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

Pathophysiology

The pathophysiology of the Zenker's diverticulum is as follows

• Zenker's diverticula (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 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 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.
• 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.
• Various hypothesis involved in the pathogenesis of the Zenker's diverticulum are as follows

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. Nineteen patients in the sample were found to have reflux and 20 had dysmotility. These findings suggest that pharyngeal pouches are not a purely localized incoordination of the cricopharyngeal sphincter but are associated with a generalized oesophageal 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.

• 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 intrabolus pressure which leads to herniation in the Killians triangle.
• 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.

Histopathological Findings: Zenker's diverticulum

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Classification

Esophageal diverticula are classified on the basis of location into three types

1. Phrenoesophageal (Zenker's diverticulum-70%),

2. Epiphrenic (20%)

3. Thoracic and mediastinal (10%)

Almost all esophageal diverticula are acquired pulsion diverticula.

Clinical examination

Asymptomatic in patients with small Zenker's diverticulum, the severity of the symptoms is proportional to the size of the diverticulum.

Common symptoms

Dysphagia

Local pain

Food regurgitation

Halitosis

Coughing

Hoarseness

Aspiration pneumonia

Bronchitis

Less common symptoms

Pill dysphagia- pills stuck in the throat

Drooling of the saliva

Choking on the food

Globus sensation

Weight loss

Cervical borborgymi

Hemoptysis

Hematemesis

Natural history

Zenker’s diverticulum presents as a progressive dysphagia. Initially, the patient presents with minor throat irritation, foreign body sensation, and coughing. Symptoms worsen as the diverticulum enlarges, and pouch becomes large enough to contain food, sputum or even medications. Patients can complain of food regurgitation several hours after a meal and typically describe weight loss. Cachexia and malnutrition can develop with Zenker’s Diverticulum, particularly in the elderly who develop a “fear of eating” secondary to choking spells.

Links

https://throatdisorder.com/zenkers-diverticulum/

Indications

• The indications of the surgery are as follows
• Severe dysphagia
• Weight loss
• Age- Elderly

Procedure

• The steps of the procedure is as follows
• The surgery is done under general anesthesia.
• Classic rigid oesophagoscopy was performed to prove the typical location of the diverticular inlet at the posterior wall of the hypopharynx,
• Diverticular inlet is cleared for any food debris and the meticulous search for the cancerous growths should be done.
• The diverticular sac is exposed using a Weerda distending diverticuloscope.
• The anterior lip of the diverticuloscope is placed into the esophagus while the posterior lip of the diverticuloscope is passed into the diverticulum.
• The diverticuloscope is advanced to the bottom of the diverticulum.
• The tissue bridge between the esophagus anteriorly and the diverticulum posteriorly is set between the two lips of the diverticuloscope.
• An operating microscope Carl Zeiss OPMI Sensera with attached carbon dioxide laser micromanipulator is set on working distance 400 mm with the laser beam focused on the tissue bridge.
• Carbon dioxide laser Lumenis AcuPulse with super-pulse delivery in a repeat mode, coupled with an AcuSpot micromanipulator, until 2009. Since March 2010, a robotic digital AcuBlade scanning micromanipulator system was used.
• The esophageal mucosa is protected from accidental laser injury by a moist swab.
• Using the laser at 5–10 W, the septum is transected at the midline down to the bottom of the diverticular sac. Occasionally electrocautery was used to control bleeding. * A feeding tube was introduced in all patients.
• Postoperative oesophagogram is performed at 5-6th day followed by a removal of the feeding tube and the discharge from the hospital on the same day or the day after.
• Antibiotic treatment with cefuroxime is routinely administered for one week following the surgery to prevent the post-operative infection.
• Control contrast esophagogram and subjective evaluation of swallowing were performed at least three months after the treatment

Complications

• Fistula
• Post operative hematoma
• Mediastinitis
• Neck emphysema
• Mucosal perforation or tearing
• Tooth fracture
• Postoperative bleeding
• Aspiration pneumonia
• Transient left recurrent laryngeal nerve paralysis
• Edema of the laryngeal inlet and left pyriform sinus

Causes

• 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, and subsequent incomplete opening of the UES, causing the protrusion of the mucosa through an area of relative weakness at the dorsal pharyngoesophageal wall.

Historical Perspective

The history of the ZD is as follows:

• 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 physiopathology of this diverticulum.
• In 1877 Zenker and Ziemssen reviwed 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.
• 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.
• In some cases this procedure led to very satisfactory results, although at least one complete recurrence was documented by Waggett and Davis [17] in a patient after a fit of violent sneezing.
• Diverticulopexy was also described in this early period by Schmid, and was first performed by Hill in 1917.
• In 1910 that Stetton was able to publish a list of all cases operated on up to that time organized according to surgical technique.
• These methods included primary excision, excision after preliminary gastrostomy, invagination of the sac, mucosal destruction without excision, and two-stage excision.