Vasospasm

The leading cause of mortality and morbidity following initial rupture; may appear 4-14 days after the initial hemorrhage, leading to focal ischemia and stroke.
Treatment with the calcium channel antagonist nimodipine (60 mg PO q4h) improves outcomes, perhaps by preventing ischemic injury rather than reducing risk of vasospasm.
Cerebral perfusion can be improved in symptomatic vasospasm by increasing mean arterial pressure with vasopressor agents such as phenylephrine or norepinephrine, and intravascular volume can be expanded with crystalloid, augmenting cardiac output and reducing blood viscosity by reducing the hematocrit; this so-called “triple-H” (hypertension, hemodilution, and hypervolemic) therapy is widely used.
If symptomatic vasospasm persists despite optimal medical therapy, intraarterial vasodilators and angioplasty of the cerebral vessels can be effective.