sign in sign up
<<
Home , Diffuse esophageal spasm, Esophageal disease, Esophageal spasm, Esophageal varices, Polyp (medicine), Schatzki ring

Review for Residents

Marc S. Levine, MD Diseases of the : Stephen E. Rubesin, MD

Published online before print Diagnosis with 10.1148/radiol.2372050199 1 Radiology 2005; 237:414–427 Esophagography

adiology Abbreviations: AIDS ϭ acquired immunodeficiency R syndrome The barium esophagram is a valuable diagnostic test for evaluating structural and CMV ϭ cytomegalovirus functional abnormalities of the esophagus. The study is usually performed as a HIV ϭ human immunodeficiency virus multiphasic examination that includes upright double-contrast views with a high- LPO ϭ left posterior oblique density barium suspension, prone single-contrast views with a low-density barium RAO ϭ right anterior oblique suspension, and, not infrequently, mucosal-relief views with either density of barium suspension. The double-contrast phase optimizes the ability to detect inflammatory 1 From the Department of Radiology, or neoplastic diseases, whereas the single-contrast phase optimizes the ability to Hospital of the University of Penn- detect hiatal and lower esophageal rings or strictures. Fluoroscopic exami- sylvania, 3400 Spruce St, Philadel- nation of the esophagus is also important for assessing disorders such as phia, PA 19104. Received February 8, 2005; revision requested April 7; revi- achalasia and diffuse . This article is a review of gastroesophageal sion received April 25; accepted June reflux disease, other types of , benign and malignant esophageal tumors, 2. Address correspondence to M.S.L. varices, lower esophageal rings, diverticula, and esophageal motility disorders, all of (e-mail: [email protected]). which can be diagnosed with the aid of esophagography. The authors are paid consultants for © EZ-Em, Westbury, NY. RSNA, 2005 © RSNA, 2005

Despite the current focus on cross-sectional imaging studies such as those of computed tomography (CT) and magnetic resonance (MR) imaging, the barium examination con- tinues to be the primary radiologic modality for the evaluation of patients with , reflux symptoms, or other clinical findings of . Double-contrast esopha- grams are particularly useful for the detection of reflux disease and its complications, infectious esophagitis, esophageal , or other structural of the esophagus. The fluoroscopic portion of the examination is also useful for the assessment of esophageal motility and detection of esophageal motility disorders such as achalasia and . The purpose of this article is to review gastroesophageal reflux disease, other types of esophagitis, benign and malignant esophageal tumors, varices, lower esoph- ageal rings, diverticula, and esophageal motility disorders, all of which can be diagnosed with the aid of esophagography.

TECHNIQUE

Barium studies of the esophagus are usually performed as multiphasic examinations that include upright double-contrast views with a high-density barium suspension, prone single-contrast views with a low-density barium suspension, and, not infrequently, mu- cosal-relief views with either density of barium suspension (1). The patient first ingests an effervescent agent and then rapidly gulps high-density barium in the upright left posterior oblique (LPO) position (patient positions are described with respect to the fluoroscopic table top) to obtain double-contrast views of the esophagus, with the esophagus thrown off the spine to avoid confusion with overlapping structures. The normal distended esophagus has a thin white luminal contour in profile and a smooth homogeneous appearance en face (Fig 1). Collapsed or partially collapsed views (ie, mucosal-relief views) show the normal longitudinal folds as thin, straight, delicate structures no more than 1–2 mm in width. After having the patient turn a 360° circle to optimally coat the gastric fundus with barium, he or she is placed in a recumbent right-side-down position for double-contrast views of the gastric cardia and fundus. The cardia is often recognized by the presence of three or four stellate folds that radiate to a central point at the gastro- esophageal junction, also known as the cardiac rosette (Fig 2) (2).

414 GASTROESOPHAGEAL REFLUX folds should be recognized as a nonspe- ESSENTIALS DISEASE cific finding of esophagitis from a host of causes. Other patients with chronic re- ● Findings of reflux include fine nodular- The purpose of barium studies in patients flux esophagitis may have a single en- ity or granularity of the mucosa, ero- with reflux symptoms is not simply to larged fold that arises at the gastric cardia sions or ulcers, thickened longitudinal document the presence of a hiatal and extends upward into the distal folds, inflammatory esophagogastric or gastroesophageal reflux but to detect esophagus as a smooth, polypoid protu- polyps, and scarring with strictures, the morphologic sequelae of reflux, in- berance, also known as an inflammatory sacculations, or fixed transverse folds. cluding reflux esophagitis, peptic stric- esophagogastric (Fig 5) (10,11). tures, Barrett esophagus, and esophageal ● Esophagography can be used to clas- This is a chronically inflamed fold adenocarcinoma. These conditions are sify patients with reflux symptoms as rather than a true , so it is also discussed separately in the following sec- being at high, moderate, or low risk for known as an inflammatory pseudopolyp tions. (10,11). Because these lesions have no adiology Barrett esophagus, on the basis of spe- malignant potential, is not cific radiologic criteria. R Reflux Esophagitis warranted when barium studies reveal ● Candida esophagitis is characterized typical findings of an inflammatory Reflux esophagitis is by far the most on esophagrams by plaques or a esophagogastric polyp in the distal common inflammatory disease involving “shaggy” esophagus, whereas herpes esophagus. If these lesions are unusually the esophagus. Double-contrast esopha- esophagitis is characterized by multiple large or lobulated, however, endoscopy grams have been shown to have a sensi- and biopsy may be required to rule out a small ulcers, and human immunodefi- tivity approaching 90% for the detection tumor in the distal esophagus. ciency virus and cytomegalovirus are of reflux esophagitis because of the abil- characterized by one or more giant flat ity to reveal mucosal abnormalities that ulcers. cannot be visualized on single-contrast Scarring and Strictures ● On esophagrams, early esophageal studies (4,5). Most cases that are missed manifest as small polypoid or occur in patients with milder forms of Localized scarring from reflux esoph- plaquelike lesions or superficial spread- esophagitis, which manifest at endos- agitis may manifest on barium studies as copy as mucosal erythema and friability. ing lesions, whereas advanced esopha- flattening, puckering, or sacculation of The single most common sign of reflux the adjacent esophageal wall, often asso- geal cancers manifest as infiltrating, esophagitis on double-contrast esopha- ciated with folds radiating toward the site polypoid, ulcerative, or varicoid lesions. grams is a finely nodular or granular ap- of scarring. Further scarring can lead to ● At fluoroscopy, achalasia is associated pearance with poorly defined radiolucen- the development of a circumferential with absent and beaklike cies that fade peripherally due to edema stricture (ie, “peptic” stricture) in the dis- narrowing of the distal esophagus due and inflammation of the mucosa (Fig 3) tal esophagus, almost always located to incomplete opening of the lower (6,7). This nodularity or granularity al- above a (12). Such strictures esophageal sphincter, whereas diffuse most always extends proximally from the often appear as concentric segments of gastroesophageal junction as a continu- esophageal spasm is associated with smooth tapered narrowing (Fig 6), but ous area of disease. intermittent weakening or absence of asymmetric scarring can lead to asym- Barium studies may also reveal shallow metric narrowing with focal sacculation primary peristalsis with multiple, repeti- ulcers and erosions in the distal esopha- or ballooning of the esophageal wall be- tive, nonperistaltic contractions, some- gus. The ulcers can have a punctate, lin- tween areas of fibrosis (Fig 7) (8). Other times producing a corkscrew esopha- , or stellate configuration and are of- peptic strictures may manifest as short geal appearance. ten associated with a surrounding halo of ringlike areas of narrowing (Fig 8) that edematous mucosa, radiating folds, or could be mistaken for Schatzki rings in sacculation of the adjacent wall (Fig 4) patients with dysphagia (8). When there (8). Some patients have a solitary ulcer at is marked irregularity, flattening, or The patient is then placed in a prone or near the gastroesophageal junction, right anterior oblique (RAO) position and often on the posterior wall of the distal nodularity of one or more walls of the is asked to take discrete swallows of low- esophagus, presumably as a result of pro- stricture, endoscopy and biopsy may be density barium to evaluate esophageal longed exposure to refluxed acid that required to rule out a malignant stricture motility. Esophageal dysmotility is con- pools posteriorly when patients sleep in as the cause of these findings. sidered to be present when abnormal the supine position (9). Other patients Scarring from reflux esophagitis can peristalsis is detected for two or more of have more widespread ulceration of the also lead to longitudinal shortening of five separate swallows (3). The patient distal third or half of the thoracic esoph- the esophagus and the development of next gulps the low-density barium sus- agus, but this ulceration always extends fixed transverse folds, producing a “step- pension to optimally distend the esoph- proximally from the gastroesophageal ladder” appearance as a result of pooling agus to show rings, strictures, or hiatal junction. Thus, the presence of ulcers of barium between the folds (see Fig 7) hernias that could be missed on upright that are confined to the upper or middle (13). These folds should be differentiated double-contrast views. Finally, the pa- parts of the esophagus should suggest an- from the thin transverse striations (ie, tient is turned from a supine to RPO and other cause for the patient’s disease. “feline” esophagus) often seen for brief right-lateral positions to assess for spon- Reflux esophagitis may also manifest intervals at fluoroscopy due to transient taneous gastroesophageal reflux or for re- as thickened longitudinal folds as a result contraction of the longitudinally ori- flux induced by a Valsalva maneuver to of edema and inflammation that extend ented in patients increase intraabdominal pressure. into the . However, thickened with reflux (Fig 9) (14,15).

