part one or more of the cardiac cavities, is situated near an orifice,

is attached to the walls by a pedicle which allows it to float freely in the ventricle, or is intertwined with the valves or chordæ tendineæ. Under all these circumstances, they give rise to the signs and symptoms we have dwelt upon above, and which ordinarily make known their presence. Occasionally, however, there is such a combination of symptomatic morbid phenomena relating to different organs that we are at a loss to separate them accurately and to determine how this or that symptom is occasioned. This statement is particularly true in regard to the distinguishing symptoms which indicate the presence of terminal coagula. At a period when the fatal termination is not far removed, and when it is extremely difficult both to recognize and interpret special {732} symptoms, it is readily understood why those pertaining directly to cardiac thrombosis have not hitherto been fully and accurately described.

COURSE, DURATION, AND TERMINATIONS.--Cardiac concretions may form more or less rapidly, and in certain situations occasion death instantaneously and surely. This is eminently true of large coagula which fill up the infundibulum and pulmonary artery. Cases of this sort have been mentioned by various authors. Amongst others, we would specially direct attention to those instances in which sudden death has taken place during the puerperal state after severe post-partum hemorrhage. The patient has at times, in assuming an erect sitting posture, been attacked with a syncopal attack resulting in a few instances fatally.[45] In the same category we should include those examples in which sudden death has followed severe surgical operations.[46] Two cases of this termination, due to coagula in the right heart, are reported by Robert Lawson.[47]

[Footnote 45: _Philada. Medical Examiner_, March, 1849, paper by Charles D. Meigs; vide also Spiegelberg, _Lerbuch der Geburtshülfe_, and Lusk, _The Science and Art of Midwifery_, p. 597.]

[Footnote 46: _Med. Times and Gazette_, vol. i., 1873, p. 58; also _Pathol. Soc. Trans._, vol. xxvii. p. 70.]

[Footnote 47: _Med. Times and Gazette_, Feb. 8, 1873.]

In cardiac dilatation this mode of death is not infrequently seen. It here seems to depend mainly upon stasis of blood caused by weakened power of contractility in the right heart and "by impairment of respiratory and nutritive attraction arising from feeble respiration and arrested tissue-change" (Hayden). The post-mortem revelation has afterward shown cardiac thrombosis to be the efficient cause of death. In diphtheria[48] and pneumonia such examples are not infrequently encountered. As Austin Flint[49] remarks, however, these coagula present almost identical physical characters with those formed after death, and consequently to fix precisely the moment of their production will at best be but a matter for conjecture. According to Walshe, it would be difficult to determine whether or not some of these almost instantaneous deaths occurred as a coincidence or as an effect. Besides, it is frequently impossible to determine the length of time they have existed before completely obstructing the circulation through the pulmonary artery into the lungs, and hence causing fatal syncopal or asphyxic phenomena. Bristowe[50] goes so far even as to affirm in the great majority of cases that cardiac concretions are unaccompanied with appreciable symptoms. In this statement he includes coagula of large size entirely filling one or more of the cardiac cavities, and doubtless formed within a few hours of the final termination. To quote his own words, "We ought to require very strong testimony indeed to convince us in any case that concretions found in the heart at the time of death have caused death, still more to convince us that those clots which resemble in every point the clots which are the mere result of dying have had this effect." How different does this sound from the opinions of B. W. Richardson,[51] who attributes so many well-marked symptoms to the formation of voluminous moulded clots in the heart! And, indeed, is it not at variance with the views of a host of the best medical observers? We believe Bristowe goes too far, and that cardiac concretions are not infrequently the cause of very sudden death both in acute and chronic diseases.

[Footnote 48: Robinson, _loc. cit._]

[Footnote 49: _Diseases of the Heart_, p. 276, Philada., 1870.]

[Footnote 50: _Reynolds's System of Medicine_, vol. v. p. 113.]

[Footnote 51: "Lectures" in the _British Medical Journal_, 1860.]

There are numerous instances in which the coagulum formed in the heart is of smaller size, does not form so rapidly, and besides occupies a position in which, as it does not interfere greatly with the function of the heart, death does not of necessity immediately take place. Little by little, however, the clot is added to, and before many days have elapsed symptoms of gravest {733} import are pronounced. So usual is it for the phenomena connected with the formation of a large cardiac concretion to be accompanied by those which properly belong to another serious affection which may likewise occasion rapid death (pneumonia, endocarditis, typhoid fever, diphtheria, etc.) that we with the greatest difficulty separate the symptoms, and can assign to the intra-cardiac condition those doubtless occasioned by it.

The cases referred to above are not the only ones. Occasionally we meet with cardiac concretions after death which have evidently existed for a number of years, and sometimes without having ever revealed their presence by notable interference with the circulation or in any way affecting the habitual good health of the individual (Laennec[52]). This is perhaps not to be wondered at when the coagulum is small and situated near the apex of the heart, in one of the auricular appendages, or in such a position as not to alter the play of the cardiac valves or obstruct the orifices. But when we see a whole cavity, as an auricle, forcibly distended by an old concretion which fills its entire cavity, the absence of all symptoms during life pointing to its existence occasions much surprise. Some of these large coagula have nevertheless, by a sudden change in their position, caused instantaneous death; others again, after giving rise to obscure symptoms affecting both the pulmonary and cardiac circulation, have likewise brought about a rapidly fatal termination.[53] Sometimes, in consequence of the condensation or atrophy of the clot, the phenomena which took place suddenly with great intensity and indicated its presence became gradually modified, and we have known one remarkable instance in a youth during the third week of an attack of typhoid fever where the accidents thus occasioned completely disappeared, and the patient left the hospital apparently cured.[54]

[Footnote 52: _Dict. Encycl. des Sci. méd._, article "Concrétions sanguines."]

[Footnote 53: _Edin. Med. Journal_, April, 1868, v.--case by H. Douglas.]

[Footnote 54: What occurred in this case I am of course unable to state in a positive manner. All I know is, that the heart became suddenly obstructed, followed by weak, irregular pulse and dusky countenance, and that in twenty-four hours, under treatment with frequently-repeated doses of digitalis and carbonate of ammonia, the accidents subsided. Was there a solution and disintegration of an incompletely formed heart-clot? It seems to me probable.]

COMPLICATIONS AND SEQUELÆ.--One, if not the gravest, complication which can arise during the formation and duration of heart-clot is the production of an embolus of the pulmonary artery, completely filling up its cavity, arresting respiration, and causing sudden death by asphyxia. More frequently smaller portions of heart-clot become detached and are transported farther along by the blood-current. Finally, they become arrested in vessels of smaller calibre. In these they may remain for a short time, and then become dissolved and resorbed, leaving the calibre of the vessel free after their disappearance, or else they form permanent plugs and give rise to inflammation, coagulation, or hemorrhage. According to the investigations of Lefeuvre,[55] which are both clinical and experimental, it would appear that the obstruction of the arterial distribution to any given part is almost immediately followed by engorgement of tissue and hyperæmia of the capillaries of the affected region. Feltz[56] has further shown that this condition is brought about by reflux from the veins and paralysis of the capillaries. It is not infrequent, moreover, to find hemorrhage into the tissues as a direct sequela of this changed condition of circulation.

[Footnote 55: _Brit. and Foreign Med.-Chir. Review_, Oct., 1871.]

[Footnote 56: _Traité clinique et expérimentale des Embolies capillaires_, Strasburg, 1870.]

These are, in fact, the conditions described under the name of infarctions. Small detached particles may be detached from the cardiac clot, if it be found in the left cavity, and transported after a similar manner by the blood-current of the aorta and its divisions until finally arrested in the different {734} viscera of the economy (spleen, kidney, liver) or in the arteries of the extremities.[57] In these different situations they give rise, when finally arrested, to results which differ considerably according to the structure of the organs or tissues where they become impacted. In certain instances, carefully studied by Senhouse Kirkes, the disintegrated and puriform contents of old fibrinous coagula are carried throughout the vascular system and determine marked typhoid phenomena. The patient is attacked with irregular paroxysms of fever of intermittent type, diarrhoea, vomiting, and extreme feebleness. Kirkes explains these symptoms partly by the obstructions occasioned by small emboli, partly by a sort of poisoning due to the transformation of the fibrin. The accidents thus occasioned at times very closely resemble those which characterize pyæmia.[58] The fluid contained in the interior of the old clots, which give rise to these accidents by reason of their transformation, is thick, grumous, and puriform. It is surrounded by a sort of pseudo-cyst, and is composed mainly of altered fibrin and red and white blood-corpuscles.[59]

[Footnote 57: _Gazette hébdomadaire_, 1856. Legroux reports a case of acute rheumatism accompanied by endocarditis and followed by concretions in the left cavities of the heart, and obliterations of the arteries of the limbs by emboli without gangrene ensuing.]

[Footnote 58: _Dict. Encycl. des Sci. méd._, _loc. cit._]

[Footnote 59: _Pathol. Soc. Transact._, vol. xiv. p. 65, cases by J. W. Ogle.]

Pulmonary apoplexy and hæmoptysis often take place in connection with the presence of a fibrinous clot of the right heart. This connection, however, is not absolute, and many cases of right cardiac coagulum have been observed in which neither of these complications became manifest. When there has been pre-existent valvular disease, especially of the mitral, these sequelæ more surely follow than when there has not been this organic disease. The connection between the pulmonary apoplexy and the valvular affection is even more intimate than that of the hæmoptysis, and the same statement is also true of its relationship with cardiac thrombosis.

Upon this subject Hayden[60] writes as follows: "Pulmonary apoplexy seeming to require it as a necessary antecedent condition, while hæmoptysis, though generally associated with thrombosis in the last moments of life, frequently does occur independently of it."

[Footnote 60: _Dis. of the Heart_, vol. i. p. 529.]

The doctrine of Ludwig, as supported by Niemeyer,[61] that the pulmonary apoplexy is directly due to stasis and deposit in the capillaries of blood-corpuscles, does not appear possible if we accord faith to the researches of Waters,[62] who has shown an intercommunication between the bronchial vessels and pulmonary veins; and reasoning upon this basis we have a strong confirmation of Virchow's theory of hemorrhagic infarction (Hayden) consequent upon embolism.

[Footnote 61: _A Textbook of Practical Medicine_, 1869, vol. i. p. 156.]

[Footnote 62: _The Human Lung_, 1860, p. 201.]

PATHOLOGY AND MORBID ANATOMY.--In the great majority of cases clots presenting different physical characters are found in one or more of the cavities of the heart after death. According to the supposed time of their formation, they have been very properly divided into--1, cadaveric (post-mortem); 2, terminal (in actu mortis); 3, ancient (ante-mortem). It is important at the very beginning of the considerations which I shall make in regard to these formations to determine, if possible, the physical characters of cadaveric and terminal clots, so as to be able afterward to more clearly separate from them the true cardiac concretions or those formed at a time more or less removed from the period of death. Without much question, it is owing to the indifference or neglect of later writers in making these necessary distinctions that uncertainty has arisen in the minds of many with respect of the age of many heart-clots. The cadaveric and terminal clots would indeed have but slight pathological interest attached to them were it not that occasionally during {735} life, in a spontaneous manner, cardiac thrombosis suddenly takes place, and is always the cause of symptoms of considerable gravity and which often occasion a fatal termination.

I. Cadaveric Clots.--These present the characters of blood drawn from the arm by venesection and which is allowed to coagulate in a vase. 1. Sometimes they are large, soft, homogeneous, friable masses, distending one or more of the cardiac cavities, and having an appearance very similar to badly-cooked currant-jelly, and there is no apparent separation of the fibrin and the globules. Such an aspect is found particularly when the relative quantity of fibrin is below the normal or the blood is deficient in plasticity. In alkaline poisoning and many adynamic forms of disease this is notably the case.[63] It may likewise occur in forms of death in which there has been considerable obstruction to the circulation. 2. In a somewhat similar manner, when the blood is removed from the influences which give it life and stagnates, or is arrested within the heart, coagulation takes place and the blood separates into two layers. The upper is fibrinous, and resembles the buffy coat covering a clot after bloodletting; the under layer is mainly cruoric, and encloses within its meshes by far the larger proportion of the red globules. This latter mass always forms the lowest stratum by relation with the position of the body after death. Between these two layers, and from the fact of their smaller density, we find more of the leucocytes. This formation of blood-clot in distinct strata has been accomplished experimentally by Pasta,[64] who poured some blood of an animal into the heart of an ox and allowed it to deposit. The cruoric mass is always soft, and may be readily washed from the fibrin by a stream of water. Frequently these clots distend the cardiac cavities to such an extent that when they are opened at the autopsy a portion will fall upon the table and the rest is readily detached from them. The microscope shows the same condition of globules and fibrin in these coagula as it does in those of a venesection. According to Walshe, these cadaveric coagula are usually voluminous, jelly-like masses of fibrin of a pale straw-color, semi-transparent, and containing a quantity of serum in their meshes. Never do they show the slightest signs of stratification, and are not really adherent to the cardiac walls. Occasionally their prolongations may be intertwined amongst the papillary muscles and fleshy columns. According to Legroux, it appears difficult to understand how these large masses of fibrin become separated from the blood and deposited in the heart during life, and yet he is indisposed to regard them as a strictly post-mortem production. They are for him simply the result of the agony.[65] After death the serum is expelled from the clot in larger or smaller quantity, and for a longer or shorter time according to its own spontaneous retractility.

[Footnote 63: Magendie, "Lectures on the Blood," _Lancet_, 1839.]

[Footnote 64: _Dict. de Médecine_, t. viii. p. 560, Paris, 1868.]

[Footnote 65: _Gaz. hébdomadaire_, 1856.]

There are instances in which death has taken place very suddenly (chloroform, lightning, blow on epigastrium), and the blood remains liquid in the cardiac cavities and shows no tendency to coagulation (Walshe). The intimate cause of this condition is difficult to state, although the sudden shock to the nervous system is doubtless the main explanation. Under these circumstances the lining membrane of the heart is apt to become stained with the coloring matter of the blood.[66] At times the ventricles of the heart contain no blood at the autopsy. This is more frequently true of the left than of the right ventricle. Even then the auricles are more or less full.

[Footnote 66: Bristowe, in _Reynolds's System of Medicine_, vol. v. p. 106.]

II. Terminal Clots.--These clots are found at a period more or less removed from the time of death. It may be that they have been present in the heart many days before the fatal termination is reached, or indeed that the act of dying, when the whole organism is overcome by the {736} numerous conditions which inevitably tend in this direction, is mainly instrumental in their rapid production. Of course their outward aspect as well as their intimate structure will vary greatly with their age and with the disease which has been present. Never are they formed entirely of cruor; frequently they are composed of a large quantity of fibrin. Their coloration varies with the quantity of red globules, leucocytes, and serum shut up in the meshes of the latter. In the cruoric as well as the fibrinous clots time also works changes of coloration. In the latter by the mere expression of the fibrin the coagula become less shiny and take on a darker tint, and when deeply colored by red globules they may go through many changes of tint from a violet or red-brick color to a pink. Usually, however, these latter changes require a much longer time to be effected than is properly understood in the term terminal clot. The latter is white, with a yellow or green tint, or again of a fleshy color with spots of deeper hue upon their surface. These are nothing more than small masses of blood, although to superficial inspection they may appear vascular. In structure they may be homogeneous throughout, but this is extremely rare, for in the same clot we habitually find different parts which are evidently of different ages; and not only is this true, but what leads more to confusion in regard to the precise age of a given clot is the fact that a relatively old one is at times juxtaposed or intimately annexed to a purely cadaveric one. To make the distinction of what portion of clot has been formed some time, and what part in the agony, is occasionally almost impossible. Owing to the manner of death or to certain rapid chemical changes which may take place, the interior of terminal clots is at times softened and filled with a puriform material which is probably only softened fibrin.[67] These clots are more or less firm and elastic. They adhere quite intimately by a number of roots to the walls of the heart, and are twined around the chordæ tendineæ, the musculi pectinati, and are closely attached after this manner in the depressions between the columnæ carneæ. Sometimes they send off long projections into the large vessels which proceed from the base of the heart. These latter may be cylindrical in form and fill up the vascular calibre, or appear like so many flattened and ribbon-like strips. The elasticity of these clots is made especially evident when we attempt to tear them away from the cavities in which they are adherent. They come away in small pieces, and show a rough, irregular surface where they have been torn asunder. Upon pressure the terminal clots allow a smaller or larger amount of serum to exude from their surface, according to their age and the site of their formation. If the quantity be large, the clot is much reduced in size and changes considerably its physical characters. It must be evident, therefore, that if a clot be contained in the ventricle, and be submitted for any notable length of time to active and forcible contractions, it cannot contain any large amount of serum. In the auricles near the appendages the clot does not bear any very strong outward pressure--not much more, in fact, than it would in an aneurismal sac. Clots in this situation may have existed, therefore, for quite a time before all or even a great part of their serum has exuded (Legroux). Rarely, terminal clots are somewhat stratified. The form of these clots is variable; usually flat, they may also be globular, ovoid, or thick. As they pass through the cardiac orifices they are narrowed. At a level with the sigmoid valves the full margin of the cusps is marked upon their surface, and discoid masses, formed usually almost exclusively of fibrin, fill the cavities of the cusps and are moulded to their surface. To this condition great importance has been attached as indicating the formation of the coagula prior to death. In fact, Poullet[68] has endeavored to prove irrecusably by experiments upon animals {737} that in all cases where these masses were present the clot had been formed quite a length of time during life. Raynaud,[69] although admitting the ante-mortem foundation of these imprints, nevertheless holds that they are produced in the act of dying. The author,[70] owing to the fact that he has found more than once the amount of fibrin and globules about equally proportioned in the deposits of the sigmoid sacs, considers that they may be formed after death. In this opinion he is upheld by Walshe, who goes even farther, and states that he has seen coagula filling the right ventricle, the infundibulum, pulmonary artery, and its branches, and tightly grasped by all these parts in which this mark was apparent,[71] and yet the coagulum was certainly formed post-mortem. This opinion was further sustained by more than one case observed during life, and in which the final symptoms were not at all those usually assigned to cardiac thrombosis. According to Richardson,[72] the fact that the clot is grooved upon its surface or contains a canicula through its interior is a positive proof of the passage of the blood-current, and hence of its formation during life.

[Footnote 67: _Cycl. of Anatomy and Physiology_, p. 114, 1848.]

[Footnote 68: _Thèse de Montpellier_, 1866. In this sign Poullet also endeavored to show a distinguishing feature between clots formed within the heart and those transported from one of the large veins of the extremities and arrested in the heart. Before Poullet, these sigmoid prolongations had been mentioned by Gallard and studied by Chauveau of Lyons and Gardner of Glasgow.]

[Footnote 69: _Dict. de Méd. et de Chirurgie_, vol. viii. pp. 562 and 565.]

[Footnote 70: _De la Thrombose cardiaque dans la Diphthérie_, Paris, 1872.]

[Footnote 71: V. (after Walshe) such a specimen, No. 3636 Univ. College Museum, London.]

[Footnote 72: _On Fibrinous Deposits of the Heart_, 1860.]

Whilst attaching a certain amount of importance to the signs just mentioned as indicating the age of a clot, Parrot[73] is disposed to consider the color, consistence, intimate attachments, and histological structure of far greater importance in determining their formation some time prior to death. Usually speaking, the terminal coagula have gone through no retrogressive changes as regards their primary elements. The red globules are perhaps paler than normal, but the fibrillæ of fibrin are still distinct and the leucocytes show well-defined nuclei and do not contain any fat-granules. These coagula, both terminal and cadaveric, are found more frequently in the right than the left side of the heart (Bouillaud). For the terminal especially the right auricle is a frequent location (Parrot). This does not coincide with the following table, taken from Legroux, and which shows the relative frequency of the products in the different cardiac cavities: In 48 cases concretions were found "in all the cavities at the same time, 8 times; the right cavities and the left ventricle, 2; the left cavities and the right ventricle, 2; the two ventricles, 4; the two right cavities, 5; the two left cavities, 3; the right auricle, 1; the right ventricle, 7; the left auricle 8; the left ventricle, 8 = 48 times."

[Footnote 73: _Dict. Encyc. des Sci. méd._, Paris, 1876.]

III. Ancient Clots.--There are several varieties which differ considerably in their outward conformation and appearances, and are formed at a period more or less removed from the time of death: _(a)_ Stratified coagula, which are attached intimately to the cardiac walls, and present frequently an aspect which has been confounded with that of true vascularization. So intimate is their adherence at times that to effect their separation the scalpel has to be used, and in the attempt the endocardium is detached. This membrane is frequently affected at the level of their attachments with an alteration of atheromatous nature. The volume of these coagula differs considerably. According to the old writers, they may have become large enough to fill the cavities entirely of one side of the heart and weigh at least a pound.[74] This is evidently an exaggeration, and coagula of this size could only be formed after death. Still, very large clots, formed some time previous to death, have been carefully described by Bouillaud.[75] These should be considered very {738} exceptional cases, and according to Raynaud[76] such masses would inevitably cause immediate death. Notwithstanding this affirmation, an ancient clot so voluminous as to fill an entire cavity has occasionally been found. Such an instance is the one referred to by Parrot,[77] where the left auricle was found distended by a stratified coagulum, whilst the other cavities were relatively empty. Generally, the volume of these clots varies from that of a walnut to that of a grain of millet. Sometimes they are flattened out, cover a large surface, and extend from one cavity into another. It is extremely infrequent to encounter a coagulum which fills more than the one-third or one-half of the cavity which contains it. These coagula have different shapes. They are ovoid, globular, sessile, pedunculated. Their number is usually in inverse proportion with their volume. When they have a certain mass and occupy the cardiac cavities they are often unique.

[Footnote 74: Cited by Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p. 62.]

[Footnote 75: _Traité des Maladies du Coeur_.]

[Footnote 76: _Dict. de Médecine et de Chirurgie_, vol. viii. p. 565.]

[Footnote 77: _Dict. Encyc. des Sci. méd._, 1 Série, vol. xviii. p. 481.]

_(b)_ Warty excrescences, which deposit generally upon the surfaces or margins of the aortic or mitral valves, although they may be found adherent to other portions of the endocardium. These warty growths or vegetations are only so in appearance, for their real structure is mainly that of fibrin. Rarely do we find them in the right heart. They have a jagged mulberry or cauliflower aspect, and adhere to an otherwise healthy endocardial lining or to points where an alteration or fissure already exists. Sometimes they are in the form of rounded pedunculated masses, as described by Laennec,[78] and have given rise to no obvious symptoms during life. These deposits of fibrin should be distinguished from morbid growths and exuded lymph. The latter may be augmented in size by layers of fibrin, and may require close inspection to clearly differentiate them. The two preceding varieties of clot are often apparently due to some constitutional dyscrasia.

[Footnote 78: "Végétations globuleuses," _Traité d'Auscultation médiate_, t. ii. p. 630.]

_(c)_ Globular concretions or fibrinous cysts, the latter term being adopted on account of the well-known contents, which have a grumous or purulent appearance[79] and are of fluid consistence. They are limited by a cyst-wall, and are firmly attached to the walls of the heart either by a single pedicle or by a series of roots intertwined with the columnæ carneæ or musculi pectinati. Usually they occupy situations in the cardiac cavities somewhat removed from the direct current of the blood. The favorite situations for them are at the apex of the left ventricle or in the appendix of the right auricle. According to Rokitansky,[80] they almost invariably occupy the left ventricle, but the observations of later writers show conclusively that this is an error (Bristowe). Thus, Hayden states that in his belief the right chambers are much more frequently the seat of thrombosis than the left chambers. This difference is explained by the greater tendency to stasis in the right heart, where also there is less considerable muscular development. Of 44 fatal cases of valvular lesion, he cites 24 instances of cardiac thrombosis on the right side of the heart, and 12 instances on the left side. No case is reported by him in which the coagulum existed solely on the left side.[81] They have been found inserting upon the cardiac valves, and in this situation, owing to their pedunculated formation and varying position, have sometimes occasioned curious physical phenomena. A rare instance of this kind is cited by Walshe,[82] where, the mitral valve being perforated, the concretion caused at one time a systolic, at another a diastolic, murmur. They vary in size from a pullet's egg to that of a hazelnut, and exist singly in a cardiac cavity or are in considerable {739} numbers. When we attempt to detach them from the cardiac parietes, we frequently tear through some of their roots and leave small masses behind. When quite numerous they are also small in size, and may then be wholly lodged in the interspaces between the fleshy columns. Under these circumstances they are usually continuous with one another and extend their processes underneath the muscular bands, which are only attached by their extremities to the walls of the heart.[83] These clots have been found in the heart free of all attachments. In one such instance reported by Pitres[84] they were very numerous and were contained in all the cavities of the heart. This was a rare example. Their surface is usually smooth and the cyst-wall occasionally very thin. The cyst itself may be unilocular or divided into a number of smaller intercommunicating cavities. Occasionally, through rupture of the sac-wall, the contents have been emptied into the cardiac cavity outside. The color of these globular or ovoid concretions is buff or brick-red, and corresponds very nearly with the fluid contained in their interior. The different coloration of the contents is due mainly to the larger or smaller proportion of the coloring matter of the blood mingled with them. Sometimes these ancient concretions are covered by coagula of later formation, and it is only after close inspection that we can determine their real character. The endocardium is usually intact at their level, and rarely shows signs even of irritative inflammation. Hence we conclude that in an analogous manner with preceding forms of coagula they owe their existence to a constitutional alteration of the blood. Whilst the rule is that on section these globular concretions offer an interior consistence which is more or less softened, yet occasionally we encounter one in which the structure is homogeneous throughout, and presents very closely the appearance everywhere revealed by its external aspect. The elements, under these circumstances, of the sac-wall and the interior part of the concretion are almost identical. Under the microscope these are recognized as being mainly compound granular bodies, oil-globules, some imperfect cells, or altered blood-corpuscles surrounded by a network of fibrin. After a brief period, and in consequence of disintegration, the contents of these cysts may resemble pus and show certain differences in their constituents according to their appearance. "When white or buff-colored they consist almost solely, if not solely, of molecular matter, oil, and broken-down corpuscles, with which are frequently mixed compound granular cells and colorless acicular crystals. When presenting a brick-red or chocolate hue they exhibit, in addition to the elements just mentioned, numerous blood-corpuscles more or less altered, and consequently more or less indistinct, and occasionally also ruby-colored, rhomboidal, hæmatoid crystals."[85]

[Footnote 79: _Pathol. Society's Trans._, vol. xiv. p. 65 _et seq._]

[Footnote 80: _Path. Anat._ (Syd. Soc. trans.), vol. iv. p. 217.]

[Footnote 81: _Dis. of the Heart and Aorta_, Part ii. p. 1020.]

[Footnote 82: _Dis. of the Heart_, 4th ed., p. 106 _(b)_.]

[Footnote 83: Bristowe, in _Reynolds's System of Medicine_, vol. v. p. 107.]

[Footnote 84: _Bull. Soc. anatomique_, Feb. 5, 1875.]

[Footnote 85: Bristowe, on "Softening Clots in the Heart," _Path. Society's Trans._, vol. xiv.]

It is to the rupture of cysts of similar characters with those just detailed that may be properly ascribed pyæmic symptoms occasioned by the diffusion of their contents in the circulation.[86]

[Footnote 86: Ogle, _loc. cit._]

Coloration.--The color of ancient coagula varies from a dull white to that of a grayish, slightly yellowish, or slate tint. These extremes of color and all intermediary shades depend upon the age of the clot, the manner of its formation, the larger or smaller number of red corpuscles shut up in its fibrinous texture, and the chemical transformations it has undergone. In order that the opinion at first formed of the age of a clot by its coloration may be of some value, it is essential that this ocular examination may be further aided by the results of microscopic investigation. Occasionally, as already stated, the ancient coagula are covered by clots of late formation, but these may ordinarily be distinguished by even slight inspection.

{740} Consistence.--Usually the ancient coagula are firm, friable, and without elasticity. They are then readily detached from their insertions by traction, and always come away in small masses. On other occasions they offer considerable cohesion, and preserve their form when we attempt to tear through or break them. The degree of friability is in proportion with the regressive alteration of their substance. Sometimes the clinical history apparently indicates that a heart-clot has remained soft during several years (Walshe). Coagula, however, which have evidently been formed for a considerable period are frequently fibrinous or cartilaginous in their structure, and a deposit of calcareous material in their interior or upon their surface is occasionally found.

Organization.--The question as to whether the coagula formed within the cavities of the heart can become organized has been variously determined. Amongst those authors who speak of the progressive evolution of the clot, some admit the possibility, others absolutely deny it. That these cardiac clots are frequently coherent, firm, fibrous, or lamellated is no proof that they may become organized, since the same features prevail in the old coagula contained in an aneurismal sac. These latter, as we are aware, are readily separated from the membranous walls which surround them, and never take on a similar structure to theirs or give evidence of a new vascular formation in their interior (Legroux). Cruveilhier, Monneret, and Robin consider these coagula to be dead structures incapable of organization. Those who believe in the possibility of the clot becoming organized support their convictions by referring to certain rude resemblances with organized tissues; yet even these (Hunter, Laennec, Bouillaud) have never established their statements by any unquestioned examples. Moreover, we should remember that formerly investigations were made in a very imperfect manner. The instruments employed were insufficient and poorly adapted to accurate research of this kind. Whenever the organization of a clot was admitted, it was in connection with a preceding inflammation of the endocardium, which itself occasioned a plastic exudation. This exudation, becoming organized, was the means, according to them, of introducing a new vascular formation into the clot. According to the later researches of Virchow, Billroth, Feltz, etc., there can be no doubt as to the vascularization at times of ancient coagula contained in the vessels. In regard to cardiac coagula, we should urge the facts of their greater size and different situation as rendering their organization very improbable. Moreover, hitherto no experimenter has injected any vascular twigs in a cardiac thrombus. To sum up: whilst it appears possible that a cardiac clot may become organized in view of what has been shown to take place in vessels, still the facts thus far closely observed do not corroborate strongly this opinion, and we cannot pronounce ourselves in an absolute manner (Raynaud). Amongst the coagula least likely to become organized are the very large ones and those connected with the heart-walls by a narrow pedicle.

DIAGNOSIS.--From the preceding signs and symptoms can an accurate diagnosis be established of the presence within the cardiac cavities of fibrinous coagula? Evidently not if these formations be of small size and be situated where they do not interfere notably with the circulation. This is eminently true of those which are formed slowly in the auricular appendix or at the apex of the ventricle. In order that even a probable diagnosis of cardiac thrombosis should be made, it is essential that the coagulum should occupy a certain space, that it should be fixed near or at one of the orifices, or interfere in a perceptible degree with the valvular play. Due consideration is always to be had for etiological conditions when these can be wholly or in part known. If, for example, there be present an acute or chronic affection of the heart, and in a sudden manner, without apparent or sufficient {741} cause, the symptoms and physical signs pointing to greater disturbance of the function of this organ become developed, we naturally suspect the formation of a cardiac coagulum. And this is true, although the signs of this production are not dissimilar to those indicating structural heart disease. Thus, the rapid development of præcordial dyspnoea, of rapid, tumultuous action of the heart, of feeble, depressible, irregular pulse, and of extreme pallor or lividity of surface, combined with coldness of the extremities and extreme anxiety, gasping for breath, and jactitation, indicate under like circumstances the formation of heart-clot. This diagnosis is further confirmed when upon listening to the respiration we find that the air enters and goes out of the lungs freely, and that there is no evidence in the lungs of any sudden obstruction or inflammatory condition. Of course it is very important for the physician to be familiar with the patient's previous condition and antecedents. If the accidents just referred to become developed without these facts being known, it would be far more difficult to make a diagnosis of cardiac clot than when the accidents take place whilst the patient is being constantly watched and when the physical state never varies without being observed and noted. If there be a venous obstruction in one of the large veins of the limbs, either at the time or prior to the formation of the cardiac thrombus, the symptoms occasioned by it will give even more significance to those which show heart trouble. The same information is also afforded by sudden obstructions in different portions of the arterial channels; and whenever these embolic transports take place they show, with tolerable certainty, the pre-existence of an intra-cardiac thrombus. As we can readily understand, it is far less practicable to make the diagnosis of a clot which develops slowly, and therefore gives rise to symptoms gradually, than of one which has manifested itself more or less suddenly.

The physical signs of cardiac thrombosis as a complication of cardiac disease are not necessarily very significative. This is true, first, because there may not be an abnormal murmur owing to the weakness of the cardiac contractions; second, because (even if it be present) the murmur may be readily confounded with one already existing which is occasioned by organic heart disease. Theoretically, the first sound of the heart should be muffled by the presence of a coagulum of any notable size which interferes with the play of the valves, but this might be also occasioned by the presence of chronic cardiac valvulitis. Still, if an abnormal murmur, harsh or soft in character, become suddenly developed over the pulmonary or aortic orifice, where it was known not to have previously existed, it is a physical sign which points with much certainty to the presence of a heart-clot. Whenever the signs and symptoms given above which show disturbance in the heart's action occur in a similar sudden manner in the course of an inflammatory or cachectic disease, such as pneumonia, cancer, or phthisis, we should properly suspect the formation of an autochthonous or embolic clot in the heart. These formations arise also, not infrequently, as an instantaneous complication in the duration of acute articular rheumatism, certain of the eruptive or acute fevers[87]--_i.e._ measles, scarlatina, etc.--and the puerperal state, as we have already pointed out in another portion of this article. In pneumonia, as in the other affections just mentioned, if no fresh inflammatory area either in the lungs or in another viscus can be discovered which is sufficient to explain the occurrence of new alarming symptoms of obstructed circulation, the difficulties of a correct diagnosis are much less than if organic heart disease be present. And this is particularly true because another solution of the cause of the patient's condition is less available (Flint). Besides, if it be sure that suddenly an endocardial murmur is developed where none existed previously, this sign, {742} taken with the striking rational and other symptoms referable to the heart, is one of great corroborative value as regards diagnosis. Not only does cardiac thrombosis occur under the circumstances mentioned already when we have a certain right to expect it by reason of its relative frequency, but occasionally it will become evident by its symptoms under conditions where we have no right to look for its development. In these instances it is only by a diagnosis of exclusion that we can discover the correct interpretation of the phenomena presented. In the obstruction caused by a heart-clot developed in the right cardiac cavities there is of course stasis in the systemic venous circulation in consequence of the small quantity of blood which can pass through the heart on its way to the lungs. This condition, moreover, develops a peculiar dyspnoea which has been very striking at times, and which has been particularly considered by Richardson,[88] so as to differentiate it with an analogous but dissimilar state which prevails when the obstruction exists in the lungs or other portions of the respiratory tract. In the former case if we listen carefully to the breathing the vesicular murmur is normal in quality and pitch, although of exaggerated intensity, and the dyspnoea is evidently due to the fact that the air lacks, so to speak, a sufficient quantity of blood to arterialize it. Consequently, the surface of the body is pale rather than cyanosed, and the heart-sounds and pulse are feeble, tumultuous, or notably irregular. In the latter case the lungs are congested or there is some other evident obstruction of the larynx, trachea, or bronchial tubes which prevents the entrance into the alveoli of a sufficient quantity of blood for the purposes of hæmatosis. Hence a rapidly generalized cyanosis becomes developed, the superficial veins are generally turgescent over the surface of the body, and what with the irregular, feeble action of the heart, although its normal sounds are distinctly defined, the violent convulsive movements of the voluntary muscles, the abolition of the intelligence of the patient toward the fatal termination, we have a sufficient number of signs which point distinctly to an asphyxic state. Finally, at the end of life in the former case it is the heart which first comes to a stop, whereas in the latter the lungs are the organs which are primarily arrested in their movements. These differential signs have great practical importance. Unfortunately, there are instances in which it is extremely difficult to assign in proper degree the symptoms occasioned by the heart-clot on the one hand or obstructed respiration on the other.

[Footnote 87: Keating, _Am. Journ. Med. Science_, Jan., 1885, p. 122, v.--an able article, entitled "Heart-Clot as a Fatal Complication in the Acute Fevers of Childhood."]

[Footnote 88: _Medical Times_, vol. i. p. 330, 1856.]

We have in another place pointed out this fact where at the same time there was present a membranous deposit of diphtheritic membrane blocking up the calibre of the larynx and a cardiac coagulum distending the right cardiac cavities.[89] In like manner, there may be an inflammatory complication in the lungs themselves--_i.e._ broncho-pneumonia--which by its sudden beginning and the rapid rise in the number of the respirations and the pulse should awaken a suspicion as to the cause of these symptoms. An error in regard to the modifying influence of this accident would be possible were it not that broncho-pneumonia, even of limited extent, reveals itself by stethoscopic signs, and, moreover, would not explain all the phenomena which arise. These are: the excessive pallor, the special kind of anxiety, the weakness and inequality of the pulse, the muffled heart-sounds, and the very rapid death. In exceptional instances, when the lungs are merely affected with hyperæmia, the characteristic signs of cardiac thrombosis are more readily recognized.

[Footnote 89: Robinson, _loc. cit._, p. 48.]

That form of uræmia known as the dyspnoeic or respiratory, which has been well described by Fournier, is sometimes confounded with heart-clot. Its commencement is often sudden. Soon labored respiratory action is very marked, and approximates true orthopnoea, although there is absence of {743} pulmonary lesion. From the cardiac disturbance it can be differentiated by the pulse, the cardiac rhythm, bodily pallor, and the usual evidences of kidney disease.

The distinguishing features between pulmonary embolism or thrombosis and the deposit of fibrinous coagula in the heart are extremely difficult to delineate. At times the cardiac coagula manifest their existence quite as suddenly as does pulmonary embolism. Nothing, moreover, prevents the formation[90] at a simultaneous moment of a coagula in the veins as well as in the heart. The puerperal condition, which is a predisposing cause of an excessive relative amount of fibrin, is likewise an efficient cause of both these formations. Besides, we should add, there is no reason why the fibrinous coagulum of the heart in changing position should not throw off a plug which will block up the pulmonary artery completely. To separate these conditions or to make a diagnosis between them other than one based upon probabilities is not possible.[91]

[Footnote 90: Ball, _Des Embolies pulmonaires_, Paris, 1862.]

[Footnote 91: Vernay, _Gaz. médicale de Lyon_, Nos. des 13 Mars et 22 Mars, 1868.]

We do not consider it essential in this place to go farther and make known the signs by which we shall be able to distinguish cardiac thrombosis from certain affections of the larynx, such as laryngitis stridulosa, oedema glottidis, and membranous laryngitis, or indeed from asthma or functional disturbance of the heart. It is easy, indeed, to confound this affection with organic cardiac disease, but what we have already said should enable us to make the distinction with facility. In certain infectious diseases, and more particularly diphtheria, death by cardiac paralysis has been described. In these instances there would seem to be a real impairment, functional or organic, of the structure of the pneumogastric nerves, which is accompanied by an irregular action of the pharyngeal muscles, by vomiting,[92] extreme slowness of the pulse,[93] a remittent form of syncopal attacks, and powerless action of the heart. No such combined symptoms appear in our description of cardiac thrombosis, and they are therefore sufficient, in our opinion, to substantiate the opinion of a morbid entity which can be satisfactorily explained by recognizing solely a lesion of nerve.

[Footnote 92: Jenner, _Diphtheria, its Symptoms and Treatment_, London, 1861, p. 42 _et seq._]

[Footnote 93: Maingault, _Actes de la Société méd. des Hôpitaux_, 5^{ème} Fascicule, 1861, Obs. 40.]

In many examples of death by heart-clot the aspect of the patient is very much that of one who dies in the period of a collapse from cholera (Flint), the great difference between the two states consisting in the fact that in the latter there is no notable degree of dyspnoea.

The diagnosis between coagulum of the right and left side of the heart can be determined with some accuracy if strict attention be paid to the effect of the presence of the clot on the normal cardiac murmurs. If, for example, the clot is situated in the right ventricle, it is probable that by interference with the tricuspid play it will render the valvular sound occasioned by closure less distinct, and for this reason the first sound of the heart will not be heard as well to the right as to the left of the sternum. In a similar way, the diminution of sound at the pulmonary orifice in the left second intercostal space may be explained, for the extension of the concretion into the origin of the pulmonary artery will almost certainly prevent the perfect closure of its cusps (Richardson). In deposits of fibrin in the left cavities of the heart we naturally distinguish less well the cardiac sounds along the left border of the sternum than toward its right margin. We also have congestion of the lungs, owing to the fact that a smaller quantity of blood is able to pass through the partially-filled left heart. To this is added a tumultuous, irregular action of the heart and a feeble pulse. It is proper to add, however, that excepting cases of chronic organic heart disease with dilatation or {744} degeneration of the walls deposits of fibrin in the left heart are relatively very infrequent.

In cases of acute endocarditis we have no means usually to distinguish between the general symptoms of nervous shock and the physical signs occasioned by cardiac thrombosis on the one hand, and rupture of a valve or tendinous cord on the other. According to Walshe, this could scarcely be otherwise, as clotting to a greater or less extent must necessarily deposit around the spot where the tear takes place. In view of a case reported by Hammer[94] of sudden cardiac failure in which the symptoms prior to death pointed to possible intra-cardiac thrombosis, and where at the autopsy thrombotic occlusion of one of the coronary arteries was found, it is well to bear in mind the possibility of this rare occurrence. The principal features of this case were the suddenness of the collapse, pallor, slight dyspnoea, and extremely slow pulse, ranging from 23 to 8 to the minute!

[Footnote 94: _Abstract of Med. Science_, 1878, p. 208; _Lond. Med. Rec._, March 15th.]

PROGNOSIS.--The prognosis of fibrinous coagula in the cavities of the heart is always extremely serious. The gravity of the situation is, however, in some degree proportionate to their size, their situation, and the rapidity of their formation. Thus, for example, those which are spread out like a membrane over the interior surface of the heart, as has been noted after endocarditis, are of less serious a nature than those which are polypiform. As regards the polypiform concretions which we encounter singly, which are small and formed slowly, they will be so much more dangerous as the lobe held by the pedicle can become engaged in the orifices of the heart or the vessels which take origin from it.[95] Certain well-known observers, it is true, such as Bouillaud, Barth, Roger, Racle, Meigs, and Armand, have stated their belief that in rare instances these coagula may become dissolved and disappear. Indeed, we ourselves have become convinced in more than one exceptional case that the morbid phenomena manifested, both local and general, were but the evident proofs of the beginning of fibrinous deposit in the right ventricle of the heart, and yet we have seen these evidences change their characters and finally disappear under proper treatment, leaving the patients ultimately in as good health as they were previous to their formation.[96]

[Footnote 95: Armand, _Des Concrétions fibrineuses polypiformes du Coeur_, Paris, 1857, p. 49.]

[Footnote 96: We are more assured in regard to this possibility than we were ten years ago (v. Thesis).]

Legroux does not believe cardiac concretions can be reabsorbed, and with Cruveilhier he admits them to be dead formations. Nevertheless, he admits that fibrinous cysts may entirely disappear by a process of progressive liquefaction. Moreover, a case reported in his exhaustive article which he observed makes him acknowledge that a fibrinous coagulum may diminish, retract, atrophy, form adhesions with the cardiac walls, and thus not interfere notably with the cardiac functions.[97] The fact, however, that there may be no present suffering does not shield such a patient surely from future accidents of a serious nature brought on by his intra-cardiac condition. About the diagnosis, however, of intra-cardiac thrombi, especially when a perfect cure has been established, there always will remain an element of justifiable doubt, and particularly in those conditions where an underlying constitutional dyscrasia of grave import was present. This latter state of itself often becomes either rapidly or eventually mortal. Apart from the gravity of cardiac thrombosis in view of its evidently pernicious influence upon the heart, it is likewise a very serious affection on account of the possibility of its giving rise to embolic transports into different viscera (brain, lungs, etc.), which themselves may bring about a direct and speedy fatal termination. Even when the embolic plugs do not occasion such considerable obstructions {745} of important vascular channels as to cause rapid death, they may fill up numerous capillaries of the economy with material of a kind which shall be followed, sooner or later, by septic symptoms or those of pyæmic poisoning.

[Footnote 97: _Gazette hébdomadaire_, 1856.]

TREATMENT.--According to certain well-known authors, all curative treatment of heart-clot is useless (Bucquoy). Others, more sanguine, repose confidence in the internal use of alkalies, even when a fibrinous deposit in the cavities of the heart has commenced to form. A third class of observers, whilst they doubt the efficacy of any treatment under these circumstances in causing the disaggregation or absorption of an intra-cardiac coagulum, nevertheless believe we can limit the rapidity and size of its formation, and also retard the fatal termination, by giving time sufficient for adhesions to form with the cardiac walls. Richardson has proposed the administration of minim x doses of liquor ammoniæ at short intervals in an ounce of water, in order to dissolve existing coagula, and reports favorably upon its use. Gerhardt[98] counts upon better results from the use of a saline spray of bicarbonate of sodium of the strength of ½° to 1½°. This spray should be frequently inhaled, and in this manner, he believes, the heart is reached more directly and effectually. Successes are claimed by the use of this method of treatment. According to Flint,[99] the idea of giving any remedies with a view to dissolve solidified fibrin is absurd, whereas as a preventive treatment it is legitimate in circumstances where this state is likely to occur, and may even become an important therapeutic object.

[Footnote 98: _Deutsches Archiv für klinische Medicin_, vol. v. p. 207, summarized in the _Dublin Quarterly Journal of Medical Sciences_, May, 1869, p. 421, quoted by Walshe.]

[Footnote 99: _Diseases of the Heart_, p. 285.]

Alkaline remedies are said to have the power of holding the fibrin of the blood in solution. If this be true, they are certainly indicated to prevent coagulation. Moreover, if the fibrin in normal blood be held in solution owing to the presence of ammonia, it must be evident that this remedy is specially indicated in carrying out a secondary object of the prophylactic treatment. Bartholow[100] still maintains, however, that frequent small doses of ammonium carbonate afford the best chances of relief even when the coagulum is already formed. The latter distinguished author advises in cases which are most imminent intravenous injections of ammonia. The proportions should be one part of ammonia to three of water. The vein selected must be the jugular, and special precautions taken to avoid the entrance of air or a foreign body into the circulation. With attention to this formal indication there is little or no danger from these injections, as has been many times proven experimentally. Walshe[101] regards the use of carbonate of ammonium, combined with bicarbonate of potassium, in five-grain doses, repeated three times daily, as a mere prophylactic, but as the best, after all, we possess, and recognizes from its use the only practical outcome from the enormous sacrifices of canine life made by Magendie in his experiments to illustrate his lectures on the blood. In spite of the numerous attempts to fluidify the blood, these efforts have always remained unsuccessful (Raynaud), and Legroux, who first proposed it, in his later writings abandoned the alkaline treatment as useless. The most he affirms that can be done is to combat with energy cardiac inflammations.

[Footnote 100: _Practice of Medicine_, New York, 1880, p. 285.]

[Footnote 101: _Diseases of the Heart_, 4th ed., London, 1873.]

There is, however, a palliative medication which is indicated by the presence of the obstacles to the circulation within the heart. The general condition must be kept in view in carrying out treatment rather than the local signs. A properly combined therapeutic method in which the derivatives and counter-irritants play an important rôle offers, in Legroux's estimation, the best solacing means to oppose to the developed accidents. We must, however, maintain the patient in a quiet attitude and administer drugs which {746} shall tranquillize pain and diminish anxiety. The counsel to keep the patient absolutely at rest is of primary importance in view of the sudden fatal accidents which have frequently occurred either in getting into bed after descending from it, or in sitting up and reaching for something the patient needs. The patient should be placed in bed in a semi-recumbent position, properly supported, and arrangements must be made so that all fatigue of eating and drinking or attending to his excrementitial functions are provided against. Of course we should treat a case of cardiac thrombosis complicating a frank inflammatory condition, such as acute endocarditis, certain forms of pleurisy or pneumonia, very differently from a case in which the state is one of relative feebleness or adynamia, as in the advanced stages of diphtheria, or after profuse uterine hemorrhage during or after confinement. In the first category of cases it may be in a few rare instances that local depletion of the blood by means of leeches or venesection is still indicated, especially if the patient be one of more than usual vigorous frame. In any example of this sort it is obvious that the internal use of the alkalies, the employment of revulsives (_i.e._ dry cups), and counter-irritants over the chest (as previously mentioned), adjoined, perhaps, to the action on the emunctories by diluent drinks, are the means which offer us the best guarantee of success. But how shall we act with our second class of cases? Certainly, we ought not for one moment, with our actual physiological knowledge, to consider the propriety of taking blood from a patient thus affected. May we use the alkaline treatment with reasonable hopes of benefit in a curative way? Yes, if we employ certain of the stimulating salts, like carbonate of ammonium, or even this salt combined with moderate doses of bicarbonate of potassium. We should remember, however, that these drugs are intended particularly to combat the pathological condition of the blood which apparently underlies the formation of fibrinous concretions in the heart.

Against the possible fatty degeneration of the cardiac muscular fibre, or the functional or organic affection of the pneumogastrics, which predispose to or accompany the production of cardiac coagula, we must make use of digitalis in small, repeated doses, and nux vomica or some other preparation containing strychnine. I have on more than one occasion seen these agents do evident good,[102] and on this account am encouraged to urge their exhibition. With Hertz, we are not disposed to believe that digitalis, when given with a little precaution, and especially in urgent cases, is contraindicated by the danger feared by Gerhardt and Penzoldt, that it favors thrombosis of the right side of the heart and gives rise to new emboli.[103]

[Footnote 102: _Loc. cit._, p. 68.]

[Footnote 103: _Ziemssen's Cyclopædia_, vol. v. p. 326.]

It is almost needless to add that under like circumstances we should insist upon the frequent use of stimulants, like alcohol, chloroform, and ether, in the form of brandy, whiskey, spiritus chloroformi, or spiritus ætheris, or repeated doses of strong black coffee with one of the preceding preparations added to it. In regard to the prophylactic use of alkaline treatment continued during several days and in large or frequently-repeated doses, we advise against it for the reasons, first, that we do not know, in advance, the precise conditions in which fibrinous intra-cardiac coagula will form; and second, because though the alkalies have a well-known antiplastic action, they act as depressants to the general economy when employed in the manner mentioned, which is the sole method in which their internal use would be of some practical advantage.

Whenever we have in diphtheria a case in which there is at the same time obstruction of the glottis by a false membrane and clogging of the heart by a fibrinous coagulum, we should abstain from performing tracheotomy on account of its evident uselessness.[104]

[Footnote 104: _Medical Times_, vol. ii. p. 617.]

{747}

NEUROSES OF THE HEART.

FUNCTIONAL DISORDERS OF THE HEART'S ACTION; ANGINA PECTORIS; EXOPHTHALMIC GOITRE.

BY AUSTIN FLINT, M.D.

The neuroses of the heart are those affections relating to this organ which do not necessarily involve either inflammation or structural lesion of any of its component parts. The larger proportion of these affections may be grouped under the name functional disorders of the heart's action. The affection called angina pectoris is characterized by pain more or less intense. It is generally associated with disordered action of the heart, and also with cardiac lesions. It may, however, exist without either disordered action or lesion, and hence it is with propriety included among the neuroses of the heart. Exophthalmic goitre is invariably associated with disordered action of the heart, but it has other very marked symptomatic traits which give to it a distinctive character. The name of the affection refers to these. The cardiac disorder is, however, the most constant, and, pathologically, the most important, and therefore the affection may be considered as one of the neuroses of the heart. In this article the functional disorders of the heart's action, irrespective of angina pectoris and exophthalmic goitre, will be first considered, and afterward these two affections will receive separate consideration.

Functional Disorders of the Heart's Action.

The disorders of the heart's action which agree in respect of their functional character present marked variations as regards the manner in which the action is disordered. An account of these will be given under the name Varieties, together with the symptomatology.

VARIETIES AND SYMPTOMATOLOGY.--The term palpitation denotes a violent or tumultuous action of the heart. A type of this variety of disorder is afforded when the heart is much excited by fear or some other intense mental emotion. The fact that emotional excitement will produce in some persons notable palpitation, and in others little or no disturbance of the heart's action, illustrates differences inherent in the organ itself as regards susceptibility to disorder. These innate differences are exemplified in cases of disease. In certain persons the heart readily takes on a morbid functional disorder from causes which in other persons do not produce this effect. A peculiar susceptibility to disorder is expressed by the term irritable heart, a term introduced by DaCosta. Instead of the violence which characterizes palpitation, there may be irregularity, with notable feebleness of the heart's action. The patient often describes this variety of disorder as a fluttering of the heart. The consciousness of the disorder is less distinct than when the {748} disordered action is violent. With irregularity are generally associated increased frequency of the heart's action and præcordial distress. The degree of disorder as respects either violence or feebleness and irregularity of action differs in different cases within wide limits. Intermittence is another variety of disorder. The intermission may extend over a period of one, two, three, or more beats. It is sometimes preceded or followed by increased frequency of action, and it sometimes occurs without any other rhythmical disturbance. The patient is usually conscious of the intermittence, and it is apt to occasion great alarm, especially before the mind has become accustomed to it. The intermissions occur more or less frequently in different cases and at different periods in the same case. In the cases of palpitation in which the heart acts with violence it is not probable that the power of the heart's action is increased. The systolic ventricular movements are quick and have a spasmodic violence, without actual increase of force. The first sound of the heart over the apex under these circumstances is short and its quality valvular. The valvular element of this sound is predominant and intensified in consequence of the quickness of the systolic movements and the small quantity of blood in the ventricles when the ventricular systole takes place. Owing to the latter physical condition the range of movement of the auriculo-ventricular valves is greater and the valvular sound proportionately increased. The systolic movements of the apex against the chest-wall sometimes give rise to a ringing or metallic sound (cliquetis métallique).

A rare variety of functional disorder which has received but little attention is notable infrequency of the heart's action. The revolutions of the organ were reduced to sixteen per minute in a case reported by Thornton.[1] In 1876, I reported 5 cases, the reduction in frequency varying from 26 to 40 per minute.[2] In one of these cases there was marked intermittency, and in another case the action of the heart was irregular. With these exceptions the rhythm was regular. I have met with a few additional instances since these cases were reported. In this variety the disorder continues for several successive days, and it may be for a much longer period. A persistent infrequency sometimes remains as a sequel, recovery in other respects being complete. In one of my reported cases the revolutions were 36 for several weeks after recovery. In these instances the infrequency of the heart's action, which is sometimes a congenital peculiarity, is acquired. Hewan has reported his own case as an illustration of this fact. His normal frequency had been 72, but after a period of intense study the frequency gradually decreased, and finally remained at from 28 to 32 per minute.[3] This variety of disorder will claim distinct consideration with reference to diagnosis and etiology. It may or may not be accompanied by præcordial distress.

[Footnote 1: _Trans. Clinical Society of London_, vol. viii., 1875.]

[Footnote 2: _American Practitioner_, January, 1876.]

[Footnote 3: _London Med. Times and Gazette_, March, 1875.]

The more frequent varieties of disorder of the heart's action occur in most instances in paroxysms. The paroxysms differ widely in duration as well as in their intensity. They may last for an instant only or for many continuous days. Exceptionally the duration is much longer. I have known a persistent and very great increase of frequency of the heart's action with irregularity, and such a degree of weakness that the pulse could with difficulty be counted, to continue for several weeks, leading to oedema of the lower limbs, prostration, and pallor, so that the patient's appearance was that of one moribund. In this case before the attack and after recovery there was no evidence of any other affection than functional disorder of the heart, and to this the patient had long been subject. In another case an extremely irregular action of the heart continued unceasingly for more than two months, there {749} being no signs of either an inflammatory or a structural affection of the organ, and the functional disorder at length ceasing. As a rule, an attack of functional disorder of the heart implies a liability thereto; other attacks occur after variable intervals. This fact involves a peculiar susceptibility, or, in other words, an irritable heart.

The symptoms referable to the heart may be combined with those of coexisting affections. Disturbances of digestion are frequently associated. Paroxysms of disordered action of the heart are often accompanied by gastric flatulence, and gaseous eructations afford relief. Patients are apt to endeavor to eructate by voluntary efforts. Other evidences of indigestion are not infrequent. The mind is much disturbed, especially if previous paroxysms have not occurred. The facial expression shows anxiety. The apprehension is of organic disease of the heart and of sudden death. This apprehension is excited in a marked degree by intermittence of the heart's action. It is often extremely difficult to convince patients of the absence of immediate danger. They require to be assured of this fact over and over again, and whenever a paroxysm occurs. This statement applies even to medical men who suffer from functional disorders of the heart's action. The surface is usually cool or cold. It is sometimes bathed in perspiration--a symptom probably due, in a great measure, to the condition of mind. Exclusive of angina pectoris, paroxysms of functional disorder are not attended by præcordial pain. The paroxysms may cease either suddenly or after a gradual improvement. The cessation is abrupt in the instances in which the paroxysms last but an instant or but a few moments, and not infrequently when the paroxysms are of much longer duration the normal rhythmical action is at once resumed.

The variety of disorder characterized by diminished frequency of the heart's action is often associated with cerebral disturbance. In 2 cases cited in my paper there were severe epileptiform seizures, together with frequent epileptoid attacks; in 2 cases there was mental excitability amounting to delirium; and in 1 case there was great mental and physical prostration with gastric irritability, the latter due apparently to cerebral disturbance. In 1 case only there was no evidence of disorder of the brain. Of 3 cases which have fallen under observation since the publication of my paper, in 1 there was notable mental disturbance, the mind remaining intact in the other 2 cases.

DIAGNOSIS.--Certain facts pertaining to functional disorders of the heart's action in their ordinary paroxysmal forms render the diagnosis probable. One of these is the occurrence in paroxysms, the action of the heart being normal in the intervals. Another fact is the occurrence of the paroxysms at night oftener than in the daytime. The ability of the patient to take active exercise without exciting a paroxysm and without discomfort is evidence that the paroxysmal affection is functional. A diagnostic feature of a purely functional disorder is great apprehension connected with the disordered action of the heart. The patient is apt to feel that there is imminent danger of sudden death. So strong is this apprehension that it is sometimes difficult to overcome it by positive assertions of the absence of danger. On the other hand, disordered action of the heart, when incident to structural affections, occasions comparatively little mental disturbance; the patient suffers chiefly or exclusively from the physical ailments. In a purely functional affection the patient generally is vividly conscious of the disordered action, whereas the action in structural affections may be greatly disordered and the patient take no cognizance of it. The existence of certain causes to be mentioned under the head of the Etiology bears upon the diagnosis. The liability to functional disorders, as evidenced by previous attacks, is also to be taken into account. These facts, however, are not fully adequate for the exclusion of {750} structural affections of the heart. Moreover, the persistence in some cases of notable disorder for days, weeks, or even months, would seem to render highly probable the existence of some structural affection. The basis of a positive diagnosis is the exclusion, by the absence of their physical signs, of inflammatory affections and lesions of structure.

The physician who undertakes to diagnosticate functional disorders of the heart by symptoms alone--that is, without physical exploration--must often be in doubt, and if not prudently distrustful of his ability as a diagnostician, he is liable to commit errors which are sometimes extremely unfortunate. I was requested to see a young woman who was represented as suffering from a disease of the heart from which she might die at any moment. It was stated to me that her situation was perfectly understood by herself and her family, and that the object of my visit was simply to satisfy some of her friends. I found her in a dark room, with every arrangement to prevent the least mental excitement and physical exertion. Fearing that my questions and the examination of the chest might occasion disturbance which would prove fatal, it was proposed that one of her family be made the medium of the former, and that the latter be dispensed with. This was of course objected to on my part. My questions she answered in a feeble whisper. The examination of the chest showed the absence of all physical signs of disease. The affection was purely functional and wholly devoid of danger. I could cite from cases which have come under my observation not a few in which the error of imputing functional disorders to organic lesions has occasioned the loss of years as regards the duties and pleasures of life, together with the unhappiness incident to living in daily expectation of sudden death. With a degree of practical knowledge of auscultation and percussion sufficient to recognize the signs of inflammatory and structural diseases, and self-confidence sufficient to decide upon the absence of these signs, there is but little liability to error in the diagnosis of functional disorders.

If the apex-beat be in its normal situation, and the areas of the superficial and deep cardiac regions be not extended, the heart is not enlarged; and if there be no endocardial murmur it may be inferred that the valves and orifices are normal. The exclusion of structural lesions under these circumstances is almost positive. It is open only to the exception that certain occult lesions may exist, such as fatty degeneration and obstruction of the coronary arteries. Aside from the infrequency of these, the history and symptoms may render their existence extremely improbable. A hæmic murmur at the aortic or the pulmonic orifices or at both orifices is not uncommon. That the murmur is inorganic may generally be determined by other evidences of anæmia, by an arterial murmur in the neck, and by the venous hum. With the results of physical exploration as just stated, whatever may be the form of disorder, whatever may be its intensity, whatever may be its duration, and whatever may be the associated symptoms, it may be declared to be purely functional.

The diagnosis is less simple and easy when functional disorders occur in connection with structural lesions, but without any relation of cause and effect. Lesions affecting the valves or orifices of the heart often exist without giving rise to any appreciable disturbance. They are either innocuous or their effects do not occasion any inconvenience of which notice is taken. How often is it that an examination of the chest reveals the signs of cardiac lesions which had not been suspected by either the patient or the physician! How often are applicants for life insurance astonished when told that they are not insurable on account of the signs of a cardiac affection! Now these persons are liable to functional disorders of the heart from the causes which produce them in those with perfectly sound organs, the cardiac lesions having no part in the etiology, but perhaps contributing to render the disorders more {751} intense. The problem of diagnosis in these cases is to determine that the functional disorders are not dependent on the lesions. Were they thereon dependent they might denote grave disease, but if not thus dependent they have little or no gravity. This diagnostic problem is to be solved, in the first place, by attention to the inquiry whether the lesions are in proportion to the disturbance of the heart's action. Valvular lesions, if the heart be but little or not at all enlarged, are either innocuous or occasion small inconvenience. This fact will often suffice for the solution of the problem. Moreover, the physical signs may show that the lesions involve neither valvular insufficiency nor obstruction, or, at all events, not in a degree adequate to account for the disturbed action; in the second place, the symptoms are to be considered with reference to the inquiry whether they belong to the clinical history of structural affections or of functional disorders; and, in the third place, the existence of any of the well-known causes of functional disorders is to be taken into consideration. The error is not uncommon of attributing functional disorders to coexisting lesions when the connection is one of mere coincidence. This error may be as unfortunate as that of supposing that functional disorders denote structural affections when the latter are entirely wanting.

Certain considerations, aside from the exclusion of organic affections of the heart, apply particularly to the diagnosis of that variety of functional disorder characterized by infrequency of the heart's action. It is to be ascertained that the infrequency is not a normal peculiarity, either congenital or acquired. Napoleon the Great was a well-known instance of normal infrequency, the number of beats being 40 per minute. As a rule, if an intelligent adult person has habitually a notably infrequent pulse he becomes acquainted with the fact, and therefore if he be ignorant of such a peculiarity it may be inferred that it is not normal.

There is a curious form of functional disorder which would lead to the error of inferring infrequency of the heart's action from the pulse. The disorder is characterized by the regular alternation of a ventricular systole giving rise to a radial pulse, with one too feeble to be appreciated at the wrist. Assuming the number of ventricular systoles to be 70 per minute, in such a case the radial pulse would be 35 per minute. I have met with several examples of this form of disorder in which, as may be said, there is a regular irregularity of the heart's action. The carotid pulse in these cases represents each ventricular systole, and on auscultation of the heart's sounds there will be found to be four sounds to each radial pulse. This form of disorder is liable to lead to the error of supposing reduplication of both the first and the second sound of the heart. It is hardly necessary to add that in cases of obstructive and regurgitant lesions with feebleness of the heart's action the diminished quantity of blood expelled from the left ventricle, with some of its contractions, may be too small to produce an appreciable radial pulse. The existence of these cardiac lesions is easily ascertained by auscultation.

Infrequency of the heart's action is a well-known symptom in cases of injury of the skull and in certain intra-cranial affections. Cerebral hemorrhage, embolism, and thrombosis are easily excluded by the absence of paralysis, but the exclusion of subacute or chronic meningitis is not so easy. But infrequency of the heart's action, when a symptom of the latter affection, is accompanied by cerebral symptoms denoting compression of the brain--symptoms which are wanting when the infrequency is the characteristic of a functional disorder of the heart's action. Moreover, the absence of fever, of increased sensibility to light and sounds, and of the symptoms embraced in the clinical history of cerebral meningitis, will render the exclusion of that affection positive. The heart's action is abnormally infrequent in some cases {752} of cholæmia and of uræmia, but these affections are easily excluded. Certain drugs--namely, aconite, digitalis, and veratrum viride--diminish the frequency of the heart's action. These drugs, given to a person in health, produce, in fact, a transient effect which is equivalent to the functional disorder of the heart thereby characterized.

PATHOLOGY AND ETIOLOGY.--The neuroses of the heart are functional disorders involving the relations of this organ to the nervous system. The functional disorders of the heart's action affect the frequency, the rhythm, and the force of the cardiac movements. The pathology of these disorders would be more fully understood were our knowledge of the physiology of the heart's movements more complete. We know that contractions of the heart continue when it is separated from all its nervous connections and after removal from the body, especially in cold-blooded animals. The rhythm, frequency, and force of its normal movements are evidently dependent on influences derived through the sympathetic and pneumogastric nerves. Experiments show that the movements continue, but with increased frequency and with irregularity, after division of the pneumogastrics; hence this nerve is regarded as exercising an inhibitory and regulating influence over the action of the heart. Disorders of the heart's action from causes which pertain to the brain doubtless involve especially this nerve. Other causes act through the relations with the different organs of the body by means of the sympathetic system of nerves.

Impoverishment of the blood occasions disorder, probably by affecting the nutrition of the heart. Toxical agents in the blood enter into the pathology in certain cases.

The etiology of functional disorders of the heart's action involves, as an important factor, a predisposition inherent either in the organ or in its nervous connections. A peculiar susceptibility to the causes which induce disorder is an idiosyncrasy. Causes which produce disorder in those who have this idiosyncrasy are inoperative upon others. Some persons are liable to functional disorders of this organ all their lives, whereas some appear to be exempt from any liability thereto. In this respect the cardiac muscular fibres are analogous to those of the pulmonary bronchi. A peculiar susceptibility of the latter is requisite for the capability of having bronchial asthma. The susceptibility of the heart-muscle varies in different persons, and a reasonable supposition is that in proportion to the degree of this susceptibility will the causes of functional disorder be more readily and actively operative.

Clinical observation furnishes evidence of various causes giving rise to functional disorders of the heart. The more prominent are--over-exertion of the faculties of the mind, prolonged mental anxiety, the use of tobacco, tea and coffee taken in excess, too great indulgence in venery, the unnatural abuse of the sexual system, dyspeptic ailments, uricæmia, and anæmia. These causes are often combined in individual cases. With reference to effective treatment, inquiries should be directed in every case to facts relating to these several causes.

Long-continued violent muscular exertions are supposed to lead to functional disorders of the heart. DaCosta has described cases occurring among soldiers during the late Civil War in which the cardiac disorder seemed to him referable to severe marches. He applied the name irritable heart to the condition in these cases.[4] It is probable that mental excitement had more or less to do with the causation. Albutt, Seitz, and other observers have attributed functional disorders to over-straining of the heart by occupations which call for severe exercise of the muscles.

[Footnote 4: _Medical Memoirs of the United States Sanitary Commission_, 1867. See _Address before the Philadelphia Medical Society_, by A. Stillé, 1883, p. 18. See also _Diseases of the Heart among Soldiers_, by A. B. R. Myers, London, 1870.]

{753} Paroxysmal disorder of the heart belongs among the multifarious symptoms referable to the nervous system in cases of hysteria. It is among the toxical manifestations embraced in the clinical history of gout, being referable, when it occurs in this pathological connection, to uricæmia. It may have this causation in cases in which the ordinary gouty manifestations do not occur.

In the variety of disorder characterized by infrequency of the heart's action it may be assumed that the causative agency is exerted through the pneumogastrics. The inhibitory function of this nerve is affected in the same way as by the galvanic current in the experimental observations on animals in illustration of this function. This view is corroborated by the frequent association of this variety of disorder with notable cerebral disturbance.

PROGNOSIS.--A purely functional disorder of the heart's action may be said to be devoid of danger to life. This is a remarkable fact, taking into view the importance of the organ, together with the degree and the duration of disordered action in some cases. Of many thousand cases which have come under my observation, I am not aware of having met with a single instance in which death was fairly attributable to an uncomplicated functional disorder. It is readily understood that functional disorders superadded to, albeit not dependent upon, organic affections of the heart may contribute to a fatal termination. But the tolerance of functional disorders under these circumstances is often very remarkable.

The assurance of the absence of all danger frequently lifts from the minds of patients a heavy load of anxiety and apprehension. To be able to give such an assurance is one of the delights of medical practice. Patients often find it difficult to believe that the disorder from which they suffer can take place while the heart is organically sound. Many require very positive and repeated assurances in order to secure their belief. The question is many times asked, "How is it possible that I should suffer so much, and yet the heart be free from disease?" Another question which is apt to be asked is, "How can you ascertain so quickly that there is no disease?" In anticipation of the latter question, in order to ensure the desirable moral effect, it is sometimes good policy to prolong the examination, inasmuch as for the exclusion of all the physical signs of organic disease a few moments only are required. Another question, still, is, "Will not organic disease be likely to be produced by the functional disorders?" The physician is fully warranted in giving a negative answer. Exclusive of the cases of exophthalmic goitre, functional disorders of the heart do not involve liability to either inflammatory or structural affections.

Recurrences of functional disorders of the heart constitute the rule rather than the exception. Their frequency will depend much on the degree of the predisposition, but of course more or less on the causes therewith associated. The mental anxiety and apprehensions which they at first occasion after a time wear away, and they are at length reckoned as belonging among those annoyances of life to which may be applied the common expression, "What cannot be cured must be endured."

TREATMENT.--Prompt relief or palliation of suffering is often the immediate object of treatment when cases first come under observation. The medicinal remedies for this object are the ethereal or alcoholic stimulants, the different antispasmodics, and opium. Chloric ether and the compound spirit of ether (Hoffman's anodyne) often act efficiently. An eligible prescription is the combination of one of these with an equal part of the compound tincture of lavender, of which a teaspoonful, properly diluted, may be given after short intervals. Brandy, whiskey, or some other form of spirit in many cases will afford prompt relief. It should be given not much diluted. These remedies {754} are especially indicated in paroxysms of irregular or intermittent and enfeebled action of the heart. They are less adapted to cases in which the heart's action is violent. Of antispasmodics, valerian, the valerianate of ammonia, camphor, and asafoetida are appropriate. Some one of the preparations of opium is to be employed if the disorder be not relieved by other remedies. Of the different forms of opiate, codeia is the least objectionable, and perhaps as efficient as any other. With a view to promptness of relief in certain cases of severity, morphia may be administered hypodermically. Other palliative measures are a sinapism to the præcordia, and, if the extremities be cold, a mustard pediluvium. Of the efficacy of the ice-bag applied over the heart, which is recommended by German writers, I cannot speak from personal observation. The testimony in behalf of its usefulness is, to say the least, sufficient for resorting to it without apprehension of doing harm. In some cases of obstinate persistence of disorder the opportunity is afforded for trying in succession the various remedies which have been named. Digitalis is sometimes useful. Concomitant disorders which may have originated or which tend to keep up the disordered action of the heart are to be appropriately treated. Flatulence and other ailments referable to indigestion and constipation not infrequently are in this category. Paroxysms may be sometimes arrested by certain mechanical means, such as pressure upon the abdomen, holding the breath after a deep inspiration, and compression of the vagus and sympathetic nerves in the neck.

In some cases of functional disorder there is a persistent increase of the frequency of the heart's action without irregularity in rhythm. The action of the heart in these cases is the same as in cases of exophthalmic goitre, the enlargement of the thyroid body and the prominence of the eyeballs which characterize the latter affection being wanting. In these cases aconite in small doses is to be recommended. From one minim to three minims of the tincture of the root may be given, repeated after intervals of four or six hours and continued indefinitely. In cases the opposite to the foregoing--namely, those in which the disorder is characterized by infrequency of the heart's action--a rational indication is to give remedies with a view to excite the heart. In the cases which have come under my observation alcoholics have had but little effect upon the heart, although apparently useful as regards the nervous symptoms which are apt to accompany this variety of cardiac disorder. As this disorder does not, as a rule, occasion distress, the patient perhaps not being conscious of any disturbances of the heart's action, and as the infrequency does not appear to involve danger, the treatment may be directed to fulfilling other symptomatic indications.

Positive assurances of the absence of danger have often a potential influence in relieving paroxysms of functional disorder. The disorder is not infrequently increased and kept up by mental apprehension, and these assurances therefore do away with an active causative agency. They are also useful in the way of preventing the recurrence of paroxysms. It is evident that in order to exert this moral influence the physician must be competent to decide that the disorder is purely functional. He can so decide only if he have confidence in his ability to exclude inflammatory and structural affections or to determine that the disorder is not dependent on lesions which may coexist. If he have not sufficient confidence in his opinion, he will naturally and properly not give positive assurances, and a lack of positiveness will be likely to lead the patient to infer that the disorder is not devoid of danger. The good effect of certain measures of treatment is in part attributable to a mental influence. This is legitimately a therapeutic object here as in other affections.

The more important part of the treatment in the majority of the cases of functional disorders of the heart's action is that which relates to prevention. {755} The preventive treatment, in addition to the moral influences already referred to, consists chiefly in removing as far as practicable the causes of the disorder. The predisposition cannot be removed, but the causes which are auxiliary thereto in producing disorder are, to a greater or less extent, controllable.

Prolonged mental anxiety is often inseparable from the events of life. "Therein the patient must minister unto himself" The voluntary exercise of the mental faculties, however, can be restrained within physiological limits. Tobacco can be abstained from, and, as a rule, total abstinence is easier than moderate indulgence. Tea and coffee can be used moderately if at all. Dyspeptic ailments are amenable to appropriate dietetic and medicinal treatment. On no account should the diet be reduced below the requirements for ample nutrition. Anæmia, which exists in a large proportion of cases, especially in women, calls for chalybeate tonics, to be continued persistently as long as the blood remains impoverished. It is needless to add that in these cases the causes of the anæmia are, if possible, to be removed, and that chalybeates are to be supplemented by proper dietetic and regiminal treatment. Sexual excess and abuses are to receive adequate attention. There can be no question as to unnatural sexual excitation. But a question often arises in individual cases concerning the physiological limitations of natural indulgence. These limitations probably differ widely in different persons. They are, however, always exceeded if the indulgence exceed the instinctive demand--that is, if its increase be made an object for voluntary efforts. Long-continued and violent muscular exertions should be interdicted. Uricæmia or the gouty diathesis claims appropriate remedies and hygienic regulations.

Several of the various causes just recapitulated are frequently combined, so that the preventive treatment is by no means always limited to the removal of a single cause. The treatment will prove successful in proportion as the efforts to remove the causes are effectual.

Angina Pectoris.

The name angina pectoris was introduced by Heberden in 1768 to designate a group of symptoms which from that date has been regarded as constituting an individual affection. The word angina, signifying strangulation, has but little pertinency in this application of it, and various other names have been proposed in its stead. For the most part these are based on pathological views which are either erroneous or hypothetical, and at the present time the name angina pectoris is generally adopted in all countries.

The affection may be defined as a paroxysmal neuralgia, the pain of which is seated within or near the præcordia, shooting thence in most cases into the left shoulder, and extending downward to a greater or less extent into the left upper extremity, the right upper extremity being sometimes similarly affected. In some instances the pain extends to the lower limbs; the paroxysms often accompanied by a feeling of anguish and of impending death, the affection in the great majority of cases being incident to organic disease of either the heart or the aorta and involving liability to sudden death.

SYMPTOMATOLOGY.--The foregoing definition embraces the prominent traits of a severe paroxysm. The pain may extend into situations other than those mentioned--namely, in different directions throughout the chest, into the neck, the jaws, and the temples, the abdomen, and the groin. In describing the pain patients use such terms as constricting, tearing, burning, etc. Perhaps in its most severe form there is no disease attended with more intense suffering. It is related that the description of the affection by Heberden led to a communication to him from an unknown correspondent who gave an account of his own case, and bequeathed to Heberden his body to be {756} examined after death. The examination was made by John Hunter, who himself fell a victim to the affection. An analogous instance occurred in my own experience. A patient was led by the intensity of his sufferings to request that I should make a post-mortem examination in his case, with the hope that something might be thereby ascertained which would prove useful to others. This request was complied with. Associated with the pain in severe paroxysms is what has been called a breast-pang, giving rise to a sensation as if death were at hand. A choking sensation, which is implied in the name angina, is an occasional symptom, resembling the globus hystericus. Respiration is not obstructed, but the patient may voluntarily restrain the respiratory movements lest they increase the suffering. Dyspnoea, if present, is thereby produced. During the continuance of the paroxysm the patient refrains from movements of the body or limbs, keeping a fixed position and grasping some firm support in order better to remain motionless while the pain lasts. A sensation of numbness in the affected limbs accompanies the pain. The circulation is usually more or less disturbed. There is sometimes increased and sometimes diminished frequency of the pulse. The action of the heart is often intermittent and otherwise irregular. It may be strong, but oftener it is weak. At the beginning the arterial tension has been found to be increased, but later is diminished. The face is generally pallid, but sometimes livid. The disturbances of the circulation are often modified by coexisting organic disease of the heart, but superadded are those of functional disorder incident to the paroxysm. The countenance is haggard and anxious. The surface of the body is cold, and may be bathed in perspiration. The mind remains unaffected. The paroxysms usually commence suddenly, and, as a rule, so end. Eructations of gas are apt to follow their cessation, together with a free discharge of limpid urine. The duration of a paroxysm may be but a few seconds; it is rarely longer than a few minutes. When it appears to be protracted for a considerable period, there is generally a series of attacks occurring in quick succession, instead of one continuous paroxysm.

There is much variation in different cases as regards the severity of the paroxysms, and the mildest offer a striking contrast to the severest, the essential symptomatic characters of the affection, however, being preserved. In mild paroxysms the pain is comparatively slight, the anguish or heart-pang is less, and the heart's action may be but little or not at all disturbed. Such paroxysms occasion annoyance without great suffering. Different cases, and the same case at different times, exemplify varying degrees of severity.

Recurrences of angina take place as a rule, to which there are but few exceptions. The intervals between the paroxysms vary in different cases, and often in the same case. Their recurrence is not governed by any law of periodicity. Generally, they are at first infrequent, and their frequency increases slowly. With increase in frequency their severity is apt to be increased. At first, and for a certain length of time, they are occasioned by some apparent exciting cause. A common cause is the exertion of walking, especially against a current of wind. Often for a considerable period patients are exempt whenever they are at rest. Sooner or later, in most cases, attacks are produced by other causes, such as a fit of anger or other mental emotion, and finally without any appreciable existing cause. I have known attacks to be caused by the act of swallowing solid food, so that eating became a source of terror to the patient. They occur in some cases during sleep. Occurring after intervals of a few moments, the affection in this respect resembling certain cases of tic douloureux, it doubtless would be difficult by any description to convey an adequate idea of the lamentable condition of the patient.

On account of the wide range of the gradations as regards the degree of severity or mildness, of the diversity of symptoms referable to the different {757} forms of disease of the heart with which the affection may be associated, and of the varied disorders which may be accidentally connected, the clinical picture of angina is by no means uniform. There is, however, no practical advantage in making formal varieties of the affection. Eulenberg makes four different types, their differential characters being based on the different nerves supposed to be especially affected, as follows: 1st, excito-motor cardiac angina; 2d, regulator angina; 3d, excito-motor sympathetic angina; and 4th, vasomotor angina. Assuming that there is ground for these pathological distinctions (which, to say the least, admits of doubt), in a practical point of view they involve difficulties not compensated for by important bearings on diagnosis and treatment. One point of distinction, however, has important bearings--namely, the existence of angina with or without organic disease of the heart. It cannot be doubted that in the vast majority of cases angina is incident to some form of cardiac lesion. That it may exist without any appreciable lesion is admitted. The propriety of recognizing it as a functional disorder rests on the latter fact.[5] Practically, the coexistence of organic disease of the heart or otherwise, and, if organic disease exist, its nature and extent, are points which it is important to take into account in the diagnosis with reference to prognosis and treatment.

[Footnote 5: Of 71 cases analyzed by Gauthier, in 3 only was the affection to be regarded as purely functional. Vide Eichhorst.]

DIAGNOSIS.--The diagnostic points in cases of angina are the præcordial seat of the pain, its radiations thence into the shoulder and upper extremity, generally of the left side, the character of the pain, the accompanying anguish and sense of impending death, the coexisting disorder of the heart (which occurs as the rule), and the voluntary immobility of the body. These are positive criteria which, if marked, render the diagnosis easy and certain. The diagnosis is further substantiated by finding the signs of organic disease of the heart, especially if there be lesions at the aortic orifice or within the aorta. Well-marked angina is in itself strong presumptive evidence of organic disease of the heart. Not infrequently the existence of the latter is for the first time discovered by an examination suggested by the occurrence of an attack of angina. The cases in which the diagnosis involves difficulty are those in which certain of the above-mentioned diagnostic points are either wanting or not well marked.

The affections which may be mistaken for angina are gastralgia and intercostal neuralgia. In gastralgia the pain is seated below the præcordia. It may radiate in different directions, but does not extend to the upper extremities, and is not accompanied by irregularity of the heart's action. The patient writhes and changes the position of the body in the effort to obtain relief. There is not a sense of impending death. The paroxysms are of much longer duration than those of angina. These differential points should suffice for the discrimination.

An acute attack of intercostal neuralgia does not differ so widely from angina, but the differential points are generally distinctive enough for a positive diagnosis. The pain in intercostal neuralgia is not seated in the præcordia. It does not shoot into the upper extremities; it is increased by the act of inspiration; the peculiar anguish of angina is wanting; the action of the heart is likely to be regular; and the diagnosis is confirmed by finding tenderness over circumscribed areas in the intercostal spaces anteriorly, laterally, and posteriorly.

Cardiac lesions in cases of angina are to be excluded by finding no physical signs of their existence. But it is to be remembered that angina is not infrequently associated with lesions not readily recognized by signs--to wit, obstruction of the coronary arteries and fatty degeneration of the heart. Persistent feebleness of the heart's action and symptoms other than angina {758} incidental thereto render it probable that one or the other or both of these lesions exist. It is probable that these lesions have been overlooked in examinations after death in some of the cases in which angina has been reported as not connected with any organic affection of the heart.

PATHOLOGY AND ETIOLOGY.--The paroxysms of angina have the distinctive traits of neuralgic affections as regards the character of the pain, its extension in the course of sensory nerves, the occurrence of intermissions, the absence of fever, the functions of digestion and assimilation remaining often unaffected, and the attacks not always being referable to any exciting cause. The association of the affection, as a rule, with organic disease of the heart is evidence of course of some pathological connection. What is this connection? A difficulty in answering this question arises from the fact that the affection is associated not with any one lesion, but with different lesions. It may be associated with obstruction (usually from calcification) of the coronary arteries, with insufficiency of the aortic valves, with rigidity from calcareous degeneration of the aorta, with aortic aneurism, and with fatty degeneration of the heart, these different morbid changes existing either singly or more or less of them in combination. The question then resolves itself into another--namely, What is the pathological condition common to these different lesions which stands in a special etiological relation to angina? It is a logical conclusion that the affection must depend upon some condition which is common to these lesions. The association with the lesions is too frequent to be explained by mere coincidence. The etiological relation involves evidently a condition which exists only in a small proportion of the cases of these lesions. This statement is a logical deduction from the great infrequency of angina and the frequency of these varieties of organic disease of the heart. I submit, as the most rational theory, that the pathological condition on which the angina depends is ischæmia of the heart. This theory is supported by the frequency of the instances in which in cases of angina the coronary arteries are obstructed; by the fact that not very infrequently this is the only lesion found after death (two instances having fallen under my own observation within the past year); by the association with aortic insufficiency and rigidity of the aorta, lesions which interfere materially with the supply of blood to the heart if it be admitted that the blood is driven into the coronary arteries, not during the ventricular systole, but by the recoil of the arterial coats in the ventricular diastole; and by the association with fatty degeneration of the heart when, owing to the weakness of the heart's action, the supply of blood to the muscular structure of the heart must be diminished. That the sudden withdrawal of a supply of blood to a part may occasion neuralgia is shown by the intense pain in the limb which directly follows embolism of the femoral artery. Moreover, general anæmia, as is well known, favors the recurrence of neuralgia in various situations.

The cardiac nerves in which the pain is seated are doubtless sensory fibres of the pneumogastrics. Their anatomical connections with the brachial plexus will explain the extension of pain to the left upper extremities. To account for the pain in parts which have no direct connection with the cardiac nerves, it may be assumed that in angina, as in other neuralgic affections, a centripetal influence conveyed to the nervous centres may occasion pain referable to different situations. This explains the shifting of pains which is one of the diagnostic traits of neuralgia. The explanation of the disturbed rhythm of the heart's action so often coexisting with the neuralgic pain is not more difficult than in cases of functional disorder disconnected from angina. For what is to be said of the rationale the reader is referred to that portion of this article which treats of Functional Disorders of the Heart.

{759} Angina, as a purely functional affection--that is, not symptomatic of any organic lesion of the heart, and not due to any structural change in, nor mechanical pressure upon, nerves--is obscure as regards its pathology and etiology, but not more so than many other neuralgic affections. As already stated, cases in which it is thus purely functional are few in number--fewer even than has been supposed, because there is reason to believe that lesions have been overlooked. Moreover, cases which have been reported render it probable that in some instances in which the heart has been found free from appreciable lesions nerves entering into the cardiac plexuses may be the seat of structural changes or may be subject to pressure from a morbid growth. But there are cases in which no lesions are discernible during life, and in which the existence of lesions is disproved by complete recovery. The affection under these circumstances must be regarded as purely functional. There is no positive knowledge of the etiology in these cases. The affection has been attributed to gout, to hysteria, to the action of cold, to the use of tobacco, and to other causes. These causes may have a certain amount of agency, but there is an unknown intervening link in their etiological connection concerning which, in the present state of our knowledge, it is useless to speculate.

Age and sex have an undoubted influence in the etiology. The affection very rarely occurs under middle life, and it occurs in men much oftener than in women.

PROGNOSIS.--As a very rare exception to the rule, a single paroxysm only may occur, the patient living for many years without any recurrence. Recurring paroxysms sometimes are separated by long intervals--weeks, months, and years. In the majority of cases, however, paroxysms recur with more and more frequency and with increasing severity. Under these circumstances death may take place after a long period of suffering.

The liability to sudden death is an important point in the prognosis. This may occur in the first paroxysm. An instance has fallen under my observation within a few months, there having been no signs previously indicative of disease of the heart. Calcareous obstruction of the coronary arteries was the lesion found after death. A person subject to paroxysms of angina must be considered as in more or less danger of sudden death with the recurrence of each paroxysm. The physician should be sufficiently impressed with the importance of this fact. While it is doubtful whether it be the physician's duty to apprise the patient of the fact, the danger should always be communicated to some discreet relative or friend. To do this is a duty which the physician owes to himself as well as to the patient. If he omit it, he exposes himself to censure should sudden death unexpectedly take place. The mildness of the paroxysms which have already occurred does not afford a positive security against the liability to a severe and fatal paroxysm. But it is a hopeful consideration that paroxysms may recur more or less frequently for an indefinite period without proving fatal. At this time I am cognizant of three cases in which paroxysms have recurred frequently for several years, the patients, with that exception, having had fair health. Let not the physician, therefore, predict with positiveness that a patient with angina will die sooner or later in a paroxysm. The uncertainty is a ground of encouragement as well as for apprehension.

The coexistence of organic disease of the heart and the nature of the cardiac lesions have a very important bearing on the prognosis. The danger is in proportion to the importance of these. Recovery is never to be expected when the affection is associated with well-marked cardiac lesions, and there is always great danger in the recurrence of paroxysms when the associated lesions are in themselves dangerous. Lesions which give rise to free aortic regurgitation and to fatty degeneration of the heart involve more or less {760} danger of sudden death, irrespective of angina. It is evidence of greatly increased danger if paroxysm of angina be superadded.

During a paroxysm of angina the immediate danger is to be estimated by the symptoms denoting disturbance of the heart's action. The danger is great in proportion as the action of the heart is feeble, irregular, or intermitting. Per contra, the danger is less in proportion as the deviation from the normal force and rhythm is small. It may be said that there is no danger so long as the heart's action remains unaffected, but the disturbance may be slight or wanting at the outset of a paroxysm and afterward become fatally great.

A favorable prognosis may be entertained when there are no signs of cardiac lesion, and when there is little or no disturbance of the heart's action during the paroxysms. Let it be borne in mind that such cases are exceptional and extremely rare. Let it also be borne in mind that lesions especially apt to be associated with fatal paroxysms may be latent--namely, obstruction of the coronary arteries and fatty degeneration. The latter fact renders it proper that a favorable prognosis should always be formed with a reservation, while the fact that recovery takes place in a few well-marked cases of angina renders it improper to withhold encouragement whenever lesions are not discoverable and the paroxysms are not accompanied by alarming symptoms referable to the heart's action. The long tolerance of the affection in some cases is not to be lost sight of with reference to the encouragement which may be fairly derived therefrom.

The immediate cause of sudden death in a paroxysm is probably an arrest of the heart's action in diastole, or such a degree of diminution of the force of its action that the accumulation of blood within its cavities induces paralysis from distension.

TREATMENT.--It is important that a paroxysm of angina be treated as soon as possible, not alone with a view to the relief of pain, but to remove immediate danger. If the physician be present, an opiate in a form to act promptly should be given either by the mouth or hypodermically; the latter mode is to be preferred. Laudanum or a solution of a salt of morphia is the most eligible form if given by the mouth. If the heart's action be weak and irregular, a diffusible stimulant is indicated. If at once available, chloric ether, Hoffman's anodyne, and the compound tincture of lavender act efficiently. If these be not at hand, an alcoholic stimulant should be given, diluted but little, and the doses repeated at short intervals until the paroxysm ends and the disturbed action of the heart has ceased. The duration of paroxysms is generally so short that a physician is rarely present unless they recur after brief intervals. A patient, therefore, subject to angina should be provided with remedies and instructions as to their use at the instant a paroxysm occurs. The amyl nitrite, first recommended in this affection by Brunton, is a remedy of signal benefit in some cases. From two to five minims may be inhaled at the commencement of the paroxysm. It is especially indicated when the characters of the pulse denote arterial tension. Caution is to be exercised in its use if there be notable weakness of the heart's action. Sinapisms, stimulating embrocations, and fomentations applied to the chest have a certain measure of utility, but they should not take the place nor delay the use of remedies which are more efficient.

A still more important object of treatment than relief in the paroxysms is their prevention. During the intervals this object claims assiduous attention. First in importance is the avoidance of all exciting causes. Bodily exercise is to be kept within the limits required in order to incur no risk of a paroxysm being produced. The same precaution applies to mental excitement. Unhappily, this is not as easy as the avoidance of muscular exertion. John Hunter's saying, that his life was at the mercy of any scoundrel who chose to {761} insult him, proved a prediction. He fell dead on receiving an insult from one of his colleagues at St. George's Hospital. Sexual intercourse I have known to prove an exciting cause. Excesses in eating and drinking are in this category. The diet, however, is not to be reduced below the full requirements for nutrition, and wine or spirits, as conducive to digestion, are in some cases serviceable. The use of tobacco is to be interdicted.

Coexisting affections which have no special pathological connection with the angina may act as auxiliary causes, and therefore claim attention. Gout is to receive appropriate treatment. Anæmia especially is to be removed. This condition strongly conduces to the development and the continuance of neuralgic affections. Chalybeate remedies and the dietetic treatment are called for if this condition coexist. It is a rational indication to supply the heart with good blood if it be true that angina depends on an ischæmic condition of this organ.

Associated cardiac lesions are to be treated according to symptomatic indications, as in cases in which angina does not occur. Digitalis may be used under the proper restrictions. I have known this remedy to prove highly useful in preventing the recurrence of paroxysms. Nux vomica is sometimes useful as a cardiac tonic.

Various drugs have had repute as empirical remedies. Of these may be mentioned the preparations of zinc, arsenic, the nitrate of silver, phosphorus, the bromine salts, the iodide of potassium, and quinine. There is no proof that these remedies have any special therapeutical effect in this affection, but that they are sometimes useful there is abundant testimony. Trial should be made of them, with proper care in their administration. Electricity in the form of the induced and of the constant current has been advocated as not only serviceable, but as effecting in some instances a permanent cure.[6] Beard and Rockwell have found general faradization useful in a few cases.[7]

[Footnote 6: Vide Eulenburg in _Ziemssen's Cyclopædia_, vol. xlv. p. 54.]

[Footnote 7: Vide _Medical and Surgical Electricity_.]

Exophthalmic Goitre (Graves' Disease; Basedow's Disease).

This affection is characterized by three striking symptomatic events--namely, persistent increase of the frequency of the heart's action, enlargement of the thyroid body, and protuberance of the eyeballs. The name exophthalmic goitre relates to the last two of these three events. It is defective, inasmuch as it does not include the increased frequency of the heart's action, which is the primary one of the three events, and the only one which is never wanting. As an individual affection it was first described by Graves in 1835, although cases in which these events were associated had been previously reported. Parry collected 7 cases in which the affection of the heart was associated with thyroid enlargement, and in 1 of these cases exophthalmia existed. An account of these cases was published in 1825. The name Graves' disease, proposed by Trousseau, has been adopted by French, English, and American writers. Basedow's disease is the name given to the affection by German writers. The affection was described by Basedow in 1840 under the name Glotz augenkrankheit.

There are cases in which one of the events in this symptomatic triad is wanting, the cases in other respects corresponding to the affection. The exophthalmia is the event oftenest wanting, the goitre, the functional disorder of the heart, and the associated phenomena being the same as if protuberance of the eyeballs coexisted. In some instances the goitre alone is wanting. The name exophthalmic goitre is not strictly applicable to these cases, but that the affection is essentially the same as when the three events {762} are present cannot be doubted. It is a chronic affection, being in the great majority of cases of long duration. Exceptionally, it is developed suddenly and disappears after a few days. In these cases the affection has been distinguished as acute, but its claim to be so called rests exclusively on the shortness of its duration.

SYMPTOMATOLOGY.--Of the three cardinal events, the increased frequency of the heart's action is the first in the order of time. This precedes the other events usually for several weeks or even months. The frequency varies in different cases within wide limits--namely, from 90 or 100 to 150 beats, and even more, per minute. There is notable variation at different times in the same case. Generally, the frequency is greatly increased by exercise and mental emotions. In other words, irritability of the heart is in most cases a marked feature. As a rule, there are none of the disturbances of action, in other respects than frequency, which are found in cases of functional disorder not associated with exophthalmic goitre. The action may be intermittent or in other respects irregular, but in most cases the rhythm is not disturbed. The patient is conscious of the heart's action, and is annoyed by it, especially under any excitement; but there is not that distressing sense of the disorder which is felt in the paroxysms of palpitation with irregularity of action considered in the first division of this article. At the outset and for a considerable period there are no signs of any organic disease of the heart, or if the latter be present the association is accidental; the disordered action, as far as it relates to the affection under consideration, is purely functional. At a later period there may be enlargement of the heart as a result of long-continued increased activity of function. From the first cardiac murmurs are generally present at the base and over the body of the heart. These are blood-murmurs due to coexisting anæmia.

Following the increased frequency of the heart's action, after a variable period enlargement of the thyroid body occurs. The enlargement may be rapid, but in most cases it takes place slowly, and ceases when it has reached a moderate degree. Cases are exceptional in which the degree of enlargement is such as to occasion any obstruction to respiration. Almost invariably both lobes of the thyroid body are enlarged, but the enlargement is generally not equal on the two sides, and, as a rule, it is greater on the right side. The enlarged lobes are soft at first, afterward becoming hard. The subcutaneous veins over them are often distended. Pulsation of their arteries is apparent to the hand and to the eye. A systolic arterial blowing murmur and a continuous hum are heard when the thyroid region is auscultated. In some instances the murmur is like that of an aneurismal varix. As a rule, murmurs are heard over the carotid artery and the jugular vein. A thrill or fremitus is often felt by the hand placed upon the thyroid body. The thyroid enlargement is due at first chiefly to dilatation of the arteries and veins. Hyperplasia of the fibroid tissue occurs afterward, and then the enlarged gland becomes hard to the touch. The size of the enlarged thyroid body is often found to vary considerably at different times--a fact attributable to varying degrees of the dilatation of the vessels and of the consequent hyperæmia.

A notable protuberance of the eyeballs has sometimes been observed to take place suddenly, but, as a rule, it is at first slight and increases slowly. The degree of protuberance varies considerably in different cases. When marked, the patient has a remarkable staring expression. Both eyeballs are alike protuberant with very rare exceptions.[8] The pupils are unaffected and {763} vision is not impaired. The protuberance is sometimes so great that the globes cannot be covered by the eyelids. Under these circumstances inflammation of the conjunctiva ensues, and perforation of the cornea has been known to occur. The eyeballs can be pressed backward into the sockets without a degree of force which occasions pain, but the protuberance returns directly the pressure is discontinued. In most, but not in all, cases the consensual movements of the upper eyelid and the globe, when the latter is moved upward or downward, are impaired; that is, the movements of the lids do not follow those of the globes. That this symptom is not to be accounted for by the exophthalmia is shown by the fact that it is not a symptom when the protuberance of the eyeball is caused by an intra-orbital tumor. The symptom therefore has diagnostic significance. The ophthalmoscope shows the veins of the retina to be dilated and tortuous, with, in some instances, visible pulsation of the retinal arteries. Anatomical conditions to which the exophthalmia is, in a measure at least, referable, are enlargement of the intra-orbital vessels by hyperæmia and an increased amount of post-ocular fat. Paresis of the straight muscles, induced by stretching, is probably an important factor when the protuberance is great. These muscles have in some instances been found to have undergone fatty degeneration.

[Footnote 8: Allan McLane Hamilton, in his work on _Nervous Diseases_, cites a case reported by Yeo, in which the exophthalmia effected only the left eye, and the goitre was limited to the right thyroid body. Cases of unilateral goitre with bilateral exophthalmia have been observed.]

Anæmia is usually associated with the foregoing cardinal symptoms. It is sometimes wanting. This was true of a case recently under my observation. If anæmia does not exist, the blood-murmurs referable to the heart and vascular system may be absent. If anæmia exist in a marked degree, there are present certain symptomatic phenomena referable thereto--namely, neuralgic pains in different situations, want of physical and mental endurance, hysterical manifestations, depression of spirits, etc. Mental irritability is apt to be a prominent trait of the affection. This may in a great measure be referred to sensitiveness occasioned by the exophthalmia. Owing to this, patients often avoid observation as much as possible. They naturally, women especially, are led to brood over the calamity of such a singular and conspicuous deformity. Breathlessness on exercise is a symptom more or less marked according to the increase in the frequency of the heart's action and the impoverishment of the blood. The appetite and digestion may or may not be impaired, and hence there may or may not be emaciation. It cannot be said that the affection is accompanied by fever, although in a certain proportion of cases the temperature of the body is half a degree or a degree above the normal range. Reports of cases embrace a considerable number of concurrent symptoms which are occasionally present, such as cephalalgia, insomnia, vertigo, amenorrhoea, neuralgia, unilateral sweating, etc. These have no special connection with the affection, but are incident to associated pathological conditions.

DIAGNOSIS.--The three phenomena which distinguish this affection are so obvious as well as characteristic that a diagnosis cannot well be avoided, after a description derived from books or lectures, when the first case presents itself in practice. The wonder is that the affection had not been clearly pointed out prior to the writings of Graves and Parry. Any difficulty in diagnosis relates to cases in which either the exophthalmia or the enlargement of the thyroid body is wanting, or to the incipiency of the affection when its characteristics are not fully developed. The bilateral protuberance of the eyeballs, the absence of local symptoms other than those caused by the exposure of the conjunctiva when the eyelids fail to cover the globes, the mobility and normal size of the pupils, the want of the normal consensus in the movements of the eyelids and the globes, and the replacement of the latter by moderate pressure, are the diagnostic points which distinguish the exophthalmia in this affection from that incident to intra-orbital tumor. The moderate increase of the thyroid body, its softness to the touch, its notable variations in volume at {764} different times, its pulsation and the auscultatory murmurs which it generally furnishes, are diagnostic points distinguishing the enlargement in this affection from that of bronchocele. The persistent frequency of the heart's action is not less marked when either of the two phenomena just referred to is wanting than when both are present. The degree of frequency varies, but more or less increase is a constant symptom; and it is a symptom not likely to be present in either exophthalmia or in goitre unassociated with Graves' disease.

Aside from the symptomatic triad, the clinical history offers in different cases considerable diversity. The diverse inconstant symptoms as they occur in other pathological conditions are without diagnostic significance. A large proportion are incident to the anæmia so often associated with the affection under consideration.

PATHOLOGY AND ETIOLOGY.--Inasmuch as the persistent frequency of the heart's action is the first event in the order of time, the thyroid enlargement and the protuberance of the eyeballs being epiphenomena, it seemed a rational supposition that the latter events were dependent on the cardiac disorder. This view was held by Graves and his colleague, Stokes. A supposition much more rational is that the three events are united by a common causation. Anæmia has been supposed to be the causative condition. This supposition is disproved by the fact that anæmia does not exist in all cases. Moreover, anæmia is a pathological condition of frequent occurrence, whereas the affection under consideration is extremely rare. It is, however, very probable that anæmia may play an important auxiliary part in the causation, as it does in all the neuroses. With the knowledge of the sympathetic and vaso-motor nerves which has been acquired since the date of Graves' discovery, the pathology seems clearly to involve these components of the nervous system. This pathological view is perhaps generally held at the present time. But to interpret all the phenomena satisfactorily by reference to the known functions of these nerves is not easy. Vaso-motor paresis will account for the dilatation of the vessels, which is an important anatomical element in the enlargement of the thyroid body and the exophthalmia. On the other hand, acceleration of the heart's action is not an effect of paresis, but of excitation. To account for this incongruity there have been different hypotheses, which it does not fall within the scope of this article to discuss. Some autopsies have shown anatomical changes in the cervical sympathetic and its ganglia, but in others no morbid appearances have been found. Whether the pathology involves peripheral nerves alone or a central morbid condition in the spinal cord or the medulla oblongata is an undecided question. For facts and arguments bearing on the different points of inquiry relating to the pathological seat and character of the affection the reader is referred to other works.[9] I will only add that in view of the fact of the exophthalmia and the goitre being, in the vast majority of cases, bilateral, it seems rational to suppose the pathological nervous condition to be central rather than peripheral. This is assuming that the three cardinal events involve a common causative condition, and not that the exophthalmia and goitre are dependent on the cardiac disorder. The termination in a certain proportion of cases in recovery goes to show that the affection does not necessarily involve structural lesions, and hence that it is properly included among the neuroses. The constancy and prominence of the disordered action of the heart render it proper to consider the affection in connection with the neuroses of that organ.

[Footnote 9: For a résumé, vide article by Eulenburg in _Ziemssen's Cyclopædia_, vol. xiv.]

In the etiology of Graves' disease sex and age have a decided influence. In very much the larger proportion of cases the patients are women. The proportion of 2 to 1, which is stated by some writers, is not sufficiently large. Out of 20 or more cases which have fallen under my observation, in 1 {765} only was the patient of the male sex. The disease is extremely rare under puberty and after middle age. Between these extremes of age there is no special predilection of the disease for any particular period of life.

Of causes which are independent of sex and age we have no positive knowledge. In particular cases the disease has been attributed to traumatic causes, to fright or other kinds of mental excitement, to sexual excess, etc. The evidence of a causative relation in these cases is simply a post-hoc connection which obtains in but a single instance or at most in a few instances. Etiological speculations, in the absence of ascertained facts, are, to say the least, useless, and it is the most politic as well as the fairest statement to say that in the present state of our knowledge we have no adequate data for determining the causation of the affection.

PROGNOSIS.--Graves' disease has no direct fatal tendency. It may not interfere with fair health for a long period. It diminishes the ability to tolerate other diseases, and in this way indirectly it threatens life. If it supervene upon organic disease of the heart, the gravity of the latter is thereby increased and its progress hastened. It induces, as a result of long-persistent increased activity of the action of the heart, enlargement of this organ. Sooner or later, if the disease continue, dilatation predominates over hypertrophy of the heart, and then occur the evils incidental to the inability of this organ to carry on the circulation adequately. Want of breath on exercise, and at length constant dyspnoea, become sources of suffering. Generally, dropsy finally ensues, and thus, indirectly, the affection leads to a fatal result. In most cases, however, death is caused by some intercurrent malady before the effect upon the heart is sufficient to occasion grave symptoms. Aside from the effect upon the heart, the affection does not seem to involve an intrinsic tendency to any particular complication.

The affection tends to long continuance. I have not met with an instance of its rapid development and its disappearance after a brief duration. Instances of complete recovery are rare; that is, the exophthalmia and the goitre do not disappear entirely, and the action of the heart does not become perfectly normal. A close approximation to complete recovery is not very infrequent, and in some instances all traces of the affection disappear.

The cases offering most in the way of a favorable prognosis are those in which there is not great acceleration of the action of the heart, this organ being free from organic disease, and those in which, exclusive of the affection under consideration, there are no marked unhealthful conditions. Impaired appetite, lack of digestive power, defective nutrition, and persistent anæmia are unfavorable prognostics. Any important antecedent disease affects of course the prognosis unfavorably.

TREATMENT.--From what has been stated in relation to the etiology of Graves' disease, it follows that there are no known special causative indications in the treatment. It is, however, a rational consideration that anything in the habits and surroundings of patients which is prejudicial to health has perhaps some agency either in causing or in maintaining the affection. It is therefore an important part of the treatment to remove all causes of ill-health which can be ascertained. The treatment, in this point of view, will embrace injunctions respecting mental occupations and excitement, a proper proportion of time devoted to out-of-door life, an adequate diet, avoidance of dietetic excesses, moderation in the use of alcohol, the disuse of tobacco, the regulation of sexual indulgence, etc. Without going farther into details, the object, in general terms, is to place the patient under the best attainable hygienic conditions.

Any disorders which coexist may possibly be involved, if not in the causation, in the persistence of the affection. They claim, therefore, appropriate treatment. Diminution of appetite and difficulties relating to digestion are {766} to be treated by measures which must vary according to the circumstances in each case, and which need not be here considered. Uterine troubles are to be removed. These have been supposed to stand in a special causative relation to the affection. The anæmic condition which is so frequently associated (in addition to the removal of its causes, if these be ascertained and if they be removable) calls for the long-continued use of chalybeate preparations in conjunction with dietetic and regiminal treatment. In a case under my observation in which recovery took place the patient took two grains of reduced iron three times daily for three years. It is generally advisable to change from time to time the preparation of iron, partly for the moral effect of giving a new remedy in order to secure perseverance on the part of the patient, and in part because, irrespective of this effect, changes seem to be of use. The prevalent idea that iron is not well tolerated is to be overcome by assurances, argument, and, if necessary, by stratagem. It is certain that in most, if not all, instances this idea is a delusion. The anæmia in this affection, as in other pathological connections, is only to be overcome by the long-continued, uninterrupted employment of chalybeates conjoined with the other measures of treatment. This should be clearly stated to patients in order to forestall discouragement and neglect of the treatment advised.

Hydropathic packing and the needle-bath have been highly recommended. A patient of mine who has recovered apparently derived benefit from daily sea-bathing. The propriety of these measures is to be determined by the glow and feeling of invigoration to which they give rise if they be useful. Should these effects not follow, daily sponging of the body with cold or tepid water, to which may be added sea-salt or alcohol, may be substituted. Mental diversion is an important hygienic measure. The patient should be urged to conquer the feeling of mortification which prevents social enjoyments and disposes to brooding over the malady.

The enlargement of the thyroid body naturally suggests the employment of iodine. This local affection, however, is very different from bronchocele or goitre occurring independently of Graves' disease. Experience shows that iodine employed either topically or for its constitutional effect is useless if not injurious. Many years ago a case was related to me by a non-medical friend in which thyroid enlargement had been treated by the application of iodine. Remarkable prominence of the eyes soon followed, which was attributed to the iodine, and the physician fell under censure which, as I suspect, he was not prepared to meet by an acquaintance with Graves' disease. If the thyroid enlargement be sufficient to occasion tracheal obstruction or give rise to great deformity, the injection into the gland of a solution of ergotin may be resorted to. William Pepper has effected a complete reduction of the thyroid enlargement by this measure, in addition to ergot given internally. He employed a solution of ninety-six grains of ergotin to an ounce of distilled water, of which from six to ten minims were injected weekly by means of a needle introduced from half an inch to an inch in depth.

For the relief of the exophthalmia, gentle compression upon the eyes by a compress and bandage during sleep has been recommended. Aside from this, the indications for local treatment relate to the inflammation which is liable to be produced by insufficient covering of the eyeballs by the eyelids and by the impaired consensual movements of the latter with the former. The patient should, as far as practicable, abstain from reading, writing, and other uses of the eyes which involve strain.

Insomnia and general nervous irritability may call for palliative treatment. Opiates should if possible be withheld, owing to their effect upon appetite and digestion, and also on account of the risk of forming the opium habit. Other hypnotics and nervines are to be preferred, but it is best to be {767} chary in the use of these. The bromides are perhaps the least objectionable of the remedies given to tranquillize the nervous system and promote sleep, but their prolonged use is detrimental.

The most important part of the remedial treatment relates to the accelerated action of the heart. Cardiac sedatives are rationally indicated, and experience confirms their usefulness. All writers recommend digitalis in order to diminish the frequency of the heart's action. A difficulty pertaining to this drug is its liability to disturb the stomach, and the consequent necessity for discontinuing its use. It is proper to give it a fair trial. In my experience aconite has proved more satisfactory. In a case already referred to two grains of reduced iron and one minim of the tincture of aconite constituted the medicinal treatment. These remedies, without any increase of dose, were continued for three years. At the end of this period the patient was in excellent health and had gained in weight forty pounds; slight exophthalmia and goitre only remained. In another case the treatment consisted exclusively of the tincture of aconite in doses gradually increased to seven minims three times daily. Chalybeates were not given in this case, because the patient was not anæmic. The remedy was continued most of the time for two years. The recovery is complete except that the heart is irritable and moderate prominence of the eyeballs remains. The treatment has been discontinued in this case for the past two years. Of veratrum and gelsemium as cardiac sedatives, which have been recommended in this affection, I have no practical knowledge. In paroxysms of unusual violence of the heart's action German writers recommend the application of cold to the præcordia by means of the ice-bag.

Galvanization of the sympathetic is strongly advocated by German writers--namely, Eulenburg, Dusch, Guttmann, Von Chvostok, Meyer, Leube--and in this country by Bartholow and others, as not only useful, but sometimes effecting a cure. The following extract from a treatise by Bartholow embraces rules for the employment of this therapeutic agent: "Recent cases treated efficiently by galvanism are relieved permanently or their course and progress much modified. During exacerbations, which constitute a prominent feature of the clinical history, the passage of a sufficient galvanic current through the pneumogastric immediately lessens the cardiac excitement. In the treatment for curative results a mild current is held to be most efficient (Chvostok). An electrode--the anode--is placed in the angle behind the jaw, and the cathode on the epigastrium, and a stabile current is allowed to flow for three to five minutes. The cervical spine should also be galvanized. It may be included in a circuit by placing the anode over the vertebræ in turn whilst the cathode rests on the epigastrium. Stabile may be varied by labile applications. The faradic current may be used successfully. An instance of this kind has come under my notice. The first published cases illustrating the curative value of galvanism were those of Chvostok (1871), who followed with a series of examples the next year, when Meyer also reported several cases. In 1874, I read a paper before the medical section of the American Medical Association advocating this plan of treatment, and illustrated its advantages by the details of five cases. In 1878, Vizioli, in a paper on electropathy, amongst others narrated several cases of Basedow's disease cured. In making the claim for the curative power for electricity the reader should understand that uncomplicated cases only are referred to."[10] Rosenthal gives the following directions: "The ascending stabile galvanic current, from one to ten elements, is passed through the cervical sympathetic (the anode in the mastoid fossa and the cathode upon the upper cervical ganglion) for eight to ten minutes at a time. The current is also directed transversely across the thyroid tumor, or an ascending current may {768} be applied to the cervical and upper dorsal vertebræ."[11] Guttmann states that temporary reduction of the frequency of the heart's action is first produced, but by persisting in the electrical treatment the reduction becomes permanent, together with progressive improvement as regards the exophthalmia and the thyroid enlargement.[12]

[Footnote 10: _Medical Electricity_, by Roberts Bartholow, M.D., LL.D., etc., Philadelphia, 1881.]

[Footnote 11: _Clinical Treatise on the Diseases of the Nervous System_, by M. Rosenthal, translated by L. Putzel, M.D., New York, 1878.]

[Footnote 12: Vide article entitled "Basedowsche Krankheit," in _Real-Encyclopedie_, Wien and Leipzig, 1880.]

{769}

DISEASES OF THE PERICARDIUM.

BY J. M. DACOSTA, M.D., LL.D.

Pericarditis.

The diseases of the pericardium, with a few exceptions, belong to the inflammatory variety, and, as a rule, are the consequences or accompaniments of other inflammatory diseases of the circulatory system or of parts near the heart. The most common of the pericardial affections is pericarditis, which may be simple or secondary, and acute or chronic.

Pericarditis may occur upon either the visceral or the parietal layer of the membrane, and may attack any portion or several or all parts at the same time, being thus circumscribed or general. Usually, the whole or a large part of the pericardium is affected. Pericarditis is further characterized by effusions or exudations, which may be either fluid or semi-solid, and in consequence of the varied character of these exudations subdivisions are often made, such as the serous, fibrinous, sero-fibrinous, purulent, sero-purulent, and hemorrhagic forms. Pericarditis is generally marked by an effusion of fluid, the exception being designated as dry pericarditis, in which serum or other thin exuded material is almost or entirely absent.

Simple acute or idiopathic pericarditis is comparatively rare, and some authorities doubt its existence, believing that the pericardial inflammation is always secondary, plausibly supposing that the primary affection has escaped detection. Bamberger and Hayden, for instance, are of this opinion. I am, however, certain that I have met with several instances of true acute idiopathic pericarditis. Cases of so-called simple pericarditis are really often due to injury. It may not be easy in many cases to determine the traumatic or other condition in which the apparent simple acute pericarditis originated. The weight of evidence is so much in favor of traumatism as a preceding and efficient cause of simple acute pericarditis that a diligent search should always be made for the same. But even these doubtful examples are comparatively rare; and pericarditis is in the vast majority of instances secondary, and not difficult to identify as such. By some, traumatic pericarditis is classed with simple pericarditis as a variety, although not idiopathic.

Inflammation of the pericardium is governed by all the laws which control inflammatory processes elsewhere, being either acute, subacute, or chronic. The subacute form probably exists frequently, but escapes detection on account of the latency of the symptoms. The acute form is the most readily recognized. If not relieved, it passes into the chronic disease, which may be of long duration. The passage from one kind to the other is so gradual as to make it almost impossible to determine when one stops and the other begins, though it may be stated that after an acute attack has continued for from two to three weeks the chronic form is established. The chronic affection may begin, however, insidiously, or develop out of the subacute variety.

CAUSES.--The causes of pericarditis are numerous, and range from simple {770} cold and injuries to the thorax to those diseases of which it becomes a companion, whether the seat be remote from, or in immediate juxtaposition to, the pericardium. Simple cold as a cause of pericarditis is, as has already been indicated, very much questioned. Though a very rare, I believe it a possible, cause. Other causes of simple pericarditis may be blows upon the breast, as with the fist; crushing or compression, as in railway accidents; penetrating wounds, as from gunshot or knife; and injury from foreign bodies in the oesophagus, such as pins, false teeth, etc. Buist[1] records a case of a man who swallowed a plate with artificial teeth attached. The plate, becoming lodged in the oesophagus, finally penetrated the pericardium posteriorly and produced fatal pericarditis. A similar case is recorded by Flint.[2]

[Footnote 1: _Charlestown Medical Journal and Review_, Jan., 1858.]

