Darren S. Bryan and Jon O. Wee
This chapter is a revision and update of that included in previous editions of the TSRA Review written by Kevin Koomalsingh (2nd edition) and Ryan A. Macke (1st edition).
Anatomy
The esophagus is a muscular conduit that runs from the pharynx to the stomach. Its length measures approximately 25 cm in men and 23 cm in women. Proximally, it is fixed to the cricoid and distally, to the diaphragm. It lies in the posterior mediastinum and runs a sigmoidal course: starting left of midline then coursing to the right and returning to the left just before traversing the diaphragm. On lateral projection, the esophagus follows the curve of the vertebral column, except at the hiatus where it courses anteriorly. Anatomically, it is subdivided into cervical, thoracic, and abdominal portions.
The cervical esophagus is roughly 5 cm in length and lies between the hypopharynx and the thoracic inlet. Using surface anatomy, it extends from the inferior border of the cricoid to the suprasternal notch. The upper esophageal sphincter (UES), which controls the entry of a food bolus, is found at the proximal extent of the cervical esophagus. The posterior cricoid cartilage forms the anterior wall of the UES, while the cricopharyngeus muscle forms the posterior wall. The cricopharyngeus blends intimately with both the inferior pharyngeal constrictor (cephalad) and inner circular muscle layer (caudad). The cervical esophagus is bounded anteriorly by the posterior membranous trachea, laterally by the carotid sheaths, the recurrent laryngeal nerve (RLN), and posterior portion of thyroid, and posteriorly by the buccopharyngeal fascia. Two important spaces exist in this area: the retropharyngeal and paraesophageal spaces. Each space provides a channel for potential pathogens to spread to the mediastinum. Access to the cervical esophagus is typically via the left neck, medial to the anterior border of the sternocleidomastoid (SCM) followed by lateral retraction of the SCM and carotid sheath. The surgeon should be aware of the RLN that runs in the tracheoesophageal groove.
The thoracic esophagus is approximately 20 cm long and lies between the thoracic inlet and the diaphragm. It runs posterior to the trachea until the angle of Louis (sternomanubrial junction). Here, it courses posterior to the left main stem bronchus (LMSB) and carina and descends to the right of the thoracic aorta. At the level of the inferior pulmonary vein, it returns left of midline and veers anteriorly to the aorta as it traverses the hiatus. This supra-diaphragmatic segment of the thoracic esophagus is prone to injury as it lacks adjacent organ support.
The abdominal esophagus extends from the esophageal hiatus to the gastro-esophageal junction and is approximately 3 cm in length. It lies in a groove on the posterior surface of the left liver. The phrenoesophageal membrane is a fibroelastic membrane that is a continuation of the transversalis fascia. It converges and envelops the abdominal esophagus proximally (through the hiatus), and distally (onto the stomach). It provides a protective sleeve whereby the diaphragm and esophagus can move independently of one another. Weakness of this ligament contributes to the pathologic conditions of GERD and hiatal hernia. The diaphragmatic crura start as ligamentous extensions from both sides of the upper lumbar vertebral bodies. They course cephalad and fuse at the esophageal hiatus. The right crus is larger and thicker and divides into a superficial segment that lies to the right and a deeper segment that lies to the left of the hiatus, just lateral to the left crus. The left crus runs along the left side only. Inferiorly, the left and right crura join to form the median arcuate ligament, which sits above the celiac artery.
The lower esophageal sphincter (LES) is not as anatomically distinct as the UES and is composed of thickening of the circular esophageal fibers near the gastroesophageal junction. It is located approximately 40 cm from the incisors, is 2-3 cm in length, and contains tonically contracted smooth muscle. In concert with the diaphragmatic crura, the phrenoesophageal ligament, intra-abdominal esophagus, and angle of His, it generates a resting pressure of 14-34 mmHg. Unlike the UES, it is neurohormonally regulated and a likely culprit in the pathogenesis of GERD. Other contributory factors for development of GERD include: the length of intra-abdominal esophagus, the level of insertion of the phrenoesophageal membrane, and elevated intra-abdominal pressures.
