| Invited Lecture(JSGE) |
| Thu. October 31st 9:00 - 9:30 Room 12: Kobe International Conference Center Main Hall |
| Portal hypertension in cirrhosis: Risk stratification and management | |||
| Guadalupe Garcia-Tsao | |||
| Yale University / VA-CT Healthcare System | |||
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| Cirrhosis is the end stage of any chronic liver disease and is classified into two clinical stages: compensated and decompensated, with a stage of "further" decompensation having been described more recently. Decompensated cirrhosis is defined by the presence of a clinically-evident decompensating events, specifically, ascites, variceal hemorrhage, or hepatic encephalopathy. While the median survival in compensated cirrhosis is 12 years, once a decompensating event develops, it decreased to <2 years. Portal hypertension is the main consequence of cirrhosis and the main driver of decompensation. It results from increased intrahepatic resistance and increased portal venous inflow. Portal hypertension is defined by a hepatic venous pressure gradient (HVPG) > 5mmHg. However, an HVPG of ≥10mmHg is the strongest predictor of the development of varices and clinical decompensation and is therefore used to define "clinically significant portal hypertension (CSPH)". Because HVPG is an invasive method, non-invasive methods using liver stiffness measurements (LSM) by transient elastography and platelet count have been studied and validated. A LSM of >25 kPa or LSM between 20-25 kPa with platelet count <150/mm3 or a LSM between 15-20 kPa with a platelet count <110/mm3 rules in CSPH in most etiologies of cirrhosis. This applies to most patients with cirrhosis except obese patients with metabolic-associated cirrhosis in whom the diagnostic accuracy can increase using body mass index. Additionally, for all etiologies, the presence of gastroesophageal varices on endoscopy and/or the presence of porto-systemic collaterals on cross-sectional imaging are both indicative of CSPH. The usefulness of the non-invasive measures relies on being able to better triage and identify the population at risk of cirrhosis decompensation/death to target therapies aimed at preventing decompensation as well as avoiding unnecessary procedures like such as endoscopy in very low risk population. Non-selective beta-blockers (NSBB) decrease portal pressure and have been shown to decrease the incidence to decompensation in patients with CSPH (measured by HVPG). Of the NSBB, carvedilol is preferred because, when compared to propranolol, it has added benefit in reducing portal pressure and preventing decompensation. Current guidance documents recommend that patients with cACLD and evidence of CSPH (mostly non-invasively using liver stiffness measurements or evidence of collaterals or varices on imaging/endoscopy) should receive treatment with carvedilol to prevent clinical decompensation. In patients who cannot take NSBB (intolerant or who have contraindications), the previous recommendations are valid, that is, to perform an upper endoscopy and ligate high-risk varices (large and/or with red signs) if these are present. |
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