Figure Restrictive transfusion, vasoactive drug, prophylactic antibiotic, endoscopy within 24 hours — TIPSS if refractory.
Acute upper GI bleed : RESUSCITATE (ABC, restrictive transfusion Hb 70; intubate if encephalopathic) → Glasgow-Blatchford Score (0 = low-risk outpatient; high = ICU + endoscopy) → Endoscopy within 24h (adrenaline + clips for ulcers; band ligation for varices). Variceal : vasoactive (terlipressin/octreotide) + prophylactic antibiotics (ceftriaxone) + band ligation → TIPSS if refractory. Non-variceal : PPI (pantoprazole) + endoscopic therapy → surgery/IR if refractory. Tranexamic acid: HALT-IT trial — NO benefit (do NOT give routinely) . Mortality 10% (non-variceal); 15-30% (variceal).
[3]
[4]
[3]
SAQ — Upper GI bleed: Glasgow-Blatchford risk stratification 10 minutes · 10 marks
Reveal all A 71-year-old man presents to the emergency department with two episodes of melaena overnight and one episode of coffee-ground vomit. He has known ischaemic heart disease (prior NSTEMI, on aspirin 100 mg daily) but no known liver disease. He is alert and orientated (GCS 15). Heart rate 108/min, blood pressure 96/58 mmHg, respiratory rate 22, SpO2 96% on room air. Initial Hb 78 g/L, platelets 180 x 10^9/L, INR 1.1, urea 14.5 mmol/L, creatinine 110 micromol/L, lactate 2.4. Venous pH 7.32. Acute upper GI bleeding is suspected.
a Calculate this patient's Glasgow-Blatchford Score (GBS), list its components, and explain how the score alters his disposition. (5 marks)
b Outline your transfusion and pharmacotherapy in the period BEFORE endoscopy. (3 marks)
c When should endoscopy occur and what Forrest grade would prompt dual endoscopic therapy? (2 marks)
[1]
SAQ — Variceal versus non-variceal upper GI bleeding 10 minutes · 10 marks
Reveal all Two patients are admitted simultaneously with suspected upper GI bleeding. PATIENT A: 55-year-old man with alcohol-related cirrhosis (Child-Pugh B, score 9), known oesophageal varices, presents with torrential haematemesis, drowsy (GCS 13), HR 122/min, BP 82/48 mmHg, Hb 70 g/L, platelets 58 x 10^9/L, INR 1.8. PATIENT B: 68-year-old woman on long-term NSAIDs for osteoarthritis, three episodes of melaena, alert, HR 96/min, BP 110/70 mmHg after 1 L crystalloid, Hb 88 g/L, normal liver function and coagulation.
a Contrast the PRE-ENDOSCOPY pharmacological and supportive management of these two patients. (5 marks)
b Describe the endoscopic therapy, and the definitive / rescue options if bleeding persists, for each patient. (3 marks)
c Justify your approach to tranexamic acid in upper GI bleeding with reference to the relevant trial. (2 marks)
[4]
Clinical pearls
High-yield upper GI bleed points for CICM/FFICM exam
Glasgow-Blatchford Score — pre-endoscopy risk. (1) THE SCORE (0 = low-risk; high = high-risk): (a) Blood urea (elevated — digested blood -> protein -> urea). (b) Haemoglobin (low — bleeding). (c) Systolic BP (low — hypovolaemia). (d) Pulse (high — hypovolaemia). (e) Comorbidity (cardiac, hepatic, renal). (f) Syncope, melaena, hepatic disease, cardiac failure. (2) USE: (a) Score 0 = LOW-RISK (suitable for OUTPATIENT — don't admit if stable + score 0 — safe discharge + early endoscopy as outpatient). (b) Score ≥1 = NOT low-risk (admit). (c) High score (≥7-8) = HIGH-RISK (ICU + urgent endoscopy + transfusion). (3) ADVANTAGE: uses PRE-ENDOSCOPY variables (available at presentation) -> triage BEFORE endoscopy. (4) VALIDATION: multiple studies — score 0 has <1% need for intervention + <0.5% mortality -> safe outpatient. (5) PRACTICE: calculate GBS at presentation — guides disposition (outpatient vs ward vs ICU) + urgency of endoscopy. (6) Rockall score (post-endoscopy — includes endoscopic findings — predicts mortality + rebleeding) — use AFTER endoscopy.[2]
