Dysphagia

Edward Hurtte, MDa, Jocelyn Young, DO, MS

b
,
C. Prakash Gyawali, MD, MRCPa,*

KEYWORDS
 Oropharyngeal dysphagia  Esophageal dysphagia
 Gastroesophageal reflux disease  Achalasia  Aspiration  Stroke

KEY POINTS
 There are two types of dysphagia, oropharyngeal and esophageal, which can be differen-
tiated with a careful history.
 Initial test of choice for evaluation of oropharyngeal dysphagia is a modified barium swal-
low, as neuromuscular etiologies are more common than structural etiologies.
 Esophageal dysphagia is predominantly caused by structural or mucosal mechanisms,
hence endoscopy with biopsy and potential for dilation is most cost effective as the initial
test.
 When no structural etiology is identified on endoscopy and/or barium radiography in
esophageal dysphagia, a high-resolution manometry study can identify motility disorders.
 Specific management of esophageal dysphagia may require referral to a
gastroenterologist.

INTRODUCTION

Dysphagia is the medical term used to describe difficulty swallowing. Dysphagia refers
to a subjective sensation of difficulty in the transit of food from mouth to stomach.1,2
Dysphagia includes difficulty initiating a swallow (termed oropharyngeal dysphagia) as
well as the sensation of food being stuck anywhere along the length of the tubular
esophagus (termed esophageal dysphagia). Oropharyngeal dysphagia can result
from abnormal neural or muscular function of the muscles involved with transfer of
food in the mouth, pharynx (back of the throat), and through the upper esophageal
sphincter (UES). Diseases that involve the tubular esophagus cause esophageal
dysphagia. There are very limited population studies available to determine the prev-
alence of dysphagia, but the overall prevalence can be estimated from that acquired
from a population cohort of over 7000 residents of Olmstead County, MN, where a

a
Division of Gastroenterology, Washington University School of Medicine, Campus Box 8124,
660 South Euclid Avenue, St Louis, MO 63110, USA; b United Health Services Hospitals, Johnson
City, NY, USA
* Corresponding author.
E-mail address: cprakash@[Link]

Prim Care Clin Office Pract 50 (2023) 325–338

[Link] [Link]
0095-4543/23/ª 2023 Elsevier Inc. All rights reserved.

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326 Hurtte et al

prevalence of 3% was reported, with a higher prevalence in individuals with heartburn

(6%) or regurgitation (11%).3 The incidence and prevalence of dysphagia increases
with age. Prevalence ranges from 5.5% to 8% in persons over the age of 50 years,
and is most common in hospitalized and nursing home patients.4,5 Dysphagia is
considered an alarm symptom warranting evaluation as ominous etiologies are
possible in addition to benign mechanisms; besides, dysphagia can impact adequate
nutrition and can contribute to weight loss.
When a patient presents with dysphagia, it is imperative for the physician to take a
careful history to differentiate which type of dysphagia is more likely, as investigation
and management differ between oropharyngeal and esophageal dysphagia. Dysphagia
needs to be distinguished from odynophagia, defined as pain during swallowing. Ody-
nophagia may arise from infection or inflammation in the throat or esophagus, and rarely
from obstructive processes. Dysphagia also needs to be distinguished from globus
sensation, defined as a constant sensation of tightness or foreign body sensation at
the back of the throat or neck.2 Globus typically does not impair swallowing and is
thought to result from increased perception or hypervigilance in the throat or upper
esophagus. In contrast, dysphagia only occurs when attempting to swallow or during
the process of swallowing. Globus is occasionally seen in reflux disease; additionally,
esophageal mucosal or motor disorders need to be excluded.6
Within each oropharyngeal and esophageal dysphagia, there are two broad groups
of etiologies, neuromuscular and structural. Neuromuscular causes dominate in
oropharyngeal dysphagia, while structural causes are far more common than neuro-
muscular dysfunction in esophageal dysphagia. The prevalence of each type of
dysfunction dictates the order of investigative studies, which is why the tests of choice
differ in oropharyngeal versus esophageal dysphagia.

