Chapter 038. Dysphagia (Part 1) ppsx
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Chapter 038. Dysphagia
(Part 1)
Harrison's Internal Medicine > Chapter 38. Dysphagia
Dysphagia: Introduction
Dysphagia is defined as a sensation of "sticking" or obstruction of the
passage of food through the mouth, pharynx, or esophagus. However, it is often
used as an umbrella term to include other symptoms related to swallowing
difficulty. Aphagia signifies complete esophageal obstruction, which is usually
due to bolus impaction and represents a medical emergency. Difficulty in initiating
a swallow occurs in disorders of the voluntary phase of swallowing. However,
once initiated, swallowing is completed normally. Odynophagia means painful
swallowing. Frequently, odynophagia and dysphagia occur together. Globus
pharyngeus is the sensation of a lump lodged in the throat. However, no difficulty
is encountered when swallowing is performed. Misdirection of food, resulting in
nasal regurgitation and laryngeal and pulmonary aspiration during swallowing, is
characteristic of oropharyngeal dysphagia. Phagophobia, meaning fear of
swallowing, and refusal to swallow may occur in hysteria, rabies, tetanus, and
pharyngeal paralysis due to fear of aspiration. Painful inflammatory lesions that
cause odynophagia may also cause refusal to swallow. Some patients may feel the
food as it goes down the esophagus. This esophageal sensitivity is not associated
with either food sticking or obstruction.
Physiology of Swallowing
The process of swallowing begins with a voluntary (oral) phase that
includes a preparatory phase during which a food bolus suitable for swallowing is
prepared and a transfer phase during which the bolus is pushed into the pharynx
by contraction of the tongue. The bolus then activates oropharyngeal sensory
receptors that initiate the deglutition reflex. The deglutition reflex is centrally
mediated and involves a complex series of events. It serves both to propel food
through the pharynx and the esophagus and to prevent its entry into the airway.
When the bolus is propelled backward by the tongue, the larynx moves forward
and the upper esophageal sphincter (UES) opens. As the bolus moves into the
pharynx, contraction of the superior pharyngeal constrictor against the contracted
soft palate initiates a peristaltic contraction that proceeds rapidly downward to
move the bolus through the pharynx and the esophagus. The lower esophageal
sphincter (LES) opens as the food enters the esophagus and remains open until the
peristaltic contraction has swept the bolus into the stomach. Peristaltic contraction
in response to a swallow is called primary peristalsis. It involves inhibition
followed by sequential contraction of muscles along the entire swallowing
passage. The inhibition that precedes the peristaltic contraction is called
deglutitive inhibition. Local distention of the esophagus from residual food
activates secondary peristalsis.
Muscles of the oral cavity, pharynx, UES, and cervical esophagus are
striated and are directly innervated by the lower motor neurons carried in the
cranial nerves. Oral cavity muscles are innervated by the Vth and the VIIth cranial
nerves and the tongue muscles by the XIIth cranial nerve. Pharyngeal muscles are
innervated by the IXth and the Xth cranial nerves.
The UES consists of constrictor and dilator muscles. The constrictor
muscles include the cricopharyngeus and inferior pharyngeal constrictor muscles.
The dilator muscles include a number of suprahyoid muscles including the
geniohyoid muscle. The constrictor muscles are innervated by the Xth cranial
nerves and the dilator muscles are innervated by the XIIth and also the Vth and the
VIIth cranial nerves. The UES remains closed owing to the elastic properties of its
wall and to neurogenic tonic contraction of the cricopharyngeus muscle. Inhibition
of the vagal excitatory activity in the central nervous system relaxes the
cricopharyngeus, and contraction of the dilator muscles opens the UES by causing
upward and forward displacement of the larynx.
The neuromuscular apparatus for peristalsis is different in cervical and
thoracic parts of the esophagus. The cervical esophagus, like the pharyngeal
muscles, is composed of striated muscles and is innervated by lower motor
neurons in the vagus (Xth cranial) nerve. Peristalsis in the cervical esophagus is
due to sequential activation of the vagal motor neurons in the nucleus ambiguus.
In contrast, the thoracic esophagus and LES are composed of smooth-
muscle fibers and are innervated by excitatory and inhibitory neurons within the
esophageal myenteric plexus. Neurotransmitters of the excitatory nerves are
acetylcholine and substance P, and of the inhibitory nerves are vasoactive
intestinal peptide (VIP) and nitric oxide. Separate groups of parasympathetic
preganglionic nerve fibers in the Xth cranial nerve arising from its dorsal motor
nucleus project onto the inhibitory and excitatory postganglionic myenteric
neurons. Patterned activation of inhibitory followed by excitatory vagal pathways
is responsible for peristalsis, which consists of a sequence of inhibition
(deglutitive inhibition) followed by contraction. The LES relaxes, with deglutitive
inhibition, at the onset of esophageal peristalsis.
The LES is closed at rest because of its intrinsic myogenic tone, influenced
by excitatory and inhibitory nerves. The function of the LES is supplemented by
the striated muscle of the diaphragmatic crura, which surrounds the LES and acts
as an external LES.
