Arterialization of the Portal Vein: A Potentially Graft-Saving Strategy to Optimize Veno-Arterial Inflow in Liver Transplantation

Introduction: The dual vascular inflow of liver grafts in liver transplantation (LT) is increasingly recognized as crucial to achieving adequate graft function in deceased donor LT (DDLT). Portal hyperperfusion is the most common, leading to decreased intrahepatic adenosine and arterial vasoconstriction via the hepatic artery buffer response. Splanchnic vasodilators, splenic artery embolization, or splenectomy are all recognized among other treatments. However, the management of portal hypoperfusion is less well described, with only isolated case reports describing the augmentation of portal venous (PV) inflow. This is the largest series describing PV arterialization as a strategy to save liver grafts by bolstering portal inflow. Methods: Patients at a single transplant center (Cleveland Clinic Abu Dhabi, UAE) were included (2018–2024). Intra-operative portal vein and hepatic artery flows are measured in all cases using a MediStim vascular flow device, and liver-vascular ultrasounds are obtained routinely post-transplant. Surgical PV arterialization is used as a short-term measure when adequate portal vein flow cannot be achieved using conventional techniques. Cases were performed using end-to-side anastomosis of a cadaveric iliac artery graft from the recipient infra-renal aorta (n = 3) to the recipient PV as an additional inflow in Y-configuration or using a conduit from the donor splenic artery to the donor PV (end-to-side) with the standard PV-anastomosis also functioning. Results: Four patients were deemed to have inadequate portal flow in the early post-LT (range POD1-7, n = 3) or intra-operative (n = 1) periods. All patients had laboratory and/or visual evidence of inadequate liver function secondary to portal hypoperfusion at the time of the decision to pursue arterialization. PV flows before arterialization were 500–590 mL/min [31–39 mL/min/100 g] and 1.4–2 L/min [93–133 mL/min/100 g] after arterialization. Arterialization grafts (n = 3) were ligated on post-arterialization days 2–7. At the conclusion of modulation, PV flows were 1.1-2.3 L/min [73–147 mL/min/100 g] with maintained HA flows 120–495 mL/min, highlighting the relative adaptability of liver graft and PV compliance after augmentation. All four patients are symptom-free with intact liver graft function at a range of 6–18 months post-LT. Graft survival of 100% compares favorably to all-comers after LT in the same setting (1-year GS = 96%, log-rank p = 0.874). Conclusions: Arterialization of the portal vein is a viable and graft-saving strategy for PV hypoperfusion in LT. Surgeons may pursue this approach in the scenario of inadequate portal vein perfusion without other identifiable causes, such as PV thrombus or port-systemic shunts, with a plan for arterial shunt reversal 1–7 days after placement based on flow assessment.