GC036 Coffee Ground Vomitustarry Stool: Upper GI Bleeding
Upper gastrointestinal bleeding is hemorrhage originating proximal to the ligament of Treitz, classically presenting with coffee-ground emesis (hematemesis of partially digested blood) and melena (black, tarry stools).
Upper GI bleeding (UGIB) is one of the most common and dangerous GI emergencies you will encounter. This lecture by Dr. Michael Cheung (GC 036) systematically walks you through: what UGIB is, how patients present, what causes it, how to assess the patient, what investigations to order, how to manage both variceal and non-variceal bleeding, and—unique to this lecture—what to do when the source remains elusive (obscure GI bleeding). A companion surgical/severe UGIB lecture (GC 198) reinforces severity grading.
Why this matters for exams: UGIB is perennially tested in HKUMed summatives—SAQs, minicases, and MCQs. Examiners love asking about definitions, risk stratification scores, transfusion thresholds, timing of endoscopy, post-endoscopic management (especially aspirin resumption), and the workup of obscure GI bleeding. The 2021, 2022, and 2025 summatives all had direct UGIB stems [1][2][3].
Learning Objectives (directly from lecture):
- Define upper GI bleeding and related terminology
- Recognize presentations of UGIB
- Understand the etiology (variceal vs non-variceal)
- Perform initial patient assessment (history, PE, investigations)
- Apply risk-stratification scores
- Manage UGIB (resuscitation, transfusion, pharmacotherapy, endoscopy)
- Approach obscure GI bleeding (VCE, enteroscopy, Meckel's scan, etc.)
Upper GI bleeding: bleeding from a source proximal to the ligament of Treitz. [4]
The ligament of Treitz (suspensory muscle of the duodenum) is the anatomical landmark separating duodenum from jejunum. Everything from the mouth/esophagus down to the duodenojejunal (DJ) flexure is "upper GI."
| Term | Definition | Why It Matters |
|---|---|---|
| Small bowel (SB) bleeding | Bleeding distal to ampulla of Vater and proximal to ileocecal valve (ICV) | Overlaps with UGIB in D3/D4; important for obscure GI bleed workup |
| Overt GI bleeding | Passage of visible blood (hematemesis, melena, hematochezia) | Clinically obvious—triggers immediate workup |
| Occult GI bleeding | Blood not detected by naked eye; presents as iron-deficiency anemia ± positive FOBT | Subtle; chronic slow bleeds; think malignancy screening |
| Obscure GI bleeding | Source unknown despite OGD + colonoscopy ± SB evaluation | Traditional: after OGD + CLN + SB radiology. Strict: after adding VCE + enteroscopy |
Exam Trap: Obscure vs Occult
Obscure ≠ Occult. Obscure means you've looked and can't find the source (can be overt or occult). Occult means invisible bleeding. Obscure bleeding can present as visible blood (obscure overt) or as anemia/FOBT+ (obscure occult). Examiners test this distinction.
2. Presentation
Presentation depends on the volume and location of bleeding. [4]
| Presentation | What It Looks Like | Anatomical Source |
|---|---|---|
| Hematemesis | Vomiting fresh red blood | Upper GI tract (proximal to DJ flexure) |
| Coffee-ground emesis | Vomitus resembling ground coffee | Upper GI—blood oxidized by gastric acid → methemoglobin (brown-black granular appearance) |
| Fresh blood from NG tube | Aspirated blood | Upper GI tract |
| Coffee-ground aspirate from NG tube | Upper GI tract | |
| Melena | Black, tarry, loose, sticky, malodorous stool | Upper GI tract down to proximal colon |
| Hematochezia | Bright red or maroon blood per rectum | Usually lower GI, BUT can be massive UGIB with rapid transit |
Melena: Heme is oxidized by intestinal bacteria into hematin → black color. Blood acts as a cathartic → patients describe loose stool/diarrhea. [4]
Fresh vs old melena: Fresh melena = jet-black tarry liquid stool (active ongoing bleeding). Old/stale melena = black-grey, dull, mixed with normal stool (bleeding has stopped) [5].
