Gastrointestinal Bleeding

Meet the patient

A 64-year-old man is brought to the emergency department having vomited fresh red blood twice at home. He is pale, sweaty, heart rate 118, blood pressure 92/58, and his wife says the toilet bowl has been black for two days. He takes ibuprofen daily for his knees and has never had an endoscopy.^[1]

This is a major upper GI bleed until proven otherwise, and the next two hours are decided by three questions that govern every GI bleed: is he shocked?, is the source upper, lower, or obscure?, and is there a varix or an aortic graft in the history? Get those three right and the algorithm runs itself.^[1]

The ligament of Treitz — where upper becomes lower

A single anatomical landmark frames the whole topic. The ligament of Treitz — the suspensory muscle of the duodenojejunal flexure — divides upper from lower GI bleeding, and the presentation usually telegraphs which side of it you are on.^[1]

• Upper GI bleeding — above the ligament of Treitz (oesophagus, stomach, duodenum). Presents as haematemesis (fresh red blood), coffee-ground vomit (acid-altered blood), or melaena (black, tarry, foul-smelling stool).
• Lower GI bleeding — below the ligament of Treitz (jejunum, ileum, colon, rectum, anus). Presents as haematochezia (fresh red or maroon blood per rectum).^[1]

A third category earns its own line: obscure GI bleeding — bleeding that remains unlocalised after a good-quality OGD and colonoscopy, the lesion usually hiding in the small bowel (angiodysplasia, GIST, Crohn disease, Meckel diverticulum), hunted by capsule endoscopy then device-assisted enteroscopy.^[1]

^[1]

Read the colour, but trust the patient — never the colour alone

The gut handles blood differently depending where it sits and how long. Each appearance maps to a mechanism, and the table is a viva staple — but the single trap beneath it is that colour is not a reliable guide to the source in an unstable patient.^[1]

• Haematemesis (fresh red blood) — blood in the stomach unaltered; active, brisk UGIB.
• Coffee-ground vomit — blood altered by gastric acid to haematin; a slower or recently stopped UGIB.
• Melaena (black, tarry, foul-smelling stool) — blood digested by acid and bacterial action; even a modest volume of upper-GI blood loss produces it.
• Haematochezia (fresh red or maroon blood per rectum) — blood that transited too quickly to be digested; usually LGIB — but a brisk massive UGIB with rapid transit can also present as haematochezia.^[1]

The non-GI mimics you must never call a GI bleed: haemoptysis (coughed-up frothy bright blood, alkaline, mixed with sputum); epistaxis or dental bleeding swallowed then vomited or passed (inspect the nose and oropharynx); and black stool that is not melaena — iron, bismuth (Pepto-Bismol), liquorice, beetroot, blueberries — none foul-smelling or sticky, and a faecal immunochemical test is negative.^[1]

Resuscitate first, endoscope second — the bundle before the scope

Every GI bleed is a resuscitation until proven otherwise, and the scope waits for the perfusion. Run ABCDE before you book anything.^[1]

• A — Airway. Protect from aspiration, above all in active haematemesis with reduced consciousness (alcohol, hepatic encephalopathy). Intubate early if the airway is unprotected — aspiration is the immediate danger.
• B — Breathing. High-flow oxygen; assess respiratory rate and SpO2.
• C — Circulation. Two large-bore peripheral cannulae; bloods including group and crossmatch; balanced crystalloid titrated to perfusion; a urinary catheter in the unstable patient; the restrictive transfusion strategy below.
• D — Disability. GCS for encephalopathy from hypoperfusion, or hepatic encephalopathy in a cirrhotic.
• E — Exposure. Full examination including rectal examination — melaena confirms UGIB even when haematemesis is absent.^[1]

The restrictive transfusion strategy is the single most counter-intuitive rule in the topic, and the trial that settled it is core exam material. Villanueva and colleagues (NEJM 2013) randomised 921 patients with severe acute upper GI bleeding to a restrictive strategy (transfuse when the haemoglobin fell below 7 g/dL) versus a liberal strategy (transfuse below 9 g/dL): 6-week survival was higher with the restrictive strategy (95% vs 91%; hazard ratio for death 0.55), and further bleeding occurred in 10% versus 16%. Within the first 5 days the portal-pressure gradient increased significantly in the liberal group but not in the restrictive group — the over-transfusion effect to explain in the viva.^[5]

