Makindo Medical Notes

Related Subjects: |Achalasia |Oesophageal Carcinoma |Diffuse Oesophageal spasm |Diffuse Oesophageal Perforation - Rupture |Gastro-Oesophageal Reflux |Barrett's oesophagus

Barrett's oesophagus is a premalignant condition where the normal lining of the oesophagus is replaced by tissue similar to that of the intestine, typically due to chronic inflammation associated with gastro-oesophageal reflux disease (GORD). This tissue change increases the risk of developing adenocarcinoma.

Flat cells elongate
Reprogrammed, a change of fate
Acid splashes burn
Battered, scarred, loss of order
Scarlet tongues GE border
@DrCindyCooper

About

• Barrett’s oesophagus is characterised by the replacement of the normal distal squamous epithelial lining with metaplastic columnar epithelium.
• Endoscopically visible above the gastro-oesophageal junction (GOJ) (≥1 cm) and confirmed histopathologically from oesophageal biopsies.

Aetiology

• Primarily caused by gastro-oesophageal reflux disease (GORD), leading to chronic acid exposure and tissue change.
• Metaplasia occurs as squamous epithelium is replaced by tall glandular columnar cells.
• Risk factors: Male gender, age >45, history of reflux symptoms, Caucasian ethnicity, obesity (especially abdominal), and smoking.

Risk Factors for Malignancy

• Presence of GORD symptoms
• Male sex, age over 45
• Length of Barrett's oesophagus >8 cm
• Early onset of Barrett's
• Presence of ulceration or stricture

Investigations

• Endoscopy: Replaces the grey and pale squamous epithelium with pink columnar epithelium, which can be seen through an endoscope.
• Biopsy: Confirms the diagnosis and assesses for dysplasia or carcinoma. Multiple biopsies (2 cm apart) are performed to capture dysplasia, which can be patchy. Dysplasia is graded as No dysplasia, Low-grade dysplasia, or High-grade dysplasia. Indocarmine spray may assist in identifying dysplastic areas.

Management

• Dietary Changes: Reducing GORD through diet (avoid spicy foods, citrus, caffeine, and alcohol), weight loss (especially abdominal fat), elevating the head of the bed, and smoking cessation.
• Proton Pump Inhibitors (PPIs): Reduce acid production; long-term use is often necessary. H2-Receptor Antagonists are alternatives but generally less effective than PPIs.
• Endoscopic Surveillance: Regular endoscopies to monitor for dysplasia or early cancer, with frequency based on dysplasia grade and risk factors.
• Endoscopic Treatments:
  • Radiofrequency Ablation (RFA): Uses heat to destroy abnormal cells, reducing cancer risk.
  • Endoscopic Mucosal Resection (EMR): Removes larger areas of abnormal tissue or early-stage cancer.
  • Cryotherapy: Freezes and destroys abnormal tissue as an alternative to RFA.
• Oesophagectomy: Considered in cases of high-grade dysplasia or early oesophageal cancer; involves removing part or all of the oesophagus (a major procedure with significant risks).

Screening (NICE Guidelines)

• Offer high-resolution white light endoscopic surveillance with Seattle protocol biopsies:
  • Every 2 to 3 years for people with long-segment (≥3 cm) Barrett's oesophagus.
  • Every 3 to 5 years for those with short-segment (<3 cm) Barrett's oesophagus with intestinal metaplasia.
• Tailor surveillance frequency based on the patient’s age, sex, family history of oesophageal cancer, and smoking history within recommended intervals.
• Do not offer surveillance for short-segment Barrett's (<3 cm) without intestinal metaplasia (confirmed at 2 endoscopies).
• Use high-dose PPIs; although evidence on efficacy in altering progression is limited, they are standard in management.
• For patients with an indefinite diagnosis for dysplasia: optimise anti-reflux treatment and re-endoscope in 6 months. If no definite dysplasia is found on subsequent biopsies, follow the surveillance protocol for non-dysplastic Barrett’s oesophagus.

References

• British Society of Gastroenterology Guidelines on the Diagnosis and Management of Barrett’s Oesophagus