Thromboelastometry in patients with advanced chronic liver disease stratified by severity of portal hypertension

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ORIGINAL ARTICLE

Thromboelastometry in patients with advanced chronic liver disease stratified by severity of portal hypertension Pierre Raeven1 · Joanna Baron‑Stefaniak1 · Benedikt Simbrunner2,3 · Alexander Stadlmann2,3 · Philipp Schwabl2,3 · Bernhard Scheiner2,3 · Eva Schaden1 · Ernst Eigenbauer4 · Peter Quehenberger5 · Mattias Mandorfer2,3 · David Marek Baron1 · Thomas Reiberger2,3  Received: 20 June 2020 / Accepted: 6 September 2020 © The Author(s) 2020

Abstract Background  Rotational thromboelastometry (ROTEM) has been studied in patients with advanced chronic liver disease (ACLD) without considering the impact of portal hypertension. We evaluated the influence of the hepatic venous pressure gradient (HVPG) on ROTEM results in patients with ACLD. Methods  Cross-sectional study; ACLD patients undergoing HVPG measurement within the prospective Vienna Cirrhosis Study (NCT03267615) underwent concomitant ROTEM testing. Results  Among 159 patients (68% male; Child–Pugh-A: 53%, Child–Pugh-B: 34%, Child–Pugh-C: 13%), 21 patients (13%) had a HVPG between 6 and 10 mmHg, 84 patients (53%) between 10 and 19 mmHg, and 54 patients (34%) ≥ 20 mmHg. Child–Pugh-C patients (vs. Child–Pugh-A and vs. Child–Pugh-B patients, respectively) showed longer clot formation time (CFT: median 187 s vs. 122 s vs. 122 s, p = 0.007) and lower maximum clot firmness (MCF: median: 45 mm vs. 56 mm vs. 56 mm, p = 0.002) in extrinsic thromboelastometry (EXTEM), while platelet counts were similar across Child–Pugh stages. In the overall cohort, ROTEM parameters did not differ by severity of portal hypertension. However, among compensated Child–Pugh-A patients, MCF decreased with increasing portal pressure, i.e. in higher HVPG strata (HVPG 9–10 mmHg: median MCF: 59 mm vs. HVPG 10–19 mmHg: 56 mm vs HVPG ≥ 20 mmHg: 54 mm, p = 0.023). Furthermore, patients with short CFT and high MCF in EXTEM had higher levels of lipopolysaccharide-binding protein, C-reactive protein, and procalcitonin, as well as higher leukocyte counts (all p  15 kPa, HVPG > 5 mmHg, or histologic F3/F4 fibrosis) and written informed consent. Data sets collected from 336 patients between June 2017 and May 2019 were screened. Exclusion criteria

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Hepatology International

were missing/inconclusive HVPG measurements, missing ROTEM results, presence of acute decompensation, severe alcoholic hepatitis, acute-on-chronic liver failure, hepatocellular carcinoma, liver metastasis, congestive heart failure, previous liver transplantation or transjugular intrahepatic portosystemic shunt. Finally, 159 patients were included in the current study. Patients under non-selective beta-blockers (NSBB) treatment (n = 30) were included in the analysis, as we expected a limited effect of NSBB on ROTEM. NSBB were paused in 26 patients 5 days prior to HVPG measurement. The interruption of NSBB treatment for baseline HVPG measurement is a routine clinical practice at our institution, we are not aware of any bleeding events that occurred in this context. The safety of this approach is also supported by pr