Differential diagnosis of esophageal disease on esophagography

This review article will present 

a gamut or pattern approach to 

the <strong>diagnosis</strong> <strong>of</strong> <strong>esophageal</strong> 

<strong>disease</strong>s. 1,2 For most patients, analysis 

<strong>of</strong> the radiographic findings in combination 

with consideration <strong>of</strong> the clinical 

history leads to the <strong>diagnosis</strong> or a 

graded differential <strong>diagnosis</strong>. 3 

Dr. Rubesin is a Pr<strong>of</strong>essor <strong>of</strong> Radiology 

and member <strong>of</strong> the Gastrointestinal 

Radiology Section, and Dr. Levine 

is a Pr<strong>of</strong>essor <strong>of</strong> Radiology and Chief 

<strong>of</strong> the Gastrointestinal Radiology Section 

at the Hospital <strong>of</strong> the University 

<strong>of</strong> Pennsylvania in Philadelphia, PA. 

October 2001 

<strong>Differential</strong> <strong>diagnosis</strong> 

<strong>of</strong> <strong>esophageal</strong> <strong>disease</strong> 

on esophagography 

Stephen E. Rubesin, MD and Marc S. Levine, MD 

Normal esophagus 

The normal esophagus is a muscular 

tube covered by nonkeratinized squamous 

epithelium. The esophagus lies 

in the neck and mediastinum. The 

aorta, left mainstem bronchus, and posterior 

border <strong>of</strong> the heart impress upon 

the wall <strong>of</strong> the esophagus. During double-contrast 

esophagography, the barium-etched 

contour is visible as a 

smooth, white line (figure 1). En face, 

the barium-coated <strong>esophageal</strong> mucosa 

is smooth and featureless, fading to 

gray. 1 The squamocolumnar junction 

with the stomach may be seen as a 

zigzag line, also known as the Z line. 

Small <strong>esophageal</strong> ulcers 

A wide variety <strong>of</strong> <strong>disease</strong>s are associated 

with small <strong>esophageal</strong> ulcers

FIGURE 1. Normal esophagus. The luminal 

contour is manifest as a smooth, straight 

white line (white arrow). The mucosal surface 

has a featureless, gray appearance en 

face (black arrow). 

have a round, stellate, linear, or serpentine 

configuration. Rarely, herpes 

esophagitis may develop in immunocompetent 

patients. In this self-limited 

form <strong>of</strong> herpes esophagitis, the ulcers 

manifest as smaller, punctate collections 

<strong>of</strong> barium. 7 

Drug-induced esophagitis is primarily 

a contact esophagitis caused by 

a variety <strong>of</strong> medications, including 

tetracycline or its derivatives, quinidine, 

potassium chloride, non- 

FIGURE 2. Small <strong>esophageal</strong> ulcers in herpes 

esophagitis. Many small punctate collections 

<strong>of</strong> barium surrounded by radiolucent halos 

(arrows) are seen in the midesophagus. The 

clinical history <strong>of</strong> AIDS in this patient enables 

the radiologist to make a <strong>diagnosis</strong> <strong>of</strong> viral, 

especially herpes, esophagitis. (Reproduced 

with permission from Levine MS, Laufer I. 

Esophagus. In: Levine MS, Rubesin SE, 

Laufer I. Double Contrast Gastrointestinal 

Radiology. 3rd ed. Philadelphia: WB Saunders 

Co.; 2000:90-126. 1 ) 

steroidal anti-inflammatory agents, 

and alendronate sodium. If little or no 

water is used during ingestion <strong>of</strong> these 

medications, pills may transiently 

lodge in the esophagus at the level <strong>of</strong> 

normal extrinsic impressions, includ- 

Table 1. Causes <strong>of</strong> 

<strong>esophageal</strong> ulcers 

Small <strong>esophageal</strong> ulcers 

(1 cm in diameter) 

Cytomegalovirus 

Human immunodeficiency virus 

Carcinoma 

Drug-induced 

Barrett’s ulcer 

Sclerotherapy for varices 

ing the aortic arch, the left mainstem 

bronchus, and the left atrium. Typically, 

small, shallow ulcers will be 

clustered together in the mid-esophagus. 

8,9 These ulcers usually heal within 

7 to 10 days after cessation <strong>of</strong> the 

<strong>of</strong>fending medication. 

