Chapter XIX: Part 19

The same early hyperæmia accompanies the development and growth of tubercle, whether it come from the bronchioles, the blood-vessels, or alveolar walls. Trasbot[48] says: "A tubercle is found to be developed along a small artery, most frequently at the angle formed by a terminal division of the vessel--some around a capillary, around which it forms a kind of bead, or in the network of an anastomosis, which envelops it on every side. Vessels are more numerous in the tissues round the nodules and in the septa or interstices of the large masses than in the healthy connective tissue: there the vascularity is often so great as to be mistaken for inflammation."

[Footnote 48: Quoted by Creighton Bevine, _Tuberculosis in Man_, p. 133.]

Hamilton,[49] speaking of the formation of tubercle in the alveolar wall and cavity, says: "Capillary blood-vessels, filled with blood-corpuscles, are drawn into it, and in this stage are distinctly visible. They are all much engorged, and occasionally minute extravasations are visible, the blood-corpuscles being thrown into the alveolar cavity." The chance of an earlier obliteration of vessels is greater under these circumstances than where the process begins in any other structure. The final result is that combination of catarrhal and tubercular products characteristic of mixed phthisis.

[Footnote 49: _The Pathology of Bronchitis, Catarrhal Pneumonia, Tubercle, etc._, 1883.]

As increased vascularity accompanies and surrounds the nascent tubercle, so vascular neo-formations accompany or are intermixed with the obliterated zone of vessels, as long since described by Guillot and recently substantially confirmed by Ewart. The former says:[50] "There result numerous and inextricable anastomoses, which extend incessantly, and of which the whole forms a mass of vessels proportional in extent to the age of the tubercles and cavities that they entirely surround."

[Footnote 50: _L'Expérience_, vol. i. p. 553.]

{281} There ensues a connection between this system and that forming on the false pleural membranes, and a supplementary function of supply for regions outside of the area of obliterated vessels and for walls of cavities is established. Considering the want of vitality of new formations generally, it is quite probable that these become sources of hemorrhage occasionally. Successive extensions of the diseased regions reduce the amount of this supply, so that the converse follows--comparative anæmia of the lung involved and diminished tendency to hæmoptysis in some of its forms.

These observations, involving considerations of predisposition and its tangible forms, do not apply to the important class of cardiac hæmoptysis. The factors here are increased venous tension, pulmonary hyperæmia of mechanical rather than vital origin, sclerosed or atheromatous vessels, capillary ectasis, and embolic obstruction of the pulmonary artery with resultant infarction, etc.

SYMPTOMS.--The definition requires that the blood be pure or unmixed, yet the coarse physical appearances may vary a good deal. The color is usually a bright red, but may be dark or venous in hue. There is sufficient inconstancy in color to prevent its being reliable in distinguishing the special source of the bleeding, though usually the bright color is of bronchial and the dark of pulmonary origin. If bright red at the onset, it loses some if not the whole of its brightness as the attack progresses or is subsiding, sometimes because of retention in the air-passages. The mass is more or less frothy, and varies in density and specific gravity, in diffluence or adhesiveness, the latter quality increasing in proportion to congestive or inflammatory conditions, whether in the early or later stages. This is dependent on the increase of the plastic, fibrinous, or reactive elements in the blood and adjoining tissues. The mass may lie in a circumscribed or in a splashy form in the bottom of the vessel, circumstances of distance and force of ejection, as well as of physical quality, producing the variations. The quantity varies greatly, both as to the amount at each act of expectoration and as to the amount during all of them. The whole amount throughout an average attack of initial hæmoptysis might be placed at about one and a half to two ounces. Such would be called moderate but decided hemorrhage. The extremes would range between a teaspoonful and several pounds, and the time consumed in the attack may vary between the time taken up by one or two ejections and several months. The intervals between the successive ejections will vary from a few minutes to twenty-four hours or more in a case lasting a week. The manner of ejection is sometimes by a single effort of hawking or throat-scraping or clearing, sometimes by a slight hacking cough or by a vigorous effort of expulsion; at other times the outflow is so rapid through the mouth and nostrils that it resembles vomiting and may suggest a hemorrhage of the stomach.

