Overview of dysphagia in adults

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Literature review current through: Jun 2015. | This topic last updated: Jan 08, 2014.
INTRODUCTION Dysphagia suggests the presence of an organic abnormality in the
passage of solids or liquids from the oral cavity to the stomach. Patients' complaints range from
the inability to initiate a swallow to the sensation of solids or liquids being hindered during their
passage through the esophagus into the stomach.
This topic will review the initial evaluation of patients with dysphagia and diagnostic testing in
patients with esophageal dysphagia. The pathogenesis, diagnosis, and evaluation of patients
with oropharyngeal dysphagia are discussed separately. Our recommendations are largely
consistent with the American Gastroenterological Association guidelines [1,2].
(See "Oropharyngeal dysphagia: Etiology and pathogenesis" and "Oropharyngeal dysphagia:
Clinical features, diagnosis, and management".)
DEFINITIONS
Dysphagia is defined as a subjective sensation of difficulty or abnormality of swallowing.
Odynophagia is defined as pain with swallowing.
Globus sensation is defined as a persistent or intermittent nonpainful sensation of a lump
or foreign body in the throat with the occurrence of the sensation between meals and
the absence of dysphagia, odynophagia, an esophageal motility disorder, or
gastroesophageal reflux as the cause of symptoms. These criteria must be fulfilled for the
last three months with symptom onset at least six months before a diagnosis of globus
sensation can be made [3]. (See "Globus sensation".)
Dysphagia can be classified as follows:
Oropharyngeal dysphagia Oropharyngeal or transfer dysphagia is characterized by
difficulty initiating a swallow. Swallowing may be accompanied by coughing, choking,
nasopharyngeal regurgitation, aspiration, and a sensation of residual food remaining in the
pharynx. (See "Oropharyngeal dysphagia: Etiology and pathogenesis", section on 'Etiology
and pathogenesis' and "Oropharyngeal dysphagia: Clinical features, diagnosis, and
management".)
Esophageal dysphagia Esophageal dysphagia is characterized by difficulty swallowing
several seconds after initiating a swallow and a sensation of food getting stuck in the
esophagus.
EVALUATION Dysphagia is an alarm symptom that warrants immediate evaluation to define
the exact cause and initiate appropriate therapy. Dysphagia in older adult subjects
should not be attributed to normal aging. Aging alone causes mild esophageal motility
abnormalities, which are rarely symptomatic [4].
History The first step in evaluating patients with dysphagia is to try to determine by careful
questioning if the symptoms are due to oropharyngeal or esophageal dysphagia (table 1) [5].
Patients with oropharyngeal dysphagia have difficulty initiating a swallow and often point toward
the cervical region when asked to identify the site of their symptoms.
Oral dysfunction can lead to drooling, food spillage, sialorrhea, piecemeal swallows, and
dysarthria.

Pharyngeal dysfunction can lead to coughing or choking during food consumption, and
dysphonia. In contrast, patients with esophageal dysphagia have difficulty swallowing several
seconds after initiating a swallow and a sensation of food getting stuck in the suprasternal notch
or behind the sternum. While retrosternal dysphagia usually corresponds with the location of the
lesion, suprasternal dysphagia is commonly referred from below [6]. The evaluation of patients
with oropharyngeal dysphagia to determine the etiology is discussed in detail separately.
(See 'Definitions' above and "Oropharyngeal dysphagia: Clinical features, diagnosis, and
management", section on 'Definitions' and "Oropharyngeal dysphagia: Clinical features,
diagnosis, and management", section on 'Determining the etiology'.)
In patients with esophageal dysphagia, a critical component of the medical history is
determining the types of food that produce symptoms (solids, liquids, or both) and the temporal
progression of symptoms (algorithm 1).

Dysphagia to both solids and liquids from the onset of symptoms is probably due to a motility
disorder of the esophagus. In contrast, dysphagia for solids that later progresses to involve
liquids is more likely to reflect mechanical obstruction [7].
Progressive dysphagia, beginning with dysphagia to solids followed by dysphagia to liquids, is
usually caused by cancer or a peptic stricture. Symptoms of peptic strictures are usually
insidious and gradually progressive, whereas those due to a malignancy progress more rapidly
[8]. Symptoms correspond to the caliber of the stricture; dysphagia to solids is usually present
when the esophageal lumen is narrowed to 13 mm or less. Intermittent dysphagia is most often
related to a lower esophageal ring or web. Patients with motility disorders may also exhibit
progressive dysphagia (usually those with achalasia or scleroderma) or may
exhibitintermittent/nonprogressive dysphagia (usually those with hypertensive lower esophageal
sphincter, diffuse esophageal spasm, or nonspecific motility disorders).

