Summary

Upper gastrointestinal bleeding (UGIB) is defined as bleeding originating proximal to the ligament of Treitz, encompassing the oesophagus, stomach, and duodenum. It is a common medical emergency with significant morbidity and mortality, accounting for approximately 50-100 hospital admissions per 100,000 population annually. The clinical presentation ranges from occult bleeding with iron deficiency anaemia to life-threatening haemorrhage with haemodynamic collapse. UGIB is classified as variceal (15-20%) or non-variceal (80-85%), with the latter predominantly caused by peptic ulcer disease (35-50%), erosive disease (15-25%), and Mallory-Weiss tears (5-15%). Management requires rapid assessment, resuscitation, risk stratification using validated scores (Glasgow-Blatchford, Rockall), and endoscopic intervention within 24 hours for most patients. Mortality has improved significantly with advances in endoscopic therapy, proton pump inhibitors, and organised multidisciplinary care, but remains 6-14% overall and up to 20-30% for variceal bleeding. [1,2,3]

Key Facts

• Definition: Bleeding from a source proximal to the ligament of Treitz (oesophagus, stomach, duodenum)
• Incidence: 50-150 per 100,000 population per year [PMID: 31884016]
• Mortality: Overall 6-14%; variceal bleeding 15-30% [PMID: 29653741]
• Peak Demographics: Elderly (70% are >60 years); Male:Female 2:1
• Commonest Cause: Peptic ulcer disease (35-50% of non-variceal)
• Most Dangerous: Variceal bleeding (highest mortality)
• Pathognomonic Feature: Haematemesis (fresh or coffee-ground) ± melaena
• Gold Standard Investigation: Oesophagogastroduodenoscopy (OGD)
• First-line Treatment: Resuscitation, PPI, endoscopic haemostasis
• Prognosis Summary: Re-bleeding 5-15%; 30-day mortality ~5-10%

Clinical Pearls

Diagnostic Pearl: Melaena indicates at least 50-100mL blood loss and blood has been in the GI tract for >8 hours. Haematochezia usually indicates lower GI source UNLESS patient is haemodynamically unstable (then consider massive upper GI bleed).

Examination Pearl: A rectal examination is MANDATORY - fresh blood on PR with haemodynamic instability often indicates massive upper GI bleed, not lower GI bleed.

Treatment Pearl: PPI infusion (omeprazole 80mg bolus then 8mg/hr for 72 hours) reduces re-bleeding rate after endoscopic therapy - give AFTER endoscopy confirms high-risk stigmata, not before.

Pitfall Warning: Normal NG aspirate does NOT exclude upper GI bleeding - up to 15% of duodenal bleeds have negative NG aspirate due to pyloric closure.

Mnemonic: Causes of UGIB: VOMITED - Varices, Oesophagitis, Mallory-Weiss, Iatrogenic (drugs), Tumour, Erosions, Duodenal/gastric ulcer.

Why This Matters Clinically

Upper GI bleeding is one of the most common GI emergencies encountered in acute medicine. Rapid recognition and appropriate management can be life-saving - delays in resuscitation or endoscopy significantly increase mortality. The condition is increasingly relevant as population ages and anticoagulant/antiplatelet prescribing rises. For examinations, UGIB is a favourite acute scenario testing resuscitation, risk stratification (Glasgow-Blatchford vs Rockall), endoscopic findings interpretation, and management of both variceal and non-variceal causes. Medico-legally, failure to perform timely endoscopy, inadequate resuscitation, or delayed senior involvement in unstable patients are common pitfalls. [4,5]

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Structured Approach

General Appearance:

• Level of consciousness (AVPU or GCS)
• Pallor (conjunctival, palmar creases)
• Distress, diaphoresis
• Evidence of chronic liver disease (see below)

Vital Signs - PRIORITY:

• Pulse: Rate (tachycardia >100), rhythm (AF common in elderly)
• Blood pressure: Hypotension (<100 systolic), postural drop (>20mmHg)
• Respiratory rate: Tachypnoea (compensatory, metabolic acidosis)
• Oxygen saturation: May be reduced with shock
• Temperature: Fever suggests infection (SBP, aspiration)
• Urine output: Catheterise if in shock

Cardiovascular:

• Heart sounds, murmurs (chronic anaemia → flow murmur)
• JVP: Low with hypovolaemia; high may indicate cardiac failure
• Peripheral perfusion: CRT, temperature, pulses

Abdominal Examination:

• Inspection: Distension, scars, caput medusae
• Tenderness: Epigastric (PUD), generalised (perforation)
• Masses: Gastric cancer, pancreatic mass
• Organomegaly: Hepatomegaly, splenomegaly (portal HTN)
• Ascites: Shifting dullness (cirrhosis)

Rectal Examination - ESSENTIAL:

• Stool colour: Melaena (black, tarry, offensive), fresh blood, normal
• Masses: Rectal cancer (separate issue)