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 415 adiology R

Figure 4. Upright LPO spot image from dou- ble-contrast esophagography shows reflux esophagitis with small linear ulcers (black ar- rows) in distal esophagus just above hiatal her- Figure 3. Upright LPO spot image from dou- nia (white arrows). ble-contrast esophagography shows reflux esophagitis with extensive granularity of lower esophagus due to edema and inflammation of mucosa. as a highly specific sign of Barrett esoph- agus, particularly if the pattern is adja- cent to the distal aspect of a midesopha- Figure 1. Upright LPO spot image from dou- Barrett Esophagus geal stricture (see Fig 10) (18). The retic- ble-contrast esophagography shows normal ular pattern is characterized by tiny esophagus with smooth homogeneous appear- Barrett esophagus is characterized by barium-filled grooves or crevices resem- ance en face. progressive columnar metaplasia of the bling the areae gastricae in the . distal esophagus caused by chronic gas- Patients are classified at moderate risk troesophageal reflux and reflux esophagi- tis. Barrett esophagus is thought to de- for Barrett esophagus when a barium study velop in about 10% of all patients with reveals esophagitis or peptic strictures in reflux esophagitis (16). Double-contrast the distal esophagus (17). These radio- esophagrams can be used to classify, on graphic findings reflect chronic inflamma- the basis of specific radiologic criteria, tory disease and scarring; the decision to patients with reflux symptoms as being perform endoscopy in this group should be at high, moderate, or low risk for Barrett based on the severity of symptoms, the esophagus (17). Patients are classified at age, and the overall health of the patient. high risk when a barium study reveals a Finally, patients are classified at low midesophageal stricture (Fig 10) or ulcer risk for Barrett esophagus when barium or a reticular pattern of the mucosa (usu- studies reveal no structural abnormalities ally associated with a hiatal hernia (regardless of the presence or absence of and/or gastroesophageal reflux) (17). In reflux or a hiatal hernia). The majority of such cases, endoscopy and biopsy should patients are found to be in the low-risk be performed to help obtain a definitive category, and the prevalence of Barrett Figure 2. Recumbent right-side-down, lateral diagnosis. Although a reticular mucosal esophagus is so small in this group that spot image of normal gastric cardia shows stel- late folds radiating to central point (white ar- pattern has been found in only 5%–10% such individuals can be treated empiri- row) at gastroesophageal junction. Note hood- of all patients with Barrett esophagus cally for their reflux symptoms without ing fold (black arrows) above cardia. (18,19), this finding has been recognized the need for endoscopy (17).

416 ⅐ Radiology ⅐ November 2005 Levine and Rubesin adiology R

Figure 5. Prone RAO spot image from single- contrast esophagography shows inflammatory esophagogastric polyp as enlarged fold (small ar- rows) extending upward into distal esophagus, Figure 7. Upright LPO spot image from dou- where it terminates as a smooth polypoid protu- ble-contrast esophagography shows asymmet- berance (large arrow). Inflammatory polyps are ric peptic stricture in distal esophagus above thought to be a sign of chronic reflux esophagitis. hiatal hernia (small black arrows), with saccu- lation of wall both en face (large black arrow) and in profile (large white arrow). Note fixed transverse folds (small white arrows) from as- INFECTIOUS ESOPHAGITIS Figure 6. Upright LPO spot image from dou- sociated longitudinal scarring of distal esoph- ble-contrast esophagography shows smooth agus above the stricture. Candida Esophagitis tapered segment of concentric narrowing (white arrows) due to peptic stricture in distal Candida albicans is the most common esophagus above a hiatal hernia (black arrow). cause of infectious esophagitis. It usually occurs as an opportunistic infection in possible to differentiate these conditions immunocompromised patients, particu- on the basis of the clinical and radio- larly those with acquired immunodefi- Glycogenic acanthosis is another com- graphic findings. ciency syndrome (AIDS), but Candida mon condition affecting elderly people. During the past 2 decades, a much esophagitis can also result from local In glycogenic acanthosis, cytoplasmic more fulminant form of candidiasis has esophageal stasis caused by severe esoph- glycogen accumulates in the squamous been encountered in patients with AIDS, ageal motility disorders such as achalasia epithelial cell lining of the esophagus, who may present with a grossly irregular and (20). Only about 50% of which causes focal plaquelike thickening or “shaggy” esophagus caused by innu- patients with Candida esophagitis are of the mucosa (23,24). Glycogenic acan- merable coalescent pseudomembranes found to have thrush, so the absence of thosis may manifest on double-contrast and plaques, with trapping of barium be- oropharyngeal disease in no way ex- studies as multiple small nodules or tween the lesions (Fig 13) (25). Other pa- cludes this diagnosis. plaques (Fig 12) (23,24). The major con- tients with achalasia or scleroderma may Candida esophagitis usually manifests sideration in the differential diagnosis is develop a “foamy” esophagus, with innu- on double-contrast studies as discrete Candida esophagitis. However, the nod- merable tiny bubbles layering out in the plaquelike lesions that are seen as linear ules of glycogenic acanthosis have a barium column; this phenomenon pre- or irregular filling defects that tend to be more rounded appearance, whereas the sumably results from the yeast form of oriented longitudinally and are separated plaques of Candida esophagitis tend to fungal infection (26). When typical find- by normal mucosa (Fig 11) (21). Double- have a more linear configuration. Also, ings of Candida esophagitis are encoun- contrast esophagrams have been found candidiasis usually occurs in immuno- tered on double-contrast esophagrams, to have a sensitivity of 90% for the detec- compromised patients with odynopha- patients with these findings can be tion of Candida esophagitis (21,22), pri- gia, whereas glycogenic acanthosis oc- treated with antifungal agents such as marily because of the ability to show curs in older individuals with no esoph- fluconazole, without the need for endos- these plaques. ageal symptoms. It therefore is usually copy.

