Volume 3 — DISEASES OF THE RESPIRATORY SYSTEM. (continued 10)

It is probable, however, that, in addition to the propulsive power exercised on the blood by the contraction of the heart, another agency affecting its passage through the lungs is the interchange of gases in respiration; and therefore any interference with the reception of oxygen and the elimination of carbonic dioxide may tend to retard the blood-flow, and thus favor stasis or passive congestion. In this way the inhalation of impure air, especially air containing an undue amount of carbonic dioxide, may occasion passive hyperæmia.

Pulmonary oedema is never a primary affection, but is always due to some preceding disease. In the first place, it may, as already stated, take its origin directly from congestion of the lungs, the walls of the obstructed vessels allowing the transudation of serum, which will collect in the air-cells and connective tissue and also in the mucous membrane of the terminal bronchi. In an early stage it may be present in the walls only of the alveoli without being effused into their cavities.

Another cause of pulmonary oedema is obstruction of the circulation of a part of a lung, such as may take place in pneumonia or miliary tuberculosis, the vessels of other parts becoming distended by backward pressure, so that the serum of the blood will exude into the air-cells or interstitial tissue. When this occurs in pneumonia it may be a most alarming and dangerous complication.

Still another and very frequent cause of pulmonary oedema is Bright's disease in its different forms, in which the oedema occurs as a part of the general dropsy incident to these affections. In acute congestive nephritis it may come on very rapidly, constituting acute pulmonary oedema. Hertz remarks that an acute oedema may take place in the course of an acute nephritis, as has been reported by Lebert, but that such an occurrence is not frequent.¹ The writer of this article has himself seen several cases of acute pulmonary oedema occurring as a part of the dropsy of scarlet fever.

¹ Ziemssen's Cyclop., v. p. 279.

More frequently it is met with in chronic albuminuria, and varies in amount from time to time, as dropsical effusions elsewhere do in this condition.

Attacks of asthmatic dyspnoea are not uncommon in the course of Bright's disease, especially in cases of chronic contracted kidney. They are described as uræmic asthma, and are referred by some writers to the action of the depraved blood on the centres of respiration. This explanation may be correct in some cases, but it seems likely that they are due in part to dropsical oedema of the bronchial mucous membrane, the connective tissue, or the air-cells. A weakened condition of the heart, such as is apt to occur in advanced periods of Bright's disease, has probably some share in determining the oedema.

In any case of oedema, according to its situation, whether it is in the connective tissue, the bronchial mucous membrane, or the air-cells, and according also to the amount in which it is effused, it will interfere more or less with breathing. If there be interstitial infiltration with swelling of the bronchial mucous membrane, lessening the calibre of the tubes, there may be merely some embarrassment of respiration; but if the effusion invade any considerable number of the air-cells, urgent dyspnoea will be produced. Oedema is generally most abundant at the lower part of the lungs, and is not uncommonly associated with pleural effusion, the two conditions being due to the same cause; and then the interference with respiration is greater and more perilous.

SYMPTOMS.—It is possible that a slight degree of pulmonary congestion may exist when the circulation is hurried without the occurrence of any other symptoms except moderate acceleration of the breathing. Under such circumstances, however, the existence of congestion cannot be proved. When it is brought about in greater degree, either by over-action of the heart or sudden recession of blood from other parts, the earliest and most prominent symptoms are a sense of oppression in the chest and quickened, laborious respiration, which may rapidly increase until the dyspnoea becomes most urgent and distressing. The heart's action grows more hurried, the pulsations in the carotid and temporal arteries are strongly felt, and the face is deeply flushed. Cough is always present, at first dry in character and afterward accompanied with expectoration of frothy mucus, which may be tinged with blood or may be even mingled with a considerable amount of bright-red blood.

The different appearances of the expectoration are probably due to the fact that in some cases the distended pulmonary capillaries allow the transudation of blood-corpuscles, and in others they are actually ruptured by the strain, so that pure blood escapes from them.

If the congestion is due to weakened action of the heart, with remora of the venous circulation, and is passive in character, the symptoms may be less acutely developed and less urgent than they are in the active form; indeed, in some cases in which very considerable portions of the lung are involved there may be no excessive dyspnoea while the patient is quiet, in consequence of the organism having become gradually accustomed to the imperfect respiration.

As the congestion increases, however, and the lungs become more affected, the signs of malaëration are more conspicuous. Dyspnoea is more oppressive, the face and surface generally, especially the lips and extremities, become cyanotic and cold, and the patient perishes from apnoea and from coma occasioned by oedema of the brain or medulla or stasis of blood in the cerebral veins, the respiratory centres being paralyzed. With the occurrence of somnolence the efforts to free the air-passages from fluid by coughing and expectoration grow less and less as the sensibility is obtunded.

When the congestion is not very extensive the amount of air in the lungs is not lessened sufficiently to materially affect the percussion note, which may remain resonant, though it may have a somewhat tympanitic quality. The vesicular murmur is still heard, but it is rather rough in character. When the general symptoms indicate a graver degree of congestion there will be corresponding changes in the physical signs; resonance will be lessened, or even replaced by dulness, in consequence of the filling of the alveoli with serum or blood; and the respiratory murmur will be completely masked by coarse and fine mucous râles. If the dulness is very marked, bronchial breathing and bronchophony may be observed. Elsewhere in parts not involved in the congestion exaggerated or puerile breathing may be heard from the supplementary action that takes place there.

The physical signs may vary as to their situation with the patient's position as the blood in the congested vessels and the serum in the alveoli and connective tissue gravitate from side to side. But when the change described as hypostatic pneumonia has taken place, and the affected portion of the lung has become condensed in texture, position has little or no influence on the physical signs, which will still remain even when the affected side is kept uppermost.

When oedema of the lungs is produced by serous effusion invading the air-cells, there is some degree of dulness on percussion, especially at the lower part of the chest. Respiratory murmur is feeble or suppressed, and fine moist râles are heard, with an intermixture at times of the true crepitant râle. These signs are generally heard on both sides, but when an area of oedema is due to pneumonia the signs may be present only on the affected side.

COURSE AND TERMINATIONS.—Acute congestion of the lungs depending on over-action of the heart or a sudden recession of blood may cause death in a short time, or may disappear, either spontaneously or under appropriate treatment, almost as suddenly as it has come on. The abatement of the symptoms is generally attended with profuse serous expectoration, and sometimes with hemorrhage, by which the congested vessels are relieved, so that they return to their natural state.

When acute oedema of the lungs is due to Bright's disease in the acute or one of the chronic forms, it is often quickly fatal, though if properly treated it may disappear. When a consequence of chronic renal disease it is apt sooner or later to return. Chronic passive hyperæmia and chronic oedema of the lungs admit of only temporary relief, because they are occasioned by such diseases of the heart or kidneys as are themselves generally incurable; and they are very sure to recur, even though they may be relieved for a time. It is not uncommon in cases of this sort to see the symptoms of chronic oedema suddenly aggravated by the occurrence of an acute attack, which is the immediate cause of death.

PATHOLOGY AND MORBID ANATOMY.—The pathological appearance of a congested lung varies according to the form of the congestion and the manner in which it has been occasioned. Acute congestion may occur very suddenly from some of the causes that have been mentioned, and may disappear with equal rapidity, leaving no traces behind. But sometimes, from the extent of the congestion, respiration is interrupted to such a degree that life is quickly destroyed. In such cases the affected portion of the lung is of a dark color from being engorged with blood, which flows from it if an incision is made. The part is heavier and crepitates less than normal lung-tissue. The bronchial mucous membrane is apt to be hyperæmic, as might be expected from the communication that exists between the pulmonary and bronchial vessels, and the tubes themselves are filled with mucus and sometimes with frothy and bloody serum.