[Footnote 2: _Diseases of the Heart_.]

By far the most common form of pericarditis may be termed secondary, which, like simple pericarditis, may be divided into the acute and chronic forms. It is termed secondary or consecutive, because it follows as a result either of impoverishment of the system or a pre-existing disease, constitutional or local. There are, however, exceptions to this rule; for we meet with cases of secondary pericarditis in which pericarditis preceded the onset of, and then continued associated with, the other manifestations of the disease which determined it. We see this sometimes in the history of acute rheumatism.

The disease of the pericardium is often the result of contiguity, but is much oftener determined by constitutional causes. Why the pericardium should be the particular membrane selected to take on inflammation as a complication to other affections has baffled the best endeavors of the most careful inquirers to determine. The diseases affecting the pericardium by continuity or contiguity of texture are chiefly myocarditis, tubercle of the lung and mediastinal glands, cancer of the same structures, pleurisy, pneumonia, and cancer of the oesophagus. On fibroid disease of the heart pericarditis is a frequent attendant.[3] The diseases affecting the pericardium by a special election, and which are remote from the membrane, are, principally, acute articular rheumatism, Bright's disease, inflammation and other diseases of the liver, phlebitis, typhus, typhoid and eruptive fevers, scurvy, and acute alcoholism. Without doubt, by far the most frequent cause of pericarditis is acute articular rheumatism. Pericarditis does not occur in chronic rheumatism, and it is doubtful whether it may be occasioned by gout, notwithstanding the decided and weighty opinion of Hayden that this is an efficient cause.

[Footnote 3: It was found in more than half the cases published by Fagge in _Transactions of the Path. Soc. of London_, vol. xxv.]

Acute pericarditis resulting from acute articular rheumatism has some peculiarities which it is well to bear in mind. It comes on early in the disease. We also know of its great frequency as a result of rheumatism, although the rheumatism be mild; for the intensity of the rheumatic inflammation is no measure of the extent or severity of the pericarditis. Nor does the number of joints involved nor their location give any idea of the greater or lesser liability of the pericardium to participate in the inflammatory action. Neither does the frequency of the rheumatic attacks bear any direct relation to the pericardial involvement; although experience has shown that the first attack usually is the one most likely to be the cause of pericarditis, while succeeding ones may or may not produce fresh seizures of pericarditis, or an aggravation of the disease where it has remained as the result of previous attacks of rheumatism.

Clinical literature is notably deficient in the reports of pericarditis ending in recovery, while the recorded cases of death from the disease as verified by autopsies are most numerous. Yet, although pericarditis is a serious malady, it is not commonly fatal; and this is especially true of the pericarditis of acute rheumatism. But it is a frequent disorder. Sibson,[4] with large experience {771} and patient observation, has collected and tabulated facts from many sources. In that particular variety of pericarditis which is the accompaniment of acute articular rheumatism he found that in 326 cases of acute rheumatism admitted into St. Mary's Hospital, about one-fifth of the cases (63) had pericarditis, which was accompanied in 54 cases by endocarditis; and only in one-fourth of the whole number (79) was there neither pericarditis nor endocarditis. One-third of the whole number of cases (108) had endocarditis, and a fourth (76) had threatened endocarditis, the signs being transient or imperfect. It is notable that the majority of the cases, regardless of sex and occupation, occurred prior to the twenty-fifth year of age; and what is equally notable is that the severity both of the joint and the heart affections was greatest at or before the same year. Of the 63 cases of pericarditis in rheumatism, there were 35 males and 18 females; of these, 11 males and 14 females were from sixteen to twenty years of age, and the fatal cases were all under the twentieth year.

[Footnote 4: _Reynolds's System of Medicine_, vol. iv.]

Pericarditis happens most frequently between the first and second weeks of acute rheumatism, although there are instances in which it occurs later, and occasionally it follows a sudden subsidence of the disease. It may be observed coincident with the onset of the rheumatic attack, and even preceding it by several hours. Latham has pointed out how acute pericarditis is more to be looked for when acute rheumatism is shifting and inconstant in its seat than when it is fixed and abiding.

Having now looked at rheumatic pericarditis, we may examine the pericarditis of some other disorders. In that class of affections known as Bright's disease of the kidney the serous membranes are liable to take on inflammatory action. A particular preference for the pericardium seems to exist, and the affections are the cause of pericarditis next in frequency to acute rheumatism. The tendency varies, however, with the particular kind of disease of the kidney which may be present. Pericarditis is common in the contracted kidney; in amyloid degeneration it is rare.[5] Where uræmia happens, it is apt to be developed. In warm climates it is less usual as an accompaniment than it is in cold and damp. But whether this be the full explanation of the varying frequency of pericarditis as an attendant upon Bright's disease in different countries is doubtful. There is, however, certainly, as we learn from the elaborate inquiry of Sibson, a varying ratio. The complication is, he proves, more frequent in Germany than in England, least frequent in France.

[Footnote 5: _Ziemssen's Cyclopædia_, vol. xv. p. 629.]

Let us now take into consideration other diseases which in their course have strong, although less-marked, tendencies to involve the pericardium. As a class, the eruptive fevers, especially scarlet fever, may present a pericardial lesion. This is owing to the fact that the serous membranes generally are liable to become inflamed in these conditions; but another element in the production of acute pericarditis may probably be found in the congestion of the kidneys which is apt to occur. Pericarditis is not commonly present early in these diseases, but rather in their later stages, when the body is enfeebled by the specific poison and the skin is susceptible to the slightest variation of temperature. It is then that the weakest and most vulnerable part will be attacked, and the pericardium may prove to be the most vulnerable part.

Other diseases which will cause pericarditis are those dependent upon dyscrasia of the blood, as in the diatheses, injuries attended by shock, and those conditions in which there is a great drain from the system. Perhaps the diathesis most apt to induce pericardial inflammation is the scorbutic, in which the impoverished and relaxed state of the system frequently manifests itself by inflammatory lesions of a low grade. In injuries or diseases {772} where there is excessive suppuration the system is so weakened that a low form of pericarditis is prone to develop itself. Diseases of the respiratory organs, as phthisis, pneumonia, or pleurisy, also enteric inflammations, will sometimes produce pericarditis. Indeed, any disease dependent upon or attended by a greatly deteriorated condition of the blood may cause pericarditis; for the health of the heart itself is determined by the quality of the vital fluid from which it draws its own sustenance in common with all other structures of the body, and any vitiated state of the blood seems to make a special impression upon the heart itself, its membranes as well as its structure.

MORBID ANATOMY.--In acute pericarditis the serous membrane first becomes injected with blood, and the injection, starting at a single or at several points, may become diffuse. If the engorged vessels do not relieve themselves, infiltration of lymph into the transparent serous layer follows, producing thickening and opacity as well as slight roughness. Consequent upon this there is further congestion, the membrane becomes red, with possibly here and there points of inflammation of greater intensity than that surrounding the original lesion; and at these places the vessels may give way and cause a hemorrhage into the sac or there are little spots of ecchymosis in the membrane. Usually there is a drying up or a partial suspension of the serous secretion from the turgid membrane, but before long the secretion generally recurs, and is even increased in quantity. Upon the surface of the serous membrane patches of coagulable lymph, more or less extended, are at the same time exuded. Under the microscope the bundle of fibres of connective tissue of the membrane appear swollen and broken up, and the proliferation starts which, as it progresses, determines the new growth and the villosities. Portions of the exuded lymph may be washed off and be found as shreds in the serum. The appearance of the lymphous deposit, as just indicated, is not always that of a plain smooth layer, but may be velvety and villous, like the lining of the small intestine, or it may be more roughened, or it may be honeycombed, as the interior of the stomach of the calf, or be in ragged shreds of varying sizes, either single or in bunches. Again, it may assume a lace-like texture, as of fibres coarsely woven together, or it may appear as if the threads were attached at one end to the pericardium and at the other floating free. All of these various forms are largely due to the heart, which in its action presses and rubs the lymph-covered surfaces together and keeps the softish exudation in constant agitation. One layer of lymph may be superimposed upon another until the deposit becomes very thick. It is this lymph which, existing before fluid is effused to any extent, determines what clinicians recognize as the dry or plastic stage of pericarditis.

Generally, however, there is effusion of considerable liquid, occasioning what is termed the stage of effusion. The fluid poured out is serous, alkaline, and albuminous, of a pale-yellow color, and transparent, but it may be opaque and milky. It may have flocculi floating in it, be stained any shade of color from red to brown by the coloring matter of the blood or by exuded blood-corpuscles, and may also contain pus. The quantity of fluid varies from a few ounces to several pints, but the latter amount is rare. The fluid is usually composed of the watery and saline elements of the blood, with a small quantity of albumen and a trace of fibrin. If the amount of fluid be small, the opposing surfaces of the pericardium come together, and the lymphous layer, becoming more or less organized by the presence of blood-vessels in it, makes attachments to the opposite wall; in this manner adherent pericardium is produced. The adhesion may vary in extent from the slightest filamentous attachment to complete obliteration of the pericardial sac; and it may be readily peeled off, or it may be so closely united as to become a part of the tissue upon which it lies. As the disease progresses the serum and, in exceptional cases, the fibrinous deposits may be entirely reabsorbed and leave {773} but little evidence of the previous inflammation. The white milky-looking spots often found in autopsies are regarded by many as the remains of cured pericarditis, but they are more likely the result of nutritive changes and consequent tissue-alteration. Fibrinous deposits are not always entirely removed. In complete adhesion of the pericardium they may be considerably reduced, but the sac never regains its normal appearance, and when the adhesions are partial they remain permanently.

The formation, density, and organization of the lymph depends largely upon the cause of the pericarditis. The more acute the attack and the greater the constitutional disturbance, the more likelihood there is of rapid effusion of lymph and of its speedy organization, whether it form adhesions or not. Where the fibrin is exuded under the influence of a subacute or chronic disease, the formation will be slow, paler, less highly organized, softer, and if adhesions form they will be less strong.

The heart participates in the inflammation of the pericardium, and if it be for any time subjected to the presence of the fluid effusion its walls degenerate and a granular atrophy occurs. Besides this, in extensive and firm adhesions there is likely to be primary hypertrophy followed by dilatation, the walls being enfeebled by degeneration, and, it may be, becoming thinner. At first, the effort to overcome the pressure of the pericardial effusion produces the hypertrophy; then the more or less complete binding down of the walls of the heart, preventing complete systole and weakening their inherent elasticity, and the pressure upon the coronary vessels, depriving the heart of the blood necessary for its healthful existence, are the causes of the degeneration and wasting of the walls and of the dilatation of the cavities.

Pus in the pericardium, as a result of pericarditis, may appear very early in the inflammatory attack, or it may occur after the effusion of lymph and serum. It may happen but in small amounts smeared over the surface of the membrane, or be profuse in quantity. Pus may also arise from small abscesses in the tissue of the heart bursting through the pericardium. It may be the result of injuries to the pericardium or to the inflamed membrane, or it may originate in the migration and proliferation of the leucocytes of the blood. The microscope in doubtful cases gives us the best idea of their prevalence and quantity, as well as of the amount of blood-corpuscles present. Where pus alone exists it is yellow and creamy; but with an excess of serum or fibrin it may be thinner or thicker in consistence, the entire heart being bathed in the fluid.

The lesions of chronic pericarditis differ but little from the acute, except as to their inception or the initial stage. The change from the acute to the chronic form may occur in a very few days, or even in less time, and an autopsy would not reveal anything to determine the fact. Pericarditis in any form is apt to be associated with pleurisy, and adhesions between the pericardium and adjacent pleura are common. In some instances the distended sac is adherent to the back of the chest. By its pressure on the lung and the oesophagus it may produce secondary lesions in them as well as in the phrenic nerves.

SYMPTOMS.--The symptoms of pericarditis may be so slight as not to attract attention. Where they are noticeable we find pain or a sense of uneasiness or of pressure, with or without tenderness in the pericardial region. The pain or uneasiness is not infrequently accompanied by pain or tenderness in the epigastric region when pressure is made upon it. This arises from the contiguity of the part and the pressure of the diaphragm against the inflamed and tender pericardium. The pain is sometimes preceded by a chill of varying severity, and is followed by febrile symptoms of greater or less intensity; but these may be so slight as to escape observation altogether except by taking notice of the markings of the thermometer.

{774} Yet the thermometric record, although indicative of fever, has nothing characteristic. It is, I think, more influenced by the conditions under which pericarditis happens than by the pericardial inflammation itself. Often the fever-curve is marked by decided remissions, and as the result of the pericarditis alone does not attain a high degree. In the aged, Charcot has pointed out that the temperature of the body is lowered in some instances of acute pericarditis. The setting in of pericarditis in acute rheumatism was observed by Lorain to depress the thermometric marking, and Brouardel has noted the same effect at the onset of pericarditis in typhoid fever.[6]

[Footnote 6: Constantin Paul, _Maladies du Coeur_, Paris, 1883, p. 130.]

The action of the heart is increased in frequency and force, as indicated by observing the impulse and the pulse at the wrist. There may be present, in different degrees, difficulty of breathing or a sense of suffocation; difficulty in swallowing; also cerebral disturbance, as headache, dizziness, sleeplessness, mental depression, fear of impending death. Besides these we may meet with hiccough and nausea and vomiting. But any or all these symptoms may also occur in myocarditis and in endocarditis, and are therefore not of themselves diagnostic; they only serve as indicators of the direction in which to seek the cause of disturbance. Some of the latter symptoms may be so aggravated, particularly those manifested by the nervous system, that attention is absolutely diverted from the seat of the disease. Indeed, they are often very misleading; and I cannot even agree to Hayden's statement[7] that with few exceptions the symptoms of pericarditis take precedence of the physical signs, though they cannot be regarded as sufficiently distinctive to warrant a positive diagnosis. Doubtless these symptoms, however suggestive of pericarditis, may be found to depend upon other causes. With so little, then, of a positive nature to assist us in our search, we should be always at great loss were it not for the physical signs.

[Footnote 7: _Diseases of the Heart and Aorta_.]

PHYSICAL SIGNS.--The chief of these are determined by inspection of the chest, by palpation, by auscultation, and by percussion.

Inspection.--In inspection of the chest the age of the patient is to be regarded in the interpretation of the appearances. In pericarditis with effusion we are apt to find a change in the shape of the chest--a bulging in the region of the heart, even though the effusion be somewhat small in quantity. This change is more apparent when it occurs in young persons, where the chest-walls are very elastic. In those advanced in years, in whom the costal cartilages are more or less ossified and the elasticity of the rib materially altered, or where the chest-walls are bound down by pleuritic adhesions, the shape of the chest may be materially altered and yet not be very apparent. The intercostal distension is in any case a matter for investigation. The chest shows a bulging in the pericardial region, slightly diminished by a dorsal decubitus and but little influenced by the acts of respiration.

Palpation.--This gives us an idea of the amount and outline of the tenderness, which is often found to correspond with that of the inflamed pericardium. It also enables us to determine to some extent the limit of distension of the pericardium, the location of the heart, and the shape of the sac. We also ascertain the impulse of the heart. Now, at first this is somewhat increased, although it is apt to be irregular. As effusion of liquid takes place, the heart is displaced generally backward and upward, and the impulse becomes indistinct or imperceptible. A slight wavy, irregular motion diffused over considerable part of the cardiac region may take its place.

Percussion.--During the dry stage, unless a very considerable amount of lymph be extravasated, the natural percussion dulness in the cardiac region is not appreciably altered. When the pericardium becomes distended with fluid the cardiac dulness increases markedly, particularly in a transverse {775} manner; and as the pericardium is conoidal in shape, but its position the reverse of that of the heart, its base resting upon the diaphragm, with its distension a roughly pyramidal outline of dulness is found, the apex being near the root of the vessels, the base upon the diaphragm. A great deal of stress has been laid on this shape of the percussion dulness--much more, I think, than in point of fact is warranted, for it is not always to be distinctly made out. Rotch[8] has called attention to the dulness being early manifest in the fifth intercostal space of the right side, and in all large effusions it is sure to extend across the sternum. It may, when the sac is much distended, reach as high as the first rib, as low as the seventh rib, and below the ensiform cartilage, and the line of the lower dulness may become continuous with that of the displaced liver. The dulness may extend on the left side backward almost to the spinal column and across the sternum to the right nipple. The dulness is somewhat influenced by position; changing from side to side alters the line of the fluid.

[Footnote 8: _Boston Medical and Surgical Journal_, 1878, vol. xcix.]

Auscultation.--Pericarditis is not discoverable without the signs by auscultation, and it is the interpretation of these signs which enables us to distinguish the various stages. We must bear in mind that, roughly speaking, there is first a stage of suspension of the serous secretion, and consequent dryness of the pericardium; secondly, effusion of lymph or fibrin; thirdly, effusion of serum or sero-pus. Now, the question arises whether we can distinguish the first effect of the inflammation on the serous membrane, which, indeed, may be exceedingly short in duration, limited to a few hours. From the fact of there being a suspension of secretion and absorption of that which has been normally secreted, it becomes evident that, the parietal pericardium coming into direct contact with the visceral layer, certain sounds will be caused by the friction of the heart in its action. Can we discern them? Great differences of opinion have been expressed with reference to this; indeed, it has even been questioned whether sounds would be or would not be produced. Stokes doubted the competency of simple dryness of the pericardium to generate friction phenomena. Collin, on the contrary, held that this is actually the condition of the pericardium indicated by the new-leather sound. To this Walshe makes assent. Hayden[9] says: "I have never met with a case which would warrant me in asserting that a state of simple dryness and vascularity of surface may give rise in the pericardium to veritable friction sound. I do not, however, deny the possibility of an occurrence which, theoretically, would seem not improbable. In every instance, without exception, in which I have had the advantage of determining by post-mortem examination of the body the condition of the serous surface of the pericardium, where friction sound of indubitable pericardial origin had existed during the patient's last illness, I have found lymph in greater or less quantity effused upon the surface." My own experience is entirely in accord with this. Theoretically, I grant the possibility. Practically, I have never seen it; and in the suspected cases lymph has always been found, with the single exception of a case in which the friction sound had disappeared nearly a week before death, which resulted from kidney lesion, and where it was reasonable to infer that the lymph had been absorbed.

[Footnote 9: _Diseases of the Heart and Aorta_, Philada., 1875, vol. i. p. 327.]

The friction sound, then, is the sign of exudation. Since it was originally described by Stokes in 1833 it has been likened by different observers to familiar objects, such as the crackling of parchment and the new-leather sound. It is generally most evident at the base of the heart, is considerably influenced by pressure, is more often double than single, frequently resembles a double cardiac murmur, and justifies the name of a to-and-fro sound given to it by Watson. The friction sounds change from time to time according to {776} the character, quantity, and stage of the exudation, ceasing altogether when adhesions have taken place or fluid has been effused, to return again as the fluid is absorbed, and to cease when recovery has taken place. They exhibit an inspiratory rhythm very much intensified by full inspiration. Although, as the place of election of the inflammation is at the base of the heart, we are apt to find the friction there earliest as well as longest, this is not invariable; for, as above stated, the morbid process may begin anywhere in the continuity of the pericardium.

Next to the friction sound, the most valuable signs in pericarditis are derived from the muffling of the cardiac sounds. This is particularly valuable in the stage of effusion, for prior, notwithstanding the friction phenomena are somewhat obscure, they do not render the sounds of the heart fainter to any material degree. The cardiac sounds become less and less distinct as the fluid increases. The heart sounds cease to be audible, just as is the case with the friction sound, from below upward, beginning to be indistinct at the apex of the heart. Gradually and lastly, the sounds of the aorta and pulmonary valves are lost, but not entirely, unless there be a large amount of fluid pushing up the pericardium at its attachment around the roots of the great vessels, and the second sound at these valves is scarcely ever wholly gone. Sudden effusions of large quantities of fluid are so rare that the progressive extinction of the cardiac sounds becomes an important element in diagnosis and prognosis. It has already been noted that the friction sounds linger around the base of the heart; this may happen with even considerable effusion. As regards the character of the fluid influencing the distinctness of the cardiac sounds, I think it may in general terms be stated that if the effusion be dense, sero-purulent, or purulent, the sounds of the heart are, in proportion to the size of the effusion, relatively more obscured than when this is thin.

DIAGNOSIS.--The diagnosis of pericarditis, as before remarked, cannot be determined by any but physical signs, and even these signs may not be sufficient for us to come at once to a positive conclusion: the refinement of perception necessary to detect and properly interpret the delicate changes which occur in some cases is still lacking to us. In reviewing the general diagnosis of pericarditis we must bear certain facts in mind. The acute malady has a very dissimilar origin. It usually sets in with a fever, ordinarily not of high grade, which may be preceded by a chill of differing intensity; the pulse is decidedly accelerated and of varying regularity, not uncommonly strikingly irregular; on the other hand, the nervous phenomena may be the most prominent. Craigie[10] observed long ago in a case of pericardial inflammation in a girl of fourteen that the only prominent symptom besides the symptom of fever was constant tossing of the extremities and person, jactitation similar to the motions of the dance of St. Vitus. Roeser of Bartenstein observed the same symptom in a child of nine years. There is at times early delirium, very frequently considerable restlessness, with more or less of an anxious expression of countenance. Quickened rather laborious breathing is often early observed, and so is pain in the præcordial region directly under or near the sternum, perhaps extending to the left shoulder, acute, severe, and shooting, increased by pressure and motion, and, as Peter[11] has pointed out, associated with pain in the phrenic nerve, elicited by pressure between the two insertions of the sterno-mastoid and also found on each side of the xiphoid appendix. But the pulse may be regular, the breathing not perceptibly accelerated or laborious, and even the important symptom, pain, may be wanting from the beginning to the end of the disease. This occurs in the so-called latent cases.

[Footnote 10: _Elements of the Practice of Physic_, Edinburgh, 1837, vol. ii. p. 151.]

[Footnote 11: _Clinique Médicale_.]

Since pericarditis is frequently attendant upon certain classes of diseases, {777} as acute articular rheumatism, Bright's disease of the kidneys, the eruptive fevers, it behooves the physician to be on the alert and examine the heart, even though nothing point to its involvement. Reminded of this fact, we must seek for those signs which will enable us to diagnosticate early the cardiac disease. And in any case the first sign of importance detected will be, in all probability, the friction sound, generally, but not invariably, first heard at the base, and prone to mask the natural sounds of the heart. At all events, this is the case when the friction sound is localized at the apex of the heart, as it occasionally is, before there is very marked development of the lymph-deposit; it is then, too, that from its softness the friction may be mistaken for a regurgitant mitral murmur. The friction may at times be felt by applying the hand to the region of the heart. This friction fremitus is, however, far from constant, and can hardly be considered of much diagnostic value, notwithstanding the high authority of Stokes, who looked upon it as distinguishing pericarditis from valvular disease. Prior to the existence of the friction sound we may suspect pericarditis by the sense of general distress and the dropping of pulse-beats or the otherwise altered cardiac rhythm. But the diagnosis is presumptive; the friction phenomena make it positive. Until the quantity of fluid is sufficient to separate the two walls of the sac the rubbing sound will be apparent. The friction sound never disappears suddenly, and this gradual disappearance points to the formation of fluid and may be regarded as a truly diagnostic sign. The fluid, following the laws of gravitation, seeks the most dependent portion of the sac, which it more or less fully distends; in consequence, the disappearance of the friction begins at the bottom of the sac and at the apex of the heart and gradually extends upward to the base. Adhesions of the pericardium will modify and may entirely prevent the formation of the friction sounds. If the adhesions be local, and if no lymph-deposit be present between them, there can be no friction; so also where the adhesion is general the friction sound is destroyed. Where local adhesions and portions of free surface more or less covered by the lymph exist, the heart, being allowed sufficient motion, produces friction sounds which may be found anywhere over its surface except at the points of adhesion. From the character of these sounds the location and the extent of the adhesions and of the cardiac movements may be determined, for "the rhythm of the pericardial friction sound is as the natural movement of the portion of the heart engaged and the mobility of the opposed surfaces," says Hayden[12] very truly.

[Footnote 12: _Diseases of the Heart and Aorta_.]

In weighing the value of friction sounds in diagnosis, especially in determining whether they are produced in the pericardium and not in the adjacent pleura, we have the simple, though not infallible, method of discrimination of letting the patient cease breathing for a moment and then ausculting the heart: they persist if pericardial. This test will fail, however, in case a portion of the pleura adjacent to the pericardium also be covered with lymph: then the heart's motion, transmitted through the pericardium, may produce pleuritic friction even while the lung is at rest. In such a case if a friction fremitus be felt it will pass beyond the cardiac area, while in pericarditis without associated pleurisy it will not be likely to extend farther than the normal limit of cardiac dulness. The pericardial friction sound may be sometimes noticed more or less extensively over the whole chest in children, and also in adults with hypertrophy of the heart, but this is far from being usual. There may be a friction sound produced by the action of the normal heart in an inflamed roughened pleura. This is very difficult to distinguish except by the attending symptoms. The sound is perceived near the apex of the heart. It is not apt to occur with each beat of the heart, and may be absent in held expiration.

{778} In the diagnosis of pericardial effusion, when at all extensive, we have, in judging of the amount of fluid in the pericardium, to take into account the increasing dyspnoea with a decided suffocative tendency, the dizziness, the pallor or lividity of the countenance, the swollen cervical veins, the bluish nails, the heart flutterings, the weak, rapid, and irregular pulse, the drowsiness or tendency to mental wandering. But the physical signs of the effusion above detailed are of the greatest value, although they give us but little information as to the character of the fluid. Even in large effusions the friction sound may not disappear from the base. Indeed, Balfour[13] records as the result of his observation that "however large may be the effusion, basic friction, if it have once existed, is never effaced." It is stated that when the amount of fluid does not entirely fill the pericardium there may be a splashing sound, and the location of the sound, as well as that of the percussion dulness, will be changed by changing the position of the patient's body. I have never observed this splashing sound. The extent of percussion dulness is no absolute sign of the extent of effusion. The area of cardiac dulness may be materially influenced by the following circumstances: the anterior margins of the lungs which overlap the front of the heart may, from emphysema, give rise to percussion resonance over the heart, even though considerable effusion have taken place; the anterior margin of the lungs, becoming solidified and having strong pleuritic attachments to the pericardium and anterior chest-wall, may increase the dulness over the heart and prevent the recognition of the effusion in the pericardium; effusion in the pleural cavity of one or both sides may produce similar results. Balfour[14] in fact mentions a case of his own in which the pericardial dulness was merged in the pleuritic dulness, and careful auscultation failed at any time to detect friction sound; the coexistence of pericarditis was surmised, but could not be detected. After death the pericardium was found to be distended with reddish serum, and both its surfaces were coated with shaggy, blood-stained lymph. Such cases are unusual, yet I have met with a similar instance. Lastly, a growth in the anterior mediastinum may be the means of masking or being mistaken for pericardial effusion by changing the dulness in the cardiac region and altering the cardiac sounds, or it may, by obstructing the circulation, cause effusion. When an effusion of fluid takes place into a partially adherent pericardium, the area of cardiac dulness may be irregular or restricted, or both, the shape and size depending on the length and strength of the adhesions.

[Footnote 13: _Diseases of the Heart_.]

[Footnote 14: _Ibid._]

Some of the results of large effusions show themselves on other organs. The backward pressure of the fluid upon the bronchi, trachea, aorta, and oesophagus interferes with their functions and actions. There may be bronchial or blowing respiration heard over the lung, due to compression of the parenchyma. The fluid around the heart prevents free motion of the organ, although not to so great an extent as in adherent pericardium; complete diastole does not occur; the auricles and ventricles are not completely filled; the systemic and pulmonary circulations become engorged, and pressure is exerted upon the coronary arteries, thus disturbing the nutrition of the heart. The irregular action of the heart occasions at times a vibration which is more or less apparent to the touch. Percussion of the liver shows enlargement of the viscus; this is due to the obstruction of the ascending vena cava, which prevents a free emptying of its blood into the right auricle, and consequently causes a backing up of the blood in the gland. If the pericardial effusion press upon the anterior portion of the chest, it may produce pain and aggravate all the other symptoms, such as the pulmonary oppression, the dizziness, the hurried respiration, the increase of pulse. Water, blood, or pus in the pericardial sac gives rise to the same physical signs as serous effusion, and {779} cannot be distinguished from it with any degree of certainty, although a careful consideration of the general symptoms presented may enable us to make a guess which can only be proved or disproved by an autopsy.

Having endeavored to show the most prominent features characterizing pericarditis in its various stages and bearing in a general way on its diagnosis, we shall examine some of the special maladies which are liable to be confounded with it. The diseases most likely to be mistaken for the acute inflammatory stage of pericarditis are inflammation of the pleura and of the endocardium. They are liable to occur from the same causes, and may be--indeed, often are--concurrent. Pleurisy gives rise to many of the symptoms of pericarditis. The chief difference is in the physical signs, some of which, however, are alike in kind, although different in locality; for in pericarditis they are confined to the region of the heart: in pleurisy they are spread over the whole side of the chest and are most perceptible at the back. This is true of the dulness, and for the most part of the friction sound, which when of pericardial origin is very rarely heard posteriorly. Then stopping the act of breathing if the sound be pleural suspends it. At times, however, as above described, we meet with cases in which a friction sound discovered over the heart may in reality be produced in the adjoining pleura. To confound the dulness on percussion caused by liquid in the pericardium with that due to liquid in the pleura is, from the different site of the liquid, not likely to happen unless the effusion be extremely large; for ordinarily a pericarditis uncomplicated with pleurisy or with pleuro-pneumonia does not change the clear sound at the back of the chest nor enfeeble or abolish there the breath sounds and the vocal fremitus. Besides, effusion into the pleura, if it give rise to a flat sound anteriorly, does not occasion the special præcordial bulging, and shows the sounds of the heart unaltered unless the pericardium contain fluid also.

Acute pericarditis is likely to be confounded with acute endocarditis. The chief difference consists in the physical signs--the friction sounds and signs of effusion in pericarditis, the blowing sounds, the slight alteration of percussion dulness in endocarditis, and the fact that in this disease the abnormal murmurs are often transmitted beyond the cardiac region and heard in the carotids and subclavian, and are far less changeable in character and in pitch.

There are other affections with which pericarditis is likely to be confounded, such as gastric irritation and acute inflammation of the brain. When pericarditis resembles gastric disorder the thoracic symptoms may be latent, but the disease produce the manifestations of extreme gastric irritation or inflammation. There are nausea and vomiting, and tenderness on pressure in the epigastric region, yet no disease of the stomach may be present. An examination of the cardiac region for the physical signs of pericarditis should be made in every case of persistent vomiting or of hiccough.

Where the symptoms are chiefly cerebral, the cardiac disease may be overlooked; indeed, in both endocarditis and pericarditis the insomnia and the active delirium may throw all the other symptoms into the shade. The violent disturbance of the brain may have its origin, in part at least, in the contaminated state of the blood which occurs in the affections, as rheumatism or Bright's disease, with which pericarditis is often associated. But it is possible also that it may be due to a coexisting endocarditis of which the products are washed into the brain. In ulcerative endocarditis cerebral manifestations are especially common, and there may be acute mania of the most violent type, as in the case reported by Sioli.[15] Sibson in his exhaustive analysis points out what I have known to happen in more than one instance, that the desponding and taciturn--or, as he calls it, sombre--delirium of pericarditis lasts from two to three weeks to as many months. Indeed, it may terminate {780} in confirmed insanity. Any form of nervous disturbance having its centre of disorder in the cerebro-spinal axis and of any degree of intensity may be seen in cases of pericarditis, whether produced as a consequence of rheumatism, of albuminuria, or by other causes. The cases with marked nervous symptoms are apt to present high temperature, 105° or more.

[Footnote 15: _Archiv für Psychiatrie_, Bd. x.]

The diagnosis of pericarditis from hypertrophy of the heart is made by remembering that in pericarditis we find friction sound, præcordial bulging, peculiar enlargement of percussion area, enfeebled impulse and heart sounds, besides the presence of pain, of fever, of dyspnoea. In hypertrophy the area of percussion dulness is enlarged, but the shape is normal; the impulse and heart sounds are strong; no pain or fever, no friction sounds exist. The chance of mistaking dilatation of the heart for pericarditis is much greater. In the early stage of pericarditis the area of percussion dulness is generally similar in size and shape to the dulness in dilatation. But soon the difference both in size and shape of the cardiac area becomes marked, the shape being pyramidal or pyriform in pericardial effusion, while in dilatation the increase is lateral and does not extend beyond the point of impulse. There is no friction sound in dilatation; and if the first sound be weakened, though it may be also sharp and short, the second sound is everywhere distinct, unlike the muffling of the cardiac sounds, except at the base, in pericardial effusion.

Tumor of the anterior mediastinum, whether solid or fluid, may become a source of perplexity in determining the diagnosis of pericarditis; for by the interposition of the morbid mass between the chest-wall and the heart the cardiac dulness is increased and the heart sounds are lessened in distinctness and perhaps in force; though if the tumor be solid and very dense the sounds may be intensified. Pericarditis may also be associated with a tumor, and a diagnosis under such circumstances is attended with great difficulty. A tumor of the anterior mediastinum is comparatively rare, and seems to be more frequent in females than in males, although the statistics are meagre and not conclusive. There may be displacement of the heart in any direction as the result of pressure from the growth. Should this be equable in front of the heart, the diagnosis becomes one of doubt, for the same alteration of the shape of the chest may be present as in pericarditis with effusion. If the tumor be malignant or scrofulous, tumors of a similar character may be found in the neck, axilla, or elsewhere, and aid us in arriving at a correct conclusion.

The differential diagnosis of pericarditis from inflammation of the anterior mediastinum will cause at times no slight difficulty. However, inflammation of the anterior mediastinum is infrequent. It may come on without assignable cause or as the result of injuries. It may be produced by extension of inflammation from adjacent parts, as in pericarditis; it does not appear in association with, or as a consequence of, other diseases, such as rheumatism, renal diseases, scurvy, or the exanthemata, as is so largely the case with pericarditis. The symptoms resemble those of pericarditis, and there is likely to be chill, followed by fever, substernal pain and weight, pain on pressure over the sternum, accelerated action of the heart. Respiration is more or less difficult and painful, on account of the movements of the cartilages and intercostal muscles. The disorder in respiration becomes the more decided when the inflammation has extended to the pleura; there is also pain on pressure in the epigastrium. The physical signs of mediastinitis may be precisely similar to those of pericarditis. The extension of the inflammation to the adjacent parts produces the characteristics of uncomplicated inflammation of these parts, and under such circumstances the distinction is far from being easily made; the pleuritic and pericardial friction sounds which are developed will naturally be ascribed to affections of the pleura and pericardium alone. In accumulation of pus in the mediastinum no little uncertainty {781} will exist in determining the difference between this and pericardial effusion. The percussion dulness may extend beyond the area of the heart, and take the form of the area in effusion into the pericardial sac. It is true, however, that in purulent collections in the mediastinum the shape of the percussion dulness is often more elongated, extending upward to the sterno-clavicular articulation. Should the accumulation be large, we meet with difficulty of respiration and of deglutition from pressure, as in pericarditis with effusion or in hydropericardium; and there may be elevation of the sternum and intercostal bulging. Abscess of the mediastinum tends to point at an intercostal space; it may also do so in the scrobiculus cordis: the impulse of the heart is weakened or entirely lost and the heart sounds are distant and obscured. There is apt to be hectic, with headache, delirium, and syncope. In fact, there is no symptom of pericarditis or of hydropericardium which may not also be found in acute mediastinitis or in the accumulation of pus in the mediastinum. Where the inflammation can be traced to an injury, as a blow upon the sternum, or where there exists caries or necrosis of the sternum, the diagnosis is greatly facilitated. The inflammatory symptoms, while of all grades of intensity, are, as a rule, more intense in the forms of mediastinitis than in any of the acute stages of pericarditis. In cases of fibrinous mediastinitis associated with fibrinous or fibro-purulent pericarditis, Kussmaul has called attention to the diagnostic value of a pulse intermitting at regular intervals simultaneously with inspiration, the pulsus paradoxicus.

PROGNOSIS.--The prognosis of pericarditis is exceedingly variable, depending largely upon the primary cause, the intensity, the stage and duration of the attack, the prior condition of the individual, and his surroundings. The general prognosis is favorable to life: though some of the older writers were disposed to look upon it as a highly dangerous disease, it is clearly one from which recovery is frequent. In many autopsies of individuals who have subsequently died of other disease the evidences of cured pericarditis have been found. By cured it is not wished to convey the idea that the pericardium was restored to the condition it was in prior to the inflammatory attack, but that the inflammation had ceased without injurious consequences. There may be recurrent attacks, and they are frequently of a subacute character; even when fibrinous deposit and attachments continue to exist, it often happens that the movement and functions of the heart are not interfered with. Unless the disease be exceedingly severe in the acute stage, the prognosis is decidedly favorable. When the attack is very severe there are strong reasons for believing that the structure of the heart is also involved, and death ensues chiefly from the latter complication.

Should adhesions take place, the prognosis is unfavorable in proportion to their extent, though to this rule there are decided exceptions. If effusion rapidly develop, the prognosis becomes at once unfavorable, death resulting in a short time from sudden pressure upon the heart and its palsy. If, however, the effusion accumulate slowly, the parts become tolerant, and a large amount of fluid may be thrown out without fatal consequences. Where death occurs it usually comes on slowly, and the immediate cause is from the pressure of the large effusion upon the heart, preventing its free diastole. The lungs become engorged with venous blood, and asphyxia of the heart ensues. There is apt to be general dropsy in such cases, particularly oedema of the lower limbs and accumulation of fluid in the serous cavities, as in the pleuræ, and the patient becomes gradually exhausted. If effusion of serum be accompanied by pus or by blood, or if there be pericarditis with pus or blood alone, the prognosis is unfavorable. Balfour,[16] however, states that recovery is not impossible in purulent pericarditis, "for the elements of pus are more or less present in every pericarditis, and pus may be only a transitional {782} stage, and may result in the breaking down of cell-elements, the formation of a pathological cream, and its complete absorption, and the perfect cure of the disease." The caseous formation, or even the pathological cream, is rarely met with, and cannot be detected prior to death. Burrows[17] records a case in which there was a layer of concrete pus over a small space in a pericarditis of seven days' duration. Pericarditis with large amount of membrane, whether this be coated with pus or not, and even without liquid effusion into the sac, is always of grave prognosis; so are cases with high temperature, cases complicated with pneumonia, cases in which the dyspnoea is of intensity disproportionate to the local symptoms, and in which the pulse is not in unison with the impulse of the heart.

[Footnote 16: _Diseases of the Heart_, 1876, p. 299.]

[Footnote 17: _Disorders of the Cerebral Circulation_, London, 1846, p. 187.]

The pathological changes in pericarditis are such that it is quite impossible to determine by the special signs or symptoms of the affection between simple pericarditis and a pericarditis the result of transmission from diseases in adjacent organs, as pleurisy or pneumonia, or as a complication of rheumatism or Bright's disease, except by the history and the general features of the case. Yet the prognosis is vastly different. The prognosis of simple pericarditis without carditis is good. Pericarditis in acute articular rheumatism is generally favorable as to life, and is nearly as favorable as simple pericarditis. Balfour[18] states that he has records of 1968 cases of disease treated in the Royal Infirmary, 70 of which were cases of acute rheumatism, with but 1 fatal case of rheumatic pericarditis. My general experience of the favorable character of rheumatic pericarditis without marked involvement of the deeper structures of the heart corresponds with this. I except, however, the comparatively rare cases with high temperature. A temperature of 105° is always grave. The prognosis of pericarditis in Bright's disease is, speaking in general terms, as unfavorable as that of the pericarditis of acute rheumatism is favorable. The pericarditis of poisons, of pyæmia, or of scurvy is, as a rule, a very serious malady. In the exanthemata recovery is the rule, unless there be extensive pleurisy or pneumonia as a complication.

[Footnote 18: _Op. cit._, p. 288.]

In injuries, such as in rupture or puncture, the prognosis must depend upon the extent and the character of the injury, the condition of the patient, and whether or not the puncturing body has been removed from the wound. Generally, these must be regarded as unfavorable cases, although paracentesis of the pericardium is now accepted as a proper operation and is attended with comparatively little risk. The cerebral symptoms occurring in pericarditis can hardly in themselves be regarded as unfavorable to life, but they are unfavorable when associated with high temperature and when considered in connection with full recovery of the mental powers. Relapses and recurrences of pericardial attacks have strongly fatal tendencies. Age and sex contribute materially to the prognosis. The very young and the aged are unpromising subjects; and Sibson[19] has shown that while females are somewhat more liable than males to acute articular rheumatism, males are more often attacked with rheumatic pericarditis; also that endocarditis accompanies pericarditis more frequently in males than in females, while simple endocarditis is more frequent in the female than in the male. He also shows that while pericarditis affects the two sexes below the age of twenty-one in nearly equal proportions, after the twenty-fifth year males are three times oftener subject to it than females. The disease is greatly modified by occupation as well as by age. Thus, Sibson has pointed out that female domestic servants under twenty-one years of age are extremely prone to acute rheumatic pericarditis, endocarditis, and carditis, as they are often unequal to labor and fatigue, and are easily affected by draughts and by exposure to wet and cold.

[Footnote 19: _A System of Medicine_, by Reynolds.]

{783} The causes of death in pericarditis are various. Death may occur in a few hours after the attack by the rapid effusion of a large quantity of fluid, compressing and causing mechanical paralysis of the heart; or it may happen from syncope due to the patient making sudden exertion, as in getting out of bed, more especially if there be a large amount of fluid in the pericardium; or, again, it may be owing to paralysis of the heart from disturbance of the cardiac centres, or to fatty degeneration of the cardiac walls largely induced by the inflammatory condition. Again, a fatal termination may be caused by pneumonia or extensive congestion of the lungs, or by a large quantity of fluid in the pleura, having its origin really in the pressure exerted on the veins and the other structures by the pericardial effusion; or death may result from non-aëration of the blood and from general exhaustion.

TREATMENT.--In the treatment of acute pericarditis the first thing to insist upon is absolute rest--rest of body, rest of mind; all effort, all fatiguing conversation, is to be avoided. The diet should be of an easily-digested kind, nourishing, but given in small quantities at a time, so as not to distend the stomach. Milk, eggs, animal broths, with occasionally just enough solid food to gratify the wish of the patient, constitute the best diet. Further, from the very outset the cause of the malady should be clearly kept in view and the treatment directed in accordance. As so many cases have their origin in rheumatism, an antirheumatic treatment has usually to be carried out. But here let me at once record the more than uselessness of the salicylates. They have no influence when pericarditis has arisen, and if salicylic acid or its compounds are being given, they should at once be stopped. The alkalies have a far better action. Again, speaking in general terms, opium in moderate doses, to keep the nervous system quiet and to moderate the general discomfort, is of wide applicability and signal use; few are the cases which its steady, judicious employment will not benefit. Especially is this witnessed in the earlier stages and before marked effusion occurs.

The treatment of acute pericarditis is much influenced by the stages of the malady--whether it is seen in the stage with plastic exudation; whether this exudation markedly persist and but little liquid effusion takes place; whether the effusion is copious. Now, in the earlier stages and before decided effusion bloodletting was at one time much in vogue, but it has been by general consent abandoned, at least general bloodletting has. Local bloodletting is still employed by some, and I am sure I have known a few cups to the præcordial region or leeches there applied relieve the pain and make the action of the heart more regular. It is, I think, in robust subjects and in the early stages decidedly to be recommended. Mercurials, like general bloodletting, have fallen into disuse. Cases of pericarditis have been seen to originate in those whose gums were touched by mercury, and it does not prevent effusion. Certainly, in pericarditis with Bright's disease the remedy must not be thought of; but under other circumstances, in lingering cases with extensive plastic deposits, or in effusions that remain uninfluenced, it is worth a trial.

The application of cold to the cardiac region, either in the shape of cold compresses frequently changed or of a bladder of ice, is very much lauded by some of the French and German physicians. Gendrin's method consists in keeping a bladder of ice over the heart for from one to three hours until the pulse and temperature come down to about a normal condition. As these rise it is from time to time reapplied, although for a shorter period; and it is thought to influence both the pain and the inflammation. I have not seen the latter effects from it; and for the pain it is less trustworthy than the more commonly employed hot-water applications and poultices. Digitalis is in the earlier stages an admirable remedy. Its use in small, frequently-repeated doses will render the action of the heart more regular and reduce {784} its frequency. Friedreich[20] and Bauer[21] both recommend its employment in large doses, to be suspended when the pulse becomes slower or irregular. Notwithstanding it might be thought particularly valuable in marked effusions alike from its tonic action on the heart and its diuretic powers, my clinical experience is against it under such circumstances. It is far inferior to the free use of stimulants.

[Footnote 20: _Die Krankheiten des Herzen_.]

[Footnote 21: "Diseases of the Pericardium," _Ziemssen's Cyclop._]

When there is decided effusion diuretics are our main dependence, and squills and tartrate or acetate of potassium are most employed. The acetate of potassium is very serviceable--half an ounce or more in twenty-four hours in broken doses. Nor need we wait for the occurrence of the effusion to begin with this remedy. An occasional hydragogue cathartic is also indicated where the strength of the patient permits; but care must be enjoined not to let him rise to go to stool. In lingering effusions iodide of potassium, not less than forty grains daily, and repeated blisters are employed. The latter remedy may also be used early in the case where the friction sound is extensive, and a large blister then is better than a small one.

A state of things is at times met with in which the pulse is weak, the extremities cool, the effusion large, the impulse of the heart very faint, the heart evidently struggling. There is but one remedy for this--the free use of stimulus, whiskey or brandy or wine, whichever is best taken. Nor do cerebral symptoms contraindicate--on the contrary, they more decidedly indicate--stimulants. Tonic doses of quinine and hypodermics of brandy aid in this stage. Should the symptoms still prove unyielding and the effusion large, the question of puncturing the pericardium will arise; and as a means at least of gaining time the operation is strongly indicated. Its manner of performance and its general results have been carefully studied by John B. Roberts, and to his remarks in this volume the reader is referred. We cannot be too careful to be on the lookout for the pulmonary complications, pleurisy or pneumonia, which are so apt to be found in acute pericarditis. They require prompt treatment, but they ill bear depressants. They demand, among other means, often quinine, and the greatest attention in sustaining the action of the heart and in keeping the kidneys actively at work. When the dyspnoea is very great, and there is considerable pleural as well as pericardial effusion, it is best to tap the pleura. I have several times given this advice in cases in which it was under discussion to tap the pericardium, and after the relief afforded to the lung the pericardial affection has yielded to remedies.

Chronic Pericarditis.

Chronic pericarditis, as such, requires but little consideration here, since its main features have been discussed in this article under other heads.

Chronic pericarditis is divided from the acute by a very shadowy line: a few hours of the acute disease may terminate in the chronic form, as in acute inflammatory affections elsewhere, or the malady may follow an attack of acute pericarditis of several weeks' duration, or it may be chronic from the beginning. In the first case the pericardium is the organ primarily affected, generally from cold, or the lesion is dependent upon some acute inflammatory disease adjacent or remote, as carditis, pleurisy, mediastinitis, or upon rheumatism. In pericarditis the result of the exanthemata, of Bright's disease, of scurvy, of tuberculosis of the lungs or elsewhere, of profuse drainage from abscesses or injuries--of, in fact, any wasting disease or fault in the economy associated with malnutrition--the pericarditis may be subacute at first, and is then apt to become chronic.

{785} The symptoms are slow of development, and are not usually rapidly productive of discomfort. They are in the main the same as those of the acute affection, although less decided, and the thermometer may mark a normal degree or but little above the normal. The physical signs of effusion of fluid, the presence of pus and blood or of adhesions, have all been discussed under their proper heads. The prognosis is, generally speaking, not as favorable as in the acute form; it depends very much upon the cause, the duration of the case, and the character of the fluid. In the treatment great attention must be paid to the cause as well as to getting rid of the effusion and relieving any direct oppression of the heart the result of the pressure of the fluid. If this cannot be done by medical means, or if there be reason to believe that the collection is purulent, paracentesis is indicated. Adhesions are not, or are but very seldom, removed by any special treatment directed to them. Indeed, it is by adhesions that most of the cases of pericarditis with lymphous effusion get well. When adhesions have disappeared after these attacks of inflammation, it has been through the efforts of nature, and nothing is left but the milk spots to testify to the previous condition of the membrane. But these, it must be remembered, are also the result of altered nutrition in the membrane, and do not in themselves bespeak a chronic pericarditis.

Adherent Pericardium.

Early in this article adhesions were mentioned as one of the results of pericardial inflammation, and it was stated that the exudation may appear in spots or extend over the visceral or parietal layers of the pericardium or over both, and become organized tissue filled with blood-vessels, gluing the walls together, and completely obliterating the sac. Limited adhesions are much more common than those which are extensive or complete. The intensity of the inflammation offers no indication of the probability of the formation of adhesions. The position of the body will materially assist in the adhesion of one point in preference to another, more especially if the body should retain a certain posture for any length of time; for the heart naturally gravitates to the most dependent part, and these portions coming into apposition will form attachments. If these are not too large and firm they may become broken, their torn ends being absorbed or remaining as pendent shreds or patches.

When the adhesions are long and flexible, the motion of the heart is not interfered with; but when they are short, firm, and extensive, the heart labors to perform its duties, without hope of relief. If the adhesions do not contract, the heart retains its shape, and diastole is easy; but in its systole the difficulty is marked, for besides the effort to expel the blood there is restraint of motion, with great loss of energy in drawing to itself the unyielding pericardium. If the pericardium be adherent to the pleura and other surrounding parts, the obstacle is increased and the sternum and costal cartilages are drawn inward and the diaphragm upward. It is to this effort of the heart in systole that the hypertrophy which is often found with pericardial adhesions has been attributed; and in the main I believe this view to be correct. But a number of distinguished observers have denied that the pericardial adhesion is the cause, and think that the cardiac hypertrophy is more probably accidental or dependent upon valvular disease the result of endocarditis, or upon a condition of myocarditis which, however slight, may coexist and lead to inflammatory deposit in the walls, and consequent hypertrophy. It is not difficult to understand how with altered walls dilatation, another consequence of pericardial adhesion, may be caused. Adhesions to the more resisting chest-wall and diaphragm prevent the approximation of {786} the cardiac walls and also the complete closure of the valves. The weakened cardiac walls begin to yield: this will be assisted by the traction of the adhesions on the walls and by the persistent engorgement of the cavities of the heart resulting from inability to empty themselves as completely as when in the normal condition. Another element will be that of shrinkage of the heart-walls, which comes on when the adhesions become so firm and produce so much pressure by contraction that the nutrition of the organ is materially interfered with. But the problem is by no means an easy one to solve, and it seems to me that there is more than one factor influencing it, and that in cases with predominant dilatation the altered heart-walls play, most likely, the prominent part.

Now, even as to the fact of hypertrophy occurring there is far from unanimity. To cite, by way of illustration, the opinion of a few observers. This condition has been asserted by Chevers[22] and by Barlow[23] to be the usual and normal result of complete adhesion of the pericardium to the heart and consequent obliteration of the sac. Hope[24] very emphatically states: "I have never examined, after death, a case of complete adhesion of the pericardium without finding enlargement of the heart, generally hypertrophy with dilatation." Stokes,[25] on the other hand, writes: "Without denying that generally adhesion may induce hypertrophy and dilatation, experience leads me to doubt that such an effect necessarily or even commonly follows the condition indicated. I have often found the heart in a perfectly normal condition with the exception of an obliterated pericardium." He adds: "It has been stated to me by Smith that he has found general adhesion of the pericardium coinciding with atrophy or with hypertrophy of the heart in nearly equal frequency. In some of the cases of atrophy the change was simple, consisting essentially in a diminished volume, with perhaps a paler color of the heart, while in others a true fatty degeneration had commenced." Bauer[26] records that "as a rule the heart is found in a more or less marked condition of degeneration and atrophy. The bundles of muscular fibres show evidences of fatty degeneration, or even of hyalin and pigment degeneration, or the appearances are those of an interstitial myocarditis, with its results." To my mind, I repeat, the state of the muscular walls seems of great importance, and it may explain the varying condition of hypertrophy and dilatation found in association with the pericardial adhesions in such a differing manner.

[Footnote 22: _Guy's Hospital Reports_, vol. vii. p. 421.]

[Footnote 23: "Gulstonian Lectures," _London Med. Gazette_, 1844, pp. 755, 756.]

[Footnote 24: _Diseases of the Heart_.]

[Footnote 25: _Diseases of the Heart and Aorta_.]

[Footnote 26: _Ziemssen's Cyclopædia_, vol. vi. p. 634.]

It is strongly held by some that hypertrophy is occasioned more by the valvular disease that may coexist than it is by adherent pericardium. Sibson[27] tells us that "when pericardial adhesions are associated with valvular disease the heart is always enlarged. It was so in twenty-five out of twenty-six cases, and in the remaining instance, a case of mitral constriction, the heart was rather large." Undoubtedly, this combination is not unusual, but there may be the most marked hypertrophy with adherent pericardium without valve affections. I have met with several such instances, and Blache[28] has recorded three of striking character.

[Footnote 27: _A System of Medicine_, by Reynolds, London, 1877, vol. iv. p. 440.]

[Footnote 28: _Maladies du Coeur chez les Enfants_, Thèse de Paris, 1869.]

Adherent pericardium may occur at any age. It has been found by Behier as the result of chronic pericarditis in an infant of eleven months.[29]

[Footnote 29: Constantin Paul, _Maladies du Coeur_, Paris, 1883.]

The SYMPTOMS of adherent pericardium are uncertain; the physical signs are the only means we have of determining its existence, and even these signs are far from invariable or well defined. In marked cases, on inspection of the præcordial region, it will be noticed that there is more or less complete {787} absence of the heart's impulse against the chest-wall. This is due to the fixed or restrained condition of the heart, particularly of its apex, and to the interposition of a layer of plastic lymph, and possibly of some fluid. There is sometimes a prominence of the costal cartilages over the heart, and the organ itself may be abrupt and jogging in its motion. The intercostal spaces to the left of the sternum are indented, and there is a drawing in of the lower portion of the sternum and attached cartilages with each systole of the heart, giving rise to a wavy movement in the epigastrium.

The application of the hand over the heart detects the impulse, but this is diminished in force and extends over a larger area than in health. The pulse is usually accelerated and irregular in its rhythm. When palpitation of the heart occurs--and this is far from a constant sign--it is dependent upon pressure at the origin of the great vessels. In some cases there is pulsation in the liver, also pulsation in the epigastrium, and venous pulsation in the vessels of the neck. The regularity of form of the chest in its rise and fall during the acts of respiration will be interfered with if the adhesions be extensive.

The position of the heart is but little changed from the normal, though of necessity the organ is more or less fixed in its position by the adhesions. No matter what posture the patient may assume, the apex-beat of the heart remains unchanged where bound by the adhesions; this is especially the case if the adhesions have extended to the pleura. The apex-beat may be entirely masked; but if it be in its normal site, a depression of the intercostal space during the systole of the heart occurs, caused by traction upon the intercostal muscle at that point. If the pleura be implicated, greater expansion of the upper and outside portion of the left side of the chest in inspiration takes place. In a certain proportion of cases the position of the heart is more oblique than normal.

On auscultation the sounds of the heart are found to be more distant and muffled, though generally less so than in effusions of fluid into the pericardium. They may be very faint; at least the first sound may be, on account of the degeneration of the walls of the heart, and murmurs may exist from attending valvular lesions. The sounds of the heart may be reduplicated. Skoda and Friedreich laid great stress on this. But reduplicated heart sounds are not pathognomonic of any affection.

It has been stated that partial adhesions may exist in such form as not to prevent the free surfaces of the pericardium from rubbing against each other, and friction sounds will result, but as the adhesions become general these sounds will disappear.

The cardiac percussion dulness is but slightly increased unless there be also hypertrophy or dilatation. The area of cardiac dulness is lessened during inspiration, because the anterior margins of the lungs extend nearly to the middle line over the front of the heart. This is so even in pericarditis with adhesions, unless the adherent pericardium be attached to the front of the chest and the pleura be also adherent; then the area of absolute dulness remains unchanged during the respiratory acts.

The cardiac impulse will be found at times to be increased by the traction of the adhesions in the pericardium and adjacent parts; at others the impulse is diminished. A disproportion between the marked beating of the body of the heart against the chest-walls and the feeble impulse of the apex has a diagnostic significance--one much greater than a double impulse. The point of cardiac impulse mostly remains unchanged. A depression at and near that point, noticeable during the systolic action of the heart, is among the more certain of the signs of adherent pericardium. When the adhesions extend to the pleura, this systolic dimpling is greater, and becomes often very marked; and it is questionable whether it occurs to any extent without pleural adhesions also existing. Often the apex-beat of the heart does not change {788} with the change of position of the patient. The chest remains normal in shape unless altered by extensive and strong adhesions to the adjacent parts. Under such circumstances there is depression of the fifth and sixth intercostal spaces, the epigastrium is sunken, and the sternum and cartilages are flattened or drawn in; this becomes most apparent during the systole of the heart. The inspiratory bulging is greatest on the right side in consequence of the fixation of the diaphragm.

Hypertrophy or dilatation and valvular disease, if associated with adherent pericardium, modify of necessity both the signs on percussion and auscultation. The aortic and mitral valves are the ones particularly affected. It is when these complications exist, rather than merely from the pericardial adhesion, that we find more or less dyspnoea or orthopnoea and a sense of faintness and dizziness, an anxious expression of countenance, imperfect aëration of the blood, lividity of the lips, dropsy, and difficulty of swallowing.

There is much uncertainty in the DIAGNOSIS of partially adherent pericardium; for the friction sound may be present, the impulse normal, the heart's action unrestrained, there may be no impeded respiration, and the patient may present none of the physical signs of adhesions. Indeed, under any circumstances the diagnosis of adherent pericardium is not a very trustworthy one. More than one of the physical signs mentioned must exist to warrant anything like a positive opinion, and the disease may be latent.

William H. Webb[30] has recorded a case of complete obliteration of the pericardial sac by inflammatory adhesions, associated with enormous hypertrophy of the heart and valvular disease, in which there were no symptoms nor physical signs to lead to a suspicion of the true state of things.[31]

[Footnote 30: I take this opportunity of acknowledging the valuable aid I have received from Dr. Webb in preparing this essay on affections of the pericardium.]

[Footnote 31: _Philadelphia Medical Times_, vol. ii.]

The PROGNOSIS of adherent pericardium depends rather upon the secondary consequences, upon the condition of the muscular walls, the hypertrophy, the dilatation, the coexistence of valvular disease, than upon the adherent pericardium itself. Yet there is a tendency to sudden death caused by it. In 115 instances of sudden death, Aran has recorded 9 of complete pericardial adhesion.

The TREATMENT must be that of the consequences with careful attention to the state of the muscular walls. Digitalis is indicated in cases with dilatation and flabby walls. Early in the case repeated small blisters and a course of iodide of potassium may be tried. But it is doubtful whether any useful result will be accomplished.

Hæmopericardium.

Hæmopericardium, or blood or blood and serum in the pericardial cavity, is rarely met with except as a result of rupture of the heart, injury to the pericardium by perforation or crushing, aneurisms, and in pericarditis occurring in diseases of a low type with degeneration of the blood, as in scurvy and purpura hæmorrhagica.

In rupture of the heart the effusion of blood into the sac is rarely rapid, and death is not immediate unless the rupture be large. Rapid distension of the pericardium with blood speedily causes death by embarrassing the action of the heart and by producing anæmia of the brain. Thus the rupture of an aneurism into the pericardial sac is of necessity quickly fatal. Penetrating wounds may be the cause of a bloody accumulation in the pericardium and give rise to serious symptoms. But the injury is not always fatal, since large vessels are not likely to be cut; the {789} hemorrhage is slow, thus permitting the pericardium to accommodate itself to the fluid; and if the amount of blood be not very large, it may be ultimately absorbed. Crushing injuries to the chest may produce effusion of blood into the pericardium by lacerating small vessels, and may burst the coronary arteries if they be diseased. The foregoing are traumatic causes; the true hæmopericardium is due to the effusion of blood or blood and serum in diseases of malnutrition and in dyscrasias which have special tendencies toward the serous membrane, particularly to the pericardium. This does not take note of the bloody effusions or of a certain amount of blood in the serum which may occur in the course of acute pericarditis; but rather of those diseases, such as scurvy, purpura, and chronic alcoholism, in which the blood is broken down, the tissues weakened, the degenerated vessels rupture or are no longer able to contain their contents, and in which the blood or bloody serum accumulates speedily in the pericardium, without or with but slight previous inflammation.

The physical signs of hæmopericardium are the same as in other effusions into the sac, with this difference--that in the traumatic kind the area of cardiac dulness is rapidly increased, while at the same time the fluid never reaches the bulk of other effusions, for before this can happen death occurs. Friction phenomena are not perceived. There are as symptoms dizziness and faintness, drowsiness, difficulty of breathing, sense of præcordial oppression, weak pulse, and, when myocarditis exists, pain in the heart. The prognosis generally is unfavorable. Death, if not the direct result of the causes producing hæmopericardium, is due to the hemorrhage or to failure of the heart.

The TREATMENT consists in absolute rest, in giving readily-digested food, and in supporting the action of the heart; for this purpose stimulants may be required, unless something in the history of the case forbid. Of course it will also be important to keep the emunctories, especially the kidneys, freely at work, and to modify the condition of the blood in the cases associated with dyscrasias. The mineral acids and ergot are remedies to be borne in mind.

Hydropericardium.

Hydropericardium is the presence of serous fluid in the pericardium of greater quantity than the normal, not dependent upon inflammation--a pericardial dropsy. To constitute this it must be more than an ounce or two; it must be sufficient to be recognizable during life.

The fluid in hydropericardium very rarely reaches the extreme quantity effused in pericarditis. It is alkaline in its reaction and of a pale straw color, or it may be of a deeper yellow and opaque, the color and opacity depending upon the presence of hæmatin, biliary coloring matter, and epithelium. It is chiefly water. According to the analysis of Gorup-Besanez, there are of water, 95.51; albumen, 2.46; fibrin, 0.08; organic matter, 1.27; inorganic salts, 0.95.

Hydropericardium is apt to occur in conjunction with dropsies in other parts, particularly with hydrothorax. It may be the result of local stasis in the veins and lymphatics of the heart and pericardium or of neighboring parts; or it is more usually the sequela, forming part of a diffused dropsy, of certain general diseases, as of the exanthemata, particularly scarlet fever; or is the accompaniment of Bright's disease of the kidneys; or of obstructive diseases of the liver; or of affections of the thoracic viscera which impede the circulation of blood through the heart and lungs. The walls of the heart become soft and flabby, and are consequently weakened; the circulation in the coronary arteries and veins is sluggish.

It is almost invariably a chronic affection, coming on insidiously, and its {790} existence may not be suspected until the disorder is well advanced, when some symptom, suddenly developed, directs attention to the heart.

After death the serous pericardium is found to be opaque, somewhat thickened, and to have an anæmic appearance. The opacity is due either to interstitial deposit or to the swelling of the epithelium.

The DIAGNOSIS of hydropericardium is surrounded by similar difficulties to that of pericardial effusion. It presents the same physical signs as this disease, except the friction at the base, and can only be distinguished by the history of the case and the attending general features.

The PROGNOSIS depends upon the extent of the dropsy and the cause producing it; in point of fact, more upon the latter. The prognosis is apt to be unfavorable when the disease is occasioned by any of the exanthemata or by Bright's disease.

The TREATMENT is that of the disease occasioning it and of the dropsy of which it forms part.

Pyopericardium.

Pus may accumulate in the pericardium as a result of pericarditis, and this has been already described. Further, metastatic or pyæmic abscesses occur occasionally in the tissue of the heart, and may be sufficiently superficial to burst into the pericardium, provided the patient survive the constitutional disturbance long enough. Morgagni observed numerous small abscesses form in the pericardium in consequence of inflammation. Abscesses in the lung and pleura may rupture and discharge their contents into the pericardial sac, and the communication may heal. Thus, Balfour[32] records a case of a boy aged thirteen who had evidences of effusion into the pericardium. Paracentesis of the pericardium was performed, and thirty ounces of pus were drawn off. While there was no evidence of communication with an abscess external to the pericardium, yet an abscess was found at the base of the right lung which was partially adherent to the sac. A communication which was closed up by the subsequent pericarditis was believed to have existed. The quantity of pus does not often reach the amount just mentioned. The fact is, a small quantity may be attended by fatal consequence. There may be pus in the pericardium when death is occasioned by diseases involving the general system, as in scurvy, erysipelas, pyæmia.

[Footnote 32: _Diseases of the Heart_.]

The SYMPTOMS of pyopericardium are those of acute or chronic pericarditis, with marked depression. The physical signs are the same. Indeed, there is no certainty in the diagnosis. Where there is, the operation of paracentesis is strongly indicated. Free incision of the pericardium has been recently practised by Rosenstein and by Samuel West[33] for purulent pericarditis.

[Footnote 33: _The Lancet_, Dec., 1883.]

Pneumopericardium.

Pneumopericardium, or accumulation of air in the pericardial sac, is a very rare affection. Yet Laennec[34] has stated that in his opinion air as well as fluid accumulates in the pericardium in all diseases just prior to death. Pneumopericardium may be associated with fluid, and may or may not be attended with inflammation of the pericardium. As the pericardium is a closed sac, air does not readily gain entrance. But it may do so through perforations of the walls by stabs or gunshot wounds, or by openings communicating with the oesophagus, lung, or stomach. Air is then drawn into {791} the sac during the contractions of the heart. Cases are on record of perforation of the sac with a knife,[35] and through the oesophagus by means of a sword swallowed by a juggler.[36] Sometimes the perforations communicate with organs that contain gas, as the stomach or intestine or the oesophagus. Graves has recorded a case in connection with abscess of the liver. When the pericardial sac is intact, the distending gas may arise from decomposing fluid in the pericardium: it is supposed that it may even be secreted by the blood of the coronary vessels. Pure air, such as we breathe, is never developed in the sac.

[Footnote 34: _Traité de l'Auscultation mediate_, chap. xxiii.]

[Footnote 35: Flint, _Diseases of the Heart_.]

[Footnote 36: Walshe, _Diseases of the Heart_.]

The accumulation of air in the pericardium which is sometimes noticed after death has been declared by many to be the result of the death-struggle. But it most likely occurs shortly before life ceases. In such cases the source of the air or gas must be the blood, for it is well known that blood contains several gases which may leave the corpuscles and fluid in which they are held mechanically.

The DIAGNOSIS of the condition under consideration is difficult, since we must chiefly depend upon the signs elicited by percussion. The general indications are a feeling of oppression in the præcordia, a sense of suffocation, fluttering of the heart; these, however, would only point to some functional disturbance. Percussion shows a preternatural resonance over the heart, the area of cardiac dulness being restricted and indistinct in proportion to the amount of air or gas contained in the sac. Emphysema of the margins of the lungs which overlap the front of the heart may give the same resonant sound, but it is not likely that emphysema of the lungs would be confined to their margins only.

Uncomplicated pneumopericardium is not frequently met with, for the affection is usually associated with fluid accumulations, and with the percussion resonance there will be other phenomena presently to be noted. On auscultation the heart sounds have a ringing character.

Pneumo-hydropericardium.

This, too, is a disorder of great rarity, and may be considered one of the curiosities of clinical experience. It is indeed an unsolved problem whether pneumo-hydropericardium ever exists except as a result of the ingress of air from without the body or from an adjacent organ through an opening made into the pericardium. Nearly all the cases that have been reported have upon careful investigation exhibited the evidence of perforation either by mechanical means or by ulcerative action.

The SYMPTOMS of the accumulation of gas or air in the pericardium associated with fluid are largely, if not entirely, the same as in pericarditis with effusion. There is the same sense of oppression in the chest, irregular rapid action of the heart, pain in the præcordial region, difficulty of breathing, and there may be febrile excitement.

These symptoms are thus not of much diagnostic value unless accompanied by the physical signs indicative of the disease. They are præcordial bulging, diminished cardiac impulse, and the sounds elicited by percussion and auscultation which show the presence of air and fluid. On percussion we have clear or tympanitic resonance in the cardiac region, somewhat modified, especially at the lower parts, by the dulness from the fluid, and very changeable with the altering postures of the patient. On auscultation the signs are variable. Laennec placed great reliance on fluctuation audible with the action of the heart and on deep inspiration, the heart sounds being heard at a distance. We may also find what has been called a splashing or a {792} churning splash, or the sounds of the heart may be extremely ringing, and even metallic; there may be a combination of sounds, as in the case recorded by Stokes,[37] where "they were not the rasping sounds of indurated lymph or the leather creak of Collin, nor those proceeding from pericarditis with valvular murmurs, but a mixture of various attrition murmurs with a large crepitating and gurgling sound, while to all these phenomena was added a distinct metallic character." In the case recorded by John F. Meigs[38] loud splashing or churning sounds were audible three or four feet distant from the heart; while Reynier[39] directs particular attention to an intermittent sound, at first metallic, and resembling a water-wheel.

[Footnote 37: _Diseases of the Heart and Aorta_.]

[Footnote 38: _Amer. Journ. Med. Sci._, Jan., 1875.]

[Footnote 39: _Arch. génér. de Méd._, Mai, 1880.]

In point of DIAGNOSIS we must be very careful not to confound the resonance transmitted from a distended stomach to the cardiac region with pneumo-hydropericardium. The rapid action of the heart and shortness of breath due to the gastric distension may further mislead, and the heart sounds may become sharply defined--the second more ringing. I have several times been called upon for an opinion in cases of the kind which were supposed to be pneumo-hydropericardium. Cavities situated near the heart may also present transmitted cardiac sounds of metallic timbre.[40]

[Footnote 40: Bauer, _Diseases of the Pericardium_.]

The PROGNOSIS is always very grave, yet cases of recovery have been reported in instances of traumatic origin.

The TREATMENT is that of pericarditis, with great attention to sustaining the action of the heart. This is chiefly effected by stimulants. Opium for its quieting effect is also indicated. In cases of marked cardiac pressure paracentesis has been recommended.

Cancer of the Pericardium.

Cancer of the pericardium is one of the rarest of all cancerous affections, never occurring as a primary disease, but consequent on cancer in some other part of the body, generally on cancer adjacent to the heart. It may be the result of direct extension of cancer or of secondary formations. In cancer of the pericardium the parietal layer of the sac is the one always attacked. The extension of the disease from the bronchi and mediastinal glands, from the lungs, pleura, oesophagus, and stomach, is the common cause. Cancer will under certain conditions produce lymphous exudation and adhesions and serous, hemorrhagic, and even purulent effusions. When lymph is thrown out friction sound exists and adhesions may follow. Serous effusion with little or no inflammation is generally present in cancer of the pericardium, and results from the obstruction in the vessels caused by pressure or by direct extension of the disease to the vessels. If the effusion be hemorrhagic, it can be attributed to the same cause. Pus is generally the result of erosion of vessels and membrane.

The DIAGNOSIS of cancer of the pericardium is practically impossible, for the physical signs are essentially the same as in pericarditis from other causes, the darting, lancinating pain excepted; yet even the pain may not be sufficiently typical to lead us to a correct conclusion. Therefore, as a rule, the existence of the disease can only be suspected, or regarded as very probable in consequence of the general features of the malady.

The rarity of this affection is seen in the summary given in _Ziemssen's Cyclopædia_. Köhler noted 6 cases of cancer of the pericardium in 9118 autopsies; Günsburg found 1 case of cancer in 1700 autopsies; and Willigk, 7 cases in 477 autopsies of persons dying of cancer.

Death, which is the result in all cases, is generally by exhaustion. Other {793} diseases of a nature allied to cancer also attack or involve the pericardium, such as lymphadenoma or lymphosarcoma in the mediastinum; the pathology is practically the same as that of cancer, and the general symptoms and the termination are alike.

Hydatids[41] give rise to growths which occasion a surmise of cancer; so do those white calcified bodies formed in concentric layers known as cardiliths. Neither has any diagnostic signs by which it can be distinguished.

[Footnote 41: See Rokitansky's _Pathological Anatomy_, and Klob, "Zeitschrift der K. K.," _Gesellschaft der Aertze zu Wien_, 1860.]

Tubercular Pericarditis.

Tubercular pericarditis is an exceedingly uncommon affection. Laennec only met with 2 instances of it, Louis with but 1 case. It is never primary, being always associated with tubercle in some other part of the body. Among the earlier records we find the case of Baillie,[42] who mentions "a case of two or three scrofulous tumors growing within the cavity of the pericardium." The case had tubercles in the lungs, and died with all the symptoms of phthisis, nothing indicating the presence of tumors in the pericardium prior to death.

[Footnote 42: _Morbid Anatomy_, 5th ed., London, 1818, pp. 11, 17.]

Tubercle in the pericardium may remain latent or excite inflammation which gives rise to the same physical signs and local phenomena as when the pericarditis is of idiopathic origin. The tubercle is mostly found beneath the serous layer of the pericardium, either cardiac or parietal, and sometimes in the adhesions, and bears a close resemblance to tubercular disease of the meninges, the peritoneum, and pleura. It must be understood, however, that pericarditis may happen in a tubercular person without being due to a deposit of tubercle in the pericardium; and a deposit may occur in the adhesions in a case of pericarditis in a tubercular person brought on by other causes than a tubercular development in the pericardium, as the instances reported by Burrows show.[43] Tubercular disease of the pericardium may be due, as Weigert has proved, to infection by contiguity from the lymphatic glands of the thorax. The pericardium may be free from tubercle, yet the purulent fluid in it be filled with tubercle bacilli.[44] Vaillard[45] declares the pericarditis to be dry in the majority of cases. The disease generally happens under forty years of age, but in Mickle's[46] case the patient died at the age of fifty-four.

[Footnote 43: _Med.-Chir. Trans._, vol. xxx. p. 77.]

[Footnote 44: Kast, _Virchow's Archiv_, June, 1884; see also _Medical News_, Aug., 1884.]

[Footnote 45: _Journ. de Méd. de Bordeaux_, 1880, l. x.]

[Footnote 46: _London Lancet_, May 26, 1883.]

The differential DIAGNOSIS of tubercular pericarditis cannot be made, as there is no positive physical sign distinguishing this form from any other. If pericarditis either in its acute or advanced stage occur in a tubercular person, and if there be neither rheumatism, Bright's disease, nor pleuro-pneumonia, and if the person have not been subjected to any injury in the præcordial region, the pericardial affection may be presumed to be due to tubercle, but only an autopsy would afford certain proof.

The PROGNOSIS is always unfavorable.

The TREATMENT is that of chronic pericarditis, sustaining the failing nutrition as well as we can by cod-liver oil and other nutrients.

{794}

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.

BY JOHN B. ROBERTS, A.M., M.D.

The operative treatment of pericardial exudations and transudations has received a new impetus within the last fifteen or twenty years from the investigations of Trousseau,[1] Roberts,[2] Hindenlang,[3] Fiedler,[4] West,[5] and others. Reference to the works of these writers will furnish the reader with the history and statistics of such operations, and with those details that I have not deemed necessary to incorporate in the present article.

[Footnote 1: _Clinical Medicine_.]

[Footnote 2: _New York Med. Journ._, Dec., 1876, with analysis of 41 cases; also _Paracentesis of the Pericardium_, Philada., 1880; _Trans. Am. Med. Ass'n_, 1880; and elsewhere.]

[Footnote 3: _Deutsches Archiv für klinische Medicin_, 1879.]

[Footnote 4: _Samml. klin. Vortr._, No. 215, Leipzig, 1882.]

[Footnote 5: _Medico-Chirurgical Transactions_, 1883.]

In all cases of bloody, serous, purulent, or aërial effusions into the pericardium, that present dangerous symptoms of heart failure, operative interference should be undertaken as soon as it is evident that medication is not lessening the embarrassment of the central organ of circulation. It is bad practice to delay the operation, which will generally be aspiration, until exhaustion, pulmonary engorgement, pericardial changes, and degeneration of the cardiac muscle render permanent relief impossible. The tendency is to wait, instead of affording immediate relief of the distressing symptoms by prompt resort to pericardicentesis. Clinical experience has abundantly shown that when the pericardial fluid is evacuated, dyspnoea, cyanosis, irregularity of the pulse, and the other threatening symptoms are lessened; and usually at once.

The time for aspiration depends less on the amount of fluid than would at first be supposed, because the sudden effusion of a moderate amount of serum will exert more pressure upon the heart than a much larger quantity poured out in so gradual a manner as to allow the pericardium to become stretched. Aspiration should therefore be performed in all cases of pericardial effusion, in which dangerous symptoms of heart embarrassment occur, as soon as medication fails, and without regard to the supposed quantity of fluid. This should be the practice without regard to any other visceral lesion that may be present as a complication, except in the case of pleural effusion.

When pleural effusion of considerable amount coexists, the pleural sac should be aspirated first, because of the difficulty of discriminating between respiratory distress due to pulmonary pressure and that resulting secondarily from interference with cardiac action, and because the evacuation of the pleural effusion seems at times to lead to absorption of the fluid in the {795} pericardium without resort to operation. This rule applies to pleurisy of the right side as well as of the left.

In dropsy of the pericardium from renal disease I admit that the transudation is at times absorbed with great rapidity, and that aspiration does not directly affect the primary disease; but still, tapping should be done if the failure of circulation and respiration seems to be dependent on the effusion. Pepper's case[6] of recovery after pericardicentesis affords corroborative evidence of the propriety of this advice. Before operation the urine was albuminous and contained tube-casts, but these symptoms entirely disappeared in the course of a few weeks.

[Footnote 6: _Medical News and Library_, Philada., March, 1878; and _Am. Journ. Med. Sciences_, April, 1879.]

When the amelioration of symptoms following the operation is not permanent because reaccumulation takes place, repetition of the operative procedure is demanded. It is better, in my opinion, to vary somewhat the point of puncture, lest the heart be wounded at the second tapping because of adhesion of the parietal to the visceral pericardium at the original point of puncture. Should repeated tapping be required in serous effusions, I should at the time of the third operation inject into the sac, after removing the serum, a solution containing tincture of iodine, alcohol, or carbolic acid, with the purpose of modifying the secreting surface and producing pericardial adhesion. Universal pericardial adhesion has been found by examination subsequent to cure by aspiration; and in a number of cases intra-pericardial injections have been made without preventing, or apparently interfering with, recovery.

The fluid injected ought probably to be concentrated, as the object to be obtained is pericarditis of a grade that will furnish plastic exudation instead of serum. Undiluted but liquefied carbolic acid, such as is used in treating hydrocele of the vaginal tunic of the testicle, would be the proper agent were it not for the possibility that its contact with the heart-walls might induce dangerous cardiac spasm. The strength of the fluid to be injected, as well as its utility, will have to be determined by future observation. Aran used fifteen grammes of tincture of iodine (French), one gramme of iodide of potassium, and fifty grammes of distilled water, and his patient recovered. Malle injected a solution of tincture of iodine "five times weaker than that recommended for hydrocele operations," but suspended the operation quickly because of the excessive pain in the cardiac region produced by the injection. Violent inflammatory symptoms arose. The patient died of diarrhoea before the exact result of the injection could be determined, though the indications were that cure by pericardial adhesion was about to take place. The autopsy seemed to confirm this belief.[7] It must be remembered also that his operation was done by trephining the sternum, which may have had something to do with the inflammatory reaction, though the injection was not made until the sixteenth day after the original operation.

[Footnote 7: _De la Paracentèse du Péricarde_, par Michel Labrousse, Thèse No. 107, 1871, pp. 22, 27.]

When aspiration has shown the pericarditis to be purulent, a free incision should be made, an antiseptic drainage-tube of good size introduced, and the cavity washed out daily with antiseptic solutions of carbolic acid (1 to 40) or corrosive sublimate (1 to 2000). In fact, pericardial effusions should be managed exactly as pleural effusions by tapping, injection, or drainage, according to the character of the contents of the sac. I have advocated this course since 1876, and it has been justified by the cases of Villeneuve, Jürgensen, Viry, Rosenstein, West, Partzevsky,[8] and Savory. Although these operators did not all practise free incision, yet the study of their cases shows the absence from danger and the propriety of such incision. As far as I {796} know, no cases of purulent pericarditis have recovered after simple aspiration. The case of Rosenstein and that of West, however, did recover after incision and drainage; and in that of Villeneuve, which was originally serous, there remained a fistulous track discharging pus for nearly six months, when spontaneous closure and cure resulted. Gussenbauer has successfully treated pyopericardium following acute osteo-myelitis at the shoulder by resection of five ribs and washing out the sac with a thymol solution.[9]

[Footnote 8: See _Lond. Med. Rec._, Feb. 15, 1883.]

[Footnote 9: _Wien. med. Wochenschr._, Nov. 21, 1884, quoted in _Medical News_, Philada., Jan. 17, 1885.]

Pericardial fistules, due to spontaneous or operative evacuation, should be managed by dilatation, with compressed sponge, and irrigation of the cavity with astringent or disinfectant solutions. Some supposed pericardial fistules may be pleural fistules, or sinuses opening into small pockets between the parietal and visceral layers of an adherent pericardium, or entirely external to the pericardium in new tissue occupying the mediastinum. Such sinuses should be laid open with the scalpel, and compelled to granulate from the bottom. Sinuses dependent upon diseased rib, sternum, or cartilage should be laid open, and the necrotic or carious structure removed by burr or chisel.

Incision of the pericardium under antiseptic precautions may be useful, and is justifiable as a diagnostic procedure in grave cases when doubt exists between a large pericardial effusion and a dilated heart. The wound will scarcely increase the danger if the pathological condition be cardiac dilatation, and may save life if effusion be the cause of the threatening symptoms. The case of Vigla upon which Roux operated shows the value of such procedures.[10]

[Footnote 10: Trousseau's _Clinical Medicine_.]

Aspiration is the method to be employed at first in all instances of pericardicentesis. Incision is to be reserved for the second step in purulent pericarditis, for diagnostic purposes, and for the extraction of foreign bodies, and similar operative designs. The best point for aspiration is usually in the fifth interspace, just above the sixth rib, and about five or six centimeters (2-2¼ inches) to the left of the median line of the sternum. In a child it should be a little nearer the sternum. The point advised is outside of the line of the internal mammary artery, is in a wide portion of the intercostal space, corresponds with the notch in the border of the left lung, is low enough to preclude wounding the auricle, high enough to avoid the diaphragm, and does not approach the point where a cartilaginous band often joins the fifth and sixth costal cartilages. Both layers of the pleura will probably be pierced by the aspirating-needle at this point, but this is not an important complication, and can only be avoided with anything like certainty by going close to the sternum, which is objectionable on other grounds.

The aspiration may be performed by using the pump and the ordinary needle or trocar which is furnished by instrument-makers in the aspirator-case. In cases of emergency or for mere exploratory puncture the common hypodermic syringe and needle will answer the purpose. The puncturing instrument should be clean and anointed with carbolized oil, and in all cases the vacuum-chamber should be attached to the needle or trocar as soon as its point is buried beneath the skin, in order that a flow of fluid may indicate the moment at which the pericardial sac is entered. Abrasion of the heart, which may occur from contact with the needle-point when the fluid is almost entirely evacuated, is not very important, but should be avoided if possible by deflecting or partially withdrawing the needle, or by using Roberts's improved pericardial trocar or that suggested by Pepper. The instrument figured in my monograph on _Paracentesis of the Pericardium_ was too large {797} for use. The improved instrument here figured is no larger than a moderate-size aspirating-needle. It consists of such a needle, flattened at its upper extremity to give the surgeon a firm hold, within which slides a canula. The distal end of the canula, made flexible by a spiral, when thrust beyond the point of the needle curves downward, and thus prevents the point of the puncturing instrument injuring the heart when the sac is nearly emptied. During penetration of the thoracic wall the canula is retracted, so that the flexible end is contained within the needle, and the perforation at the end of the canula allows the fluid to escape as soon as the sac itself is punctured. The canula is then thrust forward until the sharp point of the needle is guarded. This movement brings a lateral fenestra in the canula opposite a similar opening in the needle, and thus provides a second orifice for the escape of fluid in case the terminal one becomes occluded. The external end of the canula has a square shoulder to prevent rotation within the needle, and should be tight enough at that point to preclude entrance of air. The canula finally terminates in a ground end for attachment to the aspirator-tube. The needle--or outer canula as it may be called--is marked on the surface to show the number of centimeters concealed in the tissues. If the inner canula is suspected to be clogged with shreds of lymph or with thick pus, it can be withdrawn without disturbing the needle. The attachment may then be made to the latter as if it were an ordinary aspirating-needle, or the inner tube being cleaned may be reinserted. This is an important element, gained by using a double aspirating-trocar; for plugging is not uncommon in pericardicentesis done for chronic inflammation of the sac.

Beverley Robinson of New York has still further modified[11] my trocar. His additions may have improved the instrument if they do not unduly complicate it. Pepper, after operating upon his case, had made a delicate double canula, the inner tube of which was furnished with a fine needle-point. After introduction the inner tube was withdrawn until its point was sheathed.[12]

[Footnote 11: _New York Med. Record_, March 29, 1884.]

[Footnote 12: _Medical News and Library_, Philada., March, 1878.]

It is said that at the meeting of the Italian Medical Association at Pisa in 1878, Baccelli proposed a new method of puncture; but the account given by Severi[13] in speaking of Baccelli's cases indicates that his proposal referred not to a method of operating, but to a method of selecting the point of puncture.

[Footnote 13: _Lo Sperimentale_, Aprile, 1881, p. 392.]

It must also be remembered that failure to obtain fluid when pericardial effusion existed has occurred because the needle had been passed through a costal cartilage, and was thus plugged by a disk of cartilage. The manner in which the intercostal spaces are narrowed and changed in direction by the curving upward of the anterior portion of the ribs and by the curvature of the cartilages should be impressed upon the operator.

If failure to obtain fluid occurs, and the diagnosis remains quite certain from the symptoms, withdrawal of the needle and puncture in another position should be done or an incision of an exploratory kind made.

{798} In pericardicentesis care must be taken not to thrust the needle or trocar into the heart. This may happen even in quite careful hands. If the right ventricle is entered, venous blood will escape through the canula; if the needle is buried in the cardiac muscle, no fluid or blood can escape. The violent movements communicated to the needle will usually indicate that the needle is either in contact with the heart or thrust into its tissue. Of course such movements will occur from cardiac contact when most of the fluid has been withdrawn; but are not to be expected immediately after the introduction of the puncturing instrument unless the fluid is very small in amount, the needle deeply inserted, the pericardium adherent at the point of puncture, or the diagnosis of fluid an error.

Puncture of the heart has occurred accidentally during pericardial tapping without doing any harm, and has been suggested as a proper surgical procedure in certain cardiac conditions. Still, it is an accident to be avoided by the use of proper trocars and pumps, by the selection of a proper site of operation, by the adaptation of the suction power as soon as the point of the trocar or needle is buried beneath the skin, and by other precautions that will suggest themselves. In thick, oedematous, or fatty chest-walls no fluid will be reached perhaps until a depth of four or five centimeters (about two inches) has been attained by the point of the puncturing apparatus.

I must call attention to the fact that West[14] records a case of pericardial tapping occurring at St. Bartholomew's Hospital in 1874 where a trocar and a canula were introduced through the fourth left space near the edge of the sternum, and caused death in five minutes from hemorrhage into the pericardium, due to tearing of the right ventricle. The position chosen and the form of instrument may have had to do with this unfortunate result, of which the details are not given.

[Footnote 14: _Med.-Chir. Trans._, 1883, pp. 259, 275.]

A few words on cardicentesis, or intentional heart-puncture, may here be appropriate. It has been suggested as a means for rapid abstraction of blood from the right heart in intense pulmonary and cardiac engorgement, and for the abstraction of air after air-embolism has occurred from wounds of the large venous trunks. It has been known for years that aspiration and similar punctures of the heart are comparatively harmless. Roger accidentally withdrew 200 grammes of blood from the right ventricle of a boy of five years without doing harm. Hulke seemed to benefit a case of pleuro-pneumonia by accidentally aspirating the right heart. Cloquet, Bouchut, Steiner, and Legros and Onimus have made similar observations on the absence of danger from such wounds. Westbrook of Brooklyn, Corwin,[15] Dana,[16] and apparently Janeway of New York, have performed intentional cardiac aspiration in moribund patients without causing any noticeable harm. The contributions of Westbrook,[17] Roberts,[18] and Leuf[19] on this topic, as well as that of Senn[20] on air-embolism and its treatment, will interest those who wish further information.

[Footnote 15: _N.Y. Med. Record_, March 10, 1883, p. 263.]

[Footnote 16: _Ibid._, Feb. 3, 1883, p. 140.]

[Footnote 17: _Ibid._, Dec. 23, 1882.]

[Footnote 18: _Philada. Med. News_, Jan. 13, 1883.]

[Footnote 19: _Amer. Journ. Med. Sci._, Jan., 1885, p. 79.]

[Footnote 20: _Trans. Amer. Surg. Ass._, 1885, and _Annals of Surgery_, St. Louis, 1885.]

* * * * *

The results of operations for pericardial aspiration or incision are exceedingly good when the frequent postponement of the operation till the patient is almost moribund is recollected. Elaborate statistical tables would be out of place in this volume; and, besides, it seems almost impossible to get a complete collection of the cases. Hindenlang, West, and I have published {799} and analyzed long lists of cases collected from various sources, and I have now references to more, but this tabulation seems unnecessary, as the practical points to be derived from their study are well proved by the previous work done. In addition to the bibliographical notes already given, I add for the use of inquirers in this field two recent monographs--one by a German,[21] the other by a French writer.[22]

[Footnote 21: _Ueber Paracentese des Herzbeutels_, Gerhard Beck, Würzb., 1882, p. 33 (Thesis).]

[Footnote 22: _Contribution à l'Étude de la Paracentèse du Péricarde_, H. Ferraud, Bordeaux, 1883.]

{800}

DISEASES OF THE AORTA.

BY G. M. GARLAND, M.D.

Acute Aortitis.

The existence of inflammation of the membranes of the aorta was mentioned by Galen and other early writers, but it was not until 1824 that a systematic treatise on this subject was published. Since that time the subject has received more attention, but the results obtained are unsatisfactory. There is grave doubt, according to many writers, as to the existence of acute aortitis independent of other lesions, although it is recognized that the aorta may participate in inflammation of the neighboring organs. Even then, as Powell says, "the aorta is very slow to share in such processes, and when it does so the inflammation is very chronic and limited, giving rise to no special symptoms." Peter treats the subject at length, and after enumerating certain so-called symptoms of acute aortitis, confesses that these symptoms are merely the ordinary phenomena of angina pectoris, and these two affections cannot be distinguished from each other. It must be concluded for the present, therefore, that acute aortitis is rare, and that we know of no symptoms which are characteristic of it.

Atheroma of the Aorta.

Atheroma of the aorta is the result of chronic endarteritis, and is always of slow development. The process may be limited to the intima or it may extend to the middle and outer tunics. Beginning with a thickening and softening of the wall, it finally develops plates of calcareous deposit. These plates are most numerous in the region of the aortic valves, and diminish in number as the artery proceeds from that point. The descending portion of the aorta is relatively free from these patches, but they reappear again near or at the bifurcation.

ETIOLOGY.--Atheroma is one of the ordinary products of old age, and is therefore one expression of senility. Heredity probably exerts some influence, and certain cachexias predispose to an early occurrence of the process. Gout and syphilis render one especially prone to it. High pressure and strain are also important factors. Continuous hard toil is more productive of atheroma, according to Allbutt, than intermittent work. The pre-albuminuric stage of Bright's disease, which is characterized by high arterial pressure, is frequently productive of atheroma.

SYMPTOMS.--When the inner coat alone is affected, there are no symptoms of this disease. According as the degeneration extends deeper and involves the middle and outer tunics, the aorta begins to dilate, and the symptoms may vary from the slightest feelings of discomfort upon exertion to the most violent attacks of palpitation and pain.

{801} Usually, at the beginning the symptoms are very obscure. A slight dyspnoea on exertion, or palpitation, or dyspeptic troubles are the chief complaint. The presence of these troubles in a man of fifty years or over, whose heart and kidneys present nothing abnormal, and in whom the smaller arteries of the extremities feel hard and calcareous, may excite the suspicion of atheroma of the aorta. There are no distinctive physical signs. Some writers speak of a short post-systolic murmur over the aorta beyond the valves, which may be audible only when the heart is acting strongly.

The aorta is almost invariably dilated, and Peter says that this dilatation may be traced by percussion. According to him, the normal aortic dull area measures from two to five centimeters transversely in the male, and from two to four centimeters in the female. He says that he has seen cases of atheroma where he was able to determine a dull aortic area of eight centimeters in diameter. If the inflammation extend from the aorta to the neighboring nerves, the patient may suffer from the ordinary symptoms of angina pectoris.

TREATMENT.--This disease cannot be cured by drugs. The physician's task is to regulate the habits of the patient, to remove so far as possible all conditions which tend to aggravate and increase the trouble, and to alleviate incidental symptoms of distress.

Thoracic Aneurism.

DEFINITION.--The origin of the term aneurism is buried in obscurity, and the theories which have been advanced regarding it are not very satisfactory. Montanus thought it was derived from _a_ privative, and _neuron_, a nerve. Oetius declares it is from _aneurisma_, an enlargement, from _eurumo_, I dilate. Coale thinks a ready origin is offered in the words _aneu_, without, _rusmos_, a series, course, or succession, from _ruo_, I flow.

Aneurism of the aorta is a local dilatation of that vessel. When all the arterial tunics persist unruptured in the tumor, it is a true aneurism. When one or more of the tunics are torn in the process of expansion, it becomes a false aneurism. When all the tunics of the artery rupture and the blood escapes into the neighboring cellular tissue, it becomes a diffuse false aneurism. The internal and middle coats of an artery may burst, and the blood escape into and coagulate in the space between the middle and external tunics, and this is termed a dissecting aneurism. In rare instances of this type of aneurism the blood finds a second opening, and returns into the artery again, thus forming a double tube for a short distance.

In former times great stress was laid upon the distinction of aneurism according to the number and combination of persistent tunics, and we read of the mixed internal and the mixed external type. These points have less clinical importance, however, than a proper appreciation of the size and shape of a tumor, because all aneurisms are false after they exceed a certain size. When an aneurism involves the entire periphery of the aorta, it may be cylindrical, fusiform, or globular in shape, and receive names accordingly. When it is a mere bulging on one side of the artery it is saccular in shape. Obviously, the opening into the fusiform aneurism is quite or nearly the entire length of the tumor, whereas in the false saccular type the orifice may be reduced to a mere puncture of the arterial wall. The size of the orifice is a matter of great importance, particularly in connection with the question of operative interference, and therefore it will be referred to later. The sacciform and fusiform aneurisms are often combined together, or, in other words, it is quite common to find a lateral bulging superimposed upon a local dilatation of the artery; but such grouping is not necessary, as either form appears {802} without the other. It is not uncommon also to find one bulbous aneurism superimposed upon another, the dependent aneurism in this case being of the false or diffuse type. The second aneurism often lies outside the chest-wall, and it is connected with the mother aneurism by a narrow opening or channel.

Varicose aneurism is a false aneurism formed by communication between the aorta and the vena cava, the pulmonary artery, the right auricle, or the right ventricle. It is almost without exception rapidly fatal and not amenable to treatment.

Occasionally the aorta will present alternate bulgings upon one side and the other, so that the vessel appears to wind in its course. This condition is called cirsoid aneurism, but it has nothing in common with external aneurism of the same name.

The size of an aneurism is variable, like its shape, but in general the true aneurism rarely exceeds the size of an egg (Jaccoud). Beyond this size one or more of the coats give way, and the aneurism becomes false, in which condition it may grow as large as an adult's head if the patient lives long enough to allow such development. Balfour refers to two rare forms of aneurism--the intravalvular, which is situated within the aortic valves and above the ventricle, and the intervalvular, which is still more rare, and is situated between the valves themselves. The symptoms of these aneurisms are merely those of valvular lesion, and therefore present no differential points for diagnosis.

ETIOLOGY.--Local weakness of the aorta submitted to sudden strain is unquestionably the most frequent cause of aneurism. It is rare to find an aneurism in an otherwise healthy aorta, and some authors go so far as to assert that aneurism never occurs without preceding degenerative changes in the arterial wall. Naturally, strain is the physiological burden of the aorta, and this strain tends sooner or later to degeneration of the arterial tunics. Then, given a weakened spot, the ordinary occurrences of every-day life are sufficient to precipitate disaster. A sneeze, a cough, some sudden exertion of the body in lifting or moving, have been the starting-points of aneurism. All accumulated testimony indicates that sudden strain is more dangerous than prolonged uniform strain, and therefore some occupations are more productive of aneurism than others. Inasmuch as age, sex, occupation, and personal habits influence the development and nutrition of the aorta, it is obvious that they must exert an important influence upon the occurrence of aneurism.

All records agree that aneurism is pre-eminently a casualty of middle life, and a glance at the accompanying table, which I have prepared from an analysis of 69 reported cases, shows that the disease is most common between thirty and fifty years of age:

From 20 to 30 years of age, 4 cases. " 30 " 40 " " 21 " " 40 " 50 " " 29 " " 50 " 60 " " 14 " " 60 " 70 " " 1 case. Youngest case, 20 years of age. Oldest " 72 " "

Crisp analyzed 551 cases, and reports 398 between the ages of thirty and fifty.

Beneke has found in his records of arterial measurements that the pulmonary artery greatly exceeds the aorta in circumference up to the age of thirty. After that period the aorta begins to increase with relatively greater rapidity, until in the forties it exceeds the pulmonary artery in size, and it maintains its superiority from that time forward. The aorta continues to increase in circumference throughout life, but after the age of fifty this increase is considered a senile dilatation rather than an actual growth. It is interesting to {803} note that the era of greatest liability to aneurism coincides with that of most rapid aortic development.

Sex furnishes a distinction in the frequency of aneurism. In 82 cases I found that only a seventh were females; Crisp registers less than an eighth. The radically different occupations and habits of women may contribute somewhat to their relative immunity from aneurism, and their physiological development also seems in their favor. Beneke states that the blood-pressure during childhood is about the same for both sexes. From puberty onward it is greater in the male. This is due to the fact that after puberty the volume of the heart relative to the length of the body is less in the female than in the male, and at the same time the main arteries of the body relative to the length of the body are only a trifle narrower in women than in men. The pulmonary artery, indeed, is relatively a trifle wider in women than in men. It follows from this that the blood-tension in both the large vessels emerging from the heart is less in the female than in the male.

In general terms, it may be said that those people who are exposed to heavy labor, as mechanics, laborers, soldiers, porters, cabmen, etc., are more liable to aneurism than those who are less exposed to such straining efforts. Fixture of the chest during effort brings greater strain upon the heart and aorta, and therefore men who wield heavy hammers and sledges are especially liable to aortic disease. Constriction of the neck or forcible extension of the same during exertion is dangerous, because it thus happens that the arteries are stretched in their long diameter at the same instant that the blood-wave is expanding them laterally, and they are thereby subjected to double strain. I knew of a trotting horse which was killed by this very combination of strain upon the aorta. At the end of a trial of speed the animal refused to stop; whereupon a groom sprang forward, seized him by the bit, and threw his head strongly upward and backward. His carotids and aorta were thus stretched to full length at the moment when his heart was acting with great force. The horse dropped dead, and the autopsy revealed a rupture of the aorta.

The frequency of aneurism among the soldiers of the English army was long the subject of anxiety and thought to English surgeons. Finally, some bright man recognized one cause in the dress of the soldiers. They were obliged to wear a high stock, which constricted the neck and kept it stretched, and their trappings were adjusted so as to keep the body in a stiff and unnatural position. These objectionable details of the dress have been removed, and it is now claimed that aneurism is much less common in the army.

Syphilis and gout undoubtedly contribute to the formation of aneurism, because they both dispose to degenerative processes in the arterial tunics. Some writers, however, have laid too much stress upon syphilis. It was claimed that this disease was the cause of the great frequency of aneurism in the English army. Barwell, however, calls attention to the fact that aneurism has been 13½ times more frequent per 1000 men in the army than in the navy, and yet no one maintains that syphilis is more common in the army than in the navy.

SYMPTOMS.--The diagnosis of aneurism of the aorta may be one of the easiest problems of clinical medicine, or it may present difficulties which defeat the most skilful diagnosticians. A large number of aneurisms utter no sign of their existence, and are only revealed by the manner of death or by an autopsy. Again, the so-called signs of aneurism are so indefinite in character, and so associated with other pathological conditions, that the greatest confusion often befogs their interpretation. Mistakes therefore arise in two ways: either aneurism is diagnosed as present when it is absent, or it is declared absent when present. Robin reports the case of a vigorous young man upon whom several of the most eminent clinicians of {804} Paris diagnosed aneurism of the aorta, and yet a rest of a few days sufficed to remove all symptoms of that disease. Three candidates for the diploma of the Royal College of Physicians and Surgeons in England recently declared a case of loculated pleurisy to be aneurism of the aorta, and B. W. Richardson says he has "seen at least seven persons suffering severe mental anxiety from the belief that they were fatally struck with aneurism," and yet they were free of such disease. Balfour says: "There is only one phenomenon positively characteristic of thoracic aneurism, and that is the existence in some part of the thorax of a pulsating tumor other than the heart, which beats isochronously with it, and at least as forcibly, and which at each pulsation expands in every direction." And yet simple dilatation of the aorta, combined with mental excitement, will so increase the thoracic pulsations as to simulate aneurism. It is necessary, therefore, that a patient during an examination should be as quiet as possible, both in mind and body, and if any doubt exist regarding the significance of the symptoms present, the patient should be kept in bed for a few days in order to allay the arterial excitement.

The phenomena produced by an aneurism are naturally divided into two groups: 1. The direct symptoms, which are confined to the limits of the tumor itself, and which are termed the physical signs. 2. The indirect symptoms, which are due to the influence of the tumor upon neighboring organs, and which present themselves often at remote points as signals of distress within. This influence of the tumor upon its environment is purely mechanical and due to pressure, and the resulting symptoms vary according to the particular organ or function involved. These symptoms are therefore classified as the physiological signs.

Pain is one of the earliest and most troublesome of the pressure symptoms of aneurism. It is due to a stretching of the nerve-filaments in the aortic wall and to the pressure of the tumor upon neighboring organs, especially the vertebral column and sternum. When due to nerve-stretching, the pain is neuralgic in character, and is not necessarily confined to the chest. It may appear in the back, and is intensified by coughing or sneezing. It may be rheumatic in type, and affect the arm and shoulders for several months before other aneurismal signs develop. In such cases the right arm and shoulder appear to be most often affected. Sometimes the pain cannot be located, but is referred indefinitely to the chest, or it may accompany acts of deglutition. As a rule--and this point is important--this form of pain from an aneurism exhibits wide variations of intensity and is usually intermittent. Exercise, coughing and sneezing, mental excitement, or anything which increases the activity of the circulation or raises the blood-tension, increases the pain. It may resemble angina pectoris in location and radiation, but it differs essentially otherwise. It is more continuous, and is associated with less anxiety, which is such a conspicuous element of angina.

When the pain is due to erosion of the vertebræ or sternum, it is more steady and gnawing. It is still liable to violent exacerbations, and excitement of all kinds increases it. Oftentimes the pain is so excessive that the sufferer cannot lie down or obtain relief in any position. This is especially the case with aneurism of the abdominal aorta. Bennet reports the case of a patient who poisoned himself to be free from the terrible pain, and deaths by exhaustion from pain and distress are not uncommon.

Numerous other accidents besides pain arise from pressure upon the neighboring veins. Balfour says that severe dyspnoea, vomiting, and flatulency are frequently caused by pressure of an aneurism upon the pneumogastric nerves, and that these symptoms may be relieved by gently rubbing the tumor. Hiccough and paralysis of one-half the diaphragm are caused by pressure upon the phrenic nerve. Occasionally destructive inflammations of {805} the lung and pleura occur with aneurism, and these have been attributed to pressure upon the pneumogastric nerves and the pulmonary plexus. Palpitation of the heart is likewise often produced in a similar manner. Sometimes the patient is conscious of a pulsation in the tumor itself. Pressure upon the intercostal nerves will produce herpes zoster, and cicatricial records of such attacks are found upon patients with aneurism. Implication of the sympathetic nerves produces modifications of the pupils according as the nerves are merely irritated or paralyzed. In the first case the radial muscles of the iris become permanently contracted and the pupil is dilated. In the second case the radial muscle becomes paralyzed and the pupil is contracted. Jaccoud says that this succession of changes is not rare, and he has watched cases progress through both pupillary stages. The nerves affected are those which emerge from the cilio-spinal region, which extends, according to Budge and Waller, from the sixth cervical to the sixth dorsal, or, according to Brown-Séquard, as low as the tenth dorsal vertebra. From the anterior roots of this region nerve-filaments pass through the cervical sympathetic to the iris. The difference in the pupils is often so slight that it requires very careful measurement to detect it. The application of atropia will assist in the examination, because that drug has very incomplete influence upon the affected pupil. The pupil is also much less sensitive to light, but it contracts more strongly than the normal eyes in its accommodation for near objects. Robertson cautions against conclusions based upon mere casual observance of the eyes, because 1 person in every 14 has one pupil naturally smaller than the other.

Myosis is not pathognomonic of aneurism. It denotes merely some trouble with the cilio-spinal nerves. The nature of that trouble must of course be determined by the other associated symptoms of the case. The contraction of the pupil is sometimes accompanied by paleness of the corresponding side of the face and neck, while at other times the same region may be swollen, oedematous, and perspiring. These symptoms are due to local vascular changes from interference with, and disorganization of, the vaso-motor nerves which govern these regions. Remote local paralysis sometimes utters the first warning of aneurism, and such cases are usually very striking. Paralysis of the recurrent laryngeal is the most frequent of this group of signs. Urquhart reports a case where for some months the chief symptom was a falling of the head on the breast, as if it had been forcibly drawn down by the sterno-cleido-mastoids. Another patient was supposed to have rheumatism, but he soon became paralyzed on the right side and lost his speech. He recovered somewhat, but died subsequently from bursting of the tumor into a pulmonary cavity. Tufnell says if an amaurosis occur suddenly look for valvular disease of the heart or for aneurism of the aorta.

Dyspnoea.--The dyspnoea produced by an aneurism may vary from a slight difficulty of breathing on exertion to the most marked orthopnoea. It is produced by--_a_, direct pressure upon the trachea or bronchi; _b_, pressure upon the recurrent laryngeal or the vagus. The two forms of trouble are easily discriminated by physical examination. In cases of pressure upon the respiratory tubes auscultation reveals very characteristic signs. The constriction of the tube causes a peculiar harsh sound, which, heard only in inspiration at first, becomes audible later in expiration as well. If the pressure is upon the trachea, the sounds will be heard equally in both lungs; whereas if only one bronchus is involved, the sounds will be confined to the corresponding side. If a bronchus be completely occluded by pressure, then the peculiar breath-signs will disappear, and complete respiratory silence reign instead. The dyspnoea of this origin is greatly relieved by motion and by certain positions of the body. In capillary bronchitis, pneumonia, asthma, etc. the patient sits with the head thrown back and the shoulders raised, whereas a patient with tracheal compression finds greater relief in leaning across the {806} back of a chair, with his head resting upon his arms folded on a table, and the nights are passed in this position. Again, the pressure dyspnoea is subject to sudden and excessive variations. Any excitement which increases the cardiac activity and the blood-tension will excite dyspnoea, whereas rest and repose diminish it. This form of dyspnoea is likewise accompanied by loud stridulous breathing, and by harshness and a metallic quality of the voice. The stridor and dyspnoea bear no direct relation to the size of the tumor, because a small tumor pressing upon the side of the trachea, where the cartilaginous rings are thinner and less resistant, will produce more discomfort than a larger tumor directly in front. Where the compression of an air-tube is considerable, it usually provokes inflammation of the mucous membrane, and the secretions thereby engendered are liable to collect behind the obstruction and increase the distress for breath. Cases are reported where, tracheotomy having been performed, a catheter was pushed by the obstruction and the backed-up secretion allowed to escape, to the great relief of the sufferer. One case is recorded where the examining physician was able to see by the aid of a laryngoscope an inward projection of the wall of the trachea, which pulsated with each heart-beat.

The dyspnoea arising from pressure upon the recurrent laryngeal and vagus may begin in two ways--either by a sudden paralysis of both vocal cords, or by a preliminary spasm of the cords due to nerve-irritation. When both cords are paralyzed, which is very rare, the voice is entirely obliterated and the dyspnoea is intense and continuous. The complete paralysis may be associated with choking at meals. When only one cord is paralyzed, the breathing is not materially affected, though the voice is altered in a characteristic manner.

If the compression of the nerves mentioned simply irritates them, then the phenomenon of laryngeal spasm occurs. The voice becomes high, squeaking, and false or whispering, with a muffled falsetto. Jaccoud describes a condition where the nerves of the two sides are not uniformly affected, and therefore the cords are not equally tense in their spasm. The result of this difference of tension and vibration is a peculiar commingling of high and low tones, which produces a very discordant and unpleasant sound to the ear. Jaccoud terms this la voix bitonale. The dyspnoea from spasm persists through both inspiration and expiration, whereas with paralysis of the cords the inspiration is alone or mainly affected. The cough in these cases is phenomenal in its character, being very loud and metallic, often barking, and it is very distressing to the patient and to all who hear it.

When a bronchus is compressed the percussion note on the corresponding lung is higher in pitch and tympanitic. The inspiratory murmur is ordinarily diminished, but bronchial breathing may (rarely) occur. The coincidence of bronchial breathing with tympanitic resonance is an eccentric combination of a very paradoxical character. The cough is almost pathognomonic, with a loud barking, distressing metallic clang. Such a cough is still more suggestive when combined with the high, shrill, whistling vox anserina. The amount of expectoration is at first small, consisting of glairy, frothy mucus. Later it becomes more copious and muco-purulent, and may even be rusty and red. The presence of bloody sputa with an aneurism is always grave, because it raises suspicion of a so-called weeping aneurism which is approaching rupture.

Dysphagia.--This is a common symptom with aneurism, but it is not so constant in appearance as it is with other mediastinal tumors. It appears more often when the aneurism is situated upon the transverse portion of the aorta. It is frequently painful, but always variable in severity, and may disappear for long intervals at a time. Lying upon the face usually relieves the difficulty, while it is aggravated by reclining upon the back. Fluids are usually {807} swallowed more easily than solids. Hayden says that a feeling of sharp pain in a particular part of the gullet in swallowing when aneurism is present indicates erosion of the mucous membrane and early perforation.

Pressure upon Veins.--Localized oedema and cyanosis are two common symptoms of aneurism of the aorta. The sudden eruption, the limited distribution, and the terrifying effect of these symptoms render them especially interesting. They are due to pressure of the tumor upon the veins near the heart, and particularly upon the superior vena cava. Dujardin-Beaumetz says that, thanks to the vena azygos, compression of the superior vena cava produces simply a varicosity of the neck and upper part of trunk. Should the vena azygos be simultaneously blocked, then the oedema and cyanosis will spread over the entire head, neck, arms, shoulders, and upper trunk--_i.e._ over all parts drained by the superior vena cava. Only two such cases have been reported, however. One case was seen by Piorry and one by Dujardin-Beaumetz. In the latter case the oedema and cyanosis of parts named above came on suddenly without apparent cause. The face was swollen, blue, and covered with red patches, and the eyes were injected. The ears were cold; the abdomen and lower limbs retained their normal color. The contrast between the upper and lower portions of the body under these conditions is very striking.

Balfour says that "a thick oedematous collar covered with large veins surrounding the root of the neck" is indicative of compression of the superior vena cava.

Pressure upon the brachio-cephalic veins produces oedema and cyanosis of the head and upper extremities; oedema of the glottis has occurred under such conditions. Sudden swelling of one arm, unaccompanied by inflammation, is suspicious of aneurismal compression of the corresponding vein, especially if it comes on suddenly after exertion. Compression of the descending vena cava or right auricle may give rise to congestion and dropsy of the lower part of the body, but these are later symptoms.

Pressure upon the thoracic duct is relatively rare. It may cause emaciation, but loss of flesh with aneurism is more often due to obstruction of the oesophagus or to dyspepsia and the exhaustion from pain and sleeplessness.

Pressure upon Bones.--Pressure of a tumor on neighboring bones causes absorption and dislocation of the same. The clavicles, sternum, and ribs are rapidly eroded by the aneurism, and are pushed forward and disarticulated. Pressure upon the spinal column causes absorption of the vertebræ and of the cartilages, until oftentimes the cord is laid bare and even subjected to direct pressure.

Inspection.--Inspecting a person suspected of aneurism, one should examine the pupils, the color of the skin, the condition of the veins of the head, neck, and arms, all movements of the neck and chest, and especially the contour of the front part of the chest.

The conditions of the pupils, skin, and veins have all been described, but the movements of the neck and chest require notice here. Any area of pulsation apart from the normal apex-impulse should be critically marked and examined. Fulness or beating in the episternal notch is significant. Cheesman reports a case where a curious pulsation was occasionally communicated to the larynx and the tongue by an aneurism situated beneath the manubrium. Every now and then the thyroid cartilage would rise and fall, and the tongue would pulsate backward and forward with each beat of the aneurism.

Inspection of the larynx quickly determines the presence or absence of paralysis of the cord, and may sometimes reveal pulsating tumors pressing upon the trachea. While inspecting the shape of the chest it is best to stand upon one side of the patient and look across the surface of the thorax. In {808} this way slight deviations from the symmetrical become most readily apparent. If any abnormal point seems to pulsate, the fact can be rendered more obvious by pasting bits of paper upon the suspected spot and around its immediate neighborhood. Viewed thus in an oblique light, the relative movements of these pieces may be easily discerned. If a tumor be present and the diagnosis established, one should carefully note the color and condition of the skin over the prominence. As the tumor develops pressure the skin becomes tense and glossy. Then it turns red, and may be covered with livid spots and even ecchymoses. In later stages a black dried scale of flesh may be all that seems to restrain the heaving blood. Weeping of blood may take place for some time before the final break.

Palpation.--Given a prominence of the chest-wall or a localized pulsation in the abdomen, the next step is to examine the suspected part with the hands. Any tumor lying across an artery will move forward and backward with each pulsation of the artery, and conditions of this kind have been repeatedly diagnosed as aneurism. An aneurismal tumor, however, is distensile as well as pulsatile. Every tumor, therefore, should be grasped as far as possible between the two hands, to determine if it distends with each beat.

When one cannot reach the sides of the tumors in front, one can resort to Stokes's plan. Place the flat of one hand upon the front of the chest, and the other hand upon the back. By this means the expansile character of the pulsation may sometimes be determined.

Many intra-thoracic aneurisms present a double impulse or two distinct blows to the hand during the cardiac systole; and when these blows are too faint to be felt, they may still be registered by the sphygmograph. This double impulse is not characteristic of aneurism of the aorta, because it may also be felt in aneurisms of the large branches of the arch. Bellingham thought that the second blow was due to a reflex wave from the aortic valves, and was therefore diastolic in rhythm. Jaccoud, however, showed that it occurs even with great insufficiency of the aortic valves, thus excluding reflex waves. François Frank also proved that both blows were systolic in rhythm. He thinks they are due to the fact that the blood enters the aneurism en deux temps. The blood, rushing in at the beginning of the systole, gives a sudden distension of the partially relaxed sac-walls, and thus causes the first impulse. Then the bulk of the blood-waves, following more slowly on account of greater resistance, produces a second elevation more or less pronounced.

Balfour states that aneurismal pulsations are usually more forcible than those of the heart, and that this point has not received the attention which it merits. If the sac contains much fibrin the impulse is feebler than that of the heart.

W. S. Oliver describes a new sign of aneurism and the method for detecting it. Place the patient in the erect position and direct him to close his mouth and elevate his chin to the fullest extent. Grasp the cricoid cartilage between the fingers and the thumb, and push it gently upward. If an aneurism of the arch of the aorta be present, its pulsation will be plainly transmitted up the trachea to the hand. The act of examining will also increase the laryngeal distress if such be present.

