Barrett Oesophagus

Replacement of the normal squamous epithelium of the distal oesophagus by columnar epithelium with intestinal metaplasia (goblet cells), as a response to chronic acid and bile reflux; it is the main precursor of oesophageal adenocarcinoma.

• Length: long segment (3 cm or more), short segment (1 to less than 3 cm); endoscopic extent is recorded as circumferential and maximum length of columnar lining.
• Found in about 5 to 15% of patients with chronic reflux undergoing endoscopy and about 1 to 2% of adults; risk factors: age over 50 years, male sex (about 2 to 3 times), white ethnicity, central obesity, smoking, hiatus hernia, family history, and chronic reflux of more than 5 years.
• Progression: annual risk of adenocarcinoma is about 0.1 to 0.5% for non-dysplastic disease, about 0.5 to 1% for low grade dysplasia, and about 6 to 19% for high grade dysplasia.
• Mechanism: chronic injury from acid and bile leads to a change in progenitor cells and reprogramming to columnar epithelium, then dysplasia and cancer through sequential genomic changes (TP53 loss, CDKN2A loss).

Heartburn, regurgitation (the usual symptoms of reflux); about 10 to 40% have no reflux symptoms.

• Dysphagia, odynophagia, weight loss and bleeding suggest stricture or cancer.
• Examination is normal.
• Differential diagnosis: reflux oesophagitis, hiatus hernia, inlet patch (gastric heterotopia), eosinophilic oesophagitis, gastric intestinal metaplasia at the cardia, oesophageal cancer, achalasia.
• Complications: oesophageal ulcer, peptic stricture, bleeding, dysplasia, oesophageal adenocarcinoma, and rarely perforation.

Upper endoscopy with high-definition white light and narrow-band imaging: salmon-pink columnar mucosa extending proximal to the gastro-oesophageal junction (the upper end of the gastric folds); measure the circumferential and maximum lengths.

• Biopsy: four-quadrant biopsies every 2 cm along the segment (every 1 cm if dysplasia is known or suspected) plus targeted biopsies of any visible lesion (nodule, ulcer, irregular mucosa) first; histology confirms intestinal metaplasia (goblet cells).
• Dysplasia is graded (none, indefinite, low grade, high grade) and confirmed by a second expert gastrointestinal pathologist; biopsies are best taken after 8 to 12 weeks of proton pump inhibitor therapy to settle inflammation.
• Staging endoscopic ultrasound and CT for suspected invasive cancer.
• Tests for reflux (pH-impedance monitoring: acid exposure time of more than 6% is abnormal) only when antireflux surgery is considered.

Acid suppression: omeprazole 20 to 40 mg once daily (twice daily if symptoms or erosive oesophagitis persist), long term, taken 30 minutes before breakfast; esomeprazole 40 mg daily gives similar effect; this controls symptoms and may lower progression, although proof of cancer prevention is limited.

• Lifestyle: weight loss if obese, stop smoking, avoid late meals (3 hours before lying down), raise the head of the bed by 15 to 20 cm, reduce alcohol, fat and large meals.
• Aspirin chemoprevention: aspirin 300 mg daily with esomeprazole 40 mg daily has been explored, but evidence is limited and the bleeding risk must be balanced; give aspirin 75 mg when it is already needed for cardiovascular disease.
• Antireflux surgery (laparoscopic fundoplication) is for symptom control in refractory reflux or large hiatus hernia; it does not remove the need for surveillance.
• Endoscopic surveillance (with four-quadrant biopsies every 2 cm):
  • Short segment (less than 3 cm) without dysplasia: every 3 to 5 years.
  • Long segment (3 cm or more) without dysplasia: every 2 to 3 years.
  • Indefinite dysplasia: repeat endoscopy after 8 to 12 weeks of optimised proton pump inhibitor treatment and review by an expert pathologist.
  • Surveillance may stop in patients with limited life expectancy or unfit for treatment.
• Dysplasia and early cancer (managed in expert centres):
  • Visible lesion: endoscopic mucosal resection or endoscopic submucosal dissection for staging and treatment.
  • Confirmed low grade dysplasia: radiofrequency ablation (preferred; about 90% eradication of dysplasia and about 80% of metaplasia in 3 to 4 sessions) or endoscopic surveillance every 6 months.
  • High grade dysplasia or intramucosal cancer: endoscopic resection of visible disease then radiofrequency ablation of the remaining Barrett segment; cryotherapy as an alternative.
  • Submucosal invasion with high-risk features, or invasive cancer: oesophagectomy or oncological treatment.
  • After ablation: omeprazole 40 mg twice daily; endoscopy with biopsies at 3, 6 and 12 months and then yearly; strictures (about 5 to 8%) are treated with balloon dilatation to 15 to 18 mm.
• Special groups: women, young patients (surveillance risk is lower; consider individual risk); pregnancy (alginates, famotidine 20 mg twice daily, omeprazole 20 mg daily; defer endoscopy); elderly (individualise surveillance); renal impairment (famotidine 10 to 20 mg daily); anticoagulated patients (plan biopsies and ablation with the haematology team).
• Red flags: dysphagia, weight loss, haematemesis or melaena, odynophagia, anaemia, new nodules or ulceration, dysplasia.
• Follow-up: surveillance endoscopy every 3 to 5 years for short segment disease, every 2 to 3 years for long segment disease, every 6 months for low grade dysplasia without ablation, and yearly after ablation; review of symptoms and proton pump inhibitor dose yearly.