Zenker’s Diverticulum
Christopher Prichard , M.D.
May 6, 2004

The first case of Zenker's diverticulum was actually described in 1764 by the English surgeon, Ludlow, but it was not until 1877 that the German pathologist, Friedrich Albert von Zenker, described all 23 cases that had been presented in the literature until that time and then added 11 of his own. His description of the anatomy was so elegant that the diverticulum came to bear his name. This slide shows the sketch in Zenker's original paper of one of the diverticula that he presented.

There are a number of different types of foregut diverticula. They are often called esophageal diverticula, which is somewhat of a misnomer because Zenker's and other diverticula are actually in the hypopharynx. But the foregut diverticula has several ways to classify them, one of which is based on their etiology. They are typically classified as traction or pulsion diverticulum, and Zenker was the initial person to describe the pulsion diverticulum.

A traction diverticulum is formed due to external traction on the wall of the digestive tract resulting in the pouch formation, whereas the pulsion diverticulum is formed because of an imbalance of intraluminal force combined with the strength of the digestive tract wall. Foregut diverticula can also be classified based on their anatomic location, one of which is the midesophageal diverticulum, another described as the epiphrenic diverticulum. There are small transitory diverticula which appear throughout the swallowing cycle and then disappear; and then, of course, the hypopharyngeal diverticulum or Zenker's diverticulum.

Zenker's diverticulum is often called the pharyngoesophageal or hypopharyngeal diverticulum. It is a posterior outpouching in the hypopharynx, and it is actually a false diverticulum. That is, the wall of the diverticulum consists only of mucosa and submucosal tissue. It is a pulsion diverticulum formed by an imbalance of forces, which we will discuss in a moment, and it typically occurs in an anatomic region known as the Killian's triangle. When discussing the anatomy relevant to a Zenker's diverticulum, there are two areas that are important to look at. The first is in the posterior wall of the hypopharynx. In this region there are three inherent areas of weakness: one that is formed by a triangle at the inferior border of the cricopharyngea with the superior oblique fibers of the esophagus. This is referred to as Laimer's triangle. A second inherent weak point is between the oblique and the transverse fibers of the cricopharyngeus muscle: this is referred to as the Killian-Jamieson area, where lateral or Killian-Jamieson diverticula can form. Then, finally, the most significant area is the Killian's triangle, which is formed by the inferior-most fibers of the inferior constrictor muscle with the superior border of the cricopharyngea, and this is thought to be where the Zenker's diverticulum develops.

The second anatomic region that is important for consideration is the functional structure of the upper esophageal sphincter. This is a functional anatomic structure composed primarily of the cricopharyngeus muscle but also with the inferior fibers of the inferior constrictor as well as the superior fibers of the cervical esophagus. This is important functionally in that it has a high resting tone, about 55-60 mmHg, in the anterior posterior direction. It maintains this tone but relaxes about 100 msec prior to presentation of a bolus.

Normal swallowing is a highly complex coordinated series of events which, when undertaken correctly, seems to be taken for granted; but when there is dysfunction it is distinctly noted. It consists of three phases. The first is the oral phase, which consists of a preparatory phase of mastication followed by lubrication and formation of the bolus, which is then propagated past the faucial pillars into the oropharynx. This is the only voluntary phase of swallowing. The most fixed and critical phase of swallowing is the second or pharyngeal phase, which begins after passage of the bolus past the faucial pillars. This is the most critical phase because it is where the junction of the respiratory system and the digestive tract occurs. In this phase there is closure of the nasopharynx, constrictor contraction propelling the bolus inferiorly, as well as airway protection, which primarily occurs by closure of the glottis and vestibule as well as by elevation of the larynx and anterior displacement of the epiglottis. Then there is relaxation of the cricopharyngeus. This moves to the third and final phase, which is the esophageal phase, beginning with the opening of the UES and then pharyngeal peristaltic waves. A modified barium swallow gives us a good look at the level of coordination of these phases with a smooth swallow. You will see the velopharyngeal elevation and closure, the elevation of the larynx, and the propulsion of the bolus into the cervical esophagus.

