["Critical-illness" polyneuropathy and -myopathy]. / 'Critical-illness'-polyneuropathie en -myopathie.

Critical-illness polyneuropathy and myopathy (CIPNM) can be considered a part of the syndrome of multiple organ dysfunction. CIPNM is the commonest cause of muscle weakness acquired in the intensive care unit. Its incidence is 35-80% during prolonged mechanical ventilation. For a (differential) diagnosis, electrophysiological investigations are usually necessary, and sometimes a muscle biopsy. CIPNM may be induced by triggering of the immune response leading to increased vascular permeability with tissue invasion of inflammatory cells and local damage. There is a relation between myopathy and medication, notably corticosteroids. Clinical improvement usually follows when the CIPNM patient survives the underlying disease, but weaning from artificial ventilation is often difficult, and rehabilitation prolonged.

Critical illness polyneuropathy and myopathy (CIPNM): evidence for local immune activation by cytokine-expression in the muscle tissue.

In a longitudinal prospective study a muscle biopsy was taken from 30/32 (33%) of the 98 patients who developed critical illness polyneuropathy and myopathy (CIPNM). Neuropathic changes were found in 37%, myopathic in 40%, and a combination in 23% of the biopsies. The immunohistopathology showed macrophages and Th-cells in 40% and 60% of the muscle biopsies respectively. Small mainly perivascular infiltrates contained macrophages and Th-cells. ICAM-1, VCAM and MAC were found on the vascular endothelium in 58%, 53% and 79% respectively. In all biopsies there was an upregulation of both HLA-I and HLA-DR. Proinflammatory cytokines and TNFalphaR75 were also produced locally (IL-1beta in 71%, IFN-gamma in 40%, IL-12 in 73%, TNFalphaR75 in 90%). The anti-inflammatory cytokine IL-10 was simultaneously expressed in 96% of the biopsies. HLA-DR, TNFalphaR75 and IL-10 differed significantly when compared with control muscle biopsies. Our data provide evidence that small numbers of activated leukocytes producing both pro- and anti-inflammatory cytokines infiltrate skeletal muscle of CIPNM patients. We propose that the local balance of leukocyte activities is of importance in the pathophysiology of muscle weakness in CIPNM.