Acute Oesophagitis

1. Clinical Overview

Summary

Acute oesophagitis represents sudden-onset inflammation of the oesophageal mucosa, most commonly secondary to gastro-oesophageal acid reflux, but with important alternative aetiologies including infectious, medication-induced (pill oesophagitis), caustic injury, and eosinophilic causes. The condition affects approximately 5-20% of adults in Western populations, with gastro-oesophageal reflux disease (GERD) being the predominant cause in immunocompetent individuals. [1,2]

The pathophysiology varies by aetiology: reflux oesophagitis results from lower oesophageal sphincter dysfunction allowing retrograde acid exposure; infectious oesophagitis occurs predominantly in immunocompromised hosts (Candida albicans, herpes simplex virus, cytomegalovirus); pill oesophagitis develops when medications (particularly doxycycline, bisphosphonates, NSAIDs, potassium chloride) cause direct mucosal injury; and eosinophilic oesophagitis represents a chronic immune-mediated condition increasingly recognised as a distinct entity. [3,4]

Clinical presentation typically includes heartburn, regurgitation, dysphagia, odynophagia, and chest pain. Severity ranges from mild mucosal erythema to severe ulceration, stricture formation, and Barrett's metaplasia. Endoscopic grading systems (Los Angeles classification for GERD, Zargar classification for caustic injury) provide standardised assessment and prognostic information. [5,6]

Management is cause-specific: proton pump inhibitors (PPIs) form the cornerstone of reflux oesophagitis treatment, with superior efficacy compared to H2-receptor antagonists; infectious causes require targeted antimicrobial therapy; pill oesophagitis necessitates medication discontinuation and supportive care; caustic injuries may require surgical intervention in severe cases. [7,8]

Prognosis is generally excellent with appropriate treatment, though chronic GERD-related oesophagitis carries risks of stricture (10-15%), Barrett's oesophagus (8-20%), and progression to adenocarcinoma (0.12-0.5% annually in Barrett's patients). Early recognition and evidence-based management are crucial to prevent complications and improve outcomes. [9,10]

Key Facts

Clinical Pearls

"The Four Cardinal Causes" — GERD (70-80%), medications (10-15%), infections (5-10% in immunocompromised), and caustic ingestion (rare). Always identify the underlying cause to guide specific therapy.

"Pill without water = oesophagitis" — Doxycycline, alendronate, NSAIDs, and potassium chloride are classic culprits. Always advise: take with ≥200mL water, remain upright ≥30 minutes, avoid bedtime dosing.

"White plaques = Candida until proven otherwise" — In immunocompromised patients presenting with odynophagia and oral thrush, empirical fluconazole is reasonable while awaiting endoscopy/culture confirmation. [11]

"PPI trial is diagnostic and therapeutic" — 4-8 week PPI trial with ≥85% symptom improvement strongly suggests GERD-related oesophagitis. Lack of response mandates endoscopy to exclude alternative diagnoses. [12]

"GERD ≠ Eosinophilic oesophagitis" — Key differentiators: EoE presents with dysphagia/food impaction > heartburn, ring/furrow endoscopy, ≥15 eosinophils/HPF on biopsy, minimal PPI response, younger males. GERD shows typical reflux symptoms, LA classification findings, excellent PPI response. [13]

"Zargar Grade ≥IIb predicts strictures" — In caustic ingestion, endoscopic Zargar classification guides prognosis: Grade I (normal) = no stricture; Grade IIa (erythema/friability) = 17% stricture risk; Grade IIb-III (ulceration/necrosis) = 50-83% stricture formation. Early CT may outperform endoscopy. [6]

Why This Matters Clinically

Acute oesophagitis represents a spectrum from benign self-limiting inflammation to potentially life-threatening complications requiring urgent intervention. GERD-related oesophagitis affects up to 20% of Western adults and constitutes the most common reason for gastroenterology referral, with direct healthcare costs exceeding $10 billion annually in the United States alone. [1]

The condition matters clinically because:

1. Diagnostic challenge: Substantial symptom overlap exists between GERD, eosinophilic oesophagitis, functional dyspepsia, and cardiac ischaemia. Appropriate investigation prevents misdiagnosis and inappropriate treatment.

