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Define Barrett's Oesophagus. Describe its diagnosis, management and treatment.

General Surgery · Final Professional

The Concept — Metaplasia from Reflux

Barrett's oesophagus is a metaplastic change in the lining of the lower oesophagus, in which the normal stratified squamous epithelium is replaced by columnar (intestinal-type) epithelium. It is a direct consequence of chronic acid reflux (GORD): the squamous lining, not built to withstand acid, adapts by changing into a more acid-resistant columnar type. Its great importance is that this metaplasia is premalignant — it is the recognised precursor of oesophageal adenocarcinoma.

The Pathway to Cancer

Barrett's mucosa can progress through a stepwise sequence of metaplasia → low-grade dysplasia → high-grade dysplasia → adenocarcinoma. Although the annual risk of cancer for any individual is small, it is significantly higher than in the general population, which is the rationale for surveillance. This is why chronic reflux is not dismissed as trivial.

Diagnosis

Barrett's is identified at upper GI endoscopy, where the columnar mucosa appears as salmon-pink tongues extending up from the gastro-oesophageal junction (in contrast to the pale squamous lining), and confirmed by biopsy showing intestinal metaplasia. Biopsies are also assessed for the presence and grade of dysplasia, which determines management.

Management

Management has two aims — control the reflux and monitor for (or treat) neoplastic change. Patients are given long-term proton pump inhibitors and enrolled in surveillance endoscopy with biopsies at intervals determined by the length of Barrett's and the presence of dysplasia. Dysplasia is treated endoscopically — by radiofrequency ablation and endoscopic mucosal resection (EMR) of visible lesions — which can eradicate dysplastic Barrett's and prevent progression to cancer.

WHO and How to Surveil

Not everyone with reflux develops Barrett's, and not all Barrett's needs the same follow-up. Surveillance intervals depend on the length of the Barrett's segment and the grade of dysplasia, with non-dysplastic short-segment disease reviewed infrequently and dysplastic disease managed intensively. Systematic quadrantic biopsies along the segment are taken to detect dysplasia that may not be visible.

Treatment of Dysplasia

The advent of endoscopic therapy has transformed management: endoscopic mucosal resection removes visible nodular lesions for accurate staging, and radiofrequency ablation destroys the remaining dysplastic Barrett's mucosa, allowing normal squamous epithelium to regrow. This can eradicate high-grade dysplasia and early cancer without the major morbidity of an oesophagectomy, provided the disease is caught before it invades deeply.

The Bottom Line

Barrett's oesophagus is columnar metaplasia from chronic reflux and the premalignant precursor of adenocarcinoma; it is managed with long-term PPIs and surveillance endoscopy, with dysplasia treated endoscopically by radiofrequency ablation and mucosal resection.

A Note on Risk Stratification

The clinical value of Barrett's is that it identifies a group who can be watched so that cancer is caught early, but the risk must be kept in perspective: for most patients with non-dysplastic Barrett's the annual risk of progression to cancer is low (well under 1%), so surveillance is balanced against its burden. Risk is higher with long segments, male sex, and any degree of dysplasia — factors that intensify surveillance and, for dysplasia, trigger endoscopic treatment. Reassurance for the low-risk majority is as much a part of management as vigilance for the few.

Metaplasia is the adaptive change that carries the malignant risk.

AspectDetail
ChangeSquamous to intestinal columnar metaplasia
CauseChronic acid reflux
RiskAdenocarcinoma of lower oesophagus
ManagementSurveillance endoscopy, PPI, ablation if dysplasia

KEY POINT

Key points TO remember

  • Barrett's oesophagus = metaplasia of lower oesophageal squamous epithelium to columnar (intestinal) epithelium, caused by chronic GORD.
  • Premalignant: metaplasia → low- then high-grade dysplasia → adenocarcinoma.
  • Diagnosed at endoscopy (salmon-pink columnar tongues) + biopsy (intestinal metaplasia ± dysplasia).
  • Manage with long-term PPIs + surveillance endoscopy; treat dysplasia endoscopically (radiofrequency ablation, EMR).

EXAM TIP

Sources: Bailey & Love's Short Practice of Surgery.

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