Esophagus - Anatomy and Development - GI Motility Online

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Review
PART 1 Oral cavity, pharynx and esophagus
GI Motility online (2006) doi:10.1038/gimo6

Published 16 May 2006
Esophagus - anatomy and development

Braden Kuo, M.D. and Daniela Urma, M.D.
About the contributors (/gimo/contents/pt1/authors/gimo6.html)
View article related content (#relatedcontent)
Key Points
The adult human esophagus is an 18- to 25-cm long muscular tube that has
cervical, thoracic, and abdominal parts.
The esophagus wall is composed of striated muscle in the upper part, smooth
muscle in the lower part, and a mixture of the two in the middle.
The myenteric plexus is well developed in the smooth muscle, but is also present in
the striated muscle part of the esophagus.
The function of the myenteric plexus in the striated esophagus is not well
understood.
Esophagus develops from foregut and by week 10 is lined by ciliated epithelial cells.
Beginning at 4 months, the ciliated epithelium starts to be replaced by squamous

epithelium. At either end of the esophagus the ciliated epithelium gives rise to
esophageal glands.
The upper esophagus is derived from branchial arches 4, 5, and 6, but the
derivation of the lower esophagus is not known.
The development of various elements of esophageal wall requires coordination of a

variety of genes and mediators.
Esophageal peristalsis appears in the first trimester, and gastroesophageal reflux

can be documented in the second trimester.
Introduction
From mouth to stomach, the food conduit consists of the oral cavity, pharynx, and
esophagus. The esophagus serves as a dynamic tube, pushing food toward the stomach,
where digestion and absorption can take place. Mucus produced by the esophageal mucosa
provides lubrication and eases the passage of food. Active peristaltic contractions propel
residual material from the esophagus into the stomach. During vomiting and reflux, the
esophagus also serves as a passageway for gastrointestinal (GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) ) contents traveling
retrograde from the stomach or small intestine.
Embryology
The first stages of life are divided into the embryonic and fetal periods. The embryonic
period extends from fertilization to week 9. The fetal period lasts from the end of the week
9 to birth. From days 0 to 14, the human embryo develops into a bilaminar disk of
ectoderm and endoderm, with the endoderm forming the lining of the yolk sac. The
endoderm is the scaffold for the future digestive tract. The ectoderm gives rise to
epidermis and neural plates. Through the neurulation process, the neural plates evolve to
neural tube and neural crest cells. The neural tube is the precursor for the spinal cord and
brain. The neural crest cells, placed between the dorsal neural tube and the overlying
epidermis, migrate out to form the peripheral nervous system by week 4. On day 15, the
third embryonic layer, the mesoderm, appears and provides the substrate for the
connective tissue, angioblasts, smooth muscle, and serosal layers of the gut. By day 21, the
mesoderm is thickened and forms longitudinal masses called the paraxial mesoderm. By
day 28, the paraxial mesoderm fragments progressively from cranial to caudal into cubes
of tissue called somites. This process ends with the formation of 33 to 35 somites by day 31
of embryo development.1 (#B1)
Mesoderm proliferation and segmentation, which takes place between the endoderm and
ectoderm, induces numerous transformations in the endoderm.2 (#B2) At the same time,
the human embryo elongates craniocaudally and folds laterally. The dorsal part of the yolk
sac, composed of endoderm, is compressed by the lateral folding of the embryo and is
incorporated as a rim during the fourth week. Thus the human embryo becomes a "body
cylinder" dividing the yolk sac into intraembryonic and extraembryonic parts.3 (#B3) The
intraembryonic part is the origin of digestive tube and its accessory glands. The
extraembryonic part regresses and disappears around week 12. At this point, the early
digestive system divides into foregut, midgut, and hindgut.
Gut development takes place in four major patterned axes: anterior-posterior, dorsal-
ventral, left-right, and craniocaudal. Each axis development is based on the epithelial-
mesenchymal interactions mediated by specific molecular pathways.4 (#B4) Thus, growth
factors such as Wnt5a (expressed by mesoderm), endodermal proteins Six2/Sox2, as well
as Hoxa-2, Hoxa-3, and Hoxb-4 control esophageal development in the anterior-posterior
axis.5 (#B5) These factors affect both the esophageal environment and the neural crest cells
by making the environment more permissive for neural crest cells and by preparing the
neural crest cells to migrate within the esophagus4, (#B4) 5 (#B5) (Figure 1 (#f1) ).
Figure 1: Primordial gut. (/gimo/contents/pt1/fig_tab/gimo6_F1.html)

(/gimo/contents/pt1/fig_tab/gimo6_F1.html)
a: Lateral view of a 4-week embryo showing the
relationship of primordial gut to yolk sac. b: Drawing of
median section of the embryo showing the early digestive
system and its blood supply. The primordial gut is a long
tube extending the length of the embryo. Its blood vessels
are derived from the vessels that supplied the yolk sac.
(Source: Moore KL, Persaud TVN. The Developing
Human, 7th ed. Philadelphia: Elsevier, Inc., 2003:256).
Full size image (49 KB)

