Mallory–Weiss syndrome
Mallory–Weiss syndrome (MWS) is a condition characterised by non-transmural, longitudinal mucosal lacerations (Mallory–Weiss tears) at the gastroesophageal junction, frequently following forceful retching, vomiting, or other causes of abrupt increases in intra-abdominal pressure. These tears are typically confined to the mucosa and submucosa, distinguishing them from full-thickness oesophageal rupture (Boerhaave syndrome).
Patients often present with:
- Haematemesis (bright red or coffee-ground emesis) – in ~85% of cases
- Melena, dizziness, or syncope in cases of significant blood loss
- Preceding retching or vomiting due to alcohol, gastrointestinal illness, or other triggers
- Occasionally epigastric or retrosternal pain; symptoms of shock in severe cases
Notably, up to 25% of patients have no identifiable risk factor or prodromal vomiting.
The syndrome results from sudden rise in intra-abdominal pressure transmitted across the gastroesophageal junction, leading to mucosal shear injury. This is often due to:
- Repetitive forceful vomiting or retching
- Coughing, convulsions, or straining
- CPR or endoscopic instrumentation (iatrogenic)
Tears typically occur along the gastric side of the lesser curvature or distal oesophagus, where mechanical tension and anatomic fixation converge. These are usually 2–4 cm in length.
Aetiology and Risk Factors
- Alcohol excess: present in 50–70% of cases
- Hyperemesis gravidarum, bulimia nervosa
- Hiatal hernia (variable association)
- GERD
- NSAID use, anticoagulation, cirrhosis with portal hypertension
- Endoscopy, TEE, or other transoesophageal procedures (iatrogenic)
- CPR-associated gastric insufflation and pressure injury
While historically tied to alcoholism, MWS is now recognised across a broad clinical spectrum, including teetotalers, young pregnant women, and post-operative patients.
Investigation
Initial evaluation focuses on stabilisation and risk stratification in suspected UGIB:
- Vital signs, orthostatic hypotension, signs of shock
- CBC: haemoglobin/hematocrit
- Renal function: BUN/Cr (upper GI bleeding may elevate BUN)
- Coagulation profile
- ECG and troponin if syncope or cardiac risk
Definitive diagnosis: Upper endoscopy (EGD): diagnostic and often therapeutic
- Single or multiple linear mucosal lacerations
- Active bleeding, adherent clot, or stigmata of recent haemorrhage
Differential Diagnosis
- Boerhaave syndrome – transmural oesophageal rupture; severe chest pain, mediastinal air, sepsis
- Oesophageal varices – cirrhotic patients; requires urgent banding or sclerotherapy
- Peptic ulcer disease
- Gastric or oesophageal malignancy
- AVMs or Dieulafoy lesion
Management
The majority of Mallory–Weiss tears (up to 90%) are self-limited and resolve without intervention.
Pharmacologic:
- IV PPIs (e.g., pantoprazole) to reduce gastric acid and stabilise clots
- Antiemetics to prevent further retching (e.g., ondansetron)
- Correct coagulopathy if present
Endoscopic therapy (for active bleeding or high-risk lesions):
- Epinephrine injection
- Thermal coagulation (MPEC, bipolar probe)
- Haemoclip application
- Band ligation in some settings
History of the Mallory–Weiss tear
1833 – Johann Friedrich Hermann Albers (1802–1865) published Über stechende Geschwüre der Speiseröhre und der Atemwege (“On perforating ulcers of the oesophagus and the airways”) He described penetrating oesophageal ulcers, often complicated by fistulae into the trachea and bronchi, identified at postmortem. Though distinct from Mallory–Weiss lacerations, this was the first systematic account of oesophageal ulcer disease.
..schrecklich endende Oesophagitis veranlasst, den Weg dieser Bildung nehmen und eine Öffnung zwischen Schlund und Luftröhre veranlassen…(“…a terribly ending oesophagitis takes this course, leading to an opening between the oesophagus and trachea…”)
Albers 1833
1879 – Heinrich Quincke (1842–1922) reported three cases of oesophageal bleeding due to ulceration, two of which were fatal.
