-producing, its bearing on this effusion may yet be regarded as uncertain.

It is common to speak of heart dropsy in such a way as to imply that disease of the heart alone can produce abdominal effusion. I doubt it. I even doubt whether the heart alone can cause the anasarca that is so often attributed to it. In following a great multitude of heart diseases from the time they were recognized to their termination, I have been struck with the ease with which the patients attend to their business, sometimes even laborious business, for years--in one instance fifty years--with almost no complaint, and how rapidly their condition changes as soon as albumen and casts appear in the urine. I have been compelled by these observations to ascribe the anasarca and oedema that makes this last stage of heart disease so distressing to the kidneys, and not to the heart. Double pleuritic effusion is not uncommon under these circumstances, but every physician must have noticed the rareness of troublesome abdominal {1175} dropsy, while there is sometimes--perhaps often--a little effusion; and when in the exceptional cases there has been much, it was almost always accounted for by a dropsy-producing change in the abdominal organs, not, perhaps, discovered during life; so that for me, while they produce overwhelming effusions in other parts of the system, they are minor agents in the production of ascites. Phthisis is occasionally attended, toward its close, by oedematous legs and albuminous urine, but I cannot report any important relation between these and peritoneal effusion. I can say the same of chronic bronchitis. I record this negative testimony regarding the two last-named diseases, because I find them enumerated among the causes of abdominal dropsy.

Cancer may invade the portal vein, tumors of adjacent parts other than those of the liver, or an aneurism may compress it and cause dropsy. Hydatid tumors may do this. Diseases of the pelvic organs, both acute and chronic, may produce it, but then the disease would fall into the class of those produced by chronic or subacute peritonitis.

DaCosta thinks he has lately had a case of chronic peritonitis attended by ascites. It was in a woman thirty years of age, who had been thrown with force upon the frame of an iron bedstead, striking the lower part of the bowels. Pain and tenderness followed. These were not confined to the injured part, but extended to the whole abdomen; and there was menorrhagia. After a time there was fluid effusion in the peritoneal cavity, which slowly increased till her state demanded relief from tapping. The fluid after this operation did not return. The pain and tenderness were constant symptoms all through. She slowly improved, and at the time the case was reported it was believed that she would soon be discharged from the hospital. The only doubt which DaCosta finds regarding the diagnosis is in the facts that the liver was diminished in size and that the spleen was moderately enlarged, and he admits the possibility that an adventitious capsule of the liver may have caused the ascites, but believes that it was dependent on chronic peritonitis.

Acute peritonitis subsiding into chronic, with increase of fluid effusion, as I have already said, I am not familiar with. That occurring in cancerous and tuberculous peritonitis has already been considered. But in relation to these some facts regarding frequency of occurrence, collected by Bristowe, are worth quoting. He says that in 48 cases of tubercular peritonitis, dropsy was found in 12, and that in 22 of peritoneal cancer, 12 had more or less ascites. He further adds, regarding cirrhosis, that of 46 cases observed post-mortem, there was dropsy in only 20. This is not surprising, as in all the diseased conditions of the liver that produce dropsy the anatomical changes must reach the point at which there is considerable portal obstruction before the effusion will occur.

The amount of fluid found in ascites varies greatly. In some it may remain for a long time stationary at four or five quarts; in others the suffering caused by an accumulation of nine or ten quarts will demand its removal; and in a few cases twenty quarts have been removed in one operation. It is in cirrhosis that the largest quantity is found, and it is in this disease and in cancerous peritonitis that the most frequent tappings are required. The quality of the fluid also varies markedly: from being almost as clear and thin as spring-water it may be almost ropy, or in color greenish or yellowish or slightly red; it is very likely to contain {1176} albumen; and it is probable that a further study of its microscopic elements may enable us to resolve doubts regarding the cause of the effusion. It very often contains blood-corpuscles.

Bristowe finds from hospital records that ascites occurs in about equal frequency in males and females, but, as everybody has noticed, that hepatic dropsy is much more frequent in men than in women. Ascites, he says, is most frequent between the ages of thirty and fifty, and next between twenty and thirty and between fifty and sixty, but is not uncommon above the latter age; and it occurs in children.

SYMPTOMS.--In general, ascites is easily recognized by the swollen state of the bowels: a well-rounded swelling when the patient stands or sits, but spread out in the flanks when he lies on his back; the fulness of the side on which the patient may be lying, and the flattened condition of the opposite side,--belong to this disease, and as a group to no other. The results of percussion are significant in the movement it causes in the fluid, and for the resonance or flatness it produces. When the patient lies on his back, tapping with the finger-ends on one side of the abdomen sends a wave of the fluid across to the other side, where it is perceived as a gentle blow by the applied fingers of the other hand. If the abdomen is not full, this wave will be produced at the upper level of the fluid, but not above that. If this wave cannot be sent across the body, it may be found on either side by percussing above and feeling for it below; percussion also teaches where the fluid is, and where it is not, by the dull sound it produces. It is rare in ascites that the intestines do not float on the surface of the fluid, at least from the umbilicus upward, and there give a loud percussion sound, while toward the back, and often toward the pelvis, it is dull, or even flat; changing the position of the body, the resonance will be uppermost and the dulness in the most dependent part. Then the softness or impressibility of the abdomen till the tension becomes great is noticeable. The changed position of the fluid as the body is turned from side to side is important. A very small quantity of fluid can be detected in this manner. The patient is placed on his right side and percussion is made in the right flank: there is dulness, while in the left flank there is resonance. The patient turns on to the left side: dulness now changes position, and is on the left, and on the right resonance. If it is feared that some undetected fluid remains in the pelvic cavity, the pelvis may be raised by pillows and the same examination repeated, or he may be placed in the knee-and-elbow position referred to by Bristowe, and the percussion will then be made upward in the umbilical region. In some cases the contraction of the mesentery will not allow the intestines to rise through a large amount of fluid and float on it; but such cases are almost confined to the cancerous and the tuberculous varieties of the disease; and as in these the symptoms are grave, the physician will probably have visited his patient many times before this contraction will embarrass him. Besides, when mesenteric contraction occurs there is a very strong probability that the omentum will also be contracted, be rolled up, and lumpy; as this can almost always be felt above the level of the umbilicus, he has in it an explanation of the absence of resonance on the fluid. It has happened that oedema of the abdominal walls or fatty accumulations there have given a delusive though feeble fluctuation on percussion. In such cases, if the patient make moderate pressure with the back of a small book in {1177} the course of the median line, that kind of wave will be broken, while a wave in the abdominal cavity will not be prevented. When there is considerable distension of the abdomen by fluid, weak spots in the abdominal wall often yield and make a tumor. This is very common at the umbilicus, where a little bladder is lifted half an inch or more above the general curve of the abdomen. The fluid frequently follows the track of hernias. In females it has been known to press the anterior wall of the vagina backward and downward, so as to make it protrude at the vulva. It has, in one of my own cases, by downward pressure caused complete prolapse of the uterus. It is very often attended by oedema of the lower limbs. This is accounted for by the pressure of the abdominal fluid on the veins that return the blood from these parts, or in cirrhosis by contraction of the ring or notch through which the vena cava passes in the liver. If there is general oedema, the cause will probably be found in disease of the kidneys; or if in one limb, in pressure or thrombosis of one iliac vein. As the disease advances the accumulating fluid forces the diaphragm upward, diminishes the breathing room, and threatens the life still more. Then the patient cannot lie down in bed, but spends his nights as well as days in an easy-chair, and sleeps leaning forward on a support for his forehead. The veins on the abdominal surface will fix attention. With almost any large tumor in the cavity they become more or less enlarged. But in cirrhotic dropsy this becomes more striking than in any other affection. The enlargement is attended by a reversion of the blood-current on the lower half of the abdomen. This is early shown by emptying an inch or two of a vein with the finger, drawing it either upward or downward, and noticing from which direction it is refilled when the pressure is removed. The pelvic veins do not readily discharge their blood by the natural channels, and by anastomosing branches it is forced over the surface of the abdomen and into the thoracic veins, these latter becoming in turn greatly enlarged. The appetite is commonly poor, the digestion flatulent, the pulse accelerated. Emaciation is gradual or rapid. The urine is commonly scanty, and in cirrhosis of a reddish hue. The skin is apt to be dry, particularly so in simple chronic peritonitis. The tongue has no characteristic fur, and is often, almost always toward the close, dry. The mind is not affected till near the end; then often the patient is delirious, commonly mildly. Diarrhoea is not uncommon, and even dysentery has been observed. The result is almost always unfavorable, or, as has been said, lethal.

The diagnosis is not often difficult. When, as in chronic peritonitis and in tuberculous peritonitis, the fluid is confined in a sac or sacs, each particular pool will be yielding to pressure, but elastic, and will give the percussion wave, though it may extend but a short distance. To distinguish ovarian dropsy--ovarian cysts, as it is now called--from ascites may require a few words. Ovarian tumors of all kinds are found to be more prominent on one side when they rise from the pelvis than on the other. This is not the case with ascites. The uterus and its appendages lie in front of the pelvic intestine, and when any of them ascend above the pelvis they must occupy the same relative position. In other words, a large ovarian cyst must lie in front of the intestines, while intestinal resonance should be found behind and in the sides. But if the ovarian cyst does not occupy the whole height of the bowels, intestinal resonance {1178} may exist above it, and the dulness may be found below, bounded by a portion of a circle, and sometimes the cyst walls are resisting enough to allow its boundaries to be ascertained by the fingers. This cyst can also be felt in the vagina; and the uterus, instead of being pressed down, is sometimes lifted upward, so that it cannot be reached in the vagina, but can be felt through the abdominal walls just above the pelvic bones. A condition more troublesome than this is when ovarian cyst and ascites occur together. Then the posterior or lateral resonance is lost when the patient lies on her back, but can be found on one side when she lies on the other. In that concurrence, in dorsal decubitus it is possible by pressure or a little blow to send a wave of the ascitic fluid over the front of the cyst. This can be seen as well as felt. Should the patient take the knee-and-elbow position, the intestinal resonance may be restored in both flanks.

TREATMENT.--In opening the chapter on the treatment of ascites it is usually said, Give principal consideration to the diseased conditions that have caused the dropsy; in other words, cure cirrhosis, cancerous peritonitis, tubercular peritonitis, heart disease, and the secondary affections of the abdominal organs, release the liver from the dangerous compression to which it is subjected, and all will go well. But they do not inform us how these impossibilities--at least in most cases impossibilities--are to be achieved. It is true that the physician would not shrink hopelessly from the treatment of simple chronic peritonitis. But this is one of the rarest causes of ascites. A physician in a long lifetime may not have seen a case. It is true, ascites is a symptom, always a secondary, or even a tertiary, affection; and theoretically there can be no better advice, but practically it cannot amount to much. Then, if the cause cannot be removed, it remains to do our best to relieve the patient of his load and strive to prolong his life to its utmost possible limit. In doing this the physician will often find himself able to give gratifying relief, and once in a great while to rejoice in a cure.

The three great emunctories, the skin, the bowels, and the kidneys, are chiefly appealed to for relief in this as in other serous accumulations. Most physicians prefer to use the diuretics--first, because if they will act at all, they act so quietly and produce so little debility that whatever can be gained by them is obtained at small cost to the system. The form of ascites that most resists diuretics is that which originates in cirrhosis. Often a full trial of them, with suitable changes from time to time, is of no avail, yet now and then the kidneys yield to persuasion and act freely. The saline diuretics and digitalis are most in favor with some. In the early part of the present century a pill composed of squill and digitalis in powder, and calomel, each one grain, given three times a day, was almost universally chosen. In place of the calomel the blue mass was often preferred. When this prescription had produced a little ptyalism the mercurial was omitted and the squill and digitalis continued. It has often been observed in dropsies of all kinds that diuretics act better after a little mercurial action is set up in the system. The diuretic that I most frequently prescribe is made of the carbonate of potass. ounce ss and water ounce vj; to a tablespoonful of this a tablespoonful of fresh lemon-juice is added. This is taken every two hours, and at the same time a dessertspoonful of the infusion of digitalis or more is taken three times a day. This is an {1179} old prescription. Sometimes the old sal diureticus is used. This is the acetate of potassium. It is not always kindly received by the stomach. At Bellevue Hospital the following is much used: viz. infusion of digitalis, ounce iv; bitartrate of potash, ounce j; simple syrup, ounce ss; and water added to make a pint. This is taken pretty freely. But it would require many pages to exhaust the diuretics. I will only add that I have more confidence in the salts of potash and soda, singly or combined, aided by digitalis and a mercurial, than in any others.

The diaphoretics that are most efficient are warm water and steam. A foot-bath long continued and frequently repeated, the patient covered with blankets, and the water kept at 90° or warmer, are very effectual in producing perspiration. Bricks heated or hot water in bottles, or potatoes heated, and enveloped in damp cloths and laid alongside of the body and limbs, form an extemporaneous vapor-bath of considerable efficiency. A vapor-bath can be easily extemporized in the following way: Have a kitchen vessel furnished by the tinman with a cover which has an inch tube fitted to this and bent so as reach the floor six feet from the fire. The pot should have a capacity of a gallon or more, and should be kept boiling briskly. Meantime, the patient, in his night-dress, has a double blanket brought over his shoulders from behind, and another from before, and fastened. Now he takes a chair (wooden), under which the steam is delivered. The blanket from behind is kept off his body by the back of the chair, and the front one by his knees. The steam, shut in in this way, soon brings on a sweat, and when it is sufficiently active the front blanket is thrown off, and the patient wrapped in the rear one and put to bed, when the sweating can be regulated by blankets. This is better than what is called the alcohol sweat, for in that the patient is bathed in carbonic acid gas as well as heat. A patient is sometimes enveloped in a hot, wet blanket with good effect. Pilocarpine has come into use lately as a sudorific. I have witnessed its effects many times and can testify to its certainty as a sudorific; but it is too debilitating for common use. Digitalis has sometimes acted with extraordinary power in this way, but there are grave risks in administering large doses.

Among the cathartics that may be used in ascites, it has seemed to me that the milder hydragogues are safest. One ounce of Epsom salts with a drachm of the fluid extract of senna can be taken every second or third day for months, if need be, with little reduction of strength, and sometimes with an increase of it. I had charge of a young man in the hospital in whom cirrhosis was unquestionable, and dropsy at one time extreme, in whom the abdominal veins had made furrows that would receive the little finger, who was wholly relieved by a drastic dose of elaterium every second day. I saw him three years after his discharge, and then his health was good. Notwithstanding this, I prefer the milder medicines.

Bristowe has seen no cures from either sudorifics, diuretics, or purgatives. I have seen one or more from each of those agents, all cirrhotic. He "has seen cures occasionally from mercury, iodide and bromide of potash, copaiba, and a combination of fresh squills and crude mercury." I agree with him in his statement that counter-irritants are useless, making exception for chronic peritonitis and the early stage of the tubercular variety. He thinks quinia, iron, and cod-liver oil are useful.

{1180} Paracentesis in almost every case will at length become necessary, and the question comes whether it should be practised early or late. If it be delayed till the oppression of the breathing makes it imperative, the walls of the abdomen will be so stretched as to present little resistance to the reaccumulation of the fluid, and a second tapping will be required in fifteen to twenty-five days. A bandage is a poor substitute for muscular contraction. If, on the other hand, the fluid is withdrawn before the muscularity is not stretched out of the muscles, then accumulation will be less rapid and the patient will be spared the suffering which large accumulations cause. But tapping is not always an innocent operation. It is sometimes followed by acute peritonitis. By the early tapping this risk is oftener taken. Reginald Smith suggests the use of a small canula by which only ten or twenty ounces of the fluid can escape each hour. This mode, he thinks, removes the danger of syncope and makes the bandage needless.

Hemorrhagic Effusion

in the peritoneum is a topic on which there is little to be said. A primary effusion of this kind probably does not occur. In hæmatophilia, where the mucous membrane of the nose and wounds bleed dangerously, there is no record of spontaneous bleeding into the peritoneal cavity. The same thing can be said of that very rare disease which has been called bloody sweat. An unmarried lady applied to me fifteen years ago with this disorder. The blood would ooze out at hundreds of points on the inner face of the arm; these would run together and drop off the arm, or the same thing would occur on the chest and in the bend of the knee. This would continue for two or three minutes, and then cease of itself, but to recur in one or more, rarely several, places. For years this habit continued. There was no irregularity of the menses. I could find no visceral disease; there was no nose-bleed. She lost strength, but only moderately. This kind of bleeding continued for several years. She is now approaching fifty years of age, and for the last two or three years has had no recurrence of the bleeding. There was never anything in this case to lead to the suspicion of peritoneal or other serous hemorrhage. In the few similar cases on record there is the same absence of all evidence of internal bleeding.

It has already been said that a certain amount of blood, as shown by its corpuscles, is to be expected in cancerous ascites, and with less uniformity in tubercular ascites, and not unfrequently in hepatic dropsy, as well as in acute peritonitis. This may not deserve to be called hemorrhage, on account of the moderate quantity of blood that is effused; but aside from that which results from rupture of blood-vessels it is about the only kind of it with which we are familiar.

Scurvy, and conditions of the blood analogous to those produced by that disease, make it almost certain that if pleurisy or pericarditis occurs while these conditions exist, it will be hemorrhagic. I am not, personally, acquainted with a single instance in which peritonitis in this condition has occurred. Copeland, however, says that hemorrhage in peritonitis has been noticed by Broussais and others. The blood is mixed {1181} with the serum and stains the surface of the false membrane, as in hemorrhagic pleurisy and pericarditis, and the disease is of an asthenic type, "occurring in the hemorrhagic diathesis." "The symptoms are inflammatory from the beginning, and rapidly pass into those indicating great depression; the pulse becomes rapid, small, and soft, death quickly supervening, with convulsions, cold and damp extremities and surface," etc.

Copeland has himself not seen a case, and regards its occurrence as very rare. Delafield states that "Friedreich describes two cases occurring in patients with ascites who had been frequently tapped. He says that both the parietal and visceral peritoneum was covered with a continuous membrane of a diffuse, yellowish-brown color, mottled with small and large extravasations of blood. The membrane was thickest over the anterior abdominal wall. It could be separated into a number of layers. These layers were composed of blood-vessels, masses of pigment, branching cells, and fibrillated basement substance. In many places the extravasated blood was coagulated in the shape of round, hard, black nodules. The new membrane could be readily stripped off from the peritoneum, and there were no adhesions between the visceral and parietal portions of the peritoneum."

The erosions of abdominal cancer sometimes open vessels of considerable size, causing large hemorrhage into this cavity and sudden death.

When aneurisms of the abdominal aorta rupture, they sometimes flood the abdominal cavity; oftener they open into the structures under the peritoneum on the left side, and make a large flat tumor extending from the point of rupture downward to the brim of the pelvis, and even beyond it.

A gentleman whose health was usually good, thirty-five years of age, felt an unwonted exhaustion and feebleness creeping over him. His countenance became pale, his pulse rapid, growing smaller and smaller. It seemed certain that there was hemorrhage somewhere, but until it was noticed that the bowels were growing tumid and hard there was nothing to guide us to its seat. Even then we were left to conjecture regarding the bleeding vessel. This sinking continued for thirty-six hours. After death it was found that a small aneurism had been formed on one of the vessels of the omentum, not larger than a small walnut, and had ruptured by a very small opening, and that it was by this small opening that life had oozed away.

Bleedings from stabs and other wounds of the bowels, from lacerations of the liver, spleen, uterus, and sometimes of the kidneys, should be mentioned in this connection; but as they, for the most part, fall into the hands of the surgeons, this is not the place to give the details regarding them.

{1182}

DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA).

BY SAMUEL C. BUSEY, M.D.

DEFINITION.--Tabes mesenterica may be briefly defined to be tuberculosis of the mesenteric glands. This definition may seem too limited, because it recognizes the identity of tuberculosis and scrofulosis of the lymph-glands, and excludes those hyperplastic conditions which do not certainly undergo the cheesy degeneration. It is supported, however, by the absence of any essential difference in the histological changes which take place in tuberculous and scrofulous (Wagner) lymph-glands; by the frequent simultaneous occurrence of each in the same subject; by the secondary development of tubercles during the course of scrofulous affections; and by the fact that the cheesy transformation is alike common to both these conditions of new formations. Schüppel maintains that the presence of tubercles is necessary to the production of the cheesy metamorphosis of lymph-glands, and that "scrofulous glands are always tuberculous glands." In this view Rindfleisch coincides, and expresses the belief that the inflammatory and hyperplastic changes are secondary to the formation of the tubercles. Birch-Hirschfeld asserts that cheesy degeneration of the mesenteric glands is always accompanied by tubercular formations.

This definition is therefore adopted as the expression of the result of the most recent investigations. It must, nevertheless, be admitted that a few equally competent observers deny the identity of the tuberculous and scrofulous new formations in lymph-glands. It must also be conceded that occasionally hyperplastic processes in the lymph-glands undergo the cheesy metamorphosis independent of tubercular development.

SYNONYMS.--The differences of opinion, especially among the older authors, in regard to the nature of this disease are very distinctly indicated in the varying significance of the numerous synonyms, of which the following list is only a part: Atrophia mesenterica; Atrophia infantum (Hoffmann); Febris hectica infantum (Sydenham); Scrofula mesenterica (Sauvages); Paralysma mesentericum (Good); Physconia mesenterica (Baumes); Mesenteritis chronica (Stewart); Mesenteric fever, Hectic fever, Marasmus (Underwood); Carreau, Entero-mésentérite of the French; Darrsucht der Kinder and Gekröschwindsucht of the Germans; Tubercles of the mesentery; Tuberculous disease of the abdomen; Phthisis mesenterica; Tabes glandularis; Tabes scrofulosa; Macies infantum; Pædatrophia; and Rachialgia mesenterica.

{1183} Some of these synonyms indicate the theoretical and unsupported opinions of their authors, and others refer merely to a symptom. The name carreau refers to a hardness of the abdomen; physconia, to the presence of a non-fluctuating and non-sonorous abdominal tumor; and that of entero-mésentérite presupposes a secondary origin from a primary enteritis. Good classes it among his numerous varieties of mesenteric turgescence, but characterizes this special form as a scrofulous turgescence always associated with the strumous diathesis. The terms tabes and atrophy originated when the nomenclature of disease was derived from symptoms, and not from pathology.

HISTORY AND PATHOLOGY.--The history of tabes mesenterica is coeval with that of scrofula and pulmonary consumption. The ancient authors recognized the existence of a chronic disease of the mesenteric glands, characterized by enlargement and induration, followed by destruction of the gland-parenchyma, which was associated with digestive disturbances, emaciation, hectic fever, and usually terminated in death. At first, the degenerative process was regarded as suppurative. But as the study of scrofula progressed, and frequent observations were made of the occurrence of disease of the external lymphatics and of the mesenteric glands in the same subject, disputes arose as to the identity of the two affections. These controversies led to the general acceptance of the belief that the scrofulous degeneration of lymph-glands and the process of destruction in tabes mesenterica were identical. Consentaneous with these investigations, and for a long time subsequent, even down to a very late period, which is, perhaps, not yet concluded, the relation of scrofulous disease of the lymph-glands to pulmonary consumption was discussed and studied with great assiduity. As the knowledge concerning these diseases advanced, and the results of investigations were accepted, the doctrine of the identity of the morbid processes in scrofulous disease of the external glands and mesenteric phthisis became firmly established. The history of scrofulosis and tuberculosis cannot be separated. The connection and identification of the two processes have been subjects of constant discussion from the discovery of tubercle to the present time. Occasionally, the dividing-line seemed definitely fixed. Then would follow the general acceptance of the doctrine of identity. With the discovery of miliary tubercle a determined reaction took place against this view, and for a while many regarded scrofulosis merely as a form or stage of tuberculosis. As the conclusions in regard to these questions changed, so did the opinions concerning the true nature of tabes mesenterica change, until, finally, the investigations of Rindfleisch, Schüppel, and others seem to have established the tuberculous nature of the disease. Many authors of a comparatively recent date have applied the term tuberculosis to this condition, not because they knew or believed the development of true tubercle was a constant or essential characteristic, but because they regarded the words scrofulosis and tuberculosis as synonymous.

Notwithstanding the obscurity in which, for so long a time, the pathology of this disease was involved, certain facts well known to the earliest writers have been confirmed by continuous observation down to the present. Its secondary character has been so uniformly recognized that some of the older authors based its origin upon the absorption and conveyance along the lymphatic vessels to the glands of some peccant material originating {1184} in a primary focus of disease. The constant coexistence with scrofulous affections and pulmonary consumption had long ago established the direct and primary relation of these diseases to tabes mesenterica, and authors of recent date, though not so generally holding the opinion that it is always an intercurrent complication of these maladies, yet maintain its secondary development. Even Schüppel, whose investigations and conclusions lead in the direction of an idiopathic origin, admits that the only primary element is the tuberculosis, which finds its cause in some peripheral irritation.

In the earlier times, as now, tuberculosis of the mesenteric glands has been observed during every period of life from birth to advanced old age, but then, as at the present time, the greater number of cases were known to occur during infancy and childhood. But few cases have been observed during the earlier months of life or before weaning. Between the ages of two and eight years is the period of greatest frequency. Though rarer during the later years of childhood, the older the child the more rapid its progress to a fatal termination. Nursing infants are not exempt, but those nursed by healthy mothers are much less liable than the wet-nursed. Among hand-fed infants it is not an uncommon disease, but it is much more common among the farmed-out children. While, as has been stated, the greatest number of cases occur in those between two and eight years of age, statistics show that the liability to it increases from the age of two and a half years up to the eighth, and, according to some authors, up to the tenth year. At the latter age there is a remarkable diminution in the number of cases. This fact is probably due to the greater prevalence of the acute diseases of the respiratory organs and of the exanthematous diseases among children during this period of life. Some have attributed it to the more rapid development and increased functional activity of the mesenteric glands. This circumstance might afford a plausible explanation for the apparent sudden increase in frequency after the completion of the second year because of the independent subsistence of children at that age, and the additional duties imposed upon the alimentary tract and its dependencies; still, if this were so, the period of greatest frequency ought to begin at an earlier age and more nearly correspond with the time of weaning. It is, however, a fact that tubercularization of the mesenteric glands is more frequently associated with chronic intestinal inflammation in those over one year than in those under that age. This fact, together with the greater liability of artificially-fed infants, would seem to connect, at least in such cases, its secondary origin with some primary irritation of the intestinal canal.

Authors are not yet agreed in regard to the relative frequency of this disease in boys and girls, though opinions predominate in favor of the greater number among the males. The statistics of Rilliet and Barthez and Schmalz show a decidedly greater prevalence among boys.

The comparative frequency of tuberculosis of the mesenteric glands cannot be determined. Louis found disease of the mesenteric glands in one-fourth of the autopsies of persons dying of phthisis; in 100 adults dying of the same disease Lombard found tuberculosis of these glands in 10; and in the bodies of 100 tuberculous children he found the glands tuberculous in 34 cases. In the Hôpital des Enfants Maladies tubercles were found in the mesentery of one-half of the children dying of {1185} tuberculous affections. In the bodies of children dying of tuberculous disease in the Children's Hospital of Washington tuberculous degeneration of the mesenteric glands has been found in two-thirds of the cases, and without a single exception in those dying of rickets. Authors differ also, and the statistics are equally unreliable, in regard to the relative frequency of tubercularization of the bronchial and mesenteric glands. The general opinion seems to be in favor of the greater frequency in the bronchial glands. In a majority of cases both sets of glands are found diseased.

The geographical distribution of tabes mesenterica is as universal as that of scrofula and pulmonary phthisis. No country or climate is exempt, yet there is no locality in which it is endemic. It has been observed among all civilized nations, in the cold regions as well as in the tropical countries. Wherever scrofulous and phthisical diseases are known, there also are found cases of tabes mesenterica. Livingstone has stated that scrofula is unknown in some regions in Central Africa, and other travellers have made similar statements in regard to some Indian tribes. The statistics of the Children's Hospital of Washington show a far greater frequency among the African race than among the whites. It belongs to no class or condition of life, but occurs more frequently among the children of the squalid than among the children of the affluent and well-to-do.

ETIOLOGY.--Predisposing Causes.--Modern as well as the older authors have very generally accepted the conclusion that a constitutional tendency or liability to this disease is its most frequent and potential etiological factor. This predisposition may be either inherited or acquired. The ancients called it the strumous, and the more recent writers the scrofulous or tuberculous, diathesis. Lugol maintained that this diathesis is begotten of old and syphilitic fathers, and others state that children of parents nearly related and of those broken down by disease and excesses may inherit it. That it is transmitted by scrofulous and phthisical parents no one can doubt, but as yet it cannot be defined to be anything more than a peculiarity of the constitution which may exhibit abnormal reactions against irritating influences. The scrofulous habit is believed to be indicated by physical appearances which represent two extremes. The erethic form is characterized by a feeble and delicate frame; deficient muscular development; transparent, smooth, and florid skin; light hair and blue eyes, large pupils; precocious intellect and sanguine temperament; the torpid form, by a large head; large and tumid upper lip; soft and flaccid flesh, bloated appearance; short and thick neck; muscular incapacity, tumid abdomen, and sluggish intellect. Some of these features are more frequently symptoms of the actual disease than of the existence of a predisposition to it, and, except so far as they may refer to a primary scrofulous or pulmonary disease, cannot be accepted as indicative of the presence of a constitutional tendency to tuberculosis of the mesenteric glands. A tumid abdomen, rapid emaciation, and anæmia are far more valuable signs of the disease of these glands.

Bad air and bad food are also important predisposing causes. They are conditions to which the children of the poor, especially in large cities, are constantly exposed. Insufficient protection from climatic influences, neglect of person, and unhygienic surroundings must be classed in the same category. It is claimed that vitiated air, unwholesome habitation, {1186} insufficient or improper food, squalor and filth may cause the constitutional tendency, as they will certainly precipitate the development of the disease in those predisposed to it.

Exciting Causes.--The border-line between the predisposing and exciting causes cannot be positively fixed. The presence of tuberculosis or of some form of scrofulous disease in some other part of the body so constantly precedes the development of tuberculosis of the mesenteric glands, even in those who have not exhibited the characteristic phenomena of the scrofulous diathesis, that such affections must be regarded as exciting as well as predisposing causes. No one can doubt the frequent infection of the mesenteric glands in cases of pulmonary tuberculosis. The probability of systemic infection from a single focus is universally admitted. These facts and circumstances do not exclude the possibility of localized tuberculosis of the mesenteric glands. Whether such exclusively local development of tubercles ever occurs independent of the scrofulous diathesis cannot be determined, but that the disease does find its exciting cause in inflammatory conditions of the intestinal mucous membrane cannot be doubted. Schüppel, who asserts the primary development of the tubercle-formation in lymphatic glands, does not claim an idiopathic origin, but admits the necessity of a primary peripheral irritation in direct connection with the affected gland. The intimate connection between diseases of the intestinal mucous membrane and of the mesenteric glands is established beyond a doubt. Vogel and Steiner assert that tabes mesenterica is a common result of enteritis folliculosa. A primary inflammatory process may not contain any element which could be classed as tubercle, yet it may excite secondary tuberculosis of the glands. Whether such a result only occurs in those who may have acquired or inherited the predisposition is yet undecided. In many of the cases of tabes mesenterica tuberculous ulcers are found in the intestines, but it cannot be claimed that such ulcers are always the primary foci of tuberculous development. If primary, it is not difficult to understand how the virus may be transmitted to the glands.

It has been claimed that certain articles of food will produce the disease. Potatoes and rye bread in large quantities and a coarse vegetable diet have been mentioned among the exciting causes. Deficiency in the quantity of food is a much more frequent cause than inferiority in quality, yet there can be no doubt that any and every article of diet that will set up catarrhal inflammation of the intestinal mucous membrane may become a cause. Irritation of the mucous membrane of the alimentary tract, induced by coarse, stimulating, or imperfectly-digested food, or by the improper and frequent use of purgative medicines, may give rise to disease of the glands; and, even though the irritation may in itself be trivial, its long continuance or frequent renewal may prove sufficient, especially in those in whom the predisposition is present. Malarial and exanthematous diseases have also been considered exciting causes, and among the latter class measles and scarlet fever, because of the inflamed condition of the intestinal mucous membrane which they leave, are the most frequent. Difficult dentition and whooping cough must also be classed in this category.

Recently attention has been called to the probable transmission of the disease through the milk of diseased cows, but further investigation and {1187} more reliable data are necessary to establish this connection. Klebs has deduced the conclusion from recent experiments that the use of the milk of cows in advanced phthisis will always produce tuberculosis, which begins as an intestinal catarrh and extends to the mesenteric glands.

Some of the older authors believed that the cure of some chronic diseases of the skin and mucous membranes and the suppression of chronic discharges might induce tuberculosis of the mesenteric glands; but these conditions are now known to be most frequently the initial manifestations of the scrofulous diathesis, and the mesenteric complications are far more likely to occur when these primary foci are neglected and the patient is left to suffer the unabated progress of the disease.

MORBID ANATOMY.--It is not usual to find all the glands of the mesentery affected at once, nor of those affected all in the same stage of disease. Newly-affected glands may be found alongside of others in an advanced condition. In the first stage the glands are enlarged, but rarely exceeding the size of a filbert; they are firm, but not inelastic. This change consists in hyperplasia of the gland-constituents. Microscopic examination shows abundant cell-proliferation, but the cells are badly constructed and prone to undergo retrogressive metamorphosis. The cells accumulate in clusters without any intercellular substance, and compress the lymph-sinuses and blood-vessels.

The second stage is characterized by the commencement of the cheesy degeneration. The glands enlarge and coalesce in clusters, sometimes forming large masses of hardened and inelastic glands. On section they exhibit in the beginning foci of cheesy material imbedded in the gland-parenchyma. In the further progress of the change the whole gland is transformed into a homogeneous yellowish substance. In this condition there are found on microscopic examination globular corpuscles, nuclei, shrivelled cells, sometimes giant-cells, and most frequently tubercles. The tubercles are usually found in the follicular substance. Birch-Hirschfield says the cheesy formations in secondary tuberculous mesenteric glands are only found in discrete foci, and the tubercles occur in the follicular substance imbedded in relatively normal tissue. The cheesy transformation is, according to Virchow, a necrobiosis of the hyperplastic gland-elements, but Schüppel insists that it is the result of tubercular development. After a time the cheesy masses soften, and the glands are converted into sacs containing a purulent fluid mixed with débris. In this condition they are most frequently coalesced in bunches, sometimes forming large tumors. The intervening walls may break down and the whole bunch be transformed into one large sac filled with purulent fluid and débris. Occasionally these masses of agglutinated glands become adherent to the abdominal parietes or to the intestines. Rupture of their walls may occur, and the contents may be emptied into either the peritoneal cavity or the intestines. When communication with the intestines takes place, it is usually through an ulcer on the mucous surface. It is probable that the cheesy substance may sometimes be absorbed, as Virchow thinks, by gradual softening proceeding from the surface toward the centre.

It is believed that these degenerated glands sometimes undergo the cretaceous transformation. Such an instance has been reported by Carswell: "The patient, who when a child had been affected with tabes {1188} mesenterica and also with swellings of the cervical glands, some of which ulcerated, died at the age of twenty-one years of inflammation of the uterus seven days after delivery. Several of the mesenteric glands contained a dry cheesy matter mixed with a chalky-looking substance; others were composed of a cretaceous substance; and a tumor as large as a hen's egg, included within the folds of the peritoneum, and which appeared to be the remains of a large agglomerated mass of glands, was filled with a substance resembling a mixture of putty and dried mortar, moistened with a small quantity of serosity. In the neck, and immediately behind an old cicatrix in the skin, there were two glands containing, in several points of their substance, small masses of hard cretaceous matter." Calcareous concretions have been observed by Andral and others in the mesenteric glands in cases of chronic pulmonary disease; and Soemmering records several observations of a tartar-like substance found in devastated mesenteric glands in cases of rickets.

The morbid appearances in tabes mesenterica are not usually confined to the changes in the glands. In very many cases the evidences of disease of the peripheral glands are quite manifest, and in much the larger number of cases pulmonary phthisis and disease of the bronchial glands are present. The adjacent abdominal organs may also be involved. These consecutive morbid changes are succinctly set forth in the following notes of an autopsy taken from the records of the Children's Hospital of Washington, D.C. The subject was a negro boy aged ten, who had been taken sick a year previous to his death with a bad cold and cough, followed several months afterward by enlargement and suppuration of the cervical glands on both sides: "The body was greatly emaciated, the lips and teeth covered with sordes. Cheesy masses were scattered throughout the substance of both lungs. The right lung was firmly adherent to the thoracic walls, the left adherent at apex. The liver was enlarged and adherent to all adjacent tissues, and contained many cheesy nodules scattered throughout its substance and over the surface. The gall-bladder was distended with bile. The spleen was normal in size, very dark, and filled with cheesy masses. The pancreas contained many similar masses. The peritoneal cavity contained a quantity of muddy fluid. The peritoneum was dark in color, studded with tubercles, and ulcerated in a few places. The stomach and intestines were distended with gas; the walls of stomach thickened, the inner surface covered with a shiny mucus; in its lower wall was one large ulcer, penetrating to the peritoneal coat and measuring three-fourths of an inch in diameter. The peritoneal coat was thickly studded with nodules resembling tubercles. The small intestines were gangrenous in a few places; on the inner surface were found fourteen ulcers, varying in size from one-fourth to one and one-fourth inches in diameter, with elevated edges and red bases; two penetrated the peritoneal coat. This coat contained very many tubercles. On the mucous surface of the large intestines there were seven large ulcers, similar in appearance to those found in the small intestines. Some of Peyer's patches were ulcerated. The mesenteric glands, some as large as walnuts, were filled with cheesy material, and the mesentery was dotted over with small masses of similar matter."

In two of the reported cases of chylous effusion into the peritoneal cavity the rupture of the lacteals was caused by degeneration of the {1189} mesenteric glands; and in several other cases the rupture was produced by the presence of tumors, apparently formed by the agglomeration of numerous degenerated glands.

Several cases of fatty diarrhoea from mesenteric phthisis have been reported. Of these the most conclusive is the case of Hall.[1] The clinical history of the case and the detection of enlarged mesenteric glands in the umbilical and hypogastric regions placed the diagnosis beyond a doubt. It was, however, verified by the discovery of several vomicæ in the lungs, and of mesenteric glands "universally enlarged and affected with strumous disease. The intestinal mucous membrane was dotted with patches of ulceration, with here and there prominent masses of strumous deposit on the surface."

[Footnote 1: _Guy's Hospital Reports_, vol. i., 3d Series, 1855, p. 371.]

SYMPTOMATOLOGY.--It is not possible to describe a definite and uniform clinical history of this disease. As a secondary complication of pulmonary phthisis and scrofulous affections the preliminary symptoms are so constantly identified with the development and progress of these maladies that, as a rule, the initial stage cannot be recognized by any special assemblage of symptoms. In any tuberculous or scrofulous child the possible implication of the mesenteric glands may be predicated upon any array of symptoms that would establish the presence of these classes of disease. And even in the absence of the rational and direct signs of such affections, in those exhibiting the physical evidences of the strumous diathesis, more especially when it is inherited, the symptoms of any trivial departure from health, such as the catching of cold, irritation of the alimentary tract, or protracted convalescence from any of the exanthematous or intestinal diseases, may constitute the initial history of tabes mesenterica. In such subjects debility and anæmia, from whatsoever cause they may apparently result--and, in fact, any manifest lowering of the standard of health, whether gradual or precipitate, and without assignable cause--may mark the beginning of the process of change in the parenchyma of the glands that will terminate in tuberculosis. The later as well as the earlier history may be completely masked by the symptomatology of other diseases belonging to the tuberculous class; and so grave, as a rule, are such primary and coexisting affections that definite recognition of this complication or localized extension of the systemic infection becomes more a matter of skilful diagnosis than of practical utility.

But in those cases where disease of the respiratory organs and of the bronchial glands can be excluded the general symptomatology becomes of paramount importance. And in view of the value of prophylactic measures which may be employed to arrest, limit, or delay the localized tuberculosis of these glands, the precursory symptoms may be of special significance. This condition may be characterized by languor and dulness or marked debility and anæmia, with loss of color, attended with flatulence, stomachal disturbance, frequent eructations consisting mainly of mucus, a sense of uneasiness in the abdomen after the ingestion of food, a variable appetite, sometimes voracious and occasionally depraved. Sometimes a dislike for fatty foods is a prominent symptom. The tongue may be coated, the breath is usually foul, and some have said the body emits an acid odor. If these symptoms occur in a child of the {1190} scrofulous diathesis, or be directly or remotely associated with a previous gastro-intestinal disease, or occur or persist during the convalescence of some of the acute affections of infancy and childhood which stand in etiological relation to this disease, they may justify a reasonable presumption of commencing change in the mesenteric glands. This presumption will be strengthened by emaciation, a more marked disturbance of the digestive function, attended with fetid and occasionally whitish stools, a tumid belly, and deep, lancinating abdominal pains of short duration, recurring at long intervals and neither relieved nor aggravated by pressure or an evacuation. Some have attributed special importance to a chalky appearance and loss of consistency of the stools, indicating the suspension of absorption by the lacteals. There may also be slight evening fever. Later, the enlargement of the belly increases, the emaciation becomes more marked and rapid, the appetite more variable, sometimes very voracious, the alvine discharges more fetid or less consistent, sometimes putty-like, and generally irregular or constipated. The febrile exacerbations are more decided, and sometimes chills may occur at irregular intervals. When, in addition to these symptoms, either during the earlier or later stages, the enlargement of the glands can be detected, the clinical picture is complete. In consequence of the tympanitic distension of the abdomen, which usually increases with the progress of the disease, it is impossible in a majority of cases to detect the glandular enlargement; especially is this true when the affected glands are separate; but, as frequently happens during the last stage, when large tumors are formed by the coalescence of a number of diseased glands the diagnosis may be easily determined. In the absence of the discovery of enlarged glands the diagnosis cannot be considered positive. They are usually most readily found in the region of the umbilicus, and may in some cases, even when the tension of the abdomen is very great, be detected by grasping the abdomen with the hand and compressing it between the fingers and thumb so that the enlarged glands will be brought in close contiguity to the walls and be felt immediately under the fingers. If a tumor should be present and the peritoneal cavity be free from fluid, its locality may be recognized by a sense of resistance and circumscribed area of diminished resonance, and then definitely outlined by palpation. Underwood says: "Indigestion, costiveness or purging, irregular appetite, flushed cheeks or a total loss of color, impaired strength and spirits, remitting fever, and a hard and tumid belly, with emaciated limbs, are amongst the more common symptoms, attending at one period or other, of this disease."

When the diagnosis has been made out, it is not impossible to determine the stage of the disease. The progressive intensity of the symptoms, with rapid emaciation as a rule, bears a definite relation to the progress of the morbid changes taking place in the glands. It must, however, be borne in mind that children have died of tabes mesenterica who had enjoyed excellent health up to the moment of death, and the autopsy disclosed the condition of the glands, which had not been suspected during life. In the case previously cited, in which the autopsy exhibited such grave lesions of the stomach, liver, spleen, pancreas, and intestinal mucous membrane, the clinical phenomena were at no time commensurate with the gravity of the morbid changes.

{1191} DIAGNOSIS.--In the absence of the proof of the presence of enlarged glands or of a tumor the diagnosis cannot be positively determined. The enlargement and tympanitic distension of the abdomen do not necessarily establish the existence of glandular disease, for they are present in a great many conditions of ill-health in children. Nor is the coexistence of a tumid belly, emaciation, and fever sufficient, for they are found in other tuberculous and in gastro-intestinal diseases. The discovery of enlarged discrete glands by palpation, as before described, in connection with such disturbances of nutrition as have been set forth, constitute the strongest presumption in favor of tabes mesenterica. The presence of enlarged glands unaccompanied by the ordinary symptoms of the tuberculous or scrofulous processes is inconclusive, because the glandular hypertrophy may be a simple hyperplasia, entirely independent of any tendency to retrogressive metamorphosis. There is usually some tenderness on pressure, but this may be present in any disease of the abdominal viscera. When the glands are of sufficient size, they may, by pressure, produce secondary derangements. Cramps in the legs may be caused by pressure on nerves. Oedema of the legs and dilatation of the superficial abdominal veins may result from compression of venous trunks. "If," says Eustace Smith, "these veins are seen to ramify on the abdominal surface and to join the veins on the thoracic walls, tabes may be suspected in the absence of chronic peritonitis and enlargement of the liver." Ascites may be present, but is not a necessary result of disease of the glands.

When a tumor has been discovered by palpation, it is necessary to determine its glandular nature. If situated about the umbilicus, in front of the spinal column, if irregular, hard, and feeling like a congeries of irregularly-rounded nodules, the evidence is very decided in favor of its glandular origin. But care must be taken to exclude tumors formed by fecal accumulations and masses attached to the omentum. Omental tumors are usually more movable, better defined, more superficial, and regular in form. Cancerous masses sometimes simulate glandular tumors. The general history of the case and the age of the patient are usually sufficient to make a diagnosis by exclusion. Rilliet and Barthez distinguished a cancerous pancreas by the presence of vomiting, jaundice, and abdominal pains.

The writer has many times based a conjectural diagnosis--which was verified by a post-mortem examination--upon the presence of a tumid abdomen, increasing emaciation, with the history of a protracted gastro-intestinal catarrh, and an irregular febrile curve characterized by frequent subnormal temperatures. He has also observed a number of cases of protracted diarrhoea in children, accompanied with extreme emaciation, notwithstanding the appetite was good, sometimes even voracious, and the food taken was ample, nutritious, and easily digested, in which the stools, varying from two to three, or twice as many, daily, were whitish, leaden, or slate-colored, sometimes semi-fluid, at other times containing lumps or masses of putty consistence, presenting to the naked eye a greasy appearance and to the touch a fatty feel, and at the autopsy has found only thinness and transparency of the coat of the small intestines and degenerated mesenteric glands.

PROGNOSIS.--The prognosis is decidedly unfavorable. So far as is known to the writer, there is but one recorded case of recovery in which the {1192} diagnosis was indisputable and the fact of a cure was established by an autopsy. This was the case reported by Carswell, before referred to. The older and some of the modern authors have claimed many recoveries, but it must be manifest to every student of pathological anatomy that the mistaken diagnoses must have been nearly if not quite as numerous as the cases of cure. The writer has not witnessed a single case of recovery, but he has observed very many cured cases of disease which exhibited all the subjective and objective symptoms of tuberculosis of the mesenteric glands, save and except those by which its existence can alone be definitely and positively established. The case of Carswell demonstrates a remote possibility of cure by the cretaceous metamorphosis of the degenerated glands in a subject exhibiting the scrofulous diathesis. In view of this isolated observation, one cannot refuse to accept a similar possibility in cases in which the disease may be localized and confined to a few of the glands. In such cases, if recognized previous to the formation of cheesy foci, the possibility of staying, limiting, and perhaps occasionally curing, the disease should not be regarded as absolutely hopeless; yet the opportunities of examining the glands in the first stage of change has so rarely occurred that no one is authorized to assert that the hyperplasia is the true picture of the condition in which those in the advanced stage had its beginning; nor has any one claimed to have witnessed the progressive stages of resolution taking place in such glands.

The cretaceous transformation is an accepted though remote possibility, and absorption by means of gradual softening of the cheesy masses is perhaps a reasonable hypothesis. But even if either of these processes was an occasional termination of the disease, it could only lessen its gravity and prolong life, with an incomplete recovery, in those few cases in which the tuberculous or scrofulous changes were confined to a less number of glands than was necessary to maintain the nutrition of the body. For while there is no serious obstacle to the flow of chyle through the glands in the condition of simple hyperplasia, it is completely obstructed in those transformed into cheesy masses or purulent collections. The channels through the glands must sooner or later be obliterated by the presence of the abundant cell-proliferation which characterizes the initial stage of change in this disease. For if the compression is sufficient to cut off the supply of blood, it must prove equally destructive to the complex system of lymph-paths. To the impermeability of the glands must the emaciation and exhaustion which mark the course of the disease, to a greater or less degree according to the number of glands involved, be due.

If the investigations of Schüppel should be verified, and the primary tubercle-formations be accepted as the initial stage of change, the prognosis will be less favorable, but a distinct line of demarcation may be established between two classes of cases in each of which cheesy transformation may occur, but in one the tubercle-formations may be primary, and in the other secondary. In the latter class the prognosis may be more favorable, because treatment may be effective if commenced prior to the beginning of the retrogressive metamorphosis.

COURSE, DURATION, AND COMPLICATIONS.--When tabes is a complication of pulmonary or bronchial phthisis, or when either of the latter {1193} diseases appears as an intercurrent affection during the course of a primary localized tuberculosis of these glands, the glandular degeneration runs a more rapid course. When it appears as an extension of external scrofulous affections or finds its cause in gastro-intestinal irritation, its course is usually less rapid. The number of glands involved greatly influences its duration. The mechanical impediment to nutrition offered by a large number of impermeable glands promotes rapid emaciation and exhaustion. The condition of the mucous coat of the alimentary tract offers many considerations that affect its course and duration. Follicular enteritis hastens, and tuberculous ulceration of the mucous membrane speedily brings, the case to a fatal termination.

Some of the older authors refer to the frequent complication of rickets with tabes mesenterica, and the writer in numerous post-mortem examinations of the bodies of children dying of rickets has invariably found cheesy mesenteric glands. In view of the fact that rickets is constantly associated with disturbance of the alimentary tract, it should not be a surprise to find the glands in such close contiguity to, and having vascular communication with, the diseased mucous surface in a condition of hyperplasia. Simple hypertrophy is probably a common complication in cases which terminate by recovery, but there must be some element of cause, other than inflammation of the mucous membrane of the intestines, that determines the retrogressive metamorphosis. Several of the older authors have classed rickets in the category of strumous diseases, and it may be that in the fatal cases tuberculosis of the mesenteric glands is a local expression of this diathesis.

TREATMENT.--The treatment consists, for the most part, in methods of prevention and palliation. The tendency to disease of the lymphatic glands in scrofulous children is so constant that it is important to remove all sources of irritation and to combat all influences likely to hasten or promote the localization of the constitutional condition. All chronic discharges and diseases of the skin and mucous membrane, the continuance of which might produce glandular complications, should be cured as speedily as possible, slight colds should receive prompt attention, and catarrhal inflammations of the respiratory organs should be arrested as quickly as the resources of science will permit. The alimentary tract demands constant and careful observation. Trivial disorders should not be neglected: the causes should be ascertained and removed. Digestion and nutrition should be maintained at a healthy standard. The hygiene of person, dwelling, and sleeping apartments merits constant and intelligent supervision.

As stated above, tabes of the mesenteric glands is so frequently secondary to other diseases of a scrofulous nature that the danger lies in the failure to arrest or cure such affections. It is unfortunately too true that some of them are often beyond the resources of medical skill, but in many cases the initial manifestations of the strumous diathesis are either entirely neglected or inappropriately treated. In many such cases the final and fatal complication of mesenteric phthisis could be prevented. The treatment of these affections belongs properly to the subjects of tuberculosis and scrofula, to be found in other parts of this System of Medicine.

Localized tuberculosis of the mesenteric glands is so often, either {1194} directly or indirectly, connected with catarrhal inflammations of the gastro-intestinal mucous membrane that the cure of these affections cannot be too strongly insisted upon as an effective method of prevention. This is especially true with children exhibiting the physical signs of the strumous diathesis. When it is inherited from a diseased mother, it may be necessary to resort to artificial feeding before the proper time for weaning has been reached. In such cases no uniform rule can be arbitrarily followed. The condition of both mother and child must be considered, and cases will occur which will demand the exercise of the most cautious discretion and diligent observation.

When the disease has become established but little can be accomplished. In such cases the treatment refers to the palliation of symptoms and the maintenance of nutrition. Pain, when present, must be relieved--if necessary by anodynes, either given internally or applied in the form of cataplasms. Most often it is due to the coexisting disease of the intestinal mucous membrane or to the ingestion of unsuitable foods. The diet should be regulated and limited to nutritious and easily-digested articles. Sometimes, even in cases of advanced degeneration of the glands, great benefit may be temporarily obtained by attention to the diet. Diarrhoea should be controlled, but when dependent upon tuberculous ulcerations of the intestinal mucous membrane but little can be done toward delaying the fatal termination. When a large number of glands are affected, it will be necessary to limit the diet to such nutrient fluids as may be absorbed from the stomach.

The medical treatment is confined to a few remedies. Faulty nutrition is the predominant factor, and the drugs employed should be directed to the improvement of the assimilative functions. The lacto-phosphate of iron in the form of syrup, or the phosphates in the form of the compound syrup, sometimes prove valuable tonics. The lacto-phosphate may be given in combination with cod-liver oil. This latter, either internally or by inunction, is the most valuable and universally applicable of all remedies. The mistake is very frequently made of giving too large quantities. Few children can digest as much as a drachm administered three times a day. In Washington it is usually given in the form of the phosphatic emulsion, and has proved in the service of the Children's Hospital a valuable and effective remedy in the nutritional disorders of children. Of the chalybeates, the syrup of the iodide of iron is by far the most valuable; this may be given alone or in combination with cod-liver oil. It is specially indicated when anæmia is a marked characteristic. Some recent reports favor the employment of pancreatized foods. The ointment of the iodide of lead has been highly extolled as a local application to the belly. The nature of the disease should be constantly borne in mind, and all depressing agencies should be sedulously avoided.

{1195}

INDEX TO VOLUME II.

A.

Abdomen, enlargement of, in rachitis, 153 state of, in ascites, 1176 in cancerous peritonitis, 1169 in cirrhosis of liver, 994 in cholera morbus, 722 in chronic peritonitis, 1162 in dysentery, 796, 804 in enteralgia, 661 in intestinal catarrh, 679, 706, 707 in tabes mesenterica, 1190 in tape-worm, 940 tetanic spasm of, in dilatation of stomach, 595 tenderness of, in tubercular peritonitis, 1165, 1166

Abdominal bandage, use of, in dilatation of stomach, 609 belt, use of, in constipation, 654 distension, in acute peritonitis, 1141 glands, disease of, 1182 swelling, in intestinal indigestion, 627 tenderness, in intussusception, 848 veins, abnormal anastomoses of, in thrombosis and embolism of portal vein, 1096 prominence of, in ascites, 1177

Abortions, frequent, significance, in diagnosis of hereditary syphilis, 310

Abortive treatment of acute gout, 134

Abscess in acute pancreatitis, 1118 in local peritonitis, 1159, 1160 of joints in gout, 116 of liver, 1002 discharge of, into neighboring organs, 1007 influence on causation of acute peritonitis, 1138 in dysentery, 801 of rectum, a cause of fistula in ano, 897 of tonsils, 383 peri-anal and peri-rectal, 703, 895

Abscesses, number, in suppurative hepatitis, 1006 peritoneal, in perforation of simple ulcer of stomach, 499 seat of, in acute peritonitis, 1136 in typhlitis and perityphlitis, 817

Acanthocephali, the, 949

Acaris autumnalis of anus, 892

Acetate of lead, use of, in hemorrhage from bowels, 834 in purpura, 193 in simple ulcer of stomach, 526

Acetonæmia in diabetes mellitus, 205, 206

Acetone and alcohol in diabetic urine, 209

Acid, lactic, theory of origin of acute rheumatism, 23 nitrate of mercury, use of, in anal fissure and ulcer of rectum, 912 in cancrum oris, 343 salicylic, use of, in acute rheumatism, 51-59 uric, theory of origin of gout from, 112, 113

Acini of pancreas, anatomy, 1113

Acne complicating gout, 121

Aconite, use of, in acute intestinal catarrh, 689 in acute pharyngitis, 397, 398 in acute rheumatism, 64 in parenchymatous glossitis, 364 in tonsillitis, 388

Actual cautery, use of, in cancrum oris, 343

Acupuncture in hydatids of liver, 1109

Acute yellow atrophy of liver, 1023

Addison's disease, influence on causation of chronic intestinal catarrh, 700

Adenomata of stomach, 578

Adhesions, formation of, in abscess of liver, 1007 in gastric cancers, 566 peritoneal, in chronic intestinal catarrh, 703

Age, influence of, on causation of abscess of liver, 1003 of acute yellow atrophy of liver, 1024 of amyloid liver, 1041 of ascites, 1176 of biliary calculi, 1063 of cancrum oris, 339 of carcinoma of liver, 1034 of catarrhal stomatitis, 322 of cholera morbus, 720 of cirrhosis of liver, 990 of cirrhosis of stomach, 612 of constipation, 639 of diabetes mellitus, 203 of dilatation of stomach, 592 of functional dyspepsia, 438, 439 of entero-colitis, 732 of fatty liver, 1047 of fistula in ano, 897 of gastric cancer, 534 of gout, 110 of intestinal cancer, 869 of acute intestinal catarrh, 670 of chronic intestinal catarrh, 699 of intestinal indigestion, 623 of intestinal obstruction, 847 of macroglossia, 350 of muscular rheumatism, 74, 75 of organic stricture of oesophagus, 423 of diseases of pancreas, 1114 of parenchymatous glossitis, 360 of phosphorus-poisoning, 1030 of prolapse of rectum, 881 of pseudo-membranous enteritis, 764 of rachitis, 141 of rheumatism, 20 of rheumatoid arthritis, 141 of scrofula, 233 of scurvy, 169 of simple ulcer of stomach, 483 of spasmodic stricture of oesophagus, 419 of aphthous stomatitis, 326 of stomatitis ulcerosa, 336 of tabes mesenterica, 1184 of thrush, 332 of tonsillitis, 380 of typhlitis, 815

Agnew's rectal chemise in hemorrhage from rectum, 927

Air, impure, influence on causation of acute intestinal catarrh, 670 of rachitis, 143 of scurvy, 170 of scrofula, 232 vitiated, influence on causation of entero-colitis, 728-730 of tabes mesenterica, 1185, 1186

Albumen in urine of jaundice, 978

Albuminoid degeneration of pancreas, 1128

Albuminuria complicating gout, 123 in diabetes mellitus, 208 in intestinal indigestion, 628 in gastric cancer, 551 influence of, on causation of acute peritonitis, 1138

Alcohol, abuse of, influence on causation of enteralgia, 660 of gout, 111 of gastric cirrhosis, 612 of acute chronic gastritis, 470 of intestinal indigestion, 625 of chronic oesophagitis, 416 of diseases of pancreas, 1114, 1121 of simple gastric ulcer, 488 influence on causation of abscess of liver, 1005 of biliousness, 966 of cirrhosis of liver, 991 of lithæmia, 969 of acute oesophagitis, 410 of organic stricture of oesophagus, 423 of chronic pharyngitis, 402 of acute and chronic intestinal catarrh, 671, 672, 700 use of, in acute yellow atrophy of liver, 1030 in cholera morbus, 725 in cholera infantum, 761 in dysentery, 810 in functional dyspepsia, 439 in entero-colitis, 761 in hemorrhage from bowels, 834 in intestinal ulcerations, 829 in acute pancreatitis, 1120 in acute pharyngitis, 398 in acute rheumatism, 69

Alcoholism, influence on causation of fatty liver, 1047

Alimentation, hypodermatic, in simple ulcer of stomach, 525 rectal, 928 in organic stricture of oesophagus, 425

Alkalies, use of, in amyloid liver, 1045 in diabetes mellitus, 229 in functional dyspepsia, 458 in enteralgia, 666 in fatty liver, 1050 in gout, 132 in intestinal disorders of rachitis, 161 in acute intestinal catarrh, 693 in lithæmia, 972 in muscular rheumatism, 77 in acute oesophagitis, 416 in acute rheumatism, 60 in scrofula, 252 in simple ulcer of stomach, 527 and salicylates, combined use of, in acute rheumatism, 61

Alkaline carbonates, use of, in chronic gastritis, 477

Almond food, use of, in rickets, 223

Aloes, use of, in constipation, 655 in functional dyspepsia, 458 in hemorrhoids, 923

Alopecia, circumscribed, in rachitis, 156

Alum, use of, in constipation, 656 in enteralgia, 665 in hemorrhage from bowels, 834 in acute intestinal catarrh, 696

Alvine discharges of cholera morbus, 722

Amenorrhoea, in simple ulcer of stomach, 495

Ammonia, use of, in suppurative pylephlebitis, 1101

Ammonium chloride, use of, in chronic pharyngitis, 406

Amphistomum hominis, 949

Amyloid degeneration, gastric, influence on causation of dilatation of stomach, 590

Amyloid degeneration of mucous membrane in chronic intestinal catarrh, 705

Amyloid liver, 1040

Anæmia in chronic articular rheumatism, 71 in chronic intestinal catarrh, 709 in gastric cancer, 552 in intestinal indigestion, 629 in tabes mesenterica, 1189 influence of, on causation of chronic gastritis, 471 of functional dyspepsia, 439 of gastralgia, 460 of gastric hemorrhage, 582 of intestinal indigestion, 623 of simple ulcer of stomach, 487 pernicious, influence of, on causation of hemorrhage from bowels, 832

Anæmic murmurs in acute rheumatism, 36

Anasarca, in cirrhosis of liver, 995

Anastomoses of veins, abnormal, in cirrhosis of liver, 996 of abdominal veins, abnormal, in embolism and thrombosis of portal vein, 1096

Anatomy of pancreas, 1112 of rectum and anus, 879

Anatomical peculiarities of scrofulous tissue, 238

Anchylostomum duodenale, 955

Aneurism of gastric vessels in simple ulcer of stomach, 511

Aneurisms, miliary, of stomach, 579

Angina, 390

Angiocholitis from biliary concretions, 1077

Ankylosis following gonorrhoeal rheumatism, 106 from chronic articular rheumatism, 71 in general rheumatoid arthritis, 81

Annular form of dilatation of oesophagus, 431, 432 of gastric cancer, 562

Anomalies in form and position of stomach, 617

Anodyne applications in rheumatoid arthritis, 100

Antimony-poisoning, as a cause of cirrhosis of the liver, 991 influence of, on causation of fatty liver, 1047

Antiphlogistic treatment of acute gout, 133

Antiseptics, use of, in stomatitis ulcerosa, 338

Antispasmodics, use of, in enteralgia, 665

Anal fissure as a cause of hemorrhage from bowels, 830 fistula, 897 openings, abnormal, 880

Anus, abscess of, 880 imperforate, 877 and rectum, cancer of, 902 fissure of, 888 scrofulous and tuberculous affections of, 901 spasm of, 909 syphilis of, 900 ulceration of, 893

Aorta, aneurismal dilatation from pressure in pancreatic diseases, 1116

Aperient, mineral waters, use of, in functional dyspepsia, 458

Appendix vermiformis, lesions of, in entero-colitis, 738

Appetite, capricious, in cirrhosis of liver, 993 in tabes mesenterica, 1189 impaired, in carcinoma of liver, 1038 in catarrh of bile-ducts, 1053 in catarrhal stomatitis, 323 in cholera infantum, 742 in cirrhosis of stomach, 613 in constipation, 646, 647, 853 in dilatation of stomach, 543 in dysentery, 796, 804 in chronic gastritis, 473 in gastric cancer, 538 in chronic intestinal catarrh, 707 in intestinal ulcer, 826 in simple ulcer of stomach, 494 in stomatitis ulcerosa, 339 in typhlitis and perityphlitis, 818, 819 state of, in diabetes mellitus, 204 in acute rheumatism, 27 in muscular rheumatism, 76 in rheumatoid arthritis, 83 in scurvy, 177

Aphthous stomatitis, 325 ulcerations in morbid dentition, 373

Armies, prevalence of dysentery among, 785, 786

Arseniate of sodium, use of, in jaundice, 982

Arsenic, effect of, on rectum, 910 use of, in amyloid liver, 1046 in catarrh of bile-ducts, 1057 in constipation, 654 in diabetes mellitus, 227 in dilatation of stomach, 609 in enteralgia, 665 in functional dyspepsia, 457 in gastralgia, 462 in hepatic glycosuria, 975 in chronic intestinal catarrh, 715 in lithæmia, 973 in organic stricture of oesophagus, 425 in pseudo-membranous enteritis, 775 in chronic articular rheumatism, 74 in rheumatoid arthritis, 98

Arsenic-poisoning as a cause of cirrhosis of liver, 991 influence of, on causation of fatty liver, 1067

Arteries, increased width of, in rachitis, 139

Arthritis deformans, 84 gonorrhoeal, 102 rheumatoid, 78

Articular symptoms of chronic gout, 121

Articulations, lesions of, in acute rheumatism, 46 condition of, in scurvy, 179

Artificial feeding, influence of, on causation of entero-colitis, 731 production of gastric ulcer, 514

Ascaris lumbricoides, 952 mystax, 954 vermicularis, 950

Ascites, 1173 in cancerous peritonitis, 1169 in carcinoma of liver, 1037 in carcinoma of pancreas, 1126 in cirrhosis of liver, 995 in cirrhosis of liver, treatment, 1001 in echinococcus of liver, 1104 in Filaria sanguinis, 964 in gastric cancer, 553 in hyperæmia of liver, 987 in local peritonitis, 1161 frequency in amyloid liver, 1044 sudden development of, in thrombosis and embolism of portal vein, 1096

Aspirator, use of, in abscess of liver, 1022 in hydatids of liver, 1107

Astringents, use of, in mercurial stomatitis, 348 in stomatitis ulcerosa, 338

Atmospheric changes, influence of, on causation of tonsillitis, 380

Atonic dyspepsia, 436

Atrophy, acute yellow, of liver, 1023 of abdominal viscera in dilatation of stomach, 600 of gastric walls in dilatation of stomach, 599 of hepatic cells in cirrhosis, 992, 993 of intestinal walls in chronic intestinal catarrh, 704 of kidneys in cirrhosis of liver, 999 of liver in hydatids of, 1102 of liver from occlusion of biliary passages, 1088 of nerve, as a cause of paralysis of oesophagus, 429 of oesophagus in organic stricture, 424 of stomach, 566, 616 of testes in diabetes mellitus, 202 of tongue in chronic parenchymatous glossitis, 367

Auscultatory percussion in ascites, 1174

B.

