principles of deglutition || zenker’s diverticulum

495R. Shaker et al. (eds.), Principles of Deglutition: A Multidisciplinary Text for Swallowing and its Disorders, DOI 10.1007/978-1-4614-3794-9_35, © Springer Science+Business Media New York 2013

35 Zenker’s Diverticulum

Ian J. Cook

I. J. Cook , MBBS, MD(Syd), FRACP (�) Director Neurogastroenterology and Motility Service and Swallow Centre, Department of Gastroenterology and Hepatology, St George Hospital , Sydney , Australia

Professor of Medicince, Faculty of Medicine, University of New South Wales, Sydney , Australia e-mail: [email protected]

Abstract

There is now strong evidence that acquired Zenker’s diverticulum arises in most cases secondary to a poorly compliant, but normally relaxing, UES which cannot fully distend during the process of sphincter opening. This gives rise to increased hypopharyngeal intrabolus pressure during the phase of trans -sphincteric bolus fl ow; pressure which is imparted to the area of relative muscular weakness (Killian’s dehiscence) just proximal to the cricopharyngeus. This combination of factors gives rise to posterior herniation of the pouch over many years. The restricted opening of the cricopharyngeus is a result of muscle fi bre degeneration and fi broadipose tissue replacement. For this reason, cricopharyngeal myotomy is the essential component for successful surgical treatment of the condition. The precise aetiology of this myopathic process affecting the cricopharyn-geus is unknown and may be multifactorial. However, an underlying myo-sitis with a predilection for the cricopharyngeus muscle is likely to be one such factor in some cases.

Keywords

Zenker’s diverticulum • Bilobed pharyngeal pouches • Bilobed with one opening • Pouches with separate necks • Bilobed pouch • Laryngocoele • Upper oesophageal sphincter (UES) • Dysphagia • Swallowing • Pathophysiology

496 I.J. Cook

Introduction and Historical Perspective

The fi rst reported case of a posterior pharyngeal diverticulum was published by Ludlow [ 1 ] . He reported the case of a 65-year-old man with ema-ciation and progressive dysphagia resulting in his demise 13 days after presentation; arguably has-tened by attempted therapies which included blind dilatations with a whale bone and swallow-ing a “great quantity of quicksilver”. It was not until a century later that a systematic anatomical description of the entity was published by Zenker and von Zeimsen in 1878 [ 2 ] . They reviewed 22 cases from the literature, all con fi rmed by autopsy and an additional fi ve of their own cases (Fig. 35.1 ). They elegantly showed that the sac constitutes a herniation of mucosa and submu-cosa posteriorly between the inferior constrictor and cricopharyngeus muscles at a point of the pharynx that “… has lost the support of the muscular fi bres which usually sustain it, in consequence of some local in fl uence upon the same ” and that there are no muscle fi bres on the diverticulum itself. The focal region of relative lack of muscular support was subsequently termed Killian’s dehiscence; the roughly triangu-lar region bounded by the inferior fi bres of the inferior constrictor and the superior fi bres of the cricopharyngeus [ 3 ] .

De fi nition and Anatomical Considerations

Pharyngeal diverticula are most conveniently classi fi ed according to their anatomical site. Broadly speaking, these anatomical structures can be lateral or posterior and they can lie above (pharyngeal) or below the cricopharyngeus (cervical oesophageal). The lateral pharyngeal diverticula are quite distinct entities from the posterior (Zenker’s) diverticulum.

The typical Zenker’s diverticulum herniates posteriorly just proximal to the cricopharyngeus (Fig. 35.2 ). Although it protrudes posteriorly, as it grows in size it may track to one side or the

other but tends to be left sided in the majority. The reason for this is unclear but an anatomical consideration that may explain it in part is the greater potential space between the concavity of the cervical oesophagus and the left carotid artery compared with the right [ 4 ] . While the pouch generally has a single opening into the hypophar-ynx, a number of anatomical variations have been reported including three different types of bilobed pharyngeal pouches: bilobed with one opening [ 5 ] ; two separate pouches with separate necks [ 6 ] and a bilobed pouch separated by a septum with two necks [ 7 ] (Fig. 35.3 ).