In patients with small <strong>esophageal</strong> 

ulcers, the clinical history provides 

the key to the <strong>diagnosis</strong>. Patients with 

herpes esophagitis are usually 

immunosuppressed. If drug ingestion 

is the cause <strong>of</strong> the ulcer, a clinical history 

<strong>of</strong> using the <strong>of</strong>fending medication 

can usually be elicited. Finally, 

patients with reflux-induced ulcers 

usually have a history <strong>of</strong> heartburn, 

and the ulcers are usually located in 

the distal esophagus near the esophagogastric 

junction. These patients also 

usually have other radiographic findings 

<strong>of</strong> reflux esophagitis. 2 

Large <strong>esophageal</strong> ulcers 

The most common causes <strong>of</strong> large 

<strong>esophageal</strong> ulcers, those >1 cm in 

diameter, are human immunodeficiency 

virus (HIV) and cytomegalovirus 

(CMV) in immunocompromised 

patients, primarily patients with 

acquired immunodeficiency syndrome 

(AIDS). 13-16 HIV ulcers some- 

12 ■ APPLIED RADIOLOGY October 2001

FIGURE 3. Large <strong>esophageal</strong> ulcers due to 

HIV. This patient with odynophagia has 

large (>1 cm) ulcers (large black arrows) in 

the distal esophagus. Barium etches the 

undulating margins (arrowhead) <strong>of</strong> the 

ulcers. A halo <strong>of</strong> edema (white arrow) surrounds 

the craters. This patient recently 

underwent seroconversion for HIV. Endoscopic 

biopsies <strong>of</strong> the ulcers failed to identify 

cytomegalovirus, so HIV esophagitis 

was a <strong>diagnosis</strong> <strong>of</strong> exclusion. 

October 2001 

FIGURE 4. Squamous cell carcinoma. This 

smoker and drinker has a large ulcer (long 

arrow) surrounded by a lobulated, thickened 

edge (short arrows). The ulcer is 

deeper than a viral-induced ulcer and the 

edge is much thicker and more lobulated 

than a viral-induced ulcer. Squamous cell 

carcinoma was diagnosed histologically. 

Table 2. Mucosal nodules and plaques 

Cause Comment 

Candida Discrete plaques in immunosuppressed patient 

Reflux esophagitis Poorly defined nodules, associated hiatal hernia 

and gastro<strong>esophageal</strong> reflux 

Glycogenic acanthosis Asymptomatic patient 

Superficial spreading Coalescent plaques in focal area 

cancer 

times occur near the time <strong>of</strong> clinical 

presentation and seroconversion. The 

ulcers in CMV and HIV esophagitis 

(figure 3) tend to be large, flat, ovoidshaped 

barium collections or bariumetched 

craters. 14,16 Endoscopic biopsy 

specimens are necessary to distinguish 

CMV or HIV ulcers, as the 

treatment for each <strong>of</strong> these infections 

is different. Esophageal ulceration due 

to HIV is a <strong>diagnosis</strong> <strong>of</strong> exclusion, so 

this <strong>diagnosis</strong> can be made only when 

endoscopic biopsies, brushings, and 

cultures are negative for CMV. 

Other common causes <strong>of</strong> large 

<strong>esophageal</strong> ulcers include carcinoma 

(figure 4), drug-induced ulcers, or 

Barrett’s esophagus 3,17,18 (Table 1). 

However, these ulcers tend to be 

deeper than viral-induced ulcers, and 

their edges are frequently thickened 

and lobulated. In such cases, biopsy 

specimens may be necessary to 

exclude neoplasia. 

Mucosal nodules and plaques 

Mucosal nodules and plaques are 

elevated lesions <strong>of</strong> varying size. 

Plaques are usually discrete, irregular 

or ovoid elevations that barely protrude 

above the mucosal surface. Nodules 

are smaller elevations and are 

more rounded than plaques. The morphology 

<strong>of</strong> the elevations in combination 

with the clinical history allows a 

specific <strong>diagnosis</strong> to be made in most 

patients (Table 2). 

Candida esophagitis most frequently 

manifests as numerous small, 

discrete, ovoid or linear plaque-like 

elevations aligned parallel to the longitudinal 

folds <strong>of</strong> the esophagus (figure 

5). 19 In mild-to-moderate Candida 

esophagitis, the plaques are separated 

by intervening segments <strong>of</strong> normal 

mucosa. In more severe cases, the 

plaques may carpet the esophagus. In 

even more severe cases, confluent 

plaques, pseudomembranes, and barium 

burrowing beneath the inflammatory 

detritus may produce a grossly 

irregular appearance <strong>of</strong> the contour in 

APPLIED RADIOLOGY ■ 13

FIGURE 5. Candida esophagitis. This 

immunosuppressed patient with odynophagia 

has small, irregular, discrete plaque-like 

elevations (arrows) aligned parallel to the 

longitudinal folds <strong>of</strong> the esophagus. The 

plaques are separated by intervening segments 

<strong>of</strong> normal mucosa. 

pr<strong>of</strong>ile and the mucosal surface en face, 

the so-called “shaggy esophagus.” 

When plaques and pseudomembranes 

slough, large ulcers may form, but these 

are almost always present on a background 

<strong>of</strong> diffuse plaque formation. 

Candida albicans is the most common 

cause <strong>of</strong> infectious esophagitis. 