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 417 adiology R

Figure 8. Upright LPO spot image from dou- ble-contrast esophagography shows short ring- Figure 10. Upright LPO spot image from like peptic stricture (white arrow) in distal double-contrast esophagography shows mild esophagus above a hiatal hernia (black arrows). Figure 11. Upright LPO spot image from ringlike constriction (large white arrows) in Although this stricture could be mistaken for a double-contrast esophagography shows multi- midesophagus in a patient with Barrett esoph- , it has a longer vertical height ple discrete plaquelike lesions (arrows) in the agus. Also note distinctive reticular pattern than does a true Schatzki ring. esophagus in a patient with Candida esophagi- (black arrows) extending distally from the tis. Note how plaques have a linear configura- stricture, a classic radiographic sign of Barrett tion and are separated by normal intervening esophagus. This patient also has fixed trans- mucosa. verse folds (small white arrows) just above the stricture due to longitudinal scarring in this region. combination of ulcers and plaques that mimic Candida esophagitis (27). Herpes esophagitis in otherwise healthy patients manifests as innumerable tiny The herpes simplex virus is another fre- ulcers clustered together in the quent cause of infectious esophagitis (27). midesophagus below the level of the left Most patients with this virus are immuno- main (28). The ulcers are even compromised, but herpes esophagitis may smaller than those in immunocompro- occasionally develop as an acute self-lim- mised patients with herpes esophagitis, ited disease in immunocompetent individ- presumably because these individuals uals (28). Herpes esophagitis initially leads have an intact that pre- to the development of small mucosal ves- vents the ulcers from enlarging. icles that rupture to form discrete punched-out ulcers. As a result, herpes Cytomegalovirus Esophagitis esophagitis may manifest on double-con- trast studies as small superficial ulcers Cytomegalovirus (CMV) is another against a background of normal mucosa cause of infectious esophagitis that oc- (27,29). The ulcers can have a punctate, curs primarily in patients with AIDS. stellate, or ringlike configuration and are CMV esophagitis may manifest on dou- often surrounded by radiolucent mounds ble-contrast studies as multiple small ul- of edema (Fig 14). In the appropriate clin- cers or, even more commonly, as one or ical setting, the presence of small discrete more giant flat ulcers that are several cen- ulcers without plaques should be highly timeters or more in length (30). The ul- Figure 9. Upright LPO spot image from dou- suggestive of herpes esophagitis, because cers may have an ovoid or diamond- ble-contrast esophagography shows thin trans- ulceration in candidiasis almost always oc- shaped configuration and are often sur- verse striations due to transient contraction of longitudinally oriented muscularis mucosae in curs against a background of diffuse plaque rounded by a thin radiolucent rim of patient with “feline” esophagus. This finding is formation. As the disease progresses, how- edematous mucosa. Because herpetic ul- often associated with gastroesophageal reflux. ever, herpes esophagitis may manifest as a cers rarely become this large, the pres-

418 ⅐ Radiology ⅐ November 2005 Levine and Rubesin adiology R

Figure 12. Upright LPO spot image from double-contrast esophagography shows multi- Figure 14. Upright LPO spot image from dou- ple small plaques and nodules in midesopha- ble-contrast esophagography shows multiple gus in an elderly patient with glycogenic acan- small superficial ulcers (arrows) in midesophagus thosis. Note how nodules have a more of a patient with herpes esophagitis. rounded appearance than the fungal plaques Figure 13. Upright LPO spot image from dou- in Figure 11. ble-contrast esophagography shows shaggy esophagus of fulminant Candida esophagitis in a patient with AIDS. This shaggy contour re- sults from innumerable pseudomembranes and plaques, with trapping of barium between ence of one or more giant ulcers should lesions. suggest the possibility of CMV esophagi- tis in patients with AIDS. However, the differential diagnosis also includes giant human immunodeficiency virus (HIV) upper body (31,32). The diagnosis is es- ulcers in the esophagus (see next sec- tablished by obtaining endoscopic bi- tion). Because CMV esophagitis is treated opsy specimens, brushings, or cultures to with relatively toxic antiviral agents such rule out CMV esophagitis as the cause of as ganciclovir, endoscopy (with biopsy the ulcers. Unlike CMV ulcers, HIV-re- specimens, brushings, or cultures from lated esophageal ulcers usually heal the esophagus) is required to confirm the markedly after treatment with oral ste- presence of CMV infection before these roids (31,32). Thus, endoscopy is re- patients are treated. quired in HIV-positive patients with gi- ant esophageal ulcers, to differentiate HIV Esophagitis esophagitis caused by HIV and CMV so that appropriate therapy can be insti- HIV infection of the esophagus can tuted. lead to the development of giant esoph- ageal ulcers indistinguishable from those caused by CMV esophagitis. Double-con- DRUG-INDUCED ESOPHAGITIS trast esophagrams typically reveal one or more large ovoid or diamond-shaped ul- Tetracycline and doxycycline are the two Figure 15. Upright LPO spot image from cers surrounded by a radiolucent rim of agents most commonly responsible for double-contrast esophagography shows giant edema (Fig 15), sometimes associated drug-induced esophagitis in the United diamond-shaped HIV ulcer (arrows) in the with a cluster of small satellite ulcers States, but other causative agents include midesophagus in HIV-positive patient with odynophagia. Although CMV esophagitis can (31,32). Occasionally, these individuals potassium chloride, quinidine, aspirin or produce identical findings, endoscopic brush- may have associated palatal ulcers or a other nonsteroidal antiinflammatory ings and biopsy specimens revealed no evi- characteristic maculopapular rash on the drugs, and alendronate sodium (33–35). dence of CMV.

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 419 adiology R

Figure 16. Upright LPO spot image from double-contrast esophagography shows two small superficial ulcers as ring shadows (ar- rows) in midesophagus. This patient had drug- induced esophagitis after taking doxycycline.

