Endovascular management of portal steal syndrome due to portosystemic shunts after living donor liver transplantation

Abstract

Background and Aim: After liver transplant, pre-existent porto-systemic shunts (PSS) may persist, causing "portal steal," leading to graft dysfunction, hepatic encephalopathy (HE), and eventual rejection. In recipients of small-for-size transplant liver grafts, shunts may be created intraoperatively, facilitating diversion of portal flow to systemic circulation to avoid ill-effects of portal overperfusion. These iatrogenic shunts may also subsequently lead to portal steal. We aim to evaluate safety and efficacy of endovascular techniques in management of portal steal due to PSSs in living donor liver transplantation (LDLT) recipients. Methods: Between 2013 and 2020, we encountered five LDLT recipients with large PSS, who presented with graft dysfunction and/or HE. One patient had a surgically created shunt and four had spontaneous shunts, not surgically ligated during transplant. Endovascular techniques including plug-assisted or balloon-occluded retrograde transvenous obliteration (PARTO/BRTO) or covered inferior vena cava (IVC) stent grafts were to occlude these PSS and counter the portal steal in all patients. Technical success and clinical outcomes at 1-year-follow-up were assessed. Results: Imaging showed large PSS causing portal steal syndrome in all five patients. IVC stent graft was used to isolate the shunt in two patients and PARTO/BARTO was performed in three patients. One patient had guarded prognosis due to multiple organ dysfunction and died 5 days after endovascular procedure. At 1-year follow up, graft functions normalized in four patients with no recurrence of HE. No procedurerelated complications were seen. Conclusion: Endovascular techniques can be safely and effectively used to counter portal steal syndrome in LDLT recipients, thus avoiding surgical re-exploration in these patients.

EUS-guided coil placement and cyanoacrylate glue injection for gastric variceal bleeding with obvious spontaneous portosystemic shunts

“…Esophageal and gastric varices can lead to the formation of a gastrorenal or splenorenal shunt, which becomes interlinked with the systemic circulation. [ 18 ] The clinical significance of spontaneous portosystemic shunt formation is that on the one hand, the shunt can share part of the portal vein pressure, whereas on the other hand, gastric variceal bleeding after the formation of the shunt channel increases the risk of ectopic embolization during endoscopic embolization treatment, and the formation of spontaneous portosystemic shunts channel makes the treatment of gastric variceal bleeding very difficult. [ 19 ] A study of 700 patients with cirrhosis combined with portal hypertension demonstrated spontaneous portosystemic shunts in 16.86% of patients (gastrorenal shunt in 7.14% and splenorenal shunt in 8.43%).…”