This case report emphasizes several important and timely clinical points. First, despite the fact that the patients presented with foreign body impaction, linear furrows, white exudates, and dense esophageal eosinophilia, the pediatric gastroenterologists did not make the virtually reflexive diagnosis of EoE. Linear furrows are a nonspecific representation of inflammation that likely represent edema of the esophageal mucosa.³ Whitish material on the esophageal mucosa can represent Candida, swallowed food, anesthetic spray, and eosinophilic pus.⁴ The physicians recognized a growing body of literature supporting the fact that all of these features can be seen in any inflammatory esophageal disease, including GERD and EoE.⁵ Thus, the exclusion of the more common disease, GERD, with 2 months of high-dose proton pump inhibition was appropriate and indicated.⁶

Second, the pediatric gastroenterologists knew that the diagnosis of EoE was a possibility and, thus, obtained biopsies. EoE is an increasingly common disease. Young children typically present with the chronic symptoms of vomiting, feeding dysfunction, or abdominal pain,⁷ whereas adults, most often males, present with the stereotypical pattern of dysphagia and food impaction.⁸ In some circumstances, patients may present acutely, as in these cases, with esophageal foreign body impaction. Our work, and that of others, has shown that a significant number of patients presenting with food impaction, particularly when recurrent, have histopathologic features of EoE.^9-13 The importance of obtaining a mucosal sample at the time of foreign body removal cannot be overemphasized, even though the procedure may be inconvenient, as it is frequently performed in the middle of the night and often without nursing assistance. In many institutions, including our own, the responsibility of extraction rotates daily between the surgeon and the gastroenterologist. In other institutions, this duty lies only in the hands of the surgeon. In these circumstances, the foreign body is typically extracted without pausing to obtain biopsies to determine the underlying cause. If this occurs, the diagnosis may be missed and patients may go untreated for years, potentially leading to complications such as esophageal stricture, small-caliber esophagus, or crepe-paper esophagus. In our institution, surgeons have agreed to obtain biopsies to entertain the possibility of EoE as a potential diagnosis.

Third, prior to presentation, both of these children were reportedly asymptomatic and without obvious eating problems. It is frequently wondered how children can be asymptomatic with this degree of esophageal inflammation and whether these children could be underweight or have unidentified feeding dysfunction. Our experience, and that of others, suggests that children and adults with EoE frequently have adapted to esophageal malfunction with a variety of changes in the manner in which they eat. Identification of this adaptive behavior requires asking probing questions.^14-17 For instance, the simple question “Do you have any problems swallowing or eating?” will frequently be met with the immediate answer of “No.” More revealing would be a series of additional, more specific questions such as: “How long does it take you to finish a meal?”; “How long do you chew your food?”; “Do you need a glass of water to finish a meal?”; “Do you cut your food into small bites?”; “Are you the last person to leave the table?”; “Do you avoid eating foods such as bagels or meats?”; and “Do you feel isolated because it takes you a long time to eat?” Answers to these questions will often be in the affirmative and represent evidence of significant lifestyle accommodations that have been made to compensate for esophageal dysfunction.

Finally, the pathophysiology of this presentation has been debated in the literature. Esophageal dysmotility leading to esophageal spasm^18-20 and mucosal remodeling^21,22 resulting in fixed anatomic lesions have both been suggested. An alternative theory relies on the concept that EoE is a food allergic disease.^23,24 In this light, one wonders whether the acute impaction of a coin could be related to a hypersensitivity reaction to the metal in the coin. It would be interesting to obtain skin testing for zinc and copper to determine whether the children in this case report showed reactivity. Taking this idea one step further, one wonders whether children who suffer from food impaction should undergo skin testing for impacted food proteins. For instance, if a patient develops a food impaction with a piece of beef steak, it may be possible that this represents an acute hypersensitivity response to beef proteins that led to esophageal edema. In addition, it could be possible that a break in the esophageal mucosa contributed to the initiation of this illness. Acid, trauma, or other agents could contribute to increasing mucosal permeability and exposure of the local immunologic milieu to luminal antigens.^25,26 Alternatively, could the use of proton pump inhibitors (PPIs) actually contribute to the generation of this disease?²⁷ Interestingly, the widespread use of PPIs has increased in parallel with the prevalence of EoE, though a causative relationship has not been identified.