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REVIEW ARTICLE
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Esophageal introitus (with videos)
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Shou-jiang Tang, MD, Ruonan Wu, MSE
Jackson, Mississippi, USA
For GI endoscopists and otolaryngologists, esophagealintroitus (EI) is an arbitrary yet overlapping boundary.Many times, the term EI is used interchangeably withpharyngoesophageal sphincter or upper esophagealsphincter.1-2 In this review, the authors broadened thedefinition of EI to cover the lower part of the hypopharynxposterior to the larynx, the esophageal opening posteriorto the cricoid prominence, and the area between the bilat-eral pyriform fossae and the cervical esophagus (Fig. 1).Although much pathology can be observed within this re-gion, careful and systemic examination of the EI often isnot stressed enough during GI endoscopic training andpractice. The authors demonstrate its anatomy, endo-scopic findings, and pathologies within EI and their man-agement. Dysphagia is a common symptom in patientswith oropharyngeal or esophageal pathologies and isgenerally categorized into 2 types of dysphagia: oropha-ryngeal and esophageal.3 We prefer the term pharyngoeso-phageal dysphagia to describe dysphagia occurring withinthe EI,4 whereas oropharyngeal dysphagia more specif-ically refers to symptoms related to oropharyngeal pathol-ogies, such as myasthenia and thyrotoxicosis. Therefore,dysphagia may be categorized into 3 types: oropharyngeal,pharyngoesophageal, and esophageal. Esophagealdysphagia refers to symptoms related to esophageal pa-thologies distal to the EI. The complete 1-hour digitalvideo content pertaining to this review was publishedrecently by the American Society for GastrointestinalEndoscopy and is available at http://portal.asge.org/
ns: EI, esophageal introitus; TEF, tracheoesophageal fistula.
E: All authors disclosed no financial relationships relevantcation.
This video can be viewed directlyfrom the GIE website or by usingthe QR code and your mobiledevice. Download a free QR codescanner by searching “QR Scanner”in your mobile device’s app store.
2015 by the American Society for Gastrointestinal Endoscopy36.00i.org/10.1016/j.gie.2014.09.065
ROINTESTINAL ENDOSCOPY Volume 81, No. 2 : 2015
products/details.aspx?catidZ3&prodidZ408. With permis-sion, selected video footages are included in this review.
ANATOMY AND ENDOSCOPIC EXAMINATION
The EI muscles include the inferior pharyngealconstrictor, cricopharyngeus, and cervical esophagus(Fig. 2).1-3,5-7 The length of EI is about 3 cm to 5 cm, andthe cricopharyngeus is the main component of theseclosure muscles. The cricopharyngeus is a striated muscleand is responsible for the high pressure zone within theEI. The cricopharyngeus is innervated by branches of thevagus nerves and recurrent laryngeal nerve. Swallowing isaccomplished when the cricopharyngeus muscle relaxes,and pharyngeal pressure is sufficient to propel a bolusthrough the open sphincter. EI contractions can be inducedwith either esophageal distension mediated by the vagova-gal reflex or pressure on the pharyngeal mucosa mediatedby a glossopharyngovagal reflex.1-2 Functional evaluation ofthe EI can be obtained with videofluoroscopic swallow ex-amination, manometry, scintigraphy, and electromyog-raphy.2,5-8 However, a range of normal values remainscontroversial and their utility uncertain.2 The manometricevaluation of the upper esophageal sphincter is difficultconsidering the short zone of interest and the rapid move-ment with swallowing or any stimulation including that ofthe catheter. Videofluoroscopic evaluation is the mostconvenient of the currently available methods.
The authors recommend that endoscopic examination ofthe EI start from the oropharynx. Normal endoscopic exami-nation and various postoperative anatomies of the EI aredescribed in Video 1 (available online at www.giejournal.org). At the inlet of the oropharynx, the soft palate, uvula,bilateral palatine tonsils, and pharyngoepiglottic folds canbe found (Fig. 3). At the root of the tongue, vallate papillaeand lingual follicles can be observed as well. At the hypophar-yngeal inlet, the endoscopist should see the pyriform fossa,aryepiglottic fold, cuneiform tubercle, and corniculate tuber-cle on each side (Fig. 4). From posterior to anterior direction,the midline anatomic landmarks are the posterior pharyngealwall, postcricoid recess, interarytenoid notch, laryngeal inlet,vocal cords, epiglottis, and vallecula. The esophageal openingis located between the bilateral pyriform fossae and down inthe postcricoid recess. The cricopharyngeus muscle is locatedat the level of the esophageal opening, which usually is
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Figure 1. Oropharynx, hypopharynx, and cervical esophagus.Figure 2. Closure muscles of the esophageal introitus or upper esopha-geal sphincter muscles: inferior pharyngeal constrictor, cricopharyngeus,and cervical esophagus. The cricopharyngeus is the main component ofthese closure muscles.
