Mallory-Weiss Tear

1. Overview

A Mallory-Weiss tear is a longitudinal mucosal or submucosal laceration occurring at or near the gastro-oesophageal junction (GOJ), typically caused by a sudden and forceful increase in intra-abdominal pressure transmitted to the distal oesophagus and gastric cardia. First described by G. Kenneth Mallory and Soma Weiss in 1929 following post-mortem examinations of patients with alcoholism who had experienced haematemesis, the condition represents a distinct clinical entity accounting for 5-15% of all acute upper gastrointestinal bleeding episodes. [1,2]

The classic presentation involves an initial episode of forceful, non-bloody vomiting or retching, followed by the subsequent appearance of haematemesis—bright red blood or "coffee-ground" material. This temporal sequence is pathognomonic and helps distinguish Mallory-Weiss tears from other causes of upper GI bleeding such as peptic ulcer disease or oesophageal varices. The condition is most commonly associated with excessive alcohol consumption, which predisposes to both the precipitating event (vomiting) and potentially complicates haemostasis through coagulopathy or thrombocytopenia. [3,4]

The majority of Mallory-Weiss tears (approximately 80-90%) are self-limiting and cease bleeding spontaneously without requiring therapeutic intervention. However, approximately 10-20% of cases require endoscopic haemostasis, and a small proportion (less than 5%) may necessitate angiographic or surgical intervention for ongoing bleeding. The key clinical challenge lies in distinguishing Mallory-Weiss tear from Boerhaave syndrome, a full-thickness oesophageal perforation that represents a life-threatening surgical emergency with significantly different management and prognosis. Understanding the pathophysiology, risk stratification, and evidence-based management of Mallory-Weiss tears is essential for emergency physicians, gastroenterologists, and general surgeons managing acute upper GI bleeding. [5,6]

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2. Epidemiology

Incidence and Prevalence

Mallory-Weiss tears account for 5-15% of all acute upper gastrointestinal bleeding presentations, making them the third or fourth most common cause after peptic ulcer disease, oesophageal varices, and erosive gastritis. The reported incidence varies geographically and is influenced by local patterns of alcohol consumption and access to early endoscopy. Population-based studies estimate an annual incidence of approximately 4-10 cases per 100,000 population. [1,7]

Demographics

Age Distribution: Mallory-Weiss tears predominantly affect young to middle-aged adults, with peak incidence between 30-50 years of age. This contrasts with peptic ulcer bleeding and variceal haemorrhage, which typically occur in older populations or those with established chronic liver disease, respectively. Paediatric cases are rare but have been reported, particularly in adolescents with eating disorders (bulimia nervosa). [12,13]

Sex Distribution: There is a male predominance with a male-to-female ratio of approximately 2-4:1. This sex difference is largely attributed to higher rates of alcohol misuse in males, though non-alcoholic precipitants (hyperemesis gravidarum, chemotherapy-induced vomiting) result in a more balanced sex distribution in some series. [3,14]

Ethnic and Geographic Variation: Limited data exist on ethnic differences, though incidence appears higher in populations with elevated alcohol consumption rates. Geographic variation correlates with local drinking patterns and cultural practices.

Risk Factors and Precipitants

Temporal Patterns: Incidence may be higher during winter months (correlating with viral gastroenteritis outbreaks) and following holidays/celebrations (increased alcohol consumption).

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3. Aetiology & Pathophysiology

Anatomical Considerations

The gastro-oesophageal junction represents a transition zone between the stratified squamous epithelium of the oesophagus and the columnar epithelium of the gastric cardia. This region is subjected to considerable mechanical stress during episodes of retching and vomiting due to several anatomical factors:

1. Fixed proximal attachment: The oesophagus is relatively fixed at the diaphragmatic hiatus
2. Mobile distal segment: The gastric fundus and cardia are more mobile
3. Pressure differential: High intra-abdominal pressure transmitted to a relatively low-pressure thoracic compartment
4. Vascular anatomy: Rich submucosal plexus vulnerable to laceration

Location of Tears: The majority of Mallory-Weiss tears occur:

• Right lateral wall of the distal oesophagus (most common, ~80-85%)
• Lesser curvature of the gastric cardia (~10-15%)
• Bilateral or multiple tears (~5-10%)

