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Rhabdomyolysis

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Overview

Rhabdomyolysis describes any disease process that leads to skeletal muscle damage and breakdown, leading to the release of intracellular components such as potassium ions, myoglobin, and creatine kinase (CK).

Release of these components into the bloodstream can lead to electrolyte disturbances, acute kidney injury (AKI), metabolic acidosis, and disseminated intravascular coagulation (DIC). Myoglobin is directly nephrotoxic to the kidneys and can precipitate within them, leading to AKI.

Causes

Any condition that can cause damage to muscle tissue can cause rhabdomyolysis:

  • Any overexertion of muscle
  • Trauma and compartment syndrome
  • Epilepsy, particularly status epilepticus
  • Chronic alcohol excess
  • Drugs, such as statins (especially if co-prescribed with macrolides)
  • Myositis
  • Collapses and falls, particularly in the elderly and those who have had a long lie

Presentation

The features of rhabdomyolysis are non-specific:

  • ‘Tea-coloured’, dark urine – due to myoglobinuria
  • Myalgia and muscle weakness
  • Fever, malaise, nausea, and vomiting
  • Features of complications:

There may be a history of a cause, such as overexertion, seizures, or a fall with a long lie, particularly in the elderly.

Investigations

  • Urine dipstick:
    • May be positive for blood
  • Urine microscopy:
  • Urea and electrolytes (U&Es):
    • Increased potassium – due to release from skeletal muscle tissue
    • Hypocalcaemia – due to myoglobin binding to calcium
    • Disproportionately elevated creatinine – suggesting intrinsic renal damage
  • Serum or urinary myoglobin levels:
    • Increased
  • Serum creatine kinase (CK) – the most specific test to diagnose rhabdomyolysis:
    • Must be increased to >5 times normal or >1,000 IU/L

Management

  • 1st-line: fluid rehydration – dilutes nephrotoxins and reduces myoglobin-induced renal damage
  • Treat hyperkalaemia
  • Urinary alkalinisation is sometimes considered
  • Renal replacement therapy may be necessary

Complications

  • Acute kidney injury (AKI):
    • Myoglobin is nephrotoxic and also precipitates in the kidneys which may lead to damage.
  • Electrolyte disturbances:
    • Hyperkalaemia – due to potassium release from skeletal muscle, which can lead to ventricular arrhythmias
    • Hypocalcaemia – due to myoglobin binding to calcium, which can lead to arrhythmia and tetany
    • Metabolic acidosis – due to the release of lactic acid and other organic acids from damaged muscle tissue
  • Disseminated intravascular coagulation – due to the release of substances activating clotting from damaged muscle tissue

Prognosis

  • Early diagnosis and treatment is associated with a very good prognosis

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