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located at 14 to 15 cm as measured from the incisor teeth, atabout the level of the C-6 vertebra.
On endoscopy, the normal mucosa lining of the EI issquamous and appears whitish pink or silver-red in color,smooth, and with fine vascular patterns (Fig. 5). Thevascular patterns and mucosal pathology can be bettervisualized and demarcated under digital chromoendo-scopy, such as narrow-band imaging. Normally, we shouldnot observe much mucus accumulation within the EI.
Glycogenic acanthosisIn about 3% to 4% of patients undergoing upper endos-
copy, we see glycogenic acanthosis9-11 (Fig. 6). Glycogenicacanthosis appears as focal or multifocal whitish smoothplaques a few millimeters in size, and they are hyperplasticsquamous epithelium with abundant intracellular glycogendeposits. Mild glycogenic acanthosis is a normal benignfinding and is not associated with inflammation. Extensiveglycogenic acanthosis can be associated with Cowden’ssyndrome.11
Gastric mucosal heterotopiaGastric mucosa heterotopia in the cervical esophagus is
frequently underdiagnosed, and its prevalence rate is about2%.12-14 The heterotopic mucosa is mostly consists ofcardiac-fundic gland–type gastric mucosa.12-13 Under whitelight endoscopy, it appears as a flat or slightly raisedsalmon-colored patch, also called the inlet patch. The inletpatch can be singular or multiple. Gastric mucosal heteroto-pia is best observed under digital chromoendoscopy(Fig. 7). Occasionally, circumferential gastric heterotopia,or inlet segment, can be found.14 In one study, the preva-lence of Helicobacter pylori infection in the patch was25%.12 Gastric column heterotopia and metaplasia (as inBarrett’s esophagus) are different. Heterotopia generallymeans displacement of tissue in an abnormal location dur-ing embryologic development, whereas metaplasia repre-
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sents conversion or transformation of one type of adulttissue into another after birth.13 In contrast to Barrett’sesophagus, gastric mucosa heterotopia should not be re-garded as a precancerous lesion.12 Malignant transformationto adenocarcinoma is exceedingly rare.12 Inlet patch andinlet segment generally do not cause symptoms and are sim-ply incidental findings. It is unknown why the majority ofthese patients with inlet patch are asymptomatic. Occasion-ally, symptoms may arise and are regarded as a result of theacid produced by the parietal cells.13,15 The symptomsinclude retrosternal burning sensation, pharyngoesophagealdysphagia and/or odynophagia, globus sensation, throat irri-tation, hoarseness, and coughing. Esophageal stricture andweb can develop within the inlet segment. There are noclinical guidelines on whether and when to obtain endo-scopic biopsy specimens for heterotopic tissue confirma-tion. Most inlet patches are in fact asymptomatic, androutine biopsies to confirm the presence are unnecessary.Endoscopic biopsy should be performed in adult patientswith throat or introital symptoms, mucosal findings suspi-cious of squamous dysplasia or other neoplasm, infection,ulceration, stricture, fistula, or mass lesion. Asymptomaticinlet patch or inlet segment requires neither specific therapynor endoscopic surveillance. In patients with throat or in-troital symptoms suspicious of a causal relationship withacid secretion from the heterotopic mucosa, histologicconfirmation by biopsy and proximal pH measurementscan aid diagnosis and guide therapy.15 Because the pro-posed therapy is minimally invasive, it is reasonable toskip pH testing if the suspicion is strong and the patientagrees. Management of symptomatic lesions can start withproton pump inhibitor therapy. If optimal symptomatic con-trol cannot be achieved, endoscopic ablation with bipolarcoagulation, argon plasma coagulation, or a radiofrequencyablation device can be attempted. One study suggests thatthe globus sensation caused by an inlet patch can respondto endoscopic argon plasma coagulation ablation therapy.16
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Figure 4. Endoscopic image at the hypopharyngeal inlet: pyriform fossa,aryepiglottic fold, cuneiform tubercle, and corniculate tubercle on eachside. From posterior to anterior direction, the midline anatomic land-marks are the posterior pharyngeal wall, postcricoid recess, interarytenoidnotch, laryngeal inlet, vocal cords, epiglottis, and vallecula. E, epiglottis;VC, vocal cord; AEF, aryepiglottic fold; Cu, cuneiform tubercle; Co, corni-culate tubercle; IAN, interarytenoid notch; PPW, posterior pharyngealwall.