Affected individuals typically ingest the medication with little or no water imme- diately before going to bed. The capsule or pill then usually becomes lodged in the midesophagus, where it is com- pressed by the adjacent aortic arch or left Figure 17. Upright LPO spot image from double-contrast esophagography shows radia- main bronchus. Prolonged contact of the tion stricture as a long segment of smooth esophageal mucosa with these medica- tapered narrowing (arrows) in upper thoracic tions presumably causes an irritant con- esophagus. This patient had undergone medi- astinal irradiation. tact esophagitis. Affected individuals Figure 18. Prone RAO spot image from may present with severe odynophagia, single-contrast esophagography shows but marked clinical improvement usually long smooth stricture (arrows) in the tho- occurs after withdrawal of the offending racic esophagus caused by lye ingestion. agent. teoclast-mediated bone resorption, used Also note cardiac pacemaker wires. The radiographic findings in drug-in- to prevent osteoporosis in postmeno- duced esophagitis depend on the nature pausal women) may cause severe esoph- of the offending medication. Tetracy- agitis with extensive ulceration and stric- cline and doxycycline are associated with tures that are usually confined to the dis- ment (42). Ulceration and decreased lu- the development of small shallow ulcers tal esophagus (41). minal distensibility are other frequent in the upper or middle part of the esoph- findings (42). The extent of disease con- agus and are indistinguishable from RADIATION-INDUCED forms to the margins of the radiation those in herpes esophagitis (Fig 16) ESOPHAGITIS portal. Most cases of acute radiation (36,37). Because of their superficial na- esophagitis are self-limited, but some ture, these ulcers almost always heal Aradiationdoseof5000cGyormoreto patients may have progressive dyspha- without scarring or strictures. In contrast, the mediastinum may cause severe in- gia due to the development of radiation potassium chloride, quinidine, and non- jury to the esophagus. Acute radiation- strictures 4–8 months after completion steroidal antiinflammatory drugs may induced esophagitis usually occurs 2–4 of radiation therapy (43). Such stric- cause more severe esophageal injury lead- weeks after the initiation of radiation tures typically appear as smooth ta- ing to the development of larger ulcers therapy (42). The mucosa typically has pered areas of concentric narrowing and possible stricture formation (38–40). agranularappearancebecauseofedema within a preexisting radiation portal Alendronate sodium (an inhibitor of os- and inflammation of the irradiated seg- (Fig 17).

420 ⅐ Radiology ⅐ November 2005 Levine and Rubesin CAUSTIC ESOPHAGITIS

Whether accidental or intentional, inges- tion of lye or other caustic agents causes marked esophagitis, eventually leading to extensive stricture formation. Liquid lye causes liquefactive necrosis, resulting in the most severe form of caustic injury to the esophagus (44). Endoscopy is usu- ally performed as the primary diagnostic test to help assess the extent and severity of esophageal injury after ingestion of a caustic agent. If esophageal perforation is adiology suspected, however, a radiographic study

R with water-soluble contrast material should be performed to document the presence of a leak. Such studies may also reveal marked edema, spasm, and ulcer- ation of the affected esophagus. As the esophagitis heals, follow-up barium stud- ies have a major role in helping deter- mine the length of developing strictures, which typically involve a longer segment of the esophagus (Fig 18) than does scar- ring from other types of esophagitis (44). Patients with chronic lye strictures also have an increased risk of developing Figure 19. Upright LPO spot image from double-contrast esophagography shows leio- squamous cell carcinoma of the esopha- myoma as a smooth submucosal mass (black gus (45), so a new area of mucosal irreg- arrows) in the midesophagus. Note how lesion ularity or nodularity within a preexisting forms slightly obtuse angles with adjacent lye stricture on a barium study should esophageal wall. Also note kissing artifact (white arrows) due to apposition of opposing raise concern about the possibility of a Figure 20. Upright LPO spot image from esophageal walls. superimposed carcinoma. double-contrast esophagography shows giant fibrovascular polyp as smooth sausage-shaped mass (black arrows) expanding the lumen of OTHER ESOPHAGITIDES the upper thoracic esophagus. Note polypoid tis include Crohn disease, tuberculosis, distal tip (white arrow) of polyp. Fibrovascular , chronic graft- polyps usually arise from the region of the Alkaline reflux esophagitis is caused by cricopharyngeus muscle. (Reprinted, with per- versus-host disease, Behc¸et syndrome, reflux of bile or pancreatic secretions into mission, from reference 50.) the esophagus after partial or total gas- and, rarely, skin disorders involving the trectomy (46). This form of esophagitis is esophagus, such as epidermolysis bullosa characterized on barium studies by mu- dystrophica and benign mucous mem- cosal nodularity or ulceration or, in se- brane pemphigoid (44). ally present with dysphagia, depending vere disease, by distal esophageal stric- on the size of the tumor and how much it tures that often progress rapidly in length BENIGN TUMORS encroaches on the lumen. Leiomyomas and severity over a short period of time usually manifest on esophagrams as a (46). The risk of developing alkaline re- Benign tumors of the esophagus compose smooth submucosal mass etched in flux esophagitis can be decreased by per- only about 20% of all esophageal neo- white, which forms a right or slightly forming a Roux-en-Y reconstruction to plasms (47). The majority are detected as obtuse angle with the adjacent esopha- minimize reflux of alkaline secretions incidental findings in asymptomatic pa- geal wall when viewed in profile (Fig 19) into the esophagus after partial or total tients. Squamous are the most (49). As a result, these lesions may be gastrectomy. common benign mucosal tumor in the indistinguishable from other mesenchy- is an uncom- esophagus. These lesions usually appear on mal tumors such as fibromas, neurofibro- mon cause of esophagitis and stricture double-contrast esophagrams as small mas, and hemangiomas (except that formation in the distal esophagus. It has sessile polyps with a smooth or slightly leiomyomas are more likely on empirical been postulated that the strictures result lobulated contour (48). Some papillomas grounds). from severe reflux esophagitis caused by may be difficult to distinguish from small Fibrovascular polyps are rare benign constant reflux of acid around the tube esophageal cancers on the basis of the ra- tumors consisting of varying amounts of into the distal esophagus (44). Affected diographic findings, so endoscopy is re- fibrovascular and adipose tissue covered individuals sometimes develop marked quired for a definitive diagnosis. by squamous epithelium (50). Fibrovas- esophageal strictures that show rapid In contrast, leiomyomas are the most cular polyps usually arise near the level of progression in length and severity on se- common benign submucosal tumor in the cricopharyngeus muscle, gradually rial barium studies (44). the esophagus. Affected individuals are elongating over a period of years as they Other uncommon causes of esophagi- usually asymptomatic but may occasion- are dragged inferiorly by means of esoph-

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 421 adiology R

Figure 21. Upright LPO spot image from double-contrast esophagography shows early esophageal in profile as plaquelike le- sion (black arrows) with flat central ulcer (white arrows) on left lateral wall of the midesophagus. Figure 24. Upright LPO spot image from double-contrast esophagography shows ad- vanced esophageal carcinoma as polypoid mass (white arrows) with a large area of ulcer- ation (black arrows) on the right posterolateral wall of the distal esophagus (small rounded defects abutting mass are air bubbles).