2. Malignancy risk: Chronic reflux oesophagitis drives Barrett's metaplasia development in 8-20% of patients, with subsequent adenocarcinoma risk of 0.12-0.5% annually—a cancer whose incidence has increased 600% over five decades. [9,10]

3. Quality of life: Oesophagitis symptoms significantly impair quality of life, sleep, and productivity. Evidence-based PPI therapy provides rapid symptom relief in 70-85% of patients within 4-8 weeks. [7]

4. Preventable complications: Stricture formation (10-15%), bleeding (2-5%), and perforation (rare) are preventable with early recognition and treatment. Pill oesophagitis, entirely preventable through proper medication administration, causes significant morbidity when missed. [4]

5. Immunocompromised populations: Infectious oesophagitis in HIV/AIDS, transplant recipients, and chemotherapy patients requires specific antimicrobial therapy. Empirical treatment without confirmation risks therapeutic failure and drug resistance.

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2. Epidemiology

Incidence & Prevalence

Reflux Oesophagitis:

• Population prevalence: 5-20% (Western countries) [1]
• GERD symptom prevalence: 18-28% (weekly symptoms) [2]
• Among GERD patients undergoing endoscopy: 30-40% have oesophagitis [2]
• Increasing trend: +5% per decade (1995-2015), attributed to obesity epidemic

Infectious Oesophagitis:

• General population: less than 1%
• HIV/AIDS patients (CD4 less than 100): 15-30% [11]
• Solid organ transplant recipients: 5-10%
• Haematologic malignancy/chemotherapy: 10-20%
• Candida: 70-80% of infectious cases
• HSV: 10-15% of infectious cases
• CMV: 5-10% of infectious cases (primarily CD4 less than 50)

Pill Oesophagitis:

• Estimated incidence: 3.9 per 100,000 population annually [4]
• Likely underreported (many cases managed empirically)
• Most common medications: Doxycycline, alendronate, NSAIDs, KCl, ferrous sulphate
• Female predominance (2:1), median age 60-70 years

Caustic Oesophagitis:

• Rare in Western countries (accidental/intentional ingestion)
• Incidence: 1-2 per 100,000 population
• Bimodal age: children (less than 5 years, accidental) and adults (> 40 years, intentional/psychiatric)

Eosinophilic Oesophagitis (Distinct Entity):

• Prevalence: 50-100 per 100,000 (increasing recognition) [13]
• Male:female = 3:1
• Peak age: bimodal (children/young adults 20-40 years)

Demographics

Risk Factors

GERD-Related Oesophagitis:

Modifiable Factors:

• Weight loss (≥10% body weight) reduces GERD symptoms by 40-50% [14]
• Smoking cessation improves LES pressure within 4-6 weeks
• Elevating head of bed (15-20cm) reduces nocturnal reflux episodes by 50-70%
• Avoiding late meals (≥3 hours before lying down) reduces reflux

Infectious Oesophagitis Risk Factors:

• HIV/AIDS (CD4 less than 100 cells/μL): OR 10-20 for Candida/CMV
• Corticosteroids (prednisone ≥20mg/day > 2 weeks): OR 5-10
• Chemotherapy (particularly neutropenia less than 500): OR 8-12
• Solid organ transplant (immunosuppression): OR 6-10
• Broad-spectrum antibiotics (> 2 weeks): OR 3-5 for Candida
• Diabetes mellitus (poor control): OR 2-3 for Candida
• Inhaled corticosteroids (without spacer/rinsing): OR 2-4 for Candida

Pill Oesophagitis Risk Factors:

• Taking medication without water: OR 5-10
• Supine position immediately after medication: OR 4-6
• Pre-existing oesophageal disease (stricture, dysmotility): OR 3-5
• Large capsule/tablet size (> 10mm diameter): OR 2-3
• Bedtime dosing: OR 2-4
• Advanced age (> 65 years): OR 1.5-2 (delayed transit)

High-Risk Medications for Pill Oesophagitis: [4]

1. Doxycycline (most common, 35-40% of cases)
2. Bisphosphonates (alendronate, risedronate): 20-25%
3. NSAIDs (especially slow-release): 15-20%
4. Potassium chloride: 10-15%
5. Iron supplements (ferrous sulphate): 5-10%
6. Others: Quinidine, ascorbic acid, theophylline, tetracycline

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3. Pathophysiology

Molecular Mechanisms by Aetiology

A. Reflux Oesophagitis: The Acid Injury Cascade

Step 1: Lower Oesophageal Sphincter (LES) Dysfunction

• Normal LES pressure: 15-35 mmHg (prevents reflux)
• In GERD: Reduced to less than 10 mmHg or transient LES relaxations (TLESRs)
• Mechanisms: Hiatal hernia, obesity (mechanical), smoking/alcohol (neurohormonal)
• Result: Retrograde flow of gastric contents (pH 1-2) into oesophagus (pH 6-7)

Step 2: Mucosal Barrier Disruption

• Normal oesophagus: Squamous epithelium with tight junctions, mucin layer
• Acid exposure: H+ ions penetrate intercellular spaces → cellular acidification
• Pepsin activation: Degrades proteins, amplifies mucosal injury
• Bile acids (in duodenogastro-oesophageal reflux): Detergent effect on cell membranes
• Result: Epithelial cell damage, inflammation

Step 3: Inflammatory Response

• Damaged epithelial cells release cytokines: IL-1β, IL-6, IL-8, TNF-α
• Recruitment of inflammatory cells: Neutrophils, eosinophils, lymphocytes
• Oxidative stress: Reactive oxygen species (ROS) production
• Prostaglandin/leukotriene release: Amplify inflammation
• Result: Mucosal oedema, erythema, erosions

Step 4: Chronic Exposure and Metaplasia

• Repeated acid injury triggers epithelial cell proliferation
• Activation of CDX2 gene: Drives intestinal metaplasia
• Barrett's oesophagus: Replacement of squamous epithelium with columnar (goblet cells)
• Further progression: Dysplasia → adenocarcinoma (via p53, EGFR pathways)
• Result: Metaplasia-dysplasia-carcinoma sequence [9,10]

Los Angeles Classification (Endoscopic Severity): [5]

• Grade A: ≥1 mucosal breaks ≤5mm, not extending between mucosal folds
• Grade B: ≥1 mucosal breaks > 5mm, not extending between mucosal folds
• Grade C: Mucosal breaks extending between ≥2 mucosal folds, less than 75% circumference
• Grade D: Mucosal breaks extending ≥75% of oesophageal circumference

Prognostic Significance:

• Grade A/B: 70-80% heal with standard-dose PPI (20-40mg daily)
• Grade C/D: May require high-dose PPI (40-80mg daily), longer duration
• Grade C/D: Higher stricture risk (15-20% vs 5% for Grade A/B)

B. Infectious Oesophagitis: Pathogen-Specific Mechanisms

Candida Oesophagitis (Most Common): [11]

• Predisposing factors: CD4 less than 200, antibiotics, corticosteroids, diabetes
• Pathogenesis:
  • Candida albicans colonises oropharynx → spreads to oesophagus
  • "Yeast-to-hyphae transition: Hyphae invade epithelial cells"
  • "Release of proteinases and phospholipases: Tissue degradation"
  • "Host immune response (if intact): Neutrophil recruitment, inflammation"
• Macroscopic: White plaques/pseudomembranes, adherent to mucosa, cannot be washed off
• Microscopic: Yeast and pseudohyphae invading squamous epithelium
• Clinical: Odynophagia > dysphagia, often with oral thrush (50-70%)

Herpes Simplex Virus (HSV) Oesophagitis:

• Predisposing factors: CD4 less than 200, chemotherapy, transplant
• Pathogenesis:
  • HSV-1 (rarely HSV-2) reactivation or primary infection
  • Viral replication in squamous epithelial cells → cytolysis
  • Multinucleated giant cells, intranuclear inclusions (Cowdry type A)
  • Inflammation and ulcer formation
• Macroscopic: Small, discrete, punched-out ulcers (mid-distal oesophagus)
• Microscopic: Multinucleated cells, ground-glass nuclei, eosinophilic inclusions
• Clinical: Severe odynophagia, fever common

Cytomegalovirus (CMV) Oesophagitis:

• Predisposing factors: CD4 less than 50, solid organ transplant, severe immunosuppression
• Pathogenesis:
  • CMV infects endothelial cells and fibroblasts (not epithelium directly)
  • Vascular thrombosis → ischaemic ulceration
  • Viral cytopathic effect: "Owl's eye" inclusions in enlarged cells
• Macroscopic: Large, deep, linear ulcers (distal oesophagus)
• Microscopic: Enlarged cells with intranuclear/cytoplasmic inclusions
• Clinical: Odynophagia, GI bleeding (ulcers deep), systemic CMV common

Diagnostic Differentiation on Endoscopy:

