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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
Published on: August 30, 2020
[Disturbances of the hemostatic system in patients with aneurysmal subarachnoid hemorrhage]
A I Baranich1, I A Savin1, T F Tabasaranskiy1
1Burdenko Neurosurgical Institute, Moscow, Russia.
Subarachnoid hemorrhages due to rupture of cerebral aneurysms are characterized by high mortality. More than 25% of patients who have survived the first hours after aneurysmal SAH (aSAH) develop delayed cerebral ischemia that is one of the main causes of disability. The mechanisms underlying delayed ischemia have not yet been fully understood. Previously, the development of vasospasm was believed to be the only cause for development of delayed ischemia. In recent years, there has been evidence that hemostatic system disorders typical of this category of patients are the cause of cerebral artery thrombosis, which is one of the main pathophysiological mechanisms for the development of delayed cerebral ischemia. This review presents an analysis of published papers on hemostasis disturbances in patients with aSAH, their pathophysiological mechanisms, and their role in the development of cerebral ischemia.
Subarachnoid hemorrhages due to rupture of cerebral aneurysms are characterized by high mortality. More than 25% of patients who have survived the first hours after aneurysmal SAH (aSAH) develop delayed cerebral ischemia that is one of the main causes of disability. The mechanisms underlying delayed ischemia have not yet been fully understood. Previously, the development of vasospasm was believed to be the only cause for development of delayed ischemia. In recent years, there has been evidence that hemostatic system disorders typical of this category of patients are the cause of cerebral artery thrombosis, which is one of the main pathophysiological mechanisms for the development of delayed cerebral ischemia. This review presents an analysis of published papers on hemostasis disturbances in patients with aSAH, their pathophysiological mechanisms, and their role in the development of cerebral ischemia.
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