Pharmacologic Management of Subarachnoid Hemorrhage.

World Neurosurg

Division of Neurosurgery, Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

Published: July 2015

AI Article Synopsis

  • Subarachnoid hemorrhage (SAH) often leads to poor functional outcomes, particularly in younger patients, with no preventive pharmacological treatments currently available.
  • The main pharmacological focus for SAH is preventing delayed cerebral ischemia (DCI), with nimodipine as the only evidence-based treatment, while other potential drugs have not shown significant efficacy.
  • There is a need for further research to identify effective pharmacotherapies for DCI and improve overall functional outcomes in SAH patients.

Article Abstract

Subarachnoid hemorrhage (SAH) remains a condition with suboptimal functional outcomes, especially in the young population. Pharmacotherapy has an accepted role in several aspects of the disease and an emerging role in several others. No preventive pharmacologic interventions for SAH currently exist. Antiplatelet medications as well as anticoagulation have been used to prevent thromboembolic events after endovascular coiling. However, the main focus of pharmacologic treatment of SAH is the prevention of delayed cerebral ischemia (DCI). Currently the only evidence-based medical intervention is nimodipine. Other calcium channel blockers have been evaluated without convincing efficacy. Anti-inflammatory drugs such as statins have demonstrated early potential; however, they failed to provide significant evidence for the use in preventing DCI. Similar findings have been reported for magnesium, which showed potential in experimental studies and a phase 2 trial. Clazosentane, a potent endothelin receptor antagonist, did not translate to improve functional outcomes. Various other neuroprotective agents have been used to prevent DCI; however, the results have been, at best inconclusive. The prevention of DCI and improvement in functional outcome remain the goals of pharmacotherapy after the culprit lesion has been treated in aneurysmal SAH. Therefore, further research to elucidate the exact mechanisms by which DCI is propagated is clearly needed. In this article, we review the current pharmacologic approaches that have been evaluated in SAH and highlight the areas in which further research is needed.

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Source
http://dx.doi.org/10.1016/j.wneu.2015.02.004DOI Listing

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