Figure 6.37 Reflux esophagitis with ulceration. (A) Double‐contrast view shows shallow linear and punctate ulcers (arrows) in the distal esophagus above a hiatal hernia.
Source: Reproduced from Levine [73], with permission.
(B) Double‐contrast view in another patient shows a single flat ulcer (arrow) on the posterior wall of the distal esophagus.
Source: Reproduced from Levine MS. Radiology of the esophagus. Philadelphia: WB Saunders, 1989, with permission.
Figure 6.38 Reflux esophagitis with thickened folds. Double‐contrast view shows considerably thickened folds in the esophagus caused by edema and inflammation extending into the submucosa. Compare this image to the normal appearance of the longitudinal folds in Figure 6.35B.
Source: Reproduced from Levine MS. Radiology of the esophagus. Philadelphia: WB Saunders, 1989, with permission.
Figure 6.39 Reflux esophagitis with inflammatory esophagogastric polyp. Prone single‐contrast view shows a prominent fold arising at the cardia and extending into the distal esophagus as a smooth polypoid protuberance (arrow). This appearance is characteristic of an inflammatory esophagogastric polyp.
Figure 6.40 Scarring of distal esophagus with fixed transverse folds. Double‐contrast view shows minimal narrowing of the distal esophagus above a hiatal hernia. Also note sacculation (white arrows) of the wall and pooling of barium between transverse folds (black arrows), producing a “stepladder” appearance.
Source: Reproduced from Levine MS and Laufer I. The upper gastrointestinal series at a crossroads. AJR Am J Roentgenol1993; 161:1131–1137, with permission.
Eosinophilic esophagitis
Eosinophilic esophagitis (EoE) has been recognized as an increasingly common inflammatory condition of the esophagus, occurring predominantly in young men with long‐standing dysphagia and recurrent food impactions, often associated with an atopic history, asthma, or peripheral eosinophilia [102]. The diagnosis of EoE can be confirmed on endoscopic biopsy specimens showing more than 20 eosinophils per high‐power field [102, 103]. The etiology is uncertain, but many authors believe that EoE develops as an inflammatory response to ingested food allergens in predisposed individuals [102, 103]. As a result, symptomatic patients often have a marked clinical response to treatment with steroids or elemental diets.
Figure 6.41 Peptic stricture. Double‐contrast view shows a smooth, tapered area of concentric narrowing (arrow) in the distal esophagus above a hiatal hernia.
Source: Reproduced from Gilchrist et al. [85], with permission.
The diagnosis of EoE may by suggested on barium studies by the presence of segmental esophageal strictures, sometimes associated with distinctive ring‐like indentations, producing a so‐called “ringed esophagus” [104] (Figure 6.53). The radiographic diagnosis may also be suggested by the development of a “small‐caliber esophagus” manifested by a long but variable‐length segment of narrowing in the thoracic esophagus that has smooth contours, tapered margins, and a mean diameter of 20 mm or less [105] (Figure 6.54), so 20 mm appears to be a useful threshold diameter for the diagnosis of EoE on barium studies.
Lichen planus
Lichen planus is a chronic inflammatory condition involving the skin, mucous membranes, and, less commonly, the esophagus. Esophageal involvement predominantly occurs in elderly women with long‐standing dysphagia and associated skin lesions [106], but 50% of these patients experience dysphagia before the development of cutaneous disease [107]. Esophageal lichen planus may be manifested on barium studies by segmental strictures in the cervical or thoracic esophagus or, even more commonly, by a small‐caliber esophagus with diffuse, smooth esophageal narrowing (Figure 6.55) indistinguishable from that in EoE (see Figure 6.54) [108]. However, EoE typically occurs in young men with an atopic history, asthma, and/or peripheral eosinophilia [102], whereas lichen planus occurs in elderly women, often with associated cutaneous lesions. When esophageal lichen planus is suspected on the basis of the clinical and radiographic findings, the diagnosis can be confirmed on endoscopic biopsy specimens showing a lymphocytic infiltrate with keratinocyte degeneration and characteristic Civatte bodies (i.e. necrotic keratinocytes) [109].
Figure 6.42 Feline esophagus. Double‐contrast view shows delicate transverse folds as a transient finding in the esophagus. Contrast this image to the fixed transverse folds in the distal esophagus in Figure 6.40.
Radiation esophagitis
A radiation dose of 5000 cGy or more to the mediastinum may cause severe injury to the esophagus. Acute radiation esophagitis usually occurs two to four weeks after the initiation of radiation therapy [110]. This condition may be manifested by ulceration or by a granular appearance of the mucosa and decreased distensibility resulting from edema and inflammation of the irradiated segment [110] (Figure 6.56A). The extent of disease conforms to the margins of the radiation portal. Most cases of acute radiation esophagitis are self‐limited, but some patients may have progressive dysphagia due to the development of radiation strictures four to eight months after completion of radiation therapy [111]. These strictures typically appear as smooth, tapered areas of concentric