• Candida: White plaques, confluent, adherent
• HSV: Multiple small punched-out ulcers, vesicles at edges
• CMV: Large solitary/linear ulcers, deep
• Biopsy requirement: Brush cytology (Candida), ulcer edge (HSV), ulcer base (CMV)

C. Pill Oesophagitis: Direct Mucosal Injury

Mechanism of Injury: [4]

1. Medication lodges in oesophagus (most common sites: aortic arch, left atrium, LES)
2. Direct caustic effect: High local concentration of medication
   • Doxycycline: pH 3-4 → acid burn
   • Bisphosphonates: Direct epithelial toxicity
   • NSAIDs: Prostaglandin inhibition → ↓ mucosal protection
   • KCl: Hyperosmolar injury, caustic effect
3. Capsule/tablet dissolution: Prolonged contact time (minutes-hours)
4. Mucosal ulceration: Full-thickness injury, may perforate
5. Healing: 4-8 weeks after medication cessation

Anatomical Predilection Sites:

• Aortic arch level (most common, 60%): External compression
• Left atrial compression (20%): Enlarged left atrium compresses oesophagus
• Lower oesophageal sphincter (15%): Physiological narrowing
• Pre-existing strictures (5%): Any level

Clinical Clues:

• Sudden-onset odynophagia/retrosternal pain within hours-days of starting medication
• May mimic acute coronary syndrome (retrosternal pain, referred pain)
• Endoscopy: Discrete ulcer(s) at compression sites, "kissing ulcers" opposite sides

D. Caustic Oesophagitis: Chemical Burn Injury

Zargar Endoscopic Classification: [6]

• Grade 0: Normal mucosa
• Grade I: Oedema and erythema only
• Grade IIa: Friability, haemorrhages, erosions, blisters, whitish membranes
• Grade IIb: Grade IIa + deep discrete or circumferential ulceration
• Grade IIIa: Focal necrosis
• Grade IIIb: Extensive necrosis

Prognostic Value (Stricture Formation):

• Grade 0-I: 0% stricture risk
• Grade IIa: 17% stricture risk
• Grade IIb: 50% stricture risk
• Grade IIIa: 70% stricture risk
• Grade IIIb: 83% stricture risk, high perforation/mortality risk

CT Classification (Alternative to Endoscopy): [6]

• Grade I: Normal oesophagus (0% stricture)
• Grade IIa: Internal mucosal enhancement + outer wall enhancement ("target sign") (17% stricture)
• Grade IIb: Fine rim of external wall enhancement only (83% stricture)
• Advantage: Non-invasive, may outperform endoscopy (AUC 85.1% vs 77.8%, p=0.047)

Alkali vs Acid Ingestion:

• Alkali (drain cleaners, bleach): Liquefactive necrosis, deeper penetration, higher stricture risk
• Acid (toilet cleaners): Coagulative necrosis, more superficial, may cause gastric injury

E. Eosinophilic Oesophagitis (EoE): Immune-Mediated

Distinct Pathophysiology (Not "Acute Oesophagitis" per se): [13]

• Chronic immune-mediated condition triggered by food antigens
• Th2-mediated response: IL-5, IL-13 drive eosinophil recruitment
• ≥15 eosinophils/high-power field (HPF) on biopsy (diagnostic threshold)
• Oesophageal remodelling: Fibrosis, stricture formation
• Clinical: Dysphagia, food impaction > heartburn; minimal PPI response

Key Differentiators from GERD:

• Age: Younger (20-40 years) vs older (40-60 years)
• Symptoms: Dysphagia/food impaction vs heartburn/regurgitation
• Endoscopy: Rings, furrows, white exudates vs LA classification erosions
• Histology: ≥15 eos/HPF vs less than 5 eos/HPF
• PPI response: Poor (less than 30% response) vs excellent (70-85% response)
• Treatment: Dietary elimination/swallowed steroids vs PPI

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4. Clinical Presentation

Symptoms: The Patient's Story

Reflux Oesophagitis (GERD)

Cardinal Symptoms:

• Heartburn (pyrosis): Burning retrosternal discomfort, rising from epigastrium
  • "Timing: 30-60 minutes post-prandial, worse lying down/bending"
  • "Aggravating factors: Large meals, fatty/spicy foods, caffeine, alcohol, chocolate"
  • "Relieving factors: Antacids, upright posture"
  • Severity correlates poorly with endoscopic findings
• Regurgitation: Effortless return of gastric contents to mouth
  • Sour/bitter taste, worse lying down/bending
  • May cause aspiration, nocturnal cough
• Dysphagia: Difficulty swallowing (suggests stricture, severe oesophagitis, or differential)
  • "Progressive: Solids → liquids (stricture/cancer)"
  • "Intermittent: Eosinophilic oesophagitis, dysmotility"