Histopathological studies con fi rm the original descriptions of Zenker and von Ziemsen that the pouch itself is lined by strati fi ed squamous epi-thelial mucosa and submucosa which is often surrounded by fi brous tissue [ 8 ] . Muscle fi bres

Fig. 35.1 Preserved autopsy specimen of a large diver-ticulum from the fi rst case series described by Zenker and von Zeimsen [ 2 ] . This specimen currently resides in the Museum of Pathological Anatomy, Erlangen. (The autopsy specimen of the very fi rst case described by Ludlow still exists in the pathological collection of the Royal In fi rmary, Glasgow)


are notably absent except in some cases in the region of the neck of the diverticulum. Rarely, a squamous carcinoma or carcinoma in situ is found (see below).

Proximal, lateral pharyngeal diverticula are frequently bilateral, are more common in the elderly and occur at the level of the vallecula in an area of relative weakness through the thyrohyoid membrane at a site that is relatively poorly supported by cartilage or muscle (Fig. 35.4 ). Lateral diverticula may be a congeni-tal pharyngocele or, more commonly, acquired pulsion diverticula. Congenital lateral pouches are true branchial cleft cysts representing an embryological remnant of the third pharyngeal pouch corresponding to the thyrohyoid mem-brane [ 9 ] . The area of relative weakness is

bounded by the hyoid bone superiorly, at a site where there is incomplete overlap of the thy-rohyoid muscle anteriorly and the inferior con-strictor muscle inferiorly [ 10 ] . At this site the thyrohyoid membrane is also perforated by the superior laryngeal artery, and the internal laryn-geal branch of the superior laryngeal nerve. Lateral pharyngeal diverticula rarely cause symp-toms and they are a common incidental fi nding [ 10, 11 ] . However, there are sporadic case reports of successful alleviation of dysphagia following surgical ligation or removal of a lateral pharyn-geal diverticulum [ 12, 13 ] .

Occasionally lateral diverticula can originate just below the cricopharyngeus and herniate through an area of relative weakness lateral to the point of inser-tion of the longitudinal muscle of the oesophagus

Fig. 35.2 A typical Zenker’s diverticulum seen in lateral ( left ) and anteroposterior views ( right )

498 I.J. Cook

onto the cricoid cartilage [ 14 ] . These proximal lat-eral cervical pouches are sometimes termed Killian–Jamieson diverticula and may be confused with a true Zenker’s because of their close proximity to the cricopharyngeus (Fig. 35.5 ). However, they gener-ally extend anterior to the cervical oesophagus as it enlarges while a Zenker’s will not. Killian–Jamieson diverticula are much less common than Zenker’s and are also less likely to cause symptoms with one study attributing symptoms to this diverticulum in 19 % of patients studied [ 15 ] .

Epidemiology

A community study in the UK reported an annual incidence of 2 per 100,000 people per year [ 16 ] . However, the true prevalence is unknown and may be higher than this as many have minimal or no symptoms. For example,

Fig. 35.3 Unusual bilobed posterior pharyngeal pouch seen in an oblique view with single neck arising proximal to the cricopharyngeus

Fig. 35.4 Lateral pharyngeal pouch seen in the proximal pharynx—a distinct entity not to be confused with a pos-terior (Zenker’s) diverticulum

Fig. 35.5 Lateral cervical (Killian–Jamieson) diverticu-lum. This pouch protrudes laterally and below the cri-copharyngeus (see text)—not to be confused with a posterior (Zenker’s) diverticulum


several radiological studies report 0.1–2 % inci-dence in otherwise asymptomatic individuals [ 17, 18 ] . Zenker’s diverticulum is more com-mon in males than females by a factor of 3:1 [ 19 ] . The condition is very uncommon under the age of 40; extremely rare under the age of 30 and is generally con fi ned to the geriatric popula-tion with a median age of presentation in the seventh to eighth decades in various studies [ 20, 21 ] . However, congenital pharyngeal pouches have been reported, some with a family history, suggesting that a congenitally enlarged or weak-ened Killian’s triangle may be a factor in some [ 22– 24 ] . There are few reports of racial differ-ences but it appears to be more common in Europeans than Asians, possibly related to dif-ferences in neck length and it is more common in Northern than Southern Europe [ 25 ] .

