Chapter 044. Abdominal Swelling and Ascites (Part 4)

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Chylous ascites refers to a turbid, milky, or creamy peritoneal fluid due to the presence of thoracic or intestinal lymph. Such a fluid shows Sudan-staining fat globules microscopically and an increased triglyceride content by chemical examination. Opaque milky fluid usually has a triglyceride concentration of 11.3 mmol/L (1000 mg/dL), but a triglyceride concentration of 2.3 mmol/L (200 mg/dL) is sufficient for the diagnosis. A turbid fluid due to leukocytes or tumor cells may be confused with chylous fluid (pseudochylous), and it is often helpful to carry out alkalinization and ether extraction of the specimen. Alkali tend to dissolve cellular...

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Chapter 044. Abdominal Swelling and Ascites (Part 4) Chylous ascites refers to a turbid, milky, or creamy peritoneal fluid due to the presence of thoracic or intestinal lymph. Such a fluid shows Sudan-staining fat globules microscopically and an increased triglyceride content by chemical examination. Opaque milky fluid usually has a triglyceride concentration of >11.3 mmol/L (>1000 mg/dL), but a triglyceride concentration of >2.3 mmol/L (>200 mg/dL) is sufficient for the diagnosis. A turbid fluid due to leukocytes or tumor cells may be confused with chylous fluid (pseudochylous), and it is often helpful to carry out alkalinization and ether extraction of the specimen. Alkali tend to dissolve cellular proteins and thereby reduce turbidity; ether extraction leads to clearing if the turbidity of the fluid is due to lipid. Chylous ascites is most often the result of lymphatic disruption or obstruction from cirrhosis, tumor, trauma,
tuberculosis, filariasis (Chap. 211), or congenital abnormalities. It may also be seen in the nephrotic syndrome. Rarely, ascitic fluid may be mucinous in character, suggesting either pseudomyxoma peritonei (Chap. 291) or rarely a colloid carcinoma of the stomach or colon with peritoneal implants. On occasion, ascites may develop as a seemingly isolated finding in the absence of a clinically evident underlying disease. Then, a careful analysis of ascitic fluid may indicate the direction the evaluation should take. A useful framework for the workup starts with an analysis of whether the fluid is classified as a high (transudate) or low (exudate) gradient fluid. High-gradient (transudative) ascites of unclear etiology is most often due to occult cirrhosis, right-sided venous hypertension raising hepatic sinusoidal pressure, Budd-Chiari syndrome, or massive hepatic metastases. Cirrhosis with well-preserved liver function (normal albumin) resulting in ascites is invariably associated with significant portal hypertension (Chap. 301). Evaluation should include liver function tests and a hepatic imaging procedure (i.e., CT or ultrasound) to detect nodular changes in the liver suggesting portal hypertension. On occasion, a wedged hepatic venous pressure can be useful to document portal hypertension. Finally, if clinically indicated, a liver biopsy will confirm the diagnosis of cirrhosis and perhaps suggest its etiology. Other etiologies may result in hepatic venous congestion and resultant ascites. Right-sided cardiac valvular disease and
particularly constrictive pericarditis should raise a high index of suspicion and may require cardiac imaging and cardiac catheterization for definitive diagnosis. Hepatic vein thrombosis is evaluated by visualizing the hepatic veins with imaging techniques (Doppler ultrasound, angiography, CT scans, MRI) to demonstrate obliteration, thrombosis, or obstruction by tumor. Uncommonly, transudative ascites may be associated with benign tumors of the ovary, particularly fibroma (Meigs' syndrome) with ascites and hydrothorax. Low-gradient (exudative) ascites should initiate an evaluation for primary peritoneal processes, most importantly infection and tumor. Tuberculous peritonitis (Table 44-1) is best diagnosed by peritoneal biopsy, either percutaneously or via laparoscopy. Histologic examination invariably shows granulomata that may contain acid-fast bacilli. Since cultures of peritoneal fluid and biopsies for tuberculosis may require 6 weeks, characteristic histology with appropriate stains allows antituberculosis therapy to be started promptly. Similarly, the diagnosis of peritoneal seeding by tumor can usually be made by cytologic analysis of peritoneal fluid or by peritoneal biopsy if cytology is negative. Appropriate diagnostic studies can then be undertaken to determine the nature and site of the primary tumor. Pancreatic ascites (Table 44-1) is invariably associated with an extravasation of pancreatic fluid from the pancreatic ductal system, most commonly from a leaking pseudocyst. Ultrasound or CT examination of the pancreas followed by visualization of the pancreatic duct by
direct cannulation [viz., endoscopic retrograde cholangiopancreatography (ERCP)] usually discloses the site of leakage and permits resective surgery to be carried out. An analysis of the physiologic and metabolic factors involved in the production of ascites (detailed in Chap. 301), coupled with a complete evaluation of the nature of the ascitic fluid, invariably discloses the etiology of the ascites and permits appropriate therapy to be instituted. Acknowledgment Dr. Kurt J. Isselbacher was the co-author of this chapter in previous editions. Further Readings Lipsky MS, Sternbach MR: Evaluation and initial management of patients with ascites. Am Fam Physician 54:1327, 1996 [PMID: 8816576] McHutchison JG: Differential diagnosis of ascites. Semin Liver Dis 17:191, 1997 [PMID: 9308124] Parsons SL et al: Malignant ascites. Br J Surg 83:6, 1996 [PMID: 8653366]
Pinto PC et al: Large volume paracentesis in nonedematous patients with tense ascites: Its effect on intravascular volume. Hepatology 8:207, 1988 [PMID: 3356400] Runyon BA: Management of adult patients with ascites due to cirrhosis. Hepatology 39:841, 2004 [PMID: 14999706] Bibliography Rector WG Jr, Reynolds TB: Superiority of the serum ascites–albumin difference over the ascites total protein concentration in separation of "transudative" and "exudative" ascites. Am J Med 77:83, 1988