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Surgical anatomy of the stomach
In terms of function, the stomach mixes and stores food and is an expansion of the alimentary tract between the esophagus and the duodenum. This muscular hollow viscus produces acidic gastric juice (mucus and HCl) and enzymes, which predigest some elements of the ingested food, and portions the chyme into the duodenum.
Usually, the stomach is located immediately inferior to the diaphragm in the left upper quadrant and epigastrium. Location, size and shape of the stomach vary from person to person and may differ substantially, depending on age, filling condition and body position. The moderately filled stomach has a mean length of 25-30 cm and can hold 1.5 liters, in extreme cases up to 2,5 liters.
Within the abdominal cavity the stomach is held in position and stabilized by ligaments inserting at the liver and spleen Its convex aspect forms the major curvature (curvatura major gastrica) and its concave aspect the lesser curvature (curvatura minor gastrica). Its anterior wall is termed paries anterior gastrica and its posterior aspect paries posterior gastrica.
Since the stomach is an intraperitoneal viscus, it is covered by the gastric serosa (tunica serosa gastrica), and only the posterior aspect of the cardia is free of serosa. Stomach rotation shifts the embryonic mesogastrics from their former sagittal position to a frontal location. The lesser omentum originates at the lesser curvature and extends to the hepatic portal, while the greater omentum originates at the greater curvature and courses to the transverse colon, spleen and diaphragm.
The stomach displays the following portions:
Entrance of stomach / Cardia / Ostium cardiacum
The superior opening of the stomach, where the esophagus enterst the stomach, is 1-2 cm long. It is characterized by a marked transition from the mucosa of the esophagus to that of the stomach.
Gastric fundus / fundus gastricus
Superior to the level of entrance of the esophagus the fundus arches cephalad, which then is called gastric fornix (fornix gastricus). Usually, the fundus is full of air which is swallowed automatically when ingesting food. In the erect position the fundus is the highest point of the stomach, and on abdominal films its trapped air is evident as the “gastric bubble”. A notch (incisura cardialis) clearly delimits the fundus from the entrance of the stomach.
Body of the stomach / Corpus gastricum
The main portion of the stomach is taken up by the gastric body. The deep mucosal folds (plicae gastricae) found here extend from the cardia to the pylorus and are also known as “magenstrasse”.
Pylorus / Pars pylorica
This portion begins with the extended pyloric antrum, followed by the pyloric canal, and terminates at the actual pylorus. It is formed by the pyloric sphincter (m. sphincter pyloricus), a strong circular layer of muscle which closes off the inferior gastric orifice (ostium pyloricum). The pylorus closes off the gastric outlet and periodically lets some of the chyme pass into the adjacent duodenum.
Layers and structure of the gastric wall
Under the microscope the gastric wall displays a characteristic layered structure with the following sequence from the inside out:
- The internal aspect of the gastric wall is lined by mucosa (tunica mucosa). The gastric mucosa is made up of three sublayers: The lamina epithelialis mucosae produces viscous neutral mucus which protects the gastric mucosa against mechanical, thermal and enzymatic injury. This is followed by the loose connective tissue coat of the lamina propria mucosae into which the gastric glands (glandulae gastricae) descend. The outermost layer of the mucosa is the small lamina muscularis mucosae which can change the relief of the mucosa.
- The gastric mucosa is followed by a loose layer of connective tissue (tela submucosa gastrica), which houses not only a dense network of blood and lymph vessels but also a nerve plexus (plexus submucosus or Meissner plexus) which controls gastric secretion. Although this plexus is independent of the central nervous system (CNS), the latter may affect the former via the autonomic nervous system.
- Next is the marked tunica muscularis with its three sublayers, each comprising muscle fibers coursing in different directions: The inner layer of small oblique muscle fibers (fibrae obliquae), then a circular layer (stratum circulare) and finally the outermost longitudinal layer of muscle fibers (stratum longitudinale). These muscles effect the peristalsis of the stomach and ensure thorough mixing of the chyme with the gastric juice. Muscular function is controlled by a nerve plexus, the plexus myentericus or Auerbach plexus, in between the circular and longitudinal layers. Just like the plexus submucosus, this plexus is mostly autonomous but is also affected by the autonomic nervous system.
- Next is another layer of loose connective tissue (tela subserosa gastrica).
- The peritoneum (tunica serosa) covering the external aspect of the stomach is its final layer.
