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急性脑损伤后高肾上腺素状态的表现。

Manifestations of the hyperadrenergic state after acute brain injury.

机构信息

Department of Neurology and Neurocritical Care, Oregon Health and Science University, Portland, Oregon 97239, USA.

出版信息

Curr Opin Crit Care. 2012 Apr;18(2):139-45. doi: 10.1097/MCC.0b013e3283513290.

DOI:10.1097/MCC.0b013e3283513290
PMID:22322258
Abstract

PURPOSE OF REVIEW

Hyperadrenergic activity leading to autonomic dysfunction after acute brain injury is an underrecognized, yet important source of complications following a variety of neurologic injuries. Autonomic dysfunction may prolong ICU stay and increase healthcare costs driven by extensive diagnostic workups and/or ensuing complications. In this review article, we intend to illustrate commonalities between various hyperadrenergic states in acquired brain injury. Specifically, this review will focus on autonomic dysfunction in two common conditions in the neurocritical care unit, traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH).

RECENT FINDINGS

Elevated levels of catecholamines have been well documented in SAH and to a lesser extent in paroxysmal sympathetic hyperactivity, hinting at the underlying increased sympathetic tone in both disease states. The resultant hyperadrenergic state may manifest with vital sign alterations, or end-organ dysfunction such as heart failure. Neuroimaging and limited clinical data have elucidated some information regarding underlying mechanisms, but the gaps in understanding have thus far limited prospective clinical trials. A multitude of therapeutic options to reduce adrenergic tone have been employed with varying degrees of success.

SUMMARY

The pathophysiology of autonomic dysfunction is incompletely understood and treatment options are few. However, recognizing hyperadrenergic commonality in disparate neurologic disease may facilitate novel inquiries into lesion localization and therapeutics. It is possible that adrenergic blockade may diminish or abrogate end-organ dysfunction in TBI and SAH.

摘要

目的综述

急性脑损伤后导致自主神经功能障碍的高肾上腺素能活性是多种神经损伤后并发症的一个未被充分认识但重要的来源。自主神经功能障碍可能会延长 ICU 停留时间,并增加医疗保健成本,这是由广泛的诊断检查和/或随之而来的并发症驱动的。在这篇综述文章中,我们旨在说明获得性脑损伤中各种高肾上腺素能状态之间的共同性。具体来说,本综述将重点关注神经危重症监护病房中两种常见疾病的自主神经功能障碍,即创伤性脑损伤(TBI)和蛛网膜下腔出血(SAH)。

最新发现

儿茶酚胺水平升高在蛛网膜下腔出血中得到了很好的记录,在阵发性交感神经兴奋中则记录较少,这表明这两种疾病状态下的交感神经张力都增加了。由此产生的高肾上腺素能状态可能表现为生命体征改变或心力衰竭等终末器官功能障碍。神经影像学和有限的临床数据已经阐明了一些关于潜在机制的信息,但迄今为止,理解上的差距限制了前瞻性临床试验。已经采用了多种减少肾上腺素能张力的治疗选择,但成功率各不相同。

总结

自主神经功能障碍的病理生理学尚未完全了解,治疗选择也很少。然而,在不同的神经疾病中识别出高肾上腺素能的共性可能有助于对病变定位和治疗进行新的研究。肾上腺素能阻断可能会减少或消除 TBI 和 SAH 中的终末器官功能障碍。

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