Where the tonicity of the pulmonary vessels has been impaired by sickness, age, or other debilitating influences, passive congestion of the lungs is very likely to ensue if the heart become weakened; and as the effect of gravity will aid in determining the stasis of the blood, the resulting congestion is in life most marked in the lower and posterior regions of the lungs, where the changes are chiefly found after death. As gravity may thus determine the congestion to one part of the lungs, so a change in the patient's position may cause it to disappear from where it was first manifest and to appear in another part which has become most dependent. The condition thus brought about is known as hypostatic congestion. One of the consequences of passive hyperæmia thus induced is a transudation of the serum of the blood into the air-cells and connective tissue of the lungs; and this is one way in which pulmonary oedema may be occasioned. When hypostatic congestion has lasted for some time, it may no longer be affected by changing the patient's position; and when this is the case it may be accompanied by exudation of fibrin into the air-cells and by proliferation of epithelium, thus producing the condition termed hypostatic pneumonia.

All three of these states may be present in one lung at the same time, one portion being passively congested, another oedematous, while the most dependent part may be the seat of hypostatic pneumonia.

The congested parts of the lungs are very dark in color, in some cases almost black; blood flows freely from a section through them, and serum exudes from the alveoli and interstitial tissue when oedema exists. If the altered condition of the lung has lasted for some time, the texture of the affected part may be so firm as to resemble that of the spleen; whence this change is sometimes termed splenization. In this condition dark-red points consisting of extravasated blood may be seen scattered about. If the state already described as hypostatic pneumonia exists, the affected part is still more firm and dense in texture, and presents a granular appearance on section from the exudation of fibrin which has probably taken place, so that it resembles a portion of a lung that has been the seat of an inflammatory process from the first.

DIAGNOSIS.—The diagnosis of pulmonary congestion in its different forms, and of pulmonary oedema, is in general not difficult if the symptoms of the causative diseases are carefully observed. Acute pulmonary congestion coming on suddenly, and not preceded by any other affection, needs to be distinguished from the early congestive stage of pneumonia, which it somewhat resembles from the slightly impaired resonance on percussion and the dyspnoea that may occur in both diseases. The chief points of distinction between the two affections are the absence in congestion of initial chill, of pain in the side, and of rise of temperature; all of which are in general present in pneumonia. As the case advances the divergence between the two affections will be wider.

The diagnosis of acute oedema and of chronic congestion and oedema is based upon the physical signs belonging to them, taken in connection with the symptoms of cardiac and renal disease with which they are associated.

Capillary bronchitis bears some resemblance to pulmonary oedema, since in both affections there are moist subcrepitant râles; but in capillary bronchitis there is no such loss of percussion resonance as occurs in pulmonary oedema, and, moreover, fever is not present in oedema, as it is in the inflammatory affection. The character of the expectoration is also different in the two diseases, being thicker and more tenacious in bronchitis and serous or watery in oedema. From hydrothorax, oedema is distinguishable by the shifting line of dulness and by the absence of râles in hydrothorax.

PROGNOSIS.—Acute congestion of the lungs is always a serious affection, and, as already stated, terminates fatally in some cases in a short time. In the majority of instances, however, it disappears spontaneously or under suitable treatment, and the lungs are in general restored to their integrity. It may result in pulmonary hemorrhage, from which recovery may take place, or which may give rise to hemorrhagic infarction, the blood being drawn into the alveoli.

Passive congestion being a secondary affection, its prognosis depends upon the diseases which occasion it.

In pulmonary oedema the prognosis is always very grave. When occurring suddenly as a consequence of acute congestive nephritis, it may wholly disappear under proper treatment, and if the kidney affection is likewise cured there will be no further return of the pulmonary complication. When it comes on in the course of chronic renal disease, it may disappear and recur from time to time, but it is apparently not often the direct cause of death by itself. Sometimes, however, it is associated with cerebral oedema and other conditions which together occasion a fatal termination. When due to pneumonia, oedema adds very much to the gravity of the affection, and may be the immediate cause of death.

TREATMENT.—The treatment of acute pulmonary congestion consists in the use of means to check the undue flow of blood into the engorged lungs. Of these the best, if the patient be seen promptly and the strength of the pulse admit of it, is general bloodletting, by which the mass of the blood is lessened and the action of the heart and pressure within the blood-vessels are lowered, so that both the amount of blood in the hyperæmic vessels and the force with which it reaches them will be diminished.

This measure may be also useful in the way of preventing or checking acute pulmonary oedema by lessening the blood-pressure. Should venesection be thought inadmissible, cups may be applied to the chest in front or behind, and at the same time the volume of the blood may be temporarily lessened by placing ligatures around the thighs, so as to check the flow of blood in the veins near the surface. Revulsion from the congested vessels of the lungs may also be effected by mustard foot-baths or the application of mustard poultices to the chest. Aconite may be serviceable by controlling over-action of the heart, and may be given in the dose of 1 or 2 drops of the tincture of the root at intervals of half an hour until some effect on the circulation is produced.

It is of importance to remove any blood or serum that may be present in the air-cells and smaller bronchi; and for this purpose one of the quickly-acting and non-depressing emetics may be given, such as apomorphia hypodermically or the sulphate of zinc or turpeth mineral by the mouth. Respect must be had to the condition of the patient's strength in ordering an emetic, since if there be much prostration, or if the interference with respiration has seriously depressed the heart, more harm than good might result from its use. Expectorants may somewhat later supplement the action of emetics, or serve to keep up the good effects gotten from them by helping to remove the residual fluids from the air-passages. Among the best of these are the syrup of senega and the carbonate or hydrochlorate of ammonium.

Passive congestion of the lungs, being dependent upon a weakened condition of the circulation, requires the use of means to sustain and reinforce the heart's action. The alcoholic and ammoniacal stimulants are here of great importance, and digitalis may be of sovereign efficacy, especially in cases where the congestion is associated with dilatation and attenuation of the heart. The power possessed by this drug of increasing arterial pressure, and thus producing diuretic action, may render it further serviceable when the congestion is accompanied with oedema, as in this way the serous infiltration may be absorbed and removed. From 10 to 20 drops of the tincture or from 2 to 4 drachms of the infusion of digitalis may be given every two hours until some effect on the pulse or the kidneys is noticed. If the stomach should not bear digitalis well in either of these forms, as is the case with some patients, the alkaloid digitalin in the dose of ¹/60 grain may be given. The convallaria recently introduced as synergistic with digitalis may be substituted for it, and in the dose of from 20 minims to 1 drachm of the fluid extract it will be found not uncommonly to be an efficient heart-tonic. Like digitalis, too, it possesses diuretic power from the increased arterial pressure that it occasions.

Passive pulmonary congestion may assume a chronic form in connection with chronic cardiac and renal disease, and without presenting urgent symptoms may cause almost constant embarrassment of respiration in greater or less degree. Under such circumstances the preparations of iron are helpful by enriching the blood and increasing the tone of the heart. One of the best preparations is the mixture of acetate of iron and ammonium,² known as Basham's mixture, which combines diuretic with chalybeate action. This may be given in the dose of from 1 to 4 drachms.

² U. S. Pharm., 1882.

It is of great importance in all cases of passive congestion and of hypostatic pneumonia to change the patient's position from time to time, so as to counteract the influence of gravity and relieve dependent portions of the lungs.

Pulmonary oedema occurring in an acute form in the course of either congestive nephritis or chronic renal disease may seriously imperil life, and therefore it demands prompt and bold treatment. When it results from acute nephritis, it is more immediately dangerous than when dependent on chronic disease of the kidneys; yet in this acute form it may admit of perfect cure if proper remedial measures be at once instituted. Cups may be applied to the loins with the view of relieving the engorged kidneys and enabling them to resume their work of removing fluid from the body. In cases where the strength of the pulse is sufficient, it may even be good practice to abstract blood by the lancet to the amount of six to eight ounces. According to Oppolzer,³ this treatment may be proper even when somnolence indicates oedema of the brain, provided there be no irregularity of respiration or intermission in the pulse—signs which contraindicate bloodletting.

³ Ziemssen's Cyclop., v. p. 285.

Active diaphoretics are among the best medicinal agents to be employed, their good effects being due to their derivative action and to the large discharge of fluid from the skin which they occasion, thus promoting the removal of what is effused in the lungs. The fluid extract of jaborandi in the dose of from 20 minims to a drachm, or the hypodermic injection of ¹/8 to ¹/6 grain of nitrate or muriate of pilocarpine, frequently causes prompt and profuse perspiration. The writer is confident that he has seen life saved by the use of this drug when it has been in urgent peril from pulmonary oedema. In the absence of this agent, or along with it, the hot-air bath, which can almost always be extemporized in an efficient form, may serve to promote or increase fluid discharge from the skin. If the patient's strength is sufficient, one of the hydragogue cathartics may be given, and among them the most prompt and active is elaterium in the dose of ¹/12 to ¹/8 grain every four hours. The action of this drug must be carefully watched and its depressing tendency guarded against by the use of alcoholic stimulants.