Associated symptoms or findings such as heartburn, weight loss, hematemesis, coffee ground
emesis, anemia, regurgitation of food particles, and respiratory symptoms can further help to
narrow the differential diagnosis (algorithm 2). As an example, chronic heartburn in a patient
with dysphagia may be a clue to the presence of complications of gastroesophageal reflux
disease, such as erosive esophagitis, peptic stricture, and adenocarcinoma of the esophagus.
However, the absence of heartburn does not rule out reflux-related complications, since
approximately one-fourth of patients with peptic stricture and at least one-third of those with
adenocarcinoma of the esophagus have no history of heartburn [9,10]. Furthermore, more than
40 percent of patients with achalasia complain of retrosternal burning consistent with heartburn
[11]. (See "Complications of gastroesophageal reflux in adults" and "Clinical manifestations and
diagnosis of achalasia", section on 'Clinical manifestations'.)
Diagnostic testing Diagnostic testing to determine the etiology of esophageal dysphagia
should be based upon the medical history (algorithm 2).

Diagnostic testing in patients with oropharyngeal dysphagia is discussed in detail separately.

(See "Oropharyngeal dysphagia: Clinical features, diagnosis, and management", section on
'Determining the etiology'.)
Upper endoscopy Patients with esophageal dysphagia should be referred for an upper
endoscopy [12]. In addition to its diagnostic value, endoscopy offers an opportunity to obtain
tissue samples to determine the etiology, and to perform a therapeutic intervention (eg, dilation
of an esophageal ring). (See "Esophageal rings and webs", section on 'Treatment'.)

Barium swallow We perform a barium swallow in the following patients:

As the initial test (prior to upper endoscopy) in patients with a history or clinical features
suggestive of a proximal esophageal lesion (eg, surgery for laryngeal or esophageal
cancer, Zenker's diverticulum, or radiation therapy), a known complex (tortuous) stricture
(eg, prior caustic injury or radiation therapy) [2]. In these patients, intubation of the
proximal esophagus during endoscopy is done relatively blindly, thereby risking perforation
due to upper esophageal pathology. However, it is important to note that performing a
barium swallow prior to an upper endoscopy in such patients has not been demonstrated
to decrease the rate of endoscopic complications or improve outcomes [1].
Following a negative upper endoscopy in patients in whom a mechanical obstruction is
suspected, as lower esophageal rings or extrinsic esophageal compression can be missed
by an upper endoscopy [13].
Patients should be instructed to drink barium in the prone-oblique position; maximal distension
of the esophagogastric junction is achieved by having the patient swallow barium rapidly in
association with a variety of respiratory maneuvers [14]. In addition, asking the patient to
swallow 13 mm barium tablets or a solid bolus, such as a marshmallow or bread, may be helpful
for demonstrating subtle lesions in patients with persistent or intermittent solid food dysphagia
[15,16].
Motility testing Motility testing should be performed in patients with dysphagia in whom
(quem) upper endoscopy is unrevealing and/or an esophageal motility disorder is suspected.
Although certain motility disorders (eg, achalasia) can be strongly suspected based upon their
characteristic radiographic appearance when in advanced stages (image 1), confirmation with a
motility study is required to establish the diagnosis [2,13,17,18]. A nonspecific motility disorder
or achalasia can be detected in up to 50 percent of patients with nonstructural dysphagia
[19,20]. (See "Motility testing: When does it help?" and "Clinical manifestations and diagnosis of
achalasia" and "Clinical manifestations and diagnosis of achalasia", section on 'Evaluation'.)

