Mallory-Weiss Syndrome

Detailed Overview

Accountable for roughly 5-15% of all non-variceal upper GI bleeds. The classic presentation involves a patient experiencing repeated bouts of non-bloody vomiting or retching, abruptly followed by hematemesis. It is strongly associated with alcohol binge drinking, bulimia nervosa, or gastroenteritis. Unlike Boerhaave syndrome (a full-thickness esophageal rupture), Mallory-Weiss tears are incomplete tears and generally carry a much lower mortality rate. Most tears heal spontaneously within 48 to 72 hours with supportive care and acid suppression, though endoscopic intervention is occasionally required for active bleeding.

Epidemiology & Demographics

Primarily affects adults, particularly males aged 40-60. Highly prevalent among heavy alcohol users. Accounts for 5-15% of acute upper GI bleeds.

Etiological Mechanism

A sudden, massive increase in intra-gastric pressure transmitted to the esophagus during violent retching/vomiting against a closed glottis.

Primary Causes

Forceful vomiting/retching (emesis) from alcohol intoxication, cyclic vomiting syndrome, eating disorders, or hyperemesis gravidarum.

• Alcohol Abuse: Frequent binge drinking leads to severe gastritis and subsequent retching.
• Hiatal Hernia: Found in a high percentage of patients; structural weakness predisposes mucosa to tearing.
• Eating Disorders: Bulimia nervosa involving self-induced vomiting.
• Chronic Cough: Severe coughing fits can elevate intra-abdominal pressure enough to cause a tear.

During a severe emetic episode, there is a sudden, rapid, and uncoordinated increase in intra-abdominal and intra-gastric pressures. This pressure overcomes the tone of the lower esophageal sphincter. The stomach contents violently hit the relatively narrow gastroesophageal junction. The stress causes a longitudinal tear in the mucosa and submucosa, usually on the gastric side of the squamocolumnar junction. The submucosal arterial plexus is disrupted, resulting in arterial bleeding (hematemesis). Because the muscularis layer remains intact, perforation into the mediastinum does not occur.

Characteristic Clinical Presentation

• Hematemesis: Vomiting bright red blood or "coffee-ground" material.
• Antecedent Retching: History of severe non-bloody vomiting prior to the onset of hematemesis.
• Epigastric Pain: Mild to moderate central abdominal/chest pain.
• Melena: Dark, tarry stools may appear 24-48 hours later as swallowed blood traverses the GI tract.

Physical Examination Signs

• Tachycardia and hypotension (if significant blood loss has occurred).
• Normal abdominal exam (no peritoneal signs, differentiating it from Boerhaave syndrome).
• Pallor and diaphoresis in acute shock.

• Hemorrhagic Shock: Massive blood loss leading to hypoperfusion, end-organ damage, and potential death.
• Aspiration: Inhalation of blood or vomitus into the lungs causing aspiration pneumonitis.

Diagnostic Criteria & Guidelines

Diagnosis is established by direct visualization of single or multiple linear, reddish mucosal lacerations at or near the gastroesophageal junction via Esophagogastroduodenoscopy (EGD).

Differential Diagnosis

• Bleeding Esophageal Varices
• Peptic Ulcer Disease (PUD)
• Boerhaave Syndrome (full thickness rupture, surgical emergency)
• Dieulafoy Lesion

Laboratory Tests & Biomarkers

• Complete Blood Count (CBC): Initial hemoglobin may be normal; drops after fluids are given. Hematocrit defines severity of blood loss.
• BUN/Creatinine Ratio: Elevated (>30:1) due to digestion and absorption of blood urea in the GI tract.
• Coagulation Profile (PT/INR): Assessed especially in cirrhotics to correct coagulopathy.

Imaging Modalities & Findings

• EGD (Endoscopy):
• Chest X-Ray:

• Self-limiting
  Bleeding stops spontaneously; vital signs are stable.
• Active Bleeding
  Continuous hematemesis requiring transfusion and urgent endoscopic intervention.

Second-Line & Adjunctive Therapy

Urgent Endoscopy (within 24 hours) for active bleeding. Endoscopic hemostasis achieved via multipolar electrocoagulation, epinephrine injection, or placement of endoscopic clips (hemoclips).

Surgical & Procedural Management

Rarely needed. Open gastrotomy with surgical over-sewing of the tear or angiographic embolization of the left gastric artery is reserved for massive, refractory bleeding failing endoscopy.

Recommended Lifestyle Changes

• Cessation of alcohol consumption.
• Treatment of underlying eating disorders or hyperemesis.
• Eat smaller meals to prevent gastric over-distension if hiatal hernia is present.

Patient Counseling & Advice

Reassure that the tear heals rapidly on its own, but emphasize the necessity of avoiding alcohol and controlling vomiting to prevent recurrence. Warn that the stool will be black for a few days due to digested blood.

Follow-Up & Monitoring Schedule

Transition to oral PPI (e.g., Omeprazole 40 mg daily) for 2-4 weeks. Follow-up CBC to ensure stable hemoglobin.

Preventive Strategies

Aggressive early use of antiemetics in patients with gastroenteritis or chemotherapy. Alcohol use disorder treatment.

Excellent. Recurrence rate is low (<10%), and most heal within 48 hours. Mortality is heavily linked to underlying comorbidities rather than the tear itself.