Peptic strictures due to acid reflux (GERD) are the most common cause of benign esophageal strictures and represent about 70% of all such cases [1]. Clinically significant, longstanding acid exposure leads to erosive esophagitis with subsequent cicatrization leading to stricture formation and luminal narrowing (Fig. 6.2a, b). Poor esophageal motility and clearance of swallowed (or refluxed) contents and a dysfunctional lower esophageal sphincter contribute to the erosive esophagitis and stricture formation [2]. The presence of a hiatal hernia and delayed gastric emptying may also play a role in increased acid exposure and an increased risk of stricture formation. Peptic strictures are estimated to occur in about 10–20% of all patients with GERD. While peptic strictures can occur at any age, older white males are at highest risk.

The morbidity associated with peptic esophageal strictures can be significant. The most common symptoms patients report are heartburn, dysphagia, odynophagia, food impaction, weight loss and chest discomfort/pain. Persistent, refractory GERD, recurrent dysphagia, food impaction, weight loss and even aspiration pneumonia present real clinical challenges in this patient population. Barrett’s esophagus frequently coexists in these patients and confers neoplastic risk over the long term as well. Atypical presentations of peptic esophageal strictures include chronic unexplained cough, regurgitation and asthma. As expected, peptic strictures are more commonly found in patients with systemic sclerosis and Zollinger–Ellison syndrome.

Webs and rings are structural abnormalities of the esophagus that are often asymptomatic but may cause significant symptoms of dysphagia, regurgitation and aspiration. An esophageal ring is defined as a concentric, smooth, circumferential extension of normal esophageal tissue causing luminal narrowing. An esophageal ring can be found anywhere along the esophagus, but it is usually found in the distal esophagus. Several theories exist regarding the pathophysiology and development of esophageal webs and rings. These include congenital defects (defects in embryologic development), autoimmune, inflammation and iron-deficiency (Plummer–Vinson syndrome)-related etiologies. In general, these are best described as congential or acquired.

Three types of lower esophageal rings exist, and they are classified as type A, B or C [3]. The most common and clinically significant ring is the “B” ring, also known as Schatzki’s ring, which is primarily composed of mucosa and submucosa. The Schatzki ring is typically located at or just above the squamocolumnar junction and appears as a sharp, ring-like luminal narrowing in the distal esophagus [4, 5] (Fig. 6.3a, b).

It is postulated that GERD and esophageal dysmotility may have a role in the development of a Schatzki’s ring. Other causes of lower esophageal rings include pill-induced rings, benign pemphigoid and mediastinal radiation.

Upper esophageal rings or “webs” have been described in association with the Plummer–Vinson and the Paterson–Brown–Kelly syndromes, both associated with iron-deficiency anemia and upper esophageal post-cricoid webs. Other associated features are koilonychia, cheilosis and glossitis. Pharyngeal and cervical esophageal cancers have been associated with this condition as well. Periodic screening for esophageal cancer in these patients is recommended. Upper esophageal webs have also been reported in patients with chronic graft versus host disease (GVHD) after bone marrow transplantation (Fig. 6.4a–c).

Esophageal webs have also been reported in association with some dermatologic conditions, including pemphigoid, epidermolysis bullosa, Stevens–Johnson syndrome and psoriasis. Webs may also be seen in patients with Zenker’s diverticulum and esophageal duplication cysts.

Esophageal webs and rings are found in about 10–15% of routine barium studies.

Esophageal rings are most commonly found in Caucasians, and webs are more common in females. Dysphagia is the most common presentation, and it is typically described as “intermittent” and predominantly for solids. Most patients will report a history of GERD and/or a history of prior endoscopic intervention for symptoms.

Approximately 10–15% of patients referred for dysphagia evaluation are found to have EoE. EoE is an inflammatory condition mediated by eosinophils, and the majority of affected adults are young men in the third and fourth decades. The most common symptoms are dysphagia, food impaction and atypical chest pain. Diagnostic criteria have been proposed for EoE which include: [6].

Patients with EoE may have a history of additional allergic or autoimmune phenomena (e.g., allergic rhinitis, asthma and eczema). The most common presenting symptoms include dysphagia and food bolus impaction, the latter typically requiring urgent endoscopic intervention. Esophageal strictures may be focal or involve a long segment of the esophagus (Fig. 6.5).

