Case Presentation:

A 39–year–old woman was admitted for severe gastroesophageal reflux (GERD) with nausea and emesis. The patient had 20 years with heartburn which evolved to intermittent episodes of food impaction requiring multiple esophageal dilatations for the past 7 years, the last in 2009 complicated with an esophageal perforation and therefore refused subsequent dilatations. She has been using fluticasone, omeprazole, dexlanzoprazole, and famotidine simultaneously and metoclopramide. Despite treatment, symptoms have been persistent, requiring multiple admissions for intravenous fluid hydration with subsequent placement of a port catheter. Her medical history is relevant for POTS on midodrine and fludrocortisone, diverticulitis s/pp partial colectomy, cholecystectomy, and appendectomy. She has no history of asthma or atopy. She has been evaluated by an Allergy specialist with no significant findings. An endoscopy revealed grade B erosive esophagitis, a 4 cm hiatal hernia and bilious reflux. Esophageal biopsy showed basal cell hyperplasia and intraepithelial eosinophils (up to 20 per high power field in the distal esophagus and up to 25 per high power field in the proximal esophagus) consistent with eosinophilic esophagitis (EoE). A pH monitoring showed multiple reflux episodes. Esophageal manometry revealed a hypotensive lower esophageal sphincter (basal 6.9 mmHg (normal 10–35 mmHg)). Barium swallow revealed slight diffuse esophageal narrowing but a 13 mm barium tablet passed easily through the esophagus. The patient was felt to have both severe GERD based on reflux testing, and EoE based on >25 eosinophils per field in the proximal esophagus. Sucralfate was added with mild symptomatic improvement. Thoracic surgery evaluated the patient and scheduled for Nissen fundoplication. Pulmonary function tests, echocardiogram and cardiac stress test were normal. The patient is scheduled to continue with medical treatment for EoE after surgery.


Eosinophilic esophagitis is an increasingly common diagnosis which should be considered as a possible contributor in patients with refractory GERD, dysphagia and food impaction. This combination could have contributed to her esophageal injury as perforation is more likely in EoE than other causes of stricture. Histopathologic findings include eosinophil count of =15 eosinophils per high powered field despite acid suppression with a PPI for one to two months or a negative pH study. In this case, given the failure of medical therapy, complex antireflux surgery was warranted.


Patients with severe GERD may have eosinophilic esophagitis as well which can make the patient refractory to treatment and in this case could have contributed to perforation. Surgery can control the GERD, but therapy for eosinophilic esophagitis needs to be continued postoperatively.