What is the pathophysiology of Zenker diverticulum?

Updated: Oct 16, 2020
  • Author: Joel A Ernster, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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The pathologic process in Zenker diverticulum involves herniation of the esophageal mucosa posteriorly between the cricopharyngeus (CP) muscle and the inferior pharyngeal constrictor muscles. Therefore, by strict definition, a Zenker diverticulum is a false diverticulum. The retention of food elements and secretions within the lesion’s pouch frequently leads to halitosis, regurgitation, aspiration, and dysphagia in patients. [5, 6]

Although Zenker proposed that a pulsion mechanism affects the pharyngeal mucosa above the CP muscle, no consensus exists regarding a unifying concept of the cause of Zenker diverticula. The specific abnormality of the CP muscle has not been elucidated. Hypothetical abnormalities include the following:

  • Abnormal timing of deglutition resulting in closure of the CP muscle when ideally it should be opening

  • Incomplete CP muscle relaxation

  • Elevated resting tone of the entire upper esophageal sphincter (UES)

  • Loss of CP muscle elasticity

  • CP muscle myopathy or denervation atrophy

  • Central nervous system (CNS) injury with a focal spastic CP muscle

  • CP muscle spasm in response to gastroesophageal reflux disease (GERD)

Studies to investigate the mechanism are scant. Cook histologically examined the CP muscle obtained at the time of diverticulectomy and found abundant fibrosis within the muscle. Whether this finding is a cause or a result of Zenker diverticulum is uncertain.

Kern determined that older individuals exhibit less anterior excursion of the larynx and hyoid with deglutition than younger subjects, resulting in higher hypopharyngeal intrabolus pressures in older subjects. [7] Whether this leads to Zenker diverticula over time is speculative. Van Overbeek suggested an anthropometric explanation. He felt individuals with longer necks had a larger Killian triangle, which predisposed them to formation of Zenker diverticulum. [8]

It is hypothesized that abnormal muscle activity in the cricopharyngeus results in a discoordination of the swallowing mechanism, [9, 10] which, when coupled with increased intraluminal pressure on the mucosa of the pharynx, results in the slow, progressive distention of the mucosa. As the weakest portion of this area is located posteriorly, this becomes the location of the pulsion diverticulum formation.

Zenker diverticula extend into the left neck 90% of the time. This is likely due to the slight convexity of the cervical esophagus to the left side and to the more laterally positioned carotid artery on the left side, creating a potential space for the sac.

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