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CommentaryDysphagia is a common esophageal symptom with nearly 1 in 5 subjects older than 50 years describing this

symptom in epidemiologic surveys. It is the second most common indication for upper endoscopy in the UnitedStates. There is a myriad list of possible etiologies for dysphagia. Consequently, a systematic approach to the dif-ferential diagnosis resulting in a well planned investigation is important. As described by Drs. Katzka andKochman, a carefully obtained medical history is the initial step. Upper endoscopy is almost always indicated aspart of the evaluation and treatment.

Grace Elta, MD

Editor

CLINICAL UPDATEAmerican Society for Gastrointestinal Endoscopy

Editor: Grace Elta, MD ISSN 1070-7212 Vol. 11, No. 4 April 2004

DIAGNOSTIC APPROACH FOR DYSPHAGIA David A. Katzka, MD

Michael L. Kochman, MD, FACP

University of Pennsylvania Health System

Hospital of the University of Pennsylvania

Philadelphia, Pennsylvania

Dysphagia is defined as difficulty with swallowing or a sen-

sation of the ingested food or liquid sticking or pooling at some

point above the stomach. This is in contrast to odynophagia, or

painful swallowing. Characterization of dysphagia is accom-

plished by noting the location of the sensation of food sticking,

duration of sticking sensation, occurrence with liquids (thinversus thick) and solids (soft versus hard), association with pain

or coughing, presence or absence of regurgitation, need for liq-

uids to wash down the food, and the presence of difficulty

clearing saliva.1

Depending on the etiology, dysphagia may also be accom-

panied by nonesophageal symptoms. For example, patients

with myasthenia gravis who present with dysphagia may note

greater difficulty at dinner time than with breakfast or have

other symptoms such as muscle weakness or ptosis. Patients

with a reflux-induced stricture may have a history of heartburn

or chest pain before effective proton pump inhibitor therapy.2

Patients with a proximal esophageal stricture may have a histo-

ry of pemphigus vulgaris or lichen planus. Thus, a careful his-tory in patients with dysphagia involves not only a detailed

characterization of the cardinal symptom but also the potential

associated symptoms. Finally, compensatory symptoms must

also be elicited.3 Patients with dysphagia commonly eat slowly

and chew carefully, eat small amounts in the form of snacking

or frequent small meals, may refuse to go out for meals to avoid

demonstrating potential symptoms in public, and may follow a

diet that is calorically adequate but markedly restricted from a

societal point of view.

CHARACTERIZATION, LOCALIZATION, ANDETIOLOGY OF DYSPHAGIA

The differential diagnosis of dysphagia is broad and

includes such varied etiologies as mechanical obstruction, neo-

plasm, neuromuscular diseases, and connective tissue disorders

(Table 1). Two general categories are suggested in the evalua-

tion of dysphagia. The first is an anatomic categorization into

diseases of the oropharynx and proximal esophagus and those

of the esophageal body and lower esophageal sphincter (LES).

The second categorization is into motility or anatomic causes of

dysphagia. Thus, four subgroups of dysphagia are described:

anatomic disorders of the upper esophagus, motility disorders

of the upper esophagus, anatomic disorders of the lower esoph-

agus, and motility disorders of the lower esophagus.Generally dysphagia to solids implicates a mechanical

cause, whereas dysphagia to both liquids and solids suggests

dysmotility. Almost all chronic causes of dysphagia result in

accommodation symptoms including slow eating, alteration of

diet, avoidance of social eating situations, and learned maneu-


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Abnormalities of initiation and transfer include attempts to

