# 40 - 47 Dysphagia

### 47 Dysphagia

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■FURTHER READING
Bunsawat K et al: Exercise intolerance in heart failure with preserved 
ejection fraction: Causes, consequences and the journey toward a 
cure. Exp Physiol 109:502, 2023.
Edwards JA et al: Characteristics and treatment of exercise intolerance 
in patients with long COVID. J Cardiopulm Rehabil Prev 43:400, 2023.
Houstis NE et al: Exercise intolerance in heart failure with preserved 
ejection fraction. Circulation 137:148, 2018.
McCoy J et al: Pathophysiology of exercise intolerance in chronic dis­
eases: The role of diminished cardiac performance in mitochondrial 
and heart failure patients. Open Heart 4:000632, 2017.
Ramirez MF et al: Obesity-related biomarkers are associated with 
exercise intolerance in HFpEF. Circ Heart Fail 16:010618, 2023.
Shah RV et al: Metabolic cost of exercise initiation in patients with 
heart failure with preserved ejection fraction vs community dwelling 
adults. JAMA Cardiol 6:653, 2021.
Section 6	 Alterations in Gastrointestinal 
Function
Ikuo Hirano*, Peter J. Kahrilas

Dysphagia
Dysphagia—difficulty with swallowing—refers to problems with the 
transit of food or liquid from the mouth to the hypopharynx or 
through the esophagus. Severe dysphagia can compromise nutrition, 
cause aspiration, and reduce quality of life. Additional terminology 
pertaining to swallowing dysfunction is as follows. Aphagia (inability 
to swallow) typically denotes complete esophageal obstruction, most 
commonly encountered in the acute setting of a food bolus or foreign 
body impaction. Odynophagia refers to painful swallowing, typically 
resulting from mucosal ulceration within the oropharynx or esopha­
gus. It commonly is accompanied by dysphagia, but the converse is not 
true. Globus pharyngeus is a foreign body sensation localized in the 
neck that does not interfere with swallowing and sometimes is relieved 
by swallowing. Transfer dysphagia frequently results in nasal regurgita­
tion or pulmonary aspiration during swallowing and is characteristic of 
oropharyngeal dysphagia. Phagophobia (fear of swallowing) and refusal 
to swallow may be psychogenic or related to anticipatory anxiety about 
food bolus obstruction, odynophagia, or aspiration.
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■PHYSIOLOGY OF SWALLOWING
Swallowing begins with a voluntary (oral) phase that includes prepara­
tion during which food is masticated and mixed with saliva. This is 
followed by a transfer phase during which the bolus is pushed into the 
pharynx by the tongue. Bolus entry into the hypopharynx initiates the 
pharyngeal swallow response, which is centrally mediated and involves 
a complex series of actions, the net result of which is to propel food 
through the pharynx into the esophagus while preventing its entry 
into the airway. To accomplish this, the larynx is elevated and pulled 
forward, actions that also facilitate upper esophageal sphincter (UES) 
opening. Tongue pulsion then propels the bolus through the UES, fol­
lowed by a peristaltic contraction that clears residue from the pharynx 
and through the esophagus. The lower esophageal sphincter (LES) 
relaxes as the food enters the esophagus and remains relaxed until the 
peristaltic contraction has delivered the bolus into the stomach. Peri­
staltic contractions elicited in response to a swallow are called primary 
peristalsis and involve sequenced inhibition followed by contraction 
of the musculature along the entire length of the esophagus. The 
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■PATHOPHYSIOLOGY OF DYSPHAGIA
Dysphagia can be subclassified both by location and by the circum­
stances in which it occurs. With respect to location, distinct consid­
erations apply to oral, pharyngeal, or esophageal dysphagia. Normal 
transport of an ingested bolus depends on the consistency and size of 
the bolus, the caliber of the lumen, the integrity of peristaltic contrac­
tion, and deglutitive inhibition of both the UES and the LES. Dyspha­
gia caused by an oversized bolus or a narrow lumen is called structural 
dysphagia, whereas dysphagia due to abnormalities of peristalsis or 
impaired sphincter relaxation after swallowing is called propulsive or 
motor dysphagia. More than one mechanism may be operative in a 
patient with dysphagia. Scleroderma commonly presents with absent 
peristalsis as well as a weakened LES that predisposes patients to peptic 
stricture formation. Likewise, radiation therapy for head and neck can­
cer may compound the functional deficits in the oropharyngeal swal­
low attributable to the tumor and cause cervical esophageal stenosis. 
It is worth noting that in addition to bolus transit, symptom reporting 
of dysphagia is dependent upon intact sensory innervation and cen­
tral nervous system perception. Chronicity of motor dysfunction in 
*Deceased.

