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Rhabdomyolysis
Overview
- Definition–injury-induced breakdown of skeletal muscle fibres with release of intracellular contents (e.g. creatine kinase, myoglobin, potassium, phosphate) into the circulation.
- Key complications–acute kidney injury (AKI), electrolyte/acid–base disturbances, disseminated intravascular coagulation and compartment syndrome.
- Incidence of AKI–5–65 % overall, highest after crush trauma; risk is modified by aetiology, volume status and nephrotoxic exposures.
Aetiology
| Traumatic | Non-traumatic |
|---|---|
| Crush injury (earthquakes, RTCs) | Exertional–extreme exercise, seizures, status asthmaticus |
| Prolonged limb compression / compartment syndrome (alcohol-associated immobility, prolonged operative positioning, tight tourniquet) | Temperature-related–malignant hyperthermia, neuroleptic malignant syndrome, heat stroke, profound hypothermia |
| Penetrating or blunt muscle trauma | Metabolic / genetic–inborn errors of glycogen or lipid metabolism, mitochondrial myopathies |
| High-voltage electrocution | Drugs / toxins–statins, fibrates, antiretrovirals, cocaine, amphetamines, heroin, alcohol, synthetic cannabinoids, carbon monoxide |
| Infection–Influenza A/B, SARS-CoV-2, HIV, EBV, Streptococcus pyogenes, Staphylococcus aureus | |
| Endocrine / metabolic–diabetic ketoacidosis (DKA), hyperosmolar hyperglycaemic state, severe hyponatraemia, hypokalaemia | |
| Idiopathic |
Pathophysiology
- Direct sarcolemmal disruption (trauma) or ATP depletion (metabolic / exertional) → failure of Na⁺/K⁺-ATPase and Ca²⁺-ATPase pumps.
- Intracellular Ca²⁺ overload → sustained actin–myosin contraction, activation of Ca²⁺-dependent proteases & phospholipases.
- Myocyte necrosis → leakage of CK, myoglobin and electrolytes.
- Renal injury mechanisms
- Tubular obstruction by myoglobin-Tamm–Horsfall protein casts (worse at urine pH < 6.5).
- Direct oxidative toxicity of ferri-myoglobin.
- Intrarenal vasoconstriction and hypovolaemia.
Clinical Features
Triad: myalgia, muscle weakness/swelling, dark “tea-coloured” urine (myoglobinuria > 1.5 mg dL⁻¹). Severe pain may limit passive limb movement. Systemic clues: fever, tachycardia, nausea, agitation or delirium.
Investigations
| Test | Typical finding |
|---|---|
| Serum CK | 5 000 IU L⁻¹ (diagnostic); levels peak at 24–72 h. Very high CK (> 10 000 IU L⁻¹) alone is an inconsistent predictor of mortality |
| Serum / urine myoglobin | Positive within 1–4 h of injury; may clear before CK falls. |
| Electrolytes | Hyperkalaemia, hyperphosphataemia, hypocalcaemia (early) → rebound hypercalcaemia during recovery. |
| Urea, creatinine | Rising values indicate AKI. |
| ABG & lactate | Metabolic (high-anion-gap) acidosis. |
| ECG | Peaked T-waves, widened QRS (hyperkalaemia). |
| Coagulation profile | Prolongation if severe systemic inflammation. |
Management
Treat the Precipitating Cause
- Release compression and perform prompt fasciotomy for compartment syndrome.
- Stop offending drugs; treat malignant hyperthermia with dantrolene 2.5 mg kg⁻¹ IV bolus.
- Control hyperthermia or seizures aggressively.
Aggressive Early Volume Resuscitation
- Begin within 6 h of injury.
- Isotonic crystalloids remain first-line (e.g. Plasma-Lyte, Ringer’s acetate). avoid potassium-containing fluids in marked hyperkalaemia.
- Typical rate: 15–20 mL kg⁻¹ bolus then 200–300 mL h⁻¹ (aim urine output ≥ 2-3 mL kg⁻¹ h⁻¹).
- Monitor fluid balance closely; switch to de-escalation once CK is falling and urine clears.
