The complaints of dysphagia, odynophagia, and ingested foreign body immediately implicate the esophagus. The esophagus also is often the site of pathology in patients who present with chest pain, upper GI bleeding (see chapter 75, “Upper Gastrointestinal Bleeding”), malignancy, and mediastinitis. Many diseases of the esophagus can be evaluated over time in an outpatient setting, but several, such as esophageal foreign body and esophageal perforation, require emergent intervention.

The esophagus is a muscular tube approximately 20 to 25 cm long, primarily located in the mediastinum, posterior and slightly lateral to the trachea, with smaller cervical and abdominal components, as shown in Figure 77-1. There is an outer longitudinal muscle layer and an inner circular muscle layer. The upper third of the esophagus is striated muscle, while the lower half is all smooth muscle (including the lower esophageal sphincter). The esophagus is lined with stratified squamous epithelial cells that have no secretory function.

Two sphincters regulate the passage of material into and out of the esophagus. The upper esophageal sphincter prevents air from entering the esophagus and food from refluxing into the pharynx. The lower esophageal sphincter regulates the passage of food into the stomach and prevents stomach contents from refluxing into the esophagus. The upper sphincter is composed primarily of the cricopharyngeus muscle, with a resting pressure of around 100 mm Hg. The lower sphincter is not anatomically discrete. The smooth muscle of the lower 1 to 2 cm of the esophagus, in combination with the skeletal muscle of the diaphragmatic hiatus, functions as the sphincter, with a lower resting pressure around 25 mm Hg. An empty esophagus collapses, but three anatomic constrictions affect the adult esophagus:

1. 
   

   At the cricopharyngeus muscle (C6)

   
   
2. 
   

   At the level of the aortic arch (T4)

   
   
3. 
   

   At the gastroesophageal junction (T10 to T11)

The pediatric esophagus gets two additional areas of constriction:

1. 
   

   At the thoracic inlet (T1)

   
   
2. 
   

   At the tracheal bifurcation (T6)

The innervation of the heart mirrors that of the esophagus, with visceral and somatic stimuli converging within the sympathetic system. This anatomy makes pain of esophageal and cardiac origin similar. The esophageal venous circulation includes a submucosal plexus of veins that drains into a separate plexus of veins surrounding the esophagus. Blood flows from this outer plexus in part to the gastric venous system, an important link between portal and systemic circulation. Variceal dilatation of the submucosal system can lead to massive upper GI bleeding.

Dysphagia is difficulty with swallowing. Most patients with dysphagia have an identifiable, organic cause.

Oropharyngeal (transfer) and esophageal (transport) dysphagia describe two broad pathophysiologic types. Transfer dysphagia occurs very early in swallowing (as the food bolus moves from the oropharynx through the upper sphincter) and is often reported as difficulty in initiating a swallow. Transport dysphagia is impaired movement of the bolus down the esophagus and through the lower sphincter. Transport dysphagia is perceived later in the swallowing process, usually 2 to 4 seconds or longer after swallowing is initiated, and most commonly results in the feeling of the food “getting stuck.” A history geared toward discerning transfer from transport dysphagia provides a differential of the likely underlying pathology (Table 77-1). Another useful classification scheme divides dysphagia into that due to obstructive disease and that due to motor dysfunction. Functional or motility disorders usually cause dysphagia that is intermittent and variable. Mechanical or obstructive disease is usually progressive (difficulty swallowing solids, then liquids).¹

CLINICAL FEATURES

Although often an independent symptom, dysphagia can be associated with odynophagia, which is painful swallowing (suggesting an inflammatory process), or with chest pain that is esophageal in nature, suggesting gastroesophageal reflux disease (GERD) or a motility disorder. Question the patient regarding the course of symptoms (acute, subacute, or chronic, intermittent, progressive); food patterns (solids, liquids); location; and previous disease. Transport dysphagia that is present for solids only generally suggests a mechanical or obstructive process. Motility disorders typically cause transport dysphagia for solids and liquids.

Impaction of a poorly chewed meat bolus in the esophagus is a well-recognized complication of esophageal disease. A history of dysphagia may or may not be present. An impacted food bolus can be the presenting complaint for a variety of underlying esophageal pathologies. Patients are generally accurate in identifying location if the bolus is in the upper third of the esophagus. Esophageal filling proximal to the impacted bolus can cause inability to swallow secretions and can present an airway/aspiration risk.

Focus the physical examination on the head and neck and perform the neurologic examination. Assess for signs of previous stroke, muscle disease, or Parkinson’s disease. Cachexia and cervical or supraclavicular nodes can be observed in patients with cancer of the esophagus. The physical findings are often normal in patients with dysphagia.² Watch the patient take a small sip of water. Inability to swallow water generally confirms at least a partial obstruction.

DIAGNOSIS

The diagnosis of the underlying pathology is most often made outside of the ED. Initial evaluation of dysphagia in the ED can include anteroposterior and lateral neck radiographs, which can be helpful in transfer dysphagia and cases in which the transport dysfunction seems proximal. Obtain a chest x-ray if considering transport dysphagia. Direct laryngoscopy can be used to identify proximal lesions.