Clinical Features

Presenting symptoms include dysphagia com-bined with varying degrees of regurgitation depending on the size of the pouch. Regurgitation

of undigested food is very common (80 %) [ 19 ] . While this is more frequent immediately after the meal, patients will often describe regurgita-tion of food ingested many hours earlier or at night. Aspiration symptoms, such as deglutitive cough, as well as chronic cough, recurrent chest infections and weight loss are common fea-tures. Occasionally recurrent pneumonia and weight loss may be the predominant presenting feature particularly if the pouch is large (Fig. 35.6 ). Audible gurgling during the swal-low may be present. Halitosis, due to stasis in the pouch, can be a feature. The duration of symptoms prior to presentation varies from weeks to many years. There is little published data on the natural history of this entity but the available evidence suggest that the diverticulum develops over many years with little or minor demonstrable change in pouch size over 8 years in one small, longitudinal radiological study [ 26 ] . However, even in the context of a known long-standing pouch, rapid escalation of symp-toms can be a feature even without appreciable change in pouch size (Cook unpublished). The reason for the apparent increase in symptoms is

Fig. 35.6 CXR of patient presenting with “vomiting”, unexplained recurrent bouts of pneumonia and weight loss. ( a ) A plain CXR demonstrates pneumonic changes and a

fl uid level can be seen within the upper mediastinum ( white arrow ). ( b ) After swallowing barium, the inferior margin of the diverticulum is more clearly outlined ( black arrow head)

500 I.J. Cook

not known. However, based on our current understanding of the biomechanics of the phar-ynx and sphincter in this condition, a likely explanation for this observation might be that a critical level of cricopharyngeal fi brosis and stenosis is reached.

Physical examination is usually non-contribu-tory although rarely, a palpable lump in the neck which gurgles on palpation may be evident. Features that might suggest possible malignant change include rapid symptom progression, or bleeding. Pain is rarely reported but its presence is highly suggestive of malignant change [ 27 ] .

Complications

Squamous carcinoma complicating a pouch is rare but is well described with an incidence pos-sibly between 0.4 and 1.5 % [ 27, 28 ] . Analogous with achalasia of the cardia, chronic stasis is believed to underpin the malignant change.

Haemorrhage from the pouch is rare. Benign ulceration of the mucosa within the pouch can occur and this can result in signi fi cant bleeding. Ulceration is potentially related to acid re fl ux [ 29 ] , aspirin-induced mucosal ulceration [ 30 ] , or carcinoma [ 27 ] .

Bezoar formation in the diverticulum has been reported in large pouches [ 31 ] . Fistula formation, either spontaneous between pouch and trachea or unintentional, secondary to instrumentation has been reported [ 31 ] .

Diagnosis

The most useful diagnostic test is a barium swal-low, which usually readily demonstrates the diverticulum. The radiographic study should also carefully examine the oesophagus to identify coexistent pathology that might account for or contribute to the patient’s dysphagia and regurgi-tation. For example, a large hiatal hernia or oesophageal achalasia is an alternative cause of regurgitation and dysphagia. If a diverticulum is known or suspected, a dynamic videoradio-graphic swallow study is preferable to standard

static fi lms for a number of reasons. Very small diverticula (as well as subtle cervical webs) are sometimes only seen transiently during degluti-tion and are best detected on dynamic studies replayed in slow motion. The timing and extent of aspiration, usually immediately post-swallow in a pure Zenker’s, is better appreciated in a dynamic study. Finally, if there is concomitant neuromyogenic pharyngeal dysfunction (e.g. myopathy) the only way to detect this with cer-tainty is with a video fl uoroscopic study (Fig. 35.7 ) [ 32 ] . Concurrent neuromuscular dysfunction, if present, is important to detect as it has diagnostic and prognostic implications (see below). If there is any doubt about the possible coexistence of a neuromuscular disorder (e.g. myositis), in addi-tion to a careful neurological examination, pre-liminary testing should include a plasma CPK level [ 32– 34 ] .

