Why Upper GI Bleeding Is Examined
Upper gastrointestinal bleeding (UGIB) has a mortality of 5-10% in the UK and is a common acute medical presentation. OSCEs examine it through acute management stations, data interpretation (applying the Blatchford score to decide admission), and history-taking scenarios (haematemesis history). Examiners assess resuscitation priorities, risk stratification, and knowledge of endoscopic management.
Definitions
| Presentation | Source | Features |
|---|---|---|
| Haematemesis | Above the ligament of Treitz (pylorus to duodeno-jejunal flexure) | Fresh blood or "coffee grounds" vomit |
| Melaena | Usually upper GI (can be right-sided colonic) | Tarry, black, offensive stool — requires 50-100 mL blood loss |
| Haematochezia | Usually lower GI (but brisk upper GI bleed can cause bright red PR blood) | Fresh red blood per rectum |
Causes — Peptic vs Variceal
Non-Variceal (80%)
| Cause | % of UGIB |
|---|---|
| Peptic ulcer disease (duodenal/gastric) | 35-50% |
| Mallory-Weiss tear | 5-10% |
| Oesophagitis/gastritis/duodenitis | 10-20% |
| Oesophageal/gastric malignancy | 2-5% |
| Angiodysplasia | 5% |
Variceal (20%)
- Oesophageal or gastric varices due to portal hypertension
- Usually due to cirrhosis
- Higher mortality (30-50%) than non-variceal bleeding
- Requires different management (terlipressin, antibiotics, banding)
🧠 Mnemonic
History clues to source:
- NSAIDs/aspirin/steroids + epigastric pain = peptic ulcer
- Alcohol/cirrhosis/known liver disease = varices
- Retching then haematemesis = Mallory-Weiss tear
- Weight loss, dysphagia, anorexia = oesophageal or gastric malignancy
- No symptoms + melaena in elderly = angiodysplasia or neoplasia
Immediate Resuscitation
ABCDE Approach
- 1Airway: Risk of aspiration — particularly with massive haematemesis or reduced consciousness. Position head-down lateral if vomiting. Anaesthetic review if GCS below 12.
- 2Breathing: High-flow oxygen if haemodynamic compromise.
- 3Circulation:
- IV access x2 large-bore (16G minimum)
- Bloods: FBC, U&E, LFTs, clotting, crossmatch (4-6 units initially), group and save
- Fluid resuscitation: 500 mL Hartmann's or 0.9% saline bolus if haemodynamically unstable; aim for SBP above 100 mmHg
- Target Hb 70-80 g/L with packed red cells (avoid overtransfusion — increases portal pressure in variceal bleeding)
⚠️ Red Flag
Transfusion threshold in GI bleeding: Hb 70 g/L (restrictive transfusion) except in patients with cardiovascular disease (maintain above 80 g/L) or active haemorrhage. TRIGGER trial evidence: restrictive transfusion reduces 28-day mortality in UGIB.
Glasgow-Blatchford Score (Admission Decision)
Used before endoscopy to decide whether hospital admission is needed.
| Variable | Points |
|---|---|
| Urea 6.5-7.9 mmol/L | 2 |
| Urea 8.0-9.9 mmol/L | 3 |
| Urea 10.0-24.9 mmol/L | 4 |
| Urea 25.0 or above mmol/L | 6 |
| Hb (men) 120-129 g/L | 1 |
| Hb (men) 100-119 g/L | 3 |
| Hb (men) below 100 g/L | 6 |
| Hb (women) 100-119 g/L | 1 |
| Hb (women) below 100 g/L | 6 |
| SBP 100-109 mmHg | 1 |
| SBP 90-99 mmHg | 2 |
| SBP below 90 mmHg | 3 |
| Pulse 100 bpm or above | 1 |
| Melaena | 1 |
| Syncope | 2 |
| Liver disease | 2 |
| Heart failure | 2 |
| Score | Interpretation |
|---|---|
| 0 | Low risk — may be managed outpatient; endoscopy next day |
| 1 or above | Hospital admission required |
Rockall Score (Post-Endoscopy Prognosis)
Predicts rebleeding and mortality after endoscopy.
| Variable | Score | ||
|---|---|---|---|
| Age below 60 | 0; 60-79 = 1; 80 or above = 2 | ||
| Shock: no shock | 0; pulse above 100 = 1; SBP below 100 = 2 | ||
| Comorbidity: none | 0; cardiac failure/IHD/other major = 2; renal/liver failure/metastatic cancer = 3 | ||
| Diagnosis: Mallory-Weiss/no lesion | 0; other | 1; GI malignancy = 2 | |
| Major stigmata of recent haemorrhage: none | 0; dark spot/clot | 1; blood, adherent clot, visible vessel | 2 |
Score 0-2 = low risk; 3-4 = moderate; 5 or above = high rebleeding risk.
