36 Vasospasm Management

Devi P. Patra, Ryan Hess, Evelyn L. Turcotte, Miles Hudson, Muriel T. Zaatar, Chandan Krishna, and Bernard R. Bendok

Abstract

Cerebral vasospasm is the narrowing of the intracranial vessels often seen after subarachnoid hemorrhage. Vasospasm can be focal or diffuse and can cause delayed neurological deficit which is one of the significant causes of morbidity and mortality after aneurysmal subarachnoid hemorrhage. Medical management with induced hypertension and oral nimodipine are the only current accepted medical approaches for vasospasm. Endovascular therapy is indicated when significant and prompt response is not achieved with medical therapy. Early intervention is the key for successful endovascular management, with most centers advocating treatment within 2-4 hours of onset of symptoms if not sooner depending on severity of the deficit. Intra-arterial vasodilator therapy is the primary modality of endovascular treatment. The major limitation of intra-arterial therapy is its transient effect with high relapse rate requiring multiple sessions of therapy and its propensity to potentially cause hypotension which could negate the benefits in some cases. Mechanical angioplasty is the other modality of endovascular treatment which has more durable vasodilator effect, but with higher risk of potential complications including dissection and vessel rupture. Therefore it is usually indicated for refractory vasospasm not responding to vasodilator therapy. Despite the risks of intervention, endovascular therapy is a promising modality to treat medically refractory vasospasm and spasms in patients with challenging neurological assessments due to coma and or sedation necessitated by mechanical ventilation. This treatment likely reduces the incidence of delayed neurological deficit and can improve clinical outcomes.

Key words

cerebral vasospasm - subarachnoid hemorrhage - angioplasty - endovascular - SAH

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