Inflammation, Cerebral Vasospasm, and Brain Injury in Subarachnoid Hemorrhage-A Shifting Paradigm and a New Beginning.
Inflammation, Cerebral Vasospasm, and Brain Injury in Subarachnoid Hemorrhage-A Shifting Paradigm and a New Beginning.
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DOI:
10.1097/ccm.0000000000003373
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发表时间:
2018-11
影响因子:
8.8
通讯作者:
Chou SH
中科院分区:
文献类型:
--
作者:
Chou SH
Critical care management of subarachnoid hemor-rhage (SAH) patients remains a daily challenge for intensivists. SAH comes on suddenly and unpredictably, primarily afflicts relatively young and healthy people, requires prolonged critical care support, and leaves over 50% of survivors in protracted severe disability (1, 2). Surviving the initial hemorrhage and surgical or endovascular obliteration of the bleeding aneurysm only marks the beginning of a 14–21 days long complex disease course. During this time, over 50% patients would develop cerebral vasoconstriction and~ 30% develop new neurologic deficits whereas others may accrue injuries silently because the severity of their neurologic deficit precludes adequate clinical detection of ongoing injury (3, 4). To date, there are no bedside monitors or biomarkers that can timely detect onset or reflect severity of SAH-associated brain injury (5), and intensivists often find ourselves “shooting in the dark” with fluid resuscitation, vasopressors, and ionotropic support. There is a dire need to develop biomarkers—such as lactate in sepsis—to guide goal-directed therapy in this prolonged course of brain resuscitation after SAH.Cerebral vasospasm and delayed cerebral ischemia (DCI) are important sequalae of SAH. The definitions of these two entities have varied widely in the literature, leading to much confusion over these terminologies and difficulty comparing results from different SAH clinical studies. Cerebral vasospasm often refers to narrowing of cerebral arteries seen on radiographic imaging modalities, but many studies also defined