Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

In anatomy, Zenker’s diverticulum, also pharyngoesophageal diverticulum, also pharyngeal pouch, is a diverticulum of the mucosa of the pharynx, just above the cricopharyngeal muscle (i.e. above the upper sphincter of the esophagus). It is a false diverticulum (not involving all layers of the esophageal wall). The first description of Zenker’s diverticulum dates back to 1769 by Ludlow. It was named in 1877 by German pathologist Friedrich Albert von Zenker. Esophageal diverticula are classified on the basis of location into three types: phrenoesophageal (Zenker’s diverticulum-70%) ZD, epiphrenic (20%), thoracic and mediastinal (10%). Zenker’s diverticulum is thought to be due to the result of motor abnormalities of the esophagus. The defect over the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx results in ZD. Killian’s triangle leads to an evagination of the sphincter, which may be because of the high pressures in the food bolus in the course of swallowing and the abnormalities of the upper esophageal sphincter (UES). This failure to achieve adequate diameter for effective bolus clearance leads to a subsequent increase in the hypopharyngeal pressure gradient. As the diverticulum enlarges, it may compress the pharyngoesophageal segment as well as increased stiffness and the intrabolus pressure. The risk factors of the Zenker’s diverticulum include people in their seventh and eight decades, male, GERD, pre-existing hiatal hernia, esophageal motility disorder, esophagitis, neurological disorders like a stroke. Symptoms of Zenker’s diverticulum slowly start as a oropharyngeal dysphagia progressing from solids to liquids, Regurgitation of undigested food from the diverticular sac, Pharyngeal stasis of secretions, Chronic aspiration, Halitosis, Chronic cough, sensation of a lump in the throat, Hoarseness, Cervical borborygmi. Aspiration pneumonia, Bleeding of the diverticulum, Ulceration of the diverticulum, compression of the trachea and esophageal obstruction with large diverticula, very rarely Squamous cell carcinoma of the diverticulum, Perforation of the diverticulum during the endoscopy and hence scopes with side viewing should be used to prevent perforation. While it may be asymptomatic, Zenker diverticulum often causes clinical manifestations such as dysphagia, globus sensation, regurgitation, cough, halitosis, and odynophagia. An x-ray (barium esophagogram) is the best initial imaging study in a patient suspected with Zenker’s Diverticulum. Findings on an x-ray (barium esophagogram) suggestive of esophageal diverticulum associated with ZD appear as thin projections on the anterior esophageal wall over the Killian’s triangle. No medical treatment is currently known or practiced for symptomatic Zenker diverticulum. Surgery is the most definitive therapy for the Zenker’s diverticulum. If small and asymptomatic, no treatment is necessary. Larger, symptomatic cases of Zenker’s diverticulum have been traditionally treated by neck surgery to resect the diverticulum and incise the cricopharyngeus muscle. However, in recent times non-surgical endoscopic techniques have gained more importance, and the currently preferred treatment is the endoscopic stapling i.e. closing of the diverticulum via a stapler inserted through a tube in the mouth. This may be performed through a fiberoptic endoscope. Other non-surgical treatment modalities exist, such as endoscopic laser, which recent evidence suggests is less effective than stapling.

The first description of Zenker’s diverticulum dates back to 1769 by Ludlow. It was named in 1877 by German pathologist Friedrich Albert von Zenker. The first description of Zenker’s diverticulum dates back to 1769 by Ludlow. A century later, a German pathologist, Friedrich Albert von Zenker, recognized and further characterized the pathophysiology of this diverticulum. In 1877 Zenker and Ziemssen reviewed the world literature on the Zenker’s diverticulum. In 1840 Rokitansky first described traction diverticula of the thoracic esophagus. Until 1816 publication,ZD was thought to be congenital or traumatic in origin. In 1877, von Zeimssen, professor in Munich, published “Krankheiten des Oesophagus” on the esophageal ulceration and diverticula. Preliminary thoughts on managing pharyngoesophageal diverticula originated as early as 1830, when Bell proposed the establishment of a fistula to empty the diverticulum of its contents.

