Mallory-Weiss tear and oesophageal perforation

• A Mallory-Weiss tear is a superficial, longitudinal laceration at the gastro-oesophageal junction or cardia, produced by sudden rises in intra-abdominal pressure during vomiting, retching, coughing or straining. It is a common cause of non-variceal upper gastrointestinal bleeding and most often stops bleeding on its own.
• Boerhaave syndrome is the opposite problem: a full-thickness rupture of the distal oesophagus, usually at the left wall, with spillage into the mediastinum. It is uncommon but life-threatening, because septic mediastinitis develops within hours.
• The same trigger (forceful vomiting) can produce either lesion; the difference is the depth of the wall injury, and that depth decides everything - harmless bleeding versus mediastinal sepsis and a mortality of 20 to 90 percent in published series.
• In suspected Mallory-Weiss bleeding the first step is resuscitation plus urgent upper endoscopy; endoscopic haemostasis is reserved for active bleeding or worrying stigmata. ^[1]
• In suspected full-thickness rupture the steps are early CT (often with oral contrast) plus a water-soluble contrast swallow, then prompt antibiotics, drainage and closure - endoscopic or surgical - with better results when treatment begins within 24 hours.

By the end of this page you should be able to:

1. Explain how vomiting produces a Mallory-Weiss tear, and how a Boerhaave rupture differs in depth, site and consequence.
2. Recognise both conditions from the history and examination, including why the classic Mackler triad is often absent.
3. Choose and interpret the right investigations: upper endoscopy, chest radiograph, CT with oral contrast, water-soluble contrast swallow.
4. Manage upper gastrointestinal bleeding from a Mallory-Weiss tear: resuscitation, risk scores, endoscopic haemostasis and escalation.
5. Manage an oesophageal perforation: supportive care in intensive care, antibiotics, nutrition, endoscopic closure or surgery, and the criteria for non-operative management.
6. Explain the relationship between delay in treatment and survival, with the times commonly quoted.

Mallory and Weiss described the lesion in 1929 in patients who had retched and vomited after an alcoholic binge. ^[1] The original paper noted that the tear runs longitudinally and bleeds from submucosal vessels, which is why the bleeding can be impressive even though the wall stays intact. ^[1]

Mallory-Weiss tear and Boerhaave syndrome are two points on a spectrum of pressure injury of the same region, and an overlap (both lesions in one patient) has been reported. ^[7] The deciding question is always: has the breach crossed the muscle into the mediastinum?

Oesophageal perforation itself is only the end state. It can be produced in several ways, and it helps to group the causes:

• Spontaneous (Boerhaave syndrome): barotrauma from raised pressure, about 15 percent of oesophageal perforations in the WSES surgical series, and 8 to 56 percent in reviews. ^{[8] [7]}
• Iatrogenic: endoscopy, dilatation, intubation, or thoracic surgery; the commonest single cause overall, at roughly 52 to 60 percent. ^[7]
• Trauma: penetrating or blunt injury, including the rare effort rupture from heavy lifting, defecation or childbirth. ^[7]
• Foreign body or tumour: sharp or impacted bodies, caustic ingestion, and (rarely) erosion by adjacent disease.

How often each occurs depends on setting. Mallory-Weiss tearing is common among the causes of upper bleeding: it accounts for 3 to 10 percent of cases in one clinical review, ^[3] 5 to 15 percent in another, ^[1] and 3.4 percent (125 of 3648 patients) in a recent international multicentre cohort. ^[2] Peptic ulcer bleeding is more common, but Mallory-Weiss bleeding fills a large minority of the remainder.

In the multicentre cohort the patients with Mallory-Weiss tears were younger than those with peptic ulcer bleeding (mean 61 versus 69 years) and more often men (66 versus 53 percent). ^[2] Rebleeding was lower (4.9 versus 12 percent), but 30-day mortality was similar (5.7 versus 7.0 percent), which is a useful caution against assuming that Mallory-Weiss bleeding is always trivial. ^[2]

Boerhaave syndrome is rare. Reported incidence is about 3 cases per million people per year, predominantly in middle-aged men with a history of heavy eating and alcohol. ^[7] The male-to-female ratio ranges from 2 to 1 up to 5 to 1. ^[7] It has been reported from newborns to patients over 90, but is least common in children aged 1 to 17 years. ^[7] Iatrogenic injury remains the commonest cause of oesophageal perforation overall. ^[7]

Perforation outcomes remain serious. Mortality is reported from about 20 to 90 percent depending on series and time to treatment. ^[7] Diagnosis and effective treatment within the first 24 hours are consistently associated with far better survival (see Prognosis).

