Ascites

Introduction

Ascites refers to the pathological accumulation of free fluid in the peritoneal cavity. It is most commonly a complication of cirrhosis and portal hypertension but may also be caused by malignancy, cardiac failure, infection, or other systemic diseases.

Peak Incidence

• Most common in individuals aged 50 to 60 years.
• The majority of cases in the UK are due to decompensated cirrhosis.

Pathophysiology

Ascites develops as a result of a combination of haemodynamic, hormonal, and renal abnormalities, most commonly secondary to portal hypertension from liver cirrhosis.

• Portal hypertension increases hydrostatic pressure in the splanchnic circulation, driving fluid into the peritoneal cavity.
• Hypoalbuminaemia (due to impaired hepatic synthesis) lowers plasma oncotic pressure, further encouraging fluid transudation.
• The resultant arterial underfilling is sensed by baroreceptors, leading to activation of:
  • Renin–angiotensin–aldosterone system (RAAS) – causing sodium and water retention.
  • Sympathetic nervous system – causing vasoconstriction.
  • Antidiuretic hormone (ADH) – promoting free water retention.
• Together, these responses lead to expansion of extracellular fluid volume and worsening ascites.
• In advanced stages, impaired lymphatic drainage and increased capillary permeability contribute further to fluid accumulation.

Symptoms

• Abdominal distension and discomfort.
• Early satiety (pressure effect on the stomach).
• Breathlessness due to diaphragmatic splinting.
• Weight gain secondary to fluid accumulation.
• Occasionally, loose stools or vague gastrointestinal symptoms.

Signs

Typical examination findings:

• Shifting dullness – change in percussion tone with patient repositioning.
• Fluid thrill (wave) – impulse transmission across a fluid-filled abdomen.

Associated findings based on aetiology:

• Chronic liver disease:
  • Jaundice.
  • Spider naevi.
  • Palmar erythema.
• Cardiac causes:
  • Peripheral oedema.
  • Raised jugular venous pressure (JVP).

Diagnosis

Clinical suspicion is confirmed by bedside and laboratory testing.

Blood tests:

• Full blood count (FBC):
  • Anaemia (chronic disease or malignancy).
  • Leukocytosis (suggests spontaneous bacterial peritonitis – SBP).
  • Thrombocytopenia (portal hypertension, hypersplenism).
• Liver function tests (LFTs):
  • Elevated ALT/AST in liver disease.
  • Raised bilirubin in cirrhosis or malignancy.
  • Low albumin in chronic liver disease or nephrotic syndrome.
• Urea & electrolytes (U&Es):
  • Raised urea and creatinine in hepatorenal syndrome.
  • Hyponatraemia (dilutional, due to RAAS activation).
  • Hypokalaemia (due to diuretics or secondary hyperaldosteronism).
• Coagulation profile:
  • Prolonged PT and INR in liver dysfunction.
• Other relevant blood tests:
  • Amylase/lipase (raised in pancreatic ascites).
  • Alpha-fetoprotein (AFP) if hepatocellular carcinoma is suspected.

Diagnostic paracentesis:

• Always perform in new-onset, worsening, or suspected infected ascites.
• Ascitic fluid analysis:
  • Cell count and differential: neutrophil count ≥250 cells/mm³ suggests SBP.
  • Culture and gram stain.
  • Albumin concentration.

Serum–Ascites Albumin Gradient (SAAG):

• SAAG = Serum Albumin – Ascitic Fluid Albumin
  • High SAAG (≥1.1 g/dL or 11 g/L): portal hypertension (e.g. cirrhosis, heart failure).
  • Low SAAG (<1.1 g/dL): non-portal causes (e.g. peritoneal carcinomatosis, TB, pancreatitis).

Imaging:

• Ultrasound abdomen – confirms fluid presence; guides safe paracentesis.
• CT abdomen – reserved for suspected malignancy, TB, or diagnostic uncertainty.

Complications

• Spontaneous bacterial peritonitis (SBP).
• Hepatorenal syndrome.
• Refractory ascites.
• Paracentesis-induced circulatory dysfunction – especially after removing >5 L without albumin replacement.
• Dilutional hyponatraemia – from fluid shifts or excessive diuresis.
• Umbilical hernia or hydrothorax.

Management

General principles:

• Treat the underlying cause (e.g. cirrhosis, malignancy, heart failure).
• Alcohol cessation in liver disease is critical.
• Daily weight monitoring (aim for ≤0.5 kg/day loss without oedema, ≤1 kg/day with oedema).

Dietary measures:

• Sodium restriction: <2 g/day (≈90 mmol Na⁺).
• Fluid restriction: only if Na⁺ <125 mmol/L.

Diuretic therapy:

• First-line: spironolactone 100 mg daily (can titrate up to 400 mg).
• Adjunct: furosemide 40 mg daily (can titrate up to 160 mg).
• Maintain 100:40 spironolactone:furosemide ratio to preserve potassium balance.

Therapeutic paracentesis:

• For tense or symptomatic ascites.
• If removing >5 L, give intravenous albumin (8 g per litre removed) to prevent circulatory dysfunction.
• Provides short-term symptomatic relief.

Advanced therapies:

• Refractory ascites:
  • Consider Transjugular Intrahepatic Portosystemic Shunt (TIPS) in suitable patients.
  • Liver transplantation is definitive in eligible patients.

Prophylactic antibiotics:

• Indicated for patients with:
  • Prior SBP.
  • Ascitic fluid protein <15 g/L + advanced liver disease.
• Common agents: norfloxacin or ciprofloxacin.