Oesophagitis including eosinophilic and infective causes

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Symptom quality helps but overlaps. Heartburn and regurgitation suggest reflux; dysphagia and impaction with atopy suggest eosinophilic disease; acute retrosternal odynophagia after alendronate, doxycycline or potassium suggests pill contact; painful swallowing with thrush or profound immune suppression suggests Candida, HSV or CMV. A patient may have more than one mechanism, and empiric PPI response does not erase an alarm feature.

Endoscopy in reflux shows distal breaks; eosinophilic findings include rings, furrows, exudates and oedema but may be subtle; Candida produces plaques; viral disease causes ulceration requiring histology or specific testing. Suspected eosinophilic oesophagitis requires at least six oesophageal biopsies from at least two sites because disease is patchy. In a symptomatic patient, a peak count of at least 15 eosinophils per 0.3 mm² supports the diagnosis after other causes of oesophageal eosinophilia have been considered.

Treatment links diagnosis to a measured endpoint. PPIs can induce clinical and histological remission in eosinophilic oesophagitis. Budesonide orodispersible tablets are taken after a meal, allowed to dissolve on the tongue and swallowed gradually with saliva; they must not be chewed or swallowed whole, and food, drink and oral hygiene are avoided for thirty minutes afterward. Systemic fluconazole treats oesophageal candidiasis with renal, liver, QT and interaction review. Viral therapy is specialist-led because aciclovir and ganciclovir have substantial renal or marrow toxicity.

Key points

Reflux oesophagitis causes distal erosive injury from acid exposure; eosinophilic disease is patchy immune inflammation associated with dysphagia and food impaction.
Pill injury occurs where caustic tablets lodge, especially with little water or lying down, while Candida and viral ulceration occur mainly with impaired immunity.
Endoscopy describes distribution and obtains adequate biopsies; visual appearance cannot reliably distinguish every cause.
Treat acid disease with a defined PPI course, eosinophilic disease with diet, PPI or topical steroid, and infection with organism-specific systemic therapy.
For adult eosinophilic oesophagitis, budesonide orodispersible tablets are 1 mg morning and evening for six weeks, extendable to twelve weeks if response is inadequate under the SmPC.
Mechanical dilation treats a fixed narrowing but does not suppress underlying eosinophilic or acid inflammation.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Acid exposure

Repeated gastric reflux injures distal squamous mucosa when junction competence, oesophageal clearance and salivary neutralisation cannot limit the duration of acid exposure.

Immune or infectious injury

Food-antigen driven type-2 inflammation causes eosinophilic disease, while fungal or viral invasion occurs mainly in impaired host defence.

Direct pill contact

Caustic medicines lodged by poor water intake, recumbency or narrowing dissolve against mucosa and create focal ulcers.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier disruption
Chemical or immune injury separates epithelial cells, increases sensitivity and permits erosions, bleeding or painful swallowing.
2
Eosinophilic remodelling
Chronic cytokine-driven eosinophilic inflammation causes mucosal oedema, fixed rings, subepithelial fibrosis and a narrow-calibre oesophagus prone to recurrent solid-bolus impaction.
3
Opportunistic invasion
Candida forms mucosal plaques, whereas HSV and CMV produce ulceration that can extend deeply in severe immune suppression.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Acid-predominant pattern

Distal burning, regurgitation and erosions favour reflux, but dysphagia still needs structural assessment.

Eosinophilic pattern

Atopy, long meals, avoidance of dense solids, rings and repeated food impaction suggest chronic eosinophilic inflammation.

Pill-contact injury

Sudden odynophagia after taking a known irritant with little water or before bed suggests focal medication ulceration.

Candida risk

Thrush and odynophagia after immunosuppression, antibiotics or corticosteroids raise oesophageal candidiasis.

Viral ulcer concernRed flag

Severe odynophagia with deep ulcers in transplant or advanced immune suppression needs biopsy-supported HSV or CMV treatment.

