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Continuing Education Activity

Patients subjectively define dysphagia as difficulty swallowing and objectively defined by clinicians as an impairment in swallowing that results in an abnormal delay in the transit of a liquid or solid bolus from the oral cavity to the stomach. Dysphagia may be acute or chronic, intermittent or persistent. A globus sensation may accompany it. Dysphagia may be due to abnormalities in the oropharyngeal or esophageal phases of swallowing, or it may be mixed. The underlying etiology may be a mechanical obstruction or a motility disorder. Anatomical, neuromuscular, infectious, and inflammatory diseases may all present with or contribute to dysphagia. The medical history and physical examination are critical to determining the etiology of dysphagia and will often point to a diagnosis. The management of dysphagia is dependent on the cause of dysphagia and associated conditions. This activity reviews the evaluation and management of oropharyngeal and esophageal dysphagia and highlights the role of the interprofessional team in improving care for patients with dysphagia.


  • Distinguish between oropharyngeal and esophageal dysphagia with respect to underlying etiology and clinical symptoms.

  • Apply clinical approaches in the diagnosis of dysphagia.

  • Apply current management options used in dysphagia.

  • Implement effective interprofessional team strategies for improving care coordination and outcomes in patients with dysphagia.


Patients subjectively define dysphagia as difficulty swallowing and objectively defined by clinicians as an impairment in swallowing that results in an abnormal delay in the transit of a liquid or solid bolus from the oral cavity to the stomach. Dysphagia may be acute or chronic, intermittent or persistent. A globus sensation may accompany it. Dysphagia may be due to abnormalities in the oropharyngeal or esophageal phases of swallowing, or it may be mixed.

Dysphagia is a common problem, particularly in the elderly population. The underlying etiology may be a mechanical obstruction or a motility disorder. Anatomical, neuromuscular, infectious, and inflammatory diseases may all present with or contribute to dysphagia.

The medical history and physical examination are critical to determining the etiology of dysphagia and will often point to a diagnosis. However, bedside testing, barium swallow, endoscopy, and high-resolution impedance manometry are commonly used to pinpoint a diagnosis. The management of dysphagia is dependent on the cause of dysphagia and associated conditions.

Dysphagia-associated complications include an increased risk of aspiration, aspiration-induced pneumonia, malnutrition, morbidity, and mortality. Inpatient hospital stays are frequently lengthened by dysphagia and its complications. Patients with dysphagia often report a diminished quality of life.


Dysphagia, difficulty swallowing, can be acute or chronic and may occur in either the oropharyngeal or esophageal phases of swallowing. Dysphagia may coexist with odynophagia or painful swallowing and may be accompanied by a globus sensation. A globus sensation is the subjective feeling of a lump or having something stuck in the throat; it is usually painless.

Oropharyngeal Dysphagia

Oropharyngeal dysphagia is the delay in the transit of liquid or solid bolus during the oropharyngeal phase of swallowing. A variety of anatomical and neuromuscular disorders can cause oropharyngeal dysphagia.[1] Some causes of oropharyngeal dysphagia, such as that seen in the postoperative period following cervical discectomy and fusion, are multifactorial.[2][3] 

Anatomical causes of oropharyngeal dysphagia are most commonly due to lesions that obstruct the lumen or cause external compression of the oropharynx. These include Zenker diverticulum, esophageal webs, oropharyngeal tumors and abscesses, goiters, and external compression by an aortic aneurysm called dysphagia aortica.[4]

Neuromuscular causes of oropharyngeal dysphagia are many. Dysphagia is common after cerebrovascular accidents,  including brainstem infarctions with cranial nerve involvement. In addition, the basal ganglia lesions in Parkinson disease may cause dysphagia. Head injuries, multiple sclerosis, central nervous tumors, botulism, amyotrophic lateral sclerosis, and supranuclear palsy may all cause dysphagia. Muscular disorders such as polymyositis and myopathies may cause dysphagia. Due to its effect on the neuromuscular junction, myasthenia gravis is known to cause dysphagia.