OROPHARYNGEAL DYSPHAGIA

With a careful history and physical examination, the clinician can differentiate oropha-
ryngeal from esophageal dysphagia in 80% to 85% of cases.7 The prevalence of
oropharyngeal dysphagia increases with age due to its relationships to neurologic dis-
orders including cerebrovascular events, movement disorders like Parkinson’s dis-
ease, and dementia. As many as 70% of individuals are reported to have dysphagia
following a cerebrovascular event.8

Pathophysiology
The oral phase of swallowing involves breaking down ingested food with chewing, fol-
lowed by creation of a bolus between the tongue and the palate. The pharyngeal
phase requires the oropharyngeal musculature to propel the food bolus into the
esophagus through the UES, which opens as part of the pharyngeal phase from relax-
ation of the cricopharyngeus muscle. The pharyngeal phase also involves laryngeal
elevation, and closure of the laryngeal inlet by the epiglottis, to prevent aspiration.
The oral or pharyngeal phases of swallowing can be separately compromised in
oropharyngeal dysphagia; sometimes both phases can manifest dysfunction.9 As
complex nerve–muscle integration is essential for normal oral and pharyngeal phases
of swallowing, etiologies of oropharyngeal dysphagia are commonly neuromuscular
rather than structural.5,7

Clinical Presentation
Dysphagia is localized to the high neck or back of the throat in oropharyngeal
dysphagia. Symptoms are typically reported within 1 second of attempting to swallow.

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 Dysphagia 327

Patients may complain of coughing, nasal regurgitation, or a choking sensation when

attempting to swallow9 (Table 1). Frank aspiration can lead to lower respiratory tract
infection, pneumonia, or even a lung abscess, and these could manifest as primary
presenting features.7,10 When the lower cranial nerves are compromised, additional
symptoms could include a nasal tone of voice, hoarseness, and drooling of saliva.
When oropharyngeal dysphagia is suspected, physical examination should include
inspection of the mouth and oropharynx. In addition, a careful neurologic examination
should focus on the motor components of cranial nerves V, VII, IX, X, and XII as well as
the sensory components of cranial nerves V, VII, IX, and X, since neuromuscular etiol-
ogies are often the cause of oropharyngeal dysphagia (Table 2). Neurologic deficits in
the upper and lower extremities can also coexist and can provide an important clue to
the central localization of neurologic dysfunction in oropharyngeal dysphagia. Exam-
ination of the oropharynx includes assessing for adequate saliva.
Structural processes in the nasopharynx and proximal esophagus could include
benign webs and strictures. Abnormal cricopharyngeal relaxation can sometimes
result in a Zenker’s diverticulum in the posterior pharynx. Rarely, neoplasms of the
nasopharynx, larynx, or proximal esophagus can result in dysphagia localized to the
pharynx or high neck (see Table 2).
In addition to globus sensation, xerostomia from reduced saliva production can
contribute to the sensation of oropharyngeal dysphagia (Fig. 1). Salivary gland hypo-
function results in a sensation of difficulty swallowing because of loss of saliva, which
is a lubricant for food and a swallow stimulus. Some patients manifest food aversion,
which can originate from a fear of perception of dysphagia, especially in patients with
anxiety and hypervigilance. Finally, edentulous individuals may report dysphagia from
incomplete breakdown of food boluses.

