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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Eosinophilic oesophagitis

Gastroenterology and hepatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Complete food-bolus obstruction with inability to swallow saliva, drooling or aspiration risk requires urgent therapeutic endoscopy; airway protection and local endoscopy timing take priority. Severe chest pain, fever, tachycardia, subcutaneous emphysema or deterioration after retching, impaction removal or dilation raises perforation and needs immediate CT and upper-GI surgical review. Do not push an impacted bolus blindly or rely on pharmacological relaxation when urgent endoscopic removal is required.

Overview

Recognise eosinophilic oesophagitis across food impaction and subtle adaptive eating, confirm it with adequate biopsies and combine anti-inflammatory and stricture treatment.

EoE reflects type 2 immune inflammation causing epithelial injury, remodelling and fibrosis. Untreated disease can progress from inflammatory furrows and exudates to rings, narrow calibre and strictures. The clinical clue may be dramatic impaction, but many people normalise years of slow eating and food avoidance. Reflux, infection, Crohn disease, connective-tissue disease, coeliac disease and drug reactions can also increase oesophageal eosinophils, so histology is interpreted with symptoms and distribution.

Diagnosis requires adequate sampling even when endoscopy appears normal. BSG/BSPGHAN guidance supports at least six biopsies across at least two levels, targeted to abnormalities as well as apparently normal mucosa. The histology report should provide peak eosinophil density and other features such as basal-zone hyperplasia or fibrosis where available. A failed PPI course is no longer required before the diagnosis is made, although PPIs remain a useful first-line treatment for some patients.

Practice

Two practice questions

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Gastroenterology and hepatologyOriginal SBA

Biopsy strategy in suspected EoE

A 29-year-old with recurrent meat impactions has rings and furrows at endoscopy. Which biopsy strategy best follows BSG guidance?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • BSG BSPGHAN eosinophilic oesophagitis guidelineUK diagnosis, biopsy, treatment, dilation and follow-up consensus.
  • NICE TA708 budesonide for EoEEngland commissioning recommendation for adult induction of remission.
  • Jorveza summary of product characteristicsLicensed induction dose, administration technique, maintenance options and safety information.
  • BSG oesophageal dilatation guidelineSafety framework for treating EoE-associated strictures.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Treatment is shared and long term because relapse is common when therapy stops. Budesonide orodispersible tablets have NICE support for induction in adults and a defined licensed technique; swallowed topical steroid alternatives, PPIs and elimination diets depend on age, local commissioning and patient preference. Allergy tests do not reliably identify the food drivers for elimination. Diet restriction should be supervised by an experienced dietitian to protect nutrition and avoid unsafe broad avoidance.

Key points

  • EoE is a chronic immune-mediated oesophageal disease defined by symptoms of dysfunction and eosinophil-predominant inflammation after competing causes are considered.
  • Adults commonly present with intermittent solid-food dysphagia, food impaction or chest discomfort; children may present with feeding difficulty, vomiting or poor growth.
  • Patients often adapt by chewing excessively, drinking with every mouthful, avoiding meat or bread and taking much longer to eat, so ask how they eat rather than only whether they swallow.
  • Atopy, asthma, eczema, allergic rhinitis and immediate food allergy are common associations but their absence does not exclude EoE.
  • Endoscopic rings, longitudinal furrows, white exudates, oedema, narrowing and fragile crepe-paper mucosa support EoE, yet the oesophagus may look normal.
  • Take at least six biopsies from at least two oesophageal levels under the BSG pathway because inflammation is patchy.
  • A peak of at least 15 eosinophils per high-power field supports diagnosis in the correct symptomatic context after alternative causes are assessed.
  • A PPI trial is a treatment option rather than a mandatory diagnostic exclusion; PPI-responsive eosinophilia sits within the EoE spectrum.
  • Effective options include PPI, swallowed topical corticosteroid and dietetic-led food elimination; response should be checked histologically because symptoms correlate poorly.

Aetiology

01

Food-antigen immune response

A delayed type-2 immune response to dietary antigens drives most disease, but conventional allergy tests do not reliably identify the causal foods.

02

Atopic susceptibility

Asthma, eczema, allergic rhinitis and immediate food allergy commonly coexist, reflecting shared immune predisposition without being required for diagnosis.

03

Epithelial and genetic factors

Variants affecting oesophageal barrier function and type-2 signalling interact with environmental exposure to sustain chronic eosinophilic inflammation.

Pathophysiology

  1. 1
    Type-2 cytokine activation

    Antigen exposure activates epithelial and immune signals that recruit and maintain eosinophils within the oesophageal mucosa.

  2. 2
    Mucosal injury and dysmotility

    Eosinophil mediators cause oedema, furrows, exudate and altered wall function, producing dysphagia even before fixed narrowing develops.

  3. 3
    Fibrotic remodelling

    Repeated untreated inflammation deposits subepithelial collagen and remodels muscle, creating rings, reduced calibre and focal strictures.

Clinical features and red flags

Food-bolus impactionRed flag

Meat or bread lodges after a history of intermittent solid-food dysphagia; inability to manage saliva indicates complete obstruction and requires urgent endoscopic care.

Adaptive eating behaviour

The person chews excessively, cuts food finely, avoids dry dense textures, drinks after each swallow or is consistently last to finish meals despite denying dysphagia.

Inflammatory endoscopic phenotype

Oedema, reduced vascular markings, longitudinal furrows and punctate white exudates suggest active inflammation but can be subtle or absent.

Fibrostenotic phenotype

Fixed rings, focal stricture or diffuse narrow-calibre oesophagus produces longstanding solid-food dysphagia and impaction, often with less visible exudate.

Perforation after impaction or dilationRed flag

Severe persistent pain, fever, tachycardia, breathlessness, subcutaneous emphysema or pleural signs after intervention requires emergency imaging and upper-GI surgical involvement.

Investigations

  1. 01
    Upper gastrointestinal endoscopyFirst step
    Why
    Assess impaction, inflammatory signs, calibre and focal narrowing.
    Interpretation and limitations
    Document rings, exudates, furrows, oedema and strictures using a consistent score where possible. A normal appearance cannot exclude EoE and still requires biopsies.
  2. 02
    Multi-level oesophageal biopsies
    Why
    Demonstrate patchy eosinophil-predominant inflammation adequately.
    Interpretation and limitations
    Take at least six samples from at least two levels, targeting abnormalities and separate pots according to local pathology practice. Peak density of at least 15 eosinophils per high-power field supports EoE clinically.
  3. 03
    Histopathology review
    Why
    Confirm inflammation and identify remodelling or another diagnosis.
    Interpretation and limitations
    Eosinophil microabscesses, surface layering, basal-zone hyperplasia and lamina-propria fibrosis support EoE. Candida, viral change or malignant cells redirect management.
  4. 04
    Barium oesophagram
    Why
    Define subtle long-segment narrowing or complex strictures before treatment.
    Interpretation and limitations
    It can show reduced calibre or hold-up missed at endoscopy but does not replace biopsies. A tablet or timed protocol follows the specialist question.
  5. 05

Differential diagnosis

01

Gastro-oesophageal reflux disease

Heartburn and erosive reflux may coexist; adequate biopsies and the overall clinical-endoscopic pattern distinguish eosinophilic disease from acid injury alone.

02

Peptic stricture or ring

A focal narrowing may explain solid dysphagia, but multiple-level biopsies are required because EoE mucosa can appear normal.

03

Achalasia or cancer

Liquids-and-solids dysphagia with abnormal manometry suggests achalasia, while rapid progression, weight loss or an irregular lesion raises malignancy concern.

Additional chapter-specific clues

Alternative alarm diagnosisRed flag

Rapidly progressive dysphagia, weight loss, anaemia, bleeding or an irregular mass requires urgent cancer and structural assessment even when eosinophilia is present.

Management

01Food obstructionRelieve the bolus and diagnose the causeFirst stepA patient cannot swallow food or saliva after a solid-food impaction.+
  1. 1Assess airway and aspiration risk, keep nil by mouth and arrange urgent endoscopy; investigate perforation first if severe pain, sepsis or subcutaneous emphysema is present.
  2. 2Remove the bolus with appropriate airway support rather than repeated blind pushing or delaying for unproven pharmacological therapy.
  3. 3At safe endoscopy, document rings, furrows, calibre and stricture and obtain multi-level biopsies when feasible, because EoE is a common underlying cause.
  4. 4Provide soft-diet safety advice, urgent return criteria and gastroenterology follow-up for histology and anti-inflammatory treatment.
02InductionChoose an anti-inflammatory strategySymptomatic EoE is confirmed by adequate clinical and histological assessment.+

Complications

01

Food impaction

Fibrosis and reduced calibre trap solid food, potentially preventing saliva swallowing and requiring urgent therapeutic endoscopy.

02

Stricture and narrow-calibre oesophagus

Chronic remodelling causes persistent dysphagia, adaptive restrictive eating and the need for careful dilation alongside anti-inflammatory treatment.

03

Perforation and nutritional restriction

Impaction, instrumentation or severe retching can tear the oesophagus, while unsupervised elimination diets may cause deficiency or impaired quality of life.

