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1 Anatomy andPhysiology oftheEsophagus
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The thoracic portion of the esophagus extends from the suprasternal notch to the level of the diaphragmatic hiatus. It is in this
region that the esophagus encounters a number of important intrathoracic structures including the trachea, the mainstem bronchi,
and the aortic arch. The esophagus deviates slightly to the left of
the trachea at the thoracic inlet, shifts to the right at the carina to
accommodate the aortic arch, and turns left again posterior to the
left mainstem bronchus before entering the diaphragmatic hiatus
at the level of the 11th thoracic vertebra. The two remaining narrowing points of the esophagus occur at this bronchoaortic constriction near the fourth vertebra and at the diaphragmatic hiatus.
The majority of the arterial ow is supplied to the thoracic portion
of the esophagus via the bronchial arteries and the four to six
esophageal branches of the aorta. This blood supply is supplemented by descending branches from the inferior thyroid arteries
and intercostal arteries and ascending branches of the paired inferior phrenic arteries.
The nal segment of the esophagus is the abdominal portion, a
short segment extending from the entry of the esophagus into the
esophageal hiatus of the diaphragm until its smooth transition into
the cardia of the stomach. Within the abdomen, after passing
through the esophageal hiatus, the esophagus lies in a shallow
groove of the posterior aspect of the left lobe of the liver, formally
referred to as the esophageal groove. Blood supply to this region
of the esophagus is generally provided by an ascending branch of
the left gastric artery and from both the left and right inferior
phrenic arteries.
The lower esophageal sphincter (LES) is a zone of high pressure (mean, 24mmHg) measuring approximately 3 centimeters
with intrathoracic and intra-abdominal components. This marks
the exit point of the esophagus and is at the level of the gastroesophageal junction. The LES acts in conjunction with gastric
sling bers and the crural diaphragm to protect the epithelium of
the esophagus from injury related to reuxed gastric contents
(Fig.1.1). While it does not have a truly identiable landmark, the
LES can be identied as a pressure gradient, which is higher than
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Longitudinal muscle
Distal esophageal circular muscle
rm
Circular muscles stomach
Longitudinal muscles stomach
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Circular muscle
esophagus
esophagus
Clasp fibers
Fig. 1.1 Schematic of the microscopic myoarchitecture of the circular and
longitudinal muscle layers of the lower esophageal sphincter and stomach.
(From Zifan, A., Kumar, D.Cheng, L.K. etal. Three-Dimensional Myoarchitecture of the Lower Esophageal Sphincter and Esophageal Hiatus Using
Optical Sectioning Microscopy. Scientic Reports 7, Article number: 13188
(2017))
Cross at the angle of HIS to fo
the Sling fibers on the stomach
J. Thomas and J. Kurtz
the normal gastric pressure on manometry or at the squamocolumnar epithelial junction on endoscopy. Externally, one could
say that the LES rests under the gastroesophageal fat pad or where
the circular muscular bers of the esophagus join the oblique
bers of the stomach (the collar of Helvetius).
The wall of the esophagus in its entirety is composed of
mucosa, submucosa, and a muscularis propria. In contrast to the
remainder of the gut, the esophagus lacks a serosal outer layer and
instead is invested by a thin layer of loose connective tissue. The
muscularis propria is furthermore divided into two distinct muscular layers—an inner circular layer and an outer longitudinal
layer. Histologically, the mucosa is characterized by the presence
of a stratied squamous epithelium through the majority of its
course through the cervical and thoracic portions; however, there
is seen a distal, 1 to 2 cm transition to a gastric columnar
1 Anatomy andPhysiology oftheEsophagus
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epithelium, more suited to tolerate repeated insults from gastric
contents reuxed into the lumen of the esophagus.
Physiology
The Normal Swallowing Mechanism
The completion of a single swallow involves precise movement and
function of approximately 30 muscles and nerves [1]. These neuromuscular groups are not only vital for the complete passage of food
from the mouth to the stomach, but also for airway protection during the passage of a food or liquid bolus. Commonly divided into
the oral, pharyngeal, and esophageal phases, swallowing dysfunction can lead to a variety of complications including dysphagia,
regurgitation, and aspiration. Primary motor disturbances, abnormal upper or lower esophageal sphincters, and collagen vascular
diseases can also lead to diverticula, gastroesophageal reux, stricture, or even malignancies of the esophagus.
