). At the upper end of the vestibule is a slight narrowing, or A-ring, caused by smooth muscle (internal esophageal sphincter), which can be normal or may cause slight dysphagia if hypertrophied. The B-ring is at the GE junction itself (at the lower end of the vestibule, also known as phrenic ampulla) and is not seen unless a hiatal hernia is present. The Z line may be seen as a slight narrowing at the lower end of the phrenic ampulla and represents the epithelial junction between the esophagus (squamous) and stomach (columnar) and will not be seen unless a hiatal hernia is present. Dysphagia will not occur unless the B ring in the lower esophagus is less than 12 to 13 mm, when it is known as a Schatzki∗ ring (see discussion later in chapter).
Figure 1-1 Schematic representation of lower esophageal anatomy (in the presence of a small hiatal hernia).
Techniques
Oral Contrast Studies
Although cross-sectional imaging techniques are critical for the evaluation of malignant esophageal disease for staging purposes, most esophageal abnormalities are too small and fine to be accurately evaluated by them. Contrast examination of the esophagus (usually with barium) is an appropriate tool for the evaluation of most esophageal disease, but the radiologist’s role has been greatly diminished since the advent and routine use of direct optical endoscopy. However, given that the barium swallow and upper gastrointestinal (UGI) studies can be exquisite tools for the assessment of both morphological (gross appearance of the pharynx, esophagus, GE junction) and functional esophageal abnormalities (pharyngeal function, esophageal dysmotility, gastroesophageal reflux disease [GERD]), radiologists should still be familiar with their use and imaging findings.
A UGI swallow examination is best performed with both single- and double-contrast techniques. Before beginning the examination, the radiologist should further question the patient about his or her symptoms and history. The information gleaned from the patient can offer clues and greater specificity about what the radiologist might expect, and the radiologist might then modify or tailor the examination accordingly. At this point, the radiologist should explain the procedure to the patient because compliance is crucial to obtain an optimal examination. For instance, after the initial ingestion of effervescent gas granules, the patient should try as best as possible to refrain from eructation, which might defeat the purpose of performing a double-contrast examination. Maximal esophageal and gastric distention provides better images and therefore a greater ability to detect subtle disease. In the upright position, the patient then ingests the gas granules, followed by a small sip of water to aid rapid swallowing. The goal is to prevent the granules from “fizzing” in the mouth, which reduces their distensive effect in the esophagus and stomach. The patient then swallows a cup of high-density (“thick”) barium, at which point images are taken of the gas-distended esophagus and small mucosal abnormalities can be identified. If any abnormality is identified at this point, multiple tangential views should be taken to allow the radiologist to evaluate the lesion in more detail once the examination is finished. Too often, inadequate oblique and tangential views are taken, resulting in the lesion being visible in a limited plane, which may make formal diagnosis difficult or even impossible. Frequently the examination is performed in conjunction with a UGI series with gastric and duodenal evaluation, and the radiologist will need to then concentrate on these organs while they are maximally distended with air. The radiologist should return later to a final evaluation of the esophagus using a single-contrast examination with low-density (“thin”) barium, with the patient typically in the right anterior or prone oblique position. The patient takes several sips of barium, and esophageal motility and distensibility are evaluated as the radiologist observes the stripping waves of esophageal bolus propulsion. The lower esophagus is finally evaluated for hernias and the mucosal B-ring. GERD or a hiatal hernia may not initially be evident, and the patient should be asked to perform a Valsalva∗ maneuver as a provocative measure to increase intraabdominal pressure. This action may elicit either the hiatal hernia or reflux and perhaps be the answer to the patient’s symptoms. In this position, the normal longitudinal mucosal relief images are also observed, and this observation may permit variceal visualization. Finally, the stomach and duodenum should be briefly evaluated in case the patient’s symptoms are due to disease in these organs.
If the patient’s symptom is upper dysphagia, then anteroposterior (AP) and lateral views of the upper esophagus are taken immediately after the ingestion of the effervescent granules. While the patient drinks the barium, the radiologist both observes and performs rapid sequence images (3 to 4 per second) because the barium usually passes through the esophagus too fast for the radiologist to time the exposure correctly. Therefore functional information (i.e., a cricopharyngeus spasm) and morphological disease can be obtained at the same time.