Esophageal Dysphagia

Esophageal dysphagia may be caused by mechanical obstruction of the esophagus or a motility disorder. Mechanical obstruction is characterized primarily by dysphagia with solids, whereas motility disorders have dysphagia for both solids and liquids. Esophageal dysphagia may be intermittent or continuous.[5]

Esophageal dysphagia due to mechanical obstruction is most commonly due to a Schatzki ring, esophageal stricture or webs, esophageal carcinoma, and eosinophilic esophagitis.[6] Causes of motility disorders resulting in dysphagia include esophageal spasm, achalasia, ineffective esophageal motility, and systemic sclerosis.

Rheumatological Disorders and Dysphagia

Several rheumatological disorders are known to cause dysphagia via multiple mechanisms. Each may also exacerbate dysphagia due to other causes. For example, Sjögren syndrome, an autoimmune disease affecting exocrine glands, causes dysphagia via xerostomia and changes in the motility of the proximal esophagus. Limited cutaneous systemic sclerosis (formerly CREST syndrome) is a well-known cause of esophageal dysmotility. Other commonly encountered rheumatologic disorders that may cause or complicate dysphagia are rheumatoid arthritis, systemic lupus erythematosus, and mixed connective tissue diseases.

Medication-induced Dysphagia

Several pharmaceuticals 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 result of gastroesophageal reflux disease as a side effect of medication use.[7] Additionally, medications with immunosuppressant effects predispose to the development of infectious esophagitis with subsequent dysphagia. Examples of these drugs are:

  • Antipsychotics (eg, olanzapine, clozapine)
  • Tricyclic antidepressants
  • Potassium supplements
  • Non-steroidal anti-inflammatory drugs
  • Bisphosphonates
  • Calcium channel blockers
  • Nitrates
  • Theophylline
  • Alcohol
  • Opioids

Of note, narcotic sedatives such as opioids can lead to airway compromise and can increase the risk of aspiration in patients with dysphagia. In addition, patients with psychiatric disorders or Parkinson disease, even mild disease, can develop hypercontractile or hypertensive esophageal consequences when using opioids.


Dysphagia is a common symptom, and the incidence increases with increasing age. The prevalence of dysphagia is approximately 10% to 22% in Americans aged 50 and over.[8] In patients over age 60 years, the prevalence is approximately 40%.[9] A study reported that 63% of elderly patients who denied any history of swallowing problems demonstrated abnormalities in radiologic swallow studies.[10]

The incidence of dysphagia also varies by place of assessment. In hospitalized patients, approximately 14% to 18% of patients have symptoms of dysphagia. In senior care homes, symptomatic dysphagia is reported by 30% to 60% of patients. In patients in intensive care, a recent systematic review showed that the incidence of post-extubation dysphagia (PED) was in the range of 3% to 62%.[11] In another retrospective, observational cohort study, the prevalence of PED was as much as 84%.[12] These 2 studies indicate that the incidence of PED is relatively high in patients in the intensive care unit.[13]

The incidence of dysphagia also varies according to underlying etiology. The reported frequencies of dysphagia in patients with stroke vary between 19% and 81%.[14][15] Early detection of dysphagia in these patients is critical for reducing pulmonary complications and the length of hospital stay.[16] The incidence is more common after brainstem stroke or bilateral hemispheric stroke.[17]

The incidence of dysphagia due to an underlying pathophysiologic process may also increase with increasing age. In idiopathic achalasia, which occurs in equal frequency in males and females and is commonly diagnosed at age 50, the mean incidence is approximately 0.3 to 1.6 per 100,000 people per year in adults.[18][19][20] However, the incidence in people over 80 is approximately 17 per 100,000 annually.[21]

Over the past decade, publications on swallowing disorders have increased yearly.[22]


Swallowing is a series of events that transits food from the oral cavity to the stomach. Transit from the oral cavity to the pharynx is a voluntary process that occurs via the coordinated contraction of oropharyngeal muscles. Transit of a bolus from the oropharynx through the esophagus and into the stomach is an involuntary process. Many conditions may negatively affect this process, including neurological, muscular, mechanical, infectious, and inflammatory diseases. Each may result in dysphagia.[23]