Esophageal diverticula are classified on the basis of location into three types Phrenoesophageal (Zenker’s diverticulum-70%) ZD is a defect over the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx. Epiphrenic (20%) diverticula result either from hypertonia of the lower esophageal sphincter (esophageal achalasia). Thoracic and mediastinal (10%) Thoracic diverticula are probably more often of a congenital than traction origin.

Zenker’s diverticulum (ZD) is thought to be due to the result of motor abnormalities of the esophagus. The defect over the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx results in ZD. Killian’s triangle is surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle. It is considered a pseudodiverticulum as it includes only mucosa and submucosa. Chronic strain on the Killian’s triangle leads to an evagination of the sphincter, which may be because of the high pressures in the food bolus in the course of swallowing and the abnormalities of the upper esophageal sphincter (UES). This failure to achieve adequate diameter for effective bolus clearance leads to a subsequent increase in the hypopharyngeal pressure gradient. Increased intra-bolus pressures found in patients with ZD can be secondary to impaired bolus passage combined with the gastroesophageal reflux disease (GERD) or as a result of the GERD. As the diverticulum enlarges, it may compress the pharyngoesophageal segment as well as increased stiffness and the intrabolus pressure. Increased intrabolus pressure is also increased in older patients who perform multiple swallows to achieve bolus clearance. Acid reflux is thought to lead to increased spasm of the UES which in turn increases the intra-bolus pressures during swallowing, given that swallowing is frequently distinct from episodes of acid reflux disease.

Zenker’s diverticulum (ZD) also known as pharyngosophageal diverticulum. It is an acquired sac-like outpouching of the mucosa and submucosa layers originating from the pharyngoesophageal junction. Killian’s dehiscence a pulsion of false diverticulum occurring dorsally at the pharyngoesophageal wall surrounded by the oblique inferior pharyngeal constrictor muscle and the transversal fibers of the cricopharyngeal muscle. ZD occurs due to increased intraluminal pressure in the oropharynx during swallowing, against an inadequate relaxation of the cricopharyngeal muscle. An incomplete opening of the Upper Esophageal Sphincter (UES) causing the protrusion of the mucosa through an area of relative weakness at the dorsal pharyngoesophageal wall. The pharyngoesophageal phase of swallowing is affected in ZD resulting in hindering the neuromuscular functions such as chewing, initiating the swallowing, and propulsion of the food from the oropharynx into the cervical esophagus.

The differential diagnosis of the Zenker’s diverticulum (ZD) are as follows Plummer-Vinson syndrome, reflux esophagitis, esophageal carcinoma, systemic sclerosis, achalasia, psuedoachalasia, chagas disease, esophageal candidiasis, pharyngitis and stroke.

The incidence ZD is approximately 2 per 100,000 individuals worldwide, The prevalence of ZD is between 0.01 to 0.11% per 100,000 individuals worldwide. The mortality rate is 0.3% for stapled rigid endoscopic procedures. Mortality rate for non-stapled rigid endoscopic procedures is 0.2%. ZD commonly affects middle-aged and elderly individuals, especially people in their 7th and 8th decades.There is no racial predilection to ZD. Males are more commonly affected by ZD than females. The men to women ratio is approximately 1.5 to 1. The majority of ZD cases are reported in northern Europe.

The risk factors of the Zenker’s diverticulum (ZD) are as follow people in their seventh and eight decades, male, GERD, pre-existing hiatal hernia, esophageal motility disorder, esophagitis, neurological disorders like a stroke.

There is insufficient evidence to recommend routine screening for Zenker’s diverticulum.

Symptoms of Zenker’s diverticulum slowly start as a oropharyngeal dysphagia progressing from solids to liquids, Regurgitation of undigested food from the diverticular sac, Pharyngeal stasis of secretions, Chronic aspiration, Halitosis, Chronic cough, sensation of a lump in the throat, Hoarseness, Cervical borborygmi. The patient may note food on the pillow upon awakening in the morning. Although small diverticula may not cause symptoms, larger diverticula usually are symptomatic. Both the inability of the sphincter to fully open and the extrinsic compression from the pouch itself are likely to explain the dysphagia experienced by patients. In patients with very large diverticula, a gurgling swelling in the neck can occasionally be detected on palpation.