Do not be reassured by a normal haemoglobin at presentation. Haemodilution takes hours — the initial haemoglobin reflects the concentration before interstitial fluid shifts into the intravascular space. Trend it serially, and watch the lactate as a perfusion marker that rises before the blood pressure falls.^[1]

Read the shock, not the blood pressure — the ATLS classes

A normal blood pressure does not exclude major bleeding. Healthy young adults compensate until they have lost 30 percent of their volume, and beta-blockers and pacemakers blunt the tachycardic response — assess perfusion, not the heart rate alone. Reproduce the ATLS classes of haemorrhagic shock verbatim:^[1]

^[1]

Class III and IV are decompensated shock — the blood pressure has fallen. The clinical teaching point: the pulse pressure narrows before the systolic falls, so a narrowed pulse pressure in a tachycardic patient is an early warning, not a reassuring sign.^[1]

The atypical presentations are the ones that kill the elderly, because the bleed is silent:^[1]

• The elderly present with collapse, confusion, falls, angina, myocardial infarction, or acute kidney injury, with minimal or no abdominal symptoms and a haemoglobin that may be normal initially. Always examine the rectum and check the urea-to-creatinine ratio in any unexplained collapse or confusion in an older patient.
• Diabetic or autonomic neuropathy blunts the sympathetic response; shock may be silent.
• The anticoagulated patient — a small lesion produces a large bleed; assess and reverse per agent.
• The patient on beta-blockers — no tachycardia despite major loss; assess capillary refill, lactate, and urine output.^[1]

The causes, in the order the examiner expects

Two causes dominate, and naming them first is the expected opener. For UGIB the peptic ulcer leads (a third to a half of all cases); for LGIB in older adults the diverticular bleed leads. Memorise the order.^[1]

^[1]

Upper GI causes, in descending frequency — reproduce the order:^[1]

1. Peptic ulcer disease (gastric or duodenal) — a third to a half; the single most testable cause.
2. Erosive gastritis or gastropathy (NSAID, alcohol, stress-related mucosal disease) — 15 to 20 percent.
3. Oesophago-gastric varices — 10 to 20 percent overall but disproportionately deadly, the highest single-cause mortality.
4. Mallory-Weiss tear — 5 to 7 percent; retching-induced mucosal tear at the gastro-oesophageal junction.
5. Erosive oesophagitis — about 5 percent.
6. Upper GI malignancy (gastric or oesophageal) — 1 to 5 percent; suspect with weight loss and dyspepsia.
7. Vascular lesions — angiodysplasia, GAVE (watermelon stomach), Dieulafoy, hereditary haemorrhagic telangiectasia — under 5 percent but cause disproportionate massive bleeds.
8. Aortoenteric fistula — under 1 percent but never miss: a prior aortic graft with any GI bleed is a fistula until proven otherwise.^[1]

Lower GI causes, in descending frequency:^[2]

1. Diverticular bleeding — commonest acute LGIB cause in older adults (30 to 40 percent); characteristically painless and often self-limiting.
2. Colonic angiodysplasia — about 20 percent, right-sided (caecum), elderly; associated with aortic stenosis (Heyde syndrome), CKD, HHT.
3. Ischaemic colitis — a watershed-area insult after a low-flow state; left-sided predilection.
4. Inflammatory colitis — ulcerative colitis, Crohn disease; chronic diarrhoea with mucus and pus.
5. Infective colitis — Campylobacter, Salmonella, Shigella, EHEC O157:H7, Clostridioides difficile, amoebic.
6. Neoplasia — colorectal cancer, polyps; occult bleeding with iron-deficiency anaemia and changed bowel habit.
7. Post-polypectomy bleeding — within 1 to 2 weeks of colonoscopy.
8. Anorectal causes — haemorrhoids (painless, blood on the paper), anal fissure (painful defecation), radiation proctitis.^[1]

Risk factors, know the mechanism — examiners ask why each one bleeds:^[1]

