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Barrett’s Oesophagus

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Key points ⚡
Succinct notes to superpower your revision
Barrett’s oesophagus\: abnormal change in lower oesophageal cells due to GORD; 2.3% prevalence in re
malignant, increased risk of oesophageal adenocarcinoma.
Aetiology\: chronic GORD causing metaplasia from squamous to columnar epithelium; potential progression to dysplasia
and adenocarcinoma.
Risk factors\: GORD, acid-bile re
Symptoms\: often asymptomatic; may have heartburn, regurgitation, dysphagia, haematemesis, odynophagia, chest pain,
cough.
Investigations\: upper GI endoscopy with biopsy; look for 'salmon-coloured' epithelium above the gastro-oesophageal
junction; Prague C & M classi
Management\: high-dose proton pump inhibitors, endoscopic surveillance; radiofrequency ablation for low-grade
dysplasia, endoscopic resection for visible lesions in high-grade dysplasia.
Surveillance\: no dysplasia (OGD every 3-5 years if \<3cm and intestinal metaplasia present or 2-3 years if >3cm), low-grade
dysplasia (consider ablation), high-grade dysplasia (MDT review, ablation or resection).
Complications\: 30x increased risk of oesophageal adenocarcinoma (annual incidence 0.33%); increased risk of
oesophageal strictures, treated with endoscopic dilation.
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A comprehensive topic overview

Introduction

Barrett’s oesophagus is a condition where there is an abnormal change in the cells lining the lower portion of the
oesophagus due to chronic damage from gastro-oesophageal re
It has a prevalence of 2.3% among patients with symptoms of re
Barrett’s oesophagus is a pre-malignant condition where patients have an increased risk of developing oesophageal
adenocarcinoma.
1,2,3

Aetiology

Anatomy
The oesophagus is a
border of the cricoid cartilage at the level of C6.
The oesophagus descends through the superior mediastinum of the thorax between the trachea and the vertebral bodies
of T1 and T4. It then enters the abdomen via the oesophageal hiatus at T10.
The abdominal portion of the oesophagus is approximately 1.25cm long. It terminates at the cardiac ori
at the level of T11.
4
Food is transported through the oesophagus by peristalsis (rhythmic contractions of the muscles).
4The oesophagus has three layers (Figure 1).
Adventitia\: an outer layer of connective tissue
Muscle layer\: an external layer of longitudinal muscle and an inner layer of circular muscle
Mucosa\: non-keratinised strati
Figure 1. Layers of the oesophagus.
5
Oesophageal sphincters prevent the entry of air and the re
Upper oesophageal sphincter\: striated muscle sphincter at the junction between the pharynx and oesophagus.
Produced by the cricopharyngeus muscle. Usually, it is constricted to prevent the entry of air into the oesophagus.
Lower oesophageal sphincter\: located at the gastro-oesophageal junction, to the left of the T11 vertebra. At rest, the
sphincter prevents re
During peristalsis, the sphincters relax to allow food to enter the stomach.
4
Pathophysiology
Barrett’s oesophagus is a consequence of gastro-oesophageal re
lower oesophageal sphincter, which allows re
mucosa.
Irritation of the lower oesophagus for a prolonged period causes a transformation (metaplasia) from squamous epithelium
to columnar type intestinal epithelium (Figure 2).
Occasionally, dysplasia occurs, which predisposes to malignant transformation.
1,4
Malignant transformation occurs along a metaplasia-dysplasia-adenocarcinoma sequence
Figure 2. Histopathology of Barrett's
oesophagus. Characterised by the
presence of columnar epithelium with
goblet cells.
7

Risk factors

Risk factors for Barrett's oesophagus include\:
2
Gastro-oesophageal re
Acid-bile re
Increasing age
Obesity
White ethnicity
Male sex
Recent evidence also indicates a genetic predisposition.
6Clinical features
The change from normal to premalignant cells in Barrett’s oesophagus is asymptomatic. However, patients may have
symptoms of acid re
Typical symptoms of acid re
1
Heartburn
Regurgitation
Trouble swallowing (dysphagia)
Vomiting blood (haematemesis)
Unintentional weight loss because eating is painful (odynophagia)
Less commonly\: chest pain, laryngitis, cough, dyspnoea, wheezing
For more information, see the Geeky Medics OSCE guide to gastrointestinal history taking.

