Oesophageal diverticula

• An oesophageal diverticulum is a pouch formed by the wall of the oesophagus protruding outward. Most of the clinically important ones are "false" pouches: only the inner lining (mucosa and submucosa) pushes through a gap in the muscle, unlike a "true" diverticulum in which the whole wall is involved.
• They are classified by site and mechanism into three main types: Zenker's diverticulum in the pharynx just above the cricopharyngeus muscle (a pulsion pouch); a mid-oesophageal traction diverticulum from scarring after mediastinal granulomatous disease such as tuberculosis; and an epiphrenic pulsion diverticulum just above the lower oesophageal sphincter, usually driven by an underlying motility disorder.
• Many, especially mid-oesophageal traction pouches and small Zenker pouches, cause no symptoms and need no treatment.
• The classic symptom cluster is difficulty swallowing (often to both solids and liquids), regurgitation of undigested food hours after eating, bad breath, a gurgling swelling in the neck, chronic cough or aspiration, and weight loss.
• A barium swallow is the key test. A blind nasogastric tube or endoscope can perforate a Zenker pouch, so the test is done with care. An epiphrenic pouch should always be investigated with oesophageal manometry to find the underlying motor disorder.

By the end of this page you should be able to:

1. Name the three types of oesophageal diverticulum by site and mechanism, and explain why each forms.
2. Distinguish a true diverticulum from a false (pulsion) diverticulum.
3. Predict the symptoms from the anatomy of a Zenker pouch.
4. Choose and interpret the right investigations, including when barium swallow, endoscopy and high-resolution manometry are indicated.
5. Plan management: when to observe, when to perform cricopharyngeal myotomy with diverticulectomy or diverticulotomy, and when to use flexible endoscopic septotomy or per-oral endoscopic myotomy.
6. Recognise the complications, including aspiration pneumonia, perforation and the rare risk of cancer, and adapt care to a low-resource setting.

The three main types are listed below and are compared in the table.

A true diverticulum involves all layers of the wall: mucosa, submucosa, the muscle layer (muscularis propria) and the outer adventitia. It is produced by an external force pulling the wall outward, which is why the mid-oesophageal traction type is true.

A false (pulsion) diverticulum is a herniation of only the mucosa and submucosa through a defect or weak point in the muscular layer, driven by raised pressure inside the lumen. Zenker and epiphrenic diverticula are false diverticula. On histology an epiphrenic diverticulum appears as a pseudodiverticulum lacking a muscle layer, and the same applies to a Zenker pouch.

Oesophageal diverticula are uncommon. Zenker's diverticulum is by far the type most likely to cause symptoms and present clinically.

• Zenker's diverticulum. Reported annual incidence is 2 per 100000 adults, with a prevalence of 0.01 to 0.11 percent. Prevalence is higher in Western (northern European) populations than in Asian populations, which has been attributed to anatomical and possibly racial differences in the size of Killian's triangle. It occurs predominantly in men, with about a 1.5-fold male predominance, and is most common in the seventh and eighth decades of life. Because the condition is tied to ageing, its prevalence is expected to rise as populations age. Many pouches are small and never cause symptoms, so true prevalence is probably underestimated. ^[1][2]
• Epiphrenic diverticulum. Usually detected after middle age. There is no clear difference in incidence between the sexes. The true prevalence is uncertain because many are found incidentally. ^[1]
• Mid-oesophageal traction diverticulum. These are now rare in clinical practice, because the classic cause, pulmonary tuberculosis and mediastinal granulomatous disease, is largely controlled. Small ones are often incidental. ^[1]

The primary driver is disordered motility of the upper oesophageal sphincter region. Relaxation of the cricopharyngeus is impaired, which generates an abnormally high intrabolus pressure in the hypopharynx (the lower throat). The pouch then forms at the weakest point, Killian's triangle. Contributing factors include structural change in the cricopharyngeus itself (loss of muscle fibres, more fibrous tissue and a raised collagen-to-elastin ratio), loss of tissue elasticity with ageing, and anatomical variation in the size of Killian's triangle, which may explain racial and sex differences. Gastro-oesophageal reflux may also contribute by affecting cricopharyngeal function, although this has not been investigated consistently. ^[2]

These are not pulsion pouches at all. They arise from chronic mediastinal inflammation and fibrosis that cicatricially contracts and tethers the oesophageal wall outward. Pulmonary tuberculosis and other mediastinal granulomatous diseases are the classic association. ^[1]

More than 75 percent of epiphrenic diverticula occur concomitantly with an oesophageal motility disorder, so a motility disorder should be regarded as the underlying disease rather than an incidental finding. Reported associations include failure of the lower oesophageal sphincter to relax (achalasia) and spastic disorders. The right wall of the distal oesophagus is the most susceptible site, although the reason is not known. ^[1]

