Recognise upper gastrointestinal haemorrhage, resuscitate according to physiology, apply validated risk assessment, and coordinate time-critical endoscopic and variceal treatment with safe antithrombotic and transfusion decisions.
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.
Peptic ulcer, gastritis, oesophagitis and NSAID-related mucosal injury commonly bleed through surface erosion or arterial vessel exposure.
Oesophagogastric varices and portal hypertensive gastropathy cause bleeding in cirrhosis or other portal hypertension and require immediate cause-specific therapy.
Mallory-Weiss tears, upper-GI cancer, angioectasia and procedure-related injury are alternative sources with distinct endoscopic treatment implications.
Ulceration erodes an artery, variceal pressure ruptures a collateral, or fragile neoplastic and vascular tissue begins to ooze.
Blood may be vomited fresh or altered by acid, while digestion and intestinal transit convert it into black tarry melaena.
Rapid loss reduces venous return and organ perfusion before haemoglobin equilibrates, causing tachycardia, hypotension and shock.
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.
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.
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.
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.
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.
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.
Coughing blood, respiratory symptoms or recent epistaxis suggests a pulmonary or nasopharyngeal source rather than vomiting from the gastrointestinal tract.
Fresh rectal blood usually arises distally, but brisk upper haemorrhage can traverse rapidly; instability and upper-source clues require prompt assessment.
Iron, bismuth and some foods darken stool without the sticky texture, characteristic odour or physiological effect of melaena.
Major blood loss causes myocardial demand injury, acute kidney injury, altered consciousness and multiorgan failure if perfusion is not restored.
Massive haematemesis or encephalopathy can contaminate the airway, causing hypoxia and pneumonia and complicating urgent endoscopy.
Incomplete haemostasis or persistent causal factors lead to recurrent bleeding, transfusion exposure and delayed iron-deficiency recovery.
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.
Digested blood protein and volume depletion increase urea, making a disproportionate rise supportive of an upper source. Kidney disease and catabolism limit specificity.
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.
The benefit of vasoactive treatment in likely variceal haemorrhage depends on early administration. Waiting for endoscopic proof loses the pre-endoscopy treatment window.
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.
Being reassured by a normal initial haemoglobin in a patient with active shock and haematemesis.
Delaying terlipressin and antibiotic prophylaxis until endoscopy confirms varices in a high-probability cirrhotic bleed.
Giving adrenaline injection alone as definitive endoscopic therapy for a high-risk bleeding ulcer.
Using pre-endoscopy PPI routinely for suspected non-variceal bleeding contrary to the NICE sequence.
Correcting cirrhotic INR indiscriminately with plasma without considering the balanced haemostatic state and volume harm.
Stopping anticoagulation during admission without documenting who decides and communicates the restart date.
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A patient with cirrhosis presents with large-volume haematemesis, tachycardia and hypotension. Resuscitation and urgent endoscopy are being arranged. Which additional treatment should begin at presentation?
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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.
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.
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.
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.