Summary

Barrett's Oesophagus (BO) is a pre-malignant condition in which the normal stratified squamous epithelium lining the lower oesophagus is replaced by metaplastic columnar epithelium containing goblet cells (intestinal metaplasia). This transformation occurs as an adaptive response to chronic gastro-oesophageal reflux disease (GORD). Barrett's is clinically significant because it represents the only known precursor to oesophageal adenocarcinoma (OAC), a cancer with a poor prognosis. However, the absolute risk of progression is low (0.3-0.5% per year), and most patients with Barrett's will NOT develop cancer. Management focuses on acid suppression, surveillance endoscopy, and early intervention for dysplasia.

Key Facts

• Definition: Replacement of squamous epithelium with intestinal-type columnar epithelium confirmed by histology (goblet cells = pathognomonic).
• Cause: Chronic GORD.
• Prevalence: ~2% of general population, 10-15% of GORD patients.
• Malignant Potential: 30-125x increased risk of OAC compared to general population.
• Annual Cancer Risk: 0.3-0.5% per year (lower than historically thought).
• Key Landmark: Prague C & M Classification (Circumferential & Maximal extent).
• Key Intervention: Radiofrequency Ablation (RFA / HALO) for dysplasia.

Clinical Pearls

"Salmon pink tongues": The classic endoscopic description. Pink columnar mucosa extending upwards from the Z-line (gastro-oesophageal junction) into the pale squamous oesophagus.

Goblet Cells = Barrett's: You MUST have histological confirmation of intestinal metaplasia with goblet cells to diagnose Barrett's. Columnar mucosa without goblet cells may just be "columnar-lined oesophagus" – biologically different.

The Cancer Fear is Overstated: The annual risk of progression to cancer (~0.5%) is lower than commonly perceived. Patients should be reassured but surveilled.

Dysplasia is the Danger Zone: The critical progression is: No Dysplasia → Low-Grade Dysplasia (LGD) → High-Grade Dysplasia (HGD) → Intramucosal Carcinoma → Invasive Adenocarcinoma.

Why This Matters Clinically

Barrett's Oesophagus represents a window of opportunity. Unlike most cancers, oesophageal adenocarcinoma has a known, visible precursor. By detecting and ablating dysplastic Barrett's, we can prevent cancer development. The advent of Radiofrequency Ablation (RFA) has transformed management, offering a curative, minimally invasive treatment for dysplasia without the morbidity of oesophagectomy.

Physical examination is usually normal in Barrett's unless malignancy has developed.

Signs (If Cancer Present)

Natural History

• Most Barrett's remains stable: The majority of patients will NOT develop cancer.
• Annual Progression Rate: ~0.3-0.5% per year for non-dysplastic Barrett's.
• With HGD: ~5-10% per year progress to invasive cancer.

Outcomes After Treatment

Key Guidelines

Landmark Trials

1. AIM-Dysplasia Trial (Shaheen et al., NEJM 2009)

• Question: Is RFA effective for dysplastic Barrett's?
• Finding: RFA significantly reduced progression to cancer and achieved high rates of dysplasia eradication.
• Impact: Established RFA as the treatment of choice for dysplastic Barrett's.

2. SURF Trial (Phoa et al., JAMA 2014)

• Question: RFA vs Surveillance for LGD?
• Finding: RFA reduced progression to HGD/cancer from 26% (surveillance) to 1% (RFA) over 3 years.
• Impact: Strong evidence for treating confirmed LGD with RFA.

3. AspECT Trial (Jankowski et al., Lancet 2018)

• Question: High-dose PPI +/- Aspirin for prevention?
• Finding: High-dose PPI (Esomeprazole 40mg BD) with Aspirin reduced composite endpoint of death/OAC/HGD.
• Impact: Supports high-dose PPI. Aspirin benefit modest, needs individualisation.

Barrett's in the Elderly

• Surveillance: Balance benefit vs. comorbidity. Consider stopping surveillance if life expectancy <5 years or unsuitable for treatment.
• Treatment: RFA is generally well-tolerated. Oesophagectomy high-risk in frail elderly.