The frémissement cataire, or thrill imparted to the hand by an aneurism, has been frequently described. It is very characteristic when felt, but Powers says it is not of frequent occurrence. He has felt it in eight cases of aneurism, but four of them were complicated by regurgitant disease of rheumatic origin, and all were probably of the fusiform kind.

Pulse.--Partial or total obliteration of a large vessel, dilatation of the aorta, compression of an artery by a tumor, may produce a radial pulse {809} similar to that of aneurism. Moreover, we may find the radials differing from each other in persons who are perfectly healthy. It follows, therefore, that, taken by itself, the pulse does not contribute very decisive evidence of an aneurism. When the diagnosis of an aneurism is established or confirmed by other signs, then the added evidence of the pulse does possess some value. The finger will often detect the following characteristics of an aneurismal pulse:

1. Delay.--The pulse at the wrist is normally from 11/100 to 14/100 of a second later than the cardiac impulse. With aneurism this interval may be prolonged in one or both radials, and the additional delay may amount to 4/100 of a second. This sign of delay is of most value when the pulse in one wrist loiters behind its mate. The relative delay of the impulse of the aneurism itself and of the carotid artery may give useful information. If the beat of the tumor precedes that of the left carotid, then the tumor is nearer the heart, whereas the aneurism is evidently beyond the left carotid when the beat of the latter precedes.

2. Diminution in Volume.--The pulse in one radial may be much smaller than in the other or altogether absent.

3. Diminution in Force.--The pulse of one side may convey a less sudden and less forcible blow to the finger. This diminished suddenness of the sensation imparted to the finger corresponds to the sloping up-stroke of the sphygmographic tracing.

4. Thrill.--Under certain rare and not very clearly defined circumstances the pulse imparts a sensation of thrill to the finger. Mahomed says this probably occurs when the entrance to the aneurismal sac is very narrow and the aneurism is directly in the course of the vessel. It may also be occasionally produced by the rigidity of the wall of the vessel or by a partially-dilated clot vibrating in the blood-stream.

Under the enthusiastic and elaborate study of Mahomed the sphygmograph has attained a certain degree of usefulness. Though difficult in its application and limited in its results, yet many of the points demonstrated by it are of sufficient importance to justify their consideration. The sphygmographic tracing of the normal pulse is shown in Fig. 50.

Now, the points which distinguish an aneurismal tracing from the normal are--1, a sloping up-stroke; 2, impairment or loss of the percussion wave; 3, obliteration of the secondary waves; 4, diminished volume of the curve; 5, vibratile waves; 6, a different blood-tension.

In comparing the curves shown in Fig. 51, taken from Powell's article upon aneurism, it will be noticed that the up-stroke AB is more sloping in the curve of the right wrist than in that of the left. The percussion and dicrotic waves are entirely smoothed out into an almost uniform wavy slope. As one writer has expressed it, an aneurism acts like an air-chamber in an engine, and tends to break up the intermittent pulse into a steady stream. The relative difference of the blood-tension of two arteries is determined by the relative amount of pressure required of the instrument to develop the tracing. This amount of pressure is sometimes greater and sometimes less on the affected side.

In comparing the tracings from the radials the following points are to be noted: 1. Is there any difference in the percussion waves?--_i.e._ is the up-stroke more sloping or the apex less pointed in the one than in the other? 2. Is the tidal wave equally high and sustained in both? 3. Is the dicrotic wave equally developed?

{810} If a difference exist in the tidal wave alone, it need not, and probably will not, be due to aneurism. It is the loss of the percussion wave and of the dicrotism which characterizes aneurism.

It must be conceded here that the use of the sphygmograph and the interpretation of its tracings are beset by the greatest difficulties. Mahomed, to whom I am chiefly indebted for these sphygmographic details, declares that the use of the instrument requires great care and skill, and it may easily lead to error. "No one should attempt to use it who cannot readily obtain similar tracings from the two radials of a healthy person." Great care in the application of the instrument should be exerted, and we must guard against all causes of transient excitement. It is well to let the patient see the instrument applied to others before attempting it on him, in order that he may not fear it. The patient must be placed in a comfortable position, with both arms alike, and the points of application of the instrument must be alike on the two sides. The amount of pressure on the two sides must be equal, or the difference carefully noted. Moreover, one should never be contented with one tracing, but a number on each wrist should be taken. If, then, the two radials appear to differ, the precautions must be redoubled, and the pulse tested again on another day. Inequalities of the tracings may be produced by abnormal distribution of the radials, and an old fracture or other injury of one arm may affect the flow of blood in the arm.

Paralysis of the arm, by interfering with the vaso-motor nerves, and thereby with the venous return of the blood, may alter the character of the pulse. A tumor external to the artery, either intra-thoracic or extra-thoracic, will produce aneurismal pulse and endarteritis, or congenital contraction of the aorta may so block the artery as to produce diminished pulse-waves. It may be said that the sphygmograph is incapable of distinguishing between an endarteritis and an aneurism.

On the other hand, the instrument is very useful in distinguishing between an aneurism and a tumor compressing an artery, because in the latter case the up-stroke and percussion wave remain normal, whereas in the former they are strongly modified, as described above. With aneurism of the ascending aorta both radials must be similarly affected, if at all, and in these cases the sphygmograph teaches very little. If the right radial is alone or mainly affected, then the aneurism involves the innominate and arch together. When an aneurism of the innominate includes the aorta, then the whole sac forms virtually a dilated aorta, and no difference in the radials will appear. Hence it follows as a corollary: Given an innominate aneurism, if the radials remain equal the aorta is certainly involved. When the left radial pulse is alone affected, the aneurism lies beyond the brachio-cephalic branch, and may or may not involve the left subclavian.

{811} The sphygmograph is of less avail in aneurisms of the descending portion of the thoracic aorta or of the abdominal aorta. It may be of service in affording information regarding the condition of the aorta itself with reference to an operation, and it may also be of service in determining the upper limits of an aneurism under the following conditions: A case is reported which presented all the physical signs of aneurism of the descending aorta, but the sphygmograph showed that the left radial was affected, and thereby proved that the aneurism extended as high as the left subclavian at least.

While the foregoing facts prove that the sphygmograph by itself affords very inconclusive and untrustworthy evidence, yet when the presence of a tumor and other physical signs prove the existence of an aneurism, the written pulse-record will often be the guide to the accurate placement of the tumor, and thereby will often furnish decisive indications in the selection of the method of treatment.

Auscultation.--The typical aneurismal bruit is not an ordinary souffle, but it is an accentuated booming sound of a very peculiar character. Many writers describe it as a systolic jog or shock. Occasionally this bruit de battement is double--_i.e._ one hears two shocks, so to speak, just as one feels a double impulse. No satisfactory explanation for this reduplication of murmur has yet been given. The aneurismal murmur is almost invariably systolic. Balfour reports two cases of a diastolic murmur heard with abdominal aneurism. One of these cases was observed by himself and the other by Wickham Legg.

When this peculiar booming sound is heard over a circumscribed dull patch, it is very distinctive of aneurism, but its absence possesses no eliminative value. Many aneurismal tumors are absolutely quiet, and some of them give only a soft murmur like an ordinary cardiac souffle.

Associated with the aneurismal sound one also hears the normal heart sounds much intensified. This is peculiarly noticeable of the second cardiac sound, which acquires a ringing, booming, accentuated character when heard over an aneurism. Johnson thinks that this intensification of the heart sounds is due to the sudden tension of the walls of the sac. Balfour in referring to the same phenomenon considers it of greatest diagnostic value, and thinks that proper emphasis is not ordinarily given it.

A fundamental rule in the examination of a suspected case of aneurism is to auscult over every inch of the thorax, front and back. Not only the intrinsic signs of the tumor itself are important, but all testimony from the neighboring organs must be collected and weighed. The modification of the respiratory sounds have already been mentioned. Stokes attaches great importance to this fact, that "over one lung, more rarely over both, the breath sound has often communicated to it a peculiar sonorous vibrating quality, probably by conduction from the laryngeal stridor present."

Valvular complications of the heart are not necessarily associated with aneurism. Cases are reported, however, where a tumor is situated so near the aortic orifice as to interfere with its closure, and thus induce the ordinary phenomena of aortic insufficiency.

Of course when valvular disease is coincident with aneurism the customary signs will be added to those of the tumor, and must be carefully distinguished.

Drummond of England has recently contributed a new sign of aneurism. It is a familiar fact that after sudden exertion, and with the heart acting violently, one can hear in the mouth during expiration a well-marked whiff proceeding from the glottis. Under normal conditions of the chest this whiff is only heard after exertion, and never during perfect repose. Now, Drummond has noticed that this oral whiff, as he terms it, occurs regularly in many cases of aneurism of the aorta. When the sign is well marked the {812} whiff is audible in the trachea with the mouth shut, but disappears on compressing the nostrils with the fingers. The whiff may be double, synchronous with both the expansion and contraction of the tumor. The sign does not exist in cases of valvular lesions of the heart without aneurism. As indicated above, this sign possesses a diagnostic value only when it is observed under conditions of absolute bodily and cardiac composure. One should make a patient lie quietly for a while before examining him for this sign.

Percussion.--Circumscribed dulness is always present when the tumor reaches the chest-wall. Owing to the globular shape of the tumor, its size is usually larger than the area of dulness would seem to indicate. There is no abrupt line of demarcation, but the dulness shades off gradually into the surrounding pulmonary resonance. The dull patch is most frequently situated to the right of the sternum and on a level with the second and third ribs. More rarely it may be found on the sternum or to the left of the same. If the neighboring lungs are solidified from any cause, the percussion signs of the aneurism will of course be obscured.

Localization.--When the signs of aortic aneurism are all conclusive, the next point in the diagnosis is to determine the probable seat and extent of the tumor.

In a general way, it may be stated that the physical signs of an aneurism of the ascending aorta are grouped about the upper two right intercostal spaces. Tumor of the transverse portion presents itself at the manubrium, and aneurism of the descending aorta may be detected in the upper interscapular region to the left of the spinal column. Balfour says that the aneurism is probably about the middle of the transverse portion when the point of greatest pulsation is situated at the middle of the manubrium or from that to the fourchette above, and the veins of the root of the neck are congested.

An aneurism of the left extremity of the transverse portion usually points below the left clavicle. There are many startling exceptions to these rules. One case is reported where an aneurism of the ascending aorta pointed at the left of the sternum and pressed upon the left bronchus. Another case of aneurism of the descending aorta passed behind the oesophagus and compressed the right bronchus. An innominate aneurism occupies the episternal notch, and usually appears first along the tracheal edge of the sterno-mastoid muscle. As it increases in size it will extend across the episternal notch and push out the inner end of the right clavicle. It may appear first under the end of the clavicle, but then it is at the cardiac end of the vessel and involves the aorta.

An innominate aneurism must be distinguished from a low carotid aneurism. The latter usually appears between the sternal and clavicular portion of the sterno-mastoid muscle, and its pulsations can be felt by pushing the finger into this space when the muscle is relaxed. Cockle said that he knew of no instance of a carotid aneurism distending the episternal notch. Barwell also mentions the fact that the ear on the affected side will gain color more slowly than its mate after pinching when the aneurism is situated upon the carotid.

It is always serviceable, and often essential, to determine whether an aneurism of the innominate also involves the aorta. If the tumor appears first under the sterno-costal articulation, the aneurism probably extends on to the aorta. Again, if the radials are both equal, the tumor undoubtedly includes the aorta, for reasons already explained in connection with the pulse-curves. If the right pulse alone is affected, we can eliminate aortic complication. Barwell also states that innominate aneurism involving the aorta presents the following symptoms: The pulsation, dulness, and abnormally loud heart sounds are on and to the right of the middle line. The various congestions {813} are on the left side, and do not encroach upon the right side until later. This venous symptom is especially marked on the left pectoral.

A subclavian aneurism may cause confusion when it occupies the first third of the vessel. Such an aneurism, however, is an elongated oval in shape, and is partly covered by the clavicle, and this bone will move up and down in front of it with movements of the shoulders.

I have emphasized the unreliable character of the pulse as a diagnostic sign of aneurism, but when other signs of this lesion are well marked the pulse furnishes some evidence regarding the locality of the tumor. The following summary of the pulse-signs serves as a useful guide, therefore, in examining the pulse.

1. Both radials affected alike, the aneurism is limited to the ascending aorta.

2. Right pulse more altered than the left, the aneurism involves both the aorta and the innominate artery.

3. Right pulse alone affected, the left remaining normal, the aneurism is confined to the innominate artery.

4. Left pulse not affected, the aneurism is situated beyond the innominate.

5. Both pulses aneurismal. This occurs sometimes with aneurisms of the arch which involve the large vessels.

Varicose aneurism can only be suspected by exclusion. Thurman emphasizes one symptom which is significant when heard, but it is rare. This sign is an intense superficial souffle, accompanied by a frémissement cataire, and situated over the opening of the aneurism. It is continuous in time, though louder during systole; and this element of continuity serves to distinguish it from the ordinary bruits of aortic aneurism or valvular lesions. When there is a varicose communication between the aorta and the vena cava superior or the right auricle, the souffle will be extended along the right border of the sternum, with its maximum at the level of the second intercostal space. If the aneurism opens into the pulmonary artery or the upper part of the right ventricle, the souffle will be heard along the left border of the sternum. When the signs are manifested as the result of some excessive effort, and are accompanied by præcordial pain, Thurman thinks them almost conclusive of varicose aneurism of the ascending aorta. He adds a few other symptoms likely to be present, but less characteristic of this particular lesion. These are anasarca, venous congestion, dilatation of cutaneous veins, dyspnoea even to orthopnoea, cough with sanguinolent sputa, a bounding pulse, and less frequently general feebleness, with diminution of the animal heat. These signs have a general significance, however, except when the vena cava superior is involved, and there the venous congestion and oedema occupy the upper half of the body. We have, however, previously seen such phenomena limited to the upper part of the body, resulting from pressure upon the vena cava.

T. Gallard has related a very interesting case of an arterio-venous aneurism of the arch of the aorta communicating with the vena cava superior. This case furnished all the ordinary signs of a tumor of the mediastinum with compression of the vena cava superior. It emitted a souffle which began with the first cardiac sound and persisted through the short interval of silence and to the end of the second sound. This souffle was especially pronounced at the base of the heart, and Gallard diagnosed a communication with the vein above mentioned. The autopsy revealed the accuracy of the diagnosis.

Hayden says that aneurisms opening into the heart, the pulmonary artery, or the vena cava have, so far as he knows, without exception, arisen from the ascending aorta. The simple projection of an aneurism into one or more of the chambers of the heart is attended only by symptoms of obstruction to the blood-current, and he knows of no symptom characteristic of a communication between an aneurism and the heart. When the sac opens into the {814} pulmonary artery there occur sudden and most urgent dyspnoea and blood-expectoration, without spasm or stridor. If aneurism of the ascending aorta has been primarily determined, then the sudden eruption of such symptoms would be almost pathognomonic of this accident.

DIFFERENTIAL DIAGNOSIS.--We have enumerated a large number of symptoms, direct and indirect, which are grouped about aortic aneurism. It is an unknown thing, however, for any one aneurism to present the entire group in one tableau. A few only appear in a given case, and the possible kaleidoscopic combinations of the whole number are almost infinite. There are also numerous other conditions of the thoracic organs which produce groups of phenomena closely resembling those of aneurism, and requiring critical analysis.

An aneurism is a tumor, and the majority of its symptoms are simply signs of a tumor. It is necessary, therefore, to determine whether the tumor at hand is a solid growth or an expanded vessel. This is always difficult when the tumor is beyond reach. It may be pulsatile from lying upon the aorta. The following points, therefore, should be carefully noted and tested:

1. A solid tumor may be pulsatile, but it is never distensile.

2. The shock of a solid tumor is not markedly stronger than that of the heart (Balfour).

3. There is no accentuation of the second heart sound (Walshe), nor bruit of a booming character (Hayden).

4. In the sphygmographic tracing of a tumor-pulse the up-stroke is never sloping, and the percussion wave remains well marked.

5. Variations in the position and size of a tumor, and also in the pressure phenomena, are important. An aneurism varies constantly in its size and in its mural tension; hence all its signs vary correspondingly; whereas with a solid tumor in the mediastinum the phenomena are more constantly progressive. An aneurism which is visible and palpable upon the external chest-walls will sometimes recede within the thorax, whereas solid or cancerous tumors never act thus.

Abscess of a gland in the episternal notch may closely simulate aneurism of the innominate. Mahomed and Golding-Bird report such a case. The imitation was so close in this case as to balk a number of very careful observers, and no absolute diagnosis was reached until the sudden rapid increase of the growth and of acute superficial inflammatory symptoms revealed the probability of pus. The abscess was supposed to result from the pressure of a collar-button. A companion case was reported by the same author where an actual aneurism of the innominate presented such neutral signs that no diagnosis was reached until the patient was etherized and an exploratory incision was made down to the sac. It is well to remember that an aneurism may rise and fall with deglutition and with coughing and straining when it is adherent to the trachea. A case is reported of a very vascular sarcoma attached to the manubrium sterni and projecting into the episternal notch, which presented the double murmur, pulsation, and pressure symptoms of an aneurism, and was diagnosed as such, the mistake being discovered only at the autopsy. In such very obscure cases I know of no reliable or distinctive signs on which a diagnosis may be established: the only resort seems to be to await developments. In process of time the appearance of cancerous growth in other parts of the body will often throw light upon a thoracic tumor. Occasionally aneurism of the aorta may simulate insufficiency of the aortic valves. Guttmann reports a case which presented all the classical symptoms of aortic regurgitation and none of aneurism. The autopsy revealed a large aneurism of the ascending aorta and the aortic valves intact. The aorta itself was notably dilated throughout, and it is probable that the change in the arterial walls affected the proper systolic {815} contraction of the aortic orifice, so that insufficiency resulted. Chronic endarteritis of the aorta may produce aneurismal signs. Dujardin-Beaumetz reports a case where there were contraction of the left pupil, sudden reddening of the left side of the face, transient aphonia, intermittent dyspnoea, suppression of the left radial pulse, and a double souffle along the track of the aorta; and yet the autopsy revealed simply endarteritis of the transverse portion of that vessel, without the least dilatation. Many of the symptoms of this case could be explained by the extension of the inflammation to the sympathetic nerves.

Many aneurismal signs connected with the voice, eye, and vascular supply of the heart may be produced by the implication of either vagus in neighboring inflammation. Chronic empyema of the left side will sometimes pulsate synchronously with the heart and simulate aneurism. The following points are important:

1. Such pulsations occur only on the left side.

2. There is always a disproportion between the pulsations, which are feeble, and the extent of dulness, which is large.

3. There is absence of expansile pulsations.

4. There is usually ample evidence of the presence of a pleuritic effusion, displacement of the heart, etc.

5. Aneurism may be coexistent, however, and therefore it may sometimes be advisable to make an exploratory capillary puncture before opening the chest freely.

Berard reports a case of empyema which formed a tumor on the left side of the sternum, which pulsated and looked like an aneurism. Finally, the tumor burst and discharged pus.

DURATION.--The progress of aneurism of the aorta is very rapid, and in the majority of cases the fatal termination is not delayed many months. In 40 cases where the duration of the disease was well defined, I found that 20 of them died within one year, 9 lived for two years, and 3 lingered five years. About 75 per cent., therefore, died within two years.

TERMINATION.--Rupture of the sac is a frequent cause of death. In 106 cases analyzed by me, 39 terminated in this manner. The seat of the rupture and the organs into which the blood escapes vary according to the location of the sac.

Aneurisms of the ascending aorta burst most frequently into the pericardium, right auricle, right ventricle, right pulmonary artery, and rarely externally. Tumors of the transverse portion burst into the trachea, left lung and left bronchi, left pleural cavity, oesophagus, and externally. Those of the descending aorta empty into the oesophagus, left pleural cavity, and spinal cord.

The most frequent point of rupture appears to be into the pericardium, as 13 out of 39 ruptures emptied into that cavity. It will also be noticed that the right side of the heart and the left pleura and lung are the chosen seats of hemorrhage. I found no case of rupture into the left side of the heart.

The bursting of an aneurism is not always an immediately fatal accident. The so-called weeping aneurism may pour forth small amounts of blood for weeks and months. Neligan reports a case of external rupture near the second rib on the right side which discharged blood at intervals for more than a year. At times the bleeding was with difficulty arrested, and yet the aneurism finally solidified and the patient left the hospital calling himself well. Another man with an external aneurism thought it was a blood-boil, and squeezed it with his chin to favor the flow until he fainted. The bleeding then ceased, and never occurred again. He died one year later of typhoid fever. Such cases, however, are very rare, and usually when an aneurism bursts externally the death is sudden and tragic.

{816} Rupture of a sac into the pericardium or pleural cavity may not prove fatal for several hours, and the patient will exhibit the ordinary symptoms of internal hemorrhage. Rupture into the heart or pulmonary artery causes great dyspnoea and distress, and death follows rapidly.

Aneurism may cause death indirectly by starvation from pressure on the oesophagus, or by suffocation from occlusion of the trachea. The pain and distress occasioned by the tumor may cause death from exhaustion. Pain at times is so great that the sufferers can neither lie down nor stand, and, deprived of rest and food, they wear out. A few patients die from intercurrent accidental diseases or complications, but it may justly be said that the death of a patient with aneurism is usually directly referable to the tumor itself.

TREATMENT.--Aneurisms of the aorta occasionally solidify by the formation of a clot, and thus a spontaneous cure is established. Unfortunately, however, such a result is a rare exception to the rule of steady progress to death.

A number of methods of treatment have been advocated, and some of them present here and there gleams of hope for some cases. The aim of all these methods is to produce coagulation of the blood in the sac, either by mechanical means or by the chemical action of drugs.

The introduction of fine wire has been attempted. A canula is plunged into the aneurism, and then either short pieces of wire are dropped into the sac or one long wire is pushed in. Murchison introduced twenty-six yards of steel spring into an aneurism of the ascending aorta. This method is attended with great danger, and has not been successful, and is therefore abandoned at present.

The hypodermic injection of ergotin into the sac was also recommended by Langenbeck, but it has not met with success.

Pressure upon the aorta can only be applied to cases of abdominal aneurism, and here it has been successful. The pressure must be applied under ether, and great care must be exercised not to injure the other abdominal organs.

The starvation method was first advocated by Hippocrates, and was espoused later by Valsalva. The idea of this treatment was to render the blood more coagulable by making it less watery and richer in fibrin. Valsalva commenced by bleeding a patient freely, and then reduced his meat and drink until only half a pound of pudding was allowed morning and evening. The bleedings were repeated at intervals until the patient was too weak to lift his hand from the bed on which he lay. The vital objection to this treatment is that starving renders the blood less coagulable, though it may lower tension. Copland has seen aneurisms previously quiet begin to grow and end fatally on the starving and bleeding method.

A few years ago Valsalva's method was resurrected by Tufnell, but was modified somewhat in detail. The bleeding was omitted and the starving was less vigorous. Tufnell's three rules are--rest, restricted diet, and medicine. The rest must be absolute repose in bed, and must continue two months or ten weeks at least, without the patient sitting once erect. By this means Tufnell reduces the frequency and force of the heart-beats, and thereby lessens the number of distending blows upon the interior of the aneurism. This is of course a very tedious treatment, and many patients will be unwilling to submit to it. Others who are unable to appreciate the gravity of their disease, and seek merely relief from their subjective suffering, will refuse to continue the treatment as soon as they obtain such relief. Hence the ingenuity of the physician will often be taxed to the utmost in devising means and measures for controlling refractory patients and lessening the tedium as much as possible for all.

The room of confinement should be light, cheerful, and airy, and should {817} command a view of outdoor life if possible. Tufnell urges the choice of a south room, because the presence of sunlight is very restful to the spirits, while absence of the same is depressing. The bed should be made as comfortable as possible, and with mechanical contrivances to obviate the necessity of raising the patient. It should not be too narrow, and should be of a height most convenient for the nurse attending. Tufnell recommends a large water-cushion, not over full, under the hips. The sheets and protectives should be drawn taut and pinned to the sides of the bed to prevent wrinkling. No movement should be allowed the patient except to turn upon his side now and then, and occasionally upon his face in case such movement relieves dorsal pain. A urinal and bed-pan should be at hand, and a pleasant, agreeable nurse who will be willing to read to, converse with, and amuse the patient as desired.

The diet recommended by Tufnell is as follows: Breakfast: Two ounces of white bread and butter; two ounces of cocoa or milk. Dinner: Three ounces of boiled or broiled meat; three ounces of potatoes or bread; four ounces of water or light claret. Supper: Two ounces of bread and butter; two ounces of milk or tea. This makes an aggregate of ten ounces of solid and eight ounces of fluid food in the twenty-four hours, and no more. Thirst is liable to be present at first, especially in the summer months; and this may be relieved by holding a pebble in the mouth or by occasionally sucking a piece of ice. Tufnell thinks that the diminished amount of fluids reduces the duty of the heart and renders the blood thicker and more fitted for deposit. If the patients are very intolerant and restless, it is better oftentimes to indulge them in a little more liberal diet, but only enough to appease them and keep them in control.

Medicinal Agents.--As rest is the great refrain of his method, Tufnell recommends anodynes and soperfacients at night. For mere restlessness he prescribes the following combination: Lactucarium, 20 grains; extract of hyoscyamus, 10 grams--made into six pills, two to be taken at bedtime. The bowels will naturally be constipated, owing to rest in bed, and for this he recommends compound jalap powder. Too much purgation should be avoided, as irritation of the bowels will hasten the circulation. Obstinate constipation, however, must not be allowed, or anything which can produce straining. The instant such a condition manifests itself, enemata by tepid water should be administered.

The principal symptom to contend with is pain, and for this purpose opiates should be used freely according to the exigencies of the case. In one case it was found that smoking twenty grains of stramonium at bedtime would produce a quiet night. This was discovered accidentally by the patient, who began to smoke the stramonium under the false impression that he was suffering from asthma.

Maclean recommends the use of eucalyptus globulus for the relief of the distress due to irritation of the pneumogastric nerve.

Issues and blisters upon the back are not advisable, as they interfere with the recumbent position. Relief to dorsal pain will often be obtained by change of position, by turning upon the side or upon the face. Sometimes the application of a heated flat-iron, with the protection of brown paper, over the tender portion of the spine will relieve the boring pain. Iron may be used in anæmic cases.

We have been explicit in giving the details of the Tufnell method for two reasons. In the first place, the Tufnell method means to many people simply putting a man to bed, but it also means keeping him there for a prolonged interval of time; and this is a difficult task, and one that requires great ingenuity and patience in its execution. In the second place, when any method is attempted it should be carried out conscientiously and literally in {818} every detail, and then the results obtained can be legitimately scored to the credit or discredit of the method. But it is neither fair nor honorable to pretend to follow a method, and, neglecting important details, accredit the method with the failures which follow. Tufnell claims to have cured many cases, and he declares that absolute recumbency is the price paid. With regard to the prospects in individual cases, he says that with a strong pulse at the wrist and an excessively strong action of the heart, and a healthy state of the cardiac valves and of the aorta in general, the aneurism is difficult to cure. On the contrary, when the aorta in some part of its course is dilated into a cavity, with its walls so plated with atheroma as to be passively recipient of the blood, and not capable of transmitting it with force, the cure is comparatively easy. If this be true, it would appear that the Tufnell method is best adapted to just these cases which are least amenable to the surgical methods of treatment.

The use of iodide of potash for aortic aneurism was first advised by Nélaton and Bouillaud in 1859, and this treatment has found its warmest advocate in Balfour. The points in favor of this treatment are its simplicity, the ease with which it can be carried out, and the frequent happy results which have followed its employment. The drug may be given with an infusion of cinchona in doses of 20 grains three times daily. It almost invariably lessens the amount of pulsation in an aneurism, and rapidly diminishes the subjective discomforts of the patient.

Balfour rejects entirely the starvation diet, and even bodily repose. He allows his patients to keep about their ordinary employments while under treatment. Kämmerer has shown that iodide of potash destroys the albuminates in the blood, and therefore Balfour is inclined to feed more freely than he formerly did. He avoids any unnecessary amount of fluids in the food, but as the iodide of potash produces free diuresis, this point does not require special attention. Balfour's theory is that iodide of potash lowers the blood-tension of the artery, and also brings about a thickening and contraction of the aneurismal sac. He says: "Post-mortem examinations teach us that under the influence of iodide of potassium coagula are only occasional and concomitant, and that the essential relief is obtained by thickening and contraction of the wall of the sac."

Barwell's Operation.--During the latter part of the last century a French surgeon named Brasdor conceived the idea of placing a ligature beyond an aneurism in cases where it is impossible to tie between the tumor and the heart. A few years later Wardrop carried this idea one step farther, and suggested tying the branches of an aneurismal artery when the main vessel cannot be reached, and Cockle recommended tying the left carotid for aneurism of the aorta. In this way the idea of distal ligature for aortic aneurism was worked up. The operation was attempted a number of times, but was not attended with great success at first. Recently, Barwell of England has revived the operation and elaborated its details, so that now it is attended by encouraging success. Barwell says that one should try the milder measures first, but when a case has resisted the effects of rest, diet, and medicine, then it is time to consider the practicability of surgical interference.

Barwell's operation consists in ligating the carotid and subclavian arteries, and he performs it for aneurisms of the innominate and of the aorta also. Contrary to the ordinary teaching that the inner coat of a vessel must be ruptured in order to ensure the coagulation of the blood after a ligature, Barwell declares that such a rupture of the inner coat is a positive detriment to the operation, and more likely to lead to secondary hemorrhage. He simply endeavors in his tying to bring the inner surface of the artery into contact, and hold it thus; and in order to accomplish this without cutting the arterial tunics, he discards the round ligature in favor of a flat one. {819} Catgut is unsafe, because it is liable to decompose, even in a preservative fluid, and it is also too readily absorbable in a wound. After considerable experimenting, Barwell has adopted the aorta of an ox as the best material for a ligature. The aorta should be obtained perfectly fresh from the butcher. Peel away the outer cellular coat, and then with a pair of scissors cut the middle and inner coats spirally round and round, taking care to keep the breadth equable. The ribbon thus obtained is very elastic, and must be suspended with weights (two to four pounds) attached to it. In this way, the ribbon dries in about six hours into a horny or vellum-like substance. Any irregularities of surface can be easily scraped off, and the cord stored in antiseptic gauze. About fifteen or twenty minutes before it is needed a piece of ribbon can be picked out and soaked in a 3 per cent. solution of carbolic acid, when it will be ready for use. Care should be taken not to bend these ribbons when in the dry state or fibres in them will crack and render them fragile. In view of such chances a piece should be soaked and tested by pulling. (For details regarding the surgical work of this operation one should consult the ordinary authorities upon surgery.)

The manner of the action of the distal ligature is not clear. Brasdor and Wardrop supposed that it reduces the force and velocity of the blood in the aneurism. But the tension and blood-momentum are still transmitted to the sac. Holmes thinks that a clot forms on the proximal side of the ligature and extends down the artery into the sac.

Bennet May, in a recent discussion of this operation, says that 35 cases of double distal ligature for aneurism at the root of the neck have been recorded up to the present time. In 29 operations the two vessels were tied simultaneously. In 6 cases the subclavian artery was tied at varying intervals after the carotid. 23 of these cases died outright or were hastened to a fatal termination by the operation. In 6 cases the progress of the disease was apparently not affected by the operation. A practical cure is claimed for the remaining 6 cases. One patient lived four and a half years, another three and a half years, and the remainder are living from two years downward.

It is a noticeable fact that all the recoveries except one follow operations performed since 1877, and the betterment in result is due to improvements in the method of operating. Barwell acknowledges, however, that "success in great measure depends upon a judicious selection of cases, while want of judgment or insufficient care in examination will most certainly bring a valuable operation into disrepute." He submits the following conclusions from his own experience--

I. An aneurism commencing suddenly, especially if traceable to some traumatism or over-exertion, is more likely to be benefited by operation than one arising gradually and without assignable mechanical cause.

II. Distinct sacculation is a most desirable condition; fusiform dilatation of the innominate indicates almost certainly a similar condition of the aorta and widespread arterial disease.

III. The absence of other aneurisms of the aorta should be determined if possible.

IV. Absence of rasp-sound along the aorta or any other indication of extensive atheroma should be verified.

V. Aortic incompetence (obstruction, regurgitation, or both), unless very slight, is a decided objection, as is also mitral disease or considerable hypertrophy of the heart.

VI. Patency of the vessels leading to the brain should be investigated by making a few seconds' pressure on the carotids alternately and then simultaneously.

VII. Absence of visceral disease must be ascertained.

Electrolysis.--Like all other methods of treating aneurism, electrolysis has {820} had enthusiastic advocates and bitter opponents. Cuisselli began employing it in 1846, and was able to report 4 successful cases in 1869. He says that success may be looked for when one can diagnosticate that the aneurism is slightly developed, is lateral, and communicates with the artery by a limited opening. The heart and vessels otherwise must be in good condition. Balfour recommends electrolysis as a dernier ressort in cases where an external rupture is imminent. He says that four cells of a Bunsen's battery are sufficient, as more than four cells cause pain and require the use of chloroform. Balfour inserts both electrodes. Robin, however, strongly insists that the use of both poles produces greater pain, is more destructive to the neighboring tissues, and gives unsatisfactory results in the aneurism. He advises one to place the negative electrode upon the skin outside, and introduce the positive needle. This invariably determines the formation of a coagulum which is more firm and more resistant to the finger than the ordinary clot of stagnant blood. This clot is always small, whatever the strength of the electric current, but it forms a nucleus for further coagulation in the sac. The negative pole should not be introduced into the sac, according to Robin, because it forms only a soft diffluent clot which readily breaks up and floats away. The negative pole also is much more destructive to the surrounding tissues than the positive pole, and its withdrawal is almost invariably followed by hemorrhage. The coagulation is more rapid and more energetic when the needles are oxidizable, as iron or steel.

Robin lays down the following rules for operating: The patient should lie comfortably in bed, with his shoulders elevated by pillows, and he should be cautioned not to jump or move during the operation. Three or four needles should be inserted about one centimeter and a half from each other, and about thirty millimeters in depth. One will recognize that the needles are well in the aneurism when they exhibit movements synchronous with the sac itself. One of the needles is then attached to the positive pole of the battery, while the negative pole is attached to a sponge and pressed upon the outside of the chest. The galvanic current is allowed to pass for ten or twenty minutes, when it is gradually reduced to nothing. Then the positive pole is transferred to the second needle, which is similarly treated, and so on until the three or four needles have each been used in turn. After stopping the current leave the needles quiet for some moments; then withdraw them gently, so as not to disturb the clots, cover the punctures with charpie in collodion, and apply ice or cold-water compresses if any inflammation occurs. Sometimes morphine may be required on account of pain, but the crises of pain, dyspnoea, and other painful phenomena of the aneurism are calmed almost immediately.

The cure of an aneurism by electrolysis must not be expected from one session. More often several sessions are required, but the repetitions should be separated by four to five weeks, so that time may be allowed to develop the full benefit of the preceding operation, and to heal any secondary inflammation which may have been produced.

Acupuncture.--Constantine Paul conceived the idea of applying simple acupuncture to aneurism. He treated one case as follows: Four needles were introduced into the sac, and allowed to remain there fifteen minutes. Little or no pain was experienced. In three days there was a notable diminution of anxiety and dysphagia. A second introduction was made four days later, which was followed by still greater improvement. The patient felt so much better that he insisted on leaving the hospital. Paul thinks that electrolysis and acupuncture produce an endarteritis which thickens and strengthens the pouch-wall.

{821} Abdominal Aneurism.

This lesion is much more rare than aneurism of the thoracic aorta. Among 551 cases of aortic aneurism accumulated by Crisp, only 59 were abdominal. I find no one particular point of the abdominal aorta which is especially liable to aneurism, but in general terms the upper part is more often affected than the lower. Of 103 cases noted by Lebert, only 3 occurred at or near the bifurcation. Abdominal aneurisms are twelve times more frequent in men than in women, and they are more common between the ages of twenty to forty than after that period.

They form adhesions with all the neighboring organs and tissues, and thus develop a certain number of pressure symptoms. These symptoms, however, are by no means so diversified or numerous as in the cases of thoracic aneurism.

Abdominal aneurism is invariably false after it has attained cognizable size, and it causes death in various ways. Oftentimes it kills from exhaustion by reason of intense pain, which prevents sleeping or eating. Again, by blocking up the arterial supply to neighboring organs, as in the lower aorta itself, it will cause secondary diseases which produce death. The most common termination, however, is by rupture. The sac may rupture into the peritoneum, retro-peritoneal tissue, bowels, bladder, pleural cavity, vena cava, or into the spinal column. Lebert says he has never found a case of external rupture through the skin, but Bramwell reports a case of rupture into the retro-peritoneal tissues and subsequent escape of blood through a bedsore.

SYMPTOMS.--In a large majority of cases pain in the back is the first symptom which heralds abdominal aneurism. This pain may precede the appearance of a tumor for weeks and months. At first the pain is usually due to a stretching of the nerve-plexus which surrounds the dilating vessels, and hence it is of a neuralgic character. It is intensely severe and shooting. Beginning in the lumbar region, it shoots down into the hips and knees, or through the abdomen to the epigastric and umbilical region. It is usually more or less continuous, but subject to great exacerbations. Motion, change from reclining to upright posture, acts of coughing and sneezing, increase it. One peculiarity of this pain is that it is increased by eating and drinking. This is explained by the fact that the taking of food and drink increases the amount of blood and thereby stretches still more the sensitive wall of the aneurism. The pain often obliges patients to keep in bed, and even there the relief is very slight, so that death may result from the exhaustion of sleepless days and nights.

When the aneurism encroaches upon the vertebræ there is added a gnawing, grinding pain which is constant, and is relieved but little by change of posture. Pressure upon the stomach and bowels and upon the nerve-plexuses which supply these organs produces dyspepsia, vomiting, constipation, and a tendency to accumulation of gas in the bowels. This interference with the nutrition of the body invariably causes marked cachexia, so that a patient who has suffered some time from abdominal aneurism will look as if he were affected with cancer.

Pressure upon the renal vessels causes atrophy of the kidneys and hemorrhagic impactions. Patients may die with uræmic symptoms, such as convulsions, dropsy, and stertor.

Pressure on the bladder causes painful micturition, which is a not uncommon symptom of this complaint. Pressure upon the aorta itself below the seat of the tumor will produce symptoms of obliteration of that artery, and will be treated of under that head. Rupture of an abdominal aneurism into the vena cava produces orthopnoea, pallor, and dropsy. Smith reports such {822} a case in which gangrene of the right leg followed a puncture to relieve the dropsical tension.

Physical Signs.--The aneurismal tumor often appears suddenly after a preceding interval of pain or after some sudden strain. It may show itself in the epigastrium, iliac regions, or about the umbilicus. It presents the classical symptoms of expansile pulsation and souffle. But these are often wanting. Every case should be auscultated both front and back, because the murmurs are sometimes more audible behind than in front. François Frank calls attention to the fact that manual pressure upon an abdominal aneurism will produce an increase of tension in the vessels of the lower extremities. This rise of tension is caused by the forcing of the blood in the aneurism out into the lower vessels.

If the pressure be now suddenly removed, the general pulse will almost entirely disappear for one to two pulsations. This is due to the aspiration of the elastic wall of the tumor, which goes back to its original size. The reverse of these phenomena is true in case the tumor is solid and lies across the artery.

Scheele of Dantzig draws attention to a new diagnostic sign, which he considers pathognomonic. This is a suddenly-heightened pressure in the region of the aneurism when both femorals are compressed. This test is not without danger, however, as Sandsby found in one case which he compressed for ten to fifteen seconds. There was a momentary retardation, and then increase of impulse in the tumor, with an increased loudness of the systolic murmur. Directly after, the patient complained of a sharp attack of pain which continued during the day, and that night death followed from rupture of the tumor.

DIFFERENTIAL DIAGNOSIS.--A few diseases of the chest and abdomen may simulate this affection, and require to be eliminated in the diagnosis. A gravitating empyema may present symptoms of abdominal aneurism. The distinguishing points are the signs of an effusion in the left chest, the reducibility of the tumor by pressure, and the absence of a thrill or bruit.

A case is reported of a vast aneurism of the thoracic aorta which grew downward until it pointed in the right iliac fossa. It was considered an abscess with pulsations from the iliac arteries. It would seem as if the only safeguards against mistake in such cases were great skill in examining the whole breadth and depth of every doubtful case and a knowledge of the fact that eccentric developments may occur. Aneurism of the abdominal aorta may be simulated by excessive pulsation of that vessel. This condition appears usually in nervous, weak people, and is often the occasion of great alarm. It occurs frequently in anæmia, and may follow hæmatemesis from gastric ulcer, and thus lead to a fear of a ruptured aneurism.

The diagnosis is easy if the abdominal wall is thin enough, so that the aorta can be reached and felt. If the abdomen is distended by gas, the diagnosis may be more difficult. Duckworth reports a case where it was necessary to give ether and entirely relax the muscles of the abdomen before a satisfactory examination could be made.

Finally, in examining the abdominal aorta by auscultation, one should be careful about any murmur which may be heard. It may be due simply to pressure of the stethoscope upon the vessel. Constriction at a low point of the oesophagus, which causes an accumulation of food above and a dilatation of the tube, may closely resemble aneurism. Hayden refers to a case which exhibited dysphagia, epigastric pulsation with tenderness and percussion dulness, pain in the back and shoulder, and a tearing or raking sensation at the epigastrium on attempting to swallow.

No opinion regarding an abdominal aneurism should be formed until it is certain that the bowels are not loaded with fecal accumulations. Evacuation {823} of the bowels, therefore, is a proper preliminary to an examination for abdominal aneurism. The condition of the bladder and uterus must also be carefully noted, and the bladder should be emptied.

TREATMENT.--Excellent results have been obtained by the Tufnell method. Compression of the aorta above the tumor has been recommended, and has been followed by good results. One case is reported in which the tourniquet was applied four inches above the umbilicus on three occasions, the patient being under an anæsthetic. The first session lasted half an hour, the second three-quarters of an hour, and the third for one and a half hours. The tumor was as large as a cricket-ball, and it became solid in forty-eight hours after the last application. Three weeks later there was no evidence of an aneurism to be found. Another case is reported of one compression of five hours, and another of ten and a half hours. One case in England required fifty-two hours of pressure under chloroform.

These results encourage one to persevere in repeated sessions in case of failure at first. But a word of caution must be given to avoid injury to the abdominal organs during pressure.

Rupture of the Aorta.

Although very frequent in connection with aneurism, rupture of the aorta is otherwise relatively rare. It almost never happens in a normal aorta, but a few cases are reported where the arterial wall is described as merely thin. Usually the rupture occurs at a spot weakened by atheromatous disease, and is produced by sudden strains, falls, or blows upon the chest, or by rapid exercise of the arms. Congenital narrowing of any part of the aorta will produce so much strain behind the obstruction as to cause rupture. Fernand reports such a case in a boy fifteen years old. The ascending and transverse portions were dilated, and the inner surface was covered with small red vascular plaques. The remainder of the aorta was contracted to the size of the iliac vessels.

Men and women are both liable to rupture, but the former more than the latter. One would suppose that women during the terrible strain of childbirth would be especially liable to such an accident, but I have found only one such case reported. This woman, thirty-eight years of age, died suddenly during the first stage of labor, and a living child was extracted five minutes later by forceps. The rupture was seated one and a half centimeters above the aortic valves, and reached nearly round the entire circumference of the artery. Heinricius reports the case,[1] and says that he has been unable to find any similar case recorded. I have found one case of rupture of the aorta during the sixth month of pregnancy, but not associated with any sign of labor.

[Footnote 1: _Cent. f. Gynäkol_, No. 1, 1883.]

The majority of the ruptures occur in the immediate neighborhood of the valves or within two inches of the same. It is a very rare thing to find a rupture of the transverse or descending portion of the arch. One case is reported of a girl twelve years of age who was trampled upon by a pony and never rallied. The descending aorta was found ruptured, and the tear was apparently produced by the nipping of the vessel between the vertebral column and the heads of three left ribs, which projected forward and could be protruded still farther by pressure upon the sternum.

When the inner coat of the aorta ruptures and the blood escapes, it immediately forms a pocket between the arterial tissues, and then one of two things may occur: the escaped blood may coagulate solid, and so fill up the opening and prevent further leakage. This occasionally happens; more often, {824} however, the escaped blood pushes along, dissecting apart the tissues of the artery, and advancing until it finds some point of escape. Sometimes the blood bursts back into the aorta and rejoins the main current. In such cases the separation of the tissues continues transversely until the entire circumference of the aorta is included, and then the vessel forms a double tube. When the blood does not re-enter the aorta, it may push ahead until it reaches the iliac arteries, which is not at all uncommon. While advancing in this direction the blood also dissects backward toward the heart, and finally bursts into the pericardium. Almost invariably in these cases the pericardium is found more or less full, and the pressure of a large amount of blood in the pericardium upon the heart no doubt contributes largely to the fatal result by obstructing the action of that organ.

There may be two pints of blood in the pericardium. Death by rupture is by no means instantaneous. As a rule, the victims continue to live several hours, and even days, after the initial accident.

If the escaped blood coagulates and plugs, several months may elapse before death, as in a case examined by myself. A washwoman while shaking out a heavy piece of wet cloth in November was suddenly seized with severe pain in the chest. This pain continued with other distressing symptoms which disabled her for work, but she did not die until the latter part of the following January. The autopsy revealed a rupture, plugged by a clot, two inches above the aortic valves.

Rupture is usually announced by sharp pain coming on during exertion. There may also be a sense of choking, but this is not invariable.

Generally, the head is clear, and there is no paralysis, but occasionally the patient will swoon and appear collapsed. This of course depends upon the size of the rent and the freedom of the escape of blood. The heart is excited and rapid. The pain is located in the front of the chest or in the epigastrium, and the victims are a prey to great anxiety. Excessive trembling and inability to restrain muscular movements have been noticed. Profuse sweating, together with vomiting and evacuations of the bowels, may occur. Often the only record is, "Obscure symptoms, referable to the heart." There are no characteristics or pathognomonic symptoms of rupture of the aorta. Death is the invariable result, sooner or later, and no treatment has yet been devised to remedy the evil.

Perforation of the Aorta.

This accident causes death very rapidly, but not always instantly. Instances are reported where patients, after the piercing of all the arterial coats, have lived from one hour to three days. A case is reported of a boy sixteen years old who swallowed a needle. It passed through the wall of the oesophagus into the descending aorta, where it remained impacted. Blood poured out into the connective tissue and acted as a plug. Food escaped from the oesophagus, and putrefaction, hemorrhage, and death occurred in ten days.

Occlusion of the Aorta.

Occlusion of the aorta is produced by the formation of a clot. Such clot may occur in any part of the aorta. It may extend out from the heart or from the ductus Botalli. Such localization of the clot, however, is comparatively rare, and the most common seat of occlusion is in the abdominal aorta. The clot is usually associated with an aneurism, but it may sometimes be occasioned by an atheromatous patch. The attack is always abrupt and {825} unheralded by any prodromata. The effect of the clot is to cut off the blood-supply to all organs below the obstruction and disturb the nutrition and function of the same.

SYMPTOMS.--The attack is sudden, and begins with a shooting pain in the abdomen or sometimes under the sternum. Almost immediately the patient loses power over his legs and falls completely paraplegic. At the same time there is an intense desire to stool, which rapidly increases to involuntary evacuations. This lesion may be accompanied by intense pain at the anus. The abdomen may be very tender to pressure. The head is always clear, and the inability to stand is not associated with giddiness. There is no anxiety of the face, and often no sign of distress there.

In a few moments the legs become cold and numb, and patients complain of a sense of deadness in them. The reflexes are entirely abolished. If the renal arteries are occluded the urine is suppressed at first, but reappears as soon as collateral circulation is established through the capsule. The urine rapidly becomes albuminous and foul smelling from the cystitis which develops. In the course of forty-eight hours bullæ appear upon the legs and thighs, bedsores appear over the sacrum; violent cystitis and inflammation of the rectum follow. Some patients live long enough for gangrene of the lower extremities to form.

Great thirst is present, and vomiting with hiccough may aggravate the suffering. The bodily temperature rises above 100° F., while the temperature of the legs falls. It may reach 94° F. There is usually no pulsation perceptible in the abdomen or legs, except in rare cases, when the occlusion is incomplete.

DURATION.--Death results from exhaustion, and occurs in a few days. Two weeks is a long time for life to continue under such circumstances. One case is reported, however, where the occlusion was evidently imperfect and the man survived seven months. Collateral circulation was developed, and the epigastric was mentioned as very much enlarged.

TREATMENT.--The treatment is wholly symptomatic. Pack the extremities for warmth and protect from bedsores if possible.

Stenosis of the Aorta.

PATHOLOGY.--In 1789 attention was first called to a peculiar constriction of the thoracic aorta at the insertion of the ductus arteriosus Botalli. Careful search for this lesion since that date has discovered a series of cases, so that in 1878, Kriegk was able to report 55 instances of it. This constriction is a definite, locally circumscribed lesion, always limited to the same region, and is entirely independent of all other affections of the aorta, although it may itself be the cause of atheroma and aneurism. Beyond the locality specified stenosis of the aorta is an extremely rare affection, except as the result of outside pressure or of local arteritis. Kriegk says he found only two cases of stenosis of other parts of the aorta, although he searched through forty years of medical literature. A few instances of complete obliteration of the aorta have been recorded, and some instances of universal narrowing of the aorta from congenital obstruction in the heart are given.

The constriction at the ductus Botalli is a congenital lesion, and consists of a sinking in of the superior wall of the aorta just at the insertion of the ductus arteriosus or a little above or a little below the same. This sinking may extend to and involve the origin of the left subclavian artery, but this is not usual. The lower wall of the aorta rarely exhibits any depression.

The ascending and transverse portions of the aorta, together with the main branches, become very much enlarged. As the aorta approaches the {826} constriction, its dilatation does not terminate abruptly, but the vessel tapers down to the stenosed section in a funnel shape. Beyond the stricture the descending aorta may recover its normal size or may remain smaller than natural.

In many cases the aorta, barring the stenosis, is perfectly healthy, but the increased pressure behind the obstruction tends to develop atheroma, aneurism, hypertrophy of the heart, and rupture.

Naturally, the lower part of the body must be deprived of a portion of its quota of blood except for the compensatory circulation which develops. This collateral supply may be so complete that the person affected is unconscious of any circulatory deficiency, and may live an active life to old age. An Austrian officer born with this lesion was able to serve in all the campaigns from 1790 to 1815, and then died one day sitting at a card-table. Another man lived ninety-two years with his aorta constricted. The collateral communication between the upper and lower segments of the aorta is established by means of the deep arteries of the neck, the transversus colli, the dorsalis scapulæ, the subscapularis, the intercostals, and the lumbar arteries. The internal mammary also communicates directly with the epigastric artery. These vessels become enormously dilated, so that the superior intercostal, for instance, may equal the femoral in size.

ETIOLOGY.--The lesion is a congenital one, and results from a defective development of the aorta. In early foetal life the descending aorta is a continuation of the ductus Botalli, and the aortic arch looks like an independent communicating vessel. (See fig. 52, A.) As the arch develops, however, it gradually forms a more direct union with the descending portion, until finally the longitudinal axes of the two parts form one uniform curve and the ductus Botalli becomes a side branch. At birth there is physiologically a slight nicking of the upper wall of the aorta at the point where the two sections are joined, and the stricture we are studying seems to be merely an exaggeration of this physiological mark. Just how the depression becomes established is not clear and the explanations given are not satisfactory.

SYMPTOMS.--Indications of this lesion are usually very obscure or absent, and it is only discovered at the autopsy. Severe headache is sometimes complained of, and dyspnoea, cough, hæmoptysis, and vertigo may occur if the stenosis is excessive.

Physical Signs.--One of the most marked signs is the conspicuous beating of the dilated arteries around the shoulders and ribs. These arteries may be seen and felt. If the patient is very fleshy, however, they may be {827} concealed. There is usually a marked contrast between the arteries of the upper and lower extremities. The former are full and strong, while the latter are weak and barely perceptible. In many cases it is almost impossible to feel any pulse in the abdominal aorta or in the crural arteries. A loud murmur is also described as occurring over the aorta. This murmur is post-systolic, and does not correspond to any of the ordinary aortic murmurs.

DIAGNOSIS.--This lesion has rarely been suspected, much less diagnosed, during life, but a better knowledge of its peculiarities may lead to more frequent recognition of it hereafter. When the collateral circulation is fully established, stenosis of the aorta could hardly be mistaken for anything else. The resulting excessive dilatation of the great vessels at the root of the neck may simulate aneurism, and it should be borne in mind that aneurism is liable to follow stenosis.

PROGNOSIS.--The death of most of the victims of stenosis of the aorta is directly referable to the lesion itself, although the existence of the trouble is compatible with long life and active occupation. The duration of life and the amount of suffering caused by stenosis both depend upon the amount of obstruction in the aorta and the efficiency of the collateral circulation.

In 49 cases death occurred in the following manner:

Rupture of the aorta 10 times. Rupture of the heart 3 " Sudden pulmonary oedema 4 " Cardiac failure 8 " Apoplexy 4 " Pneumonia 8 " Capillary bronchitis 4 " Paralysis 2 " Pleurisy 1 time. No cause assigned 5 times. -- 49 times.

TREATMENT.--Obviously, no treatment for the lesion itself is possible. If recognized, the existence of the sufferer may be prolonged by adopting moderation in all things as the maxim of his life. Subjective symptoms of discomfort must be combated on general principles as they arise.

{828}

DISEASES OF THE CORONARY, PULMONARY, SUPERIOR MESENTERIC, INFERIOR MESENTERIC, AND HEPATIC ARTERIES, AND OF THE COELIAC AXIS.

BY E. G. CUTLER, M.D.

DISEASES OF THE CORONARY ARTERY.

Chronic Endarteritis (Arterio-sclerosis; Atheroma).

This is the most important inflammatory disease of the coronary artery which has been observed. It resembles chronic endarteritis elsewhere, and frequently accompanies the same affection of the aorta, though it may occur alone. The disease may be general, affecting both coronary arteries equally, or one may be more involved than the other, or the disease may be confined to one vessel or to even a small branch.

ETIOLOGY.--Chronic endarteritis of the coronary arteries is especially a disease of middle and advanced life. It occurs most frequently in the male sex. The coronary artery stands fifth in the order of frequency in which the vessels are attacked. The disease is attributed to the misuse of alcoholic drinks, syphilis, chronic lead-poisoning, gout, and chronic kidney disease, by encouraging an early senescence of the tissues, and hence favoring the occurrence of the arterial change.

SYMPTOMS.--There are no symptoms which are peculiar to the disease, those which exist being due to the consecutive changes in the substance of the heart. We may divide cases for convenience of description into those with an acute course and rapid death; those pursuing a subacute course; and, finally, those having a chronic one. In the first instance, sudden death either occurs in a person apparently in perfect health after the manner of a syncope, as in one getting out of bed or standing on the street, while straining at stool, or under sudden emotional excitement. Death may not follow on the instant, but occurs in the course of a longer or shorter time. The attack begins with pressure in the cardiac region, anxiety, restlessness, streaming pain. The complaints and anxiety increase; the breath becomes short and troublesome, the pulse small, frequent, and intermittent; finally, collapse occurs, with oedema of the lung. Death takes place with either a clear mind or slight delirium. Such a fatal ending may cover a day or two or only a few hours. Almost always careful subsequent inquiry elicits the fact that for some time past respiratory or cardiac difficulties have existed, which appeared and disappeared and were not regarded as serious or suspicious. Sudden death may also occur in cases of protracted chronic heart disease following arterio-sclerosis, with an old history of the symptoms of angina pectoris, under the appearance of a fainting fit or of a severe attack of angina or oedema of the lung lasting several days. In such a case rupture of the heart may be found, with bloody infiltration of the cardiac {829} muscle and effusion of blood into the pericardium. In other cases there may be small hemorrhages, often with pronounced infarct formation and softening. In still other cases neither hemorrhage nor infarction is found, but fatty degeneration of the muscle or beginning softening. The sclerosis in such cases is usually very distinct, and affects the trunk and anterior descending branches of the left coronary artery. Sometimes it is hard to find the diseased spot, as it may be circumscribed or on a side branch. In the last-mentioned cases, where sudden death occurs in a chronic process, no post-mortem signs of acute disease are usually found. A chronic fibroid process, with atrophy, exists, which has run a tolerably latent course and leads to death under the appearance of sudden cardiac weakness.

PATHOLOGY.--There are two stages of chronic endarteritis: 1. The stage of simple thickening of the intima; 2. The stage of ulceration and the accompanying further changes.

At first, the normal smooth, shining inner surface of the intima is interrupted here and there or in long stretches by flat rounded elevations, which gradually merge into the healthy surrounding tissues, and are characterized by a paler, more transparent character, and at the same time softer but elastic consistence. The surface of these thickenings, which are frequently located at the point where branches are given off, is either perfectly smooth or slightly wrinkled. Besides these translucent spots there are similar ones which are opaque, whitish or yellowish in color, and have a somewhat rougher surface. Lastly, there are very pronounced thickenings with a yellow color. In the slighter degrees these spots occur singly. In the more pronounced cases they may take up the greater part of the surface; the wall of the vessel is thickened, the inner surface is uneven, and the vessel itself more or less dilated. In the beginning the intima retains its shining surface: after the disease has lasted a long time this is changed, and the second stage appears. Roughnesses, erosions, and ulcerations appear, or more commonly calcification of the wall. This latter appears at first as little thin layers, and finally in large shield-like plates of lime salts, which may occupy the whole circumference of the artery and change it into a stiff, bony tube. It is found where ulceration has occurred, and often without the appearance of the latter. Together with the rigidity of the wall there occurs a slight tortuousness of the vessel. At first the superficial layers of the intima are soft; next they become more sclerosed, and their tissue denser and finally striated; or disintegration, commencing deep in, may reach as far as the surface and lead to an atheromatous ulcer. A more or less abundant deposit of lime salts follows in the sclerosed layers of the intima, leading to the formation of homogeneous plates as hard as bone.

The result of the process at first is diminution of the calibre of the vessel, next diminution of the elasticity and contractility of the artery: it loses its resistance and suffers dilatation in consequence of the blood-pressure, and may attain aneurism. Or if calcification occurs early the diminution of the lumen remains, or perhaps even increases, and may reach an almost complete occlusion of the vessel.

The effects on the heart which follow this form of disease of the coronary artery, though described in another place, had best be enumerated here: 1. The flow of blood not being sufficiently interfered with to cause disease, the heart may remain unchanged. 2. Hemorrhagic infarction may result, accompanied by simple fatty degeneration or softening, which is the most frequent cause of rupture of the heart. 3. Fibrous degeneration or myocarditis may occur, leading perhaps to aneurism of the heart. 4. There may be a combination of these two--a greater or less marked fibrous degeneration, to which a fresh hemorrhagic softening is added.

DIAGNOSIS.--There are no pathognomonic symptoms of this disease, and {830} it is doubtful if a diagnosis can be arrived at. When the conditions spoken of under Etiology pertain, and certain of the symptoms mentioned in connection with the disease are present, a suspicion of chronic endarteritis of the coronary artery may be entertained with some degree of probability.

PROGNOSIS.--This must necessarily be unfavorable where the suspicion of the disease is entertained.

TREATMENT.--Little is to be expected in the way of treatment beyond mere palliation. In the rapid cases death occurs so soon that the medical attendant barely has time to reach the patient. In those cases which last longer the treatment must bear special reference to the symptoms. Pain and spasm may be allayed by opiates or by the inhalation of some anæsthetic cautiously administered, as ether or nitrate of amyl, or by the cautious use of nitro-glycerin and the application of counter-irritants, as mustard, over the cardiac region. Digitalis is to be used with the greatest caution, if at all, as its action may be positively harmful. The same is true of the bromides.

Obliterating Endarteritis.

Besides the preceding, another form of endarteritis has been met with in the coronary artery--namely, the obliterating endarteritis, more especially found in cases of syphilis and occurring in the smallest branches. It is characterized by a gradually increasing thickening of the intima through the formation of a connective tissue rich in cells, and which leads to a narrowing, or even complete closure, of the lumen of the artery. This thickening may involve one side of the artery or its whole circumference. The inner surface of the intima on microscopic examination is found to be covered by a layer of intact endothelium where occlusion is not complete. There is deposit of neither fat nor lime salts in the thickened intima. The outer coats of the artery show little change.

The disease is accompanied by indurating myocarditis. Its symptoms are those seen in this disease--namely, weakened cardiac activity, cardiac dilatation and irregularity, possibly cardiac murmurs, an accentuated pulmonary second sound, a pulse of moderate frequency, weak and non-rhythmical, dyspnoea, cough.

DIAGNOSIS.--Impossible.

TREATMENT.--Purely symptomatic.

Aneurism.

Aneurism of the coronary artery is of rare occurrence. There is no place of election for the disease, all parts and each artery being alike liable to be affected.

ETIOLOGY.--The most common cause of the affection is chronic endarteritis, where, through disease of the intima, the resistance to the blood-pressure is diminished. Embolism is another though far less frequent cause of the disease, several such cases having been reported; and other highly suggestive cases are on record in which embolism of the artery had occurred, with the production of considerable dilatation for a short distance above the obstruction.

PATHOLOGY.--This does not differ from aneurism in other vessels. The number may be from one to many, usually not more than two or three. The size is generally that of a pea, often it is smaller, and sometimes it is as large as a large nut. The termination is usually rupture with fatal hemorrhage, and in far the majority of cases this occurs into the pericardium.

{831} SYMPTOMS.--In most all of the cases I have found recorded there were no symptoms till rupture of the sac occurred, giving rise to death from hemorrhage. Then those symptoms which might be expected occurred--namely, great præcordial pain, dyspnoea, suffocation, tumultuous heart, irregular and intermittent pulse, and sudden death.

DIAGNOSIS, PROGNOSIS, and TREATMENT need not be considered, as the disease is not recognizable.

Occlusion of the Coronary Artery.

Occlusion, more or less complete, of one or both of the orifices of the coronary artery has been met with in connection with chronic endarteritis of the root of the aorta. The accompanying sclerosis may draw the orifices up like the strings of a purse, or a calcific plate may extend from one side, or perhaps, detached, may lie simply applied to the orifice. In rare cases the chief disease may be in the artery itself, one of the main trunks or a branch being affected.

The PATHOLOGY is the same as that already described under Endarteritis, stenosis being an early consequence of the process, and persisting, or even increasing, to the last.

The SYMPTOMS observed in such cases are neither peculiar nor diagnostic. They consist of those depending on the concurrent affections, as of the cardiac valves, muscular tissue, or aortic arterio-sclerosis. Prominent among them are dyspnoea, palpitation, sudden cardiac distress, painful pressure in the region of the heart, great anxiety; at last pallor of the skin, feeble cardiac impulse, indistinctness of the cardiac sounds, the right ventricle continuing to contract forcibly till the end. There is oedema of the lungs at last, and on post-mortem examination fatty degeneration of the heart-walls is found as a secondary consequence of the occlusion.

Embolism and Thrombosis.

Although these conditions are rarely found, yet a sufficient number of cases is already on record to enable us to form a tolerably good idea of the symptoms which accompany them. These latter in embolism remarkably resemble those observed in the lower animals on ligation of the coronary arteries. In the animals experimented on a rapid enfeeblement of the heart's action ensued. The phenomena occurred in the following order: First, there was retardation of the rhythmical cardiac contractions, the left ventricle being primarily affected. At first, the right ventricle beat faster, and then gradually became slow. The beats became slower and slower till they ceased, the left ventricle ceasing to contract a little before the right. The second result was a gradual loss of power of the cardiac contraction. The third result was the gradual distension of the left auricle when the left coronary artery was compressed. The auricle swelled up more and more, became bright red, and the rhythmical contractions changed to oscillatory movements, which ultimately ceased entirely. The right ventricle and auricle continued to contract powerfully, and the left ventricle feebly.

EMBOLISM.

ETIOLOGY.--Rheumatism with its attendant complications--that is, disease of the valves, and especially of the aortic valve, atheroma of the coronary artery and possibly cardiac or other thrombosis--forms the chief cause of {832} embolism, a small fragment of tissue being borne away by the current of blood.

SYMPTOMS.--These are acute paralysis of the heart's movements, pain, feeling of impending annihilation, retained consciousness, and regular respiration. Nausea and vomiting have been observed. The lips are livid, extremities cold and covered with a clammy sweat. In one case there was inability to lie down. No pulse could be felt in any of the accessible arteries, and neither apex-beat nor heart-sounds could be detected. The ear applied to the cardiac region could hear only a kind of cardiac tremor, which was very like the sound of a vibrating steel plate. There was no loss of consciousness. The respiration was regular and rhythmical, not exceeding eighteen or twenty in the minute. The patient died twenty hours after the first symptoms.

DIAGNOSIS.--Although a positive diagnosis is impossible, the negative pulmonary physical signs, the regular and rhythmic character of the respiration, and the enfeeblement of the heart's action may lead to a very strong suspicion of embolism of the coronary artery.

PATHOLOGY.--A small coagulum may stop up the main branch, usually the left anterior, of one artery, or both arteries may be occluded by a larger coagulum. In one instance an atheromatous softened patch ruptured into the anterior portion of the left coronary artery, and filled up the lumen with a soft putty-like mass (the sculptor Thorwaldsen). A fatal issue is likely to occur in a very short time, as the anastomosis cannot be sufficient for the sudden demand.

PROGNOSIS and TREATMENT need hardly be considered, as the affection is necessarily fatal in cases which can be made out.

THROMBOSIS.

The same causes which give rise to thrombosis elsewhere are operative in this case. They are chiefly arterio-sclerosis and rheumatism.

SYMPTOMS.--There have been observed slight tightness in the cardiac region, lasting a few days, or a sense of oppression or constraint at the back of the sternum. The pulse has been quickened, but is usually very much slowed and very feeble; it has been observed as low as eight beats in the minute. There is a sense of great lassitude and feebleness of all the limbs. The respiration is normal in rhythm and frequency. Auscultation reveals nothing but ordinary respiration till near a fatal issue, when moist râles indicative of oedema of the lungs are heard. Percussion gives at all times a normal resonance. There is no dyspnoea. The heart-tones are clear, though weak, if occlusion is not complete or anastomosis is perfect. (West was able to inject the arterial system of the heart completely from one coronary artery, the other having been tied.) If there is complete obstruction, we may expect to hear a fremitus such as is produced by muscular spasm instead of normal heart-sounds (observed in two cases). The skin of the body and face is cool, pallid, and covered with sweat. The visible mucous membranes are anæmic and pale. The mind is clear.

DIAGNOSIS.--The cardiac feebleness and progressive slowness, together with the absence of symptoms connected with the lungs, might lead one to suspect the presence of thrombus.

PROGNOSIS.--If a large branch of the artery is affected a fatal termination is probable. If, on the other hand, the affection occurs in a small branch, there is reason to believe that the circulation is sometimes re-established through anastomosis.

TREATMENT must be purely symptomatic.

{833} Rupture of the Coronary Artery.

This may occur independent of aneurism. There are no premonitory symptoms in some cases, death taking place suddenly. In other cases vague and irregular symptoms lead the patient to understand that he is not in perfect health. The symptoms of the disease are not characteristic. Those which have been recorded are a difficulty of breathing, a sense of constriction across the chest, or a pain and feeling of anxiety in the præcordia; a frequent, feeble, and perhaps very irregular pulse; epigastric pain and tenderness. The extremities are cold. The mind remains clear. The physical signs are increased area of flatness in the cardiac region, due to the escape of blood into the pericardium, and scarcely audible cardiac sounds. The symptoms may extend over a period varying from a few moments to several days. Usually, some of the changes indicative of arterio-sclerosis are found in the artery.

DISEASES OF THE PULMONARY ARTERY.

Acute inflammation of the coats of the pulmonary artery has only been found associated with the pyæmic process as circumscribed abscesses of the wall.

Chronic Endarteritis (Atheroma; Arterio-sclerosis).

Endarteritis of the pulmonary artery, though quite rare, is occasionally met with in persons the subject of rheumatism, gout, syphilis, or alcoholism. It is seen only when the pressure is abnormally increased in the pulmonary vessels, especially in diseases of the mitral valve. It is usually accompanied by a more pronounced disease of the aorta, but is occasionally seen alone. The extent of disease is hardly ever so great as that found in the other large vessels, and at most amounts to the presence of prominent hard yellow or gray patches in the intima, with perhaps ulcerated surfaces, and rarely containing a deposit of lime salts. Complete rigidity has been observed extending far into the lung. The wall of the vessel may be irregularly dilated and its elasticity diminished. Usually, the disease is in a much milder form, presenting perhaps a small amount of fatty degeneration of the intima, and is not infrequently associated with mitral stenosis or insufficiency (notably the former), pulmonary fibrosis or emphysema, with accompanying hypertrophy of the right ventricle. No symptoms have thus far been found to be distinctly referable to atheroma of this artery.

Dilatation and Aneurism.

Dilatation of the pulmonary artery from primary disease of its walls is of so rare occurrence that it may be merely mentioned. It depends on chronic endarteritis, just spoken of. Where, on the other hand, there is great pressure in the pulmonary circulation, as in marked mitral stenosis, or insufficiency, collapse, or emphysema of the lung, with great hypertrophy of the right ventricle, general dilatation of the pulmonary artery may take place. The artery has been found to be six and a half inches in circumference in a case of emphysema, the normal average being three and a half inches; the semilunar valves were insufficient, and the walls of the artery very much diminished in thickness. From this as a maximum all degrees of dilatation have {834} been recorded, with sometimes thickening and degeneration of the coats, at others thinning with or without degeneration.

A systolic murmur has been observed over the artery when the dilatation was considerable. The second pulmonary sound is usually strengthened (unless the elasticity of the pulmonary artery is very much diminished or the blood-pressure lowered in the right ventricle by changes of its walls, or the pulsation is very quick and irregular). A circumscribed dulness on percussion has been found in a few cases at the left edge of the sternum, when the position of the heart was normal, between the second and third cartilages. Sometimes there is a double impulse, a systolic thrill, or more often a systolic pulsation, felt in this position without any perceptible dulness, the edge of the lung being retracted and the dilated artery taking its place. It is to be borne in mind, however, that this sign (impulse, thrill, or pulsation) may be present without any dilatation of the pulmonary artery or hypertrophy of the ventricle, when inflammatory contraction of the lung has occurred or the respiration is superficial, as may happen in phthisical subjects, women, feeble and anæmic individuals, pregnant women, convalescents, and persons afflicted with acute rheumatism. In such persons the pulmonary second sound frequently seems to be unusually loud when compared with the aortic second sound, without any evidence of hypertrophy of the right ventricle being present. The determination of the position of the lung establishes the diagnosis in such cases. On the other hand, a lung dilated by emphysema may interpose and completely cover the heart and pulmonary artery, which, though dilated, may thus be masked.

Aneurism of the trunk or primary branches of the pulmonary artery, on the other hand, is an exceedingly rare disease. But few cases are on record. Aneurisms may be spindle-shaped or sacculated, of moderate size, and are usually situated on the trunk. Lividity of the face, dyspnoea, cough, dysphagia, headache, pain in the chest and epigastrium, are the principal symptoms; and a systolic pulsation (sometimes also diastolic) between the second and third left ribs near the sternum, more or less prominence here, a superficial rough systolic murmur propagated to the left and upward, a purring thrill, and flatness on percussion in the same region and a little above it, are the principal physical signs which have been recorded.

But the physical signs and symptoms above enumerated are not all present in each case, nor are they when present distinctive of pulmonary aneurism. Dysphagia is mentioned in but a single case, dyspnoea is not constant, and cyanosis was at times absent. Also, the physical signs were not constant. Even if all were present they might be produced, as has been the case, by aneurism of the left wall of the aorta, infiltrated lung-tissue, or by a solid tumor lying over the vessels. The locality of the cardiac hypertrophy and dilatation aids in establishing the diagnosis. If it is on the left side of the heart, aneurism of the aorta is indicated; if it is on the right side, pulmonary aneurism. These aneurisms tend to rupture into the pericardium sooner or later.

Dissecting aneurism of the pulmonary artery has been observed once. It was of small extent.[1]

[Footnote 1: _Bul. de la Soc. Anat. de Paris_, 1881, pp. 589-591.]

Stenosis of the Trunk or Main Branches of the Pulmonary Artery.

Narrowing of the trunk or of one of the main branches of the pulmonary artery is of very rare occurrence. It may follow compression by an aneurism of the ascending or transverse portion of the aorta, compression by tumors in {835} the mediastinum, as from new growths or enlarged glands; it may be caused by cicatricial contraction following mediastinitis, inflammation of a portion of lung or of the bronchial glands, or it may follow disease of the coats of the artery (endarteritis).

The phenomena produced by stenosis of the trunk of the pulmonary artery are similar to those found in stenosis at the orifice, which are treated of in another place. They are anæmia of both lungs, accompanied by persistent dyspnoea with occasional exacerbations (the patient assumes a horizontal position either habitually or during the paroxysm--a fact of true diagnostic importance [Chevers], as in all other forms of disease of the heart and great vessels the patient breathes easier when the shoulders are raised. But in this the dyspnoea results from insufficiency of the supply of blood to the lungs and system generally, and hence the recumbent posture affords relief by removing the impediment of gravity, and thus promotes the supply of blood to the brain), congestion, dilatation and hypertrophy of the right side of the heart, cardiac palpitation, and finally general venous congestion. Hypertrophy of the right ventricle is shown by increase in the transverse measurement of the cardiac area of flatness and increase in the force of the cardiac impulse. The artery up to the point of constriction is dilated; the second sound is abnormally loud and accentuated. Pulsation may be felt and a systolic murmur heard in the second left intercostal space (observed in the right once), propagated upward to the neck at the left of the sternum, or heard in the interscapular space close to the spinal column.

PROGNOSIS is unfavorable.

There is nothing to be gained by treatment.

Rupture of the Pulmonary Artery.

Violent effort and great excitement have been followed by rupture of the trunk or a main branch of the pulmonary artery. In the majority of cases the coats were degenerated, though this was not always the case (Chevers). Death is often instantaneous, but sometimes is delayed some hours. In one case observed by Ollivier the duration was twenty-seven hours.

Thrombosis and Embolism.

The pulmonary artery, from its position, is especially prone to become plugged, either by substances coming from other parts of the body or by coagula originating in the vessel itself. Pieces of disintegrated coagula from the systemic veins, the contents of echinococcus cysts ruptured into the venous current, fragments of new growths, are carried to the heart and pass into the pulmonary artery, or large thrombi may be detached from their position in a vein and lodge in the trunk or main branches of the pulmonary artery.

Primary thrombosis of the pulmonary artery is very uncommon. In certain septic conditions, in parturient women, in typhoid fever, and in extreme anæmia thrombosis of the pulmonary artery may occur. It commences perhaps in the right ventricle or at the pulmonary valves, though it is also seen farther up.

SYMPTOMS.--The severity of the symptoms depends on the completeness of the obstruction. There is dyspnoea, more or less marked according to the size of the thrombus or embolus, pain in the præcordia, great distress, anxiety, faintness, sense of suffocation, tightness in the chest, palpitation, lividity and extreme pallor, cold sweats, an almost imperceptible pulse, great restlessness, {836} and occasionally convulsions. The mind remains clear. The symptoms develop gradually or rapidly--in the former case depending on the slow increase of a small thrombus--and remissions are often seen; in the latter case depending on the sudden lodgment of an embolus of large size. Sometimes the symptoms are extremely marked, and death takes place in a few minutes. The appearances are not those of asphyxia, and death is usually attributed to want of arterial blood-supply to the brain and medulla oblongata, and not to suffocation or paralysis of the heart.

Percussion shows a normally resonant chest. Auscultation gives normal breath sounds with free inspiration and expiration. There is very likely a basic systolic murmur conducted along the course of the pulmonary artery, but this is not constant. The cardiac second sound and impulse are increased. At the post-mortem examination the heart is found in diastole, the left cavities and pulmonary veins empty, the right cavities filled with blood, and the cardiac veins strongly distended.

DIAGNOSIS.--The diagnosis is often uncertain. When not developing with extreme rapidity the symptoms are very similar to those caused by stenosis of the pulmonary artery, and in the suddenly fatal cases they are almost identical with rupture of the heart or rupture of a thoracic aneurism, or even angina pectoris. The history of an antecedent thrombus or of a disease of the heart which is likely to be accompanied by thrombus, together with the absence of physical signs, render a diagnosis many times probable.

PROGNOSIS.--To be regarded as of the gravest character.

TREATMENT.--In the rapid cases death occurs before anything can be attempted. In the less severe cases absolute rest must be enjoined, and free stimulation with brandy, ammonia, and ether attempted. It might be worth while to place the patient with the head lower than the body, to favor the flow of blood to the brain.

DISEASES OF THE SUPERIOR MESENTERIC ARTERY.

Aneurism.

Aneurism of both the superior and the inferior mesenteric arteries occurs. The former is the more frequent, though still a rare disease.

The symptoms are pain in the epigastric and lumbar regions, a globular pulsating tumor in the median line, the pulsation being accompanied by a bellows murmur. The tumor has been seen in at least one instance to be so large as to press on the renal arteries. Rupture is apt to take place with the signs of internal hemorrhage. The cause of the disease is the same as of aneurism elsewhere. Embolism is said to be a not infrequent precedent. The aneurism is seldom larger than a hen's egg, and is usually globular.

A positive DIAGNOSIS of the locality of the aneurism is not possible.

The TREATMENT must follow individual indications. Compression has been successful in a few instances.

Embolism.

Several cases where the superior mesenteric artery was found at autopsy to be completely occluded by coagulated fibrin were mentioned by Tiedemann in a work published in 1843. Virchow first described the characteristic {837} post-mortem appearances which follow this lesion in his _Gesammelte Abhandlungen_, and since then records of cases have been numerous.

CLINICAL HISTORY.--In by far the majority of cases there is an evident source for an embolus. Pain in the abdomen is the first symptom, and usually remains one of the most prominent throughout. At first it may be a dull aching just below the borders of the ribs, but soon there is superadded paroxysmal pain resembling colic, and which may at times even be relieved by pressure. The occurrence of this colic in cases where embolism might happen ought to put the physician on his guard for other symptoms; for, though insufficient in itself to establish a diagnosis of embolism, the presence of a colic resisting treatment in the course of cardiac disease justifies the suspicion that this may be the case. The pain is usually located near or above the umbilicus.

Intestinal hemorrhage occurs in nearly every case; death may take place before any change in color of the stools is observed or any blood appears at the anus, but on post-mortem examination blood is found in the intestine. The cause of this hemorrhage is the infarction of the intestine analogous to that which takes place in other organs supplied by end arteries, the superior mesenteric having been proved experimentally to be functionally such an artery, owing to its great length, the extent of tissue supplied by it, and the comparative smallness of the vessels with which it anastomoses on the borders of its territory. The collateral circulation is thus so long in being established that ample time is allowed for those disturbances of nutrition in the walls of the vessel which render them permeable and allow the blood to escape. In view of the hemorrhage certain other symptoms are readily accounted for, as, for example, pallor of the face and surface of the body, the considerable and rapid fall of the temperature, syncope, hæmatemesis, diarrhoea, and melæna. These two latter symptoms are important though inconstant. There is reason to believe that the first effect of the embolism is to paralyze the bowel and prevent peristaltic action. Diarrhoea is of frequent occurrence, and may be profuse, the stools remaining of their natural color; or fresh blood may be passed at first from the rectum, followed by the continuous passage of tar-like masses; or the stools may be of pulpy consistence, mixed with blood, or consisting of tarry blood. Lastly, profuse hemorrhage may take place in which the stools resemble tar-water. The character of the blood does not give any kind of clue to the locality of the lesion.

Vomiting is a frequent symptom, and may consist of altered blood of variable consistency. A fall in temperature can often be determined by the thermometer, especially after severe hemorrhage. Not rarely the temperature is normal or may be even increased, especially if secondary inflammation has set in.

Tension and tympanitic swelling of the abdomen may occur or fluid may be detected late in the case, these being evidence of peritonitis.

PATHOLOGY.--Before proceeding to consider the pathological changes occurring in embolism, a few words on the blood-supply of the intestine might perhaps render what follows clearer. The superior mesenteric artery supplies the whole of the small intestine except the first part of the duodenum; it also supplies the cæcum and the ascending and transverse colon. The inferior mesenteric supplies the descending and sigmoid flexure of the colon and the greater part of the rectum. The anastomoses are as follows: The pancreatico-duodenalis, a very small artery and a branch of the hepatic, anastomoses with the first branch of the superior mesenteric, also a very small artery and given off under cover of the pancreas. The middle colic artery anastomoses with a branch of the inferior mesenteric. Both these arteries are given off from the main trunks of the arteries.

The experiments of Litten in 1875 show that the superior mesenteric artery, {838} though not so anatomically, is functionally a terminal artery, the anastomosis not being developed with sufficient rapidity in case of extensive embolism to ensure the integrity of the circulation.

1. The result of sudden total closure by embolism of the trunk of this artery, therefore, is precisely like that of ligature of this artery in animals, and is first to produce sudden abdominal pain, attacks of colic, vomiting, uncontrollable intestinal hemorrhage, death. The intestine from the lower transverse portion of the duodenum to the middle of the transverse colon is found to be suffused, brown-red, blackish, or grayish. All the layers are swollen; innumerable capillary extravasations of small and great extent are seen, with venous hyperæmia and oedematous infiltration. In other words, there occurs necrosis with oedema and hemorrhage in all those portions of the intestines which are supplied by this artery.

2. Closure of large branches by embolism gives rise to infarction of the portion of intestine concerned, followed by death. The symptoms differ only in intensity, if at all, from the preceding. A case has been seen where there was every reason to believe that embolism had occurred, and yet the patient recovered. (The patient, suffering from acute rheumatism complicated with peri- and endocarditis, suddenly developed profuse intestinal hemorrhage of tar-like color, which was repeated twice. Colic pains, tympanites, depression of the temperature of the body, followed. At the same time symptoms of embolism of various other arteries were present. Recovery took place after eight weeks.) This result of course depended on the subsequent perfection of the collateral circulation.

3. Closure of the smallest branches may produce the same kind of symptoms as the above, though less in degree. Limited portions of intestine have been found to be in a gangrenous condition from embolism of very minute branches, more especially when the embolus extended well into the artery. In place of gangrene of the intestine ulcers of the mucous membrane have been seen independent of typhoid fever or tuberculosis. Considerable stenosis has followed such ulcers.

The affected portion of intestine in embolism is found to contain a variable amount of blood mixed with the other contents of the gut. Peritonitis, dry and limited or general and accompanied by effusion, is the rule. The mesenteric glands are found enlarged and succulent, with perhaps here and there necrosed spots. Thrombosis of the corresponding veins is not uncommon. Large collections of blood under the peritoneum and in the mesentery have been observed. The color of the mucous membrane has been slaty, and a diphtheritic appearance has been observed.

DIAGNOSIS.--The following are the most important points in forming a diagnosis: 1. A source exists from which an embolus might be derived. 2. Profuse and even exhaustive intestinal hemorrhage sets in, which can neither be explained by primary disease of the intestinal walls nor by hindrance to the portal circulation. 3. There is a rapid and considerable fall of the temperature. 4. Pain in the abdomen comes on, which may resemble colic and be very severe. 5. Finally, tension and tympanitic swelling of the abdomen occur, and there may be fluid in the abdominal cavity. 6. Evidence of embolism of other arteries may have been obtained before the symptoms of embolism of the superior mesenteric artery come on, or such evidence may appear at the same time as the latter. 7. Palpation may reveal the presence of collections of blood between the folds of the mesentery.

PROGNOSIS.--The prognosis in embolism of the superior mesenteric artery, though not absolutely bad, is exceedingly grave. It must be borne in mind that the symptoms of occlusion of one of the large branches are similar to those where the main stem is involved, while the probabilities of recovery in the former are much greater, as already explained, from the shorter extent of {839} the anastomosis. There is evidence that recovery from the immediate effects of embolism may take place even where subsequent ulceration has been so great as to cause complete closure of the intestine through cicatrization. (A case is related by Parenski where the patient was operated on for stricture of the bowel, and only at the autopsy was it discovered that the stricture was due to cicatrization from ulceration caused by embolism of one of the branches of the superior mesenteric.) There are at least three cases of recovery on record where occlusion of the main stem was supposed to have taken place; but inasmuch as the situation of the embolus cannot be determined with certainty if the patient recovers, these cases are open to the suspicion that one or more of the larger branches only were occluded. The profuseness of the hemorrhage, though it may imperil the life of the patient from exhaustion, bears no constant relation to the gravity of the case. Copious and repeated hemorrhages per anum took place in cases of recovery, while in other fatal cases this symptom was entirely absent. Extreme fetor of the stools must be regarded as of evil omen, as it may be the evidence that gangrene of the bowel has taken place.

TREATMENT.--One of the first symptoms calling for relief is the colic, which is best met by morphia given subcutaneously or by suppository. For the hemorrhage ergot by the mouth and alum enemata have proved serviceable, or the application of ice to the abdomen. The lowering of the heart's action by sedatives is to be avoided when we remember that their use would lower the blood-pressure, and thus tend to retard the establishment of the collateral circulation.

Thrombosis.

The symptoms of thrombosis have not been determined apart from embolism, and it is doubtful if the affection proves fatal unless the extent of artery involved is very considerable or the formation of the thrombus is very rapid, for the anastomosis is gradually made compensatory. In either of the latter cases the symptoms are identical with embolism, and the pathological appearances are the same. With regard to treatment, general indications must be pursued.

Endarteritis.

This disease is met with, but it is usually slight and unaccompanied by symptoms.

DISEASES OF THE INFERIOR MESENTERIC ARTERY.

Aneurism.

Aneurism of this artery has been seen after death. The diagnosis could not be made, in all probability, during life. Pain might be a prominent symptom, though not necessarily, as many of the aneurisms of the abdomen are unattended by any symptoms. Rupture is not unlikely as a termination.

Embolism.

Embolism has been observed. Sudden pain in the abdomen comes on, followed by vomiting and diarrhoea. The patient looks miserably; the {840} belly is drawn in and painful on pressure almost exclusively in the left iliac region. Severe spontaneous colic-like pains continue, with occasional vomiting and diarrhoea. At first the stools are feculent and pap-like; then they begin to smell bad, and even stink. Red blood is passed. Soon there is a mixture of blood and slimy masses. Finally, the stools are slimy, blackish, almost tar-like, and have a terrible odor, and are passed with griping and tenesmus. Occasional vomiting still continues. The pulse becomes smaller and more frequent, and gradually irregular and intermittent. Soon collapse and death follow.

The predisposing and exciting causes are the same as in embolism of the superior mesenteric artery.

The duration is usually short, lasting from a few hours to three or four days. The termination is ordinarily fatal, though doubtless cases of recovery have occurred, as stated under Embolism of the Superior Mesenteric Artery, the size and position of the embolus not precluding the possibility of the establishment of collateral circulation.

Complications are varying degrees of peritonitis, evinced by tympanites, pain, and tenderness, either localized or diffused, and later by the occurrence of effusion. Sequelæ, when the disease is not immediately or rapidly fatal, are ulceration of the colon with subsequent cicatrization and contraction.

PATHOLOGY.--The mucous membrane of the descending colon, sigmoid flexure, and rectum is somewhat swollen, strongly reddened, and contains ecchymoses and extensive suffusions of blood; or the color may be blackish or slaty and the surface sloughy.

DIAGNOSIS.--The diagnosis can only be made by exclusion. The same points are to be carefully verified as in embolism of the superior mesenteric artery, only the pain and symptoms are in a different place, and the secondary peritonitis also begins on the left.

PROGNOSIS.--The prognosis is very grave, but recovery may take place, contractions or constrictions being left behind.

TREATMENT.--The treatment combines perfect rest, the exhibition of wine, opium, vegetable astringents, and the subcutaneous injection of morphia.

ANEURISM OF THE HEPATIC ARTERY.

The tumor varies in size from a hazelnut to a child's head, and is egg-shaped. Pain in the epigastrium and right hypochondrium or upper abdominal region is a characteristic symptom. At first the pain is not severe, and is occasional, recurring after a pause of several months' duration; later it becomes very severe and lasting. The abdomen is not tender to the touch or on pressure during the remissions from the attacks of pain, but after rupture of the aneurism, whether temporary or lasting, it is very severe. The abdomen is sometimes distended, at others not. The tumor, owing to its position, cannot be felt, nor can pulsation be detected, as the wall of the aneurism consists of connective tissue and blood-clot, and the stream of blood coming from a small artery is slow. In but a single case has increase in size of the spleen and liver been observed. The functions of the stomach and intestines remain normal in spite of the pain. The locality of aneurism of the hepatic artery is such as to readily cause temporary or lasting icterus--a phenomenon which occurs in perhaps two-thirds of the cases. Rupture, with the ordinary signs of internal hemorrhage, seems to be the usual termination. Inflammatory processes or fever does not follow hemorrhage into the abdomen. {841} If perforation occurs into the gall-bladder, a gall-duct, or the intestine, the hemorrhage may appear to be moderate. In such instances repeated discharges of blood may occur from the intestine, or at the same time may be thrown off from the stomach.

There is no means of determining how long aneurism of the hepatic artery may exist without giving any kind of sign of its presence. Judging from analogy, it is very probable that a considerable time may elapse before the disease is observed. Since pain in the abdomen is the first pathological indication, and rupture the last, we may measure the probable duration of the disease by these phenomena and also by the clinical course. This was not over ten days in two cases, and in three cases it was three to four months. Since aneurisms of the hepatic artery, even when they have reached their greatest dimensions, are not palpable, the pains which appear with them have in themselves no diagnostic worth. The same is true of the icterus which appears sooner or later. It is only after rupture has occurred that all the chances are so placed that a comprehensive estimate of them may be made and a diagnosis arrived at by exclusion. The fact that the function of the stomach remains unchanged in spite of rupture (hemorrhage), and the totally unchanged character of the blood-clots vomited, enable us to locate the situation of the hemorrhage as outside the stomach. If at the same time there is an alternate relation between the occurrence and disappearance of the icterus and the hemorrhage, the inference is admissible that the latter is located in the immediate vicinity of the gall-ducts. Other peculiarities of the blood-clots passed at stool are perhaps the imprints of the valvulæ conniventes of the jejunum.

The DIAGNOSIS of aneurism of the hepatic artery is usually impossible.

Aneurisms of the splenic, renal, and other abdominal arteries are recorded, but not in sufficient numbers to warrant a detailed description of them.

DISEASES OF THE COELIAC AXIS.

Aneurism.

Aneurism of the coeliac axis, when the tumor is large, is accompanied by very much the same symptoms as aneurism of the abdominal aorta. The disease is rather uncommon.

ETIOLOGY.--Syphilis, rheumatism, and advanced age play important parts in the etiology of this disease as predisposing causes of arterial degeneration. Many persons affected have been immoderate spirit-drinkers, which of itself does not directly tend to the disease, but does so indirectly, in that it encourages an early senescence of the tissues. In the same way any debilitating conditions may act as predisposing causes. Chronic endarteritis is most frequently found at the seat of the aneurism. Secondary or exciting causes are peculiarities of occupation, as those which are laborious and require much physical exertion and entail exposure to inclemencies of the weather.

SYMPTOMS.--Pulsation is usually the first symptom observed. It is felt in the epigastrium about two and a half inches below the ensiform cartilage, or even higher, and a little to the left of the median line; or it may be midway between the ensiform cartilage and the umbilicus, on the left. It is not unfrequently of a distensile character, and is unaffected by changes in the position of the patient. It is not synchronous with the cardiac systole, but follows in rapid succession to, and terminates with, the ventricular {842} diastole. A tumor, usually globular, is felt in the region of the pulsation. It is of variable size, from that of a hen's egg to a cricket-ball, or in case of false aneurism even much larger. The tumor is slightly tender; it moves with the diaphragm, and sometimes when it presses upon the pancreas ptyalism has been observed, which in one instance was increased by external pressure on the aneurism with the hands.

Another constant symptom is pain in the left side, extending from well up in the chest to the region of the hip, or located in the lower part of the chest alone, or perhaps in the epigastrium. This pain is either constant or excited by exertion, and paroxysmal in character.

Flatness on percussion over the tumor of varying extent is observed in many cases, and a systolic bruit, perhaps of a whistling character, is heard.

The usual termination of aneurism of the coeliac axis is rupture with internal hemorrhage. The symptoms of this accident do not differ from those of the same occurrence in abdominal and thoracic aneurism, and are likewise usually fatal.

PATHOLOGY.--Strain doubtless forms an important factor in the production of this aneurism in an artery previously weakened by disease of its coats. The tumor is frequently a false aneurism, and has for walls connective tissue and the neighboring organs. When it is of large size, on account of its position it sometimes presses upon the pancreas or vertebræ, and produces absorption with consecutive symptoms. In the former case ptyalism has been observed, which perhaps may have been due to reflex action through the coeliac plexus and pneumogastric nerve, the reflex centre being the medulla oblongata with the facial origin. The wall of the aneurism is usually thin, and in some cases it has given way, leading to the formation of so-called false aneurism. Not infrequently the wall is atheromatous. The size of the aneurism varies greatly, though it is never larger than the two fists.

DIAGNOSIS.--This aneurism is apt to be confounded with aortic aneurism, and can only at times be distinguished from it by its locality and small size.

PROGNOSIS.--This must be grave if a diagnosis is made, for the ultimate result is usually rupture and hemorrhage.

TREATMENT.--The general principles recommended in treating abdominal aneurism should be followed out. It is but rarely the case that compression is admissible, and then the distal pressure is to be used. Rest and diet form the most reliable means of treatment at our command.

{843}

DISEASES OF THE VEINS.

BY ANDREW H. SMITH, M.D.

The principal affections to which the veins are liable are the following: Inflammation (phlebitis), acute and chronic; Dilatation; Narrowing or obliteration; Degeneration; Concretions.

Inflammation.

Idiopathic phlebitis occurs for the most part under one of three conditions: First, as a simple primary inflammation of the tissues composing the walls of the vessel; second, as a participation in an inflamed or diseased condition of surrounding structures; third, as the result of the absorption of poisonous material into the blood.

Like any other structure of the body, the veins are liable to inflammation as a purely local affection. It is nevertheless true that, in the acute form, this inflammation is most likely to occur in connection with certain conditions of the system which seem to act as predisposing causes, although the connection between them and the local phlebitis is not apparent. Thus it occurs (perhaps associated with more or less of lymphangitis) in the puerperal state, in phthisis, in heart disease, and in other conditions of general depression. I have met with it, for example, during recovery from pneumonia after typhoid fever and after suffocative laryngitis. Under these circumstances it constitutes the chief element in the affection known as phlegmasia dolens. Now, none of the above conditions implies, so far as is known, any source of irritation to the venous structures, much less to a limited portion of the venous system; and the only explanation of their association with phlebitis seems to be in the assumption that these conditions favor coagulation of the blood, and that, in these cases, the formation of a clot precedes the local inflammatory process. The location of this clot is probably determined by anatomical conditions.

In other cases, however, the process evidently begins in the wall of the vessel, and the formation of the thrombus is secondary. Any change which interferes with the smoothness of the inner coat, whether by loss of endothelium or by producing inequalities of the surface, will very certainly determine the deposition of fibrin and the formation of a coagulum. The glossy smoothness of the intima seems to require the most perfect nutrition of the subjacent tissues for its maintenance, and its loss produces an immediate slowing and ultimate stoppage of the blood-current. This is admirably shown by the experiments of Nicasse,[1] which demonstrate that simply denuding a portion of a vein, and thus cutting off its vascular and nervous supply, induces almost immediately the formation of a thrombus coextensive with the denuded portion.

[Footnote 1: _Des Plaies et de la Ligature des Veinse_, Thèse, Paris, 1872.]

{844} Inflammation affecting the inner coat of a vein and extending along its surface, as in the case of a serous membrane, probably never occurs. The picture of phlebitis formerly drawn, and which embraced the exudation of false membrane or the formation of pus upon the inner surface of a vein, the pus in the latter case floating off with the blood and constituting pyæmia, the formation of a clot being a later and unimportant event, has little or no resemblance to what actually occurs.

The observations upon which these assumptions were based were erroneous, as shown by Virchow, in that the staining of the intima by absorption of coloring matter from the blood was mistaken for inflammatory redness, and changes in the clot itself were confounded with exudation and suppuration. Indeed, when we reflect that the intima is not vascular, we should scarcely expect from it anything analogous to serous inflammation. The only acute process to which it appears liable is an erosion or crumbling away under the same conditions which determine, in the middle or outer coats, increased vascularity, exudation, and the formation of pus.

Thus, from some general condition favoring the coagulation of the blood we may have a thrombus formed, followed by secondary inflammation of the wall of the vessel, or, without such general condition, we may have inflammatory changes, commencing in the outer or middle coat and causing the secondary formation of a thrombus. In either case the clot shuts off the affected portion of the vein from the general circulation. Changes take place in the clot which are more properly considered under the head of thrombosis, and by which it is ultimately removed. Exudation takes place into and between the tunics which form the venous wall, the latter becoming thickened and comparatively rigid, so that when the vein is cut across its lumen remains open like that of an artery.

Sometimes pus is formed between the different coats, constituting small mural abscesses; sometimes the intima crumbles away and exposes the middle coat, which suppurates on its inner surface, and the pus mingles with the débris of the clot. In this way a larger abscess is formed, bounded by the wall of the vein and by a partly-organized coagulum on either side. These coagula sometimes break down, and fragments from them, infected by the pus and its contained micrococci, are swept on in the current of the blood until they find a lodgment, where the process begins anew, and whence it may be propagated in like manner to other and more distant parts.[2] It is only to the condition above described that the term suppurative phlebitis can properly be applied.

[Footnote 2: Ziegler, _Path. Anatomie_, Jena, 1881, p. 429.]

But, instead of a suppurative process taking place, the endothelium may be thrown off and replaced by minute vegetations of the character of granulation-tissue, which, penetrating into and blending with the clot, may temporarily or permanently occlude the vein, and the contraction which follows may ultimately leave only a fibrous cord to represent the vessel.[3]

[Footnote 3: Leroux, _Gaz. méd. de Paris_, 28 Juin, 1879.]

This process is designated adhesive phlebitis, and is one of frequent occurrence and very important in its results. It takes place in connection with suppurative phlebitis, and by closing the vessel on either side of the suppurating portion serves to prevent the pus from mingling with the general circulation.[4] By its action the largest veins, including the venæ cavæ, are occluded, and extensive and important changes in the circulation are brought about.

[Footnote 4: While this is true of a pus-cavity forming within a vein, an abscess originating outside of a vein or between the layers of the venous wall may open into the vessel at a point not protected by a clot, and the pus mingling with the blood will constitute veritable pyæmia.]

The second condition under which phlebitis occurs is that in which a vein, {845} coursing through an inflamed or diseased structure, becomes itself inflamed. This takes place most frequently in phlegmonous erysipelas and in diffused inflammation of the cellular tissue, but it may be the result of any inflammation in the neighborhood of a vein. Under these circumstances the external layer of the venous wall is first affected, and the others subsequently. Only a portion of the circumference of the vessel may be involved, and the wall may bulge inward considerably without necessitating the formation of a thrombus (Virchow). But if the nutrition of the walls is seriously impaired, the intima becomes roughened by the loss of its endothelium, the blood-current is slowed by the increased friction thus caused, and, the uneven surface favoring at the same time the adhesion of fibrin, a clot is formed, and the course thereafter is the same as when the vessel is primarily affected.

Suppuration may also take place between the vein and its sheath, and extend for a considerable distance along the vessel. The walls participate secondarily, and the vein becomes occluded as before described.

In the third class of cases, those depending upon toxic infection, the inflammation is caused by the irritation of some poisonous material circulating in the blood. The phlebitis is therefore secondary, and is to a great degree overshadowed by the general condition which accompanies it. Aside from instances in which there is a direct inoculation of a poisonous material--as, for example, the venom of a serpent--the conditions merge into those which come under the designations pyæmia and septicæmia--diseases which were formerly confounded with phlebitis, but which are now recognized as distinct from, though often coexisting with, it.

If in acute phlebitis the inflammation does not result in the formation of pus, the vein may recover its normal condition, or the walls may remain thickened and the lumen contracted, but still pervious, or it may be entirely occluded. Suppuration, however, always results in complete and permanent closure of the vein.

The symptoms of acute phlebitis are chiefly such as indicate obstruction of the vein. When a large vein, situated in one of the extremities, is the seat of the affection, there are usually severe pain of a tensive character and decided tenderness on pressure. The limb swells, sometimes to a very considerable extent, and becomes stiff and unwieldy. If a superficial vein, such as the long saphena, is affected, there will be subcutaneous oedema and pitting; but when the vessel lies beneath a firm, tense fascia, this will limit the swelling, and the limb will be hard and brawny, while the tension will greatly aggravate the pain.

When the vein is sufficiently near the surface it may be felt at the affected part as a hard cord, usually more or less knotted. The skin over it may be discolored, presenting a red or somewhat coppery hue and a streaked or mottled appearance, or the pressure from the effused serum may empty the capillaries of blood and render the skin pale and shining.

The temperature of the limb may be elevated, normal, or subnormal. In the outset, under the influence of the inflammation, there is usually increased heat, but as the tension from the oedema interferes more and more with the circulation, the temperature falls, and the limb may become colder than its fellow.

Inflammation of a limited portion of a vein may not be attended by any notable symptoms, the collateral circulation being quickly established, and the effects of the obstruction thus obviated, while, at the same time, the local symptoms are masked by the morbid conditions in the surrounding tissues which give rise to the phlebitis.

The constitutional symptoms accompanying phlebitis are those of inflammatory fever, the grade of which will depend upon the extent and severity of the inflammation. When a considerable length of vein is involved, as {846} may be the case in the form of phlebitis already referred to, which progresses along the sheath of the vessel, the irritation of the general system may be great, especially if pus is formed, when hectic or even typhoid symptoms are not uncommon.

The differential diagnosis of phlebitis in its local appearances requires only its distinction from lymphangitis. The latter disease is more abrupt in its invasion, depends almost always upon some wound or injury with which the local symptoms are directly connected, is more diffuse, affecting a network of vessels rather than a single one, and is invariably accompanied by engorgement of the lymphatic glands to which the affected vessels lead, as, in the case of the extremities, the axillary or inguinal glands.

In complicated cases the occurrence of phlebitis may not be marked by any distinctive symptoms. It may be suspected if, in the course of erysipelas, diffuse cellulitis, etc. in the neighborhood of an important vein there is a somewhat sudden increase of pain and swelling, and if an enlargement of the tributary cutaneous veins is soon observed.

The treatment of phlebitis consists in complete rest, in the use of such constitutional means as may be necessary to allay the irritation of the system, and locally in the application of leeches and warm fomentations. If, on the other hand, the local temperature is very high, the use of ice may be indicated.

Nonat, in cases of commencing phlebitis from venesection, tried the use of flying blisters over the part affected. Obtaining good results, he extended the treatment to phlebitis following typhoid fever, etc., and the morbid phenomena were at once arrested.[5]

[Footnote 5: _Gaz. des Hôp._, No. 86 (_Med. Times and Gaz._, Aug. 7, 1858).]

Much disturbance of the parts, either in examining them or in the use of frictions, etc., is to be avoided, as there are not a few instances on record in which portions of thrombi have been detached in this way, and, floating off in the current of the blood, have resulted in pulmonary and even cardiac embolism, the latter causing immediate death.[6] The tendency to oedema will be lessened by placing the affected part in a position that will favor the return of the blood by the collateral circulation.

[Footnote 6: _Lyon Médicale_, June 18, 1876 (_N.Y. Med. Rec._, Sept. 2, 1876).]

As an internal remedy the calcium sulphide is worthy of trial.[7] The administration of ammonia is thought to lessen the tendency to the formation of coagula and to promote their absorption if already formed. Abscesses occurring in superficial localities should be promptly opened, antiseptic precautions being observed. The strength of the patient should be maintained by every possible means, the danger of an extension of the mischief being proportioned to the lowering of the vital forces.

[Footnote 7: "Report of N.Y. Therapeutical Society," _N.Y. Med. Journ._, June, 1882.]

As already stated, acute phlebitis plays a very important part in the affection known as phlegmasia alba dolens or white leg. Indeed, many writers consider that it is the only essential factor in the affection. This view is strongly insisted upon by Hervieux, but the researches of Mackenzie,[8] Simpson,[9] Barker,[10] and others have shown that something more than phlebitis is embraced in the disease. Tilbury Fox claims that there is an association of lymphangitis with the phlebitis. At all events, whatever may be the exact pathology of the affection, it appears to be certain that an abnormal condition of the blood, favoring the formation of coagula in the veins, is an essential prerequisite.

[Footnote 8: _Pathol. and Treat. of Phleg. Dolens_, London, 1862; _Med. Times and Gazette_, Aug. 22, 1866.]

[Footnote 9: _Med. Times and Gazette_, Jan. 14 and 18, 1859.]

[Footnote 10: _The Puerperal Diseases_, New York, 1876.]

Phlegmasia dolens occurs chiefly in the puerperal state, and affects chiefly {847} the lower extremities; but it may affect males and non-puerperal females, and may be seated in the arms as well as the legs. Outside of the puerperal state it is met with in conditions of depressed vitality, as during convalescence from acute disease, and in those suffering from phthisis, cancer, and other cachexiæ. When one of these conditions is present a degree of venous obstruction--from pressure, for example--which would ordinarily cause merely a slight amount of oedema may result in an adhesive or even suppurative phlebitis, and the associated phenomena which form the disease in question.[11]

[Footnote 11: Murchison, _Med. Times and Gaz._, May 23, 1863, reports the case of a man recovering from typhus in whom phlegmasia dolens resulted from the pressure of a diverticulum from the bladder upon the right iliac vein.]

The preponderance of cases, however, occurring from the second to the fourth week after delivery indicates a special condition present at that time tending to produce the disease. Some cases, doubtless, are due to the cause suggested by Lee--viz. the formation of clots in the uterine veins, and the growing out of these thrombi through the hypogastric and into the iliac and femoral veins. But that this is not the only or the usual cause is proved by numerous autopsies in which no evidence of thrombosis has been found in the uterine veins. Still, the puerperal period is very generally one of vital depression, in which hyperinosis and inopexia are presumably present. To this is added another source of irritation, in the loading of the blood with the material absorbed from the uterus in the rapid reduction of its bulk which is taking place.

It is not improbable also that small amounts of decomposing blood, and even clots, may be retained in the uterine sinuses, and ultimately be forced suddenly on into the venous circulation by the pressure resulting from the shrinking of the tissues by which they are surrounded. This would explain the suddenness with which symptoms of toxæmia or embolism often occur.

The principal difference between phlegmasia dolens and simple obstructive crural phlebitis is in the degree rather than the character of the symptoms.

When, in a healthy animal, phlebitis of the crural vein is set up artificially, causing complete obstruction, there is but little pain, and only a comparatively slight effusion into the cellular tissue, and the limb pits readily. In phlegmasia dolens, on the other hand, the pain may be very severe and the oedema very great, and the limb is stiff, hard, tense, and shining, and pits only with firm and continued pressure (Barker). Moreover, crural phlebitis may occur and prove fatal without causing phlegmasia dolens.

These facts have perhaps been allowed undue weight in the argument for non-identity. It would seem that we have only to admit a depraved condition of the blood favoring thrombosis and secondary phlebitis, and disposing to more abundant effusion of a more plastic character as the result of the obstruction, and all the distinctive phenomena of phlegmasia dolens are covered. The experiment has never been tried of producing phlebitis artificially in a subject, with the blood-condition predisposing to white leg, in order to determine whether this condition would follow; but clinically it has more than once been demonstrated that in such a subject phlegmasia dolens may result from simple pressure upon the iliac vein.

The fact, too, that the disease occurs three times in four on the left side, where the iliac vein is pressed upon by the rectum and by the iliac artery, is not to be forgotten in this connection. If lymphangitis were a necessary factor in the disease, pressure upon the vein would not have such a marked causative influence.

The symptoms of phlegmasia dolens may be gathered from the preceding remarks, together with the description of the symptoms of acute phlebitis. {848} It is to be noted, however, in addition, that the majority of cases are ushered in by one or more chills, and that the progress of the case is usually marked by a tendency to profuse perspirations. In the puerperal woman lactation is generally very much interfered with or entirely suspended. "The lochial discharges seem, in very many cases, to be very little influenced by the onset and progress of this disease, but in others they have been observed to become very fetid and offensive" (Barker).

The tendency of this affection is to terminate by resolution. The hardness diminishes before the size of the leg becomes less, and with this diminution of tension the muscles regain their power. Gradually the oedema subsides, and the knotted cords which indicated the course of the affected veins disappear. If all goes well, the limb is restored in the course of three or four weeks apparently to its normal condition. Yet even in these cases the affected vein probably remains entirely obliterated, the circulation being carried on by the subsidiary vessels.

But in many cases the recovery is only partial, and for months or years the limb remains larger than its fellow, the superficial veins are enlarged, and the skin congested and of a dusky hue. Long standing or walking causes increased oedema, and there is a disposition to eczema and ulceration above the ankle.

What was said in regard to the treatment of phlebitis is applicable to that of phlegmasia dolens. As the tension subsides the application of a roller bandage will hasten the return of the limb to its normal size. But care must be taken that it is not tight enough to still further impede the already obstructed circulation. At a later period the support of an elastic stocking may be required. Constipation is to be avoided, especially in those cases in which the left lower extremity is affected, as the pressure of the loaded rectum interferes with the return circulation.

Chronic phlebitis is usually the sequel of an acute attack or else is developed in a vein already varicose. The coats of the vessel become thickened and hardened by interlamellar development of nucleated fibrous tissue, so that the walls become more or less rigid. This thickening may be partly at the expense of the lumen of the vein, thus reducing its calibre, or it may be entirely excentric. The vasa vasorum are sometimes developed in chronically-inflamed veins to a remarkable extent. Quincke states that they may attain the size of cuticular veins.[12]

[Footnote 12: _Ziemssen's Cyclopædia_, art. "Dis. of the Veins."]

Except in the case of superficial veins, in which the vessel may be felt as a hard cord, the affection cannot be recognized during life. It may be assumed to exist when the symptoms of acute phlebitis continue in a less degree, or when tenderness, without other active symptoms, is found along the course of a vein. Under these circumstances there are apt to be acute attacks of pain and swelling from the operation of slight causes, the attacks subsiding, but the chronic condition remaining through the intervals.

The treatment looks to the avoidance or removal of the causes which tend to produce acute exacerbations. Rest is of the first importance. In chronic inflammation of a superficial vein the local use of iodine or of the ointment of iodide of lead will be of service. A succession of flying blisters along the course of the vein may be employed with advantage. When there is chronic enlargement of the limb the persistent administration of potassium iodide may be useful in promoting the absorption of effused material. After the subsidence of all inflammatory action massage may be resorted to.

{849} Dilatation of the Veins.

This condition results either from undue pressure of the blood within the veins or from impaired resistance of their walls. The former condition is found in certain forms of heart disease affecting the right chambers; on the distal side of an obstruction in a vein; when collateral veins are required to carry on the circulation, the natural channel being narrowed or obliterated; and in the veins of a limb when the position is such, a great portion of the time, that the blood is forced to mount against gravity.

The second condition, that of diminished resistance of the walls, is found in enfeebled constitutions and in the degeneracy of tissue incident to advancing age. A familiar example is furnished by the enlargement of the veins on the back of the hand in old persons.

Excessive dilatation of the veins which go to make up the superior cava often results from insufficiency of the tricuspid valve. When this insufficiency exists a proportionate part of the systolic energy is expended in driving the blood back into the systemic venous circulation, and the superior cava, from the nearer correspondence of the axis of its opening with the axis of the auriculo-ventricular opening, receives the larger share. Hence with every contraction of the ventricle a direct distending force is exerted upon this vessel and its branches which they are not fitted anatomically to resist. In such cases the distended veins may reach an enormous size, and are seen to pulsate synchronously with the arteries. The distension is greatest in the neck, but affects also the veins of the chest and of the upper extremities.

Whenever a vein is obstructed, either by some process taking place within it or by pressure from without, the distal portion is more or less dilated. Examples of this are seen in the closure of veins from phlebitis and by the pressure of abdominal tumors or the gravid uterus.

Under like conditions the tributary veins also, being forced to carry more than the normal amount of blood, become enlarged. This we see constantly in the dilated veins of the abdomen when the internal vessels are pressed upon by large dropsical effusions.

The term caput Medusæ is applied to a collection of enlarged veins radiating from a common centre or arranged in the form of a corona. Such collections often occur on a small scale above the ankles, but under some conditions they assume vast proportions. When there is obstruction of the inferior cava a great mat or pad of dilated, convoluted veins may form on the abdomen or thighs. Some of these veins may be as large as the little finger.

In the erect posture the veins of the lower extremities are subject to a distending force proportioned to the height of the column of blood which they have to sustain. For short periods at a time the resistance of the walls is ordinarily sufficient to bear this pressure without yielding, but in persons whose occupation requires them to stand a considerable portion of each day, and especially in those past middle life, there is a gradual giving way, which results in increasing not only the diameter but the length of the vein.

The dilatation takes place irregularly, being greater at one point than at another, and in one place affecting the entire circumference of the vessel, while in another it produces a bulging on one side or even a pouch or diverticulum. Especially just above the valves in the veins of the lower extremities, where the diameter is naturally a little greater, the larger area gives rise to greater pressure, and more marked dilatation results. Their breadth remaining the same, the valves are no longer able to reach across the vein, and the circulation is deprived of the aid which it is their office to give. Instead of the column of blood being divided into a number of portions, each resting upon the valve beneath it, there is now a continuous column which exerts its full static pressure. Dilatation is thenceforth doubly rapid, and at the same {850} time the vein is stretched longitudinally and becomes tortuous, thus adding another impediment to the circulation. The nutrient vessels ramifying in the venous walls are pressed upon, and the nutrition of the several tunica is impaired. From this arises fatty or calcareous degeneration. Under these combined influences the walls often become so thinned that rupture takes place. But it is rare that the blood is effused into the tissues surrounding the vein, for the overlying integument or mucous membrane, atrophied from the pressure of the vein beneath, usually gives way at the same time, affording a means of escape. Even bone is not capable of resisting the continuous pressure of an enlarged vein, but may be absorbed in the same way as in the case of arterial aneurism (Bristowe).

Sometimes the dilated vein becomes thicker instead of thinner by addition to the outer tunic; probably the result of a slow inflammatory process, to which, as already stated, varicose veins are peculiarly liable.

The slow circulation, especially in pouched and tortuous veins, favors the formation of coagula which frequently close up the vein entirely, thus bringing about a spontaneous cure. Independently of this, there is a disposition to recovery when the cause is removed, and the vessel may, under favorable circumstances, regain its normal condition. If, however, the valves have atrophied, as they are apt to do after their efficiency has ceased, entire recovery is impossible.

Oedema is apt to occur in connection with dilated veins if the impediment to the circulation is considerable. Chronic ulcers of the legs, accompanied by eczema, are a very common result of a varicose condition of the superficial veins of the lower limbs; and a permanent cure can seldom be effected unless the varicose condition is first removed.

Dilatation of the hemorrhoidal veins is an important factor in hemorrhoids. But it is far from constituting the disease, as was formerly supposed, the tumors being largely made up of dilated capillaries and hypertrophied connective tissue. Indeed, in some of the worst forms of piles it is not possible to find any evidence of varicose veins in the extruded mass.

In most cases, however, these varices are present, and may be distinguished as smooth blue or purple nodules. When a hypodermic needle is thrust into one of these, the point is felt to be in a free cavity, which immediately becomes filled with a solid coagulum when a few drops of a weak solution of carbolic acid are injected--an operation which usually effects a cure.

Obstruction of the portal circulation predisposes to hemorrhoids; hence they are a frequent attendant upon diseases of the liver. The habitual presence of fecal accumulations in the rectum, pressing upon the veins, operates directly to impede the return circulation, while the straining at stool which accompanies this condition greatly aggravates the difficulty.