Signs of Chronic Liver Disease:

• Jaundice
• Spider naevi
• Palmar erythema
• Gynaecomastia
• Testicular atrophy
• Ascites
• Hepatic encephalopathy (flapping tremor, confusion)
• Caput medusae

Special Tests

Assessment	Technique	Positive Finding	Clinical Significance
Postural BP	Lying then standing for 2 min	SBP drop >20mmHg or HR rise >20	Significant volume depletion
Rectal examination	Insert gloved finger, examine stool	Black, tarry stool (melaena)	Confirms GI bleeding
Tilt test	As per postural BP	As above	Alternative method
JVP assessment	45° head elevation	Low JVP	Hypovolaemia
CRT	Blanch nailbed 5 seconds	>3 seconds to refill	Poor peripheral perfusion

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Natural History

Without treatment, mortality from acute UGIB would approach 30-40%. Even with modern management, overall mortality remains 6-14%, reflecting the elderly, comorbid population affected. Re-bleeding is the most important predictor of mortality - patients who re-bleed have 10x higher mortality than those who don't.

Outcomes with Treatment

Variable	Outcome
Overall 30-day mortality	6-14%
Variceal bleeding mortality	15-30%
Non-variceal bleeding mortality	5-10%
6-week mortality (varices)	20-40%
Re-bleeding rate	5-15% (non-variceal); 60-70% (variceal without treatment)
Need for surgery	<5% (declining with improved endoscopy)
ICU admission rate	10-20%
Length of stay	Median 3-5 days

Prognostic Factors

Good Prognosis:

• Young age (<60 years)
• No comorbidities
• Haemodynamically stable
• Mallory-Weiss tear (low re-bleed rate)
• Forrest III (clean base ulcer)
• Low Rockall score (≤2)
• Successful endoscopic therapy
• No coagulopathy

Poor Prognosis:

• Elderly (>80 years)
• Comorbidities (CCF, CKD, liver disease, malignancy)
• Haemodynamic instability at presentation
• Variceal bleeding
• Forrest Ia (spurting arterial bleeding)
• High Rockall score (≥6)
• Failed endoscopic therapy
• Malignancy as cause
• Anticoagulant use
• In-hospital bleeding (worse than community-onset)

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Key Guidelines

1. NICE NG141: GI Bleeding (2020) — UK guidance on assessment, resuscitation, endoscopy timing, transfusion thresholds. NICE [PMID: 32436678]

2. BSG Guidelines on UGIB (2019) — Comprehensive UK guidelines including risk stratification, endoscopic therapy, variceal bleeding. [PMID: 31072838]

3. ESGE Guidelines (2021) — European recommendations on non-variceal UGIB management. [PMID: 33567467]

4. AASLD Variceal Bleeding Guidelines (2017) — US guidance on variceal haemorrhage management. [PMID: 28151840]

5. ACG Guidelines on UGIB (2021) — American College of Gastroenterology recommendations. [PMID: 34091671]

Landmark Trials

HALT-IT (2020) — Tranexamic acid in GI bleeding

• 12,009 patients with UGIB or LGIB
• Tranexamic acid vs placebo
• No reduction in death from bleeding (HR 0.99); increased VTE risk
• Clinical Impact: Tranexamic acid NOT recommended for GI bleeding
• [PMID: 32563378]

TRIGGER (2015) — Restrictive vs liberal transfusion in UGIB

• 936 patients randomised
• Hb trigger <80g/L (restrictive) vs <100g/L (liberal)
• Favored restrictive strategy (lower mortality, fewer transfusions)
• Clinical Impact: Target Hb 70-90g/L; avoid over-transfusion
• [PMID: 25539052]

UK Audit (2007) — National UGIB audit

• 6,750 patients
• Identified delays in endoscopy as key contributor to mortality
• Clinical Impact: Drove improvements in out-of-hours endoscopy services
• [PMID: 17646574]

Sung et al (2007) — IV PPI after endoscopic therapy

• 767 patients with high-risk ulcer stigmata
• IV esomeprazole vs placebo
• 6.7% vs 22.5% re-bleeding at 72 hours
• Clinical Impact: High-dose IV PPI after endoscopy is standard of care
• [PMID: 17210879]

Villanueva et al (2013) — Restrictive transfusion in UGIB

• 921 patients with acute UGIB
• Hb trigger <70g/L vs <90g/L
• 45-day mortality 5% vs 9% (favoured restrictive)
• Clinical Impact: Restrictive transfusion improves outcomes
• [PMID: 23281973]

Evidence Strength

Intervention	Level	Key Evidence
Restrictive transfusion (Hb <70-80)	1a	TRIGGER, Villanueva
Early endoscopy (<24h)	1b	Multiple observational, NICE guidance
IV PPI post-endoscopy	1a	Sung et al, Cochrane reviews
Endoscopic dual therapy	1a	Cochrane review
Terlipressin for varices	1a	Cochrane review
Band ligation for O varices	1a	Multiple RCTs
TIPS for refractory varices	1b	Early TIPS trials
Tranexamic acid	1a	HALT-IT (NO benefit)

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What is Upper GI Bleeding?