The predilection for the right lateral wall is thought to relate to the anatomy of the muscular sling fibres and the acute angle of attachment at the GOJ. [23,24]

Mechanism of Injury

The pathophysiological sequence leading to a Mallory-Weiss tear involves:

1. Precipitating Event: Forceful vomiting, retching, coughing, or straining
2. Sudden Increase in Intra-gastric Pressure: Coordinated contraction of abdominal and diaphragmatic muscles against a closed glottis (Valsalva manoeuvre)
3. Pressure Transmission: Rapid distension of the gastric fundus and cardia
4. Shear Stress at GOJ: Differential movement between relatively fixed oesophagus and mobile stomach
5. Mucosal Laceration: Longitudinal splitting of mucosa and submucosa when tensile strength is exceeded
6. Submucosal Vascular Injury: Laceration of submucosal arterioles and venules leading to bleeding

The longitudinal orientation of the tear (parallel to the long axis of the oesophagus) reflects the direction of maximum shear stress during acute distension. [4,25]

Depth of Injury: Mallory-Weiss vs. Boerhaave Syndrome

A critical distinction exists between partial-thickness and full-thickness injuries:

Boerhaave syndrome is a transmural rupture, most commonly involving the left posterolateral wall of the distal oesophagus (different location from MW tear). The classic presentation is Mackler's triad: vomiting, lower chest pain, and subcutaneous emphysema. [26,27]

Association with Hiatus Hernia

The presence of a hiatus hernia is documented in 35-100% of patients with Mallory-Weiss tears, a prevalence significantly higher than in the general population (~20% of adults > 50 years). The proposed mechanisms linking hiatus hernia to MW tears include:

• Increased mobility of the GOJ, allowing greater differential movement during vomiting
• Gastric pouch above diaphragm creating a closed compartment subject to extreme pressures
• Accentuated angulation at the GOJ increasing local shear forces
• Mucosal prolapse predisposing to mechanical trauma

The association is strongest with sliding hiatus hernias and appears independent of hernia size. [16,17,28]

Molecular and Cellular Pathophysiology

At the tissue level, the integrity of the oesophagogastric mucosa depends on:

• Epithelial tight junctions: Maintain barrier function
• Extracellular matrix: Collagen (tensile strength), elastin (compliance)
• Submucosal blood supply: Healing and haemostasis

Factors reducing tensile strength:

• Chronic alcohol exposure: Impairs collagen synthesis and epithelial regeneration
• Nutritional deficiency: Vitamin C (collagen synthesis), protein deficiency
• Repeated trauma: Recurrent vomiting causing cumulative microtrauma
• Inflammation: Reflux oesophagitis weakening mucosa

When mechanical stress exceeds the mucosal tensile strength threshold, laceration occurs along lines of maximum stress (longitudinal axis). [29,30]

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4. Clinical Presentation

Classic History

The pathognomonic presentation of a Mallory-Weiss tear consists of a characteristic temporal sequence:

1. Prodromal Phase: Repeated episodes of non-bloody vomiting or retching (minutes to hours)
2. Transition: After several episodes, fresh haematemesis appears (bright red blood or "coffee-ground" material)
3. Context: Often occurs in setting of alcohol intoxication, gastroenteritis, or other causes of vomiting

This sequence—"retching first, blood later"—is highly suggestive of Mallory-Weiss tear and distinguishes it from:

• Peptic ulcer bleeding: Haematemesis without preceding non-bloody vomiting
• Variceal bleeding: May have no vomiting, or blood appears immediately
• Boerhaave syndrome: Severe chest pain predominates over bleeding

Key Historical Questions:

• "Did you vomit several times before seeing blood?" (establishes temporal sequence)
• "How much alcohol did you drink?" (most common precipitant)
• "Do you have chest pain or difficulty breathing?" (excludes Boerhaave)
• "Are you on blood thinners?" (affects bleeding severity and management)
• "Have you had similar episodes before?" (recurrence risk)

[3,4,31]

Symptoms

Volume of Haematemesis: Ranges from streaks of blood in vomitus to massive haemorrhage. Most cases involve small-to-moderate amounts (50-200ml) that cease spontaneously. [8,32]

Predisposing Circumstances

Alcohol-Related (40-75%):

• Binge drinking episode followed by prolonged vomiting
• "Dry heaving" after stomach emptied
• Associated alcohol withdrawal symptoms

