Anatomy - Myotomy and Fundoplication according to Dor, robotically assisted

Esophagus

General Characteristics

• Muscular hollow organ, approx. 25–30 cm long
• Connects pharynx (C6) with the stomach (Th11)
• Three constrictions:
  1. Upper constriction – cricoid constriction (transition pharynx/esophagus, at level C6)
  2. Middle constriction – aortic constriction (crossing with aortic arch + left main bronchus)
  3. Lower constriction – diaphragmatic constriction (esophageal hiatus, Th10)

Topographical Sections

Cervical Esophagus (C6–Th1)

• Behind the trachea
• Accompanying structure: recurrent laryngeal nerve
• Access: transcervical, ventral-lateral

Thoracic Esophagus (Th1–Th10)

• Upper mediastinum: behind trachea, in front of spine
• Middle mediastinum: behind heart and pericardium
• Crossing by aortic arch, azygos vein, left main bronchus
• Access: right-thoracic (better overview)

Abdominal Esophagus (short, 1-3 cm)

• Passes through esophageal hiatus (Th10) into the abdomen
• Empties into the cardia region of the stomach
• Accompanying structures: anterior vagal trunk (left), posterior (right)

Stomach

General & Location

• Muscular hollow organ between esophagus and duodenum
• Located in the left/middle upper abdomen, directly under the diaphragm
• Can vary greatly in size and shape depending on age, filling state, and body position
• Great interindividual differences in terms of location, size, and shape

Size & Filling Capacity

• Average length: 25–30 cm (with moderate filling)
• Storage capacity: approx. 1.5 liters, in extreme cases up to 2.5 liters

Stomach Layers and Attachment

• Located intraperitoneally; mostly covered with serosa (except dorsal cardia)
• Embryonic mesogastria rotate into a frontal position:
  • Lesser omentum: from the lesser curvature to the hepatic portal
  • Greater omentum: from the greater curvature to the transverse colon, spleen, and diaphragm
• Attachment and stabilization by ligaments that, among other things, extend to the liver and spleen

Sections of the Stomach

• Cardia (stomach entrance, upper gastric orifice, ostium cardiacum)
  • Area of 1–2 cm in which the esophagus empties into the stomach
  • Distinct transition from esophageal mucosa to gastric mucosa (clearly visible on endoscopy)
• Gastric Fundus (stomach fundus)
  • Located above the stomach entrance, bulges upward
  • Also referred to as gastric dome or fornix gastricus
  • Typically filled with air; in upright position the highest point, recognizable as “gastric bubble” on X-ray
  • Delimited from the stomach entrance by the cardiac notch
• Gastric Corpus (stomach body)
  • Main part of the stomach
  • Characterized by deep longitudinal mucosal folds (plicae gastricae) that run from the stomach entrance to the pylorus (“gastric canal”)
• Pylorus (pyloric part, pyloric sphincter)
  • Beginning with the expanded pyloric antrum, followed by pyloric canal (canalis pyloricus)
  • Ends with the actual pyloric sphincter (pylorus), where the pyloric sphincter muscle (M. sphincter pylori) is located
  • Closes the stomach outlet (ostium pyloricum) and regulates the passage of chyme into the duodenum

Formal Boundaries and Further Anatomical Features

• Greater curvature (convex side)
• Lesser curvature  (concave side)
• Anterior wall: Paries anterior; Posterior wall: Paries posterior
• Greater omentum originates from the greater curvature; Lesser omentum spans between the left hepatic lobe and the lesser curvature

Layer structure of the esophagus (from inside to outside)

1. Tunica mucosa (Mucosa)

• Lamina epithelialis mucosae: multilayered, non-keratinized squamous epithelium – mechanically protects against food and gastric acid, with a clear Z-line to the gastric epithelium 
• Lamina propria mucosae: loose connective tissue with small vessels, lymphoid tissue, and nerves 
• Lamina muscularis mucosae: thin smooth muscle layer – contracts independently of the muscularis propria 

