Esophageal Varices

1. Overview
2. Portal Hypertension and Pathophysiology
3. Causes and Risk Factors
4. Baveno VII Consensus and Diagnosis
5. Primary Prophylaxis
6. Acute Variceal Hemorrhage
7. TIPS Procedure
8. Secondary Prophylaxis
9. Research Papers
10. Connections
11. Featured Videos

Overview

Esophageal varices are dilated submucosal veins in the lower esophagus that develop as a consequence of portal hypertension, most commonly from cirrhosis.

They represent portosystemic collaterals — alternate routes formed when portal blood pressure rises and blood seeks lower-resistance pathways through the gastroesophageal junction veins.

Approximately 50% of all cirrhotic patients have varices at diagnosis; 30% will bleed within 2 years without prophylaxis.

Acute variceal hemorrhage (AVH) carries a 6-week mortality of approximately 20%, making this one of the most feared complications of chronic liver disease.

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Portal Hypertension and Pathophysiology

Normal portal pressure gradient (HVPG — hepatic venous pressure gradient) is 1–5 mmHg.

• Clinically significant portal hypertension (CSPH): HVPG ≥10 mmHg — the threshold where varices begin to develop.
• Variceal bleeding risk increases sharply when HVPG >12 mmHg; risk of first bleed becomes negligible when HVPG drops below 12 mmHg with treatment.
• Baveno VII 2021 consensus defines CSPH as HVPG ≥10 mmHg or indirect surrogates: liver stiffness ≥25 kPa by transient elastography, or 20–25 kPa combined with platelet count <150,000.

The underlying mechanism involves two converging forces:

1. Increased intrahepatic resistance — sinusoidal fibrosis and vascular remodeling from chronic liver injury.
2. Splanchnic vasodilation — nitric oxide-mediated dilation of mesenteric vessels drives a hyperdynamic circulation that sustains and amplifies portal pressure.

Together these forces create the conditions for varices to form, enlarge, and ultimately rupture.

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Causes and Risk Factors

Most Common Cause

Cirrhosis accounts for approximately 90% of cases. The leading underlying etiologies are:

• Alcohol-related liver disease
• Chronic hepatitis B or C
• NASH/MASLD (metabolic-associated steatotic liver disease)

Less Common Non-Cirrhotic Causes

• Portal vein thrombosis — extrahepatic portal hypertension, often in younger patients
• Schistosomiasis — a major cause in endemic regions of Africa, South America, and Southeast Asia
• Budd-Chiari syndrome — hepatic vein outflow obstruction
• Nodular regenerative hyperplasia — sinusoidal portal hypertension without classic cirrhosis

Risk Factors for Variceal Bleeding

• Varix size — large varices (>5 mm) carry the highest risk
• Red wale markings on endoscopy — longitudinal red streaks indicating areas of thin, tensed variceal wall
• Child-Pugh class C (decompensated cirrhosis)
• Active alcohol use — raises portal pressure acutely and impairs hepatic synthetic function

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Baveno VII Consensus and Diagnosis

The Baveno VII 2021 international consensus workshop updated the criteria for non-invasive diagnosis and management stratification of portal hypertension.

EGD (esophagogastroduodenoscopy) remains the gold standard for diagnosing and grading varices.

Screening Recommendations

• Perform EGD at the time of cirrhosis diagnosis.
• Re-screening intervals vary by compensated vs. decompensated status and response to treatment.
• Non-invasive rule-out ("Baveno VI rule"): patients with liver stiffness <20 kPa AND platelet count >150,000 can safely avoid screening EGD (very low CSPH probability).

Variceal Grading

• Small: <5 mm, minimally tortuous
• Medium: intermediate size
• Large: ≥5 mm, occupy more than one-third of the esophageal lumen

Additional Diagnostic Tools

• Capsule endoscopy — endorsed by Baveno VII as an alternative to EGD for screening in selected patients who decline or cannot tolerate standard endoscopy.
• Transient elastography (FibroScan) — liver stiffness measurement used as a non-invasive surrogate for HVPG to stratify risk without direct pressure measurement.