The use of nonionic water-soluble contrast medium, instead of barium, is warranted when there is any risk of aspiration or esophageal leak. Although barium is inert and not toxic if inhaled, it may remain within bronchi for an extended period of time. Ionic contrast medium within the bronchi is hyperosmolar and can cause pulmonary edema and generally should not be used for esophageal examination. Barium is also toxic within the mediastinum and peritoneum, hence the use of nonionic contrast medium if esophageal perforation is suspected. Water-soluble contrast medium, which is less dense than barium, may not identify small leaks. If no initial leak or aspiration is identified, it is then prudent to follow the examination with denser barium, which may identify a small, contained leak. Even if there is some leakage of barium in these circumstances, it will likely be small, given that water-soluble contrast medium failed to identify any leakage.
Contrast studies of the esophagus (including any viscus) are often effective at characterizing the nature of the lesion or abnormality. Extrinsic (extraluminal) masses tend to displace the bowel because of their mass effect and demonstrate shallow, or obtuse, margins on contrast studies (Fig.1-2). Masses that originate in the submucosa (or have an intramural origin) tend to demonstrate sharper, less obtuse margins (Fig. 1-2). Mucosal masses tend to demonstrate acute margins, sometimes pedunculated and sometimes with a stalk. Furthermore, the intraluminal contrast appearances can suggest malignancy or benignity because malignant lesions tend to demonstrate abrupt, sharp margins that are usually irregular (sometimes termed shouldering) and are often short (Fig. 1-2). Benign lesions, on the other hand, demonstrate smoother borders with little irregularity, although some larger lesions may ulcerate as they outgrow their vascular supply. These rules of thumb generally apply to the entire gastrointestinal (GI) tract.
Figure 1-2 Schematic representation of extraluminal (A), submucosal (B), mucosal (C), malignant (D), and benign (E) mass features in contrast imaging of the GI tract.
Computed Tomography
Computed tomography (CT), although still important in the evaluation of esophageal disease, is not the investigation technique of choice for most diseases unless the patient has esophageal malignancies for which it is used for staging purposes. CT can also be used to evaluate extraluminal or submucosal masses that may impinge on the esophagus because these cannot be observed directly by barium or endoscopic studies. It is also used to evaluate traumatic conditions of perforation, which are iatrogenic, traumatic, or spontaneous. Ideally the patient is asked to drink a cup of contrast material immediately before the CT to delineate the lumen.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) has even fewer applications in the esophagus given that respiratory motion artifacts are common when the chest is evaluated with MRI, although it may serve to evaluate mediastinal and paraesophageal abnormalities when CT is not indicated.
Endoscopic Ultrasound
Endoscopic ultrasound has a role in evaluation of submucosal esophageal masses but is rarely performed. Ultrasound has little use otherwise in the esophagus.
Nuclear Medicine
Nuclear medicine still has a role in the functional examination of esophageal motility and reflux disorder, particularly in children. The patient swallows technetium-99m (99mTc) sulfur colloid, and multiple dynamic views are taken to assess esophageal transit time, particularly in patients with lower esophageal sphincter abnormalities. This test may be used in patients who cannot tolerate manometric endoscopic studies. 99mTc pertechnetate is also used, particularly in children. After the patient swallows the radiolabelled liquid, multiple dynamic images are obtained for the evaluation of gastroesophageal reflux disease (GERD) or delayed gastric emptying. In an adult, however, the use of positron emission tomography (PET) or PET/CT has become more widespread. The use of PET or PET/CT in the evaluation of the esophagus itself is limited because most primary malignancies can be evaluated directly with endoscopy or by CT. However, PET or PET/CT has proved to be particularly useful in the staging and follow-up assessment of extraesophageal disease, mainly regional lymphadenopathy, which endoscopy cannot see, and CT often cannot determine whether the node is metastatic or benign, particularly if it is small.
Diverticula
Zenker Diverticulum
Zenker∗ diverticulum is a pulsion diverticulum, usually seen in the elderly, that is due to prolonged intraluminal pressure pushing the esophageal mucosa and submucosa through the medial defect (Killian dehiscence) between the horizontal and oblique fibers of the inferior constrictor muscle at the pharyngoesophageal junction. Patients usually have evidence of esophageal dysmotility and GERD. Patients usually present because of dysphagia, halitosis, and sometimes aspiration pneumonia as fetid food becomes trapped in the diverticulum and steadily enlarges it.
Zenker diverticulum is confirmed at barium swallow as a contrast-filled sac that is posterolateral to the esophagus just above C5-6 and the cricopharyngeus muscle. When it is small, Zenker diverticulum is usually detected best in the true lateral position as a small posterior outpouch, but as it enlarges, it is easy to identify as it extends laterally to avoid the cervical spine (Figs. 1-3 and 1-4). The larger the diverticulum, the greater the compression on the normal esophagus, which can become narrow.
Figure 1-3 Lateral UGI swallow in a 76-year-old woman with a small Zenker diverticulum (arrow) with a peanut lodged inside.
