Mallory-Weiss Tear: Diagnosis and Management

Introduction

A Mallory-Weiss tear is a longitudinal laceration of the mucosa and submucosa at or just below the gastro-oesophageal junction, classically produced by a sudden, forceful rise in intra-abdominal and intraluminal pressure during vomiting or retching.¹

It accounts for around 5-10% of cases of upper gastrointestinal bleeding, making it one of the more common causes after peptic ulcer disease.² It is important to recognise because, unlike most other causes of upper GI bleeding, it is usually self-limiting and carries an excellent prognosis.

Pathophysiology

During vomiting, a sudden and marked increase in intra-abdominal pressure is transmitted to the stomach and distal oesophagus. If the gastro-oesophageal junction does not relax in a coordinated way, the resulting pressure gradient across the junction shears the mucosa, producing a longitudinal tear.¹

The tear typically extends through the mucosa and submucosa, exposing the underlying submucosal arteries and veins, which is the source of the bleeding. Crucially, it does not extend through the muscular layer, which is what distinguishes it from Boerhaave syndrome (a full-thickness rupture). The presence of a hiatus hernia increases the pressure gradient across the junction and is a recognised predisposing factor.

Risk factors and precipitants

Anything causing repeated, forceful vomiting or retching can precipitate a tear:²

• Alcohol excess, particularly binge drinking - the classic association
• Hyperemesis gravidarum and severe pregnancy-related vomiting
• Infectious gastroenteritis with protracted vomiting
• Bulimia nervosa and self-induced vomiting
• Severe or paroxysmal coughing
• Chemotherapy-induced or postoperative vomiting
• Cardiopulmonary resuscitation and blunt abdominal trauma (rare)

Predisposing factors that increase the likelihood or severity of bleeding include hiatus hernia, older age, chronic liver disease with portal hypertension, coagulopathy, and anticoagulant or antiplatelet therapy.

Clinical features

The classic history is of haematemesis following an episode of forceful vomiting or retching, where the initial vomit contains no blood and subsequent vomits do. This sequence is highly characteristic and is the single most useful diagnostic clue in the history.

Other features include:

• Haematemesis, which may be fresh red blood, streaks of blood, or coffee-ground vomit
• Melaena, if enough blood has passed distally
• Epigastric or retrosternal pain, though this is usually mild
• Light-headedness, syncope or signs of hypovolaemia if bleeding is significant
• Features of the precipitating cause: alcohol intoxication, pregnancy, or gastroenteritis

Most patients are haemodynamically stable at presentation. Significant haemodynamic compromise is uncommon and should prompt consideration of an alternative or additional diagnosis.

Differential diagnosis

The key differentials are the other causes of upper GI bleeding, and in particular Boerhaave syndrome:

Other differentials include peptic ulcer disease, oesophageal varices (particularly relevant in patients with alcohol excess, who may have both), oesophagitis, gastritis and malignancy.³

Investigations

Initial investigations are those for any upper GI bleed: full blood count, urea and electrolytes, liver function tests, clotting screen, and group and save or crossmatch. A Glasgow-Blatchford score is calculated to guide the urgency of endoscopy and whether the patient can be managed as an outpatient; many patients with a Mallory-Weiss tear score low.³

Endoscopy

Upper GI endoscopy is the diagnostic investigation and confirms the diagnosis by direct visualisation. The tear appears as a single (occasionally multiple) longitudinal mucosal laceration at the gastro-oesophageal junction, often best seen on retroflexion of the endoscope in the gastric cardia.

Endoscopy also allows exclusion of coexisting pathology, which matters particularly in patients with alcohol-related liver disease, in whom varices may be present alongside the tear. If Boerhaave syndrome is suspected clinically, CT with oral contrast is performed instead of proceeding directly to endoscopy.

Management

Management follows the general principles of upper GI bleeding, but the great majority of tears require no specific intervention.

Supportive management

Around 90% of Mallory-Weiss tears stop bleeding spontaneously and heal within 48-72 hours.¹ Treatment therefore consists of IV access, fluid resuscitation and transfusion if required, correction of coagulopathy, and antiemetics to break the cycle of ongoing vomiting. Acid suppression with a PPI is commonly given to aid mucosal healing, although the evidence for this is limited.

Endoscopic therapy

Endoscopic haemostasis is indicated where there is active bleeding or a visible vessel at endoscopy. Options include adrenaline injection, mechanical clips, band ligation and thermal coagulation, often used in combination. Clipping and band ligation are generally preferred over thermal methods, given the relatively thin wall at this site.

Further measures

Angiographic embolisation of the left gastric artery is an option for the rare case of ongoing bleeding despite endoscopic therapy, with surgical oversewing of the tear a last resort. Addressing the underlying precipitant is an important part of care: alcohol advice and support, treatment of hyperemesis, or eating disorder services for patients with bulimia nervosa.

Complications

• Significant haemorrhage requiring transfusion, more likely in patients with portal hypertension or coagulopathy
• Rebleeding, which occurs in a small minority, typically within the first 24 hours
• Hypovolaemic shock and its sequelae in severe cases
• Aspiration pneumonia from vomiting, particularly in intoxicated or obtunded patients
• Progression to full-thickness perforation is very rare, but any patient with severe pain, sepsis or surgical emphysema should be reassessed for Boerhaave syndrome

Red flags

Prognosis

The prognosis is excellent. The great majority of tears stop bleeding without intervention and heal completely within a few days, leaving no long-term sequelae, and recurrence is uncommon provided the precipitating cause is addressed.² Mortality is low and, where it occurs, usually reflects comorbidity or coexisting pathology such as portal hypertension rather than the tear itself. Outcomes are worse in patients who are anticoagulated, have chronic liver disease, or present with haemodynamic compromise.