Traumatic Rhabdomyolysis

Traumatic rhabdomyolysis is skeletal muscle breakdown after crush, compression, prolonged immobilisation or high energy injury, with release of myoglobin, potassium, phosphate and creatine kinase. Diagnosis is a creatine kinase of more than five times the upper reference limit (over about 1000 units/L), and severe cases cause acute kidney injury.

Epidemiology. It complicates a large proportion of major crush injuries and is a leading cause of death after earthquakes and building collapse. The risk of renal injury rises with creatine kinase over 5000 units/L.

Causes and associations. Crush injury, prolonged limb compression after a fall or entrapment, compartment syndrome, high voltage electrical injury, burns, vascular occlusion and revascularisation, and prolonged surgery.

Pathophysiology. Muscle cell injury and failure of membrane pumps cause calcium entry, cell death and release of intracellular contents. Muscle swelling sequesters fluid, causing hypovolaemia. Myoglobin causes renal tubular obstruction, direct toxicity and renal vasoconstriction, worsened by aciduria and volume depletion. Hyperkalaemia, hypocalcaemia (early), hyperphosphataemia, metabolic acidosis, hyperuricaemia and disseminated intravascular coagulation can follow.

Presentation is muscle pain and swelling, weakness, dark brown urine and shock. Limb findings include tense compartments, pain on passive stretch, paraesthesia and pulselessness (late). Arrhythmia can result from hyperkalaemia.

Red flags.

• Potassium over 6.0 mmol/L or ECG changes.
• Oliguria, creatine kinase over 5000 units/L or rising creatinine.
• Tense compartments.

Measure creatine kinase (peaks at 24 to 72 hours, half life about 1.5 days), potassium, calcium, phosphate, urate, creatinine, bicarbonate, blood gas, lactate, coagulation, liver tests and urine for blood with no red cells (myoglobinuria). Do an ECG. Measure compartment pressures if compartment syndrome is suspected.

Differential diagnosis. Haemolysis, haematuria, drug induced myopathy (statins, fibrates), neuroleptic malignant syndrome, serotonin syndrome, malignant hyperthermia and infection.

Fluids (start as early as possible, ideally before release of a trapped limb).

• 0.9% sodium chloride 1 to 1.5 L/h for the first hours, then 200 to 500 mL/h, aiming for urine output of 200 to 300 mL/h (at least 1 mL/kg/h). Continue until creatine kinase is under 1000 units/L and myoglobinuria has cleared, usually 24 to 72 hours.
• Reduce volumes in heart failure, oliguric renal failure and older adults, and monitor for pulmonary oedema.

Not routine. Mannitol (consider 1 g/kg only in established high urine flow and normal haemodynamics), bicarbonate (use only for pH under 7.1 or severe hyperkalaemia, 50 mmol IV) and loop diuretics (only for fluid overload).

Hyperkalaemia. Calcium gluconate 10% 30 mL IV over 10 minutes for ECG changes, soluble insulin 10 units IV with glucose 25 g, and salbutamol 10 to 20 mg nebulised. Renal replacement for refractory hyperkalaemia. Treat hypocalcaemia only if symptomatic or with ECG changes, since rebound hypercalcaemia follows.

Compartment syndrome. Fasciotomy for compartment pressure within 30 mmHg of diastolic pressure (a delta pressure under 30 mmHg), or clinical compartment syndrome.

Renal replacement. For refractory hyperkalaemia, acidosis, fluid overload or uraemia. Continuous techniques are preferred in unstable patients.

Avoid nephrotoxins and NSAIDs.

Monitoring. Creatine kinase every 12 hours, potassium every 4 to 6 hours at first, urine output hourly, creatinine daily and ECG.

Referral and escalation. Intensive care, nephrology and orthopaedic or vascular surgery early.

Special groups. In children, fluid volumes are weight based (10 to 20 mL/kg boluses). In pregnancy, give the same treatment with obstetric input.