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Esophageal Varices

Clinical Subject Page

Esophageal Varices

Esophageal varices are dilated collateral veins in the esophagus that develop due to portal
hypertension, most commonly as a result of cirrhosis.

Also called

Barrett's oesophagus (British spelling)

ICD-10

I85.0

Specialty

Gastroenterology

Onset

Chronic

Reviewed

July 2026

On This Page

Overview

Esophageal varices form because increased portal venous pressure diverts blood through collateral
veins in the esophagus. Nonbleeding varices are usually asymptomatic. Variceal hemorrhage is a
life-threatening emergency requiring prompt resuscitation, vasoactive therapy, antibiotics, and
endoscopic treatment

Etiology & Risk Factors

Common Causes

  • Liver cirrhosis — most common cause
    • Chronic viral hepatitis
    • Alcohol-related liver disease
    • Metabolic dysfunction-associated steatotic liver disease
    • Autoimmune or cholestatic liver disease
  • Portal vein thrombosis
  • Schistosomiasis
  • Budd–Chiari syndrome
  • Severe right-sided heart failure or constrictive pericarditis
  • Congenital hepatic fibrosis
  • Splenic vein thrombosis, more commonly causing isolated gastric varices

Portal hypertension caused by cirrhosis, schistosomiasis, or portal vein thrombosis is a major underlying mechanism for variceal formation.

Risk Factors for Developing Varices

  • Advanced cirrhosis
  • Clinically significant portal hypertension
  • Splenomegaly
  • Thrombocytopenia
  • Decompensated liver disease
  • Ascites
  • Ongoing alcohol use
  • Progressive hepatic fibrosis

Risk Factors for Variceal Bleeding

  • Large varices
  • High portal pressure
  • Red wale marks or red signs on endoscopy
  • Advanced liver dysfunction
  • Previous variceal hemorrhage
  • Active alcohol consumption
  • Infection or acute decompensation
  • Poor liver reserve

Pathophysiology

1. Portal hypertension increases portal venous pressure.
2. Blood is diverted through collateral venous pathways.
3. Dilated submucosal veins develop in the distal esophagus (esophageal varices).
4. Increased wall tension predisposes the varices to rupture and hemorrhage.

Clinical Presentation

-Nonbleeding varices:
• Usually asymptomatic
-Acute variceal hemorrhage:
• Sudden hematemesis
• Melena
• Features of gastrointestinal bleeding
• Hypovolemic shock (in severe cases)

History Taking

  • Ask about:
    • History of cirrhosis or portal hypertension
    • Hematemesis
    • Melena
    • Previous episodes of variceal bleeding
    • Symptoms of chronic liver disease
    • Alcohol history
    • Previous endoscopic treatment
    • Use of nonselective beta blockers

Physical Examination

Assess for:
• Signs of upper gastrointestinal bleeding
• Hemodynamic instability
• Hypovolemic shock
• Clinical features of chronic liver disease and portal hypertension

Investigations

  • Initial Tests

    • Complete blood count (CBC)

    • Liver function tests (LFTs)

    • Coagulation profile (PT/INR)

    • Renal function tests and electrolytes

    • Blood type and crossmatch (if bleeding is suspected)

    Diagnostic Investigations

    Upper Gastrointestinal Endoscopy (EGD) – Gold Standard

    • Gold standard for diagnosis

    • Confirms the presence, size, and location of varices

    • Identifies high-risk stigmata (e.g., red wale signs, red spots)

    • Allows therapeutic intervention (e.g., band ligation)

    Imaging

    • Abdominal ultrasound with Doppler

      • Evaluates liver morphology

      • Assesses portal vein patency

      • Detects portal hypertension and splenomegaly

    • CT or MRI abdomen (when indicated)

      • Evaluates portal venous system

      • Assesses complications of portal hypertension

    Additional Investigations

    • Transient elastography (FibroScan) to assess liver fibrosis (selected patients)

    • Hepatitis B and C serology

    • Ascitic fluid analysis if ascites is present

Diagnosis

-Diagnosis is established by:

  • Esophagogastroduodenoscopy (EGD)
  • Patients with cirrhosis should undergo routine screening to detect varices before bleeding occurs
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Related Topics

Management

  • 1. Primary Prevention (Non-Bleeding Varices)

    • Nonselective beta-blockers (NSBBs)

      • Carvedilol

      • Propranolol

      • Nadolol

    • Endoscopic variceal ligation (EVL) for patients with large varices or those who cannot tolerate beta-blockers.

