An understanding of the normal and abnormal histology and structure is essential to the clinical care of patients with esophageal disorders. Esophageal biopsies obtained during endoscopy sample the squamous mucosa and, less commonly, the lamina propria of the esophageal wall. The histological evaluation of submucosal glands, Meissner and myenteric ganglia, and the muscularis propria depicted in Figure 1.1 traditionally requires surgical biopsy. Endoscopic ultrasonography (EUS) can evaluate the structural integrity and anomalies of deeper structures, including the muscularis propria. Endoscopic mucosal resection and per oral esophageal myotomy allow for histological evaluation of deeper mural structures. Extrinsic compression of the esophagus by adjacent mediastinal structures as shown in Figure 1.2 is better appreciated on radiographic barium examination, EUS, or cross‐sectional imaging than endoscopy. Feline esophagus is depicted in Figure 1.3 and can be mistaken for esophageal rings in eosinophilic esophagitis. The feline pattern is transient plications visualized during retching and esophageal shortening and may represent contraction of the muscularis mucosa. Upon relaxation of the esophageal musculature and luminal distension with air insufflation, the plications disappear.

Esophageal developmental anomalies include vascular lesions, duplications, and heterotopic gastric mucosa. Congenital esophageal stenosis is caused by tracheobronchial cartilaginous remnants, fibromuscular wall hypertrophy, and membranous web formation. While typically presenting in childhood, delayed presentation in adults occurs as shown in Figure 1.4. Dysphagia lusoria is caused by extrinsic compression of the thoracic esophagus by congenital anomalies of the aortic arch, most commonly by an aberrant take‐off of the right subclavian artery from the left side of the aortic arch (Figure 1.5). Congenital venous malformations illustrated in Figure 1.6 represent another vascular anomaly and are distinct from esophageal varices as vascular obstruction or portal hypertension is not present in the former. Congenital esophageal duplications assume both tubular (Figure 1.7) and cystic (Figures 1.8 and 1.9) forms. While most are apparent before the age of 1 year, 25% can present in adults with symptoms of dysphagia. Heterotopic gastric mucosa (inlet patch) shown in Figure 1.10 is a common congenital anomaly detected with a prevalence of 4% based on an autopsy series. Infrequently, this anomaly is associated with cervical esophageal stricture (Figure 1.11) and web formation (Figure 1.12). Other uncommon developmental anomalies include esophageal atresia, congenital esophageal stenosis, and bronchopulmonary foregut malformations.

Structural esophageal anomalies include esophageal rings and webs, cricopharyngeal bar, pharyngoesophageal diverticula, and diffuse idiopathic skeletal hyperostosis of the cervical spine. The most widely recognized structural anomaly is the lower esophageal mucosal or Schatzki ring that is found in about 10% of adults. It is one of the most common causes of dysphagia and food impaction, although the majority of Schatzki rings are asymptomatic. The inner diameter of the ring is a critical determinant for dysphagia and can be assessed on endoscopic retroflexed view (Figure 1.13) or ingestion of a barium tablet of known diameter. A cricopharyngeal bar is found in 5–19% of radiographic studies of the pharynx (Figure 1.14). Like Schatzki rings, the majority are not associated with dysphagia.

Figure 1.15 illustrates progressive enlargement of a Zenker diverticum with normalization of the pharyngeal outpouching following surgery. Therapeutic options for symptomatic cricopharyngeal bars and Zenker diverticula include both endoscopic and surgical approaches. Epiphrenic diverticula arise from the distal esophagus and are often associated with an underlying spastic esophageal motility disorder. With time, the diverticula can increase in size, resulting in food retention, bezoar formation, and symptoms of regurgitation (Figures 1.16–1.18).

Treatment for large or symptomatic epiphrenic diverticula is most commonly surgical and includes not only a diverticulectomy but also treatment of the underlying motility disorder. Intramural pseudodiverticulosis is a rare finding best appreciated on barium esophagram rather than upper endoscopy. The disorder results from dilation of the excretory ducts of submucosal esophageal glands and is associated with proximal esophageal strictures and esophageal candidiasis. Diffuse idiopathic skeletal hyperostosis (DISH) of the cervical spine leads to ossification of the anterolateral ligaments and enthuses. Dysphagia may result from extrinsic compression of the cervical esophagus (Figure 1.19).