Synopsis
Recognise muscle breakdown before the classic triad appears, control its cause, prevent pigment-associated kidney injury and treat potassium, compartment and thermal emergencies without harmful routine adjuncts.
- Rhabdomyolysis releases myoglobin, potassium, phosphate, urate and enzymes from injured skeletal muscle; kidney injury reflects pigment toxicity, tubular obstruction and the accompanying hypovolaemia or shock.
- Common settings include crush or prolonged immobilisation, seizures, extreme exertion, hyperthermia, limb ischaemia, infection, metabolic disturbance, toxins and drug interactions involving statins.
- Muscle pain, weakness and dark urine form a memorable triad but are often incomplete. Examine for swollen tender muscle, reduced limb perfusion, pressure injury and the precipitating neurological or thermal illness.
- Urine dipstick detects haem pigment and may be strongly positive despite few or no red cells on microscopy, supporting myoglobinuria rather than urinary bleeding.
- Creatine kinase confirms and tracks muscle injury but may rise and peak after presentation. The clinical cause, potassium, renal function, acid–base state and urine output determine immediate risk more directly than one CK number.
- Early isotonic crystalloid is important when the patient is depleted and not congested, with repeated reassessment and an individual urine-output strategy; there is no universally safe fixed volume target.
- Routine urinary alkalinisation with bicarbonate and routine mannitol are not established standard prophylaxis. Consider any exceptional use only with renal or critical-care oversight and a defined physiological indication.
- Early hypocalcaemia often reflects calcium deposition in damaged muscle and should not be corrected solely by a laboratory value; give calcium for symptoms or a separate emergency indication, and anticipate rebound hypercalcaemia during recovery.
Key red flags
Crush injury, entrapment, prolonged unconsciousness or pressure necrosis causes swollen tender muscle and systemic pigment release. Limb neurovascular compromise or pain out of proportion raises compartment syndrome and demands urgent surgical review.
Severe exercise, heat exposure, hyperthermia, collapse or altered cognition can precede rhabdomyolysis. Heat stroke is a critical illness requiring immediate cooling and multi-organ support, not merely intravenous fluid for a high CK.
A statin interaction, stimulant, antipsychotic-associated hyperthermic syndrome, serotonin toxicity, alcohol or illicit drug exposure may be causal. Look for rigidity, autonomic features and co-ingestants rather than attributing all cases to the prescribed statin.
Rapid potassium and phosphate release, metabolic acidosis and early hypocalcaemia can occur before kidney injury is fully visible. ECG change, weakness or arrhythmia determines emergency treatment, while later rebound hypercalcaemia can complicate recovery.
Investigation priorities
Confirm significant skeletal-muscle injury and determine whether release is continuing or resolving.
Management branches
Rhabdomyolysis is suspected from the setting, symptoms, pigment urine or elevated CK.
- 1. Perform ABCDE, obtain ECG, potassium, gas, renal profile, calcium, phosphate and CK, and begin continuous monitoring when hyperkalaemia or severe systemic illness is possible.
- 2. Treat hyperkalaemic membrane toxicity and redistribute potassium through the current UKKA emergency protocol while arranging definitive removal if refractory.
- 3. Restore circulating volume with isotonic crystalloid when examination supports depletion, reassessing pressure, lungs, urine output and cumulative balance after each phase.
- 4. Involve nephrology early for oliguria, rising potassium, acidosis or overload, because continued large-volume fluid may be unsafe and dialysis decisions are complication-based.