Volume 3 — DISEASES OF THE RESPIRATORY SYSTEM. (continued 11)

Beside infarctions originating in cardiac disease there are others of peripheral origin, as in the puerperal condition from phlegmasia dolens. Hæmoptysis is a rare symptom in such cases, but when it does appear it has the same basis. It is seldom severe, and soon merges into an expectoration of pneumonic character, with the clinical forms of embolic pneumonia, or possibly of abscess or gangrene of the lung.

PATHOLOGY.—Incidentally, the pathological relations of hæmoptysis have been already indicated as being connected with phthisis and cardiac disease—principally with the former. If phthisis be an infectious or specific disease, as a large and growing professional opinion claims, hæmoptysis has its specific relations with it. Few symptoms have greater differentiating force than it has. Its occurrence, outside of well-known cardiac or dyscrasic disease, removes any case of primary pulmonary disease from the category of simple inflammation. There may be much more congestion in bronchitis, more catarrhal products in simple catarrhal pneumonia, and more fibrinous or croupous exudation in pneumonia, than in the primary stages of phthisis, and yet no hæmoptysis appear. The mechanical conditions are present in greater degree, but the infective element is wanting. Its closest affinity is with apex pneumonia or alveolar catarrh, yet probably most of such cases occur without it. A blood-dyscrasia contributes an important element in the pathogenesis of hæmoptysis.

In cardiac hæmoptysis the pathology is more simple. Extreme mechanical conditions of obstruction and reversal of the circulation are reinforced by nutritive changes of the vessels and heart, until the so-called cardiac cachexia is established. There is no infective element, and such cases are seldom if ever followed by phthisical destruction.

MORBID ANATOMY.—Reference has already been made to anatomical changes having direct or indirect relation to hæmoptysis, such as those in the blood-vessels. The anatomical basis of the slight hemorrhages of the early stage of phthisis is seldom if ever discoverable. The belief in vascular fragility and congestion with special origin rests much more upon clinical reasoning than demonstration. The large hemorrhages are now and then fatal within short periods of time or instantly, and we then have the opportunity of noting the general appearance of the lungs.

It is notable that cases are not very frequent where the source of the bleeding has not been found by the most careful search. The general appearance varies according to the length of time that has elapsed since the bleeding which preceded death.

In the cases immediately fatal the tubes are filled with fresh blood, which has stained the mucous membrane and has changed the general surface of the sections of lung into a dark, mottled, or patchy color. The greater amount of blood is to be found in the lung from which it has primarily come, but in the more profuse hemorrhages, and particularly where there has been time for the struggles of the threatening suffocation, much blood may either overflow or be inhaled into the other lung and carried into the extreme portions of the air-sacs. If the flow be not overwhelming, the patient may survive long enough to allow other effects from the blood, which has by gravitation or insufflation been carried into certain parts of the lung. We are indebted to Reginald E. Thompson⁶² for the most important study of the secondary effects of the blood thus remaining. He says that the relics of blood are to be found in the presence of hard nodules, often deeply, though not always, pigmented. They are mostly found at the summit and middle part of the upper lobe, the middle axillary region, between the third and fifth ribs, close to the pleura, the anterior inferior border, and the middle part of the base corresponding to the summit of the arch of the diaphragm. "Absorption, decoloration, and fibrination go on; the outlying portions of the blood disappear; the central nodules become hard and white, and alone remain to show what has taken place." They are in some cases of varying color, slight red or of an ivory white, mottled with old blood-pigment, around the bronchioles especially, and in the shape of small black granules. Microscopically, they consist of "a group of alveola firmly packed with a semi-opaque, homogeneous fibrinous material, and there is some thickening of the alveolar tissue and also of the interlobular tissue, which thickened tissue forms the limiting capsule."

⁶² Op. cit., p. 46, etc. These researches are an important epoch in the history of hæmoptysis.

The ultimate fate of these nodules is variable. Sometimes they go on to formation of cavities, or softening occurs around the periphery or in the centre, and leads to general liquefaction of the nodule, or they may separate from the surrounding tissue by traction. Sometimes the effect of retention of the blood in the air-passages is a catarrhal pneumonia, with the ordinary anatomical proofs of it referred to in the paragraph on modes of termination of hæmoptysis.

Accepting the observations, we have the demonstration of a phthisis ab hæmoptoe.

The morbid anatomy of cases fatal from rupture of aneurisms of the branches of the pulmonary artery has been made prominent by the researches of Rokitansky and Rasmussen.⁶³ He describes small sac-like aneurisms and ectasias situated in the vessels running along the wall of the cavity. The aneurisms have the shape of a bag and an even surface. The walls of the unbroken aneurisms are of great thickness, and those of the broken ones thin. The opening is always found on the most protruding part of the sac; the edges are thin; their size varies from a pea to a small orange. Powell⁶⁴ says a microscopic section taken from a specimen in an early stage shows new connective-tissue elements, causing induration affecting the whole thickness of the wall and obscuring the distinction between the coats. The wall is brittle, becomes thinner from want of support, and yields to an inciting cause, with rupture and death as the result.

⁶³ Edinburgh Med. Journal, 1868–69.

⁶⁴ Trans. London Pathological Society, vol. xxii. pp. 54, 55.

The morbid anatomy of cardiac hæmoptysis is found mostly in two conditions—that of degenerated, atheromatous, varicose blood-vessels, brought about by the condition of chronic obstruction and increased venous tension in valvular disease; and in that of pulmonary infarction.

The first prepares the way for diapedesis or rupture, and consequent hæmoptysis. The rupture takes place in the parenchyma, or, as the anatomical details formerly given make probable, from the blood-vessels of the bronchial mucous membrane also.

Pulmonary infarction is recognized by a dark, dense, pyramidal or wedge-shaped area of varying size situated at the surface of the lung, with the base of the pyramid coming to the pleura. It is found oftener in the lower lobes and in multiple form. It is caused by an embolic obstruction of a terminal branch of the pulmonary artery; sometimes by a thrombosis or by both. A venous reflux from the neighboring districts is supposed to fill the empty vessel, and after a certain time has elapsed changes are supposed to have occurred in their walls by which the blood escapes into the air-cells and interstitial tissue. Litten's⁶⁵ explanation, sustained by his experiments, is that the venous reflux, after a closure of the pulmonary artery, is by no means necessary to the formation of an infarction. The infarction fails if the pulmonary artery and the bronchial artery, and those arteries lying outside the lungs, but in circulatory connection with them—the pleural—are simultaneously shut off. If the whole arterial supply be thus taken away, but a living connection be maintained by means of the veins, an infarction does not follow, while it immediately follows if, at the same time with the open veins and closed pulmonary arteries, the collateral or supplementary circulation be kept free. A venous reflux cannot occur so long as a circulation in the capillaries of the lung is sustained by collateral arterial branches. The explanation is that in an unobstructed circulation the entire resistance which is offered to the blood-stream in the capillaries of the lung is overcome by the pressure existing in the pulmonary artery, which, corresponding to the greater width of the capillaries, is much less than the pressure in the corporeal arteries. If the pulmonary artery becomes suddenly impermeable, the pressure in the collateral arteries, which originates partly from the bronchial artery, and partly from those outside of, but in connection with, the lungs, as the pleural, etc., is sufficient to prevent a venous reflux, but not sufficient to overcome the entire resistance in the lungs and to drive the blood beyond the capillaries into the left auricle. Then follows an accumulation and stasis of the blood in the capillaries and smaller veins, and hence results at first a hyperæmia and later a diapedesis. Litten makes another important change in Cohnheim's doctrine: he maintains that the hemorrhage appears before the integrity of the vessel-walls is impaired.

⁶⁵ Zeitschrift für klin. Med., vol. i. p. 148, Berlin, 1880.

Other fatal cases find their anatomical basis in the softening and ulcerating processes, which while forming cavities are liable to open vessels of greater or less size in their walls or trabeculæ.

The condition of the heart in phthisis is one which has an effect in influencing the occurrence of hæmoptysis. The general statement by Peacock, that the weight of the heart in phthisis, though less than in acute diseases, is greater than that in other chronic diseases, needs to be modified somewhat, as he did not make a distinction between different forms of phthisis. The more the case approaches the fibroid variety the more likelihood of some increase of size, particularly in the right ventricle. Spatz,⁶⁶ a later authority, gives as the result of his examination that phthisis diminishes the size of the left ventricle—that an absolutely compensatory hypertrophy of the right ventricle, which is apparent in special cases, does not as a rule exist, although the resultant decrease does not throughout stand in relation to the decreased weight and volume of the whole body in phthisis. The ratio between the depth of the left ventricle and circumference of the aorta is diminished; and, as this is not compensated for by hypertrophy of the walls of the ventricle, arterial tension diminishes and the pulse becomes soft and small. The chance of rupture of weak vessels by relatively excessive tension is thus much weakened in the later stages of phthisis.

⁶⁶ Deutsches Archiv für klinisch Med., vol. xxx. p. 154.

Another element capable of modifying the hæmoptysical features of phthisis is claimed by Jaccoud⁶⁷ as existing in the insufficiency of the tricuspid valve, which compensates the increased tension in the field of the pulmonary artery arising from obstruction of a considerable part of it. The amount of blood passing from the right ventricle is thus, by a reflux, proportioned to the area of obstruction in the artery, and the tension is reduced so as to prevent rupture of the weak vessels. His conclusions are based on 18 cases of measurements of the tricuspid orifice. They varied from 111 to 130 millimeters. The evidence obtainable during life was a systolic murmur heard at the ensiform cartilage and cervical venous reflux.

⁶⁷ Clinique médicale, vol. ii. p. 346, etc.

DIAGNOSIS is mostly called for with regard to the chances of hæmatemesis. Inspection of the blood is naturally an early point for attention. Its bright-red color, frothy look, freedom from extraneous matter, and its coming up by coughing are strong evidences easily acquired of its pulmonary origin. Corroborative circumstances are the family history of phthisis or hæmoptysis, the presence of pulmonary, or in fewer instances of cardiac, physical signs, the immediately premonitory symptoms spoken of before. Fever, the age of the patient, and the continuance of the discharge of blood in its later gradations of color and mixture of catarrhal elements, inspection of the mouth, fauces, and larynx, would exclude those possible sources. Each has its limitations, but together they are conclusive as against hæmatemesis. Recent and accumulating experience attributes some diagnostic value to the presence of bacilli tuberculosis in the expectorated blood. Hiller⁶⁸ reports 6 cases of hæmoptysis in which the blood showed in bacilli: 3 were completely initial. The bacilli were easily demonstrated by preparations and also by inoculation on guinea-pigs. They have also been found in the blood of cases of acute tuberculosis by Weichselbaum.⁶⁹ Resort may be had to the well-known tests for the presence of the elastic tissue of the lung in sputum.