make a swallow without success, multiple swallows for a single

bolus, nasal regurgitation, and fatigue when eating. Problems

with transfer and airway protection are associated with cough-

ing while eating, aspiration pneumonia, multiple swallows to

clear secretions, and hoarseness. Patients with oropharyngeal

dysfunction have their greatest trouble with thin liquids

because of the ability to pool and penetrate the larynx more eas-

ily than solids.Causes of oropharyngeal dysmotility are divided into neuro-

logic and myogenic causes. Associated symptoms indicating

more global cranial nerve or muscle involvement such as facial

weakness, ptosis, dysarthria, nasal or hoarse voice, or neck and

upper-extremity weakness may be present. Neurologic diseases

of the cortex affect initiation and bolus preparation (eg, cere-

brovascular accident, tumor). Diseases that affect the brain

stem and cranial nerves (eg, tumor, polio, Parkinson’s, Shy-

Drager, botulism) will affect virtually all aspects of oropharyn-

geal motility. Diseases of the spinal cord and peripheral nerves

(eg, amyotrophic lateral sclerosis) will interfere with pharyn-

geal and UES function and abnormalities of striated muscle

function (eg, polymyositis, myasthenia gravis) will cause pha-

ryngeal weakness.

Dysmotility of the oropharynx, as in cricopharyngeal bars or

poor UES compliance and opening, may result in the formation

of a Zenker’s diverticulum.4 A Zenker’s is unique in that it may

cause dysphagia from both poor UES function and mechanical

compression of the proximal esophagus by the diverticulum

itself. Pure mechanical causes of oropharyngeal dysphagia

include primary malignancies of the head and neck. Therapy

for the malignancy may lead to stricture formation, which may

be complicated by marked dysmotility of this area from sec-

ondary nerve and muscle injury due to dissection and radia-

tion.5 Extrinsic tumors may also compress the pharynx, partic-

ularly in the case of thyroid cancers.

Benign etiologies of pharyngeal, UES, and proximalesophageal stricture formation include webs, vascular compres-

sion from an aberrant congenital right subclavian artery (dys-

phagia lusoria), and stricture formation. Strictures of the prox-

imal esophagus are due to caustic ingestion, reflux,

eosinophilic esophagitis, pill-induced injury, and various skin

diseases such as pemphigus vulgaris, lichen planus, epidermol-

ysis bullosa dystrophica, and pseudoxanthoma elasticum.6 A

history of skin disease is usually present before stricture for-

mation, though proximal esophageal stricture formation may be

the initial manifestation of these dermatologic conditions.

Dysmotility causes of dysphagia in the esophageal body and

LES are less frequent than in the proximal esophagus due to the

reliance on local control mechanisms for distal esophagealfunction. As a result, there is only a short list of primary and

secondary diseases that cause distal esophageal dysmotility; the

prototypical disease is achalasia. Achalasia is classically

defined as a complete absence of esophageal peristalsis in asso-

ciation with a hypertensive LES that incompletely relaxes;

recent research has painted a more diverse definition. It has

become clear that many patients with achalasia will not have all

the classic criteria but the diagnosis may be based on a compi-

lation of clinical, radiographic, and manometric findings.

Achalasia is a disease for which accommodation is the rule and

patients often describe the compensatory mechanisms such as

vers to aid bolus passage. Acute causes of dysphagia, particu-

larly those associated odynophagia, implicate processes associ-

ated with mucosal ulceration or inflammation. Location of the

complaints is of variable value; symptoms felt in the upper

chest or base of the neck may reflect pathology in that location

but may also indicate referred pain from a distal source. On the

other hand, dysphagia felt in the lower chest tends to be more

accurate in pointing to the site of dysfunction. The symptom of

dysphagia may also reflect a sensory abnormality within the

normal parameters of bolus transport and transit such as in

functional globus.Oropharyngeal dysphagia due to motility problems may

result in regurgitation or spitting of food. This results from the

remarkably complex mechanisms involved in moving the bolus

from mouth entry to the esophagus. Three oropharyngeal phas-

es of swallowing are present: formation of the bolus through

mastication and tongue motion, initiation of the swallow with

transfer of the bolus to the oropharynx, and coordinated pas-

sage of the bolus through the upper esophageal sphincter

(UES). Abnormalities of the first phase may be associated with

drooling, complaints of inability to move the bolus to the back

of the throat, and dysarthria due to poor tongue movement.

