The upper esophageal sphincter (UES) is formed principally by the cricopharyngeus muscle (the horizontal fibers of the inferior pharyngeal constrictor) with contributions from the thyropharyngeus and the proximal esophageal circular muscle. Killian's dehiscence is the triangular area of muscular weakness between the oblique thyropharyngeus fibers and the horizontal cricopharyngeus, where Zenker diverticulum herniates posteriorly.
| Origin | Posterior cricoid lamina (cricopharyngeus component) and inferior thyroid cartilage (thyropharyngeus component) |
|---|---|
| Insertion | Posterior median raphe of the pharynx; fibres encircle the pharyngoesophageal junction |
| Nerve Supply | Vagus nerve (CN X) via pharyngeal plexus; glossopharyngeal nerve (CN IX) contribution |
| Blood Supply | Inferior thyroid artery branches |
| Actions | Maintains tonic closure of the pharyngoesophageal junction at rest (60-100 mmHg resting pressure) to prevent air entering the esophagus; relaxes during swallowing to allow the bolus to pass; prevents esophagopharyngeal reflux |
|---|
Zenker diverticulum forms through Killian's dehiscence due to UES dysfunction producing pharyngeal hyperpressure. Endoscopic stapler myotomy divides the cricopharyngeus septum between the diverticulum and the esophageal lumen. UES dysfunction (incomplete relaxation) causes dysphagia treated by cricopharyngeal myotomy or botulinum toxin injection. Laryngeal penetration and aspiration relate to UES opening timing relative to laryngeal closure during swallowing.
Division of the cricopharyngeus muscle at the UES eliminates the functional obstruction driving Zenker diverticulum formation; endoscopic stapler myotomy divides the common wall between the diverticulum and esophagus under direct vision, with cure rates exceeding 90%.