Barrett's Without Dysplasia

• Risk of Cancer: Low (<0.5%/year).
• Approach: Reassurance. Adherence to PPI. Lifestyle. 3-5 yearly OGD.
• Consider Discharge: In elderly with stable, non-dysplastic, short-segment Barrett's if surveillance not in patient interest.

Scenario 1:

• Stem: 55-year-old man with 15-year history of GORD. OGD shows 5cm segment of salmon-pink mucosa. Biopsies confirm intestinal metaplasia with NO dysplasia. What is the diagnosis and management?
• Answer: Long-Segment Barrett's Oesophagus (C?M5). No dysplasia. Lifelong PPI. Surveillance OGD every 2-3 years. Lifestyle advice.

Scenario 2:

• Stem: Barrett's patient has surveillance OGD. Biopsy shows "High-Grade Dysplasia". What is the next step?
• Answer: 1) Confirm with 2nd expert GI pathologist. 2) If confirmed, refer to specialist centre. 3) Staging CT/EUS. 4) EMR of any nodules + RFA of flat dysplasia.

Scenario 3:

• Stem: What is the Prague Classification? Give an example.
• Answer: Standardised way to describe Barrett's extent. C = Circumferential extent (cm above GOJ). M = Maximal extent (cm above GOJ). Example: C2M5 = 2cm circumferential, 5cm maximal.

Scenario 4:

• Stem: A patient asks, "What are my chances of getting cancer?" (Non-dysplastic Barrett's).
• Answer: The annual risk is about 0.5% (1 in 200). Most people with Barrett's do NOT develop cancer. We monitor you to catch any changes early.

Scenario 5:

• Stem: What is the Seattle Biopsy Protocol?
• Answer: 4 quadrant biopsies every 2cm throughout the Barrett's segment, PLUS targeted biopsies of any visible abnormalities.

What is Barrett's Oesophagus?

Barrett's Oesophagus is a condition where the lining of your food pipe (gullet) has changed. Normally, it has a pale, protective layer. In Barrett's, due to years of acid reflux, this layer has been replaced by a different, pinker type of lining that is more resistant to acid.

Is it cancer?

No. Barrett's is NOT cancer. It is a "pre-cancerous" condition, meaning there is a small increased risk of developing cancer of the food pipe over many years. However, most people with Barrett's will never get cancer.

What are my chances of cancer?

About 1 in 200 people with Barrett's (without dysplasia) develop cancer each year. We monitor you with regular camera tests (endoscopy) to catch any changes early, when they can be treated easily.

What is the treatment?

1. Acid-reducing tablets (PPI): Lifelong. Protects the lining.
2. Lifestyle: Lose weight if needed. Stop smoking. Avoid late meals.
3. Camera tests (surveillance): Every 2-5 years to check for changes.
4. If changes happen (dysplasia): We can burn away the abnormal lining with a special procedure (RFA) without needing a big operation.

What should I look out for?

Tell your doctor if you develop:

• Difficulty swallowing.
• Unexplained weight loss.
• Vomiting blood or black stools.

Key Counselling Points (For Clinicians)

1. Reassurance: "Barrett's is NOT cancer. Most people with it never develop cancer."
2. Explain the Risk: "Your annual risk is about 1 in 200. We monitor you so we can catch any early changes."
3. Importance of PPI: "The acid-reducing tablets protect your food pipe. Please take them every day."
4. Lifestyle Matters: "Losing weight and stopping smoking can reduce your risk."
5. Surveillance: "The regular camera tests are your safety net. Please attend them."
6. Dysplasia Explained: "If we find cell changes (dysplasia), we can treat it with a heat procedure (RFA) to prevent cancer."
7. Alarm Symptoms: "Tell us immediately if you have trouble swallowing, weight loss, or vomiting blood."

Quality Markers: Audit Standards (BSG)

Historical Context: Norman Barrett

Who was Barrett?

• Norman Barrett (1903-1979): Australian-born British thoracic surgeon.
• 1950: First described the condition (though initially thought it was a congenital short oesophagus).
• Irony: Barrett himself thought the columnar lining was stomach, not a metaplastic change in oesophagus.
• Recognition: Later work by Allison and Johnstone correctly identified it as oesophageal metaplasia.