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Ascites Workup

  • Author: Rahil Shah, MD; Chief Editor: Julian Katz, MD  more...
 
Updated: Jan 03, 2016
 

Approach Considerations

Abdominal ultrasonography, diagnostic paracentesis, and ascitic fluid cultures are recommended by the British Society of Gastroenterology, the European Association for the Study of the Liver (EASL), and the American Association for the Study of Liver Diseases (AASLD), particularly in the setting of supsected infection.[1]

Laparoscopy may be valuable for the diagnosis of otherwise unexplained cases, especially if malignant ascites is suspected.[4]  This may be of particular importance in the diagnosis of malignant mesothelioma.

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Laboratory Studies

In patients with new-onset ascites of unknown origin, peritoneal fluid should be sent for cell count, albumin level, culture, total protein, Gram stain, and cytology. Note the following

  • Inspection: Most ascitic fluid is transparent and tinged yellow. A minimum of 10,000 red blood cells/µL is required for ascitic fluid to appear pink, and more than 20,000 red blood cells/µL will produce distinctly blood-tinged fluid. This may result from either a traumatic tap or malignancy. Bloody fluid from a traumatic tap is heterogeneously bloody, and the fluid will clot. Nontraumatic bloody fluid is homogeneously red and does not clot because the blood has already clotted and lysed. Cloudy ascitic fluid with a purulent consistency indicates infection.
  • Cell count: Normal ascitic fluid contains fewer than 500 leukocytes/µL and fewer than 250 polymorphonuclear leukocytes (PMNs)/µL. Any inflammatory condition can cause an elevated white blood cell count. A PMN count of greater than 250 cells/µL is highly suggestive of bacterial peritonitis. [5] In tuberculous peritonitis and peritoneal carcinomatosis, lymphocytes usually predominate.
  • SAAG: The SAAG is the best single test for classifying ascites into portal hypertensive (SAAG >1.1 g/dL) and non–portal hypertensive (SAAG < 1.1 g/dL) causes. Calculated by subtracting the ascitic fluid albumin value from the serum albumin value, it correlates directly with portal pressure. The specimens should be obtained relatively simultaneously. The accuracy of the SAAG results is approximately 97% in classifying ascites. The terms high-albumin gradient and low-albumin gradient should replace the terms transudative and exudative in the description of ascites.
  • Total protein: In the past, ascitic fluid has been classified as an exudate if the protein level is greater than or equal to 2.5 g/dL. However, the accuracy is only approximately 56% for detecting exudative causes. The total protein level may provide additional clues when used with the SAAG. An elevated SAAG and a high protein level are observed in most cases of ascites due to hepatic congestion. The combination of a low SAAG and a high protein level is characteristic of malignant ascites (see Causes).
  • Culture/Gram stain: Culture has a 92% sensitivity for the detection of bacteria in ascitic fluid, provided that samples are inoculated into blood culture bottles immediately, at the bedside. In contrast, Gram stain is only 10% sensitive for visualizing bacteria in early-detected spontaneous bacterial peritonitis. Approximately 10,000 bacteria/mL are required for detection by Gram stain; the median concentration of bacteria in spontaneous bacterial peritonitis is 1 organism/mL.
  • Cytology: Cytology smears are reported to be 58-75% sensitive for detection of malignant ascites.
  • Ascitic amylase cultures/PCR are recommended for suspected pancreatitis, and mycobacterial cultures/PCR for suspected tuberculosis. [1]
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Imaging Studies

Chest and plain abdominal films

Elevation of the diaphragm, with or without sympathetic pleural effusions (hepatic hydrothorax), is visible in the presence of massive ascites. More than 500 mL of fluid is usually required for ascites to be diagnosed based on findings from abdominal films.

Many nonspecific signs suggest ascites, such as diffuse abdominal haziness, bulging of the flanks, indistinct psoas margins, poor definition of the intra-abdominal organs, erect position density increase, separation of small bowel loops, and centralization of floating gas containing small bowel.

The direct signs are more reliable and specific. In 80% of patients with ascites, the lateral liver edge is medially displaced from the thoracoabdominal wall (Hellmer sign). In the pelvis, fluid accumulates in the rectovesical pouch and then spills into the paravesical fossa. The fluid produces symmetric densities on both sides of the bladder, which is termed a "dog's ear" or "Mickey Mouse" appearance. Medial displacement of the cecum and ascending colon and lateral displacement of the properitoneal fat line are present in more than 90% of patients with significant ascites. Although obliteration of the hepatic angle as been suggested as a sign of increased intra-abdominal fluid, this finding is seen in 80% of healthy patients.

