Esophageal Disorders

Explanation
Key Concept/Objective: To understand the major causes of dysphagia
Dysphagia refers to the sensation of food being delayed in its normal passage from mouth to stomach. Patients often complain of a sensation of food "sticking." Anatomically, dysphagia may be classified as being of two kinds: oropharyngeal and esophageal. Oropharyngeal dysphagia is difficulty in initiating a swallow. Esophageal dysphagia results from difficulty transporting food down the esophagus secondary to structural or neuromuscular defects in the smooth muscle portion of the esophagus. Further history can often establish the diagnosis of esophageal dysphagia. Patients with dysphagia that primarily involves solid food typically have a structural lesion, such as a peptic stricture, ring, or malignancy. Esophageal rings tend to cause intermittent dysphagia of solid food, whereas strictures and cancer cause progressive dysphagia. Patients with both solid and liquid dysphagia are more likely to have a motility disorder like achalasia or scleroderma. The site that a patient indicates as being the location of dysphagia is of limited value. Although dysphagia in the retrosternal or epigastric areas frequently corresponds to the site of obstruction, dysphagia localized to the neck may be from obstruction either lower in the esophagus or in the hypopharyngeal area. Oropharyngeal or transfer dysphagia is an abnormality related to the movement of a food bolus from the hypopharynx to the esophagus. Patients with oropharyngeal dysphagia typically have difficulty initiating a swallow; on attempting to swallow, they immediately experience coughing, choking, gagging, or nasal regurgitation. The distinction between oropharyngeal and esophageal dysphagia is crucial, because the conditions have distinctly different causes. Oropharyngeal dysphagia is most commonly caused by disruptions in the finely coordinated act of swallowing secondary to neuromuscular dysfunction. In this setting, the symptoms may be more severe when swallowing liquids.

Explanation
Key Concept/Objective: To understand the need to rule out pseudoachalasia in patients with suspected achalasia
All patients suspected of having achalasia should undergo upper endoscopy to exclude pseudoachalasia arising from a tumor at the gastroesophageal junction. Signs and symptoms of pseudoachalasia may mimic those of classic achalasia, both clinically and manometrically. The diagnosis of pseudoachalasia should be suspected in patients of older age, those with a short duration of symptoms, and those with more significant weight loss. In patients with achalasia, at endoscopy, the esophageal body often appears dilated and tortuous. Retained secretions and food debris may be encountered. The region of the lower esophageal sphincter usually appears puckered and remains closed with air insufflation; however, with gentle pressure, the endoscope will transverse this area. The gastroesophageal junction and gastric cardia need to be examined closely for the presence of tumors to rule out pseudoachalasia.

Explanation
Key Concept/Objective: To understand the presentation of EOE
EOE has become an increasingly recognized cause of dysphagia and food impaction in young adults. Endoscopy reveals findings of multiple esophageal rings. The etiology is unclear, but GERD, a congenital abnormality, and, possibly, allergic conditions have been implicated. EOE is characterized by esophageal eosinophilia of greater severity than found in acid reflux disease. The eosinophil density required for the diagnosis of EOE is greater than 15 eosinophils per high-power field in the mucosa; in addition, for a diagnosis to be made, the eosinophils must not clear after appropriate treatment with a PPI. EOE is often associated with other atopic diseases. Patients may have a strong family history of atopy. Although current studies have not established that GERD is a causal factor in EOE, there is clearly a role for acid suppression in those patients complaining of GERD symptoms. Treatment consists of dilation with bougienage with or without acid suppression. In many cases, more than one treatment session is needed to achieve a desired esophageal lumen of 15 mm. These patients are at higher risk for painful, deep mucosal tears. Pharmacologic treatment of EOE has been shown to result in improvement of clinical symptoms and histology in the majority of patients. Therapeutic options include pharmacologic treatments, such as oral and topical corticosteroids, and leukotriene-receptor antagonists. Dietary modification and elimination have been effective in the pediatric population, suggesting that certain foods may serve as environmental triggers for the eosinophilic infiltration. Because many adults present with strictures, endoscopic esophageal dilation is another management modality. Despite these treatment options, several controversies exist in the recommended treatment strategy. Because little is known concerning the natural history of the condition, it is unclear whether the goal of therapy should be resolution of symptoms, resolution of tissue eosinophilia, or both.

Explanation
Key Concept/Objective: To understand the diagnosis of Zenker diverticulum
An esophageal diverticulum is a sac that protrudes from the esophageal wall. As in the rest of the gastrointestinal tract, a true diverticulum is one that contains all layers of the wall. A false diverticulum contains mucosa and submucosa that have herniated through the muscular wall. Esophageal diverticula are classified into four categories on the basis of anatomy: Zenker diverticula; midesophageal diverticula; epiphrenic diverticula; and intramural pseudodiverticulosis. Zenker diverticulum is often referred to as an esophageal diverticulum. However, its location is proximal to the esophagus, above the upper esophageal sphincter (UES), and should be considered a hypopharyngeal diverticulum. Zenker diverticula are believed to form as a result of an area of weaknessâ??the Killian triangleâ??that exists between the cricopharyngeal sphincter and the inferior pharyngeal constrictor muscle. The primary abnormality that leads to the development of the diverticula is incomplete relaxation of the UES. An association between Zenker diverticula and reflux has been suggested but not confirmed. Typical symptoms include oropharyngeal dysphagia, regurgitation of undigested food, halitosis, cough, and aspiration pneumonia. Barium swallow is an excellent test for the diagnosis of Zenker diverticulum. Many small diverticula are asymptomatic, but symptomatic patients with large diverticula should be offered treatment. The classic treatment is an open surgical resection of the diverticulum with division of the cricopharyngeus muscles. Another option for extremely large diverticula is diverticulopexy, or suspension of the diverticulum in a cranial direction.

Explanation
Key Concept/Objective: To understand the treatment of GERD-related cough
Chronic cough is defined as cough that persists for a period longer than 3 months. GERD is the third most common cause of chronic cough; the two most common causes of chronic cough are postnasal drip and asthma. The pathophysiology of GERD-related cough includes both irritation of the upper respiratory tract (with or without aspiration) and stimulation of an esophageal-bronchial cough reflex. Patients with chronic cough resulting from GERD have normal chest radiographs, are nonsmokers, are not on medications known to cause cough (such as angiotensin-converting enzyme [ACE] inhibitors), and have had no response to treatment of asthma and postnasal drip. Between 43% and 75% of patients with GERD-related cough do not have typical reflux symptoms. The best initial evaluation is a trial of PPIs; the trial should continue for a period of 3 months, because GERD-related cough can take that long to resolve. Although dietary modification would seem to be a reasonable treatment of GERD, there are little data available to support it as a sole therapy. Cisapride is a prokinetic serotonin-receptor agonist that has demonstrated efficacy in treating mild GERD, but it was withdrawn from the market after causing lethal cardiac arrhythmias in some patients. This patient has no alarm signs, so EGD would be premature at this point.