In looking at the physiologic properties of the swallow, an important tool is esophageal manometry. These are pressure tracings that can actually be coordinated with a modified barium swallow to obtain precise physiologic information along certain points of the swallow. This is a typical tracing of a normal esophageal manometry. You will note the progressive contractions of the pharyngeal constrictor muscles at different pressure transducers placed along the hypopharynx. Also, a critically important part of the normal tracing is the upper esophageal sphincter relaxation, which begins at approximately the initiation of the pharyngeal contraction and, in the normal swallow, lasts until nearly the complete sweeping contraction of the constrictors. Any perturbation in this coordination can lead to dysphagia and one of the primary theories as to the development of Zenker's is an incoordination of this swallowing physiology.

Now there are a number of theories as to why Zenker's form, but there is no real consensus as to the underlying problem. It may be that it is the final end result of a number of physiologic abnormalities. One of the primary theories is pharyngoesophageal incoordination which is, as we were just speaking of, an incoordination between the opening of the cricopharyngeus and the peristaltic contractions propagating the bolus through the hypopharynx. Here you will note that the pharyngeal contraction actually occurs near the very end of the upper esophageal sphincter relaxation, which is noted by the bar. Then there is upper esophageal sphincter closure, which occurs beginning during the pharyngeal contraction, so it is essentially contracting against a closed aperture leading to higher intraluminal pressures and subsequent dehiscence in the Killian's triangle. Another theory of the development of Zenker's is that of cricopharyngeal spasm, and that is that likely in response to stimulation by reflux - the cricopharyngeus muscle simply spasms down. This is a manometric tracing obtained by McConnel that shows that in the region of the black arrow, where there normally should be upper esophageal sphincter relaxation, there is a spasmodic contraction followed by a hypertonic contraction. So, contraction of the pharyngeal constrictors against this closed aperture raises the pressure and is thought to be one of the forms of development of a Zenker's.

There are a number of other theories, one of which is a theory described as cricopharyngeal achalasia in which the cricopharyngeus has a high resting tone and fails to relax. Another theory is the theory of incomplete upper esophageal sphincter opening. And all of these are variations on the same principle, that hypertonicity of the cricopharyngeus leading to increased intraluminal pressures is the physiologic cause of the Zenker's.

There are authors such as van Overbeek who argue that it is simply an anatomic abnormality, and he cites the grouping of Zenker's diverticula within certain populations as evidence that this is a genetic and anatomic abnormality. Lerut added credence to this by taking histologic sections of the cricopharyngeus muscle in patients with Zenker's showing increased fibrosis and type I collagen deposition.

Zenker's is primarily a disease of the elderly. It rarely occurs in a patient under 40 years of age. It is typically in the seventh and eighth decades. It is predominantly in males and, in routine barium swallows obtained for any purpose, radiologic studies have shown a prevalence of about 1:1,000. Now the incidence varies depending on the region that you are in. In the United Kingdom, which has the highest incidence, it is about 2:100,000 people per year. But if you look in Asia or in Africa, a case of a Zenker's diverticulum is almost never seen. So this is the evidence offered for the anatomic theory of development.

Most patients with a Zenker's present with dysphagia, between 80% and 90%. Another very common presentation is regurgitation of undigested food. The combination of regurgitation of undigested food with cervical borborygmi is almost pathognomonic of Zenker's diverticulum. Thirty to 40% will present with aspiration and a chronic cough, and up to 15% of these total patients will actually have episodes of aspiration pneumonia from this. In severely large Zenker's, you can actually see weight loss due to malnutrition and hoarseness. In addition, with large Zenker's you can see changes in the voice and neck masses, cervical borborygmi after swallowing, as well as severe halitosis, pooling of secretions, and the sequelae of pneumonia. There has been noted to be an increased association with hiatal hernia and esophageal reflux, though there have been a number of studies that try to demonstrate a causality that has been unsuccessful, but there is a reported correlation of between 30% and 90% of patients with Zenker's with evidence of gastroesophageal reflux. There is also a small but real phenomenon presented of carcinoma within a Zenker's at an incidence of about 0.4% of diverticula. Clues that tip the clinician off as to the appearance of a carcinoma would be pain or hematemesis in a patient with Zenker's, which are not typical findings in these patients.