Gastrointestinal Illness (15-30%):

• Viral gastroenteritis (norovirus, rotavirus)
• Food poisoning (Staphylococcus aureus, Bacillus cereus)
• Chemotherapy-induced vomiting

Pregnancy (Rare, less than 5%):

• Hyperemesis gravidarum (first trimester)
• Labour and delivery (bearing down)

Other Precipitants:

• Eating disorders (bulimia nervosa with chronic purging)
• Severe coughing (pertussis, bronchitis, COPD exacerbation)
• Heavy lifting or straining

[13,18,33]

Red Flag Features Suggesting Boerhaave Syndrome

Clinicians must actively exclude Boerhaave syndrome (oesophageal perforation), which requires immediate surgical consultation:

Mackler's Triad (present in only ~30% of Boerhaave cases):

1. Forceful vomiting
2. Lower chest/epigastric pain
3. Subcutaneous emphysema (neck, chest wall)

[26,27,34]

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5. Clinical Examination

Initial Assessment and Risk Stratification

Airway, Breathing, Circulation (ABC) Approach:

• Airway: Assess for active haematemesis, aspiration risk
• Breathing: Respiratory rate, oxygen saturation (hypoxia suggests aspiration or perforation)
• Circulation: Heart rate, blood pressure, capillary refill time, peripheral perfusion

Haemodynamic Status:

[35]

General Inspection

• Pallor: Suggests acute or chronic anaemia
• Jaundice: May indicate chronic liver disease (consider varices)
• Cachexia: Malignancy, eating disorder, alcohol dependence
• Intoxication: Smell of alcohol, altered mental state
• Distress: Severe pain suggests perforation (Boerhaave)

Abdominal Examination

Inspection:

• Distension (unlikely in uncomplicated MW tear)
• Surgical scars (previous upper GI surgery)

Palpation:

• Mild epigastric tenderness: Common, non-specific
• No peritonism: Absence of guarding/rigidity (peritonism suggests perforation)
• Hepatomegaly: Chronic liver disease (consider varices)
• Splenomegaly: Portal hypertension

Percussion:

• Ascites (shifting dullness): Chronic liver disease/portal hypertension

Auscultation:

• Bowel sounds usually normal

Extraabdominal Examination

Head and Neck:

• Subcutaneous emphysema: Palpate neck and supraclavicular fossae (crepitus suggests Boerhaave)
• Telangiectasia, parotid enlargement, Dupuytren's contracture: Stigmata of chronic alcohol use

Chest:

• Hamman's sign: Crunching sound synchronous with heartbeat (pneumomediastinum)
• Reduced breath sounds: Pleural effusion (left-sided suggests Boerhaave)

Peripheral:

• Signs of chronic liver disease: Palmar erythema, spider naevi, gynaecomastia, testicular atrophy, leuconychia
• Koilonychia: Iron deficiency from chronic GI blood loss

Digital Rectal Examination (DRE)

• Melaena: Black, tarry, offensive stool confirms upper GI bleeding
• Fresh blood per rectum: Suggests massive UGIB with rapid transit (severe, rare in MW)

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6. Differential Diagnosis

Haematemesis has a broad differential; the clinical context and history narrow the possibilities.

High-Risk Differentials ("Must Not Miss"):

1. Boerhaave syndrome: Transmural rupture; surgical emergency
2. Variceal haemorrhage: High mortality without urgent intervention
3. Aortoenteric fistula: Catastrophic bleeding; very high mortality

[36,37]

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7. Investigations

Bedside Investigations

Laboratory Investigations

First-Line Bloods:

Second-Line Investigations (if indicated):

• Coagulation factors: If on anticoagulation (consider reversal)
• Thrombophilia screen: Only if recurrent unexplained bleeding
• Alcohol level: Medico-legal purposes; confirms intoxication

Interpretation Pearls:

• Normal Hb does not exclude significant bleeding: Haemodilution takes 6-24 hours; initial Hb reflects baseline
• Urea:Creatinine ratio > 100: Suggests upper GI source (blood digested to urea)
• Thrombocytopenia + coagulopathy: Think chronic liver disease (consider varices)

[38,39]

Risk Stratification Scores

Glasgow-Blatchford Score (GBS): Pre-endoscopy tool to identify low-risk patients suitable for outpatient management.