Everything about this lesion follows from a single mechanism: a sudden rise in pressure inside the stomach against a closed or tightening gastro-oesophageal junction. Retching and vomiting are the classic setting, but any paroxysmal increase in intra-abdominal pressure can do it: violent coughing, hiccup spells, seizure, heavy lifting, defecation straining, asthma attacks, and the Valsalva-like effort of pushing in labour. ^[1]

Risk factors can be divided into those that increase vomiting and those that worsen the mucosa:

• Alcohol excess was the setting of the original report and remains the commonest association in clinical practice. ^[1]
• Chronic vomiting for any reason (eating disorders, gastroparesis, obstruction) opens the door.
• Helicobacter pylori and chronic peptic disease can weaken the mucosa.
• Non-steroidal anti-inflammatory drugs and anticoagulants do not create the tear but convert it into bleeding and heavier bleeding.
• Portal hypertension and cirrhosis make Mallory-Weiss bleeding more severe. ^[1]
• Iatrogenic tearing during endoscopy itself is well described: retching with the scope in place is the usual trigger. ^[1]

The tear itself is usually on the gastric side of the junction and runs longitudinally; a purely oesophageal site is uncommon. ^[3]

The pressure mechanism is similar but the physics differs. During vomiting the gastric pressure rises while the upper sphincter fails to open normally; pressure is transmitted to the oesophagus, which is a closed tube at that moment. A rapid rise of this kind, in one cadaver model requiring about 150 mmHg in the mid-oesophagus, is enough to burst the weakest part of the wall, usually the left side of the distal oesophagus; live patients are thought to generate up to 200 mmHg or more. ^[7]

A vulnerable profile can often be identified: men in the sixth and seventh decades, obese, gourmands, and consumers of fermented alcohol (beer, cider, wine) whose vomiting after a heavy meal is the classic setting. ^[7] Specific precipitants include diabetic ketoacidosis with vomiting, renal colic with vomiting, and straining at stool. ^[7] Boerhaave syndrome has also been described in pre-existing disease of the oesophageal wall, such as eosinophilic oesophagitis, Barrett oesophagus, Barrett-related ulceration, or drug-induced oesophagitis. ^[7]

Recurrent spontaneous rupture is very rare. ^[7]

The pressure-wave theory is the standard explanation. A strong contraction of abdominal muscles and diaphragm against a closed upper sphincter produces a sudden pressure step; the mucosa tears where the wall is thinnest and the pressure gradient greatest, at the junction between the squamous epithelium of the oesophagus and the columnar mucosa of the stomach. Because only the inner layers fail, the lesion is a long, shallow gash (typically a few millimetres deep) with submucosal vessels laid open. Bleeding is therefore venous and often brisk, and because the tear is under the mucosa some bleeding may track rather than show immediately. ^[1]

The mucosa heals quickly once the bleeding stops: most tears have healed at follow-up endoscopy even without treatment. ^[1]

Here the pressure step is higher, or the wall weaker, and the muscular layer tears first. The mucosal slit is usually longer than the muscular defect. ^[7] The full-thickness hole lets gastric juice, food and air flood the mediastinum, beginning with chemical (acid) injury and followed within hours by a polymicrobial mediastinitis. ^[7]

The sepsis is worth understanding because it explains the clinical picture. The initial leakage includes acid and pepsin. Mediastinal contamination is polymicrobial: the normal oesophageal flora includes viridans streptococci, Enterobacteriaceae such as Klebsiella pneumoniae and Escherichia coli, Staphylococcus aureus, anaerobes (Bacteroides, Fusobacterium, Prevotella) and Candida species in a high proportion of cases. ^[7] Tissue injury releases damage-associated molecular patterns that activate pattern recognition receptors, and the resulting cytokine storm (tumour necrosis factor alpha, interleukin-1 beta, interleukin-6) with endothelial dysfunction drives vasodilation, hypotension, myocardial depression and, eventually, immune paralysis. ^[7] Hence the patient collapses not simply from the tear but from septic mediastinitis within hours of it. ^[7]

