Table of Contents
- Location of the Esophagus
- The Three Constrictions of the Esophagus
- Wall Structure of the Esophagus
- Vascular Supply of the Esophagus
- Lymph Drainage of the Esophagus
- Innervation of the Esophagus
- The Closing Mechanism of the Esophagus
- How does Swallowing Occur?
- Swallowing Reflex
- Esophageal Peristalsis
- Diseases of the Esophagus
Location of the Esophagus
The esophagus is located behind the trachea and the heart and in front of the spine. It connects the pharynx to the stomach. The esophagus begins at the 6th or 7th cervical vertebra on the lower edge of the cricoid cartilage. The gullet also begins with the superior esophageal sphincter at the bottom of the hypopharynx (esophagus into the esophagus) adjacent to the left pyriform sinus, and then runs dorsal to the trachea in the chest area and ventral to the spine, continuing in a caudal fashion through the diaphragm. It ultimately ends at the cardia of the stomach, parallel to the 11th thoracic vertebra.
The esophagus has two gentle curves in the coronal plane. The first curve begins slightly below the beginning of the esophagus, moves to the left by the root of the neck, and returns to the midline at the level of the 5th thoracic vertebra. Access to the esophagus can be gained from the right side of the chest. The second curve is to the left and is formed as the esophagus bends to cross the descending thoracic aorta before it pierces the diaphragm. The esophagus also has anteroposterior curvatures that correspond to the curvatures of the cervical and thoracic parts of the vertebral column.
Sections of the Esophagus
The esophagus is divided into three sections: the cervical, thoracic, and abdominal parts.
The cervical part is the part of the esophagus inside the neck. It begins at the cricoid, runs ventral to the spine, and becomes the thoracic part after entering the chest cavity.
The thoracic part is the part of the esophagus in the chest and it is the longest section. It runs dorsal to the trachea in the mediastinum, and after passing through the esophageal hiatus of the diaphragm, it becomes the abdominal portion.
The abdominal portion is the part of the esophagus that leads to the stomach. It enters into the cardia of the stomach after about 1-3 cm.
The Three Constrictions of the Esophagus
Adjacent anatomical structures lead to three constricted areas in the esophagus. These constrictions are as follows:
Cervical constriction – is caused by the cricoid cartilage and is constricted by the upper esophageal sphincter until the sphincter relaxes in response to a bolus.
Thoracic/aortal constriction – is caused by the proximity of the esophagus to the aortic arch (arcus aorta) and the left main bronchus.
Diaphragmatic/abdominal constriction – is caused by the esophageal hiatus of the diaphragm.
Wall Structure of the Esophagus
The esophagus generally has the typical wall structure of the gastrointestinal tract.
Histologically, the esophagus has the following 4 concentric layers (see image below):
- Mucosal layer
- Submucosal layer
- Muscular layer
- Adventitial layer
The esophagus lacks a continuous covering layer.
Mucosal layer (mucous membrane)
The mucosa forms the innermost layer and is formed by non-keratinized stratified squamous epithelium that is consistent with that of the pharynx. The mucosal epithelium changes from squamous cell epithelium to columnar cell epithelium at the gastroesophageal junction called the “Z line” or squamocolumnar junction. It is also subjected to heavy mechanical strain.
Below the mucosa lies a smooth lamina propria that hosts capillaries, lymphatics, and the muscularis mucosae.
The second layer is formed by submucosa, and it loosely connects the mucous membrane and the muscular coat. This layer also contains the larger blood vessels, the submucosal (Meissner) nerve plexus, and the esophageal glands.
Side note on clinical presentations
This venous plexus is important for portacaval anastomoses (e.g., in cirrhosis of the liver). If the portal system is under increased pressure, it finds already present anastomoses with the systemic circulation in which to divert blood to decrease that pressure. One of these connections is between the gastric veins and esophageal veins, and esophageal varices may form. Esophageal varices are enlarged, submucosal veins in the lower third of the esophagus. This condition most often occurs in people with serious liver diseases or portal hypertension (commonly due to cirrhosis). Esophageal varices develop when normal blood flow to the liver is blocked by a blood clot or scar tissue in the liver. Patients with esophageal varices have a strong tendency to develop severe bleeding or hemorrhaging which, if left untreated, can be fatal.