The gastric glands (glandulae gastricae) located in the fundus and body of the stomach are part of the lamina propria mucosae. 1 mm2 of mucosal surface comprises up to 100 such glands. The ductal wall of the gland is lined with different types of cells:
- Mucous cells: They produce the same neutral mucus as the epithelial cells.
- Surface mucous cells: Foveolar cells are close to the surface of the gland and contain alkaline mucus, i.e., the pH of its hydrogen carbonate ions (HCO3–) is rather high. This property is rather important in controlling the gastric pH. The mucus lines the gastric mucosa and protects it against autodigestion by the aggressive hydrochloric acid (HCl) and enzymes as autodigesting proteins. This type of cells is mostly found in the cardia and fundus of the stomach.
- Chief cells: These cells produce the inactive proenzyme pepsinogen which, once released, is activated by hydrochloric acid (HCl) to the active enzyme pepsin, the latter starting the digestion of the alimentary proteins. Since the initial contact of the enzyme with hydrochloric acid is at the surface of the gland, this ensures that the glands will not be autodigested by the enzyme. This type of cells is mostly found in the body of the stomach.
- Parietal cells: Mostly found in the body of the stomach, these cells produce plenty of hydrogen ions (H+) needed in the production of hydrochloric acid (HCl). The latter has a rather low pH of 0.9-1.5. In addition, the parietal cells also produce the so called intrinsic factor. Together with vitamin B12 from the ingested food this substance generates a complex in the small intestine which is able to pass through the intestinal wall. This vitamin plays a pivotal role in erythropoiesis (gastric resection may result in anemia).
- G cells: Primarily found in the gastric antrum, these cells produce gastrin which increases HCl production in the parietal cells.
The stomach acts as a reservoir for ingested food. Since it may store food for hours, it ensures that we can meet our daily nutritional requirements with a few major meals. Peristalsis thoroughly mixes the chyme with the gastric juice, the food is broken up chemically, predigested and then portioned into the duodenum.
Arterial and venous blood supply, innervation
The arteries supplying the stomach all arise from the unpaired celiac trunk, comprise numerous anastomoses with each other and course as arterial arcades along the gastric curvatures:
- Right gastric artery arising from the hepatic artery proper and supplying the inferior portion of the lesser curvature
- Left gastric artery supplying the superior portion of the lesser curvature
- Short gastric arteries arising from the splenic artery and supplying the fundus
- Right gastro-omental artery arising from the gastroduodenal artery and supplying the inferior (right) portion of the greater curvature
- Left gastro-omental artery arising from the splenic artery and supplying the left portion of the greater curvature
- Posterior gastric artery arising from the splenic artery and supplying the posterior gastric wall.
This way, the stomach is supplied along the lesser curvature by an arterial arcade between the left and right gastric artery and along the greater curvature by another arcade between the left and right gastro-omental artery.
The 4 major veins parallel the arterial blood supply along both curvatures of the stomach. They unite to collecting veins (left and right gastric vein draining directly into the hepatic portal vein; left gastro-omental vein and the short gastric veins drain into the splenic vein; while the right gastro-omental vein drains into the superior mesenteric vein) which all drain into the portal vein.
While gastric innervation is primarily controlled by the autonomic nervous system, there are also sensory fibers: The sympathetic nervous system innervates the pyloric muscles, while the parasympathetic nervous system (vagus nerve, CN X) supplies the other gastric muscles and the gastric glands. The vagus parallels the esophagus on the left and right and passes through the esophageal hiatus in the diaphragm; on the left side it then reaches the anterior gastric wall (t. vagalis anterior), while on the right side it innervates the posterior wall of the stomach (t. vagalis posterior). The afferent signals from sensory fibers of the stomach, on the other hand, pass via the greater splanchnic nerve to the thoracic spinal ganglia.
Lymphatic drainage of the stomach parallels its arterial and venous blood supply :
- The lymphatics of the lesser curvature parallel the left / right gastric artery and drain into the left / right gastric lymph nodes
- The lymphatics from the gastric fundus parallel the splenic artery and drain into the splenic lymph nodes
- The lymphatics from the greater curvature parallel the suspension of the greater omentum and drain into the left / right gastro-omental lymph nodes
- The lymphatics from the pyloric region drain into the pyloric lymph nodes.
From these lymph nodes mentioned above the lymph then drains into the celiac nodes, the superior mesenteric nodes and the thoracic duct.
Since the pancreatic lymph nodes are another pathway for lymph drainage, tumors of the stomach may very well metastasize into the pancreas. One special sign of gastric cancer is the frequent prominent supraclavicular lymph node of the left lateral region of the neck (Virchow / signal node) which signals advanced metastasis.
