Surgical anatomy of the left lateral segment as applied to living-donor and split-liver transplantation: a clinicopathologic study.

OBJECTIVE: To evaluate intrahepatic vascular and biliary anatomy of the left lateral segment (LLS) as applied to living-donor and split-liver transplantation. SUMMARY BACKGROUND DATA: Living-donor and split-liver transplantation are innovative surgical techniques that have expanded the donor pool. Fundamental to the application of these techniques is an understanding of intrahepatic vascular and biliary anatomy. METHODS: Pathologic data obtained from cadaveric liver corrosion casts and liver dissections were clinically correlated with the anatomical findings obtained during split-liver, living-donor, and reduced-liver transplants. RESULTS: The anatomical relation of the left bile duct system with respect to the left portal venous system was constant, with the left bile duct superior to the extrahepatic transverse portion of the left portal vein. Four specific patterns of left biliary anatomy and three patterns of left hepatic venous drainage were identified and described. CONCLUSIONS: Although highly variable, the biliary and hepatic venous anatomy of the LLS can be broadly categorized into distinct patterns. The identification of the LLS duct origin lateral to the umbilical fissure in segment 4 in 50% of cast specimens is significant in the performance of split-liver and living-donor transplantation, because dissection of the graft pedicle at the level of the round ligament will result in separate ducts from segments 2 and 3 in most patients, with the further possibility of an anterior segment 4 duct. A connective tissue bile duct plate, which can be clinically identified, is described to guide dissection of the segment 2 and 3 biliary radicles.

Biliary complications of reduced-organ liver transplantation.

Reduced-organ liver transplantation for children is effective in lowering pretransplantation morbidity and mortality. Improvements in surgical technique have reduced vascular complications; however, biliary complications continue to account for significant posttransplantation morbidity. This investigation chronicles the incidence and type of biliary complications encountered with reduced-organ liver transplantation. Retrospective review of reduced-organ liver recipients over a 59-month period was performed, and biliary complications were classified as (1) missed biliary radicle, (2) anastomotic leak requiring revision, and (3) biliary stricture. From July 1992 to May 1997, 42 children received reduced-organ grafts: 32 living-donor, 8 cadaveric-reduced, 1 split-liver, and 1 auxiliary orthotopic liver transplant. Of the 42 grafts, 41 were Couinaud segments II/III and 1 was segments II/III/IV. Ten biliary complications were identified in 9 recipients (24%). Biliary complications included parenchymal radicle leaks, 5 (50%); biliary strictures, 3 (30%); and anastomotic leaks, 2 (20%). Although technical advances have reduced the incidence of biliary complications secondary to organ ischemia, parenchymal radicle leaks continue to be a source of morbidity for reduced-organ recipients. Planned exploration on posttransplantation day 7 was performed on the most recent 26 of the 42 total reduced-organ procedures as a mechanism to identify and treat early technical complications. Planned exploration as a routine component of reduced-organ transplantation has yielded a 15% incidence of discovered parenchymal leaks and a 5% incidence of discovered anastomotic leaks. This series underscores the necessity for improved anatomical studies to correctly identify duct territories and the development of accurate noninvasive methods to assess the biliary system preoperatively and intraoperatively in the application of reduced-organ liver transplantation.

Role for interleukin-1 (IL-1) in benzene-induced hematotoxicity: inhibition of conversion of pre-IL-1 alpha to mature cytokine in murine macrophages by hydroquinone and prevention of benzene-induced hematotoxicity in mice by IL-1 alpha.

Chronic exposure of humans to benzene (BZ), a myelotoxin, causes aplastic anemia and acute leukemia. The stromal macrophage that produces interleukin-1 (IL-1), a cytokine essential for hematopoiesis, is a target of BZ's toxicity. Monocyte dysfunction and decreased IL-1 production have been shown to be involved in aplastic anemia in humans. Hydroquinone (HQ), a toxic bone marrow (BM) metabolite of BZ, causes time- and concentration-dependent inhibition of processing of the 34-Kd pre-interleukin-1 alpha (IL-1 alpha) to the 17-Kd mature cytokine in murine P388D1 macrophages and BM stromal macrophages, as measured by Western immunoblots of cell lysate proteins using a polyclonal rabbit antimurine IL-1 alpha antibody. HQ over a 10-fold concentration range had no effect on the lipopolysaccharide (LPS)-induced production of pre-IL-1 alpha precursor or on cell viability or DNA and protein synthesis. Stromal macrophages obtained from the femoral BM of C57Bl/6 mice exposed to BZ (600 or 800 mg/kg body weight) for 2 days were incapable of processing the 34-Kd pre-IL-1 alpha to the mature 17-Kd cytokine when stimulated in culture with LPS. Stromal macrophages from mice coadministered BZ and indomethacin, a prostaglandin H synthase (PHS) inhibitor that has been shown to prevent BZ-induced myelotoxic and genotoxic effects in mice when coadministered with benzene were able to convert the pre-IL-1 alpha to mature cytokine. Administration of recombinant murine IL-1 alpha (rMuIL-1 alpha) to mice before a dose of BZ that causes severe depression of BM cellularity completely prevents BM depression, most probably by bypassing the inability of the stromal macrophage in BZ-treated animals to process pre-IL-1 alpha to the mature cytokine.