Extremity Reperfusion Injury

Extremity reperfusion injury is local and systemic injury after restoration of blood flow to an acutely ischaemic limb, producing muscle swelling, compartment syndrome, rhabdomyolysis, hyperkalaemia, acidosis and acute kidney injury. It is also called myonecrotic metabolic syndrome.

Epidemiology. Acute limb ischaemia has an incidence of about 1.5 in 10,000 people each year. The risk of reperfusion injury rises with ischaemia longer than 4 to 6 hours and with severity (severity class IIb or III).

Causes of the original ischaemia. Embolism, thrombosis of native vessel or graft, arterial trauma, dissection, tourniquet use and compression, and popliteal aneurysm thrombosis.

Classification. Class I viable. Class IIa marginally threatened (salvageable if treated promptly). Class IIb immediately threatened (sensory loss beyond toes, rest pain, mild or moderate motor loss). Class III irreversible (profound sensory loss, paralysis, no venous or arterial signal).

Pathophysiology. Reperfusion causes oxidative injury, neutrophil activation and increased capillary permeability, and muscle swelling in closed fascial compartments. Compartment pressure rises and compromises tissue perfusion. Potassium, myoglobin, lactate and inflammatory mediators enter the circulation.

Presentation is severe pain out of proportion, a tense swollen limb, pain on passive stretch, paraesthesia and weakness after revascularisation, with dark urine, arrhythmia or oliguria. Pulses may return while a compartment syndrome persists.

Red flags.

• Tense compartments or increasing pain after reperfusion.
• Potassium over 6.0 mmol/L or ECG changes.
• Dark urine, oliguria or falling renal function.

Clinical examination every hour in the first 24 hours. Compartment pressure measurement when examination is unreliable (sedated patient): fasciotomy is needed when the difference between diastolic pressure and compartment pressure is under 30 mmHg, or the compartment pressure exceeds 30 to 40 mmHg. Measure creatine kinase, potassium, calcium, phosphate, creatinine, bicarbonate, lactate, myoglobin in urine and full blood count. Duplex or angiography to check graft or arterial patency.

Differential diagnosis. Reocclusion or graft failure, haematoma, deep vein thrombosis and infection.

Revascularisation. Systemic heparin at once: 80 units/kg IV bolus then 18 units/kg/h (adjusted to anti-factor Xa or activated partial thromboplastin time), unless contraindicated. Then thrombectomy, catheter directed thrombolysis, bypass or amputation, as the limb class dictates. Primary amputation for class III.

Fasciotomy. Four compartment fasciotomy of the leg (or forearm decompression) for clinical or measured compartment syndrome, and prophylactically when ischaemia exceeded 4 to 6 hours, after prolonged reperfusion delay, in combined arterial and venous injury, or when frequent examination is not possible.

Metabolic care.

• 0.9% sodium chloride 1 L over the first hour and then enough to keep urine output at 1 to 2 mL/kg/h, with monitoring for pulmonary oedema.
• Hyperkalaemia: calcium gluconate 10% 30 mL IV, insulin 10 units IV with glucose 25 g, salbutamol 10 to 20 mg nebulised, and dialysis if refractory.
• Bicarbonate 50 mmol IV for severe acidosis (pH under 7.1).

Analgesia. Opioid and regional block (avoid regional block if compartment syndrome may be masked).

Monitoring. Limb neurovascular checks hourly, compartment pressures, creatine kinase every 12 hours, potassium every 4 hours, urine output hourly and creatinine daily.

Referral and escalation. Vascular surgery at once. Intensive care and nephrology for acute kidney injury or hyperkalaemia.

Special groups. In patients with heparin induced thrombocytopenia use argatroban 2 microgram/kg/min (reduced in liver impairment). In renal impairment, adjust fluids and monitor potassium.