Abstract

Early mortality after acute ischemic stroke is most frequently caused by space-occupying ischemic brain edema. In case of complete middle cerebral artery territory (MCA) infarction, including the basal ganglia, a large space-occupying postischemic edema that finally leads to herniation and brain death may occur. These patients present with almost complete hemiplegia, head- and eye-turning progressive deterioration of consciousness over the first 24 to 48 hours, and a reduced ventilatory drive. Prognosis of large MCA or hemispheric infarctions is poor: in prospective case series, 80% died from herniation despite maximum conservative therapy.1 General measures of treatment of increased intracranial pressure (ICP) after acute ischemic stroke include elevation of the head to a 30-degree angle to improve venous drainage and avoidance of both hyperthermia and hyperglycemia. As part of the specific anti-edematous pharmacological treatment, osmotherapy using glycerol, mannitol, or hyperosmolar saline solutions is used to reduce brain edema. All substances work by means of lowering ICP, but only for a limited time. The same is true for barbiturates, which may reduce critically elevated ICP reading massively, but only …

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