2. Tela submucosa

• Connective tissue layer with Glandulae oesophageales (mucous glands), which produce mucus for the swallowing process 
• Meissner plexus: enteric nerve plexus for controlling mucosal activity
• Longitudinal folds in the tissue allow expansion during swallowing; in cross-section, the lumen appears star-shaped 

3. Tunica muscularis (Muscle wall)

• Consists of two layers:
  • Stratum circulare (circular muscle)
  • Stratum longitudinale (longitudinal muscle)
• Muscle distribution:
  • upper third: striated muscle
  • middle third: mixed muscle
  • lower third: exclusively smooth muscle 
• Auerbach plexus (myenteric plexus) between the muscle layers: coordination of peristalsis 

4. Tunica adventitia / Tunica serosa

• Pars thoracica: Adventitia – loosely connecting, collagenous connective tissue, fixes the esophagus in its environment 
• Pars abdominalis (after passage through the diaphragm): covered by serosa – intraperitoneal segment with single-layered squamous epithelium 

Layers of the stomach wall from inside to outside
Under the microscope, the stomach wall shows a characteristic layer structure from inside to outside:

1. The Tunica mucosa is the mucosal layer that lines the stomach from the inside.  The gastric mucosa is divided into three sublayers: The lamina epithelialis mucosae forms a tough neutral mucus that protects the gastric mucosa from mechanical, thermal, and enzymatic damage. Below that follows the lamina propria mucosae as a sliding layer, in which the gastric glands (Glandulae gastricae) are embedded. Finally, there is a narrow lamina muscularis mucosae, a thin first muscle layer that can change the relief of the mucosa.
2. The Tela submucosa follows in the view from inside to outside of the gastric mucosa. It represents a loose sliding layer consisting of connective tissue. In the tela submucosa, there is a dense network of blood and lymph vessels, as well as a nerve fiber plexus, the submucosal plexus (Meissner plexus), which controls gastric secretion. This plexus works independently of the central nervous system (CNS) and is influenced by the autonomic nervous system.
3. This is followed by a strong Tunica muscularis, which is divided into three sublayers with fibers running in different directions: an inner layer of small obliquely running muscle fibers (Fibrae obliquae), then a circular muscle layer (Stratum circulare), and outermost an outer longitudinal muscle layer (Stratum longitudinale). This musculature is responsible for the peristalsis of the stomach, which is responsible for the constant mixing of the chyme with the gastric juice. Between the circular and longitudinal muscle layers runs a nerve fiber plexus, the myenteric plexus (Auerbach plexus), which controls the function of the musculature. Just like the submucosal plexus, this plexus works largely autonomously but is influenced by the autonomic nervous system.
4. This is followed by another connective tissue sliding layer (Tela subserosa).
5. The conclusion is formed by the Tunica serosa. The serosa is also divided into several layers. The tela subserosa is followed by the Lamina propria serosae. In this, the blood and lymph vessels as well as nerves run. In addition, there are cells of the immune defense in the lamina propria, which are referred to as milky spots (Macula lactea). The Lamina epithelialis serosae is finally directed towards the body cavity and consists of a single-layered squamous epithelium, the serosal epithelium.This layer is shiny, transparent, and ensures good slidability of the stomach relative to the adjacent organs through a thin fluid film. 

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 found per 1mm2 of the mucosal surface. Various cells are located in the wall of the glandular tube:

• Mucus cells: They produce the same neutral mucus as the epithelial cells.
• Accessory cells: These cells are located quite superficially in the gland and secrete alkaline mucus, i.e., the pH value is high due to the bicarbonate ions (HCO3- ions) contained therein. This property is important for controlling and, if necessary, regulating the pH value of the stomach. The mucus coats the gastric mucosa and thus protects against self-digestion by the aggressive hydrochloric acid (HCl) and enzymes as self-digesting proteins. This cell type is found in abundance 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 food proteins. Since the enzyme only comes into contact with the hydrochloric acid at the surface of the gland, self-digestion of the glands by the enzyme is prevented. This cell form is mainly found in the corpus of the stomach.
• Parietal cells: These cells, which are found in greater numbers in the gastric corpus, produce abundant hydrogen ions (H+ ions), which are needed for the formation of hydrochloric acid (HCl). The hydrochloric acid has a very low pH value of 0.9-1.5. In addition, the parietal cells form the so-called intrinsic factor. This substance forms a complex in the intestine with vitamin B12 from food, which can then pass through the small 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 formation in the parietal cells.

