Part V., amongst those illustrative of recovery after symptoms of

pulmonary obstruction.]

3d. Benign Form.--This form occurs frequently after the traumatisms as described by Besson.[55] Habitually we have few or no symptoms which are at all characteristic. The embolisms are capillary and remain latent. Now and then there may be a sudden attack of difficulty of breathing, accompanied by constriction of the thorax which shall probably be explained in this manner. Sometimes the sputa are slightly covered with blood, and this fact lends additional authority to the diagnosis. According to Ball, the physical evidences of the embolisms in the chest are wholly disappointing. Besson, however, finds distinct evidences of their presence in crepitant and subcrepitant râles and dulness on percussion. Levrat[56] believes we may have probable signs of the existence of capillary emboli, and cites as an example a case of traumatism in which there might be present a thrombus, and where there would be sudden hæmoptysis followed by sanguinolent sputa, and yet the examination of the chest remained negative. There are cases reported by Paget, Colin, and Feltz in which fatal terminations, caused by a succession of asphyxic paroxysms, took place just as they do after sudden plugging of the large pulmonary divisions. This is true only when the capillary embolisms are very numerous.

[Footnote 55: Paris, 1878.]

[Footnote 56: _Thèse_, Paris, 1880.]

It has been noted that secondary changes of capillary embolisms are not apt to occur in the anæmic and cachectic; in the plethoric and those affected with chronic cardiac disorders the contrary is true. According to the condition of the nervous system, to its greater or less tendency to react, there will be more or fewer chances of the capillary embolisms making their existence known by an attack of suffocation (Luzzato).

PATHOLOGY AND MORBID ANATOMY.--Pulmonary embolism gives rise to different morbid lesions. The nature of these and their extent depend in great measure upon the size, situation, and character of the plug which fills the main trunk of the pulmonary artery or one or more of its divisions. The changes of tissue which take place are of course in close relationship with the length of time which has elapsed since the embolus first migrated. They are also influenced greatly by accidents or complications which have arisen. It shall be our effort first to narrate the important considerations which pertain to simple embolus, and whether it affect a large artery or only a small vessel. After speaking of the simple variety we will refer briefly to septic and fatty emboli and also to those of other nature.

The pulmonary artery may be blocked up by a clot formed in situ. This fact has been shown to be true by many writers--_i.e._ Lancereaux, Duguet, etc. When a thrombus is present it may be occasioned by an inflammatory condition of the artery (rare), or by a dyscrasic blood-condition, or again by localized compression in the vicinity of the coagulum, as from a tumor. We may find arterial thrombosis during pulmonary phthisis, in pneumonia, in pleurisy, and in cases of cardiac dilatation or degeneration.[57] Endocarditis of the pulmonary valve and compression of the neck by enlarged ganglia have been mentioned as causes of these thrombi.

[Footnote 57: Here it is due to relative stasis of the blood.]

{383} Ordinarily, a pulmonary embolus is fixed at the point of division of the main vascular trunk. It more or less completely blocks up the calibre of the artery, and is usually situated in the midst of a soft new clot, which also covers it in front and behind. The embolus often manifests its origin from a clot contained in one of the large veins of the lower extremities. One end is rough and excavated, and fits into the coagulum we find lodged there. It is often twisted like a corkscrew, or has on its surface the mark of the valves of the vein from which it has migrated. It is white or yellow in color. If we examine the interior of an ordinary autochthonous clot, we find it softer relatively than the clot of an embolus, and, moreover, no prolongations proceed from it which fail to correspond with any vascular division. The suddenness of the accidents and the disappearance of a previous peripheric clot are strong reasons in favor of the existence of the embolus.

More emboli are carried into the right lung than into the left, on account of the larger size of the artery. The median and lower lobes are also the ones most usually affected. When the right lung is diseased the emboli are then more frequently transported on the left side. After a time an embolus goes through certain transformations. It softens at its centre, owing to degeneration of the white blood-corpuscles. The hematies disappear soon, and the fibrin also changes in structure, becoming soft and granular. This softening at the centre of the embolus must not be confounded with a purulent change which affects certain thrombi which come from or are carried to a focus of suppuration. Whenever an embolus has been a long while in the artery, a neo-membrane forms between it and the arterial wall. This neo-membrane is mainly constituted by fibrillous tissue and here and there some developed vascular twigs. As a whole, it forms a sort of cap or covering for the embolus, and finally it takes up by absorption the granular detritus which forms in the interior of the clot. We perceive from the foregoing statement that a pulmonary embolism may heal, and that the process of its cure differs in no respect from what occurs in the case of a coagulum which disappears by absorption from some other portion of the vascular system, or indeed from the surface of the serous membrane. When the embolic plug comes from a focus of suppuration or gangrene the vascular walls will probably be affected with similar alterations.

In consequence of the obstruction of the main trunk, or of the important branches of the pulmonary artery by embolic plugs, certain effects are directly produced. These are--1st, mechanical; 2d, nutritive; 3d, irritative.

Perhaps, however, before describing these effects in detail it would be well to mention certain anatomical facts with respect of the circulation of the lung which have considerable importance in view of certain morbid lesions to which we shall refer presently. It has now been proven experimentally, by the researches of Cohnheim, Litten, and Küttner, that there are no vascular communications between the pulmonary and bronchial arteries, and, further, that there are no branches coming off from the small divisions of the pulmonary artery by which a collateral circulation can be carried on when the arteries of the third order are obstructed by embolic plugs. It is also further corroborated by the investigations of the authors named that the pulmonary artery is mainly instrumental in keeping up the function of the lungs, whilst the bronchial artery is the artery of nutrition. If the latter were obstructed in any manner, gangrene of the pulmonary structure must surely follow; if the latter be ever so thoroughly closed, no death of tissue will ever result.

The mechanical effects caused by the obstruction of the main artery or of a primary division of it are much less considerable than when a smaller artery is plugged. In the first case the only observable condition is that of anæmia of pulmonary tissue. Occasionally Lancereaux has noticed atelectasis of certain lobules. The pathogeny of this condition is difficult to {384} explain, as air enters the bronchi freely, and it should not be produced without effusion taking place. If life lasts a few hours hyperæmia and oedema of lung-tissue may be caused. The latter conditions are aided if there be existing organic disease of the heart. If, now, the smaller arteries be obstructed by embolic plugs, there is a strong tendency to the formation of hemorrhagic effusions, to which the name infarctus has been very properly given by Virchow. These infarctions vary in size from that of a small nut to that of a pullet's egg, just as they implicate one or more pulmonary lobules. They are situated at the periphery of the lung underneath the pleura. They are conoid in shape, with the apex turned toward the root of the lung. They seem like hard nuts under the surface of the lung when felt with the fingers. Their color is dark-brown or black; their cut surface is granular, even more so than the surface of a lobule solidified by broncho-pneumonia. The capillaries in and around these masses are filled with red blood-corpuscles. The same is true also of the alveoli, in which we find degenerated epithelial cells in large numbers containing granules of pigment. The connective tissue about the alveoli becomes thickened, the alveolar cavities contract, and finally the infarctions are changed into a real fibrous cicatrix, in the same way as they are transformed in other viscera of the body. Prior to this stage, however, we notice that the color of the infarction has gradually changed, and that it has become pale and yellow. This is due to the fatty degeneration of the fibrin contained in the alveoli, and the same affection of the enclosed cells. May any infarctions be restored to a condition of perfect integrity? It is more than doubtful, even if the obstructing plug of the pulmonary artery disappeared very soon, because the pulmonary parenchyma beyond the clot has suffered so much from fatty changes and hemorrhage that the vessels are unequal to their function. At times, owing to the stoppage of the nutritive action of the bronchial artery, the infarction may become a cheesy mass, which soon softens and is expectorated. This leaves a cavernous opening in the lungs. Sometimes the infarction becomes infiltrated with calcareous salts. It cannot be confounded readily with other lesions, especially pulmonary apoplexy, on account of its distinct limitations. Sometimes a lobule affected with broncho-pneumonia and hemorrhage may simulate it closely. The pathogeny or mode of production of the hemorrhage in a more or less limited area of the lung which is concomitant with an embolic plug in one of the branches of the pulmonary artery is difficult to present. This fact may be explained by the different solutions afforded by various authors as to the manner in which the apoplectic condition and the embolus are correlated. Certain writers have affirmed that the embolus itself is but a secondary phenomenon, and the surrounding hyperæmic state is the real cause of its production (Laennec). Later authorities have established that this statement is rarely true, and that the embolus always occurs first and the localized congestion follows closely afterward.

Precisely the way in which the congestion or hemorrhage was occasioned has not been elucidated in a similar manner by all. Virchow years ago (1856) recognized that one or other was due to vascular stasis and reflux of venous blood from neighboring vessels; in other words, the explanation here given was the same as for infarctus of the kidney or spleen. Jürgensen regards infarctus as being similar in structure to lobular pneumonia. It has been also affirmed that owing to incomplete obstruction tissue supplied by the artery was at first anæmiated, and later, by reason of excess of backward pressure from venous trunks, it became congested or hemorrhage was effected. Duguet states that the arterial walls beyond the embolic plug become inflamed, and thus act as a cause of hemorrhage. The first effect, then, of an embolic clot being arrested in the lung is that of anæmia. Soon this state is followed by hemorrhage occasioned in the way I have mentioned. In the lung the {385} hemorrhage means of necessity rupture of a vessel; in the spleen and brain this is not so invariable. Whilst the smaller bronchi are sometimes congested, they are rarely infiltrated with blood. For this reason gangrene is not a frequent sequela of pulmonary infarctus. It is not admissible that hemorrhage should occur without rupture of the vessel in many instances, for the reason that the sanguineous effusion is not always limited to the area supplied by a given vascular division obstructed, nor is it in the centre of the lung conoid in shape. The catarrhal changes in the lungs are very constant, although usually superficial in character and only affecting the epithelium. As Cohnheim[58] has pointed out, there is a proneness to degeneration rather than to inflammatory action.

[Footnote 58: _Untersuchungen über die Embolischen Processe_, Berlin, 1872.]

Due consideration being given to the changes of tissue effected by an arrested embolus, we can more fully understand the clinical phenomena connected with them. True it is, however, that the troubles of innervation and respiration thus brought on may pass unperceived, and for the simple reason that the pathological lesion follows, as a rule, only the transport of an embolus into a small arterial division. In a similar way the intensity of the venous reflux is in direct relationship with the functions of the heart and lungs, and if either the diseased hemorrhagic effusion is rendered more certain.

It is probable that a simple embolus cannot be followed by a gangrenous focus in the lung. This result is recognized frequently when the embolus originates in a purulent deposit, whether it be the consequence of an abscess, of puerperal fever,[59] of a compound fracture, etc. The gangrenous cavity finally softens, its contents are expectorated, and the pulmonary tissue becomes indurated and cicatrizes around the excavation.

[Footnote 59: _Dublin Journ. of Med. Science_, May, 1875.]

Pulmonary embolism may at times be the occasion of a pneumonic consolidation limited to the area of distribution of an obstructed pulmonary division. Sometimes the consolidation extends beyond this limit, and is seemingly the immediate effect of neighboring irritation. When the consolidation exists near the surface of the lung, it may extend to the pleura, producing considerable effusion and pseudo-membranous deposit upon the visceral layer. Both sides of the chest may occasionally be thus affected.

Capillary emboli of simple nature have long been described. Unless they obstruct a great many vessels simultaneously, they rarely cause death (Feltz). They do not, moreover, produce hemorrhages or infarctus, inasmuch as a collateral circulation is so easily established. The principal sources of these emboli exist outside of the vascular system, and in this variety we find emboli of air, fat, of the débris of new growths, etc.

Since 1866, the period at which Zenker first directed attention to fatty emboli in the pulmonary capillaries as a complication of an accident in which a patient was crushed between two wagons, many observers have noted accidents due to these obstructing bodies. Fatty emboli may follow numerous causes (contusions, suppurations, osteomyelitis, etc.), but are more frequent and fatal after comminuted fractures of the limbs than from any other single cause (Flournoy).

Occasionally the patient will have recovered from the shock following the fracture, when he is suddenly attacked with intense dyspnoea and expires within a few hours. The only effectual remedy would seem to be immediate amputation of the limb above the seat of the fracture. When the vessels of the lungs have been examined in these instances, they have been found to contain elongated masses, several millimeters in length, possessing a particular brilliancy, "disappearing under the action of ether, and becoming a deep, black color with osmic acid."[60]

[Footnote 60: Déjerine, _Le Progrès médical; Med. Record_, Jan. 15, 1879.]

{386} Specific emboli may be followed by the mechanical effects of simple emboli, but they are also accompanied by specific phenomena which are in relation with the particular focus in which they took origin--_i.e._ purulent or septic focus, gangrenous cavity, cancerous tumor, etc.

In the region where the embolus is arrested, local alterations of tissue become developed which correspond with the nature of the changes which exist in the spot from which the embolus was derived. Very often these morbid effects are produced without any mechanical results of emboli being occasioned.

Septic emboli are observed in infectious diseases, such as pyæmia and puerperal fever, and are prone to occasion not merely mechanical effects, but equally the suppuration, liquefaction, and finally the absolute destruction of tissue. Cruveilhier has seen pulmonary embolism followed by metastatic abscesses. The formation of these was attributed by him to suppurative phlebitis affecting the capillaries.[61]

[Footnote 61: _Dict. de Méd. et de Chirurgie pratique_, vol. xxix. p. 360.]

It is admitted to-day that infectious germs causing metastatic abscesses may be transported in the pulmonary vessels without being accompanied by pulmonary emboli. It is equally true, however, that the usual means of transport for these infectious bacteria or micrococci is an embolic plug (Jeannel).

The effects produced by the septic emboli are pneumonic consolidations involving the lobules and going on rapidly to suppuration, and sometimes to gangrene. The coloration of the lobules is red, gray, tending toward yellow as the tissue shows signs of softening. The contents of the abscess are yellow or brown and contain particles of the pulmonary structure. The tissue in the vicinity is gray and infiltrated with pus.

The number of metastatic abscesses is often very considerable. Their size is usually smaller than the infarctus due to simple emboli. The smaller abscesses are found usually near the surface of the lung. When several abscesses unite into one they may attain the size of the fist.

Whenever there exists a gangrenous lesion in some portion of the body, sphacelated débris may be carried from this focus into the venous system, and finally into the lungs. Arrested in some spot of the pulmonary tissue, the embolus will give rise to gangrenous changes similar to those of the region from which it started.[62] The infarctus thus produced will assume a dark color, then become gray toward the centre, where it shows signs of softening. Later, under the form of a thick semi-fluid mixture of extreme fetid odor and dark-brownish color, it is expectorated by degrees, and leaves behind a gangrenous cavity. The process of change in this case is due to the proliferation of infectious germs. It may be, however, that the gangrenous particles transported into the lungs have the power in themselves to decompose the tissues by chemical action into more simple elements.[63] According to the later researches of Doleris, septic bacteria have been found by him in these putrid infarctions.[64]

[Footnote 62: This process was first pointed out by Cruveilhier in his work on _Phlebitis_. It remained, however, for Virchow in his _Cellular Pathology_ (p. 235, ed. Strauss), and later for Billroth in his _Surgical Pathology_, 1868, p. 395, to give greater development to this belief.]

[Footnote 63: Lancereaux, _Traité d'Anatomie pathologique_, vol. i., 1875-77, p. 14 _et seq._]

[Footnote 64: Quoted by Levrat, p. 78.]

The infecting power of cancer is certainly not equal to that of gangrene. Nevertheless, Lancereaux has shown that cancerous nodules may be produced by metastasis. This belief in the possibility of a simple embolus taking on a cancerous change, and carrying this disease to far-removed parts, has been strongly combated by Cohn. Neither experimental nor human pathology has thus far decided the subject in an absolute manner. Certain it is, {387} however, that the power of emboli from cancerous foci to carry similar disease elsewhere depends partly upon the vitality of the cancerous particles, partly upon the power of receptivity as shown by certain constitutions for developing special diseases, and which relates, after all, to the general question of dyscrasia. Langenbeck has shown that certain animals will die within a few hours after the injection of cancerous juice. On the other hand, it is known that the infective power of the juice only lasts a very brief period. Weber, Luzzato, and others have reported numerous examples of secondary tumors of similar nature developed in the lungs when epithelioma, enchondroma, sarcoma, or carcinoma existed somewhere in the body. Finally, it would appear that emboli containing hydatids in embryo have been the means of transporting these parasites into the pulmonary structure.

DIAGNOSIS.--The sudden commencement of the accidents, especially when a peripheral thrombus has existed previously in one of the large veins of the extremities, renders the diagnosis almost certain. If the patient has been suffering from the effects of a traumatism (contusion, fractures, operation on the veins of the limbs or rectum, etc.), and is almost instantaneously attacked with intense dyspnoea and a feeling of anguish which he refers to the thoracic region, we shall be able usually to eliminate other intercurrent affections and to diagnosticate the existence of pulmonary embolism.

This accident is often confounded with cardiac thrombosis. It may usually be separated from it by the following differential symptoms: Cardiac obstruction from a clot usually comes on insidiously, by degrees; the heart-beats are irregular, tumultuous, muffled, and distant; there may be a murmur from one or other of the cardiac orifices; there is no initial chill; peripheral thrombosis is not present as a rule; there is no sensation of localized obstruction in the chest.

In pulmonary embolism the début may be instantaneous and death follow in a few seconds; or, again, the beginning may be rapid, ushered in by stifling in the chest, a chill, cyanosed face, followed soon by excessive pallor, a distinct sensation of obstacle to breathing in a particular region. Percussion and auscultation may remain negative. The patient may have a succession of similar accidents, and yet finally recover. According to Ball, pulmonary embolism and pulmonary thrombosis cannot be distinguished during life. In one case which he reports where pulmonary embolism should have been present without question the autopsy showed the presence of a thrombus in the pulmonary artery. A succession of chills, general malaise, febrile excitement, the localized phenomena of pneumonia or gangrene of the lung, point indubitably to the existence of septic emboli.

The differential diagnosis between pulmonary embolism and other affections, such as angina pectoris, a foreign body in the air-passages, pneumothorax, etc., may usually be reached without much difficulty. Sometimes the paroxysmal dyspnoea with sensations of great oppression which accompanies mitral stenosis may be mistaken for pulmonary embolism. In these instances the absence of a discoverable cause of the attack in pre-existing emboli, and the presystolic murmur with marked general anæmia, may surely lead to an accurate diagnosis. It must, however, always be remembered that in mitral stenosis it is not infrequent to have cardiac coagula formed in the right auricle, which may become detached and give rise to pulmonary emboli. Under these circumstances a severe localized pain in the side of the chest has considerable diagnostic importance as pointing to the presence of a pulmonary embolus (Cohn).

When there is pre-existing cardiac disease of organic nature a syncopal attack may sometimes occasion doubt with respect of a correct diagnosis. The sudden loss of consciousness, excessive pallor, and absence of pulse will ordinarily, however, confirm the diagnosis of syncope. Rupture of the heart {388} is accompanied with symptoms of syncope rather than those of suffocation (Balzer). Emboli of the bronchial arteries are not accompanied by any characteristic symptoms which will enable us to make a differential diagnosis. There is the same sudden dyspnoea, the initial chill and hæmoptysis, as in pulmonary embolism (Penzold).

PROGNOSIS.--As will be readily understood, the prognosis is sometimes difficult to estimate and varies with many circumstances. Certain emboli, even among those which have occasioned severe symptoms, have never been recognized. Other pulmonary emboli always remain comparatively latent. In this connection we should mention those which take place in the lungs of tuberculous patients. Again, the size and seat of the embolus will always have great importance in regard to the prognosis. If the trunk or primary divisions of the pulmonary artery be suddenly and completely obstructed by emboli, sudden death will surely follow. If secondary divisions of the pulmonary artery are filled up, more or less grave symptoms will usually follow. When emboli are carried into the tertiary or still smaller branches of the artery, they may not occasion any appreciable phenomena other than a moderate and passing dyspnoea. If, however, there be a large number of small emboli carried into both lungs at the same time, it is possible that rapid death may follow their presence. It is true, however, according to certain authors, that even a large embolus blocking up the main trunk of the pulmonary artery may be followed by recovery. Such a case is that of Jacquemier, reported by Ball. Even in this case, whilst the presence of the embolus cannot perhaps be doubted, still the exact size and location may be called in question. And here we may add that in all cases of reported cure of this nature there will naturally and inevitably exist an atmosphere of legitimate doubt about the correct observations and diagnosis of the narrated facts.

What precedes relates exclusively to the existence of simple emboli. Of course if the embolus be of septic origin, it will be followed by the appearance in the lungs of foci of purulent pneumonia or of gangrenous changes of tissue which will finally produce such structural destruction as almost certainly to terminate in death.

TREATMENT.--The majority of those who have studied this subject have recognized how vain are our efforts of treatment in many instances. Pulmonary embolism is one of those accidents which we should always be prepared to admit, however, when its characteristic symptoms show themselves, and should endeavor rationally to combat by the therapeutic means in our power. Even before we have any signs present which indicate obstruction of the pulmonary circulation, we may have those which point in a very certain manner to the existence of a peripheral thrombus. This thrombus may block up completely one of the large veins of the lower extremities, and may, owing to its possible detachment and transport, be a constant menace to life. At times these peripheral thrombi are accompanied by local inflammatory symptoms which belong to phlebitis. This condition of things is not uncommon after fractures or other traumatisms. Frequently there is no evidence of any inflammatory state, and we recognize the thrombus solely by the signs which result directly from obstructed venous circulation and by the existence of a hard, indurated cord which fills the vein at a given level. Now, what are the means we have at our command to prevent the transport of this coagulum, or indeed to dissolve it, or absorb it in its place?

First, if inflammatory signs are present we should endeavor to subdue these by local applications of an emollient character, for the reason that excessive inflammation is apt to produce such changes as cause the disaggregation of the clot, and hence its detachment. In either case, whether there be or be not any local inflammatory condition, we should insist upon absolute repose and quiet. We should not permit the limb to be moved: we should be {389} extremely careful in all our manipulations of it, and only employ those which are absolutely essential. The patient should not be permitted to raise himself in bed, nor even eat or drink without assistance. These counsels are very important, since we know how frequently a very slight movement or exertion has been followed immediately by the transport of the clot, pulmonary embolism, and sudden death. In cases of fractures or severe wounds where such a peripheral clot is discovered the surgeon should be particularly careful in applying bandages and retentive apparatus. The risk of displacement of the clot is greater after several days from the time of the fracture or wound than it is at first, and it is at this period that the most careful attention should be exercised. Instances are on record in which so late as the fifty-seventh day after a fracture of the lower extremity a peripheral thrombus was transported from its original site and caused a fatal termination (Bouchard).

Some eminent writers have thought by employing a suitable medication we might hasten the solution of the peripheral thrombi and thus prevent their migration. With this view Legroux has given the acetate of lead internally and applied it in solution over the seat of the thrombus. Richardson has vaunted the use of the carbonate of ammonium in large and frequently-repeated doses as a solvent of the fibrin. By its means he believes he prevents the fibrin from precipitating from the blood, and further helps it to resorb when it has already become solid. Prevost, Dumas, and Schutzenberger recommend specially the bicarbonate of sodium, taken internally, with a view of rendering the blood more fluid and also hastening the retrogressive changes in the clot by its oxidizing power. According to Boyer, the very object which is thus sought if it were accomplished would result injuriously to the patient, since it would favor the detachment of the clot. Further, the continued use of large and frequent doses of ammonia or soda is prone to lower the general system very much, and in this manner to act to the prejudice of the patient. According to Azam, it would appear that what we most desire to effect is the organization and adhesion of the thrombus to the walls of the vessel. This can best be accomplished by fortifying the patient in every possible way and raising his nutrition to the highest attainable point. Iron, cinchona, the most nutritious food, should be freely given. Further, the greatest attention should be paid to the hygienic surroundings. The air should be purified, and if by chance the patient is suffering from a wound close attention should be given to the renewal of the dressings and the employment of a disinfectant locally applied. One of the reasons for this last counsel is because if the thrombus were detached it is important that it should be free of any septic taint and not lead to specific accidents (purulent pneumonia, gangrenous abscess). In the above enumeration we include the means usually to be employed as preventive measures against the migration of clots.

Is there any other method which can be adopted with any chance of success? Of the surgical attempts we should mention favorably in certain cases, and especially in those where the affected vein is superficial, the adoption of persistent compression between the clot and the heart. This means has been alluded to by J. Hunter[65] as far back as 1773. Ligature and section of the vein have also been supported by some writers as suitable operations to bring into use with a like intent. Unfortunately, we are obliged to make a second traumatism in order to carry out this object, and, further, we make by the ligature at least a second coagulation, which may be the origin of the very accident we seek to avoid. Nevertheless, J. Teissier[66] of Lyons reports a case {390} observed by himself in the service of Noël Guéneau de Mussey, in which a ligature was instrumental in arresting the onward progress of the clot, which otherwise would have given rise to the accidents of pulmonary embolism.

[Footnote 65: _Observations of the Inflammation of the Internal Coats of the Veins_, quoted in thesis of Levrat, p. 108.]

[Footnote 66: _Nouveaux Éléments de Pathologie et de Clinique médicale_, t. ii. p. 931, quoted by Balzer.]

In the event of pulmonary embolism taking place in spite of all preventive means employed, what shall we do in order to combat this terrible accident? According to Ball,[67] there are three indications to be observed: 1. To establish collateral circulation in the lungs; 2. To diminish local congestions; 3. To favor the resorption of the obstacle.

[Footnote 67: _Thèse_ quoted, Paris, 1862.]

The first indication cannot be effectually responded to, by reason of the fact that there is no way in which a collateral circulation can be promoted in the lung, owing to its anatomical structure.

The second indication is best observed by the application to the chest-walls of dry cups in large number, mustard poultices, turpentine, blisters. In this place we must consider the propriety of bleeding. As a result of the embolism there is arterial anæmia and venous plethora. This latter condition can be temporarily relieved by venesection. In this method, indeed, we have an immediate help for the distended and burdened heart, and we give time to the system to recuperate somewhat. We should, however, remember that bloodletting establishes a greater tendency in the system to the formation of emboli, and is therefore to be avoided. Moreover, sometimes it is decidedly objectionable on account of cardiac degeneration, anæmia, or great weakness.

When this method is contraindicated we should not hesitate to recur to the use of drastic purgatives (Jaccoud). Digitalis has been recommended, so as to regulate the cardiac action and to increase its power. Bertin has gone so far as to praise emetics and the use of the faradic current over the thoracic parietes. It seems as if these were dangerous methods to employ, since if a portion of the clot is still undetached the efforts caused by these agents would be apt to separate whatever portion remained in its original site. In order that a quantity of oxygen should be inhaled in a given time sufficient to supply the needs of the economy until a greater power of oxygenating the blood is established, the inhalation of compressed air has been vaunted. The objection to this means is merely the one which arises as we reflect how improbable it is that this agent would be at hand in a serviceable form when the sudden accidents of pulmonary embolism take place.

The third indication, to favor the resorption of the obstacle, must be virtually attended to by giving the alkalies in large doses internally. The advantages and objections to this sort of treatment we have already referred to.

After this exposition of the different means to be employed, both as preventive and curative agents of pulmonary embolism, we are obliged to recognize that very frequently they remain ineffectual. Usually the accident takes place in a very sudden manner and when we are least suspecting its advent. When the phenomena do occur which are caused by its presence, they take place so suddenly, and terminate fatally in such a brief period, that we scarcely have the time to employ the remedial agents referred to. Finally, we must admit that in presence of this complication, especially when there is complete obstruction of the trunk or primary divisions of the pulmonary artery, all our therapeutic means are without avail, and we are indeed almost powerless.

{391}

PULMONARY PHTHISIS (FIBROID PHTHISIS OR CHRONIC INTERSTITIAL PNEUMONIA).

BY AUSTIN FLINT, M.D.

DEFINITION.--Pulmonary phthisis is a chronic disease, characterized in its common form, anatomically, by a morbid product within the air-cells, in a large majority of cases progressively increasing and extending, having a tendency to cheesy degeneration and liquefaction forming collections of puriform liquid which, evacuating by ulceration into the bronchial tubes, are followed by cavities, these pathological conditions accompanied by more or less induration from interstitial morbid growth and by small granules called miliary tubercles. A comparatively rare form of the disease is characterized by the great predominance of interstitial growth, leading to notable diminution of the volume of lung by atrophy and to dilatation of the bronchial tubes. The latter form is now commonly distinguished as fibroid phthisis. This will claim separate consideration after having considered the form generally understood by the name pulmonary or pneumonic phthisis.

SYNONYMS.--Classification.--Much confusion, as regards nomenclature and classification, followed the adoption by many of the theory of Virchow that the sole characteristic of tuberculous disease is the presence of the so-called miliary tubercles. According to this theory, the morbid product which constitutes the most marked anatomical feature of the common form of phthisis is simply an inflammatory exudation. Heretofore, pulmonary phthisis and pulmonary tuberculosis were considered as convertible terms, but, adopting Virchow's theory, in a certain proportion of cases pulmonary phthisis is not a tuberculous disease. Hence arose a variety of names denoting non-tuberculous phthisis, such as chronic broncho-pneumonia, chronic lobular pneumonia, catarrhal pneumonia, cheesy pneumonia, etc. These names have shared the fate of the theory from which they originated, the latter, at the present time, having but few supporters in any country. It is convenient to distinguish the morbid product which is characteristic of pulmonary phthisis as a tuberculous product, and it will be so distinguished in this article.

The name acute pulmonary tuberculosis denotes an affection which may be sharply separated from the chronic forms of pulmonary phthisis. The acute affection is characterized by the presence, exclusively or in great abundance, of miliary tubercles. It runs a rapid course and the symptoms are those of an acute disease. The name phthisis implies a chronic affection. In a small proportion of the cases of pulmonary phthisis miliary tubercles become developed in great abundance. In these cases acute pulmonary tuberculosis supervenes upon chronic phthisis. These cases, by those who regarded phthisis in its ordinary form as a non-tuberculous affection, were designated cases of tuberculous phthisis. The fact that in cases {392} of phthisis there is a liability to the supervention of miliary tubercles as abundantly as in cases of acute tuberculosis, is to be borne in mind, but it does not seem necessary to make a distinct variety of the disease on the basis of this fact. In some cases of pulmonary phthisis the tuberculous product is notably large at the outset, and destructive changes in the lungs go on continuously with unusual rapidity. To these cases the names phthisis florida and galloping consumption have been applied.

In view of what has been stated, the classification in this article will not extend beyond a division into the common form of pulmonary phthisis and the form distinguished as fibroid phthisis. The latter form has been designated chronic interstitial pneumonia, chronic pneumonia, and cirrhosis of lung. It is to be understood that reference is had to the common form of pulmonary phthisis, except in that portion of this article which has for its heading Fibroid Phthisis.

HISTORY.--Pulmonary phthisis, in typical cases, is developed so imperceptibly that it might with propriety be included among the so-called insidious diseases. A slight dry cough is the first local symptom. This increases, and after a variable period is accompanied by the expectoration of a small quantity of mucus. The latter becomes gradually more abundant, and has the characters of the sputa in cases of bronchitis. So slow is the increase of those symptoms before they are regarded as of sufficient importance to require attention that not infrequently the patient is unable to state precisely how long they have existed. They are generally attributed to a slight cold which will take care of itself or call for only popular remedies, and the existence of a grave disease may not have been suspected until a physical examination of the chest discloses the fact that the phthisical affection has already made considerable progress. Coincident with or preceding the commencement of cough is often some obvious impairment of the general health, as indicated by diminished muscular strength and endurance, decrease in weight, pallor of the complexion, and lessened appetite. The impairment, however, may not interfere with customary occupations, and may be evident to others when the patient takes no cognizance of it.

In not a few instances hæmoptysis is the event which first awakens suspicion of an important disease. The hemorrhage generally takes place without any apparent causation, and often in the night. It may be either slight or profuse. It may occur but once, or there may be recurrences after intervals of hours, days, or weeks. The cough in some cases dates from the occurrence of hæmoptysis. In other cases the hemorrhage or hemorrhages antedate the cough for a variable period.

From the time when the symptoms and physical signs render the diagnosis of the disease positive the history in different cases presents notable variations. Comparatively, the course of the disease is continuously progressive and rapid in cases of so-called galloping consumption. The characteristics of the disease in these cases are--an unusual degree of cough with abundant expectoration, rapid breathing, frequency of the pulse, persistent pyrexia, chills or chilly sensations followed by exacerbations of fever, profuse perspirations, anorexia, rapid emaciation with decreasing muscular strength, and a fatal termination after a few months. The physical signs in these cases show a large and progressively increasing amount of solidification from the morbid product, followed quickly by destructive changes.

The disease pursues a rapid course, and ends fatally whenever acute tuberculosis supervenes. This may occur in the early part of the chronic phthisical affection or at any period during its course. The supervention of the acute disease sometimes follows a profuse hæmoptysis. The characteristics are high fever, frequency of the pulse, cyanosis, prostration, and death within a few weeks or even a few days. The physical signs which denote a large {393} extent of solidification of lung and the consequent destructive changes are wanting in these cases.

A small proportion only of cases of pulmonary phthisis fall in the category either of galloping consumption or of the supervention of acute tuberculosis. In by far the larger proportion the disease is chronic from the beginning to the end, and a fatal termination takes place after a period averaging from two to three years, the period sometimes extending to many years.

An important distinction, as regards the history of the disease, is expressed by the terms progressive and non-progressive. The disease is progressive when the local and the general symptoms denote more or less activity in the tuberculous process, the physical signs generally showing progressive extension of the pulmonary affection. It is non-progressive when symptoms and signs having the significance just stated are wanting. The disease may become non-progressive early or late, and at any period during its continuance. A stationary condition may continue indefinitely. The symptoms and signs may show processes of restoration--namely, disappearance of the tuberculous product, diminution in size, and the cicatrization of cavities. The disease is then said to be regressive. A regressive course is not extremely infrequent. It is more or less slow and may or may not end in recovery. A stationary condition, regression having taken place to a greater or less extent, is not infrequently observed. This condition may remain because the pulmonary lesions are too great to admit of restoration. In most cases the disease is not steadily progressive. It ceases from time to time to progress, the periods of non-progression varying much in duration. With each renewal of progress the physical signs generally show an addition to the tuberculous product. As a rule, this product does not increase continuously, but, as it were, by successive eruptions after intervals of time which may be either short or long.

Pulmonary phthisis in some cases ceases to progress, and regression continues, recovery taking place from an intrinsic tendency--that is, irrespective of any measures of treatment. This highly important fact has not hitherto been distinctly recognized by medical writers and practitioners. I have established it by having recorded a series of cases in which recovery took place without medicinal or other treatment and without any material change in habits of life.[1] In these cases the disease may be said with propriety to be self-limited.[2] The weight of this fact in its bearing on prognosis and treatment is obvious. That non-progression and regression ending in recovery may be brought about by judicious measures of management cannot be doubted; in other words, the disease may be arrested in a certain proportion of cases when non-progression and recovery would not have resulted from an intrinsic tendency or self-limitation.

[Footnote 1: _Phthisis, in a Series of Clinical Studies_, by Austin Flint, M.D., 1875.]

[Footnote 2: Vide "Self-limitation in Cases of Phthisis," by Austin Flint, M.D., N.Y., _Archives of Medicine_, June, 1879.]

Pulmonary phthisis proves fatal by undermining more or less slowly the powers of life. The appetite and digestion fail. There is progressive loss of weight and of muscular strength. A greater or less degree of pyrexia is persistent, with diurnal exacerbations and night perspirations, forming what is known as hectic fever. Muco-purulent matter is expectorated in abundance, with fatiguing cough. The respirations are accelerated, and there is often suffering from dyspnoea. The pulse becomes more and more frequent and weak. Oedema of the lower limbs is of frequent occurrence. The patient dies by slow asthenia, the mental faculties usually remaining intact and the patient hopeful of recovery to the last.

The history of the disease in many cases embraces tuberculous affections elsewhere than in the lungs, and other complications. The duration is often {394} shortened by some of these. The more important are tuberculosis of the intestines, tuberculous peritonitis, perforation of lung giving rise to pneumo-hydrothorax, pneumorrhagia, pulmonary gangrene, tuberculous meningitis, and chronic laryngitis affecting deglutition. The less important affections are pleurisy with effusion, thrombosis of the femoral or the iliac vein, a circumscribed non-tuberculous acute pneumonia, chronic laryngitis not affecting deglutition, intercostal neuralgia, and perineal fistula. Profuse hæmoptysis is sometimes a grave event, and may prove the immediate cause of death.

It is impossible to divide the course of pulmonary phthisis into sharply-defined stages based on anatomical changes. Often after death the lungs present in different situations all the changes which intervene between a fresh tuberculous product and cavities. The division into a stage of crudity of the product and a stage of softening is of no practical utility. There are no symptoms nor signs which are reliable for determining when softening has taken place. The existence of cavities can generally be determined by means of the cavernous physical signs, and the disease may be considered as advanced phthisis when cavities are discovered. The term incipient phthisis is used to designate an early period of the disease. Having passed the incipient or early period, and before reaching the advanced stage or stage of excavation, cases may be conveniently grouped according to the amount of the tuberculous affection. In different cases and at different periods in the same case the affection is either small, moderate, considerable, or large. Exact chronological divisions are impracticable.

ETIOLOGY.--Pulmonary phthisis, as a rule, is developed irrespective of any antecedent affection of the lungs. The researches of Louis established the fact that the phthisical affection is very rarely preceded by bronchitis, either acute or chronic.[3] My clinical studies have led to the same result.[4] That a neglected cold may eventuate in phthisis is a traditional popular error, unfortunately held also by some medical writers and practitioners. The error is to be regretted because it often interferes with hygienic management in cases of phthisis. The name chronic catarrhal phthisis proposed by Niemeyer was based upon this etiological error. It is a matter of common clinical observation that persistent bronchial inflammation leading to pulmonary emphysema, and often accompanied by asthma, involves no liability to phthisis. The long-continued inhalation of coal- and stone-dust, of the oxide of iron, and particles of other substances gives rise to bronchitis and interstitial pneumonia (pneumonokoniosis, anthracosis, siderosis, etc.), but is rarely followed by the common form of pulmonary phthisis. It is common for phthisical patients to suppose, as a matter of course, that their disease originated in a cold. In giving the previous history they often say that they took cold at a certain time. The analysis of carefully-recorded cases shows that very rarely does the disease follow directly upon an attack of bronchitis, notwithstanding that the frequency of the latter, from the law of chances, would involve an accidental concurrence in a certain proportion of cases. Acute lobar pneumonia or pneumonic fever has little or no tendency to eventuate in phthisis. This statement is sustained by the researches of Louis and by my clinical studies. In the rare instances in which phthisis follows either acute pneumonia or bronchitis, the latter diseases act only as auxiliary causes of the phthisical affection if the sequence be more than an accidental connection. This statement applies also to pleurisy with effusion. In certain of the few instances of phthisis apparently having been preceded by pleurisy it is probable that the former was the antecedent disease, occurring early in the history of the phthisical affection and retarding or arresting the progress of the latter. It may be added that there is no ground for supposing that phthisis is ever produced solely by traumatic causes acting upon the chest.

[Footnote 3: _Recherches sur la Phthisie_, 1825.]

[Footnote 4: _Phthisis, in a Series of Clinical Studies_.]

{395} It is an old doctrine that bronchial hemorrhage may be causative of phthisis. This doctrine has been recently revived by Niemeyer and some others. It is disproved by the following clinical facts: in two-thirds of the cases in which hæmoptysis antedates phthisis the development of the latter is after the lapse of a considerable period--weeks, months, or years. The instances are few in which phthisis immediately follows the hemorrhage. The occurrence of hæmoptysis during the course of phthisis, as a rule, is not followed by any increase of the phthisical affection. On the contrary, the local symptoms are not infrequently relieved by the hemorrhage. It is, however, to be remarked that hæmoptysis as a forerunner of phthisis is of much significance. In the larger proportion of cases phthisis follows its occurrence sooner or later. It is to be added, in view of the recent discovery by Koch, that bronchial hemorrhage may proceed from the same local cause which afterward leads to the development of phthisis--namely, the presence of a special micro-organism.

The etiology of pulmonary phthisis not involving any antecedent affections of the lungs nor any appreciable local causes, it would seem to follow that the disease involves either a predisposing or a causative agency elsewhere within the organism; and as, with our present knowledge, the source of this intrinsic agency cannot be localized, it is customary to say that the disease has a constitutional origin. This use of the term constitutional here, as in other instances, expresses an important fact--namely, that the disease is not purely local; that is, attributable solely to extrinsic or any appreciable causes acting on the affected part. At the same time, the term is a confession of the imperfection of our knowledge, inasmuch as it does not specify the nature of the causative or predisposing agency, nor its origin, beyond the statement that it is not local. That the constitutional agency has a special character is a logical inference from the fact that the disease may be said to have such a character. The term vulnerability does not fully express the special character of the constitutional agency. The condition of the constitution which stands in a causative relation to the disease is something more than an undue susceptibility to morbific influences of any kind--a susceptibility giving rise to diseases the nature and seat of which are accidental. The condition is one which has relation both to the character and the situation of the pulmonary affection. Such a condition is expressed by the term cachexia.

It remains to inquire whence arises this phthisical or tuberculous cachexia.

A congenital predisposition or diathesis exists in a certain proportion of cases. This is to be inferred from the number of instances in which several or many members of a household, brothers and sisters, become affected with phthisis. There may or may not be evidence that this predisposition is inherited. An inherited predisposition is to be inferred from the number of the cases in which parents or grandparents were phthisical. While statistical facts show undoubtedly heredity as involving a causative agency, making due allowance for the law of chances, it is important for the physician to bear in mind that a tuberculous parentage involves only a certain measure of liability to phthisis in the offspring. The progenitors of many healthy men and women have been phthisical. There are instances of large families of children in which many have died with phthisis, leaving, however, some who escape this disease and are in all respects healthy.[5] The question arises whether in cases of phthisis where there is lack of evidence of a congenital predisposition the diathesis may not be innate. The affirmative answer seems probable in view of the inability oftentimes to find any rational explanation on the supposition that the diathesis has been acquired. Positive data bearing on this question are of course not available.

[Footnote 5: For data on which these statements are based, vide _Phthisis, in a Series of Clinical Studies_, by the author.]

{396} Age has a decided influence on the development of phthisis. Cases in which the ages of patients are between twenty and thirty years greatly preponderate over the number in any other decade of life. Next in order as to the number of cases are the ages between thirty and forty years. The form of tuberculous disease under present consideration is rare under ten years and also in advanced life. All that can be said with our present knowledge in explanation of the influence of age is, that either an existing diathetic condition tends intrinsically to the development of the disease or that the diathesis is likely to be acquired at certain periods of life more than at other periods. Of these two explanations the former is the more rational.

Statistics show that occupations which involve sedentary habits, confinement within doors, especially in small, illy-ventilated rooms, poor or insufficient food, and prolonged mental depression, increase the liability to phthisis. The disease is developed either during or shortly after gestation in a sufficient number of cases to show that pregnancy has a causative agency. Facts appear to show a less degree of prevalence of the disease in most cold and tropical climates than within the temperate zone. It is, however, true, as stated by Ruehle, that "there are regions in all zones which are free from the disease, and, on the other hand, there is no zone in which it is not very prevalent." The prevalence is less in high than in low altitudes. Humidity of the soil has been shown by Bowditch, Buchanan, and others to enter into the etiology. In order to determine how far purely climatic agencies exert an influence either for or against the prevalence of the disease, it is necessary to take into account other associated agencies, together with an innate predisposition; and the latter especially does not admit an exact estimation.

Certain general diseases seem to involve a liability to phthisis as a sequel. This is true of rubeola and pertussis. In cases of diabetes mellitus, phthisis is considered as occurring sufficiently often to show a causative connection. In my own clinical experience, however, phthisis has not been of frequent occurrence in that disease. Typhoid fever in some cases appears to favor the development of phthisis. Some, however, have contended for the reverse of this statement. Certain affections are apparently antagonistic in their influence. In this category are pulmonary emphysema and obstructive or regurgitant valvular lesions at the mitral orifice of the heart. The disease is rarely developed in chlorotic patients. Facts go to show that alcoholism opposes its development. In opposition to current belief, my clinical studies lead me to conclude that they who have had scrofulous disease of the cervical glands in early life are not likely to become phthisical in after years. Contraction of the chest from deformity diminishes the liability to the disease.

The communicability of phthisis is a doctrine dating as far backward as the history of medicine extends. Distinguished physicians in every age have held that the disease may be communicated under circumstances which involve close proximity, as from husband to wife or vice versâ, and from patients to nurses or attendants. The contagion is supposed to be contained in the expired breath. The clinical evidence in behalf of this doctrine is the number of instances which seem to be striking examples of communicability. It is easy to collect a considerable number of such examples. But in order to constitute clinical proof of the doctrine of communicability the number must be so large as not to be accounted for on the ground of mere coincidence. A collection of isolated instances gathered from medical literature or reports from different physicians does not establish the doctrine. Owing to the great frequency of phthisis, mere coincidence suffices to account for a certain number of instances. Moreover, long-continued proximity to cases of phthisis generally involves causative agencies other than a contagium--namely, confinement within doors and mental anxiety. In my collection of 670 recorded cases of phthisis, the number of instances in which there was {397} room for the suspicion of the disease having been communicated either from the husband to the wife or from the wife to the husband amounted only to 5. In one of these instances, a wife, who became phthisical after her husband, had lost two sisters, one of whom was a twin sister, by the disease. It must be admitted that the analysis of these cases, without disproving the doctrine of communicability, fails to lend to it support, for the reason that in such a large collection of cases the number of examples of apparent communicability are so few.

A new and strong impetus was given to the discussion of the doctrine by the discovery of the inoculability of tuberculous disease. Villemin in 1865 demonstrated the fact that this disease could be communicated to rabbits and guinea-pigs by inserting beneath the skin portions of the tuberculous product. The experiments of Villemin and many others have shown conclusively that the insertion of fresh undecomposed tuberculous matter beneath the skin or within the pleural and the peritoneal cavity, or in the anterior chamber of the eye, is followed by an eruption of tubercles in these animals within two or three weeks. If tuberculous matter taken from an animal in which the disease has been produced by inoculation be inserted in another animal, the disease is transmitted to the latter. These results of inoculation, which have been abundantly confirmed in all countries, prove indisputably the communicability, by that mode, of tuberculous disease in certain animals which have a peculiar susceptibility thereto. The fact that the disease is not readily communicated to dogs, cats, and other animals shows a peculiar susceptibility to be an important factor in the successful results of inoculation. The conclusion drawn by Villemin and others from these experiments is that the disease is communicated by means of a specific virus, a term implying the existence of a contagium.

Opposed to this conclusion are experiments which appear to prove that tubercles may be produced in rabbits by inoculating them with various kinds of non-tuberculous matter. By those who adopt the doctrine of a specific virus it is contended either that true tubercles are not produced in these experiments, or that, if followed by the development of true tubercles, the production of the latter is attributable to the derivation of the virus from the laboratories in which tuberculous animals had been confined or to a contagium received directly from these animals. The introduction of non-tuberculous matter was found by Cohnheim and Fraenkel never to be followed by tuberculous disease when the experiments were repeated in places where tuberculous animals had not been confined and the animals on whom the experiments were made were isolated from those affected with tuberculosis. Cohnheim states that inoculation with portions of indurated lung, or of the nodules resulting from peribronchitis, or of the contents of bronchiectasic cavities, will not give rise to true tubercles, for the reason that, although taken from phthisical lungs, they do not contain the tuberculous virus. This distinguished pathologist, at first an opponent of the doctrine of a specific virus, afterward became a strong advocate therefor. He was led to regard a successful inoculation as affording the only criterion and reliable test of tuberculous disease; that the etiology of tuberculous disease invariably involves the presence in the system of this virus; that it exists in a latent form whenever there is an innate predisposition to phthisis; and that it may enter the system in different directions--namely, with the inspired air into the lungs, and even within the skull through the foramen of the ethmoid bone, into the small intestine by deglutition, and into the uterus with the semen. Becoming developed in any situation, the virus may remain localized, or it may be disseminated more or less extensively by means of the lymph and blood. The behavior of the tuberculous virus, according to Cohnheim, corresponds closely to that of syphilis.

Experiments made by Gerlach, Bollinger, Aufrecht, Chaveau, Leisering, {398} Harms, Gunthern and others, have shown that the disease may be communicated by incorporating tuberculous matter with food. Rabbits, guinea-pigs, dogs, calves, swine, sheep, and goats have been rendered tuberculous by these experiments. Klebs, Tappeiner, Parrot, and Puech claim to have communicated the disease by combining with the food the matter of expectoration from phthisical patients. Gerlach and Klebs have seen the disease in animals fed with milk from cows affected with the so-called pearl disease (perlsucht), which is considered to be identical with phthisis. Finally, the disease appears to have been produced by exposing animals to an atmosphere impregnated with fine particles of tuberculous matter by means of an atomizer, and by blowing into the trachea this matter reduced to a fine powder.[6]

[Footnote 6: For a summary of the experiments relating to the communicability of tuberculous disease by inoculation, by the ingestion of tuberculous matter, and by its inhalation, and for reference, the reader is referred to an article by Wm. P. Whitney in the _Boston Medical and Surgical Journal_, July 28, 1881; to the article on "Tuberculosis" by Frederick C. Shattuck in supplement to _Ziemssen's Cyclopædia of the Practice of Medicine_, 1881; to the "Cartwright Lectures," by William T. Belfield, M.D., published in the _New York Medical Record_ in February and March, 1883; and to an article by Surgeon George M. Stemberg, U. S. Army, in the _American Journal of Medical Sciences_, January, 1885.]

It is noteworthy that tuberculous disease may be produced by inoculating with the infiltrated product, with matter from miliary tubercles, or from scrofulous glands in the neck. The identity of these morbid products is thus made evident, assuming that the fact of communicability involves the existence of a specific virus.

The practical importance of the facts already ascertained respecting the communicability of phthisis is obvious. They constitute the foundation for a reasonable supposition that the disease may be communicated to man by means of the meat of tuberculous animals, by milk, and by breathing an atmosphere charged with particles of tubercle. That the instances in which the disease is communicated, however, are rare seems to be a rational inference from the difficulty of obtaining clinical proof of communicability. That susceptibility is an essential factor is made evident by the well-known predisposition pertaining to certain periods of life. It is to be considered that while the communicability of the disease to certain animals is abundantly shown by the experiments to which reference has been made, the existence of a special virus or a contagium is not as certainly established by these experiments. They leave to be settled, by further investigation, the question whether or not the communicability of the disease involves only the agency of a septic matter devoid of the special character expressed by the terms virus and contagium. Without waiting for data sufficient to settle this important question, prudence would dictate the propriety of all practicable precautionary measures.

Still more recently, and since the foregoing remarks on the communicability of phthisis were written, have appeared the remarkable experimental researches of Koch of Berlin. Koch claims to have demonstrated the constant presence in tuberculous products of a specific organism which he calls the bacillus tuberculosis, and that it is not found in non-tuberculous products. This parasite he has isolated, and by cultivation carried through several successive generations. By its introduction, after, as well as before, cultivation, into the pleural cavity, the peritoneal cavity, the anterior chamber of the eye, and in other situations, he produced tuberculous disease, not only in rabbits and guinea-pigs, but in dogs and rats, the latter animals being less susceptible than the former to tuberculous infection. In his experimental observations, animals not inoculated, placed under the same external conditions as those inoculated, did not become tuberculous. The same parasite, alike capable of infecting healthy animals, he found in miliary tubercles, in the cheesy tuberculous deposit, in scrofulous glands, and in the sputa from {399} tuberculous patients. The parasite was found not to have lost its vitality in dried sputa.[7]

[Footnote 7: For the details of Koch's researches vide his report in the _Berliner klinische Wochenschrift_, April 10, 1882; vide, also, _Verhandlungen des Congresses für Innere Medicin_, Erster Congress gehalten zu Weisbaden, 20-22 April, 1882.]

The researches of Koch had been continued for two years before the publication of the results in March, 1882. Moreover, his ability as a skilled experimental observer in the study of micro-organisms, and his sincerity as a truth-seeker, are universally admitted. Naturally, the publication of the results of his researches excited at once great interest in all countries. At the present moment (April, 1885) questions connected with the bacillus tuberculosis are more considered than any others relating to medical pathology and etiology. Thus far, the observations of competent medical mycologists are confirmatory of the results of the researches by Koch. It seems to be established that the so-called bacillus tuberculosis is uniformly present in tuberculous products, and as uniformly absent in other morbid products; that it is generally present in the sputa of phthisical patients, and never present in the sputa of non-phthisical patients; and that tuberculous disease in animals may be produced by inoculation with this organism after cultivation has been sufficiently continued to eliminate all else pertaining to the tuberculous product. On these data are based the conclusions that phthisis is an infectious disease--in other words, that it involves in its causation a specific agent capable of self-multiplication; that it is a communicable disease, and that the agent of the communication is the bacillus tuberculosis--that is, this agent is the contagium. The supposition that the presence of the bacillus is secondary to the tuberculous affection is not tenable in view of the fact that the affection is produced by the introduction of this organism after it has passed through several generations by culture out of the body.

As has been already seen, clinical experience fails to furnish positive proof of the communicability of phthisis. There are many striking instances which, taken by themselves, render it probable that the disease was communicated; but, on the other hand, there are so many cases of its development under circumstances not pointing to contagion, and of the number of persons in close proximity to tuberculous patients the proportion of those who become affected is so small, that it has seemed impossible to establish the doctrine of contagion by clinical evidence.

The insufficiency of clinical proof, however, cannot invalidate the demonstration by inoculation. Assuming it to be demonstrated that the disease involves a specific agent, and that this agent is proven to be a contagium by its capability of producing the disease when introduced into a healthy body, the conclusion as to communicability is not to be shaken by the lack of corroborative clinical evidence or by inability to explain certain facts which seem to be inconsistent with that conclusion. Having accepted a demonstrated truth, the endeavor should be to reconcile therewith facts which do not sustain it and which may appear to be opposed to it. It remains to inquire in what way the communicability of phthisis by means of a contagium vivum is to be reconciled with facts furnished by clinical experience.

If we accept the conclusion that a particular parasitical organism is the primary and efficient causative agent in the production of phthisis, the development and multiplication of this organism must require certain local conditions. Without these the parasite is innocuous. The conditions are to its development and multiplication what the peculiarities of soil are to the production of different vegetables. Of the nature of these conditions we are at present ignorant. When they exist the bacillus develops and multiplies; when they are wanting the parasite is incapable of development and multiplication. This dependence of specific morbific agents upon particular {400} conditions is exemplified in other infectious diseases. For example, the contagium of the eruptive fevers, received into the system ever so abundantly, is inoperative in some persons, and, as a rule with rare exceptions, it is never operative after the disease which it occasions has been once experienced. In these instances it is not the contagium itself which has lost the capability of producing the disease, but the conditions for its activity are wanting. Of the nature of these conditions we know as little as of those which are essential to the development and multiplication of the bacillus tuberculosis. The inoculation of animals with tuberculous matter shows that the disease is produced in some species of animals much more readily than in other species, and some animals of the same species much more than others are susceptible to this contagium. These facts are to be explained by variations in different species of animals, and in different animals of the same species, as regards the conditions required for the efficiency of the morbific agent.

The facts in the clinical history of phthisis which denote a constitutional predisposition thereto or a tuberculous cachexia are explicable by reference to the conditions requisite for the development and multiplication of the parasite. A predisposition which may be innate, inherited, or acquired involves the existence of these conditions. The latter may be greater or less in degree. The causative agencies of confinement within doors, humidity of soil, pregnancy, etc. operate by either giving rise to or increasing these conditions. If this view be correct, it is evident that the curative influence of climatic changes, alteration of the habits of life, and other hygienic agencies must be by means of an effect exerted upon these conditions; and probably it is in this way chiefly that remedies are useful. Of the essential nature of these conditions we know neither more nor less than of what consists the tuberculous cachexia. We are, of course, as ignorant of the one as of the other if it be assumed that they are identical--that, in other words, the different expressions have the same meaning. The only difference is this: If phthisis be an infectious and a communicable disease, a contagium enters into its etiology; whereas if the existence of a contagium be denied, it follows that the cachexia is itself sufficient for the causation of the disease.

In connection with the etiology of phthisis a theory which of late years has found favor with many should be referred to. It is, that this disease may be a result of the absorption of caseated non-tuberculous morbid products in different parts of the body. This theory of autochthonous infection derives but little support from clinical observation. In much the larger proportion of the cases of phthisis it is impossible to discover anywhere caseated morbid products which may be supposed to have a causative connection with the disease. To assume that, when not discovered, foci of infection nevertheless are concealed somewhere within the organism is evidently begging the question. On the other hand, how often do suppurations, necroses, and degenerated morbid products occur in different situations without being followed by phthisis!

SYMPTOMATOLOGY AND COMPLICATIONS.--Giving under this head a fuller account of the symptomatology and complications than has been already given in sketching the history of the disease, it will be a convenient arrangement to consider these topics in their relations to the different anatomical systems of the body--namely, the respiratory, circulatory (including temperature), hæmatopoietic, digestive, nervous, and genito-urinary systems.

Symptoms, etc. referable to the Respiratory System.--The dry cough which is the earliest pulmonary symptom in typical cases is to be regarded as an effect of the local irritation caused by the presence of the tuberculous product. This product, increasing and extending, gives rise to circumscribed bronchitis which causes increase of cough with expectoration. The expectoration represents this secondary bronchitis prior to the occurrence of {401} ulceration, the escape of liquefied tuberculous product, and the existence of cavities. The quantity and the characters of the matter expectorated depend on the degree and the extent of the bronchial inflammation, the latter depending on the extent of the phthisical affection. Different cases present wide variations in these respects. The frequency and severity of the cough depend in a great measure on the quantity of the matter of expectoration and its adhesiveness. The matter expectorated, at first semi-transparent mucus, becomes muco-purulent, the characters pertaining to mucus and pus being combined in varying proportions, as in cases of chronic bronchitis. Nummular sputa--so called from the resemblance in form to a coin when lying on a flat surface, the edges often serrated--are considered as casts of small cavities formed by dilated bronchi. A microscopical examination of the sputa may show elastic yellow fibres. The presence of these is almost pathognomonic of phthisis, and denotes either the process of ulceration or exfoliation of tissue from within cavities.[8] Liquefied tuberculous product appears in the matter of expectoration as a puriform fluid. It sometimes contains small semi-solid tuberculous masses. The lining membrane of tuberculous cavities furnishes a veritable purulent matter of expectoration. It is stated by Buhl that the presence of alveolar epithelium in the sputa is distinctive of phthisis; hence the name proposed by him, desquamative pneumonia. It is, however, stated by Frischl that the alveolar epithelium is found in the matter expectorated in cases of oedema and congestion of the lungs.[9] There is sometimes notable fetor of the matter of expectoration, due to putrescent decomposition of the purulent contents of cavities or to small sloughing portions of pulmonary tissue. The varieties of sputa which have been mentioned may be accompanied by a serous liquid in more or less abundance. Calcareous masses varying in size from a pin's head to a pea are expectorated in some cases. I have known several hundred to be expectorated in a single case. In the instances which have fallen under my observation these pulmonary calculi have been expectorated when the symptoms have denoted arrest and regression of the disease; and it is consistent with this fact to regard them as obsolete tubercles. They are not to be confounded with the small solid bodies sometimes formed in the follicles of the tonsils, the latter consisting of a sebaceous-like product, which is crushed, without crumbling, by pressure, and emits a fetid odor. Since the discovery of the bacillus tuberculosis by Koch microscopical examinations of sputa in a large number of cases by different observers have shown that this parasite is generally, but not invariably, present. Its abundance in the sputa appears to correspond to the rapidity with which the tuberculous affection is progressing, and examinations with reference to its presence and its abundance are of much practical utility in diagnosis and prognosis.

[Footnote 8: In order to discover the elastic fibres readily, Fenwick advises as follows: "Prepare a solution of caustic soda, about twenty grains to an ounce of distilled water. Collect all the patient has expectorated in twelve or twenty-four hours, from ten at night to ten the next morning being the best period. Pour this, previously mixed and well shaken with an equal quantity of the soda solution, into a glass beaker, and boil it over a gas or spirit-lamp, stirring it occasionally with a glass rod. A test-tube does not warm as well as a beaker. As soon as it boils pour it into a conical glass, and add four or five times the amount of cold distilled water. If the mucus is still gelatinous after boiling, you have either added too little soda or not boiled it sufficiently. The cold water carries down to the bottom of the glass any lung-tissues that may be present, where they form a slight deposit in about a quarter of an hour; if no deposit is visible, put the glass aside for two or three hours. Remove the deposit with a dipping-tube, place it in a glass cell, cover it with a piece of thin glass, and examine with a one-inch object-glass. The lung-structures will be often found clinging to hairs and other foreign bodies present in the sputa" (_Guide to Medical Diagnosis_).]

[Footnote 9: Vide Niemeyer by Seitz, tenth ed.]

Hæmoptysis occurs in a large proportion of the cases of pulmonary phthisis. {402} It occurs much oftener in the early than in a later period of the disease. As regards the number of attacks, their duration, the intervals between them, and the amount of hemorrhage, there are wide variations. Prior to the formation of cavities the hemorrhage is from the bronchial tubes (bronchorrhagia). After cavities are formed the blood comes from the interior of these. As a rule, bronchial hemorrhage is not followed by the evidence of any increase of the phthisical affection. Not infrequently a sense of relief follows. The analytical study of a large collection of cases shows that the occurrence of bronchial hemorrhage does not diminish, but apparently increases, the chances of arrest and of tolerance of the disease. This statement holds true with regard to cases in which the hemorrhage is often repeated and profuse, as well as to those in which it is slight and infrequent.[10]

[Footnote 10: Vide _Phthisis, in a Series of Clinical Studies_, by the author.]

Cavernous hemorrhage may be due to rupture or ulceration of parenchymatous bands which traverse cavities, but often it is caused by the bursting of small aneurisms in their walls. It may be so profuse as to prove fatal. Cavities sometimes become filled with coagulated blood, which, if life continue, becomes decomposed and gives rise to a grumous, fetid matter of expectoration. Bronchial hemorrhage is supposed to be caused by a circumscribed hyperæmia at the situation where the blood escapes. In a case under my observation in which death took place shortly after a profuse hæmoptysis, there was congestion limited to the middle lobe of the right lung, and the bronchial tubes in this situation contained bloody mucus, none being found elsewhere. A circumscribed hyperæmia, however, must depend upon some local cause. Probably in most instances this anterior local cause is the tuberculous product. That the escape of blood involves a change in the coats of the vessels from which it escapes is probable.

A rare event occurring in connection with hæmoptysis is the coagulation within the bronchial tubes of fibrin which may be expectorated in the form of casts of the tubes, analogous to those which characterize fibrinous or plastic bronchitis. I have met with an instance, and also with a case in which after death the bronchial tubes of an entire lobe were found to be filled with solidified fibrin. The death in this instance followed quickly a profuse hæmoptysis. There is not the danger connected with the gradual disintegration and expectoration of the coagulated fibrin which was surmised by Niemeyer.

The presence of the tuberculous product in the lungs and the processes to which it gives rise, inclusive of the secondary bronchitis, occasion no pain. Patients often strike the chest with violence, as affording to them evidence that the organs are sound. But in most cases, from time to time during the course of the disease, sharp stitch-like pains occur. They are sometimes slight or moderately severe, but they may be sufficiently intense to confine to the house or even to the bed. They last, usually, but a few days, and recur at variable intervals. They are referred generally to the upper part of the chest, often beneath the scapula. Patients are apt to imagine that the pains are rheumatic. They are symptomatic of successive, circumscribed, dry pleurisies, which are very rarely wanting in cases of phthisis, leading to the pleuritic adhesions constantly found after death. These pleurisies are secondary to the phthisical affection, and recur at epochs when new developments of the latter take place. There is no reason to suppose that they contribute in any way to the increase of the phthisical affection. On the other hand, they protect against one important event at least--namely, perforation of lung, and, as consequent thereon, pneumo-hydrothorax. In this point of view they are conservative. These pleuritic pains are to be discriminated from those of intercostal neuralgia. The neuralgic pains generally are situated lower, and the diagnostic criterion of intercostal neuralgia is {403} available--namely, the tenderness on pressure in the intercostal spaces near the median line in front, the axillary line, and the spinal column.

The respirations are more or less frequent in different cases and at different periods in the same case according to the impairment of the function of hæmatosis by the pulmonary affection and the increased frequency of the heart's action. A sense of the want of breath as implied in the term dyspnoea is, however, seldom sufficient to occasion much suffering. Even when the respirations are considerably increased in number it is rare for the patient to complain of the want of breath when at rest. A degree of muscular weakness which prevents the patient from freeing the bronchial tubes and cavities of morbid products may give rise to distressing dyspnoea. A sudden increase in the frequency of the respirations, with dyspnoea and cyanosis, when not attributable to filling of the bronchial tubes nor to pneumothorax nor pleuritic effusion, points to the development of miliary tubercles in abundance--in other words, to the supervention of acute tuberculosis.

Important complications referable to the respiratory system are laryngitis, non-tuberculous pneumonia, pleurisy with effusion, perforation of lung with pneumo-hydrothorax, pneumorrhagia, and pulmonary gangrene.

Dysphonia and aphonia, the voice being husky or hoarse and the whisper stridulous, denote laryngitis. These diagnostic symptoms are never wanting, and the laryngeal complication may be excluded if they be absent; but the extent to which the larynx is affected is of course determinable by means of the laryngoscope. The affection in some cases extending to the epiglottis, paroxysms of cough and spasm of the glottis are produced by the act of swallowing food and drinks. The interference with deglutition may be so great as to restrict seriously alimentation, and in this way may hasten a fatal termination of the disease. In the majority of cases, however, deglutition is not interfered with. There is very rarely laryngeal obstruction to respiration. The affection involves little if any liability to the supervention of acute laryngitis or oedema of the glottis.

In most cases the laryngitis occurs at a considerable period after the commencement of the pulmonary affection, this period, in a proportion of more than one-third, being from two to four years. In some instances it seems to occur coincidently with, and in some to precede, the pulmonary affection. In the latter instances it is probable that latent tuberculous disease of the lungs preceded the laryngitis. The diversity as regards the interval of time between the date of the pulmonary affection and of the occurrence of the laryngitis, the apparent coincidence in the occurrence of both in some instances, and the want of any uniformity in different cases as regards the amount of pulmonary disease and the stage of its progress when the laryngitis occurs, render it a rational conclusion that laryngitis is not dependent on the disease of the lungs, but that it proceeds from the same cause which determines the latter.

Excluding the instances in which the laryngitis involves the epiglottis and interferes with alimentation, clinical experience teaches that this complication does not diminish the chances of arrest or recovery from the pulmonary affection, and that it has no untoward influence on the duration of the disease in the cases which sooner or later end fatally.[11] As a rule, in cases which recover the voice remains permanently more or less affected.

[Footnote 11: Vide _Phthisis, in a Series of Clinical Studies_, by the author.]

Acute lobar pneumonia or pneumonic fever is sometimes an intercurrent affection in cases of phthisis. The cases are so rare as to show absence of any predisposition to that disease derived from the phthisical affection. The pneumonia ends in recovery in a proportion of cases sufficiently large to show that, as a rule, the prognosis is not unfavorably influenced by phthisis, and, as a rule also, the course of the latter is not influenced unfavorably by the {404} pneumonia. A circumscribed pneumonia is an occasional complication of phthisis. Its non-tuberculous character is shown by the rapidity and completeness of the absorption of the intra-vesicular product. This circumscribed pneumonia gives rise to physical signs which appear to denote a rapid and considerable increase of the phthisical affection. The disappearance within a short period of the added dulness on percussion, bronchial respiration, and bronchophony, is the evidence that these signs represent a circumscribed pneumonia occurring as a complication.

Pleurisy with serous effusion is not an infrequent complication at an early period in the course of the disease. There is very little if any liability to its occurrence at an advanced period, except as associated with pneumothorax from perforation of lung. It is probably secondary in certain of the cases in which the phthisical affection appears to follow the pleurisy. The pleuritic effusion appears to retard the progress of the phthisical affection. Clinical experience shows that this complication, if it be unilateral, is not an untoward event. A double pleurisy with effusion is evidence of the existence of phthisis.

Perforation of lung, giving rise to pleurisy with effusion and pneumothorax, is an event which belongs, with some exceptions, to an advanced period of the disease. The perforation is caused by rupture of the wall of a cavity superficially situated where pleuritic adhesion from circumscribed dry pleurisy had not taken place. In most instances the occurrence of the perforation is quickly followed by acute pain and orthopnoea, with notable disturbance of the circulation, fever, and prostration, these symptoms being due to the sudden entrance of air into the pleural sac, the development of acute inflammation, and rapid serous effusion. The recognition of the pneumo-hydrothorax by means of physical signs is easy. The suffering of the patient becomes less after twenty-four or forty-eight hours. In the great majority of cases death takes place within a short period; that is, within a few days or weeks. The duration of life depends on the amount of phthisical disease, together with the condition of the patient as regards strength, etc. In some instances, the perforation taking place when the phthisical affection is small and accompanied by favorable symptoms, the pneumo-hydrothorax is tolerated for a long period. The accumulation of liquid within the pleural sac sometimes causes the air to disappear, and the pneumo-hydrothorax is converted into simple pleurisy with large effusion.

Pneumorrhagia and pulmonary gangrene are very rare complications of pulmonary phthisis. The analytical study of nearly 700 recorded cases furnished but a single example of each of these complications.

Symptoms and Complications referable to the Circulatory System, including Temperature.--More or less acceleration of the pulse and elevation of the temperature of the body belong to the clinical history of pulmonary phthisis. It may be stated that the pulse and temperature are never normal if the disease be progressive. A persistent normal pulse and no elevation of temperature therefore denote arrest or non-progression of the disease. It may also be stated that the acceleration of the pulse and the increase of temperature form a good criterion of the rapidity or otherwise of the progress of the tuberculous disease, provided inflammatory complications be excluded. The disease is progressing rapidly in proportion to the frequency of the pulse and the increase of temperature.

If the disease be progressive daily exacerbations of fever take place. They occur in the afternoon usually, and continue into the evening or the nighttime, ending in perspiration which is more or less profuse. The exacerbations are often, but not always, preceded by chilly sensations, and sometimes by a well-pronounced chill which may be accompanied by rigors. During the febrile exacerbations the cheeks frequently present a circumscribed flush {405} and the eyes have a glistening appearance. The term hectic fever has long been applied to the febrile exacerbations which characterize progressive phthisis.

The febrile exacerbations sometimes occurring prior to the development of marked pulmonary symptoms may be supposed to be malarial manifestations. Recurring daily at or near the same hour, they may simulate closely the paroxysms of intermittent fever. A differential point is the existence of more or less fever between the exacerbations in cases of phthisis, whereas after a paroxysm of intermittent fever there is apyrexia. Another point is, the occurrence of exacerbations in cases of phthisis is generally after mid-day, whereas in the majority of cases of intermittent fever the paroxysms occur earlier. But of course the existence of phthisis is to be ascertained by means of the diagnostic symptoms and the physical signs. It is, however, to be borne in mind that phthisis and intermittent fever may be associated.

The profuse night-sweating which is a source of great discomfort in cases of phthisis has no fixed relation to the intensity of the fever which precedes it. The fever may be high and very little perspiration follow, and vice versâ.

Acceleration of the pulse and elevation of temperature may arise from an inflammatory complication, such as pleurisy, pneumonia, or peritonitis, and from the supervention of acute miliary tuberculosis.

To endeavor to explain the rationale of the acceleration of the pulse and the rise of temperature would require the consideration of the general pathology of the febrile state. The absorption of septic matter is probably a factor, but is hardly sufficient for a full explanation, and it would not be easy, with our existing knowledge, to explain the modus operandi of this morbific agent. The difficulty here, however, is not greater than in explaining the phenomena of fever when occurring in other pathological conditions. Here, as in other instances, there is no uniformity in the relative degree of acceleration of the pulse and the increase of temperature. The latter may be high without a proportionate disturbance of the circulation, and the reverse. Clinical experience shows a connection between a persistent high temperature and the waste of the body, and in proportion as the vital powers decrease the action of the heart is enfeebled, and a notably small and weak pulse denotes that death by asthenia is not far distant.

Thrombosis of the iliac vein on one side or on both sides is an occasional event in cases of advanced phthisis (marantic thrombosis). The effect is a considerable oedema of the lower limb or limbs. Oedema of both lower limbs, however, occurs as an effect of feebleness of the systemic circulation. If, as is sometimes observed, there be general dropsy, it denotes a renal complication, which is generally the waxy variety of chronic Bright's disease. Under these circumstances the urine is found to be albuminous.

Symptoms and Complications referable to the Hæmatopoietic System.--Pallor of the face is generally more or less marked from an early period in the history of phthisis, and it becomes, as a rule, more and more marked as the disease progresses. There is considerable variation in this respect in different cases. Impoverishment of the blood is in a great measure to be explained by the diminished ability to ingest and assimilate food. It is not, however, in all cases proportionate to defective alimentation, and therefore it is a fair inference that the disease in some other unknown way interferes with the blood-forming processes. Exceptionally, in some cases in which the disease is progressing, pallor is wanting. The complexion sometimes retains for a long time a rosy color. This is probably due to the condition of the vessels, and is not evidence of a normal condition of the blood. It is a noteworthy fact that notwithstanding the appearances denoting anæmia in cases of phthisis the venous hum in the cervical veins is, as a rule, wanting.

That the impoverishment of the blood is an effect of the disease, and that {406} it does not contribute to the progress of the tuberculous affection, may be inferred from the fact that anæmic patients are not likely to become phthisical. This fact, which has already been stated, is established by clinical observation. Nor do the diseases relating to the hæmatopoietic system, anæmia being a prominent feature in all--namely, leucocythæmia, Hodgkin's disease, pernicious anæmia, and Addison's disease--involve any special liability to phthisis. Other intercurrent affections occasion death in these diseases when it is not due exclusively to the latter.

Symptoms and Complications referable to the Digestive System.--The opinion has been held that the development of phthisis is preceded and accompanied by appreciable disorder of the digestive system. This opinion is not sustained by the analysis of carefully-recorded cases. In many, and perhaps the majority of, cases at the time of the commencement of the phthisical affection the appetite is not notably impaired and the digestive functions appear to be well performed. Sooner or later, however, the appetite fails. This symptom may be marked when the food which can be taken does not occasion evidence of indigestion. Different cases differ very much as regards the degree of anorexia. It is marked in the cases in which there is notable increase of temperature and acceleration of the pulse. It is often invincible; that is, not only is the desire for food wanting, but there is a degree of repugnance which renders it impossible for the patient to take it. It is intelligible that in these cases emaciation and exhaustion must be progressive. It is not more easy to give a pathological explanation of anorexia as an effect of phthisis than when the symptom occurs in connection with other diseases not involving either inflammation or any ascertained structural affection of the digestive organs. The symptom is probably connected with morbid changes within the gastro-intestinal or peptic glands.

Vomiting is a rare symptom in cases of phthisis, except it be produced sympathetically in paroxysms of coughing. As thus produced it is not rare. It is of importance from its interference with alimentation.

Diarrhoea is a frequent symptom. It may be due either to intestinal indigestion or to a subacute enteritis or colo-enteritis thereby induced. A waxy or fatty affection of the liver may conduce to diarrhoea by interference with the digestion of certain alimentary principles. If, however, the diarrhoea be persistent, it points to intestinal ulcerations. These are usually seated in the Peyerian and solitary glands within the small intestine, but not infrequently they are found after death in the large intestine, and in the small intestine above the portion in which the Peyerian glands are situated. The number and extent of the intestinal ulcers found after death do not always correspond to the prominence of diarrhoea as a symptom. They cannot be excluded by the fact that this symptom is not prominent. The presence of pus and blood in the dejections is evidence of ulcerations. If the ulcers be situated high up in the intestinal tract, the pus and blood may have undergone changes which render them unrecognizable by the naked eye, and the microscope is necessary to demonstrate their presence. The diarrhoea is often accompanied by griping or colic-like pains. In proportion as diarrhoea is prominent it contributes to emaciation and exhaustion. These effects are expressed by the term colliquative, which has long been applied by medical writers to exhausting diarrhoea and perspirations occurring in cases of phthisis.

Peritonitis occurs in phthisis as an acute and as a chronic affection. When acute, it is caused by intestinal perforation incident to ulcerations; this is a rare accident. It is to be inferred whenever the symptoms denote rapidly-developed acute peritoneal inflammation. The peritoneal sac contains intestinal gas. Perforation is excluded if percussion shows dulness or flatness over the site of the liver. The normal hepatic dulness or flatness on percussion is always abolished if the peritoneal cavity contains gas. A tympanitic resonance {407} over the liver, on the other hand, is not evidence of the presence of gas within the peritoneal cavity, inasmuch as this resonance may be conducted from the transverse colon distended with gas. Peritonitis from perforation is speedily fatal. In a chronic form the peritonitis may be preceded by an eruption of miliary tubercles in this situation, or the inflammation may have proceeded from intestinal ulcerations, perforation not having taken place. The local symptoms of chronic peritonitis are often not marked. The diagnosis is to be based on pain, tenderness, muscular rigidity, and the signs denoting liquid within the peritoneal sac. A chronic peritonitis may be associated with a small pulmonary affection which may not actively progress, and under these circumstances the peritoneal complication may be tolerated for a considerable period.

Peritoneal fistula may be reckoned among the complications referable to the digestive system. It occurs sufficiently often in cases of phthisis to show some pathological connection. Analysis of cases in which it occurs affords no evidence of its having an untoward influence on the course of the phthisical disease. On the other hand, there is ground for the opinion generally held that it either occasions or betokens slowness in the progress of the pulmonary affection. It follows that it is unwise to attempt to effect a cure by surgical interference. The characteristic bacilli have been found in the matter derived from peritoneal fistula, showing that this affection is tuberculous in character.

Symptoms and Complications referable to the Nervous System.--The symptoms referable to the nervous system relate to the mind. The mental faculties in most respects remain intact, except that in proportion to the general feebleness there is diminished ability to continue their exercise. The integrity of the intellect, with one exception, often remains up to the last moment of life. A marked characteristic of the disease, however, is a delusion in respect to improvement and recovery. In spite of the progressive emaciation and debility, which are obvious to every one, patients are apt to believe that their condition is becoming more and more favorable and to feel confident of restoration to health. Even medical men affected with phthisis manifest the same delusive ideas. So strong is the determination in some cases to keep up the delusion that the statements of patients in regard to their symptoms cannot be relied upon. They are sometimes offended if the physician feels it to be his duty to intimate danger. On the other hand, when patients are convinced of the nature of the disease, and that they have not long to live, as a rule they become quickly and completely reconciled thereto. Perhaps there is no other chronic disease in which the near approach of death is generally regarded with greater complacency.

Cephalalgia, delirium, and coma are symptoms which are developed in a few cases. They denote tuberculous meningitis. This is a very rare complication in the adult. When it has given rise to the symptoms just mentioned a speedy fatal termination is to be expected.

Symptoms and Complications referable to the Genito-urinary System.--Tuberculous disease of the kidneys, testicles, ureters and the prostate gland is sometimes secondary to pulmonary phthisis. The local symptoms will depend on the situation and amount of the tuberculous product, together with the destructive changes to which it gives rise. The consideration of the anatomical conditions and the symptomatology falls properly under the head of diseases of the genito-urinary system.

As already stated, the variety of chronic Bright's disease known as the amyloid or waxy is an occasional complication in cases of phthisis. The other varieties may coexist, but the coexistence is rare. There is no tendency in phthisis to these affections, and, on the other hand, they do not involve any predisposition to phthisis.

{408} As regards functional disorders of the genito-urinary system, there is nothing noteworthy which pertains to the urine. From the readiness with which often phthisical patients of either sex enter into the marital relation it may be inferred that the disease does not for a considerable period extinguish the sexual instinct. By interrogating a considerable number of patients Louis was led to conclude that in men the disease has an erotic influence.[12] Phthisical women do not readily conceive, but pregnancy is not extremely infrequent. They may give birth to healthy children. During the course of phthisis the menses, as a rule, cease, but they continue in some cases up to a late period in the history of the disease. When suspended early they may return if the disease become non-progressive. That the cessation of the menses has an unfavorable influence on the tuberculous affection is a popular error. Nothing is gained by efforts to bring about their return. Their cessation, however, is not a good omen, and their return has a favorable significance.

[Footnote 12: _Recherches sur la Phthisie_.]

MORBID ANATOMY AND PATHOLOGY.--In the definition of the common form of pulmonary phthisis were embraced the leading anatomical characteristics of the disease. For a full account of these, together with the changes referable to peribronchitis, periarteritis, endoarteritis, secondary pleuritis, and bronchitis, as well as for histological appearances, the reader is referred to treatises on morbid anatomy. The practical objects of this article will be fulfilled by stating the abnormal physical conditions incident to the morbid changes in different cases and at different periods in the same case, and by a statement of the anatomical points involved in the general pathology. Knowledge of the abnormal physical conditions is essential with reference to physical signs and the diagnosis. It has also an important bearing on the prognosis, and is not without importance in its relations to the treatment.

Certain anatomical facts may be premised, as follows: The pulmonary affection begins at or near the apex of one lung in the vast majority of cases; exceptionally it begins at the base of one lung. The affection extends from the apex downward. The extension is not continuous in respect of time, but a series of tuberculous deposits or eruptions takes place at different epochs after variable intervals. Hence it is that different sections of one lung may show all the changes which intervene between a fresh deposit and tuberculous cavities. As a rule, not long after the affection begins in one lung the other lung is affected. This rule is so constant that, although both lungs are not affected simultaneously, the affection may be said with propriety to be bilateral. The constant occurrence of secondary circumscribed pleurisies and bronchitis has been stated under the head of Pulmonary Complications.

At an early period of the disease the marked changes appreciable by physical signs usually consist of a few hardened patches or nodules varying in size from that of a pea to that of a filbert, situated at or near the apex of one lung. The physical signs are those of slight solidification--namely, some dulness on percussion, increase of vocal resonance, and broncho-vesicular respiration. The presence of the morbid deposit causes circumscribed bronchitis affecting the smaller tubes, and this complication may give rise to subcrepitant râles within the area of the tuberculous affection. The disease may end with no further increase or extension of the local affection, this termination resulting either from self-limitation or from the agency of treatment. Of this fact I have proof from cases not only studied during life, but in which appearances were noted after death. The ending of the disease and recovery after a small tuberculous deposit occur oftener than is generally supposed.

An increase and an extension of the phthisical affection occasion larger {409} areas and also a greater degree of solidification. As the amount of increase and extension within a given period varies very much in different cases, it follows that there is nothing like uniformity in these respects. Generally, the solidified portions of the lung form islands between which the tuberculous deposit is wanting. Between these islands the lung not infrequently becomes emphysematous. This vicarious emphysema explains the existence of a vesiculo-tympanitic resonance in some cases notwithstanding the solidification. Exclusive of that sign, as thus accounted for, the solidification causes a dulness on percussion proportional in degree and extent to the solidified portion of lung. The auscultatory signs of solidification are generally present--namely, either bronchial or broncho-vesicular respiration, and bronchophony or increased vocal resonance, according to the degree of solidification. The existence of bronchitis over a larger extent is represented by more abundant and coarser moist bronchial or bubbling râles. These râles do not, as has been supposed, necessarily denote that softening of the tuberculous deposit has taken place. Dry circumscribed pleurisies occurring from time to time, even from the very commencement of the phthisical affection, may give rise to a pleuritic friction murmur. The escape of the liquefied tuberculous deposit into the bronchial tubes by ulceration, added to the products of the bronchial inflammation, occasions an increase of the bubbling râles. Moreover, the liquefied tuberculous deposit is better suited for the production of bubbling sounds than the products of bronchial inflammation. Hence the abundance of the bubbling râles, taken in connection with the characters of the matter of expectoration, is evidence of the escape of liquefied tuberculous deposit.

If phthisis be progressive, the physical conditions already enumerated--namely, solidification, liquid in the bronchial tubes, pleuritic exudation--continue. They are present in both lungs. Associated with these conditions are cavities. The cavities formed in different cases differ greatly in size and number. They differ also as regards the number and the size of the openings by which they communicate with the bronchial tubes. The latter conditions are of importance with reference to the free discharge of the contents of cavities and the production of certain physical signs. Enumerating here the cavernous signs, they are--tympanitic resonance within a circumscribed space, frequently with amphoric or cracked-metal intonation, cavernous and sometimes amphoric respiration, increased vocal resonance, cavernous whisper, pectoriloquy in some instances, and, as a rare sign, metallic tinkling. An accumulation of liquid within a cavity which has free communication with the bronchial tubes gives rise to the cavernous sign called gurgling. I have met with an instance in which a loud splashing sound was produced within a cavity synchronous with the impulse of the heart, and due to the agitation of the cavity by the cardiac movements. Owing to the association of cavities with solidified portions of lung, the latter varying greatly in different cases in the extent and the degree of solidification, with the cavernous signs are combined those which represent varying degrees of solidification--namely, either dulness or flatness on percussion, either bronchial or broncho-vesicular respiration, and either bronchophony or increased vocal resonance.

In the physical conditions incident to pulmonary complications of phthisis--namely, pleurisy with effusion, perforation of lung with pneumo-hydrothorax--the reader is referred to the article on DISEASES OF THE PLEURÆ.

With reference to the general pathology of phthisis, points relating to the morbid anatomy are to be considered. There are two distinct varieties of morbid product in cases of phthisis--namely, the miliary granulations and the infiltrated deposit formerly distinguished as crude tubercle. Laennec taught that these are only varieties of essentially the same morbid product, the former being preliminary in their occurrence to the latter. Following {410} Virchow, some late writers have restricted the application of the term tubercle to the miliary granulations, regarding the infiltrated deposit as a non-tuberculous inflammatory product. Histological investigations have failed to establish an essential distinction between the two varieties. The fact that they are so constantly associated shows some close pathological connection. Both varieties undergo the same degenerative changes. Each is found by inoculation to produce tuberculous disease in certain animals. Moreover, according to the late researches of Koch and others, each contains the characteristic parasite, the bacillus tuberculosis. In view of these considerations, the doctrine of Virchow, advocated by Niemeyer and others, is not tenable, and, as already stated under the head of the Definition and Classification of pulmonary phthisis, the term tuberculous is properly applied to both varieties. There is no such affection as a non-tuberculous pulmonary phthisis. The terms pulmonary phthisis and pulmonary tuberculosis are now, as heretofore, to be regarded as synonymous.

That the pathology of pulmonary phthisis involves a predisposition or a tuberculous diathesis has been already shown by facts pertaining to the etiology. It does not in the least invalidate this logical conclusion that in the present state of our knowledge pathologists are unable to explain this diathetic condition; that is to say, in what it consists. Its recognition is not merely a matter of speculative or theoretical interest; it has an important bearing upon a rational prophylaxis and on the treatment of phthisis.

Up to a very recent date the opinion has generally been held by pathologists that the local phthisical affection may be determined entirely by a tuberculous cachexia--that the latter, in other words, may produce the affection exclusive of any local extrinsic cause; and the question has been much discussed whether or not at the outset the phthisical affection is an inflammation. But if the parasitic doctrine be accepted, a local causative agent derived from without--namely, the bacillus tuberculosis--is essential, the predisposition or the cachexia consisting of certain unknown conditions which are required for the development and the multiplication of the parasite. According to this doctrine, the extension of the local affection is due to invasions successively of different portions of the lungs, and the development of tuberculous disease in other situations is due to the migrations of this parasite. Without the presence of the bacillus, no matter in how great degree the required conditions may exist, phthisis will not occur.

Inflammatory processes, however, accompany and follow the development of the tuberculous affection. Bronchitis, peribronchitis, periarteritis, endoarteritis, interstitial pneumonia, and pleurisy are terms which denote inflammation. To these are to be added ulceration and suppuration within cavities. The infiltrated tuberculous deposit is to be regarded as an inflammatory exudation. There is an intrinsic propriety, therefore, in calling it a pneumonia. But the behavior of this deposit differs widely from that of the exudation in lobar pneumonia. In the latter affection it is readily absorbed and disappears, leaving the pulmonary structure intact, whereas in phthisis it is absorbed with difficulty, and in most cases leads to more or less destruction of the pulmonary structure. For these reasons, irrespective of histological points of difference, the term tuberculous should be used to distinguish the exudative pneumonia which is characteristic of phthisis. The term desquamative pneumonia was proposed by Buhl. The so-called cheesy degeneration of the tuberculous products--a necrotic, not an inflammatory, process--was considered by Laennec as a distinctive mark of the products. This doctrine has been disproved. Other morbid exudations and growths may undergo similar degenerative changes.

DIAGNOSIS.--It is evidently very desirable to recognize the existence of phthisis at as early a period as possible with reference to the adoption of {411} measures with a view to prevent the further development and progress of the disease. It is also very desirable, if practicable, to determine that phthisis does not exist; that is, by the absence of diagnostic points to exclude it. Difficulty of diagnosis relates almost exclusively to an early period when the phthisical affection is small. The diagnostic points pertaining to the symptoms and the physical signs in the incipiency of the disease therefore especially claim attention.

A cough of more or less duration, which was at first slight and dry, gradually increasing and accompanied by the expectoration of mucus, should always excite a suspicion of phthisis, especially if the patient's age be between twenty and thirty years. This is not the history of a chronic primary bronchitis. A cough as just described should never be considered as nervous or sympathetic without due investigation. It should not be attributed to pharyngitis, although the latter affection is found to exist. Want of breath on exercise is a symptom pointing to something more than a bronchial or pharyngeal affection. The import of these symptoms is still greater if, after the commencement of the cough or from an earlier date, there has been decrease in weight and strength. Their significance is much increased by the occurrence of hæmoptysis. Hæmoptysis followed by a persistent cough, and still more if cough preceded its occurrence, is always presumptive evidence of a phthisical affection. Occurring without having been preceded by cough, and when cough does not immediately follow, it should suggest the probability of phthisis. In the larger proportion of cases under these circumstances it is a forerunner of the diagnostic symptoms and signs of the disease. In connection with the cough a persistent increase of the temperature of the body is an important diagnostic symptom. Chilly sensations and flashes of heat are symptoms of some importance. Especially significant are pleuritic stitch-pains referable to the upper part of the chest or beneath the scapula, these being symptomatic of the circumscribed dry pleurisies which may occur at an early period of the disease. Impaired appetite, pallor of the face, and a tendency to perspire during sleep have much significance taken in connection with the pulmonary and other symptoms.

A positive diagnosis must rest on physical signs, together with more or less of the foregoing symptoms. The physical conditions which furnish the diagnostic signs are solidification of a small portion or of small portions of lung, usually at or near the apex, the presence of mucus in the small-sized bronchial tubes, and perhaps fibrinous exudation on the pleural surface within a circumscribed area corresponding to the solidified portion or portions of lung. The signs furnished by these conditions are slight dulness on percussion, a broncho-vesicular (formerly called rude or harsh) respiration, some increase of vocal resonance and of the whispered voice, subcrepitant râles, and perhaps a grazing friction murmur. It may be important to consider the physical signs of phthisis with some detail. Aside from their importance, a reason for this is that terms by which some signs are designated are not used in precisely the same sense by all medical writers.

A small phthisical affection gives rise to slight or moderate dulness on percussion. In order to appreciate this sign if the dulness be slight, attention should be paid to the pitch of the resonance as well as to the lessened intensity of resonance. The pitch is always raised. By attention to the latter character, in conjunction with the diminution of intensity, a degree of dulness may be sometimes appreciated which, without attention to the pitch, might not be determinable.[13] In determining abnormal dulness in the infra-clavicular region on one side, the normal disparity between the two sides of the chest {412} in this region must be taken into account. The resonance at the right summit, as compared with that of the left summit, is, normally, somewhat dull. Hence it is not as easy to make out an abnormal dulness at the right as at the left summit. If the relative abnormal dulness at the right summit be but slight, the question is whether there be more than a normal disparity. This question is rendered difficult by the fact that the degree of normal disparity varies somewhat in different healthy persons. In cases of doubt little reliance is to be placed on this sign alone, but it is to be taken in connection with auscultatory signs.

[Footnote 13: The author was the first to indicate the fact that dulness is always associated with elevation of pitch. Vide "Prize Essay on Variations of Pitch in the Sounds obtained by Percussion and Auscultation," _Transactions of the American Medical Association_, 1852.]

With reference to the auscultatory signs in cases of phthisis, it is to be premised that often, owing to the importance of studying the sounds derived from a limited area and of localizing morbid conditions, the use of the stethoscope is indispensable. It is impossible to meet all the requirements of physical diagnosis by immediate auscultation. After an experience of more than a quarter of a century the writer would advise the binaural stethoscope in preference to any other. For the benefit of those who are not practically familiar with this instrument, it should be added that in order to appreciate its advantages, the instrument, in the first place, must be properly constructed, and, in the second place, some practice is necessary. A sound produced within the instrument is at first an obstacle, but it is speedily overcome by use.[14]

[Footnote 14: The dissatisfaction with the binaural stethoscope so often comes from defects in its construction that it seems proper to refer to Tiemann & Co., and to Ford & Co., of New York as reliable makers of this instrument.]

A small tuberculous solidification is represented by a broncho-vesicular respiration. This sign was named and described by me in 1856. The name takes the place of the terms rudeness, harshness, and hardness--terms which are not only inadequate, but convey an erroneous idea. Quoting from another work, the characters of the broncho-vesicular respiration and its comprehensive signification are as follows: "The sign represents the different degrees of solidification of lung between an amount so slight as to occasion only the smallest appreciable modification of the respiratory sounds, and an amount so great as to approximate closely to the degree giving rise to bronchial or tubular respiration. In other words, all the gradations of respiratory modifications caused by incomplete or an inconsiderable solidification are embraced under the name broncho-vesicular. The gradations correspond to the amount of solidification; that is, they show the solidification to be either very slight, moderate, or nearly sufficient to be regarded as considerable or complete. The sign is therefore important as evidence, first, of the existence of solidification, and, second, of the degree of solidification. Analyzing this sign, the most distinctive feature is the combination of the vesicular and the tubular quality in the inspiratory sound. These two qualities may be combined in variable proportions. The pitch of the sound is raised in proportion as the tubular predominates over the vesicular quality. The expiratory sound is more or less prolonged, tubular in quality, and the pitch raised. The prolongation of this sound, its tubular quality, and the raised pitch are proportionate to the predominance of the tubular over the vesicular quality in the inspiratory sound. If the solidification be slight, the characters of the normal vesicular respiration predominate; that is, the inspiratory sound has but a small proportion of the tubular quality, and is but little raised in pitch, the expiratory sound being not much prolonged, its tubularity not marked, the pitch not high. If, on the other hand, the solidification be almost enough to give a bronchial respiration, the inspiratory sound has only a little vesicular quality, the tubular quality predominating, the pitch proportionately raised, and the expiratory sound is prolonged, high, and tubular, nearly to the same extent as in bronchial respiration. The less the solidification the more the characters {413} of the normal vesicular respiration predominate over those of the bronchial respiration; and, per contra, the greater the solidification the more the characters of the bronchial predominate over those of the normal vesicular respiration."[15] By means of the broncho-vesicular respiration a slight morbid solidification may be recognized in one of the infra-clavicular regions or over the scapula. Here, however, as with regard to percussion, an allowance is to made on the right side for a normal disparity. The respiratory sounds on the right side at the summit, as compared with those at the left, have normally the characters more or less marked of a broncho-vesicular respiration. These characters are more marked as the stethoscope is brought toward the sternum. Hence a small solidification of lung is more easily ascertained by auscultation at the left than at the right summit.

[Footnote 15: Vide _Manual of Auscultation and Percussion_, by the author; also, paper contained in the _Transactions of the International Medical Congress_, London, 1882. The broncho-vesicular respiration was called by Skoda indeterminate (unbestimmt), and this term is still used by German writers. These sounds are not indeterminate if the characters derived from pitch and quality be analytically studied; they are sounds intermediate between the normal respiratory murmur and bronchial respiration.]

Not infrequently in cases of incipient phthisis the respiratory sounds at the summit on the affected side are so weakened that their characters cannot be studied. Weakness of the respiratory murmur in these cases becomes a diagnostic sign taken in connection with other signs.

A small tuberculous deposit may increase the vocal resonance. But, again, a normal disparity between the two sides must be allowed for. The normal vocal resonance is always greater on the right side. If, therefore, it be a question as to the existence of a small tuberculous affection at the right summit, it is to be decided whether the disparity be greater than normal. A small tuberculous deposit at the apex of the left lung, on the other hand, may not increase the resonance to an equality with that at the right summit.

Attention should be paid to the whispered voice, and, still again, the two sides show a normal disparity. The sound heard with the whispered voice, which may be distinguished as the normal bronchial whisper, is louder on the right than on the left side, and somewhat higher in pitch on the left side, at the summit of the chest. If at the right summit it exceed the normal disparity, and the pitch be higher than at the left summit, the sign may be distinguished as increased bronchial whisper, and it denotes solidification. If, on the other hand, the sound at the left summit be louder than that of the right summit, there is increased bronchial whisper, representing the solidification at the apex of the left lung.[16]

[Footnote 16: The different abnormal modifications of sounds produced by the whispered voice were first named and described by the author. Vide _Manual of Auscultation and Percussion_.]

The normal points of disparity at the summit of the chest render the diagnosis of incipient phthisis by means of alterations in the resonance on percussion, the respiratory sounds, the vocal resonance, and the whispered voice a problem in some cases of not a little difficulty. In these cases an examination of the sputa for the presence of the tuberculous parasite may furnish proof of the existence of the disease. This proof may in some instances be obtained when the physical signs, together with the symptoms, do not render the diagnosis positive, and it may be sought for in order to corroborate the evidence derived from other sources. The author can testify from considerable experience to the value of an examination of sputa for bacilli in cases in which the diagnosis is not rendered positive by other signs and by symptoms. It must, however, be borne in mind that the absence of bacilli in the sputa is not sufficient to exclude phthisis, especially if but a single examination be made. In doubtful cases, if an examination of the sputa be negative, the examination should be repeated. The weight of evidence against the {414} existence of phthisis is, of course, greater in proportion to the number of examinations with negative results.[17]

[Footnote 17: The following method of staining the bacilli tuberculosis in the sputum is essentially that recommended by Ehrlich in the _Deutsche medicinische Wochenschrift_, Mai 6, 1882:

It is important that the sputum to be examined should be derived from the lungs, and should not be solely that from the upper air-passages. A small opaque particle from the sputum is to be pressed between two cover-glasses, so that when these are drawn apart a thin film will remain upon each. Each cover-glass, as soon as the film is dry, is to be passed, with the preparation upward, rather rapidly three times through the flame of a Bunsen's burner or of an alcohol lamp. The preparation is now ready for staining.

A small quantity of water in a test-tube or flask is now shaken with an excess of aniline oil (which need be only in small amount), and after a few moments is filtered through moistened filter-paper. To the clear filtrate thus obtained is to be added, drop by drop, a saturated alcoholic solution of fuchsin (gentian-violet, methyl-violet, and several other aniline colors may be substituted) until the fluid begins to be opalescent, showing that it is saturated with the coloring agent. In this manner an alkaline-aniline staining solution is prepared.

Into this staining solution the cover-glasses, having the dried films of sputum prepared as above described, are dropped, preferably so that they will float with the preparation downward. Here they remain from a half hour to twenty-four hours. If taken out in a short time, the fluid, at least for a time during the staining process, should be heated moderately over a water-bath, and in any case the process of staining is accelerated and rendered more certain by heating.

After removal from the staining fluid the cover-glass is washed for a few moments in water, and is then dipped into a mixture of one part of pure nitric acid (it should contain no nitrous acid) to about three or four parts of water. Here it remains only a few moments, when it will be found that the preparation has lost its color, although a part will be restored by the subsequent washing in water, which should be done at once. If the preparation has not been sufficiently decolorized, it may be placed again in nitric acid, but it is not necessary or desirable that it should remain there many minutes. The object of the nitric acid is to extract the color from all but the tubercle bacilli.

The preparation may now be at once examined either in glycerin or (after drying or after treatment with alcohol and oil of cloves) in balsam. Ehrlich recommends, previous to this, a staining of the background with some color other than that of the bacilli; thus, with methyline blue if the organisms are stained red with fuchsin. This staining of the background, however, is not necessary. While the ideal method of studying the stained bacilli is by means of Leis's oil-immersion lenses and Abbé's illuminating apparatus, they can usually be seen readily enough with the high powers in ordinary use, such as the one-fifth or one-sixth inch objectives of our American microscope. After staining with fuchsin the bacilli appear as short rods of a red color, frequently curved or bent.]

The adventitious sounds which have been mentioned--namely, the subcrepitant râle and the pleural friction murmur--sometimes afford valuable aid in the diagnosis. Taken in connection with the direct signs obtained by auscultation and percussion, these accessory signs when present make the diagnosis positive: they are by no means uniformly present, and therefore their absence is not proof against the existence of a phthisical affection. To these accessory signs another sign may be added--namely, an abnormal transmission of the heart-sounds within one of the infra-clavicular regions. In the middle of this region there is nearly an equal transmission of these sounds normally. Comparing the two sides as regards the two sounds respectively, the first sound is a little louder on the left, and the second sound a little louder on the right side. Now, with a little solidification the sounds may be better transmitted, so that they are abnormally loud on the affected side.

A decision that there is no physical proof of phthisis must rest on the absence of all the foregoing signs after repeated examinations of the chest.

It is not to be concluded that for a positive diagnosis of incipient phthisis all or most of the foregoing diagnostic signs must be recognized. They are not all present in all cases. Two or three of these signs, and even a single one if well marked and associated with diagnostic points pertaining to the symptoms and history, may suffice for a positive diagnosis.

It is an interesting question how small a portion of solidification may furnish signs sufficient for a diagnosis. I have the records of two cases bearing {415} on this question. A patient came under my observation at Bellevue Hospital in 1867. In the right infra-clavicular region the respiration was abnormally broncho-vesicular, the vocal resonance was increased, and there was increase of the bronchial whisper within a small circumscribed space. On these signs was based the diagnosis of a small tuberculous deposit. The case served to illustrate the signs just named to classes for practical instruction in auscultation and percussion. The patient, who was employed as a helper in the apothecary's shop, died suddenly from taking by mistake an overdose of the fluid extract of aconite. The autopsy showed at the apex of the right lung a nodule of the size of a filbert, no tuberculous deposit being elsewhere found.

A recent medical graduate, twenty-two years of age, had cough and two attacks of hæmoptysis. His father and a sister had died with phthisis. There was slight dulness on percussion on the summit of the chest on the left side, with crepitation at both summits. These were the only signs noted. This case was included among the cases of recovery reported in my work on phthisis published in 1875. He enjoyed excellent health and was notably vigorous for twenty-eight years. Death took place in 1880 from disease of the heart and kidneys. The autopsy showed at the apex of each lung a small indurated portion somewhat larger on the left than on the right side. Elsewhere there was no appearance denoting present or past pulmonary disease.

It is in only a small proportion of cases that, when patients first come under medical observation, the phthisical affection is so small as to render the diagnosis difficult. The tuberculous solidification is generally sufficient to give rise to well-marked signs. The shrinkage of the lung at the apex from interstitial growth and diminished capability of expansion may have caused a small infra-clavicular depression and restricted respiratory movements in this region. The dulness on percussion is readily recognized. The characters of the broncho-vesicular respiration are easily determined. The increase of vocal resonance and increased bronchial whisper admit of no doubt. With these signs, oftener than at an earlier period, are associated accessory signs--namely, subcrepitant râles and bubbling in larger tubes, pleuritic friction murmur, and undue transmission of the heart-sounds.

At a somewhat later period, and sometimes even when cases are first observed, the physical signs denote a still greater degree of solidification. Infra-clavicular depression and restricted movements on one side are marked. The respiration is bronchial and the voice bronchophonic. There may be pectoriloquy with the bronchophonic characters, showing that the speech is transmitted through solidified lung.[18]

[Footnote 18: Bronchophony is to be understood as a sign distinct from increased vocal resonance. In bronchophony the resonance may or may not be increased. Intensity is not a character of this sign. Its distinctive characters are concentration of the voice sound, nearness to the ear, and elevation of pitch. The terms concentration and nearness to the ear properly express what was intended by Laennec in the words "la transmission évidente de la voix à travers le stethoscope." Pectoriloquy is to be distinguished from bronchophony. These two terms are sometimes confounded. Bronchophony is transmission of the voice, pectoriloquy the transmission of speech--that is, articulate words.]

Exceptional cases are to be referred to in which over lung containing solidified portions from tuberculous deposit dulness on percussion is wanting. Not only is dulness wanting, but the resonance is greater than normal. The resonance is altered in character. With an increase of intensity the quality is in part tympanitic and the pitch is raised. This is the sign described by me many years ago under the name vesiculo-tympanitic resonance. The distinctive characters are those just mentioned--namely, increase of intensity, the quality a combination of the vesicular and the tympanitic, and more or less elevation of pitch. The name vesiculo-tympanitic expresses these characters. It is the sign of pulmonary emphysema. It denotes that portions of {416} lung situated between islands of solidification have become emphysematous. The emphysema is vicarious; that is, supplementary to the shrinkage of the portions solidified, and, added thereto, probably collapsed lobules. Were one to be governed by percussion alone in the physical diagnosis, this sign would in some cases mislead. The liability to error is avoided by taking due cognizance of the associated signs furnished by auscultation.

In cases of advanced phthisis cavities are added to tuberculous solidification. It is desirable to recognize the existence of these. In most instances the signs which may be distinguished as cavernous suffice for the recognition of cavities. The cavernous signs are furnished by percussion and by auscultation of the respiration and of the voice.

A purely tympanitic resonance within a circumscribed space points to a cavity, but a tympanitic resonance with either an amphoric or a cracked-metal intonation is more especially a cavernous sign. An amphoric or a cracked-metal resonance over a cavity may often be obtained by observing certain rules in percussion--namely, percussing with a single and rather forcible blow, the mouth of the patient being open and brought close to the ear. These signs may be rendered still more distinct by means of the binaural stethoscope, the pectoral extremity being close to the patient's opened mouth, an assistant making the percussion. These cavernous signs are not present when cavities contain much liquid or when communication with the bronchial tubes is temporarily obstructed; hence the signs are sometimes present and sometimes absent.

There is a distinctive cavernous respiratory sign. This assertion is called for by the fact that the existence of the sign is not as yet recognized by all medical writers. According to Laennec, the respiratory sounds derived from cavities resemble the bronchial respiration. From his description it would be impossible to distinguish the former from the latter. Skoda considered the cavernous and the bronchial respiration as absolutely identical; and this view is held by German writers at the present time. Walshe indicated an essential differential point pertaining to the inspiratory sound in cavernous respiration--namely, its low pitch. The fact that in purely cavernous respiration the pitch of the expiratory is lower than that of the inspiratory sound was stated by me in 1852.[19] The distinctive characters of the cavernous respiratory sign as then indicated were as follows: An inspiratory sound low in pitch and non-tubular in quality, followed by an expiratory sound still lower in pitch and non-tubular. The quality of the sound in inspiration and in expiration may be said to be blowing, after the term soufflante used by Laennec, but applied by him to a sound either bronchial or from a cavity, when the air seems to be drawn from the ear of the auscultator.

[Footnote 19: Vide "Prize Essay."]

Appreciating clearly the characters which are distinctive of cavernous respiration, it is impossible to confound this sign with bronchial respiration, both the inspiratory and the expiratory sound in the latter sign being high in pitch and tubular in quality. This cavernous sign approaches much nearer to the normal vesicular respiration. The only distinction between these two signs is the presence of the vesicular quality in the latter and its absence in the former. Hence, the only liability to error is in confounding the two. This error can only be committed when the respiratory murmur is so feeble that the vesicular quality is not readily appreciable. In order to avoid the error, the respiration should not be pronounced cavernous when the sounds are quite weak, except there be present other correlative cavernous signs.

Cavities are often situated in close proximity to lung solidified by tuberculous deposit or interstitial pneumonia: cavernous respiration and bronchial respiration are then in juxtaposition, and their differential characters are {417} rendered very distinct by contrast. Under these circumstances, however, the cavernous respiration is sometimes modified by combination with the characters of the bronchial respiration. Not infrequently a cavernous inspiration is joined to a bronchial expiration, the more intense expiratory sound representing adjacent solidification extending over the site of the cavity and drowning the weaker cavernous expiration. In another mode of combination the inspiratory sound is bronchial at the beginning and cavernous at the end. Here the cavernous sound occurs a little later than the bronchial, and the latter is supplanted by the former. This variety of broncho-cavernous respiration has been recently described by Seitz under the name metamorphosing respiratory murmur (metamorphosirendes athmungs geräusch). In like manner, the characters of the cavernous and of the normal vesicular respiration may be combined. This combination may be expressed by the term vesiculo-cavernous respiration.

The effect of a cavity upon vocal resonance is to increase its intensity without giving rise to the characters distinctive of bronchophony--namely, nearness to the ear, concentration, and elevation of pitch. Increased vocal resonance, and not bronchophony, is therefore a cavernous sign. If bronchophony be present over a cavity, it denotes adjacent solidification of lung. With the vocal resonance more or less increased the vocal fremitus appreciable on auscultation is often intensified.

A cavernous whisper has the characters of the expiratory sound in the cavernous respiration; that is, it is low in pitch and blowing or non-tubular in quality, being in contrast, as regards these characters, with a high-pitched tubular sound in whispering bronchophony. The latter sign is often found near a cavity, showing the proximity of solidified lung.

Amphoric respiration, amphoric voice, and amphoric whisper are pathognomonic signs of a cavity, provided pneumothorax be excluded. The same is to be said of metallic tinkling, a very rare cavernous sign. Gurgling within a circumscribed space is a cavernous sign of some value. Pectoriloquy--that is, the transmission of articulated words--is not, per se, a cavernous sign; that is to say, the speech may be transmitted by solidified lung as well as through a cavity. This is true alike of words spoken with the loud and with the whispered voice. It is, however, easy to determine whether pectoriloquy be or be not due to a cavity. If with the loud voice the transmitted speech be unaccompanied by the characters of bronchophony, it denotes a cavity. So, if transmitted whispered words be unaccompanied by the characters of the bronchophonic whisper, they denote a cavity. On the other hand, the transmission is by solidified lung if bronchophony and pectoriloquy be conjoined in either the loud or the whispered voice.

The shrinkage of lung incident to the formation of tuberculous cavities increases the depression apparent on inspection in the infra-clavicular region. The site of a cavity is sometimes indicated by a circumscribed bulging of intercostal spaces, within a localized area, on forced expiration or an act of coughing. A sharply-defined circumscribed depression corresponding to the area of a cavity is visible in some cases. Another effect of shrinkage of lung is to uncover the aorta in the second intercostal space on the right side, or the pulmonary artery in a corresponding situation on the left side. The pulsation of these arteries may then be perceived by the touch, and perhaps, also, by the eye. This effect should not lead to the error of inferring the existence of aneurism. Shrinkage of the upper lobe of the left lung may cause considerable elevation of the heart, also enlarging considerably the space within which is felt the cardiac impulse.

With a practical knowledge of the physical signs of which a concise account has been given, it is practicable to determine, first, the existence of phthisis in its incipiency when the tuberculous affection is small; second, during the {418} progress of the disease to ascertain the degree and the extent of the tuberculous solidification; and, third, to recognize the existence of, and to localize, cavities.

Recapitulating the signs belonging to the foregoing phases of the disease, in incipient phthisis they are slight dulness on percussion, broncho-vesicular respiration approximating to the normal vesicular or a respiratory murmur too weak for its characters to be studied, some increase of vocal resonance, increased bronchial whisper, and, as occasional accompanying signs, subcrepitant râles, pleuritic friction murmur, and abnormal transmission of the heart-sounds, more or less of these signs being limited to the summit of the chest on one side. After further progress of the phthisical affection the signs are, dulness on percussion more or less marked, either a broncho-vesicular respiration approximating to the bronchial or a purely bronchial respiration, either notable increase of vocal resonance or bronchophony, either increase of the bronchial whisper or whispering bronchophony, and moist bronchial or bubbling râles which may be either coarse or fine, or both may be combined. After the affection has advanced to the formation of cavities the cavernous signs are added to those of solidification--namely, circumscribed tympanitic resonance on percussion, cracked-metal and amphoric resonance, cavernous respiration, cavernous whisper, increased vocal resonance and gurgling. Pectoriloquy may be present before and after the formation of cavities; in the former instance the transmission of speech being by solidified lung, and in the latter through a cavity, the two modes of transmission being easily differentiated by means of the characters associated with the pectoriloquy.

An intercurrent pneumonia, not tuberculous, may lead to the error of supposing the tuberculous affection to be much greater than it is. Especially is there liability to this error if the patient have not been under observation prior to the intercurrent pneumonia. The latter may give rise to bronchial respiration and bronchophony, with notable dulness on percussion over a considerable space. If the patient have been under observation, the rapidity with which the solidification denoted by these signs has been developed is a diagnostic point. A notable diminution of the solidification within a few weeks or days is evidence that it was due to an intercurrent pneumonia. The tuberculous deposit is never absorbed with such rapidity. The following case may serve as an illustration of this complication: A man aged thirty had had for some time slight cough and want of breath on active exercise, but he had kept about, actively engaged in business, until within a few days of the date of my visit. He was then up and dressed, his chief complaint being want of breath on any exertion. The physical signs gave evidence of considerable solidification of the upper lobe of the right lung. The question was, whether the solidification was due exclusively to phthisis, or whether with this disease was associated an intercurrent pneumonia. The question was settled definitively by an examination of the chest six weeks afterward. At the time of this examination the solidification had in a great measure disappeared; there was only slight dulness on percussion, with increase of vocal resonance and feeble respiratory murmur. Meanwhile, the symptoms had denoted progressive improvement; the cough was now slight; he no longer suffered from want of breath on exertion, and he had improved as regards appetite, strength, etc. This patient consulted me seven years and four months afterward. In the mean time he had considered himself in fair health, but he had been subject to cough, and for the preceding six months the cough had been persistent. There was now dulness at the summit of the chest on the right side, with feeble broncho-vesicular respiration, increase of vocal resonance, abnormal transmission of the heart-sounds, and subcrepitant râles. He had held his weight and strength, and his appetite and digestion were good.

{419} An occasional event in cases of phthisis is obstruction of a primary bronchus from the pressure of an enlarged bronchial gland. This event may explain a degree of embarrassment of respiration out of proportion to the changes which have taken place in the lungs. The bronchial obstruction is shown by notable feebleness or by suppression of the respiratory murmur on the side of the obstruction, and an increase of the murmur on the other side of the chest. Obstruction of a primary bronchus may prevent the appreciation of morbid respiratory signs on the obstructed side.

During the progress of phthisis the symptoms concur with the physical signs in showing the progressive inroads of the disease upon the pulmonary organs. They show, more than the physical signs, the inroad upon the powers of life. They also afford evidence, in conjunction with the physical signs, of arrest of the disease. More reliance is to be placed on the symptoms than on the signs in judging of the rapidity on the one hand, or on the other hand of the slowness, of the progress of the disease. In these several points of view the consideration of symptoms comes more properly under the head of the prognosis.

The symptoms pertaining to complications of phthisis may be the first to lead patients to consult a physician. Not infrequently advice is sought for harshness or hoarseness of the voice, arising from chronic laryngitis, the cough and other symptoms which preceded this affection not having been regarded as of sufficient consequence to require medical aid. It is to be borne in mind that chronic laryngitis, when not of syphilitic origin, is generally secondary to phthisis. The chest is therefore to be examined carefully with reference to the signs of the latter.

Pleurisy with effusion may be a complication which the physician is called upon to treat. A lung compressed by liquid which fills the affected side of the chest cannot be interrogated by means of physical signs. Under these circumstances subcrepitant râles may denote a phthisical affection on the summit of the chest on the opposite side. The existence of cough and expectoration prior to the pleurisy is strong evidence of an antecedent phthisical affection. The occurrence of hæmoptysis adds greatly to the evidence.

A tuberculous patient who has not been under any treatment may apply to a surgeon to be relieved of the inconvenience of a perineal fistula. Operative interference for this affection should never be resorted to without a careful examination of the chest.

PROGNOSIS.--Whether pulmonary phthisis is ever a curable disease has hitherto been a mooted question. Prior to the time of Laennec instances of apparent cure were open to doubt on the score of diagnosis. Laennec did not admit the probability of a cure before the formation of cavities, but he gave the histories in a number of cases in which the cicatrization of cavities had taken place.[20] If by the term curability be meant a complete restoration of the portions of lung affected by tuberculous disease to the normal condition which existed prior to the disease, the doctrine of Laennec is probably true. A moderate or even a small phthisical affection leads to changes which are permanent. There remains more or less impairment of the integrity of the pulmonary organs. But if by the term be meant that all pulmonary symptoms cease, that the patient has good general health, and that the {420} damage to the lungs is not sufficient to prevent an adequate exercise of their functions, a cure may take place before as well as after the formation of cavities. Accepting the latter sense of the term curability, no one at the present time will deny the statement just made--a fact which is due, at least in a measure, to the different views in regard to the treatment of phthisis now as compared with the time of Laennec.

[Footnote 20: "Les observations contenues dans l'ouvrage de M. Bayle, ainsi que ce que nous avons dit nous-mêmes ci-dessus du dévelloppement des tubercles, prouvent suffisamment que l'idée de la possibilité de guérir la phthisie au prémier degré est une illusion. Les tubercles crus tendent essentiellement à grossir et à se ramollir. Il est peut être au pouvoir de l'art de ralentir leur dévelloppement, d'en suspendre la marche rapide, mais non pas de lui faire un pas rétrograde. Mais s'il est impossible de guérir la phthisie au premier degré, un assez grand nombre de faits mont prouvé que dans quelques cas un malade peut guérir après avoir eu dans les poumons des tubercles qui se sont ramollis et ont formé une cavité ulcéreuse" (_Traité de l'Auscultation médiate_).]

The appearances found after death in cases which may be considered as exemplifying, practically, recovery from phthisis vary according to the extent of the tuberculous affection and the stage to which it had advanced. In a case referred to in connection with the diagnosis (vide p. 407) an examination after death, nearly thirty years having elapsed from the date of recovery, showed within small circumscribed spaces at the apex of both lungs a condensed pulmonary tissue. In the following case there was a similar condition within larger spaces: The patient, a man aged about forty, was attacked with hæmoptysis in April, 1846. Soon afterward the symptoms and signs of tuberculous disease became manifest, and death took place in the following June. On examination after death the lungs were found to contain infiltrated tuberculous deposits, some of which had undergone softening, and miliary tubercles in abundance. In addition to these appearances, at the apex of each lung was a solid mass nearly as large as a hen's egg, that on the right side being somewhat larger than that on the left. The surface over these masses presented a marked depression and a puckered appearance. On dividing the masses they appeared to consist of condensed parenchyma: they were of a reddish color, friable, and contained an abundance of minute calcareous particles. They were surrounded by a thick, firm wall isolating them from the adjacent pulmonary structure. Eighteen years before his death this patient had cough and other symptoms which were regarded at the time as denoting pulmonary phthisis. He recovered, and had good health up to the fatal illness. The only exception to this statement of his previous good health was the occurrence of a perineal fistula, which was nearly cured by division of the gut nine months before the hæmoptysis.

No one can doubt that tuberculous cavities may completely cicatrize. Instances in abundance have been observed since the publication of Laennec's treatise. The gradual contraction and final closure of a cavity may be observed during life, the cavernous signs becoming less marked, and at length disappearing. At the present time I see frequently two persons who have recovered from phthisis, recovery in one taking place nearly twenty, and in the other nearly ten, years ago. In these cases the cavernous respiration was well marked in situations in which now there is a feeble vesicular murmur. In both cases there is a circumscribed depression of the chest in these situations.

Recovery may be said to take place when cavities do not cicatrize, but remain, being lined by a membraniform structure and free from morbid products. Under these circumstances cavities are innocuous. There is an approximation to recovery when cavities furnish more or less matter of expectoration, the lungs elsewhere being free from tubercles or tuberculous products.

Recovery with calcification of tubercles is illustrated by the following case: A farmer from Illinois, aged forty, consulted me in June, 1843. Within the preceding four months he had from time to time expectorated calculi, some of which were of the size of a small pea, in great numbers. A hacking cough had existed for several months before he began to expectorate the calculi. At the time of the expectoration of these the cough was severe and he raised some bloody mucus. In the intervals the cough was slight and without expectoration. The examination of the chest was negative as regards any signs of disease. Thirteen years afterward this patient came to report his condition of health. The expectoration of calculi had continued for some {421} time after his former visit; then his cough ceased, and meanwhile he had been perfectly well.

It is a question whether the tuberculous product is ever absorbed. The fact that in some instances the physical signs in life and the appearances after death give no evidence of either tuberculous deposit or cavities, and the fact that tuberculous solidification is observed to diminish or disappear when apparently the deposit has not been expectorated, render it probable that under some circumstances absorption does take place to a greater or less extent. It is doubtless true that, as a rule, the deposit is not absorbed; the tuberculous affection in this respect affords a striking contrast to non-tuberculous pneumonia.

Cases of recovery from phthisis are cited by medical writers as proving the curability of the disease. The term curability implies that recovery is due to remedial agencies. It does not therefore embrace a truth of great importance in its bearing on the prognosis and the treatment--namely, the disease in certain cases ends in recovery purely from an intrinsic tendency. My clinical studies have furnished facts which conclusively establish this important truth. Out of a large number of cases (640) recorded during a period of thirty-four years, recovery took place in 44. In 23 of these 44 cases there were no measures of treatment to which the recovery could be attributed. The disease ended favorably in these 23 cases from self-limitation. This assertion does not express a conjecture or a theory, but a logical conclusion. Self-limitation, therefore, is a highly important element in prognosis; it is a highly important factor in the treatment. The claim in behalf of phthisis of self-limitation, based on the analysis of cases of recovery, was made by me nearly a quarter of a century ago.[21] It has not as yet received that recognition in medical literature which it is desirable that it should receive in view of the importance of its practical bearings. It will enter here into considerations connected with treatment and prognosis.

[Footnote 21: Vide _American Journal of the Medical Sciences_, January, 1858.]

Recovery from phthisis involves, of course, cessation of the progress of the disease. This cessation of progress may be due either to an intrinsic tendency or to arrest by measures of management, or to both combined. Recovery may or may not follow the cessation of progress. Owing to the disposition and the extent of the tuberculous affection, reparation of the lesions does not take place. It is a useful grouping of cases into--first, those which become non-progressive and end in recovery; and, second, those in which the cessation of progress is not followed by complete recovery. It is also useful to consider as forming a third group cases in which the progress of the disease is extremely slow. The cases in the latter group are the opposite to those in which the progress of the disease is continuous and rapid, giving rise to the name galloping consumption.

There is much significance in the fact that in cases of progressive phthisis the disease does not, as a rule, advance by a steady increase, but by a series of invasions. Successive eruptions of the tuberculous affection occur. In these eruptions the affection may be either small or moderate or considerable in amount. The intervals between them may be brief or long. The disease may end with a single eruption. This may be small or even slight, and followed quickly by recovery. There is reason to believe that instances of this kind are not infrequent. The phthisical affection may have been overlooked, or it is inferred from the recovery that there was an error in diagnosis. In the great majority of cases a series of eruptions occurs, and it is in this way that the disease is generally progressive. These clinical facts, regarded from the standpoint of the parasitic origin of phthisis, are to be explained by supposing that bacterial colonies invade at successive epochs different portions of the lungs, but that in a certain number of instances there is neither invasion nor migration of the parasite. {422} The occurrence of successive eruptions is made manifest by the symptoms and the physical signs. After the occurrence of a single eruption or a series, if there be no recurrence the recovery will depend, cæteris paribus, on the amount of the tuberculous affection.

The prognosis in individual cases involves clinical points which pertain to the symptoms and signs of the pulmonary affection, and to the symptomatic phenomena referable to other of the anatomical systems of the body. The latter are of importance as representing the constitutional condition or the cachexia, and as indicating either, on the one hand, self-limitation, or, on the other hand, a progressive tendency of the disease.

Other things being equal, the smaller the pulmonary affection the better the prognosis. But assuming that the first tuberculous eruption is small, it does not follow that other eruptions may not occur more or less speedily, and, assuming a considerable or a large eruption, another may not occur. The prognosis in the latter case is of course much the more favorable. In forming a judgment in respect of the prognosis, the amount of the pulmonary affection is less to be considered than the symptoms which relate to the progressive tendency of the disease and to its tolerance by the system. An unfavorable prognosis, however, is to be based on the existence of an amount of the pulmonary affection sufficient to compromise the respiratory function, as shown by notable increase of the frequency of the respirations and by dyspnoea. Hæmoptysis, as has been seen, if unaccompanied by other symptoms which are untoward, even if the hemorrhage be profuse, is not an unfavorable event. Microscopical examinations of the sputa afford important information bearing on the prognosis. Examinations, thus far, made by different observers, show that in proportion to the abundance of the parasite in the sputa the disease may be considered as actively progressing.

Important prognostics derived elsewhere than from symptoms referable to the pulmonary organs relate especially to the circulatory system, inclusive of the temperature of the body, to the digestive system, to the hæmatopoietic system, and to nutrition. Acceleration of the pulse is an unfavorable symptom. In proportion to the degree of acceleration, either activity of the progress or a want of tolerance of the tuberculous affection, or of both combined, is to be inferred. It is of course important, if practicable, to know the patient's normal pulse as the standard for comparison in individual cases, inasmuch as the frequency in health varies considerably in different persons. A febrile temperature is especially significant as a symptom of progressive phthisis. It is the best criterion of the activity of progress. There is no constant proportionate relation between the amount of the pulmonary affection, as shown by the local symptoms and the signs, and the elevation of temperature. Nor does the degree of fever correspond always with the acceleration of the pulse. Diurnal exacerbations of fever, with more or less profuse sweating, are evidences that the disease is progressive. Both fever and the rapid action of the heart not only have symptomatic significance, but they contribute to progressive exhaustion.

Impaired power of digestion and anorexia are bad prognostics. Especially bad is a degree of anorexia in which not only no desire for food is felt, but it is so loathed as to render adequate alimentation impossible. Diarrhoea, although not dependent on tuberculous disease of the intestine, is a bad prognostic, as denoting impairment of the digestive processes. Notable pallor, whether an effect of deficient alimentation or referable to the hæmatopoietic system, weighs heavily against the expectation of improvement. A considerable emaciation has even greater weight. Whenever in the progress of the disease the patient becomes notably pale and emaciated, there is little ground for hope, especially if there be conjoined muscular debility, a rapid pulse, and a high temperature. It is unnecessary to attempt a clinical picture of the {423} disease as it is presented toward the close of life. The reality is unhappily too familiar to every observer.

The picture just referred to has another side. The disease is not always progressive. There is reason to believe that its progress is sometimes arrested. It ceases to progress in some cases from self-limitation. In a certain proportion of cases recovery takes place. What, then, is the basis for a favorable prognosis? In general terms, it is the absence of the unfavorable prognostics which have been mentioned. The prognosis is favorable in proportion as the action of the heart is but little disturbed, the temperature of the body non-febrile, the appetite and digestion but little affected, the complexion not much changed, and the nutrition of the body fairly maintained. The inference under these circumstances is that the disease does not tend to progress, and that the existing pulmonary affection is well tolerated. The ground for encouragement is greater the less in amount the pulmonary affection; but even if the symptoms and signs show the latter to be considerable or even large, encouragement is warrantable so long as there is evidence of non-progression and tolerance. It is not, however, to be forgotten that there is always more or less danger of a renewed tuberculous eruption.

The suspension of menstruation belongs among the unfavorable events, but alone it has not great significance. Its occurrence as respects the previous duration of the disease varies much in different cases. In some cases menstruation continues nearly to the close of life. The return of menstruation after its suspension for a greater or less period is a favorable prognostic.

The occurrence of certain complications is of marked importance with reference to the prognosis. Perforation of lung followed by pleurisy and pneumothorax is in most instances speedily fatal. On the other hand, simple pleurisy with effusion, in some instances at least, seems to have a favorable effect upon the pulmonary affection. Tuberculous ulcerations of the intestine preclude the expectation of improvement and hasten the fatal termination. Tuberculous peritonitis is a fatal prognostic. Chronic laryngitis, if it interfere with alimentation, is a serious complication, but if that effect be wanting it is not unfavorable as regards its significance in prognosis. Perineal fistula is not unfavorable, to say the least. Renal disease, and any accidental complication sufficient in itself to tell more or less against the powers of life, must be regarded as telling proportionately upon the prognosis.

What influence has the evidence of a congenital tendency and heredity upon the prognosis? It is commonly believed that the chances of arrest and recovery are less in proportion to this evidence. There is doubtless truth in this belief, but it has sometimes too much weight in the minds of both patients and physicians in individual cases. The disease is by no means always progressive even when the antecedents of the patient afford the strongest evidence of an innate predisposition. The following instance is given by way of illustration: In 1861 a young woman, eighteen years of age, affected with phthisis, came under my care. The disease had existed for two years, and she had tried various climates--namely, Cuba, Florida, Minnesota, Kentucky, and Ohio. The case ended fatally in 1863. The mother of this patient and two sisters had died of tuberculous disease. The father was tuberculous at the time of her death, and he died soon afterward with an intestinal complication. There remained two sisters and two brothers. The elder of the brothers, aged seventeen, was attacked in 1861 and died in 1863. The climate of Minnesota was resorted to in this case with no benefit. The younger brother, aged sixteen, in 1861 had a dry cough, which after a short time ceased, and he became apparently well and robust. The physical signs at that time showed a small tuberculous affection at the summit of the left lung. In the winter of 1863 the cough returned, and the signs now showed a tuberculous affection of the summit of the right lung. He was immediately {424} sent to Europe, and he passed the winter and spring at Nice. He returned and went to South America in 1864. He passed the winter of 1865-66 in New Orleans and France, making the voyage in sailing ships. He passed the winter of 1866-67 in St. Paul, and died in the following spring. Of the two remaining sisters, the previous history in the case of the elder, aged thirty, seemed to warrant a retrospective diagnosis of a small phthisical affection which had ceased to progress and from which she had recovered. There were slight dulness of the summit of the chest on the left side and broncho-vesicular respiration. This one of the sisters has been well for the twenty-three years which have elapsed since the date of the supposed phthisical affection. The younger of the two sisters at the age of twenty-two had a cough with small expectoration and a moderate bronchial hemorrhage in the winter of 1862. There was abnormal dulness on percussion at the summit of the chest on the right side, with weakened respiratory murmur, some crepitation, and increase of vocal resonance. After a few weeks the pulmonary symptoms ceased. In this case there was no treatment, medicinal nor hygienic; she had passed the winters in the city and summers at attractive places of resort, entering with zest into social enjoyments, and she has been in all respects well up to the time when I last saw her, in the spring of 1881, twenty years after the phthisical disease.[22]

[Footnote 22: Since that date a recurrence of the affection has taken place, but without being progressive.]

The last two cases are instances of recovery from phthisis irrespective of any medicinal or hygienic agencies; that is, a recovery by self-limitation. Considering the evidence of a family predisposition, a favorable prognosis at the outset would hardly have been justifiable. From my records of cases other instances might be selected illustrative of the caution not to allow too much weight in the prognosis, in individual cases, to the evidence of an innate predisposition.

It might be supposed, from the greater liability to phthisis between the ages of twenty and thirty years, that its occurrence at this period of life affects unfavorably the prognosis. Facts, however, do not appear to sustain this supposition. So far as the ratio of recoveries bears upon the point, the study of a limited number of cases shows it to be not larger after than before the age of thirty.[23]

[Footnote 23: Vide _Phthisis, in a Series of Clinical Studies_.]

The liability to a recurrence of the disease after recovery is important to be considered in connection with the prognosis. Of 44 cases of recovery among those which I have recorded and analyzed, recurrence had taken place in 6 up to the time of the analysis. In one of these 6 cases the disease had recurred twice. The patient recovered from the second recurrence, and is now well, more than ten years having elapsed. In all the other cases the recurrence proved fatal. The recurrence took place after periods ranging from one and a half to over six years from the date of the recovery. So far as these cases warrant a conclusion, it is that in cases of recurrent phthisis the prognosis is very unfavorable. This conclusion might be materially modified by the study of a large number of cases. The fact that after recovery there is considerable liability to a recurrence of the disease has an obvious bearing upon the prophylactic management.

Facts pertaining to the duration of phthisis come properly under the head of prognosis. Of 44 cases of recovery which I have recorded and studied, the duration varied from six months to ten years. In more than one-half of these cases the pulmonary affection was small; in 4 cases it was moderate in amount; in 10 cases it was considerable; and in 1 case it was large and advanced.[24] These facts show that the prospect of recovery is much better {425} when the tuberculous affection is small or moderate, but that a considerable and large affection does not preclude recovery.

[Footnote 24: Vide _Phthisis, in a Series of Clinical Studies_, for abstracts of the histories of these cases. Absence of all pulmonary symptoms was known to have existed in the different cases for periods between six months and twenty-seven years. Throwing out two cases in which the period was six months, and one case in which it was eight months, the average period was six years.]

Next to recovery, the course of the disease is favorable when it ceases to be progressive and life with fair health is continued for a long period. Out of the cases which I have analyzed, there were 28 in which the disease was known to have existed for periods ranging from one year and three months to twenty-five years. The duration was reckoned up to the time of the analysis or of the last information obtained. The number of years noted does not express the duration of life. The average period during which the disease was known to have been non-progressive is a fraction over eight years. The histories in these cases exemplify the fact that phthisis, when it ceases to be progressive, although recovery does not take place, is not incompatible with fair and even good general health and long life. That recovery does not take place is owing to the persistence of pulmonary lesions, such as cavities which do not cicatrize or an interstitial pneumonia with dilatation of bronchial tubes. The tuberculous disease no longer continues, but the local effects of the disease remain. Slowness of progress and prolonged tolerance are to be hoped for when the disease neither ends in recovery nor becomes non-progressive. In some cases the disease ends fatally, having existed for many years where at no time could it be said that its progress had ceased. The prolongation of life under these circumstances depends on the slowness with which the disease progresses and the ability of the system to tolerate it.

The extremes of the duration of the disease in a large collection of fatal cases are so far apart that the average period is of little practical value as bearing on the prognosis in individual cases. In the collection of recorded cases which I have studied analytically, there were 112 the duration of which from the commencement of the disease to its fatal termination was ascertained. The mean duration was about twenty-three months. Laennec found the average duration twenty-four months; Louis and Bayle, twenty-three months; Andral, twenty-four months; Sir James Clark, thirty-six months; and Williams of London, forty-eight months.

