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For further information, see CMDT Part 22-07: Rhabdomyolysis
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Essentials of Diagnosis
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Associated with crush injuries to muscle, immobility, drug toxicities, and hypothermia
Characterized by serum elevations in muscle enzymes, including creatinine kinase (CK), and marked electrolyte abnormalities
Release of myoglobin leads to direct renal toxicity
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General Considerations
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Defined as a syndrome of acute skeletal muscle necrosis, leading to myoglobinuria and markedly elevated creatine kinase levels
Can result from crush injuries, prolonged immobility, seizures, substance abuse (eg, cocaine), and medications
The presence of compromised kidney and liver function, diabetes mellitus, and hypothyroidism increase the risk of rhabdomyolysis in patients taking statins
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Serum CK > 20,000–50,000 international units/L
Elevated serum levels of AST, ALT, and lactate dehydrogenase (due to release of these enzymes from skeletal muscle)
The massive acute elevations of muscle enzymes peak quickly and usually resolve within days once the inciting injury has been removed
Urine may appear dark
Urinary dipstick test
Injured muscle cells release intracellular components, leading to electrolyte derangements, including
Hyperkalemia
Hyperphosphatemia
Hyperuricemia
Hypocalcemia
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The mainstay of treatment is
Adjunctive treatments with mannitol and alkalinization of the urine have not been proven to change outcomes in human trials
Early exogenous calcium administration for hypocalcemia is not recommended unless the patient is symptomatic or the level becomes exceedingly low in an unconscious patient
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Acute tubular necrosis due to the toxic effects of filtering excessive quantities of myoglobin, which can be exacerbated by volume depletion
Distal tubular obstruction from pigmented casts and intrarenal vasoconstriction
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