There are three physiologic areas of esophageal narrowing: the UES, the LMSB, and the esophageal hiatus. The UES is a 1-2 cm high-pressure zone at the inlet of the cervical esophagus, and it represents the narrowest segment of the esophagus. It is most prone to iatrogenic perforation, typically during upper endoscopy. The thoracic esophagus is compressed anteriorly and laterally as it intersects the aorta and LMSB. This creates a second area of narrowing with an average diameter of 16 mm. The third physiologic narrowing is at the level of the esophageal hiatus.
The esophagus is composed of 4 distinct layers: mucosa, submucosa, muscularis propria, and adventitia. The mucosa is further subdivided into squamous epithelium, lamina propria, and the muscularis mucosae. The submucosa is the strength layer and contains a majority of the vascular arcades, nerve bundles, and lymphatics. The muscularis propria is comprised of the inner circular and outer longitudinal muscle layers. The esophagus is the only part of the gastrointestinal tract that does not contain a serosal layer. Instead, it is lined by adventitia, a loose layer of connective tissue. When suturing the esophagus, it is important to anchor each tissue bite into the submucosal layer.
Esophageal contraction is accomplished through coordinated actions of the inner circular and outer longitudinal muscles. These muscles transition from striated in the upper third, to a 50-50 blend in the middle, to smooth in the distal third. The outer longitudinal muscle becomes thin and uniform before passing through the hiatus. The inner circular muscle fibers run in a transverse orientation at the cranial and caudal extents, and in an oblique direction throughout the body of the esophagus. The inner circular muscle is more robust than the outer longitudinal layer. Hence, the propulsive function of the esophagus is largely a result of the inner, circular layer. Due to the orientation of the muscle fibers around the cricopharyngeus, there are two “V” shaped areas of weakness: (i) Killian’s triangle superiorly, between the inferior constrictors and cricopharyngeus, where a Zenker’s diverticulum can originate; and (ii) Laimer-Hackermann’s triangle inferiorly, between the cricopharyngeus and outer longitudinal muscle.
The esophagus maintains a rich arterial supply and is perfused in a segmental pattern. The cervical esophagus receives branches from the inferior thyroid and smaller accessory branches from nearby arteries. The thoracic esophagus receives branches from the right and left bronchial arteries as well as direct branches from the aorta. The left gastric and inferior phrenic arteries supply the abdominal esophagus. Once the arteries have penetrated the muscular wall, they join a longitudinal network (most prominent in the submucosa) that runs the length of the esophagus. Hence, the esophagus can be mobilized for much of its length without fear of devascularization. This vascular pattern also facilitates blunt dissection during esophagectomy.
Venous drainage is also segmental and parallels arterial inflow. The cervical esophagus drains into the inferior thyroid veins. The thoracic esophagus drains into the bronchial veins and azygos system. The abdominal esophagus drains into the gastric and coronary veins. The coronary vein is an important bridge between the systemic and portal circulations, allowing for transmission of portal hypertension and formation of esophageal varices.
Esophageal innervation originates from a combination of fibers from the somatic, autonomic, and intrinsic nervous systems. Vagal afferent nerves detect mechanical distention and various intra-luminal stimuli and feedback to the nucleus solitarius. Somatic afferent nerves detect nociception and feedback to the spinal cord. Vagal efferent nerves control motor function and glandular secretions. Sympathetic efferent nerves control blood vessel constriction, UES contraction, smooth muscle relaxation and modulate peristaltic activity. At the pulmonary hilum, the right and left vagi send numerous fibers to the esophageal wall. These fibers form two esophageal plexi, an anterior and a posterior. These plexi coalesce to form the left (anterior) and right (posterior) vagi approximately 3 cm above the diaphragm. Each reformed vagus contains nerve fibers from both sides. In addition, two intrinsic plexi are found within the wall of the esophagus: Auerbach’s and Meissner’s plexi. Auerbach’s plexus is found within the muscularis propria and functions in regulating muscular contraction. Meissner’s plexus is found in the submucosa and regulates secretions and peristalsis.
