Zenker's Diverticulum
Zenker's diverticulum (ZD) is an outpouching of tissue through the Killian triangle that is believed to be caused by dysfunction of the cricopharyngeal muscle. ZD is a relatively uncommon disorder occurring in the elderly. The predominant symptom of ZD is dysphagia, and the most serious consequence is pulmonary aspiration. Videofluoroscopy confirms the diagnosis. Therapy of symptomatic ZD has evolved from an open surgical approach to less invasive transoral endoscopic techniques. Transoral endoscopic therapy using rigid instruments is performed primarily by otorhinolaryngologists, whereas transoral therapy using flexible endoscopes is performed by surgical endoscopists and gastroenterologists. The common goal of all modalities is severing of the septum between the esophageal lumen and the diverticulum containing the cricopharyngeal muscle. Although flexible endoscopic therapy was described nearly 20 years ago, it has experienced a recent resurgence paralleling the advancements of therapeutic endoscopy in other areas, such as endoscopic submucosal dissection. Direct head-to-head comparisons of rigid and flexible endoscopic therapy are lacking, and each approach has variations in techniques as well as advantages and disadvantages. In this article, we review the pathophysiology and management of patients with ZD with an emphasis on flexible endoscopic therapy.
Zenker's diverticulum (ZD) is a posterior pharyngoesophageal pouch that forms through pulsion forces in an area of relative hypopharyngeal wall weakness between the oblique fibers of the inferior pharyngeal constrictor and the horizontal fibers of the cricopharyngeus (CP) muscles. Poor upper esophageal sphincter (UES) compliance is the presumed pathophysiologic mechanism of action. This dysfunction creates a high-pressure zone eventuating in increased pulsion forces and subsequent ZD formation. This entity most commonly presents in the elderly and can be associated with a plethora of potential symptoms, of which dysphagia is most common. It has become accepted that unless a myotomy of the CP muscle is performed wholly or as part of therapy for ZD, successful amelioration of symptoms and prevention of recurrence is unlikely.
For decades, the mainstay of treatment for ZD was an open surgical approach through a neck incision with performance of myotomy of the UES and removal or suspension of the diverticulum. Over the past 4 decades, however, alternative and often preferable incisionless transoral approaches have been developed. The literature is rife with endoscopic publications, although the vast majority involves the use of rigid tube instrumentation (rigid endoscopy). Rigid endoscopic therapy became popularized after a landmark study published by Dohlman and Mattson in 1960 and is typically performed by otorhinolaryngologists. Fewer, though increasingly more common, published data are available regarding treatment using flexible endoscopy performed predominately by surgical endoscopists and gastroenterologists. In this manuscript, we focus on the pathophysiology and interventions for ZD.
Abstract and Introduction
Abstract
Zenker's diverticulum (ZD) is an outpouching of tissue through the Killian triangle that is believed to be caused by dysfunction of the cricopharyngeal muscle. ZD is a relatively uncommon disorder occurring in the elderly. The predominant symptom of ZD is dysphagia, and the most serious consequence is pulmonary aspiration. Videofluoroscopy confirms the diagnosis. Therapy of symptomatic ZD has evolved from an open surgical approach to less invasive transoral endoscopic techniques. Transoral endoscopic therapy using rigid instruments is performed primarily by otorhinolaryngologists, whereas transoral therapy using flexible endoscopes is performed by surgical endoscopists and gastroenterologists. The common goal of all modalities is severing of the septum between the esophageal lumen and the diverticulum containing the cricopharyngeal muscle. Although flexible endoscopic therapy was described nearly 20 years ago, it has experienced a recent resurgence paralleling the advancements of therapeutic endoscopy in other areas, such as endoscopic submucosal dissection. Direct head-to-head comparisons of rigid and flexible endoscopic therapy are lacking, and each approach has variations in techniques as well as advantages and disadvantages. In this article, we review the pathophysiology and management of patients with ZD with an emphasis on flexible endoscopic therapy.
Introduction
Zenker's diverticulum (ZD) is a posterior pharyngoesophageal pouch that forms through pulsion forces in an area of relative hypopharyngeal wall weakness between the oblique fibers of the inferior pharyngeal constrictor and the horizontal fibers of the cricopharyngeus (CP) muscles. Poor upper esophageal sphincter (UES) compliance is the presumed pathophysiologic mechanism of action. This dysfunction creates a high-pressure zone eventuating in increased pulsion forces and subsequent ZD formation. This entity most commonly presents in the elderly and can be associated with a plethora of potential symptoms, of which dysphagia is most common. It has become accepted that unless a myotomy of the CP muscle is performed wholly or as part of therapy for ZD, successful amelioration of symptoms and prevention of recurrence is unlikely.
For decades, the mainstay of treatment for ZD was an open surgical approach through a neck incision with performance of myotomy of the UES and removal or suspension of the diverticulum. Over the past 4 decades, however, alternative and often preferable incisionless transoral approaches have been developed. The literature is rife with endoscopic publications, although the vast majority involves the use of rigid tube instrumentation (rigid endoscopy). Rigid endoscopic therapy became popularized after a landmark study published by Dohlman and Mattson in 1960 and is typically performed by otorhinolaryngologists. Fewer, though increasingly more common, published data are available regarding treatment using flexible endoscopy performed predominately by surgical endoscopists and gastroenterologists. In this manuscript, we focus on the pathophysiology and interventions for ZD.
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