Severe Oesophagitis at Endoscopy: Causes & Management

Endoscopic Grading — Los Angeles Classification

Los Angeles classification of esophagitis — Current Surgical Therapy, 14e

Endoscopic comparison: normal mucosa vs. Grade A-B vs. Grade C-D (white light and NBI)

Causes of Severe Oesophagitis

1. Gastro-oesophageal Reflux Disease (GERD) — Most Common

• Reflux of acidic gastric contents (and sometimes duodenal bile) onto squamous mucosa
• Risk factors reducing lower oesophageal sphincter (LOS) tone: obesity, hiatal hernia, alcohol, tobacco, CNS depressants, pregnancy, delayed gastric emptying
• Histology: eosinophil and neutrophil infiltration, basal zone hyperplasia, elongation of lamina propria papillae
• Severe grades (C/D) are independent risk factors for haemorrhagic esophagitis (along with cirrhosis, anticoagulant use, poor performance status)
• Complications: ulceration, haematemesis/melaena, stricture, Barrett's oesophagus

Special case — Zollinger-Ellison syndrome / MEN1: hypersecretion of gastric acid produces LA grade D oesophagitis with concurrent hypertrophic gastric folds and postbulbar duodenal ulcers (illustrated in image panel above)

2. Infectious Oesophagitis

3. Eosinophilic Oesophagitis (EoE)

• Chronic immune-mediated disease; food antigen driven
• Endoscopic features: rings (trachealization), linear furrows, white exudates/plaques, mucosal tears, oedema, narrow-calibre lumen

• 90% of patients show ≥1 endoscopic abnormality

• Histology: ≥15 eosinophils/HPF (often much higher); eosinophilic microabscesses; surface layering
• Typically refractory to PPIs; patients are often atopic

4. Pill-Induced Oesophagitis

• Pill fails to transit into stomach, causing direct mucosal injury
• Common offending drugs: doxycycline/tetracyclines, bisphosphonates (alendronate), NSAIDs/aspirin, potassium chloride, ferrous sulphate, quinidine
• Predisposing factors: taking pills without water, supine position, elderly, reduced motility, extrinsic compression
• Range: mild irritation → frank ulceration → haemorrhage → stricture
• Clinical presentation: sudden onset retrosternal pain and odynophagia — often diagnosable from history alone

5. Chemical / Caustic Oesophagitis

• Corrosive acids or alkalis, alcohol, excessively hot fluids, heavy smoking
• Severe cases → haemorrhage, stricture, perforation
• Morphology: non-specific ulceration and acute inflammation

6. Radiation-Induced Oesophagitis

• Complication of radiotherapy to mediastinum/thorax; degree of injury proportional to total dose
• Mucosa becomes inflamed, friable, haemorrhagic
• Vascular damage adds an ischaemic component

7. Other Causes

• Graft-versus-host disease (GvHD) — post-BMT
• Crohn's disease — rare oesophageal involvement
• Desquamative skin diseases — bullous pemphigoid, epidermolysis bullosa

Management by Cause

GERD — Severe Erosive (Grade C/D)

• High-dose PPI (e.g. omeprazole 40 mg daily or twice daily) — standard treatment; reduces gastric acidity and allows mucosal healing
• Duration: 8–12 weeks for severe erosive disease, then reassess
• Repeat endoscopy after treatment is mandatory to exclude underlying Barrett's oesophagus
• Lifestyle: weight loss, head-of-bed elevation, dietary modification, avoid precipitants

• EGD is essential for diagnosis; endoscopic haemostatic therapy generally has no role unless a focal ulcer with a stigma of recent haemorrhage (SRH) is found
• If discrete visible vessel/clot: injection, thermal coagulation, or clipping
• For diffuse LA-D haemorrhagic oesophagitis where endoscopic haemostasis is not feasible: balloon tamponade (Minnesota tube) can achieve temporary haemostasis

• Indicated for: persistent symptoms despite optimal PPI therapy, patient preference, or severe/recurrent complications
• Pre-operative workup: manometry (to guide fundoplication type), pH monitoring, barium swallow
• Nissen fundoplication (360°) for normal motility; Toupet fundoplication (270° partial) for ineffective oesophageal motility
• All patients should be on maximal PPI therapy before ARS is considered

• Peptic stricture: serial endoscopic dilatation before or instead of surgery
• Barrett's oesophagus: surveillance endoscopy programme; eradication if dysplasia present

Infectious Oesophagitis

• Endoscopy with biopsies and brushings is critical — the specific agent determines therapy
• In HIV patients with oesophageal ulcers, empirical fluconazole can be trialled before endoscopy if Candida is clinically suspected

Eosinophilic Oesophagitis

1. Biopsy protocol: 2–4 biopsies from at least two levels (proximal + distal) regardless of endoscopic appearance; fixed in 10% buffered formalin
2. PPI trial first (to exclude PPI-responsive oesophageal eosinophilia)
3. Dietary elimination — six-food elimination diet (milk, wheat, egg, soy, nuts, seafood) or targeted allergy testing
4. Swallowed topical corticosteroids — fluticasone (MDI swallowed) or budesonide (viscous oral suspension) — first-line pharmacotherapy
5. Oesophageal dilatation — for symptomatic strictures or narrow-calibre oesophagus (high risk of mucosal tears — warn patients; start with small diameter)
6. Dupilumab — biologic (anti-IL-4/IL-13) approved for EoE in adults and adolescents refractory to other therapies

Pill-Induced Oesophagitis

• Stop the offending drug (switch to liquid formulation or alternative agent if possible)
• Sucralfate suspension — mucosal protective coating
• PPIs for acid suppression and symptom relief
• Counsel on prevention: take pills with full glass of water, remain upright for ≥30 min after ingestion
• Most cases resolve spontaneously in 1–2 weeks; severe ulceration → follow up endoscopy to exclude stricture

Caustic/Chemical Oesophagitis

• Supportive care; nothing by mouth initially
• IV PPIs, IV fluids
• Endoscopy within 24–48 h to assess severity (use grading system: I–IIIb)
• Severe burns (grade IIb–III): nasogastric tube feeding, IV antibiotics (if aspiration/perforation risk), surgical consultation
• Do NOT induce emesis — worsens mucosal injury
• Long-term: endoscopic dilatation for strictures; surgical oesophageal resection for severe/refractory cases

Key Takeaways

• LA grade C/D = severe oesophagitis requiring aggressive management and mandatory follow-up endoscopy after treatment
• GERD is the most common cause; high-dose PPI for 8–12 weeks is standard
• Biopsies are essential — they differentiate GERD (eosinophils predominantly distal), EoE (eosinophils throughout, ≥15/HPF), infectious (specific inclusions/organisms), and malignancy
• Immunocompromised patients presenting with odynophagia: always consider Candida, HSV, CMV — treat empirically if clinically obvious, but endoscopy with targeted biopsies is the gold standard
• Pill-induced oesophagitis is underdiagnosed — history (new medication, no water, supine ingestion) is diagnostic