June 15, 2000 Table of Contents
Evaluating Dysphagia
MICHAEL R. SPIEKER, CAPT, MC, USN, Naval Hospital, Jacksonville, Florida
Am Fam Physician. 2000 Jun 15;61(12):3639-3648.
Dysphagia is a problem that commonly affects patients cared for by family physicians in the
office, as hospital inpatients and as nursing home residents. Familiar medical problems, including
cerebrovascular accidents, gastroesophageal reflux disease and medication-related side effects,
often lead to complaints of dysphagia. Stroke patients are at particular risk of aspiration because
of dysphagia. Classifying dysphagia as oropharyngeal, esophageal and obstructive, or
neuromuscular symptom complexes leads to a successful diagnosis in 80 to 85 percent of
patients. Based on the patient history and physical examination, barium esophagram and/or
gastroesophageal endoscopy can confirm the diagnosis. Special studies and consultation with
subspecialists can confirm difficult diagnoses and help guide treatment strategies.
Complaints of dysphagia (difficult swallowing) are common, especially in aging persons. Approximately 7 to 10
percent of adults older than 50 years have dysphagia, although this number may be artificially low because many
patients with this problem may never seek medical care.1,2 Up to 25 percent of hospitalized patients and 30 to 40
percent of patients in nursing homes experience swallowing problems. 3,4
Epidemiology
Diseases of the esophagus are among the top 50 reasons that patients seek medical care and, in frequency, rank
alongside problems such as pneumonia, bronchitis and otitis media. 5 Conditions that cause dysphagia can produce
esophageal rupture, nutritional deficits and aspiration pneumonia. Elderly patients are at the highest risk of
dysphagia and its subsequent complications, especially silent aspiration.
Although the two conditions are often associated, dysphagia should be distinguished from odynophagia (painful
swallowing). In addition, care should also be taken not to confuse globus with dysphagia. Globus is the constant
sensation of a lump in the throat, although no organic defect or true difficulty in swallowing is apparent.
Anatomy and Physiology of Deglutition
Deglutition is the act of swallowing in which a food or liquid bolus is transported from the mouth through the
pharynx and esophagus into the stomach. Normal deglutition involves a complex series of voluntary and involuntary
neuromuscular contractions proceeding from the mouth to the stomach and is commonly divided into oropharyngeal
and esophageal stages.
OROPHARYNGEAL STAGE
The oropharyngeal stage of deglutition begins with contractions of the tongue and striated muscles of mastication.
The muscles work in a coordinated fashion to mix the food bolus with saliva and propel it from the anterior oral
cavity into the oropharynyx, where the involuntary swallowing reflex is triggered 6 (Figure 1a). The cerebellum
controls output for the motor nuclei of cranial nerves V, VII and XII. The entire sequence lasts about one second.
FIGURE 1A.
The tongue initially forms the food bolus (green) with compression against the hard palate.
In the posterior oropharynx, a complex and precisely coordinated succession of muscular contractions and
relaxations occurs. The soft palate elevates to close the nasopharynx, and the suprahyoid muscles pull the larynx up
and forward6 (Figure 1b). The epiglottis moves downward to cover the airway while striated pharyngeal muscles
contract to move the food bolus past the cricopharyngeus muscle (the physiologic upper esophageal sphincter and
into the proximal esophagus6 (Figure 1c). This swallowing reflex lasts approximately one second and involves the
motor and sensory tracts from cranial nerves IX and X.
FIGURE 1B.
Displacement of the food bolus into the pharynx by the tongue initiates deglutition.
FIGURE 1C.
Relaxation of the cricopharyngeal muscle (the physiological upper esophageal sphincter) permits movement of the
food bolus into the proximal esophagus.
ESOPHAGEAL STAGE
As food is propelled from the pharynx into the esophagus, involuntary contractions of the skeletal muscles of the
upper esophagus force the bolus through the mid 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 at the initiation of the swallow, and this relaxation persists until the food bolus is propelled into the
stomach. It may take eight to 20 seconds for the contractions to drive the bolus into the stomach. 7
Pathophysiology
Organic abnormalities of deglutition may be related to initiation of the swallowing reflex in the oropharynx or to
propulsion of the food bolus through the esophagus (Table 1).8
TABLE 1.