Upper gastrointestinal (GI) bleeding means bleeding from somewhere in the upper part of your digestive system - the oesophagus (food pipe), stomach, or first part of the small intestine (duodenum). This can be a serious emergency if a lot of blood is lost quickly.

The blood might come out as vomit (which can be red or look like coffee grounds) or in your stools (which turn black and sticky like tar - called melaena).

Why does it happen?

The most common causes are:

• Stomach ulcers or duodenal ulcers: Open sores that erode into blood vessels
• Varices: Swollen veins in the oesophagus that can burst (usually due to liver disease)
• Gastritis: Inflammation of the stomach lining from medications (like ibuprofen) or infection
• Mallory-Weiss tear: A small tear in the food pipe caused by forceful vomiting

How is it treated?

1. Fluids and blood: If you've lost a lot of blood, you'll receive fluids through a drip and possibly blood transfusions to replace what you've lost.

2. Camera test (endoscopy): A thin tube with a camera is passed down your throat to find where the bleeding is coming from and treat it at the same time.

3. Medications: Acid-suppressing drugs (like omeprazole) help ulcers heal. Other medications can help reduce blood flow to the bleeding area.

4. Surgery: Rarely needed, only if the bleeding can't be stopped with other treatments.

What to expect

• You'll be kept nil by mouth until the camera test is done
• You may need to stay in hospital for a few days
• You'll likely go home on acid-suppressing tablets for several weeks
• Follow-up tests may be needed to check for infection (H. pylori) or ensure healing

When to seek help

Call 999 or go to A&E immediately if you:

• Vomit blood (red or dark/coffee-ground)
• Pass black, tarry stools
• Feel faint, dizzy, or like you might pass out
• Have fast heartbeat or feel confused
• Have severe stomach pain

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Common Exam Questions

Questions that frequently appear in examinations:

1. MRCP Part 1: "A 58-year-old man presents with melaena and a Hb of 65g/L. His Rockall score is 4. What is the most appropriate transfusion target?"

2. MRCP Part 2/PACES: "Describe the Forrest classification and its prognostic significance"

3. MRCP Scenarios: "A cirrhotic patient presents with haematemesis. What is your immediate management?"

4. MCQ: "Which of the following is NOT a component of the Glasgow-Blatchford Score?" (Answer: Age - only Rockall includes age)

5. Viva: "Discuss the evidence for tranexamic acid in upper GI bleeding"

Viva Points

Opening Statement:

"Upper gastrointestinal bleeding is defined as bleeding proximal to the ligament of Treitz and is classified as variceal or non-variceal. It is a common emergency with 6-14% mortality. Management involves rapid resuscitation with restrictive transfusion, risk stratification using Glasgow-Blatchford score, and endoscopy within 24 hours. Peptic ulcer bleeding is treated with endoscopic dual therapy and IV PPI; variceal bleeding requires terlipressin, antibiotics, and band ligation."

Key Facts to Mention:

• Incidence 50-150 per 100,000; mortality 6-14%
• 80-85% non-variceal (PUD most common), 15-20% variceal
• GBS 0 = low risk, can consider outpatient management
• Transfuse if Hb <70g/L (restrictive strategy improves outcomes)
• Endoscopy within 24 hours (12 hours if variceal)

Classification to Quote:

• "Forrest classification predicts re-bleeding risk: Ia/Ib are active bleeding requiring treatment; IIa (visible vessel) has 50% re-bleed risk; III (clean base) has <5% risk"
• "Glasgow-Blatchford is pre-endoscopy; Rockall is post-endoscopy"

Evidence to Cite:

• "Villanueva et al showed restrictive transfusion (Hb trigger <70) reduced mortality vs liberal transfusion in UGIB"
• "HALT-IT trial showed tranexamic acid provides NO mortality benefit in GI bleeding"
• "Sung et al demonstrated IV PPI after endoscopy reduces re-bleeding by 60-70%"

Structured Answer Framework:

1. Definition and Epidemiology (30 seconds)
2. Causes - Variceal vs Non-Variceal (30 seconds)
3. Clinical Presentation (30 seconds)
4. Risk Stratification (45 seconds)
5. Management - Resuscitation & Endoscopy (60 seconds)
6. Prognosis (15 seconds)

Common Mistakes

What fails candidates:

• ❌ Not knowing the difference between GBS and Rockall scores
• ❌ Over-transfusing (trigger Hb should be <70-80, not <100)
• ❌ Forgetting terlipressin and antibiotics for variceal bleeding
• ❌ Not knowing the Forrest classification
• ❌ Recommending tranexamic acid (HALT-IT showed no benefit)
• ❌ Confusing variceal and non-variceal management

Dangerous Errors to Avoid:

• ⚠️ Delaying endoscopy in unstable patient
• ⚠️ Ignoring haemodynamic instability
• ⚠️ Forgetting to reverse anticoagulation in active bleeding
• ⚠️ Not involving senior team early for variceal bleeding

Outdated Practices (Do NOT mention):

• Tranexamic acid for GI bleeding — HALT-IT showed no benefit
• Liberal transfusion targets (Hb <100) — Increases mortality
• Routine NG tube insertion — Does not improve outcomes
• H2-receptor antagonists — PPIs are superior

Examiner Follow-Up Questions

Expect these follow-up questions:

1. "What is the Glasgow-Blatchford score used for?"

