ICU neuromuscular disorders

Neuromuscular disorders in the cri tical ly i l l have long been recognised, particularly in those being mechanically venti lated. First suspicions are often raised when patients fail to wean from mechanical venti lation or limb weakness is noted on stopping sedation. Disuse atrophy, catabol ic states and drug therapy (e.g. high dose steroids, muscle relaxants) are probably responsible for some cases but do not explain al l. A neuromyopathic component of mul ti-organ dysfunction syndrome may be impl icated.

Critical illness neuropathy

Neurophysiological studies have demonstrated an acute idiopathic axonal degeneration in patients wi th a flaccid weakness fol lowing a prolonged period of intensive care. Nerve conduction velocities are normal indicating no demyel ination. CSF is normal unl ike Gui l lainBarr syndrome. The neuropathy is self-l imi ting but prolongs the recovery phase of cri tical i l lness. Recovery may take weeks to years. Pyridoxine (100 150 mg daily PO) has been used in the treatment.

Critical illness myopathy

Drug induced myopathy is not uncommon in critical ly i l l patients. Steroid induced myopathy is less common as the indications for high dose steroids have been reduced. Muscle relaxants may have a prolonged effect and may be potentiated by 2 agonists. Muscle histological studies have demonstrated abnormal i ties (fibre atrophy, mitochondrial defects, myopathy and necrosis) which could not be associated wi th steroid or muscle relaxant therapy. Myopathy may cause renal damage via myoglobinuria. Critical i l lness myopathy is associated wi th various forms of muscle degeneration but is usually self-l imiting. Recovery may take weeks to years