Download PowerPoint slide (684 KB)
(/gimo/contents/pt1/slides/gimo6-pf1.ppt)
During week 4, the foregut develops a small diverticulum on its ventral surface adjacent to
the pharyngeal gut. This tracheobronchial diverticulum subsequently elongates and
separates gradually from the dorsal foregut through the formation of the esophagotracheal
septum to become the primitive respiratory tract.
The remaining part of the foregut rapidly elongates with the craniocaudal growth of the
embryonic body. In the seventh and eighth weeks, the luminal epithelium proliferates and
almost completely occludes the foregut with only residual channels persisting. Unlike
other species, complete occlusion of the foregut has not been observed in human
embryos.6 (#B6) By week 10, new vacuoles appear in the luminal cells of the foregut and
coalesce to form a single esophageal lumen with a superficial layer of ciliated epithelial
cells.1 (#B1)
During the fourth month, a stratified squamous epithelium begins to replace the ciliated
epithelium, a process that continues until birth. Residual islands of ciliated epithelium at
the proximal and distal ends of the esophagus remain and give rise to esophageal glands.1
(#B1) Thus the primitive foregut endoderm is the origin for both the future esophageal
epithelium and submucosal glands. During week 6 of gestation, the circular muscle coat
and ganglion cells of the myenteric plexus form. During week 7, blood vessels enter the
submucosa.
The smooth muscle of the lower esophagus and the lower esophageal sphincter (LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) ) are derived from
the mesenchyme of the somites surrounding the foregut. The striated muscle forming the
muscularis propria of the upper part of the esophagus and the upper esophageal sphincter
is derived from mesenchyme of the branchial arches 4, 5, and 6. This origin explains the
upper esophageal sphincter innervation by the vagal nerve (the branchial arch 5 nerve)
and by the recurrent laryngeal nerve (a branch of the vagus nerve, the branchial arch 6
nerve). The embryologic origin of the gastroesophageal junction is still controversial, but
gastric rotation together with augmentation of the fundus of the stomach are believed to
determine its formation.7 (#B7)
The middle third of esophagus consists of a mixture of smooth and skeletal muscle. The
origin of this mixture is controversial, with somites and endoderm influencing each other
by molecular mechanisms.4 (#B4) It was suggested that esophageal striated muscle arises
from the smooth muscle by a process of transdifferentiation, however, it appears that the
two muscle types may arise from two distinct differentiation pathways. When definitive
endoderm was co-cultured with somitic mesoderm, it stimulated more smooth muscle
development than skeletal muscle from the mesenchymal somitic cells.8 (#B8)
The smooth muscle differentiation begins after the neural crest cells colonize the gut and
maturates on the rostrocaudal axis.9 (#B9) Whether the circular muscle layer precedes or
appears at the same time as the longitudinal muscle layer is still controversial, but both
layers have been reported to mature into a rostrocaudal axis by week 9.9, (#B9) 10 (#B10)
At the beginning of week 4, the neural crest cells enter the foregut and migrate
rostrocaudally to reach the terminal hindgut by week 7 and give rise to the myenteric
plexus.10 (#B10) By week 6, the neural crest cells migrate centripetally through the circular
muscle layer, giving rise to submucosal plexus.
Interstitial cells of Cajal (ICC

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) ) emerge from gut
mesenchyme around week 9. By week 14, the ICC
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) s form a network
surrounding the myenteric plexus.9, (#B9) 10 (#B10) The ICC
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) s are gut-pacemakers
crucial to the generation of slow wave contractions and to neural transmission within the
gut. The ICC (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) s form
after the differentiation of smooth muscle layers. Whether ICC
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) differentiation
requires neural crest cells has not been clearly established yet, and some recent studies
identified ICC (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) in the
absence of neural crest cells.9, (#B9) 11, (#B11) 12 (#B12)
The development of concentric layers of smooth muscle, ICC

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df6) s, and neural crest
cells (as precursors of the enteric nervous system) is a coordinated process, controlled by
numerous genes and signaling molecules including transcription factors (e.g., Phox2b,
Sox10, Pax3, Mash1), components of the RET (RET proto-oncogene ) and
ET(Endothelin)-3/EDNRB (endothelin receptor type B ) signaling pathways, secreted
proteins (Hedgehog, BMPs(bone morphogenetic proteins)), neurotrophic factors (e.g.,
neurotrophin-3), and extracellular matrix (ECM) molecules (e.g., laminin).9, (#B9) 13,
(#B13) 14, (#B14) 15, (#B15) 16 (#B16) Perturbations in this coordinated process could result in
clinical morbidities such as Hirschsprung disease, where the hindgut (usually colon) is
devoid of enteric neurons and glial cells.17 (#B17)
The myenteric plexus has cholinesterase activity by week 9.5 and ganglion cells are
differentiated by week 13. Several investigators have suggested that the esophagus is
capable of peristalsis in the first trimester.18 (#B18) Three different esophageal motility
patterns have been described in the second trimester: simultaneous opening of the
esophageal lumen from the oropharynx to the lower esophageal sphincter, propulsive
peristaltic contractions, and reflux from stomach into the esophagus.19 (#B19) Although
peristaltic movements have been observed in ultrasound images during the second
trimester, at birth the propagation of the peristalsis along the esophagus and at the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is immature,
resulting in frequent regurgitation of food during the newborn period. The pressure at the
LES (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) approaches that
of the adult at 3 to 6 weeks of age.6 (#B6)
Adult Anatomy
Gross Anatomy
The esophagus is a flattened muscular tube of 18 to 26 cm from the upper sphincter to the
lower sphincter. Between swallows the esophagus is collapsed but the lumen can distend to
approximately 2 cm in the anterior-posterior dimension and up to 3 cm laterally to
accommodate a swallowed bolus.20 (#B20)
The esophagus connects the pharynx to the stomach. Beginning in the neck, at the
pharyngoesophageal junction (C5-6 vertebral interspace at the inferior border of the
cricoid cartilage), the esophagus descends anteriorly to the vertebral column through the
superior and posterior mediastinum. After traversing the diaphragm at the diaphragmatic
hiatus (T10 vertebral level) the esophagus extends through the gastroesophageal junction
to end at the orifice of the cardia of the stomach (T11 vertebral level).
Topographically, there are three distinct regions: cervical, thoracic, and abdominal. The
cervical esophagus extends from the pharyngoesophageal junction to the suprasternal
notch and is about 4 to 5 cm long. At this level, the esophagus is bordered anteriorly by the
trachea, posteriorly by the vertebral column, and laterally by the carotid sheaths and the
thyroid gland.
The thoracic esophagus extends from the suprasternal notch to the diaphragmatic hiatus,
passing posterior to the trachea, the tracheal bifurcation, and the left main stem bronchus.
The esophagus lies posterior and to the right of the aortic arch at the T4 vertebral level.
From the level of T8 until the diaphragmatic hiatus the esophagus lies anteriorly to the
aorta.
The abdominal esophagus extends from the diaphragmatic hiatus to the orifice of the
cardia of the stomach. Forming a truncated cone, about 1 cm long, the base of the
esophagus transitions smoothly into the cardiac orifice of the stomach. The abdominal
esophagus lies in the esophageal groove on the posterior surface of the left lobe of the liver.
Two high-pressure zones prevent the backflow of food: the upper and lower esophageal
sphincter. These functional zones are located at the upper and lower ends of the esophagus
but there is not a clear anatomic demarcation of the limits of the sphincters.
Structurally, the esophageal wall is composed of four layers: innermost mucosa,