Table 1. Differential diagnosis of dysphagia

Mechanical obstruction

Reflux-induced strictures

Schatzki ring

Drug- and caustic-induced strictures

Dysphagia lusoria or aortica

Gastrointestinal stromal tumors

Zenker’s diverticulum

Inflammatory

Eosinophilic esophagitis

Neoplasm

Esophageal squamous cell carcinoma

Esophageal adenocarcinoma

Gastric carcinoma

Lung cancer

Breast cancer

Neuromuscular disease

Cerebrovascular accident

Amyotrophic lateral sclerosis

Myasthenia gravis

Parkinson’s disease

PolymyositisCricopharyngeal bar

Hypothyroidism

Amyloidosis

Botulism

Polio

Shy-Drager syndrome

Connective tissue disorders

Scleroderma

Dermatologic disease

Epidermolysis bullosa

Lichen planus

Pemphigus vulgaris

Pseudoxanthoma elasticum


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slow eating, avoidance of social eating, or getting up and walk-

ing around during a meal.7 Development of esophageal diverti-

culi may be associated with LES dysfunction. Although diffuse

esophageal spasm (DES) has been viewed as a distinct entity

from achalasia, some investigators feel that it may be within the

spectrum. This appears true in certain patients and explains

their response to achalasia therapies. In contrast to DES and

achalasia, patients may develop dysphagia in association with

LES and esophageal body hypomotility, which is aperistalsiswith a wide open LES. This may be seen both in gastroe-

sophageal reflux disease and diseases that systemically affect

esophageal motility through smooth muscle and/or enteric ner-

vous system injury such as scleroderma, hypothyroidism, and

amyloidosis.

Mechanical causes of dysphagia in the distal esophagus and

LES include both malignant and benign causes. Benign causes

of stricture formation are common, with gastroesophageal reflux

being the most common cause. These patients may present with

solid food dysphagia with or without an antecedent history of

heartburn or other typical reflux symptoms. Another common

cause of dysphagia is Schatzki rings, thin membranous excur-

sions of squamous mucosa into the esophageal lumen at the gas-

troesophageal junction. Eosinophilic esophagitis, an emerging

disease most likely secondary to food allergy, caustic ingestion,

or medication-induced injury (eg, potassium, tetracycline), may

also account for benign strictures. Extrinsic processes may

result in dysphagia including aortic or right atrial compression,

mediastinal adenopathy, and lung cancer. Malignant causes of

mechanical distal esophageal dysphagia are most likely adeno-

carcinoma or squamous cell carcinoma of the esophagus.8,9

DIAGNOSTIC EVALUATION

After the history, a detailed neurologic examination, partic-

ularly of the cranial nerves and upper extremities, should be

performed, particularly in patients with suspected oropharyn-

geal causes of dysphagia (Table 2).10 The neck should be exam-ined for thyromegaly and adenopathy. Chest auscultation is

essential for evaluation of signs of pneumonia or asthma asso-

ciated with aspiration. One of the neglected aspects of the phys-

ical examination is asking the patient to eat or drink during the

examination. What is often described by the patient as normal

eating may be an amazingly abnormal process when witnessed

personally by the physician.

The next step of the evaluation is often a barium study,

though this is increasingly replaced by endoscopy in selected

cases. Often a simple barium esophagram may suffice, but fre-

quently a video barium esophagram should be ordered, partic-

ularly if there is concern for oropharyngeal dysphagia. This

allows for an anatomic and motility evaluation of the orophar-ynx and esophagus. The video swallow may also be performed

in the presence of a speech therapist to better plan potential

treatment options as therapeutic maneuvers may be performed

during the time of the study. It needs emphasis that in this era

of magnetic resonance imaging and computerized tomography,

performance of excellent-quality barium radiography is becom-

ing a lost art. As a result, the ordering physician must be aware

of the technical expertise of the radiologist performing the

examination and potentially alter one’s evaluation.