⁶⁸ Centralblatt für die med. Wissenschaft, March 24, 1883.

⁶⁹ Wiener med. Wochenschrift, No. 13, 1884.

As positive data for hæmatemesis we have the dark color of the blood, its firmer clotting, greater density and want of aëration, acid reaction, the presence of extraneous matters of food and drink, their ejection by vomiting, and pain or uneasiness at the epigastrium. As corroborative we have the less frequent occurrence of hæmatemesis, the individual history of gastric disease, such as ulcer of the stomach or presence of hepatic cirrhosis from intemperate habits, and the history of a blow on the abdominal surface: discharges of blood from the bowels are more likely to occur in hæmatemesis.

Hæmoptysis may be simulated, as by scratches or cuts on some part of the internal surface of the throat or mouth. The blood is then likely to be thinned by secretion from the mouth. Inspection would detect the imposture. The chance of blood from an epistaxis being swallowed and afterward ejected by vomiting is to be remembered. Cardiac hæmoptysis is distinguished in most cases by the presence of symptoms and physical signs of valvular, usually mitral, disease in a considerable degree of advancement. These are so pronounced as to exclude phthisical disease. Other and fewer cases occur where the hæmoptysis is the first evidence of the cardiac disease, and they require a careful exclusion of all the features of tubercular disease, so as to be able to arrive at a correct conclusion. There are no conclusive considerations pertaining to the amount and character of the blood. In the severe and copious hemorrhages there is likely to be present a marked shock.

PROGNOSIS.—Hæmoptysis usually implies phthisis existing or imminent, and yet it has in general a favorable effect on its course. This applies more to its first stage than subsequently, and more to the small than to the large hemorrhages. The gravity of the small ones increases in proportion to their frequency. The family and personal equation is of more importance than the mere quantity. We may have a slight hæmoptysis and a large increase of the morbid condition following it, and the reverse, the result depending on the individual tolerance of and susceptibility to reaction. As in the second stage the reactive elements are more potent, the small hemorrhages then are less beneficial. They are the index of activity in the destructive lesions, and yet may relieve the accompanying congestion. The easiest appreciable symptom of the progress of the disease is the fever. We may fail to properly interpret physical signs because of want of familiarity with the individual case before us. If besides more fever there be more cough, dyspnoea, and debility, the prognosis increases in gravity. These remarks will apply with more force to the large hemorrhages than the smaller ones, and are guides for prognosis in all the clinical forms of hæmoptysis. In the special clinical form, the hemorrhagic variety of phthisis, bleedings recur often and in large quantities during years, and some of the cases end with final recovery. The fever and constitutional irritation give way under seemingly very unfavorable conditions. The fact that a great part of them have no history of heredity, and that they come on at a late period of life, may account for this, because they thus escape the influences which heredity and age are known to impose upon the other classes of phthisical subjects. Some interesting conclusions have been drawn from the history of cases of profuse hemorrhages. Pollock⁷⁰ thinks that they shorten the duration of the first stage and lengthen the duration of the second and third. Out of his 351 cases, 204 occurred in the first three months of illness: 45 had remained in the first stage when examined, 142 having undergone softening, while 164 had cavities. Of 286 cases of profuse hæmoptysis classified by Williams,⁷¹ the number of cases in the first stage was 187, and the percentage of deaths was 13.95; 65 cases were in the second stage, and the percentage of deaths was 24.61; 31 were in the third stage, and the percentage of deaths was 67.74, showing increased effect of hemorrhages upon pulmonary structures advancing in destructive processes and upon constitutions being progressively undermined by them. In other clinical varieties the symptom is so clearly subordinated to the general process that it loses its prognostic importance in the established disease. There is an imminence of fatal hemorrhage in many of them, as in fibroid phthisis, cancer, abscess, gangrene, and hemorrhagic infarction of the lungs. In extra-pulmonary hæmoptysis or in that from rupture of pulmonary aneurism there is seldom opportunity for prognosis.

⁷⁰ Elements of Prognosis in Consumption, p. 139.

⁷¹ Pulmonary Consumption, p. 150.

If the condition be recognized, we can but say that the fatal attack is liable to come at any moment. In cardiac hæmoptysis the hemorrhage is an event coming toward the close of organic and obstructive changes which are not much within our control. There are minor degrees, as shown by expectoration of single small masses of dark coagulated blood and by the absence of marked aggravation of the symptoms, which do not prognosticate unfavorably for the immediate, but do show impending dangers of a future, attack. Morbid anatomy shows traces of a recovery from a number of premonitory threatenings. The elements of a serious prognosis are the appearance of a shock, increased dyspnoea, a large amount of hæmoptysis, increased perturbations in the heart-action, and increased areas of dulness or râles at certain parts of the lung other than the usual sites of consumptive disease. These and other evidences of constitutional initiation are not as available as in the other varieties mentioned.

TREATMENT.—In the cases of the mildest form very little more need be done than to keep the patient quiet. His apprehensions may require attention. They may be allayed by assuring him that the hemorrhage will be more of a security than a danger, because it is the expression of a local congestion that will be relieved by the discharge. We have found that a large dose of quinine (ten or fifteen grains) will answer the double purpose of a nervous sedative and of controlling the congestion and hemorrhage if the latter object be necessary. This suggestion becomes still more applicable in the severe forms of hæmoptysis. The dose may be repeated within twenty-four hours if needed. If congestion be manifested by its symptoms of substernal heat, soreness, oppression, dyspnoea, and cough to a greater degree, and if the hemorrhage is becoming copious and the hemorrhagic pulse developed, and the temperature elevated, the necessity of a more active interference is evident. Absolute quiet in bed, fresh air, a calm and equable behavior on the part of the family or friends in attendance so that no excitement may be reflected to the patient, are essential. The medicines selected should be such as may control the vascular excitement, and hæmostatics. Ergot will fulfil such indications. It has its limitations in its unpleasant taste, but it should be pushed to the points of tolerance. Of the fluid extract one teaspoonful should be given every hour or two until some effect is observed in slowing the pulse or checking the hemorrhage. If the stomach rebel, ergotin pills may be substituted in doses of three to five grains at the same interval. Should all the resources of ergot medication be required or the above mode of use fail or disagree, hypodermic injections may be added. Two to three grains of the extract of ergotin would form a proper dose, to be repeated every one or two hours. It has been quite the exception in our experience to have serious irritation follow the use of it in this way. Failure in this and other uses of ergot will follow because we do not administer it with sufficient freedom.⁷² Another most valuable hæmostatic is turpentine. It should also be given freely. From ten to thirty drops in an emulsion or in sugar may be given every two to four hours, according to tolerance and to the threatening character of the case. The ergot and turpentine are best alternated at intervals of one to three hours, according to the requirements of the attack. Some preparation of opium is often required to quiet cough—morphine or codeine, one-fourth grain of the former and one-half grain of the latter, repeated at intervals until their effects are obvious. By adding the use of broken ice and the external application of cold compresses frequently repeated, and, if time and strength permit, the inhalation of persulphate of iron spray twenty or thirty minims in half an ounce of water, we get a plan of treatment adapted to the urgent cases. Some recent reports have confirmed the confidence of the ancients in the use of ligatures. They may be applied to both lower limbs. A dozen dry cups may be applied to the chest. There is no occasion or time for the use of many medicines, but if a general plan, such as the above, must be changed, acetate of lead in doses of two grains every two hours would be an excellent substitute, due regard being had to the possible toxic effects from too long continuance of it in such doses; it is usual to add a little opium to it. Gallic acid is an effectual remedy for the control of different kinds of hemorrhages. Like ergot, it is usually given in too small quantities. Twenty to thirty grains must be given every two to four hours. It is better borne by the stomach, and can often be continued longer, than the medicines above mentioned.

⁷² A medical friend, T. C. Minor of Cincinnati, has in his own case used three or four drachms of the fluid at a dose, with the effect of reducing his pulse twenty beats in a few hours.

We have already noted ipecacuanha as one of the survivals of ancient practice. It has had warm advocates among modern physicians. Graves places vivisection first and ipecacuanha next in his plan of treatment. Trousseau strongly recommended it. Peter and the French practitioners also strongly endorse its use in the severe forms. We have no doubt of its efficacy. It is important to exclude if possible the existence of a pulmonary aneurism or any such source of blooding, as there are no special means by which this can be done. It is a good rule to use the ipecacuanha in the cases of early or first-stage hæmoptyses. We would give it as it is given in dysentery. Precede its administration half an hour with thirty drops of laudanum, then give ten grains in water. If vomiting comes on, repeat it in an hour, and again, if hemorrhage continue, in two hours. The usual experience is that tolerance is established after two or three doses. It has also an application in small doses of one-quarter to one-half a grain in the milder forms, with irritative cough and slight fever.

Graves calls attention especially to the excellent effect of opium in all kinds of passive hemorrhage, hæmoptysis as well, but insists that it should be given only after vivisection has been performed or when the hæmoptysis has become rather passive, or in scorbutic and similar cases. His direction on one occasion to a physician, in a case of protracted bleeding of the gums, was, "Go home and give two grains of opium immediately, and then half a grain every hour until the bleeding stops." A combination applicable to the persistent bleeding recurring day by day is the sulphate of magnesia made soluble in rose-water by the free use of dilute sulphuric acid—one teaspoonful of the former, fifteen drops of the acid, one-half to one ounce of the rose or plain water. Many other remedies might be mentioned, and among them atropia. After the bleeding has ceased it is necessary to be assured as to the condition in which the lung has been left, and to counteract, if needed, any persistence of irritation. Fever is the most valuable evidence as to this point. If it exist, the use of quinia and ergot had better be continued freely. A three-grain ergotin pill about three times daily, and five grains of quinia morning and evening, can be tolerated two or three weeks. Local irritation should be applied if physical signs or pain warrants it.

PULMONARY APOPLEXY.

BY WILLIAM CARSON, M.D.

DEFINITION.—Escape of blood into the pulmonary parenchyma, with laceration of its substance.