submucosa, muscularis propria, and adventitia. Unlike the remainder of the GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) tract, the esophagus
has no serosa.
On endoscopy, the esophageal lumen appears as a smooth, pale pink tube with visible
submucosal blood vessels. The transition from esophageal to gastric mucosa is known as
the Z-line and consists of an irregular circumferential line between two areas of different
colored mucosa. The gastric mucosa is darker than the pale pink esophageal mucosa.
Peristaltic waves can be seen during endoscopic examination.
Blood Supply
The rich arterial supply of the esophagus is segmental (Figure 2 (#f2) ). The branches of
the inferior thyroid artery provide arterial blood supply to the upper esophageal sphincter
and cervical esophagus. The paired aortic esophageal arteries or terminal branches of
bronchial arteries supply the thoracic esophagus. The left gastric artery and a branch of the
left phrenic artery supply the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) and the most distal
segment of the esophagus. The arteries supplying the esophagus end in an extensive, dense
network in the submucosa. The copious blood supply and network of potentially
anastomotic vessels may explain the rarity of the esophageal infarction.
Figure 2: Arterial blood supply of the esophagus

(Source: Netter medical illustration with permission from
Elsevier. All rights reserved.)

Download PowerPoint slide (3,186 KB)
The venous supply is also segmental. (Figure 3 (#f3) ). From the dense submucosal
plexus the venous blood drains into the superior vena cava. The veins of the proximal and
distal esophagus drain into the azygous system. Collaterals of the left gastric vein, a branch
of the portal vein, receive venous drainage from the mid-esophagus. The submucosal
connections between the portal and systemic venous systems in the distal esophagus form
esophageal varices in portal hypertension. These submucosal varices are sources of major
GI (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) hemorrhage in
conditions such as cirrhosis.
Figure 3: Venous drainage of the esophagus


Innervation
The esophagus, like the rest of the viscera, receives dual sensory innervation, traditionally
referred to as parasympathetic and sympathetic, but more properly based on the actual
nerves, vagal, and spinal21 (#B21) (Figure 4 (#f4) ).
Figure 4: Parasympathetic and sympathetic innervation of the

esophagus (/gimo/contents/pt1/fig_tab/gimo6_F4.html)

The vagal afferent neurons compose 80% of the vagal trunk and have cell bodies in the
nodose ganglia and project to the nucleus solitarius.22 (#B22) Vagal afferents merging from
the esophageal smooth muscle layer are sensitive to mechanical distention, whereas
polymodal (responding to multiple modalities of stimuli) vagal afferents with receptive
fields in the mucosa are sensitive to various osmo-, chemo-, thermo-, and mechanical
intraluminal stimuli.22 (#B22) In general, vagal afferents do not play a direct role in
visceral pain transmission, but through mechanoceptors vagal afferents transduce
pressure into painful sensations.21 (#B21)
The spinal afferents have their cell bodies in the dorsal root ganglia and terminate in the
spinal column and in the nucleus gracilis and cuneatus in the brainstem. From there, they
project, through the thalamus, to primary sensory and insular cortical areas.23 (#B23) The
spinal afferents merging from nerve endings in the muscle layer and serosa act as
nociceptors for perception of discomfort and pain and are mechanosensitive.24 (#B24) The
spinal afferents merging from intraepithelial nerve endings are involved in mediating acid-
induced pain during topical exposure to intraluminal acid.25 (#B25) Many of the spinal
afferents contain calcitonin gene-related peptide and substance P, which are
neurotransmitters that are important in mediating visceral nociception.21, (#B21) 22 (#B22)
The motor innervation of the esophagus is predominantly via the vagus nerve. The cell
bodies of the vagal efferent fibers innervating the upper esophageal sphincter and the
proximal striated muscle esophagus arise in the nucleus ambiguus, whereas fibers
destined for the distal smooth-muscle segment and the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) originate in the
dorsal motor nucleus of the vagus nerve.
The esophagus receives parasympathetic and sympathetic innervation that regulates

glandular secretion, blood vessel caliber, and the activity of striated and smooth muscle.
The parasympathetic nerve supply comes from the nucleus ambiguus and dorsal motor
nucleus of the vagus nerve and provides motor innervation to the esophageal muscular
coat and secretomotor innervation to the glands. The sympathetic nerve supply comes
from the cervical and the thoracic sympathetic chain (spinal segments T1–T10) and
regulates blood vessel constriction, esophageal sphincters contractions, relaxation of the
muscular wall, and increases in glandular and peristaltic activity.
The thin nerve fibers and numerous ganglia of the intramural myenteric and the
submucosal plexi provide the intrinsic innervation of the esophagus. The ganglia that lie
between the longitudinal and the circular layers of the tunica muscularis form the
myenteric or Auerbach's plexus, whereas those that lie in the submucosa form the
submucous or Meissner's plexus. Auerbach's plexus regulates contraction of the outer
muscle layers, whereas Meissner's plexus regulates secretion and the peristaltic
contractions of the muscularis mucosae. A network of fibers interconnects these two
plexi.28 (#B28) The ganglia of the myenteric plexus are more numerous in the smooth
muscled esophagus than in the striated muscle esophagus.29 (#B29) In the smooth muscled
esophagus, the neurons of the myenteric plexus are relay neurons between the vagus and
the smooth muscle. In the striated muscle the role of the neurons of the myenteric plexus
is largely unknown.30 (#B30)
Positron emission tomography (PET

