Keenan and Li Ka Shing Knowledge Institute of Saint Michael's Hospital and Institute of Medical Sciences and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Curr Opin Crit Care. 2012 Oct;18(5):509-17. doi: 10.1097/MCC.0b013e328357cb5e.
ICU-acquired weakness (ICUAW) is now recognized as a major complication of critical illness. There is no doubt that ICUAW is prevalent - some might argue ubiquitous - after critical illness, but its true role, the interaction with preexisting nerve and muscle lesions as well as its contribution to long-term functional disability, remains to be elucidated.
In this article, we review the current state-of-the-art of the basic pathophysiology of nerve and muscle weakness after critical illness and explore the current literature on ICUAW with a special emphasis on the most important mechanisms of weakness.
Variable contributions of structural and functional changes likely contribute to both early and late myopathy and neuropathy, although the specifics of the temporality of both processes, and the influence patient comorbidities, age, and nature of the ICU insult have on them, remain to be determined.
目前，重症加强治疗病房获得性肌无力（ICUAW）已被认为是危重病的主要并发症。毫无疑问，在危重病后 ICUAW 非常普遍，但它的真正作用，与先前存在的神经和肌肉损伤的相互作用，以及它对长期功能障碍的影响，仍有待阐明。
在本文中，我们回顾了危重病后神经和肌肉无力的基础病理生理学的最新进展，并探讨了 ICUAW 的当前文献，特别强调了肌无力的最重要机制。
结构和功能变化的不同贡献可能导致肌病和神经病的早、晚期发生，尽管这两个过程的具体时间以及患者合并症、年龄和 ICU 损伤的性质对它们的影响仍有待确定。
