Ascitis

Fisiopatologia y tratamiento

Abstract

Cirrhosis of the liver is the main cause of ascitis. Recent studies have shown in compensated cirrhotics a 40% chance to develop ascites 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 cavity (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. The most important measure to treat ascitis is sodium restriction which in 10-20% of patients is enough to eliminate the problem. In order to obtain a maximum benefit sodium intake must be less than sodium excretion, and usually requires restriction to less than 500 mg/day, however this severe restriction is impractical and few patients are able to follow it. A better regimen is a 1-2 g/day restriction associated to a judicious diuretic regimen. Water must be restricted only in the presence of hyponatremia below 130 mEq/L. When sodium restriction alone is not sufficient to movilize ascitis a diuretic regimen of spironolactone follow by furosemide is usually successful. In the few cases refractory to maximal doses of both agents, metolazona can be helpfull. The goal of the treatment is a weight loss of 1 kg per day in patients without edema. Patients with compensated cirrhosis and tense ascitis can be treated with large volume paracentesis which means removal of the total amount of ascitis in one or several occasions. It has been demostrated that this regimen when combined with intravenous colloids has few complications and allows the patients to be discharged from the hospital sooner. Finally refractory patients can benefit from a peritoneo-yugular shunt although this modality of treatment carries a mortality of 25% and a morbidity of 66%.