Figure 3. Endoscopic image at the oropharyngeal inlet: soft palate, uvula,bilateral palatine tonsils, pharyngoepiglottic folds, and posterior tonguewith its vallate papillae and lingual follicles. T, tongue; PT, palatine tonsil;U, uvula; PEF, pharyngoepiglottic fold.
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Cricopharyngeal barThe cricopharyngeal bar is a radiologic description of
the posterior bar-like impression at or below the esopha-geal opening, corresponding to the cricopharyngeus mus-cle.17-19 One study suggested that the underlyingpathogenesis of the cricopharyngeal bar as reduced crico-pharyngeus muscle compliance.17 In about 5% to 19% ofthe asymptomatic population, it can be seen on the lateralview of a barium esophagram (Fig. 8) and on videofluoro-scopic swallowing studies.18 The bar usually is an incidentalfinding and does not cause symptoms. In some patientswith a prominent bar, pharyngoesophageal dysphagia ispresent. Treatment options of symptomatic cricopharyng-eal bar or spasm include endoscopic dilation by using sa-vory dilators or injection of botulinum toxin into themuscle.19-20 Cricopharyngeal bar also can be seen inZenker’s diverticulum and is described under the divertic-ulum section. Injection of botulinum toxin is ineffective inthis setting. Cricopharyngeal achalasia is a term generallyreserved for pharyngoesophageal dysphagia caused by cri-copharyngeus muscle dysfunction.17-18 Cricopharyngealmyotomy and botulinum toxin injection can be used totreat this condition.
Esophageal rings and websIn the esophagus, although the terms rings and webs
often are used interchangeably, in fact they are differententities. An esophageal ring is circumferential or concen-tric with mucosal and submucosal involvement, whereasa web is partial or eccentric and involves the mucosa.21
A web generally appears as a membrane-like constrictionin the cervical esophagus, referred to as an esophagealor postcricoid web (Fig. 9). On the other hand, an esoph-ageal ring usually is located at the squamocolumnar
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junction in the distal esophagus. When multiple ringsare present throughout the esophagus, the terms ringedesophagus, corrugated esophagus, or feline esophagussometimes are used, and they can be caused by eosino-philic esophagitis, reflux and non-reflux esophagitissuch as graft-versus-host disease, and some autoimmuneconditions. The barium esophagram defines a web betterthan endoscopy and generally reveals a single, thinindentation. Congenital esophageal webs are rare andcan present as dysphagia or regurgitation in early child-hood.22 In adults, most esophageal webs are idiopathicand respond to endoscopic dilation if they cause obstruc-tive dysphagia. Esophageal biopsy around the webshould be considered to rule out eosinophilic esophagitisand other forms of esophagitis. In addition, the web orring can be disrupted by performing biopsy on the lesion,obviating the need for endoscopic dilatation. Plummer-Vinson syndrome, also called Peterson-Brown-Kelly syn-drome or sideropenic dysphagia, consists of a triad ofpharyngoesophageal dysphagia, esophageal webs, andiron deficiency anemia.23 Other coexisting symptomsand signs may include glossitis, angular cheilitis, and koi-lonychia. The primary therapy is iron repletion, whichusually reverses these symptoms. In case of significantobstruction of the esophageal lumen by esophagealweb or persistent dysphagia despite iron supplementa-tion, dilation or disruption of the web by biopsy isindicated. These patients should be followed closelyfor their increased risk of squamous cell carcinomaof the pharynx and the upper esophagus.23 Although sur-veillance endoscopy is recommended,23 the optimal
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Figure 5. Endoscopic images of the hypopharynx and larynx: A, Under white light. B, Digital chromoendoscopy such as narrow-band imaging.
