Tertiary contraction of the esophagus. Uncoordinated contractions are seen in the mid to distal esophagus (arrows)
Dysphagia may be caused (Table 6.1) by a neurological deficit, which is temporary with expected recovery, such as seen with a transient ischemic attack (TIA) or a cerebrovascular accident (CVA) , progressive as in neuromuscular conditions such as scleroderma or multiple sclerosis, or more static conditions which include the post polio syndrome. In scleroderma, the esophageal smooth muscle is replaced by fibrous tissue resulting in diminished peristaltic activity and resultant dysphagia (Fig. 6.2). Esophageal dysmotility may be seen in the elderly where it is known as presbyesophagus. In this condition, there is inefficient propulsion of the food bolus due to tertiary contractions in the esophagus. These result in uncoordinated contractions of the esophagus with resultant dysphagia and at times heartburn. Cognitive disability or psychosis may also result in dysphagia. Certain radiological tests are useful in distinguishing between the various abnormalities.
Scleroderma. Featureless esophagus due to markedly diminished peristaltic activity
Structural or obstructive causes of dysphagia can be accurately diagnosed with radiological tests. These include esophageal webs, diverticula, Schatzki rings, strictures, neoplasms, or an obstructed foreign body. Esophageal diverticula are outpouchings of the esophageal wall that occur at sites of anatomic weakness in the hypopharynx or the cervical esophagus adjacent to the cricopharyngeus muscle . Achalasia is a condition wherein both neurological and obstructive etiologies come into play  (Fig. 6.3a, b). A Schatzki ring is a mucosal ring in the distal esophagus at the squamocolumnar junction. This may or may not be symptomatic based on its luminal diameter. Schatzki rings are most often responsible for episodic dysphagia to solid foods. The pathogenesis is unknown and proposed theories include congenital, developmental, and post inflammatory etiologies (Fig. 6.4) . An esophageal web occurs in the proximal esophagus and is usually anterior in location and more often eccentric.
Achalasia (a, b). The proximal and mid esophagus during a double-contrast esophagram (a) shows an overly distended esophagus. A bird beak appearance of the distal esophagus (b) due to non-relaxation of the distal esophageal sphincter
Schatzki ring. A shelf-like indentation in the distal esophagus (curved arrows) which was symptomatic in this patient due to significant narrowing of the esophageal lumen
Causes of dysphagia
Post polio syndrome
Esophageal web and Schatzki ring
Benign or malignant esophageal stricture
Primary or secondary achalasia
The type of examination and frequency or need for a repeat evaluation would depend upon the pathology suspected clinically and subsequently diagnosed radiologically.
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Gamut of Imaging Tests Available in the Evaluation of Dysphagia 
Dynamic assessment: videofluoroscopic swallowing study (VSS) also known as the modified barium swallow (MVS)
Barium swallow and esophagogram
CT scan of the neck and chest
MRI of the neck
Patient Preparation for the Radiological Examination
The patient is advised to stay NPO after midnight prior to a fluoroscopic test. The patient has to be NPO for 4–6 h prior to a CT scan or MRI performed with intravenous contrast. To alleviate anxiety and to improve patient participation and cooperation, it is advisable that the referring clinician inform the patient of the nature and benefit of the examination. Any contraindications or limitations such as radiographic contrast allergy or renal dysfunction are sought out in a screening questionnaire at the time of scheduling the examination. In cases of minor contrast allergy, the patient would be pretreated with oral prednisone and diphenhydramine. At our facilities we use a 16-h pretreatment protocol where the patient receives 50 mg oral prednisone at 8 h intervals with the last dose of prednisone taken along with 50 mg diphenhydramine within 30 min of contrast administration. When the patient arrives in the radiology department, he/she is then informed in detail about the procedure. Patient participation with regard to holding still is communicated to the patient by the radiology technologist just prior to the procedure being performed and again at the precise moment when the patient is needed to comply with this request.