Interpretation:

• GBS = 0: Very low risk; may be managed as outpatient with urgent OGD within 24 hours
• GBS ≥6: Intermediate-high risk; admit for urgent endoscopy
• GBS ≥12: High risk; likely to need intervention (transfusion, endoscopy, surgery)

[42]

Rockall Score: Combines clinical and endoscopic features to predict rebleeding and mortality.

Pre-endoscopy clinical Rockall (age, shock, comorbidity) gives early risk assessment; post-endoscopy Rockall adds diagnosis and stigmata of bleeding for refined prognosis.

[43]

Diagnostic Investigations

Upper Gastrointestinal Endoscopy (OGD): Gold standard for diagnosis

Timing:

• Immediate (less than 2 hours): Haemodynamic instability despite resuscitation (GBS ≥12)
• Urgent (within 24 hours): Most patients with UGIB
• Elective (within 48-72 hours): Low-risk patients (GBS 0-1)

Endoscopic Findings:

• Single or multiple longitudinal lacerations at GOJ (80-85% right lateral wall)
• Tear length: Usually 0.5-4 cm
• Active bleeding: Arterial spurting, oozing, or visible vessel
• Recent bleeding stigmata: Adherent clot, flat pigmented spot
• Forrest Classification (for active bleeding):
  • "Forrest Ia: Spurting arterial bleeding (high rebleed risk)"
  • "Forrest Ib: Oozing venous bleeding"
  • "Forrest IIa: Visible vessel (non-bleeding)"
  • "Forrest IIb: Adherent clot"
  • "Forrest III: Clean base (low rebleed risk)"

Advantages of OGD:

• Confirms diagnosis
• Excludes differentials (varices, ulcer, malignancy)
• Allows therapeutic intervention (adrenaline injection, clips, cautery)

[9,44]

Imaging (If Boerhaave Syndrome Suspected)

Chest X-ray (CXR):

• Pneumomediastinum: Air outlining mediastinal structures
• Left pleural effusion: 80% of Boerhaave cases
• Pneumothorax: Rupture into pleural space
• Surgical emphysema: Air in soft tissues
• Widened mediastinum: Mediastinal fluid/blood

CT Chest with Oral and IV Contrast:

• Gold standard for Boerhaave diagnosis
• Direct visualization of oesophageal tear with contrast extravasation
• Pneumomediastinum, pleural effusion, mediastinal fluid
• Guide surgical approach

Water-Soluble Contrast Swallow:

• Less sensitive than CT; used if CT unavailable
• Avoid barium (causes mediastinitis if perforation present)

[26,34]

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8. Management

Initial Resuscitation

ABC Approach:

1. Airway: Position patient upright (30-45°) to reduce aspiration risk; suction available
2. Breathing: Oxygen if hypoxic; monitor SpO₂
3. Circulation: Two large-bore IV cannulae (14-16G); aggressive fluid resuscitation

Haemodynamic Resuscitation:

Transfusion Strategy:

• Restrictive transfusion (Hb target 70-90 g/L) is associated with lower rebleeding rates than liberal transfusion (Hb target 90-110 g/L) in non-variceal UGIB. [45]
• Exception: Active cardiac disease (target Hb > 80 g/L)

Correct Coagulopathy:

• Warfarin: Vitamin K 5-10 mg IV + prothrombin complex concentrate (PCC) if active bleeding
• DOACs: Specific reversal agents (idarucizumab for dabigatran, andexanet alfa for Xa inhibitors) if available
• Platelets: Transfuse if count less than 50 × 10⁹/L and active bleeding
• Cryoprecipitate/FFP: If fibrinogen less than 1.5 g/L or significant coagulopathy

[21,46]

Pharmacological Management

Proton Pump Inhibitors (PPIs):

• High-dose IV PPI: Omeprazole or pantoprazole 80 mg IV bolus, then 8 mg/hour continuous infusion for 72 hours
• Rationale: Although PPIs show clear benefit in peptic ulcer bleeding, evidence is less robust for Mallory-Weiss tears. However, they are routinely used to:
  • Stabilize clot formation (requires pH > 6)
  • Reduce risk of rebleeding
  • Standard practice for all non-variceal UGIB pending endoscopy
• Transition to oral PPI (e.g., omeprazole 40 mg BD) after 72 hours, continue for 4-8 weeks