TREATMENT.--The author premises the consideration of the treatment by stating that this article was written before sufficient time had elapsed after the publication of the researches by Koch for their confirmation by other competent observers. At the present time (May, 1885) the doctrine that phthisis depends on the presence of a special micro-organism is to be considered as probably established. The grounds for this statement have been presented under the head of the Etiology, and reference to the practical bearings of the doctrine have been introduced in connection with the Diagnosis and Prognosis. It is evident that the doctrine is likely to have important bearings on the treatment. If it be true that the origin, the extension, and the diffusion of the disease within the body require the presence and the multiplication of a particular parasite, it is evidently a rational object of treatment to effect its destruction. For this object an efficient parasiticide is to be sought after, to be administered either by inhalation or by its introduction into the blood-vessels. Already, within the short time which has elapsed since Koch's discovery, extended observations have been made with various substances which are destructive to bacteria outside of the body, but thus far without success. A difficulty as regards inhalation is in the way of a destructive agent in the form of either an impalpable powder or a vapor or a gas reaching the colonies of bacilli in sufficient quantity to effect the object, without doing injury to the tissues or inducing toxæmia. As regards the introduction of {426} parasiticides into the blood, it seems hardly probable that a toxic agent can be safely introduced in sufficient quantity to effect the object. It remains to be determined by clinical observation whether or not these difficulties are insuperable.

Efforts to destroy the parasite in another direction promise to be more effectual--namely, by the removal of the co-operating conditions on which their multiplication depends. It is to be borne in mind that the development and continuance of phthisis involves two factors, one which is the presence of the parasite, and the other the existence of those unknown conditions constituting the tuberculous predisposition or cachexia. The removal of the latter may effect the destruction of the parasite indirectly, but not less certainly than by bringing into direct contact with it a destructive agent. It is in this indirect way that the measures of treatment which experience has shown to be more or less effective may be supposed to operate. And it is to be added that those measures of treatment the usefulness of which rests on clinical observation are in no wise disproved or modified by the parasitic doctrine. At the present time the treatment of the disease is to be governed by principles which, based on reason and experience, are independent of that doctrine.

The intrinsic tendency of phthisis to be either progressive or non-progressive underlies the treatment. In a certain proportion of cases the disease tends to advance steadily and actively, as shown by the symptoms and the physical signs. In these cases treatment cannot be expected to do more than to palliate symptoms, and perhaps prolong the duration of life. These are cases of so-called galloping consumption. In a larger proportion of cases the disease does not steadily or actively advance. Remissions occur. The pulmonary affection increases, and extends by successive tuberculous invasions or eruptions after intervals variable in duration. These cases offer more encouragement for treatment. There is room to hope after each invasion that another will not take place, and that the affection which exists may be tolerated indefinitely if the cases do not end in recovery. In a minority of cases when a certain amount of pulmonary affection has taken place there is no further increase or extension. In this respect the disease ceases to progress. In some of these cases after the lapse of weeks or months all pulmonary symptoms disappear, and the patient may be said to have recovered. The probabilities of the recovery and the time required therefor vary, other things being equal, according to the amount of the pulmonary affection. In other cases recovery does not take place. More or less of pulmonary symptoms remain. The existing lesions which these symptoms represent, however, may be well tolerated, and their existence may not interfere with fair or even good general health and long life.

Whenever the disease ceases to be progressive, with or without recovery, an intrinsic tendency has more or less agency in the cessation of progress. In some instances it is certain that this result is wholly due to self-limitation. Expressing the fact in other language than that of personification, the disease may become non-progressive because the unknown, special, constitutional morbid conditions which it is customary to embrace under the name tuberculous cachexia no longer exist; or, assuming that a particular parasite is essential to the progress of the disease, this organism may cease to multiply in consequence of the non-continuance of conditions which are necessary for its multiplication. Whatever be the explanation of the tendency of the disease--to be, on the one hand, progressive, or, on the other hand, non-progressive--it must be taken into account in estimating the influence of measures of treatment. How largely an intrinsic tendency to be non-progressive is accountable for apparent success in treatment cannot be determined with precision. The evidence of its agency can only be derived from the accumulation of cases of non-progressive phthisis in which no active measures of treatment were pursued. Reference has been made to a few such cases {427} among those which I recorded during a period of thirty-four years. Some cases in addition have come under my observation since the analysis of my cases recorded up to 1875. It is evident that a large collection of such cases cannot be made by a single observer.

From what has been stated, it follows that the treatment in case of phthisis has reference especially to the constitutional conditions which stand in a proximate causative relation to the pulmonary affection. The chief objects are to arrest the disease and to keep the cachexia in abeyance. In the present state of our knowledge measures of treatment addressed directly to the pulmonary affection, albeit important, are of secondary importance when compared with those which either co-operate with or oppose the underlying intrinsic tendency of the disease as manifested in individual cases.

Proceeding to consider the treatment in cases of phthisis, a convenient division of topics is into those relating to the climatic treatment, the dietetic and regiminal treatment, and the medicinal treatment.

Climatic Treatment.--It would be impossible within the limits of this article to enter into a discussion of the various questions connected with climatic influences or to consider the relative advantages of different climates. Nor, were it possible, would this be desirable as regarded from a practical standpoint. I shall confine myself to the general considerations which bear upon the climatic treatment.[25]

[Footnote 25: For an account of the characteristics of different places of resort in different countries, and a full consideration of the subject of climate in relation to phthisis and other diseases, the reader is referred to the article entitled "Klimatstherapie" by H. Weber of London in _Handbuch der Allgemeinen Therapie_, von H. v. Ziemssen, Zweiter Band, Leipzig, 1880.]

In the analytical study of the cases of phthisis I had recorded up to the year 1875, I endeavored to draw some conclusions respecting climatic treatment from the facts contained in the histories. Temporary changes of climate entered into the treatment in 74 cases. The histories were interrogated with reference to the number of cases in which recovery took place, the number in which the disease ceased to be progressive without recovery, and the number in which the disease progressed slowly, with reference to the apparent influence exerted by climate. The changes of climate in the 74 cases were various. In a considerable number the patients traveled in Europe, visiting different places. The foreign resorts in which they sojourned for greater or less periods were Nice, Algiers, Mentone, Egypt, Nassau, Lima, Rio Janeiro, Cuba, and the West India islands. In this country the different resorts were in Minnesota, California, New Mexico, Florida, Georgia, South Carolina, Louisiana, Virginia, Kentucky, the District of Columbia, Michigan, and the Adirondacks. Colorado as a place of resort had not excited much attention prior to my making abstracts of my histories for analytical study, and for this reason it does not appear in the foregoing list. I have notes of not a few cases in which the latter climate was resorted to. It is at once evident that 74 cases distributed over so many places of resort cannot furnish adequate data for judging of the relative advantages of different climates. Nevertheless, the analysis of these cases led to an important conclusion as respects, in general, the usefulness of a temporary change of climate. Of the 74 cases, 9 ended in recovery, 13 were in the list of cases of arrested or non-progressive phthisis, and 5 were in the list of cases in which the disease was slowly progressive. In 33 cases the disease ended fatally, and in 14 cases neither the duration nor the termination of the disease appears in the histories. Moreover, of the 33 fatal cases, in 23 the histories afforded evidence of more or less benefit from the changes of climate.[26] From these facts it seemed warrantable to deduce, as a positive conclusion, that in a considerable proportion of cases a {428} change of climate has a favorable influence on phthisis. It follows also, as a corollary, that a favorable influence is exerted by a variety of climates. Indeed, it would seem, judging from these facts, that the favorable influence pertains to the change rather than to the particular climate selected. If this be true, it follows that the agencies by which a favorable influence is exerted relate to accessory or incidental circumstances more than to purely climatic conditions.

[Footnote 26: For further details vide _Phthisis, in a Series of Clinical Studies_.]

It is an absurd supposition that any climate exerts a specific influence in arresting phthisis. This statement is not in the least inconsistent with the fact that certain climatic conditions are much more favorable than others for an arrest of the disease. Dryness, equability, and purity of the atmosphere are essential elements of a favorable climate. Within late years a high altitude (4000 to 8000 feet above the ocean-level) has been deemed by many of much importance. Aside from the purity of the air incident thereto, the rarefaction is supposed to have a salutary effect by increasing the expansion of the lungs.[27] Few at the present time regard a tropical temperature as advantageous. The choice is usually regarded as lying between a cold and a warm climate, each having favorable elements aside from temperature. There is abundant testimony in behalf of each. Circumstances pertaining to cases individually must determine which to choose. A patient who in health has found cold weather more favorable to vigor and well-being than warm weather will be likely to find a cold climate more beneficial than a warm climate, and vice versâ. In order to derive benefit from a cold climate a patient must have preserved sufficient vigor to endure out-of-door life in such a climate. Confinement much of the time within doors must deprive patients of the benefit to be hoped for from a cold climate. For obvious reasons a cold climate is better suited to men than to women. With reference to the superior excellence of particular health-resorts, caution is to be exercised in weighing not only testimony either for or against their superiority, but the value of reported cases. Putting aside the chances of error in diagnosis, it is to be considered that among those who elect a particular place of resort an arrest of the disease or improvement to a greater or less extent would probably have taken place had any one of many places been selected, and perhaps if no change had been made. On the other hand, in a certain proportion of cases the disease will be progressive anywhere. A limited number of cases must not be relied upon to establish the relative advantages of particular places, especially if there be not data enough to judge of the condition of the patient in each case as regards the amount of the pulmonary affection, the temperature, pulse, and other symptoms. A few cases which have been selected to illustrate either the favorable or unfavorable influence of a particular climate are not entitled to any weight in the formation of an opinion. To gather clinical facts sufficient to determine by analytical study the actual advantage severally of different climates is a work attended by so many difficulties that it must be long before it can be accomplished. Meanwhile, in discriminating between different places of resort the physician is to be governed by rational considerations. In reality, custom and fashion have much to do in this matter. Places which were formerly in vogue as health-resorts have now fallen into disrepute. It is almost inevitable that sooner or {429} later this will be the fate of any place which becomes so popular as to attract very largely phthisical patients, owing to the aggregation of the instances in which no benefit could have been expected from climatic treatment.

[Footnote 27: On this topic the reader is referred to an article by C. Theodore Williams, entitled "The Treatment of Phthisis by Residence at High Altitudes," in the _Transactions of the International Medical Congress_, London, 1881; also to a work entitled _Rocky Mountain Health-Resorts, an Analytical Study of High Altitudes in Relation to the Arrest of Chronic Pulmonary Disease_, by Charles Denison, M.D., 2d ed., 1880.

There is much reason in the suggestion that the immunity from phthisis in situations which are sparsely settled may be due not so much to climatic influences as to the fact that these situations are free from non-climatic causes contributing to the prevalence of the disease--namely, in-door occupations, overcrowded dwellings, etc.]

There is reason to believe that the benefit derived from climatic treatment is often in a great measure due to accessory circumstances. As already intimated, this seems to be a fair inference from the number of instances of arrest of the disease, of cessation of its progress, and of notable improvement in a collection of cases in which many and varied climates had been resorted to. Under the name accessory are embraced a variety of circumstances--in fact, everything not pertaining purely to climatic agencies. The opportunity of living in the open air and freedom from the cares of business, together with relaxation and mental diversion, are in the category of accessory circumstances. These contribute largely in some cases to the benefit derived from change of climate. Patients at a health-resort are apt to carry out hygienic regulations more faithfully than when at home. In contrast to the accessory circumstances which are favorable there are those which have an unfavorable effect, such as home-sickness, ennui from lack of usual occupations, anxiety lest affairs should suffer for want of personal supervision, interruption of fixed habits, and the want of home comforts. These in some cases may go far toward counteracting the benefit from climatic influences.

All these accessory circumstances, as bearing upon individual cases, are to be taken into account in deciding the question as to the importance of climatic treatment. Of course a change of climate is important, other things being equal, in proportion as the climate in which the patient resides is humid, variable, and the atmosphere impure. So far as purely climatic influences are concerned, it may be important only that the patient escape the more trying seasons of the year--namely, the spring and the hot summer months. A malarial climate should certainly be exchanged, if practicable, for another during the season when there is danger of being infected with the malarial miasm. To avoid this cause of disease, as well as the changes of temperature, etc. incident to the spring and summer months, it may not be necessary to go very far from home. It is probably better not to go to a distant climate for a few weeks, in order that the double acclimatation caused by going and returning within such a brief period may be avoided.

It is of essential importance to take fully into account the condition of the patient as regards the pulmonary affection and the general symptoms before advising or sanctioning a change of climate which involves long journeys and separation at a distance from home and friends. There is more reason to expect benefit from a change the stronger the evidence against an intrinsic tendency of the disease to progress actively. Whenever the temperature and circulation denote activity of progress the propriety of a change is doubtful. Whenever there is great emaciation with muscular feebleness there is little ground to expect material benefit from any climate. The experiment is allowable at an advanced period of the disease only with a view to satisfy the wishes of the patient and the friends, having a full understanding with the latter in respect of the danger of dying away from home. It should be added that sometimes in cases which offer no ground for the expectation of any essential benefit journeys or voyages are well borne, and life is apparently prolonged by a change from an inclement to a genial climate.

Distance is a point to be considered in the selection of places of resort. It is often an objection to crossing the ocean that communication with relatives or friends is attended with delay and difficulty. The voyages, as a rule, are not objectionable. Our own country embraces almost every possible variety of climate, and therefore, so far as purely climatic influences are concerned, it is not necessary to resort to foreign countries. The latter, however, have for many the advantage of being made more attractive by novelty and {430} historical associations. Moreover, there are often better arrangements for comfort and enjoyment. The accessory advantages are always to be considered with reference to the particular tastes and needs in individual cases. Good food in abundance and well cooked, large and well-ventilated rooms, facilities for walking, riding, and driving, opportunities for hunting, fishing, and other out-of-door sports, ample provisions for in-door exercise in bowling, etc., agreeable society,--these are among the accessory advantages without which often the best climatic influences will prove inoperative. To these is to be added available judicious medical advice.[28]

[Footnote 28: For details concerning the health-resorts of the Riviera, Hyères, Cannes, Nice, Mentone, and others which are much esteemed in Europe, the reader is referred to a work entitled _The Riviera_, by Edward I. Sparks, London, 1879.]

A mistake often made by those who find benefit from a change of climate is to continue the change for too short a period. The benefit speedily obtained may be speedily lost when the patient is again placed under the climatic and other circumstances attending the development of the disease. It is to be borne in mind that the benefit from a change of climate does not depend on any special remedial agency, but on a combination of favorable circumstances, and that the salutary influences connected with climate are exerted not so much directly upon the lungs as upon the general system. It follows that the beneficial effect may be manifested more by increase of appetite, better digestion, greater endurance of muscular exercise, and especially gain in weight, than by immediate improvement in the pulmonary symptoms. Many patients cannot afford the loss of time and the expense of lengthened absence, and therefore are unable to make trial of change of climate. These may be consoled by the fact that not a few cases of phthisis do well without any climatic treatment. In some of the most striking of the instances of arrest of the disease which have come under my observation change of climate did not enter into the treatment. Important as is this fact, it does not conflict with the belief that additional chances of arrest and the prospect of more or less improvement are often secured by climatic treatment. It is a wise precaution for patients to reside permanently in a climate in which an arrest of the disease has taken place. Of course this is not always practicable. Its importance is attested by reason and experience, and it is the duty of the physician, according to his discretion, to suggest it. The many obstacles which are often in the way of its adoption are sufficiently obvious.

Sanitaria for phthisical patients at health-resorts are doubtless serviceable in many cases, because hygienic measures are enforced which would not under other circumstances be thoroughly carried out. An offset to this advantage is the depressing effect upon some minds of association with other patients. Owing to this moral effect it is sometimes judicious to advise patients not to go to places which, for the nonce, are especially popular, in order that they may not have before their eyes cases exemplifying all the phases of the disease, and be led to talk over symptoms with other patients affected with phthisis. As regards sanitaria, those in which the chief object is to enforce measures of hygiene are perhaps most likely to be serviceable. If these measures be secondary to some system of medication, there is room for distrust.

It is hardly necessary to say that the treatment of patients in such institutions should be under the charge of competent physicians who have not originated or adopted any peculiar notions respecting the pathology and therapeutics of the disease. As a matter of course, there cannot and should not be any restriction in either originating or adopting ideas and methods of practice, however much they may be at variance with commonly-received opinions; but a physician who appreciates his obligation to his patients will hardly feel willing that they should be made subjects for testing pathological and therapeutical novelties in behalf of which his own belief is not committed.

{431} Dietetic and Regiminal Treatment.--The dietetic treatment resolves itself into a few simple principles. It may be assumed that as much assimilation of aliment as is possible is desirable. No one probably will contend for the propriety of any restriction of diet with a view to limiting the amount of the nutritive constituents of the blood. The difficulty in this part of the treatment lies in the impairment or loss of appetite and in lack of digestive or assimilative ability. It is useless to consider whether such or such articles of food are suitable or not for phthisical patients. All wholesome articles which can be taken with any relish and digested are suitable. Nothing could be more ill advised than to direct kinds of nutriment which a patient does not like, and to enjoin avoidance of those which the patient's appetite would dictate. Pains should be taken to ascertain the articles of diet most acceptable or against which there is the least repugnance, and to excite the appetite by variety and culinary attractions. It is important not to judge too hastily of the ability to digest the food which can be ingested. The evidences of indigestion are nausea, vomiting, flatulence, acidity, and diarrhoea: whenever these symptoms are wanting it is fair to assume digestive ability. Nor should evidence of indigestion deter at once from continuing articles which appear to have occasioned it. The processes of digestion are so apt to be disturbed by extrinsic accidental circumstances that a meal which will occasion indigestion to-day may not do so to-morrow. In short, so far as regulation of the diet is concerned the patient is to be encouraged to take all kinds of wholesome food according to appetite and taste, giving to each and all a fair trial as regards digestibility. Fully aware that these views may not commend themselves to the approval of many who think that the diet should be regulated on scientific principles rather than by the instincts of the patient, I do not any the less adhere to them, believing that they are based on experience and common sense. As regards the liability, where the instincts are followed, to the over-ingestion of food and to the ingestion of food indigestible from its quality or modes of preparation, it is far better to incur whatever inconvenience may therefrom arise than the evils of inadequate nourishment. In short, the dietetic instructions to a phthisical patient may be summed up as follows: Eat of wholesome articles of food whatever the appetite may dictate; endeavor to maintain and develop appetite and relish for food by the excitement of variety in kind and in preparation; eat whenever hungry; satisfy the appetite; eat without any expectation of harm; do not hastily attribute an indigestion to any particular articles of diet; incur the risk of over-feeding rather than of the greater evil of under-feeding.

Anorexia in a degree which I have characterized as invincible--that is, an almost complete inability to take food--is one of the most discouraging of symptoms in cases of phthisis. Of course if the symptom continue the duration of life is simply a question of time and tolerance. Milk is an invaluable form of food when appetite is completely lost. The advantage sometimes of substituting for simple cow's milk buttermilk, koumiss, or milk made sour by fermentation with yeast is due wholly to these being taken more readily and more easily digested. The same is true of the substitution for the milk of the cow that of other animals--the goat, the ass, and the mare. Eggs may be given in a liquid form with milk or other fluids. Very little reliance is to be placed on the various meat-extracts (Liebig's, Valentine's, and others) as representing any considerable amount of nutriment. Meats artificially digested--that is, in the form of peptones, as in Leube's meat solution--form a valuable addition to beef-tea. Rectal alimentation may be resorted to. A. H. Smith has reported marked benefit from defibrinated blood as a form of rectal diet.[29] A French writer, Debove, has lately reported notable benefit from forced alimentation, food being injected through a tube introduced into {432} the stomach.[30] If in any way food can be introduced, in spite of the anorexia, and assimilated, there may be room to hope that a return of appetite will be among the beneficial effects. Cod-liver oil and alcoholics will be considered in connection with the medicinal treatment.

[Footnote 29: Vide _N.Y. Med. Record_, 1881, No. xix.]

[Footnote 30: Vide _Bullétin générale Report_, Paris, 1881. Another French writer more recently in the same journal, Desnos, has pointed out a source of danger in forced alimentation--namely, the occurrence of violent acts of vomiting, during which portions of food ejected from the stomach are inhaled. The danger is from asphyxia and pneumonic inflammation excited by the presence of particles of food within the smaller bronchi. In order to avoid this source of danger, food should be introduced slowly and not in too large a quantity at a time. Intolerance of the presence of the tube within the stomach is an obstacle which may be overcome by use, but in some cases it is insuperable (vide article in _Philadelphia Med. Times_, March, 1882).]

The regiminal treatment embraces changes relating to out-of-door life, exercise, occupation, clothing, etc.

Of all the changes in this category, those relating to out-of-door life and exercise are of greatest importance. In-door life and sedentary habits, if not factors in an acquired cachexia, undoubtedly favor it. This is shown by the place which these hold in the etiology and by their agency in the arrest of the disease. With respect to the latter point, the result of my analysis of recorded cases has much significance. In 44 cases change of habits from those more or less sedentary and confining within doors to those involving out-of-door life and activity entered into the treatment. In all but 4 of these cases the hygienic treatment consisted chiefly or exclusively of the change of habits mentioned. Of the 4 excepted cases, in 1 the patient passed several months in Europe; in 1 the patient passed a summer in Minnesota; in 1 the patient made several voyages to Europe; and in 1 the patient travelled in Europe. Of these 44 cases, 15 are in the list of cases of unknown duration and termination. Deducting these, the remaining number is 29. Now, of these 29 cases, 11 are in the list of cases ending in recovery; 7 are in the list of cases in which the disease was arrested or became non-progressive; and 3 are in the list of cases of slowly-progressive phthisis. Thus, only 8 out of the 29 cases were not included among those in which the course of the disease was favorable in the three aspects just named, and in more than one-third of the cases recovery took place. Of the 8 fatal cases, in all save 1 case the change of habits appeared to be beneficial. The benefit was marked in 2 of the cases, there being in 1 of them no evidence of progress of the disease for several months.[31] Moreover, the majority of the histories of the 15 cases of uncertain duration and termination show more or less improvement. In 7 of the 11 cases ending in recovery the change in habits constituted all the treatment. Making the fullest allowances for an intrinsic tendency in the disease to end in recovery, and in some instances purely from self-limitation, the foregoing facts afford ample proof that changes of habits from those more or less sedentary and confining within doors to those involving out-of-door life and activity have considerable agency in the arrest of phthisis and exert a favorable influence upon the disease when it is not arrested. There is reason to believe that the favorable influence is greater than any other class of hygienic measures, and it is probable that to this source much of the benefit derived from change of climate is to be referred.

[Footnote 31: For details of the changes of habits in these cases vide _Phthisis, in a Series of Clinical Studies_.]

The particular changes to be made in order to secure as much out-of-door life as practicable with a certain amount of exercise must of course vary in different cases. Clerks, school-teachers, mechanics whose business requires in-door life, etc., should, if possible, adopt some other occupation securing the desired objects. Students, clergymen, and men of leisure should systematically devote a fair proportion of time to exercise in the open air, and as far as {433} practicable the exercise should involve recreation. It is needless to say that the importance of change is as applicable to women as to men. Caution is sometimes necessary not to carry muscular exercise to an injurious extreme. If carried to the extent of producing great fatigue or exhaustion, it is debilitating instead of invigorating. Exercise within doors, although much less useful than when taken in the open air, is nevertheless useful. Gymnastic exercises may be recommended when other measures which are to be preferred are not available. They are inferior to rowing, horseback riding, hunting, etc. An increased expansion of the chest is apparently a desirable effect of exercise. Forced efforts of expiration to overcome a mechanical resistance, the lungs being fully inflated, constituted a method of treatment formerly in vogue, and I have met with instances in which it seemed to have been useful. In taking exercise patients are apt to imagine that in order to avoid catching cold they should go out of doors only when the weather is in all respects favorable. Precautions in this regard are often carried so far as to interfere materially with the amount of life in the open air which is desirable. It should be understood that phthisical patients are no more--and perhaps less--liable to catch cold than persons in health, and that a cold, as a rule, does not affect the progress of the tuberculous disease. These excessive precautions have arisen from the error of considering phthisis as a sequel of bronchitis. There is no ground for the great scrupulousness with which phthisical patients avoid the night air, although out-of-door life in the daytime is to be preferred.

Every practitioner has known of cases in which some remarkable changes of habits as regards out-of-door life and exercise have led to recovery, such as performing long journeys on horseback or on foot, accompanying expeditions which involved camping in the open air with hardships, etc. Several instances of this kind have come within my knowledge. In one of these the patient, a young physician who consulted me, on being told that he had incipient phthisis gave up his practice and joined a tribe of Indians in the Far West. He remained with them for more than a year, adopting all their customs, and returned in vigorous health. But in order to rough it a patient need not go to a distance from home and friends. This fact is lost sight of when physicians sanction the exposures and hardships of travel without the limits of civilization, but enjoin upon patients great care in taking exercise out-of-doors so long as they remain in their places of residence.

All who have had the opportunity of observing the effect of sea-voyages in cases of phthisis are agreed as to their utility. A long sea-voyage or a series of voyages entered prominently into the treatment of 20 of the cases which I have analyzed. In a large proportion of these cases the favorable influence was marked. This is an accessory circumstance which contributes to the benefit in many cases derived from a change of climate. It is evident that a certain proportion only of phthisical patients can avail themselves of this measure. It is to be advised especially for those who can leave home and business without anxiety, who are fond of ocean-life, and who as a matter of course are good sailors.

The supposed liability to, and danger of, catching cold often leads phthisical patients to wear an overplus of clothing. When they strip for an examination of the chest not infrequently they remove two or three undershirts, a woollen or fur chest-protector, and sometimes in addition an oiled-silk jacket. The body is kept in constant perspiration by these articles. They occasion not only discomfort, but debility. A single word expresses the governing principle in clothing--namely, comfort. Articles of dress should be so adapted to the seasons and to changes of temperature as to secure comfort. This maxim applies to persons affected with phthisis as well as to those in health. In some instances, from an erroneous theoretical notion, patients {434} make themselves uncomfortable in an opposite way. They dispense with woollen or silk underwear throughout cold seasons with the idea that the system is thereby hardened. A good non-conductor of heat next to the surface protects against changes of temperature and promotes the functions of the skin. Attention to the sense of comfort will enable the patient to avoid error in this direction as well as an overplus of clothing.

Other regiminal observances relate to ventilation and the sponge bath. The apartment in which the patient is expected to pass at least one-third of the twenty-four hours should be sufficiently large and well ventilated. Fresh, cool air in abundance is not deleterious, as it would seem to be regarded when the utmost care is taken to exclude it. It is essential to healthful sleep and invigoration. Here, again, the supposed danger of catching cold antagonizes hygienic treatment. Air should have free access to sleeping apartments in cases of disease as in health. As a measure for invigoration the sponge bath is often useful in cases of phthisis. The water used may be cool or tepid according to the sensations of the patient and the effect. It should be followed by a glow with a feeling of invigoration. The water may with advantage be made stimulating by the addition of salt or of alcohol.

Medicinal Treatment.--The medicinal treatment in cases of phthisis embraces no known remedies having a special influence over the disease; in other words, no drug has as yet been found to be an antidote to the tuberculous cachexia. Nevertheless, medicines in many cases form an important part of the treatment. They have for their objects improvement of appetite, digestion, assimilation, and nutrition, relief from complications or associated affections, and the palliation of symptoms.

Cod-liver oil is considered in this article, as is customary, in connection with the medicinal treatment. It has, however, little or no claim to be regarded as a medicine. It is a nutrient. It is a form of fat which patients often digest readily, and which evidently increases the weight of the body. That it does more than simply increase the amount of fat in the body is shown by the fact that frequently under its use the appetite, the digestion, the condition of the blood, and the nutrition of the tissues manifest improvement. These effects are not inconsistent with the statement that it is simply an article of diet. Although the claims in its behalf as a special remedy which were made forty years ago have long since been disproved, clinical experience has continued to furnish proof of its usefulness in the treatment of cases of phthisis. It should enter into the treatment wherever it is well tolerated and digested. If it occasion nausea or diminish the appetite or give rise to eructations, its use should not be persisted in. In the choice among the different varieties of the oil experience in each case is to be the guide. Some patients find the brown varieties more acceptable than the pale, and vice versâ. I have known in several instances the unrefined, coarse oil obtained at the fish-markets to be preferred. Patients should not give up this part of the treatment until the different varieties have been tried. The popular preparations in which the oil is combined with salts of lime or with some flavoring extract are sometimes tolerated by those who are, or who fancy that they are, unable to tolerate the pure oil. They have probably no advantage for those who are able or who are willing to take the pure oil. The oil should never be given in doses larger than are readily digested, and, following this rule, the doses will rarely exceed half an ounce. They are best given shortly after meals. It is a popular notion that the oil should not be continued in hot weather. The weather should have no influence on its continuance, provided it be well tolerated and digested. The addition of fifteen minims of ether to a half-ounce dose of the oil has been found to promote its digestion, and by means of this addition persons with whom the oil disagrees may be able to take it without difficulty. The ether is to be given {435} half an hour after the oil has been taken.[32] Salad oil, cream, butter, and the extracts of malt may be made to supply, in a measure, the place of the cod-liver oil in the cases in which the latter is not tolerated.

[Footnote 32: Vide report by Dr. Andrew H. Smith, chairman of Committee on Restoratives of the New York Therapeutical Society in the _N.Y. Medical Journal_, April 20, 1879.]

Embracing the varieties of spirits, wine, and malt liquors under the name alcoholics, these are to be regarded as alimentary, but also as medicines. That they are useful in certain cases of phthisis is as well established on the basis of clinical experience as any fact in practical medicine. Their usefulness in this disease, as well as in other diseases, is to be considered irrespective of questions relating to their use and abuse in health. But as bearing on the very important subject of intemperance it may be stated that, administered purely as remedies in cases of phthisis, patients do not become so addicted to them as to make it difficult to relinquish their use whenever this is advisable. This statement is based on a large experience.

Alcoholics are useful in some and not so in other cases. The question as to their usefulness is to be decided in each case by trial. If they produce a sense of comfort without any excitation of the circulation or of the nervous system, they are likely to be useful. If in lieu of a cordial effect they occasion flushing, weariness, or indisposition to exertion or discomfort of any kind, they are not likely to be useful. The quantity to be given is to be regulated by the immediate effects. There is sometimes a notably increased tolerance of alcohol. This is to be ascertained by experimental observation. The quantity of alcohol given should never occasion the least approach to alcoholic intoxication. It should be given at or near the times of taking food, or in combination with food, as in milk-punch or egg-nog.

As to the choice of an alcoholic, this is to be determined by the past and present experience in each case. Each of the many varieties of spirits, malt liquors, and wines is best suited to some cases and not to other cases. There is no rule of choice applicable to all patients. Changes in the form of alcoholics from time to time are often advisable in the same case. In the majority of cases some forms of spirits will be found best to agree. Malt liquors, either the strong or mild varieties, agree best in some cases. Of wine, some patients take with most comfort the light and some the stronger varieties. The effect upon the pulse, respiration, and other symptoms should be observed with reference to the employment of any of the alcoholics, and of the particular ones best suited in individual cases, but much reliance must be placed on the subjective symptoms. It has been proposed to substitute pure alcohol for any and all the alcoholics used as beverages, in order to give to the treatment more distinctly a medicinal character and to avoid risk of the formation of a habit which may lead to intemperance. Since, however, of the many varieties of alcoholics, some agree in certain cases and not in other cases, it is doubtful whether alcohol is able to take the place of all. This is a point to be decided by clinical observation.

Phosphorus in the form of the hypophosphite of soda and of lime was recommended about forty years ago on the theoretical ground that it favored cell-formation and retarded the rapid waste of the tissues. More recently it has been supposed to have a specific influence over tuberculous disease. It has been employed pretty largely in different countries, but without effects sustaining the claim of having a specific action. It seems to be useful, and many physicians attach considerable importance to its use.

The preparations of iodine, from their evident utility in certain scrofulous affections, and in view of the identity of scrofula and tuberculous affections, have heretofore entered largely into the treatment of cases of phthisis. From the fact that they are now but little employed in phthisical cases it may be {436} inferred that in this instance, as in many other instances, theoretical considerations have failed to find support from clinical experience.

Of arsenic it can be said that many able observers have borne testimony to its great usefulness in some cases, as manifested by improvement in appetite, nutrition, and in the powers of life generally, together with the cough and expectoration. Here, as in other instances in which it is desirable to continue the remedy for a considerable period, the doses should be small and not increased. Noël Guéneau de Mussey testifies to a remarkable efficiency in some cases of the mineral water of Bourbole, either exported or taken at the spring.

Sulphur, especially as contained in the Sulphur Springs water, has long been considered a useful remedy in phthisis as in other chronic diseases. The Sulphur Springs of our country, however, although much resorted to for other diseases, have not in phthisical cases with us the celebrity which those in Europe (of which Des Eaux Bonnes are a famous type) have with European physicians.

The symptomatic indications for medicinal treatment in cases of phthisis are many and varied. Among the most important are those relating to appetite and digestion. For the improvement of these functions the preparations of cinchona, salicin, gentian, quassia, and other of the vegetable bitter tonics, including nux vomica, may be selected, according to the choice of the physician, or given in succession. They have more or less efficiency in conjunction with the more potential hygienic measures considered in connection with the climatic, the dietetic, and the regiminal treatment. Pepsin and dilute hydrochloric acid, taken after a meal, promote its digestion, their medicinal action being, however, limited to the meal in connection with which they are administered. The tincture of the hydrochlorate of iron and other ferruginous tonics which are much used in cases of dyspepsia and indigestion are useful in cases of phthisis. The anæmia which exists so constantly in phthisical cases is an indication for their use, and there does not seem to be ground for the conjecture which has been entertained that they promote the occurrence of bronchial hemorrhage. If they had this effect it would not disprove their utility.

Pulmonary symptoms which may furnish therapeutic indications are cough and expectoration, hæmoptysis, pain in the chest, and dyspnoea. Cough is of course necessary for the removal of the morbid products within the bronchial tubes and cavities. If the act of coughing be accompanied by expectoration, palliation is not required. But often there is what may be called a superfluous cough--that is, not accompanied by expectoration. This superfluous cough may be frequent, and occur in violent paroxysms which occasion fatigue and exhaustion. Frequently the cough prevents sleep. Palliative remedies are then indicated. It is desirable, if possible, to palliate cough with remedies which do not contain an opiate, owing to the impairment of appetite and digestion caused by the latter. Simple remedies, such as the balsam of tolu, the syrup of wild-cherry bark, Turlington's balsam, etc., may suffice. If not, other narcotics than opium should be tried--namely, hyoscyamus, lactucarium, and belladonna. Fothergill recommends hydrobromic acid and the spirits of chloroform. The addition, however, of some form of opiate is often required. The paregoric elixir is the simplest form, and therefore the best if it suffice. Of other forms, perhaps codeia is in general to be preferred. Patients should be enjoined not to prolong voluntarily ineffectual coughing efforts. The disposition to cough may in a considerable degree be controlled by the will until the morbid products are in a situation to be readily expectorated. The stimulant expectorants and those which act by causing nausea are not indicated in cases of phthisis, and are objectionable in so far as they impair appetite and digestion. Stimulating medicinal {437} inhalations are of doubtful propriety, but a superfluous cough is sometimes relieved by breathing some vapor, a little laudanum or paregoric elixir having been added to the water vaporized. The continuous breathing of an atmosphere charged with carbolic acid, either by diffusing it in an apartment or the use of a respirator, is advisable if there be fetor of the expectoration.

It has been seen that bronchial hemorrhage is not, as a rule, an unfavorable event in cases of phthisis. It does not follow from this fact that the loss of blood is desirable, and therefore that the hemorrhage should not be arrested. Moreover, the loss of blood in some instances involves immediate danger. A first attack of hæmoptysis occasions great alarm and anxiety. The prostration which appears is a moral effect rather than the exhaustion caused by the loss of blood. In repeated instances after attacks of hæmoptysis have several times recurred, I have known patients to keep about as usual during an attack, giving little or no heed to it.

The internal remedies which may be employed for the arrest of hemorrhage are: Ergot or ergotin, acetate of lead, tannic or gallic acid, and the astringent preparations of iron. Ergotin has been given with good effect by subcutaneous injection, from five to ten grains in water, with or without glycerin, being injected and repeated pro re nata. Opium in some form should be conjoined in order to allay nervous excitement. A teaspoonful of table-salt taken into the mouth and repeated after intervals of a few moments is a well-known remedy during the hemorrhage. The hemorrhage is sometimes so profuse and rapid that much blood is swallowed, and may be afterward vomited. Under these circumstances, and whenever the persistence of the hæmoptysis calls for more prompt measures, cold may be applied to the part of the chest which corresponds to the seat of the hemorrhage. This may be found by means of a localized subcrepitant râle. Another measure is the inhalation of a vaporized solution of the liquid persulphate of iron. Still another and more potential measure is the temporary ligation of one or more of the members of the body, the pressure being sufficient to interrupt the flow of blood in the veins and not in the arteries. This measure must be resorted to and continued only when the physician is present. The effect is sometimes almost magical. The measure is a substitute for venesection, which was formerly employed for the arrest of bronchial hemorrhage. Cavernous hemorrhage, occurring usually late in the disease, if profuse calls for prompt measures, and the topical employment of cold will be likely to be the most promptly effective.

Pain in the chest denotes either pleurisy or intercostal neuralgia. Mild counter-irritant applications by sinapisms or stimulating liniments, with anodynes graduated to the degree of pain, are indicated. Dyspnoea, if not caused by restrained movements of the chest from pain, or by pleuritic effusion, or by an intercurrent pneumonia, may denote either rapidity and extent of the tuberculous deposit or an accumulation of morbid products within the bronchial tubes: if the latter be the explanation, acts of expectoration are to be promoted. This is not easily done if the difficulty of expectoration proceed from great general debility. The ethereal stimulants, Hoffmann's anodyne, chloric ether, and the compound spirits of lavender are advisable under these circumstances as palliatives.

Pyrexia and increased frequency of the heart's action are symptoms indicative of an active tuberculous cachexia. How far these are purely symptomatic, and how far they may conduce to the progress of the disease, cannot be determined with our present knowledge. It may be assumed that they represent something more than is represented generally by the fever which is secondary to a local inflammation. That the febrile temperature is itself causative of changes in the tissues, as well as in the functions of the body, is probable; and the muscular power of the heart must be weakened by the {438} persistent frequency of its action. A rational object in therapeutics is either the removal or the neutralization of the morbid conditions on which the pyrexia and the increased frequency of the heart's action depend. The means of effecting this object are to be determined in the future, when more is known of the morbid conditions giving rise to pyrexia; meanwhile, there are certain medicines which, as experience shows, diminish the temperature, and febrile temperature can be reduced by external means which abstract heat from the body.

At the present time data are wanting for determining the importance of antipyretic treatment in cases of phthisis. Hyperpyrexia, however, may be considered as furnishing an indication for a trial of antipyretic medication, and the most reliable of the drugs employed for that purpose is quinia. It should be given for this object in full doses, as in other instances in which it is given for an antipyretic effect. These doses should not be continued long enough to disorder the stomach. Diurnal exacerbations of fever, especially if ushered in by a chill, may sometimes be arrested, or, if not arrested, materially modified, by full doses of quinia, although there may be no ground for the suspicion of malaria.

When the skin is hot and dry, with a high axillary temperature, sponging the body may be employed and continued until the pyrexia is diminished. I am not prepared to say whether the cold bath or the wet sheet is admissible or allowable. As having some antipyretic effect, and as diminishing the frequency of the heart's action, digitalis might be expected to prove a valuable remedy to fulfil the symptomatic indications under consideration. This drug was formerly much employed in cases of phthisis. The fact that it has in a great measure fallen into disuse may be taken as evidence that the theoretical recommendations are not sustained by clinical experience. The liability to disturbance of the stomach from its use is perhaps a sufficient reason for considering it inapplicable.

The profuse night-sweating which so often occurs in the course of phthisis claims treatment. Belladonna or atropia, the oxide or sulphate of zinc, gallic acid, the acetate of lead, and aromatic sulphuric acid are internal remedies for the palliation of this symptom. Sponging the surface before bedtime with diluted alcohol, diluted acetic acid, or with spirit in which alum is dissolved should be tried. Hot vinegar largely charged with capsicum has been found to be an efficient application. The covering at night should be as light as is consistent with comfort. Brunton has found strychnine and nux vomica, given at bedtime, useful. Another remedy, recommended by Murrell, is picrotoxin. This is given in the form of a solution (1 part to 240 parts water), the doses of from one to four minims daily, the last dose given late at night.[33] Agaricus, or the common toadstool, is recommended as an efficient remedy by Wolfenden of London and J. M. Young of Glasgow. From ten to twenty grains may be given in the form of an electuary with honey, or it may be given in the form of a tincture. In both these modes it is apt to cause nausea. This objection does not apply to the isolated medicinal principle, a crystallized substance which it is proposed to designate agaracine. Of this one-twelfth of a grain is a dose, which may be repeated if required. Young is of the opinion that it is not less effective than atropia as an antihydrotic remedy, and not open to the same degree of danger from an overdose as the latter. He has found it to act also as a soporific remedy, to relieve cough, and to diminish the temperature of the body.[34] A popular remedy is cold sage tea taken at bedtime.

[Footnote 33: Vide _Supplement to Ziemssen's Cyclopædia_, 1881, p. 325.]

[Footnote 34: _Glasgow Medical Journal_, March, 1882.]

Of complications and associated diseases, one of the most frequent is disease of the intestine. Of diarrhoea not thus connected the treatment is that {439} of indigestion. As incident to tuberculous ulcerations opium and astringents are indicated. Full doses of the carbonate of bismuth, with a salt of morphia, will often prove an efficient palliative. Peritonitis, acute and chronic, pleurisy with effusion, chronic laryngitis, pneumo-hydrothorax, and cerebral meningitis are to be treated according to indications which are considered in the articles treating of these affections, making of course proper allowances for their occurrence as secondary to the phthisical disease. Intermittent fever associated with phthisis should be arrested as promptly as possible. There is no foundation for the opinion which some have held that malaria retards the progress of tuberculous disease. Clinical facts show directly the reverse. If a perineal fistula occurs in a phthisical patient, the safest policy is not to interfere with it except so far as to make it as endurable as practicable. The idea that a fistula has a salutary effect by way of revulsion has been one of the reasons for making artificially an issue in the arm or elsewhere. This was formerly much in vogue, but it has mostly, and probably deservedly, fallen into disuse.

Medical opinion is sometimes asked concerning the propriety of marriage with a phthisical man or woman. As an abstract question there need be no hesitation as to the answer. If men went about deliberately selecting wives, or vice versâ--as, for example, horses are selected--there could be no doubt that phthisis should be considered a disqualification. Husbands and wives, however, are not mated in such a way. A marriage engagement has been entered into, and afterward one of the parties becomes phthisical. The friends of the non-phthisical party, not the parties themselves, come for advice, and the adviser is sometimes placed in an awkward situation. With respect to the effect of marriage on the tuberculous party, my analysis of 17 cases, 2 only being women, did not show that it was unfavorable. Were it unfavorable, considerations of sentiment and sense of duty generally outweigh all others. A more important point relates to offspring. A hereditary tendency is entailed in some, but not in all cases. The risk incurred in this point of view having been fairly stated, the responsibility of the medical adviser is ended.

After recovery from phthisis measures for the prevention of a relapse should receive due attention. The hygienic influences which were brought to bear on the disease, and which, as it is fair to conclude, had more or less agency in effecting the recovery, are as far as practicable to remain in operation. This important injunction applies alike to cases in which an arrest of the disease has taken place, so long as it ceases to be progressive. To prevent a renewal of its progress is an object having a similar importance as the prevention of a relapse after recovery.

In concluding the consideration of the treatment of pulmonary phthisis reference is to be made to a measure to which one of our countrymen has recently given much attention--namely, the injection of tuberculous cavities. More than thirty years ago the late Brainerd of Chicago related to me a case in which he made an opening through the chest-wall into a tuberculous cavity. He had the idea that cavities might in this way be treated by local applications with advantage. Of the result in that case it is only recollected that no bad consequences followed. Probably Brainerd did not prosecute further experimental observations, as I am not aware of any publication by him on the subject. In 1873, Mosler of Germany advocated making a free opening in tuberculous cavities with a view to drainage and topical treatment. He reported 3 cases in which a drainage-tube was introduced and kept in the cavity. The practicability of the operation and the absence of any evil result were shown by his cases. The operation had been advocated and performed prior to Mosler's publication, but without exciting consideration. To William Pepper belongs the credit of injecting medicated liquids by means {440} of a small syringe and hollow needles. Pepper has reported 12 cases in which cavities were thus injected. In these 12 cases two hundred and ten injections were made. In no instance did any harm result therefrom. The injected liquid in most of the cases was a very weak solution of iodine. In some instances a weak solution of carbolic acid was used. The objects are "the disinfection of the cavities, the relief of cough, the diminution of secretion, and the modification of the morbid action of the lining surface of the cavity, so as to favor cicatrization and contraction and the prevention of infection of the constitution." The results of the treatment in the cases reported by Pepper go to show that it may contribute to these objects. His observations have opened up a new and important department in the therapeutics of pulmonary phthisis.[35]

[Footnote 35: For reports of Pepper's cases and other details vide article in the _Transactions of the American Medical Association_, vol. xxxi., 1880; also article in the _American Journal of Medical Sciences_, October, 1874.]

Fibroid Phthisis, Chronic Interstitial Pneumonia, Cirrhosis of Lung.

The characteristic anatomical feature of this variety of phthisis is the predominant growth of the pulmonary connective tissue. If, as is generally held, this hyperplasia be due to a chronic inflammatory process, the name chronic interstitial pneumonia is not inappropriate. From an analogy to the structural affection of the liver characterized by an abnormal development of Glisson's capsule, the affection was called by Corrigan cirrhosis of the lung. The propriety of regarding it as a distinct form of pulmonary phthisis is based on points pertaining to the morbid anatomy and to the clinical history.

An abnormal interstitial growth enters more or less largely as an element into the morbid anatomy in cases of the ordinary form of phthisis. It is the chief element in typical cases of fibroid phthisis. The affected lung-structure is condensed and indurated, owing to obliteration of alveoli and bronchial tubes. The affection leads to notable diminution in volume. Resulting therefrom is a compensatory dilatation of bronchial tubes. Sacculated dilatations may reach the size of an English walnut or even a hen's egg. These are known as bronchiectasic cavities. The pleura is thickened and the opposed surfaces closely adherent to each other. With these distinctive changes are usually found small cheesy tuberculous deposits or true tuberculous cavities and miliary tubercles. The latter anatomical points show relationship to the ordinary form of phthisis. Exceptional cases are those in which the interstitial pneumonia is the result purely of the local action of inhaled irritating particles (vide PNEUMONOKONIOSIS). In these cases the tuberculous characteristics may be wanting. In cases of fibroid phthisis both lungs are often affected. But the affection is apt to be confined to, or much more extensive in, one lung, so that during life it either is, or appears to be, unilateral. Exceptionally, both lungs are extensively affected. It may originate in and be limited to a lower lobe. It is stated by Trojanowsky that when the affection is unilateral it oftener begins in the upper lobe, and when bilateral the lower lobes are first affected. A series of bronchiectasic dilatations may be so closely situated as to resemble an anfractuous cavity resulting from the discharge of liquefied tuberculous deposits.

It is customary to consider this affection as occurring consecutively to acute lobar and broncho-pneumonia, to chronic bronchitis, and to pleurisy. Taking into view, however, the slow, insidious development of the affection, the infrequency of its occurrence, and the frequency of the diseases just named, a more rational conclusion perhaps is that when these diseases are associated {441} with the phthisical affection they are secondary to it. The affection occurs oftener after than during the decade in which the ordinary form of phthisis is most apt to occur--that is, after thirty years of age.

The course of the affection as regards activity of progress is strikingly different from that of ordinary phthisis in a large proportion of cases. Commencing imperceptibly, after it has advanced to a certain extent it may remain apparently stationary, or it progresses very slowly during a long period. Its duration may extend over many years. In a case for a long time under my observation it existed probably for forty years. If the lesions be not extensive enough to interfere notably with the respiratory function, it may be tolerated indefinitely. The appetite, digestion, and nutrition may be well maintained. The muscular strength may not be much impaired. The circulation, temperature of the body, and other functions may be but little disturbed. A fatal termination, if not caused by some intercurrent disease, takes place after a very gradually progressive general debility and exhaustion.

As regards the different anatomical systems of the body other than the respiratory system, it is not important to add to the foregoing sketch details of symptomatology. The important symptoms referable to the respiratory system relate to cough, expectoration, and disturbance of respiration. The cough varies according to the quantity and character of the matter to be expectorated, the difficulty of its expulsion, and the susceptibility of the patient to the reflex influences on which cough depends. The matter expectorated is muco-purulent, and in many instances it is at times extremely fetid. This is due to the putrescency of morbid products detained within the bronchiectasic cavities and bronchial tubes, owing to difficulty in effecting their expulsion. The fetor may be suggestive of gangrene. The matter expectorated, however, if examined microscopically, will not be found to contain the débris of pulmonary structure. There may be sloughing of small portions of mucous membrane, but this is probably rare. The expectoration after certain intervals of putrid sputa in considerable or great abundance, the expectorated matter during the intervals having the characters of muco-pus without fetor, is almost pathognomonic of this variety of phthisis. The repeated occurrence of the putrid sputa, the clinical history, and the physical signs render it easy to exclude abscess of the lung. The detention of morbid products within bronchiectasic cavities, and the consequent putrescent decomposition, depend of course on the difficulty with which the contents of the cavity are expelled. This difficulty is greater if the cavities be in the lower than in the upper lobe. In a case which came under my observation the affection had been known by the attending physician to have existed for fifteen years. There was more or less habitual expectoration of ordinary muco-purulent matter, but after intervals of several days a considerable quantity of intolerably fetid matter was expelled. In this case the physical signs showed the affection to be limited to the lower lobe of the left lung. There was notable retraction of the lower and lateral portions of the chest on this side; solidification of lung was denoted by bronchial respiration and bronchophony over the posterior aspect; and the cavernous respiration was perceived over a circumscribed area in the latero-posterior aspect. This patient's general condition of health was fair; he had not a morbid aspect, and he was able to perform the duties of a clerkship in one of the municipal departments.

The respirations are more or less increased in frequency, the increase, other things being equal, being in proportion to the amount of damage of the pulmonary organs, or, in other words, the extent to which the respiratory function is compromised by the lesions. These may be sufficient to give rise to much suffering from dyspnoea. This was true of a case under my observation in which both lungs were extensively affected, while the muscular {442} strength and the functions generally of the body were not greatly impaired. The embarrassment of breathing is increased by an accumulation of muco-pus within the bronchial tubes, and notable relief follows expectoration of the accumulated products. Hæmoptysis occurs in some cases, but much less frequently than in the ordinary form of phthisis. The hemorrhage is sometimes profuse. It proceeds from erosion of the walls of vessels or the bursting of small aneurisms within bronchiectasic cavities.

Cyanosis is marked in some cases. This symptom is not always in proportion to the dyspnoea; that is, the cyanotic appearance of the prolabia and face may be present when the patient does not manifest suffering from a sense of the want of breath. The cyanosis is symptomatic of distension of the cavities of the right side of the heart, this being an effect of the obstruction of the pulmonary circulation. The obstruction may lead at length to dilatation of the right ventricle and auricle. Thence arises the general dropsy which may take place at an advanced period of the history of fibroid phthisis. A tricuspid regurgitant murmur may be perceived with or before the occurrence of dropsy; also visible pulsation of the cervical veins. A frequent physical sign under these circumstances is bulbous enlargement of the ends of the fingers and sometimes of the toes. The clubbed fingers, as they are called, are symptomatic of disturbance of the circulation. They are observed in some cases of disease of the heart, phthisis not existing.

The physical conditions giving rise to physical signs are as follows: Notable shrinkage of lung; solidification, which, if the lung be much diminished in volume, may be considerable or complete in degree and extensive; dilated tubes and bronchiectasic cavities varying in size, number, and relative situations; the presence of muco-pus in more or less abundance, the quantity variable at different times within the bronchial tubes and cavities. Vicarious emphysema is more frequent than in the ordinary form of phthisis.

In typical cases of extensive and advanced unilateral fibroid phthisis the affected side is much contracted. The appearance is like that presented in some cases after recovery from chronic pleurisy. The range of respiratory movements is much diminished, the two sides presenting a marked contrast in this regard. With this one-sided contraction of the chest there may be lateral curvature of the spine, the concavity looking toward the affected side. The supposition that the contraction is in reality a sequel of chronic pleurisy is at once disproved by finding the evidence of a degree of solidification notably greater than would be incident to the mere diminution of the volume of the lung. If the affection be limited to a lobe, either the upper or lower, there may be contraction more or less marked over the portion of the chest corresponding to the affected lobe. If the two lungs be much affected, the evidence of contraction is apparent to the eye on both sides. It is rarely if ever that the two lungs are equally affected.

The signs furnished by percussion and auscultation which represent solidification of lung, the presence of air in dilated tubes or bronchiectasic cavities and emphysematous lobules, are present either separately or in various degrees of combination. Solidification from induration without dilatation, sacculated or otherwise, of tubes, or if these be filled with morbid products and without vicarious emphysema of adjacent lobules, will give dulness on percussion more or less marked and over an area corresponding to the degree and the extent of the solidification. There may be flatness over the greater part or the whole of an entire lobe. Often, however, dulness is found in some situation, and either tympanitic or vesiculo-tympanitic resonance in other situations. Over bronchiectasic dilatations a tympanitic resonance may have the amphoric or the cracked-metal intonation. On auscultation the respiration over a space more or less extensive or within separate spaces of variable extent is either bronchial or broncho-vesicular. With these respiratory signs {443} representing solidification of lung are associated either bronchophony or increased vocal resonance, and the corresponding whispering signs--namely, whispering bronchophony and increased bronchial whisper. Over bronchiectasic cavities, may be heard the cavernous respiration and whisper. These signs of cavity may be combined with those of adjacent solidification of lung, giving rise to the several varieties of broncho-cavernous respiration. Coarse mucous or bubbling râles are of frequent occurrence, and the accumulation of muco-pus within the cavities may be represented by gurgling.

By means of the foregoing signs furnished by percussion and auscultation the character of the lesions, their situation, their extent, and the physical conditions as regards the presence of morbid products within the air-cavities, are determinable. These lesions are sometimes in striking contrast to the symptoms which represent the general conditions of the patient--the pulse, temperature, emaciation, etc. The symptoms and the physical signs may seem to conflict with each other, owing to the remarkable tolerance of the disease in some cases. To the physical changes which have been stated is to be added removal of the heart from its normal situation. If the seat of the affection be the left lung, its shrinkage may be such that the heart rises into the infra-clavicular region, and the space within which it is in contact with the chest-wall is larger than when the organ is in its normal situation. The latter circumstance is to be borne in mind with reference to the error of inferring therefrom enlargement of the heart. Not only is the area of notable dulness on percussion over the heart greater than in health, but the movements of the organ are remarkably apparent to the eye and touch. If the right lung be affected, the heart may be removed to the right of the sternum, the heart-sounds being heard here with their maximum of intensity. In this abnormal situation the presence of the heart may give rise to a notable dulness on percussion, and its impulses may be both seen and felt.

The differentiation of fibroid phthisis from the ordinary forms of the disease cannot be made with positiveness so long as the anatomical changes are small or moderate in degree and extent. The chief differential point is a greater degree of depression at the summit of the chest than would be likely to occur at an early period if the affection were of the ordinary form. If the affection begin at the base of the chest, it is more likely to be the fibroid variety. In typical cases, when the affection is unilateral and has led to notable shrinkage of the entire lung, taking the physical signs in connection with the evidence of tolerance afforded by the symptoms, it may be differentiated with confidence. Age is to be taken into account in the diagnosis; patients are rarely under forty. The expectoration from time to time of fetid mucus has considerable diagnostic significance.

With reference to the diagnosis, it is to be considered that between the ordinary form of phthisis and typical cases of fibroid phthisis there is every degree of gradation as regards the combination of the anatomical characters of both. There is no sharp line of demarcation between the two varieties. In these intermediate cases to determine by means of the symptoms and physical signs the relative proportion of each variety is not practicable, nor is this a matter of much practical importance. It may be added that the coexistence of chronic laryngitis and of tuberculous disease of the intestine is proof against fibroid phthisis. There is no possibility of the restoration of a lung affected with fibroid phthisis to its normal condition; but the prognosis as regards tolerance, arrest of progress or slowness of progress, and consequently duration of life, is much better than in the ordinary form of phthisis. On this account the diagnosis is of importance. The prognosis is better the nearer the approach to the affection in typical cases. Per contra, the prognosis is less favorable in proportion as the changes characteristic of the disease in its ordinary form are associated with those characterizing fibroid phthisis. If the affection be {444} confined to a lower lobe, it may not extend beyond this limit, and the persistence of solidification of the affected lobe may not be incompatible with good general health. Of these facts the following case is an illustration: Phoebe, aged five years, came under my observation in 1864. There was at that time notable dulness on percussion over the lower lobe of the left lung, with bronchial respiration and bronchophony. She had cough and expectoration, but had not been confined to the bed or house, and her general condition of health was then fair. The treatment consisted of tonic remedies and out-of-door life. I saw her repeatedly during the next two or three years, the physical signs remaining the same, and the general health fair. In 1869 she had chorea and was treated with Fowler's solution. I did not see her again until October, 1871; she had then, and had never been free from, some cough and expectoration, but her general health had been maintained. The signs of the solidification of the lower lobe of the left lung were then present, the upper lobe remaining unaffected. In November, 1874, I noted that I had again seen her and examined the chest. The dulness on percussion over the lower lobe of the left lung continued; there was at this time absence of respiratory sound over this lobe, but the vocal resonance was greater than on the opposite side. The left side was considerably contracted. She had still some cough and expectoration, and there was some deficiency of breath on active exercise. Her aspect was healthful, and she was well developed for her age (fifteen years). Menstruation was irregular. She consulted me for this irregularity, not regarding herself as ill in other respects. About six years afterward I met her in the street, and she accosted me. Her appearance was healthful.[36]

[Footnote 36: This patient remains in fair health at the present time, May, 1883, nearly twenty years after she first came under my observation.]

The treatment in cases of fibroid phthisis differs in no essential points from that in cases of the ordinary form of the disease. The slowness of progress and the long duration show less activity of the tuberculous cachexia. Nevertheless, the cachexia either exists or has existed, and the measures relating thereto which have been considered as belonging to the dietetic and regiminal treatment are alike applicable to both varieties of phthisis. The circumstances which render changes of climate admissible, if not advisable, are much oftener present in the fibroid variety, and there is greater probability of the disease being either arrested or retarded. Medicinal treatment is to be employed with reference to therapeutic indications alike in both varieties of the disease.

The treatment by inhalations to prevent putrefactive changes in the contents of bronchial tubes and in cavities is oftener indicated by fetid sputa in cases of fibroid phthisis. The continuous breathing of the atmosphere of a room containing an antiseptic vapor requires the patient to remain within doors. A more effective method is to make use of a respirator inhaler. A portable and convenient instrument, worn over the mouth like an ordinary respirator, has been devised by W. Roberts and improved upon by H. Curschmann. In this instrument the air which is breathed passes through layers of tow moistened with the antiseptic liquid. The disinfecting agents which have been found efficient are carbolic acid, creasote, oil of turpentine, a mixture of the tincture of iodine and the compound tincture of benzoin and thymol.[37]

[Footnote 37: Vide article by William Pepper in _Transactions of the American Medical Association_, vol. xxxi., 1880.]

Prevention of Phthisis.

The number of deaths throughout the globe which are caused by pulmonary phthisis vastly exceeds the number caused by any other disease. {445} The etiology of pulmonary phthisis embraces largely causes which can be removed. Hence the disease is to a great extent preventable. Are any comments on these simple statements needed in order that the prevention of phthisis may be regarded as among the most important of the subjects belonging to preventive medicine?

It has been assumed that phthisis involves a predisposition which is in most, and perhaps in all, cases innate. Putting aside all questions relating to an acquired tuberculous diathesis, it may be assumed that the development of the phthisical affection depends in many or perhaps in most cases, more or less, and probably often in a great measure, upon causes which promote the diathetic condition. Now, many of these causes are removable, and if removed phthisis is prevented, and the prevention of a disease which may properly be called a scourge of the human family will be diminished.

Of removable causes may be mentioned humidity of the soil in places of residence; living in small unventilated dwellings; confinement within doors; breathing in close workshops or factories, and in overcrowded rooms at night, an atmosphere deficient in oxygen and contaminated with pulmonary and cutaneous emanations; working underground in mines from which light as well as pure air is excluded; a deficiency of food sufficiently wholesome and varied; impairment of the cutaneous functions from uncleanliness; and want of a proper adaptation of clothing to the climate or season. These are obvious violations of the hygienic requirements for health. It is unnecessary to cite facts to show to what extent these violations prevail in different countries. They are causes which admit of removal, however difficult may be the task. Connected with their removal are other considerations than the prevention of phthisis. But confining the attention exclusively to the latter object, how incalculable would be the saving of life and health were these causes to be removed! Much has been done within the last half century toward diminishing the mortality from phthisis by advancement in pathological and therapeutical knowledge; how much more remains to be done by preventive measures!

The prophylaxis against phthisis must date from birth. An infant should not nurse a mother who is consumptive or whose milk is of poor quality. Care is to be observed in the selection of wet-nurses. All the various articles which are sold under the name of infants' food should be discarded. Many of these are fraudulent; that is, they are not what they purport to be. But admitting that, if properly prepared, they are safe substitutes for milk and the simple farinaceous foods, there can be no guarantee for their proper preparation; and the risk is too great to rely upon articles which cannot be readily tested and for the genuineness of which dependence must be placed on irresponsible dealers.[38] There is need of much caution respecting the purity of milk, especially in cities. Much harm is not infrequently done by over-care in children's diet--that is, by denying articles which they crave, and restricting them to those which they do not like. In this matter the instincts are not to be set aside, especially in early life, when perversions of appetite and taste have not been acquired. Not infrequently from undue caution the quantity of food is restricted, and children suffer from insufficient alimentation; this is more likely to occur in our country among the wealthy than among the poorer classes. Other prophylactic provisions pertaining to exercise, out-of-door life, clothing, etc. need not here be considered.

[Footnote 38: Vide "Address by A. Jacobi on Infant Diet," _Transactions of the New York State Medical Society_, 1882.]

In order to combat the various causes which have been named, knowledge of hygienic laws must be diffused among all classes. There is a lamentable lack of information and of interest as regards matters of hygiene among the more intelligent classes. But it is not sufficient to enlighten these: the {446} knowledge must be extended, as far as practicable, to those who, in this point of view, are lower in the scale. Many persons of wealth fall in this category. The causes which are purely personal can be reached only by information diffused by means of publications, lectures, and intercourse with medical men and others. Here is a rich field for missionary labors. To overcome certain of the causes, however, the intervention of legislative authority is necessary. With reference thereto health boards, properly constituted and invested with adequate powers, should be organized in States, counties, and cities. In this way it is practicable by the prevention of phthisis to lessen greatly the rate of mortality.

Protection against the communication of the disease requires to be specially noticed. Occupying the same bed with phthisical patients and sleeping in the same room, if the latter be not enjoined by the dictates of humanity, are objectionable. They are to be objected to on the score of unhygienic influences, physical and moral, irrespective of the doctrine of a tuberculous contagium, and of course still more in view of the probabilities in favor of this doctrine. Care should be taken to exclude from the table the meat of tuberculous animals. In addition to the purity of milk in other regards, it should be ascertained that the supply is not from cows affected with tuberculous disease. Obviously, this is especially of importance with reference to infants who are bottle-fed and in childhood, when generally milk forms a much larger proportion of the diet than in after years. The ventilation of apartments occupied by phthisical patients should be attended to with reference to the possibility of the disease being communicated by the inhalation of particles of tubercle; and it may not be a needless precaution to introduce a disinfectant into the vessels which receive the matter expectorated.

{447}

SYPHILITIC DISEASE OF THE LUNG.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--Lesions of the lungs with a syphilitic impress include catarrhal inflammation of the bronchial mucous membranes, chronic inflammatory new formations, which affect especially the connective tissue, producing sclerosis or else gummatous growths.

HISTORY.--From the early part of the eighteenth century attempts have been made to create a word-portraiture representing the peculiar features of syphilitic pulmonary disease as a separate entity. It has been defined histologically and clinically from simple and from fibroid phthisis, or from cases of syphilis in which a damaged state of the general health has fostered the development of phthisis. But the question, Is there a peculiar microscopic and macroscopic anatomy, or a special symptomatology by the aid of which the cause, seat, and dissemination of pulmonary syphilis can be recognized? remains even now but partially removed from the field of debate and conjecture, although unquestionably the syphilitic poison bears intimate relation with various pulmonary processes.

ETIOLOGY.--Predisposing and Exciting Causes.--Syphilis of the lungs is a rare disease as compared with the forms of specific laryngitis, but even here Leman asserts that there is an early simple catarrh of the larynx indistinguishable from the specific catarrhs. Whistler, in recording his observations upon 88 cases of the lesions found in syphilis of the larynx, observes that catarrhal congestions in early laryngeal syphilis simulate the same lesions from ordinary causes. Schnitzler lays particular stress on the association of pulmonary syphilis with affections of the larynx and a specific bronchitis which may occur in the first two months after inoculation. Many other writers on this subject assert that laryngeal and bronchial catarrh attend the period of early skin eruptions, disappearing in consequence of an antisyphilitic treatment.

The rarity of pulmonary syphilis has been further attested by the observations of Greenfield, who states that out of 22 cases of visceral syphilis, only 1 occurred in the lung and 4 in the larynx and trachea: in these cases, while the dura mater and cerebral vessels were extensively diseased, no trace of skin affection could be found. Goodhart has collected from the post-mortem records in Guy's Hospital during twenty-two years 189 cases of visceral syphilis, but in only 38 of these chronic lung disease occurred. Phthisis associated with syphilis is usually a late secondary or tertiary process, which appears from two to five years after the infection; in rare cases ten--even twenty--years have been said to elapse before the supervention of pulmonary trouble. Cases of phthisis associated with syphilis have, however, been described as occurring within the first twelve months after infection. Further investigation may establish these cases of early pulmonary syphilis as attributable to violent systemic infection, or their etiology may be involved in the deterioration of the general health which sometimes occurs. Moreover, one {448} must remember that simple phthisis may more readily be developed in the scrofulous syphilitic, owing to the predisposition of such persons to catarrhal forms of inflammation. In the progress of syphilis there is also a tendency to catarrhal processes through anæmia and damaged general health, which may predispose certain cases to an ordinary type of phthisis. The origin of the new formation in both tubercular and syphilitic phthisis is similar--viz. the arterial, lymphatic, and the peribronchial sheaths, spreading thence to the interlobular connective tissues. It is therefore not surprising that it has been difficult to differentiate the tubercular from the specific forms of phthisis, and Goodhart asserts that there is no histological difference between syphilitic and tubercular phthisis, except that the former is more vascular.

We may assume that true pulmonary tuberculosis may be associated with syphilis, but preserves its own pathological characters; that, although we are ignorant of the exact differential histological changes, there is sufficient evidence to show that there is a distinct association between syphilis and pulmonary disease; and that syphilitic phthisis is commonly interstitial. Whether the relation be one of cause and effect, or whether the process is simply a modification of ordinary tubercular phthisis, it is impossible at present to determine. The final adjustment of the theories concerning the specific etiology of tubercular phthisis may throw further light upon the etiology of syphilitic phthisis. That gummata may be found in the lungs is a well-established fact, and by some authorities is not considered rare.

The discussion of the etiology has already indicated the relation of the predisposing and exciting causes to pulmonary processes in connection with syphilis. In certain cases of syphilis the antecedent of pulmonary changes is a laryngeal or bronchial catarrh. The relation which an active virus in the blood sustains to the process is still subject to debate. Hutchinson writes as follows: "If the infected blood were the cause of the local phenomena, it is almost certain that such phenomena will be symmetrical, because the blood is equally supplied to both sides; such is the case during the secondary stage. If, however, the symptoms result from tissue-conditions, and the blood is at the time of the outbreak free, then there is a considerable probability that local influences may take a large share in evoking them, and they will be asymmetrical--evoked by some local cause."

The existence of gummata, then, does not necessarily show that there is any active virus in the blood, because their formation is sometimes symmetrical, sometimes asymmetrical.

PATHOLOGY AND CLASSIFICATION.--The lesions of pulmonary syphilis may be divided into four classes: _(a)_ early phthisis, associated with principal interlobular proliferation; _(b)_ advanced syphilis, in which gummatous or allied formation exists; _(c)_ simple phthisis, developing in consequence of impaired general health induced by syphilis; _(d)_ inherited or congenital syphilis, occurring in infants.

_(a)_ The pathological process in the majority of cases in the adult is interstitial new formation, very often evoked by antecedent catarrhal inflammation. At first small spindle-shaped and round cells appear and develop into connective tissue, among the fibres of which blood-vessels are freely produced; the septa of the alveoli are thickened and the alveoli themselves compressed. In any morbid process in the lungs, such as tubercle, sarcoma, or cancer, the alveoli act as the inter-fascicular spaces of the connective tissue. In the same manner in syphilis the alveoli of the lungs are always in the later stages, and sometimes primarily, more or less filled with small cells, which, surrounded by the newly-formed connective-tissue fibrous framework, gives the appearance of some of the forms of simple phthisis. The smaller bronchi become narrowed, and perhaps occluded, by the pressure of the new growth which develops along their lumen. Occlusion of the bronchi may also be caused {449} by enlargement of the bronchial glands, which is one of the incidents of the syphilitic pulmonary process.

If we endeavor to nucleate the peculiar impress attributed to early syphilitic pulmonary processes, we find much that is vague. The vascularity and advanced grade of organization of the new growth are considered by Greenfield and Goodhart to be characteristic when compared with tubercular consumption, in which the original growth is bloodless and the tendency is to retrograde metamorphosis. Green and Virchow suggest that the origin of syphilitic diseases of the lungs is distinctive in this respect, that while in the ordinary forms of phthisis the fibroid is secondary or coequal in its development with changes in the alveoli and alveolar wall, in syphilis there are primarily interstitial changes. In chronic bronchitis the fibroid thickening proceeds from the bronchi. Wagner, however, maintains that implication of the alveolar wall is as common in syphilis as in ordinary phthisis.

In the general pathology of syphilis the change in the intima of the blood-vessels is characteristic: this has not yet been demonstrated in the lung, but merely the general thickening of the external coat of the vessels. When entire vesicular consolidation and breaking down occurs, the process is similar to ordinary phthisis, and indistinguishable from it.

_(b)_ In the gummatous stage the same formation of cellular and connective tissue is found as in the diffused form, with which gummata are often associated. Gummata may originate anywhere in the intervesicular tissue, usually near the visceral pleura. Sometimes they are formed near the roots of the lungs, intimately connected with the blood-vessels and bronchial sheaths. They may also be formed in the deeper layers of the costal pleura or upon the periosteum of the ribs. Owing to the peculiar anatomical formation of gummata, their subsequent history is one of combined caseous and fatty degeneration. These centres of softening may communicate with a bronchus, more or less rapid evacuation of the mass may occur, and a cavity be formed which often enlarges as the gummata break down. Contraction may ensue, leaving a small fibrous scar with cheesy cretaceous deposit, or the gummata may point externally, with or without the appearance of inflammation in the adjacent tissues, or they may remain stationary for an indefinite period. In some cases the pulmonary new formation may be a combined interstitial, gummatous, and catarrhal process; but, as a rule, the fibroid process of syphilis in the earlier stages is not accompanied by the filling of the alveoli with catarrhal cells. Gummata developed in or near the pleural sac may increase in size, and by compressing the lung simulate pleural effusions.

_(c)_ The morbid anatomy of cases in which simple phthisis develops in consequence of the vulnerability of the pulmonary tissues to the exciting causes of bronchial inflammation requires no special consideration.

_(d)_ Interstitial inflammation, gummata, and enlargement of the bronchial glands have been found in the syphilitic foetus and in very young children. It is also claimed that syphilitic disease of the lung may be one of the forms of tertiary disease which develop in children between the second dentition and maturity. Virchow and Lebert have described pulmonary gummata in children suffering from inherited syphilis. Depaul gives the cases of two children with pemphigus who had soft puriform nodules or collections scattered through the lungs. In the infant lung the highly cellular character and ready reversion to the embryonic type of structure would naturally lead to exuberant growth and rapid diffusion of the morbid process, which could not occur in the more fibrous, less cellular lung of the adult. Hence the slower growth in the latter establishes the more fibrous and limited extent of disease: in other respects the origin and distribution of the growth are identical in both cases. In the infant enlargement of the bronchial glands {450} and bronchitis leading to broncho-pneumonia, or an unusual proliferation of epithelium in the alveoli, is more frequent than in the adult.

MORBID ANATOMY.--In the earlier stages of pulmonary syphilis the macroscopic appearance of the lung is firmer at the seat of deposit than elsewhere. It is also heavier and has a smoother surface. The infiltrated parts are grayish-red or grayish-yellow, smooth, and homogeneous. Sometimes the appearance resembles pale-whitish patches invading districts of the lung. The hyperplastic material becomes converted into a tough, contracting, fibrous tissue, which radiates through the lung, drawing together the bronchial tubes and flattening them, possibly even to obliteration. The entire lung may be involved, but the changes most frequently proceed from the hilus of the organ into the interior, following the track of the bronchial radicles and the bronchial and pulmonary arteries. The lesions frequently develop near the visceral pleura, where there is more connective tissue. This accounts for the depressed puckered scars which are found on the pleural surface.

The macroscopic appearances in specific pulmonary disease differ, according to Goodhart, "both from a chronic pneumonia and from that solidification ensuing after contraction of the lung from old pleurisy, in that it is less evenly distributed, and generally less widely spread over the lobe, than they. It is nodular, rather diffused, and more symmetrical than unilateral. From miners' phthisis the appearance differs in the absence of the extreme dilatation of the bronchial tubes and more solidity from greater growth. The tissues involved are more tough and less granular than red or gray hepatization." It is possible to differentiate other forms of fibroid phthisis by noting, in addition to the above points, the presence of the syphilitic process in other viscera, and by comparing the clinical records with the post-mortem examination.

Syphilitic lesions may be found in any part of one or both lungs, but their localization at definite points in the lungs, leaving the balance free even when the lesion has proceeded to formation of cavities, may be characteristic. There is, however, a wide division of professional opinion upon the subject of the localization of the process in syphilitic pulmonary disease; some claiming the middle lobe, some a symmetrical lesion at the apices, others lesions at a definite point elsewhere than at the apices. If the pulmonary lesions are introduced by an attack of pleurisy, the process in the lungs is usually located at one or both bases. Some, however, locate the disease at the base, without mentioning an antecedent pleurisy.

Gummata are more frequently situated in the middle or lower lobes of one or both lungs, and are defined by a boundary layer of fibrous tissue. Fibroid development may ensure their adhesion to the visceral and costal pleura. They are gray or yellowish-gray, hard, well-defined nodules, of varying size and number, occurring as single large masses surrounded by normal or compressed lung. In the centre is found a diffluent material, not unlike the centre of a scirrhous nodule, similarly enclosed in a limiting fibrous investment from an inch to many inches thick. In the condition of the neighboring pulmonary substance a difference may be observed between gummatous and tuberculous nodules: the latter occur in more numerous masses, usually small, and the entire lung is more or less diseased; while in syphilis extended districts of non-affected lung occur in the neighborhood of gummata. Whenever gummatous lesions in the lungs exist a history of pustular eruptions, laryngitis, arterial lesions--in fine, some indication of general systemic syphilitic poisoning--can always be found. Fournier thinks there are five anatomical points of distinction between syphilitic gummata and tubercle: "1. Tubercle involves the upper part of both lungs; gummata one lung, and may be limited to a portion. 2. Gummata are few as a rule, solitary; tubercles sooner or later become confluent. 3. Gummata are larger than tubercles, never {451} miliary in form. 4. Gummata are always yellow or white, never transparent like miliary tubercle. 5. Until softening takes place gummata are of more equal consistence than tubercles, and if they soften do not break down, wholly owing to the capsule. Histologically, there is no difference in structure." Gummatous formations may be found on the pericardium and heart and in the thoracic and abdominal walls. Clinically, the most important pathological feature is that large districts of healthy lung are interposed between the affected districts; this is not so in ordinary phthisis.

Bronchial Lesions.--The syphilitic like the scrofulous are predisposed to catarrhal inflammation, and this may spread down the bronchial tubes, giving rise to a general bronchitis; a coexistent laryngitis may or may not exist. Enlargement of the bronchial glands is frequently combined with the syphilitic pulmonary process. When the glands are enlarged they present a firm pigmented character, varying in size from a hazelnut to an egg, and the connective tissue surrounding them is usually infiltrated. Subsequently, owing to the pressure of the mediastinal growths, the bronchi are narrowed and more or less occluded; the same effects are occasioned in the smaller bronchi by the pressure of the new growth which develops along their lumen. The effects of bronchial narrowing or occlusion produce serious mischief in the lungs proportioned to the degree of obstruction. By the retention of the bronchial secretions the air-supply to the vesicles is interfered with; emphysema with or without asthmatic symptoms or atelectasis may ensue. Further, the results of bronchial narrowing affect the circulation through the lungs, and in combination with atelectasis very intractable local bronchitis may be developed; and, with or without atheroma, hemorrhagic infarctions may occur, with a form of pneumonia which has been described by Fuchs as apneumatosis. The narrowing of the bronchial tubes in specific fibroid phthisis affords a means of differentiating this disease from non-syphilitic fibroid phthisis, in which the tubes are widened. Cases have been reported of nodules of syphilitic new formations in the mucous membrane of the superior and inferior extremities of the trachea and larger bronchi. The nodules ulcerate, and in healing cicatricial bands of fibrous tissue are formed which cause contraction of the tracheal tube transversely or diminish its length. These lesions resemble tuberculous ulceration, but they differ in the nature of the initial neoplasm by the formation of cicatricial tissue and by the tendency to stenosis of the tracheal tube. The cutaneous syphilides, mucous patches, the exostoses of the bones of the cranium help to demonstrate the connection of the marked cachexia with syphilis rather than scrofula.

SYMPTOMATOLOGY.--As the pathology of syphilitic pulmonary processes is intertwined with the pathology of many other forms of phthisis pulmonalis, so the symptoms must be common to those obtaining in other forms of pulmonary disease. They are insidious and gradual in their development, and may be classified as the subjective, the physical signs, and the objective phenomena. The subjective symptoms may be present without noticeable departure from an appearance of health. There may be difficult respiration with more or less dyspnoea, especially in the mornings and evenings, besides a sense of heaviness and oppression in the chest, with a feeling of inability to inflate the lungs. These symptoms may be increased on exertion, respiration becoming wheezing, with imperfectly-developed asthmatic attacks. Hoarseness, with varying degrees of aphonia, more or less dysphagia or unequal pupils, may be present. Nearly all of these symptoms may be accounted for as indicative of mediastinal pressure or irritation of the pneumogastric nerve by the enlargement of the bronchial glands. The catalogue of phenomena may be present in whole or in part, and the intensity of their manifestations may vary from time to time in the history of a single case. If the bronchial glands are much enlarged, a sense of discomfort, oppression, and uneasiness {452} at the root of the neck may be experienced, which increases until actual pain is felt, located in the back between the scapulæ, but sometimes radiating through the intercostal nerves around the chest. Cough, as a rule, is an early symptom, usually dry, paroxysmal, and associated with dyspnoea, or there may be bronchial catarrh, with a relative amount of expectoration. Syphilitic disease of the larynx may occur coequal with the pulmonary trouble, and some of the above symptoms may be thus explained and many others added. Rheumatic and nervous symptoms, including sleeplessness and deterioration of the blood-crasis, may testify to the syphilitic infection of the blood.

When a physical examination of the chest is instituted, thickening of the head of the periosteum of one or both clavicles, substernal tenderness, thickening of the tibial periosteum, are usually detected. Prominent among the physical signs are the evidences of enlargement of the bronchial glands. According to Guéneau de Mussey, percussion over the spinous processes of the cervical vertebræ in the course of the trachea reveals in a healthy subject a distinct tubular sound down to the point of bifurcation of the trachea at the level of the fourth dorsal vertebra. Opposite the fifth and downward we get the lower-pitched pulmonary resonance. When the tracheal and bronchial glands are enlarged, the tubular sound over the upper dorsal vertebra is replaced by dulness, which may contrast sharply above with the tracheal and below with the vesicular resonance.

The respiratory murmur will be feeble in volume and limited to inspiration, especially over the interscapular region. Over one or the other bronchus the respiratory murmur may be more high pitched than in health, and slightly exaggerated on one side or at the base of the chest. The rhythm is often jerky and paroxysmal; the paroxysms are more or less constant, but are liable at times to increase.

The additional physical signs in syphilitic phthisis, unassociated with gummata, are those shared by other forms of fibroid phthisis, and do not require particular description here, as increasing dulness, varying degrees of bronchial breathing, and bronchophony. A peculiar alveolar rustle, resembling the sound produced by the rumpling of wall-paper, has been alluded to as characteristic.

Inspection or palpation sometimes reveals changes in the contour of the chest, with displacement of the movable thoracic viscera, as in fibroid phthisis. When cavities occur, the physical signs necessarily correspond to those of other varieties of phthisis at this stage.

When a gumma is large enough to be recognized by physical examination, one finds dulness or flatness on percussion, confined to a section of the chest, and not occupying its semi-circumference, as in pleural effusions. The vocal fremitus is suppressed in proportion to the size of the gumma. The respiratory murmur is abruptly cut off over the area of flatness, but it may be only distant bronchial breathing. The vocal resonance is absent or is distant bronchophony. Around the gumma the respiratory murmur is usually very feeble or scarcely audible, generally without râles unless they are due to neighboring congestion. The percussion resonance is good or exaggerated. Proportionate vicarious functional activity prevails in the opposite lung. If the gumma be large, the heart's impulse may be displaced to the left or right, and dyspnoea may occur as in case of pleural effusions. In this stage, owing to irritation of the bronchial mucous membrane, there may be expectoration of a tough, glairy mucus, or as a gumma softens the expectoration may become purulent.

The objective phenomena vary: the chest is often well developed, the body fairly nourished, and constitutional symptoms of a severe character may be wanting. The patient may be capable of hard physical labor, even though a {453} considerable part of the lung be affected. Moxon relates a case of a man "employed in carrying sacks of grain who was suddenly killed, and who had fibroid infiltration of a great part of the left lung and part of the right, and besides scars in his liver and testes." But in some cases the complexion is pallid and waxy, indicative of cachexia associated with digestive disorders, with night-sweats, and a variable but low thermometrical record. Usually, the progress of the disease is slower in syphilitic than in tubercular phthisis, but when the systemic poisoning is grave and many other organs are coincidently involved, the progress is more rapid; but the process peculiar to syphilis is often past, and the patient suffers from simple catarrhal phthisis with formation of cavities and softening gummata. Diarrhoea and night-sweats are said to be less frequent than in ordinary phthisis, and the pulse is slower. Hæmoptysis occurs infrequently, because the process in the lungs is chiefly fibroid; but it is possible through the rupture of newly-developed blood-vessels in the new formation in the lung or hemorrhagic infarction through the rupture of atheromatous vessels.

DIAGNOSIS.--This depends mainly on the history of the cases, the prior or coexisting syphilitic lesions, especially laryngeal processes, cutaneous syphilides, exostoses, perforation of the palate, substernal tenderness, and the thickening of the tibial periosteum or that of the head of one or both clavicles. Family immunity from phthisical tendency, recovery from lesions usually incurable if they have any other than a specific origin, are suggestive of pulmonary syphilis. If a patient retains flesh and strength beyond the natural expectation considering the serious lesions of the lungs, the fact is of relative importance when considered in connection with the other diagnostic features. The distribution of specific lesions is variously located by different authors. Grandidier found induration affecting the middle lobe of the right lung in 27 out of 30 cases believed by him to be specific phthisis; the surrounding lung contained large areas free from disease. This tendency to localization in portions of the lungs, leaving large areas free from disease, is of value in diagnosis.

PROGNOSIS.--The prognosis is involved in the discovery of syphilis as the cause of the disease and on the subsequent appropriate treatment. Grave and important specific lesions, according to some authors, have yielded to the resources of art. Fournier has recorded a case where "dulness at the summit of the left lung was extensive and signs of a cavity distinct. After six weeks of antisyphilitic treatment recovery was almost complete. In this case the presence of a phagedenic ulcer of the foot was the only sign that suggested syphilis, the symptoms of the pulmonary affection being identical with those of tubercular phthisis." The principles presiding over the prognosis of the various stages of pulmonary diseases in general are applicable to syphilitic pulmonary processes.

TREATMENT.--When a case of pulmonary lesion presents itself, unless the existence of tuberculosis be demonstrated, we must ascertain if the symptoms can possibly be due to syphilis, and the line of treatment indicated in any single case must be based upon an estimate of the prominence of the specific process. The ravages of syphilis, however, often produce such loss of substance in the lung that the lesions are irreparable, and therefore we cannot always accomplish the brilliant results which usually attend an antisyphilitic treatment. If there is evidence of enlarged bronchial glands, in addition to other measures local counter-irritation is useful by means of the biniodide of mercury ointment, 16 grains to the ounce, and applied for a continued period, or a preparation of iodine with croton oil may be tried. In the main, the general principles of treatment correspond with those recognized in similar forms of pulmonary disease of a non-specific etiology.

{454}

PNEUMONOKONIOSIS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A generic term applied to pulmonary diseases due to the inhalation of particles of irritating dust.

SYNONYMS AND CLASSIFICATION.--The synonyms and classification of pneumonokoniosis have been based upon the character of the dust inhaled, using such terms as anthracosis ([Greek: anthrax], coal), disease due to coal-dust; siderosis ([Greek: sidêros], iron), due to metallic dust; chalicosis ([Greek: chalix], gravel or pebbles), due to mineral dust; tabacosis, due to tobacco-dust; and byssinosis ([Greek: byssos], cotton), due to cotton fibre and dust. A more imperfect classification has been derived from the avocations of the sufferers; for example, miners' phthisis, Sheffield grinders' rot, potters' consumption and asthma, freestone-hewers', masons', or millers' lung.

HISTORY.--From the early experiments of Cruveilhier, who injected mercury into the system and subsequently noted the pulmonary changes, down to the experiments of the present day, evidence has accumulated to show that inorganic irritant materials are capable of exciting inflammatory new formation in the lungs. The difference between the changes produced in the lungs by experimental processes and those occurring after the inhalation by artisans of inorganic materials consists in degree rather than in essential character. In pneumonokoniosis the pulmonary processes are gradually developed, and consequently the ensuing changes in the tissues represent those usually associated with the more chronic forms of pulmonary lesions, and may not only occasion phthisis, but during years of life may cripple the sufferer by engendering chronic catarrhal processes in the mucous membranes, complicated by emphysema or asthma.

ETIOLOGY.--Predisposing Influences.--Atmospheric dust is composed of organic and inorganic matter, and both have been demonstrated by many admirable experiments to be very widely diffused in the air we breathe. In most instances the injurious action of inorganic dust is augmented by the conditions of imperfect ventilation under which it is inhaled, because the amount of dust deposited in the lungs is thereby increased. Illustrations of this fact can be found in various avocations, particularly among miners. The injurious action of dust inhaled when there is imperfect ventilation is increased in proportion as there is deprivation of sunlight, both conditions tending to lower the vitality of the artisan. Again, the rigor of confinement of parents engenders a sickly or scrofulous constitution which is transmitted to their offspring, causing great mortality among the children of artisans, especially where they, in turn, are subjected to unfavorable environment.

When work is performed in constrained or stooping positions, or when proper inflation of the chest is not secured, the liability to pulmonary disease is increased.

The foregoing conditions having been considered, the injurious action of dust upon the lungs is in proportion to the quantity deposited in them. The {455} entrance of dust is, however, physiologically opposed by the action of the pulmonary cilia, although the resistance is frequently ineffectual. This inefficiency may be owing to the quantity of dust inspired or to deficient tissue-integrity in general upon which the ciliary action depends in inverse ratio.

Exciting Causes.--These vary materially in different avocations. The most injurious industries are those in which the various forms of grindstones are used, or those trades which necessitate labor in an atmosphere loaded with particles of steel, iron, or flint. In London, where millstones are made from French burr, a peculiarly hard flint quarried on the Marne to the east of Paris, and more liable to chip from its hardness and dryness than flint quarried in other places, the mortality among the artisans is said to be very much increased. Peacock, who has investigated this subject, asserts that in certain manufactories of this class the average age of those engaged is very low: of 23 apprentices the average age was twenty-four, and the longest period during which the occupation could be followed was thirteen years. The same author has also demonstrated the presence of silicious particles in the lung-tissues. In the pottery districts of England the death-rate from pulmonary diseases is greater among those who work at that avocation than among the other inhabitants.

The study of the effect upon the lungs of the inhalation of coal-dust is very important. In the coal-mining region of Cornwall the deaths from chest diseases among miners is double that of males in the community at large; the mortality of those working in lead-mines is also very great.

The black spit of pitmen, examined under the microscope, is seen to consist of mucus enclosing finely-divided particles of coal, frequently presenting the special bands of the particular coal in which the subject of the disease may have worked. The fact that coal-dust may enter the lungs in the act of breathing is corroborated by Rindfleisch, who, reporting for Traube a post-mortem made in 1860, found in the fluid expressed from the parenchyma of the lung "one of the dotted cells of coniferous wood entirely carbonized, in which he was able to count seven pores close together. This particle of charcoal-dust equalled half the diameter of an alveolus." Inhaled particles of dust first penetrate the bronchial tubes and infundibula, and, entering the alveolar parenchyma, mix with the general current of extravascular fluid, together with which they ultimately tend to reach the lymphatic vessels. On their way they must occasionally meet with corpuscular elements which have the power of permanently adopting small solid particles into their protoplasm: foremost among such elements are the stellate corpuscles of the connective tissue, next the migratory amoeboid cells, which are found in the connective tissue of the lungs as well as elsewhere, and which carry the black pigment with them wherever they go. The residual portion which escapes, being arrested by cells on its way through the lymphatic system, is carried to the root of the lung and enters the lymphatic glands of the mediastinum; here the granules meet an obstacle to their further progress, for the countless lymph-corpuscles with which the glands are stored are ready to take up as many of the charcoal particles as can by any possibility be accommodated in their protoplasm. We may conclude that the influence of inhalations of coal-dust varies in different cases, but may be considered as prominent among the exciting causes of pneumonokoniosis.

The charcoal-grinders and carriers, chimney-sweeps, moulders, iron and glass polishers, and the workers in mother-of-pearl, all suffer more or less from destruction of lung-function. Deposits of oxide of iron have been found in the lungs of operators who have for years used this substance as a polishing pigment. Merkel reports the case of a man who was employed to clean the surface of oxidized iron by scrubbing it with sand: his expectoration was grayish-black, and was found to contain small grains of magnetic {456} oxide of iron; the lungs were found to be indurated with cavities at the apices.

Many other instances of dusty avocations may be mentioned as exciting causes. The polishing of brass is sometimes effected by rollers made of canton flannel which revolve with great velocity, filling the air with fibres of cotton which are capable of acting as mechanical irritants.

In the sizing process in some cotton manufactories the material is often adulterated with clays or some sort of salt to lessen the glutinous qualities of the flour or tallow, and although the process is carried on in damp rooms to lessen the brittleness of the size, dust prevails, causing irritation of the nose, eyes, and throat. Some interesting observations have been made on this subject by James Y. Simpson, who has especially investigated the hygiene of woollen manufactories. He suggests that these artisans are comparatively healthy because of the oil absorbed while running the machines. In the manufacture of cotton it has been found that in mills where cotton containing dust and dirt is used, as the East India varieties employed in England during the American War, the respiration was affected, and the expectoration of numbers of operatives contained slaty-colored matters, found, on microscopic examination, to contain cotton fibres.

Bakers who have to deal with highly-dried biscuit flour suffer more than those using ordinary brands of flour. But when all has been said, when we consider how many persons live permanently in an atmosphere specially surcharged with dust without showing a symptom of a morbid state of the respiratory organs, and since the epithelial cells of the lungs can contain particles of coal, it demonstrates that foreign bodies may penetrate the lungs without always inducing serious changes. Mineral matter has been found by Riegel in the form of silica in the lungs of a boy aged four, constituting 2 per cent. of the ash left after incineration. In those of a day-laborer aged forty-seven it amounted to 13 per cent., and in those of a woman cook sixty-nine years old it reached 16 per cent. Accepting these figures as accurate, they show a progressive accumulation in proportion to age among individuals breathing dusty atmosphere. Traube thinks that the changes in the lungs of coal-miners may not be produced by the accumulated particles of coal, but by the chemicals contained in coal, and not found in charcoal. In a discussion of this question in London in 1869, Wilson Fox thought it remarkable that in proportion to the number of persons exposed to the inhalation of irritating substances the cases of phthisis were comparatively few, and suggested that a diathetic condition might underlie the entire pathology.

In summing up the evidence bearing on the predisposing and exciting causes of pneumonokoniosis we cannot overlook the recent discoveries of Koch and his collaborators, but may conclude that although there is increasing evidence tending to show that the bacillus tuberculosis is always present in tuberculous pulmonary processes, yet its exact etiological relation cannot be considered as established. We may still hold that when large amounts of inorganic materials are taken into the lungs, particularly if the ventilation or hygienic conditions under which the dust is inhaled are imperfect, certain diverse pulmonary processes are apt to ensue. That phthisis can be thus produced is undoubted, but the nature of the irritant has less to do with the type of the resulting disease than has an inferior or scrofulous constitution, inherited or acquired, or the indulgence in habits directly damaging to the health; since an unvarying specific cause would be more destructive than has been proven, large numbers of individuals escaping any serious effects when equally exposed.

PATHOLOGY AND MORBID ANATOMY.--Whatever be the dust inhaled, the pathological processes set up by it partake of the same essential character, though differing in intensity and in the division of pulmonary tissue {457} principally involved, while the combined inhalation of organic particles may essentially modify the results produced. Examination of the lungs has revealed deposits of various inorganic materials which have been inhaled, such as oxide of iron, indigo, snuff, silica, coal, carbon, etc. A black discoloration of the pulmonary tissue, with or without induration, enlargement, and blackening of the bronchial glands, may, however, have its origin in morbid changes independent of inhaled matter, such as defective elimination of carbon and carbonic acid, with a sort of precipitation of carbon within the tissues.

The black coloration of the lungs, especially in miners, is also partly due to the deposition of a true hæmatoidin pigment in granular form, caused by the irritating particles inhaled setting up changes in the bronchial or pulmonary tissues, resulting in the escape of the coloring matter of the blood either by rupture of capillaries or from transudation of serum. Similar discoloration is often found in cases of chronic bronchial processes independent of a dusty etiology. The most penetrating form of dust is the silicious, on account of its hard, vitreous character. German authors comment on the difference in the power of penetration of mineral coal-dust as compared with charcoal-dust, because the spiculæ of the former are elongated, sharpened splinters. The coloration of the lung from clay-dust does not diffuse itself so readily as coal-dust, yet it possesses more irritating properties and creates more damage.

The morbid anatomy of pneumonokoniosis includes nearly all the pathological processes incident to the pulmonary tissues. The bronchial lesions are those of chronic bronchitis, with thickening of the bronchial mucous membrane, associated with possible ulceration and bronchial dilatations, forming bronchiectasic cavities. These cavities are caused by combined softening of the bronchial tissues with traction from without by the newly-formed fibrous tissue. The bronchial glands may be enlarged to the size of walnuts, and are often perfectly black and gritty on section. These enlarged glands may occasion, through pressure, many changes in the pulmonary tissues. The effect of this pressure is especially manifest in the lymphatic system. The lymph-circulation is further crippled by the accumulation in the lymph-channels of the inhaled inorganic materials. These interferences with the lymph-circulation may be followed by exudation or lobular and interlobular formation of tissue; secondary to these changes the pressure upon the vesicles may cause local congestions, exudations, and even hæmoptysis. By one or all of these processes the expansile power and elasticity of the lung are slowly depreciated, emphysema develops, intertwined with the lesions of acute, subacute, or chronic bronchitis, fibroid phthisis, and atrophic emphysema. Nodules of cretaceous matter can be recognized through the lungs, which are black in anthracosis or gray in silicosis. These nodules occur from the size of a pin's head to that of a pea, and are especially found in the lungs of glass-cutters, sandstone-workers, and grinders. In these cases they consist in part of iron and in part of stone. In sandstone-workers they are composed of silica; the organ feels nodulated, very fibrous, and in some cases actually gritty. The predominant form of pulmonary change is fibroid; hardened districts of advanced cirrhosis occur measuring two inches and upward in length and width, and in depth and thickness nearly as much. These may be rounded, but are not separable from the adjacent structures, the condensation of the tissues lessening without a defining line. On section they appear tough and leathery, most pronounced along the anterior edges of the lungs, and are apt to be covered in by thickened pleura. If the nodules previously alluded to are encysted, fibrous prolongations extend from these cysts into the substance of the lung, the thickening of the lung being greatest in the septa, on the pleural surfaces, and along the course of the bronchial tubes. Sometimes subacute or chronic pleural processes coexist. The caseous masses found in tubercular fibroid phthisis are infrequent in pneumonokoniosis, but in the latter process the {458} pathological changes may be identical with the ordinary forms of phthisis, especially in those individuals who are predisposed to pulmonary affections and those in whom the pathological processes are rapid.

In anthracosis the lung is large and increased in weight; the surface of the pleura has a bluish-black color, contrasting with the coal-black color of the lungs, which are universally pigmented and contain nodules of pigment. When only small quantities of pigment are present, it presents the appearance of dark lines running between the lobules; on section these are very hard and distinct, being about the size of a millet-seed. They are universally distributed throughout the lung, and in some places appear like small masses of charcoal. Upon squeezing the organ a blackish fluid exudes which stains the hands, but the discharge which is found lying in the bronchial tubes is often yellow and muco-purulent, although the sputa during life is more or less discolored. When the distribution of the discoloration of anthracosis is investigated, it is found to closely correspond with the lymphatic distribution of the lung, and the conclusion is probably well founded that all other irritating particles pursue the same course through the pulmonary tissues. When particles of coal or pigment enter the bronchi with the air, they cannot pass through its mucous membrane, because the basement membrane and fibrous coat underlying it present an obstacle to their lodgment, whilst the cilia of the epithelium tend to prevent their retention in the bronchi; they therefore enter the vesicles, and may be found sticking to the walls. In this way the exemption of the bronchi from pigmentation, even down to the smallest ramifications, can be explained. The interlobular septa ate also the seat of great pigmentation. The germinating epithelium elevates the cells slightly above the surface, and in the interspaces between them the pigment insinuates itself, and thus enters the underlying plasmatic or lymphatic spaces; or the pigment may be incorporated into the epithelial cells, which transfer it to the underlying lymph-space. Once the pigment has found entrance to these lymphatic channels, it is carried by them through the lymphatic vessels in the sheath surrounding the bronchial tubes and the small branches of the pulmonary artery, and in the interlobular septa to the bronchial glands. In this manner the special distribution of the coloring matter in these situations is explained. The special deposit around the small branches of the pulmonary artery is owing to the double set of lymphatics, the peribronchial and the perivascular, which form an anastomosis. The perivascular set is the larger; consequently the pigment passes into them more readily, forming the nodules. Pigment is also found in small quantities around the bronchi, which can be accounted for by the anastomosis of the lymphatics. The bluish-black appearance of the pleura and the distribution of the pigment only in the deeper layers of the visceral pleura are susceptible of a similar explanation, because the deeper layers of the pleura contain lymphatic vessels which are directly continuous by means of the lobular septa with the large perivascular branches of the lymphatic system.

The consequences of the obstruction to the lymphatic and pulmonary-artery circulation may be very serious. In grave cases the lung breaks down, forming a gangrenous-like cavity, which differs from an ordinary cavity in not being rounded; it is more like a gangrene or slough. In a few cases the pathological appearances indicate phthisis, chiefly interstitial, with formation of cavities; sometimes traces of cavities are found which have cicatrized. More commonly oedema is developed in the lung and the bronchial passages. As a consequence of combined bronchial irritation from continuous inhalation of inorganic particles, and the consequent oedema, a continuous germination and shedding of the bronchial epithelium--a chronic bronchitis--associated with emphysema, is maintained. The mechanical cause of this bronchitis--more or less impediment to the vascular and lymphatic circulations by the {459} pigment deposit--is capable of explaining the persistence of various forms of bronchial processes in anthracosis and in other forms of pneumonokoniosis after the patient has ceased working in a dusty atmosphere.

SYMPTOMATOLOGY.--Pneumonokoniosis does not present a special symptomatology. The course of the various morbid processes is insidious and slowly progressive: the development of any of the forms of pulmonary disease depends largely upon the degree of exposure to the exciting causes, or the inherited tendencies, or the susceptibility to influences liable to diminish general vitality or affect the personal hygiene.

The earliest objective symptom of pulmonary lesion is cough, especially recurrent in winter, accompanied by expectoration, which is whitish, frothy, or stringy in character. Gradually the physical signs, taken together with the symptoms, indicate the various forms of bronchitis, acute, subacute, or chronic, sometimes associated with emphysema, bronchorrhoea, or bronchial dilatation. In other cases the symptomatology is that of asthma, either purely spasmodic or secondary to emphysema or cardiac degeneration. In true anthracosis dyspnoea is a marked symptom, and perhaps the accumulation of pigment may interfere with the oxygenation of the blood, or dyspnoea may be due only to an emphysematous pulmonary tissue. The sputa will be black so long as the subject is working in an atmosphere loaded with pigment.

Fibroid phthisis is frequently associated with atrophic emphysema, and the clinical history corresponds with that which is commonly observed in these diseases. Hæmoptysis is rare, but if it occurs it suggests the addition of some tubercular element; a purulent nummular sputa is a suspicious sign of similar import. The symptoms and physical signs of dry pleurisy are to be expected whenever any form of the phthisical process supervenes. The cavities in the lungs are usually bronchiectasic, unless tubercular phthisis occurs as a complication, and the physical signs need no comment. Subacute and chronic laryngitis with ulceration complicate certain cases, particularly those which have inherited or acquired a tubercular tendency.

DIAGNOSIS.--The diagnosis involves a comparative examination of the etiology and the physical signs.

PROGNOSIS.--The prognosis depends very largely upon the withdrawal of the sufferer from an unhealthy environment. In each single case the inherited tendencies, the personal constitution and habits, must be the basis for an opinion upon the gravity of the pulmonary processes and the possibilities of restoration to health. The progress of the disease may be materially retarded or arrested by withdrawal from the occupation involving the inspiration of dust, and restoration to comparative health after years of invalidism is possible for these victims of dusty avocations, even after serious damage has taken place in the lung, if suitable hygienic conditions can be obtained.

TREATMENT.--The treatment of pneumonokoniosis divides itself into the prophylactive and the curative. In works devoted to the hygiene of occupation careful directions are given in reference to methods designed to prevent the dust from entering the respiratory passages. This is partly accomplished by the use of masks or respirators, which possess the obvious disadvantages of clumsiness and interference with respiration. Various devices may be employed in different avocations to prevent the generation of dust, but the most practical plans consist in thoroughly ventilating the atmosphere, and thus preventing the dust from reaching the artisan. Aside from these, the management of the various pathological conditions must be based upon the general principles which govern the treatment of pulmonary processes.

{460}

CANCER OF THE LUNGS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A malignant disease affecting the pulmonary tissues. (Vide also MEDIASTINAL DISEASE.)

SYNONYMS.--_Fr._ Carcinome du poumon; _Ger._ Lungenkrebs.

ETIOLOGY.--Carcinomatous disease affecting the lung-tissue is exceedingly rare as a primary process, and exhibits only a feeble inclination to inoculate other portions of the body. In the majority of cases the mediastinal glands are first affected, or it appears in the lungs as secondary to disease elsewhere in the system. Metastasis is probably effected by means of particles of living cellular material which are transferred through the blood-vessels or lymphatics.

Cancer of the lung often reverses the rule that carcinoma occurs most frequently in the female, Hasse, Kohler, and Cockle giving a majority of cases among males. It has been met with in childhood and in extreme old age, but is more common in the middle periods of life, from twenty to sixty years.

PREDISPOSING AND EXCITING CAUSES.--The predisposing and exciting causes of malignant pulmonary disease are involved in the obscurity that surrounds the development of all neoplasms.

PATHOLOGICAL ANATOMY.--Clinically speaking, cancer in the pulmonary tissues includes the scirrhous or encephaloid neoplasms. The colloid, enchondromatous, or fibromatous growths have been recorded as possible tumors, but possess only a pathological interest.

Malignant disease may commence in, or ultimately implicate, one or all of the pulmonary tissues; secondary neoplasms have been experimentally produced by lodgment in the lung of living cellular particles which grew centrally by virtue of inherent cell-proliferation, independently of changes produced in the surrounding tissues. Cancer of the lungs, whether primary or secondary, usually originates near the roots of the lungs, implicating the mucous and submucous membranes of the bronchi, sometimes commencing in its small mucous follicles. The bronchial passages and the lymph-channels become the viaducts along which the growth proceeds in its march of invasion, involving most frequently the posterior portion of the middle lobe. The apices of the lungs may be implicated, but not primarily, as in tuberculosis. The mediastinal lymphatics are originally involved in an unestimated number of cases, or enlargement of these glands is coexistent with the development of pulmonary cancer. The enlargement of the mediastinal glands is sometimes moderate, but an enormous mass may be formed. (Vide MEDIASTINAL TUMORS.)

Carcinoma is found in masses varying in size from a hempseed to an orange or larger, and since its distribution follows the lymph-channels in their circuitous route through the lung, we can account for the wide distribution of the nodular masses of secondary cancer. The isolated nodules present an {461} ovoid outline, sometimes situated near the pleural surface, in contrast with the larger formations which affect the roots of the lungs.

The primary malignant formation presents a single large mass of infiltration, possibly associated with a few small nodules scattered throughout the lungs; the right lung is conceded to be the most frequently affected, but secondary cancer usually implicates both organs.

Cancer in the parenchyma of the lung may diminish or occlude the lumen of the bronchial tubes, or they may be filled with cancerous matter and their walls perforated. The development of cancer along the distribution of the bronchial passages shows us how readily chronic bronchitis may occur as a complication and form a confusing element in the diagnosis. The remaining pulmonary tissues may escape anatomical change, or from pressure atrophic or hypertrophic emphysema or collapse may ensue. These changes, together with the similarity to a fibroid phthisical process which many cases suggest, must be borne in mind in making a diagnosis. Pulmonary apoplexy, or even gangrene, is an incident in some of the clinical pictures of this disease, and embolism or thrombosis in other parts of the system may occur. The terminations of intra-thoracic cancer vary in accordance with the history of these growths elsewhere. Infiltration with blood or melanic deposition has been noticed; evacuation of the new growth through the bronchi may induce the development of cavities in the lungs, preceded or accompanied by suppuration, ulceration, or gangrene. In addition, hydro- or pyo-pneumothorax may occur by perforation or invasion of the pulmonary pleura.

Carcinoma of the pleura is usually secondary to its development in the lung, but it may be communicated from a similar process in the mammary gland by infection through the pectoral and intercostal muscles to the parietal pleura. Carcinomatous formations on the pleura are small and hard in scirrhous, but are larger in encephaloid, cancer. The minute spots of early formation are found scattered over the pleura like drops of wax. The thickened tissues, when they coalesce, undergo degeneration, and may form plaques of cartilaginous hardness. Large pleural growths may compress or nearly efface the lung, but are among the curiosities of medical literature.

Neuralgia may be occasioned when nodules impinge upon the intercostal nerves. Similar pressure is the cause of the pain in pulmonary cancer, except that induced by the pressure of mediastinal enlargement. Chronic pleural inflammation may be frequently developed by the new growth, and the diseased lung may become adherent to the inner surface of the sternum and ribs. The lung in other cases may be compressed or retracted, uncovering the heart and rendering the chest-walls smaller. The chest may be enlarged, especially if there is pleural effusion; usually the contour is unchanged.

Pleural effusions are frequent in the history of this disease: they may be passive, resulting from pressure on the azygos or hemiazygos veins, preventing the return of the blood from the pleural veins, or from mediastinal pressure. An inflammatory hydrothorax may be excited by the deposit of cancerous material in the pleura; and it is possible for these effusions to undergo purulent transformation or to become hemorrhagic. A hemorrhagic effusion when grouped with other symptoms may be considered an important evidence of malignant formation. The further history of pleural effusions in this association is usually an increase of such an amount as to necessitate removal by thoracentesis, but reabsorption is possible.

SYMPTOMATOLOGY.--The interest of the clinical observer nucleates itself around the symptomatology and diagnosis. The frequent negative results of physical examination indubitably prove that its teachings alone are insufficient for the purposes of diagnosis, so that any study of a case would be partial which did not unite the evidence yielded by physical signs with the general symptoms. The clinical evidences are more definite when the {462} neoplasms are multiple and associated with some mediastinal process than when single or absolutely primary growths. The development of the disease is insidious. Gradually the facies and general surface of a patient indicate the true nature of the malady by the characteristic cachexia. Cough is an early symptom, unimportant save that it cannot be assigned to any definite cause. It may be dry and hard, attended only by expectoration of glairy mucus, or the sputa may be purulent. Usually the amount is in ratio with the degree of coexistent bronchitis. In the latter stages of the disease the sputa may contain blood, resembling prune-juice or black-currant jelly, due to erosion of some of the blood-vessels. In this stage of softening cells characteristic of the new growth, with portions of the pulmonary structure, may be found on microscopic examination of the sputa; the appearance of the expectoration sometimes suggests fibrinous bronchitis.

When there is elevation of temperature it may present a hectic type, with night-sweats, which are stated by Walsh to be sometimes confined to the affected side. The presence of an abnormal temperature-curve is indicative of associated inflammation of the bronchial mucous membrane, the development of a pleural process or of phthisis, especially the fibroid form. The pulse becomes accelerated in ratio to the degree of these inflammations and the failure of the sufferer's strength.

The new growth determines some mechanical symptoms cognate to all intra-thoracic tumors, especially those which involve the mediastinum. Lancinating pain would presumably be a constant symptom, but is, in fact, infrequent, unless the growth or growths enlarge so as to cause pressure on the nerve-trunks, in which event pain may become a distressing symptom. Characteristic pains complicate those cases in which the pleural tissues are involved in the morbid process. Dyspnoea is a pressure-symptom of considerable import if other conditions capable of producing it, especially uncomplicated emphysema, are rigidly excluded. When the new formation is infiltrated throughout the lungs, the growth may, as in miliary tubercle, impair the aërating power of the lungs by diminishing their elasticity and increasing their density. When, however, the process is local and restricted, the dyspnoea may be due to irritation of the terminal filaments of the vagus; this being a mixed nerve composed of accelerator and inhibitory filaments, the balance of innervating power may be readily destroyed and partial or incomplete respiratory effort follow. Dyspnoea may also result from pleural adhesions or effusions, or may be secondary to direct cardial or pericardial involvement in the cancerous process. Palpitation or increased pulse-rate may be referred to irritation of the vagi, or to some of the foregoing pathological processes.

Kindred to these symptoms are the changes in the voice, which sometimes undergoes frequent variations due to irritation or pressure on the trachea or on the branches of the pneumogastric nerve, especially when mediastinal disease is present. Aphonia, huskiness, a bass voice, or high treble, one or all, may be constant or alternating harbingers of the concealed mischief. The laryngoscope will inform one whether there is direct involvement of the larynx with morbid growth. Dysphagia is to be expected if the new formation involves the regions through which the oesophagus passes, and a sacculated pouch may be formed above the compressed spot. Changes of posture may increase or diminish the pressure, and thus the dysphagia or dyspnoea may at times be more pronounced than at others. Dysphagia may also be due to swelling of the oesophagus near the location of pressure. Reflex irritation of the sympathetic ganglia may induce pupillary contractions in one or both eyes: this symptom is chiefly present when the mediastinum is involved.

The physical signs contingent on pulmonary cancer include those ordinarily indicative of bronchitis with or without atrophic emphysema, simple pleural effusion, or chronic pleurisy with retraction. By inspection a study {463} should be made of the contour of the thorax, the respiratory movement, and displacements of the intra-thoracic viscera. The thorax may appear enlarged, either from the new formation or from associated pleural effusions. It is often retracted, owing to the atrophic changes, and collapse brought about by the new formation or induced by pleural adhesions. The movements of the chest, unless there is a pleural complication, possess no distinctive character in this disease. Displacements of the heart or trachea may be expected on mechanical principles if there is mediastinal disease. General inspection may detect in the clubbed fingers evidences of venous obstruction, and sometimes an asphyxial hue of the upper portion of the body. Nearly always a general emaciation with anxious expression exists, and a tawny or lemon-hued skin indicative of the cancerous cachexia.

By palpation of the substernal or supra-clavicular spaces one may reach masses of painless, movable, glandular enlargement, but these may be easily overlooked unless a careful study be pursued. Circumscribed swellings of the thoracic walls may be detected, though not often, and the glands of the axillæ and neck may enlarge. Palpation may also reveal an inequality in volume between the radial pulses, but not so commonly as in purely mediastinal tumors or in aneurisms. Percussion and auscultation are negative or yield an area of dulness or flatness with restricted or absent respiratory murmur. When there is a single large growth the boundaries of these signs are local. If the tumors are diffused the respiratory murmur varies. In tiers of lung it is feeble or absent; elsewhere it is harsh, puerile, or bronchial. Chiefly remarkable is the fact that the character of the respiratory murmur cannot be harmonized with any other pulmonary states when the entire clinical evidence is taken. Vocal resonance corresponds with the respiratory murmur according to accepted laws. When there is pressure on the principal bronchus on one or both sides, one can detect either a snoring, increased bronchial respiration, or else, if the pressure decidedly narrows the calibre of the bronchus, the breathing becomes feeble or wheezing. Expiration may be prolonged and sonorous in character, with or without râles. The pressure is rarely equal on the two sides. The vocal resonance in these cases is ringing and brazen. Mensuration corroborates inspection. Pleural effusion from whatever cause is revealed by the ordinary signs. Enlargement of the bronchial glands, either primary or coexistent with the development of cancer in the lung, reveals itself by pressure-symptoms proportionate in their severity to the degree of bronchial enlargement. Pain, laryngeal irritation, differences in the radical pulses, tumor if the enlargement is anterior, one or all, may be present. The aorta itself may be compressed by the enlarged glands; and by the narrowing of its lumen thrill, and even systolic, murmur can appear, making a differential diagnosis from aortic aneurism very difficult. (Vide MEDIASTINAL TUMORS.) Embolism and thrombosis, with the ordinary symptoms, may complicate the course of pulmonary cancer and obscure the diagnosis.

The duration of cancer of the lung is fixed by Walsh at 13.2 months, mean average, maximum, at 27 months; minimum, at 3.5 months; but this is based on a confessedly small contingent of cases. The first symptoms, dry cough, pain in the chest, difficulty of breathing, may last for some years without alarming the patient. After the more dangerous phenomena appear the course is often more rapid. The history of cancer in the lung in the main corresponds with cases of similar types of cancer elsewhere. The grave symptoms appear earlier in cases of mediastinal cancer than in cancer of the lungs proper. Death may result from asphyxia; from bronchial obstruction; from pulmonary oedema occurring suddenly, as in chronic alcoholism; from embolism of the pulmonary artery; or from pleural effusion. Life may gradually ebb away through general asthenia with malnutrition; in some {464} remarkable cases the same result is accompanied by hectic fever and the typhoid phenomena, with evidences of tissue-disintegration.

COMPLICATIONS.--The complications of pulmonary cancer have been already outlined. They are chiefly the bronchial, pleural, and mediastinal processes. Primary cancer of the lungs possesses a feeble tendency to metastasis.

DIAGNOSIS.--The most valuable assistance is derived from a close study of the personal and hereditary history. Whenever a new growth has been extirpated, the possibility of its reappearance in the lungs should always be remembered. The most disciplined comparative analysis of physical signs may be fruitless. The origin of a primary growth from the roots of the lungs may help to interpret the physical signs, and examination of the sputa should never be omitted. In secondary cancer the history of the case may include the removal or development of morbid growths from other parts of the body. Any pulmonary symptoms in these cases become more suspicious than they would in persons in whom no signs of cancerous diathesis have ever made their appearance. This rule must not be pressed too far, for forms of pleurisy, bronchitis, and pneumonia or phthisis may be the explanation of the symptoms.

In the differential diagnosis it is a matter of universal experience that some form of chronic pleurisy is the most frequent source of doubt to the clinician. It has been said by Wintrich that vocal fremitus in cancer is more often present than absent. If there is much pleural effusion, paracentesis will be helpful in two ways. When the fluid is turbid, highly albuminous, with a large proportion of coagulable fibrin, it is an evidence of its inflammatory origin; but if it is clear and limpid, and upon standing gives but a delicate veil of pseudo-fibrin, it indicates a passive or mechanical cause. If the fluid evacuated should contain any considerable amount of blood, such a peculiarity in association with the other symptoms already indicated is to be regarded as probable evidence of the existence of cancer of the pleura. If the external veins of the thorax are enlarged, they indicate a deep-seated cause of pressure. In malignant disease with retraction there may be less deepening and narrowing of the intercostal spaces on full respiratory movement than is associated with chronic pleurisy: there is usually greater volume and nearness of the respiratory murmur, although this is more noticeable on the left than on the right side, since the liver is present in the latter. The greater severity of the local symptoms and the increase in gravity of the disease must be contrasted with the features of a disease in the decline, as is the case in chronic pleurisy. Walsh considers that "the normal position of shoulder, spine, and scapulæ distinguishes cancer from the results of simple pleurisy." In addition, we have the shorter duration of cancer, which is never over two and a half years, often less. The lemon-hued cachexia is so frequently absent that the inference from general inspection of the features is marred. From fibroid forms of pulmonary disease we have the pressure-signs, giving evidences of mediastinal new formation; also the possible prune-juice expectoration of cancer. The retraction and displacements of the intra-thoracic organs, chiefly the heart, are greater in fibroid disease than in either pleurisy or cancer.

In addition, the history of phthisis includes a higher thermometrical record, frequent hæmoptysis, and abundant sputa. Physical diagnosis in cases of phthisis reveals a destructive process involving extensive areas of pulmonary tissue in a comparatively regular sequence. The cancerous process is more local or involves the tissues in an irregular order. Moreover, the asphyxial hue and the pressure-symptoms preponderate in malignant disease. To distinguish the cancerous process from simple forms of bronchitis we may observe the frequency with which the symptoms of bronchitis recur in cancer {465} without exposure to an adequate cause; by the absence of marked tendency to hypertrophic emphysema; by the resistance to treatment; by the persistence of dyspnoea as a prominent symptom; and by the gradual development of patches of hypostatic congestion. To differentiate from aneurism we should consider the occupation of the patient, the absence of syphilis or other causes of arterial disease, the history, the location of the tumor, and the absence of the murmur. Hydatid cysts may simulate cancer, but this disease is rare in America. (Vide PULMONARY HYDATIDS.) In cancer of the liver, as that organ enlarges pulmonary symptoms may occur from irritation, and congestion or oedema be produced. We must be content to mention the possibility of error, and decide in each case after a crucial analysis of the abdominal or thoracic symptoms.

PROGNOSIS; TREATMENT.--The prognosis is fatal; the treatment purely palliative. It is quite justifiable to relieve pain by the hypodermic use of morphia, cough by chloral or the usual narcotics, and fetor of the breath may be palliated by inhalation of carbolic acid or other disinfectants. Dyspnoea may be alleviated by the use of strychnia as a respiratory stimulant--by inhalation of nitrate of amyl or small allowances of chloroform or digitalis. Paracentesis thoracis must often be resorted to in cases of pleural effusion, even although the relief it affords be temporary.

{466}

PULMONARY HYDATIDS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A disease in the lungs consequent upon the entrance into the human system of the eggs of a small tape-worm, whose usual habitat is the upper half of the small intestine of the dog.

SYNONYMS.--Tænia echinococcus; Acephalocyst. _Fr._ Kystes hydatiques du poumon; _Ger._ Lungenechinococcus.

HISTORY.--Unmistakable references to this disease are found in the writings of Hippocrates, Aretæus, Galen, and other early writers. For a long time, however, the animal character of the hydatid cyst was not recognized, but confounded with slowly-developed local dropsies of various orders and with lymphatic dilatations. Their animal nature was suspected by Hartman in 1685, but their origin was not separated from the cysticercus. In 1766, Pallas clearly distinguished the two species, and this author was followed in a more positive way by Groeze in 1782. Laennec in 1804 carefully studied the hydatid cyst as found in the sheep, recognizing even the mode of reproduction, but he erroneously described the same parasite, when existing in man, as a distinct animal, which he termed acephalocyst. Since 1821, Bremsen, Davaine, Küchenmeister, and others have definitely settled the true mode of the entrance of the Tænia echinococcus into the human system, and the subsequent development of the hydatid cysts. The development of the parasite resembles that of the cysticercus. Like the latter, the larvæ infest the bowels of certain animals, and take their further development in a different animal or species, forming vesicles which are distributed in the parenchyma of the different organs, and in this way more or less seriously compromising the functional life of the part in which they occur.

ETIOLOGY. (See article on INTESTINAL WORMS, by Leidy.)--Hydatids have been found in the human subject in all countries, but especially in France, Germany, and in the north of Europe. They are rarely found in North America, and the fact that the majority of cases seen here have occurred in foreigners favors the probability of the hydatid disease having been imported. But there are two countries where it may be said to be endemic--Iceland and Australia. Finsen found 1 out of every 43 inhabitants affected with this disease in the district of Ofjord in Iceland. Hydatids are communicated to the human race through the system of the dog, and in Iceland the proportion of these animals to the population is probably more than 1 to 3, a recent census recording 20,000 dogs to 70,000 inhabitants. Hydatids usually enter the system through the digestive and respiratory organs. The Icelanders are excessively uncleanly and careless of the laws of ventilation. In the winter season both men and women are confined to the house in company with their dogs, and in consequence the air is impregnated, and oftentimes the drinking-water contaminated, through their dejecta, which contain thousands of the eggs of the echinococci. The largest {467} number of cases occur in the agricultural districts, since the dogs are more required there than on the sea-coast.

In Australia large numbers of dogs are maintained to guard the sheep. The droppings of these animals, dried by the hot winds, are inhaled as dust. It is curious to note that in Australia, where the high winds prevail, the proportion of pulmonary hydatids is very large, while in Iceland, where the drinking-water is the principal medium of communication, the lungs are less often affected than other viscera. Finsen's records in the latter country show 255 cases; of these, 176 occurred in the liver, and only 7 in the lungs. In both Iceland and Australia women are more subject to echinococci than men. This is possibly accounted for by the facts that the women take care of the dogs and wash the vessels from which they eat, and are also less protected by hair about the mouth and nose than men.

The disease occurs most often between the ages of twenty and thirty years, but it has been found in children of four years of age. Before ten and after sixty the proportion of cases in both sexes is equal. The malady is not hereditary, but uniformity of environment accounts for the propagation in communities. Pulmonary hydatids occur as primary formations in the lungs, but may be secondary to similar growths elsewhere, especially in the liver. There is, however, scarcely a tissue in the body in which hydatids have not been found.

MORBID ANATOMY.--Hydatid cysts consist of sacs of various sizes, from that of a pea to an orange or even an adult head. They are usually globular in shape, and attached by a vascular membrane to the organ in which they are situated. The walls of the cysts are composed of a few laminæ of indeterminate membrane of varying thicknesses, commonly depending on the age of the cyst. In young cysts they occur in direct contact with the lung, but as they grow larger a thicker investment is formed, and large old cysts which have generally undergone spontaneous rupture often have a dense leathery sac. Walsh asserts that the parent cyst lies in direct contact with the lung-tissue, and, unlike that of the liver, is rarely surrounded with a thick shell or cyst-wall of pseudo-areolar tissue. The interior of the pouch is smooth and of the aspect of serous membrane without epithelial covering. The parent cyst contains daughter cysts which are single or multiple, and a liquid the proportion of which is variable. This liquid is nearly limpid, and non-coagulable by heat or acids; it deposits by evaporation crystals of chloride of sodium.

Commonly, only one hydatid tumor is found in the human lungs, although in animals multiplicity of cysts is the rule. They are usually located in the base of the lungs, and are thought to be more common on the right side, but they may occupy any portion of one or both lungs. They have been found in the pleura, the bronchi, the pericardium, and the thyroid gland. In the pleural cavity they may be attached to both the costal and the visceral pleura; in the latter case they may form an outgrowth from the lung into the pleural cavity. Authorities differ as to the condition of the neighboring lung-tissue, some stating that the cysts are rarely surrounded by healthy lung-substance, while others assert the contrary. Since the growth of the cysts is often very slow, the accommodating power of the lung is remarkable when no constitutional mischief exists. In some instances the rapid enlargement of a cyst has been accompanied by certain forms of pneumonia, secondary inflammatory lesions, congestion of the neighboring tissue, splenification, or even gangrene.

Hydatids situated either in the lung or pleura may rupture into the bronchial tubes, and thence be discharged by cough and expectoration, or they may open externally like a pleural empyema, or even rupture through the diaphragm into the intestines or peritoneum. None of the above accidents are necessarily fatal, not even the latter, unless the fluid be puriform. {468} Empyema with pneumothorax usually follows rupture into the pleura. Finsen observes that a general urticaria may follow the rupture of a cyst into a serous cavity. In old cases, after rupture of cysts, pulmonary changes may almost always be found. The ruptured cyst may become a suppurating cavity, suggesting the possible development of phthisis. In some cases hydatid formations have been described with coexisting catarrhal or tubercular disease, or these processes may occur as a complication without rupture of the cyst.

SYMPTOMS.--The symptoms of hydatid cysts are obscure, and the physical signs difficult to analyze when the cysts are small. They are more suggestive when the cyst becomes large enough to contain a pint or more of fluid. The outline of the cyst is usually globular, and is imbedded in healthy or nearly healthy lung-tissue. According to Bird, the physical signs correspond with those familiar to us in pleural effusions: absolute dulness or flatness on percussion, with absence of respiratory murmur over a space of the chest-wall not smaller than the palm of the hand; vocal fremitus and resonance are also abolished. The expansion of the chest is more or less deficient upon the affected side, but seldom with any change on mensuration.

The area of the above physical signs usually presents a rounded outline, limited by a line of demarcation so exact that it can be mapped out with pen and ink, but is unaltered by position. Their location is generally in the lateral or infra-clavicular regions; beyond the boundary-line percussion is vesiculo-tympanitic resonant or normal, and the respiratory sounds begin at the very margin of the pen-and-ink line, and, though probably harsh and puerile in character, are indicative of healthy lung-tissue.

Pulmonary hydatids can seldom be examined by palpation, but all authors allude to a frémissement or peripheral fluctuation which may sometimes, but not invariably, be detected by palpation over the intercostal spaces. Davaine directs palpation as one would palpate an abdominal cyst. The sensation of fluctuation is as though the fluid were gelatinous; when the quantity of liquid is excessive this movement is not perceptible. It is most recognizable when there is but a single hydatid in the parent cyst (Jobert). The frémissement cannot be felt when the sac has undergone atheromatous degeneration, because there is then no liquid, and the cysts are withered, agglutinated to one another, and the tumor is inelastic and hard. By auscultating the tumor while practising percussion one may hear more or less positive vibrations resembling those produced by a bass string (Briançon).

The general symptoms of pulmonary hydatids are of mechanical origin: pain, dyspnoea, cough, with duskiness of the surface, all of which are more or less marked according to the size and location of the tumor and its rapidity of growth. A phthisical appearance is possible, with deterioration of the blood-crasis and progressive loss of flesh. Marked clubbing of the finger-ends and incurvation of the nails have been noticed, all of which symptoms have disappeared after the hydatid cyst has been tapped or expectorated. Cough nearly always accompanies this disease, as it does a large pleural effusion. The expectoration is a glairy mucus, sometimes stained with blood; when local bronchitis occurs as a complication, it may become muco-purulent. There is much diversity of opinion as to the frequency of hæmoptysis, many authors looking on it as a rare symptom. According to Bird, there is seldom or never profuse hæmoptysis, though several ounces have been expectorated at a time in an aggravated case where tapping had been long delayed. The cause of hæmoptysis is usually pressure of the growing cyst upon the pulmonary veins, leading to extravasations of blood.

If dyspnoea with deficient aëration of the blood, wasting, clubbed fingers, and expectoration persist after the expulsion or death of the hydatid, the probability is in favor of some associated pulmonary inflammation. When {469} a hydatid cyst ruptures into the bronchial passages, there is serious likelihood that the patient may choke or suffocative dyspnoea supervene. The quantity of entozoal substance voided at any one time varies from a few microscopical fragments up to a pint or more of unbroken acephalocysts. The expectoration of acephalocysts may continue several months. Serious general pulmonary symptoms precede and follow this accident. When rupture has taken place into a bronchial tube, there are the usual physical signs of a pulmonary abscess or large vomica. The sac usually suppurates, and there is a constant expectoration of blood, pus, and half-putrid acephalocysts of excessive fetor, and often portions of gangrenous lung-tissue. With these symptoms the temperature is sometimes of a low, remittent type, with hectic and sweats. The symptoms resemble those of empyema or advanced phthisis, and may continue for months, until the patient, in most cases, sinks from exhaustion, unless relieved by the evacuation of the sac and its contents. When hydatids develop in the pleural cavity the signs are identical with a localized pleural effusion.

Nothing has been said to differentiate pulmonary-hydatid expectoration from cases where an hepatic hydatid cyst has burst into the lungs, and the diagnosis may be very difficult. The physical signs of enlarged liver are present, also the antecedent symptoms of disordered hepatic action, especially intestinal indigestion and the staining of the sputa with bile. If the cyst has undergone suppuration, the symptoms may be allied to those of hepatic abscess.

The nucleation of testimony favors the view that a latent or slow growth is by far the most common history of hydatids. Their duration is very variable: patients may harbor them for a long time unconsciously, even over a period of sixty years. This is corroborated by Finsen, who reports cases in which the disease lasted sixteen, eighteen, and fifty-two years, proving this by stating that these individuals had left the country where the disease was endemic, and were residing during these periods where the malady was rare.

TERMINATIONS.--30 or 40 per cent. of cases terminate in recovery if the cysts spontaneously burst, death being caused in others by suppuration and exhaustion. There is, in addition, the risk of sudden death from the rupture of a large cyst in the lung, and consequent filling up of the air-passages by its contents. The cysts may sometimes undergo atheromatous changes in which the hydatids resemble crushed grape-seeds. Microscopically, one finds a puriform fluid, plates of cholesterin, crystals of hæmatoidin, hooklets of echinococci, and débris of membranes. Again, the cysts may resemble a caseous or cretaceous tubercle without special characteristics. This may be looked on as a species of spontaneous cure. The growth of hydatid cysts may bring about by pressure such a state of chronic pulmonary engorgement that it affords a predisposing condition favoring the development of tubercular phthisis.

DIAGNOSIS.--The differential diagnosis is necessarily difficult. The nationality of the subject and the presence of a predisposing environment should always be remembered. If the disease progresses rapidly without interference, the diagnosis may be complicated by the development of patches of bronchitis or pneumonia with rusty sputa. The bronchitis is, however, local, which, taken with the physical signs of a cyst, may be suggestive. The only absolute evidence of the existence of hydatids in the lungs, whether primary or secondary, is the appearance in the sputa of the characteristic cysts or portions of them, such as fragments of the hooklets of the echinococci. This, unfortunately, occurs as a late accident in their history. If the boundaries of the cyst can be recognized, it is justifiable to resort to paracentesis, and thereby withdraw some fluid for examination. The physical signs of local serous effusion, globular in shape, not evenly {470} distributed around the circumference of the chest, is one of the best differential evidences between hydatids and pleural effusion. Moreover, there is no fever in hydatids unless after rupture, or with extensive phthisical complication, while there is a history of fever in some stage of most cases of pleurisy. Hydrothorax is differentiated through its being bilateral and by its etiology. From local encysted pleurisy the only resort is exploratory puncture and the question of the probabilities in each case. In the same way paracentesis removes doubt whether there be mediastinal tumor, solid tumor of the lung, or circumscribed pneumonic abscess; in the latter the general history of each case is helpful. From phthisis we must have recourse to the physical diagnosis already mentioned as belonging to hydatids. An unbroken cyst in the liver, high up and far back on its convex surface, may not be distinguishable from one in the base of the lung immediately over the liver or one in the cavity of the pleura.

PROGNOSIS.--According to Reynaud, this depends on--1, whether the hydatid is single or multiple; 2, whether the pressure is exercised on blood-vessels or bronchi; 3, if hydatids are discovered elsewhere; 4, size of cyst; 5, alterations in the walls of cysts; 6, whether complicated with any other disease or independent.

If there is a tendency to pulmonary phthisis, inherited or acquired, or if this disease exists as a complication, it forms an unfavorable element in the prognosis. Persons once affected with hydatids are more susceptible to a second invasion of the parasite. The practicability of treatment by tapping is also an element in the prognosis.

TREATMENT.--Naturally, the preventive treatment rationally deduced from the now distinctly-understood causes should be practised. The water-supply should be protected from sources of contamination, and in addition the inhabitants of countries where the disease is prevalent should, as far as practicable, use boiled or stone-filtered water and refrain from eating water-cresses or plants of like character wherever these are liable to be contaminated.

Many drugs have been administered, among them the bromide and iodide of potassium; solutions of salt are also said to be deleterious to the life of the echinococcus; Laennec even prescribed salt baths. Tincture of kamela has been recommended by Hjaltelin, a physician in the employ of the Danish government in Iceland. He administered it in doses of thirty drops daily to adults, continuing its use during a month or more. It has a distinctly irritating and destructive effect on the acephalocyst (Bird). Turpentine, from its well-known anthelmintic powers and ready diffusibility, has naturally suggested itself as a remedy, and according to some has proved of great service in many instances, while in others it has signally failed.

Paracentesis is generally regarded as the most efficacious treatment, and may be carried out upon the principles usually applied in the treatment of hydrothorax. Bird recommends that the trocar should be not less than six inches long and of the smallest diameter that is made, always providing that it is strong enough to bear the strain of a firm pressure. Cysts can be tapped in this manner even when they are separated from the chest-wall by quite a deep layer of lung-substance. This treatment should be practised at the earliest possible period in the life of the cyst. Speaking of the aspirator, he says that cases always do so well if tapped early enough with the simple trocar and canula that aspiration is not required. The gradual expansion of the lung as the cyst is emptied is sufficient to expel all the fluid, especially if aided by the effects of coughing. In exceptional cases of old standing, where there is a thick adventitious external wall to the cyst, which is generally closely adherent to the ribs, or again in cysts of the pleura, a free antecedent incision of the external tissues is sometimes required. It has been suggested by different authors that tincture of iodine should be injected after {471} aspiration to secure the obliteration of the cyst by inflammation. The injection of carbolic or salicylic acid under the same conditions has been practised with success by Mosler and others.

