Mallory-Weiss tear (MWT) is a mucosal laceration at or near the gastroesophageal junction (GEJ), most often caused by forceful retching or vomiting, and accounts for approximately 3–14% of cases of acute upper gastrointestinal bleeding (UGIB). [1-3] The condition is predominantly self-limiting (~90% stop bleeding spontaneously), with an overall in-hospital mortality of ~2.7%. [1][4] Male-to-female ratio is approximately 3.6:1, with a median age of 51 years. [3]
1. History
- Classic presentation: Nonbloody emesis or retching followed by hematemesis — though this classic sequence occurs in only ~29% of cases; blood with the first episode of vomiting is more common [2]
- Characterize the vomiting: onset, frequency, severity, triggers (alcohol binge, food bolus, coughing, straining, hiccups, seizures)
- Quantify bleeding: volume, color (bright red vs. coffee-ground), duration
- Ask about preceding symptoms: nausea, epigastric pain, heartburn, dysphagia
- Associated symptoms: lightheadedness, dizziness, syncope, melena, hematochezia
- Important negatives: chest pain (think Boerhaave), abdominal rigidity, fever, weight loss, dysphagia (malignancy)
- Pregnancy-related hyperemesis, bulimia, or cyclic vomiting as triggers [2][5]
2. Alarm Features
- Hemodynamic instability (tachycardia ≥100, SBP ≤100 mmHg) — associated with higher transfusion requirements and worse outcomes [6-7]
- Hematochezia in the setting of UGIB — indicates brisk, severe hemorrhage [6]
- Syncope or presyncope
- Severe chest/back pain, subcutaneous emphysema, or crepitus → suspect Boerhaave syndrome (transmural esophageal rupture), which carries 20–50% mortality [8-10]
- Signs of hypovolemic shock (altered mental status, oliguria, cool extremities)
- Ongoing hematemesis despite resuscitation
- Coagulopathy or known portal hypertension — increases rebleeding risk [6][11]
3. Medications
- Contributors/exacerbators:
- NSAIDs and aspirin (impair mucosal defense and platelet function) [4-5][12]
- Anticoagulants (warfarin, DOACs) — strongest risk factor for GI bleeding severity [12]
- Dual antiplatelet therapy (DAPT) — 2–3× increased bleeding risk vs. aspirin alone [13]
- Corticosteroids, SSRIs, aldosterone antagonists [5]
- Acute treatment:
- IV PPI (e.g., pantoprazole 80 mg bolus → 8 mg/hr infusion) — initiate on presentation [14-15]
- Antiemetics (ondansetron) to reduce further retching/vomiting
- IV crystalloid resuscitation; pRBC transfusion if Hgb <7 g/dL (or <8 g/dL with cardiac ischemia) [15]
- Cautions:
- Hold anticoagulants/antiplatelets acutely; restart timing is individualized based on thrombotic risk [14]
- Avoid over-transfusion in cirrhotic patients (may worsen portal hypertension) [11]
4. Diet
- NPO initially if active bleeding or pending endoscopy
- After bleeding cessation: advance to clear liquids → bland diet
- Avoid alcohol — the single most common precipitant (~44% of cases) [3][16]
- Avoid spicy, acidic, or irritating foods acutely
- Long-term: address underlying causes of vomiting (GERD diet modifications, small frequent meals)
- Adequate hydration to prevent dehydration from vomiting
5. Review of Systems
- GI: hematemesis, melena, hematochezia, abdominal pain, heartburn, dysphagia, odynophagia, nausea/vomiting
- Cardiovascular: chest pain, palpitations, syncope, presyncope (assess for demand ischemia from anemia)
- Respiratory: dyspnea, pleuritic chest pain, subcutaneous emphysema (Boerhaave)
- Neurologic: dizziness, confusion, altered mental status (hypovolemia, alcohol intoxication/withdrawal)
- Psychiatric: history of bulimia or self-induced vomiting
- Constitutional: weight loss, fatigue (chronic blood loss, malignancy)
6. Collateral History and Family History
- Collateral from witnesses regarding alcohol intake, vomiting episodes, and duration of symptoms
- History of eating disorders (bulimia nervosa)
- Family history of bleeding disorders, coagulopathies, or liver disease
- Social context: alcohol use patterns (binge vs. chronic), illicit drug use
- Assess for alcohol withdrawal risk if chronic heavy use [11]
7. Risk Factors
- Alcohol use — most common risk factor, present in ~44% of cases [3][16]
