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Continuing Education Activity

Dysphagia is defined as objective impairment or difficulty in swallowing, resulting in an abnormal delay in the transit of a liquid or solid bolus. The delay may be during the oropharyngeal or esophageal phase of swallowing. This activity reviews the evaluation and management of oropharyngeal and esophageal dysphagia and highlights the role of the interprofessional team in evaluating and improving care for patients with dysphagia.


  • Identify the etiology of oropharyngeal and esophageal dysphagia.
  • Describe clinical approaches for the diagnosis of dysphagia.
  • Outline current management options used in dysphagia.
  • Review the interprofessional team strategies for improving care coordination and outcomes in patients with dysphagia.


Dysphagia is defined as objective impairment or difficulty in swallowing, resulting in an abnormal delay in the transit of a liquid or solid bolus. The delay may be during the oropharyngeal or esophageal phase of swallowing. The second aspect of the definition of dysphagia is the subjective definition – the patient’s sensation of a delay in transit of a liquid or solid bolus during swallowing. Both descriptions are relevant because some patients may lose the sensation of a delay in swallowing, while objective tests could show that they have dysphagia. Also, the patient’s symptoms of a delay in swallowing may be potentiated or attenuated through sensory neural dysfunction.

Dysphagia is a common problem in the elderly, and it can occur in patients due to two leading causes. First mechanical obstructive causes such as Schatzki ring, esophageal stricture, esophageal carcinoma, or eosinophilic esophagitis. Second motility disorders of the esophagus (esophageal spasm, achalasia, and ineffective esophageal motility/scleroderma). The dysphagia could be intermittent or persistent and limited only to solid food (mechanical obstruction), or solids and liquids (motility disorders). Clinical presentation includes history and physical examination. Bedside testing, barium swallow, endoscopy, and high-resolution impedance manometry are essential for the diagnosis. Dysphagia-associated complications include increased risk of aspiration, aspiration-induced pneumonia, malnutrition, decreased life quality, and prolonged hospital or intensive care unit stay, and increased morbidity and mortality. The management of dysphagia is dependent on the cause of dysphagia and associated conditions.


Dysphagia could be during the oropharyngeal or pharyngeal phases of swallowing.

A. Oropharyngeal dysphagia is a delay in the transit of liquid or solid bolus during the oropharyngeal phase of swallowing. It could be due to three main subgroups:[1] 

  1. Neurological
  2. Muscular
  3. Anatomical
    • Neurological causes include cerebrovascular accidents (post-stroke dysphagia), brainstem infarctions with cranial nerve involvement. Other causes include basal ganglia lesions as in Parkinson disease. Also, head and neck injuries and surgery, multiple sclerosis, central nervous tumor, botulism, amyotrophic lateral sclerosis, supranuclear palsy, and degenerative cervical spine disease.
    • Muscular causes include polymyositis, muscular dystrophy, and myasthenia gravis (a lesion at the neuromuscular junction).
    • Anatomical causes include Zenker diverticulum, enlarged thyroid, esophageal web, tumors, abscess, external compression by an aortic aneurysm (known as dysphagia aortica).[2] Also, cervical discectomy and fusion may be associated with postoperative dysphagia.[3][4]

B. Esophageal dysphagia - could be due to mechanical obstruction, or motility disorders

  • Mechanical obstruction causes include Schatzki ring, esophageal stricture, esophageal carcinoma, eosinophilic esophagitis.[5]
  • Motility disorder causes include esophageal spasm, achalasia, ineffective esophageal motility, and scleroderma.

 Mechanical obstruction is associated with dysphagia only to solid food, while motility disorder causes are usually associated with solid and liquid dysphagia. The dysphagia may be intermittent (e.g., Schatzki ring, esophageal spasm) or permanent (as in esophageal stricture, carcinoma, achalasia, scleroderma, ineffective esophageal motility).[6]

C. Rheumatological disorders

  • Sjogren syndrome (occurs in one-third of patients and caused by both xerostomia and abnormal esophageal motility, mainly of the proximal esophagus.
  • Systemic lupus erythematosus
  • Mixed connective tissue disease
  • Rheumatoid arthritis
  • Systemic sclerosis (as part of the CREST syndrome)

D. Medications

Several drugs may contribute to the severity of dysphagia. The mechanisms by which these drugs may cause dysphagia include xerostomia and changes in esophageal motility. Also, dysphagia may be secondary to the development of drug-induced esophagitis or the development of gastroesophageal reflux disease. Examples of these drugs are:

