Longitudinal mucosal tear at the gastroesophageal junction following retching or vomiting, producing hematemesis.
Also known as: Mallory-Weiss syndrome, MWT, gastroesophageal junction tear
Overview
Nonpenetrating mucosal and submucosal laceration at or just below the gastroesophageal junction, typically caused by a sudden rise in transgastric pressure during forceful vomiting or retching. Accounts for 5-15% of upper GI bleeding.
Epidemiology
Most common in men 40-60 years old, with alcohol use a leading risk factor. Also seen in pregnancy with hyperemesis, bulimia, and after endoscopy.
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Question 1GastrointestinalEasy
A 55-year-old man with alcohol use disorder develops hematemesis after several episodes of forceful retching and vomiting. He reports no chest pain. Upper endoscopy shows a single linear mucosal laceration at the gastroesophageal junction. Which of the following is the most likely diagnosis?
AMallory-Weiss tear
BEsophageal varices
CPeptic ulcer disease
DDieulafoy lesion
Reveal answer & full explanation
Correct answer: A — Mallory-Weiss tear
AMallory-Weiss tear✓
BEsophageal varices
CPeptic ulcer disease
DDieulafoy lesion
Why Mallory-Weiss tear is correct
A linear, partial-thickness mucosal laceration at the gastroesophageal junction following forceful retching or vomiting is a Mallory-Weiss tear
It classically causes hematemesis after vomiting and is typically not associated with chest pain
About 90% of cases stop bleeding spontaneously and are managed supportively
Why the others are wrong
Esophageal varices — dilated submucosal veins from portal hypertension that cause brisk bleeding, but endoscopy shows tortuous veins, not a discrete linear mucosal tear (anchoring on the alcohol history)
Peptic ulcer disease — bleeding arises from a gastric or duodenal ulcer crater, not a tear at the gastroesophageal junction (premature closure on the most common cause of upper GI bleeding)
Dieulafoy lesion — a large tortuous submucosal artery that erodes through otherwise normal mucosa, causing sudden painless hematemesis with no mucosal laceration on endoscopy (confused-with-another-painless-bleeding-source)
Question 2GastrointestinalMedium
A 52-year-old man presents with three episodes of bright red hematemesis that began after a night of heavy drinking and repeated forceful vomiting of nonbloody gastric contents. He denies abdominal pain, chest pain, or prior bleeding. Vital signs show heart rate 98/min and blood pressure 124/76 mm Hg. The abdomen is soft and nontender without peritoneal signs, and an upright chest radiograph shows no free air or pneumomediastinum. Laboratory studies reveal hemoglobin 12.8 g/dL, BUN 48 mg/dL, and creatinine 0.9 mg/dL. Which of the following laboratory findings best supports an upper gastrointestinal source of bleeding?
AElevated serum lipase concentration
BElevated serum lactate concentration
CDecreased hemoglobin concentration
DElevated BUN-to-creatinine ratio
Reveal answer & full explanation
Correct answer: D — Elevated BUN-to-creatinine ratio
AElevated serum lipase concentration
BElevated serum lactate concentration
CDecreased hemoglobin concentration
DElevated BUN-to-creatinine ratio✓
Why Elevated BUN-to-creatinine ratio is correct
In upper GI bleeding, blood proteins are digested and absorbed in the small bowel, raising the BUN out of proportion to creatinine; a BUN/Cr ratio >30 (here roughly 53) strongly points to an upper source.
It fits the classic Mallory-Weiss picture: hematemesis after nonbloody retching in an alcohol user, hemodynamically stable, soft nontender abdomen, and a normal upright CXR that excludes Boerhaave perforation.
Why the others are wrong
Decreased hemoglobin concentration — quantifies blood loss but does not distinguish an upper from a lower GI source, and it can lag in acute bleeding, so the hemoglobin is still 12.8 g/dL here.
Elevated serum lipase concentration — a marker of pancreatitis; it is checked when the picture is unclear but does not localize a bleeding source and is normal in this patient.
Elevated serum lactate concentration — reflects hypoperfusion or shock from any cause; this patient is hemodynamically stable, and lactate does not identify the level of the bleed.
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Severe vomiting from any cause: gastroenteritis, chemotherapy, bulimia, hyperemesis gravidarum
Forceful coughing or seizures
NSAID use, anticoagulation
Pathophysiology
An abrupt increase in intra-abdominal pressure during retching transmits to the lower esophagus, producing a longitudinal tear in the mucosa and submucosa just below or at the gastroesophageal junction. The tear does not extend through the muscular layer (distinguishing it from Boerhaave). Bleeding originates from submucosal arteries or venous plexus.
Clinical presentation
Symptoms
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
Signs / physical exam
Usually hemodynamically stable; tachycardia and hypotension only in larger bleeds
Stigmata of chronic liver disease if associated with alcohol use
Normal abdominal exam without peritoneal signs (helps distinguish from Boerhaave)
Classic findings
Hematemesis after nonbloody emesis is the textbook history.
Differential diagnosis
Peptic ulcer disease — Most common cause of upper GI bleeding; epigastric pain, melena, NSAID/H. pylori history; visible ulcer on EGD
Esophageal or gastric varices — Cirrhosis or portal hypertension; larger volume bleed; treat with octreotide and band ligation
Erosive esophagitis or gastritis — Diffuse mucosal injury; lower volume blood loss; often related to NSAIDs, alcohol, severe illness
Dieulafoy lesion — Submucosal arteriole; recurrent, often massive bleeding with negative initial endoscopy
Malignancy (esophageal or gastric) — Weight loss, dysphagia, anemia, chronic blood loss; mass on endoscopy
Diagnostic workup
Diagnostic criteria
Visualization of a longitudinal mucosal tear at the GE junction on EGD.
Labs
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
Imaging
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
Diagnostic algorithm
flowchart TD
A[Hematemesis after retching/vomiting] --> B[Resuscitate<br/>IVF, type and screen, PPI]
B --> C{Hemodynamically stable?}
C -->|No| D[Massive transfusion<br/>activate GI bleed protocol]
C -->|Yes| E[Upright CXR<br/>rule out perforation]
E --> F{Free air or<br/>pneumomediastinum?}
F -->|Yes| G[Boerhaave concern<br/>CT + surgery consult]
F -->|No| H[EGD within 24 h]
H --> I{Active bleed or<br/>high-risk stigmata?}
I -->|Yes| J[Endoscopic clip,<br/>band, or thermal +<br/>epinephrine]
I -->|No| K[Observation<br/>PPI continued]
J --> L[Refractory: angiographic<br/>embolization or surgery]
Workup and management algorithm for suspected Mallory-Weiss tear.
Treatment
First-line
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 and require only observation
Second-line / adjunct
Angiographic embolization of left gastric artery if endoscopy fails
Surgical oversewing — rare, reserved for refractory bleeding
Rarely, progression to deeper tear or perforation (Boerhaave-like)
PANCE pearls
Classic history: nonbloody vomiting followed by hematemesis in an alcohol user.
Hiatal hernia is found in nearly all cases at endoscopy.
Most Mallory-Weiss tears stop spontaneously — endoscopy is for diagnosis and risk stratification more than intervention.
Always rule out Boerhaave with upright CXR if pain is severe or there are systemic signs.
BUN/Cr ratio >30 in a bleeding patient strongly suggests an upper source from absorbed blood proteins.
References
ACG 2021 — ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding (Laine et al., Am J Gastroenterol 2021)
ASGE 2020 — ASGE guideline on the role of endoscopy in the management of acute non-variceal upper GI bleeding (Mullady et al., Gastrointest Endosc 2020)
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