Esophagus Function

• Transport of Food and Liquid
  Peristaltic waves of the longitudinal and circular muscles transport the bolus from the hypopharynx to the stomach. In this process, the swallowing act is initially voluntary, then reflexive.
• Protection against Reflux
  Functional closure by the lower esophageal sphincter (UES = upper, LES = lower sphincter) as well as the crura of the diaphragm.
• Controlled Passage through the Diaphragm
  Coordination of swallowing act and respiratory movement.

Stomach Function

• The stomach serves as a reservoir for the ingested food. Its task is to store the food and to mix it. 
• In the stomach, the acidic gastric juice (mucus and HCl) and enzymes are produced, which pre-digest some components of the food. Subsequently, the chyme is passed portionwise through the pylorus into the duodenum. 
• It can store the food for hours and thus ensures that we can cover our daily nutritional needs with a few larger meals. 

Arterial Vascular Supply Esophagus

The blood supply of the esophagus occurs segmentally. It receives arterial blood from three main sections, corresponding to its topographic division:

The arterial supply of the stomach occurs via several blood vessels, all of which originate from the unpaired celiac trunk. These run along the gastric curvatures as vascular arcades to supply the organ and form numerous anastomoses among themselves:

• 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.

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

Venous Drainage of the Esophagus

The venous drainage of the esophagus occurs segmentally in three directions and forms an important portocaval anastomosis through its connections between the portal and caval venous systems.

Note: This portocaval anastomosis is clinically particularly significant in portal hypertension.

• Cervical: V. thyroidea inferior → V. brachiocephalica
• Thoracic: Vv. oesophageae → V. azygos / hemiazygos
• Abdominal: V. gastrica sinistra → V. portae
  ➡ Anastomoses between V. azygos and V. portae = portocaval connection (esophageal varices in portal hypertension).

Neural Supply of the Esophagus

The neural supply of the esophagus is divided into somatomotor/sensory components for the upper (striated) muscle portion and visceromotor/sensory components for the smooth muscle portion.

• Motor Function
  • Upper Third (Striated Musculature)
    • Somatomotor: N. vagus (Rr. pharyngei, R. recurrens) → voluntary initiation of swallowing
  • Middle and Lower Third (Smooth Musculature)
    • Visceromotor: N. vagus via the Plexus oesophageus → controlled by parasympathetic reflexes
• Parasympathetic Innervation
  • Source: Nn. vagi (right and left vagus)
  • Course: Form the Plexus oesophageus in the thorax → pass as Trunci vagales (anterior/posterior) through the diaphragm to the stomach
  • Function: Peristalsis, secretion, sphincter tone
• Sympathetic Innervation
  • Source: Truncus sympathicus (segments Th1–Th6) → Nn. splanchnici major/minor → Plexus oesophageus
  • Function: Inhibition of peristalsis, increase in sphincter tone
• Sensory Innervation
  • Somatosensory (pain, touch in the upper third): N. vagus, N. laryngeus recurrens
  • Viscerosensory (distension, chemical stimuli in the lower third): Vagus and sympathetic pathways → posterior horns of the spinal cord
• Surgical Relevance:
  • Injury to the N. laryngeus recurrens (e.g., during cervical esophageal mobilization) → hoarseness, risk of aspiration
  • Denervation of the lower esophagus in fundoplication or esophagectomy can lead to motility disorders

Venous Supply of the Stomach

 Parallel to the arterial supply, the 4 major veins of the stomach run along the two curvatures. Overall, they form collecting veins (V. gastrica sinistra and dextra directly into the V. portae hepatis, V. gastroomentalis sinistra and Vv. gastricae breves to the V. splenica, and V. gastroomentalis dextra to the V. mesenterica sup.), which ultimately all drain into the portal vein.

