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.
Beside infarctions originating in cardiac disease there are others of peripheral origin, as in the puerperal condition from phlegmasia dolens. Hæmoptysis is a rare symptom in such cases, but when it does appear it has the same basis. It is seldom severe, and soon merges into an expectoration of pneumonic character, with the clinical forms of embolic pneumonia, or possibly of abscess or gangrene of the lung.
PATHOLOGY.—Incidentally, the pathological relations of hæmoptysis have been already indicated as being connected with phthisis and cardiac disease—principally with the former. If phthisis be an infectious or specific disease, as a large and growing professional opinion claims, hæmoptysis has its specific relations with it. Few symptoms have greater differentiating force than it has. Its occurrence, outside of well-known cardiac or dyscrasic disease, removes any case of primary pulmonary disease from the category of simple inflammation. There may be much more congestion in bronchitis, more catarrhal products in simple catarrhal pneumonia, and more fibrinous or croupous exudation in pneumonia, than in the primary stages of phthisis, and yet no hæmoptysis appear. The mechanical conditions are present in greater degree, but the infective element is wanting. Its closest affinity is with apex pneumonia or alveolar catarrh, yet probably most of such cases occur without it. A blood-dyscrasia contributes an important element in the pathogenesis of hæmoptysis.
In cardiac hæmoptysis the pathology is more simple. Extreme mechanical conditions of obstruction and reversal of the circulation are reinforced by nutritive changes of the vessels and heart, until the so-called cardiac cachexia is established. There is no infective element, and such cases are seldom if ever followed by phthisical destruction.
MORBID ANATOMY.—Reference has already been made to anatomical changes having direct or indirect relation to hæmoptysis, such as those in the blood-vessels. The anatomical basis of the slight hemorrhages of the early stage of phthisis is seldom if ever discoverable. The belief in vascular fragility and congestion with special origin rests much more upon clinical reasoning than demonstration. The large hemorrhages are now and then fatal within short periods of time or instantly, and we then have the opportunity of noting the general appearance of the lungs.
It is notable that cases are not very frequent where the source of the bleeding has not been found by the most careful search. The general appearance varies according to the length of time that has elapsed since the bleeding which preceded death.