GC198 Profuse Vomiting Of Fresh Blood And In Shock Severe Upper GI Bleeding
Severe upper gastrointestinal hemorrhage presenting with large-volume hematemesis of fresh (bright red) blood accompanied by hemodynamic shock requiring emergent resuscitation and intervention.
This lecture (GC 198, Prof. KM Chu, Department of Surgery, HKU) focuses on the emergency surgical approach to a patient who presents with profuse vomiting of fresh blood and is in shock — the most severe end of the upper GI bleeding (UGIB) spectrum [1]. It builds upon the companion GC 036 lecture on coffee ground vomitus / tarry stool (the "less severe" UGIB lecture) and escalates the clinical urgency to a patient who is haemodynamically unstable and may die within minutes.
The lecture covers:
- How upper GI bleeding presents (the clinical spectrum from occult bleed to haematemesis with shock)
- The pathophysiology behind different presentations (why coffee ground vs. fresh blood vs. melaena)
- Causes of severe UGIB (which diagnoses bleed badly)
- History and examination priorities in a shocked patient
- Classification of haemorrhagic shock (the ATLS shock classes)
- Resuscitation (ABC, IV access, blood products, monitoring)
- The general guideline / decision pathway (ongoing vs. stopped bleeding)
- Role of endoscopy: diagnosis, risk stratification (Forrest classification), therapy
- Post-endoscopy management: monitoring for rebleeding, risk factors for recurrence
- When surgery is needed and what operations are performed
This is a surgical emergency lecture. The examiners test the management algorithm, shock recognition, Forrest classification, indications for surgery, and clinical features of ongoing/recurrent bleeding. Expect MCQs, SAQs, and minicases built around this framework.
Core Concepts from First Principles
Haemoglobin (Hb) exposed to gastric acid is oxidised to methaemoglobin, producing the characteristic brown "coffee ground" appearance. Hb exposed to gut bacteria further converts to haematin, producing the jet-black, tarry, malodorous substance of melaena. [1]
What the biochemistry flowchart shows: two parallel arrows — Acid → Hb → methaemoglobin (coffee ground) vs gut bacteria → Hb → haematin (melaena). Same starting pigment, different “processing plant,” different bedside appearance. [1]
This is the key chemical pathway the lecture emphasises:
| Step | Process | Product | Clinical appearance |
|---|---|---|---|
| 1 | Hb released from blood into stomach | Hb | Fresh red haematemesis |
| 2 | Hb + gastric acid (HCl) | Methaemoglobin | Coffee ground vomitus |
| 3 | Hb/methaemoglobin + gut bacteria (small/large bowel) | Haematin | Melaena (tarry stool) |
Why this matters clinically: The more "processed" the blood appears, the slower or more proximal/stopped the bleeding. Fresh red blood = fast active bleed. Coffee ground = slower or partially digested. Melaena = has had time to transit through the gut.
Fresh melaena = Hb + haematin (jet black, tarry, liquid, non-particulate) → indicates acute ongoing bleeding. Old melaena = haematin only (black-grey, dull, mixed with normal stool) → indicates bleeding has stopped. [1]
This distinction is clinically critical on digital rectal examination (PR exam). When the examiner asks "how do you know if bleeding is ongoing?", fresh melaena on PR is one of the key features.
The lecture explicitly pairs presentations with severity: [1]
| Ongoing / Severe Bleed | Slow / Bleeding Stopped |
|---|---|
| Haematemesis (fresh red blood) | Coffee ground vomiting |
| Fresh melaena | Old melaena |
Additional presentations mentioned:
- Fresh PR bleed (haematochezia) — usually LGIB, but can occur with massive UGIB [1][4]
- Occult bleed — patient presents with symptoms of anaemia (fatigue, dyspnoea, pallor) without visible bleeding [1]
Causes of Upper GI Bleeding
Listed in descending order of frequency: [1]
| Cause | Key Points | Likely to be severe? |
|---|---|---|
| Duodenal or gastric ulcer | Most common cause overall. Posterior D1 ulcer erodes GDA → torrential bleed | Yes |
| Gastritis | Diffuse mucosal erosions, often NSAIDs/alcohol related | Usually less severe |
| Oesophageal or gastric varices | Portal hypertension (cirrhosis). Only ~5-10% of UGIB but ~80% of mortality [5] | Yes — very severe |
| Mallory-Weiss syndrome | Mucosal tear at GEJ after violent retching/vomiting. Usually self-limiting [5] | Usually mild |
| Benign or malignant gastric tumour | Gastric cancer can present with UGIB | Yes |
The lecture specifically lists these — know them for extended matching questions: [1]
| Cause | Why it matters |
|---|---|
| Oesophagitis, oesophageal tumour | Erosive reflux or malignancy |
| Stomal ulcer | Post-gastrectomy — ulcer at anastomotic site |
| Aortoduodenal fistula | Classic "herald bleed" — small bleed then catastrophic. Think post-aortic graft surgery |
| Haemobilia | Bleeding into biliary tree (e.g. after liver biopsy, cholangiocarcinoma) |
| Haemosuccus pancreaticus | Bleeding from pancreatic duct (e.g. pancreatic pseudoaneurysm, chronic pancreatitis) |
| Vascular malformation / angiodysplasia | AV malformations in the GI mucosa; can be diffuse |
| Dieulafoy's lesion | Submucosal artery that erodes through mucosa — massive arterial bleed from a tiny mucosal defect |
| Duodenal/jejunal diverticulum, jejunal ulcer | Rare but can bleed |
High Yield: Which Causes Are Severe?