Endoscopic techniques have limited diagnos-tic capability as the opening of the pouch is not always apparent endoscopically. If a constant fi lling defect is seen radiographically, then phar-yngoscopy may be useful in ruling out a compli-cating carcinoma. However, examination by nasolaryngoscopy [ fl exible endoscopic evalua-tion of swallowing (FEES)] frequently does not detect a diverticulum. FEES will often demon-strate regurgitation from the pouch but if a pouch is suspected, barium radiography is still indi-cated. In deciding upon the mode of therapy, it is important to estimate the size (predominantly depth) of the pouch which can be “sized” in cms or relative to vertebral width [ 35 ] . For example, transoral diverticulostomy may not be feasible if the pouch is not suf fi ciently deep to accommo-date the tip of the instrument (refer Chap. 59 ).

Pathogenesis and Pathophysiology

Zenker and von Ziemssen in 1878 hypothesised that the pouch arises primarily due to relative lack of muscular support in the region immedi-ately proximal to the cricopharyngeus [ 2 ] . This roughly triangular section of the posterior pha-ryngeal wall was well described by Killian (and subsequently termed “Killian’s dehiscence”) to

http://dx.doi.org/10.1007/978-1-4614-3794-9_59


be bounded by the oblique fi bres of the inferior constrictor muscle above and the transverse fi bres of the cricopharyngeus below [ 36 ] . Zenker believed that if the region were to sustain an insult that might render it even weaker, the likelihood of herniation would be greater. Zenker went on to say, somewhat perspicaciously, that “ if there is already a stenosis of the upper end of the esopha-gus before the occurrence of any of these causes, it may be readily understood that this would favour the formation of a diverticulum, for not only would a foreign body in this case be more easily detained in the canal, but also, in conse-quence of the stasis of food caused by the steno-sis, the pressure on the weak spot must be increased ” [ 2 ] . Over the next century following that statement, there has been much debate about the pathogenesis of the diverticulum. Furthermore, while Zenker and those following postulated that

elevated hypopharyngeal pressures might have pathogenic signi fi cance, this phenomenon was not demonstrated until 114 years later [ 20 ] .

Numerous hypotheses have been put forward that might account for the proposed increased hypopharyngeal pressure. Initially it was believed that upper oesophageal sphincter (UES) incoordi-nation, speci fi cally premature sphincter closure, in some cases combined with early UES relax-ation, would cause elevated hypopharyngeal pres-sure [ 37– 39 ] . The validity of those early observations is questionable. The radiographic studies were semi-quantitative. In the manometric studies, the UES relaxation pro fi les were recorded by a discrete perfused side-hole positioned within the sphincter without appreciation of the degluti-tive axial mobility of the UES, which is known to profoundly in fl uence temporal swallowing measures [ 40– 42 ] . Other theories proposed included resting

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Fig. 35.7 Videoradiographic sequence ( a ) and corre-sponding pharyngeal manometry ( b ) in a patient presenting with dysphagia, aspiration and who was found to have pol-ymyositis and an early Zenker’s diverticulum. Each vertical dashed line in ( b) represents the time corresponding to the numbered radiographic frames in ( a) . While the sphincter relaxes completely ( b ) it has markedly restricted opening as

evident by the prominent cricopharyngeal bar ( a ). Note the weak pharyngeal stripping wave, incomplete contact of tongue base with pharyngeal wall and resulting poor pharyn-geal clearance. Hypopharyngeal intrabolus pressure (frame 2, channel 3) is increased due to the restricted opening of the upper oesophageal sphincter (UES). From R.B. Williams et al. Gut 2003;52:471–8 with permission (Fig. 3, page 474)