The treatment of old suppurating cysts is rather different. The centre of the sac, as nearly as can be judged, is fixed upon, and an incision is then made through the skin and muscles, and the largest-sized trocar and canula that will pass between the ribs is introduced into the sac. This gives exit to a quantity of pus, even chalky substances and fragments of cysts of different sizes. The opening must be free and kept patulous for some weeks, and the sac should be daily washed out with some disinfecting solution through the drainage-tube. Some delay is always necessary to allow of the separation of the parent cyst from its nidus and the gradual expansion of the lung. Immediate attempts at its removal by forceps are generally unsuccessful, and portions are very apt to be left behind. Several complications may interfere with the success of the operation. One is the unavoidable piercing of a small bronchus by the trocar. After the operation the wound of the bronchus may remain patulous and a violent paroxysmal cough comes on, with subsequent possible evacuation of the cyst through this channel. The bronchial tubes, however, have been opened in operative treatment of pulmonary cavities without serious result. When the parent cyst has progressed to maturity quite unhindered, and is stuffed full of daughter cysts, it has been recommended in such cases to introduce the stylet and endeavor with its sharp point to stir up and break down the smaller cysts as much as possible. The thermo-cautery has recently been used successfully by Mosler to afford a means of penetrating the cyst in the treatment of pulmonary hydatids. The tissues of the thoracic wall must be first divided down to the pleura, as recommended in the opening of pulmonary vomica by the thermo-cautery. Resection of the ribs should be practised in case sufficient drainage cannot be accomplished through an interspace.

Before applying to these operative measures it is desirable that adhesions should have occurred between the visceral and the parietal pleura. Fenger and Hollister recommend the introduction of a needle as a means of diagnosis: if there be adhesions, it is unaffected by respiration; if no adhesions exist, it is moved synchronously with the breathing. There are, however, no absolutely reliable signs by which this adhesion can be determined. Paracentesis of suppurating sacs has been performed in cases in which the pleural surfaces have not been adherent. In some instances the lung has been stitched to the opening in the pleura, and after partial adhesion has occurred the purulent collection has been punctured. In certain other cases, when pleural adhesions have been absent, paracentesis has not been followed by serious pneumothorax, possibly because the apposition of the pleural surfaces is maintained by the tendency to cohesion which exists, and after operative interference these surfaces are united by adhesive inflammation.

{472}

ACUTE MILIARY TUBERCULOSIS.

BY JOHN S. LYNCH, M.D.

Acute miliary tuberculosis may be defined to be an acute disease characterized by an eruption in one or all of the organs of the body of small nodular or granular masses called tubercles, attended with fever and various other functional disturbances.

The fact which Villemin and Klebs were the first to show,[1] and which hundreds of others have since verified, that tuberculosis can be conveyed by inoculation to certain animals, and the additional fact that Koch and his followers seem to have identified the infective material in the micro-organism which he has named bacillus tuberculosis, would seem to justify our placing tuberculosis, along with variola, measles, etc., among the acute contagious infectious diseases. But since some able pathologists still deny the correctness of Koch's conclusions; since in certain animals indifferent irritants have excited a disease which could not be distinguished from tuberculosis by the ablest pathologists of Europe and America; since to some species of animals even more nearly allied to man by their organism than rabbits and guinea-pigs the disease cannot be conveyed at all, and that even to some of the latter inoculation fails to transmit it; and, above all, since there is, as far as we know, not one single case on record in which the disease has been clearly and unmistakably traced from man to man in the order of infection,--we do not think that as yet we are justified in defining it as a contagious infectious disease purely and only. Everybody will take small-pox if not protected by vaccination or inoculation, and this disease may be transmitted in a modified form to many of the lower animals. The same may be said of measles, scarlatina, and nearly all other diseases known to be contagious and infectious. Since, then, so few persons take tuberculosis that the evidence of its contagiousness rests upon a vague popular belief, and since even some animals of a species known to be peculiarly susceptible to the disease fail to take it even by inoculation, we think that we are justified in assuming that there must be something else besides a contagium required to produce the disease. This is evidently a predisposition which depends upon some peculiar diathesis, cachexia, or dyscrasia, congenital or acquired. It has been assumed that scrofula constitutes the particular diathetic condition which predisposes to tuberculosis, and it is common for scrofulosis and tuberculosis to be spoken of as convertible terms. In the article on SCROFULA in this work we have already given our reasons for dissent from this view, and to that article the reader is referred. Farther on we shall give our views as to what constitutes the tubercular diathesis when we shall speak of the mode of formation of tubercle.

[Footnote 1: But Buhl had long before advanced the doctrine that tuberculosis was a resorption disease.]

While, then, we cannot as yet admit that acute miliary tuberculosis is always and only set up by a contagium, it is unquestionably true that it is in a large majority of instances caused by an infective material, which, however, {473} does not come from without, but is produced within the system. This material is the purulent detritus resulting from the softening and breaking down of the inflammatory and other cellular hyperplasias which have undergone the caseous degeneration. It seems to make little difference whether the caseous product was derived from scrofulous glandular hyperplasia, catarrho-pneumonia, inflammation of serous membranes with a cellular exudation, or ordinary cellular inflammation; the only essential prerequisites being that there shall exist a cellular exudation or proliferation, and that these cells shall undergo the caseous degeneration.

The inoculation of this material into certain species of the lower animals or its absorption into the blood of a human being predisposed to tuberculosis will, as a rule, produce tuberculosis. Koch and his disciples add to the foregoing another prerequisite--viz. that the caseous matter must contain the bacillus tuberculosis. But as the bacillus is generally found in all the cheesy inflammatory products we have mentioned, they have (ignoring Virchow's definition of tubercle) declared that all these are tubercle, thus very much enlarging the hitherto accepted doctrine upon this subject. But if any of the cheesy products are found not to contain the bacillus, then such product is not tubercle, whatever may be the apparent identity or dissimilarity in their etiology, microscopical appearances, or clinical history. This seems to us to be a begging of the whole question of the relation of the bacillus to tubercle, and in the absence of fuller experimentation and investigation involves an assumption which cannot yet be admitted.

While the absorption of caseous pus is undoubtedly by far the most frequent cause of miliary tuberculosis, it cannot be inferred that all who may happen to have foci of caseous degenerations will necessarily be attacked by tuberculosis. On the contrary, a vast majority escape, and it is almost surprising how few of those who suffer from scrofulous inflammation of glands, joints, etc. become the subjects of miliary tuberculosis. Many cases of pulmonary phthisis also, originating as a cheesy pneumonia, run their course without any distinct tubercular complication. We can only explain these exemptions from the tubercular process by supposing that in such cases the predisposition to tuberculosis does not exist--they do not have the tubercular diathesis--or that such persons possess a peculiar means of resistance to the entrance of the infecting material into their blood.

Other diseases are supposed to favor the tubercular process, either by directly exciting or increasing the predisposition to it. Among others, measles, whooping cough, and typhoid fever have been regarded as specially liable to be followed by tuberculosis. Bad air, poor or insufficient food, onanism or other forms of sexual excess, severe study with insufficient exercise, and, in short, anything which impairs the strength or lowers the vitality, have been heretofore considered as excitants or predisposers of the disease. Admitting all these causes as effective in either exciting it or increasing the predisposition to it, there still remains quite a large residuum of cases in which the disease can be traced to none of these causes, and which, for the want of more accurate knowledge, we are compelled to call idiopathic or spontaneous. Such are those cases of tubercular meningitis occurring in young children heretofore in apparent good health, and in whom no traces of caseous degeneration can anywhere be found. It is true that it may be asserted that these children may have been infected through kissing by persons suffering from pulmonary consumption; but if this were so the disease ought to be far more frequent than it is, since the habit of kissing babies is universal and consumption the most prevailing of all diseases. In the absence of any proof to the contrary, we think that we are justified in believing that these are cases of spontaneous tuberculosis, occurring in consequence of intensity of the diathesis, either inherited or acquired.

{474} Miliary tubercles are found in the form of small roundish nodules ranging in size from 1/500 to 1/250 inch (submiliary tubercles), up to the size of a millet-seed or even of a pea. When of the latter size they are always made up of a number of submiliary tubercles. Much larger masses are found usually in the lungs and in the mesentery, but these will generally be found to consist not of miliary or submiliary tubercles alone, but of cellular new formations derived from endothelial or lymphatic proliferations excited by the presence of tubercles, and therefore mixed with them. When first formed they are grayish in color, somewhat translucent, and tolerably firm to the touch (gray granulations). They soon, however, undergo partial fatty degeneration (this degeneration usually commencing in the centre of the mass), and subsequently are converted into a dry, yellowish-white, and somewhat crumbly mass which from its resemblance to cheese is called caseous. This sooner or later softens (the softening process beginning also in the centre), and the mass breaks down into a fluid detritus--tubercular pus. In some situations they never reach the caseous and purulent stage (notably in the cerebral meninges), because the interference with the organs or nerve-centres of animal life excited by their presence destroys the patient before there is time for the accomplishment of these changes. The subsequent history of tubercle depends upon the condition of the patient, his powers of resistance, the intensity of the tubercular diathesis, the injury inflicted by the first eruption, and the appearance of secondary eruptions. If all conditions are favorable, the patient placed under proper hygienic conditions and properly treated, the first eruption will also be the last, and the tubercle dries up into an earthy mass (calcareous degeneration), or it may remain for months, and even years, in its caseous stage without undergoing the softening process.

If we examine a fresh tubercle under the microscope, we find, according to Woodward[2] and Zeigler,[3] that it is usually made up of three different kinds of cells: first and most abundantly, lymphoid cells (Woodward) or white blood-cells (Zeigler); second, endothelioid cells; and third, embryonic cells. In addition to these there is often found (but not always) a few so-called giant-cells, generally occupying the centre or circumference of the tubercle, and sometimes both. These cells, which usually contain two or more nuclei and are much larger than the ordinary lymphoid cell, were thought at one time to constitute an essential histological feature of tubercle, and have been named tubercular cells. But the frequent absence of these cells in genuine tubercle has led to the conclusion that they do not possess any special significance and are purely accidental. Each submiliary tubercle is usually surrounded by a proliferating zone in which multinuclear (giant) cells and fibro-plastic or spindle-form elements can be distinguished (Cornil and Ranvier[4]). According to Rindfleisch,[5] Woodward,[6] and Zeigler,[7] the cellular elements of tubercle are always found included in a trabeculum of fine fibrillar (connective) tissue, while Cornil and Ranvier deny the existence of any such trabeculum, maintaining that its appearance is due to the action of hardening agents used for preparing it for microscopic examination. Virchow and Woodward believed that tubercle always takes its origin in a lymphatic vessel, while Rindfleisch, partially agreeing with this view, maintains that they most generally occur in the lymphatic sheaths of the blood-vessels and follow the course of the latter, and that the cells which compose the tubercle are formed by proliferation of the endothelia of the lymphatics.

[Footnote 2: _Medical and Surgical History of the War of the Rebellion_, Part 2, Medical Volume, p. 593.]

[Footnote 3: _General Pathological Anatomy_, London, 1883, p. 171.]

[Footnote 4: _Pathological Histology_, Philadelphia, p. 116.]

[Footnote 5: _Textbook of Pathological Histology_, Philadelphia, 1872, p. 125.]

[Footnote 6: _Op. cit._]

[Footnote 7: _Op. cit._, p. 168.]

{475} Zeigler has not been able to demonstrate this relation of the tubercle to a blood-vessel--that is, to an artery--but leaves us to infer that they always arise from a capillary vessel, since he maintains that the tubercle is primarily and principally made up of emigrated leucocytes.

Such is a brief résumé of our knowledge as to the histology and mode of formation of tubercle, and such are the opinions--in some particulars agreeing, in others discordant--of those whose investigations and observations the world regards as most complete and accurate. This résumé is doubtless unnecessary and out of place in this article, since this question (the histology and mode of formation of tubercle) has been already discussed in the first volume of this work; but, as in the explanation which is to follow of our views as to what constitutes the tubercular diathesis and what is the mode of formation of tubercle we shall have to frequently refer to the facts above stated, we have thought it best, in order to save repetition and too frequent reference to authorities, to give the above résumé of the present state of the views of pathologists upon the histology of tubercle.

A careful consideration of the foregoing facts ought, it seems to us, to enable us to arrive at a rational and probably correct conclusion as to the mode of formation, as well as the principal etiological factors concerned in the causation, of the miliary tubercle; and we venture to offer the following explanation of the subject as more in consonance with the facts above related than any view which we have seen upon this question:

1. Miliary tubercles always occupy a lymph-space surrounding a capillary blood-vessel. When found, as they quite often are, occupying the wall of a larger vessel, artery or vein, it is still in the lymph-sheath of a capillary of the vasa vasorum that they primarily originated. And it may be said that this is the most dangerous site a tubercle can occupy, because when softening takes place it is so apt to burst into the lumen of the vessel and so produce a general infection.

2. The tubercular process consists at first of an undue or excessive emigration of leucocytes through the walls of a capillary which runs through a lymph-space, and where, of course, the walls of the vessel are less firmly supported. Those cells whose vitality is lowered by the causes which have preceded and excited the process can neither undergo any process of differentiation nor wander on through the lymphatics; they remain in the lymph-space, which they crowd and block up, and finally by their pressure occlude, the capillary vessel from which they emigrated. Until this event occurs they still retain a feeble vitality, and even abortive attempts at proliferation are seen, which, however, only reach the stage of division of the nucleus, the body of the cell meanwhile swelling up by imbibition and thus forming the so-called giant-cell. As soon as the capillary vessel becomes occluded further addition to the incipient tubercle from this source ceases; nutrition is now entirely cut off, and the cells, dying, become a foreign substance, and soon undergo the caseous degeneration. But by their presence they now excite a quasi-inflammatory process in the endothelia lining the lymph-space, and hence we have a secondary addition to the tubercle derived from the proliferating endothelia. Lastly, the inflammatory process extends to the connective-tissue cells around the lymph-space, and embryonic cells (the only cells capable of resulting from connective-tissue inflammation) are added to the mass. This constitutes the proliferating zone, consisting of many nucleated cells and fibro-plastic and spindle-form elements, described by Cornil and Ranvier.[8]

[Footnote 8: _Loc. cit._]

As soon as one capillary vessel becomes entirely occluded, the neighboring ones become distended by a collateral hyperæmia, and the same process of cell-exudation or emigration begins; and thus the process goes on until all the capillaries supplied by a single arterial twig take part in the process, and {476} one of the larger tubercles is thus formed by an almost innumerable number of smaller (submiliary) ones. It would seem to be quite probable that the trabeculum which Rindfleisch, Woodward, and Zeigler described, and which Cornil and Ranvier denied, consists of the remains of the connective-tissue fibres which originally existed between the capillaries successively attacked by the tubercular process.

In the lungs this process is usually complicated by a true catarrho-pneumonic inflammation. The tubercle deposited beneath the lining membrane of the air-sacs sets up inflammation in that membrane, giving rise to abundant proliferation of the endothelia as well as emigration of leucocytes, so that the air-sac becomes packed with cells which may finally undergo caseation, and then cannot be distinguished from the original tubercle which started the process. If the eruption of tubercles should be very abundant, life may be destroyed by the pneumonic process before caseation has even begun in the inflammatory products. We have quite recently observed a case of this kind. A man came to the city hospital (Baltimore, Md.) who presented all the rational and physical signs of tuberculosis of the lungs. After about three weeks, during which there was only moderate fever, no notable dulness, and only a few scattered crepitant râles, the temperature suddenly rose to 104° F.; dulness appeared first over the lower third of the right lung, which rapidly extended over that side, and subsequently to the left side, and the man speedily died, comatose and cyanotic. The autopsy showed the most extensive miliary tuberculosis we had ever seen in the human lung; but in addition to the tubercles, which were found in almost every lobule of the right lung, the air-sacs were almost universally filled with a soft, purulent-like matter which oozed from the cut surface, and which could be squeezed out in enormous quantities; myriads of Koch's bacilli were found. It was interesting to note that the apparent starting-point of this tuberculosis was two small cavities in the apex of the left lung surrounded by firmly-indurated walls. Neither of these cavities was larger than the kernel of an ordinary-sized almond, and, as the induration surrounding them did not extend to the surface of the lung, their existence was not recognized before death. The man gave a history of cough and fever, which had lasted several weeks, about three years before his admission to the hospital.

More frequently, however, the reverse of the process above described takes place. That is, a catarrho-pneumonia terminating in caseation and softening sets up tuberculosis through absorption of the caseous pus. Indeed, in the case above related the order of pathological processes was, first, a catarrho-pneumonia of limited extent, a cavity or rather cavities; second, general tuberculosis; and lastly, a secondary catarrho-pneumonia caused by the tubercles. We believe, therefore, that Niemeyer's remark, that "the greatest danger for the majority of consumptives is that they are apt to become tuberculous," is not so absurd as a distinguished American author would have us believe.

The formation, then, of tubercle we believe to be an inflammatory process, in which we have--1st, an exudation of lymphoid cells (leucocytes) into the lymph-spaces, and occlusion by pressure of the capillary vessel from which the cells have escaped; 2d, inflammation and proliferation of the endothelium lining the lymph-space; and 3d, inflammation of the tissues nearest adjacent to the space. If this is simple areolar connective tissue, we have a "proliferating zone consisting of many-nucleated cells and fibro-plastic and spindle-form elements;" if a mucous or serous membrane, the usual products of inflammation of such membrane in other and ordinary cases.

But behind these processes there must exist something else which stands in the relation to them of predisposing and exciting causes. This we believe to be some anatomical and histological peculiarity, congenital or acquired, which gives to the individual that defective organization which is denominated the {477} tubercular diathesis. It seems probable that this diathesis comprises two factors--viz.: 1st, an unusual thinness, and consequently weakness, of the walls of the capillary blood-vessels, which permits and favors a too facile emigration of the leucocytes; and 2d, a diminished or lowered vitality of the leucocytes themselves.

Both of these factors may exist at the birth of the individual as an inheritance from his progenitors, or both may be produced by causes which impair the general nutrition during either intra-uterine life or during the earlier infancy of the subject. Or one of them may exist without the other, and the animal thus escape for a long time, though exposed to the exciting causes of the disease. Sternburg's guinea-pigs (animals peculiarly susceptible to tuberculosis) remained healthy while enjoying the freedom of grassy fields, although inoculated with Koch's bacilli, which were found in their blood and tissues when killed, while those that were confined in cages under bad hygienic conditions speedily succumbed after a similar inoculation.[9] If the first of these factors exist, any exhausting disease producing a dyscrasia, habits or hygienic conditions which tend to impair the nutritive functions, even psychological and emotional influences which take away the appetite for food or impair the functions of digestion--anything, in fact, which tends to degrade the quality of the blood and diminish the functional activity of the white blood-cell--may furnish the second factor constituting the tubercular diathesis. Both factors being present, it only requires an uncertain increase of the blood-pressure, causing a dilatation of the capillaries, to ensure that increased leucopedesis which constitutes the first step in the tubercular process.[10] A protracted fever, therefore, of any kind, may furnish both the second factor in the tubercular diathesis and the exciting cause of the tubercular process itself; while any fever or any irritant capable of exciting fever or reaction against its presence occurring in man or other animal that happens to have the complete tubercular diathesis may excite tuberculosis. Koch's bacillus will undoubtedly excite tuberculosis in animals (and probably also in man) that have the tubercular diathesis complete; but it does so only by exciting that inflammatory and febrile reaction against its presence in the blood which other and perhaps indifferent irritants may also excite. In rabbits and guinea-pigs confined in cages, and therefore under unnatural and unhygienic conditions, it suffices to excite the disease only to introduce the bacillus into any part of their tissues: that it will not do so in guinea-pigs that are healthy and kept under natural conditions and surroundings Sternburg's experiments, alluded to above, clearly prove. It is true that other animals that are regarded as ordinarily non-tuberculous can also be inoculated with the bacillus with affirmative results, provided the bacillus is introduced into the eye or other serous membranes; but we must not forget that the pain and injury of such an operation will almost inevitably produce that deterioration of the health and impairment of cell-vitality which we maintain constitutes so essential a part of the tubercular diathesis. That the bacillus tuberculosis is always found in tubercle is undoubtedly true; but it is there because tubercle furnishes the most favorable and congenial breeding-place for it. Some special microbe is found in almost every special inflammatory product--vibriones in the pus of abscess, gonococcus in urethral inflammation, micrococcus in diphtheria, etc.--but no one, we believe, now holds that these various microbes are the causes of these diseases, since inoculation with pure cultures have given entirely negative results. While we believe, therefore, that the bacillus of Koch can excite tuberculosis in man or animal having the tubercular diathesis, we {478} also believe that it does so because of its property of exciting that amount of irritation and reaction necessary to initiate the tubercular process--a property, however, possessed by many other irritants; and while it is probable that a few cases may be thus produced in man, a vast majority of the cases arise independently of its presence. And hence we maintain that tuberculosis is not a specific contagious disease in the sense that it is only produced by a special contagion, as small-pox and other similar diseases are.

[Footnote 9: _Journal of the American Medical Association_, vol. iv. No. 12, p. 314.]

[Footnote 10: We hold that leucopedesis is a normal physiological process that is always going on during the period of active growth of the individual, as well as during the process of repair.]

Primary acute miliary tuberculosis occurs only in the young or early adult period of life, for the reason, perhaps, that persons of the tubercular diathesis can hardly long escape the exciting causes of the disease, and so are attacked early. Persons possessing what may be called the incomplete or partial diathesis may be attacked by a secondary miliary tuberculosis at any, even the most advanced, age; but it will be found that in all such cases of late tubercularization there has occurred a direct infection of the blood by absorption of caseous detritus from a softening cheesy pneumonia or cavity. "In 28 out of 52 cases collected by Litten, it was associated with pulmonary phthisis, and this accords with general experience" (Roberts[11]).

[Footnote 11: _Practice of Medicine_, 5th ed., p. 301.]

Acute primary general miliary tuberculosis--that is, in which all or nearly all the vascular tissues are attacked at once--must be one of the rarest diseases. Such cases can only occur when the tubercular diathesis is strongly marked and exciting causes of the most active character have been applied. As a rule, tubercular eruptions occur in successive crops, attacking the more vascular organs, as the lungs, cerebral meninges, spleen, liver, serous and mucous membranes, and bones, first and usually in the order given. Laennec's law, that if tubercle is found in any other organ it will also be found in the lung, is undoubtedly true, with the single exception perhaps of tubercular meningitis. If our explanation of the causes and mode of formation of tubercle is correct, we must a priori expect to find that a tissue so soft and spongy as the lung, and which is so vascular and subject to such great and sudden alterations of pressure and relaxation, would naturally be the site of the first formation of tubercle.

SYMPTOMS AND COURSE.--It is impossible to give a clear or lucid description of acute miliary tuberculosis, since there cannot be said to be any constant or pathognomonic symptoms produced by the disease per se. The symptoms present in any given case depend upon the organs involved, and may be said to consist merely of those furnished by such organs when invaded by inflammation. Fever is present in all cases. The grade or height of this fever will depend upon the number and extent of tubercular formations, and to some extent upon the organs involved. It will generally be highest in tubercle of the serous membranes, and of the lungs next. In general miliary tuberculosis the fever is highest, and can be distinguished with difficulty from enteric fever. If the intestinal mucous membranes are involved, and diarrhoea consequently exist, the differential diagnosis will be almost impossible. The fever, following the law of nearly all inflammatory and symptomatic fevers, is usually remittent, and the remissions and exacerbations correspond to the normal diurnal variations of temperature--lowest in the morning, highest in the evening. The remissions are also usually attended with perspiration, sometimes profuse, at others moderate. The patient early falls into that condition of prostration and general exhaustion which speedily comes on in all fevers of high temperature and protracted duration expressed by the term typhoidal state. Even the pains ordinarily complained of in inflammation of various organs are not felt, or if felt at all are seldom mentioned; which perhaps helps to render the diagnosis more difficult. Almost the only exception to this is when the cerebral meninges are early affected, in which case unusually severe headache may be complained of. Cough may be present, {479} but is not more troublesome than in many cases of enteric fever, and is quite out of proportion to the lesions found in the lungs and pulmonary mucous and serous membranes. The expectoration varies, and is sometimes entirely absent. Generally, it is moderate and consists of frothy serum, occasionally streaked with blood. Hæmoptysis is said to be occasionally present, but must be extremely rare. Respiration is notably frequent early in the disease, and in the absence of pronounced physical signs of pulmonary lesions is perhaps one of the most reliable and pathognomonic signs present. Respirations are often as frequent as 60, seldom less than 30, per minute. The pulse is usually rapid, generally hard at first, but soon becoming soft and weak. The rate varies between 110 to 120 to 160 or more late in the disease.

The disease runs a rapid and invariably fatal course, often ending within the first fortnight, seldom lasting as long as two months.

Tubercles, miliary and submiliary, are found after death in almost all the vascular organs, varying much, however, in number in various organs, and often presenting different stages of development. In some, and especially in the lungs, tubercles will be found already in a state of incipient softening, others still firm and yellow (caseous), and others still grayish and semi-translucent, showing, we think, a different period of eruption, and demonstrating the correctness of our observation that miliary tubercles are always formed in successive crops.

If the tuberculosis is associated with inflammatory phthisis, and, as is the case in a majority of instances, has been caused by absorption of caseous detritus, large masses of caseous matter may be found in the lung, either in a softening condition, or cavities will be met with empty or partially filled with pus, and surrounded by indurated walls the result of interstitial pneumonia. These caseous masses and cavities are, in our view, the result of precedent catarrhs or croupous pneumonias, and not a result of the tubercular process.

Partial or local miliary tuberculosis is a much more frequent occurrence than the general disease above described. It occurs most frequently in persons under twenty-five years of age, and in a very large majority of cases between the ages of two and twenty. It occurs also most generally in the lungs first in point of frequency, in the mesentery next, and last in the cerebral meninges. Of course a secondary general tuberculosis may result in any of these cases from resorption, except in the meningeal variety, which generally destroys life before there is time for secondary infection.

Acute miliary tuberculosis may occur in the young as a consequence of measles and other exanthematous fevers, whooping cough, typhoid fever, and various other affections which seriously impair nutrition. According to our own observation, it is most likely to attack boys and girls soon after puberty who are pursuing too severe a course of study in school with insufficient exercise in the open air, and perhaps also those evil practices unfortunately too common in both sexes. Tubercular meningitis as an idiopathic affection (that is, without the previous or concurrent deposit of tubercles elsewhere) is almost exclusively met with in children between two and seven years, but secondary tuberculosis of the meninges may occur at any age. We have seen two cases of pulmonary phthisis, one of three and one of three and a half years' duration, and who bid fair to live for a long time, suddenly carried off by tubercular meningitis. Both of these persons were past thirty years of age.

Tuberculosis of the mesentery, peritoneum, and liver (for they are sometimes found in all three of these organs) is invariably either coincident with a general tuberculosis or the secondary consequence of scrofulous inflammation of the intestinal glands. Quite often here the tubercular process is associated with the scrofulous process, and large masses of caseous material will be found in the mesenteric system of glands.

{480} As in general miliary tuberculosis there are no symptoms by which the disease can be positively recognized, so too in the partial or local disease there are absolutely no pathognomonic signs. We may say in general terms that if a person who is known to have had a pneumonia which has ended in a permanent consolidation of any considerable portion of one or both lungs, and who has for some time presented the symptoms, however slight, of chronic pulmonary phthisis, is suddenly attacked with fever and night-sweats; or, if fever has already existed, the temperature rises considerably above the previous average, with increase of cough; or if an uncontrollable diarrhoea sets in; or if headache and delirium should suddenly occur--delirium out of proportion to the fever,--then we are justified in believing that tuberculosis of the lungs, mucous membrane of the bowels, or arachnoid has occurred. Or if a young person of either sex, such as above described, should, after becoming pale and anæmic, begin to have slight fever with a dry, hacking cough, at first without expectoration or with a frothy muco-serous expectoration, which for an unusual length of time continues to retain this characteristic, and this fever and cough cannot be otherwise accounted for, then the existence of pulmonary tuberculosis is rendered extremely probable, although there is neither history nor evidence of preceding pneumonia or scrofulous glandular degeneration. If a few scattered and slight crepitant râles can be heard over one or both lungs without alteration of pulmonary resonance, and the respiratory rate is much too frequent for the temperature and pulse, then the diagnosis becomes almost absolutely certain. Unfortunately, this scattered or diffuse crepitant râle is often absent, and there are absolutely no physical signs whatever of the deadly mischief going on in the lungs.

Prolonged expiratory movement is spoken of by some as one of the reliable signs of tuberculosis, but as this sign is usually present in almost all forms of chronic pulmonary disease, its significance cannot be relied upon. Or if a child over two and under ten years of age, after showing evidences of malnutrition, should suddenly be attacked with fever of moderate temperature, become restless and fretful, should frequently vomit and retch even when the stomach is empty, and begin to have convulsions, with squinting and trismus, and if old enough complain of severe pain in the head, have a rapid, frequent, but irregular or slow and intermitting pulse,--if these symptoms become exaggerated at night and somewhat mitigated in the daytime, the diagnosis of tubercular meningitis may be made with tolerable certainty.

It would take more space than is allotted to this article to describe all the phases of tuberculosis: we shall therefore summarize the symptoms of this disease by saying again that the signs and symptoms of tuberculosis are simply those of inflammation with fever and such derangements of function and other local disorders as would be furnished by inflammation of any given organ under other circumstances, except that the pain produced by tubercular inflammation is not usually so severe as in other inflammations, and hence diagnosis is not always so easy as in the latter. For it is a remarkable fact that in tubercle of the peritoneum--an organ which in a state of inflammation usually gives such excruciating pain--this symptom is often not complained of, and the existence of tuberculosis not suspected until after a post-mortem. The same may be said of tubercle of the meninges. Pain is often not complained of, and is never so severe as in ordinary meningitis.

TREATMENT.--In acute general tuberculosis no treatment will be of any avail. All that can be done is to moderate the fever and support nutrition by appropriate food. For the first, quinia in large doses is undoubtedly the best remedy. It should be given in one or at most two doses daily. Twenty grains should be given early in the morning, and this dose repeated at 1 o'clock P.M., or thirty to forty grains may be given in a single dose about 8 or 9 o'clock A.M. Antipyrine should prove a valuable antipyretic in these {481} cases, and, being probably equally effective, produces less disorder of the nervous system and digestive functions than the salt of cinchona. Judging from what we have seen of its effects in other fevers and inflammations, fifteen to twenty grains repeated about four times in the twenty-four hours should keep the temperature very near normal.

For the second indication milk and raw eggs constitute the best diet. Brandy or whiskey in the form of eggnog or milk-punch is useful, and in the latter stages indispensable. It should not be forgotten that according to the latest observations muriatic acid disappears from the gastric juice of fever patients, and that its power to digest animal food is therefore very much impaired. This should be supplied, therefore, by giving after every ingestion of milk, eggs, or other animal food ten to fifteen drops of dilute hydrochloric acid in a sufficient quantity of water. Peptone will also aid in the proper digestion of protein substances, and should therefore be added to the acid. Some of the liquid peptone sold by manufacturing chemists contains hydrochloric acid, and would therefore meet both these indications.

By these means we may doubtless prolong the life of the patient and promote his comfort or at least diminish his suffering, and if a cure is possible secure it. Tuberculosis of the mesentery and peritoneum, as well as tuberculosis of the cerebral meninges, will generally prove fatal, the one by impairing the chylo- and hæmatopoietic functions, the other by injury to the central nervous system, though Hartshorne of Philadelphia reports one case of the latter in which temporary recovery lasting one month took place, and quotes two cases by Guersant in the _Dictionnaire de Médecine_ (1839) in which also partial recovery, lasting five weeks and two months respectively, occurred. "May we not imagine, however," says Hartshorne, "that if such convalescence could last two months, it might in a case affected with nearly similar lesions be prolonged indefinitely?"[12] I am informed that a case of permanent recovery has been reported in England, but I have not been able to obtain the reference. To these I have to add a case of my own in which recovery has been maintained for a little more than nine months. In this case, a boy of twenty-six months, the convulsions were controlled for many days by hypodermic injections of morphia, while quinia was given by the mouth when possible, and otherwise by the rectum; and, though he had left hemiplegia and was for a time both blind and deaf, he recovered entirely in about six weeks, and has remained well.

[Footnote 12: _Reynolds's System of Medicine_, Am. ed., Philadelphia, 1880, vol. i. pp. 826, 827.]

In pulmonary miliary tuberculosis the treatment is by no means so hopeless if the disease is promptly recognized and actively treated. The thing to be accomplished in this case is to prevent secondary eruptions and the softening of the tubercles already formed. We know that this last can be done in caseous deposits resulting from catarrho-pneumonia, and we also know that tubercle can be maintained in a quiet state or be made to dry up by calcareous impregnation or degeneration for an indefinite time, since post-mortems often show old tubercles in one or the other of these conditions. We know of one man who carried a caseous lung for nineteen years, coughing more or less during all that time, but in a sufficiently good state of health and strength to follow his occupation of ship-carpenter, but who died at last from phthisis; while another, a farmer living in one of the Southern States, has lived in fair health, with his left lung indurated from top to bottom, for twenty-four years. There cannot be a doubt, therefore, that if secondary crops of tubercles are prevented, and a perfect state of health and general nutrition maintained, the tubercles may remain quiescent in their cheesy condition or may undergo calcareous degeneration and dry up into inert and innocuous masses incapable of further harm.

The first and most important indication, therefore, in the treatment of {482} tuberculosis is to suppress the fever; for as long as this continues new tubercles will continue to form, since the fever is both a predisposing and exciting cause. Quinia, therefore, or antipyrine, should be given as directed in general tuberculosis. The patient should be put to bed and not permitted to go about until the arrest of fever seems permanent. Nutrition should be supported and promoted also by the same means already indicated. As soon as the fever is permanently arrested (but not before) the patient should be permitted to take gentle exercise in the open air, and should be encouraged to spend as much time as possible out of doors, and if able to do so should be sent during the winter to that climate or place where, on account of its warmth and dryness, the most time can be spent in the open air.

Hypophosphites of lime and soda should be given constantly, and cod-liver oil also if the stomach can tolerate it. Large doses of the oil are useless, and often hurtful, a dessert-spoonful being quite as much as most stomachs can bear without exciting unpleasant eructations and nausea. The appetite and digestion are best excited by tincture or extract of cinchona and nux vomica. Iron we have found to be of little use, and often hurtful. We much prefer small doses of arsenic (two to five drops of Fowler's solution), and if there is much bronchitis this will be found especially useful. Some persons, however, cannot tolerate arsenic in any dose. The patient should carry a clinical thermometer, and as soon as the slightest fever is detected he should go to bed and active antipyretic treatment should be instituted, the tonics and alteratives being meanwhile suspended. If cough is troublesome (but not otherwise), one to two grains of codeia should be given two or three times a day or as often as may be found necessary. This is much preferable to morphia or other preparations of opium, which constipate the bowels, dry the mouth, impair the appetite, and so stupefy the patient that all inclination or even ability to take exercise in the open air is destroyed. Codeia is amenable to none of these objections.

Guided by these principles, we think we have successfully treated many cases of primary pulmonary tuberculosis--many in which the hereditary predisposition was strongly marked and the diagnosis unquestionable. It is true that many of these cases have relapsed and died after a variable period, but others have remained well for several years, and still others permanently.

{483}

DISEASES OF THE PLEURA.

BY FRANK DONALDSON, M.D.

Pleurisy.

DEFINITION.--Inflammation, partial or general, of one or both pleuræ.

SYNONYMS. Pleuritis ([Greek: pleuritis]) morbus lateralis; Morbus pleuriticus (Celsus); Pneumona pleuritis (Cullen). _Fr._ Pleurésie; _Ger._ Seitenstich.

HISTORY.--Pleurisy derives its name from the accompanying pain in the side, usually its most prominent symptom. In the sense in which Hippocrates used the word [Greek: pleuritis], it meant all kinds of pain in the side, especially such as are of a violent character. Pleurisy was mentioned by Celsus, and was still better defined by Galen. Æctæus, however, was the first to describe it with precision and to speak of its treatment. These ancient authors viewed the disease as seated in the layer of the pleura lining the ribs or external parietes of the chest. More modern writers contended that the disease was more frequently in the expansion of the pleura over the lungs and other parts. Boerhaave and Van Swieten contended for the separate and distinct affection of the pleura. Sydenham, Hoffman, and Morgagni believed that the pleura and the substance of the lung were generally both implicated. Pinel was the first to definitely establish the difference between pleurisy and pneumonia from the anatomical lesions. Laennec laid the foundation of our present knowledge. He was followed by Andral, Chomel, Louis, and Cruveilhier in Paris, and by Forbes and Williams of London and Stokes of Dublin. They demonstrated, by the physical signs and general symptoms during life and by the post-mortem lesions, that inflammation may commence in and be limited to the pleura in some cases, and in others that it may extend to and involve the lungs. Again, they showed that in some instances the lung may be inflamed without involving the pleura generally, yet that in the large proportion of cases the disease may originate in one organ and extend in a greater or less degree to the other, thus implicating both of them. Previous to Laennec the incomplete anatomical knowledge of the nature of the serous membrane, the pleura, as a capsule of the lungs, and the thoracic organs and walls, as well as the theoretical views of the nature of inflammation as a morbid process, led to erroneous views. Their diagnoses were made from general symptoms only. Pleurisy was considered the more common disease. Avenbrugger, Corvisart, and Laennec, by their discoveries of the accurate physical modes of exploration of chest diseases, gave far more reliable data for differential diagnosis. Now we have, in addition to the general symptoms, the modern refinements in auscultation and percussion, the delicate measurements of Woillez's cyrtometer, Ransome's stethometer, and Pravaz's and Alex. Wood's hypodermic exploring-needles to enable us to attain great accuracy in the diagnosis.

CLASSIFICATION.--Pleurisy is one of the most common diseases of the {484} respiratory apparatus. Though apparently simple, careful study shows it to be extremely complex. It occurs in very different forms and in a great many modifications, according to the producing causes and the numerous lesions which follow its course. We might classify the forms of pleurisy, according to their causes, as primary or secondary, tubercular, traumatic, etc.; or we could designate them according to their anatomical lesions, as dry pleurisy, pleurisy with effusion, general or parietal pleurisy, encysted, multilocular, purulent, hemorrhagic, etc. A methodical classification of all these forms is difficult if we attempt to base it upon the prominent characteristics or the lesions. We prefer a classification which enables us to study separately the clinical varieties which are most frequently met with, and therefore the most important. The symptomatology shows that the inflammatory process in pleurisy is of different degrees of intensity. We propose for our study to divide them into two main groups, according to the nature of the exudation:

Fibro-serous pleurisy, Acute, Chronic.

Purulent pleurisy, Acute, Chronic.

They may be local or general. When they result from disease of neighboring parts, they are generally local. Each of these groups comprehends primary and secondary varieties.

In the first, we have an exudation resembling the plasma of the blood. The effusion is not serous, for the fluid is spontaneously coagulable, whereas serum is not. It is not properly termed fibrinous, for it contains more albumen than fibrin. Fibro-serous is the most accurate term by which to designate it. The watery portion gravitates to the lowest part of the cavity, while the plastic deposit is thrown out over the two surfaces of the pleura. In the most acute forms the general symptoms, especially the pain and fever, are well marked. The exudation is at first largely fibrinous, but it is afterward more fluid in its character. In milder cases, the latent variety of the older authors, frequently designated as the subacute form, the subjective symptoms are so slight that the individual is not aware of his condition until the exudation, which is largely sero-fibrinous, mechanically interferes with his respiration. When first recognized these cases are really often chronic. They frequently remain sero-fibrinous in their character for a long time. Sometimes they become sero-purulent (the intermediary variety), and later purulent. Purulent pleurisies (empyema) are those where pus is the product of the inflammatory action. They may be acute (empyema d'emblée) or the result of transformation of acute or chronic fibro-serous pleurisies.

By this division we shall be able to take into consideration the fundamental causes of all the forms of pleurisy. Starting from the simple primary form, we shall be able to study special varieties of secondary pleurisies, such as tubercular and rheumatic.

Next, we shall examine separately the hemorrhagic variety as distinct from hæmothorax. The localized forms, such as the interlobular, diaphragmatic, and mediastinal, will be studied as varieties caused by their development in different localities.

The simplest plan to elucidate the whole subject of pleurisy is to analyze carefully, in the first place, the unquestionably acute disease, primary pleurisy, and afterward to connect with it the study of the several forms and varieties. Acute primary pleurisy has a sero-fibrinous exudation, and is the most common form of the disease. In it are best defined the usual characteristics of this inflammation. We consider this the principal type of this class, and with it shall study the development and character common to all the varieties of inflammation of the serous membrane of the thoracic cavity.

PATHOLOGICAL ANATOMY OF FIBRO-SEROUS PLEURISY.--The anatomical {485} changes in all forms of pleurisy begin by hyperæmia of the vessels of the serous membrane and of the subserous connective tissue. This is followed by an exudation of a liquid, a pseudo-membranous deposit. In acute primary cases this is first noticed on the costal pleura. The pleura itself shows, by puffiness and oedema with red points and small ecchymosed spots, that the inflammatory process has affected it. In a few hours, in acute cases, there is found a thin deposit of fibrinous lymph of a reddish-yellow tinge, with more ecchymosed spots, resulting from the rupture of fine capillary vessels. The pleura is somewhat thickened and loses its transparency, and is studded with very fine granulations. Under the microscope it is shown that the epithelial cells are swollen, that their number has been largely increased by proliferation, and that they have been detached in great quantities. The granulations are scattered over the pleural surfaces, and separate the pleura from the fibrinous deposit. The connective tissue is loaded with liquid, in which are found in increased quantity leucocytes which have migrated through the walls of the blood-vessels.

Over the surface of the pleura there is a tissue of granulations composed of embryonic cells, which are derived from the proliferation of the elements of the connective tissue. In this tissue of new formation we find new blood-vessels coming from those belonging to the subserous tissue, which advances through small points, even to the free surface of the granulations. These vessels are very thin and brittle. They sometimes rupture and cause ecchymoses of the pleura and of the false fibrinous membranes--sometimes effusions of blood, which, becoming mixed with the serum in the pleural cavity, cause hemorrhagic pleurisies. This new tissue is susceptible of organization, and of transformation progressively into a tissue analogous to that of a cicatrix. Under the plastic exudation we find abundance of embryonic cells, which become elongated and spindle-shaped in the formation of new connective tissue. This is at first tender, but may become dense and fine over circumscribed points, so as to produce bands which enclose and touch the effusion. This is the origin of the organized neo-membranes which are found on the surface of the pleura. It is, moreover, this tissue of granulations which constitutes the bands which unite the parietal to the visceral pleura, the adhesions being produced by the contact and the union of vegetations or neo-membranes developed on the two opposed layers of the pleura. The membranes form the filamentous thin bands which draw obliquely together portions of the pleural sac. These lesions are very often slight and rudimentary in simple acute pleurisy, but are found well developed in purulent pleurisy, especially when it is chronic. These are hyperplastic parenchymatous lesions of the pleura. Acute inflammation of the pleura gives rise to two distinct forms of exudation--the plastic, deposited on the free surface of the serous layers or formed in flakes in the fluid; and the serous, which falls into the dependent portions of the cavity. The plastic may exceptionally exist alone. Their formation together is the rule. Anstie questions whether the serous effusion ever occurs without the fibrinous. The plastic exudation takes the form of granulations more or less prominent, constituting a bed of very irregular rough points. So long as the period of inflammation continues, new plastic deposits are formed over the old ones. They thus increase in thickness. The neo-membranes which play such an important rôle in the natural history of pleurisies increase very rapidly. Little by little, they are transformed into firm, very resisting tissues. They may become fibrous, cartilaginous, or even calcareous in their structure. These false membranes develop more freely at first when the opposing surfaces are kept apart by the effused liquids. The rubbing of the two pleuræ together seems to impede the process of organization. According to Wagner, the lymphatics are dilated and contain a liquid poor in corpuscles. The newly-organized and vascular {486} tissues often become the starting-points of fresh inflammatory processes and of new products.

Exudations are of two kinds--liquid and pseudo-membranous. When the inflammation extends over a limited surface, the fibro-plastic exudation may be the only one; in which case the disease soon terminates with local adhesions. This is dry pleurisy, which is rarely primary in its origin. Ordinarily, the principal lesion of acute pleurisy consists in a sero-fibrinous effusion which collects in the cavity of the pleura; almost always the liquid effusion exists in decided quantity. In it there are suspended fibrinous flocculi, and on the surface of the pleura are found false membranes. The nature of the effused liquids has been thoroughly studied, ample opportunities having been furnished since thoracentesis has been so extensively used. The quantity of liquid is very variable, from a few grammes up to several liters. The terms small, moderate, and abundant are used to designate the quantity--one-half of a liter is considered a small quantity; moderate, one to one and a half liters; abundant effusion, two to two and a half liters; very abundant, when the effusion goes beyond three liters. The liquid is transparent and of yellowish-amber color. It is darker when the fluid has been some time in the chest, and resembles that of bouillon. Sometimes it has a rose tint when the liquid contains a sufficient quantity of red globules, or it may be somewhat opaque when it encloses a large proportion of leucocytes.

The presence of a few red globules does not constitute a hemorrhagic pleurisy, nor does the presence of a small quantity of leucocytes make a purulent pleurisy. It is only when they are very abundant that they severally give those characters to the effused fluid. Dieulafoy states,[1] after frequent examinations of aspirated serous fluid of acute pleurisy, simple and frank, that it contains the smallest quantity, from 500 to 600 red globules to the cubic millimeter, while the white globules were from fifteen to twenty times more numerous. In some instances he counted 1500, 2000, and even 3000, red globules to the cubic millimeter without the coloration of the liquid being sensibly modified. He adds that the liquid from the pleura has not a perceptible rose tint unless it contains from 5000 to 6000 red globules to the cubic millimeter. He concludes that there is no tendency to transformation into purulent pleurisy unless the number of red globules reaches 4000 or 5000 to the cubic millimeter. Rindfleisch (ed. 1869, Leipzig) states also that upon their number and that of the proliferated epithelial cells, with the floating flocculi, depends the convertibility of the serous into purulent effusions.

[Footnote 1: _De la Thoracentèse par Aspiration dans la Pleurisie aigue_, p. 42, Paris, 1878.]

Chemical Character of Effused Fluid.--Mehu[2] gives the composition of the fluid as closely resembling that of the serum of the blood. He found in it the same elements--water, albumen, fibrinogenous matter, salts, red globules, and leucocytes. The proportion of these principal constituents of the blood was greatly modified in the pleuritic liquid. The quantity of water was always increased. On the other hand, the quantity of substances in solution was greatly diminished. The exudation was really blood-plasma, more or less diluted, in which the relative proportion of the constituent elements varied according to the intensity of the inflammation. It has the same alkaline reaction, and it is spontaneously coagulable, owing to the presence of the fibrin which is in solution in the serum, the proportion of fibrin making it coagulate more or less rapidly. Mehu found the quantity of fibrin to vary from 09.073 to 19.276 to the kilogramme. The same mineral substances were found, but in less quantity, than in plasma of blood. The intensity of the inflammation causes alterations in the composition of the exudations. The more acute the inflammation, the greater is the quantity of albumen and of fibrinogen. The fibrinogenous matter contained in the {487} exudation is coagulated only by contact with the air. One portion of it becomes concrete in the interior of the body in the form of fibrinous flocculi, which float in the fluid, and in the false membranes, which are deposited in successive layers on the surface of the inflamed pleuræ. This coagulation takes place in a manner analogous to that of the coagulation of the fibrin in a drop of blood. These false membranes are almost always found in acute pleurisies, but their development is very variable. Sometimes they are very thin, friable, and readily disappear; again, when the inflammation is intense, they last a long time and cover thickly both pleuræ. Occasionally they envelop the effusion and produce veritable cysts and localized pleurisies. Their color is opaline or semi-transparent when recently formed, but opaque when old. Their consistence varies according to the duration of the disease. At first they are soft, impregnated with fluid, easy to tear or break; later on they become resistant and almost dry. The microscope shows these false membranes to be formed of crossed fibrillæ, with intervals containing white blood-corpuscles, with voluminous, swollen epithelial cells of serous membrane, proliferated and detached.

[Footnote 2: _Arch. général de Méd._, 1872.]

When the pleural inflammation subsides, the exudation is destined to disappear. Usually the cure is produced by the reabsorption of the effused products. The liquid part of the exudation, the serosity, is absorbed by the lymphatics, which are found frequently dilated, and some of them are filled with fibrinous coagulations and the leucocytes. The solid parts, the false membranes, concrete fibrin, and cells disappear with more difficulty. They undergo granulo-fatty metamorphosis, and are then taken up by the lymphatics.

These fibrinous false membranes are not, as was formerly supposed, susceptible of organization. It is only the neo-membranes, formed by the proliferation of the elements of the pleura, which are organized or organizable. It is these that form bridles or ligaments which attach the lung to the thoracic wall, and are susceptible of transformation into cartilage or even into bone. In chronic cases these new membranes bind the lung down, impair its expansive powers, and inflict great damage upon the respiratory force.

Care must be taken to distinguish between the neo-membranes and the plastic and liquid exudations. These last contain transitory-formed elements entangled in the fibrinous layers. They are principally lymph-corpuscles, containing solitary nuclei, together with a few epithelial cells, almost always in process of disintegration, and isolated blood-corpuscles (Fraentzel).

Distribution of Fluid.--The situation and form in which the effusions are found in the pleural cavity furnish important data for study as applicable especially to diagnosis. At the commencement of the disease the effused plastic products form a thin covering to the pleural surface--a slight cushion interposed between the lung and the thoracic wall. Later, the fluid products gravitate by their weight to the lowest portion of the cavity of the pleura; then, as they increase in quantity, they gradually rise or are drawn to the superior portion of the thorax. Once formed, these effusions are but slightly movable and but little displaced by the varying positions of the patient, unless the quantity be very great and no adhesions or bands have been made. If the effusions be of viscid consistence, or if false membranes exist, they are mechanically prevented from moving. The serous transudations of hydrothorax always occupy the most dependent portion of the cavity, but observation shows how frequently the pleuritic effusions are immovable, being maintained and suspended between the diaphragm and the lungs, and imprisoned in the situation where they form by the false membranes.

Previous to 1843 the authorities universally taught that the effused fluids in the pleural cavity obeyed, as they would in an open vessel or in a vacuum, the law of gravity. They never appeared to question but that the fluid {488} would necessarily assume its hydrostatic level, and consequently that it would reach a horizontal line in all parts of the chest. The distribution and the form which the effusions take were first studied by Damoiseau.[3] Fernet and D'Heilly[4] maintain that Damoiseau perfectly established the form and disposition which the effusions take in pleurisy. To study them well we must bear in mind, they say, three facts: the irregularly conical form of the pleural cavity; the effect of gravity; and the habitual position of the patient when lying down. Damoiseau and these authors utterly ignored the retractile force of the lung, as well as that of the diaphragm, and the resiliency of the thoracic walls, as effecting the position of the fluids in the pleural sac. If we observe that the patient at the commencement lies ordinarily on his back, the thorax being raised and more or less inclined to the horizontal position, we easily appreciate that the effusion ought to accumulate, at first, behind, in the most dependent portion of the costo-vertebral gutter, below the inferior angle of the scapula; then, as it increases in quantity, it rises and obliquely strikes the conoidal cavity, which encloses it, and makes on its surface curves resembling those of an oblique conic section (Damoiseau). As Damoiseau described the pleuritic line of flatness as a parabola, it was highest in the axillary region, where it first appears; thence, as its summit rises, its branches advance downward and outward to the sternum and the vertebral column.

[Footnote 3: _Thèse de Paris_, 1845.]

[Footnote 4: _Nouveau Dict. de Méd. et Chir._, Paris, tome xxviii., 1880.]

Since Damoiseau's first paper[5] it has been generally acknowledged that the line of flatness over the upper surface of a moderate effusion is not horizontal when the patient is in the sitting or erect posture. There has been considerable difference of opinion among the English[6] and continental writers as to the exact disposition of the fluid: some partially assent to Damoiseau's views; others, again, very materially modify them. Wintrich,[7] who was one of the first among the Germans to emphasize the percussion line of demarcation between a pleuritic effusion and a contracted lung, says: "As the exudation gradually increases, the level of the fluid does not present a line which is horizontal or parallel to the ground, but one which descends toward the ground at a more or less acute angle." Fraentzel says that the line is never horizontal. Leichtenstein and Ferber[8] maintain that the line depends upon the position of the patient early in the disease. Gee[9] holds very much to this opinion. He states that the upper limit of the surface of liquid, when it reaches as high as two inches above the nipple, is horizontal. When lower than this, the dulness forms irregular parabolic curves, which become smaller and smaller as they descend. Austin Flint[10] says, in his more recent edition: "The upper limit of the dulness or flatness, the position of the body being vertical, is not in a continuous horizontal line extending over the posterior, lateral, and anterior aspects of the chest." Flint, Wintrich, and Fraentzel speak of the line being highest behind. Calvin Ellis of Boston in two very suggestive papers[11] described a curve-line made by the upper line of the effused fluid, which radically differed from any one previously mentioned. "This curve begins, with medium effusions, relatively low down on the back, passes outward from the vertebral column, and soon turns upward and proceeds obliquely across the back to the axillary region, where it reaches its highest point. Thence it advances in a straight line, but with a slight descent, to the sternum." Powell, however, does not find {489} that the curve invariably commences at a lower level behind. G. M. Garland,[12] in consequence of the resemblance of this curve to the italic letter _S_, has named it, very appropriately, the letter _S_ curve. He adds that, according to his experience, "this curve, as described first by Ellis, may be traced, by proper percussion, in any case of free, uncomplicated pleurisy when the patient's body is erect and the amount of fluid present is not excessive. As any effusion increases in amount, the curve of its distribution gradually rises and tends to flatten out, so that it no longer presents its characteristic _S_ feature after it reaches the second rib. At this point, when the fluid occupies nearly the entire side, the curve comes quite near to the horizontal, but if some of the fluid be withdrawn by aspiration or absorption the letter _S_ curve will reappear and retreat downward in the inverse order of its advance, until with entire absorption it becomes merged into the normal boundary of the lung."[13] Garland quotes from two recent German authorities--Heitler of Vienna and Rosenbach of Breslau--to the effect that the line of flatness of the effusion extends lower on the back than it does on the side, and that there is a triangle bounded by the vertebral column, the upper curve from the bottom, and a line drawn from the summit of the curve, where there is impaired resonance over the lung from adhesions and oedema of the lung, but where there is no fluid and no flatness. Garland had previously called attention to this space, and had named it the dull triangle. He had warned all who sought to trace the true line of pleuritic flatness to be careful not to overlook this region. Heitler had likened it to a monk's hood cut longitudinally through the centre and hanging apex down. Rosenbach made this dull space, clearing up in exercise and deep breathing, as distinctive between pleurisy and pneumonia. We must expect impaired resonance on the posterior wall above the fluid, for the fibrinous deposits from exudation collect there when the patient is in the recumbent position. Garland[14] calls attention to the confused views caused by confounding the two physical signs of dulness (or impaired resonance) and flatness (absence of resonance), the latter only indicating the presence of fluid. If the differential diagnosis between the dulness on percussion over the dull triangle and the flatness over the fluid be not carefully made by delicate, light percussion, the two may easily be confounded and the fluid be thought to have arisen to a much higher level than it has. In some cases, owing to greater thickness in the walls and coverings of the chest and adhesions, it may be more difficult to draw nice distinctions in percussion sounds. This distinction can, however, be made if the percussion-stroke is used with proper delicacy and lightness, and a comparison made between the two signs, and not between them and vesicular resonance. If the percussion be strong, the vibrations are communicated from the resonant lung above the fluid, and deceive the examiner. The most effective manner of percussing is at right angles to the general direction of the curve, which is transverse across the chest. Thus examining, we have had ample opportunities of confirming the statement of Ellis and Garland that the curve line is never highest behind, even with the largest effusion. Wintrich and his German followers hold a different view. In moderate effusions it is highest in the axilla, from which point it turns downward posteriorly to touch the vertebral column at the interscapular region. In front it extends downward toward the sternum. R. Douglass Powell[15] reports cases with drawings, showing that in typical cases the fluid does not take a water-level, "but a curve, having its convexity upward in the lateral region." When the effusion becomes excessive and fills the whole cavity, there is flatness on percussion everywhere. As the fluid subsides, however, from absorption or from mechanical removal, the distribution again resumes, to a greater or less degree, its previous shape. {490} In moderate effusions there is, ordinarily, the dull triangle posteriorly, and Skodaic resonance under the clavicle in front in the anterior triangle. On the left side the lower limit of the effusion can be recognized by the flatness being in the shape of the arch of the diaphragm. In cases complicated by adhesions or by pathological changes in the lung itself the curve is changed, and in some the Ellis curve is straighter than in others. Adhesions form sometimes early in the disease. They mechanically interfere with the usual distribution of the fluid, as do catarrhal, tubercular, or pneumonic consolidations, and, indeed, emphysematous conditions. All these physical alterations of structure modify the elastic force of the lungs. According to Mohr's statistics, adhesions were wanting in 47 per cent. of the cases analyzed by himself. Garland's experiment of injecting glue and plaster of Paris, and subsequently cocoa-butter, into the pleura of living and dead dogs, and by moulds testing the curves formed, showed that if the dogs were suspended by the head the curve of flatness on percussion was very similar to the Ellis curve. On removing the casts after they had solidified, he found they closely corresponded to the shape and position indicated by the physical signs elicited before opening the chest.

[Footnote 5: _Archives générale de Méd._, 1843.]

[Footnote 6: See Hyde Salter, _Lancet_, 1865; Powell, _Trans. Roy. Med. and Chir. Soc._, vol. lix.; W. N. Stone, _Lancet_, 1877; Le Gros Clarke, _Roy. Soc. Med. and Chir._, 1872.]

[Footnote 7: Quoted by Garland, _N.Y. Med. Journal_, 1879.]

[Footnote 8: _Ibid._]

[Footnote 9: _Auscultation and Percussion_, 1877.]

[Footnote 10: _Practice of Medicine_, 1880, p. 130.]

[Footnote 11: _Boston Med. and Surg. Journ._, 1874 and 1876.]

[Footnote 12: _Pneumono-Dynamics_, New York, 1878.]

[Footnote 13: _N.Y. Med. Journal_, Nov., 1879.]

[Footnote 14: _Pneumono-Dynamics_.]

[Footnote 15: _Med. Times and Gazette_, Oct., 1882.]

Ellis's observations, and those of Garland with his experiments, have given us the most accurate views as regards the form of the curved line of flatness.

Nearly all modern authorities, including Peter, Gerhardt, and Paul Niemeyer, admit that fluids in the pleural sac assume more or less irregular curves, and not a hydrostatic, horizontal level. Whatever may be the nature and consistence of the effusion, fibro-serous, sero-purulent, or purulent, it does not behave in its distribution as if it were in an open vessel. But few writers, however, have troubled themselves to ascertain the causes of this apparently abnormal condition. They appear to have completely overlooked the facts that had been discovered in regard to the mechanics of the chest in connection with respiration and the circulation. Physiology had shown, especially by Marry's researches, the negative force of the lungs in aspirating the blood from the large venous trunks into the right side of the heart, and thus assisting the whole venous circulation. John Hutchinson[16] drew attention to the antagonism existing between the expansion of the chest by muscular action and that of the lungs and the chest-walls. Hyde Salter[17] showed that at the commencement of inspiration thoracic elasticity was favorable to inspiration, but as it advanced it became an expiratory force with lung-tension against further expansion. R. Douglass Powell[18] drew further attention to these facts in connection with respiration and its modification by disease. Le Gros Clarke[19] showed that atmospheric pressure over the abdomen kept the diaphragm in a condition of arched passive tension. He claimed that this negative force resisted the elasticity of the lung, and was the means of retaining the supplemental air in the lung and limiting the encroachment of abdominal organs.

[Footnote 16: _Trans. Med. and Clin. Soc._, 1846.]

[Footnote 17: _Lancet_, Aug., 1865.]

[Footnote 18: _Trans. Clin. Soc._, 1870.]

[Footnote 19: _Trans. Roy. Soc._, 1872.]

Douglass Powell in March, 1876,[20] in an elaborate and very suggestive paper on "Some Effects of Lung Elasticity," gives the practical bearing of these physiological facts in clinical medicine, as indicating a better insight as to the true mechanism and relative value in diagnosis of some signs of chest diseases, especially as to the importance of thoracic resilience as a force in respiration.

[Footnote 20: _Trans. Roy. Med. and Clin. Soc._, vol. lix.]

W. H. Stone early in 1877[21] reported his experiments on sheep as to the amount of negative pressure exerted by the lungs, and concluded that it was equal to four to five inches of water. He moreover showed that even when the effusion was considerable in the pleural cavity, the lung still had contractile force sufficient to support two inches of water, so that to evacuate the {491} fluid it was necessary to use external suction sufficient to overcome this lung-traction. In December, 1877, G. M. Garland[22] gave to the public the results of his observations and experiments in regard to the form of the curve of distribution assumed by the pleural fluid, and its causes. He demonstrated that "the lung, by virtue of the strength of its contractility, takes the effusion along with it in its retraction, and that thereby assumes a pneumono-dynamic instead of a hydrostatic level," and that the Ellis curve was the true line of the upper level of the fluid in free, uncomplicated pleuritic effusion. Thus the physical cause of this condition was the retractile force of the lung lifting up the fluid. This is aided by the elastic resistance of thoracic walls and the negative pressure exercised by the effused liquid. The normal line on right side of demarcation between lung and liver is the letter _S_ curve drawn out, the summit being high and the anterior branch correspondingly depressed. The modifications of this normal line in pleuritic effusions represent the effect of the negative pressure of the fluid. The decline in the Ellis curve toward the sternum shows that the elastic energy of the anterior part of the lung is feeble compared with that in the axillary region. "The layer of fluid is of less thickness above than at the base of the lung against the diaphragm. The upper surface takes its shape from the lung, which lifts it up by its retractility, and the effusion by its weight exerts a negative pressure upon the lung. The mass of the fluid is held when in moderate quantity in the supplemental space between the lower border of the lung and the diaphragm" (Garland). The atmospheric pressure from the interior of the lungs and from the exterior of the chest-wall keeps the costal and parietal surfaces of pleura together. Skoda, Powell, Stone, Homolle, and Quincke have shown the retractile energy of the lung, but the credit of drawing especial public attention to it, and of afterward elucidating the subject in its practical application to the study of pleurisy and in putting the whole subject upon a scientific basis, is unquestionably due to G. M. Garland of Boston.

[Footnote 21: _London Lancet_.]

[Footnote 22: _Pneumono-Dynamics_, Boston, 1878.]

ETIOLOGY OF FIBRO-SEROUS PLEURISY.--The etiology of acute primary pleurisy is frequently obscure. It may be hæmatic in origin, or it may be secondary, arising from pathological causes or antecedent disease. It is difficult to state with certainty whether it occurs in perfectly healthy persons, because there may be occult pathological conditions which cannot be appreciated. However, individuals are attacked with acute pleurisy who to all appearance, both to themselves and to those around them, are healthy. Authors differ very widely as to the disease being ever caused in healthy persons by exposure to cold. The older writers bring many proofs that such is the case. Ziemssen states that he could not trace the disease to exposure to cold in a single instance in 54 cases. Anstie holds the same view. Loomis states that in all instances where it (pleuritis) has followed upon exposure he has been able to find some predisposing cause. It is undeniable that pleuritis very frequently indicates the existence of some constitutional cachexia. Vital statistics show that it is more frequent in winter and spring than at other seasons. The vicissitudes of the weather, of temperature, and other atmospheric conditions have unquestionably a marked influence on the prevalence of the disease. Drafts of air passing over the chest or over other parts of the body, particularly when the subject is surrounded in-doors with a warmer atmosphere, wet clothing, intensely cold or a raw, damp atmosphere inhaled by persons coming out of a comparatively high temperature, especially if they are improperly protected by clothing, appear to be direct causes of primary pleuritis. If individuals thus exposed are debilitated by fasting, by such medicines as mercury, iodine, iodide of potassium, by over-exertion, by free perspiration, or by previous disease, they will be still more liable to contract the disease. Overheated apartments, especially at night during the {492} sleeping hours, frequently are the direct cause of acute pleurisies or of croupal pneumonias. These cases are of such frequency that we are obliged to differ from the high authorities who consider the pleura as free from acute idiopathic inflammations as is the peritoneum.

There are numerous predisposing causes which, when examined, are found to lessen the power of resistance of the organism. Senility is an important one; so is childhood. Formerly it was supposed that pleurisy rarely attacked children. This view was prevalent because the disease often escaped detection. Of all chest diseases in children, mistakes in diagnosis are most frequently made with pleuritis.

We might suppose that this disease would be frequently met with in children, because they are oftentimes ill protected against the vicissitudes of the weather; besides, their feebleness predisposes them to feel keenly such shocks to their powers of endurance. The disease may occur at any age, and is more common under two years than was formerly supposed (Eustace Smith). Empyema is the form most frequently found in children, the effusion soon becoming purulent in them. Ziemssen tabulates the ages of 54 children whom he treated for primary pleuritis: first year of life, 3; second, 1; third, 7; fourth, 4; the remaining 39 between the ages of five and sixteen years.

Pleurisies are more frequent in males than in females, in the proportion of 5 to 3, owing to the greater exposure of the former to the exciting causes, and notwithstanding their stronger organisms. Among the predisposing causes we must not fail to give due importance to the malhygienic conditions which so powerfully impair the forces of the body. Prominent among these are sedentary occupations, imperfect alimentation, city lives, overwork of mind and body, deficient sunlight, overcrowded houses, and dampness of soil. These and many others interfere with the formative forces and lessen the power of resistance to exciting causes of pleurisy.

Traumatic pleurisies are caused by injuries or other mechanical causes. Injuries to the walls of the chest, contusions, burns, scalds, and lacerations which are superficial, frequently give rise to primary traumatic pleurisies. If the ribs are fractured, or blood, air, or pus gets into the pleural cavity, we have what has been termed secondary traumatic pleurisies.

Secondary Pleurisies.--The exciting causes of secondary pleurisies are numerous. They are pathological, and more readily appreciated than the causes of primary pleurisies. Owing to the anatomical connection between the lungs and the pleura, diseases, acute and chronic, of the former frequently give rise to pleurisies.

Among acute affections of the lungs, the several forms of pneumonia are the most frequent causes of pleurisies. Fraentzel states that we always find fibroid pneumonia associated with pleurisy as pleuro-pneumonia, even when the inflammation of the lung-tissue itself does not reach the pulmonary pleura. There is an intimate connection also between caseous pneumonia and pleurisy. This is sometimes quite circumscribed, and leads to adhesion of the pleural layers at the affected spot; sometimes it is diffused over a great part of the pleura, and it is then not infrequently associated with a considerable outpouring of different kinds of effusions. Catarrhal pneumonia rarely occurs without secondary pleuritis (Fraentzel). Pleurisies may also be caused by violent bronchial catarrhs or by hemorrhagic infarctions.

There are cases where, from the presence of tubercles under the parietal pleura, inflammatory action is set up and pleuritis ensues. Vomicæ bursting into the pleural cavity or tubercular perforation in pulmonary phthisis gives rise to pleurisies. Inflammation of the liver, cellular abscesses, and pericarditis may cause secondary pleurisies. Diffuse peritonitis is often complicated with pleurisy, the inflammatory process extending from the {493} peritoneum to the pleura, through the diaphragm, by means of the serous canaliculi. This frequently occurs in puerperal peritonitis, and is almost invariably fatal (Fraentzel). The author had a case of fatal peritonitis in a man sixty-five years of age, which originated from an empyema. There was no rupture nor perforation of the diaphragm, so that the inflammatory process must have extended from the pleura to the peritoneum by means of these canals. Malignant diseases of the mammæ, oesophagus, lungs, and hydatids produce secondary pleurisies. Eruptive fevers, especially scarlatina, variola, typhoid fevers, are among the most frequent pathological causes of secondary pleurisies. It is doubtful whether their germs pass through the circulation or through the lymph-canals, and produce local inflammation of the same nature as their own, or whether they render the pleura more sensitive to shocks of various kinds. Rheumatism, gout, and nephritic diseases are frequently followed by pleurisies. As we have rheumatic endocarditis and pericarditis, in like manner there are rheumatic and uræmic pleurisies. Alcoholism and pyæmia, septicæmia and the puerperal state, especially during the first month after parturition, are powerful predisposing causes of pleurisies, as are also any morbid conditions of the skin, kidneys, or intestinal canal which interfere with their eliminating or depurating functions. This includes all forms of blood-poisoning. Hutchinson says that children suffering from congenital syphilis are especially liable to serous inflammations, and that pleurisy is in them a not uncommon cause of death. Niemeyer denounces the impropriety of giving the name of secondary pleurisy to all cases of pleurisy occurring in subjects with broken-down constitutions or weakened by other diseases. We often meet with such cases when Bright's disease exists. Niemeyer holds that it is not dependent upon renal disease, but upon the increased predisposition for all kinds of inflammatory disease. A trifling cause will sometimes excite a pleurisy when the resistance of the organism is materially lessened by previous disease.

SYMPTOMATOLOGY.--Rational Symptoms.--These vary according to the severity of the disease. Ordinarily, attacks of acute pleurisy come on suddenly, and it rarely happens that there is any appreciable feeling of malaise. Usually the first symptom is an acute pain in the side, which alarms the patient. The significance of this severe stitch is generally appreciated, as the subject at once calls attention to his sufferings. The pain is sharp, cutting, stabbing, that causes him to hold his breath as long as possible. When he is forced to breathe, it is by the action of the superficial intercostal muscles. He endeavors to fix his diaphragm and hold it rigid in order to prevent the surfaces from coming in contact and thus increasing his agony. This causes him, necessarily, to breathe frequently in order to get sufficient air. The greater the intensity of the pain, the more frequent and shorter are the respiratory acts. The dyspnoea and the effort to lessen the pain give the patient an expression of great suffering. Usually, the pain is felt over a circumscribed spot under the nipple of the affected side. Sometimes it is experienced as low as the sixth or seventh intercostal space, but rarely posteriorly below or under the scapula or in the axilla. In children the seat of pain is not always in the chest. Their lower intercostal nerves are often affected, and the sensation being referred to the ends of these nerves where they ramify on the abdominal wall, the pain is often seated in the abdomen. Such being the case in children, care must be taken not to confound pleurisies in them with epigastric or hypochondriac irritations. In adults, the pain is rarely located in the abdomen when it is caused by pleuritis in the lower portion of the pleural surface or in that part covering the diaphragm. In children there is also much tenderness on pressure. In what has been termed subacute or latent pleurisy the stitch may be entirely absent. Valleix found pain in 40 cases out of 46. Sometimes it is absent {494} in ordinary breathing, but is brought on by sneezing or violent coughing or strong percussion. In severe cases, the effusion coming on rapidly, the pain may subside by the second day. If the effusion comes on slowly, the pain may keep up for six or eight days. The continuance of the pain always shows that the inflammatory process in the pleura is continuing, although the pulse and the temperature may be normal. The renewal of the sensation of pain after the pleurisy has passed away justifies us in the conclusion that there is a return of the inflammation. When the pain is agonizing, with signs of collapse, it is indicative of a secondary pleuritis arising in the course of a chronic caseous pneumonia. Tubercular and purulent exudations are distinguished from the sero-fibrinous by the longer duration and the greater intensity of the pain--two circumstances which afford a reliable basis for the diagnosis of such cases. The severe pain in pleuritis is probably caused by the inflammation extending to the sheaths of the nerves and to the nerve-texture itself (neuritis), as well as by inflammation of the pleura itself.

Severe attacks of acute exudative pleurisy may commence with a severe initiatory chill, followed by high fever, but ordinarily there are in pleurisy slight rigors, initial in their character. Some authors question whether they are not caused by the limited points of pneumonia connected with the pleuritis. If the rigors occur at regular intervals for days, we have reason to suspect tubercular trouble or empyema. The temperature does not run any regular course in pleurisy, nor does it bear any fixed relation to the pulse and the respiration. It usually varies from 100° to 102° F. In violent, acute cases it may reach 105° F.

Careful observations with the thermometer give us important indications by which to diagnose the nature of the pleurisies. In those of a tubercular nature the temperature continues high, from 100° to 104° F., for weeks. When the effusion becomes purulent the temperature becomes like that of hectic fever--in the morning normal, and in the evening rising to 102°, or even 103½° or 104° F. Sometimes the temperature is one or two degrees higher on the diseased side than it is on the healthy side.

As in other inflammations, the pulse in this disease varies considerably. The researches of H. Newell Martin show that there is ordinarily a constant ratio between the pulse-rate and the temperature. If the temperature be high (over 102° F.), we must expect the pulse to be as frequent as 115 or even 120 per minute. In mild cases, where the temperature does not go beyond 99.5° or 100° F., the pulse will not exceed 90 to 96. In slight cases, where the fibrinous exudation is very limited, the pulse may not exceed 80. In tubercular and purulent pleurisies the pulse may vary between 100 and 120. When there is a relapse the pulse advances as the temperature rises. Anstie has called attention to the quality of the pulse, which follows a uniform course on the whole, regard being had to the general vital condition of the patient. In the first stage of acute pains, with more or less tendency to shivering, the pulse, as tested with the sphygmograph, presents the algid form--_i.e._ the pulse-waves are very small and nearly devoid of secondary markings. As soon, however, as flushing of the face occurs, and a general sense of burning heat of the skin, the pulse passes to the true pyrexial type; the waves become large and dicrotic. The sphygmograph uniformly shows that the large and somewhat bounding pulse is always less resistant than that of health.

Jaffé-Duval[23] states that he found the temperature of the diseased side raised above that of the healthy chest. Subsequently, Peter,[24] after a long series of researches, reported some very important results as to the localized parietal temperature in cases of pleuritic effusions: (1) He found that the {495} parietal temperature, as tested by the thermometer, is always higher on the side of the pleurisy than that of the body as tested in the axilla; (2) that the elevation of the temperature increases as the effusion augments, the highest local temperature corresponding to the period of secretory activity of the inflamed pleura; (3) the rise affects both sides, but is greater over the diseased pleura; (4) the temperature falls by degrees as the effusion is reabsorbed--less on morbid side; (5) the absolute elevation of local temperature is greatest in the sixth intercostal space; (6) after paracentesis the parietal temperature is increased: this falls in a few hours where the effusion is not re-formed, but when such is the case it continues for some days. This local rise of temperature, he considers, is from hyperæmia and cell-production, caused by the traumatism from the needle added to the already-existing hyperæmia. This excessive congestion, caused by the accumulation of blood occurring when a large quantity of fluid is rapidly withdrawn, produces the syncope, pulmonary congestion, consecutive albuminous expectoration, the pain, and the oppression amounting sometimes to suffocation, and occasionally ending in death.

[Footnote 23: _Thèse de Paris_, 1875.]

[Footnote 24: _La France médicale_, 4th May, 1878.]

At the commencement in acute cases the respiratory acts become very frequent, even going to 40 or 50 per minute. They are short, interrupted, and superficial. Their frequency makes up for their incompleteness in furnishing sufficient air. The painfulness of each act forces the individual not to expand the walls of his chest more than he can avoid. Moreover, the high fever in itself produces frequent respiration. As the temperature falls the respiration becomes less abnormal. If the effusion forms rapidly, the patient may become oppressed, even when the quantity is not large. If it is thrown out gradually, the breathing is not so much interfered with until a large quantity forms, the organism becoming accustomed to the interference with the play of the lungs. The strength of the individual and the activity of his nutritive functions are materially lowered. Sometimes he breathes with difficulty, especially when he takes active exercise. The dyspnoea is very painful and alarming. The aëration of the blood is so materially interfered with that there results a large quantity of carbonic acid, which irritates excessively the respiratory nerve-centres.

During the acute stage the patient sometimes lies on his back, but more frequently on the well side, and exceptionally on the diseased side. He avoids lying on the side where the inflammation exists, because the weight of his body increases the pain. I have, however, seen patients who would persist in lying on the painful side and supporting it with their hand. It sometimes happens that a patient lies on the affected side, and will not move, because the movement gives him such acute pain. Ordinarily, he prefers to lie on the healthy side, even after the fluid has been poured out to a moderate degree, because his pain is less. When, however, the effusion has become great enough to deprive him of the use of the diseased side, he instinctively turns on that side, so as to avoid the weight of the fluid pressing upon the lung on the sound side. Moreover, he wishes to expand as much as possible the side whose respiratory force now needs to do double work. This change of position in patients has an unmistakable significance. It shows that the sufferer is aware that he is more comfortable lying on the diseased side. His physician's attention is drawn to the condition of the chest as influenced by the increased quantity of fluid pressing the air out of the lung.

Cough is not a constant symptom in pleurisy, but ordinarily it occurs at some stage of the disease. It is short, dry, and suppressed in character. It is painful, and therefore is avoided when possible, especially previous to the effusion. It disappears generally about the fourth or fifth day, when the effusion has attained a considerable amount. The cause of the cough has been generally supposed to be the exalted sensibility of the inflamed {496} pleura, but Nothnägel maintains that such is not the case. Fraentzel holds that the cough is caused by the strain on the lung-tissue and the finer bronchi when there is a slight effusion. Cough brought on by change of position is one of the characteristic symptoms of large effusions into the pleura. If the lung is completely compressed by the pleuritic effusion, then no actual strain on the alveoli or the bronchi can exist. In such cases there is no cough, but it returns when the effusion decreases in quantity, and quite violently, if this occurs suddenly, as, for instance, in puncture of the chest (Fraentzel). In the latter case the cough is probably caused by the rush of blood and the sudden expansion of the chest.

Slight frothy expectoration may exist, but ordinarily there is none whatever, unless from bronchial catarrhal complications. In that case sero-mucous fluid is expectorated in small quantity. If it becomes viscid and tinged with blood, it is caused by pulmonic involvement.

In empyema, if the expectoration becomes purulent, we ought at once to suspect the presence of some circumscribed spots of necrosis of the pleuritic covering of the lung, which have allowed the pus from the pleural cavity to filter through the lung-tissue. By careful physical examination of the chest we can ascertain whether there has been any diminution in the quantity of fluid. When, as sometimes occurs, there is actual perforation of the lung, the pus from an empyema comes in quantity, through the bronchial tubes, out of the mouth. Patients may sink from exhaustion following this discharge, or if the discharge be excessive it may fill up the bronchial tubes too rapidly for its removal by expectoration, thus causing suffocation. This danger is increased if the discharge takes place during sleep.

Cyanosis is a symptom which should cause serious alarm, for it shows that the effusion is so great as to interfere very materially with the due arterialization of the blood. When the cyanosis is accompanied by pallor, coming on suddenly in the course of a pleurisy, we may infer with considerable probability that there is a hemorrhagic exudation. But if the paleness comes on slowly during weeks or months, it may also be dependent on a simple sero-fibrinous effusion (Fraentzel). Protracted cases of effusion, especially if purulent, are associated with emaciation and loss of strength. There may exist more or less oedema of the lower extremities and of parts of the body where the patient lies down, as we have in the chronic diseases of the chest. When this oedema is limited to the affected side of the chest, whether it be extensively developed and spread over the entire half of the chest or confined to certain spots, it almost invariably justifies the diagnosis that the effusion is purulent. The effusion may, however, be purulent without the presence of this localized oedema. Occasionally, cases are met with of effusion in the left pleura where there are visible and palpable systolic pulsations in the intercostal spaces arising from the impulse of the heart or of the larger blood-vessels passing through the fluid.

Physical Signs.--Perhaps in no other disease of the chest are physical signs so important for purposes of diagnosis as they are in pleurisy. Even at the very beginning of the attack they give us valuable information. In later stages, when the effusion is in the pleural sac, they furnish, as we shall hereafter show, trustworthy data for diagnosis, prognosis, and also very valuable indications for treatment. There is no other disease of the chest where the physical changes made by the inflammatory process are so pronounced and so accessible to the senses of hearing, sight, and touch. The physical signs are so marked that, almost by themselves, they give us the pathological condition. They have been so carefully studied, and their correlative value insisted upon, that they are readily interpreted. One is often tempted to rely too much upon them to the exclusion of the proper consideration of the general symptoms.

{497} As the physical condition of the pleuræ varies much in the several stages of the disease, the physical signs must necessarily vary accordingly.

At the very beginning of the attack the sensibility of the pleuræ is augmented by the inflammation. Consequently, on inspection, it will be observed that the patient is careful to avoid the pain caused by the inflamed pleuræ rubbing together. He not only tries to avoid using the ordinary muscles (especially the intercostals) for enlarging the capacity of the lower portion of the chest, where the disease is generally found, but he retracts his chest and keeps the pleuritic side almost motionless. The well side has double work to do, and is seen to expand more fully. The patient will frequently press the lower ribs in, on the affected side, with his hand, or he will lie on that side, so as to control the expansion of the chest, or he will lie on the healthy side and bend his body over.

The respiratory movements are marked by an irregular and jerking rhythm, and are quickly made. The pain felt on inspiration is of a catching or stabbing character, and produces dyspnoea, the subject struggling for air. The diaphragm is held as fixed as possible, so as to prevent the movement of the inflamed surfaces over each other. The patient restrains as far as possible the respiratory movements, especially those of expansion and retraction. This is the condition not only at the initiation of the disease, but at the next stage, that of effusion. We meet with the same painful respiration also in dry tubercular pleurisy. Mensuration shows that the sound side of the thoracic cavity is slightly enlarged by the extra work it has to perform in the first stage. The elevation movement is noticed to be restrained when the effusion has increased to the extent of overcoming the retractility of the lung, for the diaphragm is no longer drawn up by the lung, and the effusion rises and separates the parietal and pulmonary pleuræ. The diaphragm bags from the quantity of fluid, and contracts but feebly. This condition forces the liver and the spleen down in the abdominal cavity. Gradually the jerking rhythm ceases as the effusion advances, and the characteristic stitch in the side disappears. If the effusion increases until it reaches as high as the second rib, the respiratory movements are scarcely perceptible to the eye. When it reaches its maximum, the clavicle, they appear to be arrested, but the vertical diameter is slightly altered by the action of the intercostal muscles as they endeavor to elevate the ribs, and of the diaphragm as it feebly contracts and relaxes. The pleural cavity, which in health is lubricated by about two drachms of moist serous secretion, is frequently filled to the extent of seventy, eighty, or more--even to one hundred and twenty--ounces. We cannot wonder that it should be changed in shape and diameter. All available space is filled with the fluid, and yet the serous membranes continue to throw out the secretions. The lung must lose in size by its retractile force, and when that is overcome the fluid must press in all directions. The fluid gradually rises from the surface of the pleura over the diaphragm, and the lung, by negative pressure, draws it and the fluid upward. As long as the diaphragm is arched, although the lung recedes before the effusion, it is not really compressed. When, however, the diaphragm yields and falls from the large quantity of fluid, then the fluid conquers the lung. Ordinarily, the fluid, when in excessive quantities, presses upon the lung and the bronchi until it forcibly expels the air; the lung is compressed against the vertebral column, occupying a very small space corresponding to the surface under the scapula, often not larger than from three and a half to four inches square. Inspection shows that the spaces between the ribs become flattened out, that the ribs are more widely separated, and that the spaces themselves frequently bulge. The first observable indication of great distension of the pleural cavity, sufficient to cause intra-thoracic pressure, is the depression of the diaphragm, and next the flattening of the spaces between {498} the ribs. This last is followed by increased pressure, which causes more general and marked enlargement. "This levelling of the intercostal spaces is due partly to paralysis of the intercostal muscles from serous inflammatory infiltration, and partly to the limited range of movement now possessed by the lung, which is reduced in volume by the effusion, and is no longer in contact with the thoracic parietes" (Guttman). This is especially noticed in children and young persons before the ribs become firm and resisting, the negative pressure exerted by the lung being in part annulled by the presence of the fluid. The diaphragm is notably depressed, and pushes the liver, the spleen, and the stomach below their usual point. So great is this centrifugal force that the heart's impulse may be felt in the epigastrium. The heart, when the effusion is on the left side, is frequently found over to the right of the sternum, and, in extreme cases, even in the right axilla. When the effusion is on the right side, the mediastinum is drawn over with it, and the heart is forced to the left until the apex-beat is perceived as far as one and a half inches to the left of the line drawn through the nipple, or, in some cases, to the left axilla. This rarely occurs unless we have fluid intra-thoracic pressure on the diseased side in addition to lung-traction of the healthy side. Even the costal pleura, projecting above the clavicle, may yield to pressure. Inspection reveals to the observer these striking physical alterations. Hippocrates did not fail to notice them.

1st. Mensuration shows that the semicircular, antero-posterior, and vertical measurements of the side are generally increased. According to Douglass Powell, the total circumference of the chest is always increased in effusion. 2d. Except in children, the bulging of the intercostal spaces does not occur until after the adjacent organs have been displaced by the fluid. When the effusion is large, it becomes evident, by inspection and by pressing the hand over the sides of the chest below the armpits, that there is almost immobility of the diseased side. We insist upon the importance of daily and repeated comparative measurements of the two sides as aids to diagnosis and prognosis in pleurisy. A full inspiration or a prolonged expiration will sometimes show a marked difference by measurement when it is not discovered during ordinary breathing. Woillez's cyrtometer, as perfected by Samuel Gee, is the best instrument for testing the circumference of the chest, and a pair of callipers for the diameter. The cyrtometer tracings give us the altered shape as well as circumference. It is especially valuable in the diagnosis of local empyema from basic pulmonary cavities. Care should be taken not to confound congenital deformities in the shape of the chest, such as the alar, flat or pigeon-breasted, or rachitic, with alterations produced by internal disease. It must also be borne in mind that the semi-circumference of the right side is normally greater by one-quarter to half an inch than that of the left side. By inspection of cases where large effusions have remained for long periods of time slowly absorbing--often, perhaps, not recognized--we discover marked unilateral retraction of the chest-walls, with torsion of the spine and shoulders. The adhesions preventing the lung from expanding, the alveoli become obliterated, and we have, in fact, atelectasis of the lungs. This is particularly the case in children, where the disease prevents the proper development of the side, the healthy side becoming, from supplementary work, more enlarged. Care must be taken not to confound with these the anatomical depressions met with sometimes in the anterior wall of the chest, especially at the lower portion of the sternum. The amplification of the chest takes place, to a greater or less degree, at its lower portion as soon as an appreciable quantity of liquid collects, long before it is possible to have any intra-thoracic pressure. The lung by its elasticity collapses, and the fluid is drawn upward in contact with the lung. The thoracic wall, consequently, has not, at that point, the retractile force of the lung to {499} counteract its excentric resilience. It is not then drawn in in expiration by the lungs, while it is continually being drawn outward in inspiration. The lung-traction of the parietes of the chest is feeble from the diminished size of the lung. The greater the amount of fluid, the less lung-tension; consequently, the greater the enlargement of the chest, as shown by the cyrtometer. If the lung is contracted to its utmost limit (one-third of its size, according to Powell; one-eighth, according to Rokitansky), then there could be no suction force exercised by it upon the parietes of the chest, for, being disabled in its elasticity, it literally has no power. The whole parietes of the chest on the diseased side have nothing to antagonize their elasticity, so it is kept enlarged. In addition, at this stage the fluid of itself presses against the walls of the chest in all directions.

The elastic pulmonary tissue is always, to a certain extent, on the stretch. It is striving to pull asunder the pulmonary from the parietal pleura; but this it cannot do, because the air can have no access to the pleural cavity. The five mm. of mercury elasticity of the lungs can be increased by a distension of the chest from a forcible inspiration to thirty mm. of mercury. Anything which lessens this elasticity of the lungs takes off so much from the force which interferes with the rebound of the thoracic resilience, and consequently increases the circumference of the chest. Such is the case in emphysema, oedema of the lungs, pulmonary congestion, and, curious to relate, at the outset during the pyrexial stage of acute diseases, such as pneumonia, variola, bronchitis. The enlargement of the thoracic circumference is appreciable. It, however, gradually decreases and becomes normal. This yielding of the thoracic walls is attributable to temporary engorgement of the lungs, lessening their retractile force.

At the very commencement immediate results of percussion are negative, but by delicate taps over a pleximeter there is a sound at the margins, owing to the deficient expansion, of impaired resonance and of higher pitch, and the vibrations are less full. There is also a sense of pain, owing to the increased sensibility of the costal pleuræ. As the fibrinous coatings form, the sound becomes less and less full and the normal vibrations of sound are less diffused, more circumscribed, giving to the finger, used as a pleximeter, a sense of resistance from the diminished elasticity of the lung. This is especially the case at the base over the attachment of the diaphragm. As the effusion rises from the base, the sound on percussion becomes flat. The fluid being a non-resonant body, the vibrations of the percussion taps do not extend. The sound is of high pitch, but not resonant. It has been properly designated by Skoda an empty sound, for it conveys to the ear the condition beneath, which is one of perfect airlessness. It is not simply a dull sound or one where there is not the normal resonance, but it is destitute of all resonance: it is absolutely flat. The confusion of dulness with flatness has in the past led to erroneous conclusions as to the line showing the level of the fluid in pleurisy. As high an authority as Woillez, in reference to fluid flatness, speaks of dulness as complete, absolute, or very incomplete sub-dulness! The muscular coverings of the walls of the chest or unusual amount of adipose tissue or pleuritic coatings or bands produce impairment of resonance, and sometimes marked dulness on percussion. But when the percussion wave penetrates to the lungs, there is more or less resonance. When the lung is solid from pneumonia or tubercular deposits, the sound is often very dull, but rarely flat, because it seldom happens that all of the alveoli are filled up, and even when they are the vibrations are communicated to the bronchial tubes which contain air, and in this way there is some resonance. We call particular attention to the importance of these distinctions and to the necessity of light and delicate percussion in order to test the resonance or non-resonance of the thoracic cavities. If the percussion be strong, the vibrations are conveyed {500} by the thoracic walls to the portions where there is no fluid, and thus we have impaired air-resonance, and not flatness. We have frequently seen errors of diagnosis in cases of pleurisy owing to the physician percussing with too much force. To secure accuracy, Garland[25] lays down the simple rule of percussing with great care and always in straight lines, and of percussing each line to its terminus before taking up another. Powell[26] compares the peculiar flat percussion sound of pleuritic effusion to that elicited on striking against a brick wall. The flatness is characteristic and more marked than the dulness of lung-consolidation. If we are not careful to make the distinction between impaired resonance and non-resonance, we may easily draw erroneous conclusions as to the rise and extent of the fluid in the chest. We have shown elsewhere (Pathological Anatomy of Pleurisy--Distribution of Fluid) that, as the fluid collects in the cavity, the lung contracts before it. The border above the level of the liquid contains less air, the capillary circulation is less active, and frequently there is more or less oedema, owing to its being the most dependent portion. These physical conditions impair, to a greater or less extent, the pulmonary resonance. Thus at the base above the fluid we might, on reflection, naturally expect some dulness on percussion, lessening as we recede from the fluid. Several observers have called attention to the impaired resonance over the lowest portion of lung posteriorly when the person is standing. Garland[27] termed it the dull triangle. Heitler[28] of Vienna observed this same condition in that locality, and likened it to a monk's hood cut longitudinally through the centre and hanging apex down. Rosenbach[29] of Breslau noticed that this non-resonant triangle in pleurisy would often clear up on exercise or by breathing; this fact he considered distinctive between pleurisy and pneumonia.

[Footnote 25: _Loc. cit._]

[Footnote 26: _Med. Times and Gazette_.]

[Footnote 27: _Ziemssen's Supplement_.]

[Footnote 28: _Wien. med. Wochenschr._, 1878, quoted by Garland.]

[Footnote 29: "Ein Beitrag zur phy. Diag. der Pleur.," _Berlin klin. Wochenschrift_, 1878, No. xii.]

Although the fluid first collects over the posterior portion of the diaphragm, flatness on percussion is first observed over the axillary portion of the diaphragm, because, as explained by Calvin Ellis, the conditions there are more favorable for percussion. As the effusion increases the line of flatness, when the patient is in the upright position, advances, not directly up the back and horizontally across the chest, as was formerly supposed, but across the back in a curve reaching its highest point in the axilla, from which it descends toward the sternum.[30] R. Douglass Powell[31] says the upper margin of the effusion in typical cases is not a water-level, but presents a curve having its convexity upward and in the lateral region. Since the attention of the author was first called to a careful examination of the curve of flatness as ascertained by light and delicate percussion (in the erect position), he has found it to be more or less of an Ellis curve at an early stage of the effusion. The line is sometimes better defined than at others. All observers, however, must acknowledge that at the stage of the disease when cases of chronic fibro-serous pleurisy are first seen the letter _S_ curve is not well marked. Mason states that although in some of his 200 cases this peculiarity was observed, in others the line was horizontal. When fluid fills the chest to excess and overcomes the elasticity of the lung, it gives flatness on percussion high up, even to the clavicle, and behind to the supra-spinous fossa. The fluid filling the cavity, the line of flatness becomes nearly horizontal. Then it is that percussion reveals the displacement of the diaphragm and abdominal organs. On removing the excess of fluid by aspiration or by absorption, this curved line reappears, and continues as previously.

[Footnote 30: See section on Pathological Anatomy of Pleurisy, distribution line.]

[Footnote 31: _London Med. Times and Gazette_, Oct., 1882.]

{501} Contrary to the general belief, when the fluid is moderate in quantity change of position of the patient modifies but little the area of flatness, owing to its being retained between the lung and diaphragm. Woillez[32] noticed slight mobility (never more than to the extent of one intercostal space) only in 5 of his 82 cases. He concluded that the conditions were very different from what they were in ordinary vessels outside the body. Woillez does not attempt to explain what these conditions are. Skoda acknowledged that in the majority of cases the fluid does not change its position as the patient moves. Skoda and Wintrich attribute the non-movement of fluid to adhesions. Garland, and subsequently W. H. Stone and Douglass Powell, showed that the effusions were immovable when in moderate amounts, because they were kept so by the retractility of the lung, and that the large amounts were movable because the retractility had been overcome by them. When in large quantities the fluid accumulates in depending positions of the chest. Later on in the disease, adhesions and bands mechanically interfere with the line of flatness; or if there be any disease of the lung interfering with its retractive force, the fluid may not take its usual line. These peripheral adhesions frequently occur at the upper margin, and are sometimes wavy and irregular. They often occur early in the disease, and prevent in a marked degree the fluid from yielding to the negative lung-traction.

[Footnote 32: _Mal. Aigues des Org. Resp._, Paris, 1872.]

By these bands the pleuritic fluids become sacculated in different parts of the thorax--between the lungs and the walls of the chest, between the diaphragm and lungs and the pericardium, the mediastinum, the vertebral column, and actually between the lobes of the lung. Fraentzel holds that the percussion sound is dull over the thorax whenever the effusion attains the depth of from one inch and a half to two inches between the lung and the chest wall. Garland by his experiments on dogs shows that the fluid does not thus rise between the lung and parietes, except a very thin layer, by capillary attraction, not sufficient to cause flatness on percussion or to interfere with the expansion of the lung unless the amount is very excessive, and not until the lifting power of the lung is completely overpowered. When the effusion is very large, it fills up the posterior portion of the thorax, compressing the lung against the uppermost portion of the spine or the mediastinum. The percussion sound is absolutely flat, provided the force of the blow be not too great; in that case the ribs are thrown into vibration or the vibrations extend to the sound lung. This materially impairs the dulness and may lead to error of diagnosis.

The lung may be prevented from contracting by reason of various kinds of adhesions or by means of widespread infiltrations, by emphysema, and by laryngeal stenosis. In such cases, as the effusion increases, it quickly rises in the thinner layers without displacing the organs. Fraentzel warns us that sometimes, in left-sided effusions, the lung having become adherent to the heart, the heart is drawn back with the lung away from the wall of the chest, and then it cannot be felt anywhere: the absence of the apex-beat and the feebleness of the heart-sounds may lead us to assume, incorrectly, that there is effusion in the pericardium. If the fluid collects between the external layer of the pericardium and the mediastinum, the heart is surrounded and pressed by the pleuritic effusion.

The Skodaic resonance is a remarkable tubular quality of resonance heard on percussion when the effusion extends up to the fourth rib or beyond it, nearly filling the pleural cavity. It is a high-pitched, long vibration, semi-tympanitic sound, rarely absent when, from an effusion, the lung is retracted to a very small size, but still contains some air. It is most frequently found anteriorly under the clavicle, near the sternum, because to that point the lung withdraws as long as it has any retractility left. If the air be forced {502} out of the lung by pressure, this sound is no longer heard. Flint called this peculiar tympanitic sound, heard above the level of the fluid in pleurisy, by the descriptive name vesiculo-tympanitic resonance. The vesicular, though feeble, is combined with the tympanitic quality, and the intensity of the resonance is abnormally increased. This subclavicular tympanitic sound is not peculiar to pleurisy. It exists in pneumonia preceding hepatization, and was noticed by Hudson, Graves, and Williams before Skoda called attention to it in pleurisy. Skoda's explanation of this phenomenon is now generally accepted--namely, that it comes from diminished tension of the lung-tissue, caused by diminution in the quantity of air, and consequently relaxation of lung-tension. The residuary air in the alveoli does not mix properly with the tidal column: it is indeed pent up by the narrowed diameter of the minute bronchi. Thus it becomes surcharged with carbonic-acid gas; this relaxes the air-sacs and lessens their tension. In fact, the percussion sounds are invariably tympanitic when the parietes of the organ which contains air are not stretched. When they are firmly stretched, the sound elicited by percussion becomes less and less tympanitic, and finally dull: such, we know, is the case in striking a drumhead. The chief characteristic of the sign relates to the quality of the sound; the resonance is nearly devoid of vesicular quality. A resonance absolutely non-vesicular is always tympanitic (Flint). This tympanitic sound is so constant under the clavicle that although it may be from other causes, its appearance would lead us to suspect effusion, especially in children. It is not only at the apex, but wherever the lung shrinks from pleuritic exudation and loses in tension, the percussion sound has the tympanitic quality. We find it occasionally near the sternum, and sometimes in sacculated effusions we observe it in different parts of the thorax. Traube, and subsequently Fraentzel (_Ziemssen's Cyc._), called attention to the fact that sometimes a long expiration would cause a temporary abolition of this tympanitic sound at the apex. Their explanation is that the sound is heard over the compressed lung. Garland urges that this explanation cannot be a satisfactory one, for a certain amount of pulmonary expansion is essential to the production of tympanitic resonance.

This exaggerated resonance elicited by percussion has received its name from the eminent German who wrote so much about it; but it did not escape the accurate ear of the discoverer of percussion, Avenbrugger, who clearly defined the subclavicular tympanitic resonance in pleurisy.[33] Skoda's sign, however, is not unique, for observation proves, when the lung is contracted with fluid below, that there are several varieties of resonance. Notta,[34] who was not aware of Skoda's ideas, describes the sound as hydroaérique where the lung is above the level of the fluid. Roger,[35] who called especial attention to Skoda's views, admitted that there were several varieties of tympanitic resonance heard above the fluid. He compares them to those heard on percussing over the stomach of the cadaver. Woillez[36] describes five varieties or types of sonorousness, according to their intensity, their tone, and their quality. He noticed these under the clavicle at different points above the liquid--ordinarily on the level of the second or the third rib. (1) The most common and the best defined was a short sound, dry and superficial; the tone of this was acute, with exaggeration of intensity. Williams[37] in 1841 called attention to these peculiarities. With this variety we frequently have a reverberation, pointed out by Stokes in 1837--a cracked-jar sound more or less marked. Woillez noticed this variety in 11 of his 82 cases; of this number 9 were in pleurisy of left side. (2) There was exaggeration of intensity or tympanism with a grave tone: 7 of Woillez's cases showed {503} this variety, of which 6 were on left side. (3) A subclavicular resonance, unnaturally acute, but with exaggerated intensity. (4) Exaggeration of intensity, with equal tone on both sides; only 2 patients out of 82 showed this variety. (5) Exaggerated abnormal resonance, more acute than healthy side, and with normal fulness of sound. These are all modifications of percussion sounds elicited in pleurisy and other pathological physical conditions resembling it, where there are variations of tension together with other modification of the structure of the lung. The bruit de pôt fêlé is sometimes clearly marked, as it is also in hepatization of lung.

[Footnote 33: Avenbrugger, _Ouv._, ed. de Corvisart, 1808, Paris.]

[Footnote 34: _Arch. gén. de Méd._, 1850, t. xxii.]

[Footnote 35: _Ibid._, 1852, t. xxix.]

[Footnote 36: _Mal. Aig. des Org. Resp._, Paris, 1872.]

[Footnote 37: _The Path. and Diagnosis of Dis. of the Resp. Organs_, 1841.]

Traube's Semi-lunar Space.--There is a point on the left side where we find normally a vesiculo-tympanitic sound, first pointed out by Traube and enforced by Fraentzel. It is situated at the anterior base of the left side, and is of a half-moon shape. It is bounded inferiorly by the margin of the thorax, and superiorly by a curved line whose concavity is turned downward. It begins in front, below the fifth or sixth costal cartilage, and extends backward along the margin of the chest as far as the top of the ninth or tenth rib. Its greatest breadth is from four to four and a half inches. This tympanitic sound is caused by the air in the stomach, which lies well up against the diaphragm. When the stomach is pushed down by the falling of the diaphragm, from excessive fluid, the tympanitic sound disappears. The value of this semi-lunar space in the diagnosis of pleuritic effusions has been variously estimated. Fraentzel considers it of great significance in the differential diagnosis between pleurisy and pneumonia; Ferber and Garland do not. Weil suggests that the area of this space may be diminished by filling the stomach and colon with solid or fluid food. Garland shows that as the diaphragm's depression depends upon the excess of fluid overcoming the lifting force of the lung, we may have, with a vigorous, unimpaired lung, a large amount of effusion in the pleural cavity, yet the resonance of the semi-lunar space may remain tympanitic. The condition of this semi-lunar space is of most diagnostic value in extensive left-sided effusions. The more the diaphragm is pressed down by the effusion, the smaller becomes the space of tympanitic resonance. It may gradually disappear altogether.

Auscultatory percussion may sometimes be advantageously employed to detect fluid in the pleura, especially in the younger subjects, for intercostal fluctuation may frequently be appreciated when we press carefully with the palm or surface of the finger between the ribs while the percussion shock is applied to another part of the same side. If we auscultate with a stethoscope, the chest extremity of which is made to fit in between the ribs, while another person percusses the chest, we can sometimes detect the fluctuation within the cavity of the chest.

We thus see that in the diagnosis of pleuritic effusions percussion is very valuable, perhaps the most valuable of the physical signs. We must not, however, forget that its significance may deceive us if the fluid is prevented from gravitating by pre-existing adhesions, or if it is encapsuled between the diaphragm and lung or between the lobes. Cases occasionally occur where, from fibrinous bands, the fluid is kept in the posterior part of the thorax, consequently there is pronounced clearness and fulness in front. Percussion does not enable us to diagnose the consistence of the contents of the pleura, or its nature, whether it be fibro-serous or purulent. To do this we must resort to Bacelli's method, or, still better, to exploratory punctures by the hypodermic syringe.

Palpation.--The sense of touch gives valuable physical signs in pleurisy. At the commencement, before there is any effusion of fluid, even of fibrinous deposit, we notice by palpation the decreased movement of the walls of the chest, and also the sensitiveness of the walls. When the eye cannot {504} notice modifications of the expansion and elevation movements or movements of the ribs, correct views may be formed by palpation, especially in regard to the amount of local expansion in the upper part of the chest. In the lower part, by inserting a finger in the intercostal space we notice the modification of local expansion, also the convergence of the ribs taking place coincidently with the continuance of the elevation movement. We are thus furnished with additional presumptive proofs of the impermeability of the pulmonary tissue. When fibrinous effusion exists, the hand, early in the disease, recognizes the pleuritic friction or grazing. Later on, palpation perceives the rubbing when the muscles have recovered from their temporary paresis.

As soon as the effusion begins to form we detect a lessening of the delicate vibrations of the voice as communicated to our hands, always guarding ourselves against error by remembering that the normal sound is greater in the infra-clavicular region of the right side, and that it is always weaker in children and women, unless they have shrill, weak voices, in which case it may be entirely absent. It, indeed, requires a certain sonority of voice to be felt through the walls of the chest. When we find that both sides convey the vocal vibrations to our touch, we may be sure there is no effusion of fluid. Errors are often made by applying palpation over too extensive a surface, thus reaching beyond the fluid. It is important to use light, delicate palpation, employing the finger-tips instead of the whole hand, in order to exclude the vibrations from above as we approach the confines of the effusion. This vocal fremitus is entirely lost from the base up to the point to which the fluid reaches, and later on when it separates the two pleural surfaces. This absence of vocal fremitus is one of the most valuable physical signs of pleuritic effusion. It enables us to diagnose it from nearly all cases of lung-consolidation except when caused by malignant disease. When there are considerable pleuritic adhesive bands, they interfere with the complete absence of fremitus; but in children this sign is not so reliable. With them vocal fremitus is often scarcely perceptible in health. In dry tubercular pleurisy palpation gives us the characteristic friction. Palpation detects also the rubbing of the two lymph-covered surfaces after the absorption of the fluid. When there are thick fibrinous bands extending between the parietal and pulmonary pleuræ, there may be a vocal fremitus notwithstanding the presence of a quantity of fluid in the pleural cavity.

Displacement of Adjacent Organs.--The displacement of the heart as a physical sign indicating the presence of fluid in pleurisy is one of great significance. It is indeed a cardinal sign, second only in value to percussion flatness. It is almost invariably met with. Stokes[38] stated that it was observed at an early period, and was one of the very first signs of effusion; "that it may exist even before the upper portions of the chest have become dull, and is a circumstance of constant occurrence long before any yielding of the muscular portions of the thoracic walls." The heart is displaced at the very commencement of the effusion, and its dislocation increases pari passu with the effusion. The absence of the displacement, unless it can be explained by some special circumstance which rarely occurs, such as the retention of the pericardium by old adhesions or consolidation of the opposite lung, would negative the diagnosis of unilateral effusion. In this condition there is a marked contrast with the displacement and depression of the diaphragm and the resulting alterations of position of liver, spleen, and stomach. These only occur when the effusion is in great excess--not until from the large quantity of fluid the retractility of the lung is overcome, and it is consequently unable to lift up the fluid and the diaphragm. This altered position of the diaphragm drags the heart {505} downward by means of the ligamentous attachment of the pericardial sac to its tendinous portion. The deviations from the normal positions of the heart in slight effusions can always be noticed if the exact point of the apex-beat is sought for by palpation and listened for with the stethoscope. Careful percussion will show the shifting area of flatness.

[Footnote 38: _Dis. of Heart and Aorta_, 1854, Dublin.]

Powell calls attention to a fallacy with reference to cardiac displacements in the earlier stages of effusion--that, as the base of the lung retracts, the left or the right margin of the heart, as the case may be, becomes uncovered. This may lead to an apparent delay in the displacement of the organ, the more extreme left or right boundary being now within reach of palpation. The axis of the heart is not greatly changed by an ordinary degree of effusion. It becomes a little more vertical, and in extreme cases it may become slightly twisted. Only in rare and extreme cases does the axis of the heart become altered in direction beyond the vertical line. Powell[39] found at a post-mortem a heart that had become so twisted as to present itself obliquely edgeways in front. Sibson had previously pointed out this disposition of the heart to turn over and to present its posterior surface forward in cases of effusion.

[Footnote 39: _Consumption and Dis. of Lung_, London, 1878.]

In examining into the cause and significance of the displacement of the heart in pleurisy we find that until within a few years, it was, and indeed very generally now it is, believed that the sole cause was from direct pressure of the fluid actually pushing the heart away from its normal position. Skoda, Traube, Stokes, Powell, and Garland were, we believe, the first authors to show that such was not the case, certainly in moderate effusions. The displacements take place when the amount is very small--too small to exert any positive pressure. It is true that nature places the heart in such a position that it can yield readily to slight forces. It hangs in the pericardial sac, which is suspended by the aorta, and which is bound by ligaments to the body of the third dorsal vertebra. Every change of position of the body causes certain anatomical alterations of the heart's position. Wintrich, Skoda, and Braune think that the heart swings like a pendulum from its base, and that its apex is therefore elevated with every deviation to the right or left. Lebert says the heart is first depressed by the sinking of the diaphragm, and then elevated by being pushed to the right. Fraentzel says that in displacements to the right the heart is simply pushed over, and is never elevated as Wintrich describes it. The mediastinum offers but slight resistance, and is very easily pushed to the right side, where there is no compact organ to resist, and where the cavity is larger; whereas it is with more difficulty pushed to the left, where the heart occupies so large a space.

It has been satisfactorily demonstrated that until the pleura is about two-thirds full of fluid no positive pressure is exercised upon the lungs or heart. According to Rokitansky, the lung cannot be compressed until seven-eighths of the pleural cavity is occupied by fluid. The fluid cannot be drawn off by a canula unless air enters to replace the fluid. Unless the pressure on the fluid from within the cavity is greater than that of the atmosphere we cannot draw off a large quantity: if the pressure balances that of the atmospheric air, only a few drops of fluid are discharged externally, except by forced expirations and coughs. This is the case even when the quantity reached several liters. The feebler the expiratory force the less fluid escaped. Yet the heart is displaced as soon as the effusion appears. The significance of the displacement is that it shows the presence of fluid, but does not show the measure of intra-thoracic pressure (Powell).

Garland's explanation is that the heart, with the sac and its connections, "is placed between two highly elastic bodies (the lungs) which are striving to retract in opposite directions. The heart, therefore, being acted upon on {506} either side by opposing forces, occupies a position where these forces just balance each other; and this is the status of physiological repose in the vertical position of the body. Now, when an effusion is poured into either chest, the lung of that side contracts, and thereby exhausts a certain amount of its retractile energy. The opposing lung, however, still remaining normal, immediately begins to draw the heart toward itself, and the degree of displacement thereby induced will be proportional to the diminution of energy in the compromised lung." Stokes divided displacements of the heart into excentric and concentric. The former he considered due to direct pressure of the fluid, and the latter, when from any cause there was diminution in volume of one lung, the other lung, by its increased volume, forced it over. The concentric displacements, he thought, were generally the result of some chronic disease producing atrophy of lung.

Thus we see that displacements of the heart occur at three distinct periods in the course of pleurisy, and from different causes in each case: (1st) As soon as fluid forms in the pleural sac. At this period the displacement is caused by the presence of the fluid which occupies part of the pleural cavity. The lung by its elasticity retracts. It is, consequently, of less volume and exerts less negative force upon the mediastinum and its contents than the healthy lung. The two lungs having by their equal tractile energy previously kept the heart in situ, the healthy lung draws the mediastinum out of its position in a transverse direction. Necessarily, the displacement of the heart from this cause is in proportion to the amount of fluid effused. This is the most frequent mode of displacement of the heart. It can be said to be almost always present. (2d) When the quantity of fluid is great enough to overcome the retractility of the lung and exert intra-thoracic pressure, it forcibly expels the air from the alveoli of the lung and by direct positive pressure pushes the heart aside. The displacement of the heart in this case can only be produced when the pleural sac is two-thirds or more filled by fluid. When this condition is met with, the displacement is very great, because the heart has been already displaced by lung-traction. Previous to the researches of Garland, Stone, and Powell, this was supposed to be the only manner of explaining the displacement of the heart from pleurisy. (3) Where, as illustrated by Stokes',[40] Hunt's,[41] and Chew's[42] cases, the heart is displaced toward the diseased side. This occurs more as a sequel of pleurisy in the course of the absorption of chronic or suppurative pleurisy, where by non-expansion of lung a partial vacuum is produced. The external atmosphere presses in the thoracic walls of the diseased side, and the internal atmospheric pressure from the healthy side is exerted against the mediastinum and presses the heart in that direction. Marked displacements from this cause are rare; slight displacements are more frequent. Cicatrices from healing of large cavities would have this effect. Mere consolidation of lung could not cause it.

[Footnote 40: _Dis. of Resp. Organs_.]

[Footnote 41: J. W. Hunt, _Dub. Med. Journ._, _loc. cit._]

[Footnote 42: S. C. Chew, case reported to Med. and Chi. Soc. of Md., 1883.]

Displacement of Lung.--The lung in cases of effusion is drawn up by its own retractile energy. It has been demonstrated that this force is considerable. As the effusion advances the lung recedes to a certain point, when the fluid, having overcome the retractility of the lung and having a fixed point below, actually exerts positive pressure upon the lung (Garland), and compresses the air out of the alveoli and the compressible bronchi. This compression cannot take place until the diaphragm is no longer elevated into the thorax, but is bagged down by the excessive weight of the fluid. There can be no compression of lung until its elasticity has been exhausted. The gradual effect of the continued contraction of the lung is to straighten out the letter _S_ curve. The force of lung necessarily diminishes gradually as it contracts in volume. On the other hand, the immediate effect of compression is to {507} obliterate that curve. So long, therefore, as we are able to trace a well-marked letter _S_ on the chest, we may be certain that the lung is well out of reach of compression (Garland). Peyrot[43] showed by plaster-of-Paris injections into the chests of cadavers, and then making cross-sections, that deformities of the chest are not due to a development of one side, the other remaining normal, but that they consist of a mutual adjustment of all parts. The simultaneous movement of the sternum toward the left in left-sided effusions makes the displacement of the heart appear greater than it actually is.

[Footnote 43: _Arch. gén._, Juill., 1876.]

The Diaphragm and Intercostal Spaces.--The diaphragm is not depressed below the edges of the ribs, nor do the intercostal spaces bulge until the weight of the fluid exceeds the lifting force of the lung. The admission of air into the pleural sac produces the same result. The depression of the diaphragm is due in part to the weight of the fluid, but chiefly to the diminished contractile energy of the retracted and diminished lung. The displacement of the mediastinum depends upon similar conditions. Since the traction of the lungs always affects both sides of the thorax, the movable mediastinum must follow the lung, which is still capable of contracting, and therefore with right-sided exudations the left lung will draw the parts over to itself. Only with excessive effusions in the pleural cavity does the pressure of the fluid come into activity.

The liver and spleen may be pushed below their normal position by excessive effusion after the diaphragm yields to the weight of the fluid. Woillez found the liver displaced downward in the abdominal cavity in one-fourth of the right pleurisies and only once in left-side pleurisies. The extent on the right side was from two or three centimeters to three fingers' breadth, even as far as the umbilicus.

The stomach, when the diaphragm sinks, may be pushed downward; thus the so-called semi-lunar space of Traube may be obliterated. Ferber noticed a peculiar displacement of the stomach in two cases where he had produced an artificial hydrothorax of the left side. The fundus was pushed to the right, and the stomach was folded over on itself to a certain extent. A second and marked folding-in of the greater curvature occurred near the pylorus. This condition of stomach, with left-sided pleural exudations, has been hitherto entirely neglected by authors. May not the vomiting which is often observed with excessive effusion, and which has been attributed to violent acts of coughing, be due to this doubling over of the stomach?

Auscultation.--At the commencement of acute pleurisy, when hyperæmia exists with dryness of the pleural surfaces, auscultation shows a respiratory murmur lessened in intensity and duration. There is also a jerking unevenness in the rhythm of respiration, and weakness or indistinctness of the vesicular murmur consequent upon the imperfect and irregular expansion of the lung. On the healthy side the respiratory murmur is hypervesicular, and becomes puerile and noisy in character. In from twelve to eighteen hours the plastic fibrinous deposit on one or both pleuræ causes us sometimes to hear, over circumscribed spots, at the end of inspiration and the beginning of expiration, a fine friction sound, which varies in intensity over the points of contact of the surfaces. This is especially the case in the infra-mammary, infra-axillary, and infra-scapula regions. Woillez heard friction sounds in 52 of his 82 cases. The pain in respiration makes it very jerking and irregular. The contact of the surfaces pushes aside the lymph, and thus we hear the sound at a given point at one inspiration and not at another. It is heard more distinctly during inspiration than expiration. The reason of our not hearing the friction sound at the early stage of pleurisy continuously, but with interruptions in inspiration and expiration, is because the opposed rough pleural surfaces do not continuously rub against one {508} another, but remain adherent for a few moments, until a deeper inspiration tears them asunder. The effusive stage comes on so rapidly in acute pleurisy that often when patients are examined the friction sound of the first stage has disappeared. It has been generally taught that the cause of the disappearance of the friction sound, and its subsequent reappearance as convalescence commences, are owing to the fluid separating the surfaces and its reabsorption. We have seen, from Garland's experiments and from careful clinical percussion explorations, that the fluid does not come between the two surfaces unless in very great effusion, but that it occupies the cavity between the lung and diaphragm. Stokes long since showed that there was temporary paresis of respiratory muscles, and consequently loss of movement of the surfaces over each other, which movement was necessary to produce friction sound. The reappearance of friction sounds indicates recovery of this muscular power. When heard, the friction is of the grazing variety--the most delicate form. Walshe designates it as the attrition species, and says it is audible over a limited extent of surface, occurring with occasional respirations, dry, and limited strictly to inspiration. As the effusion appears, we find, beginning with the lower border, that the respiratory murmur disappears, becoming less distinct as the effusion advances in the pleural cavity. Ordinarily, we hear no breath sounds. The absence, however, of breath sounds as a sign of pleuritic effusion is by no means a constant one. When the fluid contains many fibrinous bands, binding the lung down to the costal pleura, or when the effusion is very large and forces the air nearly out of the pulmonary tissue, pressing it into a firm mass against the vertebral column (at a point corresponding to the spine of the scapula), or when the lung is solid simply from the residual air being pressed out of it, diffused bronchial tubular breathing is heard. The tubular sound is conveyed, not ordinarily through the fluid, but by the parietes of the chest and by the solid plastic linings and adhesions. The fluid, if in large quantity and filled with fibrinous bands, may also feebly conduct the sound, which, being produced on solid surfaces, is best conducted by solids. We hear, in fact, a respiratory sound of low pitch, but tubular in quality. It is bronchial, but it differs widely from the familiar bronchial respiration observed when the lung is consolidated in pneumonia. It is a diffused distant tubular sound unaccompanied by moist sounds, soft in its quality and muffled. It has not the brazen, harsh character of pneumonic bronchial respiration. In pneumonia this sound is immediately under the ear, the lung being in contact with the inner surface of the ribs, and rendered a good conductor by its solidity, and the sound rendered louder by the increased consonating properties of the walls of the bronchi; whereas, in pleurisy, the lung is contracted above the level of the fluid, or, when the effusion is excessive, is removed from the walls by an indifferent conductor of its sounds, and the sounds are conveyed from the compressed lungs at their base by the walls of the chest, and, in a degree, by the deposits on the pleural surfaces. The bronchial breath sound which we hear over the lung, compressed by fluid, near the vertebra continues sometimes a long time after the absorption of the fluid, because the lung, deprived of air, expands slowly. If the effusion be small, we do not hear bronchial respiration, because there is sufficient air in the alveoli to prevent the conduction of the sound, the air not being compressed out by the effusion, but the whole lung being lessened in volume. If, again, the mass of fluid be very large, it prevents the free transmission of the waves of sound, and we do not hear them.

The auscultatory phenomena necessarily vary according to the amount of fluid in the cavity, the extent of the adhesions, the retraction, and the compression of the lung-parenchyma. If the compression be sufficient to prevent the air from passing down the bronchi, we do not hear bronchial respiration, {509} because where, as in health, it is not communicated to the ear (owing to its non-conduction by the lung-tissue), it cannot be produced. Douglass Powell[44] calls attention to another unusual pressure effect--altered quality of voice and cough, a husky voice, and a laryngeal quality of cough undistinguishable from that so often heard in cases of mediastinal tumor or aneurism. These disappear after paracentesis.

[Footnote 44: _Consumption and Dis. of Lungs and Pleura_, 1878.]

Above the level of the fluid, and again as absorption of fluid takes place, we have a return of the characteristic friction sound as the muscles of the chest recover their normal power. With care this sound will not be confounded with intra-pulmonary râles, which are moist sounds removed or modified by cough or expectoration. These convey to the ear the sound of bubbles of air as they pass through the mucus and the secretions of the bronchi; whereas the friction sounds are superficial noises from rough surfaces moving over each other. The mucous râles which are sometimes heard are not from the pleurisy, but from bronchial catarrh. The friction sounds heard in the stage of absorption are ordinarily coarser and more abrupt. They are unequally jerking in character, and in quality resemble osseous crepitation. In chronic pleurisy, and for a long time after the fluid is gone in acute pleurisies, we have pleuritic rubbing sounds when the walls of the chest are drawn out in full respiration. At the absorption stage we ordinarily hear the lung gradually expanding. The respiratory sounds are feeble, and frequently moist subcrepitant râles are heard in the bronchial tubes. If the effusion has been of long duration, we find the pleural surfaces so thoroughly coated with fibrinous deposit, and the lung so separated by bands from the costal pleura, that the expansion of the lung is very much impaired and the percussion dulness does not subside. Leaming and Camman of New York give numerous cases where there might well be difference of opinion as to whether the signs heard were intra-pulmonary or pleuritic. In cases where the intra-pulmonary adventitious râles resemble the extra-pulmonary frictions, the diagnosis is assisted by considering the length of the sound. The character and intensity of the friction murmur varies very much. It may be a slight grazing sound or a coarse, sharp creaking-of-leather noise. Walshe gives no less than six modifications of the friction sound, ranging from a feeble, scarcely audible noise to one of extreme loudness. Friction sound is mostly an isolated phenomenon--that is, it is not accompanied by any unnatural quality of respiratory or vocal sound. Advanced type friction consists of a series of jerking sounds, rarely exceeding three or four in number.

We must remember that sometimes, notwithstanding a considerable quantity of fluid, the lung expands, and, pushing the fluid aside, causes the rubbing of the pleural surfaces together. When unmistakable, these respiratory friction phenomena are pathognomonic of the results of pleurisy. Thus they are properly considered of great value in the diagnosis.

Pneumo-pericardial Friction Sounds.--On the left side the uneven pleural surfaces are sometimes forced together by the impulse of the heart; of course, the resulting friction sounds are cardiac in their rhythm. Then, again, fibrinous deposits on the outer surface of the pericardium are forced against those of the covering pleural layers, both by respiratory and heart impulses. Close attention to the rhythm and the positions where these sounds are heard will prevent their being considered pericardial in their nature.

The fluid may be nearly removed and yet the condensation of the superficial strata be sufficient to produce extensive and marked dulness. Under such circumstances the production of friction phenomena is inevitable. The retention of some portion of the lung surface in tolerably close proximity to the costal pleura by means of adhesions also renders the production of {510} friction sound possible, although a considerable quantity of fluid be present in the pleura. It is common to find effusion signs in the back and friction signs in front. We most frequently have friction at the base when there is absolute flatness. If the walls be separated by fluid, there can be no friction from contact. But it rarely happens that the fluid rises between the surfaces. To produce friction sounds we must have motion of rough surfaces which are in contact.

If the patient talks while we are listening in cases of small effusion we hear over the scapula, toward the spine, and between the scapula and the spine, bronchophony, as we do also when the lung is nearly deprived of air, in which case the sound sometimes has the bleating, nasal resonance designated by Laennec ægophony. In his opinion this was of constant occurrence and of great diagnostic value, but now it has been demonstrated that this sound can be heard when there is no fluid whatever, but consolidated lung. Anstie calls it one of the fancy signs of pleurisy. Ægophony is an unimportant variety of bronchophony, and not a characteristic phenomenon of pleuritic effusions. Of itself, it is not diagnostic of effusion, yet it is none the less true that it is a modification of bronchophony, and is commonly met with in cases of moderate pleuritic effusion, usually toward the upper margin of the fluid. It is difficult to state definitely the amount of fluid which usually produces it. Guttman thinks it is probably produced by the vibration of the walls of the flattened, compressed bronchi; this vibration is excited by the voice and transmitted to the thin layer of fluid which, at the upper part of the exudation, lies between the lung and the chest-wall. This tremulous movement of the sides of the bronchi gives the voice sounds a quavering, interrupted character; and, as they have to pass through a fluid medium to reach the surface, they lose in clearness and precision and acquire a nasal twang.

When the effusion is large, and we have full dilatation of the chest, all vocal resonance ceases, because the vocal vibrations go through media of such different kinds that they are lost before they reach the ear. During absorption, before the lung recovers its normal volume, we again hear bronchophony. Pleural adhesions and thickening cause the sound to be heard through the effusion when we least expect it. It is not unusual to find ægophony and bronchophony in the same lung. They are also found in some cases of pneumonia, and in some individuals, especially in children, we have between the scapula a normal resonance of the voice, with an ægophonic resonance.

Bacelli's Sign (Pectoriloquie aphonique).--This, the reverberation of the whispered voice through the fluid, is a sign of considerable value. If well marked it indicates fibro-serous fluid; its absence, however, does not show that the fluid is not of this character. (See Purulent Pleurisy.)

Auscultation is of great value as indicating with definiteness the position occupied by the effusion as it is being reabsorbed.

Heart Murmur.--From excessive accumulation of fluid in the pleural sac a systolic murmur over the base of the heart is very often heard. That it is produced by pressure or twisting of the aorta is evident from the fact that it ceases when the fluid is withdrawn.

Phonometry we have found of but little value in the diagnosis of pleurisy.

COURSE AND DURATION. Acute pleurisy is essentially a unilateral disease. It does not pursue a regularly-defined course, nor have we any critical stages, as in pneumonia. In mild cases of acute primary pleuritis the disease advances slowly and recovery is tardy. The febrile movement may be four or five days in reaching its height. It remains at this point for several days--from four to seven days; in rare instances as long as ten days.

The effusion sometimes comes on very rapidly, but ordinarily is one or two days in forming. When it appears it may be divided into (1) the stage of {511} progress, (2) stationary period, and (3) resolution. For the examination of both of these we must employ percussion, and mensuration by means of the cyrtometer, which give us exact results. Woillez in a large number of observations found that the first period lasted from eleven to twenty-four days, most frequently from fifteen to twenty days. The stationary period he found varied from twenty-four hours to several days. Frequently the reabsorption commences suddenly without any interval. Resolution is initiated from the eleventh to the twenty-fifth day, and lasts over fifteen days.

As the effusion advances the acute symptoms--rapid pulse, the elevated temperature, acute pain, and superficial dyspnoea--are materially lessened. If, however, the effusion be very great, we shall have at first painful dyspnoea, especially when the patient makes unusual exertions. This dyspnoea is ordinarily in proportion to the amount of the effusion. If there is much displacement of heart or distortion of larger blood-vessels, there is imminent danger to life. After the first few days we are often surprised at the tolerance of the whole system of the excessive amount of fluid. Absorption, after the effusion has been thrown out, is at first rapid, then it occurs more gradually; part of the liquid portion disappears, and the fibrinous portion undergoes fatty degeneration previous to absorption. The physical signs of flatness, vocal fremitus, together with the return of the displaced organs, the heart, liver, and diaphragm, to their normal positions, give us accurate means of judging of the progress toward cure. The general health shows unmistakable signs of improvement. The appetite is better, as are also the color and strength. If the effusion remains undiminished in quantity, or if it becomes purulent in character, the general appearance will show evidences of weakness and lowered vitality.

The average duration of acute primary pleurisies varies, when the effusion has not reached any considerable height, from two to four weeks. It may continue thirty or thirty-eight days--minimum duration twenty days. The absorption requires many weeks if the effusion is large or if it becomes chronic. Two months may elapse before the fluid entirely disappears. In some cases it continues, unless thoracentesis be performed, for many months. We have given the symptoms manifested when there is any renewal of the inflammatory process. In pleuritis acutissimus death may occur in ten days or two weeks from syncope, or from thrombosis caused by pressure upon the large venous trunks and consequent twisting, especially of the ascending cava, where it perforates the central tendon of the diaphragm to reach the pericardium, or by torsion of the aorta. When the effusion remains for a long time, the lung may be permanently prevented from expanding by pleuritic thickenings resulting from inflammatory products. In acute primary pleurisy the tendency is toward resolution. Louis went so far as to state that pleurisies never caused death. Trousseau, Lacaze, and others give cases where sudden deaths were produced by the quantity of fluid pressing upon the heart and blood-vessels. In subacute pleurisy (latent pleurisy of the older writers) the course of the disease is so gradual, so unattended by pain or even discomfort to the patient, that he goes perhaps weeks with considerable fluid in the cavity without being aware of it. He has probably been able to continue his occupation without intermission. It is only when he begins to feel weak and to lose flesh, and finds that his respiratory force is impaired, that he consults a physician. The rational symptoms scarcely point to pleurisy, but the physical signs of the presence of fluid are very distinctive. In this form the effusion is ordinarily greater in quantity than in the acute variety, and unless some of the fluid be taken away by aspiration, absorption is very sluggish. In these cases, if the fluid remains long in the cavity, the lung may become permanently disabled by the long continuance of the compression.

{512} In chronic pleurisy the effusions from the acute or subacute pleurisies remain unabsorbed. They ordinarily are purulent in character, but sometimes they remain sero-fibrinous many months. Purulent pleurisies may be primary as well as secondary. (See Purulent Pleurisy.)

TERMINATIONS.--Pleurisy of a fibro-serous nature terminates in (1) convalescence, (2) becomes chronic, or (3) ends fatally. Among those who are cured there are some instances where the disease is of short duration and the recovery prompt and complete. With others the disease itself is of a severer type and lasts longer. If the attack of pleurisy be secondary to another disease, especially if the latter be of a nature to profoundly affect the nutrition, convalescence is very tedious.

Acute pleurisies which are primary but rarely become chronic, but when secondary they frequently are chronic from the beginning. Heyfelder states that chronic pleurisies are three times more frequent on the left side than on the right side.

Trousseau, Bowditch, Lacaze, Behier, and others have reported sudden and unexpected deaths in cases of fibro-serous pleurisies. Not only has this resulted in cases where the fluid was excessive in quantity, but also in cases where the amount was moderate. Wilson Fox (_Brit. Med. Journ._, Dec., 1877) gathered from medical literature between 50 and 60 sudden deaths from effusions of all kinds. Syncope has been the usually assigned cause of death. Négrié[45] collected 12 cases of unexpected deaths from pleurisy, and there were but 2 of them where syncope could be assigned as the cause of the fatal termination. Of the remaining 10 cases, 3 were caused by what is invariably a grave complication, pericarditis, and 7 by clots formed in the heart or pulmonary artery. In the cases where pericarditis existed the deaths occurred as early as the eleventh or twelfth day. In the other cases death occurred as late as from the twentieth to the forty-fifth day. Woillez[46] reports 2 cases where death was produced by supervening congestion of healthy lung.

[Footnote 45: _Thèse de Paris_, 1864.]

[Footnote 46: _Loc. cit._]

COMPLICATIONS AND SEQUELÆ.--The inflammation may extend by contiguity to the lung-parenchyma, pneumonia supervening after a few days, or it may appear to come on simultaneously. It is, however, a rare complication. Lacaze[47] reported one case, and that followed thoracentesis; Lugrol reported a similar case.

[Footnote 47: _Loc. cit._]

Pneumonia does not appear to commence after the effusion has reached the point of compressing the lung. The inflammations frequently are peribronchitic and broncho-pneumonic. The mediastinum may become involved. Fraentzel states that it can never be clearly proved that simple croupous pneumonia exists as a complication of primary pleuritis on the side affected; on the sound side it occurs occasionally. Laennec taught that the compression by the fluid always tended to prevent the occurrence of pneumonia. Anstie's opinion was that when the lung is compressed to carnification it is incapable of inflammation. The most formidable way in which pneumonia may complicate pleurisy is where, considerable effusion existing in one pleura, inflammation attacks the opposite lung. It may be doubted whether this ever occurs in truly primary pleurisies: kidney disease, specific fevers, pyæmia, etc. nearly always precede it. Hyperæmia or congestion of the opposite lung, without its amounting to pneumonia, does occur, and is a very grave complication. The same may be said of double pleurisy and peritonitis as resulting from blood-poisoning. It rarely happens in primary acute pleurisy that both pleuræ become involved. When such is the case, however, it is generally tubercular in its nature, and necessarily a very grave if not a fatal complication. Walshe reports having seen 4 cases of idiopathic bilateral pleurisy in persons thoroughly healthy and perfectly free from constitutional taint of {513} any kind. In all the pericardium was involved, and in 1 the peritoneum. They were all fatal. Acute pericarditis from extension of the inflammatory process is a frequently-occurring complication. When the inflammation extends to the pericardium, the effusion is of the same character as that of the pleurisy, whether it be sero-fibrinous, purulent, or hemorrhagic. It is a complication of great gravity and is sometimes the cause of a fatal termination of the pleurisy. We have never met with endocarditis as a complication, but Fraentzel speaks of having seen it in acute pleurisy in children. Before complete carnification occurs oedema of the lungs may be produced on the diseased side or in the healthy lung. This pulmonary oedema, when it attacks the sound side, is acute, being produced by rapid pulmonary congestion, which causes free, albuminoid, and frothy expectoration, often ending in asphyxia. The serum and albumen of the blood by transudation pass into the bronchi and the alveoli, and fill them more rapidly than they can be expectorated: the subject dies by suffocation. Auscultation reveals fine vesicular râles, characteristic of oedema of the lungs, closely resembling the fine crepitation of pneumonia. Traube has named this oedema pneumonia serosa. Engorgement it certainly is, but it can scarcely be designated a pneumonia. It closely resembles the oedema we meet with after thoracentesis, which has been named by Hérard expectoration albumineuse.

Bronchial catarrhs, when complicating pleurisies, cause dyspnoea, add much to the discomfort, and protract the duration of the disease. Barth[48] speaks of dilatation of bronchi as a complication of pleurisy. Woillez[49] calls attention to a complication which has been generally overlooked by the authorities--a persistent pain which some patients suffer in the side of the chest a long time after the disease has been cured. The most dangerous complications are syncope, formation of clots, venous emboli, and exaggerated distension of the thoracic walls by the effusion.

[Footnote 48: _Mém. de la Soc. Méd. d'Obs._, Paris, 1856.]

[Footnote 49: Article "Pleurisy," _Mal. Aigu. Resp._, 1872.]

Sequelæ.--The connection of pleurisies, especially chronic, with subsequent tuberculosis, is very generally admitted. Bartholow says: "The importance of pleuritis as a cause of phthisis is hardly sufficiently recognized in inducing tubercular deposit, and by adhesion limiting the movements of the organs, and thus inducing diseases." Anstie says: "It is now well established not merely that pleurisy often occurs in phthisical lung disease, but that pleurisy itself is capable of setting up true tuberculosis even in previously healthy persons. This is specially apt to occur where purulent effusion has been allowed to remain too long in the pleura, or where paracentesis has been performed repeatedly for empyema, the wound being closed in the interval." Modern authors thus consider that a productive field is offered for the bacillus tuberculosis.

