MUSCULATURE

The muscularis propria is responsible for carrying out the organ’s motor function. The upper 5% to 33% is composed exclusively of skeletal muscle, and the distal 50% is composed of smooth muscle. In between is a mixture of both types.³ Proximally, the esophagus begins where the inferior pharyngeal constrictor merges with the cricopharyngeus, an area of skeletal muscle known functionally as the upper esophageal sphincter (UES) (Fig. 41-3A). The UES is contracted at rest and thereby creates a high pressure zone that prevents inspired air from entering the esophagus. Below the UES the esophageal wall comprises inner circular and outer longitudinal layers of muscle (see Fig. 41-2A). The esophageal body lies within the posterior mediastinum behind the trachea and left mainstem bronchus and swings leftward to pass behind the heart and in front of the aorta.¹ At the T10 vertebral level the esophageal body leaves the thorax through a hiatus located within the right crus of the diaphragm (see Fig. 41-1). Within the diaphragmatic hiatus the esophageal body ends in a 2- to 4-cm length of asymmetrically thickened circular smooth muscle known as the lower esophageal sphincter (LES) (see Fig. 41-3B).⁴ The phrenoesophageal ligament, which originates from the diaphragm’s transversalis fascia and inserts on the lower esophagus, contributes to fixation of the LES within the diaphragmatic hiatus. This positioning is beneficial because it enables diaphragmatic contractions to assist the LES in maintenance of a high-pressure zone during exercise. The LES is contracted at rest, creating a high-pressure zone that prevents gastric contents from entering the esophagus. During swallowing, the LES relaxes to permit the swallowed bolus to be pushed by peristalsis from the esophagus into the stomach.

Figure 41-3. A, Anatomic detail of the upper esophageal sphincter (UES) and its relationship to adjacent structures. B, Anatomic detail of the lower esophageal sphincter (LES) and its relationship to the diaphragm, phrenoesophageal ligament, and squamocolumnar junction.

(A, Modified from AGA Clinical Teaching Project. Esophageal disorders: Upper esophageal sphincter anatomy, slide 14, American Gastroenterological Association, 1995; B, modified from Kerr RM. Hiatal hernia and mucosal prolapse. In: Castell DO, editor. The Esophagus. Boston, Mass: Little, Brown & Company; 1992. p 763.)

INNERVATION

The esophageal wall is innervated by parasympathetic and sympathetic nerves; the parasympathetics regulate peristalsis through the vagus nerve (Fig. 41-4). The cell bodies of the vagus nerve originate in the medulla. Those located within the nucleus ambiguus control skeletal muscle, and those located within the dorsal motor nucleus control smooth muscle. Medullary vagal postganglionic efferent nerves terminate directly on the motor endplate of skeletal muscle in the upper esophagus, whereas vagal preganglionic efferent nerves to smooth muscle in the distal esophagus terminate on neurons within Auerbach’s (myenteric) plexus, located between the circular and longitudinal muscle layers.³ A second neuronal sensory network, Meissner’s plexus, located within the submucosa, is the site of afferent impulses within the esophageal wall. These are transmitted to the central nervous system through vagal parasympathetic and thoracic sympathetic nerves. Sensory signals transmitted via vagal afferent pathways travel to the nucleus tractus solitarius within the central nervous system (see Fig. 41-4); from there nerves pass to the nucleus ambiguus and dorsal motor nucleus of the vagus nerve, where their signals may influence motor function.⁵

Figure 41-4. Neural pathways of the esophagus. Extrinsic innervation is provided principally by the vagus nerve. Afferent vagal pathways carry stimuli to the nucleus solitarius, and efferent pathways originating in the dorsal vagal nucleus mediate esophageal peristalsis and lower esophageal sphincter relaxation. Ach, acetylcholine; NO, nitric oxide; VIP, vasoactive intestinal peptide.

(From Mittal RK, Balaban DH. The esophagogastric junction. N Engl J Med 1997; 336:924.)

Pain sensation arising from the esophagus is typically triggered by stimulation of chemoreceptors in the esophageal mucosa or submucosa and/or mechanoreceptors in the esophageal musculature.⁶ Central perception then occurs when these impulses are transmitted to the brain by sympathetic and vagal afferents. Sympathetic afferents travel through the dorsal root ganglia to the dorsal horn of the spinal cord, and vagal afferents travel through the nodose ganglia to the nucleus tractus solitarius in the medulla. Information from sympathetic/spinal afferents then proceeds via the spinothalamic and spinoreticular pathways to the thalamus and reticular nuclei before transmission to the somatosensory cortex for pain perception and limbic system for pain modulation. Information from vagal afferents in the medulla also travels to the limbic system and frontal cortex for pain modulation. Furthermore, because the esophageal neuroanatomic pathways overlap with those of the heart and respiratory system, in clinical practice it may be difficult to discern the organ of origin for some chest pain syndromes.⁶

CIRCULATION

The arterial and venous blood supply to the esophagus is segmental. The upper esophagus is supplied by branches of the superior and inferior thyroid arteries, the midesophagus by branches of the bronchial and right intercostal arteries and descending aorta, and the distal esophagus by branches of the left gastric, left inferior phrenic, and splenic arteries.^1–3 These vessels anastomose to create a dense network within the submucosa that probably accounts for the rarity of esophageal infarction. The venous drainage of the upper esophagus is through the superior vena cava, the midesophagus through the azygos veins, and the distal esophagus through the portal vein by means of the left and short gastric veins. The submucosal venous anastomotic network of the distal esophagus is important because it is where esophageal varices emerge in patients with portal hypertension.^1–3

The lymphatic system of the esophagus is also segmental; the upper esophagus drains to the deep cervical nodes, the midesophagus to the mediastinal nodes, and the distal esophagus to the celiac and gastric nodes. However, these lymphatic systems are also interconnected by numerous channels, accounting for the spread of most esophageal cancers beyond the region at the time of their discovery.