Complications of the Zenker’s diverticulum includes Aspiration pneumonia, Bleeding of the diverticulum, Uuceration of the diverticulum, compression of the trachea and esophageal obstruction with large diverticula, very rarely Squamous cell carcinoma of the diverticulum, Perforation of the diverticulum during the endoscopy and hence scopes with side viewing should be used to prevent perforation.

Prognosis of ZD after the intervention is good, the recurrence of the diverticulum is very rare.

While it may be asymptomatic, Zenker diverticulum often causes clinical manifestations such as dysphagia, globus sensation, regurgitation, cough, halitosis,odynophagia.

While it may be asymptomatic, Zenker diverticulum often causes clinical manifestations such as Dysphagia, Globus sensation, Regurgitation, Cough, Halitosis, Odynophagia.

Laboratory studies are not helpful in the diagnosis of the Zenker’s Diverticulum (ZD), whereas they are used for the upper esophageal webs associated with iron deficiency anemia. The laboratory tests are done to differentiate the ZD from Plummer- Vinson syndrome. Laboratory findings consistent with the diagnosis of Plummer-Vinson syndrome include the presence of iron deficiency anemia.

An x-ray (barium esophagogram) is the best initial imaging study in a patient suspected with Zenker’s Diverticulum (ZD). Findings on an x-ray (barium esophagogram) suggestive of esophageal diverticulum associated with ZD appear as thin projections on the anterior esophageal wall over the Killian’s triangle.

Zenker’s diverticulum appears as an out-pouching sac on the CT scan over the posterior esophagus in the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle.

Zenker’s diverticulum appears as an out-pouching sac on the MRI scan over the posterior esophagus in the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle. The sac is filled with, fluid, food, contrast materials.

No medical treatment is currently known or practiced for symptomatic Zenker diverticulum.

Surgery is the most definitive therapy for the Zenker’s diverticulum (ZD). If small and asymptomatic, no treatment is necessary. Larger, symptomatic cases of Zenker’s diverticulum have been traditionally treated by neck surgery to resect the diverticulum and incise the cricopharyngeus muscle. However, in recent times non-surgical endoscopic techniques have gained more importance, and the currently preferred treatment is the endoscopic stapling i.e. closing of the diverticulum via a stapler inserted through a tube in the mouth. This may be performed through a fiberoptic endoscope. Other non-surgical treatment modalities exist, such as endoscopic laser, which recent evidence suggests it less effective than stapling.

There are no established measures for the primary prevention of Zenker’s Diverticulum.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The first description of Zenker’s diverticulum (ZD) dates back to 1769 by Ludlow. It was named in 1877 by German pathologist Friedrich Albert von Zenker. The first description of Zenker’s diverticulum dates back to 1769 by Ludlow. A century later, a German pathologist, Friedrich Albert von Zenker, recognized and further characterized the pathophysiology of this diverticulum. In 1877 Zenker and Ziemssen reviewed literature on the Zenker’s diverticulum. In 1840 Rokitansky first described traction diverticula of the thoracic esophagus. Until 1816 , ZD was thought to be congenital or traumatic in origin. In 1877, von Zeimssen, a professor in Munich, published “Krankheiten des Oesophagus” on the esophageal ulceration and diverticula. Preliminary thoughts on managing pharyngoesophageal diverticula originated as early as 1830, when Bell proposed the establishment of a fistula to empty the diverticulum of its contents.

