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