When pulmonary oedema results from weakness of the heart, as in dilatation of that organ, or from chronic renal disease, all lowering measures must be avoided. Bloodletting, whether general or local, would still further depress the heart, and by increasing the hyperæmia of chronic Bright's disease would favor the further effusion of serum into the lungs. Dry cupping over the chest before and behind may be serviceable as a revulsive measure. Stimulants and tonics are called for, and digitalis or convallaria is directly indicated from the special power possessed by these agents of improving the cardiac tone and promoting the action of the kidneys by increasing blood-pressure. Digitalis has been thought objectionable when there is much irregularity of respiration, and perhaps it would be safest to postpone its administration until this symptom is relieved by the use of alcohol, ammonia, musk, or other prompt diffusible stimulants.

The writer has had repeated opportunities for observing the value of quinia given hypodermically in checking effusion of serum into the air-passages, and he would strongly recommend its use in the treatment of pulmonary oedema in the form of the hypodermic injection of the solution of hydrobromate of quinia of the strength of 4 grains to 20 minims. Of this solution 10 to 20 minims may be injected at once. If such a solution cannot be obtained, a full dose of 10 to 15 grains of the sulphate of quinia may be given by the mouth.

As in the case of passive congestion of the lungs, so in oedema, advantage may be gained by changing the patient's position from time to time, so as to prevent the constant gravitation of fluid to the same portion of the affected organs.

HÆMOPTYSIS.

BY WILLIAM CARSON, M.D.

The word means, literally, spitting of blood, from two words, [Greek: haima], blood, and [Greek: ptyô], I spit.

SYNONYMS.—If we go back far in the history of medicine, we find many synonyms, such as Hæmoptoe, Emptoe, Emptoica passio, Pneumorrhagia, Hæmorrhagia pulmonis, Crachement de sang, etc., etc.

DEFINITION.—Bronchial hæmoptysis is the spitting or expectoration of blood which has been effused into the bronchi or bronchioles from the bronchial vessels. Pulmonary hæmoptysis is the spitting or expectoration of blood which has been effused into the air-cells, the inter-alveolar and interlobular tissues. This distinction is not always practicable in diagnosis or practice. It may, however, serve for a grouping of some well-known clinical forms of hæmoptysis.

It is not possible to give indications by which the origin of blood in the lungs may be positively determined except by a reference to other symptoms than the hæmoptysis. In general, bronchial hemorrhage is characterized by a bright-red, fresh color, is aërated, unmixed, and uncoagulated. In pulmonary or parenchymatous hæmoptysis the blood is dark, non-aërated, and coagulated to some degree, and often alternates with a mixed blood and mucus sputum. These distinctions are not reliable, and must be supplemented by all of our clinical resources in the case before us. The author maintains that in the hæmoptysis of phthisis the hemorrhage in the large majority of cases is both bronchial and pulmonary. The typical parenchymatous hemorrhage is found in hemorrhagic infarction and pulmonary apoplexy, which, compared with phthisis, are rare occasions for hæmoptysis. This general statement will form the basis of what follows in this exposition.

HISTORY.—Historically, there are not many phases in the doctrine of hæmoptysis. Controversy has been chiefly confined to its relations to phthisis as cause or effect.

The simplicity and directness of observation of the ancients give a special interest to their views of hæmoptysis. They believed that it was oftener cause than effect. They found a warranty of that opinion in what they thought was a direct conversion of blood into pus, and in the irritating qualities of the latter. Hippocrates'¹ fundamental statements are, "Ex sanguinis sputo, puris sputum malum;" "Ex sanguinis vomitione tabes et puris purgatio per superiora purgatio;" "Ex sanguinis sputo puris sputum et fluor, ubi autem sputum retinetur moriuntur." Another statement of his is given in translation by Peter:² "When some of the veins of the lung are ruptured the hemorrhage is in proportion to the size of the vessel; a part, on the contrary, unless the vein be very small, diffuses itself in the lung, putrefies there, and after having putrefied forms pus. As a result, it is at one time true pus, at another pus mixed with blood, and another time it is pure blood, which is rejected; and if the vein was very full it is from it that the mass of the blood comes, and thick pus, mixed with putrefied pituitous secretion, is expectorated."

¹ Edition 1696, book 7, p. 1141, Aphorisms 15 and 16, 80 and 81.

² Clinique médicale, tome 112, p. 243. The precise locality of this quotation is not given by Peter, but it is from Hippocrates' Opera, ed. Kuhn, Leipsic, 1825, vol. ii. p. 178.

Thomas Young³ gives the following sentences from Hippocrates' Predictions and Aphorisms: "The most dangerous consumptives are cured by a rupture of the great vessel which corrodes the lungs;" "Purulent expectoration after hæmoptysis is dangerous;" "In some cases consumption originates from an effusion of blood into the lungs without hæmoptysis, especially after a strain or accidental injury; a collection of phlegmatic humors form around it by causing pain and cough, with purulent and bloody expectoration." All of these quotations show the Hippocratic doctrine distinctly, that the hæmoptysis where it appeared in a case was mostly the cause of the subsequent phthisis, and that phthisis ab hæmoptoe was not only one of the most common, but one of the most dangerous forms.

³ A Practical Historical Treatise on Consumption Diseases, London, 1815, p. 111.

The doctrine that blood effused into the lungs became pus, and produced corroding and ulcerating effects, appears in many other prominent authors between the Hippocratic writings and the nineteenth century. Celsus⁴ (30–40 A.C.) says: "Hæmoptysis is one of the causes of purulent expectoration." Galen⁵ (131–201 A.C.) says: "Phthisis is lung ulceration;" and he thinks "that in the greatest number of cases it originates in a mechanical way, through tearing of the tissue by means of an outpouring of blood in consequence of a catarrh or strain." This extract would imply that he thought the hæmoptysis in many cases secondary, but that when it did occur it had the effect which Hippocrates attributed to it, that of producing "purulence of the lungs." Sylvius⁶ (1614–1672) says: "Hæmoptysis is one of the causes of purulent expectoration."

⁴ Young, op. cit., p. 128.

⁵ Waldenburg, Die Tuberculose, p. 19.

⁶ Waldenburg, op. cit., p. 28.

Morton's⁷ (1689) language partly is: "Decantatum istud medicorum adagium, quod pus sequitur sanguinem;" and then, translated, he says: "It (the adage) appears to have originated in the fact that 'purulence' of the lungs, or phthisis pulmonalis, usually follows hæmoptysis more quickly and oftener than any other disease." In the sentence immediately following he suggests this result may be due to a putrefaction of clots that the hæmoptysis has left behind in the lungs, or to a copious effusion of humors from the whole body to the tender lungs, or to an erosion of some vessel.

⁷ Phthisiological Ed., 1727, lib. 111, chap. v. p. 95.

Another theory appears in Hoffmann's language,⁸ and was probably suggested, directly or indirectly, by Sylvius's description of tubercles: "The blood is easily extravasated into the pulmonary vesicles, stagnates there and putrefies, corrodes the neighboring parts, and finally destroys the air-passages or they are converted into nodes or tubercles." The blood becomes tubercularized, and the phthisis ab hæmoptoe is established. This idea is found at different periods, and we find a recent French author arguing against this hypothesis.

⁸ Peter, loc. cit., p. 244; Young, p. 211, Opera; Hoffmann, Physico-medica, Geneva, 1740.

The reversal of these ideas is generally acknowledged as the results of Laennec's energy and genius, yet similar opinions to his had been expressed by French and English physicians. Bayle does not place phthisis ab hæmoptoe in his classification. Desault,⁹ one of Laennec's countrymen, near a hundred years before him, "insists that tubercles constitute the essence of consumption, being generally anterior to hæmoptysis." Mudge¹⁰ says that hæmoptysis is often the consequence of the obstruction produced by tubercles. A preparation for the positive opinions of Laennec is discernible in these and other authors. His views on this particular topic were opposed by Andral. The latter modified his earliest expressions to some extent.