Anatomically the tear needs to be pictured. It occurs in about 80 to 90 percent of cases on the left wall of the distal oesophagus, between 1 and 8 centimetres in length (averaging 2.2 to 3.3 centimetres), because the muscular wall there is thin, neurovascular twigs penetrate it, and adjacent structures give least support. ^[7] The resulting mediastinal contamination spreads easily because the oesophagus sits in loose, poorly vascularised connective tissue. ^[7]

The table is a teaching summary. Real patients can have features of both. ^[7]

The classic sequence is a short bout of retching or vomiting after alcohol or food, followed immediately by haematemesis. The bleeding may start with the first vomit or after several dry retches. The blood is often bright red or mixed with dark material, and with a large tear it can be considerable and shock-inducing. Epigastric or retrosternal pain is mild. Melena may follow if the bleed is slower. ^{[1] [3]}

Most bleeds stop spontaneously. ^{[1] [3]} Even when endoscopy is normal or shows only old clot, a history of retching before haematemesis in someone without cirrhosis strongly suggests a tear that has already stopped. ^[1]

The history begins the same way (heavy meal or drinking, then vomiting) but the pain is different: sudden, violent pain in the chest, epigastrium or between the scapulae, sometimes radiating to the neck or shoulder. The patient looks shocked, breathless and cyanosed. Haematemesis is mild or absent, which is the opposite of what is taught for Mallory-Weiss bleeding and is an important clue. ^[7]

The classical Mackler triad is vomiting, chest pain and cervical subcutaneous emphysema. ^[7] In practice the full triad is present in only 10 to 50 percent of cases depending on the series, with one review estimating about 50 percent and another about 10 percent; an Australian series found chest pain in about 80 percent, vomiting in about 87 percent, and cervical subcutaneous emphysema in only about 27 percent. ^[7] Subcutaneous emphysema is the most specific finding when it is present but even it is seen in fewer than 60 percent of cases by the most optimistic estimates. ^[7]

Clues that point to perforation include dysphagia, dysphonia, pain that worsens on swallowing, Hamman sign (a crunching sound with the heartbeat), and diminished breath sounds on the side of the rupture. About 25 to 45 percent of patients do not report vomiting at presentation. ^[7] There is a particular trap: chest pain with ST-segment change on the electrocardiogram has been described, so a patient with ECG changes after vomiting still needs a perforation excluded, especially if cardiac enzymes are normal. ^[7]

Because vomiting, pain and a murmur (from mediastinal air, not from the heart) can mimic a myocardial infarction, the wrong first diagnosis is the commonest reason for delay. ^[7]

For suspected Mallory-Weiss bleeding the examination is that of upper gastrointestinal haemorrhage: tachycardia, orthostatic or supine hypotension, pallor, epigastric tenderness, and (rarely in this condition) signs of chronic liver disease. ^{[4] [5]}

For suspected perforation the examination is of a shocked, septic patient: tachypnoea, tachycardia, fever, hypotension, surgical emphysema of the neck, reduced or delayed breath sounds, and percussion dullness. Cervical and chest wall crepitus can be felt. After a few hours signs of mediastinal and then systemic sepsis appear. ^{[7] [8]}

The central differential is between the two syndromes themselves, because they share a trigger and differ only in depth. The second differential is between Boerhaave rupture and the other emergencies that produce sudden chest pain after vomiting, particularly myocardial infarction, pneumothorax, perforated peptic ulcer and aortic dissection. ^[7] The third is between Mallory-Weiss bleeding and other causes of haematemesis.

A Mallory-Weiss tear can also be mistaken at endoscopy for a Cameron ulcer, erosive oesophagitis, a Dieulafoy lesion and gastric cancer; biopsy of any non-healing lesion is required. ^[1]

Full blood count and cross-match, urea and creatinine, coagulation screen and platelets, liver function, lactate and arterial blood gas for perforation. In upper bleeding, a high urea with normal creatinine supports an upper source because digested blood is absorbed and metabolised to urea. ^[5] In perforation, leucocytosis, acidosis and rising lactate mark the move from chemical to bacterial mediastinitis. ^[7]

