ABSTRACT
The progress of intensive care medicine has dramatically improved the survival of critically ill patients, especially in patients with acute respiratory distress syndrome (ARDS) (1,2). This improved survival rate is, however, associated with general deconditioning, muscle weakness, dyspnea, depression and anxiety, and reduced health-related quality of life after intensive care unit (ICU) discharge (3-5). Deconditioning and, specifically, muscle weakness are suggested to have a key role in impaired functional status after ICU stay (3). Indeed, optimal physiological functioning depends on the upright position (6-9), so bed rest and limited mobility during critical illness result in profound physical deconditioning and dysfunction of the respiratory, cardiovascular, musculoskeletal, neurological, renal, and endocrine systems. These effects can be exacerbated by inflammation and pharmacological agents, such as corticosteroids, muscle relaxants, neuromuscular blockers and antibiotics. Denervation atrophy may also complicate critical illness and sepsis has been shown to be one of the most important determinants of critical illness polyneuropathy (10). Ginz et al. reported 20-40% reductions in involuntary muscle force of the ankle dorsiflexors upon peroneal nerve stimulation in critically ill patients who were immobilized for a week (11). These data are in line with findings in which stimulation of the ulnar nerve was used (–40% in patients, compared to controls) (12). Consecutive muscle biopsies of the tibialis anterior in critically ill patients showed 3-4% reduction per day in fiber crosssectional area in both type I and type II fibers (13). The prevalence of skeletal muscle weakness in the ICU is poorly investigated. In a prospective study, De Jonghe et al. investigated 95 of 206 patients ventilated for more than seven days. Twenty-five percent of the patients developed clinically significant muscle weakness (14). In another study, prospectively investigating patients with multiple organ failure, half of the patients developed some focal or diffuse weakness and 26% developed severe muscle weakness (15). In addition, a patient with underlying chronic disease may already have muscle weakness before being admitted to the ICU. In animal experiments, it was shown that as few as 24 hours of mechanical ventilation does induce changes in muscle regulatory factors (MyoD, myogenin), in the diaphragm, and gastrocnemius muscle (16). It is clear that these changes were induced long before the “critical illness myopathy.” Hence, it is important to realize that even in patients not formally diagnosed with critical illness myopathy, muscle dysfunction may be present.
