Oesophagus Varices

Definition | Aetiology | Pathophysiology | Risk Factors | Signs and Symptoms | Investigations | Management | Referral

Definition

Oesophageal varices are abnormally dilated submucosal veins in the lower oesophagus, which develop due to portal hypertension and have a high risk of rupture, leading to life-threatening bleeding.

Aetiology

The primary cause of oesophageal varices is portal hypertension, commonly due to:

  • Cirrhosis: e.g., alcohol-related liver disease, viral hepatitis, non-alcoholic fatty liver disease.
  • Portal vein thrombosis: can obstruct blood flow, causing increased portal pressure.
  • Budd-Chiari syndrome: hepatic vein outflow obstruction.
  • Schistosomiasis: caused by a parasite worm living in fresh water in endemic regions.this parasite is known to cause hepatic fibrosis.

Pathophysiology

  • Portal hypertension increases blood flow resistance through the liver.
  • Collateral circulation develops, including varices in the oesophagus, to bypass the obstructed liver.
  • Varices have thin walls and are prone to rupture due to high pressure, leading to massive bleeding.

Risk factors

  • Cirrhosis (any cause).
  • High portal pressure (hepatic venous pressure gradient >12 mmHg).
  • Alcohol abuse.
  • Severe liver disease (decompensated cirrhosis).
  • Previous variceal bleed (high risk of rebleeding).
  • Active infection (increases bleeding risk).

Signs and symptoms

Non-bleeding varices:

  • Usually asymptomatic and detected on endoscopy (incidental finding).
  • May cause mild dysphagia in some cases.

Acute variceal bleeding:

  • Massive, painless haematemesis (vomiting blood).
  • Melaena (black, tarry stools).
  • Signs of hypovolaemia (tachycardia, hypotension, pallor).
  • Jaundice and ascites (if underlying cirrhosis is present).

Investigations

  • Blood tests:
    • Full blood count: 🔻 low haemoglobin if bleeding; thrombocytopenia in cirrhosis.
    • Clotting screen (INR/PT): ⬆️ prolonged in liver disease.
    • Liver function tests: ⬆️ raised bilirubin, ⬆️ ALT/AST, 🔻 low albumin.
    • Urea and electrolytes: ⬆️ raised urea in upper GI bleeding.
    • Cross-match blood: in case of significant bleeding and need of potention tranfusion.
  • Endoscopy (gold standard): identifies and grades varices, assesses for active bleeding.
  • Ultrasound with Doppler: evaluates portal hypertension and liver pathology.
  • Hepatic venous pressure gradient (HVPG): used in specialist settings to assess severity.

Management

1. Acute Variceal Bleeding (Emergency):

  • ABCDE approach: secure airway, high-flow oxygen, and establish IV access.
  • IV fluid resuscitation: only if haemodynamically unstable (avoid over-resuscitation to prevent increased portal pressure).
  • Blood transfusion: if severely low haemoglobin.
  • IV terlipressin (vasopressor): can reduces portal pressure and bleeding.
  • IV antibiotics: used as it prevents infection-related complications.
  • Endoscopic band ligation (gold standard): performed urgently to control active bleeding.
  • Balloon tamponade (Sengstaken-Blakemore tube): temporary measure if endoscopy is unsuccessful.
  • Transjugular intrahepatic portosystemic shunt (TIPS): considered if band ligation fails.

2. Secondary Prevention (Post-Bleeding):

  • Non-selective beta-blockers (e.g., propranolol): to reduce portal pressure.
  • Repeat endoscopic surveillance and band ligation: routinely done until varices are obliterated.
  • TIPS procedure: also done if recurrent bleeding despite treatment.

3. Primary Prevention (For Patients with Known Varices):

  • Propranolol/carvedilol: recommended to reduce bleeding risk.
  • Endoscopic variceal ligation: considered for high-risk varices.
  • Lifestyle modifications: alcohol cessation and weight management in NAFLD-related cirrhosis.

Referral

  • Emergency gastroenterology referral: for acute variceal bleeding.
  • Hepatology referral: for assessment of portal hypertension and liver disease management.
  • Hospital a/e referral: if patient haemodynamic instability persists.