Dysphagia: Evaluation and Collaborative Management

January 15, 2021

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Volume 103, Number 2 www.aafp.org/afp American Family Physician 97

Many people occasionally experience dicult or impaired

swallowing, but they oen adapt their eating patterns to

their symptoms and do not seek medical attention.

Among

those who do seek care, the most common causes are gener-

ally benign and self-limited, and serious or life-threatening

conditions are rare. However, many older adults with pro-

gressive neurologic disease have signicant but unrecog-

nized dysphagia, which increases their risk of aspiration

pneumonia and malnourishment. In these patients, the

diagnosis of dysphagia should prompt a discussion about

goals of care. Understanding the basic pathophysiology of

swallowing and the etiologies and clinical presentations of

dysphagia allows family physicians to distinguish between

oropharyngeal and esophageal pathology, make informed

management decisions, and collaborate appropriately

with specialists.

Pathophysiology

Swallowing (deglutition) is a complex process involving

voluntary and involuntary neuromuscular contractions

coordinated to permit breathing and swallowing through

the same anatomic pathway (Figure 1).

Deglutition is com-

monly divided into oropharyngeal and esophageal stages.

In the oropharyngeal stage, food is chewed and mixed with

saliva to form a bolus of appropriate consistency in the

mouth. With the initiation of the swallow, the bolus is pro-

pelled into the oropharynx by the tongue. Other structures

simultaneously seal the nasopharynx and larynx to pre-

vent regurgitation or aspiration, and the lower esophageal

sphincter begins to relax. In the esophageal stage, the food

bolus passes the upper esophageal sphincter and enters

the esophageal body, where it is propelled by peristalsis

through the midthoracic and distal esophagus and into the

stomach through the now fully relaxed lower esophageal

sphincter.

3,4

Oropharyngeal Pathology

Oropharyngeal dysphagia is most commonly related to

chronic neurologic conditions, particularly Parkinson dis-

ease, stroke, and dementia; it is not part of normal aging.

Dysphagia: Evaluation and

Collaborative Management

John M. Wilkinson, MD; Don Chamil Codipilly, MD; and Robert P. Wilfahrt, MD

Mayo Clinic College of Medicine and Science, Rochester, Minnesota

CME

This clinical content conforms to AAFP criteria for

CME. See CME Quiz on page 79.

Author disclosure: No relevant ﬁnancial aliations.

Patient information: A handout on this topic is available at

https:// family doctor.org/condition/dysphagia.

Dysphagia is common but may be underreported. Speciﬁc symptoms, rather than their perceived location, should guide the

initial evaluation and imaging. Obstructive symptoms that seem to originate in the throat or neck may actually be caused

by distal esophageal lesions. Oropharyngeal dysphagia manifests as diculty initiating swallowing, coughing, choking, or

aspiration, and it is most commonly caused by chronic neurologic conditions such as stroke, Parkinson disease, or demen-

tia. Symptoms should be thoroughly evaluated because of the risk of aspiration. Patients with esophageal dysphagia may

report a sensation of food getting stuck after swallowing. This condition is most commonly caused by gastroesophageal

reﬂux disease and functional esophageal disorders. Eosinophilic esophagitis is triggered by food allergens and is increasingly

prevalent; esophageal biopsies should be performed to make the diagnosis. Esophageal motility disorders such as achalasia

are relatively rare and may be overdiagnosed. Opioid-induced esophageal dysfunction is becoming more common. Esoph-

agogastroduodenoscopy is recommended for the initial evaluation of esophageal dysphagia, with barium esophagography

as an adjunct. Esophageal cancer and other serious conditions have a low prevalence, and testing in low-risk patients may be

deferred while a four-week trial of acid-suppressing therapy is undertaken. Many frail older adults with progressive neuro-

logic disease have signiﬁcant but unrecognized dysphagia, which signiﬁcantly increases their risk of aspiration pneumonia

and malnourishment. In these patients, the diagnosis of dysphagia should prompt a discussion about goals of care before

potentially harmful interventions are considered. Speech-language pathologists and other specialists, in collaboration with

family physicians, can provide structured assessments and make appropriate recommendations for safe swallowing, palliative

mercial use of one individual user of the website. All other rights reserved. Contact copyrights@aafp.org for copyright questions and/or permission requests.

98 American Family Physician www.aafp.org/afp Volume 103, Number 2

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January 15, 2021

DYSPHAGIA

It may be the rst symptom of a neuromuscular disorder,

such as amyotrophic lateral sclerosis or myasthenia gravis.

