Pathological accumulation of fluid in the peritoneal cavity. Most commonly caused by cirrhosis with portal hypertension (75%). SAAG ≥11 g/L indicates portal hypertension. Managed with salt restriction, diuretics, and paracentesis.

Key Facts

  • Cirrhosis accounts for ~75% of ascites cases; other causes: malignancy (10%), heart failure (5%), TB, nephrotic syndrome, pancreatitis
  • SAAG (serum-ascites albumin gradient): ≥11 g/L = portal hypertension (cirrhosis, heart failure, Budd-Chiari); <11 g/L = non-portal hypertensive (malignancy, TB, nephrotic, pancreatitis)
  • Diagnostic paracentesis: mandatory for all new-onset ascites - cell count (SBP if neutrophils >250/mm³), albumin, protein, culture, cytology
  • SBP (spontaneous bacterial peritonitis): ascitic neutrophils >250/mm³; treat with IV ceftriaxone 2 g OD + IV albumin (1.5 g/kg day 1, 1 g/kg day 3) - reduces hepatorenal syndrome
  • Management: sodium restriction (<5 g/day = <90 mmol/day), spironolactone 100 mg OD (max 400 mg) ± furosemide 40 mg OD (max 160 mg), large volume paracentesis with albumin
  • Refractory ascites: TIPSS or liver transplant; hepatorenal syndrome: terlipressin + albumin

Overview

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 Presentation

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)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Cirrhotic ascitesCLD stigmata, SAAG ≥11USS, LFTs, ascitic tap (SAAG)
Malignant ascitesWeight loss, SAAG <11, bloody, high proteinAscitic cytology, CT
Cardiac ascitesRaised JVP, peripheral oedema, SAAG ≥11Echo, BNP
TB peritonitisFever, weight loss, SAAG <11, high lymphocytesAscitic ADA, TB culture, laparoscopy
Nephrotic syndromeProteinuria, oedema, SAAG <11Urinalysis, serum albumin
Pancreatic ascitesHistory of pancreatitis, very high amylaseAscitic amylase, CT

Diagnosis / Investigation

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

Management

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

Prognosis

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.

Other Relevant Information

SAAG Interpretation

SAAGCategoryCauses
≥11 g/LPortal hypertensiveCirrhosis, heart failure, Budd-Chiari, myxoedema
<11 g/LNon-portal hypertensiveMalignancy, TB, nephrotic, pancreatitis

SBP Diagnostic Criteria

CriterionValue
Ascitic neutrophils>250/mm³
Positive ascitic cultureConfirmatory (but ~40% culture-negative SBP)
TreatmentCeftriaxone 2 g IV OD + IV albumin
Prophylaxis (after SBP)Ciprofloxacin 500 mg OD lifelong