Myopathy in critically ill patients.

Abstract

To review myopathic changes occurring during intensive care treatment in the light of recent information about manifestation, clinical settings, pathophysiology, and histomorphologic changes. The computerized MEDLINE database, bibliography of pertinent articles, and the author's personal files. Studies were selected according to their relevance to myopathic complications in critically ill patients. All applicable data were extracted. Myopathic changes occur frequently in patients treated in the intensive care unit (ICU). Three main types have been identified: critical illness myopathy, myopathy with selective loss of myosin filaments, and acute necrotizing myopathy of intensive care. These histologic types probably represent variable expressions of a toxic effect not yet identified. Candidates for such myotoxic effects are the mediators of the systemic response in sepsis and high-dose administration of corticosteroids and muscle relaxants. The influence of these latter agents appears to be particularly important in the pathogenesis of myosin loss and myonecrosis. Experimental studies suggest that axonal damage attributable to critical illness neuropathy can be an additional factor triggering myopathies in the ICU. Muscle membrane inexcitability was recently identified as an alternative mechanism of severe weakness in ICU patients. Myopathic changes are surprisingly frequent in critically ill patients. The clinical importance of this finding is still unknown, but it is likely that weakness caused by myopathy prolongs ICU stay and rehabilitation. Because corticosteroids and muscle relaxants appear to trigger some types of ICU myopathy, they should be avoided or administered at the lowest doses possible. Sepsis, denervation, and muscle membrane inexcitability may be additional factors. Studies addressing the pathophysiology of myopathy in critically ill patients are urgently needed.