Critical illness neuromyopathy (CINM) is a common yet frequently overlooked complication in intensive care units (ICU). CINM often results in prolonged ventilator dependence and persistent limb weakness, significantly impacting patient recovery and long-term quality of life. CINM can be categorized into two primary subtypes: critical illness polyneuropathy (CIP) and critical illness myopathy (CIM). These conditions frequently arise in the context of severe sepsis, multiple organ failure, or as adverse effects of certain medications used in the ICU. This review aims to provide a concise overview of CINM, focusing on its pathophysiology, diagnostic approaches, and current clinical management strategies.
The occurrence of muscle weakness in patients with sepsis or multiple organ failure managed in the intensive care unit has been recognized with increasing frequency in the last two decades. The difficulty in examining critically ill patients may explain why this complication has been only recently recognized. This weakness is due to an axonal polyneuropathy which is called critical illness polyneuropathy(CIP). It must be differentiated from myopathy or neuromuscular junction disturbance that can also occur in the intensive care setting. Neither the cause nor the exact mechanism of CIP has been elucidated. Electrophysiological studies demonstrated an acute axonal damage of the peripheral nerves. Before the recognition of CIP, these cases were usually misdiagnosed as Guillain-Barr?syndrome. Clinical recovery from the neuropathy is rapid and nearly complete in those patients who survive. Thus, neuropathy acquired during critical illness, although causing a delayed in weaning from ventilatory support and hosptial discharge, does not worsen long-term prognosis.
Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) occur commonly in the patients who havebeen on mechanical ventilation for more than 1 week. Even in some patients diagnosed with CIP, an underlyingmyopathy may be the primary cause of the muscle weakness. The cormorbid status of CIP and CIM is called as criticalillness polyneuropathy and critical illness myopathy (CIPNM). We describe a 56-year-old man with acute quadriparesisand areflexia after systemic inflammatory response syndrome. The diagnosis of CIPNM is important to avoid unnecessaryinvestigations and unreasonably pessimistic prognosis. Electrophysiologic studies are essential for the diagnosis and forplanning further clinical management.