ARRS 2022 Abstracts

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E2030. Treatment Options for Refractory Ascites in Cirrhotic Patients: An Imaging Update
Authors
  1. Karan Singh; Avalon University School of Medicine
  2. Stephen Brown; University of Alabama at Birmingham
  3. Rakesh Varma; University of Alabama at Birmingham
Background
Ascites occur in 50% of cirrhotic patients, with an associated mortality of 50% over 2 years. Refractory ascites accounts for –10% in cirrhotic patients. The treatment strategy is based on grades of ascites according to the European Association for the Study of the Liver. There is no algorithmic approach for refractory ascites. This exhibit provides advantages and disadvantages and updates of serial large-volume paracentesis (LVP), transjugular intrahepatic portosystemic shunt (TIPS), implanted drainage devices, and an algorithm to guide the management of refractory ascites.

Educational Goals / Teaching Points
This exhibit describes the pathophysiology of refractory ascites in cirrhosis and outline the advantages and disadvantages of interventional therapies for refractory ascites. In addition, we provide a comparative analysis of clinical outcomes between the different interventional options. Lastly, we discuss a simplified algorithm for the management of refractory ascites.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
The mechanism of ascites development in cirrhosis is multifactorial and is poorly understood. The process of cirrhosis leads to conversion of the low resistance vascular bed of the liver to high resistance, increasing the portal pressure and leading to release of vasodilators, predominantly nitric oxide, which in turn causes splanchnic arterial vasodilation. As a result, there is a reduction in the effective circulatory blood volume, triggering the activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). Ultimately, aldosterone and antidiuretic hormone-induced sodium and fluid retention. The increased portal venous pressure in combination with splanchnic vasodilation alters the normal permeability of the intestinal capillaries, leading to an increased outward hydrostatic pressure and resulting in ascites. In addition, hypoalbuminemia induced by progressive cirrhosis contributes to ascitic formation.

Conclusion
The main management for ascites is dual diuretic therapy and dietary modifications. Serial LVP remains the mainstay for the management of tense ascites. TIPS should be considered early in the course for eligible patients that have refractory ascites, as it improves the quality of life and transplant-free survival. Knowing the options for management of refractory ascites guided by a simple algorithmic approach can help standardize management and improve clinical outcomes.