Ultrasonography

Real-time ultrasonography is the easiest and most sensitive technique for the detection of ascitic fluid. Volumes as small as 5-10 mL can routinely be visualized. Uncomplicated ascites appears as a homogeneous, freely mobile, anechoic collection in the peritoneal cavity that demonstrates deep acoustic enhancement. Free ascites does not displace organs but typically situates itself between them, contouring to organ margins and demonstrating acute angles at the point at which the fluid borders the organ.

The smallest amounts of fluid tend to collect in the Morison pouch (posterior subhepatic space) and around the liver as a sonolucent band. With massive ascites, the small bowel loops have a characteristic polycyclic, "lollipop," or arcuate appearance because they are arrayed on either side of the vertically floating mesentery.

Certain ultrasonographic findings suggest that the ascites may be infected, inflammatory, or malignant. These findings include coarse internal echoes (blood), fine internal echoes (chyle), multiple septa (tuberculous peritonitis, pseudomyxoma peritonei), loculation or atypical fluid distribution, matting or clumping of bowel loops, and thickening of interfaces between fluid and adjacent structures. In malignant ascites, the bowel loops do not float freely but may be tethered along the posterior abdominal wall, plastered to the liver or other organs, or surrounded by loculated fluid collections.

  • Most patients (95%) with carcinomatous peritonitis have a gallbladder wall that is less than 3 mm thick. Mural thickening of the gallbladder is associated with benign ascites in 82% of cases. The thickening of the gallbladder is primarily a reflection of cirrhosis and portal hypertension.

Computed tomography (CT) scanning

Ascites is demonstrated well on CT scan images. Small amounts of ascitic fluid localize in the right perihepatic space, the posterior subhepatic space, and the Douglas pouch (rectouterine pouch). See the image below.

This computed tomography scan demonstrates free in This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.

A number of CT scan features suggest neoplasia. Hepatic, adrenal, splenic, or lymph node lesions associated with masses arising from the gut, ovary, or pancreas are suggestive of malignant ascites. Patients with malignant ascites tend to have proportional fluid collections in the greater and lesser sacs; whereas, in patients with benign ascites, the fluid is observed primarily in the greater sac and not in the lesser omental bursae.

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Procedures

Abdominal paracentesis: Abdominal paracentesis is the most rapid and perhaps the most cost-effective method of diagnosing the cause of ascites formation. Guidelines from the American Association for the Study of Liver Diseases (AASLD) for management of adult patients with ascites due to cirrhosis advocate paracentesis in all patients with clinically apparent new-onset ascites (class I, level C recommendation).[6]

Bleeding from paracentesis is sufficiently uncommon that the AASLD does not recommend the prophylactic use of fresh frozen plasma or platelets beforehand (class III, level C recommendation).[6]

For more detailed information regarding paracentesis, including images and video, please see the Medscape article Paracentesis [in the Clinical Procedures section].

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Staging

Ascites may be semi-quantified using the following system:

  • Stage 1+ is detectable only after careful examination.
  • Stage 2+ is easily detectable but of relatively small volume.
  • Stage 3+ is obvious, but not tense, ascites.
  • Stage 4+ is tense ascites.
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Contributor Information and Disclosures
Author

Rahil Shah, MD Consulting Staff, Lebanon Endoscopy Center

Rahil Shah, MD is a member of the following medical societies: American College of Gastroenterology, American Society for Gastrointestinal Endoscopy

Disclosure: Received consulting fee from Takeda for speaking and teaching.

Coauthor(s)

Janice M Fields, MD, FACG, FACP Assistant Professor of Internal Medicine, Oakland University William Beaumont School of Medicine; Consulting Staff, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital, St John Macomb-Oakland Hosptial

Janice M Fields, MD, FACG, FACP is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, National Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors

Robert J Fingerote, MD, MSc, FRCPC Consultant, Clinical Evaluation Division, Biologic and Gene Therapies, Directorate Health Canada; Consulting Staff, Department of Medicine, Division of Gastroenterology, York Central Hospital, Ontario

Robert J Fingerote, MD, MSc, FRCPC is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Medical Association

Disclosure: Nothing to disclose.

References
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  2. Fede G, D'Amico G, Arvaniti V, Tsochatzis E, Germani G, Georgiadis D, et al. Renal failure and cirrhosis: a systematic review of mortality and prognosis. J Hepatol. 2011 Dec 12. [Medline].