The third layer is formed by circular and longitudinal muscle fibers.
Between the circular and longitudinal layers is a portion of the enteric nervous system—the myenteric plexus of Auerbach. This plexus controls the motility and peristalsis of the esophagus and the opening of the lower esophageal sphincter.
- Inner circular muscle fibers: These fibers are continuous superiorly with the fibers of the cricopharyngeal part of the inferior constrictor and inferiorly with oblique fibers of the stomach.
- Outer longitudinal muscle fibers: The longitudinal muscle fibers form a continuous covering around the entire esophagus, except posterosuperiorly, 3-4 cm below the cricoid cartilage; here, they diverge as two fascicles that ascend obliquely to the anterior aspect of the esophagus. The longitudinal layer is generally thicker than the circular layer.
The esophageal muscles are not uniform. The muscular fibers in the cranial part of the esophagus are red and consist chiefly of striated muscle. The intermediate part is mixed, and the lower part, with rare exception, contains only smooth muscle. Accessory bands of muscle connect the esophagus and the left pleura to the root of the left bronchus and the posterior of the pericardium.
The proximal one-third of the esophagus primarily consists of striated muscle. Smooth muscle predominates in the distal portion.
Side note on clinical presentations:
Laimer’s Triangle: This is a missing piece of longitudinal muscle in the dorsocranial area of the esophagus; this weak spot can lead to an increase in intraluminal pressure and an outward eversion of the mucosa and submucosa in the muscular layer and is considered a pseudodiverticulum. This pseudodiverticulum was named in 1877 by German pathologist, Friedrich Albert von Zenker, and is commonly called the Zenker diverticulum. It may be seen more frequently in elderly men who present with complaints about regurgitation of undigested, malodorous food. True diverticula are eversions of all wall layers.
The tunica adventitia is the shifting outer fascial layer that allows for free mobility of the esophagus while swallowing. It surrounds the esophagus and fills the spaces between the esophagus and surrounding organs such as the trachea, bronchi, and pleura. The following are located in this layer:
- Large supply vessels
- Lymphatic vessels
- Nerve fascicles of the vagus nerve and the esophageal sympathetic plexus
The esophagus has no serosa which makes it unique compared to the rest of the gastrointestinal tract.
Vascular Supply of the Esophagus
The three segments of the esophagus are supplied by various arteries.
Cervical – from the inferior thyroid artery (from the thyrocervical trunk)
Thoracic – from the aorta and intercostal arteries
Abdominal – from the left gastric artery (from the celiac trunk)
Venous drainage occurs through the small esophageal veins into the azygos and hemiazygos veins then into the superior vena cava.
Note: Collateral circulation—there are connections to the portal hepatic vein (portacaval anastomoses) through the right gastric vein which enlarge when blood drainage through the liver is disrupted.
Lymph Drainage of the Esophagus
The lymphatic vessels generally follow the flow of the arteries. Lymph drainage also occurs through various lymph nodes depending on the segment of the esophagus.
The cervical part drains its lymph through the deep lymph nodes of the throat (deep cervical lymph nodes) into the jugular trunk that follows the jugular veins. Metastatic disease of the upper esophagus invades the upper jugular chain.
The upper portion of the thoracic portion runs cranially through the mediastinal lymph nodes (paratracheal nodes and superior and inferior tracheobronchial nodes) into the bronchomediastinal trunk while the lower portion of the thoracic part, like the abdominal part (through the left gastric and celiac nodes), drains into the intestinal trunk.
This joins with the cisterna chyli which can be pictured as a type of “reservoir” from which the lymph flows from the thoracic duct into the left venous angle between the subclavian and jugular veins.
Innervation of the Esophagus
Like other parts of the digestive system, the esophagus is mainly controlled by the enteric nervous system (a main division of the autonomic nervous system) with the assistance of the parasympathetic and sympathetic nervous systems.