The history of the Zenker’s diverticulu (ZD) is as follows:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]}

• It was named in 1877 by German pathologist Friedrich Albert von Zenker.
• The first description of Zenker’s diverticulum dates back to 1769 by Ludlow
• One hundered years later, a German pathologist, Friedrich Albert von Zenker, recognized and further characterized the pathophysiology of this diverticulum.
• In 1877 Zenker and Ziemssen reviewed literature on the Zenker’s diverticulum.
• In 1840 Rokitansky first described traction diverticula of the thoracic esophagus.
• Until 1816 publication,ZD was thought to be congenital or traumatic in origin.
• In 1877, von Zeimssen, professor in Munich, published “Krankheiten des Oesophagus” on the esophageal ulceration and diverticula.
• Preliminary thoughts on managing pharyngoesophageal diverticula originated as early as 1830, when Bell proposed the establishment of a fistula to empty the diverticulum of its contents.
• The first recorded practice of this was by Nicoladoni in Vienna in 1877.
• An unsuccessful attempt at excision of the diverticulum, first suggested by Kluge in 1850, was performed in 1884 by Niehans.
• The first successful resection was by Wheeler in 1885, followed by additional favorable reports of von Bergmann and Kocher in 1892 and Butlin and Billroth in 1893.
• In 1896 Girard devised a method of invaginating the diverticulum into the esophagus, oversewing the resultant dimple.
• This procedure was associated with promising results, although a case of recurrence was reported by Waggett and Davis in a patient after sneez
• Diverticulopexy was first performed by Hill in 1917.
• In 1910 Stetton came up with a list of all patients that suffered from Zenker’s diverticulum along with the procedure performed for treatment.
• These methods included primary excision, excision after preliminary gastrostomy, invagination of the sac, mucosal destruction without excision, and two-stage excision.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Diverticula of the esophagus can be classified into phrenoesophageal (Zenker’s diverticulum-70%), epiphrenic, thoracic and mediastinal.

• Esophageal diverticula are classified on the basis of location into three types^[1][2][3]

• Almost all esophageal diverticula are acquired pulsion diverticula.

1. Phrenoesophageal (Zenker’s diverticulum-70%)

• ZD is a defect over the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx

2. Epiphrenic (20%)

• Epinephric diverticula result either from hypertonia of the lower esophageal sphincter (esophageal achalasia)

3. Thoracic and mediastinal (10%)

• Thoracic diverticula are probably more often of a congenital than traction origin.

Type of diverticulum	Major characteristics
Zenker’s diverticulum	Defect over Killian’s triangle Weakness in the muscular wass of hypopharynx
Traction diverticulumm	Small Mid-esophagus Motor disorder or post-inflammatory
Epiphrenic diverticiulum	Above lower esophageal sphincter Background of a motility disorder such as achlasia or diffuse esophageal spasm Nocturnal regurgitation of fluids
Thoracic diverticulum	Rare (10 % of esophageal diverticula) Dysphagia and regurgitation Due to congenital reasons, traction, pulsion and neuromuscular incoordination (functional) Epibronchial variety most common
Mediastinal diverticulum	Most commonly secondary to traction (for example from calcified lymph nodes after tuberculosis)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Zenker’s diverticulum (ZD) is thought to occur due to the result of motor abnormalities of the esophagus. A defect over the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx results in ZD. Killian’s triangle is surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle. It is considered a pseudodiverticulum as it includes only mucosa and submucosa. Chronic strain on the Killian’s triangle leads to an evagination of the sphincter, which may be because of the high pressures caused by the food bolus in the course of swallowing and the abnormalities of the upper esophageal sphincter (UES). This failure to achieve adequate diameter for effective bolus clearance leads to a subsequent increase in the hypopharyngeal pressure gradient. Increased intra-bolus pressures found in patients with ZD can be secondary to impaired bolus passage combined with the gastroesophageal reflux disease (GERD) or as a result of the GERD. As the diverticulum enlarges, it may compress the pharyngoesophageal segment as well as increased stiffness and the intra-bolus pressure. Increased intra-bolus pressure is also increased in older patients who perform multiple swallows to achieve bolus clearance. Acid reflux is thought to lead to increased spasm of the UES which in turn increases the intra-bolus pressures during swallowing, given that swallowing is frequently distinct from episodes of acid reflux disease.

