Treatment of acute hydrocephalus and cerebral ischemia after subarachnoid hemorrhage

Only recently has acute hydrocephalus after subarachnoid hemorrhage been recognized as a clinical important problem. The mortality rate in patients with acute hydrocephalus after subarachnoid hemorrhage is higher than in those without, which is mainly caused by cerebral ischemia. An explanation for the role of acute hydrocephalus in producing fatal cerebral ischemia is offered by the significant correlation between acute hydroceghalus and hyponatremia and between hyponatremia and death from cerebral ischemia, whereas cerebral ischemia is relatively rare in patients with acute hydrocephalus who do not develop hyponatremia. The relation between hydrocephalus and hyponatremia is possibly explained by enlargement of the third ventricle which could interfere with hypothalamic function. Dysfunction of the hypothalamus may result in the release of a natriuretic factor which in turn causes salt wasting and hypovolemia. This hypovolemia may contribute to the development of cerebral ischemia after subarachnoid hemorrhage. Therefore, treatment of acute hydrocephalus should not be aimed only at the reduction of cerebro-spinal fluid pressure, but also at the prevention of a negative sodium- and fluidbalance. This strategy is the subject of this thesis.