What is the role of radiology in evaluating patients with Barrett's esophagus?
M.Y.M. Chen, D.J. Ott (Winston-Salem)
Barrett's esophagus is a well-recognized entity in which the normal squamous epithelium in the distal esophagus has been replaced by a columnar epithelial lining, presumably as a result of chronic reflux esophagitis . Barrett's esophagus can be suggested endoscopically by the demonstration of reddish columnar epithelium 2-3 cm above the diaphragmatic hiatus or esophagogastric junction (EGJ), in contrast to the pale pink appearance of the adjacent squamous epithelium. The presence of columnar epithelium may be confirmed by examination of biopsy material taken from the mucosa above the EGJ. The type of columnar epithelium extension, whether circumferential or island form, does not affect the diagnostic criteria for Barrett's esophagus.
Although final diagnosis of Barrett's esophagus is dependent on endoscopic biopsy, radiologic examination, especially the double-contrast study, has played an important role in evaluation of patients with dysphagia, in diagnosis of Barrett's esophagus, and in follow-up for early detection of malignant changes.
The classic radiologic signs of Barrett's esophagus include midesophageal stricture, deep ulceration, and a reticular pattern on the mucosal surface. A variety of non specific radiologic signs are seen in patients with Barrett's esophagus [2-6]; these include gastroesophageal reflux, hiatal hernia, and thickened mucosal folds. Barrett's esophagus is more likely to be found when signs of moderate or severe esophagitis are encountered radiographically; Barrett's esophagus is found in only about 1% of patients with no esophagitis or mild esophagitis endoscopically, but in 14% of patients with severe esophagitis. On the other hand, most patients with Barrett's esophagus but with no esophagitis or only mild esophagitis are unlikely to be referred for radiologic examination.
Radiologic findings in Barrett's esophagus and their prevalence are hiatal hernia (87%), stricture (72%), thickened folds (65%), gastroesophageal reflux (60%), distal esophageal dilation (44%), esophageal ulcer (40%), and reticular pattern (23%).
Hiatal hernia has the highest frequency (75%-94%) in patients with Barrett's esophagus [2, 3]. Hiatal hernia alone poorly predicts the presence of Barrett's esophagus; however, presence of Barrett's esophagus is unusual in the absence of hiatal hernia.
Esophageal stricture is the second most common radiologic sign in patients with Barrett's esophagus and usually occurs at or below the level of the elevated squamocolumnar junction  (Figure 1). Midesophageal stricture is found in 29% and lower esophageal stricture in 42% of cases from several series [2, 3]. Although lower esophageal stricture is more common than midesophageal stricture, the latter is more specific for diagnosis of Barrett's esophagus. Patients with Barrett's esophagus and stricture are often referred for radiologic examination to document the severity of the stricture and explain the symptoms of the patient.
Figure 1. Peptic strictures in three patients with Barrett's esophagus. A. Lower esophageal stricture (S) located just above the esophageal vestibule (V) with adjacent ulcer (arrow). B. A long midesophageal stricture (S) shown on a double-contrast view. C. Intramural outpouchings (arrowhead) shown adjacent to a midesophageal stricture.
Thickened and irregular mucosal folds are a common finding (28-86%)(Figure 2) in patients with Barrett's esophagus because of their association with esophagitis. Thickened mucosal folds are best appreciated on mucosal relief films when the esophagus is collapsed.
Gastroesophageal reflux is a nonspecific sign of Barrett's esophagus and reflects its relationship with reflux esophagitis. Thus, the prevalence of reflux would be expected to be higher in this group of patients.
Barrett ulcers are present in 40% (range, 18%-54%) of patients examined radiologically and are variable in size and shape (Figure 1A). Barrett ulcers are usually deep, located either at the squamocolumnar transitional zone or below the level of stricture, and surrounded by columnar epithelium.
Erosions are found in about 25% of patients with Barrett esophagus. The erosions are shown only on double-contrast examination, and the reported prevalence of erosions is higher when double-contrast esophagography is used. Erosions are common in patients with reflux esophagitis.
Figure 2. Thickened and irregular folds in patient with Barrett's esophagus. Massive mucosal thickening (arrows) demonstrated in the distal esophagus.
Figure 3. Reticular mucosal pattern shown on double-contrast esophagram (from  with permission).
The reticular mucosal pattern has been reported in 13%-30% of patients with Barrett's esophagus who were examined with double-contrast studies (Figure 3). The reticular mucosal pattern may be specific for certain pathologic types of Barrett epithelium. However, this pattern is not specific and has been reported in patients with monilial and viral esophagitis, or superficial spreading carcinoma [5-7].
The prevalence of distal esophageal dilation ranges from 34% to 66% . Distal dilation may also be seen in patients with gastroesophageal reflux.
Some patients with Barrett's esophagus have normal radiographic results if gastroesophageal reflux, esophagitis, or the reticular pattern are absent. Most patients who have Barrett's esophagus with orad extension of island-type columnar epithelium are not referred for radiologic examination following endoscopy because esophagography is thought to be of little value in the workup of patients with simple mucosal dysplasia . However, in a recently reported study , some ectopic gastric mucosa in the esophagus could be detected as a discrete, shallow depression surrounded by a subtle, rim like elevation on double-contrast studies and as a shallow indentation on single-contrast views .