  • Antipsychotic (e.g., olanzapine, clozapine)
  • Tricyclic antidepressant
  • Potassium supplements
  • Non-steroidal anti-inflammatory drugs
  • Bisphosphonates
  • Calcium channel blockers
  • Nitrates
  • Theophylline
  • Alcohol
  • Medications with immunosuppressant effects (e.g., cyclosporin) can predispose to infective esophagitis and dysphagia
  • Opioids[7]

It is important to note here that narcotic sedatives such as opioids can lead to compromise of airway due to central effects and could increase the risk of aspiration in patients with dysphagia. The use of opiates, even in mild disease, in patients with psychiatric disorders or Parkinson disease, can develop hypercontractile or hypertensive esophageal consequences mimicking type III achalasia.


The prevalence of dysphagia varies with the underlying etiology, age of patients, sources of information (self-reported versus objective assessment), and place of assessment (community versus hospital versus ICU).

The prevalence of dysphagia is approximately 10% to 22% in Americans aged 50 and over.[8] The prevalence increases with advances in age, and it is approximately 40% in people aged over 60.[9]

In hospitalized patients, approximately 14% to 18% of patients have symptoms of dysphagia. In nursing homes, patients with symptoms of dysphagia are in the range of 30% to 60%.

The reported frequencies of dysphagia in patients with stroke vary between 19% and 81%.[10][11] Early detection of dysphagia in these patients is critical for reducing pulmonary complications and the length of hospital stay.[12] The incidence is more common after brainstem stroke or bilateral hemispheric stroke.[13]

In patients in intensive care, a recent systematic review showed that the incidence of post-extubation dysphagia (PED) from a total of 14 studies and 3520 individuals, was in the range of 3% to 62%.[14] In another retrospective, observational cohort study, the prevalence of dysphagia was up to 84%.[15] These two studies indicate that the incidence of post-extubation dysphagia is relatively high in patients in the intensive care unit.[16]

In idiopathic achalasia, the mean incidence is approximately 0.3 to 1.6 per 100,000 people per year in adults.[17][18][19]

The disease is equal in frequency in men and women, but the incidence increases with age. Achalasia is commonly diagnosed at the age of 50 years. The incidence in people over 80 years old is approximately 17 per 100,000 per year.[20]

Dysphagia is a common symptom in the elderly. A study reported that 63% of elderly patients who denied any history of swallowing problems showed abnormal swallowing evidence on radiologic swallow studies.[21]


In the elderly, dysphagia can be oropharyngeal, esophageal, or mixed dysphagia. The pathogenesis of oropharyngeal dysphagia includes dysfunction in the salivary production, loss of jaw strength, and gum and dentation problems, and age-related changes in the muscles of the jaw and the tongue resulting in poor mixing of food with saliva and delayed oral phase. In the pharyngeal phase, several age-related changes, including the threshold for laryngeal elevation, resulting in delayed pharyngeal swallowing. The esophageal phase could also be delayed in the elderly as a result of a loss of upper esophageal sphincter elasticity and function.[22]

In patients with stroke, cerebral, cerebellar, or brainstem strokes can impair swallowing function. These lesions can interrupt voluntary control of mastication and bolus transport during the oropharyngeal phase. Furthermore, cortical lesions involving the precentral gyrus cause contralateral impairment of facial muscles, lips, and tongue movements. The changes are also associated with contralateral changes in pharyngeal peristalsis. Brainstem stroke lesions are less common but result in significant swallowing compromise. Patients will lose sensations of the mouth, tongue, and cheeks, as well as the timing of pharyngeal swallow, and laryngeal elevation, glottic closure, and physiological regulation of oropharyngeal swallow; this is because of involvement of cranial nerves emerging from the brainstem.[23][24]

In patients with advanced head and neck cancer who are treated with chemotherapy containing cisplatin, and radiotherapy may develop severe dysphagia related to mucositis. Also, candida species colonize in the esophagus in more than 70% of these patients. The breakdown of the mucosal barrier leads to the failure of physiological mechanisms (provided via the mucosal epithelium and T cells to suppress the candida), leading to opportunistic candidiasis. Mucosal candidiasis causes oropharyngeal dysfunction and dysphagia.

