Ascites - From Basics to Bedside

The term ascites denotes the pathological accumulation of fluid in the peritoneal cavity. Healthy men have little or no fluid in the peritoneal cavity but women normally may have up to 20ml depending on the phase of menstrual cycle. Causes of ascites may be classified into two pathophysiologic categories: That associated with the normal peritoneum and that which occur due to a diseased peritoneum. Cirrhosis accounts for 84 percent of all cases of ascites, whereas Cardiac ascites, peritoneal carcinomatosis and mixed ascites resulting from cirrhosis and a second disease account for 10-15% of cases. Less common causes of ascites include massive hepatic metastasis, peritoneal tuberculosis, and pancreatitis and Nephrotic syndrome. Various causes of ascites are enumerated in Table 1. PATHOGENESIS Pathogenesis of ascites is different in cases with cirrhosis and without the cirrhosis. Pathogenesis in Cirrhosis Cases The presence of portal hypertension contributes to the development of ascites in patients who have cirrhosis. There is an increase in Intrahepatic resistance, causing increased portal pressure, but there is also vasodilatation of the splanchnic arterial system, which in turn results in an increase in portal venous inflow. Both of these abnormalities result in increased production of splanchnic lymph. Vasodilating factors such as vascular endothelial growth factor and nitric oxide are responsible for the vasodilatory effect. These hemodynamic changes cause activation of the RAAS with the development of hyperaldosteronism and hence sodium retention. These renal effects of increased aldosterone also contribute to the development of ascites. Sodium retention causes C H A P T E R