Some associations of Barrett's esophagus may be found during radiologic examinations. Barrett's esophagus is a common occurrence in patients with scleroderma. These patients may have low esophageal sphincter pressure, frequent reflux, and inability to clear refluxed contents from the esophagus, all contributing to development of esophagitis and complicating Barrett's esophagus. Barrett's esophagus has been reported in patients who have achalasia with esophagomyotomy. Heller esophagomyotomy may adversely affect the function of the lower esophageal sphincter, causing gastroesophageal reflux and its sequelae. Barrett's esophagus may also be found in achalasia without esophagomyotomy, possibly related to stasis .
Regression and malignant potential
Partial regression of Barrett's esophagus after antireflux surgery was reported in four patients in 1980 . In 1989, Deviere et al.  reported using omeprazole, a parietal-cell H+-K+-ATPase inhibitor for treating patients with Barrett's ulceration. In one of their patients, who had Barrett's epithelium that was seen 16 cm above the EGJ and grade 3 esophagitis, an ulcer healed after 3 months and the Barrett's epithelium regressed completely after 18 months of therapy. Esophagography may be useful in evaluating the regression of esophagitis associated with Barrett esophagus, but is of no value in judging the regression of columnar epithelium.
Barrett's esophagus is generally accepted as a precursor of esophageal adenocarcinoma. Most primary adenocarcinomas of the esophagus arise from a background of columnar epithelium. Dysplasia and carcinoma in situ may be found adjacent to the Barrett's mucosa [13-15]. The sequence of malignant changes may be initiated as severe dysplastic change, followed by carcinoma in situ, and finally invasive adenocarcinoma . The prevalence of adenocarcinoma in patients with Barrett's esophagus averages about 10% [14, 16, 17] or approximately 40 times higher than the prevalence of adenocarcinoma in the general population [16, 18]. The incidence of esophageal adenocarcinoma arising from Barrett's esophagus is about one case per 52 to 441 patient-years of follow-up [16-20]. The average age at presentation of adenocarcinoma in patients with Barrett's esophagus is 60 years old, with a range of 11 to 87 years old .
Figure 4. A. Infiltrative adenocarcinoma (arrows) with irregular narrowing in the distal esophagus arising from Barrett's epithelium. B. Endoscopic ultrasound shows the neoplastic process extending into periesophageal tissues. Two lymph nodes (L), 1 and 5 cm in caliber, are seen (from  with permission).
Figure 5. Varicoid adenocarcinoma. Barium esophagram shows the tortuous nodules and thickened mucosal folds in the distal esophagus, suggesting esophagitis. Autopsy confirmed a poorly differentiated adenocarcinoma arising from Barrett's epithelium (from  with permission).
Patients with Barrett's esophagus and persistent high-grade dysplasia found on initial mucosal biopsies are likely to develop an adenocarcinoma after 2.6 to 4.5 years . Patients with Barrett's esophagus and no dysplasia are less likely to have malignant changes. The incidence of adenocarcinoma is also related to the extent of columnar epithelium. Doubling the length of columnar epithelium in patients with Barrett's esophagus may result in a two fold increased risk for developing adenocarcinoma .
Many investigators advocate periodic endoscopic surveillance with biopsy and cytology at 6-month or yearly intervals in patients with Barrett's esophagus for early detection of cancer. Early esophageal adenocarcinoma may be found by radiologic screening in patients with Barrett's esophagus and severe dysplasia. Early adenocarcinoma arising in Barrett's esophagus may appear on a double-contrast study as a plaque-like lesion, mucosal irregularity and nodularity, or sessile polyps with a smooth or slightly lobulated contour. In patients with peptic strictures, a slight rigidity or flattening of one wall of the stricture is suggestive of early cancer. A diffuse nodularity may be present in superficial spreading type of malignancy.
The most common radiographic appearance of advanced adenocarcinoma arising from Barrett's esophagus is an irregular infiltrating stricture with an ulcerating or exphophytic mass (Figure 4). The mass usually causes complete or partial esophageal obstruction. A varicoid appearance with thickened, tortuous folds due to submucosal spread of tumor has been reported (Figure 5) [13-15]. Most adenocarcinomas arising from Barrett's esophagus are located at the level of stricture or ulceration. In addition, Barrett's esophagus and adenocarcinoma may be associated with synchronous squamous cell carcinoma in the proximal squamous-lined esophagus .
13. Haggitt RC, Dean PJ. Adenocarcinoma in Barrett's epithelium. In: Spechler SJ, Goyal RK, eds. Barrett's esophagus: pathophysiology, diagnosis, and management. New York: Elsevier Science, 1985:153-166.
21. Menke-Pluymers MB, Hop WC, Dees J, van Blankenstein M, Tilanus HW. Risk factors for the development of an adenocarcinoma in columnar-lined (Barrett) esopaghus. The Rotterdam Esophageal Tumor Study Group. Cancer 1993;72:1155-1158.