Approach to Upper GI bleed history taking and examination detail approach with investigation and enlist all possible differential from standard textbook for consultant

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"upper gastrointestinal bleeding" AND management

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Upper Gastrointestinal Bleeding - Complete Consultant Reference

Definition: Upper GI bleeding (UGIB) is any hemorrhage originating proximal to the ligament of Treitz - encompassing esophageal, gastric, and duodenal sources.
GI Bleeding Classification

1. HISTORY TAKING

A. Presenting Complaint - Characterize the Bleed

Hematemesis
  • Fresh red blood vs. coffee-ground material (digested blood indicates slower or stopped bleeding)
  • Volume: estimate in cups/liters; number of episodes
  • Presence of clots (suggests significant arterial hemorrhage)
  • Association with retching or vomiting before the bleed (Mallory-Weiss tear)
Melena
  • Black, tarry, offensive-smelling stool - confirms upper GI source in most cases
  • Age <50 with melena more strongly suggests UGIB even without hematemesis
  • Duration and number of episodes
Hematochezia
  • Bright red per rectum - typically lower GI, but ~14-15% of hematochezia cases originate from an upper GI source (usually massive UGIB)
  • If hematochezia + hemodynamic instability - always consider upper GI source
Important mimics to exclude:
  • Iron or bismuth ingestion simulates melena (stool guaiac negative)
  • Red-dyed liquid medications and beets simulate hematochezia (guaiac negative)
  • Swallowed blood from epistaxis, dental procedures, or haemoptysis

B. Associated Symptoms

SymptomClue
Epigastric pain relieved by food/antacidsPeptic ulcer disease
Epigastric pain radiating to backPosterior duodenal ulcer eroding gastroduodenal artery
Nausea, vomiting, retching BEFORE hematemesisMallory-Weiss tear
Dysphagia, odynophagia, weight lossOesophageal/gastric malignancy, severe oesophagitis
Heartburn, regurgitation (GORD history)Oesophagitis, Barrett's erosions
Jaundice, abdominal swelling, ankle oedemaPortal hypertension, variceal bleeding
Pulsatile abdominal mass, prior aortic graftAortoenteric fistula (must not be missed)
Right upper quadrant pain + bleedingHaemobilia (biliary source)
Episodic flushing, diarrhoeaCarcinoid with hepatic metastases

C. Haemodynamic Symptoms (Severity Assessment)

  • Syncope or pre-syncope (significant volume loss >15-20%)
  • Dizziness on standing (orthostatic symptoms)
  • Palpitations, chest pain (cardiac ischaemia secondary to bleeding)
  • Confusion, restlessness (cerebral hypoperfusion)
  • Oliguria, anuria

D. Past Medical History

  • Previous GI bleeding - prior episodes, their source, prior endoscopy findings and interventions (banding, injection sclerotherapy, clips)
  • Peptic ulcer disease or dyspepsia
  • Liver disease, hepatitis B/C, alcohol cirrhosis
  • Inflammatory bowel disease
  • Coagulopathy or haematological disorders
  • Renal failure (uraemia causes platelet dysfunction; raised BUN:Cr ratio can indicate UGIB itself)
  • Cardiovascular disease (relevant for transfusion threshold)
  • Prior abdominal surgery or aortic aneurysm repair (aortoenteric fistula)
  • Malignancy (known gastric, oesophageal, hepatic, or pancreatic cancer)
  • Varices - known, previously banded, TIPS procedure

E. Drug History (Critical)

  • NSAIDs and aspirin - most important risk factor for peptic ulcer bleeding; 57% of gastric ulcer bleeds and 53% of duodenal ulcer bleeds are associated with NSAID/aspirin use
  • Anticoagulants - warfarin, DOACs (rivaroxaban, apixaban, dabigatran), heparin
  • Antiplatelet agents - clopidogrel, ticagrelor, prasugrel (especially dual antiplatelet therapy)
  • Corticosteroids - especially combined with NSAIDs (synergistic ulcer risk)
  • SSRIs - inhibit platelet serotonin, impair haemostasis
  • Bisphosphonates - pill-induced oesophagitis
  • Tetracyclines, iron, potassium chloride - oesophageal/gastric erosions
  • Thrombolytics - iatrogenic haemorrhage
  • PPI/H2RA use - may partially mask symptoms