Figure 1-4 Left posterior oblique barium swallow in a 69-year-old man with a large outpouching (arrow) from the left esophagus due to a Zenker diverticulum.
There is an increased incidence of ulceration and carcinoma developing in the diverticulum. Perforation can also occur in patients because of the inadvertent placement of endoscopic instruments or nasogastric tubes.
Killian-Jamieson Diverticulum
Killian-Jamieson∗ diverticula are rare; they are observed below the level of the cricopharyngeus muscle, anterolateral to the cervical esophagus. They are also pulsion diverticula through the Killian-Jamieson space (similar to Zenker diverticula) but are much smaller than most Zenker diverticula and therefore produce symptoms and complications less commonly. They are seen as small, rounded, smooth outpouches of the lateral upper esophageal wall (Fig. 1-5). Rarely, they can be large and sometimes confused with Zenker diverticula and can even be observed with CT (Fig. 1-6).
Figure 1-5 AP (A) and lateral (B) barium swallow in a 78-year-old woman with residual contrast on either side of the upper esophagus (arrows) due to a Killian-Jamieson diverticula.
Midesophageal Diverticulum
Midesophageal diverticula are usually anterior, occurring at the level of the carina. They either are due to traction from fibrotic disease in the mediastinum (i.e., healed granulomatous disease), which retracts the whole esophagus toward the fibrotic process, or, more commonly, are due to pulsion from increased intraesophageal pressure (Figs. 1-7 and 1-8). Traction diverticula in a UGI swallow are usually narrow or triangular with a pointed apex toward the mediastinal disease. Pulsion diverticula typically have a much wider neck, are larger, and fail to empty of barium easily because they have no muscular layer (Fig. 1-9). Most patients with pulsion diverticula have evidence of motility disorders.
Figure 1-7 UGI swallow in a 70-year-old man with a small midesophageal traction diverticulum (large arrow) from prior tuberculous mediastinal adenopathy. There is also a tracheoesophageal fistula (small arrow).
Figure 1-8 UGI swallow in a 66-year-old man with a small midesophageal pulsion diverticulum (arrow).
Figure 1-9 Coronal (A) and axial (B) contrast-enhanced CT in a 66-year-old man with a midesophageal pulsion diverticulum (arrow). Contrast freely refluxes through the wide-necked orifice (arrow).
Epiphrenic Diverticulum
Epiphrenic diverticula are pulsion diverticula (i.e., the result of increased intraluminal pressure), are found most commonly just cephalad to the GE junction, and are more common in elderly patients with esophageal dysmotility. Most are discovered incidentally, but symptoms include dysphagia, reflux, and aspiration. At a UGI examination, there are obvious wide-necked outpouches in the expected location, and they can be very large (Figs. 1-10 and 1-11).
Figure 1-10 UGI swallow in a 59-year-old man with an epiphrenic diverticulum (arrow).
Figure 1-11 Axial (A) and coronal (B) CT in a 77-year-old man with a large, wide-mouthed (arrow) epiphrenic diverticulum.
Intramural Pseudodiverticula
Intramural pseudodiverticula are dilated mucous glands rather than true diverticula. These are seen as single, or more usually multiple, small, flask-like outpouchings from the esophageal lumen. They are associated with GERD and secondary stricture formation. They may be missed at esophagogastroduodenoscopy (EGD) and only observed at a UGI examination as numerous highly characteristic tiny outpouches from the esophageal lumen, typically at right angles (Fig. 1-12). When they are viewed en face, they can be mistaken for ulcer disease, but they are readily classified when viewed in the lateral plane.
Figure 1-12 Esophageal barium swallow study in a 66-year-old man with multiple pseudodiverticula (arrow) and stricture due to chronic reflux esophagitis.
Esophageal Webs and Rings
Esophageal webs and rings are usually located in the anterior upper esophagus and result from a variety of causes, which are either idiopathic or secondary to fibrosis from pemphigoid and epidermolysis bullosa, eosinophilic esophagitis, celiac disease, graft-versus-host disease, and Plummer-Vinson∗ syndrome (Figs. 1-13 and 1-14). The latter is associated with iron deficiency anemia, angular stomatitis, atrophic glossitis, and dysphagia. With lateral views with a UGI examination, these webs are seen as thin (web-like) defects at right angles to the direction of the esophageal lumen, which are usually shelf-like but can be circumferential (Fig. 1-15). Many webs are asymptomatic but can cause dysphagia. Sometimes an anterior web is combined with either posterior osteophyte impression or cricopharyngeal spasm (Fig. 1-16).
