Portal vein (PV) reconstruction is a key component for success in pediatric liver transplantation (LT). Biliary atresia (BA) often causes the native PV to become sclerotic or hypoplastic, and the… Click to show full abstract
Portal vein (PV) reconstruction is a key component for success in pediatric liver transplantation (LT). Biliary atresia (BA) often causes the native PV to become sclerotic or hypoplastic, and the portal venous flow (PVF) may decrease, whereas the collateral vessels develop and provoke a further decrease in the PVF. This negative spiral in PV circulation can complicate PV reconstruction at the time of LT. There have been several technical refinements reported in previous studies, including vein graft interposition and longitudinal venoplasty. However, aside from the techniques of PV reconstruction, collateral interruption and sufficient PVF are crucial issues that can affect the initial graft function. At the end of April 2016, we had performed 403 LTs in 389 recipients (living donor liver transplantation [LDLT], n 5 379; deceased donor LT, n 5 20; domino LT, n 5 4). PV complications occurred after LT in 23 (5.7%) patients, including PV thrombus in 4 (1.0%) and PV stricture in 19 (4.7%). Notably, 18 (4.5%) patients required reanastomosis due to intraoperative PV thrombosis, which occurred after primary PV reconstruction. Intraoperative PV thrombosis might occur due to insufficient PVF with incomplete interruption of the collaterals or inappropriate decision making with regard to the technique of PV reconstruction, especially the use of the sclerotic native PV without any technical modifications.
               
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