DDx of black stool: iron supplements, bismuth, activated charcoal, food (e.g. squid ink). [4]
Iron stools: green-black, solid/formed, often with constipation (vs melena which is loose, tarry, and extremely malodorous) [5].
Symptoms of anemia: fatigue, palpitations, dyspnea, dizziness, postural hypotension. Iron deficiency anemia, fecal occult blood +ve. [4]
| Finding | Most Likely Source | Caveat |
|---|---|---|
| Hematemesis | Upper GI | — |
| NG tube with blood | Upper GI | — |
| NG tube clean | Usually lower GI, but can still be duodenal bleeding with a competent pylorus | Don't exclude UGIB based on clean NG tube alone! |
| Melena | Upper GI down to proximal colon | — |
| Hematochezia | Lower GI, but can be massive UGIB | Always consider massive UGIB if hemodynamically unstable + hematochezia |
High Yield
A clean NG aspirate does NOT rule out upper GI bleeding. A duodenal source with a competent pylorus can bleed without blood refluxing into the stomach. This is a classic exam trick.
| Ongoing / Severe | Slow / Bleeding Stopped |
|---|---|
| Haematemesis | Coffee ground vomiting |
| Fresh melaena | Old melaena |
3. Etiology
Variceal vs Non-variceal bleeding [4]
| Category | Causes |
|---|---|
| Ulcers/Erosions | Duodenal, gastric, esophageal ulcers (account for 25–50% of non-variceal UGIB) |
| Inflammation | Gastritis, duodenitis, esophagitis |
| Tumors | Gastric, esophageal, including GIST |
| Vascular | Angiodysplasia/telangiectasia, Dieulafoy's lesion |
| Esophageal | Mallory-Weiss tear |
| Stomach | Portal hypertensive gastropathy |
| Post-surgical | Anastomotic ulcer |
| Rare | Aortoenteric fistula, hemobilia, hemosuccus pancreaticus, Crohn's disease |
Epistaxis, hemoptysis, oral bleeding lesions [4]
Always ask about nosebleeds, cough with blood, dental procedures!
Ulcers high on lesser curve and in postero-inferior wall of duodenal bulb bleed more easily. [4]
Why? The lesser curve is supplied by the left gastric artery. The posterior wall of D1 overlies the gastroduodenal artery (GDA). Erosion into GDA causes torrential bleeding [6].
Major causes of PUD:
- H. pylori
- NSAIDs/Aspirin
- Stress (ICU patients)
H. pylori, Drug-induced (aspirin/NSAIDs—LOCAL + SYSTEMIC effect), Alcohol, Stress [4]
Key aspirin points from lecture:
- Enteric-coated aspirin still causes bleeding—systemic effect (inhibits COX-1 everywhere, not just stomach)
- Almost all patients on aspirin develop mild hemorrhagic gastritis within 24 hours
- Adaptation and healing occurs
- Bleeding can be acute (first few days) or chronic (months)
- Usually self-limiting after drug removal
Stress gastritis:
- ICU patients: respiratory failure, hypotension, sepsis, renal failure, burns, peritonitis, jaundice, neurological trauma
- All have endoscopic gastritis; 2–10% have significant bleeding
VERY HIGH MORTALITY: 5–10% of cases of UGIB but 80% of mortality. [4]
This is extremely high-yield. Variceal bleeding is high-pressure bleeding (portal hypertension). Peptic ulcer bleeding is comparatively lower pressure [7].