Immunosuppression is the most frequent 

predisposing factor. Patients 

usually complain <strong>of</strong> dysphagia or 

odynophagia. Thrush in the oral cavity 

or pharynx is seen in about onehalf 

<strong>of</strong> patients. Candida esophagitis 

may also develop in patients with 

severe <strong>esophageal</strong> motility disorders, 

such as scleroderma, or in patients 

with <strong>esophageal</strong> obstruction and stasis 

due to achalasia or carcinoma. 

A B 

FIGURE 6. Mucosal changes in reflux esophagitis. (A) Mucosal nodularity. Well-defined 

radiolucent nodules carpet the mucosa <strong>of</strong> the distal esophagus (representative area <strong>of</strong> 

nodularity identified by arrow). (B) Granular mucosa and tiny ulcers. In a different patient, the 

mucosa <strong>of</strong> the distal esophagus is covered by innumerable, tiny, ill-defined radiolucencies 

(open arrows). In the more distal portion <strong>of</strong> the esophagus, tiny ulcers are visible as punctate 

dots <strong>of</strong> barium (arrows). 

Small nodules and plaques <strong>of</strong> varying 

sizes may also be seen in the 

esophagus in patients with glycogenic 

acanthosis, a common degenerative 

condition. 20,21 However, the plaques <strong>of</strong> 

glycogenic acanthosis are usually seen 

in the upper or midesophagus in a random 

distribution. In this disorder, 

glycogen is accumulated in the cytoplasm 

<strong>of</strong> cells in the upper portion <strong>of</strong> 

the squamous epithelium. Glycogenic 

acanthosis typically occurs in elderly 

individuals who have no <strong>esophageal</strong> 

symptoms and who do not have a history 

<strong>of</strong> immunosuppression or a condition 

predisposing to stasis. In contrast, 

patients with Candida esophagitis are 

usually symptomatic, and the plaques 

tend to be more linear in shape and 

aligned longitudinally along the folds. 

In some patients with reflux 

esophagitis, tiny mucosal nodules are 

seen (figure 6). 2 However, these nodules 

are more ill-defined and less discrete 

than the plaques in Candida 

esophagitis. The nodules <strong>of</strong> reflux 

esophagitis also are more confluent 

and are located in the distal esophagus, 

usually in patients with gastro<strong>esophageal</strong> 

reflux and hiatal hernias. 

Reflux esophagitis is more frequently 

characterized by poorly defined tiny 

mucosal elevations, termed mucosal 

“granularity” (figure 6B). 1,2,22,23 This 

granularity may be associated with tiny 

or linear ulcers and thickened, nodular 

folds. These changes are also usually 

associated with a hiatal hernia and fluo- 


FIGURE 7. Superficial spreading carcinoma. 

A long but focal area <strong>of</strong> confluent mucosal 

nodularity (arrows) is seen in the midesophagus. 

(Reproduced with permission from Low 

VHS, Rubesin SE. Contrast evaluation <strong>of</strong> the 

pharynx and esophagus. Radiol Clin North 

Am. 1993;31:1265-1291. 32 ) 

roscopically detected gastro<strong>esophageal</strong> 

reflux. Some patients with reflux 

esophagitis have such severe inflammation 

that plaque-like pseudomembranes 

may eventually form. 24 

A focal area <strong>of</strong> confluent mucosal 

nodularity may be worrisome for 

superficial spreading carcinoma, a 

cancer confined to the mucosa and 

submucosa (figure 7). 25,26 However, 

the nodules are not as discrete as those 

October 2001 

FIGURE 8. Reticular pattern in Barrett’s esophagus. Coned-down view <strong>of</strong> the esophagus at 

the level <strong>of</strong> the left mainstem bronchus shows a lace-like network <strong>of</strong> barium-filled grooves 

surrounding small, polygonal, radiolucent tufts <strong>of</strong> mucosa (open arrows). Distally, a striated 

appearance (large arrow) is seen. These changes were due to biopsy-proven Barrett’s 

mucosa. 

in Candida esophagitis, nor are they 

separated by normal intervening 

mucosa. Although most focal areas <strong>of</strong> 

mucosal irregularity will probably be 

caused by glycogenic acanthosis, an 

area <strong>of</strong> focal mucosal nodularity 

should be biopsied to exclude superficial 

spreading carcinoma. 

It is also difficult to distinguish a 

focal area <strong>of</strong> mucosal nodularity from 

the surface pattern termed “reticular 

mucosa,” which is seen in Barrett’s 

esophagus. 27 Barrett’s esophagus is an 

acquired condition in which there is 

progressive columnar metaplasia <strong>of</strong> 

the esophagus due to long-standing 

gastro<strong>esophageal</strong> reflux <strong>disease</strong>. The 

reticular mucosal pattern resembles 

the areae gastricae <strong>of</strong> the stomach, 

with a fine, net-like web <strong>of</strong> bariumfilled 

grooves surrounding small tufts 

<strong>of</strong> mucosa (figure 8). 