The lecture specifically highlights causes that are "more likely severe": duodenal/gastric ulcer, oesophageal/gastric varices, aortoduodenal fistula, Dieulafoy's lesion, and vascular malformations. These are discriminators in EMQs — if a question describes massive haematemesis with shock, think of these causes first.
Clinical Approach: History
The lecture organises history into two slides: [1]
| Question | Why it matters |
|---|---|
| Nature, rate, and duration of bleeding | Determines severity and urgency. Frank haematemesis vs. coffee ground vs. melaena |
| Previous episode(s) | Recurrent ulcer? Known varices? Previous endoscopy? |
| Pain | Epigastric pain → PUD. Pain worse with meals → gastric ulcer. Pain relieved by meals → duodenal ulcer. No pain → varices or Dieulafoy |
| Weight loss, anorexia | Red flags for malignancy |
| Medical conditions, liver disease, HBsAg, bleeding tendency | HBsAg carrier → chronic hepatitis B → cirrhosis → varices. Known coagulopathy → prolonged bleeding |
| History of irradiation | Radiation enteritis can cause chronic mucosal damage and bleeding |
| Question | Why it matters |
|---|---|
| Alcohol | Risk factor for gastritis, Mallory-Weiss, liver disease/varices |
| Aspirin, NSAIDs | Directly damage gastric mucosa (inhibit COX-1 → ↓prostaglandin → ↓mucosal protection). Most common drug cause of PUD |
| Anticoagulant (e.g. warfarin) | Does not cause ulcers but makes any bleed worse and harder to stop |
| Antiplatelet agent (e.g. aspirin, clopidogrel) | Same as above + aspirin also causes ulcers |
| Cardiac drugs – beta blockers | Masks tachycardia! A patient on beta blockers may not mount the expected heart rate response to hypovolaemia → you lose the earliest sign of shock |
| Iron – black stool | Iron supplements cause black stool that can mimic melaena. Key differentiator: iron stools are solid, green-black, granular on PR vs. melaena is tarry, loose, extremely malodorous [4] |
Beta-Blockers Mask Tachycardia
This is a classic exam trap. The lecture specifically lists beta blockers under drug history. If a patient on beta blockers presents with UGIB and a "normal" heart rate, you CANNOT use heart rate to exclude significant blood loss. Rely on other signs: blood pressure, urine output, GCS, base deficit.