- Gastric varices may accompany esophageal varices, or occur alone (usually in fundus)
- Cirrhosis, non-cirrhotic portal hypertension (splenic vein thrombosis if isolated gastric varices)
- Present with fresh large volume hematemesis; may present with coffee ground vomiting (rare)
Rules of 2/3 (from senior notes): [7]
- 2/3 cirrhotics develop portal HT
- 2/3 with portal HT develop esophageal varices (HVPG ≥ 10 mmHg)
- 2/3 with varices will bleed (HVPG ≥ 12 mmHg)
Near the gastroesophageal junction. Repeated retching/vomiting. Initially no blood followed by vomiting of blood. Alcohol or chemotherapy. Usually self-limiting. [4]
Causes: acid reflux (obese, middle-age, male), infectious (Candida, CMV, herpes—immunocompromised), pill-induced (tetracyclines, elderly, psychiatric patients), sclerotherapy-induced, irradiation, caustic substance ingestion. [4]
Malignancy of stomach and esophagus are uncommon causes of UGIB. Malignancy of duodenum is very rare. Bleeding usually self-limiting. [4]
Less common in stomach/duodenum than in small bowel and colon. Unusual variant: GAVE (watermelon stomach). Associated conditions: elderly, cirrhosis, chronic renal failure, radiation, scleroderma, hereditary hemorrhagic telangiectasia, aortic stenosis (Heyde's syndrome), LVAD. [4]
Heyde's Syndrome
Aortic stenosis + GI bleeding from angiodysplasia. The mechanism involves acquired von Willebrand syndrome (shear stress across the stenotic valve cleaves vWF multimers → impaired platelet adhesion at the site of angiodysplastic lesions). This is a classic exam association.
A large-caliber arteriole that protrudes through the mucosa without an overlying ulcer—causes sudden massive bleeding. Usually in the stomach (proximal, along lesser curve). Difficult to see endoscopically unless actively bleeding [5].
4. History & Physical Examination
Usual questions on onset, duration, episodes… [4]
Associated GI symptoms (critical for narrowing DDx):
| Symptom | Suggests |
|---|---|
| Epigastric pain | Peptic ulcer, malignancy |
| Vomiting e.g. after alcohol | Mallory-Weiss tear |
| Acid reflux / heartburn | Esophagitis / esophageal ulcer |
| Painful dysphagia | Esophagitis / esophageal ulcer |
| Painless dysphagia | Malignancy |
| Symptoms of cirrhosis | Variceal bleeding |
| Constitutional symptoms | Malignancy |
Risk factors to ask about:
- H. pylori infection (ask about treatment and follow-up test)
- Painkillers (NSAIDs)
- HBV / HCV (for cirrhosis → varices)
May not know they are taking these drugs! [4]
Clues:
- IHD, with "chest pain" → on aspirin
- Stroke / TIA → on aspirin/clopidogrel
- Joint pain (OA knee, gout, recent injury) → seen by ortho/dentist → given analgesic + antacid, injections
This is a classic clinical pitfall and exam scenario: the patient says "no painkillers" but is actually on aspirin for cardiovascular indications.
Drug history & allergy: antiplatelets, anticoagulants, rate-lowering drugs (beta-blockers—may mask tachycardia!) [4]
Past medical history: peptic ulcers (higher risk of recurrence), radiation, GI surgery (anastomotic ulcer) [4]
Social history: smoking, alcohol [4]
Beta-Blocker Warning
Patients on beta-blockers may NOT mount an appropriate tachycardic response to hypovolemia. A "normal" heart rate in a bleeding patient on beta-blockers can be falsely reassuring. Always check the drug history.
Assess vital signs → Confirm the complaint → General exam → Abdominal exam → PR exam → CVS exam → Respiratory exam [4]
Confirm the complaint:
- Examine the vomitus
- Examine NG tube aspirate
- (PR exam)
General exam:
- Stigmata of chronic liver disease (spider naevi, palmar erythema, jaundice, gynecomastia, caput medusae, etc.)
- Skin and oral mucosa → pallor, telangiectasia (HHT), Peutz-Jeghers pigmentation
- Cervical lymph nodes → Virchow's node (left supraclavicular) = gastric malignancy
Abdominal exam:
- Epigastric tenderness (PUD)
- Rebound, guarding → ?perforation (surgical emergency!)
