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2 Anatomy andPhysiology oftheStomach
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of the distance from the pylorus to the cardia along the greater
curvature [3]. The antrum can also be described as the portion
from the angularis incisura (seen as a notch on the lesser curve
where the stomach makes a sharp angle to the right) to pylorus.
Histologically, the antrum can be conrmed by the lack of chief
and parietal cells.
The superior aspect of the stomach is lined by the lesser
omentum, a double layer of peritoneum. This omentum extends
from the porta hepatis along the lesser curve of the stomach and
upward to contribute to the ventral mesentery of the abdominal
esophagus. The superior aspect of the lesser omentum makes up
the gastrohepatic ligament, containing the left gastric artery and
vein, hepatic division of the anterior vagal trunk, anterior and
posterior gastric divisions of the vagal trunks (nerves of Laterjet),
and lymph nodes [3]. An aberrant left hepatic artery can also be
found in the gastrohepatic ligament as it arises from the left gastric artery. The lateral, or dextral, portion of the lesser omentum
becomes the hepatoduodenal ligament, which contains the
hepatic artery, portal vein, and common bile duct—otherwise
known as the portal triad. The medial (left) portion of the lesser
omentum gives rise to the gastrophrenic ligament. The pars accida is an avascular portion of the gastrohepatic ligament overlying the caudate lobe of the liver that can be entered to expose
the right crus of the diaphragm. This allows for posterior dissection and passage of a penrose drain around the distal esophagus
to aid in retraction.
The greater omentum is a larger fold of visceral peritoneum
that hangs from the greater curvature of the stomach, overlying
the anterior surface of the small intestines, and then returns to
ascend to the transverse colon. Since it is folded on itself, it contains four layers of visceral peritoneum. The greater omentum
contains the left and right epiploic arteries along the greater curvature of the stomach. Division of the avascular plane between the
greater omentum and transverse mesocolon permits entrance into
the lesser sac and visualization of the posterior surface of the
stomach and anterior surface of the pancreatic body and tail.
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J. Borys and J. Kurtz
Complete visualization of the posterior surface of the stomach
often requires the division of short gastric arteries to aid in mobilization.
The outermost portion of the stomach is covered by the peritoneum, which forms the serosa of the stomach. Moving internally,
the next layer of the stomach is the muscularis propria or muscularis externa, which is composed of three layers of smooth muscle, an outer longitudinal, middle circular, and inner oblique layer.
The middle circular layer is noted to be the only complete muscle
layer of the stomach wall. The Auerbach myenteric nerve plexus
lies within the layers of the muscularis externa. The submucosa
overlies the muscularis externa and is a collagen-rich layer of connective tissue. Within the submucosa is a rich blood supply with
extensive anastomosis and collateral circulation in addition to the
Meissner plexus of autonomic nerves. The submucosa is the
strength layer of the gastric wall. The mucosa of the stomach is
comprised of surface epithelium, lamina propria, and muscularis
mucosa. It is this histologic layer that marks the microscopic
boundary between invasive and noninvasive gastric carcinoma.
The microscopic anatomy of the stomach helps delineate the
functionality of the stomach. The mucosa of the stomach is lined
by simple columnar glandular epithelium composed of surface
mucous cells. The luminal surface contains gastric pits, which
further contain the gastric glands that are responsible for the physiologic functions of the stomach. Within gastric pits, there are
three types of glands: cardiac, parietal, and antral glands.
Cardiac glands are found adjacent to the esophagus and contain mucous, endocrine, and undifferentiated cells, but do not contain parietal or chief cells. Parietal glands are found within the
fundus and the body of the stomach and contain parietal cells,
which are the sites of hydrochloric acid production. Parietal
glands also contain chief cells, which represent the site of pepsinogen synthesis and secretion. Antral glands occupy the mucosa
of the distal stomach and pylorus. The presence of gastrin cells is
the distinguishing feature of antral glands.
