Most patients with BE will exhibit symptoms of GERD, such as the retrosternal burning sensation known as heartburn, especially after eating. Acid regurgitation is another likely symptom. Other possible symptoms, though less common, include dysphagia and a globus sensation where patients feel as if there is a “lump” or some obstruction in their throat when there is none. Rarely, patients may be asymptomatic. Commonly, patients will have a chronic history of GERD symptoms with no other specific physical examination findings.

In January 2016, the American College of Gastroenterology (ACG) published its new clinical guideline for the diagnosis and management of BE. They now recommend screening for BE in men with at least five years of chronic GERD symptoms who also have at least two (2) additional risk factors including greater than 50 years of age, history of smoking, white ethnicity, central obesity, or a confirmed family history of BE.  Due to the extremely low prevalence of EAC in women, this population has no indications for screening except for the presence of multiple risk factors.[1][8][9]

Diagnosis of BE, as defined by the American College of Gastroenterology, requires gross endoscopic identification of columnar metaplasia, generally described as “salmon-pink” tongues of mucosal tissue, as well as pathological confirmation of intestinal metaplasia with goblet cells on biopsy evaluation. However, the British Society of Gastroenterology, as well as the GERD Society Study Committee in Japan, do not require the presence of goblet cells to diagnose BE and base the diagnosis solely on the presence of columnar metaplasia.  Due to the controversy over the significance of goblet cells, another alternative classification has been proposed, which allows the pathologist to state that there is columnar metaplasia and then further specify whether goblet cells are present or are not present. To maximize the possibility of finding BE, dysplasia, and/or carcinoma, a minimum of 8 biopsies is recommended by the ACG. The Prague C & M criteria are recommended for endoscopic grading of BE, with the most proximal extent of circumferential columnar mucosa from the GEJ being the C value, and the maximal extent of non-circumferential columnar mucosa above the GEJ being the M value.[10][11]

In cases of BE, the pathologist must determine whether dysplasia or carcinoma is present. As studies suggest that the extent of dysplasia also correlates to the risk of cancer, it may be valuable for pathologists to not only comment on the presence but also the extent of dysplasia (such as focal or diffuse). Sometimes there may be a specific concern for dysplasia if an area of nodularity or ulceration is noted on endoscopy. However, BE-related dysplasia is often flat and not apparent on endoscopy. The major histologic pattern of dysplasia is intestinal, therefore resembling an adenoma of the colon. However, non-intestinal dysplasia also exists, including foveolar and serrated patterns. Validated criteria for classification as either low or high-grade only exists for intestinal-type dysplasia, however. Low-grade dysplasia may have up to mild architectural abnormalities with cytologic atypia consisting of nuclear elongation, dense and hyperchromatic nuclei, an increased nuclear:cytoplasmic (N:C) ratio, stratification limited to the basal half of the epithelium, increased mitoses and up to the mild loss of polarity.  Features distinguishing high-grade dysplasia from low-grade include crypt crowding, full-thickness stratification, a prominent loss of polarity, and mild to marked nuclear pleomorphism.  If there is extensive regenerative change so much that the atypia present slightly overlaps with low-grade dysplasia, the pathologist may give a diagnosis of “Indefinite for Dysplasia.” Distinction between high-grade dysplasia and intramucosal carcinoma suffers from a high degree of interobserver variability, however, recommended criteria for a diagnosis of intramucosal carcinoma include the lamina propria being invaded by individual neoplastic cells with no connection to the crypts, sheeting out of malignant cells, irregular and angulated glands located in the lamina propria or muscularis mucosae, a complex anastomosing pattern of glands within the lamina propria, and/or back-to-back glands or cells in an irregular architectural pattern.[12][13]