Figure 1-13 UGI swallow in a 39-year-old woman with epidermolysis bullosa and several circumferential esophageal webs (arrow).
Figure 1-14 Barium swallow of the cervical esophagus in a 44-year-old woman demonstrates an anterior esophageal web (arrow).
Figure 1-15 UGI swallow of the upper esophagus in an 84-year-old woman with a circumferential web (arrow).
Figure 1-16 UGI of the cervical esophagus in a 60-year-old man demonstrating an anterior web (large arrow) and posterior impression (small arrow) due to cricopharyngeus spasm.
Webs can also be identified in the lower esophagus secondary to chronic GERD and are usually due to Schatzki ring. This is a relatively common finding seen in about 10% of the population and is usually asymptomatic, although about 30% of patients experience dyspeptic symptoms. It is caused by an inflammatory reaction from GERD to the esophageal B-ring, which develops a concentric narrowing resulting in luminal stricture formation, which if 13 mm or less, will likely produce symptoms. Wider rings may or may not be asymptomatic.
The rings are visualized as fixed and smooth associated with a small hiatal hernia below the rings during fluoroscopic observation after the patient swallows thin barium (Fig. 1-17). The rings can be missed on upright swallowing studies and are best elicited with the patient in the prone oblique position, the position most likely to distend the distal esophagus. The diameter of the rings can be confirmed by the patient’s swallowing a 13-mm pill in the upright position. Narrowing to 13 mm or less is considered significant, at which point the pill will become stuck at the B-ring (Fig. 1-17).
Figure 1-17 A, Barium swallow in a 64-year-old man with a Schatzki ring (short arrow). There is a small hiatal hernia with prominent gastric folds (long arrow). B, A 13-mm pill (arrowhead) failed to pass through the lower esophageal stricture.
Inflammatory Esophagogastric Pseudopolyp or Fold
An inflammatory esophagogastric pseudopolyp or fold is an extension of a thickened gastric fold protruding up into the lower esophagus and mimics the appearance of a polyp (it is sometimes termed a sentinel polyp) (Fig. 1-18). GERD is usually associated. If the fold is excessively large, a biopsy is recommended to exclude adenocarcinoma at the GE junction.
Figure 1-18 Barium swallow demonstrating mild B-ring (Schatzki) narrowing (arrows) and an inflammatory pseudopolyp (arrowheads).
Hiatal Hernias
Hiatal hernias are actually an extension of the stomach into the chest as opposed to a primary esophageal abnormality. They are differentiated into sliding (axial) or rolling (paraesophageal) types. In the former, which are far more common (up to 95% of all hiatal hernias), the upper gastric cardia and B-ring (lower esophageal mucosal ring) “slide” up through the diaphragmatic hiatus, typically more than 2 cm. The GE junction therefore lies above the diaphragm in the chest. Most sliding hernias are small and may not be observed at UGI contrast studies unless the patient is examined carefully (usually in the prone oblique position), and many are self-reducible in the erect position. Their significance, even when small, is that patients can have GERD with the resulting symptoms and potential complications. The typical sliding hernia at UGI study demonstrates several cardiac folds passing up into the chest, which may reduce back into the stomach when the patient is upright (Fig. 1-17). There may be a kink in the hiatal hernia because of compression by the adjacent diaphragm. Sliding hiatal hernias can be large with almost the whole stomach being in the chest, but the antrum pylorus remains within the abdomen (Fig. 1-19).
Figure 1-19 Chest radiograph in a 56-year-old man with a large hiatal hernia (large arrows) and gastric fluid level (small arrow). Most of the stomach resides in the chest.
Far less common are paraesophageal hernias (rolling hernias) in which the GE junction remains within the abdomen, so reflux is much less likely to occur compared with sliding hiatal hernias. Rather, the gastric fundus passes up into the chest and lies to the left of the lower esophagus (Fig. 1-20). These are generally irreducible but are more likely to be asymptomatic compared with sliding hiatal hernia, due to GERD in the more common sliding hernias. On the other hand, a variant of the paraesophageal hernia occurs when the whole stomach lies “upside down” in the chest because of volvulus, which may be obstructing or nonobstructing (see “Gastric Volvulus” in Chapter 2) and which is at greater risk of strangulation and perforation (Fig. 1-21). This is also the case with the even rarer combination of a sliding hernia and paraesophageal hernia, whereby the GE junction lies in the chest along with the gastric cardia (Fig. 1-22). Therefore, the GE junction lies in the chest with the herniated gastric fundus lying alongside and to the left of the lower esophagus.
Figure 1-20 Barium swallow in a 48-year-old woman with a paraesophageal hernia (arrow).