Differential Diagnoses of Dysphagia
Oropharyngeal dysphagia
Neuromuscular disease
Esophageal dysphagia
Neuromuscular disorders
Diseases of the central nervous system
Achalasia
Cerebrovascular accident
Spastic motor disorders
Parkinson's disease
Diffuse esophageal spasm
Brain stem tumors
Hypertensive lower esophageal
sphincter
Degenerative diseases
Nutcracker esophagus
Amyotrophic lateral sclerosis
Scleroderma
Multiple sclerosis
Obstructive lesions
Huntington's disease
Intrinsic structural lesions
Postinfectious
Poliomyelitis
Syphilis
Peripheral nervous system
Peripheral neuropathy
Motor end-plate dysfunction
Myasthenia gravis
Tumors
Strictures
Peptic
Radiation-induced
Chemical-induced
Medication-induced
Lower esophageal rings (Schatzki's
ring)
Skeletal muscle disease (myopathies)
Polymyositis
Dermatomyositis
Muscular dystrophy (myotonic dystrophy, oculopharyngeal
Esophageal webs
Foreign bodies
Extrinsic structural lesions
Vascular compression
dystrophy)
Cricopharyngeal (upper esophageal sphincter), achalasia
Obstructive lesions
Tumors
Enlarged aorta or left atrium
Aberrant vessels
Mediastinal masses
Inflammatory masses
Lymphadenopathy
Trauma/surgical resection
Substernal thyroid
Zenker's diverticulum
Esophageal webs
Oropharyngeal dysphagia
Extrinsic structural lesions
Esophageal dysphagia
Anterior mediastinal masses
Cervical spondylosis
Reproduced with permission from Castell DO. Approach to the patient with dysphagia. In: Yamada T, ed. Textbook of
gastroenterology. 2d ed. Philadephia: Lippincott Williams & Wilkins, 1995.
In oropharyngeal dysphagia, symptoms arise from the dysfunctional transfer of a food bolus in the pharynx past the
upper esophageal sphincter into the esophagus. Oropharyngeal dysphagia is most common in elderly patients and
frequently presents as part of a broader complex of signs and symptoms that lead the physician to a correct primary
diagnosis. Stroke is the leading cause of oropharyngeal dysphagia. 8
Esophageal dysphagia is caused by disordered peristaltic motility or conditions that obstruct the flow of a food bolus
through the esophagus into the stomach. Achalasia and scleroderma are the leading motility disorders, while
carcinomas, strictures and Schatzki's rings are the most common obstructive lesions.
History
Patients who have dysphagia may present with a variety of complaints, but they usually report coughing or choking,
or the abnormal sensation of food sticking in the back of the throat or upper chest when they are trying to swallow.
A carefully conducted patient history will enable the physician to identify 80 to 85 percent of the causes of
dysphagia. Specific questions about the onset, duration and severity of the dysphagia, and a variety of associated
symptoms (Table 2)9 may help narrow the differential diagnoses to a specific diagnosis or to an anatomic or
pathophysiologic-related diagnosis.
TABLE 2.
Associated Symptoms and Possible Etiologies of Dysphagia
Condition
Progressive dysphagia
Diagnoses to consider
Neuromuscular dysphagia
Sudden dysphagia
Obstructive dysphagia, esophagitis
Difficulty initiating swallow
Oropharyngeal dysphagia
Food “sticks” after swallow
Esophageal dysphagia
Cough
Early in swallow
Neuromuscular dysphagia
Late in swallow
Obstructive dysphagia
Weight loss
In the elderly
Carcinoma
With regurgitation
Achalasia
Progressive symptoms
Heartburn
Peptic stricture, scleroderma
Intermittent symptoms
Rings and webs, diffuse esophageal spasm, nutcracker esophagus
Pain with dysphagia
Esophagitis
Condition
Diagnoses to consider
Postradiation
Infectious: herpes simplex virus, monilia
Pill-induced
Pain made worse by:
Solid food only
Obstructive dysphagia
Solids and liquids
Neuromuscular dysphagias
Regurgitation of old food
Zenker's diverticulum
Weakness and dysphagia
Cerebrovascular accidents, muscular dystrophies, myasthenia
gravis, multiple sclerosis
Halitosis
Zenker's diverticulum
Dysphagia relieved with repeated
Achalasia
swallows
Dysphagia made worse with cold
Neuromuscular motility disorders
foods
Information from Johnson A. Deglutition. In: Scott-Brown WG, Kerr AG. Scott-Brown's Otolaryngology. 6th ed.
Boston: Butterworth-Heinemann, 1997.
