Abstract
Cerebral vasospasm is a prolonged but reversible narrowing of cerebral arteries beginning days after subarachnoid hemorrhage. Progression to cerebral ischemia is tied mostly to vasospasm severity, and its pathogenesis lies in artery encasement by blood clot, although the complex interactions between hematoma and surrounding structures are not fully understood. The delayed onset of vasospasm provides a potential opportunity for its prevention. It is disappointing that recent randomized, controlled trials did not demonstrate that the endothelin antagonist clazosentan, the cholesterol-lowering agent simvastatin, and the vasodilator magnesium sulfate improve patient outcome. Minimizing ischemia by avoiding inadequate blood volume and pressure, administering the calcium antagonist nimodipine, and intervention with balloon angioplasty, when necessary, constitutes current best management. Over the past two decades, our ability to manage vasospasm has led to a significant decline in patient morbidity and mortality from vasospasm, yet it still remains an important determinant of outcome after aneurysm rupture.
Highlights
RÉSUMÉ: Vasospasme cérébral : revue du sujet
Cerebral vasospasm can rarely complicate traumatic subarachnoid hemorrhage (SAH), ruptured vascular malformations, hemorrhagic brain tumors, and any condition that results in extensive bleeding into the subarachnoid space beneath the brain, in clinical practice vasospasm is by far most commonly associated with rupture of cerebral aneurysms within the basal subarachnoid cisterns
Cerebral infarction was significantly associated with increasing patient age, worse neurological condition on admission, a history of hypertension or diabetes mellitus, larger aneurysm, induced hypertension as part of management, fever, and a diagnosis of symptomatic vasospasm
Summary
One early study found no benefit from intravenous MgSO4 infusions,[121] another showed various trends toward benefit,[122] and a third suggested efficacy equivalent to nimodipine in preventing ischemic damage.[123] Several additional trials have since been completed, including several large, international, and multicenter phase 3 randomized controlled studies, Intravenous Magnesium Sulfate for Aneurysmal Subarachnoid Hemorrhage (IMASH; 327 patents enrolled) and IMASH-2 (1204 patents enrolled).[124,125] Those large trials, as well as a recent meta-analysis, found that intravenous magnesium (20 mmol MgSO4 administered over 30 minutes followed by a continuous infusion of 80 mmol MgSO4 per day for 14 days) did not increase the probability of good neurological outcome or decrease the risks of cerebral infarction, radiographic vasospasm, or mortality.[126] There is no evidence at this time to support the use of intravenous magnesium sulfate following aneurysmal SAH.
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