SYNONYMS.—Hemorrhage (pulmonaire) foyer (Jaccoud); Diffuse pulmonary apoplexy or Diffuse pneumorrhagia (Fleich); Diffuse pulmonary apoplexy (Loomis); Pneumo-hemorrhagie (Gendrin), etc.

HISTORY.—Latour¹ is quoted as being the first to use the words, "apoplexie du poumon."² Yet Duguet³ also quotes from Frank that Dolocus had a long time before employed it. It is known that cases had been described long before this, as by Corvisart in 1808, Allan Burnes in 1809, among those of this century, and by Prosper Martiano, Bonet, Morgagni, Haller, etc., among the more ancient authors.⁴ Again, Laennec gives the weight of his authority, and establishes Latour's use of the name, until, as the synonyms show, modern usage has almost abandoned it. Among the multitude of those who have treated of pulmonary apoplexy, we will have filled the requirements of this brief historical statement by mentioning Virchow and his pathological investigations into embolism, and also Cohnheim,⁵ and later Litten's⁶ studies on infarction, which have some indirect connection with pulmonary apoplexy.

¹ Histoire philosophique et médicale des Hémorrhagies, 1815, passage misquoted in L'apoplexie pulmonaire by Duguet.

² Op. cit., pp. 220, 222, and 224.

³ Op. cit., p. 11.

⁴ Duguet, p. 10, etc.

⁵ Untersuchungen über die Embolischen processe, 1872.

⁶ Zeitschrift für klinisch Medicin, Erster Band, 131.

ETIOLOGY.—Predisposing Causes.—The male sex affords predominance of cases, because of greater liability to accidents, to the various forms of ulcerative destruction of lung-tissue, and to aneurisms of the aorta and pulmonary artery.

The adult age is most exposed for similar reasons. Ogston's statistics⁷ support in a general way, but not with strictly technical force, their quotation by Herz.⁸ Omitting the last 4 of his 20 cases (2 of which were from poisoning, 1 from fracture of skull by a fall down stairs, and 1 from drowning), the average for males (12) was 56.4, and 55.3 for females (4).

⁷ Brit. and For. Med.-Chir. Rev., vol. xxxvii., 1866, p. 459.

⁸ Ziemssen's Handbook, vol. v. p. 298. Ogston says (p. 465) it did not appear, however, that any distinct rent of their substance had taken place—to any extent, at least. "When we consider that the area of the extravasation was sufficient to involve often one or two entire lobes, and that death was in most of them very sudden, the cases may be adopted as showing the action of causes similar in kind, if not in degree, to those operative in undoubted pulmonary apoplexy."

As more efficient predisposing causes than either age or sex, may be mentioned aneurisms of the aorta and pulmonary artery, amyloid degeneration of bronchial and pulmonary vessels, the influence of Bright's disease in producing disease of blood-vessels, and atheromatous diseases of the pulmonary artery.

Exciting Causes.—Penetrating and contused wounds of the chest by their direct mechanical effect, and diseases and injuries of the brain through the medium of the nervous system, may produce pulmonary apoplexy, the result in the latter case being usually an infiltration or small infarction.

SYMPTOMATOLOGY.—Pulmonary apoplexy is the least common of the two forms of distinctive pulmonary hemorrhage, the other being pulmonary infarction, already treated of under HÆMOPTYSIS. A proportion of cases is associated with mitral disease in its most advanced stages. At that time we may expect pneumorrhagia, but whether from infarction or apoplectic laceration even the event can only occasionally determine. In the latter, if hemorrhage makes its appearance it will be copious and generally overwhelming; at other times the hemorrhage may not appear, and the patient dies suddenly with possibly other indications of the internal flow. The physical signs cannot be relied on, for often the pulmonary tissue is already changed by the long-continued obstruction of circulation. Rupture of aneurism, particularly of aorta, in the great majority of cases takes place into a bronchus, and not into the parenchyma. In case of wounds of the contused variety a laceration of parenchyma occurs at times sufficient to produce marked hæmoptysis. If the blood be not ejected, there are no certain indications of what has happened. If the case be seen immediately after the accident, such physical signs as moist bubbling râles on the margin of an area of feeble or suppressed vesicular murmur, possibly attended with a dull, high-pitched percussion note over that area, would afford a strong presumption in favor of ruptured lung and consequent hemorrhage.

The same signs later might be due to a limited traumatic pneumonia. If the internal hemorrhage, whether traumatic or spontaneous, has made its way through the pleura, then, if the patient live long enough for examination, besides such symptoms as great oppression and exhaustion, the physical signs peculiar to pleural effusion may appear to a limited degree. This opportunity seldom occurs, as such a rupture produces almost invariably a fulminant and rapidly fatal result.

COURSE, DURATION, AND TERMINATION.—The course of the lighter cases is much like that of pulmonary infarction, and that of the severe forms too brief for observation. As to termination, it is quite possible there are cases of laceration so limited as to allow complete recovery, but clinical experience shows that pulmonary apoplexy is usually fatal.

PATHOLOGY AND MORBID ANATOMY.—With branches of the pulmonary vessels weakened by long-continued heart disease, or with such vessels as are found with chronic nephritis, a sudden increase of tension in them from unusual effort or excitement will precipitate a fatal rupture. Sometimes the progress of the degeneration is so insidious and complete that a rupture may occur without obvious exciting cause. This is also the natural history of aortic aneurism. An examination soon after the laceration will show a mass of blood, usually coagulated, sometimes partly fluid, lying in an irregular cavity with walls of the lacerated lung-tissue. After a longer time the lung-tissue beyond the walls of the hemorrhagic focus becomes oedematous to a certain extent. A contraction of the cavity, with change of contents, may proceed to the extent that an encapsuled mass of very small size will remain as the final result (Rokitansky).

DIAGNOSIS from bronchial hemorrhage by the probable existence of phthisical conditions and history. The quantity of blood ejected may be profuse in either case, and therefore be no criterion. From pulmonary infarction, as the other form of pulmonary hemorrhage, by the larger amount of hæmoptysis. If there be no hæmoptysis, a presumption would exist in favor of apoplexy in case of extreme dyspnoea or a fatal result. The associated diseases or causes being similar, no inference from the medical history would be reliable except in case of injuries.

PROGNOSIS.—As we meet with it in recognizable form, the result is almost invariably fatal. A qualification is allowed because of the experience of such a pathologist as Rokitansky, who describes a process of cure in a few cases. The prognosis in such would be determined partly by the severity of the antecedent or accompanying disease, as in heart lesions, and partly by the increased respiratory distress, pain, exhaustion, and hemorrhage.

TREATMENT.—As has been before intimated, a case of pulmonary apoplexy distinctive enough to be diagnosed is usually one that is beyond the reach of treatment. Remedies that may relieve dyspnoea, exhaustion, and hemorrhage are those to be relied on. External irritants, as turpentine-stupe stimulants, ergot, turpentine internally, and such other remedies as are of known effect in the treatment of the associated heart troubles and of the incidental pulmonary infarctions.

ABSCESS OF THE LUNG.

BY WILLIAM CARSON, M.D.

DEFINITION.—A circumscribed suppuration of the lung, resulting in a cavity.

SYNONYMS.—Abcés du poumon; Lungenabscess.

HISTORY.—The ancients described abscess of the lung, and placed it among the terminations of the inflammation of that organ. They believed that if the inflammation did not resolve itself by the fourteenth or twenty-first day its termination was to be by suppuration. Hippocrates, Van Swieten, and others are mentioned among those who maintained these views and consequent frequency of such cases which prevailed until physical methods and pathological investigation proved their incorrectness. J. P. Frank, Bayle, and Cayol¹ are given credit for a partial reversal of this opinion. Avenbrugger,² a pupil of Van Swieten, in describing vomicæ, divides them into two kinds—the ichorous and the purulent. By the purulent vomica he means an encysted abscess of the chest resulting from the conversion of an inflamed spot into a white, thick, glutinous, fatty matter. When these communicate with the bronchi and discharge any of their contents by expectoration, they are called open; otherwise, close or shut. He gives symptoms and signs belonging to the respective varieties. Corvisart, in his comments on these propositions, says: "In fact, the purulent vomica is always the result of an inflammation, more or less acute, of the lung." He makes distinctions between the various kinds of purulent vomica and the ichorous vomica. Laennec, as in many other subjects of which he treated, has the credit of placing this one on its modern basis, at least so far as the frequent termination of pneumonia in abscess is concerned. Among English writers Stokes deserves especial mention. Abscess was the fifth and the last of the stages of pneumonia, according to his classification. He treated largely of the perforating abscess. Traube, Trousseau, and Leyden are among those who have contributed largely to the elucidation of the subject. The latter has especially claimed for this subject a more prominent place in the literature of practical medicine, and has strongly enforced his views.

¹ Nouv. Dict. de Méd. et de Chirurgie, tome xxix. p. 394; and Leyden, "Ueber Lungenabscess," Sammlung klinische Vorträge, von Richard Volkmann, Nos. 114, 115.

² On Percussion of the Chest, a translation of Avenbrugger's original treatise by John Forbes, with comment by Corvisart, 1761–1808, pp. 38, 43, etc.

ETIOLOGY.—Predisposing Causes.—Everything tending to debilitate the constitution may become a factor in the production of abscess of the lung. Senile constitutions, Bright's disease, chronic alcoholism, diabetes mellitus, and insanity are some of the predisposing causes.

Exciting Causes.—These may be divided, as in the case of gangrene, into the pulmonary, or those originating in the lung or pleura, and the intra-pulmonary, or those originating outside of the lung or pleura. Among the former are included pneumonia and empyema, perforating and discharging into the lung, or one variety of Stokes's perforating abscess, pulmonary apoplexy, and suppurating bronchial glands, opening up a passage through the lung and bronchial tube. Either croupous or catarrhal pneumonia may be associated with or terminate in pneumonia. Among the latter, or extra-pulmonary class are included cases of embolism from the right heart, producing infarction, or from the systemic veins. These emboli carry with them the productive capacity of suppuration. Abscess external to thoracic walls, as in deep-seated mastitis, will at times perforate the walls and enter the lung. Abscesses of the liver not infrequently perforate the diaphragm, and are discharged through the lung.

Foreign bodies in the bronchi may ulcerate through them and produce suppuration of the lung, which may finally open a way externally through the chest-walls.