The sympathetic innervation occurs through post-ganglionic sympathetic fibers from:
- The stellate ganglion – the sympathetic trunk in the chest
- The thoracic ganglia II-V – The post-ganglionic fibers that extend into the esophageal plexus
Activation of the sympathetic nervous system causes inhibition of the secretion of the esophageal glands.
The parasympathetic innervation continues in the upper esophageal segment of the recurrent laryngeal nerve, and the lower portion of the esophagus is supplied by the vagus nerve.
Beneath the bifurcation of the trachea, the left and right vagal trunks merge into the esophageal plexus from which the vagal trunks proceed distally and pass through the esophageal hiatus, together with the esophagus.
The activation of the parasympathetic nervous system induces an increase in gland secretion and heightened peristalsis.
Afferent fibers containing the viscerosensory information of pain and stretching reach the brain from the esophagus through the recurrent laryngeal and vagus nerves.
The Closing Mechanism of the Esophagus
When resting, the esophageal muscles are exposed to greater longitudinal pressure and the lumen is closed (resting pressure between 10 and 30 mmHg).
The esophagus possesses closing mechanisms at both its upper and lower ends which are called the upper and lower esophageal sphincters.
Upper esophageal sphincter
The upper esophageal sphincter consists solely of striated skeletal muscle. Caudal segments of the inferior pharyngeal constrictor muscle, as well as a portion of the upper esophageal musculature, are part of its functional entity. The sphincter is innervated by the glossopharyngeal and vagus nerves. The upper esophageal sphincter is a barrier against reflux and it prevents aerophagia (the swallowing of air).
Lower esophageal sphincter
The lower esophageal sphincter is not a true sphincter. Various mechanisms interlock and form a functional entity that ultimately facilitates the sealing of the esophagus. Insufficient closing of the lower sphincter causes reflux of the stomach’s contents.
The following mechanisms form the functional sealing entity of the lower sphincter:
- Wringing mechanism – the smooth musculature in the tunica muscularis runs inward in a spiral shape along the caudal end of the esophagus.
- Angle of His – the esophagus joins with the cardia of the stomach at an acute angle which prevents the reflux of gastric juices.
- Phreno-esophageal ligament – the ligament allows the independent movement of the diaphragm and esophagus during respiration and swallowing.
- Constriction effect of the diaphragm – the sides of the diaphragm muscle located at the hiatus adhere firmly around the esophagus.
- Venous plexus – extensive venous plexuses are located in the mucosa (namely: lamina propria mucosae) and the submucosa.
The lower esophageal sphincter loosens reflexively (via the myenteric plexus) thereby allowing for the transit of food.
Functional disruptions of the sphincter resulting from an insufficient opening, leading to achalasia.
Reflux is the return flow of gastric juices into the esophagus which can become inflamed as a result (esophagitis).
Another complication of reflux disease is peptic ulcer.
Chronic reflux induces a long-lasting state of irritation that can transform the multilayered, non-keratinized stratified squamous epithelium into columnar epithelium. This restructuring of the tissue is called Barrett’s esophagus and is a precancerous condition.
How does Swallowing Occur?
From an anatomical perspective, the swallowing of food and fluids is facilitated by a highly tensile yet firmly established tissue in the esophagus.
The actual act of swallowing is a semi-reflexive process—i.e. partially voluntary and partially involuntary. The decision to swallow is voluntary; however, if the swallowed material touches the base of the tongue or the back of the throat, the swallowing reflex is triggered and becomes involuntary.
The swallowing process is subject to sensomotoric fine-tuning where it is adjusted to the consistency of the bolus. Information on the scent, taste, texture, and size of the bolus is constantly being sent to the brain. With peristaltic movements of the esophageal muscles, food ultimately makes its way to the stomach. When ingesting fluids, there are rarely any peristaltic movements of the esophagus. The upper and lower esophagus sphincters briefly open while the base of the mouth and the tongue push the fluid down into the stomach by the ‘splash swallow’ process.
The process is somewhat more complex for solid items.
The swallowing process can be divided into four different phases:
The oral preparation phase
This phase serves to break down and coat the bolus with saliva and is performed voluntarily.