6,7

Some chronic conditions, such as poor dentition, den-

tures, dry mouth (xerostomia), or medication adverse

eects, may be poorly tolerated in patients who also have

progressive oropharyngeal dysfunction. Tardive dyski-

nesia with choreiform tongue movements related to long-

term antipsychotic use may cause decompensation in older

adults; it also may cause dysphagia in younger patients.

Chronic cough related to angiotensin-converting enzyme

inhibitor use may interfere with swallowing or be

mistaken for aspiration.

Structural abnormalities (e.g., Zenker divertic-

ulum, cricopharyngeal bars or tumors, chronic

infections with Candida or herpes virus) and

extrinsic compression from cervical osteophytes

or goiter can also interfere with normal swallow-

ing (Table 1).

5-14

Esophageal Pathology

Gastroesophageal reux disease (GERD), func-

tional esophageal disorders, and eosinophilic

esophagitis are the most common causes of

esophageal dysphagia

5,15

(Table 2

1,5,13-15

). Less

common causes include medications, obstructive

lesions, and esophageal motility disorders.

GASTROESOPHAGEAL REFLUX DISEASE

GERD and recurrent acid exposure result in

changes ranging from submucosal inammation

BEST PRACTICES IN GERIATRICS

Recommendations from the Choosing Wisely

Campaign

Recommendation Sponsoring organization

Do not order “formal” swallow

evaluation in stroke patients unless

they fail their initial swallow screen.

American Academy of Nursing

Do not recommend percutane-

ous feeding tubes in patients with

advanced dementia; instead, oer

careful hand feeding.

American Academy of Hospice and

Palliative Medicine

American Geriatrics Society

AMDA – The Society for Post-Acute

and Long-Term Care Medicine

Source: For more information on the Choosing Wisely Campaign, see https://

www.choosingwisely.org. For supporting citations and to search Choosing

Wisely recommendations relevant to primary care, see https:// www.aafp.org/

afp/recommendations/search.htm.

CB D

FIGURE 1

Anatomy and physiology of deglutition. (A) Food (shown in green) is ﬁrst chewed, mixed with saliva to form a bolus

of appropriate consistency, and compressed against the hard palate by the tongue in preparation for swallowing.

(B) The food bolus is propelled into the oropharynx, where the involuntary swallowing reﬂex is triggered. This swal-

lowing reﬂex lasts approximately one second. (C) The epiglottis moves downward to cover the airway while striated

pharyngeal muscles contract to continue moving the food bolus past the cricopharyngeus muscle (the physiologic

upper esophageal sphincter) and into the proximal esophagus. This portion of the swallowing reﬂex also lasts approx-

imately one second. (D) As the food bolus is propelled from the pharynx into the esophagus, involuntary contractions

of the skeletal muscles of the upper esophagus force the bolus through the midthoracic and distal esophagus. The

medulla controls this involuntary swallowing reﬂex, although voluntary swallowing may be initiated by the cerebral

cortex. The lower esophageal sphincter relaxes from the initiation of the swallow until the food bolus is propelled

into the stomach, which may take eight to 20 seconds.

Illustrations by Miriam Kirkman-Oh

Reprinted with permission from Palmer JB, Drennan JC, Baba M. Evaluation and treatment of swallowing impairments. Am Fam Physician. 2000;

61(8): 2455-2456.

January 15, 2021

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DYSPHAGIA

TABLE 1

Causes of Oropharyngeal Dysphagia

Progressive chronic disease (geriatric

syndrome)

Stroke

Parkinson disease

Alzheimer and other dementias

Sarcopenia

Neuromuscular disease

Amyotrophic lateral sclerosis

Myasthenia gravis

Multiple sclerosis

Dermatomyositis/polymyositis (myopathies)

Antipsychotic medications*

Note: Causes are listed in order of prevalence. The relative prevalence of oropharyngeal dysphagia varies depending on the population studied;

new-onset symptoms have a relatively low prevalence among primary care outpatients, whereas chronic progressive symptoms are increasingly

prevalent among frail older patients. Some patients may have more than one cause.

*—Extrapyramidal eects from the use of antipsychotic medications (e.g., tardive dyskinesia with choreiform tongue movements) may cause dys-

phagia in younger patients and cause or aggravate other oral conditions in older patients.

Information from references 5-14.