Often referral to a gastroenterologist should be pursued

early in patients with suspected mechanical causes or non-neu-

rologic causes of dysphagia, both to aid in diagnosis and man-

agement and to exclude malignancy. Many experts support a

role for esophagogastroduodenoscopy (EGD) as the first test

for evaluating dysphagia. In some situations, this is valid, such

as in patients with a suspected Schatzki ring or peptic stricture.

Other indications for EGD as the first diagnostic test include

acute pill-induced esophagitis and suspected gastroesophageal

malignancy. Nevertheless, an endoscopy as the initial study in

some cases of dysphagia may not be the best choice for the fol-

lowing reasons: 1) motility is poorly assessed; 2) the orophar-

ynx and proximal esophagus are not well seen; 3) inadvertent

perforation of a diverticulum, particularly a Zenker’s diverticu-

lum, may occur; and 4) therapeutic procedures may be planned

in advance rather than repeating the procedure, such as endo-

scopic ultrasound for malignancy or pneumatic dilation for

achalasia.11,12 Nevertheless, endoscopy is typically an essential

part of the diagnostic evaluation and therapy, especially for dis-

orders of the esophageal body and LES.13

Esophageal manometry has been used to evaluate dysphagia

for several decades, but its clinical utility is declining. It is a pri-

mary diagnostic test for those patients with normal-appearingbarium or endoscopic studies in the context of potential DES,

achalasia, or marked esophageal hypomotility. Commonly, it is

used in conjunction with endoscopy and barium esophagram to

confirm achalasia or UES and pharyngeal dysfunction.

Manometry is also operator dependent with accuracy improv-

ing with number of studies performed on a regular basis; when

technicians or physicians perform esophageal manometry less

than several times per week, its reliability and reproducibility

may be questioned.14

Fiberoptic endoscopic evaluation of swallowing has become

a valuable tool in the evaluation of oropharyngeal causes of

dysphagia. Through this technique, a nasopharyngeal laryn-

goscopy is performed and a video obtained while the patient isswallowing various foods and dyes. Esophageal scintigraphy

by radionuclide tracer may also add supportive information to

primary studies. It is most useful when corroborating symp-

toms objectively, since food rather than barium is administered.

It is also used in many studies as an objective measure of

improvement, specifically achalasia. An emerging tool for dys-

phagia is esophageal impedance measurement.15 By measure-

ment of the conductance time between electrodes on a

transnasal esophageal catheter, esophageal transit time may be

measured and the occurrence of retrograde bolus movement

may be seen. Although it is still primarily used as a research

Table 2. Diagnostic evaluation

1. History to elicit nature of dysphagia and accompanying

symptoms.

2. Physical examination to exclude neuromuscular, dermato-

logic, and connective tissue disease.

3. Consideration for referral to gastroenterologist dependent

upon suspected etiology and care plan.

4. Barium swallow and possible video study with speech

pathologist for cases of suspected oropharyngeal disorders.

5. Endoscopy may be performed as first diagnostic and thera-

peutic step in those with suspected mid- or distal-

esophageal lesions or after barium study.


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Statements and opinions expressed in the articles and communications are those of the author(s) and not necessarily those of the Editor orPublisher. The Editor and Publisher disclaim any responsibility or liability for such material.

tool, it may replace many of the indications for esophageal

manometry in the evaluation of dysphagia.

Other complementary studies include chest radiography,

computed tomography of the chest and upper abdomen, and

endoscopic ultrasound, particularly for extrinsic or intramural

lesions. If a neurologic cause is suspected, electromyographyand magnetic resonance imaging of the brain may be needed. In

selected circumstances, specialized testing such as anti-

cholinesterase antibodies and single-fiber electromyogram for

myasthenia gravis may be helpful. Specifics of the endoscopic

therapies and medical management of the myriad disorders is

beyond the scope of this monograph.16,17

SUMMARY

Although the differential diagnosis of dysphagia is large, sim-

ple classification into mechanical versus dysmotility causes and

oropharyngeal versus esophageal locations will make diagnosis

easier. A careful history with attention to the food consistencies

that provoke dysphagia, the chronicity of the complaint, and theassociation with respiratory or neurologic symptoms helps to

focus the differential. Objective evaluation may start with a video

barium swallow with or without a speech therapist. Endoscopy

may be primarily performed in certain clinical situations, but it is

almost always performed, often for confirmation or characteriza-

tion of the diagnosis and for therapy. Other complementary test-

ing including manometry, cross-sectional imaging, and neurolog-

ic evaluation will be dictated by the specific details of the case.