Bacteria and micrococci in deposits of tonsillitis, 384 influence of, on causation of acute intestinal catarrh, 673 significance of, in cholera infantum, 744

Bandage, use of, in perihepatitis, 990

Bands and loops, formation of, in acute peritonitis, 1153

Bathing in biliary calculus state, 1079 in treatment of constipation, 651, 653 necessity of, in lithæmia, 971 value of, in scrofula, 250

Baths, use of, in diabetes mellitus, 225 in chronic intestinal catarrh, 714, 716 in intestinal indigestion, 632 in gout, 130 in gonorrhoeal rheumatism, 107 cold, use of, in acute gastritis, 470 hot, use of, in hepatic colic, 1082 in muscular rheumatism, 77 in rachitis, 163 in rheumatoid arthritis, 99 hot sand, use of, in local treatment of rheumatoid arthritis, 101 local vapor, use of, in rheumatoid arthritis, 100 mineral, use of, in rheumatoid arthritis, 99 mud, in rheumatoid arthritis, 100 warm and cold, use of, in acute intestinal catarrh, 692 salt, in rachitis, 163

Beading of ribs in rachitis, 152

Beef-essences, use of, in intestinal indigestion, 633

Beef-tea, use of, in entero-colitis and cholera infantum, 754 in rachitis, 161

Beef tape-worm, 933

Belladonna, use of, in cancerous peritonitis, 1122 in constipation, 458, 654 in enteralgia, 665 in spasmodic stricture of oesophagus, 421

Benzoate of sodium, use of, in intestinal indigestion, 636

Benzoic acid, use of, in acute rheumatism, 62

Bifid tongue, 349

Bile, action of, in digestion, 621 composition of, 1062 in pus of hepatic abscesses, 1007 in urine, tests for, 978

Bile-ducts, catarrh of, 1051

Biliary calculi, 1058 seat, 1066 origin and development, 1061-1063 number, shape, and composition, 1059-1061 impaction of, 1074 treatment of, 1079 fistulæ, 1068, 1074 form of intestinal indigestion, diagnosis, 631 passages, affections of. See _Liver, Diseases of_. occlusion of, 1082

Biliousness, 965

Bill of fare for diabetics, 221

Bilharzia hæmatobia, 948

Bismuth subnitrate, use of, in entero-colitis and cholera infantum, 759 in acute yellow atrophy of liver, 1030 in cancer of stomach, 576 in cholera morbus, 725 in functional dyspepsia, 457 in gastralgia, 463 in chronic gastritis, 478 in acute intestinal catarrh, 693 in vomiting of abscess of liver, 1021 in simple ulcer of stomach, 523

Bitartrate of potassium, use of, in ascites, 1179

Bitter waters, use of, in intestinal indigestion, 636

Black pepper, use of, in hemorrhoids, 923 in proctitis, 919 in intestinal ulcer, 827 stools in cancer of stomach, 550 tongue. See _Glossitis parasitica_.

Bladder and kidneys, influence of, on causation of gastralgia, 460

Bleeding, use of, in intestinal obstruction, 864

Blindness in scurvy, 181

Blisters, use of, in acute rheumatism, 63, 68 in cirrhosis of liver, 1002 in rheumatoid arthritis, 100, 101

Blood, alterations of, in diabetes mellitus, 206 coagulable state of, as a cause of thrombosis and embolism of portal vein, 1095 lesions, in acute yellow atrophy of liver, 1029 in cholera morbus, 721 in gout, 115 in acute rheumatism, 31 in scurvy, 173 extravasation of, into skin in scurvy, 178 presence of fat in, in diabetes mellitus, 206, 207 watery condition of, in cirrhosis of liver, 995

Bloodletting, use of, in acute intestinal catarrh, 690 in acute peritonitis, 1145

Blood-vessels, disease of, as a cause of hemorrhage from bowels, 832 lesions of, in diabetes mellitus, 200 in gout, 117 in acute peritonitis, 1133

Bloody stools in chronic intestinal catarrh, 708

Boiled-sago matter in stools of dysentery, 803

Boils, complicating diabetes mellitus, 205 and carbuncles in jaundice, 980

Bones, disease of, in hereditary syphilis, 286 lesions of, in rheumatoid arthritis, 87 in scurvy, 172, 179 of extremities, curvature of, in rachitis, 155 of face, alterations of, in rachitis, 150 rachitic, composition of, 138

Borborygmi in chronic intestinal catarrh, 706 in intestinal indigestion, 627

Bothriocephalus cordatus, 939 cristatus, 939 latus, 938

Bougies, use of, in cancer of rectum, 914 in non-malignant rectal stricture, 917 in organic stricture of oesophagus, 425 in spasmodic stricture of oesophagus, 422 in sphincterismus, 916

Bowels, compression and contraction of, as a cause of intestinal obstruction, 857 hemorrhage from, 830 increased weight of, as a cause of acute intestinal strangulation, 841 irregular, in cancer of intestines, 869 in pseudo-membranous enteritis, 765 in suppurative pylephlebitis, 1100 state of, in biliousness, 966 in catarrh of bile-ducts, 1054, 1055 in cirrhosis of liver, 993 in enteralgia, 661 in lithæmia, 970 in chronic intestinal catarrh, 706

Brain, condition of, in dysentery, 804 disease, organic, distinguished from lithæmia, 917 lesions of, in acute yellow atrophy of liver, 1026 in entero-colitis, 740 in acute intestinal catarrh, 677 in chronic intestinal catarrh, 706 in scurvy, 172 and membranes, lesions of, in acute rheumatism, 39 and meninges, condition of, in rachitis, 148, 149 and spinal cord, organic disease of, influence on causation of enteralgia, 658

Bran bread, use of, in diabetes mellitus, 223

Breast-milk, poor, influence of, on causation of entero-colitis, 731

Breath, in cancrum oris, 340 in scurvy, 177 fetor of, in catarrhal stomatitis, 323

Bright's disease, as a cause of chronic intestinal catarrh, 699 complicating chronic intestinal catarrh, 710

Bromide of ammonium, use of, in acute rheumatism, 62 of arsenic, use of, in diabetes mellitus, 247 of lithium, use of, in chronic articular rheumatism, 74 of potassium, use of, in cholera infantum and entero-colitis, 759 in diabetes mellitus, 227 in enteralgia, 665 in spasmodic stricture of oesophagus, 421 and sodium, use of, in rachitis, 163 of sodium, use of, in cholera morbus, 725 in gastralgia, 463 in acute intestinal catarrh, 698

Bronchial catarrh in trichinosis, 960 and tracheal catarrh, frequency of, in rachitis, 152

Bronchitis complicating gout, 122 chronic, complicating chronic intestinal catarrh, 709

Broncho-pneumonia, frequency of, in rachitis, 153

Bronzing of skin in diseases of pancreas, 1117

Buboes, in Filaria sanguinis, 963

Burning in gullet in phosphorus-poisoning, 1031 sensation in epigastrium in chronic gastritis, 473

Burns, external, influence on causation of acute intestinal catarrh, 670 of skin, influence on causation of intestinal ulcers, 824 of simple ulcer of stomach, 488

Bursitis, gonorrhoeal, symptoms of, 105

Buttermilk, use of, in treatment of acute intestinal catarrh, 691

C.

Cachexia in gastric cancer, 552 in intestinal cancer, 871 of scurvy, 176 influence on causation of fatty liver, 1047

Cæcum, suppuration of, as a cause of suppurative pylephlebitis, 1098

Calcification, defective, in rachitis, causes of, 138, 139 of gastric vessels, in simple ulcer of stomach, 511

Calculi, biliary, 1058 passage of, as a cause of occlusion of biliary passages, 1083 pancreatic, 1130

Calf's pancreas, infusion of, preparation, 1122

Calibre of intestines, alteration of, in chronic catarrh, 700

Calomel, use of, in Anchylostomum duodenale, 956 in catarrh of bile-ducts, 1056 in cholera morbus, 725 in entero-colitis and cholera infantum, 760 in acute gastritis, 469 in acute intestinal catarrh, 695 in jaundice, 982

Camphor, use of, in cholera morbus, 725 in acute intestinal catarrh, 698 in spasmodic stricture of oesophagus, 421

Cancer as a cause of stricture of bowels, 855 of bile-ducts, relation to biliary concretions, 1077 of gall-bladder as a cause of occlusion of common biliary duct, 1085 of intestines, 868 of liver, 1033 of oesophagus, 426 of rectum and anus, 902 of stomach, 530 and ulcer of stomach, influence on causation of chronic intestinal pancreatitis, 1121

Cancrum oris, 338

Capillary congestion in acute intestinal catarrh, 677

Carbohydrates, avoidance of, in dietetic treatment of gout, 128

Carbolic acid, use of, in cholera infantum, 761 in cholera morbus, 725 in entero-colitis, 761 in functional dyspepsia, 459 in acute intestinal catarrh, 696 in pruritus ani, 917 in tuberculous pharyngitis, 402

Carbonate of potassium with lemon-juice, in ascites, 1178

Carbonic acid, distension of stomach by, in diagnosis of gastric dilatation, 596, 601 water, use of, in chronic oesophagitis, 417

Carbuncle of tongue, 368

Carbuncles complicating diabetes mellitus, 205

Carcinoma, of pancreas, 1123 influence of, on causation of dilatation of stomach, 587 of organic stricture of oesophagus, 423 of pylorus and duodenum, as a cause of obstruction of pancreatic duct, 1130 ventriculi, 530

Cardiac affections complicating gonorrhoeal rheumatism, 106 in acute rheumatism, 28, 31 disease, chronic influence of, on causation of chronic oesophagitis, 416 of functional dyspepsia, 448 murmurs in purpura rheumatica, 189 orifice, obstruction of, in gastric cancer, 566 palpitation in constipation, 647

Cardialgia, 459 in functional dyspepsia, 449

Caries of vertebræ, influence of, on causation of chronic oesophagitis, 416

Carlsbad water, artificial, mode of preparing, 522 use of, in chronic gastritis, 477 in dilatation of stomach, 609 in simple ulcer of stomach, 522

Cartilages, lesions of, in gout, 115 in acute rheumatism, 47 in chronic articular rheumatism, 70 of joints, lesions of, in gonorrhoeal rheumatism, 103 in rheumatoid arthritis, 87

Cascara sagrada, use of, in constipation, 656

Caseation of cells in scrofula, 239

Castor oil, use of, in pseudo-membranous enteritis, 774

Casts, epithelial, in acute oesophagitis, 412

Catarrh, acute gastric, 463 chronic gastric, 470 of middle ear in hereditary syphilis, 282 tendency to, in scrofula, 245

Catarrhal gastritis, complicating simple ulcer of stomach, 502 pneumonia, frequency of, in rachitis, 153 stomatitis, 321 ulcers in acute intestinal catarrh, 676 ulcers of stomach, 529

Cathartics, abuse of, influence on causation of pseudo-membranous enteritis, 765 use of, in ascites, 1179 in enteralgia, 665 in gout, 131

Caustic drinks, influence of, on causation of organic stricture of oesophagus, 422 potash, use of, in hemorrhoids, 926

Cauterization, use of, in prolapsus ani, 919 in ulceration of oesophagus, 418 value of, in cancrum oris, 343

Cautery, actual, use of, in cancrum oris, 343

Cell-degeneration in acute yellow atrophy of liver, 1025 hepatic, in phosphorus-poisoning, 1031

Cell-growth, excessive, in scrofula, 238

Cell-proliferation, increased, in chronic intestinal catarrh, 703

Cells, caseation of, in scrofula, 239 fatty degeneration of, in scrofula, 239 of liver, atrophy of, in cirrhosis, 992, 993

Cellular growth, increased, in acute intestinal catarrh, 677

Cerebral disease, influence of, on causation of constipation, 641 hemorrhage complicating constipation, 648 inflammation, tendency to, from gastric irritation, 474 sclerosis in cirrhosis of liver, 999 symptoms of entero-colitis and cholera infantum, treatment, 759 of acute gastritis, 467 syphilis, hereditary, 304

Cerebro-spinal axis, disease of, influence on causation of oesophageal paralysis, 429

Cerium oxalate, use of, in cancer of stomach, 576

Cestodes, 931

Chancroids as a cause of follicular ulceration of rectum and anus, 895

Change of air, in cholera infantum and entero-colitis, 746, 756 value of, in dysentery, 813 of climate, benefit from, in rheumatoid arthritis, 102 value of, in acute intestinal catarrh, 688 in intestinal indigestion, 632 of residence, value of, in chronic intestinal catarrh, 715, 716

Charcoal, use of, in chronic gastritis, 478 in gastric cancer, 576

Cheek, perforation of, in cancrum oris, 341, 342

Cheesy degeneration of mesenteric glands in tabes mesenterica, 1187

Chemical theory of origin of gout, 112

Chemise, Agnew's rectal, in rectal hemorrhage, 927

Chest, alterations of, in rachitis, 152

Chilblains, tendency of scrofulous persons to, 245

Children, constipation in, treatment, 656 acute rheumatism in, peculiarities, 49

Chills in acute pharyngitis, 395 in hepatic abscess, 1008 in hepatic colic, 1071, 1072 in peri-rectal and anal abscesses, 896 in suppurative pylephlebitis, 1099 in typhlitis and perityphlitis, 818

Chloasma cachecticorum, 552

Chloral, use of, in acute rheumatism, 65 in hepatic colic, 1082 in rachitis, 163 hypodermatically, use of, in cholera morbus, 725

Chloride of gold, use of, in amyloid liver, 1046 and sodium, use of, in cirrhosis of liver, 1001

Chlorodyne, use of, in hepatic colic, 1082

Chloroform, use of, in cholera morbus, 725 in enteralgia, 665 in hepatic colic, 1082 in pruritus ani, 917 as a solvent of biliary calculi, 1081

Chlorosis, influence of, on causation of simple ulcer of stomach, 487

Cholæmia in abscess of liver, 1010 in occlusion of biliary passages, 1091

Cholagogues, use of, in lithæmia, 972 in fatty liver, 1050 in hyperæmia of liver, 988

Cholate of sodium, use of, in biliary calculi, 1081

Cholera, effect of, on rectum, 910

Choleraic diarrhoea in acute intestinal catarrh, 682 form of acute intestinal catarrh, treatment, 698

Cholera infantum, 744

CHOLERA MORBUS, 719 Synonyms, 719 Definition, 719 History, 719 Nature, 720 Niemeyer's views of, 720 Nervous origin, 720 Specific origin, 720 Relation to cholera infantum, 720 Etiology, 720 Predisposing causes, 720 Climate, 720 Geographical distribution, 720 Age, 720 Sex, 720 Exhaustion of nervous system, 720 Extreme heat, 720 Mental anxiety, 721 Exciting causes, 721 Septic material from fermentation of food, 721 Improper food, 721 Unripe fruit, 721 Ice-water, 721 Deficient gastric juice, 721 Offensive exhalations, 721 Nervous disturbance from other diseases, 721 Malaria, 721 Sewer-gas, 721 Morbid anatomy, 721 Signs of gastro-intestinal catarrh, 721 Mucous membrane, lesions, 721 Solitary glands, swelling of, 721 Peyer's patches, swelling of, 721 Blood, lesions of, 721 Kidneys, lesions of, 722 Muscular degeneration, 722 Symptoms, 722 Mode of onset, 722 Vomiting, 722 Vomit, characters, 722 Borborygmi, 722 Alvine discharges, 722 Stools, character of, 722 Pain, 722 Cramps, 722 Abdomen, state of, 722 Skin, state of, 722 Physiognomy, 722 Collapse, 722 Mental state, 722 Pulse, 723 Urine, condition of, 723 Temperature, 723 Progress and termination, 723 Tendency to recovery, 723 Mode of death, 723 Duration, 723 Diagnosis, 723 From epidemic cholera, 723 From irritant poisoning, 723 From uræmic choleriform attacks, 724 From acute peritonitis, 724 Prognosis, 724 Mortality, 724 Treatment, 724 Preventive, 724 of vomiting, 725 of heart-weakness, 725 of thirst, 725 Use of emetics, 724 of morphia, hypodermatically, 724 of friction, 724 of alcohol, 725 of ice, 725 of chloroform, 725 of opium, 725 of camphor, 725 of chloral, hypodermatically, 725 of carbolic acid, 725 of bromide of sodium, 725 of hydrocyanic acid, 725 of bismuth, 725 of calomel, 725 Diet, 725

Choleriform diarrhoea, 741

Chordo-tympani nerve, relation to causation of parenchymatous glossitis, 363

Chorea following acute rheumatism, 38 from Oxyuris vermicularis, 951

Chromic acid, use of, in syphilitic pharyngitis, 408

Chronic articular rheumatism, 69 hydrarthrosis of gonorrhoeal rheumatism, 105 gastritis, 470 glossitis, 366 gout, 120 intestinal pancreatitis, 1121 catarrh, 699 oesophagitis, 416 peritonitis, complicating simple ulcer of stomach, 502 pharyngitis, 402 form of catarrhal stomatitis, 323 of dysentery, 800 of peri-rectal and anal abscess, 896 variety of general progressive form of rheumatoid arthritis, 81

Chyluria in Filaria sanguinis, 963

Chyme, composition of, 621

Cicatricial contraction a cause of organic stricture of oesophagus, 422

Cicatrization in simple ulcer of stomach, 506 in syphilitic pharyngitis, 407 of gastric ulcer as a cause of hypertrophic stenosis of pylorus, 615 of ulcers as a cause of stricture of bowel, 855 in chronic intestinal catarrh, 703 influence on causation of occlusion of common biliary duct, 1083 of gastric cancer, 563

Cider, influence of, on causation of gout, 111

Circulation, deficient, in scrofula, 245

Cirrhosis of kidneys in gout, 117 of liver. See _Liver, Diseases of_. of stomach, 611 influence on causation of dilatation of stomach, 590

Clamp and cautery, removal of hemorrhoids by, 925 use of, in rectal polypi, 921

Cleanliness, want of, influence on causation of thrush, 332

Clergyman's sore throat, 402

Climate, change of, in entero-colitis and cholera infantum, 756 influence on causation of abscess of liver, 1002 of catarrh of bile-ducts, 1051 of cholera morbus, 720 of dysentery, 786 of hyperæmia of liver, 983 of acute intestinal catarrh, 669 of rachitis, 143 of rheumatism, acute, 19 of scrofula, 233 of simple ulcer of stomach, 485 warm, in treatment of gout, 131

Closure of hepatic vein as a cause of cirrhosis of liver, 991

Clothing, importance of proper, for prevention of chronic articular rheumatism, 73 proper, necessity of, for prevention of muscular rheumatism, 77

Clubbing of fingers in scrofula, 246

Codeia, use of, in diabetes mellitus, 226 in simple ulcer of stomach, 524

Cod-liver oil, use of, in diabetes mellitus, 228 in intestinal indigestion, 637 in chronic intestinal catarrh, 718 in pseudo-membranous enteritis, 776 in rachitis, 162 in chronic articular rheumatism, 74 in rheumatoid arthritis, 98 in scrofula, 252 in tabes mesenterica, 1194

Coffee, iced, use of, in intestinal catarrh of children, 698

Coffee-grounds vomit in gastric cancer, 546 in simple ulcer of stomach, 493

Colchicum, use of, in acute gout, 134

Cold, influence of, on causation of oesophageal paralysis, 429 of enteralgia, 658 of dysentery, 789, 790 of acute intestinal catarrh, 670 use of, in enteralgia, 665 in acute rheumatism, 66 in hemorrhage from bowels, 834 and damp, influence on causation of acute pharyngitis, 390 of catarrh of bile-ducts, 1051 of jaundice, 977 of parenchymatous glossitis, 359 of pseudo-membranous enteritis, 765 of acute oesophagitis, 410 of rheumatism, acute, 22 of chronic rheumatism, 70 of muscular rheumatism, 75 of gonorrhoeal rheumatism, 103 of rheumatoid arthritis, 88, 90, 91 baths, in acute gastritis, 470

Cold-water injections, in hemorrhoids, 924

Colic, dry, 662 hepatic, 1058, 1070 intestinal. See _Enteralgia_. nervous, 662 in acute intestinal catarrh, 679, 682

Colitis, 667, 683

Collapse in acute pancreatitis, 1119 in acute intestinal catarrh, 682 in cholera morbus, 722 in enteralgia, 662 in hemorrhage from bowels, 833 in hemorrhage into pancreas, 1129 in hepatic colic, 1071 in perforation of simple gastric ulcer, 498

Colles' law of infection of mother by syphilitic children, 263

Colloid cancer of intestine, 868 degeneration of gastric walls, in dilatation of stomach, 600 form of gastric cancer, 564 of cancer of oesophagus, 426

Colocynth, use of, in constipation, 655 in functional dyspepsia, 458

Colon, congenital stricture of, 836 dilatation of, in constipation, 644 displacement of, in constipation, 643 increased length of, in constipation, 644 lesions, in entero-colitis, 738 ulcers of, in chronic intestinal catarrh, 702 and rectum, dilatation of, from fecal impaction, 852

Colotomy, lumbar, for cancer of rectum, 915, 916

Coma, dyspnoeic, in gastric cancer, 554 in acute yellow atrophy of liver, 1027 in acute rheumatism, 38 in cirrhosis of liver, 999 in diabetes mellitus, 204, 205 in dilatation of stomach, 596

Complications of biliary concretions, 1076 of cancrum oris, 341 of constipation, 648 of diabetes mellitus, 210 of gastric cancer, 560 of gout, 121 in chronic intestinal catarrh, 709 of mercurial stomatitis, 346 of acute oesophagitis, 414 of chronic oesophagitis, 417 of parenchymatous glossitis, 362 of syphilitic pharyngitis, 407 of purpura, 190 of acute rheumatism, 31 of gonorrhoeal rheumatism, 106 of rheumatoid arthritis, 83-86 of Heberden's nodosities of rheumatoid arthritis, 86 of simple ulcer of stomach, 502 of tonsillitis, 383 of tabes mesenterica, 1193 and sequelæ of aphthous stomatitis, 329 of dysentery, 805

Compression, use of, in hypertrophy of tongue, 353 and contraction of bowel as a cause of intestinal obstruction, 857

Conception, infection of child with syphilis at moment of, 262, 267

Condensed milk, use of, in cholera infantum, 754 in entero-colitis, 754

Condurango, use of, in gastric cancer, 576

Condylomata in hereditary syphilis, 279 of rectum and anus, 901

Confluent form of aphthous stomatitis, 329

Congenital deficiency of tongue, 348, 349 nature of macroglossia, 350 malformations of rectum and anus, 879 origin of dilatation of oesophagus, 430 of organic stricture of oesophagus, 422 rachitis, 141-143

Congestion of lungs in acute rheumatism, 37 passive and active, as a cause of hemorrhage from stomach, 581

Conium, use of, in spasmodic stricture of oesophagus, 421

Connective tissue, hyperplasia of, in chronic intestinal pancreatitis, 1122 increase of, in acute yellow atrophy of liver, 1025 new, development of, in cirrhosis of liver, 992

Consanguineous marriages, influence on causation of scrofula, 234

Consistence of liver in amyloid disease of, 1042

CONSTIPATION, 638 Synonyms, 638 Nature, 638, 639 Definition, 638, 639 Etiology, 639 Age, 639 Female sex, 639, 640 Heredity, 640 Habit, 640 Occupation, 640 sedentary, 640 Acute and chronic brain disease, 641 Abuse of aperients, 641 opium, 641 Lead-poisoning, 641 Tobacco, 641 Chronic pulmonary disease, 641 heart disease, 641 liver disease, 641 Painful disease of rectum, 642 Chronic cachexiæ, 642 Wasting diseases, 642 Disorders of digestion, 642 Pancreatic disease, 642 Loss of fluids, 642 by perspiration, 642 by diuresis, 642 by diabetes, 642 by exercise, 643 Food, 643 Intestinal worms, 643 Morbid anatomy, 643 Displacement of colon, 643 Dilatation of intestines, 643 of sigmoid flexure, 643 of colon, 644 Increased length of colon, 644 Mucous membrane, intestinal, lesions of, 644 Ulcers of intestines, 644 Thinning of intestinal walls, 644 Hypertrophy of intestinal walls, 644 Fecal accumulations, 644 character, 645 Scybalæ, formation of, 645 Hemorrhoidal tumors, 645 Peri-rectal abscesses, 645 Fistulæ, 645 Symptoms, 645 Fulness and heat of rectum, 645 Appetite, impaired, 646, 647 Tongue, state, 646, 647 Flatulence, 646, 647 Abdominal distension, 646, 647 pain, 646 Stools, character, 646 Cold feet, 646 Pain in groin, 646 Varicocele, 646 Seminal emissions, 646 Urinary retention, 646 Jaundice, 646 Uterine displacements, 647 Nervous symptoms, 647 Vertigo, 647 Headache, 646, 647 Visual disorders, 647 Disorders of hearing, 647 Heart-palpitation, 647 Chilliness, 647 Menstrual disorders, 647 Anæmia and chlorosis, 647 Mental depression, 647 Hallucinations, 647 Relation of displacements of colon to suicide, 647 Fever, 647, 648 Urine, state of, 648 Skin disorders, 648 Complications and results, 648 Ulceration of intestinal mucous membrane, 648 Abscess, peri-rectal, 648 Fistulæ, 648 Hemorrhoids, 648 Intussusception, 648 Typhlitis and perityphlitis, 648 Hæmoptysis, 648 Cerebral hemorrhage, 648 Hernia, 648 Death, cause of, 649 Diagnosis, 649 From secondary constipation, 649 From rectal growths and tumors, 649 From stricture, 649 From abdominal tumors, 649, 650 From obstruction by gall-stones, 649 Of stercoral tumors, 649, 650 physical signs, 650 Prognosis, 650 Treatment, 651 Prophylactic, 651 Exercise, 651, 653 Bathing, 651 Acute form, 651 Use of purgatives, 651 enemata, 651 Chronic form, 652 Diet, 652 Use of milk, 652 Of atony of colon, 653 Use of bathing, 653 of massage, 653 of cold douche, 653 of electricity, 653 of abdominal belt, 654 of diet, 654 of mineral waters, 652, 653, 655 of strychnia, 654 of iron, 654 of belladonna, 654 of arsenic, 654 of ipecacuanha, 654 of zinc salts, 655 of enemata, 655 of cold water, 655 of water, 655 of podophyllin, 655 of rhubarb, 655 of aloes, 655 of colocynth, 655 of ox-gall, 655 of salines, 655 of Epsom salts, 655 of Rochelle salts, 655 of purgatives, mode, 656 of cascara sagrada, 656 of alum, 656 of sulphur, 656 of guaiacum, 656 of colchicum, 656 of senna, 656 of tonics, 657 In children and infants, 656 Diet, 656 Objections to vegetables, 654 Use of soap suppository, tonics, 656, 657

Constipation due to disease of spinal cord, 906 in cancer of intestine, 891 in dilatation of stomach, 594 in fissure of anus and rectum, 888 in functional dyspepsia, 450 in gastric cancer, 550 in chronic gastritis, 475 in gout, 118 in hepatic colic, 1072 in chronic intestinal catarrh, 706 in intestinal indigestion, 627 in acute pancreatitis, 1119 in acute peritonitis, 1141 in acute rheumatism, 27 in rheumatoid arthritis, 83 in simple ulcer of stomach, 494, 495 in tabes mesenterica, 1190 in typhlitis and perityphlitis, 819 significance of, in rachitis, 154 influence on causation of enteralgia, 658 of functional dyspepsia, 447 of hemorrhage from bowels, 830 of internal hemorrhoids, 884 of acute intestinal catarrh, 671 of intestinal indigestion, 625 of rectal prolapse, 881 of typhlitis, 814 as a cause of intestinal obstruction, 850 as a cause of torsion of cæcum, 853

Constitutional peculiarity, influence on causation of catarrh of bile-ducts, 1051 treatment of cancer of oesophagus, 428 of cancrum oris, 343 of enteralgia, 665 of mercurial stomatitis, 348

Contagiousness of dysentery, 793, 794 of scurvy, 169 of stomatitis ulcerosa, 336 of thrush, 332

Contraction of stomach in gastric cirrhosis, 613

Convalescence in entero-colitis, 736 in acute gastritis, treatment of, 470 in acute rheumatism, treatment of, 169 of simple ulcer of stomach, treatment of, 529 of typhlitis, treatment of, 822

Convulsions in enteralgia, 662 in chronic gastritis, 474 in hepatic colic, 1071 in acute yellow atrophy of liver, 1027 in morbid dentition, 374 in occlusion of biliary ducts, 1092 in acute oesophagitis, 414 in rachitis, 149 in rachitis, treatment of, 163, 164 in acute rheumatism, 38 in scurvy, 180 relation of, to macroglossia, 350

Cooking, defective, influence on causation of functional dyspepsia, 445 necessity of thorough, in trichinosis, 962

Co-ordination of muscles of defecation, loss of, treatment of, 916

Copaiba, use of, in hemorrhoids, 923 in chronic intestinal catarrh, 718 in cirrhosis of liver, 1001 in proctitis, 919 in pseudo-membranous enteritis, 775

Copper sulphate, use of, in pseudo-membranous enteritis, 775 in phosphorus-poisoning, 1033

Cornea in interstitial keratitis of hereditary syphilis, 299 lesions of, in chronic intestinal catarrh, 706

Corneal ulceration complicating chronic intestinal catarrh, 710

Cornil and Ranvier on causes of scrofulous inflammation, 239

Corrosive poisons, influence on causation of acute gastritis, 465 of simple ulcer of stomach, 486 sublimate, use of, in chronic intestinal catarrh, 717 in pseudo-membranous enteritis, 775 in suppurative pylephlebitis, 1101

Coryza of hereditary syphilis, 277

Cough in functional dyspepsia, 451 in acute pharyngitis, 394 in chronic pharyngitis, 404 in tuberculous pharyngitis, 401

Coughing, influence on causation of prolapse of rectum, 881

Counter-irritation, use of, in cirrhosis of liver, 1002 in acute and chronic gastritis, 469, 479 in acute intestinal catarrh, 688, 690, 698 in spasmodic stricture of oesophagus, 422 in pseudo-membranous enteritis, 776 in simple ulcer of stomach, 524

Course of biliary concretions, 1076 of acute yellow atrophy of liver, 1029 of amyloid liver, 1044 of carcinoma of liver, 1039 of cirrhosis of liver, 998 of functional diseases of liver, 967, 970, 974, 981 of hyperæmia of liver, 987 of occlusion of biliary passages, 1092 of phosphorus-poisoning, 1032 of perihepatitis, 989 of suppurative pylephlebitis, 1101 of hereditary syphilis, 273 of intestinal indigestion, 630 of cancer of stomach, 538 of dilatation of stomach, 603 of simple ulcer of stomach, 500 of acute rheumatism, 44 of gonorrhoeal rheumatism, 106

Cow's milk, impure, influence on causation of entero-colitis, 731 composition, 749, 750

Cramps in cholera morbus, 722 in diabetes mellitus, 206 muscular, in muscular rheumatism, 75

Craniotabes, occurrence of, in rachitis, 147

Creasote, use of, in enteralgia, 666 in vomiting of abscess of liver, 1021 in treatment of liver-flukes, 1110

Cretaceous degeneration of mesenteric glands in tabes mesenterica, 1189

Croton oil, effect on rectum, 910

Croupous nature of pseudo-membranous enteritis, 767, 768

Cry, peculiarity of, in thrush, 334

Cryptogam as a cause of mycotic tonsillitis, 381

Cubebs, use of, in chronic pharyngitis, 406 in pseudo-membranous enteritis, 775

Cutaneous affections complicating acute rheumatism, 42 rheumatoid arthritis, 84 eruptions of anus, 892

Cyanotic atrophy of liver, 985

Cylinder-cell epithelioma, common form of intestinal cancer, 871

Cylindrical-celled epithelial form of gastric cancer, 564

Cynanche tonsillaris, 379

Cysts of echinococci of liver (description), 1102 of hydatids of liver, contents, 1103 of mucous membrane of stomach, 579 of false membrane, in acute peritonitis, 1135 of Tænia echinococcus, character, 944 formation and origin of, in chronic intestinal catarrh, 704 formation of, from obstruction of pancreatic ducts, 1130

Cystic duct, occlusion of, effects of, 1085

Cystitis and orchitis complicating acute rheumatism, 42

D.

Dactylitis in hereditary syphilis, 291

Daettwyler's and Cohnheim's experiments in artificial production of gastric ulcers, 514

Death, cause of, in cancrum oris, 341 in chronic intestinal catarrh, 709 in constipation, 649 in dilatation of oesophagus, 432 in entero-colitis, 736 in gastric cancer, 559 in mercurial stomatitis, 347 in thrush, 334 in simple ulcer of stomach, causes of, 502 mode of, in cholera morbus, 723 in dilatation of stomach, 603 sudden, cause of, in acute rheumatism, 50

Debility in gastric cancer, 551 in tabes mesenterica, 1189 influence of, on causation of aphthous stomatitis, 326

Defecation, difficult, in cancer of rectum and anus, 904

Definition of ankyloglossia, 349 of biliousness, 965 of biliary concretions, 1058 of catarrh of bile-ducts, 1051 of occlusion of biliary passages, 1082 of cancrum oris, 338 of cholera morbus, 719 of constipation, 638, 639 of diabetes mellitus, 195 of dysentery, 777 of functional dyspepsia, 436 of enteralgia, 658 of gastralgia, 459 of acute gastric catarrh, 463 of chronic gastritis, 470 of glossitis, 354, 355, 357, 359, 367 of glossanthrax, 368 of gout, 108 of hepatic glycosuria, 973 of cancer of intestines, 868 of intestinal ulcer, 823 of jaundice, 975 of abscess of liver, 1002 of acute yellow atrophy of liver, 1023 of amyloid liver, 1040 of carcinoma of liver, 1033 of cirrhosis of liver, 990 of echinococcus of liver, 1101 of fatty liver, 1046 of hyperæmia of liver, 983 of macroglossia, 349 of morbid dentition, 371 of oesophagitis, 409 of chronic oesophagitis, 416 of carcinoma of oesophagus, 426 of dilatation of oesophagus, 430 of stricture of oesophagus, 419, 422 of ulceration of oesophagus, 418 of paralysis of oesophagus, 429 of perihepatitis, 989 of acute pharyngitis, 390 of chronic pharyngitis, 402 of tubercular pharyngitis, 400 of phosphorus-poisoning, effect on liver, 1030 of purpura, l86, 187 of pseudo-membranous enteritis, 763 of rheumatism, acute, 19 of chronic articular rheumatism, 69 of muscular rheumatism, 74 of rachitis, 137 of scrofula, 231, 232 of scurvy, 167 of cancer of stomach, 530 of cirrhosis of stomach, 611 of dilatation of stomach, 586 of acute dilatation of stomach, 610 of hemorrhage from stomach, 580 of simple ulcer of stomach, 480 of stomatitis, 321 of aphthous stomatitis, 325 of catarrhal stomatitis, 321 of mercurial stomatitis, 344 of toxic stomatitis, 344 of stomatitis ulcerosa, 336 of stomatorrhagia, 370 of tabes mesenterica, 1182 of thrombosis and embolism of portal vein, 1095 of thrush, 331 of tonsillitis, 379

Deformities in chronic gout, 121 of rachitis, treatment, 165, 166 of joints in chronic variety of general rheumatoid arthritis, 81, 82 in partial form of rheumatoid arthritis, 85, 86

Deformity in gonorrhoeal rheumatism, 104

Degeneration of pancreas, 1128 of liver, fatty, 1046 fatty and amyloid, of gastric walls, in functional dyspepsia, 451 fatty and colloid, of gastric walls, in dilatation of stomach, 600 lardaceous, of intestine, 874 of vessels in lardaceous disease of intestines, 876

Deglutition, difficult, in parenchymatous glossitis, 361 in tuberculous pharyngitis, 401 in aphthous stomatitis, 329 in mercurial stomatitis, 345 in tonsillitis, 381 impediment to, in organic stricture of oesophagus, 423 painful, in acute oesophagitis, 413 slow, in oesophageal paralysis, 429

Dejecta, influence of, on causation of dysentery, 791, 792

Delirium of enteralgia, 662 in acute intestinal catarrh, 681 in acute internal strangulation of intestines, 843 in acute peritonitis, 1142 in acute rheumatism, 37, 38

Delirium ferox, in acute yellow atrophy of liver, 1027

Demulcent drinks, use of, in acute gastritis, 469

DENTITION, MORBID, 371 Definition, 371 Synonyms, 371 Etiology and symptoms, 371 Teeth, order of normal eruption of, 372 precipitate eruption of, 372 tardy eruption of, 372 rachitis as a cause of tardy eruption of, 372 Mild cases, initial symptoms, 373 increase of saliva, 373 general, 373 Ulcerations, aphthous, 373 at point of eruption, 373 Stomatitis, catarrhal, 373 Pain, 373 Heat and tumefaction of gum, 373 Constitutional, 374 Reflex nervous symptoms, 374 Convulsions, 374 characters of, 374 cause of, 374 Paralyses, 375 Idiocy, 375 Gastro-intestinal disorders, 374 causes, 374 mechanical, 374 Otitis media, 375 Conjunctivitis, 375 Second dentition, 375 Teeth, order of eruption, 375 Symptoms, 375 Nervous system, 376 Gastro-intestinal tract, 375 Wisdom teeth, eruption of, 376 Symptoms of, 376 Diagnosis, 376 Prognosis, 376 Treatment, 376 Preventive, 376 Avoidance of cold, 376 Diet, 377 Complications, 377 Aphthous ulcerations, 377 Local, 377 Use of lancet, 377 Method of incision, 378 contraindications, 378

Dentition, influence on causation of macroglossia, 350 of aphthous stomatitis, 326 of catarrhal stomatitis, 322 of tabes mesenterica, 1186 relation to entero-colitis, 733

Deposit of thrush, microscopic appearance of, 333 in herpetic or membranous form of pharyngitis, nature of, 392

Deposits in tonsillitis, nature of, 384

Depressing emotions, influence of, on causation of scurvy, 169 of cancer of stomach, 536

Depression, mental, in chronic intestinal catarrh, 706 of spirits in functional dyspepsia, 451 of vital powers in pseudo-membranous enteritis, 765, 766

Dermalgia distinguished from enteralgia, 664

Desquamation of tongue in parenchymatous glossitis, 361

Deuteropathic form of tonsillitis, 380

Development of gastric ulcer, influence of digestive action of gastric juice upon, 512

Diabetes, influence on causation of constipation, 642

DIABETES MELLITUS, 195 Definition, 195 Etiology, 203 Nervous shock, influence on causation, 203 Mental anxiety, influence on causation, 203 Malaria, influence on causation, 203 Injury, influence on causation, 203 Heredity, influence on causation, 203 Sexual excess, influence on causation, 203 Age, influence on causation, 203 Sex, influence on causation, 203 Race, influence on causation, 204 Geographical distribution, 203 Pathology and pathogenesis, 195 Hyperæmia of liver, relation of, to, 195 causes of, 195-199 Diabetic area of medulla oblongata, result of puncture, 195 Glycosuria, artificial methods of production, 195-199 Glycogenic influence, pathology of, 196 Sympathetic nerve, relation of, to production of glycosuria, 196 Glycosuria, artificial, irritative nature of, 198 Vaso-motor nerves, influence on production of glycosuria, 196-199 Glycosuria, production of, from medicinal substances, 198 Pavy's chemical theory of production of glycosuria, 199 Morbid anatomy, 199 Nervous system, lesions of, 200 Dickinson's alterations of nervous centres, 200 Blood-vessels, lesions of, 200 Pancreas, lesions of, 200 nature of lesions, 200 disease of, relation to causation, 201 Liver, enlargement of, 201 lesions of, 201 Kidneys, lesions of, 202 Testes, atrophy of, 202 Lungs, lesions of, 202 Phthisis, complicating nature of, 202 Symptoms, 204 Initial, 204 Thirst, 204 Dryness of skin, 204 Loss of weight, 204 Pruritus of genitalia, 204 Muscular weakness, 204 Sexual appetite, loss of, 204 Appetite, 204 Dyspepsia, 204 Vision, disorders of, 204 Hearing, disorders of, 205 Temperature, 204 Carbuncles and boils, 205 Ulcerated surfaces, 205 Eczema of genitalia, 205 Urethritis, 205 Coma, 204, 205 causes of, 205, 206 mode of onset, 205 Acetonæmia, 205, 206 Nervous symptoms, 205, 206 Cramps, 206 Facial paralysis, 206 Neuralgia, 206 Blood, alterations of, 206 presence of fat in, 206, 207 source of fat in, 207 corpuscles, diminution of, 207 Urine, changes in, 207 amount of sugar in, 207 effect of diet and exercise on amount of sugar in, 207, 208 presence of inosite in, 208 specific gravity of, 208 color of, 208 odor of, 208 acetone and alcohol, presence of, 209 Albuminuria, 208 Duration, 210 Complications, 210 Phthisis, 210 Duodenal catarrh, 210 Boils and abscesses, 205, 210 Jaundice, 210 Pancreatic disease, 210 Diagnosis, 210 Tests for sugar, 211 Fehling's test, 211 quantitative, 212 Fermentation test, 212 quantitative, 213 Picric acid and potash test, 213 quantitative, 214 Indigo-carmine test, 216 quantitative, 216 precautions, 217 Test for inosite, 217 Prognosis, 217 Influence of pancreatic disease upon, 218 of age upon, 218 of phthisis upon, 218 Treatment, 218 Dietetic, 218 By skim-milk, 218 mode of administering, 219 Peptonized milk, 219, 220 Saccharine foods admissible in, 220 Foods and drinks admissible in, 220, 221 Bill of fare for diabetics, 221 Alcoholic beverages admissible, 222, 225 Gluten bread, use of, 222 Bran bread, use of, 223 Almond food, use of, 223, 224 Substitutes for sugar in food, 224 Use of bicarbonate of sodium and potassium in place of sugar, 224 Hygienic, 225 Use of mineral waters, 225, 226 Ventilation, 225 Use of baths, 225 Medicinal, 226 Use of codeia, 226 of opium, 226, 227 of ergot, 227 of bromide of potassium, 227 of bromide of arsenic, 227 of arsenic, 227 of strychnia, 227 of phosphates, 227 of iodide of potassium, 228 of tincture of iodine, 228 of nitrate of uranium, 230 of lactic acid, 228 of cod-liver oil, 228 of soap, 228 of iodoform, 229 of salicylate of sodium and salicylic acid, 229, 230 of alkalies, 229 Transfusion of blood, 229 Of neuralgia, 229

Diabetes mellitus, influence on causation of pruritus ani, 909 simple gastric ulcer, 488 relation to disease of pancreas, 1117

Diabetic area of medulla oblongata, effects of puncture, 195

Diagnosis of ascites, 1177 of biliary calculi, 1078 of catarrh of bile-ducts, 1055 of occlusion of biliary passages, 1092 of cancrum oris, 342 in cholera infantum, 745 of cholera morbus, 723 of constipation, 648 of diabetes mellitus, 210 of dysentery, 806 of functional dyspepsia, 452 of enteralgia, 663 of entero-colitis, 740 of fistula in ano, 898 of gastralgia, 461 of acute gastritis, 468 of chronic gastritis, 475 of simple gastric ulcer, 514 of superficial glossitis, 357 of chronic superficial glossitis, 367 of parenchymatous glossitis, 363 of chronic parenchymatous glossitis, 368 of glossitis parasitica, 359 of gout, 124 of hemorrhage from bowels, 833 of hepatic colic, 1078 of hepatic glycosuria, 974 of ileo-colitis, 685 of acute intestinal catarrh, 684 of chronic intestinal catarrh, 710 of ulcerations in acute intestinal catarrh, 685 of intestinal cancer, 873 of indigestion, 630 of obstruction, 858 by fecal accumulations, 860 by internal hernia, 860 by gall-stones, 860 of seat of intestinal obstruction, 861 of intestinal ulcer, 828 of lardaceous degeneration of intestines, 876 of torsion of intestines, 860 of jaundice, 981 of lithæmia, 970 of abscess of liver, 1018 of acute yellow atrophy of liver, 1029 of amyloid liver, 1045 of carcinoma of liver, 1039 of cirrhosis of liver, 999 of fatty liver, 1049 of hydatids of liver, 1104 of hyperæmia of liver, 988 of liver-flukes, 1110 of lumbago, 77 of macroglossia, 353 of morbid dentition, 376 of acute oesophagitis, 414 of chronic oesophagitis, 417 of dilatation of oesophagus, 433 of paralysis of oesophagus, 429 of organic stricture of oesophagus, 424 of spasmodic stricture of oesophagus, 420 of ulceration of oesophagus, 418 of acute pancreatitis, 1119 of carcinoma of pancreas, 1126 of obstruction of pancreatic ducts, 1131 of perihepatitis, 989 of acute peritonitis, 1143 of tubercular peritonitis, 1167 of acute pharyngitis, 396 of chronic pharyngitis, 404 of syphilitic pharyngitis, 408 of tuberculous pharyngitis, 401 of phosphorus-poisoning, 1032 of pleurodynia, 77 of pseudo-membranous enteritis, 773 of purpura, 190 of suppurative pylephlebitis, 1101 of hypertrophic stenosis of pylorus, 615 of acute rheumatism, 47 of chronic articular rheumatism, 73 of gonorrhoeal rheumatism, 107 of muscular rheumatism, 76 of rheumatoid arthritis, 92 of scrofula, 248 of scurvy, 182 of cancer of stomach, 569 of cirrhosis of stomach, 613 of dilatation of stomach, 600 of hemorrhage from stomach, 584 of simple ulcer of stomach, 514 of aphthous stomatitis, 329 of catarrhal stomatitis, 325 of mercurial stomatitis, 347 of stomatitis ulcerosa, 337 of stomatorrhagia, 371 of hereditary syphilis, 309 of bone disease of hereditary syphilis, 289, 290 of erythema of hereditary syphilis, 278 of interstitial keratitis in hereditary syphilis, 299 of nervous disease in hereditary syphilis, 304 of pemphigus in hereditary syphilis, 276 of pustular syphilides in hereditary syphilis, 279 of roseola in hereditary syphilis, 278 of tabes mesenterica, 1191 of thrombosis and embolism of portal vein, 1096 of thrush, 334 of tonsillitis, 386 of tongue-tie, 349 of tubercular ulceration of tongue, 369 of torticollis, 78 of trichinosis, 961 of typhlitis and perityphlitis, 820

Diaphoretics, use of, in ascites, 1179 in muscular rheumatism, 77

Diaphragmatic hernia, 843

Diarrhoea, in acute gastritis, 467 in chronic gastritis, 475 in gout, 118 in acute intestinal catarrh, 679, 681 in chronic intestinal catarrh, 706 in intestinal indigestion, 627 in lardaceous degeneration of intestines, 874 in intussusception, 848 in amyloid liver, 1044 in diseases of pancreas, 1115 in acute secondary pancreatitis, 1121 in carcinoma of pancreas, 1126 in tabes mesenterica, 1190 in cancer of stomach, 550 in dilatation of stomach, 594 in aphthous stomatitis, 329 in catarrhal stomatitis, 323 in trichinosis, 960 influence on causation of prolapse of rectum, 881 and dysentery complicating acute rheumatism, 42

Diarrhoeal diseases of children, mortality in, 726, 727

Diet in biliousness, 967 in catarrh of bile-ducts, 1056 in biliary concretions and hepatic colic, 1079 in cholera morbus, 725 in constipation, 652, 654 in constipation of children, 656 in diabetes mellitus, 218-224 in functional dyspepsia, 452 in dysentery, 809, 812 in enteralgia, 666 in pseudo-membranous enteritis, 776 in acute gastritis, 468 in chronic gastritis, 476 in chronic superficial glossitis, 367 in parenchymatous glossitis, 365 in gout, 127, 133 in hemorrhage from bowels, 834 in hepatic glycosuria, 975 in intestinal cancer, 874 in acute intestinal catarrh, 687, 688, 690, 692 in chronic intestinal catarrh, 714, 716 in intestinal indigestion, 633, 634 in intestinal ulcer, 829 in lardaceous degeneration of intestines, 876 in jaundice, 983 in abscess of liver, 1021 in amyloid liver, 1046 in cirrhosis of liver, 1000 in fatty liver, 1050 in hyperæmia of liver, 988 in lithæmia, 971 in morbid dentition, 376 in acute oesophagitis, 416 in chronic oesophagitis, 417 in dilatation of oesophagus, 434 in oesophageal paralysis, 430 in acute pancreatitis, 1120 in carcinoma of pancreas, 1127 in acute peritonitis, 1151 in tubercular peritonitis, 1168 in acute pharyngitis, 398, 399 in phosphorus-poisoning, 1033 in purpura, 193 in rachitis, 159 in acute rheumatism, 69 in chronic articular rheumatism, 74 in gonorrhoeal rheumatism, 107 in rheumatoid arthritis, 102 in scrofula, 249 in scurvy, 183 in cancer of stomach, 576 in dilatation of stomach, 603, 608 in simple ulcer of stomach, 519-522 in aphthous stomatitis, 330 in catarrhal stomatitis, 325 in syphilitic children, 315 in thrush, 335 in tonsillitis, 388 in trichinosis, 962

Digestion, disturbances of, in Anchylostomum duodenale, 956 in Ascaris lumbricoides, 953 in ascites, 1177 in constipation, 853 in pseudo-membranous enteritis, 765 from presence of gall-stones, 1070 in gout, 118 in hepatic glycosuria, 974 in intestinal hepatitis, 993 in intestinal ulcer, 826 in lithæmia, 969 in abscess of liver, 1013 in echinococci of liver, 1104 in fatty liver, 1048 in carcinoma of pancreas, 1125 in tubercular peritonitis, 1166 in suppurative pylephlebitis, 1100 in non-malignant stricture of rectum, 886 in acute rheumatism, 27 in gonorrheal rheumatism, 104 in muscular rheumatism, 76 in scurvy, 173 in tabes mesenterica, 1189 in tape-worm, 940 in trichinosis, 960 in typhlitis and perityphlitis, 819

Digitalis, use of, in ascites, 1179 stupes, use of, in cirrhosis of liver, 1001

Dilatation of bowel in dysentery, 812 of oesophagus, 430 in organic stricture, 424 forcible, in organic stricture of oesophagus, 426 of stomach, 586 acute, of stomach, 610 of stomach in chronic gastritis, 472 in gastric cancer, 566 in simple ulcer of stomach, 503 in anal fissure and rectal ulceration, 912 of rectal pouches, 885 in non-malignant rectal stricture, 917 and incision of rectum for sphincterismus, 916

Dilators, use of, in cancer of oesophagus, 428

Diluents, use of, in chronic gastritis, 477

Diphtheria distinguished from acute pharyngitis, 396 influence of, on causation of acute peritonitis, 438 distinguished from tonsillitis, 387

Discharges, characters of, in dysentery, 796, 803 of fistula in ano, 898 mucous, in non-malignant stricture of rectum, 886 and purulent, in ulceration of rectum and anus, 894

Disinfectants, use of, in cancrum oris, 343

Disinfection in acute intestinal catarrh, 688 of discharges of dysentery, 808

Dislocation of intestine as a cause of obstruction, 851

Displacements of stomach, 617

Dissemination of echinococcus, 944

Distomum conjunctum, 947 crassum, 948 hepaticum, 946, 1109 heterophyes, 948 lanceolatum, 947, 1109 ophthalmobium, 948 ringeri, 948 sinense, 947

Diuresis, influence on causation of constipation, 642

Diuretics, use of, in ascites, 1178

Diverticula of stomach, 617

Dogs, infection of Tænia echinococcus, liability to, from association with, 945

Douche, cold, use of, in constipation, 653

Drinking-water, dissemination of Ascaris lumbricoides by, 952 necessity of pure, in prevention of dysentery, 808

Dropsy, general, in amyloid liver, 1044 in chronic intestinal catarrh, 709 of gall-bladder from biliary calculi, 1077

Drowsiness in entero-colitis, 735, 736

Dry colic, 662

Dryness, influence on causation of dysentery, 788

Ductus communis choledochus, stenosis of, 1082 seat of occlusion of, 1083, 1084 pancreaticus, obstruction, 1129

Duodenal catarrh complicating diabetes mellitus, 210 form of gastric ulcer, etiology, 825 of intestinal cancer, symptoms, 870 of chronic intestinal catarrh, diagnosis, 711 ulcers, in chronic intestinal catarrh, 703, 713

Duodenitis, 667, 682 acute, relation to integumental burns, 682

Duodenum, congenital stricture of, 836 lesions of, in entero-colitis, 737 in acute intestinal catarrh, 674 perforation of, by gall-stones, 1068-1074

Durande's solvent for biliary calculi, 1080

Duration of catarrh of bile-ducts, 1055 of biliousness, 967 of occlusion of biliary passages, 1092 of cholera infantum, 723 of cholera morbus, 746 of diabetes mellitus, 210 of enteralgia, 660 of pseudo-membranous enteritis, 774 of parenchymatous glossitis, 362 of acute gout, 119 of paroxysms of hepatic colic, 1071 of hepatic glycosuria, 974 of cancer of intestines, 871-873 of acute intestinal catarrh, 682 of intestinal indigestion, 630 of intestinal obstruction, 862 of intestinal ulcer, 827 of acute internal strangulation of intestines, 843 of intussusception, 849 of jaundice, 981 of abscess of liver, 1017 of acute yellow atrophy of liver, 1029 of amyloid liver, 1044 of carcinoma of liver, 1039 of cirrhosis of liver, 999 of fatty liver, 1049 of hydatids of liver, 1105 of hyperæmia of liver, 987 of lithæmia, 970 of acute oesophagitis, 414 of spasmodic stricture of oesophagus, 420, 421 of carcinoma of pancreas, 1126 of obstruction of pancreatic ducts, 1131 of chronic interstitial pancreatitis, 1122 of perihepatitis, 989 of acute peritonitis, 1143 of acute pharyngitis, 395, 396 of syphilitic pharyngitis, 407 of phosphorus-poisoning, 1032 of suppurative pylephlebitis, 1101 of acute rheumatism, 44 of chronic articular rheumatism, 72 of gonorrhoeal rheumatism, 106 of muscular rheumatism, 76 of acute variety of general rheumatoid arthritis, 80 of chronic variety of general rheumatoid arthritis, 82 of aphthous stomatitis, 329 of catarrhal stomatitis, 323 of mercurial stomatitis, 346 of stomatitis ulcerosa, 337 of cancer of stomach, 559 of simple ulcer of stomach, 501 of transmission power of syphilis, 257-260 of tabes mesenterica, 1193 of thrush, 334 of trichinosis, 960 of typhlitis and paratyphlitis, 820

Dyscrasia, gouty, symptoms of, 120

Dysenteric ulceration, influence on causation of abscess of liver, 1004

DYSENTERY, 777 Definition, 777 Etymology, 777 History, 777 Ancient, 777-780 Modern, 780-784 General remarks, 784 Nature, 784 Primary nature, 784 Secondary nature, 784 Periodicity of recurrence, 784, 786 Tendency to circumscription, 785 A disease of armies, 785, 786 Etiology, 786 Climate, influence on causation, 786 Hot seasons, influence on causation, 787 Moisture, influence on causation, 788 Dryness, influence on causation, 788 Decay of animal and vegetable matter, 787, 789 Atmospheric changes, 789 Taking cold, influence on causation, 789, 790 Nervous influence, 790 Food, irritating and improper, 791 Water, impure, 791 Dejecta, influence on causation, 791 mechanical irritation of colon by, 791 propagation of the disease by, 792 Specific nature, 792 Micro-organism, influence on causation, 792 Contagiousness, 793, 794 Poison, duration of activity of, 794, 795 Pathology, 796 Local nature, 796 Discharges, characters of, 796, 803 Morbid anatomy, 797 Mucous membrane, an inflammation of, 797 Lesions of catarrhal form, 797 Mucous membrane, state of, 798 Cells, desquamation of, 798 Follicles, intestinal, alterations in, 798 Protuberances of mucosa, 798, 799 Tenesmus, cause of, 799 Of pseudo-membranous form, 799 False membranes, formation, 799 Ulcers, character and seat of, 799 Perforation, 799 date of occurrence, 800 Perityphlitis, lesions of, 800 Of chronic form, 800 Ulceration, seat and character, 800 Cicatrization in, 800 Mesenteric glands, lesions of, 801 Kidneys, lesions of, 801 Joints, lesions of, 801 Liver, lesions of, 801 abscess of, 801 Symptoms, 802 Onset, 796, 802 Pains of, 796, 802 seat and character, 802 physiognomy during, 802 Tenesmus, 796, 802 Heat of rectum, 796, 802 Vomiting, 803, 804 Strangury, 803 Prolapsus ani, 797, 803 Stools, 796, 803 character, 796, 803 bloody, 796, 803 boiled-sago matter in, 803 Fever, 796 Skin, state, 796, 804 Abdomen, state, 796, 804 Typhoid state, occurrence of, 797, 804 Tongue, state, 804 Pulse, 804 Physiognomy, 796 Appetite impaired, 796, 804 Brain, condition, 804 Pyæmia, occurrence of, 797, 804 Gangrene of intestine, 804 Complications and sequelæ, 805 Rheumatism, 805 Paralysis, 805 seat, 805, 806 Hepatic abscess, 806 Kidney disease, 806 Parotitis, 806 Hyperæsthesia of intestinal mucous membrane, 806 Diagnosis, 806 From intestinal catarrh, 807 Typhoid fever, 807 Cholera morbus, 807 Cancer of rectum, 807 Intussusception, 807 Prognosis, 807 Mortality, 807 Prophylaxis, 808 Prevention of over-crowding, 808 Cleanliness, 808 Ventilation, 808 Drinking-water, necessity of good, 808 Disinfection of discharges, 808 Food, improper, avoidance of, 808 Cold, avoidance of, 808 Treatment, 809 Rest, 809 Diet, 809, 812 Local, 809 Of ulcers, 812 Of paralysis, 813 Of abscess of liver, 813 Of rheumatism, 813 Change of air, 813 Laxatives, use of, 809 Enemata, use of, 809 Irrigation of bowel, 809 method, 809, 810 by ice-water, 810 Nitrate of silver, use of, 809, 812 Salicylic acid, use of, 809 Corrosive sublimate, use of, 809 Ipecacuanha, use of, 810 mode of administering, 811 Opium, use of, 811 Alum, use of, 810 Stimulants, use of, 812 Ergotin, use of, 812 Carbolic acid, use of, 810 Dilatation of bowel, 812 Electricity, use of, 813

Dysentery as a cause of intestinal ulcer, 824 of hemorrhage from bowels, 831

DYSPEPSIA, FUNCTIONAL, 436 Definition, 436 Synonyms, 436 Etiology, 438 Predisposing causes, 438 Depressed vitality, 438 Heredity, 438 Age, 438, 439 Anæmia, 439 Febrile states, 440 Exhaustion of nerves of organic life, 440 Mental state, influence on digestion, 437 Nervous system, influence on digestion, 437 Gastric juice, action of, 437 Privation and want, 441 Deficient gastric secretion, 441 Gastric juice, analysis of, 442 Exciting causes, 442 Errors of diet, 442 Excess of nitrogenous food, 443 Unwholesome food, 443 Over-eating, 444 Restricted regimen, 444 Defective cookery, 445 Hasty eating, 445 Imperfect mastication, 445 Irregularity in meals, 446 Spirit-drinking, 446 Hepatic disturbance, 447 Pancreatic disease, 447 Constipation, 447 Nervous sympathy, 448 Pregnancy, 448 Menstruation, 448 Uterine disease, 448 Cardiac disease, 448 Pulmonary disease, 448 Symptoms, 448 Fulness after meals, 448 Pain, seat and character, 448 Flatulence, 449 Nature of eructations, 449 Regurgitation, 449 Nature of liquids regurgitated, 449 Cardialgia, 449 Nausea and vomiting, 449 Vomiting, time of, 450 Vomit, character of, 450 Tongue, condition of, 450 Constipation, 450 Urine, condition of, 451 Gastric vertigo, 451 Skin diseases, 451 Disturbed innervation, 451 Languor and drowsiness, 451 Palpitation and cough, 451 Hypochondriasis, 451 Depression of spirits, 451 Sleeplessness, 451 Pathology, 451 Atrophy of mucous membrane of stomach, 451 Fatty and amyloid degeneration of stomachal walls, 451 Diagnosis, 452 From subacute or chronic gastritis, 452 From gastric ulcer, 452 From gastric carcinoma, 452 Treatment, 452 Removal of cause, 452 Improvement of general health, 452 Diet, 452 kinds of, 453 Use of peptonized food, 453 Exercise, 454 Fresh air, 454 Mental and moral means, 454 Travel, 455 Pain, gastric, 459 Anæmia, 457 Hepatic form, 457 Constipation, 458 Nausea and vomiting, 458 Use of bitters, 455 of nerve-tonics, 455 of nux vomica and strychnia, 455 of mineral acids, 456 of ipecacuanha, 456 of pepsin, 456 of bismuth, 457 of iron, 457 form of, 457 of silver salts, 457 of arsenic, 457 of mercury in hepatic forms, 457 of aperient mineral waters, 458 of belladonna in constipation, 458 of nux vomica in constipation, 458 of aloes in constipation, 458 of tincture of colocynth, 458 of hydrocyanic acid, 458, 459 of creasote, 458 of carbolic acid, 459 of ice, 458 of lime-water, 458 of sulphurous acid, 459 of alkalies, 458 of alcohol, 459 of hydrotherapy, 457 of electricity, 457

Dyspepsia in diabetes mellitus, 204 in gout, 118

Dysphagia, in acute oesophagitis, 413 in cancer of oesophagus, 427 in dilatation of oesophagus, 431 in organic stricture of oesophagus, 423 in oesophageal paralysis, 429 in acute pharyngitis, 394 in cancer of stomach, 546

Dysphonia, in cancer of oesophagus, 427 in organic stricture of oesophagus, 423

Dyspnoea in enteralgia, 661 in acute gastritis, 467 in chronic gastritis, 475 in dilatation of stomach, 595

Dyspnoeic coma, in gastric cancer, 555

Dysuria, complicating gout, 124 in paratyphlitis, 819 in peri-rectal and anal abscesses, 896

E.

