Volume 38, Issue 1 , Pages 17-32, January 2009
Pharyngeal Dysphagia: What the Radiologist Needs to Know
Article Outline
- Abstract
- Anatomy
- Pharyngeal Pouches and Diverticula
- Zenker's Diverticula
- Surgical Treatment of Zenker's Diverticula
- Other Diverticula
- Webs
- Benign Tumors
- Malignant Tumors
- Extrinsic Compression
- Conclusion
- References
- Copyright
Dysphagia is defined as difficulty in swallowing. Oropharyngeal dysphagia is defined as difficulty in moving the bolus from the mouth to the esophagus. The best initial evaluation of suspected oropharyngeal dysphagia is a barium study which can evaluate motility of the oropharynx and hypopharynx and provide double-contrast views that may identify structural or mucosal abnormalities. Pharyngeal diverticula, Zenker's and Killian–Jamieson diverticula, and pharyngeal pouches are readily identified on these studies. Zenker's diverticula are the commonest diverticulum implicated in pharyngeal dysphagia and typically occur in the setting of cricopharyngeal dysfunction. The radiologist must not only diagnose these diverticula but also understand the normal postoperative appearance after diverticulotomy, often confusing for the uninitiated imager. Cervical webs are a common finding in pharyngeal dysphagia and should not be mistaken for a normal postcricoid defect. Other potentially challenging diagnostic issues include correct identification of lingual hyperplasia, which mimics lymphoma, and detection of squamous carcinoma, which is more mass-like but sometimes difficult to see among the complex anatomic lines of the pharynx. All of the above abnormalities are easily differentiated from the retention cyst, the most common “mass” in the pharynx. Pathology extrinsic to the pharynx, such as tumor and cervical osteophytes, can result in secondary symptoms from mass effect. This article discusses the various radiographic findings in normal and abnormal states of the pharynx, an anatomically and functionally complicated segment of the gastrointestinal tract.
The pharynx is a complicated tube and is unique from the remainder of the gastrointestinal tract in that it is involved with respiration, speech, and swallowing. As a result, dysfunction of the pharynx can present with a myriad of symptoms, including choking, globus, and dysphagia.1, 2, 3 It is important to remember that dysphagia is defined as any perception of difficulty with swallowing and does not always indicate stricture or mass.
Anatomy
The pharynx extends from the nasal cavity to the upper esophageal sphincter, the cricopharyngeus.1, 2 It is divided into three regions: nasopharynx, oropharynx, and hypopharynx (FIG 1, FIG 2). It is formed of inner circular and outer longitudinal layers of striated muscle.

FIG 1.
Normal pharyngeal anatomy. Frontal (A), and lateral (B), views reveal vallecula (asterisks), piriform sinuses (arrows), and epiglottis (curved arrow). Note the reticular appearance at the base on the tongue (small arrow); this represents the lingual tonsil.

FIG 2.
Normal MR anatomy. Sagittal MR reveals the three anatomic regions of the pharynx: nasopharynx, oropharynx, and hypopharynx. The nasopharynx is separated from the oropharynx by the soft palate (arrow). The oropharynx is separated from the hypopharynx at the level of the hyoid (curved arrow). The cricopharyngeus, upper esophageal sphincter, is located at the C5-6 vertebral body level and separates the hypopharynx from the cervical esophagus. Vallecula (white asterisk), epiglottis (white arrow), and laryngeal vestibule (V) are easily identified.
The lingual tonsil is located at the base of the tongue and extends to the vallecula. It can undergo hyperplasia (Fig 3),4 which can be difficult to differentiate from tumor such as lymphoma (Fig 4). Lymphoma of the lingual tonsil is rare (10% versus 50-60% in palatine tonsil). Tonsillary lymphoma is almost always non-Hodgkin type and occurs in the elderly.5 Lingual hyperplasia occurs after puberty, often in the setting of chronic allergies or other inflammatory process. It can also be compensatory, such as after tonsillectomy.

FIG 3.
Lingual hyperplasia. (A) Frontal view reveals increased nodularity (asterisk) of the lingual tonsil, extending into the vallecular space (arrow). (B) Note the nodularity is symmetric, uniform, and does not have mass effect, suggesting that it represents hyperplasia and not a mass. True (t) and false (f) vocal chords delineate the intervening laryngeal ventricle (small arrow).