The effect which a severe attack may have on the patient is often notable. He becomes pale out of proportion to the amount of blood that he has lost; the pulse is full, bounding, and corresponds to what is called the hemorrhagic pulse. This is sometimes due to the mental shock, but again it is independent of any excitement on the part of the patient, or of even any sort of constitutional disturbance, as fever. We have seen it in full development in connection with a profuse hæmoptysis and a temperature of 105°. It has been noted also as part of the phenomena of hemorrhage produced by septic influences upon the vaso-motor system. Walshe's dictum is no doubt true, that there is a calm and excited variety quoad cardiac action.[51] In the former there is little vascular or mental excitement or debility, and the patient does not willingly yield to the necessary restraint.

[Footnote 51: _Diseases of the Lungs_, p. 330.]

Feebleness is an accompaniment, sometimes to a degree disproportionate to the amount of blood lost, and is an element in the shock which the patient {282} feels at so unexpected an event. The early part of the attack is usually without fever. This comes on later as a part of the reaction phenomena, and becomes then a very important prognostic symptom. We have known it, however, to range as high as 105° before the hemorrhage appeared, and without any reduction by a most obstinate continuance of the depletion.

Many cases occur without premonition. In a proportion there are symptoms precedent to the outbreak. The significance of these is often not perceived until the hæmoptysis appears. Certain subjective symptoms are common. A sense of burning, which is substernal or unilateral, corresponding to that lung which is then or shall afterward show itself affected; soreness within the same bounds; dyspnoea, rarely grossly objective; slight hacking cough for variable periods, and, more immediately antecedent, a salty taste in the mouth,--are some of these. They have their origin in a state of hyperæmia or irritation which has its outcome in catarrhal processes or hemorrhage. Which it may be will depend on certain predisposing as well as the immediately operative causes already mentioned.

Of the objective states, some importance may be attached to characteristics of the individual, such as the brunette complexion, dark hair and eyes, or to external correspondences with others of the family known to have been similarly affected.

More than the usual care is necessary in the physical examination, particularly in the use of percussion. Palpation and auscultation can be safely applied, but there might be greater difficulty in getting the patient into a good position for the actual examination. In the hæmoptysis of incipient phthisis the physical signs most usually found are deficient expansion and resonance and vesicular murmur at either apex. These are evidences of causes that had been in operation before the hæmoptysis, and indicate important physical changes at the region where they may be found. Yet they do not necessarily indicate that the bleeding has its origin at that place. Add moist bubbling râles, and the presumption becomes almost a certainty that you have found the locality of the hemorrhage. If these subside as the amount of blood expectorated gets smaller, the inference is still stronger. Successive increments of physical signs would indicate that the bleeding had been correctly located and that the lesion which gave origin to it was progressing. A proportion of cases occur where no physical sign can be found even after careful examination, so that it happens sometimes that at the period of most importance for diagnosis physical signs are not available, and when they are most distinct in the advanced cases the diagnosis is already established. They may even become embarrassing by their abundance. The true significance of the physical signs cannot be determined until the attack has subsided entirely. The termination of an attack is usually by disappearance of the congestion of which the symptoms related were the expression. The soreness and oppression beneath the sternum, the dyspnoea and fever, are relieved. The persistence of cough would not necessarily augur badly, because there is apt to be some catarrhal secretion which necessitates it. The general result is relief. If the termination is to be unfavorable, there will be an evident increase of constitutional symptoms, especially of fever, as in the case alluded to above with the high temperature. There will be a slower return to the pre-hæmoptic state and an increase of the physical signs, and you may have apparently a case of phthisis ab hæmoptoe. The impetus in a large majority of cases is from the constitutional elements which initiated the symptoms, rather than from the local cause, blood within the air-passages. Clinical experience proves that there are cases where serious and rapid injury to the lungs has followed closely upon an hæmoptysis. It is admissible to classify such as phthisis ab hæmoptoe only, in the sense that the effusion of blood in the remote parts of the lungs has brought about catarrhal pneumonia, which in those predisposed {283} ends in phthisis. Sommerbrodt's[52] experiments proved that the healthy animals recovered from the catarrhal pneumonia.

[Footnote 52: _Virchow's Archiv_, vol. lv. p. 192.]