Figure 1-21 UGI series (A) and coronal noncontrast CT (B) in a 52-year-old woman with a nonobstructing organoaxial volvulus resulting in an “upside down” stomach.
Figure 1-22 UGI series in an 86-year-old woman with a sliding hernia with the GE junction in the chest (large arrow) and paraesophageal hiatal hernia (small arrow).
Although hernias are best appreciated by UGI series, they are frequently visualized incidentally by CT, which will demonstrate a dilated lower esophagus (actually represents the gastric cardia in the chest) in the lower chest with a variable proportion of mesenteric fat surrounding the herniated stomach (Fig. 1-23). Consequently, there is a slight widening of the diaphragmatic hiatus (>15 mm). A paraesophageal hernia can also be appreciated with the herniated cardia lying alongside the lower esophagus (Fig. 1-24).
Figure 1-23 Axial (A) and coronal (B) contrast-enhanced CT in a 77-year-old woman with a sliding hiatal hernia (arrows).
Figure 1-24 UGI swallow (A) and axial (B) and coronal (C) noncontrast CT in a 60-year-old woman with a combined sliding and paraesophageal hernia (arrows). At CT the GE junction is in the chest.
Extramural Esophageal Impressions
Extramural esophageal impressions cause smooth and obtuse impressions on the esophagus similar to the extramural masses throughout the GI tract. Most causes are benign (Table 1-1). External malignant masses may ultimately distort the mucosal contour but only after transmural metastatic invasion.
Table 1-1
Extrinsic Esophageal Masses
| Benign | Malignant |
| Postcricoid impression Cricopharyngeal spasm Cervical osteophytic disease Retropharyngeal masses (e.g., goiter) Cardiomegaly Vascular anomalies (aberrant vessels, aneurysms, vascular rings) Mediastinal adenopathy (e.g., tuberculosis) |
Mediastinal adenopathy (metastases) Lung cancer Lung metastases |
Postcricoid Impression
Also known as postcricoid defect of pharyngeal venous plexus, postcricoid impression is common and not pathological, and it is caused by redundant hypopharyngeal mucosa overlying the central pharyngeal venous plexus positioned approximately at the level of C6, just below the cricoid cartilage. It varies in appearance (sometimes smooth, sometimes web-like) and is recognized by its anterior location on the esophagus.
Cricopharyngeal Spasm
This posterior esophageal impression is secondary to hypertrophy and spasm of the cricopharyngeus muscle, the lower portion of the inferior pharyngeal constrictor muscle located posteriorly at the level of C5-6 vertebral body (Figs. 1-16 and 1-25). Normally, after the primary peristaltic wave is initiated, the cricopharyngeus muscle relaxes, allowing the food bolus to pass. Failure to relax due to hypertrophy or spasm is a relatively common cause of dysphagia because the protruding muscle causes localized esophageal dysmotility and relative stricture formation. Usually, symptoms are relatively mild (many patients do not present to their physician) but can result in more marked symptoms depending on the severity of the muscular protrusion. A Zenker diverticulum may ultimately result from the localized increased intraesophageal pressure.
Figure 1-25 UGI swallow in a 56-year-old man with cricopharyngeus spasm (arrow).
Vertebral Osteophytic Disease
Anterior vertebral osteophytes or, rarely, anterior cervical disc herniation can cause discrete posterior esophageal indentations, which are usually smooth and sometimes marked (Fig. 1-26).
Figure 1-26 UGI swallow in a 75-year-old woman with pharyngeal anterior displacement due to vertebral osteophyte disease (arrow).
Retropharyngeal Masses
The cervical esophagus abuts the vertebral bodies, so pharyngeal disease that extends inferiorly and posterior to the esophagus will produce esophageal deviation. Such retropharyngeal masses include goiter, abscess, hematoma, lymphadenopathy, and parathyroid enlargement (Figs. 1-27 and 1-28).
Figure 1-27 UGI swallow in a 46-year-old woman with extramural compression of the esophagus (arrow) due to a goiter.
Figure 1-28 UGI swallow (A) and sagittal noncontrast CT (B) in a 54-year-old woman with extramural compression and deviation of the esophagus due to a retropharyngeal abscess that contains gas (arrows).
Vascular Impressions
Normally the aortic arch and left main bronchus cause smooth external compressions of the esophagus. However, ectatic or aneurysmal dilatation can cause deviation of the esophagus. There are also several congenital vascular anomalies that produce esophageal compressions, which are generally smooth and obliquely angled. Their diagnoses should be suspected by their location either by UGI examination or CT, although contrast-enhanced CT (CECT) (or MRI) will delineate the exact origin and course of the aberrant vessels.