Structural causes

Head and neck cancers

Recent surgery or radiation for head

and neck cancers (altered anatomy)

Chemoradiation-induced mucositis

and edema (short term)

Zenker diverticulum

Cervical osteophytes

Lymphadenopathy

Goiter

Cricopharyngeal bar

Oral causes

Poor dentition or dentures

Dry mouth (i.e., xerostomia)

Medications causing dry mouth (e.g., alpha

and beta blockers, angiotensin-converting

enzyme inhibitors, anticholinergics, anti-

histamines, anxiolytics, calcium channel

blockers, diuretics, muscle relaxants,

tricyclic antidepressants)

Antipsychotic medications*

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendation

Evidence

rating Comments

Patients younger than 50 years who have esophageal

dysphagia and no other worrisome symptoms should

undergo a four-week trial of acid suppression therapy

before endoscopy is performed.

9,26,27

B CAG and ACG guidelines; systematic review of seven retro-

spective cohort studies showing a positive predictive value

of less than 1% for malignancy

Patients with apparent oropharyngeal symptoms but a

negative evaluation should be referred for EGD to rule

out esophageal pathology.

C Retrospective review of 3,668 consecutive patients; distal

esophageal pathology was incorrectly perceived as arising

from the neck or throat in 15% to 30% of cases

EGD is recommended for the initial assessment of

patients with esophageal dysphagia; barium esophagog-

raphy is recommended as an adjunct if EGD ﬁndings are

negative.

9,29,30

C CAG, STS, and WGO guidelines; expert consensus based on

limited evidence and cost-analysis; EGD has greater sensitiv-

ity and speciﬁcity than barium esophagography, with greater

cost-eectiveness

For accurate diagnosis of eosinophilic esophagitis, biop-

sies from normal-appearing mucosa in the midthoracic

and distal esophagus should be requested for all patients

with unexplained solid food dysphagia.

15,17

B Expert consensus recommendation based on CAG, ACG,

and AGA guidelines; early-stage eosinophilic esophagitis

may not exhibit mucosal changes on endoscopy

Older patients with chronic illness or recent pneumonia

should be screened for dysphagia; if it is present, the

physician and patient should discuss goals of care.

22,43

C Expert consensus on dysphagia as a geriatric syndrome

ACG = American College of Gastroenterology; AGA = American Gastroenterological Association; CAG = Canadian Association of Gastroenterol-

ogy; EGD = esophagogastroduodenoscopy; STS = Society of Thoracic Surgeons; WGO = World Gastroenterology Organisation.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-

oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https:// www.aafp.

org/afpsort.

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January 15, 2021

and dysmotility to erosive esophagitis and stricture. Patients

with GERD may experience dysphagia even in the absence

of apparent mucosal damage.

EOSINOPHILIC ESOPHAGITIS

Eosinophilic esophagitis is an increasingly common inam-

matory condition triggered by food allergens.

Chronic

eosinophilic inltration leads to progressive brosis, esoph-

ageal rings and furrows, and dysmotility.

FUNCTIONAL ESOPHAGEAL DISORDERS

Like irritable bowel syndrome or functional dyspepsia,

functional esophageal disorders are thought to be caused by

abnormalities of gut–brain interaction and central nervous

system processing. People with these conditions may be

hypervigilant about minor symptoms or hypersensitive to

even physiologic amounts of acid.

Patients may report dys-

phagia, although chest pain and heartburn are more com-

mon.

ese disorders may account for many patients who

report intermittent diculties with swallowing but never

seek care,

as well as those in whom no explanation is found

even aer extensive investigations.

MEDICATIONS

Medications may cause dysphagia as a result of direct muco-

sal injury (pill esophagitis), impaired esophageal motility,

or lower esophageal sphincter relaxation and reux.

OBSTRUCTIVE LESIONS

Esophageal cancer, strictures, Schatzki rings, and webs

must be considered in patients presenting with dysphagia.

However, the prevalence of these conditions is relatively low,

particularly in patients younger than 50 years.

9,10

ESOPHAGEAL MOTILITY DISORDERS

Esophageal motility disorders such as achalasia, distal

esophageal spasm, and systemic sclerosis (scleroderma) are

rare. Similar to opioid-induced bowel dysfunction and con-

stipation, opioid-induced esophageal dysfunction, although

not as common, is being increasingly recognized.

Because

this condition is oen indistinguishable from other esopha-

geal motility disorders, its prevalence is unclear.