Table 1
Differentiation of oropharyngeal from esophageal dysphagia

Oropharyngeal Dysphagia Esophageal Dysphagia

Timing Within 1 s of swallow initiation After swallow passes through
back of throat
Localization High neck or throat Retrosternal area or sternal
notch
Associated symptoms Coughing, aspiration Heartburn
Nasal regurgitation Chest pain
Drooling Bland regurgitation of food
Hoarseness
Nasal tone of voice
Common disorders Stroke GERD
Parkinson’s disease Benign strictures
Muscular dystrophy Eosinophilic esophagitis
Brain stem disorders
Confounding Xerostomia Odynophagia
symptoms/diagnoses Globus Rumination
Food aversion Globus
Food aversion
Test of choice Videofluoroscopy Upper endoscopy
Modified barium swallow
Secondary tests Fiberoptic laryngoscopy Barium swallow
CT scan of head and neck High-resolution manometry
Blood tests for myositis,
myasthenia

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328 Hurtte et al

Table 2
Etiology of oropharyngeal dysphagia

Neuromuscular Cerebrovascular accident

Parkinson’s disease
Amyotrophic lateral sclerosis
Poliomyelitis
Brain stem disorders
Brain tumors
Polymyositis, dermatomyositis
Muscular dystrophy
Myasthenia gravis
Abnormal upper esophageal sphincter
Structural Inflammation: pharyngitis
Radiation-related strictures
Zenker’s diverticulum
Benign webs and strictures
Cervical hyperostosis
Oral, pharyngeal, and laryngeal cancer
Thyromegaly

Diagnostic Testing
When oropharyngeal dysphagia is suspected, the initial test of choice is video fluoro-
scopic contrast radiography, also termed modified barium swallow (MBS), which can
be ordered by the primary care physician (see Fig. 1). MBS provides lateral and ante-
roposterior views of the oral and pharyngeal phases of swallowing, using boluses of
varying consistency (thin liquid, thick liquid, semisolid, solid). In addition to identifying
neuromuscular dysfunction, MBS determines oropharyngeal clearance of food, and
elucidates structural abnormalities when present, including a Zenker’s diverticulum.
During the procedure, a speech pathologist instructs the patient on neck position
and maneuvers that are most likely to result adequate oropharyngeal clearance into
the esophagus without aspiration. Thus, MBS is utilized in identifying the location
and severity of oropharyngeal neuromuscular dysfunction, and determining the

Fig. 1. Algorithm for evaluation of oropharyngeal dysphagia.

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 Dysphagia 329

influence of bolus consistency and posture on bolus clearance or aspiration risk (Fig.
2). Specific swallow therapies can be recommended based on MBS findings,
including bypassing the oropharynx completely using enteral feeding when aspiration
risk is high.
MBS can be complemented by high-resolution manometry (HRM) combined with sta-
tionary impedance, which can assess pharyngeal, upper sphincter, and proximal
esophageal function in addition to distal esophageal motor physiology and pathophys-
iology11; however, this remains a research tool in most esophageal centers. Trans nasal
fiberoptic laryngoscopy or fiberoptic endoscopic examination of swallowing can deter-
mine presence of pharyngeal pooling during test swallows, as well as structural pro-
cesses in the nasopharynx, oropharynx, and larynx. Upper endoscopy visualizes the
oropharyngeal and esophageal mucosa and can identify additional mucosal and struc-
tural processes including webs, strictures, and diverticula including Zenker’s divertic-
ulum. Cross-sectional imaging (CT or MRI scans) can evaluate soft tissues in the
head and neck; these tests are also utilized for evaluation of space occupying lesions
or other abnormalities in the brain, brain stem, cervical spinal cord, and cranial nerves.
Skeletal muscle dysfunction can contribute to oropharyngeal dysphagia in rare in-
stances. These disorders include autoimmune myositides (polymyalgia rheumatica,
polymyositis, dermatomyositis, and other idiopathic myositides), muscular dystrophy,
and myasthenia gravis. In addition to inflammatory markers (erythrocyte sedimenta-
tion rate [ESR], C reactive protein [CRP]), muscle enzymes can be elevated (creatine
kinase, aldolase). Specific autoimmune markers are available for some of these disor-
ders of skeletal muscle.

