ICU · renal-metabolic

Acute Severe Rhabdomyolysis — Comprehensive ICU Management

Also known as Rhabdomyolysis · Rhabdo · Myoglobinuria · Crush syndrome · Muscle breakdown · Creatine kinase elevation · Myoglobin nephrotoxicity · Exertional rhabdomyolysis · Statin-induced rhabdomyolysis

Rhabdomyolysis — skeletal muscle breakdown releasing intracellular contents (myoglobin, creatine kinase, potassium, phosphate, urate) into the circulation → AKI (myoglobin nephrotoxicity + intratubular cast formation + volume depletion), hyperkalaemia (lethal arrhythmia), hypocalcaemia, metabolic acidosis, compartment syndrome. Causes: crush injury (trauma, building collapse, prolonged immobilisation), exertional (marathon, seizures, agitation/delirium), drugs (statins 1 — especially with fibrates/calcineurin inhibitors, illicit drugs — MDMA, cocaine, heroin), infections (influenza, legionella, coxsackie, severe sepsis), metabolic (hypokalaemia, hypophosphataemia, DKA/HHS), genetic (McArdle disease, CPT deficiency, malignant hyperthermia), inflammatory (polymyositis, dermatomyositis). Diagnosis: CK 5x ULN (1000 IU/L — typically 10,000-100,000+) + myoglobinuria (dark/tea-coloured urine + positive blood on dipstick but NO RBCs on microscopy) + hyperkalaemia + elevated AST/ALT (muscle-derived). Management: AGGRESSIVE IV FLUIDS (the 1 intervention — high urine flow — about 400 mL/h crystalloid, up to 12 L or more per day in severe crush — crystalloid, ideally balanced solution), treat hyperkalaemia (calcium gluconate + insulin/dextrose), urine alkalinisation (controversial — sodium bicarbonate mainly in acidotic patients — evidence is limited), renal replacement therapy if severe AKI (CRRT preferred), fasciotomy if compartment syndrome. Mortality: about 10 per cent overall, higher when AKI develops.

high20 referencesUpdated 26 July 202612 min readSource-verified · Sept 2026

Checked against its sources on 2 Sept 2026

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Red flags

CK ≥5000 IU/L (severe rhabdomyolysis) + dark urine + hyperkalaemia = RHABDOMYOLYSIS with high AKI risk — start AGGRESSIVE high-volume IV crystalloid immediately (about 400 mL/h, scaled up to 12 L or more per day in severe crush)
Hyperkalaemia (K ≥5.5 mmol/L, seen in 13% of severe cases) can be SEVERE and REFRACTORY — potassium is continuously released from necrotic muscle — IV calcium for ECG changes or K ≥6.5, insulin–dextrose shifts K intracellularly, nebulised salbutamol 10–20 mg adds ~1.2 mmol/L of lowering — RRT if refractory
Compartment syndrome (pain on passive stretch + tense compartment + paraesthesia; pulselessness is LATE) = SURGICAL EMERGENCY — fasciotomy is the only effective treatment; decompress when the delta pressure (diastolic minus compartment pressure) falls under 30 mmHg
Hypocalcaemia is COMMON (41% of severe cases, Ca ≤2.00 mmol/L) and usually asymptomatic — management is judicious: calcium homeostasis is biphasic, with recovery-phase REBOUND hypercalcaemia recognised — reserve IV calcium for symptomatic hypocalcaemia or hyperkalaemic ECG changes
Statins + gemfibrozil + other interacting drugs = high-risk combination for rhabdomyolysis — monitor CK and stop at first sign of muscle pain

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Practise this topic8 MCQs with explanations

Target exams

CICMFFICMEDIC

Red flags

CK ≥5000 IU/L (severe rhabdomyolysis) + dark urine + hyperkalaemia = RHABDOMYOLYSIS with high AKI risk — start AGGRESSIVE high-volume IV crystalloid immediately (about 400 mL/h, scaled up to 12 L or more per day in severe crush)
Hyperkalaemia (K ≥5.5 mmol/L, seen in 13% of severe cases) can be SEVERE and REFRACTORY — potassium is continuously released from necrotic muscle — IV calcium for ECG changes or K ≥6.5, insulin–dextrose shifts K intracellularly, nebulised salbutamol 10–20 mg adds ~1.2 mmol/L of lowering — RRT if refractory
Compartment syndrome (pain on passive stretch + tense compartment + paraesthesia; pulselessness is LATE) = SURGICAL EMERGENCY — fasciotomy is the only effective treatment; decompress when the delta pressure (diastolic minus compartment pressure) falls under 30 mmHg
Hypocalcaemia is COMMON (41% of severe cases, Ca ≤2.00 mmol/L) and usually asymptomatic — management is judicious: calcium homeostasis is biphasic, with recovery-phase REBOUND hypercalcaemia recognised — reserve IV calcium for symptomatic hypocalcaemia or hyperkalaemic ECG changes
Statins + gemfibrozil + other interacting drugs = high-risk combination for rhabdomyolysis — monitor CK and stop at first sign of muscle pain

The one-line answer

Rhabdomyolysis is skeletal muscle breakdown spilling myoglobin, creatine kinase, potassium, phosphate and urate into the circulation — producing the quartet every CICM stem tests: AKI (acute renal failure affected half of one severe-case series and about 46 per cent of a 475-patient hospital cohort), hyperkalaemia (13 per cent of severe cases at 5.5 mmol/L or above), hypocalcaemia (41 per cent at 2.00 mmol/L or below) and metabolic acidosis. Diagnose it on CK above five times the upper limit of normal or above 1000 IU/L — values may reach 100,000 IU/L — with pigmenturia; urine myoglobin is positive in only about a fifth of cases, so a negative result never excludes it. The number-one intervention is early high-volume IV crystalloid — about 400 mL/h, scaled up to 12 L or more per day of alkaline solution in severe crush; treat the hyperkalaemia (IV calcium for ECG changes or K at or above 6.5, insulin with glucose, nebulised salbutamol, dialysis if refractory), manage the hypocalcaemia judiciously — calcium is biphasic, with rebound hypercalcaemia described in recovery — and decompress compartment syndrome when the delta pressure falls under 30 mmHg.^[3]^[4]^[1]^[2]^[7]^[6]^[10]^[11]^[20]

Meet the patient

A 28-year-old man is extricated after eight hours under a collapsed wall, both lower limbs and his pelvis crushed. He arrives bradycardic at 46, blood pressure 78/50, GCS 14. The ECG shows a wide QRS with peaked T waves merging towards a sine wave. The venous gas reads K 8.2 mmol/L, pH 7.08, lactate 9, and the catheter drains dark tea-coloured urine — the severe end of the published spectrum, in which hyperkalaemia, hypocalcaemia, acute renal failure and pigmenturia cluster together.^[3]^[2]

The question that decides whether he lives the next ten minutes is the question that decides every rhabdomyolysis: is the potassium still being released from dying muscle? Because if it is, no single insulin-dextrose bolus will hold it. Hold that thought, and the fluid-first, calcium-paradox, fasciotomy-clock logic below falls into place.^[8]^[9]

References20Show

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