TextbookEmergency MedicineAcute Upper GI Bleeding

Acute Upper GI Bleeding

Acute upper GI bleeding presents with haematemesis and/or melaena. Risk stratification with the Glasgow-Blatchford score guides management, with endoscopy within 24 hours and specific treatment for variceal and non-variceal sources.

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Key Facts

~50,000-70,000 hospital admissions for upper GI bleeding per year in the UK; overall mortality ~6-8% Glasgow-Blatchford Score (GBS): GBS 0 = very low risk, can be considered for outpatient management; GBS ≥6 = high risk, requires endoscopy and admission Peptic ulcer disease is the most common cause (~35-50%); variceal bleeding accounts for ~10% but has the highest mortality (~15-20%) Endoscopy within 24 hours for all upper GI bleeds; within 2 hours for suspected variceal or haemodynamically unstable patients Rockall score: Post-endoscopy scoring system to predict rebleeding and mortality PPI therapy: Omeprazole 80mg IV bolus then 8mg/hr infusion for high-risk peptic ulcer bleeding post-endoscopy Variceal bleeding: IV terlipressin 2mg QDS + prophylactic antibiotics (co-amoxiclav) + band ligation at endoscopy Restrictive transfusion: Target Hb 70-80g/L (Villanueva trial — restrictive strategy improves survival in GI bleeding)

Overview

Key Facts

Acute upper GI bleeding is a common medical emergency. Risk stratification, appropriate resuscitation, and timely endoscopy are the cornerstones of management. The Blatchford score determines whether patients need admission, while the Rockall score predicts rebleeding and mortality.

Epidemiology

Upper GI bleeding accounts for approximately 50,000-70,000 admissions per year in the UK. Overall mortality is approximately 6-8% but varies significantly: peptic ulcer ~5%, variceal bleeding ~15-20%. Incidence increases with age. Approximately 80% of non-variceal bleeds stop spontaneously.

Aetiology

  • Peptic ulcer disease (~35-50%): Gastric and duodenal ulcers; H. pylori, NSAIDs
  • Oesophageal varices (~10%): Portal hypertension (liver cirrhosis)
  • Mallory-Weiss tear (~10%): Mucosal tear at GOJ from retching/vomiting
  • Oesophagitis/gastritis (~15%): Reflux, alcohol, NSAIDs
  • Upper GI malignancy (~5%): Gastric, oesophageal
  • Dieulafoy lesion, AVM, aorto-enteric fistula: Rare but important

Pathophysiology

Upper GI bleeding originates proximal to the ligament of Treitz. Peptic ulcer bleeding results from erosion into submucosal or deeper vessels by acid-pepsin injury. Variceal bleeding occurs from rupture of dilated portosystemic collateral veins due to portal hypertension (portal pressure >12 mmHg). The haemodynamic response includes tachycardia, hypotension, and compensatory vasoconstriction.

Clinical Presentation

Presenting Features

  • Haematemesis: Fresh blood (bright red) or coffee-ground vomiting
  • Melaena: Black, tarry, offensive stools (>50mL blood in GI tract)
  • Haematochezia: Fresh rectal bleeding (massive upper GI bleed with rapid transit)
  • Dizziness, presyncope, or syncope
  • Epigastric pain (peptic ulcer)

Red Flags

  • Haemodynamic instability (SBP <100, HR >100) — significant haemorrhage
  • Fresh haematemesis — active bleeding
  • Suspected variceal bleed (known liver disease, stigmata of chronic liver disease)
  • Anticoagulated patient — higher bleeding risk
  • Coffee-ground vomiting with tachycardia — may underestimate blood loss
  • Aorto-enteric fistula ('herald bleed' followed by massive haemorrhage) — consider if previous aortic graft

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Peptic ulcerEpigastric pain, NSAID/H. pylori historyOGD — Forrest classification
Variceal bleedLiver disease, massive haematemesisOGD — band ligation
Mallory-Weiss tearVomiting/retching then haematemesisOGD
Oesophagitis/gastritisReflux symptoms, alcohol, NSAIDsOGD
Gastric cancerWeight loss, early satiety, elderlyOGD + biopsy
Aorto-enteric fistulaPrevious aortic surgery, massive bleedCT angiography

Diagnosis / Investigation

Bedside

  • ABCDE assessment: Haemodynamic stability
  • Glasgow-Blatchford Score: Determines need for admission and intervention
  • Blood glucose: Baseline
  • DRE: Melaena confirmation

