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Rhabdomyolysis and pigment nephropathy

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Rhabdomyolysis with hyperkalaemic ECG change, shock, severe acidosis, anuria, pulmonary oedema, heat stroke, limb ischaemia or compartment syndrome requires immediate ABCDE treatment, urgent surgical or critical-care involvement where indicated, and early nephrology input; do not wait for peak creatine kinase.

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.

Key red flags

Traumatic or compression injury

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.

Investigation priorities

01
Serial creatine kinaseFirst step

Confirm significant skeletal-muscle injury and determine whether release is continuing or resolving.

Management branches

ImmediateStabilise pigment and electrolyte threat

Rhabdomyolysis is suspected from the setting, symptoms, pigment urine or elevated CK.

  1. 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. 2. Treat hyperkalaemic membrane toxicity and redistribute potassium through the current UKKA emergency protocol while arranging definitive removal if refractory.

Key medicines

Intravenous isotonic crystalloidStart promptly when hypovolaemia or major pigment burden is present, using locally approved boluses and ongoing rates titrated to perfusion, urine output, weight and respiratory reassessment.
Intravenous calcium salt for hyperkalaemic cardiac toxicityGive the calcium preparation and repeat strategy specified in the current UKKA or local resuscitation protocol when ECG toxicity is present, with immediate rhythm reassessment.
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom