Synopsis
Differentiate major causes of oesophagitis from history, endoscopy and tissue, and act urgently on caustic injury, perforation, bleeding and severe infection.
- 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.
Key red flags
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.
Investigation priorities
Identify a plausible tablet cause and prevent recurrence.
Management branches
Pain on swallowing or acute retrosternal pain suggests mucosal ulceration.
- Assess fluid intake, bleeding, sepsis and airway or perforation signs, admitting patients who cannot maintain hydration or are systemically unwell.
- Build medicine, immune, infection, reflux and radiation timelines; stop a likely injurious tablet when safe and contact its prescriber for an alternative.
- Arrange endoscopy and targeted biopsy when infection, severe ulceration, malignancy or persistent symptoms are possible, with prompt microbiology or histology requests.
- Treat the established cause and review response; lack of improvement should trigger reconsideration of co-infection, resistant organism, cancer or motility-related stasis.
Key medicines
Omeprazole for acid-mediated injuryA 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 candidiasisBNF 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.