Dysphagia can be predominately oropharyngeal or esophageal or a mixed process. As aforementioned, the incidence and prevalence of dysphagia increases with age. The pathogenesis of age-related oropharyngeal dysphagia includes dysfunction in salivary production, a loss of jaw strength, gingival and dentition problems, and age-related changes in the tongue muscles; each contributes to poor mixing of food with saliva and a delay in the oropharyngeal phase of swallowing. Age-related changes that can affect the esophageal phase of swallowing include the threshold for laryngeal elevation and a loss of upper esophageal sphincter elasticity and function.[24]

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, lip and tongue movements, and pharyngeal peristalsis. Brainstem lesions are less common but result in significant swallowing compromise due to dysfunction of the cranial nerves emerging from the brainstem. Mouth, tongue, and cheek sensations may be compromised. Alterations may occur in the timing of pharyngeal swallow, laryngeal elevation, glottic closure, and physiological regulation of oropharyngeal swallow.[25][26]

Patients with head and neck cancer treated with platinum-based chemotherapy and radiotherapy may develop severe dysphagia related to mucositis. The esophagus is colonized with Candida species in more than 70% of these patients. The breakdown of the mucosal barrier leads to the failure of protective physiological mechanisms provided via the mucosal epithelium and T-cells, leading to opportunistic candidiasis. Mucosal candidiasis causes oropharyngeal dysfunction and dysphagia.

Achalasia frequently results in progressive dysphagia. In addition, the incidence of achalasia increases with age. Several pathogenic mechanisms may contribute to the development of achalasia.

In achalasia, chronic immune-mediated ganglionitis results in the loss of the esophageal myenteric neurons normally responsible for coordinating the relaxation of the lower esophageal sphincter. The result is aperistalsis and impaired relaxation of the lower esophageal sphincter. Antibodies against myenteric neurons have been detected in the serum of patients with achalasia, particularly in patients positive for HLA DQA1*0103 and DQB1*0603 alleles.[27] Herpes simplex virus-1, measles, and the human papillomavirus may play a role in the pathogenesis of achalasia. The evidence shows that the herpes simplex virus triggers immune activation and subsequent esophageal enteric neuron loss in genetically susceptible individuals. Lastly, polymorphisms in the HLA class II molecules, vasoactive intestinal peptide receptor-1, KIT, and interleukin-10 play a role in the pathogenesis of achalasia.[28]

A relative sparing of somatic innervation of the proximal esophagus characterizes dysphagia in patients with systemic sclerosis. 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, and a discoordination of peristalsis and lower esophageal function.[29]

History and Physical

A thorough history and physical examination are critical in evaluating a patient with dysphagia. The history and physical examination will often point to the diagnosis.[30]

The medical history must include the nature of the dysphagia, the course of the problem, and whether to solids, liquids, or both. Difficulty swallowing solids predominately suggests obstruction or a mechanical problem such as esophageal webs or rings; this type of dysphagia may be intermittent. Alternatively, progressive dysphagia is more likely due to progressive stricture or malignancy. Dysphagia with liquids suggests a motility disorder such as achalasia or systemic sclerosis; if intermittent, then esophageal spasm.[30] Therefore, key topics to cover when gathering history include:

  • Onset
  • Duration and course of symptoms
  • Problems with the initiation of swallowing or after a few seconds of swallowing
  • Symptoms predominantly in the neck or chest
  • Occurrence with solids, liquids, or both
  • Self-imposed dietary changes regarding food consistency; preference for liquids or semisolids
  • Eating meals slowly
  • Throat clearance during or after meals
  • Associated coughing, choking, or postnasal regurgitation
  • History of recurrent chest infections
  • Functional decline
  • Neurological deficits 
  • Weight loss
  • Feelings of embarrassment
  • Social isolation, frustration, or depression 

Physical Signs

  • Loss of dentition or gingival disease
  • Abnormal lip closure
  • Local mucosal changes
  • Neurological changes

Difficulty initiating swallowing is more characteristic of oropharyngeal dysphagia; esophageal dysphagia usually occurs a few seconds after swallowing. Attempts should be made to distinguish between the 2 as they are often distinct pathologic processes.