Electrolyte and acid–base Control
| Problem | Treatment |
|---|---|
| Hyperkalaemia | Calcium gluconate 10 mL 10 % IV, insulin 0.1 U kg⁻¹ + 50 % dextrose, nebulised salbutamol, sodium bicarbonate if acidotic. |
| Hypocalcaemia | Replace only if symptomatic (tetany/arrhythmia); otherwise allow spontaneous correction. |
| Acidosis | Volume resuscitation ± sodium bicarbonate only for severe metabolic acidosis (target urine pH > 6.5). Routine alkalinisation not recommended. |
Renal Support
- Indications for renal replacement therapy (RRT): refractory hyperkalaemia, severe acidosis, fluid overload, oliguria with rising creatinine.
- Continuous modalities (CVVH, CVVHD) with high-cut-off membranes or adsorber (CytoSorb®) improve early myoglobin clearance but have not yet shown outcome benefit.
- Avoid nephrotoxins (NSAIDs, iodinated contrast).
Adjuncts (evidence is low)
- Mannitol and routine urine alkalinisation not supported by recent guideline or meta-analysis; reserve for selected patients with adequate hydration who fail to achieve target diuresis.
- Loop diuretics may aid diuresis once euvolaemic but do not prevent AKI
Monitoring & Supportive Care
- Serial CK, creatinine, electrolytes 6–12-hourly.
- Hourly UO; urinalysis for haem-positive dipstick with no red cells (myoglobin).
- Treat pain aggressively; consider early regional blocks for limb injuries.
- Vigilance for compartment syndrome (pain out of proportion, tense swelling, paraesthesia).
Prognosis & risk Modifiers
| Predictor of AKI / mortality | Comment |
|---|---|
| High injury burden (crush, burn, sepsis) | More muscle mass damaged → ↑ myoglobin load |
| Hypovolaemia or shock on admission | Magnifies renal hypoperfusion |
| Concomitant nephrotoxins (NSAIDs, aminoglycosides) | Independent AKI risk factor |
| CK > 10 000 IU L⁻¹ plus rising creatinine | Signals ongoing muscle injury |
| Delay > 12 h to fluid resuscitation | Associated with higher dialysis requirement |
Early, goal-directed crystalloid resuscitation remains the only intervention consistently associated with reduced AKI and mortality.
Links
- Renal Physiology
- ICU and renal disease
- Renal replacement therapy
- Contrast nephropathy
- Renal protection
Past Exam Questions
Diagnosis and Management of Dark Urine and Reduced Urine Output in an Assault Victim
A 32-year-old male is admitted to your intensive care unit. He has been the victim of a community assault. Clinical examination reveals evidence of extensive beatings with a sjambok (leather whip). His urine is dark brown in colour and his urine output is reduced.
a) What is the diagnosis? (1)
b) Describe the pathophysiology of this condition. (4)
c) Outline principles of management for this condition. (5)
References:
- Williams, J. D. and Thorpe, C. (2014). Rhabdomyolysis. Continuing Education in Anaesthesia Critical Care &Amp; Pain, 14(4), 163-166. https://doi.org/10.1093/bjaceaccp/mkt051
- Sawhney JS et al. Management of rhabdomyolysis: a practice management guideline. Am J Surg. 2021. Available from: https://www.east.org east.org
- Borrmann A et al. Kidney replacement therapies in patients with acute kidney injury and rhabdomyolysis (ReplaceRhabdo): pilot trial. Clin Kidney J. 2025. pmc.ncbi.nlm.nih.gov
- Kan CN et al. Acute kidney injury in hospitalised patients with exertional rhabdomyolysis. JAMA Netw Open. 2024. pmc.ncbi.nlm.nih.gov
- StatPearls Publishing. Rhabdomyolysis–updated 2025. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448168/
- Li Z et al. Advances in rhabdomyolysis: pathogenesis, diagnosis and treatment. Int J Clin Pract. 2025. sciencedirect.com
- Homsi R et al. Role of bicarbonate and mannitol in rhabdomyolysis–a systematic review. Kidney Blood Press Res. 2020. pmc.ncbi.nlm.nih.gov
- FRCA Mind Maps. (2024). Retrieved June 5, 2024, from https://www.frcamindmaps.org/
- Anesthesia Considerations. (2024). Retrieved June 5, 2024, from https://www.anesthesiaconsiderations.com/
Summaries:
Rhabdomyolysis
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© 2025 Francois Uys. All Rights Reserved.
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