Zenker's. The sequence is: ageing and dysfunction of the upper oesophageal sphincter region lead to high hypopharyngeal pressure at swallowing; the wall gives way at Killian's triangle between the inferior pharyngeal constrictor and the cricopharyngeus; the pouch grows posteriorly and laterally, usually to the left; food collects in it and empties slowly; the pouch may compress the true oesophageal lumen and cause dysphagia, while stagnant contents regurgitate and may be aspirated. ^[2]

Mid-oesophageal traction. Mediastinal inflammation (tuberculosis) leads to fibrosis, which shortens and tethers the outer layers of the oesophagus; the internal pressure then pouches the mucosa at that site. Because the pouch consists of the full thickness of the wall and its opening is wide, it is usually small and rarely produces symptoms. ^[1]

Epiphrenic. An underlying motility disorder (often achalasia or a spastic disorder) raises pressure above the lower oesophageal sphincter; the mucosa herniates through the muscular layer of the distal (usually right) oesophageal wall just above the sphincter; barium may pour into the pouch while the true lumen is compressed. ^[1]

Pulsion pouches (Zenker and epiphrenic) are pseudodiverticula: the mucosa and submucosa protrude through a gap in the muscle, and the muscle layer is absent in the wall of the pouch itself. A traction (Rokitansky) diverticulum, by contrast, contains mucosa, submucosa, muscle and adventitia, because the whole wall is drawn outward by external fibrosis. ^[1][2]

Zenker's and epiphrenic pouches share the same broad picture, but the details differ.

• Difficulty swallowing, usually to both solids and liquids, and often progressive. In Zenker's diverticulum this is oropharyngeal dysphagia, present from the start; both the failure of the sphincter to open and the mass effect of the pouch can obstruct. ^[2]
• Regurgitation of undigested food, sometimes hours after eating, because food was trapped in the pouch and empties late. Patients may find food on the pillow on waking. ^[2]
• Halitosis, from fermenting retained food and debris in the pouch. ^[2]
• A lump or sensation in the throat, fullness after meals, hoarseness, whistling or noise on swallowing. ^[2]
• Cervical borborygmi and a gurgling swelling in the neck on palpation with very large Zenker pouches. ^[2]
• Chronic cough, choking and chronic aspiration, which can progress to aspiration pneumonia. ^[2]
• Medication ineffectiveness, malnutrition and unintentional weight loss, when intake is poor or tablets lodge in the pouch. ^[2]
• In epiphrenic diverticulum, chest pain is a common symptom, and large pouches cause regurgitation and dysphagia that can mimic achalasia. ^[1]

Small pouches, especially traction diverticula of the mid-oesophagus, are often asymptomatic and found incidentally. ^[1]

Examination may be normal with a small pouch. With a large Zenker pouch there may be a visible or palpable swelling in the neck that gurgles on palpation, halitosis, and signs of aspiration. There are no specific cutaneous findings. The important clinical point is to recognise the aspiration risk: recurrent chest infections in an older patient with dysphagia should prompt a swallowing assessment. ^[2]

The main conditions to separate, because they present with dysphagia, regurgitation or chest pain, are pharyngeal and oesophageal cancers, peptic and corrosive strictures, achalasia and other motility disorders (which may coexist with an epiphrenic pouch rather than mimic it), gastro-oesophageal reflux disease, and cricopharyngeal or upper sphincter disorders without a pouch. A barium swallow and careful endoscopy separate them: a diverticulum has a neck and a pouch that fills with contrast, while a stricture narrows the true lumen and a cancer distorts or ulcerates the mucosa. ^[1][2]

A contrast swallow, usually barium, is the mainstay of diagnosis. It shows the size, position and shape of the pouch, the neck of the diverticulum, whether the true lumen is compressed, and the dynamics of emptying. It is the test that answers the question "where and how big?". ^[2]

Careful endoscopic evaluation is mandatory to rule out malignancy in the pouch or the oesophagus. Blind passage is dangerous: iatrogenic perforation during passage of an endoscope or a nasogastric tube through a Zenker pouch is a described complication. The pouch fills and overhangs the true lumen, so the endoscope can be mistaken into the pouch. Teach the rule: do not pass a blind nasogastric tube, and do not advance an endoscope into an unrecognised pouch; if perforation is suspected, image first. ^[2]

In epiphrenic diverticulum more than 75 percent of cases accompany an oesophageal motility disorder, so evaluation of oesophageal motility using high-resolution manometry is recommended before deciding on intervention. Manometry identifies achalasia, spastic disorders or other dysmotility that must itself be treated. Even when manometry is normal while the clinical picture suggests a motility disorder, the clinical and barium findings take precedence. ^[1]

No blood test diagnoses an oesophageal diverticulum. A chest radiograph may show an air-fluid level in the neck or mediastinum in a large, long-standing pouch, and computed tomography may be used to define anatomy before surgery, but neither is first-line. Biopsy of any suspicious mucosal lesion requires endoscopy with care.