Cause 

Table 3. Abnormal <strong>esophageal</strong> folds 

Comment 

Reflux esophagitis Other findings <strong>of</strong> gastro<strong>esophageal</strong> reflux <strong>disease</strong> 

Varices Serpentine, variable 

Varicoid carcinoma Rigid, fixed, irregular 

Lymphoma Discrete submucosal nodules 

FIGURE 9. Esophageal varices. A thickened, 

smooth, serpentine fold (long arrows) 

is seen in the esophagus at the level <strong>of</strong> the 

left mainstem bronchus. Another thickened, 

smooth, undulating fold (short arrows) is 

seen in the distal esophagus. 

FIGURE 10. Varicoid form <strong>of</strong> squamous 

cell carcinoma. Coarsely lobulated folds 

expand the lumen <strong>of</strong> the midesophagus. 

No change in the size or shape <strong>of</strong> the folds 

was seen during fluoroscopy. 

Abnormal <strong>esophageal</strong> folds 

The longitudinal folds <strong>of</strong> the esophagus 

are composed <strong>of</strong> mucosa and 

submucosa and are best seen when the 

esophagus is underdistended. Therefore, 

abnormalities <strong>of</strong> folds reflect <strong>disease</strong> 

in the mucosa and submucosa 

(Table 3). In patients with reflux 

esophagitis, thickened <strong>esophageal</strong> 

folds are frequently seen when the 

esophagus is collapsed. 1,2 These 

patients usually have other findings <strong>of</strong> 

reflux <strong>disease</strong>, including gastro<strong>esophageal</strong> 

reflux, a granular mucosa, 

and hiatal hernia. In contrast, 

<strong>esophageal</strong> varices are serpentine, 

with a smooth surface (figure 9). 

Varices may change in size with varying 

degrees <strong>of</strong> <strong>esophageal</strong> distention 

and patient position. If the folds are 

rigid, fixed, or irregular, however, the 

varicoid form <strong>of</strong> squamous cell carcinoma 

must be excluded (figure 10). 28 

Esophageal strictures 

The differential <strong>diagnosis</strong> <strong>of</strong> an 

<strong>esophageal</strong> stricture depends on the 

morphology and location <strong>of</strong> the stricture 

as well as on the clinical history. 

Benign strictures typically manifest as 

smooth, tapered areas <strong>of</strong> concentric 

narrowing (figure 11). 1 Asymmetric 

scarring may result in sacculation, 

flattening, or other deformity <strong>of</strong> the 

wall. In contrast, malignant strictures 

are manifest as eccentric narrowings, 

thicker on the side where the tumor 

originated. 23 The mucosal surface is 

irregular, with nodules <strong>of</strong> varying size 

disrupting the surface and barium 

being trapped in areas <strong>of</strong> ulceration. 

The margins <strong>of</strong> malignant strictures 

<strong>of</strong>ten appear abrupt and shelf-like (figure 

12). Unlike malignant lesions in 

the colon, however, malignant 

<strong>esophageal</strong> lesions may have sloped 

or tapered margins, as the s<strong>of</strong>t 

<strong>esophageal</strong> submucosa and muscularis 

propria provide little resistance to 

the longitudinal spread <strong>of</strong> tumor. In 

some patients, a plaque-like indentation 

<strong>of</strong> the lumen is seen (figure 13). If 


FIGURE 11. Reflux-induced stricture. A circumferential 

area <strong>of</strong> narrowing in the distal 

esophagus has a smooth, tapered contour 

(arrows) and smooth mucosa. A hiatal hernia 

(H) persists while the patient is in the 

erect position, indicating shortening <strong>of</strong> the 

esophagus due to chronic scarring. (Reproduced 

with permission from Low VHS, 

Rubesin SE. Contrast evaluation <strong>of</strong> the 

pharynx and esophagus. Radiol Clin North 

Am. 1993;31:1265-1291. 32 ) 

any mucosal irregularity or plaquelike 

flattening is identified in the 

region <strong>of</strong> an <strong>esophageal</strong> stricture, 

endoscopy and biopsy are required to 

exclude carcinoma. 

The most common causes <strong>of</strong> short 

distal <strong>esophageal</strong> strictures are gastro<strong>esophageal</strong> 

reflux and carcinoma 

(Table 4; figures 11 and 14). Long distal 

<strong>esophageal</strong> strictures are <strong>of</strong>ten due 

to severe acid exposure related to 

Zollinger-Ellison syndrome, prolonged 

nasogastric intubation, or alka- 

October 2001 

FIGURE 12. Squamous cell carcinoma. A 

malignant stricture is seen at the level <strong>of</strong> the 

aortic arch. The contour is irregular (black 

arrows). The bulk <strong>of</strong> the tumor lies on the left 

lateral wall. The stricture has an abrupt, 

mass-like margin proximally (long white 

arrow). The mucosa is nodular. Smooth, 

tapered narrowing <strong>of</strong> the <strong>esophageal</strong> wall 

(short white arrows) opposite the bulk <strong>of</strong> the 

tumor indicates the beginning <strong>of</strong> circumferential 

spread <strong>of</strong> tumor. 

line reflux esophagitis (Table 4). 

