19: Esophageal Tumors



Diagnostic pitfalls

Currently the US definition of Barrett esophagus requires endoscopically abnormal (columnar) mucosa in conjunction with histological confirmation of specialized intestinal metaplasia (presence of goblet cells). The British Society of Gastroenterology criteria allow the definition of Barrett esophagus to include other types of metaplastic epithelium, including gastric and junctional (cardiac) epithelium. Because the natural history of Barrett esophagus with regard to cancer risk is still poorly defined, limiting the definition of Barrett esophagus to the entity for which most data are available (intestinal metaplasia) has been accepted by US national society guidelines.





Management and prevention


See Table 19.1.


Table 19.1 Management of Barrett esophagus



















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.







Guidelines: Barrett’s esophagus


1. American Gastroenterological Association, Spechler SJ, Sharma P, Souza RF, Inadomi JM, Shaheen NJ. American Gastroenterological Association medical position statement on the management of Barrett’s esophagus. Gastroenterology 2011;140:1084–1091.

2. Wang KK, Sampliner RE. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett’s esophagus. American Journal of Gastroenterology 2008;103:788–797.










Diagnostic pitfalls

Low-grade dysplasia has been a source of controversy regarding the risk of cancer. While some studies report increased incidence of adenocarcinoma, other studies illustrate cancer risk to be low and similar to the risk among patients with no dysplasia. One of the reasons for the difference may be the poor inter- and intraobserver correlation in the diagnosis of low-grade dysplasia. Inflammation, which is a necessary component of gastroesophageal reflux disease, can cause morphologically similar changes to dysplasia. Risk stratification based on dysplasia will be problematic; therefore, advances in molecular techniques or other tools that more accurately describe the risk of cancer will greatly improve the effectiveness and cost-effectiveness of screening and surveillance among patients with Barrett esophagus.





Squamous Cell Carcinoma

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May 31, 2016 | Posted by in GASTROENTEROLOGY | Comments Off on 19: Esophageal Tumors

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