There is no formal scoring system or staging classification. Severity is judged by symptoms (dysphagia, regurgitation, aspiration, weight loss) and by pouch size measured on barium swallow. Small asymptomatic diverticula need no treatment. In Zenker's pouch a size above about 5 to 6 cm and a younger, fitter patient push toward excisional surgery, while small to moderate (up to about 4 cm) pouches and older, frailer patients are usually managed with myotomy or endoscopic approaches. ^[2]

The urgent issues are aspiration (presentation as aspiration pneumonia) and suspected perforation. Treat aspiration pneumonia with appropriate antibiotics, empty the pouch if possible, and refer early. If perforation is suspected after endoscopy or tube insertion, keep the patient nil by mouth, image urgently, involve surgery, and give broad-spectrum antibiotics according to local guidance. ^[2]

Observation. Small, asymptomatic pouches do not need treatment: the risk of severe complications, cancer and aspiration is low. ^[2]

Principle of treatment. The therapeutic aim is to create a communicating door between the pouch and the oesophageal lumen by transecting the common wall (septum), so the reservoir disappears and bolus clearance is restored. Because the cricopharyngeus is central to pathogenesis, cricopharyngeal myotomy is considered an essential part of treatment whatever else is done; pouch excision, suspension or inversion alone without myotomy carry a high rate of recurrence. ^[2]

Minimally invasive endoscopic septotomy (first-line in most services). Flexible endoscopic diverticulotomy or septotomy transects the common wall between the pouch and the true lumen using knives originally developed for submucosal dissection; with the D-POEM technique this is done after a submucosal tunnel, and rigid endoscopic stapling and CO2-laser approaches are also used. Endoscopic stapling has become the first-line surgical treatment in many centres: large studies show it effective in 90 to 100 percent of cases, with major complications in up to 4 percent on average and mortality below 1 percent. A meta-analysis of 11 studies (596 patients) comparing endoscopic with open surgery found that endoscopic treatment shortened procedure and hospital stay, introduced diet earlier and had fewer complications, but carried a higher rate of recurrent symptoms. ^[2][3]

Open surgery. Transcervical approach under general anaesthesia, with diverticulectomy (which allows histology of the pouch), diverticulopexy or diverticular inversion, combined with cricopharyngeal myotomy, extended by 2 to 3 cm into the oesophageal muscle in some surgical traditions. Open surgery has good mid-term results (about 80 to 100 percent clinical success) but significant morbidity and mortality (up to 30 percent and 3 percent respectively). It is preferred for large (above 5 to 6 cm) pouches, younger patients in whom malignant change is a concern, and when long-standing large pouches need inspection. Small pouches (up to about 4 cm) in older patients can be managed with diverticular inversion or suspension, and very small but symptomatic pouches with myotomy alone. Reported recurrence is 3 to 19 percent after resection, 6 to 15 percent after inversion and up to 7 percent after suspension, lower when myotomy is performed. ^[2]

Treatment targets the pouch and the underlying motility disorder. Asymptomatic, stable pouches may be observed. In symptomatic patients the usual approach is laparoscopic resection of the pouch with a myotomy through the lower oesophageal sphincter plus an anti-reflux procedure (fundoplication), since most cases have an associated motility disorder. Endoscopic alternatives include salvage per-oral endoscopic myotomy (s-POEM, myotomy opposite the pouch including the sphincter) and diverticular POEM (D-POEM, a septotomy of the pouch using the POEM technique). Long-term surgical outcomes are generally satisfactory; population data report surgical mortality of 1.6 percent for non-Zenker diverticula, with air leak (3.1 percent) as the commonest complication, and higher postoperative morbidity after thoracotomy than after laparoscopy (odds ratio 7.45). ^[1]

These are usually small and asymptomatic and require no treatment. Symptomatic cases, or pulsion-type pouches in the mid-oesophagus, are managed on the same principles as epiphrenic pouches. The underlying granulomatous disease (tuberculosis) must be treated. ^[1]

After treatment, symptoms and residual food clearance are reassessed clinically and, if needed, with a contrast swallow. Long-term recurrence is possible, particularly without myotomy, so a return of dysphagia, regurgitation or halitosis should prompt re-evaluation. Histology of any resected pouch is mandatory because of the rare risk of cancer. ^[2]