The lecture lists these signs: [1]
| Sign | What it tells you |
|---|---|
| Pallor, tachycardia, hypotension | Haemodynamic compromise — shock. Tachycardia is the earliest sign |
| Cervical lymph node | Virchow's node (left supraclavicular) → gastric malignancy (Troisier's sign) |
| Signs of chronic liver disease | Spider naevi, palmar erythema, gynaecomastia, jaundice, ascites → think varices |
| Caput medusae, splenomegaly, shifting dullness | Portal hypertension → cirrhosis → variceal bleed |
| Abdominal mass | Gastric tumour |
| PR exam – fresh and old melaena | Confirms GI bleed and indicates whether bleeding is ongoing (fresh) or stopped (old) |
This is the ATLS classification of haemorrhagic shock — tested extensively in exams: [1]
| Parameter | Class I | Class II | Class III | Class IV |
|---|---|---|---|---|
| Blood loss (% / mL) | < 15% / < 750 | 15–30% / 750–1500 | 31–40% / 1501–2000 | > 40% / > 2000 |
| Heart rate | ↔ | ↔ / ↑ | ↑ | ↑ / ↑↑ |
| Blood pressure | ↔ | ↔ | ↔ / ↓ | ↓ |
| Pulse pressure | ↔ | ↓ | ↓ | ↓ |
| Respiratory rate | ↔ | ↔ | ↔ / ↑ | ↑ |
| Urine output (mL/h) | ↔ | ↔ | ↓ | ↓↓ |
| GCS | ↔ | ↔ | ↓ | ↓ |
| Base deficit (mmol/L) | 0 to −2 | −2 to −6 | −6 to −10 | ≤ −10 |
| Need for transfusion | Monitor | Possible | Yes | Massive |
Key teaching points:
- Tachycardia is the earliest sign of shock [1] — blood pressure is maintained until Class III (compensatory mechanisms: catecholamine-driven vasoconstriction and tachycardia maintain BP until > 30% blood volume is lost)
- Pulse pressure narrows before systolic BP drops — because sympathetic vasoconstriction raises diastolic pressure first
- Base deficit is an objective marker of tissue hypoperfusion (lactic acidosis from anaerobic metabolism)
- Urine output reflects renal perfusion — a critically important monitor (target ≥ 0.5 mL/kg/hr) [1]
Why Doesn't BP Drop Until Class III?
The body compensates through the baroreceptor reflex → sympathetic activation → vasoconstriction + tachycardia. This maintains cardiac output until roughly 30% blood volume is lost. Once compensation fails, BP drops precipitously. This is why tachycardia is "earlier" than hypotension and why you must not wait for hypotension to diagnose shock.
The lecture's resuscitation checklist: [1]
| Step | Detail | Rationale |
|---|---|---|
| Secure ABC | Airway (consider ET tube if massive haematemesis + reduced consciousness), Breathing (O₂), Circulation | Standard trauma/emergency approach |
| Nil by mouth | Patient may need urgent OGD or surgery | Aspiration risk |
| NG tube in selected patients | To assess for ongoing bleeding (fresh blood aspirate) and decompress stomach | Not mandatory in all — "selected patients" |
| Large bore IV cannula | At least 14G or 16G in antecubital fossa × 2 | Flow rate ∝ r⁴ (Poiseuille's law) — large bore, short cannulae give fastest flow |
| Group O Rh-ve blood | Universal donor — use when crossmatch not yet available and patient in severe shock | Buys time while type-specific blood is prepared |
| Colloids / crystalloids | Initial volume expansion | Crystalloid (NS or Ringer's lactate) most commonly used; colloids also acceptable |
| Type & cross-match | Order immediately | Takes ~45 min for full crossmatch |
| HaemoCue | Bedside rapid Hb estimation | Guides transfusion decisions |
| CBP, R/LFT, PT/APTT | Assess anaemia severity, renal function, liver function (? cirrhosis), coagulopathy | PT/APTT essential — coagulopathy both diagnostic (liver disease) and therapeutic (needs correction) |
| Erect CXR | Rule out perforation (free gas under diaphragm) | Perforated PUD can coexist with bleeding PUD |
Why Group O Rh-Negative?
Group O = no A or B antigens → won't trigger recipient's anti-A or anti-B antibodies. Rh-negative = no D antigen → safe in Rh-negative recipients. This is used when there is no time to wait for crossmatch. Once type-specific or fully crossmatched blood is available, switch to that.
Important note from senior notes [4]: Hb does NOT accurately reflect degree of acute blood loss in the first 24 hours because haemoconcentration means both RBCs and plasma are lost proportionally. Hb only drops once the extracellular volume expands (fluid shifts or IV fluids given). So a "normal" Hb on admission does NOT mean the patient hasn't lost significant blood.
The lecture lists the monitoring parameters: [1]
| Parameter | Target/Detail |
|---|---|
| Shock chart hourly | Trending is key — a single reading means less than the trend |
| Blood pressure and pulse | Detect ongoing bleeding or response to resuscitation |
| Respiratory rate, pulse oximeter (SaO₂) | Respiratory compromise from aspiration, anaemia, or fluid overload |
| Core temperature | Hypothermia in massive transfusion is common and worsens coagulopathy ("lethal triad": hypothermia, acidosis, coagulopathy) |
| Urine output (0.5 mL/kg/hr) | Best real-time marker of end-organ perfusion. Catheterise the patient |
| Central venous pressure (CVP) | Guides fluid resuscitation, especially in patients with cardiac comorbidities |
| Cardiac monitor | Detect arrhythmias (especially in elderly patients with IHD where anaemia may trigger ischaemia) |
The lecture's core algorithm: [1]
~70–80% of ulcer bleeds stop spontaneously. The critical task is to identify the ~20% with ongoing bleeding and those in shock.