For reasons of surgical technique, the lymph node stations are grouped into 3 compartments:
- Compartment I (LN stations 1-6): All lymph node directly at the stomach; paracardiac (station 1+2), along the lesser and greater curvature (station 3+4), suprapyloric and infrapyloric (station 5+6).
- Compartment II (LN station 7-11): Lymph nodes along the major vessels: Left gastric artery (station 7), common hepatic artery (station 8), celiac trunk (station 9), splenic hilum (station 10), splenic artery (station 11).
- Compartment III (LN station 12-16): Lymph nodes at the hepatoduodenal ligament (station 12), posterior to the pancreatic head (station 13), at the mesenteric root and the mesentery (station 14+15) and along the abdominal aorta (station 16).
Pathophysiology of reflux disease
Gastro-esophageal reflux disease (GERD) results when reflux of gastric content into the esophagus effects esophageal or extra-esophageal manifestations and/or the quality of life of the patient is impaired by these symptoms. Even if the pathogenesis of GERD is multifactorial, its primary cause is insufficiency of the antireflux barrier.
Since the pressure within the abdominal cavity is higher than in the chest and this gradient increases even more during coughing and in the Valsalva maneuver, there is the physiologic tendency to propel gastric content toward the esophagus, which in turn necessitates a well functioning barrier to prevent any reflux. A functioning antireflux barrier must fulfill these essential requirements:
- Function and location of the lower esophageal sphincter (LES)
- External compression by the diaphragmatic crura
- Acute angle of His between the distal esophagus and proximal stomach
- Phreno-esophageal ligament
In terms of pathophysiology, there are 3 basic types of insufficiency of the antireflux barrier, which may be present alone or in combination:
- Transient sphincter relaxation
- Permanently low sphincter pressure
- Changes in anatomy (e.g., hiatal hernia)
While transient sphincter relaxation dominates in patients with mild reflux disease, severe GERD is a frequent sequela of hiatal hernia and/or chronically low sphincter pressure.
Transient LES relaxation
Reflux episodes in healthy persons and reflux patients with normal LES resting pressure (> 10 mmHg) may be due to transient LES relaxations not induced by swallowing. Unlike those relaxations induced by swallowing, transient relaxations are not accompanied by peristaltic esophageal activity and last longer. The difference between healthy persons and reflux patients with transient relaxations is not the relaxation rate but gastric acid reflux. In healthy persons transient relaxations rarely result in acid reflux, rather the emphasis is on gas reflux (“belching”). Transient relaxations may be caused by vasovagal reflexes which in turn are triggered by distension of the proximal stomach.
Spincter muscle and hiatal hernia
The 3–4 cm long LES is a smooth muscle segment with tonic contraction and a normal pressure of 10–30 mmHg. Its muscular contraction depends on calcium and the innervation is cholinergic. If the pressure within the abdominal cavity is higher than the sphincter pressure – particularly in abrupt increases, e.g. during coughing – or whenever the sphincter pressure is very low (0–4 mmHg), gastric content will reflux into the distal esophagus. Apart from the LES the roughly 2 cm long crura of the diaphragm also play an important role in intraabdominal pressure increases because they act as “external sphincters”.
One predisposing factor for GERD is axial hiatal hernia, where various pathophysiologic mechanisms result in acid reflux into the lower esophagus. Internal and external sphincter are separated by this anatomic shift in LES, thereby losing the sphincter effect of the diaphragmatic crura. In addition, hiatal hernia interferes with the LES function by decreasing basal pressure and increasing the number of episodes with transient relaxations. Furthermore, acid reflux into the lower esophagus is also promoted by swallowing induced sphincter relaxations, which are almost never seen in healthy persons and reflux patients without hernia.
Acid, pepsin and bile acids
Acid and pepsin play a central role in triggering esophageal symptoms and lesions. While in GERD patients the volume of acid secretion is mostly normal, acid and pepsin pass through the insufficient antireflux barrier into the acid-sensitive esophagus. The importance of the acid is underlined by the efficacy of proton pump inhibitors in GERD treatment and by the correlation of the esophageal acid exposition with the extent of erosive injuries. The damaging effect of acid and pepsin may be augmented by the bile acids (duodenogastro-esophageal reflux, DGER). At acidic pH levels conjugated bile acids result in erosions, while at alkaline pH levels unconjugated bile acids will increase the permeability of the esophageal mucosa.