The diagnostic evaluation consists of primarily the barium swallow, which shows, as in our patient, a posterior pharyngeal diverticulum with pooling of contrast. The swallow can also offer other clues. If you see intradiverticular opacification, this is most commonly related to food, but if it remains constant over a number of studies, it can be a tip-off as well to the presence of a carcinoma. A chest X-ray should be obtained in order to look for evidence of aspiration and, on occasion, large Zenker's can present as mediastinal winding on the chest X-ray. Certainly, in patients with dysphagia, the first line work-up for a patient with a Zenker's is not a modified barium swallow, but certainly patients with dysphagia will undergo modified. This is a modified barium swallow in a patient with actually two hypopharyngeal diverticula. Note the passage of contrast with the posterior pooling of contrast in this patient with a Zenker's.

There are a number of open surgical approaches to the patient with a Zenker's diverticulum, the most simple of which is a cricopharyngeal myotomy. In addition, procedures have been described for inversion of the diverticulum as well as diverticulopexy and open diverticulectomy. Diverticular inversion consists of inverting the diverticulum into the esophageal lumen and tying around the neck with a pursestring suture. Subsequently, the pouch atrophies nicely, and this is a procedure that would be used in a patient with a poor medical status who would be unable to tolerate a long general anesthetic or a patient who would not be able to withstand the complication of an open mucosal procedure such as mediastinitis. In addition, there is a procedure known as diverticulopexy which when combined with cricopharyngeal myotomy in which the diverticulum is inverted and attached against the prevertebral fascia, allows emptying of the diverticulum. This is also typically a procedure done in patients who would be unable to tolerate a long procedure or serious complications.

hen, described as the gold standard in the literature, is open diverticulectomy in which the diverticulum is removed and then a layered closure is performed. The largest series that has been presented on open diverticulectomy came out of the Mayo Clinic in which they presented 888 patients over a 30-year span. Their results were as follows: They presented significant complications of vocal fold paralysis or paresis, wound infection at rates of about 3%, as well as fistula formation at nearly 2%. Interestingly, in this paper they actually did not quote any rates for mediastinitis, which is the most feared complication of the Zenker's diverticulum; but they did have a 1.2% mortality rate and they did not give cause for specific mortalities. So it is possible that their cases of mediastinitis were hidden within this. In this series, they had a recurrence rate of 3.6%.

In 1917, Mosher introduced the concept of endoscopic diverticulectomy, but he rapidly abandoned it when his seventh patient developed a case of mediastinitis and died. It was reintroduced in 1960 by Dohlman and Mattsson who had developed special endoscopes for the procedure, and they presented a series of 100 patients with no more mortality and only a 7% recurrence rate. Then in the original Bowman procedure they used electrocautery to divide the common wall between the esophagus and the pouch. In 1993, Collard introduced the next major breakthrough in using the endoscopic GIA staple-assisted diverticulectomy. Other methods that have been used are KTP lasers, CO 2 lasers, and flexible endoscopy with electrocautery. This is the Storz diverticuloscope that is used here at The Methodist Hospital. You will note the two flanges which allow for entry into the esophagus and the diverticulum, which affords the following view. So, on endoscopy, you should see the diverticulum inferiorly as well as the esophageal lumen and the common wall that contains the cricopharyngeus muscle. This is divided using a special staple cartridge, which is modified. The standard GIA cartridge is the one below, and you will note that the cartridge with the arrow has been trimmed so that the suture line reaches the end of the pouch when it is placed in the sac endoscopically.