MUCOSA

On endoscopy the esophageal mucosa appears smooth and pink. Furthermore, the esophagogastric junction can be recognized by the presence of an irregular white Z-line (ora serrata) demarcating the interface between the lighter esophageal and the redder gastric mucosae. On biopsy, histology shows the esophageal mucosa to be lined by a nonkeratinized, stratified squamous epithelium (Fig. 41-5). This multilayered epithelium consists of three functionally distinct layers: stratum corneum, stratum spinosum, and stratum germinativum. The most lumen-oriented stratum corneum acts as a permeability barrier between luminal content and blood by having layers of pancake-shaped glycogen-rich cells connected laterally to each other by tight junctions and zonula adherens and having their intercellular spaces filled with a dense matrix of glycoconjugate material.⁷ The middle layer of stratum spinosum contains metabolically active cells with a spiny shape. The spiny shape is due to the numerous desmosomes connecting cells throughout the layer. Furthermore, this same desmosomal network maintains the structural integrity of the tissue. The basal layers of stratum germinativum contain cuboidal cells that occupy 10% to 15% of the epithelium’s thickness and are uniquely capable of replication.² Consequently, basal cell hyperplasia, defined as basal cells occupying more than 15% of epithelial thickness, is common in gastroesophageal reflux disease, reflecting an increased rate of tissue repair² (see Chapter 43). The esophageal epithelium contains a small number of other cell types including argyrophilic endocrine cells, melanocytes, lymphocytes, Langerhans cells (macrophages), and eosinophils. Neutrophils are not present in healthy epithelium.²

Figure 41-5. Esophageal epithelium. The human esophagus as shown on this biopsy specimen is lined by nonkeratinized stratified squamous epithelium. The cells of the surface (top) are long and flat and have a small nuclear-to-cytoplasmic ratio that contrasts with the cells of the basal layer (bottom), whose density, cuboidal shape, and large nuclear-to-cytoplasmic ratio account for their prominence. A subpopulation of these basal layer cells appears to have properties of esophageal stem cells.^6a Rete pegs or dermal papillae containing elements of the lamina propria normally extend into the epithelium about one half the distance to the lumen.

(Courtesy of Pamela Jensen, MD, Dallas, Tex.)

Below the epithelium is the lamina propria, a loose network of connective tissue within which are blood vessels and scattered lymphocytes, macrophages, and plasma cells (see Fig. 41-5). The lamina propria protrudes at intervals into the epithelium to form rete pegs or dermal papillae. Normally these protrude to less than 50% of the epithelium’s thickness; when greater, it also is a recognized marker of gastroesophageal reflux disease.² The muscularis mucosae is a thin layer of smooth muscle that separates the lamina propria above from the submucosa. Its functions are unclear.

SUBMUCOSA

The submucosa comprises a dense network of connective tissue, within which are blood vessels, lymphatic channels, neurons of Meissner’s plexus, and esophageal glands (see Fig. 41-2A). These glands, which vary as to number and distribution along the esophagus, consist of cuboidal cells organized as acini.⁸ They produce and secrete a lubricant, mucus, and factors such as bicarbonate and epidermal growth factor that are important for epithelial defense and repair. The secretions from these glands pass into tortuous collecting ducts that deliver them to the esophageal lumen.

ESOPHAGEAL ATRESIA AND TRACHEOESOPHAGEAL FISTULA

Esophageal atresia and tracheoesophageal fistulas are the most common developmental anomalies of the esophagus (Fig. 41-7). The former results from failure of the primitive foregut to recanalize and the latter from failure of the lung bud to separate completely from the foregut. Although the mechanisms are unclear, esophageal atresia and tracheoesophageal fistulas may result from genetic defects, such as those reported in mouse and humans (Table 41-1).¹⁰ In addition, experimental administration of the anticancer drug, adriamycin, into mouse or rat embryos commonly results in esophageal atresia and tracheoesophageal fistulas; and these defects may be accompanied by other anomalies that comprise the VACTERL group.^11–12

Figure 41-7. Esophageal atresia (A) and tracheoesophageal fistulas (B through E) are the most common developmental anomalies of the esophagus. In the most common tracheoesophageal fistula, the trachea communicates with the distal segment of the atretic esophagus (B). The next most common type is the H-type tracheoesophageal fistula, in which the trachea communicates with an otherwise normal esophagus (C). Tracheoesophageal fistulas in which the trachea communicates with both upper and lower segments of an atretic esophagus (D)

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