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Ascites = excess fluid in the abdominal cavity, is the commonest complication of cirrhosis, occurring in approximately half of all patients. It is associated with significant morbidity and mortality unless managed appropriately. For example, patients eat less due to compression of their stomach by the intra-abdominal fluid, leading to poor nutrition. In addition, the fluid can become infected.
The pathophysiology of ascites formation is understood in general, although the details are not completely defined. When the pressure in the liver sinusoids rises, because the cirrhotic liver prevents normal compliance, the extra-hepatic circulation releases vasodilators. The result is a decrease in effective arterial blood volume and the kidney responds by retaining sodium.
Retention of sodium is necessarily accompanied by retention of water. Increased pressure in the portal system increases fluid movement into the abdomen. When the retained fluid leaks into the abdominal cavity at a faster rate than can be removed by normal lymph flow, ascites accumulates.
The hallmarks of management of ascites are to decrease sodium intake and increase sodium output. We are interested in comparing more and less stringent dietary sodi.um restriction for ascites management in patients in a county hospital setting. ClinicalTrials.gov Identifier: NCT00548366
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