inhibition that precedes the peristaltic contraction is called degluti­
tive inhibition. Local distention of the esophagus anywhere along its 
length, as may occur with gastroesophageal reflux, activates secondary 
peristalsis that begins at the point of distention and proceeds distally. 
Tertiary esophageal contractions are nonperistaltic, disordered esopha­
geal contractions that may be observed to occur spontaneously during 
fluoroscopic observation.

The musculature of the oral cavity, pharynx, UES, and cervical 
esophagus is striated and directly innervated by lower motor neurons 
carried in cranial nerves (Fig. 47-1). Oral cavity muscles are innervated 
by the fifth (trigeminal) and seventh (facial) cranial nerves; the tongue, 
by the twelfth (hypoglossal) cranial nerve. Pharyngeal muscles are 
innervated by the ninth (glossopharyngeal) and tenth (vagus) cranial 
nerves.
Dysphagia
CHAPTER 47
Physiologically, the UES consists of the cricopharyngeus muscle, 
the adjacent inferior pharyngeal constrictor, and the proximal portion 
of the cervical esophagus. UES innervation is derived from the vagus 
nerve, whereas the innervation to the musculature acting on the UES 
to facilitate its opening during swallowing comes from the fifth, sev­
enth, and twelfth cranial nerves. The UES remains closed at rest owing 
to both its inherent elastic properties and neurogenically mediated 
contraction of the cricopharyngeus muscle. UES opening during swal­
lowing involves both cessation of vagal excitation to the cricopharyn­
geus and simultaneous contraction of the suprahyoid and geniohyoid 
muscles that pull open the UES in conjunction with the upward and 
forward displacement of the larynx.
The neuromuscular apparatus for peristalsis is distinct in proximal 
and distal parts of the esophagus. The cervical esophagus, like the 
pharyngeal musculature, consists of striated muscle and is directly 
innervated by lower motor neurons of the vagus nerve. Peristalsis in 
the proximal esophagus is governed by the sequential activation of 
the vagal motor neurons in the nucleus ambiguus. In contrast, the 
distal esophagus and LES are composed of smooth muscle and are 
controlled by excitatory and inhibitory neurons within the esophageal 
myenteric plexus. Medullary preganglionic neurons from the dorsal 
motor nucleus of the vagus trigger peristalsis via these ganglionic neu­
rons during primary peristalsis. Neurotransmitters of the excitatory 
ganglionic neurons are acetylcholine and substance P; those of the 
inhibitory neurons are vasoactive intestinal peptide and nitric oxide. 
Peristalsis results from the patterned activation of inhibitory followed 
by excitatory ganglionic neurons, with progressive dominance of the 
inhibitory neurons distally. Similarly, LES relaxation occurs with the 
onset of deglutitive inhibition and persists until the peristaltic sequence 
is complete. At rest, the LES is contracted because of excitatory gan­
glionic stimulation and its intrinsic myogenic tone, a property that 
distinguishes it from the adjacent esophagus. The function of the LES 
is supplemented by the surrounding muscle of the right diaphragmatic 
crus, which acts as an external sphincter during inspiration, cough, or 
abdominal straining.