Initial Evaluation

e rst step in the evaluation of a patient with dysphagia

is to distinguish between oropharyngeal and esophageal

pathology, based on characteristic symptoms. Clinical

features and their temporal prole (Table 3

13,14,22

), in addi-

tion to physical examination ndings (Table 4

13,14

), may

suggest specic diagnoses and guide further testing and

management.

TABLE 2

Causes of Esophageal Dysphagia

Gastroesophageal reﬂux disease and esophagitis

(30% to 40%)

Eosinophilic esophagitis*

Functional dysphagia

Functional esophageal disorders (20% to 30%)†

Functional heartburn

Gastroesophageal reﬂux disease (nonerosive)

Globus pharyngeus‡

Reﬂux hypersensitivity

Medications (5%)

Pill esophagitis (direct irritation associated with ascorbic

acid, bisphosphonates, ferrous sulfate, nonsteroidal anti-

inﬂammatory drugs, potassium chloride, quinidine, and

tetracyclines)

Reﬂux caused by decreased tone of lower esophageal

sphincter (associated with alcohol, anticholinergics, benzo-

diazepines, caeine, calcium channel blockers, nitrates, and

tricyclic antidepressants)

Structural or mechanical conditions (5%)

Esophageal or peptic stricture (caused by erosive esophagitis)

Foreign body or food impaction (acute-onset dysphagia)

Malignancy (esophageal or gastric cancer, mediastinal mass

with extrinsic compression)

Schatzki ring

Esophageal motility disorders (< 5%)§

Absent contractility

Achalasia

Distal esophageal spasm

Esophagogastric junction outﬂow obstruction

Hypercontractile (jackhammer) esophagus

Hypercontractile motility disorders

Opioid-induced esophageal dysfunction¶

Infections (< 5%)

Candida esophagitis

Cytomegalovirus esophagitis

Herpes simplex virus esophagitis

Rheumatologic conditions (< 5%)

Systemic sclerosis (scleroderma)

Note: Percentages are estimates of relative prevalence among pri-

mary care outpatients based on survey data and studies in dierent

populations. Some patients may have more than one condition.

*—The prevalence of eosinophilic esophagitis is increasing.

†—Functional esophageal disorders may be underrecognized;

actual prevalence is likely higher.

‡—Globus pharyngeus does not cause dysphagia, but the patho-

physiology is likely similar to functional disorders.

§—Esophageal motility disorders may be overdiagnosed; patients

may actually have other unrecognized conditions.

¶—Opioid-induced esophageal dysfunction is increasingly recog-

nized and often indistinguishable from esophageal motility disor-

ders; the exact prevalence is unclear.

Information from references 1, 5, and 13-15.

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DYSPHAGIA

Most patients with dysphagia have esophageal dysfunc-

tion caused by benign and self-limited conditions, including

functional esophageal disorders.

Oropharyngeal symp-

toms, particularly in patients without known comorbidities,

are more worrisome; they may be the initial presentation of

malignancy or neurodegenerative illness.

GLOBUS PHARYNGEUS

Globus pharyngeus, an intermittent nonpainful sensation

of a lump, foreign body, or phlegm in the neck or throat,

should be distinguished from dysphagia. Globus pharyn-

geus has a benign natural course, typically improves with

swallowing, and generally does not require further evalu-

ation beyond a careful history and examination. It is com-

monly associated with GERD or anxiety.

SYMPTOMS AND HISTORY

Patients with oropharyngeal dysphagia oen report chok-

ing, coughing, drooling, nasal regurgitation, diculty initi-

ating a swallow, or needing repeated swallows to clear food

from the mouth. ey may have hoarseness or other voice

changes, including a “wet” voice. Patients will usually accu-

rately localize their symptoms to the throat or neck.

Patients with esophageal dysfunction typically do not

have diculty initiating a swallow, but report a sensation of

food getting stuck aer swallowing. Patients with obstruc-

tive lesions report progressive symptoms occurring mainly

with solids, whereas those with motility disorders oen

have intermittent dysphagia with solids and liquids.

Regurgitation of undigested food, particularly at night, is

characteristic of achalasia or Zenker diverticulum. Painful

swallowing (odynophagia) suggests an infectious process

such as esophageal candidiasis or viral esophagitis. Distal

esophageal spasm may also cause pain with swallowing, but

this condition is much less prevalent.

RISK ASSESSMENT

Patients with dysphagia who also report weight loss, fever,

gastrointestinal bleeding, or odynophagia, or who have

unusually severe or rapidly progressive symptoms, espe-

cially older adults and those with a history of cancer or

surgery, should have a more comprehensive expedited eval-

uation. In addition to esophagogastroduodenoscopy (EGD)

and barium esophagography, the evaluation may include

laryngoscopy to check for pharyngeal lesions and computed

tomography to detect extrinsic masses.

