About 1% of people have Barrett’s oesophagus and while the risk of progression to oesophageal adenocarcinoma is low, that risk can only be managed appropriately via specialised endoscopic protocols, says Dr Matthew Stokes, a general surgeon with international sub-specialist training in upper gastrointestinal and bariatric surgery.

He explains who to investigate, when to refer, and how to advise patients about reducing their cancer risk—without causing undue alarm. 

What causes Barrett’s oesophagus?

Barrett’s oesophagus occurs when the normal squamous cell lining of the lower oesophagus converts to a columnar, intestinal-type lining in response to chronic exposure to gastroesophageal reflux (and sometimes bile reflux).  

“Over many years of exposure, those squamous cells adapt to protect themselves. And that adaptation is initially compensatory, but it does come at a cost,” Dr Stokes says—noting Barrett’s, like colorectal cancer, can gradually progress along the metaplasia–dysplasia–carcinoma pathway. 

Who should be investigated?

Dr Stokes recommends targeted screening. He advises keeping Barrett’s front of mind in key higher-risk groups, including: 

• Patients with chronic reflux, typically longer than five years (especially men over 50 years of age) 

• Those with obesity or smoking history 

• Patients with a family history of Barrett’s oesophagus or upper GI cancers. 

“These are all red flags,” he says. “These patients should very likely be encouraged to undergo an upper GI endoscopy or a gastroscopy with biopsies of any suspicious areas of the lower portion of the oesophagus and gastroesophageal junction.” 

“Ideally, that gastroscopy should be done by a specialised trained gastroenterologist or upper GI surgeon with expertise in Barrett’s oesophagus identification and treatment.”  

Importantly, only 15 to 20% of people with Barrett’s have symptomatic gastro‑oesophageal reflux disease, so absence of GORD symptoms does not exclude it.  

One biopsy is not enough

An endoscopy report that shows Barrett’s oesophagus (or columnar-lined epithelium of the lower oesophagus; intestinal cell type) based on a single biopsy is only a starting point, Dr Stokes stresses. 

“That patient ideally needs to have what’s called Seattle protocol biopsies, and that’s four quadrant biopsies every one to two centimetres of the full extent of that Barrett’s oesophagus.” 

Based on these findings, the extent of Barrett’s is described using the Prague classification—which guides risk stratification and surveillance planning. 

If a patient has a single biopsy showing Barrett’s oesophagus, Dr Stokes recommends referring them to a specialist gastroenterologist or an upper GI surgeon within three months, with definitive mapping biopsies ideally completed within six months of the initial scope. 

Surveillance intervals

Recommended surveillance periods depend on segment length and dysplasia status and will be determined by the specialist, Dr Stokes explains. 

For patients with short‑segment Barrett’s (less than 3 cm) and no dysplasia, Australian guidelines generally advise repeat endoscopy in three to five years, then every three years thereafter.  

If biopsies are indeterminate for dysplasia, endoscopy should be repeated earlier. For low grade dysplasia, repeat endoscopy should occur within six to 12 months, he notes. 

Patients with high grade dysplasia should be referred to a specialist centre for endoscopic management, he stresses. “We would consider any patient with high grade dysplasia Barrett’s oesophagus in line with someone who has early-stage oesophageal adenocarcinoma.”  

When treatment is required, about 99% of cases are now managed endoscopically, he says. Oesophagectomy is reserved for specific circumstances, such as invasive cancer or when endoscopic access is not possible (e.g., due to an anatomical variant or stricture).  

Mitigating risk of progression

Along with appropriate referral, patients with Barrett’s oesophagus should get very good control of their reflux—even if its asymptomatic, Dr Stokes emphasises.  

“That’s usually with, at minimum, a daily PPI therapy. So for example 40 milligrams of Somac or Nexium. And the patient needs to be educated on how to take their PPI properly. That means taking it 20 to 30 minutes before they commence food.”  

If timing is a compliance issue, it’s reasonable to take it before bed, he adds. 

It’s also important to manage modifiable risk factors, which include central obesity, smoking, alcohol consumption, and physical activity levels. 

While aggressive risk management is crucial, putting that risk in perspective can help limit unnecessary anxiety, he says.  

In patients with no dysplasia, risk of progression to oesophageal adenocarcinoma is 0.1–0.3% per year, he explains. This rises to about 1% per year for those with low grade dysplasia, and 5% per year for high‑grade dysplasia. 

Where does fundoplication fit in?

Anti-reflux surgery may be appropriate for some patients with Barrett’s oesophagus—but with some caveats. 

“A fundoplication is not a treatment for Barrett’s itself,” Dr Stokes explains, noting it aims to control symptoms that persist despite maximal medical therapy. 

Nor does it eliminate cancer risk. “They should continue their PPI after a fundoplication to maximally suppress acid exposure to the oesophagus, and they should not forego their surveillance,” he stresses.  

Key takeaways: 

• Investigation is appropriate for patients with reflux and Barrett’s risk factors. 

• Patents with a single biopsy suggesting Barrett’s should be referred for protocol mapping biopsies.  

• Surveillance intervals depend on segment length and dysplasia status. 

• Annual risk of progression to oesophageal adenocarcinoma varies with degree of dysplasia. 

• Risk mitigation involves tight reflux control, lifestyle modification and specialist management. 

• Patients with high‑grade dysplasia need urgent referral to a specialist centre.