Monitoring and follow-up

  • Track dysphagia, impactions and adaptive eating using explicit questions about food avoidance, meal duration, chewing and fluid chasing.
  • Repeat endoscopy with multi-level biopsies after induction and when changing a major treatment strategy; do not rely on symptomatic improvement alone.
  • Monitor weight, nutrition and food-related anxiety during elimination, with dietitian review before further restriction or reintroduction.
  • During swallowed corticosteroid treatment ask about thrush and follow adrenal or systemic monitoring when dose, duration, interactions or concurrent steroids increase risk.
  • After dilation, give written advice for expected transient discomfort and urgent review for severe pain, fever, breathlessness or haematemesis.
  • Agree a maintenance plan because untreated recurrence can resume inflammation and fibrosis even after successful induction.

Special situations

Ask how, not just whether

Compensatory behaviours can hide dysphagia. A patient who avoids steak and takes forty minutes to eat may have substantial disease while answering 'no' to swallowing difficulty.

Normal endoscopy needs biopsies

A visually unremarkable oesophagus does not exclude EoE; inadequate sampling is a common reason for delayed diagnosis.

Symptoms and histology separate

Dilation or food avoidance can improve swallowing while active eosinophilic inflammation continues, so mucosal reassessment matters.

Allergy tests do not make the menu

Skin-prick and specific-IgE tests identify immediate allergy but predict EoE trigger foods poorly; elimination should be dietetic and response-based.

Dilation is not failure

Fibrotic narrowing may need mechanical treatment even when inflammation is controlled. The error is dilation without ongoing disease modification.

Common pitfalls

  1. 01

    Discharging a food-impaction patient after removal without oesophageal biopsies or a plan to investigate EoE.

  2. 02

    Excluding EoE because the oesophagus appears normal or the patient has no known atopy.

  3. 03

    Taking one distal biopsy and missing patchy proximal disease.

  4. 04

    Using symptom response alone to claim histological remission and stop maintenance planning.

  5. 05

    Starting a broad multi-food elimination diet without specialist dietetic support and nutritional monitoring.

  6. 06

    Dilating a stricture but leaving eosinophilic inflammation untreated.

  • Dilation treats fixed narrowing but not mucosal inflammation, so combine it with anti-inflammatory management and warn about post-procedural chest pain and perforation symptoms.
    • Nutritional and dietetic assessment
    Why
    Make elimination therapy safe and sustainable.
    Interpretation and limitations
    Review weight, growth where relevant, micronutrient risk, eating disorder features and existing IgE-mediated allergy. Allergy testing alone does not select EoE trigger foods reliably.
  • 06
    Repeat endoscopy and biopsy after treatment
    Why
    Measure histological remission rather than symptoms alone.
    Interpretation and limitations
    People may compensate behaviourally despite ongoing inflammation. Timing follows the chosen induction regimen and local pathway, commonly after an adequate initial treatment interval.
    • 1
    Discuss PPI, swallowed topical corticosteroid and dietetic-led elimination using age, severity, stricture, preference, adherence and local access.
  • 2Teach the exact preparation technique: swallowed topical treatment must contact the oesophagus and food or drink restrictions after dosing follow its SmPC.
  • 3If diet is chosen, involve an EoE-experienced dietitian and use staged elimination and reintroduction with endoscopic assessment rather than indefinite unsupervised avoidance.
  • 4Repeat symptoms, endoscopy and biopsies after adequate induction because symptom relief alone does not establish mucosal remission.
    • 03FibrostenosisTreat narrowing and inflammation togetherA focal stricture, narrow-calibre oesophagus or recurrent impaction persists.+
    1. 1Define location, length and calibre through expert endoscopy or barium assessment and exclude cancer before planned dilation.
    2. 2Use graded wire-guided or endoscopically controlled dilation through an experienced service, explaining common transient chest pain and the small perforation risk.
    3. 3Continue or commence anti-inflammatory therapy because dilation does not treat the disease process driving remodelling.
    4. 4Monitor swallowing and histology, arranging repeat dilation only from objective recurrent narrowing and shared benefit-risk review.
    Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
    Topical corticosteroid that induces clinical and histological remission in adult eosinophilic oesophagitis under NICE TA708.

    Budesonide orodispersible tablet

    For adult induction, the licensed dose is 1 mg allowed to dissolve on the tongue twice daily, morning and evening, for six weeks; inadequate responders may continue to twelve weeks under specialist direction.

    Do not eat, drink or perform oral hygiene for at least thirty minutes after dosing under the SmPC. Oropharyngeal or oesophageal Candida can occur; review adrenal, interaction, hepatic and systemic steroid risks, and distinguish induction commissioning from maintenance access.

    Can reduce eosinophilic inflammation in a subset and simultaneously treats coexisting acid reflux.

    Proton pump inhibitor

    A gastroenterologist selects a full-dose licensed PPI regimen, often once or twice daily during induction according to local EoE practice, reflux burden and the current BNF; reassess rather than continuing blindly.

    Response does not mean the original diagnosis was merely GORD. Review adherence, interactions and long-term need; biopsy is usually required to demonstrate mucosal response because symptoms alone are unreliable.