GC036 Coffee Ground Vomitustarry Stool: Upper GI Bleeding

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]

Current-practice qualifier: do not insert an NG tube solely to “rule out” UGIB. It adds discomfort, has imperfect localization value, and airway manipulation should be cautious in acute variceal bleeding. Use it only when the result will change management ^[13].

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)
• The slide's “almost all patients develop mild hemorrhagic gastritis within 24 hours” describes early endoscopic mucosal injury, not clinically important bleeding in almost everyone
• 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

Lecture-era claim: the slide states “5–10% of UGIB but 80% of mortality.” Do not use 80% as a current mortality estimate. Modern series and guidelines frame outcome as 6-week mortality, typically around 10–20% overall and strongly dependent on Child–Pugh/MELD class and control of haemostasis ^[13][14].

Variceal bleeding is a portal-hypertensive emergency. The pressure-driven pathophysiology is why overtransfusion and indiscriminate plasma expansion can worsen portal pressure ^[13].

• 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)

The former “rule of 2/3” is not a safe quantitative rule: not two-thirds of all varices inevitably bleed. Bleeding risk varies with varix size/red signs, liver disease severity, and portal pressure; an HVPG ≥10 mmHg defines clinically significant portal hypertension and bleeding generally requires a gradient around ≥12 mmHg ^[13].

What the endoscopic image sequence shows (slides 35–41):

• Esophageal varices: tortuous, longitudinal, bluish submucosal columns narrowing the lumen; an active jet identifies the culprit varix.
• Band ligation: the varix is suctioned into the cap and banded, leaving a strangulated polypoid “bleb.” This is first-line endoscopic therapy for esophageal variceal hemorrhage.
• Fundal gastric varices: large grape-like submucosal mounds, often seen best in retroflexion. Their size/depth makes standard banding unreliable; cardiofundal GOV2/IGV1 bleeding is treated with tissue adhesive, with rescue TIPS or BRTO when endoscopic control fails ^[14].

Near the gastroesophageal junction. Repeated retching/vomiting. Initially no blood followed by vomiting of blood. Alcohol or chemotherapy. Usually self-limiting. ^[4]

Image recognition (slide 42): a Mallory–Weiss lesion is a linear longitudinal mucosal laceration crossing or immediately adjacent to the gastroesophageal junction, sometimes with a small adherent clot. This is different from a transmural Boerhaave rupture.

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]

Image recognition (slide 45): malignant bleeding may come from an irregular, heaped-up, friable ulcerated mass rather than a smooth punched-out peptic ulcer. Haemostasis can be difficult and tissue diagnosis is essential once safe.

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]

Image recognition (slides 47–48): an angioectasia is a small, flat, bright-red fern-like focus with radiating ectatic vessels. GAVE is an antral pattern of longitudinal red stripes radiating from the pylorus (“watermelon”) or diffuse red spots. Do not confuse GAVE with portal hypertensive gastropathy, which has a mosaic/snakeskin pattern mainly in the fundus/body and is treated by reducing portal pressure.

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].

Usual questions on onset, duration, episodes… ^[4]

Associated GI symptoms (critical for narrowing DDx):

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]

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 pinpoint or stellate blanching telangiectases on the lips and oral mucosa; ask about recurrent epistaxis and family history
• Peutz-Jeghers syndrome: dark blue-brown macules clustered on the lips/buccal mucosa (often persisting after childhood) + GI hamartomatous polyps

• 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)
• Protect the airway when consciousness is impaired or there is ongoing large-volume hematemesis; intubation is selective, not routine
• NG tube only if a specific result will alter management; it does not exclude UGIB when clear

Assess severity of hypovolemia ^[4]:

• Mild to moderate (< 15% blood volume lost): resting tachycardia
• ≥15% blood volume loss: orthostatic hypotension
• ≥40% blood volume loss: supine hypotension
• ICU admission for severe, life-threatening cases

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

Villanueva rebleeding data (highlighted on lecture slides) ^[4]:

• Overall rebleeding: restrictive 10% vs liberal 16% (HR 0.62, 95% CI 0.43–0.91, p = 0.01)
• Cirrhotic patients: restrictive 12% vs liberal 22% (HR 0.49, 95% CI 0.27–0.90, p = 0.02)
• Peptic ulcer patients: restrictive 10% vs liberal 16% (HR 0.63, 95% CI 0.37–1.07, p = 0.09 — not significant)
• Restrictive strategy also reduced need for rescue therapies (balloon tamponade, TIPS, emergency surgery)

Lecture-era exception: the slide proposes 8–9 g/dL for instability/cardiovascular disease. Current guidance keeps 7 g/dL as the usual trigger in stable patients but individualizes earlier transfusion for exsanguinating/ongoing bleeding, age, cardiovascular disease, and ischemia; a single rigid target should not replace clinical judgment ^[12][13].