⁹ Young, p. 220, Desault sur les Maladies venériennes, la Rage et la Phthisic, Bordeaux, 1733.

¹⁰ Young, loc. cit., Radical Cure for a Recent Catarrhic Cough, London, 1779, 2d ed.

The next important historical epoch in the causative relations of hæmoptysis and phthisis is in the energetic protests of Niemeyer. They were in some respects a return to the Hippocratic doctrine, in that he asserted the predominance of hæmoptysis as cause; but he gave the doctrine a basis better adjusted to a better pathology, in that he made the important element of inflammatory lesions the medium between the effusion of blood and the final purulence or ulceration (ulcus pulmonum) of the ancients. He energetically advocated the doctrine of the positive effect of effusion of blood in the bronchi or pulmonary substance in producing disorganization of the lungs, without reference to any hereditary or predisposing element or existence of tubercles.

Jaccoud¹¹ calls attention to the fact that Graves had anticipated Niemeyer in the partial revival of the Hippocratic doctrine and the teachings of Morton and Hoffmann on phthisis ab hæmoptoe.

¹¹ Clinique médicale, vol. ii. p. 302, Graves.

In a recent work¹² there is a general adhesion to the modern modifications of the Hippocratic doctrine in regard to the pathogenetic relations of hæmoptysis and phthisis. There is a decided rejection of the causative influence of tubercle in producing hæmoptysis.¹³ "The connection between pulmonary hemorrhage and tubercle stands on no pathological proof;" "From all the evidence I have been able to obtain on this point, tubercle seems to have been very unjustly credited with hemorrhage."¹⁴ He differs from others in attributing much more to the hæmophilic constitution in the production of hæmoptysis. Other phases of the history of hæmoptysis might be given. We shall allude to two only: one is the classification of the varieties. Alexander of Tralles treats of hæmoptysis under three heads: 1, Hæmoptysis by rupture; 2, by erosion; 3, by dilatation. Bricheteau¹⁵ makes four divisions: 1, constitutional; 2, accidental; 3, succedaneous; 4, critical and symptomatic. These two classifications show in themselves their origin, in that the one is representative of a local, and the other of a constitutional, pathogenesis.

¹² On Pulmonary Hemorrhage, Reginald E. Thompson, London, 1879.

¹³ Page 32, op. cit.

¹⁴ Page 33, op. cit.

¹⁵ Maladies chroniques de l'Appareil respiratoire, Paris, 1851, p. 523.

The last historical phase is the therapeutic one. We find in the practice of the present day survivals from the ancient authors. Morton recommended ligatures around the limbs to arrest hemorrhage, and bark to prevent hæmoptysis from becoming phthisis.¹⁶ Venesection, which to some extent is a modern remedy, was frequently practised by the older physicians. Erasistratus¹⁷ recommended ligatures, applied to the limbs in several places, to prevent the return of the blood to the lungs; Asclepiades thought this practice founded on an erroneous theory, but experience is in its favor. The head should be kept high, the face wetted with water, the room cool, and the patient perfectly at rest. Lietaud (1765) is cautious of employing astringents or purgatives, but recommended ligatures to the limbs and cold to the scrotum. A drachm of rhubarb was given by Fernelius in hæmoptysis. Bryan Robinson¹⁸ (1752) relates a case in which an emetic of ipecacuanha, taken three times a week, kept off hæmoptysis for eight years, while tar-water constantly brought it on. Marryat (1758, London) "advises two grains of tartarized antimony, and as much of the sulphate of copper, in half a spoonful of water." Ipecacuanha was frequently employed in hæmoptysis by the practitioners of the centuries preceding the nineteenth.

¹⁶ Young, pp. 201, 202.

¹⁷ Op. cit., p. 128.

¹⁸ Op. cit., p. 156, ed. 1660.

As an important preface to the subjects considered in this article we introduce an account of the vascular supply of the lungs.

Before entering into a statement of the distribution of the minute vessels to the lungs it is desirable, in view of the possible diseased connections between the larger bronchial and vascular trunks, to recall some points of the topographical anatomy of the latter. "The root of the left lung passes below the arch of the aorta and in front of the descending aorta. The bronchus, together with the bronchial arteries and veins, the lymphatics and lymphatic glands, is placed on a plane posterior to the great blood-vessels. The pulmonary artery lies more forward than the bronchus, and to a great extent conceals it, while the pulmonary veins are placed still farther in advance." The left bronchus "in passing obliquely beneath the arch of the aorta is depressed below the level of the pulmonary artery, which is the highest vessel."¹⁹ Practically, the chances of abnormal communications lie in the relations of the aorta, more especially the different parts of the arch, to the left bronchus and pulmonary artery, and to the trachea, of the innominate artery to the trachea, and of the glandular structures at the root of lung to the pulmonary artery.

¹⁹ Quain's Anatomy, vol. ii. pp. 897, 898.

The encroachment of aneurism of the subclavian artery on the lung, and consequent communication between it and the bronchus, is another form of accidental or extraneous hæmoptysis.

A recognized classification of the vascular systems of the lungs is into—1st, functional; 2d, nutritive. To the first belong the pulmonary arteries and veins, and to the second the bronchial arteries and veins. Both physiological and pathological experience justifies this division.

Notwithstanding the great attention and labor bestowed upon the circulation of the lungs, there are still unsettled some important points. We adopt from Küttner²⁰ some of the anatomical data applicable to our subject. The branches of the pulmonary artery follow uninterruptedly the bronchial ramifications. The mutual relations of the artery and bronchus are such that the larger vessel lying in any preparation of the lung directly next to the bronchus, and running in the same direction, can be pronounced to be a branch of the pulmonary artery. In the lungs of the embryo both lie in the same connective-tissue sheath that originates at the root of the lung, enters with them into the root of each lobule, and there spreads out. In the lobules both run not only closely alongside of each other; there appear also branches of the pulmonary artery on the bronchus itself, and press on to the mucosa of the same.

²⁰ "Beiträge zur Kentniss der Kreislaups-verhältnisse der Saugethierlunge," Virchow's Archiv, vol. lxxiii. p. 476, etc.

With the appearance of the terminal bronchiole this relation is changed. The bronchial artery, as such, ceases; the pulmonary artery—or rather its lateral branches—exclusively surround the alveolar diverticulæ on their external surfaces. At the point where the terminal bronchiole is developed into the infundibula the corresponding trunk of the pulmonary artery divides into a number of branches—"pinselförmig;" each infundibulum receives its stem, which spreads itself after the manner of a feather on its external surface. The terminal branches of the pulmonary artery cover the terminal alveoli. On every lung in which the infundibula and lobules are well distributed the terminal branches of the pulmonary artery extend beyond the borders of the infundibula and lobules into the interlobular and subpleural connective tissue, and here either lose themselves in a capillary distribution or extend to the periphery of an adjoining acinus, being lost in its capillaries.

One peculiarity of the pulmonary artery is that from a large trunk relatively fine lateral branches come. From a vessel of 0.136 mm. come branches of 0.033, 0.016, 0.011, 0.010 mm. The finest disappear immediately as vasa vasorum; the larger pass to the perivascular or peribronchial connective tissue and become capillary, or they appear on the surface of the immediately adjoining lobules and disappear in the capillary paths of the alveoli.

The terminal branches of one and the same principal artery behave differently according as they are distributed to the connective tissue or to the alveoli. In the first case they form wide meshes and narrow tubes, and are not different from the capillary terminations of the body in general. In the other case the meshes are narrow; the vessels in all of the pulmonary capillaries are wide. If these vessels are followed from their origin to their final termination, it will be seen that a considerable part of the pulmonary artery is spread in the interlobular connective tissue; that it is not exclusively a secretory vessel; that the capillary network of all the lobuli are in anastomotic connection.

