Diagnosis and Management of Barrett's Esophagus: An Updated ACG Guideline

Abstract

Barrett's esophagus (BE) is a common condition associated with chronic gastroesophageal reflux disease. BE is the only known precursor to esophageal adenocarcinoma, a highly lethal cancer with an increasing incidence over the last 5 decades. These revised guidelines implement Grading of Recommendations, Assessment, Development, and Evaluation methodology to propose recommendations for the definition and diagnosis of BE, screening for BE and esophageal adenocarcinoma, surveillance of patients with known BE, and the medical and endoscopic treatment of BE and its associated early neoplasia. Important changes since the previous iteration of this guideline include a broadening of acceptable screening modalities for BE to include nonendoscopic methods, liberalized intervals for surveillance of short-segment BE, and volume criteria for endoscopic therapy centers for BE. We recommend endoscopic eradication therapy for patients with BE and high-grade dysplasia and those with BE and low-grade dysplasia. We propose structured surveillance intervals for patients with dysplastic BE after successful ablation based on the baseline degree of dysplasia. We could not make recommendations regarding chemoprevention or use of biomarkers in routine practice due to insufficient data.

Figure 1.

Grading of Barrett’s esophagus using Prague criteria: (a) defining the circumferential extent and (b) maximal extent of the columnar-lined esophagus.

Figure 2.

Care algorithm for patients noted to have columnar mucosa in the tubular esophagus. Note the stratification of surveillance interval by length of nondysplastic BE. BE, Barrett’s esophagus; EAC, esophageal adenocarcinoma; GEJ, gastroesophageal junction; GI, gastrointestinal; HGD, high-grade dysplasia; LGD, low-grade dysplasia.

Figure 3.

Nonendoscopic Barrett’s esophagus detection devices. (a) Encapsulated and expanded Cytosponge device. (b and c) Encapsulated and expanded EsophaCap device. (d and e) Retracted and inflated Esocheck device.

Figure 4.

Algorithm for patients referred for consideration of EET. Please note that these procedures are to be performed using high-definition white light endoscopy and virtual chromoendoscopy and are generally performed after initiation of maximal acid suppressive therapy (twice-daily PPI). Resection of visible lesions should always precede ablative therapy, and this mucosal resection may upstage the BE, in which case the algorithm for the most severe histology should be followed. BE, Barrett’s esophagus; CEIM, complete eradication of intestinal metaplasia; EET, endoscopic eradication therapy; HGD, high-grade dysplasia; LGD, low-grade dysplasia; LVI, lymphovascular invasion; PPI, proton pump inhibitor.

Figure 5.

Images of band ligation endoscopic mucosal resection. (a) A lesion at the 9 o’clock position, (b) the same lesion, with borders marked with electrocautery, (c) the proximal portion of the lesion banded, and (d) complete resection of the lesion, with the absence of residual cautery markings.

Figure 6.

Suggested algorithm for post-CEIM surveillance in patients treated endoscopically for dysplastic BE. Panel a demonstrates the patient’s pretreatment long-segment BE, with a maximal extent of 9 cm and a circumferential extent of 7 cm. Panel b demonstrates the posttreatment esophagus, with previous areas of BE demonstrating neosquamous epithelium. Four quadrant biopsies are taken in the high cardia just below the Z line from the top of the gastric folds (blue dots). Four quadrant biopsies are additionally taken from each of the distal 2–3 cm of neosquamous epithelium (green dots). Biopsies taken of normal-appearing tissue above this range, even in previously long-segment disease, have not been demonstrated to have substantial additional yield for dysplasia or buried intestinal metaplasia. BE, Barrett’s esophagus; CEIM, complete eradication of intestinal metaplasia; GEJ, gastroesophageal junction. Adapted with permission from Kahn et al. (219).