Early life, influence on causation of rachitis, 141, 142 cause of tendency to scrofula in, 242

Ear disorders in hereditary syphilis, 282

Eating, hasty, influence on causation of functional dyspepsia, 445

Echinococci, seat of deposit in liver, 1102 mode of growth in liver, 1102, 1103

Echinococcus of liver, 1101

Echinorhynchus gigas, 949

Écraseur, use of, in hemorrhoids, 925

Eczema of anus, 892 of genitalia in diabetes mellitus, 205 complicating gout, 121

Eczemas, tendency to, in scrofula, 245 influence on causation of scrofula, 237

Effusions, pericardial, in acute rheumatism, treatment, 64

Elaterium, use of, in ascites, 1179

Electricity, use of, in catarrh of bile-ducts, 1057 in constipation, 653 in dysentery, 813 in functional dyspepsia, 457 in impaction of feces, 919 in gastralgia, 463 in jaundice, 983 in lithæmia, 973 in intestinal obstruction, 864 in dilatation of oesophagus, 435 in oesophageal paralysis, 430 in spasmodic stricture of oesophagus, 422 in dilatation of stomach, 608 in rheumatoid arthritis, 101

Electrolysis in hydatids of liver, 1108

Elephantiasis in Filaria sanguinis, 964

Emaciation in cholera infantum, 742 in chronic gastritis, 475 in acute intestinal catarrh, 682 progressive, in chronic intestinal catarrh, 709 in amyloid liver, 1044 in carcinoma of liver, 1038 in cirrhosis of liver, 999 in cancer of oesophagus, 427 in pancreatic diseases, 1114 in carcinoma of pancreas, 1124 in chronic intestinal pancreatitis, 1122 in obstruction of pancreatic ducts, 1131 in tubercular peritonitis, 1166 in cancer of stomach, 551

Emboli, influence of, on causation of phlegmonous form of acute oesophagitis, 411 of suppurative pylephlebitis, 1097

Embolism as a cause of hemorrhage from bowels, 831 of duodenal ulcers in chronic intestinal catarrh, 703 complicating cancer of stomach, 560 in simple ulcer of stomach, 510 of portal vein, 1095 of cerebral arteries in acute rheumatism, 39 of lungs and spleen, in scurvy, 181 influence on causation of abscess of liver, 1004

Embryo of Trichina spiralis, migration of, 959

Emetics, use of, in jaundice, 982 in cholera morbus, 724 in hepatic colic, 1082 in phosphorus-poisoning, 1033

Emotions, influence of, on production of jaundice, 976

Emphysema, diagnosis of, from abscess of liver, 1020 from perforation, in simple gastric ulcer, 509

Encephaloid carcinoma of rectum and anus, 904

Endarteritis in chronic articular rheumatism, 72

Endocarditis in acute rheumatism, 28, 33, 34 complicating gonorrhoeal rheumatism, 106

Endo- and pericarditis complicating rheumatic arthritis, 83

Enemata, anodyne, use of, in irritable rectum, 919 in impaction of feces, 918 in pseudo-membranous enteritis, 774 in carcinoma of pancreas, 1128 in rectal alimentation, amount of, 928 substances employed, 929 medicated, use of, in chronic intestinal catarrh, 714, 717, 718 nutrient, in abscess of liver, 1021 in cancer of oesophagus, 428 of tobacco, use of, in enteralgia, 666 use of, in catarrh of bile-ducts, 1057 in constipation, 655 in dysentery, 809 in enteralgia, 666 in entero-colitis, 760 in hemorrhoids, 923 in acute intestinal catarrh, 697 in intestinal ulcer, 823 in pruritus ani, 917 in seat-worms, 951

ENTERALGIA (INTESTINAL COLIC), 658 Synonyms, 658 History, 658 Nature, 658, 659 Definition, 658, 659 Etiology, 659 Heredity, 659 Sex, 659 Cachexiæ of chronic disease, 659 Morbid blood-conditions, 659 Syphilis, 660 Malaria, 660 Lead, copper, and arsenic poisoning, 660 Venereal excess, 660 Abuse of tobacco and alcohol, 660 Idiosyncrasy, 660 Reflex and sympathetic causes, 660 Ovarian and uterine irritation, 660 Disease of abdominal viscera, 660 Organic disease of brain and spinal cord, 660 Cold, 660 Indigestion, 660 Food, 660 Constipation, 660 Foreign bodies, 660 Cathartics, 660 Symptoms, 660 Pain, 660, 661 character and seat of, 660, 661 duration of paroxysms of, 660 effect of pressure on, 661 Eructations and borborygmi, 661 Nausea and vomiting, 661 Tongue, condition of, 661 Physiognomy, 661 Pulse, 661 Dyspnoea, 661 Muscular cramps, 661 Bowels, state of, 661 Abdomen, state of, 661 Micturition, painful, 661 Collapse, 662 Nervous, 662 Delirium, 662 Convulsions, 662 Vertigo, 662 Duration, 660 Varieties, 662 Alcoholic form, 662 From opium-eating, 662 Neurotic form, 662, 663 symptoms, 663 pain, 663 duration, 663 paralysis, 663 Diagnosis, 663 A true neuralgia, 663 From lumbo-abdominal neuralgia, 663 dermalgia, 664 gastralgia, 664 rheumatic pains, 664 ileus, 664 hepatic colic, 664 renal colic, 664 syphilitic colic, 664 intestinal catarrh, 664 Prognosis, 664 Termination, 664 in death, 664 in recovery, 664 Treatment, 664 Removal of cause, 664, 665 Of nervous form, 665 Flatulent form, 665 Hysterical form, 664 Preventive, 665, 666 Constitutional, 665 Local, 665 Use of bromides, 665 of iodide of potassium, 665 of iron, 665 of alum, 665 of arsenic, 665 of nitrate of silver, 665 of belladonna, 665 of valerianate of zinc, 665 of antispasmodics, 665 of opium, 665 of heat, 665 of cold, 665 of sinapisms, 665 of spinal applications, 664, 665 of cathartics, 665 of chloroform, 665 of puncturing of colon, 665 of alkalies, 666 of creasote, 666 of enemata, 666 of tobacco, 666 of phosphate of sodium as preventive, 666 Diet, 666 milk, 666

Enteritis, catarrhal, complicating gastric cancer, 560

ENTERITIS, PSEUDO-MEMBRANOUS, 763 Synonyms, 763 Definition, 763 History, 763 Etiology, 764 Age, influence on causation, 764 Sex, influence on causation, 764 Temperament, influence on causation, 764 Determinative causes, 765 Perversion of nutrition and innervation, 765 Wet and cold, 765 Food, improper, 765 Fecal impaction, 765 Cathartics, abuse, 765 Parasitic growths, relation to causation, 765 Ovarian disease, relation to causation, 765 Menstrual disorders, relation to causation, 765 Prostatic disease, relation to causation, 765 Symptoms, 765 Digestive derangements, 765 Obscurity of early, 765 Initial, 765 Irregularity of bowels, 765 Abdominal soreness, 765 Vomiting of mucus and blood, 765 Heat in rectum, 765 Depression of vital powers, 765, 766 Loss of strength, 765, 766 Pulse, state of, 766 Tongue, state of, 766 Mouth, state of, 766 Ulceration of tonsils, 766 Physiognomy, 766 Skin, state of, 766 Urine, condition of, 766 Of paroxysms, 766 Stools, character of, 766 mucous exudates in, 766 frequency of, 766 painful, 766 Pain, character and seat of, 766 Appetite, loss of, 766 Nervous disturbances, 766, 767 Hysterical, 767 Perversions of sensation, 767 Headache, 767 Special senses, perversion of, 767 Uterine disorders, 767 Pathology, 767 Views as to nature of, 767 Croupous nature of, 767, 768 Inflammatory nature of, 768 Morbid anatomy, 769 Mucous membrane, lesions of, 769 Restriction of false membrane to large intestine, 769 False membrane, characters, 769, 770 chemical characters, 772 microscopic appearance of, 770 origin from muciparous glands, 772 Diagnosis, 773 From mucous discharges of chronic diarrhoea, 773 enteritis, 773 fatty discharges of chronic hepatic and duodenal disease, 773 discharges of cholera, 773 Prognosis, 774 Cause of death, 774 Duration, 774 Treatment, 774 Of paroxysms, 774 Of intervals, 775 Local, 775 General, 775 Hygienic, 776 Diet, 776 Exercise, 776 Use of enemata, 774 of castor oil, 774 of mercury, 774 of rhubarb, 774 of sodium bicarbonate, 774 of ipecacuanha, 775 of sulphur, 775 of Plummer's pill, 775 of morphia, hypodermically, 775 of opium, 775 of nitrate of silver, 775 of sulphate of zinc, 775 of sulphate of copper, 775 of iron, 775 of nitro-muriatic acid, hot solutions locally, 775 of copaiba and cubebs, 775 of tar, 775 of arsenic, 775 of corrosive sublimate, 775 of iodide of potassium, 775 of cod-liver oil, 776 of counter-irritation, 776 of mineral waters, 776

Enteroliths, influence on causation of intestinal obstruction, 838

Enterotomy in intestinal obstruction, 867

Entorectomy in intestinal obstruction, 866

Epigastric prominence, in dilatation of stomach, 596 fulness in catarrh of bile-ducts, 1053 tenderness, in jaundice, 979 in pancreatic diseases, 1116, 1119

Epileptic attacks from Ascaris lumbricoides, 953 from tape-worm, 940

Epistaxis in occlusion of bile-ducts, 1089 in acute yellow atrophy of liver, 1028 in purpura hæmorrhagica, 188 in scurvy, 179, 180

Epithelial form, flat and cylindrical-celled, of gastric cancer, 564, 565 desquamation in acute intestinal catarrh, 677

Epithelium, detachment of, in superficial glossitis, 355 changes in, in acute oesophagitis, 411 in acute peritonitis, 1134, 1135 in chronic pharyngitis, 403 in tonsillitis, 384

Epsom salts, use of, in constipation, 655 and senna, use of, in ascites, 1179 in Oxyuris vermicularis, 951

Erethistic form of scrofulous habit, 243

Ergot, local use of, in chronic pharyngitis, 405 Use of, in diabetes mellitus, 227 in chronic intestinal catarrh, 718 in ulceration of oesophagus, 418 in purpura, 193 in stomatorrhagia, 371

Ergotin, local use, in prolapsus ani, 921 Use of, in dysentery, 812 in hemorrhage from bowels, 834 in hemorrhages of hepatic cirrhosis, 1002 in hemorrhoids, 923, 924 in intestinal ulcer, 829 in acute yellow atrophy of liver, 1030 in simple ulcer of stomach, 525

Erosions, hemorrhagic, of stomach, 529 of teeth in hereditary syphilis, 298

Errors in diet, influence on causation of functional dyspepsia, 442 of chronic gastritis, 470 of gout, 112 as a cause of jaundice, 977

Eructations in functional dyspepsia, 449 in chronic gastritis, 473 in cancer of stomach, 540 in dilatation of stomach, 593 and borborygmi in enteralgia, 661

Eruption of purpura hæmorrhagica, 188 rheumatica, 189 simplex, 187

Eruptive diseases, influence on causation of acute gastritis, 464 fevers, influence on causation of chronic gastritis, 470 of acute intestinal catarrh, 671 of scrofula, 237

Erysipelas as a cause of infantile peritonitis, 1172 complicating mercurial stomatitis, 346

Erysipelatous form of acute pharyngitis, nature, 393 of acute pharyngitis, symptoms, 396 of acute pharyngitis, treatment, 399

Erythema intertrigo, 892 of hereditary syphilis, 277 complicating gonorrhoeal rheumatism, 106

Erythematous form of acute pharyngitis, symptoms, 394

Eschar in cancrum oris, characters of, 340

Ether, use of, in hepatic colic, 1082

Etiology of ascites, 1173 of catarrh of bile-ducts, 1051 of biliary calculi, 1063 of cancrum oris, 339 of cholera morbus, 720 of constipation, 639, 850 of diabetes mellitus, 203 of dysentery, 786 of functional dyspepsia, 438 of enteralgia, 659 of pseudo-membranous enteritis, 764 of entero-colitis, 726 of fistula in ano, 897 of gastralgia, 459 of acute gastritis, 464 of catarrhal form of acute gastritis, 464 of erythematous form of acute gastritis, 465 of chronic gastritis, 470 of superficial glossitis, 355 of chronic superficial glossitis, 366 of parenchymatous glossitis, 359 of glossitis parasitica, 358 of glossanthrax, 368 of gout, 109 of hemorrhoids, 882 of internal hemorrhoids, 884 of hemorrhage from bowels, 830 of acute intestinal catarrh, 669 of chronic intestinal catarrh, 699 of intestinal indigestion, 623 of intestinal ulcer, 823 of cancer of intestines, 868 of jaundice, 975 of abscess of liver, 1002 of acute yellow atrophy of liver, 1023 of amyloid liver, 1040 of carcinoma of liver, 1033 of cirrhosis of liver, 990 of fatty liver, 1046 of hydatids of liver, 1101 of hyperæmia of liver, 983 of macroglossia, 350 of morbid dentition, 371 of cancer of oesophagus, 429 of dilatation of oesophagus, 430 of spasmodic stricture of oesophagus, 419 of organic stricture of oesophagus, 422 of ulceration of oesophagus, 418 of acute oesophagitis, 409 of chronic oesophagitis, 416 of pancreatic diseases, 1114 of acute secondary pancreatitis, 1128 of carcinoma of pancreas, 1123 of chronic intestinal pancreatitis, 1121 of obstruction of pancreatic duct, 1129 of acute diffuse peritonitis, 1136 of infantile peritonitis, 1172 of acute pharyngitis, 390 of chronic pharyngitis, 402 of tuberculous pharyngitis, 400 of syphilitic pharyngitis, 406 of proctitis, 887 of pruritus ani, 909 of purpura, 190 of hypertrophic stenosis of pylorus, 615 of rachitis, 137 of dilatation of rectal pouches, 885 of fissure of anus and rectum, 888 of neuralgia of rectum, 909 of non-malignant rectal stricture, 885 of obstruction of rectum, 889 of prolapse of rectum, 881 of ulceration of rectum and anus, 894 of peri-rectal and anal abscesses, 895 of rheumatism, acute, 19 of chronic articular rheumatism, 69 of gonorrhoeal rheumatism, 102 of muscular rheumatism, 74 of rheumatoid arthritis, 88 of atrophy of stomach, 616 of cancer of stomach, 531 of cirrhosis of stomach, 612 of dilatation of stomach, 587 of acute dilatation of stomach, 610 of hemorrhage from stomach, 580 of rupture of stomach, 618 of simple ulcer of stomach, 481 of stomatorrhagia, 370 of aphthous stomatitis, 325 of catarrhal stomatitis, 321 of mercurial stomatitis, 344 of stomatitis ulcerosa, 336 of scrofula, 232 of scurvy, 169 of tabes mesenterica, 1185 of thrombosis and embolism of portal vein, 1095 of thrush, 331 of tonsillitis, 380 of tuberculous ulceration of tongue, 369 of typhlitis, 814

Etymology of dysentery, 777

Euonymin, use of, in biliousness, 968 in intestinal indigestion, 636 in jaundice, 982 in acute yellow atrophy of liver, 1030 in hepatic colic, 1082

Eustrongylus gigas, 957

Evacuation of abscess of liver, 1021

Exacerbations, frequency of, in chronic gout, 121

Exanthemata, acute, influence on causation of tabes mesenterica, 1186

Exanthematous form of acute pharyngitis, nature, 393

Excision, in prolapsus ani, 919 in hypertrophy of tongue, 354 of rodent ulcer of rectum, 913 of cancer of rectum, 914, 915

Exercise, importance of, in biliary calculus state, 1079 in lithæmia, 971 in pseudo-membranous enteritis, 776 necessity of, in functional dyspepsia, 454 in hyperæmia of liver, 988 in treatment of gout, 130, 131 in scrofula, 252 value of, in treatment of constipation, 651, 653 in chronic intestinal catarrh, 714, 716 in intestinal indigestion, 632

Expectoration in chronic pharyngitis, 404

Extractum pancreatis, in carcinoma of pancreas, 1128 use of, in entero-colitis, 752 in chronic interstitial pancreatitis, 1122, 1123

Extravasations of blood into hepatic tissues, in hyperæmia of liver, 988

Extremities, appearance of, in rachitis, 155

Exudates in stools of pseudo-membranous enteritis, 766

Exudations, characters of, in gout, 115 fibrinous, in local peritonitis, 1160 thickness of, in tubercular peritonitis, 1167

Eye affections, complicating gonorrhoeal rheumatism, 106 diseases, complicating rheumatoid arthritis, 84

F.

Facial paralysis in diabetes mellitus, 206

False membranes, cysts of, in acute peritonitis, 1134 disposition of, in acute peritonitis, 1134 in pseudo-membranous enteritis, 766 characters of, in pseudo-membranous enteritis, 769-772 thickness of, in tubercular peritonitis, 1167

Farinaceous foods, analysis of, 750, 751 use of, in cholera infantum, 754 in entero-colitis, 753, 754

Fatigue, influence of, on causation of gonorrhoeal rheumatism, 103 and exhaustion, influence of, on causation of acute rheumatism, 22 and strain, muscular, influence of, on causation of muscular rheumatism, 75

Fat in blood of diabetes mellitus, 207 seat of deposit, in fatty liver, 1047, 1048

Fats and oils, absorption of, in digestion, 623

Fatty degeneration of pancreas, 1128 of cells in scrofulous inflammation, 239 of gastric walls in dilatation of stomach, 600 of gastric vessels, in simple ulcer of stomach, 511 gastric, influence on causation of dilatation of stomach, 590 of heart, complicating cancer of stomach, 560 infiltration of pancreas, 1128 liver, 1046 metamorphosis of pancreas, 1128 stools in diseases of pancreas, 1115, 1122, 1125, 1131

Febrile states, influence of, on causation of functional dyspepsia, 440 affections, influence of, on causation of superficial glossitis, 355 diseases, influence of, on causation of intestinal indigestion, 623

Fecal accumulations, in constipation, 644 tumor, characters of, 852 impaction, influence of, on causation of pseudo-membranous enteritis, 765 in intestinal obstruction, treatment, 863 vomiting, in gastric cancer, significance, 558 in stricture of bowel, 856, 858 in intestinal obstruction, 840, 843, 848

Feces, color, in jaundice, 978 collection of, in vermiform appendix, as a cause of typhlitis, 814 impaction of, treatment, 918 wire-drawn, in non-malignant rectal stricture, 886

Feet, deformities of, in general rheumatoid arthritis, 82

Fehling's test for sugar in urine, 212

Fermentation test for sugar in urine, 212

Fetid secretions, in gangrenous form of acute pharyngitis, 396

Fever, in catarrh of bile-ducts, 1054 in occlusion of biliary passages, 1090 in constipation, 648 in dysentery, 796 in entero-colitis, 734, 736 in acute gout, 119 in hepatic colic, 1072 in acute intestinal catarrh, 681 in chronic intestinal catarrh, 709 in jaundice, 980 in acute secondary pancreatitis, 1121 in suppurative pylephlebitis, 1099 in tabes mesenterica, 1190 in trichinosis, 960 in typhlitis and perityphlitis, 818, 819

Fibrin, amount of, in blood of scurvy, 174

Fibrinous exudations in acute peritonitis, 1133, 1134 in local peritonitis, 1160

Fibromata of stomach, 579

Filaria lentis, 964 loa, 964 medinensis, 962 restiformis, 964 sanguinis, 963 trachealis, 964

Filth, influence of, on causation of entero-colitis, 730 of tabes mesenterica, 1186

Fingers, clubbing of, in scrofula, 246

Fish as a source of Bothriocephalus latus, 939

Fissure of anus in cirrhosis of liver, 994 of anus and rectum, 888

Fistula in ano, 897

Fistulæ, biliary, 1068, 1074 in constipation, 645, 648 formation of, by gall-stones, 1068 in chronic intestinal catarrh, 703 gastro-colic, in simple ulcer of stomach, 508 gastro-cutaneous, in simple ulcer of stomach, 500 gastro-duodenal, in simple ulcer of stomach, 508 gastro-pleural, in simple ulcer of stomach, 508 in cancer of stomach, formation of, 558 in ulceration of oesophagus, 418

Fistulous openings into viscera in acute pancreatitis, 1121

Flat-celled epithelial form of gastric cancer, 565

Flatulence in constipation, 646, 647 in functional dyspepsia, 449 in acute intestinal catarrh, treatment, 693 in simple ulcer of stomach, 494 and colic in intestinal indigestion, treatment, 636

Flatulent form of enteralgia, treatment, 665

Flesh-worm, 957

Flexure of thigh upon leg in paratyphlitis, 819

Flour-ball, use of, in infant feeding, 754, 755

Fluctuation in abscess of liver, 1011

Flukes, liver, 1109

Fluke-worms, 946

Foetus in utero, syphilitic infection of mother by, 262

Follicles, changes in, in acute oesophagitis, 412 enlargement of, in chronic pharyngitis, 403 intestinal, lesions of, in dysentery, 798

Follicular pharyngitis, 402 ulcers in acute intestinal catarrh, 676 of stomach, 529 ulceration of chronic intestinal catarrh, treatment, 718 of rectum and anus, 894

Fomentations, hot, in hepatic colic, 1082

Fontanels, condition of, in rachitis, 146

Food, amount of, ingested by healthy infants, 746 certain, influence of, on causation of gastralgia, 460 improper, influence of, on causation of biliary calculi, 1065 of catarrh of bile-ducts, 1052 of cholera morbus, 721 of constipation, 643, 851 of dysentery, 791 of functional dyspepsia, 442, 443 of enteralgia, 660 of pseudo-membranous enteritis, 765 of entero-colitis, 726 of acute gastritis, 465 of parenchymatous glossitis, 360 of chronic intestinal catarrh, 700 of intestinal indigestion, 625 of diseases of pancreas, 1114 of chronic pharyngitis, 402 of rachitis, 144 of aphthous stomatitis, 326 of catarrhal stomatitis, 322 of stomatitis ulcerosa, 336 of scrofula, 232 of tabes mesenterica, 1185, 1186 inability to ingest large quantities of, in cirrhosis of stomach, 613 peptonized, use of, in functional dyspepsia, 453 in chronic interstitial pancreatitis, 1122, 1123 retention of, in dilatation of oesophagus, 431 uncooked, as a cause of intestinal worms, 931

Foods, saccharine, use of, in diabetes mellitus, 220 and drinks, admissible in diabetes mellitus, 220, 221 certain, as a cause of spasmodic stricture of oesophagus, 420 farinaceous, for infants, analyses, 750, 751 use of, in cholera infantum and entero-colitis, 753

Foreign bodies, influence of, on causation of occlusion of biliary passages, 1084 of enteralgia, 660 of chronic intestinal catarrh, 700 of typhlitis, 816, 817 as a cause of hemorrhage of bowels, 830 of chronic oesophagitis, 416

Formad on scrofulous peculiarity, 232

Formication of right leg in typhlitis and perityphlitis, 818

Frequency of stricture of bowel, 854 of intestinal ulcer, 823 of acute yellow atrophy of liver, 1023 of cancer of stomach, 532 of simple ulcer of stomach, 481, 482 of tabes mesenterica, 1184

Friction sound in perihepatitis, 989

Frictions, use of, in cholera morbus, 724

Friedrichshall water, use of, in intestinal indigestion, 636

Fruit, necessity of, for prevention of scurvy, 183

Fulness after eating in functional dyspepsia, 448 and weight in dilatation of stomach, 593

Functional dyspepsia, 436 disorders of liver, 965 diseases of stomach, 436 obstruction of bowel, diagnosed from organic, 859

Furuncular eruptions in hereditary syphilis, 280

Furunculi of anus, 892

G.

Gall-bladder, changes in, from biliary calculi, 1066 distension of, from occlusion of biliary ducts, 1085 dropsy of, from biliary concretions, 1077 from occlusion of biliary ducts, 1086 lesions of, in chronic intestinal catarrh, 705 puncture of, for relief of biliary calculi, 1081 of occlusion of biliary passages, 1094 and hepatic tubes, character of contents of, in occlusion of biliary ducts, 1085

Gallic acid, use of, in acute intestinal catarrh, 695 in chronic intestinal catarrh, 717

Gall-stones, 1058 diagnosis of presence of, 1078 impaction of, 1074 influence of, on causation of acute peritonitis, 1139 as a cause of intestinal obstruction, 839 migration of, 1067 by artificial routes, 1068, 1074 symptoms due to, 1070 passage of, a cause of perihepatitis, 989 presence of, as a cause of obstruction of pancreatic duct, 1130 symptoms due to, 1069 treatment, 1079

Galvanism, use of, in muscular rheumatism, 76

Gangrene in cancrum oris, date of appearance, 342 of tongue in parenchymatous glossitis, 362 of bowel in intussusception, 845, 849 in acute oesophagitis, 413 in acute pancreatitis, 1118 occurrence of, in tonsillitis, 383

Gangrenous form of acute pharyngitis, 395

Gas in arteries from perforation in simple gastric ulcer, 510 source of, in intestinal indigestion, 627

Gaseous distension of gut, in intestinal obstruction, tapping in, 865 eructations in dilatation of stomach, nature of, 593

Gastralgia in cirrhosis of stomach, 613 in acute rheumatism, 42

GASTRALGIA (CARDIALGIA, SPASM OF STOMACH), 459 Definition, 459 Varieties, 459 Etiology, 459 Predisposing causes, 460 Depressed vitality, 460 Nervous excitability, 460 Female sex, 460 Menstruation, 460 Anæmia, 460 Blood-poisons, 460 Malaria, 460 Gout and rheumatism, 460 Certain foods, 460 Disease of nerve-centres, 460 Exciting causes, 460 Venereal excesses, 460 Abuse of narcotics, 460 Reflex causes, 460 Affections of bladder and kidneys, 460 of uterus, 460 of ovaries, 460 Symptoms, 460 Pain, 460 character of, 460 seat of, 460, 461 hysterical phenomena, 461 tongue, 461 vomiting, 461 Diagnosis, 461 From inflammation of stomach, 461 organic gastric affections, 461 gastric ulcer and cancer, 461 rheumatism of abdominal muscles, 462 hepatic colic, 462 Prognosis, 462 Treatment, 462 Radical, 462 Palliative, 463 of chlorosis and anæmia, 462 of irritable nervous system, 463 of hysterical phenomena, 463 of pain, 463 Use of iron, form, 462 of quinine, 462 of arsenic, 462 of nux vomica and strychnia, 463 of silver salts, 463 of valerianate of zinc, 463 of bromides, 463 of electricity, 463 of bismuth, 463 of hydrocyanic acid, 463 of morphia, 463 of spirits of chloroform, 463 of hot water, 463 Travel, 463 Change of air, 463

Gastralgia distinguished from enteralgia, 664

Gastrectasia. See _Dilatation of Stomach_.

Gastric catarrh of phthisis, treatment of, 478 disease, chronic, influence on causation of atrophy of stomach, 616 fluids of cancer of stomach, absence of free hydrochloric acid in, 543 glands, alterations in chronic gastritis, 472 juice, action of, 437, 620, 621 excess of, influence on causation of intestinal indigestion, 626 erosion by, as a cause of intestinal ulcer, 824, 825 secretion, deficient, as a cause of functional dyspepsia, 441 tubules, alterations in chronic gastritis, 472 atrophy of, in atrophy of stomach, 616 in cirrhosis of stomach, 614 degeneration of, in atrophy of stomach, 616 origin of cancer of stomach from, 563, 564 ulcer, artificial production of, 514 vertigo, in functional dyspepsia, 451 walls, thickening of, in cirrhosis of stomach, 614

GASTRITIS, ACUTE (ACUTE GASTRIC CATARRH), 463 Definition, 463 Varieties, 464 Etiology, 464 Predisposing causes, 464 Of catarrhal form, 464 Mechanical, 464 Weak heart-action, 464 Organic disease of heart and lungs, 464 of liver, 464 Gout and rheumatism, 464 Malarious fevers, 464 Passive gastric hyperæmia, 465 Erythematous form, 465, 466 Frequency in children, 465 Eruptive disorders, 464 fevers, 464 Relation to brain disorders, 465 Exciting causes, 465 Catarrhal form, 465 Improper food, 465 Acrid and corrosive poisons, 465 Alcohol, excessive use of, 465 Scarlatina, 466 Morbid anatomy, 466 Difficulty in determining post-mortem changes, 466 Catarrhal form, state of mucous membrane, 466 Erythematous form, state of mucous membrane, 466 Acute form, state of mucous membrane, 466 Toxic form, state of mucous membrane, 466 Symptoms, 467 Acute toxic form, 467 Erythematous form, 467 Cholera infantum, 467 In infants, 467 Catarrhal form, 467 Pain, 467 Thirst, 467 Vomiting, 467 Vomit, character of, 467 Physiognomy, 467 Coldness of surface, 467 Prostration, 467 Pulse, 467 Temperature, 467 Hiccough, 467 Tongue, state of, 467 Urine, state of, 467 Cerebral symptoms, 467 Headache, 467 Vertigo, 467 Mental depression, 467 Dyspnoea, 467 Diarrhoea, 467 Pain after eating, 467 Diagnosis, 468 From brain disease, 468 Remittent or typhoid fevers, 468 Meningitis, 468 Peritonitis, 468 Prognosis, 468 Treatment, 468 Severe forms, 468 Rest of inflamed organ, 468 Diet, 468 Of thirst, 468 Of vomiting, 469 Mild forms, 469 Rest, 469 Diarrhoea, 469 Pyrexia, 469, 470 Pain, 469 In children, 469 Convalescence, 470 Use of ice, 468 stimulants, 469 ipecacuanha, 469 calomel, 469 sod. bicarbonate, 469 bismuth, 469 salicylate, 469 demulcent drinks, 469 hydrocyanic acid, 469 counter-irritation, 469 baths, cold, 470

GASTRITIS, CHRONIC (CHRONIC GASTRIC CATARRH), 470 Definition, 470 Etiology, 470 Functional gastric disorders, 470 Interference with portal circulation, 470, 471 Rheumatism and gout, 470, 471 Phthisis, 470, 471 Renal disease, 470 Eruptive diseases, 470 Malarious fevers, 470, 471 Alcohol, excessive use of, 470 Errors of diet, 470 Decomposition of ingested aliment, 470 Weak digestive power, 470 Injudicious medication, 470 Disease of heart and lungs, 471 Anæmia, 471 Anatomical characters, 471 Lesions of mucous membrane, 471, 472 Softening of mucous membrane, 471 Thinning of gastric walls, 471 Scirrhous state of pyloric orifice, 471 Ulceration of pyloric orifice, 472 Hypertrophy of pyloric orifice, 472 Dilatation of stomach, 472 Hypertrophy of interstitial tissue, 472 Glands, gastric, alterations in, 472 Tubules, gastric, alterations in, 472 Symptoms, 472 Of difficult digestion, 473 Pain, 473 Burning sensation in epigastrium, 473 Tenderness on pressure of epigastrium, 473 Appetite, impaired, 473 Nausea and vomiting, 473 Vomiting, time of, 473 Vomit, nature of, 473 Tongue, condition of, 473 Breath, condition of, 473 Thirst, 473 Jaundice, 474 Sympathetic nervous symptoms, 474 Mucous membranes, freedom from pain in disorders of, 474 sympathetic phenomenon in disorders of, 474 Gastric irritation, tendency to terminate in cerebral inflammation, 474 Convulsion, 474 Headache, 474 Vertigo, 474 Heart, disturbance of, 474 Dyspnoea, 475 Constipation, 475 Piles, 475 Diarrhoea, 475 Urine, state of, 475 Emaciation, 475 Diagnosis, 475 From atonic dyspepsia, 475 Gastric cancer, 476 ulcer, 476 Treatment, 476 Importance of rest, 476 Diet, 476 Milk, use of, 476 Diluents, use of, 477 mode of administering, 477 Gum-water, 477 Use of alkaline carbonates, 477 Alkaline mineral waters, 477 Carlsbad water, 477 Marienbad waters, 477 Hot water, 477 mode of administering, 478 Bismuth, 478 Charcoal, 478 Mercurials, 478 Nitrate of silver, 478 Astringents, 478 Stomach-pump, 478 Counter-irritation, 479 Mucous vomiting, 478 Constipation, 478

Gastric catarrh of phthisis, 475

Gastritis, catarrhal, complicating simple ulcer of stomach, 502 chronic catarrhal, as a cause of cirrhosis of stomach, 612 complicating gastric cancer, 560 influence on causation of dilatation of stomach, 590

Gastro-duodenal catarrh, signs of, in acute yellow atrophy of liver, 1027

Gastrodynia, 459

Gastro-intestinal canal, state of, in cancrum oris, 341 condition of, in parenchymatous glossitis, 362 in hereditary syphilis, 306 catarrh, signs of, in catarrh of bile-ducts, 1053 in carcinoma of liver, 1038 of cirrhosis of liver, treatment, 1001 signs of, in hyperæmia of liver, 986 catarrhal symptoms in jaundice, 977 disorders, influence on causation of superficial glossitis, 355 in morbid dentition, 374 lesions in tabes mesenterica, 1188

Gastro-colic fistulæ, in gastric cancer, 558 in simple gastric ulcer, 508

Gastro-cutaneous fistulæ, in simple ulcer of stomach, 500

Gastromalacia, 618

Gastro-pleural fistulæ, in simple ulcer of stomach, 508

Gastrorrhagia, 580

Gastrostomy in cancer of stomach, 578 in dilatation of stomach, 609 use of, in cancer of oesophagus, 428 in dilatation of oesophagus, 435 in organic stricture of oesophagus, 426

Gargles, use of, in acute pharyngitis, 397 in tonsillitis, 388

General progressive form of rheumatoid arthritis, symptoms, 80

Genito-urinary affections, complicating gout, 123

Geographical distribution of cholera morbus, 720 of diabetes mellitus, 203 of acute intestinal catarrh, 669 of cancer of stomach, 535 of simple ulcer of stomach, 485 of tabes mesenterica, 1184

Germ, infective, origin of acute rheumatism, 26

Glands, abdominal, diseases of, 1182 bronchial and tracheal, enlargement in rachitis, 153 changes in, in scrofula, 239, 240 gastric, alterations, in chronic gastritis, 472 of Lieberkühn, elongation of, in chronic intestinal catarrh, 703 lymphatic, enlargement of, in tuberculous pharyngitis, 401 swelling of, in acute pharyngitis, 395 mesenteric change in, in tabes mesenterica, 1187 pharyngeal, hypertrophy of, in chronic pharyngitis, 403

GLOSSITIS, 354 Definition, 354 Glossitis, superficial, 355 Definition, 355 Synonyms, 355 Etiology, 355 Teeth, irregular and jagged, 355 Tobacco, 355 Liquids, hot and acrid, 355 Nervous irritation, 355 Stomatitis, 355 Febrile affections, 355 Gastro-intestinal disease, 355 Pathology and morbid anatomy, 355 Nature, 355 Lesions, description of, 355 Epithelium, increase and detachment of, 355 Papillæ, enlargement, 355, 356 Unilateral, 356 Psoriasis linguæ, 356 Superficial ulceration, 356 Microscopic appearance, 356 Ichthyosis linguæ, 356 Relative frequency of, in smokers and non-smokers, 356 Termination in epithelioma, 356 Symptoms, 357 Local, 357 General, 357 Diagnosis, 357 Treatment, 357 Importance of treating gastric complications, 557 Local, 357 Of ulcers, 357 Removal of imperfect teeth, 357 _Glossitis Parasitica_ (_Black tongue_), 357 Definition, 357 Synonyms, 357 History, 357 Etiology, 358 Faulty nutrition, 358 Chlorate of potash, use of, 358 Syphilis, 358 Pathology and morbid anatomy, 358 Discoloration of tongue, 358 Papillæ, enlargement of, 358 Parasitic growth, 358 microscopic appearance, 358 mode of development, 358 seat of, 358 Symptoms, 359 Diagnosis, 359 Prognosis, 359 Treatment, 359 Indications, 359 Local, 359 Use of potassium chloride, 359 sodium borate, 359 _Glossitis, Parenchymatous_, 359 Definition, 359 Synonyms, 359 History, 359 Etiology, 359 Impaired health, 359 Atmospheric changes, 359 Cold and damp, 359 Age, 360 Influenza, 360 Improper and acrid food, 360 Certain plants, 360 Tobacco, 360 Acute exanthemata, 360 Disease of mucous membranes, 360 Endemic and epidemic nature, 360 Traumatic form, 360 Teeth, irregular, 360 Injuries, 360 Acrid and irritant poisons, 360 Saliva of the toad, 360 Symptoms, 360 Mode of onset, 360 Tongue, condition of, 361 enlargement of, 361 pain in, 361 desquamation of, 361 chronic induration of, 361 gangrene of, 361 Lymphatic glands, swelling of, 361 Respiration, laborious, 361 Deglutition, difficult, 361 Physiognomy, 361 Saliva, dribbling, 361 Thirst, 362 Cough, 362 Pyrexia, 362 Pulse, 362 Skin, condition of, 362 Gastro-intestinal canal, condition of, 362 Nervous system, 362 Resolution, 362 Suppuration, 362 Gangrene of tongue, 362 Duration, 362 Complications, 362 Diffused inflammation of areolar tissue between genio-hyo-glossi muscles, 362 Pathology and morbid anatomy, 363 Chordo-tympani and glosso-pharyngeal nerve, relation to causation, 363 Tongue, infiltration of, by fibrin and serum, 363 Epithelium, changes in, 363 Suppuration, nature of, 363 seat of pointing, 363 Gangrene of tongue, cause of, 363 Muscles, condition of, in diffuse inter-connective tissue inflammation, 363 Diagnosis, 363 From hypertrophy of tongue, 364 cystoma of tongue, 364 Prognosis, 364 Mortality, 364 Treatment, 364 Of mild cases, 364 Antiphlogistic, 364 Of debility, 364 Of severe cases, 365 Of localized form, 365 Diet, 365 Enemata, nutrient, 365 Abscesses, 365 Of tumefaction of tongue, 365 Of gangrene of tongue, 366 Local, 365 Use of aconite, 364 of tartar emetic, 364 of leeching, 364 of venesection, 364 of iron and quinia, 365 of deep incisions, 365 of astringents, 365 of detergent washes, 365 of spray of ammonium chloride, 365 _Glossitis, Chronic_, 366 _Glossitis, Chronic Superficial_, 366 Etiology, 366 Dyspepsia, 366 Chronic alcoholism, 366 Symptoms, 366 Pain in taking acid food, 366 Sensation of enlarged tongue, 366 Tongue, appearance of, 366 furrows of, 366 Papillæ, enlarged, 366 Ulcers, superficial, 366 Pathology, 367 Diagnosis, 367 From syphilis, 367 epithelioma, 367 Prognosis, 367 Treatment, 367 Cleanliness, necessity of, 367 Diet, 367 Exercise, 367 Avoidance of alcohol, 367 Local, 367 _Glossitis, Chronic Parenchymatous_, 367 Definition, 367 Pathology, 368 Connective-tissue hyperplasia, 368 Symptoms, 368 Tongue, induration of, 367, 368 circumscribed tumefaction of, 367, 368 loss of sensibility of, 367, 368 enlargement or atrophy of, 367, 368 chronic abscess of, 368 Pain in taking arid and sapid food, 368 Difficult articulation and deglutition, 368 Diagnosis, 368 From cystic tumor, 368 Prognosis, 368 Treatment, 368 Local, 368 General, 368 _Glossanthrax_ (_Carbuncle of Tongue_, _Malignant Pustule of Tongue_), 368 Definition, 368 Etiology, 368 Symptoms, 368 Prognosis, 368 Treatment, 368

Gluten bread, use of, in diabetes mellitus, 222

Glycosuria, artificial, methods of production, 195-199 influence of vaso-motor nerves on production, 196-199 relation of sympathetic nerve to, 196 complicating gout, 123 hepatic, 973

Gold and silver, use of, in acute yellow atrophy of liver, 1030

Gold and sodium chloride, use of, in amyloid liver, 1046 in cirrhosis of liver, 1001

Gonorrhoea complicating gout, 123 of rectum, treatment of, 918

Gonorrhoeal bursitis, symptoms of, 105 poison, influence on causation of proctitis, 888 rheumatism, 102

GOUT, 108 Definition, 108 Synonyms, 108 Classification, 108 History, 109 Etiology, 109 Predisposing causes, 109 Heredity, 109 Sex, 109 Age, 110 Temperament, 110 Vicious hygiene, influence of, on causation, 110 Luxurious living, influence of, on causation, 110 Poverty, influence of, on causation, 110, 111 Alcoholic liquors, influence of, on causation, 111 Fermented liquors, influence of, on causation, 111 Malt liquors, influence of, on causation, 111 Cider, influence of, on causation, 111 Lead-poisoning, relation of, to causation, 111 Exciting causes, 112 Errors in diet, 112 Sudden changes in temperature, 112 Traumatism, 112 Nervous exhaustion, 112 Overwork, 112 Sexual excess, 112 Pathology, 112 Theories regarding, 112 Lithæmic theory, 112 Chemical theory, 112 Defective oxidation, origin of, from, 112, 113 Uric-acid theory, 112, 113 objections to, 113, 114 Nervous theory of origin, 114 Morbid anatomy, 115 Changes in blood, 115 Uric acid, excess of, in blood, 115 Urates, deposits of, 115 Exudations, composition of, 115 location, 115 Joints, changes in, 116 Cartilages, changes in, 115 necrosis of, 116 relation of, to uratic deposits, 116 Synovial membranes, changes in, 115 Joints, hyperplasia of connective tissue of, 116 abscesses of, 116 metatarso-phalangeal, frequency of disease of, 116 most affected, 116 Blood-vessels, changes in, 117 Heart, changes in, 117 Nerves, changes in, 117 Kidneys, changes in, 117 cirrhosis of, 117 deposits in, 117 seat and character, 117 uratic deposits in, 117 Liver, changes in, 117, 118 Symptoms, 118 Prodromal, 118 Derangements of primary digestion, 118 Dyspepsia, 118 Constipation, 118 Diarrhoea, 118 Nervous symptoms accompanying, 118 Derangements of nutrition, 118 Catarrhal affections of skin, 118 mucous membranes, 118 Debility, 118 Irritability of temper, 118 Hypochondriasis, 118 Acute articular form, 119 attack, 119 Onset, 119 Fever, 119 Sleeplessness, 119 Pain, 119 Local, 119 Condition of joint, 119 Reflex muscular spasm, 119 Urine, changes in, 119 amount of uric acid in, during attack, 119 Duration, 119 Improved health following, 119 Atonic or irregular forms, 120 General symptoms, 120 Dyspepsia, 120 Urine, changes in, 120 specific gravity, 120 amount of urea, uric acid, and urates, 120 Polyuria, 120, 123 Articular symptoms, 121 Joints most affected, 121 Pain, 121 Deformities, 121 Exacerbations, frequency of, 121 Complications, 121 Skin affections, 121 Perspirations, local, 121 Seborrhoea, 121 Eczema, 121 relation of, to, 121, 122 seat and character, 122 Acne, 121 Erythematous affections, 121 Affections of mucous membranes, 122 Pharyngeal and laryngeal catarrh, 122 Bronchitis, 122 Gastro-duodenal catarrh, 122 Intestinal catarrh, 122 Genito-urinary affections, 123 Vesical catarrh, 123 Gonorrhoea, 123 Granular kidney, 123 Albuminuria, 123 importance of, 123 Glycosuria, 123 Gravel, 124 Renal colic, 124 Dysuria, 124 Diagnosis, 124 Relation of, to acute and chronic rheumatic diseases, 124 to gonorrhoeal rheumatism, 124 Importance of heredity in, 125 From acute rheumatism, 125 rheumatoid arthritis, 125 traumatic joint affections, 126 nervous arthropathies, 126 Of irregular gout, 126 Prognosis, 126 Effects of renal affections on, 127 treatment on, 127 Treatment, 127 Indications, 127 Dietetic, 127 Necessity of avoidance of carbohydrates, 128 of fermented alcoholic liquors, 128 of beer and wine, 128 of saccharine and amylaceous foods, 128, 129 Use of fatty foods, 129 of succulent vegetables, 129 of milk, 129 Proper amount of food, 129 Necessity of exercise, 130, 131 Active and passive exercise, 130 Bathing, 130 Baths, use of, 130 Climate, 130 Medicinal, 131 Of the dyspepsia, 131 Gastro-intestinal catarrh, 131 Use of pepsin and pancreatin, 131 of hydragogue cathartics, 131 of natural mineral waters, 131 of iron, 132 and potash, 132 of alkalies, 132 of lithia salts, 132 of potassium salts, 132 of sodium salts, 132 Modes of administering alkaline salts, 132, 133 Use of iodine salts, 132 of water, 133 Of acute articular gout, 133 Antiphlogistic method, 133 Expectant method, 133 By diet, 133 Local, 134 Abortive method, 134 Use of colchicum, 134 action of, 134 objections to, 134 method of administration, 135 salicylic acid and salicylates, 135 oil of wintergreen, 136

Gout, influence on causation of chronic intestinal catarrh, 699 of rachitis, 144 of rheumatoid arthritis, 89 and rheumatism, influence on causation of acute gastritis, 464

Gravel complicating gout, 124

Guaiacum, use of, in chronic articular rheumatism, 74 in tonsillitis, 388 and colchicum, use of, in constipation, 656

Guinea-worm, 962

Gummata of lungs in hereditary syphilis, 307 of rectum and anus, 900

Gummatous infiltration in syphilitic pharyngitis, 407

Gums, state of, in morbid dentition, 373 in scurvy, 177

Gum-water, use of, in chronic gastritis, 477

Gymnastic exercises, use of, in rachitis, 166

H.

Habit, influence on causation of constipation, 640 scrofulous, peculiarities of, 243, 244

Hæmatemesis in lardaceous degeneration of intestines, 875 in acute yellow atrophy of liver, 1028 in purpura hæmorrhagica, 188 in scurvy, 180 in cancer of stomach, treatment of, 577 in dilatation of stomach, 594 in hemorrhage from stomach, 586 in simple ulcer of stomach, 493

Hæmatogenous jaundice, 975

Hæmaturia in Bilharzia hæmatobia, 948 in Filaria sanguinis, 963 in purpura hæmorrhagica, 188 in scurvy, 180

Hæmophilia, influence on causation of stomatorrhagia, 370 of hemorrhage from bowels, 830 of hemorrhage from stomach, 582

Hair, growth on forehead and shoulders, in scrofula, 246

Hairs on mucous membrane of anus, 892

Hallucinations in constipation, 647

Hamamelis virginica, use of, in hemorrhoids, 923

Hand, deformities of in general rheumatoid arthritis, 82

Head, changes in, in rachitis, 146 of Tænia saginata, 934 of tape-worm, description of, 932

Headache in biliousness, 966 in catarrh of bile-ducts, 1054, 1055 in constipation, 646, 647, 853 in pseudo-membranous enteritis, 767 in chronic intestinal catarrh, 708 in intestinal indigestion, 628 in jaundice, 980 in lithæmia, 970 in acute gastritis, 467 in chronic gastritis, 475 in scurvy, 180 in simple ulcer of stomach, 494 in trichinosis, 960 and vertigo, in cancer of stomach, 554

Hearing, disorders of, in constipation, 647 in diabetes mellitus, 205 in scurvy, 181

Heart-action, cause of slowing of, in jaundice, 979

Heart affections in acute rheumatism, 28, 31 complicating chronic articular rheumatism, 72 disease, influence on causation of chronic intestinal catarrh, 700 of intestinal indigestion, 626 of simple ulcer of stomach, 487 organic, influence on causation of constipation, 641 as a cause of hyperæmia of liver, 984 disease of, as a cause of ascites, 1174 complicating simple ulcer of stomach, 503 disturbance in biliary concretions, 1077 in chronic gastritis, 474 in intestinal indigestion, 628 in rachitis, 152 lesions of, in gout, 117 in acute intestinal catarrh, 677 in chronic intestinal catarrh, 705 in acute yellow atrophy of liver, 1026 weak, as a cause of thrombosis and embolism of portal vein, 1095 and blood-vessels, lesions of, in scurvy, 172 and circulation, condition of, in scurvy, 179 and lungs, disease of, influence on causation of acute gastritis, 464 of chronic gastritis, 471 of gastric hemorrhage, 581 and membranes, lesions of, in acute rheumatism, 31-36

Heartburn in functional dyspepsia, 449 in dilatation of stomach, 593

Heat, extreme, influence on causation of cholera morbus, 720 of aphthous stomatitis, 326 of mouth, in aphthous stomatitis, 329 in stomatitis ulcerosa, 337 in rectum in pseudo-membranous enteritis, 765 use of, in enteralgia, 665 in hemorrhage from bowels, 834

Heberden's nodosities of rheumatoid arthritis, 86

Hectic in chronic intestinal catarrh, 709 in chronic form of peri-rectal and anal abscesses, 896

Hemiplegia following chronic intestinal catarrh, 710

Hemorrhage, frequency of, in scurvy, 179, 180

HEMORRHAGE FROM BOWELS, 830 General remarks, 830 Etiology, 830 Constipation, 830 Scybalous masses, 830 Hemorrhoids, 830 Anal fissure, 830 Foreign bodies, 830 Abuse of cathartics, 830 Parasites, 831 Anomalies in intestinal walls, 831 Dysentery, 831 Typhoid fever, 831 Embolism, 831 Tuberculous and syphilitic ulceration, 831 Invagination, 831 Polypi, 831 Tumors, 831 Diseases of blood-vessels, 832 Acute infectious diseases, 832 Hæmophilia, 832 Leuchæmia, 832 Anæmia, pernicious, 832 Of melæna neonatorum, 832 Morbid anatomy, 832 Symptoms, 832 Pains and borborygmi, 833 Blood, appearance of, 833 Stools, tarry, 833 Concealed form, 833 Collapse, 833 Syncope, 833 Anæmia, progressive, 833 Diagnosis, 833 of seat, 833 importance of examination of rectum in, 834 Treatment, 834 Rest, 834 Of collapse, 834 Of anæmia, 834 Diet, 834 Cold, use of, 834 Ice-water injections, 834 Ergotin, use of, 834 Opium, use of, 834 Tannic acid, 834 Tincture of iron, 834 Acetate of lead, 834 Alum, 834 Turpentine, 834 Alcohol, 834 Heat for collapse, 834 Transfusion of blood, 834 Milk, use of, 834

Hemorrhage from bowels, in intestinal ulcer, 827 mucous surfaces in acute yellow atrophy of liver, 1028 mouth. See _Stomatorrhagia_. occlusion of biliary passages, 1089 stomach, 580 rectum, 899 in cancrum oris, 341 in internal hemorrhoids, 884 in acute yellow atrophy of liver, 1030

Hemorrhages in cirrhosis of liver, 994 into pancreas, 1129 in purpura hæmorrhagica, 188 in cancer of stomach, 545 in simple ulcer of stomach, 492 in suppurative pylephlebitis, 1100 in cancer of rectum and anus, 904 in polypi of rectum, 882 sudden suppression of, as a cause of hyperæmia of liver, 984

Hemorrhagic diathesis, tendency to, in jaundice, 981 effusion into peritoneum, 1180 extravasations in acute pancreatitis, 1118 in liver tissue in acute yellow atrophy of, 1025 form of acute intestinal catarrh, treatment, 698

Hemorrhoids, 882 complicating constipation, 645, 648 external, 883 internal, 883 in chronic intestinal catarrh, 706 in intestinal indigestion, 627 in amyloid liver, 1044 in cirrhosis of liver, 994 influence on causation of hemorrhage from bowels, 830

Hepar adiposum, 1046

Hepatic calculi, 1058 colic, 1058, 1070 distinguished from enteralgia, 664 relation to malaria, 1071, 1072 disease, as a cause of hemorrhoids, 884 complicating chronic intestinal catarrh, 710 influence on causation of chronic intestinal catarrh, 700 disturbance, influence on causation of functional dyspepsia, 447 duct, cause of occlusion of, 1084 effects of occlusion of, 1085 dulness, increased, in hyperæmia of liver, 986 form of functional dyspepsia, treatment, 457 glycosuria, 973 resonance on percussion, significance, 1156 secretion, deficient, in intestinal indigestion, treatment, 635

Hepatogenous jaundice, 976

Hereditary nature of rachitis, 144 syphilis. See _Syphilis, Hereditary_.

Heredity, influence on causation of constipation, 640 of diabetes mellitus, 203 of functional dyspepsia, 438 of enteralgia, 659 of gout, 109 of cancer of intestine, 869 of chronic intestinal catarrh, 699 of intestinal indigestion, 623 of carcinoma of liver, 1033 of purpura, 191 of acute rheumatism, 21 of chronic articular rheumatism, 70 of gonorrhoeal rheumatism, 103 of muscular rheumatism, 75 of rheumatoid arthritis, 88, 91 of scrofula, 232 of cancer of stomach, 535 of tonsillitis, 380 of tabes mesenterica, 1105

Hernia, complicating constipation, 648 internal, laparotomy for, 866 strangulated, forms of, 843

Herniæ, weight, influence on causation of dilatation of stomach, 590

Hernial sacs, stomach in, 617

Herpes of anus, 892 zoster due to biliary calculi, 1078

Herpetic form of acute pharyngitis, nature and course, 392 tonsillitis, etiology, 380 form of tonsillitis, treatment of, 388

Hiccough in acute gastritis, 467 in spasmodic stricture of oesophagus, 420 in cancer of stomach, 540

Histology of gastric cancer, 563, 564, 565

History of catarrh of bile-ducts, 1051 of cancrum oris, 338, 339 of cholera morbus, 719 of dysentery, 777 of enteralgia, 658 of pseudo-membranous enteritis, 763 of acute yellow atrophy of liver, 1023 of gout, 109 of glossitis parasitica, 357 of parenchymatous glossitis, 359 of acute intestinal catarrh, 667 of macroglossia, 349 of acute oesophagitis, 409 of organic stricture of oesophagus, 422 of spasmodic stricture of oesophagus, 419 of diseases of pancreas, 1112 of paratyphlitis, 814 of acute pharyngitis, 400 of peritonitis, 1132 of introduction of opium in treatment of acute peritonitis, 1146-1151 of rheumatoid arthritis, 78 of scurvy, 167-169 of cancer of stomach, 530 of cirrhosis of stomach, 611 of dilatation of stomach, 586 of simple ulcer of stomach, 480 of tabes mesenterica, 1183 of thrush, 331 of tonsillitis, 379 of typhlitis, 814

Hoarseness in chronic pharyngitis, 404

Hob-nail appearance of hepatic surface in cirrhosis of liver, 992

Hog, Trichina spiralis in, 958

Hooklets, in fluid of hydatids of liver, significance, 1105

Hot climates, influence on causation of intestinal indigestion, 624 drinks, as a cause of acute oesophagitis, 410 influence on causation of chronic oesophagitis, 416 embrocations in typhlitis, 820 season, influence on causation of dysentery, 787 weather, intestinal affections of children in, 726

Hot-water injections in pseudo-membranous enteritis, 774 in intestinal obstruction, 860 in intestinal ulcer, 829 use of, in gastralgia, 463 in chronic gastritis, 477 in pruritus ani, 917 in sphincterismus, 916

Hour-glass contraction of stomach, 617 in gastric cancer, 566

Hutchinson on peculiarities of incisor teeth in hereditary syphilis, 293, 294

Hunyadi Jânos water, use of, in intestinal indigestion, 636

Hydatid tumors, varieties and seat, 944

Hydatids of liver, 1101

Hydrocephalus, spurious, in entero-colitis, 735

Hydrochloric acid, use of, in functional dyspepsia, 456 free, detection of, in fluids of gastric cancer, 543 use of, in dilatation of stomach, 609

Hydrocyanic acid, use of, in cholera morbus, 725 in functional dyspepsia, 458, 459 in gastralgia, 463 in acute gastritis, 469

Hydrogen peroxide, use of, in tuberculous pharyngitis, 402

Hydrophobia, influence on causation of spasmodic stricture of oesophagus, 419

Hydrotherapy, use of, in functional dyspepsia, 457

Hydrothorax, complicating gastric cancer, 560

Hygiene, bad, influence on causation of scrofula, 232 improper, influence on causation of chronic intestinal catarrh, 699

Hygienic treatment of diabetes mellitus, 225 of pseudo-membranous enteritis, 776 of intestinal indigestion, 632 of chronic interstitial pancreatitis, 1122 of obstruction of pancreatic duct, 1131 of acute rheumatism, 69 of muscular rheumatism, 77 of rheumatoid arthritis, 101 of scurvy, 183 of tabes mesenterica, 1194

Hyperæmia of liver, 983 relation to causation of diabetes mellitus, 195

Hyperplasia and atrophy of liver, in phosphorus-poisoning, 1031

Hyperpyrexia in acute rheumatism, 29, 66 of acute rheumatism, treatment of, 66-68 treatment, in acute intestinal catarrh, 692

Hypertrophy, of intestinal walls in constipation, 644 of gastric walls in stenosis of pylorus, 615 in dilatation of stomach, 599 of tongue, 349

Hypochondria in fatty liver, 1048

Hypochondriasis in functional dyspepsia, 451 in gout, 118

Hypochondrium, right, uneasiness in, from gall-stones, 1069

Hypodermatic alimentation in simple ulcer of stomach, 525 use of iron in simple ulcer of stomach, 528

Hypogastric plexus, lesions, in acute peritonitis, 1136

Hypophosphates, use of, in scrofula, 252

Hypostatic congestion of lungs in entero-colitis, 734 pneumonia, in entero-colitis, 735

Hysteria in hepatic colic, 1071 influence on causation of oesophageal paralysis, 429

Hysterical form of enteralgia, treatment, 664 origin of spasmodic stricture of oesophagus, 767 phenomena in gastralgia, 461 symptoms of pseudo-membranous enteritis, 767

I.