Flint states that "in an analysis of 47 cases, in 3 the subsequent development of phthisis was probable, although not demonstrated, and in 1 case only the occurrence of this disease as a sequel was certain." Of 53 cases reported by Blakiston, not one became phthisical during several years after recovery from the pleurisy. Flint says the effect of chronic pleurisy with effusion in a person already phthisical is to arrest or retard for a time the progress of phthisis. We have mentioned the retraction of the chest-walls with deformity of shoulders and spine, and the permanent dislocation of the heart and larger blood-vessels, as serious results, as also the orifices produced by the bursting of the empyemas outwardly. These may all in time, with judicious care and treatment, be very materially lessened, and even cured. Empyema sometimes causes destruction of the periosteum of the ribs and subsequent necrosis. It is questionable whether there are any cases of pleurisy which do not leave more or less extensive adhesions {514} between the two pleural surfaces. In many cases they do not, it is true, seem to injure seriously the general health, yet they must impair the full functions of the lungs. How frequently this is the case is shown at autopsies of persons dying of other diseases, where we find extensive adhesions when we had no reason during life to suspect that such would be the case. Adhesive bands may interfere with the expansion of the lungs and cause chronic bronchial catarrhs, ending in death. Caseous pneumonias are among the sequelæ of pleurisy. When the false membranes are thick and numerous, the lung remains impervious to air and useless. This condition sometimes produces bronchiectasis. While it is true that the lungs, when the effusion is not great enough to actually compress them, sometimes retain their expansibility for three, six, or even eight months, yet there are cases where they do not expand after being bound down for months, and then we have depression of the walls of the chest. Woillez met with 6 such cases.

DIAGNOSIS AND PROGNOSIS.--The diagnosis of the several varieties of pleurisy ought easily to be made by the due appreciation of the general symptoms and physical signs we have enumerated. Cases occur where the differential diagnosis is not free from difficulties, even to the most careful of observers. Pleurisies on the left side are more easily diagnosed than those on the right side. Most of the signs are much more frequently observed on the left than on the opposite side: some of them are rarely met with except on the left. Before the discovery of the science of auscultation and percussion pleurisy and pneumonia were frequently confounded. By their aid the two diseases may ordinarily be diagnosed with precision. In both there are chilliness, fever, cough, and dyspnoea. At the initiation of acute pleurisies, we expect for several days more or less of chilliness, but in pneumonia one, or at most two, decided rigors. The temperature in primary pleurisy rarely goes beyond 100° F. in the first twenty-four hours, whereas in croupous pneumonia, in the same length of time, it not unfrequently rises to 103° F. or 104° F. In consequence of this high temperature in pneumonia the skin becomes hot and dry, with frequently a bright spot on the cheek corresponding to the side of the diseased lung. This is not the case in pleurisies, where, on the contrary, we have a pale, anxious expression of face. The comparatively mild fever of pleurisy is continuous. We have not, as in pneumonia, the marked changes, often of two or three degrees, between the morning and evening temperatures, nor have we critical days (between the fifth and eleventh) where the fever breaks with rapid defervescence.

Pleurisy is a more prolonged disease, and is not self-limited. The cough of pleurisy is short and quick, with no expectoration, unless it is thin, frothy mucus. In pneumonia the cough is longer, and is accompanied by a tenacious expectoration, more or less free, and generally (not always) tinged with blood. The rusty-colored sputa is almost characteristic of pneumonia. At first there is a marked difference in the dyspnoea in the two diseases. In pleurisy it is superficial, because the lungs are not freely expanded in consequence of the accompanying pain. In pneumonia it is deeper and the oppression is greater. The struggle for breath in the first stage of pneumonia is frequently alarming to witness. The relative frequency of pulse and respiration is more modified in pneumonia. The stitch-like, cutting pain in pleurisy is characteristic and very circumscribed, whereas in pneumonia, unless the pleura is involved, there is little or nothing beyond a dull soreness. We have in pleurisy the restrained movement of the side affected, and corresponding increase of movement of the healthy side. Not so in pneumonia. At the beginning of croupous pneumonia we generally have the crepitant râle heard in inspiration, but not observed in pleurisy. The friction sound, if present, heard in inspiration and expiration, is equally characteristic of pleurisy. If, as sometimes happens, we do not hear either {515} the crepitant râle or the friction sound, we must be cautious in our diagnosis until we have the more definite symptoms of the next stage.

Later on in the clinical course of the diseases, in their second stage--consolidation in pneumonia and effusion in pleurisy--the physical signs enable us to make the differential diagnosis. We expect dulness in both diseases, but it is more absolute in pleuritic effusions, and to the finger, as a pleximeter, the resistance is greater. In pneumonia there is very seldom complete dulness over the whole side of the chest, for there are frequently lobules not consolidated, or spots where the solid deposit has been partially absorbed. Moreover, the area of dulness is not bounded by that peculiar curved line, with its concavity at the base behind, facing the vertebra, gradually becoming convex as it turns upward and forward toward the axilla, again descending toward the sternum, as is the case in pleuritic effusions. Changes of position of the patient may cause the fluid, when in large quantity, in pleurisy, unless prevented by fibrinous adhesions of the two surfaces, to gravitate to a greater or less degree, and thus alter the points where we have flatness on percussion. The enlargement of the thorax, the bulging of the intercostal spaces, the marked displacement of the organs, and the frequently complete obliteration of the semi-lunar space, are characteristic of excessive pleuritic effusions. The displacement of the neighboring organs, especially of the heart, is a very valuable diagnostic sign of pleurisy.

There are, however, other conditions besides the presence of fluid, such as new growths and pneumothorax, which, by increasing the contents of the chest, may produce the same result. We may also meet with cases of congenital malposition of heart or instances where infantile disease, or constrained position, necessitated by occupation, have caused malformation of the contents of the chest.

The most characteristic percussion sign of effusion in pleurisy is the semi-tympanitic (Skodaic) or amphoric resonance high up in front. In rare cases it is found in pneumonia, but it is most pronounced over the consolidated lung, whereas in pleurisy it is above the level of the fluid. The vesicular murmur is not heard below the level of the fluid, unless very feebly at its upper surface, nor indeed is the passage of the tidal column of air up and down the bronchial tubes. In pneumonia bronchial respiration and increased resonance of voice rapidly supervene; whereas in pleurisy the voice is obliterated. In pneumonia we find the characteristic loud, high-pitched, brazen bronchial respiration over the whole of the consolidated portion. When a tubular quality is given to the inspiratory murmur in pleurisy, it is a diffused, distant, and low-pitched sound from the compressed lung. There is a marked contrast between the increased vocal fremitus of pneumonia and its entire absence in pleurisy. In pneumonia there is strong bronchophony with a jarring thrill to the ear, but there is not the displacement of the adjacent organs, the increased volume of the affected side, nor the widening and bulging of the intercostal spaces, with sometimes fluctuations, perceived on auscultatory percussion, as in pleurisy.

Although both diseases are ordinarily unilateral, yet we more frequently meet with double pneumonia than with double pleurisy. It must be borne in mind that we may discover the coexistence of pneumonia and pleurisy. When this does occur special care must be taken in the diagnosis. In cases of pleurisy on the left side, sometimes the impulse of the heart forces the two surfaces of the pleura together, and causes us to hear a pleural, cardiac friction sound. It has the rhythm of the heart, and is heard when respiratory movements have been suspended. This sound is limited to the left border of the heart. Care is needed to prevent the error of diagnosing pericarditis.

The diagnosis of pleurisy from hydrothorax, or passive transudation of fluid into the cavity of the pleura from mechanical causes or blood-poisoning, depends upon the recognition of the fact that ordinarily the latter is not {516} ushered in by fever--that it is bilateral, and is frequently accompanied with dropsy in other parts of the body. Transudations being slowly developed, the lung gradually contracts, and the presence of the fluid is tolerated for a considerable time; indeed, it is not until it is excessive that it compresses the lung. Thus, dyspnoea is not ordinarily produced until the accumulation is very great.

Sometimes the diagnosis between pleurisy and intercostal myalgia, or pleurodynia, is confused and uncertain. The pain may be as intense and the respiration as jerky where there is no pleurisy, if there is great soreness of the muscles between the ribs. The pain is, moreover, accompanied by more or less rise of temperature. Oftentimes the respiration is as painful as in pleurisy, for the individual instinctively refrains from causing the muscles to contract. Usually there is greater tenderness on pressure over the walls of the chest, less fever, and the area of pain is larger in this form of muscular rheumatism. The friction sound, if present, makes the diagnosis clear. We sometimes remain in doubt for twenty-four hours.

Intercostal neuralgia less closely resembles pleurisy. It occurs without fever, generally in anæmic subjects or in those debilitated by chronic general diseases, especially uterine. The tenderness is limited to several points along the course of a nerve, at the exit of the nerve from the spinal cord, in the axillary region, and near the sternum.

Pericardial effusions and aneurisms can ordinarily be readily diagnosed from pleurisies. Their positions in the cavity are so well defined, and the accompanying physical signs are so characteristic, that they ought not to be confounded with pleuritic effusions.

Solid tumors and cysts occupying a considerable portion of the pleura or bulging into it from the mediastinum may deceive us into thinking that there is an effusion. They displace organs, press upon the lungs, or intervene between the lung-texture and the walls of the chest, thus preventing us from hearing the entrance and exit of air and the vibrations of the voice. Not containing air, we have flatness on percussion. Being solid conductors, we have with them increased vocal fremitus, whereas in pleuritic effusions it is not perceived. Ordinarily, tumors are found at the superior or central portion of the chest, and cause an irregular bulging of the walls instead of the general enlargement caused by liquid effusions. Before the discovery of the present modes of physical diagnosis intra-thoracic growths, especially cancerous ones, were frequently confounded with pleurisies by even the most careful observers. Now such errors are only occasionally committed. The history of the case, the general symptoms, absence of fever, etc. will assist us in making the differential diagnosis. A careful examination by physical exploration will give us valuable aids. The bulging produced by malignant growths is not so marked nor is it so uniform. The dulness on percussion is not so pronounced. It does not vary from changes of position of patient. The displacement of heart and other organs is not so marked. Hunt[50] calls attention to the considerable blood-stained expectoration from cancer. He calls it currant-jelly expectoration. We must look also for the characteristic signs of cancerous cachexia and enlargement of glands in the axilla and in the supra-clavicular fossa. The exploring aspirator-needle will generally enable us to arrive at an accurate diagnosis, with the assistance of a microscope to examine the fluid or solid matter withdrawn. The fluid thus obtained from cancer is generally blood-stained.

[Footnote 50: _Loc. cit._]

Inflammations of the pleuræ are sometimes caused by the presence of intra-thoracic tumors. Abscesses of the liver and echinococci cysts may ascend, and, pushing the diaphragm before them, occupy the pleural sacs, and thus simulate pleuritic effusions.

{517} Pulmonary atelectasis, caseous inflammation of the tissue of the lung, aneurisms of the large thoracic blood-vessels, may, without care, be mistaken for pleurisies. It is very important to ascertain the nature of the fluid effused into the pleural cavity, whether or not it is serous, sero-fibrinous, purulent, or hemorrhagic. Generally this can be done by careful study of the accompanying general symptoms and the clinical history of the case. If there are repeated irregular rigors from the beginning, followed by high fever and free perspirations, there is every reason to fear that the fluid is purulent. If symptoms of blood-poisoning develop, we are still more confident that there is pus. Its hemorrhagic character may be inferred when great pallor, weakness, and lowered temperature suddenly appear during an acute attack.

Bacelli's physical sign known as pectoriloquie aphonique, or the passage through the effused fluid of the whispered voice, has considerable significance as a means of testing the nature and character of the fluid. His conclusion was that, when heard, it showed the fluid was fibro-serous; when not heard, it revealed to us that the effusion was purulent or sero-purulent. Laennec had noticed that in voiceless consumptives the whispers would sometimes resound as if the patient shouted in the ear of the auscultator. R. Douglass Powell reported[51] 10 cases bearing upon the value of this sign. In 6 of these, in which the fluid was clear, 5 yielded the sign, the sixth did not. In 2 acute cases, when the effusion was purulent, the sign was heard. He adds that he has heard the sign to perfection in fetid sero-purulent effusion. Mercadie[52] claims that when pectoriloquie aphonique is heard in purulent effusions it is only at the uppermost part of the fluid near its limit, where it has become very thin from the weightier portion, the flocculi, and the leucocytes falling to the dependent portion of the sac. Care must be taken in listening for this sign. The patient must be ordered to speak each syllable slowly and in a whisper, distinctly counting up to twenty or thirty. If it be present we ought to be able to perceive that the syllables sound, to the ear, clearly articulated along the height of the effusion. The sound is caused by the transmission of the whisper without any buzzing and without continuous murmur. The maximum of intensity of this sound is heard along the vertebral gutters and along the posterior base of the pleural cavity. It becomes feeble in its distinctive character as we approach the axillary region and also immediately under the angle of the scapula. The theoretical objection has been made to this sign that its production is contrary to well-known physical laws of the conduction of sound-waves. It is said because the sound originates in the air it must be indifferently conducted by fluid; moreover, that its transmission ought to be in proportion to the density of the fluid, whereas this sound is best conducted by a thin fluid. Walshe's explanation of the greatly-increased sound-conducting power of a consolidated lung in croupous pneumonia was that it was owing to its homogeneity of structure. Bacelli avails himself of this principle to account for our hearing through a fibro-serous fluid the whispered sonorous waves, and our not hearing them when the fluid was sero-purulent or purulent. In the latter case the fluid is excessively heterogeneous, containing leucocytes in abundance, besides layers of membranes, flocculi, and blood-discs. The sound-waves are lost as they pass through these media of different density. We have found it to be a physical sign of value in the differential diagnosis of the nature of the fluid, yet its presence is not pathognomonic of serous effusions. In thin fluids it is generally heard, and ordinarily it is not found in purulent pleurisies. If well marked, it indicates a fibro-serous effusion. Its absence does not necessarily show purulent pleurisy. Its greatest value is as indicating the purulent transformation of a fibro-serous effusion.

[Footnote 51: _Trans. Int. Med. Cong._, 1881, vol. ii.]

[Footnote 52: _Thèse de Paris_, 1876.]

Thanks to modern investigations, we have in the very fine needle of the {518} aspirator, or that of the hypodermic syringe, a delicate and sure means of accurate diagnosis, not only as to the nature of the fluids, but as to that of tumors and growths which may be confounded with them. We would not use for exploration a trocar and canula. We consider it best to employ a short needle in aspiration, for fear that a delicate hypodermic needle might break. Flint states that he has known several instances of this accident. Aspiration can be performed with perfect safety, and, indeed, without any fears of unpleasant results even if we perforate an aneurism. The orifice made is so small that the tissues close the moment the needle is withdrawn after making the exploratory puncture. If care be taken to cleanse the instrument and to use Listerism that no deleterious germ be introduced, the operation is harmless. (See Purulent Pleurisy.)

Blunders in diagnosis, however, will rarely occur if an examination is conducted with great accuracy, and if we follow the course of the disease with care.

PROGNOSIS.--The prognosis of simple primary pleurisy is generally favorable, unless it is complicated with other diseases or occurs in enfeebled persons. The intrinsic tendency of the disease is to recovery. Laennec considered that the prognosis in acute pleurisy was always favorable. Pleurisy with scanty sero-fibrinous effusion is not in itself serious. Dry pleurisy is free from danger. Subacute pleurisy with large effusions, where the course of the disease is insidious and slow, is more apt to be followed by tuberculosis than the more acute cases. Louis's law, deduced from 150 cases, that patients never died from the effusion in acute pleurisies, was long since disproved by Trousseau. Lacaze du Thiers published in 1873, in his thesis, a number of cases of sudden death from large accumulation of fluid. These deaths were caused by a large amount of effusion being thrown out rapidly, and suddenly compressing the lung before the system had time to accommodate itself to the presence of the effusion. These cases, termed foudroyant, should be very carefully watched. There is danger of death from orthopnoea when the pleural cavity is completely filled, especially in latent pleurisies, where the patient, unaware of the risk, makes, perhaps, unusual physical exertions. Some deaths have been caused by oedema of the lungs and some by syncope; others, again, from thrombosis of the pulmonary artery. We must bear in mind the grave prognostic value of attacks of orthopnoea and severe dyspnoea, because they, more than the mere quantity of the fluid, show the want of tolerance in the organism. These cases demand prompt mechanical interference with the aspirator. The very rapid accumulation of the effused liquid, even if unattended by dyspnoea, is an unfavorable sign, for observation has proved that in such a case its absorption is attended with more difficulty. Bilateral pleurisies attended with considerable effusion are commonly fatal.

If there are complications with other acute diseases, such as pericarditis or pneumonia, the prognosis may be far from favorable, more particularly if pleurisies supervene when the organism has been exhausted by a long continuance of the primary disease.

If absorption begins soon after the acute symptoms subside (and we expect it to do so where the general health and strength are good), and goes on vigorously, we can with confidence predict a favorable result, especially if there be no contraction of the walls. The earlier the reabsorption takes place the more favorable the prognosis. If, however, four or five weeks pass without any perceptible diminution in the extent of the effusion, there is cause for uneasiness. Especially is it dangerous if, in addition, we have those ugly symptoms, emaciation, weakness, and hectic fever, which point to the conversion of the fluid into pus. There is the prospect of protracted formation of pus with its dangerous sequelæ, including tuberculosis from infective absorption.

{519} That these dangers can in a great measure be obviated by prompt thoracentesis ought now to be universally admitted. Anstie predicts that the experience of the next twenty years will enable us to ensure an absolute immunity from fatal results from either of these serious complications. Symptoms of oedema of the lungs or of cyanosis are bad prognostic signs; so is diminution in the amount of urine secreted, which indicates that the arteries are incompletely filled. Still worse are the symptoms of over-distension of the veins, dropsy, and the appearance of albumen, casts, and blood in the urine.

The prognosis in secondary pleurisies is much more serious. In cases where the effusion is purulent at their commencement, the prognosis is graver than when it becomes purulent after remaining some time in the cavity. This is because they are often pyæmic in their origin.

With modern treatment, however, the percentage of recovery is greater than it formerly was. When we have to contend with chronic purulent cases occurring in cachectic constitutions or in those debilitated by other illnesses, especially tubercular, the prognosis is necessarily unfavorable. The most fatal of all secondary pleurisies are those supervening in the course of pyæmia or puerperal infection. Here death is the rule, recovery the rare exception.

Pleurisies supervening on Bright's disease or nephritis, following scarlatina and idiopathic fevers, have a high rate of mortality. The modern employment of the thermometer is of the greatest assistance to us in forming our prognosis. Marked variations of temperature, whether they be below the normal or constantly high or advancingly high, have grave significance. Anstie's valuable results from the use of the sphygmograph, as giving us the favorable and the unfavorable pyrexial pulse-forms, cannot be over-estimated. We fully concur with him, "that in the dangerous secondary pleurisies the combined use, for prognostic purposes, of the thermometer and the sphygmograph is more valuable than all the other modes of observation put together." It is so because they give us accurate physical data by which we can estimate the exact condition of the patients.

Relapses, with a rapid increase in the amount of fluid after reabsorption has been active and convalescence apparent, are frequently attended with danger, because they often denote a tubercular or hemorrhagic development. A very unfavorable sign is the rapid increase in the effusion after spontaneous or artificial discharges, especially if the fluid has become fetid in its character and has the dark appearance of unhealthy, purulent matter.

TREATMENT.--The study of the natural history of acute fibrino-genic pleurisy teaches us that there is always in it a tendency toward recovery unless there is some constitutional weakness behind the disease or a large fibro-serous effusion resulting from it. We have all met with cases where patients have recovered in the course of a month or six weeks spontaneously, without any treatment. Of A. L. Mason's 200 cases, 132 recovered without having to resort to thoracentesis. It is often a harmless disease when left, as far as medical treatment is concerned, entirely to itself. Of course the body-temperature and the physical evidence of the effusion ought always to be carefully observed. The hygienic treatment ought never to be neglected. We should insist upon rest in bed in the most comfortable position to the patient. The temperature of the room should be from 65° F. to 68° F., the approximate in-door winter degree for healthy adults.[53] The body, especially the chest, should be kept quiet; all unnecessary movement should be avoided. The food ought to be nourishing in quality, easy of digestion, and in quantity sufficient to keep up healthy nutrition. Stimulants are unnecessary, but it is a mistake to withdraw water, which contributes so much to the comfort of the patient and {520} cannot injure him in the first stage. We should take care that the patient has enough sleep. If necessary, mild hypnotics should be used. The effusion results from the inflammatory process, and not from simple transudation. If the pain is very severe, we must resort to the administration of opium by mouth or to hypodermics of from one-eighth to one-sixth of a grain of morphia; this, however, should be avoided when possible, as preparations of opium impair the appetite and depress the patient. The pain ordinarily passes off in 48 hours, and can often be relieved by application of hot-water bags, turpentine stupes, or anodyne liniments. Bloodletting, general or local, is rarely necessary. Leeches will give relief to the acute pain, but opium does that more effectively. Depletory remedies are hurtful and retard convalescence, and do not control the amount of the effusion, which in itself is depletory. If the patient is seen at the initiation of the disease, a large dose of quinia (from ten to fifteen grains), especially if the temperature goes to 101° F., often has a marked effect in controlling the temperature and also the tendency to effusion. Smaller doses may be repeated every few hours. Liq. ammonii acetatis, in fluidrachm j to fluidrachm ij doses every two hours, and Apollinaris or other alkaline drinks, relieve vascular tension and promote the action of the skin and kidneys. During the pyrexia, with the effusion increasing, we endeavor to lower arterial pressure within the pleural vessels by aconite, diaphoretics, mild salines, diuretics, with complete rest of the body. Hot applications (not heavy poultices, however) may sometimes be used at short intervals, with a view of dilating the superficial vessels and thus relieving those of the interior.

[Footnote 53: _Boston City Hosp. Reports_, 3d Series, 1882.]

Under this simple treatment many patients are sufficiently well in a few weeks' time to sit up. They ought not to be permitted to move about unless there is a very small amount of effusion. Roberts[54] of University College Hospital applies adhesive strips over the chest in all cases from the beginning. Mason prefers Martin's india-rubber bandage, three or four inches wide, extending from the lower border of the ribs to the axilla, as it adapts itself better to the chest-walls and supplies an easily-regulated elastic pressure. He considers it also useful in promoting absorption after tapping. Generally in three or four weeks, in favorable cases, the effusion has been absorbed and the patient is able to resume his ordinary duties. The writer cordially endorses Anstie and Bartholow's protests against the employment of mercury for any supposed aplastic properties. It really exhausts the recuperative forces of the organism, and probably injures instead of benefiting in pleurisy.

[Footnote 54: Quain's _Medical Dictionary_.]

If the exudation be in considerable quantity, three or four weeks may be required for its absorption. If this process is sluggish, can we by medicines promote it? Mercury has lost its old reputation as a remedy for this purpose. Iodine externally, and iodide of potassium in decided doses, still retain, to a limited extent, the confidence of practitioners. Preparations of iron, especially the muriatic tincture, have had better effects in the hands of the writer than any other remedy. Large blisters cause great discomfort, and their utility is very questionable. Alkalies possess the power of dissolving exudation, and of these the most efficient is ammonia, especially carbonate of ammonium in doses of from five to ten grains. Saline laxatives, by producing watery stools, have some power in reducing the amount of fluid. Some authors recommend highly the acetate and citrate of potassium dissolved in a decoction of scoparium. J. W. Hunt[55] places most reliance upon pilocarpus pinnatus, which has given him most marked and successful results, even where other remedies have failed. He pushes it to the extent of producing extreme diaphoresis. He commences with thirty minims of the fluid extract four times daily, rapidly increasing {521} the quantity and the frequency of the doses to the extent of fluidrachm j every two hours. The one-eighth of a grain of its alkaloid, pilocarpine, given hypodermically, acts very promptly. He admits that the vital forces are so exhausted by this treatment as to require at once the administration of tonics, especially of iron with strong food. Grasset[56] reported 5 cases of effusion treated by jaborandi. They were cases of pleurisy without fever or sign of inflammation--cases which ordinarily require several blisters to produce an effect.

[Footnote 55: _Dublin Journal Med. Sci._, Dec., 1882.]

[Footnote 56: _Journal de Thérapeutique_, Avril, 1876.]

Ernest Wernaere[57] reported 7 cases of acute pleurisy where there was considerable febrile reaction. Jaborandi was effectual in every case, and the effusion rapidly disappeared after two doses of the infusion. The fever at the same time was diminished, and there was no return of it, as frequently occurs in non-inflammatory cases. It has less effect upon children than upon adults. In a case of Wernaere's only one dose was given.

[Footnote 57: _Thèse de Paris_, 1876.]

The value of counter-irritants has been frequently questioned of late years. Fly blisters give relief in limited dry pleurisy. Many practitioners have great confidence in large blisters used over the chest after the febrile stage has subsided. Woillez, in tabulating the results of the various means of promoting absorption, puts purgatives first in utility, and blisters last. Blisters, he claims, had no effect in 90 per cent. of cases. The iodide of iron, in pills, or the compound syrup of the iodide of iron and manganese, with improved digestive powers, are the best means of promoting absorption. At this period of the disease it is an advantage to lessen, within certain limits, the amount of fluid taken into the stomach, forcing the blood to abstract water by absorption from the chest. Jaborandi has the same effect by withdrawing water from the blood.

There are cases of excessive quantity of fluid, and others which resist all drugs given to promote absorption. Among these are some acute cases, but many of a subacute and chronic nature, where the effusion remains stationary, injuring respiration and often mechanically endangering life. This occurred in nearly one-third of Mason's cases.

Thoracentesis.--In studying the history of this operation we have seen how frequently, since the time of Hippocrates, it has been in favor with practitioners, and then has fallen into discredit. During the past thirty years, thanks especially to Bowditch and Trousseau, its unquestionable value has been established, and is now universally recognized. Improved knowledge of pathology, safe and easily-applied instruments, together with the discovery, by Lister, of the means of securing the operation from septic dangers, have perfected this surgical treatment. Observation in hundreds of cases has proved that, properly used, it is almost without risk. As a means of diagnosis it is the most accurate we possess; as a treatment for affording positive relief it is a boon to suffering humanity; as a method of cure it has been most successful.

Such being the estimate of its value, let us study, 1st, the indications for its use; 2d, the manner of operating; 3d, and finally, the objections founded upon the accidents that have followed its application.

The indications are met with in two conditions--that of excessive accumulation of fluid, and where there is non-absorption of the effused liquid. In going over the symptoms we have seen the effects of large collections of fluid in the pleura--how the heart is pushed out of its normal position, and how the large blood-vessels are distorted. We have called attention to the retraction and compression of the lung until in many cases it is airless, and thus not able to perform its functions. We have shown that all the adjoining organs and cavities are sometimes forcibly thrown out of the position nature placed them in. The liver is pressed forward into the abdominal cavity, and {522} the diaphragm is unable, from mechanical pressure, to ascend and contract. The mediastinum, with its contents, is materially interfered with. Observation has shown that such a state is a very dangerous one. Not only does it cause great dyspnoea, pain, and oppression, but the risk to life is imminent. In a number of instances it has caused death. Trousseau tells us of 3 deaths; Lacaze reports others. Bowditch, having seen several fatal cases produced by the quantity of fluid, worked with energy and perseverance until he was furnished by Wyman with his ingenious aspirator, of which he promptly availed himself, notwithstanding the objections he met with from others. "Ridicule," he says, "was pointed at me by some high in surgery: at first the whole medical profession was against me." He could not stand still and see men die whose lives could be saved. Chew had a patient die suddenly from this cause. Many authors mention cases of death from the large amount of fluid. Wilson Fox summed up from the records between 50 and 60 deaths from effusion in the pleural sac. Moreover, many patients have died where the disease was not recognized. The condition of the circulatory apparatus is such that we can readily understand that emboli would form in the heart, in the large blood-vessels, and in the parenchyma of the lung itself. These clots produce grave results. If they form in the pulmonary veins or in the left heart, they determine an embolic obstruction of the central artery, with all its consequences--apoplexy, hemiplegia, etc. If it forms in the right heart or in the pulmonary artery, it may produce rapid aphasia and death (Paget). Louis was certainly wrong when from his 150 cases of pleurisy he deduced the law that none died of this disease per se. It is thus a matter of the utmost importance that we should be able to recognize that there is a quantity of fluid capable of producing such serious results. The call for relief and diminution of the amount of fluid by thoracentesis is urgent. What amount is dangerous to life, and how can we arrive at an accurate estimate? To what extent can we judge by the subjective symptoms, especially by the dyspnoea? Andral and Trousseau both speak of it as a very fallacious and uncertain symptom, and by itself may be unimportant as an indication. In the beginning of the disease we find suffocating dyspnoea for a time when there is very little fluid. Diffusible stimulants and anodynes give relief. On the other hand, there are patients who with large amounts of fluid, even two quarts, walk about with but little difficulty in breathing, and attend to their pursuits unconscious of being in danger of sudden death. Bowditch[58] speaks of several fatal cases in simple pleurisy from excessive amounts, "from sudden failure of the power of the heart, with or without more or less dyspnoea." This is especially the case where the fluid forms insidiously, without marked general symptoms. When, however, we meet with dyspnoea, together with other and more reliable symptoms, it is very significant of danger, and ought to force us to resort to thoracentesis to afford mechanical relief. If we rely upon general symptoms, we may be deceived as to the amount of fluid, and serious results may follow. However, we must bear in mind that the most imperative reasons for thoracentesis are the signs of threatened failure of cardiac power. Bowditch lays down the rule that "if the dyspnoea is excessive, so as to amount to permanent orthopnoea, or if I learn that within a few hours previous to my visit there has been even one attack of momentary orthopnoea during which the patient felt as if the breath would be wholly lost, I tap immediately, provided I am sure that there is even a small quantity of fluid in the pleural cavity, and that it is apparently the chief or perhaps only cause of the orthopnoea. I fear," he says, "death may occur before my next visit." This eminent American authority on this subject lays down as the result of his vast experience the rule that "when a patient comes under {523} notice in whom a large quantity of fluid has been long effused, I advise thoracentesis as the first remedy." The author ventures to assert that where the amount is excessive there is imminent danger to life from the mechanical results of the presence of the fluid, even during the febrile stages; consequently thoracentesis is urgently necessary. I am confirmed in this view by Dieulafoy, Fernet, Clifford Allbutt, Marshall, and Cross. Barnes[59] says in all cases where the effusion is large and where dyspnoea is urgent it is better to operate at once. "It is my practice to operate at once when the chest is two parts filled with water, without waiting for urgent dyspnoea." Dieulafoy, in discussing these questions, states,[60] after consulting all the authorities accessible to him, that death has never been caused by less than two liters (equivalent to 62½ fluidounces), except in one instance reported by Blackey, where after death there was found 1500 grammes (47 fluidounces). In adults with well-formed chests he considers 1800 or 2000 grammes as the amount demanding surgical interference. He candidly acknowledges that he cannot make this an absolute rule, because the capacity of the pleural sacs must necessarily vary in different individuals according to their height, breadth, development of thoracic muscles, sex, etc.; consequently, the inconveniences and functional disturbances produced by a given quantity of fluid in the chest must be different in different persons. But how can we arrive at an accurate estimate of the amount in the chest? Dieulafoy,[61] in calculating the quantity, states that if it amounts to 1200 grammes when it reaches the sixth intercostal space, it ought to be valued at 2000 grammes when it is found at the third intercostal space. This is only approximative and unreliable. The height of liquid is not always proportional to quantity. It varies with size of chest, resistance of organs and walls, and condition of lungs. Potain insisted upon the difficulties that the pulmonary hyperæmia caused in the diagnosis, the abundance of fluid, the variable degree of yielding of the lung, and the adhesions which have drawn the walls to the lung. The true way of judging of the necessity for the operation is from the grave functional disturbances and by the definite positive physical signs which give us unmistakable indications which we dare not neglect. We can calculate the amount of the effusion by the level of the flatness on percussion, by mensuration with the cyrtometer, and of the impaired thoracic movements by the stethometer. Physical examination reveals the extent of the displacement of the heart and other viscera. The displacement of the abdominal viscera, the liver, the spleen, and the stomach shows that there must be excessive amount of effused fluid in pleura--enough to produce serious intra-thoracic pressure. This is a condition demanding surgical interference. The Skodaic resonance under the clavicle, the complete flatness being horizontal instead of giving us the Ellis curve, impaired resonance over the posterior triangle becoming absolute dulness, the presence of cavernous or amphoric respiration near the sternal-clavicular articulation, and, in rare instances, subclavian murmur from pressure upon the subclavian artery,--all these signs give unmistakable evidences that the pleural cavity is full of fluid. It is important, in considering the treatment, to form a correct estimate of the degree of intra-thoracic pressure, for Erichson has shown that the mere collapse of a lung affects but little the facility of the circulation through it; its compression or forcible collapse necessarily retards the circulation and throws extra work upon the already overburdened heart. The more precise our physical diagnosis, the more appropriate will be our treatment. Douglass Powell found the intra-thoracic pressure to vary from a -- pressure to ½ and 1½ inches of mercury at the commencement, and from -1/8 to -½, and even -1, inch mercury at the termination of paracentesis, there being in all cases a more or less considerable amount of fluid still remaining in the pleura. He states, {524} as the result of his own observations, that in recent cases the period of effusion at which the intra-thoracic pressure is converted from a -- pressure or zero to a positive pressure upon the lung and heart is marked clinically (1) by the flatness mounting up above the third cartilage (patient in sitting position), and (2) by the Skodaic resonance becoming changed from the full note to a more tubular quality. The extent of Skodaic resonance is a very valuable indication of the amount of fluid, and consequently of the propriety of operating. If this tympanitic resonance be down to the third rib, and the cyrtometer shows no decided enlargement, we had better not interfere. On the other hand, if the Skodaic sign is not heard, and instead there is flatness, we will be sure to find decided increased measurements and tubular breathing behind. Under such circumstances we may feel confident of positive intra-thoracic pressure of from one inch to one inch and a half of mercury--an amount sufficient to compress the lung and interfere with the heart's action. There is some danger of syncope, even if the patient remains motionless in bed, but if he moves about he is in imminent danger. The subject is annoyed by a straining retching cough with frothy, viscid sputa with perhaps some discolored points. The heart and the lung of the healthy side give warning of the danger, which ought never to pass unheeded. A murmur may be heard over the displaced heart, and over the lung on the unaffected side we may hear a fine crepitant râle, showing pulmonary hyperæmia and resulting oedema. The syphon or aspirator will afford, by withdrawing perhaps a quart, the necessary relief. Nature will do the rest in a large proportion of cases.

[Footnote 58: Unpublished MSS.]

[Footnote 59: _Brit. Med. Journal_, Dec., 1877.]

[Footnote 60: _Nouveau Dict. Méd._, vol. xxviii., art. "Thoracentesis."]

[Footnote 61: _Loc. cit._]

We cannot always estimate accurately the quantity of fluid by the displacement of the heart and other organs. The retractile energy of the lung is a very important factor in producing this result. A very large effusion, associated with a very powerful lung, will produce but slight displacements, while small effusions, when the lung of the affected side has lost its elasticity, will cause relatively great displacements (Garland). If there be no adhesions present, the letter _S_ curve of flatness becomes a sign of the greatest value. It marks accurately the height of the effusion. Knowing this, as well as the position of the heart and diaphragm, and the capacity of the chest, we can estimate the quantity of fluid in the pleural cavity. If in left pleurisies the heart be so pressed out of position that its apex beats to the right of sternum it is very diagnostic. With these signs, whether accompanied by dyspnoea or not, we must regard thoracentesis as imperatively called for. The presence of the febrile movement is not a counter-indication under these circumstances. The presence of a basic murmur, caused by the heart or aorta displacement, is an urgent indication for surgical interference.

There are attacks of fainting and syncope, suffocative paroxysms, with irregular and painful palpitations of the heart, with sometimes alarming threatenings of asphyxia--especially in pleurisy of the left side. These symptoms are probably due to the twisting of the inferior cava as it passes through the quadrilateral foramen of the diaphragm. The danger is necessarily increased by long continuance of the effusion. Prompt surgical treatment is indicated when we detect evidences of embarrassed circulation in the opposite lung, with a blowing quality of respiration and subcrepitant and oedemic râles.

In all cases of double pleurisy, where the total amount is sufficient to fill one whole cavity, we ought not to postpone operating. Even when the effusion is not very large, if there are other diseases of the respiratory or circulatory systems to cause grave complications, and danger of increased impairment of their functions, thoracentesis is rendered necessary. That these conditions justify thoracentesis we believe no one who has any practical experience will question. But two conditions exist where there is considerable {525} difference of opinion in regard to the propriety of operating: 1st, during the febrile stage, and, 2d, where moderate effusion remains unabsorbed.

In regard to the first of these, many authorities, even among the most enthusiastic advocates of the operation, have contended that unless there is imminent danger to life from the excessive collection of fluid, it should not be withdrawn, as it would at once re-form, and additional inflammatory action might be excited by surgical treatment. Castiaux,[62] however, strongly advocates the view that the operation by aspiration will hasten the cure of acute pleurisy and prevent the formation of the fibrinous deposits and bands which to a greater or less degree, even in moderate effusions, impair the expansion of the lungs. He relates 37 cases, almost all of which were operated upon by himself. He was successful in all of them, and the patients suffered no inconvenience or discomfort in consequence. In most of his cases the pulse and body-temperature fell (perhaps the same day, certainly the next morning), and even became normal after the operation, and the patients improved rapidly. He aspirated as soon as he detected the presence of fluid by exploratory punctures, believing that from the moment we have at our disposition sure means of relief which are harmless, it is useless to leave to nature the duty of removal--useless to leave to untrustworthy medication the relief which we can promptly give. He operated at the height of the first or inflammatory stage of the disease. He assigned as reasons for operating that he thereby relieved the lung of the compression which impairs expansion; that he removed a liquid rich in fibrin and capable of increasing the thickness of the neo-membranes; that by restoring the power to dilate he further prevented the lung from being compressed by the false membranes. These membranes cannot become organized unless they are separated by fluid. He states that he removed the fluid as completely as possible. As soon as the cavity was emptied respiration was made easy and the patient was relieved. Auscultation showed, by the vesicular murmur, that the lung had resumed its place without difficulty from top to bottom. The effusion returned, only in a few cases, with high temperature and frequent pulse, but another operation effectually arrested them. The pleurisy was cut short and puncture was considered the means of aborting the disease. The duration of the disease treated by this means was much shorter. Thus the patients were not forced to retain for months the liquid and false membranes in their chest. He states emphatically that there never supervened any accident, and especially that he never witnessed as a result the transformation of the serosity into pus, although it might appear theoretically likely to occur, as the serous membranes, already inflamed, ought to be more sensitive to injury.

[Footnote 62: _Thèse de Paris_, 1873.]

This testimony is very strong. Moutard-Martin operated upon 12 patients with fibro-serous effusions where they had existed less than ten days, and where there was more or less of fever. Out of this number, 8 had no reproduction whatever of fluid, and in 4 there was only a slight re-formation, and there was no degeneration into purulent fluid in any of them. In the other cases operated upon, where the effusions dated from twenty to sixty days, the fluid was almost always reproduced, though ordinarily to a moderate extent. He urges the prompt withdrawal of the fluid as the most successful method, especially if there is reason to suspect the formation of false membranes.

Wedal's[63] results confirm this view of the harmlessness of punctures during the febrile stage; and, more than this, they show that they hasten the cure. He operated on 17 patients from the second to the fifth day, and three times from the eighth to the tenth day. In cases of acute disease, where the patients were exempt from pulmonary or bronchial complications, the cure was not protracted beyond the twelfth day. Some were cured by the sixth day. His patients were, for the most part, vigorous men, young {526} soldiers--very favorable subjects. Ordinarily, however, as shown by J. L. Mason's[64] report of 132 cases where the operation was not performed, the duration of the attacks was weeks, and in some cases months. He considers the operation more apt to be successful if performed early in the disease, and that the existence of fever is no contraindication. The author has always pursued a more conservative course, and abstained from operating in the febrile stage unless, as in three instances, the effusion was so rapid in its formation that there was danger of serious consequences from the amount of the fluid. In these three instances the result was successful and without unpleasant sequelæ. Moutard-Martin[65] states that aspiration made during the febrile stage is in no way prejudicial to the patient. Dieulafoy[66] advises us to wait until the fever falls.

[Footnote 63: _Étude clin. des épanchments pleurit._, 1877.]

[Footnote 64: _Boston City Hospital Reports_, 3d Series, 1882.]

[Footnote 65: _Loc. cit._]

[Footnote 66: _De la Thoracéntèse dans la Pleur. Aigue_, 1878.]

To remove the effusion during the inflammatory stage does not appear to be rational treatment unless the quantity is so excessive as to endanger the life of the patient. The fluid remains limpid unless exposed to air or contact with foreign substance. When, after a time, there is some coagulation, it is only of a thin layer which covers and protects the roughened surface of the pleura. A certain amount of effusion is useful; it separates and bathes in a bland fluid the tender and inflamed surfaces, and keeps at rest the affected portion of the lung. The lung in health exercises a constant traction upon the pleural sac, the vessels of which have therefore to sustain a negative or aspiratory pressure: this being so, it is physiological that if these vessels become temporarily weakened and congested by the inflammatory process, increased exudation proceeds from them. The effect of this exudation is to neutralize lung-traction, and therefore to lessen the afflux of blood to the weakened vessels. "Fluid effusion being thus both natural and salutary, in acute pleurisy we must be watchful, but not meddlesome" (Powell). We must not hurry, but we must try if nature will not by spontaneous absorption cause it to subside. We can ordinarily do this up to the end of two or even three weeks before resorting to artificial means.

The defervescence in pleurisy, we have seen, has no fixed period, as in pneumonia. In favorable acute cases the absorption begins as soon as the temperature begins to fall. Moreover, the liquid may be absorbed, notwithstanding the continuance of fever, and the effusion may continue notwithstanding the defervescence. In the subacute form the febrile period passes by unnoticed, although the effusion is often in large quantity.

When not urgent, how long should we wait for absorption of fluid? This is a question much discussed, and not yet settled. What becomes of the effusion in the acute pleurisies?

In the first days of its formation the liquid portions of the effusion are reabsorbed by the normal vessels of the serous membranes at the points left intact and the recent vessels of the neo-membranes, but the organization of these last demands, to be complete, from two to three weeks; it is not until the end of that time that they will be most favorable to reabsorption. Dybkowsky points to the anatomical fact that the lymph-vessels are found only in those parts of the costal pleura which cover the intercostal muscles, while the portions which are reflected over the ribs are destitute of such vessels.

On the other hand, the eccentric pressure made by a considerable effusion on the pleuræ may retard their vascularization and lengthen out the work of absorption. Moreover, during the time necessary for that organization a certain quantity of coagulable fibrin is deposited on the surface of the serous membranes. The pseudo-membranous bridles are not slow in forming, and cause the adhesions which press the lung against the costal wall, the {527} vertebral gutter, and the superior parts of the thoracic cage, toward which the effusion tends to force them.

In very favorable cases the effusion may disappear by the twentieth day of the disease. In many cases, however, it lasts with the false membranes for several weeks, and not infrequently for many months. Cases are recorded by Powell and others where the effusion remained of a sero-fibrinous character for eighteen months and two years. Flint mentions two cases where the effusion was permanent, having lasted for years. Wilson Fox[67] thinks that there is but slight danger of the fluid becoming purulent from mere lapse of time unless the patient should have another fresh inflammatory attack. It must be noted, however, that such is not the case in children. Voyet[68] says that simple pleurisy in infants is transformed into purulent pleurisy with facility and extreme rapidity--so much so that when with these a serous effusion is slowly absorbed there is great danger of suppuration taking place. M. Vertiac[69] states that chronic serous pleurisy may not exist among children. In 13,000 sick children in eleven years Barthez did not have a single case. Pathological anatomy has demonstrated to us that this fluid in separating these neo-membranes on the parietal and pulmonary pleuræ increases their development. The plastic rugosities collect the fibrils of fibrin on their surface, in the same manner as they are found on the twigs in whipping the blood, and as the atheromatous deposits on the interior of blood-vessels favor the formation of emboli. These false membranes may cause a number of complications by surrounding the lung with a thick, inelastic shell. The collapse of one part of the lung diminishes necessarily the field of hæmatosis, and consequently causes a compensatory congestion of that lung, and even of the lung of the other side. This occurring in an individual predisposed to tuberculosis or in a condition to develop and cultivate the bacillus tuberculosis may start the disease. Formad[70] maintains that pleurisy is a very frequent cause of pulmonary tuberculosis. These imperfectly organized embryonic membranes cause deformities of the thorax; they are good ground for the growth of pathological products, such as cancer or tubercle; their fragile capillary vessels are the principal cause of a most troublesome form of hemorrhagic pleurisy. (See HEMORRHAGIC PLEURISY.) If the lung be compressed but a short time, it does not undergo irreparable injury, but if for a considerable time, the thickened organized membrane, with the effusion, causes a more or less considerable atelectasis, binding down the lung and preventing its expansion. The author holds that the effusion, after the fever has subsided, is, in itself, a foreign and troublesome element; for even with a medium effusion we are not exempt from unpleasant results.

[Footnote 67: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 68: _Thèse de Paris_, 1870.]

[Footnote 69: _Ibid._, 1865.]

[Footnote 70: Paper read before the Baltimore Clinical Society, February, 1883.]

Although, in moderate effusions, there is no compression of the lung, yet there is necessarily collapse of it pari passu with the amount of fluid. This interferes with its retractive power--the aspiration force, as it has been called--by which the venous blood is drawn into the right side of the heart. T. B. Curtis of Boston calls attention to this very important fact, and shows that the result must be disturbance of circulation, with imperfect blood-supply to the heart, interrupted cardiac action, feeble arterial tension, together with venous repletion and stagnation. In consequence of this condition there is a diminution of the quantity of urine, and, as generally occurs where there is venous congestion, a small quantity of albumen, cyanosis, etc. Fraentzel, Traube, and Lichtheim attribute the venous stagnation, etc. to obstruction in the pulmonary circulation resulting from pressure exercised by the effusion. Curtis and Garland hold that these bad symptoms are not caused by pressure, but by the diminished pulmonic retractility which exercises the negative pressure of emptying the large venous trunks.

{528} Such being the ill-effects of the retracted lungs, is it well to allow even a moderate amount of fluid to remain in the pleural sac after Nature has failed to remove it? Besides, the presence of liquid alone displaces the organs, especially the heart and lungs; adhesions form and keep them in an abnormal condition. The retracted lung, bound down by bands, becomes enfeebled, loses its suppleness, and is rendered rigid, seriously impairing respiration. There exist three factors--false membranes, adhesions,[71] and interstitial pneumonia--which tend to seriously disable the lung and even to produce complete atelectasis pulmonum. We must bear in mind that there is some danger of the fluid becoming purulent, especially if a fresh inflammatory attack should occur. The less time a pleurisitic effusion lasts, the sooner the patient will be placed beyond the probability of these serious injuries to the process of hæmatosis. It is but right to give Nature an opportunity, assisted by iron, salines, diuretics, iodine, and even blisters, in cases of moderate effusion. The rapidity of Nature's work in many cases in removing large quantities of fluid here and elsewhere is wonderful. But if she does not act, we ought not to let our patient become feeble and depressed in his nutrition, or perhaps maimed for life, by not withdrawing the fluid. Sometimes the absorbents only half do their work of removing the fluid, and leave a quantity in the chest. Under these circumstances tonics, good diet, and change of air will complete the absorption.

[Footnote 71: According to Wilson Fox, the density of the adhesions and false membranes is determined within the first fortnight of the effusion.]

The question arises, How long shall we wait for absorption? Test first, by exploratory puncture, the nature of the fluid: if it is fibro-serous day after day, try by the cyrtometer the size of chest and by percussion the exact amount of flatness. If there is no evidence of any decline of the effusion in two weeks, slowly withdraw some of the fluid. This will start the absorbents into activity, for the natural absorbing power of the pleura is diminished when it has been unduly stretched for some time. The layer of lymphatics subjacent to the pleura and communicating by stomata with the pulmonary lymphatics, together with the other absorbent vessels, appear to be unable to remove the fluid. We maintain that the pressure on the orifices of the lymphatics is often too great for absorption to take place, and that by removing the pressure we can start the absorbents into activity. Aspiration under these circumstances shortens the duration by several weeks and hastens convalescence. J. W. Hunt[72] advises that we should wait two or three weeks before operating. Loomis[73] says if the fluid remains stationary for one week, or is increasing when the cavity is half filled, we must operate. Barnes[74] would only wait a few days if the chest is half full, to see if absorption will begin to remove it. When the chest is two-thirds full, he advises immediate surgical interference. Oxley[75] advises a delay of three or four weeks before operating. Anstie's[76] rule is to postpone operating for one month. T. Clifford Allbutt's[77] general rule is, if an effusion rises above the angle of the scapula, and abides in that quantity or increases for two or three weeks in spite of adequate treatment, it must be drawn off, whether the patient be embarrassed by it or not. Bowditch[78] says: "If the effusion does not subside under the medical treatment, and the symptoms have not lessened after two or at the utmost four weeks, I have, after long experience, been led to the following general rules for my own guidance: 1st. I never allow any time to elapse before performing thoracentesis after a decided and prominent dyspnoea appears, or if a sudden and very threatening orthopnoea occur, or if I find the chest has become full or more than half full of fluid in a perfectly latent manner {529} during a month of illness. 2d. After there is dulness to the angle of the scapula, with the other rational and physical signs of pleuritic effusions, I tap within four weeks, even if the patient seems quite comfortable, if the line of dulness does not get lower and seem to subside under the treatment. I think fatal mistakes are made by delaying too long before tapping." The author prefers ordinarily to wait for the subsidence of the fever in acute cases, unless the effusion is in dangerous quantity. The practitioner must continually use the thermometer as well as observe physical phenomena and general symptoms. Cyrtometric tracings give very valuable indications as to the activity or non-activity of the absorbent vessels. After the fever subsides the fluid may be regarded as a foreign body doing harm to the two principal organic functions upon which the nutrition of the animal frame is dependent--respiration and circulation. It is from this standpoint that Dieulafoy[79] advises, if absorption is slow or difficult after two or three days, that the fluid should be aspirated. The greatest success has been obtained in cases where the fluid has been present but a short time. The number of fatal cases is increased by delay of operation. Toussaint's cases show this:

4 deaths in 176 cases operated upon between 1st and 20th day. 6 " 80 " " " " 20th and 60th " 1 " 7 " " " " 60th and 120th "

In the quiet kind of pleurisy, formerly designated the subacute or latent, thoracentesis is especially applicable. Ordinarily, when the practitioner is consulted, there is considerable fluid, without any febrile movement. Here we are in duty bound to assist nature. Iron in the form of the tincture of the chloride and the syrup of the iodide are our best remedies. We cannot give the patients the tonic influence of outdoor air with exercise, because there is danger in their moving about; but they should have an abundant supply of nourishing food, with light wines. Absorption is very inactive and sluggish. Even with moderate effusion to the extent of one-third of the pleural cavity, we cannot let the fluid remain too long. Pidoux designated this form of pleurisy as the thoracentesis variety.

[Footnote 72: _Loc. cit._]

[Footnote 73: _Dis. Resp. Org., etc._, 1875.]

[Footnote 74: _Loc. cit._]

[Footnote 75: _N.Y. Med. Ex._, Sept., 1882.]

[Footnote 76: _Syst. Med._]

[Footnote 77: Quain's _Dict. Med._]

[Footnote 78: Unpublished MSS.]

[Footnote 79: _La Thoracent. par Asp. dans les Pleur. Aigues_, 1878.]

Conclusions.--1st. The author wishes to be distinctly understood as not advocating aspiration simply because there is an effusion, as a mere matter of routine, for its indiscriminate employment is undoubtedly attended with risk. He does claim that its performance is imperatively called for when the pleural cavity is full or nearly so; when there is much displacement of the heart or other viscera; when the patient is suffering from serious dyspnoea and danger of syncope, and when there are complications of disease of any kind of the other side or of the heart; finally, when there is double pleurisy. Bowditch states that he has seen thoracentesis give great relief in effusions following Bright's disease and cardiac diseases.

2d. He thinks that in acute cases, after the subsidence of the fever, if the pleura is one-third full of fibro-serous fluid, Nature will probably do her work of removal promptly. If she shows no sign of doing so, we should come to her assistance in about ten days or two weeks, and draw off a portion of the fluid--enough to relieve pressure and to encourage the absorption of what is left in the sac.

3d. In the subacute or chronic fibro-serous effusions it is not well to wait over three weeks before operating. As he shall show in the study of the dangers and objections, he considers the operation a perfectly safe one if the simple rules now generally observed by operators are faithfully carried out.

In studying the advisability of operating where there are not urgent indications we must ever bear in mind that while it takes a large quantity of {530} fluid to compress the lung, the retracted lung may, by neo-membranes, be kept to its diminished volume. As long as the lung is able to lift up the fluid and the diaphragm it is in no danger of atelectasis. It is in a state of physiological rest. In a subject of bad constitution interstitial changes may indicate an earlier operation, but, if an effusion exists on the side on which there is already lung disease of a phthisical nature, we should be loath to interfere; for "experience has shown that an effusion checks, and sometimes arrests, the tubercular process" (Powell).

Contraindications.--These are principally in connection with the general condition of the patient. If it is such that there is no hope of his rallying, if he is very old, or if he has intervening croupal pneumonia, the operation is not justifiable. If the quantity of fluid is not large and does not interfere with organic functions, we can wait for some time.

Mode of Operating.--The old trocar method of operation is now abandoned. It was not always an easy one, was painful, and there was more or less danger of cutting the intercostal artery, of introducing air, and of establishing, by the size of the puncture, a fistulous orifice. If, perchance, the lung was perforated by the trocar, pneumothorax was established. In some cases of sacculated and limited effusions, and in chronic cases where the membranes were thick, it was not effectual, and if the fluid was not reached, the operator hesitated to introduce the trocar elsewhere. When the fluid flowed through the trocar, it came frequently in jets with painful coughs. The above operation was quite a formidable one. Now thoracentesis is always performed with very fine perforated needles attached to aspirators of some modern pattern, and guarded by Fitch's dome-trocar or Castiaux's protected point. We employ Dieulafoy's Potain's bottle-aspirator, Castiaux's of Paris, or Raumussen's of Copenhagen. Flint recommends the use of Davison's syringe. We fear it would be found too rough an instrument for so delicate an operation. The points of attachment of the bulb with the tubing are not sufficiently air-tight. The valves are very imperfect, and easily get out of order. In our efforts to pump out the fluid we might throw air in, and with it particles of organic matter.

The operator has his choice among no less than thirty-odd instruments similar to Dieulafoy's. They all work upon the same principle--the close operation, the withdrawal of the fluid by aspiration. The needle or trocar must be capillary: the smallest that is effective is the best--say a half millimeter in diameter--in order to make the orifice as minute as possible.

If we prefer the syphon, we must use a larger canula than we employ for aspiration--one of four millimeters in diameter. It should have two outlets--one straight, for the trocar, and one at an angle, for the attachment of the tubing. It should also be guarded by an air-tight collar. Into the syphon tubing a T-tube may be inserted for the purpose of attaching a side tube to be connected with a mercurial manometer, by means of which the exact intra-thoracic pressure may be observed during the operation. The syphon tube should be long enough to provide a fall of one, two, or three feet, as may be necessary. A fall of twelve to eighteen inches is usually enough, as we wish to remove the fluid slowly. We can easily increase the force by lengthening the tube. If the canula should become obstructed, lowering the basin suddenly will probably remove the piece of lymph. The trocar can be pushed again through the canula if necessary. In case the aspirator should be needed, the end should have a metallic joint affixed to it. In all the instruments used, absolute cleanliness should be observed. The tubing previous to operation should be filled with a solution of carbolic acid (1:40).

In cases of rapid effusion, especially during the febrile stage and when the intra-thoracic pressure of fluid is great, some prefer using the feeblest form of aspiration. Southey's capillary trocar, with drainage-tubes attached, is used as a syphon for this purpose. The fluid is drained off {531} through a narrow india-rubber tubing which is placed under water to prevent air being drawn into it. Ordinarily, the use of the fine aspirating-needle without much force, and slowly drawing off the fluid, answers the same purpose. The fear some have expressed, of the danger of injuring the lung by the force of the rarefied space, is more theoretical than real. Even with a canula of the size that Southey employs there is some danger of leaving a fistulous orifice, for it has to be kept in for hours. If the smallest tube is used, from which the fluid simply comes in drops, the operation consumes five or even ten hours. Southey speaks of cases where the flow was kept up for twenty-four hours. Unless aspiration is resorted to, flocculi may easily stop up the canula, and then we are compelled to reintroduce the trocar, and afterward to reattach the tubing. Oxley, who thinks that the best results are obtained by the use of these tubes, acknowledges that so much time was consumed that he inserts four canulas, drawing off 44 fluidounces of fluid in one hour and ten minutes, thus defeating the object of using this method, which was to draw off the fluid very slowly, so as to enable the lung to expand gradually and healthfully.

There are cases where, to withdraw the fluid, more suction force than is usually employed with the syphon has to be used in order to antagonize the negative force exercised by the traction of the lung and the passive tension of the diaphragm. The author recently had a case where, notwithstanding the presence within the right pleural sac of a quantity of fluid large enough to obliterate the Skodaic resonance under the clavicle, not a drop could be drawn out by a syphon attached to a canula of 2 mm. in diameter. Having no additional tubing to increase the force of the syphon at hand, he used Dieulafoy's rack aspirator, ½ mm. in diameter, and drew off a quart of fluid--enough to relieve the symptoms of oppression. Stone reports a case of the kind where, although there were two quarts of fluid in the pleural sac, no fluid could be drawn out with a syphon exerting a force of 1½ pounds to the square inch, or one-tenth of an atmosphere. In the same case there was actually, in inspiration, a negative pressure exercised by the lung of two inches of water. Stone mentions another case where a boy fifteen years of age died from the quantity of fluid, which would not flow out when tapped. If he had had an instrument by which he could have used aspiration he would have saved the life.

The value of this syphon method has within a few years grown much in favor. It is simple and inexpensive. It allows the fluid to be drawn out with a uniform and feeble aspiratory force. The flow is very slow, which gives the lung time to expand gently, and the displaced organs to return gradually to their normal position. With the manometer attached we can judge accurately as to the intra-thoracic pressure. The size of the canula has to be larger than when we employ the aspirator--4 mm.--whereas with the latter we use ½ mm. or 1 mm. in diameter. If by any accident the lung should be perforated, the larger orifice would not be as harmless and insignificant as the smaller one. It must be borne in mind, especially in cases of long standing, that the neo-membranes are very vascular, and that with a 4 mm. perforator we may rupture the blood-vessels and complicate matters by the escape of blood into the pleural cavity. It is claimed that when the canula and syphon tubes have been introduced the patient can be left in charge of the nurse. This, the author thinks, should never be done, for nurses are rarely competent to judge whether a sufficient amount has been withdrawn, nor are they fit to assume the responsibility of acting in cases where promptness of treatment may be of the utmost importance. The operator or a competent substitute must remain until the operation is over. The withdrawal of fluid must, moreover, be slow, for slowness contributes in a great degree to lessen the dangers. Fraentzel recommends testing the force of the {532} aspirator in the palm of the hand. Garland[80] employs needles which are 1-2 mm. in diameter and remove only 50 to 100 grammes per minute. The thoracic pressure must be relieved by the withdrawal of only enough fluid to effect that purpose. It has been objected that the negative force of the aspirator is uncertain. It is a well-founded objection, yet we can employ with it a feeble force by exhausting only a portion of the air from the cylinder or bottle, and thus remove the fluid cautiously and very deliberately. It is admitted that if there is no intra-thoracic pressure the fluid will not flow out unless we introduce air or negative force. We claim that the syphon and the aspirator with capillary needles, employed with the precautions dictated by modern experience, are both safe and effective. Ordinarily, we prefer the bottle aspirator of Potain, or Dieulafoy's instrument with the manometer attachment.

[Footnote 80: "Dis. of Pleura," in _Ziemmsen's Appendix_.]

Modern aspirators, if in perfectly good order, completely prevent the possibility of septic contamination by admission of air. Unclean needles and canulæ can--and we fear formerly often did--convert sero-fibrinous into purulent pleurisies. A case came under Powell's observation in which carelessness in this respect apparently led to decomposition of the fluid, suppurative pleurisy, and ultimately to the death of the patient. Before operating we ought always to test the instrument, and see that it works well by passing carbolized water through it. The points should be put in the flame of a spirit-lamp, and then dipped in carbolized water and glycerin--not in oil, which may be rancid. The hands and clothes of the operator should not be overlooked in this regard. The atmosphere of the room should previously be completely cleansed by ventilation, and afterward purified by atomization of disinfectants. We must not, in a word, incur the slightest risk of converting a simple inflammatory effusion of fibro-serous fluid, a mild disease, into a suppurative inflammation, a very troublesome, dangerous one.

A needle of not larger diameter than 1 millimeter (No. 2) should be connected with the end of the tubing. Next turn the stopcocks which shut off the barrel from the tubing on both sides, producing a vacuum in the receiver. The patient should then be placed in the recumbent position in bed, with his head and chest raised. We prefer this position, as the easiest for the patient at the time of operation and less apt to produce syncope or faintness. He can, without being moved, lie down in the horizontal position, which he should maintain for at least two hours. Bowditch has, without any accident, had his patients to sit during operation sidewise in a chair, with one arm resting upon a pillow placed upon the top of the back. The operation is accompanied with so little pain that it is not necessary to use either general or local anæsthesia. Some surgeons advise before operating the administration of a small dose of morphia hypodermically, or a stimulating drink of whiskey. We are not in the habit of using either. We have generally allowed patients to take a good meal of easily-digested food (milk if they consent) about two hours previous to the operation. Whiskey and ammonia we have ready in case of need. If we find it necessary to use a 4-mm. canula for syphon, it may be best to spare the pain of its introduction by local anæsthesia by ether, or by rhigoline in Richardson's spray, or by applying a piece of ice surrounded by salt, as suggested by Powell.

The point of puncture should vary according to the quantity of fluid. If the fluid is excessive, we can operate as high up as the fifth intercostal space on the right side and the seventh on the left. We can choose a lower intercostal, but as it is not proposed to draw off all the fluid, the higher operation is preferable. If the chest is two-thirds full, we can take the seventh or sixth intercostal space on the right side and eighth on the left. If only one-third of the cavity is occupied by fluid, we can go as low as the eighth intercostal {533} on right and left sides, on a level with the angle of the scapula in the axillary line. If the quantity of liquid is so great as to force the abdominal viscera, especially the liver and the spleen, below their normal position, we may be safe in puncturing below the seventh intercostal space. But if such is not the case, the diaphragm may easily be touched on a level with even the seventh intercostal space. Aran plunged a trocar into the liver when operating through the seventh intercostal space. Ch. Bernard impinged upon the peritoneum at the same point. Woillez and Paul Barbille recommend the fifth intercostal space. Cruveilhier advises the third or fourth as being the point of the spontaneous openings. The author usually inserts the needle in the sixth intercostal space in the mid-axillary line: it is out of reach of the diaphragm and is accessible when the patient lies in the position in which he prefers placing him. The space is sufficiently wide and the parietes thin. Before operating the point must be examined carefully by percussion, auscultation, and palpation, so as to be accurate in the diagnosis that there is fluid at that point, and that nothing can be injured--lung, heart, or diaphragm.

Before inserting the needle the skin should be wiped over with an antiseptic solution. The skin being drawn up, the nail of the left index finger serving as a director, the point, having been first made aseptic, is introduced along the upper margin of the lower rib, taking care not to injure the periosteum--not by a boring motion, but by a sharp push, giving it a downward direction instead of a perfectly straight one, so as to avoid striking the lung. When the fluid is reached the stopcock is turned, so as to convert the needle into an aspirator. The index tells us whether we have struck the fluid, and its nature is shown. In chronic cases, where the bands are thick and partitions are firm, we may not find the fluid the first time. In such cases the needle is withdrawn and another point selected. The author had a case where he made no less than eight punctures before getting the fluid. At the last insertion of the needle he found it, and drew off a large quantity. The patient feels relieved in a very short time. As the fluid flows out the aspirating force should be only sufficient to draw it out slowly and gently. It is well to stop for a few minutes after aspirating about 4 fluidounces to watch the effects. The fluid running in a very small stream, we give the lung time to accommodate itself to its altered condition. The lung by this process is led, rather than forced, to resume its normal position. It is a difficult matter to fix the quantity that ought to be drawn off at one time. This must vary according to the circumstances of each case. Our rule has been to draw off more when the pleurisy is acute than when it is chronic. The long continuance of the fluid in the cavity has so impaired the lung's capability of expansion by the adhesive bands or compresses that the sudden withdrawal of a large quantity is attended with risk. If the patient bears the operation well, we may remove much more than if the contrary is the case. The amount withdrawn at the first operation should vary from 8 fluidounces to 16 fluidounces in a child, and 12 fluidounces to 24 fluidounces for an adult. We must bear in mind, as to the quantity to be removed, that ordinarily there is more or less danger of producing fresh engorgement of the capillaries and hyperæmia of the lung in removing a large quantity; and, moreover, it is unnecessary. We wish to remove the intra-thoracic pressure upon the lung and to promote the absorption of the fluid. The manometer will tell us accurately whether it is necessary to take out one, two, or three pints. If nature does not in due time remove what is left, the operation can be again resorted to. Slowness in the withdrawal of the fluid, as well as the small quantity drawn, lessens the probability of any unpleasant effects. Bowditch says: "I always draw with great deliberation. I pull so lightly upon the handle of the piston that it seems as if the fluid itself were pressing out from the chest and pushed the piston upward, my hand simply following that impulse. The instant that the patient becomes {534} restless, especially if he have any constriction or sharp pain in the chest, I withdraw the tube, even if a large quantity of fluid remains. If I do this, I find the patient is soon relieved, and in most cases nature appears stimulated even by the withdrawal of a very small part of the effusion. The absorbents begin to act well, and the fluid that is left is speedily removed."

One point is of the utmost importance: the needle should be instantly withdrawn at the onset of dyspnoea, constriction, much cough, or any tendency to syncope. These symptoms are warnings we should never neglect. This is the time to administer stimulants, and ordinarily the patient soon recovers from these effects. We must not, especially in cases of long duration, expect to find much expansion of the lung until next day. The greatest success has followed cases treated by early operation and partial removals, repeated, if necessary, every day or two until absorption is commenced.

The needle should be taken out suddenly, the operator having previously turned the stopcock, and the skin allowed at once to fall over the orifice, which is so small that no air can enter. It is indeed obliterated at once. It may be well, however, to put some collodion over it, with a small compress. The patient ought not to be permitted to move for twenty-four hours after the operation. He should lie quietly in bed and partake of simple nourishment. The removal of fluid causes the return of friction sounds and of pleuritic pain. Nature slowly does her work of absorbing the fibrinous bands. The breath-sounds in some cases are not heard for weeks, or even months, after the operation. Complete recovery being slow, and the shock to the organism very serious, the patient should thoroughly re-establish his health and strength before reassuming his active duties. A protracted rest in an invigorating climate or a sea-voyage should be advised. If the lung is slow to expand, the patient should frequently practise long, deep inspirations.

Dangers of and Objections to the Operation.--Thoracentesis as a means of relieving suffering humanity has from time to time been praised and proscribed, even in this century. Boyer operated several times, and never saved a single case. Dupuytren had only 2 successful cases in 50. He said he preferred that his patients should die by the hand of God rather than by the hand of man. Sir Astley Cooper had only 1 successful case, Gendrin not 1 out of 20 cases. Davis saved two-thirds of his cases. The eminent W. W. Gerhard of Philadelphia looked upon the operation as nearly always attended by fatal results. What a contrast to modern views and clinical results! Since Bowditch and Trousseau popularized the operation, and Dieulafoy improved the aspirating instruments, there is now no difference of opinion as to the imperative necessity of operating in cases where there is, from the quantity of fluid, imminent danger to life. Up to Nov., 1882, Bowditch[81] had operated 386 times in 245 cases, without a single fatal result, and with only 1 case in which alarming symptoms supervened. Dieulafoy's[82] cases in 1878 amounted to 150, without the shadow of an accident. My colleague, S. C. Chew, has never met with any unpleasant result from his operations. The author has had 84 cases, with 138 operations, without any unpleasant result beyond temporary cough and slight dyspnoea. Fraentzel[83] had 85 different cases, with 164 operations. A. L. Mason[84] performed 122 operations in 70 cases, with no unfavorable result which could be attributed to the operation in any instance, but usually with great and permanent relief. In 42 of his cases 1 operation was all that was necessary. So common is the operation that cases are not reported unless there is something to attract attention to them. As illustrative of the great interest taken in the operation see the number of writers on the subject and the numberless articles in medical journals, and the modifications of instruments of all kinds connected with aspiration {535} and drainage. Such being the case, we ought not to be surprised that some operators may have used the aspirator-needle when they ought not to have done so--that some should have neglected the simple rules now insisted upon as the result of experience.

[Footnote 81: Unpublished MSS.]

[Footnote 82: _Tho. Pleu. Aig._, 1878.]

[Footnote 83: _Ziemssen's Cyc._, vol. iv.]

[Footnote 84: _Loc. cit._]

Although thoracentesis by aspiration is always a harmless operation in itself, there are dangers and accidents which may follow. They may be slight, serious, and sometimes even fatal. The number of deaths which have been the result of the operation, however, is small compared to that of persons dying from the effusion whose lives might have been saved by the withdrawal of fluid. Thoracentesis was frequently made use of without accident, and was considered a perfectly safe operation until Terrillon[85] called attention to an accident which occurred sometimes after operating, a complication which Pinault[86] had mentioned in 1853--the albuminoid expectoration. Terrillon reported 2 cases of sudden and rapid death with that symptom. Several similar cases, resulting in death, had been previously reported. Dieulafoy has collected from different sources reports of 6 deaths with albuminous expectoration, caused by acute oedema of the lungs brought on apparently by the operation of thoracentesis in twenty-four to thirty-six hours. In one of these cases (Gérard's) death occurred in ten minutes; in another (Gombault's) in fifteen minutes; in another (Bouveret's) in two hours; in Behier's in four hours. Terrillon's cases, where there was this frothy, albuminoid, and sometimes bloody expectoration, numbered 16, of which 6 were fatal. The patient is attacked with cough and oppression, with the characteristic expectoration. Auscultation shows the fine subcrepitant râles of oedema of the lungs, mingled with tubular quality and ægophony. Gradually, in favorable cases, the cough subsides, respiration is re-established, and in one hour the danger has passed. In fatal cases the cough becomes irregular and jerky, the agony increases, and the patient throws up the yellowish and albuminous expectoration in quantity varying from 50 grammes to (in one case reported by Moutard-Martin) 1 liter. The intensity of the dyspnoea and its duration vary very much--from twelve to twenty-four hours.

[Footnote 85: _Thèse de Paris_, 1872.]

[Footnote 86: _Ibid._, 1853.]

There has been considerable discussion among different authors as to what produce this serious condition. The view sustained by Hérard[87] is the one generally admitted to be correct--viz. that it is from rapid congestion and acute oedema of the lung, and not from the passage of serous effusions of the pleura through the bronchi. Foucart[88] relates a similar case of albuminous expectoration occurring in heart disease. This condition could not be produced by perforation of the lung, for the pre-existing vacuum renders the aspirator-needles the safest to introduce, because if there is fluid present it at once flows out and warns the operator not to push the implement farther in. In no autopsy has the orifice made by the needle been found, nor has it ever been known to produce pneumothorax. The quantity of albuminous sputa is out of all proportion to the orifice made. In several cases of reported perforation these symptoms did not occur. After the lung has been a long time compressed by an effusion, and when, in consequence of the expulsion of the liquid, it retakes its normal proportions, there occurs a rush of serum which is expelled by the bronchi. Hérard has seen patients in whom he could not find more than traces of liquid after the puncture, and who at the end of a half hour or an hour expectorated 500 to 1000 grammes of fluid which did not come from the pleura. That oedema of the lungs, or serous exudation from the capillaries into the walls and on the free surface of the alveoli, is a result of hyperæmia and pulmonary congestion is admitted by Robin, Bernard, Niemeyer, Jaccoud, and others. We have first congestion of the lung, then oedema resulting from it, ending in free albuminous expectoration, {536} which comes not only sometimes from the diseased side, but from the healthy side, owing to pressure against the mediastinum and the other lung. This is an accident the possibility of which should be always before us in operating. No precaution ought to be neglected which will ward it off. It is instructive to analyze Terrillon's cases as to the cause of the oedema. As he considers that the aspirator, by draining out the lung, is likely to produce this unfortunate result, it is satisfactory to find that of the 16 cases where this unpleasant symptom was found, 12 were where the old trocar (Reybard's) was used without aspiration, and 4 where aspirators were used. Of the 6 fatal cases collected by Terrillon, 3 were with the trocar and 3 with the aspirator. Five out of the 6 fatal cases are found to have been not simple pleurisies, but pleurisies with complications, such as heart disease, bronchitis, tuberculosis, numerous adhesions, double pleurisy. The same may be said of the benign cases. In addition to these complications, large quantities of fluid had been drawn out at one time. Dieulafoy challenges his confrères to produce an instance of death from this cause when the fluid removed did not exceed 1200 grammes. His rule now is never to withdraw more than 1000 grammes of liquid at one time, and in large effusions to empty the sac by several operations. The older and more complicated the effusion, the more rigorous should be the rule, because there is great danger in thoracentesis when the fluid has existed long enough to have compressed the lung to a serious extent by bands. All careful operators now follow this rule. It is dangerous, and withal unnecessary, to draw off large quantities at a time. The gradual removal of fluid diminishes the risk of syncope where a sudden withdrawal may be serious in its effects. The effect is to suddenly deprive the lung of pressure which has for weeks perhaps made it anæmic. The blood rushes into the empty vessels, the air into the alveoli, and violent congestion and consequent oedema result. If, on the contrary, we draw out moderate quantities at different times with the capillary needle, which is so small that its introduction is harmless, the lung resumes progressively the functions it has lost, and the circulation gradually enters. Thus there is no risk of congestion.

[Footnote 87: _Acad. Méd._, 30 Juillet, 1872.]

[Footnote 88: _Thèse de Paris_, 1875.]

In examining the fatal cases reported by different authors, Foucart, Dieulafoy, Mercier, Lerebenthel, and Gagnet, we find other modes of death in addition to those by oedema of the lung, such as asphyxia and pulmonary emboli, and, as connected with the heart, syncope and cardiac thrombosis. In most of the cases these accidents resulted indirectly from the operation in twenty-four hours or a longer time. In a case reported by Guyot it occurred three days afterward. Congestion by itself may cause sudden and rapid death by determining asphyxia.

There are other lung causes which produce sudden death following thoracentesis, such as atelectasis, consecutive to effusion; secondary pneumonia, caseous or not; pulmonary tubercles. Besnier reports a case of gangrene of the lung following paracentesis. Of the 8 cases collected by Dieulafoy which may be put into this category, we find death from pericarditis, cardiac clot, and from thrombosis of the pulmonary artery. Death from the heart may be due to old lesions, to syncope, or to the presence of clots in the heart or small circulation. Stokes has given fatty degeneration of the heart as a cause of death in simple pleurisy without operation. Syncope, with death after operation, is caused by the sudden return of the heart to its normal position. The heart being pushed out of position, the larger blood-vessels are distorted, and the course of the circulation is severely interfered with. A very slight cause will arrest the circulation. By aspiration the mechanical cause is removed, but a small embolus, may, by the increased force of blood, be carried into the pulmonary circulation. Death by emboli in the capillaries of the lungs is very similar to death {537} from clots in the right side of the heart and at the origin of the pulmonary artery. These clots may be formed in the pulmonary vessels, or may be transported in the small circulation to points more or less distant. Potain in 1861, and Vallin in 1869, reported sudden deaths from effusion in the pleural sac, causing embolism of the cerebral artery. How far aspiration is responsible for accidents of this kind it is difficult to decide. Were they caused by thoracentesis or notwithstanding the operation? They are unquestionably the cause of death without the operation in excessive effusions. The conditions which produce these results ought to be well considered previous to operation. We notice that in most of these cases large quantities of fluid were withdrawn--2000 grammes (Legroux), 3 liters (Vallin), 3500 grammes (Guyot), 1500 grammes (Chaillon and Goquel). The withdrawal in cases of long standing of such large quantities had, beyond a doubt, considerable influence in producing the fatal result. Bowditch[89] addressed letters to 60 physicians, living in 31 of the States and 2 in Canada--representative men--asking if they had ever seen or heard of fatal results following thoracentesis by aspiration. Of this number, 53 replied in the negative, and 7 in the affirmative. "Upon an analysis, however," he states,[89] "of the circumstances under which death occurred in these last, I found nothing to shake my confidence in the operation, provided it be performed with proper precautions during and subsequent to the tapping. In no one of these cases had the operation been the sole cause of the fatal result." "In 4 there was extra motion on the part of the patient after operation, and in the other 3 the disease had been allowed to continue without aid from a surgeon long after the operation was needed. In 1 the operation was a forlorn hope. One patient died on the table from anæsthetics." Bowditch adds: "These cases should not lessen our confidence in the operation, but simply teach us caution on three points--namely: do not delay too long; be very careful to direct the patient not to move, if possible, for twenty-four hours after operation; be cautious of using anæsthetics." Bowditch, from 29 fatal cases collected from Otto Leichtenstein,[90] from his own knowledge, and from European literature, tabulates the causes of death in American and European practice: 7 of these cases were caused by extra-exertion after operation; 3 from cyanosis and coma; 4 from spray injections; only 1 from syncope; and 2 from albuminoid sputa. He quotes the final remark of Leichtenstein: "Death or any serious symptoms are so rare that they ought not to have the least influence upon our estimate of this most benign and blessed operation." Bowditch states that there were only 7 deaths in this country (as far as he could ascertain), and 29, or four times as many, in Europe, although the operation has been done much more frequently here and for a much longer time. Does not this show that in this country, in following Bowditch's precepts of great care and deliberation, the operation has been more successful? He never ceased in his lectures and writings to caution us to suspend the withdrawal of fluid the moment the patient begins to suffer in breathing, even in the slightest degree. Of course there may have been other cases occurring in American practice of fatal results, of which no reports were made to Bowditch.

[Footnote 89: Unpublished MSS., 1882.]

[Footnote 90: _Deutsches Arch. für klin. Med._, vol. xxv., 1880.]

The author has carefully gone over Leichtenstein's collected cases, and he finds a number of deaths mentioned by other European authors which are not included in his list. (The reader is referred to the theses of Terrillon,[91] Foucart,[92] Foster,[93] Dieulafoy,[94] Mercier,[95] Pinault,[96] Wilson Fox,[97] and others.) Terrillon alone reports 6 deaths with symptoms of oedema of the lungs following thoracentesis. Leichtenstein does not mention any deaths from embolism, {538} such as are quoted by Goquel, Chaillon, and Woillez. In his collection he gives only 1 death by syncope, whereas Dieulafoy comments upon 4 as found recorded by Trousseau and other French authorities. Toussaint's[98] statistical tables of 300 cases, collected from other sources, give 14 deaths. Wilson Fox collected between 30 and 40 deaths connected with thoracentesis. Besnier stated in 1876 that the mortality from pleurisy in the French hospitals had greatly increased since the practice of thoracentesis had been largely followed. It is difficult to account for this in the face of the statements made by so many of its innocuousness when properly guarded: it may be explained by the fact that suppurative pleurisies are often confounded with those of a fibro-serous nature and treated by simple aspiration. Many fatal cases of empyema are complicated with phthisis; formerly these were added to the mortality for phthisis; where paracentesis was performed upon them they were added to the pleurisy column. Bearing in mind that chronic pleurisies, serous and purulent, are frequently consecutive to diabetes, Bright's disease, chronic alcoholism, cirrhosis of the liver, and other organic diseases, patients die of the primary lesions, though they have been relieved of the secondary ones. These statistics may record the deaths as resulting from pleurisy, for which there was operative interference, instead of from the organic diseases.

[Footnote 91: _Loc. cit._]

[Footnote 92: _Loc. cit._]

[Footnote 93: _Clin. Obs._]

[Footnote 94: _Loc. cit._]

[Footnote 95: _Thèse de Paris_, 1876.]

[Footnote 96: _Ibid._, 1855.]

[Footnote 97: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 98: _Thèse de Paris_, 1878.]

Formerly, when trocars and canulas of considerable diameters were used, only extreme necessity from peril to life made surgeons consent to operate. We claim that by capillary needles, gentle force, and protected points all the old objections are obviated. As Anstie says, there is no opposition to the modern operation by men who have fairly tried Bowditch's practice. Only theorists who are afraid of its imaginary results and men too timid to act hesitate to make use of it. We have discussed elsewhere (Purulent Pleurisy) the danger of admitting air into the pleural cavity, but we insist that in the close method, with capillary needles, there is no danger whatever of air entering. The puncture is so very small that it closes at once by the elasticity of the structure of the chest, just as the knuckle of the intestine in hernia closes after the needle has drawn gases and fluid out of it.

Another objection urged against puncture of the pleura in such cases is the possibility of perforating the lung by fine needles, thus letting air into the cavity and causing cough.[99] Marotte read a memoir on the subject to the Academy in 1872. He reported 4 cases, in all of which there were only temporary effects, no serious ones. Dieulafoy[100] says: "I have been witness to the puncturing of the lung several times, and I have never seen any accident supervene under any circumstances. I have thoroughly convinced myself that punctures performed with a No. 1 needle, diameter half a millimeter, are harmless, and experiments on animals have given me the same results." He even suggests aspirating a few grammes of blood from a congested lung in the first stage of pneumonia, and thus practising local bloodletting. The author has 3 times pricked the lung in aspirating--twice with a No. 2 needle, diameter 1 millimeter, where a few drops of blood were drawn into the instrument, and they did not even produce a cough or the slightest inconvenience. The third time was with a No. 4 needle (2 millimeters). From this puncture some air escaped into the pleura, and for a few days there was evidence of pneumothorax. It then disappeared entirely, the air being absorbed. The case was a circumscribed empyema, which entirely recovered.

[Footnote 99: Allbutt, _Quain's Dict. Med._, 1883.]

[Footnote 100: _Treatise on Pneumatic Aspiration_, Eng. trans., p. 256.]

It will be noted that throughout the discussion of this important subject liberal use has been made of a valuable communication specially prepared by Henry I. Bowditch for this purpose, and embodying the mature results of his study and experience of thoracentesis. It seems not only to establish conclusively the claim that to him, in conjunction with Wyman, is due the {539} great credit of introducing the principle of aspiration, but also to how great an extent it was through his persevering and skilful advocacy and performance of the operation that it became so firmly established in America upon a true scientific basis.

Purulent Pleurisy.

DEFINITION.--Purulent pleurisy is that disease in which the pleura secretes pus instead of fibro-serous fluid, as in simple pleurisy.

SYNONYMS.--Pyothorax; Empyema; Suppurative pleurisy.

HISTORY.--The term empyema was applied originally to any internal collection of pus--[Greek: en] and [Greek: pyon]. It is now restricted to pus in the pleural sac. The ancients, from the time of Hippocrates, diagnosed and treated empyema by thoracentesis and pleurotomy. They were familiar with the fact that it would sometimes discharge through the bronchi and make an orifice through the walls of the chest, and discharge outwardly. Their views of its pathology and its connection with other forms of pleurisy were necessarily crude and indefinite. Of late years, owing to the aids given by exploratory punctures, purulent pleurisies have been thoroughly investigated. Townsend[101] divided the disease into four varieties, all of which are from degenerations of acute serous pleurisies, from increase of intensity of the inflammatory phenomena, or from modification of the secretion of the serous membrane. More modern researches have shown that frequently such is the case, and that purulent pleurisies often succeed serous pleurisies. The liquid when first thrown out is serous and limpid in character, and afterward becomes cloudy, opaline, then more and more opaque and purulent, owing to the pus being freely secreted and mixing with the fibro-serous effusion. In a certain number of cases, however, the effused liquid has from the first the appearance and anatomical composition of purulent fluid--d'emblée purulente. This has been shown by autopsies in cases of women who died in childbed from suppurating pleurisies, and in persons attacked with pyogenic fever, not simply from deposits of pus, but where an inflammatory period, of longer or shorter duration, preceded the deposit.[102] Dieulafoy[103] showed that in all effused liquids in the pleural sac there were present red globules and leucocytes.[104] Laboulbène[105] has established the fact that the exuded fluid in all pleurisies, even those apparently serous, contained, from the time of their formation, purulent globules. All cases, then, are historically purulent; but clinically serous and purulent pleurisies are distinct in their progress, termination, and treatment. Purulence is not always the sign of chronicity of pleural inflammation. It may, and does, show itself in many instances from the very commencement of the attack. Wilson Fox[106] shows there is but little natural tendency in serous effusions to undergo purulent transformations. He thinks in the vast majority of cases suppurative pleurisies are so at early periods of disease. He states the proportion of primary suppurative pleurisies as from 14 to 20 per cent. It is when the number of leucocytes, from the intensity of the inflammation or modification of the process, discolors the fluid and gives to it its distinctive properties, that we use the name of purulent pleurisy. Verliac[107] states that all chronic cases in infants become purulent.

[Footnote 101: Article "Empyema," _Cyc. Prac. Med._, vol. ii.]

[Footnote 102: _Pleurisie purulente_, (Moutard-Martin), Paris, 1872.]

[Footnote 103: "De l'Examen histologique des Liquides, etc.," _Soc. Méd. des Hôp._, 1878.]

[Footnote 104: See section on Hemorrhagic Pleurisies.]

[Footnote 105: _Traité d'Anatomie path._, Paris, 1872.]

[Footnote 106: _Brit. Med. Journ._, Dec., 1877.]

[Footnote 107: _Thèse de Paris_, 1865.]

ETIOLOGY.--The causes of purulent pleurisies are divided into local or traumatic, which are well ascertained and defined; and the general, the {540} action of which is uncertain. Among the first are wounds of the chest, fractures or caries of the ribs, phlegmonous abscesses of the walls of the chest, effusions of blood, pathological liquids, pulmonary gangrene, rupture of tubercular cavities, and other injuries from adjacent organs, especially of those where pus is discharged into the cavity, for the presence of pus engenders pus. Thoracentesis has been accused of converting serous into purulent pleurisies by the admission of air into the pleural cavity. If the atmosphere admitted is contaminated by germs, we must acknowledge that such a result is possible. By the older methods, previous to the adoption of Reybard's protected canula, such a result may have been produced. We can thus, in a measure at least, account for the great mortality in cases operated upon. But since the adoption of the protected orifices of the small aspirating trocar of Wyman and the capillary perforating needles of Dieulafoy, we question whether, with such an insignificant puncture and the complete exclusion of air, thoracentesis can be justly accused of producing such serious mischief. Trousseau[108] earnestly denied such a deleterious effect of the operation in his day. We have now not only the results obtained by Demarquay, Leconte, and Manotte of injecting air into the pleural cavities of inferior animals, but we have the bold experiments of Matice, who, convinced that air could not have any bad influence, actually had the audacity to perform the operation a number of times, allowing the air to enter freely through the canula. From numerous observations there resulted the fact, unsuspected by many, that air, penetrating freely to replace the liquid extracted, never gave rise to purulence in pleurisy; that, owing to its rapid absorption, it did not in the least interfere with the expansion of the lungs; in short, that it produced no accident whatever. While admitting the force of Matice's conclusions, we think it preferable to avoid the possibility of doing harm.

[Footnote 108: _Loc. cit._]

GENERAL CAUSES.--We have shown that secondary pleurisies frequently occur in the course of convalescence from eruptive diseases, measles, small-pox, and especially scarlet fever, and that they are purulent in their nature. The puerperal condition predisposes to suppurative inflammations of the serous membranes, and pleurisies in lying-in women are almost always purulent. In rheumatism, gout, and delirium tremens, and albuminuria as a rule, the pleuritic effusion is serous. It is purulent in persons suffering from severe injuries and among men exhausted by over-work or by alcoholic excesses, or protracted obscure diseases, such as typhoid fever and pyæmia. Analyses of the cases in which purulent transformation has occurred show that tubercles of the lung have only a minor influence in its production--only 34 per cent. of the whole number. Attimont's[109] observations were founded upon 130 cases, 80 of which recovered; of the remaining 50 that died, he found tubercle in only 9 cases. Sometimes malhygienic conditions and insufficient alimentation may account for them. Men are more subject to this disease than women in the proportion of 8 to 1,[110] and young children oftener suffer from purulent pleurisy than adults. It is not easy to explain the transformation of serum into pus in pleuritic effusions that have existed for some time where there have been no grave symptoms. Imprudent exposure, affecting the general health, may thus produce disastrous results. This occurs so frequently that purulent pleurisies are generally called chronic pleurisies. There are cases where neither local nor general conditions explain the transformation of serous into purulent effusions in the chest.

[Footnote 109: _Thèse de Paris_, 1869.]

[Footnote 110: E. Moutard-Martin.]

PATHOLOGICAL ANATOMY.--This is shown by an examination of the effused liquid, the different solid detritus that it contains, the false membranes, the pleura, the lung, and the thoracic wall itself. The liquid effused is purulent in character. It contains a greater or less number of leucocytes, {541} some red globules, and voluminous granular cells, besides crystals of the fatty acids and plates of cholesterin. The pus is mixed with the serosity in varying quantities. The liquid may be slightly opaline or greenish-yellow, and sometimes gray. It may be thin or thick, with heavy flocculi, so as to pass with difficulty through a canula. The liquid is, ordinarily, inodorous, but it may be strong, and even fetid, where it has been in contact with air. In very few cases of old standing can the pus be regarded as active, the corpuscles being, as a rule, dead or having undergone fatty degeneration. Active suppuration is also more readily set up in a pleura which has already yielded pus.

Purulent effusions, independent of contact with air, may become in a short time the seat of putrid transformations. False membranes undergo alterations which produce fetid gases. The air, with its germs, its humidity, and heat, the three grand factors in putrefaction, is thrown in contact with substances of a putrescible composition. Marshall[111] holds that sero-fibrinous effusions appear to have a greater tendency to quick decomposition when air is admitted into the pleural sac than the sero-purulent or purulent products. Pus, he considers, is more stable and less inclined to rapid putrefaction than sero-albuminous fluid. In quantity it varies from a very small number of grammes to five or even six liters. By examining the fluid first drawn out we can predict, by the number of leucocytes present, whether the pleurisy will continue to be serous or will become purulent. If subjected to the influence of ammonia, it will become thready, just as happens when pus is suspended in water, if the fluid contains many of these pus-elements. The purulent fluid may fill the whole or occupy but a small part of the cavity, or again the interlobular spaces only may contain the fluid, the cavity itself being empty. False membranes are almost constantly present and adherent to the parietal or pulmonary pleura; we find them also floating in the liquid. These false membranes may be more or less voluminous. The flocculi, which may be as large as an egg, undergo transformation when air is admitted, and become horribly fetid. They may give rise to septicæmic symptoms. When we see these enormous masses in the cavity, and are unable to get rid of them by suction, we do not wonder that their presence should poison the patient and the case become incurable. Pleurotomy is the only effective mode of getting rid of these dangerous masses, with sometimes gangrenous portions of pleural or lung-tissue. These false membranes frequently form pouches and divisions for isolated quantities of fluid. The false membranes are partly adherent and partly free, especially in cases where there are pulmonary or thoracic fistula. These false membranes differ in acute purulent pleurisies from those found in pleurisies of long standing. They are but feebly adherent to the pleura, and have a slight rose coloration. In old pleurisies the false membranes are of greater density, sometimes from 6 to 8 mm. in thickness. They are more adherent, and cannot be separated, and have a grayish color. The physical state and position of the lung and disposition of the adjoining structures are very similar to what they are in serous effusions. In but few cases do the false membranes envelop the whole of the lung. They pass over one part, and on to the costal pleura. The pulmonary tissue is condensed, sometimes absolutely impermeable to air, so that it will actually sink when dropped in water, being in a state of atelectasis. In cases of shorter duration it is found crepitant throughout its structure. Brouardet[112] called attention to the inflammation in the under-pleural cellular tissue, as well as in the interlobular connective tissue, forming interstitial pneumonia, which determines condensation of this tissue and its retraction after the manner of cicatrices, and afterward its inextensibility. These explain the retraction of the thoracic walls and the narrowing of the chest.

[Footnote 111: _Loc. cit._]

[Footnote 112: "Interstitielle Pneumonie," _Soc. Méd. des Hôp. Bullétin_, 1872.]

{542} The most serious complication of this disease is the pleuro-bronchial fistula[113] by which the fluid escapes through the lung. The firm adhesions between the lungs and walls, forming enclosed pockets, contribute in no small degree to the incurability of purulent pleurisy. These pockets cannot be emptied thoroughly, nor can the washings be made to penetrate them. The purulent secretion exercises a destructive action over the tissues surrounding it, as well as upon the viscera and walls of the chest: the soft parts become inflamed and abscesses form; the intercostal muscles suffer atrophy and undergo fatty degeneration, external openings occurring from ulceration. The latter are found less frequently than pleuro-bronchial fistula. This external perforation is habitually in front, in the upper intercostal spaces, which, near the sternum, are very wide and not protected by external intercostal muscles. The fifth intercostal is the most frequent locality. There may be one or several openings. They may be caused by the pus ulcerating through the parietal walls, or abscesses may be produced in the walls and burst externally. Exceptionally, the emptying of the liquid is by ulceration of the diaphragm into the abdomen, causing fatal peritonitis. Some years since the author saw, in consultation, a patient where the autopsy proved this condition. Rare cases have been reported where the fluid escaped into the pericardium, into the mediastinum, and into the opposite pleural cavity (Fernet[114]). Bouveret[115] relates a number of cases in which the discharge of pus took place through such unusual channels as the oesophagus, the stomach, the intestines, and the pelvis of kidneys; also where the pus perforated the posterior cul-de-sac of the pleura and appeared in the posterior walls of the abdomen. In the last cases, he states, it may point in the groin, the lumbar region, the buttocks, or even in the thigh.

[Footnote 113: See section on Pneumothorax.]

[Footnote 114: _Loc. cit._]

[Footnote 115: _Journal de Méd._, Dec. 16, 1882; _N.Y. Med. Rec._, March, 1883.]

SYMPTOMS.--In a large number of cases of purulent pleurisy the general symptoms do not differ materially from those of fibro-serous pleurisies. Sometimes, however, they do. This is according to whether they are acute purulent or chronic purulent pleurisies.

In acute purulent pleurisy the disease commences in the same way as the ordinary acute fibro-serous pleurisy. Indeed, the first effusion is ordinarily serous in appearance, and afterward it becomes purulent. We have the initial chilliness more or less marked, accompanied by the characteristic pain in the side and dry cough, the fever keeping up, even as high as 103° to 104° F.; and soon the signs of an effusion supervene. In a few days, ordinarily, in acute fibro-serous pleurisies, the febrile exacerbation disappears. Graves[116] states that the extent of a pleurisy is not augmented after twenty-four hours. In acute purulent pleurisy the fever persists in spite of treatment; the effusion increases, sometimes less rapidly than in the serous variety, but in a continuous manner. If thoracentesis is performed about the eighth or tenth day, we notice that the fluid is opaline and contains a large quantity of pus. After this the fluid is reproduced, and as it forms the fever continues; the skin is hot and dry, the appetite impaired, and sweats appear during the night. In examining carefully the thoracic walls we find oedema of the diseased side. Later on there will probably be oedema of the lower extremities.

[Footnote 116: _Clin. Méd._, edited by Neligan.]

Chronic purulent pleurisy is marked by symptoms somewhat different. It commences in a similar manner to that of acute pleurisy, with fever, but in a few days the fever disappears. In the evenings there may be some febrile action with slight chills. It is remarkable that frequently vast collections of purulent fluid do not give rise to chills. The fluid augments progressively, but sometimes very slowly, and often it appears to remain stationary for a long time. This condition continues sometimes for many months. The {543} patients are pale and feeble, although they may get up and walk until the quantity is increased to such an extent as to impair their breathing capacity. Then the forces of the body by degrees diminish, and the appetite is impaired to a serious extent. The face becomes pale and the lips discolored. From time to time diarrhoea supervenes and oedema of the chest-walls is noticed, and general anasarca comes on without albumen in the urine. If nature does not open an orifice through the parietes of the chest or through the bronchi for the discharge, the patients finally succumb in the last degree of wasting with profuse sweats and fetid colliquative diarrhoea.

PHYSICAL SIGNS.--These, with some modifications, are very similar to those of ordinary sero-fibrinous pleurisy. We have the same dilatation of the chest, but it is more frequently localized. The oedema of the thoracic walls is almost characteristic of the presence of pus in the pleural cavity. We may, however, meet with it in fibro-serous pleurisy and in cachectic subjects on the side of decubitus. Then, again, there are cases of purulent pleurisy where it does not occur. It must be looked for with care, especially at the lateral portion beneath the armpit.

Mensuration and percussion afford especial evidences of purulent pleurisy, and frequently they discover encysted points.

The tubular quality of respiratory sounds is more pronounced, as are also the amphoric characters at the apex, caused by long-continued pressure of the compressed lung around the large bronchi. Ægophony is less frequently heard, the bronchophony is distant and less distinct, and vocal fremitus is more completely abolished. The non-transmission to the ear of the whispered voice through the walls of the chest (Bacelli's sound) in purulent pleurisy is a sign of considerable significance in tracing the transformation from serous fluid into pus. We must, however, bear in mind that when the sero-fibrinous effusion contains fibrinous flocculi, it has the same effect as a purulent fluid in interfering with the passage of the voice. (See article ACUTE PLEURISY.)

DIFFERENTIAL DIAGNOSIS can be but indifferently reached by considering the points mentioned. An exploratory puncture enables us to decide with certainty as to the nature of the fluid. Without this the diagnosis is often very difficult. In acute purulent pleurisy the diagnosis is most difficult, especially at an early period, because the general symptoms and the local signs resemble closely those of ordinary pleurisy. When, however, the disease is further advanced, and we have the earthy aspect of countenance with oedema of the thoracic walls, we can be nearly positive in our opinion. Moutard-Martin[117] speaks of this localized oedema at the level of the fluid as a certain indication of the purulent character of the fluid. But this oedema, as he admits, does not always exist. It is wanting in many cases, and it may be found in cases of sero-fibrinous effusion where the patient has been lying on the side, and in other cases of advanced cachectic disease. Formerly, there were many more errors of diagnosis, which were only discovered at autopsies, but now, thanks to aspiratory punctures, the diagnosis is much more accurate, and indicates to us the rational treatment. In both varieties of purulent pleurisy there is a tendency to discharge by making orifices through the walls of the chest or through the lung. This is nature's mode of spontaneous cure. The most common is the pleuro-bronchial fistula, and the period of the disease at which this accident may occur is very variable. Woillez[118] cites a case where it occurred as early as the twenty-eighth day; ordinarily it occurs at a much later period, sometimes as late as the eightieth day. It comes on early in purulent pleurisy. In infants the perforations take place as early as in fifteen or twenty days, and are favorable to the cure in one-half of the cases. Saussier in 29 {544} perforations of this kind counted 15 cures. The symptoms of this accident are easy of recognition. They vary according as the pleuritic effusion is diffused through the whole pleural cavity or is limited, encysted, or interlobular. In the first variety, where we have the physical evidences of the presence of pus, suddenly, during a paroxysm of coughing, the pus is forced up through the bronchi, and the patient in a very short time expectorates a considerable quantity, varying from a few grammes to a liter or more. The quantity thus thrown off depends upon the diameter of the fistula. It may be excessive, as in a case recently observed by the author where suffocation was produced, causing syncope, asphyxia, and death, the flow being so rapid as to fill up the bronchi to such an extent that the patient could not get rid of it. In many cases the pus is brought up more gradually, with successive coughs or with changes of position. Frequently vomiting is produced by the flow from the vomica. After the first instantaneous evacuation of pus (ordinarily continuous, sometimes intermitting) purulent expectoration takes place. The patient may pass hours without any discharge, when suddenly a severe cough brings up a quantity of pus, and again may spend days without further expectoration. Pleuro-bronchial fistulæ may have a valvular character, so that air may or may not be admitted into the pleural sac as the pus is discharged. With or without the formation of pneumothorax there is a tendency to cause putridity of pus. In cases of children, who swallow their expectoration, it often produces a very troublesome diarrhoea. The course of the disease and its prognosis are necessarily altered according to conditions met with. When the air does not penetrate, we observe that the diseased side becomes depressed and the swelling, previously noticed, disappears. The flatness on percussion diminishes or disappears entirely. On auscultation we have coarse râles, sometimes just inside the fistulous orifices, sometimes at a considerable distance. The general symptoms, as well as the physical signs, improve, and the case advances slowly toward cure. Ordinarily, the pus expectorated from the pleura, when free from contact with the air, is odorless, but it is rarely as unpleasant as in bronchial dilatations, unless it is long retained in the cavity, when putrefaction ensues. When the air enters from the bronchi, it frequently acquires a disgusting odor. If the air enters the pleura and takes the place of the pus, the chest remains enlarged. Indeed, it sometimes increases in size to such an extent as to cause suffocation unless the pus and gas are withdrawn. The valve made by the false membrane allowing the air to enter the cavity, but not to escape from it, causes the fluid to accumulate rapidly, and we have pneumothorax to a very painful degree. The diaphragm is pushed down, and, if the disease is on the right side, the liver is forced down, and descends to a level with the umbilicus.

[Footnote 117: _Purulent Pleurisy_, 1872.]

[Footnote 118: _Traité Clin. des Mal. Aigues des Organes Resp._, 1872.]

The collection of gas and fluid may be in such excess as to produce a concavity of the upper surface of the liver, while the organ is forced down into the abdomen. E. Moutard-Martin[119] explains this extreme condition by the fact that the fistulous orifice being at the superior portion of the lung, the air having equalized the interior pressure with the exterior pressure, the liquid obeys the laws of gravity, and depresses the diaphragm. The fluid thus does not reach the level of the pulmonary fistula. Under these circumstances the expectoration may cease altogether unless the patient, by change of position, allows it to flow outward through the orifice.

[Footnote 119: _Loc. cit._]

The physical signs of this condition of pyo-pneumothorax are very marked and characteristic. Above the level of the fluid there is ordinarily a great exaggeration of resonance on percussion, especially at first. At the end of a few days, however, this resonance is sometimes materially modified, and we have obscurity of the percussion vibrations. Percussion, by itself, may lead {545} us into error of diagnosis which the other modes of physical exploration will correct.

On auscultation we hear the amphoric murmur, which is sometimes of great intensity, and at others so feeble and distant as to require great attention on the part of the auscultator. These varieties of the amphoric respiratory sound appear to depend more upon the position of the pleuro-bronchial fistula, and upon the greater or less free circulation of air through the fistula, than upon the extent of the cavity (E. Moutard-Martin). This sound and the amphoric voice are the two principal auscultatory phenomena. There is also the vibrating metallic tinkling produced always in expiration. Although the physical cause may exist, this latter is by no means a constant sign. It may disappear for hours, and even days together, and then be heard for a short time. Sometimes it is only heard when the patient coughs suddenly and violently. When heard it is a very valuable indication of the presence of a pleuro-bronchial fistula. Auscultatory percussion gives us a still more valuable diagnostic phenomenon--the metallic amphoric reverberation--especially if we percuss with a metallic percussor over a metallic pleximeter. The Hippocratian splashing caused by succussion is a more characteristic sign of pyo-pneumothorax than any other we have mentioned. Other signs may fail, and often this is the only sign present. Almost all the symptoms and signs that have been considered characteristic of the presence of pus may coexist with a perfectly limpid sero-fibrinous effusion. We may even have in serous effusions a high, fluctuating temperature, profuse sweats, and quick pulse lasting several weeks. On the other hand, purulent effusions may be associated with symptoms of so mild a character as to lull suspicion. Previous to the application of exploratory punctures for purposes of accurate diagnosis, purulent pleurisies were confounded with the milder disease until so far advanced as to be too late for effective treatment. Now we can without risk discover purulent pleurisies at their very commencement, and before they reach the point of great danger to the subject we can relieve them by thoracentesis, and afterward pursue the treatment for a radical cure.

Limited, circumscribed pleurisies, such as are found at the base of the surface of the diaphragm and in the interlobular fissures, as well as those involving the pleural cavity itself, may empty their contents through the bronchi. As we have shown, the diagnosis of these forms is often very obscure and difficult. The fine capillary exploring-needle is a safe, and often a reliable, means of diagnosis. It may happen that we can only guess at the nature of the disease until, after a protracted cough, there is ejected by the mouth a quantity of pus, and the diagnosis is made clear. We may perhaps discover a point of flatness at the base or about the centre of the lung, but often this flatness is very incomplete, because the collection of pus does not always reach the thoracic wall. It may, indeed, be separated from it by healthy lung-texture. Auscultation may discover coarse râles or even gurgling with cavernous respiration. The voice sometimes has the character of pectoriloquy, at other times of bronchophony: the cavity is rarely large enough or the walls sufficiently firm to give the amphoric tone. Under these circumstances there is neither metallic tinkling nor Hippocratian succussion. The diagnosis of bronchial fistulas caused by encysted pleurisies may be confounded with tubercular cavities or with dilated bronchi. The exact position, however, of the lesion, the rapid manner of the first purulent expectoration, and the nature of the pus expectorated, will enable us always to arrive at an accurate diagnosis. We must remember that in bronchial dilatation the disease is developed by degrees, and the patients do not expectorate suddenly a notable quantity of pus; tubercular caverns are ordinarily at the summit. The mode of expectoration is different, and the matter expectorated does not present the same purulent and homogeneous characters. {546} The general health is very different where encysted pleurisies exist from what it is in patients suffering from tubercular cavities. In the former case it is comparatively good; there are no profuse night-sweats, diarrhoea, etc. Perforation through the thoracic walls may take place at a period more or less remote from the commencement of the disease. The first indication of this result is, ordinarily, a pain over a limited point of one or two of the intercostal spaces, followed, in a few days or a week, by a raised sensitive point on the surface, without change of color of the covering skin. This may remain a long time in an unchanged condition, but generally it increases gradually until it becomes soft and fluctuating, reducible by pressure, but increased in size by efforts to cough or by forcible expectorations. The skin over the raised point becomes thin with a purplish tinge; suddenly, from some effort to cough or unusual exertion requiring suspension of breath, it bursts and gives exit to a quantity of pus far out of proportion to the size of the small tumor. Sometimes there are several such points in the same subject, appearing simultaneously or consecutively, especially if the discharge is not free through the first one. Ordinarily, there is but one which appears on the anterior portion of the chest about the fifth intercostal space or in the intra-mamillary line. These orifices sometimes close and then reopen. Of 18 cases of empyema necessitatis collected by John Marshall,[120] 1 occurred in the sixth intercostal space and 17 in the fifth, and 6 of his own cases in the fifth, beneath the nipple. This is, as he states, the weak point of the chest, relatively unprotected by the adjacent muscles. The internal intercostal muscle, the weakest portion of the great pectoral, and the thin fascia, are the only coverings at that point. There is valid reason why special bulging and spontaneous perforation should occur there. The spot also corresponds nearly with the middle of the pleural cavity when distended. The fifth intercostal space is wider than those below, and its limiting ribs, held to the sternum, give firmness to its borders--conditions which help the thinness of the walls in determining the place of perforation. In children perforation often takes place in the very wide second intercostal space. The perforation, although it may contract in size, persists and remains a fistulous canal, permitting air to enter and to escape. The fluid rarely becomes fetid unless there is a pleuro-bronchitic fistula or air is otherwise freely admitted. Sometimes when the orifice is oblique, the air does not enter at all. When the purulent effusion escapes through the thoracic walls, the patient experiences at once manifest relief. The respiration becomes better, the fever decreases, the sweats disappear, the appetite improves, and the general condition is decidedly ameliorated. This improvement persists as long as there is free discharge, but if from any cause it ceases, we have a return of serious symptoms. If no air enters, percussion and auscultation show the gradual disappearance of the evidences of disease; but if air enters we have the signs of pyo-pneumothorax, amphoric breathing, metallic and succussion sounds. The diagnosis of parietal openings is comparatively easy: the quantity of pus, its odor, with the physical signs, show its nature. With care this form of pleural opening is distinguishable from a fistula made by caries of the ribs or by vertebral abscesses, and not communicating with the pleura. The existence of a thoracic fistula does not prevent the formation of pleuro-pulmonary fistula, and reciprocally a parietal fistula can be found where the other has been previously formed. The abscesses following purulent pleurisies and empyema have been long recognized. Hippocrates mentioned them as contributing to a favorable prognosis in empyema.

[Footnote 120: _London Lancet_, March, 1882.]

Pulsating empyema is where the lesion is situated in the neighborhood of the heart or of the aorta, which transmit their impulse. They are also sometimes called pulsating tumors, rising and falling with alternate movements of {547} inspiration and expiration (Stokes, Graves, and Aran). These cases strongly simulate aneurisms. According to Fraentzel, the fluid is always purulent. In 1 case reported by him, and in 2 cases seen by Traube, pericarditis with effusion was present. Douglass Powell mentions two well-marked cases of pulsation in the left supra-mammary region where the diagnosis between effusion and aneurism was very difficult, but where paracentesis removed a large quantity of fluid and the signs of pulsation ceased. In these cases there was present neither pus nor pericarditis.

TERMINATIONS.--If allowed to take its natural course, pulsating empyema almost always ends in death from exhaustion or syncope, or by discharging through the lungs or through the intercostal spaces. Formerly, it was oftener fatal than now, but it is still justly considered the gravest form of pleurisy. We have seen that exceptionally it is cured by becoming encysted. It may be cured by spontaneous openings into the lungs, and more rarely by fistulous orifices[121] through the walls of the chest. Is it possible for the disease to be cured by the absorption of the pus? The bearing of this inquiry upon the treatment cannot be over-estimated. If absorption can remove the pus, we may safely leave it in the pleural cavity. If the pus cannot be taken up by the absorbent vessels, we ought promptly to make use of radical measures and evacuate it. The literature on this point gives us few reliable cases. Spontaneous cure can rarely be produced by absorption. Douglass Powell[122] writes that "the spontaneous disappearance of such effusions is too uncommon to be expected, and the process of reabsorption is one too full of peril to be anticipated with anything but dread. It is indeed an attempt at such absorption that occasions the most characteristic hectic symptoms." Surgical intervention is the rule. The writers previous to the introduction of exploratory punctures speak of cases where purulent pleurisies were diagnosed and the effusions were absorbed. We have shown that the differential diagnosis between serous and purulent effusions is very uncertain when made from the general symptoms and physical signs. Even Trousseau, with all his skill and vast experience, made the mistake of diagnosis, and performed the operation of pleurotomy in a case of serous effusion, and his patient died. There are well-authenticated cases where, after thoracentesis, small quantities of pus left behind have been absorbed, especially in children. That purulent pleurisies have been effectively cured by the pus becoming encapsuled has been demonstrated by autopsies of persons dying from other causes. E. Moutard-Martin reports a case where, after withdrawing with an exploratory trocar a few drops of pus, and thereby establishing the diagnosis of purulent pleurisy, he was unavoidably prevented from opening the chest. Two months afterward he found the effusion had entirely disappeared. He states that this was the only case he had ever seen of a spontaneous cure without evacuation. Douglass Powell has seen one case which has satisfied him as to the possibility of a local empyema becoming absorbed. Wilson Fox reports another similar case. Chronic pleurisies in childhood are almost invariably suppurative, yet Barthez and Rilliet report 7 out of 13 recovered. It must be, and generally is, admitted that cure by pus undergoing retrogressive fatty degeneration, and then being absorbed, is possible, but it rarely occurs. Should the more fluid portion be absorbed, the inspissated pus remaining on the pleural surface may at some future time, upon softening, give rise to secondary tubercular or purulent collections. It is also true that cure is quite often effected by spontaneous evacuation through the lungs and through the walls of the chest. This is especially the case {548} in interlobular effusions and in cases sacculated by adhesions. Such cure is explained by the fact that adhesive inflammation, assisted by the elasticity of the lung on both sides, glues together the walls, isolates the fluid, and prevents air from entering, thus preventing the pus from putrefying.

[Footnote 121: In Andral's 8 cases of bronchial perforation there were only 3 deaths--a mortality less than by artificial opening previous to the application of Listerism.]

[Footnote 122: _Dis. of the Lungs and Pleura_, London, 1878.]

In cases of pulmonary perforations the probabilities of a favorable termination by absorption of gas, evacuation of fluid and the contents of the chest, are greater where air does not enter the cavity. The presence of air, especially if stagnant, in contact with the pus, makes a serious complication, causing putrefaction of the pus and consequent septicæmia, with all its dangers. The discharge of the purulent collection, through the parietes of the chest, after the manner of an ordinary abscess, is ordinarily made through the anterior part of the thorax, but it may take place in any part. At first this mode of evacuation, empyema necessitatis, is a great relief, but cures rarely result from it. Most frequently, owing to the imperfect evacuation through the tortuous canal and the entrance of air mingling with the pus, death supervenes unless the surgeon enlarges the orifice or produces a new one, and thoroughly empties the sac and persistently washes it out. From statistics collected by Wilson Fox, the mortality is not so great from spontaneous parietal openings as was formerly supposed. Of Andral's cases there were 2 deaths in 25. Goodhart had 11 cases, all of which recovered. Ewald lost 3 of his 6 cases. Cases of empyema necessitatis should be treated as artificial openings with every possible antiseptic precaution. The mortality would thus be decreased. The chances of cure by absorption are so small that when nature shows no tendency to either of the two spontaneous modes of cure, there is great danger of a fatal termination through hectic fever. The time for this result varies from a few weeks to months. When in empyema we have fistulous orifices they sometimes remain open for years. Near them are local points of depression, caused by external atmospheric pressure. When acute purulent pleurisy follows a low fever, such as typhoid or scarlet, a fatal termination may result in a short time; in other cases it is many months before the patient dies from exhaustion.

We cannot forbear to urge the importance of promptly and definitely settling the diagnosis by exploratory aspiratory punctures. Properly guarded, no evil can result, whereas a positive diagnosis enables us to act promptly with effective mechanical means of relief. It is undeniable that purulent effusions in the pleural cavity are very serious in their results, and are followed by death unless Nature or the surgeon evacuate them. Even when Nature does so, it is often imperfectly done, and the termination may be death unless we assist her to get entirely rid of the fluid.

PROGNOSIS.--Formerly the prognosis in every case was of extreme gravity. The condition was looked upon as of necessity fatal. Surgeons despaired of a successful result in operating. Now, thanks to thorough drainage and Listerism, unless the case is an old chronic empyema, we are hopeful of cure and a favorable prognosis may be given. We may look for good results where the disease is early recognized and promptly treated. J. G. Blake[123] cured 16 in a total of 19 cases. Since 1869 he cured 9 out of 10 cases. Homer[124] saved 26 out of 52. Feidler[125] treated 112 patients, only 25 of whom died (all advanced tubercular cases); 21 were restored to good health; 66 (tubercular) were cured so far as return of effusion was concerned. Israel[126] had 10 recoveries out of 11 cases. A. T. Cabot[127] reports 11 recoveries out of 14 cases. Of the fatal cases, 2 died of phthisis; the third had existed four years.

[Footnote 123: _Med. and Surg. Rep. Boston City Hospital_, 2d Series.]

[Footnote 124: Quoted from _Med. Times_, Philada., Aug., 1883.]

[Footnote 125: _Ibid._]

[Footnote 126: Quoted from Dabney, _Amer. Journ. Med. Sciences_, Jan., 1883.]

[Footnote 127: _Bos. Med.-Surg. Journ._, Aug. 16, 1883.]

{549} When purulent pleurisy follows fibro-serous effusions, and when it occurs in vigorous children, the prognosis is more hopeful than when it is preceded by scarlet fever or occurs in subjects debilitated by diseases which have exhausted the recuperative forces of the body. Empyema of tubercular origin has necessarily a grave prognosis. In persons in advanced life the prognosis is very unfavorable. If hectic fever or septicæmia occur, the prospects of cure are comparatively slight. In cases of empyema necessitatis much depends upon the power of resistance of the patient, and upon whether the matter is discharged before it has produced caries of the ribs, sternum, or spine, or has prostrated the vital powers. If these sequelæ have been produced, the condition of the body is most unfavorable to the restoration of health. If the pus in pyothorax has been discharged through the bronchi, though it may give temporary relief, it is attended with great danger, and if the discharge continues it will gradually wear out the patient's strength.

TREATMENT.--The diagnosis being established, we at once realize the great responsibility of treating a disease of such gravity. In many other diseases of serious import we trust Nature to do her part toward cure; here, as we have shown, we find her unable to come to our assistance. One of the large serous cavities, connected as it is with the lungs, is not only disabled, but contains a deleterious fluid which cannot remain in a closed cavity without sooner or later affecting the processes of nutrition. We can do little by medical treatment save to sustain the organism by tonics and reparatory agents; we can give wine, quinine, arseniate of soda, and cod-liver oil; we can administer a sustaining diet and place the patient in the best hygienic and sanitary condition. We cannot conscientiously hold out to the patient a prospect of cure by medicines.

There is danger in resorting to the expectant plan of treatment. We lose valuable time, and finally we shall be forced to resort to surgical operations, which in fact constitute the modern treatment of purulent pleurisy. By them only are we able to promote the primary objects of our treatment, which are to get rid of the purulent matter and to stop the suppurative inflammation. We thus endeavor to obliterate the pleural cavity and promote the expansion of the lungs.

Surgical Treatment.--This has been the treatment which has been most effectively used from the time of Hippocrates to modern times. There has been, and still is, great diversity of opinion as to the best modes of withdrawing the pus contained in the pleural cavity, but it is settled that when the diagnosis is certain the fluid must be removed--if not by spontaneous openings, by artificial means. We must except to this rule cases of suppurative pleurisy of phthisical origin. Bowditch years ago stated that in this class of cases it was advisable not to make permanent openings into the chest. In these the suppuration does not stop, and the operation appears to hasten the fatal issue of the disease. Wilson Fox demonstrates from statistics that the mortality in phthisical cases is increased by operations.

There is no room for discussion as to the indications, as in cases of simple sero-fibrinous pleurisy. There is only one thing necessary to be ascertained--the certainty of pus in the cavity. This is shown by the pointing or by pus abstracted by exploratory puncture. The more promptly we act, the greater the prospect of cure. As Powell[128] emphatically says, "The prognosis is practically hopeless without surgical help. We must adopt some surgical measures or take upon ourselves responsibility for a large mortality." Bowditch, Trousseau, Hamilton Roe, Anstie, Parker, Marshall, and Moutard-Martin all concur as to the necessity of surgical interference. Clifford Allbutt[129] says: "If pus or septic material be present in the body, we must not {550} rest until it is removed. I therefore dislike and reprobate all tampering with an empyema."

[Footnote 128: _Loc. cit._]

[Footnote 129: _Brit. Med. Journ._, Dec., 1877.]

We propose to mention, as briefly as we can in justice to the subject, the several modes of operating, together with our conclusions and the results obtained by us and by others of much larger experience.

Modes of Operating.--These are numerous, but they may be divided into three classes: First, the simple immediate evacuation of the fluid by subcutaneous thoracentesis with the ordinary trocar or with an aspirator of some kind, without allowing the flow to be continuous: this is the closed method; secondly, the open method--the operation by incision with a bistoury, and the introduction of permanent canulæ or of drainage-tubes of metal, of hard rubber, or of soft tubing; thirdly, the more radical treatment by free incision (pleurotomy) with or without washings or injections by the aid of syphons. With all these modes of operating the strictest antiseptic precautions should be taken.

Thoracentesis.--For this operation we have a choice between the ordinary hydrocele trocar, the trocar protected by a soft valve at the orifice (Reybard's instrument), Jules Guérin's or Wyman's aspirating pumps, Dieulafoy's previous-vacuum aspirator with capillary needles, and numerous modifications by others of Dieulafoy's, including Potain's, and Reynard's modification of Potain's, or we can have recourse to Potain's, Southey's, or Williams's syphon. If we select the trocar (Reybard's), we prepare the instrument by cleansing it thoroughly and Listerizing it. Reynard[130] recommends a hypodermic of morphia previous to operation, to prevent the painful cough. The simplest method is to pass the aspirator needle through the flame of a spirit-lamp, and subsequently to plunge it in carbolic-acid solution. We spray with a carbolized solution the point of puncture, which should be at the sixth intercostal space, when possible, in the axillary line. Powell prefers a lower opening, in the seventh or eighth intercostal space and in the posterior axillary line. He wishes to completely empty the pleural cavity of pus and promote the obliteration of the abscess-sac by the descent of the lung as it re-expands, and by the return of the heart to its normal position: these processes converge toward the lower and postero-lateral position. We ordinarily prefer local anæsthesia by sprays of ether or rhigoline or by cocaine hypodermics to anæsthesia by inhalation. After drawing up the skin, so as to be able to close the orifice by the flap after the operation, we direct the trocar by the nail of the left index finger; we, with a quick movement, insert the trocar to the extent of three or four centimeters. By this quick insertion we do not run the risk of stopping the canula with the thick membranes. We allow the fluid to flow out slowly, but as completely as possible. In fibro-serous effusions we only draw off sufficient to remove intra-thoracic pressure, to avert the dangers caused by that pressure, and promote the process of absorption. In suppurative pleurisy, while we aim at relief from pressure, we wish to get rid of a fluid which is itself deleterious. Consequently, our object is to prevent absorption and to ward off the formation of fistulous outlets through the lungs or the parietes of the chest. Therefore we endeavor to completely evacuate the pus, and, as far as possible, to prevent its re-formation. While we desire to remove all the fluid if we can, we must not run any risk by doing so. If the cough annoys the patient, and the elasticity of the walls and the pressure from the displaced organs do not continue to force out the fluid, we had better stop the flow temporarily or renew the operation next day. We must desist if the cough becomes very persistent. We prefer Dieulafoy's aspirator or Potain's modification for the simple evacuation of the fluid, unless we wish to wash out the pleura; then we employ Potain's or Williams's (of Boston) syphon, because either can be applied {551} with greater effect. It is best not to take needles of too small a diameter, for the flocculi may easily choke them. We prefer No. 2 (1 millimeter) or No. 3 (1 millimeter and a half). By using the small-sized dome-trocar we avoid the possibility of injuring the lung. Care must be taken in removing the canula to withdraw the aspiratory force by turning the stopcock; otherwise we may draw the pus into the texture of the walls and establish fistulous openings. In using the common trocar fistulæ have frequently been made, causing a serious complication.

[Footnote 130: _Brit. Med. Journal_, Sept., 1881.]

Thoracentesis thus performed has often cured empyemas, especially in children. We find instances mentioned by Lacase, Duthiers, Dieulafoy, Lebert, Hamilton Roe, and others. It has been demonstrated that the operation is sometimes effective without resorting to injections and washings of the pleural cavity. Bouchet[131] reports a case in a child following typhoid fever, where he aspirated thirty-three times and cured the patient; another case, a child four years of age, after two operations; another child, seven years of age, after six aspirations. Guérin[132] reported several cases. M. Fouson[133] reported 19 cases of children treated by aspiration with success. The younger the child, the greater are the chances of success. He advised complete emptying of the cavity. Lewis Smith[134] prefers the use of an aspirator in operating upon children. He does not think it necessary to remove all the pus present. Cordet Gassicourt[135] reports cases of three infants, each of whom was cured by one aspiration. C. Gerhardt of Würtzburg[136] recommends in children complete evacuation of purulent fluid, through incisions and washings, avoiding entrance of air. Adolph Bajincke of Berlin[137] states that aspiration with antiseptic treatment is often successful in children. He advises, if after two or three aspirations the fever returns and the fluid increases, that free incisions be made, with injections of salicylic acid (3 per cent.), with antiseptic dressings. He recommends the removal of only a portion of the fluid. A. Jacobi[138] mentioned having in a single year 3 cases of empyema in young children, each of which required but a single aspiration; the quantity of pus in 1 case amounted to 300 or 400 grammes. The flexibility of the young ribs causes sufficient sinking in of the thorax to promote recovery. F. Richardson[139] advises two aspirations before incisions. R. W. Parker,[140] London, takes Richardson's view. He strongly advocates antiseptic precautions and injections of quinine (5 grs. to ounce j) and injection of filtered and carbolized air into the pleural cavity. Austin Flint[141] advises that aspiration should be used first, but if not successful, then incisions should be made at the base of the thorax and a tent introduced to keep the orifice open. Anstie[142] gives similar directions. According to Bowditch,[143] "whenever the pus is pure there is no immediate call for thoracotomy, for patients at times get well after simple aspirations. Youth and recent uncomplicated disease favor this. Heretofore, after three aspirations the author has resorted to thoracotomy." Dabney[144] says that aspiration occasionally gives good results, even in adults. S. C. Chew reported the case of an adult (twenty-five years of age) cured of empyema by one aspiration of sixteen ounces, and also a case of a child three years of age after three aspirations. Barnes[145] reports a case of a patient nineteen years of age who recovered after four aspirations of large quantities of pus. J. G. Blake[146] reports a case (boy ten years of age) where one aspiration of ten ounces accomplished a cure. He adds that in children repeated withdrawals of pus by aspiration are justifiable, but in adults after {552} one unsuccessful operation he advises permanent opening. Dupuytren[147] cured a case after seventy-three aspirations. The author has had 3 cases perfectly cured by aspiration: a child eleven months old, after three operations; a child of five years, after five operations; a boy sixteen years of age, after two operations.

[Footnote 131: _London Lancet_, 1860.]

[Footnote 132: _De la Thoracentèse par asp. dans la Pleu. Pur._, 1871.]

[Footnote 133: _Thèse de Paris_, 1877.]

[Footnote 134: _Diseases of Children_.]

[Footnote 135: _Soc. de Thér._, 26 April, 1882.]

[Footnote 136: _Trans. Int. Med. Con._, vol. iv.]

[Footnote 137: _Ibid._]

[Footnote 138: _Ibid._]

[Footnote 139: _Ibid._]

[Footnote 140: _Ibid._]

[Footnote 141: _Clinical Medicine_.]

[Footnote 142: _Reynolds's Sys._, vol. ii.]

[Footnote 143: Unpublished MSS.]

[Footnote 144: _Amer. Journ. Med. Sci._, Oct., 1882.]

[Footnote 145: _Brit. Med. Journal_, Dec., 1877.]

[Footnote 146: _Med. and Surgical Reports Boston City Hospital_, 2d Ser., 1877.]

[Footnote 147: Altimont, _loc. cit._]

Such being the record, we are in duty bound to try simple aspirations before making use of the more radical modes of treatment. The character of the fluid as drawn off by the exploring-needle furnishes valuable indications. Should it be found laudable and inodorous, we had better aspirate once or twice before resorting to the free incision. It can do no injury, and we thus enable the lung to expand, diminish the size of the cavity, and prepare for the more radical operation. In children we ought to try this mode repeatedly unless we have symptoms of emaciation and hectic approaching; in adults only two or three times. The operation is simple, painless, without danger, and occasionally perfectly effective. If the fluid re-forms quickly--and it sometimes does with astonishing rapidity--or there are evidences of depression from fever, sweats, and diarrhoea, we must promptly have recourse to one of the effective surgical methods producing free drainage. It is undeniable that the treatment by thoracentesis is frequently unsuccessful, notwithstanding repeated operations.

In sero-fibrinous effusions the close method is the most successful, but in purulent effusion this is not ordinarily the case, and we are forced to employ the open method to produce free, continuous discharges, as the purulent fluid re-forms rapidly.

Open Methods.--Of these we have--(1) drainage through a single orifice by the introduction of a permanent canula or soft india-rubber tube; (2) drainage through two openings; (3) use of syphon; (4) pleurotomy; (5) drainage by resection of ribs. Each of these modes has its advocates. They have all been frequently used with varying results. Each has its advantages and disadvantages.

The first point to be noted about these modes of operation is, that we cannot prevent the introduction of a greater or less amount of air to replace the fluid, and therefore it is of primary importance that we should always render the air aseptic. The incision must be made after thoroughly cleansing the point to be opened. The bistoury, the canula, the dressings, the receptacles of the pus, the sponges, and everything connected with the operation, should be purified to prevent the possibility of the contamination of the pleural cavity and its contents. At each subsequent dressing all these precautions should be renewed. Antiseptic gauze of six or eight layers in thickness, with finely-combed oakum or salicylated cotton, ought to be placed over and around the orifice for an area of twelve inches. In this way what little air enters after the operation may be rendered thoroughly aseptic.

Lister[148] recommends that the coverings of gauze should be in eight folds if the drainage be excessive--that these be charged with a disinfectant composed of one part of carbolic acid to four parts of resin and pure paraffin. The dressings, he directs, should be kept in place by elastic bandages. This treatment stops suppuration promptly, and converts the discharge into one of a serous nature. His views have been amply confirmed. A. T. Cabot[149] recommends that the dressings be covered with a piece of mackintosh large enough to project in every direction. In his cases he found it acted as a valvular fold, forcing the air and pus out and preventing air from entering.

[Footnote 148: "Lectures on Clin. Surgery, etc.," _London Lancet_, Dec., 1879.]

[Footnote 149: _Loc. cit._]

Drainage by Canula through a Single Orifice.--The patient, having had about three hours previously a good substantial meal of easily-digested food, is placed in a semi-recumbent position, leaning over toward the healthy side. {553} Before selecting the point of puncture, the side ought to be first washed with soap and water, so as thoroughly to remove all dirt and epithelium débris, and then bathed in a 1:20 solution of carbolic acid. As there is to be but one opening through which the fluid is to pass, it is desirable to have it low down. The eighth intercostal space, somewhat behind the posterior axillary line, is ordinarily the best point for the puncture. Lower than that we may encounter the diaphragm, and, as we must use a trocar of considerable size, we may inflict serious injury. As we desire to completely empty the pleural cavity, a higher point would not be as effective. After having satisfied ourselves of the presence of fluid at the point selected by the physical exploration, we ought always to insert, as a crucial test, a new exploratory hypodermic needle which has been rendered aseptic. Ordinarily, it is not necessary or expedient to resort to etherization, unless in case of a child, for local anæsthesia by cocaine hypodermically, by rhigoline or the ether spray, or by the application of a small piece of ice covered with salt (as suggested by Powell), will render the incision painless. It is needless to add that a weakened heart, a sluggish capillary circulation causing a cyanotic appearance, and marked dyspnoea contraindicate the employment of etherization. We prefer cutting through the integument with a bistoury, and then inserting the trocar, which must be pushed with a thrust through to the pleura. All of the pus should be allowed to escape, unless cough, oppression, or threatening syncope should be noticed, in which case it is better to insert the tube and arrest the flow by a cork. The outward flow should be rendered slow by covering the orifice with the dressings and allowing the fluid to soak into them. The tube should only be long enough to go well through the parietes into the pleural sac; otherwise it acts as an irritant, and interferes with the adhesion of the two pleural surfaces, which is necessary for the obliteration of the pus-secreting cavity and the expansion of the lung. The tube should be kept in position by a hard-rubber shield attachment, with bandages previously soaked in disinfectants applied around the body, and several layers of carbolized gauze. The firm canulæ, metallic or hard rubber, straight or curved, as proposed by Woillez and Dieulafoy, are now generally abandoned. These admit air either by the sides of the opening or through their canals, and they sometimes produce, at their extremities, local ulceration through the lung or even through the diaphragm, and cause peritonitis. Their only advantage consists in the facilities they offer for washing out the cavity. With canulæ made of soft india-rubber there is no danger of injuring the lung, etc. They are not painful to the patient, and they can be protected by valvular strips of gold-beater's skin or some soft substance at their orifices. Through these india-rubber tubes we can inject all fluids and washes, except those containing iodine. It has been proved by Dujardin-Beaumetz[150] that iodine hardens india-rubber, renders it extremely brittle, and destroys its elasticity in a short time, even after a contact of forty-eight hours. In a case of Bucquoy's[151] the tube underwent such alterations that it could only be extracted by a long and painful operation. If these tubes are in use when iodized fluid is to be injected, they must be temporarily removed, and a metallic one, with arrangements for a double current, substituted during the process of washing. If the canulæ are to be kept in permanently, they must be of large size, so as to allow free flow outward of fluid.

[Footnote 150: Quoted by Dieulafoy, _Pneum. Asp._, English ed.]

[Footnote 151: _Ibid._]

After the operation the patient should always remain in bed in an easy, comfortable position, with the orifice covered by the dressings. His diet should be of an easily-digested and nutritious character. His temperature, pulse, and the condition of his secretions should be carefully watched. Ordinarily, it is not well to reopen the discharge-tube for three days. The same antiseptic precautions should be used then as at the operation, {554} and a fresh tube inserted. The pus secreted ought, if the case be one of recent origin, to be small in quantity and without odor. After a few days it is best to allow the fluid to flow out on the dressings as it forms, which is done by turning the patient well over on his side. An occasional cough assists the discharge. Should the odor become putrid or gangrenous, or hectic symptoms show that the secretion is profuse and has no free exit, it becomes necessary at once to use washings and injections of simple warm water or warm water feebly alcoholized--1:45 or 1:80--or feebly iodized solutions. The greatest care should be taken with these washings that very gentle force be employed. (See Pleurotomy.) This mode of operating is most effective in recent cases, for it gives the best opportunity to the lung to expand. It is the easiest to perform, and, subsequently, the least troublesome. If it be found ineffective, an additional orifice can be made and a fenestrated tube inserted, or the orifice can be enlarged by a free incision. There have been many successful cases of this mode of operating, but, as the author has sometimes found, it is difficult to establish free drainage, which is most important for the success of the treatment. The result of his experience has been that, in chronic cases especially, the two-opening drainage or free incision without tubes (pleurotomy) has finally to be employed. Powell recommends, after removing intra-thoracic pressure by aspiration or syphon, in a day or two to completely evacuate the fluid under the antiseptic spray and insert a tube for a few days only; then to allow the wound to heal, and await results, trusting nature to secrete a fibro-serous fluid which can be easily absorbed.