In achalasia, several mechanisms are involved in the pathogenesis, including the following:

  1. Immune-mediated ganglionitis: Chronic ganglionitis results in the loss of the esophageal myenteric neurons. These neurons are normally responsible for the coordination of the relaxation of the lower esophageal sphincter. The pathological changes result in aperistalsis and impaired relaxation of the lower esophageal sphincter. Antibodies against myenteric neurons have been detected in the serum of patients with achalasia,[25] especially with the presence of HLA DQA1*0103 and DQB1*0603 alleles.
  2. It is possible that viruses such as herpes simplex virus 1 (a neurotropic virus), measles, and human papillomavirus play a role in the pathogenesis of achalasia. However, the current evidence shows that herpes simplex virus (HSV)-1 triggers immune activation and subsequent esophageal enteric neuron loss in genetically susceptible individuals.
  3. Gene polymorphisms in the HLA class II molecules, vasoactive intestinal peptide receptor 1, KIT, and interleukin 10 play a role in the pathogenesis of achalasia.[26]

The dysphagia in patients with systemic sclerosis is characterized by a relative sparing of somatic innervation of the proximal esophagus. The lesion usually involves impairment of innervation of the distal esophagus. The motility disorder in these patients is characterized by

  • Normal proximal esophageal motility
  • Reduced or absent lower esophageal sphincter pressure
  • Ineffective distal esophageal body peristalsis
  • In-coordinated peristalsis and lower esophageal function[27]

History and Physical

History and physical examination are extremely important for the diagnosis of dysphagia. Common related symptoms are:[28]

  • Choking and coughing
  • Eating meals more slowly
  • Throat clearance during or after meals
  • A feeling of food stuck in the mid-chest or the throat
  • Frequent pulmonary infections
  • Weight loss
  • Changes in diet consistency of food, preference to liquids and semisolids
  • Neurological changes

Physical signs include:

  • Loss of dentition
  • Abnormal lip closure
  • Local changes
  • Neurological changes

Oropharyngeal dysphagia should be differentiated from esophageal dysphagia. Each should be considered as a distinct group.

The presence of one or more of these symptoms can predict oropharyngeal dysphagia:[29]

  • A delay in oropharyngeal initiation of swallowing
  • Deglutitive cough
  • Nasal aspiration during swallowing
  • There is a need for a repetitive swallow to clear the nasal secretion

Patients with oropharyngeal dysphagia should be considered for a barium swallow. They should also be referred to a neurologist, otolaryngologist, and speech pathologist for further assessment.

Dysphagia can be of acute onset as in stroke. However, in most other conditions causing dysphagia, the symptoms are slowly progressive. Patients who find it difficult to swallow solid food usually suffer from obstruction such as esophageal web, ring, or stricture. Patients who struggle to drink liquids are more likely to have dysphagia due to neurological lesions.


In patients with clinical evidence of nasopharyngeal regurgitation and oropharyngeal dysphagia, the initial test may be a clinical swallow evaluation performed by a speech pathologist. However, this test has its limitations and may miss over 50% of patients with significant aspiration, as seen in videofluoroscopy.[30]

The second test recommended in these patients is a modified barium swallow, which aims at assessing the degree of dysphagia and aspiration.

Patients with signs suggestive of malignancy such as weight loss, bleeding, and oropharyngeal dysphagia should undergo head and neck evaluation and a laryngoscopic examination of the pharynx and larynx, particularly look at oropharynx and Zenker diverticulum. Zenker diverticulum is typically diagnosed by an esophagogram.

Other investigations that may be used for the assessment of these patients are:

  1. Fiberoptic endoscopic evaluation of swallowing (FEES) [31]
  2. Computed tomography of the head and neck and the chest to rule out malignancy

Fiberoptic endoscopic evaluation of swallowing and video-fluoroscopic swallowing study are both considered to be the gold standard for evaluation of Parkinson disease-related dysphagia. In addition, high-resolution manometry may be a helpful tool.[32]

Patients with no supra-esophageal symptoms and negatively modified barium swallow, negative FEES findings, and clinical evidence of esophageal dysphagia should be referred to a gastroenterologist for a barium video-esophagogram. This assessment should cover both the anatomy (strictures or tumor) and motility function of the esophagus (such as achalasia). Esophagoscopy is mandatory in patients suspected to have achalasia to exclude pseudo-achalasia or other forms of esophageal obstruction. Endoscopic findings such as esophageal dilatation and retention of food are not diagnostic of achalasia.