For haematemesis from a suspected Mallory-Weiss tear, upper endoscopy (oesophagogastroduodenoscopy) is both diagnostic and therapeutic. ^{[1] [3] [4]} It should be done after haemodynamic stabilisation; the standard guideline position is that hospitalised patients with upper gastrointestinal bleeding undergo endoscopy promptly, and the ACG 2021 guideline contrasts endoscopy at 6 to 24 hours with no improvement from pushing earlier, while emphasising that resuscitation comes first. ^[5] Transfusion in hospitalised patients is suggested at a haemoglobin of 7 g/dL, and risk assessment such as the Glasgow-Blatchford score identifies very-low-risk patients who can go home. ^{[5] [6]}

Endoscopy shows a longitudinal mucosal tear at the gastro-oesophageal junction, or an ulcer at the site; the diagnosis is made when that appearance is seen. ^[3]

For perforation, endoscopy is not a first-line investigation. It has high sensitivity but can worsen the injury and amplify mediastinal contamination. ^[7] It is reserved for selected patients in whom the diagnosis remains uncertain, or for therapeutic stenting. ^{[7] [8]}

Chest radiograph comes first in suspected perforation. It may show pneumomediastinum (retrocardiac V-shaped air collection, often called Naclerio sign, in about 20 percent of cases), left pleural effusion, hydropneumothorax, atelectasis or subcutaneous emphysema. ^[7] Plain film is insensitive and non-specific, so a normal chest radiograph does not exclude perforation. ^[7]

Contrast swallow is the investigation specifically asked for. It is recommended by the American College of Radiology when perforation is suspected and it localises the breach and its output. ^[7] Important limitations:

• Missed leaks: 10 to 20 percent of perforations are missed when barium is used, and 22 to 50 percent when water-soluble contrast is used; one review reports 10 to 38 percent false-negative contrast studies overall. ^[7]
• The procedure depends on patient cooperation, positioning and swallowing, all of which can be poor in a shocked or intubated patient.
• Barium swallow carries a risk of aspiration and pulmonary oedema, while water-soluble contrast has the lower sensitivity.
• Crucial safety rule: if perforation is suspected, use water-soluble contrast first. If that study is negative but suspicion remains, repeat with barium to improve sensitivity. ^[7]

Contrast-enhanced CT of the chest and abdomen with oral contrast is the preferred investigation and is considered the gold standard for diagnosing spontaneous oesophageal rupture. Sensitivity is reported at 92 to 100 percent. ^[7] It gives the level and size of the breach, mediastinal collection, mediastinitis and pleural involvement, and in many cases gives enough information to drop the contrast swallow altogether, saving time. ^[7] Typical signs include pneumomediastinum, pneumothorax (often left-sided), pleural effusion, periaortic air, thickened oesophageal wall and oral contrast extravasation. ^[7]

Ultrasound has a limited role: it may find subcutaneous emphysema or collections, but literature support is patchy. ^[7]

There is no formal score for either condition. Severity is set by three things: haemodynamic stability, the depth/extent of the lesion, and the time since onset. A few numbers are useful to quote:

• Mortality by delay in Boerhaave syndrome. Diagnosed within 24 hours, mortality can be reduced to 6.2 percent in one review, and another reports 14 versus 27 percent for treatment within versus beyond 24 hours; treatment started within 24 hours gives about a 75 percent chance of survival; after 48 hours survival falls to roughly 40 to 60 percent (50 percent in one review), and after 72 hours to 10 percent. ^[7]
• In-hospital mortality after Mallory-Weiss bleeding is uncommon but not zero: about 5.7 percent in one international cohort, similar to peptic ulcer bleeding. ^[2]
• Rebleeding after Mallory-Weiss bleeding occurs in about 4.9 to 10.7 percent of patients depending on the cohort (17 of 159 in one series), and is associated with shock at presentation and active bleeding seen at endoscopy; other reported risk factors are coagulopathy, low haemoglobin, cirrhosis, and intensive care admission. ^{[1] [2]}
• Endoscopic haemostasis for Mallory-Weiss bleeding: reported initial haemostasis is 94 to 100 percent for haemoclip placement, 100 percent for band ligation, 93 to 100 percent for injection therapy, and 77 percent for thermal coagulation. ^[1]
• Active bleeding is seen as oozing in about 26 percent and a clean base in about 26 percent of Mallory-Weiss cases in the international cohort; 42 percent of patients received endoscopic therapy, and 90 percent of those received injections. ^[2]
• Candida is found in 58 percent of oesophageal flora samples in Boerhaave studies. ^[7] Whether empiric antifungal cover is needed is a local decision.