F. Social History

  • Alcohol use - quantity and pattern (alcoholic cirrhosis, erosive gastritis, Mallory-Weiss)
  • Smoking (impairs mucosal defense, NSAID use risk)
  • Overseas travel (portal hypertension from schistosomiasis in endemic areas)
  • Occupation and stress levels

G. Family History

  • Hereditary haemorrhagic telangiectasia (HHT/Osler-Weber-Rendu)
  • Peutz-Jeghers syndrome
  • Familial polyposis
  • Gastric malignancy

2. PHYSICAL EXAMINATION

A. Immediate Assessment - Haemodynamic Status

Vital Signs (assess severity and shock)
FindingSignificance
HR >100 bpmModerate-severe blood loss (>15-20% volume)
SBP <100 mmHgSignificant haemodynamic compromise
Postural hypotension (>20 mmHg SBP drop on standing)15-20% volume depletion
Paradoxical bradycardiaCan occur even in profound hypovolemia (vasovagal)
TachypnoeaTissue hypoperfusion, lactic acidosis
Reduced pulse pressureEarly compensated shock
TemperatureFever may suggest infectious aetiology, sepsis
Important caveat: Beta-blockers prevent tachycardia; patients with baseline hypertension may have "normal" blood pressure despite significant volume loss. Younger patients compensate better - vital signs may remain normal until >30% volume loss.

B. General Inspection

  • Pallor (anaemia)
  • Diaphoresis, cold clammy skin (shock)
  • Agitation, confusion (cerebral hypoperfusion)
  • Jaundice (liver disease)
  • Cachexia (malignancy)
  • Nutritional status

C. Skin and Peripheral Signs

SignDiagnosis suggested
Spider naevi (>5), palmar erythemaChronic liver disease/cirrhosis
Jaundice, caput medusaePortal hypertension
Gynaecomastia, testicular atrophyCirrhosis
Petechiae, purpura, ecchymosesCoagulopathy, thrombocytopenia, vasculitis
Telangiectasias on lips, oral mucosa, fingertipsHHT (Osler-Weber-Rendu)
Perioral pigmentation (lips, buccal mucosa)Peutz-Jeghers syndrome
Dermal neurofibromas, cafe-au-lait spotsNeurofibromatosis
Acanthosis nigricansGastric adenocarcinoma (paraneoplastic)
Virchow's node (L supraclavicular)Gastric malignancy
Sister Mary Joseph nodule (umbilical)Intra-abdominal malignancy
Ear, Nose and Throat Exam
  • Exclude epistaxis, posterior nasal bleeding as source of swallowed blood producing coffee-ground emesis - this accounted for 2.2% of UGIB in the UCLA CURE database

D. Cardiovascular Examination

  • Signs of heart failure (JVP, pulmonary oedema) - relevant for fluid resuscitation and Blatchford score
  • Peripheral vascular disease (may coexist with aortic pathology)

E. Abdominal Examination

  • Inspection: Scars (previous surgery, aortic repair), distension, visible peristalsis, caput medusae
  • Palpation:
    • Epigastric tenderness (peptic ulcer, gastritis)
    • Hepatomegaly (cirrhosis, hepatic malignancy)
    • Splenomegaly (portal hypertension, haematological disorder)
    • Abdominal mass (gastric/pancreatic malignancy, lymphoma)
    • Pulsatile epigastric mass (AAA - risk of aortoenteric fistula)
    • Ascites (cirrhosis, malignancy)
  • Percussion: Shifting dullness (ascites), liver dullness
  • Auscultation: Bowel sounds (hyperactive in UGIB due to blood in intestine acting as cathartic)

F. Rectal Examination

  • Examine stool colour: bright red (hematochezia), maroon, or black tarry (melena)
  • Guaiac (FOB) testing of stool
  • Assess for rectal masses, haemorrhoids

