Peri-operative medical management of cerebral vasospasm

The physiological mechanism of cerebral vasospasm after aneurysmal subarachnoid hemorrhage remains elusive and its treatment can be challenging. Traditionally, 'triple-H' therapy and the calcium channel blocker, nimodipine, are used to treat cerebral vasospasm. However, as the etiology of vasospasm is unraveled, investigative pharmaceutical agents that stop the development and attenuate the severity of cerebral vasospasm, are being investigated in clinical trials.

In this manuscript, we review the clinical presentation and characteristics of cerebral vasospasm after aneurysmal subarachnoid hemorrhage and the utility of hyperdynamic therapy and pharmacotherapies.

Triple-H therapy improves cerebral perfusion and improves neurological outcome during clinically evident cerebral vasospasm. Nimodipine is the accepted standard medication used to reduce the incidence of cerebral vasospasm, but more importantly, has a neuroprotective effect during hypoxia. Other medications such as magnesium sulfate, HMG-CoA reductase inhibitors and enoxaparin, are also being trialed with some promising results.

Endovascular administration of intra-arterial anti-spasmodic agents and balloon angioplasty are becoming more commonly utilized at institutions where endovascular therapy is available. However, triple-H therapy and nimodipine remain the accepted first-line of treatment for cerebral vasospasm after aneurysmal subarachnoid hemorrhage.