The TREATMENT of external varicose veins belongs properly to the province of surgery. When the dilatation can be traced to changes occurring in any of the internal organs, treatment should be directed to removing the cause or mitigating its effects. A constipated habit should be corrected and the hepatic circulation be promoted.

The presence of ascites will call for the use of diuretics or purgatives or of the aspirator. In cases having a cardiac origin much good may often be accomplished, for a time, by the judicious use of digitalis.

In all cases advantage is to be taken of position to aid the circulation as far as possible.

In the case of superficial veins the application of moderate and evenly-distributed pressure is of much service.

{851} Narrowing of a Vein.

This condition may occur as the result of inflammation which has stopped short of occlusion.

Under the name of hypovenosity has been described a condition of the saphenous system in which there is a deficiency in the number and size of the veins. The outlines of the limb (bone, muscle, etc.) are effaced, the skin is dusky, the limb brawny, and there are no veins visible. The motion of the limb is painful and difficult. There is degeneration of the superficial veins, collateral dilatation of the deep veins, and ultimately atrophy of the muscles.

Exercise, frictions, and hot applications are to be employed. Rest and bandaging as a mode of treatment aggravate the disease.[13] The affection is of rare occurrence.

[Footnote 13: J. Gay, _Lancet_, Nov., 1871.]

Occlusion of Veins.

Venous occlusion results very frequently from adhesive phlebitis. It is also brought about by the presence of cancerous or other tumors. The complete arrest of the current of blood through a vein rarely produces the serious results which may occur from a like obstruction of an artery. The aggregate diameter of the venous system is much greater than that of the arterial, and the venous walls are much thinner and more distensible. Hence an adequate collateral circulation is more readily established. In a healthy individual and in a healthy condition of the part simple occlusion of a vein produces only a moderate oedema of the tissues on the distal side of the obstruction. In unhealthy conditions, however, as already pointed out in discussing phlegmasia dolens, very serious results may follow.

Occlusion of either the superior or the inferior vena cava is of not very rare occurrence. It may be the result of pressure from a cancerous or other growth,[14] which is the most frequent cause, or in the case of the inferior cava it may be brought about by a thrombus gradually extending upward in one of the iliac veins until it reaches the bifurcation, when a thrombus in the other iliac is occasioned by the partial obstruction of its entrance into the cava. These united thrombi then extend upward into the cava, producing complete occlusion. This is an occasional event in phlegmasia dolens.

[Footnote 14: Watson describes a case arising from pressure from hydatids of the liver.]

Occlusion of the superior cava is less frequent than that of the ascending. It is nearly always the result of pressure from an intra-thoracic tumor, and its symptoms are more or less masked by those directly referable to the growth. There are, however, great dilatation of the veins and oedema of the tissues of the head and neck and of the upper part of the thorax. These symptoms in a case in which there are physical signs of a substernal growth would afford a strong presumption of obstruction of the cava.[15]

[Footnote 15: Stocks, _Med. Times and Gaz._, April 22, 1876; Williams, _Tr. Dublin Path. Soc'y_, July, 1878.]

The glandulæ concatenatæ of the neck are apt to be enlarged from the chronic engorgement. Watson mentions a case in which this added so much to the volume of the neck as to give a superficial resemblance to goitre.

Occlusion of the inferior vena cava produces, if life is continued, an immense dilatation of the veins of the abdomen and of the thighs. By compressing the abdominal veins it can be seen that the blood-current is reversed, flowing upward through vessels anastomosing with the intercostal and internal mammary veins. Internally, the circulation is carried on chiefly by the azygos, which may become as large as the normal cava.

{852} There is usually, but not always,[16] an extreme degree of ascites, together with anasarca of the lower half of the body. After a time, however, as the tributary circulation becomes established, the effusion will be reabsorbed.

[Footnote 16: _Le Progrès Médical_, May 26, 1877; _Med. Record_, July 28, 1877.]

If the obstruction involves the portal vein, the ascites will be still more marked. In this case there is also enlargement of the spleen. When the cava is occluded above the point at which it receives the renal veins, congestion of the kidneys results, which in time produces interstitial change. Yet even here the establishment of the collateral circulation may be sufficiently prompt to avert the danger.

Anomalies of the cava are occasionally observed. Osler has reported a case in which the inferior cava was represented only by a fibrous cord. The condition was probably congenital.[17] Greenfield mentions a case in which the descending cava was absent, both brachio-cephalic trunks passing into the heart by the coronary sinus.[18]

[Footnote 17: _Journal of Anatomy and Physiology_, April, 1879.]

[Footnote 18: _Med. Times and Gazette_, April 22, 1876.]

If the cause of the occlusion of either cava be not such as of itself to destroy life, the patient may get on with some degree of comfort for many years. The establishment of the collateral circulation sometimes keeps pace with the increasing obstruction, so that little or no ascites or oedema occurs.[19]

[Footnote 19: Turpin, "Obliteration Inf. Vena Cava," _N. O. Med. and Surg. Journal_, 1881, p. 575.]

The TREATMENT of obstruction of either of the venæ cavæ can, as a rule, be only palliative. In the great majority of cases the cause is entirely beyond our reach. All violent muscular exertion, making an excessive demand upon the circulation, should be avoided. While the blood should not be impoverished, as that would favor dropsical effusions, the patient, on the other hand, should not be allowed to become plethoric through the influence of his enforced sedentary habits. The diet should therefore be light and digestible, and over-feeding should be carefully avoided. The occasional use of saline purgatives may be required. Dropsical accumulations may call for the administration of diuretics or drastic cathartics, and perhaps for tapping.

Occlusion of the vena portæ, by obstructing the return of the blood from the intestines, gives rise to rapid and abundant effusion into the abdominal cavity. As the gastric vein cannot empty itself, there is congestion of the stomach, often ending in hemorrhage, the blood being both vomited and passed by stool. The spleen also is enlarged by passive engorgement, its vein depending upon the portal for an outlet. This assemblage of symptoms renders the diagnosis almost positive.[20] There is no enlargement of the liver unless the hepatic vein is also involved.

[Footnote 20: An interesting case is reported by A. A. Smith in the _N.Y. Med. Journal_, January, 1880.]

Paget maintains that the occlusion of the principal vein of a limb may result in an increased growth of some of the tissues, especially of the muscles.

Degenerations.

Fatty degeneration is rarely observed in the veins, but it occasionally occurs in those which have long been subjected to excessive strain, which by compressing the nutrient vessels affects the nutrition of the walls.

Calcification is less rare. It results in the formation of plates or rings which closely resemble bone in their structure. Such plates may not unfrequently be felt in old superficial varicose veins. Sometimes these formations project as spines into the lumen of the vessel, and, coagula forming about them, a thrombus is the result.[21]

[Footnote 21: See preceding reference.]

{853} Cancer of the veins is rare as a primary affection, but it is not uncommon when the vessel traverses a cancerous mass. The morbid process readily penetrates the thin wall of the vessel, and cancerous nodules form on the inside and become the starting-point of thrombi which are soon permeated and supplanted by the heterologous growth. This is sometimes moulded to the shape of the vein, and fills it for some distance in the form of a cylindrical plug. Fragments may be swept away in the blood-current and give rise to secondary cancer at the point of arrest in the liver or lungs. Virchow has described a case of primary sarcoma of the inferior cava.

The existence of syphilitic lesions in the veins has not been satisfactorily demonstrated. It is positively denied by some authorities, while certain appearances found in the veins, especially of new-born children, are attributed by other writers to syphilitic inheritance.

Phlebolithes.

Vein-stones are roundish, oval, or cylindrical bodies found in the veins or in pouches connected with the veins, or sometimes in the connective tissue adjacent to a vein. Their size varies from that of a hempseed to that of a nutmeg. Externally they are white, but when divided they are found of a yellowish color at the centre. There is generally a central cavity, around which are disposed concentric laminæ such as are observed in vesical calculi. Chemically, these bodies are composed of an animal substance in which are deposited phosphate and carbonate of lime, and sometimes magnesia. The inner part is hard and brittle, the outer softer and more earthy.

Usually, phlebolithes are found loose in the vein, but if large they may be firmly impacted in the vessel, causing complete obstruction. Sometimes the outer portion is of a gelatinous texture, from which a delicate mesh extends to the wall of the vein and becomes incorporated with it.

Frequently these concretions occupy sacs or diverticula connected with the vein. Occasionally these sacs become detached from the vessel and are absorbed and removed, and the stone, then entirely outside of the vein, becomes enveloped in a fibrous cyst formed from the surrounding connective tissue.

Some doubt exists as to the manner in which these concretions are formed, but the probability is that a small clot first forms in the vessel, and that around this, as a nucleus, successive layers are deposited from the plasma of the blood. These layers then undergo chalky transformation by the deposit within them of salts of lime and magnesia. These formations seem to be conditioned by a slow current in a dilated vein. Hence they are most frequently found in the enlarged pelvic veins of old people, and especially about the neck of the bladder in those suffering from prostatic enlargement. They are also found in the varicose veins of the extremities.

Except in superficial situations they are usually not recognized during life. They seldom produce discomfort, and therefore rarely call for treatment. When accessible they may be excised if requisite, the vein being secured above and below if not already permanently occluded.[22]

[Footnote 22: Rokitansky, _Path. Anat._, Philadelphia, 1858.]

{854}

THE CAISSON DISEASE.[1]

BY ANDREW H. SMITH, M.D.

[Footnote 1: This article is mostly drawn from a report by the writer on _The Effects of High Atmospheric Pressure, including the Caisson Disease_, published in 1873 by the New York and Brooklyn Bridge Company.]

Persons exposed for a considerable time to a greatly increased atmospheric pressure are liable, after the pressure is removed, to certain morbid effects which comprise what is known as the caisson disease. It is observed principally in those employed in submarine operations by the aid of compressed air, and who labor for hours together in what is termed by engineers a caisson. The pressure varies with the depth at which the work is carried on, and reaches sometimes fifty or more pounds to the square inch. The disease rarely if ever occurs when the pressure is less than fifteen pounds, and its severity is, other things being equal, in direct ratio to the increase in the density of the atmosphere.

SYMPTOMS.--These are, in the order of their frequency, intense neuralgic pain in one or more of the extremities, and sometimes in the trunk; epigastric pain; nausea and vomiting; more or less complete paralysis, which may be local or general; headache; vertigo; and coma.

The pain, which is often very severe, is usually paroxysmal, exacerbations and remissions occurring at short intervals. It may come on suddenly in its full severity, or it may be slight at first and rapidly increase until it becomes absolutely intolerable, "as if the flesh were being torn from the bones." The pain begins most frequently in the knees, extending rapidly to the legs and thighs, but the upper extremities may be first attacked. Sometimes the most severe pain is felt in the spine, and especially in the lumbar region. There is usually some tenderness with the pain, and a stiffness of the muscles of the affected limbs.

Epigastric pain occurs in a considerable proportion of the cases. It is often very severe, and if not relieved by treatment is liable to be followed by nausea and vomiting. The vomiting is usually limited to the ejection of the contents of the stomach, but it may persist, sometimes even after the pain has ceased. Vomiting accompanied by giddiness may occur without epigastric pain, and is then probably of cerebral origin. Paralysis, to a greater or less degree, occurs with considerable frequency, the percentage of cases increasing in proportion to the pressure of the atmosphere to which the patients have been exposed and the duration of the exposure. It affects most frequently the lower half of the body, but it may include the trunk or one or both arms. In rare cases an arm alone is affected.

The paralysis is of sensation as well as motion. It comes on soon after the invasion of the pains, but affords no relief from them. Thus, while pinching or pricking occasions no pain, the part may still be the seat of exquisite suffering. Paralysis may, however, occur in cases in which the pain is very slight or entirely absent. The paralysis varies in degree from a transient {855} weakness of the limbs and slightly impaired sensation to complete loss of motion and sensation in the affected part. Even the minor degrees generally affect the bladder.

Symptoms of a transient character are often observed depending upon changes in the brain. They consist of headache, dizziness, double vision, incoherence of speech, and sometimes syncope. They usually pass off in a few hours. In fatal cases, however, coma is the usual forerunner of death.

The duration of the caisson disease is from three or four hours to six or eight days. When paralysis occurs it may continue for weeks, or it may pass off within twelve hours. The cases marked only by neuralgic pains do not generally last more than six to twelve hours, though some continue five or six days. Death occurs only in cases which are severe from the first and show symptoms of cerebral or spinal effusion.

MORBID ANATOMY.--The constant lesion in fatal cases of caisson disease is congestion of the brain or spinal cord. This congestion may be pretty evenly distributed or it may vary in intensity in different localities. This is especially true as regards the cord. It affects both the meninges and the substance of the brain or cord. In most cases there is more or less of serous effusion into the arachnoid. The tissues of the scalp and those surrounding the spinal column are sometimes engorged.

When sufficient time elapses before death the brain may be softened in spots. This is probably due to the occlusion of vessels by coagula formed during the primary congestion.

Congestions also occur in other localities, and especially in the solid abdominal viscera. The liver and spleen have been found engorged in nearly every case. Jaminet has found clots of blood in the kidneys.[2] The mucous membrane of the stomach, intestines, and bladder is often injected and marked with patches of ecchymosis. The lungs in cases of true caisson disease, though occasionally found in a state resembling red hepatization, seldom present any other change than simple hypostatic congestion.

[Footnote 2: _Physical Effects of Compressed Air_, p. 20.]

PATHOLOGY.--It is probable that the pathology of this disease is not entirely uniform in all cases. Doubtless the chief element in it is the congestions already described, and especially of the brain and spinal cord. The mechanism, therefore, of these congestions becomes a subject of paramount importance.

It was suggested by François[3] that the morbid phenomena might be due to the liberation in the vessels of air which had been absorbed by the blood while under pressure, but which was set free again when the pressure was removed. This theory has been reasserted by Paul Bert,[4] with this difference: that he claims that bubbles of nitrogen instead of air are the cause of the interruption of the circulation. These bubbles he has discovered after death in the vessels of the brain and cord. But he states that when the pressure does not exceed five atmospheres three minutes allowed for the restoration of the normal pressure will be found to prevent the formation of these globules of nitrogen. Now, we find the caisson disease occurring when the pressure does not exceed two atmospheres and when six to eight minutes are allowed for locking out.[5] It would seem that under these conditions the gas should escape through the lungs as rapidly as it is disengaged from the blood. Moreover, we find that the attack often comes on several minutes or even hours after leaving the caisson. During this time any free nitrogen in the blood should be constantly becoming less by diffusion through the {856} pulmonary membrane, and if enough were not present at first to cause obstruction, such an effect could scarcely take place at a later period.[6]

[Footnote 3: _Annales d'Hygien publique et de Méd. legale_, t. xiv., 1860.]

[Footnote 4: _Comptes Rendus_, August, 1872, and February and March, 1873.]

[Footnote 5: _I.e._ passing from the caisson into the open air through the lock, or antechamber, where the pressure is gradually reduced.]

[Footnote 6: In a private letter to the writer, T. Lauder Brunton suggests that a bubble of air might pass from a larger vessel, which it had only partially obstructed, into a smaller branch, which would be entirely occluded by it, or that additional nitrogen might be disengaged when the pressure was lessened by relaxation of vascular tension.]

It is also very difficult to reconcile with Bert's theory the fact of the comparative immunity from danger which results from repeated exposures to the effects of compressed air. If the action were that of purely physical causes, habit could make no difference. The obstruction of the vessels, as described by Bert, is a condition of which the system could never become tolerant by frequency of repetition.

In the writer's view, the explanation is to be found in the changed conditions of the circulation, which result first from the increased pressure upon the surface, and then from the sudden removal of the pressure. While the subject is in the caisson the blood is driven from the peripheral vessels toward the interior of the body, where the pressure is less than at the surface.[7] It is also forced from the more compressible tissues into the solid and resisting organs, such as the liver and kidneys; and lastly, it flows toward bony cavities, for the reason that their walls resist the effect of direct pressure, and equilibrium of pressure can be restored within them only by an afflux of blood. Thus the distribution of the blood is everywhere changed, and the size of the vessels is no longer determined by the muscular action of their walls, but by the amount of blood forced into them, the vital action which should regulate the circulation being entirely overpowered and set at naught by an overwhelming physical force operating from without. The vessels become merely passive tubes, distended in some places where they are protected from pressure, and compressed in others where the tissues about them are compressible. By this transfer of blood from one part to another the equilibrium of pressure is restored and the circulation goes on, though without any regard to the physiological demands of the different organs. There is no stasis anywhere so long as pressure and counter-pressure are equal, thus allowing fair play for the action of the heart.

[Footnote 7: This is shown by the marked pallor of the skin and the shrunken and wrinkled appearance of the hands.]

If, now, the external pressure is suddenly removed, what will be the result? Vessels which have been compressed and almost emptied of blood will now offer new channels through which the blood can rush, and vessels overcrowded with blood, with their walls paralyzed by over-distension, will have the current within them slowed almost or quite to the point of stopping. The vessels of the brain and spinal cord, being within bony walls, where the direct pressure of the condensed air could not affect them, will be found the most distended and the most helpless to relieve themselves. They will get little aid from the vis a tergo of the circulation, for the blood will find easier courses by other ways, vascular tension being almost nil and the vaso-motor system out of use.

The longer the sojourn in the caisson has been, the more entirely passive the vessels will have become, and the longer will be the time they will require to resume their normal condition. At some points the circulation will be greatly slowed or entirely interrupted, and nerve-elements lying beyond and deprived of their blood-supply will express their want by pain or paralysis. Areas of stasis once formed will be likely to extend, and may thus affect nerve-elements which at first escaped. This would explain those cases in which the attack is deferred until some time after leaving the caisson.

It is readily conceivable that in persons beginning work when the pressure is slight and continuing day by day, as the pressure slowly increases the {857} vessels should acquire the power of adaptation to the variations in the amount of their contents, since this is only an extension of the physiological principle which we see exemplified in all organs having an intermittent function.

The influence of the trophic system of nerves also, as the connecting link between central nerve-lesions and peripheral vascular disturbances, must not be forgotten in this connection. Suspension of function in trophic cells, either in the cerebral cortex or in the anterior horns of the cord, could easily be brought about by the action of the mechanical causes already described, and would result in areas of vaso-motor paralysis and consequent congestion at the termination of the corresponding nerve-fibres. The proneness of the large joints, and especially the knees, to be attacked is suggestive, in view of the like circumstance in chronic degeneration of the cord.

CAUSES.--The one essential cause without which the disease can never be developed is transition to the normal atmospheric pressure after a prolonged sojourn in a highly-condensed atmosphere. Hence we have to consider two elements, pressure and time, the danger in these cases being as the degree of pressure to which the person has been exposed multiplied by the duration of the exposure.

But inasmuch as a prolonged sojourn in the caisson does not in every case produce the disease (many of the men employed escaping it entirely), it follows that there must be concurrent causes which determine its development.

The first of these is a special predisposition. This is occasionally strongly marked, some persons being affected by a short exposure to a low pressure from which there would generally be experienced no inconvenience whatever.

Perhaps the most frequent exciting cause of the caisson disease is too rapid locking out. Indeed, it is altogether probable that if sufficient time were allowed for passing through the lock the disease would never occur. But what is sufficient time for one is too short for another; and all that can be done is to fix upon a duration for the process which shall be proportioned to the pressure, and as great as is consistent with the circumstances, and then to see that the rule is rigidly observed. At least five minutes should always be allowed for each additional atmosphere of pressure.

Newness to the Work.--Unquestionably, the liability to the caisson disease is greatest in those exposed for the first time to the influence of the compressed air. New hands are very apt indeed to suffer more or less during the first week. Those least affected are such as begin work when the pressure is comparatively slight, and continue without intermission as the pressure increases. It seems that the system after a time becomes adapted to the changed conditions, and is protected in a measure from their effects. Nevertheless, some serious cases occur among old hands, especially when for any reason their stay in the caisson is prolonged beyond the usual time, thus showing that their immunity is merely relative. A sudden increase of pressure also, even though very slight, is certain to develop new cases, men thoroughly inured to the work often being affected under such circumstances.

Fulness of Habit.--During the progress of the work on the East River Bridge in 1872 the writer, who had medical charge of the men, observed that among those taken sick there was a very marked preponderance of men of heavy build and with a tendency to corpulency. Of 39 men of this build, only 3 escaped illness, while of 53 lank and spare men 25 escaped. Of the 39 stout men, 8 were more or less paralyzed; of the 53 slender men, only 2 were paralyzed. The deaths, 3 in number, were all of heavy men.

These figures show unmistakably that a tendency to fulness of habit renders work in a compressed atmosphere much more hazardous. Persons of this build have more fluids in the body, the distribution of which is changed by the pressure in the manner before stated, and it is therefore not surprising {858} that the effect upon them should be greater than upon lean and sinewy persons, whose bodies contain a minimum of fluid.

Severe Exertion immediately after Leaving the Caisson.--As at the moment of going out of the compressed air the system undergoes a violent reaction, it is manifestly unfitted to bear in addition a severe tax upon the muscular strength. Hence the ascent of a long flight of stairs immediately after leaving the air-lock is as wrong in theory as it has proved bad in practice. Triger, whose apparatus at Chalonnes was so arranged that the ascent of the ladder took place in the compressed air, the lock being placed at the top instead of the bottom of the shaft, found that the men ascended a distance of seventy feet without becoming in the least out of breath--making the ascent, in fact, more easily than if it had been in the open air.[8]

[Footnote 8: _Comptes Rendus_, t. xiii., 1841.]

The Abuse of Alcohol.--Several writers have remarked that habitual drinkers are more likely to be affected than those who used spirits moderately or not at all. It is stated by the director of the work at Douchy[9] that the attacks from which the men suffered were "almost always coincident with some excess committed in the interval of the shifts." It is easy to perceive that, as the disease is characterized by cerebral congestion, the abuse of alcohol, which has a tendency to produce the same result, would act as a predisposing cause.

[Footnote 9: _Annales d'Hyg. pub. et de Méd. legale_, 1854.]

Entering the Caisson Fasting.--Jaminet insists very strongly upon the influence of this cause, and cites instances to prove his position. Several cases corroborative of his views occurred under the observation of the writer. One of the rules for the men working in the New York caisson prohibited entering the compressed air without having taken food, and in addition to this each new hand was especially cautioned as to the danger of disregarding this precaution, and the foremen were directed to use every effort to secure its observance. Yet, notwithstanding all this, a number of very severe attacks were found to be coincident with, if not dependent upon, violations of this rule. In these cases epigastric pain and retching were prominent symptoms.

TREATMENT.--The treatment of this disease will depend upon the severity of the case and the presence or absence of gastric symptoms or of paralysis. If we have to deal with the neuralgic pains only, the chief reliance must be upon anodynes administered with a liberal hand. Fortunately, the pain, though very severe while it lasts, is in most cases of short duration, the attack passing off usually in a few hours. It is therefore quite practicable to keep the patient under the influence of morphine during the whole time, and thus enable him to escape entirely all extreme suffering. But large doses will be required, the intense pain inducing a remarkable tolerance of the drug. Half a grain may be given at the outset, and a quarter of a grain every half hour afterward until relief is obtained. When employed hypodermically somewhat smaller doses may be used.

In some instances the very best results are obtained from hypodermic injections of atropine at the seat of pain, but in other cases they fail to procure relief, and, upon the whole, atropine is inferior to morphine.

Jaminet, regarding the affection as wholly the result of exhaustion, relies entirely upon stimulants and concentrated nourishment, ignoring the aid of anodynes altogether. It is difficult to see the reason for this, even admitting to the fullest extent his theory of the disease, for nothing can be more exhausting than the intolerable pain which characterizes this affection, and nothing could act more promptly as a restorative than an efficient anodyne.

Starting from the theory already given as to the mode in which the disease is produced, the writer was led to the idea that benefit would be derived from {859} the use of an agent that would induce contraction of the capillaries, and thus correct the want of tone which was considered to lie at the foundation of the difficulty. For this purpose ergot was employed, with the belief that it would be useful, first, by contracting the vessels of the brain and spinal cord and relieving their congested state; and, secondly, by restoring tone to the superficial vessels, and thus imparting vigor to the circulation.

An extended trial warrants him in saying that the results justified the theory. In his hands, though not always successful, ergot was certainly very useful in a considerable number of cases. He has seen very severe pain completely relieved within half an hour after the administration of a drachm of the fluid extract. In other instances unsteadiness of the limbs, which seemed about to usher in paralysis, yielded promptly to one or two doses. A teaspoonful of the fluid extract may be given, and the dose repeated in half or three-quarters of an hour, unless the pain is relieved.

Frictions, with or without stimulating liniments, are very generally resorted to, and seem sometimes to give momentary relief, but it appears to be rather by occupying the attention of the patient than by any action occasioned in the part. In some instances, when the pain is confined to a particular locality, having the part immersed in hot water will afford temporary relief. But the use of the general hot bath is not advised, as it is unsafe to increase the already existing relaxation of the vessels. In several of Jaminet's cases paralysis came on while in the hot bath. In two of the writer's cases cold was applied to the spine, with apparent benefit in each.

Epigastric pain is almost always relieved at once by the use of an alcoholic stimulant with ginger, as employed by Jaminet.

Vomiting is best treated with sinapisms to the epigastrium and swallowing small bits of ice.

When paralysis occurs it is to be treated on general principles. Cups or leeches, with douches and frictions to the spine, may be useful; and, if the case be protracted, the use of strychnine may be called for. Electricity may be of service in preserving the nutrition of the muscles. The bladder will almost certainly be involved, requiring the constant use of the catheter.

The cerebral symptoms which occasionally occur are, with the exception of coma, so transient in their nature as to call for no special treatment. Coma, when it takes place, is to be managed according to the circumstances of the case, as when proceeding from other causes. If accompanied by a full, strong pulse, venesection may be expedient.

There remains to be considered a plan of treatment originally suggested by Pol, and carried out to some extent by Foley--viz. returning the patient at once into the compressed air. Foley says, as the result of his experience, "A true specific is returning to the caisson, through which means all such accidents (pains, vertigo, etc.) speedily disappear. It is to be resorted to unhesitatingly in all threatening cases, and the pressure should be admitted rapidly." But the means of access to the caisson are usually such that it would be difficult to remove a patient into it, even if he could be comfortably cared for while there or if his presence would not interfere with the work. It would therefore be desirable to have facilities for employing compressed air at some point above ground which would be easily accessible.

Of course the secondary effects which arise in protracted cases would not be capable of direct relief by simply reproducing the physical conditions existing in the caisson. The most that might be hoped for in such cases would be that the pressure might result in giving a new impulse to the circulation in the congested part, and thus favor resolution.

Reasoning from his view of the pathology of the disease, Bert has proposed the inhalation of oxygen in order to displace the free nitrogen from the blood by diffusion. Experiments upon animals demonstrated that the sounds {860} produced in the heart by the presence of free nitrogen speedily disappeared when the animal was made to inhale oxygen, the nitrogen diffusing into this gas much more readily than into common air. But, though immediate death was averted by this expedient, paralysis nevertheless occurred, and the post-mortem examination showed the presence of bubbles of nitrogen in the vessels of the cord.

{861}

DISEASES OF THE MEDIASTINUM.

BY EDWARD T. BRUEN, M.D.

Inflammation of the Mediastinum.

SYNONYMS.--Mediastinitis. _Fr._ Médiastinite; _Ger._ Mediastinitis.

Lesions caused by inflammatory processes in the mediastinum may, theoretically, occur in the duplicatures of the pleura, separating the pleural from the mediastinal cavity. This condition may terminate in resolution or in effusion of plastic lymph, as in a case reported by Wildemann, in which the anterior mediastinum was filled with layers of solid exudation, the pericardium inflamed, and its cavity distended by six ounces of pus. The effusion appeared to have been occasioned by long-continued pressure on the sternal region. The process is practically unrecognizable during life, or at least possesses no described clinical features.

Abscess of the Mediastinal Space.

Galen has alluded to trephining of the sternum for caries or necrosis inducing the formation of pus; and Petit[1] has furnished many instances of mediastinal abscess from the warfare of preceding centuries.

[Footnote 1: _Traité des Maladies chirurgicales_, tome i. p. 143.]

ETIOLOGY.--I. Predisposing Influences.--Mediastinal abscess is very rare, at least of such dimensions as to simulate tumor. The condition is sometimes idiopathic, possibly due to sudden exposure to cold,[2] or is associated with the rheumatic diathesis, but in these cases some forgotten injury may have been received.

[Footnote 2: Gunther, _Oesterreich Zeitschrift f. Prak. Heilk._, 1859; Gross, _System Surgery_.]

Symptomatic or secondary purulent collections may occur in connection with operations upon the neck, as tracheotomy, also from softening gummata or glanders, or they may be due to a constitutional cause, the so-called metastatic inflammation of the mediastinal connective tissue in the course of pyæmia.

Scrofulous suppuration of the lymphatic glands may result in secondary abscess.[3]

[Footnote 3: Bristowe, _Path. Soc. Trans._, London, vol. ix. p. 46.]

II. Exciting Causes.--The mediastinum has been penetrated by balls and sabres, and in one case the shaft of a carriage passed through the anterior space, yet without damage to the contained viscera. Gunshot fracture of the sternum, recorded in the history of the Civil War in America, seems to have been very rarely followed by suppuration, even though the tissues have been exposed to such a degree as to render the arch of the aorta distinctly visible.

The anterior mediastinum may be threatened with inflammation, which may sometimes terminate in abscess, as in cases of caries, necrosis, or fracture of the sternum.

{862} Warner[4] reports a case in a boy aged thirteen in which two weeks after fracture of the sternal bone a separation of the edges of the fracture was observed, the interval being occupied by a tumor of considerable size, which contracted and dilated with as much regularity as the heart. It receded on palpation, and on removal of the pressure the tumor immediately resumed its former size. It subsequently ruptured, discharged the contents of an abscess, and the patient recovered.

[Footnote 4: _Amer. Journ. Med. Sci._, Apr., 1873.]

Goodhart[5] records a case of acute mediastinal abscess resulting apparently from injury produced by the sticking of a piece of meat in the oesophagus. A case illustrating the possibilities of direct injury to this region by a blow or fall has been recorded by Bennett. In a middle-aged lady, previously in good health, an abscess slowly formed and presented a prominence over the upper part of the sternum. Two months before the lady had fallen in going up stairs, and struck the sternum against the stone edge of the stairs. These examples have been selected because they seem to cover the possibilities of directly determining causes.

[Footnote 5: _Path. Trans._, London, vol. xxvii.]

SYMPTOMS.--There are three separate groupings under which the symptoms may be classified: _(a)_ The latent symptoms, which include chiefly manifestations of intra-thoracic irritation or pressure; _(b)_ the fulminating phenomena; _(c)_ the physical signs.

As a rule, mediastinal abscess is accompanied from first to last by deep-seated and gradually increasing pain and tenderness on pressure over the sternum; but it may be a sense of constriction and oppression with boring or throbbing sensations. Sometimes there is merely a sense of uneasiness about the chest, with pains of a rheumatic or neuralgic character in the shoulders or neck, brought about by irritation of the intercostal and humeral nerves. The general health may be impaired, and irritation of the pneumogastrics may be manifested by dyspepsia, nausea, vertigo, syncope, headache, dyspnoea, and inability to lie down. Laryngeal irritation is shown by cough, or spasm, with dryness of the throat; a frothy mucus may be expectorated, with occasional rigors, sweatings, and irregular febrile movement. When abscess follows severe injuries, such as fracture or wounds, distinct evidences of phlegmon appear, possibly within a week, accompanied by intermittent fever with rigors, and a sense of weight and oppression in the front of the chest, with pain in coughing and drinking, or breathlessness, "as if one had been running" (Petit).

The pressure symptoms of mediastinal abscess are never so grave as in other forms of mediastinal tumor, since the diffluent contents of an abscess occasion less compression of the mediastinal viscera, or when the intra-thoracic tension is excessive it seeks a channel by which the pus is evacuated. The pressure symptoms are least marked when the abscess is located in the anterior mediastinum.

There may be, on inspection, a distinct prominence over the upper part of the sternum, with or without redness or oedema. Palpation may enable one to recognize fluctuation on the borders of the sternum with tenderness. The tumor may pulsate, but the pulsation never acquires the expansile character of aneurism. Dulness on percussion may be marked, and, according to Daudé, the dulness under the sternum may undergo a change by alteration of the position of the patient. The heart sounds may be heard distantly and indistinctly. The respiratory murmur may be whistling over the region of the trachea, and in the chest a few moist râles may indicate venous congestion, with exudation into the bronchial passages; otherwise the condition of the lungs will probably be normal. The entire series of pressure symptoms common to intra-thoracic growths may be present, especially if the {863} posterior mediastinum is invaded, and may correspond with those of mediastinal tumors in general.

DURATION AND PROGNOSIS.--The causal relations of abscess in the mediastinum are so various that it is only possible to decide the question of duration after weighing the possibilities of treatment. The persistence of the abscess is also decidedly governed by the thoroughness of the drainage after opening has been affected.

The PROGNOSIS depends upon the etiology and the fulfilment of the indications for treatment by drainage. Pressure on the heart and the great vessels which proceed from its base, the descending aorta, oesophagus, the pneumogastrics, and the internal thoracic circulation, must be considered as complications adverse to a favorable prognosis unless speedy relief is possible. Prominent pressure symptoms indicate an implication of the intra-thoracic glandular system.

COMPLICATIONS, TERMINATION.--The abscess may open into any of the internal viscera--the trachea, bronchi, or oesophagus. A favorable case terminating by rupture into the latter passage is reported by Bennett. At first a teaspoonful of bright fluid blood was coughed up, and the day following from two to three ounces of purulent matter followed. The discharge of pus continued five weeks, the sternal swelling subsiding pari passu.

The pleura and pericardium have both been recorded as points of outlet. The pus can even sink down into the inguinal or lumbar region. Spontaneous external opening is said to occur most frequently on a level with the second rib to the left of the sternum.

DIAGNOSIS.--The differential diagnosis between abscess and other mediastinal growths will be considered in the section on Mediastinal Tumors.

TREATMENT.--The exploratory puncture is to be recommended if a fluctuating tumor appear presenting the general symptoms of abscess. Rest, local sedative applications, and the relief of pain are positive indications. Petit, Agnew, and others have applied the trephine to the sternum in search of pus, with a satisfactory result. It is, however, generally conceded that it is better to wait until pointing occurs, as the area of the sternum is so limited that in all probability matter forming behind it would speedily make its way to the surface in an intercostal space at one of the margins of the bone. If the abscess be deeper or due to scrofulous or syphilitic caries of the sternum, the matter which forms may escape into the neck or through perforations of the bone. The latter may be congenitally present or due to disease. Caries, necrosis, or fracture of the bone may make trephining obligatory, or the same indication may prevail if a dependent flow of pus sufficient to drain the cavity is not otherwise obtainable.[6]

[Footnote 6: Chassaignac, _Traité de la Suppuration_, tome ii. p. 330.]

A similar line of treatment would be indicated if there was no tendency to external pointing, and evacuation into the viscera seemed threatened.

Excision of the whole or part of the sternum for abscess, cancer, or other causes seems to have been fairly successful. Heyfelder[7] had collected, in 1863, 18 established cases, in which there were 17 recoveries and 1 death.

[Footnote 7: _Traité des Resections_, traduit de l'Allemand avec Additions et Notes, par le Docteur Boekels, Strasburg et Paris, 1863.]

Adhesions usually prevent a double pneumothorax, even when the sternum and ribs have been resected. Unilateral pneumothorax is not necessarily fatal.

Mediastinal Tumors.

ANATOMY.--The mediastinum is the space which the two pleural sacs leave between them in the antero-posterior plane of the chest, and which {864} contains all the thoracic viscera except the lungs. It is subdivided into three parts--the anterior, middle, and posterior mediastinum. A superior mediastinum has also been described. The space between the pleural sacs occupied by the heart enclosed in the pericardium, the vena cava superior, the ascending aorta, the pulmonary arteries and veins, the phrenic nerves with their accompanying arteries, and the bifurcation of the trachea and roots of the lungs with some bronchial glands, takes the name of the middle mediastinum.

The anterior mediastinum is narrow in the middle, where the edges of the lungs nearly meet, wider above, where the lungs diverge, and widest of all below, for the same reason. It is very shallow from before backward, and it is limited posteriorly by the anterior layer of the pericardium, in front by the sternum, with the fifth, sixth, and a small portion of the seventh costal cartilages, and by the triangularis sterni muscle. The region is occupied simply by connective tissue, save in its upper part, where lies, when it still persists, the shrivelled remnants of the thymus body. It also contains a few lymphatic glands and the left internal mammary artery and vein.

The superior mediastinum is bounded by a plane passing through the lower part of the body of the dorsal vertebra behind and the junction of the manubrium and the gladiolus in front. Its upper limit corresponds to the superior aperture of the thorax. The contents of this space are the transverse portion of the arch of the aorta and its three large branches, the trachea and oesophagus, the thoracic duct, the innominate veins, upper part of the superior vena cava, left recurrent laryngeal nerve, phrenic, pneumogastric, and cardiac nerves, with lymphatic glands and remains of the thymus body.

The posterior mediastinum is triangular in shape, placed in front of the lower border of the fourth dorsal vertebra downward, and bounded anteriorly by the pericardium and roots of the lungs. The lateral boundaries are formed by the pleuræ. The space contains the descending thoracic aorta: in front of the aorta the oesophagus with the pneumogastric nerves, the left in front, the right behind. On the right of the aorta is the vena azygos major; between this vein and the aorta is the thoracic duct; superiorly is the trachea; inferiorly are the splanchnic nerves and the posterior mediastinal lymphatic glands.

DEFINITION.--There are three principal forms of morbid growths in the mediastina--sarcoma, lymphoma or lymphadenoma, and carcinoma. Hyperplasia of the mediastinal glands also may arise, intertwined with various diseases, such as phthisis (especially the form known as pneumonic), pertussis, aneurism, rachitis, and syphilis. Enlargement of the lymphatic glands may occur in connection with the scrofulous diathesis, or similar enlargement associated with primary subacute or chronic bronchitis and the varieties of catarrhal fever and influenza.

Allusion in this place will only be made to the rare instances in which uncomplicated enlargement of the thoracic glands occurs in the mediastinal spaces. Aneurism, abscess, and pericardial effusions will be referred to only in so far as they affect differential diagnosis.

Mediastinal tumors, however, include certain forms which have the interest of pathological curiosities rather than possessing a clinical importance. Cysts in this region are rare, mostly of embryonic origin (dermoid), and contain epithelial structure, such as hair, sebaceous and sweat-glands, teeth, and occasionally bone, cartilage, and other tissues. These cysts often develop rapidly and may attain great size. Lipomata[8] occur as the result of an undue increase of the mediastinal fat, and are associated with accumulation of the same in the pericardium and in the system at large. Such tumors are rare and of very gradual development. Kronlein[9] has described a congenital lipoma of the {865} anterior mediastinum in a child aged one year, which found its way through an intercostal space and then rapidly increased in size. Fibromata, osteomata, and enchondroma are also possible mediastinal and pulmonary tumors, but are seldom met with. Exostoses may form upon the internal surface, and gummata upon the anterior and posterior surfaces of the sternum.

[Footnote 8: Reigel, _Virchow's Arch._, vol. xlix.]

[Footnote 9: Langenbeck, _Klinic_, p. 157.]

PATHOLOGY AND MORBID ANATOMY.--Pulmonary processes associated with bronchial catarrh frequently lead to enlargement of the bronchial glands, because, owing to the impervious character of the basement membrane of the bronchial passages, the mucous and epithelial portion of the exudation is expectorated, and that portion of the exudate which occurs from the bronchial blood-vessels is absorbed and carried by means of the pulmonary lymphatics to the bronchial glands. Tubercular deposits frequently occur in the glands of the posterior, and much less frequently in those of the anterior, mediastinum.

Independently of the above conditions, caseating bronchial glands have been found as complications of scarlatina with nephritis or tubercular meningitis. An interesting case of this condition has been reported as following an abscess in the glands at the root of the neck as a sequel to measles nine months before.[10] Riegel also mentions an instance in which some of the mediastinal glands were enlarged to the size of hen's eggs. The trachea was compressed at the point of bifurcation, so that its calibre was reduced to one-third its natural size. This case was free from other glandular enlargements. Coupland has described a case in a boy four years of age, in whom the cervical glands were enlarged and idiopathic hyperplasia of the bronchial glands was suspected. Autopsy: On raising the sternum a collection of indurated glands was found in the anterior mediastinum, and over the root of the right lung one of these glands had broken down into a cheesy mass. A chain of enlarged lymphatics accompanied the right bronchus. The largest caseous mass had ulcerated through the trachea just above the origin of the right bronchus by an aperture measuring half an inch along the axis of the tube, while for half an inch above its lumen was compressed. In this case the right lung was solidified and contained cheesy matter, with a cavity at the apex. The father of the child had also suffered from increase in the glandular tissues.

[Footnote 10: See _Path. Soc. London_, 1884.]

The historical literature of intra-thoracic morbid growths has been exhaustively reviewed in a monograph by Cockle, but until within the last fifteen years little attempt was made to separate mediastinal tumors into definite groups.

Our present knowledge on this subject was first shaped by Virchow,[11] since which period numerous cases have been recorded.

[Footnote 11: _Virchow's Archiv_, Bd. xciii. Heft 3.]

Sarcoma of the Mediastinum.--Primary sarcomatous growths are relatively uncommon. In 7566 cadavers examined at the Marine Hospital at Kronstadt there were found 158 malignant tumors, 127 being carcinomatous, the other 31 being sarcomatous. In 24 cases reported by Kahnlich, 13 occurred in the anterior mediastinal region, and a similar location was found in a case reported by the writer,[12] also in one instance reported by West.[13]

[Footnote 12: _Philada. Med. News_, March 15, 1884.]

[Footnote 13: _Path. Soc. London_, 1883.]

The anterior mediastinal space is a favorite location for the origin of the purely sarcomatous form of tumor. Sarcoma may arise from a persistent thymus (as in cases reported by Gee, Church, and Powell), from the parietal or visceral layers of the pericardium or pleura, from the periosteum of the sternum, or from the mediastinal connective tissue.[14]

[Footnote 14: Kahnlich, _loc. cit._, describes 13 as originating in the connective tissue of the anterior mediastinum, 5 in the periosteum of the sternum, and 1 in the pericardial substance.]

{866} [Illustration: FIG. 53. 1, tumor; 2, aorta; 3, right ventricle of heart.]

In a disease of this rare nature we can best formulate an idea of the character of the growths by the recital of a few typical cases. In an autopsy made by the writer, on removing the sternum and cartilages they were found to be adherent on the right side to a mass which occupied the anterior mediastinum (see Fig. 53). The growth was seven inches long, measuring from the sternal notch, and terminated in a somewhat diffused thickening of the visceral pleura, which covered the anterior margin of the upper and middle lobe of the right lung. The growth was two and a half inches broad. It overlaid the aorta, pulmonary artery, and the vessels of the neck. The calibre of the trachea was slightly diminished. The glands of the neck were unaffected on either side. The posterior mediastinal glands were very slightly enlarged along the sides of the trachea and upper bronchi. Laterally, at the lower portion of the growth, the pulmonary pleura was thickened at the line of contact with the tumor, but the lungs were free from any traces of disease. The new formation was of fibrous consistence, of a gray-white color, and through its centre a softened tissue was found. Microscopic examination showed the growth to be composed of medium-sized lymphoid cells mixed with spindle-shaped cells, and imbedded in a homogeneous stroma or a stroma which consisted of reticulated fibres and wavy fibrous tissue. Other portions of the body were normal.

In West's case the tumor also occupied the anterior mediastinum, extending toward the second left intercostal space. The mass was about the size of a boy's head, soft, cellular, and adherent to the upper lobe of the left lung; it also rose into the episternal notch and left supra-clavicular fossa. The brachial plexus and vessels of the left side, subclavian and carotid arteries, the jugular and innominate veins, were imbedded in the tumor. The left bronchus and a portion of the trachea were flattened. The left phrenic and left pneumogastric nerves passed through the mass, and on dissection were found much thickened as they ran through the tumor. The tenth nerve measured {867} three times its normal diameter, and was pushed out of its course nearly an inch from the carotid. The recurrent laryngeal was also thickened; the right pneumogastric and phrenic nerves were not involved. The heart lay beneath the tumor; nodules of the new growth were found upon the anterior surface of the heart and along the vessels issuing from it. No secondary deposit was found in the lungs except at the margin of the left upper lobe, into which the tumor spread directly. The spleen, liver, kidneys, and lumbar glands were normal.

Microscopic examination determined the growth to be a round-celled sarcoma, the thickening of the nerves being due to infiltration by similar small-celled growth.

In primary sarcoma of the mediastinum--and the same is true of lymphadenoma--the invasion of the various intra-thoracic organs is chiefly by continuity or direct spreading of the growth. The lymphatics of the neck are very rarely implicated in this form of malignant disease; and while in lympho-sarcoma the glands may be involved, they are not so frequently as in cancerous processes. Sarcomata of the mediastinum with implication of the lungs and pleura are more frequently secondary processes; indeed, the lungs would seem never to be the seat of primary sarcoma. The pleural tissues, however, may be primarily involved. Lepine, Birch-Hirschfeld, Böhme, Eppinger, Schultz, Greenish, and others have reported cases in which the growths were abundantly distributed in the pleural tissues as primary formations. The point of origin is believed to be either directly from the ordinary connective-tissue cells or from the endothelium of the lymphatics.

Secondary sarcomata may form in the mediastinum or in the lungs within a month or so long as a year after the removal of tumors from other parts of the body, probably by metastasis prior to the removal. In some of these cases the seat of original growth and the neighboring glands may be entirely healthy.

In a typical case of multiple osteoid sarcoma of the lung reported by West fleshy vegetations were found on the visceral pleura: upon the parietal pleura, over the seventh rib, two inches from the spine and growing from it, was a lobular spongy mass as large as an orange, but perfectly disconnected with the parts beneath. The right lung was irregular in shape, owing to the presence of masses of new growth in its different parts. The middle lobe seemed almost completely converted into the new growth. Between the lower lobe and the diaphragm, but attached to the lung, was a mass the size of a cricket-ball, covered with a dark, laminated, but easily separated coagulum. The tumor occupied the upper lobe of the left lung, forming an irregular oval mass six by four and a half inches. It was white in color, and adherent to its upper border was compressed lung-tissue. There were also four or five independent nodules situated near the surface, and of a white color. The lower lobe contained one medium-sized growth and four or five small ones. The bronchial glands were not involved. The tumors appeared soft and spongy, but on incision they were found so hard that a knife could scarcely divide them.

Frequently, the lungs are found infiltrated with sarcomatous nodules of a soft consistency, varying in size from a walnut to an orange. To sum up: primary sarcomata may be the round- or spindle-celled variety; but myeloid sarcomata also occur, chiefly as secondary growths. (See Fig. 54.)

Lympho-sarcoma of the Mediastinum.--Lympho-sarcoma, lymphoma, or lymphadenoma is the form of malignant process which probably includes the majority of cases of primary mediastinal growth. It is sometimes, however, a part of a more general disease, affecting more or less the whole glandular system.

{868} Murchison[15] classified the first case of this disease involving the intestines, liver, mesentery, and heart. The same observer the following year described a case in which the glands of the neck, mediastinum, axillæ, and spleen were involved. Wunderlich has recorded a case of malignant mediastinal disease which commenced in the glands of the neck; but the cervical glands may be enormously enlarged without implication of the bronchial.

[Footnote 15: _Path. Soc. Trans._, London, vols. xx. and xxi., together with a summary of the literature of the subject.]

The general disease dates back to the time of Hodgkin, Bright, and Wilkes, and was then known as anæmia lymphatica. It has been specifically described by Virchow,[16] Cornil, and Ranvier as independent of leukæmia, and was designated lymphadénie. It was noticed by Trousseau under the title of adénie, and Ogle and numerous clinical observers since have also recorded cases.

[Footnote 16: _Die Krankhaften Geschwülste_, Band ii. p. 376.]

As a mediastinal growth the characteristics of lympho-sarcoma can be made more vivid by the reproduction of one of the first cases recorded of this disease. On removing the sternum and cartilages they were found adherent to a mass occupying the anterior mediastinum. The morbid growth reached backward to the trachea, surrounding it with a thickness posteriorly of a quarter of an inch; it extended downward to the bifurcation of the trachea, and, involving the superior prolongation of the pericardium, invaded and greatly thickened the parietal part of that membrane, covering the heart at {869} its upper half. The diseased structure reached upward to the root of the neck, involving the anterior mediastinal glands, and surrounded the trachea by a thin layer as high as the thyroid cartilage. Some of the glands on each side of the neck were affected as high as the angle of the jaw. Laterally, the morbid growth extended on each side to the line of junction of the cartilages with their ribs, displacing the anterior margin of the lung. The pulmonary pleura was involved and thickened at the line of contact, and the right lung at the upper part of its anterior margin was invaded from the pleura by white, fibrous-looking branched bands. At the lower part of the anterior lobe the lung was also invaded from the pericardium. Some of the glands at the root of the lung were involved by extension, but they were not generally affected, nor was the lung invaded except to the limited extent above mentioned. The heart and pericardium were free from disease.[17]

[Footnote 17: Powell, _Path. Trans._, vol. xxi., London.]

The malignant growths of the mediastinal region implicate the surrounding structures so rapidly that it is, as a rule, quite impossible to determine, even after death, the starting-point of the disease; and while lymphadenoma can originate in the same tissues as the other forms of sarcoma already alluded to, yet it in most cases probably originates in the lymphatics of the anterior or posterior mediastinum.

In reference to the location of this form of morbid growth, we find, on consulting a series of cases reported by Fenwick, Eve, Payne, Peacock, Powell, Murchison, Bennett, Dickinson, that the region for principal development seems to be the anterior mediastinal space, although in several instances the posterior mediastinal region was also involved.

The characteristics of the growth of lymphadenoma are the involvement by continuity of all adjacent tissues, thus affording a contrast to secondary sarcomata. The glands of the neck are sometimes invaded, but are unaffected in a considerable proportion of cases. The lungs may be involved slowly, the growth following the lymphatic paths along the bronchial or vascular sheaths. The malignancy of lympho-sarcoma is unquestionable, but as a local growth it is less so than when the process is general; it is less malignant than cancer or certain forms of sarcoma.

Carcinoma of the Mediastinum.--Primary carcinoma of the mediastinum, as separated from the foregoing groups, is relatively rare; even as a secondary growth the same is true, unless it directly penetrates the chest-wall from a cancerous breast. The cancerous growths present a special peculiarity in the fact that they incorporate all the tissues with which they come in contact, and are followed by contraction. Carcinoma often originates in the lymph-tissue at the root of the lung, and may form a mass which may involve the bronchial glands, lower part of the trachea, the right and left bronchi, and surround the aorta and oesophagus. Scirrhous cancer frequently originates in the tissues at the root of the lung surrounding the bronchi and vessels, compressing them, and extending by branching rays through the lung-substance toward the periphery, following the course of the large bronchi, the lymph or arterial vessels. Carcinomatous formation may also originate in the follicles of the mucous glands of the bronchial tubes, and the mucous membrane of the same is frequently ulcerated by extension of the morbid process. The mucous membrane of the bronchi may be covered with villous-like formations springing from the surrounding growth.[18] Obstruction of the bronchial lumen by carcinomatous growth may prevent the expectoration of the bronchial secretions, and dilatation of the bronchial tubes may be consecutive. These dilated tubes may become filled with pus from associated bronchitis or forms of catarrhal pneumonia.

[Footnote 18: See cases by Bennett and Williams, _Lond. Path. Trans._, vols. xix. and xxiv.; also Burrows, _Med.-Chir. Trans._, vol. xxvii.]

{870} The special pathological characteristics of cancerous growths are that they exist most frequently in the posterior mediastinum, and therefore exert special pressure on the respiratory passages. Again, they are subject to contraction, by which the various pulmonary structures are fused together. Hard, nodulated, cervical glands usually appear in the supra-clavicular spaces, affording special contrast in this respect with the pure sarcomata. Since, in general, the same tissues may be affected as in lympho-sarcoma or other processes affecting the bronchial glands, a positive diagnosis can usually only be made by a microscopic study of the growth. Only one lung is usually implicated, while the sarcomata spread by extension in all directions and may involve both lungs.

The effect upon the lungs of mediastinal pressure on the bronchial tubes may be very serious. Collapse of the bronchial tubes and oedema of the lungs may ensue, or subacute catarrhal inflammation with consolidation--a process which has been described by Fuchs as a form of pneumonia under the title of apneumatosis. The affected tissues not uncommonly break down by necrotic disintegration, which may lead to the formation of cavities sometimes erroneously described as resulting from softening of cancerous nodules.

Pleural effusions are prominent in the clinical history of malignant intra-thoracic disease, and especially in mediastinal processes. These effusions are consequent on pressure on the intra-thoracic circulation, or may be traceable to inflammation, either developed by irritation of the contiguous morbid process or extension of the same upon the serous membrane. Purulent pleural collections have been noted in certain cases, and they may be hemorrhagic. In 31 cases in which the character of the effusion was mentioned, 6 only were tinged with blood. This characteristic is therefore simply of relative importance. Pericardial effusion is also possible from causes similar to those operating upon the pleural tissues. Pressure may occasion dilatation or thrombosis in the vena cava. The vessels of the neck suffer, either directly from pressure inducing dilatation, or by being converted into rigid tubes, allowing of no adaptation to the amount of blood passing through them. There may be corresponding collateral swelling of the azygos or hemi-azygos veins, and at the same time collateral circulation is established between the jugular and the subclavian on the one side and the azygos and hemi-azygos on the other through the superior intercostal veins. The external thoracic veins may, in some cases, become enlarged, and infrequently compression of the inferior cava may occasion effusion into the abdominal cavity and cause oedema of the lower extremities. Morbid growths have occasionally invaded the spinal canal and excited sufficient pressure to occasion paralysis.[19]

[Footnote 19: Bennett, _loc. cit._]

There are certain forms of mediastinal and pulmonary tumors very seldom met with; for example, fibromata and osteomata,[20] the latter sometimes occurring as an exostoses springing from the posterior surface of the sternum. Dermoid cysts of this region, as in the lungs, are also most unique. Mohr records the case of a woman æt. twenty-eight who had spat up hair since her sixteenth year. In the left lung was found a cyst which communicated with the bronchus. Inside of it was found several rounded knobs, here and there pedunculated, varying in size from a nut to a hen's egg, consisting of fibrous tissue provided with sebaceous and sweat-glands, and from which sprang numerous long hairs. The remaining contents consisted of fat and balls of hair. Teeth, bone, and cartilage can sometimes be recognized in these cysts.[21]

[Footnote 20: _Die Krankhaften Geschwülste_, ii. p. 102; Förster, _loc. cit._, p. 105; Wagner, _Arch. für Physiol. Heilk._, 1859, p. 411; Luschka, _Virchow's Arch._, Bd. x. p. 500; Förster, _Ibid._, Bd. xiii. p. 105; Didardier, _L'Union méd._, 1867, No. 83.]

[Footnote 21: _Nederland Weekblat. vor Geneesk._, 1851, p. 44.]

{871} Enchondroma may occur in the mediastinum or lungs; it is rare as a primary process, but is more often found as secondary to enchondromata of the bones.[22]

[Footnote 22: Lebert, _Physiol. Pathol._, ii. p. 213; also, Förster, _Virchow's Arch._, xiii. p. 106.]

ETIOLOGY.--Predisposing and Exciting Causes.--The etiology of morbid growths in the mediastinum, as elsewhere, is subject to debate and conjecture. The most practical query relates to location--viz. that sarcomatous growths originate in the anterior mediastinum, and carcinoma more frequently in the posterior.

The trade of shoemaker was followed by several subjects of sarcoma observed by the writer. These men were accustomed to press the last against the sternum. With a pure family history free from taint of malignant disease the etiology of sarcomata may be more readily linked with some cause of irritation than is the etiology of cancerous tumors. This irritation may be a blow or other direct injury or some local irritation, as antecedent inflammatory process in the lungs, bronchial mucous membrane, or pleura. Intemperance, insufficient food, and over-exercise have been noticed in rare instances as antecedents. In reference to lympho-sarcoma, preceding causal irritation may have existed, but in two-thirds of the cases the etiology is obscure. Hereditary transmission has not been distinctly proven in regard to any of the forms of sarcomata. The etiology of cancerous tumors is still more vague, though possibly the previously-named conditions may have preceded the growth. Louis, speaking generally upon intra-thoracic cancer, places it fourth in the scale of comparative frequency of organs affected--viz. uterus, stomach, liver, and lungs. The history of the removal of a morbid growth may attest the secondary character of some growths apparently primary.

In the question of age and sex the autopsies at Kronstadt already referred to show that in 158 malignant growths 127 were carcinomatous; 81 occurred in men of an average age of fifty-three, and 46 in women of an average age of fifty-six. So we may conclude that carcinomatous growths occur after the middle period of life. In 31 cases of sarcomatous tumors, 20 occurred in men of an average age of thirty-eight, and 11 in women of an average age of forty-eight. Powell gives 24.8 as the mean age for the occurrence of mediastinal growths in general. As a rule, a mediastinal tumor recognized at a relatively early period of life, before the thirtieth year, is most likely to be one of the forms of sarcomata. Sarcomatous tumors, however, sometimes occur in the aged; for example, in a woman æt. seventy-six (Laboriou[23]) and in a woman over sixty reported by Wilson.[24] The question of liability through sex is somewhat uncertain, but while these growths may occur in either, a slight preponderance exists in favor of the male sex, especially if the growth be a lympho-sarcoma.

[Footnote 23: _Virchow's Arch._, _loc. cit._]

[Footnote 24: _Trans. Path. Soc. Philada._, Jan., 1884.]

SYMPTOMS.--In studying the semeiotic characteristics of mediastinal growths an accurate history of the case is a prerequisite of paramount importance to a correct understanding of the essential features of the malady. It should be borne in mind that no single fact determined by the methods of physical diagnosis has special pathological significance, but simply indicates certain definite physical conditions in the region under examination. The purely objective physical signs are so closely intertwined with the general symptoms of morbid process that any study is partial which does not recognize this combination. Both physical signs and general symptoms must be in turn considered in connection with a thoughtful analysis of the processes of morbid anatomy, because symptomatology is the study of the expression of pathological changes. The general nutrition of patients suffering from primary sarcoma or lympho-sarcoma is often good in the early stages of the disease unless the oesophagus is pressed upon or implicated, and at the last {872} patients may even die in a well-nourished condition. Indeed, the special import of the peculiar respiratory disturbance with pain seems set at naught by the appearance of fair health. In some cases of sarcoma or lympho-sarcoma, however, emaciation is progressive, though slower than in cancerous growths.

When cancer itself is primary, the ordinary characteristic train of disturbances of nutrition, with cachexia, follows, and then emaciation is rapid and decided. The loss of nutrition with anæmia is more marked in secondary sarcoma, and in cases of secondary cancer cachexia is the rule.

In reviewing the clinical history attention is specially directed to the development of the mediastinal growth by the gradual increment of subjective sensations of shortness of breath, with a sense of discomfort or tightness in the chest, with or without radiating pains. The respiratory phenomena present great diversity, yet the neurotic character of the dyspnoea is characteristic. Rest or change of posture may remove all oppression, or on the least exertion dyspnoea may be at once manifested. With limited physical signs there may be great distress of breathing or orthopnoea, while in many cases with unquestioned evidence of tumor there may be only a little quickening of respiration. As a rule, tumors of the anterior mediastinum are less characterized by dyspnoea than those involving the posterior space. The dyspnoea depends upon the size and seat of the tumor, and increases day by day with its growth; but in certain cases the tumor is so placed that pressure on the trachea, bronchus, or direct pneumogastric irritation may induce severe paroxysmal attacks of dyspnoea, with laryngeal symptoms resembling the condition so common in aneurismal tumors. Pressure symptoms, traceable to irritation of the pneumogastrics, are, however, as a rule, less marked than in aneurism. Pressure on the trachea without implication of the laryngeal nerves can occasion many of the symptoms usually assigned to the latter cause.[25] Even when the tenth nerves have been surrounded or involved by the growth, special symptoms may be absent, although in other cases serious phenomena follow, such as vomiting or other gastric disturbance, or even inability to swallow; sometimes palpitation, angina, irregular action, or tendency to faintness may follow implication of the cardiac plexus.

[Footnote 25: Bristow, _St. Thomas's Hosp. Rep._, vol. lxxi.: "Influence of Pressure on Trachea without Implication of the Recurrent Laryngeal Nerves."]

The symptom of pain is usually far less than in cases of aneurism, since it is only in rare instances that the chest-walls become eroded by the outward pressure of the tumor, as so frequently occurs in aneurism. Moreover, the growth more readily adapts itself to the contour of the chest, and tends to envelop rather than compress organs or nerves. From the time that pressure commences, either on the trachea, bronchi, or intra-thoracic nerves, cough is more or less constant. It may, however, be due to pulmonary changes occasioned by the pressure or actual involvement of the lung by the growth. Cough is an earlier symptom when the growth is situated in the posterior mediastinum than when it is located anteriorly. It is usually laryngeal and ringing in timbre, and may occur paroxysmally, as in pertussis. It is ineffectual, dry, or attended with only scanty mucous or frothy expectoration. The sputa may be tinged with blood, or profuse hæmoptysis is a possible symptom. A microscopic examination of the sputa in a case of intra-thoracic tumor is always important, because portions of the morbid growth may be found, or by perforation of the trachea or oesophagus the pus from a mediastinal abscess may be mixed with the sputa. Mediastinal tumors are not, as a rule, characterized by febrile symptoms. Inflammatory complications of the lungs or pleura may account for the exceptional thermometric variations. Cases have been reported by Bennett and Church in which there was persistent elevation of temperature, with daily fluctuations and rapidity of pulse and respiration. In one instance of lympho-sarcoma the paroxysms of fever corresponded with the periods of {873} growth in the enlarged glands, but in this case the lymphatics of the general system were also implicated. From the fact that the growths are strictly mesial, dysphagia is a far more common and persistent symptom than in aneurism, especially in growths of the posterior mediastinum. When the growth is situated in the anterior mediastinum the dysphagia is less frequent; but it must be borne in mind that prolongations of the tumor may occasion lateral oesophageal pressure, or narrowing of the lumen of the oesophagus can occur from pressure upon the trachea by the growth. Exceptionally, dysphagia may be due to implication of the oesophagus in the new growth. (See Cancer of the Lung.) Neural influences may increase the dysphagia, in which case it is doubtless a reflex phenomenon and is associated with hiccough or vomiting. The passage of a bougie can be readily effected in such cases.

In reference to the foregoing pressure symptoms one fact deserves recognition--viz. that in aneurismal tumors the pressure symptoms are subject to variations in intensity due to changes in the intra-aneurismal tension, while in morbid growths in the mediastinum the pressure symptoms exhibit a progressive tendency, advance upon the same lines, and are more constant than in aneurism. With this principle in mind, the additional pressure symptoms in doubtful cases of mediastinal growth must all be considered; for instance, in some histories recorded by Rossbach the pupils could be dilated by firm pressure on the tumor above the clavicle. The pulses in the brachials or radials may be unequal, and variations of rhythm, volume, and rate may be noted as evidences of pressure, which may occasion thrombosis by retarding the circulation in the innominate, subclavian, or azygos vein. The blood may reach the heart by the collateral circulation elsewhere described or by the dilated mammary superior and inferior epigastrics and the inferior vena cava. Pressure may therefore give rise to cyanosis, oedema of the upper or lower portions of the body, with enlargement of the superficial veins, or dropsy may be traceable to hydræmia.

PHYSICAL SIGNS.--When mediastinal tumors are of small size, physical signs may afford no help in making a diagnosis, and they will always vary according to the location of the growth.

Inspection may reveal venous repletion of the veins of the face and neck, with distension of the superficial veins of the chest; the latter symptom is more frequently obvious than in aneurism. In the case of sarcoma represented by Fig. 53 the foreign growth was so limited to the mesial line as not to involve the vessels or create pressure symptoms upon them. If the anterior mediastinum is implicated, there may be circumscribed alterations in the contour of the chest. Prominence of the upper piece of the sternum and of the sternal attachment of one or more ribs may be recognized. The sternum itself may appear thickened upon palpation of the notch. One side of the chest may be larger than the other above the nipple-line; the affected side, however, may be smaller, since vicarious respiratory function may create distension. The usual changes in the contour of the chest-walls will indicate pleural effusions. (See Cancer of the Lungs.) Since tumors of the anterior mediastinum overlie the aorta, transmitted pulsation may be detected in rare instances; this pulsation can be differentiated from aneurismal vibrations by the absence of the sense of expansile pulsation characteristic of dilated aorta or aneurism, but it sometimes closely resembles that yielded by an aneurismal sac thickly lined by coagulum.

Lympho-sarcoma and cancer are often accompanied by painless, movable glandular enlargements, recognizable by palpation in the supra-clavicular spaces; but the absence of the glandular implication in sarcomata is conspicuous; swelling occasionally manifests itself in the suprasternal notch. Tumors of the posterior mediastinum must attain considerable size before {874} they can be recognizable by the foregoing methods. Growths in the latter space are those especially liable to complication by pleural effusion in one or both sides. Mediastinal growths may occasion collapse of the lung, or cirrhotic processes or pleural adhesions may diminish the circumferential measurements of the chest. The heart may be displaced backward, downward, to the left or to the right side; and since in aneurism, uncombined with valvular disease, little cardiac displacement occurs, this sign is of importance. Rarely, as in Cotton's case in Brompton Hospital, the heart may be fixed in situ by the extension of the growth on both sides of it.

Percussion.--It has been observed that a very small tumor may, from its particular site, at a very early stage give rise to symptoms both of pressure and disordered innervation of great severity, whilst another may attain considerable magnitude before the patient experiences any distress or any decided evidence of pressure is manifested. It is equally true that percussion and auscultation may be most valuable, or, on the other hand, indefinite. The degree of dulness occasioned by a morbid growth in the anterior mediastinum is dependent on its size, large growths yielding flatness; but when the tumors are small the osteal resonance of the sternum is simply hardened. Respiratory percussion is available if the growth lies anteriorly. The full, clear resonance of full-held inspiration contrasts with the increased dulness developed when the lungs are stripped from the mediastinal space by forced expiration. The boundaries of the growth on either side of the sternum may be defined by percussion, and it is possible that the greater part of one side may be occupied by the new formation. The adjacent tissues are involved by direct invasion, or indirectly by extension along the bronchus from behind forward, thus involving the middle tier of the lung. Mediastinal tumors therefore in their mode of growth yield a contrast with pleural effusions, because the latter usually advance steadily from below upward. When the growth is located in the posterior mediastinum, percussion should be practised after the manner recommended by Mussey to facilitate recognition of enlarged bronchial glands. (See Pulmonary Syphilis.) The apices, humeral, scapular, basic, or marginal regions often yield a tympanitic type of resonance, since they are often in a condition of vesicular emphysema. The pericardial sac may be distended with effusion or implicated in the growth, and an area of pyramidal dulness with the base above may be recognizable.

Auscultation.--In growths situated anteriorly, in the mesial line, one of the most forcible lessons may be impressed by the distance and obscurity of the second sounds of the heart over the aortic and pulmonary artery, cartilages, or the upper piece of the sternum. The cardiac sounds may be transmitted downward, and can be heard distinctly in some abnormal position. Even a murmur can occur due to compression of the aorta, or pericardial friction. The respiratory murmur will probably seem feeble and distant over one or both apices, and whistling near the trachea.

If the posterior mediastinal space be involved, the respiratory murmur may represent some type of bronchial breathing, or if the lumen of the trachea or one of the bronchi be decidedly lessened, the respiratory murmur may be whistling, feeble, or suppressed over the affected side. Over the other bronchus the respiratory murmur may be more high-pitched than in health, and slightly exaggerated. The rhythm is often jerky and paroxysmal; the paroxysms are more or less constant, but are liable at times to increase. Auscultation should be especially practised over the roots of the lungs or in the neighborhood of the second dorsal vertebra. Frequently it can be demonstrated, both by auscultation and percussion, that there is diminished air-supply to one or other of the lungs, while the respiratory murmur is not sufficiently changed for classification. The respiration may acquire a stridulous or sibilant character, most marked on expiration, but {875} less often than in aneurism, because there is a greater tendency to occlusion of the bronchi. It should always be remembered that the lung undergoes very various and opposite changes as the result of pressure on the bronchi, interrupting the entrance and egress of air from the lobules, and the physical signs of emphysema, infarction, congestion, or consolidation may exist in one or the other side. The ordinary methods of physical examination indicate the existence of pleural effusions, but large growths extending from the mediastinum or originating in the lung may so closely simulate such effusions that a positive diagnosis can be arrived at only by paracentesis.

When tumors exist in the form of very small nodules as diffused sarcomata, no changes in the character of the respiration may be noted. Friction râles and pleuro-pericardial frictions may be heard in some cases. Distension of the bronchial tubes from pressure may occasion the dilatation of the distal bronchial passages and pulmonary lobules with retained muco-purulent secretions. The cross-sections of the bronchi have been described as multiple abscesses. Areas of collapse or slow inflammation with softening of the secondary inflammatory product can follow. The bronchial pressure may prevent the sufficient transit of air through the bronchi to create râles, or moist râles indicative of tracheo-bronchitis or oedema may abound.

The study of the vocal resonance and fremitus presents nothing novel, but corresponds with the generally-understood principles.

DURATION.--It is very difficult to determine accurately the duration of malignant diseases of the mediastinum, since for a long time the patient may be quite free from any local subjective symptom, even though a growth may have attained to a considerable size. Moreover, intra-thoracic malignant disease, especially in the non-cancerous varieties and if the digestive tract be normal, may be unattended by any of those symptoms commonly associated with malignant process, such as a peculiar tint of skin, progressive and great emaciation, or the aspect of suffering. Sarcomatous tumors usually grow rapidly, as in a case related by Jaccoud, in which death occurred within eight days after admission to the hospital. Prior to this time the patient had suffered from no objective symptoms whatever, although when admitted there was physical evidence of a large growth extending from the clavicle to the nipple.[26] West records a fatal case at two and a half months; Horstman, one in which the disease originated on the right of the sternum, as evidenced by a very small area of dulness; the entire right side of the thorax was invaded within five weeks.[27] Berevidge reports a case of sudden death from hæmoptysis in a man aged sixty-four years, who up to that time had appeared healthy, and only a few days before had complained of a slight cough and a feeling of oppression in the chest. At the autopsy two cancerous masses the size of a hazelnut were found, one of which overlaid a bronchus which was ulcerated to a considerable extent. The bronchi were filled with blood. Virchow mentions a case the duration of which was only two months. Walsh, speaking of malignant growths in general, assigns three and a half months as the minimum duration of these cases.

[Footnote 26: _Leçon de Clin. méd._, p. 636, Paris, 1867.]

[Footnote 27: _Trans. Path. Soc. London_, 1883.]

Undoubtedly, the duration will depend on the freedom from pressure upon the oesophagus, or from interference with digestion due to pneumogastric irritation, or from malignant processes in the stomach or intestines. Pain, and consequent loss of sleep, will also accelerate the termination of any case. Lebert assumes an average duration of thirteen months, and Walsh states the maximum duration in intra-thoracic malignant processes at twenty-seven months. The soft secondary malignant sarcomata or carcinomata grow more quickly, and have a relatively shorter course, than the harder forms of the same species. Lymphadenoma may persist a long time, and appear for a while to be stationary and unattended by any serious impairment of the general {876} health, but the cases are exceptional. The persistence of fibrous, fatty, or cystic tumors depends chiefly on the mechanical inconvenience occasioned by them. All forms of malignant intra-thoracic disease, however, are steadily progressive to a fatal termination. Death commonly arises from the gradual increase in seriousness of the pressure symptoms. Inability to lie down, harassing cough, want of sleep, all tend to induce fatigue which may prove fatal. Deficient aëration of the blood may occasion stupor, or sudden simultaneous pleural and pericardial effusion or general pulmonary oedema may terminate the scene. In exceptional instances death has resulted from laryngeal spasm or from acute hypertrophy of the thyroid gland with tracheal occlusion. In a remarkable case reported by Bennett paroxysmal dyspnoea had been the only symptom of intra-thoracic disease for a few months, when suddenly a severe seizure occurred which persisted uninterruptedly for three days, till weakness and exhaustion terminated in death by asphyxia. In this case the thyroid gland was found enlarged to the size of a double fist, but the enlargement was mainly below the sternum and along the sides of the trachea, which was literally surrounded by the greatly-enlarged and firm lateral lobes of the thyroid, so as to be completely flattened laterally. The structure of the thyroid appeared healthy, but very firm, and the enlargement was due solely to hypertrophy, and not to cystic or other disease, nor was there any exophthalmos.[28] Death is possible from sudden asthmatic attack, or, more rarely of all, by hæmoptysis.

[Footnote 28: See "Cancerous and Other Intra-thoracic Growths," Bennett, _The Lumleian Lect._, 1872, p. 169.]

PROGNOSIS.--The prognosis is invariably unfavorable, and must continue so unless the more recent attempts for removal of primary growths in the anterior thoracic regions yield grounds for a more hopeful outlook. We may also hope that some remedy may influence or control the development of lymphoma. Considerable relief may be obtained by rest, suitable feeding, careful regulation of the digestive system, and such hygienic measures as may seem most available.

DIAGNOSIS.--From Aneurism.--When we consider that in the diagnosis of aneurism of the aorta every sign and symptom has in turn been found fallacious in the ever-varying conditions under which aneurisms appear, and that one is forced to say that aneurism has no pathognomonic signs or symptoms, the difficulties in the way of the diagnosis of intra-thoracic morbid growths may be recognized. Moreover, the diversity in the peculiarities of each case, the multifarious character of the pressure symptoms and physical signs, and the absence of a precise order of phenomena peculiar to tumors in this situation, may render a positive diagnosis in the early stages very difficult.

Aneurism in the absence of unequivocal signs of its existence may be excluded on the following grounds: the absence of conditions which predispose to disease of the coats of the arteries--_i.e._ syphilis, alcoholism, Bright's disease, rheumatism, laborious avocations, violent exercise. Aneurism may occur at any age, but it is rare before the age of thirty years, and most prevalent between the ages of forty and fifty years. Aneurism is also less frequent in the female sex. The distal pressure symptoms of aneurism are more variable than in other morbid growths of the mediastinum, and especially dysphagia is less constant. Great emaciation without intense pain is adverse to the diagnosis of aneurism, while severe pain with occasional exacerbations is favorable to this diagnosis. However, instances of morbid growths are recorded in which intercosto-humeral neuralgia was an initial symptom.

"An extensive area of dulness must in aneurism mean a large sac, and with such a large tumor we should almost invariably get marked expansive pulsation. Again, aneurismal sacs, before they produce extensive dulness in {877} any portion of the parietes of the chest, point, as it were, in some particular direction, becoming distinctly prominent and producing an eccentric motion around them in consequence of the thoracic parietes being absorbed or yielding at the point of greatest pressure" (Graves). Hæmoptysis may occur not only from aneurismal leakage, but from the effects of pressure of morbid growths upon a bronchus or the invasion of the same by the malignant process. Blood-spitting cannot therefore be regarded as an important differential symptom. Unless valvular disease be associated with aneurism, the displacement of the heart is less frequent in aneurism than in morbid growths.

From Abscess.--The etiological relation in this process is traumatic, or mediastinal abscess occurs in connection with caries or fracture or after an operation in the neighborhood of the throat or neck, or of suppurative disease elsewhere in the thorax, as abscess of the lung or empyema. The pain in cases of abscess is deep-seated, constant, slowly increasing, rather than the paroxysmal pain of aneurism or solid tumor. The febrile movement may afford decided aid in the diagnosis, but it is also true that high temperature may mark the progress of lymphadenomata, as in Bennett and Sutton's case, in which from Jan. 11th to Feb. 28th the thermometrical wave vibrated between 103.5° maximum, with a pulse of 148 per minute, to 100.5° minimum, with a pulse of 108. In this remarkable case sweating was also a prominent feature; and a somewhat similar example has been recorded by Murchison. In corresponding circumstances the existence of secondary processes in the lungs or elsewhere, with enlarged glands in the neck, may prevent error. In mediastinal abscess there will probably be a tendency to point, with the appearance of a fluctuating, circumscribed, superficial tumor at the sternal border or adjacent to this bone. There may also be tenderness on pressure associated with the pain, and an oedematous condition of the tissues of that portion of the sternal region covering the tumor, although this symptom sometimes attends malignant new formations. Pulsation may accompany abscess, but will be of the transmitted variety. In suspicious cases the sternal bone can be drilled and an exploratory needle introduced into the tumor.

The general diagnosis of mediastinal tumor can be more easily made upon the basis of regional invasion. But in any suspicious case an elaborate and thorough clinical history is an essential prerequisite. In proportion as one completes the natural history of a case of obscure intra-thoracic disease the more likely one is to approach by exclusion a correct interpretation of the existing physical signs and symptoms.

Growths in the Anterior Mediastinum.--Tumors located in the anterior mediastinal space overlie the heart and aorta, and consequently the heart-sounds, especially the second, may be indistinct or muffled; or the second sounds may be audible in some new situation, owing to displacement of the heart. The sternal region may be distinctly prominent or bulged, and at the notch the bone may appear thickened. The resonance in the interscapular regions remains unimpaired, but over the sternum percussion should yield a very dull sound if the growth be large, but when a comparatively small tumor exists the sternal resonance will be hardened and high-pitched. An additional explanation of this modification exists in instances where the growth is not adherent to the sternum and the bone is arched over the tumor.

The respiration may be whistling or stridulous if the stethoscope is placed over the trachea, and over one or other apex anteriorly the respiratory murmur may be feeble or blowing, in proportion to the volume of air which is permitted to enter the chest. Posteriorly, the respiratory murmur may be unaffected at first, although as the growth advances evidence of pressure on the bronchial tubes may be detected over the interscapular region. The superficial veins of the chest may be enlarged, especially those below the level of the upper segment of the sternum. Dysphagia is usually slight in {878} proportion to the other pressure symptoms or entirely absent. It may be simply a symptom of irritation of the intra-thoracic nerves or due to enlargement of the glands of the mediastinum.

Mediastinal growths usually develop in the middle line; they spread in all directions, especially laterally, but avoid at first the roots of the lungs. Pressure is rather exercised upon the parts in the mesial line. They reach a large size and grow with great rapidity, producing symptoms rather as a consequence of their size than by virtue of contractile properties.

From Pericarditis.--A possible pericarditis may be mistaken for a tumor of the anterior mediastinum. The diagnosis of pericarditis must be sustained by evidence showing the dependence of this process upon rheumatism, syphilis, nephritis, or propagated inflammation. The distension of the pericardial sac due to pericarditis exhibits a definite outline. The dulness of a tumor is irregular, with a tier of dulness upon a higher level than in effusion. The absence of various pressure signs is marked in pericarditis, while disturbance of the heart's rhythm is more frequent. Kussmaul states that there are two signs characteristic of chronic pericardial inflammation with thickening and adhesion--viz.: a "complete or almost complete failure of the radial pulse during inspiration, and simultaneously visible swelling of the great veins of the neck, instead of the collapse that usually takes place during this portion of the expiratory act. Adhesion of the great vessels to the sternum, either directly or through the medium of the pericardium, is supposed to account for these phenomena."

Febrile movement is usually present in pericarditis, and, while a possible temporary feature in new growths, is not persistent unless complicated by inflammation in the pulmonary tissues. Finally, the progress of the case will often decide the question.

Growths in the Posterior Mediastinum.--In growths located in the posterior mediastinum one or the other bronchus is one of the earliest structures implicated by the pressure, because in these cases the chief mass of tumor is found at the root of the lung. Secondary lesions in the lungs directly traceable to pressure are frequent, but unilateral, although secondary cancer from malignant lesions elsewhere than in the lungs may be bilateral. Pressure symptoms as a class occur early, are grave, constant, and progressive. Percussion according to directions of Guéneau de Mussy may be made available. Abolition or great impairment of breath and voice sounds over one or other posterior aspect of the chest is the rule, since these tumors are prone to contraction. Sometimes the respiratory murmur is whistling or blowing if the bronchial pressure is less decided. Progressive emaciation and cachexia are commonly present, not only from the inherent tendencies of the disease, but also depending upon the disturbance of the functions of many important organs which have been encroached upon by the tumor. The exclusion of a malignant disease of the oesophagus is very difficult. The passage of a bougie might determine the seat of obstruction, and thus assist in the diagnosis, but great caution must be observed lest penetration of the softened tissues occur. (See Cancer of Oesophagus.)

From Pleural Effusion.--The greatest difficulty may be experienced in deciding between uncomplicated pleurisy and effusion complicated by morbid growth.

Aside from the history of the case and state of nutrition, paracentesis may aid the diagnosis, since, if the fluid is turbid, highly albuminous, with a large proportion of coagulable fibrin, it is an evidence of inflammatory origin; but if it is clear, limpid, and on standing gives but a delicate veil of pseudo-fibrin, it indicates a passive or mechanical cause. Hemorrhagic exudation is only of relative importance. The recognition of pleural friction râles over parts flat on percussion will be an evidence of tumor. Hæmoptysis in this {879} association would negative the idea of simple effusion. The presence of signs of pressure on central parts is indicative of tumor (Walsh), but Powell has recorded an instance of simple pleural effusion accompanied by husky voice and laryngeal cough; and also an instance in which, from a similar cause, there was increased size, tortuosity, and throbbing of the radial and brachial arteries on the affected side without oedema of the limb, yet probably attributable to obstruction of the return circulation.

Enlarged glands in the neck, or enlarged veins with evidence of thrombosis of the descending vena cava, would indicate tumor. Dulness from a tumor itself might resemble sacculated effusion, yet there might be retraction in place of distension of the chest, and particularly characteristic dulness in the mediastinal region as compared with the circumferential regions, or peripheral patches of resonance may be suggestive and lead to critical revision of the symptoms.

From Chronic Pneumonia.--Mediastinal growth invading the lung from its root has been mistaken for chronic pneumonia. Walsh lays stress on the following signs as distinguishing tumor: 1. A tendency to increase instead of diminution of bulk of the affected side. 2. Implication of the mediastinum, with dyspnoea out of proportion to the extent of consolidation. 3. Different characters of respiration in the two diseases. To these may be added pressure symptoms in general in cases of tumor, with displacement of the heart toward the side unaffected by the pulmonary process. Hæmoptysis is very often a concomitant of bronchial pressure, but occurs so frequently in basic pneumonia, especially in the syphilitic, that it is devoid of importance except from the standpoint of relative investigation. With reference to symptoms of bronchial irritation without assignable cause, we should always do well to remember the observation of Stokes, that they may be characteristic of disseminated morbid process.

Differentiation of Malignant Growths.--The younger the patient the more probable the existence of lymphoma or sarcoma. The majority of primary tumors of the mediastinum are lymphomatous, and when the growths originate in the anterior space they are almost certainly lympho-sarcoma or sarcoma. Widespread enlargement of the lymphatic glands, with or without enlargement of the spleen, indicates a lymphadenoma.

Finally, primary lympho-sarcoma or sarcoma tends to spread by extension of the process by continuity of structure, although secondary forms of the process present lesions distributed through the lungs.

The evidence in favor of sarcoma may be drawn from exclusion of the other forms of morbid process, from the rapidity of the growth, and from the history of previous operative interference for the removal of foreign growth, especially if the previous disease were sarcomatous.

Carcinomata may be suspected in cases in which there has been an hereditary predisposition to carcinomatous disease or the previous or concomitant existence of cancerous disease in the mammæ or elsewhere, particularly if the period of life is relatively advanced. The development of the tumor may be more slow than other forms of growth, and is associated with tendency to progressive emaciation in the absence of evidences of direct pressure on the oesophagus and the existence of cachexia. Carcinomatous disease is more commonly coincident with the presence of hard, nodular, immovable masses in the neck.

Cystic tumors present signs of fluctuation. Syphilitic gummata must be diagnosticated by exclusion and the existence of the syphilitic history. The possibility of substernal thickening due to syphilis, with reflex disturbances, particularly oesophageal spasm, must be borne in mind.

Those rare forms of disease due to hyperplasia or caseous deposit in the thoracic glands, independent of pulmonary disease, must be recognized by {880} exclusion. The fact must be remembered that with great enlargement of glands in the neck and elsewhere the bronchial glands may remain constantly unaffected.

TREATMENT.--From the inaccessible location of these growths but little assistance can be rendered by surgery. The progress of this branch of science has of recent years included resection or excision of the sternum or some of the ribs for the removal of growths involving the mediastinum or pleura. Küster[29] has successfully made partial resections of the sternum for the removal of mediastinal tumors, and the entire bone has been excised by König[30] in a case of sarcoma. The pericardial and both pleural cavities were opened in the course of the dissection; the wound became gangrenous, and the heart was afterward surrounded with pus: notwithstanding this, the wound slowly healed and the patient ultimately recovered. In cases treated by this method pleural adhesions usually prevent double pneumothorax; portions of the ribs have been resected with the sternum, and have been succeeded by unilateral pneumothorax, and recovery has ensued. (See Fig. 55.)

[Footnote 29: _Berliner klinische Wochenschrift_, No. 20, 1883, pp. 127, 136, 274.]

[Footnote 30: _Centralblatt f. Chir._, No. 42, 1882.]

Paracentesis must sometimes be practised to relieve accumulation of fluid in the pleural sacs in instances in which dyspnoea is serious, and life may be prolonged by repeatedly practising this operation. Reflex laryngeal irritation, or paroxysmal dyspnoea with stridulous breathing, requires the use of inhalations or atomization of antispasmodics, and among the most useful of these are ether and chloroform. This group of neural symptoms can sometimes be markedly palliated by hypodermic use of morphia with atropia. But too often the symptoms are caused by actual pressure, and not by nerve-irritation, and this mode of treatment is futile, and therefore these measures should be employed with caution.

{881} Sleeplessness, cough, bronchial or other pulmonary complications, must be managed upon general principles. The local pains may be met by local treatment, such as mustard sinapisms or soothing lotions; even blisters may secure temporary relief. The digestive system should be carefully studied, and assimilable and appropriate food should be selected. In lymphadenoma combinations of iodine with arsenic, as in Donovan's solution, may be tried, but, unfortunately, the utmost aid from present resources consists in a palliative and expectant policy.

{882}

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.

BY WILLIAM OSLER, M.D.

INTRODUCTION.

The blood is a fluid tissue composed of cells floating in an albuminous plasma, and it differs from other tissues not less in the arrangement of its elements than in the activity of the changes which go on in it. It is the mart into which is poured from the alimentary canal the commodities needed in nutrition, and the elements of the body select from it the various materials which they require, giving in exchange those chemical combinations which result from the metabolism of the tissues. In spite of ceaseless changes, a uniformity of composition is one of the most striking features of the blood in health. This is maintained, as regards the constituents of the plasma, by the activity of the organs which regulate income and expenditure--the alimentary canal and liver on the one hand, and the kidneys, lungs, and skin on the other; while histological uniformity is maintained by the adenoid or cytogenous tissue throughout the body, the function of which is to replace the wornout blood-corpuscles.

The corpuscles form rather less than one-half by weight of the blood. The plasma contains about 90 per cent. of water, which holds in solution proteids in the form of serum, albumen, and the fibrin-forming factors; sugar in traces; creatin, hypoxanthin, and urea; various fatty bodies in small amount; salts, chiefly sodium; and gases. The corpuscles (red) consist of hæmoglobin (90 per cent.), proteid bodies, and traces of lecithin and cholesterin.

So far as we know at present of the function of these two portions of the blood, the plasma ministers to the general nutrition of the tissues, while the corpuscles (red) are chiefly concerned with respiratory processes, acting as the carriers of oxygen and carbonic oxide.

We shall first give a brief account of the histological characters of the blood, and of the relation of the groups of adenoid or cytogenous tissue to the corpuscles.

Two forms of corpuscles are usually described, but we can recognize four varieties of blood-corpuscles in the body: (1) red, (2) white, (3) nucleated red, and (4) the hæmatoblasts (Hayem), or blood-plates of Bizzozero.

(1) Red Corpuscles.--In each cubic millimeter of plasma there are about 5,000,000 red cells. The percentage may vary within health limits from 90 to 110. The corpuscles are circular, non-nucleated, biconcave disks, homogeneous, to ordinary inspection structureless, and consist of a colorless stroma which is possibly reticulated, and a red coloring matter, the hæmoglobin. In {883} health they are tolerably uniform in size, about 7.9 µ[1] in diameter, or in English measurement 1/3200 of an inch (Gulliver). Even in normal blood there may be slight variations in size between 6.5 µ and 8.5 µ, the average, according to Hayem, being 7.5 µ.

[Footnote 1: µ is used to signify a micro-millimeter or 1/1000 part of a millimeter.]

(2) Colorless or white corpuscles, nucleated masses of protoplasm, with an average diameter of 10 µ, or about 1/2500 of an inch. The majority have a finely granular protoplasm, but in a few the granules are coarse and do not completely fill the clear protoplasm. The ultimate structure is reticular (Heitzman). Erhlich[2] has shown by their varying reaction to eosin that there are chemical differences among the colorless cells quite unrecognizable by other means. In healthy blood they display active amoeboid changes at ordinary temperatures. Their protoplasm does not, as is commonly stated, rapidly disintegrate, but if kept at a medium temperature retains its vitality, as shown by movements, for hours. The number per cubic millimeter is from 8 to 15 millions, and the ratio to the red is variously computed as 1 to 300 or 1 to 500.

[Footnote 2: _Frerichs find Leyden's Archiv_, Bd. i.]

(3) Nucleated red corpuscles, which occur in the blood of the foetus and the infant, gradually diminishing until at the third or fourth year they disappear. In the adult they do not occur in the blood in health, but are normal constituents of the red marrow of the short bones. They measure from 1/1500 to 1/2000 of an inch, and are of somewhat variable intensity of color, often quite as deep as the ordinary red forms. There may be two or even three nuclei, not colored, grouped together, often eccentric, and in some instances protruding from the cell.

(4) The hæmatoblasts of Hayem, the blood-plates of Bizzozero, the elementary or intermediate corpuscles, are small discoid colorless corpuscles about 3 µ in diameter, and are normal constituents of healthy blood. When the blood is withdrawn, they aggregate together into irregular clumps or masses, which have long been known as Schultze's granule-masses. It can be readily demonstrated in new-born rats or kittens, in which these masses abound, that the corpuscles composing them are isolated in the vessels, and only run together when the blood is drawn. The statement is commonly made that the granule-masses of Schultze result from the disintegration of the white corpuscle (of the red, Erhlich), but half an hour's study of the question in a new-born rat will convince any competent histologist that we have here to do with a separate blood-element.[3] It appears to have important relations with the production of fibrin.

[Footnote 3: Consult _Proceedings Royal Society_, 1874; _Centralblatt f. d. Med. Wissenschaften_; _Medical News_, 1882, 2; Bizzozero, _Virchow's Archiv_, Bd. xi.; Hayem, _Recherches sur l'Anatomie normal et pathologique du Sang_, Paris, 1878.]

Of the origin and life-history of the red corpuscles during post-embryonic life we have still much to learn. They are stated to develop--

(1) From colorless corpuscles, the lymph-cells or leucocytes. In the lymph-glands, the Malpighian bodies of the spleen, in the thymus, or the adenoid tissue of the tonsil, of the lymph-elements in the intestines and other regions, colorless cells are constantly being manufactured, and the general belief has been since Hewson's time that the red corpuscles develop in some way or other from these leucocytes. How or where has not yet been settled. It does not apparently go on in the blood, or we should surely catch, in the many observations and with the excellent powers now in use, a glimpse of the birth of one of them. Some observers (Johnstone[4]) maintain that they develop from the granular protoplasm of the adenoid reticulum by a process of budding. This may be so, but we should expect to find the lymph in the efferent {884} vessels and of the thoracic duct much more rich in red cells than is usually the case, and in specimens of healthy glands we should find young-looking elements such as he describes.

[Footnote 4: _Seguin's Archiv_, vol. vi.]

(2) From the nucleated red corpuscles. In the embryo this undoubtedly takes place, and as the weeks of development proceed, the ordinary red forms gradually predominate. In the child the red nucleated cells disappear early, and are then found only in the red marrow. So far as my observations go,[5] they apparently originate from colorless marrow-cells, which gradually become more homogeneous, and hæmoglobin develops in the protoplasm. The nucleus degenerates and disappears, when the cell has the appearance of an ordinary red disk. Rindfleisch thinks that the nucleus of the nucleated red is extruded in the development. It is possible that from these nucleated red corpuscles cells may originate in another way--viz. by budding. This I have seen and sketched in the marrow-cells,[6] and Malassez has studied the same process.[7] The gemmæ are small, and sprout from the protoplasm, not the nuclei, and when they break off they resemble the microcytes which occur so abundantly in certain anæmic states. Bizzozero[8] holds that these nucleated red corpuscles are independent elements which do not develop from the colorless marrow-cells. They multiply by fission, and develop into the ordinary red forms with the disappearance of the nuclei. Several recent investigations support this view.[9]

[Footnote 5: _Centralblatt f. d. Med. Wissensch._, 1878.]

[Footnote 6: _Trans. Am. Ass. Ad. Science_, 1882.]

[Footnote 7: _Archives de Physiologie_, 1882.]

[Footnote 8: _Centralblatt f. d. Med. Wissenschaften_, Bd. xix.]

[Footnote 9: _Fortschritte der Medicin_, 1885, No. 1.]

(3) Hayem believes that the red corpuscles develop from the small hæmatoblasts, but, so far as I know, his observations have never been confirmed. He states that in normal blood they occur in the proportion of about 1 to 20 red. In all states of blood reparation they increase greatly. He describes a hæmatoblastic crisis as occurring after hemorrhage, fevers, etc., when the number of these elements rapidly augments, and is succeeded by the addition of many small pale-red corpuscles, which he looks upon as intermediate between the hæmatoblasts and the ordinary red forms.

The colorless corpuscles are regarded as the direct offspring of the cells of the follicular cords in the lymph-glands and adenoid tissue, but whether by process of division of existing leucocytes or by sprouting from the endothelial places, or from the protoplasm in the fibres of the reticulum, remains to be settled.

The nucleated red corpuscles are in the healthy adult confined to red marrow, in which they probably develop from colorless cells, and may be regarded, as Neumann originally suggested, as transitional or intermediate forms between white and red cells. In anæmic states they may occur in the spleen and in the lymph-glands.

Of the origin of the hæmatoblasts or blood-plates we know absolutely nothing. They occur most abundantly under two most opposite conditions--in the young growing animal just entering upon life, and in the diseased, cachectic, wornout animal just preparing to abandon it.

Our knowledge of the relation of the cytogenetic organs to blood-formation may be thus briefly stated: The spleen certainly takes part in the development of colorless corpuscles, but its participation in red blood-formation is more doubtful. The nucleated red or embryonal forms do not occur, at least in any numbers, in health, though some observers have noted that after a repeated bleeding the organ was swollen and contained many such cells, as if it was the seat of an active development. Though the opinion prevails widely that the spleen is one of the important organs in the formation of red corpuscles, the evidence for this belief is of an exceedingly scanty nature.

The lymphatic glands and the adenoid tissue in other regions are the seats {885} of constant production of colorless corpuscles, but of their relation to the red corpuscles there is the same lack of information as in the spleen. I do not know of any corroboration of the observation of Johnstone above mentioned, and in any case the number of red cells in the efferent vessels of a lymph-gland is so small--and indeed in the thoracic duct itself--that we cannot believe they are produced as red corpuscles in large numbers within the lymphatic system.

The red bone-marrow, as pointed out by Neumann[10] and Bizzozero,[11] appears to be the seat of blood-formation, and in the adult body is the only region in which the embryonic or nucleated red cells are found. It is a tissue similar in many respects to the spleen, and, though confined to the short and flat bones, the total amount in the body is very considerable. In the young it also fills the long bones. The evidence of the development of red corpuscles in the marrow rests upon the constant presence of nucleated cells infiltrated with hæmoglobin, and of their fission. Forms undergoing the process of karyokinesis can be seen without difficulty. In excessive hemorrhage, natural or induced, it appears to undergo an active proliferation, and in the long bones a red marrow may replace the fatty tissue.

[Footnote 10: _Centralblatt f. d. Med. Wissenschaften_, 1868.]

[Footnote 11: _Ibid._, 1868.]

The liver is doubtless the seat of blood-destruction, for the bile-pigments and leucocytes with red corpuscles in their interior have been found in its tissue. Nicolaides[12] has shown that in the blood of the hepatic vein there may be a reduction of from one million to one million and a half of red corpuscles per c.m. In the embryo Neumann[13] has shown that it may be the seat of the production of corpuscles, but there is no satisfactory evidence that in the adult this ever takes place.

[Footnote 12: _Archives de Physiologie_, 1882.]

[Footnote 13: _Archiv der Heilkunde_, xv.]

The remarkable rapidity with which, after a profuse bleeding, the normal proportion of red corpuscles is reached shows with what activity the development may proceed, and how favorable the conditions must be for their production. After the loss of a large quantity of blood the manufacture of new corpuscles may proceed at the rate of 30,000, 40,000, or even 50,000 a day.

What becomes of the red corpuscles? Here, again, is a question not satisfactorily settled. We do not know the average length of life of corpuscles. They are supposed to be short-lived--three weeks, according to Quincke. The need for their dissolution is assumed to provide pigment for the various secretions and tissues, and we occasionally see a few cells in the blood with a pallor which may be regarded as an indication of senility.

Positive evidence, however, of their destruction is afforded by the occurrence of the so-called corpuscles containing red corpuscles, which occur normally in red marrow and in the spleen, and under some circumstances in the lymphatic glands and liver. The red cells undergo gradual transformation into a yellow granular, and finally black, pigment. In normal spleen and marrow the numbers found are very variable; in fevers and cachectic states they may be in extraordinary numbers. Quincke and his pupil Peters[14] have studied with great care this process of transformation of the red corpuscles and accumulation of the pigment in the cells of the marrow, spleen, liver, and lymph-glands, to which the term siderosis is applied. These pigment-granules are in the form of an iron albuminate, and are used in the development of new corpuscles. Thus, after repeated bleedings in animals, they may disappear completely in the restoration of the blood, while in animals into whose vessels blood has been transfused or injected subcutaneously the iron-containing cells in the various organs are very numerous, and even the cortical cells of the kidney contain numerous granules.

[Footnote 14: _Deutsches Archiv f. klin. Med._, Bds. xxv., xxvii., xxxii., xxxiii.]

The amount of hæmoglobin in 100 grammes of healthy blood is {886} 13.45 grm. (Preyer). Malassez estimated the quantity in a cubic millimeter of blood at between 0.125 and 0.134 milligramme, and, taking the corpuscular richness at from 4,000,000 to 4,600,000, he has estimated approximately the amount of hæmoglobin in each corpuscle.

PLETHORA.

General and persistent polyæmia or plethora has scarcely a place in recent pathology. Formerly it was thought that either from over-production or lowered expenditure the total amount of blood accumulated and filled the blood-vessels to an abnormal extent. The amount of blood undergoes, within limits, constant daily alterations, and after a full meal the vessels are in a state of plethora compared with their condition at the end of a ten hours' fast. If a plethysmograph could be devised to record graphically the variations in the total quantity of blood, each ingestion of food or drink into the vessels would be followed by a rise, and each interval by a gradual decline. So long as the organs of secretion and excretion are active the quantitative and qualitative condition of the blood is maintained at a tolerably uniform standard in each individual. At different periods of life the relation of blood-weight to body-weight varies. In the new-born the blood amounts to one-eighteenth part by weight of the body, while in the adult the average is from one-twelfth to one-fourteenth; so that in the infant there is a condition of comparative plethora. There are no reliable observations on the proportion of blood- to body-weight at respective ages, but there appears to be a reduction in old age. In women it is stated that just before each menstrual period there is a state of polyæmia.[15]

[Footnote 15: Mary Putnam Jacobi, _The Question of Rest for Women_, New York.]

Worm-Müller[16] and Cohnheim[17] have made some very interesting experiments on this question of plethora. By transfusion in dogs a state of artificial plethora is readily established, and the animals stand the injection of as much as 10 or 12 per cent. of the body-weight of blood, above which quantity a fatal result ensues. After an injection of 20 or 30 per cent. of the total amount of blood, the superfluous plasma and corpuscles are got rid of in a few days, while with a larger injection of 60 to 80 per cent. it takes two or three weeks before the normal state is again reached. The albuminous and nitrogenous materials are largely got rid of by the urine, which increases rapidly in quantity and also in the amount of urea. The excess of corpuscles gradually disappears, and the hæmoglobin becomes deposited, as Quincke has shown, in the form of small granules in the cells of the liver, spleen, and bone-marrow.

[Footnote 16: _Transfusion and Plethora_, Christiania, 1875.]

[Footnote 17: _Allgemeine Pathologie_, 2te Auflage.]

In a similar way, it is reasonable to think that the body is quite capable of disposing of surplus albuminous materials in over-fed, lazy individuals with active digestion, whose red faces, full vessels, and bounding pulses give the impression of a distended circulatory system, and whom we term plethoric. Their appearance is the result rather of blood-distribution than of actual increase in the total volume, and there is no evidence that under any circumstances a rich and abundant diet without much exercise can permanently increase the amount of blood. It was formerly held that the healing of an old sore or the cessation of an accustomed discharge or loss of blood, by diminishing expenditure while the blood-making power was maintained, could induce plethora if no local disorder was excited "before the vessels {887} in general reached a state of plethoric tension." Of such a condition, and of the plethora apocoptica that was thought to occur after the amputation of a limb, we do not hear much now, and the prevalent opinion of pathologists is expressed by Cohnheim, when he says "that, except as a transitory state, polyæmia does not occur under any circumstances." What, then, is the meaning of the full-blooded, rubicund condition which we see in some men, not necessarily large feeders, but often with vigorous active constitutions and perfect types of health? The appearance of plethora is caused chiefly by the distension of the superficial vessels; the circulation of the skin is remarkably active, particularly in the face, and it is probable that we have here to deal with local peculiarities of the vessels or of their innervation, and not with any general augmentation of the total blood-mass. It may be, however, that in such persons there is a plethora of certain of the constituents of the blood--viz. the red corpuscles--and there may be a state of polycythæmia rubra, as it has been called, in which the percentage of red cells is increased. In several such cases I have found, as has been previously noted, the number of red corpuscles considerably over the average. A relative increase in the number of red corpuscles also occurs in those sudden and excessive losses of fluid, as in cholera, in which the blood may become thick and sticky from the great reduction in the plasma, particularly of the water and salts--anhydræmia--or in cases in which the income of fluid is greatly restricted. Henry (F. P.) has recorded a case[18] of stenosis of the cardia, in which, with great emaciation, the corpuscles per c.m. were 5,525,000.

[Footnote 18: _Archives of Medicine_, New York, vol. vii.]

The condition known as hydræmic plethora develops whenever there is a great reduction in the number of corpuscles, as after a hemorrhage, or when the blood has been impoverished by long-standing suppuration, albuminuria, or in the growth of large tumors. So also when the secretion of urine is diminished, as in some cases of Bright's disease, and at the same time charged with albumen, the blood may become very watery; but in these states there is not an absolute increase in the entire blood, but only a relative excess of the water. Occasionally, this great excess can be noticed in the blood-drop as it comes from the finger-tip; the corpuscles do not fill the entire drop, and consequently leave irregular areas unoccupied by the red disks.

ANÆMIA.

A reduction in the amount of the blood or of its corpuscles occurs under a great variety of circumstances. Broadly speaking, we can recognize two great clinical and pathological groups of cases: I. Those induced by causes acting upon the blood itself; and, II. Those induced by disturbance in the functions of the blood-making organs.

I. Of causes acting directly upon the blood, we shall consider--

1st. Hemorrhage, traumatic or spontaneous. A high grade of anæmia may be quickly produced by loss of a large quantity of blood, and the reduction is in all the constituents; there is a true oligæmia. If the amount lost be excessive, death results from the diminution in the total volume of blood and general lowering of the arterial pressure. If the hemorrhage is sudden and profuse, as from a large vessel, the loss of four or five pounds of blood, or even less, may be sufficient to induce fatal syncope. In hemorrhage into the pleura or peritoneum from rupture of aneurisms, etc., it is rare to meet with more than three or four pounds of clot and serum; seven and a half {888} pounds is the largest amount I know of shed into one of the cavities (pleura) by rupture of an aneurism. When the bleeding extends over several days, the amount lost may be very much greater. In cases of hæmophilia extraordinary accounts are given of the amount collected in the course of a few days. In a case of hæmoptysis a patient lost over ten pounds by measurement in one week, and then recovered from the immediate effects. After the most severe hemorrhages the reduction in the number of red corpuscles is not nearly so great as in forms of idiopathic anæmia. Thus in the case just mentioned at the termination of the week of bleeding there were 1,390,000 red corpuscles to the cubic millimeter. In any single bleeding a fatal result follows the loss of one-third or one-half of the total blood-volume. The process of regeneration of the blood goes on with astonishing rapidity, and in some bleeders a week or ten days will suffice to re-establish the normal amount. The restitution begins even during a hemorrhage by the absorption of lymph from the tissues under the lowered pressure in the vessels. The dryness and stickiness of the serous membranes after death from a profuse hemorrhage is usually very marked. The water and saline constituents of the blood are readily restored by absorption from the gastro-intestinal tract. The albuminous elements are also quickly renewed, but it may take weeks or months before the number of corpuscles reaches the normal standard. Indeed, this condition of oligocythæmia, as it is called, may persist, grow worse, and ultimately prove fatal. The microscopical characters of the blood after severe hemorrhage are not much changed, except as regards the white corpuscles, which are relatively increased, and the fibrin network, which is much less marked than in health. The white corpuscles may be very slightly reduced in number per cubic millimeter--a fact to be accounted for either by a relatively diminished loss during the bleeding, owing to their adhesiveness and wall-loving properties, or to a quick restitution from the lymph which is poured into the blood-stream. It has been observed both in dogs and men by Lyon[19] that after a severe hemorrhage the number of red per cubic millimeter diminished for several days after the bleeding had been checked. How and where does the regeneration of red corpuscles take place after a severe hemorrhage? One would think that under these circumstances, if any, we should be able to get information which might be of service in determining the problem of blood-development; but, in spite of the numerous experiments on the subject, we are still far from a knowledge of full details. The observations of Neumann,[20] Litten and Orth,[21] Bizzozero,[22] Lepine,[23] and others appear to prove conclusively that the bone-marrow plays an important part in the formation of the new red disks, becoming lymphoid, losing its fat, and the nucleated red cells increase enormously. The same process has been observed in many cases in man. In a case of profuse metrorrhagia with profound anæmia Neumann[24] found the marrow in all the bones of a rich raspberry red, full of the nucleated forms, which were also very abundant in the blood, and more in the vena azygos than in the aorta. The evidence in favor of the active participation of the spleen is not so conclusive. Neumann[25] concludes that the spleen takes no share in the process, and holds that the nucleated red cells found in it are probably derived from the bone-marrow. Bizzozero, on the other hand, has found the spleen swollen and showing signs of lively blood-formation. He states that after removal of the spleen the restitution of the red corpuscles takes place much more slowly. Pouchet, on the contrary, says the regeneration goes on just as rapidly without the spleen. {889} Of the action of the lymph-glands there is even less evidence. They have been found swollen, but in traumatic anæmia I do not know of any observations on their swelling and conversion into a red spleen-like tissue, such as have been found in some cases of idiopathic anæmia.

[Footnote 19: Of Norwich, Conn.: _Virchow's Archiv_, lxxxiv.]

[Footnote 20: _Archiv der Heilkunde_, Bd. x.; _Frerichs and Leyden's Archiv_, Bd. iii.]

[Footnote 21: _Berliner klin. Wochenschrift_, 1877, li.]

[Footnote 22: _Centralblatt f. d. Med. Wissenschaften_, 1879, xvi.]

[Footnote 23: _Revue Mensuelle de Méd. et de Chirurg._, 1877.]

[Footnote 24: _Loc. cit._]

[Footnote 25: _Loc. cit._]

The microcytes which occur in numbers in blood in some cases of traumatic anæmia have been regarded as young developmental forms, but there is a great diversity of opinion as to their real nature, and their connection with productive blood-processes is somewhat doubtful.

Cohnheim suggests[26] that after a profuse hemorrhage the rapid consumption of red corpuscles may be reduced, in which case we need not suppose such an active development; but the fact noted by Lyon[27] and others of the increased reduction after a bleeding is against the view. In any case, if Quincke is right in assuming that the average life of a red corpuscle is only three or four weeks, what is the restitution of a couple of millions of corpuscles per cubic millimeter in comparison with the monthly renovation of the entire mass?

[Footnote 26: _Loc. cit._]

[Footnote 27: _Loc. cit._]

In the regeneration of the blood the development of the hæmoglobin does not keep pace with that of the corpuscles, so that they may, even when normal in amount, have a lowered hæmoglobin percentage, indicated under the microscope by a paleness in the cells.

2d. There is a large group of cases in which the anæmia is induced by a long-continued drain on the albuminous material of the blood--pus in a chronic suppuration, albumen in Bright's disease, prolonged lactation, etc. Rapidly-growing tumors act in the same way.

3d. The anæmia of inanition, brought about by defective food-supply or by conditions of the digestive organs which interfere with the proper reception and preparation of nourishment, as cancer of the gullet, chronic dyspepsia, etc. The reduction in the blood-mass may be extreme, but the plasma suffers proportionately more than the corpuscles, which even in the extreme wasting of cancer of the oesophagus may not be reduced more than one-half or three-fourths.

4th. Toxic anæmia, induced by the action of certain poisons in the blood, such as lead, mercury, and arsenic among inorganic substances, and the virus of syphilis and malaria among organic poisons. They act by increasing the rate of consumption of the red corpuscles, and the reduction may be considerable. The gradual impoverishment of the blood in pyrexia may be in part due to the toxic action of the fever-producing agent on the blood itself; but in this there is probably also disturbance of function in the blood-making organs.

The last three groups comprise what are known as secondary anæmias, and the condition of the blood is characterized by an increase in the water and diminution in the albuminous elements; the fibrin is often increased, and the network which separates, as seen under the microscope, is unusually dense; the white corpuscles are not much increased; there is rarely microcytosis or poikilocytosis; the reduction in the number of red corpuscles is not so great; hemorrhages do not often occur; when fever is present it is due to the disease or some complication, and is not the pyrexia of anæmia; and, lastly, they are more or less amenable to the action of iron and other remedies.

II. A consideration of the anæmias induced by disturbance in the blood-making organs themselves presents difficulties proportionate to our ignorance of the details of hæmatogenesis. We may regard, as above stated, the spleen, the general lymphatic tissue, and the marrow as the sites of production of corpuscles which are passed into the circulation fully formed. Certain of these organs--the spleen and marrow particularly--are also concerned with blood-destruction as well as blood-elaboration; but there is evidence to show[28] that {890} they, to use an ordinary simile, consume their own smoke, using the waste products for the purpose of further manufacture. Looking now upon the hæmatogenetic tissues as a single organ scattered through the body, let us consider what general disturbances of function it may suffer comparable to those met with in other structures. We can evidently suppose the physiological activity to be diminished or increased, and we should expect to find corresponding to these changes equivalent alterations in the character of the blood. Unfortunately, our knowledge of the normal processes as they go on in these tissues is so scanty that it amounts to a discussion upon the disturbances of a function itself imperfectly understood.

[Footnote 28: Quincke, quoted above.]

With diminished functional activity in an organ we commonly meet with reduction in volume, the one depending on the other: now, the only instance in the blood-making organs in which a decrease in size and diminished functional activity go together is in the senile atrophy in which the spleen becomes small, the marrow more fatty, and the lymph-glands sclerotic, and in consequence the blood also is reduced in amount; but this is only a part of the general failure of nutrition in old age. Pathologically, there is no such well-recognized condition of uniform atrophy of spleen, lymph-gland, and bone-marrow, with a corresponding general reduction in the elements of the blood. Certain cases of idiopathic anæmia come close to it, in which these parts are wasted, but there are other differences which make the two conditions scarcely comparable. In fact, as we shall see, diminished activity in blood-making is usually associated with an increase in what we call hæmatogenetic tissues. Of increased functional activity in these parts we know very little, apart from the changes met with in cases of traumatic anæmia, in which the hyperplasia of the spleen and bone-marrow may be regarded as intimately connected with the rapid development of red corpuscles.

One fact is evident: that a progressive increase in the cytogenic tissues, local or general, is associated with disturbance in the process of blood-formation, and sooner or later induces anæmia. Thus, progressive enlargement of the spleen or of the lymph-glands or marked hyperplasia of the marrow, either singly or combined, is invariably accompanied with alteration in the characters of the blood. Even in those rare instances in which the lymphoid elements of the tonsils and fauces or of the gastro-intestinal canal are chiefly involved the same change may take place.

The nature of the process in the organs is of a hyperplastic character. In the spleen the pulp at first increases and the Malpighian bodies enlarge, but ultimately there is such a development of the fibrous reticulum that the consistence is greatly augmented and the organ becomes indurated. Histologically, there is very little distinction to be made between forms of chronic enlargement of this organ. In the lymph-glands there is increase in the cells; the tissue becomes more succulent, and is in a state of hyperplasia which may terminate in a great development of the fibrous elements, with induration. So also with the bone-marrow: in the short and flat bones, where in the adult a reddish or slightly fatty tissue exists, the fat disappears entirely, and the long bones, normally filled with yellow marrow, become occupied with a red-gray or greenish-gray cytogenous tissue not unlike spleen-pulp, and in many instances more consistent than the red marrow of early life.

A reduction in the number of red corpuscles is the chief and most constant change in the blood; anæmia seems to be the invariable result, whether the spleen, marrow, or lymph-glands are affected singly or together, and is the central feature in the entire group of cases. This diminution in the red cells may or may not be accompanied by an increase in the white corpuscles, which in some cases may be so striking as to be regarded as the special blood-change, and is, as a rule, permanent, though it may be a variable or even a transitory state.

{891} The general and histological differences between forms of hypertrophy of these blood-making organs are exceedingly slight, and in their clinical features they present a large number of symptoms in common; indeed, we may say that all the important symptoms are present, whether the spleen is affected alone or with the lymph-glands and bone-marrow, or whether these parts are independently involved, and whether there is simple reduction in the red or with it an increase in the white corpuscles. Such common features are--the progressive anæmia with its group of circulatory symptoms; the irregular febrile reaction, essential fever of anæmia; the absence of marked emaciation; the tendency to effusions of serum; the progressive debility; the occurrence of hemorrhages; gastric and intestinal disturbances; and resistance to treatment.

The affections characterized pathologically and clinically by so many similar features are known and recognized as distinct diseases under the names leukæmia, Hodgkin's disease or pseudo-leukæmia, splenic anæmia, and idiopathic anæmia (some cases); and we shall now consider these a little more closely.

First, of the hyperplasias of the cytogenic tissues associated with simple anæmia. The various groups, spleen, lymph-glands, and marrow, may be involved singly or together; usually one is first affected, and the others, if at all, subsequently. Progressive enlargement of the spleen induces sooner or later anæmia, the anæmia splenica of Griesinger. These cases are by no means rare: certain of them represent the final stage of a malarial intoxication, but there are others in which the enlargement seems causeless. There may also be hyperplasia of the bone-marrow, less often of the lymph-glands. The anæmia may be profound, and the clinical picture is that mentioned above. Two cases of it under my care died of hæmatemesis. The diagnosis of this affection from splenic leukæmia rests solely on the microscopical examination of the blood. It is also classed as the splenic form of Hodgkin's disease or pseudo-leukæmia.

Primary enlargement of the lymph-glands with anæmia constitutes Hodgkin's disease or pseudo-leukæmia, in which there may be general hyperplasia of the lymphatic elements throughout the body, with nodular growths of adenoid tissue in other organs. The spleen and marrow are not often affected. Here, too, the diagnosis from lymphatic leukæmia rests with the microscope.