FIG 4.
Lingual lymphoma. Frontal (A), and lateral (B), radiographs reveal increased nodularity of the lingual tonsil. However, unlike hyperplasia, this nodularity is larger, less uniform, and has well-defined, mass-like borders (arrows).
Pharyngeal Pouches and Diverticula
Lateral pharyngeal pouches (FIG 5, FIG 6) are transient protrusions of pharyngeal mucosa through areas of weakness of the lateral pharyngeal wall, most common in the region of the tonsillar fossa or the thyrohyoid membrane, where the superior laryngeal artery and vein perforate the membrane. Pouches are more common in the elderly, are typically bilateral, and in almost all cases are asymptomatic. Pharyngeal diverticula (Fig 7) persist and are most common in wind instrument players, glass blowers, etc, secondary to prolonged increased pharyngeal pressure. They are usually unilateral and can be symptomatic, with choking, cough, dysphagia, and regurgitation.

FIG 5.
Pharyngeal pouch. Frontal radiograph reveals bilateral, small pharyngeal pouches (arrows). Pouches are transient, present only with increased pharyngeal pressure, such as during Valsalva, phonation, or swallowing. They are almost always asymptomatic.

FIG 6.
Asymmetric pharyngeal pouches. Frontal spot image reveals small left pharyngeal pouch (arrow) and even smaller right protrusion (small arrow).

FIG 7.
Pharyngeal diverticulum. Frontal radiograph reveals unilateral, persistent pharyngeal diverticulum (arrow) with air–fluid level. These are typically seen in patients with abnormally increased pharyngeal pressure.
Zenker's Diverticula
Zenker's diverticulum is a pulsion diverticulum that arises in the hypopharynx just proximal to the cricopharyngeus. It is most common in older men. Although it protrudes from an intrinsic area of anatomic weakness (Fig 8), it is thought to be secondary to cricopharyngeal dysfunction (Fig 9)6, 7, 8, 9 and resultant elevated pharyngeal pressure. The diverticulum originates in the hypopharynx but extends inferiorly (Fig 10), trapping food and liquid within the sac. The distended sac may compress the cervical esophagus, resulting in dysphagia, halitosis, and regurgitation. Complications include aspiration pneumonia (Fig 11) and, rarely, bleeding, fistula, and development of squamous cell carcinoma secondary to the chronic inflammation. This risk should be considered if there is a sudden increase in symptom severity or hematemesis8, 9 but does not warrant removal in asymptomatic patients.9 Patients with a Zenker's diverticulum are also at increased risk of perforation with endoscopic procedures (Fig 12).

FIG 8.
Killian's dehiscence. Killian's dehiscence (triangle of Killian) located between the inferior pharyngeal constrictors and the cricopharyngeus. It is an area of anatomic weakness in the hypopharynx, serving as the origin of Zenker's diverticula. (Reprinted from van Overbeek,6 with permission from Annals.)

FIG 9.
Cricopharyngeal bar. Lateral radiograph reveals failure of relaxation of the cricopharyngeus (asterisk). Although this patient has not developed a Zenker's diverticulum, ballooning at Killian's dehiscence is seen posteriorly (arrow).

FIG 10.
Large Zenker's diverticulum. Oblique view reveals large Zenker's diverticulum, extending inferiorly and compressing the cervical esophagus.

FIG 11.
Zenker's diverticulum with aspiration. Lateral view reveals moderate size Zenker's diverticulum (asterisk) with flap-like cricopharyngeus (arrows). This is also referred to as the “party” wall, separating the diverticulum from the cervical esophagus. Note aspirated barium (curved arrow) extending along the anterior trachea.

FIG 12.
Perforated Zenker's diverticulum. Lateral radiograph reveals extravasated contrast and gas extending along prevertebral space (arrows) in this patient who had bronchoscopy with perforation of Zenker's diverticulum.
Surgical Treatment of Zenker's Diverticula
Treatment of Zenker's diverticulum may be done by traditional open surgical or endoscopic techniques including the following10, 11:
Since Zenker's diverticulum is thought to arise at least in part as a complication of abnormal relaxation of the cricopharyngeus, cricopharyngeal myotomy has had a long standing history in the treatment of Zenker's diverticula and is usually performed in conjunction with the above procedures.12 However, this does not address the diverticulum itself, which can cause symptomatic compression of the adjacent cervical esophagus. In the past, diverticulum invagination was performed for smaller diverticula, while diverticulopexy (Fig 13) and diverticulectomy were utilized for larger diverticula. Now, endoscopic techniques are allowing intervention with lower morbidity and mortality. This is particularly important since most of these patients are elderly and have other comorbidities.

