ICU-acquired weakness: mechanisms of disability

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.