Ice, use of, in cholera infantum, 762 in cholera morbus, 725 in entero-colitis, 762 in acute gastritis, 468 in acute intestinal catarrh, 689, 690, 693, 698 in intestinal ulceration, 829 in acute pancreatitis, 1120 in acute pharyngitis, 397 in acute oesophagitis, 416 in rectal hemorrhage, 927 in cancer of stomach, 576 in simple ulcer of stomach, 525 in aphthous stomatitis, 330 in catarrhal stomatitis, 325 in tonsillitis, 388 local use of, in intestinal obstruction, 864 locally, in proctitis, 919

Ice-bag, use of, in typhlitis and perityphlitis, 822

Ice-water, influence on causation of cholera morbus, 721 injections in dysentery, 810 in hemorrhage from bowels, 834 in hemorrhage from rectum, 927

Icterus, 925

Icthyosis linguæ, 356

Idiocy and cretinism, relation to macroglossia, 350

Idiopathic causes of gastric hemorrhage, 582 pancreatitis, acute, 1118 tonsillitis, 379

Idiosyncrasy, influence on causation of enteralgia, 660 of acute intestinal catarrh, 671 of intestinal indigestion, 623

Ignipuncture, use of, in hypertrophy of tongue, 354

Ileitis, 667, 683

Ileo-cæcal valve, lesions of, in entero-colitis, 737 variety of intussusception, 846

Ileo-colitis of acute intestinal catarrh, lesions of, 674

Ileum, lesions of, in entero-colitis, 737

Ileus, distinguished from enteralgia, 664

Impacted feces, influence on causation of ulceration of rectum and anus, 894

Impaction of biliary calculi, 1074 of foreign bodies, as a cause of intestinal obstruction, 837

Impurities of air, influence on causation of entero-colitis, 728-730

Incision, deep in parenchymatous glossitis, 365 in fissure of anus, 912 in fistula in ano, 922

Incisions, use of, in acute pharyngitis, 397

Incisor teeth, Hutchinson on peculiarities of, in hereditary syphilis, 293, 294

Indigestion. See _Functional Dyspepsia_. influence on causation of constipation, 642 of enteralgia, 660 in atrophy of stomach, 616

Indigo-carmine test for sugar in urine, 216

Individual predisposition, influence on causation of gastric cancer, 537

Induration of tongue in chronic parenchymatous glossitis, 367 in tubercular ulceration of tongue, 369

Infants, treatment of constipation in, 656

Infants' foods, farinaceous, analysis of, 750, 751

Infantile peritonitis, 1172

Infection, syphilitic, of child at moment of conception, 262, 267 during birth, 269 during utero-gestation, 267 of mother by foetus in utero, 262

Infectious diseases, acute, as a cause of hemorrhage from stomach, 581

Infiltration, fatty, of pancreas, 1128

Infiltrating form of carcinoma of liver, 1034

Inflammation, scrofulous, Cornil and Ranvier on causes of, 239

Inflammatory affections of pancreas, 1118 diseases of stomach, 436 nature of syphilitic pharyngitis, 406 nature of rachitis, 137, 138 theory of origin of gastric ulcer, 512

Inflation of stomach, value, in diagnosis of gastric cancer, 549

Ingluvin, use of, in simple ulcer of stomach, 525

Inhalations, steam, use of, in acute pharyngitis, 397, 398

Injection of bowel in intestinal obstruction, 864 of ice-water in hemorrhage from rectum, 927 subcutaneous, of oil, in simple ulcer of stomach, 525

Injections of hot water, in intestinal ulcer, 829 uterine, influence on causation of acute peritonitis, 1140

Injury, influence on causation of acute intestinal catarrh, 673 of acute oesophagitis, 411 of diseases of pancreas, 1114 of acute peritonitis, 1140 of acute pharyngitis, 391 of rheumatoid arthritis, 91 of scrofula, 236 of cirrhosis of stomach, 612 of rupture of stomach, 618 of simple ulcer of stomach, 486

Injuries, influence on causation of diabetes mellitus, 203 of parenchymatous glossitis, 360

Inosite in diabetic urine, 208 test for, in diabetic urine, 217

Inspissated bile, 1058 treatment of, 1079

Intellect, state of, in rachitis, 149

Intermarriage of scrofulous persons, 249

Intermittence of pain in simple ulcer of stomach, 491

Intermittent fever, complicating chronic intestinal catarrh, 710 influence on causation of simple gastric ulcer, 488

Internal hemorrhoids, symptoms of, 883 strangulated hernia, forms of, 843

Interstitial hepatitis, 990 keratitis in hereditary syphilis, 299 pancreatitis, chronic, 1121

INTESTINES, CANCER OF, 868 Definition, 868 Etiology, 868 Forms of, 868 Scirrhous, 868 Lympho-sarcoma, 868 Cylinder-cell, 868 Colloid, 868 Primary, 868 Secondary, 868 Relative frequency, 868 Seat, 869 of secondary form, 869 Age, influence of, on causation, 869 Sex, influence of, on causation, 869 Heredity, influence of, on causation, 869 Exciting causes, 869 Symptoms, 869 Vagueness of early symptoms, 869 Irregular bowels, 869 Undefined pains, 869 Physiognomy, 869 Tumor, presence of, 869 character of, 870 pain in, 870 pulsation of, 870 Of duodenal form, 870 pain in, 870 vomiting in, 870 Of lower intestine, 870 constipation, 871 stools, bloody and mucous, 871 sudden disappearance of symptoms from softening of tumor, 871 Oedema, 871 Wasting, 871 Cachexia, 871 Duration, 871, 873 Morbid anatomy, 871 Cylinder-cell epithelioma most common form, 871 Method of growth, 872 Scirrhous form, method of growth of, 872 Ulceration in, 872 Colloid form, method of growth of, 872 Invasion of neighboring parts, 873 Secondary to hepatic cancer, 873 Melanotic sarcoma, secondary to tumor of eye or skin, 873 Diagnosis, 873 Of duodenal form, 873 from pyloric cancer, 873 Tumor, significance of, 873 from fecal tumor, 873 Significance of cancerous fragments in stools, 873 Prognosis, 873 Death, cause of, 873 Treatment, 874 Diet, 874

INTESTINES, LARDACEOUS DEGENERATION OF, 874 Synonyms, 874 Frequency, 874 Symptoms, absence of specific, 874 Diarrhoea, 874 Hemorrhage from bowels, 874 Hæmatemesis, 875 General condition, 875 Death, cause, 875 Morbid anatomy, 875 Seat of degeneration, 875 Mucous membrane, lesions of, 875 Iodine test, 875 Methyl-aniline-violet test, 875 Method of testing, 876 Ulceration and enlargement of mucous surface, 876 Microscopic appearance of lardaceous materials, 876 Degeneration of the vessels, 876 Diagnosis, 876 Prognosis, 876 Treatment, 876 Incurability of, 876 Diet, 876 Of diarrhoea, 876 Bismuth subnitrate, use of, in large doses, 876 Of hemorrhage, 876

INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER, 726 _Entero-colitis_, 726 Etiology, 727 Summer heats, 727 Season, 727, 728 Vitiated air, 728-730 nature of impurities in, 729 gases, 729 organic matter, 729 Over-crowding, 730 Filth, 730 Improper food, 731, 732 Artificial feeding, 731 Poor breast-milk, 731 Impure cow's milk, 731 Age, influence on causation, 732 Relation of dentition to, 733 Symptoms, 733 Onset, 733 Stools, characters of, 733, 734, 736 Tongue, state, 733 Vomiting, 733 significance of date of appearance of, 733, 734 Vomit, characters, 733 Pulse, state of, 734, 736 Fever, 734, 736 Skin, state of, 734, 736 Kidneys, state of, 734 Skin eruptions, 734 Hypostatic congestion of lungs, 734 pneumonia, 735 Spurious hydrocephalus, 735 symptoms, 735 Convalescence, 736 Death, cause of, 736 Wasting, 736 Drowsiness, 735, 736 Morbid anatomy, 736 Hyperæmia of mucous membrane, 737 Duodenum, lesions of, 737 Jejunum, lesions of, 737 Ileum, lesions of, 737 Ileo-cæcal valve, thickening of, 737 Ulcers, 737, 738 seat of, 737, 738 Mucous membrane, softening of, 737 Colon, lesions of, 738 Solitary glands, enlargement of, 738 Peyer's patches, enlargement of, 738 Appendix vermiformis, lesions of, 738 Mesenteric glands, enlargement of, 739 Stomach, lesions of, 739 Mouth, lesions of, 739 Liver, lesions of, 739 Lungs, lesions of, 740 Brain, lesions of, 740 Diagnosis, 740 Significance of abdominal tenderness, 740 Prognosis, 741 Mortality, 726, 727 _Cholera Infantum, or Choleriform Diarrhoea_, 741 Nature, 744 Relation to thermic fever, 745 Symptoms, 741 Onset, 741 Stools, 741 characters of, 741 Vomiting, 742 Appetite, impaired, 742 Thirst, 742 Tongue, state of, 742 Temperature, 742 Restlessness, 742 Loss of strength, 742 Emaciation, 742 Urine, state of, 742 Pulse, state of, 742 Stupor, 742 Morbid anatomy, 742 Rilliet and Barthez on lesions, 742 Stomach, lesions of, 743, 744 Intestinal canal, lesions of, 743, 744 Bacteria, significance of, 744 Diagnosis, 745 Prognosis, 745 Duration, 746 Treatment, 746 Preventive, 746 Weaning, time for, 746 Change of air, 746, 756 Amount of food ingested by healthy infants, 746 Curative, 747 Diet, 746, 748 Milk, use of, 749 Woman's milk, composition of, 749, 750 Cow's milk, composition of, 749, 750 Farinaceous foods, analyses of, 750, 751 Cow's milk, objections to, 749, 751 Peptonized milk, use of, 751, 753 Mode of peptonizing, 752 Oatmeal and barley as diluents, 753 Farinaceous foods, use of, 753 Flour-ball, use of, 754, 755 Liebig's foods, use of, 754 Nestle's food, use of, 754 Ridge's food, use of, 754 Condensed milk, use of, 754 Beef-, mutton-, and chicken-tea, use of, 755 Necessity of cleanliness, 756 Change of climate, 756 Medicinal, 757 Of first stage, 757 Purgatives, use of, 757 Sodium benzoate, use of, 757, 761 Sodium bicarbonate, 757 Opium, use of, 758, 759 Mist. cretæ, use of, 758 Bismuth subnitrate, use of, 758 Of cholera infantum, 759 Of cerebral symptoms, 759 Bromide of potassium, use of, 759 Of second stage, 759 Pepsin, use of, 760 Calomel, use of, 760 Lactopeptin, use of, 760 Enemata, use of, 760 Argenti nitratis, use of, 761 Alcohol, use of, 761 Of vomiting, 761 Lime-water, use of, 762 Carbolic acid, use of, 761 Ipecacuanha, use of, 762 Ice, use of, 762 Liquor ferri nitratis, use of, 762

Intestinal canal, lesions of, in cholera infantum, 743, 744 state of, in catarrh of bile-duct, 1054

INTESTINAL CATARRH, ACUTE, 667 Synonyms, 667 History, 667 Nature and classification, 668 Inflammatory nature, 668 Etiology, 669 Geographical distribution, 669 Race, 669 Sex, 669 Age, 670 Climate, 669 Summer heats, 669 Sudden changes of temperature, 670 Cold, 670 External burns, 670 Impure air, 670 Sewer gas, 670 Temperament and idiosyncrasy, 671 Previous attacks, 671 Sedentary, life, 671 Abuse of tobacco and alcohol, 671, 672 Constipation, 671 Eruptive fevers, 671 Uræmia, 671 Malaria, 671 Chronic wasting diseases, 671 Phthisis, 671 Improper and excessive food, 671, 672 Irritant and caustic poisons, 672 Drastic purgatives, 672 Foreign bodies, 672 Impure water, 672, 673 Injury, 673 Emotional influence, 673 Lesions of nerve-centres, 673 Micro-organisms, 673 Bacteria, 673 Morbid anatomy, 673 External appearance of intestines, 673 Distension of colon and cæcum, 673 of small intestines, 673 Color of intestines, 673 Serous membrane of intestines, lesions of, 674 Appearance of intestinal contents, 674 Intestinal mucous membrane, lesions of, 674 Mucous membrane, seat of inflammation of, 674 Ileo-colitis, 674 Duodenal mucous membrane, lesions of, 674 Hyperæmia of mucous membrane, 674 Swelling and softening of, 675 Villi, lesions of, 675 Solitary glands, lesions of, 675 Peyer's patches, tumefaction of, 675 Ulcers, catarrhal, 676 follicular, 676 seat of, 676 Mucous collections, 676 Vibrios and bacteria, 676 Mesenteric glands, enlargement of, 677 Liver, lesions of, 677 Spleen, lesions of, 677 Kidneys, lesions of, 677 Lungs, lesions of, 677 Heart, lesions of, 677 Brain, lesions of, 677 Pathological histology, 677 Congestion of capillaries, 677 Transudation of serum, 677 Rupture of small vessels, 677 Increase of mucus, 677 Origin of mucus, 677 Increased cellular growth, 677 Formation of ulcers, 677 Desquamation of epithelium, 677 Symptoms, 677 Mild forms of, 678 Onset of, 678 Pain, 678 Stools, character of, 678 Tongue, dryness of, 678 Duration of, 678, 681 Severe forms of, 678 Pain and colics, 679, 682 Borborygmi, 679 Tympanites, 679 Abdomen, intumescence of, 679 tenderness of, 679 soreness on moving, 679 pain in, 679, 682 Diarrhoea, 679, 681 Number of stools, 679 Character of stools, 680, 681, 682 Color of stools, 680, 681, 682 Blood in stools, 680, 681, 682 Odor of stools, 680 Tongue, condition of, 680, 681 Thirst, 680, 681 Nausea and vomiting, 681 Fever, 681 Urine, condition of, 681 Paraplegia and muscular contraction, 681 Delirium, 681 Physiognomy, 681 Emaciation, 682 Collapse, 682 Pulse, 682 Duration, 682 In children, 682 Loss of strength, 682 Choleriform diarrhoea, 682 Varieties due to seat, 682 Acute duodenitis, 682 relation to integumental burns, 682 symptoms, 682 ileitis, 683 jejunitis, 683 symptoms, 683 colitis, 683 symptoms, 684 bloody stools, 684 tenesmus, 684 Proctitis, 684 symptoms, 684 burning in rectum, 684 tenesmus, 684 mucous stools, 684 Diagnosis, 684 Of ileo-colitis, 685 Of follicular ulceration, 685 In children, 686 From typhoid fever, 676, 685, 686 dysentery, 686 enteralgia, 686 abdominal rheumatism, 686 lead colic, 686 peritonitis, 686 Prognosis, 687 Treatment, 687 Prophylactic, 687 Change of climate, 688 Disinfection, 688 Proper clothing, 688 When arising from cold, 688 heat, 688 undigested food, 689 Bright's disease, 689 phthisis, 689 Value of rest, 690 of counter-irritation, 688, 690, 698 Of thirst, 690 Of hyperpyrexia, 692 Of flatulence, 693 Of diarrhoea, 693 Of ulcers, 698 Of hemorrhagic form, 698 Of choleraic form in children, 698 in adults, 698 Of duodenitis, 698 By rectum, 697 Diet, 687, 688, 690 in children, 692 of convalescence, 692 Use of blood-letting, 690 of milk, 690, 691 of buttermilk, 691 of koumiss, 691 of eggs, 691 of beef-tea, 691 of raw-beef, 691 of milk, 690, 691 of poultices, 688, 690 of sinapisms, 688, 690 of ice, 689, 690, 693, 698 of warm and cold baths, 692 of aconite, 689 of quinia, 692 of jaborandi, 688 of bismuth, 693 of alkalies, 693 of mineral acids, 693, 694, 695 of opium, 689, 693, 698 of oxide of zinc, 694 of chalk mixture, 694 of lime-water, 694 of cassava-water, 694 of sugar of lead, 694 of calomel, 695 of bichloride of mercury, 695 of vegetable astringents, 695 of gallic acid, 695 of tannic acid, 695 of ipecacuanha, 695 of coto-bark, 696 of alum, 696 of sulphate of copper, 696 of nitrate of silver, 696, 698 of oxide of silver, 696 of iron, 696 of carbolic acid, 696 of creasote, 696 of salicylic acid, 696 of sulpho-carbolate of calcium, 696 of enemata, 697 of irrigation of large intestine, 697 of iced coffee in children, 698 of bromides, 698 of spirits of camphor, 698

INTESTINAL CATARRH, CHRONIC, 699 Etiology, 699 Age, 699 Sex, 699 Heredity, 699 Bad hygiene, 699 Overwork, 699 Chronic wasting diseases, 699 Phthisis, 699 Bright's disease, 699 Gout, 699 Addison's disease, 700 Syphilis, 700 Malaria, 700 Disease of heart and lungs, 700 liver, 700 Improper food, 700 Alcohol, 700 Foreign bodies, 700 Chronic lesions of bowels, 700 Morbid anatomy, 700 Intestines, seat of lesions, 700, 701 alteration in calibre, 700 Intestinal walls, hypertrophy, 700 Mucous membrane, lesions of, 700 alteration in color, 701 of ileum, swelling of, 701 hypertrophy of villi, 701 Solitary glands, alterations in, 702 Peyer's patches, alterations in, 702 Colon, ulcers of, 702 seat and character, 702 perforating, 702 Presence of pseudo-membrane, 702 Veins, varicose condition, 702 Duodenal ulcer from external burns and chronic Bright's disease, 703 from embolism, 703 Adhesions, peritoneal, 703 Suppuration of duodenum, 703 Chronic proctitis, lesions, 703 Mucous membrane, condition, 703 Inflammation of peri-rectal tissue, 703 Abscesses, 703 Fistulæ, 703 Pathological histology, 703 Increased cell-proliferation, 703 Hypertrophy of tissue, 703 Glands of Lieberkühn, elongation of, 703 Mode of formation of ulcers, 703 cicatrization of ulcers, 703 Formation of cysts, 704 origin, 704 polypoid growths, 704 seat, 704 Atrophy of intestinal walls, 704 seat, 704 mucous membrane in, 705 Amyloid degeneration of mucous membrane, 705 Peritoneum, lesions, 705 Mesenteric glands, enlargement, 705 Liver, lesions of, 705 abscess of, 705 Gall-bladder, lesions of, 705 Spleen, lesions of, 705 Pancreas, lesions of, 705 Kidneys, lesions of, 705 Heart, lesions of, 705 Lungs, lesions of, 706 Pleura, lesions of, 706 Cornea, lesions of, 706 Brain, lesions of, 706 Symptoms, 706 Mild forms, 706 State of bowels, 706 Signs of intestinal indigestion, 706 Time of appearance, 706 Fulness, 706 Colicky pains and borborygmi, 706 Constipation, 706 Diarrhoea, 706 Abdomen, state of, 706 Depression of spirits, 706 Hemorrhoids, 706 Severe forms, 707 Tongue, state, 707 Appetite impaired, 707 Time of appearance, 707 Pain, 707 Abdomen, state, 707 Tympanites, 707 Diarrhoea, 707 quantity, 707 Stools, appearance, 707 bloody, 707 mucous, 708 composition, 708 micrococci and bacteria in, 708 unaltered food (lientery), 708 Headache, 708 Depression, 708 Vertigo, 708 Sleeplessness, 708 Palpitation, 708 Urine, state, 708 Progress and termination, 709 Progressive emaciation, 709 Anæmia, 709 Cuticle, dryness of, 709 Fever, 709 Hectic, 709 Pulse, 709 Death, cause, 709 Complications, 709 Dropsy, general, 709 Oedema of one extremity, 709 Chronic bronchitis, 709 Phthisis, 709 Pneumonia, 709 Peritonitis, 710 Tuberculosis, 710 Bright's disease, 710 Intermittent and remittent fever, 710 Hepatic disease, 710 Ulceration of cornea, 710 Sequelæ, 710 Chronic intestinal indigestion, 710 Tabes mesenterica, 710 Constipation, 710 Stricture, intestinal, 710 Paralysis, 710 Para- and hemiplegia, 710 Diagnosis, 710 Of primary from secondary diarrhoea, 711 From chronic dysentery, 711 Of locality of lesion, 711 Of duodenal form, 711 Of catarrh of jejunum and ileum, 712 Of catarrh of colon, 712 Of stage of inflammatory process, 712 Of follicular ulceration, 712, 713 Of duodenal ulcer, 713 From tuberculous ulceration, 713 From cancerous ulceration, 713 Prognosis, 713 Treatment, 714 Preventive, 714, 715 Of cause, 714 Mild forms, 714 Diarrhoea, 715 Constipation, 714 Of follicular form, 715 ulceration, 718 Rest, 716 Change of residence, 715, 716 Baths, 714, 716 Sitz baths, 716 Permanent baths, 716 Exercise, 714, 716 Diet, 714, 716 Milk, 716 Use of stimulants, 716 wines, 716 purgatives, 714, 715 mineral waters, 714, 715 Rockbridge alum water, 714, 717 iron, 714, 715, 717 bitter tonics, 715 quinia, 715 mineral acids, 715 strychnia, 714, 715 medicated enemata, 714, 717, 718 rectal irrigation, cold water, 717 arsenic, 715 bismuth, 715, 717 liquor pancreaticus, 714 mineral astringents, 717 nitrate of silver, 717, 718 opium, 715, 718 turpentine and copaiba, 718 ergot, 718 cod-liver oil, 718 corrosive sublimate, 717 gallic acid, 717

Intestinal catarrh, complicating gout, 122 influence on causation of tabes mesenterica, 1186 colic. See _Enteralgia_. contents, in acute intestinal catarrh, 674 dilatation, in constipation, 643 disorders, influence on causation of catarrhal stomatitis, 322 of thrush, 332

INTESTINAL INDIGESTION, 620 Nature, 620 Physiology of intestinal digestion, 620 Action of saliva, 620, 621 of gastric juice, 621 Chyme, composition of, 621 Action of bile, 621 of pancreatic juice, 622 of trypsin, 622 Peristalsis, cause of, 622, 623 Action of liver, 623 Absorption of peptones and sugar, 623 of oils and fats, 623 Etiology, 623 Sex, 623 Age, 623 Heredity, 623 Idiosyncrasy, 623 Anæmia, 623 Rachitis, 623 Syphilis, 623 Febrile diseases, 623 Strumous diathesis and phthisis, 624 Want of exercise, 624 Sexual excess, 624 Impure air, 624 Mental overwork, 624 Worry and anxiety, 624 Wealth, 624 Sedentary occupations, 624 Tight-lacing, 624 Hot climates, 624 Over-eating, 624 Indigestible food, 625 Excess of starchy food, 625 Alcohol, abuse of, 625 Condiments, abuse of, 625 Irregularity in meals, 625 Imperfect mastication, 625 Tobacco, abuse of, 625 Constipation, 625 Excess of gastric acid, 626 Obstruction of bile-ducts, 626 Pancreatic disease, 626 Disease of heart and lungs, 626 of intestines, 626 Symptoms, 626 Forms, 626 Acute form, 626 Chronic form, 627 Time of appearance after eating, 627 Pain, 627 character and seat of, 627 Tympanites and borborygmi, 627 Fulness after eating, 627 Gas, source of, 627 Abdominal swelling, 627 Constipation, 627 Stools, character of, 627 Diarrhoea, 627 Hemorrhoids, 627 Tongue, state of, 628 Nervous system, state of, 628 Depression of spirits, 628 Sleeplessness, 628 Headache, 628 Vertigo, 628 Anxiety and worry, 628 Mental power, impaired, 628 Paralysis, 628 Sensibility, modifications of, 628 Faintings, 628 Heart disturbance, 628 Palpitation, 628 Circulation, languid, 628 Cold extremities, 628 Urine, state of, 628 lithates in, 628 albuminuria, 628 Perversion of sexual function, 629 Anæmia, 629 Skin eruptions, 629 Liver, functional disorder of, 629 Course, 630 Duration, 630 Termination, 630 In deterioration of health, 630 In organic disease, 630 In phthisis, 630 Diagnosis, 630 From gastric dyspepsia, 631 Of varieties of, 631 Of pancreatic form, 631 Of biliary form, 631 Prognosis, 631 Treatment, 632 Of acute form, 632 Of chronic form, 632 Hygienic, 632 Change of climate, 632 Exercise, 632 Thorough mastication, 632 Swedish movements, 632 Bathing, 632 salt-water, 632 Russian, 633 Regularity in eating, 633 Diet, 633, 634 Milk, use of, 633 Koumiss, use of, 633 Beef-essences, 633 Foods to be avoided, 635 Use of wine, 634 Mineral waters, 634, 636 Use of pre-digested foods, 635 of pancreatic extract, 635 mode of administering, 635 Of deficient hepatic secretion, 635 Of flatulence and colics, 636 Of constipation, 636 Of strumous form, 636 Use of ipecacuanha, 636 of euonymin, 636 of sanguinarin, 636 of podophyllin, 636 of sulphate of sodium, 636 of benzoate of sodium, 636 of iron, 636 of quinia, 636 of strychnia, 636 of mineral acids, 636 of bitter waters, 636 of Friedrichshall waters, 636 of Hunyadi Jânos, 636 of cod-liver oil, 637

INTESTINAL OBSTRUCTION, 835 Classification, 835 Congenital strictures and malformations, 836 Strictures, 836 seat, 836 of colon, 836 sigmoid flexure, 836 duodenum, 836 malformations, 837 of anus and rectum, 837 _Impaction of Foreign Bodies_, 837 Nature of substances found in intestines, 837, 838 Stony concretions (enteroliths), 838 Gall-stones, 838 Symptoms, 839 Modes of discharge of, 839 By vomiting, 839 By ulceration, 839 Peritonitis from, 839 Of inflammation, 839 Remote results of, 840 Impaired health, 840 Emaciation, 840 Of impaction from gall-stones, 840 Pains, colicky, 840 Vomiting, 840 Prostration, 840 Signs of disordered liver, 840 _Acute Internal Strangulation, Twisting, etc._, 840 Seat of twisting, 840 Conditions necessary to production, 841 Elongated mesentery, 841 Increased weight of bowel, 841 Inflammation of elongated bowel, 841 Symptoms, 841 Prodromal, 841 Signs of intestinal disorder, 841 Actual attack, 841 Other modes of strangulation and twisting, 841, 842 Forms of internal strangulated hernia, 843 Diaphragmatic hernia, 843 Symptoms, 843 Suddenness of onset, 843 Nausea and vomiting, 843 Pains, 843 Tympanites, 843 Of peritonitis, 843 Delirium, 843 Duration, 841, 843 _Intussusception, Invagination_, 844 Without symptoms, 844 Morbid anatomy of, 844 Diminished lumen of bowel, 845 Inflammation, changes produced by, 845 Sloughing of invaginated parts, 845 Gangrene and ulceration in, 845 Seat, 846 Ileo-cæcal variety, 846 Method of production, 846 Frequency in relation to sex, 847 in relation to age, 847 Mechanism of, 847 Local paresis and tenesmus of bowel, 847 Length of, 848 Symptoms, 848 Onset of, 848 Pain, characters of, 848 effect of pressure upon, 848 Vomiting, 848 Vomit, fecal, 848 Diarrhoea, 848 Stools, characters of, 848 Abdominal tenderness, 848 Tumor, presence of, 848 Tympanites, 848 Urgency of symptoms, relation to locality and degree of constriction, 848 Suddenness of acute cases, 848 Gangrene of invaginated portion, 849 Date of separation of sequestrum, 849 Of chronic cases, 849 Duration, 849 Abatement of symptoms before death, 849 _Constipation_, 850 Number of fecal evacuations in health, 850 Etiology, 850 Sex, 850 Sedentary life, 850 Rapid loss of fluid, 851 By kidneys, 851 lungs, 851 skin, 851 Food, improper, 851 Bile, deficiency of, 851 Dislocations of intestines, 851 Nervous diseases, 851 Hysteria, 851 Paralysis of muscular coat of intestine, 851 Chronic debilitating diseases, 852 Loss of sensibility of colon and rectum, 852 Fecal impaction, 852 Tumor, fecal, characters of, 852 Dilatation of colon and rectum, 852 Symptoms, 853 Torsion of cæcum, 853 Internal strangulation from, 853 Digestive disturbances, 853 Appetite, impaired, 853 Headache, 853 Pain, colicky, 853 Diarrhoea, 853 Evolution of gases, 853 Mental depression, 854 Nervous symptoms, 854 Pain in legs, 854 in back, 854 Strength, loss of, 854 of obstruction from, 854 _Stricture of bowel_, 854 Frequency of, 854 Seat of, 855 From cicatrization of ulcers, 855 cancer, 855 Symptoms, 856 Intestinal disorders, 856 Colicky pains, 856 Paroxysmal pain, 856 Of rectum, 856 Determination of, by digital examination, 856 _Compression and Contraction of Bowel_, 857 From abdominal tumors and cysts, 857 From adhesions of chronic peritonitis, 857 Seat of, 857 Symptoms, 857 Insidiousness of onset of, 858 Intestinal disorders, 858 Exhaustion, 858 Distinguished from stricture, 858 Differential diagnosis, 858 From external strangulated hernia, 858 functional obstruction of bowel, 859 Of congenital occlusion, 859 Of obstruction by foreign bodies, 859 by gall-stones, 860 by internal hernia, 860 by torsion, 860 uneven distension of abdomen in torsion, 860 fecal accumulation, 860 abdominal tumors, 861 Of seat of obstruction, 861 Of pain, significance of, 861 Significance of constipation, 862 of vomiting, stercoraceous, 862 Duration, 862 Mortality, 862 Relative frequency of deaths by different forms, 862 Treatment, 862 Purgatives, uselessness and danger, 862, 863 Quicksilver, use of, 863 Opium, use of, 863 method of administration, 863 Of fecal impaction, 863 Castor oil, use of, in, 863 Of invagination low in rectum, 864 Ice, locally, use of, 864 Bleeding, use of, 864 Electricity, use of, 864 Abdominal taxis, 864 Injection of warm water, 864 Replacement of pressing tumors or organs, 864 Stimulants, use of, 865 Quinia, use of, 865 Tapping of gut, in gaseous distension, 865 Surgical, 865 Laparotomy, 865 in invagination, 866 mortality, 866, 867 in internal hernia, volvulus, etc., 866 Entorectomy, 866 Enterotomy, 867 method of performing, 867

Intestinal tract, condition in rachitis, 153 trichina, 959 tube, ulceration and suppuration of, as a cause of suppurative pylephlebitis, 1097, 1098

INTESTINAL ULCER, 823 Synonyms, 823 Definition, 823 Etiology, 823 Frequency, 823 Toxic form, 823 Mineral acids, 823 Syphilis, 823 Traumatic form, 823 From hardened feces and foreign bodies, 823 intestinal parasites, 823 use of enemata, 823 burns of skin, 824 dysentery, 824 tuberculosis, 824 typhoid fever, 824 arrest of circulation, 824 erosion of gastric juice, 824, 825 Of duodenal form, 825 frequency, 825 tendency to perforation, 825 cicatrization, 825 Symptoms, 825 Indefinite nature of, 825 Pain, 826 character, 826 Appetite, loss, 826 Failure of general health, 826 Digestive disturbances, 826 Nausea and vomiting, 826 Diarrhoea, 827 Stools, character, 827 effect of seat of ulcers upon, 827 Hemorrhage of bowel, 827 black and tarry stools in, 827 Duration, 827 Diagnosis, 828 From intestinal catarrh, 828 carcinoma, 828 enteralgia, 828 hemorrhage of gastric ulcer, 828 Prognosis, 828 Treatment, 828 Diet, 829 Of vomiting, 829 Of pain, 829 Of hemorrhage, 829 Of peritonitis, 829 Of constipation, 829 Alcohol, use of, 829 Bismuth, use of, 829 Sodium bicarbonate, use of, 829 Oxide of zinc, use of, 829 Purgatives, use of, 829 Ice, use of, 829 Hot-water injections, use of, 829 Cataplasms, use of, 829 Opium, use of, 829 Ergotin, use of, 829 Turpentine, use of, 829 Prophylaxis against recurrence, 829

Intestinal ulcers, in hereditary syphilis, 306

INTESTINAL WORMS, 930 Varieties, 930 Mode of access to body, 931 Frequency in relation to uncooked food, 931 unfiltered waters, 931 uncleanliness, 931 _Cestodes, or Tape-worms_, 931 Description of mature worm, 931 head, 932 Sexual apparatus of, 932 Description of embryo or proscolex, 932 Mode of dissemination, 932, 933 Species, 933 Tænia saginata, 933 Synonyms, 933 Characteristics, 934 Length, 934 Head, 934 Sexual organs, 934 Rapidity of growth, 934 Number of eggs, 934 Sources, 934 Eating of underdone beef, 935 Tænia solium, 935 Synonyms, 935 Characteristics, 935 Sexual organs, 934, 935 Head, 935 Source, 936 Rapidity of growth, 936 Tænia cucumerina, 937 elliptica, 937 nana, 937 tenella, 938 flavopunctata, 938 madagascariensis, 938 Bothriocephalus latus, 939 Synonyms, 938 Countries where most prevalent, 938 Characteristics, 939 Sexual organs, 939 Sources, 939 From fish, 939 Bothriocephalus cordatus, 939 cristatus, 939 Symptoms of tape-worms, 939 Local, 940 Pruritus ani, 940 Dyspeptic, 940 Headache, 940 Nausea, 940 Abdomen, queer sensation in, 940 Colicky pains, 940 Vertigo, 940 Tongue, state, 940 Fainting, 940 Chorea, 940 Epileptic fits, 940 Uterine disorders, 940 Treatment, 941 Importance of removal of head, 940 Method of examining evacuations, 940 Preliminary, 941 Oil of turpentine, use of, 941 mode, 941 Male fern, use of, 941 mode of, 941 Pomegranate-bark, use of, 941 mode, 941 Pelletierin, use of, 942 Kousso, use of, 942 Koussin, use of, 942 Pumpkin-seeds, use of, 942 Santonin, use of, 942 Quinia, use of, 942 Prophylaxis, 942, 943 Tænia echinococcus, 943 Synonyms, 943 Description of, 943 head, 943 sexual organs, 943 Shortness of life, 943 Mode of dissemination, 944 Migration from intestinal canal, 944 Hydatid tumors, seat, 944 varieties of, 944 Cysts, forms of, 944 characters of, 944 contents of, 944 effects of, 945 Infection, liability to, proportioned to association with dogs, 945 Treatment, 945 Tænia acanthotrias, 945 _Trematodes, or Fluke-worms_, 946 Varieties, 946 Distomum hepaticum, 946 Synonyms, 946 Tendency to inhabit liver, 946 Physical characters, 946 Snail as a home during youth, 947 Rarity in man, 947 Animals most affected, 946, 947 lanceolatum, 947 Synonym, 947 Physical characters, 947 sinense, 947 conjunctum, 947 Symptoms of fluke-worms, 947 Signs of obstruction of bile-ducts, 947 Treatment, 948 heterophyes, 948 crassum, 948 ringeri, 948 ophthalmobium, 948 Bilharzia hæmatobia, 948 Synonyms, 948 Geographical distribution, 948 Mode of introduction to body, 948 by water, 948 by vegetables, 948 Symptoms, 948 Hæmaturia, 948 Treatment, 949 Amphistomum hominis, 949 _The Acanthocephali, or Thorn-head Worms_, 949 Echinorhynchus gigas, 949 Limited to hog, 949 _The Nematodes, or Thread-worms_, 949 General description of, 949, 950 Varieties, 950 Oxyuris vermicularis, 950 Synonyms, 950 Physical characters, 950 of female, 950 of male, 950 Number of eggs, 950 Description of eggs, 950 Modes of dissemination, 951 of introduction to body, 951 Symptoms, 951 Itching of anus, 951 periodic, nature of, 951 Onanism from, 951 Nervous disturbances, 951 Intestinal catarrh, 951 Epileptic fits from, 951 Chorea from, 951 Treatment, 951 Purgatives, use of, 951 Epsom salts and senna, 951 Tincture of aloes, 951 Enemata, 951 Suppositories, medicated, 951 Ascaris lumbricoides, 952 Synonyms, 952 Physical characters, 952 of female, 952 of male, 952 Number of eggs, 952 Mode of infection, 952 by drinking-water, 952 Geographical distribution, 953 Small intestine, most frequent habitat, 953 Migrations of, 953 Symptoms, 953 Digestive disorders, 953 Flatulence, 953 Abdominal pains, 953 Tongue, state of, 953 Appetite, impaired, 953 Nervous disorders, 953 Epileptic fits, 953 Treatment, 953 Wormseed, 954 oil, 954 Santonin, 954 Ascaris mystax, 954 Triocephalus dispar, 954 Synonyms, 954 Physical characters, 954 Symptoms, 954 Treatment, 954 Leptodera stercoralis, 954 Synonyms, 954 Physical characters, 955 Mode of infection, 955 Treatment, 955 Anchylostomum duodenale, 955 Synonyms, 955 Geographical distribution, 955 Physical characters, 955 Mode of introduction to body, 955 Symptoms, 955 A source of wasting diseases, 955 Mode of onset, 955 Debility, 956 Palpitation, 956 Digestive disorders, 956 Emaciation, 956 Prognosis, 956 Treatment, 956 Calomel and turpentine, 956 Prophylaxis, 956 Strongylus longevaginatus, 956 Eustrongylus gigas, 957 Physical characters, 957 Animals infested by, 957 Trichina spiralis, 957 Mode of infection, 958 Date of discovery in muscles, 958 Animals most frequent in, 958 Hog, 958 Rat and mouse, 958 Cats, 958 Muscular trichinæ, 958 Appearance of infected meat, 959 of trichinæ in muscle, 959 Muscular trichinæ, decay of, 959 size of, 959 duration of life of, 959 Intestinal trichinæ, 959 Physical characters, 959 Embryos, method of migration to muscles, 959 Symptoms, 959 Initial, 960 Appetite impaired, 960 Thirst, 960 Diarrhoea, 960 Vomiting, 960 Headache, 960 Prostration, 960 Constipation, 960 Muscular, 960 swellings, 960 Muscles, pain in, 960 painful and difficult motion of, 960 Bronchial catarrh, 960 Fever, 960 Sweating, 960 Insomnia, 961 Formication, 961 Oedema, 961 Peritonitis, 961 Pleuritis, 961 In children, 961 mildness of, 961 Duration, 960 Diagnosis, 961 From gastro-intestinal catarrh, 961 From cholera, 961 From rheumatism, 961 Prognosis, 961 Treatment, 961 Purgatives, 962 Diet, 962 Prophylaxis, 962 Necessity of thorough cooking, 962 Filaria medinensis, 962 Synonyms, 962 Geographical distribution, 962 Physical characters, 962 Mode of introduction to body, 963 Symptoms, 963 abscesses, 963 Treatment, 963 Filaria sanguinis, 963 Synonyms, 963 Geographical distribution, 963 Physical characters, 963 Mode of entrance to blood, 963 Habitat in lymphatic vessels, 963 Symptoms, 963 Hæmaturia, 963 Chyluria, 963 Buboes, 963 Ascites, 964 Elephantiasis, 964 Lymphangiectasis, 963 Treatment, 964 Prophylaxis, 964 Filaria loa, 964 restiformis, 964 oculi humani, Filaria lentis 964 trachealis, 964

Intestinal worms, influence on causation of constipation, 643 of acute peritonitis, 1140 of proctitis, 887

Intra-uterine rachitis, 141-143

Intussusception. See _Intestinal Obstruction_. complicating constipation, 648 and invagination as a cause of intestinal obstruction, 844

Inunctions of mercury in hereditary syphilis, 316 of oil in simple ulcer of stomach, 527

Invagination. See _Intestinal Obstruction_. as a cause of hemorrhage from bowels, 831 intestinal, laparotomy in, 866

Invasion, order of, in gonorrhoeal rheumatism, 104

Iodide of iron, in tubercular peritonitis, 1168 use of, in rheumatoid arthritis, 98 in scrofula, 251 in tabes mesenterica, 1194 of mercury, ointment, in lithæmia, 973 in amyloid liver, 1046 in cirrhosis of liver, 1002 of potassium, use of, in diabetes mellitus, 228 in enteralgia, 665 in pseudo-membranous enteritis, 775 in amyloid liver, 1045 in chronic oesophagitis, 417 in organic stricture of oesophagus, 425 in tubercular peritonitis, 1168 in syphilitic pharyngitis, 408 in acute rheumatism, 62 in chronic articular rheumatism, 74 in muscular rheumatism, 77 in gonorrhoeal rheumatism, 107 in rheumatoid arthritis, 98 in hereditary syphilis, 316

Iodine, injection of, in hydatids of liver, 1108 use of, in diabetes mellitus, 228 in hepatic glycosuria, 975 in chronic pharyngitis, 405 in rheumatoid arthritis, 100 in scrofula, 251 in typhlitis and perityphlitis, 822 test for amyloid liver, 1043 for lardaceous degeneration, 875 and olive oil, locally, in tubercular peritonitis, 1168 salts, use of, in gout, 132

Iodoform, use of, in diabetes mellitus, 229 in tuberculous pharyngitis, 402 in aphthous stomatitis, 330

Ipecacuanha, use of, in biliousness, 968 in constipation, 654 in dysentery, 810 in functional dyspepsia, 456 as antiemetic, in entero-colitis and cholera infantum, 762 in pseudo-membranous enteritis, 775 in acute gastritis, 469 in hepatic colic, 1082 in acute intestinal catarrh, 695 in intestinal indigestion, 636 in jaundice, 982 in biliousness, 968

Iridin, use of, in hepatic colic, 1082 in acute yellow atrophy of liver, 1030 in hyperæmia of liver, 988

Iritis, complicating gonorrhoeal rheumatism, 106 in hereditary syphilis, 281

Iron, use of, in catarrh of bile-ducts, 1057 in constipation, 654 in functional dyspepsia, 457 in enteralgia, 665 in pseudo-membranous enteritis, 775 in gastralgia, 462 in parenchymatous glossitis, 365 in acute intestinal catarrh, 696 in chronic intestinal catarrh, 714, 715, 717 in intestinal indigestion, 636 in acute yellow atrophy of liver, 1030 in amyloid liver, 1046 in cirrhosis of liver, 1002 in fatty liver, 1051 in acute pharyngitis, 398 in purpura, 194 in pruritus ani, 917 in acute rheumatism, 63 in chronic articular rheumatism, 74 in gonorrhoeal rheumatism, 107 in rachitis, 162 in dilatation of stomach, 609 in simple ulcer of stomach, 528 and potash, use of, in gout, 132 tinct. of chloride, use of, in hemorrhage from bowels, 834 in pain of simple gastric ulcer, 524

Irrigation of bowel in dysentery, 809 in jaundice, 983 in typhlitis, 821 intestinal, in acute catarrh of intestines, 697 in intestinal obstruction, 863, 864

Irritable rectum, treatment, 919

Irritant poisoning, diagnosis from cholera morbus, 723

Irritating medicines as a cause of acute oesophagitis, 410

Itching of anus in seat-worms, 951 at extremities of alimentary canal in tape-worm, 940

J.

Jaborandi, use of, in acute intestinal catarrh, 688 in chronic pharyngitis, 406 effect on rectum, 911

Jaundice. See _Liver, Diseases of_. in biliousness, 966 in catarrh of bile-ducts, 1054 in occlusion of biliary passages, 1087, 1089 from constipation, 646 complicating diabetes mellitus, 210 in chronic gastritis, 474 in hepatic abscess, 1009, 1013 in hepatic colic, 1073 in acute yellow atrophy of liver, 1027 frequency, in amyloid liver, 1044 in carcinoma of liver, 1038 in cirrhosis of liver, 993 in fatty liver, 1049 in hydatids of liver, 1102, 1104 in hyperæmia of liver, 986, 987 in disease of pancreas, 1116 in obstruction of pancreatic duct, 1131 in carcinoma of pancreas, 1125, 1126 in perihepatitis, 989 in phosphorus-poisoning, 1032 in suppurative pylephlebitis, 1100 complicating gastric cancer, 560

Jejunitis, 667, 683 and ileitis of chronic intestinal catarrh, diagnosis, 712

Jejunum, lesions of, in entero-colitis, 737

Joint, condition of, in acute gonorrhoeal arthritis, 105 in acute gout, 119

Joints, abscesses of, in gout, 116 alterations of, in chronic articular rheumatism, 71 condition of, in purpura rheumatica, 189 in acute rheumatism, 27 in chronic articular rheumatism, 71 in acute variety of general rheumatoid arthritis, 80 in chronic variety of general rheumatoid arthritis, 81 in partial form of rheumatoid arthritis, 85 lesions of, in dysentery, 801 in gout, 116 in acute rheumatism, 46 in chronic articular rheumatism, 70 in gonorrhoeal rheumatism, 103 in rheumatoid arthritis, 86 in scurvy, 172 most affected in gout, 116, 121 in acute rheumatism, 27 in chronic articular rheumatism, 72 in gonorrhoeal rheumatism, 104

K.

Keratitis, interstitial, in hereditary syphilis, 299

Kibbie's cot, use of, in acute rheumatism, 67

Kidneys, amyloid degeneration of, in rachitis, 153 condition of, in occlusion of biliary passages, 1090 in entero-colitis, 734 in acute rheumatism, 42 in hereditary syphilis, 308 enlargement of, in amyloid liver, 1044 in rachitis, 140 diseases of, as a cause of ascites, 1174 complicating dysentery, 806 influence on causation of hemorrhage from stomach, 582 lesions, in cholera morbus, 722 in diabetes mellitus, 202 in dysentery, 801 in gout, 117 in acute intestinal catarrh, 677 in chronic intestinal catarrh, 705 in acute yellow atrophy of liver, 1026 in phosphorus-poisoning, 1031 in rachitis, 154 in scurvy, 173 uratic deposits in, in gout, 117

Kidney-worm, 957

Koumiss, use of, in treatment of acute intestinal catarrh, 691 in intestinal indigestion, 633

Kousso and koussin, use of, in tape-worm, 942

Kyphosis in rachitis, nature of, 151

L.

Lactic acid, use of, in diabetes mellitus, 228 origin of acute rheumatism, 23

Lacto-peptin, use of, in cholera infantum and entero-colitis, 760

Lacto-phosphate of iron, in tabes mesenterica, 1194

Lacto-phosphates, use of, in scrofula, 252

Lancing, in morbid dentition, method of, 378

Languor and drowsiness, in functional dyspepsia, 451

Laparotomy in intestinal obstruction, 865 in perforating form of typhlitis, 822 question of, in perforation of gastric ulcer, 527

Lardaceous degeneration of intestine, 874

Laryngismus stridulus in rachitis, 149

Larynx, disease of, in hereditary syphilis, 308 displacement of, from hypertrophy of tongue, 351 oedema of, in mercurial stomatitis, 346 and pharynx, lesions of, in mercurial stomatitis, 347 gangrene of, complicating cancrum oris, 341

Latham's hyperoxidation theory of origin of acute rheumatism, 24

Laxatives, use of, in dysentery, 809 in pseudo-membranous enteritis, 774

Lead colic distinguished from acute intestinal catarrh, 686

Lead-poisoning, influence on causation of constipation, 641 of oesophageal paralysis, 429

Lead, sugar of, use of, in acute intestinal catarrh, 694 copper, and arsenic poisoning, as a cause of enteralgia, 660

Leeches to epigastrium in acute pancreatitis, 1120

Leeching, in parenchymatous glossitis, 364 in perihepatitis, 990 in acute pharyngitis, 398

Lemon-juice, use of, in acute rheumatism, 63

Leptodera stercoralis, 954

Leube's beef-solution, use of, in simple ulcer of stomach, 520

Leuchæmia, influence on causation of hemorrhage from bowels, 832

Liebig's foods for infants, 754

Lienteric stools, in chronic intestinal catarrh, 708

Ligaments, lesions of, in rheumatoid arthritis, 87

Ligation in fistula in ano, 922 in polypi of rectum, 921 in hypertrophy of tongue, 354 of hemorrhoids, 924

Ligature of upper extremities, in hemorrhage of simple gastric ulcer, 526

Lime, elimination of, in rachitis, 138

Lime-juice, use, in scurvy, 183, 184 salts, use of, in rachitis, 162 water, local use, in hemorrhoids, 923 use in entero-colitis and cholera infantum, 762 in acute intestinal catarrh, 694

Lip, upper, thickness of, in scrofula, 246

Lipæmia in diabetes mellitus, 207

Lipomata of stomach, 579

Lipuria, in diseases of pancreas, 1115 in carcinoma of pancreas, 1125

Liquor ferri nitratis, use of, in entero-colitis, 762

Lithæmia, 968

Lithæmic theory of origin of gout, 112

Lithia salts, use of, in gout, 132

Lithium bromide, use of, in chronic articular rheumatism, 74

Liver, action of, in process of digestion, 623 amyloid degeneration of, in rachitis, 153 changes in, from occlusion of biliary ducts, 1086 condition of, in catarrh of bile-ducts, 1053 degeneration of, complicating simple ulcer of stomach, 503

