Patients with cirrhosis have significant abnormalities in their fluid and electrolyte balance; this is manifested mainly by the development of ascites and edema. Ascites is the most common complication of patients with cirrhosis and its development constitutes the first and most important manifestation of the disease. With disease progression, patients with advanced cirrhosis and severe urinary sodium retention develop refractory ascites, a condition in which patients do not respond to diuretics or develop severe side effects to these that preclude their use. This condition occurs in 5–10% of cases admitted to the hospital for treatment of ascites. Approximately half of these patients will die within 1 year if not transplanted; therefore, the best therapy is liver transplantation in suitable candidates. During the last two decades, significant advances have been made in regard to pathogenesis and treatment of refractory ascites. The re-introduction of therapeutic paracentesis with plasma expansion in the 1980s was a milestone in the treatment of these patients. In addition, the introduction of transjugular intrahepatic portosystemic shunts as a therapy for refractory ascites has certainly provided a reasonable alternative for those patients with preserved liver function and unwilling to undergo several taps per month. This article will discuss the pathophysiology, clinical features and therapy of refractory ascites in cirrhosis.

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