Some patients with Crohn’s <strong>disease</strong> 

may also develop long distal 

<strong>esophageal</strong> strictures. A wide variety 

<strong>of</strong> conditions cause mid<strong>esophageal</strong> 

strictures (Table 4). 29-34 The combination 

<strong>of</strong> the clinical history, physical 

examination findings, and radiographic 

appearance <strong>of</strong> the strictures 

<strong>of</strong>ten enables a specific <strong>diagnosis</strong>. 

Strictures related to reflux 

esophagitis are usually seen in the distal 

esophagus. Some reflux-induced 

A 

B 

FIGURE 13. Plaque-like adenocarcinoma 

<strong>of</strong> the distal esophagus. (A) Spot image <strong>of</strong> 

the distal esophagus obtained with the 

patient in a left posterior oblique position 

demonstrates a focal area <strong>of</strong> coarse 

mucosal nodularity en face (arrows) above 

a small hiatal hernia. (B) Spot image <strong>of</strong> the 

distal esophagus obtained with patient now 

turned into the right posterior oblique position. 

A plaque-like lesion (arrows) is seen in 

pr<strong>of</strong>ile on the posterolateral wall. 


Table 4. Causes <strong>of</strong> 

<strong>esophageal</strong> strictures 

Short distal <strong>esophageal</strong> 

strictures 

Reflux-induced 

Carcinoma 

Crohn’s <strong>disease</strong> 

Schatzki ring 

Long distal <strong>esophageal</strong> 

strictures 

Nasogastric intubation 

Zollinger-Ellison syndrome 

Alkaline reflux esophagitis 

Crohn’s <strong>disease</strong> 

Mid<strong>esophageal</strong> strictures 

Barrett’s esophagus 

Radiation damage 

Caustic ingestion 

Primary or metastatic cancer 

Drug-induced stricture (especially 

potassium chloride) 

Esophageal intramural pseudodiverticulosis 

Benign mucous membrane pemphigoid, 

epidermolysis bullosa 

Graft versus host <strong>disease</strong> 

strictures are smooth and tapered (figure 

11). However, other refluxinduced 

strictures are associated with 

enough asymmetric scarring to cause 

sacculation in the area <strong>of</strong> tapering. 

These sacculations due to scarring 

should not be confused with ulcers. 

Other reflux-induced strictures may 

be associated with such severe scarring 

and <strong>esophageal</strong> shortening that a 

hiatal hernia is even present in the 

erect position. 

In the presence <strong>of</strong> a hiatal hernia 

and gastro<strong>esophageal</strong> reflux, a 

benign-appearing mid<strong>esophageal</strong> 

stricture or reticular pattern should be 

strongly suggestive <strong>of</strong> Barrett’s 

esophagus. 30 Strictures associated 

with Barrett’s esophagus are more frequently 

seen in the distal esophagus, 

however. Patients with distal 

<strong>esophageal</strong> strictures and reflux 

changes have a moderate risk <strong>of</strong> Bar- 

FIGURE 14. Short distal <strong>esophageal</strong> adenocarcinoma. 

A short, tapered stricture 

(arrows) <strong>of</strong> the distal esophagus is eccentrically 

located and has a slightly irregular 

contour. Obstruction is manifested by proximal 

<strong>esophageal</strong> dilatation. 

rett’s esophagus, between 20% and 

40%. 30 Patients with reflux esophagitis 

alone have about a 10% risk <strong>of</strong> Barrett’s 

esophagus. 30 Conversely, a very 

low risk <strong>of</strong> Barrett’s esophagus is present 

if the <strong>esophageal</strong> mucosa is 

smooth, if a stricture is not seen, and if 

only gastro<strong>esophageal</strong> reflux or a 

hiatal hernia is present. 

Schatzki rings are <strong>of</strong> unknown etiology, 

possibly related to gastro<strong>esophageal</strong> 

reflux. They are thin (1 to 

3 mm in thickness), symmetric rings 

at the esophagogastric junction, frequently 

seen above a small hiatal hernia 

(figure 15). 31 Schatzki rings are 

best demonstrated in the prone position 

and are sometimes detected only 

with a solid bolus. 32 Rings

FIGURE 16. Esophageal intramural pseudodiverticulosis. 