Swallowing: Oral Phase
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Further subdivided into the oral preparatory and propulsive stages,
the oral phase functions to ready a bolus of food or liquid for passage from the oral cavity to the pharynx. A contrast exists between
the oral phase of liquid swallowing versus solid food swallowing,
characterized in the oral preparatory with sealing of the posterior
pharynx by the tongue and soft palate during swallowing of liquids,
whereas the cyclical movement of the jaw and palate during chewing requires an open passage between the mouth and pharynx. In
the propulsive stage of the oral swallowing mechanism, in the case
of liquids, the tongue lifts to meet the hard palate, while the posterior aspect of the tongue simultaneously lowers away from the soft
palate propelling the bolus posteriorly into the pharynx.
Solid food boluses are better described via a staged transport
model in the oral phase, termed the “Process Model of Feeding”
[2]. In stage 1 of this model, the tongue carries the food to the
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surface of the lower teeth for food processing via mastication, a
process which requires cyclical motion of the jaw, tongue, palate,
and hyoid bone in a coordinated fashion in order to adequately
process the bolus [3]. Stage 2 transport is initiated by the anterior
tongue meeting the hard palate and propelling the bolus posteriorly to the pharynx, mirroring the propulsive stage for liquids.
Importantly, dysfunction/discoordination in the oral phase of both
solids (uncoordinated movement of the jaw and tongue) and liquids (inability to form an adequate seal between the posterior
tongue and soft palate) can lead to premature entry of a food bolus
in the pharynx leading to complications such as choking, regurgitation, and aspiration.
J. Thomas and J. Kurtz
Swallowing: Pharyngeal Phase andFunction
oftheUpper Esophageal Sphincter
The pharyngeal phase is a short, coordinated phase, which generally is complete within a single-second timeframe. This phase
involves both food passage through the pharynx and the upper
esophageal sphincter and functions to protect the airway as the
bolus passes through the pharynx. During this phase, as the food
or liquid bolus meets the pharynx, the soft palate elevates to cover
the nasal passages and prevent entry into the nose. Simultaneously,
the posterior tongue retracts to force the bolus against the structure of the pharynx, while the pharyngeal musculature contracts
in a superior to inferior sequence to drive the bolus downward.
Dysfunction in this phase of swallowing carries a risk for aspiration secondary to inadequate bolus passage through the pharynx
and insufcient protection of the airway during this process.
Important to a discussion of esophageal physiology, this phase
also includes the opening of the upper esophageal sphincter,
which remains closed at rest [4]. There are three distinct factors,
which impact the adequate relaxation and opening of the upper
esophageal sphincter including relaxation of the cricopharyngeus,
contraction of suprahyoid and thyrohyoid musculature (allowing
the laryngeal complex to be pulled anteriorly), and sufcient pressure from the incoming bolus. The relaxation of the upper esopha-
1 Anatomy andPhysiology oftheEsophagus
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geal sphincter is unique as it requires active opening via
contraction of the suprahyoid and relaxation of the thyrohyoid
musculature rather than a passive opening process [5].
9
Swallowing: Esophageal Phase andtheLower
Esophageal Sphincter
The esophageal phase is characterized by the passage of a food
bolus along the length of the esophagus toward the gastroesophageal junction. In contrast to the pharyngeal phase, the esophageal
phase of swallowing is a process of peristalsis, wherein control is
regulated by the function of the autonomic nervous system. This
difference in the function of swallowing is mirrored in anatomic
changes via changes in the muscular composition of the esophagus— the pharyngeal phase takes place primarily in the pharynx
and cervical esophagus, which is primarily striated muscle (under
conscious control), whereas the thoracic esophagus demonstrates
a transition to smooth muscle (under autonomic control). After a
bolus is passed through the upper esophageal sphincter, a peristaltic wave is ultimately responsible for carrying the bolus through
the esophagus to the lower esophageal sphincter, at which time
the food bolus nally passes into the stomach, terminating the
swallowing mechanism.