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Blood Supply, Lymphatics, andInnervation
Blood Supply
The stomach is richly vascularized with extensive collateralization from the four main arteries: left and right gastric arteries and left and right gastroepiploic arteries, depicted in
Fig.2.2. The left gastric artery is the rst major branch, origi-
Fig. 2.2 Vascular supply of the foregut. The stomach is shown reected
cephalad and the pancreatic duct is exposed. (From Yeo C: Shackelford’s surgery of the alimentary tract, ed. 8, Philadelphia, 2019, Elsevier)
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J. Borys and J. Kurtz
nating from the celiac trunk in approximately 90% of individuals. The left gastric artery travels along the lesser curve of the
stomach, providing 1–3 esophageal branches as it travels to the
gastric cardia [4]. The right gastric artery most commonly
branches off the proper hepatic artery, but, alternatively, may
branch off the left hepatic artery or common hepatic artery.
The right gastric artery also travels along the lesser curvature
of the stomach and eventually anastomosis with the left gastric
artery. Traveling along the greater curvature, the left gastroepiploic artery typically branches from the splenic artery and
the right gastroepiploic artery most commonly branches from
the gastroduodenal artery. The right gastroepiploic artery anastomoses along the greater curvature and each epiploic artery
supplies short gastric arteries that perfuse the greater curvature
of the stomach. The gastroepiploic arteries also supply the
greater omentum. The right gastroepiploic artery deserves a
special mention for its fundamental importance in foregut surgery. In settings of total or near-total gastrectomy, the right
gastroepiploic artery will often serve as the sole blood supply
for a gastric conduit serving as a neoesophagus. It is recommended that all surgeons aim to preserve this vessel during
foregut surgery of any kind. The extensive vascular supply
ensures a rich collateral network that allows adequate stomach
perfusion, even with ligation of three out of four vessels [5].
This fact has led to the study of ischemic conditioning prior to
esophagectomy to improve the neovascularization of the new
conduit. This also, unfortunately, means that gastric hemorrhage cannot be controlled by simple ligation of the gastric
artery.
Venous drainage of the stomach parallels the arterial ow in
most cases, with the left and right gastric arteries draining into the
portal vein, the right gastroepiploic artery draining into the superior mesenteric vein, and the left gastroepiploic draining into the
splenic vein.
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Lymphatics
Lymphatics of the stomach are divided into four zones, as noted
below [2]. Zone III, the superior gastric zone, is the largest area of
drainage. Despite the described zones, it should be noted that gastric cancers may metastasize to any of the four nodal groups,
regardless of the location of the cancer. Nodal metastasis is the
most important prognostic factor regarding curable gastric cancer
and is the best predictor of recurrence and overall survival [6].
The extent of lymphadenectomy varies between Eastern and
Western countries, but given the important prognostic implications, this topic is subject to ongoing research.
Zone I: Inferior gastric → drains into subpyloric and omental
nodes.
Zone II: Splenic → drains into pancreaticosplenic nodes.
Zone III: Superior gastric → drains into superior gastric nodes.
Zone IV: Hepatic → drains into suprapyloric nodes.
Innervation
The stomach receives both parasympathetic and sympathetic
innervations. The sympathetic innervation originates from the
T5–T10 thoracic splanchnic nerves that reach the celiac plexus.
This innervation conducts afferent impulses that mediate sensation and pain.
Parasympathetic innervation is provided by the vagus nerve.
As the vagus nerve descends inferiorly through the thorax, the left
and right vagal nerves travel parallel with the esophagus. Both
trunks divide into several branches around the esophagus, several
centimeters distal to the tracheal bifurcation. These branches then
coalesce above the esophagus hiatus, forming a periesophageal
plexus. From this plexus, the left and right vagal trunks divide as
they pass through the esophageal hiatus. The left vagus nerve is
found along the anterior surface of the esophagus, and the right
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vagus nerve travels posteriorly, lying between the esophagus and
the aorta. This anatomic arrangement is often remembered with
the acronym “LARP” (left anterior, right posterior). A truncal
vagotomy is when both the right and left vagus nerves are divided
above the level of the GE junction.
