Common aspects of all postulated mechanisms for the development of ascites in liver disease involve a combination of sodium retention and portal hypertension (Lingappa, 2003). Portal hypertension can arise from hepatic venous outflow blockage caused by nodules and fibrosis in the liver (Wongcharatrawee & Garcia-Tsao, 2001). Three possible effects of portal hypertension are (1) diversion of the vascular volume to the lymphatics, resulting in overloading of the lymphatic drainage and weeping of fluid into the peritoneum; (2) portal-to-systemic shunting causing irritants that are normally cleared by the liver to be released into circulation where they initiate activities that decrease renal perfusion and increase renal tubular sodium resorption; or (3) endothelin-1 secretion, causing renal vasoconstriction, decreased glomerular filtration rate, and sodium retention. Regardless of the causal mechanism involved, depletion of the intravascular volume activates the renin-angiotensin-aldosterone system and vasopressin, causing sodium and water retention, which further contributes to fluid accumulation (Lingappa, 2003).

Several mechanisms have been proposed for the development of malignancy-associated ascites. Patients with liver cancer may develop portal hypertension, resulting in ascites formation in much the same way as those with cirrhosis (Kichian & Bain, 2004). In addition, tumors that have seeded the peritoneum may release high levels of vascular endothelial growth factor (VEGF) that increase capillary permeability. Zebrowski, Liu, Ramirez et al. (1999) showed that VEGF protein levels were markedly increased in malignant ascites compared to levels in ascites associated with cirrhosis and that inhibiting VEGF activity decreased endothelial cell permeability in vitro. Further, animal studies show that ascites recurrence can be blocked by inhibiting VEGF expression (Stoelcker, Echtenacher, Weich et al., 2000). When the vascular permeability increases, proteins enter the peritoneal cavity. In mice, proteins in the peritoneal cavity make ascites worse by functionally impairing lymphatic drainage (Nagy, Herzberg, Masse et al., 1989). These proteins also increase the oncotic pressure pulling in more fluids via osmosis. In addition, obstruction or invasion of lymphatic channels by tumors may lead to chylous ascites (Kichian & Bain, 2004).

The accumulation of abnormal amounts of fluid in the peritoneal cavity causes many uncomfortable symptoms. Pain occurs due to stretching or compression of tissues. Also, inflammation from a peritoneal infection may cause severe pain. Increased pressure on the stomach causes early satiety and nausea. Constipation, due to pressure on the bowel, is also a common complication of ascites. Dyspnea may result from pressure on the diaphragm and leakage of ascitic fluid into the pleural space (Kichian & Bain, 2004).

Abdominal radiographic studies, ultrasound, and computed tomography scans do verify the presence of free fluid in the abdomen, but these tests are generally not required after a thorough history and physical examination. On radiography, ascites appears with hazy or ground-glass features, distended and separated loops of bowel, and poor definition of abdominal organs (Hostetter et al., 2005; Kichian & Bain, 2004).

Cytology and examination of the protein concentration of the peritoneal fluid are tests that assist in determining the cause of ascites. However, in end-of-life care, the cause is often evident, so a diagnostic paracentesis is rarely required. More commonly, the peritoneal fluid is examined for cell count, Gram stain, and culture to select the appropriate antibiotic intervention when infection is suspected.