CRITICAL CARE OUTCOMES: Edited by Margaret S. HerridgeICU-acquired weakness mechanisms of disabilityDos Santos, Claudia C.; Batt, JaneAuthor Information 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 Correspondence to Dr. Dos Santos, Critical Care Medicine and Clinician Scientist, Assistant Professor of Medicine, St Michael's Hospital/University of Toronto, 30 Bond Street, Toronto, ON M5B 1WB, Canada. Tel: +1 416 946 0420; e-mail: [email protected] Current Opinion in Critical Care: October 2012 - Volume 18 - Issue 5 - p 509-517 doi: 10.1097/MCC.0b013e328357cb5e Buy Metrics Abstract 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. © 2012 Lippincott Williams & Wilkins, Inc.