Sagittal view of the pharynx
Musculature of the pharynx
Hard palate
Soft palate
Oral pharynx
Oral cavity
Valeculae
PART 2
Cardinal Manifestations and Presentation of Diseases
Epiglottis
Tongue
Laryngeal
pharynx
(hypopharynx)
Mylohyoid ms
Hyoid bone
Hyoid bone
Esophagus
Thyrohyoid
membrane
Vocal cord
Transverse
arytenoid ms.
Cricothyroid
membrane
Cricoid cartilage
FIGURE 47-1  Sagittal and diagrammatic views of the musculature involved in enacting oropharyngeal swallowing. Note the dominance of the tongue in the sagittal view 
and the intimate relationship between the entrance to the larynx (airway) and the esophagus. In the resting configuration illustrated, the esophageal inlet is closed. This is 
transiently reconfigured such that the esophageal inlet is open and the laryngeal inlet closed during swallowing. (Adapted from PJ Kahrilas, in DW Gelfand and JE Richter 
[eds]: Dysphagia: Diagnosis and Treatment. New York, Igaku-Shoin Medical Publishers, 1989, pp. 11–28.)
combination with defects in peripheral sensory perception may reduce 
patient-reported dysphagia in patients with achalasia.
Oral and Pharyngeal (Oropharyngeal) Dysphagia 
Oral-phase 
dysphagia is associated with poor bolus formation and control so that 
food has prolonged retention within the oral cavity and may seep out of 
the mouth. Drooling and difficulty in initiating swallowing are charac­
teristic signs. Poor bolus control also may lead to premature spillage of 
food into the hypopharynx with resultant aspiration into the trachea, 
evident as swallow-induced cough or regurgitation into the nasal cavity. 
Pharyngeal-phase dysphagia is associated with retention of food in the 
pharynx due to poor tongue or pharyngeal propulsion or obstruction 
at the UES. Signs and symptoms of concomitant hoarseness or cranial 
nerve dysfunction may be associated with oropharyngeal dysphagia 
that is associated with neurologic disorders.
Oropharyngeal dysphagia may be due to neurologic, muscular, 
structural, iatrogenic, infectious, and metabolic causes. Iatrogenic, 
neurologic, and structural pathologies are most common. Iatrogenic 
causes include surgery and radiation, often in the setting of head and 
neck cancer. Neurogenic dysphagia resulting from cerebrovascular 
accidents, Parkinson’s disease, and amyotrophic lateral sclerosis is 
a major source of morbidity related to aspiration and malnutrition. 
Medullary nuclei directly innervate the oropharynx. Lateralization of 
pharyngeal dysphagia implies either a structural pharyngeal lesion or 
a neurologic process that selectively targets the ipsilateral brainstem 
nuclei or cranial nerve. Advances in functional brain imaging have 
elucidated an important role of the cerebral cortex in swallow func­
tion and dysphagia. Asymmetry in the cortical representation of the 
pharynx provides an explanation for the dysphagia that occurs as a 
consequence of unilateral cortical cerebrovascular accidents.
Oropharyngeal structural lesions causing dysphagia include Zenk­
er’s diverticulum, cricopharyngeal bar, and neoplasia. Zenker’s diver­
ticulum typically is encountered in elderly patients. In addition to 
dysphagia, patients may present with regurgitation of particulate 
food debris, aspiration, and halitosis. The pathogenesis is related to 
stenosis of the cricopharyngeus that causes diminished opening of 
the UES and results in increased hypopharyngeal pressure during 
swallowing with development of a pulsion diverticulum immediately 
above the cricopharyngeus in a region of potential weakness known as 
Killian’s dehiscence. A cricopharyngeal bar, appearing as a prominent 

