Management of vasospasm in subarachnoid hemorrhage

Delayed cerebral ischemia and the vasospasm: concepts and history The early brain injury from aneurysmal rupture is associated with substantial morbidity and mortality, including the risks of rebleeding, elevations in intracranial pressure, and development of hydrocephalus. However, even those surviving this initial period after subarachnoid hemorrhage (SAH) in good clinical condition may subsequently deteriorate, developing neurological deficits and/or cerebral infarction. This process is termed delayed cerebral ischemia (DCI) and is the major contributor to secondary brain injury and residual neurological disability in survivors of SAH (1). Pathologic narrowing of proximal intracranial arteries was first noted after SAH with the advent of cerebral angiography in the 1950s (2). This phenomenon, termed cerebral vasospasm, has been associated with neurological deterioration (3), reductions in cerebral blood flow (CBF) (4), and ischemic brain lesions (5). Angiographic vasospasm develops in as many as two-thirds of patients after SAH, with peak onset 4-10 days post-bleeding and usually regresses by the third week (6). The association of vasospasm with neurological deficits and DCI has fostered the interchangeable but misleading use of these terms. Vasospasm should be reserved to only describe the vascular/radiographic abnormality (7).