9,25

TABLE 3

Questions to Assist in the Localization and Diagnosis of Dysphagia

“What about swallowing?”

Eective initial question for screening; as eective as longer

screening instruments for prompting further questioning.

“What happens when you swallow? Does swallowing

make you cough?”

Feeling that food is stuck suggests esophageal origin,

regardless of the perceived location.

Trouble initiating a swallow, choking, coughing, or

nasopharyngeal regurgitation suggests oropharyngeal

dysphagia.

“How long has this been occurring? Is it getting worse?

Do you hesitate to go out to eat because of it?”

Acute symptoms may be caused by pill esophagitis, infec-

tion, or foreign body impaction.

Intermittent symptoms suggest intermittent use of

medications or opioids, esophageal motility disorders, or

inconsistent denture use.

Progressive or worsening symptoms suggest malignancy.

Dysphagia may lead to social isolation.

“Do you have trouble chewing your food?”

Bruxism and jaw pain suggest temporomandibular joint

arthritis or pain disorders.

Trouble chewing food suggests poorly ﬁtting dentures,

dental disease, or xerostomia.

Weakness with chewing suggests myasthenia gravis, giant

cell arteritis, or myopathy (dermatomyositis).

Information from references 13, 14, and 22.

“What gets stuck? Solids only? Solids and liquids?”

Trouble with liquids and solids suggests an esophageal motility

disorder (e.g., achalasia).

Trouble with liquids only suggests oropharyngeal pathology.

Trouble with solids only suggests a mechanical obstruction of the

esophagus, either intrinsic (stricture, web, or tumor) or extrinsic

(mediastinal mass or thyromegaly).

“Do you have any other symptoms?”

Dyspepsia suggests a complication of reﬂux (e.g., stricture).

Halitosis with regurgitation may be due to an esophageal diverticu-

lum or achalasia.

Weight loss from dysphagia suggests neoplasia or advanced disease.

“What medications do you take, including over-the-counter

medications? Do you smoke? How much alcohol do you drink? Do

you use opioids?”

Nonsteroidal anti-inﬂammatory drugs, potassium chloride, anticho-

linergics (including over-the-counter antihistamines or medications

for overactive bladder), tricyclic antidepressants, tobacco, and

alcohol can cause xerostomia and diculty swallowing.

Opioids can reduce esophageal motility.

Use of proton pump inhibitors or histamine H

blockers suggests

complications from gastroesophageal reﬂux disease.

“Do you have asthma or any food or environmental allergies?”

Positive response should prompt consideration of eosinophilic

esophagitis; random biopsies should be obtained during esophago-

gastroduodenoscopy to evaluate for this diagnosis.

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DYSPHAGIA

Isolated dysphagia does not nec-

essarily require immediate testing.

Patients younger than 50 years are

considered low risk, particularly if they

have had intermittent symptoms of

GERD or dyspepsia for more than six

months. Testing may be safely deferred

in these patients pending a treatment

trial, such as a four-week course of a

proton pump inhibitor.

9,26,27

Patients with oropharyngeal symp-

toms, hoarseness, or coughing pro-

voked by swallowing sips of water must

be evaluated for malignancy and other

obstructive lesions, as well as aspiration

risk. ey should be referred to an oto-

rhinolaryngologist or an appropriately

trained speech-language pathologist

for further imaging or formal swal-

lowing studies.

e specic screening

instruments and tests used, as well as

the health professionals administer-

ing them, vary based on local practice,

expertise, and resources.

Patients with persistent symptoms

and a negative oropharyngeal evalua-

tion should be referred for EGD to rule

out esophageal pathology.

Because

of overlapping sensory innervation,

the actual level of obstruction may be

lower than perceived by the patient; in

up to one-third of cases, symptoms in

the throat or neck are caused by lesions

in the distal esophagus.

Esophageal Dysphagia

TESTING

EGD is the recommended initial test

for patients with suspected esopha-

geal dysphagia, followed by barium

esophagography if EGD ndings are

negative.