The esophagus contains two large interconnecting systems of lymphatics spanning the length of the esophagus: a small arcade in the mucosal layer, and a more robust system in the submucosa. Esophageal malignancies extending to the submucosa or beyond can thus spread extensively and quickly. Not surprisingly, lymph can transit and drain anywhere along the course of the esophagus to pharyngeal, mediastinal and abdominal lymph nodes
Swallowing is a coordinated and complex process that can be divided into three phases: (i) oral phase, (ii) pharyngeal phase, and (iii) esophageal phase. The oral phase initiates the process and is voluntary, while the other phases are not. The pharyngeal phase delivers the food bolus to the UES. Contraction of the pharyngeal constrictors initiates a reflex arc in the swallowing center that results in relaxation of the UES. After the food bolus transits the UES, the pressure immediately increases to twice resting pressure to prevent reflux, before gradually returning to baseline. The body of the esophagus is not tonically contracted and relies on peristaltic contractions to propel food down its length. The food bolus passes through the esophagus via primary and secondary peristaltic waves before reaching the LES. At the LES, a similar reflex arc causes relaxation of this high-pressure zone for approximately five seconds as the bolus enters the stomach. This transient relaxation allows normal physiologic periods of reflux. Many hormonal substances lead to LES relaxation, including secretin, cholecystokinin, glucagon, gastric inhibitory peptide, vasoactive intestinal peptide, and neurotensin, while gastrin causes LES contraction.
Primary peristalsis is initiated voluntarily by swallowing, and encompasses all phases of the swallowing reflex, including the oral-pharyngeal phase, UES relaxation, thoracic esophageal peristalsis, and LES relaxation. Mylohyoid muscle contraction marks swallow initiation. The myenteric (Auerbach’s) plexus coordinates lumen-occluding waves throughout the thoracic esophagus. Somatic fibers become activated in a cranial to caudal fashion and the food bolus is propagated distally at a rate of 3-6 cm/second, with the entire “primary peristaltic activity” lasting 10-15 seconds. Patient posture, viscosity of the food bolus, and resistance to movement in the esophagus all contribute to the speed, duration, and amplitude of the contractile wave.
Secondary peristalsis occurs following primary peristalsis and involves only esophageal contraction without the pharyngeal phase or UES relaxation. It functions to clear the esophagus of any residual food bolus, and as such, is triggered by esophageal distention. Secondary peristalsis is propagating and coordinated.
What were once known as tertiary peristaltic waves are non-propagating and uncoordinated contractions. They occur following primary and secondary peristalsis and are not seen in normal states. They occur in higher frequency in diseased states.
Deglutative inhibition is a phenomenon that inhibits peristaltic contractions during rapid successive swallowing, such as that which occurs when drinking liquid. Because a single esophageal contraction during primary peristalsis can last 8-10 seconds, a second swallow within that time may result in a food or liquid bolus meeting an occluded lumen. Instead, via deglutative inhibition, a wave of inhibitory impulse precedes esophageal contraction, allowing for the esophagus to remain without contractions and patent until the final swallow in a series.
Suggested Readings
- Kuo B, Urma D. Esophagus-anatomy and development. GI Motility online 2006.
- Bryan DS, Ferguson MK. “Overview: Anatomy and Pathophysiology of Benign Esophageal Disease.” Sugarbaker’s Adult Chest Surgery. Sugarbaker DJ, Bueno R, Groth SS, Loor G, Wolf AS, Williams M, Adams A. Third Edition. New York, NY: McGaw Hill; 2020.
- Komanapalli C, Cohen J, Sukumar M. Exposure of the cervical esophagus. CTSNet, Inc. 2010, Jan. https://www.ctsnet.org/article/exposure-cervical-esophagus