The pathophysiology of the Zenker’s diverticulum is as follows:^{[1][2][3][4][5][6][7][8][9]}

Killian’s dehiscence

• Zenker’s diverticulum (ZD) is thought to be due to the result of motor abnormalities of the esophagus.
• ZD is a defect over the Killian’s triangle, a point of weakness in the muscular wall of the hypopharynx.
• Killian’s triangle is surrounded by the cricopharyngeal sphincter and oblique fibers of the inferior constrictor of the pharyngeal muscle.
• ZD should be considered a pseudodiverticulum as it includes only mucosa and submucosa.

Chronic straining

• Chronic strain on the Killian’s triangle leads to an evagination of the sphincter, which may be because of the high intra-luminal pressures caused by the food bolus in the course of swallowing and the abnormalities of the upper esophageal sphincter (UES).
• This failure to achieve adequate diameter for effective bolus clearance leads to a subsequent increase in the hypopharyngeal pressure gradient.
• Increased intrabolus pressures found in patients with ZD can be secondary to impaired bolus passage combined with the gastroesophageal reflux disease (GERD) or as a result of the GERD.

Enlargement of Zenker’s diverticulum

• As the diverticulum enlarges, it may compress the pharyngoesophageal segment as well as causing increased stiffness and the intrabolus pressure.
• Increased intrabolus pressure is also increased in older patients who perform multiple swallows to achieve bolus clearance.

Hypotheses for mechanism of development of Zenker’s diverticulum

Various hypothesis involved in the pathogenesis of the Zenker’s diverticulum are as follows:^{[9][10][8][11][12][13][14]}

1. Zenker’s diverticulum is a disorder of diminished upper esophageal sphincter, incomplete sphincter opening is probably the cause of dysphagia. Increased hypopharyngeal pressures throughout swallowing are probably important in the pathogenesis of the diverticulum.
2. The nemaline bodies and red ragged fibers are usually the normal cricopharyngeous findings, whereas the Zenker’s diverticulum is characterized by adipose tissue deposition and degeneration of the fiber these structural modifications can impair the UES opening and dysphagia ensues.
3. The pharyngeal pouches are not a purely localized incoordination of the cricopharyngeal sphincter but are associated with a generalized esophageal muscle dysfunction.
4. Acid reflux induces longitudinal esophageal shortening, which in turn increases the chance for the development of herniation between two spatially associated structures, the pharyngeal constrictors and cricopharyngeus muscles, leading to the development of Zenker diverticulum.
5. Zenker’s diverticulum is thought to result from disordered coordination among the pharynx and upper esophageal sphincter.
   • Manometric studies of the upper esophagus were used in testing the hypothesis of dysmotility in the formation and growth of a Zenker’s diverticulum; however, the data have provided conflicting evidence.
   • Manometric studies show that resting upper esophageal sphincter strain is normal in some patients with Zenker’s diverticulum and decreased in others. Abnormal premature relaxation and contraction of the upper esophageal sphincter seen in some patients with Zenker’s diverticulum may be accompanied with the aid of pharyngeal contractions against a closed sphincter.
   • This abnormality is thought by a few investigators to be the cause of Zenker’s diverticulum, but not by others who have found normal upper sphincter relaxation.
6. In summary, in-coordination of pharyngeal contraction and UES opening has also been variably demonstrated by some investigator.

Abnormal esophageal motility

• All the above-mentioned hypotheses lead to herniation within the Killian’s triangle, inclusive of disorders associated with altered UES function, unusual esophageal motility, esophageal shortening.
• This leads to the creation of a sac with a narrow neck that can trap liquid and food, the distended sac may compress the cervical esophagus.
• Impaired bolus passage leads to increases intra-bolus pressure which leads to herniation in the Killian’s triangle.

Role of acid reflux

• Acid reflux is thought to lead to increased spasm of the UES which in turn increases the intrabolus pressures during swallowing, given that swallowing is frequently distinct from episodes of acid reflux disease.

On gross pathology, esophageal diverticulum or a sac are characteristic findings of Zenker’s diverticulum.