The setting is upper gastrointestinal haemorrhage. Management follows the current ACG 2021 and ESGE 2021 non-variceal upper bleeding guidance, plus the international consensus statement of 2019: ^{[4] [5] [6]}

1. Airway and circulation. Large-bore intravenous access, monitoring, and oxygen. Resuscitation comes before endoscopy. ^[5]
2. Bloods. Full blood count, coagulation, liver and renal tests, lactate, cross-match. Transfuse at a haemoglobin threshold of 7 g/dL in hospitalised patients, or a higher threshold if there is cardiovascular or other serious disease. ^[5]
3. Risk score. Glasgow-Blatchford score in the emergency department; very-low-risk patients (score 0 or 1, with less than about a 1 percent risk of hospital-based intervention or death) can often be discharged for outpatient management. ^{[5] [6]}
4. Acid suppression and anti-emetic. Proton-pump inhibitors are standard in upper gastrointestinal bleeding, and a proton-pump inhibitor with an anti-emetic is logical after a Mallory-Weiss tear because both reflux and vomiting can reopen the tear, although evidence specific to Mallory-Weiss bleeding is limited. ^[3]
5. Endoscopy within about a day. Hospitalised patients should undergo endoscopy promptly after stabilisation. ^[5]
6. Endoscopic haemostasis only if needed. See the flowchart below and the indications above.

Most Mallory-Weiss bleeding stops without endoscopic treatment. ^{[1] [3]} Endoscopy is needed to find patients who have active or visible bleeding, and to catch the rare refractory case.

From the review by Kim, ^[1] with technique-based detail:

• Indication. Endoscopic treatment is needed for active bleeding (spurting, streaming or oozing) and is reasonable for stigmata of recent haemorrhage (non-bleeding visible vessel, adherent clot) if bleeding has recurred or the patient has coagulopathy. ^{[1] [3]}
• Injection therapy (adrenaline/epinephrine, with or without a sclerosant). Simple and inexpensive, effective, but the bleeding stops by mechanical compression rather than by the drug; on its own rebleeding ranges from 5.8 to 44 percent. ^[1] Epinephrine can cause ventricular tachycardia and hypertensive crisis through systemic absorption, so avoid it in coronary artery disease. ^[1]
• Thermal coagulation. Multipolar electrocoagulation has improved haemostasis but repetitive coagulation carries the risk of transmural injury and perforation because the tear is thin and lacks a serosal layer. ^[1]
• Argon plasma coagulation. Non-contact, superficial and therefore safer against perforation, but coagulation is less effective in a wet, bleeding field. ^[1]
• Haemoclip placement. Effective and safe in non-fibrotic tissue; technically difficult at the gastro-oesophageal junction, and clips can detach because of high-amplitude contractions at that site. ^[1]
• Endoscopic band ligation. Technically straightforward, effective for large tears with a single band, with excellent primary haemostasis and rebleeding rates in comparative studies. One review describes it as probably the most efficient method, but ACG 2021 and ESGE 2021 accept mechanical, injection or thermal techniques depending on the lesion, operator experience and safety considerations. ^{[1] [4] [5] [3]}
• Combined therapy (epinephrine injection plus a mechanical method) is generally preferred where a second modality is available; prior epinephrine injection can produce oedema that interferes with clip placement. ^[1]

For healing and prevention of rebleeding after haemostasis, band ligation and haemoclipping are roughly equivalent (primary haemostasis 100 percent both; rebleeding about 6 versus 10 percent). ^[1]

Escalation: if bleeding continues or recurs despite one or two endoscopic attempts, move to surgery or angiographic embolisation (transcatheter arterial embolisation). ^{[1] [3] [5]} Angiographic embolisation has the lower complication rate and is favoured when it is available, after failed endoscopy. ^[5]

The same general actions apply to every perforation regardless of cause: resuscitate, control contamination, close the breach, drain and support nutrition. ^{[7] [8]}

