PULMONARY APOPLEXY.
BY WILLIAM CARSON, M.D.
DEFINITION.—Escape of blood into the pulmonary parenchyma, with laceration of its substance.
SYNONYMS.—Hemorrhage (pulmonaire) foyer (Jaccoud); Diffuse pulmonary apoplexy or Diffuse pneumorrhagia (Fleich); Diffuse pulmonary apoplexy (Loomis); Pneumo-hemorrhagie (Gendrin), etc.
HISTORY.—Latour1 is quoted as being the first to use the words, "apoplexie du poumon."2 Yet Duguet3 also quotes from Frank that Dolocus had a long time before employed it. It is known that cases had been described long before this, as by Corvisart in 1808, Allan Burnes in 1809, among those of this century, and by Prosper Martiano, Bonet, Morgagni, Haller, etc., among the more ancient authors.4 Again, Laennec gives the weight of his authority, and establishes Latour's use of the name, until, as the synonyms show, modern usage has almost abandoned it. Among the multitude of those who have treated of pulmonary apoplexy, we will have filled the requirements of this brief historical statement by mentioning Virchow and his pathological investigations into embolism, and also Cohnheim,5 and later Litten's6 studies on infarction, which have some indirect connection with pulmonary apoplexy.
1 Histoire philosophique et médicale des Hémorrhagies, 1815, passage misquoted in L'apoplexie pulmonaire by Duguet.
2 Op. cit., pp. 220, 222, and 224.
3 Op. cit., p. 11.
4 Duguet, p. 10, etc.
5 Untersuchungen über die Embolischen processe, 1872.
6 Zeitschrift für klinisch Medicin, Erster Band, 131.
ETIOLOGY.—Predisposing Causes.—The male sex affords predominance of cases, because of greater liability to accidents, to the various forms of ulcerative destruction of lung-tissue, and to aneurisms of the aorta and pulmonary artery.
The adult age is most exposed for similar reasons. Ogston's statistics7 support in a general way, but not with strictly technical force, their quotation by Herz.8 Omitting the last 4 of his 20 cases (2 of which were from poisoning, 1 from fracture of skull by a fall down stairs, and 1 from drowning), the average for males (12) was 56.4, and 55.3 for females (4).
7 Brit. and For. Med.-Chir. Rev., vol. xxxvii., 1866, p. 459.
8 Ziemssen's Handbook, vol. v. p. 298. Ogston says (p. 465) it did not appear, however, that any distinct rent of their substance had taken place—to any extent, at least. "When we consider that the area of the extravasation was sufficient to involve often one or two entire lobes, and that death was in most of them very sudden, the cases may be adopted as showing the action of causes similar in kind, if not in degree, to those operative in undoubted pulmonary apoplexy."
As more efficient predisposing causes than either age or sex, may be mentioned aneurisms of the aorta and pulmonary artery, amyloid degeneration of bronchial and pulmonary vessels, the influence of Bright's disease in producing disease of blood-vessels, and atheromatous diseases of the pulmonary artery.
Exciting Causes.—Penetrating and contused wounds of the chest by their direct mechanical effect, and diseases and injuries of the brain through the medium of the nervous system, may produce pulmonary apoplexy, the result in the latter case being usually an infiltration or small infarction.
SYMPTOMATOLOGY.—Pulmonary apoplexy is the least common of the two forms of distinctive pulmonary hemorrhage, the other being pulmonary infarction, already treated of under [HÆMOPTYSIS]. A proportion of cases is associated with mitral disease in its most advanced stages. At that time we may expect pneumorrhagia, but whether from infarction or apoplectic laceration even the event can only occasionally determine. In the latter, if hemorrhage makes its appearance it will be copious and generally overwhelming; at other times the hemorrhage may not appear, and the patient dies suddenly with possibly other indications of the internal flow. The physical signs cannot be relied on, for often the pulmonary tissue is already changed by the long-continued obstruction of circulation. Rupture of aneurism, particularly of aorta, in the great majority of cases takes place into a bronchus, and not into the parenchyma. In case of wounds of the contused variety a laceration of parenchyma occurs at times sufficient to produce marked hæmoptysis. If the blood be not ejected, there are no certain indications of what has happened. If the case be seen immediately after the accident, such physical signs as moist bubbling râles on the margin of an area of feeble or suppressed vesicular murmur, possibly attended with a dull, high-pitched percussion note over that area, would afford a strong presumption in favor of ruptured lung and consequent hemorrhage.
The same signs later might be due to a limited traumatic pneumonia. If the internal hemorrhage, whether traumatic or spontaneous, has made its way through the pleura, then, if the patient live long enough for examination, besides such symptoms as great oppression and exhaustion, the physical signs peculiar to pleural effusion may appear to a limited degree. This opportunity seldom occurs, as such a rupture produces almost invariably a fulminant and rapidly fatal result.
COURSE, DURATION, AND TERMINATION.—The course of the lighter cases is much like that of pulmonary infarction, and that of the severe forms too brief for observation. As to termination, it is quite possible there are cases of laceration so limited as to allow complete recovery, but clinical experience shows that pulmonary apoplexy is usually fatal.
PATHOLOGY AND MORBID ANATOMY.—With branches of the pulmonary vessels weakened by long-continued heart disease, or with such vessels as are found with chronic nephritis, a sudden increase of tension in them from unusual effort or excitement will precipitate a fatal rupture. Sometimes the progress of the degeneration is so insidious and complete that a rupture may occur without obvious exciting cause. This is also the natural history of aortic aneurism. An examination soon after the laceration will show a mass of blood, usually coagulated, sometimes partly fluid, lying in an irregular cavity with walls of the lacerated lung-tissue. After a longer time the lung-tissue beyond the walls of the hemorrhagic focus becomes oedematous to a certain extent. A contraction of the cavity, with change of contents, may proceed to the extent that an encapsuled mass of very small size will remain as the final result (Rokitansky).
DIAGNOSIS from bronchial hemorrhage by the probable existence of phthisical conditions and history. The quantity of blood ejected may be profuse in either case, and therefore be no criterion. From pulmonary infarction, as the other form of pulmonary hemorrhage, by the larger amount of hæmoptysis. If there be no hæmoptysis, a presumption would exist in favor of apoplexy in case of extreme dyspnoea or a fatal result. The associated diseases or causes being similar, no inference from the medical history would be reliable except in case of injuries.
PROGNOSIS.—As we meet with it in recognizable form, the result is almost invariably fatal. A qualification is allowed because of the experience of such a pathologist as Rokitansky, who describes a process of cure in a few cases. The prognosis in such would be determined partly by the severity of the antecedent or accompanying disease, as in heart lesions, and partly by the increased respiratory distress, pain, exhaustion, and hemorrhage.
TREATMENT.—As has been before intimated, a case of pulmonary apoplexy distinctive enough to be diagnosed is usually one that is beyond the reach of treatment. Remedies that may relieve dyspnoea, exhaustion, and hemorrhage are those to be relied on. External irritants, as turpentine-stupe stimulants, ergot, turpentine internally, and such other remedies as are of known effect in the treatment of the associated heart troubles and of the incidental pulmonary infarctions.