   • Answer: Pre-endoscopy risk stratification. Predicts need for intervention. Score of 0 identifies very low-risk patients who may be managed as outpatients.

2. "How would you manage anticoagulated patient with GI bleeding?"

   • Answer: Withhold anticoagulant. Warfarin: IV vitamin K 5-10mg + PCC if INR >5 or severe bleeding. DOAC: consider specific reversal (idarucizumab for dabigatran, andexanet for factor Xa inhibitors) if life-threatening. Resume anticoagulation when safe - timing depends on indication and bleeding risk.

3. "What is the evidence for PPI therapy in UGIB?"

   • Answer: Pre-endoscopy PPI does not reduce mortality or re-bleeding. POST-endoscopy high-dose IV PPI (80mg bolus + 8mg/hr x 72h) significantly reduces re-bleeding (Sung et al - 6.7% vs 22.5%). Give AFTER endoscopy confirms high-risk stigmata.

4. "When would you consider TIPS?"

   • Answer: For refractory variceal bleeding after failed endoscopic therapy (2 attempts). Also consider early/pre-emptive TIPS in high-risk cirrhotic patients (Child-Pugh B with active bleeding or C<14) within 72 hours - evidence from early TIPS trials.

5. "What are the components of the Rockall score?"

   • Answer: Age (0-2), Shock status (0-2), Comorbidity (0-3), Endoscopic diagnosis (0-2), Major stigmata of recent haemorrhage (0-2). Maximum 11 points. Score ≤2 low risk; ≥8 high risk.

6. "How do you differentiate upper from lower GI bleeding clinically?"

   • Answer: UGIB: Haematemesis (fresh/coffee-ground), melaena; raised urea:creatinine ratio (>100). LGIB: Fresh PR bleeding (haematochezia), normal urea. BUT: Massive UGIB can present with haematochezia + shock. PR exam essential in all GI bleeds.

7. "What is the difference between Type 1 and Type 2 gastric ulcers?"

   • Answer: Johnson classification: Type I (lesser curve, not acid-related), Type II (body + duodenal, acid-related), Type III (prepyloric, acid-related), Type IV (high lesser curve near GEJ). Types II-III have high acid; Type I low acid.

8. "Describe the management of a Dieulafoy lesion"

   • Answer: Rare cause (~1-2% UGIB). Large submucosal artery with minimal ulceration. High re-bleed risk. Endoscopic therapy: mechanical clips preferred (more durable), adrenaline injection, APC. May require repeat endoscopy or surgery/angioembolisation if refractory.

Additional Viva Scenarios

Scenario 1: Unstable Variceal Bleeding

"A 52-year-old man with known alcohol-related cirrhosis (Child-Pugh B) presents with massive haematemesis. He is confused, BP 85/50, HR 125, cold and clammy. What is your management?"

Structured Answer:

1. Airway: This patient is confused with massive haematemesis - high aspiration risk. Call anaesthetics for potential intubation before endoscopy. Left lateral position while waiting.

2. Breathing/Circulation: High-flow oxygen. 2x large bore IV access. Bloods urgently including crossmatch 6 units. Crystalloid initially (avoid >2L), transfuse to Hb 70-80g/L. This is variceal until proven otherwise.

3. Specific therapy:

   • Terlipressin 2mg IV bolus NOW
   • Ceftriaxone 1g IV (reduces mortality)
   • Correct coagulopathy if possible (avoid overcorrection in cirrhosis)

4. Endoscopy: Urgent within 12 hours after initial stabilisation. Band ligation for oesophageal varices.

5. If bleeding continues: Sengstaken-Blakemore tube as bridge. Contact hepatology for TIPS (within 72 hours in high-risk Child B/C).

6. Post-endoscopy: Continue terlipressin for 5 days, propranolol for secondary prevention, surveillance OGD.

Scenario 2: Peptic Ulcer with Visible Vessel

"A 68-year-old woman on aspirin and ibuprofen for osteoarthritis presents with melaena. OGD reveals a 1.5cm gastric ulcer with a non-bleeding visible vessel. What is your management?"

Structured Answer:

1. Endoscopic therapy: This is Forrest IIa (50% re-bleed risk without therapy). Dual therapy with adrenaline injection + haemoclips OR adrenaline + thermocoagulation.