To determine the genuineness of any such special case, we should be able to include inherited or acquired predisposition; to prove priority of the hæmoptysis to cough, dyspnoea, and fever, and that these followed soon after the bleeding; and to show that the age at the time of the occurrence was not the phthisical age. If a direct or mechanical cause can be found for the bleeding, the proof would be still stronger. Most of the cases depended on to prove phthisis ab hæmoptoe or hemorrhagic phthisis (Powell) do not answer to these requirements. In the 8 cases reported by Sokolowski[53] are summarized these features, and they give strong support to the conception of a phthisis ab hæmoptoe. The mode of termination by sudden death is by syncope, and suffocation cannot be said to be very frequent. There have not been more than 3 suddenly fatal cases (within a half hour) in the Cincinnati Hospital records in a period of fifteen years: 22 cases are given in the second medical report of Brompton Hospital, where the cases of phthisis are very numerous; Powell's table[54] has 15 cases, which happened at the Brompton Hospital between February, 1868, and November, 1870. The cases which we have collected as occurring since that amount to about 20. T. Williams[55] says that of 198 patients who died, 4 died of profuse hæmoptysis. Thompson[56] says that of 383 deaths occurring in the hospital (Brompton) during three years, 26 were from fatal bleeding--a percentage ranging between 2 and 6 in the two series.

[Footnote 53: _Berlin. klin. Wochenschrift_, 30 Sept., 1878.]

[Footnote 54: Vol. xxii., _Lond. Path. Soc. Tr._]

[Footnote 55: _Med.-Chir. Trans._, vol. liv.]

[Footnote 56: _Loc. cit._, p. 115.]

The symptomatology given above is a general one. Looked at with reference to the varieties of hæmoptysis, the assignment would be to the earliest or initial attacks. Assuming five varieties--1, the simple or idiopathic; 2, the congestive; 3, the ulcerative; 4, the cavernous; 5, the extra-pulmonary--it would belong to the simple or to the congestive form.

Under the first may be included those cases which occur without any heredity or traceable cause, are not accompanied by fever, soreness, dyspnoea, or physical signs, and which further observation shows are not followed by pulmonary disease. Such cases are rare, yet clinical records afford them. Time is so important an element in the diagnosis that the presumption would be against such a classification at the time of the call for treatment. They have probably developed the hemorrhagic element of phthisis, and by otherwise vigorous constitutions are protected from its further evolution.

The congestive form is the one with which we most often meet, and is essentially the expression of the predisposing element mentioned as one of the agencies of heredity. Unlike the idiopathic variety, it has its positive symptoms, so familiar to the practitioner. Special clinical forms, as the hæmoptysis of pregnancy, the so-called vicarious cases, the earliest attacks in the hemorrhagic variety of phthisis, the hæmoptysis of plastic bronchitis (which has a phthisical element in it), that of hydatids of the lung preliminary to the opening of the hydatid, and probably others, such as cancer of the lung, may be placed in this category. Hysterical hæmoptysis is a term of doubtful propriety, because facts show that the tubercular diathesis has close affinities with the neuropathic heredity,[57] and hence that the hæmoptysis arises from the tubercular and not the neuropathic element. From this point of view it has its congestive origin, and can be properly classified under this head.

[Footnote 57: J. Grasset, _Brain_, vols. vi. and vii.]

The ulcerative form is familiar to us in the second stage of phthisis. It is more subordinated to the constitutional features, fever, hectic, and debility, to the purulent expectoration, and to the easily-determined physical signs. {284} Notwithstanding the apparently increased chance of profuse hemorrhage, the quantity of blood is often quite small and apt to be accompanied with a mixed sputum. It is not so florid as in the congestive form. Some of the most copious hemorrhages in this stage arise from the presence of the hemorrhagic diathesis or are found in persons of full and plethoric habit. They will recur at intervals of once or twice a year for many years, and some of them finally cease, with a remainder of physical signs. The physical signs usually indicate nothing more than consolidation of the lung for a long time. They are dulness, bronchophony, bronchial breathing, and mucus or crackling sounds over a limited area in the upper part of the chest. In the slow cases of pulmonary fibrosis there is now and then a small amount of ulcerative action to produce hæmoptysis. We have seen cases fatal by a suffocating quantity without discovery of the actual source.

In cavernous hæmoptysis there are striking facts which give this class a great interest. It includes most of the suddenly fatal cases which shock families or hospital inmates. It comes from rupture of small aneurisms in the walls of old cavities. A less dangerous form is that from small granulations or vessels in the walls of recent cavities or from small vessels in their trabeculæ. The elucidation of hemorrhage and death from pulmonary aneurism is of the later acquisitions in our knowledge.[58] A distinction between the ulcerative and pulmonary aneurism forms is not always practicable. A detection of the aneurism by auscultation has not been recorded, though it is at times quite large. In the latter form you may have, as in the former, repeated attacks of hemorrhage before this fatal one. The most decisive indication in favor of the aneurismal source of the bleeding, besides frequent and abundant hemorrhage, would be the proofs of a chronic cavity. In Powell's[59] 15 cases of fatal hæmoptysis 3 were without discoverable source; of the other 12, 3 were immediately fatal; in the remaining 9 the previous attacks of hæmoptysis occurred at periods varying from eighteen months to two days. The aneurisms were all in the left lung except 2: 6 occurred in individuals with family histories of phthisis; 3 with such histories; 2 are negative or doubtful of fatal hæmoptysis.