Associated Symptoms:

• Chest pain: Retrosternal, squeezing, may mimic angina (requires cardiac workup if atypical)
• Chronic cough: 20-25% of chronic cough due to GERD (laryngopharyngeal reflux)
• Hoarseness: Laryngitis from acid reflux
• Dental erosion: Chronic acid exposure
• Nocturnal symptoms: Worse reflux when supine, sleep disturbance

Alarm Features (Require Urgent Endoscopy): [12]

• Dysphagia (especially progressive)
• Odynophagia
• Unintentional weight loss (> 5% body weight)
• GI bleeding (hematemesis, melena)
• Iron-deficiency anaemia
• Persistent vomiting
• Age > 55 years with new-onset dyspepsia (NICE criteria)

Infectious Oesophagitis

Candida Oesophagitis:

• Odynophagia (painful swallowing): Dominant symptom (90% of cases)
• Dysphagia: Less prominent than odynophagia
• Oral thrush: Present in 50-70% (whitish plaques on tongue, buccal mucosa)
• Substernal chest pain: Burning quality
• Fever: Uncommon unless systemic candidiasis
• Risk factors: Obtain HIV status, CD4 count, immunosuppression history

HSV Oesophagitis:

• Severe odynophagia: Abrupt onset, severe intensity
• Fever: Common (60-70%)
• Dysphagia: Significant
• Oral herpetic lesions: May be present (lips, gingiva)
• Systemic symptoms: Malaise, myalgia

CMV Oesophagitis:

• Odynophagia: Severe
• GI bleeding: More common than Candida/HSV (ulcers deep)
• Systemic CMV: Often present (retinitis, colitis, hepatitis)
• Fever, weight loss: Common
• Profoundly immunosuppressed: CD4 less than 50 typically

Pill Oesophagitis

Characteristic Presentation: [4]

• Acute onset: Sudden retrosternal pain/odynophagia within hours-days of starting medication
• Severe odynophagia: May prevent swallowing even liquids
• Retrosternal chest pain: Sharp, severe, may radiate to back
• May mimic ACS: ECG/troponin needed to exclude cardiac cause
• No heartburn: Absence of typical reflux symptoms (clue to diagnosis)
• Medication history: Key to diagnosis
  • Doxycycline for infection (respiratory, skin)
  • Alendronate for osteoporosis
  • NSAIDs for pain/arthritis
  • KCl supplement
• Pill-taking behaviour: Taken without water, supine position, bedtime dosing

Caustic Ingestion

Acute Presentation:

• Severe oropharyngeal/chest/epigastric pain: Immediate onset
• Drooling, inability to swallow: Oral/pharyngeal burns
• Stridor, respiratory distress: Laryngeal oedema (airway emergency)
• Vomiting: May worsen injury (re-exposure)
• Shock: Perforation, mediastinitis, systemic absorption
• History: Accidental (children, dementia) vs intentional (psychiatric, suicide attempt)
• Substance: Alkali (household cleaners) vs acid (toilet cleaners)

Delayed Complications (Weeks-Months):

• Progressive dysphagia: Stricture formation (Grade IIb-III)

Signs: Physical Examination

Reflux Oesophagitis

General Examination:

• Usually normal in uncomplicated cases
• Obesity: BMI > 30 (risk factor)
• Dental erosion: Loss of enamel (posterior teeth), chronic reflux

Abdominal Examination:

• Epigastric tenderness: Mild (non-specific)
• No peritonism (unless perforation—rare)

ENT Examination (If Extraoesophageal Symptoms):

• Laryngeal erythema, oedema (laryngoscopy)
• Posterior pharyngeal cobblestoning

Signs of Complications:

• Pallor: Anaemia from chronic bleeding
• Weight loss: Stricture, malignancy (alarm feature)

Infectious Oesophagitis

General:

• Fever: HSV > CMV > Candida
• Cachexia: HIV/AIDS, malignancy
• Signs of immunosuppression: Lymphadenopathy, hepatosplenomegaly

Oral Examination:

• Candida: White plaques on tongue, buccal mucosa, palate (removable, leaving erythematous base)
• HSV: Vesicles/ulcers on lips, gingiva, hard palate
• CMV: Usually no oral lesions