Neural Supply of the Stomach 

The neural supply of the stomach is predominantly under the autonomic nervous system. There are also sensory fibers: The sympathetic system supplies the musculature of the pylorus, the parasympathetic system (N. vagus X) supplies the remaining stomach musculature and the glands of the stomach. The N. vagus 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 (Tr. vagalis anterior), and the posterior surface on the right side (Tr. vagalis posterior). Sensory fibers from the stomach, however, run afferently via the N. splanchnicus major to the thoracic spinal ganglia.

Lymphatic Drainage Pathways of the Esophagus

• Cervical → paratracheal, deep cervical LN
• Thoracic → tracheobronchial, paratracheal, paraesophageal LN
• Abdominal → left gastric, celiac LN
• Relevance in Esophageal Carcinoma: frequently multisegmental lymphatic drainage

Lymphatic Drainage Pathways of the Stomach

The draining lymph vessels of the stomach run parallel to the arterio-venous supply of the organ:

• The lymph of the lesser curvature drains parallel to the left / right gastric arteries into the left / right gastric nodes,
• from the gastric fundus, the lymph flows parallel to the splenic artery into the splenic nodes,
• the lymph of the greater curvature drains parallel to the attachment of the greater omentum to the right / left gastro-omental nodes,
• from the pyloric region, the lymph drains into the pyloric nodes.

From the mentioned regional lymph nodes, the lymph subsequently flows into the celiac nodes, the superior mesenteric lymph nodes and the thoracic duct.

Another drainage pathway for the lymph is provided by the pancreatic nodes, so that tumors of the stomach can indeed metastasize to the pancreas. As a peculiarity of gastric carcinoma, a noticeable lymph node (Virchow's lymph node) is repeatedly found in the left lateral neck region, which indicates advanced metastasis.

For surgical reasons, the lymph node stations of the stomach are divided into 3 compartments:

• Compartment I (LN Group 1-6): all LN directly at the stomach: paracardial (group 1+2), along the lesser and greater curvature (group 3+4), supra- and infrapyloric (group 5+6).
• Compartment II (LN Group 7-11): LN 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): LN at the hepatoduodenal ligament (group 12), behind the pancreatic head (group 13), at the mesenteric root and the mesentery (group 14+15) as well as along the abdominal aorta (group 16).

The lower esophageal sphincter (LES), also called gastroesophageal sphincter or cardiac sphincter, is a ring-shaped muscle at the transition between the esophagus and the stomach. Its main function is to prevent the backflow of gastric acid and food chyme into the esophagus.

Function of the lower esophageal sphincter:

Closure mechanism:

• The muscle ring remains tonically contracted at rest (i.e., it is tense) and ensures that stomach contents do not flow back into the esophagus.
• The resting tone is regulated by the autonomic nervous system (primarily the vagus nerve) and hormonal factors.

Opening during swallowing:

• During swallowing, the LES relaxes reflexively to allow food to pass into the stomach.
• This relaxation is triggered by complex neuronal control, in which inhibitory neurotransmitters such as nitric oxide (NO) and VIP (vasoactive intestinal peptide) play a role.

Prevention of reflux:

• After the passage of food, the muscle contracts again to retain the stomach contents.
• This is supported by the pressure difference between the chest and abdominal cavity as well as the angle between the esophagus and stomach (so-called angle of His).

Involvement in peristalsis:

• The lower esophageal sphincter works together with the esophageal peristalsis to efficiently transport food into the stomach.

Clinical relevance:

• An insufficiency (weakness) of the lower esophageal sphincter can lead to gastroesophageal reflux disease (GERD), causing gastric acid to rise into the esophagus and result in heartburn.
• An overactivity or malfunction can lead to achalasia, a condition in which the sphincter does not relax properly, making swallowing difficult.

In summary, the lower esophageal sphincter is an essential muscle for digestion and the protection of the esophagus from aggressive gastric acid.