[Footnote 58: Williams says that Peacock and Fearn of Derby were the first to record instances of pulmonary aneurism in England. Stark in his works edited by J. C. Smyth, 4th Lond. ed., 1788, p. 31 (quoted by Young, _loc. cit._, p. 331), relates a case of diseased lungs in which sudden death took place from the bursting of an aneurism of the pulmonary artery.]

[Footnote 59: Vol. xxii., _Path. Soc. Trans._, London.]

We have a table of cases collected from reports made since Powell's--in all 21. In 10 the aneurisms were in the left lung, 8 were in the right, and in 3 the place of the aneurism was not designated; 16 were in males, 4 in females, and 2 not noted. The relation of heredity to phthisis was not noted, except in 1, which was affirmative. In 2 there was no previous attack of hæmoptysis. The longest interval between the first and fatal attack was four years: 7 were immediately fatal. From both collections we have 33 aneurisms of the pulmonary artery in cavities, 20 being in the left lung; 10 were in the right. Most of the aneurisms were situated in the upper lobes, as might naturally be expected. Powell's opinion was that there were good grounds for saying that the more chronic and quiescent the cavity, and the more unilateral the disease--the more nearly, in short, it approached the type of fibroid phthisis--the more probable it was that the hemorrhage, if it occurred in any quantity, proceeded from a pulmonary aneurism. Taking 15 cases from our list the duration of which could be fairly named, the average was about seventeen months. The average duration of Powell's cases was about twenty-four months. Most of our cases were bilaterally affected, and only 2 were positively stated to have been of the fibroid variety. Yet, practically, {285} the clinical features enumerated by Powell form the best standard by which to determine the source of the fatal hemorrhage. Copious hæmoptysis, with great chronicity and quiescence of phthisis and cavernous physical signs, points to aneurism of the pulmonary artery within the cavity.

In the class of extra-pulmonary hæmoptysis are included those cases of ulceration and rupture of aneurisms of the aorta and its branches into some portion of the air-passages, and the necessary discharge of blood therefrom. Experience justifies a classification of this kind. Cases have occurred where the pulmonary symptoms and signs have been so prominent as to have obscured those of the coexistent and causal aortic aneurism until the fatal hæmoptysis revealed the mistake. Still others of simultaneous tubercular disease of the lungs and aortic aneurism are reported. J. W. Ogle[60] reports a case where the patient had had cough for seven years, at first attended with hæmoptysis, dyspnoea, and palpitation, and afterward consolidation of the left lung, and where death was produced by rupture of aortic aneurism into the right bronchus. Bronchitis and pneumonia have been treated without suspecting the real cause until a similar event occurred. Janeway and Loomis[61] also give instances of aortic aneurism and phthisical deposits with doubtful diagnoses in the same persons. We have seen an instance where illness began with cough, frothy and then purulent expectoration, then loss of flesh and strength and pain in side, fever to 102, dulness below right clavicle, and then a number of large hemorrhages, and finally a fatal one, all of the hemorrhages depending on an aneurism of the internal carotid artery discharging into the mouth. The chances of these irregular clinical associations must, then, be borne in mind. Careful examination only will enable us to eliminate the doubtful features.

[Footnote 60: _Lond. Path. Soc. Trans._, vol. xvii. p. 104.]

[Footnote 61: _N.Y. Med. Rec._, vol. vii. p. 304.]

In a collection of 33 aortic aneurisms discharged through the air-passages, 9 had histories of hæmoptysis previous to the last one. These discharges were more or less copious, and, considering the physical signs of phthisis obvious in some, and recollecting that aneurisms were not recognized, the clinical features were such as to produce if not justify a diagnosis of intrapulmonary hæmoptysis. Of the 33, 16 opened into the left bronchus, 14 into the trachea, 2 into the right bronchus, and 1 is given without special designation of the point of communication. Of 2 aneurisms of the arteria innominata, both opened into the trachea. Aneurisms of the subclavian have also been known to have discharged through the apex of the lung. These clinical and anatomical facts point to a large predominance of symptoms and lesions connected with the left lung where the pulmonary organs are at all affected. In our own table, while 18 had marked lesions and symptoms pertaining to the left, only 6 had them connected with the right lung. These figures are too limited to be decided, but so far as they go they tend to prove a greater amount of left-lung lesion in extra-pulmonary than in cavernous hæmoptysis.