  3. Weniger M, D'Haese JG, Angele MK, Kleespies A, Werner J, Hartwig W. Treatment options for chylous ascites after major abdominal surgery: a systematic review. Am J Surg. 2016 Jan. 211 (1):206-13. [Medline].

  4. Han CM, Lee CL, Huang KG, et al. Diagnostic laparoscopy in ascites of unknown origin: Chang Gung Memorial Hospital 20-year experience. Chang Gung Med J. 2008 Jul-Aug. 31(4):378-83. [Medline]. [Full Text].

  5. Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results?. JAMA. 2008 Mar 12. 299(10):1166-78. [Medline].

  6. [Guideline] Runyon BA, American Association for the Study of Liver Diseases. Management of adult patients with ascites due to cirrhosis: update 2012. National Guideline Clearinghouse. Available at http://guideline.gov/content.aspx?id=45103&search=ascites. Accessed: Nov 6, 2014.

  7. Gines P, Cardenas A. The management of ascites and hyponatremia in cirrhosis. Semin Liver Dis. 2008 Feb. 28(1):43-58. [Medline].

  8. Ginès P, Wong F, Watson H, et al, for the HypoCAT Study Investigators. Effects of satavaptan, a selective vasopressin V(2) receptor antagonist, on ascites and serum sodium in cirrhosis with hyponatremia: a randomized trial. Hepatology. 2008 Jul. 48(1):204-13. [Medline].

  9. Bellot P, Welker MW, Soriano G, von Schaewen M, Appenrodt B, Wiest R, et al. Automated low flow pump system for the treatment of refractory ascites: a multi-center safety and efficacy study. J Hepatol. 2013 May. 58(5):922-7. [Medline].

  10. Sola-Vera J, Minana J, Ricart E, et al. Randomized trial comparing albumin and saline in the prevention of paracentesis-induced circulatory dysfunction in cirrhotic patients with ascites. Hepatology. 2003 May. 37(5):1147-53. [Medline]. [Full Text].

  11. Lata J, Marecek Z, Fejfar T, Zdenek P, et al. The efficacy of terlipressin in comparison with albumin in the prevention of circulatory changes after the paracentesis of tense ascites--a randomized multicentric study. Hepatogastroenterology. 2007 Oct-Nov. 54(79):1930-3. [Medline].

  12. Singh V, Kumar R, Nain CK, Singh B, Sharma AK. Terlipressin versus albumin in paracentesis-induced circulatory dysfunction in cirrhosis: a randomized study. J Gastroenterol Hepatol. 2006 Jan. 21(1 pt 2):303-7. [Medline].

  13. Mercadante S, Intravaia G, Ferrera P, Villari P, David F. Peritoneal catheter for continuous drainage of ascites in advanced cancer patients. Support Care Cancer. 2008 Aug. 16(8):975-8. [Medline].

  14. Courtney A, Nemcek AA Jr, Rosenberg S, et al. Prospective evaluation of the PleurX catheter when used to treat recurrent ascites associated with malignancy. J Vasc Interv Radiol. 2008 Dec. 19(12):1723-31. [Medline].

  15. Sorrentino P, Castaldo G, Tarantino L, Bracigliano A, Perrella A, Perrella O, et al. Preservation of Nutritional-status in Patients with Refractory Ascites due to Hepatic Cirrhosis who are Undergoing Repeated Paracentesis. J Gastroenterol Hepatol. 2011 Dec 6. [Medline].

  16. Guo TT, Yang Y, Song Y, Ren Y, Liu ZX, Cheng G. Effects of midodrine for patients with ascites due to cirrhosis: systematic review with meta-analysis. J Dig Dis. 2015 Dec 2. [Medline].

  17. Seike M, Maetani I, Sakai Y. Treatment of malignant ascites in patients with advanced cancer: peritoneovenous shunt versus paracentesis. J Gastroenterol Hepatol. 2007 Dec. 22(12):2161-6. [Medline].

  18. Wallerstedt S, Olsson R, Simren M, et al. Abdominal tenderness in ascites patients indicates spontaneous bacterial peritonitis. Eur J Intern Med. 2007 Jan. 18(1):44-7. [Medline].

  19. Tapper EB, Bonder A, Cardenas A. Preventing and treating acute kidney injury among hospitalized patients with cirrhosis and ascites: a narrative review. Am J Med. 2015 Dec 24. [Medline].

 
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This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
Peritoneovenous shunt.
Massive ascites.
 
 
 
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