Description

• Accumulation of fluid in the peritoneal cavity; may occur in conditions that cause generalized edema
• Refractory ascites; 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.

Epidemiology

• Children: most commonly associated with nephrotic syndrome and malignancy
• Adults: cirrhosis (81%), cancer (10%), heart failure (3%), other (6%)

Incidence
~50–60% of cirrhotic patients develop ascites within 10 years (1). The presence of ascites in cirrhotic patients is a poor prognostic indicator with a survival rate of 50% at 2 years.

Prevalence
10% of patients with cirrhosis have ascites.

Etiology and Pathophysiology

• Portal hypertension versus nonportal 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)
  • Cirrhosis is the most common cause of ascites in the United States.
  • 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 (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)
  • Most ascites is due to portal hypertension leading to backward transmission of increased pressure to the visceral capillary bed with subsequent dilation and shift of fluid to the peritoneal cavity. This dilation further increases portal pressures and decreases systemic blood volume with resultant hypotension. Systemic hypovolemia stimulates neurohormonal mechanisms (renin angiotensin system and antidiuretic hormone) for sodium retention as an attempt to compensate for decreased systemic volume and pressure.

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.