• NSAIDs and aspirin inhibit cyclo-oxygenase, stripping the mucosal prostaglandin and mucus-bicarbonate barrier — the dominant iatrogenic cause.
• Antiplatelets and anticoagulants increase bleeding severity rather than causing it.
• Helicobacter pylori drives chronic gastric inflammation and ulceration.
• Critical illness, major trauma, severe burns (Curling ulcer), severe head injury (Cushing ulcer), mechanical ventilation over 48 hours — stress-related mucosal disease.
• Chronic liver disease and portal hypertension — variceal and portal-hypertensive gastropathy bleeding.
• Prior peptic ulcer or prior GI bleed — the highest baseline risk.^[1]

How each lesion bleeds — the mechanism

The peptic ulcer bleeds by eroding a submucosal artery. Two lesions are high-yield because the artery they hit is large: the posterior duodenal ulcer erodes the gastroduodenal artery, and the posterior gastric wall (high lesser-curve) ulcer erodes the left gastric artery. Both are classic causes of massive UGIB.^[1]

The two dominant insults — H. pylori and NSAIDs — converge on the same endpoint of impaired mucosal defence. H. pylori colonises the mucus layer, secretes urease (hydrolysing urea to ammonia to survive), and induces chronic neutrophilic gastritis with interleukin-8, TNF-alpha, and reactive oxygen species. NSAIDs block COX-1, stripping the PGE2 and PGI2 that maintain the mucus-bicarbonate barrier, mucosal blood flow, and epithelial restitution. Stress-related mucosal disease in critical illness (Curling ulcer in burns, Cushing ulcer in head injury) arises from splanchnic hypoperfusion and acid back-diffusion.^[1]

Why blood raises the urea: digested blood protein is broken down to amino acids and absorbed, and the liver converts the amino nitrogen to urea. A raised urea with a normal creatinine is a bedside clue to UGIB — and a favourite viva question.^[1]

Variceal bleeding is the deadliest mechanism because a thin-walled collateral is under high pressure and cannot constrict. Portal hypertension opens the collaterals at the gastro-oesophageal junction into varices. The ESGE thresholds to reproduce:^[9]

• HVPG over 10 mmHg — clinically significant portal hypertension; the threshold at which variceal bleeding risk and prophylaxis decisions turn.
• HVPG over 20 mmHg — marks the high-risk patient in whom pre-emptive TIPS within 72 hours must be considered after an acute variceal haemorrhage.^[9]

The Mallory-Weiss tear is the one with the sequence. A longitudinal mucosal tear at the gastro-oesophageal junction from a sudden rise in intra-abdominal pressure during retching — classically after an alcohol binge, bulimia, hyperemesis gravidarum, or prolonged coughing. The sequence the examiner rewards is retching first, then haematemesis.^[1]

The vascular lesions each carry a teaching hook. Angiodysplasia — ectatic thin-walled submucosal vessels, classically the caecum and right colon in older adults, painless and recurrent. Heyde syndrome is the triad of aortic stenosis, gastrointestinal angiodysplasia, and acquired von Willebrand disease (type 2A) — high-shear flow across the stenotic valve cleaves the large von Willebrand factor multimers needed for platelet adhesion in the high-shear microvasculature, producing both the lesions and the bleeding diathesis; valve replacement may resolve both. GAVE (watermelon stomach) — linear vascular streaks radiating from the pylorus, chronic iron-deficiency anaemia in older women, treated by argon plasma coagulation. Dieulafoy lesion — an aberrant large-calibre submucosal artery in the proximal stomach eroding without an underlying ulcer, causing painless massive haematemesis in an otherwise fit patient.^[1]

Diverticular bleeding is the commonest LGIB mechanism, and its anatomy explains its behaviour. Colonic diverticula are pseudodiverticula (mucosa and submucosa herniating through the muscularis at vessel-entry points). A vasa recta artery running over the dome is exposed at the neck and erodes into the lumen. Despite the left-sided predominance of diverticulosis, right-sided diverticula bleed more often — their necks are wider and the vasa recta more exposed. Characteristically painless haematochezia, with about 80 percent stopping spontaneously and about a quarter rebleeding.^[2]

Ischaemic colitis follows a low-flow state hitting the watershed areas — the splenic flexure (Griffith point) and the rectosigmoid junction (Sudeck point), which sit at the junctions of vascular territories (superior and inferior mesenteric arteries, and inferior mesenteric and internal iliac). The injury ranges from reversible colopathy to gangrene.^[1]