[47,48]

Antiemetics:

• Essential to prevent further retching and rebleeding
• Ondansetron 4-8 mg IV (avoid in prolonged QT)
• Metoclopramide 10 mg IV TDS (prokinetic, aids endoscopy)
• Cyclizine 50 mg IV/IM TDS (if ondansetron contraindicated)

Prokinetics (Pre-endoscopy):

• Erythromycin 250 mg IV 30-60 minutes before OGD
• Promotes gastric emptying, improves endoscopic view
• Meta-analysis shows reduced need for repeat endoscopy

[49]

Avoid:

• NSAIDs: Exacerbate bleeding, impair platelet function
• Aspirin: Withhold temporarily unless very high cardiovascular risk (discuss with cardiology)

Endoscopic Management

Indications for Therapeutic Endoscopy:

• Active bleeding at endoscopy (Forrest Ia, Ib)
• High-risk stigmata (visible vessel, adherent clot)
• Rebleeding after initial cessation
• Haemodynamic instability despite resuscitation

Endoscopic Haemostasis Techniques:

Combination Therapy:

• Adrenaline + clip or adrenaline + thermal superior to adrenaline alone
• Current guidelines recommend combination therapy for high-risk lesions

[9,50,51]

Technique for Injection Therapy:

1. Inject 1:10,000 adrenaline (1 mg in 10 ml saline) in 1-2 ml aliquots
2. Inject in four quadrants around bleeding point (total 5-10 ml)
3. Aim for visible blanching and tamponade effect
4. Follow with mechanical therapy (clips) for durable haemostasis

Endoscopic Clips:

• Through-the-scope metal clips applied to approximate tear edges
• Particularly effective for linear lacerations
• Remain in place for 1-2 weeks, then spontaneously dislodge

Interventional Radiology

Angiography and Embolisation:

• Reserved for refractory bleeding despite endoscopic therapy
• Selective catheterisation of left gastric artery or short gastric vessels
• Embolisation with coils or gelfoam
• Success rate 80-90%, but risk of ischaemia/stricture

[52]

Surgical Management

Indications (very rare, less than 1-2% of cases):

• Failure of endoscopic and angiographic haemostasis
• Torrential bleeding precluding endoscopic visualisation

• 6-8 units of blood transfused with ongoing bleeding

Surgical Options:

• Laparotomy and gastrotomy: Direct visualisation and oversewing of tear
• Oesophageal/gastric resection: Extremely rare, only if extensive injury

Mortality: Surgical intervention for MW tear is rare; when needed, mortality is 5-10% (reflects severity of underlying bleeding and comorbidities).

[53]

Specific Clinical Scenarios

Pregnancy (Hyperemesis Gravidarum):

• Multidisciplinary approach (obstetrics + gastroenterology)
• Fluid resuscitation crucial (risk of fetal compromise)
• Endoscopy safe in pregnancy if indicated
• PPIs category B (safe); avoid NSAIDs

Anticoagulated Patients:

• Reverse anticoagulation as above
• Higher rebleeding risk
• Endoscopic therapy often required

Chronic Liver Disease/Portal Hypertension:

• Difficult to distinguish MW tear from variceal bleeding pre-endoscopy
• May coexist (portal hypertensive gastropathy)
• Manage as per variceal protocol until OGD confirms MW tear

[18,22]

Post-Procedure Care

Admit for Observation:

• High-risk patients (GBS ≥6, endoscopic intervention, ongoing bleeding risk)
• Monitor vital signs 4-hourly
• Daily FBC to monitor haemoglobin

Continue PPI:

• IV infusion 8 mg/hour for 72 hours (if high-risk stigmata)
• Transition to oral PPI 40 mg BD for 4-8 weeks

Antiemetics:

• Regular antiemetics for 24-48 hours to prevent rebleeding
• Avoid triggers (oral intake initially NBM, then clear fluids → light diet)

Alcohol Withdrawal Prophylaxis (if indicated):

• CIWA-Ar scoring
• Chlordiazepoxide reducing regimen
• Thiamine supplementation (Pabrinex)

Discharge Planning:

• Low-risk patients (GBS 0-1, Forrest III lesion) may be discharged after 24 hours observation
• Arrange outpatient follow-up
• Lifestyle advice (avoid alcohol, NSAIDs)

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9. Complications

Immediate Complications

Late Complications

Mortality

Overall Mortality:

• Uncomplicated MW tear: less than 1%
• With significant comorbidity (liver disease, cardiac disease): 3-6%
• Requiring surgical intervention: 5-10%

Mortality is significantly lower than other causes of UGIB (peptic ulcer 5-10%, varices 15-20%), reflecting the self-limiting nature in most cases and younger patient demographic.