A barium esophagogram is relatively simple and of low cost and is considered the first line of investigation of esophageal dysphagia.[33] A timed-barium esophagogram is helpful in the diagnosis of achalasia. It can help in objectively document treatment outcomes and early detect recurrence.[34]

Other investigations recommended in patients with esophageal dysphagia are:[35]

  1. Esophagogastroduodenoscopy (EGD), which can help in the diagnosis of esophagitis, webs, rings, esophageal strictures, and tumors
  2. Esophageal manometry, which is usually needed in patients with chronic dysphagia
  3. High-resolution esophageal manometry is helpful in the diagnosis of achalasia (the presence of incomplete relaxation of the esophagogastric junction together with the absence of organized peristalsis is consistent with the diagnosis of achalasia).

Based on high-resolution esophageal manometry, there are three subtypes of achalasia that can be identified:

  • Type I: characterized by low intra-esophageal pressure (classic achalasia)
  • Type II: characterized by pan-esophageal pressurization
  • Type III: characterized by high-amplitude spastic contractions

Identifying the subtype of achalasia can guide the choice of therapy.[36]

Treatment / Management

Oropharyngeal dysphagia associated with myasthenia gravis responds to treatment with anticholinesterase inhibitors.

A speech therapist usually sees patients with oropharyngeal dysphagia. The management plan may include:

  • Elimination of certain food consistencies from the diet
  • Adjustment of meal bolus seizes
  • Use of techniques such as chin-tuck, head-turn, and supraglottic maneuvers to help in minimizing/preventing aspiration. Also, strengthening and coordinating muscles involved in swallowing.

Gastroscopy tube may be indicated in patients who fail to respond to the above-stated measures.[1]

Most patients with stroke will regain their swallowing function within 1 to 2 weeks after infarction.

In patients with advanced Parkinson disease, dysphagia does not respond to the dopamine precursor L-DOPA treatment. Measures discussed earlier should be applied.

Patients with Zenker diverticulum are usually managed surgically by cricopharyngeal myotomy through the oral route. However, if the patients have mild symptoms, dilatation of the upper esophageal sphincter may be indicated.[37]

Patients with dysphagia related to head and neck tumors will require long-term swallow rehabilitation. Usually, their dysphagia continues despite the surgical excision of the tumor mass, radiation therapy, or chemotherapy.[38]

Patients with a mild esophageal stricture are usually managed by controlling their esophageal reflux and by endoscopic esophageal dilatation.

Dysphagia caused by esophageal malignancies is usually esophageal adenocarcinoma secondary to longstanding reflux disease. In these patients, the development of Barrett metaplasia and dysplasia is a precursor to cancer. Esophageal squamous carcinoma typically occurs in the upper-mid esophagus and is related to smoking and alcohol drinking. Patients with esophageal malignancy are usually managed by a team of surgeons, gastroenterologists, and radiation oncologists, and the rehabilitation team.[39]

Patients with achalasia are treated with:

  • Pharmacotherapy-nitrates, calcium-channel blockers (e.g., nifedipine 10 to 20 mg sublingual 15 to 30 minutes before meals). It acts by lowering the lower esophageal sphincter resting pressure. Side effects include hypotension, headache, dizziness in about one-third of patients.
  • Botulinum toxin A is usually used by direct injection in 4 to 8 quadrants into the lower esophageal sphincter during endoscopy.[40] More than 80% of patients have a clinical response. However, remission occurs within one year in 60% of patients
  • Pneumatic dilatation- this involves tears of the lower esophageal sphincter using air-filled balloons under fluoroscopic guidance. However, nearly one-third of patients have a recurrence of their symptoms in 4 to 6 years. Pneumatic dilatation is contraindicated in patients with poor cardiopulmonary status or have comorbidities that prevent surgical intervention should esophageal rupture occurs, and surgical intervention needed.
  • Laparoscopic Heller myotomy – surgical myotomy of the distal esophageal muscle and lower esophageal sphincter. Laparoscopic Heller myotomy, when combined with fundoplication, results in a significant reduction of reflux.[41] The surgery is safe, with a reported mortality of 0.1%. The main complication is perforation of the esophagus or gastric mucosa.
  • Peroral-endoscopic myotomy (POEM):[42] This procedure involves a high-definition upper endoscope. POEM takes approximately two to three hours, and patients have to stay in the hospital for two to three days for monitoring and to receive intravenous antibiotics.[43]