Risk-stratify — GBS at the door, Rockall at the scope

Two scores divide the labour, and using them in the right order is itself a viva answer. The Glasgow-Blatchford Score uses only pre-endoscopy variables and triages at the front door; the Rockall adds the endoscopic findings and predicts mortality.^[1]

Glasgow-Blatchford Score — pre-endoscopy, predicts the need for intervention

The GBS is the front-door score because it needs no endoscopy. A score of 0 identifies patients who may be managed as outpatients; a score of 1 or more means inpatient endoscopy.^[3]

^[1]

Score range 0 to 23. A score of 0 means consider outpatient management with a low threshold for safety-net review; 7 or more flags a high risk of needing intervention (transfusion, endoscopic therapy, surgery). The GBS is more sensitive than Rockall for identifying low-risk patients safe for discharge; its weakness is low specificity — many low-GBS patients are still admitted.^[1]

Rockall — with endoscopy, predicts mortality and rebleeding

The pre-endoscopy Rockall can be done at the front door; the full Rockall adds the endoscopic component.^[4]

Pre-endoscopy Rockall:^[1]

^[1]

Endoscopic additions (full Rockall):^[1]

^[1]

A full Rockall of 0 carries very low mortality and rebleeding risk; 3 or more is high risk, with rebleeding and mortality rising steeply. The Rockall is better at predicting death than the GBS but needs endoscopy and is less useful for triage.^[1]

AIMS-65 — predicts in-hospital mortality

The five admission factors, each scoring 1 (maximum 5): Albumin under 3.0 g/dL; INR over 1.5; altered Mental status; Systolic blood pressure 90 mmHg or lower; age over 65. The score predicts in-hospital mortality — in the derivation cohort, mortality was 0.3% with no risk factors and 31.8% with all five.^[10]

Forrest classification — the endoscopic stigmata that decide therapy

The Forrest classification is the single most reproduced endoscopic table in GI bleeding exams. It grades the stigmata of recent haemorrhage in a peptic ulcer and directly dictates whether you treat:^[1]

^[1]

High-risk ulcers (Forrest Ia, Ib, IIa) get endoscopic therapy plus the post-haemostasis PPI infusion; low-risk ulcers (Forrest IIc, III) need no endoscopic therapy and can be considered for early discharge on oral PPI.^[1]

Investigations — bloods, scope, and the angiography fork

The immediate blood panel does three jobs: quantify the loss, localise the source indirectly, and guide reversal.^[1]

• Full blood count — haemoglobin (may be normal initially; trend it serially); MCV low points to chronic occult loss; platelets low flags portal hypertension.
• Urea and creatinine — a raised urea with a normal creatinine points to UGIB (digested blood protein converted to urea); a raised creatinine is AKI from hypovolaemia or hepatorenal syndrome.
• LFTs and albumin — deranged LFTs and low albumin flag chronic liver disease and a variceal risk (Child-Pugh and MELD are the risk-stratification tools in suspected variceal bleeding).
• Coagulation (PT/INR, APTT, fibrinogen) — raised INR means cirrhosis, warfarin, or DIC; guides reversal.
• Group and save or crossmatch — crossmatch the unstable patient; DOAC and warfarin levels guide the reversal agent.
• Venous gas and lactate — acidosis and raised lactate signal hypoperfusion.^[1][9]

Endoscopy and radiology, by the question being asked:^[1]

• OGD — first-line for UGIB, diagnostic and therapeutic; within 24 hours of presentation, and within 12 hours where variceal haemorrhage is suspected (after resuscitation).^[1][9]
• Erythromycin 250 mg IV, 30 to 120 minutes before OGD — a prokinetic that clears intragastric blood and clots and improves the view and yield; ACG suggests erythromycin infusion before endoscopy, and the RCT evidence showed better stomach cleansing and visualisation.^[1][9][11]
• Colonoscopy — for the admitted LGIB patient ACG recommends a nonurgent colonoscopy; an urgent colonoscopy within 24 hours has not been shown to improve outcomes such as rebleeding.
• CT angiography — an increasing role in severe LGIB: ACG highlights CTA for severe bleeds and gives management guidance for a positive CTA.^[2]

The UGIB definitive bundle — combination therapy, then the PPI infusion^[1]

A high-risk bleeding ulcer gets three things at endoscopy, in this order: adrenaline, a mechanical or thermal method, then the 72-hour PPI infusion. The recurring trainee error is adrenaline alone.^[1]

