Acute Aortic Occlusion

Acute aortic occlusion is sudden, complete obstruction of the abdominal aorta, usually infrarenal, from embolus or in situ thrombosis. It causes acute ischaemia of both legs and the pelvis, with risk of renal, mesenteric and spinal cord ischaemia, and it is a vascular emergency with high mortality.

It is rare, accounting for under 5% of acute limb ischaemia, but mortality is 20 to 50% and amputation or paraplegia complicates many survivors. Delay in diagnosis is common because it mimics spinal cord or neurological disease.

Causes by frequency:

• Embolism from the heart (atrial fibrillation, left ventricular thrombus, endocarditis, atrial myxoma, prosthetic valve thrombus) or from aortic atheroma (saddle embolus).
• In situ thrombosis on atherosclerotic aorta, hypoplastic aorta (young women who smoke), aortic aneurysm, aortitis, or aortic dissection with malperfusion.
• Hypercoagulable states: heparin induced thrombocytopenia, antiphospholipid syndrome, malignancy, polycythaemia, severe infection including viral infection.
• Low flow states with cardiogenic shock, cocaine use, and iatrogenic causes (intra-aortic balloon pump, endovascular devices, clamp injury).

Severity grading by limb threat:

• Viable: no sensory loss or weakness, audible arterial Doppler signals.
• Marginally threatened: minimal sensory loss, no weakness; salvageable if treated promptly.
• Immediately threatened: sensory loss beyond the toes, mild to moderate weakness, rest pain; needs immediate revascularisation.
• Irreversible: major tissue loss, profound paralysis and anaesthesia, absent Doppler signals, rigor.

Pathophysiology.

Sudden obstruction removes flow to the pelvis and legs, with no time for collaterals. Muscle ischaemia causes rhabdomyolysis, and reperfusion releases potassium, myoglobin, lactate and acid, leading to hyperkalaemia, acute kidney injury, arrhythmia and multi-organ failure.

A saddle embolus lodges at the bifurcation. In situ thrombosis occurs on a diseased wall, where collaterals have developed over time, so symptoms may be less severe.

Occlusion at or proximal to the renal arteries or involving the mesenteric vessels adds renal and bowel ischaemia, and spinal cord ischaemia produces paraplegia.

Sudden severe pain in both legs (or one leg at first), the buttocks or the lower back, with pallor, coldness, mottling that may extend to the abdomen, absent femoral and distal pulses, paraesthesia and weakness or paralysis. Abdominal pain, bloody diarrhoea (mesenteric ischaemia) and anuria (renal ischaemia) occur. Hypotension and shock appear with dissection or cardiac source. Paraplegia with absent leg pulses is often misdiagnosed as spinal cord compression or stroke.

Rapid investigations (do not delay revascularisation for imaging when the diagnosis is clear):

• Clinical diagnosis, with handheld Doppler of the femoral and pedal vessels.
• CT angiography of the aorta and iliofemoral run off (as soon as the patient can be scanned, ideally within 30 minutes), showing level, length, cause (embolus, thrombus on plaque, dissection, aneurysm), and renal and mesenteric vessel status.
• ECG (atrial fibrillation, infarction), troponin, bedside echocardiography (source of embolus, left ventricular thrombus, vegetation, aortic root).
• Blood tests: lactate, potassium, creatinine, creatine kinase, urine myoglobin, blood gas, full blood count and platelets, coagulation screen, group and cross-match, glucose, liver tests.
• Thrombophilia screen and antiphospholipid antibodies before heparin if possible, without delaying treatment. Platelet count fall of 30 to 50% after heparin should prompt heparin induced thrombocytopenia assessment.

Differential diagnosis.

• Aortic dissection with malperfusion and ruptured abdominal aortic aneurysm.
• Spinal cord infarction, cauda equina syndrome and Guillain-Barre syndrome.
• Bilateral iliac artery or femoral embolism, and severe acute deep vein thrombosis with phlegmasia.
• Cardiogenic shock with cold peripheries.

Minutes 0 to 10.

• Resuscitation bay with continuous monitoring, oxygen to SpO2 over 94%, two large bore intravenous lines.
• Unfractionated heparin 80 units/kg intravenous bolus (usual 5000 units), then 18 units/kg/h, with aPTT 1.5 to 2.5 times control at 6 hours. If heparin induced thrombocytopenia is known or suspected, give argatroban 2 microgram/kg/min intravenously (0.5 microgram/kg/min in hepatic impairment or critical illness; maximum 10 microgram/kg/min) with aPTT 1.5 to 3 times baseline.
• Analgesia: morphine 2.5 to 5 mg intravenously, repeated by response, or fentanyl 25 to 50 microgram intravenously. Antiemetic ondansetron 4 mg intravenously (check QTc).
• Warm the patient and protect the legs with cotton wool wrapping. Do not apply heat.
• Call the vascular surgeon and anaesthetist immediately and alert the operating theatre and interventional radiology.