9,29,30

EGD directly visualizes

the esophageal lumen and mucosa; can

detect obstructive lesions, infections,

inammatory conditions, and reux

esophagitis; allows for stricture dilata-

tion and biopsy; and is generally more

cost-eective than barium esophagog-

raphy. However, barium esophagogra-

phy is preferred over EGD for detecting

subtle narrowing or esophageal webs

TABLE 4

Physical Examination for Dysphagia

Examination

component Physical ﬁndings Potential diagnosis or consideration

General

Mental status Obtunded or intoxicated Transient and self-limited dysco-

ordination of swallow; address

underlying causes

Nutritional state Cachexia Neoplasia

Overall ﬁtness Sarcopenia Chronic disease

Strength Weakness/fatigability Myasthenia gravis

Integumentary

Skin inspection Needle tracks or sores;

cold, clammy skin

Substance use or opioid-induced

esophageal dysfunction

Sausage digits or Ray-

naud phenomenon

Connective tissue disease (e.g.,

scleroderma)

Head, eyes, ears, nose, and throat

Eyes Ptosis (fatigable), diplopia ALS

Mouth Cervical or supraclavicu-

lar lymphadenopathy

Infectious esophagitis or malignancy

Dry mouth (xerostomia) Connective tissue disease, medica-

tion adverse eect, or tobacco use

Poor dentition, poorly

ﬁtting dentures

Inability to comfortably or eectively

form a food bolus precludes safe

deglutition

Thyromegaly or goiter Extrinsic esophageal compression

Tongue deviates, tongue

fasciculations

ALS or cranial nerve defects

Observe a

swallow

Coughing, choking, or

drooling

Drooling and nasopharyngeal

regurgitation suggest oropharyngeal

localization; coughing conﬁrms an

aspiration risk

Speech Weak or breathy voice,

dysarthria

Vocal cord pathology or ALS

“Wet” voice Laryngeal aspiration (likely chronic)

Abdominal

Inspection Signs of portal hyper-

tension (e.g., varicosities,

jaundice, distension)

Esophageal varices causing dyspha-

gia by mass eect and peristalsis

disruption

Palpation and

percussion

Organomegaly Malignancy

Neurologic

Cranial nerves Absent gag reﬂex Cranial nerves IX and X aected

Asymmetric facial motor

ﬁndings

Cranial nerves V, VII, and XII share

sensory and motor control over the

muscles of expression and the tongue

Gait Abnormal gait Weakness generalizes to swallowing

ALS = amyotrophic lateral sclerosis.

Information from references 13 and 14.

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DYSPHAGIA

that may be amenable to dilatation, as well as extrinsic com-

pression of the esophagus. Patients on anticoagulant therapy

should undergo barium esophagography rst to determine

whether a dilatation procedure is needed, which requires

stopping anticoagulant therapy. However, routine biopsies

can generally be done in these patients without discontinu-

ing therapy.

For accurate diagnosis of eosinophilic esophagitis, biop-

sies from the midthoracic and distal esophagus, even if

the mucosa appears to be normal, should be requested for

all patients with unexplained dysphagia.

15,17

Although the

endoscopist or radiologist may suspect achalasia or a hyper-

contractile motility disorder based on EGD or barium esoph-

agography ndings,

high-resolution esophageal manometry

is required to denitively diagnose these conditions.

33,34

AVOIDING OVERDIAGNOSIS

Recent research has suggested that although high-resolution

esophageal manometry is important for the diagnosis of

achalasia, it may result in overdiagnosis of esophageal

motility disorders and lead to overtreatment with invasive

endoscopic therapies.

Many patients who are thought to

have hypercontractile motility disorders may actually have

functional esophageal symptoms unrelated to manometric

ndings.

Testing for these uncommon motility disorders

can be safely deferred for at least a few months to allow for

a trial of optimal medical management of more common

conditions. Delayed diagnosis of achalasia does not increase

the risk of esophageal cancer.

INITIAL TREATMENT

Patients with GERD symptoms, esophagitis, or peptic stric-

ture should undergo acid suppression therapy with standard

doses of proton pump inhibitors for eight to 12 weeks.

38,39

Patients with eosinophilic esophagitis may also respond to

this regimen, but most require elimination diets, topical ste-

roids, or both.

40,41

For patients with functional dysphagia, functional chest

pain, heartburn, or globus pharyngeus, reassurance about

the benign and self-limited nature of these conditions,

mindful eating, avoidance of trigger foods or situations,

and a trial of acid suppression may be helpful. Tricyclic anti-

depressants, which modulate esophageal visceral hyper-

sensitivity and hypervigilance, are somewhat eective in

reducing symptoms.

e dosages used in dyspepsia trials

were 25 mg of amitriptyline or 50 mg of imipramine per

day.