A patient's general health information should be reviewed, including long-term illnesses, current prescription
medications, and alcohol and tobacco use. While the literature does not describe dysphagia caused by nonprescription drugs, it is always reasonable to inquire about this. Commonly prescribed medications can cause
dysphagia in either the oropharyngeal or esophageal stages of swallowing (Table 3).10,11 Antibiotics (doxycycline
[Vibramycin], tetracycline, clindamycin [Cleocin], trimethoprim-sulfamethoxazole [Bactrim, Septra]) and
nonsteroidal anti-inflammatory drugs are the most common causes of direct mucosal injury to the esophagus, while
potassium chloride tablets can cause the most severe injury. Anticholinergics, alpha adrenergic blockers,
angiotensin-converting enzyme (ACE) inhibitors and many short- and long-acting antihistamines can cause
xerostomia.
TABLE 3.
Medications Associated with Dysphagia
Medications that can cause direct esophageal mucosal injury
Antibiotics
Doxycycline (Vibramycin)
Tetracycline
Clindamycin (Cleocin)
Trimethoprim-sulfamethoxazole (Bactrim, Septra)
Nonsteroidal anti-inflammatory drugs
Alendronate (Fosamax)
Zidovudine (Retrovir)
Ascorbic acid
10
Potassium chloride tablets (Slow-K)*
Theophylline
Quinidine gluconate
Ferrous sulfate
Medications, hormones and foods associated with reduced lower esophageal sphincter tone and
reflux
11
Butylscopolamine
Theophylline
Nitrates
Calcium antagonists
Alcohol, fat, chocolate
Medications associated with xerostomia
11
Anticholinergics: atropine, scopolamine (Transderm Scop)
Alpha adrenergic blockers
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Antiarrhythmics
Disopyramide (Norpace)
Mexiletine (Mexitil)
Ipratropium bromide (Atrovent)
Antihistamines
Diuretics
Opiates
Antipsychotics
*—Especially the slow-release (SR) formulation.
Information from Boyce HW. Drug-induced esophageal damage: diseases of medical progress. [Editorial]
Gastrointest Endosc 1998;47:547–50, and Stoschus B, Allescher HD. Drug-induced dysphagia. Dysphagia
1993;8:154–9.
A carefully conducted patient history should answer two general questions: (1) is the dysphagia oropharyngeal or
esophageal in nature and (2) is it caused by mechanical obstruction or a neuromuscular motility disorder? 8 Figure 28
presents an algorithmic approach to the history.
Differential Diagnosis of Dysphagia
FIGURE 2.
Differentiating symptoms of dysphagia.
Information from Castell DO. Approach to the patient with dysphagia. In: Yamada T, ed. Textbook of
gastroenterology. 2d ed. Philadelphia: Lippincott Williams & Wilkins, 1995.
OROPHARYNGEAL LOCALIZATION
Patients with oropharyngeal dysphagia present with difficulty in initiating swallowing and may also have associated
coughing, choking or nasal regurgitation. The patient's speech quality may have a nasal tone. These dysphagias are
most often associated with stroke, Parkinson's disease or other long-term neuromuscular disorders. Local structural
lesions are less common.
ESOPHAGEAL LOCALIZATION
Patients with esophageal dysphagia present with the sensation of food sticking in their throat or chest. The patient's
description of the perceived location of the obstruction often does not correlate well with actual pathology,
especially if the perceived location is in the cervical area. Motility disorders and mechanical obstructions are
common. Several medications have been associated with direct esophageal mucosal injury while others can decrease
lower esophageal sphincter pressures and cause reflux (Table 3).10,11
NEUROMUSCULAR MOTILITY DISORDERS
Patients with neuromuscular dysphagia experience gradually progressive difficulty in swallowing solid food and
liquids. Cold foods often aggravate the problem. Patients may succeed in passing the food bolus by repeated
swallowing, by performing the Valsalva maneuver or by making a positional change. They are more likely to
experience pain when swallowing than patients with simple obstruction. Achalasia, scleroderma and diffuse
esophageal spasm are the most common causes of neuromuscular motility disorders.
MECHANICAL OBSTRUCTION
Obstructive pathology is typically associated with dysphagia of solid food but not liquids. Patients may be able to
force food through the esophagus by performing a Valsalva maneuver, or they may regurgitate undigested food.
Close questioning of the patient may reveal a change in diet to one of predominantly soft foods. Rapidly progressive
dysphagia of a few months' duration suggests esophageal carcinoma. Weight loss is more predictive of a mechanical
obstructive lesion.12 Peptic stricture, carcinoma and Schatzki's ring are the predominant obstructive lesions.