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After transverse incision at upper pole of the umbilicus establish pneumoperitoneum and then insert 10 mm laparoscope. Insert four 5 mm trocars under transillumination in a semicircle superior to the umbilicus, one each in the left and right medioclavicular and anterior axillary line. Work through both medial 5 mm trocars, while the left lateral trocar is used for the liver retractor and the right lateral trocar for a grasper holding the stomach. Anti-Trendelenburg position of the patient and OR Table tilted slightly to the left.
Incising the greater omentum and exposing the right crus of the diaphragm
Lifting up the left hepatic lobe with a liver retractor reveals the esophageal hiatus. Dissection with the harmonic scalpel begins by incising the lesser omentum at the pars flaccida while simultaneously pulling the stomach up to the left to the free margin of the right crus of the diaphragm. Now expose the gastroesophageal junction at the right crus while evading the posterior vagal trunk.
Exposing the left crus of the diaphragm
Mediastinal mobilization of the distal esophagus
Now dissect the distal esophagus in the mediastinum, with the harmonic scalpel and also bluntly, so that it is exposed circucumferentially over a distance of at least 10 cm; in the end 4 cm - 5 cm of the esophagus should rest tension-free in the peritoneal cavity. Dissection is markedly facilitated by encircling the esophagus and the posterior vagal trunk with a tape.
In order to prevent the subsequent hiatoplasty from constricting the terminal esophagus, insert a 40F gastric tube as bougie for calibration purposes. Adapt both crura of the diaphragm posterior to the esophagus by interrupted sutures whose knots are tied extracorporeally and then guided into proper position with a knot pusher (hangman’s knot). Use non-absorbable sutures size 0. The video clip demonstrates the first of a total of three sutures.
- The sutures must include the peritoneal cover of the crura of the diaphragm which frequently pulls back to the side during dissection.
- In very large hiatal hernia and upside-down stomach with the risk of volvulus, the hiatus may be constricted further by additional sutures anterior to the esophagus.
Mesh augmentation of the esophageal hiatus
In large defects, particularly in para-esophageal hernias, mesh augmented hiatoplasty is recommended to prevent wrap dislocation into the mediastinum.
Here, a keyhole-like opening is cut into a 6 cm x 8 cm biomesh, which is placed around the esophagus like a collar. Fixate the mesh with absorbable tacks.
- Non-absorbable meshes may result in serious complications. Esophageal erosion, mesh migration into esophagus and stomach.
- Mesh fixation at the hiatus with spiral tacks is not exactly safe because injuries to the pericardium and coronary vessels have been reported. When in doubt about where to place the tacks, fixate the mesh with fibrin sealant.
Mobilizing the gastric fundus
After removing the encircling tape prepare for the fundoplication by mobilizing the entire gastric fundus along the greater curvature with division of the proximal gastrosplenic ligament. In oder to apply tension to the short gastric vessels, pull the stomach to the right with judicious use of force. Divide these vessels successively with the harmonic scalpel. Full mobilization of the proximal stomach requires that all posterior retroperitoneal adhesions with the fundus must be divided. The space created posteriorly must be large enough to accommodate the fundus pull-through later on.
For the 360° fundoplication pull the mobilized fundus posterior to the esophagus to the right with an atraumatic grasper. The inserted gastric tube calibrates the wrap and prevents esophageal constriction while performing the actual plication. Construct a short floppy Nissen fundoplication with the anterior and posterior wall of the gastric fundus. Fixation comprises 2 interrupted seromuscular sutures whose knots are tied extracorporeally and guided into proper position with a knot pusher, just as in the hiatoplasty. This step, too, relies on non-absorbable sutures size 0 (here: Ethibond®).
- The shoeshine maneuver can facilitate wrap positioning: In order to verify the correct position and length of the mobilized fundus, loosely pull the fundus back and forth posterior to the esophagus, just as you would when polishing shoes.
- The vagal trunk will remain within the wrap.
- The proximal wrap suture takes a seromuscular bite trough the anterior cardiac wall. It therefore defines the length of the intraabdominal segment of the esophagus and prevents wrap slippage.
- As demonstrated in the video clip, the bite into the anterior cardiac wall should be on the right of the cardia and not on its anterior aspect because this is where the anterior vagal nerve usually courses.
- The wrap is floppy enough if, after removal of the gastric tube, a 5 mm grasper can slip easily between the esophagus and wrap.
Leak testing, drainage
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