Quincke, then in Kiel, published Ulcus oesophagi ex digestione. He described three cases of oesophageal ulceration in the distal oesophagus, unrelated to carcinoma, corrosives, or trauma. Two patients died of massive haematemesis, one developed perforation into the pleura, and another had cicatricial stricture.
Quincke proposed the term “ulcus ex digestione” to describe an ulcer caused by the action of gastric juice upon the oesophageal mucosa, analogous to simple gastric ulcer. This was an early demonstration of oesophageal ulcer as a primary lesion and the first to connect it to fatal haematemesis.
Die beschriebenen drei Fälle zeigen… dass im unteren Theil der Speiseröhre Geschwüre vorkommen… die durch die verdauende Einwirkung des Magensaftes entstanden sind… und daher mit dem sogenannten einfachen Magengeschwür auf eine Linie gestellt werden müssen – Quincke 1879
The three cases described show… that ulcers do occur in the lower part of the oesophagus… arising from the digestive action of gastric juice… and must therefore be placed on the same line as the so-called simple gastric ulcer – Quincke 1879
1898 – Georges Dieulafoy (1839–1911)
Described two fatal haematemesis cases due to similar lesions.
1929 – Mallory and Weiss (George Kenneth Mallory & Soma Weiss)
Published their landmark report in American Journal of the Medical Sciences, describing 15 cases of “hemorrhages from lacerations of the cardiac orifice of the stomach due to vomiting” with histopathological confirmation of mucosal tears extending into the muscularis layer.
“Massive gastric hemorrhage with haematemesis due to 2–4 fissure-like lesions… characteristic around the circumference of the cardia” – Mallory & Weiss, 1929
1932 – Mallory & Weiss
Reported an additional six cases and clarified the link to vomiting-induced mucosal trauma.
1952 – Palmer
Suggested that the condition should be diagnosable clinically and visualised via endoscopy—years before it became practice.
1953 – Decker, Zamcheck, and Mallory
Reviewed 11 cases with postmortem analysis, expanding clinical understanding and raising questions about non-alcohol-related cases.
1955 – E. Gale Whiting
Performed the first successful surgical treatment of Mallory–Weiss tear.
1956 – Hardy
Performed the first endoscopic diagnosis of MWS, cementing the diagnostic utility of endoscopy.
1960s–1970s – Prevalence confirmed
Various studies (e.g., Holmes 1966; Miller 1970) documented incidence rates of 3–5% in upper GI bleeds, recognising the syndrome’s clinical significance.
Modern era (post-1980s)
Endoscopic haemostasis established as first-line treatment. Studies clarified risk factors, epidemiology, and spontaneous healing rates.
Associated Persons
- George Kenneth Mallory (1900–1968) – American pathologist; co-described the syndrome.
- Soma Weiss (1899–1942) – Hungarian-born American physician; co-described the syndrome.
- Heinrich Irenaeus Quincke (1842–1922) – Earlier documented oesophageal ulcer cases.
- E. Gale Whiting (dates unknown) – First successful surgery for MWS.
- John Decker (dates unknown) – Published pivotal autopsy-based series in 1953.
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References
Historical references
- Albers JFH. Über stechende Geschwüre der Speiseröhre und der Atemwege. Journal der Chirurgie und Augenheilkunde 1833; 19: 1-9
- Quincke H. Ulcus oesophagi ex digestione. Deutsches Archiv für klinische Medicin. 1879; 24: 72-79.
- Dieulafoy G. Exulceratio simplex. L’intervention chirurgicale dans les hématémèses foudroyantes consécutives à l’exulcération simple de l’estomac. Bulletin de l’Académie nationale de médecine 1898; 39: 49-84.
- Dieulafoy G. Exulceratio simplex. Clinique médicale de l’Hôtel-Dieu de Paris, 1898: II.
- Carr JC. The Mallory-Weiss Syndrome. Clin Radiol. 1973 Jan;24(1):107-12
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