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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.

Oesophagitis: reflux, pill, infective and caustic

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

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Time-critical presentation

Drooling, stridor, respiratory distress, shock, severe chest or abdominal pain, haematemesis, subcutaneous emphysema or peritonism after caustic ingestion requires immediate airway, toxicology and upper-GI surgical assessment. Do not induce vomiting, attempt chemical neutralisation or give anything orally without expert advice. Severe odynophagia with sepsis, neutropenia or inability to swallow fluids also needs urgent admission. Suspected perforation should go directly to CT and the regional oesophago-gastric team; routine diagnostic endoscopy can worsen an uncontrolled perforation.

Overview

Differentiate major causes of oesophagitis from history, endoscopy and tissue, and act urgently on caustic injury, perforation, bleeding and severe infection.

Reflux oesophagitis results from acid and pepsin exposure, classically affecting distal mucosa with breaks graded by the Los Angeles system. Pill injury is usually focal where transit slows, often in the mid oesophagus near external compression, and depends on caustic properties plus contact time. Infective disease reflects host susceptibility: Candida, HSV and CMV dominate, while bacterial causes are unusual. Caustic injury can involve pharynx, oesophagus, stomach and airway and may later produce stricture or malignancy risk.

History should identify tempo, odynophagia versus mechanical dysphagia, immune status, recent antibiotics or steroids, HIV risk, transplant or cancer therapy, every tablet and how it is swallowed, radiotherapy and the exact chemical exposure. Endoscopic appearance guides but does not always diagnose. Biopsy the ulcer edge for viral cytopathic change and appropriate mucosa for Candida, and request microbiology when relevant. A normal-looking mouth does not exclude deep caustic injury or oesophageal infection.

Practice

Two practice questions

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Gastroenterology and hepatologyOriginal SBA

Unsafe response to corrosive ingestion

An adult deliberately swallows a concentrated drain cleaner and develops drooling, chest pain and stridor. Which immediate action is most appropriate?

Choose one answer, then submit
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Sources and review status5 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.

  • NICE CG184 reflux and dyspepsiaAcid-mediated oesophagitis management and alarm-feature investigation.
  • Alendronic acid summary of product characteristicsOfficial swallowing instructions and oesophageal-injury warnings.
  • BNF fluconazole drug monographCurrent UK oesophageal-candidiasis regimen and safety information.
  • UKHSA National Poisons Information Service overviewOfficial access route to TOXBASE and specialist poisons advice.
  • GOV.UK sodium hypochlorite toxicologyCurrent official corrosive-exposure and delayed-sequelae information.

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 follows cause. Acid suppression heals reflux injury; the offending tablet is stopped or reformulated with safer administration; fluconazole treats most oesophageal candidiasis; viral disease requires specialist antiviral decisions and immune-status management. Caustic injury is not treated with a generic PPI-and-discharge approach: consult TOXBASE or NPIS, secure the airway, image for perforation and coordinate the timing of expert endoscopy or surgery. Evidence for routine corticosteroids or prophylactic antibiotics to prevent caustic stricture is insufficient and agent-specific advice takes precedence.

Key points

  • Oesophagitis is a mucosal injury pattern; reflux, tablets, infection, caustic exposure, radiation and immune disease require different treatments.
  • Heartburn and regurgitation favour reflux, while odynophagia is a stronger clue to ulceration, infection, pill injury or severe erosive inflammation.
  • Pill oesophagitis follows prolonged mucosal contact, commonly after a tablet is swallowed with little water or immediately before lying down.
  • Bisphosphonates, tetracyclines, potassium chloride, iron, NSAIDs and selected antimicrobials are recognised culprits, but a full medicine timeline is essential.
  • Candida often produces white adherent plaques in immunocompromised people; HSV causes discrete ulcers and CMV typically larger linear ulcers, but histology and context confirm.
  • Oropharyngeal thrush supports oesophageal candidiasis but can be absent; odynophagia in advanced immunosuppression deserves prompt assessment.
  • Caustic injury severity is not reliably predicted by oral burns or early symptoms, and damage may evolve after ingestion.
  • Do not induce emesis or neutralise an acid with alkali after a corrosive exposure because re-exposure, heat and aspiration can increase injury.
  • Endoscopy should describe distribution and severity and obtain site-appropriate biopsies; infection, malignancy and eosinophilic disease may coexist or mimic one another.