Physical Examination
A general physical examination and focused organ- or symptom-specific examinations based on the patient's history
often identify the etiology of dysphagia.
Neurologic evaluation should include assessments of the patient's mental status, motor and sensory functioning,
deep tendon reflexes and cranial nerves, and a cerebellar examination. Patients with impaired cognitive functioning
and those who are under sedation should be carefully assessed, because these neurologic states can interfere with
swallowing. Motor and sensory examinations may reveal a new stroke or identify a long-term illness. Special
attention should be focused on the cranial nerves that are associated with swallowing, particularly the motor
components of cranial nerves V, VII, IX, X and XII, and sensory fibers from cranial nerves V, VII, IX and X. A
decreased gag reflex is associated with an increased risk of aspiration.13 A “wet voice” may suggest long-term
laryngeal aspiration, while a weak, breathy voice may indicate vocal cord pathology.
Adequate saliva production results in a pink, well-hydrated oral cavity. Certain medications induce xerostoma
preventing adequate mixing and propulsion of the food bolus into the posterior oropharynx (Table 3).10,11 A tongue
blade and handheld mirror allow indirect inspection of the soft palate and vocal cord mobility. Physicians who are
skilled in nasopharyngoscopy can directly view the vocal cords and hypopharynx. Bimanual palpation of the floor of
the mouth, tongue and lips with a gloved hand detects masses and abnormal motor function. Examination of the
teeth can reveal signs of inflammation or other structural disorders.
Observing the patient swallowing a variety of liquids and solids can be helpful. The patient should demonstrate
enough neuromuscular control to chew food, mix it into a bolus with saliva and propel it to the posterior pharynx
without choking or coughing. Elevation of the larynx during the swallowing reflex protects the airway and opens the
upper esophageal sphincter. Normal laryngeal ascent can be palpated by placing the index finger above the patient's
thyroid cartilage when the patient swallows. The cartilage should move cephalad against the physician's finger.
Thyroid masses and lymphadenopathy that cause obstructive dysphagia can be palpated on examination of the neck.
A widened anteroposterior chest diameter and distant breath sounds are signs of chronic obstructive pulmonary
disease, which could be caused by long-term aspiration. The patient's abdomen should be examined for masses and
organomegaly. The presence of occult blood in the stool may be a sign of neoplasms or esophagitis.
Laboratory Evaluation
Initial laboratory evaluations should be limited to specific studies based on the differential diagnosis generated after
the completion of a history and physical examination. A complete blood count screens for infectious or
inflammatory conditions. Thyroid function studies may detect hypo- or hyperthyroid-associated causes of dysphagia
(e.g., Grave's disease or thyroid carcinoma). Other studies should be based on specific clinical conditions.
Special Studies
Although a patient history and physical examination identify the etiology of dysphagia in most patients, further
testing may be indicated to confirm the diagnosis or to establish the patient's risk of aspiration (Figure 314 and
Table 4). Subspecialists in radiology or gastroenterology will most often conduct these tests. Some centers have
multidisciplinary dysphagia teams available to offer comprehensive diagnostic evaluations and therapeutic
interventions.
Evaluation of Dysphagia
FIGURE 3.
An algorithmic approach to the diagnostic evaluation of dysphagia.
Adapted with permission from Trate DM, Parkman HP, Fisher RS. Dysphagia. Evaluation, diagnosis, and treatment.
Prim Care 1996;23:417–32.
TABLE 4.
Adjunct Studies to Evaluate Patients with Dysphagia
Barium swallow studies
Suspected obstructive lesion (e.g., Schatzki's ring, tumor)
Suspected esophageal motility disorder
Double-contrast upper gastrointestinal evaluation
Suspected esophageal mucosal injury
Evaluation of oropharyngeal anatomy and function (fluoroscopy)
Suspected gastroesophageal reflux disease
Gastroesophageal endoscopy
Suspected acute obstructive lesion (impacted food bolus)
Evaluation of the esophageal mucosa
Confirmation of a positive barium study with biopsies or cytology
Manometry
Abnormality not identified on barium study or by endoscopy
pH monitoring
Suspected gastroesophageal reflux disease
Videoradiography
Suspected risk of aspiration
NASOPHARYNGOSCOPY
Nasopharyngoscopy is particularly useful in evaluating patients with oropharyngeal dysphagias. This procedure
quickly identifies structural masses and lesions, and assesses laryngeal sensitivity to contact. Overuse of topical
anesthetics can anesthetize the pharynx and confuse the interpretation. Under direct observation from the level of the
soft palate, the physician assesses oral containment of a colored fluid bolus in the mouth and observes pooling of
fluids around the vallecula or clearing of the fluid from the oropharynx into the esophagus. Patients who show
aspiration without cough are at high risk of pulmonary complications.