[10,11]

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10. Prognosis & Outcomes

Natural History

Spontaneous Haemostasis: The majority of Mallory-Weiss tears (80-90%) cease bleeding spontaneously without requiring therapeutic intervention. Bleeding typically stops within 6-24 hours of presentation due to:

• Vasoconstriction
• Platelet plug formation
• Fibrin clot stabilisation

Healing Timeline:

• Mucosal re-epithelialization: 48-72 hours
• Complete healing: 7-10 days
• Endoscopic appearance: Scar may be visible for 2-4 weeks

[5,8]

Factors Predicting Outcome

Good Prognosis:

• Young age (less than 50 years)
• No significant comorbidity
• Normal coagulation
• Forrest III lesion (clean base) at endoscopy
• GBS 0-2

Poor Prognosis:

• Advanced age (> 70 years)
• Coagulopathy, anticoagulation, thrombocytopenia
• Chronic liver disease (portal hypertension, coagulopathy)
• Active bleeding at endoscopy (Forrest Ia, Ib)
• GBS ≥12
• Comorbid cardiorespiratory disease

[43,54]

Recurrence

Recurrence Rate: less than 5% overall

Risk Factors for Recurrence:

• Persistent precipitating cause (ongoing vomiting, bulimia nervosa)
• Chronic alcohol misuse
• Large hiatus hernia (increased mechanical stress)

Prevention:

• Address underlying cause (alcohol cessation, treat hyperemesis, manage eating disorder)
• PPI therapy (4-8 weeks)
• Avoid NSAIDs

[13,55]

Long-Term Outcomes

Quality of Life: Excellent; most patients return to baseline health without long-term sequelae.

Long-Term Complications: Rare

• Oesophageal stricture (less than 1%): May require endoscopic dilatation
• Chronic anaemia: Only if recurrent bleeding

Follow-Up:

• Routine endoscopic follow-up not required for uncomplicated cases
• Repeat OGD only if recurrent symptoms, persistent anaemia, or alarm features (dysphagia, weight loss)

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11. Prevention & Screening

Primary Prevention

Alcohol Reduction:

• Single most effective preventive measure (addresses most common precipitant)
• Brief intervention in ED/acute setting
• Refer to alcohol services if dependence identified

Avoid Precipitants:

• Early antiemetic use in gastroenteritis, chemotherapy, pregnancy
• Treat underlying cause of vomiting promptly

Optimise Coagulation:

• Review anticoagulation/antiplatelet therapy
• Avoid NSAIDs in at-risk individuals

Secondary Prevention (After First Episode)

Lifestyle Modifications:

• Alcohol abstinence or significant reduction
• Avoid binge drinking
• Avoid NSAIDs, aspirin (if not essential)

Pharmacological:

• PPI therapy: 40 mg omeprazole OD for 4-8 weeks
• Treat reflux disease: Reduce mucosal inflammation at GOJ

Eating Disorders:

• Multidisciplinary management of bulimia nervosa
• Psychiatry, psychology, dietetics input

Screening

No population-based screening is indicated (condition is acute and unpredictable).

High-Risk Groups:

• Patients with recurrent vomiting (chemotherapy, eating disorders): Educate about risk, early presentation if haematemesis

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12. Evidence & Guidelines

Key Guidelines

1. NICE Guideline NG141: Acute Upper Gastrointestinal Bleeding in Over 16 s: Management (2016, updated 2020)

   • Risk stratification with GBS
   • Timing of endoscopy
   • Transfusion thresholds
   • PPI therapy recommendations [56]

2. British Society of Gastroenterology (BSG): Guidelines on the Management of Acute Upper Gastrointestinal Bleeding (2015)

   • Endoscopic management strategies
   • Combination therapy for high-risk lesions [57]

