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Hepatology
Gastroenterology

Ascites

High EvidenceUpdated: 2025-12-24

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Red Flags

  • Spontaneous bacterial peritonitis (SBP)
  • Tense ascites with respiratory compromise
  • Hepatorenal syndrome (rising creatinine, oliguria)
  • New onset encephalopathy
  • Bloody ascites (malignancy or trauma)
Overview

Ascites

1. Clinical Overview

Summary

Ascites is the pathological accumulation of fluid in the peritoneal cavity. Cirrhosis with portal hypertension is the most common cause (75-85%), followed by malignancy, heart failure, and other causes. The serum-ascites albumin gradient (SAAG) differentiates portal hypertensive causes (SAAG ≥11 g/L) from non-portal causes (SAAG less than 11 g/L). Management of cirrhotic ascites involves sodium restriction, diuretics (spironolactone ± furosemide), and therapeutic paracentesis for tense or refractory ascites. Spontaneous bacterial peritonitis (SBP) is a life-threatening complication requiring prompt recognition and antibiotic treatment.

Key Facts

  • Prevalence: 60% of cirrhotic patients develop ascites within 10 years
  • Most common cause: Cirrhosis (75-85%)
  • SAAG ≥11: Portal hypertension (cirrhosis, cardiac, Budd-Chiari)
  • SAAG less than 11: Non-portal (malignancy, TB, pancreatitis, nephrotic)
  • Mortality: 50% 2-year mortality in cirrhosis with ascites
  • Key treatment: Salt restriction + Spironolactone ± Furosemide

Clinical Pearls

The SAAG Rule: SAAG ≥11 g/L = portal hypertension (treat like cirrhosis). SAAG less than 11 g/L = exudative (investigate for malignancy, TB, other causes). SAAG is more accurate than the outdated transudate/exudate classification.

Tap Early, Tap Often: Any patient with cirrhosis presenting unwell should have a diagnostic paracentesis to exclude SBP. Fever, abdominal pain, encephalopathy, and worsening renal function are often the only signs.

The 100:40 Ratio: Spironolactone 100mg to furosemide 40mg is the traditional starting ratio. Increase together to maintain sodium and potassium balance.

Why This Matters Clinically

Development of ascites marks decompensated cirrhosis — a significant prognostic milestone. Early detection and treatment of SBP prevents sepsis and hepatorenal syndrome. Refractory ascites requires consideration for TIPS or liver transplant referral.


2. Epidemiology

Incidence & Prevalence

  • In cirrhosis: 60% develop ascites within 10 years of diagnosis
  • First decompensation: Ascites is the most common first decompensation event
  • Prevalence: Ascites affects ~5% of hospitalised patients

Demographics

FactorDetails
AgeIncreases with age (cirrhosis, cardiac causes)
SexReflects underlying cause (alcohol-related in males)
EthnicityVaries with cirrhosis prevalence
GeographyHigher in regions with high alcohol or viral hepatitis rates

Causes of Ascites

SAAG ≥11 g/L (High Gradient)SAAG less than 11 g/L (Low Gradient)
Cirrhosis (75-85%)Peritoneal carcinomatosis
Cardiac failureTuberculous peritonitis
Budd-Chiari syndromePancreatic ascites
Portal vein thrombosisNephrotic syndrome
MyxoedemaSerositis (e.g., SLE)
Massive liver metastasesBowel obstruction or infarction

3. Pathophysiology

Mechanism (Cirrhotic Ascites)

Step 1: Portal Hypertension

  • Cirrhosis increases intrahepatic resistance
  • Portal pressure rises (HVPG greater than 10 mmHg = clinically significant)
  • Splanchnic vasodilatation occurs

Step 2: Arterial Underfilling

  • Splanchnic vasodilatation leads to relative hypovolaemia
  • Activates RAAS, sympathetic nervous system, ADH
  • Sodium and water retention

Step 3: Fluid Shifts

  • Hydrostatic pressure forces fluid into peritoneum
  • Low oncotic pressure (hypoalbuminaemia) exacerbates transudation
  • Lymphatic drainage capacity exceeded

Step 4: Ascites Formation

  • Net fluid accumulation in peritoneal cavity
  • Sodium retention perpetuates fluid accumulation

Classification

GradeDescriptionClinical Features
Grade 1MildDetected only by USS
Grade 2ModerateVisible distension, shifting dullness
Grade 3Severe (Tense)Marked distension, tense abdomen, respiratory compromise

4. Clinical Presentation

Symptoms

Signs

Red Flags

[!CAUTION] Red Flags — Urgent investigation and treatment if:

  • Fever, abdominal pain, or tenderness (SBP)
  • Worsening encephalopathy
  • Rising creatinine (hepatorenal syndrome)
  • Respiratory distress (tense ascites)
  • Bloody ascites (malignancy, trauma)

Abdominal distension (progressive)
Common presentation.
Weight gain
Common presentation.
Dyspnoea (diaphragm elevation)
Common presentation.
Early satiety, nausea
Common presentation.
Ankle swelling (peripheral oedema)
Common presentation.
Reduced mobility
Common presentation.
5. Clinical Examination