FIG 13.
Diverticulopexy. Lateral radiograph reveals suspension of the Zenker's diverticulum superiorly (arrow). This improves diverticular emptying and relieves extrinsic cervical esophageal compression, reducing aspiration risk and dysphagia, respectively.
The diverticulotomy was originally described by Mosher in 1917 and subsequently Dohlman in 1935. Diverticulotomy involves division of the common wall located between the hypopharynx and Zenker's diverticulum (Fig 14). It can be performed with cautery, CO2 laser (Fig 15),13 or more recently, a stapler. Preoperative radiographic evaluation is important as it helps determine the most appropriate procedure. Those with small diverticula do not benefit as much with endoscopic stapling.14 Surgical complications include laryngeal nerve damage, perforation, mediastinitis, infection, fistula, pharyngeal stenosis, and recurrence.15 Radiographically, patients who have undergone endoscopic diverticulotomy do not demonstrate a significant anatomical change as the diverticulum has not been resected. In comparing pre- and postoperative patients, ideally, the height of the party wall and fluid level in the diverticulum will be reduced (Fig 16).16 However, this is often difficult to judge and patients should be followed clinically.17

FIG 14.
Endoscopic stapling diverticulotomy. (A) Drawing of a large Zenker's diverticulum demonstrates dysfunctional cricopharyngeus, creating a flap-like party wall between the diverticulum and cervical esophagus. (B) Lateral spot image reveals similar configuration of diverticulum and flap-like cricopharyngeus. (C) Endoscopic stapling device straddles the party wall, with one limb in the esophagus and the other in the diverticulum, simultaneously making an incision in the party wall with three rows of staples along each cut edge (arrows, D). Note, it is recommended that this procedure not be performed for diverticula less than 3 cm, because of purchase needed by the endoscopic device for an adequate cut and staple line. (Color version of figure is available online.)

FIG 15.
Endoscopic CO2 laser diverticulotomy. Endoscopic images reveal party wall before (asterisk) and after (arrows) endoscopic laser division (A and B, respectively). (Reprinted from Takes et al,13 with permission from John Wiley & Sons, Inc.) (Color version of figure is available online.)

FIG 16.
Endoscopic diverticulotomy. (A) Patient before endoscopic diverticulotomy. (B) After diverticulotomy, diverticulum is slightly smaller, but still retains an air–fluid level. Patient's symptoms dramatically improved, although aspiration persists (arrows).
Other Diverticula
Killian–Jamieson diverticula arise from the proximal anterolateral cervical esophagus (Fig 17), also in a location of anatomic weakness. They are smaller, less common, less likely to cause symptoms, and less likely to be associated with secondary aspiration or gastroesophageal reflux disease than Zenker's diverticula.18

FIG 17.
Killian–Jamieson diverticulum. Frontal, A, and lateral, B, radiographs reveal diverticulum (arrow) extending from the anterolateral cervical esophagus. Killian–Jamieson diverticula originate below the cricopharyngeus, unlike the Zenker's diverticula, which originate in the hypopharynx above the cricopharyngeus.
Webs
Webs are thin mucosal folds most frequently located along the anterior wall of the lower hypopharynx and proximal cervical esophagus. Webs appear as 1 to 2 mm in width shelf-like filling defects (FIG 18, FIG 19). Occasionally, webs are circumferential. Cervical webs have been linked to conditions such as gastroesophageal reflux disease, epidermolysis bullosa dystrophica, or benign mucus membrane pemphigoid.19 Some evidence supports an association between cervical esophageal webs and iron deficiency anemia (Plummer–Vinson syndrome), but this is a disease seen in Northern Europe, not the United States. It is important not to confuse the postcricoid defect (Fig 20), a normal variant, with a web. The postcricoid defect is normal redundant mucosa seen along the anterior wall of the hypopharynx. It changes with peristalsis and is not circumferential, unlike webs that are a fixed circumferential or partially circumferential defect.

FIG 18.
Hypopharyngeal web. Lateral radiograph reveals a focal ring-like stricture (curved arrow) in the hypopharynx, at the level of the cricopharyngeus. Note mild proximal ballooning and jet effect (small arrows), suggesting significant narrowing. Also, there is laryngeal penetration (curved arrow).

FIG 19.
Cervical web. Focal ring-like web in the cervical esophagus (arrows) is located caudle to the cricopharyngeus (asterisk).