Management
Management of oropharyngeal dysphagia necessitates a multidisciplinary team
approach that includes the primary care physician, speech pathologist, nutritionist,
gastroenterologist, neurologist, and sometimes rheumatologist. When specific abnor-
malities are found, these are targeted. Examples of specific management include
 Endoscopic dilation for webs and strictures
 Diverticulectomy for Zenker’s diverticulum, and
 Anti-inflammatory agents or steroids for myositides.
However, most of the central and peripheral neurologic causes may not be
amenable to specific treatment, and management of individual symptoms, food
transit, and nutrition will be of key importance in these instances.

Fig. 2. Images from videofluoroscopy performed for oropharyngeal dysphagia. (A). Pharyn-
geal residue due to a poorly relaxing cricopharyngeus muscle. (B). A small Zenker’s divertic-
ulum with retained contrast in the posterior pharynx. (C). Aspiration of barium resulting in
bronchial opacification.

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330 Hurtte et al

The goals of management include minimizing the risk of aspiration and maintaining
adequate nutrition. When aspiration risk is not deemed to be high, neck positioning
and altering food consistency can be of value in achieving management goals (see
Fig. 1). Speech pathologists can assist with specific food consistency recommenda-
tions, optimal positioning, and strengthening exercises. If maintaining adequate nutri-
tion becomes challenging, or if aspiration risk is high, enteral feeding on a temporary or
permanent basis may be necessary.

ESOPHAGEAL DYSPHAGIA

Esophageal dysphagia refers to dysphagia arising from disruption of bolus transit

within the tubular esophagus after the bolus has traversed the UES. Structural causes
are far more frequent than disorders involving nerves or muscles (Table 3). Therefore,
luminal narrowing of the esophagus (strictures), mucosal inflammation from reflux dis-
ease or other inflammatory disorders, tumors within the esophagus, and compression
of the lumen from intramural or extrinsic causes, and rarely, neoplasms of the esoph-
agus can contribute to esophageal dysphagia. Benign strictures are often encoun-
tered, most often related to gastroesophageal reflux. Idiopathic benign strictures
such as the Schatzki ring at the squamocolumnar junction can cause intermittent solid
food dysphagia. Mucosal infiltration of eosinophils (eosinophilic esophagitis) can
result in compromise to the esophageal lumen from mucosal inflammation, wall stiff-
ness, and fibrosis. Eosinophilic esophagitis is thought to be triggered by dietary and/or
environmental allergens in predisposed individuals. Pill induced inflammation can also
result in strictures with the most common culprits being
 Nonsteroidal anti-inflammatory agents
 Doxycycline
 Alendronate
 Quinine, and
 Potassium supplements
Pill esophagitis can also be a consequence of other types of strictures, or motor
obstruction.

Table 3
Etiology of esophageal dysphagia

Structural Benign webs and strictures

Gastroesophageal reflux disease
Eosinophilic esophagitis
Esophageal cancer
Past esophageal surgery (fundoplication)
Paraesophageal hernia
Lichen planus
Extrinsic compression
Caustic injury
Radiation-induced strictures
Vascular compression (dysphagia lusoria)
Neuromuscular Achalasia spectrum disorders
Distal esophageal spasm
Hypercontractile esophagus (Jackhammer)
Chagas disease
Scleroderma, mixed connective tissue disease

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 Dysphagia 331

Less common are disorders involving esophageal neuromuscular function. The most
consequential of these disorders is achalasia, where the lower esophageal sphincter
(LES) fails to relax during swallowing, from abnormal esophageal inhibitory nerve func-
tion. This is typically associated with absent or abnormal peristalsis in the esophageal
body proximal to the esophagus. Less frequently, the esophageal smooth muscle dem-
onstrates exaggerated or premature contraction, loosely termed esophageal spastic
disorders. Advanced motor disorders like achalasia are irreversible, and treatment typi-
cally involves disruption or surgical incision of the LES to relieve the obstruction. Some
forms of esophageal motor obstruction can be a consequence of opioid use, and the
resulting motor pattern can mimic some forms of achalasia. Other motor disorders man-
ifest weakness of both esophageal body smooth muscle as well as the LES. In extreme
situations, the muscle generates no force and is unable to generate peristalsis. Although
dysphagia may be a symptom with these hypomotility disorders, there is no true
obstruction, and the esophagus can clear its contents with the help of gravity as long
as the patient eats while upright. Reflux is a more important consequence, and postural
measures are typically recommended to avoid reflux-induced complications.

