A 3-year-old male was hospitalized for dehydration secondary to stomatitis. He had had poor oral intake for 2 days prior to admission, and his mother noted that the child appeared lethargic and was refusing to drink. He had vomited twice but had no hematemesis or bilious emesis. He was noted to have increased episodes of drooling at home. The child’s medical history was significant only for eczema and mild reactive airway disease that was treated with triamcinolone cream and nebulized albuterol, respectively. He had no previous symptoms of stomatitis and had no history of caustic ingestion. Family history was noncontributory. On physical exam, the patient was tachycardic with a pulse of 150 beats per minute, and his blood pressure was 121/86 mm Hg. Although he was alert, he had multiple erythematous ulcers in the oral-pharyngeal region. Serum electrolytes, blood urea nitrogen, and creatinine were normal. His blood count demonstrated a white blood cell count of 26 900 cells/mL (78% granulated neutrophils), hemoglobin 14.4 g/dL, hematocrit 41%, and platelet count of 545 000. A throat culture was negative for Group A Streptococcus, and a neck radiograph did not demonstrate abscess formation. He was given intravenous fluids to prevent dehydration, intravenous ketorolac for pain, and intravenous acyclovir for a presumed diagnosis of herpes simplex virus (HSV) stomatitis based on his clinical findings. The patient was discharged after 3 days, and at the time of discharge, his oral lesions were in various stages of healing. He returned to his primary care physician 2 weeks after hospital discharge with dysphagia, odynophagia, and a significant decrease in oral intake. He had no fever, weight loss, or diarrhea. His oral ulcers had completely resolved, and the remainder of his physical exam was within normal limits. A repeat neck radiograph demonstrated a prevertebral soft tissue prominence and distinct epiglottis and aryepiglottic folds, possibly consistent with edema. The patient was placed on a trial of lansoprazole and demonstrated no clinical improvement, so esophago gastroduodenoscopy (EGD) was performed, which revealed a narrow esophageal stricture less than 5 mm in diameter located just below the upper esophageal sphincter (Figure 1A). The endoscope could not be advanced beyond the stricture. Esophageal biopsies revealed a zone of parakeratosis, but no inflammation or giant cell formation (Figure 1B), and a culture and polymerase chain reaction testing of esophageal tissue were negative for HSV, consistent with a resolved infection. A barium esophagram demonstrated a narrowing of the upper esophagus consistent with a stricture, as well as a long segment of narrowing throughout the esophagus (Figure 2). These findings prompted serial dilation using a Savary dilator system (Cook Medical, Bloomington, IN) under fluoroscopic examination. After serial dilations, the patient had marked improvement in swallowing, and a repeat barium esophagram demonstrated a dilated esophagus. A subsequent immune workup for this child was found to be normal, and the patient recovered with good oral intake.