LIVER, DISEASES OF, 965 Functional Disorders, 965 _Biliousness_, 965 Definition, 965 Pathogeny, 965 Malarial poison, effect on functions of liver, 965 Metals, effect on functions of liver, 965 Food, improper, influence of, on causation, 966 Alcoholic and malt liquors, 966 Symptoms, 966 Physiognomy, 966 Tongue, state of, 966 Breath, state of, 966 Appetite, impaired, 966 Nausea, 966 Bowels, state of, 966 Headache, 966 Vertigo, 966 Conjunctivæ, yellow, 966 Jaundice, 966 Course, 967 Duration, 967 Termination, 967 Treatment, 967 Prophylaxis, 967 Diet, 967 Skimmed milk, use of, 967 Blue-pill, 967 Rochelle and Epsom salts, 967 Euonymin, use of, 968 Ipecacuanha, 968 Podophyllin, 968 Calomel, dose of, 968 Phosphate of sodium, 968 Mineral waters, 968 _Lithæmia_, 968 Definition, 968 Pathogeny, 968 Hepatic action in formation of uric acid, 969 Albuminoid food, over-consumption of, 969 Luxurious habits, 969 Sedentary life, 969 Alcoholic and malt liquors, 969 Symptoms, 969 Digestive disturbances, 969 Appetite, capricious, 969 Tongue, state of, 969 Bowels, state of, 970 Oxaluria, 970 Nervous symptoms, 970 Headache, 970 Nausea, 970 Mental depression, 970 Vertigo, 970 Skin, state of, 970 Urticaria, 970 Urine, state of, 970 Pain in back, 970 Course, 970 Duration, 970 Termination, 970 Prognosis, 970 Diagnosis, 970 from gastro-duodenal catarrh, 970 from organic brain disease, 971 Treatment, 971 Diet, 971 Avoidance of fatty, starchy, and saccharine articles, 971 of wine and malt liquors, 971 Food, allowable, 971 Exercise, 971 Sea-bathing, 971 Nitric acid, use of, 972 Alkalies, use of, 972 Purgative mineral waters, 972 Phosphate of sodium, 972 Mercurials, 972 Podophyllin, 972 Euonymin, 972 Arsenic, 973 Quinine, 973 Sponge-baths, 973 Iodide of mercury, locally to hepatic region, 973 Electricity, 973 Of hypochondriasis, 973 _Hepatic Glycosuria_, 973 Definition, 973 Pathogeny, 973 Symptoms, 973 Digestive disturbances, 974 Increased urination, 974 Urine, condition of, 974 specific gravity of, 974 tests for sugar in, 974 Course, 974 Duration, 974 Termination, 974 Prognosis, 974 Diagnosis, 974 From gastro-duodenal catarrh, 974 From lithæmia, 974 From diabetes, 974 Treatment, 974 Diet, 975 Exercise, 975 Medicinal, 975 Nux vomica, 975 Fowler's solution, dose, 975 Phosphate of sodium, 975 Carbolic acid, 975 Bismuth, 975 Tr. iodine, 975 _Jaundice_ (_Icterus_), 975 Definition, 975 Etiology, 975 Disorganization of the blood, 975 Non-disposal by liver of biliary material, 976 Absorption of biliary material by blood, 976 Emotions, influence of, on causation, 976 Obstruction from hyperæmia of bile-ducts, 977 from spasm of muscular fibre of ducts, 977 gastro-duodenal catarrh, 977 errors in diet, 977 rich food, 977 cold and wet, 977 malaria, 977 Symptoms, 977 Premonitory, 977 Signs of gastro-duodenal catarrh, 977 Yellowness, seat of appearance, 977 mode of extension, 978 Feces, discoloration of, 978 Urine, condition of, 978 color of, 978 tests for bile, 978 albumen in, 978 urea in, 979 Liver, condition of, 979 Epigastrium, tenderness of, 979 Pulse, state of, 979 Heart, slowing of, 979 cause, 979 Temperature, 980 Fever, 980 Nervous disturbances, 980 Nutrition, disturbances of, 980 Vision, modifications of, 980 Xanthopsy in, 980 Headache and vertigo, 980 Mental depression, 980 Wakefulness, 980 Pruritus of skin, 980 Boils and carbuncles, occurrence of, 980 Xanthelasma vitiligoidea of skin, 980 plane form, 980 tuberose form, 981 Hemorrhagic diathesis, 981 Course, 981 Duration, 981 Prognosis, 981 Diagnosis, 981 Importance of ascertaining condition of gall-bladder, 982 Treatment, 982 Of nausea, 982 Diet, 983 Rectal irrigation, 983 Emetics, use of, 982 Ipecacuanha, 982 Calomel, 982 Cholagogues, use of, 982 Podophyllin, 982 Euonymin, 982 Phosphate of sodium, 982 Arseniate of sodium, 982 Mineral waters, 982 Nitric acid, 983 Nitro-muriatic acid, 983 locally, 983 Electricity, use of, 983 Structural diseases of liver, 983 _Hyperæmia of Liver_, 983 Definition, 983 Etiology, 983 Digestive process, 984 Food, over-indulgence in, 984 Sedentary life, 984 Sudden suppression of hemorrhages, 984 Menstrual period, 984 Mechanical, 984 Heart disease, organic, 984 Pulmonary disease, chronic, 984 Climate, 984 Malaria, 984 Pathological anatomy, 985 Enlargement of liver, 985 Portal vein, changes in, 985 Extravasations of blood in hepatic tissue, 985 Mechanical form, 985 Nutmeg liver, 985 Cyanotic atrophy of, 985 Atrophy of hepatic cells, 985 Sclerosis of central vein, 985 Symptoms, 986 Signs of gastro-intestinal catarrh, 986 Hypochondrium, right, fulness of, 986, 987 pain in, 986, 987 Increased hepatic dulness, 986 method of determining, 986 Urine, state of, 986, 987 Jaundice, 986, 987 Stools, condition of, 986, 987 Ascites in nutmeg liver, 987 Mental depression, 987 Course, 987 Duration, 987 Termination, 987 Prognosis, 988 Diagnosis, 988 Treatment, 988 Diet, 988 Skim-milk, 988 Exercise, 988 Bathing, 988 Mineral waters, saline laxative, 988 Phosphate of sodium, 988 Cholagogues, 988 Digitalis, use of, when due to organic heart disease, 988 _Perihepatitis_, 989 Definition, 989 Pathogeny, 989 As an extension from other parts, 989 Passage of gall-stones, 989 Traumatic causes, 989 Tight-lacing, 989 Symptoms, 989 Pain in right hypochondrium, 989 Hepatic colic, 989 Jaundice, 989 Friction sound, 989 Course, 989 Duration, 989 Termination, 989 Diagnosis, 989 From pleuritis, 990 Treatment, 990 Leeching, 990 Turpentine stupes, 990 Bandage, use of, 990 Morphia for pain, 990 _Interstitial Hepatitis--Sclerosis of Liver: Cirrhosis_, 990 Definition, 990 Etiology, 990 Age, influence of, on causation, 990 Sex, influence of, on causation, 991 Alcohol, influence of, on causation, 991 Syphilis, influence of, on causation, 991 Malaria, influence of, on causation, 991 Obstruction of bile-ducts, 991 Closure of hepatic vein, 991 portal vein, 991 Arsenic and antimony, 991 Phosphorus, 991, 992 Extension of inflammation in perihepatitis, 992 Pathological anatomy, 992 Increased size of liver, 992 Development of new connective tissue, 992 Monolobular form, 992 Multilobular form, 992 Contraction of connective tissue, 992 Decreased size of liver, 992 Hobnail appearance of surface, 992 Portal veins, lesions of, 992 Atrophy of hepatic cells, 992, 993 Symptoms, 993 Insidious development, 993 Digestive disturbances, 993 Jaundice, 997 Appetite, capricious, 993 Nausea and vomiting, 993 Bowels, state of, 993 Stools, state of, 994 Hemorrhoids, 993 Fissure of anus, 994 Abdomen, state of, 994 Flatus, accumulation of, 994 Hemorrhages, 994 Spleen, enlargement of, 994 Ascites, 995 Blood, watery condition of, 995 Anasarca, 995 Oedema, general, 995 Anastomoses of veins, 996 Physical signs, 996 Auscultation, 996 Mode of examining liver, 996, 997 Size of area of dulness, 997 Physiognomy, 997 Skin, color and state of, 997, 998 Urine, state of, 998 Ulcers of stomach and intestine, 999 Thrombosis of portal vein, 999 Nervous disturbances, 999 Cerebral symptoms, 999 Coma in, 999 Emaciation, 999 Kidneys, atrophy of, 999 Cerebral sclerosis, 999 Course, 998 Duration, 999 Terminations, 999 Prognosis, 999 Diagnosis, 999 From amyloid disease, 1000 hydatids, 1000 cancer, 1000 acute yellow atrophy, 1000 Treatment, 1000 Prophylaxis, 1000 Diet, 1000 Of malarial cause, 1000 Of overgrowth of connective tissue, 1000 Of gastro-intestinal catarrh, 1002 Of dropsical effusions, 1001 Of ascites, 1001 Of diarrhoea, 1002 Local, 1002 Of hemorrhage, 1002 Chloride of gold and sodium, 1001 of mercury, 1001 Phosphate of sodium, 1001 Vapor bath, 1001 Digitalis stupes, 1001 Copaiba, 1001 Pilocarpine, 1001 Hydragogue cathartics, 1001 Tapping, 1002 Bismuth, 1002 Opium, 1002 Ergotin, 1002 Iron, 1002 Counter-irritation, 1002 Dry cups, 1002 Blisters, 1002 Ung. hydrarg. iod. rubri, 1002 _Suppurative Hepatitis--Abscess of Liver_, 1002 Definition, 1002 Etiology, 1002 Climate, influence on causation, 1002 Sex, influence on causation, 1003 Age, influence on causation, 1003 Temperament, influence on causation, 1003 Traumatism, 1003 Wounds, 1003 State of portal and hepatic veins, 1004 embolism, 1004 Source of emboli, 1004 Ulceration and dilatation of bile-ducts, 1005 Proctitis, 1004 Dysenteric ulceration, 1004 Food, improper, 1005 Alcohol, 1005 Malarial influence, 1005 Pathological anatomy, 1005 Initial lesions, 1005 in cells, 1005 in vessels, 1005 From embolism, lesions of, 1005 Tropical form, lesions of, 1006 development of, 1006 Size of purulent collections, 1006 Formation of limiting membrane, 1006 Number of abscesses, 1006 Seat of abscesses, 1006 Contents of abscesses, 1007 Presence of bile in pus, 1007 Absence of limiting membrane, 1007 Pointing of abscesses, 1007 method of, 1007 Formation of adhesions, 1007 Pus, modes of escape, 1007 escape into neighboring organs, 1007 Processes of healing, 1008 Condition of liver outside of abscess, 1008 Symptoms, 1008 Systemic, 1008 Onset of, 1008 Chills, 1008 Temperature, 1008 Pulse, 1009 Fever, type of, 1008 typhoid form of, 1009 Sweating, 1009, 1010 General malaise, 1009 Flesh, loss of, 1009 Skin, color of, 1009 Jaundice, 1009, 1013 Mental condition, 1009 Cholæmia, 1010 Stupor, 1010 Wakefulness, 1009 Hypochondria, 1010 Urine, state of, 1010, 1014 Absence of general, 1010 Local, 1010 Change in size of liver, frequency of, 1010 Enlargement, 1010 Seat of purulent collection, 1011 Tumor of epigastrium, 1011 Fluctuation, 1011 Pain, 1011, 1012 seat of, 1011 character of, 1012 in right shoulder, 1012 Decubitus, characteristic, 1012 Nausea and vomiting, 1013 Tongue, state of, 1013 Relation to dysentery, 1014 Cough, 1014 Respiration, 1014 Pleuritis, 1014 Pleuro-pneumonia, 1014 Singultus, 1015 Pericarditis, 1015 Course, 1014 Usual point of discharge, 1016 Discharge into pleural cavity, 1016 pericardium, 1016 peritoneal cavity, 1016 intestines, 1016 Duration, 1017 Termination, 1017 Effect of mode of discharge upon, 1017 Recovery by absorption of pus, 1018 Fatty degeneration of pus, 1018 Mortality, 1017 Prognosis, 1018 Diagnosis, 1018 From echinococcus, 1018 dropsy of gall-bladder, 1019 cancer of liver, 1019 abscess of abdominal wall, 1019 empyema, 1020 intermittent fever of hepatic colic, 1020 Value of puncture of right lobe in, 1020 Treatment, 1020 Aborting, 1020 use of quinia in, 1020 Of septicæmic fever, 1020 Of dysentery in, 1020 Of vomiting, 1021 Local, 1021 Evacuation of pus, 1021 Puncture, exploratory, 1021 harmlessness of, 1021 effects of, 1022 mode of, 1022 Aspirator, use of, 1022 mode of using, 1022 Poultices, use of, 1023 Quinia, use of, 1020 Ipecacuanha, 1020 Soda powders, 1020 Bismuth, 1021 Creasote, 1021 Diet, 1021 Stimulants, 1021 Nutrient enemata, 1021 _Acute Yellow Atrophy_, 1023 Definition, 1023 History, 1023 Etiology, 1023 Frequency, 1023 Age, influence on causation, 1024 Sex, influence on causation, 1024 Pregnancy, influence on causation, 1024 Depressing emotions, 1024 Syphilis, 1024 Pathological anatomy, 1025 Change in size, 1025 Capsule, state of, 1025 Hemorrhagic extravasations in liver-tissue, 1025 Bile-ducts, lesions of, 1025 Microscopic appearance of hepatic tissue, 1025 Cell-degeneration, 1025 Connective tissue, increase of, 1025 Spleen, lesions of, 1026 Peritoneum, lesions of, 1026 Mesenteric glands, swelling of, 1026 Stomach and intestines, lesions of, 1026 Kidneys, lesions of, 1026 Heart, lesions of, 1026 Brain, lesions of, 1026 Symptoms, 1026 Prodromata, 1026 Duration of, 1027 Signs of gastro-duodenal catarrh, 1027 Jaundice, 1027 Toxæmic period, 1027 Dilatation of pupil, 1027 Excitement with delirium, 1027 Coma, 1027 Convulsions, 1027 Sensibility, disturbances of, 1028 Motility, disturbances of, 1028 Hemorrhages from mucous surfaces, 1028 Epistaxis, 1028 Hæmatemesis, 1028 Temperature, 1028 Pulse, condition of, 1028 Tongue, condition of, 1028 Nausea and vomiting, 1026, 1027, 1028 Constipation, 1028 Skin disorders, 1028 Urine, state of, 1027, 1028 Blood, changes in, 1029 Course, 1029 Duration, 1029 Termination, 1029 Diagnosis, 1029 From catarrhal jaundice, 1029 Acute phosphorus-poisoning, 1029 Treatment, 1030 Quinia, use of, 1030 Phosphate of sodium, 1030 Euonymin, use of, 1030 Iridin, use of, 1030 Purgatives, 1030 Bismuth, 1030 and carbolic acid, 1030 Ergotin, use of, 1030 Alcohol, use of, 1030 Iron, 1030 Phosphorus, 1030 Gold and silver, chloride of, 1030 Of nausea and vomiting, 1030 Of hemorrhage, 1030 _The Liver in Phosphorus-poisoning_, 1030 Definition, 1030 Pathogeny, 1030 Age, 1030 Women, frequency in, 1030 Tissues, biliary staining of, 1031 Extravasation of blood in mucous and serous membranes, 1031 Spleen, enlargement of, 1031 Liver, hyperplasia and atrophy of, 1031 cell-degeneration, 1031 Bile-ducts, lesions of, 1031 Mucous membrane of stomach, lesions of, 1031 Kidneys, lesions of, 1031 Symptoms, 1031 Resemblance to acute yellow atrophy, 1031 Of local irritation of poison, 1031 Burning in gullet, 1031 Nausea and vomiting, 1031 Systemic, 1031 Vomiting, 1031 Vomit, characters of, 1031 Stools, characters of, 1031 phosphorescent, 1031 Hepatic dulness, increase of, 1032 Jaundice, 1032 Liver, enlargement of, 1032 Nervous disorders, 1032 drowsiness, 1032 delirium, 1032 convulsions, 1032 Temperature, 1032 Pulse, state of, 1032 Urine, state of, 1032 Course, 1032 Duration, 1032 Termination, 1032 Diagnosis, 1032 From acute yellow atrophy, 1032 Treatment, 1033 Emetics, 1033 Decoction of flaxseed, 1033 Slippery elm, 1033 Oil of turpentine, 1033 Sulphate of copper, 1033 Transfusion, 1033 Diet, 1033 Of inflammatory symptoms, 1033 _Carcinoma of Liver_, 1033 Definition, 1033 Etiology, 1033 Heredity, 1033 Age, 1034 Sex, 1034 Morbid anatomy, 1034 Primary form, 1034 Hepatic enlargement, 1034 Microscopic appearances, 1035 Secondary form, 1034, 1035 frequency of, 1035 Metastasis in, 1035 forms of, 1035 from face, 1035 stomach, 1035 intestines, 1035 nodes, number of, 1035 size, 1035 changes in, 1036 Atrophy of hepatic structure, 1035 Infiltrating form, 1034 Pigment form, 1035 Tumors, shape and size, 1034 Sarcomas, 1036 Symptoms, 1036 General history of, 1036 Liver, condition, 1037 mode of examining, 1037 Ascites, 1037 Peritonitis in, 1037 Pain, seat and character, 1038 Vomiting in secondary form, 1038 Jaundice, frequency, 1038 Skin, state, 1038 Physiognomy, 1038 Emaciation, 1038 Strength, loss, 1038 Urine, condition, 1038 Signs of gastro-intestinal catarrh, 1038 Appetite, impaired, 1038 Course, 1039 Duration, 1039 Termination, 1039 Diagnosis, 1039 From amyloid disease, 1040 From echinococcus, 1040 From cirrhosis, 1040 From syphilis, 1040 Treatment, 1040 _Amyloid Liver_, 1040 Definition, 1040 Etiology, 1040 Suppuration of bone, 1041 Syphilis, 1041 Chronic malarial infection, 1041 Pulmonary cavities, 1041 Age, 1041 Sex, 1041 Cachexia from development of new formations, 1041 Temperament, 1041 Frequency in lymphatic individuals, 1041 Pathological anatomy, 1041 Origin of amyloid deposit, 1042 Mode and order of deposit, 1042 Size and shape of liver, 1042 Consistence of, 1042 Iodine test for, 1043 Mode, 1043 Condition of hepatic tissues not invaded, 1043 Symptoms, 1043 Liver enlargement, 1043 Cachexia, 1043 Jaundice, frequency, 1044 Ascites, frequency, 1044 Hemorrhoids, 1044 Diarrhoea, 1044 Stools, 1044 black, 1044 Vomiting in, 1044 Vomit, bloody, 1044 Spleen, enlarged, 1044 Kidney, enlarged, 1044 General dropsy, 1044 Hydræmia, 1044 Urine, state, 1044 Emaciation, 1044 Course, 1044 Duration, 1044 Prognosis, 1045 Diagnosis, 1045 From fatty liver, 1045 hydatid disease, 1045 cancer, 1045 Treatment, 1045 Of cause, 1045 Alkalies, use of, 1045 Iodides, use of, 1046 Ung. hydrarg. iod. rubri, 1046 Chloride of gold and sodium, 1046 silver, 1046 arsenic, 1046 iron, 1046 Diet, 1046 Of nausea and vomiting, 1046 _Fatty Liver--Fatty Degeneration of Liver_ (_Hepar Adiposum_), 1046 Definition, 1046 Etiology, 1046 Sex, 1047 Phthisis, 1047 Cachexiæ, 1047 Alcoholism, 1047 Poisoning by phosphorus, 1047 arsenic, 1047 antimony, 1047 Pregnancy, 1047 Deficient oxidation of fat, 1046, 1047 Sedentary life, 1047 Pathological anatomy, 1047 Liver, enlargement of, 1047 shape and size, 1047 anæmic condition of, 1047 seat of fatty deposit, 1047, 1048 Symptoms, 1048 Dyspeptic disturbances, 1048 Stools, character, 1048 Circulation, feeble, 1048 Pulse, condition, 1048 Sleeplessness, 1048 Mental depression, 1048 Hypochondria, 1048 Jaundice, 1049 Urine, state, 1049 Area of hepatic dulness, 1049 Course, 1049 Duration, 1049 Termination, 1049 Prognosis, 1049 Diagnosis, 1049 From amyloid liver, 1049 cancer, 1050 Treatment, 1050 Of digestive disturbances, 1050 Diet, 1050 Cholagogues, 1050 Phosphate of sodium, 1050 Sulphate of manganese, 1050 quinia, 1051 iron, 1051 Tinct. nux vomicæ, 1050 Nitric acid, 1050 Alkalies, 1050 Permanganate of potassium, 1051 Affections of Biliary Passages, 1051 _Catarrh of Bile-ducts_, 1051 History, 1051 Definition, 1051 Etiology, 1051 Peculiarity of constitution, 1051 Climate, 1051 Malaria, 1051 Cold and wet, 1051 Disturbances of portal circulation, 1052 Extension from duodenum, 1052 Food, improper, 1052 Condiments and sauces, 1052 Alcoholic and malt liquors, abuse, 1052 Pathological anatomy, 1052 Seat of catarrh, 1052 Mucous membrane of ducts, lesions of, 1053 swelling of, 1053 Finer ducts, lesions of, 1053 Liver, condition of, 1053 Symptoms, 1053 Signs of gastro-duodenal catarrh, 1053 Tongue, state of, 1053 Appetite impaired, 1053 Epigastrium, fulness of, 1053 Abdomen, state of, 1054 Intestinal canal, state of, 1054 Diarrhoea and constipation, 1054, 1055 Stools, characters of, 1054, 1055 Urine, state of, 1054, 1055 Nervous disturbances, 1054, 1055 Headache, 1054, 1055 Vertigo, 1054, 1055 Febrile movement, 1054 Jaundice, 1054 Course, 1055 Duration, 1055 Termination, 1055 Diagnosis, 1055 Treatment, 1056 Diet, 1056 Diarrhoea, 1056 Constipation, 1056 Mercury, use of, 1056 Calomel, use of, 1056 Phosphate of sodium, 1057 Silver and zinc salts, 1057 Arsenic, 1057 Iron, 1057 Quinia, 1057 Permanganate of potassium, 1057 Mineral acids, 1057 Enemata, 1057 Electricity, 1057 _Biliary Concretions, Gall-stones, Hepatic Calculi, etc._, 1058 Definition, 1058 Formation, 1058 From inspissated bile, 1058 Of calculi, 1059 shape, 1059 number, 1059 color, 1059 size, 1059 composition, 1060 nucleus, 1060 body of, 1061 rind, 1061 specific gravity, 1061 origin and formation, 1061-1063 composition of bile, 1062 reaction, 1062 Etiology, 1063 Age, 1063 Sex, 1064 Social state, 1064 Malarial influence, 1064 Season, 1065 Obesity, 1065 Starchy, fatty, and saccharine foods, 1065 Irregular meals, 1065 Retardation to flow of bile, 1066 Mental emotion, 1066 Situation and destiny of gall-stones, 1066 Spontaneous disintegration of, 1066 Gall-ducts, dilatation of, from, 1067 -bladder, changes in, from, 1066 dilatation of, 1067 adhesions, 1067 cancer of, 1067 hypertrophy of, 1067 -stones, migrations of, 1067, 1068 ulceration into neighboring organs by, 1068 Formation of fistulæ, 1068 Symptoms due to presence of gall-stones at their original site, 1069 Uneasiness in hypochondrium, 1069 Pain, 1069 in shoulder, 1069 in right side of neck, 1069 Gastralgia, 1069 Vertigo, 1070 Migraine, 1069 Headache, 1070 Digestive disturbances, 1070 Symptoms due to migration by natural channels (hepatic colic), 1070 Time of occurrence of paroxysms, 1070 Paroxysm, onset of, 1070, 1071 Pain, seat and characters of, 1070 Physiognomy, 1071 Nausea and vomiting, 1071, 1072 Pulse, state of, 1071 Collapse, 1071 Duration, 1071 Nervous disturbances, 1071 Hysteria, 1071 Convulsions, 1071 Chills, 1071, 1072 Periodicity of paroxysms, 1071 Relation to malaria, 1071, 1072 Fever, 1072 Constipation, 1072 Jaundice, 1072 duration of, 1073 After paroxysm, 1073 Stools, 1073 search for calculi in, 1073 method, 1073 Passage of inspissated bile, 1073, 1074 Recurrence of attacks, 1074 Impaction of calculi, 1074 point of, 1074 peritonitis from, 1074 adhesions, 1074 Migration by artificial routes, 1074 into neighboring organs, 1074 into stomach, 1074 into intestines, 1074 into duodenum, 1074 Biliary fistulæ, formation of, 1075 Course, 1075 Migration without symptoms, 1075 Obstruction of bowels from, 1075 Symptoms of presence in intestinal canal, 1076 Vomiting of gall-stones, 1076 Complications, 1076 Local inflammation, 1076 Dropsy of gall-bladder, 1077 Angiocholitis, 1077 Relation to cancer of ducts, 1077 Heart disturbance, 1077 Initial murmurs, 1077 Reflex nervous disorders, 1078 Herpes zoster, 1078 Death from lodgment of calculus in Vater's diverticulum, 1078 from vomiting, 1078 Diagnosis, 1078 From gastralgia, 1078 hepatalgia, 1079 flatulent colic, 1079 renal colic, 1079 Treatment, 1079 Of calculus state, 1079 Of inspissated bile, 1079 by sulphate of soda, 1079 Diet, 1079 Exercise, 1079 Bathing, 1079 Alkaline mineral waters, 1079 Phosphate of sodium, 1080 Of biliary calculi in situ, 1080 Manipulation of gall-bladder, 1080 Faradization, 1080 Ether and turpentine (Durande's remedy), 1080 Chloroform, 1081 Cholate of sodium, 1081 Ox-gall, 1081 Puncture of gall-bladder, 1081 Removal of contents of gall-bladder by puncturing, 1081 Of paroxysms of hepatic colic, 1081 Of pain, 1081 Morphia and atropia, hypodermically, 1082 dose of, 1082 Emetics, 1082 Hot fomentations, 1082 Hot baths, 1082 Chloroform, 1082 Ether, 1082 Chlorodyne, 1082 Chloral, 1082 Purgatives, 1082 Cholagogues, 1082 Ipecacuanha, 1082 Euonymin, 1082 Iridin, 1082 _Occlusion of Biliary Passages--Stenosis of Ductus Communis Choledochus_, 1082 Definition, 1082 Pathogeny, 1082 Of cystic duct, 1083 Of common duct, 1083 Passage of calculi, 1083 Catarrhal inflammation, 1083 Cicatrization of ulcers, 1083 Impaction of biliary calculi, 1084 Foreign bodies, 1084 Of hepatic duct, 1084 Seat and cause of occlusion in common duct, 1083, 1084 Pressure of tumors, 1085 Cancer of gall-bladder, 1085 of pylorus, 1085 Enlarged lymphatic glands, 1085 Effects of occlusion of cystic duct, 1085 Retention of secretion in gall-bladder, 1085 Effects of occlusion of hepatic duct, 1085 Catarrhal state, 1085 Distension of hepatic tubes with sero-mucus, 1085 Dilatation of ducts, 1086 Rupture of ducts, 1086 Changes in liver, 1086 Cell-degeneration, 1086 Symptoms, 1086 Of cystic duct, 1086 Dropsy of gall-bladder, 1086 Of hepatic duct, 1086 Jaundice, 1086, 1087 sudden disappearance of, 1087 Pruritus, 1087 Eczema, 1087 Xanthelasma, 1087 Increased area of hepatic dulness, 1087 Tenderness of hypochondrium, 1087 Enlargement of liver, 1087 Hepatic secretion, state of, 1087 Atrophy of liver, 1088 Enlargement of gall-bladder, 1087 Digestive disturbances, 1088 Appetite, state of, 1088 Tongue, state of, 1088 Thirst, 1088 Nausea and vomiting, 1088 Vomit, characters of, 1088 Bowels, irregular, 1088 Stools, characters of, 1088 color of, 1088 Kidneys, state of, 1090 Urine, state of, 1089, 1090 Albuminuria, 1090 Casts, 1090 Pulse, state of, 1089 Hemorrhages, 1089 Epistaxis, 1089 Hæmatemesis, 1089 Fever, 1090 intermittent form, 1090 distinguished from malaria, 1090 temperature, 1091 duration, 1091 Cholæmia, 1091 Nervous disturbances, 1092 Headache, 1092 Mental depression, 1092 Xanthopsia, 1092 Paralysis, 1092 Convulsions, 1092 Course, 1092 Duration, 1092 Termination, 1092 Prognosis, 1092 Diagnosis, 1092 Puncture of gall-bladder in, 1092 Exploration of gall-bladder, 1093 Mode of puncture, 1093 Of dilated gall-bladder from aneurism, 1093 from hypertrophic cirrhosis, 1093 Treatment, 1094 Fracture of impacted calculus, 1094 mode of, 1094 Solution of impacted calculi by puncture of gall-bladder, 1094 Diseases of Portal Vein, 1095 _Thrombosis and Embolism of Portal Vein; Stenosis; Pylephlebitis_, 1095 Definition, 1095 Causes, 1095 Coagulable state of blood, 1095 Weak heart-action, 1095 Impeded circulation from external pressure, 1095 Of adhesive pylephlebitis, 1095 Symptoms, 1096 Sudden formation of ascites, 1096 enlargement of spleen, 1096 passive congestion of gastro-intestinal mucous membrane, 1096 Catarrh of gastro-intestinal mucous membrane, 1096 Nausea and vomiting, 1096 Hemorrhages, 1096 Abdominal veins, abnormal anastomoses of, 1096 Course and termination, 1097 Diagnosis, 1097 Treatment, 1097 Copaiba, 1097 Pilocarpine, 1097 Leeches, 1097 _Suppurative Pylephlebitis_, 1097 Pathogeny, 1097 Ulceration and suppuration of intestinal tube, 1097, 1098 Multiple abscess of liver, 1097, 1098 Typhlitis, 1097, 1098 Traumatic injuries of intestine, 1097 Formation of emboli, 1097, 1098 Changes in vein-wall, 1098 Production of thrombi, 1098 Formation of secondary hepatic abscesses, 1098 Suppuration of cæcum, 1098 of rectum, 1098 Symptoms, 1099 Of primary lesion, 1099 Of secondary result, 1099 Chills, 1099 Pain, seat and character, 1099 Fever, 1099 periodic form, 1099 Temperature, 1100 Digestive disturbances, 1100 Vomiting, 1100 Hemorrhages, 1100 Tongue, condition of, 1100 Irregular bowels, 1100 Jaundice, 1100 Course, 1101 Duration, 1101 Termination, 1101 Diagnosis, 1101 Treatment, 1101 Ammonia, use of, 1101 Quinine, 1101 Corrosive sublimate, 1101 Parasites of the Liver, 1101 _Echinococcus of Liver_, 1101 Definition, 1101 Etiology, 1101 Migration of embryo from intestine, 1102 Pathology, 1102 Symptoms, 1102 Number of, 1102 Seat of, 1102 Atrophy of liver, 1102 Jaundice, 1102, 1104 Growth, mode of, 1102, 1103 Characters of vesicles, 1103 Contents of vesicles, 1103 Multilocular form, 1103 Hydatid tumor, characteristics of, 1104 Ascites, 1104 Enlargement of spleen, 1104 Digestive disturbances, 1104 Diagnosis, 1104 Characters of fluid, 1105 Hooklets in fluid, 1105 From abscess of liver, 1105 Duration, 1105 Termination, 1106 Treatment, 1106 Prophylaxis, 1106 Boiling and filtering of water, 1106 Therapeutical, 1106 Removal of vesicle, 1107 by incision, 1107 Puncture, 1107 Aspirator, use of, 1107 Injection of iodine, 1108 Electrolysis, 1108 Acupuncture, 1109 _Distomum hepaticum_ (_liver-flukes_), 1109 Description, 1110 Mode of access to man, 1110 Diagnosis, 1110 Symptoms, 1110 Treatment, 1110 Parasiticides, use of, 1110 Creasote, 1110 Bichloride of mercury, 1110 Thymol, 1110 Parasites in Portal Vein, 1111

Liver, diseases of, as a cause of ascites, 1173 of pancreatic hemorrhage, 1129 influence on causation of constipation, 641 of functional dyspepsia, 447 of acute gastritis, 464 enlargement of, in rachitis, 139 in hereditary syphilis, 283 functional disturbance of, in intestinal indigestion, 629 hyperæmia of, relation to causation of diabetes mellitus, 195 lesions of, in diabetes mellitus, 201 in dysentery, 801 in entero-colitis, 739 in gout, 117, 118 in acute intestinal catarrh, 677 in chronic intestinal catarrh, 705 in scurvy, 173 in tabes mesenterica, 1188 secondary growths of, in gastric cancer, 556

Lobe of ear, ulceration of, in scrofula, 246

Local causes of gastric cancer, 537 nature of dysentery, 796 peritonitis, 1159 symptoms, of superficial glossitis, 357 of abscess of liver, 1010 of chronic articular rheumatism, 71 of rheumatoid arthritis, 80, 81, 85 of thrush, 334 treatment of cancrum oris, 343 of enteralgia, 665 of parenchymatous glossitis, 365 of chronic parenchymatous glossitis, 368 of superficial glossitis, 357 of chronic superficial glossitis, 367 of glossitis parasitica, 359 of acute gout, 134 of intestinal obstruction, 864 of abscess of liver, 1021 of cirrhosis of liver, 1002 of morbid dentition, 376 of chronic oesophagitis, 417 of cancer of oesophagus, 428 of organic stricture of oesophagus, 425 of spasmodic stricture of oesophagus, 421 of ulceration of oesophagus, 418 of perihepatitis, 990 of acute peritonitis, 1151 of acute pharyngitis, 397 of syphilitic pharyngitis, 408 of purpura rheumatica, 194 of acute rheumatism, 68 of chronic articular rheumatism, 74 of muscular rheumatism, 76, 77 of gonorrhoeal rheumatism, 107 of rheumatoid arthritis, 100 of aphthous stomatitis, 330 of mercurial stomatitis, 348 of stomatitis ulcerosa, 338 of hereditary syphilis, 317 of thrush, 335 of tonsillitis, 387 of typhlitis and perityphlitis, 822

Locality, influence on causation of scrofula, 233

Loop-shaped form of stomach, 617

Lumbago, 77

Lumbar colotomy for cancer of rectum, 915

Lumbo-abdominal neuralgia, distinguished from enteralgia, 663

Lung disease, chronic, influence on causation of constipation, 641

Lungs, condition of, in rachitis, 152 in hereditary syphilis, 307 gangrene of, complicating cancrum oris, 341 gummata of, in hereditary syphilis, 307 hypostatic congestion and pneumonia of, in entero-colitis, 734 lesions of, in diabetes mellitus, 202 in entero-colitis, 740 in acute intestinal catarrh, 677 in chronic intestinal catarrh, 706 in scurvy, 172 in tabes mesenterica, 1188

Lupoid ulcer of rectum, 889

Luxurious living, influence of, on causation of gout, 110

Lymphangiectasis in Filaria sanguinis, 963

Lymphatic glands, caseation of, in scrofula, 239, 240 changes of, in scrofula, 239, 240 in tabes mesenterica, 1187 swelling of, in cancrum oris, 342 in parenchymatous glossitis, 361 in catarrhal stomatitis, 323 in mercurial stomatitis, 346 in tonsillitis, 382

Lympho-sarcoma of intestine, 868

M.

Macroglossia, 349

Magnesium sulphate, use of, typhlitis and perityphlitis, 822

Malaria, influence on causation of biliary calculi, 1064 of catarrh of bile-ducts, 1051 of cholera morbus, 721 of diabetes mellitus, 203 of enteralgia, 660 of gastralgia, 460 of gastric hemorrhage, 582 of acute intestinal catarrh, 671 of chronic intestinal catarrh, 700 of jaundice, 977 of abscess of liver, 1005 of amyloid liver, 1041 of cirrhosis of liver, 991 of hyperæmia of liver, 984 of tabes mesenterica, 1186 relation to hepatic colic, 1072 to causation of rachitis, 145

Malarial form of acute pharyngitis, symptoms, 395 poison, influence on causation of biliousness, 965 of acute pharyngitis, 391

Malarious fevers, influence on causation of acute and chronic gastritis, 464, 470

Male fern, use of, in tape-worm, 941

Malformations, congenital, of anus and rectum, 837, 879

Malignant pustule of tongue, 368 stricture and ulceration of rectum and anus, 902

Malt extracts, use of, in rachitis, 162 liquors, influence on causation of biliousness, 966 of catarrh of bile-ducts, 1052 of gout, 111 of lithæmia, 969

Manganese sulphate, use of, in fatty liver, 1050

Manipulation of gall-bladder to dissolve biliary calculi, 1080

Marasmus, influence on causation of atrophy of stomach, 616

Marriage of syphilitics, 255, 265, 269

Marriages, consanguineous, influence on causation of scrofula, 234

Massage, use of, in constipation, 653 in rheumatoid arthritis, 101

Mastication, imperfect, influence on causation of functional dyspepsia, 445 of intestinal indigestion, 625

Maternal ill-health, influence on causation of infantile peritonitis, 1172

Maxillary bones, alterations of, in rachitis, 150

Meals, irregular, influence on causation of functional dyspepsia, 446

Measles of tape-worm, 932

Mechanism of intussusception, 847

Medina-worm, 962

Medulla oblongata, effects of puncture of diabetic area, 195

Medullary form of gastric cancer, 563 of gastric cancer, histology, 563

Melæna, in simple ulcer of stomach, 492, 493 neonatorum, etiology, 832

Melænamesis in gastric cancer, 545

Melanotic sarcoma of intestines, secondary to tumor of eye or skin, 873

Melituria in chronic intestinal pancreatitis, 1122 in obstruction of pancreatic ducts, 1131

Membranous form of acute pharyngitis, symptoms, 395 of acute pharyngitis, treatment, 399

Meningitis, distinguished from acute gastritis, 468 in acute rheumatism, 39

Menstrual disease, influence on causation of pseudo-membranous enteritis, 765 disorders from constipation, 647 influence of, on causation of rheumatoid arthritis, 90 of aphthous stomatitis, 326 of simple ulcer of stomach, 487

Menstruation, influence on causation of functional dyspepsia, 448 of gastralgia, 460 scanty, in scrofula, 245 suppression of, influence on causation of disease of pancreas, 1114

Mental anxiety, influence on causation of cholera morbus, 721 and shock, influence on causation of diabetes mellitus, 203 condition, in hepatic abscess, 1009 in acute peritonitis, 1142 in scurvy, 176 in scrofula, 245 depression in occlusion of biliary ducts, 1092 in constipation, 647, 854 in chronic intestinal catarrh, 708 in intestinal indigestion, 628 in jaundice, 980 in fatty liver, 1048 in hyperæmia of liver, 987 in lithæmia, 970 influence on causation of chronic pharyngitis, 403 emotion, influence on causation of biliary calculi, 1066 spasmodic stricture of oesophagus, 419 state, in cancrum oris, 341 in cholera morbus, 722 influence on digestion, 437 on causation of functional dyspepsia, 437 overwork, influence on causation of intestinal indigestion, 624 power, impaired, in intestinal indigestion, 628

Mercuric chloride, use of, in tonsillitis, 388 in acute yellow atrophy of liver, 1030

Mercury, use of, in biliousness, 967 in catarrh of bile-ducts, 1056 in functional dyspepsia, 457 in pseudo-membranous enteritis, 774 in entero-colitis and cholera infantum, 760 in scrofula, 251 in hereditary syphilis, 315 in syphilitic pharyngitis, 408 bichloride, effect on rectum, 911 use of, in acute intestinal catarrh, 695 in dysentery, 809 in cirrhosis of liver, 1001 in amyloid liver, 1046 in treatment of liver-flukes, 1110 in chronic pharyngitis, 406

Mercurial ointments, use of, in pruritus ani, 917 in typhlitis and perityphlitis, 822 stomatitis, 344

Mercurials, use of, in ascites, 1178, 1179 in hyperæmia of liver, 988 in chronic gastritis, 478 in jaundice, 982 in lithæmia, 972 in acute peritonitis, 1151

Mesenteric glands, changes in, in tabes mesenterica, 1187 cheesy degeneration of, in tabes mesenterica, 1187 enlargement of, in entero-colitis, 739 in acute intestinal catarrh, 677 in chronic intestinal catarrh, 705 in acute yellow atrophy of liver, 1026 lesions of, in dysentery, 801

Mesentery, elongated, as a cause of acute intestinal strangulation, 841

Metals, certain, influence on causation of biliousness, 966

Metamorphosis, fatty, of pancreas, 1128

Methyl-aniline-violet test for lardaceous degeneration, 875

Metastasis in gastric cancer, frequency of, 567 in carcinoma of liver, 1035 occurrence of, in tonsillitis, 383 secondary pancreatitis from, 1120 tendency to, in medullary form of gastric cancer, 563

Metastatic abscesses, complicating mercurial stomatitis, 346

Miasmatic origin of acute rheumatism, 26

Micturition, painful, in enteralgia, 661

Micro-organisms, influence on causation of dysentery, 792 of acute intestinal catarrh, 673

Micrococci and bacteria in stools in chronic intestinal catarrh, 708

Migraine complicating rheumatoid arthritis, 84

Migration of embryo from intestinal canal, in hydatids of liver, 1102 of biliary calculi by artificial routes, 1068, 1074 of echinococcus, 944 of gall-stones by artificial routes, 1068, 1074 symptoms due to, 1070

Migrations of Ascaris lumbricoides, 953 of gall-stones, 1067

Miliary aneurisms of stomach, 579

Milk of diseased cows as a cause of tabes mesenterica, 1186 condensed, use of, in cholera infantum and entero-colitis, 754 peptonized, use of, in entero-colitis and cholera infantum, 751, 753 in functional dyspepsia, 453 in chronic interstitial pancreatitis, 1123 mode of preparing, 1123 use of, in constipation, 652 in diabetes mellitus, 218 in dysentery, 809 in functional dyspepsia, 453 in enteralgia, 666 in entero-colitis, 749 in acute and chronic gastritis, 468, 476 in treatment of gout, 129 in hemorrhage from bowels, 834 in acute intestinal catarrh, 690, 691 in chronic intestinal catarrh, 716 in intestinal indigestion, 633 in jaundice, 983 in amyloid liver, 1046 in cirrhosis of liver, 1000 in rachitis, 159 in cancer of stomach, 576 in dilatation of stomach, 608 in simple ulcer of stomach, 519

Milk-leg in paratyphlitis, 820

Mineral acids, use of, in catarrh of bile-ducts, 1057 in chronic intestinal catarrh, 715 in intestinal indigestion, 636 in scurvy, 184 in acute intestinal catarrh, 693, 694, 695 baths, use of, in rheumatoid arthritis, 99 poisoning, influence on causation of atrophy of stomach, 616 waters, alkaline, use of, in biliary calculus state, 1079 in chronic gastritis, 477 natural, use of, in gout, 131 saline laxative, use of, in hyperæmia of liver, 988 use of, in biliousness, 968 in constipation, 652, 653, 655 in diabetes mellitus, 225, 226 in pseudo-membranous enteritis, 776 in chronic intestinal catarrh, 714, 715 in intestinal indigestion, 634, 636 in jaundice, 982 in lithæmia, 972 in rheumatoid arthritis, 99 in typhlitis, 822

Mist. cretæ, use of, in entero-colitis and cholera infantum, 758

Mitral murmurs due to biliary calculi, 1077

Moisture, influence on causation of dysentery, 788

Monolobular form of interstitial hepatitis, 992

Mono- or uniarticular rheumatism, 49

Morbid anatomy of catarrh of bile-ducts, 1052 of cancrum oris, 341 of cholera infantum, 742 of cholera morbus, 721 of constipation, 643 of diabetes mellitus, 199 of dysentery, 797 of pseudo-membranous enteritis, 769 of entero-colitis, 736 of acute gastritis, 466 of chronic gastritis, 471 of parenchymatous glossitis, 363 of superficial glossitis, 355 of glossitis parasitica, 358 of gout, 115 of hemorrhage from bowels, 832 of interstitial hepatitis, 992 of acute intestinal catarrh, 673 of chronic intestinal catarrh, 700 of cancer of intestine, 871 in lardaceous degeneration of intestine, 875 of intussusception, 844 of abscess of liver, 1005 of amyloid liver, 1041 of carcinoma of liver, 1034 of fatty liver, 1047 of hyperæmia of liver, 985 of macroglossia, 352 of acute oesophagitis, 411 of chronic oesophagitis, 416 of cancer of oesophagus, 427 of dilatation of oesophagus, 432 of paralysis of oesophagus, 429 of organic stricture of oesophagus, 424 of spasmodic stricture of oesophagus, 420 of ulceration of oesophagus, 418 of carcinoma of pancreas, 1123 of acute pancreatitis, 1118 of chronic interstitial pancreatitis, 1121 of acute diffuse peritonitis, 1133 of tubercular peritonitis, 1167 of acute pharyngitis, 391 of chronic pharyngitis, 403 of syphilitic pharyngitis, 406 of tuberculous pharyngitis, 400 of hypertrophic stenosis of pylorus, 615 of acute rheumatism, 46 of chronic articular rheumatism, 70 of gonorrhoeal rheumatism, 103 of muscular rheumatism, 74 of rheumatoid arthritis, 86 of atrophy of stomach, 616 of cancer of stomach, 560 of cirrhosis of stomach, 613 of dilatation of stomach, 599 of hemorrhage from stomach, 583 of simple ulcer of stomach, 503 of aphthous stomatitis, 326 of catarrhal stomatitis, 323 of mercurial stomatitis, 346 of stomatitis ulcerosa, 336 of scrofula, 238 of scurvy, 171 of tabes mesenterica, 1187 of thrush, 332 of tonsillitis, 383 of typhlitis, 814 dentition, 371 growths of pancreas, 1123 influence on causation of organic stricture of oesophagus, 423

Morbus maculosus Werlhofii, 188

Morning vomiting in chronic gastritis, 473 in cirrhosis of liver, 993

Morphia, effect on rectum, 911 use of, in cholera morbus, 724 in dysentery, 811 in enteralgia, 665 hypodermatically, in pseudo-membranous enteritis, 775 in gastralgia, 463 in acute intestinal catarrh, 693 in intestinal obstruction, 863 in organic stricture of oesophagus, 425 in perihepatitis, 990 in tuberculous pharyngitis, 402 in acute rheumatism, 65 in muscular rheumatism, 76 in typhlitis, 822 and atropia, hypodermic use of, in hepatic colic, 1082

Mortality of cholera morbus, 724 of dysentery, 807 of entero-colitis, 726, 727 of hereditary syphilis, 272, 273 of parenchymatous glossitis, 364 of abscess of liver, 1017 of intestinal obstruction, 862 of acute peritonitis, 1143 of acute rheumatism, 50 of cancer of stomach, 532, 535 of simple ulcer of stomach, 502 of typhlitis and perityphlitis, 820, 821

Mouth, diseases of, 321 hemorrhage from, 370 lesions of, in entero-colitis, 739 state of, in pseudo-membranous enteritis, 766 in aphthous stomatitis, 329 in gangrenous stomatitis, 340 in mercurial stomatitis, 345 in ulcerous stomatitis, 337

Movements, passive, in chronic forms of rheumatoid arthritis, 100

Mucous collections in acute intestinal catarrh, 676 discharges in non-malignant stricture of rectum, 886 membranes, affections of, in gout, 118 atrophy of, in functional dyspepsia, 451 condition of, in proctitis of chronic intestinal catarrh, 703 in thrush, 333 hypertrophy of, in chronic oesophagitis, 416 of bile-ducts, lesions of catarrh of, 1053 intestinal, lesions of, in cholera morbus, 721 in constipation, 644 gastric, lesions of, in acute gastritis, 466 lesions of, in pseudo-membranous enteritis, 769 in chronic gastritis, 471 in acute intestinal catarrh, 674 in chronic intestinal catarrh, 700 in lardaceous degeneration of intestines, 875 in catarrhal stomatitis, 324 in mercurial stomatitis, 347 in cirrhosis of stomach, 614 in organic stricture of oesophagus, 424 in typhlitis, perityphlitis, 814 miliary infiltration of, in tubercular pharyngitis, 400 softening of, in chronic gastritis, 471 state of, in dilatation of stomach, 600 in dysentery, 798 of anus, hairs on, 892 of ileum, swelling of, in chronic intestinal catarrh, 701 of stomach, microscopic appearance of, in gastric cirrhosis, 614 patches, appearance of, in syphilitic pharyngitis, 407 of hereditary syphilis, 278 stools, in chronic intestinal catarrh, 708 in proctitis, 684 vomiting of chronic gastritis, 478

Mud-baths, use of, in rheumatoid arthritis, 100

Multilobular form of interstitial hepatitis, 992 of hydatid tumor of liver, 1103

Mumps, acute secondary pancreatitis metastasic of, 1121

Muriatic acid, use of, in cancrum oris, 343 dilute, in functional dyspepsia, 456 in acute intestinal catarrh, 693, 694 in chronic intestinal catarrh, 715 in intestinal indigestion, 636

Murmurs, hæmic, in gastric cancer, 553 heart, in purpura rheumatica, 189 in acute rheumatism, 28, 35

Muscles, discovery of Trichina spiralis in, 958 fatty degeneration of, in tuberculous pharyngitis, 401 lesions of, in chronic articular rheumatism, 71 in rheumatoid arthritis, 88 in scurvy, 172 pain of, in trichinosis, 960 swelling of, in trichinosis, 960 wasting of, in acute variety of general rheumatoid arthritis, 80

Muscular coat, hypertrophy of, in chronic oesophagitis, 417 of stomach, hypertrophy of, in gastric cirrhosis, 614 contraction in acute intestinal catarrh, 681 cramps in enteralgia, 661 degeneration, lesions, in cholera morbus, 722 hypertrophy in dilatation of oesophagus, 432 rheumatism, 74 spasm in acute variety of general rheumatoid arthritis, 80 trichinæ, 958 weakness in diabetes mellitus, 204

Musk and asafoetida, in spasmodic stricture of oesophagus, 421

Mutton-tea, use of, in entero-colitis and cholera infantum, 755

Myalgia complicating gonorrhoeal rheumatism, 106

Mycotic form of tonsillitis, 381, 386 theory of origin of simple ulcer of stomach, 513 parasite of, 386

Myocarditis in acute rheumatism, 34

Myomata of stomach, 578

Myo-sarcomatous tumors of stomach, 578

N.

Narcotics, abuse of, influence on causation of gastralgia, 460 use of, in cancer of oesophagus, 428

Natiform skull, significance of, in hereditary syphilis, 312

Nature of cholera infantum, 744 of cholera morbus, 720 of constipation, 638, 639 of dysentery, 784 of enteralgia, 658, 659 of pseudo-membranous enteritis, 767, 768 of growth in glossitis parasitica, 358 of acute intestinal catarrh, 668 of intestinal indigestion, 620 of acute pharyngitis, 391 of rachitis, 137 _et seq._ essential, of syphilis, 256

Nausea, in Ascaris lumbricoides, 953 in biliousness, 966 in catarrh of bile-ducts, 1053 in acute gastritis, 467 in chronic gastritis, 473 in simple ulcer of stomach, 494 in dysentery, 803 in cancer of stomach, 540 and vomiting in functional dyspepsia, 448, 449 in pseudo-membranous enteritis, 765 in enteralgia, 661 in acute intestinal catarrh, 681 in intestinal obstruction, 843, 854 in intestinal ulcer, 826 in jaundice, 977 in acute yellow atrophy of liver, 1026, 1027, 1028 in cancer of liver, 1038 in cirrhosis of liver, 993 in acute pancreatitis, 1119 in phosphorus-poisoning, 1031 in tape-worm, 940 in thrombosis and embolism of portal vein, 1096 in trichinosis, 960

Necrosis of cartilages in gout, 116 of inferior maxilla in mercurial stomatitis, 346

Necrotic ulcers of stomach, 529

Nematodes, the, or thread-worms, 949

Nephritis, chronic, complicating gastric cancer, 560 parenchymatous, in hereditary syphilis, 308

Nerve, atrophy of, as a cause of cancer of oesophagus, 429 disease of, influence on causation of oesophageal paralysis, 429

Nerve-centres and nerves, disease of, in hereditary syphilis, 302

Nerves, lesions of, in gout, 117 of organic life, exhaustion of, as a cause of functional dyspepsia, 440

Nervous affections in acute rheumatism, 37 treatment, 65 complicating rheumatoid arthritis, 84 centres, hemorrhagic extravasations into, in scurvy, 180 colic, 662 disease in hereditary syphilis, diagnosis of, 304 disorders in Ascaris lumbricoides, 953 in constipation, 647 in phosphorus-poisoning, 1032 disturbances in catarrh of bile-ducts, 1054, 1055 due to biliary calculi, 1078 from occlusion of biliary passages, 1092 as a cause of cholera morbus, 721 of pseudo-membranous enteritis, 766, 777 of hepatic colic, 1071 in jaundice, 980 in lithæmia, 970 in cirrhosis of liver, 999 in Oxyuris vermicularis, 951 in tape-worm, 940 excitability, influence on causation of gastralgia, 460 exhaustion, influence of causation of cholera morbus, 720 of gout, 112 form of enteralgia, treatment of, 665 influence on causation of dysentery, 790 origin of acute rheumatism, 24 of rheumatoid arthritis, 92 symptoms from constipation, 854 of diabetes mellitus, 205, 206 of enteralgia, 662 reflex, in morbid dentition, 374 sympathetic, in chronic gastritis, 474 system, condition of, in parenchymatous glossitis, 362 influence on digestion, 437 lesions of, in diabetes mellitus, 200 state, in intestinal indigestion, 628 theory of origin of gout, 114

Nestle's food for infants, 754

Neuralgia in diabetes mellitus, 206 treatment, 229 complicating chronic articular rheumatism, 72 gonorrhoeal rheumatism, 106 of rectum, 909

Neurotic form of enteralgia, 662, 663 origin of pruritus ani, 909 of spasmodic stricture of oesophagus, 419 theory of origin of gastric ulcer, 512

Niemeyer's views of origin of cholera morbus, 720

Nitrate of uranium, use of, in diabetes mellitus, 230

Nitric acid, cauterization with, in irritable rectum, 919 use of, in cancrum oris, 343 in fatty liver, 1050 in jaundice, 982 in lithæmia, 972 in prolapsus ani, 920 in anal fissure and rectal ulceration, 912 local use of, in hemorrhoids, 926

Nitro-muriatic acid, local use of, in jaundice, 983 in pseudo-membranous enteritis, 775

Nitrogen, elimination of, in rachitis, 130

Nitrogenous food, excess of, as a cause of functional dyspepsia, 443

Nodes, periosteal, in gonorrhoeal rheumatism, 105

Nodosities in acute rheumatism, 43 Heberden's, of rheumatoid arthritis, 86

Nodular tubercular infiltration of tongue, 369

Nodules, number and size of, in carcinoma of liver, 1035

Non-cancerous tumors of stomach, 578

Non-malignant tumors of stomach, 578 of stomach, distinguished from malignant, 572 stricture of rectum, 885

Nose, flattening of, in hereditary syphilis, 277

Nostalgia, influence of, on causation of scurvy, 169, 170

Nursing of syphilitic children, necessity of maternal, 315

Nutmeg liver, 985

Nutrient enemata, use of, in simple ulcer of stomach, 519 suppositories, 929

Nutrition, defective, in mother, a cause of rachitis, 143

Nutritive enemata in organic stricture of oesophagus, 425

Nux vomica, use of, in functional dyspepsia, 455, 458 in constipation of functional dyspepsia, 458 in gastralgia, 463 in hepatic glycosuria, 976 in jaundice, 975 in fatty liver, 1050 in paralysis of oesophagus, 430 in acute pharyngitis, 399 in dilatation of stomach, 609

O.

Oatmeal and barley as diluents of milk for infants, 753

Obesity, influence on causation of biliary calculi, 1065

Obstruction, intestinal, 835 of bile-ducts, as a cause of jaundice, 977 as a cause of cirrhosis of liver, 991 in carcinoma of pancreas, 1124 to flow of bile as a cause of biliary calculi, 1066 intestinal from bands and loops of acute peritonitis, 1153, 1154 of orifices of stomach in gastric cancer, 566 of pancreatic duct, symptoms of, 1129 of pylorus and duodenum following acute pancreatitis, 1119 of rectum, 889

Occlusion of biliary passages, 1082 of cystic duct, pathogeny, 1082

Occupation, influence on causation of constipation, 640 of acute rheumatism, 20 of mercurial stomatitis, 344 of simple ulcer of stomach, 486

Odor of diabetic urine, 208 of mouth in stomatitis catarrhalis, 323 of stools, in acute intestinal catarrh, 680 in chronic intestinal catarrh, 708

Oedema, in gastric cancer, 553 in cancer of intestines, 871 in diseases of pancreas, 1116 in trichinosis, 961 of glottis, in tonsillitis, 383 of larynx in mercurial stomatitis, 346 treatment, 348 of lung, complicating gastric cancer, 560 of one extremity in chronic intestinal catarrh, 709 of skin in scurvy, 178 of vulva in cirrhosis of liver, 995 general, in cirrhosis of liver, 995

OESOPHAGUS, DISEASES OF, 409 _Oesophagitis_, 409 Definition, 409 Synonyms, 409 _Oesophagitis, Acute_, 409 Definition, 409 Synonyms, 409 History, 409 Etiology, 409 Of idiopathic catarrhal form, 410 Predisposing causes, 410 Cold and moisture, 410 Rheumatism, 410 Hot drinks, 410 Tobacco and alcohol, 410 Irritating medicines, 410 Of deuteropathic catarrhal form, 410 As an extension of catarrhal pharyngitis, 410 Pseudo-membraniform, 410 Traumatic form, 410 from injury, 411 Phlegmonous form, 411 from disease, 411 from injury, 411 from emboli, 411 from fits of anger, 411 Pathology and morbid anatomy, 411 Nature of inflammatory process, 411 Epithelium, changes in, 411 thickening and desquamation of, 411 Epithelial casts of tube, 412 Follicles, swelling and hypertrophy of, 412 ulceration of, 412 Pseudo-membranous form, 412 Seat and character of pseudo-membrane, 412 Variolous pustules, 412 Phlegmonous form, 412 Purulent infiltration in submucous connective tissue, 412 Diffuse form, 413 Mode of escape of pus, 413 Gangrene, 413 Symptoms, 413 Painful deglutition, 413 Substernal pain, 413 Pain over vertebræ, 413 Dysphagia, amount and character of, 413 Of pseudo-membranous form, 414 Expulsion of shreds of membrane, 414 Of phlegmonous form, 414 Convulsions from pressure on pneumogastric nerve, 414 Duration, 414 Complications and sequelæ, 414 Diagnosis, 414 From dorsal myelitis, 414 Value of auscultation, 414 of catheterism, 415 From spasm and stricture, 415 From carcinoma, 415 Prognosis, 415 Treatment, 415 Of mild form, 415 Of severe cases, 416 Of pyrexia, 416 Of traumatic form, 416 Use of anodynes, 416 of ice, 416 Diet, 416 Alkalies, 416 _Oesophagitis, Chronic_, 416 Definition, 416 Synonym, 416 Etiology, 416 Sequel of acute form, 416 Abuse of alcohol, 416 Hot drinks, 416 Chronic pulmonary and cardiac disease, 416 Foreign bodies, 416 Caries of vertebræ, 416 Pressure of tumors, 416 Pathology and morbid anatomy, 416 Hypertrophy of mucous membrane, 416 of muscular coat, 417 Abscess and ulceration, 417 Diffuse inflammation of connective tissue, 417 Symptoms, 417 Complications and sequelæ, 417 Stricture, 417 Diagnosis, 417 From spasm and stricture, 417 From carcinoma, 417 Prognosis, 417 Treatment, 417 Constitutional, 417 Diet, 417 Abstinence from alcohol, 417 Sinapisms and revulsives, 417 Use of iodides, 417 of carbonic acid waters, 417 Of pain, 418 Local, 417 Use of astringents, 417 Mode of applying astringents, 418 Cauterization of painful spots, 418 _Oesophagus, Ulceration of_, 418 Definition, 418 Etiology, 418 Sequel of inflammation, 418 Symptoms, 418 Sanguinolent products, expulsion of, 418 Perforation into trachea, 418 into mediastinum, 418 Pathology and morbid anatomy, 418 Deep-seated ulcers, 418 Fistulæ, 418 Diagnosis, 418 Prognosis, 418 Treatment, 418 Constitutional, 418 Of hemorrhage, 418 Cauterization of ulcers, 418 Use of ergot and turpentine, 418 _Oesophagus, Stricture of_, 419 Definition, 419 _Spasmodic Stricture_, 419 Definition, 419 Synonyms, 419 History, 419 Etiology, 419 Neurotic origin, 419 Hysterical origin, 419 Sex, 419 Age, 419 Mental emotion, 419 Organic diseases, relation of, to, 419 Pregnancy, 419 Gout and rheumatism, 419 Hydrophobia, 419 Symptoms, 419 Spasm, seat of, 419, 420 Inability to swallow, 420 Spasm, relaxation of, 420 causes of, 420 certain foods as a cause, 420 Dysphagia not complete, 420 Pain, 420 Hiccough, 420 Time of regurgitation of food, 420 Duration, 420, 421 Pathology and morbid anatomy, 420 Diagnosis, 420 From organic spasm, 421 Prognosis, 421 Frequency of recurrence, 421 Treatment, 421 Causal, 421 General, 421 Use of valerian, 421 of oxide of zinc, 421 of bromide of potassium, 421 of camphor, 421 of musk and asafoetida, 421 of belladonna and conium, 421 Local, 421 Bougie, use of, 421 mode of using, 421 Use of counter-irritation, 422 of electricity, 422 _Organic Stricture_, 422 Definition, 422 Synonym, 422 History, 422 Etiology, 422 Congenital, 422 Cicatricial contraction, 422 Injury, 423 Scalds, 422 Caustic drinks, 422 Syphilis, 423 Morbid growths, 423 Carcinoma, 423 Spirituous liquors, 423 Sex, 423 Age, 423 Symptoms, 423 Impediment in deglutition, 423 Regurgitation of food, 423 Pain, 423 Dysphonia, 423 Suffocative symptoms, 423 Pathology and morbid anatomy, 424 Lesions of mucous membrane, 424 Thickening of mucous membrane, 424 Lesions of muscular tissue, 424 Seat of strictures, 424 Number of strictures, 424 Forms of strictures, 424 Dilatation of oesophagus, 424 Atrophy of oesophagus, 424 Diagnosis, 424 Auscultation in, 424 Value of bougies, 424, 425 Necessity of excluding aneurism, 425 Prognosis, 425 Treatment, 425 General, 425 Use of iodides, 425 Nutrient enema, 425 Malignant form, 425 Use of arsenic, 425 of morphia, 425 Pain, 425 Local, 425 Bougies, use of, 425 mode of applying, 425, 426 Forcible dilatation, 426 Oesophagotomy, 426 _Oesophagus, Carcinoma of_, 426 Definition, 426 Synonym, 426 Etiology, 426 Varieties, 426 Spheroidal-celled, 426 Squamous-celled, 426 Colloid, 426 Symptoms, 427 Dysphagia, 427 Regurgitation of food, 427 Vomiting, 427 character of, 427 Emaciation, 427 Pain, 427 character of, 427 seat of, 427 Dyspnoea, 427 Perforation of larynx, 427 of lungs, 427 of pleura, 427 of large vessels, 427 Pathology and morbid anatomy, 427 Seat, 427 Involvement of adjacent structures, 427 Diagnosis, 428 Prognosis, 428 Treatment, 428 Constitutional, 428 Local, 428 Use of stomach-tube, 428 of opium, 428 of nutrient enemata, 428 of dilators, 428 Gastrostomy, 428 _Oesophagus, Paralysis of_, 429 Definition, 429 Synonyms, 429 Etiology, 429 Impairment of nerve-function 429 From atrophy of nerve, 429 Pressure from tumors, etc., 429 Disease of nerves, 429 of cerebro-spinal axis, 429 Syphilis, 429 Plumbism, 429 Shock and fright, 429 Cold, 429 Hysteria, 429 Symptoms, 429 Dysphagia, 429 Slow deglutition, 429 Pain, 429 Salivation, excessive, 429 Pathology and morbid anatomy, 429 Diagnosis, 429 From paralysis of pharynx, 430 Value of auscultation, 430 Prognosis, 430 Treatment, 430 Diet, 430 Mode of feeding, 430 Use of strychnia, 430 ignatia amara, 430 electricity, 430 _Oesophagus, Dilatation of_, 430 Definition, 430 Synonyms, 430 Etiology, 430 Congenital origin, 430 Mechanical origin, 430 Paralysis of muscular coat, 430 General form, 431 Annular form, 431 Pouched form, 431 Retention of food, 431 Symptoms, 431 Dyspepsia, 431 Presence of a tumor, 431 Regurgitation, 431 time of, 432 Of annular form, 432 Odor of breath, 432 Perforation, 432 Death, cause of, 432 Pathology and morbid anatomy, 432 General form, 432 Muscular hypertrophy, 432 Size of dilatation, 432 Annular form, 432 seat, 432 Pouched form, 432 nature, 433 seat, 433 size, 433 Diagnosis, 433 Value of auscultation, 434 Prognosis, 434 Treatment, 434 Use of stomach-tube, 434 Diet, 434 Constitutional, 435 Use of stimulants, 435 strychnia, 435 electricity, 435 Operative measures, 435 Gastrostomy, 435

Oesophageal stenosis in atrophy of stomach, 616

Oesophagoscope, use of, in diagnosis of gastric hemorrhage, 584

Offensive exhalations, influence on causation of cholera morbus, 721

Oïdium albicans of thrush, nature, 333

Oil of amber, locally, in hemorrhoids, 923 of turpentine, use of, in tape-worm, 941 of wintergreen, use of, in acute gout, 136 in acute rheumatism, 59 of wormseed, use of, in Ascaris lumbricoides, 954

Oils and fats, absorption of, in digestion, 623

Ointment of iodide of lead, use of, in tabes mesenterica, 1194 of red iodide of mercury in amyloid liver, 1046 in cirrhosis of liver, 1002

Oleum gaultheria, use of, in acute rheumatism, 59

Oligo-articular form of rheumatoid arthritis, 84

Olive oil and iodine, locally, in tubercular peritonitis, 1168

Onanism from Oxyuris vermicularis, 951

Onset of cholera infantum, 741 of cholera morbus, 722 of entero-colitis, 733 of acute gout, 119 of intestinal catarrh, 678 of acute variety of general rheumatoid arthritis, 80 of chronic variety of general form of rheumatoid arthritis, 81 of partial form of rheumatoid arthritis, 85 of tubercular peritonitis, 1165 of typhlitis and perityphlitis, 818 mode of, in acute pharyngitis, 394 in tonsillitis, 381

Operative measures in tonsillitis, 388 in dilatation of oesophagus, 435 in cancer of stomach, 577 in stenosis of pylorus, 609

Opium, abuse of, influence on causation of constipation, 641 -eating as a cause of enteralgia, 662 use of, in cholera morbus, 725 in diabetes mellitus, 226, 227 in dysentery, 811 in enteralgia, 665 in pseudo-membranous enteritis, 775 in entero-colitis and cholera infantum, 758, 759 in hemorrhage from bowels, 834 in acute intestinal catarrh, 689, 693, 698 in chronic intestinal catarrh, 715, 718 in intestinal obstruction, 863 in intestinal ulcers, 829 in cirrhosis of liver, 1002 in cancer of oesophagus, 428 in acute pancreatitis, 1120 in chronic interstitial pancreatitis, 1122 in acute peritonitis, 1146 in cancerous peritonitis, 1172 in perforative peritonitis, 1156 in acute pharyngitis, 397, 398, 399 in cancer of stomach, 576 in simple ulcer of stomach, 524, 527 in mercurial stomatitis, 348 in typhlitis and perityphlitis, 822

Ophthalmia, influence on causation of scrofula, 237

Organic changes, minor, in stomach, 611 disease, influence on causation of acute gastritis, 464 influence on causation of gastric hemorrhage, 580 of thoracic and abdominal viscera, a cause of ascites, 1173 of stomach, 480 stricture of oesophagus, 422

Origin of biliary calculi, 1061-1063 of cholera morbus, 720 of false membranes, in pseudo-membranous enteritis, 772 of gastric ulcer, hemorrhagic infiltration theory of, 512 of gastric ulcer, inflammatory theory of, 512 mycotic theory of, 513 of simple gastric ulcer, neurotic theory of, 512 nervous, of rheumatoid arthritis, 92 specific, of rheumatoid arthritis, 92 spontaneous, of acute peritonitis, 1136, 1137

Osteo-chondritis in hereditary syphilis, 288

Osteo-periostitis in hereditary syphilis, 291

Osteophytes in hereditary syphilis, 289 formation of, in rheumatoid arthritis, 87

Otitis, influence on causation of scrofula, 237 media, in morbid dentition, 375

Otorrhoea in hereditary syphilis, 282, 283

Ovarian cysts, distinguished from ascites, 1177 rupture of, influence on causation of acute peritonitis, 1140 disease, influence on causation of pseudo-membranous enteritis, 765 disorders, influence on causation of gastralgia, 460 and uterine irritation, influence on causation of enteralgia, 658

Over-crowding, influence on causation of entero-colitis, 730

Over-distension, as a cause of rupture of stomach, 618

Over-eating, as a cause of functional dyspepsia, 444 influence on causation of intestinal indigestion, 624

Overwork, influence on causation of chronic intestinal catarrh, 699 of functional dyspepsia, 444

Oxaluria, 970

Ox-gall, use of, in biliary calculi, 1081 in constipation, 655

Oxidation, deficient, in hepatic disease, 1051, 1057 as a cause of fatty liver, 1047 defective, origin of gout from, 112, 113

Oxyuris vermicularis, 950

P.