Restrictive transfusion — Hb 70 (Villanueva trial). (1) VILLANUEVA (2013, NEJM): RCT — RESTRICTIVE (transfuse if Hb <70) vs LIBERAL (transfuse if Hb <90) in acute UGIB. RESULT: (a) RESTRICTIVE had HIGHER survival (5% vs 9% mortality at 45 days). (b) RESTRICTIVE had LESS rebleeding (more rebleeding in liberal — from increased blood volume -> raised portal pressure -> variceal rebleeding). (c) RESTRICTIVE had LESS adverse events (transfusion reactions, circulatory overload — TACO). (2) RATIONALE: (a) Liberal transfusion -> EXPANDS blood volume -> raises PORTAL VENOUS pressure (in variceal bleed) -> disrupts clot -> REBLEEDING. (b) Also: transfused blood has IMPAIRED platelet function (stored) + dilutional coagulopathy -> worse haemostasis. (3) RECOMMENDATION: RESTRICTIVE strategy — transfuse if Hb <70 g/L (target 70-90). (4) EXCEPTIONS (transfuse more liberally): (a) MASSIVE bleeding (exsanguinating — haemodynamic instability — transfuse freely — massive transfusion protocol). (b) CARDIOVASCULAR disease (ischaemic heart disease — may need Hb 80-90 for oxygen delivery). (c) Older/ frail (less reserve). (5) PRACTICE: Hb 70 threshold for stable UGIB; higher (80-90) for massive bleeding or cardiac disease. (6) KEY: 'one unit at a time' (transfuse, recheck, transfuse again if needed) — avoid over-transfusion.[5]
Variceal bleed — vasoactive + antibiotics + banding. (1) VASOACTIVE (TERLIPRESSIN/OCTREOTIDE): (a) TERLIPRESSIN (vasopressin analogue — 2 mg IV q4h) — reduces portal pressure (splanchnic vasoconstriction -> reduced portal flow -> reduced variceal pressure -> stops bleeding). (b) OCTREOTIDE (somatostatin analogue — 50 mcg bolus + 50 mcg/hr) — similar. (c) START IMMEDIATELY (if cirrhosis/known varices — don't wait for endoscopy confirmation). (d) Continue 2-5 days (until endoscopic therapy + stabilisation). (e) SIDE EFFECTS: terlipressin -> ischaemia (coronary, mesenteric, digital), hyponatraemia. (2) PROPHYLACTIC ANTIBIOTICS (CEFTRIAXONE): (a) Cirrhotics are IMMUNOCOMPROMISED (bacterial translocation from gut -> infection during bleed). (b) Infection worsens bleeding (coagulopathy + portal pressure). (c) PROPHYLACTIC ceftriaxone (1 g IV daily for 7 days) REDUCES infection + MORTALITY (multiple trials). (d) START IMMEDIATELY (if cirrhosis). (3) ENDOSCOPIC BAND LIGATION: (a) Rubber bands on varix -> strangulates -> sloughs (over days). (b) FIRST-LINE for oesophageal varices. (c) REDUCES rebleeding + mortality (vs sclerotherapy). (4) EARLY TIPSS (pre-emptive): (a) For HIGH-RISK cirrhotics (Child-Pugh C 10-13 OR Child B with ACTIVE bleeding) — Baveno VII. (b) TIPSS within 72h of admission (pre-emptive — before refractory). (c) REDUCES rebleeding + mortality (vs banding alone) in this high-risk group. (d) DISCUSS with hepatology/interventional radiology. (5) KEY: variceal bleed = vasoactive + antibiotics + banding (+ early TIPSS for high-risk).[4]
