Eosinophilic Esophagitis
An allergic inflammation of the esophagus causing severe swallowing difficulties and episodes where food gets stuck in the chest.
Emergency Management: Esophageal food impaction: Emergent EGD is required to extract or gently push the food bolus into the stomach. Avoid using glucagon or meat tenderizers, which are ineffective and risky.
Eosinophilic Esophagitis (EoE) is a chronic, immune-mediated, or antigen-mediated clinicopathologic disease of the esophagus. It is characterized clinically by symptoms of esophageal dysfunction (predominantly dysphagia and food impaction) and histologically by dense eosinophilic infiltration of the esophageal squamous epithelium.
Detailed Overview
EoE represents a Th2-mediated allergic response triggered by food or aeroallergens. Over time, the chronic eosinophilic inflammation causes esophageal remodeling, leading to fibrosis, stricture formation, and loss of esophageal compliance. It is increasingly recognized as a major cause of dysphagia in young adults and failure to thrive in children. Management requires a multidisciplinary approach involving gastroenterology, allergy/immunology, and dietetics.
Epidemiology & Demographics
Rapidly increasing incidence, currently estimated at 1 in 2,000. It most commonly affects Caucasian males (male-to-female ratio 3:1). Can present at any age, but peak diagnoses are in childhood and the 3rd to 4th decades of life.
Etiological Mechanism
A complex interplay of genetic susceptibility and environmental antigen exposure. Associated with atopic diathesis; over 70% of patients have concurrent asthma, allergic rhinitis, eczema, or IgE-mediated food allergies.
Primary Causes
Driven by exposure to food allergens (most commonly dairy, wheat, egg, soy/legumes, nuts, and seafood) and occasionally aeroallergens (pollen, dust mites), leading to local allergic inflammation.
Exposure to allergens triggers esophageal epithelial cells to secrete TSLP and IL-33, which activate Th2 cells to release IL-5, IL-4, and IL-13. IL-5 promotes robust eosinophil recruitment and survival in the esophageal mucosa. Eosinophils degranulate, releasing major basic protein (MBP) and eosinophil cationic protein, which cause direct tissue damage. Chronic inflammation activates fibroblasts via TGF-beta, leading to subepithelial collagen deposition, smooth muscle hypertrophy, and ultimately irreversible strictures and reduced esophageal motility.
Diagnostic Criteria & Guidelines
Requires an Upper Endoscopy (EGD) with biopsies. Diagnosis demands: 1) Symptoms of esophageal dysfunction, 2) Eosinophil-predominant inflammation with ≥15 eosinophils per high-power field (eos/hpf) isolated to the esophagus, and 3) Exclusion of other causes of esophageal eosinophilia (e.g., PPI-responsive EoE is now considered part of the EoE spectrum rather than a separate exclusion).
Proton Pump Inhibitors (PPIs) (e.g., Omeprazole 20-40 mg BID for 8 weeks). If symptomatic and histologic response occurs, maintain on lowest effective dose. If PPIs fail: Topical swallowed corticosteroids. Fluticasone propionate (MDI without spacer) 440-880 mcg BID, sprayed into mouth and swallowed. Alternatively, Budesonide oral suspension 1-2 mg daily mixed with a thickener (like Splenda/honey) to coat the esophagus.
Second-Line & Adjunctive Therapy
Dietary elimination: Six-Food Elimination Diet (SFED) removing milk, wheat, egg, soy, nuts, and seafood. Reintroduce sequentially with repeat endoscopies to identify the trigger. Biologics: Dupilumab (IL-4/IL-13 receptor blocker) 300 mg subQ weekly is FDA-approved for EoE in patients ≥12 years old weighing ≥40 kg.
Surgical & Procedural Management
Endoscopic esophageal dilation (bougie or balloon) is required for symptomatic strictures. It carries a higher risk of mucosal tearing in EoE compared to other strictures, so gentle dilation over multiple sessions is preferred.
Patient Counseling & Advice
Emphasize that the topical asthma inhaler (fluticasone) must be SWALLOWED, not inhaled. Advise the patient to avoid eating or drinking for 30 minutes after taking the medication to allow it to coat the esophagus. Warn about the chronic nature of the disease and the need for long-term maintenance therapy.
Follow-Up & Monitoring Schedule
Repeat EGD with biopsies 8-12 weeks after starting or changing a medical or dietary therapy to document histologic remission (<15 eos/hpf).
Preventive Strategies
No primary prevention exists. Secondary prevention of strictures is achieved via strict adherence to maintenance medication or diet.
Chronic disease. Without maintenance therapy, symptoms and histologic inflammation invariably recur. Adherence to therapy leads to excellent symptom control and prevents fibrotic complications.