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]
- GORDGastro-oesophageal reflux disease
- 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 GORDGastro-oesophageal reflux disease 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:
- 1st line: full-dose PPIProton pump inhibitor for 4 weeks
- 2nd line: H2 receptor antagonist (e.g. ranitidine, famotidine, nizatidine) / long-term PPIProton pump inhibitor
Prevention of Malignant Transformation
All patients should be offered endoscopic surveillance (including biopsy)
- Every 2-3 years for long-segment
Long-segment Barrett's esophagus is when the segment of columnar metaplasia is 3 cm or longer.
(≥3 cm) - Every 3-5 years for short-segment (
Short-segment Barrett's esophagus is when the segment is less than 3 cm in length.
<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)
The only reason that Barrett’s oesophagus needs intervention is if histology shows dysplasia. If not, no intervention is needed other than regular surveillance
Do NOT offer the following to prevent progression of Barrett’s oesophagus to dysplasia / cancer
- Aspirin
- Fundoplication (anti-reflux surgery)
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 GOJGastro-oesophageal junction) | Upper / mid oesophagus |
| Risk factors | Strongest risk factors
Other risk factors
|
Strongest risk factors:
Other risk factors:
|
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)
The pattern / trend of dysphagia is important:
- In oesophageal cancer (or other mechanical causes of obstruction, e.g. stricture, ring), the dysphagia is persistent and progressively gets worse, and there is dysphagia predominantly to solid (solid affected first, then liquid later)
- In oesophageal motility disorders, the dysphagia classically affects both solid and liquid (predominantly liquid) from the onset, and the dysphagia fluctuates (comes and goes)
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
Some non-specific biochemical changes:
- ↑ Platelet (thrombocytosis) – platelets are an acute-phase reactant
They can therefore be elevated in any cause of inflammation, including cancer.
The association is strongest for lung, colon, stomach, ovarian, and esophageal cancers, where thrombocytosis is often present at diagnosis and correlates with advanced stage and poorer prognosis.
- ↓ Haemoglobin – can be seen in any GI cancer
Management
Guidelines regarding cancer management are complicated, here are some key concepts (sufficient/simplified for exams):
- T1a stage (confined to mucosa) → offer endoscopic resection; otherwise oesophagectomy 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:
- 1st 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)
- 1st line: chemoradiotherapy
- 2nd line:
- Chemotherapy
- Oesophageal stenting
- Palliative radiotherapy
To manage oesophageal luminal obstruction:
- Oesophageal stenting (provides immediate dysphagia relief), or
- Radiotherapy
References
NICE guideline Oesophago-gastric cancer: assessment and management in adults