Based on the high-resolution esophageal manometry results, three subtypes of achalasia can be identified. The identification of the subtype forms the basis of achalasia treatment. These are organized as follows:

  • Types I and II: pneumatic dilatation, laparoscopic Heller myotomy, or POEM.
  • Type III: POEM is the preferred treatment.[42][44]

Because the etiology of dysphagia due to diffuse esophageal spasm (DES) is unknown, and usually patients present with a range of different manifestations and pathology, the treatment of these patients is directed at the symptoms rather than cause treatment.[45] Drugs such as concentrated peppermint oil, nitrates, phosphodiesterase-5 inhibitors, calcium channel blockers, and tricyclic anti-depressants may be used. Other treatments, such as peroral endoscopic myotomy, botulinum toxin, and esophageal dilatation, may be considered.

Scleroderma can cause aperistalsis or low-amplitude esophageal contractions of the distal esophagus as well as a hypotensive lower esophageal sphincter. Usually, these patients have dysphagia to both solids and liquids. The treatment is focused on symptomatic management. No pharmacological intervention has been shown to be promising. Prokinetic agents (metoclopramide, erythromycin, bethanechol, buspirone, and domperidone), which stimulate gut peristalsis, may help.[46] Non-pharmacological approaches, such as acupuncture stimulation,[47] transcutaneous electrical nerve stimulation (TENS) may be indicated in the management of advanced cases.

Differential Diagnosis

Dysphagia can be due to many different causes. Whenever a patient comes with dysphagia following differentials should be kept in mind:

  • Diffuse esophageal spasm
  • Esophageal cancer
  • Eosinophilic esophagitis[48]
  • Hiatal hernia
  • Parkinson disease
  • Zenker diverticulum
  • Multiple sclerosis
  • Paterson-Kelly syndrome
  • Dysphagia lusoria is a type dysphagia that develops in childhood, due to compression of the esophagus by vascular abnormality. Usually, there is an aberrant right subclavian artery arising from the left side of the aortic arch, or a double aortic arch, or other rare anomalies.
  • Benign strictures
  • Esophageal webs and rings
  • Esophageal reflux[49]


The prognosis of dysphagia depends upon underlying etiology. Dysphagia in stroke patients normalizes gradually and may take from three weeks to approximately six months or longer. In the case of achalasia pneumatic dilatation and laparoscopic myotomy are effective. In the case of obstructive causes of dysphagia, like esophageal rings, webs, or tumors, surgical management leads to better outcomes.


Dysphagia impairs quality of life. Following are the other complications associated with dysphagia:

  • Social isolation because of cough, embarrassment, and difficulties in swallowing
  • Pulmonary complications due to chronic aspiration, particularly pneumonia
  • Dehydration, malnutrition
  • Reduced rehabilitation after injury or illness[50]

Deterrence and Patient Education

Patient education depends on the underlying etiology of dysphagia. Patients or their caregivers are advised to feed in an upright posture with neck flexed because it will prevent chances of aspiration and helps in swallowing. Patients with dry mouth are given artificial saliva or lubricants to help in swallowing. Patients are advised not to talk while eating. Different exercises to help in swallowing are taught by the speech therapist to the patients. High caloric food should be taken.

Pearls and Other Issues

Oropharyngeal dysphagia should be differentiated from esophageal dysphagia. Each should be considered as a distinct category. While medical history and clinical examination are essential for making such a differentiation, investigations are helpful in identifying the underlying cause under each of these two categories.

Enhancing Healthcare Team Outcomes

The majority of patients with dysphagia may present to the primary care provider or the emergency department. The public, nurses, pharmacists, and patients should be educated about dysphagia. At schools, students with severe disabilities, or orthopedic impairments may require help because of dysphagia. In essence, the school support team in such schools may need a speech-language pathologist with adequate training in swallowing evaluation and management. No one should provide such services without proper official up-to-date training in this area—a team of speech therapists, neurologists, otolaryngologists, oncologists, dietitians, and nurses usually manage patients with oropharyngeal dysphagia. Surgeons, gastroenterologists, radiation oncologists, and rehabilitation teams usually manage patients with esophageal malignancy.

Article Details

Article Author

Samy A. Azer

Article Editor:

Ravi K. Kshirsagar


6/11/2022 12:01:48 AM

PubMed Link:




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