eMedicine Specialties > Radiology > Gastrointestinal

Barrett's Esophagus

Author: Narain Srinivas, MD, Consulting Staff, Department of Radiology, Forbes Regional Hospital
Contributor Information and Disclosures

Updated: Jul 24, 2008

Introduction

Background

Barrett's esophagus is a metaplastic disorder in which specialized columnar epithelium replaces healthy squamous epithelium. Barrett's metaplasia is the most common cause or precursor of esophageal carcinoma. The rate of esophageal adenocarcinoma is increasing in the Western world, and it is associated with a poor prognosis, mainly because individuals present with late-stage disease.

Numan R. Barrett (1903-1979), after whom the entity is named, was a distinguished thoracic surgeon in London. In 1950, Barrett wrote an article entitled Chronic Peptic Ulcer of the Oesophagus and "Oesophagitis." He concluded that most of the cases are examples of congenital short esophagus. He suggested that this was a separate entity from reflux esophagitis.1

In Leeds, England, in 1953, Allison, a thoracic surgeon, and Johnstone, a radiologist, published an article entitled The Oesophagus Lined With Gastric Mucous Membrane. They suggested the term Barrett's ulcers to describe ulcer craters in the columnar cell–lined esophagus.

In 1957, Barrett published another article entitled The Lower Esophagus Lined by Columnar Epithelium, which he presented as a lecture at the Mayo Clinic. He now accepted the view of Allison and Johnstone that this condition involves a columnar cell–lined esophagus and not an extension of the stomach into the mediastinum. His conclusion that a columnar cell–lined esophagus is congenital was later disproved.

For excellent patient education resources, visit eMedicine's Cancer and Tumors Center. Also, see eMedicine's patient education article Cancer of the Mouth and Throat.

Related eMedicine topics:
Barrett Esophagus and Barrett Ulcer
Esophageal Cancer
Gastroesophageal Reflux Disease

Related Medscape topics:
Resource Center GERD
Resource Center Barrett's Esophagus Resource Center
CME  Optimizing Clinical Outcomes and Patient Compliance in the Management of GERD
CME  Role of Reflux Monitoring in the Evaluation of Patients With Suspected GERD
CME  Applications of Acid-Suppression Therapy in GERD/Acid-Related Disorders
CME Endoscopic Treatment of Dysplasia and Early Cancer of the Esophagus and Esophago-gastric Junction
CME Study Supports Use of Proton Pump Inhibitors as Chemoprevention in Patients With Barrett's Esophagus
CME What's New in Barrett's Esophagus?

Pathophysiology

Barrett's esophagus is an acquired condition, secondary to chronic gastroesophageal reflux (GER) damage to the esophageal mucosa (see Image 2). Its origin probably involves multipotential undifferentiated cells. Remnants of the heterotopic gastric epithelium may be seen in the subcricoid area, termed the inlet patch, which has no malignant potential.

Classically, Barrett's esophagus has 3 histologic types of epithelium: (1) specialized columnar (intestinal metaplasia), (2) gastric, and (3) junctional. Although controversy exists, intestinal metaplasia of any length is the current criterion for the diagnosis of Barrett's esophagus .

Localization of the metaplasia to the distal 2-3 cm of the esophagus defines short-segment Barrett's esophagus. The pathophysiology of short-segment Barrett's esophagus is uncertain. Recent data suggest that it occurs as a complication of GER disease (GERD), although patients with short-segment Barrett's esophagus have a less severe form of GERD than patients with long-segment Barrett's esophagus.

Frequency

United States

Esophagitis secondary to gastroesophageal reflux (GER) is the most common medical condition in Western countries. Among the 30% of adults who have heartburn at least once a month, a third have endoscopic evidence of esophagitis. In 10% of patients with esophagitis, the condition progresses to Barrett's metaplasia. Approximately 0.5-2.0% of adults in the Western world have Barrett's metaplasia.

