Last updated: November 16, 2023

Summarytoggle arrow icon

Ascites is the abnormal accumulation of fluid within the peritoneal cavity and is a common complication of portal hypertension (e.g., due to liver cirrhosis, acute liver failure) and/or hypoalbuminemia (e.g., due to nephrotic syndrome). Other conditions resulting in ascites include chronic heart failure, inflammation of abdominal viscera (e.g., pancreatitis), and malignancies. Clinical features include progressive abdominal distention, shifting dullness, and a positive fluid wave test. Abdominal pain may be present in ascites due to acute inflammation. Diagnostics are aimed at identifying the underlying etiology and determining whether the ascitic fluid is infected. They include imaging (e.g., with abdominal ultrasound or CT abdomen and pelvis), which is used to identify free intraperitoneal fluid and possibly the underlying cause, and diagnostic paracentesis with ascitic fluid analysis. The serum-ascites albumin gradient (SAAG), or the difference between albumin levels in serum and ascitic fluid, is essential to determine the underlying cause. A high SAAG indicates that the ascites is secondary to portal hypertension. An ascitic fluid neutrophil count ≥ 250 cells/mm3 indicates spontaneous bacterial peritonitis (SBP), which should be urgently managed with empiric antibiotic therapy. Management of ascites involves identifying and managing the underlying cause as well as dietary sodium restriction and diuretic therapy. Additionally, tense ascites and refractory ascites require therapeutic paracentesis. Liver transplant is a treatment option for patients with cirrhosis who develop ascites. Transjugular intrahepatic portosystemic shunts (TIPS) and peritoneovenous shunts are advanced treatment options for refractory ascites, which carries a high risk of mortality.

Etiologytoggle arrow icon


Pathophysiologytoggle arrow icon

Pathogenesis of ascites [4][5]



Portal hypertension





The primary mechanism that leads to ascites in cirrhosis is portal hypertension. Hypoalbuminemia can contribute to the formation of, and exacerbate, ascites in cirrhosis.

Clinical featurestoggle arrow icon


Subtypes and variantstoggle arrow icon

Chylous ascites

Hemorrhagic ascites

Pancreatic ascites

Diagnosticstoggle arrow icon

Diagnostics are used to confirm the presence of ascites, assess the severity, determine the underlying etiology, and evaluate for complications. [8]

Imaging [9][10]

Abdominal ultrasound with Doppler (initial study of choice)

CT abdomen and pelvis [8]

  • Indications: to work up for the underlying cause as needed; examples include [8][11]
  • Findings

Laboratory studies [9]

The choice of laboratory studies should be guided by the pretest probability of the suspected underlying etiology.

Ascitic fluid analysis [5][8][9]

Sampling technique

  • Obtained via diagnostic paracentesis
  • See “Paracentesis” for further details on indications, contraindications, steps, troubleshooting, and complications of this procedure.


Routine peritoneal fluid analysis

Differential diagnoses of ascites based on SAAG and ascitic fluid total protein [6][8]
Ascites due to portal hypertension Ascites due to other causes
  • ≥ 1.1 g/dL
  • < 1.1 g/dL

Ascitic fluid total protein levels

Additional studies

Occult SBP is common in patients with ascites and cirrhosis, and delays in diagnosis increase the risk of death. [17]

Classificationtoggle arrow icon

The International Ascites Club classifies the severity classification of ascites as follows: [2]

  • Mild ascites (grade 1): ascites only detectable by ultrasound
  • Moderate ascites (grade 2): moderate abdominal distention
  • Large ascites (grade 3): marked abdominal distention

Treatmenttoggle arrow icon

Approach [5][8][9]

Obtain hepatology consult for patients with new-onset ascites and known or suspected liver disease.

Medical and supportive therapy [5][9][18]

This section details the management of ascites due to cirrhosis. Medical and/or supportive management of other causes of ascites (e.g., heart failure, nephrotic syndrome, peritoneal carcinomatosis, tuberculosis) are outlined in the respective articles for these conditions.

Salt and fluid restriction

  • Dietary sodium restriction: 2 g/day or 88 mEq/d (2 g of sodium = 5 g of salt)
    • Recommended for all patients
    • Advise patients to restrict the amount of salt in home-cooked meals and to avoid precooked and prepackaged food.
    • Consider referral to a nutritionist for counseling.
  • Fluid restriction: 1 L/day (only if serum Na+ < 125 mEq/L)


Combination diuretic therapy is associated with more rapid ascites reduction and a lower risk of potassium imbalance than monotherapy. [11][18]

Diuretics should be used with caution in patients with severe hyponatremia, hepatic encephalopathy, and/or renal function deterioration.

Empiric antibiotic therapy [5][9]

Antibiotic therapy for patients with cirrhosis and ascites is recommended in the following situations:

Monitoring [9][18]

  • Monitor weight, blood pressure, nutritional status, serum electrolytes, and renal function.
  • Goals of diuretic therapy
    • Patients without peripheral edema: weight loss of up to 0.5 kg/day
    • Patients with significant peripheral edema
      • Maximum recommended weight reduction: 1 kg/day
      • Once edema has resolved, daily weight loss should not exceed 0.5 kg/day
  • Discontinue or adjust the dosage of diuretics if adverse effects develop (e.g., hyponatremia, hyperkalemia, renal dysfunction).

Therapeutic paracentesis [9][18][19]

See “Paracentesis” for further details on indications, contraindications, steps, troubleshooting, and complications of therapeutic paracentesis.

Management of refractory ascites [9][18][22]

Ascites is considered refractory if it does not respond to treatment or recurs after therapeutic paracentesis despite dietary sodium restriction and high-dose diuretic therapy. The following recommendations apply to refractory ascites in patients with cirrhosis.

Half of all patients with cirrhosis who develop refractory ascites die within a year. Do not delay referral for surgical management. [9]

Complicationstoggle arrow icon

We list the most important complications. The selection is not exhaustive.

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Referencestoggle arrow icon

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  2. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
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  15. Lizaola B, Bonder A, Trivedi HD, Tapper EB, Cardenas A. Review article: the diagnostic approach and current management of chylous ascites. Aliment Pharmacol Ther. 2017; 46 (9): p.816-824.doi: 10.1111/apt.14284 . | Open in Read by QxMD
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