AHA/ASA卒中后腦水腫管理指南  內容預覽：

    The emergence of brain swelling is the most troublesome and even life-threatening consequence of a large-territory isch - emic stroke. Brain swelling occurs as a result of loss of func-tion of membrane transporters, causing sodium and water influx into the necrotic or ischemic cell, leading to cytotoxic edema.

    Unrelenting swelling disrupts the blood- brain barrier （BBB）；therefore, a component of vasogenic edema may coexist.The development of clinically significant cerebral edema is expected only in large-territory cerebral infarcts and can be observed by the clinician in 3 ways: a rapid and fulminant course （within 24–36 hours）， a gradually progressive course（over several days）， or an initially worsening course followed by a plateau and resolution （about a week）。

    Currently, no methods are available to predict the course of brain swelling reliably. There is a clinical perception that when brain swell-ing occurs in the cerebral or cerebellar hemisphere, medical management to reduce brain swelling is not successful in changing outcome. Therefore, a decompressive craniectomy is offered to relieve the mass effect of the swollen hemisphere on the thalamus, brainstem, and network projections to the cortex, manifested mainly by a decreased level of arousal.

    Decompressive craniectomy for cerebral edema after ischemichemispheric stroke has significantly increased in US hospitals.

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