The complaints of dysphagia, odynophagia, or ingested foreign body
immediately implicate the esophagus. The esophagus also is often
the site of pathology in patients presenting with chest pain, upper
GI bleeding (see Chapter 78, Upper Gastrointestinal Bleeding), malignancy, and mediastinitis. Many diseases of
the esophagus can be evaluated over time in an outpatient setting,
but several, such as esophageal foreign body and esophageal perforation,
must be addressed emergently.
The esophagus is a muscular tube approximately 20 to 25 cm long.
The majority of the esophagus is located in the mediastinum, posterior
and slightly lateral to the trachea, with smaller cervical and abdominal
components as well, as shown in Figure 80-1.
There is an outer longitudinal muscle layer and an inner circular
muscle layer. The upper third of the esophagus is made up of striated
muscle. From the lower half down, the esophagus is all smooth muscle
(including the lower esophageal sphincter). The esophagus is lined
with stratified squamous epithelial cells that have no secretory
Anatomic relations of the esophagus (seen from the left
side). The esophagus is about 25 cm (10 in.) long. The distance
from the upper incisor teeth to the beginning of the esophagus (cricoid cartilage)
is about 15 cm (6 in.); from the upper incisors to the level of
the bronchi, 22 to 23 cm (9 in.); and to the cardia, 40 cm (16 in.).
Structures contiguous to the esophagus that affect esophageal function
Two sphincters regulate the passage of material into and out
of the esophagus. The upper esophageal sphincter prevents air from entering
the esophagus and food from refluxing out of the esophagus into
the pharynx. The lower esophageal sphincter regulates the passage
of food into the stomach and prevents stomach contents from refluxing
into the esophagus. The upper sphincter is composed primarily of
the cricopharyngeus muscle. Additional tone is variably provided
by the inferior pharyngeal constrictor muscle and the cervical esophagus.1 The
upper sphincter has a resting pressure of around 100 mm Hg. The
lower sphincter is not discretely identifiable on an anatomic basis.
The smooth muscle of the lower 1 to 2 cm of the esophagus, in combination
with the skeletal muscle of the diaphragmatic hiatus, functions
as the sphincter, with a resting pressure of 25 mm Hg. The pressure
within the resting lower sphincter is a major source of esophageal
symptoms and is discussed below under Gastroesophageal Reflux Disease.
Three major anatomic constrictions exist within the adult esophagus
and are important when there is an esophageal foreign body or food
bolus impaction: at the cricopharyngeus muscle (C6), at the level
of the aortic arch (T4), and at the gastroesophageal junction (T10
to T11). The pediatric esophagus has two additional areas of constriction:
the thoracic inlet (T1) and the tracheal bifurcation (T6). An empty,
collapsed esophagus has no apparent constrictions, and the narrow
areas are only apparent with esophageal filling.
The innervation of the heart mirrors that of the esophagus, and
a convergence of visceral and somatic stimuli occurs within the sympathetic
system. This is the anatomic basis that makes esophageal and cardiac
chest pain notoriously similar, as discussed in the section Chest
Pain of Esophageal Origin.2
The esophageal blood supply is derived from several arterial
sources. The inferior thyroid artery, small branches of the thoracic
aorta, and ascending branches from the left gastric and inferior
phrenic arteries supply the esophagus throughout its length. The
esophageal venous circulation includes a submucosal plexus of veins
that drains into another plexus of veins surrounding the outside
of the esophagus. Blood flows from this outer plexus into the inferior
thyroid, azygos, coronary, and gastric venous systems, the latter
an important link between portal and systemic circulation. Variceal
dilatation of the submucosal system can lead to massive upper GI
bleeding, reviewed in Chapter 78, Upper Gastrointestinal Bleeding.3
Dysphagia is difficulty with swallowing. Most patients with dysphagia
have an identifiable, organic cause.
The two broad pathophysiologic groups of dysphagia are transfer
dysphagia and transport dysphagia.4 Transfer
dysphagia occurs very early in swallowing (as the food
bolus moves from the oropharynx through the upper sphincter) and
is often reported as difficulty in initiating a swallow. Transport
dysphagia is impaired movement of the bolus down the esophagus
and through the lower sphincter. Transport dysphagia is perceived later
in the swallowing process, usually 2 to 4 seconds or longer after
swallowing is initiated, and most commonly results in the feeling of the food’s “getting
stuck.” This initial differentiation between transfer and
transport dysphagia provides a valuable framework regarding the
likely underlying esophageal pathology (Table
80-1). Another useful classification scheme divides dysphagia
into that due to obstructive disease and that due to motor dysfunction. Functional
or motility disorders usually cause dysphagia that is intermittent
and variable. Mechanical or obstructive disease is usually progressive
(difficulty swallowing solids, then liquids).
Table 80-1 Dysphagia
| Save Table
Table 80-1 Dysphagia
|Transfer Dysphagia (Oropharyngeal)||Transport Dysphagia (Esophageal)|
|Discoordination in transferring bolus from pharynx to esophagus||Improper transfer of the bolus from the upper esophagus into
|Swallowing symptoms—gagging, coughing, nasal regurgitation,
inability to initiate swallow, need for repeated swallows||Swallowing symptoms—food “sticking,” retrosternal
fullness with solids (and eventually liquids), possibly odynophagia|
|Risk of aspiration present||Risk of aspiration present, generally less pronounced than
in transfer dysphagia|
|Long term—weight loss, malnutrition, chronic bronchitis,
asthma, multiple episodes of pneumonia||Long term—malnutrition, dehydration, weight loss,
systemic effects of cancer|
|Neuromuscular disease (80%)—cerebrovascular
accident, polymyositis and dermatomyositis, scleroderma, myasthenia
gravis, tetanus, Parkinson’s disease, botulism, lead poisoning,
thyroid disease||Obstructive disease (85%)—foreign body,
carcinoma, webs, strictures, thyroid enlargement, diverticulum,
congenital or acquired large-vessel abnormalities|
|Localized disease—pharyngitis; aphthous ulcers;
candidal infection; peritonsillar and ...|
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