Cerebral Ischemia and secondary brain damage

Regulation of cerebral blood flow

Cerebral ischemia after intracranial hemorrhage has several causes. Normally, cerebral blood flow is kept fairly constant, despite changes in cerebral perfusion pressure over a mean arterial pressure range of approximately 50 to 150 mmHg, by a process termed autoregulation. Cerebral perfusion pressure is defined as the difference between mean arterial pressure and intracranial pressure. Cerebral blood flow may be markedly increased by a rise in PaCO2, secondary to vasodilatation. Autoregulation is lost during hypercapnia.

Global ischemia

Following intracranial hemorrhage, the autoregulation reflex is also lost and cerebral blood flow becomes passively dependent upon cerebral perfusion pressure. Thus systemic hypotension and respiratory difficulties can affect both cerebral perfusion pressure and cerebral blood flow. Therefore provision of an adequate airway, mean arterial pressure, and gas exchange are mandatory for optimal management.

Focal ischemia

Around the hematoma there is a zone of ischemic tissue, which itself is surrounded by a penumbra of functionally impaired but recoverable neuronal tissue. Treatment directed at prevention of global ischemia will also lessen this focal ischemia and thus minimize neuronal death.

Intracranial pressure

Intracranial pressure is commonly increased after intracranial hemorrhage. It is elevated by both the actual space-occupying effect of an intracerebral hematoma and cerebral edema. Cerebral edema, defined as an abnormal collection of fluid within the brain substance, develops secondary to cerebral ischemia. Hydrocephalus, a dilatation of the ventricular system, will also increase intracranial pressure. Intraventricular hemorrhage into the third or fourth ventricle with obstruction of cerebrospinal fluid outflow is usually responsible, but a cerebellar hemorrhage may cause extrinsic compression of the fourth ventricle in the posterior fossa. Identification and prompt treatment of raised intracranial pressure are again important in preservation of cerebral perfusion pressure.

Cerebral vasospasm

Peculiar to subarachnoid hemorrhage is a phenomenon termed cerebral vasospasm, i.e. narrowing of the cerebral arteries in response to the presence of subarachnoid blood and its breakdown products. It begins immediately, but manifests its clinical effects on day 3 following subarachnoid hemorrhage, peaks at days 6 to 8, and then gradually subsides after the second week. It causes cerebral ischemia and continuing or new neurological deficit. The diagnosis is clinical, but changes can be detected on angiography and serial blood velocity studies using transcranial Doppler ultrasonography. Treatment is prophylactic with use of the calcium antagonist nimodipine. Established vasospasm can be treated by raising cerebral perfusion pressure with blood volume expansion and pressor agents.

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