Clinical Presentation
With esophageal dysphagia, food may be swallowed normally, but may get stuck in
the neck or chest. Localization of esophageal dysphagia can vary depending on the
site of the abnormality causing dysphagia. Even though the abnormality may be at
the bottom end of the esophagus, the sensation of food being stuck may be felt higher
up in the chest or even in the neck region (see Table 1). However, it is important to note
that esophageal dysphagia never localizes lower than the site of obstruction. Some-
times, swallowed food may be regurgitated back into the mouth when it may taste
like the food just eaten. This should be differentiated from reflux of gastric content,
which is often sour and bitter.
With structural disorders, dysphagia is initially reported with solids and not with liq-
uids. With tight obstructions, difficulty with liquids can develop, but difficulty is typically
worse with solids, especially dry solids and pills. Symptoms of reflux disease such as
heartburn may coexist, since reflux is the most common cause of esophageal strictures
causing dysphagia. Rarely, a food bolus may block the lumen of the esophagus, termed
food impaction. This is seen with tight strictures, and especially with eosinophilic esoph-
agitis. Food impaction can manifest as a total inability to swallow, including liquids, and
requires urgent endoscopy for dis-impaction of the food bolus. In contrast,

Fig. 3. Test results in a patient with achalasia. (A). Barium swallow demonstrating a dilated
esophagus with a tapered distal esophagus indicating a closed LES. (B). Endoscopic image
showing a tight and puckered LES. (C). HRM Clouse plot showing no esophageal body peri-
stalsis, and no relaxation of the LES with swallows. (D). Two images from a FLIP study
showing a tight, non-relaxing LES.

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332 Hurtte et al

neuromuscular dysfunction such as achalasia and motor disorders result in dysphagia

to both solids and liquids. These symptoms slowly develop over time in achalasia,
where relaxation of the LES during swallowing is incomplete (Fig. 3). Therefore, the con-
dition may be difficult to diagnose at the outset, but symptoms can become severe
enough to result in weight loss. Sometimes, achalasia-like disorders develop from can-
cers at the esophagogastric junction, termed pseudo-achalasia, where symptoms
similar to achalasia develop over a short period of time, and with profound weight
loss. Neuromuscular disorders of the esophagus, particularly spastic disorders and
some forms of achalasia, may also be associated with atypical chest pain; in these in-
stances, it is important to rule out a cardiac cause of chest pain before attributing this
symptom to the esophagus.

Diagnosis
A careful history can differentiate esophageal dysphagia from oropharyngeal
dysphagia. The patient typically reports food being stuck somewhere between the
neck and the epigastrium, for varying periods of time before the food passes (see
Table 1). There may be a regurgitation of the ingested food, and the patient may
sometimes induce regurgitation for relief. Some patients develop pain or discomfort
when the food is stuck and may report pain during eating as their primary symptom.
As strictures and other structural or mucosal processes are the most frequent
mechanisms of esophageal dysphagia, evaluation requires consideration of gastro-
esophageal reflux disease (GERD) in the etiology.11 Dysphagia is an alarm symptom,
especially in patients with GERD symptoms, and indicates a need for invasive evalu-
ation for strictures, esophagitis, and other complications of GERD, all of which can
cause dysphagia.12,13 Eosinophilic esophagitis (EoE) is an important differential diag-
nosis for a structural cause of esophageal dysphagia.14 Consequently, upper endos-
copy is a common investigative procedure performed in the setting of alarm
symptoms (Fig. 4).
Endoscopy has several advantages over barium radiography in the evaluation of
esophageal dysphagia. Endoscopy not only identifies reflux-induced (peptic)

Fig. 4. Algorithm for evaluation of esophageal [Link] eosinophilic esophagitis is

diagnosed.

