Crush Injury Associated Acute Kidney Injury

Crush injury associated acute kidney injury is kidney failure from traumatic rhabdomyolysis after prolonged compression of muscle (crush syndrome). It is a leading cause of death after earthquakes, building collapse, mining accidents and conflict, and in disasters up to 50% of those with crush syndrome develop acute kidney injury, with up to half of those requiring dialysis. It is preventable when fluid resuscitation begins before release from entrapment.

Crush syndrome typically requires compression of a large muscle mass (thigh, buttock, calf, or both legs) for 1 hour or more (usually more than 4 to 6 hours). Sustained pressure causes ischaemia and sarcolemmal failure; on release, reperfusion floods tissue with oxygen, producing oxidant injury and massive influx of calcium, sodium and water into cells, with efflux of potassium, myoglobin, phosphate, urate, creatine kinase and lactate into the circulation.

Pathophysiology of the injury:

• Third space sequestration of up to 10 to 15 L of fluid in damaged muscle (hypovolaemic shock)
• Myoglobin filtration with cast formation and haem mediated tubular toxicity in acidic, concentrated urine
• Renal vasoconstriction from hypovolaemia, endothelin, angiotensin II and nitric oxide scavenging
• Hyperkalaemia (sudden cardiac arrest within minutes of extrication), hyperphosphataemia, hypocalcaemia (calcium deposits in injured muscle), metabolic acidosis, hyperuricaemia
• Compartment syndrome, disseminated intravascular coagulation, sepsis and multi-organ failure

• Initially deceptively well ("smiling death"): alert, with intact distal pulses and minimal pain while the limb is compressed
• After release: swelling, pain, paraesthesia, weakness or paralysis of the limb, tense compartments, skin blistering and ecchymosis
• Hypotension and shock from fluid sequestration and bleeding; tachycardia
• Dark red brown urine, oliguria then anuria
• ECG changes of hyperkalaemia (peaked T waves, widened QRS, sine wave) and ventricular arrhythmia; sudden death
• Hypothermia, hypoxia, acidosis; tetanus prone wounds

Red flags: compression over 4 hours, both legs involved, hypotension, ECG changes, anuria or urine output below 0.3 mL/kg/h, tense compartments with loss of pulses, creatine kinase above 20 000 U/L, potassium above 6.0 mmol/L, pH below 7.2.

• Triage: duration of entrapment, body parts compressed, vital signs, urine colour and output, limb neurovascular status.
• Creatine kinase (peaks at 24 to 72 hours; above 5000 U/L predicts renal failure, above 75 000 U/L has been reported in survivors), potassium (4 to 6 hourly initially), calcium, phosphate, urate, creatinine, urea, bicarbonate, lactate, blood gas, coagulation, full blood count.
• Urine dipstick positive for blood with few red cells; urine pH and output hourly.
• ECG monitoring.
• Compartment pressure measurement when clinically suspected (delta pressure below 30 mmHg).
• Imaging for associated injuries.

Differentials: haemorrhagic shock without crush syndrome, sepsis, myocardial infarction, spinal injury, hypothermia, drug intoxication.

Before and during extrication (field management)

• Establish intravenous or intraosseous access before the limb is released.
• Start isotonic saline 1 L/h (10 to 15 mL/kg/h in adults; 15 to 20 mL/kg/h in children) before release; continue 1 to 1.5 L/h for the first 24 hours (aim for 6 to 12 L in the first day) with a urine output target of 200 to 300 mL/h (about 3 mL/kg/h) until myoglobinuria clears.
• Potassium containing fluids (Ringer lactate) are used in practice but isotonic saline is preferred when potassium cannot be measured.
• Adding sodium bicarbonate 50 mmol to every second litre keeps urine pH above 6.5 and counters acidosis and hyperkalaemia; stop if arterial pH exceeds 7.5 or serum bicarbonate exceeds 30 mmol/L.
• Mannitol 1 to 2 g/kg intravenously over 30 minutes (maximum 200 g in 24 hours), only if urine flow is established (above 20 mL/h) after fluid loading and the patient is not overloaded; stop if no diuresis in 2 hours.
• Cardiac arrest on release: treat hyperkalaemia first (calcium chloride 1 g, insulin 10 units with glucose 50 g, bicarbonate 50 mmol, salbutamol nebulised).
• Tourniquet: apply proximal to the compressed limb before release only when amputation is planned or severe haemodynamic instability is expected; release it once fluid resuscitation is under way unless amputation is performed.
• Analgesia: ketamine 0.1 to 0.3 mg/kg intravenously or fentanyl 25 to 50 microg intravenously; avoid NSAIDs.

Hospital management

• Hyperkalaemia: calcium gluconate 10% 10 to 20 mL over 10 minutes, repeat for persistent ECG changes; insulin 10 units with glucose 25 to 50 g; salbutamol 10 to 20 mg nebulised; bicarbonate 50 mmol; sodium zirconium cyclosilicate 10 g three times daily for up to 48 hours; early dialysis for potassium above 6.5 mmol/L unresponsive to medical therapy or rising by more than 0.5 mmol/L/h.
• Hypocalcaemia: do not correct unless symptomatic (tetany, arrhythmia) or when treating hyperkalaemia; rebound hypercalcaemia appears 1 to 3 weeks later in recovery.
• Wound care, tetanus prophylaxis, antibiotics for open wounds (cefazolin 2 g every 8 hours, with metronidazole 500 mg every 8 hours for contaminated wounds).
• Fasciotomy only for confirmed compartment syndrome (pressure above 30 mmHg or delta pressure below 30 mmHg, or loss of distal pulses and neurological deficit); avoid prophylactic fasciotomy because open wounds raise infection and bleeding risk; amputation for non-viable limbs or life threatening sepsis.
• Monitor urine output, central venous pressure and chest examination; reduce fluids when oliguria with overload develops.

Renal replacement therapy

• Indications: refractory hyperkalaemia, pH below 7.15, overload, uraemic symptoms, oliguria persisting beyond 24 hours with rising creatinine.
• Haemodialysis daily initially (blood flow 200 to 300 mL/min, high flux dialyser); continuous therapy for unstable patients; heparin free or citrate anticoagulation in bleeding or fresh wounds. Peritoneal dialysis is a poor option in abdominal injury or hyperkalaemia but is used when haemodialysis is unavailable.
• Renal recovery typically occurs within 2 to 6 weeks; plan dialysis capacity for disaster settings.

Disaster logistics. Triage patients with entrapment longer than 4 hours for early fluid therapy; stockpile saline, bicarbonate, calcium, dialysis supplies; establish a remote advisory team for renal disaster response.

Follow up. Creatinine, creatine kinase and urine monitoring until stable; creatinine and albumin:creatinine ratio at 3 months; rehabilitation for neurological and limb sequelae.