Gastrointestinal · PANCE / PANRE

Esophageal Varices

Dilated submucosal esophageal veins from portal hypertension; high-risk source of upper GI bleeding.

Also known as: esophageal varices, variceal hemorrhage, variceal bleeding, gastroesophageal varices

Overview

Dilated submucosal veins of the distal esophagus, formed as portosystemic collaterals in response to portal hypertension. Variceal hemorrhage is a life-threatening complication of cirrhosis.

Epidemiology

Develop in ~50% of cirrhotic patients; prevalence rises with severity of liver disease (Child-Pugh class). First-bleed risk 10-15%/yr in patients with medium/large varices without prophylaxis. Six-week mortality after variceal bleed 15-25%.

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Question 1GastrointestinalMedium
A 65-year-old male with cirrhosis has large esophageal varices that have not bled. He declines endoscopic variceal banding. Which of the following medications is most effective for primary prophylaxis of variceal bleeding?
  • AFurosemide
  • BMetoprolol
  • COctreotide
  • DCarvedilol
Reveal answer & full explanation
Correct answer: D — Carvedilol
  • AFurosemide
  • BMetoprolol
  • COctreotide
  • DCarvedilol

Why Carvedilol is correct

  • For primary prophylaxis of variceal bleeding, nonselective beta-blockers (NSBBs) or endoscopic variceal ligation (EVL) are equally effective; with banding declined, an NSBB is the choice.
  • NSBB options include propranolol 20-40 mg BID, nadolol 40-80 mg daily, and carvedilol 6.25-12.5 mg BID; carvedilol is often preferred because its combined alpha-1 plus beta blockade reduces hepatic venous pressure gradient (HVPG) more than selective agents.
  • Target heart rate on NSBB therapy: 55-60 bpm.

Why the others are wrong

  • Furosemide — a diuretic used for ascites management with no role in variceal prophylaxis (right-organ-wrong-target).
  • Metoprolol — a cardioselective beta-1 blocker; lowering the HVPG requires nonselective blockade so that unopposed alpha activity constricts the splanchnic bed, and beta-1 selective agents are therefore not recommended for variceal prophylaxis (right-class-wrong-agent).
  • Octreotide — used for acute variceal bleeding only, not for prevention (confused-with acute management).

Additional high-yield points

  • Combining NSBB plus EVL is not superior to monotherapy for primary prophylaxis.
  • Transjugular intrahepatic portosystemic shunt (TIPS) is reserved for secondary prophylaxis after EVL and pharmacotherapy failure.
Question 2GastrointestinalMedium
A 61-year-old man with cirrhosis presents with hematemesis. He is resuscitated and started on octreotide and ceftriaxone. Which of the following is the most appropriate definitive intervention?
  • ABalloon tamponade as definitive care
  • BUpper endoscopy with band ligation
  • CIntravenous proton pump infusion
  • DTransjugular portosystemic shunt now
Reveal answer & full explanation
Correct answer: B — Upper endoscopy with band ligation
  • ABalloon tamponade as definitive care
  • BUpper endoscopy with band ligation
  • CIntravenous proton pump infusion
  • DTransjugular portosystemic shunt now

Why Upper endoscopy with band ligation is correct

  • Hematemesis in cirrhosis is variceal until proven otherwise; band ligation is the definitive first-line endoscopic therapy.
  • Endoscopy within 12 hours both diagnoses the bleeding source and treats it after vasoactive (octreotide) and antibiotic therapy are started.
  • Banding controls active bleeding and is repeated to obliterate varices, reducing rebleeding.

