Barrett esophagus (BE) is a condition in which the stratified squamous epithelium of the esophagus is replaced by intestinal columnar epithelium, a process called intestinal metaplasia (IM). Dr. Norman Barrett, an Australian thoracic surgeon, characterized the findings in an article that he published in 1950.¹ In 1953, the association was made between BE and gastroesophageal reflux disease (GERD) by the English thoracic surgeon Dr. Philip Allison.² The etiology of BE is accepted to be due to chronic exposure of the esophageal epithelium to gastroduodenal refluxate. The importance of BE is its potential to progress and develop into adenocarcinoma. The association between BE and esophageal adenocarcinoma was established in a case report in 1975 by Dr. Alan Farnsworth, a cardiac surgeon, in which he identified adenocarcinoma in a segment of BE.³

Multiple factors have been identified that lead to an increased risk of developing BE. These include age over 50 years, male gender, white race, elevated body mass index (BMI), intra-abdominal distribution of body fat, hiatal hernia, and chronic GERD.⁴ BE is diagnosed by endoscopic biopsy and histologic examination which identifies the IM (Fig. 41-1).

Progression of BE to cancer is recognized as a continuum through dysplasia to cancer. As such, the histologic examination of this disease is often classified into BE without dysplasia, BE with low-grade dysplasia (LGD), and BE with high-grade dysplasia (HGD). Progressive severity of dysplasia leads to a higher risk for the development of esophageal cancer. BE without dysplasia has a 0.5% per year risk of developing into esophageal cancer, whereas BE with LGD has a 1.4% per year risk and BE with HGD has a 6% per year risk.⁵ It is this strong association between BE and esophageal adenocarcinoma that has driven the aggressive surveillance and treatment of BE.

The goal of surveillance is to reduce mortality of a disease by early diagnosis. In the case of BE, the goal of surveillance is to reduce the mortality due to esophageal cancer. The risk of developing esophageal cancer in the general Western population is low; therefore, routine endoscopic screening has not been recommended. For patients who have risk factors for BE as described earlier, there is some data supporting screening endoscopy. Therefore, the American College of Gastroenterology recommends that screening endoscopy in this patient population should be individualized.⁶

For patients already diagnosed with BE, it is a common practice to perform endoscopic surveillance to search for signs of progression to cancer. Although this makes intuitive sense, there is a lack of randomized clinical trials to identify the true effectiveness of endoscopic surveillance in patients with BE. There have, however, been population studies that have shown the practice to lead to earlier detection and associated improved survival rates of esophageal adenocarcinoma in patients with BE who had endoscopy prior to diagnosis of cancer.⁷ Therefore, the current recommendations by the American Gastroenterological Association (AGA) are as follows: for patients with BE without dysplasia, endoscopic surveillance should be performed every 3 to 5 years. For patients with BE and LGD, endoscopic surveillance is recommended every 6 to 12 months. For patients with BE and HGD who do not undergo intervention, surveillance is recommended every 3 months.⁶ It should be noted that in order for endoscopic surveillance to be effective, adequate surveillance involves taking four quadrant biopsies every 1 to 2 cm along the affected length of esophagus in addition to biopsies of any irregular appearing mucosa (Table 41-1).

The goals for treatment of BE are (1) to decrease or eliminate gastroduodenal reflux into the esophagus, primarily to improve the associated symptoms of GERD and potentially to limit progression or cause regression of BE and (2) to directly eliminate Barrett metaplasia and dysplasia (via resection or ablation), thereby decreasing the risk for development of esophageal adenocarcinoma. The methods by which to achieve these goals are continuously evolving and in certain clinical scenarios, still remain somewhat controversial.

Control of Reflux

Medical Therapy

There are several ways to reduce and eliminate gastroduodenal reflux. Medical therapy, in the form of proton pump inhibitors, has been shown to be very effective for neutralizing gastric acid and controlling acid reflux symptoms. In addition, there are several studies that have shown that medical therapy can cause modest regression of BE. Regression is often defined in several ways, including decrease in the length of BE, down-grading of Barrett dysplasia, and complete elimination of IM. The regression rates have been reported to be from 19% to 41% depending on the definition of regression. Practitioners should be aware, however, that there can be progression of BE while on medical therapy. Reported rates of progression to dysplasia range from 1.8% up to 31%. Similarly, rates of progression from BE to esophageal adenocarcinoma have been reported to be from 1.6% to 7.4% while on medical therapy. Therefore, acid and symptom control with proton pump inhibitors alone should be used in conjunction with endoscopic surveillance to monitor for regression or progression of disease.

Antireflux Surgery

Antireflux surgery has been offered to patients who have failed medical treatment, usually defined as breakthrough symptoms, or progression or continuation of esophageal damage due to reflux. The technical details of the various types of antireflux operations are discussed in detail in other chapters. Laparoscopic Nissen fundoplication is the most common operation performed, but all operations described for the treatment of GERD may be used in patients with BE.

The use of antireflux surgery to change the natural history of BE is controversial. While there are no randomized controlled trials that show superiority of laparoscopic antireflux surgery over medical therapy for causing regression of BE or preventing the development of esophageal adenocarcinoma, there are some retrospective studies that suggest there may be a benefit of surgery.⁸ In a recent review of the literature, we found that on average, 11.1% of patients who underwent medical therapy progressed to dysplasia compared to only 3.4% of patients who had antireflux surgery.⁹ Similarly, 4.1% of patients undergoing medical therapy for BE progressed to adenocarcinoma compared to only 0.7% of patients who had antireflux surgery. Although these are selective case studies and few were established to compare medical and surgical therapy, the trends do suggest a possible benefit from antireflux surgery. Despite the improved symptomatic responses to surgery compared to medical therapy and the apparent decreased rates of regression of BE and progression to adenocarcinoma, the regression is still incomplete and progression to adenocarcinoma still occurs.¹⁰ Therefore, surveillance endoscopy should still remain as an important component of treatment for BE after antireflux surgery (Table 41-2).