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 Dysphagia 333

strictures that cause dysphagia, but can also provide management using balloon or
bougie dilators during the same procedure.12 Peptic strictures are seen more often
in older patients, patients with long-standing untreated reflux symptoms, and those
with a hiatus hernia, although the incidence is decreasing with the widespread use
of proton pump inhibitors (PPIs).15 Endoscopy also provides the characterization of
esophageal mucosal injury (Fig. 5), seen as longitudinal or circumferential erosions
in the distal esophageal mucosa, which can result in dysphagia even without the pres-
ence of strictures or other processes.16 The Los Angeles (LA) Classification descrip-
tively characterizes reflux esophagitis into four grades from A through D. Using the
LA grading system, patients with LA Grades C or D esophagitis are more likely to pre-
sent with dysphagia (43%), compared to LA Grades A or B (43% vs 36%, P <.001).16
About 10% to 15% of patients with chronic GERD can develop Barrett’s esophagus,
where metaplastic columnar mucosa replaces the normal squamous esophageal mu-
cosa in the distal esophagus. Barrett’s esophagus is a risk factor for esophageal
adenocarcinoma, which can cause luminal compromise and dysphagia. Therefore,
there is a role for endoscopic screening of patients with long-standing GERD, as iden-
tification and ablation of dysplasia within Barrett’s esophagus can reduce the inci-
dence of esophageal adenocarcinoma. In this context, Caucasian men
aged >50 years, with obesity, smoking, and a family history of esophageal cancer
carry the highest risk for Barrett’s esophagus and esophageal adenocarcinoma.17,18
Endoscopy also serves to diagnose esophageal cancer when present and is part of
the staging of cancer (using endoscopic ultrasound), and the palliation of cancer (us-
ing stents).
An important condition associated with dysphagia and food bolus impaction is
eosinophilic esophagitis (EoE),19 symptoms of which can overlap with GERD. Diag-
nosis of EoE is contingent on the finding of eosinophilia (>15 eosinophils per high po-
wer field) on esophageal biopsies, which makes endoscopy the test of choice in the
evaluation of esophageal dysphagia as biopsies can be taken (see Fig. 5).
Barium radiography is very sensitive for the identification of subtle strictures and
rings in the esophagus, particularly when a standard barium swallow is combined
with a 13 mm barium pill swallow, or a marshmallow or cookie impregnated with
barium.20 Barium studies can also accurately define hiatus hernias, particularly para-
oesophageal hernias, as these can contribute to dysphagia. A timed upright barium
study, where x-rays are taken in the upright position 1 minute and 5 minutes following
administration of 8 oz of semiliquid barium, can demonstrate if esophageal emptying is
compromised from obstruction at the esophagogastric junction. Barium studies,
therefore, complement endoscopy and alternate evaluation methods such as

A B C

Fig. 5. Endoscopic images of findings in patients with esophageal dysphagia. (A). Peptic
stricture in the distal esophagus, with esophagitis. (B). Corrugated, ringed esophagus in
eosinophilic esophagitis. (C). Growth protruding into the lumen in esophageal cancer.