G. Nasogastric Aspirate (Bedside Procedure)

  • Positive aspirate (bloody, maroon, or coffee-ground): confirms UGIB; high-risk lesions more likely
  • Negative clear aspirate: does NOT exclude UGIB - intermittent bleeding, pyloric spasm, or oedema can prevent duodenal blood reflux; only positive in ~23% of patients with occult UGIB without hematemesis
  • Bilious aspirate: suggests pylorus is patent; duodenal source is less likely if no blood
  • Visual inspection is more reliable than guaiac testing of aspirate (traumatic insertion causes false positives)
  • Note: No evidence that NG tube passage provokes variceal bleeding

3. INVESTIGATIONS

A. Immediate Bloods (Resuscitation Phase)

TestRationale
FBC/CBCHb, Hct (may be normal initially due to haemoconcentration - not a reliable acute indicator), WCC, platelets
Group and Screen / Cross-matchSingle most important test; order 4-6 units PRBCs
Coagulation (PT/INR, APTT)Especially if on anticoagulants or known liver disease; correct if INR elevated or platelets <50,000
Urea and ElectrolytesBUN:Cr ratio - a ratio ≥30 strongly suggests upper GI source (digested Hb raises BUN)
Liver Function TestsBilirubin, albumin, transaminases - assess for chronic liver disease
GlucoseHypoglycaemia in liver failure
CalciumHypercalcaemia associated with Zollinger-Ellison syndrome
Serum lactateRising lactate = severe illness and predictor of in-hospital mortality
ABGMetabolic acidosis, base deficit - assessment of tissue perfusion
ECGExclude silent myocardial ischaemia precipitated by blood loss, especially in elderly or known CAD
Blood culturesIf sepsis suspected
Key Biochemical Clue:
Digested blood is absorbed as urea, raising the BUN level. A BUN:Cr ratio ≥30 suggests an upper GI source even when the presentation is atypical. - Frameworks for Internal Medicine

B. Imaging

InvestigationIndicationNotes
Chest X-rayFree air (perforation), aspiration pneumonia, cardiac sizeLimited routine value; not needed absent specific indication
Plain abdominal X-rayPerforation, obstructionLimited; contraindicated if EGD planned
Barium studiesContraindicatedBarium impairs subsequent endoscopy and angiography
CT Abdomen/Pelvis with contrastSuspected aortoenteric fistula, malignancy, complicationsHigh sensitivity for active bleeding if rate >0.3 ml/min; helps plan intervention
CT Angiography (CTA)Active bleeding not controlled by endoscopy; identifies source before formal angiography
Mesenteric AngiographyFailed endoscopy; active arterial bleeding; allows therapeutic embolizationDetects bleeding at >0.5 ml/min; CO2 + contrast used
Tagged RBC ScintigraphyIntermittent/obscure bleeding; detects at >0.1 ml/minDoes not allow immediate therapy
Ultrasound abdomenLiver size, portal hypertension, ascites, masses
Portal venous pressure studiesHVPG for portal hypertension quantification

C. Endoscopy - The Gold Standard

Upper GI Endoscopy (EGD/OGD)
  • Diagnostic and potentially therapeutic
  • Perform within 24 hours of presentation after adequate fluid resuscitation in most patients with overt bleeding
  • Earlier (within 12 hours) for high-risk patients (haemodynamic instability, suspected varices)
  • Allows Forrest classification of peptic ulcer lesions
Forrest Classification (peptic ulcer - endoscopic risk stratification):
ClassAppearanceRebleed Risk
IaActive arterial spurting~90%
IbActive oozing~10-20%
IIaNon-bleeding visible vessel (NBVV)~50%
IIbAdherent clot~33%
IIcFlat pigmented spot~5-10%
IIIClean base ulcer~<5%
Prokinetic pre-treatment: Erythromycin 250 mg IV or metoclopramide 10 mg IV 20-120 minutes before endoscopy improves gastric visualization by promoting gastric emptying of blood/clots.
Endoscopic hemostasis options:
  • Injection therapy: adrenaline (epinephrine) 1:10,000; tissue adhesives (cyanoacrylate for varices)
  • Mechanical: hemoclips, band ligation (varices and Mallory-Weiss)
  • Thermal contact: electrocoagulation, thermocoagulation (heater probe)
  • Thermal non-contact: argon plasma coagulation (APC), laser photocoagulation

