Ascites is a pathologic collection of fluid in the peritoneal cavity. The most common cause is cirrhosis, accounting for approximately 75% to 80% of cases. 
Patients present with abdominal distension; fluid may be detected on physical examination with shifting dullness. Ultrasound, computed tomography scan, or magnetic resonance imaging can confirm the diagnosis. In the majority of patients the history and examination will provide important clues as to the etiology of ascites (e.g., signs of chronic liver disease or cardiac failure). Causes include diseases that lead to portal hypertension, hypoalbuminemia, and neoplasms.
In cirrhosis, ascites forms due to renal dysfunction and abnormalities in portal and splanchnic circulation. Sodium retention is a major factor in pathogenesis.  Splanchnic arterial vasodilatation (secondary to hepatic fibrosis) leads to increased lymph formation, activation of the renin angiotensin system and sympathetic nervous system, and release of antidiuretic hormone. This causes renal sodium and water retention. There is increased resistance to portal flow resulting in portal hypertension, collateral vein formation, and shunting of blood to the systemic circulation.  About 50% of patients with cirrhosis develop ascites within 10 years.  
Other causes of portal hypertension that may be associated with ascites include congestive heart failure, constrictive pericarditis, alcoholic liver disease, fulminant hepatitis, subacute hepatitis, massive liver metastasis, and Budd-Chiari syndrome.
Conditions causing hypoalbuminemia such as nephrotic syndrome and protein-losing enteropathy may result in ascites. Peritoneal diseases including infectious peritonitis and malignancies can also cause ascites.
Professor of Clinical Medicine
Perelman School of Medicine
University of Pennsylvania
KDR declares that he has no competing interests.
Assistant Professor of Medicine
Associate Medical Director, Liver Transplant
Drexel University College of Medicine
Hahnemann University Hospital
VP declares that he has no competing interests.
Dr Kenneth D. Rothstein and Dr Vishal Patel would like to gratefully acknowledge Dr Srikrishna Nagri and Dr Sury Anand, previous contributors to this topic.
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