Step 1: Is there shock? → Resuscitate immediately Step 2: Is bleeding ongoing? → Rapid assessment and urgent endoscopy Step 3: Has bleeding stopped? → Standard history, examination, investigation, then elective endoscopy
Features Suggestive of Ongoing Bleeding
The lecture lists 5 features: [1]
- Haematemesis
- Fresh melaena
- Tachycardia
- Fresh per rectal bleeding
- Fresh blood aspirated from NG tube
These are the same features tested in SAQs asking "list clinical features suggestive of recurrent/ongoing bleeding."
Three roles per the lecture: [1]
- Verify bleeding source — what is the cause and where is it?
- Stratify risk of rebleeding — Forrest classification
- Therapy — definitive or temporising haemostasis
Forrest Classification (Endoscopic Stigmata of Recent Haemorrhage — ESRH)
This is the most testable classification in this lecture: [1]
| Forrest Class | Description | Rebleeding Risk |
|---|---|---|
| Ia | Spurting (arterial jet) | 80–90% |
| Ib | Oozing | 30% |
| IIa | Non-bleeding visible vessel | 20–50% |
| IIb | Adherent clot | 20–30% |
| III | Clean base | 0–2% |
Clinical significance:
- Forrest Ia, Ib, IIa → require therapeutic endoscopy (high rebleeding risk)
- Forrest IIb → controversial; most guidelines recommend removing the clot and treating the underlying lesion
- Forrest III → no endoscopic therapy needed → start feeding, plan early discharge [1]
Exam Discriminator: Forrest IIa vs III
A question may describe an ulcer with "a raised, pigmented protuberance in the base but no active bleeding." This is Forrest IIa (visible vessel) — rebleeding risk up to 50% — and it DOES need endoscopic therapy. A "clean, white base with no stigmata" is Forrest III — rebleeding risk < 2% — and needs no intervention. The distinction between these two determines management.
Acute Treatment: Bleeding Peptic Ulcer
Per the lecture: [1]
- Start feeding
- Early discharge
| Method | Technique | Mechanism |
|---|---|---|
| Injection method | Adrenaline (1:10,000) | Local vasoconstriction + tamponade from volume injected. Does NOT provide definitive haemostasis alone — always combine with another method |
| Thermal method | Heater probe | Coagulation of the bleeding vessel through heat |
| Mechanical method | Metal clip (haemoclip) | Physical closure of the vessel |
Standard practice: Combination therapy (injection + thermal OR injection + clip) is superior to monotherapy.
H₂ blocker, PPI → hasten healing of ulcers. PPI infusion. [1]
- PPI infusion (e.g. omeprazole/esomeprazole 80 mg bolus then 8 mg/hr for 72 hours) is the standard after endoscopic therapy for high-risk ulcers. The rationale: gastric acid impairs clot stability. By raising intragastric pH > 6, PPI allows clot stabilisation over the ulcer base, reducing rebleeding.
- H₂ blockers are less effective than PPIs at maintaining high pH but are mentioned in the lecture as "hasten healing."
The lecture emphasises: look out for rebleeding in the first 3 days. [1]
Signs of Possible Rebleeding:
- Increasing pulse rate
- Haematemesis
- Pass fresh melaena again
- Fresh blood aspirated from nasogastric tube
- Drop in haemoglobin level
Risk Factors for Recurrent Bleeding
Two slides of risk factors — all high yield for SAQs: [1]
| Factor | Why |
|---|---|
| Shock on presentation | More severe initial bleed → larger vessel involved |
| Hb < 8.0 g/dL on presentation | Indicates significant blood loss |
| Transfusion required | Proxy for severity |
| Age > 60 years | Impaired physiological reserve, more comorbidities, atherosclerotic vessels that don't contract well |
| Comorbidity | Cardiac, renal, liver disease → less tolerance for rebleed |
| Coagulopathy | Impaired clot formation → harder to stop bleeding |
| Factor | Why |
|---|---|
| Patient already hospitalised | Stress ulcers, sicker patients, delayed presentation |
| Large ulcer | More tissue destruction, higher chance of eroding into a vessel |
| Ulcer on posterior D1 | Posterior wall of first part of duodenum overlies the gastroduodenal artery (GDA) — erosion into GDA causes torrential, life-threatening haemorrhage |
| Ulcer on higher posterior lesser curve | Overlies the left gastric artery — similarly dangerous |
The Gastroduodenal Artery — Classic Viva Question
"Which vessel is at risk when a posterior D1 ulcer bleeds?" → Gastroduodenal artery (GDA). The GDA runs behind the first part of the duodenum. A deep posterior duodenal ulcer erodes through the duodenal wall into the GDA, causing massive arterial haemorrhage that endoscopy may not control → surgical indication.
