Portal Hypertensive Ascites: Current Status
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PORTAL HYPERTENSION (J GONZALEZ-ABRALDES AND E TSOCHATZIS, SECTION EDITORS)
Portal Hypertensive Ascites: Current Status Savio John 1 & Lawrence S. Friedman 2,3,4,5
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Ascites is defined as the pathological accumulation of excess free fluid within the peritoneal cavity. This review article summarizes the pathogenesis and management of ascites due to cirrhosis and portal hypertension. Recent Findings The development of ascites signifies the transition from a compensated to a decompensated phase of cirrhosis. Management of ascites in patients who fail conventional therapy is a topic of ongoing research, as the only definitive treatment in such cases is liver transplantation. Summary The latest recommendations on sodium restriction, the use and discontinuation of diuretics, novel treatment modalities including the placement of a transjugular intrahepatic portosystemic shunt (TIPS) and automated low-flow ascites pump (Alfapump®), and discontinuation of beta receptor antagonists in refractory ascites are discussed in a concise and practical way for the general practitioner involved in the care of patients with end-stage liver disease. Keywords Ascites . Portal hypertension . Decompensated cirrhosis . Paracentesis . Refractory ascites . TIPS
Introduction
Epidemiology
Ascites is defined as the pathological accumulation of excess free fluid within the peritoneal cavity. Ascites has been considered a sign of liver disease at least since the time of Hippocrates. The development of ascites signals the transition from a compensated phase of cirrhosis to a decompensated phase and is associated with a 2-year mortality rate of 50% [1–3].
Ascites is present at the time of diagnosis of cirrhosis in 20–60% of patients [4]. The cumulative probability of developing ascites in patients with cirrhosis of any cause ranges from 35 to 50% within 5 years [2, 4]. In patients with cirrhosis caused by viral hepatitis, the frequency is lower, with an estimated range of 5–6% per year [5]. Nevertheless, ascites is the most common initial decompensating event in patients with hepatitis C virus (HCV)– related cirrhosis [3].
This article is part of the Topical Collection on Portal Hypertension
Etiology * Lawrence S. Friedman [email protected] 1
State University of New York Upstate Medical University, Syracuse, NY, USA
2
Harvard Medical School, Boston, MA, USA
3
Tufts University School of Medicine, Boston, MA, USA
4
Department of Medicine, Newton-Wellesley Hospital, 2014 Washington Street, Newton, MA 02462, USA
5
Massachusetts General Hospital, Boston, MA, USA
Ascites may be due to portal hypertension or to a nonportal hypertensive cause. The most common cause of portal hypertensive ascites is cirrhosis; other causes include heart failure, alcohol-associated hepatitis, Budd-Chiari syndrome, acute liver failure, sinusoidal obstruction syndrome, massive liver metastasis, acute fatty liver of pregnancy, myxedema, and portal vein thrombosis
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