1. Airway and breathing. Oxygen and, if shocked or distressed, intubation and ventilation. Position the patient head-down if intubated to limit mediastinal contamination. ^[8]
2. Circulation. Aggressive fluid resuscitation with blood if haemorrhage is present. ^[8]
3. Nothing by mouth and nasogastric decompression with gentle suction. ^[7]
4. Broad-spectrum intravenous antibiotics without delay. The septic mediastinitis is polymicrobial, so cover aerobes and anaerobes (a third-generation cephalosporin or piperacillin-tazobactam plus metronidazole is typical; local protocols vary). ^[7] Early empiric antibiotics are described as a critical pillar. ^[7]
5. Proton-pump inhibitor infusion to reduce gastric content and acidity, plus adequate analgesia and anti-emetics to stop further vomiting. ^[7]
6. Imaging without postponing antibiotics: chest radiograph then CT with oral contrast (and contrast swallow if CT is equivocal). ^[7]
7. Surgical involvement early. Even where non-operative management is contemplated, care should be under an experienced oesophageal team with round-the-clock surgical and radiological cover. ^[8]

Endoscopic stenting and clipping have transformed recent practice. Covered self-expanding metal stents (often placed with adjunctive drainage) seal the perforation and can avoid resection; case series and narrative reviews report growing use, including in Boerhaave syndrome. ^[7] Haemoclips and sutures can close small defects, and for oesophageal perforation clip placement on both edges has been described. ^[1] Endoscopic vacuum therapy is another option in specialist centres. ^[7]

Non-operative management is appropriate only when strict criteria are met, and almost all criteria come from the WSES 2019 guidelines: ^[8]

• early presentation (less than 24 hours);
• no clinical or laboratory signs of sepsis;
• contained perforation (intramural, minimal extravasation with drainage) on CT or contrast study;
• no massive pleural contamination, and a cervical or thoracic location;
• no pre-existing oesophageal disease;
• an expert oesophageal team available for continuous monitoring, with 24-hour surgical and radiological cover.

Source control by stent with pleural drainage, rather than operation, is used when these criteria are met. ^[8]

Surgery remains the mainstay of Boerhaave syndrome in most centres. Upfront surgery is advised immediately when there is extensive pleural or mediastinal contamination or clinical deterioration. ^[8] For a fit patient presenting within 24 hours, primary repair (and drainage of the mediastinum and pleura) gives the best results; delayed presentation (beyond 24 hours) reduces the chance of successful primary repair even if it does not always increase mortality. ^{[7] [8]} If repair is not feasible, or presentation is late with tissue necrosis, oesophagectomy with delayed reconstruction or exclusion-diversion may be needed. ^{[7] [8]}

Where a laparotomy or thoracotomy is undertaken for other reasons and an oesophageal injury is suspected, it should be sought directly, by intraluminal instillation of methylene blue or by endoscopic insufflation. ^[8]

Drainage of mediastinal and pleural collections (tube thoracostomy or image-guided drains) is mandatory even when the breach is closed. ^[7] Nutrition is given parenterally, or by jejunostomy feeding tube, avoiding oral intake while the repair seals. Radiological confirmation (contrast study) that the leak has sealed is required before oral feeding is restarted. ^{[7] [8]}

• Rebleeding in about 10.7 percent overall (5.8 to 44 percent after epinephrine injection alone); risk factors as above. ^{[1] [2]}
• Complications of endoscopic therapy: ventricular tachycardia or hypertensive crisis after epinephrine injection; perforation after injection or thermal coagulation; clip detachment. ^[1]
• Rarely, extension to a full-thickness Boerhaave rupture (a transitional case). ^[7]
• Special care in cirrhosis, where bleeding is heavier and outcomes worse. ^[1]

• Septic mediastinitis, pleural empyema, abscess formation, adult respiratory distress syndrome, and multi-organ dysfunction. ^[7]
• Leak after repair or stent migration/failure, stricture and fistula formation. ^[7]
• Late outcomes include reduced quality of life, swallowing problems and the need for re-operation. ^[7]

Mallory-Weiss bleeding: most patients do well. The clot organises, the tear heals within days, and recurrence is uncommon. Mortality follows age, haemodynamic compromise, cirrhosis and comorbidity rather than the tear itself, as the 5.7 percent 30-day mortality figure shows. ^[2]

Boerhaave syndrome: the single most important prognostic factor is time to diagnosis and treatment. ^[7] The figures in common use are treatment within 24 hours giving a mortality around 6.2 percent in one review (another reports 14 to 27 percent) and a survival around 75 percent, versus roughly 40 to 60 percent survival at 48 hours and 10 percent at 72 hours. ^[7]

• Minimise the triggers: control alcohol, treat provoking cough, vomiting or reflux, and review medications that predispose to haematemesis.
• Anti-emetics before and during endoscopy reduce iatrogenic tearing from retching. ^[1]
• Chronic acid suppression and, where relevant, eradication of Helicobacter pylori are reasonable after a bleeding tear in patients with mucosal disease, though this is extrapolation rather than direct evidence. ^[1]
• There is no screening test for either condition. Prevention is prevention of vomiting and of mediastinal spread once a breach occurs.

