Mo1238 Thromboelastography for Predicting Differences in Cirrhosis-Associated Coagulopathy

AGA Abstracts

Mo1237

Mo1239

Patient-Reported Health-Related Quality of Life Outcomes Independently Predict Death, Transplant, Hospitalization and Hepatic Encephalopathy in Cirrhosis Kavish Patidar, Leroy R. Thacker, James B. Wade, Melanie B. White, Ariel Unser, Edith A. Gavis, James Hovermale, Richard K. Sterling, R. Todd Stravitz, Douglas M. Heuman, Arun J. Sanyal, Mohammad S. Siddiqui, Puneet Puri, Velimir A. Luketic, Scott C. Matherly, Jasmohan S. Bajaj

Inpatient-Onset Primary Esophageal Variceal Hemorrhage: Risk Factors and Mortality Bradley Confer, Mohannad Dugum, Thimmaiah G. Theethira, Ibrahim A. Hanouneh, Rocio Lopez, Nizar N. Zein Background: Hemorrhage from esophageal varices (EV) is a leading cause of mortality in patients with cirrhosis. Limited data is available on the risk factors and specific mortality related to inpatient-onset primary esophageal variceal hemorrhage (IOPEVH). As with other conditions occurring in the inpatient setting, we hypothesize that IOPEVH would have higher mortality despite the potential quicker time to therapy. Aim: Determine the incidence, risk factors and mortality associated with IOPEVH. Methods: A historic cohort study evaluating cirrhotic patients with medium to large EV and no prior history of EV hemorrhage. IOPEVH was defined as EV hemorrhage within the first 48 hours of hospital admission. Three groups of patients were identified: 1- IOPEVH, 2- other forms of EV hemorrhage 3no hemorrhage. All patients were followed from sentinel endoscopy to liver transplant, last follow-up or death. Univariable competing risks analysis was used to assess factors associated with EV hemorrhage including IOPEVH. A survival analysis was performed to assess differences between the three groups. Results: A total of 238 patients were included in the study. Average age was 53 years, 72% were male, mean MELD score was 14, 63% were on betablockers and 41% were on rifaximin. 7.6% had EV hemorrhage and 4% had IOPEVH. The three groups had no significant differences in rates of beta-blocker use, EV banding and time from banding to hemorrhage. Specific risk factors for IOPEVH included female gender and higher MELD, INR and bilirubin. Importantly, patients with IOPEVH had a significantly lower 5-year survival rate (11%) than patients with other forms of EV hemorrhage (67%) (p=0.001) and those with no hemorrhage (92%) (p<0.001) (Figure 1). Conclusion: Cirrhotic patients who experience IOPEVH have a higher 5-year mortality rate compared to cirrhotics patients with other forms of EV hemorrhage and those who do not hemorrhage. Prospective clinical trials are needed to confirm these results and guide therapeutic strategies.

