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  • Accumulation of fluid in the peritoneal cavity; may occur in conditions that cause generalized edema
  • 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%), other (6%)

~50–60% of cirrhotic patients develop ascites within 10 years (1).

10% of patients with cirrhosis have ascites.

Etiology and Pathophysiology

  • Portal hypertension versus nonportal hypertension causes
    • Cannot reliably establish/confirm etiology without paracentesis
    • Serum-ascites albumin gradient (SAAG): (serum albumin level: ascites albumin level) helps to differentiate causes
  • High portal pressure (SAAG ≥1.1)
    • Cirrhosis
    • Hepatitis (alcoholic, viral, autoimmune, medications)
    • Acute liver failure
    • Liver malignancy (primary or metastatic)
    • Elevated right-sided filling pressures from heart failure or constrictive pericarditis
    • Hepatic venous thrombosis (Budd-Chiari syndrome)
    • Portal vein thrombosis
  • Normal portal pressure (SAAG <1.1)
    • Peritoneal carcinomatosis
    • Tuberculosis
    • 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)
  • Pathophysiology is best described for portal hypertensive (typically cirrhotic) ascites.
    • Reduced renal and carotid perfusion activates systemic vasoconstrictors and antinatriuretic mechanisms. This stimulates the sympathetic nervous system and renin-angiotensin-aldosterone system to retain sodium and water.
    • Most ascites is due to portal hypertension, with preferentially dilated splanchnic vasculature causing systemic hypotension.

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