2. Post-endoscopy: IV PPI infusion (omeprazole 80mg bolus then 8mg/hr x 72 hours) - Sung et al evidence.

3. Medications: Stop ibuprofen permanently. Discuss aspirin with cardiology - if primary prevention, stop; if secondary prevention (prior MI/stent), may need to continue with PPI cover.

4. H. pylori: Test (CLO test/stool antigen) and treat if positive.

5. Monitoring: Monitor for re-bleeding (continued melaena, haemodynamic instability). Consider repeat OGD in 24-48 hours if high-risk for re-bleeding.

6. Discharge: On PPI (omeprazole 40mg BD) for 8 weeks. Repeat OGD to confirm healing and exclude malignancy (gastric ulcers can be malignant).

Scenario 3: Low-Risk UGIB

"A 45-year-old man presents with coffee-ground vomit after a night of heavy drinking. He had severe retching before the vomiting. He is haemodynamically stable. Hb 138g/L. What is your management?"

Structured Answer:

1. Assessment: This sounds like Mallory-Weiss tear (history of vomiting/retching then haematemesis). Stable haemodynamics, normal Hb.

2. Risk score: Glasgow-Blatchford Score: Urea normal (0), Hb normal (0), BP normal (0), no melaena (0), no syncope (0), no liver/heart disease (0). GBS = 0.

3. Management: GBS 0 is very low risk. Can be considered for outpatient management with early outpatient OGD (within 24 hours) or discharge with PPI and return precautions.

4. Advice: Return if fresh haematemesis, melaena, light-headedness, or any concerning symptoms.

5. Follow-up: Most Mallory-Weiss tears heal spontaneously. PPI for symptomatic relief.

Specific Causes - Extended Detail

Peptic Ulcer Disease (35-50% of non-variceal UGIB):

Aetiology:

• H. pylori infection: 70-80% of DU, 60-70% of GU
• NSAIDs/Aspirin: 20-25% of PUD; risk increased 4-6x
• Stress ulcers (ICU patients): Cushing's ulcer (brain injury → ↑acid); Curling's ulcer (burns → mucosal ischaemia)
• Zollinger-Ellison syndrome: Gastrin-secreting tumour → multiple ulcers, often atypical locations

Locations and Arterial Supply:

• Duodenal ulcer (first part): Gastroduodenal artery erosion → massive bleeding
• Gastric ulcer (lesser curve): Left gastric artery
• Posterior DU: Most dangerous location for bleeding
• Giant ulcers (>2cm): Higher complication rate

H. pylori Testing:

• Acute setting: CLO test (urease test) on biopsy - may have false negatives with recent PPI
• Alternative: Stool antigen test, urea breath test (after PPI stopped)
• Must test ALL PUD patients and eradicate if positive

Oesophageal Varices:

Pathophysiology:

• Portal hypertension: HVPG >10mmHg → variceal formation; >12mmHg → bleeding risk
• 40-60% of cirrhotics have varices; 30% will bleed
• Wall tension: ∝ (pressure × radius) / wall thickness → large varices at high pressure rupture

Classification:

• Grade 1: Small, straight veins
• Grade 2: Enlarged, tortuous, <1/3 of lumen
• Grade 3: Large, occupying >1/3 of lumen
• Red wale marks: High-risk stigmata for bleeding

Primary Prevention:

• All cirrhotics should have screening OGD
• Large varices (Grade 2-3) or red wale marks: Non-selective beta-blocker (propranolol, carvedilol)
• If beta-blocker intolerant: Prophylactic banding

Secondary Prevention:

• Non-selective beta-blocker (propranolol 40-160mg/day, target HR <60)
• Repeat banding until varices eradicated (every 1-2 weeks)
• Combination: Beta-blocker + banding is superior

Gastric Varices:

Classification (Sarin classification):

• GOV1: Continuation of oesophageal varices along lesser curve - treat as oesophageal
• GOV2: Extension to gastric fundus - cyanoacrylate glue injection
• IGV1: Isolated in fundus - cyanoacrylate; consider TIPS/BRTO
• IGV2: Isolated elsewhere in stomach

Treatment:

• Glue injection (cyanoacrylate histoacryl) for GOV2/IGV1
• Band ligation less effective for gastric varices
• TIPS: For refractory/recurrent gastric variceal bleeding
• BRTO (Balloon-occluded Retrograde Transvenous Obliteration): Alternative to TIPS

Mallory-Weiss Tear:

• Classically: Alcohol binge → retching/vomiting → haematemesis
• Location: Gastro-oesophageal junction (mucosal tear)
• Usually self-limiting (80-90% stop spontaneously)
• Endoscopic therapy only if active bleeding
• Low re-bleed risk (<5%)
• PPI not strictly necessary but often given for symptom relief

Oesophagitis/Erosive Disease:

• LA Grade A-D classification
• Usually minor bleeding (iron deficiency anaemia rather than acute UGIB)
• Treat with PPI; address underlying cause
• If severe ulcerative oesophagitis: exclude malignancy

Gastric Malignancy:

• 2-4% of UGIB
• Risk factors: H. pylori, smoking, family history, pernicious anaemia
• Often presents with weight loss, anaemia, anorexia
• Biopsy essential (multiple biopsies from ulcer edge)
• All gastric ulcers need repeat OGD to confirm healing and exclude cancer
• Endoscopic therapy may be needed for bleeding but surgery for definitive treatment

Angiodysplasia/Vascular Ectasias:

• More common in elderly, renal failure, von Willebrand disease
• Cherry-red flat lesions at endoscopy
• Can cause chronic blood loss rather than massive bleeding
• Treat with APC (argon plasma coagulation)
• Recurrence common; may need repeat treatment

Dieulafoy Lesion:

• Rare (~1-2%) but important cause
• Large submucosal artery with minimal overlying ulceration
• Location: Typically lesser curve, 6cm from GEJ
• Intermittent massive bleeding; may be hard to locate
• Treatment: Haemoclips, thermocoagulation, injection
• High re-bleed rate; may need surgery/angioembolisation

Special Populations

Elderly (>80 years):

• Higher mortality (10-20% vs 5% in younger)
• More comorbidities affecting management
• Higher aspirin/anticoagulant use
• Atypical presentations (confusion, collapse)
• Lower threshold for admission and monitoring
• Be cautious of transfusion targets (avoid TACO)

Cirrhotic Patients:

• Coagulopathy: Do NOT aim for normal INR (synthetic dysfunction, not true coagulopathy)
• Thrombocytopenia: Platelets >50 for active bleeding
• Infection: Antibiotics reduce mortality - give routinely
• Hepatic encephalopathy: Blood is protein load - lactulose/rifaximin
• Hepatorenal syndrome: Monitor renal function closely
• Child-Pugh/MELD score guides prognosis

Anticoagulated Patients:

Anticoagulant	Reversal	Notes
Warfarin	Vitamin K 5-10mg IV + PCC 25-50 units/kg	Target INR <1.5
Dabigatran	Idarucizumab 5g IV	Specific reversal agent
Rivaroxaban/Apixaban	Andexanet alfa Or PCC 50 units/kg	Andexanet if available
Heparin	Protamine sulfate	1mg per 100 units heparin
LMWH	Protamine (partial reversal)	50-60% reversal

When to Resume Anticoagulation:

• Depends on indication (AF vs mechanical valve vs recent VTE)
• Low bleeding risk (Forrest IIc-III): 48-72 hours
• High bleeding risk (Forrest Ia-IIa): 7-14 days
• Discuss with haematology/cardiology as appropriate

Pregnancy:

• UGIB rare in pregnancy
• Common causes: Mallory-Weiss (hyperemesis), oesophagitis, PUD
• Endoscopy safe (preferably left lateral position, avoid propofol in first trimester)
• PPI safe in pregnancy
• Foetal monitoring if significant bleeding

Massive Transfusion Protocol

Definition: Transfusion of ≥10 units pRBC in 24 hours, or 4+ units in 1 hour

Activation Criteria:

• Active bleeding with haemodynamic instability
• Anticipated need for ongoing transfusion
• Hb rapidly falling despite transfusion

Protocol:

1. Activate massive transfusion protocol (MTP) with blood bank
2. Initial pack: 4 units pRBC + 4 units FFP + 1 platelet pool (may vary by institution)
3. Ratio: Target 1:1:1 (pRBC:FFP:platelets) based on trauma data
4. Adjuncts: Calcium (citrate binds calcium), fibrinogen concentrate if fibrinogen <1.5
5. Point-of-care testing: TEG/ROTEM to guide component therapy
6. Avoid hypothermia (blood warmer), acidosis (correct shock)
7. Surgical/IR intervention if bleeding source not controlled

Complications of Massive Transfusion:

• Hypothermia
• Hypocalcaemia (citrate toxicity)
• Hyperkalaemia (stored blood has high K+)
• Coagulopathy (dilutional, consumptive)
• TACO (transfusion-associated circulatory overload)
• TRALI (transfusion-related acute lung injury)
• Iron overload (chronic transfusion)

Discharge Planning and Follow-Up

Before Discharge:

• Haemodynamically stable for >24 hours
• No active bleeding (no fresh melaena)
• Eating and drinking
• Oral PPI prescribed (4-8 weeks)
• H. pylori test result available or arranged
• Medication review (stop NSAIDs, review anticoagulation)
• Patient education on warning signs

Follow-Up:

• GP within 1 week
• Repeat OGD for gastric ulcers (exclude malignancy) - typically 8 weeks
• Confirm H. pylori eradication (if treated) - stool antigen 4+ weeks after treatment
• Variceal screening/surveillance as per hepatology protocol