An anatomical investigation shows that between the branches of the pulmonary artery no anastomoses exist. It is, however, proved that under certain conditions connections between the larger branches of the artery may occur. This artificial connection is favored through peculiarities of terminal branching: wherever two parallel branches of the pulmonary artery are followed, it will be seen that the terminal branches lie alongside of each other without anastomosis. One can be convinced of that, and, further, that the capillaries of only one or two alveoli separate them. These unusually short capillaries between two arteries are those in which differences of pressure in one or the other artery produce wide connections. Küttner agrees so far with those observers who think that between the larger branches of the pulmonary artery no wide anastomoses exist already formed. In this sense the pulmonary artery can be designated a terminal artery; on the other side, however, it must not be forgotten that such connections can arise at any time, and the artery there loses the type of a so-called terminal artery.

He further remarks that the vascular-district supply of the pulmonary artery is not so limited as Cohnheim and Litten believe; that, more than that, some branches of it pass from one lobule to the adjoining one; that others are distributed in the subpleural and interlobular connective tissue and in the bronchial wall.

If the lung of an animal be injected from the pulmonary artery, there is produced a complete filling of the vessels of the bronchial wall and into the subepithelial layer—a fact the more interesting that a similar event can scarcely be produced by a filling of the bronchial artery.

Pulmonary Vein.—Only at the root of the lung do the bronchus, pulmonary artery, and pulmonary vein lie close to each other. In the continuance of the same the artery and the bronchus remain close by each other, but the vein pursues its own course. The branches of the same are, from the hilus to their capillary termination, situated in the interlobular connective-tissue paths. They form on the external margins of the lobules wide blutbuchten, in which the veins of the infundibula enter with short stems. The artery lies intralobular—the vein interlobular. The bronchial veins connect not only with branches of the azygos and superior cava, but also with those of the pulmonary vein.

Bronchial Vessels.—The variety of origin of the bronchial arteries is notable. Whatever their origin, they follow with their chief trunk the bronchus into the parenchyma of the lung, and give off insignificant lateral branches to the connective-tissue layers. There is still another kind of artery, which divides independently in the connective tissue of the lungs, without resting on the bronchial walls; they come from the oesophageal, mediastinal, and pericardial arteries, branch in the mediastinal pleura, appear with these at the hilus of the lung, and form partly an independent mesh of pleural arteries, and partly spread themselves in the interlobular connective tissue.

All the vessels of the serous membranes of the diaphragm can contribute in many ways blood to the hilus of the lung: the unusually fine-branched arteries appear in this way to be in condition to compensate for obstructions (or lesser). The bronchial arteries in comparison with the other vessels of the lungs give off sparingly lateral branches; among the most interesting are the branches which spring directly from the trunks of the bronchial artery, pass through the peribronchial connective tissue, appear at the adjoining infundibula, and lose themselves in capillary terminations.

The capillary districts of the bronchial arteries pass immediately into those of the pulmonary. It is a fact that besides the pulmonary artery the bronchial artery provides the infundibula and alveoli with blood. If the bronchial artery springing from the intercostal and internal mammary arteries be ligated or cut, leaving open the vessels of the mediastinal pleura, and the lung be injected from the abdominal aorta, a mere inspection will show a filling of the parenchyma of the lung; anastomoses between the pleural arteries and the intra-acinous trunks of the pulmonary arteries can be recognized. There is an anastomotic connection between the pleural branches of the pulmonary and bronchial arteries.

The bronchial, as also the pulmonary, artery can be filled by means of the fine arterial branches from the mediastinal pleura.

The principal branches of the bronchial arteries go to the bronchi; at the alveolar passage they here stop as such; their capillaries become continuous with those of the pulmonary artery. The greater part of the few collateral branches nourish the submucous peribronchial and perivascular connective tissue, the nerves, the lymphatic vessels; the smaller part enter the alveoli of other bronchial systems and become capillary.

The branches going to the lung with the mediastinal pleura spread themselves in the pleura and interlobular connective tissue, nourish the large subpleural and interlobular lymphatic vessels, but lose themselves in capillary distribution on the alveoli and infundibula.

The pleural and bronchial arteries anastomose partly with each other and partly with branches of the pulmonary artery.

With reference to the branches of the pulmonary artery going to the bronchi, it may be said that they, without giving special branches to the external layer of the bronchi, press on to the basal membrane and form a compact capillary network in common with the proportionately few branches of the bronchial artery.

Amidst differences of opinion, as between Küttner, Lalesque, and Cohnheim and Litten, there is a concurrence as to the chances of supplementary function by anastomoses between channels that are ordinarily separate. Küttner admits a modified form of terminal arrangement in the pulmonary artery, but at the same time claims an amount of potential connection that is liable to come into actual operation and suspend, if not destroy, the terminal type.

The correlation of both functional and nutrient vessels is so intimate that we believe there is no conclusive argument against the actual transfer of office from one to the other in certain strained conditions of disease; Virchow's experiment proves it.

The wonderful delicacy and distensibility of the enormous network of pulmonary vessels (relation of uncovered space in the alveoli to that covered by the vessels being 50 out of 200, Kuss); their capacity of response to great variations of supply and tension; the prompt supplementary function proven by Litten²¹ to belong to the tracheo-oesophageal, pericardial, phrenic, and pleuro-mediastinal arteries, and their equilibrium under the sensitive changes of the aortic system; the slower submission of the lesser circulation to the peripheral impressions, which markedly affect the aortic system; the facts verified by Lichtheim²² that on closure of any portion of the pulmonary artery the same quantity of blood will pass through the portion remaining open as before; that this is brought about through increase of pressure in the sections still open, and through the simultaneous increased rapidity of circulation and distension of the vessel walls; and that this mechanism is able to compensate for obstruction of three-fourths of the pulmonary artery,—are important factors in the anatomical and physiological relations of hæmoptysis.

²¹ "Ueber den Hämorrhagischen Infarct," Zeitschrift für klinische Medicin.

²² Die Störungen des Lungenkreislaufs, by L. Lichtheim, Berlin, 1876, p. 65.

ETIOLOGY.—The natural history of hæmoptysis is practically that of phthisis: exceptions to this will be noted hereafter. As heredity is largely a determining influence in the latter, it may be assumed that it qualifies its principal symptoms. More or less uniformity prevails in the transmission of normal or abnormal conditions, and we seem to find an illustration of the latter in the correspondence between the percentages of hereditary phthisis and those of hæmoptysis in such cases. Reginald Thompson²³ says that "out of 1064 cases of well-marked inherited phthisis, 426 suffered from hæmoptysis." In his calculation he omitted all those in which the disease began with hæmoptysis. Had these then been included, they would have raised the percentage over that shown by the figures, which is slightly above 40. The rate would not then be much below that given as an average of cases of hereditary phthisis. This percentage of cases of hæmoptysis in hereditary phthisis is a sufficiently uniform transmission to prove the influence of heredity. Its influence is shown not only in the number of transmissions, but in the transmission of types; so that, as we have a family type of phthisis, we may have a family type of hæmoptysis, such as the cases where all the phthisical members of a family are subject to hæmoptysis of uniform characteristics, instances where the same uniformity in type is transmitted, and instances where the phthisical heredity appears to have its survival in moderate and transient attacks of hemorrhage.

²³ The Causes and Results of Pulmonary Hemorrhage, p. 110.

Atavism is also seen in some family histories. We have in view such an instance, where the marked hæmoptysical tendencies of one generation skipped the next to reappear in the third.

A special study of the relation of cases of copious hæmoptysis to different forms of heredity has been made by Reginald Thompson. His table is as follows:

COPIOUS HÆMOPTYSIS.

Age at which attack commenced.

Cases. 5 10 15 20 25 30 35 40 45 50 55 60 65

Mother 123 ... ... 27 30 34 18 8 2 3 1

Father 102 1 4 16 22 24 19 9 4 1 ... 1 1

Non-hereditary 105 ... 2 14 20 24 16 12 8 5 2

He claims that this table shows that of the cases of direct heredity, cross-heredity, and non-heredity, those who were the subjects of cross-heredity—that is, those from the mother—were more liable to copious hæmoptysis than either the cases of direct heredity or of non-heredity; and the numbers of the two latter so closely correspond as to show that heredity from the father has little influence as regards hemorrhage. The conclusion he draws from the table is that "an heredity is drawn from the mother which differs from that derived from the father, and to this must be attributed the excess of cases of copious hæmoptysis."

