Romanian Neurosurgery (Sep 2010)
Cerebral vasospasm - theoretical remarks
Abstract
Vasospasm is a serious complication of subarachnoid hemorrhage and it can cause ischemic brain injury (referred to as “delayed ischemia”) and permanent brain damage due to lack of oxygen in parts of the brain. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. About one third of all people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those suffer permanent damage as a result. It is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm. A protocol referred to as “triple H” is often used as a measure to treat vasospasm when it causes symptoms; this is the use of intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation) and hemodilution (mild dilution of the blood). Nimodipine is routinely used as prophylaxis against delayed ischemic neurological deficits associated with vasospasm. If the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer vasodilator medication: endovascular infusion of vasodilatory substances such as papaverine, or of calcium channel blockers such as verapamil; angioplasty may also be performed.