The largest series in the literature of endoscopic staple-assisted diverticulectomy comes out of Duke where they presented 150 patients on whom they performed this procedure. Their average hospital stay was less than a day, and the OR time was about thirty minutes. They presented that the average patient was advanced to a clear diet in about six hours, and 88% of their patients long term had either complete resolution or significant improvement in their symptoms; but they did have a recurrence rate of 10.9%. Of their complications, the most common was chipping of teeth due to the endoscope, followed next by postoperative fever. And only about 2% of their total patients had a severe complication of a pneumonia, perforation of the sac, or vocal fold paresis, which subsequently resolved. They had no mortality, and they had no cases of mediastinitis. In this paper, Scher went on to compare all of the cases presented in the literature from 1990 to 2002 of endoscopic and open diverticulectomy. You will note the data for average surgery length, average time to p.o. intake, and average hospitalization was significantly decreased in the patients undergoing the endoscopic technique. As well, comparing the morbidity and mortality, the endoscopic technique was noted to have about half the total significant morbidity, as well as a significantly lower mortality; but in terms of resolution of symptoms and recurrence rates of the diverticula, he found that these were about the same.

Mark Urken at Mount Sinai did a similar study just with 16 of his patients, 8 of whom had an open procedure and 8 of whom had the endoscopic procedure, and he did a charge analysis. It is interesting in that his data for surgery length, time to p.o. intake, and hospital stay were very similar to the data accumulated by Scher. And when he broke down the hospital charges for these patients, it is interesting that the OR charges for the endoscopic and open procedure were about the same, thought primarily due to the added expense of the endoscopic equipment, but that the hospital expenses of the patients were about one-fourth of that of the open diverticulectomy patients.

Our patient was taken to the Operating Room and direct laryngoscopy was performed with an anterior commissure scope which revealed a good view; so subsequently the Storz diverticuloscope was introduced, which revealed the esophageal lumen, the Zenker's pouch, and the common wall between the two. Subsequently, endoscopic staple-assisted diverticulectomy was performed. Here you see the stapled margin of the diverticulum with continuity between the esophagus and the pouch. A Dobbhoff tube was placed intraoperatively, and the patient was transferred to the floor. He was started on clears on postoperative day #1, which he tolerated well. He remained afebrile, his Dobbhoff tube was removed, and he was discharged home on postoperative day #1.

In summary, Zenker's diverticulum is a surgically correctable anatomic cause of dysphagia. Though the exact physiologic mechanism is not thoroughly understood, it is possible that this is a common final result of a number of physiologic abnormalities. Endoscopic repair offers significant advantages in appropriate patients. Given the aging population, it is likely that this will become an increasing clinically significant entity in the future.

Case Presentation:

F.M. is an 84-year-old gentleman from El Paso who presents with seven years of progressively worsening dysphagia. Over the past two years he has had increasing difficulty swallowing, and frequently feels that food is getting stuck in his throat. He recently has begun regurgitating undigested food 15 to 20 minutes after eating. He also notes some weight loss, as well as symptoms of reflux. He denies fevers, cough, or odynophagia.

Physical examination was notable for marked pooling of secretions. There was mild erythema of the hypopharyngeal mucosa. He had normal true vocal fold mobility bilaterally, and was noted to have a sensitive gag reflex. The neck was soft and had no palpable masses.

A complete blood count and Chem-7 were within normal limits. A chest x-ray was unremarkable except for some minimal fibrocalcific scarring the right apex.

A barium swallow was obtained which revealed a large hypopharyngeal pouch which filled with contrast. A diagnosis of Zenker’s diverticulum was established.

The patient was taken to the operating room and underwent direct laryngoscopy with good visualization of the esophagus, diverticulum, and common wall. A Storz diverticuloscope was introduced and an endoscopic diverticulectomy performed using the GIA stapler without complication. A Dobhoff tube was placed under direct visualization.

The patient was started on clear liquids on post-operative day one. He remained afebrile and tolerated clears, and was subsequently advanced to a soft diet. His Dobhoff tube was discontinued on post-operative day one, and he was discharged home.

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