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334 Hurtte et al

manometry and functional lumen imaging probe (FLIP) in the evaluation of esophageal
dysphagia.
When no structural etiology is found in the evaluation of esophageal dysphagia, or if
endoscopy and/or barium findings lead to suspicion of a motility disorder, an esoph-
ageal manometry can be performed.20 HRM is the current standard, where a catheter
with multiple circumferential high sensitivity sensors is introduced through an anesthe-
tized nostril into the esophagus and positioned with a few sensors located in the stom-
ach. Topographic images of esophageal peristalsis and sphincter function can be
displayed and interrogated with software tools. HRM is the gold standard for the diag-
nosis of motility disorders, particularly achalasia, using the Chicago Classification
v4.0, a hierarchical algorithm that defines criteria for diagnosis.21 The combination
of impedance with HRM, termed high-resolution impedance manometry can allow
the bolus to be visualized, and can demonstrate abnormal bolus transit if present.
The newest esophageal investigative procedure is FLIP.22 This incorporates imped-
ance methodology, with pairs of electrodes on a catheter encased in a compliant
balloon. The catheter is placed through the mouth after sedated upper endoscopy
and positioned with the balloon straddling the esophagogastric junction. With volu-
metric distension of the balloon using an electrolyte-containing fluid, cross-sectional
area, and lumen diameter can be measured throughout the esophagus and across
the esophagogastric junction. The relationship between cross-sectional area and dis-
tending pressure (measured using a sensor incorporated into the catheter) is depicted
as the distensibility index (DI).22 Low DI (combined with low opening diameter) is seen
with abnormal LES relaxation associated with achalasia spectrum disorders. Normal
DI with low diameter defines a structural process such as a stricture, while both DI
and diameter are within normal range if there is no obstructive element. Topographic
plots of diameter against time across the evaluated segment of the esophagus can
demonstrate esophageal secondary peristalsis, which can provide clues to esopha-
geal body motor function.
Thus, endoscopy, barium radiography, HRM, and FLIP provide complementary in-
formation in the evaluation of dysphagia.
If no structural or motor abnormalities are identified on esophageal testing, the sensa-
tion of dysphagia could be perceptive from increased visceral sensation, and functional
dysphagia can be diagnosed.2 Psychiatric co-morbidities such as anxiety, depression,
and somatoform disorders are common among patients with functional gastrointestinal
disorders. Dysphagia is the least common functional esophageal disorder, accounting
for only 2.4% of adults presenting with dysphagia in a large tertiary care center,23 and
requires exclusion of esophageal mucosal processes including eosinophilic esophagi-
tis, gastroesophageal reflux disease, and major motor disorders.2

Treatment
For the most part, treatment of dysphagia depends on the cause. Some general mea-
sures that are often recommended include changing the consistency of food, as soft
food items or liquids may traverse a narrowed esophageal lumen better than hard, dry
solids. Patients are advised to eat in the upright position and push solids down with
sips of fluid when necessary. Standing up and/or raising arms above the head can
straighten the esophagus and may allow intrathoracic pressure with breathing to
compress the esophagus and empty contents into the stomach. When nutrition is
compromised, the esophagus may need to be bypassed in favor of enteral feeding
into the stomach or small intestine through feeding tubes.
As strictures are often encountered as a mechanism for esophageal dysphagia,
endoscopic therapy can be provided at the index endoscopy, using either through-

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 Dysphagia 335

the-scope balloon dilators, or bougies passed either over a guide wire placed during
endoscopy (Savary-Guillard dilators) or passed blind (Maloney dilators).24 When long,
narrow strictures are encountered, fluoroscopy can provide a road map for placement
of a guide wire, especially when the stricture is not traversed with the endoscope.
Rarely, stents are placed for the management of refractory strictures, but
these need to be anchored in place when used for benign strictures. Perforation rates
are higher with malignant obstruction, and are rare with benign processes like
strictures.25
Acid suppression using a PPI is typically part of the management, as most strictures
are related to reflux disease.26 Strictures and luminal narrowing can also be seen with
EoE, where management starts with either PPI or topical steroid, sometimes comple-
mented with the elimination of some or all the most common food items associated
with EoE (milk, gluten, tree nuts, seafood, eggs, soy).27,28 Recently, dupilumab has
been approved by the Food and Drug Administration (FDA) for the management of
EoE at a dose of 300 mg weekly administered subcutaneously.29 Treatment of inflam-
mation first using these measures makes endoscopic dilation much more effective in
EoE. When endoscopic dilation is required, chest pain is the most frequent adverse
effect requiring analgesics, and perforation is rare.
Among other benign etiologies, pill esophagitis is treated with discontinuation of the
offending medication, and infectious esophagitis is treated with specific agents
directed at the infectious agent.
Motility disorders with abnormal LES relaxation such as achalasia require disruption
or surgical incision of the LES for durable symptom relief. This can be achieved
through forceful pneumatic or hydraulic dilation, myotomy of the LES through the
abdominal route (laparoscopic Heller myotomy), or myotomy through the esophageal
route (per oral endoscopic myotomy or POEM).30 Reflux can be a consequence and
may require management with PPI. Temporary benefit can be achieved with the injec-
tion of botulinum toxin into the LES during endoscopy, and this can be used as a
bridge to durable management, or as the primary management option when the pa-
tient is a poor candidate for invasive management. Rarely, esophagectomy is per-
formed for a massively dilated esophagus. Feeding past the esophagus using a
gastrostomy tube is an alternative.
Malignant obstruction of the esophagus requires targeted management that can
include neoadjuvant chemoradiation and/or surgical resection with a gastric pull-up.
Palliation of inoperative tumors may include placement of a stent to keep the esoph-
ageal lumen open.