Lateral
pterygoid
plate
Superior constrictor
Stylohyoid process
Digastric (post. belly)
Stylohyoid ligament 
Buccinator
Stylopharyngeus        
Mylohyoid
Glossopharyngeus       
Styloglossus
Digastric
(ant. belly)
Middle constrictor
Hyoglossus
Thyrohyoid membrane
Inferior constrictor
Thyroid cartilage
Cricopharyngeus
Cricothyroid
membrane
Esophagus
Cricoid cartilage
indentation behind the lower third of the cricoid cartilage, is related 
to Zenker’s diverticulum in that it involves limited distensibility of the 
cricopharyngeus and can lead to the formation of a Zenker’s diver­
ticulum. However, a cricopharyngeal bar is a common radiographic 
finding, and most patients with transient cricopharyngeal bars are 
asymptomatic, making it important to rule out alternative etiologies of 
dysphagia before treatment. Furthermore, cricopharyngeal bars may 
be secondary to other neuromuscular disorders that impair opening 
of the UES.
Since the pharyngeal phase of swallowing occurs in less than a 
second, rapid-sequence fluoroscopy is necessary to evaluate functional 
abnormalities. Adequate fluoroscopic examination requires that the 
patient be conscious and cooperative. The study incorporates record­
ings of swallow sequences during ingestion of food and liquids of vary­
ing consistencies. The pharynx is examined to detect bolus retention, 
regurgitation into the nose, or aspiration into the trachea. Timing and 
integrity of pharyngeal contraction and opening of the UES with a 
swallow are analyzed to assess both aspiration risk and the potential 
for swallow therapy. Structural abnormalities of the oropharynx, espe­
cially those that may require biopsies, also should be assessed by direct 
laryngoscopic examination.
Esophageal Dysphagia 
The adult esophagus measures 18–26 cm in 
length and is anatomically divided into the cervical esophagus, extend­
ing from the pharyngoesophageal junction to the suprasternal notch, 
and the thoracic esophagus, which continues to the diaphragmatic 
hiatus. When distended, the esophageal lumen has internal dimensions 
of about 2 cm in the anteroposterior plane and 3 cm in the lateral plane. 
Solid food dysphagia becomes common when the lumen is narrowed 
to <13 mm, but also can occur with larger diameters in the setting of 
poorly masticated food or motor dysfunction. Circumferential lesions 
are more likely to cause dysphagia than are lesions that involve only a 
partial circumference of the esophageal wall. The most common struc­
tural causes of dysphagia are Schatzki’s rings, eosinophilic esophagitis, 
and peptic strictures. Dysphagia also occurs in the setting of gastro­
esophageal reflux disease without a stricture, perhaps on the basis of 
altered esophageal sensation, reduced esophageal mural distensibility, 
or motor dysfunction.
Propulsive disorders leading to esophageal dysphagia result from 
abnormalities of peristalsis and/or deglutitive inhibition, potentially

affecting the cervical or thoracic esophagus. Since striated muscle pathol­
ogy usually involves both the oropharynx and the cervical esophagus, 
the clinical manifestations usually are dominated by oropharyngeal 
dysphagia. Diseases affecting smooth muscle involve both the thoracic 
esophagus and the LES. A dominant manifestation of this, absent peristal­
sis, refers to either the complete absence of swallow-induced contraction 
(absent contractility) or the presence of nonperistaltic, disordered con­
tractions. Absent peristalsis and failure of deglutitive LES relaxation are 
the defining features of achalasia. In distal esophageal spasm (DES), LES 
function is normal, with the disordered motility restricted to the esopha­
geal body. Absent contractility combined with severe weakness of the LES 
is a pattern commonly found in patients with scleroderma.
APPROACH TO THE PATIENT
Dysphagia
Figure 47-2 shows an algorithm for the approach to a patient with 
dysphagia. 
HISTORY
The patient history is extremely valuable in making a presumptive 
diagnosis or at least substantially limiting the differential diagnoses 
in most patients. Key elements of the history are the localization of 
dysphagia, the circumstances in which dysphagia is experienced, 
other symptoms associated with dysphagia, and progression. Dys­
phagia that localizes to the suprasternal notch may indicate either 
an oropharyngeal or an esophageal etiology as distal dysphagia is 
referred proximally about 30% of the time. Dysphagia that local­
izes to the chest is esophageal in origin. Nasal regurgitation and 
tracheobronchial aspiration manifest by coughing with swallow­
ing are hallmarks of oropharyngeal dysphagia. Severe cough with 
swallowing may also be a sign of a tracheoesophageal fistula. The 
presence of hoarseness may be another important diagnostic clue. 
When hoarseness precedes dysphagia, the primary lesion is usually 
laryngeal; hoarseness that occurs after the development of dyspha­
gia may result from compromise of the recurrent laryngeal nerve by 
a malignancy. The type of food causing dysphagia is an important 
Dysphagia localized
to neck, nasal
regurgitation, aspiration,
associated ENT symptoms
Oropharyngeal dysphagia
Esophageal dysphagia
Propulsive
Propulsive
Structural
Structural
Myogenic
Neurogenic
• Cerebral vascular
 accident 
• Parkinson’s
• Amyotropic lateral
 sclerosis
• Brainstem tumor
• Guillain-Barré
• Huntington’s chorea
• Post-polio syndrome
• Multiple sclerosis
• Cerebral palsy
• Zenker’s diverticulum
• Neoplasm
• Cervical web
• Cricopharyngeal bar
• Osteophytes
• Congenital abnormalities
• Post head and neck surgery
• Chemotherapy mucositis
• Radiation
• Corrosive injury
• Infection
• Myasthenia gravis
• Polymyositis
• Mixed connective
 tissue disorders
• Oculopharyngeal
 muscular dystrophy
• Paraneoplastic
 syndrome
• Myotonic dystrophy
• Sarcoidosis
FIGURE 47-2  Approach to the patient with dysphagia. Etiologies in bold print are the most common. ENT, ear, nose, and throat; GERD, gastroesophageal reflux disease.

