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Cocaine-induced rhabdomyolysis masquerading as myocardial ischemia.
American Journal of Medicine 1989 May
PURPOSE: Cocaine abuse has recently emerged as a major problem among young adults, and is increasingly associated with a variety of medical complications. In view of recent reports demonstrating that illicit cocaine use may cause rhabdomyolysis, we reviewed the collective experience of a university-affiliated medical center to identify patients with cocaine-induced rhabdomyolysis.
PATIENTS AND METHODS: Among hospital admissions due to acute cocaine abuse during the period June 1987 through June 1988, we identified seven patients who exhibited biochemical evidence of skeletal muscle injury. Six of these patients presented within one hour of free-basing cocaine with complaints of thoracic skeletal muscle pain. Hospital admission was prompted by the suspicion of myocardial ischemia or infarction. The remaining patient was incidentally found to have an elevated serum level of creatine phosphokinase (CPK) after abusing cocaine and was hospitalized to exclude a cardiac origin.
RESULTS: Serum CPK levels in the seven patients rose to a mean peak value of 16.1 +/- 3.6 mu kat/L, and returned toward normal within 72 hours. A cardiac origin for the elevated CPK values was excluded by negative results of determinations of CPK-MB fractions.
CONCLUSION: Rhabdomyolysis must be added to the every-growing list of medical complications associated with the illicit use of cocaine. Skeletal muscle injury may be a more common complication of cocaine abuse than has previously been appreciated, escaping medical attention when the clinical manifestations are relatively mild. The importance of recognizing this clinical entity lies in the potential confusion with myocardial ischemia. This point is illustrated by the fact that each of our patients was hospitalized to exclude the possibility of cocaine-induced myocardial infarction. Cardiac ischemia could not be differentiated from skeletal muscle injury solely on the basis of clinical assessment.
PATIENTS AND METHODS: Among hospital admissions due to acute cocaine abuse during the period June 1987 through June 1988, we identified seven patients who exhibited biochemical evidence of skeletal muscle injury. Six of these patients presented within one hour of free-basing cocaine with complaints of thoracic skeletal muscle pain. Hospital admission was prompted by the suspicion of myocardial ischemia or infarction. The remaining patient was incidentally found to have an elevated serum level of creatine phosphokinase (CPK) after abusing cocaine and was hospitalized to exclude a cardiac origin.
RESULTS: Serum CPK levels in the seven patients rose to a mean peak value of 16.1 +/- 3.6 mu kat/L, and returned toward normal within 72 hours. A cardiac origin for the elevated CPK values was excluded by negative results of determinations of CPK-MB fractions.
CONCLUSION: Rhabdomyolysis must be added to the every-growing list of medical complications associated with the illicit use of cocaine. Skeletal muscle injury may be a more common complication of cocaine abuse than has previously been appreciated, escaping medical attention when the clinical manifestations are relatively mild. The importance of recognizing this clinical entity lies in the potential confusion with myocardial ischemia. This point is illustrated by the fact that each of our patients was hospitalized to exclude the possibility of cocaine-induced myocardial infarction. Cardiac ischemia could not be differentiated from skeletal muscle injury solely on the basis of clinical assessment.
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