Barrett’s oesophagus refers to metaplasia of the oesophageal epithelial lining; whereby normal stratified squamous epithelium is replaced by simple columnar epithelium.
The prevalence ranges from 0.5-2% in the Western world. Around 10% of patients with gastro-oesophageal reflux disease (GORD) will have already developed Barrett’s oesophagus by the time they seek medical attention.
In this article, we shall look at the causes, clinical features and management of Barrett’s oesophagus.
Metaplasia is the abnormal reversible change of one cell type to another. In Barrett’s oesophagus, the normal stratified squamous layer is replaced by simple columnar epithelium.
The vast majority of cases are caused by chronic gastro-oesophageal reflux disease. The epithelium of the oesophagus becomes damaged by the reflux of gastric contents, resulting in a metaplastic transformation. This in turn increases the risk of developing dysplastic and neoplastic changes.
The distal oesophagus is most commonly affected. On endoscopy, the oesophagus appears red and velvety, with some preserved pale squamous islands. Diagnosis relies on biopsy demonstrating the presence of simple columnar epithelium within the oesophagus.
The risk factors for developing Barrett’s oesophagus include:
- >50yrs of age
- Hiatus hernia
- Family history of Barrett’s oesophagus
The typical presentation of Barrett’s oesophagus is a history of chronic gastro-oesophageal reflux disease. Features include retrosternal chest pain, excessive belching, odynophagia, chronic cough and hoarseness.
Always check for red flag symptoms (dysphagia, weight loss, early satiety, malaise and loss of appetite) for any underlying malignancy – although remember that these are late symptoms of malignancy, so may be absent.
Examination will be unremarkable.
Barrett’s oesophagus is a histological diagnosis. Patients who undergo endoscopy for chronic or resistant GORD (or to exclude malignancy), should have a biopsy taken of the oesophageal epithelium and sent for histological analysis.
The length (squamo-columnar to gastro-oesophageal junction) and degree of dysplasia are important in classification, and should be recorded on each endoscopy:
- A length <3cm is classed as short segment, whereas 3cm or longer is classified as a long segment.
- Grades of dysplasia include no dysplasia, indefinite for dysplasia, low grade dysplasia and high grade dysplasia.
Once a patient is diagnosed with Barrett’s oesophagus, they require lifelong monitoring via endoscopy.
All patients with Barrett’s oesophagus should be commenced on a proton-pump inhibitor (typically high dose, and twice-daily). Any medication that affects the stomach (such as NSAIDs) should be stopped. In addition, the patient should be provided with lifestyle advice to reduce the acidic stimulus on the squamous cells – which drives the metaplastic change.
The major risk of Barrett’s oesophagus is progression to adenocarcinoma. Therefore, all patients with confirmed Barrett’s oesophagus must undergo regular routine endoscopy. Example guidance is given in Table 1.
A recent study compared anti-reflux surgery with medical treatment in GORD patients with Barrett’s oesophagus. It found that a higher percentage (15.4%) of patients who underwent anti-reflux surgery had eventual regression of Barrett’s oesophagus, compared with medically managed patients (1.9%).
|Table 1 – Routine Endoscopy in Barrett’s Oesophagus|
|No dysplasia||Every 2-5 years||–|
|Low grade dysplasia||Every 6 months||Repeat endoscopy with quadrantic biopsies every 1cm.
There is no consensus on long-term surveillance in this group.
|High grade dysplasia||Every 3 months||If a visible lesion is present, endoscopic ablation with mucosal resection (EMR) or radiofrequency ablation should be considered|
Premalignant lesions are resected with EMR or endoscopic submucosal dissection, which limits the need for oesophagectomy.
If carcinoma is discovered on routine endoscopy, then oesophagectomy may be indicated. Adenocarcinomas detected on routine screening for Barrett’s oesophagus are typically early-stage lesions and have a better prognosis than those discovered outside of any screening program