Refer patients with persistent dysphagia, regurgitation or weight loss, any pouch described as large (over 5 to 6 cm), a Zenker pouch with aspiration symptoms, an epiphrenic pouch (all need physiologic assessment and planning), or alarming symptoms suggesting cancer. Cervical surgery and oesophageal surgery should be directed to units that perform them regularly. ^[1][2]

• Aspiration pneumonia from chronic aspiration of pooled pouch contents, the most important threat. ^[2]
• Perforation, usually iatrogenic during passage of an endoscope or nasogastric tube, or spontaneously with mediastinitis in advanced disease. ^[2]
• Bleeding, fistula, vocal cord paralysis and pharyngocutaneous fistula after surgery. ^[2]
• Malnutrition, medication ineffectiveness and weight loss. ^[2]
• Cancer in a diverticulum is rare. In Zenker's diverticulum the reported incidence is 0.5 percent, attributed to chronic irritation and inflammation. A sudden worsening of dysphagia, aphagia or new alarm symptoms (haemoptysis, haematemesis, local pain) should raise suspicion and prompt careful endoscopy with biopsy. Endoscopic stapling does not allow histology, so this risk is one reason large, long-standing pouches are more often excised. ^[2]

Small asymptomatic pouches often remain stable for life. Treated symptomatic Zenker's diverticulum has a good outcome: open surgery gives good or excellent results in most patients and endoscopic stapling is effective in 90 to 100 percent of cases, with lower complication and mortality rates. Recurrence is uncommon when myotomy is performed. In epiphrenic disease the prognosis depends partly on the underlying motility disorder and its treatment, but surgical outcomes are generally good. ^[1][2][3]

There is no screening programme, since most pouches are asymptomatic and not dangerous. Reducing aspiration risk in older patients with dysphagia (swallowing assessment, careful feeding) is the main practical preventive measure, together with treating the underlying motility disorder and mediastinal tuberculosis where these are present. ^[1][2]

• Older adults. Zenker's diverticulum is a disease of the seventh and eighth decades, and patients are often frail. Minimally invasive endoscopic approaches are preferred in this group because of lower morbidity and mortality. ^[2]
• Patients with mediastinal tuberculosis. Mid-oesophageal traction diverticula may regress or remain stable once infection is controlled; underlying disease must be treated. ^[1]
• Immunocompromised patients can present with mediastinal granulomatous disease and similar traction pouches; management is individualised.

• Barium swallow is often available even where endoscopy is limited, and it is the test that establishes the diagnosis. Learn to recognise a pouch filling with contrast in any patient with progressive dysphagia, regurgitation or halitosis. ^[2]
• Where endoscopy is available, the first priority is to visualise the pouch without perforating it: pass the instrument under direct vision, and avoid blind nasogastric tubes. ^[2]
• In the absence of surgery, attention to aspiration prevention (positioning at meals, texture modification, oral hygiene) and treatment of underlying tuberculosis can relieve symptoms and reduce harm. Open or endoscopic surgical treatment, where needed, requires referral to a centre with experience; epiphrenic and large Zenker pouches in particular benefit from surgical care. ^[1][2]

• An oesophageal diverticulum is a pouch of the oesophageal wall; "false" pulsion pouches (Zenker, epiphrenic) lack a muscle layer, while a "true" mid-oesophageal traction pouch involves the whole wall.
• Zenker's diverticulum is a posterior pulsion pouch through Killian's triangle, above the cricopharyngeus, driven by impaired upper sphincter relaxation.
• Mid-oesophageal (Rokitansky) diverticulum is a true traction pouch from mediastinal granulomatous scarring, classically tuberculosis, and is now rare.
• Epiphrenic diverticulum is a distal pulsion pouch, usually right-sided, associated with an underlying motility disorder in more than 75 percent of cases.
• Typical features: progressive dysphagia to solids and liquids, regurgitation of undigested food hours later, halitosis, neck lump or borborygmi, chronic cough and aspiration, weight loss.
• Barium swallow is the key test; endoscopy is needed to exclude malignancy but blind passage risks perforation, as does a blind nasogastric tube.
• Manometry is essential in epiphrenic pouches to identify the underlying motility disorder.
• Small asymptomatic pouches are observed. Treatment demands cricopharyngeal myotomy plus, according to size and fitness, endoscopic septotomy or diverticulectomy; epiphrenic pouches also need treatment of the motility disorder.
• Complications include aspiration pneumonia, perforation, and rarely cancer (0.5 percent in Zenker's pouch); histology of every resected pouch is required.
• Endoscopic treatment shortens hospital stay and complication rates compared with open surgery but carries a higher rate of recurrent symptoms.

Oesophageal motility disorders. Gastro-oesophageal reflux disease. Dysphagia and odynophagia. Infectious oesophagitis. Oesophageal cancer. Aspiration pneumonia. Tuberculosis (mediastinal granulomatous disease).