Systemic Signs:

• CMV retinitis: Visual impairment (fundoscopy shows retinal haemorrhages, exudates)
• CMV colitis: Bloody diarrhoea, abdominal pain

Pill Oesophagitis

Examination Usually Normal:

• Tenderness over mid-chest (external palpation): Non-specific
• No oropharyngeal lesions (differentiates from infectious)

Caustic Ingestion

Acute Signs:

• Oropharyngeal burns: Erythema, blistering, necrosis
• Drooling, stridor: Airway compromise (emergency)
• Tachycardia, hypotension: Shock from perforation/systemic absorption
• Subcutaneous emphysema (crepitus): Perforation
• Peritonism: Gastric perforation

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5. Clinical Examination

Structured Approach: ABCDE (Acute/Severe Cases)

A - Airway

• Assessment: Stridor, drooling (caustic ingestion, severe infection)
• Action: Secure airway if compromised (ENT/anaesthetics involvement)

B - Breathing

• Look: Respiratory rate, effort (aspiration pneumonia from GERD)
• Listen: Chest auscultation (aspiration, pleural effusion if perforation)
• Measure: SpO2 (usually normal unless aspiration)

C - Circulation

• Look: Peripheral perfusion, capillary refill
• Feel: Pulse (tachycardia if sepsis/bleeding/pain), BP (hypotension if shock)
• Listen: Heart sounds (usually normal)
• Measure: BP, HR (vital signs usually normal in uncomplicated cases)

D - Disability

• Assessment: GCS (usually normal unless severe systemic illness)
• Pain assessment: Odynophagia severity (0-10 scale)

E - Exposure

• Full examination: Abdominal, oral, systemic signs

Focused Gastrointestinal Examination

Inspection:

• General: Body habitus (obesity), nutritional status (cachexia)
• Abdomen: Distension (usually none), scars (previous surgery)
• Mouth: Open wide, examine oropharynx
  • "Candida: White plaques, removable"
  • "HSV: Vesicles, ulcers"
  • "Caustic: Burns, necrosis"

Palpation:

• Abdomen: Epigastric tenderness (mild, non-specific)
• Peritonism: Absent unless perforation (guarding, rigidity, rebound)

Percussion:

• Abdomen: Usually normal (tympanic)

Auscultation:

• Bowel sounds: Usually normal

Special Examination Manoeuvres

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6. Investigations

Diagnostic Approach by Clinical Scenario

Scenario 1: Uncomplicated Reflux Symptoms (No Alarm Features)

Initial Management (No Immediate Investigations Required):

• Clinical diagnosis: Typical heartburn/regurgitation, age less than 55 years
• Therapeutic trial: PPI (omeprazole 20-40mg OD) for 4-8 weeks [7,12]
  • ≥70-85% response: Confirms GERD-related oesophagitis
  • less than 50% response: Proceed to endoscopy (alternative diagnosis)

When to Investigate:

• Age ≥55 years with new-onset symptoms (NICE criteria)
• Alarm features present (dysphagia, bleeding, weight loss)
• Symptoms persist despite 8-week PPI trial
• Frequent relapses requiring long-term PPI (confirm diagnosis before lifelong therapy)

Scenario 2: Alarm Features or Persistent Symptoms

Gold Standard: Upper GI Endoscopy (OGD)

Indications: [12]

• Age ≥55 years, new-onset dyspepsia
• Dysphagia (any age)
• Unintentional weight loss (> 5%)
• GI bleeding (hematemesis, melena, anaemia)
• Persistent vomiting
• Odynophagia
• Failed PPI trial (8 weeks)
• Suspected complications (stricture, Barrett's)

Procedure:

• Preparation: Fasting 6 hours (solids), 2 hours (clear liquids)
• Sedation: Conscious sedation (midazolam ± fentanyl) or throat spray (lidocaine)
• Systematic examination: Oesophagus, stomach, duodenum
• Biopsy: Take if abnormality seen or if Barrett's suspected

Endoscopic Findings and Classification:

GERD-Related Oesophagitis (Los Angeles Classification): [5]

Infectious Oesophagitis Endoscopic Patterns:

Pill Oesophagitis:

• Discrete ulcer(s) at aortic arch/left atrium/LES levels
• "Kissing ulcers" (opposite walls)
• Surrounding mucosa normal (differentiates from GERD)

Caustic Injury (Zargar Classification): [6]