anatomic barrier to prevent these cancers from spreading rapidly into the mediasti- num. Patients with esophageal carcinoma Figure 23. Upright LPO spot image usually present with dysphagia, but this is from double-contrast esophagography alatefindingthatdevelopsafterthetumor shows advanced infiltrating carcinoma as has invaded the esophageal wall, peri- irregular area of narrowing, with mucosal nodularity, ulceration, and shelflike mar- esophageal lymphatics, or other mediasti- gins (arrows) in midesophagus. nal structures. As a result, most patients have advanced lesions at the time of diag- nosis, with a 5-year survival rate of less than 10% (52). Histologically, 50%–70% of pear on barium studies as smooth, expan- these tumors are squamous cell carcino- sile, sausage-shaped masses that expand mas, and the remaining 30%–50% are ad- the lumen of the upper and middle por- enocarcinomas (53). tions of the esophagus (Fig 20) (50). Le- Squamous cell carcinoma most com- sions composed predominantly of adi- Figure 22. Upright LPO spot image from monly develops in patients with a long- double-contrast esophagography shows super- pose tissue may appear as -attenuation standing history of alcohol and/or tobacco ficial spreading carcinoma as focal area of mu- lesions on CT images, whereas lesions consumption, whereas adenocarcinoma cosal nodularity (arrows) in midesophagus, containing greater amounts of fibrovas- virtually always arises against a back- without a discrete mass. Note how nodules cular tissue may have a heterogeneous ground of Barrett mucosa in the esopha- merge with one another, producing a conflu- appearance with areas of fat juxtaposed ent area of disease. gus. The reported prevalence of adenocar- with areas of soft-tissue attenuation (50). cinoma in patients with Barrett esophagus is about 10% (54). Because these tumors MALIGNANT TUMORS develop by means of a sequence of progres- ageal peristalsis. In rare cases, affected in- sively severe epithelial , many in- Esophageal Carcinoma dividuals may have a spectacular clinical vestigators advocate endoscopic surveil- presentation, with regurgitation of a Esophageal carcinoma constitutes about lance of patients with known Barrett fleshy mass into the or mouth 1% of all cancers in the United States and esophagus to detect dysplastic or early car- or even asphyxia and sudden death if the 7% of all gastrointestinal tumors (51). Early cinomatous changes before the develop- regurgitated polyp occludes the dissemination of tumor occurs because the ment of an advanced adenocarcinoma (50). Fibrovascular polyps typically ap- esophagus lacks a serosa, so there is no (54).

422 ⅐ Radiology ⅐ November 2005 Levine and Rubesin Double-contrast esophagography has a sensitivity of greater than 95% in the de- tection of (55), a num- ber comparable to the endoscopic sensi- tivity of 95%–100% when brushings and biopsy specimens are obtained (53). Early esophageal cancers are usually small pro- truded lesions less than 3.5 cm in size. These tumors may manifest on double- contrast studies as plaquelike lesions (of- ten containing flat central ulcers) (Fig 21), sessile polyps with a smooth or slightly lobulated contour, or focal irreg-

adiology ularities of the esophageal wall (56). Early adenocarcinomas may also manifest as a R localized area of wall flattening or irreg- ularity within a preexisting peptic stric- ture (53). Superficial spreading carci- noma is another form of early esophageal cancer characterized by poorly defined nodules or plaques that merge with one another, producing a confluent area of disease (Fig 22) (56,57). Advanced esophageal usu- ally appear on barium studies as infiltrat- Figure 25. Upright LPO spot image from ing, polypoid, ulcerative, or, less com- double-contrast esophagography shows vari- coid carcinoma as lobulated submucosal lesion monly, varicoid lesions (53). Infiltrating in the distal esophagus that could be mistaken carcinomas manifest as irregular luminal for varices. However, this lesion had a fixed narrowing with mucosal nodularity or ul- appearance at fluoroscopy and an abrupt prox- ceration and abrupt shelflike borders (Fig imal demarcation (arrows) from normal esoph- 23). Polypoid carcinomas appear as lobu- agus. lated intraluminal masses or as polypoid ulcerated masses (Fig 24). Primary ulcer- ative carcinomas are seen as giant menis- channels. These satellite metastases may coid ulcers surrounded by a radiolucent appear as polypoid, plaquelike, or ulcer- rind of tumor (58). Finally, varicoid car- ated lesions separated from the primary cinomas are those in which submucosal Figure 26. Prone RAO spot image from tumor by normal mucosa (53). Tumor spread of tumor produces thickened, tor- single-contrast esophagography shows also spreads subdiaphragmatically to the tuous, longitudinal defects (Fig 25) that uphill as serpiginous proximal stomach via submucosal lym- defects in lower esophagus. This patient mimic the appearance of varices (59). phatics. Metastases to the gastric cardia had portal . Varicoid tumors have a fixed configura- and fundus may appear as large submu- tion, however, whereas varices change in cosal masses that often contain central size and shape at fluoroscopy. Also, vari- ulcers (62). ces rarely cause dysphagia because they involve the esophagus include leiomyo- Appropriate treatment strategies for are soft and compressible. Thus, it is usu- , malignant melanoma, and Ka- esophageal carcinoma depend on accu- ally possible to differentiate these condi- posi sarcoma. rate staging of the tumor with the aid of tions on the basis of the clinical and ra- CT, MR imaging, or endoscopic sonogra- diographic findings. VARICES phy. Tumor staging is beyond the scope Squamous cell carcinoma and adenocar- of this review. Uphill Varices cinoma of the esophagus cannot be reli- ably differentiated on barium studies. Nev- Uphill varices are usually caused by Other Malignant Tumors ertheless, squamous cell carcinoma tends with hepatofugal to involve the upper or middle part of the Non-Hodgkin lymphoma and, rarely, flow through dilated esophageal collat- esophagus, whereas adenocarcinoma is lo- Hodgkin lymphoma may involve the eral vessels to the superior vena cava. Up- cated mainly in the distal esophagus. Un- esophagus. Esophageal lymphoma may hill varices may cause marked upper gas- like squamous cell carcinoma, adenocarci- manifest on barium studies as submuco- trointestinal tract . Varices ap- noma also has a marked tendency to in- sal masses, polypoid lesions, enlarged pear on barium studies as serpentine vade the gastric cardia or fundus and folds, or strictures (63). Spindle cell car- longitudinal filling defects in the distal composes as many as 50% of all malignant cinoma (formerly known as carcinosar- half of the thoracic portion of the esoph- tumors that involve the gastroesophageal coma) is another rare tumor; it is charac- agus (Fig 26) (65). They are best seen on junction (60,61). terized by a bulky polypoid intraluminal mucosal-relief views of the collapsed Esophageal carcinomas can metasta- mass that expands the lumen of the esophagus while the patient is in a prone size to other parts of the esophagus via a esophagus without causing obstruction RAO position, with use of a high-density rich network of intramural lymphatic (64). Other rare malignant tumors that barium suspension or barium paste to in-

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 423 adiology R

Figure 28. Schatzki ring. (a) Prone RAO spot image from single-contrast phase of esophagog- raphy shows Schatzki ring as smooth, symmetric, ringlike constriction (white arrow) in distal esophagus directly above a hiatal hernia (black arrows). (b) Upright LPO spot image from double-contrast phase of same examination shows mild narrowing of distal esophagus without demonstration of the ring because of inadequate distention of this region.