Figure 6. Endoscopic images of the glycogenic acanthosis: A, Under white light. B, Digital chromoendoscopy. Glycogenic acanthosis appear as focal ormultifocal whitish smooth plaques of a few millimeters in size.
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surveillance interval is unknown because of the uncom-mon nature of this syndrome.
StenosesEtiologically, stenoses or strictures within the EI can be
categorized into two types: (1) intrinsic stenoses causedby inflammation, infection, fibrosis, neoplasia, and anasto-mosis; or (2) extrinsic stenoses from external neoplasticinvasion or compression from surrounding lymph nodeenlargement or vertebral osteophytes. Inflammatory con-ditions include peptic injury, caustic substance ingestion,medication, radiation, iatrogenic, autoimmune, and idio-pathic disease processes. Although GERD causes a major-ity of the esophageal strictures, the stenosis usually is inthe distal to mid esophagus. In a recent review, the overallrisk of pharyngoesophageal stricture after treatment forhead and neck cancer was 7.2%: 5.7% after conventionalradiation and 16.7% after intensity modulated radiationtherapy.24 Nonobstructive or nonstructural causes of phar-yngoesophageal dysphagia include neuromyogenic dys-motility after stroke, Parkinson’s disease, myositis,myasthenia, and thyrotoxicosis.3-4 Most benign strictureswithin the EI are amenable to endoscopic interven-tions.25-27 In case of complete postradiation obstructionwithin the EI, combined antegrade and retrograde endos-copy (CARE) with pharyngoesophageal puncture (PEP) by
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using a stiff wire end, needle-knife, and biopsy forcepscan be attempted.25-26 For complex stenoses involvingdysmotility, a multidisciplinary approach is recommended,with a team involving a GI endoscopist, speech patholo-gist, nutritionist, and, at times, a surgeon.
Foreign body impactionAlthough the majority of ingested foreign bodies
will pass spontaneously, impaction of foreign bodiesin the esophageal introitus is a medical and endoscopicemergency.28-30 If the foreign body is suspected in thehypopharynx, an otolaryngologist is generally called bythe emergency department staff. A GI endoscopist is calledif the foreign body cannot be located in the hypopharynxor is suspected in the esophagus from the beginning.Commonly found objects include fish bones, chickenbones, pieces of glass, dental prostheses, coins, and nee-dles.29 The aims of the initial patient assessment are toidentify the type of object, its location, and the presenceof any associated adverse events. Radiographic evaluationis helpful to confirm the location of foreign bodiesand associated adverse events. Plain films of the neckand chest commonly will show the location of radiopaqueobjects. Both anteroposterior and lateral views are neces-sary, because some radiopaque objects overlying the verte-bral column may be visible only on the lateral view.
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Figure 7. Endoscopic images of the gastric mucosa heterotopia or inletpatch in the cervical esophagus under digital chromoendoscopy.
Figure 8. On barium esophagram, the cricopharyngeal bar (arrow) ap-pears as a post bar-like impression at or below the esophageal opening,corresponding to the cricopharyngeal muscle.
Figure 9. On barium esophagram, an esophageal web (arrow) appearsas a thin indentation in the cervical esophagus.
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Multidetector row CT is superior to plain radiographs forthe detection of pharyngoesophageal foreign bodies andprovides additional information for the management ofcomplicated cases (Fig. 10).29 In cases of pointed or sharpobject ingestion, symptoms and signs suggestive of perfo-
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ration, infection, abscess formation, or other coexistingconditions, CT is recommended. CT also is useful inexcluding potential vascular structures and evaluatingextraluminal conditions near the object. Emergent endos-copy is indicated in (1) foreign-body impaction withinthe esophageal introitus (Fig. 11), (2) esophageal obstruc-tion when the patient is unable to swallow secretions, and(3) disk batteries and sharp-pointed foreign bodies in theesophagus.28,30 In general, esophageal foreign bodies andfood impactions without complete obstruction should beremoved within 24 hours (urgent endoscopy). For sharpor pointed objects, commonly used over-the-scope devicesfor mucosa and/or airway protection include foreign bodyhood protectors, banding device caps, and friction-fitcaps. In the authors’ experiences, foreign body hood pro-tectors and banding device caps are inexpensive and versa-tile devices for removing sharp or pointed objects. Formost foreign bodies in the EI, rigid endoscopic removalby an otolaryngologist is equally effective and safe as a flex-ible endoscopic approach. For foreign bodies impacted inthe cervical esophagus, flexible endoscopy is probablymore convenient.
