Diverticula are acquired, focal pouches of oesophageal wall consisting of mucosa and variably attenuated muscular coat. They may occur anywhere in the oesophagus between the pharyngo-oesophageal junction and the lower oesophageal sphincter. Adults are usually affected, the incidence increasing with age.

Two different types of diverticula are recognized on the basis of their pathogenesis. Pulsion diverticula form as localized herniations due to increased luminal pressure in patients with motility disorders or chronic oesophageal obstruction, and provide an ‘escape route’ for pressure and swallowed food. Traction diverticula develop at the level of tracheobronchial lymph nodes as a result of granulomatous inflammation with secondary involvement of the adjacent oesophagus and subsequent contracture of scar tissue. Diverticula occur predominantly in three anatomical locations. Zenker's or pharyngo-oesophageal diverticulum is a pulsion defect of the posterior mucosa between the inferior pharyngeal constrictor muscle and the cricopharyngeal sphincter due to simultaneous inco-ordinate contraction. Mid-oesophageal lesions are typically traction diverticula and lie close to subcarinal, paratracheal, or hilar lymph nodes. Epiphrenic diverticula are found in the lower oesophagus above the diaphragm, and are also of the pulsion type. The upper thoracic oesophagus is rarely affected by diverticula. Pulsion defects are more likely to interfere with oesophageal function and produce symptoms. As a result, symptoms occur regularly in Zenker's diverticula, often in epiphrenic diverticula, and rarely in traction diverticula.

Some 70 to 80 per cent of all oesophageal diverticula requiring surgical therapy are Zenker's diverticula. The principal physiological defect leading to formation of a pharyngo-oesophageal diverticulum is a loss of co-ordination during the second stage of swallowing. The oblique course of the inferior pharyngeal constrictor muscle and the horizontal direction of the cricopharyngeal sphincter create an unsupported triangular region devoid of muscle in the posterior wall (Fig. 1) 907. Normally, the cricopharyngeal sphincter relaxes during contraction of the pharyngeal constrictors, allowing propulsion of food. In patients with Zenker's diverticulum the sphincter is closed during the pharyngeal contraction. Although not every swallow may demonstrate this disco-ordinate pattern, its cumulative effects expose the muscle-free area to high pressures, eventually leading to the formation of a pouch. It is unclear whether this disorder arises from a primary or secondary dysfunction of the cricopharyngeal sphincter. Gastro-oesophageal reflux, although suspected to cause reflex contraction of this muscle, is not associated with increased cricopharyngeal pressures.

Symptoms occur early in the course of pouch formation and are progressive. Patients complain of dysphagia and gurgling noises during swallowing. As food is retained in the pouch, fetor oris and spontaneous regurgitation of its undigested contents develop. Respiratory complications are frequent, including aspiration, asthma, pneumonia, and, occasionally, lung abscess. Pressure of the pouch on the recurrent laryngeal nerve may cause hoarseness. As the pouch increases in size, a soft mass may be palpated in the neck. Neglect of symptoms may result in weight loss, cachexia, and respiratory compromise. Perforation is rare and usually due to iatrogenic injury. One-third of patients have associated oesophageal functional disorders, such as hiatal hernia, diverticula elsewhere in the oesophagus, achalasia, or diffuse spasm. Nevertheless, radiographic contrast studies (Fig. 2) 908 are usually sufficient to arrive at the diagnosis and to delineate the rest of the oesophagus: motility studies are generally not required. Oesophagoscopy is indicated when there is complete obstruction or if malignancy is suspected, since cancers occasionally occur in the pouch.

Zenker's diverticulum requires treatment regardless of diverticulum size. Symptoms do not improve with other forms of therapy, and the hazards of regurgitation and aspiration increase with pouch enlargement. Myotomy and diverticulectomy are the two elements of successful surgical therapy. If the pouch is small, cricopharyngeal myotomy alone relieves symptoms. The cricopharyngeal muscle is divided vertically in the posterior midline, dissecting the mucosa over half the circumference to prevent recurrent obstruction. If the pouch is well developed, diverticulectomy is performed during the same operation to remove the cause of regurgitation (Fig. 3) 909. Care must be exercised to avoid over-excision of oesophageal mucosa and creation of a defect too large to close without tension or stenosis. Some surgeons prefer diverticulopexy with fixation to the prevertebral fascia to obliterate the lumen of the sac.

Myotomy and diverticulectomy produce excellent results. In a follow-up study from the Mayo Clinic, over 90 per cent of patients were asymptomatic. Operative mortality was 1.2 per cent and complications, including recurrent laryngeal nerve palsy, usually of transient nature, and oesophagocutaneous fistula arising from the suture line, which closed spontaneously with adequate drainage, affected 4.9 per cent of patients.

This entity is relatively uncommon, representing 10 to 20 per cent of all oesophageal diverticula. The male to female ratio is 2 : 1. Epiphrenic diverticula occur usually in the lower oesophagus within 10 cm of the diaphragm and project as solitary lesions into the right chest; left-sided or multiple lesions may be encountered. The resulting pouch is from 2 to over 10 cm in diameter and often has a narrow neck. Most epiphrenic diverticula are associated with functional motor disturbances, and some cause organic obstruction. Symptoms due to the diverticulum, however, develop in fewer than half of all patients. Patients present with dysphagia, regurgitation, and epigastric or chest pain. Occasionally, examination is prompted by aspiration with choking or coughing. Because these complaints are frequently associated with other benign oesophageal disorders, symptomatic patients should undergo complete evaluation including barium swallow (Fig. 4) 910, motility studies, and endoscopy.

Appropriate therapy in patients with symptoms consists of surgical resection of the diverticulum and alleviation of underlying motor or organic disorders (Figs. 5 and 6) 911,912. Access to the oesophagus is provided by posterolateral thoracotomy, usually on the left. The diverticulum is exposed and resected, closing the defect in the oesophagus. Distal obstruction should be excluded preoperatively, because it jeopardizes the closure of the oesophagus and may result in recurrence of the diverticulum. In most cases, an oesophageal myotomy extending from the site of the diverticulum distally to the lower oesophageal sphincter is required. If motility studies demonstrated motor dysfunction due to diffuse spasm, a long myotomy extending from the lower oesophageal sphincter to the aortic arch is performed. Any associated hiatal hernia is repaired, albeit cautiously because of the risk of recurrent obstruction. The individualized operative approach to each of these conditions emphasizes the need for a thorough preoperative understanding of the pathophysiology based on motility and other functional studies. Postoperatively, the oesophagus remains decompressed with a nasogastric tube until a Gastrografin study after 1 week has confirmed the absence of a leak.

These diverticula occur as a result of granulomatous necrosis of tracheobronchial lymph nodes due to tuberculosis or histoplasmosis. The oesophagus is involved because of its proximity to the inflammation. Fixation of a transmural segment of oesophageal wall, followed by cicatricial contraction of the involved nodes and peristaltic extension of the surrounding oesophagus results in the formation of a true diverticulum. The sac is typically located on the left side, has a broad neck, and points upward. For this reason, it is rarely filled with food particles and rarely causes symptoms. Fistulization to the airway and haemorrhage are rare complications. Bleeding into the oesophagus originates most often from erosion of small bronchial or oesophageal vessels, but communication with the superior vena cava and exsanguination have been reported. Symptomatic patients should undergo local excision of the diverticulum with closure of the oesophagus and separation from the tracheobronchial tree with a vascularized tissue flap of intercostal muscle or pericardial fat.

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