[Acute rhabdomyolysis: a case report and literature review]. / Akutna rabdomioliza, prikaz bolesnika i pregled literature.

ABSTRACT

Acute rhabdomyolysis is a syndrome characterized by the lesion of skeletal muscle resulting in subsequent release of intracellular contents into the circulatory system, which can cause potentially lethal complications. These contents include myoglobin, creatine phosphokinase, potassium, aldolase, lactate dehydrogenase and glutamic-oxaloacetic transaminase. There are numerous causes that can lead to acute rhabdomyolysis and many of patients present with multiple causes. The most common potentially lethal complication of rhabdomyoloysis is acute renal failure. In this article we present a case of a patient that developed clinical signs of acute rhabdomyolysis after consumption of heroin and alcohol. After approximately nine hours of alcohol and heroin induced coma he had acute compartment syndrome of the right arm, and clinical and laboratory signs of acute rhabdomyolysis with acute renal failure as a complication of rhabdomyolysis. Acute rhabdomyolysis developed in the patient as the result of acute compartment syndrome, with direct toxic activity of alcohol and diamorphine. During the period of coma, due to lying in particular position over a long period of time, pressure upon the certain part of the body caused muscle compression and capillary occlusion in fascial compartments, which led to ischemia. Upon pressure relief and beginning of tissue recovery, post ischemic compartment syndrome occurred with subsequent rhabdomyolysis. Getting out of coma the patient started to complain of severe pain in the right arm, which clinically worsened on passive stretching of the limb, with the loss of sensation and weakness. Laboratory findings showed high levels of creatine phosphokinase as the most sensitive marker of muscular damage. The peak of creatine phosphokinase level can be predictive for the development of acute renal failure because myoglobin level may return to normal within 6 hours after muscle injury. The peak of creatine phosphokinase (186.080 U/L; normal range 0-177) was recorded at 12 hours of admission. Other pertinent laboratory results such as urea, creatinine, prothrombin time, alanine aminotransferase and aspartate aminotransferase were also changed significantly. The peak of potassium level before dialysis was 6.8 mmol/L. Emergency fasciotomy of the anterior and posterior compartment syndrome was performed by a team of physicians after clinical examination. The second look debridement was performed at 48 and 72 hours. The plastic surgical procedure was performed 4 weeks later. On admission the patient also had oliguria with dark brown pigment in his urine. Arterial blood gases revealed metabolic and respiratory acidosis. The patient was hypovolemic and IV rehydratation with crystalloids, sodium bicarbonate and mannitol started immediately upon admission. Despite therapy his urine output decreased. Hemodialysis was initiated at serum potassium level of 6.8 mm/L and continued until his urine output returned to normal in three weeks. The patient was discharged from the hospital after six weeks, with normal urine output, without functional abnormality in his upper right limb. Acute rhabdomyolysis should be considered as a possibility in any patient with prolonged imobilization while in coma as well as in any intoxicated patient. Of course, creatine phosphokinase is the most sensitive indicator of muscle injury and the degree of creatine phosphokinase elevation correlates with the amount of muscle injury and disease severity. Other laboratory findings can help identify common complications of rhabdomyolysis such as acute renal failure, metabolic derangements and disseminated intravascular coagulopathy.