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  • Title: Optimal central venous pressure during the neohepatic phase to decrease peak portal vein flow velocity for the prevention of portal hyperperfusion in patients undergoing living donor liver transplantation.
    Author: Ryu TH, Jung JY, Choi DL, Han YS, Kim JD, Kim JH.
    Journal: Transplant Proc; 2015 May; 47(4):1194-8. PubMed ID: 26036552.
    Abstract:
    BACKGROUND: The association between intraoperative systemic hemodynamic status and preventing portal hyperperfusion, which induces shear stress on the sinusoidal endothelial cells of liver grafts, resulting in poor graft function in live-donor recipients, has not been identified. This study evaluates the effects of systemic hemodynamic parameters (SHPs) during the neohepatic phase on changes in hepatic hemodynamic parameters (HHPs) between the neohepatic phase and the 1st postoperative day. METHODS: Thirty-eight patients undergoing living donor liver transplantation (LDLT) were enrolled in this study. HHPs (flow velocities of portal vein and hepatic artery) were measured immediately after hepatic artery and bile duct reconstruction and on the first postoperative day. SHPs (mean arterial pressure, central venous pressure [CVP], cardiac index, stroke volume variation, stroke volume index, systemic vascular resistance index, and central venous oxygen saturation) were recorded and averaged for 5 minutes after the measurement of HHPs. The relationships between the SHPs and HHPs were assessed using linear or quadratic regression analysis. RESULTS: Peak portal vein flow velocity (PVV) decreased on the 1st postoperative day in 24 patients (63%). There was an inverted-U relationship between CVP and the percentage change in PVV (R(2) = 0.241, P = .008). According to the quadratic regression model, the PVV maximally decreased at a CVP of 7.8 mm Hg. No significant correlations were found between the other SHPs and HHPs. CONCLUSIONS: Maintaining CVP (approximately 8 mm Hg) during the neohepatic phase was clinically beneficial in decreasing PVV to prevent portal hyperperfusion in the early postoperative period of LDLT.
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