SYMPTOMATOLOGY.—The symptoms of abscess of the lung, as may be inferred from the enumeration of causes, are divisible into two categories—one including those symptoms with which the abscess may be associated, but which do not necessarily prognosticate it; and the other including the symptoms which indicate the abscess as a fact accomplished. In the simplest and most frequent clinical form, that following pneumonia, the early symptoms would be those of a severe and irregular form, as shown by very troublesome and uncontrollable cough or unusual pain or respiratory embarrassment, high fever, but at that time fairly typical pneumonic temperature, great prostration, etc. These may all diminish in due time, and mostly do without suppuration following. A return of pain, dyspnoea, fever, and general distress should awaken suspicion, yet they may be the result of an extension of pneumonia to other portions of the lungs. Rigors and sweats and increased depression would point to a suppurative process and under such circumstances to the lung as the locality. We cannot, then, positively predict an abscess. It is suspected when a more or less copious eruption of purulent discharge occurs suddenly, and sometimes the discharge is so abundant and pus-like that any other alternative than abscess is very remote; at other times the discharge is small in quantity. The proof of physical cavernous signs is the final step. This is often difficult. A slightly greater increase of lung-density, probably at the middle or upper part, with imperfect bronchial breathing, the appearance of a few moist râles or crepitus, the gradual increase of these and merging into coarser crepitus, and revelation of more or less of the cavity signs, is the physical history of many cases of abscess of the lung. Others have a much more pronounced course, such as the cases of so-called gangrenous abscess—a sort of connecting link between gangrene and abscess of the lung. The breaking down of tissue is ostensibly very sudden, and the cavernous signs are very soon unmistakable. Other clinical forms are the pyæmia, to be distinguished by the antecedent history, which will reveal a source for infectious emboli. The abscesses are usually multiple and small, so that their precise locality cannot be made out. The proof of infectious transportation is sudden pneumonic symptoms, as pain, tinged and finally purulent expectoration. Rupture into pleura may occur and produce empyema. Rupture of hepatic abscess and discharge through the lungs is also a clinical form shown by this antecedent event, pointing to hepatic inflammation. The egress of the pus is sometimes through a narrow track, and not by a reservoir within the pulmonary tissue; at other times the lung is really excavated. The discharge of pus is usually copious and paroxysmal. Leyden recognizes as his third class a form of chronic abscess, or one coming on during a case of chronic pneumonia and bearing great resemblance to a variety of phthisis. Its general symptoms are much the same as in the acute variety, differentiated by the element of time.

COURSE.—It may be said, in a general way, that the etiology has much to do with its course. If the cause be pneumonia, the course will be such as the detail of symptoms already given shows. In some unknown way the natural course of the disease is interrupted, and what promises to be an average case is followed by the characteristic features of abscess. If pyæmia be the precedent condition, a peculiar form of pneumonia, embolic in origin, appears, and abscesses again follow. Greater septicity and rapidity of destruction are probable sequences. The perforating abscesses are subject to modifying influences of mechanical effect, such as gravitation and the resistance of tissues, and have their peculiar course, which is often marked by great chronicity.

TERMINATION.—In the course of seventeen years the reports of the Cincinnati Hospital show that there have been 6 cases of abscess of the lung treated there. Of these 4 died and 2 were discharged as improved. These figures show the infrequency of such cases, and also represent a greater mortality than probably occurs in the non-hospital class. We know of no large statistics which show what is the percentage of recoveries. Our own experience in private practice gives a majority of recoveries. They were cases following typhoid fever, croupous and catarrhal pneumonia, and hepatic abscess. A termination in a chronic cavity now and then happens: perforation of the pleural cavity, with subsequent pyo-pneumothorax, discharge externally through an intercostal space, or even extension into the abdominal cavity, are among the actual events of such abscesses.

DURATION.—The duration of an ordinary case is subject to wide variations between one and six months. A few cases are recorded of several years' duration. Previous constitutional condition has much to do with this element. The degree of infectiousness in the pyæmic class is important as to time. The abscesses become a subordinate condition in the fate of the case. In this connection we may also refer to Leyden's third variety, a so-called chronic abscess.

PATHOLOGY.—A close parallelism, etiologically and otherwise, is observable up to certain points between gangrene and abscess of the lung. Both are products of, or associated with, pneumonia. That which finally determines whether the result shall be gangrene or abscess is unknown to us. In the article on GANGRENE OF THE LUNG some investigations are referred to which point to a probable solution in the existence of specific forms having special pathogenetic force. The tendency of experimental and clinical investigations is to connect the suppurative process closely with the product of specific germs. Ogston in 65 cases of acute abscess found micrococci present in all of them. Obstruction of blood-vessels in the centre of the pneumonic area or on the margin of the abscess walls is an important anatomical element in the production of abscess, and it is claimed that it is often due to colonies of micrococci within their calibre; so that it is probable that there are both mechanical and biological or chemical influences at work. If the view of the zymotic and infectious character of pneumonia be tenable, the contingency of an abscess developing in its course would seem not very remote. Yet the proportion of cases of abscess from pneumonia is not more than 2 per cent. Leyden's high authority supports the idea of the essential and specific differences in the chemical and morphological peculiarities of gangrene and abscess of the lung, but the subject is as yet on a hypothetical basis.

MORBID ANATOMY.—The fresh cavity, generally in the upper lobe, has rough, ragged, and irregular walls, and may have bridles of the more resistant structures, as bronchi and vessels, crossing it. Such a cavity is quite likely to contain portions of undissolved parenchyma or more or less malodorous pus. The older cavity becomes smoother walled, and of more regular limits and cleaner contents. A gradation from granular hepatization through congested to crepitant tissue is almost uniform in the varieties of abscess, whether simple or pyæmic. In addition, some peculiarities are observable in the latter. These are usually several, varying in size from a pea or less to a walnut, some round and others wedge-shaped; others lying superficially and forming slight elevations on the pleural surface. In proportion to the curative progress the cavity will contract and disappear, occasionally leaving behind a cicatricial mark. A lining pus-secreting membrane will sometimes form, resulting in such a limitation of morbid action and such a disappearance of reactionary symptoms as to make the disease entirely local, but quite chronic.

DIAGNOSIS.—The more or less sudden and copious expectoration of pus, without a specially offensive odor, in the course of a case having up to that time the history of a pneumonia, would be considered as due to the development of an abscess in the lung. Some degree of fetor in breath and expectoration is observed, but it is far different from that of gangrene. The detection of the débris of lung-structure in coarse particles, and the microscopic discovery of elastic lung-tissue, are important diagnostic points in contradistinction from the solution of tissue that gangrene usually effects upon the parenchyma of the lung. According to Leyden's³ very complete investigations, the microscope reveals fatty crystals, mostly in roundish fragments, of the size of the epithelium of the lung and of a brilliant structure; pigment-débris of a yellowish-brown or brownish-red color; hæmatoidin and bilirubin, which Traube thought were due to hemorrhagic infarction, but which Leyden has observed in all of his cases; and, lastly, micrococci, in the well-known form of the round, granular micrococci colonies, which differ from those in gangrenous fragments in that they show very little movement and do not give the iodine reaction.

³ "Ueber Lungenabscess," Volkmann's klin. Vorträge, p. 994.

Difficulties of diagnosis arise in the case of an empyema discharging through the bronchi, or of an encysted empyema discharging through the third or fourth intercostal space in front; also, between abscess of the superior portion of the liver and one in the base of the lung, or between the latter and a pyo-pneumothorax. Very careful study of the history in each case is of the first importance. Where this is not attainable the difficulty is often much increased. In the case of the empyema the discharge is more profuse at each time, the whole amount in a given period is much greater, and the time of opening is much delayed beyond that of the pneumonic abscess. Trousseau gives the case of a child who brought up for more than six months 200 grammes of pus daily. He makes children an exception to the rule as to the late opening of the pleural abscesses. In the encysted empyema discharging either internally or externally the difficulties are greater. A portion of the lung-tissue may be so near behind the deposit of matter as to make the physical signs confusing if the pus has opened externally. Some of these and of the interlobular deposits it is almost impossible to diagnose.

In hepatic abscess opening into the lung and bronchi the discharge is copious, dirty brown, paroxysmal, and will generally, on careful observation, show the bile color or its chemical reactions or some microscopic débris of the liver. In Leyden's third class, or the chronic abscess arising in the course of chronic pneumonia, the history is so much like that of some forms of phthisis as scarcely to serve in diagnosis. He thinks there are some macroscopic and microscopic appearances which may serve for diagnosis. There are in the expectoration dark and compact pieces of greenish-black color, not unlike plugs of pus, and larger, black-pigmented fragments of parenchyma, from a pin's head to a hempseed in size. Microscopically, they consist of a close and strongly-pigmented parenchyma, which seldom reveals alveolar structure. They show fatty degeneration and cholesterin plates. This class of cases is mostly without fever. The application of the bacilli-tuberculosis test would seem to offer some assistance in diagnosis.

PROGNOSIS.—A grave prognosis may be formulated if there be a history of feeble constitution, and especially if it be further impaired by habits of intemperance, if the patient belong to either extreme of age, if there has been a recent debauch, or if there be wide variation from the typical form of pneumonia. Variations will be shown in such a complexus of symptoms as follows: fever of low grade, subject to extremes in range; feeble and frequent pulse, but not so marked as in gangrene of the lung; dyspnoea, objective and subjective; typhoid depression; tongue dryish; delirium; copious and fetid or difficult expectoration; physical signs of extensive lesion, such as a large cavity with a large outlying pneumonic area. A favorable prognosis would be conditioned on the appearance of a fewer number of these symptoms or on their evolution in a milder form.

The capacity of the patient to endure a long-continued suppurative discharge is principally determined by his natural vigor and his ability to assimilate food, other elements, such as extent of injury to the lung, being the same. A well-defined superficial cavity would be more favorable, because within surgical relief.

In the pyæmic variety the force of the infectious element will determine largely the result. Chills and sweats are important prognostic elements in such a case.

In the secondary abscesses of either the empyematous or hepatic variety prognosis is grave—more so in the latter than in the former, because surgical procedure would be more promising in the former, and because of the implication of an organ so liable to destructive inflammation as the liver. A long and tedious course of suppuration is possible in either. The dangers in an established abscess arise from liabilities to septic infection and exhaustion consequent on want of reparative power and persistent suppuration.