Bloods

  • FBC: Hb (may be normal initially in acute bleed — haemoconcentration), platelets
  • U&Es: Raised urea disproportionate to creatinine (absorbed blood proteins)
  • LFTs: If liver disease/variceal bleed suspected
  • Coagulation (INR): Anticoagulated patients, liver disease
  • Group and crossmatch: 2-6 units depending on severity
  • Lactate: Tissue perfusion marker

Imaging

  • OGD (oesophagogastroduodenoscopy): Within 24h (within 2h if variceal or haemodynamically unstable)
  • CT angiography: If endoscopy fails to identify source or is not feasible
  • Mesenteric angiography: Therapeutic embolisation if endoscopy fails

Special Tests

  • H. pylori testing: Urease test at endoscopy, stool antigen, or urea breath test
  • Forrest classification: Endoscopic classification of peptic ulcer bleeding risk

Management

Non-pharmacological

  • Resuscitation: ABCDE, large-bore IV access (×2), fluid resuscitation
  • Restrictive transfusion: Target Hb 70-80g/L (Villanueva trial — liberal transfusion increases rebleeding and mortality)
  • Correct coagulopathy: FFP if INR >1.5; platelets if <50 × 10⁹/L; vitamin K if warfarin

Pharmacological

Non-variceal bleeding:

  • PPI: IV omeprazole 80mg bolus then 8mg/hr infusion for 72h if high-risk ulcer at endoscopy
  • H. pylori eradication: If positive — triple therapy (e.g., amoxicillin 1g BD + clarithromycin 500mg BD + PPI for 7 days)
  • Stop NSAIDs: Permanently if possible; lowest dose + PPI if essential

Variceal bleeding:

  • IV terlipressin 2mg QDS (reduces portal pressure) — continue for up to 5 days
  • Prophylactic antibiotics: Co-amoxiclav 1.2g IV TDS (or ciprofloxacin if penicillin allergic) for 5 days — reduces mortality
  • Endoscopic band ligation: Within 2 hours; variceal banding for oesophageal varices
  • Sengstaken-Blakemore tube: Temporary tamponade if bleeding uncontrolled pending endoscopy/TIPSS

Anticoagulated patients:

  • Warfarin: Vitamin K + PCC (Beriplex) — target INR <1.5
  • DOAC: Discuss with haematology; may need specific reversal agents

Surgical/Interventional

  • Endoscopic therapy: Clip application, adrenaline injection, thermal coagulation, band ligation
  • Interventional radiology: Embolisation for refractory non-variceal bleeding
  • TIPSS (Transjugular Intrahepatic Portosystemic Shunt): For refractory or recurrent variceal bleeding
  • Surgery: Rare — oversewing of bleeding ulcer if endoscopy and IR fail

Referral Criteria

  • GBS ≥6 — admission, endoscopy within 24h
  • GBS 0 — consider outpatient endoscopy and discharge with safety net
  • Suspected variceal bleed — urgent endoscopy within 2h, hepatology involvement
  • Rebleeding after endoscopic therapy — repeat endoscopy, consider IR or surgery

Prognosis

  • Overall mortality: ~6-8% for all upper GI bleeding
  • Peptic ulcer: ~5% mortality; ~15-20% rebleed rate after endoscopic therapy
  • Variceal bleeding: ~15-20% mortality per episode; ~60% rebleed within 1 year without secondary prevention
  • GBS 0: Very low risk (<1%) of adverse outcome — safe for outpatient management
  • Restrictive transfusion: Reduces 45-day mortality (Villanueva RCT)
  • H. pylori eradication: Reduces ulcer recurrence from ~60% to <5%

Other Relevant Information

Glasgow-Blatchford Score (GBS)

ParameterScore
Hb (men): 120-129 → 1; 100-119 → 3; <100 → 6
Hb (women): 100-119 → 1; <100 → 6
Urea: 6.5-7.9 → 2; 8-9.9 → 3; 10-25 → 4; >25 → 6
SBP: 100-109 → 1; 90-99 → 2; <90 → 3
HR ≥100 → 1
Melaena → 1
Syncope → 2
Liver disease → 2
Heart failure → 2

Forrest Classification of Peptic Ulcer Bleeding

ClassAppearanceRebleed Risk
IaSpurting haemorrhage~55%
IbOozing haemorrhage~55%
IIaVisible vessel (non-bleeding)~43%
IIbAdherent clot~22%
IIcFlat pigmented spot~10%
IIIClean base ulcer~5%