502 I.J. Cook

UES hypertonia [ 43 ] , failure of UES relaxation [ 44 ] , and a second swallow against a closed sphincter [ 38, 45 ] . There has been no consistent demonstra-tion of any of these phenomena and a number of early manometric studies reported normal UES tone, deglutitive relaxation and coordination [ 46, 47 ] . Indeed a number of subsequent manometric studies, accounting for sphincter radial asymme-try and axial mobility, reported normal or low basal UES tone, normal UES relaxation, and nor-mal pharyngo-sphincteric coordination during the swallow [ 20, 48 ] .

A combined videoradiographic and manomet-ric study in which 14 patients were compared with nine age-matched healthy controls demon-strated that the maximal opening of the UES, in both sagittal and transverse planes, is signi fi cantly restricted in patients with Zenker’s diverticulum [ 20 ] . That study also demonstrated conclusively a markedly increased hypopharyngeal intrabolus pressure during the phase of trans -sphincteric bolus fl ow and that this elevated pressure domain is in continuity with the neck of the diverticulum (Figs. 35.8 and 35.9 ). That study also demon-strated normal resting UES tone and complete sphincter relaxation during the swallow.

Additionally, they found no sphincter incoordina-tion between pharyngeal contraction and sphinc-ter relaxation and opening. These fi ndings con fi rm that the underlying disorder is one of loss of muscle compliance of the UES but that the innervation and central control of the constrictors and cricopharyngeus muscle is normal as evi-denced by complete and normally coordinated deglutitive sphincter relaxation.

Further con fi rmatory evidence for the primary defect being a loss of UES compliance came from histopathological and in vitro muscle studies. In a prospective histopathological study, cricopharyngeus and inferior constrictor muscle specimens obtained at the time of cricopharyn-geal myotomy from patients with Zenker’s were compared with control tissue obtained at autopsy from non-dysphagic individuals [ 49 ] . When compared with controls, the cricopharyngeus muscle from Zenker’s patients demonstrated marked fi broadipose tissue replacement, muscle fi bre degeneration, and segmental necrosis with macrophage myophagia (Fig. 35.10 ). Two of 14 specimens demonstrated additional in fl ammatory changes. Although healthy cricopharyngeus muscle has markedly different morphological

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Fig. 35.8 Intraluminal manometric traces in a patient with Zenker’s diverticulum (two right panels) showing much higher intrabolus pressure waves ( stippled ) than those seen in the healthy aged control subject ( left panel). Note that when the patient swallowed the second time to clear

residual bolus from the pharynx, this lower volume bolus was associated with a lower (but still abnormal) intrabolus pressure and a shorter interval of trans-sphincteric bolus fl ow ( black bar ). From I.J. Cook et al. Gastroenterology 1992;103:1229–35 with permission (Fig. 3, page 1,232)


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Fig. 35.9 Correlation of manometry ( top ) and radio-graphic tracings ( bottom ) from the same patient as previ-ous fi gure during a larger (20 mL) barium bolus swallow. Note the extremely high intrabolus pressure ( left ) in con-tinuity with the open sphincter and the neck of the pouch ( white dot represents pressure recording site). Indeed, the intrabolus pressure in this case exceeds the peak pha-

ryngeal contractile pressure which results in peristaltic “failure” and retrograde escape of the bolus ( centre panel). The patient swallowed a second time shortly thereafter ( right panel) and cleared most of the residual bolus but not before a small amount of aspiration occurred. From I.J. Cook et al. Gastroenterology 1992;103:1229–35 with permission (Fig. 4, page 1,233)