D. Scoring Systems

Blatchford Score (Pre-endoscopy - guides need for intervention):
VariablePoints
BUN ≥6.5 mmol/L2-6
Hb (men)1-6
Hb (women)1-6
SBP <110 mmHg2
SBP 100-109 mmHg1
Pulse ≥100/min1
Melena1
Syncope2
Liver disease2
Heart failure2
Score 0 = low risk for intervention needed (safe for outpatient management)
AIMS65 Score (Pre-endoscopy mortality):
  • Albumin <3.0 g/dL
  • INR >1.5
  • Mental status altered
  • SBP <90 mmHg
  • Age >65 years Score ≥2 associated with higher mortality, longer stay, greater cost
Complete Rockall Score (Post-endoscopy):
VariableScore
Age <600; 60-79 = 1; ≥80 = 2
Shock: none; tachycardia; hypotension0/1/2
Comorbidities: none; cardiac failure/IHD; renal/liver/metastatic cancer0/2/3
Endoscopic diagnosis0-2
Endoscopic SRH (stigmata of recent haemorrhage)0 or 2
Score 0-2: low risk (safe early discharge); Score ≥5: high risk (close monitoring needed)

4. DIFFERENTIAL DIAGNOSIS - COMPLETE ANATOMICAL CLASSIFICATION

(From Sleisenger & Fordtran's, Goldman-Cecil Medicine, Tintinalli's Emergency Medicine, and Yamada's Textbook of Gastroenterology)

ESOPHAGEAL CAUSES

Variceal
  1. Oesophageal varices - portal hypertension; most common variceal source; accounts for ~22% of severe UGIB overall; variceal bleeding is cause of UGIB in cirrhotic patients 59% of the time
  2. Gastro-oesophageal varices type 1 (GOV1) - extend along lesser curve
  3. Gastro-oesophageal varices type 2 (GOV2) - extend along greater curve toward fundus
Mucosal/Inflammatory 4. Reflux oesophagitis (erosive) - GORD-related; 4-13% of UGIB 5. Pill-induced oesophagitis - NSAIDs, bisphosphonates, tetracyclines, iron, potassium, quinidine 6. Infectious oesophagitis - Candida, CMV, HSV, HIV-related 7. Radiation oesophagitis 8. Caustic/chemical oesophagitis - alkali ingestion
Mechanical/Structural 9. Mallory-Weiss tear - longitudinal mucosal laceration at gastro-oesophageal junction; classic: vomiting/retching before hematemesis; 4% of severe UGIB; associated with alcoholic binge, DKA, chemotherapy, Valsalva (cough, seizure) 10. Boerhaave syndrome - full-thickness oesophageal perforation (rare but life-threatening)
Neoplastic 11. Oesophageal carcinoma (squamous cell or adenocarcinoma) - smoking, alcohol, Barrett's oesophagus, GORD
Vascular 12. Oesophageal Dieulafoy lesion - calibre-persistent submucosal artery (rare but catastrophic)