This patient has a long, 

tapered mid<strong>esophageal</strong> stricture (large 

arrow). Many small flask-like outpouchings 

(“pseudodiverticula”) are seen lateral to the 

barium-filled <strong>esophageal</strong> lumen (representative 

outpouchings identified by small arrows). 

pouchings are associated with a long 

cervical or upper thoracic <strong>esophageal</strong> 

stricture (figure 16). 33 In the more 

common form <strong>of</strong> <strong>esophageal</strong> intramural 

pseudodiverticulosis, however, 

the outpouchings are associated with a 

short, distal, reflux-induced stricture. 34 

Primary or metastatic cancers are 

frequent causes <strong>of</strong> mid<strong>esophageal</strong> 

strictures. Some squamous cell carcinomas 

have an elongated, circumferentially 

infiltrating appearance (figure 

12). An eccentric, annular lesion may 

be seen with a coarsely lobulated contour 

and barium trapped within tumor 

nodules. Adenocarcinomas <strong>of</strong> the 

esophagus arise in dysplastic columnar 

epithelium within Barrett’s 

October 2001 

FIGURE 17. Subcarinal lymph node metastases 

from breast carcinoma. Spot image <strong>of</strong> 

the midesophagus obtained with the patient 

in a near lateral position demonstrates a 

smooth-surfaced mass pressing on the 

subcarinal esophagus. 

mucosa. Adenocarcinomas are found 

most frequently in the distal esophagus. 

Adenocarcinomas can have an 

infiltrative (figure 14), plaque-like 

(figure 13), ulcerative, or polypoid 

appearance. Unlike squamous cell 

carcinomas, adenocarcinomas have a 

marked tendency to invade the gastric 

cardia and fundus. Metastases to the 

esophagus most frequently involve 

the subcarinal region due to direct 

invasion by tumor from subcarinal 

lymph nodes (figure 17) or from the 

left mainstem bronchus. 

Polypoid intraluminal masses 

A wide variety <strong>of</strong> polypoid masses 

are seen in the esophagus (Table 5). 35-41 

Table 5. Causes <strong>of</strong> polypoid 

intraluminal masses 

Benign 

Foreign body 

Inflammatory esophagogastric 

polyp 

Squamous papilloma 

Fibrovascular polyp 

Leiomyoma 

Malignant 

Squamous cell carcinoma 

Adenocarcinoma 

Spindle cell carcinoma 

Small cell carcinoma 

Primary malignant melanoma 

Polypoid masses are demonstrated 

radiographically as radiolucent filling 

defects in the barium pool (figure 18) 

or as barium-etched lines within the 

<strong>esophageal</strong> lumen. Polypoid masses 

must first be distinguished from foreign 

bodies (figure 19). The clinical 

history is crucial for the <strong>diagnosis</strong> <strong>of</strong> 

foreign bodies. These patients typically 

complain <strong>of</strong> abrupt-onset dysphagia 

or odynophagia during eating 

and the sensation that food is stuck in 

the substernal region. The polypoid 

filling defect <strong>of</strong> the foreign body may 

be associated with an irregular meniscus 

<strong>of</strong> barium superiorly. Perforation 

is uncommon, usually occurring after 

the impaction has been present longer 

than 24 hours. A repeat esophagram 

should be performed after the foreign 

body has been removed to exclude an 

<strong>esophageal</strong> stricture or motor disorder 

as the cause <strong>of</strong> the food impaction. 

Squamous papillomas are the most 

common benign mucosal tumor <strong>of</strong> the 

esophagus (figure 18), appearing as 

small, sessile, slightly lobulated 

polyps. The esophagus is one organ <strong>of</strong> 

the gastrointestinal tract in which true 

leiomyomas form. Most tumors arising 

in the mesenchyme are undifferentiated 

gastrointestinal stromal 

tumors <strong>of</strong> unknown malignant potential. 

Leiomyomas, however, are true 


FIGURE 18. Squamous papilloma. A 

pedunculated polyp (thick arrow) is seen in 

the barium pool. Barium fills the interstices 

(thin arrow) <strong>of</strong> the head <strong>of</strong> the polyp. The 

pedicle (arrowhead) has a smooth surface. 

Pedunculated polyps are typically squamous 

papillomas or adenomatous polyps 

arising in Barrett’s mucosa. (Reproduced 

with permission from Rubesin SE. Gallery 

<strong>of</strong> double contrast terminology. Gastro Clin 

North Am. 1995;24:259-288. 23 ) 

proliferations <strong>of</strong> smooth muscle and 

are the most common submucosal 

mass in the esophagus. Granular cell 

tumors are another rare cause <strong>of</strong> submucosal 

masses in the esophagus. 36 

Polyps at the esophagogastric junction 

are frequently related to chronic 

gastro<strong>esophageal</strong> reflux <strong>disease</strong>, termed 

“inflammatory esophagogastric” or 

“sentinel” polyps. 40 These polyps are 

smooth-surfaced enlargements atop a 

thickened rugal fold at the gastric car- 

FIGURE 19. Kielbasa stuck in the esophagus 

above an <strong>esophageal</strong> stricture. A triangular 

radiolucent filling defect with an 

irregular contour (black arrow) lies proximal 

to a smooth, tapered stricture (white arrow) 

<strong>of</strong> the distal esophagus. With the patient 

standing in an erect position, the presence 

<strong>of</strong> a hiatal hernia (H) indicates <strong>esophageal</strong> 

shortening. This patient with long-standing 

gastro<strong>esophageal</strong> reflux symptoms had 

been eating a sausage. The stricture was 

discovered at the time <strong>of</strong> the food impaction. 

dia. If any surface irregularity is seen, 

however, endoscopy must be performed 

to exclude a malignant tumor at 

the cardia or in Barrett’s esophagus. 