Most often at the level of the abdominal esophagus, the left
vagus nerve gives off a hepatic branch to the liver, which travels
within the lesser omentum and innervates the liver and biliary
tract. The remaining left vagal bers travel along the lesser curve
of the stomach as the anterior nerve of Latarjet, typically identied 0.5–1.0cm from the lesser curvature. Anywhere from 2 to 12
branches supply the anterior stomach wall.
The right, or posterior, vagal nerve branches into the celiac division and innervates the posterior surface of the stomach. The criminal nerve of Grassi is the rst branch from the right/posterior nerve
and is known for being a potential cause of recurrent ulcers when
left undivided in vagotomies. Division of right and left vagus nerves
distal to the celiac and hepatic branches is described as a selective
vagotomy. Highly selective vagotomy is accomplished by selective
division of the vagus nerves, known as the crow’s feet, which supply the corpus and fundus while maintaining more proximal innervation.
J. Borys and J. Kurtz
Physiology
The functionality of the stomach is dependent on the various peptides that are released from specialized cells. Gastrin is produced
by G cells, located in the gastric antrum. Gastrin is the major hormonal regulator of the gastric phase of acid secretion. Secretion of
gastrin has trophic effects on the parietal cells and gastric enterochromafn cells. Parietal cells, which produce hydrochloric acid,
are stimulated by gastrin, acetylcholine from the vagus nerve, and
histamine from enterochromafn-like cells. Therefore, via different mechanisms, acid secretion can be decreased by surgical
removal of G cells with antrectomy, vagotomy, and/or medications.
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As food enters the stomach, the resultant gastric distention
activates cholinergic neurons and stimulates gastrin release. As
the food bolus empties through the pylorus, gastric distention
decreases. This leads to the cessation of cholinergic stimulation,
and the gastrin stimulates the production of somatostatin, which,
when released, provides negative feedback for gastrin release.
Gastrin is inhibited in environments of pH less than 3. A gastric pH greater than 3 will lead to hypergastrinemia. This is seen
in patients with pernicious anemia in the setting of chronic achlorhydria, which leads to increased gastrin release. While the mechanism has not been denitively elucidated, chronic gastric infection
with Helico pylori infection has been shown to cause increased
gastrin release. It is thought that the presence of proinammatory
cytokines has been shown to stimulate gastrin release.
Hypergastrinemia can also be seen in patients being treated with
acid- reducing agents such as proton pump inhibitors due to the
lack of negative feedback on gastrin release by luminal acid. The
lack of acid leads to a lack of somatostatin, which leads to a lack
of inhibition of G cells and increased, uninhibited gastrin release.
Hypergastrinemia can also be seen in patients with retained gastric antrum or Zollinger–Ellison syndrome.
Somatostatin is considered an inhibitor of gastric peptides.
Somatostatin is produced by D cells located in the fundus and
antrum. Somatostatin release is stimulated by antral acidication.
Somatostatin has an inhibitory effect on the secretion of acid from
parietal cells. Somatostatin release is inhibited by acetylcholine
from vagal bers.
Histamine is stored in the acidic granules of enterochromafn
cells and stimulates parietal cells to release hydrochloric acid.
Pepsinogen is a precursor to pepsin, a proteolytic enzyme
secreted by chief cells and functions to initiate protein
digestion.
Intrinsic factor is produced by the parietal cells within the gastric mucosa. The release of intrinsic factor is necessary for the
absorption of cobalamin (vitamin B12) from the ileal mucosa.
This is of clinical relevance, as total gastrectomy can lead to
cobalamin malabsorption due to loss of intrinsic factor. Atrophic
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J. Borys and J. Kurtz
gastritis can lead to similar effects due to a lack of intrinsic factor
production by the gastric mucosa.
