Background
The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the condition of pathologic fluid collection within the abdominal cavity. Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle. This article focuses only on ascites associated with cirrhosis.
See the image below.
This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites. For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center and Heart Center. Also, see eMedicine's patient education articles Cirrhosis, Hepatitis B, Hepatitis C, and Congestive Heart Failure.
Pathophysiology
The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation.
The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.
The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia.
The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis.
Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites.
Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.
Epidemiology
Mortality/Morbidity
Ambulatory patients with an episode of cirrhotic ascites have a 3-year mortality rate of 50%. The development of refractory ascites carries a poor prognosis, with a 1-year survival rate of less than 50%.[1]
Sex
Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle.
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].
[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].
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].
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.
Gines P, Cardenas A. The management of ascites and hyponatremia in cirrhosis. Semin Liver Dis. Feb 2008;28(1):43-58. [Medline].
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].
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].
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].
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].
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].
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].
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].
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].
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].
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].
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.
Cardenas A, Bataller R, Arroyo V. Mechanisms of ascites formation. Clin Liver Dis. May 2000;4(2):447-65. [Medline].
[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].
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].
Jeffery J, Murphy MJ. Ascitic fluid analysis: the role of biochemistry and haematology. Hosp Med. May 2001;62(5):282-6. [Medline].
Oguntona SA, Alebiosu CO. Current concepts in the management of refractory cirrhotic ascites. Niger J Med. Jul-Sep 2006;15(3):197-202. [Medline].
Pauly RP, Sood MM, Chan CT. Management of refractory ascites using nocturnal home hemodialysis. Semin Dial. Jul-Aug 2008;21(4):367-70. [Medline].
Reynolds TB. Ascites. Clin Liver Dis. Feb 2000;4(1):151-68, vii. [Medline].
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.
Wong F, Blendis L. Hepatorenal failure. Clin Liver Dis. Feb 2000;4(1):169-89. [Medline].