DiverticulaDiverticula are uncommon in the EI, and they generally
are of 4 types: lateral pharyngeal or laryngopharyngealdiverticulum,31-34 Zenker’s diverticulum,35-39 posttraumatic
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Figure 10. A, On emergent endoscopy, a bony foreign body with adherent meat is seen impacted within the esophageal introitus. B, Successful endo-scopic removal revealed the foreign body to be a wish bone.
Figure 11. On CT, a linear calcified foreign body (arrow) is seenimpacted within the esophageal introitus.
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diverticulum or pseudodiverticulum,40 and Killian-Jamieson diverticulum41-43 (Video 2, available online atwww.giejournal.org). Diverticula in the EI and esophagusare best studied by barium esophagram. Endoscopy canmiss small lesions. In addition, a videofluoroscopic studycan reveal the dynamics of the diverticulum in relationshipto the EI during observed swallowing. Lateral pharyngealdiverticula or pharyngoceles are rare (Fig. 12). It is a pro-trusion in the piriform recess or in the vallecula. It canbe unilateral or bilateral. The presumed etiology is pharyn-geal overpressure from dysphagia. The treatment is surgi-cal or endoscopic.33-34 Zenker’s diverticulum is theprotrusion of pharyngeal mucosa through the posteriorwall of the pharynx through the Killian triangle, limitedinferiorly by the cricopharyngeal muscle and laterally bythe thyropharyngeal muscle (Fig. 13).35 Bilateral Zenker’sdiverticulum is rare.39 Posttraumatic diverticulum canmimic Zenker’s diverticulum.40 The primary etiology ofZenker’s diverticulum is thought to be the increased intra-luminal pressure secondary to cricopharyngeal spasm. Zen-ker’s diverticulum can cause dysphagia, regurgitation ofundigested food, post-swallow hypopharyngeal reflux,
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cough, and aspiration. Zenker’s diverticula often can createdifficulty in esophageal intubation during endoscopy. Iatro-genic perforation and submucosal dissection within theesophageal introitus have been reported.44 Rigid and flex-ible endoscopic treatment for Zenker’s diverticula focuseson releasing the cricopharyngeal spasm by performing di-verticulotomy on the septum.35-38 Flexible endoscopicdiverticulotomy is safe and effective37-38 (Fig. 14). Killian-Jamieson diverticulum, also called lateral cervical esopha-geal diverticulum, protrudes through a muscular gap(Killian-Jamieson triangle) in the anterolateral wall of thecervical esophagus inferior to the cricopharyngeus, supe-rior to the circular muscle of the esophagus, and lateralto the longitudinal muscle of the esophagus (Fig. 15).41-42
Killian-Jamieson diverticulum arises inferior and lateralto the Zenker’s diverticulum. Unlike Zenker’s diverticulum,Killian-Jamieson diverticulum does not have a cricophar-yngeal bar or septum. The pathogenesis of Killian-Jamieson diverticulum is unclear. It is likely to be acquired.The treatment is surgical or endoscopic for symptomaticKillian-Jamieson diverticulum.42-43
IschemiaBecause of the rich vascular supply of EI, ischemia or ne-
crosis of EI is not common. Acute esophageal necrosis, alsocalled black esophagus, can be observed in patients withsystemic hypotension or shock, severe caustic substanceinjury, local infection, or inflammation leading to reductionin esophageal blood perfusion (Fig. 16). Elderly patients areparticularly susceptible.45 Diffuse ulcerations with tissuefriability and dark pigmentation of the esophagus areseen on upper endoscopy, and there are histopathologicfindings of mucosal necrosis. The most pronounced endo-scopic findings usually are present in the distal third of theesophagus, likely because of superimposed acid refluxinjury. The most common presenting symptom is acute up-per GI bleeding. The treatment is supportive care,hemodynamic stabilization, and aggressive acid suppres-sion.45 The mortality associated with acute esophageal ne-crosis usually is related to coexisting illnesses rather thanfurther esophageal adverse events such as perforation.
