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      Comparison of the Postoperative Liver Function Between Total Intravenous Anesthesia and Inhalation Anesthesia in Patients with Preoperatively Elevated Liver Transaminase Levels: A Retrospective Cohort Study

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          Abstract

          Background

          Anesthesia and surgery may deteriorate liver function in patients with elevated liver enzyme levels; therefore, in these patients, choosing anesthetics with less hepatotoxicity is important.

          Methods

          This retrospective study investigated the effect of total intravenous anesthesia (TIVA) versus inhalation anesthesia (INHA) on the postoperative liver function in patients with preoperatively elevated liver enzyme levels (aspartate transaminase [AST] or alanine transaminase [ALT] >40 U/L) who underwent non-hepatic surgery under general anesthesia. We compared the changes in enzyme levels within 24 hrs before and after surgery.

          Results

          In 730 patients (TIVA: n=138; INHA: n=592), the baseline characteristics were comparable, except for higher comorbidity rates in the TIVA group. The median anesthesia and operation times were significantly longer in the TIVA group because approximately 50% of the TIVA group (vs 19.7% of the INHA group) underwent neurosurgery, which had a relatively longer operation time than other surgeries. Intraoperative hypotensive events and vasopressor use were more frequent in the TIVA group. After 1:4 propensity score matching (TIVA: n=94; INHA: n=376), the baseline characteristics and surgical variables were comparable, except for longer anesthesia time. Before matching, postoperative AST and ALT changes were significantly lower in the TIVA group than in the INHA group. After matching, only the ALT change was significantly lower after TIVA than after INHA [median (interquartile range), −16.7 (−32 to −4) % vs −12.0 (−28.6–6.5) %, P=0.025].

          Conclusion

          TIVA may be safer for patients with preoperatively elevated liver transaminase levels.

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          Most cited references 33

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          Strategies for safer liver surgery and partial liver transplantation.

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            Morbidity and Mortality in Cirrhotic Patients Undergoing Anesthesia and Surgery

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              Progressive necrosis after hepatectomy and the pathophysiology of liver failure after massive resection.

              Mortality after hepatectomy in rats increases markedly beyond the classic 2/3 resection from which complete recovery is the rule. Because an extremely small hepatocyte population can theoretically sustain life, we hypothesize that lethal liver failure after subtotal resection could be due to progressive injury occurring in the remnant liver. The obligatory increase in portal blood through the small remnant may be central to the pathogenesis because of sinusoidal injury and Kupffer's cell activation. To test this hypothesis an experimental study in rats was undertaken to characterize liver cell injury after lethal (85%) and nonlethal (70%) hepatectomy. One hundred thirty Wistar rats were divided into three groups: control group (Sham laparotomy, n = 30), 70[5] hepatectomy group (n = 50), and 85% hepatectomy group (n = 50). Five rats in each group were killed for blood and liver collections from 15 minutes to day 14 after hepatectomy. Survival, histologic characteristics, serum activities of aspartate (AST) and alanine (ALT) aminotransferases and arginase were determined; serum level of tumor necrosis factor-alpha (TNF-alpha) and plasma level of prostaglandin E2 (PGE2) were measured by enzyme-linked immunosorbent assay. Whatever the extent of resection, hepatic injury, as demonstrated by increased serum levels of arginase, ALT, and AST, was observed. The kinetics of arginase release after hepatectomy mimicked quite well those of AST and ALT, representing a reliable marker of hepatocyte injury. A significantly higher, more prolonged blood release of enzymes was observed after 85% hepatectomy than after 70% hepatectomy. Because of a very short half-life the rise in arginase several hours after hepatectomy seems to indicate ongoing liver damage distinct from the surgical injury. Significant elevations of TNF-alpha were detected that were much more severe after 85% hepatectomy. PGE2 levels that increased significantly after 70% resection remained depressed after 8% hepatectomy. Light microscopy demonstrated extensive patchy necrosis after 85% hepatectomy. A pattern of progressive necrosis of the remnant liver was identified with Kupffer's cell dysfunction. We hypothesize that failure of down-regulation of TNF-alpha production by PGE2 could contribute to the pathophysiology of liver injury in the remnant after massive hepatectomy. These events may be initiated in part by the dramatic increase of portal flow through a too small remaining liver, and a pathologic mechanism may be amenable to pharmacologic manipulation.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                TCRM
                tcriskman
                Therapeutics and Clinical Risk Management
                Dove
                1176-6336
                1178-203X
                05 April 2020
                2020
                : 16
                : 223-232
                Affiliations
                [1 ]Department of Anesthesiology and Pain Medicine, Korea University Guro Hospital, Korea University College of Medicine , Seoul, Republic of Korea
                Author notes
                Correspondence: Byung Gun Lim Email bglim9205@korea.ac.kr
                Article
                248441
                10.2147/TCRM.S248441
                7147612
                © 2020 Oh et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 2, Tables: 3, References: 36, Pages: 10
                Funding
                This work was supported by a Korea University Guro Hospital Grant (O1903961).
                Categories
                Original Research

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