A double aortic arch, the most common form of vascular ring, passes on both sides of the trachea and joins posterior to the esophagus. Barium studies of the esophagus demonstrate bilateral impressions anteriorly and a smooth posterior impression. A right-sided aortic arch, of which there are several types, is recognized by smooth leftward displacement of the barium-filled esophagus in the midthoracic region.
An aberrant right subclavian artery occurs in approximately 1 in 200 individuals and is due to the aberrant origin of the right subclavian artery, usually from a left-sided aortic arch, such that the vessel now has to reach the right axilla by crossing behind the esophagus at an oblique angle. Less commonly, it arises from a right aortic arch. It may be asymptomatic but can cause dysphagia (also known as dysphagia lusoria∗). The diagnosis is best made by arterial phase CT where the aberrant vessel is readily observed crossing behind the esophagus (Fig. 1-29). At UGI examination, there is a classic smooth posterior impression angled upward from the left to the right (Fig. 1-29). An aberrant left subclavian artery is part of a right-sided arch and has similar, but reverse, findings to an aberrant right subclavian artery because it passes from the right and behind the esophagus as it traverses toward the left axilla (Fig. 1-30).
Figure 1-29 AP (A) and lateral oblique (B) UGI swallow and axial (C) and coronal (D) contrast-enhanced CT in a 35-year-old man. UGI demonstrates a slanting esophageal impression due to an aberrant right subclavian artery (arrows, A and B). CT demonstrates the aberrant vessel passing posterior to the esophagus on the axial view and cephalad to the right on coronal MIP (maximum intensity projection) imaging (arrows, C and D).
Figure 1-30 AP (A) and lateral (B) barium swallow in a 17-year-old male adolescent with aberrant left subclavian artery. The vessel passes posteriorly and obliquely up and to the left of the esophagus (arrows).
An aberrant left pulmonary artery is an anomaly resulting from the left lung being supplied from the right pulmonary artery, rather than the left pulmonary artery. Because of the location of its origin, this aberrant left pulmonary artery has to cross to the left side of the mediastinum and in doing so causes an anterior extrinsic compression of the thoracic esophagus at the level of the carina, giving the name to the so-called pulmonary sling.
Extramural Mediastinal Masses
Mediastinal lymphadenopathy (benign or malignant) can cause anterior extrinsic impressions on the esophagus, which it may deviate if it is large enough. Other mediastinal masses that cause anterior esophageal impressions include bronchogenic and duplication cysts. Cardiomegaly, particularly left atrial enlargement, causes esophageal deviation if it is significantly dilated. Traction anomalies, including pulmonary fibrotic disease, also cause esophageal deviation (Fig. 1-31).
Figure 1-31 UGI swallow in a 56-year-old man with right-sided esophageal deviation (arrow) due to traction from diffuse right-sided fibrotic pulmonary tuberculosis.
Submucosal Esophageal Masses
Esophageal submucosal masses cause smooth esophageal impressions but are less obtuse than extraluminal masses. There are several well-recognized causes, but appearances at UGI series usually cannot be distinguished from one another (Table 1-2). CT may help, but small, benign masses generally cannot be differentiated, either. However, when masses are malignant or large, some CT features can aid the diagnosis.
Table 1-2
Esophageal Submucosal Masses
| Benign | Malignant |
| Varices | Metastases |
| Cyst | Lymphoma |
| GIST | Kaposi sarcoma |
| Hemangioma | Malignant GIST |
| Lipoma | |
| Neurofibroma | |
| Fibrovascular polyp | |
| Granular cell tumor |
GIST, Gastrointestinal stromal tumor.
Benign Submucosal Masses
Esophageal Varices
Esophageal varices are most commonly secondary to increased portal venous pressure (usually hepatic cirrhosis) with varices in the lower esophagus; these are sometimes termed uphill varices because of their caudal to cephalad direction of blood flow. Increased venous pressure is relieved by diverting blood away from the obstruction to the lower pressure of the esophageal venous system, usually the middle to lower third of the esophagus (Fig. 1-32). Venous return from the portal vein is via the coronary vein (left gastric) into the lower esophageal plexus with blood flowing with a cephalad direction and then from esophageal veins into the azygous vein and superior vena cava (SVC). As part of the same venous plexus, it is often associated with gastric fundal varices.
Figure 1-32 UGI examination (A) and axial contrast-enhanced T1-weighted MRI (B) in a 53-year-old man with a serpiginous esophageal filling defect caused by large esophageal varices (arrows), a complication of cirrhosis. Note the liver atrophy and diffuse ascites.