Aetiology

01

Reflux and tablet contact

Acid reflux and prolonged mucosal contact with bisphosphonates, tetracyclines, iron, potassium or NSAIDs commonly cause chemical oesophageal injury.

02

Infective inflammation

Candida, herpesviruses and other infection occur particularly with immunosuppression, diabetes, antibiotics or impaired oesophageal clearance or mucosal injury.

03

Caustic and immune injury

Alkali or acid ingestion causes immediate tissue necrosis, while eosinophilic and other immune disorders create chronic inflammatory oesophagitis.

Pathophysiology

  1. 1
    Barrier disruption

    Acid, direct chemical contact, pathogens or immune mediators injure stratified squamous epithelium and expose sensory nerve endings.

  2. 2
    Ulcerative inflammation

    Oedema, erosions and ulcers cause heartburn, odynophagia, dysphagia and sometimes bleeding or impaired oral intake as inflammation deepens.

  3. 3
    Deep injury and remodelling

    Severe caustic or infective damage can perforate, while repeated healing deposits fibrosis and creates a stricture.

Clinical features and red flags

Reflux oesophagitis

Heartburn, regurgitation and distal mucosal breaks occur without a discrete tablet relationship; severe grades may bleed, scar or conceal Barrett mucosa beneath inflammation.

Pill oesophagitis

Sudden odynophagia and retrosternal pain begins after a high-risk tablet taken with little fluid or at bedtime, often with a focal mid-oesophageal ulcer.

Candida oesophagitis

Progressive odynophagia or dysphagia in immunosuppression accompanies adherent white plaques, with or without oral candidiasis; systemic illness suggests invasive or alternative infection.

Viral ulcerative oesophagitisRed flag

Severe odynophagia, chest pain and discrete or linear ulcers occur in profound cellular immunosuppression; HSV and CMV require correctly targeted biopsy and distinct antivirals.

Caustic aerodigestive injuryRed flag

Drooling, oral pain, dysphagia, stridor, chest or abdominal pain, vomiting and haematemesis follow corrosive exposure, but severe internal injury can occur without dramatic oral burns.

Perforation or mediastinitisRed flag

Abrupt severe pain, tachycardia, fever, shock, subcutaneous emphysema, pleural fluid or pneumomediastinum demands emergency CT and specialist surgical treatment.

Investigations

  1. 01
    Detailed medicine and swallowing historyFirst step
    Why
    Identify a plausible tablet cause and prevent recurrence.
    Interpretation and limitations
    Record formulation, start date, water volume, posture and dysphagia preceding the prescription. Delayed transit from achalasia or stricture increases contact injury and needs investigation.
  2. 02
    Upper gastrointestinal endoscopy
    Why
    Assess mucosal severity, obstruction and competing disease.
    Interpretation and limitations
    Distal erosions favour reflux; focal mid-oesophageal ulcer suggests pill injury; plaques or patterned ulcers suggest infection. In caustic injury, timing and safety are decided with toxicology and upper-GI specialists.
  3. 03
    Oesophageal biopsies
    Why
    Confirm infection, immune disease, malignancy or another histological cause.
    Interpretation and limitations
    Sample the appropriate part of viral ulcers and plaque-bearing mucosa, clearly stating suspected organisms and immune status. Superficial exudate alone may be nondiagnostic.
  4. 04
    Full blood count, renal, liver and inflammatory tests
    Why
    Define immune compromise, sepsis, bleeding and medicine safety.
    Interpretation and limitations
    Neutropenia or anaemia increases urgency; renal dysfunction alters fluconazole and antiviral regimens. Normal markers do not

Differential diagnosis

01

Acute coronary syndrome

Retrosternal pain with exertional or autonomic features requires cardiac assessment, even when reflux or swallowing symptoms are also present.

