Key Facts

Ascites is the most common decompensation event in cirrhosis and is associated with significant morbidity, mortality, and reduced quality of life. Its development marks a critical prognostic threshold.

Epidemiology

Approximately 50% of patients with compensated cirrhosis develop ascites within 10 years. Once ascites develops, 1-year mortality is ~40% without transplant. Refractory ascites has ~50% 1-year mortality.

Aetiology

• Portal hypertension-related (SAAG ≥11): cirrhosis (75%), alcoholic hepatitis, heart failure, Budd-Chiari, portal vein thrombosis, myxoedema
• Non-portal hypertensive (SAAG <11): peritoneal carcinomatosis (10%), TB peritonitis, nephrotic syndrome, pancreatitis, serositis (SLE, FMF)

Pathophysiology

In cirrhosis: portal hypertension → splanchnic vasodilation (NO-mediated) → effective arterial underfilling → activation of RAAS, sympathetic nervous system, and ADH → renal sodium and water retention → ascites formation. Simultaneously, portal hypertension increases splanchnic capillary hydrostatic pressure and reduces capillary oncotic pressure (hypoalbuminaemia) → transudation into peritoneal cavity. Lymphatic drainage is overwhelmed, and ascites accumulates.

Clinical Features

• Abdominal distension (detectable clinically when >500 mL)
• Shifting dullness (most sensitive clinical sign for ascites)
• Fluid thrill/wave (large volumes)
• Weight gain
• Peripheral oedema
• Dyspnoea (diaphragmatic splinting)
• Abdominal wall hernias (umbilical, inguinal — risk of incarceration)

Red Flags

• Fever with ascites (SBP)
• Abdominal pain with ascites (SBP, perforation, malignancy)
• Rapidly increasing ascites (portal vein thrombosis, HCC, SBP)
• New ascites in known cirrhotic (investigate for cause)
• Bloody ascites (malignancy, trauma, HCC rupture)

Bedside

• Diagnostic paracentesis: mandatory for ALL new-onset ascites and ALL admissions with ascites
  • Cell count: neutrophils >250/mm³ = SBP (treat immediately)
  • Albumin: calculate SAAG (serum albumin − ascitic albumin)
  • Total protein: <15 g/L = high SBP risk; >25 g/L = consider cardiac, TB
  • Culture: inoculate blood culture bottles at bedside (aerobic + anaerobic)
  • Cytology: if malignancy suspected
  • Amylase: if pancreatic ascites suspected
  • ADA (adenosine deaminase): >40 IU/L suggests TB peritonitis

Bloods

• LFTs, albumin, INR: liver function
• U&Es, creatinine: renal function (hepatorenal syndrome risk)
• Sodium: often low (dilutional)
• FBC: infection screen
• 24-hour urinary sodium: <30 mmol/day suggests sodium retention (unlikely to respond to diuretics alone)

Imaging

• USS abdomen: confirms ascites (can detect <100 mL), liver/spleen assessment, PVT, HCC
• CT abdomen: if malignancy suspected, complex ascites
• Echocardiography: if cardiac cause suspected

Non-pharmacological

• Sodium restriction: <5 g/day (<90 mmol/day) — most important dietary intervention
• Fluid restriction: only if sodium <125 mmol/L
• Daily weights: target weight loss 0.5 kg/day (no peripheral oedema) or 1 kg/day (with peripheral oedema)
• Alcohol abstinence: reduces portal pressure

Pharmacological

• First-line diuretics: spironolactone 100 mg OD (increase by 100 mg every 3-5 days, max 400 mg) ± furosemide 40 mg OD (increase by 40 mg, max 160 mg) — maintain 100:40 ratio
• Monitor: U&Es, creatinine, weight; stop/reduce if AKI, Na <120, K+ derangement, encephalopathy
• SBP treatment: ceftriaxone 2 g IV OD for 5-7 days (or co-amoxiclav if local resistance); IV albumin (1.5 g/kg on day 1, 1 g/kg on day 3) reduces hepatorenal syndrome and mortality
• SBP prophylaxis: long-term norfloxacin 400 mg OD or ciprofloxacin 500 mg OD if: (1) previous SBP, (2) ascitic protein <15 g/L with renal/liver dysfunction, (3) GI bleed in cirrhosis
• Hepatorenal syndrome (HRS-AKI): terlipressin 1-2 mg IV QDS + albumin 20-40 g/day (target MAP >65 mmHg)

Surgical/Interventional

• Large volume paracentesis (LVP): for tense/symptomatic ascites; drain up to 15-20L; replace with albumin 8 g per litre drained (if >5L removed)
• TIPSS: for refractory ascites (diuretic-resistant or diuretic-intractable); improves ascites control in ~70%; risk of encephalopathy ~30%
• Indwelling peritoneal catheter (PleurX): palliative option for refractory malignant or cirrhotic ascites
• Liver transplantation: definitive treatment for cirrhotic ascites

Referral Criteria

• Hepatology: all new cirrhotic ascites
• Transplant assessment: diuretic-resistant or first episode of SBP (poor prognostic marker)
• Interventional radiology: TIPSS assessment
• Oncology/palliative care: malignant ascites

Development of ascites in cirrhosis is a major prognostic event — 1-year mortality ~40%, 5-year mortality ~50-60% without transplant. SBP carries ~20% in-hospital mortality and ~70% 1-year mortality. Refractory ascites: ~50% 1-year mortality. HRS-AKI: very poor prognosis (mortality >80% without treatment; ~40% with terlipressin + albumin). TIPSS improves survival in selected patients with refractory ascites. Liver transplantation is the only definitive cure.

SAAG Interpretation

SBP Diagnostic Criteria