- Abdominal mass → malignancy
- Liver and spleen size → cirrhosis/portal hypertension
- PR exam → confirm melena, assess stool color
Cardiovascular exam:
- Aortic stenosis → Heyde's syndrome (angiodysplasia + AS)
Special signs from lecture slides:
- Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu): multiple telangiectases on lips, tongue, fingers
- Peutz-Jeghers syndrome: perioral melanin pigmentation + GI hamartomatous polyps
CBC, RFT, LFT, Clotting profile, Type & Screen/Cross-match, CXR (erect), ECG, CT Abdomen [4]
| Investigation | Key Points |
|---|---|
| Hemoglobin | In acute bleeding, usually normal (hemodilution hasn't occurred yet) |
| MCV | Low → slightly chronic with iron deficiency, or thalassemia. High → ?macrocytosis from liver disease/alcohol |
| Platelet count | Low in cirrhosis (hypersplenism), DIC |
| RFT | Urea abnormally higher than creatinine — blood proteins digested in GI tract → absorbed as urea; hallmark of UGIB |
| LFT | Baseline; deranged in cirrhosis |
| Clotting profile | Prolonged INR in liver disease, warfarin use |
| Type & Screen | Essential for potential transfusion |
| CXR (erect) | Look for free gas under diaphragm (perforation) |
| ECG | Rule out ACS (anemia-induced demand ischemia) |
| CT Abdomen | If suspect perforation, even if CXR does not show free gas |
High Yield: Disproportionately Raised Urea
In UGIB, blood in the GI lumen is digested like protein → amino acids absorbed → converted to urea by liver → serum urea rises disproportionately to creatinine. A urea:creatinine ratio > 100:1 (in SI units) is suggestive of UGIB. This is a classic exam point and helps localize bleeding to upper GI.
Pre-endoscopic Rockall score (blood pressure, pulse, age, comorbidities). Glasgow-Blatchford score. [4]
| Score | Components | Purpose |
|---|---|---|
| Pre-endoscopic Rockall | Age, shock (BP + pulse), comorbidities | Predicts mortality before endoscopy |
| Glasgow-Blatchford Score (GBS) | Hb, urea, BP, pulse, melena, syncope, liver disease, heart failure | Predicts need for intervention (transfusion, endoscopy, surgery); GBS = 0 may be managed as outpatient |
The GBS is particularly useful in the emergency department to decide who needs admission vs. who can safely go home.
7. Management
Resuscitation → History/PE/Ix → Treatment (Blood, Other measures, Upper Endoscopy)- ABC approach
- Large-bore IV access (at least 2 × 16G antecubital), send bloods including T&S
- IV fluids (crystalloid initially)
- Monitor vitals, urine output (Foley catheter)
- NG tube if indicated (to confirm/characterize bleeding)
Restrictive strategy (transfuse when Hb < 7 g/dL) is superior to liberal strategy (transfuse when Hb < 9 g/dL). [4]
The landmark Villanueva et al. NEJM 2013 trial showed:
- Restrictive strategy had lower mortality (HR 0.55, 95% CI 0.33–0.92)
- Also lower rebleeding rates
- Mechanism: overtransfusion raises portal pressure → worsens variceal bleeding; also causes volume overload
Exceptions—transfusion threshold less certain; a level of at least 8–9 g/dL is recommended for: (1) Hemodynamically unstable patients, (2) Underlying cardiovascular diseases, especially acute coronary syndrome. [4]
High Yield: Transfusion Threshold
Default: Restrictive (Hb < 7 → transfuse). Exception: IHD/ACS → aim Hb 8–9 g/dL. This was directly tested in the 2025 MCQ Q33 [3].
Correct coagulopathy and thrombocytopenia: INR < 1.5 and platelet count > 50 × 10⁹/L [4]
- Use of FFP in cirrhosis is controversial (INR in cirrhosis doesn't reflect true coagulation status because both pro- and anti-coagulant factors are reduced)
IV proton pump inhibitors (PPIs) in active bleeding: Esomeprazole 80 mg bolus, then 8 mg/hour infusion. Reduces bleeding stigmata of peptic ulcer and need for endoscopic hemostatic intervention. [4]
Why IV PPI before endoscopy? Acid destabilizes blood clots. By raising gastric pH > 6, you allow clot stabilization, which can downgrade the endoscopic appearance (e.g., from active bleeding to a clean-base ulcer) and reduce the need for intervention.
