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Rhabdomyolysis — AKI and hyperkalaemia ⚠️ 💧
Rhabdomyolysis — AKI and hyperkalaemia ⚠️ 💧
Skeletal-muscle breakdown releases myoglobin, potassium and phosphate; pigment-associated kidney injury and early dysrhythmia are major threats.
🔎 Recognise
Think of crush injury, prolonged immobility, seizures, intense exertion, heat injury or drug/toxin exposure. Pain, weakness and dark urine are variable, not obligatory.
🛟 First actions
Assess ABCDE, check ECG if potassium may be abnormal, measure urine output and arrange early senior/renal discussion for severe illness. Individualise isotonic fluid replacement to perfusion and cardiac/renal tolerance.
🧪 Investigations and reassessment
Measure CK, potassium, creatinine, calcium, phosphate and acid–base status; repeat according to severity. Investigate and stop the precipitant when possible.
⚠️ Common pitfalls and escalation
A reassuring initial creatinine does not exclude evolving AKI. Avoid automatic aggressive fluids in patients with cardiac failure and do not neglect compartment syndrome in injured limbs.
UK reference: NICE NG148 AKI principles. Focused editorial source check, 7 November 2026; this is not independent clinical or pharmacy sign-off. Verify current local policy, BNF/BNFC and specialist advice before treatment. Not a prescribing protocol.
Related guides: Acute kidney injury — FY quick guide ⚠️ 💧 · Hyperkalaemia ✅
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