Confusable diagnoses · PANCE / PANRE

Esophageal Varices vs Mallory-Weiss Tear

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Esophageal Varices and Mallory-Weiss Tear are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.

Esophageal Varices vs Mallory-Weiss Tear at a glance

  • Esophageal Varices: Dilated submucosal esophageal veins from portal hypertension; high-risk source of upper GI bleeding.
  • Mallory-Weiss Tear: Longitudinal mucosal tear at the gastroesophageal junction following retching or vomiting, producing hematemesis.

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Question 1GastrointestinalMedium
A 54-year-old man with alcohol-related cirrhosis is admitted with massive hematemesis. Upper endoscopy reveals large esophageal varices with active bleeding, which is controlled with band ligation. He receives octreotide and prophylactic ceftriaxone and stabilizes. He is discharged but, against advice, does not return for follow-up and takes no further medications. Over the following year, which of the following complications is most likely to develop?
  • AOliguric hepatorenal syndrome
  • BWorsening hepatic encephalopathy
  • CSpontaneous bacterial peritonitis
  • DRecurrent variceal hemorrhage
Reveal answer & full explanation
Correct answer: D — Recurrent variceal hemorrhage
  • AOliguric hepatorenal syndrome
  • BWorsening hepatic encephalopathy
  • CSpontaneous bacterial peritonitis
  • DRecurrent variceal hemorrhage✓

Why Recurrent variceal hemorrhage is correct

  • After a first variceal bleed, rebleeding occurs in roughly 60-70% of patients within 1 year when no secondary prophylaxis is given, making it by far the most likely complication in this untreated patient.
  • Standard secondary prophylaxis is a non-selective beta-blocker (carvedilol or nadolol) PLUS serial band ligation every 2-4 weeks until the varices are obliterated; this patient received neither.
  • Per Baveno VII, combined beta-blocker plus endoscopic variceal ligation is continued long term after an index bleed, with TIPS reserved for failure of combined therapy.

Why the others are wrong

  • Spontaneous bacterial peritonitis is a real high-risk event during the acute bleed and prophylactic ceftriaxone lowers it, but across a full untreated year rebleeding is the dominant, near-inevitable event.
  • Worsening hepatic encephalopathy is commonly precipitated by a GI bleed and occurs in decompensated cirrhosis, yet it is less consistently the first complication than rebleeding without prophylaxis.
  • Oliguric hepatorenal syndrome is a late complication of advanced decompensated cirrhosis, often triggered by SBP or large-volume paracentesis, and is far less likely than rebleeding in this scenario.
Question 2GastrointestinalMedium
A 52-year-old man with heavy alcohol use presents after vomiting bright red blood. Earlier that evening he had several bouts of forceful nonbloody retching, followed by hematemesis. He is hemodynamically stable with a soft, nontender abdomen and no chest pain or subcutaneous emphysema. Upright chest radiograph shows no free air or pneumomediastinum. Upper endoscopy reveals a longitudinal mucosal tear at the gastroesophageal junction with a hiatal hernia. Which of the following best explains the findings?
  • AElevated portal venous pressure dilating thin-walled submucosal veins
  • BAbrupt rise in transgastric pressure tearing the mucosa and submucosa
  • CAcid-peptic erosion eroding through the wall into a submucosal artery
  • DMucosal ischemia from splanchnic vasoconstriction during retching
Reveal answer & full explanation
Correct answer: B — Abrupt rise in transgastric pressure tearing the mucosa and submucosa
  • AElevated portal venous pressure dilating thin-walled submucosal veins
  • BAbrupt rise in transgastric pressure tearing the mucosa and submucosa✓
  • CAcid-peptic erosion eroding through the wall into a submucosal artery
  • DMucosal ischemia from splanchnic vasoconstriction during retching

Why Abrupt rise in transgastric pressure tearing the mucosa and submucosa is correct

  • A Mallory-Weiss tear results when forceful retching causes a sudden surge in intra-abdominal and transgastric pressure that is transmitted to the lower esophagus.
  • This produces a longitudinal laceration limited to the mucosa and submucosa at or just below the gastroesophageal junction; bleeding arises from submucosal arteries or the venous plexus.
  • A coexisting hiatal hernia (present in 40-100% of cases) is thought to predispose by allowing a greater pressure gradient across the GE junction.

Why the others are wrong

  • Elevated portal venous pressure dilating thin-walled submucosal veins describes esophageal varices, which cause larger-volume bleeds in cirrhosis or portal hypertension and appear as dilated venous columns, not a discrete linear tear, on EGD.
  • Acid-peptic erosion eroding through the wall into a submucosal artery describes peptic ulcer disease, the most common cause of upper GI bleeding, driven by acid with H. pylori or NSAIDs and seen as a discrete ulcer crater rather than a retching-induced tear.
  • Mucosal ischemia from splanchnic vasoconstriction during retching does not produce a discrete linear laceration: this patient is hemodynamically stable, and ischemic injury of the distal esophagus (acute esophageal necrosis) follows hypotension or a low-flow state and appears endoscopically as circumferential black mucosa.
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Side-by-side comparison

FeatureEsophageal VaricesMallory-Weiss Tear
At a glanceDilated submucosal esophageal veins from portal hypertension; high-risk source of upper GI bleeding.Longitudinal mucosal tear at the gastroesophageal junction following retching or vomiting, producing hematemesis.
Classic presentationMassive painless hematemesis in a known cirrhotic — variceal bleed until proven otherwise.; 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); Hemodynamic…Hematemesis after nonbloody emesis is the textbook history.; Hematemesis (bright red or coffee-ground) following a bout of nonbloody vomiting or retching; Epigastric or retrosternal pain (less prominent than Boerhaave); Melena if bleeding is significant or delayed presentation; Lightheadedness, syncope if hemodynamically significant;…
Workup / key labsCBC, 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); 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…Visualization of a longitudinal mucosal tear at the GE junction on EGD.; CBC, BMP, LFTs, coagulation studies, type and screen; BUN/Cr ratio (often elevated in upper GI bleed from absorbed blood); Lactate and lipase if clinical picture is unclear
ImagingUpper 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)…Upright CXR if any concern for perforation (free air, pneumomediastinum) — must exclude Boerhaave; Upper endoscopy (EGD) — diagnostic and therapeutic; performed within 24 h; CT chest/abdomen if EGD inconclusive or perforation suspected
First-line treatmentResuscitation: 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…Supportive care: IV fluids, transfuse for hemoglobin <7 g/dL (or <8 if cardiovascular disease), correct coagulopathy; IV proton pump inhibitor: pantoprazole 80 mg bolus then 8 mg/h infusion, or intermittent dosing; Antiemetics: ondansetron or metoclopramide to prevent further retching; Most tears (80-90%) stop bleeding spontaneously; a…

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Full outlines

Esophageal Varices Mallory-Weiss Tear All 514 diagnoses

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