Introduction
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.
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.
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%.
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.
Clinical
History
- Patients with ascites often state that they have recently noticed an increase in their abdominal girth.
- Because most cases of ascites are due to liver disease, patients with ascites should be asked about risk factors for liver disease. These include the following:
- Long-term heavy alcohol use
- Chronic viral hepatitis or jaundice
- Intravenous drug use
- Multiple sexual partners
- Homosexual activity with a male partner, or heterosexual activity with a bisexual male
- Transfusion with blood not tested for hepatitis virus: in the United States, screening of donated blood for hepatitis B virus (HBV) began in 1972; reliable testing of the blood supply for hepatitis C virus (HCV) began in 1992 in developed countries
- Tattoos
- Living or birth in an area endemic for hepatitis
- Patients with alcoholic liver disease who alternate between heavy alcohol consumption and abstention (or light consumption) may experience ascites in a cyclic fashion.
- When a patient with a very long history of stable cirrhosis develops ascites, the possibility of superimposed hepatocellular carcinoma (HCC) should be considered.
- Obesity, hypercholesterolemia, and type 2 diabetes mellitus are recognized causes of nonalcoholic steatohepatitis, which can progress to cirrhosis.
- Patients with a history of cancer, especially gastrointestinal cancer, are at risk for malignant ascites. Malignancy-related ascites is frequently painful, whereas cirrhotic ascites is usually painless.
- Patients who develop ascites in the setting of established diabetes or nephrotic syndrome may have nephrotic ascites.
Physical
The physical examination in a patient with ascites should focus on the signs of portal hypertension and chronic liver disease.
- Physical findings suggestive of liver disease include jaundice, palmar erythema, and spider angiomas.
- The liver may be difficult to palpate if a large amount of ascites is present, but if palpable, the liver is often found to be enlarged. The puddle sign may be present when as little as 120 mL of fluid is present. When peritoneal fluid exceeds 500 mL, ascites may be demonstrated by the presence of shifting dullness or bulging flanks. A fluid-wave sign is notoriously inaccurate.
- Elevated jugular venous pressure may suggest a cardiac origin of ascites. A firm nodule in the umbilicus, the so-called Sister Mary Joseph nodule, is not common but suggests peritoneal carcinomatosis originating from gastric, pancreatic, or hepatic primary malignancy.
- A pathologic left-sided supraclavicular node (Virchow node) suggests the presence of upper abdominal malignancy.
- Patients with cardiac disease or nephrotic syndrome may have anasarca.
Causes
- Normal peritoneum
- Portal hypertension (serum-ascites albumin gradient [SAAG] >1.1 g/dL)
- Hepatic congestion, congestive heart failure, constrictive pericarditis, tricuspid insufficiency, Budd-Chiari syndrome
- Liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic failure, massive hepatic metastases
- Hypoalbuminemia (SAAG <1.1 g/dL)
- Nephrotic syndrome
- Protein-losing enteropathy
- Severe malnutrition with anasarca
- Miscellaneous conditions (SAAG <1.1 g/dL)
- Chylous ascites
- Pancreatic ascites
- Bile ascites
- Nephrogenic ascites
- Urine ascites
- Ovarian disease
- Portal hypertension (serum-ascites albumin gradient [SAAG] >1.1 g/dL)
- Diseased peritoneum (SAAG <1.1 g/dL)
- Infections
- Bacterial peritonitis
- Tuberculous peritonitis
- Fungal peritonitis
- Human immunodeficiency virus (HIV)-associated peritonitis
- Malignant conditions
- Peritoneal carcinomatosis
- Primary mesothelioma
- Pseudomyxoma peritonei
- Hepatocellular carcinoma
- Other rare conditions
- Familial Mediterranean fever
- Vasculitis
- Granulomatous peritonitis
- Eosinophilic peritonitis
- Infections
More on Ascites |
 Overview: Ascites |
| Differential Diagnoses & Workup: Ascites |
| Treatment & Medication: Ascites |
| Follow-up: Ascites |
| Multimedia: Ascites |
| References |
| Further Reading |
| Next Page » |
References
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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://www.guideline.gov/summary/summary.aspx?doc_id=5259&nbr=003590&string=ascites.. 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].
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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].
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Further Reading
Related eMedicine Topics
- Ascites [in the Pediatrics: Surgery section]
- Chylous Ascites
- Cirrhosis
- Hepatorenal Syndrome
- Paracentesis [in the Clinical Procedures section]
- Portal Hypertension
Clinical Trials
- Albumin 4 gr/L vs 8 gr/L in the Prevention of Post-Paracentesis Circulatory Dysfunction
- Alternatives to Large Volume Paracentesis Study
- Sodium Restriction in the Management of Cirrhotic Ascites
- Study of the Trifunctional Antibody Catumaxomab to Treat Recurrent Symptomatic Malignant Ascites
- TIPS With Coated Stents for Refractory Ascites in Patients With Cirrhosis
- Trial of Sunitinib for Refractory Malignant Ascites
- Vasoconstrictors as Alternatives to Albumin After LVP (Large-Volume Paracentesis) in Cirrhosis
National Guideline Clearinghouse
- Diagnostic laparoscopy for liver diseases. In: Diagnostic laparoscopy guidelines. Society of American Gastrointestinal and Endoscopic Surgeons - Medical Specialty Society. 1998 Apr (revised 2007 Nov). 5 pages. NGC:006841
- Management of adult patients with ascites due to cirrhosis. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization. 1998 Jan (revised 2004 Mar). 16 pages. NGC:003590
- The role of transjugular intrahepatic portosystemic shunt in the management of portal hypertension. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization. 2005 Feb. 15 pages. NGC:004222
- Ultrasonographic examinations: indications and preparation of the patient. Finnish Medical Society Duodecim - Professional Association. 2000 Apr 18 (revised 2007 Jan 11). Various pagings. NGC:005501
Keywords
ascites, fluid collection, fluid accumulation, fluid retention, distended abdomen, portal hypertension, hypoalbuminemia, hepatic congestion, congestive heart failure, constrictive pericarditis, tricuspid insufficiency, Budd-Chiari syndrome, liver disease, cirrhosis, alcoholic hepatitis,
nephrotic syndrome, protein-losing enteropathy, severe malnutrition, anasarca, chylous ascites, pancreatic ascites, bile ascites, nephrogenic ascites, urine ascites, ovarian disease, bacterial peritonitis, tuberculous peritonitis, fungal peritonitis, HIV-associated peritonitis, malignancy, peritoneal carcinomatosis, primary mesothelioma, pseudomyxoma peritonei, hepatocellular carcinoma, HCC,
familial Mediterranean fever, vasculitis, granulomatous peritonitis, eosinophilic peritonitis, alcohol use, chronic viral hepatitis, jaundice, intravenous drug use, blood transfusions, alcoholic liver disease, obesity, hypercholesterolemia, type 2 diabetes mellitus, nonalcoholic steatohepatitis, gastrointestinal cancer, malignant ascites, cirrhotic ascites, nephrotic ascites, palmar erythema, spider angiomas, puddle sign, Sister Mary Joseph nodule, gastric malignancy, pancreatic malignancy, hepatic primary malignancy, left-sided supraclavicular node, Virchow node