Fig. 35.10 ( a ) Normal cricopharyngeus muscle ( left ) obtained from autopsy specimen compared to that from a patient with Zenker’s diverticulum obtained at the time of myotomy ( b ) ( right ). When compared with the normal cricopharyngeus (CP) muscle, the muscle from patient

with Zenker’s demonstrates muscle fi bre dropout (due to necrosis, as evidenced by scattered degenerative fi bres); greater fi bre size variability and a markedly increased fi broadipose tissue replacement. (H & E × 200)

and histological appearances to limb skeletal muscle [ 49, 50 ] , the degenerative and fi brotic changes identi fi ed in the muscle from Zenker’s patients, if present in a limb muscle, would be

consistent with a primary myopathic process and accounts for the previously demonstrated loss of compliance of the UES in these patients. Lerut et al. also showed abnormal contractile properties

504 I.J. Cook

in isolated cricopharyngeal muscle from patients with Zenker’s in that stimulated isolated cri-copharyngeus muscle strips in vitro demonstrated diminished time to peak twitch, reduced contrac-tile velocity and lower amplitude contractions when compared with control tissue [ 51 ] . These alterations in biomechanical properties would also be consistent with the observed muscle fi bre drop out and fi brosis.

Further evidence that poor cricopharyngeal compliance underpins Zenker’s diverticulum and accounts for the observed increase in deglutitive intrabolus pressure comes from systematic exami-nation of the biomechanical properties of the phar-yngo-oesophageal junction before and after cricopharyngeal myotomy. Cricopharyngeal myo-tomy, effectively a curative surgical procedure, normalises both the extent of UES opening and hypopharyngeal intrabolus pressure in these patients (Fig. 35.11 ) [ 52 ] . In that study, the rela-tionship between maximal UES calibre and hypo-pharyngeal intrabolus pressure only approximated that of healthy aged controls following the surgery consistent with normalisation of UES compliance

by myotomy (Fig. 35.12 ). That study also demon-strated that an adequate myotomy is the essential component of treatment, irrespective of what is done with the pouch itself. Unless the intrabolus pressure is normalised by myotomy, the clinical result may be suboptimal (Fig. 35.13 ).

Aetiology

A wide range of conditions have been reported in association with Zenker’s [ 31 ] . Some of these may be chance associations and for most, sup-portive evidence for a causative link is lacking or minimal. Laryngocoele, benign tumours of phar-ynx or oesophagus have been reported rarely. Myositis has been reported and systematically studied (see below). There are several case reports of a pouch developing after anterior cervical spine fusion [ 53, 54 ] . Presumably this relates in part to a degree of adhesive fi xation of the poste-rior pharyngeal wall to the cervical prevertebral fascia inducing a traction component to the region. The long-standing associations among

BEFORE SURGERY

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Fig. 35.11 Pharyngeal manometric tracings from a patient with Zenker’s diverticulum before and after cri-copharyngeal myotomy. The stippled segment of the pres-

sure trace represents the hypopharyngeal intrabolus pressure domain which is very prominent preoperatively and which normalises after myotomy


Fig. 35.12 Plot of relationship between upper oesophageal sphincter (UES) opening and hypopharyngeal intra-bolus pressure before and after surgery. Note that the pre-operative compliance curve is shifted to the left and is

steeper—indicative of poor sphincter compliance. Following surgery, the location and gradient of the curve is indicative of normalisation of sphincter compliance following myotomy

Fig. 35.13 Postoperative manometric tracing ( a ) and bar-ium radiograph ( b ) in a patient who underwent diverticulec-tomy but in whom dysphagia was only partially relieved. Note the persistent post-cricopharyngeal restriction ( arrow )

indicating that the myotomy was incomplete. Note the manometric tracing showing persistently elevated intrabolus pressure ( stippled ) indicating persistently poor sphincter compliance

hiatal hernia, re fl ux and pharyngeal pouch, as well as the signi fi cance of it, remain unresolved.