Videofluoroscopic Swallowing Study (VSS)
Procedure: The patient is positioned seated facing laterally facing the speech pathologist (Fig. 6.5). Various consistencies of liquid barium and barium-coated solid foods are used to test the patient’s swallowing ability. This test is performed in conjunction with the speech and swallowing therapist, thereby allowing the therapist the opportunity to assess the patient for the potential usefulness of and the type of swallowing therapy to be utilized.
Patient positioned facing the speech pathologist with the image intensifier lateral to the patient so as to obtain a lateral view of the oral cavity and pharynx during VSS
The following conditions may be diagnosed with this test:
Laryngeal vestibular penetration or frank aspiration (Fig. 6.6).
Aspiration. Lateral view (a) of the pharynx and larynx with aspiration of barium which has penetration below the level of the vocal cords (arrow). P pyriform fossa, T subglottic trachea. AP view of the neck and chest (b) shows aspiration of barium into the right main and lower lobe bronchus (curved arrow)
If aspiration is detected, if silent or with elicitation of a cough reflex
Objective severity of dysphagia
Lack of elevation of the larynx and closure of the airway, for example, after surgery for head and neck carcinoma
Barium Swallow with Esophagogram
Procedure: Thick barium (barium sulfate suspension 250 w/v) is given orally to the patient with him standing, in order to assess the oropharynx and hypopharynx. This step also allows the evaluation for any aspiration prior to continuing on with the rest of the examination. The patient then swallows effervescent granules chased with small sips of water, following which with thick barium. The air produced by the swallowed granules and the barium create a double contrast within the esophagus with demonstration of excellent mucosal detail of the esophageal lining. This is important in the assessment of mucosal irregularities or ulcerations. Conditions such as reflux esophagitis (Fig. 6.7) or the nature of a stricture, namely, irregular or smoothly contoured, may come to light at this stage of the examination. The patient is now guided into an RAO position on the fluoroscopic table (Fig. 6.8). He drinks thin barium (barium sulfate suspension 70 w/v) in continuous sips with a wide bore straw, so as to maximally distend the esophagus. The position of the patient who is lying on the table in an RAO position allows for the assessment of true peristaltic activity, having eliminated the influence of gravity.
Esophagitis. Punctate foci of barium pooling within the esophageal mucosa in a patient with reflux esophagitis
RAO position during a single-contrast esophagram. The patient drinks thin barium from a wide bore straw while lying in this prone oblique position
The relevant normal anatomy of the pharynx and esophagus as it appears on the barium swallow and esophagogram is reviewed . The pharynx comprises of the oropharynx and hypopharynx which are separated by the pharyngoepiglottic fold. The cricopharyngeus muscle marks the beginning of the esophagus. In the normal pharynx, one sees symmetric valleculae and pyriform sinuses. The valecullae are recesses between the tongue base and epiglottis, divided by the median glossoepiglottic fold (Fig. 6.9). The pyriform sinuses are lateral recesses arising from the lateral laryngeal walls and extending into the hypopharynx bilaterally. The normal esophagus is smoothly contoured, extending from the cricopharyngeus muscle at the C5–C6 levels to the gastroesophageal junction. Smooth linear mucosal folds are observed in a normal esophagus. Saccular termination of the esophagus is physiologic and is termed the esophageal vestibule (Fig. 6.10a–c).
Normal pharyngeal anatomy. A small amount of barium is seen pooling within the valleculae (V) which appear symmetric. The valecullae are separated by the median glossoepiglottic fold (solid straight arrows). Barium also outlines the pyriform sinuses (P). The tongue base is outlined (thin white arrows)
Normal anatomy of the esophagus. (a) Normal mucosal relief in a double-contrast esophagram. (b) Uniformly distended esophagram during a single-contrast esophagram. (c) Appearance of the esophageal ampula which is the normal distended distal portion of the esophagus (arrows)
This test pinpoints the location of a lesion, from the tongue base to the gastrointestinal junction. It also assesses the distensibility of the esophagus at the site of a stricture which is useful information to aid in distinguishing benign from malignant strictures. This is a very useful test to evaluate the success of a dilatation procedure for a benign esophageal stricture and should the patient’s symptoms recur to evaluate the need for repeat intervention.
