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Pathogenesis of ascites in patients with cirrhosis

José Such, MD, PhD
Bruce A Runyon, MD
Section Editor
Keith D Lindor, MD
Deputy Editor
Kristen M Robson, MD, MBA, FACG


Ascites is defined as the pathologic accumulation of fluid in the peritoneal cavity [1]. It is the most common complication of cirrhosis, which is the most common cause of ascites in the United States, accounting for approximately 85 percent of cases [1]. Within 10 years after the diagnosis of compensated cirrhosis, about 50 percent of patients will have developed ascites [2].

The development of ascites is the final consequence of a series of anatomic, pathophysiologic, and biochemical abnormalities occurring in patients with cirrhosis. The two older theories of ascites formation, the underfill theory [3] and the overflow theory [4], appear to be relevant at different stages of the natural history of cirrhosis [5]. However, the most recent theory, the arterial vasodilation hypothesis, appears to match best with the actual hemodynamic data and has become the most widely accepted theory [6].

The formation of ascites is governed by the same principles as edema formation at other sites: net capillary permeability and the hydraulic and oncotic pressure gradients. (See "Pathophysiology and etiology of edema in adults".)


The development of portal hypertension (PHT) is the first step toward fluid retention in the setting of cirrhosis. Patients with cirrhosis but without PHT do not develop ascites or edema [7]. A portal pressure >12 mmHg appears to be required for fluid retention [7,8]; on the other hand, ascites will usually disappear if portal pressure is reduced below 12 mmHg, eg, after a surgical or radiologic portosystemic shunt [9]. Sinusoidal hypertension appears to be required for fluid retention to occur; presinusoidal portal hypertension, as in portal vein thrombosis, does not result in ascites formation in the absence of another predisposing factor.

PHT leads to profound changes in the splanchnic circulation. Although it was formerly thought that PHT was due solely to a mechanical obstruction to portal flow, data from animal models provide evidence for a component of increased portal venous inflow as a consequence of splanchnic arterial vasodilation [10,11].

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Literature review current through: Nov 2017. | This topic last updated: Dec 16, 2015.
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