Area Editoriale
Cirrhosis, most frequently caused by hepatitis C or alcoholism, was the 12th leading cause of death in the United States in 2000, accounting for more than 25,000 deaths. Ascites is the most common complication of cirrhosis and is associated with a poor quality of life, increased risks of infections and renal failure, and a poor long-term outcome. In recent years, important advances have been made in the management of cirrhosis and ascites.Pathophysiology of Ascites
The chief factor contributing to ascites is splanchnic vasodilatation.4 Increased hepatic resistance to portal flow due to cirrhosis causes the gradual development of portal hypertension, collateral-vein formation, and shunting of blood to the systemic circulation. As portal hypertension develops, local production of vasodilators, mainly nitric oxide, increases, leading to splanchnic arterial vasodilatation. In the early stages of cirrhosis, splanchnic arterial vasodilatation is moderate and has only a small effect on the effective arterial blood volume, which is maintained within normal limits through increases in plasma volume and cardiac output. In the advanced stages of cirrhosis, splanchnic arterial vasodilatation is so pronounced that the effective arterial blood volume decreases markedly, and arterial pressure falls. As a consequence, arterial pressure is maintained by homeostatic activation of vasoconstrictor and antinatriuretic factors, resulting in sodium and fluid retention. The combination of portal hypertension and splanchnic arterial vasodilatation alters intestinal capillary pressure and permeability, facilitating the accumulation of retained fluid within the abdominal cavity. As the disease progresses, there is marked impairment in renal excretion of free water and renal vasoconstriction — changes that lead to dilutional hyponatremia and the hepatorenal syndrome, respectively.