01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Forceful contraction against a closed glottis raises intra-abdominal pressure while negative intrathoracic pressure acts across the junction. The mucosa splits, most often on the gastric side of the gastro-oesophageal junction, and a submucosal vessel may bleed. Alcohol-related retching is a familiar association, but gastroenteritis, pregnancy, migraine, coughing, eating disorders, chemotherapy and any cause of persistent vomiting can precipitate a tear. Anticoagulants, antiplatelets, liver disease and thrombocytopenia do not create the lesion but can magnify blood loss and complicate haemostasis.
Presentation ranges from a small streak of bright blood after vomiting to haemodynamic collapse. Melaena can follow slower bleeding. The clinician must maintain a broad differential including peptic ulcer, varices, malignancy, severe oesophagitis and swallowed blood. The history of retching is particularly dangerous if it closes thinking: variceal haemorrhage can itself trigger vomiting, and transmural rupture can follow the same pressure event. Examine for shock, chronic liver disease, abdominal tenderness, crepitus and respiratory compromise while resuscitation proceeds.
Endoscopy confirms the linear junctional laceration, excludes competing sources and provides treatment when bleeding persists. A visible but dry tear without a high-risk bleeding feature is usually managed conservatively. When endoscopic haemostasis fails, interventional radiology or surgery is uncommon but must be available through escalation pathways. Acid-suppressive treatment after endoscopy follows the actual lesion and endoscopic stigmata under NICE non-variceal guidance; NICE does not support routine acid suppression before diagnostic endoscopy for suspected non-variceal bleeding.
Key points
- A Mallory-Weiss lesion is a longitudinal mucosal laceration near the gastro-oesophageal junction produced by a sudden pressure gradient during retching, vomiting, coughing or straining.
- The typical history is repeated non-bloody emesis followed by fresh haematemesis, but the sequence is absent in some patients and cannot replace endoscopy.
- Most tears stop bleeding spontaneously, yet active arterial oozing, shock, coagulopathy or major comorbidity can make haemorrhage clinically important.
- Initial care follows the same ABC, access, blood sampling, transfusion and risk-assessment principles as any acute upper-GI bleed.
- The Glasgow-Blatchford score supports pre-endoscopic risk assessment; only appropriately low-risk patients considered against local criteria should avoid admission.
- NICE advises endoscopy immediately after resuscitation for unstable severe bleeding and within twenty-four hours for other admitted upper-GI bleeds.
- A clean non-bleeding tear usually needs no endoscopic haemostasis, while active bleeding can be treated with clips, thermal methods or injection as an adjunct under expert care.
- Adrenaline injection should not be used as sole definitive haemostasis for a non-variceal lesion because combination treatment is more durable.
- Severe pain or systemic illness after vomiting suggests Boerhaave syndrome, and a negative endoscopy for bleeding does not make perforation safe to ignore.
- Preventing recurrence means treating the cause of vomiting, reviewing alcohol and medicines, and giving clear return advice rather than prescribing acid suppression automatically.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Forceful retching or vomiting
Repeated emesis creates the classic pressure gradient across the gastro-oesophageal junction, often after alcohol-related illness, gastroenteritis or another vomiting trigger.
Coughing and straining
Severe coughing, seizures, labour or other abrupt rises in intra-abdominal pressure can produce the same superficial junctional laceration.
Bleeding susceptibility
Antithrombotic therapy, coagulopathy and portal hypertension may increase haemorrhage severity, although they are not required for the tear to form.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Abrupt pressure gradient
Forceful gastric contraction against a relatively closed junction stretches the mucosa at the distal oesophagus and gastric cardia.
- 2Longitudinal mucosal laceration
The lining splits without full-thickness rupture, exposing submucosal vessels and causing fresh upper-GI bleeding into the lumen.
- 3Spontaneous haemostasis
Most tears stop as vessels contract and clot, while continued retching, arterial involvement or coagulopathy prolongs bleeding.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Several episodes of forceful non-bloody vomiting are followed by fresh haematemesis, often with less pain than the amount of blood initially suggests.
Tachycardia, hypotension, cool peripheries, delayed capillary refill, syncope, confusion or oliguria indicate significant haemorrhage requiring immediate resuscitation and escalation.
Disproportionate chest or upper-abdominal pain, breathlessness, fever, crepitus or pleural findings after vomiting is more consistent with perforation than an isolated mucosal laceration.
A small self-limited haematemesis episode with normal observations and no major comorbidity may prove low risk, but formal scoring and senior review precede outpatient care.
Melaena, postural dizziness or falling haemoglobin can continue after visible haematemesis stops and warrants reassessment rather than reassurance from an empty vomit bowl.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Serial physiological observationsFirst step - Why
- Recognise shock and response to resuscitation in real time.