Why the others are wrong

  • Transjugular portosystemic shunt now — TIPS is salvage for endoscopy-refractory or recurrent variceal bleeding, not the initial definitive step (right-step-wrong-time).
  • Balloon tamponade as definitive care — Tamponade is only a temporizing bridge to endoscopy or TIPS in uncontrolled bleeding, not definitive therapy (premature closure on a rescue device).
  • Intravenous proton pump infusion — PPI infusion is the answer for peptic-ulcer bleeding; it does not control variceal hemorrhage (right-drug-wrong-source).
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Risk factors

  • Cirrhosis of any etiology (alcoholic, viral hepatitis B/C, MASH/NASH, autoimmune, hemochromatosis, Wilson, primary biliary cholangitis)
  • Non-cirrhotic portal hypertension (portal vein thrombosis, schistosomiasis, congenital hepatic fibrosis)
  • Hepatic vein thrombosis (Budd-Chiari)
  • Predictors of bleeding: large varices, red wale signs on EGD, decompensated cirrhosis (Child-Pugh B/C), HVPG >12 mmHg

Pathophysiology

Increased intrahepatic resistance (fibrosis, regeneration nodules, vasoconstriction) plus splanchnic vasodilation raises portal pressure. When the hepatic venous pressure gradient (HVPG) exceeds 10 mmHg, portosystemic collaterals develop. Variceal rupture occurs when wall tension (Laplace's law: pressure × radius / wall thickness) exceeds tissue tolerance — typically HVPG >12 mmHg.

Clinical presentation

Symptoms

  • Asymptomatic until rupture
  • Hematemesis (frank red blood or coffee-ground)
  • Melena or hematochezia (if brisk)
  • Light-headedness, syncope, fatigue
  • Symptoms of cirrhosis: jaundice, abdominal distension, confusion (encephalopathy)

Signs / physical exam

  • Hemodynamic instability: tachycardia, hypotension, orthostasis
  • Stigmata of chronic liver disease: spider angiomata, palmar erythema, gynecomastia, caput medusae, splenomegaly, ascites, asterixis
  • Pallor, cool extremities if hypovolemic shock

Classic findings

Massive painless hematemesis in a known cirrhotic — variceal bleed until proven otherwise.

Differential diagnosis

  • Peptic ulcer bleed — Most common cause of UGIB overall; epigastric pain, NSAID/H. pylori; visible vessel or active bleed on EGD
  • Mallory-Weiss tear — Hematemesis after retching/vomiting; linear mucosal tear at GEJ
  • Erosive esophagitis/gastritis — Diffuse erosions; usually less severe bleeding
  • Dieulafoy lesion — Recurrent massive bleeding from small submucosal vessel; often proximal stomach
  • Aortoenteric fistula — Prior aortic graft; herald bleed followed by massive hemorrhage; CT angiography
  • Gastric varices — Often fundic; isolated or with esophageal varices; cyanoacrylate glue rather than banding
  • Portal hypertensive gastropathy — Snake-skin mosaic pattern; chronic anemia more than acute bleed

Diagnostic workup

Labs

  • CBC, type and crossmatch (4+ units PRBCs)
  • BMP, LFTs (AST/ALT, bilirubin, albumin), INR, PT/PTT
  • Lactate, ABG
  • Blood and ascitic fluid cultures (high risk of SBP)

Imaging

  • Upper endoscopy (EGD) — diagnostic and therapeutic; perform within 12 h of admission for suspected variceal bleed
  • Abdominal ultrasound with Doppler — confirms cirrhosis, portal vein patency, splenomegaly
  • CT abdomen if suspect alternative source or portal vein thrombosis
  • MRE or vibration-controlled transient elastography (FibroScan) for non-invasive staging of fibrosis

Other studies

  • Variceal screening EGD in newly diagnosed cirrhosis (Baveno VII allows deferral if liver stiffness <20 kPa and platelets >150,000)
  • Surveillance EGD every 1-3 yr based on size and presence/absence of decompensation

Diagnostic algorithm

flowchart TD
  A[Suspected variceal bleed<br/>known/likely cirrhosis] --> B[Resuscitate<br/>2 large-bore IVs<br/>Restrictive Hgb ~7]
  B --> C[Octreotide IV<br/>+ Ceftriaxone 1g]
  C --> D[EGD within 12h]
  D --> E[Endoscopic<br/>band ligation]
  E --> F{Hemostasis<br/>achieved?}
  F -->|Yes, high-risk<br/>Child-Pugh C<14<br/>or B with active bleed| G[Early TIPS<br/>within 72h]
  F -->|Yes, lower risk| H[Secondary prophylaxis:<br/>NSBB + serial EVL]
  F -->|No| I[Rescue TIPS<br/>± balloon tamponade<br/>as bridge]
Acute variceal hemorrhage management — Baveno VII / AASLD pathway.