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Figure 12. A lateral pharyngeal diverticulum, or laryngopharyngeal diverticulum, or pharyngocele is seen as a protrusion in the piriform fossa: A, B, Onbarium swallow study. C, On endoscopy. AP, anteroposterior; L, lateral.
Figure 13. A Zenker’s diverticulum protrudes through the pharyngeal mucosa above or through the cricopharyngeus: A, B, On barium swallow study. C,On endoscopy. AP, anteroposterior; L, lateral.
Figure 14. Endoscopic image of the Zenker’s diverticulum after flexibleendoscopic diverticulotomy with a needle-knife. A nasogastric tube isseen in the esophageal lumen.
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Postoperative esophageal conduit ischemia or necrosis is anuncommon but serious adverse event of esophageal sur-gery.46 Postoperatively, surgeons should have a highindex of suspicion for this adverse event. Unexplainedtachycardia, respiratory failure, leukocytosis, or any
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evidence for graft or anastomotic leakage should prompta search for conduit ischemia. The diagnosis is made bycontrast study, endoscopy, or direct operative inspection.
Proximal esophageal (downhill) varicesProximal esophageal varices, often called downhill
varices, generally develop in patients with superior venacava obstruction and/or superior vena cava syndrome,with reversal of the normal blood flow direction in theupper esophageal plexus.47-48 The etiology of superiorvena cava syndrome in reported cases includes intravenouscatheter–related thrombosis, systemic venulitis, medias-tinal fibrosis, carcinoma of the lung or thyroid gland, intra-thoracic goiter, surgical ligation of the superior vena cava,and metastatic carcinoma or mediastinal mass of unknownorigin. Bleeding from the downhill varices is rare. Endo-scopic band ligation and injection sclerotherapy havebeen reported for proximal variceal bleeding. Because ofits hemodynamics, band ligation can be started from theproximal end within the introitus (Video 3, available onlineat www.giejournal.org).
Inflammation and infectionThe symptoms associated with the inflammation and
infection within the EI can include pharyngoesophagealdysphagia, odynophagia, sore throat, throat irritation,
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Figure 15. A Killian-Jamieson diverticulum, also called a lateral cervical esophageal diverticulum, protrudes through the anterolateral wall of the cer-vical esophagus inferior to the cricopharyngeus: A, B, on barium swallow study. C, On endoscopy. AP, anteroposterior; L, lateral.
Figure 16. Endoscopic image of the acute esophageal necrosis or “blackesophagus.” Diffuse ulcerations with tissue friability and dark pigmenta-tion are shown.
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cough, GI bleeding, or spitting of blood. Common nonin-fectious etiologies include GERD, recurrent vomiting,acute radiation mucositis, chronic radiation injury, esopha-gitis desiccans superficialis,49 eosinophilic esophagitis,caustic substance ingestion, toxic fume inhalation, graft-versus-host disease,50 pemphigus vulgaris,51-52 benignmucous membrane (cicatricial) pemphigoid,53-54 epider-molysis bullosa dystrophica,55-56 Crohn’s disease, anddrug-induced mucositis.57
EI can be involved in graft-versus-host disease after allo-geneic bone marrow transplantation.50 On endoscopy,inflammation, erosion, and esophageal webs can be seen.The diagnosis is confirmed by random and targeted biopsy.
EI can be associated with certain skin diseases, such aspemphigus vulgaris, benign mucous membrane (cicatri-cial) pemphigoid, and epidermolysis bullosa dystrophica.Pemphigus is characterized by cutaneous and mucosalblistering. Pemphigus vulgaris, the most common andimportant variant, is an autoimmune blistering diseasecharacterized by circulating pathogenic immunoglobulin
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G antibodies against desmoglein 3.51-52 Vesiculobullouslesions and ruptured bullae with mucosal denudation canbe seen within the EI (Fig. 17). The role of endoscopy isto confirm EI involvement and to rule out other condi-tions. Current treatment is largely based on systemicimmunosuppression by using systemic corticosteroidswith other immunomodulators. Cicatricial pemphigoid isa rare systemic autoimmune subepidermal bullous diseaseprimarily involving mucous membranes.53-54 Histologically,there are subepidermal blisters and erosions that heal withscarring. EI involvement is uncommon, and it occursusually in patients with established ocular disease. Theclassic endoscopic findings include erosions and scarring,esophageal webs or strictures, and blister formations afterdilation or trauma (Fig. 18). Despite immunosuppressivedrugs, some patients need endoscopic dilatation totreat the symptomatic dominant esophageal strictures.Through-the-scope endoscopic balloon dilatation ispreferred by us in this situation in order to avoid or mini-mize extensive blister formations after dilatation with aSavary dilator or a bougie. Epidermolysis bullosa acquisitais a subepidermal blistering disorder associated with auto-immunity to type VII collagen, which is the collagen local-ized to anchoring fibrils within the dermoepidermaljunction of skin.55-56 Inflammation, bullous eruption, ulcer-ation, scars, webs, and strictures can be observed in EI.