Patients undergoing brachytherapy or external beam radiation for head and neck, breast or thoracic malignancies (including esophageal malignancy) are at risk of developing radiation-induced esophageal strictures (Fig. 6.6a, b). Radiation-induced chronic ischemia leads to fibrosis and chronic radiation esophagitis, which leads to esophageal stricturing. Neuromuscular injury from radiation exposure may also contribute to symptoms due to concomitant dysmotility.

In some cases, radiation-induced strictures can be quite complex anatomically and present a significant clinical challenge. The vast majority of such patients present with slowly progressive dysphagia and weight loss in the setting of a remote history of radiation exposure to the chest. Some patients may have odynophagia and chest discomfort as well.

Any cervical or mediastinal pathology or anatomic anomaly may cause an extrinsic compression of the esophagus with resultant luminal compromise and stenosis. A number of vascular abnormalities can cause focal areas of esophageal narrowing resulting in dysphagia [7, 8] (Fig. 6.7). Some examples are:

In addition to the above, cervical spine osteophytes can also cause severe esophageal narrowing resulting in significant dysphagia, particularly in the older patient (Fig. 6.8). Inflammatory mediastinal pathology (e.g., tuberculosis, fibrosing mediastinitis) can cause traction mediated esophageal luminal distortion and narrowing which can be very difficult to manage, especially in the setting of longstanding chronic fibrosis.

Endoscopic and surgical intervention in the esophagus can also commonly result in stricture formation. Any esophageal surgery with subsequent primary anastomosis (i.e., esophago-gastric, esophago-jejunal) whether performed for a benign or malignant condition can result in postoperative anastomotic stricture formation (Fig. 6.9a, b). The risk may be greater in elderly patients, those who received radiation and in patients who have repeated surgical interventions, anastomotic, leaks and local mediastinal inflammation/infection.

Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection and endoluminal ablation for Barrett’s and related neoplasia are also well-recognized causes of esophageal stricture formation. Both radiofrequency ablation and cryoablation of the esophagus carry about a 5–7% risk of esophageal stricture formation [9]. With endoscopic resection, the risk increases in direct proportion to the circumference of the esophagus resected, with circumferential resection carrying the highest risk of stricture formation. Most of these strictures are focal and present with dysphagia as the main symptom [10] (Fig. 6.10a–c).

Ingestion of a caustic substance can lead to severe esophageal injury and strictures, the degree of which depends on the nature of the ingested agent, the volume ingested and the duration of contact between the agent and the esophagus mucosa (Fig. 6.11). A majority of ingestions occur in children accidently. In adults, psychiatric illness, suicidal intent and alcoholism are common underlying reasons for ingestion, although accidental ingestion also occurs rarely in adults. Alkali causes more esophageal injury and acid causes more gastric/duodenal injury. Extensive transmural injury and inflammation can progress to severe fibrosis and stricturing over time in up to one-third of patients [11]. Patients may develop dysphagia, odynophagia and chest pain over a variable period of time from the initial injury (2 months to several years later). Patients who have experienced lye ingestion are at increased risk of development of squamous cell carcinoma of the esophagus.

Peptic disease remains the most common cause of inflammation and benign stricture formation in the pyloric channel and duodenum, although the overall incidence has dramatically decreased over the last several decades due to increased eradiation of H Pylori infection and H2 blocker and PPI use [12]. Local tissue inflammation and edema, when untreated, result in fibrosis and tissue deformity, resulting in luminal narrowing at the pyloro-duodenal channel which in turn causes gastric outlet obstruction. Patients present with early satiety, nausea, vomiting and chronic weight loss. They may report a history of NSAID use or a prior history of peptic ulcer disease.

Crohn’s disease of the stomach and foregut is relatively uncommon, with a reported incidence of <5% in all patient’s with this disease. The vast majority of patients have concomitant disease in the lower gastrointestinal tract. Crohn’s disease in the stomach and duodenum tends to involve contiguous areas in the gastro-duodenal channel, thereby leading to luminal narrowing and outlet obstruction. Stricture formation and, rarely, fistulas in this location can be problematic, and the symptoms may be insidious. Given that it is an uncommon entity, many patients may not be diagnosed accurately until there is advanced disease with significant symptomatology.