- D3.541 - Who takes the patient with eosinophilic esophagitis (EoE) and acute laryngeal edema?

Background: A 41-year-old female with no atopy, no asthma, no food allergies presents to the emergency department with sudden severe throat tightness, difficulty inhaling, and a sensation of “air being blocked at the top of the throat.” Symptoms began during a stressful work meeting, not after eating. Chronic cough for 18 months, labeled as “post-viral”; intermittent globus sensation. Non-smoker, no alcohol, very rare episodes of GERD symptoms managed with self-medication. She has had three similar episodes in the past year, each resolving spontaneously within 1–2 hours.

Case Presentation: Initial Assessment of Vital Signs revealed HR - 102 bpm, RR - 28/min, SpO₂ - 92%, and BP of 142/90 mmHg. Physical exam showed dysphonia; inspiratory stridor, normal oropharynx, skin without urticaria and clear lungs. Emergency Laryngoscopy was marked by Findings with striking asymmetry: unilateral arytenoid edema; edema of the false vocal fold on the left; normal right side; no erythema and no paradoxical vocal fold motion. This pattern is not typical for allergies, reflux, or anaphylaxis. Neck CT scan excludes any mass, abscess, or vascular anomaly. Digestive endoscopy surprisingly reveals patchy esophageal rings, subtle linear furrows with no strictures. Biopsies show 18–22 eosinophils per high-power field, consistent with EoE.

Results/Discussions: This case is atypical because most EoE patients have dysphagia or food impaction. This patient had none. Laryngeal edema is unilateral. Allergic or inflammatory edema is usually symmetric. Episodes are stress-triggered. Suggesting a functional or neurogenic component. Normal eosinophil count and IgE which makes allergic causes less likely. EoE discovered incidentally because the esophageal findings were subtle and not clinically suspected along symptomatic self-medication.

Conclusions: Possible explanations are: EoE-related neurogenic inflammation affecting laryngeal sensory pathways; shared inflammatory mediators (IL‑5, IL‑13, eotaxin‑3) sensitizing laryngeal tissue; subclinical microaspiration from esophageal dysmotility; atypical laryngeal hypersensitivity syndrome triggered by esophageal inflammation; stress-induced laryngeal edema in a patient with underlying eosinophilic disease. This is the kind of case where ENT, GI, and allergy specialists disagree on the mechanism, but need to work as a team for acute and long-term management.