A High Portal Venous Pressure Gradient Increases Gut-Related Bacteremia and Consequent Early Mortality After Living Donor Liver Transplantation. Issue 4 (April 2018) - Yao, Siyuan
Abstract : Background: Portal hypertension (PHT) is defined as a portal venous pressure gradient (PVPG) exceeding 5 mm Hg, which results in severe clinical manifestations. However, the validity of intraoperative PVPG monitoring and the association between PHT and bacterial translocation after liver transplantation remain unclear. Methods: In this retrospective study, 223 patients who underwent primary adult-to-adult living donor liver transplantation from 2008 to 2015 were divided into 2 groups based on the PVPG at the end of the operation: high PVPG (>5 mm Hg, n = 69) and low PVPG (⩽5 mm Hg, n = 154). The clinical factors were compared between the groups, and the association between a high PVPG and posttransplant bacteremia/bacterial infections was investigated. Results: The high PVPG group had a significantly higher incidence of bacteremia (46% vs 24%, P < 0.001), higher 90-day mortality rate (20% vs 7%, P = 0.002), and poorer 1-year survival (71% vs 86%, P = 0.006). The high PVPG group had a particularly higher incidence of bacteremia caused by "gut bacteria" including Enterobacteriaceae, Bacteroides spp., and Enterococcus spp. (29% vs 12%, P = 0.003). Multivariate analysis showed that a PVPG greater than 5 mm Hg (odds ratio, 2.55; 95% confidence interval, 1.18-5.55; P = 0.017) was an independent predictor of bacteremia due to gut bacteria. Conclusions: Monitoring of the PVPG is clinically meaningful for predicting patients' prognosis. In particular, a high PVPG with a threshold of 5 mm Hg at the end of adult-to-adult living donor liver transplantation may increase gut-related bacteremia through the mechanism of bacterial translocation, resulting in early mortality. Abstract : This study identifies a correlation between portal vein gradient and bacterial translocation. This evidence is supportive of the hypothesis that inflammation and impaired host defenses of the small or stressed liver contributes to the pathology of "small for size" syndrome. Supplemental digital content is available in the text.