Pain, abdominal, in Ascaris lumbricoides, 953 colicky, in stricture of bowel, 856 from presence of biliary calculi, 1069 in cholera morbus, 722 in constipation, seat, 646 seat and character of, in dysentery, 802 in functional dyspepsia, 448 in enteralgia, 660, 661 effect of pressure upon, 661 in pseudo-membranous enteritis, 766 in fistula in ano, 898 in gastralgia, 460 of gastralgia, treatment of, 463 in acute gastritis, 467 in chronic gastritis, 473 in parenchymatous glossitis, 361 in chronic parenchymatous glossitis, 368 in acute gout, 119 in chronic gout, 121 in acute gonorrhoeal arthritis, 105 in hepatic colic, seat and character, 1070 treatment of, 1081 in acute intestinal catarrh, 678, 679, 682 in chronic intestinal catarrh, 706, 707 in cancer of intestines, 870 in intestinal indigestion, 627 in acute internal strangulation of intestines, 843 abdominal, in obstruction of intestines by gall-stones, 840 in intestinal ulcers, 826 treatment, 829 in intussusception, 848 in legs, from constipation, 854 in abscess of liver, 1011, 1012 in carcinoma of liver, seat and character, 1038 in right hypochondrium, in hyperæmia of liver, 986, 987 in back, in lithæmia, 970 in morbid dentition, 373 seat of, in acute oesophagitis, 413 in cancer of oesophagus, 427 in organic stricture of oesophagus, 423 in spasmodic stricture of oesophagus, 420 in oesophageal paralysis, 429 in diseases of pancreas, 1116 seat and character of, in carcinoma of pancreas, 1125 in acute pancreatitis, 1119 in chronic interstitial pancreatitis, 1122 in obstruction of pancreatic ducts, 1131 in acute pharyngitis, 394, 395 seat of, in perihepatitis, 989 in cancerous peritonitis, 1169 character and seat of, in acute peritonitis, 1141 in chronic peritonitis, 1162 in proctitis, 887 in suppurative pylephlebitis, seat and character of, 1099 in non-malignant stricture of rectum, 886 in cancer of rectum and anus, 903 characters of, in fissure of rectum and anus, 888 in peri-rectal and anal abscesses, 896 in ulceration of rectum and anus, 893 in acute rheumatism, 27 in chronic articular rheumatism, 71 in arthralgic form of gonorrhoeal rheumatism, 104 in rheumatic form of gonorrhoeal rheumatism, 104 in muscular rheumatism, 75 in chronic articular form of gonorrhoeal rheumatism, 105 in chronic variety of general rheumatoid arthritis, 81 in Heberden's nodosities of rheumatoid arthritis, 86 seat and character of, in cancer of stomach, 539 in cancer of stomach, treatment of, 576 in dilatation of stomach, 593 in acute dilatation of stomach, 610 in simple ulcer of stomach, 488 treatment, in simple ulcer of stomach, 524 muscular, in scurvy, 177 abdominal, in tapeworm, 940 in tonsillitis, 381, 382 in tubercular ulceration of tongue, 369 in typhlitis and perityphlitis, 818

Palate, soft, appearance of, in acute pharyngitis, 391-395 in tonsillitis, 381 paralysis of, in acute pharyngitis, 395 in tonsillitis, 383

Palpitation, in functional dyspepsia, 451 in chronic intestinal catarrh, 708 in intestinal indigestion, 628 in dilatation of stomach, 595

Pancreas, condition of, in hereditary syphilis, 306 disease of, relation to diabetes mellitus 201

PANCREAS, DISEASES OF, 1112 History, 1112 Anatomy and physiology, 1112 Position, 1112 Wirsung, canal of, 1113 Acini, 1113 Relation of head to ductus choledochus, 1113 Pancreatic juice, properties of, 1113 Etiology, general, 1114 Sex, 1114 Age, 1114 Alcohol, 1114 Tobacco, 1114 Food, improper, 1114 Suppression of menstruation, 1114 Injury, 1114 Secondary organic disease of thoracic abdominal viscera, 1114 Symptomatology, general, 1114 Objective, 1114 Emaciation, 1114 Excessive salivation, 1114 Diarrhoea, 1115 Fatty stools, 1115 Stools, undigested striped muscular fibres in, 1116 Subjective, 1116 Epigastrium, abnormal sensations in, 1116 Pain, seat and character, 1116 From pressure, 1116 Of ductus choledochus, 1116 Jaundice, 1116 Of portal vein, 1116 Oedema, 1116 Aneurismal dilatation of aorta, 1116 Of stomach, 1116 Vomiting, 1116 Of duodenum, 1116 Relation to diabetes mellitus, 1117 Of solar plexus, 1117 Bronzing of skin, 1117 Physical signs, 1117 Method of examination, 1117 Palpation, 1117 Percussion, 1118 Auscultation, 1118 Inflammatory Affections of Pancreas, 1118 _Acute Idiopathic Pancreatitis_, 1118 Morbid anatomy, 1118 Hemorrhagic extravasations in, 1118 Abscesses of, 1118 Pus, character of, 1118 Secondary peritonitis, 1118 Gangrene, 1118 Symptoms, 1118 Onset, 1118 Tongue, 1119 Constipation, 1119 Appetite, impaired, 1118 Physiognomy, 1119 Vomiting, 1119 Temperature, 1119 Pain, 1119 Pulse, 1119 Collapse, 1119 Epigastrium, tenderness of, 1119 Peritonitis, 1119 Obstruction of stomach, duodenum, and bile-duct, following, 1119 Diagnosis, 1119 From biliary colic, 1119 acute gastric catarrh, 1119 gastritis, 1120 Treatment, 1120 Rest, necessity, 1120 Diet, 1120 Ice and leeches to epigastrium, 1120 Opium, 1120 Of pain, 1120 Of vomiting, 1120 Alcohol, 1120 _Acute Secondary Pancreatitis_, 1120 Etiology, acute infectious diseases, 1120 Metastasis, 1120 Morbid anatomy, 1120 Cells, changes in, 1120 Symptoms and course, 1120 Rigors, 1121 Metastatic of mumps, 1121 Fever, 1121 Pain, 1121 Diarrhoea, 1121 Fistulous openings into viscera, 1121 Treatment, 1121 _Chronic Interstitial Pancreatitis_, 1121 Etiology, 1121 Closure of duct of Wirsung, 1121 Extension from other organs, 1121 Cancer and ulcer of stomach, 1121 Alcoholism, 1121 Syphilis, 1121 Pressure of tumors, 1121 Morbid anatomy, 1121 Hyperplasia of connective tissue, 1121 Atrophy of connective tissue, 1121 Of syphilitic hyperplasia, 1122 Symptoms and course, 1122 Emaciation, 1122 Fatty stools, 1122 Melituria, 1122 Pain, 1122 Presence of a tumor, 1122 Duration, 1122 Treatment, 1122 Hygienic, 1122 Of pain, 1122 Diet, 1122 Peptonized milk, use of, 1123 mode of preparing, 1123 gruel, 1123 broth, 1123 Ext. pancreatis, use of, 1122, 1123 Watery infusion of pancreas, use of, 1122 Purgatives, use of, 1122 Opium, 1122 Morbid Growths of Pancreas, 1123 _Carcinoma of Pancreas_, 1123 Etiology, 1123 Morbid anatomy, 1123 Primary forms, 1123 Method of growth, 1124 Wirsung's duct, obstruction of, 1124 Tumor, shape and seat of, 1124 Extension to other organs, 1124 Common bile-duct, obstruction of, 1124 Secondary forms, 1124 Limitation to head of gland, 1124 Seat of primary growth, 1124 Symptoms and course, 1124 Emaciation, 1124 Debility, 1124 Physiognomy, 1124, 1125 Temperature, 1125 Pulse, 1125 Pain, 1125 seat and character of, 1125 Stools, fat in, 1125 Jaundice, 1126 Urine, fat in, 1125 Tumor, presence of, 1125 Salivation, 1125 Pyrosis, 1125 Eructations, 1125 Epigastrium, burning and weight in, 1125 Thirst, 1125 Tongue, state of, 1125 Appetite, impaired, 1125 Nausea and vomiting, 1125 Vomit, characters of, 1126 Stools, bloody, 1126 Diarrhoea, 1126 Of secondary carcinoma of liver, 1126 Dropsy, 1126 Ascites, 1126 Duration, 1126 Prognosis, 1126 Diagnosis, 1126 From gastric cancer, 1127 From hepatic disease, 1127 From tumor of enlarged gall-bladder, 1127 From aneurism of aorta, 1127 From carcinoma of omentum, 1127 of transverse colon, 1127 From chronic pancreatitis, 1127 Treatment, 1127 Diet, 1127 Ext. pancreatis, use of, 1128 Enemata, 1128 _Sarcoma and Tubercle of Pancreas_, 1128 Degenerations of Pancreas, 1128 _Fatty Degeneration of Pancreas_, 1128 Fatty infiltration, 1128 Fatty metamorphosis, 1128 _Albuminoid Degeneration of Pancreas_, 1128 _Hemorrhages into Pancreas_, 1129 From chronic disease of liver, 1129 of heart and lungs, 1129 From rupture of vessels of gland, 1129 Appearance of gland, 1129 Symptoms, 1129 Vomiting, 1129 Collapse, 1129 Pulse, feeble, 1129 Pulsating tumor, presence of, 1129 Treatment, 1129 _Obstruction of Pancreatic Duct_, 1129 Etiology, 1129 From pressure from without, 1129 Sclerosis and carcinoma of head, 1129 Of gland, 1129 Gall-stones, 1130 Carcinoma of pylorus and duodenum, 1130 Canal of Wirsung, catarrh of, 1130 Pancreatic calculi, 1130 causes of, 1130 size and shape, 1130 composition, 1130 seat of, 1130 Dilatation of canal from, 1130 Cysts of canal, 1130 contents of, 1130 Cell-structure, changes in, 1130 Symptoms and course, 1131 Presence of a tumor, 1131 Emaciation, 1131 Stools, fatty, 1131 Jaundice, 1131 Melituria, 1131 Pain, 1131 Duration, 1131 Diagnosis, 1131 From hydatid of liver, 1131 From distension of gall-bladder, 1131 Treatment, 1131 Hygienic, 1131 Diet, 1131 Anodynes, use of, 1131 Paracentesis of cysts, 1131

Pancreas, lesions of, in diabetes mellitus, 200 in chronic intestinal catarrh, 705 in scurvy, 173 in tabes mesenterica, 1188

Pancreatic calculi, composition of, 1130 size and shape, 1130 disease complicating diabetes mellitus, 210, 1117 influence of, on causation of constipation, 642 of functional dyspepsia, 447 extract, use of, in entero-colitis and cholera infantum, 752 in functional dyspepsia, 453 in intestinal indigestion, 633, 635 form of intestinal indigestion, diagnosis, 631 juice, properties of, 1114 in diseases of pancreas, 1122, 1123, 1128

Pancreatin, use of, in chronic interstitial pancreatitis, 1122, 1123

Papillæ, enlargement of, in glossitis parasitica, 358 in superficial glossitis, 355, 356

Papular eruption of hereditary syphilis, 278

Paracentesis in ascites, 1180 in obstruction of pancreatic duct, 1131

Paralyses in morbid dentition, 375

Paralysis, facial, in diabetes mellitus, 206 complicating dysentery, 805 following chronic intestinal catarrh, 710 in intestinal indigestion, 628 of muscular coat as a cause of intestinal obstruction, 851 in dilatation of oesophagus, 430 of oesophagus, 429 of palate in acute pharyngitis, 395 in tonsillitis, 383 of rectum in chronic heart disease, 908 in spinal meningitis, 908 of rectum in vertebral fracture, 908 in scurvy, 180

Paraplegia in acute intestinal catarrh, 681 following chronic intestinal catarrh, 710

Parasite of thrush, nature of, 333 of mycotic form of tonsillitis, 386

Parasites as a cause of hemorrhage from bowels, 831 in portal vein, 1111 influence on causation of intestinal ulcer, 823 of the liver, 1101

Parasitic conditions of anus, 892 growths, influence on causation of pseudo-membranous enteritis, 765

Parasiticides, use of, in treatment of liver-flukes, 1110

Paratyphlitis, 814

Parenchymatous glossitis, 35

Parents, syphilitic, treatment of, 260, 261, 314, 315

Paresis, influence on causation of dilatation of stomach, 590

Parotitis complicating dysentery, 806

Paroxysms of hepatic colic, date of appearance, 1070 treatment of, 1081 of pseudo-membranous enteritis, symptoms of, 766

Partial form of rheumatoid arthritis, symptoms of, 84

Passive movements in chronic forms of rheumatoid arthritis, 100

Pathenogenesis of cancer of stomach, 568 of simple ulcer of stomach, 512

Pathogenesis of diabetes mellitus, 195 of rheumatoid arthritis, 92

Pathogeny of biliousness, 965 of occlusion of biliary passages, 1082 of hepatic glycosuria, 973 of lithæmia, 968 of perihepatitis, 989 of the liver in phosphorus-poisoning, 1030 of suppurative pylephlebitis, 1097

Pathological anatomy of acute yellow atrophy of liver, 1025 histology of acute intestinal catarrh, 677 of chronic intestinal catarrh, 703

Pathology of cancrum oris, 341 of diabetes mellitus, 195 of dysentery, 796 of functional dyspepsia, 451 of pseudo-membranous enteritis, 767 of superficial glossitis, 355 of chronic superficial glossitis, 367 of parenchymatous glossitis, 363 of chronic parenchymatous glossitis, 368 of glossitis parasitica, 358 of gout, 112 of hydatids of liver, 1102 of macroglossia, 352 of acute oesophagitis, 411 of chronic oesophagitis, 416 of cancer of oesophagus, 427 of dilatation of oesophagus, 432 of organic stricture of oesophagus, 424 of spasmodic stricture of oesophagus, 420 of oesophageal paralysis, 429 of ulceration of oesophagus, 418 of acute pharyngitis, 391 of chronic pharyngitis, 403 of syphilitic pharyngitis, 406 of tuberculous pharyngitis, 400 of purpura, 191 of acute rheumatism, 23 of rachitis, 137 of aphthous stomatitis, 326 of catarrhal stomatitis, 323 of stomatitis ulcerosa, 336 of mercurial stomatitis, 346 of bone disease, in hereditary syphilis, 286-288 of enlarged liver in hereditary syphilis, 283, 284 of scrofula, 238 of scurvy, 173 of tabes mesenterica, 1183 of thrush, 332 of tuberculous ulceration of tongue, 369 of tonsillitis, 383

Pavy's chemical theory of production of glycosuria, 199

Peliosis rheumatica, 189

Pelletierin, use of, in tape-worm, 942

Pelvic inflammations, influence on causation of acute peritonitis, 1140

Pelvis, deformities of, in rachitis, 153

Pemphigus in hereditary syphilis, 274 diagnosis of, 276

Pepsin, use of, in functional dyspepsia, 456 in entero-colitis, 760 in dilatation of stomach, 609 and pancreatin, use of, in gout, 131

Peptones and sugar, absorption of, in digestion, 623

Peptonized food, use of, in functional dyspepsia, 453, 454 milk, use of, in entero-colitis and cholera infantum, 751, 752 in acute intestinal catarrh, 691 in intestinal indigestion, 633 in chronic gastritis, 476 in chronic interstitial pancreatitis, 1123 in simple ulcer of stomach, 520 preparation of, 1123

Perchloride of iron in hemorrhage from rectum, 927

Percussion in diseases of pancreas, 1118 in dilatation of stomach, 598 in cancer of stomach, 572 auscultatory, in ascites, 1174

Perforation in dysentery, 799 in cancer of oesophagus, 427 in dilatation of oesophagus, 432 in cancer of stomach, 558 frequency of, 558 in simple ulcer of stomach, 496 treatment of, 527 in typhlitis and perityphlitis, 819 treatment of, 822 into mediastinum in ulceration of oesophagus, 418 into trachea in ulceration of oesophagus, 418 of cheek in cancrum oris, 341, 342 of pericardium in simple ulcer of stomach, 500 of stomach and intestines by gall-stones, 1068, 1074 of transverse colon in simple ulcer of stomach, 500

Perforations of intestinal canal as a cause of peritonitis, 1138

Perforative form of peritonitis, 1154

Peri-anal and peri-rectal abscesses, 895 treatment of, 918

Peri-articular form of gonorrhoeal rheumatism, symptoms of, 105 tissue, lesions of, in acute rheumatism, 47

Pericarditis, complicating gastric cancer, 560 in abscess of liver, 1015 in acute rheumatism, 28, 33, 34

Peri- and endocarditis in acute rheumatism, treatment of, 63, 64

Perihepatitis, 989 as a cause of cirrhosis of liver, 992

Periodicity of recurrence of dysentery, 785

Peristalsis, cessation of, in acute peritonitis, 1142 intestinal, cause of, 622, 623

Peristaltic movements of stomach in gastric dilatation, 596

Peritoneal abscesses, in simple ulcer of stomach, 507 adhesions as a cause of compression and contraction of bowel, 857

Peritoneum, condition of, in hereditary syphilis, 307 lesions of, in chronic intestinal catarrh, 705 in cirrhosis of stomach, 614 in simple ulcer of stomach, 506 secondary growths of, in gastric cancer, 557

Peritonism, relation to peritonitis, 1152

PERITONITIS, 1131 History, 1131 _Peritonitis, Acute Diffuse_, 1133 Morbid anatomy, 1133 Collections of fibrin on intestines, 1133 Blood-vessels, lesions, 1133 Peritoneum, thickening of, 1134 Serous effusions, 1134 False membrane, disposition of, 1134 fatty degeneration of, 1134 cysts of, 1135 Epithelium, changes in, 1134, 1135 Pus, character of, 1136 Abscesses, seat, 1136 Solar plexus, lesions, 1136 Hypogastric plexus, lesions, 1136 Etiology, 1136 Spontaneous origin, 1136, 1137 Albuminuria, influence on causation, 1138 Pyæmia, influence on causation, 1138 Diphtheria, influence on causation, 1138 Perforations of intestinal canal, 1138 of appendix, 1138 Abscess of liver, 1138 Gall-stones, 1138, 1139 Ulcers of stomach, 1139 of dysentery, 1139 of typhoid fever, 1139 Fecal accumulations, 1139 Injury from operations, 1140 Rupture of ovarian cysts, 1140 Tumors, presence of, 1140 Urine, infiltration of, 1140 Pelvic inflammations, 1140 Intestinal worms, 1140 Vaginal and uterine injections, 1140 Traumatism, 1141 Symptoms, 1141 Pain, 1141 characters and seat, 1141 absence of, 1143 Pulse, 1141 Respirations, 1141, 1142 Abdominal distension, 1141 Tympanites, 1141 Constipation, 1141 Vomiting, 1141 Vomit, green, 1141 Peristalsis, cessation of, 1142 Temperature, 1142 Physiognomy, 1142 Mental condition, 1142 Delirium, 1142 Urine, condition, 1142 Relation to peritonism, 1152 Consequences, 1152 Formations of bands and loops, 1153 Constipation from, 1153 Obstruction, intestinal, from, 1153, 1154 Mortality, 1143 Duration, 1143 Diagnosis, 1143 From hepatic colic, 1144 renal colic, 1144 intestinal colic, 1144 Treatment, 1144 History of, 1145 Bloodletting, 1145 Opium, 1146 history of introduction of, 1146 method of administration, 1148 amount necessary, 1148, 1149 cautions in using, 1150 use of, in Bright's disease, 1150 origin of, 1151 Purgatives, use of, 1151 Mercurials, use of, 1151 Diet, 1151 Operative measures, 1152 Puncture of intestine, 1152 Of puerperal form, 1146, 1149 Peritonism, 1152 _Peritonitis from Perforation_, 1154 Seat of, 1154 From perforation of stomach, 1155 Symptoms, 1155 in typhoid fever, 1155 seat, 1155 Of intestines, 1155, 1156 Hepatic resonance of percussion, significance in, 1156 Treatment, 1156 Rest, 1156 Opium, 1156 _Local Peritonitis_, 1159 Seat, 1159 Purulent form, 1159 Symptoms, 1159, 1160 Diagnosis, 1159 Of abscesses, 1159, 1160 pus, fecal odor of, 1160 discharge of, mode, 1160 Fibrinous exudations, 1160 seat, 1160 Formation of contractile capsule on liver, 1160, 1161 Ascites from, 1161 _Chronic Peritonitis_, 1161 Possibility of, 1161 Symptoms, 1162 Vomiting, 1162 Pain, 1162 Temperature, 1162 Pulse, 1162 Constipation and diarrhoea, 1162 Abdominal tenderness, 1162 Abdomen, sacculation of fluid in, 1162 _Tubercular Peritonitis_, 1165 Symptoms, 1165 Onset, 1165 Remissions in, 1165 Fever, 1165 Temperature, 1165 Pulse, 1165, 1166 Tympanites, 1165, 1166 Digestion, disturbances of, 1166 Abdomen, tenderness of, 1165, 1166 Emaciation, 1166 Diagnosis, 1166 Significance of cough, 1167 Morbid anatomy, 1167 False membranes, thickness of, 1167 Lungs, lesions of, 1168 Prognosis, 1168 Fatality of, 1168 Treatment, 1168 Iodide of potassium, 1168 Iodine and olive oil, locally, 1168 Iodide of iron, 1168 Diet, 1168 _Cancerous Peritonitis_, 1168 Etiology, 1168 Disseminated carcinoma, most frequent cause, 1168 Case illustrating, 1168, 1171 Vomiting, 1170 Pain, 1169 Urine, condition of, 1170 Physiognomy, 1169 Ascites, 1169 fluid, characters of, 1169 Abdomen, state of, 1169 Diagnosis, 1171 From tubercular peritonitis, 1171 Treatment, 1172 Opium, 1172 Belladonna, 1172 _Infantile Peritonitis_, 1172 Etiology, 1172 Scarlet fever, 1172 Erysipelas, 1172 Age, 1172 Syphilis, 1172 Ill-health of mother, 1172 Visceral disease, 1172 Symptoms, 1173 Treatment, 1173 _Ascites_, 1173 Etiology, obstruction to portal circulation, 1173 Liver disease, 1173 Heart disease, 1174 Kidney disease, 1174 Phthisis disease, 1175 Chronic peritonitis, 1175 Acute peritonitis, 1175 Sex, 1176 Age, 1176 Symptoms, 1175 Amount of fluid, 1175 Abdomen, state of, 1176 effect of position on, 1176 Respiration in, 1177 Abdominal veins, prominence of, 1177 Digestion, derangements of, 1177 Appetite, impaired, 1177 Emaciation, 1177 Urine, condition of, 1177 Skin, condition of, 1177 Tongue, condition of, 1177 Mental state, 1177 Diagnosis, 1177 From ovarian cysts, 1177 Auscultatory percussion in, 1174 Treatment, 1178 Diuretics, use of, 1178 Carbonate of potash and lemon-juice, 1178 Bitartrate of potash, 1179 Digitalis, 1179 Diaphoretics, 1179 Vapor bath, 1179 Pilocarpine, 1179 Cathartics, 1179 Epsom salts, 1179 Ext. senna, 1179 Elaterium, 1179 Mercurials, 1178, 1179 Paracentesis, 1180 method, 1180 Hemorrhagic effusion of peritoneum, 1180 Scurvy as a cause of, 1180 Erosions of abdominal vessels, 1181 Aneurisms, 1181 Traumatism, 1181 Symptoms, 1181

Peritonitis, chronic, influence on causation of dilatation of stomach, 590 complicating chronic intestinal catarrh, 710 acute rheumatism, 42 cancer of stomach, 560 simple ulcer of stomach, 502 acute, distinguished from cholera morbus, 724 distinguished from acute intestinal catarrh, 686 from acute gastritis, 468 in acute intestinal strangulation of intestines, 843 in intestinal ulcer, treatment, 829 in perforation of simple gastric ulcer, 499 in trichinosis, 961 secondary, in acute pancreatitis, 1118, 1119

Perityphlitis. See _Typhlitis_.

Permanent teeth, disease of, in hereditary syphilis, 293

Permanganate of potassium, use of, in catarrh of bile-ducts, 1057 in fatty liver, 1051

Perspiration, excessive, as a cause of constipation, 642 in acute rheumatism, 27, 30 in rheumatic form of gonorrhoeal rheumatism, 104 of head in rachitis, 146

Perspirations, local, complicating gout, 121

Perverted nutrition, the essential character of scurvy, 173

Pessary, dilated gum, in prolapsus ani, 920

Peyer's patches, degeneration of, in hereditary syphilis, 306 lesions of, in cholera morbus, 721 in entero-colitis, 738 in acute intestinal catarrh, 675 in chronic intestinal catarrh, 702

PHARYNX, DISEASES OF, 390 _Pharyngitis, Acute_, 390 Definition, 390 Synonyms, 390 Etiology, 390 Diathetic cause of, 390 Scrofula, 390 Rheumatism and gout, 390 Syphilis, 390 Age, 390 Cold and damp, 390 Malarial poison, 391 The exanthemata, 391 Drugs, 391 Injury, 391 Pathology and morbid anatomy, 391 Acute form, nature of, 391 Phlegmonous form, nature of, 391 course of suppurative process, 301 Ulcerative form, nature of, 392 Membranous or herpetic form, nature and course, 392 deposit, nature of, 392 vesicles of, 392 Gangrenous form, nature of, 392 course of, 392 description of ulcerative process, 393 Erysipelatous form, nature of, 393 extension from lips and skin, 393 Exanthematous form, 393 of variola, 393 of measles, 394 of scarlatina, 394 Symptoms, 394 Erythematous form, 394 Mode of onset, 394 Pain, 394 Dysphagia, 394 Skin, state of, 394 Pulse, 394 Temperature, 394 Cough, 394 Glands, swelling of, 395 Localization of inflammatory process, 395 Rheumatic form, 394 Malarial form, 395 Phlegmonous form, 395 Constitutional, 395 Local, 395 Paralysis of palate, 395 Ulcerative form, 395 Constitutional, 395 Headache, 395 Local, 395 Membranous form, 395 Constitutional, 395 Chills, 395 Pain, 395 Local, 395 Duration, 395 Gangrenous form, 395 Constitutional, 395 Temperature, 395 Pulse, 395 Pain, 395 Local, 395 Fetid secretions, 395 Odor of breath, 396 Diarrhoea, 396 Mode of death, 396 Erysipelatous form, 396 Constitutional, 396 Local, 396 Duration, 396 Diagnosis, 396 From scarlatina, 396 diphtheria, 396 Prognosis, 396 Treatment, 397 Of simple form, 397 General, 397 Local, 397 Phlegmonous form, 397 General, 397 Local, 397 Gargles, 397 Medicated sprays, 398 Leeching, 398 Rheumatic form, 398 Ulcerative form, 398 Gangrenous form, 398 Diet, 398 Traumatic form, 399 Diet, 399 Erysipelatous form, 399 Diet, 399 Membranous form, 399 Diet, 399 Exanthematous form, 399 Use of aconite, 397, 398 of astringents, 397, 398 of steam inhalations, 397, 398, 399 of ice, 397 of medicated powders, 398 of iron and quinia, 398 of alcohol, 398 of opium, 397, 398, 399 Incisions and scarification, 397 Tracheotomy, 398, 399 _Pharyngitis, Tuberculous_, 400 Definition, 400 Synonyms, 400 History, 400 Etiology, 400 Pathology and morbid anatomy, 400 Nature of ulcerative process, 400 Ulcers, description of, 401 Mucous membrane, miliary infiltration of, 400 Extension to oesophagus, 401 Muscles, fatty degeneration, 401 Lymphatic glands, enlargement of, 401 Symptoms, 401 Pain in swallowing, 401 Cough, 401 Pyrexia, 401 Wasting, 401 Diagnosis, 401 Significance of intense pain in swallowing, 401 Prognosis, 401 Death, cause of, 402 Treatment, 402 Iodoform and morphine, insufflations of, 402 Hydrogen peroxide, locally, 402 Carbolic acid, use of, 402 General, 402 Rectal alimentation, 402 _Pharyngitis, Chronic_, 402 Definition, 402 Synonyms, 402 Etiology, 402 Predisposing causes, 402 Overcrowding, 402 Sedentary occupation, 402 Food, improper, 402 Tobacco, 402 Alcohol, 402 Voice, improper use of, 402 Relation to chronic inflammations of other mucous membranes, 402, 403 Uterine disturbances, 403 Mental depression, 403 Exciting causes, 402 Pathology and morbid anatomy, 403 Nature of, 403 Structures involved, 403 Epithelium, desquamation of, 403 Glands of pharynx, dilated and hypertrophied, 403 Follicles, enlargement, 403 Papillæ of base of tongue, enlargement of, 403 Of folliculous variety, 403 Involvement of glands, 403 Projections on mucous membrane, 403 nature of, 403, 404 engorgement of capillaries at base of, 404 Viscid mucus, secretion of, 404 Dry catarrh, atrophic form, 404 Symptoms, 404 Cough, 404 Expectoration, 404 Hoarseness, 404 Hemming, 404 Sensations of throat uncomfortable, 404 Absence of symptoms, 404 Diagnosis, 404 Prognosis, 404 Treatment, 405 Of catarrhal form, 405 Constitutional, necessity of, 405 Use of mild astringents, 405 of sprays, medicated, 405 Mode of making applications, 405 Of folliculous form, 405 Constitutional, 405 Strong solutions of silver nitrate, 405 of iodine, 405 Use of ergot, locally, 405 Destruction of enlarged follicles, 405 Use of medicated sprays, 406 of mercuric chloride, 406 local, 406 Counter-irritation, 406 Chronic atrophic form, 406 Use of cubebs, 406 of jaborandi, 406 ammon. chloride, 406 pyrethrum, 406 _Pharyngitis, Syphilitic_, 406 Definition, 406 Synonyms, 406 Etiology, 406 Pathology and morbid anatomy, 406 Varieties of, 406 Secondary manifestations, 406 Inflammatory nature of, 406 Mode of spread, 406 Mucous patches, 407 microscopic appearance of, 407 Ulceration, occurrence of, 407 Tertiary manifestations, 407 Gummatous infiltration, 407 seat of, 407 Course of the process, 407 Ulcerations, nature and seat of, 407 Cicatrization, 407 Hereditary manifestations, 407 Symptoms, 407 Course of, 407 Duration of, 407 Complications, 407 Sequelæ, 407 Cicatricial stricture, 407 Diagnosis, 408 Prognosis, 408 Treatment, 408 Use of mercury, 408 potassium iodide, 408 necessity of large doses, 408 Local, 408 Use of sulphate of copper, 408 of chromic acid, 408

Pharyngeal nerve, relation to causation of parenchymatous glossitis, 363 phthisis, 400 and laryngeal catarrh in gout, 122

Pharyngitis in acute rheumatism, 42

Phlegmasia alba dolens complicating gastric cancer, 560

Phlegmatic form of scrofulous habit, 243

Phlegmonous form of acute oesophagitis, 414 of acute pharyngitis, 395 treatment of, 397

Phosphate of sodium, use of, in biliary calculi, 1080, 1081 in biliary calculus state, 1080 in catarrh of bile-ducts, 1057 in biliousness, 968 as a preventive of enteralgia, 666 in jaundice, 982 in lithæmia, 972 in acute yellow atrophy of liver, 1030 in cirrhosis of liver, 1001 in fatty liver, 1050 in hyperæmia of liver, 988

Phosphates, use of, in diabetes mellitus, 227

Phosphoric acid, elimination of, in rachitis, 138

Phosphorus, use of, in acute yellow atrophy of liver, 1030 in cirrhosis of liver, 1001 in rachitis, 165

Phosphorus-poisoning as a cause of cirrhosis of liver, 991, 992 influence on causation of fatty liver, 1047 the liver in, 1030 resemblance to symptoms of acute yellow atrophy of liver, 1031

Phthisis as a consequence of intestinal indigestion, 630 complicating diabetes mellitus, 210 chronic intestinal catarrh, 709 influence on causation of ascites, 1175 of fistula in ano, 897 of chronic gastritis, 470, 471 of acute intestinal catarrh, 671 of chronic intestinal catarrh, 699 of intestinal indigestion, 624 of fatty liver, 1047 of rheumatoid arthritis, 90 of simple ulcer of stomach, 487 nature of, complicating diabetes mellitus, 202 pharyngeal, 400

Physical signs of pancreatic disease, 1117

Physick's encysted rectum, 885

Physiognomy in cholera morbus, 722 in dysentery, 796 in enteralgia, 661 in pseudo-membranous enteritis, 766 in hepatic colic, 1071 in cancer of intestines, 869 in acute intestinal catarrh, 681 in acute gastritis, 467 in parenchymatous glossitis, 361 in carcinoma of liver, 1038 in cirrhosis of liver, 997 in carcinoma of pancreas, 1124, 1125 in acute peritonitis, 1142 in cancerous peritonitis, 1169 in scrofula, 243, 244 in scurvy, 176 in gastric cancer, 552 in simple ulcer of stomach, 496 of syphilitic children, peculiarities of, 313

Physiology of intestinal digestion, 620 of pancreas, 1112

Physostigma, use of, in lithæmia, 973 in constipation, 655

Picric acid and potash test for sugar in urine, 214

Pigment form of carcinoma of liver, 1035

Piles. See _Rectum and Anus, Diseases of_. in chronic gastritis, 475

Pilocarpine, use of, in ascites, 1179 in acute intestinal catarrh, 688 in cirrhosis of liver, 1001 in chronic articular rheumatism, 74

Placental syphilis, pathology of, 271, 272

Plane vitiligoidea of skin in jaundice, 980

Pleura, lesions of, in chronic intestinal catarrh, 706

Pleuræ, lesions of, in scurvy, 173

Pleural cavities, perforation of, in simple ulcer of stomach, 500

Pleuritis, complicating gastric cancer, 560 distinguished from perihepatitis, 990 in hepatic abscess, 1014 in acute rheumatism, 37 in trichinosis, 961

Pleurodynia, 77

Pleuro-pneumonia in hepatic abscess, 1014

Plumbism, relation of, to gout, 111

Pneumonia, complicating cancrum oris, 341 chronic intestinal catarrh, 709 gastric cancer, 560 embolic, complicating simple ulcer of stomach, 503 frequency of, in rachitis, 153 hypostatic, in entero-colitis, 735 in acute rheumatism, 37 in hereditary syphilis, 307

Pneumo-pericardium, in simple gastric ulcer, 508

Podophyllin, use of, in biliousness, 968 in constipation, 655 in functional dyspepsia, 458 in intestinal indigestion, 636 in jaundice, 982 in lithæmia, 972 in hyperæmia of liver, 988 in fatty liver, 1050

Point of discharge in hepatic abscess, 1015, 1016

Pointing of hepatic abscesses, 1007

Poison of dysentery, duration of activity, 794, 795

Poisoning, phosphorus, influence on causation of fatty liver, 1047

Polyarticular form of rheumatoid arthritis, 80 inflammations of acute diseases, relation of, to acute rheumatism, 23

Polyphagia, in dilatation of stomach, 593

Polypi, as a cause of hemorrhage from bowels, 831 influence on causation of prolapse of rectum, 881 of rectum, 882 treatment, 921 of stomach, 578

Polypoid growths, formation and origin of, in chronic intestinal catarrh, 704

Polyuria in irregular gout or gouty dyscrasia, 120, 123

Pomegranate-bark, use of, in tape-worm, 941

Pork measle-worm, 935

Portal circulation, obstructed, influence on causation of chronic gastritis, 470 obstruction of, a cause of ascites, 1173 vein, changes in, in hepatic hyperæmia, 985 congestion of, as a cause of hemorrhage from stomach, 581 diseases of, 1095 parasites in, 1111 stenosis of, 1095 symptoms of pressure of, in disease of pancreas, 1116 thrombosis and embolism of, 1075 lesions of, in cirrhosis of liver, 992

Post-mortem, nature of gastromalacia, 618

Potassium bromide, in acute intestinal catarrh of children, 698 in diabetes, 227 in laryngismus stridulus, 163 chlorate, influence on causation of glossitis parasitica, 358 local use of, in hemorrhoids, 923 in morbid dentition, 376 in acute pharyngitis, 397-399 use of, in aphthous stomatitis, 330, 331 in mercurial stomatitis, 348 in stomatitis ulcerosa, 338 in glossitis parasitica, 359 citrate, use of, in muscular rheumatism, 77 iodide, in pseudo-membranous enteritis, 775 in scrofula, 252 in syphilis, hereditary, 316 in syphilitic pharyngitis, 408 salts, use of, in gout, 132 in acute rheumatism, 60

Pouched form of dilatation of oesophagus, 431

Pouches, rectal, dilatation of, 885

Poultices, use of, in acute intestinal catarrh, 688, 690 in abscess of liver, 1023 in acute rheumatism, 68 in muscular rheumatism, 76 in rheumatoid arthritis, 100 in tonsillitis, 388 in simple ulcer of stomach, 527 in typhlitis, 822

Poverty, influence of, on causation of gout, 110, 111 of rheumatoid arthritis, 91 of simple ulcer of stomach, 486 of tabes mesenterica, 1186

Pre-digested foods, use of, in intestinal indigestion, 635

Predisposing causes of cholera morbus, 720 of functional dyspepsia, 438 of gout, 109 of scrofula, 232

Pregnancy, influence on causation of functional dyspepsia, 448 of acute yellow atrophy of liver, 1024 of fatty liver, 1047 of spasmodic stricture of oesophagus, 419 of rheumatoid arthritis, 90 of aphthous stomatitis, 326 and lactation, influence on causation of scrofula, 237

Preliminary treatment of tape-worm, 941

Premonitory symptoms of jaundice, 977

Pre-natal treatment of rachitis, 158

Prevention of hereditary syphilis by treatment of parents, 260, 261

Preventive treatment of cholera morbus, 724 of enteralgia, 665 of entero-colitis and cholera infantum, 746 of chronic intestinal catarrh, 714, 715 of morbid dentition, 376 of rachitis, 158 of hereditary syphilis, 314 of scrofula, 249 of mercurial stomatitis, 347 of tabes mesenterica, 1193 of thrush, 335

Primary disease of rectum and anus, 881 form of cancer of liver, 1034

Privation and want, influence on causation of functional dyspepsia, 441

Procidentia of rectum, 881

Proctitis, 667, 684. See _Rectum and Anus, Diseases of_. influence on causation of abscess of liver, 1004

Prodromal symptoms of gout, 118

Prodromata of typhlitis and perityphlitis, 818

Prognosis of Anchylostomum duodenale, 956 of occlusion of biliary passages, 1092 of cancrum oris, 342 of cholera infantum, 745 of cholera morbus, 724 of constipation, 650 of diabetes mellitus, 217 of dysentery, 807 of enteralgia, 664 of pseudo-membranous enteritis, 774 of entero-colitis, 741 of gastralgia, 462 in acute gastritis, 468 of parenchymatous glossitis, 364 of chronic parenchymatous glossitis, 368 of glossitis parasitica, 359 of chronic superficial glossitis, 367 of glossanthrax, 368 of gout, 126 of hepatic glycosuria, 974 of acute intestinal catarrh, 687 of chronic intestinal catarrh, 713 of lardaceous degeneration of intestines, 876 of intestinal cancer, 873 of intestinal indigestion, 631 of intestinal ulcer, 828 of jaundice, 981 of lithæmia, 970 of abscess of liver, 1018 of acute yellow atrophy of liver, 1029 of amyloid liver, 1045 of cancer of liver, 1039 of cirrhosis of liver, 999 of fatty liver, 1049 of hyperæmia of liver, 988 of macroglossia, 353 of morbid dentition, 376 of oesophageal paralysis, 430 of acute oesophagitis, 415 of chronic oesophagitis, 417 of cancer of oesophagus, 428 of dilatation of oesophagus, 434 of organic stricture of oesophagus, 425 of spasmodic stricture of oesophagus, 421 of ulceration of oesophagus, 418 of carcinoma of pancreas, 1126 of tubercular peritonitis, 1168 of acute pharyngitis, 396 of chronic pharyngitis, 404 of syphilitic pharyngitis, 408 in tuberculous pharyngitis, 401 of purpura, 193 of hypertrophic stenosis of pylorus, 615 of rachitis, 157 of congenital malformations of rectum and anus, 880 of acute rheumatism, 50 of chronic articular rheumatism, 73 of gonorrhoeal rheumatism, 106 of rheumatoid arthritis, 95 of scrofula, 248 of scurvy, 182 of cancer of stomach, 575 of cirrhosis of stomach, 614 of acute dilatation of stomach, 610 of dilatation of stomach, 603 of hemorrhage from stomach, 585 of rupture of stomach, 618 of simple ulcer of stomach, 518 of aphthous stomatitis, 330 of catarrhal stomatitis, 325 of mercurial stomatitis, 347 of stomatitis ulcerosa, 338 of stomatorrhagia, 371 of hereditary syphilis, 309 of iritis in hereditary syphilis, 281 of nervous disease in hereditary syphilis, 304 of tabes mesenterica, 1191 of tongue-tie, 349 of syphilitic ulceration of tongue, 370 of tonsillitis, 387 of trichinosis, 961 of typhlitis and perityphlitis, 820

Progress and termination of chronic intestinal catarrh, 709

Prolapse of rectum, 881

Prolapsed hemorrhoids, treatment of, 924

Prolapsus ani, in dysentery, 797, 803 treatment of, 919

Propagation of dysentery by dejecta, 791

Prophylactic treatment of acute intestinal catarrh, 687

Prophylaxis in biliousness, 967 of dysentery, 808 of Filaria sanguinis, 194 of cirrhosis of liver, 1000 of tape-worm, 942, 943 of trichinosis, 962

Propylamine, use of, in acute articular rheumatism, 62 in chronic articular rheumatism, 74

Proscolex of tape-worm, 932

Prostatic disease, influence on causation of pseudo-membranous enteritis, 765

Prostration in acute gastritis, 467 in obstruction of intestines by gall-stones, 840 in trichinosis, 960

Prurigo podicis of anus, 892

Pruritus in jaundice, 980 in occlusion of biliary passages, 1087 of genitalia in diabetes mellitus, 204 ani, 909 treatment, 917 in Oxyuris vermicularis, 951 in tape-worm, 940

Pseudo-membrane, seat and character, in acute oesophagitis, 412

Pseudo-membranous enteritis, 763 form, of dysentery, lesions of, 799 of acute oesophagitis, etiology, 410 symptoms, 414

Pseudo-paralysis in hereditary syphilis, 289, 312

Psoriasis linguæ, 356

Puerperal form of acute peritonitis, treatment, 1146, 1149

Pullna water, use of, in intestinal indigestion, 636

Pulmonary affections in acute rheumatism, 36 complicating gonorrhoeal rheumatism, 106 rheumatoid arthritis, 84 artery, enlargement of, in rachitis, 139 cavities, influence on causation of amyloid liver, 1041 congestion in acute rheumatism, 37 disease, influence on causation of functional dyspepsia, 448 of chronic intestinal catarrh, 700 of intestinal indigestion, 626 chronic, influence on causation of chronic oesophagitis, 416 influence on causation of hyperæmia of liver, 984

Pulsating tumor of epigastrium, in hemorrhage into pancreas, 1129

Pulsation, epigastric, in cancer of stomach, 553

Pulse, characters of, in acute peritonitis, 1141 in tubercular peritonitis, 1165, 1166 state of, in occlusion of biliary passages, 1089 in cancrum oris, 341 in cholera infantum, 742 in cholera morbus, 723 in dysentery, 804 in enteralgia, 661 in pseudo-membranous enteritis, 766 in entero-colitis, 734, 736 in acute gastritis, 467 in parenchymatous glossitis, 362 in hepatic abscess, 1009 in hepatic colic, 1071 in acute intestinal catarrh, 682 in chronic intestinal catarrh, 709 in jaundice, 979 in acute yellow atrophy of liver, 1028 in fatty liver, 1048 in acute pancreatitis, 1119 in carcinoma of pancreas, 1125 in acute pharyngitis, 394, 395 in phosphorus-poisoning, 1032 in cancer of stomach, 553 in tonsillitis, 381 in typhlitis and perityphlitis, 819

Pumpkin-seeds, use of, in tape-worm, 942

Puncture, exploratory, in abscess of liver, 1021 in hydatids of liver, 1107 of colon, in enteralgia, 665 of gall-bladder as a means of diagnosis of occlusion of biliary passages, 1092 for relief of biliary calculi, 1081 of impacted calculus, 1094 of intestine in acute peritonitis, 1152 of right lobe, value of, in diagnosis of abscess of liver, 1020, 1021

Pupil, dilatation of, in acute yellow atrophy of liver, 1027

Purgatives, abuse of, influence on causation of acute intestinal catarrh, 672 use of, in constipation, 651, 656 in entero-colitis and cholera infantum, 757 in hepatic colic, 1082 in impaction of feces, 918 in chronic intestinal catarrh, 714, 715 in intestinal ulcer, 829 in acute yellow atrophy of liver, 1030 in acute peritonitis, 1151 in chronic interstitial pancreatitis, 1122 in seat-worms, 951 in trichinosis, 962 uselessness of, in intestinal obstruction, 862, 863

PURPURA, 186 Definition, 186, 187 Etiology, 190 Heredity, influence on causation, 190 Hereditary predisposition to, 191 Specific nature, 191 Pathology, 191 Forms, 187 Symptoms, 187 _Purpura Simplex_, 187 Mode of onset, 187 Eruption, character, 187 duration, 187 General condition, 187 _Purpura Hæmorrhagica_ (_Morbus Maculosus Werlhofii_), 188 Mode of onset, 188 Eruption, character and seat, 188 Epistaxis, occurrence of, 188 Hæmatemesis, occurrence of, 188 Hæmaturia, occurrence of, 188 General condition, 188 Duration, 189 Temperature, 189 _Purpura Rheumatica_ (_Peliosis Rheumatica_), 189 Mode of onset, 189 Joints, condition of, 189 Pains in joints, 189 Eruption, character and seat, 189 duration, 189 Cardiac murmurs, 189 _Sub-varieties_, 189 In children, 190 Purpura urticaria, 190 Purpura papulosa, 190 Complications, 190 Gangrene of intestines, 190 Diagnosis, 192 From scurvy, 192 From hæmophilia, 192 From effusions and ecchymoses of acute exanthemata, 192 From erythema nodosum, 192 From erythema multiforme, 192 Prognosis, 193 Treatment, 193 Of mild cases, 193 Diet, 193 Necessity of quiet, 193 Of complications, 194 Of purpura rheumatica, local, 194 Use of sulphuric acid, 193 of acetate of lead, 193 of ergotin, 193 of turpentine, 193 of iron, 194 Transfusion of blood, 194

Purpura hæmorrhagica, complicating gastric cancer, 560 in children, 190 papulosa, 190 urticaria, 190

Purulent form of local peritonitis, 1159 infiltration, in phlegmonous form of acute oesophagitis, 413

Pus, characters of, in acute peritonitis, 1136 evacuation of, in abscess of liver, 1021 mode of escape, in phlegmonous form of acute oesophagitis, 413 of acute pancreatitis, character of, 1118 of hepatic abscesses, 1007

Pustular syphilides in hereditary syphilis, 279 diagnosis of, 279, 280

Putrefaction, influence on causation of dysentery, 787, 789

Pyæmia complicating mercurial stomatitis, 346 influence on causation of acute peritonitis, 1138 occurrence of, in dysentery, 797, 804

Pylephlebitis, 1095 in simple ulcer of stomach, 502 suppurative, 1097

Pylethrombosis, in gastric cancer, 560

Pylorus, cancer of, influence on causation of occlusion of common biliary duct, 1085 distortion of, as cause of dilatation of stomach, 588 hypertrophic stenosis of, 615 Synonyms, 615 Etiology, 615 Cicatrization of gastric ulcer, 615 Morbid anatomy, 615 Hypertrophy of gastric walls, 615 Fibrous tissue, new growth of, 615 Symptoms, 615 Of chronic gastritis, 615 Presence of a tumor, 615 Diagnosis, 615 Prognosis, 615 Treatment, 615 hypertrophy and ulceration of, in chronic gastritis, 472 obstruction of, in gastric cancer, 566 influence on causation of dilatation of stomach, 587 resection of, in dilatation of stomach, 609 scirrhous state of, in chronic gastritis, 471 spasm of, influence on causation of dilatation of stomach, 588 stenosis of, in simple ulcer of stomach, 503 influence on causation of dilatation of stomach, 587

Pyo-pneumothorax subphrenicus in perforation of simple ulcer of stomach, 499

Pyrethrum, use, in chronic pharyngitis, 406

Pyrexia in acute gastritis, treatment of, 469, 470 in parenchymatous glossitis, 362 in acute oesophagitis, treatment of, 416 in tuberculous pharyngitis, 401 in catarrhal stomatitis, 323 in mercurial stomatitis, 346

Pyrosis in functional dyspepsia, 449

Q.

Quicksilver, use of, in intestinal obstruction, 863

Quiet, necessity of, in purpura, 193

Quinia, use of, in ascites, 1179 in catarrh of bile-ducts, 1057 in dysentery, 812 in functional dyspepsia, 457 in gastralgia, 462 in parenchymatous glossitis, 365 in gout, 135 in acute intestinal catarrh, 689, 692 in chronic intestinal catarrh, 715 in intestinal indigestion, 636 obstruction, 865 in lithæmia, 973 in acute yellow atrophy of liver, 1030 in abscess of liver, 1020 in aborting abscess of liver, 1020 in amyloid liver, 1045 in cirrhosis of liver, 1000 in fatty liver, 1051 in acute pharyngitis, 398 in pruritus ani, 917 in purpura, 194 in suppurative pylephlebitis, 1101 in rectal paralysis of malarial origin, 908 in acute rheumatism, 61 in chronic articular rheumatism, 74 in gonorrhoeal rheumatism, 107 in rheumatoid arthritis, 98 in gangrenous stomatitis, 344 in tape-worm, 942 in tonsillitis, 388

Quinsy, 379

R.

Race, influence on causation of diabetes mellitus, 204 of cancer of stomach, 535 of acute intestinal catarrh, 669 of scrofula, 235

RACHITIS, 137 Definition, 137 Etiology and pathology, 137 Inflammatory nature of, 137, 138 Defective calcification, causes of, 138, 139 Lime, method of elimination, 138 Phosphoric acid, method of elimination, 139 Nitrogen, method of elimination, 139 Anatomical causes, 139 Arteries, increased width of, influence on causation, 139 Artery, pulmonary, enlargement of, influence on causation, 139 Thoracic and abdominal viscera, relation to causation, 140 Liver, enlargement of, 139 Spleen, enlargement of, 140 Kidneys, enlargement of, 140 Direct causes, 140 Early life, influence on causation, 141, 142 Climate, influence of, on causation, 143 Air, bad, influence of, on causation, 143 Defective maternal nutrition, influence of, on causation, 143 Intestinal catarrh, influence of, on causation, 144 Improper food, influence of, on causation, 144 Pulmonary diseases, influence of, on causation, 144 Hereditary nature of, 144 Gout, influence of, on causation, 144 Syphilis, influence of, on causation, 144 Malaria, influence of, on causation, 145 Intra-uterine and congenital forms, causes and symptoms, 141-143 Symptoms, 146 Mode of development in infants, 146 in older infants, 146 Head, appearance of, 146 sweating of, 146 condition of sutures, 147 of fontanels, 147 of cranial bones, 147 Craniotabes, 147 Cranial sclerosis, 148 Brain and meninges, condition of, 148, 149 Brain compression, 149 Intellect, state of, 149 Convulsions, 149 Laryngismus stridulus, 149 Face, alterations in, 150 Maxillary bone, lower, changes in, 150 Teething, anomalies of, 150, 151 Vertebral columns, changes in, 151 Kyphosis, occurrence of, 151 Ribs, changes in, 152 tenderness of, 152 beading of, 152 Chest, alterations in shape, 152 Heart and lungs, condition of, 152 Pneumonia, catarrhal, frequency of, 153 Bronchial and tracheal catarrh, tendency to, 152 glands, enlargement of, 152 Abdomen, enlargement of, 153 Pelvis, deformities of, 153 Liver, changes in, 153 degeneration, amyloid, 153 Spleen and kidneys, degeneration, amyloid, 153 Tonsils, enlargement of, 153 Tongue, condition of, 153 Stomach, condition of, 153 Intestinal tract, condition of, 153 Constipation, significance of, 154 Kidneys, changes in, 154 Extremities, appearance of, 155 bones of, changes in, 155 Bones, curvatures of, 155 causes of, 155 Skin, disorders of, 156 Alopecia, circumscribed, 156 Of rachitis, acute, 156 Nature, 156 Prognosis, favorable nature of, 157 Influence of complications on, 158 Treatment, 158 Preventive, 158 Pre-natal, 158 Of intestinal disorders, 158 Diet, 159 Milk, use of, 159 mode of administration, 159, 160 Weaning, proper time for, 160 Of craniotabes, 162 perspiration, 162 laryngismus stridulus, 163 convulsions, 163, 164 complications, 164 constipation, 164 by diet, 164 by strychnia, 164 deformities, 165, 166 by gymnastic exercises, 166 by mechanical apparatus, 166 Use of alkalies, 161 of acids, 161 of baths, salt, 163 hot, 163 mode of applying, 163 of beef-tea, 161 mode of preparation, 161 of bromides of potassium and sodium, 163 of chloral hydrate, 163 of cod-liver oil, 162 of iron, 162 of lime, 162 of lime-water, proper dose, 161 of malt extracts, 162 of phosphate of lime, 162 of phosphorus, 165 Fresh air, value of, 163 Sea-bathing, value of, 163

Ranvier and Cornil on causes of scrofulous inflammation, 239

Rat and mouse, Trichina spiralis in, 958

Raw beef, use of, in acute intestinal catarrh, 691

Rectal alimentation, 928 conditions necessary to success, 928 emptiness of bowel, 928 time of administering, 928 syringe, variety of, 928 amount of enemata, 928 frequency of enemata, 928 substance employed, 929 contraindications, 929 use of nutrient suppositories, 929 in gastric cancer, 576 in organic stricture of oesophagus, 425 heat and fulness, in constipation, 645 inflammation, 887 irrigation in dysentery, 809 in chronic intestinal catarrh, 717 in jaundice, 983 pouches, dilatation of, 885 treatment in acute intestinal catarrh, 697

RECTUM AND ANUS, DISEASES OF, 877 Forms of, 877 Anatomy of, 877-879 _Congenital Malformations_, 879 Imperforate anus, 879 Abnormal anal openings, 880 Absence of anus, 880 Greater liability of males to, 880 Prognosis, 880 Treatment, 880 _Primary Diseases of Rectum and Anus_, 881 _Prolapse and Procidentia of Rectum_, 881 Etiology, 881 Age, infancy and senility, 881 Worms, 881 Diarrhoea, 881 Constipation, 881 Coughing and crying, 881 Loss of tone of anus and rectum, 881 Abuse of cathartics, 881 Urethral stricture, 881 Polypi, 881 Tumors, 881 Symptoms, 881 Size, 881 Appearance of mucous membrane, 881 _Polypi of Rectum_, 882 Varieties, 882 Gelatinoid form, 882 Fibroid form, 882 Nature, 882 Physical characters, 882 Symptoms, 882 Frequent desire to stool, 882 Heat and tenesmus, 882 Hemorrhage, 882 Number, 882 Seat, 882 _Hemorrhoids or Piles_, 882 Etiology, 882 Abnormal state of blood-vessels, 882 External, 883 Sex, influence of, on causation, 883 Age, influence of, on causation, 883 Exciting causes, 883 Tendency to inflammation, 883 Obliteration of vessels in, 883 Structure of, 883 Symptoms, 883 Pain, 883 Tenesmus, 883 Inability to urinate, 883 Suppuration of, 883 Internal, 883 Physical characters, 883 Structure of, 883 Color, 883 Etiology, 884 Constipation, 884 Diseases of liver, 884 Abdominal tumors, 884 Horseback riding, 884 Dysentery, 884 Diarrhoea, 884 Sedentary life, 884 Age, 884 Sex, 884 Rich food, 884 Symptoms, 884 Pain, 884 Tenesmus, 884 Spasm of sphincters, 884 Hemorrhage, 884 Weight and fulness, 884 _Dilatation of the Rectal Pouches_, 885 Rarity of, 885 Causes, 885 Symptoms, 885 Weight and uneasiness of rectum, 885 Pain, 885 Mucus, increased secretion of, 885 Exploration of bowel with blunt hook, 885 _Non-malignant Stricture of Rectum_, 885 Nature, 885 Etiology, 885 Traumatism, 885 Following operations, 885 Secondary of pelvic inflammation, 885 of syphilis, 885 Constipation, 886 Sex, influence of, on causation, 886 Symptoms, 886 Physical characters, 886 Violent straining at stool, 886 Wire-drawn feces, 886 Irregular bowels, 886 Appetite, impaired, 886 Digestive disturbances, 886 Pain, 886 Mucous discharges, 886 Seat, 886 of syphilitic, 886 Characters of syphilitic, 886 _Proctitis_, 887 Frequency, 887 Etiology, 887 Intestinal worms, 887 Rhus toxicodendron, 887 Gonorrhoeal poison, 888 Unnatural intercourse, 888 Symptoms, 887 Pain, 887 Tenesmus, 887 Mucous and bloody discharges, 887 _Fissure of Anus and Rectum_, 888 Frequency, 888 Character, 888 Position, 888 Etiology, 888 Uterine disease, 888 Frequency in women, 888 Constipation, 888 Syphilis, 888 Symptoms, 888 Pain, 888 Spasm of sphincters, 888 Mental depression, 889 _Rodent or Lupoid Ulcer of Rectum_, 889 Frequency, 889 Seat, 889 Characters, 889 Symptoms, 889 Pain, 889 Spasm of sphincters, 889 _Obstruction of Rectum_, 889 Etiology, 889 Foreign bodies, 889, 890 Sex, 889 Loss of nervous and muscular tone, 889 Impaction of feces, 889 Concretions, 890 Enteroliths, 890 composition, 890 Gall-stones, 891 Intestinal worms, 891 Tumors, pelvic, 891 Symptoms, 891 Appetite impaired, 890 Digestive disturbances, 890 Melancholia, 890 Vomiting, 890 Tenesmus, etc., 890 Sloughing of rectum, 891 _Cutaneous Eruptions and Parasitic Conditions of Anus_, 892 Eczema, 892 Erythema intertrigo, 892 Prurigo podicis, 892 Herpes, 892 Furunculi, 892 Hairs on mucous membrane, 892 Sarcoptes hominis, 892 Acarus autumnalis, 892 Rhus toxicodendron, 892 _Ulceration of Rectum and Anus_, 893 Frequency, 893 Etiology, 894 Syphilis, 894 Struma, 894 Traumatic, 894 Foreign bodies, 894 Impacted feces, 894 Symptoms, 893 Initial, 893 Diarrhoea, 893 Stools, character, 893 Pains, 893 Muco-purulent discharges, 894 Sphincters, loss of power in, 893 Abscesses, formation, 893 Ulcers, physical character, 893 Enlargement of rectal glands, 893 _Follicular Ulcerations_, 894 Etiology, 894 Origin, 894 From chancroidal invasion, 895 Symptoms, 895 _Peri-anal and Peri-rectal Abscess_, 895 Etiology, 895 Acute form, 895 Anatomical causes, 895, 896 Sex, influence on causation, 896 Cold and wet, 896 General debility, 896 Hepatic disorders, 896 Symptoms, 896 Sudden onset, 896 Chills, 896 Heat and fulness, 896 Pain, 896 Dysuria, 896 Appetite impaired, 896 Malaise, 896 Chronic form, 896 Etiology, 896 From traumatic causes, 896 ulceration of rectum, 896 Seat, 896 Symptoms, 896 Hectic, 896 Emaciation, 896 Slow formation, 896 Difficult to heal, 897 _Fistula in Ano_, 897 Great frequency, 897 Etiology, 897 Abscesses, 897 From traumatic causes, 897 Age, 897 Male sex, 897 Phthisis, 897 Forms, 897 complete, 897 incomplete, 897 Multiple, 897 Seat of external opening, 897 internal opening, 898 Course, 898 Discharges, character of, 898 Pain in, 899 Diagnosis, 898 Use of probe, 898 _Hemorrhage from Rectum_, 899 Primary and Secondary, 899 _Secondary Diseases of Rectum and Anus_, 900 _Syphilis of Rectum and Anus_, 900 Frequency, 900 relative, in the sexes, 900 Seat and character, 900, 901 Mucous patches, 900 Gummatous deposits, 900 Condylomata, 901 _Scrofulous and Tuberculous Affections_, 901 Pathology of tubercular form, 901 Description and course, 901 Causation from ingestion of morbid products of tuberculous lungs, 902 Seat, 902 _Cancer, Malignant Stricture and Malignant Ulceration_, 902 Forms, 902 Relative frequency of forms, 903 Sex, influence on causation, 903 Age, influence on causation, 903 Scirrhous, method of growth, 903 Pain in, 903 Difficult defecation, 904 Odor of patient, 904 Exhaustion, 904 Encephaloid, rapid growth of, 904 hemorrhage in, 904 Lymphatic glands, enlargement of, 904 Disease of rectum, by extension from colon, 904 Ulceration of rectum following typhoid fever and dysentery, 905 Ulceration from mechanical causes, 906 _Effects of Abnormal Conditions of Spinal Cord and Membranes on Rectum and Anus_, 906 Constipation in, 906 Loss of control, 907 Paralysis of rectum in pressure myelitis, 907 rectal, in spinal meningitis, 907 in fracture of vertebræ, 908 Sphincters, condition of, in convulsions of epilepsy, 908 Paralysis, in chronic heart disease, 908 in malaria, 908 _Spasm of Rectum and Anus_, 909 _Pruritus Ani_, 909 Etiology, 909 Neurotic origin, 909 Digestive derangements as causes, 909 Overwork, 909 Spinal irritation, 909 Worms, 909 Rheumatism, 909 Diabetes mellitus, 909 _Neuralgia of Rectum_, 909 Frequency of, 910 Causes of, 910 Malaria, 910 Reflex, 910 Uterine disease, 910 Symptoms, 910 _Effect of Cholera and Certain Poisons and Remedies on Rectum_, 910 Of cholera, 910 Of arsenic, 910 Of corrosive sublimate, 910 Of croton oil, 910 Of strychnia, 911 Of morphia, 911 Of jaborandi, pain in rectum, from, 911 Of mineral acids, 911 Treatment, therapeutical and surgical, 911 Of anal fissure, 911 Cauterization with nitrate of silver, 912 Incision and dilatation, 912 Of rectal ulcer and deep anal fissure, 912 Cleanliness, 912 Bougies of soap, 912 Cauterization, 912 Glycerite of tannin, 912 Astringent, 912 Red precipitate ointment, 912 Use of acid nitrate of mercury, 912 Nitric acid, 912 Incision, 912 method of, 913 Dilatation, method of, 912 Of tuberculous ulcer of rectum, 913 Of chronic ulcer of rectum, 913 use of Ward's paste, 913 Of rodent ulcer, 913 excision in, 913 Of cancer of rectum, 913 use of anodynes, 913 enemata of warm water, 914 bougies, use of, 914 excision, 914, 915 method of, 915 lumbar colotomy, 915 method of, 916 Of dilatation and inflammation of rectal pouches, 916 incision, 916 Of loss of co-ordination in muscles of defecation, 916 Of sphincterismus, 916 Use of purgatives, 916 of hot hip-baths, 916 of bougies, 916 of incision and dilatation, 916 Of pruritus ani, 917 Use of enemata, 917 of carbolic acid, 917 of turpentine, 917 of hot water, 917 of sulphate of zinc and alum, 917 of chloroform, 917 of iron and quinine, 917 of mercurial ointment, 917 of tincture gelsemium, 917 Of non-malignant rectal stricture, 917 Use of bougies, 917 of dilatation, 917 Of syphilitic form, 917 Of peri-anal and peri-rectal abscess, 918 Use of poultices, 918 of incision, 918 Of gonorrhoea of rectum, 918 Astringent injections, 918 Of impaction of feces, 918 Use of dilatation of sphincter, 918 of enemata, 918 of purgatives, 918 of iron and quinine, 919 of electricity, 919 Of irritable rectum, 919 Anodyne enemata, 919 Cauterization with nitric acid, 919 Of concretions of rectum, 919 Of proctitis, 919 Use of copaiba, 919 of black pepper, 919 of ice, locally, 919 Of prolapsus ani and procidentia, 919 Use of astringent solutions, 919 of anal pad and T-bandage, 920 of cauterization, 920 method, 920 of excision, 920 method, 920 of dilated gum pessary, 920 of ergotin, locally, 920, 921 of strychnia, locally, 921 of nitric acid, locally, 920 of nitrate of silver, 920 Of polypus, 921 Ligation, 921 Clamp and cautery, 921 Of fistula in ano, 921 Palliative, 921 Operative, 921 by incision, 922 by ligation, 922 methods, 922 question of operation in phthisical cases, 922 Of hemorrhoids, 923 Palliative, 923 Astringent ointments, 923 Enemata of potassium chlorate, 923 of lime-water, 923 Use of copaiba, 923 of black pepper, 923 Oil of amber, locally, 923 Use of hamamelis virginica, 923 of ergotin, 923, 924 of aloes, 923 of cold water, 924 Rest after defecation, 924 Of prolapsing, 924 Operative, 924 Of external, 924 Of internal, 924 by strangulation, 924 method, 925 by clamp and cautery, 925 by écraseur, 925 by caustics, 926 by nitric acid, 926 by caustic potash, 926 Of hemorrhage from rectum, 926 Ice, use of, 927 Injections of ice-water, 927 of perchloride of iron, 927 Use of tampon, 927 method, 927 of Agnew's rectal chemise, 927 of ligature, 927

