Isn't dysphagia in the patient with a Zenker's diverticulum related to cricopharyngeal dysfunction rather than to the pouch ?
M.B. Orringer (Ann Arbor)
Zenker's or cricopharyngeal diverticula are pulsion diverticula which form as a result of abnormally increased intraluminal pressure. Most often, this is the result of incoordinated swallowing, an extremely complex action which requires, among other things, coordination of pharyngeal contraction, upper esophageal sphincter relaxation, and propagation of the peristaltic wave down the esophagus. A number of terms have been used to define the condition in which there is abnormal function of the upper esophageal or cricopharyngeal sphincter. However, such terms as cricopharyngeal chalasia, achalasia, or spasm can rarely be substantiated objectively, since in most patients, standard esophageal manometry fails to demonstrate true hypotonicity or hypertonicity of the upper esophageal sphincter or failure to relax with swallowing. This shortcoming of standard manometry, however, may be circumvented by newer « sleeve » manometric recording devices [1,2]. Radiographic documentation of impaired swallowing may require sophisticated cine fluoroscopic techniques.
Given the limitations of standard diagnostic procedures in defining upper esophageal sphincter dysfunction; however, the patient's history often becomes the most important indicator of disordered cricopharyngeal dysfunction. These patients may present with a typical symptom complex of cervical dysphagia, expectoration of excessive saliva, hoarseness due to distortion of the vocal cords by spastic cricopharyngeal muscle, and weight loss . This is a classic presentation of cricopharyngeal motor dysfunction which may occur in patients with no identifiable cricopharyngeal diverticulum, for example, those who have had a recent bulbar cerebral vascular accident that results in cricopharyngeal motor dysfunction and markedly impaired swallowing. The presence of a pharyngoesophageal (Zenker's diverticulum) on barium swallow examination is, in my opinion, presumptive evidence of upper esophageal sphincter dysfunction.
Regardless of our inability to objectively document motor dysfunction of the upper esophageal sphincter in these patients, a relative functional obstruction must be present for the « blow out» of mucosa and submucosa through the muscular wall of the esophagus to occur. If one considers the anatomic aspects of this problem, virtually no other conclusion can be drawn, (figure 1) The upper esophageal or cricopharyngeal sphincter is the lower most portion of the inferior pharyngeal constrictor. The oblique fibers of the thyropharyngeus muscle, the upper portion of the inferior pharyngeal constrictor, are separated from the more horizontal folds of the cricopharyngeal sphincter by a point of potential weakness (Killian's triangle), which is the site of formation of the Zenker's diverticulum. It
Figure 1. Formation of pharyngoesophageal (Zenker's) diverticulum. Left herniation of the pharyngeal mucosa and submucosa occurs at the point of transition (arrow) between the oblique fibers of the thyropharyngeus muscle and more horizontal fibers of the cricopharyngeus muscle (Killian's triangle). Center and right— as the diverticulum enlarges, it dissects toward the left side and downward in the superior mediastinum in the prevertebral space. (From Orringer MB. Diverticula and miscellaneous conditions of the esophagus. In : Textbook of Surgery — 13th Edition (1986) Sabiston DC Jr, Ed. WB Saunders, Philadelphia, pp 726-731.
is absolutely reliable that the diverticulum will be found proximal to the cricopharyngeal muscle fibers.
The logical conclusion which must be drawn from this is that there is incoordination of the upper esophageal sphincter with swallowing resulting in increased intraluminal pharyngeal pressure proximal to the sphincter and a subsequent outpouching of the mucosa and submucosa at the point of potential weakness in the pharyngeal wall just proximal to the sphincter.
To attack the diverticulum surgically without relieving the distal obstruction from neuromotor dysfunction is to ignore the underlying cause of the patient's complaint. It is the degree of cricopharyngeal motor dysfunction, not the size of the diverticulum, which determines the severity of the patient's complaint of dysphagia. That is, some patients with 1 or 2 mm diverticula proximal to a «tight » upper esophageal sphincter may complain of severe dysphagia, while those with a 3 or 4 cm pouch may have relatively little dysphagia. Impaired cricopharyngeal motor function is the key to understanding the symptoms of dysphagia in these patients, and as is true of all pulsion diverticula, it is the underlying motor dysfunction causing obstruction and formation of the pouch which must be relieved if the problem is to be treated successfully.
It was long ago recognized that when operating upon pulsion diverticula of the thoracic esophagus, a concomitant esophagomyotomy is mandatory if serious complications of unrelieved obstruction (blow out of the suture-line) are to be avoided . The case is no different with pharyngoesophageal (Zenker's) diverticula. Pulsion diverticula recur because the underlying obstruction responsible for their formation was not relieved at the initial operation.
2. Kahrilas PJ, Dodds WJ, Dent J, Hogan WJ, Arndorfer RC (1987) The effect of sleep, spontaneous gastroesophageal reflux and a meal on LIES pressure in normal human volunteers. Gastroenterology 94: 466-471.