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Primary Prophylaxis

The goal of primary prophylaxis is to prevent the first variceal bleed in patients who have never bled.

Non-Selective Beta-Blockers (NSBBs)

• Propranolol (target: reduce resting HR by 25% or to 55 bpm) or nadolol — older agents, well-established efficacy.
• Carvedilol 6.25 mg/day — preferred for CSPH with varices per Baveno VII; provides greater portal pressure reduction than propranolol or nadolol and also reduces hepatic inflammation via alpha-1 blockade.
• Caution: propranolol and nadolol are contraindicated or used cautiously in refractory ascites (may reduce renal perfusion); carvedilol carries the same caution.

Endoscopic Variceal Ligation (EVL)

• Preferred for medium/large varices or when NSBBs are intolerated or contraindicated.
• Repeat EGD every 2–4 weeks until varices are eradicated, then surveillance every 3–6 months.

Combined Therapy

NSBB + EVL combined is not superior to either alone for primary prophylaxis (unlike secondary prophylaxis, where combination is standard of care).

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Acute Variceal Hemorrhage

Acute variceal hemorrhage (AVH) is a medical emergency with approximately 20% 6-week mortality even with optimal treatment.

Resuscitation Principles

• Restrictive transfusion strategy: target hemoglobin 7–8 g/dL — overtransfusion raises portal pressure and increases rebleeding risk.
• Airway protection: consider elective intubation before endoscopy in encephalopathic or actively vomiting patients.

Early Pharmacotherapy (Start Before Endoscopy)

Initiating vasoactive therapy before endoscopy reduces active bleeding and improves outcomes:

• Octreotide: 50 mcg IV bolus, then 50 mcg/hr infusion for 3–5 days (splanchnic vasoconstriction reducing portal inflow).
• Terlipressin: 2 mg IV every 4–6 hours — reduces portal pressure via V1 receptor-mediated splanchnic vasoconstriction; the only vasoactive agent with demonstrated mortality benefit in randomized controlled trials.
• Antibiotics: IV ceftriaxone 1 g/day for 5–7 days — reduces spontaneous bacterial peritonitis risk and mortality; shown superior to oral norfloxacin in advanced cirrhosis in a landmark New England Journal of Medicine RCT.

Endoscopy Within 12 Hours

• EVL is preferred over endoscopic sclerotherapy — equivalent hemostasis with fewer complications (strictures, ulcers).
• For gastric varices (type 2): cyanoacrylate glue injection or TIPS preferred over EVL.

Salvage Therapy (Failure to Control or Early Rebleeding Within 5 Days)

• TIPS — highly effective rescue therapy; see dedicated section below.
• Balloon tamponade (Sengstaken-Blakemore tube or Linton-Nachlas) — bridge only, maximum 24 hours; significant complication risk (aspiration, esophageal necrosis).
• Self-expanding metal stents (Danis stent) — emerging bridge therapy with lower complication profile than balloon tamponade.

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TIPS Procedure

The transjugular intrahepatic portosystemic shunt (TIPS) creates a direct channel between the portal vein and hepatic vein via a covered metal stent deployed through the liver parenchyma, bypassing the high-resistance sinusoidal circulation.

Hemodynamic Effect

Portal pressure gradient typically falls from 18–22 mmHg to <12 mmHg after TIPS — below the threshold for variceal bleeding.

Early TIPS (High-Risk Patients)

Early TIPS within 72 hours of AVH (ideally within 24 hours) in high-risk patients — Child-Pugh B with active bleeding or Child-Pugh C <14 — dramatically reduces rebleeding and improves survival compared to standard NSBB + EVL. This was established by Garcia-Pagan et al. in the landmark 2010 NEJM trial.