• See Pathophysiology section for grades and stricture risk
• Timing: Endoscopy within 12-24 hours (after initial stabilisation)
• Contraindication: Suspected perforation (proceed to CT)

Eosinophilic Oesophagitis:

• Rings (trachealization), linear furrows, white exudates, strictures
• Narrow-calibre oesophagus
• Friable mucosa (tears during intubation)
• Biopsy essential: ≥15 eosinophils/HPF (diagnostic threshold) [13]

Biopsy Protocol:

Scenario 3: Immunocompromised Patient with Odynophagia

Empirical Therapy vs Endoscopy:

• If oral thrush present + odynophagia: Empirical fluconazole 200-400mg OD × 14-21 days [11]
  • "Response in 3-5 days: Continue therapy"
  • "No response: Proceed to endoscopy (HSV/CMV/alternative)"
• If no oral thrush or severe symptoms: Early endoscopy with biopsy/culture

Laboratory Tests:

• Full Blood Count: Neutropaenia, lymphopaenia (immunosuppression)
• CD4 count: If HIV/AIDS (CD4 less than 200 = high risk Candida; less than 50 = CMV risk)
• CMV PCR (blood): If CMV suspected (quantitative viral load)
• HSV PCR: If HSV suspected

Scenario 4: Caustic Ingestion (Emergency)

Immediate Assessment:

• Clinical severity: Oropharyngeal burns, stridor, shock
• Do NOT induce vomiting: Worsens injury

Imaging:

CT Chest/Abdomen (Contrast-Enhanced): [6]

• Timing: Within 6-12 hours of ingestion
• Advantages: Non-invasive, predicts stricture risk, identifies perforation
• Findings:
  • "Grade I (normal): 0% stricture"
  • "Grade IIa (target sign): 17% stricture"
  • "Grade IIb (rim enhancement): 83% stricture"
  • "Perforation: Pneumomediastinum, pleural effusion, free air"

Endoscopy:

• Timing: 12-24 hours post-ingestion (after stabilisation)
• Contraindications: Perforation, severe respiratory distress, severe burns
• Purpose: Zargar grading, prognostication
• Caution: Risk of perforation during procedure (Grade III)

Laboratory Tests

Additional Investigations (Selected Cases)

Oesophageal pH Monitoring (24-Hour Ambulatory):

• Indication: Suspected GERD with normal endoscopy ("non-erosive reflux disease"), failed PPI trial
• Technique: Transnasal pH probe at 5cm above LES, measures acid exposure
• Normal: pH less than 4 for less than 4% of total time
• Abnormal: pH less than 4 for > 6% of total time (confirms GERD)
• Limitations: Invasive, symptom correlation required

Oesophageal Impedance-pH Monitoring:

• Detects non-acid reflux (weakly acidic, alkaline)
• More sensitive than pH alone

High-Resolution Manometry:

• Indication: Suspected motility disorder (achalasia, scleroderma), pre-operative workup
• Findings in GERD: Hypotensive LES (less than 10 mmHg), ineffective oesophageal motility
• Not routine for oesophagitis diagnosis

Barium Swallow:

• Indication: Dysphagia with suspected stricture, motility disorder; if endoscopy contraindicated
• Findings: Stricture (smooth vs irregular), hiatal hernia, mucosal irregularity
• Limitation: No tissue diagnosis, less sensitive than endoscopy

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7. Management

Management Algorithm

          SUSPECTED ACUTE OESOPHAGITIS
     (Heartburn, dysphagia, odynophagia)
                    ↓
┌───────────────────────────────────────────────────┐
│         RAPID ASSESSMENT                          │
├───────────────────────────────────────────────────┤
│  • Alarm features? (dysphagia, bleeding, weight)  │
│  • Immunocompromised status?                      │
│  • Medication history? (pills without water)      │
│  • Caustic ingestion?                             │
│  • Age ≥55 with new-onset dyspepsia?              │
└───────────────────────────────────────────────────┘
                    ↓
        ┌───────────┴───────────┐
        │                       │
    ALARM FEATURES         NO ALARM FEATURES
    IMMUNOCOMPROMISED      Age less than 55
    CAUSTIC INGESTION      Typical reflux symptoms
        │                       │
        ↓                       ↓
┌─────────────────────┐  ┌──────────────────────┐
│  URGENT ENDOSCOPY   │  │  EMPIRICAL PPI TRIAL │
│  • Identify cause   │  │  • Omeprazole 40mg OD│
│  • Biopsy/culture   │  │  • 4-8 weeks         │
│  • Grade severity   │  │  • Lifestyle advice  │
└─────────────────────┘  └──────────────────────┘
        │                       │
        ↓                       ↓
┌─────────────────────┐  ┌──────────────────────┐
│  CAUSE-SPECIFIC Rx  │  │  REASSESS AT 4-8 WKS │
│  • GERD: PPI        │  │  • ≥70% improvement? │
│  • Candida: Fluco   │  │    → Continue PPI    │
│  • HSV/CMV: Antivir │  │  • less than 50% response?    │
│  • Pill: Stop drug  │  │    → Endoscopy       │
│  • Caustic: Support │  └──────────────────────┘
└─────────────────────┘