The oral transportation phase
This phase includes the closing of the lips and jaws as well as the beginning of the lifting of the velum to the nasopharynx. It is a voluntarily triggered and reflexive process.
The pharyngeal phase
The pharyngeal phase begins when the bolus has passed through the pharyngeal isthmus and describes the transportation of the bolus through the pharynx while protecting the airways by lifting the glottis against the epiglottis; this phase is reflexive (swallow reflex).
The esophageal phase
This phase describes the transportation of the bolus through the esophagus into the stomach; this phase is reflexive.
The broken-down, saliva-coated bolus is passed over the tongue toward the pharynx. If the bolus makes contact with the base of the tongue or the back of the throat, afferents in the glossopharyngeal and vagus nerve cause the stimulation of the deglutition center in the medulla oblongata—the pharyngeal muscles are subsequently activated.
During the swallowing process, the upper and lower airways are sealed and respiration ceases.
Closing of the upper airways
The closing of the upper airways when swallowing is ensured by Passavant’s bar. The superior pharyngeal constrictor muscle contracts and produces a bulge-like swelling of the lateral and posterior epipharyngeal wall. Together with the backward motion of the velum, the bulge seals the nasopharynx during swallowing.
Side note: Velum paralysis
If the velum is paralyzed, as may be the case in diphtheria, this closing mechanism becomes insufficient, and food and fluids may enter the nose. Fortunately, because of vaccines, diphtheria has nearly been eradicated.
Closing of the lower airways
The vocal folds and epiglottis close, the base of the mouth tightens, and the larynx is lifted upward causing a closure of the lower airways.
If the airways are secured, the upper esophageal sphincter opens by way of the vagus nerve, and primary esophageal peristalsis is initiated.
The mid and lower pharyngeal constrictor muscles contract, moving the bolus to the esophagus. After the bolus has entered the esophagus, the upper esophageal sphincter closes, and the airways reopen.
The bolus then “slides” downward toward the stomach because of gravity and the peristaltic motions of the esophageal muscles.
Primary esophageal peristalsis describes the contractive waves of the esophageal muscles toward the lower esophageal sphincter.
Secondary esophageal peristalsis is caused by the stretching of the esophageal wall induced by the bolus.
The lower esophageal sphincter must relax for a bolus to enter the stomach which occurs reflexively under the control of the myenteric plexus.
Important USMLE question.
Lower esophageal sphincter tone is lowered by:
- GIP (gastric inhibitory peptide)
- Progesterone (pregnancy heartburn)
A tone reduction of the lower esophageal sphincter leads to insufficient closing which can cause heartburn. Fat, alcohol, coffee, and nicotine all lower the muscle tone of the lower esophageal sphincter.
Lower esophageal sphincter tone is increased by:
- Substance P
Achalasia is a degenerative disease that leads to expansion of the esophagus upon insufficient relaxation of the lower esophageal sphincter.
After entering the cardia, the lower esophageal sphincter closes again. Passage of one bolus of solid food takes between 5 and 25 seconds.
Diseases of the Esophagus
Reflux disease is also known as gastroesophageal reflux disease (GERD).
This widespread disease describes a chronic condition of increased reflux of gastric juices into the esophagus which may lead to regurgitation, retrosternal pain, and hoarseness.
Since the mucous layer of the esophagus does not offer enough protection against the aggressive action of gastric juices, esophagitis or erosion (ulcers) may result. The cause of reflux disease is related to a dysfunction of the lower esophageal sphincter.
Reasons for decreased muscle tone may include:
- Endogenous substances (e.g., progesterone during pregnancy)
- Stimulants and depressants (such as nicotine, caffeine, and alcohol)
- Poor nutrition (excessive sugar, fat, or carbonated beverages)
- Vitamin B12 deficiency
- Stress (activating an increase in the sympathetic nervous system)
- Increased pressure on the lower esophageal sphincter due to increased intra-abdominal pressure (pregnancy, obesity, digestion problems, lying down)
- Hiatal hernias
Therapy is contingent on the triggering factors and primarily consists of removing these triggers. Stress-induced discomfort can often be improved by learning relaxation procedures and avoiding poor nutrition habits. Surgery may be necessary for severe or chronic progression.
