Haematemesis, melaena and upper GI bleeding

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Upper gastrointestinal bleeding arises proximal to the ligament of Treitz and commonly presents with haematemesis or melaena; brisk bleeding can produce maroon stool or haematochezia. Coffee-ground material indicates blood altered by acid but does not quantify current rate. Distinguish swallowed epistaxis and haemoptysis from true vomiting, yet treat uncertainty physiologically. Ask about syncope, stool, pain, retching, liver disease, alcohol, previous ulcer or varix, NSAIDs, antiplatelets, anticoagulants and cardiovascular comorbidity. Examination seeks shock, postural change when safe, cool peripheries, encephalopathy, ascites, stigmata of chronic liver disease and abdominal tenderness.

Resuscitation and diagnosis run in parallel. Secure access, send crossmatch and serial laboratory tests, monitor urine output and correct hypothermia. Blood products are not prescribed by one early haemoglobin because acute loss initially removes plasma and cells together. Use local major-haemorrhage support for exsanguination, and a restrictive red-cell strategy for most stable patients while individualising coronary ischaemia and ongoing shock. Platelet and coagulation correction depends on active bleeding, counts, medicine effect and planned intervention; indiscriminate plasma for a mildly prolonged INR in cirrhosis may not restore balanced haemostasis and can worsen portal pressure.

Risk tools standardise but do not replace judgement. The Glasgow-Blatchford score uses presentation variables to identify intervention risk; NICE allows consideration of early discharge when it is zero and no other concern exists. Endoscopy identifies cause, treats ulcer stigmata or varices and provides a post-endoscopy Rockall component. Failure or rebleeding leads to repeat endoscopy, interventional radiology or surgery according to lesion and expertise. Variceal bleeding is a portal-hypertension emergency requiring vasoactive therapy, antibiotics, band ligation and consideration of TIPSS; secondary prevention and alcohol or liver-care planning begins before discharge. Every bleed needs a plan for H pylori, NSAID modification and safe antithrombotic restart.

Key points

Assess circulation and airway before debating ulcer versus varix; massive haematemesis and encephalopathy create a high aspiration risk that may require anaesthetic airway control.
Two large-bore venous cannulae, blood count, renal and liver profiles, coagulation, group-and-save or crossmatch, lactate and frequent observations support resuscitation, but haemoglobin may initially appear normal.
Use the Glasgow-Blatchford score at first assessment and the full Rockall score after endoscopy; a score supports disposition but never overrides active shock or clinical concern.
Transfuse according to the overall clinical picture and current restrictive strategy, individualising for exsanguination, ischaemic heart disease and active instability rather than chasing a normal haemoglobin.
Unstable severe bleeding needs endoscopy immediately after resuscitation; other admitted upper GI bleeds should undergo endoscopy within 24 hours under NICE guidance.
Suspected variceal bleeding requires terlipressin and prophylactic antimicrobial therapy at presentation, with urgent endoscopic band ligation and early specialist discussion of rescue or pre-emptive TIPSS.
Do not give acid suppression before endoscopy routinely for suspected non-variceal bleeding under NICE; after endoscopic stigmata and haemostasis, use the recommended PPI regimen.
Review anticoagulants and antiplatelets immediately, balancing haemostasis against thrombotic indication with haematology, cardiology and endoscopy input; reversal is context specific.
Endoscopic haemostasis requires combination or mechanical/thermal therapy appropriate to the lesion, followed by monitoring for rebleeding and radiological or surgical rescue when necessary.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Peptic and erosive disease

Peptic ulcer, gastritis, oesophagitis and NSAID-related mucosal injury commonly bleed through surface erosion or arterial vessel exposure.

Portal hypertensive bleeding

Oesophagogastric varices and portal hypertensive gastropathy cause bleeding in cirrhosis or other portal hypertension and require immediate cause-specific therapy.

Tears, tumours and vascular lesions

Mallory-Weiss tears, upper-GI cancer, angioectasia and procedure-related injury are alternative sources with distinct endoscopic treatment implications.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Mucosal or vascular disruption
Ulceration erodes an artery, variceal pressure ruptures a collateral, or fragile neoplastic and vascular tissue begins to ooze.
2
Intraluminal blood transit
Blood may be vomited fresh or altered by acid, while digestion and intestinal transit convert it into black tarry melaena.
3
Circulatory compromise
Rapid loss reduces venous return and organ perfusion before haemoglobin equilibrates, causing tachycardia, hypotension and shock.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Haemorrhagic shockRed flag

Tachycardia, hypotension, narrow pulse pressure, cool peripheries, oliguria, altered mentation or raised lactate indicates inadequate perfusion. Beta-blockers and pacing can blunt tachycardia, so trends and end-organ signs matter.

Variceal haemorrhageRed flag

Known cirrhosis, portal hypertension, previous varices, ascites, splenomegaly or thrombocytopenia with significant upper bleeding raises varices. Assume and treat early because infection and rebleeding risks are high.

Peptic ulcer bleeding

Epigastric symptoms, NSAID or aspirin exposure, H pylori and previous ulcer support gastroduodenal ulcer. Endoscopic active bleeding, visible vessel or adherent clot determines haemostatic and post-procedure treatment.