Patient Education:

• Avoid NSAIDs permanently (or with strong PPI protection if essential)
• Signs of re-bleeding: Black stools, vomiting blood, dizziness
• Take PPI as prescribed
• H. pylori treatment importance
• Alcohol advice (especially if varices)

Quality Metrics and Audit Standards

Key Performance Indicators:

• Time to endoscopy (target: <24h for all, <12h for high-risk)
• Pre-endoscopy risk stratification (GBS documented)
• Post-endoscopy risk score (Rockall documented)
• H. pylori testing rate for PUD
• Appropriate transfusion (restrictive strategy)
• Rebleeding rate (<10%)
• 30-day mortality (<10%)
• Antibiotics in variceal bleeding (>90%)

BSG Quality Standards:

• OGD within 24 hours of presentation
• Dual endoscopic therapy for high-risk stigmata
• IV PPI infusion post-endoscopy for high-risk ulcers
• H. pylori testing and eradication
• Documentation of endoscopic findings and therapy

MCQ Practice Questions

Question 1: A 62-year-old man presents with haematemesis. He has a history of atrial fibrillation on apixaban. His Glasgow-Blatchford Score is 12. Which of the following is the MOST important initial step? A. Immediate endoscopy B. IV omeprazole infusion C. Reversal with andexanet alfa D. Resuscitation with IV fluids and blood products E. CT angiography Answer: D - Resuscitation takes priority. Haemodynamic stabilisation must precede all other interventions. Anticoagulant reversal is considered for life-threatening bleeding after resuscitation is initiated.

Question 2: Which of the following Forrest classifications has the HIGHEST risk of rebleeding without endoscopic therapy? A. Forrest Ia (spurting haemorrhage) B. Forrest IIa (visible vessel) C. Forrest IIb (adherent clot) D. Forrest IIc (flat pigmented spot) E. Forrest III (clean base) Answer: A - Forrest Ia (spurting haemorrhage) has 90% rebleeding risk without intervention. Forrest Ib (oozing) 10-30%, IIa 50%, IIb 25-30%, IIc 7-10%, III <5%.

Question 3: A 55-year-old cirrhotic patient with Child-Pugh C cirrhosis presents with massive variceal haemorrhage. Despite two endoscopic band ligation attempts, bleeding continues. What is the NEXT most appropriate step? A. Repeat band ligation B. Balloon tamponade as bridge to TIPS C. Emergency surgery D. Increase terlipressin dose E. CT angiography with embolisation Answer: B - Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporising measure for refractory variceal bleeding as a bridge to TIPS. Surgery carries very high mortality in decompensated cirrhosis.

Question 4: Which of the following drugs has been shown in a large RCT to provide NO mortality benefit in upper GI bleeding? A. Terlipressin B. Omeprazole C. Tranexamic acid D. Octreotide E. Ceftriaxone Answer: C - The HALT-IT trial (2020, n=12,009) demonstrated that tranexamic acid does NOT reduce mortality in GI bleeding and may increase venous thromboembolism risk.

Question 5: A patient with an INR of 6.5 on warfarin presents with haematemesis and a BP of 85/50. PCC is administered. What is the target INR for reversal in life-threatening bleeding? A. <3.0 B. <2.5 C. <2.0 D. <1.5 E. <1.0 Answer: D - Target INR <1.5 for life-threatening bleeding. PCC (prothrombin complex concentrate) 25-50 units/kg is preferred over FFP as it provides rapid, complete reversal.

OSCE Station Guidance

Station Type: Acute Management Scenario (8 minutes)

Scenario: You are the medical registrar on-call. A 58-year-old man has been brought to resus with a 2-hour history of coffee-ground vomiting and fresh haematemesis. He has a background of alcohol dependence and liver disease. Observations: HR 125, BP 85/60, RR 24, SpO2 94% on air, GCS 14/15.

Expected Actions:

1. Request A-E assessment structured approach (airway first)
2. High-flow oxygen application
3. 2x large bore IV cannulae (grey/brown gauge)
4. Urgent bloods: FBC, U&E, LFT, coagulation, crossmatch 6 units
5. Crystalloid bolus 500mL while awaiting blood
6. Recognise likely variceal bleeding from history
7. State terlipressin 2mg IV stat
8. State antibiotic (ceftriaxone 1g IV)
9. Contact gastroenterology for urgent endoscopy
10. Consider anaesthetic input for airway protection

Examiner Questions:

• "What scoring system would you use pre-endoscopy?" (GBS)
• "What transfusion target would you aim for?" (Hb 70-80g/L)
• "What is the drug of choice for variceal bleeding?" (Terlipressin)
• "When should endoscopy be performed?" (Within 12 hours for variceal)

Station Type: Communication Skills (8 minutes)

Scenario: Mr Smith, 72 years old, has been admitted with a bleeding peptic ulcer successfully treated endoscopically. He is on aspirin and naproxen for chronic pain. Explain the diagnosis and ongoing management.