Non-variceal ulcer — Forrest classification + dual therapy. (1) FORREST CLASSIFICATION (endoscopic appearance — predicts rebleeding + guides therapy): (a) Ia: ACTIVE spurting bleeding (highest risk — treat). (b) Ib: ACTIVE oozing (high — treat). (c) IIa: NON-BLEEDING visible vessel (high — treat). (d) IIb: NON-BLEEDING adherent clot (moderate — may remove + treat). (e) IIc: NON-BLEEDING flat pigmentation (low — observe). (f) III: CLEAN base (lowest — no treatment — will heal). (2) ENDOSCOPIC THERAPY (for Ia, Ib, IIa — high-risk): (a) ADRENALINE INJECTION (1:10,000 — into submucosa around ulcer) — vasoconstriction + tamponade. (b) THERMAL (heater probe, bipolar coagulation) — coagulate vessel. (c) CLIPS (haemoclips — mechanical closure). (d) COMBINATION (adrenaline + thermal/clips — DUAL therapy — BEST — reduces rebleeding vs monotherapy). (3) FOR IIb (adherent clot): may REMOVE clot (snare/water jet) + treat underlying vessel (if high-risk patient). (4) FOR IIc, III (low-risk): NO endoscopic therapy (will heal with PPI). (5) POST-ENDOSCOPY: PPI infusion (80 mg bolus + 8 mg/hr for 72h — for high-risk Forrest Ia/Ib/IIa — reduces rebleeding). (6) H. PYLORI: test (biopsy — rapid urease test or histology) — if positive -> ERADICATION (triple therapy — PPI + amoxicillin + clarithromycin — 14 days — prevents recurrence). (7) STOP NSAIDs (if cause — switch to paracetamol).[1]
HALT-IT trial — tranexamic acid NO benefit. (1) HALT-IT (2020, Lancet): RCT — TRANEXAMIC ACID (1 g IV bolus then 3 g/24h for 24h) vs placebo in acute GI bleed (upper + lower — 12,000 patients). RESULT: (a) NO difference in DEATH from bleeding (3.7% vs 3.8%). (b) NO difference in rebleeding. (c) MORE thromboembolic events (venous, seizures) in TXA group (trend — not significant but concerning). (2) CONCLUSION: TRANEXAMIC ACID does NOT benefit acute GI bleed — DO NOT give routinely. (3) RATIONALE (why it failed): (a) GI bleed is not primarily fibrinolytic (unlike trauma/postpartum — where TXA helps — CRASH-2, WOMAN). (b) The bleeding stops with endoscopic/mechanical therapy (not fibrinolysis-dependent). (4) CURRENT: DO NOT give TXA for UGIB (no benefit + possible harm — thrombosis). (5) EXCEPTION: may consider in MASSIVE bleeding (if fibrinolysis contributing — but evidence weak — discuss). (6) KEY: this is a RECENT landmark trial — changed practice (TXA was previously used — now not recommended).[3]
PPI — pantoprazole infusion. (1) PROTON PUMP INHIBITOR (PPI — pantoprazole, esomeprazole): (a) Mechanism: irreversibly inhibits H+/K+ ATPase (proton pump) in parietal cells -> raises gastric pH -> stabilises clot (acid dissolves clot -> rebleeding). (b) DOSE: 80 mg IV BOLUS + 8 mg/hr INFUSION (for 72h after endoscopic therapy in high-risk ulcer). (c) EVIDENCE: (i) REDUCES rebleeding + need for surgery (meta-analyses — Odutayo 2018 BMJ). (ii) BUT: 2019 International Consensus — recommends AGAINST routine pre-endoscopy PPI for ALL (no mortality benefit — selective for high-risk). (iii) POST-endoscopy PPI for HIGH-RISK ulcers (Forrest Ia/Ib/IIa) — standard. (2) PRE-ENDOSCOPY: (a) OLD practice: PPI for ALL UGIB (to stabilise clot before endoscopy). (b) CURRENT: SELECTIVE — may give (reduces rebleeding + need for surgery) but DON'T delay endoscopy for PPI. (c) If low-risk (GBS 0 — may not need PPI pre-endoscopy). (3) POST-ENDOSCOPY: (a) HIGH-RISK ulcer (Forrest Ia/Ib/IIa + endoscopic therapy) -> PPI infusion 72h (reduces rebleeding). (b) Then ORAL PPI (pantoprazole 40 mg daily for 4-8 weeks — heal ulcer). (4) LOW-RISK (Forrest IIc, III — no therapy) -> oral PPI (heal ulcer). (5) SIDE EFFECTS: (a) Hypomagnesaemia, hypocalcaemia (PPIs reduce absorption). (b) Increased C. difficile (PPIs alter gut flora). (c) Increased fractures (calcium absorption). (d) Acute interstitial nephritis. (6) DON'T use long-term unnecessarily (risks).[6]
