Venous outflow reconstruction in living-donor liver transplantation for Budd-Chiari syndrome involving vena cava

Abstract

Ironically, the hepatic vena cava is mostly involved in Budd-Chiari syndrome in the Asia-Pacific region, whereas living-donor liver transplantation is predominant, which cannot replace the hepatic cava. Hata and colleagues introduced a new surgical technique for venous reconstruction in living-donor liver transplantation, providing a novel solution to this longstanding dilemma.

FIGURE 1

Schematic illustration of our surgical technique. (a) The pericardium is opened, in which the IVC root is taped and secured. Then the congested liver is excised en bloc with the hepatic IVC under veno‐venous (VV)‐bypass assistance as needed (VV‐bypass is sometimes unnecessary in chronic BCS with well‐developed collaterals, typically azygos and/or hemiazygos veins). To prevent splanchnic congestion, the portal vein is also cannulated to return the splanchnic venous outflow to the superior vena cava via VV‐bypass. (b) On a back‐table, the hepatic cava is isolated/retrieved from the explanted liver. (c) After examining the lesion from the outside, the cava is everted and also scrutinized from the luminal side. After resecting the diseased portion and then returning the inside/outside eversion, only the healthy part of auto‐IVC graft is harvested. (d) Further, to make doubly sure, the cranial side is inverted inferiorly, and the originally caudal end of the auto‐cava, that is, the part farthest from the BCS lesions, is anastomosed to the IVC root in the pericardium or directly to the right atrium if the IVC root is affected. (e) Then the liver graft is put‐in, and the HV is anastomosed to the healthy auto‐transplanted cava in an end‐to‐side fashion. The remaining gap of IVC is interposed with an artificial graft, if necessary. BCS, Budd–Chiari syndrome; HV, hepatic vein; IVC, inferior vena cava.

FIGURE 2

Pre‐ and intraoperative images of the IVC lesion and reconstruction. (a, b) Early/arterial and delayed/venous phases of coronal scan images, respectively, of the preoperative dynamic CT focusing on the IVC lesion. In this case, the IVC lesion was more clearly delineated in the early rather than delayed phases, but not enough to completely identify all the lesions. (c) A representative image showing IVC inspection from inside the vessel (lumen side). Under good direct vision on a back‐table, the lesions, for example, obliterated, thrombosed, fibrotic, or even just thickened, can be easily and reliably identified. (d) An image representing IVC reconstruction using the harvested auto‐IVC graft, corresponding to Figure 1d. In this case, a ringed expanded polytetrafluoroethylene (ePTFE) graft was used for IVC interposition. (e) An image displaying HV anastomosis of a right hemi‐liver graft to the auto‐transplanted cava using continuous suture with 5–0 prolene. It is also important to open the IVC wide enough to create a large anastomotic orifice extending halfway around the right (graft) side. This procedure intrinsically reduces the potential risk of post‐transplant BCS recurrence by using the autologous IVC that is confirmed healthy from both inside and outside the vessel. Furthermore, to ensure extra safety, the cranial and caudal ends of the harvested auto‐IVC are reversed, and the originally caudal end, which is farthest from the BCS lesion and thus considered the healthiest, is anastomosed to the IVC root in the pericardium, that is, the most downstream anastomosis. The patient was discharged 3 weeks post‐transplant with no surgical complications. She has been doing well for 2 years afterward with no BCS recurrence. BCS, Budd–Chiari syndrome; CT, computed tomography; HV, hepatic vein; IVC, inferior vena cava.