Authors' Reply

Abstract

We read with eager anticipation Haas et al.'s report, 1 but we consider their diagnosis of nontraumatic rhabdomyolysis to be in direct conflict with the details of their case report. The authors appropriately point out that alcohol and other drugs likely pose a direct toxic effect at the level of the myocyte, but most reported cases of toxin-associated rhabdomyolysis are complicated by extremes of core body temperature, seizures, or other muscular injury from direct trauma or prolonged immobilization. 2-4 The case reported by Haas et al. clearly describes traumatic skeletal injury because "the patient became extremely agitated, needing complete body (4-point) restraint." A careful examination of the authors' references, including the thorough review from 1989, demonstrates that "[r]habdomyolysis should be considered in any patient who has been…fighting restraints, agitated, or undertaken other strenuous exertion." 4 Alcohol-and drug-associated rhabdomyolysis occurring from skeletal injury sustained while struggling against restraints is a common phenomenon recognized in the emergency medicine literature. 5 Furthermore, it cannot be concluded that the patient's clinical deterioration was solely the result of an anticholinergic overdose. The patient's progressive excitation (as his alcohol level declined) and long history of alcohol abuse raises the possibility that alcohol withdrawal further complicated his increased agitation. All cases of toxin-induced agitation, whether from acute intoxication or withdrawal, benefit from liberal administration of intravenous sedative therapy to restore inhibitory tone to the central nervous system. Physical restraint of any sort, as demonstrated in this case, may lead to traumatic skeletal injury, nephrotoxicity, and even death.