Splanchnic vasoconstrictors (if underlying cirrhosis): Terlipressin / octreotide. For suspected variceal bleeding (e.g., known varices, symptoms/signs/lab results). [4]
- Terlipressin: V1 vasopressin analog → splanchnic vasoconstriction → reduces portal pressure
- Octreotide: somatostatin analog → similar mechanism
- Start BEFORE endoscopy, continue 2–5 days post-OGD [7]
Antibiotics (if underlying cirrhosis): 3rd generation cephalosporins (esp advanced cirrhosis), quinolones. [4]
Why antibiotics? GI bleeding in cirrhotics carries a very high risk of spontaneous bacterial peritonitis (SBP) and sepsis. Prophylactic antibiotics reduce bacterial infections (Chavez-Tapia meta-analysis [4]) and mortality. In advanced cirrhosis, 3rd-gen cephalosporins (e.g., IV ceftriaxone) are superior to quinolones (Fernandez et al. 2006: infection rate 33% vs 11% with cephalosporins, HR 3.71 for quinolone group) [4].
After stabilization: [4]
- Within 24 hours if hemodynamically stable
- Within 12 hours if hemodynamically unstable
- Within 12 hours if suspected variceal bleeding
Injection with adrenaline, heater probe, hemoclips, argon plasma coagulation (APC), band variceal ligation / sclerotherapy, n-butyl-2-cyanoacrylate (tissue adhesive—for gastric varices) [4]
| Modality | When Used |
|---|---|
| Adrenaline injection | Achieves initial hemostasis (tamponade + vasoconstriction); always combine with a second modality |
| Heater probe | Thermal coagulation of bleeding vessel |
| Hemoclips | Mechanical compression of vessel |
| APC | Superficial thermal ablation; good for angiodysplasia, GAVE |
| Band ligation | First-line for esophageal varices |
| Sclerotherapy | Alternative to banding; more complications |
| Cyanoacrylate glue | For gastric varices (too large/deep for banding) |
Continue PPIs. Resume aspirin ASAP once endoscopic hemostasis has been achieved in those with high cardiothrombotic risk: 1–3 days, certainly within 7 days. [4]
Why resume aspirin early? The Sung et al. Ann Intern Med 2010 trial showed:
- Recurrent ulcer bleeding: aspirin 10.3% vs placebo 5.4% (NS, p=0.25) → slightly higher rebleeding, but…
- All-cause mortality: aspirin 1.3% vs placebo 12.9% (HR 0.2, p=0.005) → massive mortality benefit
The thrombotic events typically occur at days 7–30, usually between days 7–10. So delaying aspirin beyond 7 days risks a thrombotic event (MI, stroke) that is far more lethal than a rebleed.
Eradicate H. pylori. Long-term PPIs if concomitant aspirin use. [4]
High Yield: Post-Bleeding Aspirin Management
Resume aspirin within 1–3 days (max 7 days) after endoscopic hemostasis in high cardiothrombotic risk patients. Delaying aspirin beyond 7 days significantly increases mortality from thrombotic events, which outweighs the small increase in rebleeding risk.
Although not explicitly tabulated in GC 036, Forrest classification appeared in the 2022 minicase (Forrest IIa) [2]. Understanding it is essential:
| Forrest Class | Description | Rebleeding Risk | Need Endoscopic Rx? |
|---|---|---|---|
| Ia | Spurting hemorrhage | ~55% | Yes |
| Ib | Oozing hemorrhage | ~55% | Yes |
| IIa | Non-bleeding visible vessel | ~43% | Yes |
| IIb | Adherent clot | ~22% | Controversial (attempt to remove clot) |
| IIc | Flat pigmented spot | ~10% | No |
| III | Clean-base ulcer | ~5% | No |
9. Obscure GI Bleeding Workup
When OGD and colonoscopy (± SB radiology) fail to identify a source, the lecture walks through additional modalities:
Detects bleeding at 0.5–1 mL/min. Contrast extravasation detected only during active bleeding. Localizes bleeding in 50–72% with massive hemorrhage but only 25–50% when bleeding has slowed/stopped. Advantage: therapeutic also. Complications: catheter site, thromboembolism (ischemic bowel), contrast (allergy, nephropathy). [4]
Detects bleeding at 0.3 mL/min. Contrast extravasation only during active bleeding. No therapeutic interventions. Complications: contrast allergy, nephropathy. [4]
CTA is more sensitive than conventional angiography (lower threshold: 0.3 vs 0.5–1 mL/min) and non-invasive, so often done first. If CTA is negative, conventional angiography is likely also negative.