Differentiating between a fixed peptic stricture (Fig. 6.11) and lack of relaxation of the distal esophageal sphincter in cases of achalasia (Fig. 6.3b) may be confidently accomplished with the help of the esophagram .
Smoothly contoured benign distal esophageal stricture. (a) Peptic stricture (bracket) caused as a result of scarring and fibrosis due to long-standing reflux esophagitis. (b) Holdup of a barium tablet at the stricture
We will now discuss some of the conditions that can be identified using barium swallow and esophagram tests. Lesions at the tongue base, valleculae, or pyriform sinuses cause high dysphagia. Tongue base or vallecular lesions may be detected by flexible endoscopy in the otolaryngologist’s office. However, lesions of the valleculae or pyriform sinuses may at times be first picked up on a barium swallow, obtained by the primary care physician for a patient presenting with early symptoms of dysphagia.
There are several entities that may cause extrinsic compression on the esophagus and thereby result in symptoms of dysphagia. A hypertrophied cricopharyngeus muscle causes indentation of the posterior esophageal wall and thereby results in difficulty swallowing (Fig. 6.12). Cervical vertebral osteophytes along the anterior margins of the vertebral bodies most commonly occur at the C5 to C7 levels. The presence of osteophytes allows less room for esophageal distention when the food bolus approaches that segment of the esophagus (Fig. 6.13a, b). In the mediastinum, an ectasia or aneurysm of the aorta may cause extrinsic compression on the thoracic portion of the esophagus (Fig. 6.14). Mediastinal fibrosis due to a variety of causes including post-radiation fibrosis or following chronic inflammatory disease may limit the distensibility of the thoracic esophagus resulting in dysphagia of varying degrees.
Indentation of a hypertrophied cricopharyngeus muscle (solid arrow) resulting in narrowing of the lumen of the cervical esophagus.
Extrinsic compression by cervical osteophyte. (a) Large anterior marginal osteophytes at C4-C6 (arrow). (b) Cervical vertebral osteophytes in a different patient indenting the barium column during a single-contrast esophagram (asterisk)
Ectatic aortic knob (solid arrow) causes mild narrowing of the cervical esophagus due to an extrinsic compression effect
Esophageal diverticula are outpouching of the esophageal wall. They occur at sites of anatomic weakness in the hypopharynx or cervical esophagus, adjacent to the cricopharyngeus muscle [2, 6]. A Zenker’s diverticulum (Fig. 6.15) is a posterior esophageal diverticulum that occurs along the mid-posterior esophageal wall, just superior to the cricopharyngeus muscle. This is often seen in patients who have a prominent cricopharyngeus muscle. A Killian-Jamieson diverticulum occurs along the anterolateral wall of the cervical esophagus and is inferior to the cricopharyngeus muscle (Fig. 6.16a, b). Radiological findings help distinguish between these diverticula based not only on the posterior or lateral position of the sac but also on the relationship of the diverticulum to the cricopharyngeus muscle. Diverticula may or may not be symptomatic, which is usually based on the size of the diverticulum. The presence of a diverticulum may cause halitosis and dysphagia. Food entrapment within the diverticulum and esophageal dysmotility on account of the diverticulum or delayed reflux of food or liquid from the sac may all contribute to the development of symptoms. A mid-esophageal diverticulum may be formed by mediastinal adhesions and is a traction diverticulum (Fig. 6.17). It is formed due to extrinsic traction occurring as a result of fibrosis and scarring adjacent to the esophageal wall. An epiphrenic diverticulum is a distal esophageal diverticulum along the lateral esophageal wall and is usually a pulsion diverticulum, occurring as a result of asymmetric pressure along the esophageal wall (Fig. 6.18). The epiphrenic diverticulum is often associated with a hiatal hernia.
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