Barrett’s Oesophagus

Definition

Barrett’s oesophagus is characterised by the replacement of the normal stratified squamous epithelium of the lower oesophagus with a metaplastic columnar epithelium.

Aetiology

Key risk factors: ^[Ref]

• GORD
• Male
• White race
• Obesity
• Smoking

 

The above risk factors are also shared with oesophageal cancer.

Clinical Features

Barrett’s oesophagus is typically asymptomatic and does not have specific clinical features of its own. ^[Ref]

 

Clinical features of concurrent GORD are common.

Complications

Barrett’s oesophagus can be a precursor to oesophageal adenocarcinoma (risk is low: <1% per year).

Investigation and Diagnosis

Barrett’s oesophagus is most often identified incidentally during upper GI endoscopy.

 

Endoscopic (gross) appearance: ^[Ref]

• Barrett’s oesophagus: salmon-coloured, velvety mucosa extending above the gastroesophageal junction into the distal oesophagus
• Normal:  pale, glossy mucosa

 

Histology confirms Barrett’s oesophagus by the presence of specialised intestinal-type epithelium: ^[Ref]

• Columnar epithelium
• Goblet cells
• Crypt-like glandular structures

Management

Symptomatic Relief

Management is as per GORD guidelines:

• 1^st line: full-dose PPI for 4 weeks
• 2^nd line: H2 receptor antagonist (e.g. ranitidine, famotidine, nizatidine) / long-term PPI

Prevention of Malignant Transformation

All patients should be offered endoscopic surveillance (including biopsy)

• Every 2-3 years for long-segment (≥3 cm)
• Every 3-5 years for short-segment (<3 cm)

 

If biopsies taken during endoscopic surveillance of Barrett’s oesophagus show dysplasia → perform endoscopic intervention

• High-grade dysplasia → endoscopic resection followed by ablation of any remaining tissue
• Low-grade dysplasia → endoscopic ablation (usually radiofrequency)

Oesophageal Cancer

Types

There are 2 histological 2 subtypes of oesophageal cancer, with different pathologies and risk factors. Oesophageal adenocarcinoma is now the most common subtype in Western countries. ^[Ref1][Ref2]

Feature	Adenocarcinoma	Squamous cell carcinoma
Location	Lower oesophagus (near the GOJ)	Upper / mid oesophagus
Risk factors	Strongest risk factors GORD Barrett’s oesophagus   Other risk factors Male sex Smoking Obesity Low fruit / vegetable diet	Strongest risk factors: Smoking Alcohol   Other risk factors: Achalasia Hot beverages Nitrosamines (rich in fish)

Clinical Features

Key common clinical features: ^[Ref]

• Progressive dysphagia (initially to solids, then to liquids)
• Constitutional symptoms (e.g. weight loss)
• Dyspepsia

 

Odynophagia is possible, but not common, usually with ulcerated or infiltrative lesions. (Note that prominent odynophagia is classically associated with oesophageal candidiasis)

Investigation and Diagnosis

Primary Care – Suspected Upper GI Cancer Pathway

Refer using a suspected cancer pathway referral if:

• Dysphagia, or
• ≥55 y/o AND weight loss AND upper abdominal pain OR reflux OR dyspepsia

 

Other less important points (less commonly examined):

• Consider a non-urgent upper GI endoscopy in those with haematemesis
• Consider a non-urgent upper GI endoscopy in those who are ≥55 y/o AND any of the following
  • Treatment-resistant dyspepsia
  • Upper abdominal pain + low haemoglobin
  • High platelet count + nausea / vomiting / weight loss / reflux / dyspepsia / upper abdominal pain
  • Nausea or vomiting + weight loss / reflux / dyspepsia / upper abodminal pain

Secondary Care

Gold standard test: upper GI endoscopy with biopsy

 

Test for staging (after diagnosis is established): PET/CT scan

 

Barium swallow can show the classic apple core sign (the circumferential constricting lesion in the oesophagus resembles the shape of an apple core after the fruit is eaten)

• However, note that barium swallow is not routinely used as 1st line diagnostic modality
• It is usually performed when endoscopy is inappropriate /anatomical assessment / other motility disorders are considered

Management

Guidelines regarding cancer management are complicated, here are some key concepts (sufficient for exams, but over-simplifies the guidelines and actual management):

• T1a stage (confined to mucosa) → offer endoscopic resection; otherwise oesophagoestomy is most likely necessary
• For those who surgery is not appropriate (e.g. unresectable, not fit) → chemoradiotherapy
• To manage oesophageal luminal obstruction → oesophageal stenting

 

Key information to guide management:

• Stage 1 oesophageal cancer includes T1a / T1b + N0 + M0 (tumours that are limited to invasion of the mucosa or submucosa without regional lymph node involvement or distant metastasis)
  • T1a: invasion limited to the mucosa (lamina propria / muscualris mucosa)
  • T1b: invasion limited to the submucosa

Stage 1 Oesophageal Cancer

Resection is the preferred definitive management:

• 1^st line: endoscopic resection + ablation of residual tissue
• If  T1b + high-risk features (incomplete endoscopic resection / pathological evidence of lymphovascular invasion / deep submucosal invasion) → oesophagectomy

Advanced Oesophageal Cancer (Beyond Stage 1)

If the patient is fit for surgery, offer:

• Oesophagectomy, and
• Lymph node dissection, and
• Chemotherapy and/or radiotherapy

Palliative Management

The following applies to those who are not a candidate for surgery (e.g. unfit, unresectable, metastatic disease)

• 1^st line: chemoradiotherapy
• 2^nd line:
  • Chemotherapy
  • Oesophageal stenting
  • Palliative radiotherapy

 

To manage oesophageal luminal obstruction:

• Oesophageal stenting (provides immediate dysphagia relief), or
• Radiotherapy

References