Peristaltic contractions can be categorized as either primary (initiated by a swallow) or secondary (initiated by distension of the
esophagus). Tertiary contractions have also been described as nonprogressive, nonperistaltic, monophasic, or multiphasic, simultaneous waves. These represent uncoordinated contractions of smooth
muscle responsible for esophageal spasm. It is believed that both
the circular and longitudinal layers of the muscularis propria play
distinct roles in peristalsis. While the circular musculature serves to
contract and force the food bolus toward the stomach, it is hypothesized that the longitudinal layer serves to shorten the esophagus
and increase the diameter of the esophagus ahead of an oncoming
bolus [6]. Immediately following relaxation of the upper esophageal sphincter, the lower esophageal sphincter relaxes and a contraction wave is generated sequentially along the esophageal body
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until it reaches the lower esophageal sphincter. Complex neuronal
interactions along the length of the esophagus are responsible for
this contraction. The amplitude and frequency of contractions are
modied by a number of factors including temperature, bolus size,
and viscosity. Additionally, in well- spaced swallows, the esophageal contraction responds in a 1:1 ratio, whereas swallows taken in
rapid succession will inhibit contraction until the nal swallow in a
sequence. It is believed that these modications are mediated by
vasovagal and neuromuscular reexes.
The lower esophageal sphincter (LES) marks an important
limiting factor in the speed and completeness of the esophageal
phase of swallowing and representing an important pathophysiologic landmark in foregut disorders including gastroesophageal
reux and achalasia. The LES, composed of portions of the
esophagus, stomach, and diaphragmatic crura, has a resting pressure, which ranges between 15 and 35mmHg. Peristaltic waves
alone do not generate enough force to open the LES. Vagalmediated relaxation of the LES occurs in increments of approximately 5 to 10s to allow passage of a food bolus, starting at the
initiation of the peristaltic wave and remaining in the relaxed
position for several seconds following passage of a bolus; however, there are also spontaneous relaxations of the LES, which
occur intermittently and remain a common cause of gastroesophageal reux disease [7].
J. Thomas and J. Kurtz
Complex Innervation andNeuronal Control
oftheEsophagus andEsophageal Peristalsis
As previously discussed, the upper esophageal sphincter is composed of striated muscle bers stemming from both the cricopharyngeus muscles and the esophagus. This sphincter complex
receives its innervation from the glossopharyngeal nerve, branches
of the vagus nerve, portions of the ansa cervicalis, and sympathetic innervation from a portion of the cervical ganglion. Motor
function of the upper esophageal sphincter is primarily derived
1 Anatomy andPhysiology oftheEsophagus
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from the vagus nerve, with lower motor neurons located in the
nucleus ambiguus, via the superior laryngeal and recurrent laryngeal nerve branches [8]. It is the swallow mechanism and introduction of a food bolus (swallow-induced peristalsis), which
activates the lower motor neuron of the nucleus ambiguus of the
brainstem, which allows for peristalsis of the striated muscle of
the upper esophagus and the function of the upper esophageal
sphincter [9]. While a number of neuropeptides have been shown
to be present at the endplate of these motor neurons, acetylcholine
acting on nicotinic receptors is thought to predominate the motor
function of the sphincter [10].
Esophageal peristalsis is regulated by autonomic nerves
located in the intramural enteric nervous system. Derived from
both vagal motor efferent bers and sympathetic inputs, this
plexus is located between the inner circular and outer longitudinal
smooth muscle layers of the esophagus. It is widely accepted that
this plexus contains both excitatory and inhibitory neurons, which
result in either the synchronized contraction, or relaxation, of the
esophageal body. Both the excitatory contractile and inhibitory
neurons in this plexus do appear to be innervated by separate sets
of preganglionic vagal bers [11]. Peristalsis of the esophagus is
the result of precise, coordinated movement between the inner
circular and outer longitudinal muscular layers of the esophagus
controlled by these neural inputs.
The LES, located at the distal end of the thoracic esophagus, is
innervated by both vagal parasympathetic and splanchnic sympathetic nerve bers. It is important to note that it is the vagal input
that is vital for the reexive relaxation required for the passage of
a bolus through the sphincter [12]. Based on several studies into
the neuronal control of the LES, it has become apparent that the
resting tone of the LES is primarily myogenic in nature with
excitatory input from the vagus nerve. However, the vagus nerve
also provides an inhibitory effect on the sphincter eliciting relaxation. This has been supported by studies demonstrating that
vagotomy results in contraction of the LES, while stimulation of
vagal efferents results in LES relaxation [13].
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J. Thomas and J. Kurtz
References
1. Matsuo K, Palmer J.Coordination of mastication, swallowing and breathing. Jpn Dent Sci Rev. 2009;45:31–40.
2. Palmer J, Rudin N, Lara G, Crompton A.Coordination of mastication and
swallowing. Dysphagia. 1992;7:187–200.
