The term “esophagus” derives from the Greek root “oisein” (to carry) and “phagos” (to eat). The esophagus’ intricate components perform in symphony to provide a muscular conduit between the pharynx and stomach. Even small deviations in structure can lead to dysfunction. Benign esophageal lesions can obstruct the esophageal lumen and produce symptoms. This chapter discusses esophageal development and anatomy as well as the pathophysiology of benign esophageal diseases. Chapter 29 details the surgical and endoscopic approaches to these diseases. Motility disorders and congenital esophageal diseases are discussed in more detail in Chapters 33 and 51, respectively.
The esophagus and trachea both form from a medial ventral diverticulum arising from the primordial foregut at approximately day 22 or 23 of fetal development (Fig. 28-1). The foregut divides into trachea and esophagus during week 4. The stomach bud forms posteriorly shortly thereafter. Both the trachea and esophagus elongate between days 23 and 34 or 36. It is thought that esophageal lengthening occurs by ascent of the pharynx rather than descent of the stomach. By approximately day 36, the trachea and esophagus have completely separated.1
The esophageal wall is derived from both endoderm and mesoderm. The endoderm forms the epithelium and glands, whereas the mesoderm eventually forms the muscular layers, connective tissue, and angioblasts. During the seventh and eighth weeks of development, the esophageal epithelium proliferates to fill the lumen, leaving only small irregular channels open. These channels grow to form vacuoles, which then coalesce to create one lumen by the 10th week of gestation (Fig. 28-2). Ciliated epithelium initially lines the embryological esophagus, but it is replaced by the fourth month of gestation by stratified squamous epithelium. By the sixth week, the mesenchymal circular muscular coat forms, and the splanchnic mesenchyme surrounds the esophagus and trachea. The splanchnic mesenchyme enables the formation of the smooth muscle of the lower esophagus. The longitudinal musculature forms during weeks 9 through 12, and the muscularis mucosa forms by week 16. Blood vessels start to enter the esophageal wall in week 28, but the lymphatic capillaries do not form until the third to fourth month of gestation.1
Congenital anomalies of the esophagus occur in 1 in 3500 births and typically are the result of a genetic defect or maternal event. They are more common in premature infants, and 60% are associated with other congenital anomalies, including VACTERL syndrome (associated vertebral, anal, cardiac, tracheal, esophageal, renal, and limb congenital anomalies).2 For further information regarding congenital anomalies of the esophagus, including atresia, stenosis, clefts, and tracheoesophageal fistula, see Chapter 51.
Esophageal terminology can be classified by function, anatomy, or surgical divisions. Anatomically, the esophagus is divided into cervical, thoracic, and abdominal portions. Surgeons further classify esophageal anatomy based on therapeutic approach and adjacent structures as cervical, proximal, middle, distal thoracic, and abdominal.
The esophagus ranges from 21 to 34 cm in length from the cricopharyngeus to the lower esophageal sphincter (LES), with an average length of 23 cm in females and 28 cm in males. The cervical esophagus ranges from 3 to 5 cm in length, the thoracic portion 18 to 22 cm, and the abdominal portion 3 to 5 cm. The distance from the incisors to the cricoid cartilage is 13 cm.3
Nonkeratinizing, stratified squamous epithelium lines most of the esophageal lumen. This mucosa contains only alveolar serous glands, which are small, tubular mucus glands originating from the submucosa. In the terminal esophagus, cardiac glands, much like those found in the stomach, project through the epithelium to form papillae. Endoscopically, the transition between the esophageal squamous mucosa and the columnar gastric mucosa starts as four-to-six pink tongues projecting up through the paler distal esophagus at what is known as the “Z-line” just proximal to the esophagogastric junction. Replacement of the distal esophageal squamous mucosa by columnar epithelium is diagnostic of Barrett esophagus, a premalignant condition.3 For further information on Barrett esophagus, see Chapter 41.
The lamina propria mucosa lies deep to the mucosa and consists of an areolar, elastic, and collagenous network of fibers that contains small blood vessels, follicles, and mucus glands. The muscularis mucosa is a thin layer of smooth muscular bundles. The submucosa consists of loose areolar connective tissue and elastic and collagen fibers with numerous blood vessels, lymphatics, nerves (including Meissner plexus), and deep mucus glands (Fig. 28-3).
The pharyngeal and esophageal muscles coordinate to form coordinated contractions to make swallowing and speech possible. Pharyngeal muscle is striated, whereas the esophagus transitions to more smooth muscle as it descends past the level of the carina and the lower two-thirds of the esophagus. The tunica muscularis is composed of oblique muscle fibers in a single layer in the pharynx, but two layers throughout the esophagus: a longitudinal outer layer and circular inner layer. The circular layer is an extension of the cricopharyngeus muscle.3
The upper esophageal sphincter (UES) acts as the gatekeeper for entry of a food bolus from the pharynx to the esophagus during swallowing. The posterior cricoid cartilage forms the anterior wall of the UES, and a muscular sling of the lower inferior pharyngeal constrictor forms the posterior UES. This sphincter functions to prevent esophageal distension during respiration and to prevent reflux, as it remains in a tonic state of contraction with 30 to 142 mm Hg of pressure between episodes of swallowing.