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df9) ) and functional
magnetic resonance imaging (fMRI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df3) ) have been used to
map the central nervous system projections from the esophagus. Esophageal stimulation
at the subliminal and liminal levels is sensed peripherally and transmitted to the brain for
further processing and modulation. Esophageal sensory innervation is carried by the vagus
nerve to the nodose ganglion and projects through the brainstem, through the thalamus, to
terminate in the cortex.26, (#B26) 27 (#B27) Regions that are activated by esophageal
stimulation include secondary sensory and motor cortex, parieto-occipital cortex, anterior
and posterior cingulated cortex, prefrontal cortical cortex, and the insula.31 (#B31)
Lymphatics
Lymphatic drainage in the esophagus consists of two systems: the lymph channels and
lymph nodules. (Figure 5 (#f5) ).
Figure 5: Lymphatic drainage (/gimo/contents/pt1/fig_tab/gimo6_F5.html)


The lymph channels begin in the esophageal tissue space as a network of endothelial
channels (20–30 m) or as blind endothelial sacculations (40–60 m).32 (#B32) The
location of the lymphatic capillary origin is not known precisely. Some authors propose
that precapillary spaces exist in the lamina mucosa, but others contend that there is an
absence of true lymphatic capillaries in the upper and middle levels of the lamina
mucosa.6 (#B6) Electron microscopic studies show anastomotic lymph capillaries in the
lower mucosal levels and small lymphatic vessel in the submucosa.
Lymph capillaries drain into collecting lymph channels (100–200 m) that continue
through the esophageal muscular coat and are distributed parallel to the long axis of the
esophagus. Paired semilunar valves within the collecting channels determine the direction
of flow. The collecting lymph channels merge into small trunks that open into the regional
lymph nodes.
As with esophageal innervation, the lymphatic drainage of the esophagus differs in the
striated and smooth muscle regions. The lymphatics from the proximal third of the
esophagus drain into the deep cervical lymph nodes, and subsequently into the thoracic
duct. The lymphatics from the middle third of esophagus drain into the superior and
posterior mediastinal nodes. Lymphatics of the distal third of the esophageal follow the left
gastric artery to the gastric and celiac lymph nodes. There are considerable
interconnections among these three drainage regions primarily owing to the dual
embryologic origin of lymphatic pathways from branchiogenic and body mesenchyme.7,
(#B7) 32 (#B32) The bidirectional lymph flow in this region is responsible for the spread of
malignancy from the lower esophagus to the upper esophagus.

Musculature of the Esophagus
The muscular coat consists of an external layer of longitudinal fibers and an internal layer
of circular fibers (Figure 6 (#f6) ). The longitudinal fibers are arranged proximally in
three fasciculi. The ventral fasciculus is attached to the vertical ridge on the posterior
surface of the lamina of the cricoid cartilage by the tendocricoesophageus. The two lateral
fasciculi are continuous with the muscular fibers of the pharynx. The longitudinal fibers
descend in the esophagus and combine to form a uniform layer that covers the outer
surface of the esophagus.
Figure 6: Musculature of the esophagus


The circular muscle layer provides the sequential peristaltic contraction that propels food
toward the stomach. The circular fibers are continuous with the inferior constrictor muscle
of the hypopharynx; they run transverse at the cranial and caudal regions of the
esophagus, but oblique in the body of the esophagus. The internal muscular layer is thicker
than the external muscular layer. Below the diaphragm, the internal circular muscle layer
thickens and the fibers become semicircular and interconnected, constituting the intrinsic
component of the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) .
Accessory bands of muscle connect the esophagus and the left pleura to the root of the left
bronchus and the posterior of the pericardium. The muscular fibers in the cranial part of
the esophagus are red and consist chiefly of striated muscle; the intermediate part is
mixed; and the lower part, with rare exceptions, contains only smooth muscle.
Upper Esophageal Sphincter
The upper esophageal sphincter (UES

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df10) ) is a high-pressure
zone situated between the pharynx and the cervical esophagus (Figure 7 (#f7) ). The UES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df10) is a
musculocartilaginous structure composed of the posterior surface of the thyroid and
cricoid cartilage, the hyoid bone, and three muscles: cricopharyngeus, thyropharyngeus,
and cranial cervical esophagus. Each muscle plays a different role in UES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df10) function.33 (#B33)
These three muscles spread upward, posteriorly, where they insert into the esophageal
submucosa after crossing the muscle bundles of the opposite side. The thyropharyngeus
muscle is obliquely oriented, whereas the cricopharyngeus muscle is transversely oriented.
Between these two muscles, there is a zone of sparse musculature—the Killian's triangle,
from which Zenker's diverticulum might emerge.
Figure 7: Upper esophageal sphincter and upper esophageal

musculature (/gimo/contents/pt1/fig_tab/gimo6_F7.html)

The cricopharyngeus (CP

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df1) ) muscle is a striated
muscle attached to the cricoid cartilage. It forms a C-shaped muscular band that produces
maximum tension in the anteroposterior direction and less tension in lateral direction.34
(#B34) Structurally, biochemically, and mechanically, the CP
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df1) is different from the

surrounding pharyngeal and esophageal muscles. It is composed of a mixture of fast- and
slow-twitch fibers, with the slow fibers being predominant and having a diameter of 25 to
35 m. The CP (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df1) is
suspended between the cricoid processes, surrounds the narrowest part of pharynx, and
extends caudally where it blends with the circular muscle of the cervical esophagus.
The cervical esophagus contains predominantly striated muscle fibers, but occasionally
smooth fibers are found in the center of the muscle.33 (#B33) The muscle fibers are
arranged in two layers: the external layer containing longitudinal arranged fibers, and the
internal layer containing circular or transversely arranged fibers. The external longitudinal
layer of the cervical esophagus originates from the dorsal plane of the cricoid cartilage
constituting a sparse muscle area: the Laimer's triangle. The external longitudinal layer
courses down the length of the entire esophagus. At its distal end the longitudinal fibers
become more oblique and end along the anterior and posterior gastric wall.35 (#B35) The
internal circular layer of muscle originates at the level of cricoid cartilage and in
descending forms incomplete circles.35 (#B35)
Upper esophageal sphincter function is controlled by a variety of reflexes that involve

