Ascites Workup

  • Author: Rahil Shah, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jan 4, 2012
 

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.
    • 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.[2] 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.
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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 inThis 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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Other Tests

  • Laparoscopy may be valuable for the diagnosis of otherwise unexplained cases, especially if malignant ascites is suspected.[3] This may be of particular importance in the diagnosis of malignant mesothelioma.
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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 (grade II-3 recommendation).[4]

Bleeding from paracentesis is sufficiently uncommon that the AASLD does not recommend the prophylactic use of fresh frozen plasma or platelets beforehand (grade III).[4]

For more detailed information regarding paracentesis, including images and video, please see the eMedicine 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 and American Society for Gastrointestinal Endoscopy

Disclosure: Takeda Consulting fee Speaking and teaching

Coauthor(s)

Janice M Fields, MD  Consulting Staff, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital, William Beaumont Hospital, St. John Macomb-Oakland Hospital

Janice M Fields, MD 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, and National Medical Association

Disclosure: Salic Pharmaceuticals Honoraria Review panel membership

Specialty Editor Board

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, Canadian Medical Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

James L Achord, MD  Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine

James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

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, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

References
  1. 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. Dec 12 2011;[Medline].

  2. [Best Evidence] 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. Mar 12 2008;299(10):1166-78. [Medline].

  3. 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. Jul-Aug 2008;31(4):378-83. [Medline]. [Full Text].

  4. American Association for the Study of Liver Diseases. Management of adult patients with ascites due to cirrhosis. National Guideline Clearinghouse. Available at http://guideline.gov/summary/summary.aspx?doc_id=5259. Accessed March 20, 2009.

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

  6. 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. Jul 2008;48(1):204-13. [Medline].

  7. 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. May 2003;37(5):1147-53. [Medline]. [Full Text].

  8. 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. Oct-Nov 2007;54(79):1930-3. [Medline].

  9. 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. Jan 2006;21(1 pt 2):303-7. [Medline].

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

  11. 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. Dec 2008;19(12):1723-31. [Medline].

  12. 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. Dec 6 2011;[Medline].

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

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

  15. Albornoz L, Motta A, Alvarez D, et al. Nitric oxide synthase activity in the splanchnic vasculature of patients with cirrhosis: relationship with hemodynamic disturbances. J Hepatol. Oct 2001;35(4):452-6. [Medline].

  16. Amadon MN, Arroyo V. Ascites and spontaneous bacterial peritonitis. In: Schiff ER, Sorrell MF, Maddrey WC, eds. Schiff's Diseases of the Liver. 8th ed. Philadelphia, Pa: Lippincott Raven; 1999:503-44.

  17. Cardenas A, Bataller R, Arroyo V. Mechanisms of ascites formation. Clin Liver Dis. May 2000;4(2):447-65. [Medline].

  18. [Best Evidence] D'Amico G, Luca A, Morabito A, Miraglia R, D'Amico M. Uncovered transjugular intrahepatic portosystemic shunt for refractory ascites: a meta-analysis. Gastroenterology. Oct 2005;129(4):1282-93. [Medline].

  19. Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology. Feb 2001;120(3):726-48. [Medline].

  20. Jeffery J, Murphy MJ. Ascitic fluid analysis: the role of biochemistry and haematology. Hosp Med. May 2001;62(5):282-6. [Medline].

  21. Oguntona SA, Alebiosu CO. Current concepts in the management of refractory cirrhotic ascites. Niger J Med. Jul-Sep 2006;15(3):197-202. [Medline].

  22. Pauly RP, Sood MM, Chan CT. Management of refractory ascites using nocturnal home hemodialysis. Semin Dial. Jul-Aug 2008;21(4):367-70. [Medline].

  23. Reynolds TB. Ascites. Clin Liver Dis. Feb 2000;4(1):151-68, vii. [Medline].

  24. Runyon B. Approach to the patient with ascites. In: Yamada T, Alpers DH, Laine L, Owyang C, Powell DW, eds. Textbook of Gastroenterology. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1999:966-91.

  25. Wong F, Blendis L. Hepatorenal failure. Clin Liver Dis. Feb 2000;4(1):169-89. [Medline].

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