This difference will be seen in the following table, which shows the number of cases occurring before and after thirty:

Cases. Before age of 30. After age of 30.

Mother 123 91 32

Father 102 65 37

Non-hereditary 105 60 45

He thinks the explanation is to be obtained from the statistics of hæmophilia, which show a large proportion of transmissions from mothers to sons, and that we have here a strong argument connecting copious hæmoptysis, not with tubercle, but with hæmophilia.

His next table is one of 125 cases of double heredity, calculated upon the same basis as the others, that of 400:

Cases. 5 10 15 20 25 30 35 40 45 50 55 60 65

Double heredity 125 ... 3 20 40 23 15 12 9 1 1 1

Calculated to 400 ... 10 74 128 75 48 37 29 3 3 3

which shows a close approximation to the table of cases of cross-heredity from the mother, and that the calculated number for 400 cases of double heredity are almost identical with that of the actual number of 400 cases of cross-heredity between the ages of fifteen and twenty-five—in the first case being 202, in the second 203—and the calculated number of cases before thirty amount to 287, not quite equal to actual number for cases of cross-heredity, which is 294. He concludes that these cases do not show a greater tendency to hemorrhage than is shown in cases of direct and non-heredity. We may accept these figures and calculations as important without endorsing the conclusion which they are intended to sustain—viz. that such hæmoptyses are essentially of hæmophilic origin. It may be stated as a general opinion that hæmophilia does not especially manifest itself in pulmonary hemorrhages, and that hæmophilic families are not specially liable to phthisis.

The hemorrhagic diathesis, as distinguished from the specific bleeders' heredity, does not often manifest its activity through the lungs, and, as correlative, phthisis does not often show hemorrhages in other organs than the lungs.²⁴ Leudet has met in 244 cases of phthisis 9 times hemorrhages in other organs than the lungs; oftenest by the intestine, the skin, the nasal mucous membrane; more rarely by the brain and urinary organs; 10 times between the muscles of the abdominal walls. These considerations suggest that the phthisical hæmoptysis is distinct from that of hæmophilia or the hemorrhagic diathesis, and has an independent origin.

²⁴ "Rémarques sur la Diathese hémorrhagique," Mém. Soc. de la Biologie, 1859, p. 179.

Some facts in regard to the previous diseases of patients admitted into the Brompton Hospital with phthisis are given in the second medical report of that institution, which may have a bearing on the special features, such as hæmoptysis. Among 1973 patients admitted, 275 were found to have suffered with well-marked attacks of rheumatism, and 16 had acute symptoms of it while in the hospital, making a larger number than of any other disease, fevers coming next with 238. The connection of forms of hemorrhage with so-called rheumatism suggests a possible influence of that kind in favoring hæmoptyses during the evolution of phthisis. We know of no facts collected with the view of studying this relation. If such a conclusion were sustained, it would tend to confirm the view connecting hæmoptysis with hæmophilia or the hemorrhagic diathesis.

Williams²⁵ gives a statement qualifying the assumption that the hemorrhagic variety of consumption specially originates in family predisposition, for in 72 cases out of 1000 tabulated cases of phthisis family predisposition was present in only 25 instances. This percentage is scarcely small enough to exclude a predisposition.

²⁵ Pulmonary Consumption, p. 157.

Considering hæmoptysis in this aspect, as a result of heredity, does not account for all the cases with which we meet. We are surprised occasionally by the appearance of pulmonary hemorrhage where heredity of phthisis cannot be traced. Such persons present the aspect of a vulnerable state; they yield readily to a phthisical invasion. Some of the so-called cases of phthisis ab hæmoptoe are found in this class, yet they may have inherited a phthisical predisposition, brought about by various degenerating influences acting on their ancestors, such as antihygienic surroundings, bad air, insufficient food, frequent childbearing, and excessive nursing. The heredity is not in special symptoms, but in a predisposition which needs only some exciting cause for a specific symptomatology that may be carried forward to the next generation.

One individual may himself yield to the same degenerating influences, and live with more or less of an acquired predisposition until similar exciting causes reveal his specific weakness. Another may find that he has a phthisis directly acquired from a single attack of severe illness without the aid of any element of heredity or of the acquired predisposition. The gradation would then be inherited predisposition, acquired predisposition, and acquired phthisis. Hæmoptysis may find its origin in these several relations of heredity. Combined, they represent the law of uniformity and the law of variation in hereditary transmissions. If these general observations be correct, they show that the ordinarily stated percentage of transmission of hæmoptysis in inherited phthisis does not express the totality of influence operating in the production of hæmoptysis. Something must be subtracted from the so-called non-inherited phthisis and added to the inherited form.

When we attempt to express the relation of acquired or non-inherited phthisis to hæmoptysis, we find no sufficient data. Thompson's table above given is assumed by him as showing that the influences superinducing hæmoptysis in the non-hereditary class are equivalent to the heredity operating through the father, which is quite subordinate.

R. Thompson²⁶ states that out of 1064 of his cases of well-marked inherited phthisis, 426 had hæmoptysis; of 1016 when phthisis was not known to be inherited, 558 had hæmoptysis.

²⁶ Loc. cit., p. 110. In a later work Thompson (Family Phthisis, London, 1884) states that the general effect of the paternal inheritance is to reduce the number of cases of copious bleeding for the total period of life, but an excess is observed for the special period between twenty and twenty-five; that in the inheritance of the females from the father the number of cases of bleeding is large, the number of the copious cases being twice as many as the moderate. The effect of double heredity upon males was to make the cases of copious bleeding numerous, and that nearly half the total number of cases were disposed to bleed. In females there was an increase in the number of cases of moderate amount. As regards acquired phthisis among males, that hæmoptysis is a well-marked feature, and nearly three-fourths are cases of copious bleeding; as to acquired phthisis among females, that the number of cases is considerably smaller, the reduction being marked in the cases of copious bleeding.

In a collection of cases of phthisis taken from the Cincinnati Hospital records, amounting to 1266, there were of

Cases of hæmoptysis 475, or 37.51 per cent.

" phthisis, with family history of same 332

" hæmoptysis in same 127, or 38.25 "

" acquired or non-inherited phthisis 934

" hæmoptysis in same 348, or 37.25 "

In 10 cases there was a family history of hæmoptysis; that is, of a general family peculiarity in that direction. These percentages show no great difference between the relations of inherited and non-inherited phthisis to hæmoptysis, the inherited exceeding by 1 per cent. that of the non-inherited form.

Without here attempting a comprehensive statement of what the predisposition, transmitted or acquired, is, we may mention two influences of important force—a tendency to fragility of vessels and to the catarrhal disposition. It is sufficient to speak of the fact that in no other disease of the lungs than phthisis have we as a common feature this vascular fragility. It differentiates the disease and the symptoms. If it appear in any of them, it should at once excite a suspicion of the phthisical constitution. That it does appear in some such cases without ulterior effects does not invalidate the general statement. It may be put down as a part of the phthisical habit directly concerned in the liability to hæmoptysis. The proof of this proposition is more clinical than anatomical.

The attempt to prove that it is hæmophilic rests upon the application of a few histological examinations of hæmophilic vessels to the phenomena of phthisical hæmoptysis. The assumption of identity has only the doubtful force of analogy. Histological examinations of the vessels in the earliest stages of phthisis and hæmoptysis are too rare to afford sufficient data. In the latter stages the condition is too complex, because of positive inflammatory and ulcerative processes.

Although alterations in the vessels in the early stage of simple inflammation cannot be histologically demonstrated, yet they must exist in order to allow diapedesis. So with early phthisis: in the pre-hæmoptoic stage the alterations are not demonstrated, yet that such disorder of function must have accompanying structural change underlying the phenomena of the initial hæmoptysis is in accordance with physiological and pathological doctrines, and has much consistent clinical force. When we presuppose a delicacy of, or injury to, the blood-vessels of a part, there is the imminence of not only a rupture, and consequent hemorrhage, but of those changes which, leading through stasis and congestion, come to be inflammatory, and which affect still further the vascular structures and adjoining parenchyma.

