This article introduces the pathogenesis and relevant anatomy of Zenker diverticulum. The clinical symptoms and relevant investigation are presented along with the various therapeutic interventions including open and endoscopic approaches. Techniques to perform the myotomy and diverticulectomy are expanded on and include traditional suture ligation, endoscopic stapling devices, microlaryngoscopic CO 2 laser and flexible LISA laser. The article concludes with a management algorithm for this entity based on the size of the diverticulum.
Key points
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Zenker diverticulum is a pseudodiverticulum through Killian triangle between the oblique and fundiform parts of the cricopharyngeus.
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It is thought to be caused by repeated incoordination between upper esophageal sphincter relaxation and pharyngeal contraction resulting in increased intraesophageal pressure and subsequent pseudoherniation through Killian triangle.
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It is most commonly presents in males in their seventh and eighth decades.
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The most common symptoms are dysphagia, regurgitation of food, and halitosis.
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It is seen on esophagram as a cricopharyngeal bar and associated diverticulum that can vary in size.
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Most diverticula, both small and large, can be successfully treated endoscopically with minimal morbidity and a 95% success rate.
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Open surgery is reserved for failed endoscopic treatment or inability to obtain adequate endoscopic exposure.
Introduction
Zenker diverticulum (ZD) is an outpouching of mucosa without muscle through a dehiscence in a triangular area of weakness within the cricopharyngeus (CP) muscle, on the dorsal wall of the hypopharynx, and is therefore more correctly classified as a pseudodiverticulum. Originally described in Great Britain by Ludlow as an autopsy finding in 1769, a more detailed description was put forth by the German Pathologists Zenker and von Ziemssen in 1877. They proposed the generally accepted pathophysiology of “forces within the lumen acting against restriction”. Later, in 1907, Killian observed this pharyngeal pseudodiverticulum as emanating posteriorly in the midline between the thyropharyngeus above and the CP below ( Fig. 1 ).
Introduction
Zenker diverticulum (ZD) is an outpouching of mucosa without muscle through a dehiscence in a triangular area of weakness within the cricopharyngeus (CP) muscle, on the dorsal wall of the hypopharynx, and is therefore more correctly classified as a pseudodiverticulum. Originally described in Great Britain by Ludlow as an autopsy finding in 1769, a more detailed description was put forth by the German Pathologists Zenker and von Ziemssen in 1877. They proposed the generally accepted pathophysiology of “forces within the lumen acting against restriction”. Later, in 1907, Killian observed this pharyngeal pseudodiverticulum as emanating posteriorly in the midline between the thyropharyngeus above and the CP below ( Fig. 1 ).
Anatomy
The inferior pharyngeal constrictor consists of 2 muscles, the thyropharyngeus and the cricopharyngeus . The latter muscle has 2 components, the oblique, or superior part of the CP and the fundiform, or inferior part of the CP. Both the superior and inferior portions arise bilaterally from the posterolateral border the thyroid lamina. Although the superior fibers meet at a median raphe on the posterior border of the hypopharynx, the inferior fibers circle the esophageal lumen without attaching to a median raphe. The triangular area between these components is defined as Killian triangle and is the triangle through which ZD herniates. This should be differentiated from the Killian-Jamieson diverticulum, located more inferolaterally, in close proximity to the recurrent laryngeal nerve, between the inferior CP muscle above and the superior border of the longitudinal muscle fibers of the proximal esophageal muscle below.
Pathophysiology
The upper esophageal sphincter (UES) is approximately 1 cm in craniocaudal dimension and is principally formed by the CP. The CP, which is contracted at rest, generates the zone of maximal UES pressure with a resting pressure of 60 mm Hg and 30 mm Hg in the sagittal and transverse dimensions, respectively. As originally proposed by Zenker, it is generally accepted that the repeated dyscoordination between UES relaxation and pharyngeal contraction during deglutition, known as circopharyngeal dysfunction (CPD), causes increased intra-esophageal pressure and contributes to the anatomic weakness of the posterior pharyngeal musculature, thereby predisposing to the development of a pseudodiverticulum. Various age-related changes in deglutition contribute to cricopharyngeal dysfunction and support the presentation of ZD in a relatively older population. These include dyssynchronous oral and pharyngeal phases of swallow, degenerated Auerbach plexus and delayed anterior displacement of the hyoid as well as on overall decreased elevation of the hyolaryngeal complex. Similarly, cricopharyngeal achalasia, incomplete or delayed CP relaxation, premature UES closure, and neuropathic injuries leading to uncoordinated deglutition may also contribute to an elevated UES pressure and predispose to the development of a ZD. Although gastroesophageal reflux (GERD) has been implicated in the development of ZD by some, it is difficult to differentiate GERD as a cause or effect of CPD or ZD. Certainly, histologic studies of the cricopharyngeus of ZD demonstrate fibrosis, increased collagen deposition, and fat replacement, which confirm the hypothesis of a poorly compliant cricopharyngeal system.
Symptoms
ZD is a relatively rare entity with a reported prevalence of 0.11%, presenting most commonly in men in their seventh or eighth decades. Symptoms relate to the size of the pharyngeal diverticulum and most commonly manifest as dysphagia. Other symptoms include regurgitation of undigested food, halitosis, aspiration, gurgling in the throat, neck mass, dysphonia, and malnutrition.
Signs
Most patients do not have pertinent clinical signs on physical examination. However, a minority of patients with very large diverticulum may present with malnutrition, dysphonia, a soft swelling on the left side of the neck known as Boyce sign, cervical borborygmi, or crepitus. Although the diagnosis is suspected based on history, it is confirmed by esophageal studies ( Fig. 2 ).
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