Symptoms Predictive of Oropharyngeal Dysphagia [31][32][33]

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

Symptoms Predictive of Esophageal Dysphagia

  • Symptoms occur a few seconds after initiation of the swallow
  • Associated regurgitation of undigested food
  • Dysphagia felt more within the chest   

Although oropharyngeal dysphasia is commonly seen in the geriatric population, a history of smoking or alcohol use, with or without unintentional weight loss, should suggest the possibility of underlying malignancy.[32]

Regurgitation of undigested food, hoarseness of voice, halitosis, the feeling of fullness in the throat, and history of aspirations may suggest Zenker diverticulum, which is believed to be the result of weakness in the cricopharyngeal muscle.[33]


As discussed above, a thorough history and physical examination often point to a diagnosis and are critical steps that guide further evaluation and management of dysphagia. Attempts should be made to determine if the dysphagia is oropharyngeal, esophageal, or mixed.[34]

Oropharyngeal Dysphagia

In patients with clinical evidence of oropharyngeal dysphagia, the initial test may be a clinical swallow evaluation performed by a speech pathologist or bedside nurse. However, this test has limitations and may miss over 50% of patients with significant aspiration.[35] Early detection of oropharyngeal dysphagia using screening tools may play a role in reducing complications, particularly in the older population.[36] Multiple bedside evaluation screening tools are available. However, they lack predictive value for aspiration, are of limited consistency, and are not validated.[37][38]

After the initial bedside clinical swallow evaluation, two instrumental tests are often used to assess oropharyngeal dysphagia.[32] The videofluoroscopic swallow study (VFSS) allows direct visualization of bolus passage by evaluating swallow physiology, swallow efficiency, and aspiration risk through the two-dimensional view.[39] Even though this study has significant diagnostic value, there is a need to develop scientific tools to increase reliability and decrease interreader variability, which is a limitation of this study.[40] Fiberoptic endoscopic evaluation of swallowing (FEES) is performed by passing an endoscope through the nares to observe the nasopharynx, oropharynx, and larynx to allow direct visualization and detailed analysis of swallow structures and their function during intake of food with various consistencies.[41]

Which test is chosen is dictated by patient characteristics. To perform VFSS, patients must be able to sit upright and must be able to travel to the radiology department. In contrast, FEES can be done at the bedside.[32] A recent systematic review shows that FEES is more sensitive to detecting penetration, residues, and aspiration than VFSS.[42] However, either is the gold standard for assessing Parkinson disease-related dysphagia. In addition, high-resolution manometry may be a helpful tool to complement other diagnostic strategies to evaluate upper esophageal sphincter pathology, particularly in patients with globus sensation.[43][44]

Patients with signs of malignancy, such as weight loss or bleeding, in addition to oropharyngeal dysphagia, should undergo a head and neck evaluation and a laryngoscopic examination of the pharynx and larynx. Particular attention should be paid to the oropharynx and any potential evidence of a Zenker diverticulum. An esophagogram typically diagnoses Zenker diverticulum. In addition, computed tomography of the head and neck may be considered to rule out any suspected malignancy.

Esophageal Dysphagia

Patients with no supra-esophageal symptoms, unremarkable modified barium swallow or FEES, and clinical evidence of esophageal dysphagia should be referred to a gastroenterologist for a barium video-esophagogram. This assessment should cover the anatomy and motor function of the esophagus. Barium esophagogram is relatively simple and low-cost and may be considered the first line of investigation over endoscopy in esophageal dysphagia. Endoscopy is associated with risks such as aspiration, particularly in elderly patients.[45] A timed barium video-esophagogram is also helpful in the diagnosis of achalasia. It can help objectively document treatment outcomes and detect recurrence early.[46] Barium video-esophagogram should also be considered the initial test when carcinoma, esophageal rings or strictures, or severe reflux esophagitis is suspected; it has 90% to 95% sensitivity in these conditions.[47][48]

The choice of the initial test must be based on patient characteristics and shared decision-making. The combined barium esophagogram and endoscopy approach may be the best in specific scenarios.[49] Many gastroenterologists recommend endoscopy as an initial test since most patients who underwent an esophagogram require endoscopy eventually.[50] Endoscopic evaluation offers additional benefits of therapeutic interventions such as dilation and biopsies.