Is there a form of anæmia dependent upon hyperplasia of the bone-marrow--an anæmia medullaris? In 1875, Pepper and Tyson[29] found affection of the marrow in idiopathic anæmia, and Pepper suggested that this might be the starting-point of the disease, which could thus be regarded as a medullary form of pseudo-leukæmia. Cohnheim in 1876[30] described the same condition, and I had an opportunity of examining several cases.[31] Granting that the marrow is a tissue which shares in the blood-making functions, it seemed reasonable to suppose that a general hyperplasia of its elements might disturb the processes of hæmatosis and produce anæmia, just as in hyperplasia of the spleen and lymph-glands. Two facts soon came to light which seem opposed to this explanation of the pathology of idiopathic anæmia. A hyperplasia of the marrow was found in cases of chronic disease with wasting, and cases of idiopathic anæmia were described in which the marrow was normal. The numerous observations of the past five or six years have not brought us nearer to a solution of the problem. The observations of Neumann,[32] and those of Litten and Orth,[33] on the changes in the marrow in chronic diseases have been abundantly confirmed, and a red lymphoid marrow may be met with in various cachectic states. This, too, I have frequently seen, {892} yet it is in my experience rare to find such marked, rich hyperplasia of the marrow, such an entire absence of fat, as in some cases of idiopathic anæmia. In 9 autopsies in typical cases at Montreal, not parturition cases, the marrow of the long bones was lymphoid and red in 6; in 1 it was not examined; in 1, which I did not see, the marrow was stated to be normal; and in 1, an old woman over sixty years of age, the marrow of the short bones was rich in lymphoid cells and nucleated red corpuscles, and the long bones contained a grayish gelatinoid--atrophic--marrow. It does not appear possible with our present knowledge to arrive at a satisfactory conclusion on this question. Some regard the marrow-change as the consequence, others as the cause, of the anæmia. Both Cohnheim[34] and Pye-Smith[35] regard those cases of idiopathic anæmia in which the marrow-changes are pronounced as cases of anæmia medullaris.

[Footnote 29: _American Journal Med. Sciences_, 1875, ii.]

[Footnote 30: _Virchow's Archiv_, Bd. lxviii.]

[Footnote 31: _Centralblatt f. d. Med. Wissenschaften_, 1877, Nos. 15 and 28; 1878, No. 26.]

[Footnote 32: _Berl. klin. Wochenschrift_, 1877, xlvii.]

[Footnote 33: _Ibid._, 1877, li.]

[Footnote 34: _Loc. cit._, Bd. i. S. 467.]

[Footnote 35: _Loc cit._]

Next of the parallel series of hyperplasias of the blood-forming organs with anæmia, plus an increase of the colorless corpuscles--leukæmia. Here, too, we have the three forms--splenic, lymphatic, and medullary.

The splenic leukæmia is the most common, and in its general features is identical with splenic anæmia, the excess of white corpuscles being the only distinguishing feature. It is almost invariably associated with changes in the marrow.

The lymphatic leukæmia may arise in connection with hyperplasia of the lymph-glands or of the adenoid elements in the alimentary tract--tonsils and Peyer's glands. It is much less common than lymphatic anæmia or Hodgkin's disease, and there are not many uncomplicated cases on record. Apparently, a very limited bunch of glands--cervical--may induce the change in the blood.[36] Medullary changes are almost invariably associated with a great increase of colorless corpuscles in the blood, and a myelogenous form of leukæmia is now, owing chiefly to the investigations of Neumann, well established. Indeed, he would regard the change in this tissue as the primary and important, and those in the lymph-glands and spleen as secondary.

[Footnote 36: Gowers, _Reynolds's System of Medicine_, art. "Leucocythæmia."]

The hyperplasia, either lymphadenoid in character or pyoid, may result in the expansion and softening of the bones, with the production of irregular tumor-like masses.

We have, then, the following group of anæmias induced by a primary disturbance of function in the blood-making organs:

PRIMARY OR | Leucocytic | Splenic, | CYTOGENIC | | Lymphatic, | Leukæmia. ANÆMIA. | | Medullary, | | | Non-leucocytic | Splenic, Anæmia splenica. | Lymphatic, Hodgkin's disease. | Medullary, Idiopathic anæmia (certain cases).

There remain for consideration the relation of the tissue-change to the anæmia and the nature of the leucocytosis; but until the chief facts in the development of the corpuscles are thoroughly known we cannot expect a satisfactory solution of these problems.

The anæmia may be explained on the view of diminished production (anæmatosis) or increased consumption of the red corpuscles (hæmophthisis). We know nothing of the intimate processes connected with lessened production, but as anæmia so constantly accompanies the hyperplasia, we assume they are intimately connected with each other, and the diminution in the number of corpuscles in some way the result of disturbed functional activity in the blood-making organs. An increased consumption of corpuscles in anæmia is {893} indicated by the presence in large numbers of cells containing red blood-corpuscles in the spleen and marrow, and occasionally in the lymph-glands; by the increased amount of iron which has been found in the liver; and in some cases by the deep color of the muscles and an intensification of the color of the urine. Either a failing production with normal rate of consumption, or a normal output with heightened destruction, would produce anæmia. Possibly, in some instances, both factors may prevail. Quincke's interesting observations[37] may enable us to determine the cases in which one or other has been dominant. Where there is great destruction we shall expect to find the granules of iron albuminate in the spleen, bone marrow, and liver-cells, possibly in the cells of the cortex of the kidneys, and the iron reaction should be present.

[Footnote 37: _Loc. cit._]

The relation of the hyperplasia of the cytogenic tissues to the increase in the colorless corpuscles is even more obscure. A prime difficulty is the circumstance that apparently identical tissue-changes may be associated with either a leucocytic or non-leucocytic anæmia. The splenic hyperplasia of leukæmia and of anæmia splenica are histologically identical. The excess of white corpuscles may be due either to over-production or to failure in their transformation into red. That they develop in the hyperplastic spleen, marrow, and lymph-glands is not to be doubted, and it seems reasonable to attribute the excess to the hyperplasia. Their variable size, as spleen or lymph-glands are chiefly affected, was early observed by Virchow, and when the marrow is involved there may be many large leucocytes similar to the larger marrow-cells. Virchow's original explanation, that the excess of colorless cells was due to a failure in their transformation into red corpuscles, rests upon the presumption that such a transformation is the normal process--a view not fully established. If this is the case, we should expect to find some relation between the increase of the white and the decrease in the red, but this is not always constant; as a general rule, with a diminution of the white there is an increase in the red, but the red and the white cells may increase or diminish in numbers simultaneously, or, again, the leucocytes may be greatly reduced while the red corpuscles remain about stationary. Griesinger,[38] Biesiadecki,[39] and others regard the increase in leucocytes as a primary blood-change. Several recent French writers support this view, as Renant,[40] who believes that the unequal size of the leucocytes indicates their division in the blood, and Variot.[41] One of the most interesting features in connection with an increase in the colorless cells is that it may be only transitory, and a case which clinically and pathologically may present the features of idiopathic anæmia to-day may to-morrow present the characters of leukæmia; a case of splenic anæmia may become one of splenic leukæmia, or vice versâ. Thus, in Litten's oft-quoted case--about which there can be no doubt[42]--of acute anæmia of three weeks' duration, an enormous increase of colorless corpuscles took place, and finally a ratio of one white to four red was reached. Quite as interesting is the case of Fleischer and Penzoldt,[43] in which for eight months the patient presented the ordinary symptoms of anæmia lymphatica or Hodgkin's disease, and then, before death, the blood became intensely leukæmic, the ratio 1:9. Still more so as the case of Goodhart's,[44] in which, with an enlarged spleen and lymphoid growths in liver and kidneys, there were variations in the number of corpuscles every few days--at one time great excess of white, at another no increase whatever. Again, a case may early come under observation as one of leukæmia, with a ratio of 1:20 or 1:30, and in the course of a few months, with persistence or even aggravation of {894} the general symptoms, the normal ratio of white to red may be reached. This was the history in one of the Montreal cases.[45]

[Footnote 38: _Virch. Archiv_, Bd. v.]

[Footnote 39: _Wien. Med. Jahrbuch._, 1876.]

[Footnote 40: _Archives de Physiologie_, 1881.]

[Footnote 41: _Thèse de Paris_, 1882.]

[Footnote 42: _Berl. klin. Wochenschrift_, 1877.]

[Footnote 43: _Deutsches Archiv f. klin. Medicin_, Bd. xxvi.]

[Footnote 44: _Clin. Society's Transactions_, London, 1877.]

[Footnote 45: Howard, _Montreal General Hospital Reports_, vol. i. p. 39.]

It seems questionable whether such a variable feature as increase in the colorless corpuscles should be permitted to separate diseases which have all essential characters in common. We shall probably, however, continue for a long time to speak of these conditions as separate and distinct, but it is evident that as time goes on, and our knowledge of the diseases and of blood-development increases, the identity of many of them will be acknowledged, and we shall find that here, as so often the case in natural history, the multiplication of species has been the result of imperfect information, and that as points of resemblance in essential characters and development are studied minor differences disappear.

With reference to the general tissue-changes in anæmia there are two points of interest: The metabolism of the proteids is increased, as shown by the increased excretion of urea, and owing to defective exudation the decomposition of the fats is lessened; hence the retention of fat, or even increase, in anæmic persons. The influence of repeated small bleedings in hastening the fattening of cattle has been known since the time of Aristotle, and horse-dealers still affirm that there is nothing like bloodletting to put an animal into good condition.

CHLOROSIS

is a special form of anæmia distinguished by certain etiological and anatomical peculiarities. In the first place, it is a disease of the female sex; cases in the male are of extreme rarity. In the majority of instances it is associated with disturbed menstrual function or with the evolution of the reproductive organs at the period of puberty. Occasionally it occurs in pregnant women and in children. It is a common disease among the ill-fed, overworked young girls in large towns who are confined all day in close, badly-lighted rooms or who have to do much stair-climbing. Girls of the better classes are by no means exempt; indeed, some writers speak of it as specially prone to affect the higher ranks of life. Lack of proper exercise, good food, and fresh air, the mental stimulation of unhealthy literature, and masturbation, are important factors. Emotional and nervous symptoms may be prominent--so much so that the disease is regarded by some as a neurosis.

The anatomical peculiarities relate to the blood and circulatory system. There is anæmia, but the impoverishment is less in the number than in the corpuscular richness in hæmoglobin. This fact, first pointed out by Duncan,[46] has been abundantly confirmed. Thus, for example, in one case, with a globular richness of 85 per cent., the hæmoglobin was only 52 per cent., and in another, with 92 per cent. of red, the hæmoglobin percentage was as low as 64. The numerous investigations of the past few years[47] have, among other points, fully established this as perhaps one of the most striking features in chlorosis. The color-value of the individual corpuscle is very much reduced. Of 22 observations of Hayem, the average number of red corpuscles was {895} 3,740,000, and the hæmoglobin reduced to about 50 per cent. In Laache's 13 cases the average percentage of corpuscles was 72, and of hæmoglobin 45. This author has pointed out that in certain cases with all the clinical symptoms of chlorosis well marked there may be very slight reduction in the corpuscles or hæmoglobin; and such he terms pseudo-chlorosis. The red corpuscles in chlorosis vary much in size. Very large forms--giant red cells--are common, and microcytes are sometimes to be seen; but there is not the extreme irregularity in size and outline of the blood in idiopathic anæmia. The presence of a large number of young, imperfectly-formed corpuscles, especially as regards the hæmoglobin, is the distinguishing feature of chlorotic blood. Hayem and Willcocks both regard the average corpuscular diameter to be lower than normal, though many large forms occur. The color of the red corpuscles is noticeably pale, and the marked deficiency in hæmoglobin can be observed in individual corpuscles as well as in the blood-mixture prepared for counting. Quinquaud found the serum normal in quality, but the solids were slightly reduced in amount. Hunt[48] has shown that there are peculiar inter-menstrual oscillations in the blood in chlorotics. There is usually a fall in numbers just before the flow, but the individual value remains good; subsequently the number rises, but the color-value is not maintained (Willcocks). Virchow[49] pointed out that in many cases of chlorosis there was a defective development of the circulatory system, either congenital or resulting in failure of the normal rate of growth; the parts remained infantile. The heart and arteries were small, the walls of the latter thin, and the calibre of the aorta narrowed. In some instances there was found a compensatory hypertrophy of the heart. Defective development of the uterus and ovaries has also been noted, but these changes on the part of the circulatory and generative organs are not constant features in chlorosis.

[Footnote 46: _Sitzungsbericht d. Kais. Akad. d. Wissenschaften zu Wien_, 1867.]

[Footnote 47: Leichtenstern, _Hæmoglobingehalt des Blutes_, Leipzig, 1878; Hayem, _Recherches sur l'Anatomie, etc. du Sang_, 1878; Malassez, _Archives de Physiologie_, 1877; Moriez, _La Chlorose_, Paris, 1880; Laache, _Die Anämie_, Christiania, 1883; Willcocks, _Practitioner_, 1883.]

[Footnote 48: _Lancet_, ii., 1880.]

[Footnote 49: _Ueber die Chlorose_, etc., Berlin, 1872.]

The SYMPTOMS of chlorosis are those of anæmia of moderate grade. As in idiopathic anæmia, the subcutaneous fat is in full, or even extra, amount. The complexion is most peculiar, neither the blanched aspect of hemorrhage nor the muddy pallor of grave anæmia; but there is a curious yellow-green tinge in marked cases which has given the name to the disease ([Greek: chlôros]), and also its popular designation, the green sickness. Breathlessness, palpitation, and tendency to fainting are due to the anæmia. Digestive troubles are also common, and the appetite is often depraved. There are venous and cardiac murmurs. The menstrual functions are almost always deranged, and there may be hysterical and nervous manifestations. Relapses are not uncommon. The intimate pathology of the disease is unknown. In its insidious onset, sometimes causeless, and in certain features of the blood-state, it resembles pernicious anæmia, but it differs from it in many essential particulars. The association with menstrual disorders, the hypoplasia of the circulatory and generative organs in some cases, the favorable course and response to suitable treatment, as well as the sex and period of life, are features peculiar to chlorosis. Then, again, the anæmia is not so intense, and the relation of the hæmoglobin is just the reverse; in chlorosis the individual corpuscles are deficient in hæmoglobin, while in idiopathic anæmia the reverse appears to be the case.

Some regard the blood circulatory and uterine condition as the expression of a congenital defect leading to the formation of a diathesis--and in certain cases this may be so--but some of the most marked cases I have seen have been in girls of healthy families, who after a healthy childhood developed chlorosis at puberty, from which, under suitable treatment, they recovered to become robust and vigorous women. The almost specific action of iron suggests failure of the digestion or assimilation of the minute traces of this substance which are contained in our ordinary foods, and from which {896} the iron of the corpuscles must be derived. Zander[50] holds that it is largely due to a defect in the hydrochloric acid of the gastric juice, by which the iron-holding compounds are dissolved, and claims that in chlorosis the administration of this remedy after eating fulfils every indication and enables the iron in the foods to be converted into an absorbable compound.

[Footnote 50: _Virchow's Archiv_, lxxxiv.]

The condition of the blood-making organs themselves throw no light on the PATHOLOGY of the disease.

The TREATMENT of chlorosis requires special mention. Iron may be regarded as a specific when given in sufficient doses. I have found Blaud's formula, as given in Niemeyer's textbook (ferri sulph. potass. carb. et tart. aa ounce ss; tragacanth q. s. Make ninety-six pills. Two or three pills to be taken three times a day), the most satisfactory method of administering the drug. Under their use I have repeatedly seen the number of the red corpuscles per cubic millimeter double in a fortnight; and it is one of the most interesting therapeutic phenomena to watch with the hæmacytometer the progressive development and increase of red corpuscles under the influence of fifteen or twenty grains of iron daily. Other forms may be used--reduced iron, dialyzed, the lactate, the tinct. of the perchloride--and it does not really make much difference which form is employed so long as enough is administered. Dilute hydrochloric acids or the vegetable acids may be given, and special attention should be devoted to dietetic and hygienic regulations.

MELANÆMIA

is a condition characterized by an accumulation of granular pigment in the blood and various organs, particularly the spleen, liver, marrow, and brain. It is almost invariably associated with prolonged malarial infection, and the pigment results from the transformation of the hæmoglobin of the corpuscles, many of which undergo destruction as a direct consequence of the influence of marsh miasm. Very exceptionally, however, the dark particles are extraneous, and result from the passage of carbon-granules into the circulation in cases of intense anthracosis. Soyka[51] met with a case of this kind in which the coal particles were distributed throughout the spleen, liver, and kidneys. In blood the pigment occurs either free in the form of fine granules or in cloud-like collections of various sizes and shapes, often surrounded by a hyaline margin, or it occurs enclosed in cells. The free pigment, not often met with, is either molecular or in the form of irregular particles which may equal a red corpuscle in size. Aggregations of the granules are not uncommon, forming various-sized masses which may be imbedded in a hyaline substance. More commonly the pigment is contained in cells, ordinary leucocytes or large flattened--endothelial--cells derived from the spleen or liver. The color varies from yellowish-brown to a deep black. Except during periods of intense malarial infection and in the most severe and chronic cases melanæmia is rarely observed. In most ordinary cases of intermittent one may seek in vain for the pigment-granules, and I have examined many chronic cases with well-marked ague-cake with negative results. In other instances the pigment is found during or after a paroxysm; and this is the period when an examination of the blood should be made. The greatest care and cleanliness should be exercised in obtaining the blood-drop; and it should be remembered that in some of the glass slips used for microscopic purposes {897} irregular brownish flakes may occur which I have known to be mistaken for pigment.

[Footnote 51: Quoted by Hindenlang, _Virchow's Archiv_, lxxix.]

The melanæmia is but the expression of extensive destruction of corpuscles and accumulation of pigment in the spleen, liver, and bone-marrow; and these organs in cases of fatal intermittent or remittent fevers may present important changes. In the spleen, which is usually enlarged and indurated, the pigment is chiefly in the vicinity of the arteries and veins, the tissues about which may be absolutely black, and in both stroma and pulp innumerable cells are found filled with blood-corpuscles and blood-pigment in all stages of transformation to melanin. The color of the organ may be of a deep reddish-brown, or in very chronic states gray or even a dark olive. In the liver the dark granules are chiefly at the periphery of the lobules, fixed within the connective-tissue elements and leucocytes, not in the liver-cells themselves. It may be abundant about the portal branches, staining the connective tissue of Glisson's sheath, and it is also met with in the vicinity of the hepatic veins. When much affected the liver may have a deep bronze tint. As Arnstein has shown,[52] the bone-marrow may present similar changes and have a grayish-brown color. There may be deep pigmentation of peritoneum and omentum. The deposition of the granules in and about the vessels of the cortex cerebri may give a slate-gray color to the brain, or even a graphite tint in very severe cases. The capillaries have been found occluded with cells filled with the pigment-granules. The kidneys--particularly the Malpighian tufts--the mucous surfaces, and the skin may also be the seat of pigmentary deposition. These coarse changes in the organs in chronic malaria were known to the older writers, and in Bright's _Medical Observations_ a beautiful representation is given of the condition of the brain. To American physicians, with their extensive experience of malarial fevers, these changes were well known, and Stewardson of the Pennsylvania Hospital gave an admirable description of them in 1841;[53] and from the same institution in 1868 came another important contribution to the subject by Meigs, Pepper, and Rhoads.[54] Meckel[55] and Virchow[56] gave the first satisfactory explanation of the discoloration, showing that it was due to pigment, which might also be free in the blood. Frerichs in his well-known work on the liver gave an exhaustive account of the coarse and microscopical appearances.

[Footnote 52: _Virchow's Archiv_, lxi.]

[Footnote 53: _Am. Journal Medical Sciences_.]

[Footnote 54: "On the Morphological Changes of the Blood in Malarial Fever," _Penn. Hospital Reports_, 1868.]

[Footnote 55: _Deutsche Klinik_, 1850.]

[Footnote 56: _Virchow's Archiv_, Bd. i.]

There is still some difference of opinion as to the mode of origin of the pigment. Most writers hold that it results from the destruction of the red corpuscles in the spleen and liver, and from these situations the pigment gets into the blood; but more recently Arnstein[57] and Kelsch[58] have urged the view that the melanæmia is the primary process, the destruction of corpuscles going on in the blood itself, and the particles and coloring material taken up by the leucocytes are transformed into melanin, and then the cells collect in the spleen, liver, and bone-marrow, producing the condition of melanosis. It is probable that the older view is the true one, and we may regard the process as an exaggeration or intensification, under the stimulus of the malarial poison, of the normal process of blood-destruction which goes on in the spleen and bone-marrow, and under some circumstances in the liver and lymph-glands. We can often trace in the cells of these organs the stages of transformation from red corpuscles to melanin-granules, just as can be done in the tissues in the neighborhood of an extravasation, where also the process is chiefly intracellular (Langhans). On the other hand, in those very states in which the red corpuscles are destroyed in the blood and the hæmoglobin set free, we do {898} not find melanæmia. It happens occasionally in fevers that we meet with colorless cells in the blood containing red blood-corpuscles, which in time would be transformed into pigment, but, so far as we know, such a condition has not been observed in the blood in malaria. The connection between the fever paroxysm and the appearance of the pigment in the blood depends, most likely, on changes in the volume of the organs under the influence of the fever, whereby cells containing the pigment are dislodged and get into the circulation. This explains, too, their rapid appearance in some cases with the onset of a paroxysm. No doubt, as Virchow originally taught and as well shown in Gussenbauer's[59] observations, the pigment may result from the diffusion of the coloring matter and gradual precipitation of it in the granular form within the protoplasm of colorless cells; but of the occurrence of such a process in the circulating blood in malaria we have no satisfactory evidence, and we incline to the belief that the melanosis of the organs is the primary condition, while the melanæmia is secondary and inconstant.

[Footnote 57: _Loc. cit._, and _ibid._, lxxi.]

[Footnote 58: _Archiv de Physiologie_, 1875.]

[Footnote 59: _Virchow's Archiv_, lxiii.]

Occasionally, in cases of extensive melano-sarcoma, pigment-granules may be found in the blood in large numbers, and even appear in the urine and be deposited in the organs and skin. In a few instances also free pigment has been observed in the blood in Addison's disease.

PROGRESSIVE PERNICIOUS ANÆMIA.

DEFINITION.--Extreme and progressive anæmia developing without evident or apparently adequate cause.

SYNONYMS.--Idiopathic anæmia (Addison); Essential anæmia (Lebert); Anæmatosis (Pepper).

HISTORY.--During the first two or three decades of this century cases of severe and fatal anæmia were noted by Andral and others, but the credit of having given the first accurate series of cases belongs to Walter Channing of Harvard, who in the _New England Quarterly Journal of Medicine_ for 1842 published a paper entitled "Notes on Anhæmia, particularly in connection with the Puerperal State and with Functional Disease of the Uterus, with Cases."[60] Any one who reads this communication will be convinced that Channing's description, particularly of the seven cases occurring in the puerperal state, is that of the disease to which Gusserow and Biermer have more recently directed attention.

[Footnote 60: My attention was accidentally called to Channing's observations in the Periscope of Hall's _British-American Journal_ for 1845. Since then Musser, in the _Med. News_, Oct. 7, 1882, has given a valuable abstract of the paper.]

In Addison's monograph on the suprarenal capsules (1855) there is a brief but clear account of the disease, which he speaks of as follows: "For a long period I had from time to time met with a very remarkable form of general anæmia occurring without any discoverable cause whatever--cases in which there had been no previous loss of blood, no exhausting diarrhoea, no chlorosis, no purpura, no renal, splenic, miasmatic, glandular, strumous, or malignant disease. Accordingly, in speaking of this form of anæmia in clinical lectures, I, perhaps with little propriety, applied to it the term idiopathic, to distinguish it from cases in which there existed more or less evidence of some of the usual causes or concomitants of the anæmic state." As early as 1843 this acute observer had spoken in his clinics of this condition.[61]

[Footnote 61: McKenzie, S., _Lancet_, 1879, ii.]

{899} The physicians at Guy's appear to have been well acquainted with the disease, and in 1857 Wilks described cases under the heading "Idiopathic Fatty Degeneration." To the labors of Zurich professors we are indebted for much of our knowledge. That versatile clinicist Lebert, then at Zurich, published in 1853 cases of puerperal chlorosis, and we owe to him the excellent designation of essential as applied to these cases of anæmia (1858). It was in 1871-72 that the communications of Gusserow[62] and Biermer[63] aroused a very general interest in the disease. Gusserow's cases, like some of Channing's, were in connection with pregnancy. Biermer, thinking he was dealing with a previously unknown affection, gave it the name of progressive pernicious anæmia. In the past ten years the literature of this form of anæmia has enormously increased. In Germany, in addition to the articles in the encyclopædias (Ziemssen's, Eulenberg's) and innumerable contributions and dissertations, two important monographs have appeared by Müller (Zurich, 1877) and Eichorst (Leipzig, 1878). In France, Hayem, Lepine, and others have published important observations. In England, the Guy's Hospital physicians, Taylor and Pye-Smith, in the _Hospital Reports_ (1878-83) have fully established Addison's claim to having given a clear account of the disease. Important contributions have been made by Stephen Mackenzie, Coupland, Bramwell, Bradbury, and others. In this country Pepper in 1875 brought the disease to the notice of the profession and suggested the name anæmatosis. Howard (R. P.) of Montreal at the Centennial Medical Congress (1876) gave a full account of the affection, the existence of which he had long recognized and taught. Musser[64] has reviewed the American literature, and has given a tabular synopsis of 39 cases which have been recorded in this country.

[Footnote 62: _Archiv f. Gynäkologie_, ii.]

[Footnote 63: _Correspondenzblatt für Schweizerische Artze_, 1872.]

[Footnote 64: _Proceedings of Philadelphia County Med. Society_, 1885.]

ETIOLOGY.--The disease is widely distributed, and there are no special geographical influences. In Germany and certain of the Swiss cantons--Zurich particularly--the cases seem to occur more frequently than in England or America. In this country it can scarcely be called one of the rare diseases, although up to January, 1885, Musser[65] could collect only 39 cases. During ten years in Canada I saw 16 cases, most of them with colleagues at Montreal.

[Footnote 65: _Loc. cit._]

That bad hygienic conditions have much to do with the induction of the disease is shown by the records of Zurich and Berne, where the cases have been very numerous among the lower classes, who are hard worked, ill fed, and poorly housed. Possibly here other unknown causes may be at work, as the conditions which prevail in the Zurich canton are not unknown in other countries. In Ireland, where the peasants have poor food and wretched houses, the disease does not appear to be common. In the Montreal cases the subjects were chiefly of the upper or of the higher mechanic classes.

The age most subject to the disease is the adult period; cases are rare under twenty and over fifty. In Pye-Smith's table of 103 selected cases there were only 6 under fifteen years of age; 4 between fifteen and twenty; 29 between the twenty-first and thirtieth years; 26 cases between the thirty-first and fortieth years; 21 between the forty-first and fiftieth years; 13 between the fifty-first and sixtieth; and only 4 above sixty. The youngest case I have seen was in a girl of twenty, and oldest in a woman over sixty. The youngest case on record was at the fifth year.[66]

[Footnote 66: Quoted in _Am. Journ. Med. Sci._, Jan., 1885.]

Sex.--If we exclude all cases in women directly connected with the puerperal state, primary idiopathic anæmia is more frequent in men than in women. Of the 16 Montreal cases, 4 were dependent upon parturition, and of the remainder, 9 were in men and only 3 in women. But most of the {900} collected figures include the parturition cases, and the women are in excess; thus, of 93 cases from the Swiss clinics at Zurich and Berne, 67 were females. Eichorst's figures are 65 women and 30 men. Of 110 cases collected by Coupland, 56 were men and 54 women. In Pye-Smith's careful tabulation of 103 selected cases, 48 were men and 59 women.

As observed by Channing, Lebert, and Gusserow, pregnancy and parturition are important factors in the production of a grave form of anæmia. In the majority of cases the symptoms develop post-partum, often, but not necessarily, in consequence of loss of blood during delivery. Obstinate vomiting during pregnancy and prolonged lactation may bring about the same condition. Of 29 cases of this sort in Eichorst's table, in 19 the symptoms developed during pregnancy and in 10 after delivery.

Gastric and intestinal disturbance, dyspepsia, vomiting, and diarrhoea have occurred in a number of cases prior to the development of the anæmia.

In some instances loss of blood, chronic discharges, ulcers, or other sources of drain have been present.

In not a few cases there has been mental worry, grief, or fright. This has been specially noted by Wilks and Howard, and more recently by Curtin.[67] It does not seem probable that malaria has any predisposing influence.

[Footnote 67: "Nervous Shock as a Cause of Pernicious Anæmia," _Med. Times_, Philada., April 4, 1885.]

It is by no means always the ailing or delicate who are attacked; many of the cases have occurred in men previously strong and robust.

After excluding all these factors, which prevail in a considerable proportion, there still remain cases without, as Addison says, any discoverable cause whatever--cases to which in our present knowledge we may apply the term idiopathic. These may be primary, and the others, in which some one or other of the above-mentioned causes appears to have prevailed, secondary anæmias, the latter to be distinguished from a host of other sequential anæmias only by the fact of a progressive and pernicious course.

Of 91 observations collected by Eichorst, in 24 cases the disease appeared to have come on spontaneously, and 67 as the result of various causes: pregnancy and parturition, 29; digestive troubles, 24; loss of blood, etc., 7; bad hygienic conditions, 7.

SYMPTOMS.--The classical description of Addison must ever be quoted in this connection: "It makes its approach in so slow and insidious a manner that the patient can hardly fix a date to the earliest feeling of that languor which is shortly to become so extreme. The countenance gets pale, the whites of the eyes become pearly, the general frame flabby rather than wasted, the pulse perhaps large, but remarkably soft and compressible, and occasionally with a slight jerk, especially under the slightest excitement. There is an increasing indisposition to exertion, with an uncomfortable feeling of faintness or breathlessness in attempting it; the heart is readily made to palpitate; the whole surface of the body presents a blanched, smooth, and waxy appearance; the lips, gums, and tongue seem bloodless; the flabbiness of the solids increases; the appetite fails; extreme languor and faintness supervene; breathlessness and palpitations are produced by the most trifling exertion or emotion; some slight oedema is probably perceived about the ankles; the debility becomes extreme--the patient can no longer rise from his bed; the mind occasionally wanders; he falls into a prostrate and half-torpid state, and at length expires: nevertheless, to the very last, and after a sickness of several months' duration, the bulkiness of the general frame and the amount of obesity often present a most striking contrast to the failure and exhaustion observable in every other respect."[68]

[Footnote 68: Monograph on _Disease of Suprarenal Capsules_, p. 3.]

The mode of onset is variable: in many cases there are etiological {901} conditions, such as pregnancy, loss of blood, etc., which for weeks or months precede, and perhaps determine, the development of the anæmia. There may have been mental worry or shock, and after a prolonged period of ill-health the anæmic symptoms become marked. Failure of strength, lassitude and disinclination for exertion, with shortness of breath and palpitation and an increasing pallor, accompanied by headache, giddiness, and dyspepsia, are the symptoms for which the patient seeks advice.

The condition of the skin is remarkable in pronounced cases: the color is rarely a deep white or ashen, as in the pallor of fear or fainting or the bloodlessness from hemorrhage, but there is a peculiar lemon tint, a light straw-yellow or grayish-yellow color, which may be mistaken for a mild icterus. This is one of the most characteristic features of the disease.

The subcutaneous fat does not waste; on the contrary, the fatty panniculus may increase, and, as Addison remarked, there may be a bulkiness of the frame. Actual emaciation is very uncommon.

Slight oedema is present in the feet, particularly toward the close, and it may extend up the legs, but rarely reaches a high grade. Occasionally it may appear in the face and hands.

Cutaneous hemorrhages in the form of small petechiæ are liable to appear on the legs and arms, not often on the trunk.

The sweat secretion is not affected, but in several instances, as in other chronic affections where death is protracted, a cadaverous odor has been perceived from the skin or breath.

The blood, as expressed, often with difficulty, from the finger-tip, has not the rich color of health, but is pale, like a light claret. The corpuscles usually fill the drop, and we do not see, as in certain cachectic states, an extreme degree of hydræmia in which the red corpuscles do not entirely occupy the plasma. It is sometimes difficult to get a drop of blood from the finger-tip, and to do so the arm should hang by the side and may be squeezed from the shoulder downward to press the blood into the hand. The microscopical characters of the blood are as follows:

(1) The red cells present a great variation in size, and there can usually be seen _(a)_ large giant forms, the megalocytes measuring 8, 11, or even 15 mm.: these are not often very numerous, and may show irregular foldings at the edges; _(b)_ medium-sized disks, such as are usually found in the blood: these always predominate; _(c)_ small round cells, microcytes, 6, 4, or even 2 mm. in diameter, and of a deep color. They are rarely absent in typical cases, though varying in number at different periods. The color of the large and medium-sized corpuscles may be much less intense than normal.

(2) In addition to the variation in size, the corpuscles show a remarkable irregularity in form--an irregularity which, so far as my observation goes, is never met with to the same extent in other conditions. They may be elongated and rod-like, scarcely recognizable as blood-disks. Balloon and kidney shapes are common. One end of a corpuscle may retain its shape, while the other is extended as a pointed or blunt process. The normal concavity may be lost on one side and deepened on the other. Many of the large forms are longer than broad, often quite ovoid, and with sinuous margins. The microcytes are either globular or present a pit-like depression on one surface. To this condition of irregularity of the corpuscles in size and form Quincke has given the name poikilocytosis ([Greek: poikilos], variously shaped). It possibly depends on an altered state of the serum; I have failed to produce it with dilution. The corpuscles in the blood of idiopathic anæmia do not form such well-defined rouleaux as in health.

(3) The colorless corpuscles may be relatively increased, but are usually diminished to some extent. They present no very special changes in form or stricture. Larger forms may occasionally occur, but I have not noted their {902} presence, specially the cases in which the marrow was found red and lymphoid after death. In two cases the majority of the corpuscles at several observations were smaller than normal. The amoeboid movements are active.

(4) In only two instances, in the cases I have examined, were nucleated red corpuscles present, and these very scanty. They have been noted by several observers. Ehrlich states[69] that they are present in all cases.

[Footnote 69: _Berl. klin. Wochenschrift_, 1880.]

(5) Schultze's granule masses, composed of the hæmatoblasts or blood-plates, are either absent or very scanty. In some cases not a trace of them could be found, and in others they are less abundant than in health. In this respect the blood offers a marked contrast to that of various cachectic states, and also to leukemia, in which the masses are sometimes very numerous. Leube,[70] however, has recorded a case in which they were abundant.

[Footnote 70: _Ibid._, 1879.]

(6) The fibrinous network between the corpuscles is thin and indistinct. The Cercomonas globulus and Cercomonas navicala, described by Klebs[71] as occurring in pernicious anæmia, are possibly peculiar to Prague.

[Footnote 71: _Real Encyklopädie_, art. "Flagellata."]

The reduction in the number of the red corpuscles is the special feature of the disease, the diminution reaching far below that met with after the most severe hemorrhage. Instead of a corpuscular richness of 5,000,000 per cubic millimeter, the number may be reduced to one-quarter, or even one-tenth. In the more extreme anæmia from hemorrhage, in cancer or in phthisis, the reduction rarely reaches as low as 1,500,000, while this figure is common in pernicious anæmia, and in advanced cases may sink below 1,000,000, or even to 500,000. This latter figure is exceptional. In only 2 cases have I counted the number so low as this. In a case of Quincke's the red were reduced to 143,000 per c.m., and, strange to say, the man recovered. Great variations may occur from month to month in the course of the disease. An increase in the number is not always associated with an improvement in the patient's condition.

The hæmoglobin is also greatly reduced, but not in proportion to the reduction in the red corpuscles. The relative coloration of the corpuscles is increased, and this seems as marked a feature in pernicious anæmia as the relative reduction is in chlorosis.[72] Owing to the fact that the hæmoglobin value of individual corpuscles is increased, the anæmia is never quite so intense as the number of corpuscles would appear to indicate.

[Footnote 72: Laache, _Die Anämie_, Christiania, 1883; _Deutsche Medicin Wochenschrift_, 1884, No. 43.]

The circulatory system presents many symptoms of importance. When the patient is recumbent and at rest, the heart's action is quiet, but on exertion or excitement the action becomes rapid, and there are palpitation, fluttering, and sometimes painful sensations in the cardiac region. Stairs are particularly trying to these patients. There may be slight enlargement of the heart, indicated by an increased area of visible pulsation, and an impulse in the third or fourth left intercostal space, near the sternum, is frequently seen. The hæmic or functional murmurs are usually present, variable in intensity and site, most often heard at the base and in both aortic and pulmonary areas, but also at the apex. Indeed, their variability is often puzzling; sometimes it would seem that there might be a murmur at each orifice, at another limited only to one; and for the bruit to be present at one examination and absent at the next is not uncommon. In several of Eichorst's cases there was a variable diastolic murmur at apex or base.

The larger arteries pulsate visibly--so much so that at times it suggests the water-hammer pulsation of aortic insufficiency. The carotid pulsation may be most evident, and still more so in the abdominal aorta, the throbbing of which may be very distressing to the patient. A systolic arterial murmur may be heard in all the arteries. The pulse is soft, compressible, usually {903} rapid (80 to 100 or over), depending a good deal on the position and state of excitement. One is sometimes surprised in these cases to find a full and at the same time very soft pulse. It may be dicrotic.

The venous hum is well marked, and is rarely absent except after prolonged rest in bed, when both cardiac and venous murmurs may disappear, to return at once on making the patient stand up. Channing, in the paper already referred to, speaks of the thin, scanty state of the blood, and yet notes the prominent appearance of the veins beneath the skin, particularly about the hands and wrists.

Hemorrhages occur very frequently. Epistaxis is most common, and may have preceded for years the onset of the grave anæmia. It may recur repeatedly and be a source of constant drain, or ultimately be the cause of death. From other mucous surfaces bleeding is not so common. I have seen one case in which there were for months repeated small hemorrhages from the bowels, and bleeding from the gums has been observed in several cases. The petechiæ on the skin have already been referred to. Retinal hemorrhages, as first noticed by Biermer, are very common. They are numerous and small, scattered around the disk. They are not peculiar to any special form, but are liable to occur in severe anæmia from any cause.

Respiratory symptoms are not prominent: a short cough may be present, but the only special feature is the shortness of breath, which is often early and troublesome, and depends on the condition of the blood, not of the lungs. There may be a very distressing and persistent sense of insufficient aëration (Pepper). Toward the close hydrothorax may develop.

The gastro-intestinal system is in the majority of cases more or less deranged. Dyspepsia may precede for years the anæmia, and may persist throughout the illness. There is loss of appetite, amounting sometimes to a positive repulsion toward all forms of nutriment. Nausea and vomiting are rarely absent throughout the illness, and there are some cases in which the gastric symptoms are so marked as to suggest a primary stomach lesion as the atrophy to which Fenwick[73] has called attention, or even arouse a suspicion of cancer.

[Footnote 73: _Lancet_, 1877, ii.]

Diarrhoea is also a frequent symptom, and in some cases hastens the fatal result. There may be melæna, and in Müller's monograph a case is given in which leucin and tyrosin were found in the stools.

The urine is pale, acid, and of low specific gravity. Occasionally it becomes darker in color. The urea may be diminished, but it has been found increased in some cases by Quincke, Eichorst, and Laache. The uric acid is more commonly increased, and the phosphoric acid. The percentage of iron has been found larger than normal. Albumen is rarely found. Peptones, leucin, and tyrosin may be present (Laache). Blood does not often occur.

Fever is not a constant symptom; some cases run their course without any elevation, but there is usually slight febrile reaction of an irregular, remittent type, an evening elevation of two or three degrees, and a morning remission to the normal standard. There may be a week or ten days of fever, and then a long spell without any. Toward the close there is commonly an elevation, occasionally depression, of temperature, as in one case reported by Müller in which it sank to 24.8° C.

COURSE.--In the majority of cases the disease runs a steadily downward course, well indicated by the terms progressive and pernicious. In almost every case periods of temporary improvement occur. Recovery is possible, and Pye-Smith[74] gives a summary of 20 undoubted cases which got well. The lactation and parturition cases stand a better chance of recovery than others. {904} The average course of the affection is from six to twelve months; there are rapid cases in which a fatal termination may be reached in a few months, and there are others which drag on for two, or even three, years, periods of improvement alternating with relapses. Death is usually by asthenia. It may be hastened by hemorrhage from the nose or bowels or by persistent vomiting or diarrhoea.

[Footnote 74: _Guy's Hospital Reports_, 1883.]

MORBID ANATOMY.--The body is not often emaciated; usually, indeed, the panniculus adiposus is well developed. The peculiar lemon tint of the skin is present in the majority of cases, and there may be petechiæ. The voluntary muscles may appear normal, but are often of an intense flesh color, more like horse muscle. In six cases the words "rich red color" and "remarkably deep red color" occur in my notes. In other instances they are pale. When the cavities are opened the general pallor of all the organs is most striking. The serous surfaces are smooth and glistening, and occasionally present ecchymoses. The amount of fluid may be increased. The mucous membranes are pale; minute hemorrhages are not uncommon.

The heart is in many cases large and flabby, in others normal, and in a few undersized. The pericardial fluid may be in excess, and the subpericardial fat is often increased. The flaccid relaxed state of the walls is very noticeable, and on opening the chambers the amount of blood is always very slight. In one case I could only obtain two drachms from the right heart, and between three and four from the left. There may be small clots entangled with the chordæ tendineæ of the valves. The muscle-substance is pale, of a faded-leaf, light-yellow color, and beneath the endocardium, particularly of the left side and of the papillæ, there are flaky spots (tabby mottling) of fatty degeneration. The peculiarities of general fatty degeneration of the heart are nowhere better seen than in these cases. The valves and orifices are usually normal. The intima of the aorta may show fatty changes. The smaller arteries and veins contain most of the blood.

The lungs are crepitant, pale, with a slight bloody oedema at the bases. The fluid expressed has often a yellowish tinge. Exudation into the pleural cavities is common. The air-passages do not offer any special changes.

The liver is of normal size, pale and generally fatty, not invariably; in none of Eichorst's cases was this a marked feature. Quincke and others have found the amount of iron increased.

The mucous membrane of the gastro-intestinal tract is pale, covered with a thin mucus, and may present ecchymoses. Post-mortem solution of the gastric mucosa is common, and I have seen oedema of it. Fatty degeneration of the cells of the peptic tubules is common, and they may be in an atrophic state, as well described by Fenwick.[75] Ecchymoses of the small and large bowel are common; ulceration is rare. In a few instances the lymphatic elements of the mucosa have been found swollen. Extensive atrophy of the mucosa has been found associated with degeneration of the nerve-elements, but these changes, as shown by the observations of Nothnagel[76] and Schleimpflug,[77] are not uncommon in many other conditions.[78]

[Footnote 75: _Loc. cit._]

[Footnote 76: _Beiträge zur Phy. u. Path. des Darms_, Berlin, 1884.]

[Footnote 77: _Zeitsch. f. klin. Med._, ix., 1885.]

[Footnote 78: Sasaki, _Virchow's Archiv_, 96.]

The blood vascular organs have naturally received special attention. The spleen offers, as a rule, no important changes; the size is variable, rarely enlarged, occasionally reduced in size, but for the most part normal. The smallest I have seen was in one of Howard's cases, in which the organ weighed only one ounce and five drachms. In the 51 autopsies noted in Howard's paper the spleen was stated to be normal in 36 and enlarged in 13. Ten ounces is the heaviest I have seen. The spleen-tissue is moderately firm, of a light brown-red color. I have never noticed either the extreme softening of an acute splenic swelling or the hardness of chronic induration. {905} The histological characters present nothing special. Cells containing red corpuscles occur, but not in such numbers as in cases of acute splenic swelling from fever. I have seen the nucleated red corpuscles in several instances.

The lymph-glands are, as a rule, normal in size and appearance. In three instances I found them decidedly smaller than normal, and in two they had a rich deep-red color, and on section looked more like spleen-tissue than lymph-gland. Weigert has noted the same appearance.[79] In one of the cases there were nucleated red corpuscles in the glands, as has been observed by Rindfleisch in a case of rickets,[80] and more recently in tuberculosis.[81]

[Footnote 79: _Virchow's Archiv_, Bd. lxxix.]

[Footnote 80: _Archiv f. Mikros. anatomie_, Bd. xxiii.]

[Footnote 81: _Med. News_, xiv. No. 23.]

The fatty tissue of the long bones is in many instances replaced by a red marrow resembling that of the short bones of the adult and the entire osseous system of the infant. This was first noticed by Pepper in 1875,[82] and has since been frequently observed. The color is usually of a reddish-purple when fresh, becoming a bright red on exposure. Sometimes there is a grayish-red appearance. It may not be universally distributed in the long bones, and the change would appear to proceed from the trunk toward the periphery--a direction the reverse to that in which the red marrow of the child becomes fatty. In many cases the marrow has been found normal; in others, the change known as gelatinoid has been observed. In five Montreal cases I found the marrow of the long bones lymphoid, in one gelatinoid, and in two the long bones could not be examined. It must be borne in mind that the short and flat bones of the adult contain a red lymphoid marrow mixed with a variable amount of fat, in which nucleated red corpuscles can always be found.

[Footnote 82: _American Journal of Medical Sciences_, lxx.]

The brain and cord present an intensely anæmic appearance; the membranes are relaxed and oedematous, and petechiæ may exist. The convolutions are often wasted, and the amount of cerebro-spinal fluid increased. No important changes have been found in the substance.

The ganglia of the sympathetic system have been examined by Queckett in one of Addison's cases and found fatty. Wilks and others have found them normal. Brigidi[83] has described an increase in the interstitial tissue and pigmentation of the cells. In two instances I found nothing abnormal. Sasaki[84] has described marked degenerative changes in Auerbach's and Meissner's plexuses in two cases of pernicious anæmia.

[Footnote 83: _London Med. Record_, 1878.]

[Footnote 84: _Loc. cit._]

The kidneys are usually pale and without special change beyond the fatty degeneration. Quincke has found the amount of iron increased. The suprarenals have in several instances been found very small. The sexual organs show no constant changes.

PATHOLOGY.--Under the general subject of Anæmia the pathology has been discussed at sufficient length. After excluding pregnancy, parturition, lactation, and inanition cases, as partaking more of the characters of secondary anæmia, we can recognize three groups of cases: First, those in which the bone-marrow has been found extensively affected--cases of anæmia medullaris; second, cases in which a primary atrophic change in the mucous membrane of the stomach appears to have been the starting-point of the trouble; and, third, cases in which after death no special changes have been found sufficient to explain the anæmia. To the latter the term idiopathic is applicable, and possibly they may be instances of hæmophthisis due to increased destruction of the corpuscles from causes unknown at present.

DIAGNOSIS.--A case in which anæmia comes on without obvious cause and without enlargement of the spleen, and progressively increases in spite of remedies, diet, change of air, etc., may be regarded as one of an idiopathic or essential character. If the case goes on to a fatal termination, the designation of pernicious is appropriate. I would place some reliance on the {906} microscopical examination of the blood, and would consider the presence of microcytes with great irregularity in the ordinary red corpuscles strong confirmatory evidence. The absence of wasting, the peculiar lemon tint of the skin, the occurrence of epistaxis and retinal hemorrhages, would render a diagnosis certain.

In that class of cases so well described by Fenwick,[85] Nothnagel,[86] and Nolen,[87] in which there has been an interstitial inflammation of the gastric mucosa and atrophy of the glands, the question has not yet been decided how far this condition is to be considered causal, and how far a part of the general disturbance of nutrition. The clinical picture may be identical with that of idiopathic anæmia, and in some of the cases the gastric symptoms have been so marked that the relation of the atrophy and the anæmia has evidently been that of cause and effect. And yet in these cases there does not appear to be the pronounced emaciation of inanition anæmia. In other instances the diarrhoea and chronic intestinal trouble may, with or without gastric participation, bring about a similar condition.

[Footnote 85: _Loc. cit._]

[Footnote 86: _Deutsches Archiv f. klin. Med._, xxiv.]

[Footnote 87: _Centralblatt f. d. Med. Wissenschaft._, xx.]

Profound anæmia may arise during or after pregnancy, and a considerable proportion of the cases on record have been in this connection.

From ordinary cases of Hodgkin's disease, anæmia lymphatica, there could be no difficulty in making a diagnosis if the superficial glands were enlarged. In splenic anæmia, if the enlargement was not great, there might for a time be uncertainty, which the progressive increase of the organ would remove. Neither in anæmia splenica nor lymphatica are we so likely to meet with the microcytes or irregular corpuscles.

Chlorosis occurs chiefly in young girls, and is amenable to treatment.

From the various cachexias--malarial, syphilitic, metallic--the history will commonly afford grounds for a diagnosis, and in these states, as in latent cancer, the wasting is apt to be more pronounced than in essential anæmia. Cases of gastric cancer are occasionally met with which simulate closely pernicious anæmia, and the diagnosis may be doubtful for months.[88]

[Footnote 88: Richard Neale, _Practitioner_, 1883.]

The enteritis and hemorrhages caused by the presence of Anchylostoma duodenale in the intestines may produce an aggravated form of anæmia resembling closely the form under consideration. It prevails among the workers in mines and tunnels, hence the name miner's anæmia or anchylostomiasis. The diarrhoea and the detection of the ova or worms in the discharges would afford grounds for a diagnosis.[89]

[Footnote 89: _Trans. of the International Med. Congress_, London, 1881, vol. i. 437.]

The PROGNOSIS is unfavorable, particularly in those cases which have arisen without any cause or previous ill-health. In the cases arising from defective food, etc.--inanition anæmias--pregnancy, or lactation, the outlook is less grave. Of the 64 Zurich cases in Müller's monograph, 7 recovered, and of Quincke's 31 cases, 11 recovered. Pye-Smith gives a table of 20 recorded cases of recovery.[90] Great improvement may occur, or even recovery for a period of several years, after which the disease may recur and prove fatal. This was the history in a case under the care of Wilkins at the General Hospital, Montreal.

[Footnote 90: _Loc. cit._]

TREATMENT.--The designation pernicious applied by Biermer indicates the hopeless character of the disease in perhaps a majority of the cases; of late the records happily show a considerable percentage of recoveries. Thus, Pye-Smith has collected 20 cases in which convalescence was established after severe and profound anæmia, belonging undoubtedly to the class here considered. The intractable nature of a case and the resistance to ordinary treatment are points which may first suggest to the practitioner the fact that he is dealing with a something more than simple anæmia.

{907} Hygienic and dietetic regulations are of the first importance. Cases appear to have got well with change of air and a better diet after resisting all ordinary means. In other instances no benefit whatever has been derived from residence at the sea or in the mountains. As a rule, the cases are best treated at home. The greatest care must be exercised in the regulation of the diet, which should be light and nutritious. So long as the digestion keeps tolerably active there is hope: anorexia, vomiting, and other dyspeptic symptoms are among the most troublesome and serious features. The bitter tonics, hydrochloric acid, and pepsin may be administered. But the stomach may fail absolutely and reject even the smallest amount of liquid food, and rectal alimentation must be employed. The gastric symptoms have been specially marked in cases in which there has been found post-mortem atrophy of the peptic glands. In certain of these cases the problem of feeding will tax to the uttermost the resources of the physician. Rectal injections of blood (fresh or dried), as recommended by A. H. Smith, I have found beneficial in several cases. Intestinal symptoms--diarrhoea, flatulence, and in some cases melæna--call for treatment.

Of medicines, arsenic is the most important, and in the form of Fowler's solution should be employed in small and increasing doses. We are indebted to Bramwell[91] for pointing out the great value of this medicine, and in certain cases it acts almost as a specific. In 8 of the 20 cases of recovery noted by Pye-Smith the improvement seemed due to the arsenic. Padley[92] has collected in the literature 48 cases treated without arsenic, of which 42 were fatal, while of 22 cases treated by arsenic 16 recovered, 2 improved, and only 4 proved fatal. The testimony of recent observers is very strongly in favor of this drug as the most efficacious we possess in this grave disease. The use should be continued long after the convalescence is apparently established; indeed, it should be given at intervals for many months after recovery, as there are dangers of relapse. There are cases which are not benefited by arsenic, even when well borne. Finlay[93] has recently reported a case which was cured by iron after the failure of arsenic.

[Footnote 91: _Edinburgh Med. Journal_, 1877.]

[Footnote 92: _Lancet_, 1883, ii.]

[Footnote 93: _Lancet_, 1885, i.]

Iron, as a rule, seems quite useless in the majority of these cases. I have frequently seen the percentage of red corpuscles gradually sink under its administration, and then rise in a remarkable way when the arsenic was employed. This is in curious contrast to the effect of this drug in the various secondary anæmias and chlorosis in which it is rightly regarded as a specific. The cases which are benefited may have a different etiology, and where the arsenic does not succeed some form of iron should be given, as Finlay's case, just mentioned, shows that there are instances where it cures after the failure of the arsenic.

Broadbent advises the use of manganese when the anæmia is associated with uterine or menstrual trouble. Phosphorus has been extensively employed, and occasionally with benefit.

When all remedies have been tried in vain the question of transfusion of blood arises. As a substitute for the intravenous transfusion the blood has been injected into the peritoneum: this has been practised in Italy with success.[94] The subcutaneous injection has also been used, and lately the inhalation of a spray of blood has been recommended.[95] In four or five instances intravenous injection has succeeded, but in the majority of cases it has proved useless. Von Ott's[96] interesting researches show that the injected blood-corpuscles and albuminous materials always undergo destruction in the blood, and a 6/10 per cent. solution of common salt seems to answer just as well, and is much more available and less dangerous.

[Footnote 94: _Practitioner_, vol. xxxi.; Ponfick, _Berl. klin. Wochenschrift_, 1879.]

[Footnote 95: _Med. News_, 1885, i.]

[Footnote 96: _Virchow's Archiv_, Bd. xciii.]

{908} The injection of milk, as first practised in cholera by my preceptors, Bovell and Hodder[97] of Toronto, has also been employed in anæmia (Pepper, Wulfberg).

[Footnote 97: _Canadian Journal of Science_, 1854.]

LEUKÆMIA.

DEFINITION.--A disease characterized by a great and persistent increase of the colorless corpuscles of the blood, associated with enlargement of the spleen, lymphatic elements, and bone-marrow.

SYNONYM.--Leucocythemia (Bennett).

HISTORY.--Our knowledge of this affection dates from the description of two cases by Craigie and Bennett in the October number of the _Edinburgh Medical Journal_ for 1845. The altered state of the blood was thought to be due to the presence of pus--a suppuration of the blood. In the November number of Froriep's _Notizen_ for 1845, Virchow described a case in which the proportion between the red and white corpuscles seemed reversed, and the blood had in consequence a grayish-white appearance. He attributed the condition to an increase in the colorless corpuscles. A case of Rokitansky's is referred to in this article. In 1846, Fuller described a case before the Medico-Chirurgical Society of London, in which the increase in the colorless corpuscles was noted during life and after death.

In the August and September numbers of _Medicinische Zeitung des Vereins für Heilkunde_ (1846) Virchow reviewed these four cases, and insisted upon the fact that the colorless cells in the blood were not pus, and vindicated a place in pathology for the white blood-corpuscle. In the January number (1847) of the same journal he gives further cases of white blood which he had collected in the literature--cases of Bichat (1801), Velpeau (1827), Caventon (1828), Andral (1839), Barth (1834),[98] and several others--and discussed the conditions under which the colorless elements might increase and the relation of the spleen to the white cells. In the same year (1847), in the first volume of his _Archiv_, Virchow proposed the name leukæmia. Vogel in 1849 diagnosed a case during life.[99]

[Footnote 98: Donne (_Cours de Microscope_, 1844), who examined Barth's case, seems to have been the first to recognize that the colorless cells were blood- and not pus-corpuscles. See note by Gowers in _Lancet_, i., 1878.]

[Footnote 99: _Virchow's Archiv_, Bd. iii.]

Bennett in 1851 collected additional cases, and gave the name of leucocythemia to the disease, and in 1852 published a monograph entitled _Leucocythemia; or, White-celled Blood, in Relation to the Physiology and Pathology of the Lymph-gland System_. He claimed priority in the discovery of the condition, and for several years a lively paper war raged between the Edinburgh and the Berlin professors.

At this distance of time and place we can, now that the clouds of controversy have blown away, see the truth. Bennett certainly described cases before Virchow, but only in a manner similar to that in which Bichat, Velpeau, and others had previously done, and he distinctly stated his belief that the grayish-white color of the blood was due to pus. Virchow from the first grasped the idea that the altered state of the blood was due to an increase in the colorless cells, and he first suggested the relation between their increase and the condition of the spleen and lymph-glands, and he first gave a satisfactory name to the disease; so that, while acknowledging the great and valuable services of Bennett, we must, perforce, recognize the greater merit {909} of Virchow, and recognize his priority in the scientific description of the disease and in giving to it a suitable name. The further investigations of Virchow enabled a splenic and a lymphatic form to be recognized, and many years later Neumann[100] described the myelogenous variety.

[Footnote 100: _Archiv der Heilkunde_, Bd. xi.]

FORMS OF THE DISEASE.--According as the pathological changes are located in the spleen, lymph-glands, or marrow we speak of splenic, lymphatic, and medullary or myelogenous forms; but it is very exceptional for pure unmixed varieties to occur. More commonly, the spleen and marrow, or these with the lymph-glands, are involved. The disease may begin and make great progress in one of these regions, or be confined to it for months, before appearing elsewhere. The spleen is most often affected, and with it the marrow. According to many recent writers, the myelogenous form is the most general, and certainly the marrow is rarely found unchanged. The unmixed lymphatic variety is not of frequent occurrence. An intestinal form, characterized by swelling of the solitary and agminated lymph-glands and the general adenoid tissue of the bowel, has been described by Behier.[101] In a few instances the tonsillar and pharyngeal lymph-elements have been early, perhaps primarily affected, and Kaposi has recently recorded a case[102] under the name lymphoderma perniciosa, in which the lymphatic elements of the skin were first involved.

[Footnote 101: _L'Union médicale_, 1869.]

[Footnote 102: _Wiener Med. Jahrbücher_, 1885.]

ETIOLOGY.--We know scarcely anything of the causes of the disease, but it is usual to take into account certain factors which may possibly influence its production, such as climate and country, age, sex, etc.

Climate and Country.--The disease appears to be more common in temperate regions; not many instances are reported from the tropics. It does not appear to be often met with in India. It is, I think, more common in Europe than in this country. The determination of its prevalence is rendered difficult by the fact that many cases reported simply as enlarged spleen, without any examination of the blood, have possibly been leukæmia. It does not seem to be more common in the southern part of this continent.

Age.--No age appears exempt. Cases are recorded in infants of eight or ten weeks and in men of sixty-nine and seventy years of age. The youngest case I have seen was in a suckling of eight months. The majority of cases occur at the middle period of life, from thirty to forty. After the fiftieth year the cases diminish very much in number.

Sex.--Males are more prone to the affection than females, in the proportion of at least 2 to 1. Of 11 cases which I saw in Montreal, only 3 were in females; of 200 cases collected in the literature, 135 were in males and 65 in females (Birch-Hirschfeld[103]).

[Footnote 103: _Lehrbuch der Path. Anatomie_, 2te Auf., 1883.]

Social and sanitary conditions do not appear to have much influence, though the lower and middle classes furnish the majority of the cases. Mental worry and depression are specially mentioned as predisposing causes in some cases.

Previous Disease.--In women it has frequently been noticed that disturbance in the menstrual and sexual functions has preceded the onset of the disease. The climacteric period has the greatest number of cases, and in a few instances the disease had developed during pregnancy.

The hemorrhagic diathesis has been noted in many cases, and the patient may have been the subject of slight hemorrhages for years. In one case of Howard's[104] the lad had been subject to nose-bleeding as a child, and his mother and one sister had been much troubled in the same way.

[Footnote 104: _Montreal Gen. Hosp. Reports_, vol. i., 1880.]

Malaria.--On account of the frequency of chronic splenic tumor in malarial infection, inquiries are always carefully made in any suspected case as to the occurrence of intermittent fever. An intimate connection is believed by {910} certain writers to exist between the affections, and a few cases seem to have followed directly upon chronic malaria. In Mosler's statistics of 112 cases there were only 4 in which the sequence was well marked.[105] In Gowers' 150 cases there was a history of malaria in 30.[106] In the Montreal cases there was an account of malaria in 3 certainly--possibly in a fourth. In the reports of 33 American cases there were only 6 with a history of malarial attacks within twelve years from the date of the onset of leukæmia. Guiteras of Key West (now of Charleston, S.C.) states that it is a rare affection in the South. Schmidt of New Orleans writes me that it is not uncommon in Louisiana, but there are very few cases reported in Southern journals.

[Footnote 105: _Die Leukæmie_, Berlin, 1872.]

[Footnote 106: _Reynolds's System_, art. "Leucocythæmia."]

Syphilis appears to have been in a few cases closely connected with the onset of the disease.

Injury.--Many patients give an account of a blow or strain in lifting. In 3 cases which I have seen the patients laid great stress on this. One had received a kick in the side from a horse, and the two others had strained themselves in lifting. De Chapelle[107] has dealt specially with this feature in the etiology of the disease.

[Footnote 107: _De la Leukémie dans ses Rapports avec la Traumatisme_, Paris, 1881.]

Previously-existing splenic enlargement does not seem, as we might expect, to predispose to leukæmia. It is rare for a case of simple chronic hyperplasia of the spleen--from malaria, for instance--to terminate in leukæmia.

The disease occurs in the lower animals, and cases have been described in horses, dogs, oxen, cats, swine, dogs, and mice. The majority of cases have been in dogs.[108] A study of the comparative pathology of the disease has not thrown any light on the etiology.

[Footnote 108: Siedamgrotzky, _Ueber die Leukæmie bei den Hausthieren_, Leipzig, 1878; Bollinger, _Virchow's Archiv_, lix.; _London Med. Record_, vol. ii., 1874.]

SYMPTOMS.--A division of the disease into two or three stages has been made by some writers, but as no special regularity is observed in the sequence of events, we need only recognize a period of development, in which the disease gradually becomes established, and a final period of cachexia, when there are symptoms of profound blood-change and the viscera are involved.

The mode of onset is insidious. In the majority of cases there is failure in health and strength, and the patient seeks advice for progressive enlargement of the abdomen with dragging pain in the side, or for the shortness of breath, the enlarged lymph-glands, the pallor, or the various symptoms of anæmia, as headache, palpitation, and dizziness. Bleeding at the nose is common. Vomiting and diarrhoea may be early symptoms, and in a few cases oedema of the face and feet has been noted early in the disease. Occasionally the first symptoms to attract the attention of friends or physician are of a serious nature--a sudden hemorrhage, for example. In one of Howard's cases the lad had played lacrosse two days before the onset of the fatal hæmatemesis, and in another case, a girl, there was early and fatal hemorrhage from the stomach before the condition of splenic enlargement was suspected.

Digestive System.--Gastric symptoms are rarely absent in the form of oppression after eating, nausea, and vomiting; the latter may be an early and troublesome feature. The appetite is variable, and when the spleen is greatly enlarged the mechanical pressure is apt to cause uneasy feelings after eating.

Diarrhoea is common, and may come on very early in the disease (Case I.[109]), and it is a frequent cause of death. The stools are usually thin and catarrhal, not often dysenteric, but melæna occurs in many cases. The diarrhoea may be due to a dysenteric process in the colon (Case II.), and tenesmus may {911} be present. It has not been noted that the diarrhoea is more frequent when the lymph-glands of the intestines are involved.

[Footnote 109: These figures refer to Montreal cases, some of which I saw with my colleague, Palmer Howard, others with John Bell, Lachapelle, and G. T. Ross.]

The liver shows no alterations in the early stage, but as the disease advances it is almost invariably enlarged. Jaundice is not often present, but there may be recurrent attacks (Case II.), due either to catarrh of the ducts or to pressure of glands in the hilus. Ascites is a variable feature; a slight degree is not uncommon as part of a general dropsy dependent upon the blood-condition, but in some cases it is a prominent symptom and calls for frequent tappings (Case IX.). In some cases it is due to pressure of leukæmic growths in the branches of the portal vein or the liver, or of enlarged glands upon the trunk at the hilus. The ascites is not always hepatic; like the hæmatemesis and melæna, it may be of splenic origin and occur without any disturbance in the portal vein or liver. Leukæmic peritonitis has been met with.[110]

[Footnote 110: Willcocks, _Proceedings of Conn. Med. Soc._, 1874.]

Nervous System.--Headache, dizziness, and attacks of fainting are common, and due chiefly to the anæmia. In some cases the headache is severe and persistent. The intelligence is well preserved; only toward the close is there rambling delirium. Mental disturbance may occur, and in one case the patient committed suicide. Some writers speak of special sadness and moroseness. This I have never noticed; on the contrary, in most of the cases I have seen the patients seemed specially tranquil and resigned. Coma may come on suddenly from cerebral hemorrhage (Case X.).

Sleep is not usually disturbed; some patients doze incessantly.

Special Senses.--Weak vision is often complained of, due to the anæmia, sometimes to the leukæmic retinitis. Blindness rarely supervenes, even when the retinal changes are extensive. Marked intolerance of light may be present.

The condition of the retina is variable. There may be simply turbidity and swelling of the retina, with large and tortuous veins, or more commonly with the opacity there are hemorrhages, such as occur in profound anæmia from any cause. A peculiarity, however, of the extravasations in some cases of leukæmic retinitis is the appearance produced by the aggregation of colorless corpuscles, often in the centre of the hemorrhage, so that there is a yellow or white nucleus and a zone of red. The collections of colorless corpuscles may indeed have the characters of small leukæmic growths. In one case (XI.) throughout the retinæ were numerous small raised opaque white bodies one to two millimeters in diameter, some of them surrounded by rings of extravasation. There was no swelling of the disk.

Deafness has been frequently observed, and may appear early. It was specially noted in the cases of Edes,[111] Morrill,[112] Seguin,[113] and Pepper,[114] and DaCosta.[115] No satisfactory explanation has been given, and the suggestion that it is due to hemorrhage has not, so far as I know, been confirmed by autopsy. Noises in the ears may be very troublesome, and even be so bad as to disturb hearing and necessitate the writing of questions (Case XI.).

[Footnote 111: _Boston Med. and Surg. Journal_, 1871.]

[Footnote 112: _Loc. cit._]

[Footnote 113: _Archives of Scientific and Practical Medicine_, New York, 1873.]

[Footnote 114: _Med. and Surg. Reporter_, 1883, 48.]

[Footnote 115: _Ibid._, 1874.]

Blood-vascular System.--In a well-marked case the blood-drop squeezed from the finger-tip is more or less turbid, of a reddish-brown or in extreme cases chocolate-brown color.

The blood should be examined in a thin layer, and for this purpose it is better to take a small than a large drop. A rough estimation of the proportion of white corpuscles can be much better obtained when a uniform thin layer is beneath the top cover. The red corpuscles, as a rule, present no striking changes, no special alterations in size or shape. Microcytes are {912} occasionally seen, and now and then larger forms, but the extreme variations of pernicious anæmia are rarely met with. They are reduced in number, but not often to a great extent. A reduction below 2,000,000 to the cubic millimeter has been exceptional in cases which I have examined. In only one did the number sink to 1,500,000 per c.m. Laache[116] has noted a case in which, with enlargement of the spleen and a ratio of white to red of 1:17, the number of red corpuscles was little if at all reduced.

[Footnote 116: _Die Anämie_, Christiania, 1883.]

The colorless corpuscles are enormously increased. Instead of eight to ten millions per c.m., as in normal blood, they may reach 500,000 per c.m. or even 700,000 per c.m. The ratio of white to red cells may be 1:20, 1:10, 1:4, or they may even equal or exceed the red. Without a proper apparatus (Gowers, Malassez, or Zeiss) an accurate estimate is impossible, and it is chiefly upon the rough-and-ready method that the statements are made of the white exceeding the red in numbers. It is very seldom indeed that this is the case, and even in extreme leukæmia the ratio does not often reach 1:3 or 1:2. In none of my observations did the ratio rise to 1:1; the highest was 1:2. Cases are on record in which the white have exceeded the red: Sörensen's,[117] where the red per c.m. were 470,000 and the white 680,000, and in an interesting observation of Fleischer and Penzoldt,[118] as a mean of 57 accurate counts, the ratio of white to red was 115:100. The corpuscles have the natural grayish-white appearance of leucocytes, but differ in certain points from normal white blood-cells. The variations in size are greater: in normal blood only a few may be seen less than 1/2800 or 1/3000 of an inch, but in leukæmia on a single slide there may be colorless cells with the extreme measurements of 1/2000 and 1/3500. In ordinary cases we meet with--(1) cells of the average size, about 1/2800 of an inch in diameter, like normal corpuscles, with two or three nuclei and fine granular protoplasm; (2) smaller forms, 1/3000 of an inch and under, with single nuclei, resembling rather lymph-cells, and they were believed by Virchow to indicate special involvement of the lymph-glands, but they are present in all forms, though possibly more prevalent in the lymphatic variety; (3) large forms, 1/2000 to 1/1500 of an inch, with bold nuclei and bearing a close resemblance to the marrow-cells. They are not always present, and are believed to originate in the marrow.

[Footnote 117: _Virchow-Hirsch's Jahresber._, 1874.]

[Footnote 118: _Deutsches Archiv f. klin. Med._, Bd. xxvi.]

Cafavy states[119] that the colorless corpuscles of leukæmia do not display active amoeboid changes, indicating thereby a diseased and enfeebled condition of protoplasm. I find a note made in Sanderson's laboratory in 1873 on the very sluggish and imperfect movements of the colorless corpuscles in a case of leukæmia in University College Hospital. In Case V. the note on one day is, "Active amoeboid changes," and in two other cases since Cafavy's paper I have seen the protoplasmic movements tolerably active, but not in all equally. Possibly the leucocytes from the marrow do not move so freely as the others; normal marrow-cells have very feeble amoeboid powers. Ehrlich[120] has observed that the number of leucocytes in leukæmic blood which contain granules reacting with eosin is very great, whereas in normal blood very few occur.

[Footnote 119: _Lancet_, ii., 1880.]

[Footnote 120: _Zeitschrift f. klin. Med._, Bd. i.]

Nucleated red blood-corpuscles, such as occur in the blood of the foetus and in the red marrow of the adult, have been found in leukæmic blood by Klebs, Mosler, and others. I have observed them in four cases. They are scanty, usually isolated, rarely more than one or two in a field; often, indeed, many fields must be searched before finding one. On two occasions (Case IX.) they might be called numerous--three or four in each field of the No. 9 immersion lens.

Schultze's granule-masses, the aggregations of the discoid hæmatoblasts, are {913} present in variable numbers, sometimes very numerous. I have examined slides in which they were absent. A curious mistake was made by a writer in the _Lancet_ (1878, ii.) when he described these as a hitherto unnoticed feature of the blood in leukæmia.

The fibrin network which separates between the corpuscles is usually very thick and dense.

Peculiar crystals, elongated octahedra or spindles, of variable size and bright-white appearance, separate very commonly on a slide of leukæmic blood, particularly if kept surrounded with oil or paraffin for twenty-four hours. They are known as Charcot's crystals, and are identical with those which occur in the bone-marrow, in semen, and in sputum in some cases of bronchitic asthma. White of Boston described them well in 1859,[121] and believed they were produced by the separation of a neutral principle which he named leukosin. I can confirm Zenker's observation,[122] that they form sometimes in the colorless cells.

[Footnote 121: _Boston Medical and Surg. Journal_.]

[Footnote 122: _Deutsches Archiv f. klin. Med._, xviii.]

Leukæmic differs from ordinary blood, and from that of other anæmic or cachectic states, by the readiness with which the hæmoglobin crystallizes. Often if a slide is kept and prevented from evaporating by a rim of paraffin, beautiful plates of hæmoglobin will crystallize.

The pulse is always quickened--80 to 100, and in the final stages 110-130--usually soft and compressible, and not always small in volume. The heart's action is readily excited. A systolic murmur is not infrequent at the apex; basic hæmic murmurs are not so often heard as in anæmia, but a venous hum in the neck is generally present. The apex-beat of the heart may be pushed up an interspace by the enlarged spleen. Oedema of the ankles and feet from the feeble circulation is constantly met with, particularly toward the close, and there may be general anasarca. Effusion into the pleural cavities is not common.

Hemorrhages are among the most constant features of the disease, and may occur at any time, early or late, in the course. The tendency to bleeding is greater in this than in any of the allied affections. Epistaxis is the most frequent form, and may precede the development of the disease for months or years. Hæmatemesis may carry off a patient early (Case II.), or even before the nature of the trouble is suspected (Case VI.). Hemorrhage from the bowel is common. Hæmoptysis and hæmaturia are rare. Bleeding from the gums may be present (Cases V. and VII.). In women there may be profuse menstruation. Petechiæ on the skin are frequent; occasionally there are large extravasations beneath the skin or between the muscles. Hemorrhage into the brain may prove quickly fatal (Case X.), and the extravasations into the retinæ may impair vision.

The respiratory system offers few special symptoms. The shortness of breath on exertion is due in great part to the anæmia, and progressively increases with the advance of the disease. The free action of the diaphragm is hampered by the enlarged spleen. There may be cough from bronchitis, and toward the end signs of oedema at the bases of the lungs. Pneumonia is not uncommon as a final complication.

The temperature in the early stages presents very slight variations, but when the disease is advanced there is always fever of the remittent or of the continuous type. There is usually a morning remission, and an evening exacerbation which reaches 101° or 103°. Periods of pyrexia may alternate with prolonged intervals of freedom from fever. In some cases the febrile movement is very slight throughout the entire course.

Genito-urinary System.--The urine is usually normal in amount, pale, strongly acid, and its specific gravity above the normal. Considerable variations occur in individual cases. Sediments of lithates are very common. {914} The urea presents no constant changes; sometimes it is increased, at others diminished, the quantity depending probably on the food and the presence or absence of fever. The quantity of uric acid excreted seems always to be increased, due either to a lessening of the oxidation processes in consequence of the reduced number of red corpuscles, or, as Salkowski suggests, it stands in relation to the existing splenic tumor; but observers have not found the amount proportionately increased in other forms of splenic enlargement, and the cause of the constant increase is still doubtful. Hypoxanthine, lactic, formic, acetic, and hippuric acids have been found, but their presence is neither constant nor apparently of special import. Albumen may be present. Sugar is rare. Hæmaturia, as before observed, very seldom occurs. Cystitis may arise and be troublesome (Case XI.).

A curious symptom in connection with the generative system is priapism, of which a number of cases have been recorded. Edes[123] narrates the case of a boy of fifteen in whom obstinate priapism was the first symptom. Longuet[124] reports a case of six weeks' duration. Saltzer[125] mentions five cases, in one of which the condition persisted for seven weeks, and Peabody[126] gives a case in which it lasted six weeks. It is not definitely settled whether the priapism is due to thrombosis in the corpora cavernosa or to irritation of the nervi errigentes.

[Footnote 123: _Boston Med. and Surg. Journ._, 1871.]

[Footnote 124: _Progrès méd._, 1875.]

[Footnote 125: _Berliner klin. Wochenschrift_, 1879.]

[Footnote 126: _New York Med. Journ._, 1880, xxi.]

In women there are the usual menstrual irregularities consequent upon a grave constitutional disease. Occasionally the flow is excessive; more commonly it is interrupted altogether.

Blood-glandular System.--Slow increase in the volume of the spleen, causing a sense of weight in the left hypochondrium, is an early symptom in many cases. Patients do not usually come under observation until the enlargement is established and the organ can be felt below the costal border. Pain and tenderness over the organ are very common, though sometimes it is painless throughout. Palpation often elicits a creaking fremitus due to the rubbing together of the adhesions. The gradual enlargement causes an evident increase of girth in the lower thoracic and upper abdominal zones, and marked prominence of the left hypochondrium. The tumor extends to the right and downward, and may occupy a large portion of the abdomen, extending even to the pelvis. When there is no ascites the edge can be easily felt with the anterior notch or notches. The pressure of a large spleen causes distress after a full meal, and by its mechanical effect may even compress the bowels and produce fatal obstruction.[127] The effect upon the heart and respiration has already been noticed. The adhesions may interfere with the depression of the organ during a deep inspiration. The size varies in an inexplicable way, considering the indurated fibroid nature of the enlargement. It may be perceptibly larger after a meal.[128] A hemorrhage or free diarrhoea may reduce the size very much, as in Morrill's case.[129] A murmur may occasionally be heard, and an enlarged spleen has been known to pulsate.[130]

[Footnote 127: Collins, _Brit. Med. Journ._, 1882, i.]

[Footnote 128: Johnson, _Lancet_, 1870, Jan.]

[Footnote 129: _Bost. Med. Journ._, 1877.]

[Footnote 130: Gerhardt, _Zeitschrift f. klin. Medicin_, Berlin, Bd. iv.]

Lymphatic Glands.--In the great majority of cases the lymph-glands are but slightly if at all involved. Even when they are affected it is rare to see such large bunches as in Hodgkin's disease. When they are growing there may be pain and tenderness, and if large they may be a source of inconvenience, but severe pressure symptoms are not often witnessed. Enlargement of the glands in the superficial groups is readily detected, but the deep-seated collections in the mesentery and retro-peritoneum can rarely be palpated unless of considerable size. Mediastinal lymph-tumors in leukæmia are exceptional. In none of the cases I have seen were the lymph-glands {915} greatly enlarged. It is stated that in children the lymphatic variety is more common than in adults.

There may be tenderness over the bones, and in rare instances swelling, but unless the tenderness is marked and accompanied by some local expansion or softening, we cannot determine positively the existence of the myelogenous variety. The sternum, ribs, and flat bones are most often affected, and there may be great irregularity and deformities, as in a case I saw with Riess of Berlin. It is well to bear in mind that in perhaps the majority of persons there is a tender spot upon the sternum which may cause marked wincing when touched firmly. No reliance should be placed upon tenderness without swelling or softening. Such tenderness may exist, and post-mortem the marrow be found normal;[131] and, on the other hand, there may be extensive changes in the bone-marrow without any tenderness (Litten).

[Footnote 131: _Deutsches Archiv f. klin. Med._, xxvi.]

MORBID ANATOMY.--There may be extreme wasting. Dropsy of the feet is common, and ascites may be present.

A noteworthy feature is the full amount of blood in the heart and blood-vessels, usually in the form of large coagula. In one case (XI.) the weight of clots alone in the heart-chambers, not including what came from the veins, was 620 grammes. The portal, cerebral, pulmonary, and subcutaneous vessels were also greatly distended with clots. The portal vein just above the union of the branches measured eleven centimeters in circumference.

The blood is usually clotted in the heart and vessels, and the aggregation of the colorless corpuscles densely infiltrating the fibrinous clots and the serum gives a pus-like appearance, so that it has not infrequently happened, as in Virchow's memorable case, that the observer on opening the right auricle believed for the moment that he had cut into an abscess. The leukæmic clots often have a peculiar greenish color, and resemble somewhat the fat of the turtle. Similar coagula may fill the veins of the brain and abdominal viscera. The tendency of the white corpuscles to aggregate together, and the subsidence of the red to the lower part of the heart-chambers and vessels, may give an appearance of more intense leukæmia than actually exists. The reaction of the blood is usually acid. The chemical constitution has been carefully studied, but with no very satisfactory results. Hypoxanthine, lactic acid, leucin, tyrosin, a mucin-like body, and a gelatinous substance have been described, but none of them may be regarded as characteristic of the disease. The octahedral crystals are thought by some to be tyrosin,[132] but Schreiner[133] says they consist of the phosphate of an organic base, the composition of which is not yet settled.

[Footnote 132: Huber, _Archiv der Heilkunde_, Bd. xviii.]

[Footnote 133: _Liebig's Annalen_, cxciv.]

The specific gravity of the blood is lowered, 1036 to 1049. The water is increased. The fibrin in many observations has also been found increased; 4.8 per 1000 was the average of ten observations by Bennett. The albumen and the salts have not often been estimated. The former is stated to be diminished. The fatty bodies have been found in excess of the normal quantities.

The heart is often pushed up by the large spleen; the pericardium, more rarely the endocardium, may present ecchymoses, and the fluid may be in excess. In a few instances leukæmic growths have been met with. The chambers are usually distended, the walls soft, and a moderate grade of fatty change is very common. No special alteration has been met with in the blood-vessels. I have seen extensive fatty degeneration of the intima and small arteries.

In the great majority of cases the spleen is increased in size, but the shape is retained. It is usually of a deep violet-red color, and strong adhesions may unite it to the abdominal wall, diaphragm, or stomach. The capsule {916} may be greatly thickened, forming a firm fibro-cartilaginous investment. The vessels are enlarged, particularly the veins at the hilus. The weight may vary from two to eighteen pounds. The largest on record is given by Langley Browne[134]--18½ pounds. Six or seven pounds is an average weight. The length may vary from seven to twenty inches, and the breadth eight to twelve. The organ is in a condition of chronic hyperplasia--hard, firm, cuts with resistance, and displays a uniform reddish-brown surface on which the trabeculæ are more or less prominent. There may be hemorrhages or infarcts, and it is not uncommon to see regions of yellow or rusty-brown staining, indicating where an extravasation had occurred. As a rule, no trace of the Malpighian bodies can be seen. Grayish-white, circumscribed lymphoid tumors may occur throughout the organ, contrasting strongly with the reddish-brown matrix. The process of gradual enlargement is a simple hyperplasia. In the early stage, not often seen, there is swelling of the pulp, increase in the cell-elements, without the firmness and induration of the fully-developed leukæmic organ. Rupture may occur at this period from the intense hyperæmia. The Malpighian bodies are enlarged and prominent by their grayish-white color. A gradual and progressive induration results from the increase in the adenoid network and the fibrous trabeculæ. A section shows the enormous development of the fibrous elements. The cells may be scanty, only two or three in meshes, or, indeed, the reticulum may be so close that only a single cell is enclosed. As a rule, the hyperplasia extends over the whole organ, and the Malpighian bodies become involved and lose their distinctness. In only one of the cases which I have examined were they at all prominent. Leukæmic new growths in the spleen are rare.

[Footnote 134: _Lancet_, 1877, ii.]

Uncomplicated cases of the lymphatic form are very uncommon: usually they enlarge with the spleen, and in the majority of instances the hypertrophy is not extensive, scarcely ever reaching the high grade seen in Hodgkin's disease. The groups of cervical, axillary, mesenteric, and inguinal are most frequently affected; the bronchial and mediastinal but rarely. The bunches of glands are not usually larger than walnuts, moderately soft, isolated, movable; large matted groups do not often occur. They may vary a good deal in size during the course of the disease, often diminishing notably before death. In chronic cases they may become very indurated. The leukæmic lymphadenitis is a simple hyperplasia, and the soft glands may look, on section, of a normal gray color or may have a deep gray-red appearance. Hemorrhages may occur, and twice I have seen the enlarged glands deeply hyperæmic. Histologically, the appearance is very like a normal gland, only the lymph-spaces are more closely packed. In the harder glands the fibrous reticulum is much increased, the capsule thickened, and the section more grayish in color. Caseation or suppuration rarely occurs, and invasion of contiguous parts is most exceptional.

The tonsils and the lymph-follicles of the tongue, pharynx, and mouth have been found much enlarged.

The bone-marrow is usually the seat of important changes, which in some cases appear early and persist as very prominent features of the disease. The most constant alteration is a uniform substitution of a grayish-red or gray-green puriform-looking tissue for the normal red and fatty marrow of the long and short bones. The entire medulla may resemble the consistent matter which forms the core of an abscess, and the term pyoid applied to this condition by German authors well expresses the general characters. More rarely the marrow has a reddish-brown hue. The difference depends largely on the number of colorless corpuscles, which in the pyoid form are enormously increased, and there are but few red cells. Ponfick has met with dark-red, dense hemorrhagic infarctions in leukæmic marrow. The condition of the {917} bones is variable; usually, the compact and cancellated tissues appear normal, but the hard shell may be much thinned and expanded, the cancellæ widened, and the whole substance rendered spongy. In marked cases there may be localized swellings which are tender, and even yield, on firm pressure. The sternum and ribs are most frequently affected in this way. There are instances in which the bone-marrow has not been involved, and in one case there was osteo-sclerosis.[135] Histologically, the chief change is hyperplasia of the colorless marrow-cells, which in the pyoid variety compose the chief part of the tissue. They vary much in size and appearance. Three forms can usually be recognized: large granular cells with distinct nuclei; medium-sized cells, like colorless blood-corpuscles; and smaller forms, like lymph-cells, with large nuclei and a narrow zone of investing protoplasm. The red corpuscles and microcytes are in variable numbers. In one case the latter were very abundant. Nucleated red corpuscles are very constant elements. Corpuscles containing red blood-corpuscles are not so numerous as in ordinary red marrow, nor, as a rule, are the myeloplaques abundant. Charcot's crystals are always to be found--if not at first, when the marrow is quite fresh, certainly later, when decomposition has begun.

[Footnote 135: Heuck, _Virchow's Archiv_, lxxviii.]

The thymus is rarely affected, and even in children is not often swollen. A few cases of enlargement have been recorded.

The thyroid is even less frequently involved.

In one case the suprarenal capsules were large and swollen,[136] and in addition to the leukæmia there was bronzed skin. Hemorrhage, caseous degeneration, and in one instance rupture,[137] have been noted.

[Footnote 136: Barclay, _Lancet_, 1863, i.]

[Footnote 137: Fleischer and Penzoldt, _loc. cit._]

In the digestive system the stomach rarely presents any changes other than catarrhal. Even when death has occurred from hæmatemesis the mucous membrane may be pale, without erosion, hemorrhage, or ulceration (Cases II. and VI.). In a few instances lymphatic growths have been described. In many cases the intestines have been the seat of leukæmic tumors which have originated in the solitary and agminated glands of Peyer. Occasionally the lymphoid infiltration is diffuse in the mucosa and not confined to the follicles. Ulceration may occur in the patches, and in a few cases the bowel lesions have been so pronounced that the term intestinal leukæmia seemed justifiable.[138] The cæcum and colon may also present these new growths, and in a few cases dysenteric processes have been observed (Case II.). The peritoneum has been found covered with small lymphoid growths. In Willcocks' case of lymphatic leukæmia[139] there were growths on the surface of the stomach and gastro-splenic omentum. Blood may be found in the cavity from rupture of the spleen. Ascitic fluid is common. Fibroid thickening, induration, and adhesions are very often met with, particularly in the neighborhood of the spleen.

[Footnote 138: Behier, _loc. cit._]

[Footnote 139: _Loc. cit._]

The liver is very commonly enlarged, pale, smooth, and retains the normal shape. It may be greatly increased in size, as in case of Walshe's, where it weighed 13½ pounds. The substance is usually firm, of a grayish-brown color, or even marbled. Two chief changes have been met with--a diffuse leukæmic infiltration and numerous small leukæmic tumors. The infiltration may be very slight, and not noticeable with the naked eye, or it may be in the form of irregular scattered areas of a yellowish-white appearance, not distinctly isolated, but merging into the hepatic tissue. When moderate, a section shows the columns of liver-cells to be separated by wide spaces occupied by leucocytes, which are partly within and partly outside of the capillaries. The accumulation of these elements produces atrophy of the liver-cells, and their aggregation and increase in certain regions produce the grayish-white areas, in the midst of which traces of liver-tissue may be found. {918} The defined leukæmic growths are small, not often attaining a large size, and may resemble tubercles. They are usually situated in the interlobular tissue, and consist of lymphoid cells in a well-defined reticulum, and they possibly have a different origin from the diffuse infiltrations.

Fatty degeneration of the liver-cells is a very common change.

The respiratory system is not often the seat of important lesions. Lymphoid growths have been found in the mucous membrane of the trachea and bronchi, and occasionally in the lungs, in which situation they may closely resemble tubercles, but differ from them in not tending to caseate or soften. Oedema of the bases of the lung is almost always found. Many patients are carried off by a low pneumonia. The greenish leukæmic clots projecting from the cut ends of the vessels may give a very curious appearance to the section of the lung. The pleural surfaces may be the seat of lymphoid growths.

The kidneys are usually pale, often enlarged, and show signs of parenchymatous swelling. The capillaries, like those of the liver, may be distended with leucocytes, and leukæmic tumors may occur, generally situated in the cortex and ranging in size from a pea to a cherry. In none of the cases I have examined were there any special changes in these organs beyond slight enlargement and filling of the capillaries with leucocytes.

The generative organs are usually normal. No changes have been found to account for the persistent priapism met with in certain cases.

The meninges of the brain, the veins, and sinuses, are often filled with grayish clots. Occasionally meningitis has been found, with exudation of lymph. The small vessels of the brain may be plugged with leucocytes, forming thrombi, from which softening results. Cerebral hemorrhage may prove rapidly fatal. In Case X. of the Montreal series the patient died suddenly, and without any premonition, with a huge apoplexy of the ventricles and posterior part of the hemispheres.

Leukæmic growths in the skin have been described.

The leukæmic tumors demand further consideration. They are not common. In 10 of the 11 Montreal cases careful post-mortem examinations were made, and in not one were there definite new growths. In Case I. there was diffuse leukæmic infiltration of the liver, the histological characters of which were carefully studied. In the 157 cases collected by Gowers[140] there were only 13 instances of leukæmic nodules in the liver, and 10 in the kidneys. They are still more uncommon in the lungs. In the spleen--unlike this organ in Hodgkin's disease--they are very rarely seen. The nodules consist of leucocytes in a meshwork of delicate reticular tissue. Their mode of origin has been much discussed. There can be no doubt, I think, that they are new growths of lymphoid tissue of local origin. Possibly they start from accumulations of colorless corpuscles which pass out of the capillaries. In the infiltration of the liver one sees diffuse collections which resemble new growths, but which have evidently resulted from the aggregation in and outside of the capillaries of enormous numbers of leucocytes, which cause the atrophy of the cells of the organ. Doubtless, they multiply in loco by a process of fission, and these aggregations may themselves be foci for the origin and development of colorless cells which pass into the blood-current and augment the number.[141] Quite recently Bizzozero has studied the development of these leukæmic new growths, and has shown clearly that the cells which compose them are in process of active fission.

[Footnote 140: _Loc. cit._]

[Footnote 141: "On the Histology of Leucocythæmia," _Canada Medical and Surgical Journal_, 1876.]

The COURSE OF THE DISEASE is slow and chronic, a matter of months and years. There are exceptional instances in which the disease has proved fatal in a few weeks; this occurs sometimes in children,[142] but acute leukæmia is {919} very rare. In a table of 63 cases collected by Gowers, in which the date of the first symptoms was fixed with tolerable accuracy, the duration was less than one year in 13 cases; from one to two years in 16; from two to three years in 19; from three to four years in 9; from 4 to 5 years in 3; and five years and upward in 3 cases. The course is rarely uniform, but periods of improvement occur in which the fever subsides, the painful sensations in the abdomen diminish, the appetite improves, and the spleen reduces in volume. Such intervals, corresponding to the administration of certain drugs, are apt to lead to therapeutic errors. A patient may sometimes get about for months, and even attend to a light business, with an enormous spleen and a ratio of white to red corpuscles of 1 to 6 (Case VIII.). Hemorrhages, high fever, profuse diarrhoea, and the occurrence of dropsy shorten the course. Toward the close there is great muscular debility, and usually a wandering delirium.

[Footnote 142: Golitzinsky, _Jahrb. f. Kinderheilkunde_, 1860-61.]

In the majority of cases death is by asthenia--a gradually progressive weakness and ultimate failure of the heart. Diarrhoea and hemorrhage hasten the fatal result. A profuse hemorrhage may cut off a patient early or after the disease is well established. Cerebral hemorrhage was noticed in 6 of 60 cases in which Gowers was able to ascertain accurately the cause of death. A few are carried off by pleurisy or pneumonia or peritonitis after tapping.

Pyæmia and rupture of the spleen are mentioned as causes of death in some cases.

The DIAGNOSIS of leukæmia rests upon the determination of a great and persistent increase in the colorless elements of the blood. Cases of Hodgkin's disease and of splenic anæmia, almost identical in general features, can only be distinguished by an examination of the blood. I should say that in any case we can speak of the blood as leukæmia when the ratio of white to red cells falls below 1 to 50. Some writers hold that to determine leukæmia the ratio should be at least 1 to 20, but when the study of the variations in the proportion of the corpuscles in any case extends over weeks or months, we not uncommonly find that the ratio, which, at one observation may be 1 to 8, or 1 to 10, a week later may be 1 to 60 or 80, or even 150. Indeed, the state of the blood is a variable factor, and too close attention to it has diverted our minds from the broad features which this disease has in common with others. For practical clinical purposes we have to distinguish ordinary lieno-lymphatic leukæmia from--(1st) chronic malarial infection with splenic hypertrophy; (2d) from cases of non-malarial splenic enlargements with anæmia; (3d) from general lymphadenoma or Hodgkin's disease. The history in malarial cachexia, the absence of lymphatic enlargement, and the blood-condition will usually be sufficient for purposes of a diagnosis. Great increase in the white blood-corpuscles is not often seen in the chronic splenic tumor of malaria; indeed they may be much diminished in number. Toward the end in very chronic cases the clinical picture may be very similar: the large abdomen, possibly ascites, dropsy of the feet, and irregular fever may resemble closely splenic leukæmia, and the absence of an increase in the colorless corpuscles may be the only marked difference. From anæmia splenica there is still greater difficulty, and I have seen instances in which the absence of an excess of the colorless corpuscles in the blood formed the sole criterion: the hemorrhages, the dropsy of feet and abdomen, retinal extravasations, the general cachexia, and the fever were identical with those of leukæmia. Still greater may be the difficulty of separating certain cases of lymphatic leukæmia from general lymphadenoma or Hodgkin's disease; but in the latter affection the glandular enlargement is usually greater and altogether a more prominent feature, and the spleen is not so often increased in size. There may, however, be a considerable increase in the number of the white corpuscles, 1 to 150 or 1 to 100 red, and cases do occur which appear intermediate {920} or transitional in character, and upon which judgment must be reserved until the progress of the case decides the question.

Pure cases of myelogenous leukæmia are almost unknown; if the osseous symptoms are not marked the course is very like that of pernicious anæmia. Indeed, there are two interesting cases on record in which the progressive anæmia seemed to pass into leukæmia. In Litten's case[143] the patient presented the symptoms of profound anæmia, and five days before death the blood became markedly leukæmic. There was no enlargement of spleen or lymph-glands, but the bone-marrow was intensely leukæmic--_i.e._ of the pyoid form. In the case reported by Leube and Fleischer[144] the patient, aged thirty, four months after her confinement became anæmic and the left leg was swollen. Though at first only anæmic, subsequently the ratio of white to red corpuscles rose to 1 in 10. Gangrene of the leg supervened, necessitating amputation, from the effects of which she died. There was no affection of spleen or lymph-glands, but the marrow was of the red lymphoid variety. A gastric ulcer was also present. This was no doubt a case of post-partum anæmia aggravated by the presence of ulcer of the stomach, and the great interest of the case lies in the transition of the anæmia into leukæmia.

[Footnote 143: _Berliner klin. Wochenschrift_, 1877.]

[Footnote 144: _Virchow's Archiv_, lxxxiii.]

There are certain general conditions, accompanied by an increase in the colorless corpuscles, which must be distinguished from leukæmia. In suppuration there may be marked leucocytosis; so also in cancer and protracted cachectic states, as phthisis. In cases with large cancerous masses about the stomach and omentum, or where, as occasionally happens in chronic phthisis, there is a greatly enlarged amyloid spleen, if the white blood-corpuscles are much increased, care may be necessary to escape a mistake in diagnosis. In diphtheria the colorless elements may be much increased. Bouchat says that in some instances there may be an acute leukæmia.[145] In puerperal fever also the condition of leucocytosis is not uncommon.

[Footnote 145: _Gazette des Hôpitaux_, 1877.]

The PROGNOSIS is in the highest degree unfavorable, and in those cases, few, indeed, in number, in which there were symptoms like leukæmia and which disappeared under treatment, the doubt remains whether they were true examples of the disease. When once established, the spleen and glands enlarged, the hemorrhages and dropsies present, and the blood condition marked, death is the only termination to be expected. Specially unfavorable signs are a tendency to hemorrhage, persistent diarrhoea, early dropsy, rapid increase in the splenic tumor, great excess of colorless corpuscles, and high fever. Temporary improvement may occur for weeks or even months, and the white blood-corpuscles reduce in number, but such breaks are usually transient.

TREATMENT.--If, as some writers hold, chronic malarial poisoning is an important factor in the induction of leukæmia, we should take special pains with patients so affected, and endeavor by the use of quinine and arsenic to free the system and reduce the volume of the spleen. There certainly may be danger of the development of leukæmia in any case of chronic splenic tumor, though my own experience has been that in these cases the production of anæmia of high grade, without increase in the white blood-corpuscles, is more common. It is a mistake to suppose that anæmia always accompanies chronic splenic enlargement: it may persist for years with a percentage of red corpuscles little if at all below normal, but grave anæmia or leukæmia are probabilities to be dreaded.

In an early stage, when the spleen is moderately enlarged, the lymph-glands scarcely swollen, and the leucocytosis not intense, there is a hope that by the persistent use of quinine, iron, and arsenic a cure may be effected; but when the disease is fully established and the leukæmia marked, a recovery {921} is rarely if ever witnessed, and the treatment is largely palliative and symptomatic. To reduce the volume of the spleen various remedies are recommended, and so long as the organ is only moderately enlarged and hardened some of them may be beneficial. Quinine should be given a full and prolonged trial, as undoubtedly under its use the organ may reduce in size. As anæmia is almost always present, iron may be administered at the same time. That the quinine has any special influence over the production of the white corpuscles, as some think, I have not been able to satisfy myself. To be of use, it must be employed early and in large doses. Ergotin internally and by injection into the spleen has been recommended. I have not seen any permanent benefit from its use. Local measures, such as inunction of biniodide of mercury ointment over the spleen, the interrupted voltaic current, the application of cold, either ice or the cold douche, may be employed. Moderate reduction in the volume may be effected by these means--most effectually by the electricity and mercurial inunction.

Arsenic should always be given a trial, and pushed for several months in increasing doses. Several cases are reported in which the improvement lasted for many months. Direct injections into the spleen are also of service. Phosphorus, from which much was expected after the favorable reports of Broadbent and Wilson Fox, has not proved of much value. There are very curious remissions in the course of the disease which render therapeutical deductions somewhat fallacious. I have seen the most marked improvement occur without any special treatment: ascites and dyspnoea disappear, the white corpuscles decrease in number, and the patient from a bed-ridden, wretched condition get up, attend to light duties, and walk half a mile to hospital (Case IX.). In Case VIII. there were also during eighteen months remarkable variations, depending more on the state of the gastro-intestinal canal than the blood condition.

Transfusion has proved useless. Leukæmic blood to the amount of several ounces has been withdrawn and other healthy blood substituted.

Excision of the spleen has been frequently practised in leukæmia. Collier[146] gives a résumé of 16 cases, and concludes that it is a useless and unjustifiable operation, as all of them proved fatal. A successful case, however, is reported from Italy. If performed early, there is a possibility of success, but when the organ is enormously enlarged and the blood intensely leukæmic, the conditions are most unfavorable.

[Footnote 146: _Lancet_, 1882, i.]

Gastric symptoms and diarrhoea call for careful treatment, as the comfort of the patient depends largely on the condition of the primæ viæ. Hemorrhage is frequent, and is a dangerous symptom, particularly when it depends upon engorgement of the portal system, and calls for appropriate remedies. Purgatives are to be employed with caution. The dragging pain in the left hypochondrium, and the sense of weight and distension after eating, are very distressing, and the splenic pain may require sedatives. Inhalations of oxygen relieve the dyspnoea and have been found to check the progress of the disease.

HODGKIN'S DISEASE.

DEFINITION.--A disease characterized by progressive hyperplasia of the lymph-glands, sometimes also of the spleen, with anæmia and the development of secondary lymphatic growths in various parts of the body.

SYNONYMS.--Pseudo-leukæmia; General lymphadenoma; Malignant {922} lymphoma (Billroth); Lympho-sarcoma (Virchow); Adénie (Trousseau); Desmoid carcinoma (Wagner); Anæmia lymphatica (Wilks); Lymphatic cachexia (Mursick); Adenoid disease (Southey).

HISTORY.--Morgagni and other writers mention cases of enlargement of the lymph-glands proving fatal, but Hodgkin of Guy's Hospital first called special attention to the subject in a paper before the Medico-chirurgical Society of London,[147] entitled "On Some Morbid Appearances of the Absorbent Glands and Spleen." Some of the cases then described were undoubtedly examples of scrofulous glands, but four at least were instances of the disease which now bears his name; and at the meeting of the London Pathological Society in 1878, when a discussion on lymphatic disease took place, Wilks exhibited the original specimens collected by Hodgkin. Other cases were recorded in England by several observers, and in 1856, Wilks[148] reported several examples of enlarged lymph-glands with growths in the spleen associated with anæmia, but without any leukæmia; and again in 1865 this observer published additional cases,[149] and gave the name of Hodgkin's disease to the affection characterized by enlargement of the lymph-glands, growths in the spleen and other organs, and anæmia. The cases and discussions contained in the _Transactions_ of the Pathological Society of London and Gowers' exhaustive article in _Reynolds's System of Medicine_ embrace the most valuable of the English contributions. In Germany, Virchow described the cases under the term lympho-sarcoma, and in his work on tumors gave a full account of the histology. Billroth gave the term malignant lymphoma to these growths to distinguish them from local non-infective lympho-sarcomas. Cohnheim and Wunderlich used the term pseudo-leukæmia to express the distinction between these cases and leukæmic enlargements.

[Footnote 147: _Transactions_, vol. xvii., 1832.]

[Footnote 148: _Guy's Hospital Reports_, 3d Series, vol. ii.]

[Footnote 149: _Ibid._, vol. ix.]

In France, Trousseau described it under the term adénie, and Ranvier used the term lymph-adénie. In America many cases have been described, and one of the first and fullest analyses of recorded observations is by J. H. Hutchinson in the _Transactions_ of the College of Physicians of Philadelphia, Series 3, vol. i.

ETIOLOGY.--No satisfactory etiological relations have been determined in the disease.

Age has an important predisposing influence. The majority of the cases are young persons. In Gowers' table of 100 cases, 30 were under twenty years, 34 between twenty and forty, and 36 above forty. Most of the cases I have seen have been in young adults.

Sex has a still more marked influence; at least three-fourths of all cases are in males, the proportion being considerably higher than in leukæmia--75 per cent. in Gowers' tables, and 40 out of 58 in Hutchinson's tables.[150]

[Footnote 150: _Loc. cit._]

Heredity has in a few instances been adduced as a possible cause, but not, I think, on very reliable grounds. In two cases (II. and III.[151]) the patients were each a twin. It might be supposed that members of tuberculous families, or those who had suffered from scrofulous enlargements when young, would be more liable to the disease, but the cases in which such connection can be traced are very few in number.

[Footnote 151: These figures refer to cases of which I have notes.]

Antecedent syphilis has been noted in a few instances.

Exposure, intemperance, bad food, etc. are possible predisposing causes.

Local irritation, which so often produces lymphatic swellings, appears to stand occasionally in causal connection with the development of general lymphadenoma. Trousseau lays particular stress upon this, and gives instances in which chronic irritation of the skin, otorrhoea, chronic nasal or pharyngeal catarrh, irritation of a decayed tooth, gave rise to local gland swelling which preceded the general development of the disease. But this {923} is a comparatively rare affection, and think of the hundreds of instances met with of local lymphatic irritation!

SYMPTOMS.--Enlargement of the lymphatic glands in the neck, axillæ, or groins is the earliest symptom noticeable in the great majority of cases. This may be quite painless at first, and the patient seeks advice on account of the disfigurement or the inconvenience felt in adjusting the collar. Occasionally the anæmic and constitutional symptoms first attract attention. When the trouble begins in the deeper groups--bronchial, mesenteric, or retro-peritoneal--pressure effects are the first complaint, and there may be great obscurity and uncertainty about the nature of the case. Thus, the first symptom may be dyspnoea, with pain in the chest, or pain in the abdomen with swelling of the legs and shooting pains in the course of the nerves; or in rare cases symptoms of a totally different nature may be among the first to attract attention. Thus in J. H. Hutchinson's case there was paraplegia from pressure of a secondary growth, and the same was observed in a case which I dissected at the Montreal General Hospital (Case VI.). But such are very exceptional, and in the great majority swelling of the superficial glands is the earliest phenomenon. In rare instances the tonsils and pharyngeal adenoid tissue have been first affected.

Hemorrhage is not an early symptom. Epistaxis has been noted, but not with the frequency with which it occurs in leukæmia.

With the progressive enlargement of the glands the patient becomes anæmic, and finally cachexia is developed.

The Lymphatic System.--In an early stage it is difficult or impossible to distinguish the affection from syphilitic or scrofulous adenitis. The gradual increase in the size and the involvement of other groups, and the oncoming anæmia, will alone in certain cases render a decision possible. In the cervical group, in which the trouble usually begins, the chain of glands on one side becomes enlarged--perhaps only those just above the clavicle, or in some instances the posterior ones are also affected. They are isolated, movable, and not, as a rule, tender. Months, or even years (three years, Case VII.), may elapse before the enlargement becomes general or affects the other side. With their increase in size and number the separation between the glands, at first evident, disappears, and they form distinct groups or bunches. Thus the submaxillary set, those of the anterior triangle, and those of the posterior may form irregular aggregations of various sizes. Ultimately, huge tumors may develop which obliterate the neck, extending upon the shoulders and over the clavicles and sternum. When these grow inward, toward the trachea, great dyspnoea may be produced, and the pressure may be so extreme that tracheotomy must be performed.

The skin becomes involved, and ulcerates. Usually it is freely movable over the masses. The pharynx and oesophagus may be compressed, and occasionally the carotids. The submaxillary tumors may limit the movement of the jaws.

Next to the cervical, the axillary glands are most frequently involved. If small, no inconvenience is felt, but when large bunches occur there is great pain in moving the arms, and pressure upon the brachial or axillary veins may cause swelling of the limbs. The tumors may pass far out, almost to the nipple.

The inguinal glands are not so often involved. In only one of the ten cases which I have seen were they affected, but they may form large and even pendulous tumors, as well shown in the cases of Surgeon-Major Porter.[152]

[Footnote 152: Figured in _Path. Soc. Trans._, xxix.]

Of the internal glands, those of the thoracic cavity are most often attacked. The chain in the posterior mediastinum may be involved and surround the aorta or compress the gullet; or they may pass up the trachea to the {924} neck, and involve the thyroid (Case V.). When the bronchial group is enlarged there are signs of pressure on the tubes, dyspnoeal attacks, and serious implication of the lung (Case VI.) In the mediastinum there may be large masses covering the aorta, extending over the pericardium, and producing bulging of the sternum and ribs, perhaps pulsation, and ultimately erosion of the bones and outward projection of the tumors (Cases II. and III.). There may be considerable pressure upon the veins and obstruction to the flow in the superior cava and jugulars.

In the abdomen the mesenteric glands are often affected, and if the belly-walls are thin can be readily felt. The continuous chain of retro-peritoneal glands may be greatly enlarged, and extend from the diaphragm into the pelvis, surrounding the aorta, cava, and nerves. When the patient is thin there may be no difficulty in detecting these, but when there is an enormously thick panniculus the diagnosis may be impossible, as in Case I., in which intense lumbar and sacral pain and swelling of the legs were the only symptoms. The matting of organs in the pelvis caused by these growths may be a source of great difficulty in the diagnosis, as in a case in which I saw an eminent and careful surgeon open the abdomen to extirpate a uterus for fibroids, and found general lympho-sarcoma of the retro-peritoneal and pelvic glands.

It is probably in connection with affection of the abdominal glands that the bronzing of the skin occurs which is mentioned in a few instances. It was well marked in Case IV. of my series.

The glands present great variations in the rate of growth and there may be fluctuations from month to month. They may diminish rapidly, and almost disappear from a region to develop again in a few weeks. The enlargements may diminish very much before death.

The spleen does not present the almost constant enlargement of leukæmia, and in the majority of cases cannot be felt below the ribs. Moderate hyperplasia is common, but I have never seen the large splenic tumor. In some instances it has been found extending into the umbilical region, and if there are secondary lymphoid growths the surface may be very irregular.

The thyroid may be enlarged; it was so in Cases II. and IV., and in Case V. the growth in the glands of the neck involved the right lobe.

The thymus has also been found affected; indeed, the disease may, according to Virchow, sometimes begin in the gland.

Blood and Circulation.--The blood presents the characters of anæmia, and as a rule the more advanced the glandular trouble the greater the impoverishment. The red corpuscles are reduced in numbers one-half or even three-fourths, but never, in my experience, to the extent in pernicious anæmia. The lowest number per cubic millimeter which I have counted was in Case II., when on one occasion the numbers sank to 2,100,000 per c.m. There may be most advanced disease without great anæmia. In one case (IV.) with enormous enlargement of the cervical and axillary gland there were 4,250,000 to the c.m., and during his three weeks' stay in the hospital the numbers were never much reduced. So also in Case III. there was not profound anæmia to within two months of the patient's death.

The red corpuscles are usually uniform in size. I have never seen extreme poikilocytosis, though occasionally the microcytes have been numerous. The colorless corpuscles are not greatly increased, although there may be moderate leucocytosis, as in Case IV., in which the ratio of white to red kept about 1:150. A condition of actual leukæmia may be induced. The corpuscles may be smaller than usual, and present the characters of the blood in lymphatic leukæmia. I have not met with nucleated red corpuscles in any of the cases which I have examined.

The granule-masses of Schultze are in variable numbers.

{925} Cardiac weakness and palpitation are common, due chiefly to the anæmia. The mediastinal growths in some cases cause great embarrassment from pressure. Fatty heart-muscle is an almost constant sequence of the anæmia. The pulse is quickened--80-110, or, if much fever, 120-130. Hæmic murmurs may be heard at the base of the heart, and the venous hum at the root of the neck is often very distinct. Pressure of the tumors upon the nerves may influence the heart's action, and in one case in which sudden death took place it may have been due to interference with the innervation of the heart by pressure on the nerve-trunks.

Respiratory System.--Shortness of breath from the anæmia is common, particularly on exertion. When the tracheal and bronchial glands are affected urgent attacks of dyspnoea may occur and suffocation be induced. Pressure on the pneumogastric or recurrent laryngeal may cause hoarseness or aphonia. The gland-tumors may invade the lung, or there may be secondary growths. These are not usually large enough to induce symptoms. The shortness of breath may be caused by pleuritic effusion, which may be an early symptom and the one for which the patient is sent to hospital (Case X.). It is due to pressure on the azygos and intercostal veins.

Fever is observed in nearly all cases; even in the early stages slight elevation of temperature may be noted. When the disease is firmly established the fever is a marked feature. It may be of an irregular hectic type, with morning remissions--this is, I think, the most common--or it may be continuous, with an evening exacerbation. More rarely there are ague-like paroxysms, with rigor, hot and sweating stage (Case I.), and during these the fever may rise to 104° and glands may become more swollen. The range is never very great, rarely exceeding 103°.

Digestive System.--Difficulty in swallowing may result from the enlargement of the lymph-follicles at the base of the lungs and of the tonsils and pharyngeal adenoid tissue. This may be so great as to necessitate feeding with a tube. There may be early gastric trouble when the mesenteric and abdominal glands are first affected--dyspepsia, nausea, and vomiting. Secondary tumors of the stomach are not common. The loss of appetite and feeble digestion, prominent symptoms in so many cases, are largely due to the anæmia.

Diarrhoea is not met with so frequently as in leukæmia; it may come on toward the close and carry off the patient. New growths in the intestine may produce severe attacks and sometimes hemorrhage. Obstinate constipation may be the result of pressure.

The liver is rarely enlarged, and there are not often hepatic symptoms. The new growths do not produce irregularity in the enlargement. Pressure of enlarged glands at the hilus may cause jaundice and ascites.

Genito-urinary System.--The urine is usually clear and presents no striking changes. Reaction acid; albumen may be present. The testicles may be the seat of secondary growths.

Nervous System.--Headache, giddiness, and noises in the ear are common, and are dependent upon the anæmic state. Southey[153] has noticed delirium and coma in some cases.

[Footnote 153: _Barth. Hospital Reports_, vol. ix.]

Special Senses.--Deafness is not uncommon, caused by pressure of the large glands in the neck or by the growth of adenoid tissue about the pharynx, closing the Eustachian tube. Inequality of the pupils has been noted, from pressure of a gland on the sympathetic. Retinal hemorrhages are uncommon.

Skin.--There may be definite secondary lymphatic tumors apart from direct infiltration by continuity.[154] Bronzing may occur (Case IV.). Papular rashes may be very troublesome. Subcutaneous oedema of feet and eyelids may occur when the anæmia is very profound.

[Footnote 154: Greenfield, _Path. Soc._, xxvii.]

{926} MORBID ANATOMY.--The Lymph-glands.--Virchow made the division into the hard and soft varieties, the difference depending on the proportion between the cells and the adenoid reticulum. Where the cells predominate the growth is soft--may be semi-fluctuating--but when the stroma is much hypertrophied the glands are hard, firm, and feel like organs in a state of chronic induration. The great majority of the cases are of the soft variety. When first affected the glands may be hard, and as the development proceeds become less consistent; but there are cases in which they maintain their firmness and solidity throughout.

When examined in the early stage the individual glands are more or less isolated, perhaps not larger than almonds or walnuts, adherent by their capsules, but readily separated and movable. Even when death has been caused, some groups may generally be found in this state, as it is rare for all to be equally developed. When advanced, the glands fuse together, distinction is lost between them, and the bunch may form a large tumor the size of an orange or even a cocoanut. When of moderate size the section may show normal-looking gland-substance, and the distinction between cortical and medullary portions may be well preserved. When much enlarged the section has usually a grayish-white appearance, smooth, and of variable consistence, either firm and dry or soft and juicy. The vascularity is not often marked, and extravasation and areas of congestion are not seen so frequently as in some actively-growing neoplasms of the lymph-glands.

The capsules are thinned, and may disappear in the fusion of contiguous glands, traces being seen on the section as strands of connective tissue. About large groups the capsular tissues may be much condensed, forming a very firm investment. The growth may perforate the capsule and invade contiguous parts--muscle, skin, or the solid organs.

The chief changes which the tumors may undergo are fibroid induration, suppuration, and caseation. The gradual increase of the stroma may give a high degree of density, and the gland on section may present a smooth, glistening appearance. Suppuration is most frequently seen when the growth reaches the skin; it may point and an abscess discharge. In the deep glands the formation of pus is not often met with. Caseation is extremely rare. Hemorrhages may take place from rupture of the thin-walled vessels.

The chief characters of the lesions in the different groups have been dealt with in the section on Symptoms. The superficial glands are most often attacked, and the cervical or axillary may form huge masses before there are any signs of internal trouble. The superficial and deep cervical groups may be uniformly affected, the muscles lifted and wasted, and vessels and trachea surrounded by a solid mass. Sometimes all distinction between the tissues is lost, and the carotids run in the midst of the new growth, which may extend far out beneath the trapezius and down into the chest or over the clavicle on to the outside. When the neck is not primarily affected the groups are more isolated, and can be traced as chains of enlarged glands along the trachea and the carotids continuous with those of the axillæ and mediastinum.

The axillary group is next involved in the order of frequency, and the masses when large grow out under the pectorals and back beneath the scapulæ and high into the fossa, compressing the axillary vessels and causing great swelling of the arm. In Case VII. the growth infiltrated the neighboring muscles and eroded the humerus and neck of the scapula, perforated the blade, and exuded on its outer surface. Though an enormous mass, the vessels were not infiltrated, and only moderately compressed. The inguinal glands when very large may obstruct the femoral artery and vein, and seriously interfere with the circulation in the legs.

