Approach to anatomic variations of the graft portal vein in right lobe living-donor liver transplantation.

Right lobe living-donor liver transplantation (LDLT) is often not attempted in donors with anomalous portal venous branching (APVB). The authors describe their experience with portal vein (PV) reconstruction in 17 cases of APVB in right lobe LDLT. From July 1997 to December 2001, 214 right liver LDLT were performed at the Asan Medical Center. Seventeen of the donors had APVB and successfully underwent right lobectomy. The APVB were type II (trifurcation) in nine cases, type III (independent posterior segmental branching from main PV trunk) in seven, and unclassified in one. All 17 donors and recipients are alive, with good liver function. In type II APVB, the donor PV branches were obtained with separate openings that were joined as a common orifice at the back table in two, with a discoid-patch single opening in four, and with one common opening in three. In type III APVB, the donor PV were divided with two openings in four and with a discoid-patch single opening in three. The discoid-patch defect in the remnant PV was repaired with a vein patchplasty in two donors and resected with end-to-end anastomosis in five. However, one donor developed portal vein thrombosis (PVT) that was managed successfully by re-exploration and insertion of a metallic vascular stent. Of the four type III APVB obtained with two separate PV openings, the first two liver grafts were each reconstructed as double PV anastomoses. One of them required re-exploration because of PVT. In the two succeeding cases, a Y-graft interposition technique using a cryopreserved cadaveric iliac vein or the recipient's own portal confluence was successfully applied. To minimize the risk of PVT in donors with APVB, discoid-patch excision followed by repair with vein patchplasty or segmental resection should be avoided. Individual division of the PV branches creating two separate openings instead is recommended. To decrease the recipient's risk of PVT, interposition Y-graft venous reconstruction at the back table is superior to double PV anastomoses.

Safety of anti-hepatitis B core antibody-positive donors for living-donor liver transplantation.

Serologic evidence of resolved hepatitis B virus (HBV) infection (HBV surface antigen negative, anti-HBV core antibody [HBc] positive) in a liver donor can be regarded as an occult infection with episomal HBV in the liver. The purpose of this study was to evaluate the safety of anti-HBc-positive living donors. Between March 2001 and January 2002, 127 donors underwent hepatectomy for living-donor liver transplantation at Asan Medical Center. They were classified as members of an anti-HBc-positive group (n=50) or an anti-HBc-negative group (n=77). The two groups were subdivided into right lobectomy (n=86) and left lobectomy (n=34) groups to compare operative risk. Perioperative clinical profiles were compared by anti-HBc status and extent of donor hepatectomy. There were no statistical differences of preoperative liver function and liver steatosis between the anti-HBc-positive and anti-HBc-negative groups. Operation time and blood loss did not show any differences between the hepatectomy-matched anti-HBc-positive and anti-HBc-negative groups. Postoperative recovery of liver function, incidence of complication, and regeneration rate of the remnant liver after right lobectomy also did not show significant differences. The anti-HBc-positive group did not exhibit any adverse preoperative, intraoperative, or postoperative outcomes compared with the anti-HBc-negative group. This indicates that anti-HBc-positive donors can be assessed to have the same degree of risk for donor operation as anti-HBc-negative donors.

Transjugular intrahepatic portosystemic shunt for intractable posthepatectomy ascites.

We report two cases of transjugular intrahepatic portosystemic shunt for control of intractable ascites after resection of cirrhotic livers. The first case was a 46-year-old male who had undergone right lobectomy of the liver for a small hepatocellular carcinoma. His liver function had recovered within a week after the operation, but ascites drainage of 1-4 L/day persisted for more than a month despite vigorous medical therapy. We performed transjugular intrahepatic portosystemic shunt on the 49th postoperative day and the pressure gradient between the right atrium and the left portal vein was reduced to from 21 mmHg to 6 mmHg. Thereafter, ascites became responsive to diuretic therapy and was well controlled without complication. Second case of a 54-year-old male patient who had undergone left lateral segmentectomy due to a small hepatocellular carcinoma presented intractable ascites of 1-3 L/day, which was also effectively controlled after transjugular intrahepatic portosystemic shunt performed on the 34th postoperative day, though there was an episode of hepatic encephalopathy stage 1. Based on our limited experience, hepatectomized patients suffering from prolonged intractable ascites despite a favorable profile of liver function may be candidates for transjugular intrahepatic portosystemic shunt with an acceptable risk of hepatic failure and procedure-related complication.

A case of primary non-function following adult-to-adult living donor liver transplantation.

We report a case of primary non-function of graft liver following adult-to-adult living donor liver transplantation. The recipient was a 43-year-old male with hepatitis B-associated liver cirrhosis. The donor was a 28-year-old brother of the recipient. We transplanted a left lobe graft from the donor weighing 550 g, in which 20% macrovesicular steatosis was observed. Total ischemic time was less than 40 minutes. The recipient presented a marked impairment of coagulation profile and marked elevation of liver enzymes without any evidence of flow disturbance of the liver vessels, which was very similar to the clinical course of primary non-function following cadaveric donor liver transplantation. We performed retransplantation using a cadaveric whole liver graft on the second day after the initial operation and the recipient survived without any complications. A resected graft liver specimen showed total necrosis of hepatocytes without intravascular thrombosis. We concluded that failure of the living donor graft was due to primary non-function occurring in the adult recipient.