5 Centralbl. f. d. med. Wissensch., June 23, 1883.
6 Arch. Ital. de Biologie, 1883, iii. 2, and i. 1.
7 Ibid., 1883, iii. 2.
In chronic congestion and enlargement of the spleen from malarial poisoning the removal of the patient to a non-malarious locality will always materially assist in the recovery of health.
Hemorrhagic Infarction of the Spleen.
The investigations of Virchow, and more recently of Cohnheim, into the pathogenesis and pathology of hemorrhagic infarction have afforded an easily intelligible explanation of the causes of the frequency of this morbid process in the spleen. A moment's reference to the anatomy of the splenic blood-vessels will show that the conditions most favorable to the production of hemorrhagic infarction in the presence of an exciting cause are here afforded. Instead of terminating in a capillary network with free and abundant anastomoses, the splenic arteries end in fine pencils, opening, not into capillaries leading to venous radicles, but into vascular spaces in which traces of both afferent and efferent blood-vessels gradually become effaced. These arterioles have no other vascular communications than with the small arteries, the terminal extremities of which they are. This arrangement may be very perfectly demonstrated in injected spleens where the material has been imperfectly driven through the vascular system of the organ, so that wedge-shaped areas of successful injection become sharply defined. This distribution of the blood-vessels renders the area supplied by each almost completely dependent upon it for efficient nutrition, and almost certain to become structurally altered if its lumen should become in any manner obstructed. To this arrangement of the arteries and arterioles upon one side is added, upon the other, a valveless condition of the splenic veins, whereby regurgitation may readily occur. We have here, therefore, evidently conditions most favorable to the development of hemorrhagic infarction.
The process through which hemorrhagic infarction occurs has been definitely observed by Cohnheim. The area of the distribution of the obstructed artery or arteriole, receiving no blood-supply from anastomosing branches, undergoes disintegration. The walls of the blood-vessels as far as the nearest communicating branch participate in the process of disorganization. After a while a backward movement of the blood-current begins in the nearest still pervious vessels, and is continued into the obstructed vessels, through whose disintegrating walls the blood escapes and the hemorrhagic infarction is established. The future course of the infarct depends almost entirely upon the nature of the causes that brought it about.
In the spleen, as in other organs, the causes of hemorrhagic infarction may be widely different, though an essential condition of each is that it be competent to produce plugging of the blood-vessel. The most important cause is probably ulcerative endocarditis, in the course of which minute fragments of the endocardium or of the vegetations that have formed upon it, especially of the neighborhood of the valves, in consequence of inflammation, constitute the emboli. The plugs largely consist of fibrinous matter enveloping colonies of micrococci, or they may be derived from detached portions of thrombi, or from solid particles that may have in any way gained access to the circulatory current, as from endarteritis, from atheroma, primary emboli in the pulmonary circulation, etc.
Hemorrhagic infarction has also been described by Ponfick8 as occurring in relapsing fever and originating in the veins, and not to be referred to any of the already-mentioned causes. It is thrombotic in origin, and due to some peculiarities of the morbid processes of the affection.
8 Virchow's Archiv, Bd. lx.; Mosler, Ziemssen's Cyclop., viii. p. 443.