02

Eosinophilic oesophagitis or cancer

Food impaction, multiple rings or eosinophil-rich biopsies support EoE, while rapid progression, weight loss or irregular narrowing raises malignancy concern.

03

Achalasia or other motility disorder

Mixed-consistency dysphagia, retained saliva and diagnostic manometry indicate propulsion or junction failure rather than mucosal inflammation alone.

Management

01OdynophagiaClassify ulcerative oesophagitisFirst stepPain on swallowing or acute retrosternal pain suggests mucosal ulceration.+
  1. 1Assess fluid intake, bleeding, sepsis and airway or perforation signs, admitting patients who cannot maintain hydration or are systemically unwell.
  2. 2AlternativeBuild medicine, immune, infection, reflux and radiation timelines; stop a likely injurious tablet when safe and contact its prescriber for an alternative.
  3. 3Arrange endoscopy and targeted biopsy when infection, severe ulceration, malignancy or persistent symptoms are possible, with prompt microbiology or histology requests.
  4. 4Treat the established cause and review response; lack of improvement should trigger reconsideration of co-infection, resistant organism, cancer or motility-related stasis.
02Caustic ingestionProtect the airway and avoid harmful first aid

Complications

01

Bleeding and nutritional compromise

Ulcerated mucosa can bleed and painful swallowing may prevent adequate fluid and calorie intake, causing anaemia, dehydration and weight loss.

02

Peptic or caustic stricture

Fibrotic healing narrows the lumen and produces progressive solid-food dysphagia, sometimes requiring repeated specialist dilation to restore swallowing.

03

Perforation and mediastinitis

Deep caustic necrosis, severe infection or instrumentation can disrupt the full wall, causing pleuromediastinal contamination, sepsis and shock.

Monitoring and follow-up

  • Reassess odynophagia, ability to drink, bleeding and systemic signs early; worsening pain or sepsis should trigger perforation imaging and admission.
  • After reflux or pill injury, ensure symptoms resolve and investigate persistent dysphagia for stricture, EoE, malignancy or a motor disorder.
  • During fluconazole or antiviral therapy, monitor renal, liver, blood-count and interaction risks at the frequency appropriate to drug and immune status.
  • Following significant caustic injury, specialist follow-up should address nutrition, stricture symptoms, repeat endoscopic or radiological assessment and psychological support.
  • Verify that an offending medicine and safer administration instructions are recorded across primary care, pharmacy and the original prescribing service.

Special situations

Odynophagia changes the differential

Pain during transit points toward active mucosal ulceration or infection more strongly than uncomplicated motor dysphagia, although overlap occurs.

Location offers a clue

Pill ulcers often occur where the oesophagus is externally narrowed, while reflux injury predominates distally; neither distribution is independently diagnostic.

The mouth can look normal

Absence of thrush does not exclude Candida oesophagitis, and absence of oral burns does not exclude important corrosive injury below.

Biopsy site matters

HSV cytopathic change is usually sought at ulcer edges, while CMV-infected stromal cells are often found at the ulcer base; communicate the differential to pathology.

Do not neutralise corrosives

Attempted acid–alkali neutralisation can release heat and provoke vomiting, repeating mucosal exposure and aspiration. Specialist poisons advice is safer.

Common pitfalls

  1. 01

    Calling severe odynophagia reflux without reviewing immune status, tablets and infectious causes.

  2. 02

    Continuing alendronate after dysphagia or retrosternal pain despite product advice to stop and seek review.

  3. 03

    Diagnosing CMV or HSV solely from ulcer shape and prescribing toxic antivirals without appropriate tissue evidence.

  4. 04

    Inducing vomiting or attempting chemical neutralisation after caustic ingestion.

  5. 05

    Using normal oral examination findings to reassure against serious oesophageal corrosive injury.

  6. 06

    Performing routine endoscopy before CT and surgical discussion when perforation is suspected.

