Esophageal diverticula are unusual but interesting abnormalities that can develop in any part of the esophagus. The most common esophageal diverticulum occurs in the cervical region and is known as a Zenker diverticulum. An esophageal diverticulum may also occur in the midesophagus near the pulmonary hilum or as an epiphrenic diverticulum near the gastroesophageal junction. There are two categories of esophageal diverticula—pulsion and traction. Each has a distinct etiology. Pulsion diverticula are the most common type in the United States, and develop as a consequence of a motility abnormality in the esophagus distal to the site of the diverticulum.¹ They are false diverticula since they are not composed of the entire wall of the esophagus, but instead the mucosa herniates or protrudes through the muscle layers (Fig. 30-1).

The other type, traction diverticula, develop secondary to inflamed mediastinal lymph nodes, and represent a true diverticulum since all layers of the esophageal wall are involved. The prevalence of all types of diverticula increases with age.

Pulsion diverticula are the most common type of diverticula, and the most common pulsion diverticulum is a Zenker diverticulum. These develop in the cervical region secondary to repetitive pharyngeal pressure on boluses of food that are held up by a dysfunctional cricopharyngeus muscle.² Over time, this pressure causes a posterior herniation of the esophageal mucosa through Killian dehiscence, a weak point at the junction of the inferior constrictor and cricopharyngeus muscles. Epiphrenic diverticula are also pulsion diverticula. These develop secondary to a motility disorder in the distal esophagus, most commonly at the gastroesophageal junction and most commonly achalasia.³ Radiographically, pulsion diverticula typically have a wide neck, rounded contour, and retain contrast material on a barium swallow (Fig. 30-2). Symptoms associated with pulsion diverticula are often initially related to the underlying motility abnormality, but as the size of the diverticulum increases the symptoms may become more attributable to the pouch itself. Thus, while dysphagia is often the primary initial symptom, as the pouch enlarges, regurgitation may become more prominent. It is not unusual for these symptoms to lead to a misdiagnosis of gastroesophageal reflux disease before the diverticulum itself is identified (Fig. 30-3). However, careful questioning will usually elicit the key information that the regurgitated material tastes bland, not bitter, since the regurgitated food or fluid was trapped in the pouch and never made it to the stomach. Other symptoms attributable to a diverticulum are halitosis, cough, and aspiration of debris retained within the pouch. The larger and more proximal the pouch, the more troublesome these symptoms may be for patients.

Traction diverticula are caused by granulomatous inflammation of mediastinal lymph nodes, and occur most commonly in areas where tuberculosis or histoplasmosis is endemic. The inflamed nodes attach to the esophagus, and as the acute inflammation subsides, the nodes contract, pull on the esophagus, and create a conical outpouching. Traction diverticula are true diverticula, since the entire wall of the esophagus is involved. In contrast to pulsion diverticula, traction diverticula tend to have a pointed tip on radiographs and empty well on barium swallow (Fig. 30-4). Symptoms generally are less significant compared to patients with a pulsion diverticulum, and are related to the diverticulum or mediastinal inflammation since there is no underlying motility abnormality.

Surgery is the only effective therapy for esophageal diverticula. Dilation of the cricopharyngeus muscle has been attempted in patients with Zenker diverticulum with limited success. Even if the dilation is helpful, it only addresses the dysphagia component of the patient’s symptoms. The surgical plan for patients with a pulsion diverticulum includes myotomy of the dysfunctional esophageal muscle adjacent and distal to the diverticulum and either excision or suspension of the diverticulum based on its size and location. Failure to divide the dysfunctional muscle leads to a high rate of recurrence and increases the risk of a leak from the suture or staple line if the diverticulum has been excised.⁴ For patients with a symptomatic traction diverticulum, only excision of the diverticulum is necessary, but the fibrotic nodes that caused the diverticulum can make the dissection tedious. Approaches to both pulsion and traction diverticula include the traditional open techniques and more recent transoral, laparoscopic, and thoracoscopic minimally invasive options. Given the absence of effective nonsurgical therapy and the relative safety of most of these procedures, symptomatic patients with an esophageal diverticulum should be considered for surgical therapy regardless of age.

The physical examination of patients with an esophageal diverticulum generally is unrevealing, even when a large Zenker diverticulum. However, if a transoral approach for correction of a Zenker diverticulum is being considered, it is important to assess the ability of the patient to adequately open the mouth and extend the neck.⁵

The best way to visualize an esophageal diverticulum is with a barium swallow.⁴ Our preference is a video swallow esophagogram, since in addition to showing the size and location of the diverticulum, it provides information about the efficacy of bolus transport by the esophageal body and the presence of a hiatal hernia or other abnormalities. Upper endoscopy is useful both to measure the size and location of the diverticulum, and to evaluate the esophageal mucosa for any abnormalities, particularly in elderly patients where it is essential to rule out malignancy.

Esophageal manometry is important to evaluate the underlying motility abnormality. It is usually necessary to pass the motility catheter using endoscopic guidance, as the catheter may otherwise coil in the diverticulum. Motility studies in patients with a Zenker diverticulum are often normal and are not necessary. The upper esophageal sphincter is composed of skeletal muscle, in contrast to the smooth muscle of the lower esophageal sphincter, and standard motility techniques lack sufficient sensitivity to reliably detect the underlying abnormality. Motility findings that might be present in a patient with a Zenker diverticulum include an increased bolus pressure in the pharyngeal contraction wave (evidence of outflow obstruction distally) and mistimed or incomplete relaxation of the cricopharyngeus with a swallow.² Most patients with a Zenker diverticulum are elderly, and the cause of the cricopharyngeal dysfunction is usually related to prior neck injury, radiation, or neurologic abnormalities such as a stroke. Young patients (<50 years old) with a Zenker diverticulum often have no predisposing factors, but frequently have symptoms of gastroesophageal reflux disease. This raises the possibility that proximal reflux can induce dysfunction of the cricopharyngeus muscle and lead to the development of a Zenker diverticulum. Certainly, reflux should be considered and further evaluated if present in an otherwise healthy patient under age 50 who presents with a Zenker diverticulum.

Transcervical Cricopharyngeal Myotomy and Diverticulectomy or Suspension

The traditional approach for repair of a Zenker diverticulum is transcervical, with the patient positioned supine and the neck extended. An incision is made in the left neck along the anterior border of the sternocleidomastoid muscle. The sternocleidomastoid muscle and carotid sheath are retracted laterally. The omohyoid, sternothyroid, and sternohyoid muscles are divided to facilitate exposure of the cervical esophagus. The Zenker diverticulum will be located posterior to the cricoid cartilage. The diverticulum is sheathed in multiple layers of fibrous tissue that must be teased apart to permit exposure of the base of the diverticulum (Fig. 30-5).