- Hiatal hernia — strongly associated; present in ~20% of MWS cases [1][4][17]
- Forceful/prolonged vomiting or retching from any cause
- Reflux esophagitis (comorbid in ~24%) [1]
- Coagulopathy or anticoagulant use — increases severity and rebleeding risk [6][16]
- Portal hypertension/cirrhosis — more severe bleeding, higher rebleeding and mortality [6][11]
- Aspirin/NSAID use [4]
- Male sex, age 40–60 years [3]
- Other causes of forceful vomiting: chemotherapy, gastroparesis, pregnancy (hyperemesis), severe coughing, straining, CPR, seizures
8. Differential Diagnosis
- Boerhaave syndrome (transmural esophageal rupture) — the critical cannot-miss diagnosis. Distinguished by severe chest/back pain, subcutaneous emphysema, pneumomediastinum, Mackler triad (vomiting, chest pain, subcutaneous emphysema). Mortality 20–50% [8-9]
- Peptic ulcer disease — most common cause of UGIB; epigastric pain, NSAID/H. pylori history [7]
- Esophageal varices — in patients with known liver disease/cirrhosis; typically more massive bleeding [11]
- Erosive esophagitis — heartburn, dysphagia; usually less severe bleeding [7]
- Dieulafoy lesion — painless, massive, intermittent UGIB from aberrant submucosal vessel [7]
- Gastric/esophageal malignancy — weight loss, dysphagia, older age
- Aortoenteric fistula — history of aortic graft; herald bleed followed by massive hemorrhage [18]
- Hemobilia — post-hepatobiliary procedure or trauma
9. Past Medical History
- Prior episodes of UGIB or MWT
- Known hiatal hernia, GERD, peptic ulcer disease
- Liver disease/cirrhosis (increases severity) [11]
- Coagulation disorders (hemophilia, thrombocytopenia, von Willebrand disease)
- Chronic kidney disease/hemodialysis (increased MWS risk with even mild vomiting) [19]
- Prior GI surgeries, endoscopic procedures
- Cardiovascular disease (relevant for demand ischemia from acute blood loss) [20]
10. Physical Exam
- Vitals: Tachycardia, hypotension, orthostatic changes — assess hemodynamic stability first [7]
- General: Pallor, diaphoresis, altered mental status
- HEENT: Dry mucous membranes; look for subcutaneous emphysema in the neck (Boerhaave) [10]
- Chest: Hamman sign (mediastinal crunch on auscultation — Boerhaave); decreased breath sounds (pleural effusion)
- Abdomen: Typically soft and non-tender in MWT; epigastric tenderness may suggest PUD; peritoneal signs suggest perforation
- Rectal: Stool color — melena, hematochezia, or occult blood
- Skin: Stigmata of chronic liver disease (spider angiomata, palmar erythema, jaundice, caput medusae)
11. Lab Studies
- CBC — hemoglobin/hematocrit (note: initial Hgb may not reflect true blood loss for hours) [7]
- BMP — BUN:creatinine ratio (elevated BUN suggests upper GI source from digested blood)
- Coagulation panel (PT/INR, PTT) — assess for coagulopathy [14]
- Liver function tests — screen for underlying liver disease [14]
- Type and screen/crossmatch — prepare for potential transfusion
- Lactate — marker of tissue hypoperfusion in significant hemorrhage
- Troponin — consider in elderly or patients with cardiac risk factors; up to 19% of UGIB patients have troponin elevation from demand ischemia [20]
12. Imaging
- Imaging is generally not required for suspected MWT — diagnosis is made by upper endoscopy (EGD) [2][21]
- CT chest with oral contrast — indicated if Boerhaave syndrome is suspected (pneumomediastinum, pleural effusion, esophageal wall thickening, extraluminal contrast) [10][22]
- CT angiography — may be considered in massive UGIB when endoscopy is not feasible or fails to localize bleeding [18]
- Chest X-ray — may show pneumomediastinum, subcutaneous emphysema, or left-sided pleural effusion (Boerhaave) [22]
13. Special Tests
- Glasgow-Blatchford Score (GBS) — validated for risk stratification in UGIB; GBS of 0–1 identifies patients who may be safely managed as outpatients [3][7][15]
- AIMS65 score — predicts mortality in UGIB
- Shock Index (HR/SBP) — useful for predicting transfusion need in MWS [3]
- Upper endoscopy (EGD) — gold standard for diagnosis and therapy; tears appear as longitudinal mucosal lacerations at the GEJ, most commonly on the lesser curvature/left lateral wall of the gastric cardia [2-3]
