Dysphagia is the sensation that something is impeding the normal passage of swallowed material. Patients with dysphagia often complain that ingested material “gets stuck” or “just won’t go down right.”

Dysphagia can be caused by intrinsic disorders of the oropharynx and/or esophagus that mechanically narrow the lumen through inflammation, fibrosis, or neoplasia (e.g., peptic stricture, eosinophilic esophagitis, esophageal cancer), by extrinsic disorders of the oropharynx and/or esophagus that mechanically narrow the lumen by compression, encasement or invasion (e.g., lung cancer, enlarged mediastinal lymph nodes, abnormal blood vessels that compress the esophagus), or by neuromuscular “motor” disorders that disrupt peristalsis in the oropharynx and/or esophagus (e.g., myasthenia gravis, achalasia).

It has been estimated that the cause of dysphagia can be determined with an accuracy of approximately 80% based on a careful history alone. Most patients who complain of dysphagia can be found to have an underlying organic disorder, and only infrequently is dysphagia a “functional” symptom.

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Also known as:Difficulty swallowing

What disease states can produce these signs or symptoms?

Oropharyngeal dysphagia

Oropharyngeal dysphagia should be suspected in patients who complain of any of the following symptoms: (1) Difficulty initiating a swallow, (2) nasopharyngeal regurgitation, (3) choking and coughing with swallowing, and (4) a sensation that residual material remains in the pharynx after swallowing.

Esophageal dysphagia

Esophageal causes of dysphagia should be suspected in anyone who complains of dysphagia without the oropharyngeal symptoms, as listed in Table I.

Table I.
Mechanical lesions Oropharyngeal tumorsZenker’s diverticulumCervical osteophytes
Neurologic disorders Cerebrovascular accidentsParkinson’s disease
Skeletal muscle disorders Polymyositis/dermatomyositisMuscular dystrophies
Neuromuscular transmission disorders Myasthenia gravis

What urgent or emergent measures should be initiated even before the diagnosis is established?

The symptom of dysphagia virtually always warrants prompt evaluation, but dysphagia infrequently requires urgent evaluation. The exception to this rule is food impaction. Patients who have mechanical narrowing of the esophagus from any of the diseases listed in Table II may develop a food impaction if they swallow a solid bolus that is too large to pass through the area of narrowing. Such a bolus can completely obstruct the lumen of the esophagus to the point that patients cannot swallow their oral secretions. Such patients are at risk for pulmonary aspiration, and endoscopy should be performed as soon as possible – and certainly within 12 hours – to remove the obstructing material.

Table II.
Esophageal mucosal diseases Gastroesophageal reflux disease (peptic stricture)Eosinophilic esophagitisSchatzki ring/esophageal websEsophageal tumorsCaustic injury (e.g., lye ingestion, pill esophagitis)Radiation injuryInfectious esophagitis
Extrinsic diseases that compress the esophagus Chest tumors (e.g., lung cancer, lymphoma)Infections with mediastinal lymphadenopathy (e.g., tuberculosis, histoplasmosis)Vascular anomalies (dysphagia lusoria)
Diseases affecting esophageal smooth muscle or its innervation AchalasiaSclerodermaOther motility disorders

What is the appropriate initial diagnostic approach to identify the specific underlying disease?

Answers to the following key questions can direct the evaluation and management of patients with dysphagia.

  • 1. Are there symptoms of oropharyngeal dysfunction? Oropharyngeal dysphagia should be suspected in patients who complain of any of the following symptoms: (1) Difficulty initiating a swallow, (2) nasopharyngeal regurgitation, (3) choking and coughing with swallowing, and (4) a sensation that residual material remains in the pharynx after swallowing. If any of these symptoms are prominent, evaluation for oropharyngeal dysfunction may precede tests for esophageal disorders. Videofluoroscopy, in which a motion recording is made of swallows involving barium suspensions and barium-coated materials, is an excellent technique for assessing oropharyngeal function. Depending on the predominant symptom, patients with oropharyngeal dysphagia may require evaluation by a neurologist or otolaryngologist.

  • 2. Is the dysphagia for solid foods, liquids, or both? Esophageal mucosal diseases and extrinsic compressing diseases cause dysphagia by narrowing the esophageal lumen. Such narrowings generally do not restrict the passage of liquids and, consequently, these diseases characteristically cause dysphagia only for solid foods. Dysphagia for both solids and liquids suggests an esophageal motility disorder, especially achalasia. In achalasia, there is no peristalsis in the body of the esophagus to propel swallowed material, and there is persistent contraction of the lower esophageal sphincter, which causes a complete mechanical obstruction of the distal esophagus.

  • 3. Where does the patient perceive that ingested material sticks? Patients with dysphagia due to a lesion that narrows the esophageal lumen often perceive that swallowed material sticks at or above the level of the lesion. It is very uncommon for patients to perceive that swallowed material sticks at a level substantially below that of the obstruction. Thus, a history that food sticks above the suprasternal notch is of little value in localizing the obstruction because this sensation could be caused by a lesion located anywhere from the pharynx to the most distal esophagus. If the patient localizes the obstruction to a point below the suprasternal notch, however, the dysphagia is very likely due to an esophageal disorder.