Medication-induced stricture (pill mucositis) oftenoccurs at the anatomic narrowing: esophageal opening,middle one third behind the left atrium, and the gastro-esophageal junction. The most common culprit medica-tions are nonsteroidal anti-inflammatory drugs, ironsupplements, tetracycline, doxycycline, alendronate, potas-sium chloride, ascorbic acid, and quinidine.57
Infectious esophagitis generally develops in immuno-compromised patients, with candidiasis being the mostcommon infection.58-62 Less-common infections includeherpes simplex and cytomegalovirus esophagitis.58-60
When obtaining tissue diagnosis, physicians should ensurethat biopsy specimens are taken from both the ulcer edgeand base. In herpes infection, the viropathic changes tendto be present at the ulcer margins, whereas viropathic
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Figure 17. A, Image of vesiculobullous lesion and ruptured bullae on the skin of a patient with pemphigus vulgaris. B, Endoscopic image of similarlesions within the esophageal introitus.
Figure 18. Endoscopic images of the esophageal introitus in a patient with mucous membrane (cicatricial) pemphigoid. A, The endoscopic findingsinclude blister formations after dilation or trauma. B, Erosions, scarring, esophageal webs, or strictures.
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findings are present within the ulcer base during cytomeg-alovirus infection. Other infectious agents or infectionsinclude HIV, actinomycosis, aspergillosis, histoplasmosis,and tuberculosis. Immunocompromised patients also candevelop phlegmonous esophagitis and infectious necro-tizing esophagitis.63-64 They are rare and associated withhigh mortality. These are suppurative bacterial infections,and the most common pathogens are Streptococcus,Staphylococcus, Escherichia coli, Haemophilus influen-zae, Proteus, and Clostridia.
FistulasFistulas within the EI include pharyngocutaneous,
pharyngo-respiratory, esophagopleural or esophagome-diastinal, and esophagorespiratory or tracheoesophagealfistulas (TEF).65-67 The development of a pharyngocutane-ous fistula after oncologic head and neck surgery is aserious adverse event and is common after major hypo-pharyngeal and laryngeal ablative surgery.65 It was recom-mended that these patients are best treated with regionalmyocutaneous flaps or free tissue transfers at expert cen-ters.65 TEF is a congenital or acquired communicationbetween the trachea and esophagus. Most patients with
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congenital TEFs are diagnosed immediately after birth orduring infancy. Acquired TEF occurs secondary to malig-nant disease (neoplasms of the esophagus, lung, andtrachea), infection (tuberculosis, aspergillosis), ruptureddiverticula, and trauma. Post-intubation TEF infrequentlydevelops after prolonged mechanical ventilation with anendotracheal or tracheostomy tube. Infrequently, trau-matic TEF develops after tracheostomy and is related toimproper tracheal incision (Fig. 19). Improperly positionedtracheal tubes exert posterior pressure against the esoph-agus, resulting in a TEF. The prognosis is generally poorin these patients. Endoscopic interventions with mechani-cal tissue approximation (such as the over-the-scope clip-ping devices), tissue adhesive application, and temporaryor permanent stenting have been reported with variablesuccess rates.68
NeoplasmsOver 95% of hypopharyngeal cancers are squamous
carcinomas, which usually present as infiltrating ulcerativelesions.69-70 The most common site for hypopharyngealcancer is the piriform sinus, followed by the postcricoidregion and the posterior pharyngeal wall (Fig. 20). The
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Figure 20. Endoscopic images from a patient with hypopharyngeal squamous cell carcinoma. A, The hypopharynx and larynx. B, Piriform sinus. Themost common site for hypopharyngeal cancer is the piriform sinus, followed by the postcricoid region and the posterior pharyngeal wall.