Lecture-era target: “INR < 1.5 and platelets > 50 × 10⁹/L.” This may be relevant to selected anticoagulant-associated bleeds/procedures but is not a universal target in cirrhosis.

• In advanced liver disease, PT/INR does not measure the rebalanced haemostatic state. Baveno VII advises against routine FFP in acute variceal bleeding because it does not reliably correct haemostasis and can cause volume overload/worsen portal pressure ^[13].
• Platelet/fibrinogen correction in uncontrolled variceal bleeding is individualized; there is no evidence that a fixed count alone predicts failure of haemostasis ^[13].
• Temporarily withhold anticoagulants during uncontrolled major bleeding and use drug-specific reversal only when severity, timing, renal function, and thrombotic risk justify it; involve the relevant specialty early ^[16].

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. High-dose IV PPI can downstage ulcer stigmata and reduce endoscopic therapy, but has not shown the same benefit for mortality/rebleeding and must not delay endoscopy ^[12]. If the source is variceal, stop empiric PPI after OGD unless another indication exists ^[13].

Large clot burden: consider IV erythromycin 250 mg 30–120 minutes before OGD (if no contraindication such as major QT risk); it improves gastric clearance and visualization ^[13][14].

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 in cirrhosis/advanced chronic liver disease with acute variceal hemorrhage: current ESGE guidance recommends ceftriaxone 1 g IV daily for up to 7 days, modified for allergy, local resistance, cultures, and antimicrobial policy ^[14].

Why antibiotics? GI bleeding in cirrhotics carries a very high risk of spontaneous bacterial peritonitis (SBP) and sepsis. Prophylactic antibiotics reduce bacterial infections and mortality. The Chavez-Tapia meta-analysis (Aliment Pharmacol Ther 2011) showed a pooled RR 0.43 (95% CI 0.19–0.97, p = 0.04) for bacterial infection with antibiotics vs control ^[4]. In advanced cirrhosis, 3rd-gen cephalosporins (e.g., IV ceftriaxone) are superior to quinolones — Fernandez et al. 2006: infection rate 33% (norfloxacin) vs 11% (ceftriaxone), HR 3.71 (95% CI 1.47–9.34), p = 0.003 ^[4].

After haemodynamic resuscitation:

• Nonvariceal UGIB: early OGD within 24 hours. Routine urgent OGD within 12 hours does not improve outcomes; ≤6/≤12-hour OGD is reserved for patients who remain unstable despite adequate resuscitation ^[12].
• Suspected variceal hemorrhage: OGD within 12 hours once resuscitated; if instability persists, perform as soon as safely possible with airway and critical-care support ^[13][14].

Injection with adrenaline, heater probe, hemoclips, argon plasma coagulation (APC), band variceal ligation / sclerotherapy, n-butyl-2-cyanoacrylate (tissue adhesive—for gastric varices) ^[4]

The slide montage shows the instrument-to-lesion match: injection needle for temporary control, coaptive thermal probe pressed onto the vessel, and a clip closing the vessel mechanically. Epinephrine is never definitive monotherapy for a bleeding ulcer—follow it with thermal or mechanical haemostasis. Current ESGE 2026 guidance also recognizes an over-the-scope clip as a first-line alternative for selected high-risk ulcer stigmata ^[12].

For varices, combine vasoactive medication with endoscopic therapy. Use EBL for esophageal varices and tissue adhesive for cardiofundal GOV2/IGV1. Consider pre-emptive TIPS within 72 hours (ideally within 24 hours) for high-risk patients (Child–Pugh C < 14, or Child–Pugh B > 7 with active bleeding, or HVPG > 20 mmHg) ^[13][14].

Peptic ulcer after successful endoscopic haemostasis: give high-dose PPI for 72 hours (continuous infusion or an accepted high-dose intermittent IV/oral regimen), then usually oral PPI twice daily for the early healing period ^[12].

Aspirin depends on indication. For secondary cardiovascular prevention, do not routinely interrupt aspirin; if it was held, the ACG–CAG guideline advises resumption on the day endoscopic haemostasis is confirmed, while ESGE advises as soon as possible (preferably within 3–5 days) ^[12][16]. For primary prevention, reassess and usually discontinue rather than automatically restart.