Some squamous cell carcinomas 

have a polypoid (figure 20) rather than 

infiltrating appearance. 38,39 Small cell 

carcinomas are rare tumors that typically 

manifest as small, centrally 

ulcerated masses in the midesophagus. 

37 Spindle cell carcinomas are usually 

large, polypoid masses that 

FIGURE 20. Polypoid squamous cell carcinoma. 

A 1.5-cm lobulated lesion (arrow) 

arises from the left anterolateral wall <strong>of</strong> the 

midesophagus. 

expand the <strong>esophageal</strong> lumen without 

causing significant obstruction. 39 

Despite the relatively noninfiltrating 

appearance <strong>of</strong> spindle cell carcinomas, 

5-year survival rates in these 

patients are as dismal as in those 

patients with squamous cell carcinomas. 

Rarely, primary malignant 

melanoma <strong>of</strong> the esophagus may be 

manifest as a bulky, polypoid intraluminal 

mass indistinguishable from 

spindle cell carcinoma. 41 AR 


REFERENCES 

1. Levine MS, Laufer I. Esophagus. In: Levine 

MS, Rubesin SE, Laufer I. Double Contrast Gastrointestinal 

Radiology. 3rd ed. Philadelphia: WB 

Saunders Co; 2000:90-126. 

2. Levine MS. Radiology <strong>of</strong> esophagitis: A pattern 

approach. Radiology. 1991;179:1-7. 

3. Rubesin SE, Laufer I. Pictorial glossary <strong>of</strong> double 

contrast radiology. In: Gore RM, Levine MS 

(eds). Textbook <strong>of</strong> Gastrointestinal Radiology. 2nd 

ed. Philadelphia: WB Saunders Co; 2000:44-66. 

4. Levine MS, Laufer I, Kressel HY, Friedman 

HM. Herpes esophagitis. AJR Am J Roentgenol. 

1981;136:863-866. 

5. Levine MS, Loevner LA, Saul SH, et al. Herpes 

esophagitis: Sensitivity <strong>of</strong> double-contrast esophagography. 

AJR Am J Roentgenol. 1988;151:57-62. 

6. Rubesin SE, Levine MS, Laufer I. Odynophagia. 

In: Thompson WM, ed. Common Problems in 

Gastrointestinal Radiology. Chicago: Year Book 

Medical Publishers; 1989:108-117. 

7. Shortsleeve MJ, Levine MS. Herpes esophagitis 

in otherwise healthy patients: Clinical and radiographic 

findings. Radiology. 1992;182:859-861. 

8. Creteur V, Laufer I, Kressel HY, et al. Druginduced 

esophagitis detected by double-contrast 

radiography. Radiology. 1983;147:365-368. 

9. Bova JG, Dutton NE, Goldstein HM, Hoberman 

LJ. Medication-induced esophagitis: Diagnosis by 

double contrast esophagography. AJR Am J 

Roentgenol. 1987;148:731-732. 

10. Gohel V, Long BW, Richter G. Aphthous 

ulcers in the esophagus with Crohn colitis. AJR 

Am J Roentgenol. 1981;137:872-873. 

11. Collazzo LA, Levine MS, Rubesin SE, Laufer I. 

Acute radiation esophagitis: Radiographic findings. 


12. Levine MS. Drug-induced disorders <strong>of</strong> the 

esophagus. Abdom Imaging. 1999;24:3-8. 

13. Levine MS, Loercher G, Katzka DA, et al. 

Giant HIV-related ulcers in the esophagus. Radiology. 

1991;180:323-326. 

14. Sor S, Levine MS, Kowalski TE, et al. Giant 

<strong>esophageal</strong> ulcers in HIV-positive patients: Clinical, 

radiographic and pathologic findings. Radiol- 

October 2001 

ogy. 1995;194:447-451. 

15. Levine MS, Woldenberg R, Herlinger H, Laufer 

I. Opportunistic esophagitis in AIDS: Radiographic 

<strong>diagnosis</strong>. Radiology. 1987;165:815-820. 

16. Balthazar EJ, Megibow AJ, Hulnick D, et al. 

Cytomegalovirus esophagitis in AIDS: Radiographic 

features in 16 patients. AJR Am J 

Roentgenol. 1987;149:919-923. 

17. Gloyna RE, Zornoza J, Goldstein HM: Primary 

ulcerative carcinoma <strong>of</strong> the esophagus. 