FIG 20.
Postcricoid defect (arrow). Lobular filling defect along the anterior wall of the hypopharynx should not be confused with a web. This filling defect changes with peristalsis, and there is no proximal ballooning or jet effect to suggest significant stenosis.
Benign Tumors
Although not neoplastic, retention cysts are the most common benign mass lesions in the pharynx (Fig 21).20 They are small, round or ovoid, well-circumscribed, smooth-surfaced submucosal masses, best seen on frontal views of the pharynx. They are typically located in the valleculae or along the aryepiglottic folds. These cysts are thought to result from dilation of mucus glands in the lamina propria or deeper layers due to retained secretions and chronic inflammation. Usually asymptomatic, cysts larger than 1 cm may cause dysphagia.

FIG 21.
Retention cyst. Similar well-defined round filling defect is seen in the left vallecula. Retention cysts are almost always asymptomatic.
Other benign pharyngeal masses may cause dysphagia due to local space-occupying effects. Common lesions encountered are lipomas, papillomas, neurofibromas, fibrovascular polyps, and granular cell tumors. Fibrovascular polyps typically arise near the cricopharyngeus muscle and may be quite long (Fig 22).21, 22 On occasion, these tumors can be regurgitated and have been reported to cause dyspnea or, rarely, asphyxia.23

FIG 22.
Fibrovascular polyp. (A) Esophagram reveals lobular filling defect in the mid and distal thoracic esophagus (long arrow). Note the long stalk, which extends from the hypopharynx, where most fibrovascular polyps originate (short arrows). (B) Intraoperative specimen reveals elongated fibrovascular polyp. (Color version of figure is available online.)
Malignant Tumors
Squamous cell carcinoma is by far the most common malignant tumor of the pharynx. Tongue base squamous cell carcinomas may extend into the valleculae, pharyngoepiglottic fold, or palatine tonsil and may penetrate deep into the tissue of the tongue. Fluoroscopically, ulcerative tumors are seen as irregular contrast collections extending anteriorly, disrupting the normal smooth contour of the tongue base. Polypoid tumors project posteriorly and laterally into the oropharynx and are best demonstrated during phonation (Fig 23). By the time tongue base squamous cell carcinomas are symptomatic, they are usually extensive with nodal metastases, and prognosis is poor.

FIG 23.
Squamous cell carcinoma. (A) Frontal radiograph reveals lobular filling defect in the left vallecula (arrow) with obliteration of the left piriform sinus. (B) Lateral radiograph reveals mass obliterating the entire left piriform sinus (arrows). (C) Cross-sectional imaging reveals mass (asterisk) in left piriform sinus displacing the hypopharynx to the right.
Extrinsic Compression
Dysphagia can sometimes result from extrinsic compression from space-occupying lesions within the pharynx or neck. Bulky lymphadenopathy and vertebral osteophytes24 are common etiologies. Less common sources are benign tumors like lipomas or rare malignant soft-tissue tumors such as sarcomas.
Large syndesmophyte/osteophyte complexes in diffuse idiopathic skeletal hyperostosis can cause pharyngeal dysphagia (“DISHphagia”) (Fig 24).25 There are several mechanisms of dysphagia caused by osteophytes.26, 27, 28, 29 First, large osteophytes cause direct mechanical blockage of the esophagus or hypopharynx. Second, dysphagia may even be caused by small osteophytes, if they are located at the fixed points of the esophagus (cricoid cartilage at the C6 level). Third, osteophytes may cause an inflammatory reaction around the esophagus. Fourth, neuropathy can result from osseous impingement.

FIG 24.
DISHphagia. (A) Frontal image from a barium swallow reveals extrinsic compression along the right hypopharynx (arrow). (B) Lateral view reveals a large anterior syndesmophyte complex in this patient with diffuse idiopathic skeletal hyperostosis (asterisks). (C) Sagittal reconstructed CT images revealing anterior displacement of the hypopharynx and cervical esophagus by the large bony protuberances. Postsurgical image after syndesmophytes surgically resected reveals decreased displacement of the hypopharynx on the frontal (arrow), (D) and lateral (E) views.
Conclusion
The pharynx is an anatomically and functionally complicated segment of the gastrointestinal tract. The radiologist must be familiar with the normal, abnormal, as well as postoperative, radiographic findings of the pharynx.
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doi:10.1067/j.cpradiol.2007.08.009
© 2009 Mosby, Inc. All rights reserved.
Volume 38, Issue 1 , Pages 17-32, January 2009