afferent inputs to the motor neurons innervating the sphincter. These reflexes elicit either
contraction or relaxation of the tonic activity of the UES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df10) . Inability of the
sphincter to open or discoordination of timing between the opening of the UES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df10) with the pharyngeal
push of ingested contents leads to difficulty in swallowing known as oropharyngeal
dysphagia.33 (#B33)
Lower Esophageal Sphincter
The lower esophageal sphincter is a high-pressure zone located where the esophagus
merges with the stomach (Figure 8 (#f8) ). The LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is a functional unit
composed of an intrinsic and an extrinsic component. The intrinsic structure of LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) consists of
esophageal muscle fibers and is under neurohormonal influence. The extrinsic component
consists of the diaphragm muscle, which functions as an adjunctive external sphincter that
raises the pressure in the terminal esophagus related to the movements of respiration.
(Figure 9 (#f9) ). Malfunction in any of these two components is the cause of
gastroesophageal reflux and its subsequent symptoms and mucosal changes.36 (#B36)
Figure 8: Gastroesophageal mucosal junction and muscular

arrangement at the lower esophagus

Figure 9: Diaphragmatic crura and esophageal opening viewed from

below (a) and as viewed from above (b).
The esophageal opening is created by a loop of right crux
of the diaphragm. (Source: Netter medical illustration with
permission from Elsevier. All rights reserved.)

The intrinsic component of the LES

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is composed of
circular layers of the esophagus, clasp-like semicircular smooth muscle fibers on the right
side, and sling-like oblique gastric muscle fibers on the left side.37 (#B37) The circular
muscles of the LES (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7)
are thicker than the adjacent esophagus. The clasp-like semicircular fibers have significant
myogenic tone but are not very responsive to cholinergic stimulation, whereas the sling-
like oblique gastric fibers have little resting tone but contract vigorously to cholinergic
stimulation.37 (#B37)
The extrinsic component of the LES

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is composed of the
crural diaphragm, which forms the esophageal hiatus, and represents a channel through
which the esophagus enters into the abdomen. The crural diaphragm encircles the
proximal 2 to 4 cm of the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) , and determines
inspiratory spike-like increases in LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) pressure as
measured by esophageal manometry.38 (#B38)
The endoscopic localization of the LES

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is different from the
manometric localization. The endoscopic localization of the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is presumably
determined by changes in the esophageal mucosa color owing to transition from
nonstratified squamous esophageal epithelium to the gastric mucosa, changes known as
the Z-line. A study correlating manometric and endoscopic localization of the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) (Z-line) found that
the functional location of LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) was 3 cm distal to the
Z-line.39, (#B39) 40 (#B40)
Three-dimensional (3D) manometric measures of the lower esophageal high-pressure zone

showed a marked radial and longitudinal asymmetry, with higher pressures toward the left
posterior direction. Radial pressures peak at the respiratory inversion point during
esophageal manometry where inspiration converts from a positive pressure as measured
by pressure sensors to a negative pressure as the pressure sensor enters the intrathoracic
cavity. The high-pressure zone appears to coincide with asymmetric thickening of the
muscular layer at the gastroesophageal junction, which corresponds to the gastric "sling"
fibers and to the semicircular "clasp" fibers.41 (#B41)
The LES (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is

innervated by both parasympathetic (vagus) and sympathetic (primarily splanchnic)
nerves, with the vagal pathways being essential for reflex relaxation of LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) .42 (#B42) Vagal
sensory afferents from the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) and distal esophagus
end in nucleus tractus solitarius of the hindbrain. The motor innervation of the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is topographically
provided through preganglionic fibers from the dorsal motor nucleus of the vagus. The
dorsal motor nucleus and the tractus solitarius nucleus form a dorsal vagal complex in the
hindbrain that coordinates reflex control of the sphincter.42 (#B42)
Histology
Light Microscopy
The wall of the esophagus consists of four layers: mucosa, submucosa, muscularis propria,
and adventitia. Unlike other areas of the GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) tract, the esophagus
does not have a distinct serosal covering. This allows esophageal tumors to spread more
easily and makes them harder to treat surgically.43 (#B43) The missing serosal layer also
makes luminal disruptions more challenging to repair.
The mucosa is thick and reddish cranially and more pale caudally. It is arranged in
longitudinal folds that disappear upon distention. It consists of three sublayers:
Mucous membrane: a nonkeratinized squamous epithelium. It covers the entire