High-resolution esophageal manometry, which is preferred over conventional manometry, also plays a role in evaluating esophageal dysphagia. It is helpful in the diagnosis of achalasia, diffuse esophageal spasm, jackhammer esophagus, and esophagogastric junction outflow obstruction[47][51]

Treatment / Management

Treatment of dysphagia should be tailored towards the underlying etiology and individualized based on patient characteristics. The treatment goals for dysphagia are to reduce mortality and morbidity due to aspiration, pneumonia, malnutrition, dehydration, and psychological impairments. A multidisciplinary approach must involve primary care and specialty clinicians, nurses, speech therapists, dieticians, and caregivers using compensatory and rehabilitative strategies to promote quality of life and regain physiologic swallowing, respectively.[52] Comprehensive dysphagia management is essential, particularly in the geriatric population, patients with dementia, Alzheimer disease, stroke, and Parkinson disease.[53][54]

Clinicians should be aware of the psychological impacts of dysphagia on patients, including depression, anxiety, frustration, fear, vulnerability, and embarrassment. Educating patients and their caregivers about coping strategies and addressing their social needs is important.[55][56]

Swallowing techniques such as head tilt, chin-tuck, head rotation, and supraglottic maneuvers have shown some benefit in minimizing or preventing aspiration; however, there is contradictory evidence of their efficacy.[52][53] Swallowing rehabilitation, including strengthening exercises and skills-based training, can be done by speech therapists.[57]

Dietary modifications such as texture-modified food and thickened liquids may help patients with dysphagia. Due to the lack of data, the evidence supporting dietary modification is not strong, and the immediate and long-term effects of thickened liquids are uncertain.[58][59] Other dietary considerations that should be considered, particularly in patients with dementia or those who have had a stroke, include timing, frequency, bolus size, patient preferences, food additives, caregiver knowledge, and patient attentiveness. The lack of consistent terminology for different food textures among various countries poses a significant challenge for future studies to pool the evidence.[60]

Peripheral stimulation, such as thermal, tactile stimulation at the base of the tongue and soft palate or transcranial magnetic stimulation, is a simple, safe, and noninvasive strategy that may help dysphagia due to neurological causes. However, the utility of these therapies remains uncertain in geriatric patients.[52] In patients with dysphagia due to stroke, neuromuscular electrical stimulation and traditional swallowing therapies may have potential benefits.[61] However, if the patients have mild symptoms, dilatation of the upper esophageal sphincter may be indicated.[62] Most patients with stroke-induced dysphagia will regain their swallowing function within 1 to 2 weeks after infarction.

Cricopharyngeal myotomy or dilation can be considered in patients with cricopharyngeal dysphagia or Zencker diverticulum. This can often be done via the oral route. However, if the patients have mild symptoms, dilatation of the upper esophageal sphincter may be indicated.[62] 

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

Structural causes such as benign esophageal strictures can be treated in various ways. If the stricture is mild, control of underlying gastroesophageal reflux may be adequate, with or without endoscopic dilation. Refractory cases can be treated with steroid injection, incision, or stent placement. 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.[63] Dysphagia caused by an esophageal malignancy is usually managed by a team of surgeons, gastroenterologists, medical and radiation oncologists, and the rehabilitation team.[64]

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

Because the underlying pathophysiology of dysphagia due to diffuse esophageal spasm is unknown, treatment is directed at controlling patient symptoms.[65] 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 and a hypotensive lower esophageal sphincter. Usually, these patients have dysphagia with both solids and liquids. The treatment is focused on symptomatic management. No pharmacological intervention has been shown to be promising. Prokinetic agents that stimulate gut peristalsis, such as metoclopramide, erythromycin, bethanechol, buspirone, and domperidone, may help.[66] Non-pharmacological approaches, such as acupuncture stimulation or transcutaneous electrical nerve stimulation (TENS), may be indicated in the management of advanced cases.[67]


