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April 1972

Drugs, Coma, and Myoglobinuria

Author Affiliations

From the Spiller Neurological Unit (Drs. Penn and Rowland) and the Department of Medicine (Dr. Fraser), Hospital of the University of Pennsylvania, and the Department of Neurology (Drs. Penn and Rowland), Philadelphia General Hospital, Philadelphia.

Arch Neurol. 1972;26(4):336-343. doi:10.1001/archneur.1972.00490100066006

Myoglobinuria was proved in four patients in coma after drug ingestion or injection and was suspected in four others because of the very high serum enzyme concentrations, including creatine phosphokinase, and renal insufficiency. The variety of drugs used suggests that this is not a direct effect of specific drugs but is due to several effects of coma. Pressure upon dependent muscles in immobile individuals is probably primarily responsible, but ischemia, anoxia, hypotension, hypothermia, and acidosis contribute. In five patients there was residual evidence of pressure or traction injury to ulnar, peroneal, and sciatic nerves or to the brachial plexus. The syndrome can be recognized in comatose individuals if dependent limbs are swollen and indurated. In any comatose patient, routine determination of serum enzymes and evaluation of the urine for myoglobin would permit early recognition of this syndrome; forced diuresis might decrease the incidence of renal damage, the most threatening complication of myoglobinuria.

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