    2. Acute Variceal Bleeding

    Initial Stabilization

    • Airway protection if indicated

    • Oxygen therapy

    • Two large-bore IV lines

    • Fluid resuscitation

    • Restrictive blood transfusion strategy (target Hb ≈ 7–9 g/dL)

    Medical Therapy

    • Vasoactive drugs

      • Octreotide

      • Terlipressin

    • Prophylactic intravenous antibiotics

      • e.g., Ceftriaxone

    Endoscopic Therapy

    • Endoscopic variceal ligation (EVL) – First-line treatment

    • Endoscopic sclerotherapy if band ligation is unavailable or unsuccessful

    Rescue Therapy

    • Balloon tamponade (temporary bridge)

    • Transjugular intrahepatic portosystemic shunt (TIPS) for uncontrolled or recurrent bleeding

    3. Secondary Prevention

    After recovery from the first bleed:

    • Combination of:

      • Nonselective beta-blocker

      • Repeated endoscopic variceal ligation

    • Evaluate for liver transplantation in patients with advanced cirrhosis

    Diagnosis is established by:
    • Esophagogastroduodenoscopy (EGD)
    Patients with cirrhosis should undergo routine screening to detect varices before bleeding occurs

    • Treat the underlying cause of portal hypertension

    • Manage chronic liver disease

    • Alcohol cessation (if alcohol-related liver disease)

    • Liver transplantation for end-stage liver disease

Complications

• Variceal hemorrhage
• Hypovolemic shock
• Recurrent bleeding

Prognosis

  • The prognosis depends on the severity of the underlying liver disease and whether bleeding occurs.
  • Early screening and appropriate primary and secondary prophylaxis reduce the risk of recurrent
    hemorrhage.

Key Points / Clinical Pearls

• Esophageal varices are caused by portal hypertension, most commonly due to cirrhosis.
• Nonbleeding varices are usually asymptomatic.
• EGD is recommended for screening in patients with cirrhosis.
• Acute bleeding presents with hematemesis, melena, and may cause hypovolemic shock.
• Acute management includes stabilization, vasoactive drugs, antibiotics, and urgent endoscopic
therapy.
• Persistent bleeding may require balloon tamponade or emergent TIPS.
• Primary prophylaxis includes NSBBs or EVL.
• Secondary prophylaxis includes NSBBs, EVL, and selected use of TIPS.

  • Meseeha M, Tian C, Attia M. National Center for Biotechnology Information (NIH). Esophageal Varices, StatPearls.
  • Kaplan DE, Ripoll C, Thiele M, et al. AASLD Practice Guidance on Risk Stratification and Management of Portal Hypertension and Varices in Cirrhosis. Hepatology. 2024;79:1180-1211. PMID: 37870298.
  • de Franchis R, Bosch J, Garcia-Tsao G, Reiberger T, Ripoll C; Baveno VII Faculty. Baveno VII - Renewing Consensus in Portal Hypertension. J Hepatol. 2022;76:959-974. PMID: 35120736.
  • MedlinePlus, National Library of Medicine (NIH). Esophageal Varices: Medical Encyclopedia.
  • Singh S, Chandan S, Vinayek R, Aswath G, Facciorusso A, Maida M. Comprehensive Approach to Esophageal Variceal Bleeding: From Prevention to Treatment. World J Gastroenterol. 2024;30:4602-4608. PMID: 39575399.