On microscopic histopathological analysis, Zenker’s diverticulum presents with the following findings:

• Psuedo diverticulum
• Only mucosa and submucosa present
• Chronic submucosal inflammation
• Epithelial atypia or dysplasia
• Squamous cell carcinoma of esophagus (in advanced cases)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

Zenker’s diverticulum (ZD) also known as pharyngosophageal diverticulum. It is an acquired sac-like outpouching of the mucosa and submucosa layers originating from the pharyngoesophageal junction. Killian’s dehiscence a pulsion of false diverticulum occurring dorsally at the pharyngoesophageal wall surrounded by the oblique inferior pharyngeal constrictor muscle and the transversal fibers of the cricopharyngeal muscle. ZD occurs due to increased intraluminal pressure in the oropharynx during swallowing, against an inadequate relaxation of the cricopharyngeal muscle. An incomplete opening of the Upper Esophageal Sphincter (UES) causing the protrusion of the mucosa through an area of relative weakness at the dorsal pharyngoesophageal wall. The pharyngoesophageal phase of swallowing is affected in ZD resulting in hindering the neuromuscular functions such as chewing, initiating the swallowing, and propulsion of the food from the oropharynx into the cervical esophagus.

ZD is caused by^{[1][2][3][4][5][5]}

• Zenker’s diverticulum also known as pharyngosophageal diverticulum.
• It is an acquired sac-like outpouching of the mucosa and submucosa layers originating from the pharyngoesophageal junction.
• Since it involves only the mucosa and submucosa it is a false diverticulum.
• Killian’s dehiscence– pulsion false diverticulum occurring dorsally at the pharyngoesophageal wall bounded by the propulsive oblique inferior pharyngeal constrictor muscle and the transversal fibers of the cricopharyngeal muscle
• ZD occurs due to increased intraluminal pressure in the oropharynx during swallowing, against an inadequate relaxation of the cricopharyngeal muscle,
• A subsequent incomplete opening of the UES, causing the protrusion of the mucosa through an area of relative weakness at the dorsal pharyngoesophageal wall.
• ZD cause the disorder of the pharyngoesophageal phase of swallowing.
• The neuromuscular functions such as chewing, initiating the swallowing, and propulsion of the food from the oropharynx into the cervical esophagus.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The differential diagnosis of the Zenker’s diverticulum (ZD) are as follows Plummer-Vinson syndrome, reflux esophagitis, esophageal carcinoma, systemic sclerosis, achalasia, psuedoachalasia, chagas disease, esophageal candidiasis, pharyngitis and stroke.

Dysphagia

Oropharyngeal dysphagia

Esophageal dysphagia

Solids only

Solids and Liquids

Solids only

Solids and Liquids

•Zenker’s diverticulum •Neoplasm •Webs

Neurogenic

Myogenic

Pain

•Achalasia •Scleroderma •DES

•Myasthenia gravis •Connective tissue disorder •Myotonic dystrophy

No

Yes

Heart burn

Barium swallow

Mental status

•Pill esophagitis •Caustic injury •Chemotherapy

Yes

No

Impaired

Normal

Non progressive

Progressive

Sac

Webs

Mass

Scleroderma

•Achalasia •DES

Stroke

•ALS •Parkinsonism

•Rings •Webs

•Strictures •Cancer

Zenker’s diverticulum

Plummer-Vinson syndrome

Carcinoma

Chest pain and manometry

Barium swallow

Weight loss

Increase LES pressure

Rings

Webs

Yes

No

Rapid

Slow

Achalasia

DES

Cancer

Strictures/GERD

Zenker’s diverticulum must be differentiated from other diseases that cause dysphagia such as reflux esophagitis, esophageal carcinoma, systemic sclerosis, esophageal spasm, pseudoachalasia, stroke, esophageal candidiasis and Chagas disease.^{[1][2][3][4][5][6][7][8][9][10][11]}