• Combination therapy — adrenaline (epinephrine) 1:10 000 injection in four quadrants around the bleeding point PLUS a mechanical or thermal method (through-the-scope clip, heater probe, bipolar electrocoagulation, argon plasma coagulation). Adrenaline alone is inferior to combination therapy and carries higher rebleeding.
• Adherent clot (Forrest IIb) — consider removing the clot to expose the lesion, then treat the visible vessel.
• Low-risk ulcers (Forrest IIc, III) — no endoscopic therapy; oral PPI.^[1]

Post-haemostasis, the PPI infusion is the dose every candidate must reproduce verbatim.^[6]

^{[6] [8]}

The Lau 2000 NEJM trial established this regimen with omeprazole — an 80 mg bolus then 8 mg/hour for 72 hours after successful endoscopic haemostasis reduced recurrent bleeding within 30 days (6.7% vs 22.5%) — and Sung 2009 confirmed it with esomeprazole (rebleeding within 72 hours 5.9% vs 10.3%). After the infusion, the trials continued with oral omeprazole 20 mg/day for eight weeks (Lau) or oral esomeprazole 40 mg/day for 27 days (Sung); ACG recommends high-dose PPI for 3 days after haemostasis, then twice-daily oral PPI for the first 2 weeks after endoscopy.^[6][8][1]

After successful haemostasis, two follow-up steps prevent recurrence: test and treat Helicobacter pylori (urea breath test or stool antigen at 4 weeks — biopsy-based tests are unreliable in acute bleeding and on a PPI), and continue the oral PPI while addressing ongoing risks (stop NSAIDs, alcohol advice, anticoagulation review). Eradication of H. pylori prevents rebleeding.^[1]

Lesion-specific endoscopic therapy:^[1]

• Mallory-Weiss tear — usually self-limiting; clip or thermal therapy if actively bleeding.
• Dieulafoy lesion — endoscopic clip, band ligation, or thermal coagulation.
• GAVE — repeated argon plasma coagulation; refractory cases use oral iron, thalidomide, or antrectomy.
• Angiodysplasia — argon plasma coagulation; treat the trigger (aortic valve replacement in Heyde syndrome).
• Upper-GI malignancy — palliative endoscopic therapy (argon plasma, self-expanding metal stent); definitive oncology or surgery.
• Aortoenteric fistula — surgical emergency, not endoscopy first; vascular surgery for graft repair.^[1]

If endoscopy fails or rebleeds, escalate without watching the patient bleed into the night. A repeat endoscopy (second-look) is reasonable for rebleeding; beyond that, surgical or radiological rescue — under-running of the bleeding vessel (the gastroduodenal artery), partial gastrectomy, or mesenteric angiographic embolisation.^[1]

The variceal bundle — start at first suspicion, do not wait for the scope

In any suspected variceal bleed, the vasoactive drug and the antibiotic are started at the time of presentation — before endoscopy confirms varices. This is the bundle that separates a pass from a fail.^[9]

• Vasoactive drug — terlipressin, octreotide, or somatostatin, started at presentation and continued for up to 5 days. Watch for ischaemia and hyponatraemia with terlipressin.^[9]
• Antibiotic prophylaxis — ceftriaxone 1 g/day IV for up to 7 days for all patients with advanced chronic liver disease and acute variceal haemorrhage (adjusted to local resistance and allergies). In advanced cirrhosis with gastrointestinal haemorrhage, IV ceftriaxone was more effective than oral norfloxacin at preventing proved or possible infection (11% vs 33%) and spontaneous bacteraemia or peritonitis (2% vs 12%).^[9][13]
• Endoscopic therapy — endoscopic band ligation (EBL) for acute oesophageal variceal haemorrhage; cyanoacrylate injection for acute gastric cardiofundal variceal bleeding. Endoscopic evaluation within 12 hours of presentation, once resuscitated.^[9]
• Restrictive transfusion — threshold at or under 7 g/dL, with a post-transfusion target of 7 to 9 g/dL.^[9]
• Rescue and pre-emptive TIPS — for persistent bleeding despite vasoactive plus endoscopic therapy, urgent rescue TIPS. Pre-emptive TIPS within 72 hours (preferably within 24) for high-risk patients: Child-Pugh C at or under 13, Child-Pugh B over 7 with active bleeding despite vasoactive drugs, or HVPG over 20 mmHg. The early-TIPS RCT in these high-risk patients cut failure to control bleeding or rebleeding (1 vs 14 patients) and death (4 vs 12).^[9][12]