99mTc sulfur colloid and 99mTc pertechnetate-labeled autologous RBCs. Detects bleeding at 0.1–0.5 mL/min (as little as 5 mL intraluminal blood). Allows sequential scans → increases probability of identifying bleeding site. Caveat: delayed scan may identify site of blood pooling only, not actual bleeding site. [4]
This is the most sensitive radionuclide test for slow/intermittent bleeds. The key advantage is that you can re-image over hours because the tagged RBCs circulate.
Capsule + transmitter → receiver/recorder → workstation. Examines entire small bowel. Diagnostic only. Complications: capsule retention (strictures). [4]
Indications: Obscure GI bleeding, non-stricturing small-bowel Crohn's disease, celiac disease, hereditary polyposis syndromes (Peutz-Jeghers, FAP with duodenal polyps). [4]
Contraindications: Known/suspected GI obstruction or strictures, swallowing disorders, severe motility problems, uncooperative patients. [4]
VCE diagnostic yield 53% vs CTE 40%. VCE better for vascular and inflammatory lesions. CTE better at detecting SB masses. Negative CTE → positive VCE in 57%. Negative VCE → positive CTE in 50%. VCE and CTE are complementary examinations. [4]
DBE: working length 200 cm, overtube 140 cm. Reaches 240–360 cm distal to pylorus, 102–140 cm proximal to ICV. [4]
The balloon system prevents stretching of the looped intestine, allowing stepwise "accordion" advancement deep into the small bowel. Can be performed antegrade (oral) or retrograde (anal).
| Feature | DBE | SBE |
|---|---|---|
| Operators needed | Two | One or Two |
| Speed | Slower intubation | Faster intubation |
| User-friendliness | ++ | +++ |
| Depth of insertion | ++++ | ++ |
| Total enteroscopy rate | ~78% (Japan) | ~25% |
With an accessory channel and tip deflection capability, biopsy and therapeutic interventions are possible: bleeding, mucosal neoplastic lesions. [4]
Remnant of omphalomesenteric duct, arising from antimesenteric surface of middle-to-distal ileum. [4]
Rule of 2's:
- 2% of population
- M:F = 2:1
- Within 2 feet from ICV
- 2 inches in length
- 2% develop complications, usually before age of 2
- Lined by 2 types of mucosa: intestinal + heterotopic (gastric, duodenal, pancreatic, colonic)
Ectopic gastric mucosa → acid secretion → ulcer/bleeding adjacent to or downstream from the diverticulum. [4]
Meckel's Scan:
- IV 99mTc pertechnetate (affinity for gastric mucosa) → scintigraphy
- Meckel's diverticula lacking gastric mucosa will NOT be seen
- Does not detect active bleeding
- Most useful in children and young adults
11. Integration with Related Material
From GC 092 and senior notes: Posterior duodenal ulcers erode into the GDA → torrential hemorrhage. Anterior duodenal ulcers → perforation (different complication axis). Modified Johnson classification for gastric ulcers is not directly tested here but useful background [8].
NSAIDs are particularly dangerous in elderly patients—often prescribed for musculoskeletal pain without adequate PPI cover. Always ask about OTC medications, TCM, and drugs prescribed by other specialists.
The 2025 MCQ Q34 tested precipitants of hepatic encephalopathy—bleeding gastric ulcer was the most likely answer because GI bleeding provides a protein load that is converted to ammonia [3].
12. Likely Exam Questions
-
A 72-year-old man on aspirin for IHD presents with melena. Hb 7.4 g/dL. What is the appropriate transfusion strategy?
- Restrictive strategy (transfuse at Hb < 7 g/dL) is the standard
- BUT this patient has IHD → aim Hb 8–9 g/dL → packed cell transfusion is indicated
- The 2025 MCQ tested exactly this [3]
-
Name 4 clinical features suggestive of recurrent bleeding after endoscopic hemostasis (from 2021 SAQ [1])
- Hematemesis, fresh blood from NG tube, fresh melena, hematochezia, tachycardia, hypotension, drop in Hb
-
What immediate action is needed for a patient with hematemesis, BP 90/60, pulse 100?
