Upper Gastrointestinal Bleeding (Adult)

1. Overview

Upper Gastrointestinal Bleeding (UGIB) is defined as haemorrhage originating proximal to the Ligament of Treitz (oesophagus, stomach, or duodenum). It is a major medical emergency, accounting for ~50-100 admissions per 100,000 population annually. [1]

The condition is broadly stratified into Non-Variceal (85%)—predominantly Peptic Ulcer Disease (PUD)—and Variceal (15%)—resulting from portal hypertension, usually due to cirrhosis. Variceal bleeding carries a significantly higher 30-day mortality (~15-20%) compared to non-variceal causes (~2-5%). [2]

Management has been refined by the Baveno VII consensus for varices and the NICE/ESGE guidelines for PUD. The paradigm shift of the 2020s includes the strict use of Restrictive Transfusion (Villanueva trial), the avoidance of Tranexamic Acid (HALT-IT trial), and the use of Haemostatic Powders (Hemospray) as a bridge to definitive therapy. [3]

2. Epidemiology

The Risk Profile

• Age: Mortality rises exponentially in those > 60 years due to comorbid disease.
• The "Drug Surge": 50% of non-variceal bleeds are associated with NSAID or Aspirin use.
• The "Weekend Effect": National audits show higher mortality for patients admitted on weekends, likely due to delayed access to therapeutic endoscopy. [4]

Incidence and Mortality

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3. Aetiology & Pathophysiology

⚠️ THE 7-STEP MOLECULAR MECHANISM (Non-Variceal/PUD)

1. Mucosal Barrier Disruption: H. pylori (via VacA/CagA toxins) or NSAIDs (via COX-1 inhibition) deplete protective prostaglandins (PGE2).
2. Acid-Pepsin Digestion: Loss of the bicarbonate-rich mucus layer exposes the epithelium to luminal acid (HCl) and pepsin.
3. Vessel Erosion: Chronic ulceration penetrates the muscularis mucosae, eventually eroding into a submucosal artery (e.g. Gastroduodenal artery in posterior DU).
4. Haemorrhage & Clot Inhibition: At the low pH of the stomach (less than 5.0), Pepsin actively degrades fibrin clots and prevents platelet aggregation, perpetuating the bleed.
5. Haemodynamic Compensations: Hypovolaemia triggers baroreceptors, causing a catecholamine surge (Tachycardia/Vasoconstriction) and RAAS activation.
6. Splanchnic Steal: Systemic vasoconstriction shunts blood away from the gut to protect the heart/brain, which can exacerbate mucosal ischaemia and increase ulcer size.
7. Azotaemia: Massive protein loading from digested blood leads to an isolated rise in Urea, while Creatinine remains normal (Urea:Cr ratio > 100). [5, 6, 7]

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4. Clinical Presentation

Symptoms

• Haematemesis: Fresh red (active) or "coffee-ground" (digested by HCl).
• Melaena: Black, tarry, offensive stools. (Note: Requires > 50mL blood to stay in gut for > 8 hours).
• Haematochezia: Bright red blood per rectum; usually LGIB but indicates massive UGIB if accompanied by shock.

Physical Signs

1. Shock Index (HR/SBP): If > 1.0, indicates significant occult blood loss.
2. Stigmata of CLD: Jaundice, spider naevi, and splenomegaly (highly suggestive of varices).
3. Epigastric Tenderness: Suggestive of PUD.
4. Rectal Examination: Mandatory to confirm melaena and exclude lower sources. [8]

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5. Investigations

The Pre-Endoscopy Risk Score: Glasgow-Blatchford (GBS)

• GBS 0-1: Safe for outpatient management.
• GBS ≥6: High risk of requiring blood transfusion or endoscopic intervention. [9]

Laboratory Workup

• Hb: May be normal initially (it takes 24-48h for haemodilution to occur).
• Urea: Significantly elevated in UGIB vs. LGIB.
• Coagulation: Check INR (Warfarin) and Platelets.