^{[9] [9]}

Reversing anticoagulation — by agent

Assess and reverse per agent, weighing bleeding against thrombotic risk.^[2]

• Warfarin (vitamin K antagonist) — reverse with four-factor prothrombin complex concentrate (4F-PCC); compared with plasma it gave faster access to the GI procedure in VKA-associated GI bleeding. ACG addresses reversal agents for life-threatening LGIB on vitamin K antagonists and DOACs.^[17][2]
• Dabigatran — idarucizumab (5 g IV as two 2.5 g boluses): in RE-VERSE AD patients with major GI bleeding it reversed dabigatran activity rapidly and completely in nearly all, with bleeding cessation within 24 hours in 68.7%.^[14]
• Apixaban, rivaroxaban, edoxaban (factor Xa inhibitors) — andexanet alfa (80% excellent or good haemostasis in the ANNEXA-4 final report); where cost or availability limits it, 4F-PCC achieved 73% haemostatic efficacy in factor-Xa-inhibitor GI bleeding.^[15][16]
• Antiplatelets — ACG gives updated recommendations on resuming antiplatelet and anticoagulant medication after LGIB cessation; hold and liaise with cardiology when a recent coronary stent is in play.^[2]

The never-miss mimics — three lesions that hide

Three lesions are disproportionately lethal because they are missed. Name each, and the single discriminator that exposes it.^[1]

• Aortoenteric fistula — a prior aortic graft or aneurysm repair with any GI bleed, often a "herald" small self-limiting bleed days before an exsanguinating one. Surgical emergency, not endoscopy first — endoscopy may miss the fistula in the duodenum. The discriminator: the graft history.
• Dieulafoy lesion — painless, massive haematemesis in an otherwise fit patient; an aberrant large-calibre submucosal artery, usually the proximal stomach along the lesser curve, with no underlying ulcer. The discriminator: the otherwise-well patient and the absence of an ulcer.
• Heyde syndrome — aortic stenosis with angiodysplasia and acquired von Willebrand disease (type 2A); high-shear flow cleaves the large vWF multimers. The discriminator: the aortic stenosis murmur; valve replacement may resolve the bleeding.^[1]

Lower GI bleeding — the colonoscopy-versus-angiography fork

After resuscitation, LGIB forks on haemodynamic stability.^[2]

• Stable patient (bleeding stopped or small-volume) — ACG recommends a nonurgent colonoscopy for most patients requiring inpatient colonoscopy; an urgent colonoscopy within 24 hours has not been shown to improve rebleeding or other outcomes. Colonoscopy is diagnostic and therapeutic.
• Severe or ongoing LGIB — CT angiography, whose role ACG now emphasises in severe LGIB, localises the source and guides transcatheter embolisation; ACG also sets management for a positive CTA.^[2]

How GI bleed patients come to harm — the preventable list

• A brisk UGIB labelled LGIB because the blood was fresh per rectum — the OGD is delayed and the duodenal ulcer keeps bleeding.^[1]
• Over-transfusion of a variceal bleed raising portal pressure and worsening the bleeding (Villanueva).^[5]
• Antibiotics omitted in a cirrhotic with a variceal bleed — ceftriaxone prophylaxis is a strong recommendation, and the trials show fewer infections with it.^[9][13]
• Adrenaline alone for a bleeding ulcer — rebleeding that combination therapy would have prevented.^[1]
• An aortoenteric fistula sent for endoscopy instead of vascular surgery.^[1]
• Aspiration in active haematemesis because the airway was not protected early.^[1]
• Rebleeding in the first 72 hours missed because the patient was not monitored or kept on the PPI infusion.^[6]
• H. pylori never tested or treated after an ulcer bleed — recurrence.^[1]

The trials and scores that set the standard

^{[5] [6] [8] [12]}

The scores carry their own citation. Rockall (Gut 1996) derived and validated the mortality and rebleeding score; Blatchford (Lancet 2000) derived the pre-endoscopy score that identifies low-risk patients safe for outpatient care; AIMS65 (Saltzman, Gastrointest Endosc 2011) predicts in-hospital mortality from five admission variables; ESGE (Endoscopy 2022) sets the current variceal bundle — vasoactive drugs, ceftriaxone, erythromycin, 12-hour endoscopy, band ligation, and pre-emptive TIPS.^{[3][4][10][9]}

