You are in: eMedicine Specialties > Radiology > GASTROINTESTINAL Barrett's EsophagusArticle Last Updated: Jul 24, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 13
  Author: Narain Srinivas, MD, Consulting Staff, Department of Radiology, Forbes Regional Hospital Narain Srinivas is a member of the following medical societies: American College of Radiology and Radiological Society of North America Editors: Neela Lamki, MD, Professor, Department of Radiology, Sultan Qaboos University, Oman; Adjunct Professor, Department of Radiology, Baylor College of Medicine; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; 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; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Clinical Assistant Professor of Radiology, University of Washington Medical School Author and Editor Disclosure Synonyms and related keywords: Barrett's esophagus, Barrett esophagus, Barrett's metaplasia, Barrett metaplasia, BE, esophageal carcinoma, chronic gastroesophageal reflux, chronic GER, gastroesophageal reflux disease, GERD INTRODUCTIONSection 2 of 13
  BackgroundBarrett'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. PathophysiologyBarrett'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. FrequencyUnited StatesEsophagitis 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/MorbidityBarrett'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. RaceWhites have the highest risk of Barrett's esophagus, and blacks have the lowest risk. SexMales have a higher risk of Barrett's esophagus than females. AgePeople older than 45 years have the highest risk for BE, and those younger than 40 years have the lowest risk. Clinical DetailsTypical 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 ExaminationWhen 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 TechniquesPositive 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. DIFFERENTIALSSection 3 of 13
Other Problems to Be ConsideredWhen 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. RADIOGRAPHSection 4 of 13
FindingsA specific diagnosis of Barrett's esophagus can be suggested if a proximal esophageal stricture, deep penetrating ulcer, or reticular mucosal surface pattern is seen on the esophagogram (see Image 1). Although esophageal ulceration in Barrett's esophagus can occur anywhere along the columnar epithelium, classically it involves the most proximal portion at or near the squamocolumnar junction, well above the cardia and even as high as the aortic arch. Unlike the shallow ulcerations that usually are caused by reflux esophagitis in the squamous epithelium, a Barrett ulcer tends to be deep, penetrating, and identical to a peptic gastric ulcer. Stricture formation usually accompanies the ulceration. At times, no ulceration is evident, and only a smooth, tapered stricture is present. The stricture forms at the squamocolumnar junction. The Barrett stricture tends to be short and tight, typically causing eccentric narrowing of the lumen in contrast to the smooth, symmetric, and circumferential luminal narrowing in peptic strictures. A specific sign of Barrett's esophagus is the ascending or migrating stricture, in which progressive upward migration of both the squamocolumnar junction and the level of the stricture is depicted on serial esophagograms. A delicate reticular pattern extending inferiorly for a variable distance from the level of a stricture has been described as a radiologic sign of Barrett's metaplasia. However, this appearance is nonspecific, and it has been observed in other conditions such as candidiasis, viral esophagitis, superficial spreading carcinoma, and areae gastricae in a small hiatal hernia. A sliding hiatal hernia with gastroesophageal reflux (GER) commonly is seen in patients with Barrett's esophagus. However, in most patients, a variable length of normal-appearing esophagus separates the Barrett ulcer from the hiatal hernia. This finding is in contrast to that of reflux esophagitis, in which the distal esophagus is abnormal down to the level of the hernia. Another radiologic sign that raises the possibility of Barrett's esophagus is a focal defect in the esophageal contour at least 4 cm proximal to the esophagogastric junction. The contour defect is believed to be an early stage of a midesophageal stricture, a classic feature of Barrett's esophagus. Esophageal contour defects caused by Barrett's esophagus simulate normal variations in the caliber of the esophagus. Optimal distention of the esophageal lumen and varying obliquity may be necessary to confirm the presence of restricted distensibility and to identify fixed transverse folds. Subtle contour defects can be observed more readily on double-contrast images because fixation of the esophageal wall may be more conspicuous than on images obtained with a single-contrast technique. Radiographic findings in short-segment Barrett's esophagus are less specific. In one study, 70% of patients with short-segment Barrett's esophagus had reflux esophagitis, peptic scarring or strictures, or both on double-contrast esophagograms, and 30% had only hiatal hernias or strictures as radiographic findings. Degree of ConfidenceFindings of Barrett's esophagus on a double-contrast esophagogram must be confirmed with esophagogastroduodenoscopy (EGD) and biopsy. False Positives/NegativesThe fine reticular pattern inferior to the stricture in some patients with Barrett's esophagus also may be observed when the areae gastricae, which is the normal appearance of the gastric mucosa on a double-contrast image, is visualized within a small hiatal hernia. CT SCANSection 5 of 13