Endoscopic Management
Timing: Endoscopy within 24 hours of presentation for all patients requiring hospital admission. Immediate endoscopy (within 12 hours) for haemodynamic instability.
Endoscopic treatments for non-variceal bleeding:
- Adrenaline injection (1:10,000)
- Thermal coagulation
- Clipping
- Combination therapy (two modalities) — reduces rebleeding vs monotherapy
Pre-endoscopy IV PPI:
- Omeprazole 80 mg IV bolus then 8 mg/hour infusion
- Reduces blood/clot around ulcer, improves endoscopic view
- Continue for 72 hours post-endoscopy for high-risk ulcers (Forrest Ia-IIb)
Variceal Bleeding — Specific Management
🧠 Mnemonic
ABCT — variceal bleeding:
- A irway (aspiration risk — consider intubation early)
- B and ligation — endoscopic (definitive treatment)
- C eftriaxone 1 g IV OD for 7 days (antibiotics reduce mortality in cirrhosis)
- T erlipressin 2 mg IV QDS (vasoconstrictor — reduces portal pressure; start before endoscopy)
Terlipressin is the vasoactive drug of choice. Start immediately when variceal bleeding suspected — do not wait for endoscopy.
Sengstaken-Blakemore tube: Balloon tamponade for uncontrolled variceal haemorrhage as a bridge to definitive treatment (TIPS or surgery). Only by experienced operators.
TIPS (Transjugular Intrahepatic Portosystemic Shunt): Decompresses portal system in refractory variceal bleeding.
Frequently Asked Questions
"What is the significance of elevated urea in upper GI bleeding?"
Blood in the upper GI tract is digested and absorbed as amino acids. The resulting nitrogenous compounds are metabolised to urea — causing a disproportionate rise in blood urea relative to creatinine. A urea:creatinine ratio above 100 (when both in mmol/L) suggests an upper GI source. This is one of the Blatchford score variables and a useful clinical clue even before endoscopy.
"Why do we avoid aggressive fluid resuscitation in variceal bleeding?"
Over-transfusion increases portal venous pressure, which increases blood flow to varices and worsens haemorrhage. A restrictive transfusion strategy (Hb target 70-80 g/L) and avoiding large crystalloid boluses reduces portal hypertension. In the Child-Pugh C cirrhotic, even a slight increase in portal pressure can be life-threatening.
"What is a Mallory-Weiss tear?"
A linear mucosal tear at the gastro-oesophageal junction, typically caused by forceful or repeated retching and vomiting. The classic history is fresh haematemesis after a bout of vomiting — often in the context of alcohol excess. Most Mallory-Weiss tears stop bleeding spontaneously. Endoscopic treatment is reserved for those with active bleeding or high-risk stigmata.
"When should surgery be considered for GI bleeding?"
Interventional radiology (embolisation) is preferred over surgery as first-line rescue therapy for non-variceal UGIB failing endoscopic treatment. Surgery is reserved for when radiology is unavailable or fails. Indications: continued haemodynamic instability despite resuscitation, failure of two endoscopic attempts, or rare situations where the anatomy or pathology (e.g., a posterior duodenal ulcer eroding the gastroduodenal artery) favours surgical access.
"How do NSAIDs cause peptic ulcers?"
NSAIDs inhibit cyclo-oxygenase-1 (COX-1), reducing prostaglandin synthesis in the gastric mucosa. Prostaglandins normally stimulate mucus and bicarbonate secretion, maintain mucosal blood flow, and inhibit acid secretion. Without this protection, gastric acid and pepsin cause mucosal erosion and ulceration. Selective COX-2 inhibitors (celecoxib) have lower GI toxicity but increased cardiovascular risk. Co-prescription of a PPI reduces (but does not eliminate) NSAID-associated GI risk.
Related Posts
- Abdominal Examination OSCE — assessing for signs of chronic liver disease and haemorrhagic shock
- Blood Results Interpretation OSCE — interpreting FBC, clotting, and LFTs in acute GI bleeding
- Jaundice History OSCE — liver disease and cirrhosis as background to variceal bleeding