Mallory-Weiss tear

Haematemesis following repeated retching suggests a mucosal junctional tear, often self-limiting. Continued haemodynamic compromise or substantial bleeding still requires ordinary resuscitation and endoscopic evaluation.

Aorto-enteric fistulaRed flag

A herald bleed followed by massive haemorrhage in a patient with previous aortic graft or aneurysm is a vascular catastrophe. Immediate vascular surgery and appropriate CT angiography take priority over routine endoscopy sequencing.

Rebleeding after haemostasisRed flag

New haematemesis or melaena with pulse rise, hypotension, falling haemoglobin or increasing urea after initial control suggests recurrence and needs repeat resuscitation and urgent endoscopy or radiological rescue.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

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 observations and shock assessmentFirst step
Why
Quantify perfusion, airway risk and response to resuscitation before and after haemostasis.
Interpretation and limitations
Trend pulse, blood pressure, mental state, capillary refill, urine output and lactate. A temporarily normal pressure after fluid does not establish bleeding control.
02
Full blood count and crossmatch
Why
Establish baseline cell counts, prepare compatible blood and follow haemoglobin and platelet trajectory.
Interpretation and limitations
Initial haemoglobin may underestimate acute loss. Interpret serial values with administered fluid, active bleeding and physiology; the crossmatch request should reflect anticipated urgency.
03
Renal, liver and coagulation profiles
Why
Assess urea rise, organ dysfunction, cirrhosis severity and factors affecting medicines, transfusion and intervention.
Interpretation and limitations
Disproportionate urea supports upper bleeding but is non-specific. INR in cirrhosis does not fully describe haemostasis; anticoagulant type and timing need separate assessment.
04
Glasgow-Blatchford score
Why
Stratify need for hospital intervention using presentation findings before endoscopy.
Interpretation and limitations
Calculate accurately after initial data are available. A score of zero may support early discharge only in a clinically suitable patient with reliable follow-up; active bleeding or instability overrules it.
05
Upper gastrointestinal endoscopy
Why
Locate bleeding, classify stigmata, provide haemostasis, diagnose varices and obtain selected tissue after stabilisation.
Interpretation and limitations
Unstable severe bleeds require immediate endoscopy after resuscitation; other admitted patients within 24 hours. Findings determine PPI, repeat endoscopy, TIPSS, radiology or surgery.
06
CT angiography
Why
Localise active bleeding or identify a vascular catastrophe when endoscopy fails, is unsuitable or an aorto-enteric fistula is suspected.
Interpretation and limitations
Active extravasation can direct embolisation. A negative study during intermittent bleeding does not end monitoring; protocol and haemodynamic safety require radiology discussion.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Haemoptysis or swallowed blood

Coughing blood, respiratory symptoms or recent epistaxis suggests a pulmonary or nasopharyngeal source rather than vomiting from the gastrointestinal tract.

Lower-GI bleeding

Fresh rectal blood usually arises distally, but brisk upper haemorrhage can traverse rapidly; instability and upper-source clues require prompt assessment.

Non-blood dark stool

Iron, bismuth and some foods darken stool without the sticky texture, characteristic odour or physiological effect of melaena.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Front doorResuscitate and risk-stratifyFirst stepHaematemesis, coffee-ground vomit or melaena is reported or observed.

1Begin ABCDE, assess aspiration and encephalopathy, obtain two adequate venous lines, monitor continuously and send urgent crossmatch and organ profiles.
2Give warmed blood and fluids according to physiology and the local haemorrhage protocol, correcting hypothermia and major metabolic disturbance without over-resuscitating portal hypertension.
3Calculate Glasgow-Blatchford score while contacting the endoscopy team, but base level of care and timing on active bleeding, comorbidity and response.
4Review NSAIDs, antiplatelets and anticoagulants immediately and obtain specialist advice for reversal and later restart.

02Variceal suspicionTreat before visual confirmationSignificant upper bleeding occurs with cirrhosis or portal-hypertension features.

1Start terlipressin and prophylactic intravenous antimicrobial treatment at presentation unless contraindicated, using current BNF and local liver guidance.
2Resuscitate carefully, involve gastroenterology, anaesthesia and critical care, and perform urgent endoscopy with band ligation for oesophageal varices.
3DefinitiveIf haemostasis fails, use the locally supported bridge such as balloon tamponade or covered stent only with expert airway and monitoring, and refer urgently for TIPSS or other definitive rescue.
4After control, arrange secondary prophylaxis, liver decompensation bundle, alcohol support and transplant consideration where appropriate.

03Non-variceal bleedLink endoscopic stigma to treatmentEndoscopy identifies peptic ulcer or another non-variceal source.

1DefinitiveUse endoscopic haemostasis appropriate to active bleeding or high-risk stigmata, avoiding adrenaline injection as the sole definitive modality.
2Give the recommended PPI regimen after endoscopy for stigmata of recent haemorrhage and test for H pylori with a valid follow-up eradication plan.
3Monitor for rebleeding; arrange repeat endoscopy, then interventional radiology or surgery when endoscopic control fails or bleeding recurs.
4Remove avoidable NSAID exposure and make a shared, documented plan for necessary aspirin or anticoagulant resumption.

