Anatomy - Fundoplication, laparoscopic according to Toupet

The stomach is, formally speaking, a dilation of the digestive tract located between the esophagus and the intestine, tasked with storing and mixing food. This muscular hollow organ produces acidic gastric juice (mucus and HCl) and enzymes that partially digest some components of the food, subsequently transferring the chyme in portions to the small intestine.
The stomach is usually located in the left and middle upper abdomen directly beneath the diaphragm. The position, size, and shape of the stomach vary greatly from person to person and depending on age, state of fullness, and body position. When moderately filled, the stomach is on average 25-30 cm long and has a storage capacity of 1.5 liters, and in extreme cases, up to 2.5 liters.
The stomach is anchored and stabilized in the abdominal cavity by ligaments that extend to the liver and spleen, among others. It forms the greater curvature (Curvatura major) with its convex side and the lesser curvature (Curvatura minor) with its concave side. Its anterior wall is referred to as Paries anterior, and its posterior wall as Paries posterior.
The stomach is intraperitoneal and thus covered by serosa, with only the dorsal cardia free of serosa. The embryonic mesogastria move from their original sagittal position to a frontal one due to the rotation of the stomach: The lesser omentum extends from the lesser curvature to the hepatic portal, while the greater omentum spreads from the greater curvature to the transverse colon, spleen, and diaphragm.
The stomach can be divided into different sections:

• Cardia / Ostium cardiacum:
  The upper gastric mouth is an area of 1-2 cm where the esophagus opens into the stomach. Here, the sharp transition from the esophageal mucosa to the gastric mucosa can usually be well recognized with an endoscope.
• Fundus gastricus:
  Above the gastric entrance, the fundus arches upward, also known as the "gastric dome" or Fornix gastricus. The fundus is typically filled with air that is involuntarily swallowed during eating. In an upright person, the fundus forms the highest point of the stomach, so in an X-ray, the collected air appears as a "gastric bubble." Opposite the gastric entrance, the fundus is demarcated by a sharp fold (Incisura cardialis).
• Corpus gastricum:
  The main part of the stomach is formed by the gastric body. Here, deep longitudinal folds of the mucosa (Plicae gastricae) extend from the gastric entrance to the pylorus and are also referred to as the "gastric street."
• Pars pylorica:
  This section begins with the expanded antrum pyloricum, followed by the pyloric canal (Canalis pyloricus), and ends with the actual pylorus. Here lies the pyloric sphincter muscle (M. sphincter pylori), formed by a strong circular muscle layer, which closes the lower gastric mouth (Ostium pyloricum). The pylorus seals the gastric outlet and periodically allows some chyme to pass into the subsequent duodenum.

Stomach Wall
Under the microscope, the stomach wall shows a characteristic layer structure from the inside out:

• Internally, the stomach wall is lined by mucosa (Tunica mucosa). The gastric mucosa is divided into three sublayers: The lamina epithelialis mucosae produces a viscous neutral mucus that protects the gastric mucosa from mechanical, thermal, and enzymatic damage. Below it follows the lamina propria mucosae, which contains the gastric glands (Glandulae gastricae). Lastly, there is a narrow lamina muscularis mucosae that can alter the relief of the mucosa.
• The gastric mucosa is followed by a loose connective tissue layer (Tela submucosa), consisting of connective tissue with a dense network of blood and lymph vessels, as well as a nerve fiber plexus, the submucosal plexus (Meissner's plexus), which controls gastric secretion. This plexus operates independently of the central nervous system (CNS) but can be influenced by it through the autonomic nervous system.
• Next is a strong tunica muscularis, divided into three sublayers with fibers running in different directions: an inner layer of small oblique muscle fibers (Fibrae obliquae), then a circular muscle layer (Stratum circulare), and an outer longitudinal muscle layer (Stratum longitudinale). This musculature ensures the peristalsis of the stomach, responsible for the constant mixing of chyme with gastric juice. Between the circular and longitudinal muscle layers runs a nerve fiber plexus, the myenteric plexus (Auerbach's plexus), which controls the function of the musculature. Like the submucosal plexus, this plexus operates largely autonomously but is influenced by the autonomic nervous system.
• This is followed by another connective tissue layer (Tela subserosa).
• The peritoneum as the serous membrane (Tunica serosa) forms the conclusion.

