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For further information, see CMDT Part 22-07: Rhabdomyolysis

Key Features

Essentials of Diagnosis

  • 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

General Considerations

  • 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

Clinical Findings

  • Myalgias

  • Weakness

  • May be asymptomatic

  • Use of statins is an important cause of rhabdomyolysis

    • The cytochrome P450 liver enzymes metabolize all statins except for pravastatin and rosuvastatin

    • The following medications block the action of cytochrome P450 and can increase the risk of rhabdomyolysis when used with statins (but no increased risk when used with pravastatin or rosuvastatin):

      • Protease inhibitors

      • Erythromycin

      • Itraconazole

      • Clarithromycin

      • Diltiazem

      • Verapamil

    • The likelihood of rhabdomyolysis also increases when statins are used with niacin and fibric acids (gemfibrozil, clofibrate, and fenofibrate).


  • 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

    • Positive for "blood" but without red blood cells on urinary sediment

    • This false-positive result is due to detection of myoglobin

  • Injured muscle cells release intracellular components, leading to electrolyte derangements, including

    • Hyperkalemia

    • Hyperphosphatemia

    • Hyperuricemia

    • Hypocalcemia


  • The mainstay of treatment is

    • Aggressive volume repletion with 0.9% normal saline (i.e. > 4 L/day)

    • Removal of offending agents if medications are thought to have caused the disorder

  • 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



  • 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


  • Myopathic complications of statins usually resolve within several weeks of discontinuing the drug

When to Refer

  • Clinically meaningful rhabdomyolysis requires immediate attention and inpatient management, so affected patients should not be referred to outpatient nephrology consultation unless to follow up after a hospital admission


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