Cerebral vasospasm after subarachnoid hemorrhage: An update

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.

Incidence of Vasospasm, Outcome, and Quality of Life after Endovascular and Surgical Treatment of Ruptured Intracranial Aneurysms: Results of a Single-Center Prospective Study in Switzerland

“…The reason for these findings in our small series is nevertheless unclear. Possible factors influencing these observations might include the lack of removal of the clot in the subarachnoid space in patients treated with endovascular techniques and the meticulous treatment of ICP in cases of cerebral edema [22,[49][50][51].…”

Perspectivas en el tratamiento del vasospasmo cerebral inducido por hemorragia subaracnoidea

“…El déficit neurológico isquémico tardío o también llamado "delayed ischemic neurological deficit (DIND)" causado por el VC sigue siendo una complicación que se presenta en un 20 al 30% de los pacientes que ingresan con el diagnóstico de una HSA 33 . En series contemporáneas, del 15 al 20% de estos pacientes sufren un accidente cerebrovascular (ACV) o mueren a causa del vasospasmo a pesar de un tratamiento agresivo 17,31,33,48 . El presente artículo tiene como objetivo presentar una actualización de las diferentes modalidades terapéuticas en desarrollo e investigación que serán tema de discusión y lectura obligada en el futuro próximo.…”

Recommendations for Stroke Management: Update 2003

“…Angiographic vasospasm has a typical temporal course, with onset 3 to 5 days after the hemorrhage; maximal vasospasm is expected at 5 to 14 days, and gradual resolution over 2 to 4 weeks 240 . In about one half of cases, vasospasm is manifested by the occurrence of a delayed neurological ischemic deficit, which may resolve or progress to cerebral infarction (with acute or subacute development of focal or generalized symptoms) 241 .…”