Cirrhosis can lead to abdominal fluid accumulation (ascites) and subsequent
distention and weight gain. This article seems to suggest that liver
transplantation is the solution.

Fluid retention in cirrhosis: pathophysiology and management
A. Kashani, C. Landaverde, V. Medici and L. Rossaro

From the Department of Internal Medicine, Division of Gastronterology and
Hepatology, University of California, Davis Medical Center, 4150 V Street - PSSB
3500, Sacramento, CA, 95817, USA


Abstract

Accumulation of fluid as ascites is the most common complication of cirrhosis.
This is occurring in about 50% of patients within 10 years of the diagnosis of
cirrhosis. It is a prognostic sign with 1-year and 5-year survival of 85% and
56%, respectively. The most acceptable theory for ascites formation is
peripheral arterial vasodilation leading to underfilling of circulatory volume.
This triggers the baroreceptor-mediated activation of
renin-angiotensin-aldosterone system, sympathetic nervous system and nonosmotic
release of vasopressin to restore circulatory integrity. The result is an avid
sodium and water retention, identified as a preascitic state. This condition
will evolve in overt fluid retention and ascites, as the liver disease
progresses. Once ascites is present, most therapeutic modalities are directed on
maintaining negative sodium balance, including salt restriction, bed rest and
diuretics. Paracentesis and albumin infusion is applied to tense ascites.
Transjugular intrahepatic portosystemic shunt is considered for refractory
ascites. With worsening of liver disease, fluid retention is associated with
other complications; such as spontaneous bacterial peritonitis. This is a
primary infection of ascitic fluid caused by organisms originating from large
intestinal normal flora. Diagnostic paracentesis and antibiotic therapy plus
prophylactic regimen are mandatory. Hepatorenal syndrome is a state of
functional renal failure in the setting of low cardiac output and impaired renal
perfusion. Its management is based on drugs that restore normal renal blood flow
through peripheral arterial and splanchnic vasoconstriction, renal vasodilation
and/or plasma volume expansion. However, the definitive treatment is liver
transplantation.

taken from:
http://qjmed.oxfordjournals.org/cgi/content/abstract/101/2/71

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