1. Pathophysiology and Neurogenic Dysfunction

Degeneration of the Myenteric Plexus

• In the pathogenesis of achalasia, there is a progressive degeneration of inhibitory neurons in the myenteric plexus (Auerbach's plexus).
• These neurons produce nitric oxide (NO) and vasoactive intestinal peptide (VIP), which physiologically mediate relaxation of the lower esophageal sphincter.
• Due to their loss, the activity of the cholinergic excitatory neurons predominates, leading to a persistent increase in tone of the LES.

Absent Peristalsis in the Esophagus

• The coordinated peristalsis of the esophagus is disrupted by the degeneration of inhibitory neurons.
• Instead of normal, sequential contractions, non-peristaltic, simultaneous contractions occur.
• This leads to a functional obstruction at the gastroesophageal junction.

2. Functional Effects

Hypertension of the Lower Esophageal Sphincter

• Normally, the resting tone of the LES decreases during swallowing through inhibitory signals from the myenteric plexus.
• In achalasia, the sphincter remains contracted because the nitrergic inhibitory signals are absent.
• The resting pressure of the LES is pathologically elevated (≥ 35 mmHg in HRM).

Aperistalsis of the Esophagus

• Propulsive peristaltic waves are absent in the distal esophagus.
• This leads to uncoordinated muscle activity and lack of bolus propulsion.
• Patients suffer from dysphagia, regurgitation, and weight loss.

3. Pathogenetic Hypotheses

• Autoimmune Reaction: Association with HLA-DQ genotypes suggests an immune-mediated destruction of inhibitory neurons.
• Infection Theory: An infection with herpes viruses (HSV-1) or Trypanosoma cruzi (Chagas disease) could trigger neuronal degeneration.
• Genetic Factors: Familial cases are rare, but there are indications of genetic predisposition.

5. Clinical Consequences

• Untreated, achalasia leads to progressive dilation of the esophagus (megaesophagus).
• Increased risk for aspiration, secondary esophagitis, and squamous cell carcinoma.

Conclusion

Achalasia is a primary, neurodegenerative disease of the esophagus with absent inhibitory control of the lower esophageal sphincter and consecutive aperistalsis. 

Achalasia is mainly classified according to the Chicago Classification (High-Resolution Manometry) into three types. Additionally, there is an etiological classification into primary and secondary achalasia.

1. Classification according to the Chicago Classification (Manometry-based)

This classification is based on High-Resolution Esophageal Manometry (HRM) and describes different functional forms of achalasia:

- Type I (classic achalasia)

• No relevant peristalsis of the esophagus
• Increased lower esophageal sphincter (LES) resting pressure with absent relaxation
• Absence of contractions in the tubular esophagus
• Expanded lumen possible (advanced stages → megaesophagus)
• Treatment: Pneumatic dilation, laparoscopic myotomy or POEM

- Type II (panesophageal pressure increase)

• Uncoordinated contractions with increased intraluminal pressure increase (“compression pattern”)
• Uniform pressure increases over the entire esophagus
• Best prognosis for interventions (e.g., myotomy or dilation)
• Treatment: Pneumatic dilation, laparoscopic myotomy (very good success prospects)

- Type III (spastic achalasia)

• Spastic, high-amplitude contractions in the distal esophagus
• High intraluminal pressure with irregular, sometimes painful contractions
• Lowest success rate for dilation, therefore often surgical or endoscopic myotomy (POEM) necessary
• Treatment: POEM or extended myotomy (Heller myotomy with further distal extension of the incision)

2. Etiological Classification

In addition to the functional classification, achalasia can also be classified according to the cause:

- Primary Achalasia

• Idiopathic degeneration of the myenteric plexus (Auerbach's plexus)
• Unknown cause, presumably autoimmune-related

- Secondary Achalasia (Pseudoachalasia)

• Cause due to external factors, e.g.:
  • Malignancies (gastric carcinoma, esophageal carcinoma, mediastinal tumors)
  • Chagas disease (Trypanosoma cruzi → damage to the enteric nervous system)
  • Postoperative or post-radiation damage
  • Autoimmune diseases (e.g., paraneoplastic syndromes)

Summary

1. Chicago Classification (Type I–III, based on manometry)
2. Etiological Classification (Primary vs. Secondary Achalasia)

These classifications help in choosing the therapy and assessing the prognosis.