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ESSENTIALS OF DIAGNOSIS

ESSENTIALS OF DIAGNOSIS

  • Associated with crush injuries to muscle, immobility, drug toxicities, and hypothermia.

  • Characterized by serum elevations in muscle enzymes, including creatine kinase, and marked electrolyte abnormalities.

  • Release of myoglobin leads to direct renal toxicity.

GENERAL CONSIDERATIONS

Rhabdomyolysis is a syndrome of acute skeletal muscle necrosis resulting in markedly elevated plasma creatine kinase levels and myoglobinuria. Excessive urinary myoglobin can cause intrarenal vasoconstriction and pigmented tubular cast formation leading to intrarenal obstruction and ATN. Rhabdomyolysis can result from crush injuries, prolonged immobility, seizures, substance abuse (eg, cocaine), and medications (especially statins); concomitant volume depletion in these settings increases risk of rhabdomyolysis and associated ATN. The presence of kidney or liver disease, diabetes mellitus, and hypothyroidism increase the risk of rhabdomyolysis in patients taking statins. The cytochrome P450 liver enzymes metabolize all statins except for pravastatin and rosuvastatin. In patients taking statins, the risk of rhabdomyolysis is increased in the presence of kidney or liver disease, diabetes, hypothyroidism, concurrent use of niacin and fibrate-containing therapy; risk is also increased with concurrent statins (except pravastatin and rosuvastatin) with drugs that inhibit cytochrome P450 (including protease inhibitors, erythromycin or clarithromycin, itraconazole, diltiazem, and verapamil).

CLINICAL FINDINGS

A. Symptoms and Signs

Patients with rhabdomyolysis may have myalgia, weakness or both, though it is not uncommon for them to be asymptomatic. Urine may appear dark due to the presence of myoglobin.

B. Laboratory Findings

Rhabdomyolysis of clinical importance commonly occurs when serum creatine kinase exceeds 16,000–50,000 IU/L. Often, there are elevated serum levels of other skeletal muscle enzymes including AST, ALT, and LD. The acute muscle enzymes elevations peak quickly and usually resolve within days once the inciting injury has resolved.

The classic laboratory finding in rhabdomyolysis is a urine dipstick test that is positive for “blood” but without RBCs on microscopy; the false-positive result is due to detection of myoglobin rather than hemoglobin. Additionally, rhabdomyolysis causes injured muscle cells to release intracellular components, leading to electrolyte derangements (including hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia).

TREATMENT

The mainstay of treatment is aggressive volume repletion with 0.9% normal saline (ie, more than 4 L/day) and removal of any offending medications thought to have caused the disorder. Adjunctive treatments with mannitol and alkalization of the urine have not been proven to change outcomes. As patients recover, calcium can translocate from tissues to plasma, so early exogenous calcium administration for hypocalcemia is not recommended unless the patient is symptomatic or the level becomes exceedingly low in an unconscious patient; calcium repletion can cause precipitation of calcium phosphate given the frequently concurrent hyperphosphatemia.

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

WHEN TO REFER

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