Surveillance plan strategies have a history of being arbitrary and not validated by strong prospective clinical studies with a 2014 study, even concluding that there is no association between surveillance and decreased EAC-related deaths. Based on their systematic review of the literature and evaluation of the level of evidence, the ACG made several changes to the recommended management of BE in its newest guidelines. High-definition white-light endoscopy is a novel endoscopic technology that is now recommended for routine use in surveillance beyond electronic chromoendoscopy. For non-dysplastic BE, the current ACG recommendation after the initial diagnosis is to follow up with surveillance every 3 to 5 years. The patient should also be placed on once-daily proton pump inhibitor therapy, regardless of the presence of reflux symptoms, due to evidence of a chemopreventive effect of proton pump inhibitors, where the risk of progression to neoplastic BE is reduced compared to no acid suppression or H2 blockers. Due to the significant impact on management, if BE is associated with dysplasia, the ACG emphasizes the importance of confirming a dysplasia diagnosis with a second pathologist with extensive experience in BE-related neoplasia. Patients with confirmed low-grade dysplasia can now be considered for endoscopic ablative therapy or can follow a 6 to 12-month interval surveillance plan.  For patients with confirmed high-grade dysplasia with endoscopic mucosal abnormalities, endoscopic mucosal resection followed by ablation of the remaining BE mucosa is recommended.  If no mucosal abnormality is visible, in other words, the mucosa is flat; radiofrequency ablation therapy is considered sufficient for low- or high-grade dysplasia as well as carcinoma. Cryotherapy is another option of ablative therapy.  It is necessary to continue surveillance of patients after ablative therapy, as multiple treatments are often required to ensure complete elimination of the lesional tissue. Surgical therapies such as esophagectomy are not the preferred initial approach to management for high-grade dysplasia or intramucosal cancer, as the procedure has a high risk of morbidities, though should be considered if intramucosal cancer has poor prognostic factors, such as lymphovascular invasion or poor differentiation or if cancer involves the submucosa. Patients with significant comorbidities that limit their likely survival may not benefit from endoscopic therapies, with risks of the procedures being greater than potential gains.[14][15]

• Acute gastritis

• Antral web Cholelithiasis

• Chronic gastritis

• Coronary artery atherosclerosis

• Esophageal cancer

• Esophageal mobility disorders

• Esophageal spasm

• Esophagitis

• Gall stones

• Helicobacter pylori infections

There is no longer any question that if Barrett esophagus is left untreated, it can develop into an adenocarcinoma. However, the risk of progression is very slow, and most patients will not develop a malignancy. However, at the same time, it should be noted that the number of cases of adenocarcinoma has steadily increased over the past three decades.[16]

The role of diet in the etiology of Barrett esophagus remains inconclusive but it is recommended that patients lower the intake of meat. In addition, patients should avoid oily foods, alcohol, caffeinated beverages, chocolate, acidic juices, vinegar and carbonated drinks.

The American College of Gastroenterology recommends upper endoscopy to detect or screen for Barrett esophagus after age 50.

Since not all patients will progress from BE to cancer, an essential area of research is the development of reliable risk-profiling methods to identify patients at higher risk and who will benefit more from therapies. The use of biomarkers to risk-stratify patients is currently undergoing extensive research, with DNA content abnormalities and TP53 and CDKN2A genetic alterations showing the most promise to date.  At this time, though, there is not enough evidence to recommend them for use in routine practice. Novel sampling techniques for screening that show promise include transnasal endoscopy and cytosponge. Many more on-going and future studies should add to our current knowledge base regarding BE and its best management.

The incidence of adenocarcinoma of the esophagus is increasing in most western nations, and most believe this is due to Barrett's esophagus. The progression of the lesion to cancer is slow, but once cancer occurs, the prognosis is very poor. Over the years, multiple societies have developed guidelines for screening, surveillance, and management of Barrett's esophagus.[9][17] Since most patients may have no symptoms or symptoms of reflux, suspicion of Barrett should always be high, especially in high-risk populations. Unfortunately, many gastroenterologists and surgeons have been performing upper endoscopies, but there is no clear-cut evidence revealing that this procedure can detect esophageal cancer early or prevents cancer. Unnecessary endoscopies also lead to high healthcare costs. Thus, the recommendations are that one follow strict guidelines for surveillance based on patient risk factors, rather than empirically performing endoscopy in all patients. An interprofessional approach with a team composed of pathologists, thoracic surgeons, radiologists, gastroenterologists, and general surgeons will permit individualization of care and the best results. The nurse's role is vital in educating the patient about reflux and ways to prevent it. The pharmacist should ensure that the patient is adequately treated for reflux and has a referral to a gastroenterologist.[18][19] Pharmacists will verify all anti-acid medication strategies (e.g., PPIs, H@ receptor blockers, etc.), verifying dosing, drug interactions, counseling patients on administration and adverse events, and reporting back to the prescriber with any concerns. [Level V]

Outcomes

There are many case series reporting on Barrett's outcomes, which are good to excellent. However, there are very few studies on long-term outcomes. Even though there are several types of treatments for Barrett and GERD, there is no solid evidence to indicate which one is the best or most effective. With the ability to deliver laser and radio-frequency wave therapy via the endoscope, more long-term studies are needed to determine not only the safety of these procedures but also their effectiveness in preventing the progression of Barrett's esophagus to a malignancy.[20] [Level V]