ICU-acquired weakness:  mechanisms of disability.
OBJECTIVE
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.


RESULTS
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.


CONCLUSIONS
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.
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. claudia.santos@utoronto.ca
Claudia C
CC
Dos Santos
Jane
J
Batt
D016638:Critical Illness; D006233:Persons with Disabilities; D006801:Humans; D007362:Intensive Care Units; D018908:Muscle Weakness / Q000209:etiology* / Q000517:prevention & control; D018482:Muscle, Skeletal; D009133:Muscular Atrophy; D018384:Oxidative Stress; D015995:Prevalence; D059748:Proteolysis; D012121:Respiration, Artificial; D012307:Risk Factors