GASTRIC CAUSES

Ulcers/Erosions 13. Gastric ulcer (peptic) - ~38% of all severe UGIB; NSAIDs, H. pylori, aspirin 14. Gastric erosions/erosive gastritis - NSAIDs, alcohol, stress, salicylates, radiation 15. Stress-related mucosal disease (SRMD) - critically ill patients: sepsis, trauma, burns (Curling's ulcer), CNS injury (Cushing's ulcer), mechanical ventilation 16. Cameron ulcers/erosions - linear erosions on the crest of gastric folds in a hiatus hernia; often occult; associated with large sliding hiatal hernias
Variceal/Portal Hypertensive 17. Gastric varices - fundal varices particularly dangerous (large calibre, high-pressure); isolated gastric varices (IGV1, IGV2) 18. Portal hypertensive gastropathy (PHG) - mosaic snake-skin mucosal pattern; diffuse oozing 19. Gastric antral vascular ectasia (GAVE) / Watermelon stomach - parallel red stripes radiating from pylorus; associated with cirrhosis, systemic sclerosis, bone marrow transplant
Vascular 20. Dieulafoy lesion - calibre-persistent artery in gastric submucosa; 70% occur within 6 cm of gastro-oesophageal junction on lesser curve; 3.2% of severe UGIB; recurrent, often massive, difficult to find endoscopically 21. Gastric angiodysplasia/Angioectasia - 4% of severe UGIB; associated with Heyde's syndrome (aortic stenosis + angiodysplasia), chronic renal failure, von Willebrand disease
Neoplastic 22. Gastric adenocarcinoma - weight loss, anorexia, dysphagia, Virchow's node 23. Gastric lymphoma (MALT/DLBCL) - H. pylori associated 24. Gastrointestinal stromal tumour (GIST) - submucosal, may erode and bleed 25. Carcinoid tumour (neuroendocrine tumour) - rare gastric carcinoids 26. Leiomyoma/leiomyosarcoma - submucosal
Iatrogenic/Post-procedure 27. Post-polypectomy bleeding 28. Post-endoscopic mucosal resection (EMR) / ESD bleeding 29. Post-gastrostomy tube bleeding 30. Post-bariatric surgery - anastomotic ulcers (marginal ulcers) at gastrojejunostomy
Systemic/Infiltrative 31. Amyloidosis - gastric mucosal infiltration 32. Eosinophilic gastroenteritis 33. Ménétrier disease - hyperplastic gastropathy with protein-losing enteropathy

DUODENAL CAUSES

  1. Duodenal ulcer (peptic) - most common single cause; posterior DU erodes gastroduodenal artery causing catastrophic haemorrhage
  2. Duodenal erosions/duodenitis - NSAIDs, H. pylori, Crohn's disease
  3. Duodenal Dieulafoy lesion - less common than gastric; affects 2nd/3rd part of duodenum
  4. Duodenal angiodysplasia/Angioectasia
  5. Duodenal carcinoma - periampullary carcinoma
  6. Ampullary carcinoma
  7. Duodenal GIST/stromal tumour

SPECIAL/RARE CAUSES

Biliary/Pancreatic 41. Haemobilia - bleeding into biliary tree; causes: hepatic artery pseudoaneurysm (post-trauma, post-biopsy, post-ERCP), hepatic artery aneurysm, cholangiocarcinoma, gallbladder malignancy; classic Quincke's triad: RUQ colic + jaundice + haematemesis/melaena 42. Haemosuccus pancreaticus (Wirsungorrhagia) - bleeding into the pancreatic duct; causes: splenic artery aneurysm, pseudocyst erosion, pancreatitis; bleeds intermittently through ampulla of Vater
Vascular 43. Aortoenteric fistula (AEF) - primary (AAA eroding into duodenum) or secondary (post-aortic graft reconstruction - 3rd part of duodenum most common site); presents with "herald bleed" followed by catastrophic haemorrhage; must always be considered in patient with prior aortic surgery 44. Splenic artery aneurysm - rare; may rupture into stomach 45. Hepatic artery aneurysm - ruptures into bile duct (haemobilia)
Systemic/Haematological 46. Coagulopathy - anticoagulant therapy, DIC, haemophilia, von Willebrand disease 47. Thrombocytopenia - ITP, TTP, drug-induced, hypersplenism 48. Vasculitis - Henoch-Schonlein purpura, polyarteritis nodosa
Hereditary Vascular 49. Hereditary haemorrhagic telangiectasia (HHT) / Osler-Weber-Rendu syndrome - autosomal dominant; telangiectasias on lips, buccal mucosa, nasal mucosa, GI tract; can cause massive UGIB 50. Blue rubber bleb naevus syndrome - cutaneous + GI haemangiomas
Genetic/Syndrome-related 51. Peutz-Jeghers syndrome - hamartomatous polyps; perioral pigmentation 52. Gardner's syndrome - colorectal and upper GI polyposis 53. Zollinger-Ellison syndrome (gastrinoma) - hypersecretory state; multiple, refractory peptic ulcers in atypical locations (distal duodenum, jejunum); hypercalcaemia (MEN1)
Swallowed Blood (Pseudohaematemesis) 54. Epistaxis (posterior nasal bleeding) - 2.2% of apparent UGIB 55. Oropharyngeal/dental bleeding 56. Haemoptysis - swallowed blood from pulmonary/bronchial source