Disease	Signs and Symptoms								Barium esophagogram	Endoscopy	Other imaging and laboratory findings	Gold Standard
	Onset	Dysphagia			Weight loss	Heartburn	Other findings	Mental status
		Solids	Liquids	Type
Plummer-Vinson syndrome	Gradual	+	–	Non progressive	+/-	–	Glossitis Koilonychia	Normal	Thin projections on the anterior esophageal wall Multiple upper esophageal constrictions	Direct visualization of esophageal webs Superior to esophagogram	Videofluoroscopy shows mucosal and submucosal foldings	Triad of Iron deficiency anemia Esophageal webs Glossitis
Esophageal stricture	Gradual Sudden onset	+	–	Progressive	+/-	+/-	Odynophagia Cough Chest pain	Normal	Sacculations Fixed transverse folds Esophageal intramural pseudodiverticula	Mucosal edema Circumferential thickening in GERD Pale mucosa with white exudate in lymphocytic esophagitis Swelling and hemorrhagic congestion in caustic ingestion	Manometry may show dysmotility CT scan for staging malignant strictures	Barium esophagogram
Diffuse esophageal spasm	Sudden	+	+	Non progressive	+	+	Chest pain	Normal	Nonperistaltic and nonpropulsive contractions Corkscrew or rosary bead esophagus	Inconclusive	Manometry shows high-amplitude esophageal contractions CT scan may show hypertrophy of esophageal muscles	Manometry
Achalasia	Gradual	+	+	Non progressive	+/-	–	Regurgitation of undigested food Chest pain	Normal	“Bird’s beak” or “rat tail” appearance Dilated esophageal body Air fluid level (absent peristalsis) Absence of an intragastric air bubble	Dilated esophagus Residual food fragments Normal mucosa	Residual pressure of LES > 10 mmHg Incomplete relaxation of the LES Increased resting tone of LES Aperistalsis	History of dysphagia with positive endoscopy and manometry
Systemic sclerosis	Gradual	+	+	Progressive	+/-	+	Muscle and joint pain Raynaud’s phenomenon Skin changes	Normal	Dysmotility Patulous esophagus	Mucosal damage Peptic stricture (advanced cases)	Positive serology for Antinuclear antibodies Rheumatoid factor Creatine kinase ESR	Skin biopsy
Zenker’s diverticulum	Gradual	+	–		+/-	–	Food regurgitation Halitosis Cough Hoarseness	Normal	Thin projections on esophageal wall over Killian’s triangle	Outpouching of posterior pharyngeal wall Exclude the presence of SCC	CT & MRI shows out-pouching over the posterior esophagus in the Killian’s triangle	Barium esophagography
Esophageal carcinoma	Gradual	+	+	Progressive	+	+/-	Lymphadenopathy Cachexia	Normal	Irregular stricture Pre-stricture dilatation	Esophageal obstruction Staging of disease	CT and PET scan is an optional test for staging of the disease	Biopsy
Stroke (Cerebral hemorrhage)	Sudden	+	+	Progressive	+	+/-	Dysarthria Limb weakness Fatigue	Impaired	Pooling of contrast in the pharynx Aspiration of barium contrast into the airway	Reduced opening of upper esophageal sphincter Reduced larynx elevation	CT without contrast shows acute hemorrhage as a hyperattenuating clot	CT without contrast
Motor disorders (Myasthenia gravis)	Gradual	+	+	Progressive	+/-		Ptosis Diplopia Fatigue	Normal	Stasis in pharynx and pooling in pharyngeal recesses	Velopharyngeal insufficiency Delayed swallowing function	CT may show anterior mediastinal mass (thymoma) Positive tensilon test	Anti–acetylcholine receptor antibody test
GERD	Gradual Sudden onset	+	–	Progressive	+/-	+	Cough Hoarseness	Normal	Free acid reflux Esophagitis with scarring Strictures Barrett’s oesophagus	Erythema, erosions and ulceration Barrett’s esophagus	Esophageal manometry may show decreased tone of LES	24 hour esophageal pH monitoring
Esophageal web	Gradual	+	+/-	Progressive	–	+/-	Findings of the underlying cause such as iron deficiency anemia or bullous pemphigoid	Normal	Symmetrical narrowing of the esophagus	Smooth membrane not encircling the whole lumen	Videofluoroscopy shows mucosal and submucosal foldings	Barium esophagogram