Although in fl ammatory changes were found in only 14 % of myotomy specimens in those undergoing surgery [ 49 ] , these samples are

likely to represent a late stage in the condition in which fi brosis predominates. The cricopharyn-geus would appear to be quite sensitive to in fl ammation as evidenced by the loss of UES compliance in patients presenting with dysphagia

506 I.J. Cook

in whom myositis was subsequently found to be the cause [ 32 ] . The mean time from symptom onset to diagnosis of in fl ammatory myopathy in that study was 55 months. Of even greater poten-tial relevance in that retrospective case–control study was that 69 % of myositis cases had a restrictive disorder of the cricopharyngeus (bar or circumferential stenosis) and 24 % of all patients had Zenker’s diverticulum; a signi fi cantly greater proportion than was seen in controls (6 %) with a neurogenic pharyngeal dysphagia [ 32 ] . There is an additional case report of a Zenker’s associated with polymyositis [ 55 ] . However, a number of case reports in patients coming to myotomy for dysphagia suggest that myositis can be very focal, apparently con fi ned to the cricopharyngeus and can cause stenosis of the sphincter [ 56– 58 ] .

There are a number of reports of an apparent increased association with hiatal hernia, includ-ing one case–control study [ 59, 60 ] . A number of studies report an association with re fl ux dis-ease [ 43, 60– 63 ] . Re fl ux and hiatal hernias are very common conditions; the latter particularly in the geriatric population in which pharyngeal pouches are most prevalent. Hence, a chance association among these conditions will be common. The mechanisms potentially responsible for such a putative link are speculative and, as yet, lack proof. One notion is that the hiatal hernia alone or re fl ux per se increases resting tone within the UES. While abrupt pressurisation of the oesophagus during spontaneous re fl ux events generally triggers re fl exive UES relaxation, some re fl ux events can induce increased basal UES tone [ 64, 65 ] . However, these events do not impair deglutitive UES relaxation—the critical time domain during which the swallow-related increased intraluminal pressure is acting on the posterior pharyngeal wall [ 65 ] . Others have pos-tulated that oesophageal shortening, as a conse-quence of re fl ux events and/or in association with hiatus hernia formation, put differential axial traction on the relatively untethered cri-copharyngeus compared with the inferior con-strictors [ 63 ] . They postulate that this differential axial mobility, due to the better anchoring of the inferior constrictors through its median raphe,

would tend to open up the region of Killian’s triangle. In the absence of more plausible patho-genetic mechanisms and until objective demon-stration of such mechanisms is found, the potential causative link with GERD must remain highly speculative [ 66 ] .

Summary

There is now strong evidence that acquired Zenker’s diverticulum arises in most cases sec-ondary to a poorly compliant, but normally relax-ing, UES which cannot fully distend during the process of sphincter opening. This gives rise to increased hypopharyngeal intrabolus pressure during the phase of trans -sphincteric bolus fl ow; pressure which is imparted to the area of relative muscular weakness (Killian’s dehiscence) just proximal to the cricopharyngeus. This combina-tion of factors gives rise to posterior herniation of the pouch over many years. The restricted open-ing of the cricopharyngeus is a result of muscle fi bre degeneration and fi broadipose tissue replacement. For this reason, cricopharyngeal myotomy is the essential component for success-ful surgical treatment of the condition. The pre-cise aetiology of this myopathic process affecting the cricopharyngeus is unknown and may be multifactorial. However, an underlying myositis with a predilection for the cricopharyngeus mus-cle is likely to be one such factor in some cases.

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16. Laing MR, Murthy P, Ah-See KW, et al. Surgery for pharyngeal pouch: audit of management with short and long term follow up. J R Coll Surg Edinb. 1995; 40:315–8.

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19. Jamieson GG, Duranceau AC, Payne WS. Pharyngo-oesophageal diverticulum. In: Jamieson GG, editor. Surgery of the oesophagus. Edinburgh: Churchill Livingstone Press; 1988. p. 435–43.

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principles of deglutition || zenker’s diverticulum

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