Vasospasm After aSAH

For those who survive the initial event of aneurysmal rupture, the leading cause of morbidity and mortality has changed over the past 25 years. Previously, early rebleeding was the main culprit, but this has been minimized by early surgical repair (96). Today, cerebral vasospasm is the greatest threat to functional brain recovery and life. In fact, 7% of patients die of vasospasm (97), 7% have severe neurologic deficits associated with vasospasm (98), and another 20% have delayed ischemic neurologic deficits secondary to vasospasm (98). Although CT/CTA perfusion techniques are increasingly utilized (99,100), symptomatic vasospasm refractory to medical management therapy must be evaluated with 4-vessel cerebral angiography. Invariably, an angiographic vasospasm pattern is evident in most SAH patients on days 4 through 12. Balloon and chemical angioplasty with selective intra-arterial bolus injection of vasodilators are the options. The clinician guides the decision to treat. If the severe vasospasm involves the ICA, A1, or M1 segments, angioplasty has been shown to be technically feasible, with durable results and significant clinical improvement. If more distal cerebral artery involvement is detected, selective intra-arterial infusion of vasodilators has been shown to improve parenchymal perfusion by reducing the degree of vasospasm and, thus, improve outcome scores.

Papaverine is the only FDA-approved intra-arterial vasodilator. It is short lived but not without risk. Reported complications include rapid increases in intracranial pressure (which typically return to normal with discontinuance of papaverine infusion) (101), transient neurologic deficits (including mydriasis) (102), brain stem depression (103,104), monocular blindness (105), seizures (105,106), thrombocytopenia (107), precipitation of embolic crystals (108), and paradoxic exacerbation of vasospasm that leads to cerebral infarction (109). In fact, at higher concentrations, papaverine can precipitate in blood, which can also be embolic.

These issues have led clinical investigators to try other vasodilatory agents, with most interest centered around calcium entry blockers, such as nimodipine (110 ), nicardipine (111 ), and verapamil (112), which have shown promise in small numbers of patients. Duration of their effects is not known; however, because the drugs are infused locally, some believe their molecular nature causes deep penetration into the brain tissue, resulting in the desired prolonged effects. Best results might be obtained when treatment is begun within 2 hr of the onset of symptoms (113), but positive results might be seen up to 24 hr after onset (114,115).

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