Myoglobinuric renal failure is another serious and potentially fatal complication of compartmental syndromes. Myoglobin is released from damaged muscle cells in amounts related to the severity of the muscle damage. If the damaged muscle is perfused, myoglobin enters the circulating blood and is filtered by the kidney. Muscle ischemia of 4 hours gives rise to significant myoglobinuria, which reaches a maximum approximately 3 hours after the circulation is restored, but which persists for as long as 12 hours. Significant myoglobinuria produces myoglobinuric renal failure, which may be due to a direct toxic effect of myoglobin, to renal vasoconstriction, to precipitation of myoglobin in the renal tubules, or to a combination of these factors.
Most hospitals have sensitive and specific assays for urinary myoglobin.
If these are not available, dark urine may usually be attributed to myoglobinuria if the benzidine or hemastix tests are positive in the absence of pink serum and microscopic hematuria. If myoglobinuria is suspected, one should endeavor to maintain a high urinary output to dilute the effect of myoglobin on the kidney. Because myoglobin is less soluble in acid urine, precipitation may be minimized by the maintenance of an alkaline urine through the administration of lactate or bicarbonate. If renal failure ensues, prompt institution of dialysis may be required. Whereas myoglobinuric renal failure may complicate any compartmental syndrome, it appears to be most common after compartmental syndromes produced by prolonged limb compression in a drug-overdosed patient.