FindingsCT scanning is not the modality of choice for the diagnosis of Barrett's esophagus. However, CT scans obtained for reasons other than the evaluation of Barrett's esophagus may incidentally reveal a deep Barrett ulcer in the mid-to-distal esophagus.6 In addition, in the event of transformation in an area of Barrett's metaplasia to esophageal adenocarcinoma, CT may reveal a focal esophageal soft-tissue mass.7 In patients with these findings, CT is useful in staging the cancer and in predicting its response to treatment. Degree of ConfidenceAn esophageal ulcer or a mass lesion found incidentally on CT scans must be further evaluated with endoscopy and, probably, biopsy because these findings are nonspecific and may occur in other conditions.8 A deep ulcer is a nonspecific finding and may be present in other conditions such as esophagitis related to human immunodeficiency virus (HIV) or cytomegalovirus (CMV) infection. Unless contiguous involvement of surrounding tissues exists, distinguishing between a malignant neoplasm and a benign lesion, such as a leiomyoma, may be difficult. False Positives/NegativesBecause CT has a poor yield in the detection of mucosal lesions, it is not the appropriate test, by itself, for the diagnosis of Barrett's esophagus. MRISection 6 of 13
FindingsMRI, like CT, does not have a role in the diagnosis of Barrett's esophagus. MRI is an evolving modality, and imaging techniques may be refined in the future to permit detection of esophageal ulcers and mass lesions with certainty. ULTRASOUNDSection 7 of 13
FindingsUltrasound (US) also is not the modality of choice in the diagnosis of Barrett's esophagus. However, endoscopic US is used to evaluate early submucosal or mucosal cancer in the surveillance of patients with Barrett's esophagus.9, 10 Intraluminal US may reveal an esophageal neoplasm, which is depicted as a solid mass lesion that disrupts the normal layers of the esophagus. In addition, extension of the neoplasm beyond the confines of the esophageal wall also may be determined with US. Degree of ConfidenceFindings at intraluminal esophageal US performed for reasons other than the investigation of Barrett's esophagus warrant further evaluation with endoscopy and biopsy. NUCLEAR MEDICINESection 8 of 13
FindingsRadionuclide examination with intravenously administered technetium-99m pertechnetate may show uptake by the gastric type of mucosa; this uptake may be observed in Barrett's metaplasia. However, because intestinal metaplasia of any length is the currently accepted modality for the diagnosis of Barrett's esophagus, the significance of a positive finding on a pertechnetate scan is uncertain. In addition, nuclear scanning is not the investigation of choice in the diagnosis of Barrett's esophagus. Positive uptake in an area of Barrett's metaplasia may be incidentally observed on scans obtained for reasons other than the assessment of Barrett's esophagus. Degree of ConfidencePositive pertechnetate uptake in the region of the esophagus suggests the presence of gastric mucosa. This finding should be evaluated further with endoscopy and, probably, biopsy. False Positives/NegativesBecause intestinal metaplasia of any length is the currently accepted modality for the diagnosis of Barrett's esophagus, the significance of a positive finding on a pertechnetate scan is uncertain; it signifies ectopic gastric mucosa in the esophagus. In addition, uptake may be observed in remnants of the heterotopic gastric epithelium in the subcricoid area, termed inlet patch, which has no malignant potential. Sufficient care must be taken to ensure that positive uptake does not represent the passage of swallowed saliva through the esophagus. This finding can be confirmed by asking the patient to drink a glass of water and then by imaging the lower chest again. In addition, because Barrett's metaplasia may consist of only intestinal metaplasia without the presence of gastric mucosa, no uptake of technetium-99m pertechnetate may occur in the region of Barrett's esophagus. ANGIOGRAPHYSection 9 of 13
FindingsAngiography has no role in the diagnosis of Barrett's esophagus. INTERVENTIONSection 10 of 13
Patients with gastroesophageal reflux (GER) symptoms for more than 5 years, particularly those aged 50 years or older, should undergo esophagogastroduodenoscopy (EGD) for the detection of Barrett's esophagus.11 When erosive esophagitis visually obscures the squamocolumnar junction, reevaluation after the esophagitis heals may be needed for clear recognition and accurate biopsy of Barrett's esophagus. With the recognition of Barrett's esophagus as a premalignant lesion, the crucial issue is surveillance. The goal of surveillance is to detect dysplasia.12 Dysplasia occurs on the background of metaplasia, but it is not the ideal marker for selecting patients with a high risk for adenocarcinoma. Mutations in the p53 gene and DNA aneuploidy are among promising markers that may well precede the development of dysplasia. Approximately 40% of patients who have high-grade dysplasia without cancer, according to endoscopic biopsy findings, are found to have adenocarcinoma at esophagectomy. The technique of obtaining 4-quadrant biopsy samples in every 2-cm section of the Barrett's esophagus generally is accepted. Multiple biopsy samples from areas of normal-appearing Barrett's esophagus are necessary because of the multicentric nature of the dysplasia. In patients with high-grade dysplasia, EGD surveillance is needed every 3 months. If an experienced pathologist confirms the presence of high-grade dysplasia during the second EGD, patients should undergo esophagectomy. In patients with low-grade dysplasia, surveillance is needed every 6-12 months. The surveillance interval should be lengthened to every 2-3 years when the results of 2 successive annual EGDs reveal nondysplastic epithelium. Although dysplasia and cancer can develop in patients with short-segment Barrett's esophagus, the incidence of cancer in these patients is not known. Until the risk of cancer is specifically defined in these patients, endoscopic surveillance is not recommended in those with short-segment Barrett's esophagus. Radiologic intervention has no role in the management of BE. However, after esophagectomy, balloon dilatation may be performed with fluoroscopic guidance if a stricture develops at the anastomotic site. Medical/Legal Pitfalls
See also the Medscape topic Medical Malpractice and Legal Issues. FURTHER READINGSection 11 of 13
Esophagus, Carcinoma - Radiology MULTIMEDIASection 12 of 13
REFERENCESSection 13 of 13
Article Last Updated: Jul 24, 2008 | ||||||||||||||
