Mallory-Weiss tear (MWT), also known as Mallory-Weiss syndrome (MWS), is characterised by a tear or laceration in the distal oesophagus and proximal stomach, which are usually associated with forceful reaching. The incidence of Mallory-Weiss tear among patients presenting with upper gastrointestinal bleeding ranges from 3 to 15%. The patient presents with haematemesis, which is usually self-limiting, ceasing spontaneously in 80% to 90% of patients.


  • Incidence: 8.00 cases per 100,000 person-years
  • Peak incidence: 50-60 years
  • Sex ratio: 1:1
Condition Relative
Gastro-oesophageal reflux disease625.00
Mallory-Weiss tear1
Perforated peptic ulcer0.88
<1 1-5 6+ 16+ 30+ 40+ 50+ 60+ 70+ 80+


The pathogenesis of Mallory-Weiss tear is not completely understood. It has been proposed that mucosal lacerations develop secondary to a sudden increase in oesophageal intraluminal pressure which results in tearing of the underlying submucous venous or arterial plexus.

Predisposing conditions
  • Alcoholism
    • 40% to 80% of the patients diagnosed with MWT have a history of heavy alcohol use.
  • Hiatal hernia
    • Present in 40% to 100% of people with MWT, retching increases the potential for mucosal laceration by creating a higher pressure gradient, in these patients. However, in >40% of patients, an identifiable risk factor is not found
  • Other risk factors include bulimia nervosa, hyperemesis gravidarum, and gastroesophageal reflux disease (GERD)
Precipitating factors
  • Severe vomiting
  • Coughing
  • Blunt abdominal trauma
  • Strained defecation
  • Oesophageal instrumentation

Clinical features

Patients with Mallory-Weiss tear mostly present with acute onset of gastrointestinal bleeding with
  • Haematemesis (85%)
    • consists of a small and self-limited episode, which varies from flecks or streaks of blood mixed with gastric contents and/or mucus, blackish or 'coffee ground', to bright-red bloody emesis after a bout of retching, vomiting, coughing, straining.

Other less common symptoms include
  • Postural/orthostatic hypotension
    • Light-headedness/dizziness due to a sudden drop in blood pressure caused by bleeding.
  • Melaena
    • Usually associated with upper gastrointestinal bleeding proximal to the ligament of Treitz.
  • Dysphagia
  • Haematochezia
  • Abdominal pain
  • Signs of anaemia
    • Rare in acute Mallory Weiss tear. Low haemoglobin at presentation may be indicative of co-existing comorbidities. Signs of anaemia include pallor, tachycardia, dyspnoea, and fatigue.

There are no specific physical signs to Mallory-Weiss tear, and the signs are similar to any other hemorrhagic conditions or shock.


Mallory-Weiss syndrome should be suspected in patients with upper gastrointestinal bleeding and a history of vomiting or retching.

Initial laboratory investigation
  • FBC, including haematocrit to assess the severity of the initial bleeding episode and to monitor patients.
    • Usually normal in an acute setting; however, anaemia may range from mild to severe in rare cases
  • Coagulation studies and platelet counts to detect coagulopathies and thrombocytopenias (routine platelet count, prothrombin time, and activated partial thromboplastin time).
    • Typically normal
  • Liver function test to rule out liver disease
    • Typically normal, except in a patient with underlying or co-existing liver disease
  • Renal function, urea, creatinine, and electrolyte levels (to guide intravenous fluid therapy).
    • Urea may be high in a patient with ongoing bleeding
  • Cross-matching/ blood grouping and antibody screen (potential blood transfusion)
Other tests to consider
  • ECG, troponin, creatinine kinase (should be considered in patients with a history of CAD, symptoms of cardiac ischaemia, massive bleeding, or multiple comorbidities)

Diagnosis of aetiology:
  • Upper endoscopy: It should be performed in all patients after stabilisation. It is the test of choice for diagnosis and treatment and should be done within 24 hours.
    • Finding include single and longitudinal tear that typically appears as a red longitudinal break in the mucosa.

Differential diagnosis

Mallory-Weiss tear should be differentiated from other causes of upper GI bleeding.