3. American College of Gastroenterology (ACG): Guidelines for Management of Patients with Ulcer Bleeding (2012)

   • Applicable principles for non-variceal UGIB including MW tears [58]

4. European Society of Gastrointestinal Endoscopy (ESGE): Non-Variceal Upper Gastrointestinal Hemorrhage Guidelines (2021)

   • Pre-endoscopic management
   • Endoscopic techniques
   • Post-procedure care [59]

Landmark Studies and Key Evidence

Epidemiology and Natural History:

• Kortas et al. (2001): Retrospective study of 105 MW tear patients; 84% stopped bleeding spontaneously, 16% required endoscopic therapy. Hiatus hernia present in 94%. [16]
• Knauer (1976): Classic case series describing presentation and outcomes; established less than 5% mortality. [10]

Endoscopic Management:

• Park et al. (2004): Endoscopic band ligation effective for MW tear with active bleeding; 92% primary haemostasis. [60]
• Laine & Peterson (1994): Meta-analysis showing combination endoscopic therapy superior to monotherapy for non-variceal UGIB. [51]

Risk Stratification:

• Blatchford et al. (2000): Development and validation of Glasgow-Blatchford Score; GBS=0 identified low-risk patients suitable for outpatient management (sensitivity 99%). [42]
• Rockall et al. (1996): Rockall score combining clinical and endoscopic variables predicts mortality and rebleeding in UGIB. [43]

Transfusion Strategy:

• Villanueva et al. (2013): NEJM randomized trial showing restrictive transfusion strategy (Hb target 70 g/L) superior to liberal strategy (90 g/L) in acute UGIB; lower mortality and rebleeding. [45]

PPI Therapy:

• Lau et al. (2007): High-dose IV PPI reduces rebleeding and need for surgery in peptic ulcer bleeding; extrapolated to all non-variceal UGIB. [47]
• Neumann et al. (2012): Cochrane review confirming PPI benefit in non-variceal UGIB. [48]

Boerhaave Syndrome Diagnosis:

• de Schipper et al. (2009): CT sensitivity 100% for Boerhaave diagnosis vs. 50% for CXR. [34]

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13. Common Exam Questions

Written Exam (SBA/MCQ)

Question 1: A 35-year-old man presents with haematemesis. He reports drinking 10 pints of lager last night, followed by vomiting 6-7 times. The first 5 episodes contained food and bile, but the last episode contained fresh blood. Observations: HR 95, BP 125/80, RR 16, SpO₂ 98% (air). What is the most likely diagnosis?

Answer: Mallory-Weiss tear (classic history: alcohol, repeated non-bloody vomiting → haematemesis)

Question 2: A patient with a suspected Mallory-Weiss tear has a Glasgow-Blatchford Score of 0. What is the most appropriate management?

Answer: Urgent outpatient endoscopy within 24 hours (GBS 0 = very low risk, safe for outpatient management)

Viva Voce Questions

Q1: "Tell me about Mallory-Weiss tears."

Model Answer: "A Mallory-Weiss tear is a longitudinal mucosal or submucosal laceration at the gastro-oesophageal junction, typically caused by a sudden increase in intra-abdominal pressure from forceful vomiting or retching. It accounts for 5-15% of acute upper GI bleeds and classically presents with haematemesis following repeated non-bloody vomiting, often in the context of alcohol intoxication. The tear is partial-thickness—involving only mucosa and submucosa—which distinguishes it from Boerhaave syndrome, a full-thickness oesophageal perforation. Around 80-90% of Mallory-Weiss tears cease bleeding spontaneously, with the remainder requiring endoscopic haemostasis using adrenaline injection, clips, or thermal coagulation. Prognosis is excellent with mortality below 1% in uncomplicated cases."

Q2: "How do you distinguish Mallory-Weiss tear from Boerhaave syndrome?"

Model Answer:

Q3: "What is your approach to managing a patient with a Mallory-Weiss tear and active bleeding at endoscopy?"