TIPSS — for refractory variceal. (1) TIPSS (TransJugular Intrahepatic Portosystemic Shunt): (a) PROCEDURE: interventional radiology — jugular vein -> hepatic vein -> create channel (with stent) through liver to PORTAL vein -> shunts portal blood to systemic (bypasses liver) -> reduces PORTAL PRESSURE -> stops variceal bleeding. (b) INDICATIONS: (i) REFRACTORY variceal bleeding (failed band ligation + vasoactive). (ii) EARLY (pre-emptive) TIPSS — for high-risk cirrhotics (Child C 10-13 or Child B + active bleeding) — within 72h — Baveno VII — reduces rebleeding + mortality. (iii) Refractory ascites, hepatic hydrothorax, Budd-Chiari (other portal hypertension complications). (2) ADVANTAGE: reduces portal pressure -> definitive for variceal bleeding. (3) DISADVANTAGES: (a) HEPATIC ENCEPHALOPATHY (shunts blood PAST liver -> toxins (ammonia) reach brain -> confusion/coma — 30-50% develop). (b) LIVER FAILURE (shunts reduce liver perfusion -> worsens function). (c) HEART FAILURE (increased venous return -> volume overload). (d) PROCEDURE complications (bleeding, infection). (4) CONTRAINDICATIONS: severe heart failure, severe encephalopathy, severe liver failure (MELD >18-25 — too sick), polycystic liver, tumour. (5) POST-TIPSS: monitor encephalopathy (treat with lactulose, rifaximin), liver function. (6) LIVER TRANSPLANT: if end-stage cirrhosis — curative (resolves portal hypertension + liver disease). (7) PRACTICE: TIPSS for refractory variceal (or early high-risk) — discuss with hepatology/IR.[4]
Massive transfusion protocol — for exsanguinating UGIB. (1) ACTIVATE if: massive bleeding (haemodynamic instability despite resuscitation, Hb dropping rapidly, visible exsanguination). (2) RATIO 1:1:1 (RBC:plasma:platelet — PRCT trial — trend to fewer deaths from exsanguination vs 1:1:2). (3) TRANEXAMIC ACID: (a) In TRAUMA (CRASH-2) — within 3h reduces mortality. (b) In GI BLEED (HALT-IT) — NO benefit. (c) In MASSIVE GI bleed — may consider (if fibrinolysis contributing — but evidence weak — discuss). (4) CALCIUM: transfused blood contains citrate (anticoagulant) -> chelates Ca2+ -> hypocalcaemia -> monitor + replace (calcium chloride/gluconate). (5) WARM: prevent hypothermia (worsens coagulopathy). (6) CORRECT ACIDOSIS (worsens coagulopathy). (7) TARGET: Hb >80, platelets >50, fibrinogen >1.5, INR <1.5, ionised Ca2+ >1.0. (8) DON'T delay definitive therapy (endoscopy/surgery/IR/TIPSS) for transfusion — transfuse WHILE preparing definitive. (9) MORTALITY: high (massive bleeding — often variceal or large ulcer with arterial bleeder).[1]
