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Kufe DW, Pollock RE, Weichselbaum RR, et al., editors. Holland-Frei Cancer Medicine. 6th edition. Hamilton (ON): BC Decker; 2003.

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Holland-Frei Cancer Medicine. 6th edition.

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Malignant ascites can occur in patients with colon, pancreatic, breast, and lung primaries with the development of peritoneal carcinomatosis.202 The life expectancy of such patients is generally limited to weeks to months after the onset of ascites. Of the three major complications of liver cirrhosis—hepatic encephalopathy, ascites, and variceal hemorrhage—ascites is the most common.203 The development of ascites in the natural history of chronic liver disease in the absence of malignancy is an important landmark as approximately 50% of patients with ascites succumb in 2 years.204

Clinical Manifestations

The earliest evidence of ascites is an increase in abdominal girth accompanied by weight gain. Ascites is usually evident on clinical evaluation, based on abdominal distention and flank dullness, and is frequently associated with leg edema. The presence of a full and bulging abdomen should lead to percussion of the flanks. If the flank dullness is found, then “shifting” should be checked for. Approximately 1,500 mL of fluid must be present to detect dullness.205 In supine patients, sacral edema is an important clue. Pain accompanied by ascites suggests a malignant cause for fluid accumulation. Abdominal ultrasonography may be required to determine with certainty if fluid is present in the abdominal cavity. Ultrasonography can detect as little as 100 mL of fluid in the abdomen. Approximately 4% to 10% of patients with ascites also develop pleural effusions, with two-thirds of the effusions being right-sided. Pleural fluid may be present with minimal or no ascites. Inguinal or umbilical hernias may accompany ascites.

Peritoneal carcinomatoses causes ascites by the exudation of proteinaceous fluid from tumor cells lining the peritoneum.202 In rare cases, massive liver metastasis can cause ascites by portal hypertension. Tumor-induced portal vein thrombosis and underlying cirrhosis-related portal hypertension are also responsible for ascites in the patients with portal hypertension. Chylous ascites because of malignant lymphoma is caused by lymphatic obstruction. Malignancy should be suspected as a cause of ascites in patients with a history of cancer. Breast, lung, colon, and pancreatic primary malignancies are most commonly complicated by ascites.202 Underlying liver disease is the cause of ascites formation in approximately 80% of cases. Approximately 5% of patients have “mixed” (ie, having two or more causes) ascites. Tables 155-4 and 155-5 list other causes of ascites.

Table 155-4. Subtypes of Malignancy-Related Ascites.

Table 155-4

Subtypes of Malignancy-Related Ascites.

Table 155-5. Classification of Ascites by Serum-Ascites Albumin Gradient.

Table 155-5

Classification of Ascites by Serum-Ascites Albumin Gradient.


A diagnosis of ascites is suspected on the basis of history and physical examination, but the final confirmation is based on successful abdominal paracentesis. Sampling ascitic fluid in all patients with new-onset ascites is necessary. The practice of ordering every conceivable test on ascitic fluid is strongly discouraged as it can be very expensive and as it may be more confusing than helpful. A cell count with differential, albumin assessment (in addition to serum albumin), and culture in blood culture bottles should be the routine. Cytology of ascitic fluid is an important test in cancer patients. Total protein, glucose, lactate acid dehydrogenase (LDH), amylase, and Gram stain tests are optional. A few other tests (eg, tuberculosis smear and culture; tests for triglyceride and bilirubin) should be ordered in the proper clinical setting.

Nonneutrophilic ascitic fluid is transparent and slightly yellow to amber. The opacity of most cloudy fluid specimens is caused by neutrophils. Bloody ascites may result from traumatic tap or from ascites secondary to hepatocellular carcinoma or peritoneal carcinomatosis. Dark brown ascitic fluid may indicate biliary perforation or leak. The upper limit of an absolute polymorphonuclear leukocyte (PMN) count in uncomplicated cirrhotic ascitic fluid is usually 250/mm3. Any inflammatory process can result in an elevated ascitic-fluid white blood cell (WBC) count. Spontaneous bacterial peritonitis (SBP) is the most frequent cause of an increased WBC count with PMN predominance. Tuberculous peritonitis and peritoneal carcinomatosis give rise to an increased WBC count but with lymphocyte predominance. The serum-ascites albumin gradient (SAAG) has been proved in multiple studies to categorize ascites better than the total protein concentration (transudate/exudate) and other parameters. The difference between the serum and ascitic-fluid albumin concentrations correlates directly with portal pressure.206 The calculation of the SAAG involves measuring the albumin concentration of serum and ascitic-fluid specimens and subtracting (it is not a ratio) the ascitic-fluid value from the serum value. The serum albumin is nearly always the largest value, barring laboratory error. A SAAG of > 1.1 g/dL is diagnostic of portal hypertension, with 97% accuracy.207 Conversely, if the SAAG is < 1.1 g/dL, the patient does not have portal hypertension (with 97% accuracy) and malignancy is generally the cause. The etiology of ascites can be classified according to whether the associated SAAG is high or low (see Table 155-4).

Hepatocellular carcinoma, massive liver metastases, and malignant lymphoma causing ascites by lymphatic obstruction, are generally not associated with positive cytology. Positive cytology of ascitic fluid for malignant cells should only be expected in cases with peritoneal carcinomatoses. Chylous ascites has a high triglyceride concentration, usually higher than the serum. A triglyceride level should be obtained routinely in the presence of milky ascitic fluid. An ascitic-fluid bilirubin level greater than the serum level of bilirubin suggests a bile leak into the ascitic fluid.


The serum-ascites albumin gradient can be very helpful diagnostically, as well as in therapeutic decision making. Patients with low-SAAG ascites (malignant ascites falls into this category) usually do not have portal hypertension and do not respond to salt restriction or to diuretics,208 except in cases of nephrotic syndrome. The mainstay of the treatment of nonovarian (lung, breast, colon, and pancreatic) peritoneal carcinomatosis is outpatient therapeutic paracentesis as these patients have a poor prognosis. For malignant ascites, the frequency of large-volume paracentesis is dictated by the patient's symptoms. Patients with an ovarian malignancy may respond well to surgical debulking and chemotherapy. Antituberculous therapy is the mainstay of treatment for tuberculous ascites. High-SAAG ascites usually responds well to diuretics and measures for maintaining sodium balance. Fluid loss and weight change are directly related to sodium balance. A realistic dietary sodium restriction of 2 g/d (= 2,000 mg/d = 88 mmol/d) should be the goal. Fluid restriction is not necessary when treating most patients who have cirrhotic ascites. Approximately 10% of patients with cirrhotic ascites are refractory to standard medical treatment with diuretics and salt and fluid restrictions. Patients who cannot tolerate diuretics because of complications are also regarded as having refractory ascites. Large-volume paracentesis is safe and effective for the treatment of refractory ascites. The incidences of hyponatremia, hypotension, hepatic encephalopathy, and renal impairment are lower for patients treated with paracentesis than for those treated with diuretics. The current recommendations are that intravenous albumin should be administered when large-volume paracentesis is repeatedly performed. Peritoneovenous shunting has fallen out of favor as a consequence of excessive complications and poor patency rates. Transjugular intrahepatic portosystemic shunts (TIPS) can also be considered in patients with refractory ascites. Finally, liver transplantation is the only lifesaving therapy for all patients who present with refractory ascites and severe liver dysfunction in the absence of underlying malignancy.

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Copyright © 2003, BC Decker Inc.
Bookshelf ID: NBK12901


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