Cerebral vasospasm after subarachnoid hemorrhage: An update

TLDR

Symptomatic vasospasm, the leading cause of morbidity after subarachnoid hemorrhage, typically develops 4–12 days post‑bleed, correlates with thick basal cistern clots, presents with gradual neurological decline, and may be worsened by hyponatremia. The study reviews mechanisms of smooth‑muscle contraction and relaxation and experimental efforts to elucidate the nature of vasospasm. Current effective therapy for symptomatic vasospasm involves volume expansion with colloid or blood, raising systemic blood pressure, and lowering intracranial pressure.

Abstract

Abstract Symptomatic vasospasm, or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction, is currently the most important cause of morbidity after acute subarachnoid hemorrhage. The development of vasospasm is directly correlated with the presence of thick blood clots in the basal subarachnoid cisterns, which can be detected by an early computed tomographic scan. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. The onset is gradual, occurring over hours or days. There is typically a gradual deterioration of the level of consciousness, accompanied by focal neurological deficits that are determined by the arterial territories involved. Hyponatremia frequently occurs and may exacerbate the symptoms. The patients are usually volume depleted, and therefore many authorities now treat them with replenishment and expansion of their intravascular volume with colloid and blood. Volume expansion, together with elevation of the systemic blood pressure and reduction of the intracranial pressure when elevated, constitute the only currently available effective therapy for symptomatic vasospasm. The cause of vasospasm remains obscure. Mechanisms of smooth muscle cell contraction and relaxation and experimental efforts to elucidate the nature of vasospasm are reviewed.