1.44: Surgery for Pharyngeal Pouch / Zenker's Diverticulum

OPEN ACCESS ATLAS OF OTOLARYNGOLOGY, HEAD & NECK OPERATIVE SURGERY

SURGERY FOR PHARYNGEAL POUCH / ZENKER’S DIVERTICULUM

Daniel Schuster, James Netterville, Johan Fagan This chapter provides an overview of management of Zenker’s divertula (ZD), including detailed surgical technique, with an emphasis on effective therapy and management. Zenker, a German pathologist, first reported 27 hypopharyngeal pulsion diverticula in 1878. 1 In 1907, Killian, described the triangular dehiscence between the cricopharyngeus and inferior constrictor muscles that is the anatomic site of formation of Zenker’s Diverticula. 2 (Figure 1) Although there is a role for open surgery, management has evolved to effective, safe endoscopic techniques with proven low morbidity.

Etiology

The etiology has been debated for more than a century. Historically, authors have theorized that trauma, congenital upper esophageal strictures, thyroid goiter, or foreign bodies may play role. 3 Gastroesophageal reflux, cricopharyngeal achalasia, persistently elevated resting tone of the cricopharyngeus, structural abnormality of the cricopharyngeus muscle, and central or peripheral neurologic disease have also been proposed as contributing or causal factors, though convincing evidence is lacking. 3 However, it was Zenker who correctly described it as a pulsion diverticulum and put earlier theories to rest. 1 Since that time most authors agree that anatomic predisposition plays a central role in the pathogenesis, though the exact aetiology is still a subject of debate. It is now widely accepted that dysfunction of the cricopharyngeus muscle plays a central aetiological role. High intraluminal pressures at the level of Killian’s triangle result in herniation of esophageal mucosa and submucosa through this area of inherent muscular weakness. Some advocate that high intraluminal pressures produced by incoordination of the inferior constricttor muscle against a closed cricopharyngeus is responsible, while others state that high pressures are a result of the anatomic relationship between the relatively wide hypopharynx and a narrower esophageal inlet through which food boluses pass. 5 Killian’s triangle itself is of variable size, and patients with larger areas of inherent muscular weakness are likely more predisposed to a ZD.

Pathophysiology

1.pngFigure 1: Red arrow shows where ZD extrudes through Killian’s dehiscence (blue) between the inferior constrictor and the cricopharyngeus muscles 2.pngFigure 2: Cricopharyngeal bar (CP) containing the cricopharyngeus muscle, which separates esophagus (O) from ZD 3.pngFigure 3: Barium swallow of ZD. Note location of cricopharyngeus muscle (arrows) in upper part of party wall between esophagus and ZD; and how buccopharyngeal fascia contains the diverticulum (green line) ZD is a pulsion diverticulum or herniation of esophageal mucosa and submucosa through Killian’s triangle, which is immediately proximal to the cricopharyngeus muscle (Figures 1, 2, 3). Of surgical importance is that the entire diverticulum is contained within the buccopharyngeal fascia, which itself is not involved in the formation of the diverticulum (Figure 3). The buccopharyngeal fascia is in effect displaced posteriorly by the posterior wall of the diverticulum, creating a safer plane to divide the “party wall” (that contains the cricopharyngeus) without penetrating the fascia and entering the prevertebral space (Figure 3). This anatomic relationship between the ZD and the surrounding buccopharyngeal fascial layer is the key to understanding how the upper digestive tract remains separated from the retropharyngeal space when incising the anterior wall of the diverticulum, or in the case of an isolated endoscopic cricopharyngeal myotomy. Disrupting this fascial layer could theoretically increase the likelihood of developing mediastinitus. However, when endoscopically dividing a hypertrophic cricopharyngeus muscle in the absence of a ZD, the buccopharyngeal fascia is situated immediately behind the cricopharyngeus muscle, and great care has to be taken to preserve this fascial layer when completely dividing the cricopharyngeus muscle. Despite initial fears that this fascia could not be preserved during endoscopic cricopharyngeal myotomy, Chang et al demonstrated in a cadaveric study that the buccopharyngeal fascial layer remained histologically intact with carbon dioxide (CO2) laser cricopharyngeal myotomy. 4

Clinical Presentation

ZD occurs predominantly in the elderly; it is rarely seen in patients

Special Investigations

Diagnosis is confirmed with a contrast swallow and videofluoroscopy (Figure 3). Laryngoscopy is done to rule out other causes of dysphagia, as well as to document vocal cord dysfunction. Preoperative evaluation must include assessment of the function of the lower esophageal sphincter, as cricopharyngeal myotomy in patients with an incompetent lower esophageal sphincter places them at risk of developing severe gastroesophageal and laryngopharyngeal reflux.

Surgical Anatomy

A ZD is a thin-walled sac lined by stratified squamous epithelium with a thin layer of fibrous submucosa. The muscular layer of the hypopharynx is absent from its wall. The posterior mucosal herniation passes through Killian’s dehiscence/ triangle and is located between the inferior fibers of the inferior pharyngeal constrictor and the superior edge of cricopharyngeus muscle (Figures 1, 3). The common (party) wall contains the cricopharyngeus at its upper edge and separates the esophagus from diverticulum (Figures 2, 3). It is important to understand that after the ZD herniates through Killian’s dehiscence, it expands posterior to the cricopharyngeus and the superior esophageal muscles layers but is still contained within the perioesophageal fascia. This protective layer of investing facia surrounding both the esophagus and ZD is the key to endoscopic division of the cricopharyngeus muscle and the entire party wall between the ZD and the esophagus. Without this fascial layer, saliva would be likely to track into the mediastinum causing mediastinitis.

Treatment