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 lecture's trial explains why prolonged interruption of secondary-prevention aspirin is dangerous: the modest rebleeding signal was outweighed by fewer deaths. Apply that conclusion only to patients with a genuine cardiovascular indication.

Test for and eradicate H. pylori. If an acute-bleed test is negative, repeat later because bleeding and PPI exposure can cause false negatives. Confirm cure at least 4 weeks after antibiotics, holding PPI/PCAB for 2 weeks and bismuth/antibiotics for 4 weeks before the test ^[17]. Long-term gastroprotection depends on ongoing aspirin/NSAID need and bleeding risk.

Recurrent ulcer bleeding: repeat OGD with endoscopic re-treatment first. If the second endoscopic attempt fails, proceed to transcatheter arterial embolization; surgery follows failed/unavailable embolization ^[12].

Current-practice synthesis ^[15]:

Capsule endoscopy should be performed as early as possible after an overt bleeding episode—ideally within 48 hours—to maximize yield. Routine second-look OGD/colonoscopy before capsule is not required, though a targeted repeat is reasonable when the first examination was incomplete or suspicion remains high ^[15].

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]

Image recognition (slide 55): active extravasation appears as a focal cloud/puddle of contrast outside the expected arterial tree that enlarges on later frames. Catheter angiography is invasive but can immediately convert diagnosis into superselective embolization.

Detects bleeding at 0.3 mL/min. Contrast extravasation only during active bleeding. No therapeutic interventions. Complications: contrast allergy, nephropathy. ^[4]

CTA is fast, non-invasive, and usually precedes catheter angiography in active significant bleeding. A negative scan means there was no detectable extravasation during acquisition; it does not exclude intermittent bleeding.

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.

Its limitation is imprecise localization: blood can move before delayed images are acquired. In a patient with significant ongoing bleeding, CTA is generally faster and more actionable; tagged RBC scanning has a narrower role for intermittent low-rate bleeding when localization will guide subsequent angiography.

Capsule + transmitter → receiver/recorder → workstation. Examines entire small bowel. Diagnostic only. Complications: capsule retention (strictures). ^[4]

Indications: Suspected small-bowel bleeding, non-stricturing small-bowel Crohn's disease, celiac disease, hereditary polyposis syndromes (Peutz-Jeghers, FAP with duodenal polyps). ^[4][15]

Contraindications/precautions: Known or suspected obstruction/stricture and major swallowing risk require an alternative delivery or patency assessment. Established Crohn disease should generally have a patency capsule before VCE ^[15].

What the capsule slides show: normal landmarks include a small papillary ampulla and benign pale nodular lymphoid follicles. Bleeding lesions include shallow punched-out small-bowel ulcers and flat red angioectasias/AVMs with fresh blood nearby. Capsule retention is seen as a persistent radiopaque capsule on abdominal radiograph/CT; if there is no acute obstruction, device-assisted enteroscopy can often retrieve it ^[15].

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]

These percentages are lecture-era pooled estimates, not universal test characteristics. The practical distinction remains useful: capsule is first-line for mucosal/vascular lesions, while CTE is valuable for mural masses, Crohn-related stenosis, and when capsule retention is a concern ^[15].

Reading the CTE images (slide 68): neutral oral contrast distends and separates small-bowel loops; scrutinize multiplanar views for focal hyperenhancement, asymmetric wall thickening, a mass, a transition/stricture, and mesenteric vascular change. CTE shows the bowel wall and extra-luminal disease that capsule cannot.

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).

The diagrams show the push–pull cycle: advance the scope, inflate the tip/overtube balloons to anchor, withdraw to pleat bowel onto the overtube, then repeat. Capsule location and transit time help choose oral (proximal) versus anal (distal) access.

The device-performance numbers above come from early, operator-dependent lecture studies and should not be treated as present-day universal superiority estimates. The clinically important point is that both approaches permit biopsy and haemostasis; route and platform depend on lesion location and local expertise.

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
• Ectopic gastric mucosa is present in < 25% of Meckel's diverticula ^[4]
• Meckel's diverticula lacking gastric mucosa will NOT be seen
• Does not detect active bleeding
• Most useful in children and young adults

The “< 25%” figure refers to the lecture's estimate across all diverticula. Bleeding Meckel diverticula are enriched for ectopic gastric mucosa, which is precisely what the scan detects; a negative scan therefore cannot exclude Meckel diverticulum, especially in adults.

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].