This chapter presents images from a selection of diseases of the esophagus not covered elsewhere in the textbook, including trauma, foreign body impaction, corrosive and pill esophagitis, lymphocytic esophagitis, acute esophageal necrosis, and rare manifestations of systemic and dermatological diseases.

Mallory–Weiss tears, mucosal lacerations at the gastroesophageal junction (GEJ) caused by a sudden rise in intraabdominal pressure during vomiting or retching, may cause upper GI hemorrhage. Hemostatic treatment is warranted for either active bleeding or stigmata of recent bleeding seen at endoscopy (Figure 14.1). Careful antegrade and retrograde views of the GEJ are mandatory, as these tears can be subtle (Figure 14.2).

Perforation of the esophagus following procedures such as pneumatic dilation of the lower esophageal sphincter or bougie dilation of an esophageal stricture should be suspected with chest pain, fever, or the presence of subcutaneous air (Figure 14.3). An esophagram with a water‐soluble agent prior to the use of barium is recommended for initial testing. Spontaneous rupture of the esophagus, Boerhaave syndrome (Figure 14.4), is life threatening, requiring immediate management.

Esophageal intramural hematomas typically derive from mechanical trauma to the esophagus. On endoscopic evaluation, a bluish or violet mass protruding into the esophageal lumen is seen, sometimes in association with superficial ulceration (Figure 14.5). These often resolve spontaneously.

The esophagus is the most common site of foreign body impaction. Underlying structural or motility abnormalities of the esophagus predispose to foreign body impaction in individuals; qualities of individual objects may also predispose to impaction whether or not an underlying abnormality of the esophagus is present. When food bolus impaction is encountered, an attempt at advancement under endoscopic guidance into the stomach is reasonable. Frequently, examination of the cleared esophagus reveals a Schatzki ring, peptic stricture, or signs of eosinophilic esophagitis (Figure 14.6).

Sharp bone fragments can impale the esophageal wall causing local trauma (Figure 14.7). Underlying strictures predispose solid objects, like fruit pits, to become stuck (Figure 14.8). Patients with psychiatric disease may swallow a panoply of unusual objects, including so‐called “sporks,” which are challenging to remove and can cause local ulceration (Figure 14.9). Coins, most commonly swallowed inadvertently by pediatric patients, may become lodged in the esophagus. Because they are radiopaque, a plain radiograph can identify these objects. When coins have not spontaneously passed 24 hours after ingestion, endoscopic removal is warranted (Figure 14.10).

Pill esophagitis describes chemical irritation of the esophagus from a medication tablet. Some medications may become stuck in the esophagus and cause local inflammation or erosions without an underlying esophageal structural or motility disorder. In other cases, an underlying esophageal disorder may be the cause (Figure 14.11).

Purposeful or accidental ingestion of corrosive substances, particularly strong alkali solutions found in some cleaning products, can lead to caustic esophagitis. Long‐term sequelae of caustic ingestion include persistent esophageal strictures and increased risk of esophageal squamous cell carcinoma. Endoscopy can grade the injury, which ranges from mucosal erythema, to sloughing and ulceration of the mucosa, to frank esophageal necrosis (Figure 14.12).

Acute esophageal necrosis or “black esophagus” is typically characterized by circumferential necrosis of the esophagus. Endoscopically, the esophageal mucosa appears blackened, and involvement typically stops abruptly at the gastroesophageal junction (Figure 14.13). The necrotic esophageal epithelium is friable with underlying hemorrhagic tissue. This condition can be reversible but associates with high mortality owing to the substantial burden of comorbid illness found in these patients, and subsequent strictures can be challenging to treat.

Lymphocytic esophagitis (LyE) is a newly described condition characterized clinically by esophageal symptoms such as dysphagia, heartburn, or chest pain, and histologically by an intense, lymphocyte‐predominant inflammatory infiltrate in the esophageal mucosa in the absence of granulocytes (Figure 14.14). A range of endoscopic findings can be seen in LyE, including esophageal rings, strictures, furrows, plaques, erosive esophagitis, erythema, and nodularity (Figures 14.15 and 14.16).

Systemic diseases can affect the esophagus in rare instances. Sarcoidosis can cause extrinsic esophageal compression from enlarged lymph nodes, infiltration of the esophageal wall resulting in an achalasia‐like syndrome, and esophageal strictures or mucosal nodularity (Figure 14.17). The chronic transmural inflammation of Crohn’s disease can narrow the esophagus and create sinus tracts and deep ulcerations. In some instances, esophagotracheal or esophagobronchial fistulae develop and cause recurrent pneumonitis, pneumonia, or empyema, which may require endoscopic or surgical management (Figure 14.18).

While graft‐versus‐host disease (GVHD) more commonly affects the lower GI tract and the liver, it can affect the esophagus. Diagnosis is made histologically, which also excludes opportunistic infections in these immunosuppressed patients. Esophageal erythema or friability, as well as webs or strictures, can be seen on endoscopic examination and barium studies can show strictures (Figures 14.19 and 14.20). Behçet syndrome, characterized by oral and genital aphthous ulceration and ocular inflammation, also rarely affects the esophagus (Figure 14.21). Primary or secondary amyloidosis may cause dysphagia due to amyloid deposition in esophageal muscle or nerves (Figure 14.22). Additionally, esophageal intramural pseudodiverticulosis can be seen with concomitant disorders including HIV, esophageal motility disorders, and eosinophilic esophagitis. The finding is rare, may be asymptomatic, and may be associated with dysphagia and stricture formation (Figure 14.23).

Finally, blistering dermatological diseases can rarely involve the esophagus. Pemphigus vulgaris, due to autoantibodies against desmoglein‐3 in keratinocytes, can cause esophageal blistering (Figure 14.24). Bullous pemphigoid is caused by IgG autoantibodies directed against the basement membrane of the squamous epithelium. Esophageal involvement by bullous pemphigoid is also rare, but it can result in esophageal mucosal sloughing and upper GI bleeding (Figure 14.25). Benign mucous membrane pemphigoid (BMMP) is due to deposition of autoantibodies in the basement membrane of the esophageal mucosa, leading to tense blisters with subsequent scarring and stricturing (Figures 14.26 and 14.27

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