Investigations

The main investigation for Barrett’s oesophagus is an upper gastrointestinal endoscopy with biopsy.
At endoscopy, Barrett’s oesophagus is characterised by the replacement of the paler squamous epithelium with ‘salmon-
coloured’ columnar epithelium above the gastro-oesophageal junction (GOJ).
The length (in centimetres) of changes to the epithelium is measured and helps inform subsequent management and
surveillance.
The minimum length of epithelial changes required for a diagnosis is 1cm above the GOJ.
Figure 3. Endoscopic image showing the
characteristic colour changes of
epithelium in Barrett's oesophagus.
8
The Prague C & M classi
The Prague C & M classi is used to determine disease severity\:
C\: circumferential extent of disease. The distance from the GOJ to the highest location metaplasia is present
around the entire circumference of the oesophagus
M\: distance from the GOJ to the highest location of metaplasia
Example\: C3 M5
The higher the numbers, the more severe the disease and the greater the risk of malignant transformation.
9

Management

Patients with Barrett's oesophagus are o
They are also o
9,10
Table 1. The management of Barrett's oesophagus.Initial endoscopy

Management
No dysplasia
Low-grade
dysplasia
High-grade
dysplasia
High-de
(oesophago-gastro-duodenoscopy/OGD) and biopsies
taken every 2cm on initial detection.
If \<3cm and gastric metaplasia present\: repeat OGD
and consider discharging
If \<3cm and intestinal metaplasia present\: repeat OGD
every 3-5 years
If > 3cm\: repeat OGD every 2-3 years
If con
ablation is recommended.
MDT discussion and repeat endoscopy at a specialist
centre.
Options include are\:
Radiofrequency ablation if no visible lesion
Endoscopic resection if visible lesion present

Complications

Compared to the general population, patients with Barrett’s oesophagus have a 30x increased lifetime risk of developing
oesophageal adenocarcinoma.
11
However, the absolute risk of Barrett’s oesophagus progressing over time and developing into oesophageal
adenocarcinoma is fairly low (annual incidence of 0.33%).
12
Barrett’s oesophagus has been associated with an increased risk of oesophageal strictures. This occurs due to acid re
and is treated with endoscopic dilation.

References

BMJ Best Practice. (n.d.). B a r r e t t’ s O e s o p h a g u s . [online] Available from\: [LINK]
Spechler, S.J. and Souza, R.F. (2014). Barrett’s Esophagus. T h e N e w E n g l a n d J o u r n a l o f M e d i c i n e , 371, pp.836–845.
Pophali, P. and Halland, M. (2016). Barrett’s oesophagus\: diagnosis and management. B M J , p.i2373.
OpenStax. The Mouth, Pharynx, and Esophagus. Available from\: [LINK]
Goran tek-en. I m a g e s h o w i n g l a y e r s o f o e s o p h a g u s . License\: [CC BY-SA 4.0]
P, Fitzgerald RC; Genome-wide association studies in oesophageal adenocarcinoma and Barrett's oesophagus\: a large-
scale meta-analysis. Lancet Oncol. 2016 Oct;17(10)\:1363-1373.
Mikael Häggström, M.D. M i c r o s c o p i c i m a g e s h o w i n g h i s t o l o gy o f B a r r e t t’ s O e s o p h a g u s . Samir. E n d o s c o p i c i m a g e o f c h a n g e s s e e n i n B a r r e t t’ s O e s o p h a gu s . License\: [Public License\: domain]
[CC0 1.0]
Fitzgerald, R.C., di Pietro, M. and Ragunath, K. (2013). British Society of Gastroenterology guidelines on the diagnosis and
management of Barrett’s Oesophagus. G u t , pp.1–36. Available from\: [LINK]
NICE, Endoscopic radiofrequency ablation for Barrett's oesophagus with low-grade dysplasia or no dysplasia. Available
from\: [LINK]
Solaymani-Dodaran, M. (2004). Risk of oesophageal cancer in Barrett’s oesophagus and gastro-oesophageal re
53(8), pp.1070–1074.
Desai, T.K., Krishnan, K., Samala, N., Singh, J., Cluley, J., Perla, S. and Howden, C.W. (2011). The incidence of oesophageal
adenocarcinoma in non-dysplastic Barrett’s oesophagus\: a meta-analysis. G u t , 61(7), pp.970–976.Reviewer
Dr Leo Alexandre
Consultant Academic Gastroenterologist

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Investigations
Management
Complications
Source\: geekymedics.com