01OverviewDefinition, clinical context and the essential points that orientate the chapter.
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.
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.
- 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.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Reflux and tablet contact
Acid reflux and prolonged mucosal contact with bisphosphonates, tetracyclines, iron, potassium or NSAIDs commonly cause chemical oesophageal injury.
Infective inflammation
Candida, herpesviruses and other infection occur particularly with immunosuppression, diabetes, antibiotics or impaired oesophageal clearance or mucosal injury.
Caustic and immune injury
Alkali or acid ingestion causes immediate tissue necrosis, while eosinophilic and other immune disorders create chronic inflammatory oesophagitis.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Barrier disruption
Acid, direct chemical contact, pathogens or immune mediators injure stratified squamous epithelium and expose sensory nerve endings.
- 2Ulcerative inflammation
Oedema, erosions and ulcers cause heartburn, odynophagia, dysphagia and sometimes bleeding or impaired oral intake as inflammation deepens.
- 3Deep injury and remodelling
Severe caustic or infective damage can perforate, while repeated healing deposits fibrosis and creates a stricture.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Heartburn, regurgitation and distal mucosal breaks occur without a discrete tablet relationship; severe grades may bleed, scar or conceal Barrett mucosa beneath inflammation.
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.
Progressive odynophagia or dysphagia in immunosuppression accompanies adherent white plaques, with or without oral candidiasis; systemic illness suggests invasive or alternative infection.
Severe odynophagia, chest pain and discrete or linear ulcers occur in profound cellular immunosuppression; HSV and CMV require correctly targeted biopsy and distinct antivirals.
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.
Abrupt severe pain, tachycardia, fever, shock, subcutaneous emphysema, pleural fluid or pneumomediastinum demands emergency CT and specialist surgical treatment.
05InvestigationsWhat to request, why it matters and how to interpret it.
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
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.
- 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.
- 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.
- 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 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.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute coronary syndrome
Retrosternal pain with exertional or autonomic features requires cardiac assessment, even when reflux or swallowing symptoms are also present.
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.
Achalasia or other motility disorder
Mixed-consistency dysphagia, retained saliva and diagnostic manometry indicate propulsion or junction failure rather than mucosal inflammation alone.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01OdynophagiaClassify ulcerative oesophagitisFirst stepPain on swallowing or acute retrosternal pain suggests mucosal ulceration.+
- 1Assess fluid intake, bleeding, sepsis and airway or perforation signs, admitting patients who cannot maintain hydration or are systemically unwell.
- 2AlternativeBuild medicine, immune, infection, reflux and radiation timelines; stop a likely injurious tablet when safe and contact its prescriber for an alternative.
- 3Arrange endoscopy and targeted biopsy when infection, severe ulceration, malignancy or persistent symptoms are possible, with prompt microbiology or histology requests.
- 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 aidA corrosive chemical has been swallowed or strongly suspected.+
- 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.
- 2Do not induce vomiting, neutralise the chemical or blindly insert tubes; contact TOXBASE or NPIS with exact product and exposure details.
- 3Obtain urgent CT and upper-GI surgical or gastroenterology review to select safe endoscopy and intervention timing, while treating shock, pain and aspiration.
- 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.+
- 1Discontinue or substitute the culprit with the responsible prescriber, balancing bone, infection or cardiovascular treatment needs against mucosal injury.
- 2Advise swallowing tablets with sufficient water while upright and avoiding administration immediately before bed, using the exact product instructions.
- 3Investigate pre-existing dysphagia, stricture or achalasia if the tablet lodged despite correct technique or if symptoms fail to resolve.
- 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+
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.
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.
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.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Bleeding and nutritional compromise
Ulcerated mucosa can bleed and painful swallowing may prevent adequate fluid and calorie intake, causing anaemia, dehydration and weight loss.
Peptic or caustic stricture
Fibrotic healing narrows the lumen and produces progressive solid-food dysphagia, sometimes requiring repeated specialist dilation to restore swallowing.
Perforation and mediastinitis
Deep caustic necrosis, severe infection or instrumentation can disrupt the full wall, causing pleuromediastinal contamination, sepsis and shock.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- 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.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
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.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling severe odynophagia reflux without reviewing immune status, tablets and infectious causes.
- 02
Continuing alendronate after dysphagia or retrosternal pain despite product advice to stop and seek review.
- 03
Diagnosing CMV or HSV solely from ulcer shape and prescribing toxic antivirals without appropriate tissue evidence.
- 04
Inducing vomiting or attempting chemical neutralisation after caustic ingestion.
- 05
Using normal oral examination findings to reassure against serious oesophageal corrosive injury.
- 06
Performing routine endoscopy before CT and surgical discussion when perforation is suspected.