Treatment

First-line

  • Resuscitation: 2 large-bore IVs, restrictive transfusion to Hgb ~7 g/dL (avoid over-transfusion — raises portal pressure)
  • Vasoactive agent — octreotide 50 mcg IV bolus then 50 mcg/h × 3-5 days (or terlipressin where available) — START BEFORE EGD if suspected
  • Prophylactic IV antibiotic — ceftriaxone 1 g daily × up to 7 days (reduces SBP, rebleeding, and mortality)
  • Endoscopic variceal band ligation (EVL) within 12 h — preferred over sclerotherapy
  • Cyanoacrylate injection for gastric varices
  • Correct coagulopathy judiciously — overcorrection has not shown benefit; platelets if <50,000
  • Airway protection (intubation) for active hematemesis or altered mental status

Primary prophylaxis (no prior bleed, medium/large varices)

  • Non-selective beta-blocker — propranolol, nadolol, or carvedilol — titrate to HR 55-60 or maximum tolerated dose
  • OR endoscopic variceal band ligation every 2-4 weeks until eradication
  • Carvedilol preferred in compensated cirrhosis per Baveno VII

Secondary prophylaxis (after first bleed)

  • Combination non-selective beta-blocker + serial EVL (every 2-4 weeks until obliteration, then surveillance every 3-6 months)
  • Lifelong therapy
  • TIPS for failure of combined therapy

Second-line / adjunct

  • TIPS (transjugular intrahepatic portosystemic shunt) — rescue therapy after failed endoscopic control; early/preemptive TIPS within 72 h reduces mortality in high-risk patients (Child-Pugh C <14, or B with active bleeding)
  • Balloon tamponade (Sengstaken-Blakemore, Minnesota, or Linton tubes) — temporizing bridge to definitive therapy; maximum 24 h
  • Self-expanding covered metal esophageal stent — alternative to balloon tamponade
  • Liver transplantation evaluation

Complications

  • Hemorrhagic shock and death
  • Spontaneous bacterial peritonitis (SBP) — high risk; prophylactic ceftriaxone reduces incidence
  • Hepatic encephalopathy precipitated by GI bleed (lactulose, rifaximin)
  • Aspiration pneumonia
  • Hepatorenal syndrome
  • Rebleeding (60-70% within 1 yr without secondary prophylaxis)

PANCE pearls

  • Start octreotide and ceftriaxone BEFORE endoscopy whenever variceal bleed is suspected — both reduce mortality.
  • Restrictive transfusion strategy (Hgb target ~7) reduces rebleeding and mortality vs liberal strategy (Villanueva, NEJM 2013).
  • Early TIPS (within 72 h) in high-risk patients (Child-Pugh C <14 or B with active bleeding on endoscopy) reduces mortality (García-Pagán, NEJM 2010).
  • Beta-blocker contraindications relative in advanced cirrhosis: refractory ascites, SBP, hypotension (SBP <90), or AKI — discontinue if these develop.
  • Carvedilol lowers portal pressure more than propranolol and is preferred in compensated cirrhosis (Baveno VII).
  • Variceal screening can be deferred in compensated cirrhosis with liver stiffness <20 kPa AND platelets >150,000 (Baveno VI/VII criteria).

References

  • Baveno VII 2022 — de Franchis R et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76:959-974
  • AASLD 2017 — Garcia-Tsao G et al. Portal Hypertensive Bleeding in Cirrhosis: Risk Stratification, Diagnosis, and Management. Hepatology 2017;65:310-335
  • Restrictive Transfusion — Villanueva C et al. Transfusion Strategies for Acute Upper Gastrointestinal Bleeding. NEJM 2013;368:11-21
  • Early TIPS — García-Pagán JC et al. Early Use of TIPS in Patients with Cirrhosis and Variceal Bleeding. NEJM 2010;362:2370-2379

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