What are the causes of ascites?

Causes of Ascites

Cirrhosis is the most common cause of ascites, accounting for approximately 75-85% of cases, with the remaining cases caused by conditions such as malignancy, heart failure, tuberculosis, pancreatic disease, and nephrotic syndrome. 1, 2

Classification Based on Serum-Ascites Albumin Gradient (SAAG)

The SAAG is the most useful test to determine the underlying cause of ascites, with an accuracy of approximately 97%.

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

• Cirrhosis (most common cause)
• Alcoholic hepatitis
• Heart failure
• Budd-Chiari syndrome
• Portal vein thrombosis
• Massive liver metastases
• Liver involvement in right heart failure 1

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

• Peritoneal carcinomatosis
• Tuberculosis peritonitis
• Pancreatic ascites
• Nephrotic syndrome
• Serositis in connective tissue diseases
• Bowel obstruction or infarction 1

Pathophysiology of Ascites Formation

Two key factors are involved in the pathogenesis of ascites:

1. Portal hypertension: Increases hydrostatic pressure within hepatic sinusoids, favoring fluid transudation into the peritoneal cavity 1

   • Progressive collagen deposition and nodule formation in cirrhosis alter normal vascular architecture
   • Activated hepatic stellate cells may dynamically regulate sinusoidal tone and portal pressure

2. Sodium and water retention: Inability to excrete adequate sodium leads to positive sodium balance 1

   • Arterial splanchnic vasodilation causes decreased effective arterial blood volume
   • Activation of vasoconstrictor and sodium-retaining systems (sympathetic nervous system and renin-angiotensin-aldosterone system)
   • Renal sodium retention leads to expansion of extracellular fluid volume and ascites formation

Diagnostic Approach

Initial Investigations

• Diagnostic paracentesis with:
  • Ascitic fluid cell count and differential
  • Total protein and albumin measurement
  • SAAG calculation
  • Culture (bedside inoculation into blood culture bottles)
  • Neutrophil count to rule out spontaneous bacterial peritonitis 1

Additional Tests Based on Clinical Suspicion

• Amylase (if pancreatic origin suspected)
• Cytology (if malignancy suspected)
• Glucose and lactate dehydrogenase (if secondary bacterial peritonitis suspected)
• Mycobacterial culture (if tuberculosis suspected) 1

Imaging

• Abdominal ultrasound to evaluate:
  • Liver appearance
  • Pancreas and lymph nodes
  • Presence of splenomegaly (suggesting portal hypertension) 1

Management Considerations

The treatment of ascites depends on its cause:

For Cirrhotic Ascites

• Sodium restriction (2000 mg/day)
• Diuretic therapy:
  • Spironolactone (aldosterone antagonist) counteracts secondary aldosteronism 3
  • Loop diuretics may be added for resistant cases
  • Monitor for complications including hyperkalemia, hyponatremia, and renal impairment

For Refractory Ascites

• Large volume paracentesis with albumin infusion
• Transjugular intrahepatic portosystemic shunt (TIPS)
• Liver transplantation for eligible candidates 4, 5

For Non-Portal Hypertensive Ascites

• Treatment directed at the underlying cause
• Low SAAG ascites generally does not respond to sodium restriction and diuretics 1

Special Considerations

• Alcohol-induced liver disease: Abstinence from alcohol can dramatically improve the reversible component of alcoholic liver disease and make ascites more responsive to medical therapy 1

• Monitoring: Daily weight monitoring is essential to assess diuretic efficacy and prevent adverse effects; weight loss should not exceed 0.5 kg/day in patients without peripheral edema 1

• Hyponatremia: Fluid restriction is generally not necessary unless severe hyponatremia is present 1

• Hepatic impairment: Spironolactone can cause sudden alterations of fluid and electrolyte balance which may precipitate impaired neurological function and worsening hepatic encephalopathy 3

The development of ascites is associated with poor prognosis and impaired quality of life. Patients with cirrhosis and first onset of ascites have a probability of survival of 85% during the first year and 56% at 5 years without liver transplantation 4.