Rhabdomyolysis

On this page
  1. Direct answer
  2. What you must remember
  3. A statin, a macrolide and dark urine
  4. Where the exam tries to catch you
  5. Frequently asked questions
  6. Related topics

Direct answer

Rhabdomyolysis is the breakdown of skeletal muscle that releases creatine kinase, myoglobin, potassium and phosphate into the circulation. Creatine kinase is the most useful marker and often rises above five times the upper limit of normal, while myoglobin injures the kidney through tubular obstruction and direct toxicity. Management is early isotonic fluid to maintain a brisk urine output, with monitoring of potassium, calcium and creatinine and removal of the cause.

What you must remember

  • Key marker: creatine kinase, often in the thousands, peaking within one to three days of injury.
  • Myoglobinuria: a dipstick positive for blood with few or no red cells on microscopy is the classic clue.
  • Common causes: crush injury, prolonged immobilisation, seizures, heat stroke, exertion, alcohol and cocaine.
  • Drug causes: statins, especially with fibrates, clarithromycin or azole antifungals; stop the offending drug first.
  • Genetic causes: glycogen storage disorders and carnitine palmitoyl transferase deficiency present with exercise-related episodes.
  • Fluids: early high-volume isotonic saline aiming for a brisk urine output; the evidence for bicarbonate and mannitol is weak.
  • Calcium trap: early hypocalcaemia is followed by rebound hypercalcaemia in recovery; treat only if symptomatic or with hyperkalaemia.

A statin, a macrolide and dark urine

A 56-year-old diabetic man on atorvastatin 40 mg is admitted with pneumonia and started on clarithromycin. Four days later he has thigh pain, weakness and dark urine, with creatine kinase of 22,000 U/L, creatinine risen from 1.1 to 2.4 mg/dL, potassium 5.9 mmol/L and low calcium.

  1. Read the urine. The dipstick is positive for blood but microscopy shows few red cells, which confirms myoglobinuria.
  2. Stop the culprits. The statin and clarithromycin are stopped at once, and intravenous saline is started.
  3. Watch potassium and the heart. Potassium and the electrocardiogram are monitored, and sodium bicarbonate is not given routinely.
  4. Examine the limb. The thigh is examined for compartment tension, because a swollen, tense muscle group needs surgical opinion.
  5. Trend the markers. Creatine kinase is trended until it falls, and dialysis is reserved for refractory hyperkalaemia, acidosis or volume overload that the kidney cannot manage.
  6. Judge recovery. Recovery is judged by falling creatine kinase, stable potassium and a urine output that stays adequate once intravenous fluids are reduced.

Where the exam tries to catch you

Rhabdomyolysis questions turn on look-alike findings and drug interactions.

  • Trap: assuming a positive dipstick always means haematuria. Correct: myoglobin and haemoglobin both turn the dipstick positive, and only microscopy separates them.
  • Trap: diagnosing hepatitis from an AST-predominant pattern. Correct: muscle injury raises aspartate aminotransferase more than alanine aminotransferase.
  • Trap: calling mild creatine kinase rises rhabdomyolysis. Correct: rises after vigorous exercise or intramuscular injection are not rhabdomyolysis, and the threshold matters.
  • Trap: forgetting the interacting drugs. Correct: fibrates, macrolides, azoles and ciclosporin each raise statin levels and can precipitate toxicity.

Frequently asked questions

What urine finding distinguishes myoglobinuria from haematuria?

In myoglobinuria, the urine dipstick is positive for blood but microscopy shows few or no red blood cells, because myoglobin is a pigment and not a cell. In true haematuria, microscopy reveals red cells. This dissociation is the classic clue to rhabdomyolysis.

Which drug combinations commonly cause rhabdomyolysis?

Statins combined with fibrates, clarithromycin or azole antifungals commonly cause rhabdomyolysis because they raise statin levels. Stopping the statin is the first step, along with the interacting drug. Patients with renal or hepatic impairment are more vulnerable.

Why is hypocalcaemia seen early in rhabdomyolysis?

Calcium is deposited into damaged muscle early on, so serum calcium falls in the acute phase. Hypocalcaemia is usually not treated unless it causes symptoms, arrhythmia or hyperkalaemia. Rebound hypercalcaemia can occur in recovery.

Is urinary alkalinisation with sodium bicarbonate proven in rhabdomyolysis?

Urinary alkalinisation with sodium bicarbonate is not proven to prevent kidney injury in rhabdomyolysis. Many clinicians use fluids alone, aiming for a brisk urine output. Over-alkalinisation can cause hypocalcaemia and should be avoided.

What is the most sensitive marker for skeletal muscle injury?

Serum creatine kinase is the most sensitive marker of skeletal muscle injury, rising within hours and peaking within a few days. Its level correlates with the extent of muscle damage. Creatine kinase is not specific to muscle, so the source should be considered.

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