DIFFERENTIAL DIAGNOSIS OF ESOPHAGEAL DYSPHAGIA Esophageal dysphagia

arises within the body of the esophagus, the lower esophageal sphincter, or cardia. A large
number of conditions are associated with esophageal dysphagia, the most common of which will
be reviewed here (table 2). The differential diagnosis of oropharyngeal dysphagia is discussed
in detail, separately (table 3). (See "Oropharyngeal dysphagia: Clinical features, diagnosis, and
management", section on 'Determining the etiology'.)
Intraluminal causes
Food impaction Food impaction is by far the most common cause for acute dysphagia in
adults. The estimated annual incidence is 13.0 per 100,000 and with a higher incidence in
males as compared with females (1.7:1) [21]. The incidence increases with age, especially after
the seventh decade. Patients usually develop symptoms after ingesting meat (most commonly
beef, chicken, and turkey), which completely obstructs the esophageal lumen, resulting in
expectoration of saliva [22]. The food bolus can be removed using grasping devices (either en
bloc or piecemeal, depending upon the consistency of the bolus), or it can be gently pushed into
the stomach using an endoscope [21,23]. Endoscopic management of food impaction is
discussed in detail separately. (See "Ingested foreign bodies and food impactions in adults",
section on 'Food bolus'.)
Intrinsic causes
Esophageal stricture Peptic stricture is a complication of acid reflux, which occurs in
approximately 10 percent of patients with gastroesophageal reflux disease (GERD) who seek
medical attention [24,25]. The development of peptic strictures among patients with reflux has
been associated with older age, male gender, and longer duration of reflux symptoms [26]. In
addition to GERD, peptic strictures have been observed in a number of other conditions that
lead to increased esophageal acid exposure (eg, systemic sclerosis, Zollinger-Ellison syndrome,
nasogastric tube placement, and Heller myotomy for achalasia).
Patients with a variety of other disorders, such as infectious esophagitis, postsurgical resection
for esophageal or laryngeal cancer, caustic ingestion, pill esophagitis, and radiation exposure,
may develop narrowing of the esophagus that is similar to a peptic stricture despite its nonpeptic
origin.
Eosinophilic esophagitis Up to 15 percent of patients being evaluated for dysphagia with
endoscopy are found to have eosinophilic esophagitis [27-29]. Adults and teenagers frequently
present with dysphagia and food impactions [27]. A number of endoscopic findings have been
associated with eosinophilic esophagitis including stacked circular rings, strictures, linear
furrows, white papules and a small caliber esophagus. Individual endoscopic features
suggestive of eosinophilic esophagitis have low sensitivity ranging from 15 to 48 percent but
high specificity ranging from 90 to 95 percent [30]. The diagnosis of eosinophilic esophagitis is
established by upper endoscopy and esophageal biopsy which demonstrates an increased
number of eosinophils (>15 per high power field). (See "Clinical manifestations and diagnosis of
eosinophilic esophagitis", section on 'Endoscopy'.)
Esophageal webs and rings Esophageal webs and rings can partially or completely
compromise the esophageal lumen [31]. They can be solitary or multiple.
An esophageal web is a thin mucosal fold that protrudes into the esophageal lumen and
is covered with squamous epithelium. Webs most commonly occur anteriorly in the
cervical esophagus, causing focal narrowing in the postcricoid area (image 2).

Esophageal rings are typically mucosal structures but in rare cases are muscular. Rings
are found at the gastroesophageal junction, are smooth, thin (<4 mm in axial length), and
covered with squamous mucosa above and columnar epithelium below (picture
1 and image 3) [32].
Patients with esophageal rings and webs have intermittent dysphagia for solids. Esophageal
rings have been described in association with iron deficiency (the Plummer-Vinson or PatersonKelly syndrome) in which case anemia, koilonychia, or other manifestations of iron deficiency
may be present (image 4) [33].
An esophageal web/ring is diagnosed on barium swallow and upper endoscopy and appears as
a focal, thick constriction of variable luminal diameter [34]. Rings are usually found at or a few
centimeters above the squamocolumnar junction. Endoscopy is less sensitive than the barium
esophagram in detecting esophageal rings and a ring may be missed unless the lower
esophagus is widely distended [35]. The caliber of a muscular ring changes during peristalsis,
distinguishing it from a peptic stricture or mucosal ring. (See "Esophageal rings and webs",
section on 'Clinical presentation and diagnosis'.)
Carcinoma Cancer of the esophagus or gastric cardia is associated with rapidly progressive
dysphagia, initially for solids and later for liquids. In addition, patients may have chest pain,
odynophagia, anemia, anorexia, and significant weight loss.
An achalasia-like syndrome (pseudoachalasia) has also been described in patients with
adenocarcinoma of the cardia due to microscopic infiltration of the myenteric plexus or the
vagus nerve [36]. Certain features increase the likelihood that the patient has pseudoachalasia
due to malignancy [37]. These include short duration of symptoms (less than six months),
presentation after age 60, excessive weight loss in relation to the duration of symptoms, and
difficult passage of the endoscope through the gastroesophageal junction. In such cases,
endoscopic ultrasonography with fine-needle aspiration (EUS FNA) should be performed to
diagnose an underlying malignancy. (See "Clinical manifestations and diagnosis of
achalasia" and "Epidemiology, pathobiology, and clinical manifestations of esophageal cancer".)
Radiation injury Patients undergoing radiation therapy for thoracic or head and neck tumors
are at risk for developing esophagitis and esophageal strictures. In the acute setting, patients
may develop esophagitis resulting in dysphagia and odynophagia. In some patients, chronic
ischemia and fibrosis lead to chronic radiation esophagitis, which may present as esophageal
ulcerations or strictures in the proximal esophagus [38]. Although controversial, another
potential cause of dysphagia in patients who have received thoracic radiation is a motility
disorder [39,40]. (See "Gastrointestinal toxicity of radiation therapy", section on 'Esophagitis'.)
Lymphocytic esophagitisbv Lymphocytic esophagitis is characterized by the presence of a
dense peripapillary lymphocytic infiltrate and peripapillary spongiosis involving the lower twothirds of the esophageal epithelium and the absence of significant neutrophilic or eosinophilic
infiltrates [41]. While lymphocytic esophagitis is being increasingly recognized on histopathology
in adults and has been associated with dysphagia, it is unclear if it is a distinct clinical entity and
its etiology is unknown [42-44].
In one retrospective study of 129,252 adults who had undergone an upper endoscopy, 0.1
percent had lymphocytic esophagitis on biopsy [42]. As compared with patients with normal
esophageal biopsies, patients with lymphocytic esophagitis were significantly more likely to be
older (63 versus 55 years) and to have presented with dysphagia (53 versus 33 percent), and
were significantly less likely to have GERD (19 versus 38 percent).