  • A patient who develops dysphagia, odynophagia, retrosternal pain or new heartburn while taking alendronate should stop it and seek medical review under the SmPC advice.
    • exclude local ulceration or perforation.
  • 05
    HIV and cause-directed immune assessment
    Why
    Identify an underlying acquired or treatment-related immunodeficiency.
    Interpretation and limitations
    Offer HIV testing with consent in an appropriate presentation and review transplant, chemotherapy and steroid exposure. Treating infection without addressing immune cause invites recurrence.
  • 06
    CT neck, chest and abdomen with contrast
    Why
    Detect perforation, necrosis, mediastinal contamination or associated injury.
    Interpretation and limitations
    Extraluminal gas, collections, pleural contamination and wall non-enhancement guide urgent intervention. A normal radiograph cannot safely exclude early perforation.
  • 07
    TOXBASE or National Poisons Information Service advice
    Why
    Obtain agent-specific caustic risk and management guidance.
    Interpretation and limitations
    Provide exact product, concentration, amount, time, symptoms and co-exposures. Household and industrial formulations differ, so generic bleach assumptions can be unsafe.
    • A corrosive chemical has been swallowed or strongly suspected.
    +
    1. 1Use an ABCDE approach, remove contaminated clothing safely, keep the patient nil by mouth and involve anaesthesia early for drooling, voice change, stridor or respiratory distress.
    2. 2Do not induce vomiting, neutralise the chemical or blindly insert tubes; contact TOXBASE or NPIS with exact product and exposure details.
    3. 3Obtain urgent CT and upper-GI surgical or gastroenterology review to select safe endoscopy and intervention timing, while treating shock, pain and aspiration.
    4. 4Plan nutritional support and later stricture follow-up for significant injury, with safeguarding or mental-health assessment when exposure was deliberate.
    03Medication preventionStop recurrent pill injuryTablet-associated oesophagitis is likely or confirmed.+
    1. 1Discontinue or substitute the culprit with the responsible prescriber, balancing bone, infection or cardiovascular treatment needs against mucosal injury.
    2. 2Advise swallowing tablets with sufficient water while upright and avoiding administration immediately before bed, using the exact product instructions.
    3. 3Investigate pre-existing dysphagia, stricture or achalasia if the tablet lodged despite correct technique or if symptoms fail to resolve.
    4. 4Use a time-limited acid-suppression or mucosal-healing plan when clinically indicated, and document the reaction to prevent inadvertent re-exposure.
    Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
    Heals reflux erosions and may support healing after selected pill injury once the offending medicine is addressed.

    Omeprazole for acid-mediated injury

    A common licensed adult regimen for reflux oesophagitis is 20 mg orally once daily for four weeks, extending to eight weeks or using 40 mg daily for severe disease under product guidance.

    Acid suppression does not treat Candida, viral infection or transmural caustic necrosis. Investigate alarm symptoms, review interactions and reduce to the lowest effective maintenance dose after healing.

    Systemic antifungal treatment for established or strongly suspected oesophageal Candida infection.

    Fluconazole for oesophageal candidiasis

    BNF adult treatment is 200–400 mg orally or intravenously on day one, then 100–200 mg once daily for 7–21 days, with longer treatment in selected severely immunocompromised patients.

    Adjust for renal function and review QT prolongation, liver injury, pregnancy and major CYP interactions, including anticoagulants. Failure should prompt endoscopy, susceptibility or alternative-organism assessment rather than blind prolongation.

    Targets biopsy-supported viral oesophagitis in immunocompromised patients; the organism determines therapy.

    Antiviral treatment for HSV or CMV

    Use intravenous or oral aciclovir for HSV and ganciclovir or valganciclovir for CMV only through the infection or transplant-specific specialist regimen, adjusted for renal function and immune status.

    Aciclovir can crystallise in kidneys and needs hydration and renal adjustment; ganciclovir can cause profound marrow suppression and is teratogenic. Do not treat by endoscopic appearance alone when tissue can safely clarify the virus.