• Cirrhosis and portal hypertension. Mallory-Weiss bleeding is heavier and more likely to need intervention. ^[1] Large varices and portal hypertension can make thermal coagulation hazardous. Boerhaave syndrome is managed on the same principles, but coagulopathy must be corrected before repair. ^[7]
• Children. Both are rare. Boerhaave is least common at ages 1 to 17. ^[7] If a child presents after vomiting with chest pain or shock, imaging to exclude perforation is mandatory.
• Pregnancy. Vomiting in pregnancy (hyperemesis gravidarum) is a recognised trigger of both. Care is multidisciplinary: obstetrics, gastroenterology and surgery.
• Older adults. Outcome in both conditions tracks comorbidity and physiological reserve more than chronology.

• In a setting with endoscopy available only in working hours, the emphasis shifts to resuscitation, blood, intravenous proton-pump inhibitors, anti-emetics, and early transfer for any high-risk endoscopic stigmata or suspected perforation.
• A Mallory-Weiss tear that has stopped bleeding can be observed without endoscopy if the history is typical and the patient stabilises; but any haemodynamic compromise, cirrhosis or active bleeding still requires endoscopy. ^[1]
• Suspected perforation should be suspected clinically (retching, severe pain, shock; crepitus) and investigated with a plain chest radiograph while arranging transfer. Water-soluble contrast swallowing is the standard confirmatory test and a CT with oral contrast is the most reliable; in hospitals without CT, a contrast swallow and a plain chest film plus clinical judgement remain standard. ^[7]
• If surgery is not available locally, the priority is urgent transfer after antibiotic cover and decompression; survival in Boerhaave syndrome falls steeply after the first day. ^[7]

Non-variceal upper gastrointestinal bleeding; upper endoscopy and its complications; gastrointestinal bleeding; thoracic trauma; mediastinitis; the Glasgow-Blatchford score; portal hypertension and varices; acid-peptic disease.

• A Mallory-Weiss tear is a superficial, non-perforating longitudinal tear at or near the gastro-oesophageal junction, produced by sudden raised intra-abdominal pressure during vomiting, retching, coughing or straining; it is a common cause (about 3 to 15 percent) of upper gastrointestinal bleeding. ^{[1] [2] [3]}
• Most Mallory-Weiss bleeding stops spontaneously; endoscopic haemostasis is reserved for active bleeding or high-risk stigmata, with band ligation and haemoclip both excellent and thermal coagulation riskier against perforation. ^{[1] [3]}
• Gastric-side tears are far more common than purely oesophageal ones; cirrhosis and portal hypertension make bleeding heavier. ^[1]
• Boerhaave syndrome is a full-thickness distal oesophageal rupture (usually the left wall) from raised pressure; it is uncommon (roughly 3 cases per million per year) but carries a 20 to 90 percent mortality. ^[7]
• The two share a trigger but differ in depth: mild pain and massive haematemesis (Mallory-Weiss) versus severe pain and mild or absent blood (Boerhaave). ^[7]
• The Mackler triad (vomiting, pain, cervical surgical emphysema) is present in only 10 to 50 percent of Boerhaave cases. ^[7]
• Water-soluble contrast swallows miss 22 to 50 percent of perforations; barium misses 10 to 20 percent; CT with oral contrast has 92 to 100 percent sensitivity. ^[7]
• Suspected perforation needs NPO, broad-spectrum antibiotics, proton-pump inhibitor, analgesia, early drainage and closure; endoscopic or surgical according to contamination and time since onset. ^{[7] [8]}
• Non-operative management by stent and drainage is only for carefully selected patients seen early. ^[8]
• Best outcomes in Boerhaave syndrome follow diagnosis and treatment within 24 hours. ^[7]