Patient-reported outcomes such as the measures of health-related quality of life (HRQOL) in PROMIS (Patient Reported Outcomes Measurement Information System) tools are important to evaluate effectiveness of treatments. However their additive role in predicting outcomes in cirrhosis beyond current prognostic models is unclear. Aim: Analyze the additive impact of PROMIS HRQOLtools in predicting time to death/transplant, all hospitalizations and hepatic encephalopathy (HE)-related hospitalizations in cirrhosis.Methods: Outpt cirrhotics were administered PROMIS computerized tools for 11 domains (anger, anxiety, depression, physical function, pain behavior & impact, sleep & wake disturbances and social activities & roles). PROMIS scores, MELD score, HE status, age, sex & alcoholic cirrhosis etiology were then entered into a Cox-regression model for times to composite death/transplant, nonelective hospitalizations & HE-related hospitalization. To analyze additive impact of PROMIS scores beyond HE, a separate PROMIS+HE only model was studied for the same outcomes. Results: 207 cirrhotics (57 yrs, MELD 12, 64% men, 29% HE, 44% HCV, 18% alcohol, 24% NASH) were enrolled. HE pts had a higher MELD (16 vs 10, p<0.0001) & were impaired on all PROMIS tools (p<0.001) compared to no-HE pts except anger, anxiety & depression. Follow-up: Pts were followed for 38mths (IQR 22-47 mths), during which 35% had death/transplant (20% transplant/15% died), 33% were hospitalized & 12% were hospitalized for HE. Model with all variables: Time to death/transplant: HE, MELD & 4 PROMIS domains (Anger, fatigue, pain behavior & wake disturbances) were significantly predictive. Time to hospitalization: MELD with 2 PROMIS domains (Anger, Physical function) were predictors. Time to HE-related hospitalization: MELD, Anger, depression, sleep & wake disturbances were predictive. Age, gender & alcohol etiology were not predictors for any outcome.HE+PROMIS model: Time to death/transplant: HE with anger, fatigue, physical function, pain behavior & wake disturbance were predictors. Time to hospitalization: HE, anger, depression, pain impairment & physical function. Time to HE-hospitalization: HE, anger, depression, sleep & wake disturbances were predictive. Thus PROMIS results add to prognostication provided by HE alone.Conclusions: Patient reported HRQOL outcomes add to current prognostic models in cirrhosis since PROMIS results are associated with development of death/transplant & hospitalizations independent of HE status & liver disease severity. Inclusion of patient-reported outcomes could improve our study of cirrhosis research effectiveness and encourage inquiry into HRQOL issues. Mo1238 Thromboelastography for Predicting Differences in Cirrhosis-Associated Coagulopathy Robert Cheng, Ria Kanazaki, Nicholas A. Shackel, Geoffrey W. McCaughan Background Thromboelastography (TEG) is used to predict blood transfusion requirements in liver transplant surgery. It measures viscoelastic properties of blood during different phases of coagulation. Although cirrhotic patients are coagulopathic, some paradoxically develop thrombosis. We assessed coagulation properties of cirrhotic patients of varying aetiology and evaluated for predictors of thrombosis. Methods Biochemical and clinical data were acquired from 219 consecutive patients on the Australian National Liver Transplant Unit registry, including: TEG scores [K time (K), R time (R), alpha angle (AA), maximal angle (MA)], coagulation studies (INR, APTT, fibrinogen), full blood count, creatinine, thrombotic complications, cause of cirrhosis, and MELD score. Disease aetiology and MELD scores were compared against each parameter using unpaired t-test. Results Patients fell into two distinct groups: 33 had cholestatic liver disease (primary biliary cirrhosis and primary sclerosing cholangitis); 225 had non-cholestatic liver disease. When comparing cholestatic liver disease to non-cholestatic liver disease, the platelet count in x109/L (142 ± 16 vs 80 ± 3.7, p<0.0001), fibrinogen level in g/L (3 ± 0.21 vs 1.8 ± 0.06, p<0.0001), and INR (1.6 ± 0.08 vs 2.2 ± 0.09, p<0.0001) were significantly different. For TEG, K (2.7 ± 0.36 vs 3.8 ± 0.16, p=0.005), MA (63 ± 2 vs 47 ± 0.7, p<0.0001) and AA (58 ± 2.4 vs 49 ± 0.9, p<0.001) were significantly different. MELD was not significantly different (21 ± 0.9 vs 20 ± 0.6, p=0.99). When TEG was compared against laboratory coagulation studies, in non-cholestatic liver disease all TEG items strongly predicted elevated INR and decreased fibrinogen and platelet count. In cholestatic liver disease only MA had similar significant correlations with INR, fibrinogen and platelet count. None of the cholestatic liver disease patients developed portal vein thrombosis (0/33). 7% of non-cholestatic liver disease patients (15/225) developed portal vein thrombosis. Significant predictors of thrombosis were low APTT (p=0.02), low platelet count (p=0.048), and presence of HCC (p=0.009). TEG did not significantly predict portal vein thrombosis. Conclusion We found significant differences between coagulation profiles of cholestatic versus non-cholestatic liver disease. In noncholestatic liver disease all TEG items significant predicted elevated INR and descrease in fibrinogen and platelets. In cholestatic disease, on MA had the same significant correlations. Therefore in cholestatic liver disease, MA is a useful independent predictor of changes in INR, platelet count, and fibrinogen level. Significant predictors of portal vein thrombosis in non-cholestatic liver disease patients included low APTT, low platelet count, and presence of HCC.

AGA Abstracts

Mo1240 Spleen and Liver Volumes Are Strongly Correlated With Elevated Hepatic Venous Pressure Gradient in Patients With Non-Cirrhotic Portal Hypertension Ohad Etzion, Akeem Adebogun, Jason Eccleston, Ahmed M. Gharib, David E. Kleiner, Meral Gunay-Aygun, Richard Childs, Sergio Rosenzweig, Ivan J. Fuss, Harry Malech, Warren Strobe, Gulbu Uzel, Christa Zerbe, Steven M. Holland, Theo Heller, Christopher Koh Background: Elevated hepatic-venous pressure gradient (HVPG) is a predictor of clinical outcome in patients with cirrhosis, but has not been as extensively evaluated in non-cirrhotic portal hypertension (NCPH). Objectives: To investigate whether spleen and liver volumes as assessed by cross sectional imaging are correlated with HVPG measurements in patients with viral hepatitis and systemic diseases with suspected NCPH.Methods: Patients who had a transjugular liver biopsy with HVPG measurements between 2003-2013 for clinical care at the NIH Clinical Center were retrospectively evaluated. Patients with sickle cell disease were excluded. Epidemiologic, anthropometric, laboratory and imaging data were retrieved from the closest time point to HVPG measurement. Liver and spleen volumes were calculated from cross sectional computed tomography (CT), or magnetic resonance imaging (MRI) sections. Spleen (SBMI) and Liver (LBMI) volumes were adjusted to body mass index (BMI). Pearson's correlation coefficient was computed to assess the relationship between study variables.Results: Eighty-four patients were evaluated, 74% were males, with a mean age of 37±18.2 years. Primary clinical diagnoses included immunodeficiencies (50%), malignancies (19%), viral hepatitides (19%), and other systemic disorders (12%). HVPG was elevated in 68% of subjects, with a mean value of 7.3 ±4.7mm/Hg; clinically significant portal hypertension (≥ 10 mm/Hg) was identified in 23% of patients. Significant histologic fibrosis (Ishak >2) was seen in 21% of patients with elevated HVPG. In the entire cohort, SBMI significantly correlated with HVPG (r=0.42, p=0.0002), as did LBMI (r=0.40, p= 0.0004). SBMI and

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