Table 1

Differential diagnoses of upper gastrointestinal bleeding

Microscopic featuresMacroscopic featuresClinical features
Dieulafoy lesionNormal surface gastric mucosa aside from defect
Histologically normal, tortuous submucosal artery with an abnormally large arterial diameter (1–3 mm)
Small mucosal defect varying from 2 to 5 mm, with a fibrinoid necrotic base
Mucosal erosion ~1–5 mm; 75% within 6 cm of the GOJ
Attached thrombus may be seen
Absence of inflammation at the edge of the mucosal defect
<1% of UGIBs
Intermittent painless melaena and haematemesis
M:F 2:1
Duodenal ulcerMucosal ulceration that can penetrate into submucosa and muscularis propria, or perforate onto the serosal surface; degree of surrounding fibrosis relative to chronicity
Background mucosal changes depend on aetiology, for example, Helicobacter pylori gastritis or NSAID-related reactive gastropathy (see below); most other causes, for example, peptic, have non-specific microscopic features
Mucosal defect ~2–4 cm
Diffuse, erythematous mucosal borders
Bleeding vessel or adherent clot sometimes visible in ulcer base
~50% of UGIBs
Symptoms: epigastric abdominal pain, belching, anorexia, haematemesis
Risk factors: H. pylori infection, smoking, NSAIDs, steroids, vagal tone (Cushing’s ulcer), burns (Curling’s ulcer), Zollinger-Ellinson syndrome (rare)
Gastric ulcerMucosal defect ~2–4 cm
Smooth base with perpendicular borders
Bleeding vessel or adherent clot sometimes visible in ulcer base
Oesophageal varicesLarge dilated submucosal veins
Expanded submucosa with elevation of mucosa above normal tissue
±Haemosiderin-laden macrophages
±Fresh blood
Dilated submucosal vessels in ‘columns’
Commonly in distal oesophagus
Small (1–2 mm) or large (1–2 cm)
5%–10% of UGIBs
Haemorrhage risk:
Size of varices
Anticoagulants
Active alcohol use
Systemic infection
Volume resuscitation can precipitate further haemorrhage—aim for stability and Hb >80 g/L
GastritisMicroscopy depends on aetiology, for example, H. pylori gastritis (usually antral but may be pan-gastric; bacteria highlighted by histochemistry); NSAID-related reactive gastropathy (foveolar hyperplasia, fibromuscular lamina propria expansion, paucity of inflammation); acute gastritis (mucosal oedema, haemorrhage and superficial erosions)Mucosal erythema and oedema, typically associated with friability and superficial mucosal ‘breaks’ (erosions)10%–20% of UGIBs
Heterogeneous phenomenon; the Sydney system or the Operative Link for Gastritis Assessment staging system may be useful in diagnostics/prognostics.
Common aetiology: H. pylori colonisation, NSAIDs, alcohol, critical illness
Treatment should comprise H. pylori eradication, antacid therapy and cytoprotective agents.
Mallory-Weiss tearLongitudinal mucosal lacerations of the distal oesophagus/proximal stomach, with surrounding haemorrhage and acute inflammatory reactionLongitudinal mucosal lacerations with or without active bleeding and adherent clot
Occasionally healing tears may appear as superficial ‘blood blisters’
Up to 10% of UGIBs
More common in the young
Predisposing factors include alcoholism and hiatus hernia
Haematemesis initiated by severe coughing or retching
Non-bleeding tears may be managed conservatively, with acid suppression and antiemetics.
  • GOJ, gastro-oesophageal junction; Hb, haemoglobin; NSAID, non-steroidal anti-inflammatory drug; UGIBs, upper gastrointestinal bleeds.