Barrett’s Esophagus (BE) is thought to be a complication of longstanding gastroesophageal reflux disease (GERD). In BE, metaplasia of the distal esophagus’ normal squamous epithelium to columnar-lined intestinal mucosa occurs. Metaplastic changes of BE may be suggested by upper endoscopy, or potentially capsule endoscopy, but confirmation requires biopsy of the columnar-appearing mucosa showing intestinal metaplasia.

BE is the major risk factor for developing adenocarcinoma of the esophagus and is considered a pre-malignant condition. BE is felt to be an adaptation to, and ultimately a complication of, longstanding GERD.

BE is suggested on upper endoscopy when there is extension of salmon-colored mucosa into the esophagus extending >1cm proximal the gastroesophageal junction (GEJ). Diagnosis is confirmed with biopsy evidence of intestinal metaplasia. High-grade dysplasia, low-grade dysplasia and adenocarcinoma can also be seen on biopsy and confirm underlying BE but are not required to make the diagnosis of BE.

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Adenocarcinoma or erosive esophagitis can cause a false negative biopsy. However, this is only clinically important in erosive esophagitis. Re-endoscopy should be considered after healing of erosive esophagitis with PPI therapy for 8-12 weeks to definitively confirm or exclude BE, particularly if the initial indication for endoscopy was suspected BE.

In patients with suspected BE and lack of intestinal metaplasia biopsy, a repeat endoscopy should be considered in 1-2 years.

Historical features have been identified as risk factors associated with the development of BE. These include longstanding GERD, male gender, age greater than 50, tobacco use, Caucasian race, and central obesity.

Numerous clinical studies analyzing prevalence data for BE have produced a wide range of estimates. A study in Sweden determined the prevalence of BE in that population to be 1.6%. Small autopsy studies in the United States identify the prevalence to be one quarter to one half of that. Estimates from a simulation model and confirmed by the National Cancer Institute’s SEER data suggest the prevalence of BE in the general US population to be 5.6%.

Erosive esophagitis can mask identification of intestinal metaplasia in biopsy specimens. If BE is suspected, is a known prior diagnosis or is the primary indication for endoscopy and biopsy then erosive esophagitis should be healed prior to biopsy to eliminate this masking effect.

There are no physical examination findings that confirm BE. However, an increased body mass index (BMI), specifically central obesity, correlates with an increased risk.

The potential mechanism for increased visceral adiposity causing BE is likely both mechanical (increased risk of GERD in abdominal obesity) and biochemical (increased adipocytokines).

Currently, there are no non-tissue based biomarkers available to risk-stratify or diagnose patients with BE. While many tissue biomarkers for risk of adenocarcinoma development in BE are under investigation, none are available at this time. Hence, no laboratory evaluation is recommended for either screening, diagnosis, prognosis, or surveillance of BE.

There are no imaging studies recommended. The diagnosis of BE is made by upper endoscopy findings of columnar epithelium in the esophagus with biopsy confirmation of intestinal metaplasia.

Although screening for BE was not recommended in the 2008 American College of Gastroenterology (ACG) Practice Guidelines, they have since published updated screening guidelines in 2015.

Summary of screening recommendations:

  • Screening for BE may be considered in males with chronic (>5 yrs.) symptoms of GERD and two or more risk factors (listed in IIA).

  • Screening for BE in females is not recommended.

  • Screening of the general population (no chronic GERD symptoms and no risk factors) is not recommended.

No additional studies are useful in diagnosing BE. Radiographic imaging, esophageal manometry, and potential hydrogen (pH) monitoring are not helpful in diagnosing BE.


No immediate management is necessary for BE. However, given the potential for progression to esophageal adenocarcinoma, surveillance or endoscopic eradication therapy will be needed based on histologic findings.

Endoscopic management of BE begins with a close inspection of the BE mucosa. Management algorithms have been developed for nonnodular BE and nodular BE. Patients with nodular BE on upper endoscopy should undergo endoscopic mucosal resection (EMR) with histologic findings determining subsequent management. If findings of EMR demonstrate no dysplasia, surveillance endoscopy can be resumed. However, if EMR demonstrates low or high grade dysplasia (LGD, HGD) endoscopic ablative therapy is warranted.

Patients with nonnodular BE and no dysplasia should resume surveillance endoscopy with biopsies. Those with LGD or HGD should receive endoscopic eradication therapy.

GERD symptoms, if present, can be managed acutely with acid suppression. Once-daily proton pump inhibitor (PPI) therapy is appropriate initial management. Twice-daily PPI therapy is not recommended unless needed to manage symptoms not controlled on daily therapy.



D. Long-term management.

Several cohort studies now suggest that subjects with BE maintained on PPI therapy have a decreased risk of progression to neoplastic BE, even without GERD symptoms. Therefore, patients with BE should receive longterm, once-daily PPI therapy.

Aspirin or NSAIDs should not be routinely prescribed to patients with BE as an antineoplastic strategy.

The goal of surveillance endoscopy is to identify dysplasia and early adenocarcinoma before lesions become symptomatic improving chances to treat for cure. Retrospective data show statistically significant survival benefit with surveillance endoscopy in patients with adenocarcinoma of the esophagus. Thus, surveillance endoscopy should be performed in appropriately selected patients.

Patients should have a 5-year or greater life expectancy, a good understanding of surveillance and their disease, and a willingness to adhere to the recommended surveillance regimen. Since esophagitis can decrease the diagnostic yield of biopsy, GERD symptoms should be controlled with PPI therapy and any known esophagitis should be healed prior to surveillance endoscopy and biopsy.