Besides these changes initiated in the blood-vessels, there are others of close relation to the phthisical constitution, which begin in the vulnerable epithelial elements of the bronchial mucous membrane and of the air-cells. They are the evidences of the dispositio catarrhalis, which received its name from the old observers, and the validity of which has been confirmed by modern pathological and clinical researches.

It is responsible for the great susceptibility to catarrhal affections of the bronchi and air-cells which lays the foundation for chronic catarrhal pneumonia.

These two elements, of fragility of vessels and of the catarrhal tendency, are the tangible instruments of heredity. They are also the factors of the acquired predisposition.

The Vienna Hospital reports, running through more than fifteen years, and embracing more than 20,000 cases, give as the ages most liable to hæmoptysis those between eighteen and twenty-nine years. No statistics as to sex are given.

Of 1266 cases of phthisis²⁷ taken without selection from the records of the Cincinnati Hospital, there were

Between 10 and 20 years 81; in this class, hæmoptysis 20

" 20 " 30 " 459; " " " 208

" 30 " 40 " 363; " " " 143

" 40 " 50 " 191; " " " 62

" 50 " 60 " 110; " " " 28

" 60 " 70 " 45; " " " 9

Over 70 " 7; " " " 1

Age not stated 10; " " " 4

1266 475

²⁷ We desire to acknowledge the services of Walter A. Dun, then a resident physician at the Cincinnati Hospital, in collecting these cases from the hospital books.

Ware in Mass. Med. Soc. Proc. gives ages in 317 cases:

43 up to 20

139 between 20 and 30

77 " 30 " 40

Of Pollock's²⁸ 351 cases of profuse hæmoptysis,

43 were under 20 years of age.

168 between 20 and 30 " "

100 " 30 " 40 " "

40 over 40 " "

These figures from widely-different sources testify to the fact that the greatest number of cases of hæmoptysis occurs between twenty and thirty years of age, or at least with a variation of only about a year from those extremes. The possibility of hæmoptysis, if we may judge by cases reported, lies anywhere between sixteen days of age and the limit of life. A case of hæmoptysis in a child sixteen days old is alluded to in Nouv. Dict. de Méd. et de Chirurg.²⁹ The oldest on the list of the Vienna Hospital reports is seventy-two. In our Cincinnati Hospital list we have 7 over seventy years. Others have reported cases beyond these figures.

²⁸ Prognosis in Consumption, p. 311.

²⁹ Vol. xxix. p. 391.

A case of death from pulmonary aneurism and hæmoptysis in a child aged two and a half years is reported in London Path. Soc. Trans.;³⁰ also one by Powell³¹ of a child seven months old from a similar rupture—illustrations of the remark that children are subject not so much to initial as to terminal hæmoptysis.

³⁰ Vol. ii. p. 35.

³¹ Med. Times and Gaz., June, 1874.

As to the relations of sex to the amount of hæmoptysis, we have the Table XI. from the second medical report of the Brompton Hospital:

Males. Females. Males. Females. Total.

Below drachm j in quantity. 843 700 55 83 1681

From drachm j to drachm iv. 616 482 34 69 1201

From ½ oz. to 4 oz. 429 268 13 21 731

Above 4 oz. 343 153 9 7 512

Entirely absent. 588 193 74 65 920

2819 1796 185 245 5045

These results correspond with the general one stated by Williams,³² that large hemorrhages occurred in 34.76 per cent. of males, and in only 17.67 per cent. of females. In the above table, where quantities of blood above four ounces were noted, the male figure is more than double that of the female. As regards exemption, it is stated that of the cases of decided phthisis which had been free from hæmoptysis, about five-sevenths were males, and under two-sevenths females. In general it may be said that females are more liable to small and males to the larger hemorrhages.

³² Treatise on Consumption, p. 156.

Of 268 females in our Cincinnati Hospital list, 44 had hæmoptysis—about 13 per cent. Of 998 males, 431 had hæmoptysis, or about 43 per cent.

In the second Brompton Hospital report³³ it is stated that "many of the most violent attacks of this nature (sudden fatal terminations) have depended on a sudden rise in the temperature." The peculiar prevalence of hæmoptysis on the coasts of some warm countries has long since been noted. Archibald Smith,³⁴ in giving his practical observations on the diseases of Peru, says: "There appears to be a general predisposition to this disease, hæmoptysis." An intelligent individual, himself a sufferer while then a resident on the lower portion of the North American south-western coast, has given me the same statement. Pasley³⁵ says at least 10 per cent. of the cases of phthisis in Trinidad which die in the hospital terminate in a profuse hæmoptysis; the quantity of blood varies from 15 to 70 or 80 ounces, and the duration of life from the beginning of the hæmoptysis till the end five to fifteen minutes. Of Ware's cases,³⁶ 83 were in winter, 101 in spring, 69 in summer, 102 in autumn, or 185 in autumn and winter, 170 in spring and summer. In four months of warm weather, June, July, August, and September, 97 cases; in October, November, December, and January, 134; in February, March, April, and May, 124—an average of 129 for the eight cold months, an excess of 32 cases, or about 33 per cent.; in the transition seasons, spring and autumn, 101 and 102. The highest numbers were in March and November, 38 and 39; lowest number in June, 18. These are the only figures obtainable as to our climate, and they do not agree with those given by R. E. Thompson's table,³⁷ showing the prevalence of hæmoptysis as to months in 1000 well-marked cases:

Jan., Feb., Mar., Apr., May, June, July, Aug., Sept., Oct., Nov., Dec.,

67 61 90 95 112 130 128 64 64 55 81 63

The summer months of June and July show the largest numbers, and the months of December, January, and February lesser numbers. The decrease in August is explained in great measure by the diminution in attendance. It is possible that other elements of climate besides temperature may account for this difference between American and English figures.

³³ Page 17.

³⁴ Edinburgh Med. and Surg. Journ., vol. liv., 1840.

³⁵ Brit. Med. Journ., Jan. 10, 1880, p. 53.

³⁶ Mass. Med. Soc., 1860.

³⁷ On Pulmonary Hemorrhages, p. 114.

A more correct opinion as to the effect of altitude is developing. Archibald Smith³⁸ more than forty years ago testified to the good effects of removal from the coast to the high sierras of Peru in cases of phthisis with hæmoptysis. His own instances of great improvement following removal to high levels, 5000 to 8000 feet, are conclusive. He also gives instances where renewals of hemorrhagic attacks followed the return to the coast. It was the custom for physicians to send their consumptive patients to the sierras without reference to their hemorrhagic attacks.

³⁸ Loc. cit.

Similar testimony is accumulating in this country. The Colorado regions are supplying, through their physicians, much material bearing upon the effect of altitudes on hæmoptysis. H. K. Steele of Denver, Col., writes, June, 1883, that "it is the opinion in the profession generally, and I endorse it, that this country acts beneficially in the hæmoptysis of phthisical patients." Jacob Reed, Jr., says³⁹ that not only does the ascent to this altitude (6000 feet) not predispose to pneumorrhagia in consumptives, but that "hemorrhagic cases do well here; in most cases the bleedings becoming less frequent, in many cases ceasing altogether." By letter May, 1883, he says these cases number between 500 and 600, and he feels justified in the positive statement that not only does altitude not precipitate hæmoptysis, but that "those suffering from this symptom are benefited here, their bleeding becoming less frequent and less in quantity." He makes an exception of florid cases in active progress or old cavities waking up to new action.

³⁹ "Altitude in Reference to Pneumorrhagia," an analysis of 70 cases, read at the eighth annual convention of the Colorado Med. Soc., 1878, p. 66.

Denison,⁴⁰ after an analysis of 90 cases of hæmoptysis out of 202 of phthisis, says: "The advantages of high altitudes are pre-eminently for hemorrhagic cases in the first stage, while hemorrhagic cases with excavations, especially if the bleeding has been recent and softening is in progress, should be interdicted from going to great elevations."

⁴⁰ Rocky Mountain Health Reports, p. 140.

He also quotes Herman Weber⁴¹ as recommending "alpine climates, not only as a prophylactic measure against hæmoptysis, but also as a means to promote the cure of the effects of the inflammatory processes resulting from pulmonary hemorrhage."

⁴¹ Hæmoptysis as a Cure of Inflammatory Processes and Phthisis, with Remarks on Treatment.