18. Levine MS, Rothstein RD, Laufer I. Giant 

<strong>esophageal</strong> ulcer due to Clinoril. AJR Am J 

Roentgenol. 1991;156:955-956. 

19. Levine MS, Macones AJ, Laufer I. Candida 

esophagitis: Accuracy <strong>of</strong> radiographic <strong>diagnosis</strong>. 

Radiology. 1985;154:581-587. 

20. Berliner L, Redmond P, Horowitz L, Ru<strong>of</strong>f M. 

Glycogen plaques (glycogenic acanthosis) <strong>of</strong> the 

esophagus. Radiology. 1981;141:607-610. 

21. Glick SN, Teplick SK, Goldstein J, et al. 

Glycogenic acanthosis <strong>of</strong> the esophagus. AJR 

Am J Roentgenol. 1982;139:683-688. 

22. Graziani L, Bearzi I, Romagnoli A, et al. Significance 

<strong>of</strong> diffuse granularity and nodularity <strong>of</strong> 

the <strong>esophageal</strong> mucosa at double-contrast radiography. 

Gastrointest Radiol. 1985;10:1-6. 

23. Rubesin SE. Gallery <strong>of</strong> double contrast terminology. 

Gastro Clin North Am. 1995;24:259-288. 

24. Levine MS, Cajade AG, Herlinger H, Laufer I. 

Pseudomembranes in reflux esophagitis. Radiology. 

1986;159:43-45. 

25. Itai Y, Kogure T, Okuyama Y, Akiyama H. 

Superficial <strong>esophageal</strong> carcinoma: Radiological 

findings in double-contrast studies. Radiology. 

1978;126:597-601. 

26. Levine MS, Dillon EC, Saul SH, Laufer I. Early 

<strong>esophageal</strong> cancer. AJR Am J Roentgenol. 

1986;146:507-512. 

27. Levine MS, Kressel HY, Caroline D, et al. Barrett 

esophagus: Reticular pattern <strong>of</strong> the mucosa. 

Radiology. 1983;147:663-667. 

28. Yates CW, LeVine MA, Jensen KM. Varicoid 

carcinoma <strong>of</strong> the esophagus. Radiology. 

1977;122:605-608. 

29. Levine MS, Borislow SM, Rubesin SE, 

O'Brien C. Proximal <strong>esophageal</strong> stricture caused 

by Motrin. Abdom Imaging. 1994;19:6-7. 

30. Gilchrist AM, Levine MS, Carr RF, et al. Barrett’s 

esophagus: Diagnosis by double-contrast 

esophagography. AJR Am J Roentgenol. 

1988;150:97-102. 

31. Levine MS, Rubesin SE. Radiologic investigation 

<strong>of</strong> dysphagia. AJR Am J Roentgenol. 

1990;154:1157-1163. 

32. Low VHS, Rubesin SE. Contrast evaluation <strong>of</strong> 

the pharynx and esophagus. Rad Clin North Am. 

1993;31:1265-1291. 

33. Cho SR, Sanders MM, Turner MA, et al. 

Esophageal intramural pseudodiverticulosis. 

Gastrointest Radiol. 1981;5:9-16. 

34. Levine MS, Moolten DN, Herlinger H, Laufer I. 

Esophageal intramural pseudodiverticulosis: A 

reevaluation. AJR Am J Roentgenol. 1986;147:1165- 

1170. 

35. Olmsted WW, Lichtenstein JE, Hyams VJ. 

Polypoid epithelial malignancies <strong>of</strong> the esophagus. 


36. Rubesin SE, Herlinger H, Sigal H. Granular 

cell tumors <strong>of</strong> the esophagus. Gastrointest Radiology. 

1985;10:11-15. 

37. Levine MS, Pantongrag-Brown L, Buck JL, et 

al. Small-cell carcinoma <strong>of</strong> the esophagus: Radiographic 

findings. Radiology. 1996;199:703-705. 

38. Levine MS, Laufer I, Yamada A. Tumors <strong>of</strong> 

the esophagus. In: Levine MS, Rubesin SE, 

Laufer I. Double Contrast Gastrointestinal Radiology. 

3rd ed. Philadelphia: WB Saunders Co; 

2000:126-148. 

39. Levine MS. Other malignant tumors <strong>of</strong> the 

esophagus. In: Gore RM, Levine MS (eds). Textbook 

<strong>of</strong> Gastrointestinal Radiology. 2nd ed. 

Philadelphia: WB Saunders Co; 2000:435-451. 

40. Bleshman MH, Banner MP, Johnson RC, et 

al. The inflammatory esophagogastric junction 

polyp and fold. Radiology. 1978;128: 589-593. 

41. Yoo CC, Levine MS, McLarney JK, Lowry MA. 

Primary malignant melanoma <strong>of</strong> the esophagus: 

Radiographic findings in seven patients. Radiology. 

1998;209:455-459.

Differential diagnosis of esophageal disease on esophagography

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