🏥 Emergency Briefcase · Clinical guide

Rhabdomyolysis

Interactive diagnostic, risk-stratification, treatment and monitoring guidance for emergency clinicians.

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Time-critical findingsLife-threatening hyperkalemia, acute kidney injury, severe acid-base disturbance, shock, compartment syndrome or rapidly progressive systemic illness require immediate stabilization.
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What is rhabdomyolysis?

Core process

Skeletal-muscle breakdown releases creatine kinase, myoglobin, potassium, phosphate and other intracellular contents. Complications may include acute kidney injury, electrolyte emergencies, dysrhythmia and compartment syndrome.

Clinical pearl: The classic triad of muscle pain, weakness and dark urine is uncommon. Maintain suspicion when the mechanism fits.

Pathophysiology

  • Muscle membrane injury and cellular necrosis
  • Myoglobin filtration and tubular toxicity
  • Volume depletion and renal vasoconstriction
  • Potassium and phosphate release
  • Calcium shifts during injury and recovery

Common causes

TraumaticCrush injury
Prolonged immobilization
Burns
Electrical injury
Compartment syndrome
PhysiologicStrenuous exercise
Heat illness
Seizures
Infection
Ischemia
Medication/toxinStatins
Cocaine/amphetamines
Alcohol
Antipsychotics/NMS
Serotonergic toxicity
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Diagnostic approach

Clinical checklist

Muscle pain/tenderness
Weakness
Dark urine
Oliguria
Heat/exertion
Trauma/immobility
Drug/toxin exposure
Compartment findings

Initial studies

  • CK with serial trend
  • Creatinine/BUN and electrolytes
  • Calcium, phosphate and bicarbonate
  • Urinalysis: heme-positive with few/no RBCs supports myoglobinuria
  • ECG when potassium is abnormal or toxicity is severe
  • Etiology-directed testing

Diagnostic interpretation

FindingInterpretationCaveat
CK ≥5× upper limit of normalCommon working definitionAbsolute threshold depends on laboratory ULN and clinical context
Urine dipstick positive for blood with few/no RBCsSuggests pigment/myoglobinAbsence does not exclude rhabdomyolysis
HyperkalemiaPotentially immediate lethal complicationRepeat unexpected values and obtain ECG without delaying treatment when unstable
Rising creatinineRenal injury/evolving AKIRisk depends on multiple variables, not CK alone
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McMahon Risk Score

Predicts risk of the composite outcome of renal replacement therapy or in-hospital mortality using admission values. It supports—but does not replace—clinical judgment.

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Enter admission values

Use the score with renal function, electrolytes, hemodynamics, urine output and overall trajectory.

Published risk bands: scores below 5 were associated with low risk, while scores of 10 or more were associated with substantially higher risk. The original outcome was renal replacement therapy or death—not AKI alone.

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Treatment priorities

Treat the cause and stop ongoing injuryControl hyperthermia, seizures, ischemia, agitation, toxin exposure and pressure-related injury.
Use goal-directed isotonic crystalloidStart early when clinically appropriate, then titrate to perfusion, urine output, renal function and volume status. Avoid fixed high rates in patients at risk for overload.
Treat hyperkalemia immediately when indicatedStabilize myocardium with IV calcium for ECG changes; shift potassium with insulin/dextrose and beta-agonist therapy; arrange definitive removal when needed.
Manage complicationsAssess for compartment syndrome, severe acidosis, dysrhythmia, disseminated intravascular coagulation and evolving renal failure.

Fluids

Balanced crystalloid or normal saline may be selected based on the patient and local protocol. Reassess frequently. Urine-output goals are individualized; commonly used adult targets are approximately 1–3 mL/kg/hour, capped near 300 mL/hour in trauma guidance.

Bicarbonate and diuretics

Routine bicarbonate or mannitol to prevent AKI is not supported by strong evidence. Consider bicarbonate for another clear indication, such as selected severe metabolic acidosis or hyperkalemia.

Calcium

Early hypocalcemia is often observed without replacement unless symptomatic or needed for cardioprotection in life-threatening hyperkalemia. Rebound hypercalcemia may occur during recovery.

Renal replacement therapy

Base dialysis on standard clinical indications—refractory hyperkalemia, severe acidosis, volume overload, uremic complications or progressive renal failure—not CK or myoglobin level alone.

Do not anchor on the CK.

Disposition and therapy should integrate kidney function, potassium, acid-base status, volume status, urine output, cause, comorbidities and follow-up reliability.

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Monitoring and disposition

Laboratory trend

  • CK until clearly declining
  • Creatinine and BUN
  • Potassium and bicarbonate
  • Calcium and phosphate
  • Additional tests driven by cause

Clinical trend

  • Urine output and volume status
  • Serial extremity/compartment exam
  • Core temperature when indicated
  • Cardiac monitoring for hyperkalemia
  • Neurologic status and strength

Recovery signals

  • Cause controlled
  • Stable/improving renal function
  • Electrolytes stable
  • Adequate urine output
  • Symptoms and CK trending appropriately

Disposition framework

Discharge is not defined by one universal CK cutoff. Consider clinical stability, normal or improving renal function/electrolytes, controlled etiology, oral hydration, functional status, reliable follow-up and the likelihood of rebound or delayed toxicity.

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Clinical references

Reference links are provided for professional education. Follow current local protocols, specialist guidance and patient-specific clinical judgment.

Emergency Briefcase · Professional education only; not a substitute for patient-specific medical judgment.