Mortality/Morbidity

Barrett's metaplasia leads to most, if not all, esophageal and gastroesophageal-junction adenocarcinomas, with an annual rate of neoplastic transformation of 0.2-2%. Once cancer is diagnosed, patients have a median survival of less than 1 year; less than 10% of patients survive for longer than 5 years despite combined chemotherapy and surgery.2

Conventional clinical risk factors for Barrett's adenocarcinoma are neither sensitive nor specific enough for the classification of individuals with a high risk. Therefore, surveillance is required for all patients with Barrett's metaplasia who are surgical candidates, but this approach is neither feasible nor cost-effective.

Race

Whites have the highest risk of Barrett's esophagus, and blacks have the lowest risk.

Sex

Males have a higher risk of Barrett's esophagus than females.

Age

People older than 45 years have the highest risk for BE, and those younger than 40 years have the lowest risk.

Presentation

Typical symptoms described in gastroesophageal reflux disease (GERD) are heartburn (eg, retrosternal burning, a tight sensation radiating toward the neck) and acid regurgitation (ie, unpleasant return of sour or bitter gastric contents to the pharynx). Less common symptoms include water brash (ie, hypersalivation associated with an episode of esophageal acid exposure), dysphagia (ie, difficulty in swallowing), and a globus sensation (ie, sensation of a lump in the throat). The common typical symptoms of heartburn and acid regurgitation often occur after eating, especially after ingesting large meals.

Preferred Examination

When heartburn or acid regurgitation is the dominant symptom, the specificity is sufficiently high to diagnose gastroesophageal reflux disease (GERD). If no additional indication for further evaluation exists, patients may be confidently treated for GERD without undergoing confirmatory tests.

The preferred radiologic examination for Barrett's esophagus is a double-contrast esophagography.3 Imaging modalities that yield less information include nuclear medicine technetium-99m-pertechnetate scanning, endoluminal ultrasonography (US), chromoendoscopy,4  and CT scanning.

Limitations of Techniques

Positive findings on a double-contrast esophagogram suggest a diagnosis of Barrett's esophagus, in correlation with the clinical history. However, an endoscopic examination with biopsy is required to confirm the diagnosis because columnar metaplasia is diagnosed at microscopy.5 In addition, the features that suggest columnar metaplasia are not always present on the esophagogram. A Barrett stricture without the other features cannot be distinguished from the other etiologies of a stricture.

Differential Diagnoses

Other Problems to Be Considered

When a smooth stricture is the main feature, the following should be considered: corrosive stricture, stricture after prolonged nasogastric intubation, Crohn disease, Behcet syndrome, and radiation-induced stricture.

When a reticular mucosal appearance is present distal to the area of ulcerations, the following should be considered: candidiasis, superficial spreading carcinoma, glycogenic acanthosis, and areae gastricae in a small hiatal hernia.

More on Barrett's Esophagus

Overview: Barrett's Esophagus
Imaging: Barrett's Esophagus
Follow-up: Barrett's Esophagus
Multimedia: Barrett's Esophagus
References
Further Reading

References

  1. Cameron AJ. The history of Barrett esophagus. Mayo Clin Proc. Jan 2001;76(1):94-6. [Medline].

  2. Moayyedi P, Burch N, Akhtar-Danesh N, Enaganti SK, Harrison R, Talley NJ. Mortality rates in patients with Barrett's oesophagus. Aliment Pharmacol Ther. Feb 15 2008;27(4):316-20. [Medline].

  3. Levine MS. Radiology of esophagitis: a pattern approach. Radiology. Apr 1991;179(1):1-7. [Medline].

  4. Curvers W, Baak L, Kiesslich R, Van Oijen A, Rabenstein T, Ragunath K, et al. Chromoendoscopy and narrow-band imaging compared with high-resolution magnification endoscopy in Barrett's esophagus. Gastroenterology. Mar 2008;134(3):670-9. [Medline].

  5. Miehlke S, Morgner A, Aust D, Madisch A, Vieth M, Baretton G. Combined use of narrow-band imaging magnification endoscopy and miniprobe confocal laser microscopy in neoplastic Barrett's esophagus. Endoscopy. Feb 2007;39 Suppl 1:E316. [Medline].

  6. Noh HM, Fishman EK, Forastiere AA. CT of the esophagus: spectrum of disease with emphasis on esophageal carcinoma. Radiographics. Sep 1995;15(5):1113-34. [Medline].

