Other causes of ascites include malignancy, heart failure, tuberculosis, alcoholic hepatitis, Budd‐Chiari syndrome, and nephrogenic ascites. In patients with cirrhosis, ascites due to portal hypertension (PHT) is primarily related to an inability to excrete adequate amounts of sodium into urine, leading to a positive sodium balance. This is the case at the early stages of hepatic decompensating when ascites is responsive to a reduced intake of dietary sodium and to moderate doses of diuretics.Ĭirrhosis is the most common cause of ascites, representing 85% of all cases of ascites. For easily‐controllable ascites, on the other hand, the volume of fluid that spills into the peritoneal cavity can be reduced below this absorption threshold. Thus, the development of clinically significant ascites occurs when the rate of ascites formation exceeds the rate of ascites reabsorption.
However, the daily absorption of fluid from the peritoneal cavity back to the circulation is limited, and the maximum absorption of fluid out of the peritoneum is approximately 850 mL/d. Furthermore, the constituents of the fluid are in dynamic equilibrium with those of the plasma. With ascites, this fluid is not static within the peritoneal cavity, but is rather in a continuous exchange with the circulation through a large capillary bed under the visceral peritoneum, with about half the volume entering and leaving the peritoneal cavity every hour. Normally, the peritoneal cavity contains 25–50 mL of ascitic fluid, which allows for the movement of bowel loops past one other and helps hydrate serosal surfaces. Ascites is defined as the pathological accumulation of excess fluid in the peritoneal cavity.
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