Infectious esophagitis Patients with infectious esophagitis, especially due to herpes

simplex virus (HSV), usually present with odynophagia and/or dysphagia [45,46]. Other causes
of infectious esophagitis include cytomegalovirus (CMV) and Candida species.
Although Candida species are the most common fungal cause of esophagitis, other fungal
infections including cryptococcosis, histoplasmosis, blastomycosis, and aspergillosis have rarely
been described [47]. Other pathogens, such as mycobacteria and nocardia, occasionally cause
esophagitis [47,48]. (See "Herpes simplex virus infection of the esophagus", section on 'Clinical
manifestations' and "Herpes simplex virus infection of the esophagus", section on
'Diagnosis' and"Clinical manifestations of oropharyngeal and esophageal candidiasis", section
on 'Esophageal candidiasis'.)
Extrinsic causes
Cardiovascular abnormalities A number of vascular anomalies can cause dysphagia by
compressing the esophagus ("dysphagia lusoria") but are rare [49]. Some of the aberrant
vessels form complete rings, while others form incomplete rings around the esophagus [50].
(See "Vascular rings".)
Complete vascular ring anomalies include a double aortic arch, right aortic arch with
retroesophageal left subclavian artery and left ligamentum arteriosum, and right aortic arch
with mirror-image branching and left ligamentum arteriosum [50]. Dysphagia lusoria is
rare. Extrinsic compression of the esophagus may be noted on barium swallow, and the
diagnosis can be established by endoscopic ultrasonography or CT scan [49].
Incomplete vascular ring anomalies include retroesophageal right aberrant subclavian
artery and anomalous left pulmonary artery [50].
In older adults, severe atherosclerosis or a large aneurysm of the thoracic aorta can
result in impingement on the esophagus and produce dysphagia ("dysphagia aortica").
When symptoms are intractable, surgical intervention should be considered. When due to
congenital causes, symptoms usually develop during childhood, but they may also develop in
adults.
Most subjects with an aberrant subclavian artery are symptom-free throughout their lives [51].
However, coughing, dysphagia, thoracic pain, or even Horner's syndrome may develop at an
older age [52]. In infants, there is an increase in pulmonary infections and respiratory
abnormalities.
Enlargement of the left atrium may cause dysphagia in patients with mitral valve disease [53].
This is due to extrinsic compression by the enlarged atrium, resulting in partial luminal
obstruction at the mid to lower third portion of the esophagus [54].
Motility disorders
Achalasia Primary achalasia is a disease of unknown etiology in which there is a loss of
peristalsis in the distal esophagus and a failure of lower esophageal sphincter (LES) relaxation
with swallowing (image 1 andimage 5). (See "Pathophysiology and etiology of achalasia".)

