Work

Splenic artery embolization reverses non-occlusive hepatic artery hypoperfusion syndrome by enhancing the hepatic arterial buffer response

Year: 2026

Type: article

Abstract: Purpose Nonocclusive hepatic artery hypoperfusion syndrome (NOHAHS)—formerly splenic artery steal syndrome—is an underrecognized complication following liver transplantation characterized by arterial insufficiency despite hepatic artery patency. The pathogenesis is driven by maladaptation of the hepatic arterial buffer response (HABR) rather than true steal. This study evaluates the hemodynamic and clinical sequelae of splenic artery embolization (SAE) for NOHAHS. Methods Twelve patients with graft dysfunction without an alternative cause, patent hepatic artery with elevated resistive index (RI) or slow end-diastolic flow, and dominant splenic circulation were included in this single-center retrospective study. Hemodynamic parameters were calculated using Doppler-derived flow measurements, including hepatic artery flow (HAF), portal vein flow (PVF), and HAF:PVF buffer ratios. Hepatic function biomarkers were assessed up to 12 months post-SAE. Results SAE significantly improved HAF (mean HAF: 91.0 ± 58.0 to 162.4 ± 133.4 mL/min; RI: 0.79 ± 0.10 to 0.72 ± 0.09; P < 0.01) while simultaneously reducing PVF (mean PVF: 1768.5 ± 824.4 to 1021.6 ± 520.0 mL/min; P < 0.01), resulting in a 2.7-fold increase in the buffer ratio (HAF:PVF ratio: 0.068 to 0.190; P < 0.01). Sustained improvements in serum bilirubin and albumin were observed after SAE ( P < 0.05). Procedure-related complications included two cases of non-occlusive splenic vein thrombosis and one splenic abscess. Conclusion SAE enhances the HABR via reciprocal modulation of hepatic artery and portal vein inflow to improve graft function in NOHAHS. These findings strengthen the HABR theory of graft inflow modulation and support the effectiveness of SAE as a treatment for NOHAHS in the post-transplant period.

Source: Journal of Liver Transplantation

DOI: 10.1016/j.liver.2026.100347