Diagnosis of oropharyngeal dysphagia uses a variety of tools. Traditional barium swallow is often recommended as a first test. Video esophagography is a specialized form of barium swallow study in which videotaped images are played at low speed to allow detailed analysis. Manometry and esophagoscopy are also used, depending on the clinical picture.² If a foreign body is suspected, the diagnostic evaluation takes yet another path (see later section, “Swallowed Foreign Bodies and Food Impaction“).

Neoplasm

Neoplasms are a common cause of both transfer and transport dysphagia. The esophagus or surrounding structures can be the primary site. A large majority of esophageal neoplasms are squamous cell; the remaining are adenocarcinomas. Risk factors for squamous cell disease include alcohol, smoking, achalasia, and previous ingestion of caustic material with lye. Barrett’s esophagus predisposes to adenocarcinoma. Surgery and radiation therapy for head and neck cancer are also important associations.³

There is usually a fairly rapid progression of dysphagia from solids to liquids (6 months). Bleeding is another sign suggesting neoplasm. Assume neoplasia in patients >40 years old with new-onset dysphagia. Definitive diagnosis is made by endoscopy with biopsy.

Anatomic Causes

Esophageal stricture develops as a result of scarring from GERD or other chronic inflammation. Generally strictures occur in the distal esophagus proximal to the gastroesophageal junction and may interfere with lower sphincter function. Symptoms may build over years and are often noted solely with solids. Stricture can serve as a barrier to reflux, so heartburn may decrease as dysphagia increases. Evaluation involves ruling out malignancy, and treatment is dilatation.⁴

Schatzki ring is the most common cause of intermittent dysphagia with solids. This stricture near the gastroesophageal junction is present in up to 15% of the population, and most are asymptomatic. A ring may form over time in response to GERD. Food impaction in the esophagus is a frequent presenting event with a Schatzki ring. The treatment is dilatation.⁴

Esophageal webs are thin structures of mucosa and submucosa found most often in the middle or proximal esophagus. They can be congenital or acquired. Esophageal webs also occur as a component of Plummer-Vinson syndrome (along with iron deficiency anemia) and can be seen in patients with pemphigoid and epidermolysis bullosa. Treatment is dilatation.

Diverticula can be found throughout the esophagus. Pharyngoesophageal or Zenker’s diverticulum is a progressive out-pouching of pharyngeal mucosa, just above the upper sphincter, caused by increased pressures during the hypopharyngeal phase of swallowing. Symptom onset is often after age 50, as most diverticula are acquired rather than congenital. Patients complain of typical transfer dysfunction or halitosis and the feeling of a neck mass. Diverticula can also be seen in the mid or distal esophagus, the latter usually in association with a motility disorder.⁵

Neuromuscular and Motility Disorders

Neuromuscular disorders typically result in misdirection of food boluses with repeated swallowing attempts. Liquids, especially at the extremes of temperature, are generally more difficult to handle than solids, and symptoms are often intermittent. Stroke is the most common cause of this type of dysphagia. Oropharyngeal muscle weakness is often the mechanism, although upper sphincter dysfunction can also contribute. Polymyositis and dermatomyositis are also common causes of transfer dysphagia.

Achalasia is a dysmotility disorder of unknown cause and the most common motility disorder producing dysphagia. Impaired swallowing-induced relaxation of the lower sphincter is noted, along with the absence of esophageal peristalsis. Symptom onset is usually between 20 and 40 years of age. Achalasia may be associated with esophageal spasm and chest pain and with odynophagia. Associated symptoms can include regurgitation and weight loss. Dilation of the esophagus can be massive enough to impinge on the trachea and cause airway symptoms.⁶ Therapy includes reduction of lower sphincter pressure by oral medications, endoscopic injection of botulinum toxin into the muscle of the sphincter, dilatations, or surgical myotomy.

Diffuse esophageal spasm is the intermittent interruption of normal peristalsis by nonperistaltic contraction. Dysphagia is intermittent and does not progress over time. Chest pain is a common symptom. Therapy involves control of acid reflux and consideration of smooth muscle relaxants and/or antidepressants, although effectiveness is unclear.⁶

Esophageal dysmotility is the excessive, uncoordinated contraction of esophageal smooth muscle. Clinically, chest pain is the usual presenting symptom of esophageal dysmotility. The onset is usually in the fifth decade. Pain often occurs at rest and is dull or colicky, and stress or ingestion of very hot or very cold liquids may serve as triggers. Acute pain may be followed by hours of dull, residual discomfort. Many patients also have dysphagia, usually intermittent. Pain from spasm may respond to nitroglycerin. Calcium channel blockers and anticholinergic agents can also be used. The other motility disorders commonly recognized include ineffective esophageal motility, hypertensive lower esophageal sphincter, and nutcracker esophagus. Nutcracker esophagus is a motility disorder in which there are high-amplitude, long-duration peristaltic contractions in the distal body of the esophagus or the lower sphincter. The cause is unknown.⁶