Drainage by two openings, as first effectively employed by Chassaignac, is made by the introduction, through a large covered canula, of a tube of india-rubber, perforated with holes, drawn out at another orifice. The tube has its two extremities on the outside, and one posterior, in the eighth or ninth intercostal space, and the other in front, in the seventh intercostal space, after the withdrawal of the canula. The anterior orifice is first made, and a long curved probe with a bulb at the end is passed through backward and downward until it strikes the posterior lowest intercostal space. The operator cuts down on the probe, which points outward. To this end the fenestrated drainage-tube is securely fastened, and is then drawn out through the first orifice. Both ends are retained out of their orifices, by a shield firmly fixed on the tube, for at least an inch. The pus flows out little by little, but continuously, through one or other orifice, according to the position of the patient. This is the most effective method to prevent accumulation. Unfortunately, false membranes and flocculi sometimes stop up the orifices in its walls, the pus does not flow out as it is formed, and there are all the evils of air and fluid mixed and retained in the serous cavity. It is, however, generally admitted that by this system of drainage a number of cases have been cured; but it is not often employed as a primary operation, as we wish to avoid, if possible, the irritation which may result from the presence of so much tubing in the chest. Moreover, it is not the best operation if there is any hope of the lung expanding again. In old chronic cases we cannot hope for more than very limited expansion.

Gross[152] speaks of drainage-tubes as harsh and dangerous. Flint, Sr.,[153] prefers free incisions, with introduction of tents, to drainage-tubes. Dabney[154] considers continuous drainage in some form vastly preferable in the majority of cases. Israel[155] had 10 cases recover out of 11 treated by thorough and continuous drainage. Cheadle believes that a large collection will certainly require a free opening in the end, and the sooner the pus is let out the better.

[Footnote 152: _System of Surgery_, vol. ii.]

[Footnote 153: _Clin. Med._]

[Footnote 154: _Amer. Journ. Med. Sci._, Oct., 1882.]

[Footnote 155: Quoted by Dabney.]

Chassaignac's method of drainage will answer well unless, as frequently {555} happens, the purulent pleurisies contain large fibrinous masses, hydatid pouches, or pieces of sphacelous débris.

Syphons, as used in purulent pleurisies, have some very decided advantages. Potain's ingenious instrument, based upon the syphon principle, enables us alternately to empty the pleural cavity into a basin of water, and, by reversing the instrument, to inject the water into the pleural cavity, thus washing out as often as necessary and with ease the purulent collection and cleansing the cavity. Potain's syphon is composed of an india-rubber tube 30 centimeters in length, to be introduced and remain in the pleural cavity. This tube is introduced through the canula, after the withdrawal of the trocar, to the depth of at least 20 centimeters, in order that its extremity should reach the posterior wall, the tube having been previously filled with water. The outer extremity is put into a basin containing water. The part of the tube at the outside of the orifice is closed by a serre-fine just beyond the shield, as is also the extremity in the water. Another tube is connected with the chest portion. This can be used for introducing water to wash out the pleura. The syphon of Potain has very decided advantages over the metallic and hard-rubber drainage-tubes. It prevents the introduction of air and enables us completely to empty the cavity; it permits us to wash out the cavity as frequently as is necessary without fatigue to the patient, without pain, and without change of position, and thus prevents attacks of coughing. All this is done slowly, and the flow can be arrested at any moment by means of the stopcocks. Where repeated washings are required the patient himself can perform them with ease. With the other modes the washings are practised with difficulty. The improved syphon by F. H. Williams of Boston is simple in construction, of small size, and inexpensive. Revilloid of Geneva (1882) reports 10 cases thus treated, of which 6 were cured. Bénard[156] reports 8 cases treated by syphon, of which 4 were cured. Goodhart's[157] statistics are not favorable to the use of the syphon. Of his 28 cases thus treated, 10 died; in only 6 did the syphon method alone effect the cure. Powell[158] objects to the syphon method, because by it the chest cannot be drained unless the lung expands completely or air is freely allowed to enter the pleura. These conditions are impossible in such cases with a single opening and a single tube. Moutard-Martin, while speaking of the advantages of Potain's syphon, admits that in chronic cases where there are pieces of false membrane and flocculi floating in the fluid the tube may be clogged up, just as occurs in the metallic tubes and the drainage-tubes. The patient may thus die by retention of pus and by putrid absorption, unless pleurotomy is employed. It must be borne in mind that the syphon is a weak aspirating instrument. It ought to be 10 meters long to possess an aspirating force equal to that of a pneumatic pump (water being taken as the standard), and its long arm should measure from 7 to 8 meters, in order that its aspiratory force should equal that of a good pneumatic aspirator. Thus we see how weak is the aspirating power of a syphon which only measures the space which separates the bed of the patient from the floor. The ordinary aspirator can be easily changed into a syphon. The descending arm of the tube must be emptied by a stroke of the piston; the current is then established and the stream becomes continuous (Dieulafoy[159]).

[Footnote 156: _Thèse de Paris_, 1871.]

[Footnote 157: _Guy's Hospital Reports_, 1877.]

[Footnote 158: _Loc. cit._]

[Footnote 159: _Trea. Pneum. Aspiration_, Eng. trans., 1873.]

While all prominent modern authorities admit the value in some cases of double metallic tubes, of those of hard rubber, of drainage-tubes, and of syphons, with thorough and complete antiseptic treatment, yet observation has taught us that there are many disadvantages and uncertainties. The drainage-tube may give rise to considerable irritation and prevent the closing of the sac--a very important aid to the cure. If the flow is retarded, the {556} fluid may decompose. Therefore it is well to remove the tube frequently, to wash, cleanse, and renew it. The admission of air and stopping up of tubes, the feeble force employed, the putrid pseudo-membranes, and sometimes sphacelous débris, cause, in many instances, fatal results. It frequently happens that at first, when trying the simple aspirations, we find a whitish laudable pus which subsequently becomes thick and fetid. We use drainage-tubes and Williams's syphon, with strict adhesions to Listerism, and yet there may ensue continuous fever, emaciation, sweats, drawn face, and general oedema. We resort to detergent washes, with salicylate of sodium, of tincture of iodine, very diluted, yet the patients get worse and the tubes become obstructed. There is not sufficient free flow of the contents of the chest.

Pleurotomy.--We naturally shrink from freely opening the chest. It is right to try the simpler methods--aspiration, tubes to remain in the chest, drainage, use of syphons--but we are forced in many cases of chronic empyema to use pleurotomy, the thoracotomy of Bowditch, the operation of l'empyème of the ancients. It consists of a wide opening into the thorax between two ribs, permitting the escape of the effused liquids. If the orifice is large enough, we can remove from the cavity of the pleura not only the pus, but the large fibrous masses, gangrenous débris, hydatids, and putrefying material which produce septicæmia and death. The literature of this subject shows that bad results have ensued from this operation, and again and again it has been abandoned, but now that we can, by means of large openings, freely wash out the cavities, and can apply injections of antiseptic and alterative medicines to the suppurating surfaces, many lives are saved. Hippocrates' dogma as to the danger of free and rapid evacuation of pus had often a dangerous influence in preventing a thorough emptying of the sac. The object of this radical operation must be kept in view--to evacuate the pus by a free current, to permit the discharge of plastic products and organic débris, and to allow easy and frequent washings with healing and purifying injections. By these means we arrest suppuration, obliterate the sac, and allow the lung to expand. For this purpose wide orifices should be boldly made. They should be made where the chest bulges most, but not always at the most dependent portion. Ordinarily, the eighth intercostal space, somewhat behind the posterior axillary line, has been the one selected, because it has been supposed that thereby the cavity could be most effectually drained. The author has usually punctured higher, in the seventh intercostal space on the left and in the sixth on the right side, for the fifth and sixth ribs being more fixed, there is less danger of subsequent approximation. We cannot always determine the exact position of the diaphragm. The lung may be bound down by old adhesions to the diaphragm, and thus the latter may be injured by too low an incision; we can, moreover, better adapt the position of the patient to enable the matter to flow out from a higher orifice. Cases have occurred where the liver has been perforated on the right side by low punctures. In health the uppermost point of the diaphragm may be as high as the fifth space on the left side or the fourth space on the right. The cure does not depend upon the exact position of the puncture, because we expect to insert a mouth-tube to keep the orifice open, and probably resort to washings. It is not by its weight only that we expect the fluid to escape; incessant movements of the thorax assist in forcing the fluid through the tubes. Marshall[160] urges the fifth space on the right side, and as near the weak point of the chest under the nipple as possible. On the left the pericardium must be carefully avoided. He advises that the operation should never be lower than the sixth or seventh intercostal interval. Douglass Powell prefers a lower puncture, in the seventh or eighth space in the posterior {557} axillary line. In the punctures lower down the tube as it ascends rubs upon the diaphragm and protracts the healing, and the orifice closes too early. The emptying of the sac and the washings can be thoroughly attended to higher in the chest. The weak point selected by nature for empyema necessitatis ought always to be examined to see if there be any thinning of the wall, for if that be the case, the puncture should be made there. The incision should be made on a plane somewhat below that of the aponeurotic and muscular portions of the chest, to prevent the liquids from infiltrating into the subcutaneous cellular tissue. If we ascertain first by exploratory puncture that there is pus lower down, it is safe to operate at that point. The exterior orifice should be wider and larger than the interior, and not parallel with it, in order to avoid the gaseous infiltration in the tissues by the respiratory movements. Care must be taken that the bistoury should pass close to the upper border of the inferior rib, to avoid the intercostal artery. In making the incision--about 6 centimeters in length--should the artery be cut, it can easily be remedied by torsion. We raise the skin, and thus make a flap over the orifice. The bistoury should not be introduced with one cut through the soft textures, as recommended by Woillez, but layer by layer should be cut through. This secures avoiding the intercostal artery, and gives a larger exterior than interior cut, thus preventing danger of liquid infiltration. We can be guided by the index finger, and feel the textures as we cut down upon them. Under a continuous spray to thoroughly purify the air that may enter, a free opening should be made large enough to allow the finger to be introduced. As air enters the fluid contents escape through the orifice, protected by antiseptic dressings of gauze, oakum, and salicylated cotton. At first it is well to remove the dressings containing the pus twice daily; later, once daily will be sufficient. The orifice must be kept patent by a short, wide tube with a fine wire around it. We can thus, by changing the position of the patient, get rid of the contents of the chest cavity. If there should be fetidity, it is desirable to use washes of warm water first, and afterward of feebly-alcoholized water--a solution of salicylate of soda, chlorinated soda, or permanganate of soda. Cabot[161] had most success in the use of sol. chlorinated soda, one part to twelve or fifteen of water, for purposes of injection. The average time that the tubes remained in, with his cases, was only twenty-four days. His favorable results he imputed to the mechanical action of the india-rubber covering over the antiseptic dressings.

[Footnote 160: _Loc. cit._]

[Footnote 161: _Loc. cit._]

Resection of Ribs.--The ancient operation of resection of ribs, dating back to Celsus, is strongly advocated by Pietavy, Thomas of Birmingham, Lane, and other modern writers as affording the best means of thoroughly evacuating the pleural cavity of its purulent contents and of keeping up constant drainage. John Marshall[162] reports 4 cases where he resected the ribs to make permanent openings. In all of these cases the walls became gradually firm and new bone was formed. He concluded that the removal of a portion of one rib was not sufficient, but that a large space through four ribs is the proper size for the opening, that the sixth rib is the essential one to deal with, and that from one and a half to two inches of bone should be taken away. In one case he performed a subcutaneous division of costal cartilage with a view to weakening the thoracic walls and allowing them to fold in. A number of cases are reported of resection of ribs, with varying success, by Ewald,[163] Taylor, House,[164] and Thomas.[165] Taylor[166] advises the removal of the periosteum to prevent the rapid re-formation of bone. If after the puncture the rigidity of the ribs seems to keep up the discharge, and the lung does not expand to meet the rib, a resection of a considerable portion of two or three ribs may be {558} made for relief. If, again, in the progress of the case the adjoining ribs have fallen in and have approximated, and thus become a source of pain in retaining a permanent drainage-tube, a portion of rib may be resected. The principal object of resection of ribs is to favor their falling in, for a sufficient orifice can thus be made between the ribs for the discharge. The upper two-thirds of the breadth of a rib may be trephined in order to give more room for exploration, evacuation, ablution, and prolonged drainage. This is the operation of Esthander,[167] who thus treated successfully 5 of his 6 cases operated upon. Fenger of Chicago[168] operated in this manner on fourth, fifth, and sixth ribs.

[Footnote 162: _London Lancet_, March, 1882.]

[Footnote 163: "Med. Soc. Berlin," _Lon. Med. Rec._, 1876.]

[Footnote 164: _London Med. Record_, Aug., 1876.]

[Footnote 165: _Trans. Clin. Soc._, vol. xiii.]

[Footnote 166: _Brit. Med. Journ._, Feb., 1881.]

[Footnote 167: "Resection du Côltes de Emp.," _Revue Mens. de Méd. et Surg._, 1879, vol. B.]

[Footnote 168: _Med. News, Philada._, Sept., 1882.]

Jacobi[169] says that resections ought not to be practised upon children. W. A. Lane,[170] from the observation of 5 cases of empyema in children, strongly recommends that a portion of rib or ribs be removed at first, and the cavity thoroughly drained from the beginning. It assists, he argues, the cure by promoting the falling in of the ribs, the expansion of the lungs, and the ascent of the diaphragm. In children the difficulty in securing free drainage is that the spaces between the ribs are small, and after the cavity is opened they become much more contracted; soft tubes thus become compressed, and hard tubes cause much local irritation. Resection of ribs enables the operator to keep the orifice open and have perfect drainage. The opening should be large enough to allow the introduction of the finger and of an india-rubber tube of sufficient diameter to give free passage to the contents of the chest, without the tube being displaced by movement of the ribs. In only one of Lane's cases was trouble caused by rapid increase of bone. He operated as low as the ninth intercostal space in the axillary line, taking care always, by the hypodermic syringe, to ascertain that there was pus at that point. He divided the periosteum longitudinally, and removed with cutting forceps about three-quarters of an inch of rib. After he had thoroughly cleared out the cavity he introduced a short india-rubber tube, so that its inner end should not project into the cavity. Wire sutures were passed deeply through the intercostal tissues and tube, and, to render the position of the tube more secure, soft pins were fixed through the wall of the tube, and attached to them were pieces of elastic surrounding the chest.

[Footnote 169: _N.Y. Med. Record_, Jan., 1881.]

[Footnote 170: _Guy's Hospital Reports_, vol. xli., 1882.]

If necessary in order to have uninterrupted free drainage, children as well as adults should have their ribs resected. The important point in operating is to secure free exit to the fluid and purification of the cavity by the necessary washings by the open method. Pleurotomy by resection of ribs is almost universally acknowledged to be the most effective treatment, for it promotes most rapidly the agglutination of the pleural surfaces and the expansion of the lung.[171]

[Footnote 171: Lawson Tait strongly advocates this same method of treatment in peritonitis. He has performed laparotomy successfully in 20 cases, using washings and drainage-tubes (_Bost. Med. and Surg. Journal_, Aug. 16, 1883).]

Good drainage is the essential consideration after the operation. We must prevent putrefaction or fetid decomposition in the pleural contents. So long as pus is retained within the sac, it does not putrefy, but putrefaction follows contact with the putrefactive agencies which abound in ordinary air, as shown by Pasteur and Tyndal. These are solid particles floating in the atmosphere. Although air must be admitted, it should be rendered aseptic. The drainage-tube, which should be just long enough to go thoroughly into the cavity, by itself is in many cases insufficient. The upper part of the cavity may retain on its surface pus and flocculi which may prove dangerous. By the syphon we can fill the cavity slowly with medicated tepid water without shock and {559} without risk of tearing away the neo-membranes. Woillez[172] advises that pleurotomy should be promptly used whenever pus is found. Béhier advocates the same treatment. E. Moutard-Martin,[173] whose authority is high from his great experience and conservatism, advises us always to commence the treatment with thoracentesis by aspiration. He says, if the fever persists and the general condition grows worse, he does not hesitate to resort to pleurotomy. The author's more limited experience coincides with his. I. Marshall[174] states as his opinion that purulent pleurisies require the immediate or early adoption of the open method. In fibro-serous pleurisy we wish to restore the physiological condition of the pleura, whereas in purulent cases the object is to obliterate the sac by adhesions throughout the surfaces, just as abscesses are cured. It is necessary that the costal and pulmonary pleura and that of the diaphragm should be brought closely in contact. This is produced simultaneously by the dilatation of the lung and the diminution in every way of the pleural cavity. The dilatation is produced by the disappearance of the intra-pleural pressure and the pressure in the opposite direction from the bronchial surfaces. This last depends upon the condition of the lung and of the visceral pleura. If the lung has been long compressed, it is almost carnified and reduced to a state of foetal atelectasis. It rarely happens that the bands which bind the lung down do not in time undergo granular fatty degeneration and disappear. This enables the lung to expand, if not to its original size, yet sufficiently to occupy the cavity, reduced in size by the approach of the walls. The heart, which previous to the operation was thrown more or less out of its normal position, comes back from the empty side, and often passes the position that it normally occupied. The lung follows the heart. The whole mediastinum finds itself altered in its position and in its contents. The depressed diaphragm rises promptly to its old position in the pleural cavity. The liver, spleen, and the rib-wall undergo striking modifications. We do not expect the lung to dilate to its full extent, as after aspirations in simple pleurisies. The lung, indeed, is already impaired in its movement. We admit air in order to secure treatment to these surfaces. When air is admitted into the normal chest, the lung is retracted to about one-half its size. In serous effusions we fear free admissions of air, because it assists in compressing the lungs, and may contain germs which promote suppuration. We must bear in mind that we may have double pleurisy from the pus producing pleural necrosis at the point of contact of the pleural sacs about the middle of the sternum opposite the middle of the third rib. Elsewhere there is no such danger, for the pleural surfaces remain a long distance from each other.

[Footnote 172: _Bul. Soc. Méd. des Hôp._, 26 April, 1872.]

[Footnote 173: _Pleurisie purulente_, 1872.]

[Footnote 174: _Loc. cit._]

Why should we postpone pleurotomy, with or without resection of ribs, until we have used the drainage-tube, canula, etc.? The impression is that this operation is attended with danger, whereas ordinarily, with care, such is not the case. In pleurotomy there is not the same danger of serious accidents as in thoracentesis, especially as performed by canulas and trocars. Pleurotomy never causes acute oedema of the lung. The forcible unfolding of the lung, with rush of blood to vessels that have been almost emptied by compression, does not occur under these circumstances. After the large openings of the chest the causes of the forced expansion of the lung do not exist. The diminution of the pressure on the mediastinum, the re-establishment of the thoracic aspiration, and consequently the more free access of venous blood into the right heart, favorably influence the general circulation. The pulse increases in force, the cyanosis is dissipated, frequently within a few hours, and the anasarca disappears in a few days.

Theory and observation show beyond a doubt that in all cases where {560} there exists a decided intra-pleural tension pleurotomy of the thorax modifies efficiently the circulatory and respiratory functions. Instead of causing suffocation, it diminishes almost always, and that instantly and remarkably, the dyspnoea. In 1868, Maisonneuve[175] made the startling announcement, which he claimed was nevertheless rigidly true, that of 100 patients who die after surgical operations, 95 are poisoned by organic substances absorbed. He claimed that the liquids exuded from the surface of wounds become corrupt when exposed to the external air, and that subsequently they undergo morbific changes and become formidable poisons. If, he said, we can prevent the dead liquids from putrefying, the gravest operations could be performed without danger. No one who studies the results of empyema in the past can question that the greatest danger is from the blood-poisoning known as septicæmia, caused by the absorption of the septic infection by the lymphatics.[176] No matter what may be the nature of septicæmia, it is sufficient that the vast surfaces of the pleura produce certain prurient secretions, which, when absorbed and carried into the circulation, cause hectic fever with its results. We claim that there is less danger from putrid absorption when free incisions are made than from those only large enough to introduce a drainage-tube. Rome[177] collected 49 cases, but of these 10 contained fetid pus; 9 of the number had been treated by one or many, even up to fifteen, aspirations. He concludes that the surgical interventions, other than pleurotomy, provoked in the purulent liquid of the pleura putrid fermentations in one-fifth of the cases. The products of this fermentation irritate actively the serous membrane, and cause an abundant suppuration intractable in its nature, and there is imminent danger of rapid exhaustion and hectic fever. One-third of Rome's cases contained solid pieces which could not be removed in any other way than by making free incisions. Although subserous cavities are not perfectly analogous to phlegmonous abscesses, yet they closely resemble each other. Histologically, the inflammatory process and its phases are the same, but there is this difference--absorption of the deleterious products is more active. Why allow a warm abscess to be transformed into a cold abscess, which will open later spontaneously after having caused grave disorders? We have seen how frequently large collections of pus sooner or later open either through the lung or through the chest-walls. If an opening has to be made, the more promptly the better. In the first stage, especially in acute purulent pleurisy, the slight neo-membranes and fibrinous deposits, barely solid, readily undergo granular fatty degeneration, and are absorbed if relieved of the pus. In this stage the two folds of the pleura are in their best condition for becoming adherent to each other, and by obliteration of the pleural cavity to end the disease. If acute empyema be treated early and gently before the lung is compressed or injured, with free opening and constant drainage, the patient being in a recumbent position on face or side, the pleura needs no washings. The orifices made spontaneously are frequently insufficient to completely empty and to keep up the current of pus as it forms. In bronchial fistula, unless the air is prevented from coming from the lung into the pleura by a valvular opening, we have frequently to resort to pleurotomy. If in empyema necessitatis the orifice partly closes or is not free enough, we must not hesitate to enlarge it or make a counter-opening to enable the matter to flow out. In tubercular pyo-pneumothorax, where the purulent fluid has been the primary lesion and has perforated the lung, the operation is not indicated. E. Moutard-Martin's treatise was founded upon 17 subjects, 5 of whom died and 12 were cured. Of the 12 cured, 2 had bronchial fistula in pneumothorax without any sign of tubercle; 5 had permanent fistulous openings and discharged {561} occasionally a few drops of pus; 7 were cured without fistula. Blake[178] reported 19 cases treated by permanent openings, with 15 "cured and much relieved." He operated by making incisions from one to two inches long, parallel with the ribs, between the seventh and eighth ribs, a little inside of the scapula. His practice was to keep the orifice open. He used either a spiral wire covered with gutta-percha or a gum-elastic catheter fastened to a shield and kept in position by adhesive plasters. Martin Oxley[179] by pressing open the incision with a pair of dressing forceps introduced a silver or india-rubber tracheotomy-tube to keep the orifice open. He related several instances where pieces of tubing fell into the cavity and remained there without injury for months, and in one case as long as several years. Dabney[180] urges with force the importance of our having a continuous discharge of pus as far preferable to its daily removal, "not only because it seems less liable to become fetid, but because, as the two surfaces of the pleura have to come together and heal by granulations, the retention of pus would delay this process by keeping the costal and pulmonary surfaces apart." Thorough drainage by two orifices or a wide incision kept open by two tubes is more effective than a simple drainage-tube. Antiseptic precautions are essential to ensure success at every stage of the operation.

[Footnote 175: _London Prac._, 1868.]

[Footnote 176: Ranney, _Annals of Anat. and Surgery_, 1881.]

[Footnote 177: _Thèse de Paris_, 1882.]

[Footnote 178: _Boston City Hospital Reports_, 2d series.]

[Footnote 179: _Liverpool Medico-Chirurg. Journal_, January, 1882; _N.Y. Medical Abstract_.]

[Footnote 180: _American Journal Med. Sciences_, Oct., 1882.]

Value of Injections and Washings.--The object of injections is to enable us thoroughly to wash out the cavity and to promote adhesions between the pleural surfaces. The chief danger being from septicæmia, it is of the greatest importance that the pus should not be allowed to remain in the cavity longer than can be avoided. The body-temperature, taken twice daily, is one of the best means of ascertaining the extent of the re-formation of pus. Stagnant pus, mingled with air, will undergo fermentation and cause putridity; hence the great value of incessant drainage through unobstructed tubes. When the pus is free from unpleasant odor and runs freely, it is not necessary to use washings or injections of any kind, for the cavity will purify itself. Washings and injections have sometimes been found very injurious and irritating, and sudden deaths have been attributed to them. If flocculi form, washings of tepid water with a very small percentage of alcohol or of salicylic acid (1 per cent.), used without force for fear of rupturing some of the recently-formed capillaries, are useful. When modifying injections are used, the patient ought to lie on the opposite side. In this way all the diseased parts are reached by the fluid. An ordinary syringe should not be used, but a Thudicum bottle or a fountain syringe: either of these can be raised sufficiently high to allow a gentle flow into the cavity. If the discharge becomes fetid, injections of solution of permanganate of potash (1 or 2 grains to ounce j) or of tinct. of iodine (1:4) in water ought to be used. The author has never seen any results of poisoning from the use of carbolic acid, but he has always used a feeble solution, 2 or 3 per cent. Dabney had symptoms of carbolic-acid poisoning in one of his cases where he used a 2 per cent. solution, notwithstanding the fact that he had taken every precaution to ensure its prompt return. A. T. Cabot[181] mentions a case of carbolic poisoning in a boy four years of age produced by a feeble solution of one part to thirty of water used only to cleanse the instruments, tubes, and hand of the operator. Kuster's[182] experiments show that anæmia and septic and pyæmic fevers predispose the system to carbolic-acid poisoning. He recommends an 8 per cent. solution of chloride of zinc. Chlorate of potassium drachm j to pint j has been used with benefit. The medical journals contain so many reports of the serious, and even fatal, results from absorption of carbolic acid when thrown into abscesses {562} that we are compelled to abandon it in favor of other injections. B. W. Richardson long since showed the great value of iodine as a disinfectant. It not only corrects the fetor of decomposed pus, but at the same time lessens the secretion from the walls. The first injections should be weak, gr. 4 or 5 of iodine and iodide of potassium to a pint of water. Liq. iodinii com., ounce ss to ounce iv, ought not to be used until the surfaces have become accustomed to the action of iodine. Injections of medicated fluid ought not to be used unless they are absolutely necessary, because in some instances they have produced fainting attacks and epileptiform seizures with alarming convulsions. These results have followed injections of different fluids--borax, carbolic acid, iodine, permanganate of potassium, and even warm water. Similar phenomena have followed the injection of the bladder, the uterus, and even from passing a catheter. The shock may have been too sudden or the injection too forcible or the fluid too cold. A. L. Mason[183] suggests that it is probably owing to sudden irritation of the lymphatics through the great splanchnic nerve, with anæmia of the brain. Paralysis of the limbs after convulsions makes the theory of embolic origin probable. These accidents must not make us underrate the great value of frequent washings with injections when rendered necessary by the approach of putrid infection. The number of these washings should depend upon the urgency of the symptoms, and antiseptic injections should not be employed unless we find evidences of fetor, because of one great objection: they do not favor the expansion of the lung.

[Footnote 181: _Loc. cit._]

[Footnote 182: Quoted by Dabney, _loc. cit._]

[Footnote 183: _Boston City Hospital Reports_, 2d Series.]

Cases of long-standing compression of the lung could hardly result in complete re-expansion, but the general health will be recovered and the chest, contracted by approximation of the pleural surfaces from the walls being pressed in or ribs resected, will cease to secrete pus. If fever persists, with diarrhoea, sweats, emaciation, and fetid suppuration, it shows that the washings are not sufficient in number. They can be repeated as often as every three or four hours, to be decreased in frequency as the patient improves. Under frequent washings Feyrot[184] reports favorable results in almost hopeless cases. Time is very precious when these symptoms of exhaustion or septicæmia set in, as it is of the utmost importance that we should endeavor to prevent promptly the absorption of the putrid products, the inevitable effects of which are to produce, before long, fatty and amyloid degeneration of the principal viscera. The most effective way of using detergent fluids is by syphons through two tubes perforated at their extremities and fastened with shields. A Thudicum douche-bottle or a fountain syringe can easily be used by patients themselves as often as is required. The orifice and the tubes should be protected by thorough and rigid antisepticism. As the case improves the cavity gradually gets smaller, the two pleuræ become adherent, and the quantity of fluid lessens until only a small amount flows out. Every eight or ten days we carefully draw out the tubes by degrees, until we have only a little canal beneath the walls. We can thus let the orifice heal slowly, for the sac is obliterated and the patient cured.

[Footnote 184: _Thèse de Paris_, 1876.]

In the hands of Boyer, Delpech, Dupuytren, and Sir Astley Cooper the bistoury gave bad results, but as now used, with all modern appliances and antiseptic precautions, it affords infinite relief and many cures. We claim that by early pleurotomy, with Listerism scrupulously used at every stage of the operation, and if necessary with detergent washings, the mortality from this extremely grave disease can be very materially lessened.

Double Pleurisy.

Pleurisy may occur on both sides at the same time. Double pleurisies are secondary, not primary, and result from rheumatism, or still more frequently, {563} according to Louis, from tuberculosis. In 150 cases of pleurisy quoted by him, there were no bilateral cases which were not produced by rheumatism, gangrene, or tuberculosis. A double pleurisy in a previously healthy person creates a strong suspicion of tubercular origin. There is generally an interval of some days before the attack of one side is followed by that of the other. When effusion takes place the dyspnoea is very great. Death is imminent unless the fluid is withdrawn by aspiration. Maintenon[185] states that the inflammation may be so intense and the fever so high as to destroy life before the effusion is thrown out. The physical signs are the same as in unilateral cases. The effusion is never so great on one side as on the other. The progress of disease is rapid, and the result is almost always fatal.

[Footnote 185: _Thèse de Paris_, 1873.]

Diaphragmatic Pleurisy.

The serous lining of the upper surface of the diaphragm may be involved in an ordinary pleurisy, or inflammation may be limited to it without involving either the pulmonary or the parietal membrane. In this latter case we have modifications of the characteristic symptoms and physical signs. Functional disturbances and special symptoms enable us to diagnose it. There is a febrile movement with occasional delirium, and some of the prominent symptoms, but without the physical signs to indicate the exact locality. The pain is intense, and dyspnoea exists even to the extent of orthopnoea and respiratory anguish, the respiration jerky and convulsive. The pain comes on suddenly in one of the hypochondriac regions, extending up to the attachments of the diaphragm to the costal surfaces. The pain is intense, and increased by full inspirations, by physical efforts, by vomiting, and even by the eructations of wind. The position of the patient attracts attention: as he sits with the trunk inclined forward, he has an anxious and distressed expression of countenance, sometimes accompanied by nausea and vomiting with singultus. Pressure elicits a characteristic tenderness; if applied under the false ribs, it causes suffering. The phrenic nerve is painful on pressure practised over the accessible points of its course, between the two inferior bands of the sterno-cleido-mastoid at the base of the neck. There are also painful irradiations in the cervical plexus above the clavicle and in the scapular region. Pressure over a circumscribed spot of the epigastric region causes a sharp agony of pain. This point is at the intersection of two lines--one, the external border of the sternum; the other, at the osseous portion of the second rib. Guéneau de Mussey[186] has named this the diaphragmatic bottom. This pain extends sometimes to the vertebra and upward to the first intercostal space. Auscultation and percussion at the base of the lung give us some results: impaired expansion of the lung at the base and dulness on percussion; the diaphragm is in a great degree immobile, owing partly to the pressure upon it, and partly to a paresis from inflammation of its upper serous covering (Stokes[187]). When the inflammation is on the right side, we may find an icteroid tint, with vomiting, delirium, etc., with the liver pushed below its normal position in the abdomen. The inflammation of the pleural covering of the diaphragm may be caused by sero-hepatitis extending through the diaphragm (Copeland[188]).

[Footnote 186: _Archiv. de Méd._, 1879, vol. ii.]

[Footnote 187: _Dis. of Chest_, 1837.]

[Footnote 188: _Dict. Med._, vol. iii., edited by Lee.]

If the effusion is confined to the space between the lung and diaphragm, the diagnosis is obscure. There may indeed be cases where we have but few of the symptoms already mentioned. If the fluid is not confined to this portion, but flows into the pleural cavity, it gives great relief, and the result is favorable. Diaphragmatic pleurisy may, however, end in death, either by its discharge into the peritoneal cavity or by constitutional disturbances.

{564} Interlobular and Mediastinal Pleurisies.

The effusion is sometimes confined by adhesions between two lobes. The mediastinal variety is situated between the pleural boundary of the mediastinum and the adjacent portion of the pulmonary serous membrane. It is but rarely met with, and may be diagnosed by local symptoms. The flatness on percussion in the interlobular variety is very circumscribed. Both forms cause local pains, but in the mediastinal variety the pain is very deep and perceptible at the middle of the sternum, and is increased by the respiratory movements. In both varieties there is more or less fever. If either variety exist on the left side, the condition of the pericardium must be carefully examined, as pericarditis may be confounded with it. These limited collections of fluid may burst into a bronchus and be expectorated.

Multilocular Areolar Pleurisies.

Multilocular encysted collections of fluid in the pleural cavity are due to the partitions made by pseudo-membranes which divide the pleura into subcavities. These occur generally in subjects who have had previously dry or adhesive pleurisies. They are more serious than ordinary pleurisies. We meet with them in aspirating, when, after draining off the fluid from the base of the pleural cavity, we find the lung expanding, but above that point there is absence of respiratory murmur and of other physical signs indicating the presence of fluid. Reybard[189] divides multilocular pleurisy into three varieties, with varying symptoms and physical signs, according to whether it exists at the upper, middle, or lower portion, right or left side. Owing to the thickness and distribution of neo-membranes, it is frequently difficult to localize the points of collections of fluid. Aspiration is the most accurate means of ascertaining the exact point and extension of the effusion.

[Footnote 189: _Bullétin Acad. Méd._, 1879.]

Rheumatic Pleurisy.

HISTORY.--The recognition of the fact that we can have local manifestations of rheumatism in the texture of the lung itself, of the bronchi, and of the pleura is of comparatively recent date. There had been indefinite, loose statements, or rather suggestions, in some of the writers in the early part of the century, such as Chomel and Andral, as to the possibility of rheumatism appearing in the pulmonary textures; but we believe that the first definite description of the disease was made by T. H. Buckler of Baltimore in 1865.[190] He claimed that the white fibrous tissue of the bronchi could be the seat of rheumatism, as well as similar textures about the joints. He illustrated his views by cases observed and reported by himself. He showed how, as a result, there were symptomatic engorgements, more or less solid, of the pulmonary parenchyma or rheumatic pneumonia. In 1854, Black[191] found crystalline particles of uric acid and of urate of soda deeply imbedded in the thin white fibrous tissue of bronchi. Buckler showed the metastatic character of rheumatic inflammation in the bronchi and lungs as elsewhere. Buckler's subsequent papers[192] published in connection with this subject, show remarkable success in treatment of fibro-bronchitis and rheumatic pneumonia based upon his views of their pathology.

[Footnote 190: _Fibro-Bronchitis and Rheumatic Pneumonia_.]

[Footnote 191: _Edin. Med. Journal_, 1854.]

[Footnote 192: _Boston Med. Journal_, 1882, and _Amer. Med. Journal_, Oct., 1882.]

SYMPTOMS.--We find rheumatic pleurisy coming on in the course of {565} rheumatic fever with the characteristic mobility of the points of inflammatory action. Laseque[193] gives the symptom with accurate details--the acute pain in the side of the chest without cough or expectoration. He describes the pain as differing from that of ordinary pleurisy, in that the extent of pain is greater and not so limited, due to the fact that the rheumatism invades the aponeurotic tissue which forms the covering to the intercostal muscles. It persists longer and is wider spread. The dyspnoea is caused by the inability to move the respiratory muscles and by the disease invading the aponeurotic centre of the diaphragm.

[Footnote 193: "Pleurésie rheumatismale," _Arch. Gén. de Méd._, 1873.]

The rapidity of the inflammation causes the sudden pain and the accompanying effusion in even a few hours. In a well-defined case recently seen by the writer in a lady forty-seven years of age the rheumatism literally jumped from a large joint to the pleura, giving rise to a severe pain, without cough or expectoration, with an increase of 2° of temperature and 20 beats of pulse. There was a moderate effusion. In forty-eight hours, under the influence of an initiatory dose of quinine (20 grains), followed by free doses of salicylate of sodium, the attack subsided and the friction sound at the base of the lung disappeared. This case did not follow the rule mentioned by Senx,[194] that the disease, upon leaving the pleura of one side, appears in the same manner on the other. It sometimes goes to the pericardium and endocardium from the pleura. Chomel[195] insisted upon the frequent examination of the heart to ascertain whether this had occurred.

[Footnote 194: _De la Pleurésie rheumatismale_, Paris, 1878.]

[Footnote 195: _Art. Pleurésie Dict._, in 30 vols., 1842.]

Rheumatism of the pleura does not always appear and disappear suddenly. It sometimes is gradual in progress and slow in recovery. It usually occurs when we have manifestations elsewhere, but the pleura may be the point first attacked, as is more frequently the case in pericarditis.

DIAGNOSIS.--The diagnostic signs are hereditary or personal tendency to the disease, the character of the local pain, the mobility of the disease, violence of pain and its rapid disappearance, and the existence of profuse sweats. Suppuration rarely occurs.

PROGNOSIS is in its nature serious, not from the intensity of the disease, but from its being a visceral rheumatic affection. It is, moreover, frequently double, and may recur often in the same subject.

TREATMENT is that of rheumatism elsewhere--salicylic acid and its salts, alkalies with opiates. Thoracentesis is rarely indicated, because mechanically the effusion does not seriously impede respiration: if the pericardium be involved, it may be necessary in order to relieve the pleura or the pericardium.

Hemorrhagic Pleurisy.

DEFINITION.--Pleurisy complicated by hemorrhage. Hemorrhagic pleurisy is the union of an ordinarily slight hemorrhage in the pleura with inflammation of that membrane (Laennec).

ETIOLOGY AND PATHOLOGY.--These must be studied together, because the pathology of the disease explains its etiology. While hæmothorax designates hemorrhage into the pleural cavity without inflammation, hemorrhagic pleuritis involves necessarily the idea of inflammation accompanied by effusion of blood, whether this occurs before, during, or subsequently to the inflammation. We cannot assign the name hemorrhagic pleurisy simply because there may be slight red coloration of the effusion. Microscopic researches have shown that all effusions, even the simplest, contain more or less white and red blood-corpuscles. The presence of a certain number of the red discs no more justifies us in calling the pleurisy hemorrhagic than the presence of {566} the leucocytes would entitle us to call it purulent pleurisy. Dieulafoy[196] states that there can be from 500 to 4000 red globules to the cubic millimeter without producing any coloration. They must reach 5000 before they will really attract attention. He says, however, that when the number of red corpuscles reaches 2000 the effusion is "histologically hemorrhagic," because the presence of blood is analogous to the state of engorgement or congestion of the first stage of pneumonia or other phlegmasia, and constitutes a particular phase of pleurisy which must produce purulent matter. The name hemorrhagic pleurisy ought to be used when the number of red blood-corpuscles is sufficient to enable us, by the unaided vision, to detect the presence of blood. We may, however, find a fluid in the pleural sac which is red and yet does not contain blood-discs, but their coloring principle, the dissolved hæmatin. Jaccoud[197] designates this condition pseudo-hemorrhagic pleurisy. Vulpian and Charcot explain the slight discoloration by the presence of hæmatin crystals, which, having been imbedded in the false membranes, escape into the flow of the chest. Nolais[198] included both of these discolored effusions among the varieties of hemorrhagic pleurisies: "Hemorrhagic pleurisies include all those of which the liquid borrows the red coloring matter of the blood." Moutard-Martin (R.)[199] divides hemorrhagic pleurisy into three varieties: simple, as produced in simple, acute, or subacute pleurisy; tubercular; and cancerous. Trousseau[200] considered all hemorrhagic pleurisies as caused by cancer. Beigel[201] states positively that in cancerous pleurisy the effusion is limpid with a yellowish tinge. Walshe[202] held the same views. Nolais, Moutard-Martin (R.), and Fernet satisfactorily demonstrated that such is not the case, but that the hemorrhagic effusion may be simple and independent of any organic disease. It may be produced by acute inflammations of the pleura as well as by cancer of the lung or pleura. It may be connected with pleuro-pneumonia or miliary tubercle. It comes, although more rarely, from fevers, such as measles, and from certain dyscrasiæ due to renal, hepatic, or even splenic lesions. When hemorrhagic pleurisy follows hæmothorax, the blood, after remaining liquid at least one or two hours, initiates the inflammatory action which has, according to Ch. Nélaton,[203] for its object the encystment of the clot. Cornil and Ranvier[204] claim that the cyst is caused by the retracted clot, and that after absorption of the serosity this cyst may become organized. The presence of air causes fetidity of the blood and purulent pleurisy.

[Footnote 196: _De la Thoracentèse par Aspiration dans la Pleurésie aigue_.]

[Footnote 197: "De l'Humorisme ancien comparé à l'Humorisme moderne," _Thèse de Concours_, 1863; _Gazette Méd._, 1860, quoted by Nolais.]

[Footnote 198: _Thèse de Paris_.]

[Footnote 199: _Thèse de Paris_, 1878.]

[Footnote 200: _Clin. Méd._]

[Footnote 201: _Reynolds's Syst. of Med._, 1871.]

[Footnote 202: _Dis. of the Chest_.]

[Footnote 203: _Thèse de Paris_, 1880.]

[Footnote 204: _Path. Anatomy_.]

We may have hemorrhagic effusions occurring simultaneously with acute pleurisy, with pulmonary congestions, pneumonias, and apoplexy of the lung. They are caused by the violence of the inflammation with local plethora, producing a sanguinary stasis--a mechanical result of intense congestion. Moutard-Martin (R.) states that in these cases the red globules come through the walls of the blood-vessels, as do the leucocytes, by diapedesis. Jaccoud[205] admits that the blood-vessels are altered by the inflammation, perhaps also by the derangement in the vaso-motor innervation. The tissue of the pleura is penetrated by both red and white blood-corpuscles, and the blood-vessels and lymphatics are dilated, red corpuscles being found in lymphatics. By far the greatest number of hemorrhagic pleurisies are secondary to pleural inflammations, either resulting from acute causes or from cancerous or tubercular disease, or from diseases causing a dyscrasia of the blood, such as nephritic diseases, hepatic, cardiac, scorbutic affections, or alcoholic excesses. The secondary result of these pleurisies is the formation of neo-membranes, fibrous {567} in their nature, which pathological anatomy shows contain, as they become organized, abundant blood-vessels with thin and brittle walls. A slight exciting cause is all that is necessary to produce their rupture. The primary cause is the false membrane, and, in some cases, vascular granulations, which have rapidly formed, perhaps in twenty-four hours--conditions eminently favorable to the production of hemorrhage. In cancerous, tubercular, and dyscrasial conditions of the blood, the blood-vessels are especially weak and easily give way, owing to the defective nutritive properties of the blood itself, just as, in typhoid fever, we have nasal and intestinal hemorrhage, and in typhus, petechiæ. In 200 cases collected by Moutard-Martin[206] there was found intra-pleural effusion in three-eighths of the cases. Only one-third of that number were hemorrhagic. In 42 cancers observed between 1872 and 1876, 35 were without pleural effusion, 1 only was hemorrhagic. M. Moutard-Martin reports 34 observations of hemorrhagic pleurisy produced by cancer, 19 by tubercle, and 31 following simple pleurisy. Of these last there were 7 cases of effusion complicated with a pneumonia, 3 with a cirrhosis, 6 with a cardiac affection: all except 12 of these cases had some complication. Most of these (12) recovered, so he had not the autopsies to verify his diagnosis. Rayer[207] cites 4 cases of bloody effusion in the pleura occurring in the course of a nephritis. Poutin[208] reports 1 in renal sclerosis. M. Natalis-Guyon[209] reports an epidemic of measles where many infants died of hemorrhagic pleurisy. Marguerite cites 13 cases complicating pneumonia, granulations, chronic pleurisy, small-pox, etc.

[Footnote 205: _Clin. Méd._]

[Footnote 206: _Loc. cit._]

[Footnote 207: _Traité des Mal. des Reins_.]

[Footnote 208: _Soc. Clin. de Paris_, 1879.]

[Footnote 209: _Soc. Méd. des Hôpitaux_.]

Rilliet and Barthez[210] say that it is common to find in infants considerable discoloration of effused serum in variolic and other organic poisons. It seems fair to conclude that hemorrhagic pleurisy may occur in a large number of cases where the blood has undergone alterations, but to produce it, it is necessary that the pleura should have been rendered vulnerable by pre-existing causes, because it ordinarily resists, better than many other membranes, the hemorrhagic tendency. If we admit the existence of tubercular or cancerous hemorrhagic pleurisies, we ought not to consider those as simple which are produced under the influence of the other causes that we have mentioned. The tubercular granulations are deposited either on the pleural surface or in the parenchyma of the lung near the surface, the most frequent locality being in the thickest parts of the organized false membranes. The rupture of their blood-vessels causes the escape of blood into the pleural cavity. The effusion, more or less discolored, rarely exceeds a liter in quantity. Effused blood from cancerous origin may either come from rupture of the vessels in the growths themselves by ulceration, or from the neo-membranes in their vicinity.

[Footnote 210: _Traité des Mal. des Enfants_, t. iii.]

The primitive seat of the cancer is rarely in the pleura, but most frequently in the lung, the cancer being of secondary formation arising primarily from ganglions of the mediastinum. Hemorrhagic pleurisy may be caused by laceration of the newly-formed blood-vessels in the neoplasms by aspiration or by the lung expanding too suddenly. We conclude that hemorrhagic pleurisy is generally owing, directly or indirectly, to vascular neo-membranes which are produced in simple, in tubercular, and cancerous pleurisies.

SYMPTOMS.--The symptomatology of this form of pleurisy does not differ materially from that of other varieties. We cannot attach much importance to the initiatory symptoms nor to the march of the disease. If the quantity of blood be great, we must expect general weakness, pallor, and even fainting. We may have oedema of the walls, as in purulent pleurisy, and exceptionally in serous pleurisy. Ordinarily, however, hemorrhagic pleurisy is more extensive, and limited to the inferior part of the chest, owing to the interference with the venous circulation. If cancerous in its origin, we shall have dyspnoea {568} and violent intercostal neuralgia from pressure of the tumor. When the effusion is formed in the pleural sac, the physical signs already enumerated indicate its presence. Some authors, especially Fernet, Moutard-Martin, Alcoud, and Guéneau de Mussey, attach considerable significance to Bacelli's whisper-pectoriloquy as showing that the effusion is not serous in character. Nolais questions this view, and says that this sound ought to be heard whenever there is blood, whereas they state it is heard only at the base or summit of fluid. When hemorrhagic pleurisy results from tuberculosis, it is never from the ordinary ulceration form, but always from the acute miliary, non-ulcerating variety. We must not, therefore, expect to be aided in our diagnosis by the progress and symptoms of pulmonary phthisis. We may, however, detect uncertain, indefinite symptoms which are hard to interpret as indicative of tuberculosis. The effusion is rarely excessive in this variety, whereas when resulting from cancer it is often very abundant and is rapidly reproduced.

DIAGNOSIS.--We may suspect the presence of hemorrhagic effusions, but only by exploratory punctures can we arrive at certainty of diagnosis. We must bear in mind that we may withdraw with the aspirator-needle some drops of blood at its insertion and at the close of the exploration from the highly vascular neo-membranes or from the lung itself. Having ascertained the nature of the fluid, the differential diagnosis must be made as to the cause, simple, tuberculous, or cancerous. We must study the manner of access of the disease, and especially ascertain if its invasion was violent, with a quantity of blood (d'emblée), or whether it came from the neo-membranes. In the simple variety there are the ordinary acute or subacute symptoms of pleurisy, without any preceding symptoms. In cases of tubercular origin we have to aid us a small quantity of fluid effused and the insidious character of symptoms. In cancerous cases we must expect to find traces of hereditary or of personal taint which may have affected the general health. We must look for cancer elsewhere, and examine carefully to see if there be any tumor of the mediastinum or intra-thoracic pressure, or any infiltration of the lymphatic glands, especially above the clavicle. The fluid drawn in the exploration ought to be examined microscopically, for we may detect evidences of cancer. Walshe[211] cites a case where encephaloid débris was thus discovered. Other authors also give similar cases.

[Footnote 211: _Diseases of the Chest_.]

PROGNOSIS.--This depends upon the nature of the disease producing it. When caused by the newly-formed membranes connected with simple serous pleurisy it is ordinarily not serious, for the mere presence of blood in the pleura has no bad influence over the restoration of health. It is more the intensity of inflammation, with the quantity of blood effused, that indicates gravity of prognosis. Dieulafoy[212] considers the prognosis as unfavorable in the hémorrhagie d'emblée form, drawing the distinction between this and the histologically hemorrhagic. He thinks that every purulent pleurisy was at first hemorrhagic, and the presence of pus shows greater intensity of inflammation. Homolle[213] also states that the pleurisies rich in red globules are ordinarily very acute, and, in consequence of that fact, predisposed to purulence. Purulency is not the sole cause of danger. We fear compression of the lungs, and still more septicæmia. In the tubercular and cancerous forms the prognosis must be very serious. When the hemorrhagic pleurisies arise in the course of organic diseases of the heart, kidney, and liver, they are of grave import.

[Footnote 212: _Loc. cit._]

[Footnote 213: _Rev. des Sci. Méd._, 1880.]

TREATMENT.--If the quantity is excessive, local applications and ergot ought to be employed to arrest the flow. If the dyspnoea and oppression are great, it is best to draw off at least some of the fluid. If the quantity be not large enough to embarrass respiration, we must expect nature to absorb {569} it, or by local inflammation to encyst it. Lacaze[214] reports a case where a fistula was established, and the case was cured. Dieulafoy gives another case where six punctures were made, and no less than 6 liters, in all, were withdrawn. He injected afterward a solution of 4 grammes of sulphate of zinc to 400 grammes of water, and the patient was cured. In the first stage of the disease we use palliatives--morphia hypodermically, bromides, and chloral--if indicated. During febrile symptoms of acute cases we refrain from withdrawal of fluid unless it is excessive. The question of thoracentesis has been discussed in regard to simple pleurisies. The same rules apply, a fortiori, when the nature of the fluid is hemorrhagic. Ordinarily, the abundance of fluid, and the dyspnoea which results therefrom, indicate the operation. We prefer not to draw off the fluid completely--only enough to relieve the embarrassment of respiration--because we destroy the equilibrium of pressure on one side against the neo-membranes and the compressed lungs on the other. Congestion of the lung may thus be produced with albuminoid expectoration. Moutard-Martin (R.) coincides with Dieulafoy in limiting the amount to be withdrawn to one liter. Of course the fluid is slowly aspirated. After part of the fluid is withdrawn, what remains is absorbed, remains stationary, or increases in quantity. We repeat the operation, and slowly draw off greater quantities of fluid if it returns; especially in cancerous cases, where the effusion is often very large, the operation gives great relief. It is rarely large enough in tubercular cases to justify thoracentesis.

[Footnote 214: _Thèse de Paris_, 1851.]

Tubercular Pleurisy.

Tubercular pleurisy may be acute or chronic. It may occur during the course of ordinary tubercular disease of the lung, by extension of the disease from the lung to its serous covering, or it may proceed from tubercular deposit on the pleura independently of any previous disease of the lung. Acute tubercular pleurisy may be dry and situated at the summit of the chest, or may be what is called accidental pleurisy. Dry pleurisy is almost constant in tuberculosis of the lung. Its existence is, in itself, a powerful presumption of pulmonary phthisis, especially when it is situated at the apex. In tuberculosis pleuritic inflammation is lighted up by slight and scarcely appreciable causes. Its commencement is insidious, with little or no pain or fever: indeed, it is with subacute symptoms that the disease slowly advances. The first intimation the patient has of the disease is the impairment of his breathing-power by the presence of fluid. The fluid is not generally in large quantities, and is serous or sero-fibrinous, and sometimes sero-purulent. Latent pleurisy of the older writers was frequently tuberculous in its origin. This form of tuberculosis may precede or follow the deposit of tubercles in the lung-tissue. The tubercles may be deposited to a slight extent in the tissue of the lung, and their presence is shown by an irritating cough only when the pleurisy approaches insidiously. The tubercular granulations over the visceral pleura are extended to the parietal surface also, and notably to the circumference of the fibrous leaflet of the diaphragm--an especial point of elevation for the secondary products.

This disposition of tubercular lesions of the pleura is one of the most striking examples of what is called infection from contiguity, and is a powerful proof of the infective property of tubercular products which from an initial nucleus is propagated from point to point. Acute tuberculosis of the pleura is one of the most common manifestations of acute phthisis. It more frequently causes acute than subacute pleurisy. Chronic tuberculosis almost always produces purulent pleural effusions. It is much {570} more common in infants than in adults, and is sometimes met with in children from three to ten years of age (Barthez et Rilliet[215]). Tubercles may be developed in the intra- or extra-serous membrane. Among old people the tubercle sometimes appears first in the recent false membranes produced by pleuritis (as associated with caseous pneumonia, or genuine tuberculous processes in the lungs), or in connection with tubercles of other organs (Fraentzel[216]). The advance of this disease is habitually slow, or at least not accelerated by the development of other tubercular diseases. The diagnosis is often accompanied with great difficulties, for the disease may be confounded with chronic or with purulent pleurisy, especially if these are developed in a tuberculous subject. In both cases we have hectic, night-sweats, emaciation, etc. Thoracentesis alone can give definite results when the effusion is in considerable quantity. When suppurative pleurisy supervenes in tuberculous subjects, the prognosis is very grave. Should the pus be sufficient in quantity to embarrass respiration, it can be drawn off cautiously by aspiration. The open method of drainage and free incisions should not be used, for experience has shown that they injure instead of benefiting the patients.

[Footnote 215: _Mal. des Enfants_.]

[Footnote 216: _Ziemssen's Cyc._, vol. iv.]

Hydrothorax.

From [Greek: hydôr], water, and [Greek: thôrax], the chest.

DEFINITION.--Dropsy of the chest. The accumulated fluid in the pleural cavity which resembles the serum of the blood is not the product of inflammation, but is caused by mechanical obstruction to the circulation or by blood-poisoning. Hydrothorax is never idiopathic, but invariably secondary, resulting from disease, not of the pleura, but of the circulatory system or of the blood itself.

HISTORY.--Before pathological anatomy had been accurately studied, effusions resulting from inflammatory processes in the pleura were confounded with simple hydrothorax, which is not a variety of pleurisy. Royer[217] and Laennec[218] divided hydrothorax into idiopathic and symptomatic; Darwell[219] adopted in a great measure their views. They did not draw the distinction between the passive transudation of serum, constituting the condition known as hydrothorax, and exudations resulting from idiopathic pleurisy. Before physical modes of exploring the chest were used there was great uncertainty in the diagnosis of collections of fluid in the pleural cavity.

[Footnote 217: _Dict. de Méd._, 1832.]

[Footnote 218: _Dis. of Chest_, Forbes's edition.]

[Footnote 219: _Cyc. Pract. Med._]

ETIOLOGY.--Dropsical effusion in the thorax is produced by the same causes which give rise to collections of watery fluid in other serous cavities and in the connective tissue, constituting general anasarca. Primary among the causes is obstruction of the venous circulation in the walls of the chest or in the lungs. Mitral disease, especially insufficiency with dilatation, deranges the normal circulation in the lung and its serous coverings, producing hyperæmia, oedema of the lung, and finally serous effusions into the pleural sac. General dropsy results. According to Fernet,[220] in dropsies resulting from mitral disease oedema of the lungs and hydrothorax always precede all other oedemas. Fraentzel,[221] on the contrary, states that it does not occur until there is no longer any room for the transuded fluid in the deeper portions of the subcutaneous tissues. Other diseases of the heart produce hydrothorax. Whenever there is abnormally high venous pressure, which invariably follows dilatation of the right side after compensatory hypertrophy has reached its limit, and the heart literally yields to the backed current of blood, we must expect dropsical results. Intra-thoracic tumors, aneurisms, emphysema, and sclerosis of the {571} lung cause hydrothorax by pressing upon the venous trunks and upon the thoracic duct without producing general dropsy. Chronic diseases, such as cancerous disease, chronic malaria, etc., produce great exhaustion and give rise to general hydræmia. Especially is this the case in chronic disease of the kidneys, such as the several varieties of nephritis and amyloid degeneration, where there has been a loss of albumen for a long time and the blood-serum has been rendered poorer in solid constituents. Hydrothorax is not a disease, but a symptom resulting from a variety of causes which produce physical exosmosis of the serum of the blood.

[Footnote 220: _Nouveau Dict. Méd._, vol. xxviii.]

[Footnote 221: _Ziemssen's Cyc._, Amer. trans., vol. iv.]

PATHOLOGICAL ANATOMY.--Hydrothorax being merely dropsy of the thoracic cavity, there is no lesion of the pleura. There is a collection varying from 100 grammes to many liters of fluid in the cavity. It differs from the effusion in subacute pleurisy in its small quantity of fibrin, in having far less of albuminoid material, and no white blood-corpuscles. The water collects almost always in both sides of the chest, more on the side on which the patient lies in bed. In the recumbent position the fluid gravitates posteriorly more than the effusions of pleurisy. In the upright position it will follow Ellis's curved line more regularly than in effusions resulting from pleurisy, for there are no adhesion-bands interfering with its doing so. The fluid is limpid, of a light-yellow or citron color. Its composition resembles that of the plasma of the blood, but it contains more water and less of the constituent elements. Alex. James[222] found that the amount of mineral matter was the same in dropsical fluids in all parts of the body, and that the organic albuminoid substances were larger in quantity in the pleura than in any other cavity. The amount of organic substances varied directly in accordance to the degree of pressure on the different capillary vessels. The anatomical changes in the pleura and the subpleural connective tissue are similar to those found in other collections of dropsical fluid. They are swollen and thickened by maceration with water. They become opalescent and less firm of texture. The lungs retract as the fluid increases in quantity. As the filtrates collect in both pleural sacs, the lungs do not forcibly collapse. The patient would sink at once were this the case. The arch-tension of the diaphragm is but rarely overcome, and consequently we must not expect to find the liver and spleen pushed down, especially when there is fluid in the peritoneal cavity. The position of the heart, unless there is a marked difference in the collections of the two sides, is but little altered, the retractive force of both lungs being impaired.

[Footnote 222: _Med. Times and Gazette_, Jan., 1880.]

SYMPTOMS.--The general accumulation of watery fluid is not attended by any pronounced symptom until it has reached the point of interfering mechanically with the normal play of the lungs. At first dyspnoea is only perceptible on increased physical exercise. When the quantity is excessive, the individual suffers when perfectly quiet. The patient, until the fluid is excessive, lies on his back as the most comfortable position, but as the quantity increases he is often obliged to sit up in bed.

The dyspnoea is ordinarily much more oppressive than in pleuritic effusions, because both lungs are compressed. There is no rise of temperature, no pain in the side, no tenderness on pressure, no acceleration of the pulse, and but rarely any cough, as there is in pleurisy. The dyspnoea often becomes very painful, and may even produce orthopnoea, being accompanied by short and frequent acts of breathing. Where there are very large amounts of fluid the mechanical interference with the breathing is so great that cold sweats, cyanosis, and asphyxia follow, the pulse becoming smaller and more feeble until the patient dies.

The physical signs are, in general, the same as those of pleuritic effusions, especially the subacute form, with some slight variation. Inspection {572} and mensuration do not aid us as in pleurisy, for in hydrothorax the accumulation of fluid is bilateral instead of unilateral. The tension is not sufficient to dilate the walls of the chest. Palpation shows absence of vocal resonance, but not invariably, for we are unable to compare the two sides. We must remember that we have oedema of the walls of the chest, which would partially prevent the thoracic vibrations from being felt. Percussion flatness is not as absolute as it is in pleurisy, unless the fluid is in excessive quantity, for the tension of the fluid is feebler and the lung contains more air. The lung is never completely compressed, as in pleurisy, there being no fibrinous bands to constrict it. The percussion vibrations, unless very lightly made, are communicated to the lung; and so there is dulness instead of flatness. The absence of fibrinous bands permits the fluid to change its position with the varying postures of the patient. This rarely occurs in pleuritic effusions after the first few days. Finally, Skodaic tympanic resonance at the apex is but seldom met with in simple hydrothorax.

Auscultation.--The presence of fluid between the lung and parietes prevents us from hearing the vesicular murmur. The distant bronchial respiration is rarely heard in hydrothorax, as it is in pleurisy, because the lungs are not completely deprived of air, and when present is less intense. Ægophony is frequently heard over the upper limit of the fluid, the whispering voice being transmitted through the fluid. Owing to pulmonary oedema there are subcrepitant râles, but never pleuritical friction sounds.

DIAGNOSIS.--Ordinarily, the diagnosis ought to be made without difficulty. The only disease with which there can be any danger of confounding it is subacute pleurisy. The principal points of differential diagnosis have been enumerated above. In subacute pleurisy (latent pleurisy) we have, in less intensity, the ordinary pleuritic symptoms. The pleuritic friction murmur is present, and a fluid containing the products of inflammation. Very exceptionally is subacute pleurisy double, whereas hydrothorax is almost invariably so.

The history of the case enables us to arrive at an accurate diagnosis. The withdrawal of a small quantity of fluid with a fine perforated needle, and its chemical and microscopical examination, will complete the diagnosis in doubtful cases.

Oedema of the lung can scarcely be confounded with hydrothorax. The absence of the physical evidences of water in the cavity, and the crackling sound heard in auscultation, are distinctive of oedema.

PROGNOSIS.--The prognosis is always serious, but it depends upon the nature of the disease producing the dropsy. If this can be removed, the collection of water may disappear. But, unfortunately, the circulatory diseases which produce it are generally chronic and incurable. The fluid can, by general treatment and mechanical means, be reduced, and the life of the patient prolonged and made comparatively comfortable. Sooner or later a large number of cases must succumb.

TREATMENT.--The treatment should first be directed to the primary disease causing the dropsy. If heart disease be the promoting cause, we must, by means of digitalis, endeavor to promote compensating hypertrophy, and by arsenic and iron improve the quality of the blood. If Bright's disease be the cause, the skimmed-milk diet, with iron and manganese, must be given with remedies which lessen the hydræmic condition of the blood. Digitalis, diuretics, jaborandi, and drastic purgatives give decided results. Of all purgatives, elaterium in decided doses (¼ grain), guarded by conium or hyoscyamus, causes most relief by producing free watery stools. Mechanical means must be resorted to without hesitation. It is best first to remove the fluid from the lower extremities by the insertion of Southey's capillary canula with caoutchouc tubing attached. Large quantities of water may {573} thus be drawn off without local irritation, erysipelatous in its nature, being produced. Thoracentesis by aspiration averts death very often, and gives the greatest possible relief when the effusion is large enough to produce dyspnoea. In a case under the author's care life was prolonged many months and large quantities of fluid were removed. Altogether, there were twenty-two operations and 1563½ ounces of water removed. As often as every week one or other side had to be emptied, the quantity removed each time varying from 49 ounces to 112 ounces. For two months previous to death filtrates collected in the abdominal cavity also, and had to be frequently withdrawn.

Pneumothorax.

DEFINITION.--A collection of atmospheric air or of gas in the pleural cavity. Pneumothorax ([Greek: pneuma] and [Greek: thôrax]).

In ancient times gaseous collections were frequently noticed in serous cavities, especially on opening the chest for empyema and at post-mortem examinations. The presence of air resulting from laceration of the lungs by fractured ribs was known and designated as emphysema thoracis. Air in the pleura was considered as an accidental complication which occurred with empyema or as formed after death. Morgagni and others mentioned the presence of gas as formed in the pleural cavity. Itard[223] was the first to speak of it as a disease and to name it pneumothorax. Owing to the imperfect knowledge of pathology at that period, he attributed the production of the air to the decay of the lung from chronic suppuration, and to the decomposition of the long-retained pus. Laennec was the first to give an accurate anatomical and clinical account of the disease.

[Footnote 223: _Thèse de Paris_, 1803.]

HISTORY.--Pure pneumothorax--that is, pneumothorax caused by the presence of air alone in the pleura--is but rarely met with, except for a short time, when it has been introduced from without by traumatic injuries. The irritating effects of gas, unless it comes in small quantities through the ribs from wounds in the chest-walls, are very frequently followed in a short time by the production of a quantity of serosity or of pus. If air is introduced into the pleural cavity from perforation of the lung, there is also liquid matter from the lungs of such a character as at once to provoke inflammatory action. Such a condition is then denominated hydro-pneumothorax or pyo-pneumothorax. The latter was, in fact, recognized by Hippocrates by the sign of succussion, though not so designated.

ETIOLOGY.--Laennec divided pneumothorax into three distinct varieties: 1st, essential pneumothorax, resulting from the spontaneous formation of gas in the pleural cavity; 2d, pneumothorax from putrid decomposition of liquids effused into the pleura; 3d, pneumothorax by perforation, due to rupture into the pleura or to an accidental opening by which atmospheric air or gas from the lungs is introduced into the pleural cavity. This division, having Laennec's high authority, was for a long time generally received. It has now been established that the pleuræ cannot secrete air.

Proust[224] collected 25 cases of so-called spontaneous pneumothorax, and showed that they could all be otherwise satisfactorily explained. In some cases errors of diagnosis had been made by mistaking tympanitic sonority at the anterior-superior portion of the chest, or the existence of the amphoric breathing found in pleurisy, for pneumothorax. Some were cases of pneumonia in which tympanitic percussion resonance deceived observers. Then, again, there was found, among the cases cited, pneumothorax resulting from rupture of a tubercular cavity or of a hydatid. In tubercular cases Proust found that the orifices made were so small--no larger, as Gairdner of {574} Edinburgh had stated, than a pin's point--that they could not be detected, or that they had cicatrized before the post-mortem examination, or perhaps closed by adhesive false membranes. Other investigations by Ewald[225] and Jaccoud[226] have confirmed Proust's views that essential pneumothorax does not occur. Researches in pathological physiology disprove the possibility of a serous membrane producing a secretion of gas or of its passing from the blood through the capillary walls. We therefore conclude that pneumothorax from secretion of air within the pleura is contrary to physiological facts generally accepted, and is disproved by pathological investigations.

[Footnote 224: _Ibid._, 1862.]

[Footnote 225: Quoted by Fraentzel, _Ziemssen_, vol. iv.]

[Footnote 226: _Gaz. hébd._, 2^{ème} serie, 1864.]

The second variety in Laennec's division--namely, where the gas results from decomposition of fluid in the pleural cavity--has been supported by such high authorities as Hughes Bennett, Townsend, Wunderlich, and Jaccoud. Yet it is difficult to understand how it could occur. The contact of air appears to be necessary for the decomposition of serum and pus in the pleural cavity. While shut up in a cavity coated with neo-membrane, a fluid may certainly remain undecomposed for a long time, and undergo decomposition as soon as taken out of the cavity. Recent researches in regard to putrid fermentations appear to confirm the view that the presence of air is absolutely necessary to produce that effect.

We believe, therefore, that perforation, with rupture of the visceral or parietal layer of the serous membrane, causing the introduction of air into the pleural cavity, is the invariable cause of pneumothorax and of hydro-pneumothorax. The causes of the rupture are in the lung, in the pleura, or in the adjoining organs. They may be traumatic or non-traumatic: the latter may be perfectly designated pathological causes, because the pneumothorax is always secondary, following upon a pre-existing pathological condition.

Traumatic pneumothorax may take place in consequence of an injury to the thoracic walls, of an exterior injury, or of a penetrating wound. The parts may be so bruised that pleural necrosis gives rise to sloughs and resulting openings. Fracture of ribs may tear the lungs, and allow air to enter the connective tissue and produce local emphysema. Violent contusions, as in a case recently observed by the author, produce laceration of the lung without the rib or costal pleura being injured.

Non-traumatic or Pathological Causes.--Laennec taught that pulmonary tuberculosis was the most frequent cause of pneumothorax; and further observation has demonstrated the correctness of this view. Walshe states that such is the case in 90 per cent. of the cases of perforation of the lung. In 131 observations reported by Saussier,[227] 81 were from pulmonary phthisis, principally from caseous pneumonia. Fraentzel[228] says, from his own observation, that 90 out of 96 cases of pneumothorax are produced by vomicæ on the surface of the lungs in the course of caseous pneumonia. Grisolle states that nine-tenths of the cases result from rupture of a lung-cavity. Fuller[229] reports 22 cases, in 18 of which the disease was produced by tubercular ulceration. Chambers,[230] at St. George's Hospital, reports that 21 out of 23 were tubercular. Fernet[231] states that pneumothorax results in nine-tenths of the cases from some of the forms of pulmonary phthisis.

[Footnote 227: _Thèse de Paris_, 1841.]

[Footnote 228: _Ziem. Cyc._, vol. iv.]

[Footnote 229: _Dis. of the Chest_, p. 226.]

[Footnote 230: _Dec. Pathologicum_, cap. v. sec. v.]

[Footnote 231: _Nouveau Dict._, vol. xxviii.]

Ordinarily, pneumothorax is unilateral; only exceptionally is it met with on both sides. In tubercular cases it is twice as common on the left side as on the right (Condrin[232]). In the total of 146 cases reported by Louis, Walshe, and Powell, 94 were on the left side; whereas when it is consecutive to a pleuritic effusion it is almost always on the right side--17 out of 18 (Saussier[233]).

[Footnote 232: _Thèse de Paris_, 1882.]

[Footnote 233: _Ibid._, 1841.]

{575} In tubercular cases perforation of the lung may occur at any period of the disease; the most frequent time, however, is that of the softening or while excavations are being formed, where adhesions have not yet protected the two sides by binding them together with neo-membranes. It may come from a small cavity. Andral met with cases where only a few tubercles existed. Townsend reported a case where one tubercle burst immediately under the pleura. The superior lobe of the lung is where the perforation generally occurs, because it is there that the tubercular lesion ordinarily commences and is most advanced (Louis). It is least frequent in chronic fibroid phthisis and most often met with in acute pneumonic phthisis. Douglass Powell[234] reports cases where sinuses extended from cavities, and finally burst into the pleura. Sometimes the rupture occurs at the base of the superior lobe, about the third or fourth rib; it may happen, however, at any point of the lung; it has even occurred at the base of the lung lying on the diaphragm (Houghton[235]).

[Footnote 234: _Med. Times and Gaz._, Jan. and Feb., 1869.]

[Footnote 235: _Cyc. Pract. Med._, vol. iii.]

Saussier[236] shows by the following table the relative frequency of the principal causes of pneumothorax in 131 cases:

Pneumothorax with phthisis . . . . . 81 " " empyema . . . . . 29 " " gangrene . . . . . 7 " " pulmonary emphysema 5 " " apoplexy . . . . . 3 " " hepatic fistula . 2 " " hydatids . . . . . 1 " " hæmothorax . . . . 1

[Footnote 236: _Thèse de Paris_, 1841.]

Empyema ranks second as a producing cause of pneumothorax. Ordinarily, by direct necrosis of the parietal pleura, an orifice is made through which the pus is evacuated through the bronchi, and air in inspiration enters the pleural cavity by the bronchial fistula. Pyothorax is converted into pyo-pneumothorax. The valvular opening may, however, be closed by inspiration so that air cannot enter, or adhesions may limit a portion of the pleura, and then we have a circumscribed pneumothorax. Empyema, by producing ulceration of the thoracic walls and pointing exteriorly (emphysema necessitatis), leaves fistulæ through which air enters the pleural cavity.

Gangrene of the lung by sloughs allows air to penetrate. Bronchiectasic cavities sometimes become the seat of putrefactive changes and ulcerations through the lungs into the pleura. Infective emboli being arrested in the smaller peripheral branches of pulmonary arteries, air enters the cavity; it is thus that pneumothorax arises in various kinds of surgical diseases when infective emboli pass into the circulation (Fraentzel). Flint[237] reports a well-marked case of pneumothorax, lasting less than one month, where there was every reason to suppose that it had been caused by rupture from interstitial emphysema. W. T. Gardner had previously reported a similar case. Saussier found emphysema was a cause in only 5 out of 131 cases. Fraentzel speaks of emphysema as rarely being a cause. Perforation of the oesophagus, ulcerative, cancerous, or traumatic from the use of bougies, produces pneumothorax. Suppurating bronchial glands--a case of which was met with by the author--bursting into the cavity produce pneumothorax. Hydatids of the lungs, abscesses of the abdomen, sometimes coming even from the cæcum and from the liver, burst into the pleural cavity and introduce air. Echinococcus cysts of the liver are occasionally emptied into the pleural cavity.

[Footnote 237: _Practice of Medicine_, ed. 1881; _Series of Amer. Clin. Lectures_, article "Pneumothorax," 1875.]

{576} Pneumothorax is more than four times as frequent in men as in women. One-third of the whole number of cases occurs in persons between the ages of twenty and thirty years; one-tenth between the ages of ten and twenty; one-twelfth between thirty and forty (Saussier[238]). Although pneumothorax has a number of exciting causes, yet they are all comparatively rare except pulmonary tuberculosis and purulent pleurisy.

[Footnote 238: _Thèse de Paris_, 1841.]

PATHOLOGICAL ANATOMY.--In traumatic pneumothorax and simple cases, such as from the bursting of emphysematous alveoli, the presence of air is the only pathological product. If the pleura and adjoining organs are not diseased, the rupture or tearing cicatrizes rapidly, and the air disappears in a few days by absorption. If a quantity of air be admitted, the pneumothorax may last for months; yet if the pleura is healthy, the air itself will not produce local changes. If blood or morbid products flow in with the air, then inflammatory changes occur, and we have deleterious products effused. Demarquay and Leconte[239] demonstrated the innocuousness of introducing air into healthy pleural sacs of dogs, having injected it repeatedly into the same dogs without any unpleasant result. These observers analyzed the air after it had remained in the chest, and confirm Davy's[240] researches as to the changes in its condition. The oxygen diminished gradually, and finally disappeared, while carbonic acid replaced it to nearly the same amount. This air from the pleura approximated in composition to the air of expiration. When blood and bronchial secretions with pus are thrown into the pleura, they promptly produce more serious results, especially intense suppurative pleurisy. Duncan[241] found in a case of pyo-pneumothorax a fetid gas to contain 26 parts of sulphuretted hydrogen and carbonic acid and 74 parts of nitrogen. Secondarily, lesions are produced--hydro-pneumothorax and pyo-pneumothorax. In other cases, the pleura having been previously the seat of chronic disease with purulent effusion, this latter undergoes fetid changes and septicæmia results. Under these circumstances the pathological changes are similar to those we have described as found in empyema. We find like increase of tissue-formation, of pus, and of the development of the gases, sulphuretted hydrogen and sulphydrate of ammonia, which give rise to a horrible fetidity. The quantity of air varies very much, as does the amount of fluid: there may be a small quantity of air and much fluid, or the reverse.

[Footnote 239: _Gaz. Méd._, 1864.]

[Footnote 240: _Phil. Trans._, 1823.]

[Footnote 241: _Edin. Med. and Surg. Journal_, 1827.]

The opening into the pleural cavity may be direct or oblique: if direct, it remains open; if oblique, it is generally more or less valvular. The symptoms, prognosis, and treatment vary accordingly. Through a patent orifice the air enters in inspiration, and goes out with the expired air from the lungs. As it cannot accumulate, there can be no positive air-pressure within the pleura. If, however, the orifice be valvular, although the air enters it does not escape, for it presses upon the valve and closes it. If the valvular fold be perfect, the air soon becomes excessive in quantity, and exerts dangerous pressure upon the lung and adjacent organs. By means of a trocar, attached by tubing to a water-pressure gauge, Douglass Powell[242] ascertained post-mortem the degree of intra-pleural pressure present in 16 cases of pneumothorax. In 4 out of these cases the pressure was nil. In 12 there was more or less intra-pleural pressure present, varying in degree from 1¾ to 7 inches of water.

[Footnote 242: _Medico-Chir. Trans._, 1876.]

Unless the lung be mechanically prevented, the entrance of air into the pleural cavity at once produces a retraction of the lung, owing to its elasticity. There is no compression of the lung unless the air is increased in quantity by each inspiration, and, having no exit, accumulates; then the lung may be forced against the spinal column and the residual air actually {577} forced out of the alveoli. Powell[243] questions whether the intra-thoracic pressure excited in pneumothorax is ever equal to what is sometimes the case in pleurisy: the highest he had ever met with in pneumothorax was 7 inches of water. Garland,[244] in repeating Damoiseau's experiments in testing the effects of the introduction of air into the pleural cavity, found that the air did not penetrate between the lung and the lateral chest-walls until the lower border of the lung had retracted upward the distance of several ribs.

[Footnote 243: _Loc. cit._]

[Footnote 244: _Loc. cit._]

One of the most pronounced effects constantly observed in pneumothorax is the immediate displacement of the heart to a greater extent than in pleurisy. Gaidy,[245] as far back as 1828, described displacement of the heart as an important sign of pneumothorax. He related a case where, at the moment of the perforation, the woman was conscious of the heart's beat having been transferred to the right of the sternum. Powell[246] out of 17 cases found the heart displaced in 16: in the seventeenth the unruptured lung was so consolidated that it could not collapse. In pneumothorax of the right side a careful examination is sometimes required to detect the displacement of the heart. The apex can be discovered at a considerable distance to the left of the nipple, with the right ventricle drawn to the left edge of the sternum. It has been generally believed that the cause of this displacement was the intra-pleural pressure of the air, but this does not satisfactorily explain it, for there can be no pressure until the elasticity of the lung has been overcome. In 13 of Powell's cases there was great displacement of the heart with different degrees of intra-pleural pressure. In 3 cases there was great displacement of the heart with no intra-pleural pressure. The same author[247] showed, experimentally, that the elastic tension of one lung, when unopposed by that of the other, was sufficient to draw aside the mediastinum, and with it the heart. He thus demonstrated that these displacements are by no means necessarily a sign of intra-pleural pressure, since they may occur to the right of the sternum without there being any pressure. Clinically, we know that the admission of air into the pleural cavity immediately and constantly displaces the heart, unless the opposite lung be consolidated or otherwise injured in its resiliency. This occurs even when the patent orifice of the perforation prevents the accumulation of any quantity of air. There is not enough air to produce direct pressure, but there is enough to impair the elastic traction of the lung, and thus to destroy the equilibrium of traction which keeps the heart in its normal position. The healthy lung by its unimpaired tractile force immediately draws over the heart. Skoda[248] maintains that "air does not enter the pleural cavity simply at the cost of the torn and retracted lung, but the sound lung also retracts to such a degree as to move the mediastinum." Garland's experiments[249] conclusively demonstrate that the air in pneumothorax is powerless to exert an appreciable lateral displacing force until the lung has completely collapsed; and this does not ordinarily occur. There can be, he says, but one cause of constant and early displacement of the heart--the elastic force of the opposing lung, which draws it over to itself. He adds that "the explanation of the greater displacement of the heart in pneumothorax is that the air, having practically no weight, cannot exert upon the heart the negative pressure which an effusion evidently would."

[Footnote 245: _Arch. Gén. de Méd._, tome xvii., 1828.]

[Footnote 246: _Medico-Chirurg. Trans._, vol. lix.]

[Footnote 247: _British Med. Journal_ and _Med. Times and Gazette_, July, 1869.]

[Footnote 248: _Auscultation and Percussion_, Eng. trans.]

[Footnote 249: _Loc. cit._]

The fluid in hydro-pneumothorax is very rarely of a serous character. Saussier found but 1 such example in 169 cases. It is almost always purulent pneumothorax, and frequently it has a very offensive fetid odor from putrid decomposition. Mixed with pus there are sometimes found masses of {578} pseudo-membranes, débris of lung, and gangrenous patches, as in purulent pleurisies. The fistulous orifice through which the air has entered is not always easily found, being often hid away among false membranes. It is small and tortuous, and can only be discovered by placing the lung under water and blowing air through the bronchial tubes. Sometimes the orifices close and the air becomes encysted, interlobular, or diaphragmatic. There is sometimes only one opening; again, there may be several. Nolais reports a case where there were six openings. Orifices with lacerated edges are met with, varying in length from one to ten or twelve centimeters. It must be borne in mind that perforation can take place without producing pneumothorax. Saussier found this occurred in 2 out of 74 cases, and in 8 out of 29 resulting from pleurisy. Fériol and Guéneau de Mussey give similar cases.

SYMPTOMS.--The initiatory symptoms of pneumothorax vary according to the cause which produces it. When the effusion of air into the pleural cavity is from perforation of a diseased lung (most frequently tuberculous, more rarely gangrenous or from an abscess), the first symptom is a sudden agonizing pain in the side, accompanied with dyspnoea amounting almost to suffocation. In rare instances, where strong old adhesions limit the pneumothorax, there may be only slight pain, without dyspnoea. The rush of a moderate quantity of air into the cavity causes the lung to collapse; but should the amount of air be excessive, it will render the symptoms of oppression most intense, for it will compress the lung and heart and obstruct the capillary circulation in the lung. Such must be the case, for there is no aspiration of blood from the large veins, and no aëration of blood in the lung. The patient often feels as if the chest were being torn away, and the expression of his countenance betrays distress and alarm. If the orifice be large and valvular, preventing the escape of the air, the air accumulates rapidly and completely forces the air out of the lungs, and death shortly follows, sometimes in a few hours. There is no rise of temperature or fever. On the contrary, the temperature very frequently falls one or two degrees below the normal in consequence of the sudden collapse, the pulse from exhaustion being very frequent and feeble, accompanied by cold sweats. The voice becomes exceedingly feeble and whispering. In many cases the patient does not sink at once from the shock of the perforation, but becomes less oppressed, although he suffers considerably, being unable to lie flat in his bed. Respiration is not only frequent (sometimes 60 per minute), but the dyspnoea is oppressive and distressing to witness. Fever follows invariably, and sometimes with great rapidity, caused by pleuritis. When this occurs, the patient again suffers from dyspnoea as the purulent fluid accumulates in the pleura and gradually dropsy comes on. These cause dyspnoea and cyanosis. The position of the patient, leaning forward, supporting his elbows on his knees, indicates his agony and difficulty in breathing; the pain appears to go through and produce local hyperæsthesia, and the patient dies from the empyema with hectic and oedema of the lungs. The pleurisy excited may be simply serous in its products, even when it is tuberculous in origin. Usually, however, it is purulent, and we must then expect to find the grave symptoms we have enumerated in speaking of empyema with hectic and septicæmia.

PHYSICAL SIGNS.--These are well distinguished and marked, and lead easily to its diagnosis. Inspection shows the side to be immovable and the dilatation permanent; the spaces between the ribs are obliterated and the shoulder raised. There is no rhythmical expansion and contraction of the walls of the chest, the diaphragm is not elevated, and the liver and stomach are kept down. Air continues to enter the cavity, until the quantity is so great that its tension is equal to the atmospheric pressure. The contrast between this condition and that of the healthy side is very great. In the former the breathing is labored, with painful muscular contraction in the walls and whole side. {579} Percussion over the chest gives a hyper-resonant sound, with a graver-pitched tympanitic resonance. There is but little sense of resistance to the finger, owing to the elasticity of the contained air. When fluid is secreted in the second stage we have absolute flatness at the base over a horizontal level, and tympanitic resonance above. The pitch of this last sound varies according to the tension of the gas contained in the chest and the correlative tension of the thoracic walls. If this tension be feeble, the pitch is higher; if it be extreme, the tone will be drum-like, muffled, acute, and the tympanitic character will be less easily perceptible. It may happen that the pitch will be so high that we may be misled and think there is flatness. It is not true flatness, but a clean and high-pitched sound, very different from the tympanitic sound usually found; it is sometimes remarkably metallic in character. With auscultatory percussion, using a solid pleximeter, we have the prolonged metallic resonance which Trousseau appropriately named the bruit d'airain.

The area of hyper-resonance and flatness on percussion is changed with the altered position of the patient. The fluid, obeying the law of gravitation, takes its hydrostatic level, and when the patient's chest is upright is horizontal. Hyper-resonance is often pronounced over the sternum, and sometimes infringes upon the healthy side. When the disease is on the left side it obliterates the normal dulness over the cardiac area.

Palpation.--Thoracic vibrations of the voice are not felt over the portion of the chest containing air, nor over that containing fluid. This absence of vocal fremitus is very characteristic. The hand detects that the heart has been displaced toward the sound side and that the abdominal viscera are pushed down.

Auscultation.--The auscultatory phenomena vary according to the cause of the pneumothorax and the size and direction of the orifice. In tubercular cases, where perforation has produced a large, free opening, as the air passes in and out of this large pleural cavity with firm walls (the lung having collapsed perhaps to one-third or less of its normal size), we have the physical conditions which give marked amphoric and metallic respiratory sounds, with absence of respiratory murmur. The amphoric breathing is of greatest intensity near the point of perforation, which ordinarily is at the mammary or upper scapular region, and is found in both inspiration and expiration. The cough and the whispered voice give the characteristic metallic quality. There is also metallic tinkling produced by droppings of fluid in the cavity, by the shaking of the body, or by vocalization. Even when the orifice in the lung is closed we may have amphoric echo, from sounds produced in the bronchi, and passing through a cavity filled with air. The intensity of these sounds varies in different cases. Sometimes they are very loud; in other cases they are feeble and seem distant from the ear. The fine metallic tinkling may be heard at one moment and disappear at the next. These amphoric and metallic sounds, heard at different points, are characteristic of pneumothorax with free openings. When, however, the orifice from tubercular perforation is small, oblique, or valvular, the respiratory murmur is inaudible, except perhaps at the very apex of the lung, and we cannot perceive any adventitious auscultatory phenomena beyond a faint, distant, hollow sound.

There is, in both kinds of orifices, the well-known splashing Hippocratian succussion sound on shaking the chest. The latter is pathognomonic of hydro-pneumothorax, and is sometimes heard when no other sign is present. The hands applied over the surface of the chest feel the fluctuations of the fluid striking against the interior walls. When pneumothorax follows purulent pleurisy we do not find immediately the pronounced symptoms nor the physical phenomena heretofore described as occurring when it is produced by rupture from the lung into the pleural cavity. The condition {580} of the parts is very different. Pus is present in considerable quantity in the cavity, and the ulceration of the costal pleura and the soft walls of the chest allows the fluid to flow outward and air to enter the cavity. Or there may be necrosis of parietal pleura into a bronchus and consequent discharge of pus through the mouth. The lung is already disabled. The violent pain in the side and the dyspnoea are no longer found. Indeed, the exact time of the rupture and commencement of the discharge is frequently unknown to the patient himself. The symptoms of entrance of air into the pleural cavity may not occur for some time. The patient who has had empyema is made more uncomfortable; the discharge through the mouth is offensive, and its quantity and its character call attention to the chest, in which percussion shows the presence of air; auscultation gives amphoric breathing, and succussion demonstrates the presence of air and fluid in the pleural cavity. Very soon, however, the presence of air produces putridity of the secretion, with loss of appetite, fever, diarrhoea, and the other alarming symptoms of pyo-pneumothorax. In some instances the pleura discharges its contents and heals over. There is another variety of pneumothorax, which is ordinarily attended with only temporary inconvenience, and which may soon disappear, leaving the patient no worse than before the attack. This variety of pyo-pneumothorax may be produced by the sudden rupture of emphysematous vesicles, by coughing, or even without any unusual force in the expiratory effort, the alveoli having become extremely thin and brittle by degeneration of their walls. For the minute the pain is violent and the dyspnoea great, but it soon subsides, and in a few days the gas may be all absorbed, unless it is in large quantity. If the pleura is healthy and the lung not otherwise diseased, the rupture may not cause any inflammatory action, fever, or effusion. The rupture may heal over entirely, or if some inflammatory effusion is produced it will probably be rapidly absorbed. In exceptional cases pleurisy may be excited and the case become prolonged. While the air remains in the pleura we have the physical signs characteristic of pneumothorax--displaced heart, as shown by palpation and auscultation, tympanitic percussion resonance, amphoric breathing, and succussion.

DIAGNOSIS.--Ordinarily, there should be no difficulty in diagnosing pneumothorax, no matter how it is produced. We have simply to consider well the already-mentioned modes of the commencement of the disease, and give due value to the characteristic physical signs, especially displacement of the heart, hyper-resonance on percussion, absence of vocal fremitus, amphoric respiration, succussion, and decided shifting of flatness and resonance on change of position. When all these signs are present, each being in itself almost characteristic, there can be but little question. Obstruction of a large bronchus would be followed by absence of health sounds and intense dyspnoea, but we should not have the other physical signs of pneumothorax. Extensive emphysema would produce some of the signs--exaggerated resonance on percussion and enlargement of the side. Emphysema, however, is bilateral, and the resonance over an emphysematous lung has not the same pronounced tympanitic quality as in pneumothorax. The enlargement in emphysema is more under the clavicle; the breathing not amphoric; the normal murmur, although enfeebled, is never completely annulled; and the heart is not displaced. Large superficial pulmonary cavities with firm but thin walls give us several of the physical signs of localized pneumothorax, such as amphoric respiration and metallic tinkling; but the succussion sound is never heard over them. The tympanitic percussion is rarely so pronounced in a cavity as in pneumothorax, and in the latter there is never the cracked-jar sound. In phthisical cavities of large size there probably would be depression instead of enlargement of the chest. The situation will ordinarily enable us to make the differential diagnosis, for localized pneumothorax is almost always low {581} down in the thorax, and the pulmonary cavities but rarely below its middle third. The progress of the case and clinical history would clear up the diagnosis. If a circumscribed pneumothorax was present with phthisis, the diagnosis might be difficult. Powell calls attention to the similarity of some of the signs of acute congestion rapidly supervening at the base of a comparatively sound lung to those of pneumothorax. But in the former the resonance, although high-pitched, is not truly tympanitic, and the heart is not displaced. There is no other disease of the chest where we find in such close proximity the two extremes of percussion sounds--flatness from the secondary effused fluid, and the tympanitic resonance above. If delicate, slight percussion is used, the line of demarcation can be clearly defined; if, however, the force of the percussion stroke be even of moderate intensity, the flatness is mingled with the tympanitic quality, as it is in percussing from the left lobe of the liver to the stomach.

PROGNOSIS.--The prognosis is unfavorable and always uncertain. During the first few days after the rupture of the pleura it is especially bad, though it becomes less so as time goes by. There are cases where the perforation and its results appear to prolong life. "If the opposite lung be healthy, we may hope that arrest of the pulmonary disease may convert the case into one of chronic empyema" (Powell). But, unfortunately, the rupture often occurs when the patient is emaciated and dying of chronic lung ulceration. Cases of pyo-pneumothorax produced in advanced phthisis or by gangrene of the lung are almost invariably fatal. The most unpromising cases at first sometimes prove the least serious, and, again, those that appear at the commencement slight, contrary to expectation, die. Much depends upon the condition of the other lung and the position of the perforation. If the other lung be healthy and the perforation low down, the chances of recovery are better. The progress is most favorable in the cases where the rupture occurs from emphysema. When from purulent pleurisy the discharge passes through a bronchus, the orifice may heal and in due time plastic material be thrown over it, and the air and fluid be left in the pleura. Cases are reported where the orifice remains open and pneumothorax lasts for a long time. Laennec reported one case where the patient lived six years. Fuller[250] reports another where the orifice was open at the end of eleven months, another nineteen months, and another twenty-seven months. We have mentioned Demarquay and Marotte's experiments of the innocuousness of air injected into the pleura. Air is harmless, as they have shown, in the pleura, unless sulphuretted hydrogen or sulphite of ammonia be developed. Fuller says the prognosis is very unfavorable when the effusion is large, with great displacement of the organs. Flint considers pneumothorax occurring as a complication of phthisis as almost hopeless. It is important to ascertain promptly the nature and direction of the opening, whether it be free or valvular.

[Footnote 250: _Diseases of Chest._]

TREATMENT.--This is in a great measure palliative. Hypodermics of morphia or opiates relieve the agony and lessen the shock caused by the perforation. Alcoholic and diffusible stimulants may sustain the heart in its struggle against the effects of dislocation and impaired circulation. Care must be taken not to depress the powers of reaction by too much morphia. Hot water in india-rubber bags applied to the chest gives great relief. Alcoholic stimulants must be given to prevent sinking from exhaustion. When the distension from air is excessive, paracentesis gives marked relief, the lives of patients having been prolonged for days by it. If the opening is valvular, to prevent the air from accumulating in excessive quantity Reybard's protected gold-beater's skin trocar may be used and kept in the chest. Otherwise fine aspirators may be employed, which would seem to be harmless, and the {582} operation be repeated whenever necessary. Larger points and the trocar should never be used, as there is danger of making a permanent fistulous orifice, as well as of injuring some blood-vessels or the lung itself. After the excess of air has been removed by aspiration the affected side should be strapped to control the inspiratory movements on renewal of positive pressure. Anstie[251] recommends drachm ss doses of ether every three or four hours. Fernet[252] recommends inhalation of oxygen. If fluid should compress the chest, some of it must be removed by aspiration, but care must be exercised, for the presence of fluid is conservative in its effects. Its pressure stops up the orifice and promotes its healing. If it becomes fetid, pleurotomy, with detersive washes, ought to be resorted to. Food should be frequently administered, with quinine and cod-liver oil, and good hygienic surroundings prescribed.

[Footnote 251: _Reynolds's System of Medicine_, vol. iv.]

[Footnote 252: _Nouveau Dict. Méd._, vol. xxviii.]

Hæmothorax.

DEFINITION.--Accumulation of blood in the thoracic cavity unconnected with inflammation of the pleuræ.

ETIOLOGY.--Hæmothorax may be caused by traumatic injuries, by the bursting of an aneurism, from ulceration through the walls of the aorta of the vena cava, or from the veins of the pleura. It may be caused by laceration of the intercostal arteries in penetrating wounds. In very rare cases a profuse bleeding takes place in caseous pneumonia or in gangrene of the lungs, and bursts into the pleural cavity (Fraentzel). Cancer of the lung or pleura may, by pressure, produce absorption and destruction of the walls of the blood-vessels, and cause discharge of their contents into the pleural cavity. Sir Thomas Watson[253] reports a case where enormous hæmothorax caused enlargement of the left side, pushing the heart to the right of the sternum from caries of two ribs with ulceration through an intercostal artery. The blood never escapes from the lung into the pleura when there is considerable pulmonary apoplexy.

[Footnote 253: _Practice of Medicine_, vol. ii.]

PATHOLOGICAL ANATOMY.--Blood is found coagulated to a greater or less degree in the pleural cavity, and the lesion producing the hæmothorax can generally be found; the remains of blood may be found even after it has been some time effused. If the hemorrhage does not prove fatal, it may all be absorbed, or it may by its presence cause local inflammation of the pleural membrane.

SYMPTOMS.--The symptoms are those of perforation into the chest--sudden intense pain on the diseased side, with internal hemorrhage, great pallor, feeble circulation, cold extremities, and syncope. Patients often die in a few minutes. If the hemorrhage is moderate in quantity, they revive and the circulation returns, but they complain of feelings of suffocation and oppression. Slowly the general strength returns and the patient recovers.

SEQUELÆ.--Most modern surgeons admit that serious hemorrhages into the pleura come from the thoracic walls, or from the blood-vessels in the neighborhood of the hilum, or from those which accompany the bronchial diseases of the second or third order. Hæmothorax is always consecutive to some primary lesion. Where it is caused by penetrating wounds or by the bursting of blood-vessels in the lungs, air enters the cavity and becomes mixed with the blood, producing a complication in the form of hæmato-pneumothorax. This frequently gives rise to pyo-pneumothorax with a collection of purulent and ichorous fluid.

DIAGNOSIS.--The previous history of the case, together with the characteristic symptoms we have mentioned, enables us to diagnose hæmothorax from {583} pneumothorax, which commences in a similar way. The only other condition likely to be confounded with it is effusion in pleurisy, the physical signs of which are somewhat the same. If the blood remains uncoagulated we shall have absence of vesicular murmur, with dulness on percussion, absence of fremitus, and no friction sound. The introduction of a fine hypodermic needle enables us to be certain of the nature of the fluid.

The PROGNOSIS is always serious. If the cause of the hemorrhage is the bursting of an aneurism, death supervenes in a short time. Hæmothorax, when caused by penetrating wounds, unless they produce hemorrhage, is not necessarily serious. The blood may entirely disappear in a few weeks. Entrance of air with the blood renders the prognosis more serious. Secondary pleurisy is not ordinarily severe unless pus forms.

TREATMENT.--If time is allowed, every effort must be made by local and general treatment to arrest the hemorrhage--ice-bags and hot-water bags ought alternately to be applied to the chest and between the scapula; the patient to be kept in the horizontal position and made to rest quietly; ice taken by mouth; small doses of morphia and large doses of ergotin must be given promptly hypodermically, as the stomach is in no condition to absorb remedies readily. If the accumulation be excessive and continues to embarrass the respiration very much, we recommend free incisions to take out sufficient blood to relieve the pressure and great dyspnoea. Unless danger is imminent, this is a hazardous experiment, as letting in atmospheric air among blood-clots may seriously complicate the condition. Should pleuritis or other complications occur, they must be rationally treated.

Growths in the Pleural Cavity.

Some authors mention various tumors which are rarely met with in the pleural cavity, and which are not peculiar to the serous membrane of the pleura. Among them may be placed sarcomas, fibro-sarcomas, and epithelioma. Their presence in other organs may assist in the diagnosis. Other varieties exist more or less connected with chronic pleurisies. Among these are fibromas, cartilaginous and osseous formations. Rokitansky speaks of lipomas as deposited on the costal pleura. The only varieties which we think it necessary to call attention to are cancer and hydatids.

CANCER OF THE PLEURA.--Cancer of the pleura is not a very rare disease, but ordinarily it is a secondary formation, coming from cancerous disease of the mediastinum, of the lung, or of some abdominal organ. Some authors doubt whether it is primary even in the lungs and mediastinum. It certainly is not often met with as a primary disease of those organs. Lebert[254] had only seen 6 observations, in 447 cases of cancer, involving the mediastinum, the pleura, and the lungs. Walshe[255] reported 29 cases of primitive cancer of the respiratory organs; in 18 cases one lung was diseased with its pleura, and in 13 the right lung. Lépine[256] in 1869 communicated a very curious case of primary cancer of the pleura in a child ten years of age. The right pleural cavity was filled by a white scirrhous tumor. Darolles[257] (1874) reported another example of primary cancer of the pleura, which afterward spread to the lung. Andral, Vidal, and Lebert reported cases where the tumors appeared to develop simultaneously in the pleura and other organs. Primary cancer of the pleura may exceptionally occur, but ordinarily the disease results from its extension step by step, or else distant propagation, from lungs, breast, mediastinum, or the abdominal organs. Most frequently the secondary {584} cancer appears more or less independently of the primitive tumor, and is seen in the form of disseminated points on the surface of one or both folds of the pleura. This propagation of cancer is now generally admitted to be through the intermediary of the lymphatic system; in fact, the lymphatics are themselves attacked by the degeneration, and they are seen, particularly on the surface of the pleura, in the form of white small cords. Some modern pathologists consider that the serous cavities are lymphatic cavities, which can, just as the vessels themselves, serve as ways of generalizing the disease (Cornil and Ranvier, Charcot, Lépine, and Virchow).

[Footnote 254: _Traité Prac. Mal. des Cancereuses_, Paris, 1851.]

[Footnote 255: _Nature and Treatment of Cancer_, London, 1846.]

[Footnote 256: _Bull. de la Soc. Anat._, 1869.]

[Footnote 257: Quoted by Fernet, _Nouveau Dict. Méd._, vol. xxviii.]

PATHOLOGICAL ANATOMY.--Primary cancer of the pleura is ordinarily encephaloid and multiple. Extended infiltration is very rarely found. Lebert reports one case in an infant of seven months. The multiple masses are ordinarily soft and pulpy, varying in volume from the size of a grain of millet-seed to that of a small nut. The aspect is yellowish-white. The juice is rarely pressed out of them. Under the microscope we see large cells and multiple cells with their nuclei. The small granulations or the lenticular masses are flat, resembling drops of wax. We may have solid bodies possessing all the characters of scirrhous, encephaloid, and colloid, grayish, or gelatinous structure. These cancerous productions are generally vascular, especially in the encephaloid variety. Their rupture frequently produces hæmothorax and hemorrhagic pleurisies. The bronchial glands, and finally the cervical glands, often become involved.

SYMPTOMS.--The symptoms of pleural cancer, especially of the smaller and secondary deposits, are often obscure and indefinite. They are not sufficiently definite to attract attention during life. If the masses are scirrhous and large, they press upon the lungs, impede respiration, and give rise to dyspnoea. If the disease is propagated from the lungs or breast, we may suspect cancer where we have a dull pain with some cough. Pain, indeed, is constant, but not violent, unless the nodules excite local inflammation. When scirrhous tumors press upon the intercostal nerves, the pain is very persistent. External pressure over the points gives rise to pain. The dyspnoea increases as the size of the tumor increases. The expectoration is occasionally bloody. The physical signs are sometimes characteristic--dulness on percussion, absence of respiratory murmurs, friction sounds, no vocal fremitus.

DIAGNOSIS.--Generally very difficult. The progress of the disease is ordinarily slow, and follows its development in other portions of the body. Cancerous cachexia, degeneration of the glands above the clavicle, hæmothorax, and hemorrhagic pleurisy, together with dry cough and persistent intercostal neuralgia, are, when present, valuable aids to diagnosis. Extensive caseous pneumonia and pleuritic effusions may be confounded with cancer of the pleura. These tumors may not be at the base, but in the middle of the thorax; dulness may not exist at the base as is invariably the case in pleurisy. The position of the body does not affect the limit of dulness in cancer.

The PROGNOSIS is always very serious, the disease being invariably fatal. In Walshe's cases the duration of the disease was from three and one-half months to twenty-seven months; average duration, thirteen and one-fifth months. One-fourth of his cases occurred between the ages of fifty and sixty years.

The TREATMENT is palliative--opium and other narcotics, and locally chloroform and aconite for the intercostal pains. When effusion results from cancerous inflammation the aspirator may be used to relieve the great oppression caused by the quantity of fluid.

{585} Hydatids of the Pleura.

Trousseau[258] considered hydatids of the pleura a comparatively rare disease. He believed that when found in the cavity it was frequently caused by cysts of the lung which had fallen into the pleural cavity. Vigla[259] mentions 3 cases. Davaine[260] met with 25 cases of hydatids, only 1 of which he believed originated in the pleural cavity. The acknowledged greater frequency of these hydatids in the right inferior lobe of the lung, gives probability to Dolbeau's[261] view that "they frequently proceed from cysts on the convex surface of the liver." Hearn[262] reports 75 cases collected from various observers as intra-thoracic, 15 of which were in the pleura, in the subserous tissue, between the parietal pleura and thoracic wall.

[Footnote 258: _Clin. Med._, vol. i., Philada. ed.]

[Footnote 259: "Des Hydàtides intrathor.," _Arch. gén._, 1855.]

[Footnote 260: _Traité des Entozoaires, etc._, Paris, 1860.]

[Footnote 261: _Thèse de Paris_, 1856.]

[Footnote 262: _Thèse de Paris_, 1875.]

PATHOLOGICAL ANATOMY.--In the greater number of cases, as examined at autopsies in Hearn's reports, the tumor was formed by a voluminous pocket occupying a large part or the whole of the cavity of the pleura. The walls of the envelope were formed of a transparent or slightly opaline and whitish membrane composed of numerous thin layers, containing on its interior surface the echinococci. In the interior of the cyst there was a limpid hyaline liquid with living parasites. Nothing different was noticed in cysts from those found elsewhere, except the absence of the usual adventitious membrane--a fact previously noticed by Davaine. When the cysts are very large they press upon the lung and adjoining organs just as is the case with large effusions in the pleural cavity. The heart, moreover, is pushed to one side, out of its normal position; the lung is compressed and diaphragm depressed.

SYMPTOMS.--The first appearance of cysts of the pleura causes but little disturbance of the functions of the lung. It is scarcely appreciable until it interferes with the play of the other organs. The three prominent symptoms are the pain, the dyspnoea, and the cough. The pain occupies the exact point where the tumor is situated, and radiates from that point. Once developed, it persists with tenacity throughout the duration of the disease. This persistence of the pain is indeed an important characteristic of the disease, and is a sign of value in the diagnosis between hydatids and pleuritic effusions. The dyspnoea increases progressively with the volume of the tumor. The cough is not heard as frequently as when the cysts occur in the lungs. It is dry, and does not cause hæmoptysis.

DIAGNOSIS.--Physical signs must be marked to enable us to distinguish fluid cysts of the pleura from cysts in the lung or effusions in the pleural cavity. When the hydatid tumor has attained sufficient size to cause pain and dyspnoea it generally presses outward the walls of the chest after the lung has been compressed. It does not occupy the base of the cavity, as the effusions do, and the dilatation has a globular form. Trousseau[263] has given several examples in which this shape determined the diagnosis. With this arching of the chest the immobility of the chest is an important sign. Vocal fremitus is diminished or totally abolished, and percussion elicits absolute flatness. These two physical signs assist us in making the diagnosis between hydatids and pleurisy. The auscultatory phenomena, from similar physical conditions, closely resemble those of pleuritic effusions. It must be borne in mind that sometimes hydatid cysts are complicated by pleuritic inflammations, caused by their presence. The diagnosis is unquestionably complicated by difficulties that are not removed unless the cysts burst through a bronchial tube and discharge a transparent and clear fluid in which the microscope shows the presence of echinococci. Such hydatid expectoration is a pathognomonic {586} sign of the existence of an intra-thoracic cyst. Hydatids of the liver may press the diaphragm far up into the pleural cavity without bursting through it. Trousseau maintained that without bursting they may make a passage for themselves through the distended, attenuated fibres of the muscular portion of the diaphragm, for the progress of these cysts is necessarily slow. We must not hesitate to make an exploratory aspiration to determine with certainty the nature of the fluid.

[Footnote 263: _Loc. cit._]

PROGNOSIS.--The prognosis is certainly very serious, but not so bad as when cysts of the same nature are situated in the lungs. Their spontaneous cure may be effected by bursting through a bronchus or even through the walls of the chest. The patient may, however, die from asphyxia during the discharge through the lungs. When not evacuated they may produce death by compression of the lungs.

TREATMENT.--If the disease is recognized previous to its making an opening through a bronchus, it can be treated safely and effectively by aspiration. Bird[264] reports a number of cures by this operation in Australia. Trousseau advises extreme caution, even in regard to exploratory punctures, unless adhesions have taken place between the tumor and the walls of the chest, for he fears the escape of fluid into the cavity of the chest and consequent purulent pleurisy. It is well to remember that this great practitioner was not aware of the innocuousness of capillary punctures and aspiration. If the bronchus has been perforated, we must hope for spontaneous cure. If empyema be caused by the tumor pleurotomy must be used as recommended by Moutard-Martin[265] and Vigla,[266] and constant washing of the pleuræ must be used. This treatment gives us reasonable assurance of success.

[Footnote 264: Quoted by Hearn.]

[Footnote 265: _Purulent Pleurisy_.]

[Footnote 266: _Loc. cit._]

History of Thoracentesis.

Thoracentesis ([Greek: thôrax], chest, and [Greek: chentein], to pierce) is the operation for the evacuation of collections of fluid, serum, pus, or blood from the pleural cavity.

Among the ancients, dating back to the time of Hippocrates, it was practised, and was known as the operatio empyematis. Hippocrates uses the word [Greek: empyon], signifying, literally, an internal collection of pus just above the cavity of the peritoneum, above the diaphragm. Subsequently he speaks of empyema of blood, empyema of serum, empyema of gas, but not of pus, applying the term to the operation, which he employed principally for empyema necessitatis. Subsequently the name empyema was used, as now, to designate a purulent collection in the pleural cavity.

If we may credit the story which has descended from mythological times, the operation for empyema had its origin in an accident. It is related that a certain Phalereus, who was attacked with what was denominated an ulcer on the lungs, was pronounced by all his physicians to have an incurable disease. In his despair he exposed himself in battle so that he might be slain; the enemy's weapon, however, pierced his side, making an opening through which the pus escaped, and he recovered.[267]

[Footnote 267: Cicero, _De Naturâ Deorum_, lib. iii. cap. 28.]

It is certain that from the most remote periods the chest was opened when collections of pus were formed. Galen states that the ancients employed actual cautery for that purpose. He reports that Euryphon de Cinde by this means saved the life of Cinesias, son of Evagoras.[268] The details into which Hippocrates and his school entered in regard to the operation show that it was frequently performed in their day. It is very remarkable that many of the more important precautions in the operation were observed by {587} Hippocrates. We find from the _Aphorisms_ that the operation was considered the only means of cure,[269] and that when these precautions were observed, and the fluid was white and of good quality, the patients recovered.[270] The principal precautions were not to delay the operation after the existence of pus was recognized, and to draw off the liquid. He further states that if the serous fluid in dropsy of the chest or pus in empyema should be drawn off too rapidly the patient would die. So impressed were the disciples of Hippocrates by this view that they adopted the operation of perforating a rib instead of cutting through the intercostal space, because they could with more ease stop up the orifice and regulate the outward flow of the fluid. The later Hippocratians preferred cutting instruments to actual cautery. Hippocrates, if unable to discover the locality of the fluid in the thorax by succussion, applied over the walls of the chest a linen compress which he soaked in earth of Eretria and warm water, and concluded that the collection existed at the points where the earth commenced to dry!

[Footnote 268: _Comm. in Aphor. Hipp._, lib. vii.]

[Footnote 269: _Aphorisms_, lib. vii., Aph. 44.]

[Footnote 270: _Ibid._, lib. vi., Aph. 27.]

When these signs failed, he cut through the most prominent rib at the base of the chest and toward the back. He made a large incision through the rib, but only a small one the size of a thumb-nail through the tissue beneath the rib. After allowing a small quantity of pus to escape, he introduced a tent of undressed flax, with a piece of thread attached to it. This he withdrew twice daily, to allow the pus to flow. At the end of two days he permitted the remaining pus to be discharged, and inserted a tent of linen. To prevent the lung, habituated to the presence of fluid, from drying too rapidly he injected wine and oil through a canula. When the excavated fluid was thin (serous?) he replaced the tent by a tube of tin, and when it ceased to secrete fluid he shortened each day the length of the tube, so that the cicatrization of the wound extended from the inner end of the orifice.[271] The genius of Hippocrates cannot but excite our admiration, as it did Laennec's, who selected as the subject of his thesis "The Doctrines of Hippocrates as applicable to the Practice of Medicine." Can it have been Hippocrates's modes of physical explanation that suggested to Laennec the idea that led to his great discovery of auscultation?

[Footnote 271: _De Morbis_, lib. i. p. 448.]

Hippocrates's operations were made by boring through the rib or with a red-hot iron or a bistoury cutting through the intercostal space. Galen (A.D. 150) had his pyulcon with which to draw out the fluid. Galen and Roger of Parma bored through the sternum. Many of the ancient surgeons, such as Eumphon of Cnidos, Paul of Ægina, Celsus, Solinger, divided the soft parts by caustics and the knife after laying bare the pleura. Blunt instruments were sometimes used, such as sounds. Celsus in his latter years lost confidence in the operation, and it fell into discredit among the Greeks and the Romans, by whom it seems to have been nearly abandoned. In the Middle Ages the question was discussed whether it was better to open the chest by steel or by fire in traumatic pleurisies. Trousseau states that about the sixteenth century the operation of trepanning the ribs was revived. About the same time the detersive injections which had been recommended by Galen were again advocated, especially by Fabrice d'Aquapendente. The operation was unpopular among the greatest surgeons, and but seldom resorted to except in extreme cases. Notwithstanding the servile obedience to tradition in those days, some important points were advocated in regard to the propriety of allowing the openings for empyema to remain unclosed for an indefinite period. From the seventeenth to the eighteenth century the operation of paracentesis was the topic of many surgical treatises.

Early in the seventeenth century practitioners became less distrustful of {588} puncturing the chest, and were led to believe in the harmlessness of the operation (Trousseau). As a consequence of this tendency, physicians began to study the question of puncturing the chest in hydrothorax. In 1624, Gérome Goulée alleged that he succeeded more frequently in hydrothorax than in abdominal paracentesis. Twenty years later, Zacutus Lucitanus asserted that paracentesis was as necessary in cases of serous effusion into the chest as incision in empyema. In 1663, Robin and Duval recommended thoracentesis as the best treatment for hydrothorax. Some time afterward this practice was put in force by Willis. Lower also mentions a case, and subsequent authors quoted these cases as an encouragement to the performance of paracentesis of the chest for the removal of serous effusions. Jean de Vigo brought out again the pyulcon. Druin about the year 1665 proposed the use of the trocar as a substitute for the actual cautery in opening the chest.

In 1658, Bontius for the first time took up in a precise manner the subject of the introduction of air into the pleural cavity. He declared there was no danger from it. Bartholin maintained the opposite opinion. The indications for the operation were laid down, but they were necessarily very imperfect. In proportion as attention was directed to the question of the admission of air, the manner of operating was modified. In 1669, Scultetus discussed thoracentesis in his work _Armamentarium Chirurgicum_. He made use of a trocar, with a bladder at the external orifice, principally to prevent the introduction of air, as Reybard later used a piece of cat's intestine and a bladder of gold-beater's skin. Scultetus used the sypho, a common syringe, for injecting the chest, and also the [Greek: pyoulchon] ([Greek: pyon], pus; [Greek: elchô], to draw out), or pyulcon, for drawing out matter, as its name indicates. This was practically the syphon. Scultetus describes the operation by incision with his gladeolo salicet longo, and by puncture with the canula et acus, both figured in his plates; so also his drainage-tubes, with directions for shortening them as the cavity heals, and the long tubes, which probably acted by gravitation after the manner of the syphon. Aspiration was made by the mouth, by cups, and by syringes affixed to a canula or catheter.[272]

[Footnote 272: These facts were kindly furnished me by Morrill Wyman, who carefully examined Scultetus' work (edition 1672) in the Harvard Library.]

It is thus evident that more than two hundred years ago aspiration was used to evacuate fluid from the pleural cavity. Trousseau says that "at that period aspiration and suction were used for this purpose--timidly pursued, in accordance with Scultetus' example; and that it became afterward in vogue with the masters of surgical art."

Palfin preferred the trocar to incision for treatment of hydrothorax. In 1707, Anel wrote a book on the art of sucking wounds without using the mouth. Bourdelin (1742) rejected the trocar for fear of injuring the lung. That Scultetus' practice was continued is evident from the work of Laurence Heister (1742), who described puncture of the chest, with drawings of exhausting syringes for the removal of pus or serum.

In 1765, one hundred years after Druin's use of the trocar, when perforation by actual cautery was abandoned, Lurde timidly advocated it on account of his fear of wounding the lung. He advised the operator to close the canula with the finger at each inspiration, leaving it open during expiration, so as to prevent the entrance of air. Chopart and Desault opposed the use of the trocar as a coarse mode of operation, involving the risk of wounding the intercostal artery and lung (Trousseau). Van Swieten at the end of the last century questioned the advisability of using the trocar. Later, in 1796, Benj. Bell,[273] in cases of thoracentesis, used india-rubber bottles fitted to the opening for the same purpose, first compressing them and then allowing them to expand by their elasticity. He strongly recommended paracentesis {589} of the pericardium when the amount was so excessive as to cause death. He gives exact directions how and where to operate.

[Footnote 273: Vol. v.]

Isbrand de Diéonerbrock[274] plunged a bistoury between the fifth and sixth ribs, and introduced into the wound a silver canula large enough to fit the orifice, and stopped the canula with a tent which he withdrew each day. Jean Scultetus[275] recommended several different canulas, some of silver, some of gold. He also invented syringes, straight and curved, to absorb the pus or make injections into the chest. Scultetus operated in the sixth intercostal space; he raised a piece of skin, so that it might lap over the orifice after the operation. He used a tent until the eleventh day, when he inserted a canula. After Scultetus, Lamzweerden[276] used suction, and contended that it was very successful. Paul Barbette[277] considered thoracentesis as indispensable in empyema and hydrothorax. He maintained that it was less dangerous than the puncture for ascites. F. Hoffmann at the commencement of the eighteenth century[278] gave his full and complete approbation to the operation performed according to the accepted rules. Dominique Anel[279] was an avowed partisan of the suction of the effused fluids in the chest. He had seen soldiers very successfully suck, with the mouth, wounds of the chest. He invented different syringes and other machines to pump out the effused fluids, some of which were very large, with canulæ whose orifices were very wide and of different shapes.

[Footnote 274: _Medic. Morb. Pectoris Hist._, 2.]

[Footnote 275: _Armam. Chir._, Paris, vol. i. p. 20, quoted by Sprengel.]

[Footnote 276: _Appendix ad Sculpt. Armen_, 1671, quoted by Sprengel.]

[Footnote 277: _Chirurgia_, lib. iii. cap. 2, Geneva, 1688, quoted by Sprengel.]

[Footnote 278: _Medicina consultatoma_, vol. i., 1721.]

[Footnote 279: _L'art de Sucer les plaies sans se servir de la bouche d'un Homme_, Amst., 1707.]

Laurence Heister[280] (1742) acknowledged that Anel's syringes were valuable in pumping out the fluid from the middle or lower part of the chest, but not when paracentesis was performed in the higher portions between the second and third ribs. Heister gives[281] drawings of exhausting syringes for the removal of pus or serum. C. G. Ludwig published[282] a new apparatus invented by a surgeon named Bucer to pump out the fluids contained in the chest. This machine was composed of canulæ, to which was adapted a bowl to receive the liquid as it was withdrawn. Ludwig claimed that the especial advantage of this instrument was that it pumped all the fluid out at one time, without the operator being annoyed by any disagreeable odor. Leber[283] proposed a similar instrument which was easier of application. A. T. Richter demonstrated the inutility of all these inventions; the blood, he said, would be drawn out with the fluid and by coagula stop up the canula. Valentin (1772) objected to the use of these pumps as applied to chest fluids.

[Footnote 280: _Chirurgie_, Th. i. Buch. i. Kap. 10, p. 89.]

[Footnote 281: _Ibid._, p. 72.]

[Footnote 282: _Diss. de Vul. Pectoris_, Leip., 1768.]

[Footnote 283: Quoted by Sprengel, p. 60, vol. ix.]

In the latter part of the eighteenth century there were numerous English and continental writers on the subject of paracentesis. Among them were J. W. Belquer, Sharp Mohrenheim, Richter, Ponteau, Callisen, Pierre Cooper, Allemoth, Zellar, and Audouard. Some of these preferred the trocar to the bistoury. Some were in favor of prompt action, and others objected to the operation unless there were threatening symptoms. Valentin urged that the presence, on the surface of the chest, of oedema and ecchymosed spots was a certain indication of fluid effusion.

During the first twelve years of this century the operation seems to have fallen into disuse. In 1808, Audouard objected to the Hippocratian method, which had been practised for centuries, of drawing out small quantities at a time, for fear that the sudden withdrawal of a large quantity would produce a vacuum in the chest. He maintained, and proved, that sudden and {590} complete evacuation had no such result. In 1811, Corvisart[284] drew attention to thoracentesis. In 1812, Larrey discussed its merits. Charles Bell[285] preferred the trocar to the other methods in hydrothorax when he could be positive of the presence of fluid, but he stated that he preferred first to introduce the bistoury. He operated in the sixth intercostal space, but in empyema he preferred to make the puncture higher up. Samuel Cooper[286] recommended as small an orifice as possible for the evacuation of serum, but larger and wider ones for pus and blood.

[Footnote 284: _Maladies du Coeur_, 1811.]

[Footnote 285: _System of Operative Surgery_, vol. ii. p. 194.]

[Footnote 286: _Dictionary of Surgery_, p. 749.]

In tracing the history of this important operation we have shown that it has been performed from the time of Hippocrates, and that it has been held in different degrees of estimation by the numerous authors who have discussed it--that sometimes it has been popular, and again regarded unfavorably.

Récamier operated, but unsuccessfully. Up to the period we have now reached (1816) great difficulty of accurate diagnosis existed, and crude notions of physiology prevailed. Errors of diagnosis as to the character of the fluid when present, and still more as to its existence in the chest, frequently led to unpleasant results. Laennec's genius so completely cleared up the differential diagnosis of all diseases of the chest, including pleurisy, that men grew less timid. Laennec[287] himself was a strong advocate of the operation; he advised it in acute pleurisy where dyspnoea, threatening life, supervened, and in chronic cases where other remedies failed. He proposed to apply a piston cupping-glass over the wound after the discharge of liquid, and to produce a vacuum in the chest more or less quickly, continuously, and completely according to effects.

[Footnote 287: _Traité d'Auscultation mediate_, 1818.]

As Bowditch[288] states, "We should be groping in the same dark way, and perhaps getting into the chest by caustic pastes or by actual cautery, had not Laennec discovered for us auscultation, with all its admirable powers of diagnosis of thoracic affections."

[Footnote 288: Unpublished communication to the writer, 1882.]

In 1815, Blondel practised puncture of the chest with a bistoury. Gendrin performed the same operation in acute pleurisy in 1831, but with only bad results. Townsend[289] (1833) acknowledged that the operation had fallen into disuse, as much from uncertainty of diagnosis as from any experience of its general danger. He gives the results of Thomas Davies's operations--8 out of 10 successful cases in empyema, with 9 fatal cases in pneumothorax with effusion (probably tubercular), and 3 fatal cases in hydrothorax. Davies used a grooved needle to determine the presence of the liquid, its quality, and the thickness of the walls. After the operation his practice was to inject a weak solution of chloride of lime, which he found to have the effect of diminishing the discharge and correcting its character. Crompton[290] (1834) had 3 successful cases out of 10.

[Footnote 289: _Cyc. Prac. Med._, vol. ii. p. 43.]

[Footnote 290: _Ibid._, vol. iii. p. 400.]

Robert Law[291] pronounced paracentesis more successful in chronic than in acute pleurisy. Townsend doubts whether the admission of air was hurtful; he quotes Nysten and Spies's experiment, showing that air introduced into healthy pleuræ was invariably absorbed in a few days.

[Footnote 291: _Ibid._, 1834.]

Townsend[292] and Law, as well as C. I. B. Williams,[293] speak of the different kinds of syringes that have been proposed to draw off the fluids.[294] Dupuytren proposed (1814) the introduction of a small canula with a very flexible substance at its outward extremity, such as the bladder of some domestic animal, which would allow fluid to escape, and at the same time would oppose the entrance of air into the chest. Becker (1834) published a work in which he investigated the nature of the false membranes in pleurisy, and showed that the {591} access of air did not produce unpleasant results. He reported 2 successful cases out of 3 of operation.

[Footnote 292: _Ibid._]

[Footnote 293: _Library of Pract. Med._, 1841.]

[Footnote 294: Boyson, _Thèse de Paris_, 1814.]

R. Townsend[295] wrote an elaborate paper in 1833 on empyema, in which he applied the principles of physical diagnosis. He cites numerous cases of thoracentesis, and speaks of the operation as easy of execution, productive of little pain to the patient, generally followed by immediate relief, and as having been in numerous instances crowned with complete success. Robert Law[296] (1834) speaks discouragingly of the operation in consequence of the "unavoidable admission of air into the inflamed cavity." He considered the operation of tapping the chest more likely to be successful in chronic than in acute pleurisy.

[Footnote 295: _Cyclop. Prac. Med._, vol. ii., 1833, London.]

[Footnote 296: _Ibid._, vol. iii., 1834.]

In 1835, Faure[297] read his paper on thoracentesis before the Academy of Medicine of Paris, which attracted a great deal of attention. Contradictory opinions were given by prominent members as to the value of the operation. The debate was prolonged, and no definite conclusion was reached. Laennec, although he had recommended the operation in excessive effusions and in chronic cases, was yet timid, and his advice had not the overwhelming influence that it should have had. Becker of Berlin in 1834 wrote his paper on chronic pleurisy, in which he also laid down the principles of diagnosis by means of auscultation and percussion. He detailed 5 cases which he had operated upon. To Thomas Davies is due the credit of having in 1835 recommended the use of the exploring-groove needle to ascertain the nature of the pleuritic effusions, but Powell claims that Sir Benj. Brodie first suggested it. Ringer first recommended the use of the hypodermic syringe for that purpose. Stokes[298] insisted upon the evils attending paracentesis, among which he mentions the converting of serous into purulent effusions.

[Footnote 297: _Bullétin de l'Académie de Médecine_, 1838, tome i. p. 62.]

[Footnote 298: _Dis. of Chest_, Dublin.]

Watson's lectures on practice, delivered in 1836-37, show that while he was much interested in the operation, the necessity of which he discusses with his characteristic ability, yet his conservatism led him to put prominently forward the dangers and evils connected with it. According to these two prominent English practitioners, only imminent peril to life justified the operation. Guérin[299] in 1841 applied his subcutaneous method of operation to empyema. He drew fluids from the chest by a suction-pump applied to a canula, using a curved trocar and canula to prevent injury to the lung.[300]

[Footnote 299: _Essai sur la Méthode Sous-cutanée_, Paris, 1841.]

[Footnote 300: Drawings of the trocar and canula, with the aspirators, are shown in Jacob and Bongeré, _Med. operatoire_.]

Reybard in 1837 took up Dupuytren's suggestion, and used gold-beater's skin as a valvular means of excluding air at the mouth of the canula; this is now known as Reybard's canula apparatus, and was the one used and highly recommended by Trousseau. Stanski in 1839 invented an apparatus for drawing off air from the chest, working on the principle of aspiration. Bowditch states[301] that while in Paris from 1832 to 1835 he never saw a case of pleurisy in Louis's, Chomel's, Andral's, or Trousseau's wards where thoracotomy was performed or even suggested. Medical opinion was either indifferent or in actual opposition at that time. H. I. Bowditch of Boston relates[302] that he saw 2 cases of effusion in the pleural cavity in 1839, in which he proposed thoracentesis, but the surgeons would not operate: both of these patients died. He was convinced at the time that their lives might have been saved. Schuh of Vienna published his work on the _Influence of Auscultation and Percussion on Practical Surgery_, in which he boldly maintained that paracentesis was a radical cure in cases of chronic thoracic effusion, no matter how originating. This work had a great influence in advancing {592} the popularity of the operation of thoracentesis. Subsequently, Schuh and Skoda, both professors at Vienna, published[303] a monograph on the treatment of pleurisies, especially by surgical means, which, as Trousseau acknowledged, has become a classical work in Germany, and occupies a distinguished place in the history of paracentesis of the chest. They admitted that when the effusion is not excessive in quantity, and there are no complications, recovery generally takes place. When the effusion is excessive even, it may in time disappear, but it may prove a matter of months or years. They advised that the operation should be performed when there was no marked improvement for three weeks. These authors refuted the arguments urged against the operation, and gave details as to the mode of operating. The Germans were the first to consider the puncture as a means of radical cure in pleuritic effusions: Becker, Schuh, and Skoda gave it a decided impulse. Hope's[304] paper endeavored to prove that pleuritic effusions did not require surgical interference, but would yield to general treatment.

[Footnote 301: Unpublished MS., 1883.]

[Footnote 302: _American Journal Med. Sciences_, April, 1852.]

[Footnote 303: _Medicinische Jahrbücher der K. K. Oesterreich Staates_, 1841.]

[Footnote 304: "Notes on the Treatment of Chronic Pleurisy," in _Medico-Chir. Review_, London, 1841.]

Thus we see that up to 1841 these unsettled controversies over the dangers and advantages of the operation were still going on. Fred. Bird's results in 1843 proved the possibility of its successful employment, doubted up to that time in England. Trousseau's attention was strongly drawn to the necessity of the operation of thoracentesis as early as 1832, when he attended a case at the Hôtel Dieu that died from excessive pleuritic serous effusion. Louis, from the observation of 150 cases of simple pleurisies that had recovered, had enunciated the law that pleurisy is never the immediate cause of death. This fact, together with Récamier's want of success, had so prejudiced the minds of French practitioners against the operation that it was loudly condemned in acute cases of effusion and in all cases of hydrothorax. Having no fears of fatal termination in pleurisy, they saw naturally no necessity for surgical interference. Trousseau states that it was not until after he had witnessed three patients die from acute pleurisy that he ventured to operate (Sept. 11, 1843). He did not summon a consultation, for fear of being thwarted. It was so successful that he was emboldened to operate without hesitation. After his third operation he read his memoir to the Academy of Medicine in 1843. Trousseau in these memoirs maintained the proposition which extensive observation has now after forty years fully sustained, that dyspnoea and orthopnoea may occur when the effusion is in moderate quantity, and that they may be absent when the effusion is considerable, especially if it has formed slowly. Furthermore, that the signs that constantly indicate the gravity and imminent danger of effusions, and which consequently demand the operation, are the displacement of the heart (whence results syncope), displacement of the mediastinum, depression of the spleen and of the liver, acceleration and feebleness of the pulse, and an anxious countenance.

The next year (1844) Trousseau read another memoir on the same subject. He used the trocar with Reybard's gold-beater's skin at the orifice. While he was popularizing the operation and laying down the indications which called for its performance, several English observers[305] were turning their attention in the same direction. The paper by Hughes and Cock[306] showed that they had been operating in Guy's Hospital for four or five years, and with great success, using a simple trocar and canula of the diameter of one-twelfth of an inch. They imputed their success to the small size of the instrument used, which allowed the fluid to flow slowly and never permitted air to enter the chest during respiration. They gave a tabular account of 20 operations. Hamilton Roe[307] at that time was operating successfully with the trocar. {593} Roe's paper was replete with information and with practical suggestions. He tabulated 39 cases where syncope (one great objection which had been urged against the operation) did not occur even once. He disproved another popular objection, that there was great danger of the admission of air into the pleural sac. Owing to the size of his trocar, a considerable quantity of air entered the pleura during his operations, and in some of them so freely as to produce all the physical signs of pneumothorax, but in none of them did it produce any permanently evil effects. In one instance only was even temporary inconvenience caused. When the fluid was ascertained by the exploring-needle to be purulent, he advised the immediate performance of the operation. In acute cases he recommended a delay of three weeks as the time for testing nature's powers of absorbing the fluid. He advised the closing of the orifice after operation. This author gave an account of his 24 cases. He concluded by stating that the operation is not more dangerous than any other which is performed upon the human body, and that the evil consequences supposed to attend it are imaginary rather than real, inasmuch as it was only fatal in 1 out of 24 cases, and does not produce even temporary inconvenience. Thompson in the same year justly condemns the practice of leaving the canula in the orifice--a proceeding he considers as capable of converting a serous into a purulent fluid. In 1848,[308] at the request of H. I. Bowditch of Boston, J. M. Warren operated by the usual method recommended in the works on surgery. Partial relief was obtained, but the amount of suffering undergone by the patient during the operation, and the fact that an aperture was usually left open by this method, decided Bowditch that he would never recommend it unless under very urgent circumstances. Soon after this, Stone operated with the common trocar and canula, by the advice, in consultation, of Bowditch. In 1849, Bowditch saw another death resulting from effusion where he had advised the operation, but the consulting surgeon would not consent.

[Footnote 305: _London Medical Gazette_, 1847.]

[Footnote 306: _Guy's Hospital Reports_, vol. ii., 1844.]

[Footnote 307: _London Lancet_, 1844, copied into _Amer. Journal Med. Sciences_, Oct., 1845.]

[Footnote 308: Bowditch, _Amer. Journal Med. Sciences_, April, 1852.]

To illustrate the opposition Bowditch found in the United States, he quotes[309] a remark of W. W. Gerhard, the distinguished auscultator of Philadelphia, "that he should be as willing to have a bullet shot through his chest as to have paracentesis performed on one of his patients."

[Footnote 309: Unpublished MS., 1882.]

About 1850,[310] Bowditch saw the paper published by Hughes and Cock, and it determined him in future to try the trocar they had used or something like it.[311] "Fortunately, a few weeks before (April 10, 1850) M. Wyman had a sudden and severe case with large effusion and intense orthopnoea. Death was threatening, yet Wyman felt called upon by public opinion, medical and lay, to summon a prominent practitioner from Boston. They both agreed that the patient was in extreme danger, and Wyman urged tapping with an exploring-trocar. It was decided to postpone surgical interference until next day, when another meeting would be held, the consulting physician returning to Boston to advise with the ablest men of the faculty and render their decision the following forenoon. That was done, and it was found that no prominent practitioner in Boston would consent to the idea of tapping. Nevertheless, the oppression was so severe, and death so imminent unless the patient could be relieved by some means, that the country physician agreed to Wyman's proposal that an exploring-trocar should be introduced. The fluid flowed out imperfectly, but some relief and no harm resulted" (Bowditch). Two days after this, Wyman operated again with the exploring-trocar and a suction-pump. Wyman[312] demonstrated to John Homans on the 23d of February, 1850, that the chest could be safely punctured with his instrument and the serum evacuated in acute pleurisy.

[Footnote 310: _Ibid._]

[Footnote 311: _Ibid._]

[Footnote 312: Private letter to author, 1883.]

Although suction, as we have shown, was used as far back, probably, as Galen (second century), by Scultetus in 1662, and was in use in 1707, as {594} shown in Anel's work, in 1742 in Laurence Heister's work, by Ludwig and Lehren in 1768, again in 1796 (Benj. Bell), yet it had been abandoned and lost sight of, with the exception of Laennec's suggestion of its application in the form of a cupping-glass over the orifice of puncture, until Guérin (1841) used it. The author followed Trousseau's clinics in 1849 and 1850, and saw him repeatedly operate with Reybard's canula guarded by gold-beater's skin, but never with Guérin's suction apparatus. The French seemed to have lost sight of it until 1865, when Guérin, at the French Academy, recalled attention to it, showing how he aspirated liquids, instead of allowing them to flow outward after the puncture. His apparatus consisted of a curved trocar, the end of which was made tapering and sharp enough to puncture the thorax through the skin and the muscles; of a pump, the piston of which was perfectly adjusted to produce a vacuum; and of an adjuster at the extremity of the pump, consisting of a stopcock which enabled the operator alternately, without removing the instrument, to aspirate the fluid and evacuate it into a basin. Wyman's pump, invented in 1850, was arranged very much in the same way, only it contained valves which were opened and closed by the movement of the barrel, to enable the operator to suck out the fluid and then force it out of the pump. After the operation the skin, being drawn over and closing the orifice, acted as a valve which prevented at the same time the entrance of air and the escape of fluid. Dieulafoy, in November, 1869, invented his aspirator, which is based upon the same principles as those used by Guérin (1841) and by Wyman and Bowditch (1850)--namely, pneumatic aspiration, which the vacuum of the air-pump supplies. Guérin's instrument was large and costly. Wyman's trocar was of a very small diameter, being only one-twenty-fourth of an inch, and the canula but little larger. This was attached, at first, directly to the aspirating syringe, afterward by means of a flexible tube. With this apparatus Wyman demonstrated that tissues could be safely punctured and cavities evacuated without the admission of atmospheric air, that the wound, causing but a drop or two of blood, was followed by no inflammation, and that no dressing was required. The smallest trocar used previously to Wyman's was that of Roe, which was one-twelfth of an inch in diameter. From 1850, Bowditch appreciated the great value of Wyman's invention, as shown in one of the first operations on a patient of his. He adopted and practised it. His position as professor of diseases of the chest, and his great reputation in that branch, gave him an extensive practice and brought him many cases of pleurisy. He met with great opposition from the surgeons and prominent practitioners of the country, but his results were so favorable that he forced an unwilling and an unbelieving profession to accept, as he expresses it, "the beautiful thought of Wyman of thoracentesis or aspiration with a fine needle." "I considered the operation so simple, and yet so effectual, and never harmful, that I deemed it my duty to print cases illustrative of its value." Bowditch had been for eight or ten years endeavoring to get some effective plan of opening the chest without risk. He readily caught at Wyman's plan, and he operated so frequently and successfully as to demonstrate its value to the medical public both of this country and of Europe. As he states,[313] it was, in fact, what he had been for years longing for--viz. a simple and painless, or almost painless, operation for removing fluids from the thorax--one that could be done without danger and leave no open wound. Bowditch relates[314] that when he visited Europe, nine years after his first publication of cases, he showed the instrument in England, Scotland, France, and Germany, and that he met with very indifferent recognition of its value. Only W. T. Gardner of Edinburgh and Budd of London seemed to appreciate the plan. They had instruments made after the American pattern. All others had no faith in the operation. In Paris his old master, Louis, smiled {595} incredulously at his enthusiasm for it and doubted its necessity. At Vienna Skoda turned with apparent scorn and left the room as Bowditch was demonstrating its employment. The Parisian authors, Woillez, Peter, Moutard-Martin, Peyrot, and others, do not even mention Bowditch, but give Trousseau alone the credit of popularizing thoracentesis.