Model Answer: "Initial resuscitation following ABC principles: large-bore IV access, fluid resuscitation targeting systolic BP > 100 mmHg, correct any coagulopathy, and crossmatch blood. I would start high-dose IV PPI (omeprazole 80 mg bolus then 8 mg/hour infusion) and antiemetics to prevent rebleeding. At endoscopy, if active bleeding is present—Forrest Ia or Ib—I would perform combination endoscopic therapy: adrenaline 1:10,000 injection in four quadrants around the tear, followed by mechanical haemostasis with haemostatic clips to approximate the tear edges. This combination approach has superior efficacy compared to monotherapy. Post-procedure, I would admit for observation, continue IV PPI for 72 hours, monitor haemoglobin, and provide alcohol cessation advice. If endoscopic haemostasis fails, interventional radiology (angiographic embolisation) or rarely surgery would be considered."

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14. Clinical Pearls & Pitfalls

Clinical Pearls

✅ "Retching First, Blood Later": This temporal sequence is pathognomonic for Mallory-Weiss tear

✅ "Mallory-Weiss Bleeds, Boerhaave Perforates": Remember the depth difference (partial vs. full thickness)

✅ "90% Stop Spontaneously": Most cases self-resolve; avoid overtreatment

✅ "Think Hiatus Hernia": Present in up to 100% of cases; increases shear stress at GOJ

✅ "GBS 0 = Outpatient": Safe to discharge with urgent outpatient OGD if Glasgow-Blatchford Score is zero

✅ "Combination Endoscopic Therapy": Adrenaline + clips superior to adrenaline alone for high-risk stigmata

Common Pitfalls

❌ Missing Boerhaave Syndrome: Always assess for chest pain, surgical emphysema, and systemic toxicity

❌ Assuming Normal Hb = No Bleeding: Haemodilution takes hours; initial Hb reflects baseline, not acute loss

❌ Forgetting Antiemetics: Rebleeding from ongoing vomiting is preventable—use regular antiemetics

❌ Delaying Endoscopy in High-Risk Patients: GBS ≥12 or haemodynamic instability requires urgent (less than 2 hours) OGD

❌ Liberal Transfusion: Restrictive strategy (Hb target 70 g/L) reduces rebleeding and mortality

❌ Ignoring Alcohol Withdrawal: Chronic drinkers at risk of withdrawal seizures—prophylactic benzodiazepines

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15. Patient/Layperson Explanation

What is a Mallory-Weiss Tear?

A Mallory-Weiss tear is a small split in the lining of the food pipe (oesophagus) where it joins the stomach. It happens when you vomit or retch very forcefully, which puts a lot of pressure on this area and causes the lining to tear slightly. Think of it like overstretching a piece of fabric until it splits.

What Causes It?

The most common cause is drinking too much alcohol, which makes you vomit repeatedly and violently. Other causes include:

• Severe vomiting from food poisoning or stomach bugs
• Very bad morning sickness in pregnancy
• Violent coughing

What Are the Symptoms?

The typical pattern is:

1. You vomit several times (without blood)
2. Then you notice blood in your vomit (bright red or like coffee grounds)
3. You might have mild tummy pain

Is It Serious?

Usually not. About 9 out of 10 people with a Mallory-Weiss tear stop bleeding on their own without needing any treatment other than fluids and medications to stop vomiting.

However, seek urgent medical help if you:

• Vomit a large amount of blood
• Feel dizzy, faint, or very unwell
• Have severe chest pain (this could be a different, more serious problem)

How Is It Diagnosed?

You'll have a camera test (endoscopy) where a doctor passes a thin, flexible tube with a camera down your throat to look at the tear. This is usually done while you're sedated so you don't feel it.

What Is the Treatment?

For most people:

• Fluids through a drip in your arm
• Medications to stop vomiting
• Medications to reduce stomach acid
• Observation in hospital for 24 hours

If the bleeding doesn't stop:

• The doctor can use the camera to inject medication or apply small clips to stop the bleeding
• This is successful in over 90% of cases

How Long Does Recovery Take?

The tear usually heals within 2-3 days. You'll be advised to:

• Avoid alcohol
• Avoid aspirin and anti-inflammatory painkillers (like ibuprofen) for a few weeks
• Take stomach acid tablets for 4-8 weeks

Can It Happen Again?

It's uncommon to get another tear unless you continue vomiting frequently. If you have an alcohol problem or eating disorder, getting help for these conditions will prevent it happening again.

What's the Difference from Boerhaave Syndrome?

This is a more serious condition where the tear goes all the way through the wall of the food pipe, rather than just the lining. It causes severe chest pain and requires surgery. Mallory-Weiss tear is much less serious and rarely needs surgery.

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