Update on the Management of Subarachnoid Hemorrhage

Katja E Wartenberg

Disclosures

Future Neurology. 2013;8(2):205-224. 

In This Article

Future Perspective

The majority of the recommendations for the management of patients with SAH are based on the consensus opinions of experts in the field.[29,56] There are many open-ended questions such as the efficacy of antifibrinolytic therapy and the optimal blood pressure goal to prevent rebleeding prior to aneurysm repair, the efficacy of intensive glucose control and its target range, the impact of maintained normothermia on outcome after SAH, the optimal hemoglobin target after SAH and during DCI and the optimal therapy regimen for neurogenic stunned myocardium. New endovascular techniques such as intra-aortic balloon pumps and counterpulsation entered the field of DCI management. Current prevention of DCI and neuroprotection trials include intracisternal application of thrombolytic therapy to decrease the clot burden, and consequently the incidence of delayed cerebral ischemia, early placement of lumbar drainage to reduce subarachnoid blood, intrathecal application of magnesium sulfate, intraoperative implantation or intraventricular use of nicardipine prolonged-release implants (pellets), transfusion of packed red blood cells, administration of erythropoetin as well as randomized, controlled outcome studies of statins and human albumin. The common aim of the reduction of blood clots in the subarachnoid space or the local and systemic application of neuroprotective agents is the reduction of delayed cerebral ischemia along with an improvement of clinical outcome. Most of these trials are designed as safety studies. The STASH trial (recruiting) and the ALISAH II trial (under review) are Phase III trials aimed at improving outcome.[218,301] The best monitoring technique and triggers for neuroimaging and intervention for DCI in poor-grade SAH patients needs to be studied. With the application of multimodality monitoring, including intracortical electroencephalography electrodes, more light is shed into the pathophysiology of secondary injury after SAH such as spreading depolarizations, a wave along the cortex characterized by swelling of neurons, distortion of dendritic spines, a large change of the slow electrical potential and silencing of brain electrical activity (spreading depression), seen as a cause or a sign of DCI. Physiological derangements are noted and interpreted. The role of spreading depolarizations in DCI and potential therapy targets for physiological derangements detected by multimodality monitoring now need to be clarified and defined.

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