Antifibrinolytic therapy for intracranial aneurysms.

Abstract

I T HAS long been known and it has been recently documented in an admirable fashion 7 that patients who sustain a subarachnoid hemorrhage from a ruptured berry aneurysm have a tendency to rebleed, that this tendency is minimal during the first 2 days, rises to a maximum about the end of the first week, falls to a relatively low level during the third week, and to a very low figure after the third month. Pathologically speaking, what does this mean? It probably means that the initial hemorrhage stops by means of the formation of a blood clot (possibly aided by arterial spasm), that this blood clot is intact for 2 days and then shows evidence of dissolution. Dissolution may allow a second hemorrhage to occur. If the second hemorrhage does not occur early, fibrous tissue and endothelial repair take place, thus providing the patient once more with a reasonable, if perhaps restricted, life expectancy. Therapeutically, there is little that can be done for the patient's initial hemorrhage beyond good medical and nursing care and the occasional evacuation of an intracranial hematoma. Most effort has been directed toward preventing the incidence and consequent mortality and morbidity of the second and subsequent hemorrhages. The classical surgical methods of clip, ligature, and encapsulation are well known. Medical reduction of blood pressure has also been advocated. 17 Another reasonable method that suggests itself is a prolongation of the duration of the naturally occurring hemostatic blood clot within and about the wall of the aneurysm. This prolongation might be expected to provide protection against hemorrhage while fibrous tissue and endothelial repair got under way. In the course of experimental work u designed to induce controlled thrombosis within intracranial aneurysms, we noted that electrically induced thrombi in the femoral artery