inner surface of the esophagus, except the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) , where both
squamous and columnar epithelium may coexist. The mucous membrane is
composed of
stratum basale, including basophilic cells that can divide and replenish the
superficial layers
stratum intermedium
stratum superficialis.
Lamina propria: a thin layer of connective tissue
Muscularis mucosa: a thin layer of longitudinally, irregularly arranged smooth
muscle fibers. The muscularis mucosa extends through the entire esophagus and
continues into the rest of the GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) tract, being
much thinner in the proximal part of the esophagus than in its distal part.44 (#B44)
At the pharyngeal end of the esophagus, the muscularis mucosa is represented by a
few scattered smooth muscle fibers. Caudally, approaching the cardiac orifice, the
muscularis mucosa forms a thick layer. The muscularis mucosa separates the
lamina propria from the submucosa and retracts when it is sectioned during
surgical procedures.
Submucosa
The submucosa contains connective tissue as well as lymphocytes, plasma cells, nerve cells
(Meissner's plexus), vascular network (Heller plexus), and mucous glands. The esophageal
glands are small racemose glands (which have acini arranged like grapes on a stem) of
mucous type. Their secretion is important in esophageal clearance and tissue resistance to
acid.45 (#B45)
Muscularis Propria
The muscularis propria is responsible for motor function. The upper 5% to 33% is
composed exclusively of striated (skeletal) muscle, and the distal 33% is composed of
smooth muscle. In between there is a mixture of both, called the transition zone.
Functionally the transition zone can be observed with manometry as a region where there
is no significant contraction amplitude during a peristaltic contraction that travels down
the body of the esophagus.46 (#B46)
Adventitia
The adventitia is an external fibrous layer that covers the esophagus, connecting it with
neighboring structures. It is composed of loose connective tissue and contains small
vessels, lymphatic channels, and nerve fibers.
Developmental Anomalies
Tracheoesophageal Fistula and Atresia
Tracheoesophageal fistula and esophageal atresia are the most frequent congenital
esophageal abnormalities. Tracheoesophageal fistula results from defects in the separation
of the respiratory tract from the foregut. Esophageal atresia results from failure of the
primitive gut to recanalize during week 8. Five types of congenital esophageal atresia with
or without tracheoesophageal fistula have been recognized32 (#B32) : (Figure 10 (#f10) ).
Figure 10: Main types of tracheoesophageal fistulae

The figure shows both tracheoesophageal fistula (A-E) and
tracheal abnormalities ( F-J). Note that A-E do not
correspond with the classification of the type of
tracheoesophageal fistula. A shows type C, B type B, C type
D, D type E, and E type A tracheoesophageal fistula,
respectively. (Source: Netter medical illustration with
permission from Elsevier. All rights reserved.)

Type A—pure esophageal atresia (7.6%)

Type B—esophageal atresia with proximal tracheoesophageal fistula (0.8%)
Type C—esophageal atresia with distal tracheoesophageal fistula (86.5%)
Type D—esophageal atresia with proximal and distal tracheoesophageal fistula
(0.7%)
Type E—"H-type" tracheoesophageal fistula without esophageal atresia (4.4%)
The most common variant is type C, with an incidence of 86.5%. It presents as a blind
esophageal pouch with a fistula between the trachea and the distal esophagus. The fistula
often enters the trachea close to the carina.
The second most common anomaly is type A, pure esophageal atresia without
tracheoesophageal fistula.
Esophageal atresia with tracheoesophageal fistula occurs in one in 3000 to one in 5000
births. In 93% cases of esophageal atresia there are associated malformations (VACTERL)
and in 7% esophageal atresia is found as a solely malformation.47 (#B47) The VACTERL
association describes the following more commonly associated combination of defects:
vertebral, anorectal, cardiac, tracheal, esophageal, renal, and limb. When studies over the
last 30 years had been conducted, there were no changes in the incidence of
tracheoesophageal fistula and esophageal atresia, but decrease in the subsequent mortality
had been found.48 (#B48)
Clinically, esophageal atresia should be suspected when polyhydramnios is present in the
mother. Polyhydramnios develops as a consequence of the inability of the fetus to swallow
and thus absorb amniotic fluid. On physical examination of the newborn, a scaphoid
abdomen and the regurgitation of saliva are indicators of GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) obstruction. If rapid
onset of choking, coughing, and regurgitation are present at the first feeding, suspicion of
esophageal atresia is raised. When esophageal atresia is suspected, a nasogastric tube
insertion should be attempted. Failure to pass a nasogastric tube into the stomach,
together with chest radiography showing air/contrast collection in the upper esophageal
segment, confirms the diagnosis of esophageal atresia. If atresia is present, an inserted
nasogastric tube will typically stop at 10 to 12 cm.
The atretic upper esophagus ends in a blind pouch, and the trachea communicates with the
distal esophagus. Air enters the GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) tract via the
tracheoesophageal fistula and the newborn presents clinically with a gas-filled abdomen
and frequent aspiration pneumonias due to gastric reflux into the respiratory tract through
the fistula. Confirmation of the type of esophageal atresia is obtained by esophagography
with or without bronchoscopy.
Treatment of esophageal atresia and tracheoesophageal fistula is surgical, and the

procedure depends on the type of esophageal atresia and the distance between the two
esophageal segments. Thus, if the distance between the esophageal segments is short, end-
to-end anastomosis is the preferred surgical procedure. If the distance between segments
is long, lengthening of the upper esophageal segments in some cases can be achieved using
bougienage or intraoperative myotomy.47 (#B47) A colonic segment may be inserted
between the esophageal segments when the lengthening of the upper esophageal segments
is not possible or adequate.
The results of surgical correction are generally excellent when the esophageal
malformation is an isolated anomaly. Overall outcome is determined by the associated
genetic malformation, age of infant, and birth weight.47 (#B47) Postoperative
complications develop more often in very premature and premature infants, with term
infants having a higher survival rate and better prognostic than preterm infants.49 (#B49)
Long-term outcome after esophageal atresia repair indicates that the most significant
problems are GI (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) and
respiratory symptoms. Reported incidence of these types of complications in adults and
children varies from 30% to 60%, with respiratory infections being more severe in
childhood and eventually improving through adolescence.50 (#B50) The most frequent GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) complications are
gastroesophageal reflux disease (GERD
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df4) ) (48%) and
dysphagia (43%).50 (#B50)
Gastroesophageal reflux disease symptoms may be alleviated by pharmacologic treatment

or with time, owing to the patient's accommodation with the medical condition, but there
is a higher risk of developing chronic esophagitis and Barrett's metaplasia compared to the
normal population.51 (#B51) This increased risk is owing to impaired esophageal luminal
acid clearance. Nissen fundoplication is the preferred surgical treatment for GERD
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df4) , postesophageal
atresia repair, with a 15% to 30% failure rate and requirement for reoperation.52 (#B52)
Dysphagia, owing to esophageal dysmotility, has been found to be the most troublesome
GI (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) symptom, with
negative impact on the quality of life in adults who have been treated for esophageal
atresia as infants.53 (#B53)
The aesthetic aspects of the surgical treatment are now becoming more important in adults
with esophageal atresia owing to good functional results of applied treatments.53 (#B53)
Congenital Esophageal Stenosis