[Footnote 313: Unpublished MSS., 1883.]

[Footnote 314: _Ibid._]

Trousseau's first publication was in 1843, and yet in 1859 there was no general adoption of the operation, nor was there until 1869, when Dieulafoy rediscovered Wyman's wonderful improvement of the application of negative force to draw out fluids from the chest.

In estimating the value of the substitution of aspiration for the trocar-and-canula method, we must bear in mind that with the latter there was danger of the introduction of air into the thoracic cavity, of the production of fistulous orifices, and the too rapid, and therefore dangerous, evacuation of the fluid. Moreover, there are cases where the trocar and canula is not effectual, although the quantity effused be considerable--where, indeed, the fluid cannot flow out, although the canula be pushed in actual contact with the fluid. The explanation of this is now understood. The fluid is kept in the pleural sac by a negative pressure of from 4 to 5 inches of water (Stone), 6 millimeters mercury (Donders), 5 millimeters mercury (M. Foster), exercised by the lung in its elastic contraction, and by the passive tension of the arched diaphragm. The fluid has no tendency to flow out, and this suctional pulmonary force must be antagonized by an external suctional force, that of aspiration, before the fluid can be withdrawn.

The invention can best be appreciated from the standpoint reached by modern investigations of the physics of the living mechanism of the chest. The principle of applying suctional force in pleurisy is in imitation of nature's gentle methods in connection with respiration. We have shown that most of the dangers connected with aspiration are caused by not taking into consideration the adjustment of lung-tension with thoracic resilience, and consequently of using too great negative force and withdrawing the fluid too rapidly and in too great quantity.

Thoracentesis by aspiration, with greater or less force as may be necessary, is now placed upon a scientific basis. We claim that this modern method is an American invention--that Morrill Wyman was the discoverer and H. I. Bowditch the utilizer of the discovery. As such they may be regarded as benefactors of the human race.

It is extraordinary that Trousseau never alluded to Bowditch's operations, and that Dieulafoy should never have heard of them. Fraentzel acknowledges that Bowditch was the first to introduce aspiration into practice. The Germans have been very slow in appreciating its value. Fraentzel states that he did not use it until 1871, and that it was not until 1879 that it had in Germany any ardent supporters. Bowditch[315] has now operated 387 times upon 246 patients without any unpleasant result.[316] The distinctive points in Dieulafoy's ingenious modification of the aspirator are that the needles are very fine, even one-half of a millimeter in diameter; that the barrel of the exhausting pump is of glass; that there is a pre-existing vacuum; that we are not compelled to jar the side of the patient by the process of pumping, and moreover by turning the cock we produce at once a vacuum in the needle itself, and know with certainty the moment the fluid is reached, and can see it flow through the glass index in the tubing, even if it be in drops. We can judge of the nature of the fluid, whether it be serum, pus, or blood. The minuteness of the needle is a great cause of safety, because it allows the fluid to flow so gradually that the lung has time to expand slowly. We can in an instant arrest the flow of the fluid by turning the stopcock, and if necessary by drawing out the needle. By giving the needle a downward direction after it {596} enters the cavity, we prevent the point from pricking the lung. So small an orifice is made that even if the needle does touch the lung, there is no danger, for the orifice closes over at once. As Dieulafoy claims, "the fineness of the needle guarantees the harmlessness of the puncture." Castraux's concealed point (invented in 1873), and Fitch's (of Nova Scotia) protected canula (invented in 1873), are valuable additions to the aspirator-needle. These dome-trocars, as they are called, prevent the possibility of injuring the lung, for the sharp-pointed needle, after it has penetrated the pleural cavity, is at once, by a slight movement, converted into a blunt-pointed needle with an orifice near the end. With these very fine needles the force is sufficient to draw up the thickest fluids. We are compelled to admit that Dieulafoy's instrument is a great advance on any other that has been invented. Its simplicity, its easy application, its safety, have rendered paracentesis a harmless operation and one of great value in serous effusions. While Guérin and Wyman may both claim priority of invention, all must admit that Dieulafoy has improved upon their ideas and given us a beautiful and effective instrument. There have been proposed, since Dieulafoy showed his instrument in 1869, no less than forty other aspirators, modifications in form or dimensions of his apparatus. Of these, to us the most valuable is Potain's bottle aspirator, with which aspiration can be so easily and effectually employed. It is simple and cheap. An india-rubber cork accurately fitting a strong bottle is perforated for two tubes each having a stopcock. One of the tubes fits on the end at the exit in the basin, and the other is adapted to an aspirating syringe.

[Footnote 315: _London Lancet_, vol. ii., 1879.]

[Footnote 316: Letter to author, 1883.]

One of the most important of the improvements to the aspirator-canula is the addition--first suggested in 1858 by Charles Thompson,[317] and afterward adopted by Potain, Powell, and Fraentzel--of a lateral tube for the outflow connected with the main canula through which the trocar passes. By this improvement, in case the canula is clogged up, the trocar can be pushed down to remove the obstruction without danger.

[Footnote 317: _Med. Times and Gazette_, 1858.]

The principle of aspiration is now well established, and the indications for its use are becoming more defined and more accurate. New applications as a means of diagnosis, as well as of treatment, daily render it more valuable.

To guard against the dangers shown by modern experience to be sometimes attendant upon the operation of aspirating the pleura (see Dangers of Thoracentesis), it is now generally admitted that the removal of the contents of the chest should be slow and gradual; and that, ordinarily, it is safest at one operation to remove only a portion of the effused liquid. Our object should be to remove pressure and allow nature by absorption to take away the remainder, for positive pressure is an urgent indication for thoracentesis. It is therefore of primary importance to properly estimate the quantity present, and thus to test the intra-thoracic pressure. Great care and caution must be used, because if we extract too much the operation may be followed by serious results.[318] Large-sized canulæ should never be used, for fear of too rapid withdrawal of fluid. It has been demonstrated that even with a capillary perforated needle we can exercise more negative pressure than is safe, especially toward the close of the operation, when there supervenes a negative pressure exerted by the fluid remaining in the pleural cavity. It is from these well-known facts that we recognize the great value of Potain's ingenious addition to the aspirator of a manometer of extreme simplicity, a kind of barometer or cuvette, which is placed along the tube which withdraws the fluid. If we are not satisfied with this new safety improvement of the aspirator, we may adopt Douglass Powell's suggestion (_On Consumption, etc._) {597} of fitting into the bottle a pressure-gauge, so as to know at any moment what degree of aspiration is being used.

[Footnote 318: _Trans. de l'Assoc. pour l'Adv. des Sciences_, 6th Session, 1877.]

The syphon method has been of late years very extensively used, especially by Southey, W. H. Stone, and Garland, A. T. H. Waters, Wilks, Oxley, and habitually by Douglass Powell. It is a feeble aspirating force, which has very decided advantages. It is effective, and acts slowly and uninterruptedly with a gentle and uniform negative pressure. Its action allows the lung gradually to expand and the displaced organs slowly to resume their normal position. It thus in many cases furnishes us with a safe means of thoracentesis. (See Surgical Treatment, in Pleurisy.)

{598}

{599}

DISEASES OF THE CIRCULATORY SYSTEM.

DISEASES OF THE SUBSTANCE OF THE HEART.

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.

CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.

CARDIAC THROMBOSIS.

NEUROSES OF THE HEART.

DISEASES OF THE PERICARDIUM.

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.

DISEASES OF THE AORTA.

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

DISEASES OF THE VEINS.

THE CAISSON DISEASE.

DISEASES OF THE MEDIASTINUM.

DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM.

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.

DISEASES OF THE SPLEEN.

DISEASES OF THE THYROID GLAND.

SIMPLE LYMPHANGITIS.

{600}

{601}

DISEASES OF THE SUBSTANCE OF THE HEART.

BY WILLIAM OSLER, M.D.

Malpositions of the Heart.

We shall consider only such alterations as affect the whole organ; faulty position of individual parts comes under the section upon Malformations. It may, however, be mentioned that cases are known of complete transposition of the chambers, the pulmonary artery and cavæ being connected with the left, the aorta and pulmonary veins with the right side, the valves being also transposed.[1]

[Footnote 1: Pazannuzzi, _London Med. Record_, 1877.]

Malpositions of the heart result either from errors of development, or, more commonly, from changes in contiguous organs, usually the effect of disease.

Of the congenital anomalies only a few are of practical interest. The heart may be placed vertically in the chest, as in the foetus, the apex beating at the lower end of the sternum; or, more rarely, the organ lies transversely. Dextrocardia, the condition in which the heart is on the right side of the body, is much more important, and is usually associated with the transposition of the abdominal viscera--situs inversus viscerum. In these cases the apex-beat is in the region of the right nipple; a distinct area of dulness can be obtained to the right of the sternum, in which situation the heart sounds are loudest; and, lastly, there is pulmonary resonance in the place of normal cardiac dulness. In the great majority of cases--70 out of 78[2]--the abdominal organs are also transposed, the liver on the left side, the spleen on the right; but in a few instances the heart alone has been misplaced, and under such circumstances care is needed to diagnose the condition from dislocation of the organ due to old-standing lung disease with retraction.

[Footnote 2: Gruber, _Virchow's Archiv_, 1865.]

More serious congenital malpositions, but of less practical importance, are the cases of ectopia cordis, which may exist in all grades, from simple failure of closure in the sternum--fissura sterni--to the most extreme condition, in which the naked heart lies outside the chest-wall. Hodgen[3] and March[4] have each described remarkable examples of the latter condition. In other instances the heart lies free in the neighborhood of the neck, or it may be in a congenital umbilical hernia.

[Footnote 3: _American Practitioner_, xviii. p. 107.]

[Footnote 4: _Trans. of the New York State Medical Society_, 1859.]

The malpositions with which we are more immediately concerned arise from disease of the heart itself or its membranes, or from disease of contiguous organs.

We judge of the situation of the heart by the site of the apex-beat, by the position and extent of the area of dulness, and by the character of the sounds. So constant in health is the position of the apex-beat in the fifth intercostal {602} space that in our examination of the heart we seek first to determine its existence as affording the most important information of the normal situation of the organ. The area of dulness is a much more variable guide, depending as it does so greatly on the degree of distension of the lungs. When, as sometimes happens, neither apex-beat nor area of dulness can be obtained, the position of maximum intensity of the heart sounds becomes an important indication.

In regard to the effect of respiratory movements in the position of the heart, with each inspiration it is drawn down slightly by the descent of the diaphragm, and it is separated from the chest-wall by the inflation and descent of the left lobe of the lung--in deep inspiration to such a degree as to obliterate the area of dulness and to prevent the systolic impulse from reaching the intercostal space.

The effect of gravity on the position of the heart is well illustrated by the more forcible and extended beat when the chest is bent forward or when the person is turned toward the left side--procedures frequently resorted to when from any cause the apex-beat is obscure.

Of diseases of the heart itself, dilatation and hypertrophy are very common causes of displacement, and in general enlargement the organ may occupy a very considerable part of the left side of the chest, and the apex-beat in the seventh or eighth space in the axillary line. Hypertrophy of the left ventricle alone pushes out the apex-beat, while enlargement of the right ventricle gives a stronger impulse toward the left border of the sternum and a more marked pulsation below the ensiform cartilage. Hypertrophy and dilatation of the auricles increase the width of the cardiac dulness, and may cause marked pulsation in the second and third spaces on either side of the sternum.

In pericardial effusion the heart is pressed backward and the apex slightly raised.

To understand clearly the effects upon the position of the heart of disease of contiguous organs, we must bear in mind their mutual relations. Situated in the mediastinum between the lungs on either side, it is subject to the elastic traction of these organs, which counterbalance each other, but if from any cause the elastic tension of one lung is suppressed, as in pneumothorax or in pleural effusions, then the other lung may also collapse to a slight degree, and pull over the mediastinum and with it the heart. The pericardium is firmly fixed below to the diaphragm, chiefly to the central tendon, to a slight extent also to the muscular substance, but the union with the diaphragm is so intimate that there can be but little movement of the attached portion. The mobility of the heart is measured by that of the mediastinum and pericardium, and through these alone the displacing forces act. The limits of dislocation are determined by the attachments of the central tendon, of the inferior cava, and the great vessels at the root. Within the pericardium the heart has a certain degree of mobility, but this is confined, as regards pressure or traction effects, to rotation upon its axes.

Of the malpositions due to changes in contiguous organs, the following may be considered:

Changes in the Chest-wall.--The gradual incurvation of the ribs and costal cartilages in some cases of rickets may alter the position of the heart.

Curvature of the spine, particularly cases which narrow to a great extent the upper outlet of the thorax, may produce very considerable displacement of heart and great vessels. There may be areas of extensive pulsation on either side of the sternum, and the condition may simulate aneurism of the aorta, as in a case reported by Bramwell.[5]

[Footnote 5: _Lancet_, 1878, i.]

In certain affections of the lungs the position of the heart is much altered. {603} In emphysema, when extensive, the apex is directed more to the right, and the organ is somewhat lower than normal, on account of the depressed condition of the diaphragm. The heart may also occupy a more transverse position. The area of cardiac dulness may be greatly reduced by the distended left lung, and there is usually forcible epigastric pulsation, due to the lower position of the organ and the hypertrophy of the right ventricle which almost always accompanies emphysema.

The most marked displacement is produced by fibroid induration of the lung, with contraction--cirrhosis. As the process of condensation goes on, the chest-wall is gradually flattened, and the mediastinum, with the heart, drawn toward the affected side. When the left lung is involved, the heart may be completely to the left of the median line, and is usually drawn upward as well. There may in such cases be a very wide area of impulse, as the heart occupies the position of the left lung in front. In cirrhosis of the right lung the organ is drawn toward the right side, and the area of visible impulse may be in the third and fourth interspaces to the right of the sternum. In the process of slow traction the heart revolves upon itself and the left chambers come uppermost. In many cases of chronic phthisis, when the anterior margin of the left lung is involved, the retraction from induration may leave a large portion of the heart exposed and increase the area of visible pulsation; sometimes, when there is much contraction of the upper lobe, the organ is drawn up and to the left, and the apex-beat may be in the fourth interspace.

The pressure of a pneumonic lung may depress the diaphragm and draw down the heart.

Abnormal conditions of the pleuræ are frequent causes of cardiac displacements. In pneumothorax there is collapse of the lung on the affected side, and the elastic traction of the sound lung draws over the mediastinum and heart. It is not that the heart is pushed over, as so often stated, but the tension of the other lung, being unopposed, pulls the mediastinum toward the sound side. Later, when, as usually happens, effusion takes place, the pressure assists in the displacement. In pleuritic effusion dislocation of the heart to one side is almost constant if the amount of fluid is at all considerable. Here pressure plays the most important part, and the heart is gradually pushed over by the effusion; but the elastic tension of the lung on the sound side is also concerned in the result. In right-sided effusion the whole organ may be to the left of the median line, and from the depression of the diaphragm it is usually lower in the chest, so that the apex-beat may be in the sixth, rarely the seventh, interspace in the axillary line. When the exudation is on the left side, the dislocation is more marked, and there may be a cardiac impulse at the right nipple or even beyond it. A common error is to regard the pulsation as due to the apex, but it is invariably caused by some portion of the right chambers, usually the ventricle. Even in the most extensive effusion the apex is probably never pushed beyond the right border of the sternum, and the relative position of apex and base is not changed. This I have carefully noted in several autopsies.[6]

[Footnote 6: Fig. 76 of Sibson's article on "Displacements of the Heart" in _Reynolds's System of Medicine_ gives an incorrect idea of the position of the organ in these cases, as the apex is represented as beating beneath the right nipple.]

In the gradual absorption of a pleuritic effusion, serous or purulent, the heart may not only regain its normal position, but is in many instances drawn toward the affected side by the contracting false membranes.

Of conditions of the mediastinum producing displacement, two only need be mentioned--aneurism and tumor. Very large aneurisms of the arch usually press the heart downward, and its axis may be transverse; but much depends on the direction of growth, and a slight lateral and downward dislocation is most frequently met with. Tumors do not necessarily {604} cause displacement, but when large there may be some dislocation in the direction of the growth of the mass. Most extensive masses of mediastinal cancer may occur without any disturbance of the position of the heart.

Diseases of the abdominal viscera not uncommonly produce dislocation of the heart, generally upward. Extensive peritoneal effusion, gaseous or fluid, forces up the diaphragm, and with it the heart, which may assume the transverse position, and the apex beat as high as the third interspace. Gas much more readily than fluid rapidly lifts the diaphragm and produces upward dislocation of the heart. Diaphragmatic hernia of intestines or stomach may push the heart up or to one side.

Conditions of the liver not infrequently affect the position of the heart. Abscess or hydatid cysts of the left lobe may push the organ up and to the left. More rarely large hepatic tumors drag the diaphragm down, and with it the heart. Very great splenic enlargement, as in leukæmia, may push up the diaphragm and lift the heart.

Other abdominal growths, as large retro-peritoneal and ovarian tumors or aneurism of the abdominal aorta, may occasionally produce the same effect. Knowsley Thornton has given in Fothergill's work on the _Heart_ an excellent account of the upward displacement of the heart in ovarian disease.

As a very rare circumstance, the heart is displaced by accidental injury to the chest-walls. The case which Stokes relates of this kind was probably, as he subsequently suggested, due rather to the effects of the pleuritic effusion which followed the accident.

The dislocations of the heart when gradually induced rarely disturb to any serious extent the functions of the organ.

Myocarditis.

Inflammation of the heart-muscle is rarely primary; usually it is associated with endo- or pericarditis, strain,[7] embolic processes, disease of the arteries, or the presence of certain poisons--diphtheritic, rheumatic, etc.--in the blood.

[Footnote 7: Some French writers refer specially to the occurrence of myocarditis from strain or prolonged muscular exercise--myocardite des surmenes. Peter (_Maladies du Coeur_, Paris, 1883) gives two cases (without autopsy), and quotes a case from Revilliod, whose work (_La Fatigue_, Lausanne, 1880) I have not been able to consult.]

We may recognize three forms--acute suppurative, acute interstitial, and chronic myocarditis. By many writers the parenchymatous degeneration so frequent in fevers is regarded as an inflammation, but it is the result of a process which we can scarcely term inflammatory.

Acute suppurative myocarditis is almost invariably associated with pyæmia or with malignant endocarditis, and in most instances may be regarded as embolic. In severe pyæmia from any cause foci of suppuration are not infrequently met with in the walls of the ventricles. There may be multiple abscesses or a single purulent collection varying in size from a pea to a walnut. Numerous miliary abscesses are not so often met with in ordinary pyæmia as in endocarditis. If large, the abscess may burst into the heart or into the pericardium and excite inflammation of this membrane; or, indeed, without perforation, as I saw in one instance. The calcareous nodules occasionally found in the muscle-substance have been regarded as healed abscesses. Suppurative myocarditis is a frequent result of malignant endocarditis, and we meet with it either in the form of miliary abscesses, scattered in numbers through the substance, or as large solitary abscesses at the bases of vegetative outgrowths or in connection with excavating ulcers of the endocardium, valvular or mural. The small embolic abscesses vary in size from {605} a pin's head to a pea, and may occur in extraordinary numbers in the muscle-substance of all the chambers. They present usually a central grayish-white focus of suppuration surrounded by a zone of deeply-congested and hemorrhagic tissue. Microscopically, there is a central infiltration of leucocytes with destruction of the muscle-fibres, and in every instance colonies of micrococci can be readily discovered. These abscesses are identical in character with those occurring in the kidneys, intestines, and brain. Sometimes at the base of large endocardial outgrowths, particularly of the aortic segments, abscesses are found extending deep into the muscle-substance, and even perforating the wall. These occur most often in the left ventricle, but occasionally in the right, as in a case of stenosis of the pulmonary valves at the Montreal General Hospital, in which there was an abscess cavity in the wall of the right ventricle the size of a marble, situated at the base of some endocardial vegetations. The acute ulcer of the heart is of the nature of a suppurative myocarditis, having its starting-point, in the great majority of cases, in the endocardium. It may perforate the wall of the ventricle, as in the cases of Mackenzie[8] and Keating.[9] The blood-pressure in the abscess-cavity may dilate the wall, and form what is known as acute aneurism of the heart.

[Footnote 8: _Path. Soc. Trans. London_, xxxiii.]

[Footnote 9: _Trans. of the College of Physicians of Philadelphia_, 1879.]

Acute interstitial myocarditis occurs in connection with the infectious fevers, and also with pericarditis, more rarely endocarditis. It is characterized by the presence of numerous round cells in the interfibrillar tissue, multiplication of the corpuscles, and degeneration, granular or fatty, of the muscle-fibres. The coarse appearances are--a relaxed state of the cardiac walls, pale or turbid condition of substance, in extreme instances a sodden, soft friable state, so that the muscle readily tears on pressure. In acute pericarditis the superficial myocardium, for a line or two beneath the membrane, frequently presents this condition in a typical manner; it looks pale and turbid, contrasting strongly with the deeper parts, and on examination presents infiltration of leucocytes, swelling of the interstitial tissue, sometimes effusion of blood-corpuscles, and a swollen, granular, or fatty state of the muscle-fibres. Although the process may be intense, suppuration rarely occurs, whereas in myocarditis supervening upon inflammation of the endocardium it is, as we have seen, not uncommon. A similar diffuse interstitial process is met with in many of the fevers. In rheumatism, typhus, scarlet fever, small-pox, and diphtheria the myocardium may be found relaxed and soft, the chambers dilated, the substance pale, easily torn, in some instances extremely soft; and this condition has been variously described as inflammatory or degenerative. While not denying that such a state of the muscle-fibre may be brought about by the action of the fever or the influence of some specific poison without any signs of inflammatory action, yet in other instances changes have been found which are evidently of the nature of a myocarditis. In these cases the intermuscular connective tissue is swollen, infiltrated with round cells and nuclei, the vessels are dilated, and often there are minute extravasations and the muscle-fibres are granular and fatty, with indistinct striæ and nuclei. As Leyden[10] has pointed out, this condition probably affords an explanation of some of the cases of sudden death in diphtheria. It may occur without the coarse or microscopic appearance of degeneration of the muscle-fibres, and when of any duration may produce areas of atrophy. Though usually diffuse, it may be patchy and limited in distribution. Martin[11] has described in cases of sudden death in diphtheria and typhoid fever an acute endarteritis of the small branches of the coronary arteries, which probably has a close relationship with this acute interstitial myocarditis.

[Footnote 10: _Zeitschrift für klinische Medicin_, Bd. iv.]

[Footnote 11: _Revue de Médecine_, 1881.]

{606} The SYMPTOMS of acute myocarditis are those of cardiac weakness and irritability, and it is the conditions under which these occur which make us suspect involvement of the myocardium rather than any special features pertaining to the disease. We may reasonably suspect its presence in a case of rheumatism, puerperal fever, or other specific fever when the patient complains of cardiac distress or actual pain, with shortness of breath, and on examination we find a weakened impulse, feeble, indistinct first sound, and a small, irregular pulse. The area of heart-dulness is increased, and there may be a murmur due to muscular incompetence. There is usually fever, but this is generally due to the primary affection. The symptoms are those of a weak and dilated heart, and are peculiar only in the mode of onset and the circumstances under which they arise. A point of note observed by Stokes is the weakening or disappearance of organic murmurs during an attack of acute myocarditis. In acute pericarditis grave implication of the myocardium may be suspected when the pulse gets small and rapid, dyspnoea urgent, and the cardiac pain is increased. Such symptoms, in the absence of copious effusion, would appear to indicate extension of the inflammation to the heart-muscle. Even the occurrence of suppuration has no distinctive symptoms, as it almost invariably occurs as part of a pyæmic process, and the cardiac weakness which supervenes may be regarded as an outcome of the septic or febrile condition. The bursting of an abscess into the pericardium will excite violent pericarditis. In the case of Kortüm, referred to by Friedrich,[12] an abscess in the septum burst into the ventricle; the symptoms, which developed suddenly during a lecture, were a sense of constriction in the chest, dyspnoea, and lividity, and death occurred in six hours.

[Footnote 12: _Virchow's Handbuch_, Bd. v.: "Herzkrankheiten," S. 275.]

The DIAGNOSIS can rarely be made with certainty; at the best we can suspect its presence under the conditions above mentioned.

The course of suppurative myocarditis is always unfavorable, but the fatal termination of the case is usually dependent on concomitant causes. The possibility of recovery in some instances of abscess of the heart is suggested by the occurrence of caseous and cretaceous masses, probably the remnants of collections of pus.

The chief danger in interstitial myocarditis is heart paralysis and sudden death, as occur in diphtheria and occasionally in rheumatism. From mild grades of the disease recovery may take place, and even when general and severe it has often been some indiscretion which has induced the collapse, as sudden sitting up in bed or getting out to attend to the calls of nature. Possibly the slight intramuscular scars and spots of atrophy furnish evidence of past acute myocarditis.

When suspected, the TREATMENT should consist of absolute rest, muscular and mental, with careful feeding and stimulation. If a rheumatic case upon the alkaline or salicylate treatment, the remedies should be stopped. I saw sudden death from heart failure in a case of acute rheumatism in which during four days the full alkaline treatment of Fuller was followed, and in which, by mistake, a much larger quantity of the bicarbonate of soda was given each day than had been intended. Strychnia and small doses of quinine may be given. Shall digitalis be employed in acute myocarditis? Upon this point authorities differ. If we regard it as simply increasing the force of the muscular contractions, we can understand the fear of straining a weakened heart; but digitalis has important trophic influences, and, while it stimulates the vigor of the contraction, improves the nutrition of the heart-muscle and renders it better able to contract. After all, the question amounts to the giving of digitalis in dilatation, and with a weak first sound and feeble action the careful administration, in conjunction with stimulants, will be found beneficial. Peter[13] speaks highly of the application of a blister in the region of the heart.

[Footnote 13: _Loc. cit._]

{607} Chronic Myocarditis (Fibroid Heart).

A condition characterized by the substitution in areas of variable extent of a fibrous connective tissue for the muscular substance. It is an interstitial growth, comparable to the cirrhosis of other organs, and the muscle-elements in the affected regions are wasted or entirely destroyed. The process may occur in a mild grade throughout the organ, but it is more common to find it distributed in certain parts which seem specially prone to this form of degeneration.

The conditions under which it is most likely to occur are those which we find in connection with arterio-sclerosis. It is an affection of adult and advanced life, and is met with most frequently associated with disease of the coronary arteries. In chronic valvular affections it is very common, and may be part of the so-called cyanotic induration or an extension from the thickened endocardium. Sometimes it seems a part of a general arterio-capillary fibrosis. In a few cases there is direct extension from the pericardium. Rheumatism is in this way indirectly responsible; possibly some of the cases are directly traceable to acute interstitial myocarditis occurring in this disease. Chronic alcoholism, syphilis, and gout are prominent factors in the etiology. Some of the most marked cases give no clue in the history or habits of any conditions which we could reasonably connect with the disease. Males are more often affected than females. The tendency to arterio-sclerosis seems to run in some families. Mental anxiety is not without influence, and when the disease is established seems very liable to bring on the anginoid attacks. The situation and extent of the fibrosis are very variable. The papillary muscles and the columnæ carneæ of the left ventricle are most frequently affected, less often the corresponding structures on the right side. The middle portion of the muscular bundles and the apices of the papillæ are first involved. In the latter the process may extend almost to their bases, but on section it will be found that it is more advanced in the superficial than the deep parts. This change is very common in cases of valvular disease with hypertrophy, especially mitral stenosis, but it often occurs in elderly persons who have had no special heart symptoms.

Beneath patches of pearly-white thickened endocardium local fibrosis may occur, often seen at the upper part of the septum in left ventricle, and in the dilated and thickened left auricle of mitral stenosis, and occasionally in other parts. This is usually regarded as an extension from a chronic endocarditis. More rarely the fibrosis extends from a thickened pericardium, but cases are on record of the conversion of the outer layers of the muscular fibres into a firm, hard tissue. We frequently meet with scattered areas of fibrosis in septum and ventricular walls without any implication of peri- or endocardium. During foetal life an endo-myocarditis may occur in the conus of the right ventricle, less frequently in the left, and produce very great narrowing by the gradual contraction of the newly-formed tissue. But the condition to which the term fibroid heart can be most properly given is an extensive affection of the left ventricle, involving most commonly the anterior wall near and at the apex and the lower part of the septum. In these cases there may be marked bulging at the apex, and on section the wall cuts with great resistance, and a dense fibrous tissue of a grayish-white appearance occupies the position of the myocardium. In extreme cases a large part of the septum and anterior wall is in this state, and may present only traces of muscular tissue. There is usually thinning, sometimes thickening, of the affected portions, and the septum bulges toward the right ventricle. The endocardium is opaque, often much thickened, and directly continuous with the fibrous tissue. The columnæ carneæ may be narrow and flattened, and the lacunæ {608} between them very small. The chamber is usually dilated. The upper third of the septum and the base and posterior wall of the ventricle in such cases present a marked contrast to the affected parts, and may look natural, but more commonly are hypertrophied. The other chambers may not show any special change or there may be scattered areas of fibrosis. The thinning and dilatation at the apex and septum are the conditions which precede and lead to the formation of cardiac aneurism. The valves may be normal, but in many cases there is sclerotic endocarditis and retraction. The histological appearance varies much with the stage of the process. When early or where advancing, the muscle-bundles are seen separated by round and elongated cells. The process is usually more marked about groups of fibres, which gradually become isolated by the increase of the growth, and in this way one often sees streaks or patches of muscle-tissue surrounded by the fibrous elements. The destruction of the muscle-cells is apparently by pressure; they gradually waste and present the condition of brown atrophy, the pigment of which remains and indicates the position of the fibres. The intimate pathology of the process is of great interest. Doubtless in some instances we may attribute the fibrosis to an extension of an indurative process from the endo- or pericardium, but the researches of Tautain,[14] Martin,[15] Huber (Karl),[16] and others have thrown a new light on the subject, and it seems probable that in most instances the fibroid degeneration is associated with changes in the coronary arteries. The former describes an endarteritis and a periarteritis of the small vessels, leading to disturbance of nutrition and increase of the connective tissue (sclérose dystrophique). Huber in a considerable number of cases has traced the connection between the arterio-sclerosis, chiefly of the smaller twigs, and the indurative process. The region supplied by the obliterated arteriole is in the condition of an infarct and undergoes an anæmic necrosis, and subsequently by a proliferating myocarditis is transformed into a fibroid area. The condition is well described and figured by Ziegler.[17] Why this obliterating endarteritis should be so limited in the majority of cases to the vessels of the left ventricle is not very clear. The parts most distant from the aorta seem most liable to the process, as the apex and the tips of the papillæ; and it is interesting in this connection to note that the left coronary artery is more frequently diseased than the right.

[Footnote 14: _Thèse de Paris_, 1878.]

[Footnote 15: _Revue de Medicine_, 1883.]

[Footnote 16: _Virchow's Archiv_, Bd. lxxxix.]

[Footnote 17: _Pathologische Anatomie_, Lief. ii., 1884.]

In the milder grades of fibrous myocarditis, when only the apices of the papillæ and thin layers beneath the endocardium are involved, the heart does not appear to be seriously affected; but when of any extent the vigor and force of the contractions are impaired, and the ventricle is unable to do the work of a healthy muscle. Compensatory hypertrophy is not readily established, possibly on account of the arterial sclerosis on which many of the cases seem to depend, although in rare instances, as in a specimen referred to by Quain,[18] there may be very great muscular hypertrophy. Dilatation of the left ventricle is much more apt to follow, as the fibroid walls have not the resisting power of muscular tissue, and the patients finally present a clinical picture of heart failure. The gradual yielding of the fibroid region may result in aneurism.

[Footnote 18: "Lumleian Lectures," _Lancet_, 1872, i.]

There are no characteristic symptoms to indicate the condition. The fibroid heart is a weak heart, and it is scarcely possible to distinguish it from fatty degeneration. A feeble, irregular, sometimes slow, pulse, dyspnoea on exertion, and painful anginoid attacks--symptoms which may have persisted for many years--are special clinical features in many cases. In a patient I examined some years ago for Palmer Howard of Montreal--a typical instance of the condition under consideration--the first symptoms began eight years before death with angina, and there were repeated attacks of cardiac asthma. {609} A careful study of the case was made by Howard[19] extending over several years, and weak heart, dyspnoea on exertion, and anginoid attacks were the prominent symptoms.

[Footnote 19: "Fibroid Disease of the Heart," _Canada Med. and Surgical Journal_, vol. viii., 1880.]

Several very careful studies of the disease have been made within the past few years.[20] Among the symptoms the following may be specially considered. The first place seems accorded by all to the cardiac weakness, and in consequence the pulse is feeble. By some (Rühle) irregularity is regarded as a special feature (delirium cordis), but Ebstein refers to three cases in which the pulse was always regular. Juhel-Renoy also speaks of it as frequent and regular. In many cases the number of beats appears about normal; in others there is a great increase; while in a third set the pulse may be very slow, sinking to 40 or 50 per minute. It is evident that in regard to regularity and frequency of the pulse there are very great differences. In this connection it is interesting to refer to the case of thrombosis of the coronary artery reported by Hammer,[21] in which the pulse sank to 8 per minute.

[Footnote 20: Rühle, "Zur Diagnose der Myocarditis," _Deutsches Archiv f. klin. Med._, Bd. xxii.; Ebstein, _Zeitschrift für klinische Medicin_, Bd. vi.; Leyden, _Ibid._, Bd. viii.--a most important and exhaustive article; Welch, in a paper read before the Medical Section of the American Medical Association, Washington Meeting, 1884; Juhel-Renoy, _Archives gén. de Médecine_, Juillet, 1883.]

[Footnote 21: _Wiener Med. Wochenschrift_, 1878, No. 5.]

Angina is a most important symptom; attacks may recur for years, and death may take place in a paroxysm. Asthmatic attacks are very common: a feeling of impending suffocation, and gasping for breath amounting in some instances to urgent dyspnoea. Oedema of the lungs may occur in these attacks. Fainting and pseudo-apoplectic attacks are frequent symptoms. The physical signs are not very definite or constant. The apex-beat may be displaced and weak, perhaps unrecognizable. With an increase in the area of dulness this is a sign of dilatation. A systolic murmur at the apex is not infrequent. There may be the bruit de galop; gradual heart failure, with general dropsy, is the mode of termination in a considerable number of cases.

The DIAGNOSIS can rarely be made with certainty. The combination of weakened heart, atheromatous arteries, and angina attacks occurring in a person above fifty years of age is certainly suggestive of the existence of this condition; but, as will be seen, this group of symptoms occurs also in fatty degeneration, although the anginoid attacks are probably not so frequent.

In spite of the admirable clinical memoirs above referred to, we are still in need of careful studies of an extensive series of cases, whereby we can get information which will enable us to distinguish more clearly than we can at present the diseases of the myocardium from one another. In this respect our pathological knowledge is in advance of our clinical.

The TREATMENT is largely that of cardiac dilatation and angina, which will be elsewhere considered. The condition is a chronic one, and often associated with hypertrophy, and many of the symptoms are dependent upon failing compensation. Under such circumstances digitalis is indicated, but when there are attacks of angina caution must be exercised in its use.

The Degenerations of the Heart-Muscle.

Under this division we shall consider the following conditions, all of which are characterized by an alteration in the quality and an impairment of function in the affected tissue: 1. Anæmic necrosis; 2. Parenchymatous degeneration; 3. Fatty changes, infiltration and degeneration; 4. Brown atrophy; 5. Amyloid degeneration; 6. Hyaline degeneration; and 7. Calcareous degeneration.

{610} 1. Anæmic necrosis is a condition which results in the heart-muscle when a branch of the coronary artery is blocked either by a thrombus or an embolus, or is obliterated by a progressive sclerosis. The region supplied by the affected vessel is deprived of blood and undergoes a process of infarction. In some instances the tissue is not infiltrated with blood, as in an ordinary infarct, but has a pale yellowish color and is very soft. When there is extravasation the color is more reddish-brown. Histologically, the muscle-cells are found in a state of granular degeneration, and on staining the nuclei do not take the tint, and the whole tissue ultimately assumes the homogeneous granular aspect of coagulation necrosis. There may be fatty degeneration in the contiguous muscle-fibres, and finally, as with infarcts in other organs, fibroid induration takes place. This process, as before mentioned, plays an important part in the production of the fibroid patches scattered through the myocardium. When fresh, the softening of the affected region may be marked, and the name myomalacia cordis which Ziegler[22] has suggested is so far suitable, but it seems more appropriately applied to that condition of general softening of the organ met with in severe fevers. This process most frequently affects the left ventricle, and if extensive may lead to rupture.

[Footnote 22: _Loc. cit._]

The clinical aspects of this condition, as induced by sclerosis of the coronary arteries, have been recently studied with great care by Leyden.[23] In acute cases death occurs in a few hours with symptoms of intense angina pectoris and heart failure. The subacute cases are characterized by recurring anginoid attacks lasting from a few minutes to half an hour. There may be attacks of asthma with heart weakness, and signs of oedema of the lungs. The clinical picture is that of angina pectoris, and the patient may have had similar attacks on previous occasions.

[Footnote 23: _Zeitschrift f. klin. Med._, Bd. vii., 1884.]

2. Parenchymatous Degeneration.--The relation of inflammation of the heart-substance to this degeneration is still somewhat indefinite. I have under Myocarditis described an acute interstitial form characterized by inter-fibrillar swelling with exudation and proliferation of corpuscles, and often granular or fatty degeneration of the muscle-cells. These changes may certainly be regarded as inflammatory, and they are met with either in association with endo- or pericarditis or in connection with specific fevers. Under the term parenchymatous degeneration or cloudy swelling Virchow described[24] a change of frequent occurrence in the heart-muscle and elsewhere, which I think should be distinguished from myositis, although the two processes may lead to alterations difficult to distinguish macroscopically. It is characterized by a pale, turbid state of the cardiac muscle, general, not limited, and a relaxed, soft, brittle condition of the walls. The turbidity and softness are the special features; there are no peri- or endocardial changes--simply the loss of color and consistence. It is the softened heart of Laennec and of Louis; and Stokes speaks of an instance in which "so great was the softening of the organ that when the heart was grasped by the great vessels and held with the apex pointing upward, it fell down over the hand, covering it like the cap of a large mushroom."[25] Microscopically, the fibres are indistinct, the protoplasm occupied by fine granules which obscure the striæ, and sometimes the nuclei. Proliferative changes rarely occur, although swelling and multiplication of the nuclei and the interstitial cells have been described. The granules may be extremely minute, or so large that they are mistaken for fat. They are generally uniform in size, and are scattered irregularly through the fibres. In extreme grades the entire fibre may be occupied by them, and no trace of structure can be seen. Dilute acids and alkalies dissolve the granules, but they resist the action of ether, indicating their albuminous nature. This condition is met with in the infectious diseases--typhoid, {611} typhus, small-pox, pyæmia, remittent fever, etc.--particularly when the disease is protracted and the temperature high. Apparently, we must regard it as an expression of the effect of the poison upon the metabolism of the fibres, inducing a separation of albuminous particles in a granular form. That the high temperature alone does not produce it is demonstrated by its absence in many other diseases in which this condition prevails. The relation to fatty degeneration is not clear. It would appear to precede the development of this change.

[Footnote 24: _Archiv_, vi.]

[Footnote 25: _Diseases of the Heart_, Am. ed., p. 373.]

The effect of this degeneration is virtually the same as that of myocarditis, already described. It produces the weak heart of fever so well described by Stokes,[26] with indistinct impulse, feeble or imperceptible first sound, and progressive diminution of contractile power. There is often a great reduction in the number of beats, which may sink to 40 or 50 per minute. In severe cases of typhoid fever we often have an opportunity of studying the progressive enfeeblement of the heart with weakening or disappearance of the first sound.

[Footnote 26: _Loc. cit._, chap. vii.]

To Stokes we are indebted for the suggestion of the use of alcohol in this condition, and the experience of the past forty years has fully confirmed this practice of the Dublin school.

3. Fatty Heart.--Two conditions of the heart are recognized under this heading--viz. fatty infiltration and fatty degeneration.

Fatty Infiltration.--Cor adiposum, Lipomatosis cordis, and Fatty hypertrophy or overgrowth are synonyms found in the older and more recent works.

A condition in which there is an excess of fat beneath the pericardium and a growth of the same between the fibres of the myocardium. There is normally a certain amount of fat in the cardiac groves, particularly the auriculo-ventricular, and along the coronary arteries. An excess is not infrequently met with in connection with general atrophy, whether the result of disease or the natural decay of old age. Here it serves as padding, and has no pathological significance. In very corpulent persons there is always much subpericardial fat; it forms a part of the general obesity, and in this state an excessive accumulation may lead to a dangerous or even fatal impairment of the contractile power of the heart. Obesity is the expression of a morbid tendency, generally hereditary, to the deposition of fat in the connective tissues. A sedentary life and the consumption of food rich in carbohydrates favor this tendency, but we see it arise under conditions just the opposite when the predisposition to polysarcia is marked. Males are more usually affected than females, at least in Great Britain and Germany.

In the inspection of the bodies of very corpulent persons we find the mediastinum occupied by masses of fat which may completely cover the pericardium. The entire heart may be enveloped in a thick sheeting of fat, through which not a trace of muscle-substance can be seen. Along the groves, the regions of normal deposit, the layer may be an inch or more in diameter. In some cases the muscle-substance beneath seems but slightly involved; there may be superficial infiltration and penetration of columns of fat between the bundles, but the thickness of musculature is normal, and apart from the excessive deposition there is not much amiss. In other instances the muscle-substance is seriously affected; on section of the ventricular wall the fat is seen to infiltrate the entire muscle, separating strands of fibres and reaching almost to the endocardium. There may be places, indeed, in the thinner parts of the ventricular walls in which there appears to be complete substitution of the muscle by fat. Even the papillary bundles may contain adipose tissue. The chambers are usually dilated and the entire organ soft and relaxed. Microscopically, the fat-cells are everywhere {612} seen infiltrating the muscle-tissue, separating the fibres and inducing atrophy. In some cases, even when the condition is advanced, the muscle-fibres appear normal, but in the majority fatty degeneration is also present. Often in these cases the coronary vessels will be found atheromatous.

The SYMPTOMS of fatty overgrowth will depend greatly on the degree of infiltration, the state of the muscle-fibres--whether normal or degenerated--and on the presence or absence of coronary atheroma. Many very fat persons enjoy excellent health and have actively beating hearts, which fail them only on severe exertion, when they get out of wind and experience cardiac distress, perhaps palpitation. The pulse is good and the heart sounds are clear. The signs of heart failure (which may be due either to excessive infiltration or secondary degeneration of the muscle, or both combined) in obese persons are generally very marked--breathlessness on slight exertion, amounting oftentimes to dyspnoea; attacks of asthma of a distressing nature coming on without cause or after a full meal; cough, with or without bronchitis; dizziness and pseudo-apoplectic attacks. Sudden death from syncope or rupture of the heart is common. Dropsical symptoms and cyanosis may supervene. The physical signs are those of heart weakness; impulse imperceptible or very diffuse; area of dulness increased, but often hard to delimit, with fat chest-walls and fatty mediastinum; sometimes a soft systolic murmur at apex; radial pulse rapid, weak, and irregular, in some instances very slow.

The DIAGNOSIS of the condition with such a series of symptoms in an excessively stout person can offer but little difficulty.

The TREATMENT in the early stage should be directed to reducing the general obesity, and such persons should be warned against taking too violent exertion or subjecting the heart to unusual strain. Moderate exercise, mental quietude, and careful dieting may do much toward postponing heart failure, which, when established, calls for the treatment which shall be described under Dilatation.

Fatty Degeneration.--An anomaly or disturbance of nutrition in which minute particles of fat accumulate in the protoplasm of the muscle-fibres, and impair the functional activity of the organ.

This is one of the most common of post-mortem conditions, and in mild grades is met with in a great variety of diseases. The fat is a product of the metabolism of the protoplasm of the muscle-fibres, and in a normal state it (or its immediate antecedents) is oxidized; but when either there is increased transformation or reduced oxidation the products accumulate in the protoplasm, and are evident as minute molecules or as distinct fine oil-droplets. The condition of cloudy swelling or parenchymatous degeneration appears in many cases to precede that of fatty degeneration, and sometimes the granules are of such a size, so abundant, and resemble fat so closely that chemical tests alone can distinguish between them.

A practical division of fatty degeneration is into--1, cases in which the process has attacked a normal heart; and 2, cases in which we find it associated with valvular disease and hypertrophic states of the muscular walls.

In the first group we have _(a)_ The degeneration which accompanies the failing nutrition of old age, of wasting diseases, and of cachectic states. _(b)_ The fatty change in the heart-muscle so often a sequence to, or coexisting with, the parenchymatous degeneration of fevers. _(c)_ The extreme fatty degeneration so constantly associated with profound anæmia. _(d)_ Certain poisons, particularly phosphorus; arsenic, lead, and antimony also act in the same way. The slow poisoning by alcohol is a very frequent cause of a gradually fatty degeneration of the heart. And _(e)_ some local causes are important in inducing this change in the previously normal organ. Pericarditis is almost invariably associated with involvement of the superficial myocardium, {613} either inflammatory or degenerative. Disease of the coronary arteries is a frequent and important cause of fatty metamorphosis. When due to the general conditions above mentioned, the affection is widely distributed in the organ; when the result of gradual narrowing of the vessels by atheroma, the distribution is in the regions supplied by the affected vessels.

The second group comprises those cases in which the fatty degeneration involves the muscle-substance in a condition of hypertrophy, and is an important element in inducing the disturbance of compensation upon which so many heart symptoms depend. Here the process may be more local, affecting, for example, the left ventricle chiefly, as in the hypertrophy from aortic valve disease or in association with contracted kidneys, or the right ventricle in chronic lung affections and mitral stenosis. More rarely we find the process confined chiefly to the auricles, but there may be advanced changes of this nature in the hypertrophied left auricle in mitral stenosis. The fatty degeneration of an hypertrophied heart may be induced by any of the general causes above referred to, but there are also special ones to which it is liable. The chronic congestion which accompanies a dilated heart affects the walls of the organ as well, and diminishes the vigor of the coronary circulation. In emphysema and in mitral stenosis, and other diseases which induce a dilated state of the right heart, fatty degeneration, sometimes combined with fibroid change, is, as Jenner pointed out,[27] very common. This state of the right chambers also interferes with the proper oxygenation of the blood in the lungs, and so acts in a double way. Degenerative changes in the coronary arteries are specially prone to accompany valvular diseases, on which the majority of cases of hypertrophy depend, and we have here one of the most serious causes of fatty degeneration in this state. And, finally, we see this change in some hypertrophied hearts without being able to ascertain any exciting cause: a nutritive breakdown occurs, of which the fatty degeneration is the expression. Possibly in such cases the trophic nerve-influences may be at fault.

[Footnote 27: _Medico-Chirurgical Transactions_, xliii.]

Defective oxidation, in whatever way brought about, seems the common factor in all forms of fatty degeneration. The process may be almost confined to the heart or be more or less general in the solid viscera and voluntary muscles. The diaphragm is sometimes much involved with the heart, even when the other muscles show no signs of the change. There certainly seems to be a special proneness to fatty degeneration in the heart-muscle which may perhaps be associated with its incessant activity. So great is the need of an abundant oxygen-supply that it early feels any deficiency, and in consequence is the first muscle to show nutritional changes.

Fatty degeneration is met with at all ages. I have seen it in the hypertrophied right ventricle of a new-born infant, with stenosis of the pulmonary artery. The cases dependent upon vascular changes are most frequent after middle life. Males appear more frequently affected than females. The form associated with anæmia is an exception to this rule. Stout persons are not more liable to be affected than thin ones; indeed, it is often, to use Paget's phrase, "a lean degeneration." Sedentary habits, worry, grief, and other depressing emotions are believed by some to have a predisposing influence. Persons with gouty and arthritic tendencies are more prone to this change.

The anatomical condition is very characteristic even to the naked eye, and the microscope may be required only in corroboration. It may be local or general. In the former case the left ventricle is most frequently affected, the right ventricle more rarely, and the auricles very seldom. The amount of subpericardial fat may be slight. If the process is advanced and in all the chambers, the heart looks large and is flabby and relaxed. It is pale, of a light yellow-brown tint, buff color, or, as it is sometimes expressed, a {614} faded-leaf color. The consistence is greatly diminished, and the substance tears easily and the finger can be readily thrust through the wall. Extreme grades are met with in profound anæmia and in phosphorus-poisoning. The fatty degeneration of coronary disease and of valvular affections is usually more local, and the heart has often a brownish-yellow tint from the coexistence of brown atrophy. In the left ventricle the papillary columns and the layers of muscle just beneath the endocardium are most affected, and in a curious streaked or patchy way--the tabby mottling of some authors. A similar change may be seen in the right ventricle, particularly in the hypertrophy from mitral disease. In the auricles the right may show patches on the musculi pectinati, but on the left, which is most often affected, the thick endocardium usually obscures it. Chemically, it has been shown that in fatty degeneration the heart may contain from 3 to 5 per cent. more fat than normal.

On microscopical examination of teased portions of the muscle the fibres are broken and irregular, and there is much free fat, in form of droplets, among them. The appearance of the fibres will vary with the intensity of the process; in mild grades there are minute scattered droplets in the protoplasm, not obscuring the nuclei or the striæ; but in an advanced condition the fibres seem occupied completely with minute globules, and no trace of structure can be seen. The patchy distribution of the fatty degeneration in many cases, usually evident to the naked eye, is corroborated by the microscope, and one may obtain portions of the muscle with scarcely a normal fibre, while in a contiguous bit the fibres are little if at all affected. In some instances of general fatty degeneration in anæmia, and even in fevers, as diphtheria, the process is so advanced that it is difficult to find any normal-looking fibres. Brown atrophy is a frequent accompaniment of fatty degeneration.

The effect of this change upon the heart is seen in a diminution of its functional power; the contractile force is weakened and the organ rendered incapable of doing its work efficiently. If the change occurs in a previously normal heart, much will depend on the rapidity with which it has supervened. Repeated hemorrhages or poisoning by phosphorus will induce in a few days an extreme degree of weakness rarely seen in the fatty degeneration of chronic anæmia--perhaps equally extensive. As a consequence of the enfeebled action of the heart, the arteries are not well filled during the systole, and there is anæmia of the organs. The mural weakness readily permits of dilatation, with imperfect emptying of the chambers and distension of the venous system. In hypertrophy the failing compensation is frequently due to the onset of fatty degeneration. During a sudden strain or a more continued effort than usual there may be heart failure, asystolism, or the walls may tear and sudden death occur from rupture.

The SYMPTOMS of fatty degeneration of the heart are by no means definite, being those of defective cardiac power. It is often met with post-mortem when not expected, and on the other hand we may fail to find it even when the symptoms seem to point very clearly to its existence. In chronic anæmia, in chlorosis, in fevers and wasting diseases the process may be extreme, without leading to any more marked symptoms than feeble action of the heart, palpitation on exertion or excitement, with signs of slight dilatation, and a soft mitral systolic murmur from incompetency of the valves. In cases of idiopathic anæmia, in which the fatty degeneration is perhaps more marked than in any other condition except phosphorus-poisoning, the pulse is frequently full, though soft, and regular so long as the patient is quiet. The symptoms of fatty degeneration in cases of valvular disease with hypertrophy are simply those of failing compensation, and we see the same process in the non-valvular hypertrophy of chronic Bright's disease. But, apart from these conditions, fatty degeneration occurs as part of a process of general failure {615} of nutrition, premature or senile. These form the cases of idiopathic fatty heart which seem so constantly to be associated with atheromatous changes in the coronary vessels. English writers have dealt specially with this form, which certainly appears to be more prevalent in Great Britain than on this continent or in Europe. In these cases there may be general obesity, but as often the subjects are of spare habit, with full atheromatous arteries, and other indications, perhaps, of early senility. They are usually persons who have lived freely and taken stimulants in excess. Among the symptoms believed to indicate fatty degeneration in these cases are--weak, irregular action of the heart, with a small intermittent pulse; cardiac pain, sometimes anginoid in character; dyspnoea, particularly on exertion, as in ascending an incline; signs of cerebral anæmia, indicated by vertigo or pseudo-apoplectic attacks and loss of mental power; the presence of an arcus senilis; and, as a final symptom, Cheyne-Stokes respiration.

Persistent irregularity in the action of the heart in a person with atheromatous arteries, and dyspnoea on exertion, without signs of valvular affection, are certainly suggestive of degeneration of the muscle-fibres of the heart. In some instances there has been noted a greatly diminished number of beats, 40 or 50 per minute, or even slower. Irregular action of the heart may, however, persist for years without indicating any serious mischief.[28] The yellow fatty arcus senilis is believed by many physicians to indicate a weak fatty heart, and it does occur in many persons of soft flabby habit of body with degenerated arteries and evidences of premature decay; but by itself it is of no value as a sign of vascular degeneration. It must not be confounded with the opaque white calcareous arcus not uncommon in elderly people, and met with occasionally in middle-aged persons. The Cheyne-Stokes breathing so often referred to as specially associated with fatty heart is, in my experience, a much more frequent concomitant of uræmic states.

[Footnote 28: In the spring of 1882, I saw, for Geo. W. Campbell, a gentleman aged eighty-two, a man of remarkable vigor, mental and bodily. He had an extraordinarily irregular yet full pulse, with atheromatous arteries--a condition which he assured me had been constantly present for close upon forty years, and had been a source of needless anxiety to many physicians, and for some years to himself.]

The physical signs of fatty degeneration of the heart are a weak impulse, often diffuse, and if the patient is thin the area of dulness may be found increased. In stout persons it is difficult to determine dilatation on account of the fat inside and out. The sounds on auscultation are generally weak, distant, and muffled, but in the fatty degeneration of anæmia the first will often be found sharp and distinct, though short and more like the second sound. A soft murmur, systolic in character, is not infrequently heard at the apex, and believed to be due to muscular incompetency.

The DIAGNOSIS is beset with difficulties, and in most cases we have to be content with probabilities, except in the instances due to anæmia, etc. Permanent weakness of impulse and the symptoms it entails, with signs of degeneration of tissue as shown by atheromatous arteries, are the most suggestive features, but even about them there are uncertainties. My own errors and a contemplation of those of several very eminent clinicians, taken in connection with the fact that some of the most typical cases of fatty heart which come under my observation have been instances of sudden death in persons pursuing their avocations, have made me very cautious in the diagnosis of this condition.

The PROGNOSIS depends entirely on the circumstances under which the degeneration has developed. In the weak fatty heart of chlorosis and anæmia, with a return to a normal blood-condition, the nutrition of the heart is improved and its action strengthened. Doubtless many cases of failing compensation are due to it, and a subsidence of the symptoms under {616} rest, digitalis, and careful feeding may simply mean improved nutrition of heart-muscle and disappearance of the fat which clogs its action. Where due to atheromatous changes, no permanent improvement can be expected; and in these cases, particularly if combined with fatty infiltration, rupture or fatal syncope may occur. In not a few of such cases the persons have not complained either to their physicians or friends of cardiac distress. The case of the celebrated Scotch divine, Chalmers, described by Begbie,[29] is an illustration of advanced fatty heart with sudden death in a man of extraordinary vigor of mind and body.

[Footnote 29: _Contrib. to Pract. Med._, 1862.]

The TREATMENT should be directed to the removal of the cause when possible, as the anæmia, febrile condition, etc. In all cases rest, quiet, and avoidance of excitement are to be rigidly enforced. Sudden exertions may prove instantly fatal. In the cases where there is hypertrophy with or without valvular disease, and the failing compensation is due to this cause, digitalis acts well, and should be combined with stimulants. In the senile and atheromatous cases great care must be exercised: the bowels should be kept loose, and the patient cautioned not to strain at stool or make any sudden exertion. He should lead a very quiet, regular life, and exercise great moderation in food, drink, and venery. Warm and Turkish baths are most dangerous. Iron, arsenic, and nux vomica are remedies from which benefit may be expected. Digitalis is, as a rule, contraindicated. We must remember that, as Sir William Jenner has remarked, fatty degeneration is sometimes a preservative lesion, and induces a due proportion between the cardiac strength and the arterial resistance, reducing the former when there is great atheroma and brittleness of the vessels. The application of blisters is often of use in allaying the pain, and nitrite of amyl should be given in the anginoid attacks.

4. Brown atrophy is a very common degenerative change in the heart-muscle, particularly in the hypertrophied organ of valve affections. In old people and in persons dead of wasting diseases it seems invariably present. When advanced, the color of the muscle is quite distinctive--a dark red-brown and the consistence may be greater than normal. Microscopically, the fibres present a central accumulation of brown pigment, generally arranged about the nuclei and extending up and down the cells. The cement-substance between the cells is often unusually distinct in these cases, and seems more fragile than in healthy muscle. The composition of the pigment has not, so far as I know, been determined, but it is doubtless, like that of the brown induration of the lung and red atrophy of the liver, derived from the hæmoglobin, and possibly, as in these latter conditions, is connected with feeble venous circulation.

5. Amyloid degeneration of the heart is occasionally met with, but rarely in so advanced a grade as to be recognizable macroscopically. It occurs in the intermuscular connective tissue and in the blood-vessels, not in the fibres, and occasionally may be extensive, as in a case mentioned by Ziegler.[30]

[Footnote 30: _Pathologische anatomie_, 3te Aufl., Lief. i., §59.]

6. The hyaline degeneration of Zenker is sometimes seen in the heart-muscle in cases of prolonged fever. The affected fibres are swollen, homogeneous, translucent, and the striæ very faint or entirely absent.

7. Calcareous degeneration may occur in the myocardium, involving the fibres and forming a definite calcareous infiltration of the protoplasm, as well figured and described by Coats.[31] It is a rare condition, whereas extensive calcified plates in endo- and pericardium are by no means uncommon.

[Footnote 31: _Pathology_, 1883.]

{617} Spontaneous Rupture of the Heart.

Laceration of the wall of the heart is usually associated with fatty infiltration or degeneration, most frequently the latter. It is doubtful if in any instance the healthy muscle has broken. Rare causes are--acute softening, in consequence of embolism of a branch of a coronary artery; abscess from pyæmia; or an acute ulcer of the endocardium. Cysts simple or hydatid are mentioned, but the extreme rarity of causes other than fatty changes may be inferred from the statistics of Quain,[32] who states that of 100 cases of rupture collected by him, fatty degeneration was noted (microscopically) in 77, and in the others there was softening in all but 2, or no mention was made of the condition of the wall.

[Footnote 32: _Loc. cit._]

Males are more frequently the subject of this accident than females, and the great majority of cases occur in persons over sixty years of age--two-thirds of the eases tabulated by Quain.[33]

[Footnote 33: _Loc. cit._]

The rent may occur in any of the chambers, but the most frequent site is the left ventricle on the anterior wall, not far from the septum. Statistics give, for 55 cases,[34] 43 in left ventricle, 7 in right ventricle, and 3 in right auricle and 2 in the left auricle.

[Footnote 34: Elleaumé, _Essai sur les Ruptures du Coeur_, Paris, 1857.]

The break is generally a ragged, irregular rent in the course of the fibres, and the trajét may be oblique and crossed by strands of muscle. The internal orifice may be larger than the external; the opposite is rarely the case. Two or more rents have been found. Usually the fissure is not very long--from a quarter of an inch to an inch--but there are cases of long rents extending from base to apex. Clots usually block the orifices, and the pericardium also contains large coagula. Evidence is sometimes found to indicate that the tear has occurred slowly, as attempts at repair may be present.

The wall in the vicinity of the break has usually been found in a state of degeneration, and we can readily understand how sudden and violent contractions might strain a weak part and tear the substance. Perhaps irregularity in the contractions may be an important factor, such as we may suppose occurs when a wave of contraction reaches a patch of advanced fatty change or softening from embolism.

The accident usually takes place during exertion or excitement. Many cases are reported during straining at stool, others while lifting weights, running, or during coitus. Cases are mentioned as occurring during sleep or while at rest.

There may be no preliminary symptoms, and without warning the patient falls, and with a few gasps or a cry is dead. This occurred in 71 of the 100 cases collected by Quain. In other instances there is great pain in the præcordial region, a sense of suffocation and anguish, with vomiting, and life may be prolonged several hours. In one instance the patient lived eleven days.[35] Probably in such cases there is a small rent at first which gets blocked with clots, and only a small amount of blood oozes into the pericardium with each systole. The symptoms may be those of simple heart failure, as in a case I examined for Burland of Montreal, in which the patient lived thirteen hours after the onset of the symptoms, and was able, though with difficulty, to continue his walk up a rather steep hill.[36] Death appears to occur from shock or syncope, sometimes from compression of the heart by the extravasated blood. In the case just mentioned the amount of blood in the pericardium was {618} very much less than I have seen in cases of rupture of an aneurism into this sac.

[Footnote 35: Barth, _Archiv. générales_, 1871.]

[Footnote 36: This was a case which illustrated well the latency of many cases of fatty heart. The patient was an active merchant, aged sixty, who had never complained of cardiac trouble, and had only a short time before his death effected a reinsurance upon his life for a large amount.]

In protracted cases the nausea and vomiting may for a short time lead to the supposition that the case is one of severe indigestion, but, as mentioned above, in the great majority of cases death occurs at once, and in the others there can rarely be any question of diagnosis, and still less of treatment.

Atrophy of the Heart.

DEFINITION.--A diminution in size and weight of the organ, due to degeneration and atrophy of the muscular fibres.

The old writers applied the term phthisis of the heart to this condition. The decrease is always in weight, and usually in size; it is doubtful if there is an atrophic and dilated heart in which, with the wasting, the size is maintained by the dilatation. In many of the degenerations, particularly fatty and fibroid, there is local atrophy of the muscle-fibres and yet the weight and size of the organ are not changed.

The varieties which have been recognized correspond to those of hypertrophy--viz. the simple, eccentric, and concentric forms, but the two latter are probably only conditions of contraction or dilatation in a wasted heart. The post-mortem contraction in the small left ventricle of persons dead of chronic disease may be excessive; and here, as in concentric hypertrophy, the examination must be made with care.

ETIOLOGY.--The atrophy is either congenital or acquired. The congenital atrophy which is most frequently seen in women is in association with defective development of the arterial system and the generative organs. This is occasionally very marked in chlorosis, and is described and figured by Virchow in his monograph on this subject.[37] But apart from this general hypoplasia of the heart and vessels in women, we sometimes in the post-mortem room find in a man, dead perhaps of an acute disease and without any cardiac symptoms, a heart small out of all proportion to the size and general nourishment of the body. Many of the older writers mention this. Gowers refers to a case which Allan Burns narrates, in which the heart of an adult was not larger than that of a child of six or seven. Morgagni has a similar observation.

[Footnote 37: _Ueber die Chlorose_, Berlin, 1872.]

The great majority of the cases are secondary or acquired, and are met with in the wasting diseases, as cancer, phthisis, prolonged suppuration, and diabetes. The cardiac wasting is part of the general marasmus which affects the whole body. In about half the cases of phthisis the heart is small.[38] In cancer of the pylorus the most extreme wasting has been found. Disease of the coronary arteries is an occasional cause, but it most frequently produces local atrophy or degeneration. Compression by pericardial effusion, fatty infiltration, and pericardial adhesions are mentioned as rare causes.

[Footnote 38: Quain, _loc. cit._]

A rough guess at the proportional size of the heart may be made by comparing it with the closed right fist of the person. Weighing gives the most accurate test, and in each instance regard must be had to the size of the body. In some instances the organ has weighed only two or three ounces. The heart figured by Bramwell,[39] one of the smallest on record, weighed only 2 ounces and 2 drachms. Quain[40] refers to one, from a girl aged fourteen, which weighed only 1 ounce 14 drachms.

[Footnote 39: _Diseases of the Heart_, 1884.]

[Footnote 40: _Loc. cit._]

Usually, in secondary atrophy, the visceral pericardium is wrinkled and the coronary arteries prominent and tortuous--two features of great importance in determining atrophy and in distinguishing between the acquired and {619} congenital forms. The pericardial fat is variable in amount. Microscopically, brown atrophy is the most constant change; fatty degeneration much less common. Senile atrophy may present very similar appearances. The heart may be tough and firm from an increase in the fibrous elements. The pericardial fluid I have often noticed to be much increased.

There are no characteristic SYMPTOMS. The heart-muscle may be able to fulfil the requirements of the wasted frame. A feeble impulse and diminished area of dulness may be present, but in the marasmus of middle-aged or elderly people emphysema of the anterior margin of the lung may seriously interfere with a proper examination. The increased pericardial effusion occurs toward the end. The heart sounds are feeble and the pulse weak. Palpitation is frequent, and there may be the usual signs of anæmia, dizziness, etc.

The condition may be suspected, but is rarely diagnosed during life.

The PROGNOSIS depends upon the disease to which the atrophy is secondary, to the amelioration of which also the treatment must be directed.

Hypertrophy of the Heart.

DEFINITION.--An increase in the size of the heart due to an increased thickness, total or partial, of the muscular walls.

VARIETIES.--Two forms may be recognized--simple hypertrophy, in which the cavity or cavities remain of the normal size; and eccentric hypertrophy, in which with increased thickness of the walls there is enlargement of the cavities. Dilated hypertrophy and hypertrophy with dilatation are terms by which the latter form is most frequently described.

By many writers a third variety, concentric hypertrophy, is recognized, in which there is diminution in the size of the cavity with thickening of the walls; but in these cases we have to deal with a post-mortem change--rigor mortis; and if the organ is kept for twenty-four hours or soaked in water, the so-called concentric hypertrophy will usually disappear.

The increased size may affect the entire organ, general hypertrophy; or only one side or one cavity, partial hypertrophy. The latter is the most common. Of the single chambers the left ventricle is most frequently involved, then the right. The auricles are rarely affected alone, but the left is more often than the right.

ETIOLOGY.--Disturbed innervation and increased work are the two principal causes of cardiac hypertrophy. We see hypertrophy from deranged innervation (1) in Basedow's disease (exophthalmic goitre); (2) in long-continued nervous palpitation from any cause, particularly sexual excesses; (3) certain poisons and articles of diet appear to act in this way, as tea, coffee, alcohol, and tobacco.

In all these cases there is simple over-action or increased functional activity, which, if prolonged, certainly produces some degree of hypertrophy. How this condition is brought about is not very clear. We may suppose the increased frequency of contraction to result from stimulation of the accelerator nerves, as seems probably the case in exophthalmic goitre; from irritability of the cardiac ganglia themselves, owing to the influence of such toxic agents as tea, tobacco, etc.; or from defective vagus control. Long-continued neurotic palpitation in reality causes hypertrophy by increasing the work of the heart, for under perverted stimuli the ventricular contractions are doubled in frequency--sometimes in force as well--while maintaining the circulation in normal vessels offering no increased resistance to the blood-flow.

There can be no doubt of the occurrence of actual hypertrophy as a sequence of the irritable heart induced by sexual excesses and tobacco. I had under observation on and off for several years a very emotional and {620} hypochondriacal young man addicted to venery, whose left ventricle became strongly developed and beat outside the nipple-line. His entire thoughts became centred in his heart trouble, and he travelled from one authority to another in this country and Europe seeking advice.[41] The smoker's heart rarely leads to much hypertrophy, but in young lads it may do so, and even induce more serious disease, as indicated by the presence of murmurs and signs of cardiac failure. The abuse of spirits as a cause of hypertrophy is not very clearly established. Alcoholism appears to be a factor in the production of atheroma. I have been struck by the fact that in four typical instances of so-called idiopathic hypertrophy occurring in powerfully-built workers there was a history of intemperance; and it is quite possible that this may have combined with the muscular efforts in inducing the heart disease; at any rate, it would prove an important element in hastening the final breakdown when from any cause hypertrophy had arisen.

[Footnote 41: After three or four years of most unnecessary worry in the expectation of death from heart disease, this patient has quieted into the belief that there is not anything seriously wrong with his heart, and has now rarely any indications of trouble.]

The majority of cases of hypertrophy of the heart are due to mechanical causes leading to increased resistance and increased work on the part of the organ. Under these circumstances, as in other hollow viscera, the muscle develops, gets thicker and firmer, and capable of accomplishing the extra labor thrown upon it. Defects in the valvular mechanism, obstruction, or incompetency, and increased resistance to the blood-flow in the arteries, are the most important causes of hypertrophy. The ultimate factor in all is heightened pressure within the cardiac cavities due to one of two things--increased volume of blood to be moved or difficulty in propelling the normal volume, caused by obstruction to the flow either central or peripheral.

Pericardial adhesions may impede the action of the heart, and either directly cause hypertrophy or induce dilatation and a consequent hypertrophy.

The details regarding the etiology are best considered in a study of hypertrophy as it affects the individual chambers.

Left Ventricle.--This chamber is much more frequently affected than any other, and may be involved alone or as part of a general enlargement of the organ. The more important causes are as follows:

(1) Aortic Stenosis.--To send the normal charge of blood through a narrowed orifice the muscle must contract with increased force, and to accomplish the work the walls increase in thickness. There may be simple hypertrophy without dilatation of the chamber, but in the later stages this inevitably supervenes.

(2) Aortic Regurgitation.--Curling and foreshortening of the aortic cusps permits of a backward flow into the ventricle during its diastole, with the production of dilatation and increased pressure, to overcome which the walls thicken--eccentric hypertrophy. This is one of the most common causes, and leads to enormous enlargement of the heart.

(3) Mitral Insufficiency.--In extreme grades of mitral stenosis the left ventricle is usually small, but when the curtains are curled and the patent auriculo-ventricular orifice large, there may be very great hypertrophy. Free regurgitation is always accompanied by considerable eccentric hypertrophy, due to the distension of the chamber by the extra quantity of blood forced in at each auricular systole.

(4) Pericardial adhesions, particularly when in addition to union of the layers the parietal membrane is firmly united to the pleura or to the sternum, may cause hypertrophy of the left ventricle alone, but more commonly of the whole heart.

(5) Abnormal Conditions of the Aorta.--_(a)_ Atheroma, with or without dilatation of the arch, is a cause of hypertrophy, for the heart has to {621} compensate for the loss of arterial elasticity, an important factor in the onward movement of the blood during the diastole; and, again, there is increased resistance in the wider tube. _(b)_ Great narrowing, as in the congenital coarctation just beyond the ductus arteriosus, which may produce colossal hypertrophy. Pressure upon the large vessels in the thorax by tumors may act in the same way. _(c)_ Aneurism of the aorta is not often accompanied by hypertrophy unless the valves are affected. Theoretically, it might be expected, as a large saccular dilatation would certainly appear to be a cause of increased resistance, but in uncomplicated cases the experience of most observers appears to accord with that of Stokes,[42] who states that we usually find a small heart. Occasionally, however, there is marked hypertrophy even without valvular disease.

[Footnote 42: _Loc. cit._]

(6) Kidney disease, acute and chronic, is very frequently accompanied with hypertrophy of the left ventricle. Indeed, simple hypertrophy is more often met with in chronic Bright's disease than under any other conditions. Increased blood-pressure in the smaller arteries throughout the body is now very generally acknowledged to be the immediate cause. But how this is brought about is a question not yet satisfactorily determined.

We have to deal with two sets of cases. There is the cardiac hypertrophy accompanying acute or subacute nephritis, particularly the scarlatinal. Here there are no chronic arterial changes, and the increased arterial tension appears to be due to contraction of the smaller arteries under the influence of retained excreta, which may act through the vaso-motor centre, as Ludwig observes, or possibly directly upon the unstriped fibres of the tunica media of the arteries. Bright's original explanation still holds good, I think, when he says that the altered quality of the blood "so affects the minute and capillary circulation as to render greater action necessary to send the blood through the distant subdivisions of the vascular system."[43]

[Footnote 43: _Guy's Hospital Reports_, 1836.]

The hypertrophy of the left ventricle in connection with contracted kidneys is more frequent and more marked. Traube suggested[44] that the interference with the local circulation in the kidneys by the obliteration of vessels increased the work of the heart and induced the hypertrophy, but it is much more probable that the change is a widespread one throughout the body. Gull and Sutton hold[45] that in these cases there is a condition of arterio-capillary fibrosis in which the small arteries are thickened and their calibre diminished, leading in time to a more or less widespread sclerosis in various organs, particularly the kidneys. As a result of this fibrosis, the movement of blood in the smaller vessels is much impeded, the arterial tension increased, and the work of the heart greatly augmented. On the other hand, George Johnson[46] maintains that the muscular coat of the arterioles becomes thickened under the influence of retained excreta, and they are in a state of spasm which increases the tension and heightens the blood-pressure in the left ventricle.

[Footnote 44: _Gesammelte Beiträge_, Bd. ii.]

[Footnote 45: _Medico-Chirurgical Transactions_, lv., 1872.]

[Footnote 46: _Ibid._, vol. xxxiii.]

The question can scarcely be considered settled as regards details, but the general fact of increased peripheral resistance is well established, and it is one of the most frequent causes of non-valvular hypertrophy. It may be quite marked in persons without positive evidence of renal disease as indicated by albumen or casts in the urine, but in whom the condition of arterio-capillary fibrosis is evident from the thickened state of the small arteries, the increased tension, and the firm dislocated impulse of the heart.

(7) Prolonged muscular exertion has been much insisted upon as a cause of cardiac hypertrophy by DaCosta, Myers, Albutt, Seitz,[47] and others. {622} Soldiers, blacksmiths, miners, mountaineers, and men whose occupations call for heavy and prolonged exercise occasionally develop hypertrophy of the heart, which it seems reasonable to connect with the over-use of the muscles. DaCosta's irritable heart in young soldiers appears to represent the early stage of this condition. In 38 per cent. of the cases excessive marching was the cause. He was able to confirm the existence of hypertrophy by autopsy. It is not uncommon to meet with cases of pronounced heart disease, with symptoms of failing compensation, dropsy, etc., in large, powerfully-built men who have been engaged in laborious occupations, and who are admitted to hospital with the clinical picture of chronic valvular disease. At the autopsy one is surprised to find an hypertrophied and dilated heart without valve lesion, perhaps no extensive arterial degeneration, and no kidney disease. They are called cases of idiopathic hypertrophy, but I believe that some of them, at any rate, are instances of a condition induced by prolonged muscular effort. I have had an opportunity of studying carefully four such cases, and I have seen autopsies in two other instances. As I mentioned, alcoholism may be also a factor in these cases, as most of them occur in hard drinkers.

[Footnote 47: _Die Ueberanstrengung des Herzens_, Berlin, 1875--a collection of six monographs on the subject.]

How muscular effort acts in inducing hypertrophy has been much discussed. It seems rational to suppose that prolonged action of the heart at a rate more vigorous and rapid than normal would induce enlargement of its muscle, just as constant exercise acts with others; and possibly within limits this does take place. Albutt speaks of the large red left ventricles in the Leeds iron-workers killed by accident or cut off by acute disease. No doubt the thickness of the ventricle is measured by the muscular needs of the system. Muscular contraction affects the heart in two ways: first, the venous flow is accelerated, more blood reaches the right heart, and is sent to the lungs, and more reaches the left ventricle and the systemic arteries. The fuller inspirations also favor flow to the heart. When the exercise is excessive the right heart and the venous system become still more distended, and the outflow from the peripheral arteries proportionately retarded and the tension in them increased--particularly is this the case in efforts requiring straining, as in lifting, etc.; and, secondly, the effect of muscular contraction has been shown by Traube to increase very greatly the pressure in the arteries. Gaskell, however, states[48] that when a muscle contracts its own arterioles dilate; but however that may be, the increased tension during muscular contraction can be determined in the radial by the finger, and still better by the sphygmograph, during steady contraction of the muscles of the arm. In yet a third way the blood-pressure may be increased during violent muscular efforts, particularly when the breath is held. The vaso-motor centre is stimulated by the lack of oxygen, and in consequence the blood-pressure rises in the peripheral arteries. At the end of prolonged contests we sometimes see men get pale or the left ventricle may become so embarrassed that they faint.

[Footnote 48: _Journal of Physiology_, iii.]

(8) That the heart becomes hypertrophied during pregnancy has been specially insisted upon by French writers, Larcher[49] and others. Many doubt the correctness of their deductions, but the weight of evidence seems to point unmistakably to the existence of moderate increase in the thickness of the walls of the left ventricle.[50] Cohnstein[51] connects it with the hydræmic and chlorotic conditions of the blood, so liable to develop during pregnancy.

[Footnote 49: _Archives générales_, 1859.]

[Footnote 50: McDonald, _Heart Disease during Pregnancy_, London, 1878.]

[Footnote 51: _Virchow's Archiv_, lxxvii.]

(9) Hypertrophy of the right heart in disease of the lungs or of the valves is usually followed by more or less hypertrophy of the left ventricle as well, caused by the increased work in consequence of retarded outflow into the venous system.

{623} Right Ventricle.--Hypertrophy of this chamber is most frequently met with in connection with disease of the left side of the heart; next with various chronic affections of the lungs; and lastly with valvular affections of the right side.

(1) Mitral lesions--incompetence or stenosis--are very common causes which act by increasing the resistance in the pulmonary veins and obstructing the free flow of blood in capillaries of the lung. To compensate for this defect the walls of the right ventricle increase in size, and the hypertrophy at first may be unattended with dilatation.

(2) Pulmonary Lesions.--The obliteration of any considerable number of blood-vessels within the lungs by emphysema, cirrhosis, or phthisis (sometimes), occasionally the compression of pleuritic exudation, increases the blood-pressure in the pulmonary artery and rapidly leads to hypertrophy of the right heart. Narrowing of the main branches of the pulmonary artery by the growth of tumors or an aneurism of the aorta occasionally produces the same effect.

(3) Valvular lesions on the right side are rare causes of hypertrophy in the adult, but during foetal life, when endocarditis is more prevalent in the pulmonary and tricuspid valve, stenosis or insufficiency at these orifices leads to great enlargement of the ventricle. Pulmonary stenosis is the most common lesion; incompetence is not often met with. Lesions of the tricuspid valves in the adult are almost always associated with mitral disease. When the dilated hypertrophy of the right ventricle reaches a certain grade in cases of mitral disease or pulmonary lesion, tricuspid incompetence develops.

(4) Among other causes which may be mentioned are pericardial adhesions, which some think tend specially to the production of right-sided hypertrophy and extensive pleuritic adhesions. Atheroma of the pulmonary arteries is more often a consequence than a cause of hypertrophy.

The auricles are usually dilated and hypertrophied; simple hypertrophy is probably never seen. In the left auricle this condition develops in lesions at the mitral orifice, particularly stenosis when it compensates for the obstruction. In free mitral regurgitation the hypertrophy is not so marked.

The right auricle hypertrophies when there is greatly increased blood-pressure in the lesser circulation, whether due to mitral stenosis or pulmonary lesions, and incompetency at the tricuspid orifice. Stenosis of the auriculo-ventricular orifice is a less frequent cause. The dilatation is always excessive.

MORBID ANATOMY.--In general hypertrophy the entire organ is increased in size and weight; more commonly we find the condition limited to two or three chambers or to one side. The estimation of slight grades of enlargement is difficult, but where the increase is marked the process is simple enough. The volume of the heart varies in different individuals according to their age and size. The normal heart is about the size of the closed fist, and, as Virchow suggests, a fair estimate can be made by comparing the two together. By careful weighing we get much more accurate information. The heart of an average-sized man weighs about 9 oz., of a woman about 8 oz. In great hypertrophy the organ may weigh three or four times the normal amount. A heart which weighs over 12 oz. in a man, and over 10 oz. in a woman, may be considered hypertrophied. Hearts weighing from 16 to 20 oz. are not uncommonly met with. Weights above 25 oz. are rare. The heaviest hearts on record are described by Beverley Robinson of New York,[52] 53 oz.; Dulles of Philadelphia, 48 oz.; and there are several cases described in the _Transactions_ of the London Pathological Society of the organ weighing as much as 46 oz.

[Footnote 52: _New York Medical Record_, 1883.]

{624} Next to weighing, careful measurement of the thickness of the walls is the best means of determining hypertrophy. When there is great dilatation of a chamber the walls, though actually thick, may look proportionately thin; and on the other hand, when rigor mortis is present the cavity may be very small and the walls appear enormously thick. In this case measurements should not be made until the heart has been soaked in water and thoroughly relaxed. The normal thickness of the left ventricle is about half an inch (12 or 13 millimeters), being thicker toward the base. It is well to measure in two or three places, not including the papillary muscles. A thickness of 10 lines or over (20 to 25 mm.) indicates hypertrophy. It is rare to meet with the wall thicker than 1 inch (25 mm.), even in very great hypertrophy. The right ventricle is thinner than the left, and has an average diameter of from 2 to 3 lines (4 to 7 mm.). A thickness of from 6 to 9 lines (13 to 20 mm.) may be met with in great hypertrophy. It is very rare to see a diameter of more than three-quarters of an inch, but cases are reported of a thickness of over an inch. The left auricle has a normal thickness of about a line and a half (3 mm.), which in considerable hypertrophy may be nearly doubled. The wall of the right auricle is even thinner than the left, rarely exceeding 1 line in diameter. In hypertrophy the sinus does not present a marked increase in thickness, but the appendix, particularly the musculi pectinati, may be greatly developed and measure from 2 to 3 lines in diameter.

The shape of the heart is much affected by the degree of hypertrophy in different cavities. Great enlargement of the ventricles broadens the apex, and the conical shape is lost. In the enormous hypertrophy and dilatation of aortic insufficiency the increased breadth and rotundity of the apex becomes very marked. When the right ventricle is chiefly affected, it occupies a large share of the apex, and the transverse diameter of the organ is increased. When due to mitral stenosis the contrast between the large broad right ventricle extending well to the apex and the small left chamber is very striking.

When not degenerated the muscle-tissue of an hypertrophied heart is of a deep-red color, firm, and usually cuts with slightly increased resistance. The right ventricle often has a peculiarly hard, leathery feel, which was noticed by Rokitansky. In simple hypertrophy of the left ventricle the papillary muscles and columnæ carneæ may be increased in size, but the former often appear flattened in great eccentric enlargement. The trabeculæ are usually much more developed in the right ventricle and in the appendix of the right auricle than in the left chambers. Very often the tissue looks pale, and may be soft from the occurrence of fatty degeneration.

The histological characters of the changes in hypertrophy have been much studied, particularly with a view of determining the question of numerical increase. Hepp[53] described an increase in the thickness; but most recent observers regard the hypertrophy as due to numerical increase, resulting from the development of new fibres, either by the splitting of the old ones (Rindfleisch) or their growth from interfibrillar nuclei.[54] Wilks and Moxon[55] and Gowers[56] find that the fibres are not increased in size. Letulle[57] thinks that there is a process of progressive hyper-nutrition of the fibres.

[Footnote 53: _Henle's Zeitschrift_, 1854.]

[Footnote 54: Zielonko, _Virchow's Archiv_, lxii.]

[Footnote 55: _Pathological Anatomy_, London, 1875.]

[Footnote 56: _Reynolds's System_.]

[Footnote 57: Quoted by Peter, _loc. cit._, p. 280.]

The toughness of the hypertrophied muscle is due to the increase in the connective tissue, which is more marked as a rule in the right than the left ventricle. Sometimes, indeed, it is not at all noticeable in the latter, which may be soft and tears readily with the finger.

SYMPTOMS.--Hypertrophy is a conservative process, usually secondary to some valvular or arterial lesion, and is not necessarily accompanied by any {625} symptoms. So admirable is the adjusting power of the heart that, for example, an advancing stenosis of aortic or mitral orifice may be for years perfectly counterbalanced by a progressive hypertrophy, and the subject of the affection be happily oblivious to the existence of heart trouble. Particularly is this the case with mitral stenosis and the consequent hypertrophy of the left auricle and right ventricle. While leading quiet lives and not straining the heart with violent exertion, such persons may not suffer in any way, or perhaps only experience a little shortness of breath when going up stairs. Indeed, the hypertrophy is in almost all instances an unmixed good, and many of the symptoms which arise are to be attributed to its failure, or, as we say, disturbance of compensation.

The left ventricle is most often involved, and the clinical features of hypertrophy are best seen when it is affected. Inspection may reveal decided bulging of the præcordia, producing in extreme instances marked asymmetry of the chest. This is most frequent in persons under twenty years of age, and it may occur without any pericardial adhesions, which Shroetter[58] thinks are invariably associated with this condition. The intercostal spaces may be widened, and the area of visible impulse is much increased. On palpation the character and position of the apex-beat give most important results. It is stronger, more forcible and heaving, and may lift the chest-wall. With each systole the hand or the ear applied over the heart may be visibly raised. A slow heaving impulse is one of the best signs of simple hypertrophy; when there is large dilated hypertrophy the forcible impulse is often more sudden and abrupt. A second, weaker, impulse can sometimes be felt, due possibly (as Gowers suggests) to a rebound from the aortic valves. The area of impulse is greatly increased, and the beat may be felt in the sixth, seventh, or eighth interspace from an inch to three inches outside the nipple. The downward dislocation of the apex is an important sign in hypertrophy of the left ventricle; simple outward displacement may be due to enlargement of the right ventricle.

[Footnote 58: _Ziemssen's Encyclopædia_, vol. vi.]

In moderate grades of hypertrophy, as seen in chronic Bright's disease, the apex-beat may be in the sixth interspace in the nipple-line or a little outside it.

Percussion gives an area of increased dulness, due to the much larger portion of the heart which comes in contact with the chest-wall. The dulness in the parasternal line may begin at the third rib or in the second interspace, and the transverse limits extend from half an inch to two inches beyond the nipple-line, and an equal distance beyond the middle line of the sternum. The dull region is more ovoid than in health. When carefully delimited and measured, there may be in the colossal hypertrophy of aortic valve disease an area of dulness from seven to eight inches in transverse extent. In moderate grades a transverse dulness of four inches is not uncommon.

On auscultation the heart sounds, when there is no valve disease, may not present any special changes, but the first is often prolonged and dull; but when there is dilatation as well, it may be very clear and sharp. Reduplication is not uncommon, particularly in the hypertrophy of renal disease. A peculiar clink--the tintement métallique of Bouillaud--may sometimes be heard, with the impulse most frequently just to the right of the apex-beat. The second sound is clear and loud, sometimes ringing in character or reduplicated. When the hypertrophy depends upon valvular lesions the sounds are of course much altered, and replaced or accompanied by murmurs.

The pulse of simple hypertrophy not dependent on valvular lesions is usually firm, full, and strong, of high tension, and regular. It may be increased {626} in frequency, but often is normal. In eccentric hypertrophy the pulse is full, but softer, and usually more rapid. So long as the hypertrophy is maintained the pulse is regular; one of the earliest signs of failure and dilatation is irregularity and intermittence. The various modifications of the pulse in connection with valve disease are considered elsewhere.

Among symptoms which patients complain of most frequently are unpleasant sensations about the heart--a sense of fulness and discomfort, rarely amounting to pain. This may be very noticeable when recumbent and on the left side. Actual pain in simple hypertrophy is rare, but in the irritable heart from tobacco and in neurasthenics with slight enlargement it is often a very troublesome symptom. Palpitation is not often complained of, nor do patients always have sensations from the violent shocks of a greatly hypertrophied organ; others, again, will have very uneasy feelings from a moderately exaggerated pulsation. The general condition of health has much to do with this: we are not in health conscious of our own heart's action, but one of the very first indications of nervous exhaustion from excesses or over-study is the consciousness of the heart's action, not necessarily accompanied by palpitation. Flushings of the face, noises in the ear, flashes of light, and headaches are not uncommon.

There are certain untoward effects of long-continued hypertrophy of the left ventricle which must be mentioned, chief among which is the production of atheromatous degeneration of the vessels. Particularly is this the case when the hypertrophy results from increased peripheral resistance. The heightened blood-pressure in the arteries (which is expressed by the word strain) gradually induces an endarteritis and a stiff, inelastic state of those vessels most exposed to it--viz. the aorta and its primary divisions. In overcoming the peripheral obstruction the hypertrophy "ruins the arteries as a sequential result" (Fothergill). It is in this way that prolonged muscular exertion acts injuriously, and leads to two common morbid conditions in athletes and persons whose employment necessitates violent exercise of the muscles--viz. aneurism and sclerosis of the aortic semi-lunar valves, with incompetency. Syphilis certainly does not embrace the entire etiology of aneurism, the occurrence of which in soldiers, strikers, foundrymen, etc. can be traced to arterial strain. So also with the sclerosis of the semi-lunar valves--just enough, perhaps, to produce incompetency; how common it seems to be in strong, well-built men whose excesses have been on the cinder-path or on the river! The increased aortic tension, with the more forcible recoil and closure of the semi-lunar valves, would seem to be factors in the production of this condition. Aortic incompetency is the special danger of athletes, and no inconsiderable number of the cases of this lesion occurring in men without rheumatic or syphilitic history may be traced to over-use of the muscles.

Another special danger is rupture of the blood-vessels, particularly of the brain. In the condition of general arterial degeneration associated with contracted kidneys and hypertrophied left heart apoplexy is common; indeed, we may say that in the majority of cases of cerebral hemorrhage there is sclerosis of the cerebral vessels, often with the development of miliary aneurisms, and the rupture is directly induced by the forcible action of the heart.

Hypertrophy of the right ventricle in the adult is rarely induced by valvular disease on the right side, but is a result of increased resistance in the pulmonary circulation, as in cirrhosis of the lung and emphysema, or in stenosis of the mitral orifice. When the compensation is perfect, and the hypertrophy fully maintains the equilibrium of the circulation, there are no symptoms. Extra exertion, as in ascending stairs or running, may induce shortness of breath, but in many respects hypertrophy of {627} the right ventricle is the most enduring and salutary form in the whole range of cardiac affections. For long periods of years the effects of mitral stenosis may be counterbalanced completely, and only sudden death by accident or an acute disease reveals the existence of extensive unsuspected heart disease. In the hypertrophy secondary to pulmonary disease, particularly emphysema and cirrhosis, there may be sensations of uneasiness in the cardiac region, with cough and shortness of breath; but so long as the dilatation is moderate the symptoms are not marked. With great dilatation and tricuspid regurgitation come the venous engorgement, oedema, and pulmonary troubles. The increased pressure in the lesser circulation not uncommonly leads to atheroma of the pulmonary artery, and the full state of the capillaries leads ultimately to a deposition of pigment and increase in the fibrous elements in the lung--the brown induration. Pulmonary congestion and apoplexy from thrombosis or embolism are more often associated with dilatation. Hæmoptysis may result from rupture of vessels during sudden exertion.

The physical signs of hypertrophy of the right ventricle are not so marked as those of the left. Bulging of the lower part of the sternum and left cartilages is occasionally met with. The apex-beat is forced to the left, but is not so often displaced downward. The most marked impulse may be in the epigastrium, in the angle between the ensiform cartilage and the seventh rib or beneath the cartilages of the sixth and seventh ribs. The pulsation is rarely the strong heave of left-sided hypertrophy, and is apt to be diffuse, not punctuate, particularly if there is much dilatation. In thin-walled chests there may be pulsation in the third and fourth right interspaces. The area of dulness is increased in the transverse direction, particularly toward the right, where it may extend an inch or more beyond the border of the sternum. On auscultation the first sound at the lower part of the sternum is louder and fuller than normal, but the differences are not very marked unless there is much dilatation, when it is clearer and sharper. The second sound is accentuated in the pulmonary artery on account of the increased tension, and there may be reduplication. The pulse at the wrist is usually small. The jugular pulsation occurs when there is tricuspid incompetence, which arises when the eccentric hypertrophy reaches a certain grade.

Hypertrophy of the auricles is always associated with dilatation. It is most common in the left chamber, which hypertrophies in mitral stenosis and incompetency, and assists materially in restoring the balance of the circulation and protects the lungs. There are no special physical signs, and we usually can only infer its presence by the existence of mitral stenosis and a presystolic murmur. Increased dulness may be determined at the left of the sternum, and there may be a presystolic wave in the second left interspace.

Hypertrophy and dilatation of the right auricle occur not infrequently, and are almost invariably associated with a similar condition in the right ventricle, and incompetency of the tricuspid. In emphysema, cirrhosis of the lung, chronic bronchitis, and in mitral disease, it is very common, much more so than the statement of some authors would lead us to expect. In comparison with the left auricle the greater development and hypertrophy of the appendix and its musculi pectinati is very striking. The latter may be distributed over the anterior wall of the sinus to a much greater extent than in health. There may be increased dulness in the third and fourth interspaces, with pulsation presystolic in rhythm. Usually there are signs of venous engorgement, jugular pulsation, and other evidences of dilatation of the right heart.

The DIAGNOSIS of cardiac hypertrophy does not usually present any serious difficulties. Increase in size, more forcible contraction, with displacement of {628} the apex-beat, and the character of the pulse, are the most important signs. There are certain conditions which require to be carefully distinguished. Neurotic palpitation, from whatever cause, may be accompanied with forcible contraction, but it has not the heaving impulse of genuine hypertrophy. Actual enlargement of the organ may, however, result from prolonged over-action, as in Basedow's disease, in the smoker's heart, and the irritable heart of neurasthenics, but it is usually slight. Increased dulness in the cardiac area may be due to a variety of causes, some of which may simulate hypertrophy, as pericardial effusion, aneurism, mediastinal growths, or displacement of the heart from pressure or the existence of malformation of the chest; but with the exercise of ordinary care the diagnosis can usually be made. There are two opposite conditions which not infrequently give trouble. When the left lung is retracted from pleurisy, phthisis, or cirrhosis, there is a large surface of the heart exposed, and the pulsation may be extensive and forcible, and at first sight resemble hypertrophy. There is usually in this condition some dislocation upward and to the left. The history of pulmonary or pleuritic disease, and the evident fixture of the lung on deep inspiration, will usually suffice to prevent mistake. A similar exposure of the heart occurs without any disease in very narrow-chested persons with ill-developed lungs; and here, though the area of dulness may be much increased, yet the normal position of the apex and the absence of forcible heaving impulse, pulse signs, and of any obvious cause of hypertrophy will afford satisfactory criteria for a diagnosis. Just the reverse occurs in some cases in which a moderate cardiac hypertrophy is masked by emphysema of the lungs or of their anterior borders. The area of dulness may be normal, or even diminished, and the pulsation diffuse and chiefly epigastric. The general condition, state of the pulse, and character of the sounds would help in the diagnosis, but it is sometimes a matter of no little difficulty.

The symptoms and physical signs above narrated sufficiently indicate the points of difference between hypertrophy of the two sides of the heart.

In all cases the greatest possible care should be exercised in ascertaining the presence or absence of conditions likely to cause hypertrophy.

The COURSE of a case of ordinary hypertrophy may be divided into three stages: 1st. The period of development, which varies much with the nature of the primary disease. Thus in rupture of an aortic cusp or in sudden overstrain from exertion it may require months, or even years, before the hypertrophy becomes fully developed. In these cases it may never do so, and then death results. On the other hand, in sclerotic affections of the valves with stenosis or incompetence the hypertrophy develops pari passu with the lesion, and may continue to counterbalance a progressive impairment of the valves. 2d. The period of full compensation, the latent stage, during which the heart's vigor meets all the requirements of the circulation. There may be no signs whatever of heart weakness, but the hypertrophied muscle completely equalizes the valvular or other defects. It may last an indefinite period of years. In some cases this fortunate period is never fully attained, and indications of incomplete compensation remind the individual that he has a heart affection. 3d. The period of disturbed compensation, which sooner or later awaits all victims of hypertrophy. It may come suddenly during an extra exertion, and death follow from acute dilatation; or more commonly it takes place slowly, and results from degeneration and weakening of the heart-muscle, with consequent dilatation and all its evils. There may be repeated failures before the end is reached, represented clinically by attacks of cardiac dyspnoea and dropsy.

The breaking, as it is called, of a compensatory hypertrophy may be induced by many causes. Among the most important is failure of general or local (cardiac) nutrition. In many a chronic heart case readmitted to {629} hospital, perhaps for the third or fourth time, with dyspnoea and dropsy, exposure, poor food, and whiskey are responsible for the failure. Gradual sclerosis of the coronary arteries leading to fatty or fibroid changes is a fruitful source of disturbed compensation. It is well known that during or after an acute illness, pneumonia, fever, or a bronchial attack the first symptoms of heart disease may be manifested. Mental emotions, severe grief, or fright have been known to bring on symptoms of heart failure in hypertrophy. One of the most frequent causes is sudden or prolonged muscular exertion, which may disturb a compensation perfect for years, and induce death in a few days.[59] The intimate pathology of broken compensation is not always clear. It certainly does not always depend on degeneration of the muscle-fibres, so far as microscopical examination can tell, and in many cases we are forced to conclude that the ganglia are at fault and the breakdown is nervous, not muscular.

[Footnote 59: Traube, _Gesammelte Beiträge_, Bd. iii.]

The PROGNOSIS depends entirely upon the nature of the cause which has induced the hypertrophy. When remediable or removable, the heart may return to its normal size, as after pregnancy, acute Bright's disease, and some cases of hypertrophy from deranged innervation and muscular exertion. When the cause is irremediable, as in chronic valve disease, sclerosis of the arteries, or obliteration of pulmonary capillaries, the case is quite different. Here the prognosis depends largely on the capability of maintaining in its integrity a sufficient hypertrophy to compensate for the obstruction: so long as this keeps up all is well; the evils come with failure of the hypertrophy and increase of the dilatation. Conditions of general and local nutrition are all-important factors, and when these can be supported to the highest possible degree the prognosis is favorable. Ill-health may be indicated at once by the onset of cardiac symptoms, pointing to disturbed compensation. Much depends on the seat of the original disease. Mitral stenosis carries with it as good prognosis, quo ad longevity, as aortic stenosis,[60] and the latter much better than aortic insufficiency. The nutrition of the muscle of the heart demands a full and constant supply of blood, but in aortic incompetency the rapid regurgitation does not permit of the complete distension of the coronary vessels,[61] and the strain is such that atheroma of these arteries is very apt to follow and still further diminish the blood-supply. Hence the prognosis in aortic insufficiency for enduring hypertrophy is bad. The hypertrophy which accompanies general arterial degeneration, though compensating for peripheral obstruction, carries with it certain dangers, as already {630} indicated, in the liability to cause rupture. With care such patients may survive for years, though exposed to risks other than cardiac.

[Footnote 60: Brückes held that the coronary vessels were filled in diastole alone, but there can be no question that blood also enters during the systole. The sigmoid valves certainly do not in the majority of cases cover the orifices of these arteries during this act. Undoubtedly, however, the heart-vessels are more distended in diastole. The pallor of the muscle in systole is a proof that the coronary vessels are not well filled at this period.]

[Footnote 61: This is not the usual statement, but my experience--limited, it is true--seems to point to the conclusion that mitral stenosis may also exist for many years without exciting symptoms of heart disease. It may, I think, be safely affirmed that a larger number of persons with mitral valve disease live in blissful ignorance of the existence of serious heart lesion than any other group of cardiac cases. Particularly is this the case in women. Two points have attracted my attention in this connection: the frequency with which we find evidence of stenosis--as shown by the presystolic thrill and rough murmur--in women complaining, perhaps, of shortness of breath on exertion and slight cardiac distress--symptoms which are readily relieved--and the discovery post-mortem of stenosis of the mitral orifice in cases of sudden death by embolism or from some intercurrent disease occurring in persons in whom heart disease had never been suspected. The narrowing may be extreme--an orifice only 13 millimeters in width in one case in which a woman was stricken with hemiplegia while attending to her household duties. Such cases, and they are not very uncommon, teach us how perfect compensation may be in this lesion.]

The TREATMENT of hypertrophy consists largely of measures directed toward its maintenance in a degree proportionate to the extra work which the heart has to do. In organic disease the well-being of the patient depends on this: we cannot remove the cause, but we can by careful hygienic and dietetic regulations maintain the balance between the defect and the compensation. The original lesion is usually beyond control, and the special indications are to moderate certain dangers associated with hypertrophy, and to promptly meet the earliest symptoms of heart failure. The utmost moderation in food, drink, and exercise must be enjoined. Quiet, regular habits are all important; excesses of all kind quickly lead to impairment of the heart's action. In the hypertrophy associated with arterial and renal disease a special danger exists in the tendency to rupture of vessels. In these cases vigorous heart-beat, with very high tension in the peripheral arteries, indicates mischief which may be met by taking prompt measures for the reduction of the high pressure. A brisk cathartic may avert an apoplectic attack, and there are cases in which the old practice of bleeding--formerly so much in vogue for hypertrophy--is justifiable. Palpitation and shortness of breath are among the earliest signs of failing compensation, and call for the treatment to be considered under Dilatation. The condition of hypertrophy from organic disease is not directly amenable to treatment; we cannot diminish the size of the organ, but we can regulate its action by measures which control the contractions when from any cause they become too forcible or irregular. More particularly is this the case in hypertrophy due to disturbed innervation. When vigorous, rest and the administration of cardiac sedatives, such as aconite or veratrum viride, will generally suffice to reduce the force of the contractions. The palpitation and irregular action in cases of irritable heart from over-exertion, the abuse of tobacco, or sexual excesses may subside with the removal of the cause. The steadying action of small doses of digitalis is often well seen in these cases.

Dilatation of the Heart.

DEFINITION.--An increase in the size of one or more of the chambers, with or without thickening of the walls.

VARIETIES.--Two varieties may be recognized: (1) dilatation with thickening, and (2) dilatation with thinning. Dilatation with thickening is the most common, and corresponds with the dilated or eccentric hypertrophy and the active dilatation of some writers. Those cases of dilatation with walls of apparently normal thickness--simple dilatation of authors--also belong to this category, for if the chamber is distended, and yet the walls maintain their normal diameter, they must of course be hypertrophied. The dilatation with thinning--passive dilatation--is specially met with in the auricles, and is characterized by increase in the size of the chamber and attenuation of the walls.

The diastole of the heart is partly an active, partly a passive act. The cavities behave as would rubber balls, and their distension after contraction is partly due to their elasticity. The heart is a suction- as well as a force-pump. In the ventricles, for example, after systole the active dilatation draws blood from the auricle--must do so, in fact, in the very process of dilating--and then the auricular systole completes the process, fully accomplishing the diastole. Dilatation occurs during this period, and results from distension beyond the limits of the contractile power of the wall. More blood is contained in the cavity than the muscle of the wall can {631} control--_i.e._ expel--but if the organ is healthy, hypertrophy ensues and the chamber accommodates itself to the altered condition. It is the heightened pressure during diastole which is dangerous; during systole the pressure may be extreme, and yet no dilatation may ensue, as in aortic stenosis, in which condition the size of the chamber may remain normal, and yet the walls hypertrophy to meet the greatly-increased resistance to the outflow of the blood during the systole. In the auricles, however, the increased tension during contraction may be accompanied with considerable dilatation, as in mitral stenosis.

ETIOLOGY.--There are two important causes in the production of dilatation: increased pressure within the cavities, and impaired resistance due to disease of the muscular substance of the heart. They may act singly, but are often combined. Weakened walls may yield under normal distending force, or normal walls may yield under a heightened blood-pressure, or both factors may prevail.

1. Increased endocardiac pressure--which results, as before stated, either from an augmented quantity of blood to be moved or an obstacle to be overcome--is the most frequent cause of dilatation. It does not necessarily cause it. Simple hypertrophy may be the result, as in the early period of aortic stenosis and in the hypertrophy of the left ventricle in Bright's disease.

Most of the important causes of increased endocardiac pressure have already been considered under Hypertrophy, but we may refer to one or two more particularly.

The size of the cardiac chambers is variable in conditions of health. With slow action of the heart the dilatation during diastole must be much more full and complete than with rapid action. Physiologically, the limits of dilatation have been reached when the chamber cannot be emptied during the systole. We find this as an acute, transient condition in severe exertion--during, for example, the ascent of a steep mountain. There may be great distension of the right heart, as shown by the increased epigastric pulsation, and even increase in the cardiac dulness. The safety-valve action of the tricuspid valves may here come into play, and by permitting regurgitation into the auricle relieve the lungs. Rest causes it to pass off, but if it has been extreme, the heart may suffer a strain from which it may recover slowly, or, indeed, the person may never again be able to undertake severe exertion. In the process of training the getting wind, as it is called, is largely a gradual increase in the capability of the heart, particularly the right chambers. A degree of exertion can be safely maintained in full training which would be quite impossible under other circumstances, because by a gradual process of what we may call physical education the heart has strengthened its reserve force--widened enormously its limits of physiological work. Endurance in prolonged contests is measured by the capabilities of the heart, and its essence consists in being able to meet the continuous tendency to overstep the limit of dilatation.

We have no definite information as to the nature of the change in the heart which occurs in the process of training, but it must be in the direction of increased vigor, muscular and nervous. The large hearts often noted in athletes may be due, as already mentioned, to the prolonged use of their muscles; but probably no one can become a great runner or oarsman who has not naturally a large and capable heart. Master McGrath, the celebrated greyhound, and Eclipse, the race-horse, both famous for endurance rather than speed, had very large hearts.

Over-training and heart-strain are closely connected with this question of excessive dilatation during severe muscular effort. Both mean the same thing in many cases. A man, perhaps not in very good condition, calls upon his heart for much extra work during a race or the ascent of a very steep {632} mountain, and is seized with cardiac pain and a feeling of distension in the epigastrium, and the rapid breathing continues an unusual time, but the symptoms pass off after a night's quiet. An attempt to repeat the exercise is followed by another attack, or indeed an attack of cardiac dyspnoea may come on while he is at rest.[62] For months such a man may be unfitted for severe exertion, or may be permanently incapacitated. He has overstrained his heart and has become broken-winded. We see the same thing sometimes in horses. What exactly has taken place in these hearts we cannot say, but their reserve force is lost, and with it the power of meeting the demands exacted in maintaining the circulation during severe exertion.[63] The heart-shock of Latham[64] includes cases of this nature--sudden cardiac breakdown during exertion and not due to rupture of a valve. It seems probable that some cases of sudden death in men and animals during long-continued violent efforts, as in a race, are due to over-distension and paralysis of the heart.

[Footnote 62: In _St. George's Hospital Reports_, 1872, Clifford Albutt gives his own experience.]

[Footnote 63: H. C. Wood tells me he believes that wind in athletes is in large part a question of vagus control, and that he has noticed in races of dogs used in hunting and other violent exercise the vagi are more sensitive and powerful than in sedentary breeds. He thinks that a similar difference exists between tame and wild rabbits.]

[Footnote 64: _Diseases of the Heart_, New Sydenham Soc. ed.]

In the various forms of valvular disease we meet with numerous examples of dilatation. In aortic incompetency during diastole blood enters the left ventricle from the unguarded aorta and from the left auricle, and the amount of blood at the termination of diastole subjects the walls to an extreme degree of pressure, under which they inevitably yield: in time they augment in thickness, and we have the typical eccentric hypertrophy of this condition.

In mitral regurgitation a certain quantity of the blood which should have been driven into the aorta is forced into the auricle from which it came, dilating it; and then in the diastole of the ventricle a larger amount is returned from the auricle, and with increased force, by the hypertrophied walls of this chamber. In mitral stenosis the left auricle is the seat of greatly-increased tension during systole, and dilates as well as hypertrophies; the distension too may be enormous. Dilatation of the right chamber is very common, and is produced by a number of conditions, which were considered under Hypertrophy. All circumstances which permanently increase the tension of the blood in the pulmonary vessels will cause it--mitral stenosis, emphysema, etc. The dilatation seems easily produced, but the accompanying hypertrophy may hold it in check for years. We may here refer to the extreme distension of the right chambers in pneumonia, particularly when the consolidation is extensive. The passive dilatation may be very great and the walls much thinned, and we see the same in states of asphyxia. Valvular lesions of the right heart are not frequent causes of dilatation. When the causes which bring about the dilatation act suddenly, the degree of distension may be great, and there is much more difficulty in the establishment of compensation, as in rupture of an aortic cusp.

2. Impaired nutrition of the heart-walls from degeneration or inflammation may lead to such a diminution of the resisting power that dilatation readily occurs.

In fevers the loss of tone due to parenchymatous degeneration or myocarditis may lead to a condition of acute dilatation which may prove fatal. It is a well-recognized cause of death in scarlatinal dropsy,[65] and may occur in rheumatic fever,[66] typhus, typhoid, erysipelas, etc. The myocarditis accompanying acute endo- or pericarditis may lead to dilatation, especially in the latter disease. The cavities are usually large in fatty degeneration or {633} infiltration from the relaxed and atonic state of the walls. In anæmia, leukæmia, and chlorosis the dilatation of the chambers may be considerable. In fibroid degeneration the wall generally yields where the process is most advanced, as at the left apex. The impaired nutrition in coronary disease may lead to dilatation. Under any of these circumstances the walls may yield with normal blood-pressure, or if increased tension is present the effect is the more readily produced.

[Footnote 65: Goodhart, _Guy's Hospital Reports_, Series iii. vol. xxiv.]

[Footnote 66: Samuel West, _Barth. Hospital Reports_, xiv.]

Pericardial adhesions are usually spoken of as a cause of dilatation, acting by traction from without, and we generally find in a case of extensive and firm union considerable hypertrophy and dilatation. In this condition there is usually some impairment of the superficial layer of muscle which may permit of over-distension.

MORBID ANATOMY.--Usually the condition exists in two or more chambers, and is associated with hypertrophy, the appearances of which have already been described. It is more common on the right side than on the left. Perhaps the most general dilatation which we see is in cases of aortic incompetency, in which all the cavities may be enormously distended. In mitral stenosis the left auricle is often trebled in capacity, and the right auricle and ventricle also are very capacious. The former may contain eighteen to twenty ounces of blood. In many chronic affections of the lungs the right chambers are chiefly affected. Dilatation with thinning is often the result of an acute process met with in the fevers. The walls may be very much thinner than normal, almost membranous, and the dark color of the blood may show through with distinctness. When the distension of one ventricle is very great, there may be a distinct bulging of the septum toward the other side. The shape of the organ is altered, and when the right chambers are chiefly affected it is more globular in shape. Distension of the left auricle may render it visible in the front of the heart, and the appendix may be prominent. The right auricle when enormously enlarged, as in some cases of pneumonia, in emphysema, and in leukæmia, may form a large mass occupying a considerable space in the antero-lateral part of the thorax. The walls in dilatation with thinning are flabby and relaxed, and collapse at once when cut, but in dilatation with hypertrophy they are firm, especially those of the right ventricle.

The auriculo-ventricular rings are often dilated, and there may be an inch and a half, or even two inches, of increase in the circumference. Thus, the tricuspid orifice, the circumference of which is about four and a half inches, may admit freely a graduated heart-cone of over six inches, and the mitral orifice, which is about three and a half inches normally, may admit the cone to five and a half inches or even more. Great dilatation is always accompanied with relative incompetence of the valves, so that free regurgitation into the auricles is permitted. The orifices of the cavæ and of the pulmonary veins may be greatly dilated.

The muscle-substance varies much in appearance according to the presence or absence of degenerations. The endocardium is often opaque, particularly in the auricles. The microscopical examination may show marked fatty or parenchymatous change, but in other instances of dilatation and heart failure in eccentric hypertrophy there may be no special alteration noticeable. I fully agree with Niemeyer's assertion, "that it is not possible by means of the microscope to recognize all the alterations of the muscular fibrillæ which diminish the functional power of the heart."[67] We know too little as yet of the changes in the ganglia of the heart in these conditions: as centres of control they probably have more to do with cardiac atony and breakdown than we generally admit. Degeneration of them has been noted by Putjakin[68] and others.

[Footnote 67: _Textbook of Medicine_, vol. i., Am. ed.]

[Footnote 68: _Virchow's Archiv_, lxxiv.]

{634} SYMPTOMS AND PHYSICAL SIGNS.--Dilatation produces weakness of the cardiac walls, diminishes the vigor of their contractions, and is thus the very reverse of hypertrophy. So long as compensation is maintained the enlargement of a cavity may be considerable: the limit is reached when the hypertrophied walls can no longer in the systole expel all the contents, part of which remain, so that at each diastole the chamber is abnormally full. Thus in aortic incompetency blood enters the left ventricle from the aorta as well as the auricle, dilatation ensues, and also hypertrophy as a direct effect of the increased pressure and increased amount of blood to move. But if from any cause the hypertrophy weakens, and the ventricle during systole does not empty itself completely, a still larger amount is in it at the end of each diastole, and the dilatation becomes greater. The amount remaining after systole is a cause of obstruction, preventing the blood entering freely from the auricle. Incompetency of the auriculo-ventricular valves follows with dilatation of the auricle and impeded blood-flow in the pulmonary veins. Dilatation and hypertrophy of the right heart may compensate for a time, but when this fails stasis occurs in the venous system, with dropsy. The consideration of the symptoms of chronic valvular lesions is largely that of dilatation and its effects. Acute dilatation, such as we see in fevers or in sudden failure of an hypertrophied heart, is accompanied by three chief symptoms--weak usually rapid impulse, dyspnoea, and signs of obstructed venous circulation. Cardiac pain may be present, but it is often absent.

The physical signs of dilatation are those of a weak and enlarged organ. The impulse is diffuse, often undulatory, and is felt over a wide area, and an apex-beat or a point of maximum intensity may not exist. When it does it may be visible, and yet cannot be felt--an observation of Walshe's which is very valuable. An extensive area of impulse with a quick, weak maximum apex-beat may be present. When the right heart is chiefly dilated the left may be pushed over so as to occupy a much less extensive area in the front of the heart, and the true apex-beat is not felt; but the chief impulse is just below or to the right of the xiphoid cartilage, and there is a wavy pulsation in the fourth, fifth, and sixth interspaces to the left of the sternum. In extreme dilatation of the right auricle a pulsation can sometimes be seen in the third right interspace close to the sternum, and with free tricuspid regurgitation this may be systolic in character. Whether the pulsation frequently seen in the second left interspace is ever due to a dilated left auricle is not satisfactorily determined. I have sometimes thought it was presystolic in rhythm, though it may be distinctly systolic. Post-mortem, it is rare in the most extreme distension to see the auricular appendix so far forward as to warrant the belief that it could beat against the second interspace. The area of dulness is increased, but an emphysematous lung or the full distended organ in a state of brown induration may cover over the heart and limit greatly the extent. The directions of increase were considered when speaking of Hypertrophy with dilatation.

The first sound is shorter, sharper, and more valvular in character, and more like the second. As the dilatation becomes excessive it gets weaker. Reduplication is not common, but occasionally differences may be heard in the joint sound over the right and left hearts. Murmurs very frequently obscure the sounds; they are produced by incompetency of the valves due to the great dilatation, or are associated with the chronic valve disease on which the condition depends. The aortic second sound is replaced by a murmur in aortic regurgitation; the pulmonary is accentuated in mitral regurgitation and pulmonary congestion, but with extreme dilatation it may be much weakened. The heart's action is irregular and intermittent, and the pulse is small, weak, and quick.

The DIAGNOSIS is generally easy when the physical signs, the history, and {635} the general condition are taken into account. In a case of valvular disease with hypertrophy the onset of dyspnoea and venous stasis with dropsy tell unmistakably of cardiac dilatation. Increased præcordial dulness, with a weak, diffuse impulse, is not simulated by many conditions, and one only, pericardial effusion, need be specially mentioned. This may present very serious difficulties, and indeed a dilated heart has been aspirated under the belief that effusion was present. The points to be attended to are--the greater lateral dulness in dilatation and the wavy impulse which may extend over a great part of it; in effusion the dulness extends upward and is more pear-shaped, the impulse is not so extensive, and may be tilted up an interspace or may not be visible. The sounds in pericardial effusion are muffled and distant over the dull region, but at its upper limit may be clear. The absence of friction is an important negative sign. In some cases it is extremely difficult to determine between the conditions, and I have known a weak, feeble, irregular heart, with cyanosis, and oedema lead to the diagnosis of dilatation when effusion was present.

The PROGNOSIS depends upon the cause of the dilatation. In anæmia and fevers the temporary dilatation may undoubtedly pass away with the improvement of health; but when the cause is not remediable the danger must be measured by the presence or absence of compensation. In the majority of the cases which we see the dilatation occurs in valve disease, and no symptoms of importance arise so long as the compensation is perfect. Failure of this, which may result from many causes, as already mentioned, is always serious. It may be only temporary, and with care the compensation can be re-established and the symptoms pass away. We constantly see this in the eccentric hypertrophy of the right heart from mitral disease; an attack of bronchitis suffices to disturb the compensation, and with the relief of the catarrhal trouble the dyspnoea and heart symptoms disappear.

The TREATMENT of dilatation is virtually that of chronic valvular disease, and we shall only refer to general indications. With the earliest symptoms of failure the work of the heart should be reduced to a minimum by placing the patient at rest. This in itself may suffice without any other measures. Time and again I have seen, particularly in cases of aortic insufficiency, the dyspnoea relieved and the oedema of the feet disappear and the compensation re-established by placing the patient in bed, enjoining absolute quiet and carefully regulating the diet. The importance of rest in the early stages of heart failure cannot be too much insisted upon.[69] Quiet and careful dieting may suffice for the milder attacks, but we have usually even in these to resort to heart tonics. Digitalis is the most powerful remedy we possess in restoring and maintaining compensation. Under its use the irregular, feeble, and frequent contraction becomes regular and stronger, and the embarrassed circulation is relieved. In hospital practice the same chronic heart cases may return year after year with attacks of cardiac failure, dyspnoea, dropsy, etc., and each time the rest in bed and digitalis may suffice to restore compensation. A fourth or fifth, even a sixth, attack may be safely weathered, and then the final breakdown occurs when nothing avails to combat the dilatation. Of substitutes for digitalis, caffeine and convallaria have been much used of late. Caffeine in some cases acts more promptly, which is an advantage, but its action is not so certain and not so enduring. Convallaria is very variable {636} in its action; it has succeeded in some instances in which digitalis has failed, and in others has been quite without effect. In extreme cardiac failure with great dilatation, lividity, orthopnoea, and feeble pulse, stimulants must be freely given; ether may be employed hypodermically. In this condition of final asystolism digitalis seems to have lost its influence. In the heart failure of pneumonia I have found camphor a valuable adjuvant to the diffusible stimulants. To improve the general nutrition, and with it that of the heart-muscle, iron and arsenic are most valuable adjuvants, especially in the dilatation of anæmia. The treatment of special symptoms, dropsy, dyspnoea, etc., is considered under Valvular Affections.

[Footnote 69: In Ortel's system (_Ziemssen's Handbuch der Allgemeine Therapie_, Bd. iv.) of treating heart disease exercise, particularly climbing, forms a very important part, but an analysis of his cases shows that most of them were instances of fatty heart in obese persons. It would scarcely be applicable to valvular disease. The severe exercise, he thinks, stimulates the heart-muscle and helps in the restoration of the hypertrophy. His other suggestion, the reduction of the liquids ingested, seems much more reasonable, as in this way the volume of blood to be circulated may be considerably reduced.]

Aneurism of the Heart.

This term is now restricted to local or partial dilatations of the wall of one of the cardiac cavities. Formerly, dilatation of the heart or of one of its chambers was spoken of as aneurism. This rare condition[70] is most frequently associated with fibroid degeneration, but other causes of local weakness of the walls, as ulcer, acute myocarditis, and fatty degeneration, have been present in a few cases. An instance is on record where the aneurism followed a stabbing wound of the chest.[71] The left ventricle is usually involved; very few cases occur in the other chambers. The condition may be acute or chronic.

[Footnote 70: In the index catalogue there are references to only 18 cases by American authors. In the museums of Philadelphia there are only 5 specimens--3 in the museum of the College of Physicians; 1 each in the University and Pennsylvania Hospital cabinets.]

[Footnote 71: Quoted by Legg, _Bradshawe Lecture on Cardiac Aneurisms_, London, 1883.]

Acute aneurism is met with occasionally in ulcerative endocarditis, more rarely as the result of local softening due to myocarditis or plugging of a branch of a coronary artery. In severe endocarditis perforation is, I think, more common than the production of aneurism. In one case I saw a deep excavation at the upper part of the septum produce a bulging the size of a marble in the wall of the left auricle, and in another ulceration in one sinus of Valsalva had extended into the septum, the upper part of which presented an aneurismal dilatation which had ruptured into the left ventricle. Legg considers the production of acute aneurism by the rupture of abscesses or cysts as doubtful.

Chronic aneurism is almost confined to the left ventricle, and, as Cruveilhier pointed out,[72] is the result of fibroid degeneration of the muscle. In a few instances fatty degeneration appears to have been the cause. The monographs of Thurnam,[73] Pelvet,[74] and Legg[75] give the most complete account of the disease. They are more common in men than in women, and the majority of the cases occur after middle life.

[Footnote 72: _Anatomie pathologique_, Paris, 1835-42.]

[Footnote 73: _Medico-Chirurgical Transactions_, vol. xxi., 1838.]

[Footnote 74: _Des Aneurysmes du Coeur_, Paris, 1867.]

[Footnote 75: _Loc. cit._]

The situation of the aneurism is most frequently at the apex--59 of 90 cases collected by Legg. They are usually rounded in shape, and may vary in size from a marble to a cocoanut. The sac may be double, as in a case described by Janeway,[76] or, as in a specimen in Guy's Hospital Museum, the whole wall of the ventricle may be covered with aneurismal bulgings. In the simplest form there is a rounded dilatation at the apex, and the lower part of the septum is lined with thrombi. Often the tumor is distinctly sacculated, and communicates with the ventricle by a very small orifice. The pericardium is usually thickened, and calcification may occur in the walls. Rupture seems rarely to occur--in only 7 of the 90 cases collected by Legg. Of other {637} parts of the ventricle, the septum and the undefended space at the highest part of the septum just below the aortic ring are most often involved. This latter situation is sometimes the seat of a congenital dilatation, usually a small, thin, smooth sac without thrombi, which has no pathological significance.

[Footnote 76: _N.Y. Med. Journ._, 1875, xxi.]

Cardiac aneurisms rarely produce any symptoms, and in the majority of cases have been found accompanying other conditions which have proved fatal. At the left apex the increase in dulness and area of pulsation could scarcely be distinguished from hypertrophy unless associated with marked bulging. They seldom perforate the chest-wall. Berthold (quoted by Legg) has described one connected with the right auricle which produced a pulsating tumor beneath the skin, the region of the second and third ribs.

Adventitious Products in the Heart.

Tubercle.--In general tuberculosis and in tuberculous pericarditis there may be nodules in the heart-substance, but, as a rule, this organ is very rarely the seat of tubercle. Large caseous masses sometimes occur, but unless associated with tubercle in other organs they are not to be regarded as necessarily tuberculous. Miliary granulations have been seen on the valves.

Cancer and sarcoma rarely are primary, and are not often met with as secondary growths. Sometimes a mediastinal sarcoma penetrates along the veins and involves the auricle, with or without great involvement of the pericardium. The secondary tumors may be single or multiple. In a case of cancer of the uterus I found a large mass in the wall of the right ventricle, involving also the anterior segment of the tricuspid, and partially blocking the orifice. The surface was eroded, and the pulmonary arteries contained numerous cancerous emboli. In another instance the heart was considerably enlarged by the presence of many rounded masses of colloid cancer throughout the walls. In a remarkable case of sudden death in a child I found the tricuspid orifice firmly blocked with a sarcomatous mass which I thought at first had originated in the heart, but dissection showed to have come from the renal vein, which was filled with sarcoma extending from a large tumor of the kidney. Melanotic cancer, fibromata, and myomata have occasionally been seen, and a secondary epithelial growth has been described by Paget.

Syphilis of the heart is met with in the form of gummata or as a specific arteritis leading to patches of fibroid induration. The gummous growths form tumors of variable size, which usually occupy the septum or the ventricles. Possibly many of the caseous and calcified masses not infrequently met represent obsolete gummata. The syphilitic myocarditis probably originates in an affection of the arteries, and leads to patches of fibroid induration more or less extensive. Many authors hold that syphilis plays a very important rôle in the production of fibroid heart.

Cysts.--Simple cysts are rare in the heart. I have met with two instances--one, the size of a marble, situated in the wall of the right auricle near the septum, was filled with a brownish fluid; the other, the size of a small walnut, occupied the base of the posterior segment of the mitral, and was filled with a clear fluid. Blood-cysts occasionally occur.

Parasites.--The Cysticercus cellulosæ, the larva of Tænia solium, and the hydatid or echinococcus, the larva of Tænia echinococcus of the dog, are sometimes found in the heart. The former, usually single, is extremely rare; in the hog and calf the measles, as the cysts are called, very often exist in the heart-muscle. In the recent paper by Mosler[77] references are given to 13 cases of cysticerci in the heart. The greatest number present was 19. The {638} hydatid is more common: 25 instances are mentioned in the statistics of Devaine and Cobbold, and Mosler's more recent figures only give 29. They occur in the right ventricle more frequently than in the left. Occasionally they attain a larger size and compress the heart and push back the lungs. The cyst may burst and the contents be discharged into the pulmonary artery or aorta, as in a case given by Osterlen,[78] in which gangrene of the right leg followed the plugging of the femoral by hydatid vesicles discharged into the blood by the bursting of a cyst in the left auricle.

[Footnote 77: _Zeitschrift für klinische Medicin_, Berlin, Bd. vi., 1883.]

[Footnote 78: _Virchow's Archiv_, xlii.]

{639}

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.

BY ALFRED L. LOOMIS, M.D.

Endocarditis.

DEFINITION.--Endocarditis is an inflammation of the endocardium, and may be either exudative, neoplastic, or ulcerative in character. While its different varieties are closely connected in their etiology, they are distinct in the extent, duration, character, and course of their pathological changes. They cannot be classified as acute and chronic in the ordinary acceptation of these terms, for they often so merge into each other as to render it difficult, if not impossible, to determine when they cease to be acute and become chronic; and some cases are at no time acute. It has been claimed that an acute endocarditis becomes chronic when its course is prolonged, but the advanced changes are only a stage of the acute process.

So-called acute endocarditis is accompanied by a fibro-cellular exudation into the substance of, and underneath, the endocardium, causing elevations of its surface. The better term for this variety is exudative endocarditis, it being borne in mind that the exudation does not take place upon the free surface of the membrane, but into its substance and underneath it. This form of endocarditis may be entirely recovered from, or it may lead to interstitial changes in the endocardial and myocardial tissue which will correspond to the changes usually described as those of chronic endocarditis.

Interstitial endocarditis is a better term for these changes. The disease may be the sequela of exudative endocarditis, or may be interstitial from its commencement, for the valvular changes of interstitial endocarditis are often found in those who never have had either acute articular rheumatism or exudative endocarditis, but have been the subjects of chronic rheumatism or gout.

Acute exudative endocarditis may, in certain cases, be stamped with an ulcerative process, the result of septic infection, giving rise to those pathological changes which have been described as acute ulcerative endocarditis.

HISTORY.--The history of endocarditis is restricted to modern pathology. It is not spoken of by the older medical writers. Before the sixteenth century knowledge of the structure and functions of the heart was imperfect and scanty, and its diseased conditions were altogether unknown.

The history of the pathology of cardiac disease commenced with Harvey, Lancisi, Vesalius, and Vieussens. They investigated not only the normal structure of the heart and the mechanism of the circulation, but accurately described a few of its valvular diseases.

There is little doubt but that Laennec, Senac, and Morgagni were quite familiar with the valvular diseases of the heart, but Kreisig first traced the relationship between valvular diseases and inflammation of the lining membrane of the heart.

{640} The term endocarditis was first used by Bouillaud, who had the advantage of Laennec's discovery of auscultation. Corrigan first discovered the physical signs of aortic insufficiency. The most important advance in the pathology of endocarditis is due to the investigations of Virchow and Luschka, the former developing its sequelæ or results, the latter its histological changes. Ulcerative endocarditis is of modern date, and its literature scarcely extends back twenty years. The labors of Kirk, Virchow, Charcot et Vulpian, Moxon, Eberth, and Lancereaux are all connected with the etiology and anatomical changes of ulcerative endocarditis.

The relationship of interstitial endocarditis to valvular diseases of the heart and to cardiac murmurs is a subject which at present is engaging the attention of many medical observers.

I shall describe endocarditis under three heads: 1st, Exudative endocarditis; 2d, Ulcerative endocarditis; 3d, Interstitial endocarditis.

That the pathological changes which I shall describe may be readily appreciated, I will briefly review the anatomical structure of the endocardium.

The endocardium consists of connective tissue, with numerous elastic fibrils, covered by and continuous with a layer of flattened cells. Upon this lies the endothelial layer, which disappears in twenty-four hours after death.

Luschka regards the endocardium as continuous with all the arterial tissues, but the majority of histologists consider it a continuation of the internal membrane. Some regard the endocardium and inner coat of the arteries as analogous, since both are non-vascular and have an endothelial covering upon a connective-tissue base. As endocarditis is, for the most part, limited to the valves of the heart, a knowledge of their anatomical arrangement is important.

A transverse section of a segment of an auriculo-ventricular valve shows that upon the superior or auricular surface and upon the inferior or ventricular surface there are flattened cells and endothelium, and that next to each lies a fibro-elastic layer, the superior being the thicker. These two layers are separated by connective tissue.

The layer of flat cells is thickest on the ventricular surface. The fibro-elastic tissue is thickest at the base of the valve. The semi-lunar valves have endocardium on one side and the tunica intima on the other.

Although the endocardium has no vessels of its own, the capillaries upon the cardiac walls are in contact with it. The arrangement in the valves is different, as only a few vessels ramify between the layers of the mitral valve, and none are found, normally, in the sigmoid valves.

Acute Exudative Endocarditis.

This variety of endocarditis is met with most frequently in connection with acute articular rheumatism.

In adults it usually has its seat in the left heart; in intra-uterine life it occurs in the right heart. The inflammation commences in, and seldom extends beyond, the valves and the valvular orifices, but it may involve the whole or any part of the ventricular or auricular portions of the endocardium.

MORBID ANATOMY.--The endocardium becomes infiltrated with young cells, the process beginning in the layer of flat cells. The new formative cells are developed not only from the cells of the layer immediately underneath the endocardium, but also from leucocytes. This hyperplasia, this heaping up of embryo-plastic cells, is accompanied by softening of the deeper {641} layers of the intercellular structure, and as the softening goes on the intercellular substance is destroyed.

The endothelial elements also play an active part in the processes. The masses of new cells push out the endocardium, and papillary elevations are formed, filled with a fluid whose chemical properties resemble those of mucin, since it coagulates into threads when acetic acid is added. The cone-like vegetation is surrounded in the deeper layers of the endocardium by a zone of proliferation which is never distinctly limited, but which exhibits progressive hyperplasia from the periphery toward the centre.

All these changes may have taken place in non-vascular tissue. Where the capillaries are most numerous a punctuate or arborescent vascularity is seen, and this is followed by opacity of the part which is the seat of the inflammation. After death the endocardium and lining membrane of the vessels are often stained; this staining is produced by the coloring matter from the red corpuscles, and is the result of post-mortem change.

There is no exudation upon the villous projections; the coagula found upon them are a deposit of fibrin from the blood, the projections acting as foreign bodies in the blood-current. The fibrinous deposits occur chiefly on the surface which is opposed to the current of the circulation, and sometimes they are distinctly conical; at others they have the shape of a raspberry. They occupy the parts most exposed to the friction of the blood, and are arranged on the borders of the aortic valves at a little distance from their edges, the seat being determined by the limit of the vascular network. The band of tissue which passes from the attached border of the valve to the Arantian body in the centre shows the inflammatory granulations most distinctly. They consist of a cauliflower-like bulbous extremity, connected by a constricted neck with a firm, hard base that is intimately blended with the subjacent tissue. A thin hyaline layer covers each mass. At first these granulations or vegetations are very small and numerous, so that the membrane presents a granular appearance. Later, they become larger, reaching oftentimes the size of a small pea.

Near the insertion of the tendons upon the auricular surface of the mitral valve are found irregular wreaths of vegetations which enclose the attachments of the chordæ tendineæ. Moxon has shown that the friction of the vegetations or of fibrinous clots that gather upon the vegetations may, by the irritation it produces, excite endocarditis at points remote from the valves.

The tendon of the mitral valve may show the effects of endocarditis by becoming soft and friable, and even rupturing, or the chordæ tendineæ may adhere to one another. When such adhesions occur either with agglutinations of the flaps to each other or to the heart-walls, stenosis or regurgitation may result.

In connection with these changes new vessels are developed in the substance of the mitral valve, or those that already exist become more apparent. In the semilunar valves new vessels are formed or neighboring capillaries send out prolongations into the parts destitute of vessels. This, according to Charcot, is one way in which arborescent vascularity occurs. These changes are most marked in those forms of exudative endocarditis which run an acute course.

In some instances the hyperplasia is so extensive as to interfere with nutrition, and may lead to fatty metamorphosis. A cavity is then formed filled with granular fat-cells, discrete fat-globules, and blood-pigment, whose endocardial covering ruptures, and the contents are carried into remote capillaries to cause capillary embolism and septicæmia. This has been called ulcerative endocarditis.

{642} Ulcerative Endocarditis.

Ulcerative endocarditis occurs in those diseases where there is great vital depression. It is met with oftenest in pyæmia, puerperal fever, scarlatina, and diphtheria. It has been called septic, diphtheritic, and infectious endocarditis.[1]

[Footnote 1: Jaccoud, Klebs.]

MORBID ANATOMY.--Ulcers may form in endocarditis in either one of three ways: 1st. The exudative process may be so rapid and extensive as to cut off the nutrition of the endocardium covering the apices of the papillary elevations, and ulcers result in non-septic inflammation. 2d. Degeneration of the neoplastic tissue, due either to deficient blood-supply or other causes of impaired nutrition, may so soften the villi or efflorescences that their apices will be swept away by the blood-current and ulcers thus be formed. Charcot especially insists that the ulceration of these elevations is the consequence of granular degeneration, and not of fatty metamorphosis, with which it is often confounded. 3d. The exudative process may be purulent in character, and form minute abscesses in the substance of the valves beneath the endocardium, which, rupturing, leave comparatively deep ulcers. Acute multiple abscesses in the aortic valves are of frequent occurrence in ulcerative endocarditis.

