What are the causes of ascites?

Causes of Ascites

Cirrhosis is the most common cause of ascites, accounting for approximately 85% of cases in the United States, while the remaining 15% result from various non-hepatic etiologies including heart failure, cancer, tuberculosis, and nephrotic syndrome. 1, 2

Classification by Serum-Ascites Albumin Gradient (SAAG)

The SAAG is the most useful diagnostic tool for determining the underlying cause of ascites, with a 97% accuracy in identifying portal hypertension when ≥1.1 g/dL.

High SAAG Ascites (≥1.1 g/dL) - Portal Hypertension Related

• Cirrhosis - Most common overall cause
• Alcoholic hepatitis
• Heart failure - Distinguished from cirrhosis by elevated BNP/pro-BNP levels (median 6100 pg/mL vs 166 pg/mL in cirrhosis) 1
• Budd-Chiari syndrome (hepatic vein thrombosis)
• Sinusoidal obstruction syndrome
• Acute liver failure
• Massive liver metastases causing portal hypertension

Low SAAG Ascites (<1.1 g/dL) - Non-Portal Hypertension Related

• Peritoneal carcinomatosis
• Tuberculous peritonitis
• Pancreatic ascites
• Nephrotic syndrome (exception: may respond to diuretics despite low SAAG)
• Postoperative lymphatic leak
• Myxedema (severe hypothyroidism)

Mixed Ascites

Approximately 5% of patients have "mixed ascites" with two or more concurrent causes 1. Common combinations include:

• Cirrhosis plus peritoneal carcinomatosis
• Cirrhosis plus tuberculous peritonitis
• Multiple predisposing factors (e.g., heart failure, diabetic nephropathy, and nonalcoholic steatohepatitis)

Pathophysiological Mechanisms

1. Portal hypertension pathway:

   • Increased hydrostatic pressure in portal circulation
   • Splanchnic vasodilation
   • Reduced effective arterial blood volume
   • Activation of sodium-retaining mechanisms

2. Hypoalbuminemia pathway:

   • Reduced oncotic pressure
   • Fluid shifts from intravascular to extravascular space

3. Direct peritoneal pathology:

   • Inflammation (tuberculosis, pancreatitis)
   • Malignant infiltration (peritoneal carcinomatosis)
   • Infection

Diagnostic Approach

The initial evaluation should include:

1. Diagnostic paracentesis - Essential for all new-onset ascites 1

   • Cell count and differential
   • Total protein
   • Albumin (for SAAG calculation)
   • Cultures if infection suspected

2. Imaging

   • Abdominal ultrasound with Doppler to evaluate:
     • Liver morphology
     • Portal vein patency
     • Hepatic vein patency
     • Rule out hepatocellular carcinoma

3. Laboratory tests

   • Liver function tests
   • Renal function
   • Serum albumin
   • Pro-BNP/BNP (to distinguish cardiac from cirrhotic ascites)

Clinical Pearls and Pitfalls

• Ascites mimics: Giant cysts or pseudocysts can rarely mimic ascites; imaging usually provides the correct diagnosis 1
• Obesity challenge: Physical examination for ascites in obese patients is difficult; ultrasound may be required 1
• Temporal clue: Ascites typically presents within weeks of development, whereas a slowly enlarging abdomen over months to years is more likely due to obesity 1
• Mixed ascites: Always consider the possibility of multiple causes, especially when response to therapy is suboptimal 1
• Mortality indicator: Development of ascites in cirrhosis is associated with reduced 5-year survival from 80% to 30% 1, marking transition from compensated to decompensated cirrhosis

By understanding the diverse causes of ascites and applying a systematic diagnostic approach using the SAAG, clinicians can accurately determine the underlying etiology and implement appropriate treatment strategies to improve patient outcomes.