Special populations — what changes

Cirrhosis or variceal bleed. Resuscitate with a restrictive transfusion (threshold at or under 7 g/dL, post-transfusion target 7 to 9 g/dL), start a vasoactive agent (terlipressin, octreotide, or somatostatin) plus ceftriaxone 1 g/day at presentation, and move to endoscopy within 12 hours for band ligation (cyanoacrylate for gastric varices). If bleeding persists, urgent rescue TIPS; in high-risk patients (Child-Pugh C at or under 13, Child-Pugh B over 7 with active bleeding, or HVPG over 20 mmHg) consider pre-emptive TIPS within 72 hours. Risk-stratify with Child-Pugh and MELD.^[9][12]

Anticoagulated or antiplatelet patients. Reverse the life-threatening bleed per agent: 4F-PCC for warfarin (faster to GI procedure than plasma), idarucizumab for dabigatran, andexanet alfa (or 4F-PCC where it is unavailable) for factor Xa inhibitors. Hold antiplatelets with cardiology input if there is a recent stent — do not reflexively stop all agents forever after an ulcer bleed without balancing stent-thrombosis risk; ACG sets updated recommendations on resuming antiplatelet and anticoagulant therapy after bleeding stops.^{[17][14][15][16][2]}

The elderly. Aortic stenosis with recurrent GI bleed raises Heyde syndrome (acquired von Willebrand from shear). Diverticular LGIB is common. Lower physiological reserve means early senior review.^[1]

Pregnancy. Physiological plasma expansion masks early loss; variceal bleed risk rises in portal hypertension. Manage as for the non-pregnant: ABC, restrictive transfusion, urgent OGD (safe with left lateral tilt and pulse oximetry); prefer the left lateral position to avoid aortocaval compression. Avoid NSAIDs.^[1]

CKD or dialysis. Higher bleed risk from uraemic platelet dysfunction; time endoscopy with the dialysis plan; desmopressin is sometimes used peri-procedure in uraemic bleeding under specialist advice.^[1]

The mantra

The mantra: resuscitate before you scope, restrict the transfusion, combine the therapy, and give the antibiotic and the vasoactive drug at first suspicion of a variceal bleed.^[1][5][9]

Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)ShowHide

The 64-year-old on ibuprofen who vomited fresh blood, heart rate 118, blood pressure 92/58, with melaena for two days. What is your first 30 minutes? Model: This is a major upper GI bleed — resuscitate before the scope. Airway (intubate only if unprotected), high-flow oxygen, two large-bore peripheral cannulae, bloods including group and crossmatch, balanced crystalloid, and a restrictive transfusion strategy — transfuse when the haemoglobin falls below 7 g/dL. Crossmatch because he is haemodynamically compromised. Stop the NSAID. Calculate the Glasgow-Blatchford — it will be high. Admit to a monitored bed and book OGD within 24 hours; give erythromycin 250 mg IV beforehand. The likely source is a peptic ulcer; if it is a high-risk Forrest ulcer, plan adrenaline injection plus a mechanical or thermal method plus the 72-hour omeprazole infusion, then continue the oral PPI.^{[1][5][6][11]}

Stem 2 — the cirrhotic with massive haematemesis (answer)ShowHide

A 58-year-old with alcoholic cirrhosis presents with massive haematemesis, heart rate 120, blood pressure 85/50. What do you start before the endoscopy? Model: This is a suspected variceal bleed, and the bundle starts at first suspicion — do not wait for endoscopy to confirm varices. Start a vasoactive agent (terlipressin, octreotide, or somatostatin) at presentation for up to 5 days, give ceftriaxone 1 g IV daily for up to 7 days (antibiotic prophylaxis to all patients with advanced chronic liver disease and acute variceal haemorrhage — it prevents infection), protect the airway (intubate early if encephalopathic), resuscitate with a restrictive transfusion strategy (threshold at or under 7 g/dL; post-transfusion target 7 to 9 g/dL — over-transfusion raised the portal-pressure gradient in the liberal arm of the trial), correct coagulopathy carefully, and admit to ICU. Book endoscopy within 12 hours for band ligation (cyanoacrylate glue for gastric cardiofundal varices). If bleeding persists despite vasoactive and endoscopic therapy, urgent rescue TIPS; consider pre-emptive TIPS within 72 hours if Child-Pugh C at or under 13, Child-Pugh B over 7 with active bleeding, or HVPG over 20 mmHg.^{[9][13][5][12]}