Minutes 10 to 60.

• Crystalloid (balanced solution) 500 mL boluses to restore perfusion, aiming for urine output over 1 mL/kg/h. Avoid vasopressors when possible because they worsen limb and visceral ischaemia.
• Treat hyperkalaemia (potassium over 6.0 mmol/L or ECG change): calcium gluconate 10% 10 mL intravenously over 10 minutes (repeat if ECG changes persist), insulin 10 units with 25 g glucose intravenously, salbutamol 10 to 20 mg nebulised. Check potassium hourly. Prepare for dialysis.
• Treat rhabdomyolysis: crystalloid to maintain urine output of 100 to 200 mL/h, avoiding fluid overload, and monitor creatine kinase, potassium and creatinine every 4 to 6 hours.
• Early CT angiography to define the level and extent of occlusion, limiting contrast volume when renal function is impaired.

Revascularisation (within hours; every hour of delay increases muscle loss).

• Embolic occlusion: bilateral femoral cutdown with Fogarty balloon catheter embolectomy under local or general anaesthesia, with completion angiography. Treat the source.
• In situ thrombosis on a diseased aorta: thrombectomy with endarterectomy, or aortobifemoral bypass. In unfit patients, axillobifemoral bypass. Endovascular options are aspiration thrombectomy, angioplasty and stenting, or hybrid repair.
• Catheter directed thrombolysis is reserved for marginally threatened limbs with a distal or incomplete occlusion: alteplase 0.5 to 1 mg/h by catheter (usual total up to about 40 mg) with low dose heparin 500 units/h, with fibrinogen and clinical review every 6 hours. Not for immediately threatened limbs, because it is too slow. Absolute contraindications: previous intracranial haemorrhage, ischaemic stroke in 6 months, intracranial neoplasm, active bleeding, major surgery or trauma in 3 weeks, and aortic dissection.
• Dissection related occlusion: urgent aortic repair or endovascular fenestration or stenting by the aortic team.
• Fasciotomy (four compartment, both legs) for reperfusion with tense compartments, prolonged ischaemia (over 4 to 6 hours), or rising creatine kinase and pain on passive stretch.
• Primary amputation for irreversible ischaemia, with palliative decisions when the patient is moribund.

After revascularisation. Intensive care or high dependency unit. Continue heparin infusion until oral therapy begins. Monitor for compartment syndrome, acute kidney injury, hyperkalaemia, bowel ischaemia, spinal cord injury and bleeding. Dialysis for refractory hyperkalaemia or oliguric renal failure.

Treat the cause and prevent recurrence.

• Embolic source: apixaban 5 mg orally twice daily (2.5 mg twice daily if two of age 80 or over, weight 60 kg or under, creatinine 133 micromol/L or over) or warfarin to INR 2.0 to 3.0 (mechanical valves: INR 2.5 to 3.5), long term.
• Atherosclerotic in situ thrombosis: aspirin 75 to 100 mg daily, atorvastatin 40 to 80 mg daily (LDL cholesterol under 1.4 mmol/L), blood pressure control, smoking cessation.
• Hypercoagulable state: specialist haematology, warfarin to INR 2.0 to 3.0 (higher range or avoid direct oral anticoagulants in antiphospholipid syndrome).
• Heparin induced thrombocytopenia: stop all heparin, argatroban 2 microgram/kg/min intravenously (0.5 microgram/kg/min in hepatic impairment or critical illness; maximum 10 microgram/kg/min) with aPTT 1.5 to 3 times baseline, and later warfarin once platelets are over 150 x 10^9/L.

Monitoring. Limb perfusion, compartments and neurology every hour for 24 hours, then every 4 hours. Potassium, creatinine, creatine kinase and lactate every 4 to 6 hours for 24 to 48 hours. Duplex of the graft or aorta at 1 month, 6 months and yearly.

Referral and escalation. All patients need an emergency vascular surgeon and a unit with intensive care and dialysis. Transfer immediately when these are unavailable, with heparin running and analgesia given. Involve cardiology for the embolic source.

Special groups.

• Pregnancy: rare. Use heparin, left lateral tilt, and endovascular or surgical embolectomy. Warfarin and direct oral anticoagulants are avoided.
• Young women with hypoplastic aorta: atherosclerotic in situ thrombosis is typical; smoking cessation is essential.
• Kidney impairment: contrast sparing, but do not withhold CT angiography when it changes management; reduce apixaban dose by creatinine clearance; plan dialysis.
• Older adults and frailty: discuss goals of care early, because mortality is highest in this group.