The margins of the ulcers are irregular, but well defined; the edges are swollen and thick, and their floor (the muscular substance of the heart or the fibrous layer of the valve) is infiltrated with pus.

Where there is extensive loss of substance perforation of the valve may occur. These perforations are sometimes closed or hidden by a fibrinous exudation.

The soft and friable vegetations may be torn into long shreds by a forcible blood-current, and subsequently may excite endocardial inflammation where they come in contact with the walls of the heart-cavity, or they may break off and form emboli. A fibrinous string upon a flap of the aortic valve is not infrequently driven down and back by a regurgitant current, so as to excite endocarditis in the mitral valve.

Some observers state that micrococci and bacteria are found in ulcerative endocarditis of a septic or diphtheritic origin, and they have given to it the name of mycosis endocardii. It is probable that these minute organisms are developed by the septic ulcerative process rather than that they are the cause of such processes. They appear as spheres, highly refractive, motionless, cohering in groups, without any stroma. Acids, alkalies, ether, and chloroform have no effect on them, so that they are not to be regarded as vegetable products.

The valvular ulcerations in this form of endocarditis give rise to the most diverse lesions. Masses may be detached from the diseased cardiac orifices, either from the fibrinous deposits on the valves or from ulcerations of the valves themselves, and, having entered the circulation, they will produce various symptoms in the organs and tissues to which they are carried.

It is important to make a distinction between the results produced by displacements into the blood-current of large masses and those arising from the entrance of molecular fragments. It is also to be remembered that the masses from the vegetations or ulcerated valves in ulcerative endocarditis are often stamped with a septic element which leads to the development of suppurative infarctions in different organs.

The size and site of the emboli are important, for they may be so large as to obstruct vessels of large size.

The femoral and even the external iliac may suddenly become impervious to the circulatory currents, on account of the presence of a large embolus from the heart.

{643} When the arteries in the limbs are thus plugged, the result is generally an ischæmia, terminating often in gangrene. Capillary embolism may occur in a number of organs at the same instant, and give rise to a variety of lesions. When the cutaneous capillaries are obstructed ecchymotic spots are produced, followed by cellulitis. When the cerebral vessels are obstructed softening may occur, which, if the vessels are very small, may be developed without any evidence of obstruction to the cerebral circulation. If the obstructed artery is of large size, instantaneous hemiplegia and secondary softening will result.

Capillary emboli may have their seat in the vessels of the spleen, giving rise to infarctions and suppuration.

The kidneys may also undergo analogous changes. Rayer, without knowing the origin of these changes, has given an excellent description of them under the name of rheumatic nephritis.

In addition to the local lesions arising from these arterial or capillary emboli, the septic phenomena are most important. When typhoid symptoms, deep jaundice, and symptomatic intermittent fever are associated with acute endocarditis, it establishes its ulcerative character. In acute exudative as well as in ulcerative endocarditis, when the inflammation progresses rapidly, the valves soften and become less resistant than normal. As a result, they are stretched, bulged, or torn by the stream of the circulating blood-current.

A rupture of the mitral valves will open into the auricular, and that of the aortic into the ventricular, cavity. The reason for this is to be found in the fact that when the valves are closed the blood-pressure is exerted from the left ventricle toward the mitral valve, and from the aorta toward the semilunar valves. If the blood penetrates a rent in a flap of the valves, the endocardium is puffed out, and a valvular aneurism is formed, and round or funnel-shaped aneurismal sacs may project from the valves. The bottom of one of these sacs may be perforated, and long, ragged, gray shreds, covered with fibrin, may be found hanging in the ventricular cavity.

Microscopically, the torn shreds from a valvular aneurism, the result of acute endocarditis, consist of nuclei and round cells imbedded in a mass of granular matter. There is neither connective fibrilla nor elastic tissue. When the ulceration is localized in the ventricle, the pressure of the blood may bulge out the heart-wall, and thus give rise to a so-called partial cardiac aneurism. By rupture of such aneurism communication between the different heart-cavities may be established, which will vary with the seat of the ulceration.

Acute exudative endocarditis may involve the muscular structure of the heart. Such myocarditis (or carditis) may involve the deeper structures, weaken them, and so alter their consistence that bulging and the formation of a ventricular aneurism may result. Usually such myocarditis is so slight that incomplete organization of the new embryo-plastic cells occurs and the tissue undergoes fatty changes. The results of all forms of acute endocarditis are best studied in connection with the morbid changes of interstitial endocarditis, into which they so often gradually merge.

Interstitial Endocarditis.

MORBID ANATOMY.--Interstitial (or chronic) endocarditis may be a continuation of a process which commenced in an acute exudative endocarditis, or it may be interstitial from its commencement, and be so insidiously evolved as to escape notice. The anatomical changes may sometimes be confined to the edges of the valves, at others to their base, or they may involve the entire valves, which become thickened, indurated, contracted, degenerated, and {644} adherent. It is more closely allied to rheumatism, gout, and chronic interstitial changes in other organs than either of the other varieties.

There is no part of the endocardium which is exempt from interstitial inflammation. The favorite place for its development is the endocardium of the valves and that at the apex of the left ventricle. The thickening at first may be either translucent or opaque, and the valves may become three or four times thicker than normal. In some instances, although the valves are thickened and indurated, their functional activity is not interfered with, and they offer no obstruction to the blood-current.

White, thickened, opaque spots are often irregularly scattered over the internal wall of the heart. The vegetations met with in interstitial endocarditis differ from those of the acute exudative variety in that they are less prominent and firmer. They rest upon an indurated base. Their cartilaginous consistency is due to the fact that their cellular elements are not round (as in acute exudative endocarditis), but elongated and flattened, possessing an abundant intercellular fibrillated tissue.

In and underneath the endocardium there is an increase of tissue, and upon any prominence arising from the thickening of the endocardium occur fibrin deposits. These fibrinous efflorescences assume a variety of forms, and sometimes string out into the adjacent vessels and cavities for half an inch or more. Their usual form is globular or wart-like, and their seat is on the ventricular surface of the aortic and upon the auricular surface of the mitral and tricuspid valves.

In interstitial endocarditis the cell-development is far less rapid and abundant than in the acute exudative form, and this very slowness accounts for the greater induration and thickening.

A microscopical examination of a cross-section of an indurated valve shows a number of flat cells arranged in irregular layers, having between them a fibrinous material which has in it here and there a few elastic fibres. The new formations always originate in the layer of flat cells. These changes are best marked in the fibrous zone at the valvular orifices, upon the surfaces of the valves themselves, and in the chordæ tendineæ. The new tissue, whether developed rapidly as in acute exudative, or slowly as in interstitial endocarditis, becomes fibroid and contracts, and this contraction is progressive.

As a consequence, the rigid valves, whose edges are round and hard, are drawn toward their base, and thus are made to assume a puckered appearance. A similar process in the chordæ tendineæ causes them to become hypertrophied, rigid, and cartilaginous, while they are diminished in length. In this way the valves are not only diminished in depth, but not infrequently have their free edges approximated to the cardiac walls, so that extensive valvular insufficiency is the result. This, however, does not always happen, for a thickened cartilaginous valve may have such abundant fibrinous or papillary excrescences upon it that the onward current is obstructed and extensive stenosis results.

As the thickening and rigidity of the flaps of a valve increase, their mobility is diminished, and adhesions take place between their edges which begin at their bases and progress toward their apices: so thoroughly do they become adherent that in some cases all evidence of a valvular outline is lost, and a fibrinous diaphragm is formed across the valvular orifice having only a small slit at its centre, looking and feeling like a buttonhole; hence the term buttonhole slit. The mitral opening, which will usually admit the ends of three fingers, may be so narrowed that the end of the little finger will scarcely pass through it, and the aortic opening may become so diminished as not to admit a small quill. These retractions and adhesions cause the mitral valves, with their columns and cords, to assume the form of a perforated cone.

{645} Long stringy masses of fibrin, when located on the aortic valve, sometimes form adhesions with the aortic walls, and thus is induced a sudden and extensive regurgitation.

Insufficiency and stenosis are often found at the same valvular orifice as the result of the thickening, adhesion, and retraction.

Changes at the aortic orifice usually occur after middle life, and induce more insufficiency, retraction, and adhesion than those which are limited to the mitral valve. The mitral valves are the most frequent seat of interstitial endocardial changes in early and adult life. These lesions are analogous to those characteristic of endarteritis deformans. The tendency of the lowly-organized tissue which results from interstitial endocarditis is to undergo fatty and calcareous changes.

The minute patches of fatty degeneration in the imperfectly organized tissue underneath the endocardium sometimes form atheromatous masses containing more or less granular débris. The endocardium over these patches may be destroyed, or the patches may soften and ulcerate and cause extensive destruction of the valves. Valvular aneurism may form in the same manner as has been described in exudative endocarditis. The formation of calcareous granules and plates is a very frequent termination of interstitial endocarditis.

The aortic orifice is the most frequent seat of calcareous degeneration. It is rarely associated with mitral stenosis. So extensive may this process be that little beads of chalky material may be seen studding the free edges of the valve and even extending into the cardiac cavities.

When interstitial endocarditis has its seat in the endocardium of the cardiac cavities, the endocardium will undergo changes similar to those of the valves, and the muscular walls of the heart will be the seat of interstitial myocarditis. As a result, the walls of the heart become thinner and less resistant than normal, and depressions are formed on its inner surface. The process is in reality a fibrous overgrowth, which occurs in spots varying in size from half an inch to one inch in diameter. When it extends through the entire heart-wall the columns and cords may be so shortened as to cause valvular insufficiency.

If the cardiac walls yield so that a well-defined pouch is produced, a condition results which is called aneurism of the heart. Cardiac aneurism, thus induced, is usually seated at the apex of the left ventricle; the aneurismal sac may vary in size from that of a marble to that of a closed fist, and may communicate with the ventricle by a funnel-shaped or ring-like aperture. The walls of the sac are solid and rigid; the internal surface is smooth, but it may be anfractuous. In the latter case clots adhere to its wall. Cardiac muscular fibres are found here and there in the aneurismal walls. They are mostly, however, made up of layers of flat cells, their flatness being the result of pressure.

Aneurisms at the base and in the inter-ventricular septum may result from the extension of a valvular aneurism.

ETIOLOGY.--In most instances endocarditis depends upon a constitutional dyscrasia characterized by alterations in the vital, physical, or chemical properties of the blood.

Acute exudative endocarditis rarely, if ever, occurs as a primary or idiopathic affection. It seems to have a direct connection with those diseases and dyscrasiæ in which the blood is altered either in the relative proportions of its constituents or in its physiological elements. So frequently is acute exudative endocarditis associated with acute articular rheumatism that they have often been described as one disease.

It is generally stated that acute endocarditis occurs in 50 per cent. of those who suffer with acute articular rheumatism, but the statistics of Bellevue {646} Hospital show that endocarditis complicates rheumatism in only 33 per cent. of the cases. From these statistics it is evident that a majority of the cases of acute rheumatism run their course without endocardial complication.

The irritant action of the blood, the salts of which are changed or which contains excrementitious products or a specific poison, is shown most markedly upon the valvular surface of the endocardium; and it is for this reason that the parts which are most exposed to friction of the blood-current are those which first and most extensively exhibit the pathological changes of endocarditis.

Charcot records a large number of observations in which endocarditis developed in patients with chronic rheumatism and in which it never assumed an acute form. It therefore seems evident that organic lesions of the valves from endocarditis may occur in the course of chronic as well as of acute rheumatism.

There is no disease in which a morbid blood-state exists in which endocarditis may not occur. The essential fevers, the exanthemata, diphtheria, septicæmia, pyæmia, and Bright's disease, are all conditions in connection with which endocarditis is frequently exhibited. It is met with occasionally in secondary syphilis.

Acute and chronic Bright's disease are often complicated by it. When an individual who is already the subject of valvular disease of the heart is attacked with acute rheumatism, the liability to endocarditis is much increased.

Even when rheumatism and chorea are absent, endocarditis is liable to occur when valvular disease exists. Some regard myocarditis, pericarditis, pleurisy, and pneumonia as capable of exciting endocarditis by the extension of the inflammatory process from the surface of the heart; it is questionable if it ever results from such extension. That it can be the result of traumatism is possible: Bamberger records two cases of traumatic endocarditis. Wunderlich ranks measles, next to rheumatism, as a cause of endocarditis.

In estimating the etiological importance that any disease bears in the production of endocarditis, we must remember that not every blowing sound or murmur is indicative of an inflamed endocardium. Bamberger and Niemeyer think that the excited and irregular action of the heart in children, by inducing irregular tension of the valves, may bring about a blowing sound during the course of acute rheumatism.

Acute ulcerative endocarditis is met with in pyæmia, puerperal fever, and endometritis, scarlatina, and diphtheria: it may occur as a secondary affection to some inflammatory focus located in the body--septic endocarditis.

Again, this form of endocarditis may appear without obvious cause--spontaneously or in connection with some specific form of inflammatory disease, as croupous pneumonia. Wilks calls it then arterial pyæmia. Primary ulcerative endocarditis is a name recently and perhaps more aptly given it.

Finally, ulcerative endocarditis may appear as a graft (recurrent endocarditis) upon a valve the seat of interstitial endocarditis, and have all the pathological appearances of the septic form, but none of its clinical aspects.

The majority of cases of interstitial endocarditis are the sequelæ of the exudative form. It is far more frequently associated with articular rheumatism than with any other condition. In a certain proportion of cases the process is interstitial from its onset, especially when it occurs with gout, chronic rheumatism, in alcohol-drinkers, or in the aged.

SYMPTOMS.--The subjective symptoms of acute exudative endocarditis are more obscure than those of any other disease. They are not only few and ill-defined, but they have no regular order of development. When the muscular tissue of the heart is not involved the disease may run its entire course without exhibiting a single subjective symptom.

{647} The urgent symptoms of acute rheumatism, the different phases assumed by the dyscrasiæ and acute infectious diseases in which this condition is liable to occur, so mask those of the endocardial inflammation that they are often overlooked.

When the endocardial inflammation is extensive and the muscular tissue of the heart is involved, the patient will complain of palpitation and a sense of discomfort in the region of the heart; not infrequently cardiac palpitation is accompanied by dyspnoea, and decubitus on the left side is noticed. In a small percentage of cases the palpitation is appreciable to the physician. The heart may beat with great force and its action be tumultuous, and yet the pulse not be altered in character.

The pulse, at first, is usually strong and forcible; later, it becomes rapid, small, feeble, and irregular. In some cases it is very frequent from the onset of the disease. As a rule, the force of the pulse will not correspond to the cardiac activity; for, as the muscular fibres of the heart become involved, its propelling power is diminished, and the pulse is correspondingly feeble and compressible. It may be dicrotic. The respirations are more or less accelerated, and sometimes labored, and there may be paroxysmal dyspnoea. The face may be flushed and covered with a profuse perspiration, or it may assume a dusky, pallid, ashy-gray, or slightly cyanotic hue. In rare cases there may be sleeplessness or nocturnal delirium of a typhoid type. If the muscular tissue of the heart is extensively involved, nausea, vomiting, giddiness, and syncope may be present.

When there is pain in the cardiac region, especially if it is augmented by pressure, pericarditis is usually present, and slight pain or tightness in the cardiac region is not an infrequent symptom, and is quite common when endocarditis occurs in those who are the subjects of chronic valvular disease.

The temperature in acute exudative endocarditis seldom exceeds 103° F.

When ulcerative endocarditis complicates septicæmia and a rupture of a valve occurs, a typhoid state rapidly supervenes. The patient is forced to assume the sitting position on account of the intensity of the dyspnoea, cyanosis is sudden and extreme, and the symptoms of multiple embolism make their appearance. The febrile symptoms are marked; the temperature may reach 106-107° F.; the patient becomes jaundiced; and there are frequent rigors, which, with the paroxysmal febrile attacks, simulate the icteric form of malarial fever. The spleen becomes enlarged and tender, the urine becomes scanty, dark-colored, albuminous, and of high specific gravity, and in severe cases delirium and coma occur.

Some cases of endocarditis putrida (as some German pathologists call it) are attended with nausea, vomiting, and diarrhoea. The frequency with which this form of endocarditis is associated with pneumonia certainly suggests a blood-poison of great intensity. Although it is rarely met with except in septic conditions, it may occur late in severe forms of rheumatic and traumatic endocarditis or when there has been pre-existing suppurative disease of the bones.

The symptoms which attend embolism from detachment of the fibrinous efflorescences upon the valves are due to the arrest of such a plug in an artery whose calibre is too small to admit of its passage. Beyond the obstruction the circulation is arrested; hence results either an infarction or necrosis of the part whose blood-supply is thus shut off. The organ most liable to be the seat of such emboli is the spleen, and after this the kidney and the brain. Hence the occurrence of hemiplegia with aphasia or marked cerebral symptoms in the course of acute endocarditis is indicative of cerebral embolism.

There are no positive subjective symptoms of interstitial endocarditis. There may be palpitation and a sense of uneasiness, sometimes amounting to {648} pain at the præcordial region, with irregularity in the action of the heart, but all of these, when taken together, are not sufficient for a diagnosis. This can be made only from changes in the heart-sounds produced by changes in the valves and valvular orifices.

PHYSICAL SIGNS of exudative endocarditis.--Inspection.--Upon inspection it will sometimes be noticed that the area of the cardiac impulse exceeds the normal--that it is irregular and often tumultuous. As the disease advances, the apex-beat and the impulse grow more indistinct, but never to the same extent or so suddenly as in pericarditis. In children the vessels of the neck exhibit venous stasis far more frequently than in adults.

Palpation.--At the onset of an endocarditis the cardiac impulse is more forceful than normal, and the heart-action is frequently irregular. In some instances the heart thumps violently against the chest-walls. The force of the cardiac impulse varies from day to day. The impulse is stronger when pain is present over the præcordial space. If during the entire course of the disease there is no decrease in the force of the apex-beat, it may be inferred that there is no deficiency in the muscular power of the heart. When acute endocarditis supervenes upon long-standing valvular disease, there will be an alternate increase and diminution in the area and force of the impulse. When the walls of the heart become weakened by subsequent myocarditis, or when the endocardial inflammation is itself very extensive, the force of the apex-beat is diminished. An endocardial thrill is frequently present in acute exudative endocarditis.

Percussion.--The area of cardiac dulness in endocarditis is normal, unless changes at the valvular orifice retard the outflow of blood from the lungs, and then the right-heart cavities become engorged and the area of dulness will extend beyond the normal limits. But it is to be remembered that the increase is always slight, except in those few cases where the heart-cavities are both suddenly and extensively distended with blood or masses of fibrin. Extensive myo- or endocardial inflammation may so weaken the heart-walls that they will dilate, and then percussion will reveal an enlargement in the area of cardiac dulness.

Auscultation.--On auscultation a murmur or murmurs can be heard over the various cardiac orifices. The fact that valvular disease may have previously existed makes it important, at the first visit to a patient who is suffering from acute articular rheumatism, chorea, Bright's disease, etc., to carefully examine the heart. When cardiac hypertrophy exists and valvular disease has pre-existed, it is difficult, if not impossible, to recognize acute exudative endocarditis or to determine the time of its advent if it exist. The most important and constant sign of endocarditis is a systolic murmur, its greatest intensity being over the apex; but this murmur, which is soft and blowing in character, the so-called bellows murmur, may be either ventricular or valvular. In all cases it is due to roughening or thickening of the endocardium. It often changes its point of maximum intensity during the acute period of the disease. It is developed at the onset of the disease, and when one is on the lookout for endocarditis, this will be the first evidence of its occurrence. And yet in some instances no murmur may be present during the entire course of an endocarditis.

A mitral murmur alone occurs in about 50 per cent. of cases of rheumatic endocarditis. It is usually developed early, and before it becomes distinct it is preceded by prolongation of the first sound. This is a transition sound between a normal heart-sound and a murmur. It is a feeble, wavering sound, extending over the slight interval which normally exists between the first and second sounds.

Other changes that are not murmurs, but which frequently precede them, are loud, ringing normal sounds, muffled first sound, feeble first and {649} intensified second sound, doubling of the first sound, roughness of the first sound, and a humming over the right heart.

Complete absence of the heart-sounds is a rare but possible antecedent of an endocardial murmur. A mitral murmur in acute endocarditis is usually audible over a limited area. It is the exception to hear it both in front and at the back. Very frequently it is heard most distinctly over the stomach.

When the blood becomes dammed back into the lungs, there is an extra strain upon the pulmonary semi-lunar valves, and then the second sound will be accentuated over these valves on account of the sharp shock which they sustain during diastole. With this accentuation of the second sound over the pulmonary orifice, the first pulmonic sound may be feeble or absent. A subdued or absent first sound shows tension of the artery.

Reduplication of the second sound in a mitral endocarditis is probably due to the difference in time occupied by the ventricles in emptying themselves. A tricuspid murmur occurs in 50 per cent. of the cases of acute mitral endocarditis--a pulmonic in about one-third of the cases. They are superficial and scratchy in character, and indicate a relaxed condition of the vessels and a thin condition of the blood. These murmurs are never permanent. Mitral endocarditis is accompanied by aortic murmurs in about 16 per cent. of cases. Acute mitral endocarditis occurring with chorea is as apt to become interstitial as when it is of rheumatic origin.

Aortic murmurs are usually soft and blowing, but they may be musical, whistling, or twangy. In aortic endocarditis the second sound is usually lost over the carotids. Incompetency of the aortic valves is met with only in the interstitial form of endocarditis.

In about 12 per cent. of the cases of exudative endocarditis arising from rheumatism a regurgitant murmur will be heard at the tricuspid orifice, but such murmurs are not the result of endocarditis of the right heart.

Tricuspid murmurs are present in 50 per cent. of all cases of recent mitral murmurs, in about 40 per cent. of recent aortic murmurs, and in about one-fourth of mitro-aortic murmurs. Such tricuspid murmurs are due to an increase in the slight normal insufficiency existing at the tricuspid orifice. They are of short duration, and are heard over the body of the heart over the right ventricle. Sometimes they are vibrating in character.

In children aortic endocarditis is rare; at this period obstruction at and regurgitation through the mitral orifice commonly occur together.

The physical signs of interstitial endocarditis are such as are due to those changes in the valves which will be considered under the head of Cardiac Murmurs, and their Relations to Valvular Diseases.

DIFFERENTIAL DIAGNOSIS.--Acute exudative endocarditis may be mistaken for pericarditis, and its murmur may be mistaken for the murmur produced by aortitis and for those that develop during the course of fevers.

The friction sounds of pericarditis are superficial in character, and are limited to the præcordial space, while the murmurs of endocarditis are distant, and each murmur will have its area of diffusion beyond the præcordial space. A pericardial sound is distinctly a friction, creaking, or rubbing sound; it has a to-and-fro character, while the murmur of endocarditis is soft and blowing.

Endocardial murmurs accompany the heart-sounds, while pericardial friction sounds are not always rhythmical with the heart-sounds.

The intensity of a pericardial friction is increased when the patient bends forward at the end of a full inspiration or when the stethoscope is pressed firmly over the præcordial region; and in the last-named case it becomes distinctly grazing and rubbing in character. In endocarditis these methods produce no difference in either the intensity or the character of the murmur. There is an endocardial thrill in endocarditis not present in pericarditis.

{650} As soon as effusion occurs in pericarditis the absence of pain, the alteration in the character of the pulse, the great increase in dulness, and the disappearance of the adventitious sounds will decide the diagnosis.

Aortitis has most of the symptoms of endocarditis, but in addition the pulse is more rapid, the respirations are more hurried, and pain which shoots down the spine and is increased by motion is present in the præcordial region. Not infrequently aortitis is accompanied by cutaneous hyperæsthesia.

Acute inflammation of the aorta is exceedingly rare, and in the few cases observed has been complicated by very grave diseases. Indeed, Powell, Lebert, and Rindfleisch doubt its existence.

In the _Medico-Chirurgical Transactions_ (vol. xlvii. p. 129) Moore gives a case where rigors, fever, intense and painful throbbing of the aorta, and embolic infarction of distant organs occurred, with symptoms so resembling those of endocarditis that few would venture to favor a diagnosis of aortitis during life.

The functional cardiac murmurs which occur in fevers are usually heard only at the base of the heart, while those of endocarditis are most frequent and distinct at the apex. There are no symptoms of obstruction present with febrile murmurs, while they are frequently present in endocarditis.

It is often difficult to determine whether an endocardial murmur is of old or recent origin: if during an attack of acute rheumatism an endocardial murmur is developed under daily examination, it is a certain index of acute exudative endocarditis. If a murmur exists at the first examination which is systolic, soft, and blowing in character, and not accompanied by the evidences of cardiac hypertrophy, there is good reason to believe that it is produced by an acute endocardial inflammation.

If, on the other hand, the murmur is rough in quality, diastolic, and cardiac hypertrophy exists, it cannot be regarded as a sign of acute endocarditis.

The rules for distinguishing murmurs due to interstitial endocarditis from functional murmurs will be given under the head of Cardiac Murmurs.

PROGNOSIS.--Exudative endocarditis is rarely a direct cause of death, but it seldom results in complete recovery. Acute mitral endocarditis terminates in permanent valvular disease in over 25 per cent. of the cases. The elements that will render the prognosis immediately unfavorable in any case are the symptoms of embolism or of metastasis. Sudden splenic enlargement, with tenderness over its site, albuminuria or hemiplegia, when accompanied by the physical signs of acute insufficiency or perforation of a valve with cyanosis, dyspnoea, and disturbance of the heart-rhythm, will render the prognosis exceedingly unfavorable. All these symptoms are diagnostic of acute ulcerative endocarditis, and therefore when the signs of endocarditis appear during the course of pyæmia, diphtheria, or other septic condition, the liability to these conditions must be considered.

When even exudative endocarditis is accompanied or followed by typhoid symptoms its prognosis is unfavorable. In children bronchial complications, catarrhal pneumonia, and intercurrent diarrhoea may lead to a fatal issue. Death may result from acute insufficiency of the heart or from complications.

The prognosis in interstitial endocarditis will depend upon the seat and extent of the valvular lesions which it produces. It will be more fully considered under the head of Valvular Diseases.

In cardiac aneurism death may result from rupture of the aneurismal sac, from apoplexy, or from secondary diseases in other organs.

TREATMENT.--Acute exudative endocarditis is rarely, if ever, idiopathic. It is so constantly associated with certain infectious diseases, and especially with acute articular rheumatism, that its treatment must be determined by the condition under which it occurs.

{651} In every case the patient must have absolute rest in bed in a room whose temperature should never be below 70° or 75° F. The præcordial region should be covered with flannel, and care exercised not to expose the surface when physical examination of the heart is made. Some authorities claim that an ice-bag applied to the præcordial space during the active period of an acute endocarditis will arrest and limit the inflammatory process. My own experience does not sustain the results claimed for this plan of treatment.

In rheumatic endocarditis antirheumatic remedies are indicated, the joints must be kept absolutely at rest, and such local treatment should be resorted to as will relieve pain and give the greatest comfort to the patient.

If the blood is kept alkaline, as indicated by the urine, the liability to endocarditis is diminished.

To ensure rest small doses of opium are often required; but opium cannot be administered as freely in endocarditis as in pericarditis.

During the whole course of acute endocarditis the strength of the patient must be maintained by the judicious use of concentrated nutriment, with some preparation of iron.

When endocarditis occurs with septic diseases and is attended by typhoid symptoms, or when it assumes the ulcerative form, alcoholic stimulants, quinine, and iron must be freely administered.

In endocarditis complicating Bright's disease the rapid elimination of the urea must be established. The severe pain over the præcordial space may be relieved in many subjects by the application of a few leeches to the region.

Experience proved that the employment of mercury (internally) and blue ointment (externally) to lessen the plasticity of the blood, and the internal use of iodide of potassium (for the absorption of fibrinous exudation), were harmful, before it was demonstrated that the theory on which their use was based had no foundation.

Cardiac Murmurs, and their Relations to Valvular Diseases of the Heart.

DEFINITION.--A cardiac murmur is an adventitious or abnormal sound produced within the heart or blood-vessels, either by obstruction to the blood-current, an abnormal direction of the blood-current, or by a change in the blood-constituents.

HISTORY.--The systematic study of cardiac murmurs and valvular diseases dates from the discovery of auscultation by Laennec. Previous to his discovery there are a few recorded cases where observers during the seventeenth and eighteenth centuries described forms of valvular diseases. One of the first to describe a valvular lesion of the heart was Vieussens in 1716. At the close of the seventeenth century Willis and Riverius published cases of valvular disease. In all these instances it was the aortic valves that were diseased, and the discovery of their condition was undoubtedly due to the peculiarity of the radial pulse which is so marked and striking in aortic disease.

In Friedreich's article in Virchow's _Handbuch_, "Krankheiten des Herzens," Meckel's essay of 1756 is given as the first paper on endocardial disease.

John Hunter[2] in 1794 gives a lengthened account of a most interesting case of aortic valvular disease. Senac[3] gives an account of disease of the auriculo-ventricular valves; and Allan Burns, whose work was published in 1809, describes aortic regurgitation and obstruction, and supposes that "a reflux current can produce a hissing noise, something like what is described as audible palpitation in some diseases of the heart."[4]

[Footnote 2: _Treatise on the Blood_, etc.]

[Footnote 3: _Treatise on the Heart_, 1783.]

[Footnote 4: _Obs. on some of the most Frequent and Important Dis. of the Heart_, Allan Burns, Edinburgh, 1809.]

{652} The subject of vegetations upon the valves was very fully considered by Corvisart in 1806. Corvisart was the first to mention the importance of what is now called the purring thrill. He stated that "it probably came from a difficulty experienced by the blood in going through an orifice disproportionate to the amount of fluid." Laennec regarded murmurs or bruits as the result of spasmodic contraction of the heart or arteries. Corrigan in 1829 defined murmurs as "the result of the development of currents and the intrinsic collision of the moving liquid."

In 1842, Gendrin gave cardiac murmurs as bruits de frottement endocardiaques, and established the friction theory. He also called attention to the fact that alteration in the constituents of the blood will produce murmurs which are heard in arteries of medium calibre.

Bouillaud describes a murmur as an exaggeration of the normal bruit caused by blood-friction against the segments of the heart, and he says that according to the size or condition of the orifice the murmur will be rasping, sawing, or blowing.

Chauveau states that bruit de souffle is produced by the vibration of a nei e fluide, always formed when blood rushes through a part of the circulatory system actually or relatively dilated.

This nei e fluide has its best development in anæmia, when it is termed the bruit du diable, for the jugular veins do not collapse and the volume of blood in anæmia is diminished. Chauveau's theory is applicable to anæmic murmurs, but not to all cardiac murmurs.

Hope states that "valve murmurs are produced by collision of the blood-particles against one another, or that either the liquid alone or the liquids and solids conjointly may develop murmurs."

There are many who have advocated the tension theory--viz. that an increase in tension and force can so exaggerate a normal sound as to produce a murmur. This theory has no clinical foundation. Often, however, valve-lesions may exist, and the blood-current be so weak, the propulsive force so feeble, that no murmurs are audible.

Some observers are of the opinion that spasm of the papillary muscles and chordæ tendineæ and weakening of these structures through fatty degeneration can cause temporary murmurs.

The conditions that determine the character of a cardiac murmur, its pitch, quality, and intensity, are subject to the same physical laws as govern the formation and quality of sound elsewhere. They are the rapidity and force of the moving body, the obstructions which it meets, and the physical properties of the media of conveyance. The same vibration that produces a murmur may produce an endocardial thrill, called sometimes purring thrill.

Far more important, however, than loudness, pitch, or quality of a murmur are its rhythm, its point of maximum intensity, and the area of its diffusion, all of which can best be considered in connection with the physical signs of each valvular lesion.

During a cardiac diastole the heart-cavities are all filling; just before the commencement of the cardiac systole the blood is forced from the lungs and the cavæ through the auricles into the ventricles, while the mitral and tricuspid valves are pressed against the walls of the ventricles, and no obstruction is offered to the blood-current. If, as the result of disease, any obstruction exists at either one of the auriculo-ventricular orifices, the blood as it passes through the opening will impinge on such obstruction and cause a presystolic murmur.

During a cardiac systole the filled ventricles contract; blood is thrown through the semi-lunar openings, the flaps of whose valves are pressed against the walls of the vessels, so that no obstruction is offered to the outgoing {653} current. At the same instant the auriculo-ventricular valves close their orifices, so that blood may not be forced back into the auricles.

If, as a result of disease, the semi-lunar valves should obstruct the outgoing current, or the mitral or tricuspid valves should not wholly close the auriculo-ventricular orifices, then in the one case the direct blood-current, as it passes over the obstruction at the semi-lunar orifices, would produce a systolic murmur, and in the other the backward current through the abnormal opening at the auriculo-ventricular orifice would also produce a systolic murmur.

Again, if the lungs and the aortic system (when filled at the systole) have, back of them, a semi-lunar valve that does not completely close that end of the circuit, the blood will regurgitate into the ventricles during the period of cardiac rest, so that semi-lunar incompetence will cause a diastolic murmur.

ENDOCARDIAL MURMURS.

Rhythm. Situation. Orifice. Nature. Systolic 1 Basic, Aortic, Obstructive. " 2 " Pulmonary, " " 3 Apical, Mitral, Regurgitant. " 4 " Tricuspid, " Diastolic 1 Basic, Aortic, " Presystolic 1 Apical, Mitral, Obstructive.[5]

[Footnote 5: Pulmonary regurgitant murmur (diastolic) and tricuspid obstructive murmur (presystolic) are so rarely met with that, clinically, they may be disregarded.]

The following is the order of relative frequency of cardiac murmurs: 1. Mitral regurgitation; 2. Aortic obstruction; 3. Aortic regurgitation; 4. Mitral obstruction; 5. Tricuspid regurgitation; 6. Tricuspid obstruction; 7. Pulmonary obstruction; 8. Pulmonary regurgitation. The most frequent combinations of murmurs are--1. Aortic obstruction and regurgitation; 2. Mitral obstruction and regurgitation; 3. Mitral obstruction and tricuspid regurgitation; 4. Aortic obstruction and mitral regurgitation; 5. Double valvular disease at aortic and mitral orifices (four murmurs).

It is often difficult, after having satisfied ourselves of its existence, to determine the rhythm of an endocardial murmur. To resolve this difficulty it is necessary to determine which is the first and which the second sound of the heart.

The first sound of the heart is synchronous with the carotid pulse, the radial pulse, and the apex-beat. It may be wholly replaced by a systolic murmur, but the second sound is always heard following the apex-beat, for the pulmonic and the aortic valves are never diseased at the same time.

Having determined the existence of a murmur, its rhythm, pitch, intensity, and quality, we next determine its point of maximum intensity. These points of maximum intensity for murmurs at the four valvular orifices of the heart may be briefly summarized as follows: Murmurs arising at the mitral valve are loudest at the apex of the heart or immediately above it; tricuspid murmurs are loudest over the lower part of the sternum; pulmonary murmurs, in the second left intercostal space close to the sternum; and aortic murmurs, in the second right intercostal space at the edge of the sternum and over the whole length of the body of that bone.

Valvular diseases which cause murmurs result either in a condition of the valves that allows regurgitation, or one that obstructs the onward blood-current. Valvular insufficiency arises when extensive retraction, perforation, or partial detachment of the valves prevents them from completely closing their respective orifices. And when the chordæ tendineæ have been ruptured, or when calcareous degeneration has made the valves or the parts in the immediate vicinity abnormally rigid, the regurgitant current through the aperture thus left gives rise to a regurgitant murmur.

{654} When the valves are thickened, retracted, adherent, hypertrophied, or degenerated, so that their edges are prevented from being accurately applied to the walls of the ventricles or vessels, they obstruct the current of blood, and the impinging of the blood-current against the obstruction gives rise to obstructive murmurs. These conditions--stenosis and insufficiency--are often found coexisting, but rarely in equal degree, one usually predominating sufficiently over the other as to give a dominant character to the murmur.

The lesions which produce these conditions may be temporary or permanent--temporary when they occur during the course of acute endocarditis, and permanent when they consist of a new growth either of connective, fibroid, calcareous, or atheromatous tissue, which alters the form of the valves and impairs their function. Acute and chronic valvular disease may produce the same murmurs. The effect of the valvular deformity depends entirely upon its seat.

In the study of the relations of valvular lesions to cardiac murmurs physical signs are the important factors in their diagnosis, and it is necessary always to bear in mind the normal physiological conditions which constitute a complete cardiac pulsation.

The apex of the normal heart is felt between the fifth and sixth ribs on the left side, about two inches below the nipple and one inch to its sternal side. The base of the heart is on a level with the third costal cartilages. The tricuspid valve lies behind the middle of the sternum, on a line with the articulations of the cartilages of the fourth ribs with the sternum. The mitral valve lies behind the cartilage of the fourth left rib, near the edge of the sternum. The aortic valves lie behind the sternum, a little below the junction of the cartilages of the third ribs with the sternum, near its left edge. The pulmonary valves lie behind the junction of the third left rib with the sternum.

Let it be remembered that the tricuspid orifice is the most superficial, then the pulmonary, next the aortic, and, deepest of all, the mitral orifice. Ranged from above downward, the pulmonary orifice comes first, then the aortic, then the mitral, and lastly the tricuspid.

Aortic Obstruction, or Stenosis.

Stenosis at the aortic orifice is a common cardiac lesion, and one that is always accompanied by more or less hypertrophy of the left ventricular walls.

MORBID ANATOMY.--In aortic obstruction the cardiac valves will be found to present some or all of the changes which have been described as taking place in the course of acute and interstitial endocarditis, together with degenerative changes due to atheromatous, calcareous, fibroid, fatty, or connective-tissue metamorphosis.

Sometimes the valves may be covered with thick, warty, irregular excrescences that cause loud murmurs, and yet do not seriously interfere with the outgoing blood-current. At other times stenosis of the aortic orifice may be so extensive as to almost obliterate it. When such is the case, the extent of the lesion will be measured much more by the consequent hypertrophy and its effects on the systemic circulation than by the loudness or harshness of the murmur which it produces.

Very frequently the valves are so rigid that they cannot be pressed back against the wall of the aorta, and these unyielding prominences are greater obstacles to the outgoing current of blood than vegetations on the surface of the valves.

In a few rare cases the outlet may be diminished by constriction of the {655} aorta at the point of insertion of the valves. Adhesion of the aortic valves begins at their bases and extends along their free edges to their tips; sometimes they become fused together into a mass, so that they project into the blood-stream in the form of a funnel irregular in shape and studded with calcareous nodules. The line of attachment of the valves to the aorta frequently becomes entirely obliterated.

In some instances the contraction of the valves between their points of attachment causes them to form a deep pocket or pouch, and their points of attachment may be a quarter of an inch apart.

Obstructions at the aortic orifice are frequently accompanied by atheromatous changes in the aorta, the result of chronic inflammation of its tunics--arteritis deformans.

As a result of aortic stenosis the wall of the left ventricle becomes hypertrophied. This change is a gradual one, and is called compensatory hypertrophy: it is due to the increased force required to propel the blood through the constricted orifice.

After a time insufficiency of the mitral valves is apt to occur, caused either by the extension of endocardial inflammation from the aortic valves or by the forcible pressure of blood upon the ventricular surface of the valves.

A slight thickening or roughening of the aortic valves may cause slight obstruction to the outgoing blood-current, which will interfere but little with the emptying of the ventricular cavity, and which rarely leads to hypertrophy of their walls.

ETIOLOGY.--Aortic obstruction is most frequently met with in early and advanced life, the mean age being forty-seven years. It is not uncommon in children; valvular lesions have been found in children under two years of age. It may be induced where the aorta is defectively developed, and some think that imperfect development of the trachea may lead to imperfect expansion of the chest, and thus induce disease of the aortic valve.[6]

[Footnote 6: Barlow in _Guy's Hospital Reports_, S. 1, vol. vi. p. 235.]

Its most frequent cause is acute exudative and interstitial rheumatic endocarditis. The origin of nearly all valvular disease may be traced back to an attack of rheumatic fever. Next to acute rheumatism, chorea is its most frequent cause. Bright's disease and pyæmia may cause it, and atheroma or arteritis deformans extending to the valves will give rise to valvular lesions which cause obstruction.

Any of the conditions that cause acute exudative and interstitial endocarditis may effect changes in the valves, and the tissue thus developed, undergoing atheromatous, fatty, fibroid, calcareous, or connective-tissue change, will cause obstruction.

Increased tension of the aorta may be the result of chronic spinal deformity, and may be regarded as the indirect cause of aortic stenosis.

The connection between cancer and cardiac valvular disease is to be noticed, if not as cause and effect, at least as a remarkable and noteworthy coincidence.

Women are far less subject to aortic obstruction after rheumatism than men. In men the aortic valves are subject to more pressure and strain than in women, and hence non-rheumatic disease of these valves is very common, while in women it is very rare.

Aortic disease especially occurs in men whose occupations involve repeated, sudden, and great muscular effort.

In old age the walls of the aorta are weakened, and when aortic disease is met with in young subjects it must be regarded as the result of a premature senile condition of the vessels. Allbutt says that in Leeds quite young men have aortic valvular disease, and Peacock mentions several cases where the {656} disease has occurred in young girls who have been placed at service before they were fully developed.

Sometimes the valves are found to be studded with vegetations, apparently of syphilitic origin. Corvisart and Virchow both admit the possibility of such an origin for valvular disease of the heart, but no unquestionable case has as yet been advanced in proof of it. It has been claimed that this is the reason why soldiers so frequently suffer from heart disease; but sailors are notoriously more subject to syphilis than soldiers, and heart disease is rare among them.

The reason is evidently to be found in their mode of dress: sailors wear loose clothes, soldiers have the tightest possible fitting garments. More force is required to pump the blood through the constricted vessels, hence arises more strain on the aorta and more strain on the valves.

Single, sudden muscular efforts have in a limited number of cases produced disease at the aortic orifice.

Aortic valvular disease more frequently than mitral is of non-rheumatic origin; it is slower in its development, and is more commonly met with in advanced life.

SYMPTOMS.--The subjective symptoms of obstruction at the aortic orifice are not usually well marked. Extensive aortic stenosis is not incompatible with a state of comparative good health. As the obstruction to the outflow of blood from the ventricle increases, compensatory ventricular hypertrophy enables the heart to fill the arterial system and relieve the pulmonary pressure. As soon as the ventricular hypertrophy no longer compensates for the obstruction, the arteries are inadequately filled; the left auricle cannot empty itself into the left ventricle, and hence the pulmonary vessels are abnormally full, as is also the entire venous system. The scanty arterial supply gives the pallor to the face which so frequently accompanies this condition, and syncope is liable to occur as a result of partial cerebral anæmia.

These are late effects, and in many cases do not make their appearance until the mitral valve is secondarily involved. The pulse in aortic stenosis is normal in frequency, diminished in volume and power, usually regular in rhythm, though it may be intermittent, and is compressible and jerky in character.

As a general rule, in aortic stenosis signs of arterial anæmia precede evidences of venous engorgement. The obstruction to the exit of blood is shown in the sphygmographic tracing by a slanting or oblique up-stroke, as seen in the accompanying tracing, or, as Mahomed says, "the influence of percussion is lost." Tracings of the pulse in aortic stenosis sometimes show considerable separation between the percussion and the tidal waves. In some rare instances the pulse is slowed. There may be slight palpitation, and pain in the chest may sometimes occur in paroxysms; but pain in the chest is far more common in regurgitation than in obstruction. Aortic obstruction is more frequently connected with cerebral embolism than any other valvular lesion.

The left middle cerebral artery is the most common seat of aortic cardiac emboli. The left lower limb is more subject to embolism from aortic valvular disease than the right. The splenic and renal vessels are also the frequent seat of such emboli. Sometimes embolism is due to small auricular or ventricular {657} clots that form behind the obstruction. Such clots have occluded the aortic orifice and caused sudden death.[7]

[Footnote 7: _Pathological Transactions_, vol. ix. p. 91.]

PHYSICAL SIGNS.--The physical signs of aortic obstruction are generally distinctive and easily appreciated.

Inspection.--The visible area of the cardiac impulse is abnormally increased. Very extensive increase in the area of impulse is frequently accompanied by a lifting of the chest-wall over the heart.

Palpation.--The impulse is felt to be forcible, and is sometimes accompanied by a heaving or lifting motion. The apex is displaced toward the left and slightly downward. A sensation will sometimes be imparted to the hand during systole similar to that produced on the sense of hearing by the whizzing of a missile by the ear. This is often nothing more than an intensified endocardial thrill. This systolic frémissement radiates to the ensiform process of the sternum, being most intense in the second right intercostal space.

Percussion.--The area of cardiac dulness will be increased in proportion to the displacement of the apex-beat to the left. The increase in dulness measures the amount of left ventricular hypertrophy.

Auscultation.--Aortic stenosis produces a systolic murmur which more frequently accompanies than replaces the first sound of the heart. The maximum intensity of this murmur is usually at the second sterno-costal articulation of the right side, but it may be heard with equal intensity over the whole upper part of the sternum, and followed up the aorta and along the carotids; again, it may be loudest at the xiphoid cartilage, or it may be heard with greatest intensity at the junction of the left third rib with the sternum. In most cases the first sound is heard with the murmur, but the murmur may entirely replace or obscure it. This murmur is usually loud and harsh in character, and is loudest at the beginning of the systole. Harshness is one of its distinguishing characteristics.

In pure aortic stenosis the aortic second sound may be inaudible, and is always feeble, but the pulmonic second sound will always be audible. The area of diffusion of this murmur follows the law that a murmur is propagated in the direction of the blood-current. It is conveyed along the aorta into the carotids, and one of its characteristics is that it is heard in the great vessels of the neck. It may sometimes be heard in the thoracic and abdominal aorta.

When an aortic obstructive murmur is heard at the apex its intensity is diminished, and when heard behind it is most distinct at the left of the third and fourth vertebræ near their spines, and frequently extends downward along the spine in the course of the aorta, but with diminished intensity. It is to be noted here that a systolic murmur, audible at the base, and traceable along the ascending arch toward the end of the right clavicle, is by no means limited to cases of aortic stenosis, although aortic stenosis always produces a murmur with these characteristics.

Arterial murmurs, synchronous with the cardiac systole, are far more frequent than diastolic murmurs. When the mitral or tricuspid valves are thickened or incompetent, or when the myocardium is the seat of extensive fatty degeneration, the murmur of aortic obstruction will entirely replace the first sound of the heart.

DIFFERENTIAL DIAGNOSIS.--Aortic obstruction may be mistaken for mitral regurgitation, tricuspid regurgitation; an anæmic bruit, for the murmur of a thoracic aneurism and for a murmur produced by a scabrous condition of the ascending arch of the aorta.

1. Both mitral and tricuspid regurgitation, as well as aortic stenosis, are recognized by a systolic murmur. The murmur of aortic obstruction is heard with its maximum intensity at the second right sterno-costal articulation, and {658} diminishes in intensity toward the apex. The murmur of mitral regurgitation is heard with greatest intensity at the apex-beat. The murmur of aortic obstruction is conveyed into the vessels of the neck; that of mitral regurgitation to the left, in the direction of the apex-beat, and is heard behind, between the fifth and eighth dorsal vertebræ, at the left of the spine, with very nearly the same intensity as at the apex. The pulse in aortic stenosis is hard, firm, and wiry in character, but regular, while in mitral regurgitation the pulse is irregular in rhythm as well as in force, is never incompressible, and is easily increased in frequency. Gastric, intestinal, renal, hepatic, and bronchial symptoms are present in mitral regurgitation, while the subjective symptoms of aortic obstruction are cerebral in character. The pulmonic second sound is generally feeble in aortic stenosis, while in mitral regurgitation it is intensified. The murmur of aortic stenosis is harsh; the murmur of mitral regurgitation is soft, and frequently musical in character.

2. Tricuspid regurgitation is also accompanied by a systolic murmur. But while the murmur of aortic stenosis has its maximum intensity at the right second sterno-costal articulation, the murmur of tricuspid regurgitation is very rarely heard above the third rib: this is an important diagnostic sign. Tricuspid regurgitation is accompanied by jugular pulsation, while the murmur of aortic obstruction is heard in the arterial trunks of the neck. To distinguish between intrinsic pulsation of the jugular vein and throbbing of the carotid arteries press lightly on the vessel above the clavicle; this arrests pulsation when due to tricuspid disease, while if due to aortic stenosis the result is negative. Moreover, respiration influences jugular pulsation, while it has no influence over carotid throbbing. The area of transmission of tricuspid regurgitant murmurs is not more than two inches from the point of their maximum intensity; whereas the aortic obstructive murmurs are conveyed along the sternum into the vessels of the neck. There is nothing peculiar or abnormal about the pulse of tricuspid regurgitation, while the hard and wiry pulse of aortic obstruction is quite characteristic.

3. An anæmic bruit may be mistaken for aortic stenosis, since the rhythm and seat of the bruit are often identical with those of the stenosis. Anæmia, however, produces a murmur that is heard loudest in the carotids, and is accompanied by a venous hum, the bruit du diable, which is continuous, and heard best on the right side of the neck. Thus in anæmia there are three murmurs, arterial, cardiac, and venous. In aortic disease the murmur has its maximum intensity at the second sterno-costal articulation of the right side, and is not accompanied by a venous hum. There is always more or less cardiac hypertrophy in stenosis, and an increase in the force of the apex-beat, while anæmia is attended by a feeble cardiac impulse. The murmur is soft and blowing in anæmia and harsh and rasping in aortic obstruction. The pulse is characteristic in aortic stenosis; in anæmia it may have a thrill, but is never hard and wiry. Lastly, the subjective signs of anæmia will render the diagnosis comparatively easy, especially when the hum in the veins coexists.

Aortic disease usually occurs in those who have passed middle life as a rule, and in men, while young females are the chief subjects of anæmic murmurs.

4. Thoracic aneurism may produce murmurs resembling those of aortic stenosis. The dilating impulse on palpation, the normal force of the heart-beat, the single or double bruit, the pain,--all these symptoms of thoracic aneurism are absent when aortic stenosis alone is present. Moreover, the history of the case will greatly aid in the diagnosis; and, lastly, aneurismal murmurs have their maximum intensity at the seat of the tumor, and not at the base of the heart.

5. A murmur from a scabrous state of the arch of the aorta is exceedingly {659} rare. It is located higher up than that of aortic stenosis, is not transmitted into the cervical vessels, and has its maximum intensity over the transverse portion of the arch.

Aortic Insufficiency, or Regurgitation.

Aortic insufficiency is an abnormal condition of the aortic valves which prevents their complete closure and allows a backward current of blood to flow from the aorta into the left ventricle during the diastole. This lesion is rarely found unassociated with aortic stenosis, and together they constitute one of the most important and frequent valvular lesions. It is sometimes called aortic incompetence, aortic inadequacy, and aortic reflux.

MORBID ANATOMY.--In a normal heart at diastole the aortic semi-lunar valves are firmly closed, so as to completely fill the orifice between the left ventricle and the aorta. In aortic insufficiency the valves are prevented from performing their normal function, on account of the following anatomical changes. As a result of interstitial endocarditis the valves may have been thickened, puckered, and shortened, so that they do not meet when brought into the plane of the orifice.

When the central portion of the segment is indurated, the whole valve subsequently curls up, either toward the orifice or back against the wall of the aorta, and in either case there is insufficiency of the valves. In the first case there is insufficiency with great obstruction; in the second, with but very slight obstruction.

These processes of thickening and shortening are usually the result of the train of changes which attend and follow endocardial inflammation, but they may also come as the result of an atheromatous process extending from the aorta to the valves; and it may be mentioned here that the atheromatous changes, by impairing the elasticity of the aortic walls, become a source of imperfect coronary circulation, and hence prepare the heart for that dilatation whose other causes will subsequently be described.

Regurgitation may result not so much from shortening as from adhesion of the valve-tips to the walls of the aorta. There may be depression of the valves which comes from over-extension, and then extreme insufficiency will be the result. When this pathological lesion occurs, usually only one segment is involved. Complete retroversion of the valves is a questionable lesion; still, it may occur. Again, one or more segments may be more or less detached from their points of insertion, or from the same causes a valvular aneurism or a diseased valve may be torn or ruptured, and then perforation allows a free opening for the regurgitant passage of the blood.

After extensive obstruction has existed for a long time little tunnels may form by the side of the valves and permit a regurgitant current from the aorta to the ventricle. The aortic valves are more liable to laceration than any other valves. Not infrequently the ragged edge of a lacerated or displaced aortic valve is found covered with fibrinous efflorescences of larger or smaller size.

During a cardiac diastole, normally, the blood is passing from the auricle into an empty ventricle; when, however, regurgitation has persisted for a considerable time, there will be added to the primary stream (which of itself is capable of filling the cavity of the ventricle) a regurgitant stream from the aorta, and by this combination of two streams the left ventricle becomes over-distended and permanently dilated. This dilatation occurs all the more readily since during the diastole the ventricular walls are relaxed and less capable of resisting the increased blood-pressure. Thus, permanent dilatation of the left ventricle occurs in a comparatively short time; and to overcome {660} the dilatation and the obstruction to the cardiac circulation the left ventricular walls hypertrophy. The hypertrophy goes on increasing until it compensates for the dilatation; but before this point is reached the ventricular cavity sometimes becomes very much dilated and the left heart reaches an immense size.

This dilatation and hypertrophy may be so extensive that the organ often weighs twenty or thirty ounces, a case being recorded where the enormous weight of forty-eight ounces was reached.[8] The heart is then frequently called the cor bovinum. In such cases the organ has a peculiar pointed form, the right ventricle appearing like a mere appendix. The left ventricle is thus capable of containing so much blood, and such an abnormally large amount is thrown into the aorta at each cardiac cycle, that the arterial system is largely over-filled. Hence the arteries are elongated during their pulsations more than in health, and often become distinctly flexuous with each cardiac pulsation.

[Footnote 8: See Hilton Fagge, _Diseases of the Valves of the Heart_.]

The increase in the ventricular power and in the amount of blood contained in the ventricles and thrown against the aortic walls leads to endarteritis and subsequent atheromatous degeneration of the arterial walls, and the arteries become so brittle that during excitement they may suddenly rupture and cerebral apoplexy result; aneurism is also liable to be developed under such conditions.

In the normal heart the aortic recoil is the force which propels the blood into the coronary arteries. When the aortic valves are insufficient, and furnish little or no resistance to the return blood-current, the coronary blood-supply is consequently diminished. When perfect compensation has existed for some time, it begins to fail, and dilatation again commences at the expense of the walls of the heart. This dilatation is aided, first, by the condition of the coronary arteries above referred to, and, secondly, by the fact that aortic recoil is now expended as much in driving a regurgitant current into the ventricle as in forcing blood through the coronary vessels.

In some cases atrophy of the papillary muscles allows the mitral flaps to swing back into the left auricle when increased pressure is exerted upon them. When from any one of these causes mitral incompetence becomes secondary to, and coexistent with, aortic insufficiency, all the signs of impeded venous circulation will be present. These changes will be considered under the head of Mitral Disease.

When over-distension of the left ventricle causes incomplete emptying of the left auricle, a greater or less amount of passive hyperæmia of the lungs may be present without mitral insufficiency.

ETIOLOGY.--The etiology of aortic insufficiency is similar to that of aortic stenosis. Rheumatic endocarditis is undoubtedly its most frequent cause, but it may also have its origin in sudden and violent muscular effort, atheroma of the aorta, endarteritis, congenital malformation, and enlargement of the aortic orifice. Congenital malformation or congenital non-development is, according to Virchow, a frequent cause in chlorotic females.

In many cases the atheroma that causes the incompetence is of gouty origin, especially when gouty kidneys coexist or when alcoholismus is associated with a gouty diathesis.

Sometimes aortic incompetence is the result of imperfect development of the aortic valves. A rare case is recorded in the _Pathological Transactions_ (vol. xvi. p. 77), where a young man fell from a height upon his side and tore off an entire flap of the semi-lunar valve: there was no external mark of injury, and the rupture was plainly due to the transmission of rapid vibrations from the jarred surface. Valvular inadequacy sometimes results from dilatation of the aorta at its origin.

{661} There can be little doubt but that the interstitial inflammation which gives rise to the valvular changes which allow aortic regurgitation is often excited by the violence with which the aortic valves are closed by the backward rush of blood on the aortic recoil during prolonged and violent physical exertion.

Thus, although rheumatism plays a very important part in its development, it is so far from being its sole cause that C. Hilton Fagge says that in at least half the cases of this form of valvular disease met with in London hospitals one fails to elicit a rheumatic history.

SYMPTOMS.--Rational Signs.--So long as hypertrophy of the left ventricle compensates for its dilatation, the individual will suffer little or no inconvenience, even though the regurgitation is extensive. When the regurgitant stream is a very small one there will also be little or no disturbance of the general health.

But the compensation is only maintained for a short time. When the equilibrium is lost the eccentric hypertrophy induces excessive heart-action during mental excitement or violent muscular effort. The action of the heart then becomes labored, and the patient becomes anxious, nervous, and fretful. Sufferers from aortic regurgitation are generally aware that exercise will augment all their uncomfortable symptoms. Their respirations are accelerated by moderate exercise, and are accompanied by cardiac palpitation. As the insufficiency increases attacks of headache and vertigo become more and more prolonged and severe; the patient complains of muscæ volitantes, dyspnoea, giddiness, and is compelled to sleep with his head elevated. Palpitation is now a constant symptom, and a visible carotid impulse is persistently present.

A comparatively frequent symptom of aortic regurgitation is a distinctly paroxysmal shooting or stabbing pain over the heart, in the left shoulder, or extending down the left arm. Sometimes this pain is accompanied by numbness and a peculiar whiteness of the skin along the line of the pain. In other cases the pain passes from the middle of the sternum to the right arm. This pain is increased by mental excitement and muscular exertion, and sometimes by over-distension of the stomach. In a few cases patients will complain of a sickening fluttering of the heart.

When the nutrition of the hypertrophied ventricular walls becomes markedly interfered with, or when insufficiency of the mitral valves occurs, the veins of the systemic circulation become overloaded, as is evidenced by cyanosis and dropsy; the dropsy appears first as oedema of the feet, and gradually extends upward until a condition of general anasarca is reached. The cyanosis is increased after slight exertion, and is accompanied by dyspnoea, carotid pulsation, and puffiness of the face.

In the advanced stages of the disease there is orthopnoea, sudden starting in sleep, angina pectoris, and in some cases albuminuria and enlargement and tenderness of the liver. Attacks of syncope at first occur only after active muscular exercise, but later they occur independently of it, and are extremely distressing. These patients are in danger of death at any moment, either during a state of the utmost calm or the most intense excitement; the danger is greater, however, during exertion.

The pulse is the most characteristic subjective symptom of this form of valvular lesion. It was first accurately described by Sir Dominick Corrigan,[9] and it is frequently called Corrigan's pulse. He especially said that the disease was indicated by visible pulsation of the vessels of the head, neck, and upper extremities. On account of the elongation of the arteries during their pulsation, and their becoming distinctly flexuous, the pulse is frequently called the locomotive pulse. It is large and distinct, rapidly projected against the finger, and just as quickly the arterial tension sinks to its minimum and the {662} impulse vanishes. It is sometimes accompanied by a vibrating jar, on account of which it is called the water-hammer, jerking, splashing, or collapsing pulse. Its characteristics are more apparent when the arm is raised above the head. Although slightly infrequent, quick, and jerking, it is always regular in rhythm; the radial impulse is felt a little after the apex-beat. Thus the pulse-wave of aortic regurgitation travels slowly along the arteries. This delay in the pulse is constant.

[Footnote 9: _Edin. Med. and Surq. Journ._, April, 1832.]

As soon as the systemic circulation is overloaded from insufficiency of the heart or from secondary mitral insufficiency, the pulse becomes feeble and irregular upon the slightest exertion, and may intermit, but it is still of the same peculiar jerking character. The sphygmographic tracings of this pulse show a high upstroke and absence of the dicrotic wave.

This vibrating pulse or pulse of unfilled arteries is usually possessed of fulness of volume, but when obstruction coexists it may be small and flickering unless the arteries are calcified or atheromatous. The pulse of aortic insufficiency taken by the sphygmograph resembles strongly the pouls des vieillards, but the senile pulse gives a rounded instead of a pointed summit. Still, in old age the two tracings may be indistinguishable.[10] The peculiar crochet or beak is noticeable in graphic tracings of the pulse of aortic inadequacy.

[Footnote 10: Marey, _Phys. Méd. de Circ. du Sang_, Paris, 1863.]

Stokes has described, under the designation of steel-hammer pulse, a peculiar and characteristic pulsation of the arteries which occurs in cases of acute rheumatic arthritis supervening upon chronic inadequacy of the aortic valves. The pulse is abrupt and energetic, as the rebound of a smith's hammer from the anvil; it is exhibited, however, only in the arteries adjacent to the affected joints.[11]

[Footnote 11: _Continued Fever_, 1874, p. 244.]

PHYSICAL SIGNS.--Inspection.--There is an increase in the area of the apex-beat, which is plainly more forcible and is visible over a wider area than in aortic obstruction. After compensation has ceased to balance the forces in the heart the apex-beat becomes more and more feeble and diffused. One of the most important points obtained by inspection is pulsation of the carotids and the vessels of the upper extremities. Becker and Quincke have observed pulsation of the retinal vessels in cases of extensive aortic regurgitation.[12]

[Footnote 12: _London Ophth. Hosp. Rep._, Feb., 1873.]

Palpation.--On placing the hand over the præcordial region a heaving, lifting impulse will be perceived, which is transmitted over a large portion of the thoracic walls. The apex-beat is displaced downward and toward the left, sometimes as far as the eighth rib and two and a half inches to the left of the left nipple. Occasionally a continuous diastolic thrill, equally intense during the whole of the diastole, is felt over the sternum, most distinctly at the site of the aortic valves. In some cases there is a slight pulsation in the scrobiculus cordis.

{663} Percussion.--The area of percussion dulness corresponds to the extent of the cardiac enlargement. Deep dulness is elicited below and to the left of the normal area, and its outline has more of an oval contour than in health. So soon as the cardiac dilatation exceeds the hypertrophy, the area of dulness will extend horizontally rather than vertically, and it may be carried slightly upward, the apex beating in the axillary space. The area of dulness may extend six and a half inches from right to left, and from the upper edge of the third rib to the line of the liver dulness. The superficial area of dulness is likewise increased horizontally and toward the left.

Auscultation.--Aortic regurgitation is characterized by a diastolic murmur, which may take the place of, or immediately follow, the second sound of the heart. It is very distinct at any point over the base of the heart, but usually has its maximum intensity either at the sternal end of the second right costal cartilage, in the second right intercostal space, or at the sternal junction of the third rib on the left side. It is transmitted over the sternum, and sometimes will be loudest at the xiphoid cartilage, and is thence transmitted in the direction of the apex. Its area of diffusion is greater than that of any other cardiac murmur: it is not only conducted down the sternum to the xiphoid cartilage and to the apex, but it may be heard at the sides of the chest along the spinal column, and sometimes faintly in the ascending and transverse portions of the arch, in the carotids, and in rare instances as far as the radial arteries. The murmur of aortic reflux is accompanying rather than substitutive, for the pulmonic second sound is audible at the right base.

Foster[13] regards incompetency of the posterior segment of the valve as producing a murmur which is conducted to the apex, whereas inadequacy of either or both of the anterior segments is accompanied by a murmur which is conducted to the ensiform cartilage. This point has a practical bearing on account of the relationship of the anterior segments of the valve to the coronary arteries. If the murmur indicates a lesion of the posterior flap of the valve, the prognosis will be better. When the second sound of the heart is distinct the murmur immediately follows it. Many English writers call the murmur a post-diastolic aortic murmur.

[Footnote 13: _Med. Times and Gaz._, 1873, vol. ii. p. 658 _et seq._]

Although having the greatest area of diffusion, aortic reflux has not the loudest murmur; it is soft, blowing, sometimes rough, and frequently musical. It is loudest at the beginning of diastole, gradually decreasing in intensity, although it may preserve its rushing, blowing character during all the diastole.

An aortic regurgitant murmur may temporarily disappear if a plug of fibrin closes the orifice, or if the walls of the left ventricle are the seat of extensive fatty degeneration, the aorta being rigid and inelastic.[14] When aortic stenosis coexists there will be a double murmur, audible over a very large space, having its maximum intensity at the right edge of the sternum in the second interspace.

[Footnote 14: _Brit. Med. Journ._, 30th March, 1882.]

Systolic and diastolic murmurs, though sometimes separated by a well-defined pause, may run into each other. If mitral regurgitation occurs with aortic regurgitation, each murmur retains its own location of maximum intensity. In rare instances, when two segments of the valve are healthy, a clear aortic second sound is heard, which is preceded by a faint reflux murmur. Such a murmur is said to be prediastolic in rhythm. Aortic reflux murmurs are often very indistinct, and can only be heard when the patient is in the recumbent posture. There is no necessary connection between the amount of reflux and the loudness of the murmur.

A diastolic murmur heard at or below the level of the aortic valves, chiefly {664} audible in the line of the sternum, indicates considerable aortic incompetence. If a diastolic murmur is inaudible in the carotids, it is usually preceded by a systolic murmur, which has its maximum intensity at the aortic valves or in the so-called aortic area: such a murmur indicates comparatively trifling incompetence with considerable obstruction, probably produced by calcified semi-lunar valves.

If a diastolic murmur is distinctly audible in the carotid arteries, it is invariably preceded by a loud systolic murmur in them, the systolic portion of the murmur not being very plainly audible in the aortic nor in any part of the cardiac area: this indicates very considerable incompetence with comparatively trifling obstruction.

DIFFERENTIAL DIAGNOSIS.--The diagnosis of aortic regurgitation is generally not difficult, as it rests almost exclusively upon the existence or nonexistence of a diastolic murmur. It may, however, be mistaken for aortic stenosis, for mitral obstruction, for pericarditis localized over the aorta, for aneurism of the aorta, for aneurism of the aorta immediately above the valves, patency of the ductus arteriosus, for insufficiency of the pulmonic semi-lunar valves, and, occasionally, for a rough and inelastic condition of the ascending aorta.

1st. Mitral obstruction gives a presystolic murmur, while aortic reflux produces a diastolic murmur. Mitral stenosis is accompanied by no hypertrophy or dilatation of the left ventricle, whereas these conditions are always present with aortic reflux. The quality of a presystolic mitral murmur is harsh and rough, and it has a churning, blubbering, or grinding character, while aortic reflux has a murmur of low pitch and of a soft, blowing, or musical character. Mitral stenosis is accompanied by a purring thrill which is absent in aortic regurgitation. The murmur of mitral stenosis is the longest of all the cardiac murmurs. The murmur of mitral stenosis is never heard behind, whereas that of aortic regurgitation is often heard at the sides of the chest and along the spinal column. Finally, mitral stenosis is attended by well-marked pulmonary symptoms during active physical exertion, which are rarely present in aortic insufficiency.

2d. A pericardial friction sound over the aorta has its maximum intensity over the seat of its production, and is usually audible during both the cardiac systole and diastole. In aortic regurgitation the character of the pulse, the existence of hypertrophy and dilatation of the left ventricle, and the carotid pulsation will establish the diagnosis.

3d. An aneurism at the sinuses of Valsalva is diagnosticated by the history of the case, the presence of the murmur over the pulmonary artery, the evidences of arterial degeneration, the absence of left ventricular dilatation and hypertrophy, and the peculiar jerking pulse. An aneurismal murmur is circumscribed, has a booming quality, and is usually systolic in rhythm and never transmitted to the apex of the heart.

4th. Patency of the ductus arteriosus is a rare condition: in a case where this was diagnosticated[15] the murmur was audible at the left of the sternum, was not everywhere continuous with the second sound, was only transmitted very feebly to the left, and had a wavy character, sufficient of itself to distinguish it from an aortic regurgitant murmur.

[Footnote 15: _Guy's Hosp. Rep._, Ser. 3, vol. xviii., 1872-73.]

5th. Insufficiency of the pulmonic semi-lunar valves is the rarest of all valvular lesions: the murmur should be diastolic, having its maximum intensity in the second intercostal space of the left side; it should be transmitted only downward and toward the right apex; and should not be attended by arterial pulsation, a jerking pulse, or by left ventricular hypertrophy and dilatation.

6th. A diastolic murmur in the ascending arch, due to roughening, rigidity, {665} and dilatation of the artery, is also rare, while the condition which some say can produce it is very common.

Two cases are recorded in which the diagnosis rested upon the character of the pulse, throbbing of the arteries, and the absence of hypertrophy and dilatation of the left ventricle.[16]

[Footnote 16: Bellingham _Dis. of Heart_, 1857, p. 152; also _Trans. Path. Society_, vol. iii., March, 1868, p. 3, article by Prof. Law.]

Mitral Stenosis.

Stenosis, or obstruction of the auriculo-ventricular opening of the left heart, is due partially to constriction at the base of the mitral valves, and partially to adhesions of the valve-tips or chordæ tendineæ. It usually occurs as a consequence of rheumatic endocarditis, rarely of atheromatous degeneration, and is most likely to occur in endocarditis affecting young persons.

Mitral disease is present in one-half the cases of valvular diseases of the heart. Usually, insufficiency and stenosis of the mitral orifice occur together, and stenosis probably never occurs without some insufficiency.

MORBID ANATOMY.--As a result of acute exudative or interstitial endocarditis, the valves are rendered shorter and narrower, as well as thicker and more cartilaginous, than normal. These rigid valvular projections not only obstruct the flow of blood from the auricle to the ventricle, but allow of its regurgitation from the ventricle into the auricle. In mitral stenosis there is not only thickening and contraction of the valves, but the valve-tips or the chordæ tendineæ become adherent, and sometimes each papillary muscle gives rise to a corrugated, cylindrical mass pierced with one or more slits, indicating the chordæ of which it was originally made up. The wall of the valve, especially toward its free edge, is greatly thickened, and these thickened portions are so dense that they have a distinctly cartilaginous feel. On the valvular flaps that have undergone this sclerotic change calcareous masses are very frequently developed, and are especially liable to form when a gouty diathesis exists.

When the chordæ tendineæ and papillary muscles have become adherent, the edges of the valves are drawn down toward the apex of the heart; and since the flaps are adherent for a greater or less distance upward from their bases, the valve presents a funnel-shaped appearance with its base looking toward the auricle and its apex toward the ventricle, whose smaller opening, rarely circular, usually resembles a slit with its axis in the line which unites the original segments of the valve. This button-hole slit may scarcely admit the tip of the little finger, while the normal mitral orifice permits the easy introduction of three fingers.

Annular (ring-like) stenosis is far more common at the mitral than at the aortic orifice. Hard, wart-like vegetations frequently develop on the puckered and seamed flaps, which increase the already existing obstruction. Sometimes the funnel-shaped appearance is wanting, and the flaps are stretched horizontally across, with a small opening in the centre, like a diaphragm: looked at it from the auricle, this slit is often crescentic in shape.

In cases of long standing the vegetations may become calcified. If the new tissue in the diseased valves undergoes fatty change and softens, ulcerative processes are set up and the chordæ tendineæ may rupture. On the floor of such ulcers calcareous masses and débris are frequently found.

Hayden thinks that "all funnel-shaped mitral stenosis is the result of primary acute inflammation and thickening of the valve-segments, with cohesion of their adjacent edges." Out of 62 cases of mitral stenosis, 59 assumed the button-hole form, and 3 only the funnel-shape (Fagge and Hayden).

{666} In rare instances the tendons will adhere to the wall of the heart as well as become matted together. Adjacent to the valves the endocardium will usually be found slightly thickened.

The following changes are developed in the heart and vessels as the result of mitral stenosis: The left ventricle becomes smaller, and sometimes its walls are thinner than normal. The aorta is also small and thin-walled. An almost necessary result of mitral stenosis is dilatation, with subsequent hypertrophy of the left auricle. Sometimes the auricular cavity is enormously dilated--so much so that fifty years ago Thurman described it as true aneurism of the left auricle.[17] Not infrequently the left auricular walls are from one-eighth to one-fourth of an inch in thickness. Its appendix is elongated, assuming a peculiar curved form, the aperture between it and the auricle becoming wider than normal. Moxon records a case of extensive mitral stenosis where the appendix was two and three-quarter inches long.

[Footnote 17: _Med.-Chir. Trans._, vol. iii., Ser. 2, p. 244.]

As soon as the auricular hypertrophy ceases to be compensatory and dilatation begins, the pulmonary circulation becomes obstructed, causing increased tension in and distension of the pulmonary vessels. The walls of the pulmonary vessels, especially those of the main trunk, are thickened and hypertrophied; in rare cases they have been found twice the thickness of those of the aorta.

Although mitral stenosis is a disease of youth, and atheroma one of old age, yet it not infrequently happens that even before the age of puberty atheromatous degeneration occurs in the pulmonary vessels, especially in the small branches, as a result of the increased blood-tension in the pulmonary system.[18]

[Footnote 18: _Trans. Path. Society_, vol. xvii. p. 90.]

The passive pulmonary hyperæmia which results from the obstructed pulmonary circulation may lead to those changes which collectively constitute brown induration of the lung. Another occasional occurrence, directly due to extensive mitral stenosis, is nodular hemorrhagic infarction. Hemorrhagic infarction of the lungs is in nearly every case preceded by thrombosis of the right side of the heart.

In some instances the enormously dilated left auricle may, by pressing on a bronchus, reduce its calibre one-half, and thus interfere with the functional activity of the left lung. When the pulmonary hyperæmia is extensive violent physical exertion or violent coughing may cause a rupture of one of the larger pulmonary vessels, and true pulmonary apoplexy result.

Bronchorrhoeal expectoration of large quantities of glairy mucus is a very frequent result of the intense hyperæmia of the mucous membrane of the bronchial tubes which sometimes occurs in mitral stenosis. The secretion is increased with every increase in the passive hyperæmia. The lungs are at all times so liable to congestion and oedema that any sudden or violent exercise may lead to a rapidly fatal result. Again, when the conditions enumerated have existed for some time, mitral stenosis may lead to hypertrophy of the right heart. In some rare cases the tricuspid orifice has become slightly insufficient.

ETIOLOGY.--Mitral disease is especially met with in the young, and in the child it is almost invariably a stenosis. The average age is about thirty-one; it is very rare to find it occurring after the fiftieth year of life. It seems from statistics that it is nearly twice as frequent in females as in males.

It is not infrequently of congenital origin. Acute rheumatic endocarditis is its most frequent cause. The mitral valves are more frequently affected in chorea than the aortic. In some few instances stenosis results from extension of the inflammatory process from the aortic semi-lunar valves, or prolonged aortic regurgitation and stenosis may lead mechanically to mitral disease, but not to stenosis. Niemeyer regards atheroma as an exceptional cause of mitral stenosis. No other authority regards it as a possible cause.

{667} It is a question whether scarlatina or diphtheria tends to produce in children a valvular endocarditis which is followed by mitral stenosis. It seems plausible, since in many young children it is certain that mitral stenosis has not resulted from either rheumatism or chorea. Finally, with the exception of atheroma, all the causes enumerated in the etiology of aortic stenosis may be the cause of mitral stenosis.

SYMPTOMS.--Rational Signs.--The subjective cardiac symptoms of mitral stenosis are few. There may be no such symptoms. Usually, after violent exercise there is more or less cardiac palpitation, but this will cease as soon as the auricle can relieve itself, which is readily accomplished by the patient's assuming a recumbent position on the right side with the head slightly elevated. This class of patients as a rule are pale and anæmic. There is a sharp pain frequently felt in the region of the apex, which is always suggestive of mitral stenosis. The pulse is regular and normal in character so long as the auricular hypertrophy compensates for the auricular dilatation.

When the ventricle is unable to receive and discharge its normal quantity of blood with normal regularity, the pulse becomes small in volume, feeble in force, rapid and irregular in rhythm. The sphygmograph exhibits a tracing, frequently called the mitral pulse; the sphygmograph tracing is the same as when the ventricle throws a greatly diminished blood-current into the aorta (Fig. 44). This is asystolism, and the pulse is a clear indication of the condition.

Balfour differs from other authorities in the statement that among the most remarkable subsidiary phenomena of mitral stenosis is irregularity of cardiac rhythm, which, always present in a greater or less degree, is sometimes a diagnostic phenomenon. The auricular systole commences earlier than normal on account of its hypertrophy. This premature contraction of the auricle, stimulating ventricular contraction, is indicated by a second ventricular systole which is much less forcible than the first.

The passive pulmonary hyperæmia attending the advanced stages of this form of cardiac disease causes habitual dyspnoea, which is exaggerated by physical exertion and is attended by a dry, hacking, teasing cough which resembles the so-called nervous cough.

After violent or prolonged exertion there may be bronchorrhoea, a pint of glairy, watery mucus often being expectorated in a few moments. Not infrequently severe exercise induces attacks of profuse, watery, blood-stained expectoration, indicative of pulmonary congestion and oedema. Sometimes the exertion of walking rapidly against a strong wind will induce such intense congestion and oedema of the lungs in one with extensive mitral stenosis as to cause sudden death.

Hæmoptysis is not infrequent, small quantities of pure florid blood being expectorated.

Orthopnoea is not a frequent symptom of mitral stenosis, for even in extensive and long-standing cases the pulmonary congestion is not constant, as the auricle is able ordinarily to empty itself, and only becomes engorged during active physical exertion or great mental excitement.

It should be mentioned here that the old idea, that "mitral stenosis sometimes produces hypertrophy of the left ventricle," is fallacious. In no instance can it be attributable to mitral stenosis.

{668} Physical Signs.--Inspection.--As the left ventricle does not receive its normal quantity of blood, the cardiac impulse is feeble. Sometimes it has a visible undulating movement.

Palpation.--On palpation, although the apex-beat is less forcible than normal, a distinct purring thrill will be communicated to the hand: this thrill is a constant attendant of mitral stenosis, and may be regarded as its diagnostic sign. It should be remembered, however, that a purring thrill does not always indicate mitral stenosis. It is most distinct at the apex-beat, although it may be diffused over the whole præcordial space. It either continues through the entire diastole or is only present just before the systole. It is sometimes called a presystolic thrill. It ceases with the apex-beat. The only conditions besides mitral stenosis which will cause a purring thrill at the cardiac apex are mitral regurgitation, with extensive dilatation of the left ventricle, and left ventricular aneurism; in both instances the thrill will not be presystolic, but systolic.

Percussion.--The increased size of the left auricle may cause an increase in the area of cardiac dulness upward and to the left at the inner part of the second left interspace. This increased area of dulness will only be recognized on careful percussion during expiration.

Auscultation.--Mitral stenosis is characterized by a loud churning, grinding, or blubbering presystolic murmur; this murmur is of longer duration than any other cardiac murmur, on account of the time required for the blood to pass through the narrowed and obstructed orifice. It ends with the commencement of the first sound and the apex-beat, being synchronous with the purring thrill. The murmur is heard with its maximum intensity a little above the apex-beat.

Cryan records a case where the murmur was absent, but the diagnosis of mitral stenosis was made from the other symptoms. At the autopsy the orifice would barely admit the tip of the little finger, and the absence of the murmur was accounted for by the smallness of the aperture.[19]

[Footnote 19: _Trans. Path. Society_, Dublin, Part 2, vol. iv., 1870.]

As a rule, mitral stenosis is accompanied by the loudest as well as the longest cardiac murmur. The murmur is always louder when the patient is erect than when in the recumbent posture. For a few days before death, and at any time when there is great constitutional debility, the murmur may be held in abeyance. A presystolic murmur is never present when auriculo-ventricular narrowing does not exist. When this lesion does exist it is never permanently, and very seldom temporarily, absent. A prolonged murmur and a sharp first sound indicate a funnel-shaped stenosis. A murmur immediately following the second sound, and running through the apex-beat, indicates great contraction of the orifice--diaphragmatic contraction. The murmur of mitral stenosis is very rarely, if ever, conveyed to the left of the apex-beat, and it is rarely heard more than two inches to the right of the apex. The second sound of the heart is intensified over the pulmonary valves. When mitral reflux and mitral obstruction coexist, the two murmurs run into each other, constituting a single murmur that may be mistaken for a systolic murmur. The harsh character of the presystolic element of the murmur can always be recognized.

A mitral obstructive murmur is never soft or musical, but there is a rare form of presystolic mitral which is so short as to resemble a tone. A mitral stenotic murmur does not often merge into the first sound of the heart, but is usually separated from it by a short interval. Sometimes a stenotic murmur only becomes audible when the patient sits up. In about one-third of all cases of stenosis of the mitral orifice the second sound is reduplicated. It is best heard at the apex and when the heart's action is slow. The reduplication may be temporarily absent. Pulmonary congestion efficiently accounts for {669} this reduplication. Geigel ascribes it to "non-coincidence in the closure of the valves." Guttman regards it as originating at the stenotic orifice itself. Balfour thinks that thrill and reduplication of the second sound are sufficient to make a diagnosis in the absence of murmur. Some regard the length of the pause between the murmur and the first sound as a measure of the stenosis--the shorter the pause, the greater the stenosis.

DIFFERENTIAL DIAGNOSIS.--The diagnosis of mitral stenosis is not difficult; it mainly depends upon the existence of two physical signs--the purring thrill and a loud, long, blubbering presystolic murmur.

Mitral obstruction may be mistaken for the murmur of aortic regurgitation (see page 657), for a pericardial friction located over the apex, for a prolonged systolic murmur replacing the first sound at the apex, and for a prediastolic basic murmur transmitted to the apex.

1. To diagnosticate between local pericarditis and mitral stenosis, the same methods are employed and the same rules are to be observed as were mentioned in the diagnosis between aortic reflux and local pericarditis (p. 664).

2. A prolonged systolic apexial murmur, enduring as it does for the period of the first sound, that of the short pause, and reaching the second sound, is often accompanied by a muffled second sound readily mistaken for the first. The diagnosis of this murmur rests upon its soft and blowing character, the synchronism of the murmur with the systolic impulse and carotid pulsation, and the fact that there is no murmur with the second sound at the base.

A prediastolic murmur is distinguished from a mitral stenotic murmur by its progressively diminishing intensity from the base to the apex, by its being accompanied by hypertrophy of the left ventricle, and by a jerking, irregular pulse. The preceding tracings explain themselves.

Mitral Regurgitation.

Regurgitation at the mitral orifice is due to a condition of the mitral valves which allows the blood to flow back from the left ventricle into the left auricle. The backward effects of mitral reflux are more varied than those of any other valvular lesion.

It is a common form of valvular disease, and in the majority of cases is the result of acute exudative or interstitial endocarditis.

MORBID ANATOMY.--The most common lesions which give rise to mitral regurgitation are thickening, induration, and shortening of the mitral valves. In rare instances it may occur independent of valvular disease from displacement of one or more of the segments of the valve, the result of changes in the papillary muscles, chordæ tendineæ, or the ventricular walls. It may also occur in extreme anæmia, or from relaxation of the papillary muscles and dilatation of the left ventricle, without a corresponding elongation of the papillary muscles, and from rupture of the chordæ tendineæ. In most instances, however, the valves are shortened, thickened, and indurated.

In some instances lime salts and large masses of chalky matter are found {670} imbedded in the indurated valves. In such cases the surface and edges of the valves are so rough and jagged that more or less obstruction accompanies the regurgitation.

All these changes, except calcification, may also occur in the chordæ tendineæ and columnæ carneæ. The valves may also become adherent to the walls of the ventricles, or as a result of the shrinking and shortening of the chordæ tendineæ the valve-flaps may not pass back to the plane of the orifice.

Again, the valves or the chordæ tendineæ may be ruptured, so that the valves are pressed during the cardiac systole back into the auricle. If the chordæ tendineæ which are inserted nearest the centre of the valve become lengthened, that part of the flap will be bent upon itself, having evidently yielded to the blood-pressure, and this allows of regurgitation. Sometimes, when the valves appear perfectly healthy, by the application of the water test they will be found to be insufficient.

The first effect of mitral regurgitation is dilatation of the left auricle, due to the pressure of the two blood-currents during its diastole--one from the lungs, and the other from the left ventricle. This dilatation leads to thickening and hypertrophy of the left auricular walls. Following this, the pulmonary circulation is impeded, the pulmonary vessels enlarge, and they may undergo degeneration as a result of the continued regurgitant pressure.

Passive congestion of the lungs with brown or pigment induration is an early pathological sequel of mitral regurgitation. The constant interference with the return circulation from the lungs obstructs more or less the outward current of blood to the lungs from the right ventricle. As the obstruction is a gradual one, the right ventricle becomes so hypertrophied as to overcome it. Consequently, the hypertrophied right ventricle compensates at first for the mitral regurgitation, and as long as the right ventricle is able to fully overcome the abnormal pressure of the blood in the lungs from the mitral regurgitation, so long the patients are comfortable. Sooner or later, however, the compensatory hypertrophy of the right ventricle ceases, and a secondary dilatation occurs which admits of no compensation.

This final dilatation of the right ventricle is favored by the myocardial degeneration, which occurs as a result of defective nutrition of the heart-walls; when this condition is reached the veins throughout the body are placed in a similar condition to those in the lungs.

This general venous congestion is indicated by passive hyperæmia of the abdominal viscera and by cyanosis of the surface during active physical exercise.

The liver is the organ first affected, on account of its great vascularity and from the fact that the hepatic veins do not collapse readily and possess no valves. Thus the liver becomes enlarged and stony (the nutmeg liver) as a result of the obstruction to the emptying of the hepatic vein, and when there is coexistent obstruction of the bile-ducts jaundice will be present.

This portal obstruction induces passive hyperæmia of the intestines and stomach, enlargement of the spleen, and large and painful hemorrhoidal tumors. The impediment to the return of blood from the brain causes cerebral congestion; from the kidney, renal congestion; and, finally, the obstruction to the systemic venous return leads to the accumulation of fluid in the areolar tissue and in the cavities. This dropsy generally begins in the feet and extends upward. In females the obstruction in the vena cava inferior induces derangements of the menstrual functions. Ascites, hydrothorax, hydro-pericardium, and pulmonary oedema may subsequently develop.

In addition to these changes, the dilated and hypertrophied left auricle throws an abnormal quantity of blood with abnormal force into the left ventricle during its diastole, which leads to dilatation of its cavity and necessitates a compensatory hypertrophy of the left ventricular walls. This {671} hypertrophy of the left ventricle increases the force of the reflux current, so that during excitement and active physical exertion pulmonary congestion, oedema, and cerebral apoplexy are liable to occur. In many cases of mitral regurgitation, when the venous engorgement is excessive, general dropsy is favored by the anæmia produced by the obstruction of the thoracic duct.

Friedreich maintains that the augmented tension in the venous system causes an increased resistance in the systemic arteries, which leads to left ventricular hypertrophy.

ETIOLOGY.--Mitral regurgitation may occur at any age; it is especially liable to follow rheumatic endocarditis in the young.

Acute exudative and interstitial endocarditis of rheumatic origin is the primary cause of most of the changes which lead to mitral insufficiency. These changes cause the extensive retractions and thickenings which are present in most cases.

It may occur in conditions of extreme anæmia or where there is degeneration of the walls of the left ventricle.

It is not infrequently secondary to changes at the aortic orifice, produced either by an extension of endocarditis from the aortic to the mitral valves and their appendages, or by the secondary mitral valvulitis excited by regurgitant blood-currents from the aorta.

Mitral insufficiency may also be the result of the enlargement of the left auriculo-ventricular orifice which accompanies excessive dilatation of the left ventricle.

Disease of the columnæ carneæ and chordæ tendineæ, when their structures are so weakened as to allow the flaps of the valve to pass back of the plane of the orifice, will also cause mitral insufficiency.

Ulcerative endocarditis may cause it, either by perforation and rupture of the valves or by rupture of the chordæ tendineæ.

SYMPTOMS.--During the early stage of mitral insufficiency, when the hypertrophy of the right ventricle compensates for the regurgitation, there are no rational symptoms which would lead one to suspect its existence; but when the right ventricle is unable to overcome the obstruction to the pulmonary circulation caused by the regurgitant blood-current, there will be more or less dyspnoea, accompanied by a short, hacking cough, with an abundant expectoration of frothy serum. Sometimes the watery expectoration is blood-stained.

Frequently, the blood-stained expectoration is accompanied by free hæmoptysis, although it should be remembered that profuse hæmoptysis is far more frequent with stenosis than with regurgitation at the mitral orifice. But a cough and watery expectoration with occasional dark blood-stains are usually present as an advanced symptom of mitral regurgitation. Active physical exertion increases the dyspnoea and causes cardiac palpitation.

In advanced cases the extremities, face, and lips become blue, the result of the interference with the capillary circulation, and the liver becomes enlarged and hardened--conditions easily recognized by palpation and percussion.

The patient will complain of a sense of weight and fulness in the right hypochondrium, and there will be anorexia, nausea, and a sense of oppression in the epigastrium. Sometimes the hepatic circulation becomes so obstructed that the biliary secretion is interfered with, and jaundice will be added to the cyanotic discoloration, which gives to the surface a peculiar greenish hue.

Following the hepatic derangement are frequent attacks of gastric and intestinal catarrh and evidences of embarrassed renal circulation.

The urine is diminished in quantity, high-colored, and loaded with lithates. Sometimes albumen and fibrinous or blood casts are found in it.

{672} Headache, dizziness, vertigo, stupor, somnolence, and sometimes a peculiar form of delirium of short duration, result from the passive cerebral hyperæmia induced by obstruction in the superior vena cava.

A late symptom of mitral regurgitation is dropsy, which results both from impaired general nutrition and the abnormal blood-pressure in the venous system, both together causing an exudation of the watery portion of the blood through the walls of the vessels. Dropsy, from mechanical causes having their seat in the heart, first appears in the lower extremities, the ankles becoming oedematous, and thence may extend over the whole body. For this condition to be reached it may require several years or only a few months, depending upon the general condition of the patient and the amount of the reflux. With the general anasarca the dyspnoea becomes extreme; the serous cavities of the body as well as the lungs become oedematous; erythema may occur in the region of the groins, the skin exhibiting a tendency to diffuse gangrene.

Late in the disease pulmonary hemorrhagic infarction may occur as a result of metastasis, and this, in the vast majority of cases, lights up a rapidly fatal pneumonia.

All these changes, however grave and urgent they may be, are gradual in their development, so that the condition of the patient is not so insufferable as its description would lead one to suppose.

The pulse of mitral regurgitation is at first in no respect characteristic. It remains regular in force and rhythm, but later it becomes somewhat diminished in force and volume, irregular in its rhythm, and increased in frequency, but never jerking in character. This tracing illustrates my meaning. While it remains full it is feeble and always compressible. When the heart's action is excited, it has a certain tremulousness: these last-named characteristics are to be regarded more as the result of the failure of the left ventricle than of changes in the valvular insufficiency. If a mitral regurgitant pulse has any distinctive peculiarity, it is its diminution in volume.

Coincident mitral or aortic stenosis may render the pulse regular even in extensive mitral regurgitation.

Physical Signs.--Inspection.--The area of visible cardiac impulse extends over an abnormal space, and is more or less distinct according as the right ventricular hypertrophy is moderate or extensive. Sometimes the thoracic wall is seen to rise and fall with each cardiac cycle, and not infrequently the epigastrium exhibits slight pulsation corresponding in rhythm with the heart-beats.

The epigastric pulsation is due to the right ventricular hypertrophy always found with extensive mitral regurgitation.

Skoda, Bamberger, and Leyden record a few instances in which inspection revealed a double impulse accompanying, with more or less regularity, each cardiac systole. This double impulse only occurs in aggravated cases of {673} mitral insufficiency, and arises from non-coincidence of contraction of the two ventricles.

The jugular veins appear swollen, and this is always most conspicuous when the patient is lying down.

Palpation.--The apex-beat is displaced to the left. When hypertrophy predominates over dilatation, the apex-beat is felt lower than normal. When the dilatation exceeds the hypertrophy, the apex-beat is carried outward and often slightly upward. The impulse is diffused and more or less forcible according as the right or left ventricular hypertrophy predominates. This systolic frémissement is most noticeable when the base of the heart lies close to the chest-wall from retraction of the margin of the left lung.

Purring tremor, systolic in rhythm, felt most intensely at the apex and becoming feebler the farther the hand is removed from that part, either to the right or upward, is invariably due to mitral reflux.

Hayden says that it is exceptional to have a purring thrill with simple mitral reflux. I have never found it except in those cases where left ventricular dilatation greatly exceeded the hypertrophy.

Percussion.--Percussion reveals an increase in the area of cardiac dulness, especially laterally; it extends both to the left and right of the normal line, as well as downward. The area of superficial as well as deep-seated dulness will be increased laterally and downward.

Auscultation.--Mitral insufficiency is attended by a systolic murmur which either completely or partially replaces the first sound of the heart. The quality of the murmur is variable, and not in itself as distinctive as that of mitral stenosis. It is usually a soft and blowing bellows murmur; sometimes, toward its end, the murmur will assume a distinctly musical character.

While the first sound of the heart may be heard distinctly in the early stages of mitral reflux, later the murmur in nearly all cases takes the place of the heart-sounds. Hence many English writers rightly denominate this murmur as post-systolic rather than systolic in its nascent stages. It is heard with its maximum intensity at the apex-beat. Its area of diffusion is to the left on a line corresponding to the apex-beat. It is audible at or near the inferior angle of the left scapula. It can be heard between the lower border of the fifth and the upper border of the eighth vertebra, at the left of the spine, with nearly the same intensity as at the apex. The murmur may be absent from the latter situation until cardiac hypertrophy is developed.

The second sound of the heart over the pulmonary valves is accentuated, while below the junction of the third rib with the sternum on the left side both heart-sounds are feeble. Skoda first drew attention to exaggeration of the second pulmonary arterial sound as a positive and unerring indication of mitral regurgitation.

An intensified pulmonary second sound requires a strong right ventricle and an intact tricuspid valve, and is not always present. In general terms, the area of diffusion of a mitral regurgitant murmur is toward the left of the apex-beat. Whatever may be its character, the murmur is generally loudest at its commencement. A loud systolic murmur at the apex, and not heard at the back, is probably not produced by mitral reflux.

As at the aortic orifice, so at the mitral, stenosis and regurgitation are apt to occur in the same individual, giving rise to a combined presystolic and systolic murmur, which is a continuous murmur that begins shortly after the second sound of the heart and often continues until the second sound commences. The two sounds, although mingling to form one murmur, can, in the majority of cases, be readily distinguished from each other, for the point of maximum intensity and the very limited area of diffusion of a presystolic murmur readily distinguish it from a mitral systolic which is audible in the left scapular region. It is important to recognize the existence of both these {674} murmurs in estimating the prognosis in any case. Guttman mentions a case where five distinct murmurs were combined and yet clearly distinguishable.

DIFFERENTIAL DIAGNOSIS.--It is usually not difficult to recognize mitral regurgitation. The seat and rhythm of the murmur and its area of diffusion are sufficient to distinguish it from other cardiac murmurs. The character of the pulse, the symptoms referable to the right heart, and the pulmonary complications will also assist in its diagnosis.

It may, however, be mistaken for aortic obstruction, since both give rise to a systolic murmur, for tricuspid regurgitation, for fibroid disease of the heart, and for roughening of the ventricular surface of the mitral valve or of the ventricular wall near the aortic orifice.

The diagnosis between mitral regurgitation and aortic stenosis has already been given (see page 657).

Mitral and tricuspid insufficiency both produce a systolic murmur, but a mitral regurgitant murmur has its maximum of intensity at the apex, and is conveyed toward the left axillary and scapular regions, while the maximum intensity of a tricuspid regurgitant murmur is to the right of the base of the xiphoid cartilage, and it is transmitted upward and to the right: the area of transmission establishes the diagnosis.

Pulmonary symptoms are prominent in mitral reflux, and absent in tricuspid regurgitation. The pulmonary second sound is markedly enfeebled in tricuspid regurgitation, and markedly intensified in mitral regurgitation.

Fibroid disease of the heart may produce a systolic apex murmur, but it is an exceedingly rare disease, a pathological curiosity.[20]

[Footnote 20: In the _Pathological Transactions_ (1874, vol. xxv. p. 64) Fagge records a few cases, and mentions that perhaps one positive indication of fibroid disease of the heart, rather than of a valvular lesion, may be found in its resisting treatment with greater obstinacy.]

Roughening of the ventricular wall gives rise to a murmur which has its maximum intensity at the base of the heart, and is transmitted along the aortic arch and into the vessels which spring from it in the thorax.

The vibration of an irregular chordæ tendineæ stretched across the aortic orifice, its extremities being inserted into opposite walls of the ventricle, may produce a systolic musical murmur, but the line of its transmission will correspond to that of an aortic obstruction. A systolic mitral murmur due to the sudden rupture of one or a number of the valve-flaps, of the papillary muscles or tendons, is accompanied by a loud systolic blowing murmur, which is immediately accompanied by all the urgent symptoms of acute pulmonary congestion.

Pulmonary Obstruction.

On account of the infrequency of disease of the pulmonic valves very little is known of the phenomena to which such diseases may give rise. In fact, they are so rare that there is no written history of their subjective symptoms; their diagnosis is only arrived at by exclusion, and they cannot be recognized except by the physical signs which attend them.

As has been already stated, endocarditis in the right heart is rare, except in intra-uterine life, and the various conditions of the aorta, atheroma, aortitis, etc., which I have mentioned in the etiology of aortic valvular disease have no analogues in the pulmonary vessels.

Usually, valvular disease of the right heart is the sequela of lesions in the left. It must be remembered, however, that the pulmonary artery may become atheromatous. I have already shown (see p. 666) how certain valvular diseases of the left heart may induce such a pathological condition. But even under such conditions disease of the pulmonary valves is rare. Balfour {675} believes that constriction of the pulmonary artery may occur at various periods of intra-uterine life. As a rule, the pulmonary valves are subject to no lesions except congenital malformation.

MORBID ANATOMY.--Bertin records an instance of pulmonary obstruction where the valves, distorted and adherent, formed a horizontal septum across the orifice, it being barely one-fourth of an inch.

A rigid tricuspid valve has been found to be the cause of obstruction at the pulmonary orifice, the pulmonary valves themselves being normal. A few autopsies have revealed obstructions at the pulmonary artery, caused not so much by valvular defect as by aneurisms, tumors of the pericardium or of the anterior mediastinum, enlarged bronchial glands, or pressure of a solidified lung.

The pulmonary artery may be occluded just beyond the valves by a cancerous tumor, and there are examples where a phthisical process in the left lung has induced it.

A murmur indicative of pulmonary obstruction may be produced by a cardiac thrombosis.

I have placed these statements under the head of its morbid anatomy for the reason that they cannot be appreciated and their pathological significance realized during life.

Reasoning from analogy, obstruction at the pulmonary orifice ought to be followed by compensatory hypertrophy of the right ventricle and accompanied by tricuspid regurgitation and dilatation of the right auricle.

Ormerod records 3 cases[21] where pulmonary obstruction was diagnosticated during life, and where the post-mortem proved the accuracy of the diagnosis: 2 of these cases occurred in men under twenty-eight, and the other in a woman of twenty-one. In 2 of these cases all the other cardiac valves were healthy. The pulmonic orifice would barely admit the introduction of a goosequill. Warburton Bigbie mentions a case (man æt. eighteen) where reflux and stenosis at the pulmonary orifice coexisted. There were four valves, and these were incompetent. All the other valves were normal.

[Footnote 21: _Edin. Med. and Surg. Journ._]

Congenital stenosis of the infundibulum of the right ventricle is the probable result of foetal myocarditis or of syphilis.

I have never met but two pulmonic obstructive murmurs where subsequent autopsies were obtained. In both cases it was found that the murmur had been produced by mediastinal tumors pressing on the pulmonic artery so as to diminish the calibre.

ETIOLOGY.--Pulmonary stenosis is rarely the result of endocarditis or of degenerative changes in the pulmonary artery. Bertin states that when abnormal communication between the two sides of the heart has existed, the arterial blood has excited endocarditis in the right heart.

Syphilis has been advanced as a possible cause of degenerations at the pulmonic orifice.

SYMPTOMS.--The only rational symptoms that have been noted in the few recorded cases of pulmonic disease admit of manifold explanations, and no one is either constant or diagnostic. In some cases anæmia existed, in others there were cardiac palpitation, dyspnoea, cyanosis, and dropsy; but none of these belong exclusively to a pulmonic lesion nor do they necessarily depend upon it.

Physical Signs.--Inspection, palpation, and percussion give negative rather than positive results. In a few instances palpation may give a systolic thrill confined to the second left intercostal articulation. Such a frémissement results both from roughness and contraction of the pulmonic orifice.

Auscultation.--A systolic murmur is heard with its maximum intensity directly over the pulmonic valves; it is very superficial, and consequently {676} very distinct, and it is limited in its diffusion. It is never heard at the xiphoid cartilage nor along the course of the aorta. If it has an area of diffusion, it is toward the left shoulder. The murmur is loud and soft in character, sometimes bellows. It is not audible in the vessels of the neck nor is it attended by arterial pulsation.

When phthisical consolidation partially occludes the pulmonary artery, a loud but soft systolic murmur is heard, which is sometimes high-pitched and musical, and often entirely suspended during a full inspiration. In some few instances there is a bruit de diable in the jugular veins.

DIFFERENTIAL DIAGNOSIS.--It is possible to confound a pulmonic obstructive murmur with a mitral regurgitation which is propagated upward into the left auricular appendix. But the area of a mitral regurgitant is also backward, and by this it could be distinguished from a pulmonic obstruction. Besides, in mitral disease the pulse is very different from the pulse of pulmonary stenosis.

Aortic stenosis can hardly be mistaken for pulmonary obstruction, for the arterial pulsation, the peculiar pulse, and the transmission of the murmur into the arteries of the neck will suffice to discriminate between them.

An aneurism at the sinus of Valsalva may produce a systolic pulmonary murmur by the pressure which it produces upon the pulmonary artery. It would be impossible to distinguish it from a pulmonic stenosis.

The diagnosis of pulmonary obstruction is usually reached only by exclusion.

Pulmonary Regurgitation.

This form of valvular lesion is exceedingly rare; indeed, many doubt its occurrence. The lesion seldom occurs except as the result of injury or congenital defect, and there are but few well-authenticated cases in medical literature.[22]

[Footnote 22: _Path. Trans._, vol. xvi. p. 74.]

The statement[23] that the pulmonary valves exhibit a cribriform condition nearly as often as the aortic is not sustained in this country by the results of post-mortems. In one of the cases to which I have referred (p. 675) as an example of pulmonary stenosis the valves were likewise found insufficient. In Bigbie's case (referred to on p. 675), where there were four flaps to the valve (producing obstruction), there was marked insufficiency coexisting.

[Footnote 23: _Dis. of the Heart_, Bellingham.]

The morbid anatomy, etiology, and rational symptoms do not require a separate consideration. The anatomical appearances are the same as those found in similar conditions of the aortic valves, and the etiology and rational symptoms are the same as those of pulmonic stenosis.

Physical Signs.--Theoretically, pulmonic regurgitation should be accompanied by a diastolic murmur having its maximum intensity over the pulmonic valves, and its area of diffusion should be downward and toward the xiphoid cartilage. It should be soft and blowing in character. This murmur is rarely heard alone: it is usually associated with obstruction at the same orifice or with some murmur whose origin is on the left side of the heart.

Niemeyer states that dyspnoea, hemorrhagic infarction, and consumption of the lungs have followed insufficiency at the pulmonary orifice. No other authority mentions any such symptoms, while the assignment of valvular disease as a cause of phthisis is not based upon clinical facts.

With a pulmonic regurgitant murmur there should be on palpation and percussion physical evidences of hypertrophy and dilatation of the right heart, the rationale of whose production would be identical with that which was considered in aortic regurgitation. I have never heard a regurgitant pulmonic murmur.

{677} DIFFERENTIAL DIAGNOSIS.--The murmur of pulmonary regurgitation may be mistaken for that of aortic regurgitation. The points in connection with their differentiation are fully discussed on p. 664.

The PROGNOSIS and TREATMENT are identical with those of the former lesion.

Tricuspid Stenosis.

This valvular lesion is so rare that there are no established rules for its diagnosis.

Its MORBID APPEARANCES and ETIOLOGY are the same as those of pulmonic stenosis.

The SYMPTOMS of tricuspid stenosis would be those due to obstruction to the entire venous circulation. The right auricle would be dilated, and there would be visceral enlargements in the abdomen, cyanosis of the face and extremities, scanty and albuminous urine, hemorrhoidal tumors, headache, dizziness and vertigo due to passive cerebral hyperæmia, and finally general anasarca. The few recorded cases were associated with mitral stenosis with one exception, a case of Bertin's.[24]

[Footnote 24: _Traité des Maladies du Coeur_, Obs. 17.]

In a case exhibited by Quain the tricuspid flaps, thick and opaque, were united for one-third of their extent. In the other cases the valve-flaps formed a diaphragm whose central opening varied in size, admitting only the point of one finger. In every condition of tricuspid stenosis the heart was enlarged.

Tricuspid stenosis (as in pulmonic stenosis) may be the result of pressure of tumors.

In all well-authenticated cases the chief symptoms seem to be extreme lividity, palpitation, and dyspnoea.

Physical Signs.--Inspection reveals general cyanosis. The jugulars are turgescent and exhibit presystolic pulsation. This pulsation is sometimes the only inconvenience the patient suffers.

Palpation may discover a venous thrill at the base of the neck.

Percussion may show the right auricle to be greatly enlarged, and cardiac dulness will be increased laterally and toward the right.

Auscultation.--Tricuspid stenosis should be attended by a presystolic murmur whose maximum intensity would be at the lower portion of the sternum just above the xiphoid cartilage. This murmur may be propagated faintly toward the base, but never toward the apex of the heart. It is sometimes accompanied by fremitus.

Hayden offers the following diagnostic point: The murmur of mitral stenosis (without which tricuspid stenosis never occurs) is limited to the apex region; a murmur of the same rhythm is produced at the sternum by tricuspid stenosis, "and between these two localities there is a point where no murmur can be heard."

It is unnecessary to consider its differential diagnosis.

The lesion would be diagnosticated (if at all) by exclusion, and prognosis and treatment would depend on the gravity and sequelæ of the accompanying condition--viz. Mitral Stenosis (q. v.), for the rule is, that stenosis of the tricuspid never occurs unless there is extensive mitral obstruction, and the latter condition is always the predominant one.

Tricuspid Regurgitation.

Regurgitation at the tricuspid orifice is generally secondary to mitral stenosis or regurgitation; primary disease of the tricuspid valves, however, is not infrequent.

{678} MORBID ANATOMY.--The valvular lesions which lead to tricuspid insufficiency are similar to those which produce mitral insufficiency. The valves are thickened, shrunken, and opaque, the papillary muscles are shortened, thickened, and the chordæ tendineæ undergo similar changes and are sometimes adherent.

The valves or the chordæ tendineæ and columnæ carneæ may rupture; in either case acute and extensive insufficiency results, as has been stated. Acute endocarditis of the right heart is rare in adult life, but when it occurs the tricuspid valves are its primary and principal seat.

The reason for this is found in their anatomical structure and in the tension to which they are subject in diseases of the mitral valves. They are rarely the seat of rheumatic endocarditis or calcareous degenerations.

Ulcerative endocarditis is seldom met with in the right heart. In a case recorded by Charcot and Vulpian one of the tricuspid valves was softened and perforated, presenting numerous vegetations. Scattered abscesses in the lungs were found in this case.

Any infection through emboli from the tricuspid flaps will produce secondary effects within the thoracic cavity. The first effect of tricuspid regurgitation is dilatation of the right auricle; following this there will be more or less hypertrophy of its walls. As soon as the valves in the subclavian and jugular veins are no longer able to resist the regurgitant current jugular pulsation follows. But before this occurs the tributaries of the inferior cava and the organs to which they are distributed will become greatly engorged, for they have no valves to resist the regurgitant current, as are found in the veins coming from the upper part of the body. The inferior cava and the hepatic veins sometimes become enormously distended under these circumstances, and the liver will show the peculiar section that has gained for it the name of nutmeg liver.

Following the hepatic changes, the skin assumes a dingy yellow hue. When this is combined with cyanosis it produces a peculiar greenish tint which is only met with in heart disease. The spleen enlarges and hardens; the mucous membrane of the stomach is congested, ecchymotic, and often presents numerous hemorrhagic erosions. Intestinal catarrh is subsequently developed, and the general venous congestion within the abdominal cavity is exhibited by hemorrhoids and ascites. The kidneys become congested and stony, and thrombi may form in the femoral vein and induce subsequent pulmonary infarctions.

The stasis in the veins below the diaphragm is accompanied by transudation of serum--first in the ankles, and thence the dropsy progresses upward until the patient may finally reach a condition of general anasarca. The obstruction to the general systemic circulation which results may subject the left ventricle to so much extra labor that it hypertrophies, and then we have the infrequent occurrence of disease of the left heart following that of the right.

Since tricuspid reflux has mitral disease for its principal cause in abnormal cases, the heart becomes greatly enlarged and a condition of extreme cardiac dilatation and hypertrophy is reached.

ETIOLOGY.--As has been stated, the most frequent cause of tricuspid regurgitation is mitral disease, either stenosis or regurgitation. Any condition of the lungs which will produce hypertrophy and dilatation of the right ventricle will lead to it; it is met with in extensive pulmonary emphysema, in cirrhosis of the lung, and in extensive chronic bronchitis. Balfour regards chronic bronchitis as its most frequent cause after mitral stenosis.

It is possible for any valvular disease in the left heart, when of long duration, to lead to tricuspid regurgitation. From all these causes the rationale is {679} the same: the abnormal amount of blood in the right ventricle presses with undue force against a valve, which physiologists regard as normally slightly insufficient; the stress upon the valve-flaps and the valvular attachments is such that endocardial inflammation is excited at the part subject to the greatest strain, and valvular insufficiency is the result.

It is possible for disease of the tricuspid valves to result from any of the causes which have been enumerated on p. 666 as etiological factors in valvular diseases.

SYMPTOMS.--Tricuspid regurgitation being in the majority of cases secondary to some other valvular disease or some chronic pulmonary affection, its symptoms during the early stages are vague and masked by those of the primary disease. But as soon as the valves become so insufficient that the venous return is markedly impeded, a train of symptoms is developed which has its origin in the visceral derangements already referred to.

In addition to these symptoms there may be, with extensive tricuspid regurgitation, cardiac palpitation, cardiac dyspnoea, and marked irregularity in the force and rhythm of the heart. The liver and spleen are enlarged, the skin becomes dingy, and there is obstinate constipation with hemorrhoids. The liver is likewise rendered very liable under such circumstances to attacks of interstitial hepatitis. Venous stasis is evinced by dyspepsia, nausea, vomiting, and hæmatemesis. The secretion of the kidneys is scanty, dark-colored, of high specific gravity, often containing albumen and casts.

Passive cerebral hyperæmia is marked by headache, dizziness, vertigo, and muscæ volitantes, and there is a peculiar mental disturbance which is not met with in any other form of heart disease.

Late in the disease, if the patient is placed in a horizontal position, the face becomes turgid and blue, and if he remain long in the recumbent position stupor and coma may supervene. Jugular and epigastric pulsation are characteristic physical signs.

A very late symptom is dropsy, which begins at the ankles and extends upward until there is general anasarca. It is a point to be noticed that in the dropsy from tricuspid reflux the genital organs suffer slightly if at all.

Physical Signs.--Inspection.--In extensive tricuspid disease the area of the cardiac impulse is increased more than in any other valvular lesion. This area sometimes extends from the nipple to the xiphoid cartilage, and it may reach as high as the second right intercostal space. There is a visible impulse in the jugular veins, more apparent in the right than in the left. Sometimes the veins in the face, arms, and hands, or even the thyroid and mammary veins, are seen to pulsate.

Palpation.--The apex-beat is indistinct, except in cases where there is marked hypertrophy of the left ventricle. Pulsation occurs in the epigastrium, which may be due to reflux into the enlarged hepatic veins or to the fact that the dilated and hypertrophied right ventricle so presses on the liver that the impulse is conveyed through the diaphragm with each cardiac pulsation. Guttman thinks epigastric pulsation is due wholly to reflux into the veins of the liver, and not to right ventricular pulsation.

{680} Early in the disease the impulse in the jugulars is confined to the lower part of the vessels, particularly to the sinus. Beyond this point the vein merely undulates. Later, a systolic pulsation is felt as high up as the angle of the jaw, and may be accompanied by distinct though feeble presystolic pulsation.

The liver may first simply undergo systolic depression, chiefly at the left lobe; secondly, the whole liver may have an impulse coming from an enormously dilated vena cava; and thirdly, the systolic pulsation of the veins within the organ may give to it a palpable expanso-pulsatory movement. The hepatic pulsation is rhythmical with the cardiac impulse. In rare cases it precedes jugular pulsation. Sometimes pulsation is felt in the femoral veins.

Sphygmographic tracings of the jugular pulse show it to be dicrotic.

Percussion shows an increase in the area of cardiac dulness to the right and upward, sometimes as far as the second intercostal space.

Auscultation.--The murmur of tricuspid insufficiency is heard with, or takes the place of, the first sound of the heart; it is superficial, of low pitch, blowing, soft, and faint, and is heard with the greatest intensity over the lower part of the sternum, at its left border, between the fourth and sixth ribs. It is rarely audible above the third rib or to the left of the apex-beat. This murmur is transmitted from the region at the base of the xiphoid cartilage upward and to the right from one to two inches. Sometimes it is heard only over a very limited area, and then it may be overlooked.

DIFFERENTIAL DIAGNOSIS.--A tricuspid regurgitant murmur may be confounded with that due to aortic obstruction, pulmonic obstruction, and mitral regurgitation. A tricuspid regurgitant murmur is never audible above the third rib; is not accompanied by an accentuation of the second sound over the pulmonary artery, but by jugular and epigastric pulsation; and is heard with maximum intensity near the base of the ensiform cartilage. These points are sufficient to differentiate it from an aortic or pulmonary obstructive murmur. The differential diagnosis between it and a mitral regurgitant murmur has been given.

PROGNOSIS IN VALVULAR DISEASES OF THE HEART.--Any statements as to the duration of life in valvular diseases of the heart, and their relative frequency as a cause of death (especially of sudden death), must be based upon personal observation, and necessarily will differ with different observers.

In order to establish, if possible, a basis of comparison for the different valvular lesions, I give a résumé which I have made of 81 cases, in all of which autopsies were made and the diagnosis of valvular disease verified.[25]

[Footnote 25: _Med. Rec. N.Y._, April 1, 1870, p. 66 _et seq._]

In 14 cases of various valvular lesions, each of which was accompanied by cardiac hypertrophy and dilatation, 50 per cent. of the deaths were due directly to the valvular lesion. In 1 of these, where there was stenosis at both auriculo-ventricular orifices, death was sudden.

In 15 cases of valvular disease, in which there was only cardiac hypertrophy, there were 11 deaths from the heart lesion. In 5 of these death occurred suddenly, and these 5 sudden deaths were all directly due to the heart lesion.

In 6 cases of valvular disease accompanied by dilatation alone, 4 deaths resulted directly from the heart lesion, and 2 of these were sudden.

In 15 cases where the aortic valves were involved (either calcified, rigid, or atheromatous) the heart lesion was not the cause of death in any case. Of these 15 cases, sudden death occurred but in 2; in 1 there were firm and long-standing pericardial adhesions, and in the other cerebral apoplexy.

In 12 cases of calcification of the mitral valve, no death occurred as the direct result of the valvular lesion, and there were only 2 sudden deaths, both from cerebral apoplexy.

{681} The aortic and mitral valves were diseased in 14 cases; in 2 of these only did death result from the heart lesion, and the only three sudden deaths in this class were from uræmia, apoplexy, and croupous laryngitis.

The aortic and pulmonic valves were both diseased in 3 cases which died suddenly, and in no instance was death due directly to the heart lesions.

In 2 cases there was disease at the aortic, mitral, and tricuspid orifices, and no sudden death.

Thus it will be seen that of these 81 cases, in 24 only was death due directly to the heart lesion. There were only 8 sudden deaths due directly to the heart lesion.

The results of personal, clinical, and pathological observation lead me to the opinion that the loudness, harshness, and the area of diffusion of any cardiac murmur have little to do with its prognosis.

I deduce from the above-mentioned cases that cardiac murmurs rarely necessitate a bad prognosis unless hypertrophy and dilatation coexist; but so soon as the signs of considerable dilatation and hypertrophy are present a great variety of complications are liable to occur.

In 1870, I had a patient sixty years of age with extensive aortic reflux, who had been under my observation eight years, during which time he had three attacks of pneumonia. There were no appreciable signs of cardiac dilatation in his case.

Walshe says: "The order of relative gravity, as estimated not only by their ultimate lethal tendency, but by the amount of complicated miseries they inflict, is--1, tricuspid regurgitation; 2, mitral obstruction and regurgitation; 3, aortic regurgitation; 4, pulmonic obstruction, 5, aortic obstruction."

The following are conditions which render the prognosis in each valvular lesion more or less unfavorable:

In aortic stenosis the prognosis is less grave than in any other valvular lesion. Life may be prolonged and good health enjoyed for many years. Yet it must be remembered that extensive aortic stenosis rarely exists without attendant regurgitation.

So long as the hypertrophy of the left ventricle compensates for the obstruction, the prognosis is good; but when the hypertrophied walls fail to overcome the obstruction, dilatation begins, and the ventricular systole becomes feeble and intermitting, and the arterial supply to the brain is so much diminished as to lead to cerebral anæmia.

If after sudden exertion or violent muscular effort there is interruption or great irregularity in the heart's action, sudden death may occur from a complete arrest of the ventricular systole.

Evidences of excessive hypertrophy and dilatation, the occurrence of syncope, signs of cerebral anæmia, attacks of vertigo, great muscular prostration, continued and marked paleness of the face, and irregularity of the pulse, render the prognosis exceedingly unfavorable in aortic stenosis.

If the presence of vegetations can be determined, there is danger from cerebral embolism.

When there are no evidences of alterations in the ventricular walls after an aortic obstructive murmur has existed for some time, it may be assumed that no vegetations exist on the valves, and that the murmur is not due to extensive aortic stenosis, and consequently is not dangerous to life.

When the mitral valves become involved, the combined lesions render the prognosis unfavorable.

Death may result from cerebral complications, pulmonary oedema, or cardiac degeneration.

Aortic insufficiency is a much graver form of valvular disease than aortic stenosis. It is difficult to estimate the probable duration of life in aortic {682} insufficiency, for it frequently gives rise to no symptom that would lead to its diagnosis until it is far advanced. Twenty-one days and five years are the extreme limits that have been recorded. It must always be borne in mind in estimating the factors for and against a good prognosis that in no other valvular lesion is sudden death so liable to occur. Yet the record of the cases which I have given (page 680) indicates that mitral stenosis is nearly, if not quite, as frequently a cause of sudden death.

A diseased valve can never be restored to its normal functions, and the shorter and more gushing the murmur the more extensive the regurgitation. The effects of the regurgitation must be carefully estimated before a prognosis can be given in any case. When one aortic flap is puckered and shrunken, the other two may elongate and compensate for the patency. But this occurs only in very young subjects.

Aortic regurgitation is, however, more serious in the very young than in adults. In children the valvular changes are less atrophic and more inflammatory in character.

Where the disease is met with in middle life, in those who daily undergo severe mental or bodily strain, the prognosis is unfavorable. And when in such patients there are the evidences of arterial degeneration or a tendency to it, the dangers are greatly increased, for the hypertrophied ventricle drives out the blood from its dilated cavity with greater than the normal force, and the vessels being weakened there is great danger of their rupture; hence the frequent occurrence of apoplexy and infarctions. In the very old I have seen aortic incompetence last a long time and cause little inconvenience.

Again, the prognosis is bad when cyanosis and dropsy result from the failure of a dilated and hypertrophied left ventricle to empty itself. This weakness is the result of that interference with the coronary circulation which brings about impaired nutrition, and therefore degeneration of the heart-walls.

When mitral insufficiency is secondarily induced, then obstruction to the systemic circulation leads to induration of the liver and kidneys, which interferes with the performance of their functions and hastens the fatal issue.

Sudden rupture of a valve or valvular disease that has developed very rapidly is more dangerous than when the valvular insufficiency is slowly developed. The flap or flaps involved can sometimes be determined during life, and then the prognosis will be more or less favorable according as the anterior or posterior are incompetent. In all cases the prognosis depends more upon the condition of the heart-walls and on the general nutrition than upon any other element.

When aortic regurgitation is complicated by aortic stenosis, mitral regurgitation, or by the vascular and visceral conditions resulting from the derangement of the circulation, the prognosis is exceedingly unfavorable. Death may result from embolism, apoplexy, dropsy, pulmonary oedema, from sudden cardiac insufficiency, or from visceral complications. When the radial impulse is felt a little after the apex-beat, it is always important to determine whether the action of the heart remains regular under mental excitement or violent physical exertion: if it does, the prognosis is far better than when it becomes irregular.

Mitral stenosis admits of but slight compensation; if extensive, it is always a grave disease. The prognosis in any case can be estimated by the severity of the thoracic symptoms. When physical exertion greatly exacerbates the thoracic symptoms, the prognosis is especially bad; for during violent exercise such patients are not only liable to pulmonary congestion and oedema, but to pulmonary infarctions and pulmonary apoplexy with large extravasations.

Where mitral stenosis is extensive it ranks next to aortic regurgitation in its danger of sudden death. The statistics furnished by Bellevue Hospital show sudden death to occur as often in mitral stenosis as in aortic reflux.

{683} Congenital mitral stenosis is not dangerous, and does not cause much embarrassment, for it is invariably associated with hyperplasia of the pulmonary arterial system. The later in life mitral stenosis occurs, the more unfavorable the prognosis.

Mitral regurgitation uncomplicated by any other valvular lesion gives rise to very little disturbance of the systemic or capillary circulation. It is more often fully compensated for than any other valvular lesion. The changes which lead to it are of slow growth and their tendency is to remain stationary. Patients with a moderate regurgitation at the mitral orifice suffer very little except during or after violent physical exercise, and, were it not for the slight dizziness which attends it, it would pass unnoticed. As long as the compensatory hypertrophy of the right ventricle is sufficient to overcome the obstruction to the pulmonary circulation, patients with this form of heart disease may not suffer from dyspnoea even after violent physical exercise. As regards the duration of life, the prognosis in mitral regurgitation is good. When, however, mitral stenosis and regurgitation coexist, the liability to sudden pulmonary complications becomes so great that a very guarded prognosis must be given; and it must be remembered that combined reflux and stenosis at the mitral orifice is a frequent combination.

In very many instances it is unnecessary to tell a patient with mitral reflux that he has an incurable heart disease, for with no other valvular lesion the individual may live to advanced life. But when it is combined with mitral stenosis it must be regarded as a very serious form of valvular lesion. As soon as symptoms occur that show failure of the right heart, the prognosis becomes unfavorable. Oedema of the extremities or fluid in any of the serous cavities, cyanosis, dyspnoea, and hæmoptysis, are indications of such failure.

Death may result from general anasarca, from serous effusions into the pleuræ, peritoneum, or pericardium, from pulmonary oedema and congestion, or from heart-insufficiency.

Extensive obstruction or regurgitation at the pulmonic orifice would necessarily lead to serious results, but there are no reliable data upon which the prognosis can be based.

The prognosis in tricuspid obstruction and regurgitation, when associated with mitral disease, is very grave; but it is not as bad as when it results from chronic bronchitis and pulmonary emphysema.

When in any case jugular and epigastric pulsation are marked, the changes in the various organs of the body already referred to rapidly ensue. Walshe says that "tricuspid regurgitation is the worst of all valvular lesions." Patients with tricuspid reflux are in extreme danger from intercurrent attacks of acute pulmonary hyperæmia.

Tricuspid disease, of all valvular lesions, leads most rapidly to cyanosis and dropsy.

TREATMENT.--The treatment of aortic stenosis and of aortic regurgitation may be summed up under three heads--viz. rest, diet, and regimen.

Rest is most important; it must be mental as well as physical; the appetite, emotions, and passions must be kept under perfect control: these indications are best maintained by a sedentary country life. Straining, especially when the hands are above the head, should be carefully avoided.

The stomach also must have all the rest compatible with the most perfect nutrition; it is frequently a difficult matter to combine both indications, for it should be remembered that the more perfectly the nutritive processes are maintained the longer will the cardiac muscle resist degeneration. Sugar, sweet vegetables, and animal fat must be sparingly indulged in. The food should consist of nitrogenous, albuminoid material, and should be taken in quantities that do not disturb the heart's action.

{684} In aortic incompetence patients in sleeping should assume, as nearly as possible, a horizontal posture. By lying on their backs they lower the height of the distending column of blood, and thus relieve both the cardiac circulation and the tendency to pulmonary congestion. Sometimes, when defective aortic pressure reacts injuriously on both the gastric and hepatic secretions and limits both their supply and their efficiency, moderate alcoholic stimulation may be cautiously employed to tide over a weakly period. The bowels should be gently moved once daily. That the cutaneous circulation may be active the body should be warmly clothed. Any prolonged exposure of the surface to cold is to be avoided. In winter the warm bath may be occasionally used, and in summer the patient is frequently benefited by a warm sea-water bath.

Medicinal agents are not to be resorted to until the cardiac hypertrophy fails to be compensatory. Then relief is demanded for the failing heart-power. In aortic regurgitation with feeble heart-action the tincture of digitalis and the tincture of the perchloride of iron are to be given in ten-minim doses three times a day. The iron is especially indicated whenever anæmia is evidenced. Digitalis is given to produce a sedative action, and therefore should be given in very small doses and regulated according to its effects on each patient. An infusion of the English leaves is the preparation which is most reliable, although the tincture, if fresh and well prepared, is equally good. When rapid and immediate action is demanded, digitalis may be given hypodermically. There is one guide to its use not unimportant to remember: that is, as long as it causes an increase in the flow of the urine it is safe to continue its use. When vertigo and syncope are prominent symptoms quinine and strychnia may be given with the digitalis. When the heart in aortic reflux acts with violence and rapidity, and the arteries are in a state of high tension, aconite will be found of service in quieting the heart's action. In aortic incompetence small doses of arsenic seem to have a stimulating effect, especially when given with digitalis and iron. Iron may disturb the stomach, arsenic seldom if ever does. It is always a safe rule when giving iron to administer at the same time a bitter vegetable infusion, as quassia or columba.

When the hepatic and gastric vessels are engorged, three or four leeches over the liver or epigastrium, followed by a warm fomentation, will afford temporary relief.

At no time should a large quantity of fluid be taken into the stomach. Symptoms of angina pectoris, with local pain and dyspnoea, are evidences of aortitis. This demands the application of leeches over the sternum and continued small doses of mercury.

The treatment of dyspnoea, dropsy, pulmonary oedema, and other late and distressing symptoms will be considered in connection with mitral disease. Sometimes the pain of aortic disease is so severe as to require an anodyne for its relief: opium must not be given by the mouth, but the sulphate or the hydrochlorate of morphine can be safely given hypodermically. The severe angina-like pain of aortic regurgitation can often be promptly relieved by the nitrate of amyl.

Barlowe and Fagge both advise senega and ammonia carbonate for the less severe effects of aortic reflux. They advance no reason for the use of these drugs, but their cases show that they have a markedly beneficial effect. All authorities unite in regarding aortic insufficiency as less amenable to treatment than other valvular lesions.

In all cases the idiosyncrasy of each patient should be carefully considered.

No treatment can restore a diseased valve to its normal condition, or prevent, for any considerable time, cardiac dilatation and hypertrophy when the normal function of the valves is greatly interfered with.

{685} The first step in the treatment of a serious lesion at the mitral valves is to make the patient clearly understand his exact condition, that he may see the reasonableness of the advice given, for his treatment for the most part must be carried on by himself. A patient must be fully persuaded of its necessity before he will regulate his habits and mode of life in accordance with the requirements of his case. The rules as to nutrition are the same as those to be observed in aortic stenosis and reflux. There should be a gentle and regular daily evacuation from the bowels. Straining at stool must be avoided, and any use of alcohol, strong tea, coffee, and tobacco is to be prohibited. If in either form of mitral valvular disease the patient is anæmic, iron should be given. This is given as a food to such patients, and is best administered about half an hour after meal-time. Ten or twenty grains of Vallette's mass may be given with benefit to anæmic patients two or three times a day for a long period.

Patients with mitral reflux should avoid a prolonged use of the voice, especially in speaking or singing. Small doses of quinine and strychnine, alternating with the administration of iron, are often of service. If there is anorexia, infusion of quassia or columba may be given with the iron. The triple phosphates of iron, quinine, and strychnine, or small doses of dilute sulphuric acid, will be found to improve the condition of these patients when they show signs of extreme debility.

In every case of mitral disease there comes a period when the pulmonary hyperæmia shows that the compensation of the right heart has failed. An adjustment of the heart to the circulation is now effected by the judicious administration of digitalis. Digitalis should only be given at those times when the heart-failure is imminent and there is marked pulmonary congestion. Half an ounce of the infusion every two hours for twenty-four or forty-eight hours is often required to overcome the heart-failure. The time will come when digitalis ceases to have its sustaining effect upon the heart-muscle; hence it should always be most sparingly and carefully used, and the patient should never be allowed to use it continually.

When the pulse is rapid, feeble, and irregular, more time is needed for the flow of blood into the ventricle, and greater force and regularity in the ejection of the blood from that ventricle are demanded. Digitalis fulfils all these conditions: the pulse becomes regular, beating about sixty per minute, full and forceful. The urine, before scanty, now becomes abundant and normal. Pulmonary engorgement diminishes, and commencing dropsy gradually but totally disappears.

Hayden advises ten minims of the spirits of chloroform and fifteen minims each of the tincture of digitalis and the tincture of the perchloride of iron in an ounce of water every three hours.

Whenever asystolism is present or suppression of urine is threatened, digitalis should be given whether the other indications are present or not. In most cases of mitral stenosis it is best to avoid the use of digitalis as far as possible.

The dropsy which accompanies advanced mitral regurgitation may be promptly relieved by compound jalap powder, combined with calomel in sufficient quantity to produce prompt and free catharsis. In some cases of cardiac dropsy, squill, juniper, brown cream of tartar, and copaiba act as diuretics. This latter drug is best exhibited in the form of the resin.

In mitral reflux a combination of digitalis and nitrous ether will often be found to act as a diuretic. In all cases when a diuretic is given in heart disease the loins should be cupped or warm poultices applied and the bowels freely purged. In copious hæmoptysis in cardiac disease ergotin may be given in full doses either by the mouth or hypodermically.

The hæmoptysis which accompanies pulmonary apoplexy of heart disease {686} sometimes temporarily relieves the dyspnoea. On this basis Dickenson and Fagge and other English writers recommend venesection for the relief of the pulmonary engorgement or heart-failure. Pain in the præcordial region which accompanies valvular insufficiency may sometimes be relieved by the application of leeches over the præcordial space. Hyoscyamus, hydrochlorate of morphia, nitrate of amyl, chloroform, and a belladonna plaster over the præcordial space have all been employed for the same purpose.

It is to be remembered that such pain is the cry of the heart-muscle for a higher degree of nutrition.

Bleeding in heart disease favors dropsy by thinning the blood and by diminishing the heart-power. It should never be resorted to except in great emergencies. Niemeyer advises arsenic and antimony in mitral valvular disease, but does not say in what cases or for what reason they are to be used. When in the late stages of mitral disease the free use of digitalis fails to regulate the pulse and to relieve the pulmonary engorgement, its prolonged administration does harm rather than good; but in every case of mitral disease where the drug has not been used it may be safely affirmed that its administration will give prompt relief.

If it becomes necessary to use an anodyne or hypnotic at any period in the course of mitral valvular disease, morphia hypodermically is to be preferred to all others.

The rules in regard to hygiene, diet, and exercise which have been given for the management of mitral disease are equally indicated in the management of pulmonary obstruction or regurgitation. Beyond this their treatment is purely symptomatic.

The treatment of tricuspid obstruction depends upon the gravity and sequelæ of the accompanying disease--viz. mitral. Stenosis of the tricuspid orifice never occurs until mitral obstruction is excessive, and the latter condition is always the predominant one.

The same rules of hygiene and diet which have already been given for mitral disease must be followed with the utmost care by those suffering from tricuspid reflux. The patient must lead a life of perfect quiet, and should live in a warm, equable climate. When occurring with mitral disease digitalis should not be omitted; for although the drug, by increasing the action of the heart, would seem to be injurious, yet it promotes ventricular contraction, and thus tends to relieve the tricuspid pressure. In tricuspid insufficiency with pulmonary emphysema this drug should be very cautiously exhibited, and its use or omission must depend upon the effects produced in each case. If the cerebral symptoms are exaggerated, it must be discontinued. The indications for the use of tonics, such as iron, quinine, strychnine, are the same and follow the same demands as in mitral disease. When venous engorgement demands prompt relief, drastic cathartics or the abstraction of a few ounces of blood from the arm will temporarily diminish the high venous tension. The treatment of the dropsy and the local oedema is the same as for similar condition occurring in mitral disease. There are many subsidiary remedies which will have to be employed for the relief of gastric, hepatic, and intestinal symptoms, which are often the most troublesome occurrences of this disease.

{687}

CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.

BY MORRIS LONGSTRETH, M.D.

The questions involved in the subject of the congenital defects of the heart and its great vessels and their causes are not easy of settlement. In the first place, the seat, the extent, and the consequences of the deficiency or defect are not regular or constant. Secondly, the causes and the mode and date of their origin are involved in great obscurity. Their classification either on a purely topographical or on a purely etiological basis is almost impossible on the one hand, because the changes are so irregular and varying, and, on the other hand, because our knowledge of the primary cause or causes of the alterations is quite defective. The views which at the present time find most favor arrange the various malformations into classes according to the period of development of the foetus at which the arrest or change of tissue occurred--as it were, a chronological classification. The ideas in respect to the pathology or the pathological causes of malformed hearts have undergone great changes--changing in some degree pari passu with the mode of classification, and in great degree inducing and compelling such changes.

In early times deformed hearts were looked upon as monsters, curiosities, lusus naturæ. When a knowledge of foetal development and circulation was acquired the deformed heart was compared with the heart-formation in classes of a lower grade than mammals. Such were the beliefs of comparative anatomy and physiology that it was held that the human foetus was matured by stages from the forms found in the lowest invertebrates through the various ascending scales of the animal kingdom. This classification was, on the basis of comparative anatomy, purely anatomical. The underlying thought of such pathological teaching was that in the original ovum something was left out--an actual deficiency of parts which, when developed in the natural manner, made man different from the lower animals; or else, supposing these parts to have been originally present, there was a defect of plasticity, causing a failure of the proper adhesion of symmetrical portions. Excessive development was looked upon as a surplus of parts in the ovum, and by their growth certain of the openings of the heart were prematurely closed. In this view of the pathological alterations no expression of opinion was made how the excess or deficiency of structure was occasioned: the malformation was merely a failure of the parts to rise and pass through the various grades of development--a too rapid or a too slow growth of one or more of the various parts of the foetal heart. There was no reason assigned why the human ovum had in it deficiencies or excesses of material, and thus came to resemble in one of its parts the conditions found in lower animals.