3. Hiiemae K, Palmer J.Food transport and bolus formation during complete feeding sequences on foods of different initial consistency.
Dysphagia. 1999;14:31–42.
4. Cook I, Dodds W, Dantas R, Massey B, Kern M, Lang I, etal. Opening
mechanisms of the human upper esophageal sphincter. Am J Physiol.
1989;257:G748–59.
5. Shaw D, Cook I, Gabb M, Holloway R, Simula M, Panagopoulos V, Dent
J. Inuence of normal aging on oral-pharyngeal and upper esophageal
sphincter function during swallowing. Am J Physiol. 1995;268:389–96.
6. Wood J.Physiology of the enteric nervous system. In: Physiology of the
gastrointestinal tract; 1987. p.67–109.
7. Allaix M, Patti M.The esophagus from pathophysiology to treatment. In:
Reference module in biomedical sciences. Elsevier; 2014.
8. Mittal RK.Motor function of the pharynx, esophagus, and its sphincters.
San Rafael, CA: Morgan & Claypool Life Sciences; 2011.
9. Goyal RK, Chaudhury A.Physiology of normal esophageal motility. J
Clin Gastroenterol. 2008;42:610–9.
10. Sivarao D, Goyal R.Functional anatomy and physiology of the upper
esophageal sphincter. Am J Med. 2000;108:27S–37S.
11. Mittal RK.Regulation and dysregulation of esophageal peristalsis by the
integrated function of circular and longitudinal muscle layers in health
and disease. Am J Physiol. 2016;311:431–43.
12. Hornby P, Abrahams T. Central control of lower esophageal sphincter
relaxation. Am J Med. 2000;108:90–8.
13. Goyal R, Rattan S.Nature of the vagal inhibitory innervation to the lower
esophageal sphincter. J Clin Investig. 1975;55:1119–26.
Anatomy andPhysiology
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oftheStomach
JennaBorys andJamesKurtz
Anatomy
The stomach is the most proximal abdominal organ of the alimentary tract. It is xed proximally at the GE junction and distally by
the retroperitoneal attachments of the proximal duodenum [1].
Many surgeons divide the stomach into two units: proximal and
distal gastric units. The proximal unit includes the distal esophagus, esophageal hiatus, and the proximal stomach—all of which
incorporate the gastroesophageal junction and lie at the level of
the 11th or 12th thoracic vertebra. The distal gastric unit contains
the gastric antrum, pylorus, and rst portion of the duodenum [2].
The stomach is composed of several anatomic divisions, as
shown in Fig.2.1. The gastric cardia is the portion of the stomach
2
J. Borys
Department of Surgery, Grant Medical Center, Columbus, OH, USA
e-mail: Jenna.Borys@Ohiohealth.com
J. Kurtz (*)
Valley Forge Surgical Associates, Phoenixville, PA, USA
e-mail: James.Kurtz@towerhealth.org
© Society of American Gastrointestinal and Endoscopic Surgeons
(SAGES) 2023
A. D. Patel et al. (eds.), The SAGES Manual of Physiologic
Evaluation of Foregut Diseases,
https://doi.org/10.1007/978-3-031-39199-6_2
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14
Duodenum
Pyloric antrum
ature
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J. Borys and J. Kurtz
Esophagus
Cardia
Lesser curvature
Pylorus
Fig. 2.1 Divisions of the stomach. (From Yeo C: Shackelford’s surgery of
the alimentary tract, ed. 8, Philadelphia, 2019, Elsevier)
+
+
+
+
Fundus
+
Body
Greater
curv
that extends just distal to the gastroesophageal junction. The fundus is the portion of the stomach above and to the left of the GE
junction. As the esophagus enters the abdomen at an oblique
angle, the position of the fundus creates an acute “angle of His.”
This forms an internal ap valve that helps prevent reux at the
lower esophageal sphincter. The corpus or body of the stomach
lies between the fundus and the antrum. The antrum transitions
into the thicker-walled pylorus, which then transitions distally to
the smooth, thin-walled rst portion of the duodenum.
Despite the surgical and physiologic relevance, there are no
obvious external landmarks to delineate the boundaries between
each portion of the stomach. Of important surgical relevance is
determining the junction between the body and the antrum, as
complete antrectomy is essential for acid-reducing surgery in
patients with peptic ulcer disease. Combining techniques from
multiple sources best describes the boundary as 2/5 of the distance from the pylorus to the cardia along the lesser curve and 1/8
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