TREATMENT.—The treatment of abscess differs little if at all from that of gangrene of the lung. The tendencies of the two diseases toward exhaustion and infection are similar, but are less pronounced in the former. The same remedies are necessary in both, such as stimulants, tonics, antiseptics, anodynes, and expectorants internally, inhalations and drainage externally; brandy and malt liquors as stimulants; nourishing and concentrated food at frequent intervals; quinine as tonic and antiseptic; carbolic acid and turpentine as most valuable antiseptics (the latter being also an excellent stimulant); eucalyptus in cases of profuse as well as fetid discharge; carbonate of ammonia, senega, as expectorants; morphine and codeine or anodynes to control cough; carbolic acid for inhalation; and in cases of definitely localized cavities a free opening to be made with antiseptic injections.

Successful cases of surgical interference are reported, and such treatment is now recognized as proper when the system is giving way under septic poison, evinced in chills, sweats, and great prostration, where the purulent discharge is fitful and imperfect, and where the physical signs are clear enough to show the locality of the abscess.

GANGRENE OF THE LUNG.

BY WILLIAM CARSON, M.D.

DEFINITION.—Putrid necrosis of the lung-tissue.

SYNONYMS.—Lungenbrand, Gangrene du poumon, Gangræna pulmonum.

HISTORY.—By common consent, Laennec has the credit of first identifying, naming, and classifying gangrene of the lung as a distinct disease; yet Lieutaud¹ in 1707 describes imperfectly a case of gangrene of the lung in a child: "the right lung, within and without, appeared entirely putrid." Bayle² is considered, in his section on his fourth variety of phthisis (phthisis ulcereuse), to have described a rather chronic form of gangrene of the lung. Morgagni, Boerhaave, Stoll, J. Frank, and Cullen considered gangrene as one of the terminations of peripneumonia.³ Laennec's development of the subject has only in a few directions been enlarged. His classification is universally adopted. His description is adopted generally as the most complete. There have been, however, controversies on different points, such as the relation of pneumonia and of the obstruction of the vessels to gangrene of the lung.

¹ Historia Anatomica Medica, 1787, Obs. 329, cited by Louisa Atkins, 1872.

² Bayle, G. L., Recherches sur la Phthisis pulmonaire, 1809–10, p. 30.

³ I. Straus, Nouv. Dict. de Méd. et de Chir., p. 403, etc.

In the pathology and etiology of gangrene Virchow's investigations on embolism and thrombosis opened up important relations; in diagnosis, Traube and Leyden and Jaffee; in medical treatment, also Traube; and in surgical treatment, Haley and Lawson (1879),⁴ S. C. Smith (1880), E. Bull (1881), Fengar and Hollister (1881), Mosler and Voght (1882). The antecedent development of pulmonary surgery, through important work done by Mosler, Pepper, and others, had prepared the way for special applications of it to gangrene and abscess of the lung. Spencer Wells claims to have suggested similar proceedings nearly forty years ago.

⁴ Lungen Chirurgie, Mosler, xx. p. 67.

ETIOLOGY.—Predisposing Causes.—Constitutional weakness is a common predisposing influence: it may be a primary condition, but is more often secondary or dependent on some recently-acting debilitating cause, as typhoid fever, chronic lung disease, diabetes, etc. Chronic alcoholism is a cause which, besides its effect on the system at large, may add a special one on the lungs in producing hyperæmia or drunkard's pneumonia.

Of 46 cases we have collected mostly from the Vienna Hospital report, the youngest was nineteen years old and the oldest was forty-seven years. Lebert⁵ has collected altogether 60 cases, 32 of his own and 28 of others: 19 occurred between twenty and thirty years, and 1 between thirty and forty. Huntington⁶ gives 32 cases from the Massachusetts General Hospital Record between 1857 and 1875: 9 were between twenty and thirty years, and 12 between thirty and forty; the youngest was ten years old and the oldest sixty-four. It is noticeable that these figures coincide largely with those showing the incidence of phthisis. Louisa Atkins⁷ gives, as the youngest ages among all the varieties, one of three months and another of two months.

⁵ Klinik der Brustkrankheiten, vol. i. p. 827.

⁶ Boston Med. and Surg. Journal, vol. xcv. p. 486.

⁷ Gangræna Pulmonum bei Kindern, 1872.

Of the 46 Vienna Hospital cases, 43 were male and 3 female. Huntington's cases were males 24, females 8. Of Lebert's own 32 cases, 22 were males; of the 32 others summarized by him, in 4 sex was not mentioned, and of the remainder 17 were males and 11 females. These figures show the large predominance of males in the liability to attack.

Exciting Causes.—They may be classified as pulmonary and extra-pulmonary. The influence of the alcoholic habit has been referred to above among predisposing causes: debauches are a frequent antecedent, especially in hospital cases, by means of resulting pulmonary hyperæmia and drunkard's pneumonia. Its association with croupous pneumonia may be assumed as settled after some warm disputes. The pneumonia of Bright's disease and putrid bronchitis are occasionally causative; bronchiectasies result in it not unfrequently. Extension of diphtheritic inflammation from the tracheal and bronchial mucous membrane is another form. The catarrhal pneumonia secondary to measles may produce it in children.

Embolism is the most frequent cause in the class of extra-pulmonary causes. It may be mechanical or infecting. A bronchial artery may be plugged so as to produce a gangrenous slough from mechanical cutting off of nutrition. Embolism of the pulmonary artery branches is more frequent, and by bringing about infarction and apoplexy may produce gangrene. Of the infecting variety may be mentioned emboli from the peripheral veins, as in surgical or uterine phlebitis, or from cerebral sinuses secondarily involved from otitis. Other causes acting from without on the lungs are foreign bodies, as particles of food passing beyond the trachea into the lungs, as in case of the insane or drunkards, and blows on the walls of the chest. These latter are capable of producing not only the ordinary phenomena of contusion-pneumonia⁸ but gangrene, and without evidence of external injury or fracture of the ribs.

⁸ M. Litten, p. 26, vol. v., Zeitschrift für klinische Medicin.

SYMPTOMATOLOGY.—Gangrene of the lung is the termination of a process the beginning and progress of which are not declared or cannot be followed through characteristic symptoms. Even its final occurrence may remain unknown if a communication be not established with a bronchus, which event is followed by the true symptoms, the expectoration and its odor. Whatever symptoms occur previous to that event may occur independent of it. Adopting Lebert's dictum,⁹ gangrene of the lung is not a pathological unit. As its pathogenesis varies, so does its symptomatology. A feature common to its several varieties is marked constitutional depression and variations from the typical form of the disease in which it occurs. If pneumonia, croupous or catarrhal, be the precedent or associated disease, it will be marked by soft and feeble and frequent pulse, restlessness, dulness or distress of countenance, more or less cyanosis, cool and relaxed skin, possibly delirium, dry tongue, unusual dyspnoea and pleuritic pain, copious prune-juice expectoration, irregular or non-typical temperatures. Along with these functional variations occur some in physical signs, as a lesser amount of dulness or of bronchial breathing, indicative of less structural density and corresponding exudation. A case with such an evolution may afford a presumption of an outcome in gangrene, but appearance of the characteristic expectoration and fetor is necessary to exclude it from irregular forms of pneumonia, which have no such termination. The same general remark applies to the cases of gangrene in bronchiectasic cavities. Perhaps some aggravation of the general condition may excite apprehension, but the characteristic phenomena of expectoration, odor, etc. must decide. If the cause be of embolic origin, we may expect some suddenness and perhaps shock in the beginning, and later the evidences of a more limited inflammation of the lung-tissue, such as circumscribed dulness and modified respiratory sound, which finally end in those indicating destruction of lung-tissue.

⁹ Op. cit., p. 803.

The macroscopic characters of the expectoration are those of a putrid or fetid liquid of varying shades of color, ashy gray, dirty green, or greenish-yellow, prune-juice, or more or less hemorrhagic. The odor, which is at first so fetid and penetrating, often disappears after the expectoration has been standing a while. It is separable, as first described by Traube,¹⁰ into three principal layers. The uppermost, covered with a layer of foam, consists of, first, dirty green, crumbling, confluent lumps; second, of larger, homogeneous, green muco-purulent masses; and, third, of whitish-gray, transparent, mucous masses. The second layer is formed of a colorless fluid. At the bottom is a fine yellowish-white sediment. Microscopically are found fat-acid crystals, many large fat-drops, and finely granular débris, masses of free, black pigment. It is said elastic tissue is nowhere to be found, but to this statement there are no doubt exceptions. Other bodies have been found by Leyden and Jaffee,¹¹ which they named Leptothrix pulmonalis. Kannenberg,¹² besides the above forms, found constantly infusoria of the family of monads in the sputa of 11 out of 14 cases of pulmonary gangrene. He considers them peculiar to the processes of decomposition in the lungs.

¹⁰ Gesammte Beiträge zur Pathologie und Physiologie, Zweiter Band, p. 452, etc.

¹¹ Deutsches Archiv für klin. Med., Band ii. pp. 488, etc., "Ueber putride Sputa."

¹² Virchow's Archiv, Band lxxv.; Zeitschrift für klinische Med., Band i. p. 228.

PROGNOSIS in general is unfavorable. Individually, the gravity of the case is determined by the evidence bearing on previous habits and constitution; by the violence of the onset, as shown in prostration, severe pain in the chest, dyspnoea, persistent and violent cough, delirium, feebleness and softness of the pulse; by the variations from the typical standards of croupous, or especially catarrhal, pneumonia, such as greater amount of septic or infectious or typhoidal element, non-typical and low temperatures in the early stages and also in the stage of disintegration; by the amount of the latter as shown in the physical signs of extensive lesion and in the amount of gangrenous sputum; and by the irritant effect of this in producing bronchial catarrh, and consequent catarrhal secretion, which may of itself become an element of danger in a system already much prostrated. Favorable prognosis is allowable when these conditions are being gradually reversed.

PATHOLOGY.—The pathology of gangrene of the lung is scarcely more settled than it was forty years ago, when Stokes¹³ published his eighteen propositions, embodying his experience. Obstruction of vessels and inflammatory exudations are present as important pathological conditions, but of themselves are not pathogenetic of gangrene. Other, as yet unknown, elements of putrefactive agency are present. Leyden and Jaffee's observations and those of Kannenberg have been mentioned¹⁴ as efforts to throw light upon the pathogenesis of gangrene of lung, but how far the bodies described by them precede, coincide, or follow the familiar clinical phenomena are undetermined questions. Filehne,¹⁵ in his experiments to determine the reason of the almost universal absence of elastic fibres in the expectoration of patients with gangrene of lung, comes to the conclusion that there is a ferment which, acting under alkaline conditions, destroys the fibres. The agents of this ferment he does not try to determine. Stokes anticipates the tendency of modern experimental pathology by announcing as an alternative proposition that "a process of putrefactive secretion precedes in many cases the death of lung." The constitutional debility which is so early a symptom prepares the way for such an invasion. In reference to the relation between the septic material and thrombosis in gangrene, Kohler¹⁶ affirms that the septic material produces the fibrin-ferment, and thereby capillary thrombosis. Recklinghausen thinks that a special material capable of exciting coagulation has not yet been found in gangrenous substances, but that there may be several factors, such as anæmia, changes in the vessel-wall, imbibition with foreign substances, etc. Other experiments¹⁷ and views point toward the conclusion that there are substances formed in various diseased conditions which have the power of ferments and of producing coagulation of blood in the lesser circulation.