Red flags requiring action

Recurrent food impaction or a narrow-calibre oesophagus suggests eosinophilic remodelling even when reflux symptoms coexist.
Odynophagia in an immunocompromised person raises Candida, HSV or CMV infection and requires organism-directed assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Upper-GI endoscopyFirst step
Why
Define distribution, severity, obstruction and complications.
Interpretation and limitations
Target visible lesions and obtain tissue; normal-looking mucosa does not exclude eosinophilic inflammation, and viral appearances require histological confirmation.
02
Eosinophilic oesophagitis biopsy set
Why
Detect patchy mucosal eosinophilia and establish whether the diagnostic threshold is met.
Interpretation and limitations
Take at least six biopsies from at least two oesophageal sites, including abnormal areas. In the appropriate symptomatic and exclusion context, a peak count of at least 15 eosinophils per 0.3 mm² supports EoE. Document PPI exposure and never delay emergency bolus removal for a washout; if high suspicion persists after non-diagnostic biopsies taken on PPI, plan repeat biopsies after at least three weeks off PPI when clinically safe.
03
Fungal or viral tissue testing
Why
Identify the organism causing opportunistic oesophagitis.
Interpretation and limitations
Brushings, biopsy and viral testing distinguish Candida, HSV and CMV, preventing toxic empirical treatment aimed at the wrong pathogen.
04
Immune-status assessment
Why
Find the host factor that changes infection probability and outcome.
Interpretation and limitations
Review HIV testing where appropriate, neutrophils, transplant or cancer therapy, diabetes and corticosteroid exposure while preserving confidentiality.
05
Response endoscopy and biopsy
Why
Measure mucosal healing after an adequate anti-inflammatory course.
Interpretation and limitations
Assess symptoms and repeat biopsies while the patient remains on the selected treatment, usually 8–12 weeks after starting it. Clinical remission is not a substitute for histology; a peak count below 15 eosinophils per 0.3 mm² is the practical remission threshold.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Oesophageal cancer

Progressive dysphagia, weight loss or an irregular ulcer requires targeted biopsy regardless of a plausible inflammatory trigger.

Achalasia

Retention and regurgitation from motor failure may cause secondary inflammation but require manometric confirmation after structural exclusion.

Cardiac pain

Retrosternal pain with exertion or autonomic symptoms demands cardiac assessment rather than attribution to visible mild oesophagitis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Worked case: eosinophilic diseaseTreat inflammation and calibre, then prove responseFirst stepA 28-year-old with asthma has a second meat impaction; emergency endoscopy shows rings, furrows and a fixed 12 mm narrowing.

1Remove the bolus without delaying emergency care and take six biopsies from proximal and distal oesophagus at the index procedure, documenting that the patient was taking a PPI when sampled.
2AlternativeHistology shows a peak 48 eosinophils per 0.3 mm² and no alternative mucosal cause. Because the result is diagnostic despite PPI exposure, begin shared treatment planning rather than requiring a washout merely to reconfirm a positive result.
3After consent, cautiously dilate the fixed narrowing and start budesonide orodispersible 1 mg morning and evening after meals for six weeks, with administration teaching and candidiasis review; mechanical treatment does not replace anti-inflammatory therapy.
4At six weeks swallowing has improved but intermittent dysphagia remains, so the specialist extends induction to twelve weeks within the product regimen and keeps the response endoscopy on treatment.
5At week twelve there has been no further impaction and repeat biopsies while taking budesonide show a peak 6 eosinophils per 0.3 mm². Record clinical and histological remission and agree maintenance and recurrence follow-up.

02Worked case: candidiasisUse systemic antifungal treatmentAn adult receiving chemotherapy has thrush and marked odynophagia with oesophageal plaques.

1Assess hydration, immune severity, interactions and whether endoscopic sampling is needed.
2Give systemic fluconazole using the current product and local infection regimen with renal adjustment.
3Investigate non-response for resistant Candida, HSV, CMV or another ulcerative cause.
4Confirm symptom resolution, oral intake and correction of the predisposing factor where possible.

03Worked case: pill injuryRemove the exposure mechanismOdynophagia begins after alendronate was swallowed at bedtime with little water.

