Critical illness-polyneuropathie und -myopathie

Abstract

Muscle weakness and atrophy in critically ill patients is caused by specific neuromuscular disorders arising de novo during the stay in the ICU. Among these, critical illness polyneuropathy and the several forms of ICU-associated myopathies are most prevalent. Clinical manifestations include flaccid pareses, delayed weaning from the respirator and prolonging of the rehabilitation phase. Diagnosis is made by means of electrophysiology; with regard to myopathies muscle biopsy is often needed. The pathogenesis of neuromuscular complications in the ICU is unknown. However, most authors suggest that the sepsis-associated activation of immune mechanisms (systemic inflammatory response syndrome, SIRS) plays an important role. We recently described the presence of a neurotoxic activity in the sera of patients with critical illness polyneuropathy, which could be completely reversed by NMDA antagonists. Recently, the dramatic reduction in the incidence of critical illness polyneuropathy in patients treated with intensive insuline therapy pointed to a pathogenic role of hyperglycemia. By contrast, occurrence of myopathies may be triggered by exogenous factors such as high-dose glucosteroids and non-depolarizing muscle blocking agents. The critical illness per se is unrelated to the development of neuromuscular complications. Detailed electrodiagnostic studies are desirable in patients with long-lasting ICU stays, whenever possible as weekly monitoring, to detect and follow neuromuscular complications. Steroids and muscle relaxants should be given cautiously because of their potential to trigger myopathies in ICU patients.