Figure 27. Upright LPO spot image from double-contrast esophagography shows downhill esophageal varices as ser- confined to the upper or middle part of distal esophagus is not adequately dis- piginous defects in midesophagus above the esophagus (Fig 27). Venography, CT, tended at fluoroscopy (Fig 28b), so it is the level of the carina. This patient had or MR imaging may be performed to con- important to obtain prone views of the superior vena cava syndrome. firm the presence of superior vena cava esophagus during continuous drinking of obstruction and to help determine the a low-density barium suspension (67). underlying cause. Conversely, rings can also be missed if crease mucosal adherence (65). The dif- the hiatal hernia is overdistended, result- ing in overlap of the distal esophagus and ferential diagnosis for varices includes LOWER ESOPHAGEAL RINGS varicoid carcinoma and esophagitis with hernia that obscure the ring (68). Rings thickened folds. with a maximum luminal diameter of Lower esophageal rings are a frequent more than 20 mm rarely cause dyspha- finding on esophagrams, but only a small Downhill Varices gia, whereas rings with a maximum di- percentage cause symptoms. The term ameter of less than 13 mm almost always Downhill varices are caused by supe- Schatzki ring is reserved for lower esoph- cause dysphagia (66). Studies have shown rior vena cava obstruction with down- ageal rings in patients who present with that esophagography is a sensitive tech- ward flow via dilated esophageal collat- dysphagia. Such rings are almost always nique for the detection of symptomatic eral vessels to the portal venous system located at the gastroesophageal junction. lower esophageal rings, sometimes reveal- and the inferior vena cava. Causes of Histologically, the superior surface of the ing rings that are missed at endoscopy (67). downhill varices include central cathe- ring is lined by squamous epithelium, ter–related of the superior and the inferior surface is lined by co- vena cava, bronchogenic carcinoma or lumnar epithelium. The exact pathogen- DIVERTICULA other metastatic tumors involving the esis of Schatzki rings is uncertain, but Pulsion Diverticula mediastinum, lymphoma, substernal goi- some rings are thought to develop as a ter, mediastinal radiation, and sclerosing result of scarring from reflux esophagitis. Pulsion diverticula tend to be located mediastinitis (65). Most patients with Lower esophageal rings appear on bar- in the distal esophagus and are often as- downhill varices have superior vena cava ium studies as smooth-surfaced ringlike sociated with fluoroscopic or manomet- syndrome at the time of clinical presen- constrictions 2–3-mm in height at the ric evidence of esophageal dysmotility tation. Such varices typically appear as gastroesophageal junction, almost al- (69). These diverticula are usually de- serpentine longitudinal filling defects ways located above a hiatal hernia (Fig tected as incidental findings in patients that, unlike uphill esophageal varices, are 28a) (66). The rings can be missed if the with no esophageal symptoms. However,

424 ⅐ Radiology ⅐ November 2005 Levine and Rubesin adiology R

Figure 31. Prone RAO spot image from sin- gle-contrast esophagography shows beaklike narrowing (black arrows) of distal esophagus caused by secondary achalasia. Note greater length of narrowed segment than is usually seen in primary achalasia (see Fig 30). Also Figure 29. Upright LPO spot image from dou- note metallic esophageal stent (white arrow) ble-contrast esophagography shows multiple for palliation of esophageal carcinoma, esophageal intramural pseudodiverticula as which presumably had spread to gastro- flask-shaped outpouchings (black arrows) in lon- Figure 30. Upright frontal spot image from esophageal junction via periesophageal lym- gitudinal rows parallel to the long axis of the double-contrast esophagography shows typical phatics. This image was obtained in an el- esophagus. Note how some pseudodiverticula findings of primary achalasia, with dilated aperi- derly patient with recent onset of dysphagia (white arrows) appear to be floating outside the staltic esophagus and tapered beaklike narrow- and weight loss. esophagus without apparent communication ing (arrow) of distal esophagus due to incom- with the lumen. plete opening of the lower esophageal sphincter. This image was obtained in a middle-aged pa- tient with long-standing dysphagia. high esophageal strictures (71), or they oc- a large epiphrenic diverticulum adjacent cur as an isolated finding. When strictures to the gastroesophageal junction may fill are present, these patients may present with dysphagia, but the pseudodiverticula with debris, causing dysphagia, regurgi- Esophageal Intramural themselves rarely cause symptoms. tation, or aspiration (70). Pulsion diver- Pseudodiverticula ticula appear on barium studies as Esophageal intramural pseudodivertic- rounded wide-necked outpouchings that ula consist of dilated excretory ducts of ESOPHAGEAL MOTILITY fail to empty when the esophagus col- deep mucous glands in the esophagus. The DISORDERS lapses (69). pseudodiverticula typically appear on Achalasia esophagrams as flask-shaped outpouchings in rows parallel to the longitudinal axis of Primary achalasia is an idiopathic con- Traction Diverticula the esophagus (Fig 29) (71). When viewed dition involving the myenteric plexus of en face on double-contrast esophagrams, the esophagus, whereas secondary acha- Traction diverticula occur in the the pseudodiverticula can be mistaken for lasia is caused by other underlying con- midesophagus and are usually caused by tiny ulcers. When viewed in profile, how- ditions, most commonly a malignant tu- scarring from tuberculosis or histoplas- ever, they often appear to be floating out- mor involving the gastroesophageal mosis in perihilar lymph nodes (69). Be- side the wall of the esophagus, without junction (especially carcinoma of the gas- cause traction diverticula contain all lay- apparent communication with the lumen tric cardia) (73). Primary achalasia is ers of the esophageal wall, they maintain (see Fig 29) (72). Many patients have an characterized by absence of primary peri- their elastic recoil and empty their con- isolated cluster of pseudodiverticula in the stalsis in the esophagus and incomplete tents when the esophagus collapses at distal esophagus in the region of a peptic relaxation of the lower esophageal fluoroscopy. Traction diverticula often stricture (72). In such cases, the pseudodi- sphincter, which manifests on barium have a triangular or tented appearance verticula probably occur as a sequela of studies as a tapered beaklike narrowing of resulting from traction on the diverticu- scarring from reflux esophagitis. Less fre- the distal esophagus adjacent to the gas- lum by the fibrotic process in the adja- quently, the pseudodiverticula have a dif- troesophageal junction (Fig 30) (73). In cent mediastinum (69). fuse distribution and are associated with advanced disease, the esophagus can be-