consideration. Intermittent dysphagia that occurs only with solid 
food implies structural dysphagia, whereas constant dysphagia 
with both liquids and solids strongly suggests an esophageal motor 
abnormality. Two caveats to this pattern are that despite having a 
motor abnormality, patients with scleroderma generally develop 
mild dysphagia for solids only and that patients with oropharyn­
geal dysphagia often have greater difficulty managing liquids than 
solids. Dysphagia that is progressive over the course of weeks to 
months raises concern for neoplasia. Episodic dysphagia to sol­
ids that is unchanged or slowly progressive over years indicates 
a benign disease process such as a Schatzki ring or eosinophilic 
esophagitis. Food impaction with a prolonged inability to pass an 
ingested bolus even with ingestion of liquid is typical of structural 
dysphagia. Chest pain may accompany dysphagia whether it is 
related to motor disorders, structural disorders, or reflux disease. A 
prolonged history of heartburn preceding the onset of dysphagia is 
suggestive of peptic stricture and, infrequently, esophageal adeno­
carcinoma. A history of prolonged nasogastric intubation, esopha­
geal or head and neck surgery, ingestion of caustic agents or pills, 
previous radiation or chemotherapy, or associated mucocutaneous 
diseases may help isolate the cause of dysphagia. With accompany­
ing odynophagia, which usually is indicative of ulceration, infec­
tious or pill-induced esophagitis should be suspected. In patients 
with AIDS or other immunocompromised states, esophagitis due to 
opportunistic infections such as Candida, herpes simplex virus, or 
cytomegalovirus and to tumors such as Kaposi’s sarcoma and lym­
phoma should be considered. A history of atopy increases concerns 
for eosinophilic esophagitis, which is most prevalent in Caucasian 
male patients between the ages of 20 and 40 years. Medication use 
should identify agents associated with pill esophagitis and narcot­
ics that are associated with opioid-induced esophageal dysmotility. 
Dysphagia
CHAPTER 47
PHYSICAL EXAMINATION
Physical examination is important in the evaluation of oral and pha­
ryngeal dysphagia because dysphagia is usually only one of many 
manifestations of a more global disease process. Signs of bulbar 
or pseudobulbar palsy, including dysarthria, dysphonia, ptosis, and 
Dysphagia
Dysphagia localized
to chest or
neck, food impaction
Solid and liquid
dysphagia
Solid
dysphagia
Odynophagia
Intermittent
• Schatzki ring
• Esophageal web 
• Pill esophagitis
• Infectious
 esophagitis
• Caustic injury
• Chemotherapy
 mucositis
• Sclerotherapy
• Crohn’s disease
• Behcet’s syndrome
• Bullous pemphygoid
• Lichen planus
Progressive
• Neoplasm
• GERD with weak
 peristalsis
• Achalasia (primary
 and secondary)
• Diffuse esophageal
 spasm
• Scleroderma
Variable
• Peptic stricture
• Eosinophilic
 esophagitis
• Hiatal hernia
• Extrinsic compression
• Surgical stenosis
• Radiation esophagitis
• Ringed esophagus
• Congenital esophageal
 stenosis