- Resuscitation (ABC, large-bore IV access, fluid resuscitation, type & screen, cross-match blood)
-
A patient with known cirrhosis presents with hematemesis. What pharmacotherapy should be started BEFORE endoscopy?
- IV terlipressin (or octreotide) + prophylactic antibiotics (IV ceftriaxone for advanced cirrhosis) + IV PPI
-
When should aspirin be resumed after endoscopic hemostasis for peptic ulcer bleeding in a patient with recent coronary stenting?
- Within 1–3 days, certainly within 7 days
-
Which of the following is NOT a cause of black stool? → Trick: iron tablets cause green-black stool, not true melena
-
A clean NG aspirate rules out upper GI bleeding. → FALSE (duodenal bleeding with competent pylorus)
-
The most sensitive imaging modality for slow intermittent GI bleeding is: → Tagged RBC scan (0.1–0.5 mL/min)
-
Forrest IIa ulcer—what does it mean and does it need endoscopic therapy? → Non-bleeding visible vessel → Yes
| Trap | Correct Answer |
|---|---|
| "Hb is normal so bleeding is not severe" | In acute bleeding, Hb is initially normal (hemodilution takes ≥24h) |
| "NG aspirate is clear so it's not UGIB" | Can be duodenal bleeding with competent pylorus |
| "Liberal transfusion is safer" | Restrictive is better (lower mortality, less rebleeding) except in IHD/hemodynamic instability |
| "FFP corrects coagulopathy in cirrhosis" | Controversial—cirrhotic coagulopathy is balanced |
| "Stop aspirin permanently after GI bleed" | Resume within 1–7 days—mortality benefit outweighs rebleeding risk |
| "Variceal bleeding is common" | Only 5–10% of UGIB but 80% of mortality |
| "Enteric-coated aspirin prevents GI bleeding" | No—systemic COX-1 inhibition still causes bleeding |
High Yield Summary
UGIB = bleeding proximal to ligament of Treitz. Presents as hematemesis, coffee-ground vomiting, melena, or (if massive) hematochezia. Most common cause is peptic ulcer (25–50%). Variceal bleeding is only 5–10% but causes 80% mortality. Key investigations: CBC (Hb may be normal acutely!), RFT (urea disproportionately raised), LFT, clotting, T&S, CXR erect, ECG. Risk stratify with GBS/Rockall. Management: resuscitate → restrictive transfusion (Hb < 7; Hb < 9 if IHD) → IV PPI (80 mg bolus then 8 mg/hr) → correct coagulopathy → terlipressin + abx if variceal → OGD within 24h (12h if unstable/variceal). Post-endoscopy: continue PPI, eradicate H. pylori, resume aspirin within 1–3 days. Obscure GI bleeding: VCE + CTE are complementary; DBE/SBE for therapy; Meckel's scan in young patients. Always ask about hidden NSAIDs/aspirin use!
Active Recall - Upper GI Bleeding
[1] Past papers: 2021 Fourth Summative SAQ (Q9) [2] Past papers: 2022 Fourth Summative Minicase (Case 1, Section 4) [3] Past papers: 2025 Fourth Summative MCQ (Q33, Q34) [4] Lecture slides: GC 036. Coffee ground vomitustarry stool_upper GI bleeding.pdf [5] Senior notes: Ryan Ho GI.pdf (Section 2.1.2) and Ryan Ho Fundamentals.pdf (Section 3.3.2) [6] Senior notes: Maksim Surgery Notes.pdf (Section 3.3) [7] Senior notes: Maksim Medicine Notes.pdf (Section 7 - Oesophageal varices) and Block A - Abdominal distension_ ascites and cirrhosis.pdf [8] Senior notes: Block A - Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf [9] Lecture slides: GC 198. Profuse vomiting of fresh blood and in shock severe upper GI bleeding.pdf [10] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf [11] Senior notes: Block A - Gastroenterology Interactive Tutorial.pdf [12] Past papers: 2018 Fourth Summative Minicase.pdf
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