  7. Li Y, Woodall C, Wo JM, Zheng H, Ng CK, Ray MB, et al. The use of dynamic positron emission tomography imaging for evaluating the carcinogenic progression of intestinal metaplasia to esophageal adenocarcinoma. Cancer Invest. Apr-May 2008;26(3):278-85. [Medline].

  8. Eisenberg RL. Esophageal ulceration. In: Gastrointestinal Radiology: A Pattern Approach. 1996: 45-69.

  9. Odegaard S. Searching a role for endoscopic ultrasonography in Barrett's esophageus and other acid-related or gastrointestinal motility disorders. Minerva Med. Aug 2007;98(4):409-15. [Medline].

  10. Savoy AD, Wolfsen HC, Raimondo M, Woodward TA, Noh K, Pungpapong S, et al. The role of surveillance endoscopy and endosonography after endoscopic ablation of high-grade dysplasia and carcinoma of the esophagus. Dis Esophagus. 2008;21(2):108-13. [Medline].

  11. Pondugula K, Wani S, Sharma P. Barrett's esophagus and esophageal adenocarcinoma in adults: long-term GERD or something else?. Curr Gastroenterol Rep. Dec 2007;9(6):468-74. [Medline].

  12. Wilson BC. Detection and treatment of dysplasia in Barrett's esophagus: a pivotal challenge in translating biophotonics from bench to bedside. J Biomed Opt. Sep-Oct 2007;12(5):051401. [Medline].

  13. Yamamoto AJ, Levine MS, Katzka DA. Short-segment Barrett's esophagus: findings on double-contrast esophagography in 20 patients. AJR Am J Roentgenol. May 2001;176(5):1173-8. [Medline].

  14. Ertan A, Younes M. Barrett's esophagus. Dig Dis Sci. Aug 2000;45(8):1670-3. [Medline].

  15. Glick SN. Barium studies in patients with Barrett's esophagus: importance of focal areas of esophageal deformity. AJR Am J Roentgenol. Jul 1994;163(1):65-7. [Medline].

  16. Jankowski JA, Harrison RF, Perry I. Barrett's metaplasia. Lancet. Dec 16 2000;356(9247):2079-85. [Medline].

  17. Ryan AM, Healy LA, Power DG, Byrne M, Murphy S, Byrne PJ, et al. Barrett esophagus: prevalence of central adiposity, metabolic syndrome, and a proinflammatory state. Ann Surg. Jun 2008;247(6):909-15. [Medline].

  18. Schuchert MJ, Luketich JD. Management of Barrett's esophagus. Oncology (Williston Park). Oct 2007;21(11):1382-9, 1392; discussion 1392, 1394, 1396. [Medline].

  19. SSAT patient care guidelines. Management of Barrett's esophagus. J Gastrointest Surg. Sep 2007;11(9):1213-5. [Medline].

  20. Szarka LA, DeVault KR, Murray JA. Diagnosing gastroesophageal reflux disease. Mayo Clin Proc. Jan 2001;76(1):97-101. [Medline].

Keywords

Barrett's esophagus, Barrett esophagus, Barrett's metaplasia, Barrett metaplasia, BE, esophageal carcinoma, chronic gastroesophageal reflux, chronic GER, gastroesophageal reflux disease, GERD

Contributor Information and Disclosures

Author

Narain Srinivas, MD, Consulting Staff, Department of Radiology, Forbes Regional Hospital
Narain Srinivas, MD is a member of the following medical societies: American College of Radiology and Radiological Society of North America
Disclosure: Nothing to disclose.

Medical Editor

Neela Lamki, MD, Professor, Department of Radiology, Sultan Qaboos University, Oman; Adjunct Professor, Department of Radiology, Baylor College of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Abraham H Dachman, MD, FACR, Professor, Department of Radiology, The University of Chicago School of Medicine; Director of CT, Department of Radiology, The University of Chicago Hospitals
Abraham H Dachman, MD, FACR is a member of the following medical societies: Radiological Society of North America
Disclosure: iCAD, Inc. Consulting fee Consulting; iCAD, Inc. Grant/research funds Other; GE Healtcare, Inc. Honoraria Speaking and teaching

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Clinical Assistant Professor of Radiology, University of Washington Medical School
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

 
 
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