Critical illness myopathy and polyneuropathy.
Neuromuscular weakness commonly develops in the setting of critical illness. This weakness delays recovery and often causes prolonged ventilator dependence. An axonal sensory-motor polyneuropathy, critical illness polyneuropathy (CIP), is seen in up to one third of critically ill patients with the systemic inflammatory response syndrome (usually due to sepsis). An acute myopathy, critical illness myopathy (CIM), frequently develops in a similar setting, often in association with the use of corticosteroids and/or nondepolarizing neuromuscular blocking agents. These patients are often difficult to evaluate due to the limitations imposed by the critical care setting and may be further complicated by the presence of both CIP and CIM in varying degrees. This paper reviews the clinical and electrophysiologic features of these disorders, as well as the putative pathophysiology. In the case of CIM, an animal model has provided evidence that weakness in this disorder is caused by muscle membrane inexcitability due to altered membrane sodium currents and loss of myosin thick filaments.
D000200:Action Potentials / Q000502:physiology; D016638:Critical Illness; D004576:Electromyography / Q000379:methods; D006801:Humans; D018482:Muscle, Skeletal / Q000473:pathology; D009135:Muscular Diseases / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D009218:Myosins / Q000378:metabolism; D011115:Polyneuropathies / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D012121:Respiration, Artificial; D012307:Risk Factors; D015222:Sodium Channels / Q000502:physiology; D013256:Steroids / Q000009:adverse effects / Q000627:therapeutic use
D015222:Sodium Channels; D013256:Steroids; D009218:Myosins