Ascites

ASCITES 

1. Definition

Ascites is the pathological accumulation of free fluid in the peritoneal cavity, most commonly due to portal hypertension secondary to cirrhosis.

• Clinically detectable when fluid ≥ 1.5–2 L
• Most common complication of decompensated cirrhosis

2. Epidemiology

• ~60% of patients with compensated cirrhosis develop ascites within 10 years
• Once ascites develops → 5-year survival ≈ 50%
• Major cause of hospital admission in liver disease

3. Etiology of Ascites

A. Portal Hypertension–Related (High SAAG)

• Cirrhosis (most common)
• Alcoholic liver disease
• Viral hepatitis (HBV, HCV)
• NASH
• Budd–Chiari syndrome
• Cardiac cirrhosis / constrictive pericarditis

B. Non–Portal Hypertension (Low SAAG)

• Peritoneal carcinomatosis
• Tuberculous peritonitis
• Pancreatic ascites
• Nephrotic syndrome
• Serositis (SLE)

4. Pathophysiology of Ascites

Central Concept: Portal Hypertension + Splanchnic Vasodilation

Stepwise Mechanism:

1. Portal hypertension → ↑ sinusoidal pressure
2. ↑ Nitric oxide → splanchnic vasodilation
3. ↓ Effective arterial blood volume (arterial underfilling)
4. Activation of:
   
   • RAAS
   • Sympathetic nervous system
   • ADH

5. Renal sodium and water retention
6. Fluid transudation into peritoneal cavity

Key Hypotheses (Harrison):

• Peripheral arterial vasodilation hypothesis (most accepted)
• Overflow hypothesis (obsolete)

5. Clinical Features

Symptoms

• Progressive abdominal distension
• Weight gain
• Dyspnea (↑ intra-abdominal pressure)
• Early satiety
• Lower limb edema

Signs

• Shifting dullness
• Fluid thrill
• Umbilical hernia
• Caput medusae
• Signs of chronic liver disease

6. Grading of Ascites (International Ascites Club)

7. Diagnostic Evaluation

A. Diagnostic Paracentesis (MANDATORY)

All new-onset ascites → diagnostic tap

Ascitic Fluid Analysis

8. SAAG (Serum–Ascites Albumin Gradient)

Formula:

SAAG = Serum albumin – Ascitic fluid albumin

Interpretation:

• SAAG ≥ 1.1 g/dL → Portal hypertension
• SAAG < 1.1 g/dL → Non-portal causes

SAAG is superior to total protein for etiological diagnosis 

9. Management of Ascites

A. General Measures

• Treat underlying cause
• Avoid NSAIDs
• Avoid ACE-I / ARBs in advanced cirrhosis
• Alcohol abstinence

B. Sodium Restriction

• <2 g/day (≈ 88 mmol/day)
• Water restriction only if Na <125 mEq/L

C. Diuretics-oral (First-line)

Maintain 100:40 ratio
Max doses:

• Spironolactone 400 mg/day
• Furosemide 160 mg/day

Target weight loss:

• With edema: ≤1 kg/day
• Without edema: ≤0.5 kg/day

D. Large Volume Paracentesis (LVP)

• For tense / refractory ascites
• Remove >5 L safely

Albumin replacement:

• 6–8 g albumin per liter removed

Prevents paracentesis-induced circulatory dysfunction

10. Refractory Ascites

Definition

Ascites that cannot be mobilized or recurs rapidly despite:

• Sodium restriction
• Maximal diuretics

Management

• Repeated LVP + albumin
• TIPS (Transjugular Intrahepatic Portosystemic Shunt)
• Liver transplantation (definitive)

11. Complications of Ascites

A. Spontaneous Bacterial Peritonitis (SBP)

• PMN ≥250/mm³
• Common organisms: E. coli, Klebsiella
• Treat: 3rd gen cephalosporins

B. Hepatorenal Syndrome (HRS)

• Functional renal failure
• Triggered by SBP, LVP without albumin

C. Others

• Umbilical hernia rupture
• Hyponatremia
• Respiratory compromise

12. Special Types of Ascites

A. Cardiac Ascites

• High SAAG, high protein
• Treat heart failure

B. Chylous Ascites

• Milky fluid
• Triglycerides >200 mg/dL
• Causes: lymphoma, TB

C. Pancreatic Ascites

• Very high amylase
• Low SAAG

13. Prognosis

• Ascites = marker of decompensation
• Median survival after onset ≈ 2–3 years
• Best long-term treatment: liver transplantation