About 1850, Dittrich of Erlangen, by his studies of inflammation of the heart during intra-uterine life, quite diverted public opinion from the older views of the subject. Peacock's earlier studies preceded this work by a few {688} years, and a few years later came Meyer,[1] who greatly extended the scope and influence of the inflammatory theory of Dittrich. Ten years later commenced the clinical recognition of congenital heart defects, and especially the anatomical changes in congenital narrowing of the pulmonary artery, by Von Dusch and by Mannkopff,[2] and by Stoelker.[3] Friedberg had, however, as early as 1844, published his studies of the stages of development of the circulatory organs in the human embryo, and had in accordance therewith divided the malformation of the heart into three groups, corresponding to the three periods of the heart's growth. This was the classification adopted quite independently by Peacock of London in his first publication in 1857. It was not until after Dittrich's studies[4] and Meyer's that any distinctive cause was assigned for the failure to develop.

[Footnote 1: _Virch. Arch._, Bd. xii., 1857.]

[Footnote 2: _Ann. des Charité-Krankenh. zu Berl._, 1863.]

[Footnote 3: _Diss._, Bern, 1865.]

[Footnote 4: See Dorsch's (his student) dissertation, _Die Herzmuskelentzundung als Ursache angeborner Herzcyanose_, Erlangen, 1855.]

Carl Heine,[5] and also Halbertsma, proposed a classification based on the quantitative and qualitative differences. Under the first division the former placed such changes as absence of the heart, deficiency of individual parts, abnormal smallness, atresia, and fissures; and, in the other direction, duplication of the heart as a whole or in its individual parts, and abnormal largeness. The qualitative differences were deviations of form, of position, and of the arrangement of the great vessels.

[Footnote 5: _Angeborene Atresie d. Ostium arteriosum dextrum, Beitrag z. Lehre v. d. angeborenen Herzanomalium_, Tübingen, 1861.]

Peacock's classification in his earlier edition (1858) was partly on the basis of the time at which arrest of development occurs, and partly on the degree of impediment to the circulation and the functions of the heart. In his second edition he adheres to the same classes, with slight modifications, thus: 1. Arrest of development early in foetal life (fourth to sixth week; heart with two or three cavities; single or imperfectly divided arterial trunk); 2. Arrests at a later period (sixth to twelfth week; imperfect auricular or ventricular septa; imperfect or misplaced vessels); 3. Those after the third foetal month (closure and patency of foetal passages; irregularities of valves, cavities, etc.).

Kussmaul (1865) published a very important work on malformations due to defects of the pulmonary artery,[6] and these malformations he considers under two general groups--viz. those having their origin before the ventricular septum closes, and those occurring after this period. His most valuable contribution to the subject is the importance which attaches to the distinction between primary and secondary defects or arrests of development--_i.e._ between an original alteration of growth or morbid condition, and those which follow from it as a necessary consequence. Of his classification, and of the importance of pulmonary artery malformations, a further description will be given.

[Footnote 6: _Ueber angeborene Enge und Verschluss der Lungenarterienbahn_, Freiburg, i. B.]

For study, one would wish to arrange the malformations in classes convenient for clinical purposes. For example, separate them into groups of the defects compatible with extra-uterine existence and those incompatible with adult life. Unfortunately, this division is not possible. We find many cases of defects involving originally the same seat: in one the individual lives many years, in another the obstruction immediately induces symptoms, and death soon comes. A classification according to the seat of the disease alone, if it could be made, would give the subject a simplicity equal to that of valvular heart disease in the adult. Here, however, we find such variations in the details of the alteration that if this principle of classification alone is {689} employed the confusion becomes very great. It would seem, therefore, that the principle first made use of by Kussmaul, of classifying the defects by distinguishing the primary malformations from their secondary effects, renders the subject the most simple, and at the same time affords the advantage of more readily understanding the mechanism of their production.

It will be useful to pass over seriatim, following the course of the foetal circulation, the various valves, orifices, and foetal openings to be able to comprehend which are most liable to defects or to see which defects most frequently occur, and also to find which alterations produce the greatest disturbance of the circulation.

1. The Foramen Ovale and Septum of the Auricles.--In markedly deformed hearts the entire septum may be in greater or less degree wanting, as seen in cases of the bilocular or trilocular organ. This defect is comparatively rare, and the foetus has but a short extra-uterine life. In other cases the septum is complete, but the foramen may be unusually large, and remain unclosed wholly or in part; perforations may be present, or the valve may merely fail to adhere. Of the latter cases, the patent foramen is found in conjunction with defects at other parts, while small sieve-like perforations or the mere non-adherence of the membrane--both of very common occurrence--may be owing to a temporary obstruction during the early hours of life or to any unknown cause, or may possibly be due to a reopening of the foramen from an acquired disturbance of the circulation. Opinions vary as to the mechanism of the closure of the foramen. Some consider it a passive process due to increased blood-pressure in the left auricle, coming from the entrance of the current of aërated blood from the lungs; others speak of it as an active process resulting from the excitation to contraction of the muscular fibres in the membranous valve. Whatever may be the mechanism, patency of the foramen ovale of undoubted foetal origin (excepting the minute perforations and oblique slits) must be looked upon in nearly every case as a secondary defect--secondary to an obstruction to the outflow of blood from the ventricles through the great arterial trunks, or it may be from the auricle itself through defect of the auriculo-ventricular orifice. In a vastly preponderating number of cases it results from pulmonary artery obstruction. The foramen may close, however, in such a case if an outlet is provided by the aorta through an open septum ventriculorum, or when this vessel arises from both ventricles. Narrowing or closure of the right auriculo-ventricular orifice, as a primary cause, can prevent the closure of the foramen ovale; primary narrowing of the tricuspid orifice is very rare, single or combined with other defects. In these cases the direction of the blood is from the right auricle to the left. There are, however, cases on record of patency of the foramen ovale in which the blood-current is from the left to right side, the reverse of the foetal course. Here the cause to be looked to is a congenital deficiency of the mitral orifice, or a narrowing, closure, or malposition of the aorta.

2. The Right Auriculo-ventricular Orifice and Tricuspid Valve.--A primary deficiency of this orifice and the valve guarding it very rarely occurs as a primary defect and uncombined with malformation of other parts of the pulmonary circulation. It does come in certain cases in conjunction with great narrowing of the pulmonary orifice or artery, but by no means commonly. If the pulmonary outlet is normal and in the usual position, the right auriculo-ventricular orifice is never found closed, although the leaflets have been seen defective, permitting regurgitation. In certain other cases the orifice and valve, as well as entire right ventricle, show a failure to develop, and all these parts appear shrivelled. This condition is a secondary result, due to a great deficiency of the pulmonary artery and narrowing of the pulmonary conus. The malformation of the pulmonary artery in such cases results from an unequal division of the truncus communis--the narrowing {690} of the conus generally from endo-myocarditis. The aorta is unusually large in diameter. The blood from the right auricle passes through the foramen ovale to the left side of the heart; the ductus arteriosus Botalli remains open, or in very rare cases the mixed venous blood reaches the lung through collateral channels. In rare cases the blood, in addition to the open foramen ovale, has a direct passage from the right auricle into the left ventricle.

3. The Pulmonary Artery and the Right Conus Arteriosus.--This situation presents by far the largest number of cases of congenital heart malformation of primary occurrence. The defects at this part require different interpretations according as they are found within the right ventricle or in the pulmonary artery itself. So frequent are the defects at these seats that Kussmaul bases his classification, for a large proportion of cases, on the malformation of the pulmonary artery track, and describes them as combined with defects secondarily resulting in other parts.

The narrowing or closure may exist either at the limit between the sinus and the conus of the right ventricle, the conus arteriosus may be uniformly narrowed, or the defective development may involve the orifice only or the whole length of the pulmonary artery. Many of these defects, resulting in closure or narrowing, are due, as Rokitansky was the first to show, to inflammatory changes. It is Kussmaul's great merit to have pointed to the fact that a very large proportion of all malformations owe their origin primarily to diseased conditions originating at this seat. The varieties of these defects and their secondary consequents will be described later.

4. Patency of the Septum Ventriculorum.--The degree of deficiency of the septum varies greatly. The entire partition between the ventricles may be wanting or exist in merely a rudimentary condition. Ordinarily, there is found a triangular, rounded, or oval opening in the septum close to the base of the heart, at the portion which in the normal heart consists of only a membrane (pars membranacea). Besides this usual opening, one, or even two, others may present themselves at other points of the septum, thus forming multiple communications between the cavities. In narrowing or closure of the pulmonary passage the septum is more or less deflected toward the left ventricle to allow a freer passage of blood from the right side of the heart through the open septum into the aorta. In other cases the passage of blood may be from the left ventricle into the right--the reverse of the usual direction. The defects of the septum are usually of a secondary character, dependent on primary malformation of other parts, and, as already said, chiefly those of the pulmonary track. They are of congenital origin, commencing early in foetal life, before the third month, when normally the septum closes. Hence patency of this septum furnishes in many cases a valuable means of determining the date of the primary defects with which it is found combined. This malformation, however, does very rarely stand as an isolated defect, and still more rarely it is believed to have been acquired through an ulcerative destruction (myocarditis) of a portion of the septum, either during foetal or extra-uterine life; wasting or atrophy of the membranous part is sometimes thought to have occurred. In these latter cases a misdirection of the blood-current of a marked sort rarely occurs unless the inflammatory or other changes affect the main arterial orifices.

5. The aortic and mitral orifices are very much less frequently found narrowed or obstructed as the result of congenital primary defects than the orifices and their valvular apparatus of the right heart; and, also following the rule which obtains on the right side, the mitral is less frequently affected than the aortic orifice.

6. Of the Malformations of the Great Vessels.--Such changes may come alone, though usually they are combined with simultaneous or consecutive defects in other parts of the central circulatory apparatus. Of the sorts of {691} defects or malformation which these two vessels suffer, there are two chief forms to be described: 1, such as result from an unequal division of the vessels in their formation from the truncus communis; 2, those which result in more or less complete transposition of their origins. Of the transpositions we may find two sorts: in one the vessels maintain nearly their normal relative positions to each other, but each communicates with the improper ventricle; in the other they are transposed relatively to each other and also to the respective ventricles. In the first of these classes, unequal division, one variety may be ascribed to a defective or irregular development of the septum by which the vessels are formed of unequal sizes; the other, originating later in foetal life--_i.e._ after the third month (for the septum between the vessels is completed nearly simultaneously to the ventricular septum)--results from inflammatory or other morbid change in or about the orifice and trunk of one or other vessel, causing a narrowing or closure, the other vessel showing compensatory enlargement. This form is not a true unequal division of vessels. The apparent origin of one or both vessels from the same ventricle in these cases is not a true example of transposition of the vessel, but is due to a deviation of the septum ventriculorum toward one side or the other from increased blood in the ventricle from which the outflow is more or less completely obstructed. True transpositions of the vessels, both relatively to each other as well as to the ventricles, originate very early in foetal life, and these as well as the unequally-divided vessels are primary defects, and are usually accompanied by many secondary changes. Another malformation occasionally found, involving the beginning portion of the great vessels, is a failure of complete division: the septum truncus communis remains rudimentary, and the blood of the aorta is free to mingle with that in the pulmonary artery. This defect may be accompanied with a rudimentary septum ventriculorum.

7. Ductus Arteriosus Botalli.--This foetal orifice varies greatly in the conditions which are presented; sometimes it is entirely wanting, in others patulous and even in a state of dilatation; in others, again, a short portion is patent (this state is probably comparable to failure to adhere seen in the valve of the foramen ovale or the sieve-like opening in the fossa ovalis; unlike the valve of the foramen, the ductus probably never reopens), or in yet others the ductus is closed in some cases of malformation, and in others of very similar character it remains open. It becomes difficult to explain the varied states of the duct, so dissimilar are they to other defects of development present. In none of the conditions which are presented can the malformations be regarded as of a primary character. Our surprise at certain of its conditions probably must depend on a failure to justly appreciate the primary malformation present, or else on changes in the heart and the circulation coming at a period subsequent to the date of origin of the malformation of the duct itself. When the duct is open at one end and closed at the other, the open part communicates usually with the pulmonary artery, since the closing process commences normally at the aortic extremity: the closure beginning at the pulmonic extremity is occasionally seen in malformations of heart where the blood-current has had a reverse direction through the duct.

The premature closure of the ductus arteriosus Botalli, which is spoken of by some authors, seems to be a rather unfair designation to apply to the condition. In most cases it is in reality an absence of the duct dependent on the defective development of certain of the branchial arches. In other cases the apparent premature closure is due to general uniform narrowing, almost closure, of the pulmonary orifice and vessels; in such cases the lungs are supplied by the enlarged bronchial arteries or other collateral branches. The ductus arteriosus Botalli remains patulous when the pulmonary artery is {692} narrowed or closed; in these cases the blood from the right side of the heart to reach the lungs must pass either through an opening in the septum ventriculorum or through the patent foramen ovale. The duct is generally open in cases of transposition of the main arteries, or even in cases of obstruction of the aortic orifice, or of uniform narrowing of the descending aorta or its main branches. Its usual length and its point of origin from the pulmonary artery or its branches, as well as its junction with the aorta, may vary. Two ducts have been found--one from each pulmonary branch, one of them joining the aorta as usual, the other seeking one of its branches. A distinct duct has been found arising directly from the right ventricle. None of these defects are to be considered as primary malformation, but as the secondary results from alterations of the circulation occasioned by other malformations of the heart or of its great vascular trunks.

* * * * *

Fully bearing in mind the distinction which must be made between primary and secondary defects, and the fact that congenital lesions of the orifices and valves are mostly located on the right side of the heart, let us look at various causes which are capable of producing malformations. In many cases, from the condition of the parts, it is possible to say positively that the alterations are dependent on an inflammatory process commencing in the endo-myocardium at an early period of foetal existence; this is true even after excluding cases in which the inflammatory products present may fairly be considered to be the result of defective development and not its cause. Inflammation was, as has already been shown, long ago pointed out as the cause of these obstructive malformations. Rokitansky (1844) was followed in his views by many, who asserted, probably wrongly, that this condition was the sole cause of the misdirection of development. It was considered that while in very many cases the evidences of the inflammation remained indubitable, in others, through a greater lapse of time, the inflammatory products became less distinct or were wholly removed. Thus, all defects of development may be traced as the results of some obstruction of the pathways of the foetal blood, which, on the one hand, effects the closure of certain vessels or orifices, or on the other hand maintains patent others which normally should be obliterated. It is much easier to trace these causes when they operate during the later periods of development, after the heart and great vessels have assumed the general shape they maintain, than those which operate at the earlier periods of transition. It is plain to us that an obstruction of the pulmonary artery or its branches coming before the end of the third foetal month must, by preventing the flow of blood through it from the right ventricle, maintain an opening of greater or less size in the incomplete septum ventriculorum. It is much less easy--or, in fact, impossible--to be positive about an obstruction or other change which causes the transposition or an unequal division of the great vessels, or which prevents entirely the development of either septum. Nevertheless, we can believe that some obstruction of the foetal circulation causes the former defect as well as the latter, if we may judge of so dark a question by the analogies. In fact, what would present itself as a trifling obstacle in the third or fourth month of foetal life would in the sixth week be an impassable obstruction.

It has been urged against the view that some inflammatory process is the invariable cause of the obstacle, by those who support the development theory, that, as the heart remains in a rudimentary condition, the defects result from a want of formative or plastive activity of the parts. It seems, however, as difficult to account for the want of formative activity which prevents the development of the septum or causes an unequal division of great arterial trunks as to find the traces of an obstruction. Maternal impressions or shocks have doubtless caused many headless {693} foetuses or otherwise misshapen the product of conception during the early months of development. The effect on the foetus from such shocks cannot of course be a direct nervous impression, such as those seen producing local disturbances of nutrition or of formative activity in the adult's own organism, but it is due to disturbances of the placental circulation, by which the blood-current is delayed in the foetal circuit. Such delay may result in a temporary obstruction of the blood in certain foetal vessels. A delay of the blood-current during a few hours in the early period of development of the foetus, when formation is excessively rapid, may result in changes which become permanent. The evidences of such obstruction may fade completely. Osler[7] has recently urged that it is difficult to suppose an endocarditis limited to the pulmonary valves in an embryo not more than an inch in length, and whose heart could not be above a few millimeters in size. But is it not possible to suppose an endocardial inflammation which affects at the same time, for example, the vascular orifices and the line of the rudimentary septum? The septum may thus be prevented from further development, and the orifice suffer malformation by subsequent contraction. The evidences of the inflammation would greatly lessen as the size of the heart expanded. Cannot inflammation, syphilis, or other communicable disease, from which we know the foetus suffers, be substituted for the unknown "want of formative activity"? In respect to the extent of surface involved in the foetal heart in inflammatory or other morbid processes, can we not suppose that the area exhibiting evidences of disease in the minute heart would be as restricted as in the adult heart? In rheumatic endocarditis of the adult the cause which leads to the inflammation is a general one; the evidences we find of the morbid process, however, are confined to very narrow limits. The reasons for this restriction may be the same.

[Footnote 7: _Montreal Gen. Hos. Reps._, vol. ii.]

The simple narrowing of a blood-track where direct evidence is wanting may be explained by the occurrence of a specific morbid process as satisfactorily as by an appeal to lack or excess of formative power. The real difficulty arises in the explanation of cases of transposition of the great vessels. The problem is in every way a most difficult one for solution under any supposition. If it were true that the formation of the pulmonary artery and the aorta was from the start by separate blood-channels, and these distinct vessels suffered a genuine transplantation and became attached to the wrong ventricle, the aorta to the right and the pulmonary to the left ventricle, then undoubtedly we should be compelled to accept the developmental theory as usually expressed. But it is not the case that these vessels are developed in distinct trunks: their development results from the division of a common trunk through an infolding of the walls or the gradual formation of a septum proceeding contemporaneously with the septum of the ventricles, the vessels at the same time making a half turn on their axis. A delay in the formation of either septum may result in the malapposition of the vessels to the ventricles. The septum which is probably delayed in formation is the vascular septum, since it is apparently the growth of this septum that applies the force which results in the axis rotation of the vessels. Are we again to explain the abortive formation of the vascular septum or any portion of the branchial arches by the unknown want of formative power? The want of formative power must have a cause; it does not come spontaneously. Are not inflammatory endarteritis and syphilitic lesions of the blood-channels probable causes of the contraction or obliteration of portions of the branchial arches?

Another question, dark and obscure, requires a short comment. It is commonly accepted, if an abnormal communication (speaking of small openings) exists between the two ventricles, that the septum has been prevented from {694} closing by the blood-current being diverted from its usual course through narrowing of an arterial ostium, and compelled to flow into one or the other ventricle. The patency or the closure of the ventricular septum is held as a criterion of the date of origin of the primary malformation. We know that certain ulcerations of the endo-myocardium may result in forming openings between the two ventricles, but is it not possible that a perforation may be made in the ventricular septum after it has closed by a lesion originating at an arterial ostium of the same character as one that prevented the septum from closing? The muscular tissue of the heart from the third to the sixth foetal month, and even later, is of very soft character. A rapidly-coming closure, or even temporary obstruction, of one or the other great arterial trunks would greatly increase the blood-pressure within the corresponding ventricular cavity. The ventricular septum would become stretched and thin, and might readily be perforated, so delicate is the muscular tissue.

If such a possibility is consummated, it must alter the value which has hitherto been placed on the opening in the ventricular septum as a criterion of the date of origin of the primary lesions of the great vessels which ordinarily are the cause of the patent condition of this partition.

* * * * *

It is to be seen from a review of the recorded cases of malformation of the heart that defects of the arterial outlet of the right ventricle are the primary cause of the largest number of cases. It is impossible to state the proportion of these to those at other orifices or the great vessels, so incomplete are the records and so unlike are the opinions of the reporters. It is but natural that this the more active ventricle of foetal life should exhibit more frequently defects of development, since the left ventricle in adults suffers more commonly in its valvular apparatus during its more active period.

The position at which the defects resulting in obstruction of the blood-current through the pulmonary artery may occur have been mentioned. The degree of the narrowing is of much importance--much more than the seat of the obstruction; but of still greater consequence is the date of origin of the defect of development, since on its occurrence early or late in foetal life depend the condition of the septum ventriculorum and the perfection of secondary compensatory alterations which render the heart capable or incapable of a prolonged extra-uterine life.

Narrowing or closure of the course of the blood passing through the pulmonary artery may be divided into two classes: 1, those cases in which the septum ventriculorum is imperfect to a greater or less degree; and 2, those in which it is fully formed, the separation between the ventricles being complete. The date of their origin corresponds to different periods of the development of the foetus. The earlier the obstruction comes in the normal outlet of the ventricle, the more rudimentary is the ventricular septum. The size of the opening of the septum depends on the degree of narrowing of the pulmonary outlet as well as on the date of origin of the obstruction. If the arteries are transposed in relation to the ventricles, and one of them becomes obstructed, the effect on the septum is the same, although the direction of the current through the opening is reversed. Kussmaul and others have pointed to certain exceptions which may lead to errors. In a congenital opening of the ventricular septum, isolated from other defects, an endocarditis involving the pulmonary orifice may occur subsequent to the time of the usual closure of the septum, or even after birth. It would be difficult to distinguish such a case from one of pulmonary narrowing occurring before the third foetal month. The character of the inflammatory changes and the size of the pulmonary artery beyond the point of narrowing would assist in marking the distinction. It must be remembered, however, that the pulmonary artery is {695} recorded as possessing a large size beyond the seat of narrowing in cases of undoubted congenital origin.

The alteration in the form and size of the right ventricle varies greatly according to the time at which the pulmonary obstruction originates. The ventricle seems to maintain its size, and even to become hypertrophied and dilated, when the pulmonary obstruction occurs before the closure of the septum: if the pulmonary artery is obliterated or exceedingly narrowed at a later period, the ventricle shrivels, because no blood is able to pass, and gradually more and more of the foetal current passes through the foramen ovale to the left side; if, however, the pulmonary defect is but slight, the right ventricle continues its function, becomes hypertrophied, and may dilate. In pulmonary obstruction the right ventricle changes its form somewhat in accordance with the seat of obstruction. Thus the primary obstruction may be in the pulmonary artery or its branches; or in other cases the malformation is found within the cavity of the right ventricle. The last group is spoken of as conus stenosis.

The malformations of the conus of the right ventricle may present themselves under three forms: they all act as constrictions, but alter the shape of the ventricle very variously; their effect on the circulation is practically the same, varying only with the closeness of the constriction. If an inflammatory process occur at the seat of the normal muscular constriction between the sinus and the conus, it may result in fibrous thickening and contraction; thus the normal division of the sinus from the conus becomes exaggerated and permanent. The narrowed portion may continue to exhibit evidences of endocarditis, or these may fade away, leaving a smooth surface. These narrowed parts seem to be especially liable to inflammation at a subsequent period as the bulk of the blood and the force of the circulation increase. Peacock describes a condition of narrowing due to muscular hypertrophy alone. It would seem in these cases that the hypertrophy was, in not a few of the instances, an acquired condition, and not congenital.

These cases present a heart having, as it were, a double or subdivided ventricle, comparable to that of the turtle. The condition has been described by some writers as a supernumerary ventricle. The form and size of the communication between the two portions of the ventricles vary very greatly: in some of the cases due to inflammation the passage merely admits of a large probe, and consists of a firm fibrous ring, or there may be two or more such openings. In constriction by muscular bands the opening is usually a large oval with smooth walls. In these cases the size and the condition of the walls of the so-called supernumerary ventricle present different appearances according to the degree of constriction and the size of the pulmonary opening; it is probable also that the condition of the ventricular septum influences the consecutive alteration in the parts. When the constriction is close and but little blood enters the conus, its walls are thin and flaccid, while in cases of less marked narrowing, provided the pulmonary artery remains nearly normal, the walls of the conus become hypertrophied, in conjunction with a similar development of the other parts of the right ventricle.

In other cases the entire conus may be uniformly narrowed: this change is due almost invariably to inflammatory lesions, and in many instances it is difficult to determine whether the condition is of foetal origin or whether it arose during the early months of extra-uterine life or even at a later period. Its occurrence in conjunction with other malformations would point to its origination during the developmental period. The conus may also present a constriction directly at or just beneath the valvular orifice of the pulmonary artery. This condition is almost invariably combined with some narrowing of the artery itself, and there is so constantly present evidence of inflammation of recent date that it is almost impossible to say whether the defect {696} is not due to a myocarditis originating after the developmental period. With this condition the entire conus usually presents more or less shrinkage or collapse, becoming greater as the constriction at the orifice is more marked. This collapse of the conus is to be looked upon as secondary to the primary defect at the orifice.

Closure or narrowing of the pulmonary artery trunk may be traced to many conditions acting at several different points of the course of the blood. Nearly all these conditions are caused by inflammatory lesions which result in contractions of the arterial walls. In fact, pulmonary artery defects not dependent on inflammatory changes are very obscure and difficult of explanation. In adult life we know of only two conditions which lead to obliterations of vessels; first, inflammation of the lining membrane (endarteritis); and second, stoppage of the blood-current, usually through pressure directly applied to the vascular trunk. The clots of blood which occupy the vessels form both in advance and beyond the point of pressure; hence we can look for obstruction, causing closure of the pulmonary artery, at either extremity of the blood-course. Thus, we may think of a primary conus obstruction which may secondarily have the effect of reducing the size of the pulmonary artery, but it is never obliterated through this means; nearly always some blood passes in this direction, and blood also enters the pulmonary artery from the ductus arteriosus Botalli: both conditions necessarily tend to keep the artery from complete collapse; moreover, the artery, even in cases of very narrow conus, may remain of its usual size. The same effect may be produced by narrowing of the tricuspid orifice. This condition is a very rare one, and never could lead to complete closure of the pulmonary artery unless this orifice were entirely obliterated and the septum of the ventricles remained closed. Peacock speaks of premature occlusion of the ductus arteriosus Botalli as one of the causes of narrowing of the pulmonary artery. The obliteration of this portion of the branchial arches, by preventing the blood flowing in its usual course to the descending aorta, he thinks results in narrowing the calibre of the pulmonary artery. May not the condition be equally well interpreted in a different manner? May not it be that the obstruction of the artery was the cause of collapse of the ductus? One would think it possible, if an obstruction arose in the ductus arteriosus Botalli, for the blood-current in the pulmonary artery to maintain another branchial arch patulous for its accommodation, or, failing this, to dilate the pulmonary branches and thence return to the left side of the heart. In rare cases the pulmonary artery has been found deficient in size when the lungs are malformed, either by reduction in their size as a whole or by the absence of one or more lobes. Such a cause has very little opportunity of acting with much force on the pulmonary artery during foetal life. This cause and all the others in this group are to be looked upon as secondary in their effects.

In primary defects of the pulmonary artery trunk the vast majority afford indubitable evidences of an original inflammatory causation; others are due just as positively to a defective evolution of this vessel from the common arterial trunk. Instances are on record of the complete closure of the pulmonary artery and its conversion into a ligamentous cord: these cases are very rare. In a somewhat larger number a pretty uniform narrowing, sometimes to an extreme degree, and often exhibiting thickened walls, is found. It is much more frequent to see the obstruction of the artery, due to inflammatory changes, at its valvular orifice.

Peacock describes the narrowing at the pulmonary orifice in many cases to be due to disease of the pulmonary valves, whereby the number of cusps are reduced in number, or to a membrane stretched across with small openings in its central portion; or the obstruction may consist of a duplicature of the lining of the vessels, or even to bands of muscular fibres surrounding the {697} orifice. Two valves of unequal size may be found at the orifice, giving evidence that the larger one has been formed by the adhesion of two of the normal cusps; the membranous obstruction is probably due to the union more or less complete of the three cusps. The curtains thus formed protrude into the course of the artery and form a deep circular sinus between the valves and the walls of the vessel. The opening between these adherent valves varies from a transverse slit to a tubular or barrel-shaped orifice--a tube within a tube. These diseased valves are thickened, very firm, fibrous, or even calcified. In other cases the obstruction consists of abundant warty elevations, so numerous that they are equally effective in preventing the passage of blood as the united valves. The size of the opening is sometimes extremely reduced, measuring only five millimeters in diameter. The pulmonary artery is most generally less in size than normal, but never becomes reduced to the same extent as its orifice, unless it has likewise suffered from inflammatory disease; otherwise its walls remain thin, resembling the venæ cavæ.

In addition to disease within the calibre of the vessel, Meyer, who strongly advocated the inflammatory cause for all these defects, pointed to pericarditis, occurring at the origin of the pulmonary artery and compressing the vessel, as a rare method of causation.

In a very large majority of the cases of pulmonary narrowing on record the septum ventriculorum is found to be more or less defective. In accordance with the usual principles, this defect of the septum, in conjunction with narrowing of the pulmonary artery, is held to indicate that the obstruction of the artery dates from a period of development anterior to the closure of the septum. This view was advanced by Hunter in 1783. But Peacock gives an account of many cases of pulmonary narrowing, combined with open septum ventriculorum, in which the obstruction was caused by adhesion of the pulmonary valves. It is, however, a fact that the development of the valvular apparatus is not effected until after the septum of the ventricles is completed. How, then, can we suppose valves to adhere so as to obstruct the pulmonary artery and prevent the closure of the septum when in reality the valves themselves have not developed? Does it not seem possible that in some rare cases the opening found in the septum ventriculorum is in reality a reopening? Another case is on record of open septum ventriculorum and narrowing of the pulmonary orifice in a child born of a mother who suffered a prolonged fright during the fifth month of utero-gestation. Strong mental impressions are accounted causes of malformation of the foetus, and in this case the fright, if it was the origin of the defective development of the septum, came more than two months too late.

In cases of pulmonary narrowing with open septum the aorta communicates freely with the right ventricle, or appears to arise from both ventricles, or more rarely from the right cavity alone (the deficient pulmonary artery remaining in its usual position). Many opinions have been held as to which one of the three defects is primary. Hunter's conclusion has most generally prevailed. The obstruction of the course of the pulmonary artery is looked upon as the primary defect. From the obstruction the right ventricle becomes distended, and the opening of the septum is due to the blood-pressure, which prevents the final closure. The blood-pressure also alters the direction of the septum and pushes it farther to the right. Thus the septum comes to stand directly under the aortic orifice, or by a further deviation to the left side brings that orifice wholly within the right cavity. In these simple cases the origin of the aorta from the right ventricle is not a real but merely an apparent transposition or transplantation of this vessel; the aorta has not been moved, but only the septum has been moved under its orifice, and the right ventricle has consequently become more extensive. In other cases the aorta {698} seems to move more toward the right side, usually coming also more to the front, and in other cases there is an actual transposition of these vessels. The method of this transposition will be further described.

Meckel's original theory for open septum and narrowed pulmonary artery was that the defect was primarily in the septum of the ventricles, due to a want of formative energy, and the pulmonary artery closed itself, as do other arteries, from want of use. Meyer showed that a defect of the septum was incapable of causing narrowing of the pulmonary artery, since the exit of blood is easier through the artery, from the form of the right ventricle, than through the open septum; the passage of the blood from right to left is opposed by the blood-mass in the left cavity. Heine also thought the pulmonary-artery narrowing was a secondary defect, but did not think the opening of the septum caused the narrowing. He considered the primary malformation to be a deviation of the septum to the left. The deviation of the partition before its closure brought the aorta within the left cavity, and furnished a free exit for the blood from this chamber shorter and more convenient than through the pulmonary and the ductus arteriosus Botalli to the descending aorta; the pulmonary artery collapsed for want of use, similarly to other foetal blood-courses. Hence, Heine considered that in all cases of open septum and apparent transposition of the aorta which exhibited no evidences of inflammation as a conjectural cause of narrowing or closure of the pulmonary artery the explanation was to be found in a primary deviation of the septum ventriculorum.

The difficulty in Heine's theory lies in showing the mechanism of a deviation of the septum without a primary obstruction of the flow of blood through the pulmonary artery. The hypertrophy of the right ventricle which Heine proposed as an explanation is almost certainly a secondary effect of the obstruction, and therefore cannot be supposed to originate a deviation of the septum; it is doubtful if hypertrophy can be considered as a cause of increased blood-pressure within the cavity of a ventricle under any circumstances, and certainly not as exercising pressure in a direction to cause the supposed deviation of the septum. An open septum without obstruction of the pulmonary orifice, which rarely occurs, does not produce hypertrophy of the right chamber.

The explanation of cases of open septum with obstruction of the pulmonary artery seems entirely satisfactory by Hunter's theory, or by what Kussmaul has named the engorgement theory. But when there is a real transposition of the arteries, the pulmonary placed farther to the left and behind and coming from the left cavity, the aorta in front and to the right and arising from the right or pulmonary chamber, thus changing their relative positions and their orifices exchanging ventricles, the difficulty of explanation becomes great, and the cause of the abnormal relations of the vessels cannot be traced to a simple deviation of the septum ventriculorum.

For the explanation of these cases of complete transposition of the vessels, as well as their transplantation relatively to the ventricles, Rokitansky has traced respectively the development of the two arterial trunks from the common trunk and of the septum ventriculorum. He considers that the partitioning of the arterial trunks is the governing factor in their formation, and that the ventricular septum is arranged in conformity with the septum of arterial trunks. In tracing the development of the circulatory apparatus in man there seems to be no doubt that the heart develops exactly like that of other vertebrates.

The very first rudiment of the heart is a spindle-shaped thickening of the intestinal fibrous layer of the fore part of the alimentary canal. This spindle-shaped formation then becomes a hollow pouch, and separates from the intestinal layer and lies free in the cardiac cavity. The earliest condition {699} yet seen in the human being is that from an embryo of about two weeks (Coste), in which the viscus appeared as a simple tube in the shape of a letter S--the hollow rounded pouch having slightly elongated and bent to this form, and simultaneously turned spirally on an imaginary axis, so that the posterior part of the tube rested on the dorsal surface of the anterior part. The yelk-veins connect at its posterior part, while the arteries form a continuation of its anterior extremity. The spiral turning and curving increase, and simultaneously two shallow indentations appear in the twisted pouch, transversely to its long axis, looking like kinks in a flexible tube. These indentations mark the outline of the three primitive portions of the central organ--viz. the first, with which the veins communicate, represents the future auricles; the next, the ventricles; the third portion, the common arterial trunk (aortic bulb or truncus arteriosus communis). Early in development the first section is the largest, but by the time the S is formed the middle or ventricular portion exceeds in size the auricles and their appendages. So far, the central organ remains a continuous tube, indented transversely in its course at the points which mark its future division; the blood moves through it as through a coiled tube, entering by the veins and passing out by the aortic bulb to the vascular or branchial arches; the venous entrance is posterior, the arterial exit is anterior and is directed toward the future aortic arch. This is the condition at the end of the second week. The future auricles and ventricles now form a common cavity; the indentation between them, called the auricular canal, represents the future auriculo-ventricular orifice. The future fibrous ring forming this orifice is the first to be developed of all the permanent structures of the heart; its infolding to form the two auriculo-ventricular orifices comes early, but at a later date than here spoken of. Its exact method of development is not clearly described.

Between the second and fourth weeks is exhibited an indication of the future most important step in development; this process does not really step forth until the fourth week, although superficial traces of a furrow antedate this time. This step is the division of three sections of the tube into opposite halves, a right or venous, a left or arterial half. This division results in the formation of the future septa between the auricles and between the ventricles, and separates the common arterial trunk (aortic bulb) into the future aorta and pulmonary artery. This partition is spoken of as longitudinal; but it will be seen, if the real lines of growth of the future auricular and ventricular septa are carefully regarded, that the indentations which mark their site are also transverse, as were the primitive ones for division of the auricles from the ventricles. The proximal end of the tube comes in contact with the distal portion by a further bending movement, so that these two ends go to make the left half of the heart; and the middle portion of tube, composed partly of auricle and partly of ventricle, forms the right half of the heart. This secondary indentation, commonly spoken of as longitudinal, is in reality transverse, although, from the more markedly bent condition of the tube which has come about, it does not advance in the same plane as the primitive indentation of the tube. The mechanism of the division of the aortic bulb will be described later.

This secondary indentation, which finally results in the formation of the auricular and ventricular septa, appears earlier in the ventricular cavity, about the fourth week, and later in the auricles, about the eighth week. By about the twelfth week the process of formation for the muscular partitions is completed; the septum ventriculorum normally is gradually built up, and by this time has joined itself, at the base of the heart, to the septum forming itself in the arterial bulb; thus the right and left ventricles are finally separated. The septum in the auricles is also finished in its muscular part, mostly built up from the base and posteriorly toward the roof of the cavity, {700} leaving, however, the foramen to be closed by the membrane some days after birth.

The foetal heart from the fourth week onward becomes more and more rounded in outline, and finally more or less rectangular. The auricular appendages become conspicuous and overhang the ventricles. The future left ventricle appears larger than the right, and the former projects notably leftward and downward. The aortic bulb or common trunk appears to arise wholly from the right ventricle, although the vessel communicates with both cavities, since at this period the cavities are undivided. The furrow which marks the line of the future septum ventriculorum runs to the left of the root of the common trunk; and until at least as late as the sixth week this trunk appears from the exterior to be in connection only with the future right ventricle.

As early as the sixth week, possibly earlier, a distinct furrow is seen on both sides of the common trunk running longitudinally from its root at the ventricle to its first branch (branchial arch). This indentation does not traverse directly to the ventricular furrow; in fact, at this period the ventricular furrow is not conspicuous at the origin of the trunk toward the base of the heart, the septum within not having risen as yet to the base of the ventricles. During the formation of this furrow the common trunk continues its slow partial rotation on its axis; the rotation of the other parts of the cardiac tube has ceased; the segments of the tube have come to a standstill--become, as it were, fixed and adherent to each other, the proximal to the distal end, the anterior surface to the posterior, through the previous bending of the tube on itself.

Within the common trunk Rokitansky has described the changes, as seen in cross-sections, which result in its division into a permanent aorta and pulmonary artery, and also the adaptation of the septum arteriosus trunci to the septum ventriculorum. He says that at an earlier period than here described for the external furrow appearing, on the inner surface of the truncus arteriosus communis (aortic bulb), to its left side and somewhat posteriorly, above the starting-point of the anterior limb of the septum ventriculorum, a little swelling appears, which grows toward the right and slightly forward, so that the common trunk is divided into an anterior rather left-hand, and a posterior right portion, respectively the pulmonary artery and aorta. The growth does not pass in a straight line through the lumen of the common trunk, but so that the forming septum makes a concavity posteriorly toward the aorta, and a convexity anteriorly toward the pulmonary; thus, on cross-section the aorta has the outline of the gibbous moon--the pulmonary, fitting into it, separated by the septum, of a new moon. The septum ventriculorum, as seen starting at the base of the ventricles from the fibrous ring of the auriculo-ventricular orifice (having already been built upward from the future apex of the heart), originates at a point on the posterior wall of the common ventricular cavity in exact correspondence with the starting-point of the little swelling on the inner surface of the common arterial trunk. The two septa are thus formed in apposition. The septum ventriculorum, in advancing forward to meet the other limb of the septum forming on the opposite wall of the ventricular cavity, follows the septum trunci arteriosus communis, surrounds the posterior vessel (the aorta) to its front, then passes around it to its right; the pulmonary is on the other side of the septum; the portion of the septum ventriculorum between the orifices of the vessels is the pars membranacea of the septum. The anterior portion of the septum ventriculorum forms one wall of the arterial conus of the right ventricle. Thus it happens that by the eighth week the common trunk is divided into aorta and pulmonary artery; the structure of the septum ventriculorum is so far advanced that these vascular trunks are connected with the proper ventricles, but the {701} septum ventriculorum does not close completely until about the twelfth week.

In explaining the occurrence of a transposition of the arterial trunks in accordance with the facts of their normal development, Rokitansky says, if the septum trunci, starting from the usual point of the little swelling on the inner surface of the common trunk, turns abnormally with its concavity forward (instead of backward as normally), and thus passes through the trunk, there will be established an anterior left aorta and a posterior right pulmonary, because the septum ventriculorum in its growth conforms to the direction of the septum trunci. Thus, another than the usual portion of the common trunk is partitioned off and placed in communication with the respective ventricles. This furnishes us with examples of transposition of the arterial trunks relatively to each other, but not transposed in relation to the ventricle into which they are implanted. The great majority of specimens of this sort with which we are acquainted--and Rokitansky knew no others--show an open septum. They are usually spoken of, therefore, as instances of "both vessels arising from the same ventricle (the right usually)," or of "aorta communicating with both ventricles, the pulmonary artery normally placed." Rokitansky assigns no reason for this deviation in the line of growth of the septum trunci across the lumen of the common trunk; in fact, he never examined a malformed heart during this stage of development. The deviation of the septum trunci, the primitive factor in this malformation--since to it the septum ventriculorum conforms its development--he accounts for by chance (deviation of formative energy). It seems much more probable, as it is always the pulmonary artery which must be reduced in size when the concavity of the septum trunci presents anteriorly (the aorta occupies the smaller area when the concavity of the septum is posterior), that the deviation of the septum trunci is due to some one of the many conditions (endo-myocarditis) which have already been pointed out as the cause of pulmonary-artery narrowing or closure; hence, another malformation of the heart can be thus traced to pulmonary obstruction, the evident cause of so many other defects.

For examples of transposition of the vessels, both relatively to each other and to the ventricles, with complete closure of the septum ventriculorum, Rokitansky also gives a satisfactory explanation. It is important to note the distinction between cases of closed and open septum. Transposition of the vessels with open septum are, as already shown, doubtful instances of transposition from one ventricle to the other, although the vessels may be transposed in relation to each other; furthermore, the mechanism which explains relative transposition of the vessels does not explain the implantation of the vessels into the improper ventricle. His explanation is that the starting-point of the little swelling from which the septum trunci forms is shifted to a point farther forward on the inner circumference of the common trunk, and at the same time has its concavity anteriorly, and as in the previous case decreasing also the area of the pulmonary artery; and thus the aorta comes more forward and to the right, and the pulmonary artery passes more to the left and backward. The septum ventriculorum, in conforming itself to the abnormal starting-point and direction of the septum trunci, must consequently pass across the common ventricular cavity in such direction that the aorta comes in connection with the pulmonary side of the heart, and the pulmonary artery with the systemic heart. Consequently, Rokitansky traces both the relative and the actual transposition of the arterial trunks to the deviation either of the direction or of the starting-point of the septum trunci. The deviation of the position of the little swelling on the inner surface of the common trunk, which Rokitansky supposes, is probably not an actual transference or misplacement of this point of formative energy, but in reality a failure of the common trunk (aortic bulb) to continue its axis-rotation, as it {702} normally does, after the other portions have become fixed. This premature cessation of the rotation of the common trunk would leave the starting-point of the septum trunci in a more anterior position than normal, since the trunk rotates normally in a direction to bring its left side, on which the starting-point of the septum trunci is situated, more posteriorly. A pericardial inflammatory adhesion, such as Meyer pointed out for certain cases of pulmonary artery obstruction, would fix the common trunk, prevent its proper rotation, and at the same time narrow the pulmonary orifice in certain instances. In other cases, in which the pulmonary artery is found of normal size, the septum trunci may be supposed to divide the vessel in the usual direction (concavity posteriorly as normal), whilst the septum trunci commenced to grow from an abnormal position, more anteriorly and to the left than normal (through failure of rotation); hence, as the septum ventriculorum conforms to its growth, the vessels become connected with the improper ventricle; the pulmonary, however, is not found permanently narrowed, and the septum ventriculorum is completely closed. Here the cause is a failure of the common trunk to rotate on its axis, probably from an external adhesion of its periphery.

Malformations affecting primarily the Right Side of the Heart.

In classifying defects in the course of the pulmonary artery we come to--

1. Closure or narrowing of the artery, with perfect ventricular septum.

Congenital obstruction of the pulmonary artery, with closed septum, although more rare than with open septum, is nevertheless a frequent defect. Unfortunately, it is very often impossible to distinguish with certainty whether the stenosis is essentially congenital or is acquired after birth. Complete closure is the least difficult to distinguish, because this defect very soon causes death; the prognosis in a merely narrowed orifice is much more favorable. The duration of life in complete closure never extends beyond a full year, while in undoubted congenital narrowing the age of sixty-five years has been attained.

From this atresia the most striking consequence is a reduction of size of the right ventricle, increasing almost to closure. This result is so common that Peacock thought it was the law that in atresia the right ventricle reduced itself to closure, while in stenosis it dilated and became hypertrophied. This is not the law, but only a rule of very common occurrence. Instances of eccentric and concentric hypertrophy are found among the records of these cases. Great reduction of the right ventricle results probably only when the obstruction comes very soon after the completion of the septum ventriculorum--thus at a time when the ventricle is yet very small. The wasting of the right ventricle can reach a very high degree, and when it becomes very great the tricuspid orifice is also defective. The foramen ovale and the ductus arteriosus Botalli are, in complete closure, usually found open. The obstruction may come in the conus or at the valvular orifice, or the artery is found converted into a cord.

In seven cases the duration of life varied from four days to nine months.

When the stenosis does not reach a high grade, positive clinical signs are often wanting for the determination of its existence, and the difficulty becomes greater as the age of the person advances.

Clinically, we find congenital blueness with palpitation, dyspnoea, together with the physical signs of pulmonary stenosis; these symptoms, however, may make their first appearance only on the advent of some acute disease. Sometimes they come in the first month or the first year of life, or even much later. {703} If abundant congenital compensatory changes are present, the symptoms may be postponed until further compensatory alterations become impossible; or at the narrowed orifice the development of a fresh endocarditis may determine the occurrence of symptoms. The mere increase of the body and of the mass of the blood may alter the relations of the circulation, and this disproportion may show itself with suddenness. Febrile conditions may also suddenly disorder the circulation.

The compensatory alterations which commonly are held to indicate a congenital origin of stenosis of the pulmonary artery are patulousness of the auricular septum and of the ductus arteriosus Botalli. When both of these remain open there cannot be much doubt that the date of origin is from the foetal state or in the first weeks of life. If only one of the foetal passages remains open, the ductus gives a greater surety of a foetal date than the foramen ovale. The closure of both foetal passages does not exclude a congenital origin if the obstruction of the pulmonary orifice is moderate. The patulousness of both foetal passages indicates that the defect arose at least shortly after birth, because these openings close within four or five weeks of this event. The foramen ovale alone open indicates very little with certainty, as it is so often found with one or more small openings without any probable cause. Bézot found it partially unprotected in 44 cases out of 155; Klob, 224 in 500; Wallmann, 130 in 300. Rokitansky has indicated that a strong blood-pressure not unfrequently may press the fibrous valve of the foramen strongly toward one auricle or the other, and thus lead to its atrophy in part, forming larger or smaller openings of communication between the two cavities. In doubtful cases of stenosis of the pulmonary artery such small openings are not signs of much value in determining the congenital origin of the stenosis. Unless there is a marked defect in the septum atriorum, the congenital origin of the pulmonary atresia or stenosis cannot be predicated on this ground.

Patency of the ductus arteriosus Botalli has been very rarely observed as a primary malformation. A coincidence of this as primary defect with post-natal stenosis of the pulmonary artery must necessarily be extremely rare. In persistence of the ductus art. Botalli the current passes from the aorta toward the pulmonary artery; the obstruction of the pulmonary artery conditions a dilatation with hypertrophy of the right ventricle. Reopening of the closed ductus is impossible.

The condition of the pulmonary valves as well as the diameter of the pulmonary artery itself and its branches often afford valuable points for the determination of the congenital origin of stenosis of this orifice. The greater the narrowing, or the more extreme the thinning of the wall, the earlier the coming of the obstruction.

Morgagni reported the first case of stenosis of the pulmonary orifice--in fact, the first case of congenital malformation of the heart--in a girl aged sixteen. He recognized the relationship of the open foramen ovale and the dilatation of the right ventricle as mechanical effects of the pulmonary stenosis.

2. Obstruction of the conus arteriosus dexter, with open ventricular septum.

A. The separation of the conus in the form of a so-called supernumerary third ventricle has been reported by Peacock in ten cases, and ten others have been added by Kussmaul from various sources. The degree of separation varies very greatly in individual cases: in some it is so slight that the designation becomes doubtful, while in others it is so great that the word stricture might with propriety be employed. In two cases a goosequill-sized opening existed between the sinus of the right ventricle and the conus; in others the communication between the two was multiple. The size of the supernumerary ventricle varies greatly; in one case of a girl of twelve years it would only contain a hazelnut.

{704} In most of the cases the partitioning probably commences by hypertrophy of the muscular bands which are more or less marked in normal hearts in this situation: to this, as the result of endo-myocarditis, is added cicatricial contraction of the inflammatory products, whereby the original partitioning becomes greatly increased. The preponderating frequency of the seat of the stenosis directly at the transition of the conus to the sinus increases the likelihood of this explanation of its causation.

Alteration of the valves of the pulmonary artery, probably of foetal inflammatory origin, is of very frequent occurrence with supernumerary ventricle and conus stenosis; sometimes only two cusps are found, though four cusps have been noted; they may be absent or be replaced by a ring mass formed from their union. Normal valves have been observed unaltered by inflammatory changes. The conus appears always to suffer diminution, and the pulmonary artery is found more or less narrowed according to the degree of obstruction. The sinus of the ventricle is dilated and its walls hypertrophied. The aorta, mostly widened, springs in all cases from both the ventricles, unless wholly from the right one. The foramen ovale is generally more or less widely open, although it has been found closed; the ductus art. Botalli is mostly closed. The duration of life may be long; Kussmaul reports the oldest case at thirty-eight years.

B. Of primary uniform narrowing or shrinkage of the right conus art. dext. Kussmaul reports eight cases from various sources. The conus was shortened, and formed a ring-shaped fissure, gradually reduced in size toward the orifice of the pulmonary artery. The pulmonary valves were variously changed, mostly by union of one or more of the cusps, though sometimes remaining normal in shape, though very delicate. The pulmonary artery was generally narrowed to about the width of the calibre of the conus itself, unless further change came to it from its special involvement by endarteritis.

In all cases the aorta arose from both ventricles. The right side of heart was dilated, and the right ventricular wall hypertrophied. The foramen ovale remained open. The ductus arteriosus Botalli has been found absent or closed, and the collateral circulation effected by anomalous communications, oftentimes duplicate or manifold; in most cases the ductus remains open. The oldest patient in which this form of heart has been found was twenty-five years.

C. Ring-formed narrowing of the conus, due to a muscular band. Peacock reports this defect from a girl æt. nineteen, cyanotic from birth; the constriction was situated at the bases of the valves, and was formed by a muscular band covered by fibrous tissue, and the edges of the opening were studded with warty vegetations. The pulmonary valves were two in number, probably resulting from fusion of two of the cusps; were thickened and opaque, but smooth. The index finger could be passed between the valves. The artery was of small size, but much wider than the constriction. The aorta was dilated, and arose from both ventricles through a perforation of the septum ventriculorum. The foramen ovale was closed. The ductus art. Botalli gave free passage to a crowquill. The right side of heart showed dilatation and hypertrophy of both its cavities, and the tricuspid valve was thickened and had vegetations on its auricular aspect.

3. Simple stenosis and atresia of the pulmonary artery, with open septum ventriculorum.

This class includes malformations, with stenosis or atresia of the pulmonary artery, in which the defects occur before the completion of the ventricular septum, as the result of engorgement already described, but in which no other primary congenital defect exists; thus the separation of the pulmonary artery from the truncus arteriosus communis is completed; the auricles and ventricles are marked out by their septa, though not completely divided; {705} the position of the aorta in relation to the pulmonary artery is either normal or more to its right; and there are no primary defects of any consequence in the other orifices of the heart. The simple stenosis or atresia of the pulmonary artery as thus defined is by far the most frequent malformation of the heart. Kussmaul has found about 90 described; among these are 26 cases of atresia.

As a rule, in partial obstruction the entire length of the artery, as far as the bifurcation, shows narrowing, but the greatest narrowing exists at the orifice of the pulmonary artery; only rarely are the orifice and the tube equally narrowed. Exceptionally, the tube has been found narrower just without the orifice, and later resumed its normal circumference. The walls are very often thin, like those of veins, and at times the vessel is shrunken. The valves are variously altered, often to a greater or less degree united, thickened, and opaque.

In complete closure two different conditions are seen; in some the artery itself to its bifurcation changes to a firm cord or thread; in others the tube is more or less narrowed and the orifice alone is closed.

As a rule, in stenosis and atresia of the pulmonary artery the conus is only moderately narrowed and its walls hypertrophied, while the sinus of the right ventricle is dilated and hypertrophied. The right auricle is dilated and hypertrophied. The tricuspid leaflets are clouded and thickened. The left ventricle is commonly small, and the wall not thicker than the dilated right ventricle. Sometimes the aortic and mitral valves suffer alterations of an inflammatory sort, probably of foetal origin. The shape and position of the heart are changed, but the size, as a whole, may not be much altered. The aorta may be widened, often to double the normal size. As to the origin of the aorta, it is often difficult to speak with certainty; its relative position to the pulmonary artery and to the body and axis of the heart is, as a rule, unchanged. Whether it is to be described as arising from one or both ventricles, or from the right one alone, depends on the posture which the septum ventriculorum assumes beneath its orifice. As a matter of fact, this relationship makes little difference to the flow of blood from the right ventricle, whose normal orifice is obstructed; provided the septal opening is sufficient, the flow of blood is secured and the hindrance to the circulation precluded. The opening in the septum ventriculorum may be only at the membranous portion, or it may also involve the adjacent muscular septum; the defect may be round or triangular, with its apex above and with smooth margins.

The foramen ovale has been found open in 39 cases out of 53. Its condition in this respect shows very great proportional variation in the different collections of cases. The open or closed condition of the foramen does not seem to depend on the degree of stenosis of the pulmonary artery itself. It depends, probably, more on the freedom of escape for the blood from both the ventricles through the aorta--probably also on the condition of the ductus arteriosus Botalli. The foramen ovale and ductus art. Bot. have been found closed much more frequently in stenosis than in atresia of the pulmonary artery, and the ductus is deficient or absent oftener in stenosis than in atresia. This absence of the ductus occurs in 13 per cent. of the cases, and tends to support Peacock's theory that narrowing of the pulmonary artery is the consequence of the defective development of that branchial arch out of which the ductus art. Botalli is formed.

It is of great interest to note the collateral circulation by which blood reaches the lungs when the pulmonary artery is closed. When the ductus arteriosus is open, the blood passes from the aorta into the ductus and the branches of the pulmonary artery become branches from it. When the ductus arteriosus is closed or very narrow, the bronchial arteries become {706} the means of supply for the lungs, and through them the blood passes to be aërated. Branches from the coronary arteries have been found supplying a partial channel for the blood to the lungs, as well as the oesophageal, pericardial, internal mammary, and intercostal arteries.

The duration of life is often very considerable. Thirty-seven years have been attained.

4. Combined Stenosis and Atresia of the Pulmonary Artery.--Under this division are arranged other primary defects of the heart, which are found combined with stenosis and atresia of the pulmonary artery. It is very striking how frequently this artery is narrowed or closed in defects of the heart which date from the early period of foetal life, before the division of the truncus art. comm. and of the ventricles has occurred. It is only very rarely that defects from this early period show a normal width in this vessel; in the great majority it is narrowed or closed. The aorta is rarely affected in this manner. Changes in the aorta may come also, but a complete failure or great narrowness of this circulation is so difficult to overcome by a collateral circulation--more difficult than the pulmonary circulation--that life must cease in the foetus, or at least the conditions are incompatible with extra-uterine existence.

A. Combination with partial persistence of the truncus arteriosus communis. The defects coming under this head show usually very great deficiency of the organ and its great vessels, although the heart itself in rare instances shows the proper arrangement of the cavities and their valves. The persistence of the truncus art. comm. may be complete or partial; the defect consists in the total absence or arrest of growth of the septum of the truncus, which partitions it into two portions. Normally, the two septa grow simultaneously and meet at the base of the heart. In cases of persistence of the truncus art. comm. the upper septum fails to develop. In incomplete division of the truncus the pulmonary artery suffers more than the aorta, and the former is always narrower than its fellow-vessel. This difference varies greatly. The valves of the pulmonary artery often fail entirely, and the ductus art. Botalli is many times absent.

B. Combination with cor biloculare.--Here we have a heart consisting of two cavities--one auricle and one ventricle--where no partitioning has taken effect. The defect results from the failure of the septum ventriculorum to grow; and with this, as in the former division, comes also a more or less complete failure of the septum trunci art. comm.

C. Combination with single ventricle and divided auricles (cor triloculare biatriatum).--In the cases of single ventricle with more or less complete division of the auricles the pulmonary artery generally shows narrowing to a greater or less degree; it may still be pervious, although its orifice is closed, or it may be throughout entirely obliterated. The valves may be entirely wanting. The duration of life is very short, though in a very few with effective compensatory changes it may be prolonged very considerably.

D. Combination with divided ventricle and a single auricle (cor triloculare biventriculare).--In strictness, this defect is nothing more than an open foramen ovale with some deficiency of the pulmonary artery; but, in reality, the heart is much more malformed. The whole septum atriorum is wanting; the superior or descending vena cava is doubled--one entering the left part of the common auricle, the other opening more to the right. The ventricular septum shows a greater or less defection, the pulmonary artery is narrowed, and the aorta arises from both ventricles or wholly from the right one.

E. Combination with special anomalies in the position of both the great arterial trunks.--Here come a variety of anomalies in the arrangement of the aorta and the pulmonary artery in relation to their respective ventricles and to themselves.

{707} _a_. In transposition of the great arteries, the aorta arising from the right ventricle and the pulmonary artery from the left cavity, either there comes a general transposition of all the viscera or the heart alone is reversed. Very rarely in transposition of the vessels the septum ventriculorum is closed, commonly open, and although the size of the vessels may be normal, usually their relation and position continue reversed throughout their course. In cases where the pulmonary artery is narrowed the duration of life is short. _b_. The pulmonary artery may arise from the left ventricle and the aorta from both ventricles; or, _c_, the aorta may come wholly from the right ventricle, and the pulmonary artery from both cavities; the latter vessel may be narrowed or show its normal width or even be considerably dilated. _d_. Both the great vessels may arise from the left ventricle, very much dilated, with the aorta in front of the pulmonary artery and the latter narrowed. _e_. The relation of the great arteries may be found reversed--_i.e._ the aorta in front and the pulmonary artery behind, and the aorta spring from both ventricles and the pulmonary from the right alone.

F. Combination with primary defects of other valvular orifices of the heart.

_a_. The tricuspid valve may be quite rudimentary, producing by the regurgitation thus allowed, especially when combined with pulmonary stenosis, great dilatation of the right auricle. When the pulmonary artery is narrowed the septum ventriculorum remains open; the aorta carries the blood, distributing it to the lungs by an open ductus arteriosus Botalli or a collateral circulation. The collateral circulation is less developed the greater the width of the pulmonary artery. The foramen ovale may close in such a case, but when it remains open the relief to the over-distended right auricle is very great.

_b_. Many cases of congenital stenosis and atresia of the right auriculo-ventricular orifice are reported in which the condition of the pulmonary artery is not described. In fact, it is a difficult matter to determine if the auriculo-ventricular narrowing is a primary one. Its defective size may be merely, as it were, a rudimentary condition, a failure to enlarge through disuse. When the pulmonary orifice is closed and the right ventricular cavity remains small, the tricuspid orifice is naturally small in size. There are, however, undoubted cases of tricuspid narrowing with or without stenosis of the pulmonary artery; the defect consists in a primary contraction of the fibrous ring or in the union by partial adhesions of the leaflets.

Malformations affecting primarily the Left Side of the Heart.

Primary defects of the systemic side of the heart are, for the reasons already given, very much more rarely seen than those of the pulmonary heart. In such cases the aortic conus and its orifice are found more frequently affected than the mitral orifice; both of these orifices, however, may be congenitally altered without foetal malformations at other parts of the heart being present; such cases are on record, though only sparsely scattered through the literature of cardiac diseases. Dilg[8] has recently made an important addition to this subject. He proposes a classification on a new basis for all forms of cardiac malformation; to these classes he makes conform the malformations of the left side of the heart. In the first class he places all cases dependent on an inflammatory process occurring in the foetal heart after its normal development is completed; in the second, those cases of malformation in which the deviation from the normal consists in defects of formation; in the third, those which present a combination of endo-myocarditis with defective development.

[Footnote 8: _Virch. Arch._, Bd. xci., S. 193-259, 1883: "Ein Beitrag zur Kenntniss seltener Herzanomalien in Anschluss an einem Fall von angeborner linksseitiger Conusstenose."]

{708} Among the many cases of malformation of the heart which he presents there are reports of 15 cases of stenosis of the conus, which are to be divided into two categories, in accordance with his classification. In the first group, in 7 cases the stenosis is due to an inflammatory process, and is conditioned by the results of the endo-myocarditis localized in the aortic conus. These cases must have originated at a late period of foetal life, and they correspond closely to the conditions arising in the adult organs from similar processes. In all the specimens the mitral orifice was involved, and contributed a share in the production of the conus stenosis; in all the cases the aortic valves also had suffered inflammatory changes. Here Dilg also speaks of a band-like hypertrophy of muscular fibres, marking the outlines of the aortic conus, similar to the condition described by Peacock in the right ventricle; in this condition there was no evidence of endocarditis, and the condition may have been due to cadaveric rigidity. The left ventricle presented varying conditions according to the state of the aortic and mitral valves; in some cases there was concentric hypertrophy, or, more strictly speaking, narrowing or shrivelling of the cavity with hypertrophied walls; in others dilatation existed. The other cavities of the heart were influenced by the competency of the mitral orifice, but almost always showed considerable hypertrophy and dilatation. The valvular apparatus of the right heart was not free from evidences of old inflammation, but this condition was not very marked. The ages of the reported cases reached from thirty to seventy-five years.

In the second group there are eight cases in which the defective condition of the aortic conus caused malformation of other parts of the heart. Here the conus stenosis occurred at an early period of foetal development, before the permanent structures of the heart were fully formed. The conus stenosis is to be considered as primary, the other defects as secondary. As we have already seen, the left side of the heart is much less liable to deforming causes, and when such do occur the secondary defects are less conspicuous. Thus, in only four of these cases were there such malformations of other parts of the heart as openings in the septa of the ventricles or auricles, patency of the ductus arteriosus Botalli. The defects consist more usually in what were formerly called excesses of development, such as the formation of bands below the aortic orifice; or of deficiencies of development, such as only two aortic valves. These conditions are very doubtfully due to formative excesses or deficiencies, but rather to intense inflammatory processes or other morbid conditions which have resulted in the formation of excessive cicatrices or the removal of normal parts.

Another division of cases shows narrowing of the aortic trunk itself. This condition is probably always a true defect of development; so far as these cases, collected by Dilg, show, it is unquestionably so. In narrowing or closure of the pulmonary artery trunk it is found that in some instances this condition was dependent on an endarteritis resulting in a partial occlusion of the lumen of the vessel; here, however, the aortic trunk furnishes no evidences of such a process. It must therefore be due to an unequal division of the truncus arteriosus communis. The cause and the mechanism of this unequal division of the common trunk, resulting in a reduction of the size of the aorta, are probably similar to what Rokitansky indicated for the reduction in the size of the pulmonary artery trunk.

In the specimens of aortic narrowing (no cases of complete closure are reported) from this cause and mechanism the pulmonary artery has been found unusually wide, but this condition of the pulmonary trunk is not very conspicuous, and does not necessarily result from the narrowed state of the aorta. The compensatory or secondary defect of open septum ventriculorum, or even of the auricular septum, is, in these cases, neither invariable nor necessary to a proper maintenance of the foetal or adult circulation. In fact, {709} the open ventricular septum is rare; the condition of the auricular septum is, in the reports, often not stated. The left ventricular walls commonly show a preponderance of hypertrophy over dilatation of this cavity, but in some cases the distension of the cavity is marked.

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SYMPTOMS.--The most striking symptom which occurs in malformation of the heart is the cyanosis, but the appearance of this peculiar symptom may be postponed until some time, even a long period, after birth. In the newly-born infant presenting a blue color the diagnosis rests between the not infrequent temporary failure of respiration from many causes and a defective development of the circulatory organs. In most cases the doubt is promptly solved by the voluntary or artificial efforts of breathing, whereby the cyanosis disappears. If the dark hue persists after the respiratory movements have been developed, the cyanosis may be found to depend either on cardiac malformation or an imperfect expansion of the lungs (atelectasis). The distinction between these two conditions can usually be made by a study of the respiratory movements, by the state of the heart's action and of the pulse, aided sometimes by an inspection of the outlines of the chest. In cardiac malformation respiration seems to be well performed and full, though often hurried or labored; in atelectasis this function is often found characteristically altered by being short, high, and imperfect, with imperfect distension; the ribs, instead of moving upward and outward, fall toward the median line, and the chest fails to expand transversely. In malformation the heart's action and the pulse are rapid, and a murmur can often be heard. The thoracic outline may deviate from the usual antero-posterior flattening by the sternum being prominent in cases where the heart, instead of its usual position to the left, is placed more centrally, as comes in certain defects of development. Both of these conditions may be present, and then the symptoms are mixed in character.

Cases of atelectasis, sufficiently marked to give rise to persistent cyanosis, if not relieved too frequently show a pretty rapid increase of color, becoming deeply livid, with convulsive movement, ending shortly in death. The diagnosis in such cases between a cardiac malformation and a non-expanded lung is almost impossible unless the respiration shows characteristic features. It is probable that the treatment proper for the latter would aggravate the condition of the circulation in malformation. In a majority of cases a post-mortem examination is necessary to determine whether the cyanosis is of cardiac or of pulmonary origin. In the atelectatic condition, if death comes within a few days of birth, the ductus arteriosus Botalli and the foramen ovale may both be found open, especially the latter, their time of normal closure not having arrived; in cases dying at a later period, if the foetal openings are still found patulous, the open state must be considered as dependent on the condition of the lung-tissue, since in malformation of the heart the patulous state of these foetal openings is, as has already been shown, rare as a primary defect, and, except in connection with defects of development resulting in obstruction, which operate at other points of the foetal circulation, is almost never found. In other words, an open foramen or ductus is a secondary defect, dependent, on the one hand, on a primary obstruction of the cardiac ostia, or, on the other hand, it may be on a primary atelectasis or malformation of the lungs.

If the child passes beyond the first weeks of life without exhibiting cyanosis, the subsequent occurrence of the condition becomes almost a pathognomonic symptom of cardiac or vascular malformation, unless it can be shown that the coloration is dependent on some acute disease, especially acquired valvular disease: in this connection collapse of the lung (post-natal atelectasis), too, must be remembered.

{710} It is during the first week of life that cyanosis makes its appearance in the great majority of cases of malformation of the heart, in the proportion of more than two to one of the cases. The coloration, once developed, may remain permanent and of equal intensity until death, but as less than 8 per cent. of infants with malformation die within the first week, and only 36 per cent. within the first year, this symptom usually remits. It may wholly disappear, to return on very slight provocation, such as excitement, or on exertion, on the advent of acute disease, or without apparent cause. Probably about one-fourth of those who die in infancy perish in paroxysms of dyspnoea, another quarter of acute disease, and the remaining half of convulsions; and toward death the cyanosis generally becomes very intense.

If the malformation is not of character or degree to develop cyanosis early in life, the child grows and passes through the usual stage of development, usually, however, feeble, poorly nourished, incapable of common exertion, but often without any special phenomena to attract attention, and the vice of formation is undetected unless by a special examination. There are several other symptoms frequently present in connection with malformation, but not of a pathognomonic character. Dyspnoea, though rarely occurring without cyanosis, may attract attention, and, if frequently brought on by active exercise, increases in violence, to be later accompanied with the cyanosis originally absent. Palpitation is not uncommon, especially in cases of great hypertrophy with dilatation, in hearts struggling to overcome an obstruction; in other cases it is absent or only occurs on exertion in connection with dyspnoea and cyanosis. The degree of animal heat varies greatly, judging by the various opinions expressed by writers. The sensation of patients able to express their feeling is often that of chilliness, and in some cases the surfaces of the body feel cold, although the indications of the thermometer show no great variation from the normal temperature. It is obvious that no very great variation from this standard is compatible with the long duration of life, although a depression may exist during or immediately after paroxysms of dyspnoea or cyanosis. Cough is also frequent, but is probably always due to some acquired pulmonary disease.

The physical signs offer increased facilities for the recognition of defects of development. In the early reported cases there are of course no records of these conditions, and there is therefore a lessened number of instances from which to collate the physical signs. In the early days of life it has been shown wherein the presence of a cardiac murmur may lead to the distinction between malformation and atelectasis. In later periods of life the physical signs cannot be regarded as characteristic. There are no signs by which a malformation can be distinguished accurately from an acquired cardiac disease, so that without the clinical history and a grouping of symptoms the diagnosis cannot be made from the physical examination.

Inspection and palpation of the chest often show the heart to be in an unusual position, placed more centrally under the sternum. It must be remembered that transposition of the heart to the right side is not unfrequently unaccompanied with any malformation of its ostia giving rise to symptoms; and this organ may be even more markedly displaced without being malformed, although under both these conditions irregularities of the principal trunks are usually found.

Percussion frequently shows enlargement of the area of cardiac dulness, but, on the other hand, at the post-mortem examination the heart is often found markedly defective without externally showing variation of its size or shape, or of its position within the thorax; hence in such cases no deviation from the normal will be revealed on percussion or inspection of the chest. It is probable that cardiac murmurs are not always to be detected in cases of even marked defects of development, but when present it is recorded most {711} frequently that a single murmur is heard over the base of the heart, blowing in character and systolic in time. Such a sound is probably produced by the passage of the blood through an abnormal opening between the ventricles or through the foramen ovale. Other murmurs may also be present; if the arterial ostia are defective from narrowing, roughness, or insufficiency of their valvular apparatus, abnormal sounds of different characters, diastolic or systolic in time, may be heard. Too few observations as yet exist for a general diagnostic scheme to be formulated. Auscultation of the intra-uterine heart may in the future become sufficiently accurate to enable us to prognosticate a congenital cardiac malformation or disease; there is one case on record in which a correct diagnosis was made in this way.

The ends of the fingers and toes are frequently described as bulbous. This rounding and retraction of the nails, frequently spoken of as clubbing, does undoubtedly exist in many cases, but the condition cannot be regarded as characteristic of malformation of the heart, since it comes with even more frequency in tubercular disease of the lungs, in chronic pleurisy, and in other chronic pulmonary maladies.

Lebert has recently insisted on the connection between stenosis of the pulmonary artery and tuberculosis, not merely as a coincidence, but as the cause of the development of the tubercles in the lungs. Many others have spoken of this connection, and very many are the cases recorded--perhaps nearly one-quarter of the whole number. In some cases large or small single cheesy masses exist; in others cavities form, and in rare cases a miliary tuberculosis exists, still more rarely affecting other organs than the lungs. In view of the recent dogmas of tuberculosis it is doubtful if many of these authors would at present insist on the connection between malformation of the heart and tuberculosis being other than a coincidence, since it is not apparent why such patients are more likely to be invaded by a bacillus of tuberculosis than other persons, and this organism is known to grow so readily wherever the spores chance to fall.

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DURATION OF LIFE.--In connection with certain malformations some indications have already been given in respect to the duration of life in such defects. It is, however, apparent that the degree of the obstruction to an orifice or vessel, and still more the completeness of the secondary compensatory alterations, exert a greater influence than the seat of the malformation on the continuance of life. The occasional slight isolated malformations, such as open septa without obstruction of the orifices, in themselves often entail no symptoms, and, unless combined with acquired valvular disease, exercise no influence on the duration of life; here, however, the prognosis merges entirely into the acquired malady.

Of the other conditions of malformation, narrowing of the aorta and of the aortic conus seems to be, on the whole, compatible with a longer duration of life than any other condition, and these defects cause death in the early days or months in fewer cases than similar obstructions on the right side of the heart. This result apparently comes from the fact that the left ventricle seems to possess unlimited capacity for hypertrophy, and hence is able to overcome the obstruction; when the aortic valves allow of regurgitation the compensation fails and death comes sooner. When the main branches of the aorta are defective or when the descending aorta is derived from the pulmonary artery, the duration of life is much shortened.

In cases of pulmonary narrowing in general it may be stated that the greater the obstruction the shorter the life. This rule is subject to many exceptions; so frequent are the exceptions that the rule is almost valueless for determining the life in any given case. Complete closure of the pulmonary trunk has permitted of the continuance of life for sixteen years, {712} and then ended from an intercurrent acute disease. When the septa are maintained open--when, therefore, the communications between the pulmonic and systemic sides of the heart are free--a greater age is attained than when these openings have become closed. This condition of the pulmonary artery in order to permit of a long duration of life must be coincident with a considerable development of the collateral circulation by which the blood freely enters the lungs for aëration; otherwise the compensation fails very soon.

In transposition of the main trunk relatively to the ventricles, with closure of the septum ventriculorum (very rare), life ends not many weeks after birth; if the septa remain open, which is not common, life may be prolonged for a year or two.

Cyanosis.

There are two views to be found, set in opposition to each other, to account for the peculiar blue coloration of the skin and mucous membranes in cases of malformation of the heart. The first explanation attributes the phenomenon to a general congestion of the venous system, due to the obstruction of the pulmonary artery. This view was proposed by Morgagni in connection with his, the first described, case of malformation of the heart. The other view considers that the intermingling of venous and arterial blood through any channel, but especially by means of abnormal openings in the septa, produces the blue coloration. Numerous writers have defended each of these theories of causation; from most of their observations darkness rather than light has resulted through the attempt to defend one or the other theory exclusively.

Gintrac defended the admixture theory for cyanosis, and his views became so well known that a large majority of persons conformed their belief to his teachings. This author distinguished four varieties of blue coloration: first, that due to some malformation of the heart or great vessels, by which the blood of the right side of the heart enters the systemic arterial circulation; second, likewise due to intermixture of the blood, but produced by conditions developed after birth through the re-establishment of the passages of communication or other changes in the circulation; third, where the coloration appears without direct admixture of the blood, but from organic disease of the heart; fourth, cases without malformation, from a suppression of the menses. Before the time of Gintrac, cyanosis had a very indefinite signification, and the condition was looked upon, and was classed by very many, as one of the cachexiæ, and was often spoken of as a form of icterus. He, however, held that the organic lesions of the heart and great vessels were the necessary conditions of its production, and that the mixture of the red and black blood, and the distribution of the mixed fluid by means of the arteries to all parts of the body, determined its essential character. He showed, too, that all communications between the right and left heart were not followed by cyanosis; the explanation of the absence of the blue color was that from the simultaneous contraction of the auricles and ventricles of the two sides of the heart an equilibrium was produced, and the blood did not deviate from its normal course. This result followed only when the normal exits of the blood were unobstructed. This supposition, as is apparent, is not in accord with the facts. During the filling of the ventricles, before the muscular contraction of the walls occurs, the blood has the opportunity of freely mingling if the opening between the cavities is sufficiently large: that the blood will not thus mingle when the muscular contraction acts remains to be proved. Cases of open septum ventriculorum, as an isolated defect, without obstruction of the great vascular trunks (a rare condition), are not attended with cyanosis: the absence of this symptom, as will be shown later, is readily to {713} be explained on other grounds than those supposed by Gintrac. The normal outlets of the blood are, however, almost always obstructed to a greater or less degree; and here the explanation of the absence of the cyanosis fails. In the delayed appearance of cyanosis Gintrac considered the reason to be that the venous blood differed less from the arterial in the young subject than in those of more advanced age, because, on the one hand, the aëration was more active, and, on the other hand, the deterioration of arterial blood was less marked. In other cases he points to an increase of the obstruction, through inflammatory changes, as the probable reason for the delayed appearance of the blue color; in still other cases it was supposed to be due to a disturbance of the equilibrium of the pulmonary and systemic circulation from an increase in the blood-mass. In cases of unilocular and bilocular hearts, of which the author speaks, his explanation completely fails, for here the admixture of the blood within the heart is very marked; yet such cases have been reported without cyanosis. He further believed that openings in the ventricular septum, as well as between the auricles, were effected after birth as the results of acquired cardiac disease.

Gintrac, in speaking of the causes of cyanosis, says that the condition shows no hereditary tendency; that the pregnancy during which the defective infant is developed is without noticeable phenomena; and that the confinement is normal. It is on some of these points that we are in want of accurate information. It has been pointed out that many congenital defects of the heart result from morbid processes affecting the organ during its developmental stage. These lesions are the same in kind as those which produce cardiac and vascular disease in the adult, and are likewise of a sort capable of communication from the parent to the foetus. Such diseases are found acting oftentimes temporarily in the parent; and if they acted during pregnancy, or even if present only at the time of conception, their results would rationally be expected to be displayed in the foetus. Such diseases as rheumatism and syphilis, which may be regarded as temporarily-acting maladies, would come under this class, and doubtless many others might be added to the list. The work of collecting the histories of pregnancies or the condition of the parents at or before the time of conception would be painfully tedious: such records do not exist at present, and they could be made sufficiently full only in exceptional cases; but their value in determining the causes which operate in the production of defective development of the heart cannot be too highly estimated.

The conclusions stated by Moreton Stillé[9] seem to be the first which justly cover the ground from a comparison of large numbers of cases of malformation of the heart. The first conclusion by him is that cyanosis may exist without admixture of the blood; by this was meant that no abnormal communication between the right and left sides of the heart, and no channels between the principal vascular trunks, are present. He mentions five cases of cyanosis occurring in which no means of admixture existed. The second conclusion is that there exists no proportion between cyanosis and the degree in which the blood is mixed; for this he cites four cases, some with the aorta arising from the right ventricle, others of hearts with only two cavities and the common trunk undivided, in which the cyanosis was only partial or transient. The third conclusion, the converse of the first, and reinforcing the preceding one, is that complete admixture of the blood may take place without cyanosis. The fourth, that the variation in the extent, depth, and duration of the discoloration is inexplicable by the doctrine of the mixture of the blood.

[Footnote 9: "Inaug. Thesis." _Amer. Journ. Med. Sci._, N. S., vol. viii., 1844.]

Having shown that commingling of arterial and venous blood cannot be the cause in itself of cyanosis, Stillé proceeds to the study of the other {714} theory--viz. that it is due to congestion of the general venous system resulting from some obstruction in the right side of the heart or in the pulmonary artery, impeding the passage of the blood through the heart. These structural lesions must fulfil the three following indications: 1st, that they shall be sufficient in degree to account for the symptom; 2d, that they be present in every case of cyanosis, or in their place some other cause acting on similar principles; 3d, that they shall never exist without cyanosis or without a satisfactory explanation of the exceptional occurrence. He holds that contraction of the pulmonary artery is to be taken as the type of all the lesions that may produce cyanosis, and that this type fulfils the indications given above.

Most writers since Stillé have coincided with him, or have regarded cyanosis as partly due to venous congestion and partly to commingling of arterial and venous blood. Some writers, however, have pointed to the abnormal communications between the right and left side of the heart, and asked why, if admixture of the venous and arterial blood is not the cause of cyanosis, should the admixture through such openings be found in such a large proportion of cases. Such writers have failed to distinguish between the primary and secondary defects of development. They have failed to see that the pulmonary obstruction which prevents the blood during extra-uterine life from passing to the lungs for aëration, and consequently produced the cyanosis, prevented the closure of the ventricular septum during intra-uterine life, or of the auricular septum within a few days of birth. In reply to the above question it may be pointed out, as Peacock has done, that such communications between the two sides of the heart are all important for the continuance of life, even for the shortest period, when the pulmonary artery is occluded.

It is evident, as Peacock has shown, that if Stillé's first and third conclusions are true, as the cases undoubtedly show, the theory of intermixture of the blood does not account for the condition of cyanosis. It is probable in many of these cases with abnormal openings in the septa that the intermixture of the blood is but slight, since if the pressure on the two sides of the heart is equal--and it may become equal through the establishment of a collateral circulation, although primarily it was unequal--no intermixture takes place through the defective septa. Neither does the admixture theory account for cases of intermittent or delayed cyanosis. Such cases can only be supposed to be due to a varying propulsive power or to a subsequent increase of the pulmonary obstruction. Neither does admixture account for localized cyanosis; for example, in the face or in one extremity: this condition, rare as it is, must be due to other causes. Peacock, while combating the admixture theory, considers that Stillé's conclusions in favor of the congestion theory as dependent on obstruction of the pulmonary artery are too exclusive. He discusses also the relationship of congenital cyanosis due to malformation, to cyanosis acquired through pulmonary and cardiac disease as seen in the adult, and shows why the latter condition is rarely ever as intense as the former, and also why acquired obstruction of the pulmonary artery is not necessarily productive of cyanosis. The reason of the difference he believes consists in the compensatory hypertrophy of the right ventricle, with perhaps a gradual diminution of the blood-mass, as seen in some cases.

On the whole, Peacock subscribes to the congestive theory, but thinks that the intensity of the cyanosis is modified by the capacity of the capillaries, by the period of development or duration of the obstruction, by the natural coloration of the skin, and by the color of the blood itself.

Under these two theories, and the arguments offered in support of them, there seems to be no other explanation possible of the condition of blueness, and yet the whole story of the mechanism of cyanosis does not seem clear. Partly, this is due to the incomplete knowledge of the physiology of the aëration of the blood which obtained during the most active period of the {715} discussion of cyanosis and its causation. Let us consider briefly the simplest case of cyanosis. Every child born has in one sense a temporary malformation of the heart--an open foramen ovale which does not close for several days after birth. Every child is born partially cyanotic, owing to compression of the uterine sinuses or pressure on the umbilical cord; it is completely cyanotic if there occurs premature separation of the placenta. The cyanosis continues until the child breathes. The cause of this cyanosis must be looked for, not in the temporary malformation, but in the imperfect expansion of the lungs. As soon as the respiratory function is assumed--as soon as, in other words, the pulmonary-artery branches carry a full amount of blood which becomes aërated in the lungs--the cyanosis ceases, although the foramen ovale is not yet closed.

The closure of the foramen by a trapdoor valve is, as has already been pointed out, not in accordance with the anatomical facts: turning the newly-born infant on its right side does not favor, as it is commonly supposed, the closure by gravity of a preformed swinging lid, which when it has dropped down for ever partitions the right from the left auricle. The right-sided position may favor the expansion of lungs or in other ways promote the pulmonary circulation, but in itself it does not tend to close the foramen. In fact, cyanosis does not here depend on the defective development, but on want of aëration of the blood.

Again, looking to the skin or mucous membrane, what is the condition of the blood and of the circulation which renders the parts of a blue color, and in what do they differ from the normal? In the normal state of the blood and circulation the capillaries of a given area are filled, one half with arterial blood, and the other half with venous blood; that is to say, the capillaries at the point of their origin from the arterioles contain pure arterial blood: as the blood-current proceeds outward the blood becomes progressively less and less red and more and more blue or black; when the venous radicle is reached the blood-current is of as dark a hue as it ever becomes. In general terms, therefore, it may be said, taking the average, that in a given area half the blood is venous, half arterial. Here, then, we see, with an equal mixture of the red and blue blood, nothing resembling cyanosis. It is evident, therefore, that to produce a cyanotic hue the blood must be wholly venous; the intensity of the blueness will vary with the amount of non-aërated blood present in the capillaries. But let us suppose an equal admixture of right- and left-sided blood to take place--for example, when the aorta arises from both ventricles, the pulmonary artery obstructed. It cannot be supposed that the venous blood would retain its dark hue. The contact of the two bloods within the aorta on their way to the capillaries would result in arterializing the venous blood at least one-half, so that when it arrives at the capillary network the intensely blue color of a marked case of cyanosis would have disappeared.

Besides this, there are other considerations to be taken into account to show that neither of the two exclusive theories accounts for the state of the blood and of the circulation in cyanosis. If the condition of the cyanotic parts, due to acquired valvular heart disease or various morbid states of the pulmonary tissue of an acute character be compared with the same parts in cyanosis from malformation of the heart, striking differences are discernible. If the simple condition of cyanosis of the part due to localized pressure on the veins be examined, the differences are even more perceptible. In the malformation there is an admixture of blood; in the other condition there is no opportunity for the intermingling of the currents. In the latter the cyanotic area becomes swollen, and the intensity of the color may become lessened through the oedematous condition; in the former the skin of the cyanotic infant rarely if ever presents any swelling; the veins of the part show little, {716} if any distension, as is so frequent in the latter; cases of malformation in which subsequent endocarditis with additional obstruction occurs may show oedema and swelling similar to cases of acquired valvular disease. In these cases of cyanosis the condition must be due to a want of aëration of the blood, since it never appears until such alterations of the pulmonary tissue and circulation are reached as to render it certain that the blue coloration is due to a want of aëration of the blood. Fulness of the veins and oedema may be present, but never general cyanosis.

Another important consideration in the production of cyanosis does not seem to have been fully appreciated. It is the fact that in all cases of obstruction of the pulmonary artery the collateral circulation, carried on by very varying channels, the bronchial arteries, the oesophageals, the coronaries in some cases, the internal mammaries and intercostal arteries in rare cases, or by the ductus arteriosus Botalli, which alone must be always inadequate in marked narrowing of the pulmonary trunk,--the collateral circulation must always remain insufficient for carrying sufficient blood to the lungs for aëration. Kussmaul was the first to call particular attention to this fact; and it is to this condition of insufficient channels for the blood reaching the lungs that certain cases of cyanosis must owe their causation.

Hence it must be that, in all the complex conditions found in cases of cyanosis from defective development of the heart, a want of due arterialization or aëration of the blood is at the foundation of the state as seen in the cyanotic area. Whether it results in a given case from excessive admixture of venous blood with the arterial when the current reaches the capillaries, or from venous stasis due to central obstruction, of which pulmonary-artery narrowing or closure is the type, or whether from a failure of sufficient blood to reach the lung, as where the collateral circulation remains imperfect, or as seen in certain cases of defective development of the lungs, is most difficult to ascertain. That sufficient consideration has not been given to the third possible factor in the causation of cyanosis--viz. failure of the blood to reach the lung, as distinguished from general venous congestion alone--is evident. That intermingling of the blood from the two sides of the heart must inevitably reduce the red color is certain--that in very many cases the reduction in color does not cause cyanosis can be readily understood from the consideration already offered. The cases of free admixture in which cyanosis does occur may coincide with a condition of very imperfect collateral circulation to the lungs, and hence with a low aëration of blood of the left ventricle, insufficient, therefore, to bring up the color of the blood from the right side of the heart above the cyanotic point.

Whether non-aëration of the blood from failure to reach the lungs, apart from general venous congestion, is a sufficient explanation of the cyanosis in a large majority of cases or in the whole number, is not apparent from the records of reported cases. Much more accurate post-mortem accounts, made with a view to determine the question, than at present exist will be required. In a number of well-reported cases of defective pulmonary artery with a free admixture of blood the pulmonary collateral circulation is found to be well developed, and no cyanosis had appeared, or had been but trifling and inconstant. In other cases of quite as marked pulmonary obstruction with but slight commingling of the blood through abnormal apertures and but slightly-developed collateral circulation, cyanosis has been found intense and constant. In the two conditions the possibilities for general venous congestion are about the same, though perhaps not equal, while the striking difference, apart from the admixture of the blood-current, consists in the conveniences for the aëration of the blood.

The only variety of malformation of the heart in which intense and constant cyanosis must inevitably be present is that very rare form of {717} transposition of the great trunks, the aorta springing from the right ventricle, the pulmonary artery from the left, with closure of the septum ventriculorum; the pulmonary veins enter the left auricle bearing red blood, and the venæ cavæ the right auricle with blue blood; if the ventricular septum is closed, the aorta necessarily carries blue blood to the systemic circulation, and the pulmonary artery is filled with red, carrying it back to the lungs, whence the fluid has just come. In such relation of the principal trunks, even if the ductus arteriosus Botalli and the foramen ovale remain open, cyanosis is necessarily present. The bulk of the blood in the aorta is blue: the only points in which it comes in contact with red blood are, first, at the foramen ovale: here the intermingling is not sufficient to bring it above the cyanotic color; and, secondly, at the ductus arteriosus, and here the tube is not favorably directed for a copious intermingling of the two bloods, neither can it probably ever be sufficient in itself for this purpose. Hence the aortic blood is almost wholly venous. If these two foetal openings did not persist life could not continue beyond a few hours, or even a few minutes, after birth. In such a case the cyanosis does not depend on general venous congestion, and specimens are reported of this sort in which the great vascular trunks were without obstruction, life having been maintained for a few months; adult existence is probably impossible. If, however, with such transposition of the vessels to the improper ventricle, the septum ventriculorum remains widely open, cyanosis may be absent or inconstant, because, apparently, admixture of the blood and also aëration are sufficiently free. But in cases of transposition of the vessels, or even in the much more frequent specimens without transposition, when the track to the lungs is defective either from want of a collateral pulmonary circulation or directly from impervious pulmonary artery, cyanosis becomes more intense and more constant or comes in more frequent paroxysms, irrespective of the presence or absence of evidences of general venous congestion.

It would seem to result from this grouping of facts, and looking at them from a reverse bearing to Moreton Stillé's point of view, that distal rather than proximal obstruction of the pulmonary artery, taken as a type, was the cause of cyanosis. Admixture of arterial and venous blood must reduce the redness of the arterial stream, just as certainly as red paint mixed with black varnish will render the black less intense: whether admixture alone ever produces a deep cyanotic hue of the surfaces is probably more than doubtful; that admixture will prevent constant cyanosis seems certain, when cases of complete transposition of the vessels with open septum ventriculorum are compared with those with closed septum, the other conditions remaining the same. General venous congestion from pulmonary obstruction or other causes outside the pulmonary tissue produces cyanosis, but of a sort quite unlike the typical cyanotic condition of malformation of the heart. It may therefore be doubted if the cyanosis seen in obstruction of the pulmonary artery is due to general venous congestion; it may be wholly produced by conditions on the other side of the obstruction--viz. want of aëration of the blood, which must ever remain the essential feature of cyanosis. This supposition allows of an easy explanation of the difference between cases of apparently equal obstruction of the artery, in some of which cyanosis is present and in others absent; it also allows of the explanation of inconstant or paroxysmal cyanosis where the obstruction, and consequently the venous congestion, is uniform and permanent.

{718}

CARDIAC THROMBOSIS.

BY BEVERLEY ROBINSON, M.D.

DEFINITION.--In general, this name is given to every deposit of coagulated blood or fibrin in one or more of the cardiac cavities. By its derivation ([Greek: thrombôsis], coagulation, from [Greek: thrombys], clot) it further implies the manner in which the coagulum is formed and all the morbid alterations connected with it.

SYNONYMS.--Heart-clot. _Fr._ Thrombose cardiaque; _Ger._ Blutgerinnungen im herzen; _Lat._ Thrombosis cordis; _It._ Trombo; _Sp._ Trumbo.

The definition offered is not wholly satisfactory, because, although it is accurate as far as it goes, it is not complete. It does not distinguish between concretions of different origin, etiology, mode of formation, and age. No separation is made between fibrinous deposits which increase from the beginning and layer by layer in the cavities of the heart, and those transported there from a distance and forming a nucleus for fresh deposits. To make the definition anything like exhaustive would require many references to the general history of THROMBOSIS AND EMBOLISM; we therefore direct our readers to that article for what relates to the common facts of these morbid processes, retaining for the present only those matters which relate specially to the heart.

Heart-clots may be formed--1, during life, when the patient enjoys, apparently, good health and strength; 2, toward the termination of life, when the general forces are evidently depressed, or at the final stage, when life ebbs low and the agony has appeared; 3, after death. These clots have therefore been divided into cadaveric clots, those of the agony, and ancient clots. To the clots of the agony exception is properly taken, for the reason that agony is a term employed with a somewhat badly-defined signification. At what period does it begin? Is it not frequently of different length? Does it always exist? The answers to these different questions render our objection proper, and show that we had better employ the word terminal for coagula of the second division.

Manifestly, the separate varieties of coagula have not an equal importance. The clots which are post-mortem productions are only interesting for their physical characters, which, fortunately, are well marked, and enable us at once to distinguish them from the two other varieties. The coagula in the first two divisions have an interest both clinical and pathological.

The ancient clots are invariably accompanied with signs and symptoms which should reveal their presence. As much might be affirmed for the terminal clots in the majority of instances and when the patient is not already in extremis. The pathological study of these varieties has great value, and especially in so far as it will the better enable us to distinguish the clots formed some time previous to death--be it of shorter or longer duration--from those which are but the result of the gradual stagnation of the blood-current in a weakened and wellnigh powerless organ. Amongst the clots which are formed in the venous system, some are transported, and pass {719} immediately through the heart, to be arrested finally in some of the larger or smaller arterial trunks, whilst others remain in situ in the heart, and are constantly increased by successive additions or layers of new fibrin or cruor.

The nomenclature to be desired is one which would assign different distinguishing names to each variety of coagulum, so that at once its origin, mode of formation, and perhaps too its age, should be exactly determined. The ancients employed the term polyp for deposits of every description in the heart, but such use of the word was, generally speaking, erroneous, since the true polyp is a very rare disease of the cardiac cavities. Bartholetti and Pissini first made use of it, and considered without doubt that the false polyps or fibrinous deposits in the heart were of analogous nature with the true polypi which are found so frequently in the uterus and nasal cavities. No doubt (as has been inferred) the term polyp in regard to these formations came into habitual use owing to lack of familiarity on the part of the older writers with the varied aspects of clots, as well as their ignorance of the distinct appearance offered by sections from them under lenses of great power. This mistake, therefore, is to-day not to be wondered at, if we duly consider how imperfect and unusual in olden times were pathological researches. Heart-clot was, as will be seen in the historical sketch which follows, the subject of numerous prolonged and animated discussions. As a result of these latter, it was ultimately believed that the great differences of appearance and formation which exist between coagula depend in great measure upon their relative age, and it is for this reason that the basis of distinction between their varieties rests mainly upon the period of time previous to a death at which they are formed. When we speak, however, of polypiform concretion or deposit, we approximate nearer the truth and indicate in a measure the local origin of a coagulum. Many others have employed the terms post-mortem and ante-mortem as being the only suitable terms with which to make a distinction between the coagula formed during active existence and those which are revealed only with the scalpel in the dead-house. In the consideration of this subject the symptoms shall be fully described which indicate the presence of heart-clot found during life, whilst in regard to clots formed in extremis or after death it is desirable particularly to show the pathological characters which shall definitely place them. For all that pertains to embolism of the heart we shall refer the reader, except when it is essential to mention certain details, to other articles in this work. Certain authors have erroneously, it is believed, regarded this subject of heart-clot as one of mere pathological interest, stating that the dead-house is the only place to study its origin and many of its organic effects. This opinion should be combated with vigor. Such a view is far too restricted, and it is here believed that the clinical aspects of cardiac thrombosis are worthy of attentive study, and that something better and further should be attained than merely to watch the downward course of a patient thus affected, and to bear in mind the pathological sequelæ of this disease.

HISTORICAL SKETCH.--The questions which have a present interest in regard to heart-clot are very different from those which formerly engaged medical attention. No longer are we uncertain as to the formation of these coagula during life, nor doubtful as to the various and important effects produced by their transport in different organs through the arterial and venous vessels. Thanks especially to the inaugural thesis of Legroux (1827), to those of Le Marchand and Ball (1862), to that of Bucquoy (1863), but particularly to the experimental researches of Virchow (1846-56) and to the observations of Senhouse Kirkes[1] in regard to the formation and transport of emboli into the cerebral vessels, these facts are all matters of ordinary information. There is little doubt that Galen had noted the formation of {720} intra-cardiac thrombi during life, and attributed to them interference with circulation and respiration, and, at times, sudden death. With the exception of Salius, mentioned by Morgagni as having remarked oedema due to this cause, we reach the sixteenth century before again meeting with any detailed mention of a similar pathological condition. Helidé of Padua, according to some,[2] Benivenius, according to others,[3] were the first authors to give full descriptions of cardiac polyps. This, indeed, was the term affixed for a long period to fibrinous concretions in the heart, beginning with Sebastian Pissini (Milan, 1654), who first employed it. The name took origin, without doubt, on account of their resemblance to polyps of the nasal fossæ, and perhaps to the animal thus named. It was particularly at this period that they acquired their significance, and became the subject of animated discussions between distinguished physicians of the last two centuries. Some, exaggerating their importance, attributed to them the gravest and most important symptoms, although a chronic affection of the heart or lungs present at the time was frequently sufficient to explain them; others, like Kerkring (1670) and Jos. Pasta[4] (1737), who contested the possibility of the blood coagulating during life, and believed they were invariably cadaveric formations, took from them even a pathological interest. This latter extreme opposition to reality originated very soon a mixed conviction, which was that held by Senac and Morgagni. These distinguished observers recognized that intra-cardiac thrombi formed both during life and after death, the former being rarely encountered. The later, or anatomical school, confirmed these views, but also added testimony to show that ancient and terminal concretions were not phenomena of such unusual occurrence as had been previously held. Testa (1810) and Kreyssig (1824) connected fibrinous deposits with inflammation of the heart, and the last-named writer described a disease which he named carditis polyposa. This view and that of Laennec, which attributed globular vegetations to an inflammatory cause, are in our day disproved. Amongst those authors who rendered certain the formation of cardiac clots during life, we should mention a few others whose names have a special importance in this connection as having made a special study of diseases of the central organ of circulation. These are Corvisart, Burns, Andral, and Bouillaud. Since this period the field of research has become far less limited, and investigations have been made in regard to similar coagulations in the large vessels of the body.

[Footnote 1: _Med.-Chir. Trans._, 1844, pp. 281-325.]

[Footnote 2: _Dict. de Méd. pratique_, vol. viii. p. 558.]

[Footnote 3: _Ziemssen's Cyclopædia_, vol. vi. p. 292.]

[Footnote 4: Quoted by Grisolle, _Pathologie interne_, Paris, 1865, p. 464.]

In 1856 a new era was established in regard to these formations, and especially with reference to their transport. Virchow at this period showed conclusively, after long-continued and accurate clinical observations and experimental researches, that a clot formed on the one hand in one of the large veins might be carried to the pulmonary artery and block up more or less completely the supply of blood to the lungs; on the other, that a portion of a thrombus formed in the left heart-cavity might become detached and plug completely one of the arteries of some far-removed organ, as the spleen or kidney, and thus give rise to those ultimate effects which we now understand under the name of infarction. Thus was first established the new pathological ideas which have become familiar with the words embolus and embolism. True it is that Virchow was not the first writer who had described the facts relating to the translation of portions of coagulum from one region to another of the circulatory system, and its fixation in a particular arterial branch. Already this subject had been clearly and succinctly narrated by Van Swieten. A passage in which the causes and mechanism of apoplexy are referred to gives lucid explanation of this doctrine: "Whatever causes change the blood, lymph, and the matter which supplies the spirits, so as they cannot pass freely through the arteries of the brain, but are there impacted. Such are {721} frequently--polypous concretions in the carotid and vertebral arteries, whether first formed about the heart or within the cranium itself."[5] These ideas of Van Swieten had not, however, produced any very permanent impression, and were almost forgotten, when Legroux (1827) promulgated his view in regard to the possibility of portions of coagulum being carried from the heart into different portions of the arterial system. He published, in fact, two most interesting cases of gangrene of the hand and forearm in which the efficient cause of the disease was found in an obliterating embolus of the brachial artery, which was evidently similar in its nature to the thrombus found in the heart of his patient. It is interesting to remark that Legroux's inaugural thesis, in which these facts were brought to light, was only the forerunner of some very complete articles on the subject of cardiac and vascular concretions, in which he goes over much of the ground which was covered in Germany by the work of Virchow. Legroux published his ulterior researches in the _Gazette hébdomadaire_, Paris, 1856, pp. 716 _et seq._ In fact, under the head of correspondence we find in No. 20 of the journal of this year (pp. 349 and 350) an interesting letter from Legroux to the editor, in which he claims for himself the priority of publication (Van Swieten excepted) of the facts pertaining to intra-cardiac thrombi and their effects due to transport of detached fragments into a region more or less removed from their place of development (p. 34). As this claim, according to my researches, appears justified, a part at least of the credit awarded to Kirkes, Virchow, and Schützenberger as discoverers and disseminators properly belongs to Legroux.

[Footnote 5: G. Van Swieten, _Commentaries upon the Aphorisms of Boerhaave_, Aph. mx., vol. iii. p. 159, ed. London, 1774.]

In spite, however, of these investigations, and those of Allibert (1828), Louis (1837), Baron (1838), and Paget,[6] who showed how the blood could coagulate in the heart and by transport block up the pulmonary capillaries, we cannot dispute the glory to Virchow of having in some sort created this study. Owing to his great sagacity, he was able to seal his studies and experiments with the stamp of a master-mind. The new words embolus and embolism introduced by him refer to a process which was previously but badly understood, and which now fix, as it were, a domain in modern pathology. The theory of Virchow found many advocates--many who were opposed to it in the beginning. In consequence of this it was the origin of numerous works undertaken in this new direction. Amongst the most important are the communication of Schützenberger,[7] the thesis of Lancereaux (1862), the great work of Cohn (Berlin, 1862), the article of Weber in the treatise of Pitta and Billroth--which contains recent theories about coagulation of the blood and the transformation of clots--and the memoir of Polaillon upon cardiac embolism (Paris, 1879).

[Footnote 6: _Med.-Chir. Trans._, 1844, pp. 162-188.]

[Footnote 7: _Gazette médicale de Strasbourg_, 1857.]

ETIOLOGY.--So soon as the blood is withdrawn from the influence of life it no longer remains fluid, but rapidly coagulates. Thus it is we find frequently after death coagula filling the cavities of the heart and extending in long ribbon-like bands into the larger vessels, more particularly in the veins. What occurs here is very similar to what we notice in a bowl which receives the blood of a venesection. Here the blood thickens rapidly, the clot forms, leaves the sides of the bowl, assumes the appearance of jelly more or less colored owing to the corpuscles enclosed in the meshes of fibrin, and is bathed in a quantity of ambient serum. A similar change takes place in the heart: the serum is imbibed by the tissues and the clot remains in its cavities.

Coagulation of the blood is a very complex problem. Many theories seek to explain it. On the one hand, it has been said the fibrin pre-exists in the blood, and by the fact of the slowing of the circulation, the reduction of the {722} temperature, etc. the fibrin separates from the blood and coagulates. Again, it is admitted that the fibrin does not exist formed in the blood, but that a fibrinogenous material is present which is acted upon by the hæmoglobin or globulin contained in the red globules, the leucocytes, and the corpuscles of connective tissue, and sometimes is, sometimes is not, caused to precipitate as fibrin (Virchow). The exact conditions which occasion the activity of the globulin are unknown. The reaction which takes place has been said to resemble that which takes place between amygdalin and emulsin when prussic acid is formed, or between myrosin and myronic acid when the volatile oil of mustard is produced. Further, it is stated, in accordance with accurate chemical investigations, that the plasma of the blood contains a substance called plasmin, which separates itself into fibrin which coagulates and into fibrin which remains dissolved in the blood (metalbumen, Robin). These fibrins are evidently of two kinds. The plasmin divides itself under the influence of slowing of the circulation, the action of acids, of foreign bodies, of oxygen in excess, etc.; it remains intact in a fluid condition when the vascular walls and globules are healthy, the blood circulating with normal rapidity, and in presence of alkaline principles.[8] According to Foster,[9] "Coagulation is the result of the interaction of two bodies, paraglobulin and fibrinogen, brought about by the agency of a third body, fibrin ferment." Schmidt concludes that when blood is shed a number of white and intermediate corpuscles fall to pieces, by which act a quantity of fibrin ferment and of paraglobulin is discharged into the plasma. These meeting there with the already present fibrogen give rise to fibrin, and coagulation results.

[Footnote 8: _Dict. de Méd. et de Chirurgie pratique_, vol. viii. p. 569.]

[Footnote 9: _A Textbook of Physiology_, p. 22, New York, 1880.]

As regards the formation of clots within the body, it is supposed that injured or diseased spots or foreign bodies first attract, and then, as it were, by irritation cause the death of, a certain number of corpuscles.[10] The views of Schmidt of the fibrino-plastic function of paraglobulin are not accepted by all investigators; and some authors believe that the fibrinogen as well as the fibrin ferment arises from the white corpuscles.[11]

[Footnote 10: _Pflüger's Archiv_, vi. (1872), p. 413; xi. (1875), pp. 291 and 515; xiii. (1876), pp. 93 and 146; quoted by Foster.]

[Footnote 11: Frédericq, L., _Recherches sur la Coagulation du Sang_, Bruxelles, 1877, quoted by Foster.]

According to Bristowe,[12] the frequency of sanguineous concretions does not depend upon sex, but is in a certain relation with age. He has remarked, for example, that they are proportionately more often met with at the extremes of life than toward middle age. This might be explained satisfactorily, perhaps, on the supposition that at these periods the circulation is at times very feeble, owing either to congenital feebleness on the one hand or chronic organic affections on the other. At all events, when we seek for the causes which have most influence in determining the formation of cardiac concretions previous to death, we find--I. the mechanical, or those which act specially in slowing the current of blood through the heart. These causes may exist within the heart or may be removed from it. II. The vital or pathological. These causes are of somewhat difficult determination at times, and pertain usually to affections in which there is notable blood-change, in which the quantity of the fibrin has been augmented absolutely or relatively, or to those of infectious type--viz. diphtheria; or to those constitutional in nature--phthisis, cancer, etc. III. The inflammation of the endocardium or endocarditis. This is admitted by Andral, in a note upon the etiology of cardiac concretions in the work of Laennec, as having special importance. Bouillaud also attributed their formation in certain cases to the chemical action of pus which was present in the economy.

[Footnote 12: _Pathol. Society's Trans._, vol. xiv. p. 71, quoted by Bartholow.]

{723} I. Amongst the mechanical causes we should mention all organic lesions of the heart, all obstacles in the pulmonary circulation, and possibly, by analogy, certain badly-defined lesions of the pneumogastric nerves. All the stenoses and dilatations of orifices, all irregularities of the valves or heart-walls, all depressions or roughened parts of the walls,[13] may determine the beginning of a concretion. In the same way, a small mass of fibrin deposited on a calcareous valve after transport from one of the veins of the limbs may originate a voluminous heart-clot. Dilatation of the heart, pericarditis, every cardiac change which weakens the contractile power, is a predisposing cause of cardiac thrombosis. Every organic lesion of the heart tending toward that final stage of asystolism so often encountered, and which weakens so greatly cardiac contractility; pouching of different portions of the cardiac wall, or aneurism; pressure upon the right heart by a mediastinal tumor or a sacculated aneurism of the arch of the aorta,[14]--all these have great power in producing intra-cardiac thrombi. The mechanism of these different lesions was familiar to Kreyssig, Laennec, and Hope. At the same time it must be admitted that these changes in the heart are not of themselves always sufficient to give rise to fibrinous deposits. We encounter stenoses and regurgitations at orifices very frequently, and concretions, on the other hand, are relatively rare. Moreover, we find heart-clot at times when there is no cardiac alteration. We believe, therefore, that the heart lesion is an aiding factor--that in the last moments of life, when the force of the heart's contraction is weakened and the conditions of the blood favor coagulation, they will act with special power.

[Footnote 13: _Pathol. Society's Trans._, vol. xiv. p. 71, cases by J. W. Ogle.]

[Footnote 14: Walshe, _Dis. of the Heart_, Lond., 1873.]

Among the mechanical causes which are removed or distant should be mentioned all those which interfere with the pulmonary circulation. Such are the effects left behind by pneumonia, pleuro-pneumonia, or the compression of the blood-vessels by old congestion of the lungs. In these cases, when the vis a tergo is impaired somewhat, and an obstacle is placed in the pulmonary capillary circulation, even if cardiac thrombosis does not directly result at first, we may have thrombi form in the pulmonary veins. In the same way, the nervous affections which are accompanied with slowing of the circulation tend to produce coagulation of the blood. All lesions, as we have said, of the pneumogastrics act in the same direction. In proof of this we should cite the experiments of Meyer of Bonn, of Longet, and of Blondet, who produced fibrinous concretions in the hearts of animals by tying or cutting the pneumogastric nerves. At the same time, the heart-beats became more rapid, wavering, unequal, and less energetic than in ordinary physiological conditions. After all, however, all these mechanical causes are but predisposing causes, for they do not always produce cardiac concretions. Frequently, as we have said already, the obstruction to the circulation may be present, and yet at the autopsy no fibrinous deposit be found in the heart. In order that the mechanical causes act efficiently to produce coagula, it is essential that they be aided by the conditions of the blood which favor it.

All concretions do not form with the same rapidity nor are they of the same size. At times their production is sudden, and but a few hours elapse before the fatal termination is reached. Again, it is affirmed that weeks, and even months, may pass before the concretion has reached a volume sufficient to cause entire stoppage of the heart's contractions. In the former category are found, of course, the softer, least consistent coagula--usually, however, very voluminous; in the latter are the smaller, more elastic, and resistant concretions, at times even presenting a stratified structure[15] and {724} surrounded habitually by a clot formed during the latter moments of life, and having a large proportion of cruor in its composition. The heart affected with fatty degeneration should, if we consider its weakened power and deficient contractility, be a predisposing cause of stagnation first, and finally of the formation of intra-cardiac thrombi. As a matter of observation in the dead-house, however, such hearts are not frequently accompanied with fibrinous deposits in their cavities.

[Footnote 15: According to Legroux, roughening of the walls or valves gives rise to stratified coagula of moderate size, or else to those small clots which deposit on the surface or margin of the valves (_Dict. Encycl. des Sci. méd._, article "Concrétions sanguines," Paris, 1876).]

All diseases which by their nature and duration produce great exhaustion of the vital powers tend strongly to produce fibrinous coagula in the heart. This is eminently true of those which at the same time do not occasion a diminished plasticity of the blood. It is often assumed that mere stasis in the blood-current through the heart is essential to the formation of clots in its cavities, and to lend support to this belief reference is made to the phenomena which take place in bleeding. It is not true, however, that stasis is necessary to coagulation, and the proof is afforded when we take a bundle of twigs and by beating the blood forcibly produce the separation of the fibrin. Besides a slowness of the circulation, there must be, once again, an obstacle in the heart itself, and even then polypoid concretions are not always formed.[16]

[Footnote 16: _Gaz. hébdomadaire_, Paris, 1856.]

II. The Vital or Pathological Causes.--In this class of conditions leading to cardiac thrombosis are included all diseases in which certain special changes have taken place in the blood itself. Among these we should mention, first, certain sthenic inflammatory affections in which the proportion of the plasmin (fibrin and metalbumen) is notably elevated, and in which, on this account, there is a strong tendency to the separation of fibrin from the blood and to the formation of cardiac concretions. In fibrinous pneumonia and acute rheumatism this is particularly true, and amongst the numerous accidents we have to dread in the course of these diseases none strike us with more dread than the possible production of intra-cardiac thrombi. In fibrinous pneumonia this complication is so frequent that Bouillaud has enunciated the following pathological law: "Fibrinous concretions exist constantly in patients who succumb to a frank, acute pleuro-pneumonia, well characterized, which has reached the second stage."[17] According to Raynaud, this is without question a great exaggeration, and results from the confusion this learned author evidently made between terminal clots and those formed some time previous to death. Nevertheless, there is here a proof of the great frequency of coagula occasioned by this disease, and of the strong tendency to their formation which the condition of the blood must afford. What we have said of fibrinous pneumonia and acute articular rheumatism is not true, singular to say, of lobular or broncho-pneumonia. The lesions of this form of pneumonia are those of a catarrhal inflammation of the lung, and the blood does not offer during its course the remarkable tendency to coagulation that is shown in fibrinous pneumonia. Usually, the heart-cavities and the vessels are filled after death with a liquid of a black or violet-brown color, very often sticky.[18] The fibrin in the heart-cavities in pneumonia is fibrillar, and does not present those changes which indicate that it has been deposited for a long while. Moreover, these coagula do not present physical characters which show any considerable degree of age. They are usually terminal coagula, or at least formed within a few days of the fatal termination. Do globular vegetations occur in pneumonia? At times they do, but they are at least very rare as compared with the fibrinous conditions just referred to.

[Footnote 17: _Gazette méd._, 1843, vol. xi. p. 270, quoted by Armand, _Thèse de Paris_, 1857, p. 41.]

[Footnote 18: Damaschino, _Thèse de Paris_.]

There are other general conditions in which there is a marked tendency to {725} the formation of cardiac coagula. In the puerperal state, according to Simpson, it is occasioned by the resorption of many new elements which vitiate its composition and thus occasion this result. In the poisoning following upon glanders or pyohæmia intra-cardiac thrombi are often found. Lancereaux has found in this latter disease fibrinous deposits in the right ventricle and pulmonary artery around small masses composed of pus-cells. In the different cachectic states, such as those caused by chronic Bright's disease,[19] advanced phthisis, and cancer, although we have a diminution in the proportion of red globules, there is present at the same time a relative increase of fibrin; and the consequence is that concretions are often formed in the heart. In fact, it is in these cachexiæ that we often encounter those fibrinous cysts which will be described under the title of Morbid Anatomy.

[Footnote 19: Here the retention of the excreta is an important factor in the formation of cardiac thrombosis (Bristowe).]

Many well-known authors have declared that diphtheria was very powerful in producing fibrinous concretions in the right heart some time previous to death. Among those who have written specially on this subject we would mention Winkler,[20] Richardson,[21] Meigs[22] and Robinson.[23] According to the latter writer, elastic fibrinous clots twisted in the valves and adherent to the cardiac walls are developed frequently in children at a period quite removed from that of the agony, and at a time when they are not as yet in a condition of extreme weakness. Except in exceptional instances this influence of diphtheria to produce cardiac coagula is doubted by Parrot.[24] He admits its power, particularly when it is complicated with membranous croup, and in these examples he believes the precocious formation of coagula is determined probably by the asphyxic condition. Whilst denying the influence of diphtheria, Parrot freely acknowledges that measles, especially when complicated with broncho-pneumonia, tends to produce cardiac concretions. The same tendency is recognized by Harley in the early stage of scarlet fever where there is high pyrexia.[25]

[Footnote 20: _Die Bluthlumpen dann der Häutiger Bräune_, Wien, 1852.]

[Footnote 21: _Med. Times_, vol. i. p. 23, 1860.]

[Footnote 22: _Am. Journ. Med. Sci._, April, 1864.]

[Footnote 23: _De la Thrombose cardiaque dans la Diphthérie_, Paris, 1872.]

[Footnote 24: _Dict. Encycl. des Sci. méd._, vol. xviii. p. 484.]

[Footnote 25: _Medico-Chirurg. Trans._, vol. lv.]

Notwithstanding the diminished proportion of fibrin in typhoid fever, and the impossibility of explaining, in many cases, any increase of the plasticity by local inflammatory disorders, cardiac concretions have been observed by Huss, Virchow, and Hardy.[26] Bucquoy also relates, after Huxham, an epidemic which reigned at Plymouth in 1742 amongst sailors who came from a long cruise, characterized by dyspnoea, cardiac palpitations, and intermittences of the pulse. Many of those attacked died, and at the autopsies made polypoid concretions of considerable elasticity and adherent to the walls of the heart were found. Another similar occurrence took place amongst the soldiers of the garrison of Rocroy in 1746. Quite a number succumbed after having shown symptoms similar to those of the sailors of Huxham. Cadaveric sections discovered in the left ventricle several hard, consistent cardiac thrombi.

[Footnote 26: Quoted by Bucquoy, _Des Concrétions sanguines_, Paris, 1863, p. 36.]

III. Endocarditis.--Whatever may be the opinion of different authors in regard to the frequency of endocarditis when intra-cardiac thrombi are present, it is certain that if it does exist the explanation of the presence of these deposits is clear and ample. In endocarditis we have both a local and mechanical cause and also a vital condition of fibrinous deposits in the heart. As a mechanical cause we know that often it is the cause of the stenoses of orifice which are present, and that further, by its effect in producing roughening or fissuring of surface, it offers a strongly predisposing cause of the {726} deposit of fibrin. Ulcerative endocarditis acts still more efficiently in this direction, owing to the fact that it produces its effects as much on the surface of the valve, aortic and mitral, near the adherent portion and in the neighborhood of the cardiac orifice, as between its layers. The result is, that the surface is rough, unequal, presenting often cauliflower excrescences, and showing sometimes, in the midst of a mass of fibrin that has become deposited by degrees, portions of a softened, partially-detached valve which was the nucleus of the outer layers of fibrin. Further, endocarditis of both forms acts as a vital and efficient cause of cardiac thrombosis, in that it belongs to the class of inflammatory diseases which occasions an absolute increase in the proportion of fibrin of the blood (from 25/1000, concrete fibrin 3, and metalbumen 22, to 56/1000, concrete fibrin 17, metalbumen 36); and also, more especially in ulcerous endocarditis, by the transport of infectious materials into the blood, which still further tend to cause coagulation.[27]

[Footnote 27: At times there is complete deprivation of epithelium over a limited area, and in rare cases slight ulcerations of membrane. These two conditions are efficient factors of the exudation of plastic lymph.]

SYMPTOMATOLOGY.--According to Laennec,[28] it is equally erroneous to attribute to cardiac thrombosis many symptoms which properly belong to an organic lesion of the heart (notably hypertrophy) as it is to believe that intra-cardiac thrombi never begin to form until the terminal period of life. According to him, Haller, Vinckler, Staneari, and Bonaroli[29] have observed obliterations of the internal jugular vein and carotid artery by very firm concrete fibrin, and he himself has seen a similar production in the inferior vena cava for the space of four fingers' breadth. Although these concretions were evidently formed during life, they occasioned no symptoms indicative of their presence, nor were there any obstructions in the course of the circulation which could explain their origin. Reasoning from these facts and from the phenomena which occur in aneurismal tumors, it seems highly probable that the blood should coagulate in the heart also during life. Later writers frankly admitted that coagulations in the veins caused partial dropsies, a usual instance of which is the white swelled leg, or phlegmasia alba dolens, from obliteration of the femoral vein.[30] This is not invariable, for I have seen, in patients who have succumbed to diphtheria, both venæ cavæ obstructed by coagula, without having observed during life either local or general oedema.[31]

[Footnote 28: _A Treatise on Diseases of the Chest_, p. 183, Philada., 1823.]

[Footnote 29: Quoted by Morgagni, _Epist._ 64.]

[Footnote 30: Vide Bouillaud, _Archiv. gén. de, Méd._, t. ii. et v., quoted by Hope.]

[Footnote 31: _Thrombose cardiaque dans la Diphthérie_, Paris, 1872, p. 43.]

Scarcely any contemporary author doubts that cardiac thrombosis gives rise to more or less well-defined symptoms. What these are we shall now consider. Of course we are far less liable to-day, when the diagnosis of organic cardiac disease is so accurate, to attribute to intra-cardiac thrombi the signs, physical or rational, which properly belong to them, and which ancient observers could not differentiate. Nevertheless, there are complex cases in which one is at fault even in regard to this problem.

The symptoms of cardiac thrombosis vary naturally with their size, situation, and rapidity of formation. Certain authors have affirmed, for example, that the concretions formed in an auricle cause a greater amount of interference with the circulation than those elsewhere situated. This they do partly by reason of their size and the less contractile power possessed by the auricle, partly because from the auricle prolongations are sent off which occlude the cardiac orifices. When cardiac concretions form suddenly a few days previous to death, they always aggravate all the symptoms of an obstructed circulation.[32] If the case be one of pre-existing disease of the heart, they soon obliterate the cardiac cavities and lead to a rapid fatal {727} termination. According to Grisolle,[33] when the concretions are small and form an obstacle neither to the play of the valves nor to the cardiac circulation, they are not revealed by any appreciable functional trouble. The opinion of Grisolle in regard to small coagula is also shared by Legroux, especially when they are fixed at a distance from a cardiac orifice or concealed in a sinus. When, however, the thrombi are larger and interfere more or less with the course of the blood, they occasion very marked symptoms.

[Footnote 32: Hope, _On the Heart_, p. 486, Philada., 1846.]

[Footnote 33: _Pathologie interne_, p. 467, Paris, 1865.]

Even before the days of auscultation there were certain rational signs which were dwelt upon with much force as showing the presence of cardiac concretions. Thus, Senac[34] writes that the patients thus afflicted feel a weight or oppression in the præcordial region which sometimes becomes extremely painful. Palpitations and irregularities of the pulse were also noted as symptomatic of these productions. Laennec believes that coagula of any size may be recognized; "when, in a patient who till then had presented regular pulsations of the heart, these suddenly became so anomalous, confused, and obscure that they can no longer be analyzed, we may suspect the formation of a polypous concretion."[35] He further adds that if the trouble takes place on one side alone of the heart, the fact is almost certain. When the coagula occupy the cavities of the right heart, the sounds of the left heart may remain normal whilst those of the right side are more or less distant and muffled (Legroux). Several authors, amongst whom we should mention Legroux, Bouillaud, Barth, and Roger, have mentioned amongst the physical characters which show the existence of intra-cardiac thrombi the sudden development of a blowing murmur limited to the præcordial region or propagated into the aorta. Sometimes this bruit was soft, sometimes harsh and rough. These writers have also noticed, in conjunction with grave general symptoms, the doubling of the first sound of the heart, making occasionally a sort of galloping murmur. As regards the recognition of concretions on one side alone, I acknowledge that after auscultating carefully several cases in which the autopsy showed coagula formed during life, I have been unable to note signs sufficient to justify a differential diagnosis.

[Footnote 34: _Traité de la Structure du Coeur, de son Action et de ses Maladies_, t. ii. p. 470 _et suix_, quoted by Bucquoy.]

[Footnote 35: _De l'Auscult._, t. ii. p. 597, quoted by Hope.]

The distinction appears to me difficult in like cases, for how explain that a trouble so considerable, even though it exists on one side only, should not influence the entire cardiac circulation? Moreover, it should be emphasized that the phenomena dwelt upon do not always manifest themselves when the cardiac contractions are perfectly normal. The heart-beats may be increased in frequency and the rhythm be changed. The passage, therefore, from a state of relative calm merely to that of extreme agitation is appreciated less readily. This is particularly true of the symptoms usually described as pertaining to the presence of terminal coagula. For here, at a period approximating the fatal termination, it is wellnigh impossible to determine accurately special symptoms. For this reason it is not surprising how authors have varied in their descriptions, and at best none of them are completely full and satisfactory. I have myself many times sought to recognize the blowing murmur given by Bouillaud as a physical sign of cardiac concretions, but in not a single instance have I been able to satisfy myself as to its existence. True it is that the cases I have watched with greatest care were those of children affected with toxic diphtheria, and it is possible, on account of the infrequency of valvular diseases during childhood, that more than once there may have been confusion between the signs afforded by newly-formed thrombi and those which belonged exclusively to a pre-existing disease of the endocardium.

Moreover, these murmurs have been heard and described by too many good {728} observers (Walshe, Flint, Richardson) for any small negative evidence to weigh against that which is very positive. Sometimes they have been but the exaggeration of a bruit previously heard and which characterized an organic affection of the heart. Sometimes the presence of the thrombus has caused the diminution or complete disappearance of the pre-existing structural murmur. Again, these murmurs are discovered for the first time when the other signs indicate the existence of intra-cardiac thrombi. When they are heard under these circumstances they prove positively that the coagula have sent prolongations between the cavities of the heart or into the great vessels, so as to prevent the accurate coaptation of the valves or to obstruct the onward current of the blood. In the first case a regurgitant murmur is occasioned, tricuspid or mitral, which is heard at the apex; in the second case a basic murmur is detected, which is pulmonary or aortic. Usually these murmurs are systolic, although they may in rare conditions be diastolic. The murmurs have been heard more frequently on the right side of the heart, and have pointed by their location of greatest intensity to the obstruction of the infundibulum and pulmonary orifice. They are then basic or suprabasic, and carried upward toward the infra-clavicular region on the left side. These murmurs are heard very rarely on the left side--so infrequently, indeed, that Walshe cannot affirm that he has ever observed clinically one in this region. Theoretically, of course, such murmurs may be heard at any spot in the præcordial region, and with the first or second sounds provided their size and position in relation to orifices or valves could sufficiently account for them. Whilst there can be little question that murmurs do take place in the præcordial region wholly due to the presence of heart-clot, it is probable that their frequency and diagnostic importance is less than superficial consideration would cause one to believe. Thus, Flint[36] states that "the presence of coagula may occasion an endocardial murmur, but as a rule it is wanting, probably in consequence of the enfeebled action of the heart." Richardson[37] holds an analogous opinion, and writes: "There are sometimes abnormal sounds, but it is difficult to distinguish these from murmurs the results of valvular lesions." Walshe[38] is at variance with this view, especially in regard to the thrombal de novo murmur, and has "heard such a murmur when the examination post-mortem showed the fibrinous coagulum as the only probable cause of it."

[Footnote 36: _Disease of the Heart_, Philada., 1870, p. 280.]

[Footnote 37: _The Coagulation of the Blood_, Lond., 1858, p. 428.]

[Footnote 38: _Op. cit._ (foot-note).]

Auscultation.--In the heart the single, constant sign that has been observed consists in the modified tonality of the normal sounds. These are rapid, irregular, muffled, obscured, and distant. There is notable inequality also in the strength of successive beats, which is obviously explained by the great difficulty the blood encounters in traversing the heart. Now, as I have seen in frequent autopsies that the valvular mechanism of the left heart is ordinarily free from any fibrinous deposit, it is readily understood that it can produce the two sounds normal as regards situation and time, but greatly modified in transmission.

Percussion.--Percussion, except in particular cases which are rare, and in which the cavities are much distended by their contents, will only furnish us with negative signs. When the ventricles are swollen by large coagula, the percussion dulness will be extended laterally. As the right cavity is usually the seat of the deposit, it will be particularly marked toward the right of the sternum. In those instances where the area of præcordial dulness had been determined before the formation of the fibrinous concretion this extension becomes a physical sign of great value. It is to Piorry and the use of the plessimeter that we owe whatever of exactness belongs in like cases to this method of examination.

{729} Inspection and Palpation.--The cardiac impulse may be unaffected by the presence of the thrombus, and if it has been regular in rhythm previous to its formation it may still remain so. This condition is infrequent, however, and usually the pulsations become irregular, tumultuous, and rapid. The force of successive beats will also be different. These signs can be determined by the sight and touch.

Pulse.--The characters of the pulse are variable. Sometimes it presents manifest inequalities, occasional intermittences, and is extremely frequent. It may be quite feeble in the beginning, and afterward gain in strength. Sometimes, in spite of its weakness and depressibility, it retains its regularity and its rhythm is unchanged. The coagulum existing in the cardiac cavities, especially on the right side, explains the variations of the pulse. Effectively, at each contraction of the ventricle this chamber, containing a less quantity of liquid blood, projects a smaller amount of venous blood to the lungs. Besides, this quantity is insufficient to replace the volume of revivified blood which leaves the lung with each inspiration. Soon the left cardiac cavities contract with but small power upon an amount of blood below the normal, and yet it is with this supply that the left heart must satisfy the needs of all the organs. The arteries during life become nearly empty, and it is to this condition, as well as to the lack of synchronism between the action of the two sides of the heart, should be attributed the signs we recognize in the characters of the pulse.[39]

[Footnote 39: Robinson, _loc. cit._]

In some instances of cardiac concretions the sonority of the chest remains normal. In others it is obviously augmented, and even by percussion very lightly performed a sound of raised pitch is produced. According to Richardson, this acute emphysema is the direct result of an insufficient blood-supply in the capillaries which surround the pulmonary alveoli. Whilst such a condition may often be observed amongst children, it is not unknown with adults. The affirmation, therefore, of Walshe, that it can only be observed in young people, and that in adults its place is supplied by considerable pulmonary congestion, is not exact. Since Richardson first called attention to the exaggerated sonority of the lungs in cases of heart-clot, other observers have also referred to it. Lavirotte (1864) particularly has insisted on it as a proof of fibrinous deposition in the right heart, and has demonstrated with pathological specimens that it was occasioned by the exsanguinated state of the lungs and their hyperdistension with air.[40] On the other hand, Raynaud[41] states that when the left cavities are the seat of the concretion there is considerable stagnation in the lungs, and they show signs of great congestion. Thoracic percussion becomes less resonant, and subcrepitant râles are heard in an extended area. Sometimes, even, a moderate hæmoptysis takes place. These signs of emphysema on one hand, of congestion on the other, are not spoken of by the majority of writers on this subject; yet when they are present they will serve to fix our diagnosis and render it more certain. With respect to emphysema, especially amongst children, we should mention its great frequency, and on this account perhaps proper value has not been given to it when found at the autopsy of a child whose death has been occasioned by cardiac thrombosis. When the cardiac thrombus is present in the right side of the heart, Legroux[42] has shown that there will be a more or less turgid condition of the veins of the neck, and perhaps also of the right upper limb. With this distension of the veins we shall remark, according to him, a partial or general infiltration of the subcutaneous tissues. Sometimes the oedematous condition is limited to the face and neck; occasionally it extends below the diaphragm, especially on the right side of the body. The extent of the oedema will depend upon the number and size of the prolongations which are {730} given out by the main coagulum. Occasionally these prolongations have been found not only blocking up the pulmonary artery, but also filling one or both venæ cavæ and branching out as far as the jugular and subclavian veins.

[Footnote 40: _Congrès Medico-Chirurgical_, Lyon, 1864.]

[Footnote 41: _Dict. de Méd. et de Chirurgie_, vol. viii. p. 573.]

[Footnote 42: _Gazette hébdomadaire_, 1856.]

In my own observations I have always found the veins of the neck manifest, without in a single instance reaching any great size, and never have I noticed the prominence of the eyes noted by Walshe. In these cases cyanosis was limited, and was notable in a marked degree only upon the lips, the cheeks, and in the upper extremities. The general or local infiltration of tissue I have never remarked, although closely looked for on several occasions. Some authors, indeed, have described a bluish appearance of the entire surface of the body, together with signs of general infiltration. The explanation given of these phenomena is that there is a general obstruction of the capillary circulation, and that the return of the venous blood to the cavities of the heart is rendered almost impossible. In other words, we have here a well-marked asphyxic condition. If this be true, it is only partially so, and there must be great variation in different instances of fibrinous deposition in the right heart. The rational symptom which was for me one of great value in the diagnosis of these cases was that of excessive pallor, not only of the face, but of the limbs and the entire trunk. This pallor appeared constantly to increase until the last moments of life.

Richardson indeed says the symptoms are those of syncope, not of asphyxia. The different processes of life are arrested on account of a simple absence of arterial blood, not owing to the presence of blood unfitted to reconstitute the tissues. The tendency to fainting is probably due, therefore, to the fact that the right ventricle being more or less completely filled by a fibrinous coagulum, the blood is prevented from passing through its cavity and entering the lungs. As a result, there will be but a relatively small portion of blood which becomes oxygenized after each right cardiac systole. When the clot occupies the left ventricle and auricle, there will be a reflux of blood into the pulmonary tissue, thus causing great congestion of this structure. So intense will this congestion become that occasionally hæmoptysis results and pulmonary apoplexy may be developed, due, doubtless, to rupture of the capillary vessels. This condition occurs before the right heart is much or at all obstructed by coagula. We can appreciate that the physical signs must, if properly noted, show manifestly in which cavity the clot is located. If it be in the right heart, anæmia and emphysema of the lung should follow; hence breathlessness and increased pulmonary resonance. If it be in the left cardiac cavity, the lungs become engorged very rapidly, and we should find dulness on percussion, moist râles, and perhaps an equal or even greater amount of dyspnoea.

Difficulty of breathing appears to belong as well to the symptoms which indicate cardiac thrombus on one side of the heart as to those which characterize its presence upon the other. This symptom was first accurately described by Hope, since his day by Richardson and Meigs.[43] It has something special in its features which strikes one particularly, but may deceive unless closely observed. It takes place not because the movements of the thorax are interfered with, not because the entrance of air into the lungs is prevented, for the vesicular respiratory murmur is easily distinguished, but because the amount of blood furnished by the pulmonary artery is diminished. The anguish of the patient is sometimes terrible. The nares dilate, the chest expands spasmodically with each inspiration, and the patient is agitated, moans, and shows that extreme craving for air described by Van Swieten in the summæ anxietates. Under these circumstances, Hayden[44] states, the surface is cold, and often humid with perspiration. Pain and great oppression {731} in the præcordial region have occasionally been referred to, as in the patient of Beau, who said, in placing his hand to his chest, "I have there a weight which has suddenly formed and which stifles me." Often the anxiety is extreme, and the painful sensations continue to increase steadily until death occurs. In rare instances the suffering, when it has reached a certain degree of intensity, may remain stationary, or even become considerably less. If such a respite occur, it is only temporary, however, and the anguish soon recommences. In milder cases sometimes, and apparently after dissolution or disintegration of the clot, the severe symptoms may by degrees disappear, and from this period the patient makes a steady, uninterrupted march toward recovery. I have only lately witnessed a similar example in a youth attacked with typhoid fever, which had reached the third week. There are constant and intense effort to breathe, extreme restlessness, and the patient will throw himself from one side of the bed to the other, and scarcely remain quiet for a few moments. These symptoms are usually more developed when there is concomitant cardiac disease of organic nature, and unless this be present may not be so pronounced as to concentrate attention upon them.

[Footnote 43: _Am. Journ. Med. Sciences_, April, 1864.]

[Footnote 44: Cases 106, 107, and 111.]

The brain scarcely shows the effect of congestion when the patient dozes for a few moments even in the midst of his great distress. These times of repose are frequent, but very temporary. In a little while the patient goes off in delirium or has a convulsion. Again, he relapses into coma, in which state death may take place. In some instances there has been obstinate vomiting during several days preceding a fatal termination. It is possible that this symptom favored the rapid development of the thrombus.

The preceding signs and symptoms will sometimes declare themselves suddenly in the midst of an inflammatory or cachectic affection, and will then point directly to the presence of a cardiac thrombus of considerable size which has rapidly formed, and which obstructs an orifice or interferes with the normal play of the valves. Again, there are all the physical evidences of an old organic affection of the heart, or those of acute endocarditis or pericarditis, and rapidly all the symptoms referable to the heart become greatly increased, whilst orthopnoea, pallor, and coldness of the extremities take place. If a careful examination of the chest reveals no intercurrent and pulmonary nor superadded cardiac affection, we may then fairly assume the existence of an intra-cardiac concretion. Nevertheless, we should remember that in many of these cases there is a close resemblance of the symptoms with those occasioned by a sudden rupture of one of the chordæ tendineæ in the course of acute endocarditis (Walshe).

We should not lose sight of the fact that at times a clot will form in the heart without giving rise to manifest symptoms unless the attention be specially directed to its formation. This will be true in instances where the coagulum forms slowly, is small, or occupies a place removed from orifices or valves. In a cardiac sinus, for example, a coagulum of inconsiderable size may remain fixed and latent for a long period. Such is not the case, as we already have shown, when the coagulum fills in