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 425 come massively dilated and tortuous dis- esophagitis. AJR Am J Roentgenol 1980; 25. Levine MS, Woldenberg R, Herlinger H, tally (ie, “sigmoid” esophagus). Because 135:15–19. Laufer I. Opportunistic esophagitis in 5. Creteur V, Thoeni RF, Federle MP, et al. AIDS: radiographic diagnosis. Radiology of the slow progression of symptoms, af- The role of single- and double-contrast ra- 1987;165:815–820. fected individuals typically have long- diography in the diagnosis of reflux esoph- 26. Sam JW, Levine MS, Rubesin SE, Laufer I. standing dysphagia when they seek med- agitis. Radiology 1983;147:71–75. The “foamy” esophagus: a radiographic ical attention. 6. Graziani L, Bearzi I, Romagnoli A, Pesaresi sign of Candida esophagitis. AJR Am J Secondary achalasia is also character- A, Montesi A. Significance of diffuse gran- Roentgenol 2000;174:999–1002. ularity and nodularity of the esophageal 27. Levine MS, Laufer I, Kressel HY, Friedman ized by absent peristalsis in the esopha- mucosa at double-contrast radiography. HM. Herpes esophagitis. AJR Am J Roent- gus and beaklike narrowing near the gas- Gastrointest Radiol 1985;10:1–6. genol 1981;136:863–866. troesophageal junction (74). In second- 7. Dibble C, Levine MS, Rubesin SE, Laufer I, 28. Shortsleeve MJ, Levine MS. Herpes esoph- ary achalasia caused by tumor at the Katzka DA. Detection of reflux esophagitis agitis in otherwise healthy patients: clini- on double-contrast esophagrams and en- cal and radiographic findings. Radiology gastroesophageal junction, however, the doscopy using the histologic findings as 1992;182:859–861. length of the narrowed segment is often the gold standard. Abdom Imaging 2004; 29. Levine MS, Loevner LA, Saul SH, Rubesin adiology greater than that in primary achalasia be- 29:421–425. SE, Herlinger H, Laufer I. Herpes esophagi- cause of spread of tumor into the distal 8. Levine MS. Gastroesophageal reflux disease. tis: sensitivity of double-contrast esopha- R esophagus (Fig 31) (74). The narrowed In: Gore RM, Levine MS, eds. Textbook of gography. AJR Am J Roentgenol 1988;151: gastrointestinal radiology. 2nd ed. Philadel- 57–62. segment may also be asymmetric, nodu- phia, Pa: Saunders, 2000;329–349. 30. Balthazar EJ, Megibow AJ, Hulnick D, Cho lar, or ulcerated because of tumor infil- 9. Hu C, Levine MS, Laufer I. Solitary ulcers KC, Beranbaum E. Cytomegalovirus trating this region. In some cases, barium in reflux esophagitis: radiographic find- esophagitis in AIDS: radiographic features studies may reveal other signs of malig- ings. Abdom Imaging 1997;22:5–7. in 16 patients. AJR Am J Roentgenol 1987; nancy at the cardia, with distortion or 10. Bleshman MH, Banner MP, Johnson RC, 149:919–923. DeFord JW. The inflammatory esophago- 31. Levine MS, Loercher G, Katzka DA, Her- obliteration of the normal cardiac rosette gastric polyp and fold. Radiology 1978; linger H, Rubesin SE, Laufer I. Giant, hu- (74). The clinical history also is impor- 128:589–593. man immunodeficiency virus–related ul- tant, because patients with primary acha- 11. Styles RA, Gibb SP, Tarshis A, Silverman cers in the esophagus. Radiology 1991; lasia almost always have long-standing ML, Scholz FJ. Esophagogastric polyps: ra- 180:323–326. diographic and endoscopic findings. Radi- 32. Sor S, Levine MS, Kowalski TE, Laufer I, dysphagia, whereas patients with second- ology 1985;154:307–311. Rubesin SE, Herlinger H. Giant ulcers of ary achalasia are usually older (over age 12. Ho CS, Rodrigues PR. Lower esophageal the esophagus in patients with human im- 60 years) with recent onset of dysphagia strictures, benign or malignant? J Can As- munodeficiency virus: clinical, radio- (less than 6 months) and weight loss (75). soc Radiol 1980;31:110–113. graphic, and pathologic findings. Radiol- 13. Levine MS, Goldstein HM. Fixed trans- ogy 1995;194:447–451. verse folds in the esophagus: a sign of re- 33. Kikendall JW, Friedman AC, Oyewole MA, Other Esophageal Motility flux esophagitis. AJR Am J Roentgenol Fleischer D, Johnson LF. Pill-induced 1984;143:275–278. esophageal injury: case reports and review Disorders 14. Gohel VK, Edell SL, Laufer I, Rhodes WH. of the medical literature. Dig Dis Sci 1983; Symptomatic diffuse esophageal spasm Transverse folds in the human esophagus. 28:174–182. Radiology 1978;128:303–308. 34. Coates AG, Nostrand TT, Wilson JA, Elta may manifest on barium studies as inter- 15. Furth EE, Rubesin SE, Rose D. Feline esoph- GH, Agha FP. Esophagitis caused by non- mittently weakened or absent primary agus. AJR Am J Roentgenol 1995;164:900. steroidal anti-inflammatory medication: peristalsis with repetitive, lumen-obliter- 16. Winters C, Spurling TJ, Chobanian SJ, et al. case reports and review of the literature for ating, nonperistaltic contractions that Barrett’s esophagus: a prevalent, occult com- pill-induced esophageal injury. South Med plication of gastroesophageal reflux disease. J 1986;79:1094–1097. produce a classic “corkscrew” esophagus 1987;92:118–124. 35. de Groen PC, Lubbe DF, Hirsch LJ, et al. (76). More commonly, however, these 17. Gilchrist AM, Levine MS, Carr RF, et al. Esophagitis associated with the use of patients have multiple nonperistaltic Barrett’s esophagus: diagnosis by double- alendronate. N Engl J Med 1996;335: contractions of mild to moderate severity contrast esophagography. AJR Am J Roent- 1016–1021. without a corkscrew esophagus (77). genol 1988;150:97–102. 36. Creteur V, Laufer I, Kressel HY, et al. Drug- 18. Levine MS, Kressel HY, Caroline DF, Laufer induced esophagitis detected by double- Older patients may have intermittent I, Herlinger H, Thompson JJ. Barrett contrast radiography. Radiology 1983;147: weakening of peristalsis in the distal esophagus: reticular pattern of the mu- 365–368. esophagus and multiple nonperistaltic cosa. Radiology 1983;147:663–667. 37. Bova JG, Dutton NE, Goldstein HM, contractions in the absence of esopha- 19. Chen YM, Gelfand DW, Ott DJ, Wu WC. Hoberman LJ. Medication-induced esoph- Barrett esophagus as an extension of se- agitis: diagnosis by double-contrast geal symptoms, a relatively common vere esophagitis: analysis of radiologic esophagography. AJR Am J Roentgenol manifestation of aging known as presby- signs in 29 cases. AJR Am J Roentgenol 1987;148:731–732. esophagus (78). 1985;145:275–281. 38. Teplick JG, Teplick SK, Ominsky SH, 20. Gefter WB, Laufer I, Edell S, Gohel VK. Haskin ME. Esophagitis caused by oral Candidiasis in the obstructed esophagus. medication. Radiology 1980;134:23–25. References Radiology 1981;138:25–28. 39. Levine MS, Rothstein RD, Laufer I. Giant 1. Levine MS, Rubesin SE, Herlinger H, Laufer 21. Levine MS, Macones AJ, Laufer I. Candida esophageal ulcer due to Clinoril. AJR Am J I. Double-contrast upper gastrointestinal esophagitis: accuracy of radiographic diag- Roentgenol 1991;156:955–956. examination: technique and interpreta- nosis. Radiology 1985;154:581–587. 40. Levine MS, Borislow SM, Rubesin SE, tion. Radiology 1988;168:593–602. 22. Vahey TN, Maglinte DD, Chernish SM. O’Brien C. caused by 2. Herlinger H, Grossman R, Laufer I, Kressel State-of-the-art barium examination in op- a Motrin tablet (ibuprofen). Abdom Imag- HY, Ochs RH. The gastric cardia in double- portunistic esophagitis. Dig Dis Sci 1986; ing 1994;19:6–7. contrast study: its dynamic image. AJR 31:1192–1195. 41. Ryan JM, Kelsey P, Ryan BM, Mueller PR. Am J Roentgenol 1980;135:21–29. 23. Rose D, Furth EE, Rubesin SE. Glycogenic Alendronate-induced esophagitis: case re- 3. Ott DJ, Chen YM, Hewson EG, et al. Esoph- acanthosis. AJR Am J Roentgenol 1995;164: port of a recently recognized form of se- ageal motility: assessment with synchro- 96. vere esophagitis with esophageal stric- nous video tape fluoroscopy and manom- 24. Glick SN, Teplick SK, Goldstein J, Stead JA, ture—radiographic features. Radiology etry. Radiology 1989;173:419–422. Zitomer N. Glycogenic acanthosis of the 1998;206:389–391. 4. Koehler RE, Weyman PJ, Oakley HF. Sin- esophagus. AJR Am J Roentgenol 1982; 42. Collazzo LA, Levine MS, Rubesin SE, gle- and double-contrast techniques in 139:683–688. Laufer I. Acute radiation esophagitis: ra-

