Unusual venous collateral pathways allow for reperfusion of the intrahepatic portal venous system in children with portal vein thrombosis after split liver transplantation: Clinical relevance and management implications

Abstract

PVT is the most frequent vascular complication after LT in small children, and a higher incidence has been observed in those transplanted for biliary atresia or with a LLSG. Thrombosis of the PV causes extrahepatic portal hypertension and is associated with splenomegaly and the development of venous neo‐collaterals, including gastro‐oesophageal varices and splenorenal shunts. It has also been incidentally suggested in the literature that patients who have had a Roux‐en‐Y loop for a biliary reconstruction may present with a cavernomatous transformation of the distal portion of the loop. In this study, 13 children with CEPH caused by thrombosis of the PV after LT were analysed. The study evidenced the development of two types of hepatopetal venous networks: (a) a large cavernoma along the Roux loop and around the biliary anastomosis, and (b) a network of neo‐collaterals in the gastro‐duodeno‐pancreatic area that connected to the intrahepatic portal branches directly through the liver capsule. These hepatopetal venous networks between the venous system of the surrounding organs or the omentum and the intrahepatic portal branches can be identified by radiologists. The relevance for the transplanting physician and the transplant surgeon is discussed.

Imaging findings of hepatocellular carcinoma with portal vein tumor thrombosis secondary to hepatic portal vein collateral circulation: a cross-sectional study

“…There was only one such collateral vessel in all the patients enrolled, and the incidence rate was only 1.41%, accounting for 0.8% of all the hepatic portal collateral vessels found. This may be related to the vascular variation of patients' abdominal veins or the operation involving the juxtaposition of the abdominal structure (drained by the systemic veins) and the intestinal tract (drained by the portal vein tributaries), all of which may lead to the formation of hepatic collateral circulation (20) in patients with PVTT at abnormal sites.…”