The far less common “downhill” varices form from the upper to middle third of the esophagus and are secondary to superior vena caval obstruction. Blood in “downstream” varices enters the upper esophageal plexus in a caudal direction of flow and reenters the SVC through the azygos in the thoracic esophagus. If the azygos is also obstructed (or the lower SVC), then blood continues in a caudal direction to connect with the coronary vein, then the portal system, and finally the inferior vena cava (IVC). Varices in these circumstances occur along the length of the entire esophagus.
Despite the increased venous pressures that precipitate esophageal variceal formation, esophageal varices are best visualized with the patient horizontal because the venous pressure in the upright position is not sufficient to distend the varicosities. Aside from EGD, they are best visualized when the patient is prone while drinking barium as serpiginous submucosal impressions either in the lower (uphill) or mid to upper (downhill) esophagus. They are also usually well visualized by contrast-enhanced CT or MRI, particularly in the portal venous phase after contrast enhancement as prominent submucosal contrast-filled venous plexuses (Fig. 1-32). Without the use of intravenous (IV) contrast, the esophageal wall will simply appear thickened and therefore difficult to differentiate from other esophageal abnormalities. The findings need to be differentiated from varicoid carcinoma that can also present with serpiginous submucosal fold findings (Fig. 1-33).
Figure 1-33 UGI swallow of the lower esophagus in an 84-year-old man with an infiltrative esophageal adenocarcinoma extending for several centimeters with a varicoid pattern (arrow).
Esophageal Cysts
Esophageal cysts represent foregut duplication cysts (congenital) or retention cysts (acquired). The former are usually discovered incidentally, whereas the much rarer retention cysts may be more symptomatic, arising from dilated mucous glands, usually in the distal esophagus.
At UGI, both types appear as submucosal defects, although foregut cysts may calcify and barium may occasionally fill the retention cyst, giving the appearance of a smooth and rounded mass. They are better visualized at CT as smooth submucosal hypodense lesions (Fig. 1-34).
Figure 1-34 Axial contrast-enhanced CT in a 10-year-old girl with a hypodense 1.8-cm mass (arrow) contiguous with the esophagus due to an esophageal duplication cyst.
Esophageal Submucosal Benign Tumors
Common to all these masses is their intramural or submucosal origin (Table 1-3). They therefore cause esophageal narrowing, which at UGI examination is represented by an intraluminal mass with slightly obtuse margins and generally smooth surface. Differentiation between different diagnoses by imaging alone can be difficult, and the final diagnosis is usually made after surgical resection and histological evaluation (Fig. 1-35). They vary considerably in size with gastrointestinal stromal tumors (GISTs) being the largest (up to 10 cm in diameter) (Fig. 1-36). The masses are generally well outlined by barium en face, and the overlying mucosa may ulcerate (as evidenced by barium pooling in the center of the mass) as they grow.
Table 1-3
Submucosal Benign Esophageal Tumors
| Tumor type | Features |
| GIST | Most common; smaller; may contain amorphous calcification at CT; can be large |
| Hemangioma | Reddish blue multinodular mass |
| Lipoma | Fat density on CT |
| Neurofibroma | May be associated with disease in multiple anatomical sites |
| Granulosa cell tumor | Broader-based mass |
| Hamartoma | Contains multiple tissue types (bone, cartilage, fat, muscle) |
CT, Computed tomography; GIST, gastrointestinal stromal tumor.
Figure 1-35 Single- (A) and double-contrast (B) UGI series and axial (C) and coronal (D) contrast-enhanced CT views in a 50-year-old man with a smooth submucosal esophageal impression (arrows) due to a GIST.
Figure 1-36 AP (A) and lateral (B) UGI swallow in a 31-year-old woman with a large submucosal esophageal impression (arrows) due to a GIST.
Fibrovascular Polyp
Fibrovascular polyp is an unusual, benign, submucosal neoplasm of the mid and upper esophagus and consists of fibrovascular and adipose tissue (Fig. 1-37). It may have a long stalk that then elongates in tubular fashion down the length of the esophagus. It sometimes bleeds and can be so long that it can be regurgitated into the pharynx, rarely obstructing the larynx.
Figure 1-37 AP (A) and lateral (B) UGI swallow in a 50-year-old man with an irregular filling esophageal defect due to a fibrovascular polyp (arrows).
Submucosal Hemorrhage
Submucosal hemorrhage is usually iatrogenic from endoscopic procedures or nasogastric tube placement but can be spontaneous in patients with bleeding disorders. The appearances are rarely observed at barium studies but are identified at CT, usually as a circumferential esophageal soft tissue mass, which may be hyperdense if imaged shortly after the acute hemorrhagic event (Fig. 1-38).