REFERENCES

1. Dakkak M, Bennett JR. A new dysphagia score with objective valida-

tion. J Clin Gastroenterol 1992;14:99-100.

2. Smith PM, Kerr GD, Cockel R, Ross BA, Bate CM, Brown P, et al. A

comparison of omeprazole and ranitidine in the prevention of recurrenceof benign esophageal stricture. Gastroenterology 1994;107:1312-8.

3. Blam ME , Delfyett W, Levine MS, Metz DA, Katzka DA. Achalasia: a

disease of varied and subtle symptoms that do not correlate with radi-ographic findings. Am J Gastroenterol 2002;97:1916-23.

4. Cook IJ, Gabb M, Panagopoulos V, Jamieson GG, Dodds WJ, Dent J, et

al. Pharyngeal (Zenker’s) diverticulum is a disorder of upper esophagealsphincter opening. Gastroenterology 1992;103:1229-35.

5. Silvain C, Barrioz T, Besson I, Babin P, Fontanel JP, Daban A, et al.Treatment and long-term outcome of chronic radiation esophagitisafter radiation therapy for head and neck tumors. A report of 13 cases.

Dig Dis Sci 1993;38:927-31.6. Lahoti D, Broor SL, Basu PP, Gupta A, Sharma R, Pant CS. Corrosive

esophageal strictures: predictors of response to endoscopic dilation.

Gastrointest Endosc 1995;41:196-200.7. Spiess AE, Kahrilas PJ. Treating achalasia: from whalebone to laparo-

scope. JAMA 1998;280:638-42.8. Fried RL, Brandt LJ. Endoscopic removal of post-esophagectomy sutures

facilitates esophageal dilation. Gastrointest Endosc 1994;40:394-5.

9. Honkoop P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, vanBlankenstein M, et al. Benign anastomotic strictures after transhiatal

esophagectomy and cervical esophagogastrostomy: risk factors andmanagement. J Thorac and Cardiovasc Surg 1996;111:1141-8.

10. Castell DO, Donner MW. Evaluation of dysphagia: a careful history is

crucial. Dysphagia 1987;2:65-71.11. Pfau PR, Ginsberg GG, Lew RJ, Faigel DO, Smith DB, Kochman ML,

et al. Esophageal dilation for endosonographic evaluation of malignantesophageal strictures is safe and effective. Am J Gastroenterol2000;95:2813-5.

12. Wallace MB, Hawes RH, Sahai AV, Van Velse A, Hoffman BJ. Dilationof malignant esophageal stenosis to allow EUS guided fine needle aspi-ration: safety and effect on patient management. Gastrointest Endosc

2000;51:309-13.13. Spechler SJ. American Gastroenterological Association medical posi-

tion statement on treatment of patients with dysphagia caused by benigndisorders of the distal esophagus. Gastroenterology 1999;117:229-32.

14. Philip O. Katz. Personal communication. 2003.

15. Castell DO, Vela M. Combined multichannel intraluminal impedance andpH-metry: an evolving technique to measure type and proximal extent of gastroesophageal reflux. Am J Med 2001;111 Suppl 8A:157S-9S.

16. American Society for Gastrointestinal Endoscopy Guideline.Esophageal dilation. Gastrointest Endosc 1998;48:702-4.

17. Ahmad NA, Lew RJ, Katzka DA, Ginsberg GG, Kochman ML.Endoscopic management of dysphagia: benign strictures and achalasia.ASGE Video Library, 2000.

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