Approach to Ascites

1. Pathophysiology

• Splanchnic vasodilation → increased hydrostatic pressure → fluid extravasation into peritoneum; when lymphatic return is overwhelmed, fluid accumulates
• Decreased arterial filling → activation of renin-angiotensin-aldosterone system → renal sodium and water retention → plasma volume expansion → further fluid accumulation

2. Causes of Ascites

SAAG ≥ 1.1 g/dL (Portal hypertension / Transudates)

SAAG < 1.1 g/dL (Non-portal / Exudates)

Note: Malignancy accounts for only ~10% of ascites; epithelial cancers (colon, gastric, pancreatic, ovary, breast, endometrial) cause 80% of malignant ascites.

Meigs' syndrome = benign ovarian fibroma + ascites + pleural effusion (both resolve with tumor excision).

3. Clinical Presentation

• Symptoms: Abdominal distension, discomfort, early satiety, dyspnea (respiratory compromise when severe)
• Signs:
  • Shifting dullness (most reliable clinical sign; requires ~1.5 L of fluid)
  • Fluid thrill (massive ascites)
  • Bulging flanks
  • Stigmata of chronic liver disease: spider nevi, palmar erythema, caput medusae (portosystemic shunt via umbilical vein), gynecomastia, testicular atrophy, Dupuytren's contracture

4. Diagnostic Approach

Step 1: History and Physical Examination

• History of liver disease, alcohol use, malignancy, cardiac disease, TB exposure
• Careful abdominal exam for shifting dullness, fluid thrill, hepatosplenomegaly

Step 2: Abdominal Imaging

Step 3: Diagnostic Paracentesis (FIRST investigation in new ascites)

Step 4: Calculate the SAAG

• SAAG ≥ 1.1 g/dL → Portal hypertension (97% accuracy)
• SAAG < 1.1 g/dL → Non-portal hypertensive cause

5. Management

A. Cirrhotic Ascites (Mainstay)

1. Sodium restriction - 2 g/day (2000 mg). More restrictive diets are not recommended as they compromise nutrition.
2. Diuretics:
   • Spironolactone (aldosterone antagonist) - start 100 mg/day, increase every 3-4 days up to 400 mg/day maximum. More effective than loop diuretics as first agent.
   • Furosemide - start 40 mg/day, increase to 160 mg/day maximum. Add if ascites is tense, weight loss is inadequate, or hyperkalemia develops.
   • Target weight loss: 1 kg in week 1, then 2 kg/week
   • Do NOT exceed 0.5 kg/day (without peripheral edema) or 1 kg/day (with peripheral edema)
   • Avoid ACEIs, ARBs, and NSAIDs (impair renal function and worsen hemodynamics)
3. Albumin infusion:
   • Acute infusion alone is of no benefit and risks pulmonary edema
   • Long-term albumin (40 g twice weekly × 2 weeks, then 40 g weekly) + spironolactone + furosemide reduces recurrent ascites and improves 18-month survival

B. Refractory Ascites (10-20% of patients)

• Large-volume paracentesis (LVP): Remove all or most fluid
  • Give albumin 6-8 g IV per liter removed, especially when >5 L removed, to prevent paracentesis-induced circulatory dysfunction (PICD)
• TIPS (Transjugular Intrahepatic Portosystemic Shunt):
  • More effective than LVP + albumin for preventing recurrent ascites
  • Associated with higher encephalopathy rate
  • PTFE-covered TIPS improves survival in patients requiring LVP >2×/month
• Peritoneovenous shunt: Subcutaneous silicone tube transferring peritoneal fluid to systemic circulation - for patients not candidates for TIPS or transplantation
• Automated flow pump (alfapump): Transfers ascitic fluid to bladder; reduces LVP need and improves QOL; requires surgical placement; risk of infection
• Liver transplantation: Definitive treatment

C. Spontaneous Bacterial Peritonitis (SBP)

• Infection of ascitic fluid without an identifiable surgical source (perforation, abscess, etc.)
• Mechanism: bacterial translocation from gut → mesenteric lymph nodes → bacteremia → ascitic fluid colonization (impaired Kupffer cells due to portosystemic shunting)
• Risk factors: low ascitic fluid complement, reduced immune defenses, intestinal bacterial overgrowth
• Most common organisms: Gram-negative aerobes (E. coli, Klebsiella)
• Clinical features: Fever, abdominal pain, jaundice, tenderness ± rebound; up to one-third are initially asymptomatic and present with encephalopathy, AKI, or sepsis
• Diagnosis: Ascitic fluid PMN count >250 cells/mL on diagnostic paracentesis
• Treatment: Broad-spectrum antibiotics (covering gram-negatives and anaerobes), tailored to culture results; IV albumin reduces risk of hepatorenal syndrome

D. Associated Complications

• Hepatorenal syndrome (HRS): Functional AKI from hemodynamic dysfunction in end-stage liver disease; treated with vasoconstrictors (terlipressin), albumin; indication for transplantation priority
• Hyponatremia: Fluid restrict to 1.5 L/day for serum Na <130 mEq/L; tolvaptan only as bridge to transplantation (risk of hepatotoxicity)
• Hepatic hydrothorax: Ascitic fluid migrates to pleural space (usually right side) via diaphragmatic defects

6. Summary Algorithm

New-onset ascites
        ↓
History + Exam + Imaging (USS/CT)
        ↓
Diagnostic paracentesis (all new ascites)
        ↓
Calculate SAAG
    ┌──────────────┐
    ↓              ↓
SAAG ≥1.1       SAAG <1.1
(portal HTN)    (non-portal)
    ↓              ↓
Treat cause    Cytology, TB screen,
(cirrhosis,    lipids, amylase, etc.
cardiac, etc.)
    ↓
Cirrhotic ascites:
Na restriction + spironolactone ± furosemide
    ↓
Refractory → LVP + albumin → TIPS → Transplant

Key Points Summary