Microscopic features | Macroscopic features | Clinical features | |
Dieulafoy lesion | Normal 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 ulcer | Mucosal 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 ulcer | Mucosal defect ~2–4 cm Smooth base with perpendicular borders Bleeding vessel or adherent clot sometimes visible in ulcer base | ||
Oesophageal varices | Large 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 |
Gastritis | Microscopy 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 tear | Longitudinal mucosal lacerations of the distal oesophagus/proximal stomach, with surrounding haemorrhage and acute inflammatory reaction | Longitudinal 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.