When to Refer
The initial evaluation of oropharyngeal dysphagia can be initiated by the primary care
provider, who may order MBS, and have the patient follow instructions provided by the
speech pathologist who participates in the MBS. Consultation with a neurologist may
be useful when neuromuscular etiologies are considered. Consultation with an ear-
nose-throat specialist can help rule out structural processes in the pharynx and larynx.
A gastroenterologist can help with the placement of a gastrostomy tube for enteral
feeding in instances where aspiration risk is high, or when nutrition is compromised.
Endoscopic empiric large-caliber bougie dilation is sometimes performed for
dysphagia localized to the high neck where evaluation is negative.
Esophageal dysphagia typically requires referral to a gastroenterologist, especially if
symptoms persist despite trials of acid suppression with a PPI, because endoscopy is
an alarm symptom needing invasive investigation. Endoscopy, with the potential for
biopsy and endoscopic dilation, becomes more cost effective than a barium

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336 Hurtte et al

radiograph, as an abnormal finding on barium studies will require an endoscopy for bi-
opsy and management.

SUMMARY

A thorough history is a vital starting point in the evaluation of dysphagia, as the history
can differentiate oropharyngeal from esophageal dysphagia. Mechanisms and etiol-
ogies vary widely between oropharyngeal and esophageal dysphagia. As neuromus-
cular causes dominate, evaluation of oropharyngeal dysphagia starts with MBS. In
contrast, as structural mechanisms are found more often than neuromuscular
dysfunction in esophageal dysphagia, an upper endoscopy offers both diagnosis
and therapeutic intervention, as dilation can be performed at index endoscopy.
Once the etiology is determined, specific management can be offered targeting the
cause of dysphagia, if this is available.

CLINICS CARE POINTS

 When evaluating a patient with dysphagia, take a careful history to differentiate

oropharyngeal dysphagia from esophageal dysphagia
 When investigating oropharyngeal dysphagia, request an MBS to optimize swallow
technique and food consistency, and to evaluate for aspiration
 When treating oropharyngeal dysphagia with significant aspiration or weight loss, consider
enteral feeding through a gastrostomy tube
 When a patient has esophageal dysphagia, refer for upper endoscopy before empiric acid
suppression for diagnosis of the mechanism of dysphagia, and potential therapy
 When a patient presents with a history of food impaction, consider eosinophilic esophagitis
as a diagnostic possibility
 When a patient with intermittent solid food dysphagia has normal upper endoscopy with
biopsies, consider a barium swallow including a barium pill swallow to identify subtle
strictures or other mechanical processes
 When esophageal dysphagia is not explained by endoscopy and/or barium radiography,
request an esophageal HRM to identify or rule out achalasia spectrum disorders

DISCLOSURES

No conflicts of interest exist. No funding was obtained. E. Hurtte: no disclosures; J.

Young: no disclosures; C.P. Gyawali: Medtronic, Ardelyx, Dexcel Pharma.

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