Structured Approach

Abdominal:

  • Inspect: Distension, everted umbilicus, dilated veins (caput medusae)
  • Palpate: Tenderness (SBP), hepatosplenomegaly
  • Percuss: Shifting dullness, fluid thrill
  • Auscultate: Bowel sounds (exclude ileus)

Cardiovascular:

  • JVP (cardiac ascites)
  • Peripheral oedema

Stigmata of Chronic Liver Disease:

  • Jaundice, spider naevi, palmar erythema
  • Gynaecomastia, testicular atrophy
  • Encephalopathy (asterixis)

Special Tests

TestTechniquePositive FindingPurpose
Shifting dullnessPercuss flanks; reposition patientDullness moves to dependent sideDetect moderate ascites
Fluid thrillTap one flank; feel oppositeImpulse transmittedLarge volume ascites
Puddle signKnee-elbow position; percuss umbilicusCentral dullnessDetect small volumes (rarely used)

6. Investigations

First-Line

  • Diagnostic paracentesis — All new ascites or hospital admission
  • Ascitic fluid analysis — Cell count, albumin, culture

Ascitic Fluid Analysis

TestInterpretation
Cell count (WCC)Neutrophils ≥250/mm³ = SBP
AlbuminCalculate SAAG
SAAG≥11 g/L = portal hypertension
CultureIdentify organism in SBP
CytologyIf malignancy suspected
ProteinLow (<5 g/L) = high SBP risk; primary prophylaxis indicated

Laboratory Tests

TestExpected FindingPurpose
LFTsDeranged in liver diseaseAssess liver function
AlbuminLow in cirrhosisCalculate SAAG
U&EsHyponatraemia, renal impairmentMonitor electrolytes, renal function
INRProlonged in cirrhosisCoagulopathy assessment
FBCThrombocytopenia, leukopenia (hypersplenism)Portal hypertension

Imaging

ModalityFindingsIndication
UltrasoundFree fluid, liver appearance, spleen sizeFirst-line
CT abdomenCharacterise ascites, exclude malignancyIf USS inconclusive or malignancy suspected
DopplerPortal vein, hepatic vein patencyExclude Budd-Chiari, PVT
EchoCardiac functionIf cardiac ascites suspected

7. Management

Management Algorithm

                 NEW ASCITES
                      ↓
┌─────────────────────────────────────────┐
│        DIAGNOSTIC PARACENTESIS          │
│  Cell count, albumin, culture           │
└─────────────────────────────────────────┘
                      ↓
┌─────────────────────────────────────────┐
│         CALCULATE SAAG                  │
├─────────────────────────────────────────┤
│  SAAG ≥11 → Portal hypertension         │
│             (Cirrhosis, cardiac)        │
│  SAAG &lt;11 → Non-portal                  │
│             (Malignancy, TB, other)     │
└─────────────────────────────────────────┘
                      ↓
┌─────────────────────────────────────────┐
│         CIRRHOTIC ASCITES               │
├─────────────────────────────────────────┤
│  1. Salt restriction (&lt;2g/day)          │
│  2. Spironolactone 100mg OD             │
│     ± Furosemide 40mg OD                │
│  3. Fluid restrict if Na &lt;125           │
│  4. Titrate diuretics (max 400/160)     │
└─────────────────────────────────────────┘
                      ↓
┌─────────────────────────────────────────┐
│         REFRACTORY ASCITES              │
├─────────────────────────────────────────┤
│  1. Therapeutic paracentesis + albumin  │
│  2. Consider TIPS                       │
│  3. Liver transplant assessment         │
└─────────────────────────────────────────┘

Conservative Management

  • Sodium restriction: Less than 2g (88 mmol) per day
  • Fluid restriction: Only if severe hyponatraemia (Na less than 125)
  • Avoid NSAIDs: Reduce renal perfusion
  • Alcohol abstinence: Essential if alcohol-related

Medical Management

DrugStarting DoseMax DoseNotes
Spironolactone100mg OD400mg ODFirst-line; monitor K+
Furosemide40mg OD160mg ODAdd if insufficient response
Albumin8g per litre drained (if >L)—Prevents circulatory dysfunction

Diuretic Monitoring:

  • Weight loss: Target 0.5kg/day (no oedema) or 1kg/day (with oedema)
  • Monitor: U&Es, creatinine (stop if AKI develops)

Therapeutic Paracentesis

Indications:

  • Tense/symptomatic ascites
  • Refractory ascites
  • Respiratory compromise

Technique:

  • Large-volume paracentesis (LVP): Drain to dryness
  • Give albumin if more than 5L drained (8g per litre removed)
  • Can be repeated as needed

TIPS (Transjugular Intrahepatic Portosystemic Shunt)

Indications:

  • Refractory ascites
  • Frequent need for LVP

Contraindications:

  • Severe hepatic encephalopathy
  • Very poor liver function (MELD greater than 18)
  • Cardiac failure

Disposition

  • Admit if: SBP, tense ascites with symptoms, new encephalopathy, renal impairment
  • Discharge if: Stable on diuretics, community drainage arranged if needed
  • Follow-up: Weekly weight; regular U&Es; hepatology

8. Complications

Immediate

ComplicationIncidencePresentationManagement
SBP10-30% per yearFever, pain, encephalopathyIV cefotaxime, albumin
Respiratory compromiseTense ascitesDyspnoea, hypoxiaTherapeutic paracentesis

Early (Weeks)

  • Electrolyte disturbance: Hypokalaemia (furosemide), hyperkalaemia (spironolactone)
  • Renal impairment: Over-diuresis, hepatorenal syndrome
  • Hyponatraemia: Dilutional

Late (Months-Years)

  • Hepatorenal syndrome: Type 1 (rapid) or Type 2 (slower)
  • Umbilical hernia complications: Incarceration, rupture, ulceration
  • Malnutrition: Protein loss, poor intake

9. Prognosis & Outcomes

Outcomes

VariableOutcome
2-year survival (cirrhosis + ascites)50%
Response to diuretics90%
Refractory ascites10% (poor prognosis)
Post-SBP mortality30-50% at 1 year

Prognostic Factors

Good Prognosis:

  • First episode
  • Good liver function (Child-Pugh A)
  • Response to diuretics
  • No SBP

Poor Prognosis:

  • Refractory ascites
  • Hepatorenal syndrome
  • Recurrent SBP
  • High MELD score
  • Hyponatraemia

10. Evidence & Guidelines

Key Guidelines

  1. EASL Clinical Practice Guidelines on Decompensated Cirrhosis (2018) — European Association for the Study of the Liver. J Hepatol 2018
  2. AASLD Practice Guidance on Ascites and HRS (2021) — American Association for the Study of Liver Diseases.
  3. BSG Guidelines on Ascites — British Society of Gastroenterology.

Key Trials

ANSWER Trial (2018) — Albumin for long-term ascites management

  • 431 patients
  • Key finding: Weekly albumin infusions improved 18-month survival
  • Clinical Impact: Supports long-term albumin use in refractory ascites

Evidence Strength

InterventionLevelKey Evidence
Spironolactone + furosemide1bMultiple RCTs
Albumin with LVP1aCochrane review
TIPS for refractory1bRCTs
Long-term albumin1bANSWER Trial

11. Patient/Layperson Explanation

What is Ascites?

Ascites is a build-up of fluid in your tummy (abdomen). It usually happens when your liver isn't working properly (cirrhosis) but can also be caused by heart problems or cancer.

Why does it matter?

Fluid build-up can make you uncomfortable, short of breath, and affect your appetite. It is also a sign that your liver or heart is not working well. Sometimes the fluid can become infected (called SBP), which is serious and needs urgent treatment.

How is it treated?

  1. Reduce salt: Eating less salt helps prevent more fluid building up.
  2. Water tablets (diuretics): Medications like spironolactone help your body get rid of extra fluid.
  3. Draining fluid: If there is a lot of fluid, doctors can remove it with a needle (paracentesis).
  4. Treating the cause: If liver disease is the cause, avoiding alcohol and treating hepatitis is essential.

What to expect

  • You will need regular blood tests to check kidney function and salt levels
  • Fluid may need to be drained more than once
  • Weight is monitored to track fluid loss
  • Some people need a special procedure called TIPS or a liver transplant

When to seek help

See a doctor urgently if you have:

  • Fever or abdominal pain
  • Increasing confusion or drowsiness
  • Rapid weight gain or worsening swelling
  • Difficulty breathing

12. References

Primary Guidelines

  1. European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406-460. PMID: 29653741

Key Studies

  1. Runyon BA. Management of adult patients with ascites due to cirrhosis: update 2012. Hepatology. 2013;57(4):1651-3. PMID: 23463403
  2. Caraceni P, et al. Long-term albumin administration in decompensated cirrhosis (ANSWER). Lancet. 2018;391(10138):2417-2429. PMID: 29861076

Further Resources

  • British Liver Trust: britishlivertrust.org.uk
  • NHS Ascites: nhs.uk/conditions/ascites

Last Reviewed: 2025-12-24 | MedVellum Editorial Team


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • Spontaneous bacterial peritonitis (SBP)
  • Tense ascites with respiratory compromise
  • Hepatorenal syndrome (rising creatinine, oliguria)
  • New onset encephalopathy
  • Bloody ascites (malignancy or trauma)

Clinical Pearls

  • **The 100:40 Ratio**: Spironolactone 100mg to furosemide 40mg is the traditional starting ratio. Increase together to maintain sodium and potassium balance.
  • **Red Flags — Urgent investigation and treatment if:**
  • - Fever, abdominal pain, or tenderness (SBP)
  • - Worsening encephalopathy
  • - Rising creatinine (hepatorenal syndrome)

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines