Eduovisual
Gastrointestinal
Eosinophilic esophagitis: diagnosis and treatment
— Prevalence ~1 in 2,000 in the US and rising; now the most common cause of food impaction in young adults.
— Male predominance (~3:1), peak in 20s–40s, but pediatric and older-adult cases occur.
— Strong association with atopy: asthma, allergic rhinitis, atopic dermatitis, IgE-mediated food allergy, eczema (~50–80% have atopic comorbidities).
— Young/middle-aged adult with dysphagia to solids, especially meat or bread, often with adaptive eating behaviors (cuts food small, chews excessively, drinks water with meals — the "IMPACT" behaviors).
— Recurrent food impactions requiring ED disimpaction.
— Heartburn or chest pain unresponsive to standard PPI dosing — but note PPI response no longer excludes EoE.
— Children: feeding difficulty, vomiting, failure to thrive, abdominal pain rather than classic dysphagia.
— Th2-driven inflammation with IL-5, IL-13, eotaxin-3 (CCL26) recruiting eosinophils → tissue remodeling, fibrosis, strictures, and a narrow-caliber esophagus.
— Triggers are predominantly food antigens (milk, wheat, egg, soy, nuts, seafood) and possibly aeroallergens.
Board pearl: Any adult presenting to the ED with a food bolus impaction should have EoE on the differential — outpatient GI referral for endoscopy with biopsies is the expected Step 3 disposition, even if the bolus passes spontaneously. Do not attribute recurrent "GERD-like" symptoms in a young atopic male to acid reflux alone without considering EoE.
— Solid-food dysphagia is the cardinal symptom — intermittent, often for years before diagnosis.
— Food impaction (steakhouse syndrome) — meat, bread, rice; may require endoscopic disimpaction.
— Chest pain or retrosternal discomfort, often noncardiac, sometimes mistaken for GERD or MI.
— Heartburn and regurgitation that is partially or non-responsive to PPIs.
— Adaptive eating behaviors — patients underreport dysphagia; ask specifically: "Do you cut food into small pieces? Drink water with meals? Avoid steak or bread? Take longer to eat than others?"
— Infants/toddlers: feeding refusal, vomiting, failure to thrive.
— School age: abdominal pain, vomiting, regurgitation.
— Teens: dysphagia, impaction (adult phenotype emerging).
— Atopic history: asthma, eczema, allergic rhinitis, oral allergy syndrome, IgE food allergy.
— Family history of EoE or atopy.
— Dietary triggers: worsening after specific foods (dairy, wheat).
— Medication history: prior PPI trials, dose, duration, response.
— Prior endoscopies, dilations, or impactions.
— Environmental allergens — seasonal symptom variation suggests aeroallergen contribution.
— Weight loss, anemia, GI bleeding, age >50 with new dysphagia — evaluate for malignancy or peptic stricture.
— Progressive dysphagia to liquids → consider motility disorder (achalasia).
Key distinction: EoE dysphagia is typically intermittent and solid-food predominant for years, whereas malignancy causes progressive solid-then-liquid dysphagia with weight loss, and achalasia causes both solid and liquid dysphagia from onset with regurgitation of undigested food.
— Atopic dermatitis — flexural eczematous patches, lichenification at antecubital/popliteal fossae.
— Allergic rhinitis — pale boggy turbinates, transverse nasal crease ("allergic salute"), allergic shiners (infraorbital darkening).
— Asthma — end-expiratory wheeze, prolonged expiratory phase.
— Conjunctival injection, Dennie–Morgan lines under lower lids in children.
— Generally normal in EoE — but inspect for thrush (suggests inhaled steroid use or alternative diagnosis), oropharyngeal lesions, and goiter.
— Lymphadenopathy or supraclavicular nodes → think malignancy, not EoE.
— Typically normal. Epigastric tenderness suggests peptic disease.
— Hepatosplenomegaly or mass → alternative pathology.
— Plot height, weight, BMI percentiles; failure to thrive is a pediatric red flag.
— In adults, document BMI and weight trajectory — significant weight loss is not typical of EoE and should prompt broader workup.
— Assess airway: drooling, inability to handle secretions → urgent endoscopy.
— Vitals: tachycardia and hypertension from distress are common; hypotension or fever is atypical and should prompt evaluation for perforation.
— Subcutaneous emphysema, chest pain, fever after disimpaction → suspect Boerhaave/iatrogenic perforation.
CCS pearl: A patient with acute food bolus impaction unable to manage secretions needs emergent EGD within 6 hours, NPO status, IV access, and anesthesia/GI consult — glucagon can be tried but has limited efficacy and should not delay endoscopy. After successful disimpaction, obtain biopsies during the same procedure to establish EoE diagnosis.
— Concentric rings ("trachealization" or feline esophagus) — fixed rings indicate fibrostenosis.
— Linear furrows — vertical longitudinal lines.
— White exudates/plaques — eosinophil microabscesses (mimic Candida).
— Edema — loss of vascular pattern, pallor.
— Strictures and narrow-caliber esophagus.
— Crepe-paper mucosa — fragile mucosa that tears with scope passage (high perforation risk).
— Up to 10–25% of EoE patients have normal-appearing mucosa — biopsies are mandatory even if visually normal.
— ≥6 biopsies from at least 2 esophageal levels (proximal/mid and distal) to maximize sensitivity.
— Also biopsy stomach and duodenum if eosinophilic gastroenteritis is suspected or to exclude other causes of eosinophilia.
— Diagnostic threshold: ≥15 eosinophils per high-power field (eos/HPF) in at least one biopsy.
— CBC: peripheral eosinophilia present in ~50% but not required; marked eosinophilia (>1,500) → consider hypereosinophilic syndrome, parasitic infection.
— Total IgE often elevated; specific IgE testing has limited utility for guiding EoE diet therapy.
— Consider allergy referral if atopic comorbidities are prominent.
— Barium esophagram is not required but may show small-caliber esophagus, rings, or strictures; useful when endoscopy underestimates luminal narrowing.
— CT/MRI have no role in routine EoE diagnosis.
Board pearl: A "normal-looking" esophagus does not rule out EoE — always obtain multilevel biopsies in any patient endoscoped for unexplained dysphagia or food impaction. Documentation of biopsy from ≥2 levels is the expected Step 3 standard.
— Symptoms of esophageal dysfunction (dysphagia, impaction, feeding intolerance, chest pain, heartburn).
— Esophageal biopsy showing ≥15 eos/HPF (≈60 eos/mm²).
— Other causes of esophageal eosinophilia excluded (see mimics below).
— Important change: a PPI trial is no longer required to diagnose EoE. PPI-responsive esophageal eosinophilia is now considered part of the EoE spectrum, not a separate entity.
— GERD — can cause mild distal eosinophilia (usually <15/HPF), often resolves with PPI.
— Eosinophilic gastroenteritis — eosinophilia beyond esophagus.
— Achalasia — can have secondary eosinophilia from stasis.
— Crohn disease with esophageal involvement.
— Infections: parasitic (helminths), fungal (Candida) — though Candida usually does not cause tissue eosinophilia.
— Drug hypersensitivity: pill esophagitis, hypersensitivity reactions.
— Connective tissue disease: scleroderma, vasculitis (EGPA).
— Hypereosinophilic syndrome — peripheral eos >1,500 with end-organ involvement.
— Pemphigus vegetans, graft-versus-host disease.
— Endoscopic functional luminal imaging probe (EndoFLIP) — measures esophageal distensibility; reduced distensibility predicts food impaction risk and helps guide dilation.
— High-resolution manometry — not routine; consider when dysmotility or achalasia is suspected.
— pH/impedance monitoring — reserve for atypical cases where GERD is the leading alternative.
Key distinction: GERD-associated esophageal eosinophilia is typically distal, patchy, and <15 eos/HPF and resolves with PPI; EoE shows diffuse, dense (often >15/HPF) eosinophilia at proximal and distal sites and is now defined independent of PPI response. Both can coexist — they are not mutually exclusive.
— Symptomatic remission — resolution of dysphagia, prevention of impaction.
— Histologic remission — <15 eos/HPF, ideally <6/HPF.
— Endoscopic remission — improved EREFS score.
— Prevention of long-term fibrostenotic complications — strictures, narrow-caliber esophagus.
— PPI: easiest, cheapest, ~30–50% histologic response; reasonable first-line in most adults.
— Topical corticosteroids (budesonide oral suspension, fluticasone): ~60–80% histologic response; preferred when fibrostenosis is prominent or PPI fails.
— Empiric elimination diet: avoids medication exposure; best for motivated patients; 6-food (milk, wheat, egg, soy, nuts, seafood), 4-food, or step-up 2-food (milk, wheat) approaches.
— Targeted elimination by allergy testing: poor predictive value; not recommended as primary strategy.
— Biologic (dupilumab): now FDA-approved for EoE ≥1 year old, used when conventional therapy fails or in patients with concurrent atopic disease.
— High-risk features for fibrostenosis: long symptom duration before diagnosis (each year delay → ~9% increase in stricture risk), rings/strictures on EGD, prior impactions.
— Narrow-caliber esophagus or stricture → plan for endoscopic dilation in addition to anti-inflammatory therapy.
Step 3 management: First-line therapy choice in adult EoE should be individualized: start a PPI (omeprazole 20–40 mg BID × 8 weeks) or swallowed topical steroid (budesonide 1 mg BID or fluticasone 880 mcg BID × 8 weeks), then repeat EGD with biopsies at 8–12 weeks to confirm histologic response — symptoms alone are insufficient to gauge remission.
— Mechanism beyond acid suppression: anti-inflammatory effects on eotaxin-3 expression.
— Dose: omeprazole 20–40 mg BID, esomeprazole 20–40 mg BID, or equivalent × 8 weeks induction.
— Response: ~30–50% achieve histologic remission. Responders continue lowest effective dose long-term.
— Counsel on long-term PPI risks: C. difficile, fractures, hypomagnesemia, B12 deficiency, possible CKD; benefits generally outweigh risks in confirmed EoE.
— Budesonide oral suspension (Eohilia) — FDA-approved 2024: 2 mg BID × 12 weeks induction.
— Compounded viscous budesonide (mixed with sucralose/Splenda): 1 mg BID adults, 0.5 mg BID children.
— Fluticasone MDI swallowed (not inhaled): 880 mcg BID adults; spray into mouth and swallow, no spacer.
— Patient counseling (high-yield): no food/drink × 30–60 minutes after dose; rinse mouth to prevent oral/esophageal candidiasis.
— Histologic response: 60–80%; symptomatic response similar.
— Adverse effects: candidiasis (~5–10%), minimal systemic absorption, rare adrenal suppression with prolonged high dose.
— FDA-approved for EoE in patients ≥1 year old and ≥15 kg.
— Dose: 300 mg SC weekly in adults (different weight-based dosing pediatric).
— Indicated for refractory EoE or patients with concomitant atopic disease (asthma, atopic dermatitis, CRSwNP).
— Cost and prior authorization are significant; reserve after PPI ± steroid failure.
— EoE relapses in >50% within 1 year off treatment — chronic maintenance is the rule.
— Use lowest effective dose of PPI or steroid that maintains remission; reassess periodically.
Board pearl: Always counsel patients on swallowed steroids to avoid eating, drinking, or rinsing for 30–60 minutes after dosing — this maximizes mucosal contact and is a frequent test point. Inhaler use with a spacer (for asthma technique) is wrong for EoE.
— Eliminate milk, wheat, egg, soy, nuts/peanuts, fish/shellfish × 6 weeks → EGD with biopsy.
— Histologic remission ~70%; reintroduce one food at a time with repeat EGD to identify triggers.
— Most common triggers: dairy > wheat > egg > soy.
— 2-food elimination (milk + wheat) first → if no remission, escalate to 4-food, then 6-food.
— Reduces number of endoscopies needed by ~35%.
— Highest efficacy (~90%) but poor palatability and adherence; reserved for severe refractory pediatric cases.
— Skin prick and IgE testing have poor predictive value for EoE triggers — not recommended as sole guide.
— Indicated for fibrostenotic disease: strictures, narrow-caliber esophagus, persistent dysphagia despite histologic remission.
— Modalities: through-the-scope (TTS) balloon or Savary bougie.
— Rule of "start low, go slow": begin with diameter just below estimated stricture; advance no more than 3 mm per session; target final diameter 15–18 mm.
— Risks: post-procedure chest pain (~75%), perforation (~0.3–1%), bleeding.
— Dilation treats symptoms but not underlying inflammation — always pair with anti-inflammatory therapy.
CCS pearl: In a CCS case of EoE with stricture and recurrent food impaction, the correct sequence is: EGD with biopsy → confirm EoE → initiate PPI or topical steroid → repeat EGD at 8–12 weeks → perform graded dilation if strictures persist. Dilating without histologic therapy is incomplete management. Counsel patients that mild post-dilation chest pain lasting 24–48 hours is common and expected; severe pain, fever, or subcutaneous emphysema warrants imaging to exclude perforation.
— EoE is less common but increasingly recognized in adults >65.
— New-onset dysphagia in older adults must first exclude malignancy, peptic stricture, Schatzki ring, and motility disorders — EoE is a diagnosis of inclusion after biopsy, not assumption.
— Greater polypharmacy → pill esophagitis (bisphosphonates, doxycycline, KCl, NSAIDs) can mimic or coexist with EoE.
— Atopic background may be absent; presentation often fibrostenotic due to delayed diagnosis.
— Reassess risk/benefit at each visit: fracture risk, hypomagnesemia, C. difficile, pneumonia, CKD progression, B12 deficiency.
— Check magnesium, B12 periodically with long-term use; ensure adequate calcium/vitamin D.
— Drug interactions: clopidogrel + omeprazole/esomeprazole — prefer pantoprazole if dual antiplatelet therapy required.
— Monitor for oropharyngeal candidiasis — higher risk with dentures, xerostomia, diabetes.
— Minimal systemic absorption; bone density concerns less than systemic steroids but be cautious in established osteoporosis.
— PPIs: no dose adjustment required; however PPIs may worsen CKD and cause acute interstitial nephritis — monitor creatinine.
— Budesonide and fluticasone: minimal renal excretion; no dose adjustment.
— Dupilumab: no renal adjustment.
— PPIs: reduce dose with severe hepatic impairment (omeprazole max 20 mg/day in severe disease).
— Swallowed corticosteroids: budesonide undergoes extensive first-pass hepatic metabolism — systemic exposure increases in cirrhosis; use cautiously, monitor for cushingoid features.
— Dupilumab: no hepatic dose adjustment.
Step 3 management: In an older patient on clopidogrel post-PCI who develops EoE, choose pantoprazole or rabeprazole over omeprazole/esomeprazole to avoid CYP2C19-mediated reduction of clopidogrel activation — or favor swallowed budesonide as first-line.
— EoE itself does not affect pregnancy outcomes; management focuses on symptom control while minimizing fetal exposure.
— PPIs: generally considered safe (omeprazole, lansoprazole, pantoprazole — Category B/C historically); use lowest effective dose.
— Swallowed topical steroids (budesonide, fluticasone): low systemic absorption; budesonide has the most reassuring pregnancy data (used in IBD and asthma in pregnancy).
— Dupilumab: limited pregnancy data; use only if clearly needed; shared decision-making.
— Dietary therapy: safe and preferred when feasible; ensure adequate caloric and micronutrient intake with dietitian support.
— Elective endoscopy and dilation generally deferred to postpartum unless emergent (impaction).
— PPIs and swallowed topical steroids are compatible with breastfeeding (minimal transfer).
— Presentation shifts with age:
– Infants: feeding refusal, vomiting, failure to thrive.
– Toddlers/school-age: vomiting, abdominal pain, refusal to eat solids.
– Adolescents: adult-pattern dysphagia and impaction.
— Diagnostic criteria identical (≥15 eos/HPF).
— Treatment:
– PPI: 1–2 mg/kg/day divided BID.
– Swallowed fluticasone 88–440 mcg BID (age-based) or viscous budesonide 0.5–1 mg BID.
– Dupilumab approved ≥1 year and ≥15 kg.
– Dietary therapy: elemental formula highly effective but adherence-limited; SFED widely used with dietitian.
— Growth monitoring is essential — track height/weight percentiles; involve nutrition.
— Multidisciplinary care: pediatric GI, allergist, dietitian, feeding therapist.
Board pearl: A toddler with food refusal, vomiting, and poor weight gain plus a strong atopic family history needs pediatric GI referral for EGD with biopsies — do not anchor on "picky eating" or simple GERD. Early diagnosis prevents fibrostenotic progression.
— Food bolus impaction — most common acute complication; cumulative lifetime risk ~30–55% in untreated EoE.
— Esophageal strictures — develop with prolonged inflammation; risk increases ~9% per year of diagnostic delay.
— Narrow-caliber esophagus — diffuse luminal narrowing; high impaction risk.
— Crepe-paper mucosa — fragile mucosa, spontaneous tears or tears with scope passage.
— Spontaneous esophageal perforation (Boerhaave-like) — rare but reported, particularly with forceful vomiting against fixed rings.
— Nutritional deficits and weight loss — more in pediatrics; rare in adults.
— Psychosocial impact — anxiety around eating, social avoidance, reduced QoL.
— Swallowed steroids: oral/esophageal candidiasis (~5–10%), dysphonia, rare adrenal suppression with long-term high doses; theoretical bone density effects with prolonged use.
— PPIs: C. difficile, CAP, hypomagnesemia, B12 deficiency, AKI/AIN, CKD progression, fractures, rebound acid hypersecretion on discontinuation.
— Dupilumab: injection-site reactions, conjunctivitis, eosinophilia (transient), arthralgia; rare hypersensitivity.
— Dilation: chest pain (75%), perforation (~0.3–1%), bleeding, mucosal tears.
— Perforation risk during EGD is higher than general population due to fragile mucosa and rings; small-caliber endoscopes and careful technique reduce risk.
— Untreated EoE evolves from inflammatory → mixed → fibrostenotic phenotype over years; early intervention may prevent stricturing.
— EoE is not associated with esophageal cancer — important counseling point.
Key distinction: Unlike Barrett esophagus, EoE has no documented increased risk of esophageal adenocarcinoma or squamous cell carcinoma — reassure patients, but emphasize that fibrostenotic remodeling is the real long-term threat, justifying chronic maintenance therapy.
— Acute food bolus impaction — particularly with inability to manage secretions (drooling, choking, aspiration risk).
— Severe chest pain after eating or vomiting → exclude esophageal perforation with CT chest with oral contrast or gastrografin esophagram.
— Hematemesis or signs of significant GI bleeding.
— Food impaction with airway compromise → EGD within 6 hours.
— Food impaction without airway compromise → EGD within 24 hours (do not wait for spontaneous passage beyond 24 hours due to ulceration/perforation risk).
— Suspected perforation → surgical and GI consultation; avoid endoscopy until imaging clarifies.
— Post-disimpaction observation if mucosal tear, significant ulceration, or aspiration occurred.
— Surgical admission for perforation — broad-spectrum antibiotics, NPO, urgent thoracic surgery consult; small contained perforations may be managed with stents/clips by interventional GI.
— Severe dehydration or inability to tolerate oral intake in pediatrics with feeding refusal.
— Gastroenterology — diagnosis, endoscopy, dilation, long-term management.
— Allergy/immunology — atopic comorbidities, IgE-mediated food allergy assessment, dupilumab candidacy.
— Dietitian/nutrition — elimination diets, pediatric nutritional support.
— Speech-language pathology/feeding therapy — pediatric feeding aversion.
— Thoracic surgery — perforation.
— Failure of first-line therapy (persistent ≥15 eos/HPF after 8–12 weeks) → switch or add therapy class.
— Recurrent impactions despite medical therapy → dilation; consider dupilumab.
CCS pearl: For a stable patient with food impaction whose bolus passes spontaneously in the ED, do not discharge without arranging outpatient GI follow-up and EGD with biopsies within 1–2 weeks — missing the diagnostic window is a Step 3 transition-of-care failure.
— Heartburn predominant, distal symptoms, response to PPI; eosinophilia usually <15/HPF and distal-only.
— Can coexist with EoE; both diagnoses possible.
— Older patients, long-standing GERD, distal smooth narrowing, responds to dilation + PPI; no eosinophilia.
— Lower esophageal mucosal ring; intermittent solid dysphagia, "steakhouse syndrome" — often confused with EoE.
— Dilation curative; no inflammation on biopsy.
— Dysphagia to both solids and liquids, regurgitation of undigested food, weight loss.
— Manometry: absent peristalsis, failure of LES relaxation; bird-beak on barium.
— Can have secondary mild eosinophilia from stasis.
— Age >50, progressive dysphagia, weight loss, anemia, smoking/alcohol history (SCC) or chronic GERD/Barrett (adenocarcinoma).
— EGD with biopsy diagnostic.
— Sudden odynophagia after bisphosphonates, doxycycline, KCl, NSAIDs, iron; mid-esophageal ulcers.
— Candida (white plaques, immunocompromised, inhaled steroids), HSV (vesicles, ulcers), CMV (large ulcers, AIDS).
— Eosinophilia beyond esophagus — stomach, small bowel; abdominal pain, diarrhea, ascites.
— Peripheral eos >1,500 with multi-organ involvement (skin, heart, lungs).
— Rare esophageal involvement; usually accompanies ileocolonic disease.
— Scleroderma (motility dysfunction, GERD), EGPA (Churg-Strauss) with eosinophilia and asthma.
Key distinction: EoE = young/middle-aged atopic man, intermittent solid dysphagia, ≥15 eos/HPF on multilevel biopsy; achalasia = dysphagia to solids AND liquids, manometric LES failure; cancer = progressive dysphagia + weight loss in older patient. Mismatch of these triads should redirect the workup.
— Peripheral eosinophilia >1,500/µL × 6 months with end-organ damage (cardiac, neuro, pulmonary, cutaneous).
— Subtypes: myeloproliferative (PDGFRA fusion → imatinib-responsive), lymphocytic, idiopathic.
— EoE has peripheral eos usually <1,500 and tissue infiltrate confined to esophagus.
— Asthma + eosinophilia + vasculitis (mononeuritis multiplex, sinusitis, cardiac/renal involvement); ANCA (MPO) positive in ~40%.
— May have GI involvement with eosinophilia, but systemic features dominate.
— Strongyloides, hookworm, ascaris, trichinella, anisakiasis — relevant in travel/immigrant history.
— Check stool O&P, strongyloides serology before starting systemic steroids or dupilumab in at-risk patients (risk of hyperinfection).
— Multiorgan hypersensitivity with eosinophilia 2–8 weeks after culprit drug (allopurinol, anticonvulsants, sulfas).
— Asthma, atopic dermatitis, allergic rhinitis, oral allergy syndrome, IgE food allergy.
— Coordinated care with allergist; dupilumab may treat multiple conditions simultaneously.
— Mast cell infiltration with secondary eosinophilia; flushing, GI symptoms; tryptase elevated.
— Rare; usually known IBD with new dysphagia.
— Scleroderma: dysphagia from dysmotility + severe GERD; antibodies (anti–Scl-70, anti-centromere), skin findings.
— Sjögren: dysphagia from xerostomia.
Board pearl: Before starting dupilumab or systemic steroids in a patient with eosinophilia and travel/immigration history from endemic regions, screen for Strongyloides (serology) to prevent hyperinfection syndrome — a classic Step 3 patient safety pitfall.
— PPI: continue lowest effective dose (often once daily) in responders.
— Swallowed topical steroids: continue at induction or reduced dose (e.g., budesonide 1 mg daily or BID); monitor for candidiasis.
— Dietary therapy: maintain elimination of identified trigger foods indefinitely; periodic challenges to verify persistence of trigger.
— Dupilumab: continue weekly injections; long-term durability data emerging.
— Failure of first-line therapy (persistent eosinophilia and/or symptoms at 8–12 weeks) → switch to another first-line agent (PPI ↔ steroid ↔ diet).
— Multiple failures → dupilumab.
— Persistent fibrostenosis despite histologic remission → endoscopic dilation.
— Treat coexisting asthma, atopic dermatitis, allergic rhinitis aggressively; consider dupilumab when multiple atopic conditions overlap.
— Vaccinations: routine adult schedule; live vaccines contraindicated with high-dose systemic steroids (rarely used in EoE); generally safe with topical/swallowed steroids and dupilumab.
— Recognize early dysphagia/impaction warning signs; seek care promptly.
— Eating behaviors: small bites, thorough chewing, sit upright, drink fluids with meals.
— Avoid eating large meat or bread portions, especially if rings/strictures persist.
— Medication adherence and proper administration technique (steroid swallow technique, NPO interval).
— Address coexisting GERD: weight loss if obese, head-of-bed elevation, avoid late meals.
— Limit alcohol and tobacco (mucosal irritation, GERD).
Step 3 management: At discharge or follow-up after induction therapy, document a maintenance regimen, repeat EGD plan, allergy/dietitian referrals, and patient instructions on eating behaviors — open-ended "PRN" management is the wrong answer; EoE requires structured longitudinal care.
— Repeat EGD with biopsies at 8–12 weeks after starting first-line therapy — symptoms alone are unreliable due to adaptive eating behaviors.
— Document EREFS score and eosinophil counts at each surveillance EGD.
— EGD every 1–2 years in stable patients on maintenance, more frequently after therapy changes.
— Annual office visit at minimum to reassess symptoms, adherence, atopic comorbidities, growth (peds), and medication side effects.
— Symptom-based reassessment alone is insufficient — histologic monitoring is preferred.
— PPI: periodic magnesium, B12 (with long-term use), creatinine; assess for C. difficile risk with new diarrhea; bone density if other risk factors.
— Topical steroids: oral exam for candidiasis; consider AM cortisol if cushingoid features develop with prolonged high-dose use.
— Dietary therapy: serial nutrition reviews, micronutrient assessment (calcium, vitamin D, iron in dairy/wheat elimination).
— Dupilumab: monitor for conjunctivitis (~10%), injection reactions; CBC for transient eosinophilia (usually benign).
— Growth parameters at every visit; nutrition follow-up; feeding behavior progression.
— Coordinate school accommodations for medication timing and food restrictions.
— Chronic disease framing — EoE is not curable but is controllable; analogy to asthma.
— Adherence is critical — relapse after stopping is the norm.
— Reassurance about cancer risk — no association with esophageal cancer.
— Emergency action plan for food impaction: do not force food down; seek ED if unable to swallow saliva.
Board pearl: A patient who reports "feeling great" after 8 weeks of swallowed budesonide still needs a repeat EGD with biopsies to document histologic remission — symptom resolution and histologic resolution are discordant in 30–40% of EoE patients due to adaptive eating habits.
— Discuss risks specific to EoE: higher rates of mucosal tears and perforation due to fragile, rigid esophagus; document this explicitly in dilation consent.
— Discuss anesthesia risks, especially in pediatric repeated endoscopies.
— Parents provide consent; age-appropriate assent from older children, especially for dietary restrictions and injection therapies (dupilumab).
— Address school and social impact of food eliminations — coordinate with school nurse for emergency action plan.
— Shared decision-making about long-term PPI vs steroid vs biologic — discuss known risks transparently.