Figure 1-38 Axial contrast-enhanced CT in a 66-year-old woman with esophageal hematoma and acute hemorrhage (arrow).
Malignant Submucosal Masses
These masses are rare and include metastases (most commonly melanoma, lymphoma, breast) or primary tumors, including sarcomas, mainly Kaposi sarcoma, or malignant GISTs. They often cause mucosal irregularity and ulceration if they invade through the muscularis mucosae and into the mucosa.
Mucosal Abnormalities
Both benign and malignant mucosal abnormalities are well delineated by good single- and double-contrast technique (Table 1-4). Normal esophageal mucosal folds are mostly longitudinal and extend the length of the esophagus and are best seen on collapsed rather than distended double-contrast views at UGI examination (Fig. 1-39). Conversely, transverse folds, which are also normal, are more difficult to identify and are better seen on double-contrast views. Transverse folds in the esophagus, when observed, are sometimes referred to as a feline esophagus, mimicking the normal esophageal folds observed in cats (Fig. 1-40). Thickened edematous benign folds are often seen with esophagitis from any cause, the most common being GERD (Fig. 1-41).
Table 1-4
Esophageal Mucosal Abnormalities
| Benign | Malignant |
| Esophagitis (peptic, infectious, caustic, inflammatory, drugs, iatrogenic, radiation, Crohn, Behçet) Ectopic gastric mucosa Neoplastic (leukoplakia, squamous papilloma) Glycogenic acanthosis Tylosis Epidermolysis bullosa/pemphigoid |
Esophageal carcinoma Kaposi sarcoma Malignant GIST Metastases |
GIST, Gastrointestinal stromal tumor.
Figure 1-39 Barium swallow demonstrating multiple longitudinal esophageal folds.
Figure 1-40 UGI swallow in a 77-year-old man with multiple fine transverse folds due to a feline esophagus. There is slight aspiration in the trachea and left main bronchus (arrow).
Figure 1-41 UGI swallow in a 56-year-old man demonstrating thickening longitudinal esophageal folds and subtle nodular change (arrows) due to reflux esophagitis.
Benign Mucosal Disease
Esophagitis
Esophagitis represents the most common mucosal abnormality in clinical practice predominantly because it is due to a wide variety of causes (Table 1-5). Barium studies can be diagnostic and should be performed if endoscopy is contraindicated. Some findings are subtle, and close observation of the whole esophagus is mandatory. Once an abnormality is identified, additional spot views in multiple tangential planes should be taken to maximize the ability of the examination to define the precise cause.
Table 1-5
Causes of Esophagitis
| Infectious | Herpes Candida infection CMV HIV Fungal infection Tuberculosis |
| Iatrogenic | Radiation therapy Nasogastric tube |
| Drugs | Tetracycline Nonsteroidal antiinflammatory drug Potassium Iron |
| Chemical | Reflux esophagitis Corrosives |
| Inflammatory | Crohn disease Scleroderma Pemphigoid Epidermolysis bullosa |
CMV, Cytomegalovirus; HIV, human immunodeficiency virus.
Infectious Esophagitis
Infectious esophagitis is most commonly identified in the immunocompromised host (from any cause) and includes herpes simplex, candidiasis, and cytomegalovirus (CMV).
Candida albicans causes the most common infectious esophagitis, which presents with diffuse and painful dysphagia. Most patients are immunosuppressed from either chemotherapy or immune deficiencies, particularly human immunodeficiency virus (HIV), and it is a relatively common manifestation in patients with acquired immune deficiency syndrome (AIDS). The disease may coexist with herpes or CMV esophagitis. Patients with disorders of esophageal motility and the resulting stasis (scleroderma, achalasia, and strictures) are also at risk for Candida infection. As its name suggests, the esophageal mucosa is coated with diffuse white (albicans) plaques, which can be present from the tongue (oral thrush) to the lower esophagus. Gastric hyperacidity generally prevents it from spreading below the GE junction.
The imaging findings may lag clinical findings, either with the onset of disease or after treatment (oral antifungal agents are highly effective at treating the disease). When imaging findings are present, they are usually seen from the mid to upper esophagus with multiple and diffuse raised mucosal plaques, sometimes with pseudomembranes and ulcer formation with severe disease (Fig. 1-42). The appearances can sometimes be confused with glycogenic acanthoses, which have randomly deposited mucosal abnormalities, whereas a Candida infection tends to have linear mucosal plaques (Figs. 1-42 and 1-43).
Figure 1-42 UGI swallow in 43-year-old woman undergoing chemotherapy for breast cancer and Candida esophagitis. There is a “shaggy,” plaque-like appearance to the esophageal mucosa.
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