Diagnosis

The diagnosis of rhabdomyolysis made by the measurement of serum creatine phosphokinase and serum and urinary myoglobin is usually systematic. Serum creatine phosphokinase should be at least six times the upper normal value (100 IU/l) for diagnosis. Serum creatine phosphokinase begins to rise 2 to 12 h after the injury and reaches its peak value, ranging from several hundred IU per liter in mild muscle injury to over 200 000 IU/l in the full-blown crush syndrome, 1 to 3 days after injury; the serum level slowly declines at a rate of 50 per cent every 48 h. Therefore serum creatine phosphokinase should be measured daily for at least 3 days to follow the extent of muscle destruction and its regression. If the serum creatine phosphokinase level remains elevated, ongoing muscle injury, necrosis, and/or compartment syndrome should be sought. Creatine phosphokinase isoenzymes should be assayed only in the case of concomitant heart injury, in which case the elevated MB fraction has a cardiac etiology and the MM fraction is indicative of rhabdomyolysis. The measurement of other serum muscle enzymes such as lactate dehydrogenase or aldolases, which are also elevated in acute traumatic rhabdomyolysis, is of no practical use and is not measured routinely. Heavy-chain fragments of serum myosin and cardiac troponin T have recently been shown to reach long-lasting elevations in rhabdomyolysis, but their diagnostic and prognostic usefulness has not yet been evaluated. Therefore their routine measurement cannot be recommended.

The normal concentration of serum myoglobin ranges up to 85 ng/ml, of which half is bound to an a 2 globulin. Myoglobin is an oxygen-binding respiratory protein found in muscle at a concentration of 2.5 g per 100 g of skeletal muscle. It is released from injured muscle, and it increases before creatine phosphokinase and decreases more rapidly owing to its clearance by renal excretion and its metabolism to bilirubin. A close correlation has been demonstrated between the percentage and depth of burned surface and the concentration of serum myoglobin and creatine phosphokinase. There is no correlation between serum and urinary myoglobin. Myoglobinuria appears when serum concentrations exceed 1500 ng/ml, suggesting that at least 100 to 200 g of muscle have been injured. The presence or absence of visible myoglobinuria does not reflect the extent of muscle damage. Furthermore, owing to its metabolites, a normal myoglobin serum level does not exclude the diagnosis of acute traumatic rhabdomyolysis.

Evaluation of the metabolic consequences of muscle destruction includes the measurement of serum and urinary electrolytes, including calcium and phosphorus, and renal function indices. These measurements should be repeated once daily until they are normal to monitor treatment-induced modifications.

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