Congenital esophageal stenosis represents narrowing of the esophageal lumen. It can be
located at any level of the esophagus, but is more frequent in the distal third. It appears
either as a web (membranous diaphragm) or a long segment of esophagus with a
threadlike lumen (fibromuscular stenosis). Usually, the esophageal stenosis results from
incomplete esophageal recanalization during the eighth week of human embryologic
development, but it also may result from failure of esophageal blood vessels to develop in
the affected area.32 (#B32) The presence of respiratory tissue in some esophageal stenosis
cases (as hyaline cartilage, or respiratory mucus gland) suggests an incomplete separation
of the respiratory bud as the etiology in some cases.
The incidence of esophageal stenosis is low, occurring in 1 in every 25,000 live births.54
(#B54) In a recent study, no significant changes in population characteristics of patients
with congenital esophageal stenosis were observed over the last three decades, but
mortality and postoperative complication rates decreased and associated cardiac
anomalies became by far the most important risk factor for mortality.48 (#B48)
Congenital esophagus stenosis has been classified histologically as follows:
Group I: tracheobronchial rests (cartilage, respiratory mucus glands, ciliated

epithelium)
Group II: membranous diaphragm
Group III: fibromuscular stenosis
Patients may present with aspiration and recurrent pneumonia in early infancy. Dysphagia
and regurgitation of solid food are symptoms that appear later in childhood, when more
solid foods are added to the child's diet. If the esophageal stenosis is not severe, its
diagnosis may be postponed until adulthood, when a history of long-standing solid foods
dysphagia could be documented.
Once suspicion of congenital esophageal stenosis is raised, an upper endoscopy with

biopsy and pH monitoring of the esophagus help with diagnosis and eliminate the
possibility of a stricture secondary to gastroesophageal reflux. Barium swallow typically
demonstrates narrowing of the esophagus lumen.
The first approach to treatment is with dilation, which may include bougienage or
pneumatic dilation under fluoroscopic guidance. Dilation may be diagnostic and
therapeutic. Although pneumatic dilation expands and stretches a fibromuscular stenosis,
a persistent "waist" in the balloon may indicate a cartilaginous ring and the necessity for
surgical resection. The efficacy of dilatation seems to be limited and may even result in
severe complications such as chest pain, mucosal tears, or esophageal rupture. When
pneumatic dilation fails, surgical treatment may be required for removal of the abnormal
segment.55 (#B55)
Laser lyses of webs or stenosis stenting have been described and may be attempted in
selected cases.49 (#B49)
When respiratory tissue is present on esophageal stenosis biopsy, surgical removal of the
involved segment is necessary owing to high risk of malignant transformation.55 (#B55)
Congenital Esophageal Duplication and Duplication Cyst
Foregut duplications include esophageal cysts (tubular duplications) and bronchogenic

cysts. They originate from failure of the primitive foregut to become completely vacuolated
during the embryonic life. These cyst- or tube-like structures develop independently and
rarely are in continuity with the esophagus. They can be associated with other congenital
malformations, such as tracheoesophageal fistulas, spinal abnormalities, esophageal
atresia distal to duplication, and other segmental GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) duplications (small
bowel is more frequent).56 (#B56)
Duplications of the GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) tract have three
common characteristics:
They are contiguous with some segment of the GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) tract.
They are lined by alimentary epithelium.
They have smooth muscle in theirs walls.44 (#B44)
The congenital duplication cysts represent 0.5% to 2.5% of esophageal benign tumors.57,
(#B57) 58 (#B58) Originating from foregut, they could be attached to the esophagus or to the
tracheobronchial system. They are lined by squamous columnar, cuboid, or ciliated

epithelium, surrounded by two layers of smooth muscle.59 (#B59) They are usually located
in the right posterior mediastinum. Usually they are accidentally discovered on chest
computed tomography (CT
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df2) ) scans and are
asymptomatic. Cysts may become symptomatic owing to complications such as respiratory
system compression (causing stridor, cough, or tachypnea), digestive system compression
(causing chest pain or dysphagia), cardiac compression (causing cardiac arrhythmias),
infarction, rupture, or, rarely, neoplastic dysplasia.60, (#B60) 61 (#B61)
Congenital esophageal duplications may be separated from the esophagus or may share a
common wall. Duplications may also contain gastric mucosa. Duplications of the
esophagus can be associated with vertebral anomalies and intraspinal cysts and often are
associated with intraabdominal intestinal duplications.60 (#B60)
The diagnosis of esophageal duplication can be made by CT