Airway protection — intubate if encephalopathic. (1) RISK: aspiration (haematemesis -> vomit -> aspirate -> pneumonitis/ARDS) — especially in: (a) ENCEPHALOPATHIC (cirrhosis — altered mental status — can't protect airway). (b) ACTIVE haematemesis (large volume — high aspiration risk). (c) Sedated/obtunded. (2) INDICATION for INTUBATION: (a) Encephalopathy (any degree — risk increases). (b) Massive haematemesis (ongoing — high volume). (c) Before ENDOSCOPY (if encephalopathic — protect airway during procedure). (3) PROCEDURE: (a) RSI (rapid sequence — assume full stomach — blood in stomach). (b) LARGE-BORE SUCTION (Yankauer — blood + clots). (c) HEAD DOWN tilt (let blood drain out — not into lungs). (d) Tilt patient LEFT LATERAL (if possible — blood drains). (4) BENEFIT: protects airway (prevents aspiration — a leading cause of death in UGIB) + facilitates endoscopy (safe procedure). (5) RISK: intubation has risks (oesophageal trauma, hypotension from anaesthetic, delay). (6) DECISION: balance — encephalopathic + active bleed -> intubate (benefit > risk); alert + small bleed -> don't intubate (observe). (7) PRACTICE: have LOW THRESHOLD to intubate encephalopathic cirrhotics with UGIB (aspiration is a killer).[1]
Coagulopathy in cirrhosis — correct before/during. (1) CIRRHOSIS causes COAGULOPATHY: (a) Impaired SYNTHESIS (liver makes clotting factors — II, V, VII, IX, X, XI, fibrinogen — cirrhosis -> low). (b) THROMBOCYTOPENIA (hypersplenism from portal hypertension -> platelet sequestration -> low). (c) VITAMIN K deficiency (impaired absorption — cholestasis -> low II, VII, IX, X). (d) DIC (sepsis in cirrhosis -> DIC on top). (2) ASSESS: PT/INR, platelets, fibrinogen (low in cirrhosis). (3) CORRECT (if bleeding or before procedure): (a) FRESH FROZEN PLASMA (FFP — 15 mL/kg — provides factors — correct PT). (b) PROTHROMBIN COMPLEX CONCENTRATE (PCC — more concentrated — less volume — faster — but not all factors). (c) CRYOPRECIPITATE (if fibrinogen <1.5 — provides fibrinogen). (d) PLATELETS (if <50 + bleeding — transfuse). (e) VITAMIN K (phytomenadione 10 mg IV — if vitamin K deficiency — takes 6-12h). (4) CAUTION: (a) Don't OVER-correct (cirrhosis is BOTH prothrombotic AND anticoagulant deficient — rebalanced haemostasis — correcting 'abnormal' labs may cause THROMBOSIS). (b) The INR in cirrhosis DOESN'T accurately reflect bleeding risk (the 'rebalanced' haemostasis — INR may be high but bleeding risk not proportionate). (5) PRACTICE: correct SEVERE coagulopathy (if bleeding) but don't chase 'normal' INR (balance — thrombosis risk). Thromboelastography (TEG/ROTEM) may guide (viscoelastic — better than INR for cirrhosis).[4]
Rebleeding — risk factors and management. (1) REBLEEDING (within 3-5 days of initial): 10-20% (ulcer); 60% (variceal — without secondary prophylaxis). (2) RISK FACTORS (ULCER): (a) HIGH-RISK FORREST (Ia/Ib/IIa — active bleeding/visible vessel). (b) LARGE ulcer (>2 cm). (c) HIGH-RISK LOCATION (posterior duodenal bulb — gastroduodenal artery; high gastric lesser curve — left gastric artery — near large vessels). (d) COMORBIDITY (older, cardiac, renal, shock on presentation). (e) H. PYLORI not eradicated. (f) NSAIDs continued. (3) RISK FACTORS (VARICEAL): (a) Child-Pugh C (severe cirrhosis). (b) Active bleeding at endoscopy. (c) Large varices. (d) No beta-blocker/banding. (4) MANAGEMENT: (a) REPEAT ENDOSCOPY (second attempt — may succeed — dual therapy). (b) INTERVENTIONAL RADIOLOGY (angiography + embolisation — non-variceal). (c) TIPSS (variceal — refractory). (d) SURGERY (last resort — oversew ulcer — high mortality). (5) PREVENTION: (a) ULUCER: PPI + H. pylori eradication + stop NSAIDs + endoscopic dual therapy. (b) VARICEAL: beta-blocker + band ligation (eradicate) ± TIPSS (high-risk). (6) MORTALITY from rebleeding: high (especially in cirrhotics/elderly).[1]
