Hepatic Artery Thrombosis

Hepatic artery thrombosis is occlusion of the hepatic artery or its branches by clot. It is the most serious vascular complication after liver transplantation and is rare in the native liver.

Incidence after adult liver transplantation is 2% to 9%, and higher in children (8% to 15%). Early thrombosis (within 30 days) causes graft ischaemia, bile duct necrosis, biloma, abscess and graft failure, with graft loss or death in many without urgent treatment. Late thrombosis presents with biliary strictures and recurrent cholangitis.

Risk factors are technical (small or kinked artery, difficult anastomosis, aortohepatic conduit, retransplantation), cold ischaemia over 12 hours, a small recipient, hypercoagulability, cytomegalovirus infection, ABO incompatibility, rejection and low flow states. In the native liver, causes include trauma, vasculitis, embolisation, chemoembolisation and dissection.

Pathophysiology.

The biliary tree relies on the hepatic artery for its blood supply (through the peribiliary plexus), so occlusion causes ischaemic cholangiopathy sooner than parenchymal necrosis.

The liver tolerates sudden occlusion in the native state because of portal venous flow, but the transplanted liver has no collateral supply for weeks.

Early: fever, sudden rise in aminotransferases (often over 1,000 units/L), falling graft function, sepsis, bile leak and encephalopathy. Late: cholangitis, jaundice, liver abscess and biliary strictures. Some patients are asymptomatic.

Red flags.

• Rapid rise in aminotransferases or lactate after transplant.
• Fever with abdominal pain and sepsis.
• Bile leak or liver abscess.
• Encephalopathy and coagulopathy.

Doppler ultrasound is the first test: absent hepatic artery flow or a tardus parvus waveform (resistive index under 0.5, systolic acceleration time over 80 ms). Confirm with CT angiography or catheter angiography. Send liver enzymes, bilirubin, INR, lactate, blood cultures and cytomegalovirus PCR. Magnetic resonance cholangiography shows biliary complications.

Differential diagnosis.

• Acute rejection.
• Portal vein thrombosis.
• Primary graft non-function.
• Biliary leak or stricture.
• Hepatic vein outflow obstruction.
• Cytomegalovirus hepatitis.

Revascularise urgently, ideally within hours of early thrombosis. Options are surgical thrombectomy and revision of the anastomosis, endovascular catheter directed thrombolysis, angioplasty with stenting, or arterial reconstruction. Retransplantation is needed for graft failure or irreversible biliary necrosis.

• Unfractionated heparin: 80 units/kg IV bolus (maximum 5,000 units), then 18 units/kg/h; until the vessel is secured and then until oral therapy is established; adjust to anti-Xa 0.3 to 0.7 units/mL; monitor platelets, anti-Xa, bleeding and graft function; use lower doses with active bleeding or severe coagulopathy.
• Aspirin: 75 to 100 mg orally once daily; long term after revascularisation; maximum 100 mg daily; monitor bleeding; avoid with active bleeding.
• Piperacillin-tazobactam (cholangitis or abscess): 4.5 g IV every 6 hours for 5 to 7 days after source control; maximum 18 g daily; monitor renal function and blood counts; reduce for creatinine clearance under 40 mL/min.

Drain abscesses and bilomas, and treat biliary strictures by endoscopic or percutaneous dilation and stenting.

Prevention. Meticulous anastomotic technique, intraoperative Doppler, aspirin prophylaxis after transplant, and early Doppler screening in the first week.

Monitoring. Doppler ultrasound daily in the first week after transplant, then at defined intervals, liver enzymes and lactate.

Referral and escalation. Transplant surgery and interventional radiology immediately; hepatology and critical care.

Special groups. Children need earlier and more frequent Doppler and have a higher risk, and revascularisation is attempted before retransplantation.