¹³ Dublin Quarterly Journal Med. Science, Feb. 1, 1850.

¹⁴ Op. cit.

¹⁵ "Sitzungsbericht der Phys. Med. Soc." in Erlangen Schmidt's Jahrbucher, 1877, No. 7.

¹⁶ Recklinghausen's Handbuch der Pathologie, p. 136.

¹⁷ Wooldridge, Du Bois-Reymond, Archiv Centralblatt für med. Wissenschaften, No. 41, vol. xi. 1874, p. 734.

MORBID ANATOMY.—The circumscribed variety, as it usually appears, is a cavity irregular in outline, with ragged walls, made so by the unequal invasion of the lung-tissue by the gangrenous process. Sometimes the cavity itself contains loose fragments of lung-tissue, or the contents may be of a dirty, greenish, or brownish color, with some of the odor of the expectorated matters. If the case has been a chronic one, the walls are smoother, with a more or less formed lining membrane and the contents of a less characteristic color or odor. The cavity is usually in the right lung, and in the middle or lower portion. There is much variety of statement on this point. The tissue immediately adjacent to the gangrenous walls shows more or less of the products of catarrhal pneumonia. The vessels terminating in the walls are obstructed by coagula. If the gangrenous part come to the pleural surface, belonging to what Fournet calls the superficial variety, it may produce adhesions there, or it may result in perforation, with the result that we have the products of pleuritic inflammation united with the contents of the gangrenous cavity. In multiple foci, some will show the less advanced stages of disease, such as incomplete softening and local inflammatory lesions. In the diffused variety the lesions are sometimes described as being the same except in extent. The demarcations, however, from surrounding tissue are not as well marked; the tissue is soft, breaking easily under pressure, sometimes oedematous, dark or dirty black on surface or on section of lung; at other times the surface is mottled with lighter-colored patches. A secondary result is the production of bronchitis by the contact of the irritant expectoration from the gangrenous cavity.

DIAGNOSIS.—Abscess of the lung is the disease most likely to be confounded with gangrene of the lung. In the former you do not have the same amount of profound constitutional depression; the symptoms have a more frank expression, as it were, because of better precedent conditions usually; the first eruption of matter from the abscess is more copious and sudden than the usual manner of expectoration of gangrenous sputum; the appearance of the contents of the abscess is that more nearly of healthy pus, though the latter has at times a dark dirty brown or hemorrhagic look; the separation into layers is not apt to occur; the odor is usually not so fetid; microscopically, elastic fibres are much more abundant in abscess than in gangrene of the lung. The cavernous physical signs are not reliable in either disease. There are cases in which it is impossible, and in which it is of no practical importance, to make a diagnosis between gangrenous abscess and pulmonary gangrene. Gangrene supervening in phthisical cavities is distinguished by the history of a chronic pulmonary disease in which a cavity has been previously marked. It is phthisis advanced to the destruction of tissue plus the unknown gangrenous element which has found a lodgment in a favorable place. Stagnation of cavity contents, depression of system, etc. are favoring conditions. The same remarks apply to bronchiectasic cavities and putrid bronchitis, physical signs in the latter being additional points of difference.

Our experience proves that the essential SYMPTOMATOLOGY of gangrene of lung, except the débris of lung-structure in the sputum, can occur where there was no gangrenous destruction, either circumscribed or diffuse, no bronchiectasic cavities or bronchial dilatations, and no phthisical cavity. In the case alluded to the gangrenous odor and general characters of the sputum and the separation into layers and the consolidation of tissue were present, but the post-mortem afforded no explanation of the fetid expectoration. It was a case of debauch and alcoholic excesses and exposure.

COURSE, DURATION, AND TERMINATION.—The course of this disease is essentially an acute one. Whatever the early condition be, the gangrenous element hastens its progress, as in cases beginning with the phenomena of acute pleuro-pneumonia. A pre-existing phthisical cavity will take on acute phases, also the septic element will be reinforced, and, as indicated in the enumeration of symptoms, clinical irregularities will be introduced. The early prostration is increased, and the patient dies from exhaustion after a period varying from three days to six weeks from the time the gangrene became manifest. Various complications, such as pleuritis and perforation of pleura and pneumothorax, hemorrhage, or extensive, diffused gangrene may cut short the patient's life within the average period. Occasionally the gangrenous cavity becomes chronic and the patient may live for months in imperfect health. The termination of the circumscribed variety is usually death. Diffuse gangrene is invariably fatal.

TREATMENT should be directed, first, to the known precedent states of constitutional weakness, bad habits, etc., which lay a foundation for unhealthy inflammatory processes, and for the pathogenetic elements that bring about the gangrenous and septic and exhausting conditions; second, to the special symptoms, such as severe pain in the side, harassing cough, dyspnoea, etc. Remedies of the first class are quinia, turpentine, early alcoholic stimulation, carbonate of ammonium, antiseptics, as carbolic acid, etc. An anticipation from the beginning of any irregular form of acute pulmonary disease of its termination in gangrene is impossible, and hence early treatment is necessarily general. It would be properly confined to the use of quinia, which would be useful, either before or after the gangrenous element had developed, in small doses frequently given, unless high temperature or the septic process indicate the use of large ones. Turpentine internally is desirable in proportion to the infectious or typhoidal character of the attack. Its use by inhalation is beneficial when gangrenous destruction has already taken place. Brandy or whiskey in moderate and frequent quantities, one-half to one tablespoonful every three hours, and carbonate of ammonium, meet the requirements which the tendencies to debility indicate. Milk, milk-punch, beef and chicken extracts should be given in the intervals between the administration of medicines. This general plan is applicable throughout the pre- and post-gangrenous stages. In the symptomatic treatment pain and a general respiratory distress often demand attention. Opium is then useful, both in relieving pain and moderating dyspnoea and cough. As these symptoms are often urgent in the later stages of gangrene of the lung, the treatment of the disease harmonizes both in its constitutional and symptomatic aspects. Prescriptions can also be readily prepared which contain remedies that have a decided effect in correcting the fetor of the breath and expectoration, and thus evincing an influence on the putrefactive process or ferment, which has become the prominent feature of the disease. The author recommends that carbolic acid, in the dose of one grain every four hours, be given for that purpose, and also its use by inhalation. Assistance can sometimes be given by putting the patient in such a position on the side as to promote the emptying of the cavity.

Tapping a gangrenous cavity and the introduction of drainage-tubes may be successfully resorted to. The cases suitable for such surgical treatment have been described by Fenger and Hollister¹⁸ as those where, "the presence of a gangrenous or ichorous cavity having been ascertained, it is found that notwithstanding an outlet through the bronchi for a portion of the contents of the cavity, it steadily fills up again; the partial evacuation does not relieve the patient; the infection of the healthy portions of the lung from the decomposed contents of the cavity has commenced or is evidently about to take place; the breath and expectoration continue fetid; absence of appetite; increasing weakness, with or without fever, etc." For the steps of the operative procedure reference may be made to the complete directions given by the same authors or to works on surgery. The double opening advised by the above authors would be the most efficient plan.

¹⁸ Amer. Journ. Med. Sci., Oct., 1881, p. 385.

CROUPOUS PNEUMONIA.

BY ALFRED L. LOOMIS, M.D.

SYNONYMS.—English and American: Acute sthenic exudative pneumonia; Primary lobar pneumonia; Vera peripneumonia; and Pneumonitis. Fr. Fluxion du poitine and Fièvre pneumonique; Ger. Pneumonia lobaris and Lobäre Lungenentzündung.

DEFINITION.—Croupous pneumonia is an acute general disease with a characteristic local pulmonary lesion. Anatomically considered, it is an acute inflammation of the vesicular structure of the lungs, resulting in infiltration of the alveoli, with inflammatory products, which renders them impervious to air. This condition is known as hepatization.

HISTORY.—Until the time of Laennec, pneumonia and pleurisy were described as one disease. Hippocrates said that pleurisy was "a disease quickly fatal, and characterized by sputa of various colors." Although these two diseases were undifferentiated, accurate descriptions of the lesions and objective signs of pneumonia have come to us from the earliest medical writers.¹

¹ Thucydides, The Plague at Athens, B.C. 430.

Much of the early history of this disease is interwoven with the detailed accounts of a great variety of pulmonary symptoms which occurred in the epidemics and plagues which prevailed in Eastern Europe in the centuries just preceding the Christian era, and in Western and Southern Europe during the sixteenth and seventeenth centuries. The black death has been regarded by some as an epidemic of pneumonia. While it is probable that in most of these epidemics the lung was early involved, and that its implication hastened death, yet no proof exists to sustain the belief that they were other than epidemics of typhus fever, dysentery, and those (as yet unknown) fevers which collectively were named plagues. That many of these plagues were complicated by pneumonia there is scarcely room for doubt.

French investigators were the first to separate the pneumonic process from all other morbid processes which occur in the thoracic organs. Valsalva, Morgagni, and Boerhaave gave accurate descriptions of pneumonia, but they did not sharply distinguish it from pleurisy. Bichat and Pinel separated collapse of the lung attending pleuritic effusion from inflammation of the lung-substance.² Laennec was the first to draw the line sharply between pneumonia and pleurisy, and to him, more than to any other observer, is due the credit of describing pneumonia as a distinct disease. With his labors begins a new era in the history of pulmonary inflammations.

² Nos. phil., ii., Pinel.

Grisolle's work³ is especially valuable in statistics relating to the climatic element in the development of pneumonia and its comparative frequency among different races. The elaborate treatise on the geographical distribution of pneumonia by Ziemssen has furnished data for a more accurate knowledge of its geographical boundaries. Following in the footsteps of Laennec, Chomel, Stokes, Addison, and many laborers of our own day have furnished the material from which the clinical and pathological history of pneumonia is now being constructed.

