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A High Portal Venous Pressure Gradient Increases Gut-Related Bacteremia and Consequent Early Mortality After Living Donor Liver Transplantation

Yao, Siyuan, MD1; Yagi, Shintaro, PhD1; Uozumi, Ryuji, MS2; Iida, Taku, PhD3; Nagao, Miki, PhD4; Okamura, Yusuke, PhD1; Anazawa, Takayuki, PhD1; Okajima, Hideaki, PhD1; Kaido, Toshimi, PhD1; Uemoto, Shinji, PhD1

doi: 10.1097/TP.0000000000002047
Original Clinical Science—Liver

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.

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.

1 Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

2 Department of Biomedical Statistics and Bioinformatics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

3 Department of Organ Transplant and Regenerative Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.

4 Department of Infection Control and Prevention, Kyoto University Hospital, Kyoto, Japan.

Received 22 June 2017. Revision received 22 October 2017.

Accepted 3 November 2017.

The authors declare no funding or conflicts of interest.

S.Y. and S.Y. designed the study and wrote the draft. S.Y., T.I., and Y.O. acquired the data. M.N. analyzed the data as a specialist of infection prevention. R.U. analyzed the data as a specialist of medical statistician. S.Y., T.I., Y.O. T.A., H.O., T.K., and S.U. performed living-donor liver transplantations, and followed up the patients. M.N., T.A., H.O., T.K., and S.U. contributed to editing the article. S.U. supervised the study design and revised the article.

Correspondence: Shintaro Yagi, PhD, Department of Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. (shintaro@kuhp.kyoto-u.ac.jp).

Supplemental digital content (SDC) is available for this article. Direct URL citations appear in the printed text, and links to the digital files are provided in the HTML text of this article on the journal’s Web site (www.transplantjournal.com).

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