141Observational cohort study of hepatic encephalopathy after TIPS. . - PDF document

141Observational cohort study of hepatic
141Observational cohort study of hepatic encephalopathy after TIPS. 2017; 16 (1): 140-148 female sex, comorbid diabetes mellitus (DM), non-alcoholic causes of por- ascites as the indication for TIPS,hypoalbuminaemia, high serum creatinine, hepatofugal high Child-Pugh score, high reduced and placing an uncovered stent have all Some of the stud- There has been a call for the predictorsMATERIAL AND METHODSclinical data was carefully sampled to ensure the safety ofUncovered stents were used until 2000, as stentgraftsto patients with longer life expectancy and if the patients TIPS re-TIPS HE was based on close follow up of patients after thepsychometric tests was used. No psychometric tests arepatient stay after the TIPS procedure and outpatient fol-follow up appointments at 3-6 months were made thereaf-ter. This was based on previous reports that most of theFamilies and patients were educated to contact the hepa- and NCSS 9. Statistical significance was test for categorical varia-Routhu M, et al. 2017; 16 (1): 140-148statistically associated with development of hepatic en-RESULTS Descriptive Statistics of quantitative data.MinimumM

aximumMeanUnitsP Value*P ValueAge at TI
aximumMeanUnitsP Value*P ValueAge at TIPS18.383.154.511.6Pre-TIPS Hepatic Venous Pressure0349.74.10.0810.49155430.66.3Pre-TIPS Portal Pressure Gradient64120.65.70.0490.04602913.24.40.0100.04954121.45.40.2440.376Post-TIPS Portal Pressure Gradient1248.43.90.6130.777Diameter of The Stent61410.81.2mm0.5470.837Shunt Length2016081.114.0mm0.8790.145Decompression of Shunt-5279.34.30.1380.038Systolic Blood Pressure501900.8610.548Diastolic Blood Pressure3012073.812.10.3440.471Heart Rate4814283.515.7/min.0.0370.031Sodium104152134.36.10.3950.473Serum Creatinine48740Serum Bilirubin365448.062.00.5900.579Conjugated Bilirubin043834.653.80.9560.566Alanine Aminotransferase4.7564.7 67.447.0U/L0.0100.1855.9588.261.65U/LGamma-Glutamyltransferase12929.8155.9148.9U/L0.0470.1091588.2158.8138.8U/L0.2170.440Total Protein39.997.565.912.1g/L0.5510.807Albumin14.651.930.86.5g/LInternational Normalized Ratio0.3111.50.6N/A0.9980.870Total Cholesterol0.78.13.31.20.4860.962Ammonia730962.540.60.4910.599Pre TIPS Child-Pugh Points5148.32.2N/A0.0200.479 Variables before TIPS. Categorical data.VariableP Value*P 0.4720.8860.381N/A0.6880.520 Non-co0.3020.217Two shunts used0.73

61.0000.1360.737 and Fisher´s exact tes
61.0000.1360.737 and Fisher´s exact test. Significant differences (P )143Observational cohort study of hepatic encephalopathy after TIPS. 2017; 16 (1): 140-148we have grouped the etiology of portal hypertension intoalcoholic, cholestatic, vascular/non-cirrhotic, NAFLD/after TIPS is summarized in Tables 3 and 4. In terms ofcirrhotic patients were HE free after TIPS. On the otherpatients with alcoholic liver disease did develop new HEsample: 895Pre-TIPS Encephalopathy: 66missing data regarding postTIPSEncephalopathy: 125Figure 1. Figure 2. Routhu M, et al. 2017; 16 (1): 140-148 Results of logistic regression.(Percent correctly classified = 68.0%)No HEHETotalNo HE261122383HE75158233Total336280616Model for Refractory Ascites(Percent correctly classified = 62.5%)No HEHETotalNo HE7244116HE284876Total10092192cirrhotic patients were HE free after TIPS and 65% ofpatients with viral hepatitis developed HE after TIPS.DISCUSSIONtance of age, pre-TIPS portal venous pressure, serum The pre- was associated with hepatic This is in concordance withFigure 3. Portal Hypertensive Gastropathy, 25Ascites and Others, 4145Observational coho

rt study of hepatic encephalopathy after
rt study of hepatic encephalopathy after TIPS. 2017; 16 (1): 140-148to confirm that previously reported sex differences indevelopment of HE in small samples were more likelymeet the criteria for NAFLD presents a diagnostic chal- Therefore, As patients suffering with ascites usually have, asease developed new HE after TIPS. This is in contrast We believe, that the likelihood of developing Results of Odds Ratio.Odds RatioConfidence IntervalCholestatic etiology of portal hypertensionIdiopathic liver disease as etiology of portal hypertensionRouthu M, et al. 2017; 16 (1): 140-148other mentioned studies. It is therefore difficult to The higherristics of patients who did, and who did not, develop HEIt merely describes that people with a certain baselineACKNOWLEDGMENTSThe authors would like to thank Mr Christopher West,Honorary Senior Fellow of the Department of PublicHealth and Policy, University of Liverpool, for the valuablestatistical support.ABBREVIATIONS diabetes mellitus. hepatic encephalopathy. transjugular intrahepatic portosystemic shunting.FINANCIAL SUPPORT1.American Association for the Study of Liver Diseases, Eu-ropean

Association for the Study of the Liver.
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01; 48(3):46.Biecker E, Roth F, Heller J, Schild HH, Sauerbruch T, 2007; 19(10): 846-52.Routhu M, et al. 2017; 16 (1): 140-148Observational Cohort Study of Hepatic EncephalopathyAfter Transjugular Intrahepatic Portosystemic Shunt (TIPS) Sunil Kumar Routhu, Tomas Fejfar,Vaclav Jirkovsky, Antonin Krajina, Eva Cermakova, Petr Hulek, Ladislav Hosak*** School of Psychiatry, Health Education Wessex, United Kingdom.Department of Radiology, University Hospital in Hradec Kralove, Czech Republic.Computer Technology Center, Faculty of Medicine in Hradec Kralove, Charles University in Prague, Czech Republic.ORIGINAL ARTICLEINTRODUCTIONliver insufficiency and/or portosystemic shunting; it mani- The pooled estimate of Furthermore, 10%The more severe the HE the smaller the chances ofsurvival.Mexican Association of Hepatology,Latin-American Association for Study of the Liver andManuscript received: Manuscript accepted: DOI:10.5604/16652681.1226932.Introduction and aim. ofand methods. A study Results. 257 tal hypertension contributed to the regression model. Patients age, serum creatinine, presence of diabetes mellitus and portal sion. We Key wor