The role of erythropoietin in aneurysmal subarachnoid haemorrhage: from bench to bedside.

Abstract

Subarachnoid haemorrhage (SAH) caused by a ruptured aneurysm accounts for only 5 % of strokes, but occurs at a fairly young age and carries a poor prognosis. Delayed cerebral ischaemia (DCI) is an important cause of death and dependence after aneurysmal SAH. The current mainstay of preventing DCI is nimodipine and maintenance of normovolemia, but even with this strategy DCI occurs in a considerable proportion of patients.Several drugs have been developed that have the potential to limit cerebral vasospasm and delayed ischaemic neurologic deficit, thus improving outcome for patients. However, although numerous agents can prevent arterial narrowing and/or block the excitatory cascade of events leading to ischaemic neuronal death in experimental conditions, there is still no pharmacologic agent that has been shown conclusively to improve the outcome in clinical practice.Erythropoietin (EPO) is a well-known erythropoietic hormone recently found to exert neuroprotective properties and has been shown to reduce cerebral vasospasm and infarct volume after experimental SAH. In humans, although EPO treatment did not impact the overall incidence of vasospasm, it significantly reduced the incidence of severe vasospasm, the incidence of delayed ischaemic deficits with new cerebral infarcts, and the duration of impaired autoregulation. The current study provides new evidence for the potential benefit and relative safety of EPO for the treatment of SAH in humans. Future clinical trials will hopefully provide definite evidence whether EPO treatment is beneficial in SAH patients.