The frequency of surveillance endoscopy depends on the time since initial identification of BE and degree of dysplasia identified. The 2015 ACG practice guideline details recommendations for surveillance endoscopy.

  • Patients without dysplasia: Endoscopic surveillance should take place at intervals of 3-5 yrs.

  • Patients with results indefinite for dysplasia: Repeat endoscopy after 3-6 months of PPI therapy. If repeat reading is indefinite for dysplasia, a surveillance interval of 12 months is recommended.

  • Patients with low-grade dysplasia (LGD): Endoscopic ablative therapy is the preferred treatment modality. Endoscopic surveillance every 12 months may be considered. Patients with high-grade dysplasia (HGD): Endoscopic ablative therapy Post-ablative surveillance:

    LGD: Endoscopic surveillance is recommended every 6 months in the first year, annually thereafter.

    HGD: Endoscopic surveillance is recommended every 3 months for the first year, every 6 months in the second year, annually thereafter.

Several technologies are undergoing investigation to improve the accuracy of endoscopic biopsy in identifying dysplasia. Adjunctive endoscopic imaging technologies have been developed to increase the yield of biopsy by directing the endoscopist toward areas more likely to be involved with dysplasia rather than simply using a random four-quadrant technique.

Narrow band imaging (filtering the light to exclude all but blue and green) is a technique that can be used with a high-resolution endoscope to better identify dysplasia visually during endoscopy. Similarly autofluorescence uses a blue light to identify dysplasia. Staining the tissues prior to endoscopy (chromoendoscopy) has been used but appears to be no more effective than random biopsy. Narrow band imaging, autofluorescence and chromoendoscopy image large areas of mucosa.

For smaller areas of more suspicious appearing mucosa, laser confocal microscopy can be used to direct biopsy. Laser confocal microscopy magnifies the mucosa and images cellular structures during endoscopy to identify areas more likely to be dysplastic.

PPI therapy is not without potential complications. There are numerous drug-drug interactions with the PPIs and prior to prescribing in a PPI-naive patient on other medications these interactions should be reviewed. PPI therapy has been associated with an increased risk of community-acquired pneumonia, Clostridium difficile infection and decreased dietary magnesium and vitamin B12 absorption. PPI therapy has a potential association with atrophic gastritis, other enteric infections, decreased calcium absorption, and hip fracture.

Medical therapy for symptom control with a PPI is not affected by comorbidity except in circumstances where PPI therapy alters the efficacy of another medication used for treatment of the comorbidity. Surveillance endoscopy and biopsy should be limited to patients with a life expectancy of at least 5 years.

No change in standard management.

No change in standard management.

No change in standard management.

PPI therapy may decrease serum concentrations of the active metabolite(s) of clopidogrel. The risks and benefits of using these medications in combination should be considered with each individual patient and alternative methods of acid suppression may be appropriate in patients who require clopidogrel therapy.

No change in standard management.

No change in standard management.

While immunosuppression can increase the risk of cancer development in general and case reports support an increased risk of esophageal adenocarcinoma in BE patients who are immunosuppressed following solid organ transplant, there are no general recommendations to change standard management or screening in this population.

No change in standard management.

No change in standard management.

No change in standard management.

No change in standard management.

Given the longterm nature of PPI therapy in BE, patients do not require intravenous (IV) PPI to replace oral PPI if made nil per os (NPO) while hospitalized.

BE is not an indication for hospitalization and thus should not guide discharge planning.

BE is not an indication for hospitalization and thus should not guide discharge planning.

All patients with established BE should have their surveillance plan assessed at the time of hospitalization for any reason. If surveillance has been initiated and remains appropriate or has not been initiated but is appropriate, the hospitalist should ensure the recommended surveillance plan is being adhered to as an outpatient.

Surveillance endoscopy should be scheduled as a part of discharge planning for the patient if overdue or due within 3 months. Additionally, the patient and primary care provider should be informed in the discharge documentation when surveillance is due next, for all patients. If patients have active esophagitis or uncontrolled GERD symptoms, they should be treated with PPI therapy for at least 8-12 weeks prior to any surveillance endoscopy and biopsy.




  • BE is the major risk factor for development of esophageal adenocarcinoma (but not squamous cell carcinoma of the esophagus).

  • Rates of BE conversion to esophageal adenocarcinoma depend on the degree of dysplasia.

    BE with no dysplasia: 0.33%

    BE with LGD: 0.50%

    BE with HGD: 7.0%

  • Symptomatic esophageal adenocarcinoma has a poorer overall prognosis (less than 15% 5-year survival) when compared to asymptomatic adenocarcinoma discovered via surveillance for BE (around 85% 5-year survival).

  • The process of endoscopy and biopsy, including risk and benefits should be discussed with patients who are candidates for screening endoscopy (including sedation).

  • The frequency of surveillance endoscopy depends on the results of initial endoscopy.

  • An endoscopic or surgical procedure will be recommended for high-grade abnormalities or cancer.

Patients should be willing to proceed to the recommended invasive therapy if high-grade abnormalities or cancer are identified, before embarking on a surveillance endoscopy program.



Shaheen. “ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus”. The Am J of Gastroenterology. 2015.

Hayeck, TJ. “The Prevalence of Barrett’s esophagus in the US: estimates from a simulation model confirmed by SEER data”. Dis Esophagus. vol. 23 . 2010. pp. 451-457.

Singh, S. “Acid-suppressive medications and risk of oesophageal adenocarcinoma in patients with Barrett’s oesophagus: a systematic review and meta-analysis”. Gut. vol. 63. 2014. pp. 1229-1237.