Barrett Esophagus

Background

• Barrett esophagus is a metaplastic change of esophageal mucosa from the normal esophageal squamous epithelium to the columnar-lined metaplastic epithelium compromising 3 cell types: gastric fundic epithelium, gastric cardiac junctional epithelium, and intestinal metaplasia (IM) (columnar epithelium with intestinal-type goblet cells).
• Barrett esophagus is caused by longstanding gastroesophageal reflux disease (GERD) with risk factors including GERD for > 5-10 years, age > 50 years, male sex, White race, tobacco use, central obesity, and family history of Barrett esophagus or esophageal adenocarcinoma (EAC) in a first-degree relative.
• There is no clear association between Helicobacter pylori infection and Barrett esophagus.
• The primary complications of Barrett esophagus are the development of dysplasia and the progression to adenocarcinoma.

Evaluation

• Barrett esophagus is typically identified during an upper endoscopy in patients with GERD.
  • Endoscopic findings suggesting Barrett esophagus include cephalad displacement of the squamocolumnar junction and the appearance of columnar epithelial projections into the esophagus (most guideline organizations suggest a columnar mucosal length of ≥ 1 cm for a diagnosis of Barrett esophagus).
  • Many guideline organizations agree that a diagnosis of Barrett esophagus requires biopsy confirmation of IM because of an increased risk of EAC associated with IM.
• Do not screen for Barrett esophagus by upper endoscopy in the general population with GERD, except consider screening in individuals with chronic GERD and multiple risk factors (including age > 50 years, male sex, White race, central obesity, hiatal hernia, tobacco use, and family history of Barrett esophagus or EAC in a first-degree relative) (Weak recommendation).
• In patients with esophagitis on initial endoscopic evaluation, consider a repeat endoscopy after completing 8-12 weeks of proton pump inhibitor (PPI) therapy to ensure healing and exclude the presence of Barrett esophagus.
• For screening endoscopy, consider obtaining at least 8 biopsy samples if the endoscopic appearance suggests potential Barrett esophagus to increase the diagnostic yield, following the Seattle protocol for any segments > 4 cm of 4-quadrant biopsies at intervals ≤ 2 cm (Weak recommendation).
• If the patient has short segments and 8 random biopsies are unattainable, consider at least 4 biopsies per cm of suspected circumferential Barrett esophagus and 1 biopsy per cm in tongues of suspected Barrett esophagus.
• The diagnosis of dysplastic Barrett esophagus should be confirmed by a second pathologist, preferably with expertise in Barrett histopathology (Strong recommendation).

Management

• Use once-daily PPI therapy in all patients with Barrett esophagus without contraindication to PPI use. Do not use twice-daily PPIs, except consider them in patients with reflux symptoms or esophagitis that are inadequately controlled with once-daily dosing.
• See Gastroesophageal Reflux Disease (GERD) for details on the management of concomitant GERD.
• Consider endoscopic surveillance with biopsies in patients with Barrett esophagus due to the risk for progressing to dysplasia and carcinoma (Weak recommendation), and use a shared and informed decision-making approach before starting surveillance.
  • Use a structured biopsy protocol in the surveillance of Barrett esophagus according to the Seattle protocol of 4-quadrant biopsies at intervals 1-2 cm of the involved esophageal segment to minimize detection bias (Strong recommendation).
  • Commonly recommended frequencies for endoscopic surveillance:
    • Consider performing surveillance in patients with Barrett esophagus at intervals dictated by the degree of dysplasia on previous biopsies (Weak recommendation).
    • Consider surveillance at an interval of 3 years in patients with long segments (≥ 3 cm) of nondysplastic Barrett esophagus and 5 years in patients with short segments (< 3 cm) of nondysplastic Barrett esophagus (Weak recommendation).
    • Consider surveillance every 6 months for 1 year followed by annual checks if low-grade dysplasia and endoscopic eradication therapy is not pursued (Weak recommendation).
• If low-grade dysplasia, consider endoscopic eradication therapy over surveillance (Weak recommendation); radiofrequency ablation is considered the preferred endoscopic ablative therapy.
• If high-grade dysplasia or adenocarcinoma is confined to the mucosa, offer endoscopic eradication therapy with endoscopic mucosal resection of any visible lesions followed by radiofrequency ablation of the remaining Barrett segment (Strong recommendation).
• Consider endoscopic eradication therapy compared to esophagectomy for patients with superficial submucosal adenocarcinoma and low-risk features, such as, a negative deep margin, well or moderate differentiation, and no lymphovascular invasion.