Based on high-resolution esophageal manometry results, 3 subtypes of achalasia can be identified; the subtype forms the basis of achalasia treatment.[68][69] 

Medical management can be attempted using nitrates or calcium channel blockers to decrease the resting pressure of the esophageal sphincter; side effects occur in one-third of patients and include hypotension, headache, and dizziness. Endoscopic injection of botulinum toxin A into the lower esophageal sphincter may be offered. While more than 80% of patients undergoing this intervention have a clinical response, recurrence of symptoms is common.[70] 

Procedural or surgical intervention for achalasia is the mainstay of therapy. Types I and II achalasia are best managed with pneumatic dilatation, laparoscopic Heller myotomy, or gastric peroral endoscopic myotomy (POEM). POEM is the preferred treatment for Type III achalasia. As with any procedure, there are risks and benefits with each approach.

Pneumatic dilatation uses air-filled balloons to dilate the lower esophageal sphincter 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 and those with comorbidities that prevent surgical intervention should an esophageal rupture occur.

Laparoscopic Heller myotomy of the distal esophageal muscle and lower esophageal sphincter significantly reduces reflux when combined with fundoplication.[71] The surgery is safe, with a reported mortality of 0.1%. The main complication is perforation of the esophagus or gastric mucosa.

POEM requires a highly skilled operator using a high-definition endoscope. The procedure takes approximately 2 to 3 hours, and patients must stay in the hospital for 2 to 3 days for monitoring and intravenous antibiotics.[68][72]

Differential Diagnosis

Dysphagia may be acute or chronic and can be oropharyngeal, esophageal, or mixed. There are many underlying etiologies of dysphagia.[73][74] These include but are not limited to:

  • Benign esophageal stricture
  • Cerebrovascular accident (stroke)
  • Diffuse esophageal spasm
  • Eosinophilic esophagitis
  • Esophageal malignancies
  • Esophageal webs and rings
  • Gastroesophageal reflux disease (GERD)
  • Hiatal hernia
  • Multiple sclerosis
  • Parkinson disease
  • Paterson-Kelly syndrome
  • Zenker diverticulum

A form of dysphagia that is unique to childhood is dysphagia lusoria. This form of dysphagia is due to compression of the esophagus by a vascular abnormality. The most common abnormalities are an aberrant right subclavian artery arising from the left side of the aortic or double aortic arch.


The prognosis of dysphagia depends upon the underlying etiology. For example, dysphagia in stroke patients normalizes gradually, from 3 weeks to approximately 6 months or longer. Dysphagia due to achalasia or mechanical obstruction may resolve with surgical intervention.


Dysphagia can significantly impair the quality of life of those affected. Patients with dysphagia may experience social isolation because of cough, embarrassment, and difficulties in swallowing. Dysphagia may increase the risk of chronic aspiration and pneumonia. Dehydration and malnutrition may occur. Rehabilitation after injury or illness may be reduced.[75]

Deterrence and Patient Education

Patients should be educated about the underlying etiology of their dysphagia, including any etiology-specific needs. However, patients or their caregivers are advised to feed in an upright posture with the neck flexed to help swallowing and reduce the risk of aspiration. Patients with xerostomia may benefit from artificial saliva or lubricants. Patients should be advised to refrain from talking while eating. High-caloric food should be taken. Speech therapists may teach a range of exercises to assist swallowing.

Pearls and Other Issues

Oropharyngeal dysphagia should be differentiated from esophageal dysphagia, and each should be considered a distinct category. While the medical history and physical examination are essential for making such a differentiation, investigations may help identify the underlying cause of the dysphagia.

Enhancing Healthcare Team Outcomes

Most 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, such schools' support teams 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 typically care for patients with esophageal malignancy.

(Click Image to Enlarge)
Barium swallow showing achalasia
Barium swallow showing achalasia
Image courtesy S Bhimji MD


Samy A. Azer


11/18/2023 11:04:34 AM



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