Patofiziologija zapoznele možganske ishemije ob subarahnoidni krvavitvi zaradi rupture anevrizme možganske arterije

Aneurysms of cerebral arteries are present in 1% to 2% of the total population and represent the most common cause of atraumatic subarachnoid haemorrhage. Aneurysm rupture occurs in 8 to 10 individuals per 100,000 population. Mortality of patients after aneurysm rupture is up to 50% and few can live independently after bleeding. After the rupture of a cerebral artery aneurysm, 70% of patients develop angiographic vasospasm and 30% develop an additional neurological deficit. In most cases, vasospasm occurs 3 to 14 days after aneurysm rupture. A poor baseline neurological status (Hunt and Hess score) and a large blood volume in the subarachnoid space are associated with a higher incidence of vasospasm. Various investigative methods are available for diagnosing vasospasm, each with specific advantages and limitations. Vasospasm is no longer recognised as the sole cause of delayed cerebral ischemia after cerebral aneurysm rupture; the role of the inflammatory response and the phenomenon of spreading depolarisation are also important. The calcium channel blocker, nimodipine, remains the only agent proven to be associated with a better neurological outcome in patients after subarachnoid haemorrhage. In patients after subarachnoid haemorrhage due to the rupture of a cerebral aneurysm, the appropriate therapy for extracranial complications, as well as the therapy for possible epileptic seizures, is essential.