In the cases immediately fatal the tubes are filled with fresh blood, which has stained the mucous membrane and has changed the general surface of the sections of lung into a dark, mottled, or patchy color. The greater amount of blood is to be found in the lung from which it has primarily come, but in the more profuse hemorrhages, and particularly where there has been time for the struggles of the threatening suffocation, much blood may either overflow or be inhaled into the other lung and carried into the extreme portions of the air-sacs. If the flow be not overwhelming, the patient may survive long enough to allow other effects from the blood, which has by gravitation or insufflation been carried into certain parts of the lung. We are indebted to Reginald E. Thompson62 for the most important study of the secondary effects of the blood thus remaining. He says that the relics of blood are to be found in the presence of hard nodules, often deeply, though not always, pigmented. They are mostly found at the summit and middle part of the upper lobe, the middle axillary region, between the third and fifth ribs, close to the pleura, the anterior inferior border, and the middle part of the base corresponding to the summit of the arch of the diaphragm. "Absorption, decoloration, and fibrination go on; the outlying portions of the blood disappear; the central nodules become hard and white, and alone remain to show what has taken place." They are in some cases of varying color, slight red or of an ivory white, mottled with old blood-pigment, around the bronchioles especially, and in the shape of small black granules. Microscopically, they consist of "a group of alveola firmly packed with a semi-opaque, homogeneous fibrinous material, and there is some thickening of the alveolar tissue and also of the interlobular tissue, which thickened tissue forms the limiting capsule."
62 Op. cit., p. 46, etc. These researches are an important epoch in the history of hæmoptysis.
The ultimate fate of these nodules is variable. Sometimes they go on to formation of cavities, or softening occurs around the periphery or in the centre, and leads to general liquefaction of the nodule, or they may separate from the surrounding tissue by traction. Sometimes the effect of retention of the blood in the air-passages is a catarrhal pneumonia, with the ordinary anatomical proofs of it referred to in the paragraph on modes of termination of hæmoptysis.
Accepting the observations, we have the demonstration of a phthisis ab hæmoptoe.
The morbid anatomy of cases fatal from rupture of aneurisms of the branches of the pulmonary artery has been made prominent by the researches of Rokitansky and Rasmussen.63 He describes small sac-like aneurisms and ectasias situated in the vessels running along the wall of the cavity. The aneurisms have the shape of a bag and an even surface. The walls of the unbroken aneurisms are of great thickness, and those of the broken ones thin. The opening is always found on the most protruding part of the sac; the edges are thin; their size varies from a pea to a small orange. Powell64 says a microscopic section taken from a specimen in an early stage shows new connective-tissue elements, causing induration affecting the whole thickness of the wall and obscuring the distinction between the coats. The wall is brittle, becomes thinner from want of support, and yields to an inciting cause, with rupture and death as the result.
63 Edinburgh Med. Journal, 1868–69.
64 Trans. London Pathological Society, vol. xxii. pp. 54, 55.
The morbid anatomy of cardiac hæmoptysis is found mostly in two conditions—that of degenerated, atheromatous, varicose blood-vessels, brought about by the condition of chronic obstruction and increased venous tension in valvular disease; and in that of pulmonary infarction.
The first prepares the way for diapedesis or rupture, and consequent hæmoptysis. The rupture takes place in the parenchyma, or, as the anatomical details formerly given make probable, from the blood-vessels of the bronchial mucous membrane also.
Pulmonary infarction is recognized by a dark, dense, pyramidal or wedge-shaped area of varying size situated at the surface of the lung, with the base of the pyramid coming to the pleura. It is found oftener in the lower lobes and in multiple form. It is caused by an embolic obstruction of a terminal branch of the pulmonary artery; sometimes by a thrombosis or by both. A venous reflux from the neighboring districts is supposed to fill the empty vessel, and after a certain time has elapsed changes are supposed to have occurred in their walls by which the blood escapes into the air-cells and interstitial tissue. Litten's65 explanation, sustained by his experiments, is that the venous reflux, after a closure of the pulmonary artery, is by no means necessary to the formation of an infarction. The infarction fails if the pulmonary artery and the bronchial artery, and those arteries lying outside the lungs, but in circulatory connection with them—the pleural—are simultaneously shut off. If the whole arterial supply be thus taken away, but a living connection be maintained by means of the veins, an infarction does not follow, while it immediately follows if, at the same time with the open veins and closed pulmonary arteries, the collateral or supplementary circulation be kept free. A venous reflux cannot occur so long as a circulation in the capillaries of the lung is sustained by collateral arterial branches. The explanation is that in an unobstructed circulation the entire resistance which is offered to the blood-stream in the capillaries of the lung is overcome by the pressure existing in the pulmonary artery, which, corresponding to the greater width of the capillaries, is much less than the pressure in the corporeal arteries. If the pulmonary artery becomes suddenly impermeable, the pressure in the collateral arteries, which originates partly from the bronchial artery, and partly from those outside of, but in connection with, the lungs, as the pleural, etc., is sufficient to prevent a venous reflux, but not sufficient to overcome the entire resistance in the lungs and to drive the blood beyond the capillaries into the left auricle. Then follows an accumulation and stasis of the blood in the capillaries and smaller veins, and hence results at first a hyperæmia and later a diapedesis. Litten makes another important change in Cohnheim's doctrine: he maintains that the hemorrhage appears before the integrity of the vessel-walls is impaired.