BARIUM STUDIES
A barium study (esophagram) is often the first step in evaluating patients with dysphagia, especially if an obstructive
lesion is suspected. It identifies intrinsic and extrinsic structural lesions but lacks precision in identifying the nature
of obstructive lesions. A barium study assesses motility better than endoscopy and is relatively inexpensive with few
complications; however, it can be difficult to perform in sick or uncooperative patients.
Double-contrast studies provide better visualization of esophageal mucosa. Barium marshmallows or pills localize
obstructive lesions in the mouth or esophagus. Fluoroscopy can identify abnormalities in the mouth and oropharynx
and, if observed closely, can provide some detail about function, detecting reflux and abnormal peristalsis.
ENDOSCOPY
Gastroesophageal endoscopy provides the best assessment of the esophageal mucosa. 15 Masses or other lesions
identified by barium studies should initiate esophagogastroscopy with biopsy and cytology. In patients with acute
onset of dysphagia while eating, gastroesophageal endoscopy can directly remove an impacted food bolus and dilate
strictures. Endoscopy has the added benefit of detecting infection and erosions, and providing biopsy capability.
While endoscopy does not assess motor function or subtle strictures as well as barium studies 15 (its sensitivity for
detecting Schatzki's rings is only 58 percent, compared with 95 percent for barium study), a consensus panel making
final diagnoses in patients with dysphagia found that for all dysphagia diagnoses, gastroesophageal endoscopy is
more sensitive (92 percent versus 54 percent) and more specific (100 percent versus 91 percent) than doublecontrast upper gastrointestinal radiography.16 One author suggests that the higher cost of gastroesophageal
endoscopy may be offset by lower subsequent medical costs because of its improved accuracy in diagnosing
dysphagia.17
VIDEORADIOGRAPHIC STUDIES
Patients at risk for silent aspiration (e.g., stroke, neurologic impairment) may benefit from videoradiographic studies
that are performed by a team composed of a radiologist, an otolaryngologist and a speech pathologist with expertise
in swallowing disorders.17 This evaluation uses quantifiable measures of swallows of a variety of bolus consistencies
to help objectively identify the presence, nature and severity of oropharyngeal swallowing problems and to assess
treatment options. Compared with upper gastrointestinal radiography, videoradiographic studies are better in
identifying patients with mild strictures and extrinsic compressions (e.g., tumors or osteoarthritic spurs of the
vertebrae).12 These studies are more expensive because of the special expertise, equipment and facilities required.
MANOMETRY
Manometry assesses motor function of the esophagus and is indicated if no abnormality is identified by barium
study or gastroesophageal endoscopy.18 A catheter with multiple electronic pressure probes is passed into the
stomach, measuring esophageal contractions and defining upper and lower esophageal responses to swallowing.
Manometry detects definitive abnormalities in only 25 percent of patients with nonobstructive lesions. Its use in
disorders of the oropharyngeal upper esophageal sphincter is not particularly effective, because patients do not
tolerate the procedure well.
PH MONITORING
Despite several drawbacks, esophageal pH monitoring remains the gold standard for diagnosing patients with
suspected reflux disease.19 A nasogastric probe is inserted into the patient's esophagus and records pH levels. These
levels are compared with the patient's record of symptoms over a 24-hour period to determine if acid reflux
contributes to the symptoms. Combined recordings of esophageal pH levels and intraluminal esophageal pressure
may aid in diagnosing patients with reflux-induced esophageal spasm.
OTHER IMAGING TECHNIQUES
Plain radiographic films of the chest or neck offer limited information unless structural abnormalities are noted.
Computed tomography and magnetic resonance imaging scans provide excellent definition of structural
abnormalities, particularly when used to evaluate patients with suspected central nervous system causes of
dysphagia. Ultrasonography of the pharynx and tongue offers no benefit compared with videofluorography, but
ultrasonography may aid in the evaluation of submucosal and extramural lesions of the esophagus. Radionuclide
studies may be used to evaluate transit function through the esophagus.
Final Comment
Family physicians can reduce the symptoms and risks of complications by early and aggressive evaluation and
management of stroke patients. Physicians should recommend that all patients, especially the elderly, take their
medications with a full glass of water while in an upright position well before bedtime. Patient referral is warranted
when the cause of dysphagia is unclear, when there is evidence of aspiration or if further diagnostic or therapeutic
expertise is necessary.
