Management and prevention
See Table 19.1.
Barrett’s esophagus with: | Recommendation |
No dysplasia | Endoscopic surveillance with biopsies every 3–5 years |
Low-grade dysplasia | Endoscopic surveillance with biopsies every 12 months or endoscopic therapy |
High-grade dysplasia | Endoscopic therapy (endoscopic mucosal resection, radiofrequency ablation, photodynamic therapy) |
Esophageal adenocarcinoma | Esophagectomy |
Screening and surveillance
Identification of the link between EAC and Barrett esophagus has led to the implementation of endoscopic screening and surveillance programs. The strategy proposed by several national societies includes screening patients with multiple risk factors for EAC (age 50 years or older, male sex, white race, chronic symptoms of gastroesophageal reflux disease, hiatal hernia, elevated Body Mass Index, intra-abdominal distribution of body fat) to detect Barrett esophagus using upper gastrointestinal endoscopy. If intestinal metaplasia is histologically confirmed in a region of the esophagus that has columnar-appearing mucosa, surveillance with high-resolution white-light endoscopy should be performed at intervals dependent on the presence and degree of dysplasia. Current guidelines suggest taking systematic four-quadrant biopsy specimens every 2 cm along the length of Barrett metaplasia. In addition, any endoscopic abnormalities such as erosions, nodules, or strictures should be biopsied.
Patients with no dysplasia are recommended to undergo surveillance at an interval between 3 and 5 years. Patients in whom low-grade dysplasia is diagnosed should have surveillance with four-quadrant biopsies every 1 cm performed every 12 months, or be considered for endoscopic ablation. High-grade dysplasia (HGD) must be confirmed on review by an experienced pathologist. Confirmation of HGD prompts a recommendation for endoscopic therapy using endoscopic mucosal resection, radiofrequency ablation or photodymic therapy. Visible lesions (ulcers, nodules, masses) associated with HGD should be removed by endoscopic mucosal resection techniques, which is both therapeutic and diagnostic by confirming the absence of invasive cancer. Invasive cancer should be staged using endoscopic ultrasound and treated by surgical resection.
Case–control studies illustrate a potential survival benefit from endoscopic surveillance of patients with Barrett esophagus; however, prospective studies to confirm the efficacy of surveillance are lacking.
Molecular markers for the presence of Barrett esophagus, dysplasia and cancer are under development; however, markers have not been validated to predict which patients with Barrett esophagus are at risk for progression. Furthermore, advanced imaging techniques such as chromoendoscopy have not been shown to improve the clinical outcomes of patients with Barrett esophagus and are not recommended for routine use at this time.