- Point-of-care ultrasound — assess for free fluid, IVC collapsibility (volume status), pleural effusion
14. ECG
- Obtain ECG in patients with hemodynamic instability, chest pain, elderly, or cardiac risk factors
- Look for: ST changes or T-wave inversions suggesting demand ischemia from acute anemia/hypovolemia [20]
- Sinus tachycardia is the most common finding
- Rule out ACS as a mimic of epigastric/chest pain presentation
- Up to 19% of UGIB patients develop troponin elevation; ECG helps contextualize this finding [20]
15. Assessment
Mallory-Weiss tear is a clinical-endoscopic diagnosis characterized by mucosal lacerations at the GEJ following forceful vomiting or retching. Key clinical pearls:
- Most cases are self-limiting (~90% stop spontaneously) [4]
- The "classic" history of nonbloody emesis → hematemesis occurs in only ~29% of cases [2]
- In ~35% of patients, an additional bleeding lesion is identified at endoscopy [2]
- Severity stratification depends on hemodynamic status, active bleeding at endoscopy, and comorbidities (cirrhosis, coagulopathy) [6][16]
- Complications: bleeding anemia (26%), hypovolemic shock (2.9%), and rarely progression to Boerhaave syndrome [1][8]
The following figure illustrates the endoscopic management approach for Mallory-Weiss tears and other less common causes of UGIB:
16. Treatment Plan
Initial stabilization
- ABCs; two large-bore IVs; IV crystalloid resuscitation
- Transfuse pRBCs if Hgb <7 g/dL (threshold of 8 g/dL with active cardiac ischemia); avoid over-transfusion in cirrhotics [11][15]
- IV PPI (pantoprazole 80 mg bolus → 8 mg/hr continuous infusion) [14][24]
- Antiemetics to prevent further retching
- Correct coagulopathy if present (FFP, vitamin K, platelet transfusion as indicated)
Endoscopic therapy (only for actively bleeding tears): [23]
- Epinephrine injection (1:10,000) — most commonly used; primary hemostasis ~94% [25]
- Hemoclipping — effective and widely used [1]
- Band ligation — 100% primary hemostasis in one RCT; comparable to injection [25]
- Combination therapy (injection + clipping) — used for refractory cases [1]
- Non-bleeding tears with stigmata (clot, visible vessel) generally do not require endoscopic therapy [23]
If endoscopy fails
- Transcatheter arterial embolization (interventional radiology) [14]
- Surgery — exceedingly rare (<0.1% of cases); oversewing of the tear [1]
17. Disposition
- Discharge/outpatient management: Hemodynamically stable patients with GBS 0–1, no active bleeding at endoscopy, no coagulopathy, and no portal hypertension can be managed with brief observation or outpatient follow-up [6-7]
- Admission (floor): Patients requiring transfusion, with active bleeding controlled endoscopically, or with significant comorbidities
- ICU admission: Hemodynamic instability despite resuscitation, massive hemorrhage, hypovolemic shock, need for intubation, or significant comorbidities (cirrhosis with coagulopathy) [5][11]
- GI consultation: All patients with suspected UGIB should have GI consultation for endoscopy within 24 hours; urgent/emergent endoscopy for hemodynamically unstable patients [5][15]
- Surgery consultation: Rarely needed; consider if endoscopic and angiographic interventions fail
18. Follow Up / Return Precautions
- Follow-up: GI follow-up within 1–2 weeks post-discharge; sooner if high-risk features
- Rebleeding is uncommon and typically occurs within 24 hours if it does occur; more likely in patients with coagulopathy or portal hypertension [6]
- Return precautions: Recurrent hematemesis, melena, hematochezia, lightheadedness/syncope, chest pain, shortness of breath, severe abdominal pain
- Patient counseling:
- Alcohol cessation — the most impactful modifiable risk factor [3][16]
- Avoid NSAIDs; use acetaminophen for pain
- Take PPI as prescribed (typically 4–8 weeks)
- Treat underlying cause of vomiting (GERD, gastroparesis, etc.)
- Expected recovery: Most tears heal within 48–72 hours without recurrence; long-term prognosis is excellent in the absence of underlying liver disease [2][4]
References
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