16. Ascites in Chronic Liver Disease / L.J.Scully 

Ascites is the accumulation of nonsanguinous fluid in the peritoneal cavity. 

With significant liver disease, albumin synthesis is reduced. Low serum albumin results in a decrease in intravascular osmotic pressure. This causes renal blood flow changes, resulting in sodium and water retention. Increased aldosterone levels, possibly due to decreased catabolism of this hormone by the liver, also contribute. There is a generalized salt and water retention, but the fluid accumulation may be confined to the peritoneal cavity or may be associated with peripheral edema. Ascites develops because of increased portal pressure and the transudation of fluid from the capillaries in the portal system to the peritoneal cavity. Hepatic lymph production also increases and extravasates directly into the peritoneal cavity. 

Ascites most commonly presents with increasing abdominal girth, often associated with an uncomfortable feeling of distention, and sometimes nausea and anorexia. Shortness of breath may develop, resulting from either elevation of the diaphragm or pleural effusion. Ankle edema may accompany ascites. 

Clinical examination reveals flank fullness on inspection. "Shifting dullness" or a "fluid thrill" may be elicited. Smaller amounts of fluid may be detected on ultrasound when clinical signs are absent. One should look for other signs of portal hypertension, such as dilated abdominal wall veins or an enlarged spleen. 

Newly developed ascites must have a diagnostic aspiration to determine the albumin level, cell count and cytology. The fluid should be clear and straw-colored. Occasionally, lymph can accumulate in the peritoneal cavity, causing "chylous ascites," which requires different management. Ascitic fluid may become infected, in which case the white blood cell count will be elevated in the fluid. If the fluid is sanguinous, other causes ^_ such as infection or malignancy ^_ must be sought. The serum ascites albumin gradient is the best way of confirming if the ascitic fluid is secondary to portal hypertension. In this situation the gradient is high ^_ i.e., >11 g/L ^_ whereas it is low if the ascites is due to peritoneal carcinomatosis. This is far more accurate than our previous assessment of transudative versus exudative ascites. 

Management initially includes bed rest and salt restriction. Most cases also require adding a diuretic such as spironolactone. Careful aspiration of large quantities (up to 8 L) of ascitic fluid may be necessary in some resistant cases; this can be safely performed, and if the serum albumin level is very low an intravenous infusion of albumin is given before the paracentesis.