Nontraumatic rhabdomyolysis with long-term alcohol intoxication.

Rhabdomyolysis, the disintegration of skeletal muscle, is a common cause of acute renal failure. This clinical entity occurs mainly from 2 sources: traumatic and nontraumatic. Traumatic rhabdomyolysis has been described as crush syndrome during war and natural disasters. In modern or peace time, the majority of cases of rhabdomyolysis are nontraumatic, and alcohol abuse is one of the most common causes. In many cases of alcohol-related nontraumatic rhabdomyolysis reported in the literature, patients have a typical history of short-term alcohol intoxication and alcohol-induced coma or immobilization. These patients are commonly diagnosed and treated in emergency settings because of a rapid onset of severe muscle pain and deceased urine output. In contrast, nontraumatic rhabdomyolysis with long-term alcohol abuse is rarely reported in the literature and is often overlooked because of insidious and indolent onset; the lack of coma, convulsion, and immobilization in the history; and the lack of severe muscle pain in the clinical presentation. It is especially important for family physicians to diagnose nontraumatic rhabdomyolysis appropriately, because it may be encountered in an outpatient setting with chief complaints of generalized malaise and weakness. The objectives of this case report are: (1) to clearly describe the clinical features, available diagnostic tools, and optimal treatment for nontraumatic rhabdomyolysis with long-term alcohol intoxication; (2) to increase the awareness among physicians, especially family physicians, of nontraumatic rhabdomyolysis with chronic alcoholism; and (3) eventually, to promote early recognition and treatment of this syndrome to prevent renal failure. Case Reports A 48-year-old African American man presented to our office 1 day after a witnessed syncopal episode at work, with complaint of generalized malaise, weakness, and decreased appetite. The patient, a long-term alcohol consumer, reported that he had not eaten anything in the morning and felt dizzy around noontime before passing out. There was no seizure activity or trauma reported and no history of any alteration of sensorium, no fever, no intake of acetaminophen or anti-inflammatory drugs, and no use of illicit drugs or herbal medications. Physical examination revealed a cachectic male with jaundice, tachycardic with heart rate of 120 beats/ min, and hepatomegaly to 3 cm below the right costal margin. Urinalysis at admission showed positive dipstick for blood with negative microscopic examination for red blood cells (RBCs). Serum total creatine kinase (CK) was significantly elevated with normal level of CK in cardiac muscle (CKMB) and troponin I. Other laboratory results are shown in Table 1. Once the diagnosis of rhabdomyolysis was confirmed, the patient was immediately treated with aggressive intravenous infusion of normal saline and monitored for urine output and serum total CK. The patient recovered uneventfully and was discharged with descending CK level and normal creatinine clearance.