Harvey's Garden

Rhabdomyolysis and crush syndrome

1 min read

Epidemiology

Etiology

  • Traumatic
    • Crush injury
    • Direct injury
  • Nontraumatic
    • Seizures
    • Overexertion (e.g., strenuous exercise)
    • Intoxication (e.g., cocaine, heroin, amphetamines, MDMA, alcohol, carbon monoxide, phencyclidine)
    • Skeletal muscle ischemia
    • Infection
    • Adverse drug reactions (e.g., neuroleptics, statins)

Pathophysiology

  • Rhabdomyolysis → release of the following substances:
    • Creatine phosphokinase (CPK) and serum myoglobin → pigment nephropathy → acute tubular necrosis → acute kidney injury (intrinsic)
    • Potassium → cardiac arrhythmia
    • Lactic acid → metabolic acidosis
  • Hypovolemia → ↓ renal perfusion → acute kidney injury (prerenal)
    • Hypovolemia is predominantly due to third spacing of extracellular fluid into damaged muscle tissue.
  • Reperfusion syndrome → compartment syndrome

Clinical features

Diagnostics

  • Labs:
    • ↑ Creatine Kinase (CK): Best initial test (often >1,000 U/L, can exceed 100,000).
    • ↑ Potassium (Hyperkalemia): Most immediate life-threatening abnormality.
    • ↑ Phosphate (Hyperphosphatemia).
    • ↓ Calcium (Hypocalcemia): Precipitants of calcium phosphate in damaged muscle (early phase).
    • ↑ LDH, ↑ AST/ALT.
  • Urinalysis:
    • Dipstick: Positive (+) for Blood (detects heme moiety).
    • Microscopy: No RBCs seen.
    • USMLE Pearl: Dipstick (+) for blood + Microscopy (-) for RBCs = Myoglobinuria.
  • ECG: Check for signs of hyperkalemia (peaked T waves, wide QRS).

Treatment

Graph View

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