ABSTRACT
Cirrhosis of the liver is the main cause of ascitis. Recent studies have shown in compensated cirrhotics a 40 percent chance to develop ascitis after five years of follow up. The presence of ascitis is usually associated with advanced liver disease, and higher mortality than patients with compensated cirrhosis. Many theories have been proposed to explain ascitis formation being the most important the presence of portal hypertension and sodium retention. Extravascular fluid accumulation depends directly of a balance between hydrostatic and colloid-osmotic pressure (Starling law). Hepatic sinusoids differ from splanchnic ones in regard to the presence of fenestrae, that allows albumin and other substances to flow freely from the sinusoid to the extravascular space. For these reasons the sinusoids lacks colloid-osmotic pressure, and the hydrostatic pressure regulates the flow of fluids passing through them. In cirrhosis, diffuse fibrosis and nodule formation cause functional obstruction to the hepatic blood flow, and a secondary increase in the sinusoidal pressure, that leads to exit of fluids from the sinusoids to the hepatic lymphatics and the thoracic duct. When the amount of fluid that leaves the sinusoids exceeds the capacity of the thoracic duct, fluids accumulate in the abdominal cvity (ascitis). A new theory about ascitis formation states that the first event is a diffuse peripheral arterial vasodilation that cause ineffective plasma volume that triggers the production of humoral factors directed to retain sodium in the kidney...