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Webs are thin, membrane-like structures that project into the esophageal lumen. They are covered on both sides with squamous epithelium and are most commonly found in the cervical esophagus. Webs are usually detected incidentally during barium x-rays and rarely occlude enough of the esophageal lumen to cause dysphagia. The etiology of these webs is unclear. Most are probably congenital in origin. In some instances postcricoid esophageal webs are associated with iron deficiency and dysphagia _ the so-called Plummer-Vinson or Paterson-Kelly syndrome. This syndrome is associated with increased risk of hypopharyngeal cancer and should be managed with bougienage, iron replacement and careful follow-up. Esophageal webs may also form after esophageal injury, such as that induced by pills or lye ingestion, and have also been reported in association with graft-versus-host disease. The lower esophageal or Schatzki's ring is also a membrane-like structure, but unlike webs is lined by squamous epithelium on its superior aspect and columnar epithelium inferiorly. Such a ring is quite common, being detected in up to 10% of all upper GI barium x-rays. Few produce sufficient luminal obstruction to cause dysphagia (yet a lower esophageal ring is a common cause of dysphagia). When the lumen is narrowed to a diameter of 13 mm or less, the patient will experience intermittent solid-food dysphagia or even episodic food-bolus obstruction. Treatment of a symptomatic Schatzki's ring involves shattering the ring with a large-diameter bougie or a balloon dilator.
Pharyngoesophageal diverticula are outpouchings of one or more layers of the pharyngeal or esophageal wall and are classified according to their location.
This diverticulum arises posteriorly in the midline between the oblique and transverse (cricopharyngeal) fibers of the inferior pharyngeal constrictor muscles. As this diverticulum enlarges, it usually shifts to the left of the midline. Zenker's diverticulum forms because of decreased compliance of the cricopharyngeal muscle, which results in abnormally high pressures in the hypopharynx during deglutition. If large, the diverticulum may cause dysphagia secondary to external compression of the cervical esophagus. In addition to oropharyngeal-type dysphagia, Zenker's diverticulum may be associated with effortless regurgitation of stagnant, foul-tasting food, as well as aspiration. A very large diverticulum can produce a neck mass, usually on the left side. Treatment of a symptomatic Zenker's diverticulum is surgical. Most surgeons will either resect the diverticulum or suspend it (diverticulopexy) so that it cannot fill. This is combined with cricopharyngeal myotomy. In many cases cricopharyngeal myotomy alone will alleviate symptoms. Once the cricopharyngeal myotomy has been performed, the patient has lost an important defense mechanism to prevent the aspiration of refluxed material. The patient should therefore be instructed to elevate the head of the bed in order to minimize this risk. For the same reason patients with gross GERD should not undergo cricopharyngeal myotomy unless the reflux can be controlled either medically or surgically.
Traditionally, midesophageal diverticula have been called "traction" diverticula because of their supposed etiology. They were believed to arise secondary to old mediastinal inflammation, such as tuberculosis, that caused adherence of mediastinal structures to the outer esophageal wall so that outward traction occurred during peristalsis. It now appears likely that very few midesophageal diverticula arise this way. In most there is an associated motility disorder and it is likely that this is actually a "pulsion" diverticulum formed when a peristaltic wave deteriorates into a simultaneous or spastic contraction in the smooth-muscle esophagus. Midesophageal diverticula rarely require specific therapy. Rather, only the associated motor disorder requires treatment if symptomatic.
These "pulsion" diverticula form just above the LES and are invariably associated with an esophageal motor disorder - usually diffuse esophageal spasm, with or without abnormal relaxation of the LES. Patients with these diverticula usually present with dysphagia and/or angina-like chest pain. In addition, they may complain of nocturnal regurgitation of large quantities of stagnant fluid. If symptoms are present, treatment with nitrates or calcium channel blockers may be helpful. If this is not successful, surgery is indicated. Any surgical attack on these diverticula should involve a myotomy of the spastic distal esophagus and/or LES. Resection of the diverticula alone seldom affords long-term benefit.
This disorder has a characteristic radiologic appearance consisting of numerous tiny, flask-shaped outpouchings from the esophageal lumen. There is usually an associated smooth stricture in the proximal esophagus. Patients typically present with dysphagia that responds to peroral dilation. The outpouchings are actually dilated ducts coming from submucosal glands and thus are not true diverticula. The etiology is obscure. Some cases are associated with esophageal candidiasis, but this organism does not appear to be of etiological importance.
Blunt or penetrating trauma to the chest can cause esophageal injury. In addition, esophageal instrumentation such as that used in bougienage or endoscopy may cause perforation or mucosal laceration. Severe retching or vomiting can also cause esophageal perforation (Boerhaave's syndrome) or mucosal laceration (Mallory-Weiss tear). Boerhaave's syndrome is a life-threatening condition that requires immediate surgery to drain the mediastinum and repair the defect in the esophageal wall. Patients, typically alcoholics, present with sudden epigastric and/or chest pain following a bout of vomiting and usually have fever and signs of hypovolemia or shock. The mucosal laceration of the Mallory-Weiss tear is probably better classified as a disorder of the stomach, because in most cases the laceration starts at the GE junction and extends down into the stomach. These patients present with hematemesis or melena following a bout of retching or vomiting. The bleeding usually stops spontaneously and only supportive therapy is required. If bleeding persists, endoscopically applied hemostasis or surgical intervention may be necessary.
A surprising variety of foreign bodies can lodge in the esophagus after being swallowed either inadvertently or deliberately. The three most common sites where foreign bodies become stuck are the piriform sinuses, at the aortic arch and just above the LES. The patient can usually localize the site of the obstruction quite accurately, and this can be confirmed using routine x-rays if the object is radiopaque. (However, as mentioned above, some patients may perceive the obstruction in the throat region when it is really in the distal esophagus.) Otherwise, x-rays using small amounts of water-soluble contrast media may be necessary. Most foreign bodies can be removed by an expert endoscopist. Surgery is rarely required, except when perforation has occurred. A more common clinical problem is esophageal food-bolus obstruction. This typically occurs when a patient with a motility disorder, stricture or Schatzki's (lower esophageal) ring swallows a large solid-food bolus. The patient notices immediate chest pain, usually well localized to the site of obstruction. Attempts to swallow anything further are unsuccessful and usually lead to prompt regurgitation. Many physicians will initially treat these patients with smooth-muscle relaxants such as intravenous glucagon, sublingual nitroglycerin or nifedipine; however, there is little evidence that this approach is efficacious. If the food bolus does not pass on spontaneously within a few hours, endoscopy should be performed, at which time the bolus can either be removed per os or pushed through into the stomach. These patients should not be left too long, as the bolus is capable of causing significant maceration to the esophageal mucosa. Giving the patient meat tenderizer, in an attempt to dissolve the bolus, is probably of no value and may be very harmful; papain can digest the esophageal mucosa and has been reported to cause severe hemorrhagic pulmonary edema when aspirated. |
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