Achalasia is an uncommon disorder that can occur at any age, but is usually diagnosed in
patients between 25 and 60 years. Men and women are affected with equal frequency.
Progressively worsening dysphagia for solids (91 percent) and liquids (85 percent) and
regurgitation of bland undigested food or saliva are the most frequent symptoms in patients with
achalasia. Other symptoms include chest pain, heartburn, and difficulty belching.
Findings on barium esophagram that are suggestive of achalasia include a dilated esophagus
that terminates in a beak-like narrowing, aperistalsis, and poor emptying of barium from the
esophagus. However, barium esophagram may be falsely negative in one-third of patients [55].
Manometry is required to establish the diagnosis of achalasia. Aperistalsis in the distal twothirds of the esophagus and incomplete LES relaxation on conventional manometry are
characteristic of achalasia. (See "Clinical manifestations and diagnosis of achalasia", section on
'Evaluation' and "Clinical manifestations and diagnosis of achalasia", section on 'Diagnosis'.)
Spastic motility disorders Diffuse esophageal spasm (DES), nutcracker esophagus,
hypertensive lower esophageal sphincter, and ineffective esophageal motility can cause
intermittent nonprogressive dysphagia to solids and liquids. Patients may also report associated
chest pain [56]. The barium radiographic picture includes a broad spectrum of severe nonperistaltic contractions, which may produce striking abnormalities in the barium column. These
findings have resulted in descriptions such as "rosary bead" or "corkscrew" esophagus (image
6 and image 7). However, radiographic studies may be entirely normal among patients with DES
or be abnormal in patients with normal motility; as a result, these tests are neither sensitive nor
specific. Manometry is required to establish the diagnosis of a spastic esophageal motility
disorder. The specific manometric criteria to diagnose DES, nutcracker esophagus, and
hypertensive LES are discussed in detail, separately. (See "Esophageal motility disorders:
Clinical manifestations, diagnosis, and management", section on 'Esophageal manometry'.)
Ineffective esophageal motility disorder (IEMD) is defined on manometry by at least 30 percent
of the distal esophageal amplitude contractions below 30 mmHg. In one study, approximately 30

percent of subjects with IEMD reported dysphagia. However, studies using esophageal
intraluminal impedance testing have shown that up to 68 percent of liquid and 59 percent of
viscous swallows in such patients showed normal bolus transit [57]. Overall one-third of patients
had normal bolus transit, suggesting that the manometric diagnosis of IEMD does not always
correlate with the effectiveness of esophageal function.
Systemic sclerosis (scleroderma) Patients with systemic sclerosis often have a history of
heartburn and progressive dysphagia to both solids and liquids secondary to the underlying
motility abnormality or the presence of peptic stricture, which occurs in up to 50 percent of these
patients [58]. The diagnosis of systemic sclerosis is suggested by the presence of skin
thickening and hardening (sclerosis) that is not confined to one area (ie, not localized
scleroderma). The diagnosis is supported by the presence of extracutaneous features and
characteristic serum autoantibodies. (See 'Esophageal stricture' above and "Diagnosis and
differential diagnosis of systemic sclerosis (scleroderma) in adults", section on 'Evaluation for
suspected systemic sclerosis'.)
Esophageal involvement is present in up to 90 percent of patients with systemic sclerosis (table
4) [59-61]. Scleroderma primarily involves the smooth muscle layer of the gut wall, resulting in
atrophy and sclerosis of the distal two-thirds of the esophagus [59]. As a result, the most
common motility abnormalities observed in the distal two-thirds of the esophagus are
aperistalsis or low-amplitude contractions, and low or absent lower esophageal sphincter
pressure [62]. The proximal esophagus (striated muscle) is spared and exhibits normal motility.
(See "Gastrointestinal manifestations of systemic sclerosis (scleroderma)".)
Sjgren's syndrome Approximately three-quarters of patients with Sjgren's syndrome have
associated dysphagia [63,64]. Defective peristalsis has been demonstrated in one-third or more
of patients with primary Sjgrens syndrome [65,66]. Xerostomia appears to exacerbate
swallowing discomfort but does not appear to correlate with dysphagia [63]. The diagnosis of
Sjgrens syndrome is discussed separately. (See "Clinical manifestations of Sjgren's
syndrome: Exocrine gland disease" and "Clinical manifestations of Sjgren's syndrome:
Extraglandular disease", section on 'Gastrointestinal tract' and "Diagnosis and classification of
Sjgren's syndrome", section on 'Diagnosis'.)
Functional dysphagia According to the Rome III criteria, functional dysphagia is defined as
a sense of solid or liquid food lodging (alojada)or passing abnormally through the esophagus,
absence of evidence that GERD is the cause of the symptoms, and absence of a motility
disorder. All criteria must be fulfilled for the past three months with symptom onset at least six
months prior to the diagnosis. [3,67,68].
Symptoms of dysphagia may be intermittent or present after each meal. Patients should be
reassured and instructed to avoid precipitating factors and chew well. In our experience,
symptoms may improve with time. In patients with severe symptoms despite these measures,
treatment with a calcium channel blocker, anticholinergic agent, antidepressant, anxiolytic, or
smooth-muscle relaxant should be considered. Although empiric esophageal dilation with a 50
to 54 F Maloney dilator has been demonstrated to improve symptoms in patients with functional
dysphagia in at least one randomized trial, conflicting results have also been reported [69,70].