Gastric bicarbonate is produced by the surface mucus cells that
line the gastric lumen.
Gastric acid secretion is ultimately regulated by acetylcholine,
gastrin, and histamine. Receptors for each of these are located
along the basolateral membrane of the parietal cell. Ultimately,
stimulation of any of these receptors activates that parietal cell
proton pump, an H+/K+-ATPase that exchanges cytosolic hydrogen ions (H+) for luminal potassium cations (K+). Parietal cells
also have receptors for somatostatin, which serves to inhibit acid
secretion. Gastric acid production can be prevented by receptor
antagonist for each of the three primary stimulants listed above.
There are three phases of gastric acid secretion: the cephalic,
gastric, and intestinal phases.
The gastric phase begins with the sight, smell, thought, or taste
of food, which triggers the release of acetylcholine. This phase
accounts for approximately 20% of gastric acid secretion. The
release of acetylcholine also stimulates histamine release from
enterochromafn cells, HCl release from parietal cells, and gastrin release from the G cells. The gastric phase starts when food
enters the gastric lumen, and the antral distension triggers gastrin
release. This phase accounts for 30–40% of the acid production.
The intestinal phase is activated when a food bolus enters the
small intestine. This phase accounts for 10% of the secretory
response to a meal. Eventually, luminal acidication will incite D
cells to produce somatostatin and begin the inhibitory effect on
acid secretion.
References
1. Teitelbaum EN, Hungness ES, Mahvi DM.Stomach. In: Townsend CM,
editor. Sabiston textbook of surgery. 20th ed. Pennsylvania: Elsevier;
2016. p.1188–201.
2. Skandalakis LJ, et al. Surgical anatomy and technique. New York:
Springer; 2009. p.285–94.
3. Brenkman HJF, van der Wielen N, Ruurda JP, etal. Surgical anatomy of
the omental bursa and the stomach based on a minimally invasive
2 Anatomy andPhysiology oftheStomach
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approach: different approaches and technical steps to resection and
lymphadenectomy. J Thorac Dis. 2017;9(Suppl 8):S809–16.
4. Mirilas P, Loukas M, Skandalakis LJ.Anatomic considerations in gastroduodenal surgery. In: Fisher JE, editor. Fisher’s mastery of surgery. 7th
ed. Pennsylvania: Wolters Kluwer; 2017. p.44136–5042.
5. Mulholland MW. Gastric anatomy. In: Mulholland MW, editor.
Greeneld’s surgery scientic principles and practice. 6th ed.
Pennsylvania: Wolters Kluwer; 2017. p.36715–7164.
6. Lirosi M, Biondi A, Ricci R.Surgical anatomy of gastric lymphatic drainage. Transl Gastroenterol Hepatol. 2017;2:14. https://doi.org/10.21037/
tgh.2016.12.06.
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Eect ofObesity onForegut
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Physiology
RyanLamm andFrancescoPalazzo
Introduction
Obesity has reached epidemic proportions and affects the health
of children and adults throughout the world. It is dened as a body
mass index (BMI)>30kg/m2 for adults or greater than the 95th
percentile of BMI according to the 2000 Centers for Disease
Control and Prevention growth charts [1]. The prevalence of obesity has been on the rise during the last two decades, with 40% of
the adult population in the United States and 13% of the adult
population worldwide currently considered obese [1, 2]. Obesity
is a predisposing risk factor for several morbid conditions, and
research is accumulating on the pathways that link chronic weight
gain to the onset of several pathological states. The cost of said
comorbidities has been estimated to have an impact on the US
annual healthcare cost of $147–210 billion [2].
Obesity has an impact on several aspects of human physiology
that are critical to the normal functioning of the GI tract. Several
3
R. Lamm · F. Palazzo (*)
Department of Surgery, Thomas Jefferson University Hospital,
Philadelphia, PA, USA
e-mail: Ryan.lamm@jefferson.edu; Francesco.palazzo@jefferson.edu
© 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_3
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