Gastric Glands
The gastric glands (Glandulae gastricae) are located in the lamina propria mucosae and can be found in the fundus and corpus of the stomach. Up to 100 glands are located on 1mm² of the mucosal surface. Various cells are located in the wall of the glandular tube:

• Mucous cells: They produce the same neutral mucus as the epithelial cells.
• Mucous neck cells: These cells are located quite superficially in the gland and secrete alkaline mucus, i.e., the pH is high due to the bicarbonate ions (OH- ions) contained in it. This property is important to control and, if necessary, regulate the pH of the stomach. The mucus coats the gastric mucosa, protecting it from self-digestion by the aggressive hydrochloric acid (HCl) and enzymes as self-digesting proteins. This cell type is found predominantly in the cardia and fundus of the stomach.
• Chief cells: These cells produce the inactive precursor enzyme pepsinogen, which is converted into the active enzyme pepsin by hydrochloric acid (HCl) after release and is responsible for the digestion of dietary proteins. Since the enzyme only comes into contact with hydrochloric acid at the surface of the gland, self-digestion of the glands by the enzyme is prevented. This cell form is mainly located in the corpus of the stomach.
• Parietal cells: These cells, which are found more frequently in the gastric corpus, produce abundant hydrogen ions (H+ ions) needed for the formation of hydrochloric acid (HCl). Hydrochloric acid has a very low pH of 0.9-1.5. Additionally, parietal cells produce the so-called intrinsic factor. This substance forms a complex with vitamin B12 from food in the intestine, which can then pass through the intestinal wall. This vitamin is of particular importance in erythropoiesis (removal of the stomach can lead to anemia).
• G-cells: These cells, which are preferably located in the antrum of the stomach, produce gastrin to increase HCl production in the parietal cells.

The stomach serves as a reservoir for ingested food. It can store food for hours, allowing us to meet our daily nutritional needs with a few larger meals. Through peristalsis, the food bolus (chyme) is mixed with gastric juice, chemically broken down, partially digested, and then gradually transferred to the duodenum.

The arterial supply of the stomach is provided by several blood vessels, all originating from the unpaired celiac trunk, forming numerous anastomoses among themselves, and running along the gastric curvatures as vascular arcades to supply the organ:

• Right gastric artery from the proper hepatic artery to the lower part of the lesser curvature,
• Left gastric artery to the upper part of the lesser curvature,
• Short gastric arteries from the splenic artery to the fundus,
• Right gastroepiploic (omental) artery from the gastroduodenal artery to the lower (right) part of the greater curvature,
• Left gastroepiploic (omental) artery from the splenic artery to the left side of the greater curvature,
• Posterior gastric artery from the splenic artery to the posterior wall.

Thus, the stomach is supplied by 2 vascular arcades between the left and right gastric arteries at the lesser curvature, as well as the left and right gastroepiploic arteries at the greater curvature.

Parallel to the arterial supply, the 4 major veins of the stomach run along the two curvatures. Collecting veins (left and right gastric veins directly into the portal vein, left gastroomental vein and short gastric veins to the splenic vein, and right gastroomental vein to the superior mesenteric vein) form from them, all draining into the portal vein.

The nerve supply of the stomach is predominantly under the control of the autonomic nervous system, but there are also sensory fibers: The sympathetic system supplies the pyloric musculature, the parasympathetic system (vagus nerve X) supplies the rest of the gastric musculature and the glands of the stomach. The vagus nerve runs right and left parallel to the esophagus, passes through the diaphragm via the esophageal hiatus, and reaches the anterior surface of the stomach on the left side (anterior vagal trunk), and the posterior surface on the right side (posterior vagal trunk). Sensory fibers from the stomach, on the other hand, run afferently via the greater splanchnic nerve to thoracic spinal ganglia.

The efferent lymphatic vessels of the stomach run parallel to the arterio-venous supply of the organ:

• The lymph from the lesser curvature runs parallel to the left/right gastric arteries into the left/right gastric lymph nodes,
• from the gastric fundus parallel to the splenic artery into the splenic lymph nodes,
• the lymph from the greater curvature runs parallel along the attachment of the greater omentum to the right/left gastro-omental lymph nodes,
• from the pyloric region into the pyloric lymph nodes.
  From the aforementioned regional lymph nodes, the lymph subsequently flows into the celiac lymph nodes, the upper mesenteric lymph nodes, and the thoracic duct.
  Another pathway for lymph drainage is through the pancreatic lymph nodes, allowing gastric tumors to metastasize into the pancreas. A peculiarity of gastric carcinoma is the recurrent presence of a noticeable lymph node in the left lateral neck region (Virchow's node), indicating advanced metastasis.
  For surgical reasons, the lymph node stations are divided into 3 compartments:
• Compartment I (LN group 1-6): all LNs directly at the stomach: paracardial (group 1+2), at the lesser and greater curvature (group 3+4), supra- and infrapyloric (group 5+6).
• Compartment II (LN group 7-11): LNs along the major vessels: left gastric artery (group 7), common hepatic artery (group 8), celiac trunk (group 9), splenic hilum (group 10), splenic artery (group 11).
• Compartment III (LN group 12-16): LNs at the hepatoduodenal ligament (group 12), behind the pancreatic head (group 13), at the mesenteric root and mesentery (group 14+15), and along the abdominal aorta (group 16).

