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.