1Stop the offending preparation and assess for bleeding, obstruction or perforation.
2Treat mucosal injury and modify osteoporosis therapy through the responsible prescriber.
3Teach upright administration with a full glass of water only if the medicine is later judged safe and appropriate.
4Verify healing and investigate persistent dysphagia for a stricture or another diagnosis.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Provides topical corticosteroid exposure that induces clinical and histological remission in adult eosinophilic oesophagitis.

Budesonide orodispersible tablet

For adult eosinophilic oesophagitis, take one 1 mg orodispersible tablet in the morning and one in the evening for six weeks; induction may be extended to twelve weeks if response is inadequate. Take after a meal, place on the tongue and let it disintegrate, then swallow the budesonide-rich saliva gradually. Do not chew or swallow the tablet whole, and do not eat, drink or perform oral hygiene for at least thirty minutes afterward.

Specialist initiation is required. The product should not be used in hepatic impairment and is not recommended in severe renal impairment. Avoid potent CYP3A4 inhibitors such as ketoconazole or ritonavir unless a specialist judges the combination necessary and can monitor increased systemic exposure. Check oral or oesophageal candidiasis and cumulative systemic corticosteroid effects, including adrenal suppression; maintenance and withdrawal decisions require specialist review.

Systemic antifungal therapy reaches oesophageal mucosa; topical mouth treatment alone is inadequate for established oesophageal candidiasis.

Fluconazole for oesophageal candidiasis

For adult oesophageal candidiasis, give fluconazole 400 mg orally or intravenously on day 1, then 200 mg once daily for 14–30 days. After the loading dose, use 50% of the maintenance dose when creatinine clearance is 50 mL/min or less in a patient not receiving dialysis. For the cited 2 mg/mL intravenous formulation, infuse at no more than 10 mL/min and account for its sodium and fluid load; change to oral treatment when swallowing and absorption permit.

Review interacting medicines, pregnancy, liver tests, renal function and QT risk; correct hypokalaemia, hypomagnesaemia and hypocalcaemia before treatment. The infusion contains 0.15 mmol sodium per mL. Lack of improvement should prompt culture or biopsy and assessment for resistant Candida or viral ulceration rather than automatic dose escalation.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Food impaction

Rings and fibrosis can trap a solid bolus completely, prevent saliva passage, threaten aspiration and require airway-aware urgent endoscopic removal.

Stricture

Repeated inflammatory injury heals with collagen deposition and contraction, producing progressive luminal narrowing, reduced distensibility and recurrent solid-food dysphagia.

Bleeding or perforation

Deep mucosal ulceration, prolonged impaction and endoscopic instrumentation can cause substantial haemorrhage or transmural breach with mediastinal and pleural sepsis.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track food impactions, adapted eating, weight and dysphagia separately from heartburn.
Repeat eosinophilic histology at the specialist-defined point because symptoms alone under-report inflammation.
During budesonide treatment, ask about oral or oesophageal Candida and systemic steroid effects.
For infection, monitor renal, liver, marrow or ECG parameters according to the selected antimicrobial.
After pill injury, document an alternative medicine plan and verify that administration technique is understood.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Appearance can be normal

Eosinophilic oesophagitis is histological, so a visually unremarkable oesophagus does not justify omitting biopsies.

Thrush is a clue, not a rule

Oesophageal Candida can occur without oral plaques, and thrush does not exclude simultaneous viral ulcers.

Dilation does not treat immunity

Mechanical widening relieves a stricture but persistent eosinophilic inflammation drives recurrence.

Instructions are pharmacology

Remaining upright with water for alendronate limits mucosal contact and is part of safe prescribing, not optional lifestyle advice.

11Common pitfallsFrequent interpretation and management errors.

01
Labelling recurrent food impaction as careless eating without eosinophilic biopsies.
02
Using topical oral nystatin alone for proven oesophageal candidiasis.
03
Treating deep viral ulcers by appearance without tissue when safe diagnosis is possible.
04
Describing EoE dilation as intrinsically more likely to perforate: chest pain and mucosal tears are common, but expert dilation has a perforation risk comparable with dilation for other benign oesophageal disease and must accompany anti-inflammatory treatment.

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