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The incidence ZD is approximately 2 per 100,000 individuals worldwide, The prevalence of ZD is between 10 to 110 per 100,000 individuals worldwide. The mortality rate is 300 individuals per 100,000 individuals for stapled rigid endoscopic procedures. Mortality rate for non-stapled rigid endoscopic procedures is 200 individuals per 100,000 individuals. ZD commonly affects middle-aged and elderly individuals, especially people in their 7th and 8th decades.There is no racial predilection to ZD. Males are more commonly affected by ZD than females. The men to women ratio are approximately 1.5 to 1. The majority of ZD cases are reported in northern Europe.

The incidence ZD is approximately 2 per 100,000 individuals worldwide.^[1][2][3]

The prevalence of ZD ranges from a low of 10 individuals per 100,000 individuals to a high of 110 individuals per 100,000 individuals worldwide.^[1][2][3]

• Mortality rate is 300 per 100,000 individuals for stapled rigid endoscopic procedures.
• Mortality rate for non-stapled rigid endoscopic procedures is 200 individuals per 100,000 individuals.

ZD commonly affects middle-aged and elderly individuals, especially people in their 7th and 8th decades.^[1]

There is no racial predilection to ZD.

Males are more commonly affected by ZD than females. The men to women ratio is approximately 1.5 to 1.^[1]

The majority of ZD cases are reported in northern Europe.^[1][4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The risk factors of the Zenker’s diverticulum (ZD) are old age (seneth and eighth decade of life), male gender, gastroesophageal reflux disease (GERD), pre-existing hiatal hernia, esophageal motility disorder, esophagitis, neurological disorders like a stroke.

Risk factors for ZD includes^[1][2]

• Old age (70-80 years)
• Male gender
• GERD
• Hiatal hernia
• Esophageal motility disorder
• Esophagitis
• Neurological disorders such as stroke

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

There is insufficient evidence to recommend routine screening for Zenker’s diverticulum (ZD).

There is insufficient evidence to recommend routine screening for ZD.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The development of Zenker’s diverticulum (ZD) slowly starts as a oropharyngeal dysphagia progressing from solids to liquids, regurgitation of undigested food from the diverticular sac, chronic aspiration, halitosis, chronic cough, sensation of a lump in the throat, hoarseness, borborygmi. If left untreated, ZD may lead to complications such as aspiration pneumonia, bleeding from the diverticulum, ulceration of the diverticulum, compression of the trachea and esophageal obstruction with large diverticula, perforation, very rarely squamous cell carcinoma of the diverticulum. Patients who undergo surgery have a very low rate of recurrence for ZD.

• Symptoms of Zenker’s diverticulum slowly start as a^[1]
  • Oropharyngeal dysphagia progressing from solids to liquids
  • Regurgitation of undigested food from the diverticular sac
  • Pharyngeal stasis of secretion
  • Chronic aspiration
  • Halitosis
  • Chronic cough
  • Sensation of a lump in the throat
  • Hoarseness
  • Cervical borborygmi.

• The patient may note food on the pillow upon awakening in the morning.
• Although small diverticula may not cause symptoms, larger diverticula usually are symptomatic.
• Both the inability of the sphincter to fully open and the extrinsic compression from the pouch itself are likely to explain the dysphagia experienced by patients.
• In patients with very large diverticula, a gurgling swelling in the neck can occasionally be detected on palpation.

• Complications of the Zenker’s diverticulum includes^[2][3][4][5]
• Aspiration pneumonia
• Bleeding of the diverticulum
• Ulceration of the diverticulum
• Compression of the trachea and esophageal obstruction with large diverticula
• Very rarely squamous cell carcinoma of the diverticulum
• Perforation of the diverticulum during the endoscopy. Hence scopes with side viewing should be used to prevent perforation.

Prognosis of ZD after the intervention is good, the recurrence of the diverticulum is very rare.^[6]

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