Rhabdomyolysis and Acute Renal Failure Following Carbon Monoxide Poisoning: Two Case Reports with Muscle Histopathology and Enzyme Activities

Abstract

Two patients with carbon monoxide poisoning are presented, both of whom suffered rhabdomyolysis complicated by acute renal failure. One patient, an attempted suicide, developed a compartment syndrome of the right thigh that required fasciotomy and recovered after a period of hemofiltration and hemodialysis. Muscle biopsy appearances were consistent with partial muscle infarction. The other patient, rescued from a smoke filled room, exhibited raised creatine kinase but no evidence of muscle swelling. He developed anuric renal failure and adult respiratory distress syndrome and died despite maximum intensive care. Muscle biopsy showed early evidence of muscle necrosis. In both cases there was a marked reduction of enzyme activities in the muscle biopsy consistent with metabolic derangement. Although there was a clinical compartment syndrome in the first case, there was no muscle swelling at the time of biopsy or subsequently in the second case. A direct toxic effect of carbon monoxide may thus have been an important mechanism contributing to the muscle necrosis in the second case, although local ischemia may have been an exacerbating factor in the first case.

Carbon monoxide poisoning

“…CO poisoning also may result in rhabdomyolysis and acute renal failure, potentially as a direct toxic effect of CO on skeletal muscle [63][64][65]. Cutaneous blisters [110] and noncardiogenic pulmonary edema [111][112][113] have been reported in patients with severe CO poisoning.…”

“…Cellular energy metabolism is inhibited even after normalization of CO-Hgb levels [54,60], which may explain prolonged clinical effects after CO-Hgb levels decrease [13]. Binding to myoglobin may reduce oxygen availability in the heart and lead to arrhythmias and cardiac dysfunction [13,61,62] and may contribute to direct skeletal muscle toxicity and rhabdomyolysis [63][64][65][66]. CO also stimulates guanylyl cyclase, which increases cyclic guanosine monophosphate resulting in cerebral vasodilation, which has been associated with loss of consciousness in an animal model of CO poisoning [67,68].…”

Is the Return to High-Level Athletics Possible after Fasciotomy for a Compartment Syndrome of the Thigh?

“…12 There are fewer studies that report compartment syndromes of the thigh caused by exercise 3,7,15,18,19,28,29,31,32,35,45 or related to sports injuries 6,35,44 than those that describe thigh compartment syndromes that are fracture-related, 9,21,25,34,37 iatrogenic, 4,10,27,30,39,41,42 or related to vascular impairment 13,33,38 or intoxications. 8,37…”

Carbon Monoxide Poisoning

“…CO poisoning may also result in rhabdomyolysis and acute renal failure, potentially as a direct toxic effect of CO on skeletal muscle [57][58][59]. Cutaneous blisters [106] and noncardiogenic pulmonary edema [107][108][109] reported in patients with severe CO poisoning.…”

“…Cellular energy metabolism is inhibited even after normalization of CO-Hgb levels [47,54], which may explain the prolonged clinical effects after CO-Hgb levels decrease [9]. Binding to myoglobin may reduce oxygen availability in the heart and lead to arrhythmias and cardiac dysfunction [9,55,56]; it may also contribute to direct skeletal muscle toxicity and rhabdomyolysis [57][58][59][60]. CO also stimulates guanylyl cyclase, which increases cyclic guanylyl monophosphate, resulting in cerebral vasodilatation, which has been associated with loss of consciousness in an animal model of CO poisoning [61,62].…”