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Total Hilar Exposure Maneuver for Repair of Complex Bile Duct Injury.

ABSTRACT: The reconstruction of high-level bile duct injury is challenging because exposure of the hilar area is limited and sometimes inaccessible by the Hepp-Couinaud approach. We describe a maneuver for total hilar exposure to perform complex bile duct injury reconstruction. After adhesions surrounding the liver are divided, intraoperative ultrasonography is used to delineate the hilar and intrahepatic biliary anatomy. Surgical exposure of the biliary system is achieved by our maneuver, which consists of four steps: (1) identification of landmark structures, such as the base of the umbilical fissure, the inferior edge of segment 4b, the cystic-hilar plate junction, and the right anterior portal pedicle; (2) lowering of the hilar plate; (3) hepatotomy along the right anterior pedicle; and (4) connection of the hepatotomy to the base of segment 4b. This maneuver allows the liver to be flipped upward, which facilitates clear exposure of the hilar duct and preserves the liver parenchyma. The anterior parts of the right and left hepatic duct are then opened, a wide-hepaticojejunostomy anastomosis is achieved for biliary reconstruction, and a jejunal subcutaneous limb is created. We used this maneuver for treating complex bile duct injury in six cases; none of the patients has died, and two had Clavien-Dindo grade III complications, including surgical site infection and intra-abdominal collection. The total hilar exposure maneuver is thus feasible and safe. It provides excellent exposure of both hepatic ducts and is a good surgical alternative to the Hepp-Couinaud approach in cases of high-level injury.

SUBMITTER: Wiboonkhwan NA

PROVIDER: S-EPMC8786702 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Mechanisms of the proliferation of liver are mainly studied in animal model of liver regeneration after partial hepatectomy (PH). However, the PH model involves complex regeneration mechanisms, including hemodynamic factors, cytokines, growth factors, and metabolites. Among liver metabolites, bile acid (BA) is a key signaling molecule that regulates liver regeneration. This study aimed to establish a new type of rapid liver hyperplasia model induced mainly by bile acid pathway through hepatoenteral circulation with hilar bile duct ligation (HBDL). We first established the HBDL model by ligating the bile duct of all hepatic lobes but the right lateral lobe in rabbits and compared with the PVL model and sham operation group. Changes in the liver lobe and hemodynamics were observed. Liver function and the bile acid level were also analyzed. Then we verified the HBDL model in mice. Liver function and the levels of bile acids and cytokines were tested. The protein and mRNA levels of FXR, FGF15, CYP7A1 and FoxM1b in liver tissue were also analyzed. After hilar ligation of the biliary tract, the unligated liver lobes proliferated significantly. Compared with those in the sham group, the volume and weight of the unligated right lateral lobe of the liver in the HBDL group and the PVL group increased significantly (P < 0.05). Transient liver function impairment occurred both in the HBDL group and PVL group in the rabbit model as well as the mouse models. The bile acid levels in the HBDL groups of the rabbit model and mouse model increased significantly within first week after surgery (P < 0.05). The immunohistochemistry results confirmed the proliferation of hepatocytes in the unligated liver lobe. Compared with those in the sham group, the levels of FXR, FGF15 and FoxM1b in the HBDL group were significantly increased (P < 0.05), while the expression of CYP7A1 was inhibited. Compared with those in the HBDL group, the postoperative hemodynamic changes in the PVL group were significant (P < 0.05). The levels of IL-6 and TNF-α in the HBDL group were higher than those in the sham group. The HBDL model is simple to establish and exhibits good surgical tolerance. The model has definite proliferative effect and strong specificity of bile acid pathway. This is an ideal animal model to study the mechanism of liver regeneration through bile acid pathway.

Project description:Background and aimsIn extrahepatic bile duct (EHBD) cholangiopathies, including primary sclerosing cholangitis, a reactive cholangiocyte phenotype is associated with inflammation and epithelial hyperproliferation. The signaling pathways involved in EHBD injury response are poorly understood. In this study, we investigated the role of Hedgehog (HH) signaling and its downstream effectors in controlling biliary proliferation and inflammation after EHBD injury.Approach and resultsUsing mouse bile duct ligation as an acute EHBD injury model, we used inhibitory paradigms to uncover mechanisms promoting the proliferative response. HH signaling was inhibited genetically in Gli1-/- mice or by treating wild-type mice with LDE225. The role of neutrophils was tested using chemical (SB225002) and biological (lymphocyte antigen 6 complex locus G6D [Ly6G] antibodies) inhibitors of neutrophil recruitment. The cellular response was defined through morphometric quantification of proliferating cells and CD45+ and Ly6G+ immune cell populations. Key signaling component expression was measured and localized to specific EHBD cellular compartments by in situ hybridization, reporter strain analysis, and immunohistochemistry. Epithelial cell proliferation peaked 24 h after EHBD injury, preceded stromal cell proliferation, and was associated with neutrophil influx. Indian HH ligand expression in the biliary epithelium rapidly increased after injury. HH-responding cells and neutrophil chemoattractant C-X-C motif chemokine ligand 1 (CXCL1) expression mapped to EHBD stromal cells. Inhibition of HH signaling blocked CXCL1 induction, diminishing neutrophil recruitment and the biliary proliferative response to injury. Directly targeting neutrophils by inhibition of the CXCL1/C-X-C motif chemokine receptor 2/Ly6G signaling axis also decreased biliary proliferation.ConclusionsHH-regulated CXCL1 orchestrates the early inflammatory response and biliary proliferation after EHBD injury through complex cellular crosstalk.

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Total Hilar Exposure Maneuver for Repair of Complex Bile Duct Injury.

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