The Author
MICHAEL R. SPIEKER, CAPT, MC, USN, is currently director of residency training at the Naval Hospital, Jacksonville, Fla., and is
an assistant professor at the Uniformed Services University of the Health Sciences F. Edward Hébert School of Medicine, Bethesda,
Md. He earned his medical degree at the Oregon Health Sciences University School of Medicine, Portland, and completed a family
practice residency at the Naval Hospital, Camp Pendleton, Calif.
Address correspondence to Michael R. Spieker, M.D., Naval Hospital, Family Practice, 2080 Child St., Jacksonville, FL 32214.
Reprints are not available from the author.
The opinions and assertions contained herein are the private views of the author and are not to be construed as official or as
reflecting the views of the Navy Department or the Department of Defense.
REFERENCES
1. Lindgren S, Janzon L. Prevalence of swallowing complaints and clinical findings among 50–79-year-old men and women in an
urban population. Dysphagia. 1991;6:187–92.
2. Tibbling L, Gustafsson B. Dysphagia and its consequences in the elderly. Dysphagia. 1991;6:200–2.
3. Brin MF, Younger D. Neurologic disorders and aspiration. Otolaryngol Clin North Am. 1988;21:691–9.
4. Layne KA, Losinski DS, Zenner PM, Ament JA. Using the Fleming index of dysphagia to establish prevalence. Dysphagia.
1989;4:39–42.
5. Nelson C, Woodwell D. National Ambulatory Medical Care Survey: 1993 summary. Vital Health Stat. 13 1998iiivi1–99.
6. Schuller DE, Schleuning AJ, DeWeese DD, Saunders WH. DeWeese and Saunders' Otolaryngology—head and neck surgery.
8th ed. Schuller DE, Schleuning AJ, eds. St. Louis: Mosby, 1994.
7. Logemann JA. Evaluation and treatment of swallowing disorders. San Diego: College-Hill, 1983.
8. Castell DO. Approach to the patient with dysphagia. In: Yamada T, ed. Textbook of gastroenterology. 2d ed. Philadelphia:
Lippincott Williams & Wilkins, 1995.
9. Johnson A. Deglutition. In: Scott-Brown WG, Kerr AG. Scott-Brown's Otolaryngology. 6th ed. Boston: Butterworth-Heinemann,
1997.
10. Boyce HW. Drug-induced esophageal damage: diseases of medical progress. [Editorial] Gastrointest Endosc. 1998;47:547–
50.
11. Stoschus B, Allescher HD. Drug-induced dysphagia. Dysphagia. 1993;8:154–9.
12. Kim CH, Weaver AL, Hsu JJ, Rainwater L, Zinsmeister AR. Discriminate value of esophageal symptoms: a study of the initial
clinical findings in 499 patients with dysphagia of various causes. Mayo Clin Proc. 1993;68:948–54.
13. Horner J, Massey EW. Silent aspiration following stroke. Neurology. 1988;38:317–9.
14. Trate DM, Parkman HP, Fisher RS. Dysphagia. Evaluation, diagnosis, and treatment. Prim Care. 1996;23:417–32.
15. Cooper GS. Indications and contraindications for upper gastrointestinal endoscopy. Gastrointest Endosc Clin N Am.
1994;4:439–54.
16. Dooley CP, Larson AW, Stace NH, Renner IG, Valenzuela JE, Eliasoph J, et al. Double-contrast barium meal and upper
gastrointestinal endoscopy. A comparative study. Ann Intern Med. 1984;101:538–45.
17. Castell JA, Stumacher SG, Castell DO. Approach to patients with oropharyngeal dysphagia. Gastroenterologist. 1994;2:14–
9.
18. Feussner H, Kauer W, Siewert JR. The place of esophageal manometry in the diagnosis of dysphagia. Dysphagia.
1993;8:98–104.
19. Bollschweiler E, Feussner H, Holscher AH, Siewert JR. pH monitoring: the gold standard in detection of gastrointestinal reflux
disease? Dysphagia. 1993;8:118–21.
Members of various family practice departments develop articles for “Problem-Oriented Diagnosis.” This article is one in a series
coordinated by the Department of Family Medicine at the Uniformed Services University of the Health Sciences, Bethesda, Md.
Guest editors of the series are Francis G. O'Connor, LTC, MC, USA, and Jeannette E. South-Paul, COL, MC, USA.
Copyright © 2000 by the American Academy of Family Physicians.
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