Detecting and treating microvascular ischemia after subarachnoid hemorrhage.

PURPOSE OF REVIEW

To provide an overview of the current management of cerebral vasospasm following subarachnoid hemorrhage, emphasizing the detection and treatment of delayed ischemia.

RECENT FINDINGS

Sensitive and specific monitoring methods are necessary to register the onset of cerebral vasospasm early to prevent long-term morbidity and mortality. Therefore, various techniques to measure cerebral perfusion and/or surrogate parameters have been developed. Prophylaxis with calcium antagonists such as nimodipine is administered for neuroprotection. Resolution of ongoing cerebral vasospasm can be achieved by either dilating constricted vessels or optimizing hemodynamics. Therapeutic treatment with hypertension, hypervolemia and hemodilution (HHH) has a direct influence on cerebral vasospasm, ischemic sequelae and outcome, while prophylactic HHH leads to excess complications. Other treatments, for example endothelin antagonists, statins or magnesium salts, used to prevent or treat cerebral vasospasm, are being tested. Endovascular treatment options can be used for therapy-refractory cerebral vasospasm, but they carry procedure-related risks and may be short-acting.

SUMMARY

Diagnosis of microvascular ischemia following subarachnoid hemorrhage involves clinical observation, non-invasive determination of cerebral hemodynamic variables, autoregulation studies and invasive online monitoring of cerebral oxygenation and metabolism. Nimodipine is administered prophylactically, while HHH is initiated therapeutically. New causal therapies are being evaluated.