Cognitive behavior therapy is helpful in patients with

functional dyspepsia

and may be considered if medical

therapy is ineective.

Patients with pill esophagitis should take their medication

with copious amounts of water and then remain upright for

30 minutes. If opioid-induced esophageal dysfunction is

suspected, the patient should be helped to discontinue use

or at least reduce the dosage.

20,21

Oropharyngeal Dysphagia

Up to one-half of debilitated and frail older adults have

some degree of dysphagia and silent aspiration, although

they oen are not aware of the problem. Patients who have

had a stroke and those with Parkinson disease, dementia, or

sarcopenia are at particular risk.

11,12

Dysphagia may be con-

sidered a geriatric syndrome. It is multifactorial and may be

triggered by acute insults or gradual decline; it leads to poor

outcomes such as malnutrition, social isolation, dehydra-

tion, weight loss, and aspiration pneumonia; and treatment

requires multidisciplinary interventions.

SCREENING

Although hospitalized patients are routinely assessed for

dysphagia, particularly aer a stroke, impairments in

community-dwelling older adults may not be recognized.

All patients with chronic illness or recent pneumonia

should be periodically screened for dysphagia.

e single

question “What about swallowing?” may be as eective as

more detailed screening tools.

Patients who are suciently

alert and able to follow directions may also be observed

swallowing a few sips of water.

AVOIDING OVERTREATMENT

In older patients with progressive chronic illness, a diagno-

sis of oropharyngeal dysphagia should prompt a discussion

about goals of care. e family physician is well-suited to

provide anticipatory guidance about the potential conse-

quences of dysphagia, as well as a realistic assessment of

the patient’s overall condition and long-term prospects. A

formal swallowing evaluation may be needed to guide this

discussion (Table 5).

22,44-49

Interventions for oropharyngeal dysphagia have limited

benet because of the inevitable decline in most patients.

Nasogastric tube feeding does not result in any survival

benet or reduce rates of aspiration pneumonia,

50,51

and it

is associated with signicant harms.

52,53

Hand feeding is as

eective and is generally recommended; caregivers and care

settings must promote choice and respect the preferences of

patients and their surrogates.

MULTIDISCIPLINARY EVALUATION AND

REHABILITATION

Speech-language pathologists use various tests ranging

from bedside assessment to instrumented swallowing

studies to determine specic decits, the patient’s poten-

tial for improvement, and the most appropriate dietary

104 American Family Physician www.aafp.org/afp Volume 103, Number 2

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January 15, 2021

DYSPHAGIA

TABLE 5

Swallowing Evaluation for Oropharyngeal Dysphagia

Video ﬂuoroscopic swallowing study (modiﬁed

barium swallow)

Preferred diagnostic test; more accurate than

bedside swallow assessment for detection of

aspiration and allows for more precise treatment

recommendations

44,45

Performed by radiologist and speech-language

pathologist in video ﬂuoroscopy suite

Fiber-optic endoscopic evaluation

Supplementary tool to video ﬂuoroscopic swallow-

ing study; good correlation in detection of aspiration

and bolus residue in the pharynx and pharyngeal-

laryngeal area

Trial of compensatory maneuvers using dierent

viscosities (thin liquid, thick liquid, puree, solid food)

to potentially improve swallowing eectiveness

Performed by speech-language pathologist in out-

patient/bedside setting with physician review; easy

to perform and well tolerated

Information from references 22 and 44-49.

Bedside swallow assessment

Structured observation of eating and drinking by speech-language pathol-

ogist or other trained observer

Trial swallows using dierent viscosities (thin liquid, thick liquid, puree,

solid food): check for coughing, choking, “wet” voice, or piecemeal swal-

lowing (i.e., multiple swallows per bolus)

Water-swallowing test (5 to 30 mL) or repetitive saliva-swallowing test:

check for coughing, choking, or “wet” voice

Pulse oximetry combined with trial swallows or water- swallowing test:

check for oxygen desaturation > 2% to 3%

Patient self-evaluation: selected questionnaires to assess health status,

dysphagia severity, and quality of life

Eating Assessment Tool

Single question (“What about swallowing?”) may be as eective as more

detailed screening tools

Swallowing Quality of Life questionnaire

Sydney Swallow Questionnaire

TABLE 6

Management of Oropharyngeal Dysphagia

Diet modiﬁcations

Mindful eating

Avoiding foods likely to cause dysphagia

Chewing carefully

Cutting food into smaller pieces

Drinking liquids to dilute food bolus

Eating slowly

Lubricating with sauces

Taking smaller bites

Mechanical soft diet to compensate for impaired

chewing due to weakness or poor dentition

Modiﬁed consistency diet to compensate for impaired

swallowing (thickened food and liquids with increased

viscosity and cohesiveness slow transport speed)