Surgery for Bleeding Ulcer
Indications per the lecture: [1]
| Indication | Explanation |
|---|---|
| Therapeutic endoscopist not available | If no one can do endoscopic haemostasis, proceed to surgery |
| Massive bleeding | Cannot stabilise the patient long enough for endoscopy |
| Failed endoscopic therapy | Endoscopy attempted but bleeding not controlled |
| Rebleed after endoscopic therapy | Second endoscopy can be attempted, but if this also fails → surgery |
Plication of bleeder + additional procedure [1]
"Plication" = under-running the bleeding vessel with sutures to stop the bleeding. This is the haemostatic component. But you also need to address the underlying ulcer disease.
Depends on: [1]
- Condition of patient (haemodynamically unstable → simpler surgery)
- Experience of surgeon
- Type of ulcer
| Ulcer Type | Procedure |
|---|---|
| Duodenal Ulcer (DU) | V + P = Vagotomy + Pyloroplasty |
| Gastric Ulcer (GU) | Partial gastrectomy |
Why vagotomy for DU? Duodenal ulcers are primarily caused by excess acid. Vagotomy (truncal) removes vagal-mediated acid secretion. Pyloroplasty is needed because vagotomy also denervates the pylorus, causing gastric stasis — the pyloroplasty creates a wider outlet.
Why partial gastrectomy for GU? Gastric ulcers need excision because (a) they may harbour malignancy, and (b) the ulcer itself is in the stomach and removing it removes the disease. Acid reduction alone is less effective for GU than DU.
Modern note: With PPI therapy and H. pylori eradication, acid-reducing surgery is now rare. But the lecture framework is what examiners test.
While the lecture focuses mainly on peptic ulcer bleeding, varices are listed as a major cause of severe UGIB. From the supporting material [2][5]:
| Aspect | Management |
|---|---|
| Resuscitation | Same ABC principles; restrictive transfusion (Hb target 7-8 g/dL — overtransfusion raises portal pressure) |
| Correct coagulopathy | FFP, platelets, vitamin K as needed |
| Antibiotic prophylaxis | IV cephalosporin (e.g. ceftriaxone) — reduces infection-related mortality in cirrhotic patients with variceal bleeding |
| Vasoconstrictor | IV terlipressin (splanchnic vasoconstriction → ↓portal pressure) or IV somatostatin/octreotide |
| Endoscopic therapy | Band ligation (oesophageal varices) or cyanoacrylate injection (gastric varices — too large to band) |
| Rescue | Balloon tamponade (Sengstaken-Blakemore tube) → TIPSS → surgery |
| Feature | Variceal | Non-Variceal (PUD) |
|---|---|---|
| Volume | Very large, profuse | Variable |
| Pain | Usually painless | Often epigastric pain |
| Signs of CLD | Present (jaundice, spider naevi, ascites, splenomegaly) | Usually absent |
| Drug history | Less relevant | NSAIDs, aspirin |
| Endoscopy | Varices visible | Ulcer with Forrest stigmata |
| Pharmacotherapy | Terlipressin, octreotide, antibiotics | PPI infusion |
| Endoscopic Rx | Band ligation, cyanoacrylate | Injection, thermal, clip |
| Transfusion strategy | Restrictive (Hb target 7-8) | Also restrictive but less critical |
Exam Intelligence
| Trap | Correct Approach |
|---|---|
| Hb is normal on admission → exclude significant bleed | WRONG. In acute haemorrhage, Hb is initially maintained because both plasma and RBCs are lost. Hb drops only after haemodilution (12-72h) |
| Blood pressure is normal → no shock | WRONG. BP is maintained until Class III shock (> 30% loss). Use tachycardia, pulse pressure, urine output, base deficit |
| Patient on beta blockers with HR 70 and UGIB | Don't be reassured. Beta blockers suppress tachycardia — look at other parameters |
| Forrest IIa = no intervention needed | WRONG. Visible vessel has 20-50% rebleed risk → needs endoscopic therapy |
| Forrest III = needs intervention | WRONG. Clean base < 2% rebleed → start feeding, early discharge |