Possible differential diagnoses:
  • Reflux esophagitis:
    • Similarities: presents with coffee-ground emesis and anorexia. Typical symptoms of an oesophageal disease like odynophagia, dysphagia, retrosternal chest pain, and heartburn may be present
    • Differences: ulcerations seen in reflux esophagitis are usually irregularly shaped and multiple, located in the distal oesophagus. In Mallory-Weiss syndrome there is a single and longitudinal tear.
  • Boerhaave's syndrome:
    • Similarities: Classic presentation is an episode of retching or vomiting followed by severe retrosternal pain and/or epigastric pain
    • Differences: the symptom may progress rapidly and other common symptoms may include subcutaneous emphysema, cyanosis, sepsis and shock, water-soluble contrast is helpful to localise the lesion.
  • Oesophagitis:
    • Similarities: occur concurrently with MWT and typical symptoms include odynophagia, dysphagia, retrosternal chest pain, and heartburn, together with 'coffee ground' emesis
    • Differences: a history of oesophageal reflux, recent intake of medications ( corticosteroid, tetracycline, doxycycline, ferrous sulfate. On endoscopy, mucosa irritation/inflammation, brushing is seen.
  • Peptic ulcer disease:
    • Similarities: patients may present with upper gastrointestinal (GI) bleeding or melaena, without other symptoms.
    • Differences: however, most patients describe a history of gnawing, burning, or hunger-like abdominal pain 40 to 60 minutes after eating. On endoscopy, an ulcer is seen.


Since Mallory-Weiss tear is mostly self-limited and recurrence is uncommon, the initial management is focussed on stabilising the general condition of the patient, and a conservative approach would be appropriate in most of the patients.

Immediate resuscitation of patients with active bleeding should be started at the time of admission. We assess hemodynamic stability by checking the airway, breathing, and circulation (ABC protocol).
  • Establishment of a good central or peripheral intravenous (IV) access (usually 2 lines) along with fluid replacement.
  • Packed RBCs infusion is indicated if the Hb <8 gm/dl or if the patient presents with signs of shock or severe bleeding.
  • Nasogastric decompression using NG tube could be performed, especially in patients with ongoing bleeding or those suspected of having concomitant upper gastrointestinal (GI) bleeding sources.
  • Electrolyte imbalance, if present, should be corrected appropriately.
  • Coagulation factors need to be optimised before proceeding with endoscopy.

Most patients managed conservatively are typically hospitalised until hemostasis is achieved and symptoms are resolved.

Pharmacological treatment
  • Anti-secretory therapy: PPIs or H2 antagonists are first-line therapy, given to all patients who are waiting for endoscopy and have clinically significant upper gastrointestinal bleeding. It promotes hemostasis by neutralising gastric acid and stabilising blood clots
  • Anti-emetics: considered in a patient with nausea and vomiting, which may be a cause or an aggravating factor in patients with MWT.
  • Somatostatin and its long-acting synthetic analogue octreotide: not routinely recommended for patients with non-variceal upper GI bleeding; however, they may be considered as an adjunct treatment to PPIs and endoscopy until more definitive diagnostic tests and therapeutic procedures are implemented

Once the patient is stabilised, several risk assessment and scoring systems (like Glasgow-Blatchford bleeding score and clinical Rockall score) for active bleeding should be used to stratify patients as low or high risk. Patients are classified according to who should have an endoscopic evaluation, who may be discharged with minimal risk of complications, and who should be admitted to hospital for further observation.

Endoscopic treatment: oesophagogastroscopy is the investigation of choice in all cases of upper GI bleeding. It is indicated after medical treatment is given in case of actively bleeding (spurting or oozing haemorrhage) MWT. Different modalities of treatment include the following:
  • Endoscopic band ligation (with or without epinephrine injection)
  • Haemoclip placement is an effective method to control actively bleeding lesions.
  • Thermocoagulation therapy

  • Surgery, which in practice is very rarely warranted in patients with MWT, It is usually reserved for situations where endoscopic haemostasis of bleeding has failed or transmural oesophageal perforation has occurred

Patients without risk factors for rebleeding, evidence of severe upper gastrointestinal bleeding, or endoscopic stigmata of recent bleeding can be discharged from the hospital on oral antisecretory therapy.


It may be related to the degree of blood loss or following treatment.

Severity of bleeding
  • Hypovolemic shock
    • Usually related to acuity and severity of bleeding; rare if early stabilised and treated promptly
  • Re-bleeding
    • Occurs within the first 24 hours and most often in patients with risk factors
  • Myocardial ischaemia or infarction
    • Usually related to the acuity, severity of bleeding, and associated CAD.
Following treatment or investigations
  • Oesophageal perforation
    • May present as rapidly developing mediastinitis and sepsis.
  • Vasopressin infusion-related abdominal pain
    • Abdominal pain lasting 10 to 15 minutes after vasopressor use


For most patients without any associated disease, the prognosis is generally excellent. The tear heals rapidly, usually within 48-72 hours. Bleeding is self-limited and will have stopped by the time of endoscopy.

  • The mortality rate is approximately 5% and depends upon patient age and the presence of coexisting medical conditions.
  • Risk of re-bleeding occurs in about 8% to 15% of patients.
    • It usually occurs within the first 24 hours and most often in patients with high-risk factors like old age, haematemesis and/or hematochezia at presentation, alcoholism and other comorbid illness (anaemia, chronic liver disease, coronary artery disease, chronic obstructive pulmonary disease).