Pureed diet to compensate for impaired chewing

due to weakness, poor dentition, or dry mouth with

impaired bolus formation

Tasting diet

Patient-centered approaches to feeding and environ-

ments conducive to eating should be part of usual care

for all older adults with chronic debilitating illness

*—Patients with potential for recovery and the ability to remember and follow instructions are more likely to beneﬁt from swallowing rehabilitation

than those with progressive symptoms.

†—Should be preceded by a discussion about goals of care and shared decision-making, balancing aspiration risk with quality of life.

Information from references 22 and 55-57.

Swallowing rehabilitation*

Muscular reconditioning exercises to strengthen jaw, lips, and tongue

In clinically stable patients who have potential for improvement

(e.g., after a stroke), the goal is long-term change in control of

swallowing via neuroplasticity

In patients with progressive conditions (e.g., Parkinson disease), the

goal is maintaining current swallowing status as long as possible

Compensatory safe-swallow techniques (positioning to compensate

for weakness and dysfunction)

Eating upright

Chin-tuck maneuver for patients with stroke or degenerative disease

changes pharyngeal dimensions to direct the food bolus toward the

pharynx and esophagus, compensates for delay of glottic closure,

and reduces aspiration risk during swallowing

Head-turn maneuver for patients with unilateral weakness (turning

head toward weaker side) uses gravity to push the bolus toward the

stronger side

Enteral feeding†

Nasogastric tube feeding: typically placed during the ﬁrst week after

stroke to allow for administration of nutrition and medication

Percutaneous endoscopic gastronomy: used longer term if dysphagia

persists after the ﬁrst week; best for patients with some degree of

rehabilitation potential; does not improve mortality or reduce aspira-

tion risk

January 15, 2021

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Volume 103, Number 2 www.aafp.org/afp American Family Physician 105

DYSPHAGIA

modications and swallow therapies. ickened liquids and

foods with specic textures are oen helpful in reducing

aspiration risk. Patients with the ability to remember and

follow instructions may be taught compensatory maneuvers

of the head, neck, and chin, as well as rehabilitative exercises

to promote safer swallowing (Table 6).

22,55-57

Palliative care specialists can help facilitate

patient-centered feeding. One hospice, in collaboration

with professional chefs, maintains a website featuring rec-

ipes that have been adapted to emphasize pleasurable tex-

tures and tastes.

Social connections and rituals involving

food remain important even when swallowing is no longer

possible.

This article updates previous articles on this topic by Spieker,

and by Palmer, et al.

Data Sources: We searched PubMed and Google Scholar using

the following search terms alone and in various combinations:

dysphagia, esophageal spasm, gastroesophageal reﬂux disease,

eosinophilic esophagitis, functional esophageal disorders, acha-

lasia, esophageal motility disorder, and aspiration. We exam-

ined clinical trials, meta-analyses, review articles, and clinical

guidelines, as well as the bibliographies of selected articles.

The Cochrane database and Essential Evidence Plus were also

searched. Search dates: August 2019 to July 2020.

The authors thank Darlene E. Graner, SLPD, CCC-SLP, and Emily

A. Hosﬁeld, MS, CCC-SLP, for their review of the manuscript.

The Authors

JOHN M. WILKINSON, MD, is a consultant in the Department

of Family Medicine and an associate professor in the Mayo

Clinic Alix School of Medicine, Mayo Clinic College of Medi-

cine and Science, Rochester, Minn.

DON CHAMIL CODIPILLY, MD, is a fellow in the Division of

Gastroenterology and Hepatology at Mayo Clinic College of

Medicine and Science.

ROBERT P. WILFAHRT, MD, is a consultant in the Department

of Family Medicine and an assistant professor in the Mayo

Clinic Alix School of Medicine, Mayo Clinic College of Medi-

cine and Science.

Address correspondence to John M. Wilkinson, MD, Mayo

Clinic Alix School of Medicine, Mayo Clinic College of Med-

icine and Science, 200 1st St. SW, Rochester, MN 55905

(email: wilkinson.john@ mayo.edu). Reprints are not available

from the authors.

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