— Avoid clopidogrel–omeprazole/esomeprazole combination (use pantoprazole) — a documented patient-safety pitfall.
— Screen for Strongyloides before systemic steroids or biologics in at-risk patients to prevent hyperinfection.
— ED → outpatient transition after food impaction is a high-risk handoff — ensure GI follow-up and EGD with biopsies are scheduled before discharge; missed biopsy is a sentinel diagnostic-delay event.
— Pediatric-to-adult transition at age 18–21: structured handoff to adult GI; address autonomy, insurance, adherence.
— Dupilumab cost (~$30,000–60,000/year) and prior authorization barriers — document failure of conventional therapy carefully.
— Dietitian access varies — patients without insurance coverage may default to medication; advocate for nutrition referrals.
— Health literacy: written/visual aids for steroid swallow technique improve adherence.
— No mandatory public health reporting for EoE.
— Document adverse events (perforation, anaphylaxis to biologic) through institutional and FDA MedWatch channels.
Step 3 management: A patient discharged from the ED after spontaneous passage of a food bolus without scheduled GI follow-up represents a transition-of-care safety failure. The expected board answer is to arrange outpatient EGD with biopsy within 1–2 weeks, provide written instructions, and document understanding before discharge.
Board pearl: If a vignette describes a young atopic man with dysphagia + food impaction + concentric rings on EGD, the immediate next step is multilevel biopsy — not empiric dilation, not pH testing, not barium swallow.
— 28-year-old man with asthma and eczema presents with steak lodged in his throat for 3 hours. Endoscopy disimpacts the bolus and reveals concentric rings and linear furrows.
— Best next step: obtain multilevel biopsies (proximal and distal) during the same EGD; not PPI trial alone, not barium swallow.
— Patient with dysphagia and 25 eos/HPF on biopsy responds to omeprazole BID with histologic remission.
— Diagnosis: EoE (PPI response does not exclude EoE per current criteria).
— Patient achieves remission with swallowed budesonide × 12 weeks. Asks if therapy can be stopped.
— Answer: continue maintenance; relapse rate >50% within 1 year off treatment.
— Patient on PPI BID × 12 weeks has persistent 30 eos/HPF and dysphagia.
— Next step: switch to or add swallowed topical corticosteroid, repeat EGD at 8–12 weeks.
— Persistent dysphagia despite histologic remission with stricture on EGD.
— Next step: endoscopic dilation with continued anti-inflammatory therapy.
— 3-year-old with food refusal, vomiting, poor weight gain, family history of atopy.
— Next step: pediatric GI referral for EGD with biopsies.
— EoE patient post-PCI on clopidogrel needs PPI.
— Choose: pantoprazole (not omeprazole/esomeprazole).
— Adult with EoE, severe atopic dermatitis, and asthma; failed PPI and topical steroids.
— Best therapy: dupilumab (treats all three).
— Severe chest pain, fever, subcutaneous emphysema post-dilation.
— Next step: CT chest with water-soluble contrast; broad-spectrum antibiotics; thoracic surgery consult.
— Immigrant patient before starting dupilumab — screen serology to prevent hyperinfection.
Key distinction: When stems offer "barium swallow" vs "EGD with biopsy" for new dysphagia in a young patient with atopy, EGD with biopsy is correct — barium is rarely the right answer when EoE is on the differential.
Eosinophilic esophagitis is a chronic Th2-mediated esophageal disease of young atopic patients, diagnosed by ≥15 eos/HPF on multilevel biopsy after exclusion of mimics, and managed indefinitely with PPIs, swallowed topical corticosteroids, elimination diets, dupilumab for refractory or atopic-comorbid disease, and endoscopic dilation for fibrostenotic complications — with repeat EGD required to confirm histologic remission because symptoms alone are unreliable.
Board pearl: When in doubt on Step 3, the right move for new dysphagia in a young atopic patient is EGD with multilevel biopsies, structured 8–12-week histologic reassessment, and indefinite maintenance therapy — not symptomatic-only management.