Conjoined unification venoplasty for triple portal vein branches of right liver graft: a case report and technical refinement

Anomalous portal vein (PV) branching of the donor liver is uncommon and usually makes two, or rarely, more separate PV branches at the right liver graft. Autologous PV Y-graft interposition has long been regarded as the standard procedure, but is currently replaced with the newly developed technique of conjoined unification venoplasty (CUV) due to its superior results. Herein, we presented a case of CUV application to three PV openings of a right liver graft. The recipient was a 32-year-old male patient with hepatitis B virus-associated liver cirrhosis. The living liver donor was his 33-year-old sister who had a type III PV anomaly, but the right posterior PV branch was bifurcated early into separate branches of the segments VI and VII, thus three right liver PV branches were cut separately. We used the CUV technique consisting of placement of a small vein unification patch between three PV orifices, followed by overlying coverage with a crotch-opened autologous portal Y-graft. The portal Y-graft was excised and its crotches were incised to make a wide common orifice. Three bidirectional running sutures were required to attach the crotch-opened autologous portal Y-graft. After portal reperfusion, the conjoined PV portion bulged like a tennis ball, providing a wide range of alignment tolerance. The patient recovered uneventfully from the liver transplantation operation. The CUV technique enabled uneventful reconstruction of triple donor PV orifices. Thus, CUV can be a useful and effective technical option for reconstruction of right liver grafts with various anomalous PVs.

An anomalous portal vein crossing the lesser sac and ending at the upper part of ductus venosus / 대한해부학회지

In serial sagittal sections of a fetus on week 9 (crown-rump length, 36 mm), we incidentally found absence of the usual portal vein through the hepatoduodenal ligament. Instead, an anomalous portal vein originated behind the pancreatic body, crossed the lesser sac and merged with the upper part of the ductus venosus. During the course across the lesser sac, the vein provided a deep notch of the liver caudate lobe (Spiegel's lobe). The hepatoduodenal ligament contained the hepatic artery, the common bile duct and, at the right posterior margin of the ligament, and a branch of the anomalous portal vein which communicated with the usual right branch of the portal vein at the hepatic hilum. The umbilical portion of the portal vein took a usual morphology and received the umbilical vein and gave off the ductus venosus. Although it seemed not to be described yet, the present anomalous portal vein was likely to be a persistent left vitelline vein. The hepatoduodenal ligament was unlikely to include the left vitelline vein in contrast to the usual concept.

Left-sided Gallbladder with Intrahepatic Portal Vein Anomalies: A Single Center Experiences

PURPOSE: The goal of this article was to characterize and explain the etiology of a left-sided gallbladders with intrahepatic portal vein anomalies, and these cases of this unusual anatomy were all encountered at a single center. METHODS: We reviewed the movies recorded during surgery, the database information and the preoperative radiologic examinations of 1,141 patients who underwent cholecystectomies at our institution between August 2007 and July 2010 to assess the presence of left-sided gallbladder and its combined anomalies. RESULTS: Four of 1141 patients (0.35%) were diagnosed with left-sided gallbladder. In all the cases, the gallbladder was located on the left side of the falciform ligament, under the left lobe of the liver with typical abnormal intrahepatic portal venous branching. The right posterior portal vein came directly from the main portal vein, and the right anterior portal vein originated from the left portal vein, but the ligamentum teres joined to the left branch of the portal vein in the liver. CONCLUSION: Left-sided gallbladder with intrahepatic portal venous branching anomaly resulted from the defective development of the central portion of the liver rather than from abnormal regression of the left umbilical vein with persistence of the right umbilical vein.