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6. Management: The Acute Protocol

1. Resuscitation (The "Villanueva" Strategy)

• Restrictive Transfusion: Transfuse only if Hb less than 70 g/L (Target 70-90). Exceptions: ACS or active massive exsanguination.
• Avoid Over-hydration: Excessive crystalloid increases portal pressure and precipitates variceal rupture. [10]

2. Non-Variceal (PUD) Management

1. PPI: Give 80mg Omeprazole bolus only after OGD confirms high-risk stigmata. (Pre-OGD PPI does not improve mortality).
2. Endoscopy (within 24h): Dual therapy is standard (Adrenaline injection + Clip or Thermal coagulation).
3. Forrest Criteria: Ia (Spurting) and IIa (Visible vessel) have the highest re-bleed risk.

3. Variceal Management (The "Baveno" Protocol)

1. Vasoactive: Start Terlipressin (or Octreotide) immediately upon suspicion.
2. Antibiotics: IV Ceftriaxone (decreases mortality and re-bleeding).
3. Endoscopy (within 12h): Band Ligation is the gold standard.
4. Pre-emptive TIPS: Consider within 72h for Child-Pugh B with active bleed or C patients. [11]

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7. Evidence: Landmark Trials

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8. Single Best Answer (SBA) Questions

Question 1

A 65-year-old male with known cirrhosis presents with melaena. BP 110/70, HR 95. Hb 75 g/L. What is the most appropriate transfusion management?

• A) Transfuse 2 units RBC now to target Hb > 100
• B) Wait until Hb less than 70 to transfuse
• C) Transfuse 1 unit RBC now to target Hb 70-90
• D) Give 1L Normal Saline instead of blood
• E) Start an Iron infusion
• Answer: C. Per the Villanueva trial and NICE guidelines, a restrictive strategy (target 70-90) is superior, particularly in cirrhotics where over-transfusion increases portal pressure.

Question 2

A patient with a bleeding gastric ulcer undergoes OGD showing a non-bleeding visible vessel (Forrest IIa). What is the evidence-based management after successful endoscopic dual therapy?

• A) Discharge immediately on oral PPI
• B) 72-hour continuous IV PPI infusion
• C) Start oral Amoxicillin and Clarithromycin
• D) Repeat OGD in 12 hours
• E) Start IV Octreotide
• Answer: B. For high-risk stigmata (Forrest Ia, Ib, IIa), a 72-hour high-dose IV PPI infusion significantly reduces the rate of re-bleeding (Sung et al evidence).

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9. Viva Scenario: The "Rockall" Reality

Examiner: "You have successfully banded varices in a 52-year-old. Describe your post-procedural risk assessment and follow-up."

Candidate:

1. Risk Score: I would calculate the Full Rockall Score (incorporating Age, Shock, Comorbidity, and Endoscopic findings).
2. High Risk: If the score is ≥6, the risk of re-bleeding and mortality is high; I would keep the patient on HDU/CCU for at least 48 hours.
3. Prophylaxis: I would continue Terlipressin for 2-5 days and Ceftriaxone for 7 days.
4. Secondary Prevention: I would start a non-selective beta-blocker (e.g. Carvedilol) before discharge and arrange a repeat OGD for further banding in 1-2 weeks.

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10. Patient Explanation

"Upper GI bleeding means you are bleeding from your stomach or the tubes leading to it. This can be caused by an ulcer (like a deep scratch) or swollen veins if you have liver problems. We pass a small camera down into your stomach to find the source and stop the bleed using clips or heat. It's very important that we keep your blood pressure stable but don't 'over-fill' you with blood, as that can actually make the bleeding restart. You will likely need to stay in for a few days of IV medication."

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11. References

1. Lau JWY, et al. International consensus recommendations on the management of patients with non-variceal upper gastrointestinal bleeding. Ann Intern Med. 2019. [PMID: 31634906]
2. NICE NG141. Acute upper gastrointestinal bleeding: management. 2012 (Updated 2020). NICE
3. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013. [PMID: 23281973]
4. HALT-IT Trial Collaborators. Effects of a high-dose 24-h infusion of tranexamic acid on death in GI bleeding. Lancet. 2020. [PMID: 32563378]
5. Baveno VII Faculty. Personalised care for portal hypertension. J Hepatol. 2022. [PMID: 35033617]

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Last Updated: 2026-01-05 | MedVellum Editorial Team