5. FREQUENCY SUMMARY (UCLA CURE Database - Sleisenger & Fordtran's)

CauseFrequency
Peptic ulcer (gastric/duodenal)35-40%
Oesophageal/gastric varices16-22%
Portal hypertension-related lesions4.6%
Oesophagitis (erosive)4.6-13%
Angioectasia/angiodysplasia4-6%
Mallory-Weiss tear4%
Dieulafoy lesion3.2%
GI tract neoplasm3.1-7%
Epistaxis/swallowed blood2.2%
Gastric/duodenal erosions1.2-4%
No cause found7-8%
Other (Cameron ulcers, AEF, haemobilia)~9%

6. KEY CLINICAL PEARLS FOR THE CONSULTANT

  1. Melena is an upper GI bleed until proved otherwise - even without hematemesis, melena in a patient <50 is more likely upper GI than lower.
  2. 15% of hematochezia has an upper GI source - any patient with hematochezia + haemodynamic instability needs urgent OGD.
  3. Always ask about aortic surgery - an aortoenteric fistula classically presents with a "herald bleed" followed by exsanguination. This diagnosis cannot be missed.
  4. BUN:Cr ratio ≥30 is a biochemical pointer to UGIB from intraluminal digestion of haemoglobin.
  5. Initial haematocrit is unreliable - acute haemorrhage has not had time to equilibrate; haematocrit falls only after haemodilution with IV fluids or extravascular fluid shift.
  6. Beta-blockers mask tachycardia; antihypertensives mask hypotension - do not use vital signs alone in these patients to estimate haemorrhage severity.
  7. Blatchford score 0 - patient may be safely managed as outpatient with early elective OGD.
  8. Forrest Ia/Ib/IIa - require endoscopic hemostasis (combination therapy preferred: injection + mechanical or thermal).
  9. PPI infusion - 80 mg bolus then 8 mg/hr continuous infusion for 72 hours post-endoscopic therapy in high-risk ulcers; reduces rebleeding and need for surgery.
  10. Octreotide/terlipressin - splanchnic vasoconstriction for suspected variceal bleeding; start empirically while awaiting endoscopy (octreotide: 50 mcg bolus then 25-50 mcg/hr infusion; terlipressin: 2 mg IV 6-hourly).
  11. Transfusion threshold - Hb ≤7 g/dL in most patients; ≤9 g/dL in elderly or those with cardiac comorbidities. Restrictive transfusion policy (Hb 7-8 target) is associated with better outcomes than liberal policy in peptic ulcer bleeding.
  12. H. pylori testing - test all patients with peptic ulcer bleeding (rapid urease test at endoscopy or stool antigen); eradication reduces 1-year rebleeding rate from ~33% to <5%.
  13. Prokinetics before endoscopy - erythromycin 250 mg IV 20-90 minutes before endoscopy improves visualisation significantly; should be used routinely when blood is suspected in the stomach.
  14. Rising lactate in hospital = clear predictor of in-hospital mortality; monitor dynamically.

Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease (9780323609623); Goldman-Cecil Medicine (9780323930345); Tintinalli's Emergency Medicine (9781260019933); Yamada's Textbook of Gastroenterology (9781119600169); Frameworks for Internal Medicine (9781496359308)
Recent evidence update: A 2025 systematic review (PMID 39093247) assessed prognostic scores for UGIB in the ED, confirming the continued value of Blatchford and AIMS65; a 2025 meta-analysis (PMID 40029534) on tranexamic acid found no mortality benefit for acute GI bleeding, consistent with the HALT-IT trial, and it is not routinely recommended.
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