Figure 19. A, Endoscopic image of a traumatic tracheoesophageal fistula within the esophageal introitus after tracheostomy, related to improper trachealincision. B, The fistula was managed successfully by temporary stenting by using a fully covered expandable metal esophageal stent (Evolution stent, CookMedical, Winston-Salem, NC). C, After-stenting swallow study shows no leakage.
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incidence of poorly differentiated cancer is higher in thehypopharynx than in other regions. Hypopharyngeal can-cers are difficult to catch in their earliest stages and haveone of the highest mortality rates of any head and neckcancer. Symptoms of hypopharyngeal cancer may includeswollen lymph nodes in the neck, sore throat, radiatingpain from the throat to the ears, voice change, pharyngoe-sophageal dysphagia, and odynophagia. Postcricoid can-cers are frequently circumferential and cause dysphagia,whereas cancers in the piriform sinus tend to remainasymptomatic for some time. The risk factors of hypo-pharyngeal cancer are smoking, chewing tobacco, heavyalcohol use, poor diet, and Plummer-Vinson syndrome.It should be noted that there is an increased risk of esoph-ageal cancer in patients with otolaryngeal cancers aseither synchronous or metachronous lesions or secondaryto radiation exposure. Small, early cancers of the piriformsinuses are curable with radiation therapy. Small, earlycancers of the posterior pharyngeal wall can be treatedwith larynx-preserving local excision. There is growing ev-idence and interest that the detection and resection ofearly pharyngeal and hypopharyngeal dysplasia and can-cers can be achieved with flexible endoscopy under digitalchromoendoscopic guidance.71 If a cancer extends to orarises in the cervical esophagus, laryngopharyngectomy
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and esophagectomy may be required. A gastric pull-upprocedure may be needed. Other neoplasms found inthe EI include papilloma and papillomatosis, lipoma, fi-brolipoma, adenocarcinoma, leiomyoma, granular cell tu-mor, spindle-cell carcinoma, neuroendocrine tumor, andlymphoma.
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Received May 1, 2014. Accepted September 29, 2014.
Current affiliations: Division of Digestive Diseases, Department of Medi-cine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Reprint requests: Shou-jiang Tang, MD, Associate Professor in Medicine,Division of Digestive Diseases, University of Mississippi Medical Center,Jackson, MS 39216.
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GASTROENTEROLOGY ARTICLE OF THE WEEK March 5, 2015
Tang SJ, Wu R. Esophageal introitus. Gastrointest Endosc 2015;81:270-281. [To watch the videos referenced in this article, use the following links. Note that video files are large, it may take several minutes to download.]
Video #1: https://www.dropbox.com/s/mvgmow4t5up85d5/mmc1.mp4?dl=0
Video #2: https://www.dropbox.com/s/8rd5xdpqpcapihn/mmc2.mp4?dl=0
Video #3: https://www.dropbox.com/s/l19ergf5d1yngu0/mmc3.mp4?dl=0
1. Inlet patch b. it is composed of metaplastic gastric epithelium c. can be colonized with H. pylori d. should always be biopsied to be sure there is no malignancy e. If symptomatic, ablation with APC may be effective 2. True statements regarding the cricopharyngeus include a. It is composed mainly of smooth muscle b. Is innervated by the vagus nerve and the recurrent laryngeal nerve c. Relaxes when the esophageal lumen is distended d. Esophageal manometry is an accurate way of assessing cricopharyngeus function True or False 3. Esophageal webs are visualized better by barium studies than by EGD. 4. Whitish smooth plaques in the esophagus are caused by hyperplastic squamous epithelium, is known as glycogenic acanthosis and are considered premalignant lesions. 5. Pemphigus vulgaris can affect the proximal esophagus wih ruptured bullae and mucosa denudation, if dilation is needed, balloons are preferred to Savary dilators 6. Barium studies are more sensitive than endoscopy to detect smaller upper esophageal diverticuli. 7. A cricopharyngeal bar noted on barium esophagram indicates cricopharyngeal sphincter dysfunction and usually accounts for symptoms of dysphagia 8. Iron replacement in Plummer-Vinson syndrome may be sufficient to resolve the esophageal web in some cases 9. A web only contains mucosa; a ring contains mucosal and submucosal tissue 10. Downhill esophageal varices may be a complication of superior vena cava thrombosis