³ Traité de la Pneumonie.

Recently, Jürgensen has strongly advocated the infection theory of pneumonia, and has presented strong arguments in support of his opinions. Sturges of London and Cohnheim⁴ advocate the use of the term pneumonic fever, and the former gives a most interesting general comparison between it and the affections which he regards analogous to it. Careful pathological experiments have recently been made by Heidenhain, Sommerbrodt, Schuppel, and Klebs⁵ with a view to establish the germ-theory of pneumonia.

⁴ Leçons de Chir. méd., 1877, p. 17.

⁵ Arch. für experiment. Pathol., p. 420.

The literature of the past ten years is richer in the development of facts and experimental investigations than all the centuries that have preceded; and these recent experiments, combined with modern statistics and the results of the microscope in pathological histology, have given to croupous pneumonia a separate and distinct place in the list of pulmonary diseases.

MORBID ANATOMY.—Anatomically as well as clinically, there are three recognized stages in croupous pneumonia: 1, Stage of engorgement or congestion; 2, Stage of red hepatization; 3, Stage of gray hepatization, resolution, or purulent infiltration (suppuration).

It has been claimed that the stage of engorgement is preceded by a dry stage, or "stage of arterial injection," in which the lung-tissue is dry and of a bright-red color. It is evident that congestion of the minute branches of the pulmonary artery would not give to the lung-tissue a bright-red color, and if such a condition exists it must be due to injection of the bronchial vessels. It is by no means proven that such injection ever precedes pneumonic engorgement. In the stage of engorgement that portion of the lung which is involved in the pneumonic process does not collapse when the thoracic cavity is opened. The affected portion of lung is distended and firmer than normal lung-tissue, and when pressed upon crepitates less, often remaining indented after the pressure is removed. The lung is not entirely airless, for by pressure the air can be forced from one portion of it to another. Its color is darker than normal, usually being of a brownish-red or purple. There is an increase not only in its actual weight, but in its specific gravity. On section a thin, frothy, blood-stained serum exudes, and sometimes on pressure flows freely from the cut surface; occasionally this exudation is tenacious. When alcohol is added to this fluid, it coagulates into a granular, amorphous mass.

The capillaries around the air-cells are distended, and dark blood oozes from their divided ends. Occasionally, upon close examination, there may be seen beneath the pleura and between the air-sacs small points of blood-extravasation. A portion of lung in this stage, when placed in water, does not float as near the surface as healthy lung-tissue.

When examined with the microscope, the lumen of the alveoli are seen to be diminished by the encroachment of the varicosed and tortuous capillary vessels. As a rule, the air-sacs are uniformly dilated; some, however, may be collapsed—a condition probably due to pressure during the early period of the pneumonic process. The epithelia of the alveoli are swollen, and contain a granular protoplasm with free nuclei. The air-vesicles also contain exfoliated epithelial cells and white and red blood-corpuscles. The serum which escapes into the alveoli from the distended capillary vessels is the fluid in which these cell-elements float. Since the enlarged epithelia often suffer a division of their protoplasm, embryonic mono-nucleated cells are intermingled with the other elements. It is still a disputed question whether the bronchial or the pulmonary capillaries are the chief source of the pneumonic exudation.

Physiology teaches that lung-tissue is nourished by the blood in the ramifications of the bronchial arteries, and that the pulmonary capillaries are the passive media for the interchange of gases. Hence it is claimed that the bronchial capillaries only are implicated in the inflammatory process. Virchow has shown that the pneumonic process can be completely established in places where pulmonic capillaries cannot be traced on account of the plugging of a large branch of the pulmonary artery;⁶ yet even he admits that secondarily the pulmonary vessels have much to do in the inflammatory process.

⁶ Ges. Abhang., p. 369, Virchow.

On the other hand, it is claimed that in the early stages of the pneumonic process the parts that are supplied by the bronchial capillaries are not reddened or injected, as they would be were these vessels primarily concerned in the inflammatory process. Reasoning from the above, it would seem that both sets of vessels are involved, but that usually one set is implicated at the very commencement to a greater extent than the other.

It is often difficult, and sometimes impossible, to differentiate between the anatomical appearances produced by pulmonary congestion and oedema and the first stage of pneumonia. In pulmonary congestion and oedema the fluid in the alveoli is serum, and contains none of the pathological cell-elements found in the first stage of pneumonia. The alveolar capillaries are turgid, and in this respect resemble the capillaries in pneumonic congestion, but when a stream of water flows over a portion of lung in the first stage of pneumonia its dark color remains, while in hyperæmia of a non-inflammatory character this is not the case.

On account of its color and its resemblance to liver-tissue the name red hepatization has been given to the second stage of croupous pneumonia. The lung in this stage has a dark liver or mahogany color, and is slightly mottled, the mottling becoming more marked the farther advanced is the hepatization. The color is of a brighter red when the lung is first removed from the body than after it has been exposed to the air.

The volume of the lung is increased—at times so as to bear the impress of the ribs. It is solid and firmer than normal; pressure does not indent but tears it; it is very friable, and its torn surface presents a granular appearance. Its specific gravity is increased. It is airless, and there is an entire loss of crepitation.

Upon section it is seen that the granular appearance of the cut surface is due to the pneumonic exudation which fills the alveoli. This granular appearance is not so well shown on the cut as on the torn surface. The granules can be readily removed from the air-cells by means of a fine needle. A dirty, red, viscid fluid slowly oozes from its cut surface, which is more apparent after the lung has been exposed to the air for twelve or twenty-four hours and has undergone post-mortem changes. At any time this viscid, rusty-looking material may be scraped from the cut surface, or it exudes when a portion of the lung is firmly compressed. A portion of the inflamed lung quickly sinks in water, and small spots of blood-extravasations may be seen scattered here and there throughout its substance. When a stream of water is poured over the cut surface of the implicated lung the color changes from a maroon to a gray or yellow-gray, the usual color of fibrillated fibrin.

Not infrequently the material in the infundibula and air-cells extends into the minute bronchi, but these tubes are rarely completely filled with the pneumonic exudation. When examined under the microscope the alveoli are found filled with a solid material composed of a network of fibrillated fibrin, in whose meshes are leucocytes, red blood-globules, and changed epithelia. These latter are in various forms, usually round or oval. They may, however, become quadrangular, triangular, or irregular. They are granular, and may contain a single nucleus, a nucleolus, or multiple nuclei. These cells finally become granular, and fat-globules accumulate in them. They also become discolored from imbibition of blood-coloring matter, so that in the latter part of the process there is quite an accumulation of pigment-granules, not only in the free cells, but in the fixed epithelia. The larger cells discharge their nuclei into the accumulation of corpuscular elements, and the whole contents of an alveolus present a more or less round shape. The alveolar walls remain unchanged, or are slightly thickened by the capillary turgescence. All of these different cell-elements have been regarded by different observers as characteristic of pneumonia. The red globules give the color to the consolidated lung. The pus-cells are always numerous.

The transition from red to gray hepatization is never well defined. The mottling gradually becomes more marked, so that the affected portion of lung assumes a marbled or granite appearance. As the deep-red color of the second stage fades the density of the pneumonic consolidation becomes less and less, until it is a mere pulp, breaking down under slight pressure. The decoloration is due to the pressure on the blood-vessels, to decoloration of the blood-corpuscles that were present in the second stage, and to fatty degeneration of the other cell-elements which occupied the air-sacs.

The weight and density of the affected lung-tissue are diminished, and toward the end of this stage the lung crepitates. On section a nearly uniform dirty-gray, bloodless surface is exhibited, from which flows spontaneously or upon slight pressure a dirty-white or reddish-gray puruloid fluid. The granular red hepatized look has disappeared or is very indistinct. The amount of oedema in the affected portion of the lung varies in different cases. When it is excessive a large quantity of serum exudes from the cut surface, which then exhibits a smooth, non-granular, glistening appearance, and it does not so readily break down when pressed upon as do other forms of gray hepatization. When examined under the microscope, the alveoli are seen to be filled with numerous round mono-nucleated cells, the intercellular fibrils that bound the elements together having disappeared; in other words (the fibrillated having become granular fibrin), the alveoli are filled with a fluid or semi-fluid mass in which numbers of discrete oil-globules and protein granules are freely mingled.

The granular and fatty elements are due to the rapid degenerative changes that occur in the cell-elements. In this stage leucocytes still emigrate from the blood-vessels. The masses that occupy the alveoli are now shrunken, and between them and the alveolar wall is a layer of fluid, so that in a thin section the contents of the air-sacs are readily lifted out by a camel's-hair brush. All of the affected portion of the lung is rarely in the same stage of the inflammatory process, and to distinguish red from gray hepatization, or the latter from the beginning of some of the conditions next to be mentioned, is often impossible.

The changes which take place subsequent to the stage of gray hepatization, and the modifications due to age, remain to be considered.

Croupous pneumonia may terminate—1, in resolution [recovery]; 2, in suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5, and very rarely, in chronic (fibroid) pneumonia.

1. During resolution the lung is moist, lighter than in the stage of hepatization, has a yellow or yellowish-green color, and still shows a marked loss in elasticity. On section, the lung appears to be non-granular, and a tenacious, puruloid fluid escapes when the section is pressed upon. Some oedema may still remain. When examined under the microscope the alveolar capillary vessels are seen to have returned to their normal calibre; the alveolar epithelium is restored; the cells in the air-sacs are degenerated, broken down, and resolved into a detritus. The degeneration of these cells is both fatty and mucoid, and the coloring matter of the blood gives origin to the granular pigment which is scattered throughout the disintegrated and liquefied mass. Some of the pigment is supposed to come from the connective tissue between the alveoli. In this condition the alveolar contents are either expelled by expectoration or undergo absorption, the lung being finally restored to its normal condition.

2. When purulent infiltration or suppuration of the lung occurs, its surface becomes yellow—more so than in any of the preceding conditions; it is soft, moist, and friable, and gives somewhat the sensation of an abscess. It is well described as miry.⁷

⁷ Pneumonia, Sturges, 1876, pp. 110, 113.

On section, a diffluent, purulent fluid exudes from a surface whose yellow color is due both to the large number of cells which are undergoing fatty degeneration, and to the anæmia which results from over-distension of the alveoli with these cell-elements.