These statements are sufficient to show that the view formerly prevalent, and still more or less so, that high altitudes have the effect of prolonging or favoring hæmoptysis, is not altogether correct. It should be understood as applying to the extreme heights of 10,000 or 15,000 feet, and that rapidity of transfer and unusual exertion are necessary and qualifying considerations. Jourdanet⁴² places the region of safety in phthisis about the mid-point between the level of the sea and the snow-line. The preservative level is lower in Alpine than in American regions. The line of perpetual snow in Mexico being about 4500 meters, the preservative zone would be 2250 meters. In Switzerland, where the line of snow marks 2700 meters, the same zone would be 1350 meters. No such definite limitations are attainable as regards hæmoptysis, but a correspondence of zones might be conjectured.

⁴² Influence de la Pression de l'Air, vol. ii. pp. 183, 184, 213.

The belief that pregnancy in some way favors hæmoptysis is a very old one. It has been more or less accepted by modern writers. Trousseau⁴³ gives his observations to the effect that there are women who during pregnancy, and others who during nursing, spit blood. His belief was that such hæmoptyses were not symptomatic of pulmonary tubercle nor of cardiac disease, but he classifies them as cases of hemorrhagic deviation. Peter⁴⁴ speaks of a gravid pulmonary hyperæmia, proven in part by his determination of increased local temperatures in the lower intercostal spaces. Some of his cases do not sustain his theories, and can properly be referred to puerperal accidents, such as emboli in phlegmasia alba dolens. Such cases as we have met with in connection with pregnancy or lactation have had hereditary or acquired tendencies to phthisis. We have under view a case where hæmoptysis always recurs during pregnancy and where there is a family history of phthisis. A brother has pulmonary hemorrhages preceded by inflammatory attacks, which stand in a relation to him corresponding to the pregnant hyperæmia of the sister. The well-known effects of pregnancy or prolonged lactation in developing phthisis are a sufficient explanation of this class of cases.

⁴³ Clinique Medic. Trans., vol. i. p. 531.

⁴⁴ Leçons de Clinique médicale, vol. ii. p. 664, 2d ed.

Many exciting causes are assigned by patients in explanation of a dreaded event, and some are otherwise misinterpreted. Their mode of action is not intelligible unless we keep in view the anatomical, physiological, and pathological data heretofore given. Numerous cases occur where no exciting causes can be found, such as those coming on in the quietude of sleep. The insidious agencies of the predisposing causes must be responsible. A study of many cases will show that the alleged causes have become operative only after a considerable time has elapsed, during which a congestive or inflammatory condition has appeared, the expression of a latent tendency. Dancing in a warm room or speaking long in the open air, followed in twenty-four hours by bleeding, are such instances. The physical effort was only so far instrumental as it gave a chance for the development of a potential diathetic condition. It was not the direct cause. Falls, frights, blows on the chest, heavy lifting, playing on wind instruments, and emotional excitement are sufficient to bring on a hemorrhage by direct influence, and by so increasing arterial tension as to overcome the resistance of vessels already weak. It is not intended to maintain the impossibility of rupture of healthy vessels under some circumstances, but the large provision made in the great distensibility of the pulmonary vessels and in the supplementary functions already alluded to make it necessary to be cautious in such admissions. The fact that hemorrhages from the direct causes are sometimes not followed by phthisical effects does not necessarily disprove their diathetic origin.

The effect of blows on the chest in producing hæmoptysis and phthisis has been the subject of medico-legal examinations in suits for damages. In all of such cases within our knowledge there has been the element of fright or great emotional excitement, and hence a complexity of causation. An hereditary tendency to phthisis was also present—a fact which diminished the force of the plea that the blow was alone responsible for the injuries to the health of the parties concerned.

Diseases or injuries of the brain may be mentioned as causes of pulmonary hemorrhage, which may occasionally be shown by hæmoptysis. Experimental pathology has recently thrown much light on these cases. (See PULMONARY APOPLEXY, infra.)

It may be worth while, in view of recent researches, to refer to a form of hæmoptysis closely associated with a newly-discovered parasite, named Distoma Ringeri,⁴⁵ after Ringer of Tamsui, Formosa, who discovered the parasite, but did not at once recognize its etiological relation to the endemic hæmoptysis. In a post-mortem of a man dead from rupture of an aortic aneurism he found the parasite lying on the lung-tissue, probably escaped from a bronchus. There were some small deposits of tubercle, no cavities, and slight congestion of the lungs. Manson found that these parasites were associated with a frequently-recurring hæmoptysis. Baely of Tokio⁴⁶ discovered the parasite, probably before any others. It is quite common in North Formosa and through Japan. Manson says:⁴⁷ "Endemic hæmoptysis can be readily diagnosed. There is a history of irregular, intermitting hæmoptysis, associated with a slight cough, and in the intervals of more active bleeding the expectoration once or several times a day of small pellets of viscid, brownish mucus. Examination of a small portion of the sputum with the microscope at once settles the diagnosis, sometimes as many as twenty parasites being found in a single field." Further examination is necessary to determine the manner in which this parasite produces the hæmoptysis.

⁴⁵ The Filaria sanguinis hominis and certain New Forms of Parasitic Disease in India, China, and Warm Countries, p. 134, by Patrick Manson, Amoy, China.

⁴⁶ London Lancet, Oct. 2, 1880.

⁴⁷ Ibid., p. 143.

The association of bacilli tuberculosis with hæmoptysis is proven by a number of examinations. These will be referred to in their diagnostic relations at another page. It is not intended here to imply an etiological relation, because as yet our knowledge does not point to the blood-vessels as being the special or usual habitat of bacilli or the place of their most destructive efforts.

Hydatids of the lung are a cause of hæmoptysis which may come from congestion accompanying their growth, or from their rupture and consequent opening of blood-vessels.

Before proceeding farther we shall refer more fully than before to the conditions prepared by heredity, age and sex, etc. for the action of the exciting causes. The agencies were stated to be the peculiar vulnerability of the vascular and epithelial structures of the lungs. When the morbid imminence is reinforced by an infective element, as in phthisis, certain results follow which make easy the action of the incidental causes. Because of the enormous vascularity and great delicacy of structure of the lungs, and their liability to external influences, slight external irritants in such constitutions produce more than what follows in other cases. Instead of a transient hyperæmia or mild catarrhal inflammation, we may have that fluxionary hyperæmia of which an early outcome is hæmoptysis. Experimental pathology explains such occurrences by demonstrating that while a normal vessel, as in the mesentery, will require a pressure of seventy millimeters of mercury to produce extravasation of its contents, an inflamed one will not stand more than twenty-five millimeters. If catarrhal pneumonia proceed in its phthisical form, it adds its elements of danger.

After its early stage of congestion we have the initiative processes extending from the epithelial structures of the bronchi and alveoli to the alveolar wall, which becomes thickened. By means of the double pressure of abundant epithelial and fibrinous products retained within the alveolar cells, and of the increased growth in the alveolar walls, obliterative endarteritis and obstruction of blood-supply follow, the final result of which may be destructive changes opening the way for softening and ulceration, and consequent hemorrhage.

The same early hyperæmia accompanies the development and growth of tubercle, whether it come from the bronchioles, the blood-vessels, or alveolar walls. Trasbot⁴⁸ 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."

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.

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."

⁵⁰ L'Expérience, vol. i. p. 553.

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.

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 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 ends in phthisis. Sommerbrodt's⁵² experiments proved that the healthy animals recovered from the catarrhal pneumonia.

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 Sokolowski⁵³ 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 table⁵⁴ 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. Williams⁵⁵ says that of 198 patients who died, 4 died of profuse hæmoptysis. Thompson⁵⁶ 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.

⁵³ Berlin. klin. Wochenschrift, 30 Sept., 1878.

⁵⁴ Vol. xxii., Lond. Path. Soc. Tr.

⁵⁵ Med.-Chir. Trans., vol. liv.

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.

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. 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's⁵⁹ 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.

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.

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, 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. Ogle⁶⁰ 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 Loomis⁶¹ 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.

⁶⁰ Lond. Path. Soc. Trans., vol. xvii. p. 104.

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 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.