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df2) chest exam or MRI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df8) body exam. A chest
x-ray may demonstrate a soft tissue mass with a mediastinal shift. Barium swallow can
detect tubular esophageal duplication, but miss the esophageal cyst that does not
communicate with the esophageal lumen.61 (#B61) Ultrasound can help distinguish a solid
from a cystic mass, and barium contrast study can demonstrate extrinsic compression of
the esophagus. A CT (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df2)
scan delineates anatomy of the mass prior to surgical resection, and a nuclear
(technetium) scan may help identify ectopic gastric mucosa.
Definitive treatment involves complete surgical resection of the duplication, even for
asymptomatic cysts.
Congenital Esophageal Rings
The congenital esophageal ring is a concentric extension of the normal esophageal tissue,
usually consisting of different anatomic layers including mucosa, submucosa, and
sometimes muscles. The location is variable, but most are found in the distal esophagus.
There are three types of esophageal rings: types A, B. and C.62 (#B62)
Esophageal rings may originate from incomplete vacuolization of the esophageal columnar
epithelium during early embryonic life; however, they are also associated with
immunologic63 (#B63) or inflammatory conditions (such as scleroderma, chronic graft-
versus-host disease),64, (#B64) 65 (#B65) and gastroesophageal reflux.66 (#B66)
The type A esophageal ring is a muscular ring located roughly 2 cm proximal to the
squamocolumnar junction and it represents a proliferation of the proximal border of the
LES (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) . It consisting of
three layers: mucosa, submucosa, and muscularis propria. It is the least frequent type and
usually asymptomatic.67 (#B67)
The type B or Schatzki's ring is a mucosal ring located at the squamocolumnar junction.
Because it is difficult to exactly localize the squamocolumnar junction and the LES
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) , the exact anatomic
relationship between the Schatzki's ring and squamocolumnar junction remains
controversial. Typically it is associated with the proximal margin of a hiatal hernia. It
consists of two layers, mucosa and submucosa, having squamous epithelium on its upper
surface and columnar epithelium on its lower surface.68 (#B68)
The type B ring is the most common esophageal ring and is found in 6% to 14% of subjects
undergoing an upper GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) series. No differences
in the prevalence of rings based on gender has been noticed, but they appear to be more
common in subjects over 40 years old.62 (#B62) Characteristically, Schatzki's ring causes
intermittent dysphagia for solid food, a common complication being meat impaction
(steakhouse syndrome). Esophageal rings usually exist as a single lesion but can be
multiple. Owing to its mucosal nature, Schatzki's ring has been proposed to be caused by
GERD (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df4) , but no
clinical association had been found.62 (#B62)
The type C esophageal ring is an indentation caused by the diaphragmatic crura,

sometimes seen on radiographic studies. It is never symptomatic. Routine upper GI
(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df5) series, including
barium radiography and upper esophagogastric endoscopy are diagnostic for this type of
ring. The prognosis is good, and patients with symptoms are advised to change their
dietary habits and to cut and chew all food carefully. If no improvement in the symptoms is
noticed, serial progressive dilations are recommended.62 (#B62)
Congenital Esophageal Webs
The congenital esophageal web is defined as a thin, usually eccentric, transverse

membrane. It consists of two layers, mucosa and submucosa, and is formed from
connective tissue covered by normal squamous epithelium. Its location is variable, but
most frequently is found in the cervical esophagus, where it is frequently associated with
heterotopic gastric mucosa. Most cases are asymptomatic. Intermittent dysphagia for solid
food is the usually complaint. Esophageal web occurs more frequently in females.62 (#B62)
As for congenital esophageal rings, it is thought that webs result from incomplete
vacuolization of the esophageal columnar epithelium during early embryonic life. They
were also associated with iron-deficiency conditions, blistering skin diseases (such as
epidermolysis bullosa),69 (#B69) heterotopic gastric mucosa in the upper esophagus,70
(#B70) and gastroesophageal reflux.66 (#B66)
Radiographic techniques are the most sensitive diagnostic methods and esophageal webs
may be confused with esophageal stenosis. Treatment consists of bougienage, and rarely
transendoscopic incision or surgical resection is necessary.
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What are the main parts of the esophagus?

What are the main parts of the esophagus?

How does the esophagus develop embryologically?

How does the esophagus develop embryologically?

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GI Motility online (2006) doi:10.1038/gimo6

Esophagus - anatomy and development

View article related content (#relatedcontent)

Beginning at 4 months, the ciliated epithelium starts to be replaced by squamous

The development of various elements of esophageal wall requires coordination of a

Esophageal peristalsis appears in the first trimester, and gastroesophageal reflux

Figure 1: Primordial gut. (/gimo/contents/pt1/fig_tab/gimo6_F1.html)

Full size image (49 KB)

Interstitial cells of Cajal (ICC

The development of concentric layers of smooth muscle, ICC

Structurally, the esophageal wall is composed of four layers: innermost mucosa,

Figure 2: Arterial blood supply of the esophagus

Full size image (172 KB)

Figure 3: Venous drainage of the esophagus

Full size image (201 KB)

Figure 4: Parasympathetic and sympathetic innervation of the

Full size image (197 KB)

The esophagus receives parasympathetic and sympathetic innervation that regulates

Positron emission tomography (PET

Figure 5: Lymphatic drainage (/gimo/contents/pt1/fig_tab/gimo6_F5.html)

Full size image (120 KB)

malignancy from the lower esophagus to the upper esophagus.

Figure 6: Musculature of the esophagus

Full size image (138 KB)

Upper Esophageal Sphincter

The upper esophageal sphincter (UES

Figure 7: Upper esophageal sphincter and upper esophageal

Full size image (151 KB)

The cricopharyngeus (CP

(/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df1) is different from the

Upper esophageal sphincter function is controlled by a variety of reflexes that involve

Lower Esophageal Sphincter

Figure 8: Gastroesophageal mucosal junction and muscular

Full size image (140 KB)

Figure 9: Diaphragmatic crura and esophageal opening viewed from

Full size image (114 KB)

The intrinsic component of the LES

The extrinsic component of the LES

The endoscopic localization of the LES

Three-dimensional (3D) manometric measures of the lower esophageal high-pressure zone

The LES (/gimo/contents/pt1/abbreviations/gimo6_abbreviations.html#df7) is

Mucous membrane: a nonkeratinized squamous epithelium. It covers the entire

Tracheoesophageal Fistula and Atresia

Figure 10: Main types of tracheoesophageal fistulae

Full size image (88 KB)

Type A—pure esophageal atresia (7.6%)

Treatment of esophageal atresia and tracheoesophageal fistula is surgical, and the

Gastroesophageal reflux disease symptoms may be alleviated by pharmacologic treatment

Congenital Esophageal Stenosis

Congenital esophagus stenosis has been classified histologically as follows:

Group I: tracheobronchial rests (cartilage, respiratory mucus glands, ciliated

Once suspicion of congenital esophageal stenosis is raised, an upper endoscopy with

Congenital Esophageal Duplication and Duplication Cyst