When examined under the microscope, the cells are found not only crowding the alveoli, but infiltrating the inter-alveolar tissue. This corpuscular infiltration of the alveolar walls may so interfere with their nutrition that they will undergo softening and degeneration. Whether these cells (in all respects resembling pus-cells) have emigrated from the blood-vessels or are the result of epithelial changes is still unsettled. Reason and analogy seem to point to a dual origin. Now and then these cells are pigmented. Occasionally the alveolar walls become thinned, indistinct, and finally rupture.

There has been much discussion over the term suppuration of the lung, but the appearances reported by those who uphold, as well as by those who protest against, the term are identically the same, all agreeing that the "lung is filled with pus."

3. Abscess of the lung, as a termination of croupous pneumonia, is exceedingly rare, and is always preceded by extensive cellular or interstitial oedema; small abscesses are formed by the rupture of several of the alveolar septa. It may follow purulent infiltration. These abscesses vary in size from that of a pea to one which may occupy the greater part of a lobe. They may have a thick, well-defined, irregular wall, their interior being crossed by shaggy shreds of broken-down lung-tissue, or they may form irregular excavations in softened lung-tissue. They may be single or multiple. Several abscesses are often found in the same lobe. They increase in size by peripheral growth or by fusion of several small abscesses.

Abscesses are more common in the upper than in the lower lobes; their frequency is variously estimated as 1 in 30 or 60 cases. These pus-cavities, if of small size, may ultimately close by cicatrization, in which case they may open into a bronchus of sufficient size to allow of the discharge of their contents. Under such circumstances the contents of the abscess are expectorated; interstitial inflammation is set up around their site, which after a time encloses them in a firm connective-tissue wall; contraction ensues, and finally only a line of cicatricial tissue marks their former situation. Or if no such bronchial opening occurs, the abscess becomes encapsulated in firm cicatricial tissue, and the contents undergo cheesy and calcareous transformation. Sometimes these abscesses perforate the pleura and discharge their contents into the pleural cavity, causing pyo-pneumothorax. External fistulous openings have occurred, but they are a rare termination of pulmonary abscess.

4. Gangrene is said to be a termination of croupous pneumonia in about 2 per cent. of cases, but this estimate is based on too few statistics to be wholly reliable. It is met with in bad constitutions where there is very great vital depression, in chronic alcoholismus, and in cases of intense septic poisoning. Interference with the blood-supply, causing the formation of pulmonary or bronchial thrombi, leads to its development.⁸ While usually limited to a small area of lung-tissue, it may invade large tracts, and be either circumscribed or diffuse.

⁸ Huss, Pneumonia; Carswell, Ill. El. Forms of Disease.

The gangrenous portion of the lung is changed to a dark, dirty, pulpy mass, sometimes wanting the fetor of gangrene. When the mass has become diffluent, a sort of cavity is formed, in which are found fetid fluid and shreds of gangrenous lung-tissue. Around the gangrenous mass there is a zone of gray hepatized, friable tissue, which in turn is bounded by a zone of red hepatized tissue. When the above-named zones are not present in diffused gangrene, the cavities are large, and shreds of tissue and vascular bands traverse the cavity, which swarms with bacteria. Such a gangrenous mass may lead to sloughing of the pleuræ. It has been denied that a croupous pneumonia can terminate in gangrene, but modern pathologists all support the opposite view. It may be mentioned that gangrene in croupous pneumonia of the horse is of frequent occurrence.

5. Chronic (interstitial fibroid) pneumonia may result when the process of resolution in croupous pneumonia is delayed and the inflammatory process does not advance beyond the stage of gray hepatization. In such cases the walls of the alveoli, and finally the inter-alveolar tissue, become the site of new connective-tissue developments.

The peculiarly hard and oedematous condition that sometimes marks gray hepatization is, by some observers, regarded as an intermediate stage between croupous and interstitial pneumonia. An abundant cell-production in the second or third stage of croupous pneumonia may be followed by shrivelling of the alveolar contents, and subsequent cheesy changes may bring about one form of phthisis. Whether this can ever occur independent of tubercle is still a mooted question. This is called (by those who believe in such an origin of phthisis) cheesy infiltration, and is to be differentiated from tubercular infiltration.

In childhood croupous pneumonia is not of so frequent occurrence as catarrhal. In its anatomical changes it does not differ from croupous pneumonia in adults. In old age the pneumonic changes usually begin in the upper lobes of the lung, and extend downward—the reverse of what occurs in adult life. In the stage of engorgement crepitation is usually wholly absent, and when the stage of red hepatization is reached the color is found much darker than in adults, sometimes being blue or black; the lung is much more strikingly marbled, and on section the granules, in those cases where they are present, are much larger than in adult life. Frequently in senile pneumonia the granular look is absent. Gangrene is a far more frequent termination of croupous pneumonia in old age than at any other period. The highly-rarefied condition of the lungs at this period seems to favor the development of small abscesses.

Croupous pneumonia involves either the whole lobe or a whole lung. Its most frequent seat is the lower lobe of the right lung. Its next most frequent seat is the lower lobe of the left lung, then the upper lobe of the right, the middle lobe of this lung being least frequently involved. Double pneumonia has been variously estimated as occurring in from 5 to 50 per cent. of cases, but in all probability the percentage rarely, even in epidemics, exceeds 12 or 15 (Huss, Grisolle, Barth, Ziemssen). In old age the difference in point of frequency of attack between the two sides is very slight, and some affirm that sthenic is more frequent on the right and typhoid pneumonia on the left side. Double pneumonia is more frequent in the senile period than during adult life.

The average duration of the different stages is as follows: The stage of engorgement lasts from two to three days; the stage of red hepatization, from three to five days; and the stage of gray hepatization, from two to six days. In old age the stages rapidly merge into each other, and suppuration of the lung may occur within thirty-six or forty-eight hours from the onset of the pneumonia, while it is not at all infrequent for complete red hepatization to occur within the first six or eight hours.

The changes in the pleura over a pneumonic lung are quite characteristic. An uneven, thin, downy-looking layer of plastic lymph is spread over the pleural surface, which presents a fine arborescent vascularity. At times this plastic layer may partially conceal the liver-brown color of the pneumonic lung. As the stage of gray hepatization is reached, pleuritic adhesions are apt to be formed, which subsequently undergo absorption, and thus the pleuritic changes follow, to a certain extent, those which are taking place within the lung. The cell-elements in this fibrinous meshwork are chiefly pus- and large endothelial-cells. The pleura itself is opaque, congested, and ecchymotic, and may be so thickened as to give rise to a dull note on percussion after the pneumonia has undergone resolution. If there are adhesions from previous pleurisies, or pleuritic changes that have occurred prior to the lighting up of a pneumonia, they will modify its course and termination.

The right heart is dilated, and on inspection immediately after death it is not unusual to find both ventricles filled with pale, firm clots that insinuate themselves between the columnæ carneæ and sometimes extend into the vessels. The pulmonary vessels running to the affected portion of the lung may be the seat of thrombosis. Pericarditis is so frequently found at the post-mortem of those who die of pneumonia that its occurrence must be regarded as something more than either accident or complication.

The blood is hyperinotic in croupous pneumonia, and, while the amount of fibrin is only slightly increased at the very onset, the amount obtainable goes on increasing until the eighth or ninth day; i.e. as the amount of fibrinous exudation within the alveoli augments, so does the same factor appear in greater quantity in the blood—a circumstance whose opposite condition we should expect to observe. In infectious diseases—e.g. variola—as the temperature rises the hyperinosis increases. In pneumonia, however, the pyrexia and fibrin increase in the blood and bear no relationship to each other. The amount varies greatly in every case; it has reached 10.5 in 1000.

Around the zone of pneumonic inflammation it is not infrequent to discover pulmonary oedema; and in many fatal cases extensive oedema seems to be the direct mode of death.

Temporary compensatory emphysema may occur in the neighborhood of the inflamed lobe or lobes. It may be mentioned that when emphysema has previously existed the pulmonic granules observable in the second stage are of unusually large size.

The bronchial glands are enlarged and congested, and in rare instances they may suppurate. The lymphatics of the lung are choked with fibrin and with red and white blood-corpuscles, and the deeper lymphatics contain products identical with those in the pulmonary alveoli. In both lymphatic vessels and in the lymph-glands (bronchial) at the root of the lung there are always well-marked evidences of inflammation.

The liver and spleen are congested, the latter organ especially presenting the characteristics which are found in it in cases of death from fevers.

Finally, gastro-intestinal catarrh is occasionally observed, and in rare cases it is attended by ulceration and hemorrhage. But there seems no good reason for believing that there is any connection between pneumonia and these intestinal changes. Indeed, most of the observations bearing on this point were made during cholera epidemics. Still, analogous influences might induce both at the same time.

No change in the brain accompanies pneumonia, except congestion. Pus and inflammatory products when found in the meshes of the pia-mater are in all probability due to coexisting meningitis or cerebro-spinal meningitis of an epidemic character.

ETIOLOGY.—The specific cause of croupous pneumonia is as yet undetermined, and the very existence of such a cause is still a matter of conjecture.

Among the predisposing causes age ranks first. There are three distinct periods of life in which the liability to pneumonia is greatest—viz. in early childhood, between the ages of twenty and forty, and after sixty.

Notwithstanding the fact that catarrhal pneumonia is a very common disease in childhood,⁹ the statement that croupous pneumonia is rare at this period cannot be received.¹⁰ From a number of statistical tables it appears that it is five times more frequent during the first two years of life than in the succeeding eighteen.¹¹ It is met with most frequently between the ages of twenty and forty, and after a lapse of twenty years the predisposition to it increases, pneumonia being the most fatal of all acute diseases after the sixtieth year. Nine-tenths of the deaths from acute diseases after the age of sixty-five are from pneumonia. Each year after sixty the liability to it is greatly increased.

⁹ "Die lobuläre pneumonie ist im Sänglingsalter eine ausserordenich häufige Krankheit" (Vogel, Kinderkrankheiten, p. 222).

¹⁰ "Lobäre pneumonie kommt viel seltener vor" (Vogel, loc. cit.).

¹¹ Klinik der Kreislaufs u. Athms. org., Breslau, 1856.

In early life, in what may be denominated the first period, anterior to the second year, males and females are very nearly equally affected. Between twenty and forty, the time when the condition of males and females is most diverse, the proportion is 3 males to 1 female, or at least 2 to 1. After sixty, when the hygienic condition of both sexes again differs very slightly, this proportion is less striking, and the disease is pretty evenly divided between old men and old women; still, the male sex always furnishes more cases than the female. When women work as men do, or when both sexes are huddled together (as in prisons), then the difference between them is lost.