New trends in prevention and management of cerebral vasospasm after subarachnoid hemorrhage.

Abstract

Spontaneous subarachnoid hemorrhage is a bleeding into the subarachnoid space without trauma. Aneurysms are the underlying cause in 80% of the cases. Among other causes are arteriovenous malformations, anticoagulation, vasculitis and brain tumor. Spontaneous subarachnoid hemorrhage is a serious disease where up to half of the patients die. Of those who survive, only half return to work and many have a reduced quality of life. Spontaneous subarachnoid hemorrhage is presented by severe headache with rapid onset, vomiting, confusion or disturbed consciousness, neck stiffness and sometimes seizures and complicated by cerebral vasospasm, obstructive hydrocephalus, hyponatremia, neurogenic pulmonary oedema, cardiac dysfunction and terson’s syndrome. Delayed cerebral ischemia (DCI) is a common complication of aneurysmal SAH and remains the single most important cause of morbidity and mortality in those patients who survive the initial bleed. Cerebral vaspospasm is considered the main culprit of DCI. DCI was defined as symptomatic vasospasm or the appearance of new infarction on computerized tomography (CT) or magnetic resonance (MR) when the cause was felt to be attributable to vasospasm. Clinical diagnosis of delayed ischemic neurological deficit (DIND) is made when other possible causes of neurological deterioration such as rebleeding, hydrocephalus, seizures and electrolyte abnormalities have been excluded. The presence and the amount of oxyhemoglobin and other by-product of red cell lysis(eg,bilirubin and methemoglobin) in the subarachnoid cisterns is believed to be the major trigger of the phenomena that ulti