Forrest classification — guides endoscopic therapy. (1) THE CLASSIFICATION (endoscopic appearance of ulcer): (a) I: ACTIVE BLEEDING — Ia (sputting — arterial), Ib (oozing). (b) II: STIGMATA OF RECENT BLEEDING — IIa (visible vessel — non-bleeding), IIb (adherent clot), IIc (flat pigmentation — haematin). (c) III: CLEAN BASE (no stigmata — healed/never bled). (2) REBLEEDING RISK (without treatment): Ia 55-100%, Ib 30-55%, IIa 40-50%, IIb 20-30%, IIc 5-10%, III <5%. (3) ENDOSCOPIC THERAPY INDICATED: Ia, Ib, IIa (high-risk — treat with dual therapy — adrenaline + thermal/clips). (4) IIb (adherent clot): controversial — may remove + treat underlying (if high-risk patient) or leave + PPI (if low-risk). (5) IIc, III (low-risk): NO endoscopic therapy (observe + PPI — will heal). (6) USE: guides which ulcers to treat (Ia/Ib/IIa) vs observe (IIc/III) — reduces unnecessary therapy (low-risk would heal anyway) + ensures high-risk get treatment (reduces rebleeding). (7) POST-THERAPY: PPI infusion (for high-risk Ia/Ib/IIa after therapy).[1]
Lower GI bleed — distinguish (melaena vs haematochezia). (1) UPPER GI bleed: (a) HAEMATEMESIS (vomiting blood — coffee-ground or fresh). (b) MELAENA (black, tarry stool — digested blood — from upper GI — typically proximal to ligament of Treitz). (2) LOWER GI bleed: (a) HAEMATOCHEZIA (bright red blood per rectum — fresh — lower GI — colon/rectum). (b) No haematemesis (bleeding is below stomach). (3) OVERLAP: (a) MASSIVE upper GI bleed can cause HAEMATOCHEZIA (rapid transit — blood doesn't have time to digest -> bright red — confusing — looks like lower). (b) RIGHT colon bleed can cause MELAENA (slow transit — digested — looks like upper). (4) DETERMINE SOURCE: (a) UPPER GI endoscopy FIRST (if haematemesis or melaena — upper source likely). (b) If haematochezia + haemodynamically STABLE -> consider lower GI (colonoscopy). (c) If haematochezia + SHOCK -> suspect MASSIVE upper GI (rapid transit) -> upper endoscopy first. (d) CT angiography (if obscure — identify bleeding source). (e) Tagged RBC scan (nuclear — for slow intermittent — localise). (5) LOWER GI causes: diverticulosis (most common — 40%), angiodysplasia, colitis (ischaemic, infectious, IBD), polyp/cancer, haemorrhoids, post-polypectomy. (6) MANAGEMENT: colonoscopy (diagnostic + therapeutic — clips, adrenaline), IR embolisation, surgery (if refractory).[1]
Post-discharge — H. pylori + secondary prophylaxis. (1) NON-VARICEAL (ULCER): (a) H. PYLORI ERADICATION (if positive — triple therapy — PPI + amoxicillin + clarithromycin — 14 days — CONFIRM eradication with urea breath test/stool antigen at 4+ weeks post-treatment). (b) STOP NSAIDs (switch to paracetamol; if NSAID essential + H. pylori negative -> PPI co-prescription lifelong). (c) ANTIPLATELET/ANTICOAGULANT: resume (if for cardiovascular indication — after haemostasis — usually within 7 days — balance bleeding vs thrombosis — multi-disciplinary). (d) PPI for 4-8 weeks (heal ulcer). (e) Follow-up endoscopy (if malignancy suspected — biopsy; large gastric ulcer — recheck at 8 weeks — exclude cancer). (f) SMOKING CESSATION (impairs ulcer healing). (2) VARICEAL: (a) NON-SELECTIVE BETA-BLOCKER (propranolol, nadolol, carvedilol — reduce portal pressure — reduces rebleeding — lifelong). (b) REPEAT BAND LIGATION (eradicate varices — multiple sessions q2-4 weeks until obliterated — then surveillance). (c) TIPSS (if recurrent despite beta-blocker + banding — definitive). (d) LIVER TRANSPLANT (if end-stage cirrhosis — curative). (e) ADDRESS CIRRHOSIS (alcohol cessation — rehab; treat hepatitis — antivirals for HBV/HCV; nutrition). (f) VACCINATION (hepatitis A/B, influenza, pneumococcal — prevent further liver insult). (3) PROGNOSIS: (a) Non-variceal mortality 10% (older, comorbid). (b) Variceal mortality 15-30% (Child-Pugh/MELD — cirrhosis severity). (c) Rebleeding: 10-20% (ulcer — reduced by PPI + H. pylori); 60% (variceal — reduced by beta-blocker + banding/TIPSS).[1]
Red flags
Critical upper GI bleed red flags
Glasgow-Blatchford Score : 0 = low-risk (outpatient); high = ICU + endoscopy.[2]
Restrictive transfusion : Hb 70 (Villanueva — liberal worse) — EXCEPT massive bleeding.[5]
Endoscopy within 24h (diagnostic + therapeutic).[1]
Variceal : vasoactive (terlipressin) + prophylactic antibiotics (ceftriaxone) + band ligation.[4]
Early TIPSS for high-risk cirrhotics (Child C or Child B + active bleeding) — Baveno VII.[4]
Tranexamic acid: HALT-IT — NO benefit (do NOT give routinely).[3]
Intubate if encephalopathic (aspiration protection).[1]
Forrest classification : Ia/Ib/IIa (high-risk) -> dual endoscopic therapy + PPI infusion.[1]
Massive transfusion 1:1:1 (PRCT) for exsanguinating.[1]
Prognosis
Upper GI bleed evidence and outcomes
[4]
Figure Exam overview — key physiology, red flags and first-hour management.
Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation.
Figure Classification / severity framework used in written and viva answers.
Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1: restate definition, one number examiners expect, and one absolute do-not-miss action for acute-upper-gi-bleed-glasgow-blatchford-endoscopy-tipss .
Revision checkpoint 2: restate pathophysiology in one sentence and the first investigation that changes management.
Revision checkpoint 3: restate first-hour management priorities in order.
Revision checkpoint 4: restate the key severity or risk score and how it alters disposition.
Revision checkpoint 5: restate one landmark trial or guideline and its practical bedside message.
Revision checkpoint 6: restate the most dangerous treatment trap.
Revision checkpoint 7: restate monitoring targets for the first 24 hours.
Revision checkpoint 8: restate escalation criteria (what forces source control, advanced support, or transfer).
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Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
[1] References [1] Barkun AN, et al. Management of Nonvariceal Upper Gastrointestinal Bleeding: Guideline Recommendations From the International Consensus Group. Ann Intern Med , 2019.PMID 31634917 [2] Blatchford O, et al. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage. Lancet , 2000.PMID 11073021 [3] HALT-IT Trial Collaborators Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial. Lancet , 2020.PMID 32563378 [4] de Franchis R, et al. Baveno VII - Renewing consensus in portal hypertension. J Hepatol , 2022.PMID 35120736 [5] Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med , 2013.PMID 23281973 [6] Leontiadis GI, et al. Systematic review and meta-analysis of proton pump inhibitor therapy in peptic ulcer bleeding. BMJ , 2005.PMID 15684023