Key Communication Points:

• Explain what happened (ulcer, bleeding, treated with camera test)
• Explain cause (medications damaging stomach lining)
• Explain changes needed (stop naproxen permanently, continue aspirin with PPI cover)
• Explain H. pylori testing and treatment if positive
• Warning signs for return to hospital
• Follow-up arrangements

Pathology and Radiology Interpretation

Endoscopic Appearances:

Finding	Description	Clinical Significance
Spurting vessel	Pulsatile arterial bleeding	Forrest Ia - 90% rebleed - requires immediate therapy
Oozing	Non-pulsatile bleeding	Forrest Ib - requires therapy
Visible vessel	Pigmented protuberance in ulcer base	Forrest IIa - 50% rebleed - requires therapy
Adherent clot	Blood clot covering ulcer	Forrest IIb - consider clot removal and therapy
Flat pigmented spot	Flat discolouration	Forrest IIc - low risk - medical therapy
Clean base	White/grey ulcer base	Forrest III - <5% rebleed - discharge consideration

Variceal Grading:

• Grade I: Small, straight varices
• Grade II: Moderate, tortuous varices occupying <1/3 oesophageal lumen
• Grade III: Large, coil-shaped varices occupying >1/3 lumen
• Blue colour: Higher rupture risk
• Red signs (red wale marks, cherry red spots): Imminent bleeding risk

CT Findings in UGIB:

• Active extravasation: Hyperdense contrast within stomach/duodenal lumen
• Arterial phase blush: Active bleeding visible on CT angiography
• Pseudoaneurysm: Focal outpouching from vessel, high rebleed risk
• Varices: Enlarged tortuous vessels in portal distribution
• Portal hypertension signs: Splenomegaly, ascites, collaterals

Angiographic Findings:

• Active bleeding: Contrast extravasation (requires >0.5mL/min bleeding)
• Pseudoaneurysm: Focal contrast outpouching
• Abnormal vessels: Dieulafoy lesion shows large calibre submucosal vessel
• Embolisation targets: Gastroduodenal artery (DU), left gastric artery (varices/GU)

International Comparison and Variations

UK vs USA Practice Differences:

Aspect	UK (NICE/BSG)	USA (ACG/ASGE)
Risk score	GBS preferred pre-endoscopy	GBS or AIMS65
Transfusion trigger	Hb <70g/L	Hb <70-80g/L
PPI pre-endoscopy	Not routinely recommended	May be considered
Endoscopy timing	<24h all; <12h variceal	<24h; urgent if high-risk
Vasoactive drugs	Terlipressin	Octreotide
Antibiotics in varices	Ceftriaxone 7 days	Ceftriaxone or quinolone

Australian/New Zealand Guidelines:

• GESA (Gastroenterological Society of Australia) guidelines align with international practice
• Emphasis on rural/remote considerations for transfer
• Telehealth consultation for endoscopy decision-making

European Variations:

• ESGE guidelines form basis of European practice
• Some variation in vasoactive drug choice (terlipressin vs somatostatin)
• Similar emphasis on restrictive transfusion

Historical Perspective

Key Milestones:

• 1958: First fibreoptic endoscope developed (Hirschowitz)
• 1974: Therapeutic endoscopy for UGIB introduced
• 1983: H. pylori discovered (Marshall and Warren - Nobel Prize 2005)
• 1990s: Forrest classification widely adopted
• 1996: Glasgow-Blatchford Score developed
• 2000: Rockall score refined for post-endoscopy risk
• 2010: IV PPI regimens standardised (Sung et al)
• 2013: Restrictive transfusion strategy shown superior (Villanueva)
• 2020: HALT-IT trial disproves tranexamic acid benefit

Evolution of Management:

• Historical: Surgery was primary treatment for bleeding ulcers
• 1980s-90s: Endoscopic therapy became first-line
• 2000s: PPI revolutionised acid suppression
• 2010s: Focus on transfusion targets and timing
• Present: Multidisciplinary approach, protocol-driven care

Future Directions and Research

Current Research Focus:

• AI-assisted endoscopic diagnosis and treatment
• Novel haemostatic agents (e.g., haemostatic powders, TC-325)
• Biomarkers for early rebleeding prediction
• Optimal anticoagulation resumption timing
• Personalised risk stratification
• Point-of-care coagulation testing

Emerging Technologies:

• AI-powered endoscopy image analysis for lesion characterisation
• Over-the-scope clips for larger/difficult lesions
• Endoscopic suturing devices
• Novel vasoactive agents with fewer side effects
• Remote/robotic endoscopy

Ongoing Clinical Trials:

• TRIGGER2: Optimal transfusion thresholds
• HALT-IT follow-up studies
• Anticoagulation resumption timing studies
• Novel haemostatic agent trials

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Last Reviewed: 2025-12-27 | MedVellum Editorial Team

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and current guidelines.