426 ⅐ Radiology ⅐ November 2005 Levine and Rubesin diographic findings. AJR Am J Roentgenol sensitivity of radiographic diagnosis. AJR 68. Hsu WC, Levine MS, Rubesin SE. Overlap 1997;169:1067–1070. Am J Roentgenol 1997;168:1423–1426. phenomenon: a potential pitfall in the ra- 43. Lepke RA, Libshitz HI. Radiation-induced 56. Levine MS, Dillon EC, Saul SH, Laufer I. diographic detection of lower esophageal injury of the esophagus. Radiology 1983; Early esophageal cancer. AJR Am J Roent- rings. AJR Am J Roentgenol 2003;180:745– 148:375–378. genol 1986;146:507–512. 747. 44. Levine MS. Other esophagitides. In: Gore 57. Itai Y, Kogure T, Okuyama Y, Akiyama H. 69. Levine MS. Miscellaneous abnormalities of RM, Levine MS, eds. Textbook of gastroin- Superficial esophageal carcinoma: radio- the esophagus. In: Gore RM, Levine MS, testinal radiology. 2nd ed. Philadelphia, logical findings in double-contrast studies. eds. Textbook of gastrointestinal radiol- Pa: Saunders, 2000;364–386. Radiology 1978;126:597–601. ogy. 2nd ed. Philadelphia, Pa: Saunders, 45. Appelqvist P, Salmo M. Lye corrosion car- 58. Gloyna RE, Zornoza J, Goldstein HM. Pri- 2000;465–483. cinoma of the esophagus: a review of 63 mary ulcerative carcinoma of the esopha- 70. Fasano NC, Levine MS, Rubesin SE, Red- cases. Cancer 1980;45:2655–2658. gus. AJR Am J Roentgenol 1977;129:599– fern RO, Laufer I. Epiphrenic diverticulum: 46. Levine MS, Fisher AR, Rubesin SE, Laufer I, 600. clinical and radiographic findings in 27 Herlinger H, Rosato EF. Complications af- 59. Yates CW, LeVine MA, Jensen KM. Vari- patients. Dysphagia 2003;18:9–15. ter total gastrectomy and esophagojeju- coid carcinoma of the esophagus. Radiol- 71. Cho SR, Sanders MM, Turner MA, Liu CI, nostomy: radiologic evaluation. AJR Am J

adiology ogy 1977;122:605–608. Kipreos BE. Esophageal intramural pseudo- Roentgenol 1991;157:1189–1194. 60. Levine MS, Caroline D, Thompson JJ, Kres- . Gastrointest Radiol 1981;6:

R 47. Ming SC. Tumors of the esophagus and sel HY, Laufer I, Herlinger H. Adenocarci- 9–16. stomach. In: Atlas of tumor , fas- noma of the esophagus: relationship to 72. Levine MS, Moolten DN, Herlinger H, cicle 7. Washington, DC: Armed Forces In- Barrett mucosa. Radiology 1984;150:305– Laufer I. Esophageal intramural pseudodi- stitute of Pathology, 1973;16–23. 309. verticulosis: a reevaluation. AJR Am J 48. Montesi A, Pesaresi A, Graziani L, Salmis- 61. Keen SJ, Dodd GD, Smith JL. Adenocarci- Roentgenol 1986;147:1165–1170. traro D, Dini L, Bearzi I. Small benign tu- noma arising in Barrett esophagus: patho- 73. Ott DJ. Motility disorders of the esophagus. mors of the esophagus: radiological diag- logic and radiologic features. Mt Sinai In: Gore RM, Levine MS, eds. Textbook of nosis with double-contrast examination. J Med 1984;51:442–450. gastrointestinal radiology. 2nd ed. Philadel- Gastrointest Radiol 1983;8:207–212. 62. Glick SN, Teplick SK, Levine MS, Caroline phia, Pa: Saunders, 2000;316–328. 49. Levine MS. Benign tumors of the esophagus. DF. Gastric cardia metastases in esopha- 74. Woodfield CA, Levine MS, Rubesin SE, In: Gore RM, Levine MS, eds. Textbook of geal carcinoma. Radiology 1986;160:627– Langlotz CP, Laufer I. Diagnosis of primary gastrointestinal radiology. 2nd ed. Philadel- 630. versus secondary achalasia: reassessment phia, Pa: Saunders, 2000;387–402. 50. Levine MS, Buck JL, Pantongrag-Brown L, 63. Levine MS, Rubesin SE, Pantongrag-Brown of clinical and radiographic criteria. AJR Buetow PC, Hallman JR, Sobin LH. Fibro- L, Buck JL, Herlinger H. Non-Hodgkin’s Am J Roentgenol 2000;175:727–731. vascular polyps of the esophagus: clinical, lymphoma of the : ra- 75. Tucker HJ, Snape WJ, Cohen S. Achalasia radiographic, and pathologic findings in diographic findings. AJR Am J Roentgenol secondary to carcinoma: manometric and 16 patients. AJR Am J Roentgenol 1996; 1997;168:165–172. clinical features. Ann Intern Med 1978;89: 166:781–787. 64. Agha FP, Keren DF. Spindle-cell squamous 315–318. 51. Livstone EM, Skinner DB. Tumors of the carcinoma of the esophagus: a tumor with 76. Chen YM, Ott DJ, Hewson EG, et al. Dif- esophagus. In: Berk JE, ed. Bockus gastro- biphasic morphology. AJR Am J Roentge- fuse esophageal spasm: radiographic and enterology. 4th ed. Philadelphia, Pa: Saun- nol 1985;145:541–545. manometric correlation. Radiology 1989; ders, 1985;818–840. 65. Levine MS. Varices. In: Gore RM, Levine 170(3 pt 1):807–810. 52. Silverberg E. Cancer statistics, 1985. CA MS, eds. Textbook of gastrointestinal radi- 77. Prabhakar A, Levine MS, Rubesin S, Laufer Cancer J Clin 1985;35:19–35. ology. 2nd ed. Philadelphia, Pa: Saunders, I, Katzka D. Relationship between diffuse 53. Levine MS, Halvorsen RA. Carcinoma of 2000;452–463. esophageal spasm and lower esophageal the esophagus. In: Gore RM, Levine MS, 66. Schatzki R. The lower esophageal ring: sphincter dysfunction on barium studies eds. Textbook of gastrointestinal radiol- long term follow-up of symptomatic and and manometry in 14 patients. AJR Am J ogy. 2nd ed. Philadelphia, Pa: Saunders, asymptomatic rings. Am J Roentgenol Ra- Roentgenol 2004;183:409–413. 2000;403–433. dium Ther Nucl Med 1963;90:805–810. 78. Grishaw EK, Ott DJ, Frederick MG, Gel- 54. Spechler SJ, Goyal RK. Barrett’s esophagus. 67. Ott DJ, Chen YM, Wu WC, Gelfand DW, fand DW, Chen MY. Functional abnormal- N Engl J Med 1986;315:362–371. Munitz HA. Radiographic and endoscopic ities of the esophagus: a prospective anal- 55. Levine MS, Chu P, Furth EE, Rubesin SE, sensitivity in detecting lower esophageal ysis of radiographic findings relative to age Laufer I, Herlinger H. Carcinoma of the mucosal ring. AJR Am J Roentgenol 1986; and symptoms. AJR Am J Roentgenol esophagus and esophagogastric junction: 147:261–265. 1996;167:719–722.

Volume 237 ⅐ Number 2 Diseases of the Esophagus ⅐ 427