International Cooperative Study in 1990 and based on observations of 3,521 patients (surgery performed in 83 percent), it was found at the 6-month evaluation that 26 percent had died and 58 percent had made a good recovery (Kassell et al). Vasospasm and rebleeding were the leading causes of morbidity and mortality in those who survived the initial hemorrhage. More recent series, usually from one country or one center, generally reflect these statistics except that rebleeding has been less frequent as earlier intervention has become more generally applied.
This is influenced by the neurologic and general medical state of the patient as well as by the location and morphology of the aneurysm. Ideally, all patients should have the aneurysmal sac obliterated, but the mortality is high if the patient is stuporous or comatose (Hunt and Hess scale IV or V).
The general medical management in the acute stage includes bed rest, fluid administration to maintain above-normal circulating blood volume and central venous pressure; use of elastic stockings and stool softeners; administration of calcium channel blockers to reduce infarction from vasospasm (see below); additional beta-adrenergic blockers, intravenous nitroprusside, or other medication to reduce greatly elevated blood pressure and then maintain systolic blood pressure at 150 mm Hg or less; and pain-relieving medication for headache (this alone will often reduce the hypertension). The prevention of systemic venous thrombosis is critical; it usually is accomplished by the use of cyclically inflated whole-leg compression boots. The use of antiepileptic drugs is controversial; many neurosurgeons administer them early, with a view of preventing a seizure-induced risk of rebleeding. Several small studies suggest they may be detrimental and we have generally avoided them unless a seizure has occurred.
Calcium channel blockers are used to reduce the incidence of stroke from vasospasm. Nimodipine 60 mg administered orally every 4 h is currently favored. Although calcium channel blockers do not alter the incidence of angiographically demonstrated vasospasm, they have reduced the number of strokes in each of five randomized studies, beginning with the one conducted by Allen and colleagues. Several groups use angioplasty techniques to dilate vasospastic vessels and report symptomatic improvement, but there are as yet insufficient controlled data to judge the merits and safety of this procedure.
The most notable advances in this disease have been in the techniques for the early obliteration of aneurysms, particularly the operating microscope and endovascular approaches, and in the management of circulatory volume. In the majority of patients, intravascular volume is depleted in the days after subarachnoid hemorrhage. This, in turn, greatly increases the chances of ischemic infarction from vasospasm. In part, this volume contraction can be attributed to bed rest, but sodium loss, probably resulting from the release of atrial natriuretic factor (ANF), a potent oligopeptide stimulator of sodium loss in renal tubules, may also be a factor. Hyponatremia develops in the first week after hemorrhage, but it is unclear whether this also results from the natriuretic effects of ANF or is an effect of antidiuretic hormone, causing water retention. The work of Diringer and coworkers (1988) suggests that both mechanisms are operative but it is the volume depletion, not hyponatremia per se, that is of the greatest clinical consequence.