{927} Of the internal groups, those of the thorax are most often affected, and we may have the chain in the posterior mediastinum along the aorta and the sides of the trachea and gullet, and along them pass into the neck (Case V.), or the bronchial group may be primarily attacked, with the formation of a great bunch at the fork and numerous small masses along each bronchus at the root of the lung, which may be extensively involved (Case VI.); or those of the anterior mediastinum beneath the sternum may be affected, with the production of large masses extending over the pericardium and passing even to the diaphragm. In these cases bulging of the sternum and ribs, with erosion and perforation, may occur. In Case II. the sternum was completely destroyed to a level with the fourth rib. The heart may be pushed aside and the aorta and its branches completely surrounded by growths (Cases II. and VI.). It is remarkable in these cases that great vessels do not suffer more from compression. When the abdominal glands are involved, the retro-peritoneal are most frequently enlarged, and form a continuous chain from the diaphragm to the internal rings on either side of the aorta and its branches, extending into the pelvis. Pressure effects are not common, but they may compress the ureter, causing hydronephrosis, the sacral and lumbar nerves, the iliac veins, and, as in the case I mentioned, may adhere to the broad ligaments and uterus in such a way as to deceive the most skilled gynæcologist. The mesenteric glands may present slight enlargement, but in my experience they are but little affected, even when the retro-peritoneal are of large size. When the glands at the portal fissure are involved they may compress the vein and duct. Phelps of Chateaugay, N.Y., sent me a specimen in which the glands of this region formed two huge masses the size of cocoanuts, and, so far as I could ascertain, they were primary lympho-adenomatous growths. The possibility of ovarian disease had been discussed by several consultants.

The chief change is an increase of the cells with or without thickening of the reticulum. The cells correspond to ordinary lymph-corpuscles; some may be a little larger, with darker granules and more pronounced nuclei. Giant cells are frequently met with, more often in the small glands. I have not seen them in the large soft tumors. In the early stage there may be simple hyperplasia and the relations of the lymph-paths are maintained, but when the glands are much developed the normal arrangement is disturbed and they cannot be injected. The reticulum varies much; in the very soft form it is expanded and can scarcely be found; the substance may be semi-diffluent. The firmer the structure the more evident is it, and in the hard forms the network of fibres in whose meshes the cells are enclosed can be distinctly seen and by pencilling very clearly brought out. It is not merely a thickening of pre-existing fibres, but probably there is a new development of adenoid tissue. In some cases of advanced fibroid change very few cells can be seen. The vessels passing to the glands are sometimes dilated.

Spleen.--In about 75 per cent. this organ is hypertrophied or presents lymphoid growths (Gowers). The enlargement is not often great, rarely approximating the colossal size of the leukæmic organ. It is due to either simple hyperplasia or to the presence of the new growths, sometimes to both. In the 75 cases of enlarged spleen new growths occurred in 56 (Gowers). Of the 38 cases in Hutchinson's table, 27 presented the splenic tumors. These are grayish-white bodies, ranging in size from a small pea to a walnut or larger, scattered irregularly through the substance, usually rounded in outline, but in some instances irregularly shaped. They contrast by color strongly with the red spleen-pulp. The numbers may vary from one or two to many dozens, the spleen-substance being a mere remnant between them. These masses often resemble the lymph-glands in appearance and consistence. {928} They are not encapsulated, but in immediate contact with the spleen-tissue. They originate from the Malpighian corpuscles, and may be regarded as the enlarged and developed lymph-elements in the spleen. The larger ones probably arise from the fusion of several small ones. When uniform in size and scattered throughout the organ, they may resemble coarse tubercles, but the absence of any caseation may serve to distinguish them. Their histological characters are those of the glands, lymph-corpuscles in a fibrous reticulum; the consistence depends on the preponderating element.

Amyloid degeneration was found by Gowers in two cases in the growths.

The thymus has been found involved in the mediastinal growths, and is occasionally affected primarily. The thyroid may be attacked by the cervical tumors.

The suprarenals may contain secondary growths. In Case VII. both were extensively involved.

The medulla of the long bones has been found converted into red lymphoid marrow, and in a few instances into the pyoid variety met with in leukæmia. It has been found normal in other cases.

Digestive System.--In the mouth and pharynx the lymphatic elements are very commonly affected when the cervical glands are enlarged, sometimes independently. The tonsils may form large masses, and with the follicles at the root of the tongue and at the pharynx produce great obstruction. Sloughing may occur. In the gullet and stomach secondary tumors have occasionally been seen. In Case VII. there was a flat elevated mass at the cardia beginning to ulcerate.

The small intestines may be extensively involved; the glands of Peyer enlarged and even ulcerated. In Case VII. there were over twenty ulcers in the jejunum and ileum, ranging in size from a split pea to a bean, edges elevated and indurated and the bases sloughing. The large intestines may be secondarily affected, the intertubular adenoid tissue be greatly developed and compress the crypts of Lieberkühn, and lead to thickening of the mucosa.

The liver is often enlarged, and presents scattered lymphoid tumors, rarely larger than a pea, of a white or yellow-white color, and may be readily mistaken for tubercles. They are most common beneath the capsule and in the interlobular tissue. A diffuse interacinous growth may also occur. Cirrhosis has been observed in the vicinity of the growths, and fatty degeneration.

The pancreas may be the seat of secondary masses.

Genito-urinary System.--The kidneys are very often the seat of new growths, usually small and of a character similar to those in the spleen and liver. When the disease is very rapid the tumors may be large and very vascular. The texture of the kidney is usually soft, and parenchymatous change is common. The testicles may also be the seat of adenoid growths; this was the case in one of Hodgkin's patients.

The Respiratory System.--Growths in the trachea are rare. The lungs are frequently affected, either by the direct invasion at the root from the bronchial glands (Case V.), or by numerous scattered nodules through the substance. They develop about the bronchi, and may reach the size of marbles. Intense bronchitis, oedema, and congestion may be secondary changes induced by pressure on the bronchi or trachea.

The serous membranes occasionally present lymphoid growths. Pleural effusion is not uncommon.

The heart presents no very constant changes. When the anæmia is profound it may be very fatty. It may be compressed by mediastinal growths, and has been found much atrophied. Lymphoid growths may occur in it.

The Nervous System.--The brain itself is rarely affected, but growths have been found in the dura mater. In Case VI. a secondary mass compressed the spinal cord, as in Hutchinson's case, producing paraplegia.

{929} The skin may be the seat of adenoid growths, as in Greenfield's case.[155] The growing tumors may involve it (Case IV.), and ulceration may occur.

[Footnote 155: _Loc. cit._]

COURSE, DURATION, AND TERMINATION.--Trousseau and other French writers have divided the disease into different stages--the latent and period of early development, the period of generalization, and the cachectic state; but the course of the disease is very variable, and depends much upon the position of the glandular enlargements, the rapidity of development of secondary growths, and also the constitutional peculiarities of the patient. Early and rapid growth in the mediastinal groups may produce pressure effects, and cause death before any marked anæmia--much less cachexia or the development of secondary masses in important organs, as the cord, may prove quickly fatal. In some cases the glandular enlargement rapidly spreads, and group after group is involved in the space of a few months; in others there may be hyperplasia of a single set, as the cervical on one side, for months, or even years, before the glands on the other side or in other regions become involved. The most acute cases may run a course in three or four months, the most chronic in as many years. Periods of quiescence are not uncommon, and the tumors may not only cease to grow, but actually diminish, or even disappear in a region, and this without any special treatment.

The mode of death is commonly by asthenia; cachexia is gradually developed, the anæmia becomes more profound, and finally, with local or even general dropsy, the end comes from heart failure. Very frequently the patient is cut off before grave constitutional disturbance is established, particularly by asphyxia from the pressure of enlarged glands on the trachea and bronchi or occlusion of the pharynx. Hemorrhage and diarrhoea, such common symptoms in leukæmia, are rarely seen. Coma has been the cause of death in a few cases. Oedema of the lungs, pneumonia, extensive pleuritic effusions, may hasten, and in some instances cause, the fatal result.

The DIAGNOSIS is in most cases easy; in others time alone will decide the true nature of the glandular enlargement. Of the chronic forms of adenitis which are liable to be confounded, the scrofulous is the most common. The points to be attended to in the diagnosis are--the age; scrofulous glands affecting chiefly the young and individuals presenting other signs of the so-called scrofulous habit, or there may be a well-marked family history of phthisis. In the question of age, however, it is to be remembered that there is a condition known as adult or senile scrofula, in which there may be general enlargement of the glands. Of all groups the cervical are most frequently involved in scrofula, and the submaxillary set more often than those of the anterior and posterior triangles, while in Hodgkin's disease the latter are usually affected first. The enlargement in scrofula is rapid at first, and may last for years in a group without extending; the bunches are often, even when small, welded together, and, most important of all, they tend to suppurate--a feature scarcely ever seen in true lymphadenosis. Size is an uncertain criterion. I have seen masses of scrofulous glands in the neck as large as two fists and without suppuration. A single large bunch in the neck, particularly if submaxillary, persisting for over a year or eighteen months without involvement, however slight, of the glands in the same or the opposite side or in the axillæ, is almost certainly not malignant lymphoma. On the other hand, a group of slowly-enlarging glands in the anterior cervical triangle, with gradual affection of those of the opposite side of the axillæ, particularly if in a person between twenty and thirty and becoming anæmic, would render the suspicion of Hodgkin's disease strongly probable.

In connection with this it may be mentioned that occasionally in acute {930} phthisis there may be great swelling of the glands, from a growth of miliary tubercles in them. A case of the kind was admitted into my wards in the General Hospital, Montreal: a man aged twenty-four, with great swelling of the cervical glands in both sides, tonsillitis, and sloughing pharyngitis, irregular fever, and diarrhoea, and for a time the case was believed to be one of Hodgkin's disease.

PATHOLOGY.--Local benign lymphomata occur, identical in histological characters with the tumors of Hodgkin's disease, and differing only in the absence of any tendency to extend in the neighborhood or to generalize. They are not uncommon about the neck, may grow slowly, and last for years.

The lymphatic growths of leukæmia are not in any essential particular different from those of Hodgkin's disease, and the diagnosis rests upon the examination of the blood. There are, however, certain broad differences when any considerable number of cases of the two diseases are compared. Thus the lymphatic element in leukæmia is less pronounced, the splenic and medullary forms predominate; in Hodgkin's disease exactly the reverse prevails. It is rare in leukæmia for the internal glands to be much involved, and patients do not often die from the pressure effects of the tumors. The hemorrhages so common in leukæmia, and the diarrhoea, are rare symptoms. The bone-marrow is more generally affected, and, lastly, the tendency to generalize seems greater in the growths of Hodgkin's disease.

From other forms of malignant growths in the lymph-glands there may be difficulty in the diagnosis, and even a microscopical examination may not serve to make the distinction.

Thus there is a true lympho-sarcoma, a small-celled growth of the lymph-glands, which must be distinguished, though it is hard in some cases, from the general lymphadenoma. The distinctions laid down by some writers, such as a special tendency to attack contiguous parts, and a more general distribution of the metastatic growths, will not hold, as we have seen that cases of lymphadenosis or Hodgkin's disease may attack neighboring structures, and the secondary tumors, though preferably in lymphatic textures, may occur in every organ. In the retro-peritoneum, for example, true lympho-sarcoma is not uncommon, forming large tumors which may press forward the viscera and produce a very prominent mass in the abdomen. They are not uncommon in children, and with renal sarcomas make up three-fourths of the abdominal growths of early life. But they may occur in adults and attain large size, involving adjacent organs, such as the kidneys, or, as in a case I saw a short time since, grow into the colon and cause death by gradual hemorrhage. These are local growths as regards the lymphatic system, not involving distant glands, and not often, indeed, producing metastasis.

We may recognize in the lymphatic glands--1st, the local benign growth which seems nothing more than hypertrophy, lymphadenoma, and which may persist for years; 2d, a local malignant growth, lympho-sarcoma, which invades contiguous structures and may be followed by metastasis, but there is not general involvement of the lymphatic tissues; and 3d, there is a generalized lymphoma involving groups of glands in succession, and the adenoid tissue throughout the body, usually accompanied by anæmia alone, in which case we term it Hodgkin's disease--sometimes by an excess of colorless corpuscles as well, when we call the affection lymphatic leukæmia.

PROGNOSIS.--When established sufficiently to make a sure diagnosis, the prognosis is in the great majority of cases bad; true examples of the disease rarely if ever recover. A hopeful prognosis may be given in those cases in which only a few glands are involved, and where there is any suspicion of a scrofulous habit or where the enlargement has persisted for years without {931} extending. The presence of profound anæmia, the existence of swelling in distant groups and in internal glands, are grave indications. High, irregular fever, rapid growth, and the development of cachexia are symptoms of the full establishment of the disease. The physician must not be deceived by intervals of improvement, with perhaps subsidence of the glandular swelling in places. Such breaks in the onward progress are not uncommon.

TREATMENT.--When small and localized, the question of the removal of the glands may be raised. If they persist after appropriate remedies, and if there is not grave anæmia, and other groups and the spleen are not affected, excision should certainly be performed. Circumscribed lymphadenoma, particularly of the neck, may exist for years before the glands in other regions become involved; and in such cases removal affords the best guarantee that the disease will not extend.

Local applications are of doubtful benefit. I have never seen any permanent improvement follow the persistent use of iodine, biniodide of mercury ointment, or friction with oil. Galvano-puncture has not been successful, and the same may be said of the various substances injected into the glands--iodine, arsenic, chromic acid, etc.

Internally, iodine and iodide of potassium have been extensively used, but without much benefit. Quinine, iron, and cod-liver oil are useful as tonics, but have no influence on the size of the tumors. Arsenic is the only medicine which has seemed to me of positive value, and under its use I have seen the gland-tumors decrease greatly in size. It should be given in increasing doses until some of the unpleasant effects of the drug are manifested, when a return should be made to a small dose, and again gradually increase. When well borne, large doses, 20 or 25 minims, of the liquor arsenicalis should be taken three times a day for many weeks. In two cases with moderate enlargement of the cervical and axillary glands the progress of the disease seemed arrested, and the glands certainly became smaller and softer. In the history of these cases the patients will often speak of changes in the volume of the gland quite uninfluenced by any treatment; and these fluctuations must be taken into account in estimating the value of a drug; but, making due allowance for this, the beneficial effects of the arsenic are unquestionable when given early in large doses and the administration kept up for months. Many recent writers have borne testimony to this, among them Karewski,[156] who reports three recoveries.

[Footnote 156: _Berl. klin. Wochenschrift_, 1884, 17 and 18.]

Phosphorus has been of service in the hands of Gowers and Broadbent, and when arsenic is not well borne it should be tried.

Change of air and scene has benefited some cases. The patient's strength must be supported by every possible means; fortunately, gastro-intestinal disturbance is not so marked as in leukæmia, and even with most extensive and progressive enlargement of many groups of glands the appetite may be good and the digestion excellent.

When the glands of the neck compress the trachea, or when the lymphoid elements of the tonsils and pharynx obstruct the orifice of the glottis, tracheotomy may be necessary.

HÆMOPHILIA.

DEFINITION.--An hereditary or congenital fault of constitution, characterized by a tendency to bleeding, spontaneous or traumatic, and often associated with swelling of the joints.

{932} SYNONYMS.--Hæmatophilia; Hereditary hæmorrhage; Hæmorrhagic diathesis; Idiosyncrasia hæmorrhagica. _Ger._ Bluterkrankheit, Blutsucht; _Fr._ Hémophilie. The term bleeder is applied to a patient.

CLASSIFICATION.--In this article the congenital or hereditary disease will alone be considered, to the exclusion of cases of transient hemorrhagic diathesis, the hemorrhages of scurvy, fevers, anæmia, purpura simplex, and purpura hæmorrhagica.

HISTORY.--So far as is known, the classical writers make no mention of the disease, though in the _Pharsalia_ of Lucan there is a passage, quoted by Legg,[157] which well describes the hemorrhagic diathesis. The first positive reference is in the writings of Alzaharvi, a physician of Cordova who died in 1107 A.D. A doubtful case is mentioned by Benedictus in 1539, who relates the history of a barber who bled to death from slight wounds of the nose caused by clipping the hairs. Hochstetter described a case in 1674 to which Virchow has called attention.[158] Legg[159] found a well-recorded case by Banyer in the _Philosophical Transactions_ (1743). Fordyce in 1784 described a Northamptonshire family the members of which suffered from hemorrhages.[160] With brief references to the disease by two German writers in 1793 and 1798, these scanty materials comprise the facts known at the beginning of this century.

[Footnote 157: _Hæmophilia_, London, 1872.]

[Footnote 158: _Virchow's Archiv_, Bd. xxviii.]

[Footnote 159: _Loc. cit._]

[Footnote 160: _Fragmenta Chirurgica et Medica_, London, 1784.]

To American physicians belongs the credit of the full recognition and description of the disease and the discovery of its remarkable hereditary nature.

Otto[161] gave an account of a New England family members of which had been bleeders for several generations. He also referred to a Maryland family observed by Rush. Otto appears to have been the first to note the immunity of females in bleeder families, and their tendency to transmit the disposition. In the _Philadelphia Medical Museum_, vol. i., 1805, a letter of E. H. Smith is published, written in 1794, in which he gives an account of a boy affected with the disease. Hay[162] reported the Appleton-Swain families of Reading--one of the most remarkable histories ever published of the disease. In 1817 the Buel Brothers described the Collins family,[163] and Coates[164] a family in Delaware county, Pa. Hughes[165] and Gould[166] also described notable examples. Holton, Harris, and Dunn have studied other American bleeder families, and a brief record of the local literature of the subject will be found at the end of this article.

[Footnote 161: _Medical Repository_, New York, 1803, vol. vi.]

[Footnote 162: _New England Medical Journal_, 1813, vol. ii.]

[Footnote 163: _Transactions of the Medical and Physical Society of New York_, 1817.]

[Footnote 164: _North American Medical and Surgical Journal_, Philada., vol. vi., 1828.]

[Footnote 165: _Transylvania Journal_, 1831, vol. iv., and _American Journal Med. Sciences_, 1833, vol. xxi.]

[Footnote 166: _Boston Medical and Surgical Journal_, 1857.]

In Germany, Nasse (1820), Rieken (1829), Schönlein, Canstatt, Wachsmuth, Lange, Virchow, and others added greatly to our knowledge of the disease. Grandidier published a monograph in 1855, a new edition of which in 1877[167] contains a most exhaustive account of the disease and a statistical résumé of all cases to date. In England the disease has not attracted much attention. Legg published an important monograph in 1872, and many papers of value are scattered through the _Transactions_ and journals.

[Footnote 167: _Die Hämophilie_, Leipzig, Zweite Auflage, 1877.]

In France the articles in the encyclopedias and a few theses--of which Gavoy's (1861) and Simon's (1874) are the most important--comprise the chief literature.

ETIOLOGY.--The disposition is, in the majority of cases, hereditary, but there may be a spontaneous origin, the disease appearing in the child of a family in which no previous cases had occurred. Nothing is known of the {933} conditions under which the disease may thus arise in a healthy stock. Many of such cases die early, but others live and may become the starting-points of new bleeder families. In the history of sixty families Grandidier[168] found statements of this mode of origin of the affection.

[Footnote 168: _Op. cit._, p. 136.]

The two most interesting features in the etiology relate to sex and heredity. The disease is much more common in males than females, the proportion being variously estimated at 11 to 1, or even 13 to 1. In 64 bleeder families, in 5 were sons and daughters alike affected; in 27 all the sons were bleeders; and in 6 of these there were no daughters.

There is no disease with so marked a tendency to transmission, and it may appear in four or five generations in succession. In the Appleton-Swain family of Reading, Mass., there have been cases since the early part of the last century, and F. F. Brown of that town writes me that cases still occur in the descendants.[169] Legg gives a chart of the Clitherow family, in which it has existed for the past two hundred years.[170]

[Footnote 169: The last case Brown has been able to ascertain was in a lad, Warren Coburn, aged seventeen, who died about twelve years ago. His mother's brother was a bleeder, and died of hemorrhage from a slight scalp wound after having been brought to death's door on three or four other occasions by trivial wounds. Mrs. Coburn was a daughter of Daniel Hart, whose wife was a Norton. Her mother was a Bacheller and a granddaughter of Oliver Appleton's daughter. This lad is an instance of the transmission of the disposition to the seventh generation within a period of two hundred years. Brown further states that there do not appear to be in the vicinity of Reading any Appleton or Swain families in which bleeders exist. As the tendency is chiefly transmitted through the female members of a family, who lose the patronymic by marriage, it is often difficult to trace the relationship. I think if we had fuller genealogical details we should find that several of the bleeder families now thought to be distinct belonged to the same stock.]

[Footnote 170: _St. Barth. Hospital Reports_, 1881.]

YEATON. | +----------+-------------+---------+---------+----------+ | | | | | | Son, bleeder. Daughter. Daughter. Daughter. Daughter. Daughter. | | | | | | | | | | +----------+-----+ | | | | | | | | | | Son, bleeder. Three daughters. | | | | | | | | | Son, bleeder. | | | | | | | | +------------+-----------+ | | | | | | | | | Son, bleeder. Daughter; Daughter. | | | children not bleeders. | | | | | | +-----------+-----------------+----+ | | | | | | | Son, bleeder. Daughter. Daughter. | | | | | | Son, bleeder. +-----+-----+ | | | | | | One son Four daughters. | | bled to death. | | | | +-----------+----------+----------+----------+ | | | | | | Son, bleeder. Daughter. Daughter. Daughter. | | | | | Twin boys, Son, not Son, not | bleeders. a bleeder. a bleeder. | | +--------------+-----------+----+ | | | Son, bleeder. Son, bleeder. Daughter.

In the celebrated bleeder families of Tenna, Switzerland, five generations have been affected. The modes of transmission are as follows: (1) Father {934} to son, grandson, etc. This is rare, but instances are on record. (2) Father not a bleeder, but of bleeder stock, transmits the tendency to son--very uncommon. (3) Father to daughter, granddaughter, etc.--not common. The daughters of a bleeder are usually free, though their brothers may be affected. (4) Mother a bleeder, transmits to sons and daughters. (5) Mother not a bleeder, but daughter of one, transmits to her sons, the daughters remaining free, but their sons affected. This is the most common mode of inheritance. Atavism by transmission through the female line is almost the rule, and the daughters of a bleeder, though healthy and free from any tendency, are almost certain to transmit the disposition to their male offspring. The 657 cases analyzed by Grandidier occurred in two hundred families. The chief facts of heredity are well illustrated by the preceding chart of the Yeaton family, given by Gould in the _Boston Medical and Surgical Journal_, 1857.

The Anglo-Germanic nations appear especially prone to the disease. Of 194 families in Grandidier's table, 154 were of the Teutonic stock. Records of the disease among the Latin races are rare. Jews are probably not more liable than other people, but the rite of circumcision gives an unusual opportunity for its manifestation at an early age.

The age at which the bleeding tendency first appears was determined by Grandidier in 113 cases as follows: in 63 during the first year; in 17 during the second, and up to the end of the second year in 93. It is rare for the first manifestation to occur after the twelfth year, and there was only one case in which the first bleeding appeared after the fifteenth year.

The constitution and temperament of bleeders, about which the older writers had much to say, probably present no peculiar characteristics. Some persons claim to be able to recognize bleeders even before they have manifested any tendency to hemorrhage. They are usually fresh, healthy-looking persons, with fine, soft skins, through which the superficial veins may show with more than usual distinctness. A division of cases into erethetic and atonic forms has been made by Wachsmuth and Grandidier. The mental activity of bleeders has been noted to be above the average, due, doubtless, to the fact that the liability to bleed from slight blows and cuts has made sedentary and studious habits preferred to out-of-door employments and amusements.

Families in all conditions of life are affected. Much interest was excited in the disease in England from the fact that the late Prince Leopold was a sufferer.

Climate appears to have an influence in determining attacks. Cold, damp, changeable weather is favorable, while a residence in a warm, equable climate diminishes the tendency in a very marked manner. Some patients have an extraordinary susceptibility to changes in the weather.

All observers have noted the great fertility of bleeder families. Those first born seem less liable to bleed than subsequent ones.

SYMPTOMS.--The existence of the defect of constitution may not be suspected until an uncontrollable hemorrhage follows some trivial injury or operation, or a spontaneous bleeding may occur and present great or insuperable difficulties in its arrest. The symptoms usually occur in the first years of life, and in the great majority of cases, as mentioned above, the first bleeding occurs before the fifth year. The symptoms may be grouped under three divisions (Legg, Grandidier): external bleedings, spontaneous and traumatic; interstitial bleedings, petechiæ, and ecchymoses; and the joint affections. Legg recognizes three grades of the disease. The first and most severe is characterized by bleedings of every kind, external and internal, and by troublesome joint affections: this form is most often seen in men. The second grade is less severe; there are spontaneous hemorrhages from the mucous surfaces, but no traumatic bleeding or ecchymoses and no joint {935} troubles: this form is most often seen in women. The third and lowest degree is when there is a tendency simply to ecchymoses; no dangerous bleedings occur: this form is often seen in members of bleeder families, and if in women the menstruation may be early and profuse.

External Bleedings.--The spontaneous bleedings may occur from the skin, the mucous, and in rare instances the serous, membranes. There are frequently preliminary symptoms--prodromata--such as flushing, fulness of the head, and throbbing of the arteries--signs of so-called plethora; often there is irritability of temper, but sometimes, in children, extra cheerfulness has been observed. The localities affected and the frequency are shown by the following analysis of 334 cases by Grandidier: Epistaxis, 169 times; from the mouth, 43; stomach, 15; bowels, 36; urethra, 16; lungs, 17; cerebral hemorrhage, 2; skin of head, 4; tongue and finger-tips, 4 each; tear-papilla, 3; eyelids, 2; external ear, 5; female generative organs, 10; ulcer of skin, 2; navel (long healed), 2. An odd situation for spontaneous bleeding is mentioned by Townsend,[171] in which a child bled to death from the scrotum. In many cases these spontaneous hemorrhages prove fatal--most frequently the epistaxis. The traumatic bleeding may result from blows, cuts, scratches, etc., and the blood may be effused into the tissues or discharged externally. Fatal hemorrhages have occurred from the following wounds: blow on head, 11 times; slight scratches on skin or abrasion of dermis; laceration of the frænum of the lip, slight cut (two lines deep) in a duel wound; bite of the tongue (7 cases); fall on the mouth; blow on the nose; blow of a stone on the finger; cut in paring the nail; fall on the head with meningeal hemorrhage (2 cases, brothers); and rupture of the hymen on the wedding-night.

[Footnote 171: _Boston Med. and Surg. Journal_, lv.]

After operations, trivial and severe, many fatal cases have occurred, and the statistics of the same author give the following: cutting of the frænum linguæ, 1; leeching, 5; venesection, 4; blister, 2; extraction of tooth, 12; circumcision, 8; cutting umbilical cord, 4; vaccination, 2; fistula, stone, ligation of carotid, of radial, of ulnar, of femoral arteries, amputation of arm and of thigh, 1 each; phimosis, 2. Leeching, extraction of teeth, and circumcision are most dangerous operations in bleeders.

The bleeding is always a capillary oozing, and the vessels are not seen. It may last for hours, or even many days and weeks, and the amount of blood lost may be enormous. Epistaxis may be fatal in twenty-four hours. In Coates' case a medical student lost half a gallon of blood in twenty-four hours, and in the ten days which the bleeding continued it was estimated that he lost about three gallons.

The healing of a wound in a bleeder may take place rapidly, either with or without suppuration. When the hemorrhage is large or prolonged, severe anæmia follows, from which, as a rule, the patients recover with remarkable rapidity.

The interstitial hemorrhages--petechiæ, ecchymoses, hæmatoma--may be spontaneous or the result of injuries. The petechiæ occur most frequently in the skin, particularly of parts distant from the heart--the legs and arms, less often the face. On the mucous and serous surfaces they are less common. They resemble ordinary purpuric spots, and crops may come out with symptoms of swelling and pain in the joints. Large extravasations--hæmatoma--are most frequently of traumatic origin and may follow the slightest blow, as in a case of Sir Wm. Jenner's, in which from the fall of a rubber ball on the thigh an enormous extravasation took place between the knee and trochanter.[172] They are blue, black, or reddish-black at first, and in their absorption go through the various changes in color which we notice in a bruise. These blood-tumors may occasionally arise spontaneously.

[Footnote 172: Legg, etc., p. 68.]

The arthritic affections in hæmophilia are very remarkable, and so {936} common as to form prominent features in the disease. There may be simple pain in and about the joints, or swelling with redness and signs of intense inflammation. The attacks may come on suddenly with fever, resembling closely acute rheumatism. The large joints are usually affected, the knees most often, then the elbows, ankles, and shoulders. There may be repeated attacks, and at last great crippling and deformity. The small joints are rarely affected. In cold, damp weather the attacks are most common; occasionally they follow traumatism. In addition to the joint troubles, bleeders suffer much with irregular pains in the limbs, particularly during change of weather, or these pains with arthritis may usher in an attack of hemorrhage.

Many other irregular symptoms are described in the monographs, some of which have no intimate relation with the disease. The anæmia has, of course, all the features of the traumatic form. Digestive troubles, after the bleeding, are common, and are due to the anæmia. The Buel Brothers[173] mention that in two of their cases the patients showed a marked inclination to eat sand and earth. Children with the hemorrhagic tendency pass through the ordinary diseases of infancy like others. Whooping cough is very liable to cause epistaxis. Rheumatism and scrofula are said to be common in bleeder families.

[Footnote 173: _Op. cit._]

The blood in bleeder cases is, as a rule, normal, so far as our present means of investigation enable us to decide. When a hemorrhage has continued for some time, it is thin and watery, but at the beginning of the bleeding the blood is usually rich in corpuscles and fibrin and coagulates firmly. The salts have been found increased in quantity. No change has been noted in the corpuscles, the number of which is stated by several observers to be increased. Prior to a hemorrhage there may be, according to some writers, a state of plethora or increase in the total quantity of blood, and the tolerance of the loss, so much greater in bleeders than in ordinary persons, is adduced in support of this view.

MORBID ANATOMY.--Not many changes other than those of profound anæmia have been found in the bodies of bleeders. An unusual thinness of the walls of the vessels, first noted by Bladgen in 1817,[174] has been met with in a number of cases; in a few instances hypertrophy of the heart; in others a rounded foetal shape of the organ. Within the past few years careful microscopical examination has been made of the tissues and blood-vessels of bleeders. Kidd[175] found degeneration of the muscle-fibres of the middle coat of the arteries, and the endothelium of the small arteries, veins, and capillaries was swollen, proliferated, and some of the small veins were blocked with the products. Legg[176] reports a case in which Klein made a most careful examination with negative results, and he stated that of six such examinations which had heretofore been made, in only one case (Kidd's) were important changes found. At the same meeting of the London Pathological Society, Theodore Ackland also reported a case with negative results as regards histological changes.

[Footnote 174: _Medico-Chirur. Transactions_.]

[Footnote 175: _Medico-Chirurgical Society's Transactions_, vol. lxi.]

[Footnote 176: _Lancet_, Oct. 27, 1884.]

The joint changes have been studied in a number of cases. Hemorrhage has been found in and about the capsule, and the acute swelling may be due largely to it, as was shown in Hutchinson's case,[177] in which he aspirated the joint. When it lasts any time, there is great staining of the cartilages and discoloration. There may be inflammation of the synovial fringes and erosion and destruction of the articular surfaces (Legg).

[Footnote 177: _Trans. State Med. Soc. N.Y._, 1877.]

The PATHOLOGY of the disease is unknown. No doubt two circumstances combine in hæmophilia--congenital fragibility of the vessels and a defect in coagulability of the blood--but whereon these depend we are as yet entirely ignorant. There is no evidence of the nature of the anatomical changes in {937} the vessels which permits of their ready laceration, and none on the nature of the alteration of the blood which prevents the normal thrombus formation in a wound; and in the absence of information on these points theories must necessarily be unsatisfactory, and their discussion, in a work of this practical nature, profitless.

The DIAGNOSIS presents no difficulty in members of a bleeder family, in whom slight joint trouble and petechiæ are as much manifestations of the disease as the more severe hemorrhages. In a large majority of cases the tendency becomes manifest at an early date. The spontaneous umbilical hemorrhages of infants are, as a rule, to be excluded, being dependent upon, or associated with, jaundice or syphilis or a mycosis (Weigert[178]). The hemorrhagic diathesis may develop in children or members of a healthy family and prove fatal, and the question in such cases always comes up, Are they instances of hæmophilia? There seems to be a desire to limit this term to cases of an hereditary nature only; but when a child shows a marked tendency to multiple hemorrhages, spontaneous or traumatic, which tendency persists and is not merely transitory, and particularly if there are joint troubles, I think that under these circumstances we have a genuine case of hæmophilia; and such a child, if he--it is more likely to be a male--survives and marries, may be the founder of a bleeder family. These are the congenital in contradistinction to the hereditary cases. In the histories of the bleeder families we frequently come back to the origin in a person born of a healthy stock in which there have been no hemorrhagic tendencies. On the other hand, single severe uncontrollable hemorrhages in children or adults are not to be ranked as hæmophilia unless there have been other features pointing to the existence of the diathesis. The literature abounds in cases of this kind, many of which are described as hæmophilia. In doubtful cases it is very difficult to decide, as in a case of Forscheimer brought before the Academy of Medicine of Cincinnati.[179] In the review of American literature we have excluded all cases in which the hereditary or congenital characters were not well marked.

[Footnote 178: _Cohnheim's Pathologie_, i. 382.]

[Footnote 179: _Cincinnati Lancet and Clinic_, 1884.]

It may be useful to put down here for the guidance of the practitioner the varieties of bleeding commonly met with, and which must not be confounded with hæmophilia:

(1) The umbilical hemorrhages of infants, due to jaundice or to syphilis hæmorrhagica neonatorum, etc.

(2) Purpura simplex, seen often in debilitated, rarely in healthy, children, usually confined to the legs, and in some cases I have seen it associated with rheumatic pains or swellings in the knees and ankles.

(3) Peliosis rheumatica, an affection which in the large interstitial hemorrhages and the joint swellings touches hæmophilia in a curious way. It too may show itself in several members of the same family.

(4) Purpura hæmorrhagica, Morbus maculosus Werlhöfii, a grave disease, characterized by extensive cutaneous ecchymoses, mucous hemorrhages, but not dependent on any local disease, or, so far as is known, on any specific poison. The bleedings in scurvy may be mentioned here, but there could be little difficulty in determining their nature.

(5) Infective purpura, due to the action of some specific poison--small-pox, measles, scarlet fever, cerebro-spinal fever, etc. The hemorrhages may be cutaneous and trivial, or may be in the most aggravated form of interstitial and mucous bleedings, as seen, for example, in black small-pox.

(6) Toxic purpura, as in snake-bites and many poisons, such as phosphorus.

(7) Simple hemorrhagic diathesis, under which may be included those cases in which, without any hereditary disposition or previous hemorrhagic history, there is a tendency to uncontrollable hemorrhage from a slight wound.

{938} (8) Hæmatidrosis, bloody sweats, which occur usually in hysterical or epileptic females, and are in rare instances accompanied with mucous hemorrhages.

In considering the PROGNOSIS it is well to remember that the patients rarely die in the first bleeding. The younger the individual the worse is the outlook. As above stated, the attacks are most frequent under five years of age, and of 152 boys the subject of the disease, 81 died before the termination of the seventh year (Grandidier). Legg, however, states that it is rarely fatal in the first year. The longer a bleeder lives, the greater the chance of his outlasting the tendency; but that it may persist to the end of a long life, and then prove fatal, is shown by the case of old Oliver Appleton, the first recorded American bleeder, who died at an advanced age of hemorrhage from a bedsore and from the urethra. A bleeder may have years of existence, in which the tendency seems lessened or even absent. The prognosis is always worse in a boy than in a girl. In the latter menstruation is sometimes early and excessive, but, happily, in the female members of hæmophilic families neither this function nor the act of parturition bring with them special dangers.

TREATMENT.--The prophylaxis is all-important. The members of a bleeder family, particularly the boys, must be guarded from injury as much as possible, and operations of all kinds must be avoided, except when life itself is in jeopardy. The extraction of a tooth should be absolutely prohibited. Occupations must be sought which will give the least possible risk of injury. Daughters of bleeder families should not be permitted to marry, as it is through them that the tendency is chiefly propagated, and, even if not bleeders themselves, some of their male children are certain to be affected. The question of the marriage of male bleeders is more difficult to decide, but in any case where the tendency is marked it should be prohibited.

When an injury or wound has occurred, absolute rest, cleansing the wound, and compression should first be tried. If in a favorable locality pressure on the artery may be employed, failing in this, the various styptics may be used. In epistaxis, ice, tannin, and gallic acid may be tried before plugging.

Internally, ergot seems to have been of use in several cases. Otto[180] speaks of the value of sulphate of soda in purgative doses. The perchloride of iron, 30-40 minim doses, every two hours, is advised by Legg, with a purge of sulphate of soda if there is no bleeding from the bowels. Venesection has been resorted to in several instances. Transfusion has been employed, but without benefit. The diet should be light and supporting. After the attacks the patients should take iron and cod-liver oil until the health seems restored. When possible, a residence in the South during the winter is advisable, as most cases are aggravated by the cold weather, and in any case care must be taken to protect patients against cold and wet.

[Footnote 180: _Loc. cit._]

The joint troubles must be treated on general principles.

AMERICAN LITERATURE OF HÆMOPHILIA.

Buel: _Transact. of the Med.-Physic. Society of New York_, vol. i., 1817; 1 F., 4 cases.

Coates: _North Am. Med. and Surgical Journal_, Philada., 1828, vi. p. 37; 1 F., 5 cases.

Dunn: _Am. Journal Med. Sciences_, 1883, vol. lxxxv. p. 68; 4 F.

Felt: _History of Ipswich_, 1834--Appleton family referred to.

Gould: _Boston Med. and Surgical Journal_, 1857, p. 500; 1 F., 11 cases.

Harris: _Philada. Med. Times_, 1872; 2 F., 7 cases.

Hay: _New England Journal of Med. and Surgery_, 1813, vol. ii. p. 221; 1 F., 15 or 16 cases (accurate number rather difficult to make out).

{939} Holton: _Am. Journal of Med. Sciences_, April, 1874; 1 F., 7 cases.

Hughes: _Transylvania Med. Journal_, 1831, vol. iv. p. 518, and _Am. Journal Med. Sciences_, 1833, vol. xxi. p. 543; 1 F., many cases.

Hutchinson: _Trans. State Med. Society of New York_, 1877, p. 208.

Otto: _Medical Repository_, 1803, vol. vi.; 3 F., 8 cases.

Pepper: _Philada. Med. Times_, 1881, vol. xii. p. 109; 1 case--Lancaster county family described by Dunn.

Sewell: _Med. Chronicle_, Montreal, 1857, vol. iv.; 2 F., 4 or 5 cases.

Smith: _Philadelphia Medical Museum_, 1801, vol. i. p. 284.

Traneus: _St. Louis Med. and Surgical Journal_, 1870, p. 535; 1 F., 4 cases.

Townsend: _Boston Med. and Surgical Journal_, vol. lv. p. 447; 1 F., 3 cases.

ADDISON'S DISEASE.

DEFINITION.--A constitutional affection characterized by asthenia without emaciation, a depressed circulation, gastric irritability, and usually pigmentation of the skin. In the majority of cases it is associated with a fibro-caseous degeneration of the suprarenal capsules, and in many there are changes in the abdominal sympathetic system.

SYNONYMS.--Morbus Addisonii; Bronzed-skin disease. _Fr._ Maladie d'Addison, Maladie bronzée; _Ger._ Addisonische Krankheit.

HISTORY.--In the _Halle Hospital Reports_ for 1823 Schötte describes a case, and one is also given by Bright in vol. ii. of his _Medical Reports_, 1831. A few other instances are also on record before 1855, when Addison published his monograph _On the Constitutional and Local Effects of Disease of the Suprarenal Capsules_, from which we may date our knowledge of the affection. Following close upon the work of Addison numerous observations were made in England, where the disease appears to be more common than elsewhere. Wilks of Guy's Hospital,[181] and Greenhow of the Middlesex Hospital, may be mentioned among those who in England have specially studied the disease, and the latter published an important monograph in 1875.[182] In France, besides numerous minor contributions, the exhaustive articles in the encyclopædias have been the most important publications. In Germany the monograph of Averbeck (1869) and the abstracts of Meissner in _Schmidt's Jahrbücher_ may be specially mentioned. Virchow, Griesinger, Oppolzer, Bamberger, and others have made valuable contributions. Recently Burger[183] has published a small monograph. In other European centres contributions have been made, among which may be mentioned that of Schmidt of Amsterdam, who brought forward cases in support of the view that the disease was an affection of the sympathetic ganglion. In America the first cases were reported by Ranking[184] and Taylor.[185]

[Footnote 181: In numerous communications in _Guy's Hospital Reports_ and _Trans. Path. Society_.]

[Footnote 182: "On Addison's Disease," _Croonian Lectures_.]

[Footnote 183: _Die Nebeunieren und der Morbus Addison_, Berlin, 1883.]

[Footnote 184: _Am. Journ. Med. Sci._, 1856.]

[Footnote 185: _New York Med. Journal_, 1856.]

ETIOLOGY.--The causation of the disease is unknown. Cases are more frequent in hospital than in private practice. Males are more often attacked than females; the proportion in Jaccoud's table[186] is 79 to 48, and in Greenhow's[187] analysis of 183 good cases, 119 were males and 64 females. Under ten and over fifty years of age the disease is very uncommon; the majority of the cases occur between the twentieth and the fortieth year. Greenhow {940} has called attention to the fact that in a number of instances the disease appears to have followed an injury, such as a blow upon the abdomen or back, and in several cases caries of the spine has preceded the attack. He refers also to the greater frequency of the disease in the laboring classes and those exposed to injury from over-exertion. The disease does not seem to be more prevalent among members of phthisical families, although the morbid process in the glands has been regarded as of a tuberculous nature, and it is common for other tuberculous lesions to occur in the course of the disease.

[Footnote 186: _Dictionnaire de Médecine_.]

[Footnote 187: _Op. cit._]

The disease is rare in America--apparently much more so than in England.

SYMPTOMS.--In the words of Addison, the leading and characteristic symptoms are: "Anæmia, general languor and debility, remarkable feebleness of the heart's action, irritability of the stomach, and a peculiar change of color in the skin occurring in connection with a diseased condition of the suprarenal capsules."

Although, perhaps, not the most essential, the symptoms pertaining to the skin are in the majority of cases the most prominent, and have given rise to the names bronzed skin, melasma suprarenale, etc. which have been applied to the disease. A gradual increase in the pigment of the rete mucosum, either patchy or diffuse, causes a gradual discoloration, which may ultimately reach such a degree that a previously blonde individual may have the aspect of a Malay or a mulatto. The grades of coloration may range from a light yellow to a deep brown, or even black. In some instances there is a greenish-brown tinge, to which the term bronzed is peculiarly applicable. In typical cases it is diffuse over the whole surface, but as a rule deeper on exposed parts, face, neck, and hands, and also in those regions where the normal pigmentation is most intense, nipples, scrotum, and penis, or in the vicinity of cicatrices or regions of chronic irritation. It is usually first noticed on the face, either diffuse or in spots, and the extension may be rapid or gradual, in many instances not reaching a high grade and not becoming universal. It may be absent, and is not to be regarded--as was formerly the case--as an essential feature of the disease. Patches of leucoderma may occur in connection with the pigmentation, as beautifully delineated in Pl. xi. of Addison's monograph. The pigmentation is not confined to the skin, but may extend to the mucous surfaces--mouth, conjunctivæ, vagina. In the mouth the patches may be as dark as in the dog; they are usually scattered, often on the margins of the lips and on the edges and under surface of the tongue and on the cheeks. The conjunctivæ are less often affected. The vagina may be very deeply pigmented. An intensification of the choroidal pigment has been observed. In some cases a patchy pigmentation of the serous membranes has been found, and is figured in one of Addison's original plates, and pigmentation of the nails, hair, and teeth may also occur. A variation has been observed in the intensity of the coloration with the general health of the patient. The discoloration rarely precedes the general symptoms, but more usually follows the asthenia.

Some observers have noted a peculiar odor of the breath and from the skin, particularly during the last few days of life.

Anæmia of a moderate degree may exist, but it is not, as often stated, a constant symptom. Greenhow states that "there is no real anæmia, the blood being often rich in red corpuscles, even in excess, and there is no increase in the white." No special alterations in the appearance of the corpuscles have been noted. In some instances free pigment has been found.[188] In a case recently at the hospital of the University of Pennsylvania, Hughes found the number of red corpuscles over five millions per cubic millimeter, and there were free pigment-granules in the blood.

[Footnote 188: Corput, _Gazette hébdomadaire_, 1863.]

Hemorrhages are rare; extravasations into the retinæ have not, so far as I {941} can ascertain, been observed, nor are there often the other common features of anæmia.

The pulse is frequent and small, the heart's action weak--sounds clear; a venous murmur may sometimes be heard. In some cases there appears to be a special enfeeblement of the heart and a liability to fainting attacks, and without any warning a fatal syncope may occur. Cold feet and hands result from the weak circulation, and may be a most annoying symptom.

Symptoms in connection with the respiratory system are not common. There may be dyspnoea, and the complication of phthisis may give rise to all the features of that disease. There may, however, be extensive lung trouble with but few symptoms. The temperature is rarely elevated, more often it is subnormal.

Gastric disturbances are very common--anorexia, nausea, vomiting--particularly toward the close, but they may be early and prominent features, persisting in spite of all remedies and proving the most formidable symptoms of the malady. They appear to be of nervous origin, and not referable to changes in the organ itself. It is doubtful if the case reported by Gilliam,[189] in which there was degeneration of the gastric mucosa, was Addison's disease. The state of the bowels is variable; constipation is more frequent than the normal condition. Diarrhoea is common, and may come on suddenly without obvious cause, and is a not infrequent cause of death.

[Footnote 189: _Phil. Med. and Surg. Reporter_, xxiv.]

The urine is usually pale, free from albumen, not often increased in amount. It is interesting to note, in connection with the involvement of the abdominal sympathetic, that in a few cases there has been polyuria. The nitrogenous elements may be greatly reduced, the urea to 13-20 grammes daily, and the amount of indican may be increased as much as 64-75 milligrammes in 1000 c.c. (Samuel). In one case Thudichum found the urinary pigments greatly reduced in amount, the uromelanin not amounting to more than one-twelfth the normal quantity. A recent observation of Nothnagel is of interest.[190] In a patient aged twenty, who had the typical symptoms of the disease for two years, death took place by coma and the condition of acetonuria was determined.

[Footnote 190: _Zeitschrift für klin. Med._, Bd. ix.]

The symptoms connected with the nervous system are the most prominent in the disease, and are more constant than the anæmia or the bronzing. The most marked is a depression and enfeeblement of the nervous forces, a profound asthenia out of all proportion to the general condition. The patients complain of a lack of energy, mental and bodily; the least exertion is an effort, and there is a feeling of tire and weariness with which the facial expression is quite in keeping. The fainting fits, giddiness, noises in the ears, may also be due to faulty innervation, as they occur in cases in which the anæmia is by no means advanced. Headache, lumbar and abdominal pains are frequent, and in a considerable proportion of cases there is tenderness on pressure in the lumbar region. With the advance of the disease the prostration becomes more marked, the patient remains in the recumbent posture, the voice gets weak and small, the intelligence dulled, and occasionally there is delirium. Head symptoms may suddenly supervene, and death by coma or convulsions cut short the progress even early in the disease (Pye-Smith). In Jaccoud's series convulsions were noted in 19 cases.

The disease may be said to be invariably fatal, but the course presents many variations. The majority of cases die within eighteen months of the first onset of the symptoms. B. Fenwick, in an analysis of 30 recent cases,[191] calls attention to the fact that when bronzing does not occur the course is more rapid. Thus the average duration of the non-bronzed cases was only 4.8 months, while for bronzed ones it was 23.6 months. There are acute cases {942} in which, with great weakness, vomiting, and diarrhoea, the fatal end may occur in a few weeks. Some of these rapid cases resemble typhus. Syncopal attacks, coma, or convulsions cut short not a few cases. In a few instances it is much prolonged--six years (Niemeyer) or even ten years (Greenhow). Whether recovery ever takes place is doubtful. Finney[192] has reported an apparently genuine case which got well. Some French observers (Potain) think that recovery takes place more often than is supposed. Sir Wm. Gull mentioned a case of recovery.[193] Periods of improvement lasting many months may occur.

[Footnote 191: _Path. Soc. Trans._, vol. xxxiii., London.]

[Footnote 192: _Dublin Med. Journ._, April, 1882.]

[Footnote 193: _Int. Med. Congress_ (London) _Transactions_, vol. ii.]

MORBID ANATOMY.--The panniculus adiposus and subperitoneal fat may be in normal quantity. There is rarely great emaciation, nor are the organs blanched and bloodless. The most constant lesion is in the suprarenal organs, which present a caseo-fibrous change, more rarely simple atrophy or other alterations. So frequent is the caseo-fibrous condition that some writers (Wilks) hold that it is the specific lesion of the disease. The organs are enlarged--may weigh several ounces each. The capsules are thickened, and may present caseous or even calcareous masses. The normal shape of the gland is lost, and it forms an irregular nodular mass closely adherent to contiguous parts--liver, kidney, and cava on the right side, kidney, spleen, and often pancreas, on the left. There is usually a good deal of fibrous thickening and matting in the vicinity, and the adhesions to adjacent structures may be very strong. The peritoneum often shows patches of fibroid induration. On section the diseased organ cuts with great resistance, and to the touch has an almost cartilaginous hardness. The exposed surface shows caseous masses of a yellow or grayish-white color, varying in size from a pea to a walnut, imbedded in a grayish semi-translucent fibrous tissue, pale when first cut, becoming reddish on exposure. These caseous masses may undergo softening or calcification, and pockets of pus are not uncommon. Definite small miliary granulations are not often seen, though nodular grayish-yellow bodies the size of small peas may occur. The strands of fibrous tissue which separate and enclose the caseous masses have often a very peculiar translucent, infiltrated appearance. When the cheesy lumps are small, the amount of this tissue is considerable and gives a remarkable character to the section. Wilks has described a case in which this tissue made up the entire mass. The substance of the gland is usually destroyed. The vessels and nerves can be traced to the organs where they become imbedded in the fibrous tissue.

Histologically, the soft translucent tissue consists chiefly of spindle-shaped fibre-cells, and in firmer older parts of ordinary fibrous stroma. In the immediate neighborhood of the cheesy masses there are round corpuscles--about the size of or a little larger than white blood-cells--imbedded in a fine reticulum of fibres. Giant-cells are sometimes found, but they have not been common elements in the specimens which I have examined. The caseous substance consists of granular débris in which the remains of cells and fibres can be seen. In coarse and microscopical features the lesion resembles closely local tubercular affections. The extension is by a small-celled growth, which gradually invades the adjacent parts, extending peripherally as the central portions caseate. Distinct miliary granulations are not often met with. The relation of this local growth to tuberculosis is a very interesting question. It is usually regarded as a scrofulous or tuberculous process, to which in its general features it quite conforms. I have been interested in ascertaining whether the bacillus tuberculosis existed or not in the local lesion. In Cohnheim's laboratory Karl Hüber kindly gave me an opportunity of examining the adrenals in two cases, in only one of which were the {943} bacilli evident. Since then I have re-examined the fibro-caseous tissue in Ross's case,[194] which was a most typical one, the suprarenals alone involved, and in the recent case reported by Pepper,[195] and in neither have I been able to demonstrate bacilli. Future examinations must decide whether the local affection is inflammatory or whether it belongs to the infective granulomata.

[Footnote 194: _Can. Med. Assoc. Trans._, vol. i., 1877.]

[Footnote 195: _Phila. Med. Times_, 1885.]

That other alterations may occur in cases of Addison's disease appears well established, though some still regard the caseo-fibrous change essential and specific. Atrophy of one or both glands has been frequently seen. Jaccoud gives 7 cases in his tables. Good recent cases have been described by W. B. Hadden,[196] Hebb,[197] and Goodhart.[198] The atrophy is due to a chronic interstitial process similar to cirrhosis of the liver. Hadden[199] states that the lesion is identical with that in the thyroid gland in myxoedema.

[Footnote 196: _British Medical Journal_, 1885.]

[Footnote 197: _Lancet_, 1883, i.]

[Footnote 198: _Path. Soc. Trans._, 1882.]

[Footnote 199: _Loc. cit._]

Absence of one or both the capsules has been noted by Legg, Spender, Borland[200] and Hubbard.[201]

[Footnote 200: _Boston Med. and Surg. Journal_, 1867.]

[Footnote 201: _Proceedings of Conn. Med. Society_, 1868-71.]

Cancer of the adrenals, by no means uncommon as a secondary process, rarely produces any special symptoms; but there are cases which are difficult to exclude from the category of Addison's disease. Jaccoud gives several, and in the case of Edes, often quoted,[202] the asthenia and discoloration may have been due to the capsular affection, but there was also extensive peritoneal cancer.

[Footnote 202: _Boston Med. and Surg. Journal_, 1878.]

By far the most constant morbid change after that in the adrenals is a more or less widely distributed tuberculosis, particularly of the lungs. A very considerable proportion of the cases are complicated with chronic phthisis. Regarding the disease of the suprarenals as primary, the general tuberculous affection may be secondary; and it is just in these organs, as Weigert has shown, that the veins are apt to be perforated by tubercles and systemic infection induced. The retro-peritoneal and mesenteric lymph-glands may also be tuberculous. Ulcers of the ileum may occur, and swelling of Peyer's glands and the solitary elements in the bowels is very common. In Ross's case there were numerous lymphoid infiltrations of the mucosa of the stomach, chiefly about the pylorus and cardia. The changes in the skin are confined to an increase of the pigment in the cells of the rete mucosum, most pronounced in the deeper layers and in the deeper parts in the connective-tissue cells of the papillæ and subcutaneous tissues. The condition is not to be distinguished from a deeply-pigmented scrotum or from the dark skin of the negro. The pigment resembles the ordinary coloring matter of the skin, but is possibly different from it in containing no iron.[203] Nothnagel has made[204] an exceedingly interesting study of the pigmentation in Addison's disease, and concludes that it is identical in distribution with that in the skin of the dark races; that it does not originate in the cells of the rete mucosum, but is elaborated in deeper cells, about the vessels of the cornium, and transported by them to the more superficial layers--a mode which recent observations seem to show is the normal one; and, lastly, that it is a process induced through the nervous system in some way as yet unknown.

[Footnote 203: Arnold, _Virchow's Archiv_, xxxv.]

[Footnote 204: _Loc. cit._, Bd. ix.]

The spleen has been found enlarged. The thymus gland may also persist or be much larger than normal. In Ross's case it weighed six ounces. The heart and blood-vessels do not present any constant changes: the heart has been found small in some cases. Venous engorgement of the abdominal viscera has been noted in a few cases, but it is not a common feature. It was not present in two typical cases which I have examined.

{944} In the nervous system the condition of the abdominal sympathetic has received special attention, and in a number of cases definite changes have been met with, chiefly of a sclerotic or chronic nature and intimately associated with the fibroid induration about the capsules. The nerve-cells of the semilunar ganglia are described as degenerated, deeply pigmented, and often present a new growth of connective tissue about and between the cells. There are at least thirty or more cases in which such alterations have been found. In some instances the medulla of the nerves passing from the ganglia has been found wasted and the fibres in a state of fatty degeneration. In some cases these parts have been found normal (Foa,[205] Huber,[206] Hebb,[207] and Hadden[208]). In a most typical case under Ross at the Montreal General Hospital, I could find no differences in the cells and nerves, comparing them with those of a woman dead on the same day of heart disease. More recently, I have examined a case for Pepper in which the right semilunar ganglion was imbedded in the sclerotic tissue of the right adrenal; the nerve-cells were undergoing atrophy from compression; and there were fatty changes and degenerations in the nerves connected with this ganglion. The left was uninvolved, and the cells and fibres appeared normal.

[Footnote 205: _Virchow-Hirsch_, 1879.]

[Footnote 206: _Virchow's Archiv_, 86.]

[Footnote 207: _Lancet_, 1883, i.]

[Footnote 208: _Loc. cit._]

Jacquet has described pigmentary changes in the ganglia of the cord as well as in those of the abdomen, and Guermonprez[209] alterations in the brain similar to those of senile dementia. At the Congress in 1881 at London, Semmola of Naples showed a figure illustrative of degeneration of the ganglia of the abdomen, and also an infiltration of leucocytes in the neighborhood of the central canal of the cord, from a case of Addison's disease without affection of the adrenals.

[Footnote 209: Quoted by Burger, _loc. cit._]

PATHOLOGY.--The suprarenal organs are usually grouped with the blood-vascular organs. From the number of nerve-fibres--sympathetic, pneumogastric, and even phrenic--passing to the medullary part, and from the presence of cells resembling nerve-corpuscles, Leydig and others have thought that this portion belonged to the nervous system. We know absolutely nothing of their functions. They do not appear to be essential to life, but may be removed, crushed, or destroyed with impunity, though the operation is not without danger from their close proximity to important structures. They are sometimes congenitally absent. They are proportionately larger during foetal life, but they do not appear to atrophy as age advances; indeed, it would appear from the observation of Mattei (Jaccoud) that they augment in volume with increasing years. Their chemistry has attracted much attention. Vulpian has described a material which gives a green, blue, or black color with perchloride of iron, and with oxidizing substances a rose-red; and the same observer found also hippuric and taurocholic acids. Leucin, margarin, myeline (Segilsohn), and a special coloring matter (Arnold), have been described. Henle has pointed out that the central part in the horse became of a rich brown with bichromate of potash from the reduction of the brown oxide of chromium. MacMunn's[210] observations on the spectroscopic appearance of the pigment of the suprarenals point to these glands as in some way concerned with the transformation of the effete coloring matters of the body.

[Footnote 210: Paper read before the Physiological Society of London, _Journal of Am. Med. Assoc._, 1885, March 21.]

An immense number of experiments have been made with a view of ascertaining the function of these bodies, and extirpations, crushings, etc. have been made--among others by Brown-Séquard,[211] Gratiolet,[212] Phillipeaux,[213] Harley,[214] Nothnagel,[215] the general result of which appears to be that they are not {945} important organs and that they have no influence in the production of pigment. Recently, Tizzoni[216] has stated--as Brown-Séquard had done--that pigmentation followed extirpation in the rabbit; but there is a large amount of negative evidence by most careful observers; as, for example, Nothnagel, who found no changes in 153 animals in which he had destroyed the suprarenals.

[Footnote 211: _Archives générale_, 1858.]

[Footnote 212: _Ibid._, 1856, ii.]

[Footnote 213: _Ibid._, 1858.]

[Footnote 214: _Med.-Chir. Review_, vol. xxi.]

[Footnote 215: _Zeitsch. f. klin. Med._, Bd. i., 1879.]

[Footnote 216: _Lancet_, 1884, ii.]

Various attempts have been made to explain the phenomena of the disease, to two or three of which we shall refer:

1st. That the disease is directly dependent upon destruction of the capsules and consequent abnegation of their functions. This was the view of Addison, and it appeared to be supported by the experiments of Brown-Séquard (performed shortly after the publication of Addison's memoir), who held that after extirpation of the glands pigment accumulated in the blood; which he explained on the supposition that their function was the disposal of a material in the blood readily converted into pigment. Subsequent experiments appear to have demonstrated conclusively that, like the spleen, the adrenals are not necessary to life, and that no important changes occur after their removal, or even after the induction of caseous and fibroid induration (Nothnagel). A much stronger argument against this view is found in the fact that cases have been reported in which the capsules presented little or no change.[217] Taylor[218] held that the pigmentation was induced by destruction of the cortical part of the organs, and the general nervous phenomena by involvement of the central part, which has such close relation with the nerve-structures. This view has again been advanced by B. Fenwick.[219]

[Footnote 217: Care must be exercised in the examination of apparently normal capsules. There may be extensive small-celled infiltration and destruction of the gland-elements without either reduction or increase in size.]

[Footnote 218: _Loc. cit._]

[Footnote 219: _Path. Soc. Trans._, xxxiii., 1882.]

2d. That it is an affection of the abdominal sympathetic system, induced, most commonly, by capsular disease, but also by other chronic affections which implicate the solar plexus and its ganglia. Addison hinted at this explanation, and had the ganglia examined in one of his cases, but Schmidt of Amsterdam (1859) was the first to point out the possible connection and to record a case. Many corroborative observations have since been made, and this view has the support of the leading authorities. The changes which have been met with are very varied--fibroid thickening of the sheaths with atrophy of the nerve-tubes, fatty degeneration and wasting, excessive pigmentation of the cells, myxomatous degeneration of the stroma of the semilunar ganglia, and in a few instances there have been changes in the spinal cord. The chronic caseo-fibrous process in the capsules seems specially prone to involve contiguous tissues, and the close proximity of the semilunar ganglia renders them more liable to be attacked by the sclerotic process than in other affections in the vicinity, such as aneurism or tumors. According to this view, the symptoms of Addison's disease are to be regarded as the expression of a severe nutrition disturbance caused by a morbid state of the sympathetic ganglia, or, as Semmola puts it, the entire affection, beginning with disturbance of digestion and running its course with asthenia, low temperature, and marked debility in the oxidation and nutritive processes, is a pathological demonstration of the physiological functions of the sympathetic ganglia. The pigmentation may have its origin in changes in the trophic nerves, and the pronounced debility is the outcome of the disturbed chemical activity in the tissue-elements. It is, in short, a disease of the nervous system of organic life. Greenhow, who is a strong advocate for this view, also thinks that the circulatory, respiratory, and digestive symptoms may in part be due to implication of the pneumogastrics, the peripheral branches of which are frequently {946} involved in the thickened tissues about the capsules. The feeble action of the heart, small pulse, the nausea, vomiting, and the gasping respiration, may arise reflexly from irritation of these branches.

There are about thirty cases on record in which changes have been found in the sympathetic system. Riesel[220] compares the symptoms of Addison's disease with those which follow extirpation of the semilunar ganglia in animals. There is a paralysis of the vaso-motor nerves of the abdominal viscera, induced either by degeneration of the ganglia or reflexly by irritation, and consequently the blood accumulates in these parts, and there is a corresponding spanæmia of other organs, which explains the weak circulation, anæmia and the heart symptoms, fainting, and loss of energy. Recently this theory has been advocated by F. P. Henry.[221]

[Footnote 220: _Deutsches Archiv f. klin. Med._, Bd. vii.]

[Footnote 221: _Philada. Med. Times_, 1885, No. 452.]

The occasional occurrence of pigmentation of the skin in abdominal tuberculosis, retro-peritoneal tumors, cancer of pancreas, and in uterine irritation lends support to this view.

The weak points of this view are--the doubtful nature of the changes in the ganglia and the nerves in many cases. Mere increase of the normal pigment, slight fatty degeneration or swelling, so often recorded, should not be regarded as important, for they occur under a variety of conditions. Of positive swelling and redness of the ganglia, fibroid atrophy with destruction of nerve-cells and degeneration of the nerve-fibres, there can be no doubt, but about less marked alterations opinions will differ whether they are truly morbid or not. The fact that in certain well-observed cases the ganglia and nerves were found normal is hard to reconcile with a theory that the disease is an affection of the abdominal sympathetic. Burger states[222] that there are nine cases in which changes could not be found, and there are the recent cases of Huber,[223] Hebb,[224] Foa,[225] and Hadden.[226]

[Footnote 222: _Loc. cit._]

[Footnote 223: _Virchow's Archiv_, Bd. lxxxviii.]

[Footnote 224: _Lancet_, 1883.]

[Footnote 225: _Virchow-Hirsch_, 1879.]

[Footnote 226: _Brit. Med. Journ._, 1885, i.]

Hale White's recent observations,[227] as well as those of Saundby,[228] on the histological changes in the sympathetic clearly show that many of the changes which have been described in cases of Addison's disease are common in other affections, and have probably no direct association with the characteristic symptoms of the malady.

[Footnote 227: _Ibid._]

[Footnote 228: _Ibid._, 1883, i.]

Then, again, the absence of the characteristic symptoms of Addison's disease in so many cases in which the matting and implication of the nerves seems quite as great as in capsular disease. In aneurism of the abdominal aorta in the neighborhood of the coeliac axis the tissues in the vicinity may be indurated and cicatricial, the semilunar ganglia compressed, and the nerve-fibres atrophied, without bronzing and without the constitutional symptoms. Cases, too, of retro-peritoneal cancer rarely induce pigmentation, though in some instances--as in a case of Paget's (Geo.),[229] in which there was extensive lymphadenosis with involvement of the abdominal sympathetic--the bronzing may be intense. Induration about the pancreas and stomach in cancer has induced the same change, and recently Jürgens has recorded a case of aneurism[230] of the abdominal aorta with symptoms of Addison's disease and degeneration of the sympathetic nerves.

[Footnote 229: _Lancet_, 1879, i.]

[Footnote 230: _Berliner klin. Woch._, March, 1885.]

3d. That the essence of the disease is to be sought in some injurious agent--a poison introduced from without or possibly arising within the body as a result of faulty metabolism. There is not the slightest evidence for the existence of any such specific poison, which Averbeck, in his monograph, brings forward to account for the anæmia and the local disease in the capsules.

A more plausible theory, one closely related to the first one mentioned, is {947} that the blood is gradually poisoned by the retention of some material the destruction or alteration of which it is the function of the adrenals to effect. The disease is in this view analogous to chronic uræmia.

The relation of affections of the thyroid gland to myxoedema and cretinism, and the experimental production of these conditions by the removal of the thyroid, have widened our view of the importance of the ductless glands. It is interesting to note the analogy between myxoedema and Addison's disease. In both there are distinct histological changes in the tissues--in one an increase in the mucin, in the other an increase in the pigment--and in both marked nervous phenomena: mental dulness, a progressive dementia in myxoedema, a profound asthenia in Addison's disease. We regarded the thyroid as unimportant to life until the experience of surgeons and extirpation in monkeys by Horsley demonstrated that abolition of its function was followed by a serious train of symptoms; and perhaps the experimental removal of the suprarenals in monkeys--so much more closely allied to man than the animals hitherto experimented upon--may demonstrate that these little bodies are also not without their influence upon health.

Although the view of disturbed innervation consequent upon involvement of the abdominal sympathetic meets the case, theoretically, better than any other, and is at present widely held, yet there are signs of a return to the old view of Addison, which has been so consistently advocated by Wilks.[231] The data are not yet forthcoming for a final decision of the question, but it is possible that future investigations may establish the truth of Addison's view, that suspension of the function of the glands is the essential factor in the causation of the disease. That the sympathetic may be normal in genuine cases, and again that all the symptoms of the disease may occur without affection of the adrenals, are, however, facts difficult to harmonize with either theory.

[Footnote 231: Discussions at Pathological Society of London, session 1884-85.]

DIAGNOSIS.--It is of the first importance to remember that an increase in the pigment of the skin is by no means confined to Addison's disease, and, on the other hand, that the constitutional symptoms may be present without a trace of bronzing; and in their absence a positive diagnosis cannot be made. The conditions which give rise to a deepening of the color of the skin are--(1) Abdominal growths, tubercle, cancer, lymphoma. The patches of pigmentation in such cases are usually scattered, most often about the face and forehead. Occasionally the pigmentation may be deep and extensive, as in one case I saw of abdominal tuberculosis believed to be Addison's disease. Guéneau de Mussey[232] has called special attention to the frequency of this complication in chronic tuberculous peritonitis. Pigmentation may also be on the mucous surfaces in these cases. (2) Pregnancy, in which the discoloration is usually limited to the face, the so-called masque des femmes enceinte, and which, it is to be remembered, does not always disappear with the pregnancy. Chronic uterine disease, especially fibro-myoma, is a very common cause of patchy melasma. (3) Hepatic disease, which may induce definite pigmentation as well as the yellow-brown color of jaundice. Overworked persons of constipated habit and sluggish livers may present a patchy staining about the face and forehead. (4) The vagabond's discoloration, caused by the irritation of lice and dirt, may reach a high grade, and has been mistaken in several instances for the pigmentation of Addison's disease. (5) In rare instances there may be deep discoloration of the skin in connection with melanotic cancer--so deep and general that it has been confounded with melasma suprarenale. Wagner,[233] Wickham Legg,[234] and Falls[235] have {948} described remarkable cases of the kind. The occurrence of melano-sarcoma of the choroid or skin should render the diagnosis in these cases easy enough, but if deep seated a difficulty might readily occur.

[Footnote 232: _Étude sur la Pigmentation de la Face dans la Tuberculose abdominaire_, Paris, 1879.]

[Footnote 233: _Archiv der Heilkunde_, Bd. v.]

[Footnote 234: _Path. Soc. Trans._, London, vol. xxxv., 1884.]

[Footnote 235: _Philada. Med. Times_, 1883.]

It must be borne in mind that there are cases without bronzing, in which the profound asthenia and gastric symptoms are the prominent features, and, as mentioned above, these cases seem to run a very acute course. Indeed, they have been mistaken for typhus.

TREATMENT.--As cure is out of the question, the treatment is symptomatic and directed to the avoidance of certain perils associated with the disease. We have no means of checking the progress of the capsular affection. Pepper advises counter-irritation, and in the early stages the cautery may be used. Rest of mind and body must be enjoined, and the dangers of exertion and exhaustion set before the patient. Even in the early stage fatal syncope may occur.[236] The sense of weakness and tire at times becomes greatly aggravated, and may deepen into attacks of the most profound asthenia, during which the patient should be strictly confined to bed. It is in these paroxysms that special dangers occur. General tonic measures must be employed for the support of the strength. When there is anæmia, iron may be given, and Greenhow speaks of the good effects of the citrate or perchloride given with glycerin. Arsenic, strychnia, phosphorus, have been found useful in individual cases. Galvanism has been used, but without much benefit. The paroxysms of profound asthenia call for stimulants--wine, brandy, and ammonia. The gastro-intestinal symptoms require the most careful treatment. Bismuth, hydrocyanic acid, creasote, soda-water, ice, and champagne will be found useful in allaying the vomiting and irritability of stomach, but in some cases these symptoms prove most intractable. Purgative medicines must be given with very great caution on account of the liability to profuse diarrhoea and serious collapse. The constipation, which may be obstinate, is best treated by mild enemata. The greatest care should be exercised in the diet, which should be plain and easily digested. Though the vomiting is not directly dependent upon the state of the stomach, yet indigestible food and irregularities in eating may induce the gastric attacks. When there is much irritability of the stomach the patients seem to do best on a strict milk diet.

[Footnote 236: Quite recently an active professional man consulted me for bronzing of the face and hands, and he had had one fainting spell. With the concurrence of Pepper he was advised to give up business for a year and live quietly abroad. His general condition was so good and the pigmentation so limited that there seemed just a possibility that it was not Addison's disease. He went home and prepared to follow out our advice, but a second sudden attack of syncope proved fatal.]

{949} OTHER DISEASES OF SUPRARENAL BODIES.

ANOMALIES.--There may be four glands, two on each side. More commonly, there are small supplementary organs--glandulæ succenturiatæ--situated in the neighborhood, seldom reaching the size of a pea. Grawitz has recently shown that many of the small adenomas of the kidney are in reality minute portions of suprarenal tissue which have become included in the course of the development of these organs. Fusion of the two glands has been observed (Klebs). They may be absent.[237]

[Footnote 237: Defect of adrenals is very rare. There are not a few observations in which it is stated that the right gland was absent. Now, if the examination is not made with care, and particularly if the liver is removed first, the right gland may be taken away with it closely lodged in the fossa suprarenalis, and so escape observation. Time and again have I directed the attention of the student making the autopsy to the right adrenal on the under surface of the liver.]

It is curious how liable the suprarenals are to anomalies in position or form in connection with defective development of the brain and cord. In anencephalous monsters the glands may be absent or very small.[238] In one instance I found them normal in size, but they were below, not above, the kidneys.

[Footnote 238: Lomer, _Virchow's Archiv_, Bd. xc.; Weigert, _ibid._, Bd. c.]

ATROPHY.--Extreme wasting may be met with as an accidental circumstance: there may be only a trace of gland-tissue left. Several such specimens have been found in association with Addison's disease. There may be an interstitial growth of fibrous tissue, cirrhosis, with shrinking of the organ. More often the glands are larger and harder in connection with the cyanotic induration of heart disease. It is stated by some writers that the adrenals of the negro are larger than those of the European races--a statement which I have not been able to confirm in several observations.

APOPLEXY.--In the new-born and young children congestion is not infrequent. Hemorrhage into the central medullary substance is by no means uncommon, either on one side or bilateral. The amount may be considerable, and the glands greatly distended, forming large tumors.

INFLAMMATION.--Suppuration is rare except in connection with the caseo-fibrous change already described as specially associated with Addison's disease. Abscesses in the vicinity, as from caries of the spine, may involve one or both capsules.

DEGENERATIONS.--Fatty changes are very common, particularly in the cortical layer, which then has a light-yellow color, instead of the normal dark gray-red. Yellow oil-drops appear to be normal constituents of the cells of the cortex.

Amyloid degeneration may occur, but only in connection with similar changes in other organs. The glands are enlarged, very firm, and the medullary part translucent. The iodine reaction shows it to be limited to the fibrous septa and blood-vessels.

The brown pigment of the intermediate zone, zona reticularis, may be greatly increased. Normally in man, the amount is very variable, and the deeper color may be due to congestion of the blood-vessels.

CYSTS with serous or hemorrhagic contents are occasionally found, chiefly in the cortical part. They may be multiple. Hydatid cysts have been met with.

TUMORS are not very uncommon. Cancer may attack them primarily, but more often they are involved in secondary growths after carcinoma of stomach or other organs. They are not infrequently affected in cancer of the kidneys {950} by direct extension of the growth. Sarcomas are also not uncommon, and may form large masses the size of the foetal head. They may be melanotic.

These varied pathological conditions are not usually associated with any special or distinctive symptoms, and in the great majority of cases have been unsuspected during life. The organs may be totally destroyed without inducing any of the phenomena of Addison's disease. In a few cases, however, bronzing of the skin has been met with.

{951}

DISEASES OF THE SPLEEN.

BY I. E. ATKINSON, M.D.

Morbid processes affecting the spleen have been and remain involved in great obscurity. Older writers, who were accustomed to reach their conclusions in great measure through the observation of symptoms alone, were obliged in the absence of anything like correct knowledge of anatomy, physiology, and pathology to supply from the imagination most of their theories of disease. Untrammelled by the bonds of accurate investigation and ignorant of pathological anatomy, they found no difficulty in ascribing to various parts and organs peculiar groups of symptoms, both physical and moral; and for a number of these the spleen was held responsible. We now know that many of the symptoms thus supposed to indicate splenic disease depend upon alterations in other parts of the body, and may be observed in persons possessing perfectly healthy spleens. But while we have learned that symptoms formerly supposed to depend upon splenic disorder may, in reality, have nothing to do with this organ, we still remain ignorant of many of the real symptoms of splenic disease, as well as of many of the morbid conditions that induce them. Such knowledge as we have, however, is based upon comparisons of symptomatology with dead-house revelations and the experience of the laboratory, and, while as yet imperfect, cannot fail to increase under modern methods of research.

In order to begin the study of diseases of the spleen in an intelligent manner it is manifestly necessary to have some settled ideas regarding its anatomy and physiology. No apology is needed, therefore, for the brief anatomical and physiological descriptions that follow.

The spleen is the largest of the ductless glands, and is situated in the left hypochondriac region. It is of a dark slate or bluish-gray color, and often of wrinkled appearance. It is of soft, friable structure. It rests between the stomach, diaphragm, and left kidney, and in form resembles a flattened oval. It extends from the level of the eleventh rib, beginning one or two centimeters distant from the vertebral column, downward and forward to a position about four centimeters from the point of the eleventh rib (Lushka). It is separated from the ninth, tenth, and eleventh ribs by the diaphragm. It presents two surfaces--one external and convex, facing the diaphragm; the other internal and concave, applied to the cardiac end of the stomach. The hilum divides the internal portion into two parts by a deep fissure, which marks the line of attachment of the gastro-splenic omentum. The larger and anterior part is bound to the fundus of the stomach by delicate areolar tissue, and the posterior and smaller portion to the left pillar of the diaphragm and the left suprarenal capsule. The upper portion is connected with the diaphragm by peritoneum forming a suspensory ligament. The bottom of the hilum is perforated by a number of openings for the transmission of blood-vessels, nerves, and lymphatics. The anterior border of the organ is notched and thinner than the posterior border. The pointed lower end touches the splenic flexure of the transverse colon and rests upon the costo-colic ligament. {952} The spleen varies in size and weight within wide limits. Its average weight in adults is 250 grams, its length from 11 to 13 centimeters, and its thickness from 4 to 6 centimeters (Orth). Its volume is from 150 to 180 cubic centimeters. According to Gray, the proportionate weight of this organ to that of the whole body varies from 1:320 to 1:400, gradually diminishing until old age, when the proportion becomes as 1:700.

In the vicinity of the spleen are often found a number of small bodies similar to it in structure. These are known as accessory spleens, and are usually situated in the gastro-splenic or in the greater omentum. The attachments of the viscus are not very close, and much variation in size and position is possible.

Except at the hilum the peritoneum forms everywhere one of the coverings of the spleen. Its peculiar sheath or capsule is composed of fibro-elastic tissue of a whitish color, prolongations of which extend into the substance of the organ and form the trabeculæ that constitute its supporting framework and sheaths for blood-vessels and nerves. A close meshwork is thus created in which are contained the splenic vessels and pulp. This fibrous coat and these trabeculæ contain involuntary muscular fibres. These, with the elastic fibres, provide for the changes in size that the organ undergoes. When incised, the normal spleen presents a reddish-brown color, and its substance may be readily broken down with the finger into a pulp. This pulp consists of a mass of branched intercommunicating connective-tissue corpuscles of different sizes, within the substance of which remains of red blood-corpuscles may often be detected. The interstices of these cells are filled with blood. The very large splenic artery enters the spleen by numerous branches, ramifying within the trabecular sheaths and terminating in pencils of minute size.

The external coats of the smaller arteries are converted into lymphoid tissue, which, suddenly expanding here and there, forms the bodies known as the Malpighian follicles, which are supplied with capillary vessels, and which may often be distinguished by the naked eye as points of whitish color, sometimes attaining the size of pinheads. These small arteries end in capillaries, which, according to Müller, gradually lose their cylindrical character and emerge into a system of connective-tissue corpuscles, inosculating with the corpuscles of the splenic pulp in such a manner that the blood passes into the pulp-tissue freely, and is gradually brought to the veins by the transition of this tissue into that of the blood-vascular system. The splenic lymphatics originate in the arterial sheaths and in the trabeculæ. In the former case they accompany the blood-vessels; in the latter, they communicate with a superficial network in the corpuscle. All join at the hilum and enter the neighboring lymphatic glands. The splenic nerves are from the right and left semi-lunar ganglions and right pneumogastric nerve. They accompany the branches of the splenic artery, and have been traced deeply into the tissue of the organ.

It is perfectly established that under normal conditions the volume of the spleen may vary considerably, and especially during the act of digestion, and that this does not occur through simple engorgement of the vessels. The very important experiments of Roy show that, in cats and dogs at least, the splenic circulation does not depend upon the ordinary blood-pressure, but is carried on "chiefly, if not exclusively, by a rhythmic contraction of the muscles contained in the capsule and trabeculæ of the organ."[1] This rhythmic contraction and expansion Roy observed to occur with great regularity at the rate of about sixty contractions an hour, with extremes of rapidity of rhythm of forty-six seconds for the most rapid and two minutes three seconds for the slowest. He also observed that stimulation of the central end {953} of a cut sensory nerve, or of the medulla oblongata, or of the peripheral ends of both splanchnics and both vagi, causes a rapid contraction of the spleen. Unsatisfactory as is our knowledge of splenic physiology and of its exact relations to the maintenance of life (for that the spleen is not the seat of a peculiar and exclusive function has been demonstrated by the survival of individuals after extirpation of the organ), at present certain theories of its nature find pretty general acceptance. Thus, it is considered that in the lymphoid tissue of the blood-vessels and Malpighian corpuscles leucocytes are produced--that the cells of the splenic pulp appear to take red blood-corpuscles into their interior, where their disintegration takes place. There are not sufficient grounds for believing that in the spleen red blood-corpuscles are formed. Recent observations of Tizzoni, Crédé, and Zesas have led them to the conclusion that they are made in the spleen; but Bizzozero and others deny that this occurs except after serious hemorrhage.

[Footnote 1: _Journal of Physiology_, vol. iii., 3 and 4, p. 203.]

It is impossible to detect by palpation any part of a healthy spleen. Its area may be approximately defined by percussion alone, though even by this method it is not always easy to determine its position and size. Loomis advises that the patient be placed upon his right side in order to facilitate the examination. The anterior border of the spleen is then "readily determined by the tympanitic resonance of the stomach and intestines. Inferiorly, where the organ comes into contact with the kidney, it is difficult, and often impossible, to determine its boundary. Its superior border corresponds to the line which marks the change from flatness to pulmonary resonance." The vagueness of these directions is necessitated by the difficulties of the subject, the splenic outlines being liable to frequent variations. Schuster and Mosler give excellent reasons for prosecuting the investigation with the patient in the right semi-supine position.

Acute Congestion of the Spleen.

Except within the physiological limits already referred to, acute congestion of the spleen never occurs as a primary process. Under pathological conditions it is known to take place under a great variety of circumstances, principally, however, in connection with those states of the system in which disease is supposed to depend upon some specific principle or germ. To a minor extent it is probable that splenic congestion accompanies nearly all febrile conditions, and from the border-lands of health to that highest and most intense degree of hyperæmia by which the organ acquires a volume and prominence that have caused it to be designated as acute splenic tumor, all gradations may be observed, though in many instances these may be so slight as to be incapable of recognition clinically, and are only brought to our knowledge through necroscopic examination. The congestion becomes most marked in the course of the acute specific fevers. In typhus and typhoid fevers, in small-pox, scarlatina, diphtheria, in epidemic cerebro-spinal meningitis, in acute tuberculosis, in erysipelas, puerperal fever, in conditions of blood-poisoning and in malarial fevers, more especially those of more severe type, it reaches its highest development. According to Friedreich, a form of pneumonia (differing from ordinary croupous pneumonia in its serpiginous course), acute coryza, and acute pharyngitis and tonsillitis are accompanied by enlargement of the spleen in consequence of the septic nature of these disorders. During the fever of secondary syphilis a splenic enlargement purely hyperæmic in character may sometimes be detected. Similar conditions are occasionally observed in a number of other affections. This tendency of the spleen to active congestion is to be accounted for by its peculiar anatomical structure, whereby unusual facilities for hyperæmia are {954} afforded, more especially in the infective fevers, in the course of which the organic germs which are supposed to constitute their essential principles collect in the pulp, and by their accumulation and multiplication serve to excite a more or less intense determination of blood to the part, the organisms themselves being taken up by the leucocytes and connective-tissue corpuscles composing the pulp. We can thus account for the multitudes of these organisms to be found in the splenic pulp after various infective disorders, as in relapsing fever as observed by Ponfick, in pyæmia by Birch-Hirschfeld, and in splenic fever of animals by various observers. The less intense degrees of congestion occurring during the various specific fevers and in many simple febrile disturbances are usually so slight as not to attract attention. When the hyperæmia has been unduly prolonged, as more especially occurs as a result of chronic malarial poisoning, leucocythæmia, pseudo-leucocythæmia, or Hodgkin's disease, there is a well-pronounced tendency toward permanent structural changes and the development of hypertrophy.

SYMPTOMATOLOGY.--Milder degrees of congestion do not, generally, reveal their existence by symptoms, and those of more pronounced character give for the most part signs that are vague and nearly obscured by the more prominent features of the pathological processes that occasion or accompany the splenic changes. It may happen that acute splenic tumor of considerable size may be quite painless. It has been objected, indeed, that when pain accompanies splenic enlargements it is not attributable to any sensibility of the spleen itself, but to the participation of the investing peritoneum in the morbid action or to the dragging of the enlarged organ upon the parts with which it is connected (Mosler). Patients, however, will often complain of a dull, aching pain and a sensation of weight in the left hypochondrium. Occasionally, this pain may be severe and lancinating or may extend to the shoulder. Headache and various digestive disorders--anorexia, vomiting, flatulence, and diarrhoea--may prove distressing accompaniments. Other symptoms, such as melæna, voracious appetite, vertigo, extreme anæmia with its various concomitants, etc., belong rather to conditions of protracted congestion where new formation and true hypertrophy have been developed.

It is evident that it will often be extremely difficult, and sometimes even impossible, to determine the extent to which symptoms are occasioned by the splenic congestion or by the general affection to which it owes its origin. Mosler declares that he is nearly always able to detect during the cold stage of intermittent fever a peculiar murmur over the splenic region and upward and downward in the abdominal region, which he attributes to the contraction of the splenic artery. This murmur he has not been able to perceive in chronic splenic tumors.[2]

[Footnote 2: _Ziemssen's Cyclop._, vol. viii. p. 468.]

The normal splenic area can only be defined by percussion, and congestion to a not insignificant extent may occur without revealing itself by other symptoms than increase of the extent of percussion dulness. When the organ projects beyond the margin of the ribs and can be felt by the fingers of the examiner, it is enlarged, unless the patient is the subject of displaced or of wandering spleen. But whether the enlargement be due to hyperæmia simply or to hypertrophy can only be determined by a consideration of all the concomitant circumstances. Unless under the influence of chronic irritation or as a result of mechanical hyperæmia, congestions of the spleen are commonly of sudden development and of transitory duration. In ordinary inflammations, such as pleurisy, etc., the degree of congestion is so slight as to be unnoticeable; but as an epiphenomenon of the various specific fevers the enlargement occurs rapidly and acquires a prominent interest in many cases. Acute splenic tumor, for example, is almost of constant occurrence during the course of typhoid fever, and, according to Friedreich, its presence may {955} be ascertained some days before the specific symptoms of the disease have declared themselves. A similar early development has been claimed for it in diphtheria and other affections. The congested spleen of typhoid fever and of relapsing fever, however, differs from that of most other acute disorders in returning to its normal dimensions much more slowly; and it is important to remember that until the splenic tumor has disappeared there is reason to believe the danger of relapse still imminent. In most cases the enlargement disappears pari passu with the disorder that occasioned it. In malarial fevers and in septic diseases the splenic tumor may acquire excessive dimensions. Acute splenic tumor, however, never attains the dimensions often encountered in chronic congestion and hypertrophy.

PATHOLOGY AND PATHOLOGICAL ANATOMY.--Simple splenic congestion presents at first no anatomical features differing from purely physiological hyperæmia. There is simply more blood in the dilated vessels and vascular spaces, and consequently in the viscus, than is usual. Very soon, however, there is hyperplasia of the cells of the pulp. Enlargement, tension of the capsule, and diminished consistency of the spleen appear. The color will depend upon the condition of the capsule, being most dark and blue when this is thinnest. In high grades of congestion the parenchyma upon section will be found distended and semi-diffluent, and after acute malarial fever (pernicious remittent fever), the organ may resemble a bag of half-liquid pulp. Softening in varying degree may be found after acute congestion from whatever cause. In the congestions due to some infective processes at least additional factors are introduced, although as yet definite knowledge of their exact pathogenetic influence has not been attained. The observations connecting minute organisms with the origin of these affections have been so elaborate, so carefully and conscientiously reported, extend over such wide and varied fields, that it is difficult to refuse to place reliance in them. It seems that in a number of affections the presence of these microscopic organisms is constant and essential, and that the splenic congestion that accompanies them is a direct result of their presence in the spleen itself. The micro-organisms will be found infesting the cells of the pulp, and, so far as we have definite knowledge, they show peculiar characteristics according to the particular infectious disease to which the patient succumbed. While the conditions in acute splenic tumor are identical with those of inflammation, and in the affections properly designated as septic, should the life of the patient have been sufficiently prolonged, may be found to have led to the formation of embolic centres with hemorrhagic infarctions and abscess, in infectious diseases not septic they do not prove equal to the production of suppuration. Where the action is acute, resolution will speedily follow the subsidence of the febrile process. But in prolonged hyperæmia new formation will be developed, and the enormous collection of leucocytes will give a reddish-gray color to the organ. This change will also be sometimes observed in the spleens of those in whom the infectious diseases have run a more protracted course.

DIAGNOSIS.--Acute splenic tumor, if at all pronounced, may usually be diagnosticated without much difficulty. The development of an enlargement in the splenic region, with pain and tenderness to pressure, during the course of any acute febrile disease will nearly always indicate splenic hyperæmia. It may sometimes be difficult to determine whether the tumor may not have existed prior to the invasion of the present malady. In such cases one must have recourse to the previous history of the patient, or, failing in this, must observe the behavior of the tumor upon the subsidence of the general affection.

PROGNOSIS.--The prognosis of acute congestion and acute splenic tumor will depend rather upon the exciting cause. When of simple origin it is of but insignificant importance. Even in specific fevers the spleen will in most {956} instances return to its normal volume upon the establishment of convalescence. Rupture of the spleen has been known to occur in congestion from severe malarial fever, but this is a most rare accident in the absence of traumatic influences. The congestion may become chronic, and frequently does become so, in cases where the stimulus continues to exert an influence upon the spleen, as is done in chronic malarial poisoning.

TREATMENT.--The transitory hyperæmia of a brief malarial attack or of any ordinary febrile seizure will disappear with its exciting cause, and will require no special treatment. For the acute congestions of most specific fevers but little is to be done except through attention to the general condition: it is only when pain and discomfort in the splenic region are sufficient to attract the attention of the patient that measures for the relief of the congestion will be necessary. In that most common exciting cause of it, malarial fever, patients will often complain bitterly of the pain in the left hypochondrium for some time after the febrile attack has been overcome. In such cases it may be pretty safely concluded that the poisonous influence of the malaria has not been entirely overcome, and the proper employment of quinine and other derivatives of Peruvian bark, and bitter tonics, will undoubtedly prove most serviceable. In very many cases benefit may be derived from local applications. Experiment has clearly shown that the stimulation of the splenic nerves is capable of effecting a notable reduction in the bulk of the organ. Clinical experience gives similar proofs, and cold effusions, evaporating lotions, etc. will sometimes secure prompt unloading of the spleen; indeed, Mosler considers that there is danger in treating the acute splenic tumor of typhus fever of inducing unfavorable changes by the too sudden reduction of its bulk by local applications. The use of stimulating applications to the splenic region will also prove beneficial in many cases. Among the most valuable of these will be found the tincture of iodine.

Chronic Congestion and Enlargement of the Spleen.

Within narrow limits there may be simple increase in the size of the spleen from hyperæmia, without alteration of the relations between its structural parts. The common results, however, of hyperæmia of long standing are overgrowth of the elements of the reticulum, with new formation of connective tissue and hyperplasia of the pulp-tissue. This condition of chronic enlargement or hypertrophy of the spleen may develop as a result of chronic active hyperæmia or through passive or mechanical engorgement of the portal system. Chronic active hyperæmia of the spleen is in much the greater number of instances caused by chronic malarial poisoning. It also occurs as a cause or a result of leucocythæmia and of pseudo-leucocythæmia or Hodgkin's disease, and is always associated with more or less true hypertrophy of the structural elements of the organ. Enlargement from the above-mentioned causes constitutes the vast majority of those abnormalities generally designated as chronic splenic tumor. In persons living in malarious countries, and subjected for prolonged periods to the intoxicating influence, the peculiar splenic enlargement tends to become chronic. After the earlier attacks the spleen returns more or less promptly to its normal dimensions. Usually it is only after repeated attacks of intermittent or remittent fevers, and often only after exposure to the malarious influence for years, that the splenic tumor becomes established as a permanent disorder and assumes the characteristics that have secured for it the popular denomination ague-cake. Persons living in the localities referred to may develop this enlargement without ever having had unequivocal attacks of malarial fever. They will betray, however, the effects of the poisoning by malarial neuralgias and {957} neuroses or by a well-marked periodicity in the course of simple maladies, or they will exhibit its effects by the peculiar facies and by general paludal cachexia. Under these conditions the splenic enlargement sometimes attains enormous proportions.

Splenic enlargement of considerable extent may result from mechanical hyperæmia of the portal circulation from cirrhosis of the liver. It is, however, certainly not a necessary consequence of cirrhosis, since this may exist to a pronounced degree and yet the spleen remain normal--a condition that is probably favored by extensive distribution of muscular and elastic fibres to the viscus, that enable it to a great extent to regulate its own circulation. On the other hand, the spleen may be atrophied by a fibrotic contraction of its trabeculæ, the result of long-standing hyperplasia. Chronic engorgement and enlargement of the spleen may also result from mechanical obstruction to the systemic venous circulation, especially that due to insufficiency of the mitral valve, whereby obstruction to the portal circulation arises secondarily. (The ulcerative endocarditis of septic origin is associated with splenic congestion, which is, however, always of the acute active variety, and complicated for the most part with embolic abscess and hemorrhagic infarction.)

SYMPTOMATOLOGY.--Long-continued or frequently-recurring attacks of splenic hyperæmia, occurring under the stimulus of chronic malarial poisoning or of leucocythæmia or pseudo-leucocythæmia, will ultimately induce those structural changes that result in new formation. Enlargements from the two latter diseases will be more appropriately considered elsewhere. After repeated attacks of remittent or intermittent fever or other forms of malarial intoxication the symptoms of acute will gradually merge into those of chronic congestion. They will usually prevail to a more intense degree. The dragging weight of the tumor will excite pain, and may render rest upon the right side too uncomfortable to be indulged in. Hemorrhage from the stomach and bowels may occur, and at times will be excessive. The patient may be reduced to an extreme degree by the profuse and repeated losses of blood. In the intervals of the malarial attacks the temperature will be unelevated, and the pulse may be slow and irregular, though oftener feeble and rapid. All the symptoms will be, however, commingled with those from other causes. Those of malarial cachexia will sometimes be very pronounced. The pale, sallow complexion, the pallid lips, the extreme anæmia and generally unhealthy aspect, and the general symptoms accompanying such states, the history of miasmatic fevers, of characteristic neuralgias, etc., will generally be present. Oedema may be observed, but will usually be hydræmic in origin. Anomalous symptoms due to the systemic condition will be often developed when the enlargement arises from other than malarial causes.

Under the influence of the latter cause the spleen may acquire many times its normal dimensions, and may easily be felt below the border of the ribs, where its irregularly curving and notched border will serve to identify it. The tumor sometimes becomes so large that it reveals its presence by causing a bulging and asymmetry appreciable by the patient. Here, however, congestion will have been supplanted by hypertrophy. The tumor may vary greatly in size. It may fill the left part of the abdominal cavity, reaching to the pubes and distending the belly-wall with its dense enlargement, dull upon percussion, and perhaps moving within narrow limits under the hand of the examiner. This tumor may attain a size and weight many times greater than the normal. Hypertrophy once established, it may remain more or less pronounced for years, directly occasioning unimportant symptoms. It is difficult to determine the exact influence exerted by these tumors upon the duration of life.

PATHOLOGICAL ANATOMY.--In simple hypertrophy there is both hyperplasia of the pulp and of the trabecular connective tissue. The spleen is {958} enlarged, sometimes to an extreme degree, equalling fifteen or sixteen times its normal weight.[3] Such enlargement is not observed in any other form of splenic disorder, excepting in some rare cases of leucocythæmia and tumor. Its density is also increased. The capsule is thickened, and adhesions to the surrounding parts may be quite intimate. The color of the surface is darker than normal. Upon section the structure appears dense, smooth, of a dark color (from deposit of pigment), and showing to the naked eye great increase of the trabecular tissue. The pigmentation more especially observed in malarial intoxication occurs in the intervascular cords of the pulp (Rindfleisch), where it can be seen as black, flaky masses of hæmatin (the origin of melanæmia). According to Friedreich,[4] there may be a circumscribed splenic hypertrophy, consisting of little points of granulation imbedded in the pulp. In ordinary diffuse hypertrophy all the elements are involved, though the trabeculæ show the greatest increase and encroach more or less upon the pulp. The Malpighian corpuscles may show little or no enlargement. The processes are indistinguishable from those of chronic inflammation. In hypertrophy from obstructed portal circulation the organ will be dark red and very full of blood. It sometimes happens that obstructive hypertrophy terminates in fibrotic contraction, when the connective tissue will be found to have almost completely crowded out the pulp.

[Footnote 3: Hertz, _Ziemssen's Cyc._, vol. ii.]

[Footnote 4: _Virchow's Archiv_, xxiii., 1865; _Ziemssen's Cyc._, viii., Mosler.]

DIAGNOSIS.--Decided enlargement will usually be recognized with but little difficulty. A tumor in the left hypochondrium, occupying and transgressing the normal splenic boundaries, will probably be of splenic origin. Occasionally enlargement may be simulated by a spleen of normal size displaced downward by intra-thoracic growths or effusions or by that remarkable abnormality known as wandering spleen. The course of the primary affection in the one case, and the free movability of the organ in the other, will suffice generally to guard against error. Rarely, the tumor may be due to cancer of the stomach, enlargement of the left kidney or of the left lobe of the liver, omental tumors, fecal accumulations in the colon, or ovarian tumors. The concomitant symptoms will suffice to distinguish cancer of the cardiac end of the stomach. Percussion will reveal the presence of subjacent gases, and palpation will detect the greater hardness of the gastric tumor. Enlargement of the left kidney may be due to cancer, abscess, or other causes, and may simulate splenic hypertrophy. The renal tumor may be traced farther backward, and will not present the characteristic outline of the spleen. The clinical history and symptoms will here, again, prevent error. Omental tumor is usually separated from the splenic region by an area of resonance. Enlarged liver may be traced toward the right side of the body, becoming more noticeable as the spleen is receded from. Fecal accumulation may closely resemble splenic tumor, as it does other abdominal enlargements. The doughy consistency of enlarged spleen may be like that of the fecal mass, but one may often permanently alter the shape of the latter by the pressure of the fingers, and in any case doubt may be dispelled by the use of purgatives. Ovarian tumors may be traced into the pelvis, as may also, for the most part, fibro-cystic and fibroid tumors of the uterus and its appendages.

On the other hand, recognition of splenic tumors may be prevented by gaseous distension of the stomach and bowels, by abdominal dropsy, diffuse or encysted, by fecal distension of the colon, and may, indeed, be impossible until these conditions have been remedied. Enlargement of the spleen from simple hyperplasia must also be distinguished from other forms of splenic enlargement--from splenitis, from lardaceous degeneration, from tumors, from leukæmia and pseudo-leukæmia, from syphilitic and tuberculous {959} spleen, etc. In such cases the diagnosis will rather depend upon concomitant symptoms than upon the physical characters of the enlarged organ. Percussion and palpation will not seldom enable one to determine the presence of tumor (cancer), hydatids, etc. Pressure will often serve to elicit expressions of great tenderness in splenitis; enlargements with fluid contents will be revealed by fluctuation. In the greater number of cases where the enlargement is evident, but is without distinguishing characteristics, the general condition of the patient and the history of his illness will disclose its true nature. Lardaceous degeneration will have been anteceded by prolonged suppuration, by tubercle, by scrofula, or by syphilis, and will generally be associated with the same processes in other parts. Syphilitic disease may be indicated by the history of the patient, though in this case, of course, lardaceous degeneration could only with difficulty be excluded. Tubercle, rarely giving rise to an appreciable tumor, can only be conjecturally diagnosticated from the history and general condition of the patient. The condition of the blood and of the lymphatic system in leukæmia and pseudo-leukæmia will suffice to determine the nature of the splenic enlargement. The ague-cake of chronic malarial poisoning is usually accompanied by a degree of cachexia, as is shown in the earthy pallor of the complexion. This is often sufficient to enable one to discriminate between several forms of enlargement, for it differs from the intense pallor of leukæmia by its sallow hue, and is not at all like the hue of the complexion in lardaceous disease. The cancerous cachexia, it is true, may closely resemble it, but here the history and symptoms assist in avoiding mistakes.

PROGNOSIS.--When the hyperplastic processes have amounted to true connective-tissue formation, a complete return to normal conditions will not occur after the removal of the stimulus. The permanence of the enlargement will be proportionate to the extent of organization of the hyperplastic elements. In ague-cake some reduction in size will follow the exhaustion of the malarial influence, though the spleen probably never ceases to be appreciable as a distinct enlargement. At the same time, the enlarged organ may not, of itself, exert any specially unfavorable effect upon its bearer. Not a few persons will live for years with it, and eventually die from other causes. It may be assumed, however, that the presence of ague-cake is indicative of profound malarial cachexia, by which the powers of life are much less resistant to unfavorable influences. It may be said, in a general way, that the larger the spleen the less favorable is the prognosis. It should be remembered that a considerable proportion of persons suffering from leucocythæmia have also suffered from chronic malarial poisoning, and that the enlarged spleen of this affection may possibly have begun its morbid course under the influence of malaria.

TREATMENT.--In passive congestion relief is often secured through the use of remedies that diminish portal engorgement or enable the heart to find compensation for a damaged mitral valve--conditions in which the splenic disorder is really an unimportant concomitant. In the enlargement that has for its cause chronic malarial intoxication cinchona and its alkaloids are preferable to all other remedies, not only in arresting the new growth otherwise progressive under the stimulus of the poison, but by neutralizing the latter and facilitating the absorption of the hyperplastic elements that have not already become converted into more highly-developed tissue. To effect these objects the agents must be given in fair doses (twenty grains of sulphate of quinia daily) until the malarial cachexia shall have been overcome--until the bulk of the enlarged spleen shall have been reduced to the smallest possible proportions. To bring about the desired result the treatment may have to be continued during several months, occasionally suspended upon the supervention of symptoms of cinchonism. A drug of deserved repute {960} (probably through its anti-malarial influence) is arsenic. This should be given for protracted periods. Many remedies possessing anti-malarial properties have also been recommended and employed in these conditions. Eucalyptus and eucalyptol have recently been used with promising results, though the sanguine expectations of some will hardly be realized. Iron, preferably as a sulphate or as the tincture of the chloride, is invaluable in correcting the profound anæmia always present in these cases, though its influence in reducing the splenic bulk immediately is, at best, doubtful. Remedies competent to reduce hepatic and portal engorgement will often prove beneficial. Salines and vegetable cathartics may more especially be employed, but the use of mercurials, except for occasional administration, is almost universally condemned as productive of evil consequences.

Local Treatment.--The systematic application of cold by effusion or by ice-bags will at times undoubtedly reduce the size of an enlarged spleen. Alleviation will often be afforded by solutions of nitric acid to the splenic region, and counter-irritants are of occasional service, either by means of the tincture of iodine persistently employed or by blistering fluids or plasters. These, however, should be used with great caution in debilitated subjects, as gangrene has been known to follow their application. Mosler thinks that the practice of injecting tincture of iodine, carbolic acid, etc. into the substance of the spleen is sufficiently promising to justify further experiment. The continuous electric current and electrolysis have also been recently recommended as of advantage in reducing the splenic bulk. In cases of excessive enlargement, where accompanying or consequent cachexia threatens to end in death, extirpation of the spleen has been advised and practised. While the removal of the leucocythæmic spleen is so constantly followed by death that the operation cannot be considered justifiable, it seems that the spleen enlarged from other causes may sometimes be removed with safety. In the _Lancet_ of Feb. 11, 1882, Herbert Collier tabulates all (until then) known cases of removal of the spleen for disease, 29 in number: 16 of these operations were upon leukæmic subjects, and had a fatal termination; 8 of the remaining cases recovered. Crédé[5] concludes from an analysis of 30 cases of extirpation of splenic tumor that the adult spleen may be removed without detriment; that its removal causes temporary derangement of the blood-making function; and that this is compensated for by activity of the thyroid body and red marrow of the bones. As bearing further upon the question of the practicability of splenectomy, should surgical art succeed in reducing the dangers immediately dependent upon the operation, are the highly interesting experiments of Tizzoni[6] and Griffini,[7] wherein extirpation of the spleen in dogs was followed by reproduction of true splenic tissue.

[Footnote 5: _Centralbl. f. d. med. Wissensch._, June 23, 1883.]

[Footnote 6: _Arch. Ital. de Biologie_, 1883, iii. 2, and i. 1.]

[Footnote 7: _Ibid._, 1883, iii. 2.]

In chronic congestion and enlargement of the spleen from malarial poisoning the removal of the patient to a non-malarious locality will always materially assist in the recovery of health.

Hemorrhagic Infarction of the Spleen.

The investigations of Virchow, and more recently of Cohnheim, into the pathogenesis and pathology of hemorrhagic infarction have afforded an easily intelligible explanation of the causes of the frequency of this morbid process in the spleen. A moment's reference to the anatomy of the splenic blood-vessels will show that the conditions most favorable to the production of hemorrhagic infarction in the presence of an exciting cause are here afforded. Instead of terminating in a capillary network with free and abundant {961} anastomoses, the splenic arteries end in fine pencils, opening, not into capillaries leading to venous radicles, but into vascular spaces in which traces of both afferent and efferent blood-vessels gradually become effaced. These arterioles have no other vascular communications than with the small arteries, the terminal extremities of which they are. This arrangement may be very perfectly demonstrated in injected spleens where the material has been imperfectly driven through the vascular system of the organ, so that wedge-shaped areas of successful injection become sharply defined. This distribution of the blood-vessels renders the area supplied by each almost completely dependent upon it for efficient nutrition, and almost certain to become structurally altered if its lumen should become in any manner obstructed. To this arrangement of the arteries and arterioles upon one side is added, upon the other, a valveless condition of the splenic veins, whereby regurgitation may readily occur. We have here, therefore, evidently conditions most favorable to the development of hemorrhagic infarction.

The process through which hemorrhagic infarction occurs has been definitely observed by Cohnheim. The area of the distribution of the obstructed artery or arteriole, receiving no blood-supply from anastomosing branches, undergoes disintegration. The walls of the blood-vessels as far as the nearest communicating branch participate in the process of disorganization. After a while a backward movement of the blood-current begins in the nearest still pervious vessels, and is continued into the obstructed vessels, through whose disintegrating walls the blood escapes and the hemorrhagic infarction is established. The future course of the infarct depends almost entirely upon the nature of the causes that brought it about.

In the spleen, as in other organs, the causes of hemorrhagic infarction may be widely different, though an essential condition of each is that it be competent to produce plugging of the blood-vessel. The most important cause is probably ulcerative endocarditis, in the course of which minute fragments of the endocardium or of the vegetations that have formed upon it, especially of the neighborhood of the valves, in consequence of inflammation, constitute the emboli. The plugs largely consist of fibrinous matter enveloping colonies of micrococci, or they may be derived from detached portions of thrombi, or from solid particles that may have in any way gained access to the circulatory current, as from endarteritis, from atheroma, primary emboli in the pulmonary circulation, etc.

Hemorrhagic infarction has also been described by Ponfick[8] as occurring in relapsing fever and originating in the veins, and not to be referred to any of the already-mentioned causes. It is thrombotic in origin, and due to some peculiarities of the morbid processes of the affection.

[Footnote 8: _Virchow's Archiv_, Bd. lx.; Mosler, _Ziemssen's Cyclop._, viii. p. 443.]

SYMPTOMATOLOGY.--Hemorrhagic infarction of the spleen, as such, reveals its presence by no signs during life. Its importance depends almost entirely upon the nature of its exciting cause. When this is of simple origin there is hardly ever any deleterious influence exerted upon the health of the individual. That hemorrhagic infarction was present in any given case can only be ascertained by the evidences of it discoverable after death. Rarely by its presence localized inflammation and abscess may be excited. Far different, however, is the result where the embolic material has been derived from an ulcerative endocarditis or other septic centre. In this event the infarction serves surely as the starting-point for metastatic abscess.

PATHOLOGICAL ANATOMY.--Hemorrhagic infarctions of the spleen may vary in number from one to many, and in size from that of a large shot to a bulk nearly equal to that of the spleen itself. They are usually situated at the surface of the organ in a wedge-shaped distribution, the base looking toward the capsule and causing a slight projection, the apex pointing toward {962} the deeper portions. Infarctions, however, may also occasionally occur in the central parts of the spleen. A definite wedge-shape may be destroyed by the coalescence of several neighboring infarcts.

The appearance and density of the infarction will depend very much upon its age. When recent it is of a dark-red color, of firm consistency, and of homogeneous aspect, and is surrounded by a zone of hyperæmia. As it grows older the dark color gradually fades to a paler hue, in consequence of the absorption of the color-elements of the hemorrhage, and a yellowish shade appears, from fatty degeneration of the cellular constituents. With the fading in color the infarction decreases in size; contractions and scar-formations are developed, later to become converted into bands of dense fibrous tissue. Occasionally complete fatty metamorphosis of the cellular elements may ensue and caseation of the infarct take place. The caseous mass may soften and form a cavity, or may ultimately undergo calcareous degeneration. Not very infrequently one may detect at necroscopic examinations of spleens these calcareous nodules, equal to shot or peas in size, witnesses of the bygone metamorphoses of which we are speaking. When, instead of being of simple origin, the infarct is the result of septic changes, the course is different. Coincident with or immediately preceding the hemorrhagic infarction inflammatory symptoms will develop around the embolic masses (consisting principally of fibrinous material imprisoning multitudes of micrococci), and metastatic abscess rapidly becomes established. Pus will then be commingled with the softening mass, and the microscope will reveal the swarming organisms. In the latter event the changes of the hemorrhagic infarction are much more rapid than in simple infarction, when they may be very protracted.

Splenitis.

Although it is impossible to separate acute splenic tumor and chronic splenic enlargement from the processes of inflammation, for practical purposes it is convenient to consider as splenitis only those morbid conditions in which the tendency is toward suppuration. Simple idiopathic splenitis is undoubtedly very rare, and, although formerly its symptoms were described with great detail, most recent writers are content to acknowledge an almost complete ignorance of them. Indeed, splenic abscess is often detected after death when it had not even been suspected during life.

Diffuse Splenic Abscess.--In the rare cases of idiopathic splenic inflammation the exciting cause will commonly have been a fall or blow or other violence by which the spleen has been injured, or it may have followed chronic malarial poisoning or an extension of inflammation from the capsule or neighboring parts.

SYMPTOMATOLOGY.--The rarity of this affection makes accurate description of its symptoms almost impossible. Mosler has never seen it. The descriptions of it are based, at best, upon observation of but few cases. Its onset may be sudden; more commonly it is insidious, the patient complaining of weight and dull pain in the left hypochondrium, irradiating to the left shoulder. The presence of pain depends upon the participation of the capsule in the process. Cough and dyspnoea may be present, and febrile phenomena are constantly to be observed. Vomiting, want of appetite, furred tongue, etc. will be noticeable. After a time a tumor will be detected that will, at first, almost certainly show no sign of fluctuation. Coincidently with the development of the tumor a small degree of ascites and of anasarca of the lower extremities may appear.

Up to this point the presence of abscess may only be conjectured, and indeed throughout its entire course it usually escapes positive identification. {963} Fluctuation may, however, be detected, and from its location and concomitant symptoms may reasonably be ascribed to a splenic abscess. The fluctuating tumor has been known to fill the whole abdominal cavity from epigastrium to pubes. Grisolle reports such a case where the tumor presented the appearance of ascites. In this form of splenic abscess the progress is generally insidious. Under symptoms of hectic fever, wasting, etc. the physical signs of splenic enlargement are gradually manifested until the presence of fluid may be determined. After months of suffering the patient will expire from exhaustion or from the consequences of rupture of the abscess into the abdominal or pleural cavity or into the lungs, lighting up rapidly-fatal inflammation; or, discharging into the bowel or stomach or through the abdominal wall, the abscess may temporarily improve and allow a short prolongation of a wretched life. In the event, however, of an escape of pus from the body, as through the abdominal wall, bowel, etc., recovery is possible in a very small proportion of cases. Wardell has seen such a case discharging through the abdominal parietes. Zweifel has met a similar condition. Nasse has known of recovery after the pus had been expectorated, and Webb, after discharge into the intestine. Occasionally, splenic abscess may become encapsulated and undergo caseous metamorphosis, when it may become inactive, ultimately cicatrize, or become calcareous.

PATHOLOGICAL ANATOMY.--In abscess of the spleen, when of small size, a non-metastatic origin may be recognized by the absence of micrococci from its purulent contents and of concomitant signs of blood-poisoning. When not spontaneously arrested, these abscesses attain a size not equalled by metastatic splenic abscess. The splenic substance will then be reduced to a semi-fluid or fluid mass of reddish pus enclosed within a pyogenic membrane. In extreme cases all traces of true splenic pulp and trabeculæ will be obliterated; but when the inflammatory action is less intense the trabeculæ will extend in all directions through the abscess cavity. The capsule, thickened and indurated, will have formed adhesions or will have entirely disappeared before the advancing wall of the abscess.

Embolic Abscess.

It has been shown that hemorrhagic infarction in the spleen is the result of an embolic obstruction of the splenic blood-vessels. If the embolus be simply a detached portion of an aseptic clot or fibrinous vegetation or of atheromatous degeneration, the subsequent changes will be those characteristic of the involution of hemorrhagic infarction. Under exceptional circumstances and from not understood causes inflammation and abscess may follow. These, however, are to be reckoned among the rare results of simple hemorrhagic infarction of the spleen. Altogether more frequently the embolus is derived from the ulcerative endocarditis of septic origin or from other septic centre, and consists of congeries of micro-organisms, themselves the infecting agents or the vehicles of the poison that lights up the characteristic morbid processes. A colony of these micro-organisms, lodged in and occluding splenic arteries, by the irritation of their presence and by their multiplication excite the inflammatory processes that accompany and follow the hemorrhagic infarction. Embolic splenic abscess is, then, nearly constantly a secondary result of conditions of blood-poisoning, and as such can only play a subservient part in the train of pathological events in which all parts reached by the blood-supply may be engaged. The vascular distribution in the spleen is such as to afford exceptionally favorable opportunities for the development of metastatic abscesses, and in a large proportion of spleens of those who have died from blood-poisoning they will be detected. They are rarely {964} present without the appearance of similar changes in other organs, and there is, therefore, but little difficulty in attributing them to their true cause.

SYMPTOMATOLOGY.--Unless inflammation of the splenic capsule be excited, these abscesses give rise to no pain, neither do they (except rarely) produce discoverable splenic enlargement as distinct from the general splenic enlargement always present in septic fever. Their course is usually brief, in consequence of the usually acute course of the disease that occasions them. When, in chronic pyæmia, splenic embolic abscess may develop more slowly, exceptionally palpable fluctuating tumor becomes manifest.

Fever, with all the accompanying phenomena of blood-poisoning, is present in these cases, and commonly masks any splenic alteration that might otherwise become apparent. Embolic abscess should always be suspected in blood-poisoning, though in most cases its detection could have but little influence in determining treatment.

PATHOLOGICAL ANATOMY.--Embolic abscess may develop from a hemorrhagic infarction, in which case the necrotic central mass is surrounded by a zone of inflammation which rapidly converts the whole area into a broken-down, reddish, purulent, semi-fluid matter. If the abscess supervene without the occurrence of hemorrhagic infarction, its situation is still nearly always peripheral, the wedge-shaped embolic area pointing toward the centre. It varies in size from that of a pinhead to that of a pea and larger. It consists of a necrotic centre composed of pus-cells and detritus, a surrounding mass of exudation, and a circumscribing border of hyperæmia. Microscopic examination will usually reveal swarms of micrococci. In the progress of the abscess the whole mass becomes converted into a grumous brownish fluid. The peritoneum rarely participates in the activity of the inflammation, but may form deposits of lymph over the seats of the abscesses.

Mosler[9] summarizes Ponfick's description of a peculiar splenic inflammatory process resulting from relapsing fever. It differs from ordinary embolic abscess in being limited to the splenic venous system. It may equal two-thirds of the entire spleen in bulk. It resembles in appearance embolic abscess, but the arteries remain pervious. These abscesses may heal or may enlarge and peritonitis may be excited. The possibility of their originating in a venous thrombosis is entertained by Ponfick. A peculiar inflammatory condition of the follicular tissue of the spleen has also been described by Ponfick as a result of relapsing fever.

[Footnote 9: _Ziemssen's Cyclop._, vol. iii.]