04DischargePrevent recurrence and lost resultsBleeding is controlled and the patient is physiologically ready to leave hospital.

1Confirm stable observations, oral intake, haemoglobin trajectory and absence of recurrent bleeding, and reconcile all medicines.
2Document ulcer, variceal or uncertain cause, H pylori result and treatment, acid-suppression duration and antithrombotic restart plan.
3Provide clear return advice for melaena, haematemesis, syncope or weakness and ensure gastroenterology, liver or repeat-endoscopy follow-up has an owner.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces portal inflow and improves control of acute variceal haemorrhage while urgent endoscopic treatment is arranged.

Terlipressin for suspected variceal bleeding

Start at presentation using the current BNF and local variceal-haemorrhage regimen, continuing until definitive haemostasis or the guideline maximum duration unless adverse effects intervene.

Assess ischaemic cardiovascular or peripheral vascular disease, hyponatraemia and arrhythmia risk; monitor for chest, abdominal or limb ischaemia and stop with specialist review when toxicity occurs.

Reduces bacterial infection, rebleeding and adverse outcomes associated with cirrhosis and acute variceal haemorrhage.

Prophylactic antimicrobial therapy in variceal bleeding

Give the locally recommended intravenous prophylactic regimen promptly in suspected or confirmed variceal haemorrhage, adjusted for allergy, renal function and local resistance.

Obtain cultures when infection is suspected without delaying treatment. Review for allergy, C difficile and resistance, and stop or narrow according to the liver pathway and clinical course.

Stabilises clot and reduces rebleeding after endoscopic treatment of high-risk peptic ulcer disease.

Post-endoscopy proton-pump inhibitor

After endoscopic confirmation of non-variceal stigmata of recent haemorrhage, use the NICE and locally approved high-dose regimen, then step down for the indicated healing course.

NICE does not recommend routine acid suppression before endoscopy for suspected non-variceal bleeding. Review H pylori, interactions, duration and whether long-term gastroprotection remains necessary.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Shock and organ ischaemia

Major blood loss causes myocardial demand injury, acute kidney injury, altered consciousness and multiorgan failure if perfusion is not restored.

Aspiration

Massive haematemesis or encephalopathy can contaminate the airway, causing hypoxia and pneumonia and complicating urgent endoscopy.

Rebleeding and anaemia

Incomplete haemostasis or persistent causal factors lead to recurrent bleeding, transfusion exposure and delayed iron-deficiency recovery.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Trend pulse, blood pressure, mental state, peripheral perfusion, urine output, oxygen requirement and lactate at a frequency appropriate to active bleeding.
Repeat haemoglobin, platelets, coagulation, renal function and electrolytes in context of blood loss and transfusion, avoiding a purely number-driven transfusion strategy.
Watch for recurrent haematemesis, fresh melaena, syncope or shock after endoscopy and activate the repeat-endoscopy or rescue plan immediately.
During terlipressin, monitor sodium, ECG and symptoms or signs of cardiac, gut or limb ischaemia; document contraindication review.
Track H pylori testing, eradication and valid confirmation where indicated, together with ulcer-healing and repeat-endoscopy plans.
Ensure antiplatelet and anticoagulant interruption and restart have named owners because both premature resumption and prolonged omission can cause harm.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Haemoglobin lags loss

Before plasma redistribution, whole blood is lost in similar proportions and haemoglobin can look deceptively preserved. Perfusion and bleeding rate drive early resuscitation more than the first concentration.

Urea rises above creatinine

Digested blood protein and volume depletion increase urea, making a disproportionate rise supportive of an upper source. Kidney disease and catabolism limit specificity.

Cirrhosis INR is incomplete

Reduced procoagulant and anticoagulant factors coexist in advanced liver disease. Routine plasma based only on modest INR prolongation can increase volume and portal pressure without reliably correcting haemostasis.

Terlipressin precedes scope

The benefit of vasoactive treatment in likely variceal haemorrhage depends on early administration. Waiting for endoscopic proof loses the pre-endoscopy treatment window.

A zero score is narrow

Glasgow-Blatchford zero identifies a highly selected low-risk group. Social reliability, diagnostic uncertainty, active symptoms and other admission needs still matter before early discharge.

11Common pitfallsFrequent interpretation and management errors.

01
Being reassured by a normal initial haemoglobin in a patient with active shock and haematemesis.
02
Delaying terlipressin and antibiotic prophylaxis until endoscopy confirms varices in a high-probability cirrhotic bleed.
03
Giving adrenaline injection alone as definitive endoscopic therapy for a high-risk bleeding ulcer.
04
Using pre-endoscopy PPI routinely for suspected non-variceal bleeding contrary to the NICE sequence.
05
Correcting cirrhotic INR indiscriminately with plasma without considering the balanced haemostatic state and volume harm.
06
Stopping anticoagulation during admission without documenting who decides and communicates the restart date.