Highly effective medications (antacids, H2 blockers, and proton-pump inhibitors) are available.
In esophagitis, the esophagus is inflamed due to a chronic state of irritation. Most of the causes result from the long-term effects of irritation of the mucosa as follows:
- Hydrochloric acid – GERD, constant vomiting from bulimia, etc.
- Alcohol – high percentage due to alcohol abuse
- Mucous-damaging medication
- Infections such as cytomegalovirus, herpes, and candida
Chronically untreated reflux disease may result in metaplasia of the esophageal epithelium where the normal multilayered, non-keratinized stratified squamous epithelium changes into columnar epithelium. This epithelium is resistant to stimuli, but it is also susceptible to dysplasia which may become an early stage of cancer. For this reason, Barrett’s esophagus is considered precancerous.
Esophageal cancer is more frequent in patients suffering from nicotine abuse, alcohol abuse, or an overload of nitrosamines (substances present in soy sauce, cured meats, and beer). Squamous epithelium carcinoma is more common than adenocarcinoma and occurs in the upper two-thirds of the esophagus while the GERD-related columnar epithelium type of cancer occurs in the lower one-third of the esophagus.
Normally, the esophageal hiatus is constrained by the contraction of the diaphragm during inhalation. This ensures that no stomach contents enter the esophagus as a result of the intra-abdominal pressure increase during inhalation.
In the case of a hiatal hernia, the esophageal hiatus forms a type of hernial orifice through which parts of the stomach or the entire stomach are permanently or temporarily displaced into the chest cavity. One cause of a hiatal hernia is the acquired expansion of the esophageal hiatus.
This is facilitated by age-related loss of the conjunctive tissue’s elasticity or the increase of intra-abdominal pressure, as is the case during pregnancy, obesity, or chronic coughing.
There are various types of hiatal hernias:
- Sliding hernias (axial hernias)
- Paraesophageal hernias
- Upside-down stomach
Depending on the type of hernia, the function of the lower esophageal sphincter may be disrupted which may result in heartburn. Paraesophageal hernias often cause a feeling of pressure in the chest, or shortness of breath, and have a high rate of complications like esophageal/gastric incarceration, twisted stomach, or similar conditions. Paraesophageal hernias must be treated surgically due to the high rate of complications.
With the congestion of the portal vein (e.g., resulting from cirrhosis of the liver), the blood must be re-routed (portacaval anastomoses). One of these anastomoses occurs through the esophageal veins:
- Gastric veins
- Esophageal veins
- Azygos/hemiazygos veins
- Superior vena cava
This may result in the expansion of the esophageal varices. Rupture of the varices is associated with hematemesis and represents a medical emergency.
Pulsion diverticulum / pseudodiverticulum
Pulsion diverticulum occurs as a result of increased intraluminal pressure. There are three types of pulsion diverticulum based on the location along the esophagus:
- Zenker’s diverticulum
- Mid-esophageal diverticulum
- Epiphrenic diverticulum
Pulsion diverticulum is considered a pseudodiverticulum as it does not involve all layers of the esophageal wall and does not have a muscle coat. This type of diverticulum forms through dilation in the mucosa and submucosa in the esophagus, in the weak area of Laimer’s triangle.
Traction diverticulum / true diverticulum
The traction diverticulum involves all layers of the esophageal wall and is a true diverticulum. This diverticulum forms when adjacent structures form scar tissue, pulling on the whole wall of the esophagus (e.g., parabronchial diverticula and epiphrenic diverticula).
Halitosis and dysphagia are common in traction diverticulum. They may result in regurgitation and aspiration during the night. Diverticula can easily become inflamed or form fistulae and can accumulate food particles.
A damaged myenteric plexus leads to a disruption of esophageal peristalsis and insufficient slackening of the lower sphincter, resulting in the typical “champagne glass” dilation of the esophagus.
Patients may present with complaints about difficulty swallowing, regurgitation, and a feeling of retrosternal pressure.