Stem 3 — the prior aortic graft with a herald bleed (answer)ShowHide

A 72-year-old man who had an abdominal aortic aneurysm repair three years ago presents with a small, self-limiting episode of melaena. He is now stable. What must you not do, and what must you do? Model: This is an aortoenteric fistula until proven otherwise — a prior aortic graft with any GI bleed is the classic setup, and the small herald bleed can precede an exsanguinating haemorrhage within days. Do not rely on endoscopy first — OGD may miss the fistula in the duodenum, and the diagnosis is not excluded by a negative scope. Do involve vascular surgery urgently for CT angiography and graft repair or excision. Sending this patient for a routine OGD and discharge is the preventable death.^[1]

References17ShowHide

1. [1]Laine L, Barkun AN, Saltzman JR, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding Am J Gastroenterol, 2021.PMID 33929377
2. [2]Sengupta N, Feuerstein JD, Jairath V, et al. Management of Patients With Acute Lower Gastrointestinal Bleeding: An Updated ACG Guideline Am J Gastroenterol, 2023.PMID 36735555
3. [3]Blatchford O, Murray WR, Blatchford S. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage Lancet, 2000.PMID 11073021
4. [4]Rockall TA, Logan RF, Devlin HB, Northfield TC. Risk assessment after acute upper gastrointestinal haemorrhage Gut, 1996.PMID 8675081
5. [5]Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding N Engl J Med, 2013.PMID 23281973
6. [6]Lau JY, Sung JJ, Lee KK, et al. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers N Engl J Med, 2000.PMID 10922420
7. [7]de Franchis R, Bosch J, Garcia-Tsao G, et al. Baveno VII - Renewing consensus in portal hypertension J Hepatol, 2022.PMID 35120736
8. [8]Sung JJ, Barkun A, Kuipers EJ, et al. Intravenous esomeprazole for prevention of recurrent peptic ulcer bleeding: a randomized trial Ann Intern Med, 2009.PMID 19221370
9. [9]Gralnek IM, Camus Duboc M, Garcia-Pagan JC, et al. Endoscopic diagnosis and management of esophagogastric variceal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline Endoscopy, 2022.PMID 36174643
10. [10]Saltzman JR, Tabak YP, Hyett BH, et al. A simple risk score accurately predicts in-hospital mortality, length of stay, and cost in acute upper GI bleeding Gastrointest Endosc, 2011.PMID 21907980
11. [11]Carbonell N, Pauwels A, Serfaty L, et al. Erythromycin infusion prior to endoscopy for acute upper gastrointestinal bleeding: a randomized, controlled, double-blind trial Am J Gastroenterol, 2006.PMID 16771939
12. [12]García-Pagán JC, Caca K, Bureau C, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding N Engl J Med, 2010.PMID 20573925
13. [13]Fernández J, Ruiz del Arbol L, Gómez C, et al. Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and hemorrhage Gastroenterology, 2006.PMID 17030175
14. [14]Van der Wall SJ, Lopes RD, Aisenberg J, et al. Idarucizumab for Dabigatran Reversal in the Management of Patients With Gastrointestinal Bleeding Circulation, 2019.PMID 30586692
15. [15]Milling TJ, Middeldorp S, Xu L, et al. Final Study Report of Andexanet Alfa for Major Bleeding With Factor Xa Inhibitors Circulation, 2023.PMID 36802876
16. [16]Shamiea M, Kashua A, Natour AE, et al. Prothrombin complex concentrate for reversal of factor Xa inhibitor-associated acute major gastrointestinal bleeding Am J Med, 2026.PMID 41554493
17. [17]Spector H, McRae HL, Love T, et al. Reduced Time to Procedure for Gastrointestinal Bleeding After Warfarin Reversal With Four-Factor Complex Concentrate as Compared to Plasma J Clin Med Res, 2023.PMID 36755762