Rectum, heat of, in dysentery, 802 in pseudo-membranous enteritis, 765 painful disease of, influence on causation of constipation, 642 suppuration of, as a cause of suppurative pylephlebitis, 1098 stricture of, symptoms, 856

Recurrence of spasmodic stricture of oesophagus, frequency of, 421 of tonsillitis, frequency of, 387

Reflex causes of enteralgia, 660 nervous disturbance, due to biliary concretions, 1078 symptoms in morbid dentition, 374 spasm of muscles in general form of rheumatoid arthritis, 80

Regimen, restricted, influence on causation of functional dyspepsia, 444

Regurgitation, in functional dyspepsia, 449 of food in cancer of oesophagus, 427 in dilatation of oesophagus, 432 in organic stricture of oesophagus, 423 time of, in spasmodic stricture of oesophagus, 420 in ulceration of oesophagus, 418 in acute oesophagitis, 413 in cancer of cardiac orifice of stomach, 542

Relapses, frequency of, in typhlitis and peri- and paratyphlitis, 820 influence of salicyl treatment on frequency of, in acute rheumatism, 52 tendency to, in acute rheumatism, 44, 45

Remissions in chronic variety of general rheumatoid arthritis, 82 in tubercular peritonitis, 1165

Remittent and typhoid fever, distinguished from acute gastritis, 468

Renal affections complicating acute rheumatism, 42 colic complicating gout, 124 distinguished from enteralgia, 664 disease, influence on causation of chronic gastritis, 470 influence on causation of simple ulcer of stomach, 488

Resection, in gastric cancer, 577 of pylorus, in dilatation of stomach, 609

Respiration, in ascites, 1177 in acute peritonitis, 1141 difficult, in tonsillitis, 382 laborious, in parenchymatous glossitis, 361

Rest after defecation, in hemorrhoids, 924 in hemorrhage from bowels, 834 in perforative peritonitis, 1156 importance of, in dysentery, 809 in chronic gastritis, 476 in treatment of simple ulcer of stomach, 519 local, importance in rheumatoid arthritis, 100 necessity of, in acute gastritis, 469 in treatment of heart, complications of acute rheumatism, 64 value of, in treatment of acute intestinal catarrh, 690 in chronic intestinal catarrh, 716

Restlessness in cholera infantum, 742

Results of chronic articular rheumatism, 71, 72

Retention of food in dilatation of oesophagus, 431

Rhamnus, fl. ext., use in constipation, 656

Rheumatic and arthritic diathesis, relation of, to causation of gonorrhoeal rheumatism, 103 form of acute pharyngitis, symptoms, 394 treatment, 398 of gonorrhoeal rheumatism, symptoms, 104 of tonsillitis, treatment, 388, 389

RHEUMATISM--_Acute_, 19 Synonyms, 19 Definition, 19 Etiology, 19 Climate, influence of, on causation, 19 Season, influence of, on causation, 19 Occupation, influence of, on causation, 20 Age, influence of, on causation, 20 Sex, influence of, on causation, 21 Heredity, influence of, on causation, 21 Temperament, influence of, on causation, 21 Cold and damp, influence of, on causation, 22 Fatigue and exhaustion, influence of, on causation, 22 Depressing passions, influence of, on causation, 22 Traumatism, influence of, on causation, 22 Polyarticular inflammation of acute diseases, relation of, to, 23 Pathology, 23 Theories regarding origin, 23 Lactic-acid theory, 23 Latham's theory of hyperoxidation, 24 Nervous theory, 24 Miasmatic theory, 26 Infective-germ theory, 26 Symptoms, 26 Invasion, 26 General description, 27 Local, 27 date of appearance of, 27 Joints, condition of, 27 most affected, 27 Pain, character of, 27 Tendency to invade fresh joints, 27 Description of special symptoms, 29 Temperature, 27, 29 Hyperpyrexia, 29, 66 Defervescence, mode of, 29 Digestive tract, 27 Tongue, 27 Appetite, 27 Constipation, 27 Thirst, 27 Urine, condition of, 30 amount of urea and uric acid in, 30 during convalescence, 30 Albuminuria in, 30 Saliva, condition of, 30 Perspiration in, 27, 30 Blood, condition of, 31 Complications, 31 Cardiac affections in, 28, 31 frequency of, 32 causes of, 32 occupation, 33 age, 32 date of appearance of, 28, 33 forms of, 32 relative frequency of forms of, 33 endocarditis and pericarditis, symptoms, 28, 33, 34 ulcerative endocarditis, 33 myocarditis, 34 symptoms of, 34 subacute, 35 murmurs in, 28, 35 relative frequency of different murmurs, 35 anæmic murmurs, 36 Pulmonary affections, 36 frequency of, 36 relation of, to cardiac complications, 36 pneumonia and pleuritis, 36, 37 congestion of lungs, 37 Nervous affections, 37 delirium, 37, 38 coma, 38 convulsions, 38 chorea, 38 meningitis, 39 embolism of cerebral arteries, 39 spinal inflammation, 40 causes of, 40 hyperpyrexia as a cause of, 41 intemperance, 40 rheumatic poison as a cause of, 41 Renal affections, 42 Pharyngitis, 42 Gastralgia, 42 Diarrhoea and dysentery, 42 Peritonitis, 42 Cystitis and orchitis, 42 Cutaneous affections, 42 Nodosities, 43 Position, 43 Duration, 43 Pathology of, 44 Course and duration, 44 Average duration of acute symptoms, 45 Relapses, tendency to, 44, 45 Morbid anatomy, 46 Articulations, changes in, 46 Synovial membrane, changes in, 46 Microscopic appearance of effusion, 47 Cartilages, changes in, 47 Soft parts about joints, changes in, 47 Brain and membranes, changes in, 39 Spinal cord and membranes, changes in, 40 Blood, changes in, 31 Heart and membranes, changes in, 31-36 Diagnosis, 47 From pyæmia, 47 acute glanders, 48 periostitis, 48 articular enlargements of rickets, 48 of hereditary syphilis, 48 inflammation of cerebral softening and hemorrhage, 49 of spinal disease, 49 Prognosis, 50 Mortality, 50 Cause of sudden death in, 50 Rheumatism, acute articular, in children, 49 Peculiarities of, 49 Treatment, 51 Use of salicylic acid and salicylates, 51-59 Influence of, upon joint-pains, 51, 52 on pyrexia and hyperpyrexia, 52, 55 on frequency of relapses, 52 on frequency of heart complications, 53-55 on duration, 55 Unpleasant effects of, 56 Effects of, upon the heart, 57 Heart-failure from, 57 Delirium from, 57 Albuminuria and hæmaturia from, 58 Doses of, 58 Mode of administration, 59 Use of salicine, advantages of, 58 Dose of, 58 of oil of wintergreen, 59 of alkalies, 60 Method of administration, 60 Influence of, on pain and pyrexia, 60 on duration, 60 on heart complications, 60, 61 and salicylates, relative power of, 60, 61 combined use of, 61 of quinia, 61 of potassium iodide, 62 of ammonium bromide, 62 of cold, 66 of trimethylamine, 62 of benzoic acid, 62 of chloral and morphia, 65 of lemon-juice, 63 of perchloride of iron, 63 of alcohol, 69 of blisters, 63, 68 of aconite, 64 Of complications, 63 Of peri- and endocarditis, 63, 64 Of pericardial effusions, 64 Of myocarditis, 64 Necessity of rest in heart complications, 64 Of meningitis, 65 Of nervous affections, 65 Of delirium, 65 Of sleeplessness, 65 Of hyperpyrexia, 66 by cold, 66 modes of applying, 67 Summary of treatment, 68 Diet in, 69 Hygienic management, 69 Convalescence, 69 _Subacute Articular_, 46 Symptoms of, 46 _Mono- or Uni-articular Acute and Subacute_, 49 _Chronic Articular_, 69 Synonyms, 69 Definition, 69 Etiology, 69 Primary nature, 70 Predisposing causes, 70 Heredity, 70 Acute rheumatism, 70 Cold and damp, 70 Exciting causes, 70 Symptoms and course, 71 Mild forms, 71 Pain, character of, 71 Local, 71 Creaking of joints, 71 Alteration of joints, 71 Anæmia and debility, 71 Tendency to exacerbation, 71 Influence of weather on, 71 Joints most affected, 72 General condition of, 71 Complications, 72 Cardiac disease, 72 Endarteritis, 72 Asthma, 72 Bronchitis, 72 Neuralgia, 72 Dyspepsia, 72 Results, 71, 72 Ankylosis from, 71 Thickening, 71, 72 Duration, 72 Termination, 72 Morbid anatomy, 70 Of simple form, 70 Changes in joints, 70 synovial membrane, 70 Capsule and ligaments, 70 Cartilages, 70 Muscles, 71 Diagnosis, 73 From rheumatoid arthritis, 73 From articular enlargement of spinal diseases, 73 of syphilis and struma, 73 of tubercular disease, 73 From chronic articular gout, 73 Prognosis, 73 Treatment, 73 Hygienic, 73 Importance of proper clothing, 73 Therapeutic, 73 Use of salicylates in, 73, 74 of salicylate of quinia, 74 of propylamine, 74 of trimethylamine, 74 of potassium iodide, 74 of arsenic, 74 of cod-liver oil, 74 of quinia, 74 of guiaiac, 74 of bromide of lithium, 74 of pilocarpine, 74 of iron, 74 Local, 74 Diet, 74 _Muscular_, 74 Synonyms, 74 Definition, 74 Etiology, 74 Age, influence of, on causation, 74 Sex, influence of, on causation, 75 Cold, influence of, on causation, 75 Fatigue and strain, influence of, on causation, 75 Heredity, 75 Symptoms, 75 Pain, character of, 75 effect of pressure upon, 75 Cramp, muscular, 75 Spasm, muscular, in, 75 Muscles most affected, 76 Digestive tract, 76 Appetite, 76 Constipation, 76 General, 76 Duration, 76 Diagnosis, 76 Tendency to error, 76 From organic spinal disease, 76 functional spinal disease, 76 lead and mercurial poisoning, 76 neuralgia, 76 Morbid anatomy, 74 Varieties, 77 Lumbago, 77 Symptoms, 77 Diagnosis, 77 Pleurodynia, 77 Symptoms, 77 Diagnosis, 77 from intercostal neuralgia, 77 Torticollis, 78 Symptoms, 78 Diagnosis, 78 Treatment, 76 Indications, 76 Relief of pain, 76 Use of morphia, 76 of diaphoretics, 77 of potassium iodide, 77 of alkalies, 77 of citrate of potassium, 77 of salicylates, 77 of baths, hot, 77 of galvanism, 76 Local, 76, 77 Heat, 76 Poultices, 76 Hygienic, 77 necessity of proper clothing, 77 Of lumbago, 77 Of pleurodynia, 78 Of torticollis, 78 _Rheumatoid Arthritis_, 78 Synonyms, 78 History, 78 Etiology, 88 Of general progressive form, 88 Influence of age on causation, 88 of sex on causation, 88 of cold and damp on causation, 88, 90 of heredity on causation, 88 of rheumatism on causation, 88, 89 of gout on causation, 89 of diseases of pregnancy on causation, 90 of disorders of menstruation, 90 of scrofula on causation, 90 of phthisis on causation, 90 of poverty on causation, 91 of injury on causation, 91 Of partial form, 91 Advanced age, influence of, on causation, 91 Sex, influence of, on causation, 91 Local irritation of joint, influence of, on causation, 91 Cold and damp, influence of, on causation, 91 Of Heberden's nodosities, 91 Advanced age, influence of, on causation, 91 Female sex, influence of, on causation, 91 Poverty, influence of, on causation, 91 Heredity, influence of, on causation, 91 Varieties, 79 Symptoms, 80 Of general progressive or polyarticular form, 80 Acute variety, 80 Resemblance to acute rheumatism, 80 Mode of onset, 80 General, 80 Local, 80 Wasting of muscles, 80 Reflex muscular spasm, 80 Duration, 80 Of chronic variety, 81 Mode of onset, 81 Local, 81 Pain, character of, 81 Position and shape of joints, 81 Creaking of joints, 81 Ankylosis, 81 Course and duration, 82 Remissions, 82 Deformities of upper extremities, description, 82 of hand, description, 82 of lower extremities, description, 82 of feet, description, 82 General condition, 82 Digestive symptoms, 82 Loss of appetite, 83 Constipation, 83 Skin, condition of, 83 Urine, condition of, 83 Of partial or oligo-articular form (arthritis deformans), 84 Mode of onset, 85 Local, 85 Condition of joint, 85 Deformities of special joints, description, 85, 86 Remissions, 85 Duration, 85 Of Heberden's nodosities, 86 Seat and nature, 86 Pain in, 86 Exacerbations, acute, in, 86 Complications, 83-86 Of progressive form, 83 Endo- and pericarditis, 83 Pulmonary affections, 84 Nervous affections, 84 Cutaneous affections, 84 Migraine, 84 Eye diseases, 84 Rheumatic nodules, 84 Of partial form, 84, 85 Of Heberden's nodosities, 86 Morbid anatomy, 86 Changes in the joints, 86 in synovial membranes, 86 fluid, 86 in cartilages, 87 in bones, 87 in ligaments, 87 in muscles, 88 Formation of osteophytes, 87 Frequency of ankylosis, 87 Pathogenesis, 92 Relation of, to rheumatism, 92 Nervous origin of, 92 Specific origin, 92 Diagnosis, 92 Of acute form, from subacute or chronic rheumarthritis, 92 Of chronic form, from chronic articular rheumatism, 93 Of partial form, from chronic articular rheumatism, 93 from chronic traumatic arthritis, 93 from chronic periarthritis of shoulder-joint, 93 from articular affection of locomotor ataxia, 94 from articular affections of progressive muscular atrophy, 94 From chronic gout, 94, 95 arthritis of late syphilis, 95 Prognosis, 95 Of progressive or polyarticular form, 95, 96 Of partial form, 96 Of Heberden's nodosities, 96 Treatment, 96 Unsatisfactory, 96 Indications, 96 Removal of causation, 96 Use of salicylic acid and salicylates, 97 of salicylate of quinia, 97 of sodium, 97 of potassium iodide, 98 of cod-liver oil, 98 of iodine, 98 of quinia, 98 of iodide of iron, 98 of iron, 98 of arsenic, 98 of baths, hot, 99 mineral, 99 selection of, 99 indications for, 99 mud, 100 local, 100 of anodyne applications, 100 of poultices, 100 of tinct. iodine, 100 of rest in acute forms, 100 of blisters, 100, 101 of passive movements in chronic forms, 100 of mercurial ointment, 100 of iodine ointment, 100 of vapor baths, 100 of sand baths, 101 of electricity, 101 mode of applying, 101 of massage, 100, 101 of compression by rubber bandage, 101 Hygienic, 101 Use of flannel clothing, 102 Change of climate, 102 Diet, 102 Duration of, 102 _Gonorrhoeal Rheumatism, or Gonorrhoeal Arthritis_, 102 Synonyms, 102 Etiology, 102 Non-gonorrhoeal origin, 102 Stage of gonorrhoea at which most frequent, 102 Predisposing causes, 103 Cold and damp, 103 Fatigue, 103 Rheumatic and arthritic diathesis, 103 Heredity, 103 Sex, 103 Morbid anatomy, 103 Changes in joints, 103 in synovial membrane, 103 fluid, 103 in cartilages, 103 Symptoms, 104 Joints most affected, 104 Order of invasion, 104 Arthralgic form, 104 pain in, 104 Rheumatic form, 104 mode of invasion, 104 local, 104 temperature, 104 perspiration, 104 pain, 104 digestion, 104 deformity in, 104 Acute gonorrhoeal arthritis, 105 pain in, 105 condition of joint in, 105 general, 105 Chronic hydrarthrosis, 105 joints most affected, 105 condition of, 105 formation of pus, 105 Involvement of tendons and sheaths, 105 Periarticular form, 105 pain in, 105 Gonorrhoeal bursitis, 105 Nodes in periosteum, 105 Complications, 106 Neuralgia, 106 Sciatica, 106 Myalgia, 106 Affections of the eye, 106 Iritis, 106 Erythema, 106 Cardiac affections, 106 Endocarditis, 106 Pulmonary affections, 106 Termination, 106 Followed by ankylosis, 106 spondylitis, 106 rheumatoid arthritis, 106 strumous articular disease, 106 Course and duration, 106 Prognosis, 106 Mortality, 106 Diagnosis, 107 Treatment, 107 Local, 107 General, 107 Use of iron, 107 of quinia, 107 of potassium iodide, 107 of sodium salicylate, 107 of baths, 107 Diet in, 107

Rheumatism complicating dysentery, 805 influence on causation of acute oesophagitis, 410 of pruritus ani, 909 of tonsillitis, 380 acute and chronic, influence of, on causation of rheumatoid arthritis, 88, 89 and gout, influence on causation of gastralgia, 460 of chronic gastritis, 470, 471 of acute pharyngitis, 390

Rheumatoid arthritis following gonorrhoeal rheumatism, 106

Rhubarb, use of, in constipation, 655, 656 in functional dyspepsia, 458 in pseudo-membranous enteritis, 774 in jaundice, 982

Rhus toxicodendron, eruption of anus from, 892 influence on causation of proctitis, 887

Ribs, changes in, in rachitis, 152

Rickets, as a cause of tardy eruption of teeth, 372 complicating tabes mesenterica, 1193 influence on causation of intestinal indigestion, 623

Ridge's foods for infants, 754

Rigors in hepatic abscess, 1008 in acute secondary pancreatitis, 1121

Rilliet and Barthez on lesions of cholera infantum, 742

Rochelle salts in biliousness, 967 use of, in constipation, 655

Rockbridge alum water, use of, in chronic intestinal catarrh, 714, 717

Rodent ulcer of rectum, 889 treatment of, 913

Roseola of hereditary syphilis, 277 diagnosis of, 278

Round-worms, 952

Rubeolous form of acute pharyngitis, 394

Rubber bandage, compression by, in treatment of rheumatoid arthritis, 101

Rupture of stomach, 618

Russian baths, use of, in intestinal indigestion, 633

S.

Saccharine foods, use of, in diabetes mellitus, 220

Sacculation of ductus pancreaticus, from obstruction, 1130 of fluid, in chronic peritonitis, 1162

Salicine, advantages of, in treatment of acute rheumatism, 58

Salicylate of quinia, use of in chronic articular rheumatism, 74 in rheumatoid arthritis, 97 of sodium, use of, in gonorrhoeal rheumatism, 107 in thrush, 335 and salicylic acid, use of, in diabetes mellitus, 229, 230

Salicylates, use of, in muscular rheumatism, 77 and alkalies, combined use of, in acute rheumatism, 61 relative power of, in acute rheumatism, 60, 61

Salicylic acid, use of, in acute intestinal catarrh, 696 in catarrhal stomatitis, 325 in rheumatism of dysentery, 809 and salicylates, influence of, on duration of acute rheumatism, 55 on frequency of relapses in acute rheumatism, 52 on heart complications of acute rheumatism, 53-55 use of, in acute rheumatism, 51-59 in acute gout, 135 in chronic articular rheumatism, 73, 74 in rheumatoid arthritis, 97

Saliva, action of, in digestion, 620 condition of, in acute rheumatism, 30 dribbling of, in parenchymatous glossitis, 361

Salivary glands, condition of, in scurvy, 177

Salivation, excessive, in morbid dentition, 373 in pancreatic carcinoma, 1125 diseases, 1114 in aphthous stomatitis, 329 in catarrhal stomatitis, 323 in mercurial stomatitis, 345 in stomatitis ulcerosa, 337 in tonsillitis, 382

Salted meats, influence of, on causation of scurvy, 171

Sanguinarin, use of, in intestinal indigestion, 636 in constipation, 665

Sanguine form of scrofulous habit, 243

Santonin, use of, in Ascaris lumbricoides, 954 in tape-worms, 942

Sarcinæ and bacteria in vomit of dilatation of stomach, 594

Sarcoma of pancreas, 1128 of stomach, 578 of liver, 1036

Sarcoptes hominis of anus, 892

Scalds, influence on causation of organic stricture of oesophagus, 422

Scarification in acute pharyngitis, 397

Scarlatina, influence on causation of acute gastritis, 466

Scarlatinous form of pharyngitis, 394

Scarlet fever, influence on causation of infantile peritonitis, 1172

Sciatica complicating gonorrhoeal rheumatism, 106

Scirrhous carcinoma of pancreas, secondary nature of, 1124 form of gastric cancer, 564 of intestinal cancer, 868 method of growth, 872 state of pylorus in chronic gastritis, 471 of rectum and anus, 903

Sclerosis, cranial, in rachitis, 148 of central vein, in hepatic hyperæmia, 985 of liver. See _Liver, Diseases of_.

Scolex of tape-worm, 932

SCROFULA, 231 Synonyms, 231 Definition, 231, 232 Etiology, 232 Predisposing causes, 232 Formad on the scrofulous peculiarity, 232 Heredity, influence on causation of, 232 Bad hygienic surroundings, influence on causation of, 232 Food, improper, influence on causation of, 232 Air, impure, influence on causation of, 232 Locality and climate, 233 Season, 233 Age, 233 Sex, 234 Social position, 234 Consanguineous marriages, 234 Complexion and temperament, 235 Race and nationality, 235 Acquired scrofula, 236 Exciting causes, 236 Injury, 236 The eruptive fevers, 237 Vaccination, 237 Pregnancy and lactation, 237 Eczemas, 237 Catarrhs, 237 Ophthalmia and otitis, 237 Pathology and morbid anatomy, 238 Anatomical peculiarity of tissue, 238 Excessive cell-growth in, 238 Low vitality of cells in, 239 Cornil and Ranvier on causes of scrofulous inflammation, 239 Fatty degeneration of cells in scrofulous infiltration, 239 Caseation of cells, 239 Glands, changes in, 239, 240 caseation of, 239, 240 Relation of, to tuberculosis, 240, 241, 242 Causes of tendency to appear in early life, 242 Symptoms, 243 Physiognomy of, 243, 244 Scrofulous habits, 243, 244 forms of, 243 Phlegmatic form, description of, 243 Erethistic form, description of, 243 Torpid form, description of, 243 Sanguine form, description of, 243 Features peculiar to, 245 Deficient circulation, 245 Tendency to chilblains, 245 to catarrhs and eczema, 245 Low temperature, 245 Scanty menstruation, 245 Mental condition, 245 Downy hair, growth on forehead and shoulders, 246 Cutting and ulceration of lobe of ear from ear-rings, 246 Thick upper lip, 246 Teeth, condition of, 246 Clubbing of fingers, 246 General manifestations, 246 Influence upon other diseases, 246 Modification of measles by, 247 of boils by, 247 ordinary injuries by, 247 conjunctivitis by, 248 No such disease per se, 248 Diagnosis, 248 From syphilis, 248 lupus, 248 Prognosis, 248 Treatment, 249 Preventive, 249 Intermarriage, danger from, 249 Diet, 249 Importance of breast-milk, 249 Starchy food, danger from, 249 Weaning, proper time for, 250 Air, pure, importance of, 250 Bathing, value, 250 Therapeutic, 251 Necessity of exercise, 252 Use of iodine, 251 of iodide of iron, 251 of mercury, 251 of cod-liver oil, 252 of alkalies, 252 of hypophosphites and lactophosphates, 252 Of enlarged glands, 252

Scrofula, influence on causation of acute pharyngitis, 390 of rheumatoid arthritis, 90 of tonsillitis, 380 acquired, 236 and tuberculosis, relation to tabes mesenterica, 1183, 1185

Scrofulous affections of rectum and anus, 901

SCURVY, 167 Synonyms, 167 Definition, 167 History, 167, 168, 169 Etiology, 169 Sex, influence on causation, 169 Age, influence on causation, 169 Contagiousness of, 169 Depressing emotions, influence on causation, 169 Nostalgia, influence on causation, 169, 170 Atmospheric changes, influence on causation, 170 Air, impure, influence on causation, 170 Personal habits, influence on causation, 170 Tobacco, influence on causation, 170 Drink and food, influence on causation, 170, 171 Salted food, influence on causation, 171 Morbid anatomy, 171 Post-mortem appearance of body, 171, 172 Skin, lesions of, 172 Muscles, lesions of, 172 Bones, lesions of, 172 Joints, lesions of, 172 Brain, lesions of, 172 Heart and pericardium, lesions of, 172 Blood-vessels, lesions of, 172 Lungs, lesions of, 172 Pleuræ, lesions of, 173 Digestive tract, lesions of, 173 Pancreas, lesions of, 173 Kidneys, lesions of, 173 Liver, lesions of, 173 Bladder, lesions of, 173 Spleen, lesions of, 173 Pathology, 173 Essential characters, 173 Perverted nutrition, 173 Blood, condition of, 173 amount of fibrin in, 174 of albumen, 174 of red corpuscles, 174 of salines in, 174, 175 of water, 175 alkalinity of, 175 analyses of, 175 Symptoms, 176 Mode of development, 176 Cachexia of, 176 Initial, 176 Mental condition, 176 Physiognomy, 176 Pains, muscular, 177 Appetite, 177 Breath, 177 Tongue, condition of, 177 Gums, condition of, 177 Salivary glands, condition of, 177 Skin, condition of, 176, 178 extravasations of blood in, 178 oedema of, 178 ulceration of, 178 Bones, condition of, 179 Articulations, condition of, 179 Heart, condition of, 179 Hemorrhages, frequency of, 179 Epistaxis, 179, 180 Hæmatemesis, 180 Hemorrhage from bowels, 180 Hæmaturia, 180 Serous inflammations, 180 Pericarditis, 180 Pleuritis, 180 Nervous centres, hemorrhagic extravasations into, 180 Convulsions, 180 Headache, 180 Paralysis, 180 Embolism of lungs and spleen, 181 Urine, condition of, 181 Spleen, enlargement of, 181 Visual disorders, 181 Blindness, 181 Conjunctiva, hemorrhage under, 181 Hearing, disorders of, 181 Temperature, 182 Diagnosis, 182 From skin disorders, 182 rheumatism, 182 Prognosis, 182 Treatment, 183 Preventive, 183 Hygienic, 183 Diet, 183 Necessity of fruit, 183 of milk, 183 Lime-juice, 183, 184 preparation of, 184 Ventilation, 184 Air, pure, 184 Therapeutic, 184 Use of vegetable bitters, 184 of mineral acids, 184 of hæmostatics, 185 Of stomatitis, 185 local, 185 Of hemorrhages, 185

Scurvy as a cause of hemorrhagic effusion of peritoneum, 1180

Scybalæ, formation of, in constipation, 645

Sea-bathing, value of, in rachitis, 163

Season, hot, influence on causation of dysentery, 787 of biliary calculi, 1065 of entero-colitis, 727, 728 of rheumatism, acute, 19 of scrofula, 233 of stomatitis ulcerosa, 336 of thrush, 332

Seat of abscesses in suppurative hepatitis, 1006, 1011 of deposit in lardaceous degeneration of intestines, 875 of cancer of intestine, 869 of intussusception, 846 of local forms of peritonitis, 1159 of stricture of bowel, 855

Seat-worms, 950 symptoms of, 951 treatment of, 951

Seborrhoea complicating gout, 121

Second dentition, 375

Secondary causes of disease of pancreas, 1114 character of tabes mesenterica, 1183, 1186 disease of liver in carcinoma of pancreas, 1126 of rectum and anus, 900 form of intestinal cancer, 869 of carcinoma of liver, 1034, 1035 growths, in gastric cancer, 556 pancreatitis, acute, 1120 period of hereditary syphilis, 274 ulcers of tongue, 370

Secretions in tonsillitis, character of, 385 fetid, in gangrenous form of acute pharyngitis, 396

Sedentary life, influence on causation of constipation, 640 of acute intestinal catarrh, 671 of dilatation of stomach, 592 and occupation, influence on causation of intestinal indigestion, 624 occupation as a cause of chronic pharyngitis, 402

Seminal emissions in constipation, 646

Senna, use of, in constipation, 656

Sensations, perversions of, in pseudo-membranous enteritis, 767

Sensibility, modifications of, in intestinal indigestion, 628

Septic material from fermentation of food, influence on causation of cholera morbus, 721

Septicæmic fever, in abscess of liver, treatment of, 1020

Sequelæ of cancrum oris, 341 of chronic intestinal catarrh, 710 of acute oesophagitis, 414 of chronic oesophagitis, 417 of syphilitic pharyngitis, 407 of simple ulcer of stomach, 500, 503 of tonsillitis, 383

Serous effusion in acute peritonitis, 1134 inflammations in scurvy, 180

Severe forms of chronic intestinal catarrh, 707

Sewer-gas, influence on causation of cholera morbus, 721

Sex, influence on causation of ascites, 1175 of biliary calculi, 1064 of cholera morbus, 720 of constipation, 639, 640, 850 of diabetes mellitus, 203 of enteralgia, 659 of pseudo-membranous enteritis, 764 of fistula in ano, 897 of gastralgia, 460 of gout, 109 of hemorrhoids, 883 of acute intestinal catarrh, 669 of chronic intestinal catarrh, 699 of cancer of intestine, 869 of intestinal indigestion, 623 of intussusception, 847 of abscess of liver, 1003 of acute yellow atrophy of liver, 1024 of amyloid liver, 1041 of carcinoma of liver, 1034 of cirrhosis of liver, 990 of fatty liver, 1047 of organic stricture of oesophagus, 423 of spasmodic stricture of oesophagus, 419 of diseases of pancreas, 1114 of peri-rectal and -anal abscesses, 896 of phosphorus-poisoning, 1030 of cancer of rectum and anus, 903 of non-malignant rectal stricture, 886 of acute rheumatism, 21 of gonorrhoeal rheumatism, 103 of rheumatoid arthritis, 88, 91 of tabes mesenterica, 1184 of typhlitis, 815 of scrofula, 234 of scurvy, 169 of cancer of stomach, 533 of cirrhosis of stomach, 612 of simple ulcer of stomach, 483

Sexual apparatus of the various species of tape-worm, 932, 934, 935, 939 appetite, loss of, in diabetes mellitus, 204 excess, influence of, on causation of diabetes mellitus, 203 of gout, 112 of intestinal indigestion, 624 functions, perversion of intestinal indigestion, 629 organs of Tænia echinococcus, 943

Shingles, occurrence of, in gall-stones, 1069

Shock and fright, influence of, on causation of paralysis of oesophagus, 429

Sialorrhoea in carcinoma of pancreas, 1125 in diseases of pancreas, 1114

Sigmoid flexure, dilatation of, in constipation, 643 stricture of, 836

Silver, chloride of, use of, in amyloid liver, 1046 nitrate, use of, in dysentery, 809, 812 in enteralgia, 665 in pseudo-membranous enteritis, 775 in entero-colitis, 761 in chronic gastritis, 478 in chronic intestinal catarrh, 717, 718 in spasmodic stricture of oesophagus, 422 in ulcer of oesophagus, 418 in chronic oesophagitis, 418 in prolapsus ani, 920 in acute and chronic pharyngitis, 399, 405 in simple ulcer of stomach, 523, 524 in aphthous stomatitis, 330 in mercurial stomatitis, 348 in ulcerative stomatitis, 338 salts, use of, in catarrh of bile-ducts, 1057 in functional dyspepsia, 457 in gastralgia, 463 in acute intestinal catarrh, 696, 698 in acute yellow atrophy of liver, 1030

Sinapisms, use of, in cholera infantum, 762 in cholera morbus, 724 in enteralgia, 665 in acute intestinal catarrh, 688, 690

Singultus, in hepatic abscess, 1015

Siphon process for washing out of stomach in gastric dilatation, 604

Situation of biliary calculi, 1066

Sitz-baths, use of, in chronic intestinal catarrh, 716

Size of purulent collections in abscess of liver, 1006

Skim-milk, use of, in biliousness, 967 in diabetes mellitus, 218 in hyperæmia of liver, 988

Skin affections complicating gout, 118, 121 appearance of, in cancrum oris, 342 bronzing of, in diseases of pancreas, 1117 burns of, influence of, on causation of ulcer of intestine, 824 of simple ulcer of stomach, 488 condition of, in ascites, 1177 in chronic variety of general rheumatoid arthritis, 83 in scurvy, 176, 178 diseases, chronic, cure of, as a cause of tabes mesenterica, 1187 disorders, in constipation, 648 in functional dyspepsia, 451 in intestinal indigestion, 629 in jaundice, 980 in cirrhosis of liver, 995, 998 in acute yellow atrophy of liver, 1028 in rachitis, 156 dryness of, in diabetes mellitus, 204 in chronic intestinal catarrh, 709 eruptions in entero-colitis, 734 lesions of, in scurvy, 172 state of, in cholera morbus, 722 in dysentery, 796, 804 in pseudo-membranous enteritis, 766 in entero-colitis, 734, 736 in hepatic abscess, 1009 in lithæmia, 970 in carcinoma of liver, 1038 in acute pharyngitis, 394

Sleeplessness, in functional dyspepsia, 451 in chronic intestinal catarrh, 708 in intestinal indigestion, 628

Sloughing of intestine in invagination, 845

Soap, use of, in diabetes mellitus, 228

Social position, influence of, on causation of scrofula, 234 state, influence of, on causation of biliary calculi, 1064

Sodium arseniate, use of, in catarrh of bile-ducts, 1057 in fatty liver, 1050 in lithæmia, 972 benzoate, use of, in entero-colitis and cholera infantum, 757, 761 in intestinal indigestion, 636 in acute rheumatism, 62 bicarbonate, use of, in diabetes, 230 in pseudo-membranous enteritis, 774 in acute gastritis, 469 in acute and chronic intestinal catarrh, 693, 714 in chronic gastritis, 478 in intestinal ulcer, 829 in scrofula, 252 in dilatation of stomach, 609 in cancer of stomach, 576 in thrush, 335 in tonsillitis, 388 borate, use of, in glossitis parasitica, 359 chloride of gold and, in amyloid liver, 1046 in cirrhosis of liver, 1001 salts, use of, in gout, 132 sulphite and hyposulphite in aphthous stomatitis, 330

Solar plexus, lesions of, in acute peritonitis, 1136 symptoms of pressure upon, in diseases of pancreas, 1117

Solitary glands, lesions of, in cholera morbus, 721 in entero-colitis, 738 in acute intestinal catarrh, 675 in chronic intestinal catarrh, 702

Solvent treatment of biliary calculi, 1080

Sore throat, 390

Sour-smelling perspiration in acute rheumatism, 30, 31

Spasm, muscular, in muscular rheumatism, 75 in acute variety of general rheumatoid arthritis, 80 of rectum and anus, 909 reflex muscular, in acute gout, 119 seat of, in spasmodic stricture of oesophagus, 419, 420

Spasmodic stricture of oesophagus, 419

Spasms, tetanic, in dilatation of stomach, 595

Specific nature of dysentery, 792 origin of purpura, 191 of rheumatoid arthritis, 92

Sphincter ani, loss of power in, in ulceration of rectum and anus, 893 paralysis of, in diseases of spinal cord, 907 spasm, in fissure of anus, 888

Sphincterismus, treatment of, 916

Spinal applications, use of, in enteralgia, 664, 665 cord, effects of abnormal condition of, on rectum and anus, 906 and membranes, lesions of, in acute rheumatism, 40 inflammation complicating acute rheumatism, 40 irritation, influence of, on causation of pruritus ani, 909

Spirit-drinking, influence of, on causation of functional dyspepsia, 446

Splashing sound on palpation in dilatation of stomach, 597

Spleen, amyloid degeneration in rachitis, 153 lesions of, in acute intestinal catarrh, 677 in chronic intestinal catarrh, 705 in scurvy, 173 in tabes mesenterica, 1188 in acute yellow atrophy of liver, 1026 enlargement of, in amyloid liver, 1044 in cirrhosis of liver, 994 in hydatids of liver, 1104 in phosphorus-poisoning, 1031 in thrombosis and embolism of portal vein, 1096 in rachitis, 140 in hereditary syphilis, 305

Spondylitis following gonorrhoeal rheumatism, 106

Spontaneous disintegration of biliary calculi, 1066 origin of acute peritonitis, 1136, 1137

Sprays, medicated, use of, in acute pharyngitis, 398 in chronic pharyngitis, 405, 406

Squamous-celled form of cancer of oesophagus, 426

Starchy food, influence on causation of intestinal indigestion, 625

Steam inhalations, use of, in acute pharyngitis, 397, 398

Stenosis, influence on causation of dilatation of stomach, 587 of cardia as a cause of atrophy of stomach, 616 of ductus communis choledochus, 1082 of portal vein, 1095 of oesophagus, as a cause of atrophy of stomach, 616 of orifices of stomach in gastric cancer, 566 of pylorus in carcinoma of stomach, treatment, 578 in simple ulcer of stomach, 503 hypertrophic, 615

Stercoraceous vomit, in acute internal strangulation of intestines, 843 in intussusception, 848, 849 vomiting, in enteralgia, 662 significance of, in intestinal obstruction, 862 in stricture of bowel, 856

Stimulants, use of, in cancrum oris, 344 in cholera morbus, 725 in dysentery, 812 in entero-colitis and cholera infantum, 761 in acute gastritis, 469 in chronic intestinal catarrh, 716 in intestinal obstruction, 865 in abscess of liver, 1021 in aphthous stomatitis, 331 in gangrenous stomatitis, 344

STOMACH, ATROPHY OF, 616 Etiology, 616 General inanition and marasmus, 616 Result of stenosis of oesophagus or cardia, 616 Anæmia, 616 Secondary nature, 616 Acute infectious diseases, 616 Mineral poisoning, 616 Chronic gastric disease, 616 Morbid anatomy, 616 Gastric tubules, degeneration of, 616 atrophy of, 616 Symptoms, 616 Digestive disturbances, 616 Anorexia, 616 Vomiting, 616 Anæmia, 616 _Anomalies of Form and Position_, 617 Hour-glass contraction, 617 Diverticula, from ingestion of foreign substances, 617 Loop-shaped form, 617 In hernial sacs, 617 In diaphragmatic hernias, 617 umbilical hernias, 617 Displacements, 617 by tumors, 617 by tight-lacing, 617 Twisting of, 617

STOMACH, CANCER OF, 530 Definition, 530 Synonyms, 530 History, 530 Etiology, 531 Frequency, 532 Sex, 533 Age, 534 Geographical distribution, 535 Race, 535 Heredity, 535 Simple ulcer of stomach, 536 Chronic gastritis, 536 Depressing emotions, 536 Individual predisposition, 537 Local predisposition, 537 Symptoms, 537 Course of typical cases, 538 Loss of appetite, 538 Pain, 539 Seat, 539 Effect of food on, 539 Character of, 539 Absence of, 539 Functional disturbance of stomach, 540 Eructations, 540 Breath, fetid, 540 Hiccough, 540 Tongue, appearance, 540 Vomiting, 541 Character, 541 Effect of situation of cancer on, 541 Time of, 541 In pyloric form, 541 cardiac form, 541 Frequency, 542 Cause of, 542 Vomit, characters of, 542 Gastric fluids, detection of cancerous fragments in, 542 absence of free hydrochloric acid in, 543 tests for hydrochloric acid in, 543, 544 Vomit, bloody, 545 detection of blood in, 545 coffee-grounds, 546 Hemorrhages, frequency, 545 Dysphagia, 546 Tumor, presence of, 546 frequency of, 546 method of examining for, 546-549 seat of, 548, 561 size of, 548 consistence of, 548 inflation of stomach with carbonic acid gas in diagnosis of, 549 Constipation, 550 Diarrhoea, 550 Black stools, 550 Urine, state of, 550 Albuminuria, 551 Emaciation, 551 Debility, 551 Depression of spirits, 552, 554 Anæmia, 552 Cachexia, 552 Physiognomy, 552 Oedema, 553 Ascites, 553 Pulse, 553 Epigastric pulsation, 553 Hæmic murmurs, 553 Venous thrombosis, 553 Temperature, 554 Dyspnoea, 554 Headache and vertigo, 554 Intelligence, 554 Coma, 554 dyspnoeic, 555 cause of, 555 Secondary growths, 556 of liver, 556 diagnosis of, 556, 557 growth of peritoneum, 557 Enlargement of supra-clavicular glands, 557 Perforation, 558 frequency of, 558 formation of fistulæ, 558 gastro-colic fistula, 558 Fecal vomiting in gastro-colic fistulæ, 558 Death, cause of, 559 Duration, 559 In early life, 559 Complications, 560 Jaundice, 560 Pylethrombosis, 560 Peritonitis, 560 Catarrhal enteritis, 560 Chronic diffuse nephritis, 560 Pleuritis, 560 Pericarditis, 560 Hydrothorax, 560 Pyo-pneumothorax, 560 Oedema of lung, 560 Pneumonia, 560 Embolism, 560 Aphthæ, 560 Fatty degeneration of heart, 560 Phlegmasia alba dolens, 560 Insanity, 560 Purpura hæmorrhagica, 560 Chronic catarrhal gastritis, 560 Morbid anatomy, 560 Varieties, 561 relative frequency of, 561 Method of growth, 562 Of annular form, 562 Of diffuse form, 562 Relation to coats of stomach, 562 Ulceration, 562 causes of, 562 cicatrization of, 563 Suppuration, 563 Medullary form, 563 peculiarities of, 563 histology of, 563 tendency to metastasis, 563 origin in gastric tubules, 563 Cylindrical-celled epithelioma, 564 histology of, 564 origin from gastric tubules, 564 Scirrhous form, 564 histology of, 564 Colloid form, 564 histology of, 564 Flat-celled epithelioma, 565 Secondary form, 565 peculiarities of, 565 seat of, 565 Changes, secondary, in stomach, 566 Hypertrophy of gastric wall, 566 Obstruction of orifices of stomach, 566 Atrophy of stomach, 566 Dilatation of stomach, 566 Hour-glass contraction of stomach, 566 Adhesions to adjacent organs, 566 Metastasis, 567 relative frequency of, 567 causes of, 568 Wasting of various organs, 568 Pathenogenesis, 568 Theories regarding origin, 569 Diagnosis, 569 Presence of a tumor, value in, 569 Detection of fragments of cancer in vomit, 569 Absence of free hydrochloric acid in gastric fluid, 569 Value of coffee-ground vomit, 569 From gastric ulcer, 569-571 chronic gastric catarrh, 569-571 gastralgia, 571 nervous dyspepsia, 571 fibroid induration of stomach, 571 chronic interstitial gastritis, 571 non-malignant stenosis, 571 non-malignant tumors, 572 tumors of adjacent organs, 572 of liver, 572 cancer of pancreas, 572 tumors of omentum and intestines, 573 aneurism of aorta, 573 spasm of rectus muscle, 573 pernicious anæmia, etc., 574 cirrhosis of liver, 574 of position of growth, 574 of form of growth, 574 Mortality, 574 Prognosis, 575 Treatment, 576 Diet, 576 Pain, 576 Vomiting, 576 Acid eructations and heartburn, 576 Constipation, 577 Diarrhoea, 577 Hæmatemesis, 577 Stenosis of pylorus, 578 Use of condurango, 576 of opium, 576 of ice, 576 of hydrocyanic acid, 576 of bismuth, 576 of oxalate of cerium, 576 of rectal alimentation, 576 of antacids, 576 of charcoal, 576 of washing out of stomach, 577 Surgical measures, 577 Resection, 577 Gastrostomy for stenosis, 578 _Non-cancerous Tumors of_, 578 Polypi of, 578 Adenomata, 578 Myomata, 578 Myosarcomata, 578 Sarcoma, 578 Miliary aneurisms, 579 Cysts of mucous membrane, 579 Fibromata and lipomata, 579

STOMACH, CIRRHOSIS OF, 611 Definition, 611 Synonyms, 611 History, 611 Etiology, 612 Sex, influence on causation, 612 Age, influence on causation, 612 Alcohol, abuse of, 612 Syphilis, 612 Injury, 612 Chronic catarrhal gastritis, 612 Symptoms, 612 Of chronic dyspepsia, 613 Appetite, impaired, 613 Gastralgia, 613 Inability to ingest large quantities of food, 613 Loss of flesh and strength, 613 Vomiting, 613 Vomit, characters of, 613 Diagnosis, 613 Significance of long duration of dyspepsia, 613 Value of physical examination, 613 Presence of a tumor, 613 Stomach-tube, use of, 613 From cancer, 613 Morbid anatomy, 613 Contraction of stomach, 613 Cavity of stomach, size of, 613 Thickening of gastric walls, 614 Mucous membrane, lesions, 614 Muscular coat, hypertrophy of, 614 Fibrous tissue, increase of, 614 Microscopical appearances of mucous membrane, 614 Gastric tubules, atrophy of, 614 Formation of adhesions, 614 Peritoneum, lesions of, 614 Prognosis, 614 grave nature of, 614 Treatment, 615

Stomach, condition of, in rachitis, 153

STOMACH, DILATATION OF, 586 Definition, 586 Synonyms, 586 History, 586 Etiology, 587 Stenosis of pyloric orifice, 587 Carcinoma, 587 Cicatricial growths from simple ulcer, 587 from corrosive poisons, 587 Hypertrophy of pyloric orifice, 587 Obstruction of pylorus by polypi, 587 Narrowing of pylorus by tumors of adjacent organs, 587 Congenital stenosis, 588 Spasm of pylorus, 588 Obstruction from distortion and displacement, 588 Without obstruction (atonic form), 589 Abnormal gastric contents, 589 Excessive eating and drinking, 589 use of beer, 589 Abuse of condiments, 589 of tobacco, 589 Fermentation of contents of stomach, 589 Impairment of gastric muscular force, 590 Organic changes in muscular coat, 590 Destruction by ulcers and cancers, 590 Chronic catarrhal gastritis, 590 peritonitis, 590 Degenerations (fatty, colloid, and amyloid), 590 Oedema of coats of stomach, 590 Cirrhosis of stomach, 590 Mechanical restraint of gastric movements, 590 Adhesions, 590 Weight of herniæ, 590 Impaired general nutrition, 590 Paresis from neuropathic causes, 590 Frequency of, in its causal relation, 592 Age, 592 Infrequency of atonic form among the poor, 592 Sedentary life, 592 Symptoms, 592 Disturbance of gastric functions, 592 Impaired appetite, 593 Increased appetite (polyphagia), 593 Thirst, 593 Pain, 593 Fulness and weight, 593 Eructations and heartburn, 593 Gases, nature of, 593 inflammability of, 593 Vomiting, 593 time of, 593 Vomited matters, abundance of, 593 amount of, 593 fermentation of, 594 odor of, 594 presence of micro-organisms in, 594 sarcinæ, bacteria, etc. in, 594 absence of free hydrochloric acid in, 594 presence of blood in, 594 Constipation, 594 Diarrhoea, 594 Urine, state of, 594 Dyspnoea and cardiac palpitation, 595 General condition, 595 Tetanic spasms, 595 seat of, 595 muscles of calves and abdomen, 595 of flexors of hand and forearm, 595 Coma, 596 Temperature, 596 Physical signs, 596 Prominence of epigastric region, 596 Peristaltic movements, 596 Splashing sound on palpation, 597 method of producing, 597 Percussion, 598 Auscultation, 598 Displacement of adjacent organs, 599 Morbid anatomy, 599 Degrees of, 599 Capacity, 599 Fundus, size of, 599 Oesophagus, dilatation of, 599 Hypertrophy of gastric walls, 599 Atrophy of gastric walls, 599 Fatty and colloid degeneration of muscular coats, 600 Mucous membrane, state of, 600 Atrophy of abdominal viscera, 600 Diagnosis, 600 Distension of stomach with carbonic acid gas in, 596, 601 Ingestion of water to aid, 598, 602 Stomach-tube, use of, 597, 602 Determination of lower gastric border, 598, 602 From chronic catarrhal gastritis, 603 atonic dyspepsia, 603 Prognosis and course, 603 Death, mode of, 603 Treatment, 603 Prophylactic, 603 Diet, 603, 608 Washing of stomach, 603 object of, 604 modes of, 604 apparatus used in, 604-607 siphon process, 604-606 stomach-pump, 604 frequency of, 607 objections to, 607 contraindications, 608 Of heartburn, 609 Of anæmia, 609 Of constipation, 609 Use of electricity, 608 of nux vomica, 609 of strychnia, 609 of abdominal bandage, 609 of hydrochloric acid, 609 of pepsin, 609 of sodium bicarbonate, 609 of Carlsbad water, 609 of iron and arsenic, 609 of resection of pylorus, 609 of gastrotomy, 609 _Acute Dilatation of_, 610 Definition, 610 Etiology, 610 Symptoms, 610 Pain, 610 Tympanites, 610 Vomiting, cessation of, 610 Prognosis, 610 Treatment, 610 Use of stomach-tube, 610

Stomach, functional and inflammatory diseases of, 436

STOMACH, HEMORRHAGE FROM, 580 Definition, 580 Synonyms, 580 Etiology, 580 Ulcer of stomach, 580 Cancer, 580 Traumatism, 580 Corrosive poisons, 580 Diseases of gastric vessels, 580 Aneurism of gastric arteries, 580 Varices of veins, 580 Degenerations of vessels, 581 Congestion, active, 581 passive, 581 Portal vein, 581 Pulmonary blood-vessels, 581 Heart disease, 581 Violent vomiting, 581 Acute infectious diseases, 581 Hemorrhagic diathesis, 582 Malaria, 582 Anæmia, 582 Cholæmia, 582 Bright's disease, 582 Neuropathic conditions, 582 Melæna neonatorum, 582 Bursting aneurisms, 582 Idiopathic causes, 582 Hemorrhage from nose, mouth, lungs, etc., 583 Symptoms. See _Gastric Ulcer_. Morbid anatomy, 583 Source of, 583 From diapedesis, 583 From rupture of blood-vessels (rhexis), 583 Diagnosis, 584 Significance of black stools, 584 Examination of vomit, 584 From hysterical vomiting, 584 Examination of nose and throat, 584 From oesophageal hemorrhage, 584 Use of oesophagoscope in, 584 From hæmoptysis, 584, 585 Of causes, 585 Prognosis, 585 Treatment. See _Gastric Ulcer_.

Stomach, lesions of, in cholera infantum, 743, 744 in entero-colitis, 739 minor organic changes in, 611 organic diseases of, 480

STOMACH, RUPTURE OF, 618 Etiology, 618 Injury, 618 From over-distension by solids or gas, 618 Symptoms, 618 Prognosis, 618 Treatment, 618

STOMACH, SIMPLE ULCER OF, 480 Definition, 480 Synonyms, 480 History, 480 Etiology, 481 Frequency, 481, 482 Sex, influence on causation, 483 Age, influence on causation, 483 when most frequent, 484, 485 Climate, influence on causation, 485 Geographical distribution, 485 Poverty, 486 Occupation, 486 Needle-women, cooks, and maid-servants, 486 Shoemakers and tailors, 486 Injury, 486 Corrosive poisons, 486 Pulmonary phthisis, influence of, on causation, 487 Menstrual disorders, 487 Chlorosis and anæmia, 487 Diseases of heart and blood-vessels, 487 of kidneys, 487 of stomach, 488 Diabetes mellitus, 488 Intermittent fever, 488 Abuse of alcohol, 488 Burns of skin, 488 Symptoms, 488 Pain, 488 Character, 489 Localized nature of, 489 Seat, 489 Effect of food upon, 489 pressure, 490 rest, 490 mental emotion, 490 Distribution of, 490 Intermittence of, 491 Causes of, 491 Vomiting, 491 Time of, 491 Character of, 491, 492 Causes of, 492 Hemorrhage, 492 Quantity, 492 Voided by bowels, 492 appearance of stools in, 493 Hæmatemesis, 493 Appearance of blood in, 493 Causes, 493 Hemorrhage, effect upon other symptoms, 494 Relief of pain after, 494 Sources of, 494 Of indigestion, 494 Appetite, loss of, 494 Thirst, 494 Constipation, 494, 495 Flatulence, 494 Nausea and vomiting, 494 Headache, dizziness, etc., 494 Tongue, condition, 495 Amenorrhoea, 495 Temperature, 495 General health, 496 Physiognomy, 496 Cachectic dropsy, 496 Physical signs, 496 Perforation, 496 Frequency, 497 in sexes, 497 May occur without symptoms, 497 Cause, 498 Pain in, 498 Collapse in, 498 Physiognomy in, 498 Temperature, 498 Pulse, 498 Vomiting, 498 Constipation, 498 Thirst, 498 Respiration, 498 Suppression of urine, 498 Abdomen, state of, 498 Tympanites, 498 Retraction of testicle, 498 Position of patient, 498 Death in, cause of, 499 Peritonitis in, 499 Peritoneal abscesses, 499 Pyo-pneumothorax subphrenicus of Barlow and Wilks, 499 Into pleural cavities, 500 transverse colon, 500 pericardium, 500 Sequelæ, 500, 503 Gastro-cutaneous fistulæ, 500 Stenosis of pylorus, and dilatation, 503 Complications, 502 Pylephlebitis, 502 Chronic peritonitis, 502 Catarrhal gastritis, 502 Interstitial gastritis, 502 Extension to pleura, 503 Fatty degeneration of heart, 503 Embolic pneumonia, 503 Pulmonary tuberculosis, 503 Bright's disease, 503 Heart disease, 503 Hepatic degenerations, 503 Course, 500 Forms of, 501 Latent, 501 Acute perforating, 501 Hemorrhagic, 501 Gastralgic-dyspeptic, 501 Chronic hemorrhagic, 501 Cachectic, 501 Recurrent, 501 Stenotic, 501 Duration, 501 Terminations, 501 Tendency to recovery, 501 Causes of death, 502 Mortality, 502 Morbid anatomy, 503 Ulcers, number, 503 Position, 503 Size, 504 Shape, 504 tendency to become conical, 504 Tendency to transverse extension, 504 Appearance of edges, 505 floor, 505 Microscopic appearance of surrounding tissue, 505 Cicatrization, 506 method, 506 deformities of stomach from, 506 Peritoneum, lesions of, 506 Perforations, seat, 509 Lesions resulting from, 507 Ulcerations of surrounding viscera, 507 Circumscribed peritoneal abscess, 507 Gastro-cutaneous fistulæ, 508 -colic fistulæ, 508 -duodenal fistulæ, 508 Pneumo-pericardium, 508 Gastro-pleural fistulæ, 508 Emphysema of areolar tissue, 509 time of appearance, 509 nature of the gas, 509 Gas in arteries, 510 Hemorrhage, source of, 510 Changes in blood-vessels, 510 Embolism, 510 Thrombosis of vessels about ulcer, 510 Fatty and waxy degeneration and calcification of gastric vessels, 511 Varicosities of veins, 511 Aneurism of vessels about ulcer, 511 Pathenogenesis, 512 Theories regarding development, 512 Digestive action of gastric juice on development, 512 Inflammatory theory of origin, 512 Neurotic theory of origin, 512 Theory, circumscribed hemorrhagic infiltration, 512 Disease of gastric blood-vessels, 513 Böttcher's view of mycotic origin, 513 Artificial production of, 514 Daettwyler and Cohnheim's experiments, 514 Diagnosis, 514 From nervous gastric disorders, 515 nervous vomiting, 516 gastralgia, 516 gastric crises, 517 cancer. See _Stomach, Cancer of_. chronic catarrhal gastritis, 517 hepatic colic, 517 Prognosis, 518 Treatment, 519 Removal of sources of irritation, 519 Importance of rest, 519 Diet, 519-522 Use of nutrient enemata, 519 Milk, 519 peptonized, 520 Leube's beef, solution of, 520 Beef-juice, freshly-expressed, 521 Avoidance of coarse food and fruits, 521 Of pain, 524 Of vomiting, 524 Of hemorrhage, 525 Of dyspepsia, 527 Of perforation, 527 Importance of maintaining nutrition, 527 Of anæmia, 528 Of sequelæ, 528 Of convalescence, 529 Carlsbad waters, use of, 522 method of preparing, 522 Use of stomach-tube, 523, 525 method of, 523 of bismuth, 523, 524 of argentum nitratis, 523, 524 of opium, 524 of codeia, 524 of astringents to relieve pain, 524 of tr. ferri-chlor. to relieve pain, 524 of counter-irritation, 524 of subcutaneous injection of milk, oil, and beef-tea, 525 of ice, 525 of antiemetics, 525 of ingluvin, 525 of ergotin in hemorrhage, 525 of dil. sulphuric acid in hemorrhage, 526 of acetate of lead in hemorrhage, 526 of ligature of upper extremities in hemorrhage, 526 of rubber balloon tampon in hemorrhage, 526 of alkalies in dyspepsia, 527 of poultices in perforation, 527 of laparotomy in perforation, 527 of inunctions of oil, 527 of iron in anæmia, 528 hypodermic, 528

Stomach, tubercular ulcers of, 529 typhoid ulcers of, 529 syphilitic ulcers of, 529 necrotic ulcers of, 529 catarrhal ulcers of, 529 follicular ulcers of, 529

Stomach and intestines, lesions of, in acute yellow atrophy of liver, 1026 perforation of, by gall-stones, 1068, 1074

Stomach-pump, use of, in chronic gastritis, 478

Stomach-tube, use of, in cancer of oesophagus, 428 in dilatation of oesophagus, 434 in organic stricture of oesophagus, 426 in paralysis of oesophagus, 430 in simple ulcer of stomach, 523, 525 in washing of stomach in gastric dilatation, 604 value of, in diagnosis of organic stricture of oesophagus, 424 in diagnosis of cirrhosis of stomach, 613 in diagnosis of dilatation of stomach, 597, 602