- Interpretation and limitations
- Trend pulse, blood pressure, respiratory rate, oxygen saturation, mental state, urine output and early-warning score. A normal initial blood pressure does not exclude compensated haemorrhage.
- 02
Full blood count, coagulation and organ profile - Why
- Assess anaemia, platelets, coagulopathy, urea and treatment risk.
- Interpretation and limitations
- Haemoglobin can be initially normal before redistribution, so repeat according to clinical course. Raised urea supports upper-GI blood digestion but is not source-specific; identify kidney or liver dysfunction before medicines and procedures.
- 03
Group and antibody screen or crossmatch - Why
- Prepare safe blood-component support when the bleed may be significant.
- Interpretation and limitations
- Match urgency and products to haemodynamic state, ongoing loss, comorbidity and the local major-haemorrhage protocol rather than using haemoglobin alone.
- 04
Glasgow-Blatchford score - Why
- Estimate need for intervention before endoscopy.
- Interpretation and limitations
- Calculate from presentation data and use with clinical judgement and local discharge criteria. It is not designed to identify a Mallory-Weiss tear or overrule instability.
- 05
Upper gastrointestinal endoscopy - Why
- Locate the source, characterise the tear and deliver haemostasis.
- Interpretation and limitations
- A longitudinal junctional laceration confirms the lesion. Record active spurting or oozing, adherent clot and alternative pathology; a clean stopped tear generally does not need endoscopic therapy.
- 06
CT chest and upper abdomen with contrast - Why
- Investigate oesophageal perforation rather than routine uncomplicated haematemesis.
- Interpretation and limitations
- Extraluminal gas or contrast, mediastinal fluid and pleural contamination support rupture. Arrange the protocol with radiology and upper-GI or thoracic specialists without delaying resuscitation.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Boerhaave syndrome
Severe persistent chest pain, breathlessness, fever, pleural fluid or mediastinal gas after vomiting suggests full-thickness perforation rather than a mucosal tear.
Peptic or variceal bleeding
Ulcer risk or cirrhosis may indicate another source; urgent endoscopy distinguishes a junctional laceration from ulcer or varices.
Swallowed nasopharyngeal blood
Epistaxis, oral bleeding and absence of a gastrointestinal lesion can explain apparent haematemesis, particularly after swallowed blood provokes nausea.
Additional chapter-specific clues
Known cirrhosis, portal hypertension, ascites, jaundice or prior varices requires the suspected-variceal pathway until endoscopy defines the source.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01First hourResuscitate an undifferentiated upper-GI bleedFirst stepHaematemesis or melaena occurs after retching, with or without circulatory compromise.+
- 1Assess airway, breathing and circulation, call for senior help, place appropriate large-bore IV access and monitor continuously when bleeding is severe.
- 2Send urgent bloods and group-and-screen, begin balanced crystalloid while blood is prepared, and activate the major-haemorrhage protocol for uncontrolled bleeding or shock.
- 3Review anticoagulants, antiplatelets, liver disease and comorbidity, using indication-specific reversal with haematology or cardiology input rather than indiscriminate correction.
- 4Calculate a pre-endoscopy risk score once immediate care is under way and refer to gastroenterology for timing, airway and location of endoscopy.
02Endoscopic careConfirm and control the lesionThe patient is resuscitated sufficiently for upper-GI endoscopy.+
- 1Perform endoscopy immediately after resuscitation for unstable severe bleeding or within twenty-four hours for other admitted patients, following NICE and local service availability.
- 2Inspect the junction carefully, clear clot safely and exclude peptic, variceal, malignant and inflammatory sources before attributing bleeding to a tear.
- 3Leave a clean stopped laceration without unnecessary intervention; treat active haemorrhage with a suitable mechanical or thermal method, with dilute adrenaline only as part of combination therapy when used.
- 4EscalationEscalate recurrent or uncontrolled bleeding promptly to repeat endoscopy, interventional radiology or surgery according to anatomy and local expertise.
03After haemostasisPrevent recurrence and discharge safelyEscalationBleeding has stopped and no immediate endoscopic or surgical escalation is required.+
- 1Observe physiology and repeat haemoglobin according to bleed severity, comorbidity and endoscopic findings, with re-endoscopy planning for recurrent haematemesis, melaena or shock.
- 2Identify and treat the vomiting trigger, provide time-limited antiemetic support when appropriate and review alcohol, pregnancy, infection, migraine, medicines or eating-disorder risk sensitively.
- 3Use post-endoscopy PPI only when indicated by the identified non-variceal lesion or coexisting acid injury, and resume antithrombotic therapy through a documented risk-balanced plan.
