• Ascites is the pathologic accumulation of fluid in the peritoneal cavity and the most common complication of cirrhosis (1).
  • It may occur in conditions that cause generalized edema like nephrotic syndrome, heart failure, and malignancy.
  • Amount of fluid accumulation:
    • Grade 1: Mild ascites—only detected by ultrasound (US); responsive ascites
    • Grade 2: Moderate ascites—moderate symmetric distension of abdomen; recurrent ascites
    • Grade 3: Large or gross ascites—marked distension of the abdomen; refractory ascites (RA)
      • Ascitic fluid that recurs after paracentesis or cannot be prevented by treatment
  • Men generally have no fluid in peritoneal cavity; women may have up to 20 mL depending on menstrual phase.


  • Children: most commonly associated with nephrotic syndrome and malignancy
  • Adults: cirrhosis (81%), cancer (10%), heart failure (3%), tuberculosis (TB) 2%, other (6%)
  • 50% of patients with decompensated cirrhosis develop ascites.

Approximately 50–60% of cirrhotic patients develop ascites within 10 years (2). The presence of ascites in cirrhotic patients is a poor prognostic indicator with mortality of about 44% in 5 years (1).

10% of patients with cirrhosis have ascites.

Etiology and Pathophysiology

  • Portal hypertension versus non portal hypertension
    • Cannot reliably establish/confirm etiology without paracentesis
    • Serum-ascites albumin gradient (SAAG): (serum albumin level: ascites albumin level) helps to differentiate
  • High portal pressure (SAAG ≥1.1 g/dL)—reflects portal hypertension
    • Cirrhosis, hepatitis (alcoholic, viral, autoimmune, medications), acute liver failure, liver malignancy (primary or metastatic), heart failure or constrictive pericarditis, Budd-Chiari syndrome, and portal vein thrombosis
  • Normal portal pressure (SAAG <1.1 g/dL)—excludes portal hypertension
    • Peritoneal carcinomatosis, TB, severe hypoalbuminemia (nephrotic syndrome; severe enteropathy with protein loss), Meigs syndrome (ovarian cancer), lymphatic leak (chylous ascites), pancreatitis, inflammatory (vasculitis, lupus serositis, sarcoidosis), other infections (parasitic, fungal), hemoperitoneum (trauma or ectopic pregnancy)
  • Pathogenesis of ascites in the setting of portal hypertension (cirrhotic ascites): backward transmission of increased pressure to the visceral capillary bed with subsequent dilation and shift of fluid to the peritoneal cavity
    • This decreases intravascular volume and leads to hypotension. Systemic hypovolemia triggers renin-angiotensin–aldosterone system.

Risk Factors

  • Cirrhosis—hepatitis B and C; alcohol abuse
  • Congestive heart failure (CHF); advanced kidney disease; malignancy
  • TB

General Prevention

Lifestyle—appropriate diet; physical activity; safe sexual practices; avoid alcohol misuse and hepatotoxic medications.

Commonly Associated Conditions

Nephrotic syndrome, liver cancer, heart failure

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