STOMATITIS, 321 Definition, 321 Varieties, 321 _Stomatitis Catarrhalis_, 321 Synonyms, 321 Definition, 321 Etiology, 321 Irritation of alimentary canal, 321 Local causes, 321 Foreign substances, 321, 322 Medicines, certain, 322 Morbid dentition, 322 Protracted crying, 322 Distant causes, 322 Intestinal derangements, 322 Improper food, 322 Cold, 322 Acute exanthemata, 322 Age, 322 Symptoms, 322 Initial, 322 Heat of mouth, 322 Unwillingness to nurse, 322 Painful deglutition, 323 Increased secretion, 323 Impaired taste, 323 Fetor of breath, 323 Loss of appetite, 323 Diarrhoea, 323 Swelling of lymphatic glands, 323 Pyrexia, 323 Chronic form, 323 Vomiting, 323 Duration, 323 Pathology and morbid anatomy, 323 Hyperæmia of tissues, 324 Mucous membrane, state of, 324 Tongue, engorgement of, 324 Ulcerations, 324 Congestion of palate, 324 Lips, state of, 324 Diagnosis, 325 From gastric catarrh, 325 Prognosis, 325 Treatment, 325 Correction of intestinal disturbances, 325 Local, 325 Ice, use of, 325 Salicylic acid, 325 _Aphthous Stomatitis_, 325 Definition, 325 Synonyms, 326 Etiology, 326 Age, 326 Scrofula, influence on causation, 326 Heredity, influence on causation, 326 Improper food, influence on causation, 326 Excessive heat, influence on causation, 326 Overwork, influence on causation, 326 Excessive menstruation, influence on causation, 326 Pregnancy, influence on causation, 326 Debility, influence on causation, 326 Chronic diseases, influence on causation, 326 Acute exanthemata, influence on causation, 326 Exciting causes, 326 Morbid dentition, 326 Dampness of atmosphere, 326 Personal habits, 326 Drugs, 326 Pathology and morbid anatomy, 326 Vesicles, nature of, 327 rarity of their detection, 327 Lesions, characteristics of, 327 Ulceration, anatomy of, 328 cause, 328 method of repair, 328 Lesions, seat of, 328 in confluent, 328 in discrete, 328 Symptoms and course, 328 Discrete form, 328 Confluent form, 328, 329 Constitutional, 329 Diarrhoea, 329 Vomiting, 329 In parturient women, 329 Local, 329 Heat of mouth, 329 Increased secretion, 329 Difficult mastication, 329 Duration, 329 Discrete form, 329 Confluent form, 329 Complications and sequelæ, 329 Diagnosis, 329 Of confluent form from ulcerative stomatitis, 330 Of confluent form from thrush, 330 Prognosis, 330 Of confluent form, 330 In parturient women, 330 Treatment, 330 Diet, 330 Local, 330 Use of sodium hyposulphite, 330 of ice, 330 of astringents, 330 of iodoform, 330 Of confluent form, 331 Necessity of constitutional, 331 Use of iron and quinia, 331 of stimulants, 331 of chlorate of potassium, 331 _Stomatitis Parasitica_ (_Thrush_), 331 Definition, 331 Synonyms, 331 History, 331 Etiology, 331 Innutrition, influence on causation, 332 Want of cleanliness, influence on causation, 332 Age, influence on causation, 332 Season, influence on causation, 332 Exhausting diseases, influence on causation, 332 Intestinal disorders, influence on causation, 332 Contagiousness, 332 Pathology and morbid anatomy, 332 Deposit, description of, 332 microscopic appearance, 333 seat of, 333 Parasite of, 333 Oïdium albicans, nature, 333 Mucous membrane, condition, 333 Deposit in oesophagus and larynx, 334 in intestinal canal, 334 Symptoms, 334 Initial, 334 Cry in, 334 Growth, seat of, 334 Constitutional, 334 Duration, 334 Cause of death, 334 Diagnosis, 334 Value of microscopic examination, 335 Treatment, 335 Preventive, 335 Diet, 335 Local, 335 Constitutional, 335 Use of astringents, 335 of sodium bicarbonate, 335 of sodium salicylate, 335 _Stomatitis Ulcerosa_, 336 Synonyms, 336 Definition, 336 Etiology, 336 Atmosphere, impure, 336 Uncleanliness, 336 Food, improper, 336 Measles, influence on causation, 336 Age, influence, on causation, 336 Season, influence on causation, 336 Sex, influence on causation, 336 Contagiousness, 336 Pathology, 336 Fibro-purulent infiltration of lymph-spaces, 336 Ulcers, description of, 336, 337 seat of, 336 course of, 337 Symptoms, 337 Initial, 337 Mouth, heat of, 337 Appetite, loss of, 337 Difficult deglutition, 337 Lymphatic gland, swelling, 337 Salivation, excessive, 337 Duration, 337 Diagnosis, 337 From mercurial stomatitis, 338 cancrum oris, 338 Prognosis, 338 Treatment, 338 Preventive, 338 Hygienic, 338 Air, fresh, necessity of, 338 Constitutional, 338 Local, 338 Use of antiseptics, 338 of astringents, 338 of potassium chlorate, 338 Extraction of carious teeth, 338 _Stomatitis Gangrenosa_ (_Cancrum Oris_), 338 Definition, 338 Synonyms, 338 History, 338, 339 Etiology, 339 Hygiene, improper, 339 Endemic character, 339 Age, 339 Sex, 340 Acute exanthemata, 340 Symptoms, 340 Initial, 340 Tumefaction of cheek, 340 Ulceration of cheek, 340 Odor of breath, 340 State of gums, 340 Difficult deglutition, 340 Eschar, characters of, 340 Constitutional, 341 Intelligence, 341 Pulse, 341 Appetite, 341 Gastro-intestinal canal, 341 Death, cause of, 341 Complications and sequelæ, 341 Pneumonia, 341 Lungs, gangrene, 341 Vulva, gangrene, 341 Larynx and pharynx, gangrene, 341 Hemorrhage, 341 Pathology and morbid anatomy, 341 Nature, 341 Character and seat of ulceration, 341 Ulceration, color, 342 rapidity, 341 of gums, 342 Gangrene, date of appearance, 342 Skin, appearance of, 342 Perforation of cheek, 341, 342 Glands, swelling of, 342 Diagnosis, 342 From malignant pustule, 342 Prognosis, 342 Treatment, 343 Local, 343 Cauterization, 343 by nitric acid, 343 by muriatic acid, 343 by acid nitrate of mercury, 343 by actual cautery, 343 Use of disinfectants, 343 Constitutional, 343 Use of stimulants, 344 _Stomatitis, Toxic_, 344 Definition, 344 _Stomatitis Mercurialis_, 344 Definition, 344 Synonyms, 344 Etiology, 344 Special vulnerability to toxic influence of mercury, 344 Difference in susceptibility, 344 Depraved constitution, 344 Idiosyncrasy, 344 Occupation, 344 Symptoms, 345 Subjective, 345 Gums, state of, 345 Mouth, tenderness of, 345 Teeth, state of, 345 Difficult deglutition, 345 Saliva, increase of, 345 amount secreted, 345 Lymphatic glands, enlargement, 346 Tongue, inflammation of, 346 Larynx, oedema of, 346 Gangrene of mucous membranes, 346 Necrosis of inferior maxilla, 346 Constitutional, 345, 346 Fever, 346 Cachexia, 346 Duration, 346 Complications, 346 Erysipelas, 346 Pyæmia, 346 Metastatic abscesses, 346 Pathology and morbid anatomy, 346 Nature of, 346 Microscopic appearance of detritus, 346 Ulceration of gums, 347 Characters of ulcers, 347 Mucous membrane, lesions of, 347 Tongue, inflammation of, 347 Tongue and mucous membrane, ulcers of, 347 Teeth, loosening of, 347 Larynx and pharynx, lesions of, 347 Diagnosis, 347 Prognosis, 347 Death, cause of, 347 Treatment, 347 Preventive, 347 Use of potassium chlorate, 348 of opium, 348 of astringents, 348 of detergents, 348 of enemata, nourishing, 348 of tonics, 348 Local, 348 Constitutional, 348 Of glossitis, 348 Of oedema of larynx, 348

Stomatitis, catarrhal, in morbid dentition, 373

Stomatorrhagia, 370 Definition, 370 Synonym, 370 Etiology, 370 Disease or injury, 370 Hæmophilia, 370 Vicarious of menstruation, 370 Symptoms, 371 Gums most frequent source, 371 Results, 371 Diagnosis, 371 Prognosis, 371 Treatment, 371 Use of ergot, 371 of turpentine, 371 of astringent washes, 371

Stony concretions as a cause of intestinal obstruction, 838

Stools, appearance in hemorrhage from bowels, 833 and characters of, in chronic intestinal catarrh, 707 black, in hemorrhage from bowels, 833 in intestinal ulcer, 827 in cancer of stomach, 545 in simple ulcer of stomach, 492, 493 bloody, in carcinoma of pancreas, 1126 in intestinal ulcer, 827 and mucous, in intestinal cancer, 871 characters of, in catarrh of bile-ducts, 1054, 1055 in cholera morbus, 722 in acute colitis, 684 in constipation, 646 in dysentery, 796, 803 in pseudo-membranous enteritis, 766 in acute intestinal catarrh, 678, 680-682 in chronic intestinal catarrh, 706-708 in intestinal indigestion, 627 in intussusception, 848 in intestinal ulcer, 827 in cirrhosis of liver, 994 in fatty liver, 1048 in proctitis, 887 in ulceration of rectum and anus, 893 in tabes mesenterica, 1190 condition of, in hyperæmia of liver, 986, 987 fatty, in diseases of pancreas, 1115, 1122, 1125, 1131 frequency and characters, in cholera infantum, 741 in entero-colitis, 733, 734, 736 in non-malignant rectal stricture, 886 mucous, in proctitis, 684 number of, in acute intestinal catarrh, 679 of hepatic colic, 1073 mode of searching for calculi in, 1073 phosphorescent, in phosphorus-poisoning, 1031 significance of cancerous fragments in, in malignant diseases of intestine, 873 undigested striped muscular fibres in, in pancreatic diseases, 1116

Stramonium ointment, use of, in hemorrhoids, 923 in acute oesophagitis, 418

Strangulation, acute internal, as a cause of intestinal obstruction, 840 of bowels, acute internal, 840 removal of hemorrhoids by, 924

Strangury in dysentery, 803

Stricture, cicatricial, in syphilitic pharyngitis, 407 congenital, a cause of intestinal obstruction, 835 following chronic oesophagitis, 417 of bowel, 854 following chronic intestinal catarrh, 710 of oesophagus, 419 spasmodic, 419 seat of, in organic stricture of oesophagus, 424 of rectum, symptoms, 856 malignant, of rectum and anus, 902 non-malignant, of rectum, 885 treatment, 917

Strongylus longevaginatus, 956

Structural diseases of liver, 983

Struma, See _Scrofula_. as a cause of ulceration of rectum and anus, 894

Strumous articular disease, as a sequel of gonorrhoeal rheumatism, 106 diathesis, influence on causation of intestinal indigestion, 624 form of intestinal indigestion, treatment, 636

Strychnia, effect on rectum, 911 use of, in constipation, 654-657 in diabetes mellitus, 227 in functional dyspepsia, 455 in gastralgia, 463 in chronic intestinal catarrh, 714, 715 in intestinal indigestion, 636 in dilatation of oesophagus, 435 in oesophageal paralysis, 430 in prolapsus ani, 921 in rachitis, 164 in dilatation of stomach, 609

Stupes, digitalis, use of, in cirrhosis of liver, 1001 turpentine, use of, in perihepatitis, 990

Stupor in abscess of liver, 1010 in cholera infantum, 742

Subacute articular rheumatism, 46 symptoms, 46

Substernal pain in acute oesophagitis, 413

Sucking, influence on causation of macroglossia, 350

Suffocation, from hypertrophy of tongue, 350 sensation of, in organic stricture of oesophagus, 423

Sugar, absorption of, in digestion, 623 in urine of diabetes mellitus, amount of, 207 substitutes for, in food of diabetics, 224 tests for, in diabetic urine, 211-217

Suicide, relation of displacements of colon to, 647

Sulphate of copper, use of, in acute and chronic intestinal catarrh, 696, 717 in superficial glossitis, 357 in syphilitic pharyngitis, 408 of manganese, use of, in fatty liver, 1050 of sodium, use of, in biliary concretions, 1079 in intestinal indigestion, 636 of zinc, enemata of, in chronic intestinal catarrh, 714, 717 and alum, use of, in pruritus ani, 917

Sulpho-carbolate of calcium, use of, in acute intestinal catarrh, 696

Sulphur, use of, in constipation, 656 in pseudo-membranous enteritis, 775

Sulphuric acid, use of, in purpura, 193 in simple ulcer of stomach, 526

Summer heats, influence on causation of cholera infantum, 727 of entero-colitis, 727 of acute intestinal catarrh, 669

Superficial glossitis, 355

Supporting treatment in hereditary syphilis, necessity of, 315

Suppositories, iodoform, use of, in fissure of anus, 912 medicated, use of, in seat-worms, 951 nutrient, 929

Suppuration, duodenal, in chronic intestinal catarrh, 703 of bone, influence on causation of amyloid liver, 1041 seat of, in parenchymatous glossitis, 363 symptoms of, in tonsillitis, 383

Suppurative hepatitis, 1002 pylephlebitis, 1097

Supra-clavicular glands, enlargement, in gastric cancer, 557

Surgical measures in gastric cancer, 577 treatment of intestinal obstruction, 865

Sutures of head, condition of, in rachitis, 147

Sweating, in acute rheumatism, 30, 31 in hepatic abscess, 1009, 1010 in trichinosis, 960 of head, in rachitis, 146

Swedish movements, value, in intestinal indigestion, 632

Sympathetic nerve, to production of glycosuria, 196 nervous symptoms, in chronic gastritis, 474

Symptomatology, general, of pancreatic disease, 1114

Symptoms due to migration of gall-stones, 1070 to presence of gall-stones of original site, 1069 of Anchylostomum duodenale, 955 of Ascaris lumbricoides, 953 of ascites, 1175 of catarrh of bile-ducts, 1053 of occlusion of biliary passages, 1086 of biliousness, 966 of compression and contraction of bowel, 857 of hemorrhage from bowels, 830 of stricture of bowel, 856 of cancrum oris, 340 of cholera infantum, 741 of cholera morbus, 722 of acute colitis, 684 of constipation, 645, 853 of diabetes mellitus, 204 of acute duodenitis, 682 of dysentery, 802 of functional dyspepsia, 448 of enteralgia, 660 of entero-colitis, 733 of pseudo-membranous enteritis, 765 of Filaria medinensis, 963 sanguinis, 963 of fistula in ano, 898 of fluke-worms, 947 of gastralgia, 460 of acute gastritis, 467 of chronic gastritis, 472 of superficial glossitis, 357 of chronic superficial glossitis, 357 of parenchymatous glossitis, 360 of chronic parenchymatous glossitis, 368 of glossitis parasitica, 359 of glossanthrax, 368 of gout, 118, 120 of hemorrhoids, 883 internal, 884 of hepatic colic, 1070 of hepatic glycosuria, 973 of acute ileitis and jejunitis, 683 of acute intestinal catarrh, 677 of chronic intestinal catarrh, 706 of intestinal indigestion, 626 time of appearance after eating, 629 obstruction from foreign bodies, 839 of acute internal strangulation of intestines, 840 of intestinal ulcer, 825 of cancer of intestines, 869 of lardaceous degeneration of intestine, 874 of intussusception, 848 of jaundice, 977 of lithæmia, 969 of abscess of liver, 1008 of acute yellow atrophy of liver, 1026 of amyloid liver, 1043 of carcinoma of liver, 1036 of cirrhosis of liver, 993 of fatty liver, 1048 of hydatids of liver, 1102 of hyperæmia of liver, 986 of liver-flukes, 1110 of liver in phosphorus-poisoning, 1031 of morbid dentition, 371 of cancer of oesophagus, 427 of dilatation of oesophagus, 431 of paralysis of oesophagus, 429 of organic stricture of oesophagus, 423 of spasmodic stricture of oesophagus, 419 of ulceration of oesophagus, 418 of acute oesophagitis, 413 of chronic oesophagitis, 417 of carcinoma of pancreas, 1124 of hemorrhage into pancreas, 1129 of acute pancreatitis, 1118 of acute secondary pancreatitis, 1120 of chronic interstitial pancreatitis, 1122 of obstruction of pancreatic ducts, 1131 of paratyphlitis, 819 of perihepatitis, 989 of hemorrhagic effusion of peritoneum, 1181 of acute diffuse peritonitis, 1141 of chronic peritonitis, 1162 of infantile peritonitis, 1173 of perforative form of peritonitis, 1155, 1156 of tubercular peritonitis, 1165 of peri-rectal and anal abscesses, 896 of acute pharyngitis, 394-396 of chronic pharyngitis, 404 of syphilitic pharyngitis, 407 of tuberculous pharyngitis, 401 of proctitis, 684, 887 of thrombosis and embolism of portal vein, 1096 of purpura, 187 of purpura hæmorrhagica, 188 of purpura rheumatica, 189 of purpura simplex, 187 of suppurative pylephlebitis, 1099 of hypertrophic stenosis of pylorus, 615 of rachitis, 146 of dilatation of rectal pouches, 885 of neuralgia of rectum, 910 of non-malignant stricture of rectum, 886 of obstruction of rectum, 891 of polypi of rectum, 882 of prolapse of rectum, 881 of rodent ulcer of rectum, 889 of follicular ulceration of rectum and anus, 895 of ulceration of rectum and anus, 893 of fissure of rectum and anus, 888 of acute rheumatism, 26 of chronic articular rheumatism, 71 of gonorrhoeal rheumatism, 104 of muscular rheumatism, 75 of rheumatoid arthritis, 80 of general progressive form of rheumatoid arthritis, 80 of partial form of rheumatoid arthritis, 84 of seat-worms, 951 of scrofula, 243 of scurvy, 176 of atrophy of stomach, 616 of cancer of stomach, 530 of cirrhosis of stomach, 612 of dilatation of stomach, 592 of acute dilatation of stomach, 610 of hemorrhage from stomach, 493 of simple ulcer of stomach, 488 of perforation in simple ulcer of stomach, 496 of rupture of stomach, 618 of aphthous stomatitis, 328 of catarrhal stomatitis, 322 of mercurial stomatitis, 345 of stomatitis ulcerosa, 337 of stomatorrhagia, 371 of hereditary syphilis, 273 of tabes mesenterica, 1189 of tape-worm, 939 of thrush, 334 of hypertrophy of tongue, 350 of syphilitic ulceration of tongue, 370 of tubercular ulceration of tongue, 369 of tonsillitis, 381 of trichinosis, 959 of Triocephalus dispar, 954 of typhlitis and perityphlitis, 818

Syncope in hemorrhage from bowels, 833

Synonyms of Anchylostomum duodenale, 955 of Ascaris lumbricoides, 952 of Bothriocephalus latus, 938 of cancrum oris, 338 of cholera morbus, 719 of constipation, 638 of Distomum hepaticum, 946 of functional dyspepsia, 436 of enteralgia, 658 of pseudo-membranous enteritis, 763 of Filaria sanguinis, 963 of gout, 108 of superficial glossitis, 355 of parenchymatous glossitis, 359 of glossitis parasitica, 357 of acute intestinal catarrh, 667 of lardaceous degeneration of intestine 874 of intestinal ulcers, 823 of macroglossia, 349 of morbid dentition, 371 of cancer of oesophagus, 426 of dilatation of oesophagus, 430 of organic stricture of oesophagus, 422 of spasmodic stricture of oesophagus, 419 of oesophagitis, 409 of acute oesophagitis, 409 of chronic oesophagitis, 416 of Oxyuris vermicularis, 950 of acute pharyngitis, 390 of chronic pharyngitis, 402 of syphilitic pharyngitis, 406 of tuberculous pharyngitis, 400 of hypertrophic stenosis of pylorus, 615 of rheumatism, acute, 19 of chronic articular rheumatism, 69 of gonorrhoeal rheumatism, 102 of muscular rheumatism, 74 of rheumatoid arthritis, 78 of scrofula, 231 of scurvy, 167 of cancer of stomach, 530 of cirrhosis of stomach, 611 of dilatation of stomach, 586 of hemorrhage from stomach, 580 of simple ulcer of stomach, 480 of aphthous stomatitis, 326 of catarrhal stomatitis, 321 of mercurial stomatitis, 344 of stomatitis ulcerosa, 336 of stomatorrhagia, 370 of Tænia echinococcus, 943 of Tænia saginata, 933 of Tænia solium, 935 of tabes mesenterica, 1182 of thrush, 331 of tongue-tie, 349 of tonsillitis, 379

Synovial membranes, lesions of, in gout, 115 in acute rheumatism, 46 in chronic articular rheumatism, 70 in gonorrhoeal rheumatism, 103 in rheumatoid arthritis, 86

Syphilides, pustular, in hereditary syphilis, 279

Syphilis, distinguished from carcinoma of liver, 1040

SYPHILIS, HEREDITARY, 254 Marriage of syphilitics, 255-265 Essential nature of syphilis, 256 of tertiary syphilis, 257 Duration of transmissive power, 257-260 Period when marriage is admissible, 260, 261 Treatment of married syphilitics, 260, 261, 269 Methods of infection between parents, 262, 264 Infection of mother by foetus in utero, 262 by conception, 264 Colles' law of infection of mothers of syphilitic children, 263 Modes of infection of the child, 265 From the father, 265 From the mother, 266 By infection previous to conception, 266 at moment of conception, 262, 267 during utero-gestation, 267 during birth, 269 Summary of facts in regard to transmission, 269, 270 Placental, pathology of, 271, 272 Modes of manifestation, in offspring of syphilitics, 272 Danger to offspring in untreated syphilitics, 272 Influence of interval between infection and conception on development of, 272 Mortality of syphilitic children, 272, 273 Symptoms and course, 273 Average time of appearance, 273, 274 Symptoms of secondary period, 274 Pemphigus, 274 Objections to specific origin of, 274 Arguments favoring specific origin of, 275 Description of eruption, 276 Diagnosis, 276 Coryza, 277 Symptoms of, 277 Difficulty in suckling from, 277 Flattening of nose, 277 Erythema, or Roseola, 277 Seat and character of, 277, 278 Diagnosis, 278 Papules, 278 Seat and character, 278 Mucous patches, 278 Seat and character, 278 Diagnosis, 278, 279 Danger of transmission from, 279 by nursing-bottles, etc., 279 by caresses and kisses, 279 Condylomata, 279 Seat and character, 279 Pustular syphilides, 279 Date of appearance, 279 Seat and character, 279 Diagnosis, 279, 280 Furuncular eruption, 280 Iritis, 280 Specific character, 280 Symptoms, 280 Age when most frequent, 281 Prognosis, 281 Symptoms of intermediate period, 281 Of tertiary period, 282 Ear disorders, 282 catarrh of middle, 282 Deafness, 282, 283 duration of, 283 Liver, disease of, 283 enlargement of, 283 Pathology, 283, 284 Diagnosis, 286 Bones, disease of, 286 Pathology, 286-288 Osteo-chondritis, symptoms, 288 Most attacked, 288 Pseudo-paralysis, 289, 312 Formation of osteophytes, 289 Diagnosis, 289, 290 from rickets, 289, 290 Osteo-periostitis, 291 diagnosis from non-specific form, 291 Dactylitis, 291 Varieties, 291 Diagnosis, 291 Prognosis, 291 Teeth, disease of, 292 Temporary, 292 Permanent, 293 Hutchinson on malformation of central upper incisors, 293, 294 Diagnosis from non-specific malformations, 293, 297 Erosions of, 298 Keratitis, interstitial, 299 Symptoms, 299 Complications, 299 Diagnosis, 299 from non-specific forms, 299 Age when most frequent, 300 Nerve-centres and nerves, disease of, 302 Resemblance to adult form, 303 Age and date of appearance, 304 Pathology, 304 Diagnosis, 304 Prognosis, 304 Spleen, disease of, 305 enlargement, 305 cause, 306 Gastro-intestinal tract, disorders, 306 Peyer's patches, degeneration of, 306 Intestinal ulcers, 306 Pancreas, disease of, 306 Peritoneum, disease of, 307 Lungs, disease of, 307 gummata of, 307 pneumonia, specific, 307 Larynx, disease of, 308 Testicles, disease of, 308 Kidneys, disease of, 308 Bright's disease of, 308 Parenchymatous nephritis, 308 Thymus gland, disease of, 309 Diagnosis, 309 Chief elements of, 310 Relative importance of a specific parental history, 310 Appearance of child at birth, 311 Physiognomy of syphilitics, 313 Abortions, frequent, significance of, in, 310 Prognosis, 310 Treatment, 314 Preventive, 314 Of parents, 260, 261, 314, 315 Necessity of supporting, 315 Nursing of syphilitic children, necessity of maternal, 315 Wet-nurses, for syphilitic children, question of, 315 Diet, 315 Mercury, use of, 315, 316 mode of administration, 316 inunctions of, 316 Iodide of potassium, use of, 316 Local, 317

Syphilis as a cause of infantile peritonitis, 1172 influence on causation of enteralgia, 669 of glossitis parasitica, 358 of chronic intestinal catarrh, 700 of intestinal indigestion, 623 of acute yellow atrophy of liver, 1024 of amyloid liver, 1041 of cirrhosis of liver, 991 of oesophageal paralysis, 429 of organic stricture of oesophagus, 423 of chronic intestinal pancreatitis, 1121 of acute pharyngitis, 390 of rachitis, 144, 145 of fissure of rectum and anus, 888 of non-malignant rectal stricture, 885 of ulceration of rectum and anus, 894 of cirrhosis of stomach, 612 of rectum and anus, 900

Syphilitic parents, treatment of, 314, 315 pharyngitis, 406 ulcers of stomach, 529 ulceration of tongue, 370 influence on causation of hemorrhage from bowels, 831

Syphilitics, marriage of, 255-265

Syringe, variety of, in rectal alimentation, 928

T.

TABES MESENTERICA, 1182 Definition, 1182 Synonyms, 1182 History, 1183 Pathology, 1183 Secondary character, 1183, 1186 Tuberculous nature, 1183 Relation to scrofula and tuberculosis, 1183, 1186 Age, 1184 Sex, 1184 Frequency, 1184 Geographical distribution, 1185 Etiology, 1185 Scrofulous and tuberculous diathesis, 1185 Heredity, 1185 Diet and food, improper, 1185, 1186 Filth and poverty, 1186 Malaria, 1186 Inflammation of intestinal mucous membrane, 1186 Acute exanthemata, 1186 Dentition, 1186 Whooping cough, 1186 Mild of diseased cows, 1186 Cure of chronic skin disease, 1187 Morbid anatomy, 1187 Glands, mesenteric, changes in, 1187 enlargement, 1187 cheesy degeneration, 1187 softening of, 1187 cretaceous degeneration, 1187 Spleen, lesions of, 1188 Lungs, lesions of, 1188 Liver, lesions of, 1188 Gastro-intestinal canal, lesions of, 1188 Pancreas, lesions of, 1188 Symptoms, 1189 Precursory, 1189 Debility and anæmia, 1189 Digestive disorders, 1189 Tongue, state of, 1189 Appetite, state of, 1189 Stools, characters of, 1190 Bowels, irregular, 1190 Pyrexia, 1190 Abdomen, state of, 1190 Tympanites, 1190 Tumor, presence of, 1190 Diagnosis, 1191 From fecal accumulation, 1191 tumors of omentum, 1191 Prognosis, 1191 Course, 1192 Duration, 1193 Complications, 1193 Rickets, 1193 Treatment, 1193 Preventive, 1193 Hygienic, 1193 Pain, 1194 Diarrhoea, 1194 Cod-liver oil, 1194 Iodide of iron, 1194 Lacto-phosphates, 1194 Ointment of iodide of lead, 1194

Tabes mesenterica following chronic intestinal catarrh, 710

Tænia acanthotrias, 945 cucumerina, 937 echinococcus, 943 migration of, from intestinal canal, 945 mode of dissemination of, 944 elliptica, 937 flavopunctata, 938 madagascariensis, 938 nana, 937 saginata, 933 solium, 935 tenella, 938

Tampon, use of, in hemorrhage from rectum, 927

Tannic acid, use of, in acute intestinal catarrh, 695 in hemorrhage from bowels, 834

Tape-worms, 131 method of examining evacuations for, 940

Tapping in cirrhosis of liver, 1002 of gut in intestinal obstruction, 865

Taraxacum, local use of, in pseudo-membranous enteritis, 775

Tarry stools in hemorrhage from bowels, 833

Taxis, abdominal, in intestinal obstruction, 864

T-bandage, use of, in prolapsus ani, 919

Teeth, condition of, in scrofula, 246 displacement of, from hypertrophy of tongue, 351 eruption of, in second dentition, 375 irregular and jagged, influence on causation of superficial glossitis, 355 of parenchymatous glossitis, 360 malformation of, in hereditary syphilis, 292 order of normal eruption, 372 precipitate eruption of, 372 state of, in mercurial stomatitis, 345 tardy eruption of, 372 wisdom, eruption of, 376

Teething, anomalies of, in rachitis, 150, 151

Temperament, influence on causation of pseudo-membranous enteritis, 764 of gout, 110 of acute intestinal catarrh, 671 of amyloid liver, 1041 of acute rheumatism, 21 of scrofula, 235

Temperature in occlusion of biliary passages, 1091 in cholera infantum, 742 in cholera morbus, 723 in diabetes mellitus, 204 in entero-colitis, 734, 736 in acute gastritis, 467 in jaundice, 980 in abscess of liver, 1008 in acute yellow atrophy of liver, 1028 in carcinoma of pancreas, 1125 in acute pancreatitis, 1119 in acute peritonitis, 1142 in tuberculous peritonitis, 1165 in acute pharyngitis, 394, 395 in phosphorus-poisoning, 1032 in purpura hæmorrhagica, 189 in suppurative pylephlebitis, 1100 in acute rheumatism, 27, 29 in rheumatic form of gonorrhoeal rheumatism, 104 in scrofula, low, 245 in scurvy, 182 in cancer of stomach, 554 in dilatation of stomach, 596 in simple ulcer of stomach, 495 in tabes mesenterica, 1190 in tonsillitis, 381, 382 sudden changes of, as a cause of gout, 112

Tenderness of epigastrium in chronic gastritis, 473

Tenesmus in acute colitis, 684 in dysentery, 796, 802 in polypi of rectum, 882 in proctitis, 684

Termination of catarrh of bile-duct, 1055 of occlusion of biliary passages, 1092 of lithæmia, 970 of abscess of liver, 1017 of acute yellow atrophy of liver, 1029 of carcinoma of liver, 1039 of cirrhosis of liver, 999 of fatty liver, 1049 of hydatids of liver, 1106 of perihepatitis, 989 of suppurative pylephlebitis, 1101 of phosphorus-poisoning, 1032 of gonorrhoeal rheumatism, 106 of simple ulcer of stomach, 501

Terminations of cholera morbus, 723 of enteralgia, 464 of intestinal indigestion, 630

Tertiary period of hereditary syphilis, 282 ulcers of tongue, 370

Test, Fehling's, for sugar in urine, 211 fermentation, for sugar in urine, 212 indigo-carmine, for sugar in urine, 216 for inosite in diabetic urine, 217 iodine, for amyloid liver, 1043 for lardaceous degeneration of intestines, 875 picric acid and carmine, for sugar in urine, 213

Testicle, atrophy of, in diabetes mellitus, 202 retraction of, in paratyphlitis, 819 in perforation of simple gastric ulcer, 498

Testicles, disease of, in hereditary syphilis, 308

Tests for bile in urine, 978 for free hydrochloric acid in vomit of gastric cancer, 543, 544 for sugar in diabetic urine, 211-217

Thermic fever, relation to cholera infantum, 745

Thermo-cautery, use of, in hypertrophy of tongue, 354

Thigh, flexure upon leg, in paratyphlitis, 819

Thirst in cholera infantum, 742 in cholera morbus, treatment of, 725 in diabetes mellitus, 204 in acute gastritis, 467 in chronic gastritis, 473 in parenchymatous glossitis, 362 in acute intestinal catarrh, 680, 681 treatment of, 690 in carcinoma of pancreas, 1125 in acute rheumatism, 27 in dilatation of stomach, 593 in simple ulcer of stomach, 494 in hypertrophy of tongue, 351 in trichinosis, 960 in typhlitis and perityphlitis, 818

Thorn-head worms, 949

Thread-worms, 949

Thrombi, as a cause of suppurative pylephlebitis, 1098

Thrombosis in simple ulcer of stomach, 510 of portal vein, 1095 in cirrhosis of liver, 999 venous, in gastric cancer, 533

Thrush. See _Stomatitis Parasitica_.

Thymol, use of, in treatment of Distomum hepaticum, 1110

Thymus gland, disease of, in hereditary syphilis, 309

Tight-lacing, a cause of perihepatitis, 989 displacement of stomach by, 617 influence of, on causation of intestinal indigestion, 624

Tincture of aloes, use of, in seat-worms, 951 of chloride of iron, use of, in simple ulcer of stomach, 524 of gelsemium, use of, in pruritus ani, 917 of iodine, use of, in diabetes mellitus, 228 locally, in rheumatoid arthritis, 100 of iron, use of, in hemorrhage from bowels, 834

Tobacco, abuse of, influence of, on causation of constipation, 641 of enteralgia, 660 of acute intestinal catarrh, 671, 672 of intestinal indigestion, 625 of parenchymatous glossitis, 360 of superficial glossitis, 355 of acute oesophagitis, 410 of diseases of pancreas, 1114 of chronic pharyngitis, 402 of dilatation of stomach, 589

TONGUE, ABNORMALITIES AND VICES OF CONFORMATION, 348 Congenital deficiency of, 348, 349 Bifid, 349 _Ankyloglossia_ (_Tongue-tie_), 349 Definition, 349 Synonyms, 349 Pathology and morbid anatomy, 349 Diagnosis, 349 Prognosis, 349 Treatment, 349 _Macroglossia_ (_Hypertrophy of Tongue_), 349 Definition, 349 Synonyms, 349 History, 349 Etiology, 350 Congenital nature of, 350 Age, 350 Sex, 350 Sucking, influence of, on causation, 350 Dentition, influence of, on causation, 350 Convulsions and epileptic seizures, 350 Idiocy and cretinism, relation of, to, 350 Symptoms, 350 Character of enlargement, 350 Suffocation from, 350 Saliva, increase of, 351 Thirst, 351 Larynx and hyoid bone, displacement of, 351 Ulceration of tongue, 351 Teeth, displacement of, 351 Difficult mastication, 351 Pathology and morbid anatomy, 352 Nature of, 352 Microscopic changes, 353 Size of, 353 Diagnosis, 353 Prognosis, 353 Treatment, 353 Use of bandaging and compression, 353 of leeching, 353 Operative measures, 353 Ligation, 354 Excision, 354 Ignipuncture, 354 Thermo-cautery, 354 Medication, futility of, 354

TONGUE, ULCERATION OF, 369 Tuberculous ulceration of, 369 Etiology, 369 Pathology, 369 Epithelium, shedding of, 369 Ulcer, anatomical characters of, 369 formation of, 369 Nodular tubercular infiltration, 369 Symptoms of, 369 Seat of, 369 Course, 369 Characters, 369 Induration, 369 Indolence of, 369 Saliva, increased secretion, 369 Pain, 369 Diagnosis, 369 From squamous-celled carcinoma, 369 syphilitic ulcer, 370 Treatment, 370 Syphilitic ulceration of, 370 Symptoms, 370 Secondary ulcers, 370 seat, 370 pain, 370 characteristics, 370 Tertiary, 370 sequelæ of gummata, 370 seat, 370 characteristics, 370 Prognosis, 370 Treatment, 370

Tongue, state of, in catarrh of bile-ducts, 1053 in biliousness, 966 in cholera infantum, 742 in constipation, 646, 647 in dysentery, 804 in functional dyspepsia, 450 in enteralgia, 661 in pseudo-membranous enteritis, 766 in gastralgia, 461 in acute gastritis, 467 in chronic gastritis, 473 in parenchymatous glossitis, 361 in chronic parenchymatous glossitis, 367 in chronic superficial glossitis, 366 in acute intestinal catarrh, 678, 680, 681 in chronic intestinal catarrh, 707 in intestinal indigestion, 628 in abscess of liver, 1013 in acute yellow atrophy of liver, 1028 in acute pancreatitis, 1119 in acute rheumatism, 27 in scurvy, 177 in cancer of stomach, 540 in simple ulcer of stomach, 495 in tonsillitis, 381, 383 in typhlitis and perityphlitis, 819 enlargement of, in catarrhal stomatitis, 324 in parenchymatous glossitis, 361 inflammation of, in mercurial stomatitis, 346

Tongue-tie, 349

TONSILS, DISEASES OF, 379 _Tonsillitis_, 379 Definition, 379 Varieties, 379 Synonyms, 379 History, 379 Etiology, 380 Of idiopathic form, 380 Diathetic causes, 380 Rheumatism, 380 Scrofula, 380 Heredity, 380 Chronic disease of tonsils, 380 Age, 380 Of deuteropathic form, 380 Of hepatic form, 380 Of traumatic form, 380 Of mycotic form, 381 due to cryptogam, 381 Symptomatology, 381 Onset, 381 Pulse, 381 Temperature, 381, 382 Appearance of throat, 381 Pain, 381, 382 Ears, noises in, 381 Involvement of adjacent structures, 381, 382 Appearance of soft palate, 381 of uvula, 382 Deglutition, difficult, 381 Salivation, excessive, 382 Regurgitation of liquids, 382 Glands, lymphatic, swelling, 382 Voice, alteration of, 382 Respiration, difficult, 382 Headache, 383 Tongue, condition of, 381, 383 Urine, condition of, 383 Albuminuria, 383 Termination, 383 Resolution, 383 Suppuration, 383 symptoms of, 383 Abscess, point of rupture, 383 Gangrene, 383 Metastasis, occurrence, 383 Ulceration of maxillary and carotid arteries, 383 Oedema of glottis, 383 Paralysis of palate, 383 Hypertrophy of tonsil following, 383 Complications and sequelæ, 383 Pathology and morbid anatomy, 383 Of catarrhal form, 384 Of lacunar form, 384 condition of epithelium, 384 deposit, nature of, 384 presence of micrococci and bacteria, 384 mode of subsidence, 384 Of follicular form, 384, 385 Of parenchymatous form, 385 result of lacunar form, 385 mode of subsidence, 385 Secretion, character of, 385 Presence of micro-organisms, 385 Submaxillary glands, lesions of, 385 Of herpetic form, 386 Of mycotic form, 386 nature of parasite, 386 seat of deposit, 386 subjective symptoms, 386 Diagnosis, 386 From diphtheria, 387 sore throats of cachectic conditions, 387 Prognosis, 387 Recurrence, frequency of, 387 Treatment, 387 Mild cases, 387 Local, 388 Pyrexia, 388 Pain, 388 Severe cases, 388 Rheumatic form, 388 Herpetic form, 388 Mycotic form, 389 Diet, 388 Gargles, use of, 388 Ice, use of, 388 Tincture of guaiacum, 388 of aconite, 388 Sodium bicarbonate, 388 Poultices, 388 Sodium salicylate in rheumatic form, 388 Mercuric chloride in herpetic form, 388 Operative measures, 388 Cauterization in mycotic form, 389

Tonsils, hypertrophy of, following tonsillitis, 383 ulceration of, in pseudo-membranous enteritis, 766

Torsion of cæcum from constipation, 853

Torticollis, 78 treatment, 78

Toxæmic period of acute yellow atrophy of liver, 1027

Toxic form of acute gastritis, 467 of intestinal ulcer, 823 stomatitis, 344

Tracheotomy in acute pharyngitis, 398, 399

Transfusion of blood in diabetes mellitus, 229 in hemorrhage from bowels, 834 in phosphorus-poisoning, 1033 in purpura, 194

Transmission of syphilis at moment of conception, 262, 267 by infection prior to conception, 266 during utero-gestation, 267

Traumatic causes of perihepatitis, 989 form of intestinal ulcer, 823

Traumatism, influence on causation of gout, 112 of hemorrhagic effusion into peritoneum, 1181 of abscess of liver, 1003 of non-malignant stricture of the rectum, 885 of acute rheumatism, 22 of hemorrhage from stomach, 580

Travel, value of, in functional dyspepsia, 455 in gastralgia, 463

Treatment of Ascaris lumbricoides, 953 of ascites, 1178 of Anchylostomum duodenale, 956 of Bilharzia hæmatobia, 949 of catarrh of bile-ducts, 1056 of biliary calculi in situ, 1080 calculus state, 1079 concretions, 1079 of occlusion of biliary passages, 1094 of biliousness, 967 of cancrum oris, 343 of cholera infantum, 759 morbus, 724 of constipation, 651 in children, 656 of diabetes mellitus, 218 of diarrhoea in chronic intestinal catarrh, 715 of duodenitis, 698 of dysentery, 809 of functional dyspepsia, 452 of enteralgia, 664 of nervous form of enteralgia, 665 of pseudo-membranous enteritis, 774 of entero-colitis, 746 of impaction of feces, 918 of Filaria medinensis, 963 of Filaria sanguinis, 964 of fissure of anus, 911 of fistula in ano, 921 of fluke-worms, 948 of gastralgia, 462 of acute gastritis, 468 of chronic gastritis, 475 of parasitic glossitis, 359 of parenchymatous glossitis, 364 of chronic parenchymatous glossitis, 368 of superficial glossitis, 357 of chronic superficial glossitis, 367 of glossanthrax, 368 of gout, 127 of acute articular gout, 133 of hemorrhage from bowels, 833 of hemorrhoids, 923 of hepatic colic, paroxysms, 1081 of hepatic glycosuria, 974 of lardaceous degeneration of intestine, 876 of acute intestinal catarrh, 687 of chronic intestinal catarrh, 714 of intestinal cancer, 874 of intestinal indigestion, 632 of intestinal obstruction, 862 from fecal impaction, 863 surgical, 865 of intestinal ulcer, 828 of invagination, low in rectum, 864 of intussusception, 864 of jaundice, 982 of Leptodera stercoralis, 954 of lithæmia, 971 of abscess of liver, 1020 of acute yellow atrophy of liver, 1030 of amyloid liver, 1045 of carcinoma of liver, 1040 of cirrhosis of liver, 1000 of fatty liver, 1050 of hydatids of liver, 1106 of hyperæmia of liver, 988 of liver-flukes, 1110 of lumbago, 77 of macroglossia, 353 of cancer of oesophagus, 428 of dilatation of oesophagus, 434 of organic stricture of oesophagus, 425 of spasmodic stricture of oesophagus, 421 of oesophageal paralysis, 430 of ulceration of oesophagus, 418 of acute oesophagitis, 415 of chronic oesophagitis, 417 of carcinoma of pancreas, 1127 of hemorrhage into pancreas, 1129 of obstruction of pancreatic duct, 1131 of acute pancreatitis, 1120 secondary pancreatitis, 1121 of chronic interstitial pancreatitis, 1122 of peri-anal and peri-rectal abscess, 918 of perihepatitis, 990 of acute peritonitis, 1144 of cancerous peritonitis, 1172 of infantile peritonitis, 1173 of perforative peritonitis, 1156 of puerperal peritonitis, 1146 of tubercular peritonitis, 1168 of peri- and endocarditis in acute rheumatism, 63, 64 of phosphorus-poisoning, 1033 of acute pharyngitis, 397 of phlegmonous form of acute pharyngitis, 397 of chronic pharyngitis, 404 of syphilitic pharyngitis, 408 of tuberculous pharyngitis, 402 of pleurodynia, 78 of proctitis, 919 of prolapsus ani, 919 of purpura, 193 of suppurative pylephlebitis, 1101 of hypertrophic stenosis of pylorus, 615 of rachitis, 158 of cancer of rectum, 913 of dilatation of rectal pouches, 916 of gonorrhoea of rectum, 918 of hemorrhage of rectum, 926 of irritable rectum, 919 of polypi of rectum, 913 of rodent ulcer of rectum, 913 of non-malignant stricture of rectum, 917 of ulceration of rectum, 912 of tuberculous ulcer of rectum, 913 of diseases of rectum and anus, 911 of congenital malformation of rectum and anus, 880 of acute rheumatism, 51 of chronic articular rheumatism, 73 of gonorrhoeal rheumatism, 107 of muscular rheumatism, 76 of rheumatoid arthritis, 96 local, of rheumatoid arthritis, 100 of scrofula, 249 of scurvy, 183 of seat-worms, 951 of sphincterismus, 916 of cancer of stomach, 576 of cirrhosis of stomach, 615 of dilatation of stomach, 603 of acute dilatation of stomach, 603 of hemorrhage from stomach, 585 of rupture of stomach, 618 of simple ulcer of stomach, 519 of aphthous stomatitis, 330 of catarrhal stomatitis, 325 of mercurial stomatitis, 347 of stomatitis ulcerosa, 338 of stomatorrhagia, 371 of tabes mesenterica, 1193 of Tænia echinococcus, 945 of tape-worm, 941 of thrombosis and embolism of portal vein, 1096 of thrush, 335 of tongue-tie, 349 of syphilitic ulceration of tongue, 370 of tubercular ulceration of tongue, 370 of tonsillitis, 387 of torticollis, 77 of trichinosis, 961 of Triocephalus dispar, 954 of typhlitis, peri- and paratyphlitis, 822

Trematodes, 946

Trichina spiralis, 957 appearance of meat affected with, 959 discovery of, in muscles, 958 method of migration to muscles, 959 symptoms of, 959

Trichinosis. See _Intestinal Worms_. in children, 961 prophylaxis of, 962 symptoms of, 959 treatment of, 961

Trimethylamine, use of, in acute rheumatism, 62 in chronic articular rheumatism, 74

Triocephalus dispar, 954 symptoms and treatment of, 954

Tropical form of hepatic abscess, lesions of, 1006

Trypsin, action of, in digestion, 622

Tubercle of pancreas, 1128

Tubercular peritonitis, 1165 ulcers of stomach, 529

Tuberculosis complicating chronic intestinal catarrh, 710 influence of, on causation of intestinal ulcer, 824 relation of, to scrofula, 240-242

Tuberculous affections of rectum and anus, 901 nature of tabes mesenterica, 1183, 1184 pharyngitis, 400 ulcer of rectum, treatment of, 913 ulceration, as a cause of hemorrhage from bowels, 831 of bowel, distinguished from chronic intestinal catarrh, 713 of tongue, 369

Tuberose vitiligoidea of skin, in jaundice, 981

Tubules, gastric, alterations in chronic gastritis, 472

Tumefaction of cheek in cancrum oris, 340

Tumor, fecal, characters of, 852 frequency of, in gastric cancer, 546 presence of a, in cancer of intestines, 869 in intussusception, 848 in hypertrophic stenosis of pylorus, 615 significance of, in diagnosis of cancer of stomach, 569 of cirrhosis of stomach, 613 in tabes mesenterica, 1190 in typhlitis and paratyphlitis, 819 of carcinoma of liver, shape and size, 1034 of epigastrium in abscess of liver, 1011 pulsating, of epigastrium, in hemorrhage into pancreas, 1129 significance of a, in diagnosis of intestinal cancer, 873 seat and character, in carcinoma of pancreas, 1124, 1125 in cancer of stomach, 548

Tumors, as a cause of hemorrhage from bowels, 831 of stomach, non-cancerous, 578 pressure of, as a cause of occlusion of common biliary duct, 1085 of pancreatic duct, 1129 and cysts, compression by, as a cause of intestinal obstruction, 857

Turkish baths, use of, in rheumatoid arthritis, 99

Turpentine, use of, in Anchylostomum duodenale, 956 in chronic intestinal catarrh, 718 in intestinal ulcer, 829 in ulceration of oesophagus, 418 in hemorrhage from bowels, 834 from mouth, 371 in phosphorus-poisoning, 1033 in pruritus ani, 917 in purpura, 193 in stomatorrhagia, 371 in tape-worm, 941 stupes, use of, in perihepatitis, 990 and ether, as solvents of biliary calculi, 1080

Twisting of bowels, 840 seat, 841 of stomach, 617

Tympanites, in acute internal strangulation of intestines, 843 intestinal catarrh, 679 in chronic intestinal catarrh, 707 in intestinal indigestion, 627 in intussusception, 848 in acute peritonitis, 1141 in acute dilatation of stomach, 610 in perforation of simple ulcer of stomach, 498 in tabes mesenterica, 1190

Typhlitis, influence of, on causation of suppurative pylephlebitis, 1097 stercoralis, treatment, 821 and perityphlitis in constipation, 648

TYPHLITIS, PERITYPHLITIS AND PARATYPHLITIS, 814 History, 814 General remarks, 814 Etiology, 815 Age, influence of, on causation, 815 Sex, influence of, on causation, 815 Appendix vermiformis, disease of, 815 abnormalities of size and position, 815 ulceration and stricture of, 815 collection of feces and foreign bodies in, 816 anatomical peculiarities of, 816 Constipation, influence of, on causation, 816 Paresis of muscular tissue of cæcum, 817 Foreign bodies, influence of, on causation, 817 Morbid anatomy, 817 Perforative peritonitis, lesions of, 817 Intestinal walls, thickening, 817 Mucous membrane, ulceration, 817 Abscesses, seat, 817 point of discharge, 818 Contortions and adhesions of vermiform appendix, 818 Cicatrix of vermiform process, 818 Symptoms, 818 Mode of onset, 818 Prodromata, 818 Disinclination to walk, 818 Formication and paresis of right leg, 818 Chill, 818 Collapse of strength, 818 Fever, 818, 819 Thirst, 818 Appetite, loss of, 818, 819 Pain, 818 character and seat, 818 Abdominal tenderness, 818 Tumor, presence of, 819 seat and shape, 819 Disturbance of digestion, 819 Vomiting, 819 Constipation, 819 Tongue, state of, 819 Pulse, state of, 819 Urine, state of, 819 Perforation, occurrence of, 819 causes of, 819 Of paratyphlitis, 819 Insidiousness of, 819 Flexure of thigh upon leg, 819 Perversions of sensation in right leg, 819 Dysuria, 819 Retraction of testicle, 819 Priapism, 819 Milk-leg from thrombosis, 820 Frequency of relapses, 820 Diagnosis, 820 From fecal impaction, 820 cancer, 820 invagination, 820 Duration, 820 Prognosis, 820 Mortality, 820, 821 Prophylaxis, 821 Treatment, 821 Of typhlitis stercoralis, 821 Irrigation of bowel, 821 Of abscesses, 822 Of perforative form, 822 Of indurated tumors, 822 Of convalescence, 822 Magnesium sulphate, use of, 822 Opium, use of, 822 Hot embrocations, use of, 822 Ice-bag, use of, 822 Mineral waters, 822 Mercurial ointment, 822 Iodine, 822 Laparotomy in perforative form, 822

Typhoid fever, as a cause of hemorrhage from bowels, 831 distinguished from dysentery, 807 influence of, on causation of intestinal ulcer, 824 ulcer, as a cause of acute peritonitis, 1139 of stomach, 529

U.

Ulcer, duodenal, of chronic intestinal catarrh, diagnosis, 713 gastric, influence on causation of cancer of stomach, 536 intestinal, 823 of intestine, prevention of recurrence, 829 of rectum, treatment, 912 rodent, of rectum, 889 simple, of stomach, 480 position and shape, 504 tuberculous, of rectum, treatment, 913

Ulcerated surfaces, complicating diabetes mellitus, 205

Ulceration, character and seat, in cancrum oris, 341 follicular, of chronic intestinal catarrh, 712, 713 in aphthous stomatitis, 328 intestinal, in constipation, 644 of cheek in cancrum oris, 340 of colon in chronic intestinal catarrh, 702 of gums, in mercurial stomatitis, 347 of intestines, complicating constipation, 648 of maxillary and carotid arteries in tonsillitis, 383 of oesophagitis, 418 of rectum, influence on causation of carcinoma of, 904 of rectum and anus, 893 of lobe of ear in scrofula, 246 of skin and muscles in scurvy, 178 of cancer of stomach, 562 of tongue, 369 syphilitic, 370 tuberculous, 369 of vermiform appendix, as a cause of typhlitis, 814 and dilatation of bile-ducts, as a cause of abscess of liver, 1005

Ulcerations, follicular, of rectum and anus, 894 nature and seat, in syphilitic pharyngitis, 407 of chronic form of dysentery, seat and characters, 800

Ulcerative endocarditis in acute rheumatism, 34 form of acute pharyngitis, morbid anatomy, 392 symptoms, 395 treatment, 398

Ulcerous stomatitis, 336

Ulcers, in dysentery, characters and seat, 799 in entero-colitis, seat, 737, 738 in acute intestinal catarrh, catarrhal and follicular, 676 seat, 976 treatment, 698 in chronic intestinal catarrh, mode of formation, 703 in simple ulcer of stomach, number, 503 in stomatitis ulcerosa, seat and character, 336, 337 of stomach as a cause of acute peritonitis, 1139 of stomach and intestines in cirrhosis of liver, 999

Uncleanliness, influence on causation of intestinal worms, 931 of stomatitis ulcerosa, 336

Ung. hydrarg. iod. rubri, in lithæmia, 973 use of, in amyloid liver, 1046 in cirrhosis of liver, 1002

Uni-articular rheumatism, 49

Unilateral enlargement of papillæ in superficial glossitis, 356

Unripe fruit, influence on causation of cholera morbus, 721

Uræmia, influence on causation of acute intestinal catarrh, 671

Uræmic choleriform attacks, diagnosis from cholera morbus, 724 coma, complicating cancer of stomach, 556

Uranium nitrate, use of, in diabetes, 230

Uratic deposits in kidneys in gout, 117

Urea, action of liver in formation of, 968, 969 amount of, in urine of jaundice, 979 diminished excretion of, in acute yellow atrophy of liver, 1029

Urethral stricture, influence on causation of prolapse of rectum, 881

Urethritis, complicating diabetes mellitus, 205

Uric acid, amount in urine, during paroxysms of gout, 119 in blood of gouty individuals, 115 in urine of lithæmia, 970 theory of origin of gout, 113, 114 and urates, amount of, in urine of gouty dyscrasia, 120 urea, amount excreted, in acute rheumatism, 30

Urinary retention in constipation, 646

Urine, state of, in ascites, 1177 in catarrh of bile-ducts, 1054, 1055 in occlusion of biliary passages, 1089, 1090 in biliousness, 966 in cholera infantum, 742 morbus, 723 in constipation, 648 in diabetes mellitus, 207 in dysentery, 803 in functional dyspepsia, 451 in enteralgia, 661 in pseudo-membranous enteritis, 766 in entero-colitis, 734 in acute gastritis, 467 in chronic gastritis, 475 in acute gout, 119 in gouty dyscrasia, 120 in hepatic glycosuria, 974 in acute intestinal catarrh, 681 in chronic intestinal catarrh, 708 in intestinal indigestion, 628 in jaundice, 978 in lithæmia, 970 in abscess of liver, 1010, 1014 in acute yellow atrophy of liver, 1029 in amyloid liver, 1044 in carcinoma of liver, 1038 in cirrhosis of liver, 998 in fatty liver, 1049 in hyperæmia of liver, 986, 987 in chronic interstitial pancreatitis, 1122 in acute peritonitis, 1142 in cancerous peritonitis, 1170 in phosphorus-poisoning, 1032 in acute rheumatism, 30 in gonorrhoeal rheumatism, 104 in chronic general rheumatoid arthritis, 83 in gastric cancer, 550 in dilatation of stomach, 595 in scurvy, 181 in tonsillitis, 383 in typhlitis and perityphlitis, 819 fat in, in carcinoma of pancreas, 1125 infiltration of, as a cause of acute peritonitis, 1140 presence of albumen in, in gout, 123 tests for bile in, 978 for sugar in, 211

Uterine disorders in pseudo-membranous enteritis, 767 in tape-worm, 940 influence on causation of functional dyspepsia, 448 of fissure of anus, 888 of gastralgia, 460 of chronic pharyngitis, 403 displacements from constipation, 647 injections as a cause of acute peritonitis, 1140

Utero-gestation, infection of child with syphilis during, 267 in acute pharyngitis, 391-394

Uvula, appearance of, in tonsillitis, 382

V.

Vaccination, influence on causation of scrofula, 237

Valerian, use of, in spasmodic stricture of oesophagus, 421

Vapor baths, use of, in ascites, 1179 in cirrhosis of liver, 1001 in rheumatoid arthritis, 100

Varicocele from constipation, 646

Varieties of enteralgia, 662 of gastralgia, 459 of acute gastritis, 464 of acute intestinal catarrh, 682 of rheumatoid arthritis, 79 of seat-worms, 950 of stomatitis, 321 of tonsillitis, 379

Variolous form of acute pharyngitis, 393 pustules in acute oesophagitis, 412

Vaso-motor nerves, influence on production of glycosuria, 196-199

Vater's diverticulum, death from lodgment of biliary calculi in, 1078

Veins, varicose condition of, in chronic intestinal catarrh, 702

Venereal excess, influence on causation of enteralgia, 660 of gastralgia, 460

Venesection, use of, in parenchymatous glossitis, 364

Venous walls, changes in, influence on causation of pylephlebitis, 1098

Vermiform appendix, contortions and adhesions of, in typhlitis, etc., 814

Vertebral column, changes in, in rachitis, 151 pain in acute oesophagitis, 413

Vertigo in catarrh of bile-ducts, 1054 in biliousness, 966 in constipation, 647 gastric, in functional dyspepsia, 451 in enteralgia, 662 in acute gastritis, 467 in chronic gastritis, 474 in hemorrhage from bowels, 833 in intestinal indigestion, 628 in lithæmia, 970 in cirrhosis of liver, 993 in dilatation of stomach, 595 in simple ulcer of stomach, 494 in tape-worm, 940

Vesical catarrh, complicating gout, 123

Vesicles of aphthous stomatitis, nature of, 327

Vibrios and bacteria in acute intestinal catarrh, 676

Villi, lesions of, in acute intestinal catarrh, 675 hypertrophy of, in chronic intestinal catarrh, 701

Virchow on circumscribed hemorrhagic infiltration as a cause of gastric ulcer, 512

Vision, disorders of, in diabetes mellitus, 204 yellow, in jaundice, 980

Visual disorders in biliousness, 966 in constipation, 647 in pseudo-membranous enteritis, 767 in intestinal indigestion, 628 in scurvy, 181

Vitiated air, influence on causation of cholera infantum, 728-730 of entero-colitis, 728-730

Vitiligoidea in jaundice, 980

Voice, alteration of, in parenchymatous glossitis, 361 in stomatitis parasitica, 334 in tonsillitis, 382 characters of, in cholera morbus, 722 improper use of, as a cause of chronic pharyngitis, 402

Vomit, characters of, in cholera morbus, 722 in functional dyspepsia, 450 in enteralgia, 662 in pseudo-membranous enteritis, 765 in entero-colitis, 733 in acute gastritis, 467 in chronic gastritis, 473 in hepatic colic, 1072 in cancer of intestines, 870 in intestinal obstruction from internal strangulation and twisting, 843 from intussusception, 848, 849 from impaction of gall-stones, 840 from stricture of bowel, 856 in abscess of liver, 1014 in acute yellow atrophy of liver, 1028 in cirrhosis of liver, 993 in carcinoma of pancreas, 1126 in diseases of pancreas, 1116 in acute pancreatitis, 1119 in acute peritonitis, 1141 in phosphorus-poisoning, 1031 in suppurative pylephlebitis, 1100 in dilatation of stomach, 594 in cancer of stomach, 542 in cirrhosis of stomach, 613 in simple ulcer of stomach, 491, 492 coffee-grounds, in acute yellow atrophy of liver, 1028 in phosphorus-poisoning, 1031 detection of blood in, in cancer of stomach, 545 of cancerous fragments in, in cancer of stomach, 542 presence of micro-organisms in, in dilatation of stomach, 594 spinach-colored, in acute peritonitis, 1141 stercoraceous, in enteralgia, 662 in intestinal obstruction from internal strangulation and twisting, 843 from impaction of gall-stones, 840 from intussusception, 848, 849 in stricture of bowel, 856

Vomiting in Ascaris lumbricoides, 953 in occlusion of biliary ducts, 1088 in cholera infantum, 742 treatment, 761 in cholera morbus, 722 treatment, 725 in dysentery, 803 in functional dyspepsia, 449 in enteralgia, 662 in pseudo-membranous enteritis, 765 in entero-colitis, 733 treatment, 761 in intestinal impaction of gall-stones, 840 in gastralgia, 461 in acute gastritis, 467 treatment, 469 in chronic gastritis, 473 in hepatic colic, 1070, 1071, 1072 in hemorrhage from bowels, 833 in acute internal strangulation and torsion of intestines, 843 in acute intestinal catarrh, 681 in intestinal cancer, 870 in intestinal obstruction, 843, 848, 849, 854, 856 from stricture of bowel, 856 ulcer, 826 treatment of, 829 in intussusception, 848, 849 in impaction of fecal matter, 854 in abscess of liver, 1013 treatment of, 1021 in acute yellow atrophy of liver, 1026, 1028 in carcinoma of liver, 1038 in cirrhosis of liver, 993 in cancer of oesophagus, 427 in acute oesophagitis, 413 in carcinoma of pancreas, 1126 in diseases of pancreas, 1116 in hemorrhage into pancreas, 1129 in acute pancreatitis, 1119 peritonitis, 1141, 1143 in cancerous peritonitis, 1170 in tuberculous peritonitis, 1165 in suppurative pylephlebitis, 1100 in obstruction of rectum, 890 in atrophy of stomach, 616 in cancer of stomach, 541 time of, 541 treatment of, 576 in cirrhosis of stomach, 613 in dilatation of stomach, 593 time of appearance, 593 in simple ulcer of stomach, 491 treatment of, 524 in aphthous stomatitis, 329 in typhlitis and perityphlitis, 818, 819 in trichinosis, 960 of blood in hemorrhage from bowels, 833 in cirrhosis of liver, 833 in simple ulcer of stomach, 493 of gall-stones, 1076 of segments of tape-worm, 940

Von der Velden on absence of free hydrochloric acid in fluids of gastric cancer, 543

Vulva, gangrene of, complicating cancrum oris, 341 oedema of, in cirrhosis of liver, 995

W.

Walls of intestines, hypertrophy of, in chronic catarrh, 700

Ward's paste, use of, in tuberculous ulcer of rectum, 913

Warm baths, use in constipation, 653 in acute intestinal catarrh, 692

Washing out of stomach in gastric cancer, 577 dilatation, 603 objections to, in gastric dilatation, 607 contraindications of, in gastric dilatation, 608 in simple ulcer of stomach, 523

Wasting in entero-colitis, 736 in cancer of intestines, 871 in tuberculous pharyngitis, 401 diseases, influence on causation of constipation, 642 of chronic intestinal catarrh, 699 in acute intestinal catarrh, 671

Water, impure, influence on causation of dysentery, 791 acute intestinal catarrh, 672, 673 unfiltered, influence on causation of intestinal worms, 931 use of, in constipation, 655 as a solvent, use of, in gout, 133 hot, use of, in chronic gastritis, 477

Water-brash in functional dyspepsia, 449

Weak heart-action as a cause of acute gastritis, 464

Weaning, proper time for, 160, 746

Weather, influence of, on exacerbations of chronic articular rheumatism, 71

Weight, loss of, in diabetes mellitus, 204

Wet-nurses for syphilitic children, question of, 315

Whip-worm, 954

Whooping cough, influence on causation of tabes mesenterica, 1186

Wine, use of, in intestinal indigestion, 634

Wintergreen, oil of, use in Ascaris lumbricoides, 954 in gout, 136 in liver-flukes, 1110 in Oxyuris vermicularis, 951 in acute rheumatism, 59

Wire-drawn feces in non-malignant stricture of rectum, 886

Wirsung's canal, anatomy of, 1113 catarrh of, as a cause of obstruction of pancreatic duct, 1130 dilatation of, from pancreatic calculi, 1130 duct, closure of, as a cause of chronic interstitial pancreatitis, 1121

Wisdom teeth, eruption of, 376

Woman's milk, composition of, 749, 750

Worms, intestinal, 930 influence on causation of rectal prolapse, 881

Wormseed, use of, in Ascaris lumbricoides, 954

Worry and anxiety, influence on causation intestinal indigestion, 624

X.

Xanthelasma in jaundice, 980

Xanthopsy in jaundice, 980

Y.

Yellow atrophy of liver, acute, 1023 vision, in jaundice, 980

Yellowness of skin in jaundice, mode of extension of, 977

Z.

Zinc chloride, local use of, in hemorrhoids, 926 oxide, use of, in catarrh of bile-ducts, 1057 in acute intestinal catarrh, 694 in intestinal ulcer, 829 in spasmodic stricture of oesophagus, 421 salts, use of, in constipation, 655 in acute intestinal catarrh, 697 in chronic intestinal catarrh, 714, 717 sulphate, use of, in gonorrhoea of rectum, 978 in pseudo-membranous enteritis, 775 local use of, in chronic pharyngitis, 405 in aphthous stomatitis, 330 valerianate, use of, in constipation, 655 in enteralgia, 665 in gastralgia, 463

END OF VOLUME II.