  • 4. Is the dysphagia intermittent or progressive? A lower esophageal mucosal (Schatzki) ring typically causes dysphagia that is intermittent and nonprogressive. In contrast, esophageal strictures usually cause dysphagia that progresses in frequency and severity. Benign strictures typically progress slowly (over a period of months to years) and are associated with minimal weight loss. Malignant esophageal strictures usually cause rapidly progressing dysphagia (over a period of weeks to months) with substantial weight loss.

  • 5. Is there a history of chronic heartburn? Heartburn is the cardinal symptom of gastroesophageal reflux disease (GERD), and a history of chronic heartburn suggests that dysphagia might be due to reflux esophagitis or a peptic esophageal stricture. Heartburn is not specific for GERD, however, and patients with achalasia or eosinophilic esophagitis also experience this symptom frequently.

  • 6. Has the patient taken medications likely to cause pill esophagitis? A number of medications taken in pill form are potentially caustic to the esophagus and can cause ulceration with stricture formation if they have prolonged contact with the esophageal mucosa. Common causes of pill esophagitis include certain antibiotics (e.g., doxycycline), potassium chloride preparations, nonsteroidal anti-inflammatory drugs (NSAIDs), quinidine preparations, and alendronate.

  • 7. Is there a history of connective tissue disorders? Connective tissue disorders such as scleroderma, rheumatoid arthritis, and systemic lupus erythematosus often are associated with esophageal dysmotility.

  • 8. Is the patient immunosuppressed? Infectious esophagitis occurs frequently in patients whose immune system has been compromised severely by infection with the human immunodeficiency virus, by advanced malignancy, or by organ transplantation with the administration of potent immunosuppressive drugs. Most esophageal infections are caused by one or a combination of only three organisms: candida, cytomegalovirus, and herpes simplex virus. Odynophagia (pain on swallowing) is usually the predominant symptom for patients with infectious esophagitis, but most patients experience dysphagia as well.

  • 9. Is there a history of emergency room visits for food impaction? Although virtually any of the esophageal mucosal and extrinsic diseases listed in Table II can be complicated by food impaction, this complication is especially characteristic of eosinophilic esophagitis. In addition, patients with eosinophilic esophagitis frequently have a history of atopic diseases such as asthma, eczema, and allergic rhinitis.

Endoscopic evaluation

Endoscopic evaluation is recommended for virtually all patients with dysphagia suspected to be of esophageal origin to: (1) establish or confirm a diagnosis, (2) seek evidence of esophagitis, (3) exclude malignancy, and (4) implement therapy when appropriate (e.g., esophageal dilation).

The endoscopist can obtain biopsy specimens of esophageal lesions that may establish the diagnosis of neoplasms or specific infections. Endoscopy has largely displaced barium swallow for the initial evaluation of dysphagia, and barium swallow is not needed at all in most patients with dysphagia. Nevertheless, a barium swallow can be helpful in certain situations, especially when attempting to delineate anatomic relationships between the esophagus and surrounding organs.

Endoscopic examination

May reveal no abnormalities in patients with dysphagia. The role of empiric esophageal dilation for such patients is debated. A number of reports have alleged that this practice can be beneficial. However, limited, prospective clinical studies have not shown clear-cut benefit for empiric dilation, and the American Society of Gastrointestinal Endoscopy does not advocate the practice. Nevertheless, empiric esophageal dilation remains a common clinical practice among community gastroenterologists.

What is the diagnostic approach if this initial evaluation fails to identify the cause?

Esophageal manometry generally is considered the gold standard test for diagnosing esophageal motility disorders such as achalasia. Typically, endoscopy is the first diagnostic test for patients with dysphagia, and esophageal manometry is performed to confirm the endoscopic impression that there is a motility disorder, or if the endoscopy reveals no mucosal/mechanical abnormalities to explain the dysphagia.

What is the Evidence?

Achem, SR, Devault, KR. “Dysphagia in aging”. J Clin Gastroenterol. vol. 39. 2005. pp. 357-71.

Bulat, RS, Orlando, RC. “Oropharyngeal dysphagia”. Curr Treat Options Gastroenterol. vol. 8. 2005. pp. 269-74.

Kahrilas, PJ, Smout, AJ. “Esophageal disorders”. Am J Gastroenterol. vol. 105. 2010. pp. 747-56.

Olson, JS, Lieberman, DA, Sonnenberg, A. “Empiric dilation in non-obstructive dysphagia”. Dig Dis Sci. vol. 53. 2008. pp. 1192-7.

Pandolfino, JE, Fox, MR, Bredenoord, AJ, Kahrilas, PJ. “High-resolution manometry in clinical practice: utilizing pressure topography to classify oesophageal motility abnormalities”. Neurogastroenterol Motil. vol. 21. 2009. pp. 796-806.

Spechler, SJ, Castell, DO. “Classification of oesophageal motility abnormalities”. Gut. vol. 49. 2001. pp. 145-51.

Spechler, SJ. “American gastroenterological association medical position statement on treatment of patients with dysphagia caused by benign disorders of the distal esophagus”. Gastroenterology. vol. 117. 1999. pp. 229-33.