Technical Considerations

• Covered PTFE stents (e-PTFE, e.g., Viatorr) are standard — superior long-term patency compared to bare metal stents.
• Also used for refractory ascites and hepatic hydrothorax.

Complications

• Hepatic encephalopathy — occurs in 20–35% of patients post-TIPS; results from portal blood bypassing hepatic detoxification and reaching systemic circulation directly.
• Shunt dysfunction or occlusion
• Hemolysis (shear stress on red cells through the stent)
• Cardiac volume overload (portal decompression increases venous return)

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Secondary Prophylaxis

The goal of secondary prophylaxis is to prevent rebleeding after the index hemorrhage. Without treatment, rebleeding occurs in 60–70% of patients within 1–2 years.

Combination Therapy — Standard of Care

NSBB + EVL combined is superior to either alone for secondary prophylaxis and is recommended by all major guidelines (AASLD, EASL, Baveno VII).

• NSBB: propranolol or nadolol titrated to heart rate 55–60 bpm; carvedilol if tolerated.
• EVL: repeat every 2–4 weeks until variceal eradication, then 3–6 month surveillance endoscopy.

Rebleeding Despite Combination Therapy

Patients who rebleed despite NSBB + EVL should receive TIPS, which reduces rebleeding to <10% per year.

Liver Transplantation

Transplantation ultimately addresses the underlying cause of portal hypertension. TIPS serves as a bridge to transplant in eligible patients, maintaining hemostasis while they await organ allocation.

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Research Papers

1. de Franchis R et al.; Baveno VII Faculty. "Renewing consensus in portal hypertension." J Hepatol. 2022;76(4):959–974. PMID: 35120736
2. Sarin SK et al. "Acute variceal bleeding: APASL guidelines." Hepatol Int. 2019;13(4):460–491. PMID: 31165956
3. Garcia-Tsao G, Abraldes JG et al. "Portal hypertensive bleeding in cirrhosis: AASLD practice guidance 2017." Hepatology. 2017;65(1):310–335. PMID: 27786365
4. Villanueva C et al. "Transfusion strategies for acute upper gastrointestinal bleeding." N Engl J Med. 2013;368(1):11–21. PMID: 23281973
5. Bernard B et al. "Antibiotic prophylaxis for the prevention of bacterial infections in cirrhotic patients with gastrointestinal bleeding." Hepatology. 1999;29(6):1655–1661. PMID: 10347104
6. Lo GH et al. "A prospective randomized trial of sclerotherapy versus ligation in the management of bleeding esophageal varices." Hepatology. 1995;22(2):466–471. PMID: 7543458
7. Garcia-Pagan JC et al. "Early use of TIPS in patients with cirrhosis and variceal bleeding." N Engl J Med. 2010;362(25):2370–2379. PMID: 20573925
8. Bosch J et al. "Prevention and treatment of variceal hemorrhage." Nat Rev Gastroenterol Hepatol. 2009;6(12):695–705. PMID: 19904258
9. Tripathi D et al. "UK guidelines on the management of variceal haemorrhage in cirrhotic patients." Gut. 2015;64(11):1680–1704. PMID: 25887380
10. Lo GH et al. "Endoscopic variceal ligation plus nadolol and sucralfate compared with ligation alone for the prevention of variceal rebleeding." Hepatology. 2000;32(3):461–465. PMID: 10960433
11. Rios Castellanos E et al. "Comparing terlipressin vs octreotide in acute variceal bleeding: systematic review." J Clin Gastroenterol. 2015;49(2):138–144. PMID: 24572883
12. Abraldes JG et al. "Carvedilol for portal hypertension." Am J Gastroenterol. 2012;107(2):310–319. PMID: 21989145

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Connections

• Gastroenterology
• Hepatic Encephalopathy
• Cirrhosis
• Peptic Ulcer Disease
• H. pylori
• GERD

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Featured Videos

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