- 4Before discharge confirm oral intake, follow-up, haemoglobin or iron needs and written return advice for further blood, fainting, black stools, severe pain or breathlessness.
04Pain after vomitingSeparate mucosal tear from transmural ruptureChest pain, systemic upset or respiratory findings accompany haematemesis after forceful vomiting.+
- 1Keep nil by mouth and assess for sepsis, pleural disease, crepitus and shock rather than assuming pain comes from a superficial tear.
- 2Contact upper-GI surgery and radiology early and obtain urgent CT of chest and upper abdomen using a leak-sensitive contrast protocol agreed locally.
- 3Start local perforation antimicrobials and resuscitation when rupture is suspected, avoiding forceful instrumentation before the specialist plan.
- 4Proceed to drainage and operative or endoscopic source control according to containment, physiology and expertise if perforation is demonstrated.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Proton pump inhibitor after endoscopy
Use the current NICE CG141 regimen for non-variceal bleeding with endoscopic stigmata or a licensed oral course for coexisting acid injury; route and intensity are selected from the endoscopic finding and local protocol.NICE advises against routine acid suppression before endoscopy in suspected non-variceal bleeding. Do not let PPI administration delay resuscitation, endoscopy or investigation of perforation.
Antiemetic therapy
Select a licensed antiemetic and adult dose from the current BNF according to the likely cause, route available and comorbidity, using the shortest effective course and correcting dehydration or electrolyte disturbance.Check QT prolongation, Parkinsonism, bowel obstruction, pregnancy, sedation, dystonia and interactions for the chosen agent. Persistent vomiting or distension needs renewed diagnosis, not serial symptomatic dosing.
Blood components and antithrombotic reversal
Give red cells, platelets, plasma, prothrombin complex or a specific reversal agent only through the current major-haemorrhage, haematology and drug-specific pathway, guided by physiology, laboratory results and the anticoagulant indication.Over-transfusion and unnecessary reversal can increase circulatory, thrombotic or portal-pressure risk. Involve the relevant specialist when recent coronary stenting, mechanical valve or high thrombotic risk complicates interruption.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Major haemorrhage and shock
An arterial tear or impaired haemostasis can cause substantial blood loss, syncope, myocardial strain and acute kidney injury.
Rebleeding
Failure of initial clot stability, continued vomiting or uncorrected coagulopathy can produce recurrent haematemesis after apparent improvement.
Aspiration
Active vomiting of blood can contaminate the airway, especially with reduced consciousness or heavy alcohol exposure, causing hypoxia and pneumonia.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Trend pulse, blood pressure, mental state, urine output and ongoing haematemesis or melaena after apparent haemostasis; deterioration outranks a previously low score.
- Repeat haemoglobin, platelet count, coagulation and renal profile at intervals matched to severity, transfusion and comorbidity rather than a fixed routine for every patient.
- After endoscopic treatment watch for recurrent bleeding and arrange the locally defined escalation route for urgent re-endoscopy, radiology or surgery.
- Assess nausea, oral intake and hydration, and confirm that the precipitating illness or medicine exposure is improving before discharge.
- Document when anticoagulants and antiplatelets will restart, who owns the decision and what bleeding or thrombotic features trigger earlier review.
- Give explicit warning signs of perforation because new severe chest pain, fever, breathlessness or collapse after vomiting requires emergency reassessment.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
The history suggests, endoscopy confirms
Retching followed by blood is characteristic but peptic ulcer, varices and cancer remain possible until the upper gastrointestinal tract is assessed.
Haemoglobin lags behind shock
Early whole-blood loss can leave the concentration deceptively normal, so physiology and observed bleeding guide initial urgency.
A dry tear needs restraint
Most Mallory-Weiss lesions have stopped by endoscopy; unnecessary clipping or injection adds procedural risk without clear benefit.
Adrenaline is an adjunct
Injection can slow active bleeding and improve visualisation but should be combined with a definitive mechanical or thermal method when used for non-variceal haemostasis.
Pain changes the differential
Prominent post-emetic chest pain and systemic signs should immediately raise Boerhaave syndrome, even when haematemesis is also present.
11Common pitfallsFrequent interpretation and management errors.
- 01
Labeling haematemesis as a Mallory-Weiss tear from the vomiting history and missing varices or peptic ulcer.
- 02
Waiting for haemoglobin to fall before treating a shocked patient with ongoing blood loss.
- 03
Giving routine pre-endoscopy PPI as a substitute for resuscitation and timely diagnostic endoscopy.
- 04
Using adrenaline injection alone for active non-variceal bleeding without a definitive second modality.
- 05
Discharging from a low risk score without confirming local criteria, social safety and senior clinical review.
- 06
Missing oesophageal perforation because post-vomiting chest pain is attributed to a superficial laceration.