So far we have considered the symptoms and classification of phthisical hæmoptysis. There remain those other forms of pulmonary hæmoptysis connected with cardiac disease and hemorrhagic infarction. Practically, these are reduced to the first variety, as cardiac disease is the question we have most frequently to consider in this connection. We are justified in assuming the parenchymatous origin of cardiac hæmoptysis, because it rarely appears until chronic valvular disease has prepared the way for its occurrence by its well-known degenerative effects on the pulmonary circulation whereby thrombosis appears, and because at those advanced periods emboli are often injected into the pulmonary artery capable of producing hemorrhagic infarction and consequent hæmoptysis. This latter is accompanied by aggravation of symptoms already serious--increase of dyspnoea, cardiac perturbation, and probably cough. If the hemorrhage be copious, shock may appear, and varies {286} according to the size of the obstructed vessel and the amount of hemorrhage. The patient may have some premonitions, but not of the kind noted in the initial hæmoptysis of phthisis, such as the superficial soreness, burning, or pain localized in the substernal regions. The hæmoptysis, after it has begun, continues more regularly, at shorter intervals, and for a longer time, with the coarse appearance of the blood already mentioned, such as dark, non-aërated, coagulated sputum. The quantity may equal that from the most typical bronchial or broncho-pulmonary hæmoptysis in phthisis; usually it is not copious. Fever is not an ordinary accompaniment, but may develop in consequence of increased structural lesion, as from pneumonic infiltration around a large infarction. It has not then the typical range of ordinary pneumonia, seldom going beyond 100 or 101. The physical signs exclusive of the primary cardiac lesion are those pointing to limited infiltration of lung-tissue about the middle or lower region of the lung. We have limited areas where percussion is dull, almost as much so as over pleuritic effusion, and where the respiration is very feeble or suppressed, and later a bronchial breathing adjoining as a consequence of pneumonic complication. There may be several of these areas, varying in size. Sometimes the localization by physical signs is impossible because of the hemorrhage or infarction being small and deep-seated. Pain becomes a localizing symptom when the infarction is superficial and the pleura becomes involved. The form of valvular disease most likely to produce hæmoptysis is mitral disease, especially mitral obstruction disease.

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.

{287} 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. Thompson[62] 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."

[Footnote 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. Powell[64] 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.

[Footnote 63: _Edinburgh Med. Journal_, 1868-69.]

[Footnote 64: _Trans. London Pathological Society_, vol. xxii. pp. 54, 55.]

{288} 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's[65] 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.

[Footnote 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 {289} 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.

[Footnote 66: _Deutsches Archiv für klinisch Med._, vol. xxx. p. 154.]

Another element capable of modifying the hæmoptysical features of phthisis is claimed by Jaccoud[67] 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.

[Footnote 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. Hiller[68] 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.

[Footnote 68: _Centralblatt für die med. Wissenschaft_, March 24, 1883.]

[Footnote 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 {290} 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. Pollock[70] 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.

[Footnote 70: _Elements of Prognosis in Consumption_, p. 139.]

[Footnote 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 {291} 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. {292} It is better borne by the stomach, and can often be continued longer, than the medicines above mentioned.

[Footnote 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.

{293}

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.--Latour[1] is quoted as being the first to use the words, "apoplexie du poumon."[2] Yet Duguet[3] 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's[6] studies on infarction, which have some indirect connection with pulmonary apoplexy.

[Footnote 1: _Histoire philosophique et médicale des Hémorrhagies_, 1815, passage misquoted in _L'apoplexie pulmonaire_ by Duguet.]

[Footnote 2: _Op. cit._, pp. 220, 222, and 224.]

[Footnote 3: _Op. cit._, p. 11.]

[Footnote 4: Duguet, p. 10, etc.]

[Footnote 5: _Untersuchungen über die Embolischen processe_, 1872.]

[Footnote 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 statistics[7] 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).

[Footnote 7: _Brit. and For. Med.-Chir. Rev._, vol. xxxvii., 1866, p. 459.]

[Footnote 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 {294} 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.