The LES does not have anatomy as discrete as the UES. The LES is composed in part from a thickening of the circular esophageal fibers that superimpose on each other approximately 3 cm from the gastroesophageal junction. It is not macroscopically or grossly detectable. The LES, in conjunction with the diaphragmatic crura, angle of His, and intra-abdominal length of esophagus, provides a tonic pressure of 14.5 to 34 mm Hg to prevent reflux.3 Liebermann-Meffert4 described short transverse clasp fibers and oblique sling fibers in cadavers that curve around the greater curve that aid in the sphincter effect and help account for the asymmetric anatomy of the LES. For more information regarding the pathophysiology of the esophageal sphincters, see Chapter 33.
Only loose adventitia adheres the esophagus to its surrounding mediastinum, as it has no serosa or mesentery. These loose attachments allow for considerable cephalocaudal movement during respiration.
The esophagus receives arterial blood from multiple sources as it courses through the neck, chest, and abdomen.
The superior thyroid artery gives off smaller arteries that supply the UES and pharynx. The inferior thyroid arteries supply the cervical esophagus. They give off 2 to 3 cm branches called tracheoesophageal arteries that travel inferiorly and medially on each side. The tracheoesophageal arteries subdivide into tracheal and esophageal branches, which in turn subdivide several more times before they eventually enter the esophageal wall.3
The thoracic esophagus derives its blood supply from the superior and inferior thyroid arteries superiorly and the aorta inferiorly. Both the tracheobronchial arteries and the bronchoesophageal artery originate from the aortic arch and further subdivide to provide branches to the trachea. The proper aortic esophageal arteries are unpaired and arise from the descending aorta.3
The abdominal esophagus is supplied by the left gastric artery, ascending branches from the left phrenic artery, and the splenic artery. The splenic artery delivers arterial blood to the posterior and left lateral distal esophagus. Branches from both extend beyond the diaphragmatic hiatus. The repetitive branching of the arterial supply eventually forms a rich submucosal arterial plexus that allows for ligation of extramural vessels without compromising the underlying esophagus (Fig. 28-4).
A submucosal venous plexus drains blood from the subepithelial venous network. This plexus then empties into communicating veins that traverse the muscular wall along with the perforating arteries. The superior esophagus drains into the internal jugular veins or the azygos or hemiazygos veins. The inferior veins drain into the left gastric and splenic veins. There are no valves in the esophageal venous system.3
The lymphatic system of the esophagus is poorly described. Lymph from the thoracic esophagus likely drains to paratracheal, tracheobronchial bifurcation, juxtaesophageal, and intra-aorticoesophageal nodes. The abdominal esophagus likely drains to superior gastric, pericardiac, and inferior diaphragmatic nodes. All areas of the esophageal lymph system eventually empty into the thoracic duct. Lymphatic channels are more abundant as longitudinal submucosal channels than in the muscular layers.3
The visceral autonomic nervous system innervates the esophagus, pharynx, and larynx. The sympathetic efferent pathways cause vasoconstriction, sphincter contraction, and relaxation of the muscular wall via the cervical and thoracic sympathetic chains. The parasympathetic nervous system increases glandular and peristaltic activity via the vagus (cranial nerve X). The vagus also carries somatic and visceral sensory and skeletal motor fibers to the esophagus. The superior laryngeal nerve mainly has a secretory and sensory function, but it also supplies motor branches to the larynx and cricopharyngeus muscle, which controls the timbre of the voice.3
Benign Esophageal Neoplasms
Benign esophageal neoplasms are rare lesions, most occurring in less than 0.5% of the population on autopsy. A review of 20,000 autopsies in 1962 found only 90 benign esophageal tumors, or a prevalence of 0.45%.5 The majority of benign esophageal tumors do not cause symptoms unless they become large enough to obstruct the esophageal lumen or impinge on surrounding structures. Mucosal lesions are more likely to present with symptoms, as they are more likely to obstruct the lumen. One must keep in mind a broad differential diagnosis when evaluating these patients, as these lesions can create mechanical obstruction and symptoms common to many other esophageal diseases (Table 28-1). Adult patients with cancer, gastroesophageal reflux, motility disorders, esophagitis, or even psychiatric illness can have similar presentations to these benign lesions.
|Finger-like projections of squamous epithelium|
Shelf of mucosa projecting into lumen
|Submucosal||Granular cell tumor|
|Large cells with eosinophilic granules, neural|
|Pale, yellow, firm|
Rubbery polyp, +/– feeding vessel
|Spindle cells with fibrous core|
Hypertrophied muscular ring with normal
|Fleshy compressible lesion|
Circumferential projection of rings into lumen
|Heterotopic||Inlet patch||Gastric mucosa||Pink patch, distal esophagus|
|Fluid-filled cyst under muscular layer|
Normal esophageal wall
|No communication with lumen|
Communicates with true lumen
These lesions are typically found incidentally on imaging or on endoscopy and typically do not warrant resection unless they mechanically compress mediastinal structures. Generally, removal is recommended for patients with symptoms or larger lesions.
Lesions of the Mucosal Layer
Esophageal papillomas are small (typically subcentimeter) benign sessile lesions arising from the lamina propria in the distal esophagus.6 Histologically, they have finger-like projections of squamous-lined epithelium over a core of connective tissue. Endoscopically, they appear as pale exophytic, wart-like lesions that can be mistaken for verrucous squamous cell carcinoma, granulation tissue, or papillary leukoplakia. They occur most often in the fifth decade of life.7 They rarely cause symptoms, but large lesions can cause dysphagia.