pancuronium and Necrosis

A series of recent reports have identified cases of a quadriplegic myopathy characterized by myofiber necrosis and loss of myosin filaments associated with the use of nondepolarizing muscle blocking agents and glucocorticoids. We report electrophysiological findings in 7 intensive care unit patients who developed evidence of an acute myopathy in association with the use of nondepolarizing muscle blocking agents. Several important features were identified: (i) a neuromuscular transmission deficit was observed in 3 patients up to 7 days following withdrawal of vecuronium; (ii) motor M potentials were of low amplitude, there was mild abnormal spontaneous activity on needle electromyography, and sensory conduction was relatively preserved; (iii) not all patients received glucocorticoids or were asthmatic; (iv) 2 patients given vecuronium had very high creatine kinase levels and developed acute renal failure associated with myoglobinuria; and (v) rises in motor M potentials accompanied clinical recovery. This complication of intensive care may be severe, but is reversible and possibly avoidable. Our findings implicate nondepolarizing muscle blocking agents in the development of the myopathy. Electrophysiological studies provide important prognostic guidance.

Topics: Action Potentials; Adult; Aged; Creatine Kinase; Critical Care; Critical Illness; Female; Humans; Hydrocortisone; Male; Median Nerve; Methylprednisolone; Middle Aged; Muscular Diseases; Necrosis; Neural Conduction; Neuromuscular Junction; Pancuronium; Synaptic Transmission; Ulnar Nerve; Vecuronium Bromide

A fatal case of fulminant hepatic failure that occurred in the neonatal period is reported in a premature infant born after 27 4/7-weeks' gestation. Immediately after birth the infant had severe hypoxia and hypotension resulting from birth asphyxia, hypovolemic shock, and septicemia. At autopsy, histological appearance of the liver showed virtually total hepatocellular necrosis without features of fibrosis. Although the exact cause of hepatocellular injury cannot be fully ascertained, it is assumed that hypoxia and hypotension must have been the predominant factors leading to massive hepatic necrosis.

Topics: Acyclovir; Alanine Transaminase; Aspartate Aminotransferases; Bicarbonates; Cloxacillin; Dopamine; Female; Fetal Hypoxia; Fetal Membranes, Premature Rupture; Humans; Infant, Newborn; Infant, Premature, Diseases; Liver; Male; Necrosis; Netilmicin; Pancuronium; Partial Thromboplastin Time; Penicillins; Pregnancy; Prothrombin Time; Sepsis; Shock; Sodium; Sodium Bicarbonate