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Prevention of Further Decompensation in Patients With Ascites

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Portal Hypertension VII

Abstract

Ascites are the most frequent first decompensating event in patients with advanced chronic liver disease. Pathophysiology of ascites involves portal hypertension, systemic inflammation, splanchnic arterial vasodilation, and activation of humoral vasoactive systems leading to sodium and water retention. After the occurrence of ascites, patients with cirrhosis are at high risk for further decompensation (i.e., hepatic encephalopathy, portal hypertensive bleeding, progression to recurrent/refractory ascites, spontaneous bacterial peritonitis, hepatorenal syndrome), and death. While the treatment of ascites is based on counteracting sodium and water retention with diuretics and removing ascites by paracentesis, all patients with ascites should be evaluated regarding candidacy for liver transplantation. Ultimately, the management of patients with ascites should aim at preventing further decompensation and death, targeting the underlying mechanisms that drive the development of further decompensation, such as the ongoing etiology of liver disease, portal hypertension, and abnormalities in the gut-liver axis, systemic inflammation, and splanchnic arterial vasodilation. Transjugular Intrahepatic Portosystemic Shunt (TIPS) implantation should be considered for recurrent/refractory ascites because it improves transplant-free survival. Herein, we review available strategies for the prevention of further decompensation in cirrhotic patients with ascites, including etiologic treatment, nonselective beta-blockers, TIPS, antibiotics, and albumin.

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Piano, S., Reiberger, T., Larrue, H., Bureau, C. (2022). Prevention of Further Decompensation in Patients With Ascites. In: de Franchis, R. (eds) Portal Hypertension VII. Springer, Cham. https://doi.org/10.1007/978-3-031-08552-9_49

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