ICU-acquired weakness: mechanisms of disability

被引:17
作者
Dos Santos, Claudia C. [1 ]
Batt, Jane
机构
[1] Univ Toronto, St Michaels Hosp, Keenan & Li Ka Shing Knowledge Inst, Toronto, ON M5B 1WB, Canada
关键词
critical illness myopathy; critical illness polyneuropathy; ICU-acquired weakness; mechanical ventilation; multiorgan failure; CRITICAL ILLNESS POLYNEUROPATHY; TUMOR-NECROSIS-FACTOR; HUMAN SKELETAL-MUSCLE; NF-KAPPA-B; PROTEASOME PROTEOLYTIC PATHWAY; MYOFIBRILLAR PROTEIN OXIDATION; FOXO TRANSCRIPTION FACTORS; NERVE EXCITABILITY CHANGES; HUMAN QUADRICEPS MUSCLE; GLYCATION END-PRODUCTS;
D O I
10.1097/MCC.0b013e328357cb5e
中图分类号
R4 [临床医学];
学科分类号
100218 [急诊医学];
摘要
Purpose of review 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. Recent findings 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. Summary 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.
引用
收藏
页码:509 / 517
页数:9
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