DIAGNOSIS.--The diagnosis of splenic abscess presents very often great difficulties, and is frequently quite impossible. In ordinary embolic abscess a diagnosis cannot be made with certainty. The existence of pyæmia with enlargement and pain would make it probable that splenic abscess had formed. In the larger abscesses of malarial, traumatic, or unknown origin the detection of a fluctuating tumor in the region of the spleen will suggest its true cause, but examination of the contents will alone clear up the diagnosis between the real disease and hydatid tumors, nephritic and perinephritic accumulations of fluids, etc. Even where the contents of the cavity are purulent, it will often be impossible to decide upon their splenic origin unless in the event of portions of the splenic tissue escaping at the orifice of the abscess. In cases of constant and increasing pain and tenderness in the splenic region, with enlargement, associated with general failure of health, splenic abscess may be suspected, and an exploratory puncture with the aspirating-needle may not only be justifiable, but imperatively called for. In all cases it must be remembered that splenic abscess of this character is a most rare disease.

PROGNOSIS.--Splenic abscess usually terminates fatally. The life-destroying influence, however, is not exerted through the spleen itself, for this may {965} be converted into a simple bag of semi-fluid contents, with complete destruction of all its tissue, and yet danger is to be apprehended only from the effects of suppuration or of rupture into the closed cavities or from peritonitis, etc. Of itself, embolic abscess rarely excites alarming symptoms, because, being usually of septic origin, the stress of the general condition is thrown more upon the whole body, or upon a number of its parts, of which the spleen is not the most important.

TREATMENT.--Treatment should be directed more toward prophylaxis than toward cure. In those congestions and hyperplasias that may result in abscess the remedies indicated for these conditions should be actively employed. The application of ice to the splenic region, of counter-irritants, the use of local bloodletting, the unloading of the intestinal circulation by saline purgatives, the proper employment of quinine, etc. in chronic malarial poisoning, seasonably adapted, may prevent the formation of abscess. In the event of fluctuation declaring itself, evacuation under antiseptic precautions should be practised; ordinarily, the most effective general treatment is that directed against the primary disease.

Perisplenitis.

Inflammation of the splenic capsule is a more common affection than clinical observation would lead one to suppose. It consists of a more or less localized splenic peritonitis, and its lesions are often found at the necropsy when its existence had not been suspected during life.

ETIOLOGY.--Its commonest cause is the extension of inflammation from neighboring parts. Chronic ulcer of the stomach may be the origin of chronic perisplenitis, leading to the formation of dense inflammatory deposits. Persons who have long suffered from miasmatic poisoning frequently develop strong adhesions between the spleen and diaphragm. And from the same cause the spleen may become closely adherent to the neighboring viscera. Chronic enteritis, perinephritic inflammation, and the like may excite it. It has been shown that the pain in splenic affections is nearly always due to the capsulitis present; and it is probable that much pain in the splenic region, stitches in the side, etc. are really the results of this inflammation. It can only be conjectured that in given cases one has to do with perisplenitis. Almost all that is known about it comes from the dead-house.

PATHOLOGICAL ANATOMY.--The simplest post-mortem signs of bygone perisplenitis are the unusually dense fibrous adhesions between the spleen and surrounding parts. These may vary within wide limits. Exceptionally, the spleen will be found intimately adherent to surrounding parts throughout, and can only be separated from them by tearing it away. Under these circumstances, mostly in chronic malarial subjects, the capsule will be uniformly much thickened and sac-like. The splenic tissue may be reduced to a tarry, semi-fluid pulp that oozes through the lacerated walls. Sometimes the capsule of the spleen will show localized thickenings of dense cartilage-like consistency, usually on the convex surface. According to Wilks and Moxon (p. 487), "section shows them to be laminated parallel to the surface, and the microscope reveals a fibrinous structure, the fibres being arranged in dense areolated lamellæ." The same authors consider these to be among the most decisive evidences of chronic alcoholism. They may become calcified (Orth). It is not unlikely that they may often be the effects of syphilis. They undoubtedly often occur in syphilitic subjects. The interest attaching to them is entirely a pathological one, as the affection is never detected during life, and as they probably exert no influence whatever upon the duration of life or even upon the well-being of their bearer.

{966} Lardaceous Spleen.

The spleen is more liable to lardaceous or amyloid disease than any other organ of the body. And, although in the further course of the degeneration other organs and tissues inevitably become implicated (unless the patient die of some intercurrent affection), the spleen may in the earlier stages be alone involved. In 58 cases of lardaceous disease compiled from the records of the London Hospital, the spleen was the only organ in which the degeneration was detected in 28 cases, while it remained unaffected in only 10 cases.[10]

[Footnote 10: Turner, _Transactions Patholog. Soc. Lond._, vol. xxx.]

The tendency of lardaceous disease toward generalization shows that it is under systemic and not local influence, though whether this influence is exerted in depositing preformed albuminoid material in the affected parts (infiltration), or in bringing about a special alteration in situ (degeneration), is even yet not definitely decided. Upon the one hand, the infiltration theory is upheld by Rindfleisch, Billroth, and others, while Fehr, Kyber, Cohnheim, and others consider it to be a result of tissue-metamorphosis. Cohnheim concludes that the infiltration theory could only be accepted upon the presumption that the lardaceous material is not a soluble but a corpuscular substance, or that it is only deposited in consequence of some acquired predisposition of the part. He regards the process as a local degeneration due to general causes in which the lardaceous material is derived from the pre-existing albumen of the tissues. According to Virchow and Kyber, there is brought to the tissue whose nutrition is somehow lowered a substance, between which and a malarial substance formed in loco an intimate combination occurs, the result being lardaceous material (Ziegler).

This form of degeneration involves the spleen in one or both of two ways. It may appear as scattered points throughout the splenic substance, corresponding to the Malpighian bodies and presenting a resemblance to grains of boiled sago, or in a diffused manner, constituting true lardaceous spleen, in which the entire organ appears to be involved.

ETIOLOGY.--As in lardaceous disease of other parts, by far the most common causes of its development in the spleen are prolonged suppuration, especially of bone, the suppurative processes of phthisis pulmonalis and of scrofulosis. The next most frequent causative influence is syphilis, whether accompanied by prolonged suppuration or by the cachexia so often observed in this disorder. Chronic malarial poisoning, chronic diarrhoea, chronic alcoholism, and occasionally the less-rapidly fatal malignant new growths, may induce the degeneration. Exceptionally, it has been observed where no other general disturbance of nutrition had existed. The various causes of lardaceous degeneration have in common one feature, chronicity, though Mosler quotes from Cohnheim instances where lardaceous spleen was discovered in one case five months after joint injuries had been received, and in another four months after a compound fracture of the right leg.

SYMPTOMATOLOGY.--Lardaceous disease of the spleen is usually associated with similar disease of other organs--the liver, kidneys, stomach, intestines, heart, etc.--and its symptoms are so frequently accompanied by those of the affection that has given origin to it that it must always be difficult to distinguish them as attributable to the condition of the spleen itself. Profound anæmia with an appearance of cachexia is always present in advanced cases. Milder cases may reveal themselves by no signs. The symptoms arising from other parts implicated in the degeneration may completely mask those depending upon the spleen. When the stomach is involved, vomiting and hæmatemesis even to a fatal termination may occur, or uncontrollable diarrhoea from intestinal changes may supervene. Splenic enlargement is not {967} unusually accompanied by enlargement of the liver. Ascites, however, is always a rare accompaniment.

Rarely, the spleen attains enormous size, and may then occasion sensations of weight and tension, and occasionally acute pain from implication of the capsule in inflammatory action. When the organ can be felt through the abdominal walls it will generally be hardened, painless, and with its boundaries much thicker and rounder than normal.

PATHOLOGICAL ANATOMY.--As has been already remarked, lardaceous disease of the spleen is observed in two forms. In both the spleen is enlarged and hardened. Its structure presents a tough, waxy consistence, and the organ has entirely lost its friability. In sago spleen, light-brown or grayish waxy bodies are scattered throughout the splenic structure. The pulp may remain quite healthy, or it may also be involved. These sago-like bodies correspond to the enlarged and lardaceous Malpighian corpuscles, and stand out with some prominence from the general surface. They may vary in size from that of a pinhead to that of a small pea. The color of the spleen may shade from a pale fawn color to a reddish-brown. In many cases where the parenchyma is involved there will be exhibited scattered areas of semi-transparent, wax-like material.

In the diffusely lardaceous spleen the organ is enlarged throughout, pitting to pressure, and upon section presenting a waxy, semi-translucent appearance, usually of a reddish-gray, but sometimes of a deep-red, color. Instead of a pulpy, easily broken-down condition of the splenic parenchyma, there will be found a dense tissue that can be cut into tough, glistening slices. Minor degrees of the change cannot be readily detected by the unaided eye, and even in advanced cases the judgment will often be at fault. Under these, and in fact under all circumstances a correct conclusion as to the nature of a given change can only be reached after the employment of reagents that exert peculiar influences over the lardaceous material. The action of iodine upon this material is quite characteristic. If a watery solution of iodine with iodide of potassium be applied to the cut surface of the suspected organ, the normal portions will be stained a yellowish color, while those parts that have undergone lardaceous degeneration will assume a rich mahogany red or brown, which will become violet or purple upon addition of sulphuric acid. This latter reaction is not constant, and may usually be omitted. Cornil has recently proposed as a test a solution of methyl-aniline-violet, which possesses the property of staining lardaceous matter red, while ordinary tissues will be stained a deep, bright blue. This reaction possesses the advantage of being permanent and very delicate, and on that account preferable for microscopic examination of specimens. According to Cohnheim, this reagent enables one to distinguish commencing lardaceous change.

In lardaceous disease of the Malpighian corpuscles the alteration will be found to begin in the arterial twig to which the corpuscle is attached, soon extending to the entire tissue of the corpuscle, which it causes to enlarge considerably. When the splenic pulp is attacked it is said to be the vessels of the pulp that are first involved. It is held by most pathologists (Virchow, Kyber, etc.) that the change is chiefly seated in the muscular coat of the small arteries, but that the intima is also very frequently affected, and that occasionally all the coats are involved. Thence the degeneration spreads to the cells and nuclei of the splenic tissue. Later investigations, however, seem to make it probable that the lardaceous degeneration is mostly limited to the connective-tissue trabeculæ and walls of the venous sinuses; that the pulp-cells are for the most part not implicated, but that they disappear in consequence of the pressure of the ever-increasing lardaceous material and the consequent anæmia (Cohnheim, Ziegler).

DIAGNOSIS.--This will depend more upon the history and concomitant {968} symptoms and general condition of the patient than upon any positive evidence to be gained by special reference to the spleen. In a patient predisposed to lardaceous degeneration by any of the influences enumerated above the presumption in favor of splenic lardaceous disease is strong if, in addition to splenic enlargement, there is evidence of hypertrophy of the liver and albuminuria, indications of the participation of other organs in the process, and an anæmic and cachectic appearance of the individual always observed in advanced degrees of the degeneration.

PROGNOSIS.--The prognosis is almost always unfavorable, not so much on account of the splenic condition as from the general depreciation of the powers of life. The disorder being progressive, the tendency is toward death by complications resulting from degenerations of other organs. And yet it seems quite probable that mild grades of lardaceous degeneration may be entirely recovered from occasionally; but this will be almost invariably in cases where the spleen alone is implicated. At all events, when not advanced it may be long held in abeyance. The duration of the disease generally is indefinite and may cover a space of years.

TREATMENT.--The treatment of lardaceous degeneration of the spleen will consist rather in combating its exciting causes than in efforts directed toward the condition of the spleen itself. It may, however, be possible to effect some good by resorting to remedies supposed to be useful in subduing ordinary splenic enlargement.

Echinococcus of the Spleen.

Echinococci invade the human body in the United States far less frequently than in many other countries, where the canine race occupies much closer relations with man (as in Iceland). The echinococci are the larval forms of Tænia echinococcus, a tape-worm of minute size inhabiting the intestinal tract of the genus Canis, more especially that of the dog. The ova of the tæniæ are voided in countless numbers in the feces of their hosts. Still unhatched or in an embryonic form, they are thence conveyed through the medium of water or otherwise to the stomach of man, whence the embryos (scolices) escape into the tissues and develop into ordinary hydatid cysts. Rare as is this affection in the human body, it is relatively extremely uncommon as implicating the spleen, and recorded instances of its occurrence are not numerous. Hydatids of the spleen may coexist with those of other parts, and in occasional instances are said to be secondary to these. They are commonly encountered about the middle period of life, and appear to affect the sexes in equal proportions.

In cases of multiple hydatid cysts in different parts of the body it has been asserted, upon the one hand, that a single older cyst serves as the parent cyst, germs from which become transplanted in other localities through the blood. This view receives some support from the fact that one cyst, usually seated in the liver, is commonly much larger than the others. An objection to its universal acceptance, however, as pointed out by Budd, is that it is very difficult to imagine that a germ from a larger cyst can travel through the portal vein, against the current, toward the spleen, mesentery, etc., to form a secondary cyst. On the other hand, it seems likely that an individual exposed to infection by the echinococcus would be liable to ingest many scolices at one time or on repeated occasions, and that the differences in development depend upon varying degrees of assimilative power on the part of the parasite and of the conditions of its environment.

SYMPTOMATOLOGY.--Whether echinococcus of the spleen will betray symptoms of its presence depends upon varied circumstances. Small cysts, {969} certainly, may occasion no signs, subjective or objective. Cysts may even attain very large dimensions without exciting discomfort to their bearer, and may consequently escape detection. Pain may precede the appearance of a tumor, but will be irregular and paroxysmal, increasing in severity with the growth of the cyst. The most constant annoyance, however, is that occasioned by the size and weight of the enlargement. The patient may detect its presence accidentally, or his attention may first be directed to it by his medical attendant. He may give a history of its growth during a number of years without its having occasioned more than passing uneasiness.

The tumor may exceptionally attain a large size, nearly filling the left side of the abdominal cavity. It may encroach upon the area of the thoracic cavity. Upon examination, the tumor, when of sufficient size, will be rounded, not resembling the appearance of a simply enlarged spleen. Fluctuation will be detected, and occasionally the peculiar hydatid thrill, upon the diagnostic importance of which great stress has been placed. This, however, is a very inconstant sign, and in the majority of cases is not to be discovered. Frerichs only found it where the sac was not tense and contained other vesicles. A peritoneal friction sound may sometimes be detected by the ear placed over the region of the tumor. These cysts differ from other fluctuating tumors in being of very slow growth, remaining almost without change for years, and in exciting no constitutional reaction, unless, as is quite possible, inflammation of the sac is developed, when rigors, hectic, and other symptoms indicative of suppurative inflammation will be observed. Pressure of the tumor upon the stomach may excite anorexia, vomiting, epigastric uneasiness, and gastric catarrh. If the pressure is exerted upon the portal vein or vena cava, dropsy may result; if upon the bowel, constipation may be produced.

It is possible for the development of the cyst to be arrested through the death of the echinococcus. This may occur if it is of small size. Its walls may then become calcareous, and the mass will cease to exert any injurious influence upon the host. In other cases, as a result of inflammation, rupture will take place, and the contents of the cyst, with the characteristic formations, will escape into the peritoneal, pericardial, or pleural cavities, or into the alimentary tract, the urinary passages, or even into the vena cava; or they may be discharged through the body-wall. In any of these events a fatal termination is almost inevitable. Rupture may also occur in an unaltered cyst from any sudden or excessive violence. Death will usually speedily ensue from collapse or as a result of inflammation of the peritoneum. Finally, complete recovery will sometimes be secured through treatment.

DIAGNOSIS.--Echinococcus of the spleen presents no characteristic symptoms. When the tumor is small and escapes observation, or when the fluid nature of its contents cannot be recognized, its existence cannot be determined. In larger tumors the hydatid thrill will, when present, assist the observer, and the presence of fluctuation will of course serve to exclude all solid enlargements of the spleen from consideration. Abscess will differ in its shorter course, its rapid increase in size, and its inflammatory symptoms, the general condition contrasting with the excellent condition of health usually observed in simple hydatid tumor. The diagnosis will become greatly obscured in the event of inflammation of the cyst. Certainty can only be attained through an exploratory puncture and examination of the contents of the cysts. These will consist of a clear, non-albuminous fluid, rich in sodium chloride, and revealing the echinococcus scolices and hooks and membranous shreds when examined under the microscope. Doubt may arise where inflammatory changes have made the fluid albuminous and where the scolices and hooklets have been destroyed or do not accompany the escaped fluid.

{970} MORBID ANATOMY.--The spleen may be almost destroyed by the hydatid cysts, which, usually single, may exist in large numbers. According to Wardell,[11] "they are seldom found in the pulp, usually in the gastro-splenic epiploon or in the cysts constituted of the serous investment." The cysts consist of a thick fibrous investment and an inner parenchymatous layer, from which the little heads develop in tiny vesicles. Compound systems, one enclosed within the other, are thus formed, varying from the size of a pea to that of a marble, and even very much larger. The cysts may undergo atheromatous or calcareous degeneration. In these cases the echinococci are destroyed, and the mass becomes encapsulated in a calcareous envelope and remains quiescent. The microscope will reveal the remains of the echinococci, even after long periods. Where rupture has taken place the rent in the cyst will have allowed characteristic matters to escape into the communicating parts, where they may be detected.

[Footnote 11: _Reynolds's System of Medicine_, vol. v.]

The PROGNOSIS of echinococcus of the spleen is always serious, usually most unfavorable. The best results are observed in those cases where, the cyst being small, spontaneous arrest of development has occurred. Puncture of the cyst and partial evacuation of its contents, when practicable, increase what would otherwise be almost hopeless chances of ultimate recovery in cysts of moderate and large size.

TREATMENT.--The only treatment that promises good results is the evacuation of the cyst fluid. Murchison recommends the removal of the fluid with a very small trocar, whereby the admission of air into the cavity is avoided. The withdrawal of the fluid is sufficient to destroy the life of the parasite, and in favorable cases to secure the degenerative changes of which mention has been made. The adoption of antiseptic precautions will undoubtedly increase the chances of recovery. Unfortunately, a certain number of cases will run into suppuration, when all the dangers of suppurating cavities have to be encountered, and must be treated in the usual way. Various injections into the cyst-cavity have been recommended, but they do not seem to afford better results than simple evacuation. These will probably most successfully be employed in cases where the cyst has formed inflammatory adhesions to the skin, which may be effected through the external application of caustic agents capable of exciting inflammatory changes in the deeper parts (Vienna paste, etc.). Injections may be then made through incisions carried into the cyst, without danger of exposing the peritoneal cavity. Internal medication, except for general purposes, has no efficacy in the treatment of these tumors.

Syphilis of the Spleen.

The spleen is not very frequently affected by syphilis. Nevertheless, this viscus may become the seat of syphilitic disorder during either its early or late phases. It has even been asserted by Weil that the spleen may become enlarged in the interval between the appearance of the primary sore and the first cutaneous eruption. Whatever changes the spleen may undergo during the course of early syphilis are essentially of the simple congestive type, and are comparable to the acute splenic enlargements of the ordinary specific fevers; certainly, no essentially syphilitic changes can be detected at this stage. In fact, throughout the whole secondary period the splenic derangement is of the nature of simple hyperplasia. In the later stages of syphilis there is a more permanent enlargement of the spleen, due to a chronic interstitial inflammation that should be distinguished from that very much more common result of old syphilis, lardaceous degeneration. The histological characteristics of these enlargements are not known to differ essentially from the simple chronic enlargements of the spleen already considered.

{971} It is only toward the end of the secondary period, and during tertiary syphilis and in inherited syphilis, that products essentially syphilitic can be recognized. Gummy infiltrations and tumors of the spleen have been observed by a few writers--not, however, clinically, but for the most part in the dead-house. These tumors are found scattered throughout the substance of the organ, but most commonly near its surface. They vary in number within not very wide limits, and in size from that of a pinhead to that of a pea or larger. They may be sharply circumscribed (but not encapsulated) or more diffused. The portions of the spleen affected become changed by the syphilitic material into grayish-red, homogeneous masses in recent cases. At a later stage they are "gray or grayish-yellow, homogeneous, somewhat dry, tough, almost cheesy."[12] The spleen under these circumstances is, as a whole, somewhat enlarged.[13] Gummy tumors of the spleen may be confounded with tubercle and old hemorrhagic infarction.

[Footnote 12: Wagner, Mosler, _Ziemssen's Cyclop._, vol. viii. p. 485, Am. ed.]

[Footnote 13: Gold, _Viertelj. f. Derm. und Syph._, 1880, p. 463.]

There is a form of circumscribed enlargement from new growth that is sometimes observed in the spleens of syphilitics, and which is probably of syphilitic origin, producing changes similar to certain forms already described as a variety of perisplenitis. It is situated at the surface of the spleen, and consists of hard whitish or pale-yellow plates but slightly elevated above the normal level, but of considerable superficial extent. When incised, these plates remind one of cartilage.

Splenic enlargements are common in the subjects of inherited syphilis. According to Cornil, infants syphilitic by inheritance have very frequently enlarged spleens, the capsule being inflamed and thickened and the splenic tissue abnormally hard. The organ may thus become sufficiently enlarged to be detected by palpation. Sée considers that enlargement of the spleen is present in one-fourth of all cases of inherited syphilis, and Haslund reports splenic enlargement in 58 of 154 necropsies of such infants.

The clinical signs of syphilitic spleen are almost beyond recognition, if indeed they can be said to exist. Circumstances of growth, etc. may excite the suspicion that a given splenic tumor may be syphilitic. Jullien, it is true, describes symptoms of splenic syphilis, but his views do not seem to be well founded.

TREATMENT.--In recent enlargements therapeutics may effect much in reducing the tumor, and the facility with which its reduction is effected will afford a valuable indication of the success of treatment. Gummy tumors are probably within the reach of antisyphilitic treatment, and it is not unlikely that some of the shrunken, indurated areas often detected post-mortem, and usually ascribed to infarctions, are in reality due to the cicatricial remnants of old gummata. Chronic diffuse splenic enlargements of syphilitic origin are but little influenced by treatment.

Rupture of the Spleen.

The peculiar texture of the spleen renders it especially liable to rupture--more so than any of the other abdominal viscera. By far the most common cause of splenic rupture is external violence from blows, kicks, falls, squeezing force, and wounds incised or punctured. It may be the direct result of the injury, or the rent may be made by the penetration of broken ribs or of foreign bodies. The rupture may even occur spontaneously from causes located within the organ itself. It has been previously observed that in the enlargement accompanying the acute infectious fevers, malarial fever, etc., while the distension of the capsule renders the spleen tense and elastic, {972} section through its substance will often reveal a semi-diffluent condition, the exact nature of which is not well understood, but which undoubtedly originates in excessive vascularity. This occurs especially in malarial fever and typhus. Rupture may here take place spontaneously, or, as is commonly the case, a very slight degree of violence is sufficient to produce it: a wrench, the effort to preserve a disturbed equilibrium, an otherwise insignificant blow, may determine the lesion. Pregnancy and the puerperal state may be the predisposing causes to the accident, and vomiting has been known to produce it. It has also been known to follow the softening and breaking down of a hemorrhagic infarction or the rupture of varices and aneurism. The normal spleen is only with the greatest rarity subjected to a degree of violence sufficient to rupture it, while in countries where enlargement of the spleen is of common occurrence, as from malaria, the accident occurs more frequently.

SYMPTOMATOLOGY AND COURSE.--When the rupture is of traumatic origin there may be no marks of external violence: the symptoms usually are those that follow sudden and great losses of blood, faintness, pallor following intense pain in the splenic region, frequency and weakness of pulse, sighing, coldness of the extremities, and the rapidly developing signs of profound prostration. A fatal termination usually quickly follows the rupture. Where the hemorrhage is not immediately great the patient may not succumb at once, but may live for hours, even days--nay, may even recover, as has occurred in the experience of some observers. Wilks and Moxon saw a case of splenic laceration where five ounces of laminated clot in process of absorption were found lying upon the spleen, death having occurred eighteen days after the accident in consequence of abscess of the brain. In cases where rupture has taken place, perhaps from very slight violence, in a spleen enlarged and softened from disease, the above-mentioned symptoms may have been preceded by pain and a sense of weariness in the splenic region, and by distinguishable enlargement of the organ.

PATHOLOGICAL ANATOMY.--Except in injuries caused by the penetration of foreign bodies or fractured ribs the rupture will usually be linear, and either straight, curved, angular, or stellate. If the rupture have occurred spontaneously it will probably be single, but in the event of its following violence it will most often have resulted at several places. In cases of traumatic splenic rupture in persons suffering from chronic malarial poisoning, Konaraloff[14] invariably found the rents in the lower portion of the organ, the greater ones on the outer surface, the smaller ones mostly on the inner surface near the hilum. They were widely gaping and deep. In ruptures consequent upon disease alone or slight violence to a diseased organ the spleen will usually be found enlarged, sometimes to three or four times its normal volume, with its substance softened and of a cherry-red color. In such cases signs of bruising or injury to the integument will not usually be discoverable. Splenic hemorrhage has been known to occur from the rupture of varices and aneurism, in which case characteristic appearances have been found after death. After death from rupture of the spleen the abdominal cavity will be more or less filled with blood, dark and coagulated. Though the contrary has been held, it is doubtful if multiple rupture of the spleen can be regarded as certainly indicative of a traumatic origin.

[Footnote 14: _Lond. Med. Rec._, No. 97, 1883, p. 259.]

Tubercle of the Spleen.

Tubercle not unfrequently attacks the spleen, but only as secondary to general tuberculosis. Wilks and Moxon indeed think the larger nodules of tubercle may be primary, but there seems to be no evidence in support {973} of this opinion. As a symptom of general tuberculosis, splenic enlargement from congestion, simply and quite without any specific deposit, is observed as a form of acute splenic tumor. It is at the later stages of general tuberculosis that distinct deposits of tubercle are formed in the spleen, and these are consequently almost always crude. They are generally scattered throughout the pulp, and, according to Billroth, they but rarely affect the Malpighian corpuscles. They are of very small size, and may be present in great numbers; their color is grayish and they are translucent, and only the largest show the yellow tinge of commencing fatty degeneration. According to Orth, they are not always easily distinguishable from the Malpighian bodies. Occasionally, and especially in scrofulous children, larger nodules are formed by the confluence of several tubercles that may equal a pea in size and present numerous yellow points of caseation.

It is usually impossible to diagnosticate the existence of splenic tubercle during life. After death the general splenic tissue will be darkened from hyperæmia and the tubercles surrounded by a vascular halo. When incised the tubercles will stand out from the tissue in which they are imbedded, unlike the Malpighian bodies, and when exposed to a stream of water the latter will disappear, while the tubercles will remain unaffected.

Tumors of the Spleen.

The spleen is very rarely invaded by new growths other than those already mentioned, and then almost exclusively either from direct extension from other parts or by metastasis. In pseudo-leukæmia or Hodgkin's disease the spleen is usually enlarged by a hyperplastic process quite like that of leukæmia. In that variety of this disease that has been called lympho-sarcoma, in which the spleen is invaded subsequently to the implication of the lymphatic glands, especially those of the cervical region, the Malpighian follicles may become enlarged, and even attain the size of walnuts. They contain spindle-cells and connective tissue. The trabeculæ likewise participate in the enlargement. Apart from the hyperplastic follicles thus occurring and also seen in leukæmia, small-pox, scarlatina, etc., lymphoma has been observed by Virchow, Weichselbaum, and others. The tumors consist of bright grayish-red or reddish, not sharply defined, nodules projecting from the dark-red mass of the spleen. Primary sarcoma is said to have been observed in the spleen, but malignant tumors of this organ are usually secondary growths, and even thus occurring are exceedingly rare. They are soft and very rapidly-growing sarcomata and carcinomata. As a rule, they depend upon malignant disease of the liver or abdominal glands through metastasis or by extension of growth. They sometimes grow with almost incredible rapidity. The symptoms are very obscure, and the presence of the malignant infiltration cannot be detected unless hard nodulated masses are formed, which become perceptible through the abdominal wall, as in hepatic cancer. The prognosis is always bad, and depends generally upon the existence of splenic cancer only in so far as this indicates the dissemination of the primary affection and becomes the forerunner of the cancerous cachexia. Fibroma and angioma have also been encountered in the spleen: they are both exceedingly rare. The latter has been known as a pulsating tumor (Langhans).

{974}

DISEASES OF THE THYROID GLAND.

BY D. HAYES AGNEW, M.D., LL.D.

The thyroid body occupies a very important position in the neck, being closely related to the larynx, the trachea, the carotid blood-vessels, the pneumogastric, sympathetic, and recurrent laryngeal nerves. These relations render quite intelligible the phenomena which are so frequently present when the gland becomes the subject of disease. It is richly supplied with blood-vessels from the external carotids and the subclavian arteries.

Notwithstanding the obscurity which enshrouds the physiological function of the gland, there are good reasons for supposing that its office in the animal economy is not an unimportant one: indeed, its presence, not in the vertebrata alone, but also in birds, reptiles, and fishes, tends to strengthen this conclusion. The experiments of Zesas appear to show that the thyroid body plays an important rôle in regulating the supply of blood to the brain, and also of supplementing the work of the spleen. The place, therefore, of the gland in the body as an appendage to the vascular system appears to be well chosen.

Congenital absence of the thyroid body is uncommon, though it has been noted by a few writers. Curtin[1] met with one case in which the gland was replaced by a mass of fat. Possibly in this instance the fat was the result of a morbid change in the thyroid, and not an evidence of the latter having never been present. Beach[2] furnishes another case where on dissection no trace of the gland could be found. Hyrtl speaks of the isthmus being frequently absent--a fact observed by other anatomists.

[Footnote 1: _Lancet_, 1850, vol. ii. p. 25.]

[Footnote 2: _Medical Times and Gazette_, May 30, 1884, p. 603.]

Goitre.

Various names have been employed by different writers to designate enlargements of the thyroid body. Among these may be named bronchocele, tracheocele, thyrophraxia, Derbyshire neck, struma, and goitre. Among English-speaking people the disease is generally spoken of as goitre or Derbyshire neck.

Hypertrophy of the gland may be either general or partial; when general--that is to say, involving the entire body--the term symmetrical or bilateral is employed to designate the enlargement; when confined to a single lobe, it is said to be asymmetrical or unilateral. Not unfrequently limited portions or small areas of one lobe only are affected, causing irregularities or nodosities which may be readily detected by the eye or the touch.

SYMPTOMS.--The earliest evidence of bilateral goitre is the appearance of an unusual fulness and breadth of the lower part of the neck or that part between the sternum and the larynx. This fulness extends laterally under the sterno-cleido-mastoid muscles, partially effacing the suprasternal fossa, {975} and is entirely unattended by pain, heat, redness, or other sign of inflammation. When the disease is unilateral, the swelling is seen to extend from the side of the trachea and larynx outward under the sterno-cleido muscle. The tumor, in consequence of its attachment to the trachea, follows the movements of the latter, and hence will be seen to rise and fall during the act of swallowing or of deglutition.

The progress of the enlargement varies greatly in different cases. After its first appearance it may remain quiescent for years, scarcely causing any change in the appearance of the neck which could be deemed a deformity; in other instances the growth will be progressive, attaining to the size of a goose egg, when it may again remain stationary. It is not common in the United States to meet with those excessive hypertrophies of the thyroid so common in Switzerland, where the gland extends up behind the ears, outward to the margins of the trapezii muscles, and hangs down in front of the sternum a large pendulous mass and imparting a most hideous appearance to the patient.

Pressure Symptoms and the Attendant Phenomena.--It is very remarkable to what a degree hypertrophy of the thyroid may reach without giving rise to any marked functional disturbances. This is due, no doubt, to the character of the enlargement, the cystic and vascular causing less inconvenience than the fibrous or more solid varieties. The pressure symptoms which may ensue are--first, difficulty of respiration. This is likely to follow when the central portion of the gland enlarges in common with the lateral masses, thereby causing pressure directly upon the trachea. This pressure may result in softening, and even complete absorption, of one or more of the rings of the trachea. An irritative cough may appear in the course of the hypertrophy, which is to be referred to the encroachment by the gland on the pneumogastric nerve. Hoarseness and a peculiar croaking voice are also sometimes witnessed, indicating the contact of the tumor with one or both recurrent laryngeal nerves.

Redness of the skin and elevation of temperature on one side of the neck are occasionally present, and sometimes accompanied by dilatation of the pupil of the eye corresponding to the affected side. These symptoms result from pressure upon the sympathetic nerve, and may exist in either unilateral or bilateral goitre. When associated with the latter form of the disease, the sides of the tumor will be found asymmetrical.

GEOGRAPHICAL DISTRIBUTION.--Goitre is met with in all parts of the world. There are, however, localities in which it prevails to a remarkable extent, assuming, indeed, the importance of an epidemic disease. In some portions of Switzerland, as in Savoy and in the Tyrol, there are villages in which scarcely a single inhabitant escapes. The disease is very common in Piedmont and in all deep valleys of the Alps, the Pyrenees, the Apennines, and about the foot-hills of the Cordilleras. In the valley of the Maurienne, Larrey states, nearly all the residents were subjects of goitre. According to the government reports in Piedmont and Savoy, there are 22,371 persons afflicted with bronchocele. There is a notable prevalence of the disease at Schlettstadt on the Rhine. In France the districts where the largest number of cases of goitre is observed are St. Aubin and Rosieux. These places, with others less noteworthy in the same country, it is estimated, furnish not less than 500,000 cases of the disease. In the government of Irkoutsh, which is drained by the sources of the Lena and its tributaries, there were in 1870, according to Hachine, as many as 3400 persons laboring under goitre. Among the inhabitants of Siberia antecedent to the conquest by Russia the disease was scarcely known. Its prevalence after this event was attributed to the habit adopted by the Russians of living in heated and uncleanly rooms, altogether unlike the Siberians, who spend most of their time in the open air. {976} Humboldt speaks of goitre being so common in Honda and Moussa, towns contiguous to the Magdalena River, that very few of their inhabitants escaped the disease.

In England the counties of Derbyshire, Surrey, Nottingham, and Norfolk furnish a large number of cases. In this country New Hampshire, Connecticut, Vermont, and New York are the States which supply the most examples of goitre. In Lower Canada goitre is also quite common.

In Switzerland the disease is frequently associated with mental imbecility (cretinism), though it is not at all established that between the two there exists any necessary connection, as cretinism is often met with in persons free from goitre, and the latter in those whose intellectual powers are unimpaired. Indeed, it has been observed by Burns, that in some countries where goitre is very prevalent cretinism is exceptionally rare; nevertheless, the observations of Lemon and the experiments of Horsley are of a character to leave the relation between the two still an open question.

CAUSES.--The causes of goitre are quite obscure. The disease is in some way associated with countries the topographical features of which consist in high mountains and deep valleys. In illustration of this fact we have only to cite the great prevalence of the disease in Switzerland, in the central mountainous parts of Asia, on the Himalayas and the Andes, as also in the mountains of Brazil. In Europe it may be said that goitre is much more common in the south and south-west countries than in the north and north-west. Sea-coasts are generally exempt from the disease. Bardeleben during the many years in which he acted as chief of the surgical clinic at Greifswald saw only two cases of goitre.

The use of glacier- or snow-water has been charged with the production of this evil, containing as it does large quantities of carbonic acid and other matters not generally found in pure potable water. In opposition to this view we are able to present the testimony of Captain Gerard that in those portions of the Himalayas where the inhabitants for a number of months in each year drink snow-water goitre is really less frequently observed than among those who live at the foot-hills of the same region. This coincides with what Lebert states, that if water from the regions of ice and snow constitutes a cause of goitre, then we should expect to find the disease increasing more and more as the glaciers are approached, when, really, just the reverse is the case, the subjects of such enlargements being seen in greater numbers at the bottom of valleys than in the more elevated regions. The Polar expeditions of Lenstake and Kolleweg, undertaken in the years 1868 and 1870, also contradict the supposed connection between goitre and ice-water, as not a case of the disease was reported, notwithstanding the men drank nothing else; and in Sumatra, where snow is never seen, goitre is quite common. Nor is there any satisfactory evidence that lime- or magnesia-water, also charged with exerting a determining influence in the causation of goitre, has anything to do with its existence. The testimony of Humboldt as to the rareness of the affection at Mariquita, where the water is strongly impregnated with lime salts, and my own observation that throughout the Pequea and Conestoga valleys, both limestone districts, goitre seldom occurs, are inimical to such a theory. From St. Maurice to Martiny in Wallis, Lebert speaks of goitre being very common, notwithstanding the absence of lime formation.

That water, however, does become the medium for certain materials which, taken into the system, produce enlargements of the thyroid, is unquestionably true. In corroboration of this statement we have two notable facts recorded by Frank, who says that at Rheims, where goitre was very common, quite one-half of the tumors disappeared after the source of the old water-supply was abandoned and the town supplied by a branch from the river Verle. {977} And again at Stenseifen, near Schmideberg, where goitre prevailed as an endemic, the disease disappeared on the closing of a fountain which furnished water to the inhabitants of the place.

Atmospheric causes have also been invoked in order to shed light on the production of goitre. Thus it is said that the common occurrence of the latter in very deep valleys, so overshadowed by the dense foliage of timber as to prevent a proper interchange or circulation of air, is favorable to this theory; yet as against this view we have the statement of Humboldt, who says that on the plateaus of Bogota, which are swept by constant currents of air and are quite sterile in vegetation, goitre is common.

That local or geological conditions do exist which are directly concerned in the development of endemic goitre cannot be gainsaid, and these of so active a nature that persons coming from remote districts into such goitrous centres and entirely free from all enlargements of the gland, are liable to suffer in common with the native born. Not only so, but, as has been observed by Virchow, even domestic animals in such localities become subjects of the disease.

The very careful study of this subject by Labour of Newcastle, England, furnishes strong evidence that water passing through calcareous soils alone had little if anything to do with goitre, but when such soils were impregnated with ferruginous and earthy salts the geological conditions were present for developing the disease.

Enlargement of the thyroid body is occasionally seen as one of the late manifestations of syphilis, usually bilateral and attaining in some instances a great size.

Gestation is another and not an uncommon cause of goitre, the tumor appearing in the last months of pregnancy or immediately after parturition. Three cases clearly traceable to the above cause are under the writer's care while penning this article. It is in such cases that the tumors sometimes grow with frightful rapidity. Roberts reports three cases in primiparæ, all of which ran an acute course and terminated fatally by asphyxia.

In Graves' or Basedow's disease goitre forms one of the elements in the morbid circle, and when thus associated may be regarded as a neurosis.

VARIETIES.--Goitre appears under different forms, and not unfrequently one variety is transformed into another. The following classification, resting on a pathological basis, will be adopted, namely--Follicular; Gelatinous; Cystic; Fibrous; Vascular.

In follicular goitre there is a proliferation, both in the cell-elements of the follicles and in the connective tissue constituting their walls. This general hyperplasia of the normal histological components of the gland constitutes a tumor which, for a time at least, remains quite soft and compressible, even communicating to the touch the sensation of fluctuation. The tendency, however, of the growth is not to remain long in this condition, but to become more firm and even hard to the feel.

The fibrous is often a transformation from the follicular goitre, an advanced stage in the life-history of the latter. There occurs a new formation of interstitial connective tissue, which by its accumulation and encroachment upon the follicles lessens, and finally obliterates, them to a degree which converts the gland into a fibroma. It is rare, however, to find this metamorphosis general. Generally the change is limited to portions of the thyroid, and accordingly the tumor in this variety of the disease is found hard, knotty, and incompressible at different points corresponding to the sclerosed portions. The vascularity of the fibrous variety is quite insignificant in those portions of the gland which have been the subject of this morbid change, though in other parts there is a liberal supply of blood-vessels.

Vascular goitre may also be a transformation from the follicular variety, in {978} which, with an increased hyperplasia of the follicular elements of the gland, there is a new formation of blood-vessels taking the place of the connective tissue present in the fibrous form of goitre. When the arterial element predominates, the vessels will be found to be very much dilated and anastamosing freely. These goitres are compressible, have a soft, spongy feel, sometimes pulsate, and on auscultation disclose a distinct bruit, hence the term aneurismal goitre often applied to such. In other instances the venous element predominates, when the swelling will, as in the arterial variety, be compressible and communicate to the ear a well-marked blowing sound or murmur. As the superficial veins, in common with the deep ones, are enlarged and tortuous, the surface of the tumor will often exhibit at different points a bluish appearance. In two instances, and in females of a highly-wrought nervous temperament, I have known the vascular goitre to enlarge in a few minutes to wellnigh twice its usual size, threatening the patient with suffocation for the time, and almost as quickly subside after a free emesis.

In gelatinoid goitre the follicles of the gland are distended so as to form large cavities filled with a gelatinoid- or colloid-looking substance, the product of the enclosed cells. As the distension of the follicles progresses the vascularity of the gland becomes notably less, the vessels being obliterated by the pressure. This tumor may attain a very great size, is much firmer than the vascular goitre, and to the touch has a doughy feel.

Cystic goitre is rarely such in the beginning of its history, being often an advanced stage of the follicular variety. In the transition the compartments of the latter undergo enlargement, their normal cell-contents being replaced by an albuminoid transudation from the vessels of the follicles. This process continuing, the interfollicular connective tissue disappears--a mechanical result caused by pressure. Still later, and from this cause, the walls of the adjoining follicles suffer a similar fate, and as these melt away larger cavities are formed, until at length the whole interior of the gland is converted into a number of loculi, and in some rare instances into one great sac. The gelatinoid or colloid goitre may undergo a similar transformation, and much in the same way. The fluid contents of cystic goitre vary in their physical properties as also in their chemical constitution. Generally the substance contained in the cysts is rich in albumen, has a ropy appearance resembling somewhat the white of an egg, and to the feel is viscous or unctuous, similar to that of the synovial secretion. Sometimes it is dark, resembling coffee-grounds--a condition due to the decomposition of extravasated blood derived from ruptured blood-vessels belonging to the gland. Crystals of cholesterin are also present, formed by fatty degeneration of the cells of the follicles, and mingled with a variable amount of sodium chloride. The cystic goitre is soft and fluctuating, and often grows to a large size.

* * * * *

The blood-vessels of goitre are not exempt from pathological changes, but frequently become the subjects of atheromatous and amyloid changes.

Carcinoma and Sarcoma of the Thyroid Gland.

Malignant growths of the thyroid body are comparatively rare, and when present are accompanied by symptoms sufficiently significant to differentiate them from those which are benign. In both carcinoma and sarcoma the increase of the tumor is rapid; the surface veins become very distinct, and the enlargement is general, affecting the entire gland. In addition to the above phenomena, the evil effect resulting from pressure is sooner realized and more pronounced than in goitre, and in a short time the generalization of the disease becomes apparent in the loss of flesh and strength. Should {979} the tumor be a carcinoma, there will likely follow the infection of those lymph-glands in nearest relation to the neoplasm.

EVIL EFFECTS OF GOITRE.--In this country, though goitre may grow to a large size, it is not common for patients to suffer any inconvenience other than that which results from the unsightly appearance of the tumor; hence life is not seriously imperilled by the disease. Occasionally, however, there are exceptional instances in which unpleasant and even troublesome symptoms are developed. Among these may be mentioned alteration of voice or a slight aphonia in consequence of pressure by the tumor on the recurrent laryngeal nerve. An irritating cough may also exist, and when no evidence of pulmonary trouble is present it must be referred to pressure upon the pneumogastric nerve. Dyspnoea when present results usually from pressure upon the trachea. It has been observed that when this pressure is long continued, particularly in cases of vascular goitre, some of the rings of the trachea gradually disappear, leaving only a membranous tube, which may collapse and cause the sudden death of the patient.

Hiccough and diaphragmatic spasms have also occurred when the enlargement of the gland extended laterally, in consequence of pressure on the phrenic nerve. In addition to the above phenomena there is often experienced in goitre severe neuralgic pains on the side of the neck, in the ear, and over the back of the head, and indeed in the course of any of the branches of the cervical plexus of nerves.

Occasionally I have seen a red blush of the integument on the side of the neck, answering to the largest portion of tumor, accompanied by increased heat, doubtless from the growth encroaching on the sympathetic nerve.

TREATMENT.--The treatment of goitre may be divided into constitutional and local. Too often the management of the disease is conducted in an empirical manner, every variety being subjected to the same routine of remedies. No greater mistake can be made. To attain any satisfactory success it is absolutely necessary that a correct diagnosis of the composition of the tumor shall be known. In follicular and in fibrous goitre much may be anticipated from constitutional and local measures. Those remedies which possess the property of inducing retrograde changes of structure and their subsequent absorption are the ones to be selected for administration, and among these iodine and its combinations rank highest. The compound solution of iodine, the iodide of potash, and the iodide of iron, all have their therapeutical adaptiveness. The earlier treatment is commenced the more hopeful will be the prognosis. If the patient is in all other respects in good health, and especially is somewhat fleshy or given to obesity, the compound solution of iodine should of preference be selected. At first the dose should be small, in order to test the tolerance of the stomach, not exceeding five or six drops three times a day, taken in some sweetened water, orange syrup, or curaçoa, and always about one hour after meals. Every two or three days the dose may be increased one or two drops until eighteen or twenty are taken, beyond which it is not desirable to go. It is in these forms of goitre that the burned sponge (spongia usta) was at one time very generally used as an internal remedy, half a drachm to a drachm being taken twice or thrice daily. As the virtue of the article was due to the iodine it contained, it must necessarily be inferior to the solution of the same substance.

In addition to the constitutional treatment the local use of alterative ointments will be indicated, the best of these being iodoform, iodide of lead, and iodide of mercury. Iodoform will be found most efficient employed in the following formula:

Rx. Iodoform, drachm iss; Benzoated lard, ounce j.

This ointment is to be rubbed into the goitre for fifteen or twenty minutes {980} morning and evening, after which a piece of lint smeared with the same should be laid over the tumor, covered with oiled silk, and retained in position by a strip of muslin. If the officinal iodide-of-lead ointment be used, it will be desirable to lessen its strength by the addition of a little simple cerate, as it is liable to cause severe irritation of the skin when thoroughly applied, thus neutralizing in a great measure the value of the application. Whatever unguent is selected, the application will be best made before an open fire.

There are several natural waters which can at the same time with the other treatment be taken with advantage, their efficiency being due to the iodine which they contain. The most valuable of these are Adelheid's Quelle and Wildegger. A glass of either can be drank morning and evening. If after two or three months' continuous treatment under the plan described no impression is made on the disease, or in the event of the iodine acting unpleasantly by causing symptoms of iodism, the iodide of potash should be substituted, administering three times a day from five to twenty grains of the salt dissolved in water and syrup, and well diluted.

Boinet has proposed the mixture of iodine with the food as a very satisfactory mode of introducing the drug into the system; and I suppose that it was on the strength of this suggestion that Michaud, with a view to protect the garrison of Étiennes against the prevailing goitre, ordered iodine to be baked in the soldiers' bread. In cases of goitre associated with a pale, anæmic state of the system it will often be found necessary to alternate, for a time, the remedies already directed with iodide of iron and cod-liver oil.

In follicular and fibrous goitres which prove rebellious to the plan of treatment detailed a resort may be had to injections. From eight to twenty drops of the tincture of iodine should be introduced deep into the substance of the gland by the hypodermic syringe. This procedure can be repeated every three or four days, selecting at each operation a different section of the gland, at the same time carefully watching the effect produced. Any marked elevation of temperature, local or general, accompanied by pain or stiffness of the neck, is the signal for suspending temporarily this form of medication. The favorable signs following injections are the shrinking and increasing hardness of the tumor; and so long as these processes continue progressive no repetition of injections will be necessary.

Electrolysis constitutes another therapeutic resource, applicable not only to the treatment of follicular and fibrous, but also to the vascular, goitre. This agent has been favorably employed by Chvostek of Vienna, and to some extent in this country by Baird and others. The current used by Chvostek was one from a Siemens battery of thirteen elements and strong enough to cause a moderate degree of burning. The time consumed at each sitting is not to exceed five minutes, during which the points of application must be frequently changed.

In vascular goitre, iodine, either internally or locally, effects little good. Ergot is to be preferred. From ten to twenty drops of the fluid extract should be given internally three times a day, with injections of the same amount and used in the same general manner as has been directed for the iodine.

Recently I have been using injections of carbolic acid in vascular goitre, and thus far with the most promising results. Four or five drops of a solution of the crystals of the acid dissolved in glycerin, using no more of the latter than will be barely sufficient to liquefy the crystals, should be deposited by means of the hypodermic syringe deep into different portions of the gland at intervals of four or five days. On the withdrawal of the instrument the puncture can be covered with a strip of rubber adhesive plaster. The acid when thus employed causes the tumor to shrink and become hard.

{981} Gelatinous and cystic goitres are quite intractable to constitutional remedies. They require to be attacked locally. Bonnet has tried caustic potash and chloride of zinc. The applications were made over the front wall of the tumor, and in some instances to the inner surface of the sac. The results were not of a kind to make the method a popular one. Iodine and alcohol have also been thrown into the parenchyma of the gland, and with a like unsatisfactory effect. Setons have had numerous trials. The method is an old one, having been used by Celsus, and revived from time to time by Quadi of Naples, Hutchinson, Kennedy, and Stanton. The object in using the seton is to develop in the tumor a destructive inflammation and suppuration. Any one who has witnessed a case of acute suppuration in the thyroid gland will not be anxious to repeat the experience. The purulent products are profuse, highly offensive, and tax severely the powers of the general system; and to these disadvantages may be added the risks of sloughing, hemorrhage, and septic poisoning.

The treatment which promises most in gelatinous and cystic goitre is either that practised by Gosselin or that by Morrell Mackenzie of London. The plan of Gosselin is to make a very small incision in the skin over the front of the tumor, in order to lessen the resistance to the introduction of a small trocar and canula, through the latter of which, after evacuating the cyst and washing it out with tepid water, he injects the tincture of iodine (fluidrachm j). This injection is allowed to remain about five minutes. Should its discharge be followed by a flow of blood, a second and even a third injection is made before withdrawing the canula. This operation does not materially differ from that practised by V. Dumreicher, except that this practitioner emptied the cyst with an aspirator previous to washing out the sac and injecting the iodine. The method of Mackenzie, however, has succeeded so well in practice that it is to be preferred both for efficiency and safety. In this plan perchloride of iron is substituted for iodine. One part of the iron is mixed with four parts of water, and after partially emptying the cyst with a trocar and canula at its most dependent part the fluid (fluidrachm j-fluidrachm ij) is thrown into the sac by a syringe. The canula is now plugged with a stopper that the injection may be retained. After three days the stopper is removed and the contents of the sac are allowed to flow out. In case the discharge proves to be bloody or serous, the injection is repeated; if, on the contrary, it exhibits signs of pus the iron solution is withheld, but the canula is permitted to remain, that free drainage may be maintained until the goitre has been destroyed by suppuration. During the presence of the instrument the affected part of the neck is covered by a flaxseed-meal poultice.

In gelatinous goitre, when the tumor is multilocular, after tapping and before injecting, I introduce through the canula a plunger, and by pushing it in different directions through the interior of the tumor break up the separating walls of the cysts, and thus open a way for the better diffusion of the injecting material. The plan of Mackenzie, destroying as it does the tumor by a slow chronic form of suppuration, and at the same time draining away the pus as it forms, greatly lessens the risk which might otherwise arise from diffused suppuration, bleeding, or sloughing. At the Copenhagen Congress, Mackenzie stated that he had by the method described treated 193 cases of goitre with only 2 fatal cases, the latter being those of a fibro-cystic form.

In making a comparison between the relative safety of perchloride of iron and of iodine as injections in goitre, the great superiority of the former over the latter is well brought out in the cases collected and analyzed by Schwalbe, 106 in number, for the cure of which iodine was used, death following in 5 cases and diffused suppuration in 22 cases.

When all measures fail to control the growth of a goitre, and the life of the patient is jeopardized from the effects of pressure, the case ceases to be {982} a medical one and must be relegated to the domain of surgery. Fortunately, the necessity for operation rarely occurs. It may be remarked, in closing this article, that the excision of the gland has been followed in several instances by evils greater than those for which the operation was performed. The experiments of Zesas and Horsley on lower animals, and the observations of Kocher after the removal of the thyroid in man, place the question of extirpation of goitre among the unsettled problems of surgery.

{983}

SIMPLE LYMPHANGITIS.

BY SAMUEL C. BUSEY, M.D.

ANATOMY AND PHYSIOLOGY.--The pathological relations of the absorbent system are important, because of their direct connection with the morbid processes and structural changes taking place in a variety of diseases; therefore, before discussing the subject of lymphangitis, a brief reference to the anatomy and physiology of the lymphatic system is necessary.

The lymphatic system consists of large and capillary vessels, interstitial spaces or juice-tracks, lacteals, follicles, and glands. The serous cavities are also considered lymph-chambers, and the loose cellular tissue is a vast chambered lymphatic sac communicating with lymphatic vessels. The larger vessels are divided into two classes--the superficial, which in the subcutaneous tissue accompany the veins, while in the solid viscera they lie under the capsule, and in the tubular viscera under the serous membrane; and the deep-seated vessels, which accompany the deep-seated blood-vessels, ramify through the interior of the organ in the solid viscera, and emerge at the hilus; while in the tubular viscera they lie in the submucosa, and by free anastomosis form plexuses. There is no communication between these two sets of vessels, except in the solid viscera and in the glands which may be common to both sets. Between the vessels of each set there is, however, a free anastomosis, by which large-meshed plexuses are formed. In consequence of these peculiar arrangements each set may be separately diseased, and inflammation may spread rapidly from vessel to vessel of the same set.

The lymph-capillaries are arranged in networks which lie in the meshes of the plexuses of the blood-capillaries, from which they are separated by intervening tissue-elements. Their walls consist of a single layer of endothelium resting upon elastic tissue. In their continuity they are sinuous, and are provided with an incomplete valvular arrangement.

The large vessels have three coats, not unlike the coats of the veins, and are provided with numerous valves. These valves are the more abundant in the superficial vessels, and the intervals between them grow gradually less as they approach the glands.

The whole lymph vascular system terminates either in the right or left thoracic duct.

The origin of the lymphatics has not been definitely settled. It has been demonstrated that lymph circulates in the connective-tissue interstices, and it seems to have been established that these spaces are lymph reservoirs, discharging through lymph-capillaries. It is admitted that the capillaries commence either in closely-meshed networks or lacunar spaces. Plexuses of lymphatic capillaries, corresponding with the distribution of the blood-capillaries, lie under the endothelium of the serous membranes, and are in open communication with the serous cavities through the stomata. The stomata vera are either the openings of lymph-channels communicating directly with lymph-capillaries, or discontinuities between the cells of the surface, leading {984} into superficial lymph-sinuses. The pseudo-stomata are the interstitial or intercellular cement substance, and represent the communication of the lymph canalicular system with the free surface of serous membranes.

Lymph-follicles consist of a reticulum of connective tissue, the meshes of which are crowded with cells, thus forming patches in the submucous or subserous tissue. Around these patches there is a plexus of lymph-capillaries.

Lymphatic glands are round or oval bodies situated in the course of the lymphatic and lacteal vessels. They are composed of follicular tissue, trabeculæ, and lymph-tracts, all enclosed in a capsule. No doubt exists in regard to a channel of communication between the afferent and efferent vessels through a complex system of lymph-paths which communicate more freely with the afferent than with the efferent vessels. They are very vascular.

Every lymphatic vessel passes through one or more glands before reaching the trunks. Before penetrating the peripheric fascia of a gland these vessels divide into a number of smaller ones, which are distributed upon the surface of the cortical portion, and empty directly into the superficial lymph-sinuses. A number of vessels emerge from each gland, but they are less numerous and larger than the afferent vessels. The lymph is poured through the afferent vessels into the lymph-spaces of the cortical alveoli, and thence into the channels of the medullary substance, from which it escapes, enriched in corpuscular elements, into the efferent tubes. The current of fluid passing through such a complex structure must necessarily be retarded. This relation of the glands to the lymph-current is, moreover, especially interesting in its pathological significance. Whatever enters the lymph may, if small enough, pass through the glands and be swept along with the current, but the structure of the gland is, in a mechanical sense, a filtering apparatus, interrupting the free current of the fluid and retaining the coarser particles. The lymph in passing through the glands derives constituents not previously possessed, but, nevertheless, the retention of elements which for a time might arrest the dissemination of hurtful material may eventually convert the gland into a new source of infection. This fact is illustrated in the history of malignant growths.

Perhaps the most interesting consideration connected with this relation of the lymph-glands to the fluid passing through them is presented by the anatomical arrangement of the chyle-vessels and the mesenteric glands. The lacteals, commencing as the central efferent vessels of the intestinal villi, pass between the folds of the mesentery, through several tiers of mesenteric glands, and, uniting into one or more trunks, terminate in the receptaculum chyli. During digestion these vessels are full of chyle, and during the intervals of digestion they convey lymph.

The lymphatic system may be considered an appendage of the blood vascular system. By the blood the tissues are supplied with nutriment and oxygen. By both the blood and lymph the surplus and waste are conveyed away. The current of the lymph is in a reverse direction to that of the blood-supply. The lymphatic vascular system receives through its rootlets, which are distributed through the tissues, the surplus transudation from the arterial capillaries, the products of tissue-waste and transformation, and the chyle, and empties its contents into the great venous trunks near their termini. It therefore performs the double function of absorption from without and absorption from within. In other words, it introduces into the blood the material from both the food and the air which is required for the sustenance and repair of the tissues, and conveys away the unassimilated surplus, waste, and effete material.

The forces concerned in the locomotion of the lymph are numerous. Recklinghausen believes the movement of the lymph to be mainly due to the difference between the arterial and venous blood-pressure. The greater this {985} difference the more rapid its current. The lymph canalicular system is not in vascular continuity with the blood-capillaries, and consequently the force of blood-pressure can only be communicated to the column of lymph by the passage of the plasmatic fluid into the lymphatic system by peripheral transudation and endosmosis. These are favored by the single homogeneous walls of the lymphatic plexuses and the enormous absorbing surface. These forces are essentially vis a tergo, for the difference between the arterial and venous blood-pressure is the excess of the former over the latter. To these must be added other factors, not less important or necessary, derived from the contractility of the walls of the lymphatic vessels, from the compression of the surrounding and contiguous parts, from the movements of respiration, and from the absorption of chyle. Besides these, the slowness of the movement of the lymph as compared with the rapidity of the arterial and venous blood-currents; the varying amount of pressure in the lymph vascular system, and the absence of distension in a normal condition; the entrance of the lymphatic trunks into the veins near the confluence of large branches, where the venous blood-pressure is almost inappreciable and the current is most rapid; the marked effect of active muscular movement in accelerating the flow of lymph; and the contractility of the vascular walls,--are all conditions which cannot be omitted from a consideration of the forces concerned in the locomotion of the lymph.

The supply of valves is very abundant, and they are always more numerous where pressure from surrounding and contiguous parts is most effective, though not infrequently most irregular in its operation, and consequently where isolation of small sections of the column of the fluid is most needed. The valves prevent regurgitation only so far as the superimposed column of fluid is insufficient to impair their integrity, or where there is no solution of the continuity of the vascular walls, and distension is within the limits of ordinary and normal extensibility. In cases of lymphangiectasis it is not usually necessary to look beyond the nearest neighboring and connected gland for the cause of such distension. Nature has increased the number of valves in the afferent vessels as they approach the glands, as well to modify and direct the flow as to prevent regurgitation; but if from any cause the passage of the lymph through the glands is obstructed or prevented, dilatation of the afferent vessels will ensue as a consequence. Valvular insufficiency and dilatation may exist in opposite relations to each other, either as cause or effect. The dilatation of a vessel may result from thinning or loss of contractility of its walls, caused by increased resistance to the onward movement of the fluid, and by the lesser extensibility of the intima than of the adventitia.

Lymphatic varices usually have their beginning in the vessels and extend to the plexuses, but the plexuses may be alone affected. Varicosities always extend backward from the point where the flow of the contained lymph is arrested, and may result from a repletion of each proximal intervalvular section with valvular incompetency.

The propulsive power of the heart diminishes with increased distance, due to increased friction and increasing resistance from flexures, bendings, and anastomoses, but chiefly from the increased carrying capacity of the vascular subdivisions. Hence, as the current of the lymph is in reverse relation to the capacity of the vessels, flowing, as does the venous blood, from subdivisions into trunks of diminished aggregate capacity, the velocity of the current of the lymph should be faster in the trunkal vessels than in the subdivisions. Such is the fact, though farther removed from the left heart and peripheral plasmatic circulation; and yet it is much slower in the thoracic duct than the blood-current in the venæ cavæ, which are not supplied with valves. The movement of the venous blood is in a measure due to cardiac and arterial contraction, but that force is least where the current is most rapid--in the {986} venæ cavæ. The increased rapidity of the venous blood-current as it approaches the heart must, therefore, be derived from some other source; and it is equally manifest that the velocity of the venous blood in the terminal trunks is transmitted to the column of lymph and chyle flowing from the thoracic duct into the blood-channels.

The foregoing reference to the anatomy and physiology of the absorbent system shows very conclusively the importance of its pathological relations. It is certainly concerned in the morbid processes of a variety of diseases. But not less important is the fact that it is the main channel for the diffusion of infections throughout the body. Disease may be conveyed by the lymph from a single focus to many and distant parts, whilst the intervening channel of communication may remain free from injury. Along the course of the current every gland may become an additional focus, intensifying the infectiveness of the noxious material and increasing the area of its diffusion. This is alike true of poisons introduced from without and of those originating in the system.

SYNONYM.--Angioleucitis.

DEFINITION.--Lymphangitis may be either simple or septic. As a rule, the disease is localized, but may, especially when induced by some septic poison, be widely diffused, implicating extensive areas of lymphatic tissue and extending to contiguous structures.

Simple lymphangitis may be either reticular or tubular. In the former the fine capillary network or plexus is involved; in the latter the trunkal vessels are inflamed. Very frequently both forms exist at the same time.

ETIOLOGY.--Simple lymphangitis may be either idiopathic or traumatic. It is, however, rarely spontaneous. External irritation, such as solar rays, pressure, and friction, may set up a superficial inflammation, though usually there is some form of injury--a wound, scratch, sprain, contusion, abrasion, prick, or sting of an insect. The graver forms are caused by neighboring inflammation, suppuration, and ulceration. The products of these morbid changes are absorbed and conveyed along the vessels. The inflammation may be continuous along the course of the vessel, or separated from the origin of the morbid product by an area of intervening healthy tissue. Absorption of the secretions and parenchymatous fluids of inflamed parts is an active and frequent agency in the causation of lymphangitis. It may also be caused by contiguous inflamed tissue and by obstruction of the current of the lymph. Lymph-thrombosis, from whatever cause produced, may excite inflammation at the locality of formation, which is usually in the immediate vicinity of a valve, or the thrombi may disintegrate or undergo puriform liquefaction, and thus extend and diffuse the inflammation.

Slight pricks, scratches, and abrasions, which in themselves are so trifling as not to attract attention, may admit irritating substances from without. This is a frequent cause among medical men, whose hands and fingers are constantly exposed to irritating and ichorous discharges.

Localized lymphangitis is frequently set up by specific kinds of irritation. The adenitis and periglandular inflammations in cases of scarlet fever and diphtheria are familiar illustrations. The indurated glands in syphilis and suppurating buboes in chancroid exhibit the different effects of the virus of these forms of disease. The lymphatics of the solid viscera are often inflamed when the organ is the seat of disease. Pelvic cellulitis, if not in itself a lymphangitis, may be the starting-point of a severe and extensive inflammation of the absorbents, occasionally involving both the superficial and deep-seated vessels along one or both thighs.

Age and constitution are recognized factors. Lymphangitis is more frequent in the young, and is much more easily excited in the strumous and persons in a low state of health. Unhygienic conditions predispose to its development.

{987} Lymphangitis may also find its cause in excessive exercise of function, paralysis of vessels, mechanical obstruction to the lymph-stream, lodgment of particles of cancerous or tuberculous matter in the vessels, compression from cicatrices, indurated connective tissue, tumors, diseased glands, stasis in large veins, and regurgitant heart affections.

SYMPTOMATOLOGY.--Reticular lymphangitis is characterized by rapidly-increasing localized redness, attended with a burning, throbbing pain, and usually quickly implicates the skin and its capillaries. Oedema to a greater or less extent may soon ensue, which, when present, increases the pain. Fever may or may not be present, depending in some measure upon the extent, intensity, and cause of the inflammation and upon individual peculiarities. Erythema usually represents a reticular lymphangitis with hyperæmia of the skin and its capillaries, and erythema nodosum is the same associated with lymphatic oedema. Any trivial injury may induce this form of inflammation, such as a prick or the sting of an insect, which in extent, duration, and intensity will vary with the cause, nature of the poison introduced, location, and susceptibility of the sufferer.

Tubular lymphangitis is usually a much more serious form of the disease. When the vessels of the superficial set are involved, wavy or straight irregularly reddened lines are seen along the course of the vessels, extending from the point of beginning to a single gland or ganglion, which is usually tender and enlarged. These lines feel like hard, knotted cords. The inflammation may be limited by the first tier of glands, or it may extend to one or more distant ganglia. From the inflamed gland the disease may be conveyed along the connecting branches of the deeper set of vessels, and both sets may become involved. The inflammation may also extend through the intervening tissues from the superficial to the deeper-seated vessels. When both sets are involved, the disease assumes a graver form and the symptoms are aggravated. The pain becomes more acute, and the swelling is greatly increased and more diffused. Fever may or may not be present, and is usually moderate when the inflammation is confined to the superficial vessels, but when the deeper set is implicated it often commences with a rigor and is usually considerable. When the deeper set is alone affected the red wavy, knotted lines cannot be seen, but may, unless the oedema is great, be felt. The parts are swelled, indurated, and stiffened, due in the acute stage to increased saturation of the tissues, and in the chronic stage to hypertrophy of the connective tissue. When the oedema is great the covering integument presents a glossy, shining appearance.

PATHOLOGY AND MORBID ANATOMY.--In lymphangitis the adventitia of the vessels and surrounding connective tissue are chiefly affected. The external coat is thickened, injected, and infiltrated with cells. The intima becomes opaque and is stripped of its endothelium. The lymph coagulates in the interior of inflamed vessels and blocks up the channel. These thrombi may become organized and permanently obliterate the lumen of the vessel, or they may liquefy or suppurate. Their products may enter the circulation and cause septicæmia or pyæmia. In a few instances the clots have undergone calcareous degeneration. In some instances coagula are found independently of any disease of the coats of the vessels. In such cases the coagulation has been caused by the entrance of some foreign material into the lymph-stream. The thickening and relaxation of the coats of the vessels lead to dilatation, and consequently to slowing of the current and stasis of lymph. From this may result the serious consequences of an extensive lymphangiectasia, which may involve either or both the superficial and deeper vessels of a large area or an entire extremity. In such cases enormous development of the adipose tissue usually takes place, not infrequently associated with rupture of the dilated radicals and exhaustive periodic discharges of lymph. In most of the {988} cases of lymphangiectasia and lymphorrhagia the fluid, which either accumulates in the affected area or is discharged through the ruptured orifices, presents the physical characteristics and appearance of chyle, due to the quantity of fat it contains. In some cases the fluid at first discharged is serous, and gradually changes, as the flow continues, to a chylous or milk-like fluid. In these cases there is also a tendency to frequently-recurring attacks of an erysipelatous or elephantoid inflammation. This predisposition is traceable to the structural changes produced by the previous inflammation, traumatism, or thrombosis. Inflammation and lymph-thrombosis are the pathological processes which usually cause circumscribed narrowing or complete occlusion of lymph-channels; and within the area from which the narrowed or occluded vessels originate there is lymph-stasis, dilatation of trunkal vessels, and oedema of the tissues. Lymphangitis may also cause adhesion of the internal surfaces of the vessel, fibroid transformation or calcification of their coats, and suppuration.

The alterations which take place in the lymph consist chiefly of an increased proportion of fibrin, the addition of numerous cell-elements, not unlike endothelial cells, white and occasionally red blood-corpuscles, lymphoid cells, granular matter, and a varying quantity of albumen and fat, which in a measure must owe their presence to pathological processes affecting the intima and to transformation of the inflammatory products.

All forms of inflammation of the lymphatic vessels exhibit a tendency to extend to the connective tissue. Cellulitis is almost a constant accompaniment of lymphangitis. In other cases the inflammation and consequent thrombosis and obstruction of the lymph-stream produce oedema and saturation of the tissues. Hyperplasia and sclerosis of the connective tissue follow.

Adenitis is characterized by swelling, congestion, and hardness. If resolution takes place, as is usual in all forms of simple lymphangitis, the gland or ganglion will be restored to its normal condition, though not infrequently some enlargement and firmness will remain for a considerable time, which favor recurrences from very trivial causes. It often happens, however, that structural changes occur. Exudation and suppuration may take place. Suppuration begins in the centre, and sooner or later the whole gland-structure is converted into a pus-cavity. Buboes are usually associated with periglandular abscesses. In fact, the latter are very frequently present when the glands do not suppurate, but have assumed a condition of chronic or subacute inflammation, which subsides very slowly and is subject to recurring acute exacerbations from some continuous or repeated irritation. Glands may be devastated or rendered wholly or partially impermeable, thus forming permanent and irremediable obstacles to the lymph-stream. Inflamed and swollen glands are not necessarily impermeable, but the flow of the lymph through them is undoubtedly impeded. The subacute or chronically inflamed glands may become adherent to and imbedded in a mass of indurated connective tissue, and may finally undergo calcareous or caseous degeneration.

Lymphangitis sometimes extends by contiguity of tissue to the synovial membrane of joints, most frequently the knee-joint. So likewise may synovitis and other joint affections set up a lymphangitis. In either case the tendency to suppuration is imminent.

DIAGNOSIS.--The diagnosis of the forms of simple lymphangitis is very easy. The red, wavy, corded, and irregularly-knotted lines following the course of lymphatic vessels readily distinguish it from phlebitis. These lines lead to a gland, which soon also becomes tender and swollen. Oedema soon takes place. An inflamed lymphatic vessel is much smaller and more tender to the touch than an inflamed vein, and usually lies between the injured locality and an inflamed gland. Fever is more constantly present and higher than in phlebitis.

{989} Reticular lymphangitis is usually a circumscribed inflammation, with more or less oedema, located in the region of a lymphatic network. It invades the integumental structures. It is not necessary to distinguish it from an erythema, for the latter can scarcely ever be present without implication of the lymphatic radicles. Tubular lymphangitis and lymphangiectasia, which are so frequently associated conditions and attended with oedema, present objective appearances very similar to those present in oedema from phlebectasis. Phlebectasis is excluded by the absence of pain, of dilatation of the superficial vein, and of changed color, and of a single hard cord along the course of the varicose vein; by the non-appearance of oedema in the neighborhood of the ankle and on the dorsum of the foot during the earlier stages of the disease, and its gradual extension upward. The infiltration in phlebectasis results from increased transudation in consequence of increased blood-pressure in the venous radicles, and their dilatation, or from interrupted venous circulation. The accumulated fluid is consequently watery, poor in solid constituents, and the resulting swelling presents all the characteristics of ordinary oedema. Absorption may be normal or perhaps increased, and with rest of the limb the intumescence will probably diminish or disappear. In consequence of the poverty of the transuded fluid the changes in nutrition are very slow, and the enlargement partakes more of the nature of an anasarca than of an hypertrophy; and, finally, phlebectasis is usually connected with some constitutional affection or distant local disease, and attacks the most distal parts, where the circulation is least supported by the muscles. Lymphangiectasis is most often found in circumscribed localities where the networks of lymph-capillaries are most numerously distributed. The swelling is more diffused, and is not in the form of single hard cords. It is more resistant, and the color of the surface is unchanged. It usually extends downward, and is not so much influenced by continued rest and posture. The accumulated fluid results from diminished absorption or interrupted lymph-circulation, and consists of the normal pre-existing parenchymatous fluids, the nutritive juices continually conveyed thither, and the fluids consumed by the functions of the parts saturated with organic débris. It is, however, more abundantly supplied with organic elements from both progressive and retrogressive metamorphosis. It also contains more albumen and fibrinous substances than the accumulated fluid in phlebectasis and ordinary oedema. The swelling or enlargement is formed of more consistent, coagulable, and partly organizable material, possesses greater consistence, and is nearly compact to the touch, which increases as the fluid undergoes the changes due to its retention in the parts. The development is peculiar, and not altogether unlike phlegmasia. The pus-formations which sometimes ensue partake of the nature of cold abscesses, and are located in the connective tissue. The pus-formations in phlebectasis usually begin in the venous thrombi within the dilated and enlarged veins, are associated with acute symptoms, and result, usually, in purulent absorption.

In view of later anatomical and pathological researches, it must be admitted that phlegmasia dolens is occasionally a lymphangitis, having its origin in inflammation of the vessels or areolar tissue. Some pathologists have advanced the theory that, as seen in lying-in women, it is a parametritis commencing in the cellular tissue in the immediate vicinity of the womb and extending to remoter parts. The writer saw recently, in consultation with J. Taber Johnson, a case of puerperal pelvic cellulitis associated with a firm, resistant, diffuse, painful, and tender swelling involving the inner aspect of both thighs, and extending from the groin on each side downward below the middle third of the thigh. The pelvic inflammation appeared first in the left iliac fossa, and was associated with the swelling before described on the thigh. This subsided, and was immediately followed by a similar condition {990} in the right iliac fossa, accompanied by a precisely similar intumescence on the right thigh. At no time could any enlarged, hard, or corded veins be discovered. The swellings presented the usual objective and tactile characteristics of those inflammatory affections so frequently supervening within areas abundantly supplied with lymph networks, in communication with the original lymphangitis and lymph-thrombosis. In this case the swellings were located in a region specially rich in lymph capillary networks. With the subsidence of the pelvic cellulitis the thigh intumescence on either side gradually disappeared.

Tubular lymphangitis is readily distinguished from erysipelas by the presence of the knotted and corded lymphatic vessels. Reticular lymphangitis is characterized by fine, closely-arranged red lines limited to a circumscribed area, and is usually associated with and starts from some injury. In erysipelas the redness is uniform. It does not follow the course of the lymphatic vessels, nor extend from a wound in the direction of and to a gland or ganglion of glands. The fever is usually higher and of longer duration. The inflamed surface is marked by the appearance of blebs.

PROGNOSIS.--Simple lymphangitis is usually unattended with danger unless complicated with suppurating arthritis. The disease, as a rule, runs a rapid course to recovery. It is more favorable the nearer the inflammation lies to the surface.

TREATMENT.--The treatment is both constitutional and local. The first indication is to remove the cause. The wound should be cleansed and disinfected. For this purpose solutions of carbolic or acetic acid may be employed, or it may be cauterized with caustic potash or chloride of zinc. The fever should be controlled by the employment of antipyretics. One or more full doses of the sulphate or hydrochlorate of quinia, administered at shorter or longer intervals according to the quantity given at each dose and the intensity of the fever, may be sufficient. Antipyrin is a very valuable remedy. It will reduce the fever more speedily and decidedly than the salts of quinia. If the fever is reduced and kept under control by the judicious administration of this remedy in moderate doses, the tendency of the inflammation to extend is very greatly diminished, and may be arrested. Its antipyretic effect is, however, less durable than that of the salts of quinia, but is unattended with the cerebral disturbances usually associated with the employment of quinia salts. The bowels should be kept solvent by the use of saline cathartics. The diet should be restricted during the pyrexial stage. After the acute stage has passed, tonics and improved diet may become necessary; especially will this be the case in those previously debilitated. In healthy, robust subjects it is not probable, under proper and prompt treatment, that the disease will continue long enough to endanger convalescence by serious exhaustion. When needed, iron, cod-liver oil, and the salts of quinia may be resorted to. But, after all, a good appetite and a sufficient supply of nutritious and easily-digested foods constitute the best and most available tonics. Rest of the affected part is very important, and the posture should be such as to remove pressure and relieve tension.

In the beginning of the acute stage cold applications may be employed, but, as a rule, the local treatment should be confined to the assiduous application of hot soothing and emollient fomentations, to which opium or belladonna may be added. By these means the tension of the swollen and inflamed parts, and consequently the pain, are assuaged. It is rarely necessary to employ internally any anodyne to relieve the pain; but in occasional cases, occurring in persons keenly susceptible to pain, an opiate or some less powerful anodyne may be administered. Some advise the local abstraction of blood by leeching, but it is admissible only when the pain is very acute and confined to a limited and defined area. After the subsidence {991} of the fever and acute inflammatory stage the remaining oedema and indurations may be treated with the local application of the tincture of iodine, inunction with mercurial ointment, bandaging, massage, and rest.

For the oedematous condition, which is sometimes very persistent, pressure is the most available and potential remedy. This should be secured by systematic bandaging either with a flannel or an elastic bandage. In such cases passive movement and massage or kneading of the part constitute an important and valuable auxiliary to pressure.

To allay itching, which is sometimes almost intolerable even after the acute inflammation has subsided, the part may be painted with a solution of nitrate of silver or collodion. If these fail, an alcoholic solution of benzoic acid, twenty grains to the ounce, may be employed.

If suppuration takes place, the abscess should be promptly and effectually incised. It should be thoroughly evacuated and dressed antiseptically. When this occurs a more or less tonic and supporting treatment is necessary. Iron, cod-liver oil, quinia, and stimulants may be, according to circumstances, administered. The devastating effects of suppurating cavities should be controlled by the liberal use of the appropriate remedies to arrest exhaustion and to rebuild waste.

In occasional instances the initial stage, consentaneous with the receipt of the injury, such as the sting of an insect, is marked by violent shock and threatening collapse. The writer has witnessed two such cases occurring in robust, healthy men stung by honey-bees on the forearm, where great exhaustion and alarming collapse, with violent retching, profuse diarrhoea, and agonizing pain, were accompanied by rapidly-developed inflammation and swelling at the locality of the puncture. In such cases the free administration of alcoholic stimulants seems imperatively demanded.

The general plan of treatment of acute simple lymphangitis is antiphlogistic, by the employment of remedies to reduce inflammation and promote resolution. The danger of suppuration should not be overlooked or underestimated. A single suppurating focus may widely diffuse disease and impair the entire organism. A single and apparently trivial inflammation of lymphatic tissue may be the initial stage of a fatal pyæmia or septicæmia.

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INDEX TO VOLUME III.

A.

Abdominal aneurism, 821 viscera, lesions, in catarrhal pneumonia, 358

Abscess, diffuse splenic, 962 embolic, of spleen, 963 of the lung, 296 of the mediastinal space, 861 termination of croupous pneumonia in, 311, 332

Abscesses, seat and nature, in suppurative endocarditis, 604

Accidents during tracheotomy, 156

Acephalocysts, expectoration of, in pulmonary hydatids, 469

Aconite, locally, in chronic laryngitis, 127 use, in exophthalmic goitre, 767

Acupuncture, use, in thoracic aneurism, 820

Acute general diseases, resemblance of croupous pneumonia to, 317 miliary tuberculosis, 472

ADDISON'S DISEASE, 939 Definition, synonyms, and history, 939 Diagnosis, 947 Duration, 941 Etiology, 939 Morbid anatomy, 942 Nervous system, lesions, 944 Spleen, lesions, 943 Suprarenal capsules, lesions, 942, 943 Pathology, 944 Theories regarding origin, 945-947 Symptoms, 940 Anæmia and hemorrhages, 940 Bronzing of skin, seat and characters, 940 Dyspnoea, 941 Gastro-intestinal disorders, 941 Nervous symptoms, 941 Pain, characters and seat, 941 Pulse in, 941 Urine, condition, 941 Treatment, 948

Adductors of vocal cords, paralysis of, 81

Adenitis, in lymphangitis, 988

Adherent pericardium, 785

Adhesions, pericardial, seat and characters, 785

Adults, grave form of catarrhal pneumonia in, 360

Adventitious products of the heart, 637

Ægophony, significance, in pleurisy, 510

Aërial fistula, following tracheotomy, 163

After-treatment of tracheotomy, 159

Agaricus, use, in pulmonary phthisis, 438

Age, influence on aortic obstruction, 655 on causation of acute catarrhal laryngitis, 93 of acute miliary tuberculosis, 478 of angina pectoris, 759 of aortic regurgitation, 655 of asthma, 190 of bronchitis, 157 of cardiac thrombosis, 722 of catarrhal pneumonia, 353 of croupous pneumonia, 314 of exophthalmic goitre, 764 of fatty degeneration of the heart, 613 of fibroid phthisis, 441 of fibro-serous pleurisy, 492 of gangrene of lung, 301 of hæmoptysis, 275 of hay asthma, 212 of Hodgkin's disease, 922 of laryngismus stridulus, 70 of leukæmia, 909 of mediastinal tumors, 871 of mitral regurgitation, 671 of mitral stenosis, 666 of pernicious anæmia, 899 of phthisis, 396 of pneumothorax, 576 of pseudo-membranous laryngitis, 101 of purulent pleurisy, 540 of simple lymphangitis, 986 of thoracic aneurism, 802

Air, compressed, use, in bronchial asthma, 208 moist, use, in acute catarrhal laryngitis, 97 rarefied, exhalation into, in emphysema, 246

Albuminoid expectoration following thoracentesis, 535

Alcohol, abuse, influence on causation of chronic laryngitis, 121 of the caisson disease, 858 influence on causation of fatty cardiac degeneration, 612 use, in acute miliary tuberculosis, 481 in bronchial asthma, 205 in catarrhal pneumonia, 370 in croupous pneumonia, 348, 349, 351 in endocarditis, 651 in gangrene of the lung, 305 in parenchymatous degeneration of the heart-muscle, 611 in pseudo-membranous laryngitis, 108 in pulmonary phthisis, 435

Alcoholism, influence on causation of chronic myocarditis, 607 of pleurisy, 493 of croupous pneumonia, 314

Alkalies, use, in pseudo-membranous laryngitis, 105 in rheumatic pericarditis, 783 in prevention and treatment of pulmonary embolism, 389, 390

Alkaline sprays, use, in chronic laryngitis, 125, 127

Allen's nasal forceps, 54

Altitude, influence on causation of hæmoptysis, 277, 278

Alum, use, in laryngismus stridulus, 73

Ammonium, carbonate, use, in cardiac thrombosis, 745 in croupous pneumonia, 349 in prevention of pulmonary embolism, 389 and chloride of, use, in catarrhal pneumonia, 370, 371 chloride, use, in chronic laryngitis, 124, 125

Amphoric respiration in pulmonary phthisis, 417

Amyl nitrite, use, in angina pectoris, 760 in bronchial asthma, 204 in chronic endarteritis of the coronary artery, 830 in fatty cardiac degeneration, 616

Amyloid degeneration of heart-muscle, 616 of suprarenal bodies, 949

ANÆMIA, 887 Albumen, continuous loss of, influence on causation, 887 Blood, changes in, 890, 891 Bone, spleen, lymph-glands, enlargement of, and relation to production of blood-corpuscles, 888-894 Hemorrhage, influence on causation, 887 Inanition, influence on causation, 889 Toxic causes of, 889

Anæmia in Addison's disease, 940 in exophthalmic goitre, 763 in pulmonary phthisis, 406

ANÆMIA, PROGRESSIVE PERNICIOUS, 898 Course, 903 Definition and history, 898 Diagnosis, 905 Etiology, 899 Age and sex, influence on causation, 899 Hygiene, bad, influence on causation, 899 Loss of blood, chronic discharges, etc., 900 Mental worry and anxiety, 900 Pregnancy and parturition, 900 Morbid anatomy, 904 Bones, changes in, 905 Lymph-glands, changes in, 905 Spleen, changes in, 905 Pathology, 905 Prognosis, 906 Symptoms, 900 Blood and blood-corpuscles, changes in, 901 Gastro-intestinal disorders, 903 Hæmic heart-murmurs, 902 Hemorrhages in, 901-903 Oedema in, 901 Onset, mode of, 900 Skin, changes and color of, 901 Temperature, 903 Urine, changes in, 903 Treatment, 906 Arsenic, use, 907 Diet in, 907 Iron, use, 907 Milk, injection of, 908 Transfusion of blood, 907

Anæmic necrosis of heart-muscle, 610

Anæsthesia of larynx, 65

Anæsthetics, use, in laryngismus stridulus, 73

Anatomy of tracheal region, 146, 147

ANEURISM, ABDOMINAL, 821 Diagnosis, 822 Symptoms, 821 Treatment, 822 Compression of aorta, good results of, 822

Aneurism, diagnosis of, from mediastinal tumors, 876

ANEURISM, THORACIC, 801 Definition, 801 Diagnosis, 814 From abscess, 814 From tumors, 814 Duration, 815 Etiology, 802 Age and sex, influence on causation, 802, 803 Occupation, influence on causation, 803 Syphilis and gout, influence on causation, 803 Morbid anatomy, 801, 802 Symptoms, 803 Auscultation in, 811 Bone, signs of pressure upon, 807 Bruit, characters, 811 Cyanosis and oedema, 807 Dysphagia in, 806 Dyspnoea in, 805 Frémissement cataire, frequency, 808 Inspection, 807 Localization of tumors, 812 Myosis in, 805 Of varicose form, 813 Oral whiff of Drummond, significance, 812 Pain, characters, 804 Palpation in, 808 Percussion in, 812 Physical signs in, 807 Pressure signs, 804-807 Pulse, peculiarities of, 808-810 Thrill in pulse, 809 Veins, signs of pressure upon, 807 Voice, modifications of, 806 Terminations, 815 Treatment, 816-820 Acupuncture, use, 820 Barwell's operation of ligation, 818, 819 Ergotin, hypodermic use, 816 Electrolysis, method of applying, 819, 820 Opiates, use, 817 Potassium iodide, 818 Pressure, use, 816 Starvation method, 816 Tufnell's method of rest and diet, 816, 817 Wire, introduction of, into sac, 816

Aneurism of the coeliac axis, 841 of the coronary artery, 830 of the heart, 636 of the hepatic artery, 840 of the interior mesenteric artery, 839 of the superior mesenteric artery, 836 of the pulmonary artery, 833

Aneurismal form of hæmoptysis, 284

Angina, in anæmic necrosis of heart-muscle, 610

ANGINA PECTORIS, 755 Death, cause of, 760 Definition, 755 Diagnosis, 757 Etiology, 758 Morbid anatomy, 758 Prognosis, 759 Symptoms, 755-757 Treatment, 760 Amyl nitrite, use, 760 Chalybeates, use, 760 Digitalis and nux vomica, 761 Opium and morphia, use, 760 Preventive, 760 Stimulants, 760

Angina pectoris in aortic regurgitation, 661

Anginoid attacks in chronic myocarditis, 608, 609

Anomalies, congenital, of heart and great vessels, 687 of blood-vessels of tracheal region, 147 of suprarenal bodies, 949

Ante-mortem heart-clots, character, 737

Anthracosis, appearance of lungs in, 458

Antimony, use, in bronchitis, 179, 180 in croupous pneumonia, 347

Antipyrin, use, in acute miliary tuberculosis, 480, 481 in simple lymphangitis, 990

Antiseptics, use, in croupous pneumonia, 352

Antispasmodics, use, in functional heart disease, 754 in laryngeal oedema, 116 in laryngismus stridulus, 73 in spasm of the glottis, 74

Anxiety, in cardiac thrombosis, 731

Aorta, atheroma of, 800 disease of, influence on causation of hypertrophy of the heart, 620 diseases of, 800 occlusion of, 824, 825 perforation of, 824 rupture of, 823 stenosis of, 825

Aortic arch, localization of aneurism of, 812 conus, defects of, in cyanosis, 708 obstruction, 654 regurgitation, 659 stenosis and regurgitation, treatment, 683 trunk, narrowing, in cyanosis, 708 and mitral orifices, defects of, in cardiac malformations, 690

Aortitis, acute, 800

Apex-beat, in dilatation of the heart, 634 in hypertrophy of the heart, 625, 627 normal position of, 654 significance of position of, in diagnosis of functional heart disease, 750

Apex of lung, tendency to tuberculous deposit in, 408

Aphonia, in paralysis of adductors of vocal cords, 82 in pulmonary phthisis, 403

Apomorphia, use, in catarrhal pneumonia, 371 in acute catarrhal laryngitis, 97, 98

Apoplexy of suprarenal bodies, 949 pulmonary, 293

Appetite, impaired, in pulmonary phthisis, 406

Arch of aorta, localization of aneurisms of, 812

Arsenic, use, in acute miliary tuberculosis, 482 in Addison's disease, 948 in atrophic nasal catarrh, 49 in bronchial asthma, 207 in carcinoma of larynx, 131 in chronic congestion and enlargement of the spleen, 959 in chronic laryngitis, 125 in dilatation of the heart, 636 in Hodgkin's disease, 931 in leukæmia, 921 in pernicious anæmia, 907 in pulmonary phthisis, 436

Arterio-sclerosis of the coronary artery, 828 of the pulmonary artery, 833

Artery, coronary, diseases of, 828 hepatic, aneurism of, 840 pulmonary, diseases of, 833 inferior mesenteric, diseases of, 834 superior mesenteric, diseases of, 836

Arytenoideus, paralysis of, 84

Aspiration in pericardial effusion, 776, 780 of the pleura, dangers of, 596 history, etc., 593-596

Aspirators in thoracentesis, varieties, 530, 532

Asthenic pneumonia, treatment, 351

ASTHMA, BRONCHIAL, 184 Definition, 184 Diagnosis, 198 From dyspnoea of bronchitis and cardiac disease, 198 of laryngeal affections, 199 From embolism of pulmonary artery, 200 From emphysema, 198 From spasm of diaphragm, 199 Duration, 189 Etiology, 190 Age and sex, influence on causation, 190 Cold and damp, influence on causation, 192 Enlarged bronchial glands, 191 Heredity, influence on causation, 190 Pollen of plants, vapors, gases, etc., 192 Uterine, nasal, and stomachic irritation, 193 History, 184 Morbid anatomy, 197 Pathology, 193-197 Prognosis, 200 Sequelæ, 189 Synonyms, 184 Symptoms and course, 185 of intervals, 184 paroxysms, description, frequency, and time of onset, 185-187 heart-circulation, state of, during, 188 physical signs of, 187, 188 Physiognomy of asthmatics, 186, 190 Treatment, 201 Hygienic and dietetic, 206 Locality, change of, 206 Of intervals, 206 Of paroxysms, 201 Use of arsenic, 207 of belladonna and stramonium, 203 of chloroform, 202 of cigarettes, medicated, 203, 207 of compressed air, 208 of electricity, 205 of emetics, 204 of lobelia and tobacco, 204 of morphia and chloral hydrate, 201, 202 of nitrite of amyl, 204 of nitro-glycerin, 208 of potassium bromide, 204 iodide, 207 nitrate, 203 of stimulants, 205

Asthma complicating emphysema, 239 hay, 210

Astringents, use, in chronic laryngitis, 125, 126 in laryngeal oedema, 116

Atelectasis, influence on causation of bronchial dilatation, 228

Atelectasis. See _Lung, Collapse of_.

Atheroma of the aorta, 800 of the coronary artery, 828 of the pulmonary artery, 833

Atmospheric causes of goitre, 977

Atomizer, use, in hyper- and paræsthesia of the larynx, 64

Atresia of the pulmonary artery, 702

Atropia, use, in profuse expectoration of bronchiectasis, 231 in pulmonary phthisis, 438 in the caisson disease, 858

Atrophic form of chronic nasal catarrh, 47 lobar emphysema, 248

Atrophy of suprarenal bodies, 949 of the heart, 618

Auricles of the heart, hypertrophy of, 627

Auriculo-ventricular orifice and tricuspid valve, defects of, 689 rings, condition, in cardiac dilatation, 633

Auscultation during paroxysm of asthma, 187 of mediastinal tumors, 874 in bronchial dilatation, 229 in bronchitis, 170-174 in cardiac malformation, 710, 711 thrombosis, 728 valvular disease, 657, 663, 668, 673, 675, 677, 680 in catarrhal pneumonia, 359, 360, 362, 363 in collapse of the lung, 253 in croupous pneumonia, 335, 337, 338 in emphysema, 238 in endocarditis, 648 in fibro-serous pleurisy, 507-510 in hydrothorax, 572 in mediastinal abscess, 862 in pericarditis, 775 in pneumothorax, 579 in pulmonary phthisis, 412-418 in purulent pleurisy, 543, 544 in pyo-pneumothorax, 545 in thoracic aneurism, 811

Auscultatory percussion in fibro-serous pleurisy, 503

Auto-laryngoscopy, 29

Axillary glands, enlargement of, in Hodgkin's disease, 926

B.

Bacelli's sign of pleurisy, 510, 517, 543

Bacillus tuberculosis, relation of, to acute miliary tuberculosis, 477 to hæmoptysis, 279, 280 to pulmonary phthisis, 398

Balfour's treatment of aneurism, 818

Balsams, use, in chronic bronchitis, 182

Bandage, use, in phlegmasia dolens and lymphangitis, 848, 991

Barrel-shaped chest of emphysema, 237

Barwell's operation for cure of thoracic aneurism, 818

Basedow's disease. See _Exophthalmic Goitre_.

Baths, cold, use, in bronchial asthma, 206 in croupous pneumonia, 349 hot, use, in laryngismus stridulus, 73

Belladonna, use, in pulmonary phthisis, 438 and stramonium, use, in bronchial asthma, 203

Bellocq's canula, use, in epistaxis, 52

Benign form of pulmonary embolism, symptoms, 382 growths of the larynx, 128 tumors of the trachea, 140

Benzoin, use, in chronic laryngitis, 124, 126

Bilious pneumonia, 334

Binaural stethoscope, use, in auscultation, 412

Black sputa of pitmen, 455, 459

Blaud's pills, use, in chlorosis, 896

Bleeder families, 933

Bleeding in heart disease, question of, 686

Bleedings, seat and amount, in hæmophilia, 935

Blisters, use, in acute myocarditis, 606 in capillary bronchitis, 180 in chronic phlebitis, 848 in pericardial effusion, 784 in pleurisy, 521 in thoracic aneurism, 817

Blood changes in, in croupous pneumonia, 313 in hæmoptysis, 287 in Hodgkin's disease, 924 in leukæmia, 911, 915 in pernicious anæmia, 901 condition of, in chlorosis, 894 in hæmophilia, 936 diseases of the, 882

Blood-corpuscles, changes in, in pernicious anæmia, 901 relation of spleen, lymph-gland, and bone-marrow to production, 890, 891

Blood-glandular system, diseases of, 882

Bloodletting, local and general, in pulmonary congestion and oedema, 263, 264

Blood-vessels, pulmonary, changes in, in emphysema, 243 relation of, to miliary tubercles, 474, 475

Bone-marrow, hyperplasia of, in anæmia, 892 influence on blood-formation, 885 lesions, in leukæmia, 916 in pernicious anæmia, 905

Bones, pressure upon, in thoracic aneurism, 807

Bowditch's connection with history of thoracentesis, 591-595

Brain, lesions, in croupous pneumonia, 313 in pernicious anæmia, 905 and membranes, lesions, in catarrhal pneumonia, 358 in leukæmia, 918

Breath, fetid, in chronic pharyngitis, 122

Breathing, in collapse of lung, 252

Bright's disease, complicating phthisis, 407 influence on causation of pericarditis, 771 of congestion and oedema of the lungs, 259

Bromides, use, in exophthalmic goitre, 767

Bronchi, diseases of, 164

Bronchial asthma, 184 breathing, in pleurisy, 508 catarrh, complicating emphysema, 247 influence on causation of collapse of lung, 251 glands, enlargement of, in croupous pneumonia, 313 lesions, in bronchitis, 175, 176 in catarrhal pneumonia, 357 in pneumonokoniosis, 457 lesions of syphilis of the lungs, 451 respiration in croupous pneumonia, 337

BRONCHIAL TUBES, DILATATION OF (Bronchiectasis), 227 Definition, history, and etiology, 227 Diagnosis and prognosis, 230 Morbid anatomy, 230 Symptoms, 228 Treatment, 230

BRONCHITIS, 164 Definition, 164 Diagnosis, 176 From phthisis, 177 From pneumonia, 176 Of chronic form, from emphysema, 177 Etiology, 164 Age and sex, influence on causation, 165 Cold and damp, season, etc., 166-168 Exciting causes, 168 Predisposing causes, 165 History, 164 Morbid anatomy, 175 Mortality, 165, 177 Prognosis, 177 Synonyms, 164 Symptoms--acute form, 169 Capillary form, 171 Cough, characters, 171 Dyspnoea in, 171 Physical signs of, 171 Chronic form, 174 Cough and expectoration, characters of, 174 Mechanical form, 170 Pseudo-membranous form, 173 Rheumatic form, 172 Treatment, 178 Of acute and capillary forms, 178-180 Antimony, use, 180 Counter-irritation, 178 Emetics, 180 Expectorants, 179 Quinia, use, 179 Venesection, 178 Of chronic form, 181 Alteratives, 182 Change of climate, 183 Compressed air, 183 Diet, 181 Inhalations, 182 Iron, use, 182 Of pseudo-membranous form, 180 Of rheumatic form, 180

Bronchitis and pneumonia, influence on causation of phthisis, 394 complicating emphysema, 239 tracheotomy, 162 of acute infectious diseases, influence on causation of catarrhal pneumonia, 354

Broncho-vesicular respiration, characters and significance of, 412

Brown atrophy of heart-muscle, 616 induration of lungs, 256

Bruit, in thoracic aneurism, 811

C.

Caffeine, use, in dilatation of the heart, 635

CAISSON DISEASE, 854 Definition, 854 Duration, 855 Etiology, 857 Morbid anatomy, 855 Pathology, 855 Symptoms, 854 Headache, vertigo, and coma, 855 Nausea and vomiting, 854 Pain, seat and characters, 854 Paralyses, 854, 855 Treatment, 858 Atropia, use, 858 Compressed air, 859 Ergot, use, 859 Morphia, use, 858 Of paralysis, 859

Calcareous degeneration of the heart-muscle, 616

Calcification of the vein, 852

Calcium sulphide, use, in acute phlebitis, 846

Canulas, tracheotomy, 151, 152

Cancer of adrenals in Addison's disease, 943 of the heart, 639 of the lungs, 460 of the pericardium, 792 of the pleura, 583 of the veins, 853

Capillary bronchitis, 171 emboli of lungs, effects, 385 vessels, relation to miliary tubercles, 475

Caput Medusæ, 849

Carbolic acid, danger of, in injections into pleural cavity, 561 use, in abscess of lung, 300 in gangrene of lung, 305 injections, in goitre, 980 and iodine, injections, in pericardial effusions, 795

Carcinoma of the larynx, 128 of the mediastinum, seat and characters, 869 of the nasal passages, 55 of the thyroid gland, 978 of the trachea, 141

Cardiac action, irregular, in fatty degeneration of the heart, 615 disease influence on causation of chronic splenic enlargement, 957 hæmoptysis, symptoms, 285 hypertrophy, relation to adherent pericardium, 786 murmurs, relation to valvular disease, 651 sedatives, use, in hypertrophy of the heart, 630

CARDIAC THROMBOSIS, 718 Complications and sequelæ, 733 Definition, 718 Diagnosis, 740 From dyspnoeic uræmia, 742 laryngeal affections, 743 nervous shock of acute endocarditis, 744 pulmonary embolism, 743 Duration and terminations, 732 Etiology, 721 Age and sex, influence on causation, 722 Mechanical causes, 723 Vital or pathological causes, 724 Endocarditis, influence on causation, 725 History, 719 Morbid anatomy and pathology, 734 Of ancient clots, 737 cadaveric and terminal clots, 735 Physical characters of clots, 735-740 Prognosis, 744 Synonyms, 718 Symptoms, 726 Blowing murmur of Bouillaud, significance, 730 Dyspnoea, 730 Mental condition, 731 Pain, 730 Physical signs, 727 Physiognomy in, 730 Pulse, characters, 729 Syncope, 730 Treatment, 745 Alkalies, as solvents, use, 745 Ammonium carbonate and liquid ammonia, use, 745 Counter-irritation, 746 Digitalis and nux vomica, use, 746 Intravenous injections of ammonia, 745 Rest, value, 746 Sodium bicarbonate, use, 745 Stimulants, use, 746

Cardicentesis, 798

Caseated morbid products, influence on causation of pulmonary phthisis, 400

Caseous pneumonia following pleurisy, 514 pus, influence on causation of acute miliary tuberculosis, 473

Casts of bronchi, in pseudo-membranous bronchitis, 176

Catarrh, chronic nasal, 42

Catarrhal pneumonia in children, symptoms, 359 relation of, to collapse of lung, 354, 355 tendency, influence on causation of hæmoptysis, 275

Catheterization of larynx in true croup, 107

Cavernous form of hæmoptysis, 284

Cavities, diagnosis of, in pulmonary phthisis, 416 tubercular, injection of, 439, 440

Cell-walls, changes in, as a cause of emphysema, 334

Cerebral anæmia, in aortic obstruction, 656 disturbance in functional heart-disease, 749 hyperæmia in tricuspid regurgitation, 649

Cerebral symptoms in cardiac thrombosis, 731 of croupous pneumonia, 329 of pericarditis, 774

Chest, alterations of, in pleuritic effusions, 497, 498 changes in, in emphysema, 236, 237

Cheyne-Stokes breathing in fatty degeneration of the heart, 615

Children, catarrhal pneumonia in, 359

Chills in croupous pneumonia, 320 in pleurisy, 494 in purulent pleurisy, 542

Chloral hydrate, use, in bronchial asthma, 202 in catarrhal pneumonia, 372

Chlorides, diminution of, in croupous pneumonia, 330

Chloroform, use, in bronchial asthma, 202

Chlorosis, 894 Definition and etiology, 894 Morbid anatomy, 894 Symptoms, 895 Treatment, 896

Chondritis of the larynx, 117

Chorea of the larynx, 76

Chronic bronchitis, 174 influence on causation of bronchiectasis, 228 congestion and enlargement of the spleen, 956 endarteritis of the coronary artery, 828 of the pulmonary artery, 833 interstitial pneumonia, 391, 440 lobular emphysema, 233 myocarditis, 607 pericarditis, 784 phlebitis, 848 purulent pleurisy, symptoms, 342

Cigarettes, medicated, use, in bronchial asthma, 203, 207

Circumscribed pleurisies, 545

Cirrhosis of the liver, influence on causation of splenic enlargement, 957 of lung, displacement of heart by, 603

Classification of hay asthma, 221 of pleurisy, 454 of pneumonokoniosis, 454 of pulmonary embolism, 373

Climate, change of, in acute laryngitis, 96 in chronic bronchitis, 183 influence on frequency of hæmoptysis, 277

Climatic treatment of pulmonary phthisis, 427

Clothing, proper, for phthisical patients, 433, 434

Clots, ancient or ante-mortem, of heart, characters, 737 cadaveric, in cardiac thrombosis, 735 terminal, in cardiac thrombosis, 735

Clubbing of fingers in cyanosis and cardiac malformations, 711

Cocaine, use, in chronic laryngitis, 127 in coryza, 42 in epiglottic ulceration, 112 in hyper- and paræsthesia of the larynx, 65 in morbid growths of the larynx, 131

Codeia, use, in bronchitis, 180, 182 in cough of miliary tuberculosis, 480

Cod-liver oil, use, in acute miliary tuberculosis, 482 in atrophic nasal catarrh, 49 in chronic bronchitis, 182 in chronic laryngitis, 125 in pulmonary phthisis, 434 in purulent pleurisy, 549 in ulceration of trachea, 139 in vesicular emphysema, 245

Coeliac axis, aneurism of, 841 diseases of, 841

Coffee, use, in bronchial asthma, 205 black, use, in cardiac thrombosis, 746

Colchicum, use, in rheumatic bronchitis, 181

Cold applications in epistaxis, 51 influence on causation of congestion and oedema of the lungs, 258 of pericarditis, 770 of perichondritis and chondritis of larynx, 117 use, in catarrhal pneumonia, 371 in pericarditis, 783 in reduction of temperature in croupous pneumonia, 349 in simple lymphangitis, 990 and damp, influence on causation of asthma, 192 of bronchitis, 166 of croupous pneumonia, 315 of fibro-serous pleurisy, 491 and moisture, influence on causation of acute catarrhal laryngitis, 93

Collapse of lung, 250

Color of ante-mortem heart-clots, 739

Columnæ carneæ, lesions, in chronic myocarditis, 607

Communicability of pulmonary phthisis, 396

Complications after tracheotomy, 161 of acute coryza, 41 of cancer of the lungs, 464 of cardiac thrombosis, 733 of catarrhal pneumonia, 364 of emphysema, 239 of fibro-serous pleurisy, 512 of mediastinal abscess, 864 of pulmonary phthisis, 400

Compressed air, use, in bronchial asthma, 208 in chronic bronchitis, 183 in emphysema, 245

Compression in treatment of abdominal aneurism, 823

Congenital anomalies of the heart and great vessels, 687 malpositions of the heart, 601

Congestion, acute, of spleen, 953 and enlargement of the spleen, chronic, 956 and oedema of the lungs, 258

Congestive form of hæmoptysis, 283

Contagiousness of acute miliary tuberculosis, 472 of pseudo-membranous laryngitis, 102 of pulmonary phthisis, 396-400

Conus arteriosus dexter, obstruction with open ventricular septum in cyanosis, 703

Convallaria, use, in dilatation of the heart, 635

Convulsions, in croupous pneumonia, 329 in pseudo-membranous laryngitis, 102

CORONARY ARTERY, DISEASES OF, 828 Chronic Endarteritis (Arterio-sclerosis; Atheroma), 828 Diagnosis and prognosis, 829, 830 Etiology and symptoms, 828 Pathology, 829 Treatment, 830 Aneurism of, 830 Embolism of, 831 Embolism and thrombosis of, 831 Obliterating endarteritis of, 830 Occlusion of, 831 Rupture of, 833 Thrombosis of, 832

Corpuscles of the blood, changes in, in Hodgkin's disease, 924 in leukæmia, 912 in pernicious anæmia, 901

Coryza, acute, 41

Cough in acute catarrhal laryngitis, 94 in asthma, 188 in bronchial dilatation, 228 in capillary bronchitis, 171 in cardiac malformations and cyanosis, 710 in catarrhal pneumonia, 358-361, 363 in chronic bronchitis, 174 pharyngitis, 122 in croupous pneumonia, 322 in emphysema, 236 in fibro-serous pleurisy, 495 in hydatids of pleura, 585 in laryngismus stridulus, 71 in mitral regurgitation, 671 stenosis, 667 in morbid growths of the trachea, 140 in pseudo-membranous laryngitis, 102 in pulmonary congestion in oedema, 260 phthisis, 400 treatment, 436 in purulent pleurisy, 542 in thoracic aneurism, 806 nervous, 71

Counter-irritation in acute bronchitis, 178 in atelectasis, 255 in cardiac thrombosis, 745, 746 in catarrhal pneumonia, 369 in croupous pneumonia, 347 in pericarditis, 783

Course of anæsthesia of the larynx, 67 of cardiac thrombosis, 732 of fibro-serous pleurisy, 510 of hyperæsthesia of the larynx, 163 of hypertrophy of the heart, 621 of laryngismus stridulus, 71 of leukæmia, 818 of pernicious anæmia, 903 of pulmonary congestion and oedema, 261

Crepitant râle of croupous pneumonia, 335

Crico-arytenoid muscles, hysterical paralysis of, 83

Cricotomy, 148, 156

Critical phenomena in croupous pneumonia, 331

Croup, false. See _Laryngismus Stridulus_.

Croupous pneumonia, 307

Cubebs, use, in chronic laryngitis, 124

Cyanosis, admixture theory of origin, 712 congestive theory of origin, 714 in cardiac malformation, 709 in fibroid phthisis, 442 in fibro-serous pleurisy, 496 in mitral regurgitation, 671 and congenital anomalies of the heart and great vessels, 687

Cysts, fibrinous, in cardiac thrombosis, 738 hydatid, of lungs, number and seat, 467 of suprarenal bodies, 949 of the heart, 637

Cystic goitre, 978

D.

Dangers of thoracentesis, 534

Death, cause of, in angina pectoris, 760 in croupous pneumonia, 345 in leukæmia, 919 in pericarditis, 783 in pulmonary embolism, 380, 381 in thoracentesis, 536, 537 in valvular heart disease, 681 mode of, in cardiac thrombosis, 732 in Hodgkin's disease, 929

Decubitus in fibro-serous pleurisy, 495

Definition of acute miliary tuberculosis, 472 of Addison's disease, 939 of angina pectoris, 755 of anæsthesia of larynx, 65 of bronchitis, 164 of bronchial asthma, 184 dilatation, 227 of brown induration of lungs, 256 of cancer of the lung, 460 of cardiac thrombosis, 718 of catarrhal pneumonia, 353 of chronic laryngitis, 121 nasal catarrh, 42 of collapse of the lung, 250 of congestion and oedema of lungs, 258 of croupous pneumonia, 307 of dilatation of the heart, 630 of endocarditis, 639 of emphysema, 232 of epistaxis, 50 of gangrene of the lung, 301 of hæmophilia, 931 of hæmoptysis, 266 of hæmothorax, 582 of hay asthma, 210 of Hodgkin's disease, 921 of hydrothorax, 570 of hyperæsthesia of the larynx, 62 of hypertrophy of the heart, 619 of laryngeal oedema, 112 of leukæmia, 908 of lymphangitis, 986 of mediastinal tumors, 864 of morbid growths of larynx, 128 of trachea, 139 of pericarditis, 169 of perichondritis and chondritis of the larynx, 117 of pernicious anæmia, 898 of pleurisy, 483 of pneumonokoniosis, 454 of pneumothorax, 573 of pulmonary abscess, 296 embolism, 373 hydatids, 466 phthisis, 391 of purulent pleurisy, 539 of simple tracheitis, 133 of spasm of the glottis in adults, 74 of stenosis of trachea, 142 of syphilis of the lung, 447 of the caisson disease, 854 of thoracic aneurism, 801

Deflected septum in chronic nasal catarrh, 44

Degenerations of heart-muscle, 609-616 of the suprarenal bodies, 949 of the veins, 852

Dermoid cysts of the mediastinum, 870

Delirium in croupous pneumonia, 329

Dentition, influence on causation of laryngismus stridulus, 70

Depressing influences, influence on causation of croupous pneumonia, 315

Diagnosis of abdominal aneurism, 823 of abscess of the lung, 299 of acute and chronic bronchitis, 176 of acute catarrhal laryngitis, 95 of acute congestion of spleen, 955 of acute miliary tuberculosis, 480 of acute myocarditis, 606 of acute phlebitis, 846 of Addison's disease, 947 of adherent pericardium, 788 of anæsthesia of larynx, 66 of aneurism of the coeliac axis, 842 of angina pectoris, 757 of aortic obstruction, 657 regurgitation, 664 of asthma, 198 of atrophic emphysema, 249 of bronchial dilatation, 230 of cancer of the lung, 464 of the pleura, 584 of cardiac thrombosis, 740-744 of catarrhal pneumonia, 365 of chronic congestion and enlargement of the spleen, 958 endarteritis of the coronary artery, 829 laryngitis, 124 myocarditis, 609 of collapse of the lung, 254 of coryza, 41 of croupous pneumonia, 339 of cyanosis, 709 of dilatation of the heart, 634 of echinococcus of the spleen, 969 of embolic splenic abscess, 964 of embolism of the coronary artery, 832 of the superior mesenteric artery, 838 of endocarditis, 650 of epiglottic affections, 109-112 of exophthalmic goitre, 763 of fatty cardiac degeneration, 615 infiltration of the heart, 612 of fibroid phthisis, 443 of functional heart disease, 749-752 of gangrene of the lung, 304 of hæmophilia, 937 of hæmoptysis, 289 of hæmothorax, 582 of hay asthma, 221 of hemorrhagic pleurisy, 568 of Hodgkin's disease, 929 of hydatids of the pleura, 585 of hydrothorax, 572 of hyperæsthesia and paræsthesia of the larynx, 64 of hypertrophic lobar emphysema, 243 of hypertrophy of the heart, 627 of interlobular emphysema, 249 of lardaceous spleen, 967 of laryngeal oedema, 115 of laryngismus stridulus, 72 of leukæmia, 919 of mediastinal abscess, 863 tumors, 876 of mitral regurgitation, 674 stenosis, 669 of morbid growths of the larynx, 130 of the trachea, 141 of paralysis of adductors of vocal cords, 83, 85 of tensors of vocal cords, 85, 86 of pseudo-membranous laryngitis, 103 of pericardial effusion, 778 of pericarditis, 776 of pernicious anæmia, 905 of pleurisy, 514 of pneumonokoniosis, 459 of pneumothorax, 580 of pulmonary apoplexy, 294 congestion and oedema, 262 embolism, 387 hydatids, 469 phthisis, 410 regurgitation, 677 stenosis, 676 of purulent pleurisy, 543 of simple lymphangitis, 988 tracheitis, 134 of spasm of the glottis in adults, 75 of stenosis of the aorta, 827 of the trachea, 142 of syphilis of the lungs, 453 of thoracic aneurism, 815 of thrombosis of the coronary artery, 832 of tricuspid stenosis, 677

Diaphoretics, use, in laryngeal oedema, 116 in pulmonary abscess, 264

Diaphragm, displacement of, in pleurisy, 497, 498, 507

Diaphragmatic pleurisy, 563

Diarrhoea in Hodgkin's disease, 925 in leukæmia, 910 in pernicious anæmia, 903 in pulmonary phthisis, 406 treatment, 439

Diathesis, the tubercular, 477

Diet after tracheotomy, 161 in acute miliary tuberculosis, 481 in Addison's disease, 948 in bronchial asthma, 206 in cardiac valvular disease, 683, 685 in catarrhal pneumonia, 369, 370 in croupous pneumonia, 348 in collapse of the lung, 256 in endocarditis, 651 in fatty degeneration of the heart, 616 in hay asthma, 224 in pericarditis, 783 in pernicious anæmia, 907 in pseudo-membranous laryngitis, 108 in simple lymphangitis, 990 restricted, in thoracic aneurism, 817

Dietetic treatment of pulmonary phthisis, 431

Digestive disorders in functional heart disease, 749 influence on causation of pernicious anæmia, 900

Digitalis, use, in acute myocarditis, 606 in angina pectoris, 761 in aortic disease, 684 in chronic endarteritis of the coronary artery, 830 in croupous pneumonia, 349 in dilatation of the heart, 635 in exophthalmic goitre, 767 in fatty degeneration of the heart, 616 in functional disease of the heart, 754 in hypertrophy of the heart, 630 in mitral disease, 685 in pericarditis, 783 in pulmonary congestion and oedema, 263 in vesicular emphysema, 247, 248

Dilatation of the pulmonary artery, 833 of the bronchial tubes, 227 of the heart, 630 of the trachea, 143 of the veins, 849

Diphtheria, influence on causation of anæsthesia of the larynx, 66 paralysis of the larynx, 80 of the trachea, 136

Displacement of adjacent organs in pleurisy, 504 of the heart in pneumothorax, 577

Displacements of the heart, 601-604

Disseminated form of catarrhal pneumonia, lesions, 357

Diverticular dilatation of trachea, 143

Double pleurisy, 562 pneumonia, prognosis, 343

Drainage of pleural cavity, methods of, 552-562

Dropsy in aortic regurgitation, 661 in mitral regurgitation, 672 of emphysema, treatment, 247 time of appearance in tricuspid regurgitation, 679

Drummond's oral whiff in aneurism, 812

Ductus arteriosus Botalli, defects of, in cardiac malformation, 691

Duration of anæsthesia of the larynx, 67 of asthma, 189 of cancer of the lungs, 463 of cardiac thrombosis, 732 of catarrhal pneumonia, 368 of fibro-serous pleurisy, 511 of Hodgkin's disease, 929 of laryngismus stridulus, 71 of life in cardiac malformations and cyanosis, 711 of mediastinal abscess, 863 tumors, 875 of pulmonary phthisis, 424 of stenosis of the aorta, 825 of the caisson disease, 855 of thoracic aneurism, 815

Durham's tracheotomy canula, 151

Dysphagia in chronic pharyngitis, 122 in hysterical affections of the glottis, 83 in inflammation of the epiglottis, 110 in laryngeal oedema, 114 in mediastinal tumors, 872, 873 in morbid growths of larynx, 129 in perichondritis and chondritis of the larynx, 118 in thoracic aneurism, 806

Dysphonia in morbid growths of larynx, 129 in perichondritis and chondritis of the larynx, 118 in pulmonary phthisis, 408

Dyspnoea in acute catarrhal laryngitis, 94 in Addison's disease, 941 in angina pectoris, 756 in aortic regurgitation, 661 in cardiac thrombosis, 730 in catarrhal pneumonia, 359, 360, 363 in chronic pharyngitis, 122 in croupous pneumonia, 321 in cyanosis and cardiac malformation, 710 in dilatation of trachea, 144 in fatty infiltration of the heart, 612 in fibro-serous pleurisy, 493, 495 in Hodgkin's disease, 925 in hydatids of pleura, 585 in hydrothorax, 571 in hypertrophy of the heart, 626 in laryngeal oedema, 114 in leukæmia, 913 in mediastinal tumors, 872 in mitral regurgitation, 671 stenosis, 667 in morbid growths of the larynx, 129 in paralysis of abductors of vocal cords, 88 in pernicious anæmia, 903 in pneumothorax, 578 in pulmonary embolism, 379-381 in stenosis of the trachea, 143 in thoracic aneurism, 805

E.

