Chapter 038. Dysphagia (Part 3) potx

Chapter 038. Dysphagia
(Part 3)

Oropharyngeal motor dysphagia results from impairment of the voluntary
effort required in bolus preparation or neuromuscular disorders affecting bolus
preparation, initiation of the swallowing reflex, timely passage of food through the
pharynx, and prevention of entry of food into the nasal and the laryngeal opening.
Paralysis of the suprahyoid muscles leads to loss of opening of the UES and
severe dysphagia. Because each side of the pharynx is innervated by ipsilateral
nerves, a unilateral lesion of motor neurons leads to unilateral pharyngeal
paralysis.
Neuromuscular disorders causing dysphagia are listed in Table 38-1. They
include a variety of cortical and suprabulbar disorders, lesions of the cranial
nerves in their nuclei in the brain stem or their course to the muscles, defects of
neurotransmission at the motor end plates, and muscular diseases. Some of these
disorders also involve laryngeal muscles and vocal cords, causing hoarseness.
Since the oropharyngeal phase of swallowing lasts no more than a second,
rapid-sequence videofluoroscopy is necessary to permit detection and analysis of
abnormalities of oral and pharyngeal function. However, such studies can only be
performed in a fully conscious and cooperative patient. A videofluoroscopic
swallowing study (VFSS) using barium of different consistencies may reveal
difficulties in the oral phase of swallowing. The pharynx is examined to detect
stasis of barium in the valleculae and pyriform sinuses and regurgitation of barium
into the nose and tracheobronchial tree. Pharyngeal contraction waves and
opening of UES with a swallow are carefully monitored. Manometric studies may
demonstrate reduced amplitude of pharyngeal contractions and reduced UES
pressure without further fall in pressure on swallowing (see Fig. 286-3). General
treatment consists of maneuvers to reduce pharyngeal stasis and to enhance airway
protection under the direction of a trained swallow therapist. Feeding by a naso-
gastric tube or an endoscopically placed gastrostomy tube may be necessary for
nutritional support; however, these maneuvers do not provide protection against

aspiration of salivary secretions. Gastrostomy tube feeding may actually increase
gastroesophageal reflux and lead to more aspiration. Jejunostomy tube feeding
may lessen reflux.
Dysphagia resulting from a cerebrovascular accident usually improves with
time, although often not completely. Patients with myasthenia gravis (Chap. 381)
and polymyositis (Chap. 383) may respond to treatment of the primary disease.
Cricopharyngeal myotomy is usually not helpful. Extensive operative procedures
to prevent aspiration are rarely needed. Death is often due to pulmonary
complications.
A cricopharyngeal bar results from failure of the cricopharyngeus to relax
but with normal activity of the suprahyoid muscles on swallowing. Barium
swallow shows a prominent projection on the posterior wall of the pharynx at the
level of the lower part of the cricoid cartilage (see Fig. 286-1).
A transient cricopharyngeal bar is seen in up to 5% of individuals without
dysphagia undergoing upper gastrointestinal studies; it can be produced in normal
individuals during a Valsalva maneuver. A persistent cricopharyngeal bar may be
caused by fibrosis in the cricopharyngeus.
Cricopharyngeal myotomy may be helpful in severely symptomatic case
with functional evidence of obstruction by the cricopharyngeus muscle, but is
contraindicated in the presence of gastroesophageal reflux because it may lead to
pharyngeal and pulmonary aspiration.
Globus pharyngeus mainly occurs in individuals with emotional disorders,
particularly in women. Results of barium studies and manometry are normal.
Treatment consists primarily of reassurance. Some patients with globus
pharyngeus have associated reflux esophagitis, and they may respond to treatment
of the esophagitis.

ESOPHAGEAL DYSPHAGIA

In an adult, the esophageal lumen can distend up to 4 cm in diameter. When

the esophagus cannot dilate beyond 2.5 cm in diameter, dysphagia to normal solid
food can occur. Dysphagia is always present when the esophagus cannot distend
beyond 1.3 cm.
Circumferential lesions produce dysphagia more consistently than do
lesions that involve only a portion of circumferences of the esophageal wall, as
uninvolved segments retain their distensibility.
The esophageal causes of mechanical dysphagia are listed in Table 38-2.
Common causes include carcinoma, peptic and other benign strictures, and lower
esophageal ring. Esophageal motor dysphagia may result from abnormalities in
peristalsis and deglutitive inhibition due to diseases of the esophageal striated or
smooth muscle.