| All patients with UGIB need emergency endoscopy | WRONG. ~80% stop spontaneously. Emergency OGD for those with ongoing bleeding / haemodynamic instability |
| Restrictive transfusion = a key concept | Transfuse to Hb 7-8 g/dL (not 10). Overtransfusion causes harm (esp. in varices → ↑portal pressure) |
| DU surgery = partial gastrectomy | WRONG. DU → V+P (vagotomy + pyloroplasty). GU → partial gastrectomy |
- Most common cause of UGIB → Peptic ulcer disease [1][4]
- Highest mortality cause of UGIB → Oesophageal/gastric varices [5]
- Earliest sign of shock → Tachycardia [1]
- Most dangerous ulcer location → Posterior D1 (GDA), higher posterior lesser curve (left gastric artery) [1]
- When to use Group O Rh-negative → When crossmatch not yet available and patient in severe shock [1]
- PPI infusion rationale → Raise intragastric pH > 6 to stabilise clot on ulcer
Additional Integration Points
- Replacement fluids are used to correct existing volume deficits; maintenance fluids cover daily requirements
- Aim for urine output > 0.5 mL/kg/hr as evidence of adequate resuscitation
- Crystalloids distribute to the entire ECF (only ~25% stays intravascular); colloids stay intravascular longer but have fallen out of favour due to evidence of renal harm
- Restrictive transfusion (Hb trigger 7 g/dL, target 7-9) is associated with lower mortality in UGIB compared to liberal (Hb trigger 9, target > 10)
- Especially important in variceal bleeding: overtransfusion → ↑blood volume → ↑portal pressure → ↑rebleeding
High Yield Summary
-
UGIB presentations spectrum
- Haematemesis (severe/ongoing) → Coffee ground (slower) → Fresh melaena (ongoing) → Old melaena (stopped) → Occult (chronic). The chemistry: Hb → methaemoglobin (acid) → haematin (bacteria).
-
Top causes
- PUD (most common), varices (most lethal), gastritis, Mallory-Weiss, tumours. Severe causes also include aortoduodenal fistula, Dieulafoy's.
-
Earliest sign of shock = tachycardia.
- BP doesn't drop until > 30% blood loss (Class III). Beta-blockers mask tachycardia.
-
Resuscitation
- ABC → large bore IV × 2 → Group O Rh-ve if urgent → crystalloid → crossmatch, CBP, clotting, LFT, erect CXR → monitor UO (0.5 mL/kg/hr).
-
~80% of ulcer bleeds stop spontaneously.
- Identify ongoing bleeders (haematemesis, fresh melaena, tachycardia, fresh PR bleed, NG aspirate) → urgent OGD.
-
Forrest classification
- Ia (spurting 80-90%) → Ib (oozing 30%) → IIa (visible vessel 20-50%) → IIb (clot 20-30%) → III (clean base 0-2%). Treat Ia/Ib/IIa endoscopically. III = feed and discharge.
-
Endoscopic Rx
- Injection (adrenaline) + Thermal (heater probe) or Mechanical (clip). Post-Rx: PPI infusion (80 mg bolus → 8 mg/hr × 72 hrs).
-
Monitor for rebleeding × 3 days
- ↑HR, haematemesis, fresh melaena, NG blood, ↓Hb.
-
Risk factors for rebleed
- Shock, Hb < 8, transfusion, age > 60, comorbidity, coagulopathy, large ulcer, posterior D1 (GDA), high posterior lesser curve (left gastric artery).
-
Surgery indications
- No endoscopist, massive bleed, failed endoscopy, rebleed after endoscopy. DU = V+P. GU = partial gastrectomy.
Active Recall - Severe Upper GI Bleeding
[1] Lecture slides: GC 198. Profuse vomiting of fresh blood and in shock severe upper GI bleeding.pdf [2] Senior notes: Block A - Abdominal distension_ ascites and cirrhosis.pdf (Managing Acute Esophageal Variceal Bleeding) [3] Senior notes: Block A - Introduction to GI_Hepatology investigations (LFT, Endoscopy).pdf (Causes of Acute Upper GI Bleeding) [4] Senior notes: Ryan Ho Fundamentals.pdf (Upper GI Bleeding section) [5] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf [6] Senior notes: Ryan Ho Fluids and Nutrition.pdf (Principles of Fluid Therapy) [7] Senior notes: Maksim Surgery Notes.pdf (UGIB section) [9] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Question 37)
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