Echinococcus of the spleen, 968

Effects of cardiac hypertrophy, 626 of pulmonary embolism, 383

Effusions, characters, in purulent pleurisy, 540, 541 of fibro-serous pleurisy, 487-491 of pericarditis, 772

Elaterium, use, in hydrothorax, 572

Electric illuminator, use, in laryngoscopy, 24

Electricity, use, in anæsthesia of the larynx, 68 in angina pectoris, 761 in bronchial asthma, 205 in paralysis of the larynx, 90

Electrolysis, use, in goitre, 980 in thoracic aneurism, 819

Embolic abscess of the spleen, 963

Embolism and thrombosis of coronary artery, 831 of pulmonary artery, 835 complicating cardiac thrombosis, 733 from aortic obstruction, 656 influence on causation of gangrene of the lung, 302 of inferior mesenteric artery, 839 of pulmonary artery distinguished from asthma, 200 of superior mesenteric artery, 836 relation to acute myocarditis, 604 symptoms of, in endocarditis, 647

Emetics, use, in acute catarrhal laryngitis, 97 in catarrhal pneumonia, 371 in collapse of the lung, 255 in pulmonary congestion, 263 in pseudo-membranous laryngitis, 106

EMPHYSEMA, 232 Definition and history, 232 Varieties, 232 _Interlobular or Extra-vesicular Emphysema_, 249 _Vesicular Emphysema_, 232 Acute lobular form, 232 Symptoms and treatment, 233 Atrophic lobar form, 248 Symptoms and treatment, 248, 249 Chronic lobular form, 233 Hypertrophic lobar form, 233 Complications, 239 Diagnosis, 243 Duration, 242 Etiology, 234 Changes in alveolar wall, influence on causation, 234 Expiratory and inspiratory theories of causation, 235, 236 Heredity, influence on causation, 234 Morbid anatomy, 242 Prognosis, 244 Symptoms, 236 Cough and dyspnoea, 236 Chest, shape of, 237 Physical signs, 236-238 Respiration, peculiarities of, 238 Treatment, 245 Cod-liver oil, use, 245 Compressed air, use, 245, 246 Digitalis, use, 247 Expectorants, use, 246 Expiration into expired air, 246 Iron, use, 245 Potassium, iodide, 246 Quinia hydrobromate, hypodermatically, 247 Strychnia, use, 245

Emphysema after tracheotomy, 162 distinguished from asthma, 198 following asthma, 189

Empyema, pulsating, 596 See _Pleurisy, Purulent_.

Enchondroma of the mediastinum, 871

Encysted pleurisies, 545, 546

Endarteritis, obliterating, of the coronary artery, 830 of the pulmonary artery, 833 of the superior mesenteric artery, 839

ENDOCARDITIS, 639 Definition, 639 Diagnosis, 649 From aortitis, 650 From pericarditis, 649 Etiology, 645 Acute and chronic Bright's disease, 646 Acute rheumatism, 645, 646 Pyæmia, puerperal fever, the specific fevers, etc., 646 History, 639 Morbid anatomy, 640-645 Of acute exudative form, 640 Of interstitial form, 643 Of ulcerative form, 642 Prognosis, 650 Symptoms, 646 Dyspnoea, 647 Mitral murmurs, frequency and characters of, 648 Of exudative form, 647 Of interstitial form, 647 Of ulcerative form, 647 Pain in, 647 Physical signs, 648, 649 Physiognomy, 647 Pulse, characters, 647 Tricuspid and aortic murmurs, characters, 649 Treatment, 650 Iron, use, 651 Opium, use, 651 Rest, value, 651 Stimulants, use, 651

Endocarditis, influence on causation of cardiac thrombosis, 725 ulcerative, influence on causation of splenic infarction, 961

Engorgement stage of croupous pneumonia, 308

Enlargement of the spleen, chronic, 951, 956 in lardaceous disease, 967 in syphilis, 971

Epigastric pulsation in mitral disease, 672 in tricuspid disease, 679

Epiglottis, erosion of, 110 treatment, 111 inflammation of, 109, 110 ulceration of, 111 symptoms and treatment, 112

Epistaxis, 50-52 in croupous pneumonia, 331

Ergot, use, in epistaxis, 51 in embolism of superior mesenteric artery, 839 in hæmophilia, 938 in hæmoptysis, 291 in morbid growths of larynx, 131

Ergotin, use, in aneurism, 816 in exophthalmic goitre, 766 in hæmoptysis of heart disease, 685 in hæmothorax, 583 in pulmonary phthisis, 437

Erosion of epiglottis, 110

Eruptive fevers, influence on causation of pericarditis, 771 of pleurisy, 493

Erysipelas of the trachea, 136

Ether, use, in pneumothorax, 582

Etiology of acute catarrhal laryngitis, 93 miliary tuberculosis, 473 splenic congestion, 953 of Addison's disease, 939 of anæsthesia of the larynx, 65 of aneurism of the coeliac axis, 841 of the coronary artery, 830 thoracic, 802, 803 of aortic obstruction, 655 regurgitation, 660 of asthma, 190 of atheroma of the aorta, 800 of atrophic lobar emphysema, 252 of bronchial dilatation, 227 of bronchitis, 164 of brown induration of the lungs, 256 of cancer of the lungs, 460 of cardiac malformation, 694 thrombosis, 721 of catarrhal pneumonia, 353 of chronic congestion and enlargement of spleen, 956 endarteritis of the coronary artery, 828 laryngitis, 121 of collapse of the lung, 250 of congestion and oedema of the lungs, 258 of croupous pneumonia, 324 of dilatation of the heart, 631 of the veins, 849 of embolism of the coronary artery, 831 of emphysema, 234 of endocarditis, 645 of epistaxis, 50 of exophthalmic goitre, 764 of fatty degeneration of the heart, 612 of fibroid phthisis, 440 of fibro-serous pleurisy, 491 of functional heart disease, 752 of gangrene of the lung, 301 of goitre, 976 of hæmophilia, 932 of hæmoptysis, 272 of hæmothorax, 582 of hay asthma, 212 of hemorrhagic pleurisy, 565 of Hodgkin's disease, 922 of hydrothorax, 570 of hyperæsthesia of the larynx, 62 of hypertrophy of the heart, 619 of hysterical affections of the glottis, 83 of lardaceous spleen, 966 of laryngeal oedema, 113 of laryngismus stridulus, 70 of leukæmia, 909 of lymphangitis, 986 of mediastinal abscess, 861 tumors, 871 of mitral regurgitation, 671 stenosis, 666 of morbid growths of the larynx, 127 of the trachea, 139 of paræsthesia of the larynx, 63 of paralysis of abductors of vocal cords, 87 of adductors of vocal cords, 81 of constrictors of larynx, 80 of tensors of vocal cords, 85, 86 of the whole larynx, 79 of pericarditis, 769 of perichondritis and chondritis of larynx, 117 of perisplenitis, 965 of pernicious anæmia, 899 of pneumonokoniosis, 454 of pneumothorax, 573 of pseudo-membranous laryngitis, 101 of pulmonary abscess, 296 apoplexy, 293 embolism, 374 hydatids, 466 phthisis, 394 stenosis, 675 of purulent pleurisy, 539 of spasm of the glottis in adults, 74 of stenosis of the aorta, 826 of the trachea, 142 of syphilis of the lung, 447 of the caisson disease, 857 of tricuspid regurgitation, 678

Eucalyptol, use, in bronchial dilatation, 231

Evil effects of goitre, 979

Exciting causes of asthma, 191 of bronchitis, 168 of gangrene of the lung, 302 of hay asthma, 214

Excision of the spleen, 960 of the sternum in mediastinal abscess, 863 of the thyroid gland, 981

Exercise, importance, in pulmonary phthisis, 432, 433 in chronic bronchitis, 183

EXOPHTHALMIC GOITRE (Graves' Disease; Basedow's Disease), 761 Definition, 761 Diagnosis, 763 Etiology, 764 Morbid anatomy, 764 Prognosis, 765 Symptoms, 762 Dyspnoea, 763 Digestive disorders, 763 Eyeball, protuberance of, 762 Increased heart-action, 762 Thyroid body, enlargement of, 762 Treatment, 765 Aconite, use, 766 Digitalis, use, 767 Ergot, hypodermically, 766 Ice-bag to præcordiæ, 767 Iron, use, 766, 767 Iodine, use, 766 Hydropathic packing and the needle-bath, 766 Galvanization, 767 Of exophthalmia, 766 Opiates, use, 766

Expectorants, use, in bronchitis, 179 in simple tracheitis, 135 in pulmonary phthisis, 436

Expectoration, albuminoid, following thoracentesis, 535 characters in, in acute catarrhal laryngitis, 79 in asthma, 188 in bronchial dilatation, 228 in capillary bronchitis, 171 in catarrhal pneumonia, 359-361 in croupous pneumonia, 322 in chronic bronchitis, 174 in fibroid phthisis, 441

Expectorations, characters in fibro-serous pleurisy, 496 in gangrene of the lung, 303 in pulmonary congestion and oedema, 260 in pulmonary phthisis, 401 in simple tracheitis, 133, 134 of acephalocysts in pulmonary hydatids, 469

Expiratory movement in asthmatic paroxysm, 186 theory of origin of emphysema, 235

Exploratory puncture in mediastinal abscess, 863 value, in diagnosis of pleurisy, 518 of purulent pleurisy, 543, 548

Extra-pulmonary hæmoptysis, 285

Exudations of fibro-serous pleurisy, characters, 486

Exudative endocarditis, acute, 640

Eyeball, protuberance of, in exophthalmic goitre, 640

F.

Faintings in Addison's disease, 941

False membranes of true croup, nature, 100 seat and character, in purulent pleurisy, 541

Fatality of Addison's disease, 941

Fatty degeneration of the heart, 612 of the veins, 852 infiltration of the heart, 611

Fevers, influence on causation of dilatation of the heart, 632

Fibroid heart, 607 phthisis, influence on causation of bronchial dilatation, 228

Fibroma of nasal passages, 55

Fibromata of trachea, frequency, 140

Fibro-serous pleurisy, 484

Fibrous goitre, 977

Fistula, aërial, following tracheotomy, 163 in phthisical persons, treatment of, 439

Fistulæ, pleuro-bronchial, seat and characters in purulent pleurisy, 542

Fistules, pericardial, 796

Flatness, level of, pleuritic effusions, 487, 491, 500

Fluctuation in pulmonary hydatids, 468

Flush of pneumonia, 328

Follicular goitre, 977 and fibrous goitre, treatment, 979, 980

Fomentations, use, in phlebitis, 846

Fragility of pulmonary vessels as a cause of hæmoptysis, 275

Frémissement in pulmonary hydatids, 468 cataire in thoracic aneurism, 808

Friction sounds in fibro-serous pleurisy, 507-509 in pericarditis, 775, 777

Functional heart disorders, 747

G.

Gallic acid, use, in epistaxis, 51 in hæmoptysis, 291

Gangrene of the lung, 301 influence on causation of pneumothorax, 575 complicating catarrhal pneumonia, 364 termination of croupous pneumonia in, 332

Gastric pneumonia, 334

Gastro-intestinal canal, lesions, in catarrhal pneumonia, 358 in croupous pneumonia, 313 in Hodgkin's disease, 928 in leukæmia, 917 in pernicious anæmia, 904 disorders in abdominal aneurism, 821 in Addison's disease, 941 in catarrhal pneumonia, 360, 362 in croupous pneumonia, 330 in endocarditis putrida, 647 in functional heart disease, 749 in Hodgkin's disease, 925 in leukæmia, 910 in mitral regurgitation, 671 in pernicious anæmia, 903 in pulmonary phthisis, 406 in tricuspid regurgitation, 679

Galvanism, use, in Addison's disease, 948

Galvanization, use, in exophthalmic goitre, 767

Galvano-cautery knife, use, in tracheotomy, 150 snare, use, for removing nasal growths, 56 use, for removal of nasal hypertrophies in hay asthma, 224 in chronic nasal catarrh, 44, 45, 47, 48, 50 in epistaxis, 51

Gelatinous goitre, 978 treatment, 981

General diseases, influence on causation of phthisis, 396

Geographical distribution of goitre, 975 of hay asthma, 218

Gestation, influence on causation of goitre, 977

Giddiness in Addison's disease, 941

Glacier- and ice-water, influence on causation of goitre, 976

Glands, bronchial lesions of, in bronchitis, 175

Glottis, hysterical affections of, 83 spasm of, in adults, 74, 75

GOITRE, 974 Definition, 974 Etiology, 976 Atmospheric causes, 977 Gestation and syphilis, influence on causation, 977 Glacier- and ice-water, influence on causation, 976 Geographical distribution, 975 Symptoms, 974 Treatment, 979 Electrolysis, use, 980 Ergot, use, 980 Excision of gland, 982 Injections, use, 989, 981 Iodides of lead and mercury, locally, 980 Iodine, use, 979-981 Iodoform, use, 979 local, 979 Natural mineral waters, use, 980 Of follicular and fibrous form, 979 Of gelatinoid or cystic form, 981 Of vascular form, 980 Syrup of iodide of iron, 979-981 Tincture of iron, injections, 981 Varieties, 977

Goitre, exophthalmic, 761

Gold, chloride of, use, in epiglottic erosion and ulceration, 111, 112

Gout, influence on causation of aortic regurgitation, 660 of thoracic aneurism, 803

Granulations, exuberant, complicating tracheotomy, 162

Grave form of pulmonary embolism, 380

Graves' disease. See _Exophthalmic Goitre_.

Great vessels, malformations of, 690

Gray hepatization stage of croupous pneumonia, lesions, 310

Gummy tumors of the spleen, 971

Gummata of the lung, 449, 450

H.

Hæmatemesis, distinguished from hæmoptysis, 289

Hæmopericardium, 788, 789

HÆMOPHILIA, 931 Classification, synonyms, and history, 932 Definition, 931 Diagnosis, 937 Etiology, 932 Age and sex, influence on causation, 933 Heredity, causation, 932 Morbid anatomy, 936 Pathology, 936 Prognosis, 938 Symptoms, 934-936 Blood in, 936 External bleedings, seat, 935 Interstitial bleedings, seat and characters, 935 Joints, affections of, 935, 936 Treatment, 938 Diet, 938 Ergot and iron, use, 938 Prophylaxis, 938

HÆMOPTYSIS, 266 Definition, 266 Diagnosis, 289 From hæmatemesis, 289 Etiology, 272 Age, influence on causation, 275 Bacillus tuberculosis, relation of, to, 279, 280 Catarrhal predisposition, influence on causation, 275 Exciting causes, 278 Fragility of blood-vessels, influence on causation, 275 Heredity, influence on causation, 272-275 Injury, influence on causation, 279 Pregnancy, influence on causation, 278 Sex, influence on causation, 276 Season, climate, etc., influence on causation, 277, 278 History, 266-272 Mortality, 290 Pathology and morbid anatomy, 286 Aneurisms of pulmonary artery, appearance of, 287 Heart, changes in, 288 Of cardiac hæmoptysis, 288 Of pulmonary infarction, 288 Seat of, and changes in hemorrhages, 288 Prognosis, 290 Synonyms, 266 Symptoms, 281 Frequency of attacks, 284 Of aortic aneurism discharging into air-passages, 285 Of cavernous form, 284 Of extra-pulmonary form, 285 Of hemorrhagic infarction and cardiac form, 285, 286 Of simple, congestive, and ulcerative forms, 283, 284 Physical signs, 282 Treatment, 291, 292 Absolute quiet, necessity of, 291 Astringent inhalations, 291 Ergot and turpentine, use, 291 Gallic acid, use, 291 Ice, use, 291 Ipecacuanha, use, 292 Opium, use, 291, 292 Quinia for fever following, 292

Hæmoptysis in hypertrophy of the heart, 627 in pulmonary phthisis, 401 influence on causation of pulmonary phthisis, 395

HÆMOTHORAX, 582 Etiology and pathology, 582 Symptoms, 582 Treatment, 583

HAY ASTHMA, 210 Classification, 221 Definition, 210 Diagnosis, 221 Etiology, 212 Age, sex, and heredity, influence on causation, 212, 213 Certain plants and grasses, 215, 216 Dust and animal parasites, 216 Exciting causes, 214 Heat and dryness, 214, 215 Occupation and temperament, 213, 214 Pollen theory of origin, 216-218 Predisposing causes, 212 Geographical distribution, 218 History, 210 Prognosis, 222 Symptoms and course, 218-221 Treatment, 222 Diet, 224 Climate, change of, 224 Galvanism, 224 Nasal hypertrophies, removal of, 224, 225 Nasal injections, use, 224 Quinia, use, 224

Headache and vertigo in mitral regurgitation, 672 in acute congestion of spleen, 954 in croupous pneumonia, 329 in Hodgkin's disease, 925 in leukæmia, 911

Head-reflector, use in laryngoscopy, 22

Heart and circulation, effect of asthmatic paroxysm upon, 188

HEART AND GREAT VESSELS, MALFORMATIONS OF, 687 Diagnosis, 709 Duration of life in, 709 Etiology, 692 Defects of arterial outlet of right ventricle, the most frequent primary cause, 694 Narrowing of pulmonary artery and patency of septum ventriculorum, theories of origin of, 697-702 Development of foetal heart, relation to course, 698, 700 Malformation affecting primarily left side, 707-709 Narrowing of aortic trunk, 708 Stenosis of the conus, 708 Affecting primarily the right side, 702-706 Of conus arteriosus dexter, with open ventricular septum, 703 Of pulmonary artery, combined stenosis, and atresia of, 706 Of pulmonary artery, closure of, with perfect ventricular septum, 702 Of pulmonary artery, stenosis of, with open ventricular septum, 706 Symptoms, 709 Clubbing of fingers and toes, 711 Cyanosis, 709 Dyspnoea and cough, 710 Physical signs, 710 Temperature in, 710

Heart and lung, disease, influence on causation of pulmonary embolism, 375 aneurism of, 636 atrophy of, 618 cancer of, 637 changes in, in emphysema, 240 clot, as a cause of death in croupous pneumonia, 343 condition of, in hæmoptysis, 288 cysts of, 637

HEART, DILATATION OF, 630 Definition, 630 Diagnosis, 634 Etiology, 631 Morbid anatomy, 633 Prognosis, 635 Symptoms, 634 Treatment, 635 Caffeine, use, 635 Convallaria, use, 635 Digitalis, use, 635 Rest, value of, 635

Heart disease, death from, following thoracentesis, 536 displacements of heart from, 602 influence on causation of congestion of the lungs, 258 influence on causation of hydrothorax, 570 diseases of the substance of, 601

HEART, DISPLACEMENTS OF, 602 From abdominal disease, 604 From changes in chest-wall, 602 From cirrhosis of lung, 603 From disease of pleura, 498, 504, 603 From heart disease, 602 From mediastinal tumors, 603 From pericardial effusions, 602 In pneumothorax, 577

HEART, FATTY DEGENERATION OF, 612 Diagnosis and prognosis, 615 Etiology, 612 Age and sex, influence on causation, 613 Cardiac hypertrophy, influence on causation, 613 Mineral and alcoholic poisoning, 612 Morbid anatomy, 613, 614 Symptoms, 614 Physical signs, 615 Pulse in, 615 Treatment, 616 Amyl nitrite, use, 616 Digitalis, use, 616 Iron and vegetable tonics, 616

HEART, FATTY INFILTRATION OF, 611 Diagnosis, 612 Etiology, 611 Symptoms and treatment, 612

HEART, FUNCTIONAL DISORDERS OF, 747 Diagnosis, 749 Etiology, 750 Morbid anatomy, 752 Prognosis, 753 Symptoms, 748 Cerebral disturbances, 749 Digestive disturbances, 749 Infrequency of intermittence of heart's action, 748 Palpitation, 747 Paroxysms, characters, and frequency of, 748 Treatment, 753 Aconite, use, 754 Alcohol, use, 755 Antispasmodics, use, 753, 754 Digitalis, use, 754 Opium and morphia, use, 754 Preventive, 754 Tonics, chalybeate, use, 754

HEART, HYPERTROPHY OF, 619 Definition, 619 Diagnosis, 627 Etiology, 619 Disturbed innervation, influence on causation, 619 Kidney disease, 621 Mechanical causes, 620 Morbid anatomy, 624 Prognosis, 629 Symptoms, 624 Dyspnoea, 626, 627 Physical signs, 625-627 Pulse, characters, 625, 627 Sensation, uneasy cardiac, 626, 627 Treatment, 630 Digitalis, use, 630 Sedatives, use, 630 Varieties, 619

Heart, lesions of, in Hodgkin's disease, 928 in interstitial endocarditis, 644, 645 in pernicious anæmia, 904 malpositions of, 601 murmur, cause of, in pleurisy, 510 muscle, amyloid degeneration of, 616 anæmic necrosis of, 610 brown atrophy of, 616 calcareous degeneration of, 616 degenerations of, 609-616 hyaline degeneration of, 616 parenchymatous degenerations of, 610 neuroses of, 747 normal positions of, 601, 602 palpitation of. See _Heart, Functional Disorders of._ parasites of, 637 rupture of, spontaneous, 617

Heart's action, increase of, in exophthalmic goitre, 762 mechanism of, 652

Heart, sarcoma of, 637 sounds, in adherent pericardium, 788 in pericarditis, 776 syphilis of, 637 tubercle of, 637

HEART, VALVULAR DISEASES OF, AND CARDIAC MURMURS, 651 Definition, 651 History, 651 Murmurs, 654 _Aortic Obstruction or Stenosis_, 654 Diagnosis, 657 Etiology, 655 Morbid anatomy, 654 Symptoms, 656 Cerebral anæmia, 656 Cerebral and other embolisms, 656 Murmurs, characters, 657 Physical signs, 657 Pulse, characters, 657 _Aortic Regurgitation or Insufficiency_, 659 Diagnosis, 664 Etiology, 659 Morbid anatomy, 659 Symptoms, 659 Carotid pulsation, 661, 662 Pain, characters, 661 Physical signs, 662 Pulse, characters, 661 _Mitral Regurgitation_, 669 Diagnosis, 674 Etiology, 671 Morbid anatomy, 669 Symptoms, 671 Cough and expectoration, 671 Cyanosis and physiognomy, 671 Digestive disorders, 671 Dropsy, occurrence of, 672 Headache, vertigo, etc., 672 Murmurs, seat and characters, 673 Physical signs, 672 Pulse, characters, 672 _Mitral Stenosis_, 665 Diagnosis, 669 Etiology, 666 Morbid anatomy, 665 Symptoms, 667 Hæmoptysis, 667 Murmurs, characters, 668 Pain, 667 Physical signs, 668 Pulmonary congestion, cough, etc., 667 Pulse, characters, 667 Purring thrill, significance, 668 _Pulmonary Obstruction_, 674 Diagnosis, 676 Etiology, 675 Morbid anatomy, 675 Symptoms and physical signs, 675 _Pulmonary Regurgitation_, 676 Physical signs, 677 _Tricuspid Regurgitation_, 677 Diagnosis, 680 Etiology, 678 Morbid anatomy, 678 Symptoms, 679 Cerebral hyperæmia, 679 Jugular and epigastric pulsation, 679 Physical signs, 679 Prognosis in valvular heart disease, 680-683 Treatment, 683 Arsenic, use, 684, 685 Calomel and jalap, use, 685 Diet in, 683-686 Digitalis, use, 684, 685 Ergotin, 685, 686 Hygienic, 683, 684, 686 Iron, use, 684, 685 Nitrate of amyl, use, 684, 686 Of aortic disease, 683, 684 Of dropsy, 684, 685 Of hæmoptysis, 685 Of mitral disease, 685 Of tricuspid disease, 686 Opium and morphia, use, 684, 686 Quinia and strychnia, use, 684, 685 Rest, value, 683 Squill, juniper and cream of tartar, use, 685

Heat and dryness, influence on causation of hay asthma, 214 use, in laryngismus stridulus, 73

Hemorrhage and congestion in pulmonary embolism, 384 during and after tracheotomy, 158, 162 in croupous pneumonia, 331 influence on causation of anæmia, 887 intestinal, in embolism of the superior mesenteric artery, 837 seat, in hæmoptysis, 287

Hemorrhages in Addison's disease, 940 in leukæmia, 913 in pernicious anæmia, 903 in pulmonary phthisis, 401, 402 interstitial, of hæmophilia, 935 seat and amount, in hæmophilia, 935

Hemorrhagic infarction of spleen, 960 pleurisy, 565

Hemorrhoids from obstruction of portal vein, 850

Hepatic artery, aneurism of, 840

Hepatization of croupous pneumonia, lesions, 309

Heredity, influence on causation of acute catarrhal laryngitis, 93 of asthma, 190 of emphysema, 234 of epistaxis, 50 of hæmophilia, 934 of hæmoptysis, 272-275 of hay asthma, 212 of Hodgkin's disease, 922 of pulmonary phthisis, 395 on prognosis of phthisis, 423

Hernia of trachea, 143

Herpetic eruptions of croupous pneumonia, 328

Hiccough in goitre, 979

History of Addison's disease, 939 of bronchial asthma, 184 dilatation, 227 of bronchitis, 164 of brown induration of the lungs, 256 of cardiac murmurs, 651 thrombosis, 719 of collapse of the lung, 252 of congestion and oedema of the lungs, 258 of croupous pneumonia, 307 of cyanosis and cardiac malformations, 687 of emphysema, 232 of endocarditis, 639 of gangrene of the lung, 301 of hæmophilia, 932 of hæmoptysis, 266 of hay asthma, 210 of Hodgkin's disease, 922 of hydrothorax, 570 of the laryngoscope, 19 of leukæmia, 908 of pernicious anæmia, 898 of pleurisy, 483 of pneumonokoniosis, 454 of pneumothorax, 573 of pulmonary abscess, 296 embolism, 373 hydatids, 466 phthisis, 392, 394 of purulent pleurisy, 539 of the rhinoscope, 21 of syphilis of the lung, 447

Hoarseness in acute laryngitis, 94

HODGKIN'S DISEASE, 921 Course, duration, and termination, 929 Definition and synonyms, 921 Diagnosis, 929 Etiology, 922 Morbid anatomy, 926 Lymph-glands, lesions, 926, 927 Spleen, lesions, 927 Pathology and prognosis, 930 Symptoms, 923 Blood and circulation, changes in, 924 Digestive disorders, 925 Genito-urinary system, changes in, 925 Hæmic murmurs in, 925 Lymphatic glands, enlargement of, seat and characters, 923 Skin, changes in, 925 Special senses, modifications of, 925 Spleen, enlargement of, 925 Respiratory system, disorders, 925 Treatment, 931 Arsenic, use, 931 Local, 931 Iodine and potassium iodide, use, 931 Phosphorus, use, 931 Quinia, iron, and cod-liver oil, use, 931

Hoffmann's anodyne, use, in functional heart disease, 753

Hyaline degeneration of heart-muscle, 616

Hydatids of the pleura, 585 pulmonary, 466

Hydropathic packing in exophthalmic goitre, 766

Hydropericardium, 789, 790

HYDROTHORAX, 570 Diagnosis and prognosis, 572 Definition, etiology, and history, 570 Pathological anatomy and symptoms, 571 Treatment, 572

Hygienic treatment of croupous pneumonia, 347 of pernicious anæmia, 907 of pleurisy, 519 of valvular heart disease, 683-685

Hyoscyamia, use, in catarrhal pneumonia, 372

Hyoscyamus, use, in acute catarrhal laryngitis, 98

Hyperæsthesia of larynx, 62

Hyperplasia of cytogenic tissues, relation to increase of white blood-corpuscles, 893 of spleen, lymph-glands, and bone-marrow, influence on causation of anæmia, 890, 891

Hypertrophic lobar emphysema, 233 nasal catarrh, 44

Hypertrophy of auricles of the heart, 627 of erectile tissue in chronic nasal catarrh, 44 of the heart, 619

Hypophosphites, use, in acute miliary tuberculosis, 481 in emphysema, 245 in phthisis, 435

Hypostatic pneumonia. See _Lungs, Congestion and Oedema of_.

Hysteria, influence on causation of paræsthesia of the larynx, 64

Hysterical affections of the glottis, 83

I.

Ice, use, in acute catarrhal laryngitis, 97 in laryngeal oedema, 117 in pericarditis, 783 in pseudo-membranous laryngitis, 104

Iceland, frequency of hydatid disease in, 466

Idiosyncrasy, influence on causation of cardiac functional disease, 752

Image, the laryngeal, 30 the rhinoscopic, 39

Impulse, cardiac, in adherent pericardium, 787 in aortic obstruction, 657 regurgitation, 662 in mitral regurgitation, 672 stenosis, 668 in pericarditis, 774 in tricuspid regurgitation, 679 in dilatation of the heart, 634 in hypertrophy of the heart, 625, 627

Inanition, influence on causation of anæmia, 889

Incipient phthisis, diagnosis of, 411

Indications for paracentesis of the pericardium, 794 for thoracentesis, 521 for tracheotomy, 145

Infarction, hemorrhagic, of lungs, symptoms, 286 of spleen, 960 pulmonary, lesions of, 288 in pulmonary embolism, characters and seat, 384

Infectious fevers, influence on causation of acute interstitial myocarditis, 605

Inferior mesenteric artery, diseases of, 839 tracheotomy, 148, 155

Inflammation of the epiglottis, 109 of the mediastinum, 861 of suprarenal capsules, 949 of the veins, 843

Inflammatory theory of origin of cardiac malformations, 692

Inflation of lung in atelectasis, 253, 254

Infrequency of heart's action in functional disease, 748

Inhalations, astringent, in hæmoptysis, 291 in chronic bronchitis, 182 in fibroid phthisis, 444 in pseudo-membranous laryngitis, 106 in simple tracheitis, 135 in ulcer of trachea, 139

Injections, use, in chronic enlargement of the spleen, 960 in echinococcus of the spleen, 970 in goitre, 980, 981 into pericardial sac, 795 into pleural cavity in purulent pleurisy, 551, 553, 562 of arsenic into spleen in leukæmia, 921 of tubercular cavities, 439, 440

Injury, influence on causation of hæmoptysis, 279 of paralysis of the larynx, 79

Innervation, disturbed, influence on causation of hypertrophy of the heart, 619

Innominate aneurism, localization of, 812

Inoculability of tuberculous disease, 397

Inspection in bronchitis, 163 in cardiac malformations, 710 thrombosis, 729 valvular disease, 657, 662, 668, 672, 675, 677, 679 in catarrhal pneumonia, 360, 361 in croupous pneumonia, 335, 336, 338 in endocarditis, 648 in fibro-serous pleurisy, 497, 498 in hypertrophy of the heart, 625, 627 in mediastinal abscess, 862 tumors, 874 in pericarditis, 774 in pneumothorax, 578 in thoracic aneurism, 807

Inspiratory and expiratory theories of origin of emphysema, 235

Instruments necessary in tracheotomy, 149

Insufficiency, aortic, 659

Insufflator, use, in chronic laryngitis, 126

Intercostal spaces, bulging of, in pleuritic effusion, 497, 498, 507

Interlobular emphysema, 249 pleurisy, 564

Intermittence of heart's action, 748

Intermittent pneumonia, 334

Interstitial endocarditis, 643 myocarditis, acute, 605 pneumonia, chronic, 391, 440

Iodine, locally, in acute congestion of the spleen, 956 in chronic congestion and enlargement of the spleen, 960 inflammation of the epiglottis, 110 laryngitis, 126 in exophthalmic goitre, 766 in pulmonary phthisis, 435 injection of, in goitre, 980, 981 internal use, in goitre, 979, 980 test for lardaceous spleen, 968 use, in Hodgkin's disease, 931

Iodoform, use, in chronic epiglottic inflammation, 110 in chronic laryngitis, 125

Ipecacuanha, use, in acute catarrhal laryngitis, 98 in bronchitis, 180 in hæmoptysis, 292 in laryngismus stridulus, 73

Iron, perchloride, injection of, in goitre, 981 pernitrate, use, in epiglottic ulceration, 112 syrup of the iodide of, use, in goitre, 979 use, in Addison's disease, 948 in anæsthesia of the larynx, 68 in angina pectoris, 761 in chlorosis, 896 in chronic congestion of the spleen, 960 in dilatation of the heart, 636 in endocarditis, 651 in exophthalmic goitre, 766, 767 in fatty degeneration of the heart, 616 in functional heart disease, 755 in hæmophilia, 938 in paralysis of the larynx, 91 in passive pulmonary congestion, 263, 264 in pernicious anæmia, 907 in pulmonary phthisis, 436 in valvular heart disease, 684, 685 in vesicular emphysema, 245

Irregular cardiac action in fatty degeneration, 615

Irritable heart, 747

Irritants, influence on causation of pseudo-membranous croup, 101 to pulmonary tissue, influence on causation of phthisis, 394

Ischæmia of the heart, influence on causation of angina pectoris, 758

Itching of skin and mucous membranes in hay asthma, 220, 221

J.

Jaborandi, local use, in chronic laryngitis, 125 use, in fibro-serous pleurisy, 520, 521 in laryngeal oedema, 116

Jacquemet on causes of death in pulmonary embolism, 381

Jarvis' snare for removal of nasal polypi, 54

Jaundice in mitral regurgitation, 671

Joint affections of hæmophilia, 935

Joints, lesions of, in hæmophilia, 936

Jugular pulsation in tricuspid regurgitation, 679

K.

Kidney disease, influence on causation of cardiac hypertrophy, 621 of pleurisy, 493 of pulmonary embolism, 375

Kidneys, lesions, in Hodgkin's disease, 928 in leukæmia, 918 in pernicious anæmia, 905 state of, in pseudo-membranous laryngitis, 102

L.

Lactic acid, use, in pseudo-membranous laryngitis, 106

Lardaceous spleen, 966

Laryngeal image, the, 30-33

Laryngectomy in morbid growths of the larynx, 131

LARYNGITIS, ACUTE CATARRHAL (False Croup), 92 Diagnosis, 95 From diphtheritic laryngitis, 95 From membranous croup, 95 From tubercular laryngitis, 95 Duration, 94 Etiology, 93 Pathology, 92 Prognosis, 96 Symptoms, 93 Treatment, 96 Alkalies in, 97 Apomorphia in, 97, 98 Baths, cold and sea, in, 96 Emetics in, 98 Ice in, 97 Inhalations in, 97 Narcotics in, 98 Of oedema of glottis in, 98 Potassium chlorate in, 91 iodide in, 97 Silver nitrate in, 97, 99

LARYNGITIS, CHRONIC, 121 Definition, etiology, and synonyms, 121 Diagnosis, 123 Morbid anatomy, 122 Prognosis, 124 Symptoms, 121 Treatment, 124 Ammonium chloride, use, 124 Anodynes, 127 Arsenic and cod-liver oil, use, 125 Cocaine, use, 127 Cubebs, use, 124 Inhalations, use, 126 Insufflations, use, 126 Iodoform, use, 125 Respirators, use, 126 Tar, use, 125, 126 Tracheotomy in, 127

Laryngitis, chronic tubercular, 123 syphilitic, 123 complicating pulmonary phthisis, 403

LARYNGITIS, PSEUDO-MEMBRANOUS, 100 Complications, 103 Contagiousness, 101 Diagnosis, 103 From catarrhal laryngitis, 104 From general oedema of glottis, 104 Etiology, 101 Mortality, 103 Pathology, 100 Prognosis, 103 Symptoms, 101 Treatment, 104 Alkalies in, 105 Diet in, 107 Emetics in, 106 Ice in, 104 Inhalations in, 106 Lactic acid in, 106 Massage of larynx, 107 Mercury in, 104 Pilocarpine in, 106 Quinia in, 105, 108 Stimulants in, 108 Strychnia in, 108 Tracheotomy in, 107

Laryngoscope, description of, 21 history of, 19

Laryngoscopy and rhinoscopy, 19

LARYNGOSCOPY, ART OF, 25-29 description of the laryngeal image, 30-33 methods of illumination in, 23-25 obstacles to, 28, 29 position of observer, 26 position of patient in, 26 use of electric illuminator, 24 use of head-reflector in, 22

Laryngotomy, in morbid growths of the larynx, 31

Larynx, anæsthesia of, 65 treatment, 67

LARYNX, CHOREA OF, 76 Symptoms, 76 Treatment, 77 Diseases of, 109 Disorders of motion of, 68 Exalted action of, 69 Hyperæsthesia of, 62 Treatment, 64 Lepra of, 132 Lupus of, 132 Muscles of, 59 Nerves of, 60

LARYNX, MORBID GROWTHS OF, 127 Definition and etiology, 127 Morbid anatomy, 128 Prognosis and diagnosis, 130 Symptoms, 129 Treatment, 131 Cocaine, use, 131 Laryngectomy, 131 Laryngotomy in, 131

Larynx, muscles of, 59 nerves of, 60 neuroses of, 59

LARYNX, OEDEMA OF, 112 Definition and synonyms, 112 Diagnosis and morbid anatomy, 115 Prognosis, 116 Symptoms, 113 Treatment, 116 Antispasmodics, use, 116 Astringents, use, 116 Diaphoretics, use, 116 Jaborandi, use, 116 Ice, use, 117 Morphia, use, 116 Purgatives, use, 116 Scarification, 116 Tracheotomy, 117

LARYNX, PARÆSTHESIA OF, 63 Symptoms and treatment, 64 Paresis and paralysis of muscles of, 78 Paralysis of constrictors of, 80 Perversions of sensations of, 61

LARYNX, PERICHONDRITIS AND CHONDRITIS OF, 117 Definition and etiology, 117 Diagnosis and prognosis, 120 Morbid anatomy and symptoms, 118 Treatment, 121

LARYNX, SPASM OF, IN CHILDREN (Laryngismus Stridulus), 70 Course and duration, 71 Diagnosis, 72 From true croup, 72 From simple laryngitis, 72 Etiology, 70 Pathology, 71 Prognosis, 72 Symptoms, 70 Voice in, 71 Treatment, 73 Alum in, 73 Anæsthetics, 73 Antispasmodics in, 73 Baths, hot, in, 73 Emetics in, 73 Ipecacuanha, 73 Potassium bromide in, 73

Latent pneumonia, 334, 342

Laxatives, use, in pleuritic effusions, 520

Leeches, in acute bronchitis, 178

Left ventricles, hypertrophy of, 625

Lepra of the larynx, 132

Lesions of cancer of the lung, 460, 461 of chronic congestion of the spleen, 958 of croupous pneumonia in children, 312 of fibro-serous pleurisy, 485 of lungs in pneumonokoniosis, 457, 458 in pulmonary phthisis, 408, 410 of nervous system, in Addison's disease, 944 of pulmonary hydatids, 467 Seat in syphilis of the lung, 450

LEUKÆMIA, 908 Course, 918 Definition, synonym, and history, 908 Diagnosis, 919 Etiology, 909 Age and sex, influence on causation, 909 Climate, influence on causation, 909 Malarial and previous disease, causation, 909 Syphilis, influence on causation, 910 Morbid anatomy, 915 Blood, and heart-changes in, 915 Bone-marrow, changes in, 916 Lymphatic glands, changes in, 916 Leukæmic growths, characters of, 918 Spleen, changes in, 915 Prognosis, 920 Symptoms, 910 Blood-corpuscles, changes in, 911, 912 Digestive disorders, 910 Genito-urinary disorders, 913 Hemorrhages, seat and characters, 913 Lymphatic glands and spleen, enlargement of, 914 Nervous symptoms, 911 Pulse, characters, 913 Respiratory symptoms, 913 Special senses, modification of, 911 Treatment, 920 Arsenic, use, 921 Ergot, use, 921 Excision of spleen, 921 Iron, use, 921 Quinia, use, 921 Transfusion, 921

Ligation of carotid and subclavian arteries in thoracic aneurism, 818

Lime, use, in pseudo-membranous laryngitis, 105

Liver, changes in, in tricuspid regurgitation, 678, 679 displacement of, in pleurisy, 497, 507 enlargement of, in leukæmia, 911 influence on destruction of the blood, 885 lesions, in catarrhal pneumonia, 358 in Hodgkin's disease, 928 in leukæmia, 918 in mitral regurgitation, 670

Lobelia, use, in bronchial asthma, 204

Local treatment of chronic congestion and enlargement of the spleen, 960 of chronic laryngitis, 125 of epiglottic inflammation, 109, 110 ulceration, 112 of laryngeal oedema, 116 of simple lymphangitis, 990 of ulceration of trachea, 139

Locality, change of, in bronchial asthma, 206 choice of, in treatment of hay asthma, 223

Localization of thoracic aneurisms, 812

LUNG, ABSCESS OF, 296 Definition, history, etiology, and synonyms, 296 Diagnosis, 299 Pathology and morbid anatomy, 298 Prognosis, 300 Symptoms and course, 297 Treatment, 300

LUNGS, CANCER OF, 460 Definition, 460 Diagnosis, 464 Duration, 463 Etiology and morbid anatomy, 460 Prognosis, 465 Symptoms, 461

LUNG, COLLAPSE OF (Atelectasis), 250 Definition and history, 250 Diagnosis, 254 Etiology, 250 Age, influence on causation, 251 Bronchial catarrh, relation of, to, 250, 251 Mechanism of production, 251 Thoracic effusions, influence on production of, 252 Morbid anatomy, 253 Prognosis, 255 Symptoms, 252 Treatment, 255 Diet in, 256 Emetics, question of use, 255 Expectorants, use, 255 Of congenital form, 255

LUNGS, CONGESTION AND OEDEMA OF (Hypostatic Pneumonia), 258 Course and termination, 261 Definition, 258 Diagnosis, 262 Etiology, 258 History, 258 Morbid anatomy, 261 Prognosis, 262 Symptoms, 260 Treatment, 263 Of passive form, 263 Of pulmonary oedema, 264 Use of bloodletting, general and local, 263, 264 of diaphoretics, 264 of digitalis, 263 of emetics, 263 of iron in chronic form, 263, 264 of stimulants, 263 of quinia hydrobromate, hypodermatically, 264

Lung, displacement of, in pleurisy, 506

LUNG, GANGRENE OF, 301 Course and duration, 305 Definition, synonyms, and etiology, 301 Diagnosis and prognosis, 304 Pathology and morbid anatomy, 303, 304 Symptoms, 302 Treatment, 305

Lungs, appearance of, in congestion, 262 brown induration of, 256 changes in, in hæmoptysis, 287 condition of, in pneumothorax, 576 early lesions of, in pulmonary phthisis, 408-410 lesions of, in croupous pneumonia, 308-313 in Hodgkin's disease, 928 in leukæmia, 918 in pernicious anæmia, 904 in pneumonokoniosis, 457 syphilitic disease of, 447

Lung-tissue, gross and microscopic appearance of, in catarrhal pneumonia, 356, 357

Lupus of the larynx, 132

Lymph, mechanism of circulation of, 984, 985

LYMPHANGITIS, SIMPLE, 983 Definition, 986 Diagnosis, 988 Etiology, 986 Age, influence on causation, 986 Specific irritation, 986 Traumatism, influence on causation, 986 Pathology and morbid anatomy, 987 Prognosis, 990 Symptoms, 987 Oedema, 987 Of tubercular form, 987 Pain, characters, 987 Temperature, 987 Treatment, 990 Antipyrine, use, 990 Bandage, use, 991 Cold, locally, 990 Diet in, 990 Fomentations, use, 990 Iron, arsenic, and cod-liver oil, 990, 991 Local, 990 Quinia, use, 990 Rest, 990 Silver nitrate, locally, 990

Lymphatic glands, changes in, in leukæmia, 914, 916 enlargement of, in Hodgkin's disease, 923, 926 influence on blood-formation, 884 lesions, in pernicious anæmia, 905 relation to production of blood-corpuscles, 890 swelling of, in perichondritis of larynx, 118

Lymph-spaces, seat of miliary tuberculosis in, 475

Lymph-vessels, lesions, in lymphangitis, 987

Lympho-sarcoma of the mediastinum, 867

M.

Mackenzie's method of injecting goitre, 981

Malaria, influence on causation of acute splenic enlargement, 954 of lardaceous spleen, 966 of leukæmia, 909

Malformations of left side of heart, 707 of right side of heart, 702

Malignant tumors of trachea, 141

Malign growths of larynx, 128

Malpositions of the heart, 601

Marriage of bleeders, 938 of phthisical persons, 439

Marrow of bone, lesions, in leukæmia, 916

Massage of larynx in true croup, 107

Measles, influence on causation of acute miliary tuberculosis, 473

Mechanical bronchitis, 170 causes of cardiac thrombosis, 723 of collapse of the lung, 251

Median tracheotomy, 148, 155

Mediastinal pleurisy, 564

MEDIASTINUM, DISEASES OF, 861 _Abscess of the Mediastinal Space_, 861 Complications and terminations, 863 Diagnosis and prognosis, 863 Etiology, 861 Symptoms, 862 Treatment, 863 _Inflammation of the Mediastinum_, 861 _Tumors of the Mediastinum_, 863 Anatomy of the mediastinal space, 863 Definition, 863 Diagnosis, 876 From abscess, 877 From aneurism, 876 From chronic pneumonia, 879 From pericarditis, 878 From pleurisy, 878 Of anterior growths, 877 Of posterior growths, 878 Differentiation of malignant growths, 879 Duration, 875 Etiology, 871 Pathology and morbid anatomy, 865-871 Carcinoma, characters, seat, and method of growth, 869 Lympho-sarcoma, characters, seat, and method of growth, 867 Sarcoma, characters, seat, and method of growth, 865-867 Prognosis, 876 Symptoms, 871 Cyanosis and oedema, 873 Dyspnoea, peculiarities of, 872 Pain, characters and seat, 872 Physical signs, 873 Pressure symptoms, 872, 873 Treatment, 880 Donovan's solution, use, 881 Morphia, use, 880 Paracentesis, 880 Resection of sternum, 880

MELANÆMIA, 896 Definition and etiology, 896 Morbid anatomy, 897 Pigment, mode of origin, 897, 898

Membrane of pseudo-membranous laryngitis, nature, 100 seat, 101

Membranous exudation, nature of, in pseudo-membranous bronchitis, 176

Menstrual disorders in chlorosis, 894, 895

Menstruation in fibro-serous pleurisy, 497, 498

Mental emotion, influence in evoking paroxysms of angina pectoris, 456

Mercury, use, in pseudo-membranous laryngitis, 104

MESENTERIC ARTERY, INFERIOR, DISEASES OF, 839 Aneurism, 839 Embolism, 839, 840

MESENTERIC ARTERY, SUPERIOR, DISEASES OF, 836-839 Aneurism, 836 Embolism, 836-839 Endarteritis, 839 Thrombosis, 839

Metallic tinkling in pneumothorax, 579

Meteorological conditions as a cause of bronchitis, 168

Miliary tubercles, physical characters of, 474 tuberculosis, acute, 472

Mineral and coal-dust, influence on causation of pneumonokoniosis, 455 poisoning, influence on causation of asthma, 191 of fatty degeneration of the heart, 612

Mitral disease, influence on causation of hydrothorax, 570 Prognosis, 682, 683 Treatment, 685, 686 Regurgitation, 669 Stenosis, 665 Valve, disease of, influence on causation of brown induration of the lung, 256

Morbid anatomy of acute congestion of the spleen, 955 exudative endocarditis, 640 myocarditis, 604, 605 of Addison's disease, 942 of aortic obstruction, 654 regurgitation, 659 of asthma, 197 of bronchial dilatation, 230 of bronchitis, 175 of brown induration of the lungs, 256 of cancer of the lungs, 460 of the pleura, 582 of cardiac thrombosis, 734 of catarrhal pneumonia, 354 of chronic myocarditis, 607 congestion of the spleen, 957 pharyngitis, 122 of croupous pneumonia, 308 of dilatation of the heart, 633 of fatty cardiac degeneration, 613 of fibroid phthisis, 440 of fibro-serous pleurisy, 484 of gangrene of the lung, 304 of hæmophilia, 936 of hæmoptysis, 286 of hæmothorax, 582 of hemorrhagic infarction of spleen, 961 of Hodgkin's disease, 926 of hydatids of pleura, 585 of hydrothorax, 571 of hypertrophy of the heart, 623 of interstitial endocarditis, 644 of lardaceous spleen, 967 of laryngeal oedema, 115 of leukæmia, 915 of mediastinal tumors, 865 of mitral regurgitation, 670 stenosis, 665 of morbid growths of larynx, 128 of pericarditis, 772 of perichondritis and chondritis of the larynx, 118 of pernicious anæmia, 904 of phthisis, 408 of pneumonokoniosis, 456 of pneumothorax, 576 of pulmonary abscess, 298 congestion and oedema, 261 emboli, 382 hydatids, 467 stenosis, 675 of purulent pleurisy, 540 of rupture of the spleen, 972 of simple lymphangitis, 987 tracheitis, 134 of splenitis, 963 of syphilis of the lung, 450 of the caisson disease, 855 of tricuspid regurgitation, 678 of ulcerative endocarditis, 642 of vesicular emphysema, 242

Morbid growths of the larynx, 127 of nasal passages, 52 of trachea, 139

Morphia, use, in bronchial asthma, 201 in chronic laryngitis, 127 in epiglottic ulceration, 112 in fibro-serous pleurisy, 520 in hæmothorax, 581 in hyper- and paræsthesia of the larynx, 64 in the caisson disease, 858 in ulceration of the trachea, 139 in valvular heart disease, 684, 686

Mortality of acute and chronic bronchitis, 177 of catarrhal pneumonia, 368 of croupous pneumonia, 342 of hæmoptysis, 290 of laryngismus stridulus, 72 of pseudo-membranous laryngitis, 103 of stenosis of the aorta, 827 of valvular heart disease, 680

Murmurs, blowing, in cardiac thrombosis, 727 cardiac, relation to valvular disease, 651 characters, in aneurism of the pulmonary artery, 834 in aortic obstruction, 657 regurgitation, 663 in mitral regurgitation, 668 stenosis, 673 in pulmonary stenosis and regurgitation, 675, 676 in tricuspid disease, 677, 680 and seat, in endocarditis, 648, 649 disappearance of, in acute myocarditis, 606 hæmic, in pernicious anæmia, 902 over splenic region, in splenic congestion, 954 significance, in abdominal aneurism, 822

Mucous membrane, bronchial swelling of, as a cause of asthma, 197

Multilocular areolar pleurisies, 564

Muscular exertion, influence on causation of aortic disease, 656, 660 influence on causation of hypertrophy of the heart, 622 prolonged, influence on causation of functional heart disease, 752

Muscle-substance, condition in dilatation of the heart, 633

Muscles of larynx, 59

MYOCARDITIS, 604 Etiology and morbid anatomy, 604, 605 Diagnosis, 606 Interstitial form, 605 Suppurative form, 605 Symptoms and treatment, 606

MYOCARDITIS, CHRONIC (Fibroid Heart), 607 Diagnosis, 607 Morbid anatomy and etiology, 607, 608 Symptoms and treatment, 608

Myosis, in thoracic aneurism, significance, 805

Myxoma of nasal passages, 53

N.

Narrowing of a vein, 851

Nasal catarrh, acute, 41

NASAL CATARRH, CHRONIC, 42 Atrophic form, 47 Prognosis, 48 Symptoms, 47 Treatment, 48 Arsenic and cod-liver oil in, 49 Galvano-cautery in, 48 Phosphates in, 49 From defective nasal respiration, 43-46 Deflected septum, 44 Hypertrophy of erectile tissue, 44 Osseous obstruction, 44 Treatment, 44-46 Galvano-cautery, 44-46 Iodine, use, 45 From necrosis of nasal bones, 49, 50 Inflammatory form, without hypertrophy, 46 Prognosis, 47 Treatment, 47 Electricity, 47 Silver nitrate, 47

Nasal cavities, anatomy of, 33, 35 diseases, table of, grouped by symptoms, 50 hypertrophies, removal of, in hay asthma, 225 injections in hay asthma, 224 mucous membrane, hypertrophy of, influence on causation of asthma, 193 passages, diseases of, 41 fibroma of, 55 morbid growths of, 52 myxoma of, 53 polypi of, 53 treatment, 54 sarcoma and carcinoma of, 55

Nausea and vomiting in acute congestion of spleen, 954 in Addison's disease, 941 in croupous pneumonia, 330 in pernicious anæmia, 903 in splenitis, 962

Needle-bath, in exophthalmic goitre, 766

Nervous cough, 77 lesions, of Addison's disease, 944 of Hodgkin's disease, 928 of leukæmia, 918 of pernicious anæmia, 905 symptoms of Addison's disease, 941 of Hodgkin's disease, 925 of leukæmia, 911 of pulmonary phthisis, 407

Neuralgia in hyperæsthesia of the larynx, 63

Neuroses of the larynx, 59 of the heart, 747

Night-sweats, of pulmonary phthisis, 405 treatment, 438

Nitro-glycerin, use, in bronchial asthma, 208

Nutrition, bad, influence on causation of catarrhal pneumonia, 354 impaired, of heart-walls, influence on dilatation of the heart, 632

Nux vomica, use, in angina pectoris, 761

O.

Occlusion of the aorta, 824 of the coronary artery, 831 of veins, 851

Occupation, influence on causation of hay asthma, 213 of mediastinal tumors, 871 of pneumonokoniosis, 455, 456 of pulmonary phthisis, 396 of thoracic aneurism, 803 in-door, influence on causation of bronchitis, 165

Oedema, from dilatation of veins, 850 in pernicious anæmia, 901 of glottis, 94, 103 of the lungs, 258 of thoracic walls, in purulent pleurisy, 542, 543

Onset of acute catarrhal laryngitis, 93, 94 of laryngismus stridulus, 70 of leukæmia, 910 of pseudo-membranous laryngitis, 102

Operations, various, in tracheotomy, 48

Operative treatment of pericardial effusions, 794

Opiates, use, in exophthalmic goitre, 766

Opium, use, in acute catarrhal laryngitis, 98 in croupous pneumonia, 348 in hæmoptysis, 291, 292 in pericarditis, 783 in pulmonary phthisis, 436, 437, 439 in valvular heart disease, 684, 685 and morphia, use, in angina pectoris, 760

Organization of heart-clots, 740

Orthopnoea, in mitral stenosis, 667

Osseous obstruction, as a cause of chronic nasal catarrh, 44

Over-training and heart-strain, influence on causation of cardiac dilatation, 631

Oxidation, defective, in fatty degeneration of the heart, 613

Oxygen, inhalations in true croup, 107

Ozæna, 47

P.

Pack, cold, use in croupous pneumonia, 349

Pain, characters, in croupous pneumonia, 322 in lymphangitis, 987 in mediastinal abscess, 862 in pulmonary phthisis, 402 in acute and chronic congestion and enlargement of the spleen, 954, 957 in acute phlebitis, 845 in aneurism of the coeliac axis, 842 in aortic obstruction, 656 regurgitation, 661 in caisson disease, 854 in cancer of the pleura, 584 in cardiac thrombosis, 731 in chronic endarteritis of the coronary artery, 828 in endocarditis, 647 in hydatids of the pleura, 581 in hyperæsthesia of the larynx, 62 in morbid growths of the larynx, 129 in pericarditis, 773, 774 in perichondritis and chondritis of the larynx, 118 in splenitis, 962 in stenosis of the trachea, 142 in ulceration of the trachea, 139 seat and characters, in angina pectoris, 756 in diaphragmatic pleurisy, 563 in fibro-serous pleurisy, 493 in mediastinal tumor, 872 in thoracic aneurism, 804 seat, in abdominal aneurism, 821

Palpation in cardiac malformations, 710 in cardiac thrombosis, 729 in cardiac valvular disease, 657, 662, 668, 673, 675, 677, 679 in croupous pneumonia, 335, 336, 338 in endocarditis, 648 in fibro-serous pleurisy, 503, 504 in pericarditis, 774 in pneumothorax, 579 in thoracic aneurism, 808

Palpitation in cardiac valvular disease, 656, 661, 667, 671, 675, 679 in hypertrophy of the heart, 626 of the heart, 747

Papilloma of larynx, 128, 130

Papillomata of trachea, frequency, 140

Paracentesis in endocardial effusions, 784, 794 in pulmonary hydatids, 470

Paræsthesia of larynx, 63

Paralysis in caisson disease, 854 of adductors and abductors of vocal cords, 81, 84, 86 of arm in thoracic aneurism, 810 of constrictors of larynx, 80 of muscles of larynx, 78 of posterior crico-arytenoids, 86 of tensors of vocal cords, 85, 86 of the whole larynx, 79

Parasites, influence on causation of hay asthma, 216 of the heart, 637

Parenchymatous degeneration of heart-muscle, 610

Paroxysms, frequency of, in angina pectoris, 756 in functional heart disease, 748 of asthma, description and frequency of, 185-187

Patency of septum ventriculorum, 690

Pathology of acute catarrhal laryngitis, 92 phlebitis, 843-845 congestion of spleen, 955 of Addison's disease, 944 of anæsthesia of larynx, 67 of aneurism of the coeliac axis, 842 of angina pectoris, 758 of asthma, 193 of bronchial asthma, 193 of bronchitis, 175 of caisson disease, 855 of cancer of the lungs, 460 of cardiac thrombosis, 734 of catarrhal pneumonia, 354 of chronic endarteritis of the coronary artery, 829 pharyngitis, 122 of collapse of lung, 253 of embolism of the coronary artery, 832 of the superior mesenteric artery, 837 of exophthalmic goitre, 764 of fibroid phthisis, 440 of functional heart disease, 752 of gangrene of lung, 303 of hæmophilia, 936 of hæmoptysis, 286 of hemorrhagic pleurisy, 565 of Hodgkin's disease, 930 of hysterical affections of glottis, 84 of laryngismus stridulus, 71 of mediastinal tumors, 865 of morbid growths of trachea, 140 of perichondritis and chondritis of larynx, 118 of pernicious anæmia, 905 of phlegmasia dolens, 847 of pneumonokoniosis, 456 of pseudo-membranous laryngitis, 100 of pulmonary abscess, 298 congestion and oedema, 261 emboli, 382 phthisis, 408 of simple lymphangitis, 987 tracheitis, 134 of spasm of the glottis in the adult, 75 of stenosis of the aorta, 825 of the trachea, 143 of syphilis of the lung, 448 of vesicular emphysema, 242

Pectoriloquie aphonique in pleurisy, significance, 510, 517

Percussion during paroxysm of asthma, 187 in bronchial dilatation, 228, 229 in cardiac malformation and cyanosis, 710 thrombosis, 728 valvular disease, 657, 663, 668, 673, 675, 677, 680 in catarrhal pneumonia, 359-363 in collapse of lung, 253 in croupous pneumonia, 335, 337, 338 in emphysema, 237 in endocarditis, 648 in fibro-serous pleurisy, 499-503 in hydrothorax, 572 in hypertrophy of the heart, 625, 627 in mediastinal abscess, 862 tumors, 874 in pericarditis, 774 in pneumothorax, 579 in pulmonary congestion and oedema, 260 phthisis, 411, 413, 415-418 in purulent pleurisy, 543, 544 in pyo-pneumothorax, 544 in thoracic aneurism, 812

Perforation in purulent pleurisy, 542-547 of the aorta, 824 of lung, in thoracentesis, 538

Pericardial effusions, displacements of heart, from, 602

PERICARDIAL EFFUSIONS, OPERATIVE TREATMENT OF, 794 Aspiration, method of, 796, 797 Free incisions and drainage, 795 Indications for, 794, 795 Injections into pericardium, 795 Puncture of heart, results of, 798 Results, 798 Site of puncture, 796

PERICARDITIS, 769 Definition, 769 Diagnosis, 779 From cardiac hypertrophy, 780 From cerebral affections, 779 From mediastinal tumors and inflammation, 780 From pleurisy and endocarditis, 779 Etiology, 769 Bright's disease, influence on causation, 771 Cold, influence on causation, 770 Eruptive fevers, influence on causation, 771 Rheumatism, acute, influence on causation, 770 Traumatism, influence on causation, 769, 770 Secondary causes, 770, 771 Frequency, 770, 771 Morbid anatomy, 772, 773 Prognosis, 781 Symptoms, 773 Auscultation, 775 Cerebral symptoms, 774 Friction sounds, characters, 775 Pain, 773 Percussion and palpation, 774 Physical signs of, 774 Pulse and temperature in, 774 Treatment, 783 Blisters, use, 784 Cold, locally, 783 Counter-irritation, 783 Diet in, 783 Digitalis, use, 783 Of effusion, 784 Paracentesis, 784 Potassium, bitartrate and acetate, use, 784 iodide, 784 Quinia, use, 784 Stimulants, 784

Pericarditis, chronic, 784 tubercular, 793

PERICARDIUM, ADHERENT, 785 Adhesions, seat and character, 786 Impulse in, 787 Prognosis, diagnosis, and treatment, 788

Pericardium, cancer of, 792, 793 diseases of, 769

Perichondritis of larynx, 117

Perisplenitis, 965

Peritonitis complicating pulmonary phthisis, 406

Pernicious anæmia, progressive, 898

Phlebitis, 843

Phlebolithes, 853

Phlegmasia alba dolens. See _Veins, Diseases of_.

Phosphates, use, in atrophic nasal catarrh, 49

Phosphorus, use, in Hodgkin's disease, 931 in leukæmia, 921 in pulmonary phthisis, 435

PHTHISIS, FIBROID, CHRONIC INTERSTITIAL PNEUMONIA, CIRRHOSIS OF LUNG, 440 Course and duration, 441 Diagnosis, 443 Etiology, 440 Symptoms, 441 Cough and expectoration, characters, 441 Cyanosis in, 442 Physical signs, 442 Sputa, characters, 441 Treatment, 444

Phthisis, incipient, diagnosis, 411, 413

PHTHISIS, PULMONARY, 391 Definition, 391 Diagnosis, 410 Auscultation in, 412, 416, 417 Bacilli, significance of presence in sputa, 413 Broncho-vesicular respirations, characters, 412 Dry cough, significance of, 411 Inspection in, 417 Of cavities, 416, 417 Of incipient form, 411 Of intercurrent pneumonia in, 418 Percussion in, 411, 415, 416 Stethoscope, necessity of use in, 412 Vesiculo-tympanitic resonance, characters, 415 Whispered voice, transmission of, 413-417 Etiology, 394 Age, occupation, and sex, 396 Bacillus tuberculosis, relation of, 392, 398 Bronchitis, relation of, to, 394 Communicability of, 396-398 General diseases, influence on causation, 396 Hæmoptysis, influence on causation, 395 Heredity and constitutional predisposition, influence on causation, 395 Season, humidity of soil, etc., influence on causation, 396 History, 392 Morbid anatomy and pathology, 408 Prevention, 444 Prognosis, 419 Symptoms and complications, 400 Anæmia in, 405, 406 Cough, characters, 400 Dysphonia, aphonia, and laryngitis, 403 Genito-urinary disorders, 408 Hæmoptysis, frequency and significance, 401, 402 Heart, and circulatory disorders in, 405 Intercurrent pneumonia, occurrence of, 403, 404 Nervous symptoms, 407 Night-sweats in, 404 Pain in, 402 Peritonitis, occurrence of, 406, 407 Pleurisy and pneumothorax in, 404 Respiration in, 403 Sputa, characters, 401 Temperature in, 404, 405 Vomiting, diarrhoea, and digestive disorders, 406 Synonyms, 391 Treatment, 425 Agaricus, use, in night-sweats, 438 Alcohol, use, 435 Arsenic, use, 436 Belladonna and zinc oxide, use, 438 Climatic, 427-430 Cod-liver oil, use and value, 434 Cold use, 437 Dietetic, 431 Ergotin, use, 437 Injection of cavities, 439 Iodine, use, 435 Iron, use, 436 Marriage of consumptives, question of, 439 Of cough, 436 Of diarrhoea, 438 Of night-sweats, 438 Of pyrexia, 437 Out-of-door life, necessity of, 432 Picrotoxin, use, 438 Quinia, use, 438 Sea-voyages, value, 433 Sanitaria, value, 430 Use of opium, 436, 439

Physical signs during paroxysm of asthma, 187 in emphysema, 236, 237 in fatty degeneration of the heart, 615 in mitral regurgitation, 671 in pulmonary congestion and oedema, 260, 261 regurgitation, 697 in purulent pleurisy, 543 of abdominal aneurism, 822 of acute bronchitis, 169 of acute miliary tuberculosis, 480 of adherent pericardium, 787 of aortic obstruction, 657 of aortic regurgitation, 662 of atrophic lobar emphysema, 248 of cancer of the lungs, 462, 463 of pleura, 584 of capillary bronchitis, 171 of cardiac malformations, 710 of cardiac thrombosis, 728, 741 of cardiac valvular disease, 668 of catarrhal pneumonia, 359-363 of collapse of lung, 252, 253 of croupous pneumonia, 334, 335 in children, 335, 338 of diaphragmatic pleurisy, 563 of dilatation of the heart, 634 of endocarditis, 648 of fibroid phthisis, 442 of fibro-serous pleurisy, 496 of hæmopericardium, 789 of hæmoptysis, 282 of hydrothorax, 572 of hypertrophy of the heart, 625 of mediastinal tumors, 873 of pericarditis, 774 of pneumothorax, 578 of pulmonary abscess complicating croupous pneumonia, 339 of pulmonary hydatids, 468 phthisis, 411 of pulmonary stenosis, 675 of senile pneumonia, 336, 338, 339 of stenosis of the aorta, 826 of syphilis of the lung, 452 of thoracic aneurism, 807 of thrombosis and embolism of the pulmonary artery, 836 of the coronary artery, 832 of tricuspid stenosis, 677

Physiognomy in angina pectoris, 756 in asthma, 186, 190 in croupous pneumonia, 328 in endocarditis, 647 in laryngismus stridulus, 71 in pulmonary embolism, 379-381

Picrotoxin, use, in pulmonary phthisis, 438

Pigment, seat and treatment of, in melanæmia, 896, 897

Pigmentation of Addison's disease, 940 of lungs in pneumonokoniosis, 451, 458

Pilocarpine in laryngeal oedema, 116 use, in pleuritic effusions, 521 in pseudo-membranous laryngitis, 106 in pulmonary oedema, 264

Pimpinella saxafraga, use, in acute catarrhal laryngitis, 99

Plants and grasses, certain, influence on production of hay asthma, 215

Plethora, 886

Pleura, cancer of, 583 diseases of, 483 displacement of heart from, 603 hydatids of, 585 lesions of, in croupous pneumonia, 313

Pleural cavity, morbid growths of, 583 effusions, frequency, in cancer of the lungs, 461 influence on causation of collapse of lung, 251 occurrence in course of mediastinal tumors, 870

Pleurisies, circumscribed, 545 encysted, 545, 546 multilocular areolar, 564

PLEURISY, 483 Complications, 512 Course, 510 Definition, 483 Diagnosis, 514 From abscess of liver, 516 Atelectasis, 517 Hydrothorax, 515 Intercostal neuralgia, pleurodynia, etc., 516 Pneumonia, 514, 515 Tumors and cysts, 516 Of nature of effusion, 517 Duration, 511, 512 Etiology, 491 Age and sex, influence on causation, 492 Atmospheric changes, influence on causation, 491 Of primary form, 491 Of secondary form, 491 Pulmonary affections, acute and chronic, influence on causation, 492 Rheumatism, gout, and nephritic affections, 493 Syphilis, influence on causation, 493 Traumatism, influence on causation, 492 Pathological anatomy, 484 Effused fluid, chemical characters of, 486 distribution of, 487 Exudation, seat, nature, and appearance of, 485, 486 Level of line of flatness assumed by effusion, 488, 489 Prognosis, 518 Sequelæ, 483 Symptoms, 493 Bronchial breathing, significance of, 508 Chills, frequency, 494 Cough, characters of, 495 Cyanosis, 496 Displacement of organs in, 504, 507 Expectoration, characters, 496 Friction sounds, seat and characters, 507, 509 Heart murmur in, 510 Mensuration, necessity of frequent, 497, 498 Pain, seat and characters, 493 Physical signs in, 496 Pneumo-pericardial friction sounds, 509 Pulse, characters, 494 Respiration in, 494 Skodaic resonance, seat and characters, 501 Temperature, 494 Voice sounds in, 510 Whispered voice, significance of, 510, 517 Synonyms, 483 Terminations, 512 Treatment, 519 Alkalies, use, 520 Blisters, use, 520, 521 Counter-irritants, use, 520, 521 Effusion, removal of, 520 Iron, use, 520, 521 Jaborandi and pilocarpine, 520, 521 Laxatives and purgatives, 520, 521 Opium and morphia, use, 520 Potassium iodide, use, 520 Quinia, use, 520 Rest, 519 Strapping of chest in, 520 Thoracentesis, 521 Albuminous expectoration following, 535 Contraindications, 530 Death from, causes, 536, 537 During febrile stage, question of, 525 Indications for, 521 Mode of operating, 530, 534 Secondary pneumonia and tuberculosis following, 536

Pleurisy, complicating pulmonary phthisis, 404 diaphragmatic, 563 double, 562

PLEURISY, HEMORRHAGIC, 564 Diagnosis, 568 Etiology and pathology, 565, 567 Prognosis, 568 Symptoms, 567 Treatment, 568

Pleurisy, interlobular and mediastinal, 564

PLEURISY, PURULENT, 539 Definition, 539 Diagnosis, 543 Exploratory puncture, value, 543 From tubercular cavities and dilated bronchi, 545 Of perforation, 543, 544 Etiology, 539 Age and sex, influence on causation, 540 Eruptive fevers, influence on causation, 540 Puerperal condition, the, influence on causation, 540 Rheumatism, gout, and nephritic diseases, 540 Traumatism, influence on causation, 540 History, 539 Pathological anatomy, 540 Prognosis, 548 Symptoms, 542 Physical signs, 543 Synonyms, 539 Terminations, 547 Treatment, 549 Alteratives, use, 549 By free drainage, 552-556 Injections and washing of cavity, value of, 561, 562 Modes of operating, 550 Pleurotomy, 555 Resection of ribs, 556 Surgical, 549 Thoracentesis, 550-552

Pleurisy, rheumatic, 564, 565 tubercular, 569

Pleuro-bronchial fistulæ, signs of occurrence of, in purulent pleurisy, 543

Pleurotomy, 556, 557

Pneumonia, acute lobar, complicating pulmonary phthisis, 403

PNEUMONIA, CATARRHAL, 353 Complications and sequelæ, 364 Definition, 353 Diagnosis, 365 From acute miliary tuberculosis, 367 From collapse of lung, 366 From croupous pneumonia, 366 Duration, 368 Etiology, 353 Age, influence on causation, 353 Infectious diseases complicated with bronchitis, influence on causation, 354 Mortality, 368 Pathology and morbid anatomy, 354 Bronchi, lesions, 356 Bronchial glands, lesions, 357 Lung-tissue, gross and microscopic appearance of, 356 Relation to collapse of lung, 355 Prognosis, 368 Symptoms, 358 Cardiac failure in, 363 Cough, 360, 361 Death, cause of, 362 Gastro-intestinal, 360 In children, 358 Nervous, 362 Of grave forms, in adults, 360 Physical signs, 358, 360, 362 Pulse and respiration, characters, 360, 361 Sputa, 360, 361 Temperature, 358, 360, 361 Synonyms, 353 Terminations, 368 Treatment, 368 Alteratives, use, 372 Ammonia preparations, use, 370, 371 Apomorphia, use, 371 Chloral hydrate, use, in nervous symptoms, 372 Climate, change of, 372 Counter-irritation, use, 369 Diet in, 369, 370 Emetics, use, 371 Hyoscyamia, hypodermatically, use, 372 Of gastro-intestinal disorders, 370 Of nervous symptoms, 372 Opium, use, 372 Quinia, use, 370, 371 Strychnia, use, 371

Pneumonia, chronic interstitial, 391, 440 complicating pleurisy, 512

PNEUMONIA, CROUPOUS, 307 Definition, 307 Differential diagnosis, 339 From capillary bronchitis, 340 From catarrhal pneumonia, 340 From hypostatic congestion, 340 From meningitis, 342 From pleurisy, 340 From pulmonary apoplexy, 341 congestion and oedema, 339 From typhoid fever, 342 Etiology, 314 Age and sex, influence on causation, 314 Cold, damp, season, etc., influence on causation, 314 Depressing influences, influence on causation, 315 Klebs on specific germ of, 319 Nature of, 315-318 Resemblance to acute general diseases, 317, 318 History, 307 Morbid anatomy, 308 Changes in abdominal viscera, 313 in bronchial glands, 313 in heart and blood, 313 in lung, 308-313 in pleura, 313 Prognosis, 342-345 Cause of death, 345 Mortality, 342, 343 Symptoms, 319 Alimentary tract, state of, 330 Cerebral, 329, 330 Chills, characters, in, 318 Cough, characters, in, 322 Critical phenomena, 331 Dyspnoea, characters, 321, 322 Expectoration, characters, 322 Herpetic eruptions, occurrence, 328, 329 Indicating danger, 331 Objective, 334-339 Of abscess and gangrene, 332 Of bilious and gastric form, 334 Of latent form, 334 Of purulent infiltration, 332 Pain, characters, 322 Physical signs, 334-339 Physiognomy, 328 Pulse, characters, 326, 328 Respiration, characters, 321 Sputum, characters, 322 Subjective, 319-334 Surface of body, state of, 328 Temperature in, 324 Urine, condition, 330 Synonyms, 307 Treatment, 345-352 Alcoholic stimulants, use, 348 Antiseptics, use, 352 Carbonate of ammonium, digitalis, musk, camphor, etc., use, 349 Cardiac depressants, danger, 346 Cold, use, 349 Counter-irritation, questionable utility of, 347 Diet in, 347, 348 Expectorants, use, 347 Of convalescence, 351 Of delirium, 351 Of senile variety, 351 Opium, use, 348 Quinia, use, 350 Reduction of temperature in, 349 Rest in, value, 347 Venesection, harmfulness, 346

Pneumonia, hypostatic, 258

Pneumo-hydropericardium, 791

Pneumo-hydrothorax complicating phthisis, 404

PNEUMONOKONIOSIS, 454 Definition, etiology, and history, 454 Diagnosis and prognosis, 459 Pathology and morbid anatomy, 456-459 Symptoms and treatment, 459

Pneumo-pericardial friction sound, 509

Pneumo-pericardium, 790

PNEUMOTHORAX, 573 Definition, 573 Diagnosis, 580 Etiology, 573 Age and sex, influence on causation, 576 Traumatic causes, 574 History, 573 Pathological anatomy, 576 Air, quantity, 576 Heart, displacement, 577 Opening, shape and seat, 576 Prognosis, 581 Symptoms, 578 Pain, seat and characters, 578 Physical signs, 578-580 Respiration, characters, 578 Treatment, 581, 582 Diet, 582 Opium and morphia, use, 581 Paracentesis, 581 Stimulants, 581

Pollen of plants, influence on causation of asthma, 192 theory of origin of hay asthma, 216

Polypus, nasal, 53, 54

Post-mortem heart-clots, 735

Potain's syphon, use, in purulent pleurisy, 555

Potassium acetate, use, in pericarditis, 784 bicarbonate, use, in cardiac thrombosis, 745, 746 chlorate, use, as an injection in pseudo-membranous laryngitis, 105 in purulent pleurisy, 562 bromide, use, in bronchial asthma, 204 in bronchitis, 179 in chronic inflammation of epiglottis, 110 in hyper- and paræsthesia of larynx, 64 in laryngismus stridulus, 73 in pulmonary hydatids, 470 iodide, use, in acute catarrhal laryngitis, 97, 99 in acute tracheitis, 136 in bronchial asthma, 207 in chronic bronchitis, 182 in chronic phlebitis, 848 in paralysis of the larynx, 91 in pericardial effusions, 784 in pleurisy, 520 in pseudo-membranous laryngitis, 105 in pulmonary hydatids, 470 in thoracic aneurism, 818 in vesicular emphysema, 246, 247 nitrate, use, in bronchial asthma, 203

Predisposing causes of asthma, 190 of bronchitis, 165 of gangrene of the lung, 301 of hay asthma, 212

Pregnancy, influence on causation of hæmoptysis, 278 of pernicious anæmia, 900 of pulmonary phthisis, 396

Pressure symptoms in aneurism of the pulmonary artery, 834 of abdominal aneurism, 821 of goitre, 975 of mediastinal abscess, 862 tumors, 872, 873 of thoracic aneurism, 804-807 upon aorta, for relief of thoracic aneurism, 816

Prevention of angina pectoris, 760 of phthisis, 444-446 of pulmonary embolism, 388

Preventive treatment of functional heart disease, 755

Priapism in leukæmia, 914

Prognosis in lardaceous spleen, 968 in pseudo-membranous laryngitis, 103 in simple tracheitis, 135 in valvular heart disease, 680 of acute catarrhal laryngitis, 96 congestion of the spleen, 955 of adherent pericardium, 788 of anæsthesia of the larynx, 67 of angina pectoris, 760 of asthma, 200 of atelectasis, 255 of atrophic emphysema, 249 of bronchial dilatation, 230 of bronchitis, 177 of cancer of the lung, 465 of the pleura, 584 of cardiac thrombosis, 744 of catarrhal pneumonia, 368 of chronic congestion and enlargement of the spleen, 959 of chronic laryngitis, 124 nasal catarrh from defective respiration, 46 of croupous pneumonia, 342 of dilatation of the heart, 635 of embolic splenic abscess, 964 of embolism of the superior mesenteric artery, 838 of endocarditis, 650 of epiglottic ulceration, 112 of exophthalmic goitre, 765 of fatty degeneration of the heart, 616 of fibro-serous pleurisy, 518 of functional heart disease, 753 of gangrene of the lung, 303 of hæmoptysis, 290 of hæmothorax, 583 of hay asthma, 222 of hemorrhagic pleurisy, 568 of Hodgkin's disease, 930 of hydatids of the pleura, 586 of hydrothorax, 572 of hyper- and paræsthesia of the larynx, 64 of hypertrophy of the heart, 629 of laryngeal oedema, 116 of laryngismus stridulus, 72 of leukæmia, 920 of mediastinal tumors, 876 of morbid growths of larynx, 130 of trachea, 141 of pericarditis, 781 of pernicious anæmia, 906 of phthisis, 419 of pneumonokoniosis, 459 of pneumothorax, 581 of pulmonary abscess, 300 congestion and oedema, 262 embolism, 388 hydatids, 470 of purulent pleurisy, 548 of simple lymphangitis, 990 of stenosis of the aorta, 827 of the trachea, 143 of syphilis of the lungs, 453 of ulceration of the trachea, 139 of vesicular emphysema, 244

Progressive pernicious anæmia, 898

Prophylaxis of acute catarrhal laryngitis, 96 of hæmophilia, 938 of phthisis, 444-446

Prune-juice expectoration, significance in pneumonia, 319, 344

Pseudo-membranous bronchitis, 173 laryngitis, 100

Puerperal state, influence on causation of phlegmasia dolens, 846 of pulmonary embolism, 377 of purulent pleurisy, 540

Pulmonary apoplexy, 293 Definition and history, 293 Diagnosis, etiology, and symptoms, 294 Prognosis and treatment, 295 and hæmoptysis, complicating cardiac thrombosis, 734 artery, closure of, with perfect ventricular septum, in cyanosis, 702 combined stenosis and atresia of, in cyanosis, 706

PULMONARY ARTERY, DISEASES OF, 833 Chronic endarteritis (atheroma; arterio-sclerosis), 833 Dilatation and aneurism, 833 Rupture of pulmonary artery, 835 Stenosis of trunk or main branches, 834 Thrombosis and embolism, 835, 836

Pulmonary artery and right conus arteriosus, defects of, 690 and vessels, anatomy of, relation to hæmoptysis, 269-272 disease, influence on causation of cardiac hypertrophy, 622, 623 influence on tricuspid regurgitation, 678

PULMONARY EMBOLISM, 373 Classification, 373 Death, cause of, 380, 381 Definition, 373 Diagnosis, 387 Etiology, 374 Diseases of thoracic, abdominal, and pelvic viscera, influence on causation, 375 Puerperal state, influence on causation, 377 Source of emboli, 374, 375 Surgical affections as a cause, 377 History, 373 Pathology and morbid anatomy, 382 Effects of emboli, 383 Infarctions, mechanism of production, 384, 385 Specific and septic emboli, effects, 386 Prevention of, 388, 389 Prognosis, 388 Symptoms, 378 Dyspnoea, characters of, 379-381 Of benign form, 382 Of grave form, 380 Of sudden form, 379 Physical signs, 381 Physiognomy in, 379-381 Sputa sanguinolent, in benign form, 382 Treatment, 388 Carbonate of ammonium and bicarbonate of sodium, use as solvents, 389 Counter-irritation and venesection, use, 390 Purgatives, use, 390 Surgical measures, 389

PULMONARY HYDATIDS, 466 Definition, etiology, and synonyms, 466 Diagnosis, 469 History, 466 Morbid anatomy, 467 Prognosis, 470 Symptoms, 468 Treatment, 470 Anthelmintics, use, 470 Of old suppurating cysts, 471 Paracentesis in, 470 Potassium bromide and iodide, 470 Surgical measures, 471

Pulmonary hyperæmia in mitral stenosis, 666, 667 infarction, lesions of, 288 orifice, narrowing or closure of, as a cause of cardiac malformation, 694 phthisis, 391 regurgitation, 676 stenosis, 674 vein, anatomy of, 270

Pulsating empyema, 546

Pulsation in abdominal aneurism, 822 jugular and epigastric, in tricuspid regurgitation, 679 seat of, in aneurism of the cardiac axis, 841

Pulse, characters, in chronic myocarditis, 608, 609 in endocarditis, 647 in fatty degeneration of the heart, 615 in leukæmia, 913 in pericarditis, 774 in thoracic aneurism, 808 in acute miliary tuberculosis, 479

Q.

Quinia, use, in acute congestion of spleen, 956 in acute miliary tuberculosis, 480, 482 in anæsthesia of the larynx, 68 in bronchitis, 79, 181, 182 in catarrhal pneumonia, 370, 371 in chronic congestion and enlargement of the spleen, 959 in croupous pneumonia, 350 in endocarditis, 651 in fever following hæmoptysis, 292 in gangrene of the lungs, 305 in hay asthma, 224 in Hodgkin's disease, 931 in hyper- and paræsthesia of larynx, 65 in laryngismus stridulus, 73 in leukæmia, 921 in pericarditis, 784 in pseudo-membranous laryngitis, 105, 108 in pulmonary phthisis, 438 in purulent pleurisy, 549 in simple lymphangitis, 990, 991 tracheitis, 135 in valvular heart disease, 685 hydrobromate of, hypodermic use, in pulmonary congestion and oedema, 264

R.

Ragweed, influence on causation of asthma, 215, 216

Râle crepitant of croupous pneumonia, 335 redux of croupous pneumonia, 338

Recovery from pulmonary phthisis, 420-423

Recurrence of pulmonary phthisis, 424

Redness of skin, one-sided, in goitre, 975

Reduplication of second sound in mitral stenosis, 668

Reflex causes of laryngismus stridulus, 70 symptoms of nasal polypus, 53

Regiminal treatment of pulmonary phthisis, 432

Regurgitation, aortic, 659 mitral, 669 pulmonary, 676 tricuspid, 677

Relapse in croupous pneumonia, frequency, 326

Remissions, frequency, in acute catarrhal laryngitis, 94

Remittence of pulse in croupous pneumonia, 328

Remittent pneumonia, 334

Resection of ribs in purulent pleurisy, 557-562

Resolution stage of croupous pneumonia lesions, 310

Resonance, subclavicular, in pleurisy, 501-503

Respiration, characters, in catarrhal pneumonia, 359-363 in chronic bronchitis, 171 in collapse of lung, 252 in croupous pneumonia, 321 in fibro-serous pleurisy, 495, 497 in morbid growths of trachea, 140 in pneumothorax, 578 in pseudo-membranous laryngitis, 102 in pulmonary phthisis, 403

Respirator, use, in chronic laryngitis, 126

Respiratory power, defective, relation of, to catarrhal pneumonia, 356 sounds in emphysema, 238 in purulent pleurisy, 543

Rest, absolute, necessity of, in croupous pneumonia, 347 in treatment of thoracic aneurism, 817 necessity, in endocarditis, 651 value, in cardiac hypertrophy, 630 in acute and chronic phlebitis, 846, 848 in dilatation of the heart, 636 and quiet, necessity of, in hæmoptysis, 291 value, in cardiac thrombosis, 745, 746

Retention-cysts of trachea, 141

Reticular lymphangitis, symptoms, 987

Retina, condition of, in leukæmia, 911

Reybard's trocar, use, in pneumothorax, 581

Rheumatic bronchitis, 172 pleurisy, 564, 565

Rheumatism, acute, influence on causation of endocarditis, 645 as a cause of pericarditis, 770 influence on causation of paralysis of vocal cords, 82 of valvular heart disease, 655, 661, 666, 671 and gout, influence on causation of pleurisy, 493 of purulent pleurisy, 540

Rhinoscope, history of, 21

Rhythm of endocardial murmurs, method of determining, 653

Ribs, resection of, in purulent pleurisy, 557

Rickets, influence on causation of laryngismus stridulus, 70

Right ventricle, physical signs of hypertrophy of, 627

Rigors in croupous pneumonia, 320

Rupture of splenic abscess, 963 of the aorta, 823 of the coronary artery, 833 of the heart, spontaneous, 617 of the pulmonary artery, 835 of the spleen, 971 of thoracic aneurism, 815

S.

Sacculated form of bronchial dilatation, 230

Salicylate of sodium, use, in rheumatic bronchitis, 181

Sanitaria for phthisical patients, 430

Sarcoma of larynx, 128-130 of nasal passages, 55 of thyroid gland, 978 of the heart, 637 of the mediastinum, frequency and history, 865-867

Scarification in laryngeal oedema, 116

Schrötter's tubes, use, in perichondritis and chondritis of larynx, 121 dilators, in laryngeal oedema, 117

Schultze's granule-masses, absence of, in blood of pernicious anæmia, 902 in blood of Hodgkin's disease, 924 increase of, in leukæmia, 912

Season, influence on causation of bronchitis, 168 of croupous pneumonia, 315, 316 of hæmoptysis, 277

Seat of collapse, in atelectasis, 253 of lesions, in croupous pneumonia, 312 of nasal polypus, 53 of oedema of the lungs, 260 of pulmonary emboli, 383 of rupture of the aorta, 823 of tracheal ulcers, 138

Sea-voyages, benefit upon course of pulmonary phthisis, 433 value, for relief of hay asthma, 222

Secondary nature of pericarditis, 770 pleurisies, etiology, 492

Secretion, alterations of, in chronic pharyngitis, 122

Semi-lunar ganglion, lesions, in Addison's disease, 944

Senegæ, use, in bronchitis, 179

Senile pneumonia, treatment, 351

Sensation of larynx-perversion, 61

Sensations, peculiar cardiac, in hypertrophy of the heart, 626

Septum, deflected, as a cause of chronic nasal catarrh, 44 of auricles, defects of, cardiac malformations, 689 and foramen ovale malformations, 689 ventriculorum, patency of, in cardiac malformations, 690 theories regarding patency, 699

Sequelæ of asthma, 189 of cardiac thrombosis, 733 of catarrhal pneumonia, 364 of emphysema, 239 of fibro-serous pleurisy, 512 of hæmothorax, 582

Sex, influence on causation of angina pectoris, 759 of aortic obstruction, 655 of asthma, 190 of cardiac thrombosis, 722 of chronic myocarditis, 607 of chronic pharyngitis, 121 of croupous pneumonia, 314 of exophthalmic goitre, 764 of fatty degeneration of the heart, 613 of fibro-serous pleurisy, 492 of gangrene of lung, 302 of hæmophilia, 933 of hæmoptysis, 276 of hay asthma, 212 of Hodgkin's disease, 922 of laryngeal oedema, 113 of laryngismus stridulus, 70 of leukæmia, 909 of mediastinal tumors, 871 of perichondritis and chondritis of larynx, 118 of pernicious anæmia, 899 of pneumothorax, 576 of pseudo-membranous laryngitis, 101 of thoracic aneurism, 803

Sexual excess, influence on causation of exophthalmic goitre, 765 of functional heart disease, 752 of hypertrophy of the heart, 619 avoidance of, in functional heart disease, 755

Shape of heart in hypertrophy, 624

Shoemakers, frequency of mediastinal tumors in, 871

Shrinkage of lung in pulmonary phthisis, 417

Silver nitrate, spray, use, in acute catarrhal laryngitis, 97, 99 use, in chronic inflammation of epiglottis, 110 in chronic laryngitis, 125, 126 in epiglottic ulceration, 112 in erosion of epiglottis, 111 in inflammatory non-hypertrophic form of chronic nasal catarrh, 47 in laryngeal oedema, 116 in simple tracheitis, 135

Simple lymphangitis, 983

Skin, color, in chlorosis, 895 in pernicious anæmia, 901 discoloration of, in Addison's disease, 940 state of, in croupous pneumonia, 328 tumors of, in Hodgkin's disease, 925

Skodaic resonance on percussion in pleurisy, 501-503

Sodium bicarbonate and borate, use, in chronic laryngitis, 125 sulphate, use, in Addison's disease, 938

Soil, humidity of, influence on causation of phthisis, 396

Souffle in abdominal aneurism, 822

Southey's capillary tubes, use, in hydrothorax, 572

Spasm of diaphragm, distinguished from asthma, 199 of glottis in adults, 74 of larynx in children, 70 theory of origin of asthma, 193, 194

Special senses, modifications of, in Hodgkin's disease, 925 in leukæmia, 911

Specific and septic emboli of the lungs, 386 fevers, influence on causation of acute splenic congestion, 953 germ of croupous pneumonia, 319

Sphygmograph, value, in diagnosis of thoracic aneurism, 809

Splashing sound in pneumothorax, 580

Spleen, changes in, in tricuspid regurgitation, 678, 679

SPLEEN, DISEASES OF, 952 _Acute Congestion of_, 953 Diagnosis, 955 Etiology, 953 Pathology and morbid anatomy, 955 Prognosis, 955 Symptoms, 954 Treatment, 956 _Chronic Congestion and Enlargement of_, 956 Diagnosis, 958 Etiology, 956 Malaria, influence of, 956 Pathological anatomy, 957 Prognosis, 959 Symptoms, 957 Treatment, 959 Arsenic, use, 960 Extirpation, results of, 960 Ice, locally, 960 Iodine, use, 960 Iron, use, 960 Local, 960 Quinia, use, 960 _Echinococcus of_, 968 Diagnosis, 969 Morbid anatomy, 970 Prognosis, 970 Symptoms, 968 Size and characters of the tumor, 969 Treatment, 970 _Embolic Abscess of_, 963 Diagnosis and prognosis, 964 Etiology, 963 Micro-organism, influence of, 963 Prognosis, symptoms, and treatment, 964 _Hemorrhagic Infarction_, 960 Etiology, 961 Pathological anatomy, 961 Infarcts, seat and characters, 961, 962 Symptoms, 961 _Lardaceous Spleen_, 966 Diagnosis, 967 Etiology, 966 Pathological anatomy, 967 Prognosis, symptoms, and treatment, 966, 968 _Perisplenitis_, 965 Etiology, 965 Pathological anatomy, 965 _Rupture_, 971 Pathological anatomy, 972 Symptoms and course, 972 _Splenitis_, 962 Pathological anatomy, 963 Symptoms, 962 _Syphilis of_, 970 _Tubercle of_, 972 _Tumors of_, 973

Spleen, displacement of, in pleurisy, 497, 507 enlargement of, in Hodgkin's disease, 924 in leukæmia, 914 influence of, in production of blood-corpuscles, 889 on blood-formation, 884 lesions, in Addison's disease, 943 in Hodgkin's disease, 927 in leukæmia, 916 in melanæmia, 897

Splenic abscess, diffuse, 962 enlargement in syphilis, 971

Splenitis, 962

Spot, pneumonic, 328

Spray-producers, proper, in chronic laryngitis, 125, 126

Sputa, characters, in catarrhal pneumonia, 359-361 in pneumonokoniosis, 455, 459 in pulmonary phthisis, 401 in fibroid phthisis, 441 sanguinolent, in pulmonary embolism, 382

Sputum of croupous pneumonia, 322

Starvation method of treatment of thoracic aneurism, 816

Steam, inhalations, in chronic pharyngitis, 126

Stenosis, aortic, 654 mitral, 665 of trachea, 142 of the trunk and main branches of the pulmonary artery, 834 pulmonary, 674 tricuspid, 677

Stillé, Moreton, on causation of cyanosis, 713

Stitch in the side in pleurisy, 493

Stimulants in catarrhal pneumonia, 371 use, in abscess of lung, 300 in Addison's disease, 948 in angina pectoris, 760 in cardiac thrombosis, 746 in collapse of the lung, 256 in croupous pneumonia, 348 in functional heart disease, 753 in pulmonary phthisis, 435 in pseudo-membranous laryngitis, 108 in simple lymphangitis, 991 in thrombosis and embolism of the pulmonary artery, 836

Stomach, disease of, influence on causation of pulmonary embolism, 375 displacement of, 507

Stomachic asthma, 193

Strain, influence on causation of thoracic aneurism, 802

Strapping of chest in pleurisy, 520

Stricture of trachea, 142

Strychnia, use, in acute myocarditis, 606 in Addison's disease, 948 in anæsthesia of larynx, 68 in paralysis of larynx, 91 in pseudo-membranous laryngitis, 108 in respiratory failure of catarrhal pneumonia, 371 in valvular heart disease, 685 in vesicular emphysema, 216

Subclavian aneurism, localization of, 813

Subjective symptoms of croupous pneumonia, 319

Succussion sound in pneumothorax, 579

Sudden or fatal form of pulmonary embolism, symptoms, 379

Suffocation, sense of, in laryngeal oedema, 114

Sulphur, use, in pulmonary phthisis, 436

Sulphuretted hydrogen, use, in bronchial asthma, 209

Sulphuric acid, use, in epistaxis, 51

Superior tracheotomy, 148, 153

Suppurating hydatid cysts, treatment, 471

Suppuration, influence on causation of lardaceous spleen, 966 of veins, 844, 845

Suppurative myocarditis, acute, 604

Suprarenal bodies, anomalies, 949 atrophy of, 949 changes in, in Addison's disease, 942 cysts of, 949 degenerations of, 949 inflammation of, 949 tumors of, 949

Surgical affections, influence on causation of pulmonary embolism, 376 measures in pulmonary embolism, 390 treatment of paralysis of vocal cords, 89 of purulent pleurisy, 549

Sympathetic ganglia, lesions, in pernicious anæmia, 905 system, relation of Addison's disease to, 945

Symptoms and course of asthma, 185 of bronchial asthma, 185 and treatment of atheroma of the aorta, 800 of hydropericardium, 789, 790 of pneumo-hydropericardium, 791 of pyopericardium, 790 of abdominal aneurism, 821 of acute catarrhal laryngitis, 93 congestion of the spleen, 954 coryza, 41 miliary tuberculosis, 478 myocarditis, 606 phlebitis, 845 of Addison's disease, 940 of adherent pericardium, 786 of anæsthesia of larynx, 66 of aneurism of the coeliac axis, 841 of the coronary artery, 831 of the inferior mesenteric artery, 839 of the superior mesenteric artery, 836 of angina pectoris, 755-757 of aortic obstruction, 656 regurgitation, 661 of atheroma of aorta, 800 of atrophic form of chronic nasal catarrh, 47 lobar emphysema, 248 of bronchial dilatation, 228 of brown induration of lungs, 257 of the caisson disease, 854 of cancer of the lungs, 461, 462 of cancer of pleura, 584 of cardiac malformations, 709 thrombosis, 726 of catarrhal pneumonia, 358 of chlorosis, 895 of chorea of larynx, 76 of chronic bronchitis, 174 congestion of spleen, 957 endarteritis of the coronary artery, 828 inflammation of epiglottis, 110 laryngitis, 121 myocarditis, 608 nasal catarrh due to necrosis, 49 from osseous and membranous obstruction, 44 of collapse of lung, 252 of croupous pneumonia, 319 of dilatation of the heart, 634 of trachea, 144 of echinococcus of spleen, 968 of embolic abscess of spleen, 964 of embolism of the coronary artery, 832 of the superior mesenteric artery, 837 of endocarditis, 646-649 of epiglottic ulceration, 112 of exophthalmic goitre, 762 of fatty degeneration of the heart, 614 infiltration of the heart, 612 of fibroid phthisis, 441 of fibro-serous pleurisy, 493 of functional heart disease, 747-749 of gangrene of lung, 302 of goitre, 914 of hæmophilia, 934 of hæmoptysis, 281 of hæmothorax, 582 of hay asthma, 218 of hemorrhagic infarction of spleen, 961 pleurisy, 567 of Hodgkin's disease, 923 of hydatids of pleura, 585 of hydrothorax, 571 of hyperæsthesia of larynx, 62 of hypertrophy of the heart, 624 of hysterical affections of glottis, 83 of inflammation of epiglottis, 109 of inflammatory non-hypertrophic form of nasal catarrh, 47 of lardaceous spleen, 966 of laryngeal oedema, 113 of laryngismus stridulus, 70 of leukæmia, 910 of mediastinal abscess, 862 tumors, 822 of mitral regurgitation, 671 stenosis, 667 of morbid growths of larynx, 130 of trachea, 140 of nasal polypus, 53 of occlusion of the coronary artery, 831 of the aorta, 825 of paræsthesia of larynx, 64 of paralysis of abductors of vocal cords, 87, 88 of adductors of vocal cords, 82 of central adductors of vocal cords, 85 of constrictors of larynx, 80 of external tensors of vocal cords, 86 of tensors of vocal cords, 85 of the whole larynx, 79 of pericarditis, 773 of perichondritis and chondritis of the larynx, 118 of pernicious anæmia, 900 of phlegmasia dolens, 847 of pneumonokoniosis, 458 of pneumothorax, 578 of pseudo-membranous laryngitis, 101 of pulmonary abscess, 297 apoplexy, 294 congestion and oedema, 260 embolism, 378 hydatids, 468 phthisis, 400 stenosis, 675 of purulent pleurisy, 542 of rheumatic pleurisy, 565 of rupture of the aorta, 824 of the heart, 617 of the spleen, 972 of sarcoma, carcinoma, and fibroma of nasal passages, 55 of simple lymphangitis, 987 tracheitis, 133 of spasm of the glottis in adults, 74 of splenitis, 962 of stenosis of the aorta, 826 of the pulmonary artery, 835 of trachea, 142 of syphilis of the lung, 451 of termination of pneumonia in abscess, 332 of thoracic aneurism, 803 of thrombosis and embolism of the coronary artery, 832 of the pulmonary artery, 836 of tricuspid regurgitation, 679 stenosis, 677 of ulceration of trachea, 139 of vesicular emphysema, 233, 236

Syncope and suffocation in pulmonary embolism, 379-381 in cardiac thrombosis, 730

Synonyms of Addison's disease, 939 of bronchial asthma, 184 of bronchial dilatation, 227 of bronchitis, 164 of cancer of the lungs, 460 of cardiac thrombosis, 718 of catarrhal pneumonia, 353 of chronic laryngitis, 121 of croupous pneumonia, 307 of gangrene of lung, 301 of goitre, 974 of hæmophilia, 932 of hæmoptysis, 266 of hay asthma, 210 of Hodgkin's disease, 921 of laryngeal oedema, 112 of leukæmia, 908 of lymphangitis, 986 of perichondritis and chondritis of the larynx, 117 of pernicious anæmia, 898 of pleurisy, 483 of pneumonokoniosis, 454 of pulmonary abscess, 296 embolism, 393 hydatids, 466 phthisis, 391 of purulent pleurisy, 539 of simple tracheitis, 133

Syphilis, influence on causation of abductors of vocal cords, 87 of aneurism of the coeliac axis, 841 of chronic myocarditis, 607 of goitre, 977 of lardaceous spleen, 966 of leukæmia, 910 of paralysis of adductors of vocal cords, 82 of pleurisy, 493 of thoracic aneurism, 803 of the heart, 637

SYPHILIS OF THE LUNG, 447 Definition, history, and etiology, 447 Diagnosis and prognosis, 453 Morbid anatomy, 451 Pathology, 448 Symptoms, 451 Treatment, 453

Syphilis of the spleen, 970

Syphilitic and chronic laryngitis, 123 disease of the lung, 447

Syphon process of draining pleural cavity, 555, 556 use of, in thoracentesis, 530, 531

T.

Tannic acid, use, in chronic laryngitis, 126

Tapping in gangrene of the lung, 305, 306

Tar, use, in chronic laryngitis, 124

Taste and smell, loss of, from nasal polypus, 53

Temperament, influence on causation of hay asthma, 214

Temperature, changes of, influence on causation of bronchitis, 168 diurnal variations, significance of, in diagnosis of catarrhal pneumonia, 365 in acute catarrhal laryngitis, 94 in acute miliary tuberculosis, 478 in cancer of the lung, 462 in capillary bronchitis, 171 in catarrhal pneumonia, 358, 360, 361, 363 in croupous pneumonia, 324-326 in endocarditis, 647 in fibro-serous pleurisy, 494 in Hodgkin's disease, 925 in leukæmia, 913 in pernicious anæmia, 903 in pseudo-membranous laryngitis, 102 in pulmonary phthisis, 404 in purulent pleurisy, 542 of pericarditis, 774 of the limb in acute phlebitis, 845

Termination of cardiac thrombosis, 732 of fibro-serous pleurisy, 512 of Hodgkin's disease, 929 of pulmonary hydatids, 468 of purulent pleurisy, 547 of thoracic aneurism, 815

Theories regarding causation of cyanosis, 712 origin of Addison's disease, 945 of the caisson disease, 856

Thirst in croupous pneumonia, 330

Thoracentesis, albuminoid expectoration following, 536 danger of, and objections to, 534 death from, cause, 536-538 duration of proper time to wait for absorption, 528 during febrile stage of pleurisy, 526 heart affections following, 536, 537 history of, 586 in fibro-serous pleurisy, 521 in hemorrhagic pleurisy, 569 in hydrothorax, 573 in pleurisy, indications for, 521 mode of operating, 530 in purulent pleurisy, 550 perforation of lung in, 538 point of puncture, 532-534

Thoracic aneurism, 801

Thorax, shape of, in emphysema, 236, 237

Thrill, in thoracic aneurism, 808, 809 purring, in mitral stenosis, 668, 669

Thrombosis and embolism of the pulmonary artery, 835, 836 of the coronary artery, 832 of the superior mesenteric artery, 839

Thyro-cricotomy, 148-154

Thyroid body, enlargement of, in exophthalmic goitre, 762 gland, carcinoma and sarcoma of, 978 diseases of, 974

Tinnitus aurium, from nasal polypus, 53

Tobacco, abuse of, influence of, on causation of chronic laryngitis, 121 avoidance of, in functional heart disease, 755 influence on causation of hypertrophy of the heart, 619 of functional heart disease, 752 use, in bronchial asthma, 204

Tongue-spatula, proper mode of using, 109

Tongue, state of, in catarrhal pneumonia, 360 in croupous pneumonia, 330

Tonics, use, in paralysis of larynx, 91

Toxic causes of anæmia, 889

Trachea, dilatation of, 143, 144 diseases of, 133 hernia and fistule, 143

TRACHEA, MORBID GROWTHS OF, 139 Diagnosis and prognosis, 141 Etiology, 139 Pathology and symptoms, 140 Treatment, 141

Trachea, stenosis of, 142, 143

TRACHEA, ULCERATION OF, 136 Prognosis, 139 Seat, 138 Symptoms and treatment, 139

Tracheaectasy, 143

Tracheitis, complicated, 136

TRACHEITIS, SIMPLE, 133 Diagnosis and prognosis, 134 Morbid anatomy, 134 Symptoms, 133 Treatment, 135

Tracheocele, 144

Tracheoscopy, 134

TRACHEOTOMY, 145 Accidents during, 156 After-treatment, 159 Complications arising after, 161 Cricotomy, 156 Indications for, 145 Inferior tracheotomy, 155 Median tracheotomy, 155 Methods of operating, 155, 156 Superior tracheotomy, 153 Thyro-cricotomy, 154 tube, choice, 150 removal, 161

Tracheotomy in chronic laryngitis, 128 in laryngeal oedema, 117 in paralysis of abductors of vocal cords, 88 in paralysis of larynx, 89 in pseudo-membranous laryngitis, 107 in spasm of the larynx, 75

Transfusion in pernicious anæmia, 907

Transposition of great arteries in cyanosis, 707

Traube's semi-lunar space, tympanitic sound in, in pleurisy, 503

Traumatism, influence on causation of fibro-serous pleurisy, 492 of leukæmia, 910 of lymphangitis, 986 of mediastinal abscess, 861 of pericarditis, 770 of purulent pleurisy, 540

Treatment of abdominal aneurism, 823 of acute catarrhal laryngitis, 96 congestion of spleen, 955 miliary tuberculosis, 480 myocarditis, 606 phlebitis, 846 of Addison's disease, 948 of adherent pericardium, 788 of anæsthesia of larynx, 67 of aneurism of the coeliac axis, 842 of angina pectoris, 760 of asthma, 201 of atheroma of aorta, 801 of atrophic emphysema, 249 of atrophic form of nasal catarrh, 48 of bronchial dilatation, 230 of bronchitis, 170 of caisson disease, 858 of cancer of the lungs, 465 of cancer of pleura, 584 of carcinoma and sarcoma of nasal passages, 56 of cardiac thrombosis, 745 valvular disease, 683 of catarrhal pneumonia, 369 of chlorosis, 896 of chorea of the larynx, 77 of chronic congestion and enlargement of spleen, 959 endarteritis of the coronary artery, 830 inflammation of epiglottis, 110 laryngitis, 124 myocarditis, 609 nasal catarrh due to necrosis, 50 from osseous and membranous obstruction, 44 phlebitis, 848 of collapse of the lung, 255 of coryza, 42 of croupous pneumonia, 345 of deflected nasal septum, 46 of dilatation of the heart, 635 of the veins, 850 of trachea, 144 of echinococcus of the spleen, 970 of embolic splenic abscess, 965 of embolism of the superior mesenteric artery, 839 of endocarditis, 650 of epiglottic ulceration, 112 of epistaxis, 51 of erosions of epiglottis, 111 of exophthalmic goitre, 765 of fatty degeneration of the heart, 616 of fatty infiltration of the heart, 612 of fibroid phthisis, 444 of fibroma of nasal passages, 56 of functional heart disease, 753 of gangrene of lung, 305 of goitre, 979 of hay asthma, 222 of hæmopericardium, 789 of hæmophilia, 938 of hæmoptysis, 291 of hæmothorax, 583 of hemorrhagic pleurisy, 568 of Hodgkin's disease, 931 of hydatids of pleura, 586 of hydrothorax, 572 of hyper- and paræsthesia of larynx, 64 of hypertrophy of the heart, 630 of inflammation of the epiglottis, 109 of inflammatory non-hypertrophic form of nasal catarrh, 47 of lardaceous spleen, 967 of laryngeal oedema, 116 of laryngismus stridulus, 71 of leukæmia, 920 of mediastinal abscess, 863 tumors, 880 of morbid growths of larynx, 131 of trachea, 141 of nasal polypus, 54 of nervous cough, 77 of paralysis of larynx, 88 of pericarditis, 783, 784 of perichondritis and chondritis of the larynx, 121 of pleurisy, 519 of pneumonokoniosis, 459 of pneumothorax, 581 of progressive pernicious anæmia, 906 of pseudo-membranous laryngitis, 104 of pulmonary abscess, 300 apoplexy, 295 congestion and oedema, 263 embolism, 388 hydatids, 470 phthisis, 425 of purulent pleurisy, 549 of rheumatic bronchitis, 181 pleurisy, 565 of simple lymphangitis, 990 tracheitis, 135 of spasm of the glottis in the adult, 74 of stenosis of the aorta, 825, 827 of trachea, 143 of syphilis of the lung, 453 of the spleen, 971 of thoracic aneurism, 816 of thrombosis and embolism of the pulmonary artery, 836 of ulceration of trachea, 139 of vesicular emphysema, 245 operative, of pericardial effusions, 794

Tricuspid disease, prognosis, 683 treatment, 686 regurgitation, 678 stenosis, 677 valve, defects of, in cardiac malformations, 689

Tube, tracheotomy, choice of a proper, 150 management of, after tracheotomy, 160

Tubercle, influence on causation of purulent pleurisy, 540 of the heart, 637 of the spleen, 972

Tubercles, histology, mode of formation, etc., 474-476 miliary, formation, 475, 476 physical characters, 474

Tubercular diathesis, 476, 477 laryngitis, diagnosis, 95 pericarditis, 793 phthisis, following pleurisy, frequency, 513 pleurisy, 569 process, nature, 375

TUBERCULOSIS, ACUTE MILIARY, 472 Contagiousness of, 472 Definition, 472 Etiology, pathology, etc., 472-478 Age, influence of, 478 Bacillus tuberculosis, relation to, 473 Bad air, hygiene, etc., influence of, 473 Catarrho-pneumonia, relation to, 476 Symptoms and course, 478 Of partial or local form, 479 Physical signs, 479 Temperature, 478 Treatment, 480 Antipyrine, use, 481 Codeia, use, 482 Cod-liver oil and hypophosphites, 482 Diet in, 481 Quinia, use, 480 Stimulants, 481

Tuberculosis complicating and following catarrhal pneumonia, 364 in Addison's disease, 943 relation of, to stenosis of pulmonary artery, 711 to chronic laryngitis, 123

Tubular lymphangitis, symptoms, 987

Tufnell's method of treating aneurism, 816

Tumor, aneurismal, of abdomen, characters, 822 characters of, in echinococcus of spleen, 969 presence of, in dilatation of trachea, 144 splenic, size in congestion of spleen, 954

Tumors, leukæmic, frequency, characters, etc., 918 of mediastinum diagnosed from pericarditis, 780 of suprarenal bodies, 949 of the spleen, 973

Turpentine, inhalations in acute catarrhal laryngitis, 97 use, in bronchial dilatation, 231 in hæmoptysis, 291 in pseudo-membranous laryngitis, 106 in pulmonary hydatids, 470

Tympanitic resonance in pneumothorax, 571

Typhoid pneumonia, 333

U.

Ulcer of the heart, 605

Ulceration of trachea, 136 following tracheotomy, 162

Ulcerations of epiglottis, 111 of septum as a cause of epistaxis, 51

Ulcerative endocarditis, 642 form of hæmoptysis, 283

Urine and ovarian irritation, as a cause of asthma, 193 changes in, in Hodgkin's disease, 925 in leukæmia, 913 condition in pernicious anæmia, 903 in Addison's disease, 941 in tricuspid regurgitation, 679 state of, in capillary bronchitis, 171 in catarrhal pneumonia, 360 in mitral regurgitation, 671 in pneumonia, 330

Uterus, disease of, influence on causation of pulmonary embolism, 375

V.

Valves, changes in, in aortic obstruction, 654, 655 regurgitation, 659 in mitral regurgitation, 670 stenosis, 665 condition, in tricuspid regurgitation, 678 lesions of, in acute exudative endocarditis, 641 in interstitial endocarditis, 643 in tricuspid stenosis, 675 in ulcerative endocarditis, 642

Valvular disease, influence on causation of dilatation of the heart, 632 of hypertrophy of the heart, 620, 623

Varicose aneurism, 802 signs of, 813 veins, 849

Varieties of dilatation of the heart, 630 of goitre, 977 of hypertrophy of the heart, 619

Variola, acute tracheitis in, 136

Vascular goitre, 977 treatment, 980 supply of lung, relation to hæmoptysis, 269

Vegetations in ulcerative endocarditis, 642

Vein-stones, 853

VEINS, DISEASES OF, 843 _Degenerations of_, 852 _Dilatation_, 849 Treatment, 850 Pressure, 850 _Inflammation_, 843 Diagnosis, 846 Pathology and morbid anatomy, 843-845 Formation of a clot preceding inflammation, 843, 844 Suppuration of vein, seat and character, 844, 845 Symptoms, 845 General, 845, 846 Local, 845 Treatment, 846 Blisters, use, 846 Calcium sulphide, use, 846 Fomentations, 846 Ice, use, 846 Rest and position, necessity of, 846 Phlebitis, chronic, 848 Phlegmasia dolens, 846 Puerperal state, influence on causation, 847 Symptoms and treatment, 847, 848 _Narrowing of a Vein_, 851 _Occlusion of Veins_, 851 Treatment, 852 _Phlebolithes_, 853

Veins of neck, turgidity of, in cardiac thrombosis, 730 pressure upon, in thoracic aneurism, 807

Venesection, harmfulness of, in croupous pneumonia, 346 in acute bronchitis, 178 in pulmonary embolism, 390

Venous hum in pernicious anæmia, 903

Ventricle, right, alteration in form in cardiac malformation, 695

Vesicular emphysema, 232

Vessels, great, congenital anomalies of, and cyanosis, 687

Viscera, lesions, in pseudo-membranous laryngitis, 101

Vision, distortion of, in croupous pneumonia, 329

Vital or pathological causes of cardiac thrombosis, 724

Vitality, depressed, influence on causation of croupous pneumonia, 314, 315

VOCAL CORDS, PARALYSIS OF ADDUCTORS OF, 81 Abductors, 86 Central adductors, 84 External tensors, 86 Tensors, 85 Treatment, 88 Electricity in, 90 Surgical, in, 90 Tonics in, 91 Tracheotomy in, 89

Vocal resonance in pulmonary phthisis, 413, 417

Voice, alteration of, in chronic laryngitis, 122 in dilatation of trachea, 144 in goitre, 975 in morbid growths of the larynx, 129 improper use, influence on causation of hyperæsthesia of the larynx, 62 in epiglottic ulceration, 112 in hysterical affections of glottis, 83 in laryngismus stridulus, 71 in morbid growths of trachea, 140 in paralysis of adductors of vocal cords, 82 of tensors of vocal cords, 85, 86 of whole larynx, 80 over-use of, influence on causation of chronic laryngitis, 121 sounds in fibro-serous pleurisy, 510 transmission of, in purulent pleurisy, 543, 545

Vomiting in the caisson disease, 854 in diaphragmatic pleurisy, 563 in embolism of the superior mesenteric artery, 837 in endocarditis, 647 in pulmonary phthisis, 406

W.

Waldenburg's apparatus for emphysema, 246

Wasting of pleural cavity in purulent pleurisy, 551, 553-562

Water, influence on causation of goitre, 976

Whispered voice, importance in diagnosis of pulmonary phthisis, 413, 417 transmission of, and significance in pleurisy, 510, 512

White corpuscles of the blood, increase of, in leukæmia, 912 leg, 846

Whooping cough, influence on causation of acute miliary tuberculosis, 473

Wildegger water, use, in goitre, 980

Wire, fine, introduction into sac for relief of aneurism, 816

Worms, influence on causation of laryngismus stridulus, 70

Wounds, etc., influence on causation of pulmonary embolism, 376

Y.

Yeo's respirator, use, in chronic laryngitis, 126

Z.

Zinc sulphate, use, in chronic laryngitis, 126

END OF VOLUME III.