Chapter XXVI: Part 26

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.