Barrett's oesophagus
Barrett's oesophagus is a change in the lining of the lower oesophagus caused by long-standing reflux. It is not cancer and it is not a disease in itself — it is an adaptation. Its importance lies in the fact that it is the only recognised precursor of oesophageal adenocarcinoma, and that it can be monitored. The great majority of people with Barrett's never develop cancer.
How it forms
The oesophagus is lined by squamous epithelium, well suited to the passage of food but poorly equipped to withstand acid. The stomach is lined by columnar epithelium, which is. When acid, pepsin and bile reflux repeatedly into the lower oesophagus over years, the squamous lining is damaged faster than it can repair.
The oesophagus responds by replacing it with a lining better able to survive that environment. Stem cells in the basal layer differentiate instead into columnar cells with goblet cells — intestinal metaplasia. This is a protective adaptation: the new lining tolerates acid far better, which is one reason some patients' heartburn paradoxically improves as Barrett's develops.
The cost is that this metaplastic lining is genetically less stable. Continued injury drives accumulating mutations, and a proportion progress through low-grade dysplasia, high-grade dysplasia and finally invasive adenocarcinoma. Each step takes years, which is what makes surveillance and endoscopic treatment possible.
Risk factors reflect both the reflux and the metabolic environment: chronic reflux, male sex, age over 50, white ethnicity, central obesity, smoking, and a family history. Notably, Helicobacter pylori infection is associated with a reduced risk, probably because it lowers acid production.
Symptoms
Barrett's itself causes none. Patients have the symptoms of their reflux — heartburn, regurgitation — or, in a substantial minority, no symptoms at all, which is why screening is debated and why some cancers arise in people who never complained of reflux.
New dysphagia, weight loss, vomiting, bleeding or anaemia in someone with known Barrett's requires urgent endoscopy rather than a routine one.
How the diagnosis is made
Endoscopy shows salmon-pink columnar mucosa extending above the gastro-oesophageal junction. The length is recorded using the Prague C&M classification — circumferential extent and maximal extent — because length influences risk and surveillance interval.
Diagnosis requires biopsy confirming intestinal metaplasia. Biopsies are taken systematically: four-quadrant samples every 2cm (the Seattle protocol), plus targeted biopsies of any visible abnormality. Any visible lesion matters more than random sampling, and modern practice emphasises careful inspection with high-definition and narrow-band imaging before biopsy.
Dysplasia is graded as absent, indefinite, low-grade or high-grade. Because this judgement is subjective and drives management, a diagnosis of dysplasia should be confirmed by a second expert gastrointestinal pathologist.
Surveillance
Patients with non-dysplastic Barrett's enter endoscopic surveillance, with the interval determined by segment length — longer segments are checked more often, short segments considerably less. Surveillance is continued while the patient would be a candidate for treatment should dysplasia be found, which means it is reasonable to stop in patients who could never undergo intervention.
Patients deserve the honest figure: the annual risk of progression to cancer in non-dysplastic Barrett's is low, in the region of a few per thousand per year. Surveillance is worthwhile, but the diagnosis is not a sentence, and anxiety is a genuine harm of over-dramatising it.
Treatment
Controlling reflux
Proton pump inhibitors are given to all patients, both for symptoms and because acid control probably reduces progression. Weight loss and smoking cessation matter. Antireflux surgery is an option for patients with poorly controlled reflux; it has not been shown to eliminate cancer risk, and surveillance continues regardless.
Endoscopic treatment of dysplasia
This is the major change of the past two decades, and it has largely replaced oesophagectomy for early disease.
- Endoscopic mucosal resection or submucosal dissection removes any visible lesion, providing accurate staging as well as treatment.
- Radiofrequency ablation then destroys the remaining Barrett's segment, allowing normal squamous lining to regenerate.
- The combination is standard for high-grade dysplasia and for intramucosal cancer, and is also recommended for confirmed low-grade dysplasia, where it reduces progression compared with surveillance alone.
Surgery
Oesophagectomy is now reserved for disease that has invaded the submucosa, where the risk of lymph node involvement rises sharply, or where endoscopic treatment has failed. The shift from oesophagectomy to endoscopic therapy for early neoplasia has spared many patients a major operation, and is the single most important reason to have Barrett's assessed in a unit that offers both.
Recovery and follow-up
Endoscopic treatments are day-case procedures. Chest discomfort and transient difficulty swallowing are common for a few days; stricture is the main complication and is treatable by dilatation. Treatment usually requires several sessions over months to clear the segment.
After successful eradication, surveillance continues, because recurrence occurs in a proportion of patients. Acid suppression is continued long-term.
Common questions
Does Barrett's oesophagus mean I will get cancer?
No. The great majority of people with Barrett's never develop oesophageal cancer. The yearly risk is low. Barrett's matters because it identifies the small group who should be monitored, so that any change is found at a stage when it is easily treated.
Why do I need repeat endoscopies if I feel fine?
Because the changes that precede cancer cause no symptoms. The purpose of surveillance is to find them while they can still be removed through the endoscope, without an operation.
My heartburn got better — does that mean the Barrett's improved?
Unfortunately not, and it can be misleading. The new lining tolerates acid better than the original one, so some people's symptoms ease as Barrett's develops. Symptoms are not a guide to what is happening in the lining.
Can Barrett's be reversed?
Where dysplasia is present, endoscopic treatment can remove the abnormal lining and allow normal lining to grow back, and this is very effective. For Barrett's without dysplasia, treatment is not usually recommended, because the risk it removes is small and the treatment carries its own risks.
Will I need my oesophagus removed?
Almost certainly not. Early disease is now treated endoscopically in the great majority of cases. Surgery is reserved for cancer that has grown deeper than the surface layers.
Should my family be screened?
Screening of relatives is not routine. It may be considered where there is a strong family history of Barrett's or oesophageal adenocarcinoma alongside other risk factors, and this is worth discussing individually.
Related conditions
Other conditions of the oesophagus covered on this site:
- Gastro-oesophageal reflux disease (GORD) and hiatus hernia
- Paraoesophageal hernia
- Achalasia
- Oesophageal diverticulum (Zenker's and epiphrenic)
- Benign tumours of the oesophagus
- Oesophageal cancer
- Oesophageal perforation and Boerhaave syndrome
This page provides general information and does not replace an individual medical consultation. Assessment and treatment are decided for each patient after review of their history, examination and investigations.