Gastroesophageal reflux disease (GERD) is present when reflux of stomach contents into the esophagus causes esophageal or extraesophageal manifestations and/or the symptoms impair quality of life. Although the pathogenesis of GERD is multifactorial, it is primarily due to an insufficiency of the antireflux barrier.

Antireflux Barrier

Since there is a higher pressure in the abdomen than in the thorax, and the gradient increases further with coughing and the Valsalva maneuver, there is a physiological tendency to move stomach contents towards the esophagus, necessitating a well-functioning barrier to prevent reflux. Essential requirements for a sufficient antireflux barrier include:

• Function and position of the lower esophageal sphincter (LES)
• External compression by the diaphragmatic crura
• Acute angle of His between distal esophagus and proximal stomach
• Phrenoesophageal ligament

From a pathophysiological perspective, three fundamental forms of an insufficient antireflux barrier can be distinguished, which may occur individually or in combination:

• Transient sphincter relaxation
• Permanently reduced sphincter pressure
• Altered anatomy (e.g., hiatal hernia)

While transient sphincter relaxations dominate in patients with mild reflux disease, severe forms of GERD are often associated with a hiatal hernia and/or a permanently reduced sphincter pressure.

Transient Relaxation of the LES

In healthy individuals and reflux patients with normal resting pressure of the LES (> 10 mm Hg), reflux episodes can occur due to transient, swallow-independent relaxations of the LES. Unlike swallow-induced relaxations, transient relaxations are not accompanied by peristaltic esophageal activity and last longer. What distinguishes reflux patients from healthy individuals with transient relaxations is not the frequency of relaxations, but the reflux of gastric acid. In healthy individuals, transient relaxations rarely lead to acid reflux; rather, gas reflux ("belching") is more prominent. Triggers for transient relaxations can include vagovagal reflexes induced by distension of the proximal stomach.

Sphincter Apparatus and Hiatal Hernia

The LES is a 3 – 4 cm long, tonically contracted segment of smooth muscle, with a pressure normally ranging from 10 – 30 mm Hg. Its muscular contraction is calcium-dependent, and its neural regulation is cholinergic. If the intra-abdominal pressure exceeds the sphincter pressure—especially with abrupt increases such as from coughing—or if the sphincter pressure is very low (0 – 4 mm Hg), reflux of stomach contents into the lower esophagus occurs. In addition to the LES, the approximately 2 cm long diaphragmatic crura play an important role as an "external" sphincter during intra-abdominal pressure increases.

An axial hiatal hernia predisposes to reflux disease, where various pathophysiological mechanisms lead to acid reflux into the lower esophagus. The displacement of the LES results in an anatomical separation of the internal and external sphincter apparatus, leading to a loss of the sphincter effect of the diaphragmatic crura. Furthermore, the hernia causes disturbances in LES function with a decrease in basal pressure and an increase in transient relaxation episodes. Acid reflux into the lower esophagus is also facilitated by swallow-induced sphincter relaxations, which are practically never observed in reflux patients without hernia and in healthy individuals.

Acid, Pepsin, and Bile Acids

Acid and pepsin play a central role in the induction of symptoms and lesions in the esophagus. In patients with GERD, the volume of acid secretion is usually normal, but acid and pepsin pass through the insufficient antireflux barrier into the acid-sensitive esophagus. The relevance of acid is underscored by the effectiveness of proton pump inhibitors in GERD therapy and by the correlation of esophageal acid exposure with the extent of erosive damage. The damaging effect of acid and pepsin can be potentiated by bile acids (duodenogastroesophageal reflux, DGER). At acidic pH, conjugated bile acids lead to erosions, and at alkaline pH, unconjugated bile acids increase the permeability of the esophageal mucosa.