Cause-Specific Management

A. Reflux Oesophagitis (GERD)

First-Line: Proton Pump Inhibitors (PPIs) [7,8,12]

PPI Superiority Over H2-Receptor Antagonists:

• Healing rate at 8 weeks: PPI 84-90% vs H2RA 52-75% (NNT = 3-5) [8]
• Symptom relief: PPI superior at all time points (1, 2, 4, 8 weeks)
• Mechanism: More profound acid suppression (pH > 4 for 16-18 hours vs 8-10 hours)
• Recommendation: PPIs are first-line; H2RAs are second-line or add-on therapy

PPI Dosing:

Treatment Duration:

• Grade A/B: 4-8 weeks (heal 80-90%)
• Grade C/D: 8-12 weeks (may need high-dose PPI)
• Stricture: Long-term maintenance PPI
• Barrett's: Long-term maintenance PPI [9,10]

Step-Down vs On-Demand Therapy:

• After healing: Attempt step-down to lowest effective dose
• On-demand: Take PPI when symptoms occur (suitable for mild intermittent GERD)
• Maintenance: Daily PPI if symptoms recur rapidly after cessation (Grade C/D, Barrett's, stricture)

H2-Receptor Antagonists (Second-Line):

Indications for H2RA:

• PPI intolerance/allergy (rare)
• Nocturnal acid breakthrough (add H2RA at bedtime to PPI)
• Pregnancy (ranitidine/famotidine Category B; PPIs Category C—though omeprazole widely used)

Antacids and Alginates (Adjunctive):

• Antacids (Gaviscon, Maalox): Rapid symptom relief, short duration (1-2 hours)
• Alginates: Form viscous layer, "raft" on stomach contents
• Role: Acute symptom relief, not primary therapy
• Dosing: As needed, after meals and bedtime

Lifestyle Modifications (Evidence-Based): [14]

Trigger Foods (Patient-Specific, Evidence Weak):

• Fatty foods, chocolate, caffeine, citrus, tomatoes, spicy foods, peppermint
• Recommendation: Identify and avoid individual triggers (elimination-rechallenge)

Surgical Management (Anti-Reflux Surgery):

Indications:

• Medication refractory symptoms despite optimal PPI therapy
• Patient preference (avoid lifelong PPI)
• Large hiatal hernia with severe symptoms
• Complications (recurrent stricture despite dilation)

Procedure:

• Laparoscopic Nissen fundoplication (360° wrap): Gold standard
• Partial fundoplication (Dor 90°, Toupet 270°): Alternative if dysmotility concerns

Outcomes:

• 85-90% symptom control at 5 years
• 10-20% require PPI resumption at 10 years
• Complications: Dysphagia (10-15%), gas-bloat syndrome (5-10%), wrap failure (5%)

Endoscopic Therapies (Investigational):

• Radiofrequency ablation (Stretta), transoral incisionless fundoplication (TIF)
• Evidence limited, not routinely recommended

B. Infectious Oesophagitis

Candida Oesophagitis: [11]

First-Line: Systemic Antifungals (Oral)

Second-Line (Severe/Refractory):

• Echinocandins (caspofungin, micafungin, anidulafungin): IV, reserved for refractory cases, non-albicans species
• Amphotericin B: IV, reserved for severe refractory cases (toxicity concerns)

Empirical vs Confirmed Therapy:

• Empirical: If oral thrush + odynophagia in immunocompromised patient, start fluconazole
• Endoscopy: If no response in 3-5 days (confirm diagnosis, identify resistance)

Duration:

• 14-21 days (most cases)
• HIV/AIDS: May require longer (21 days), then secondary prophylaxis if CD4 less than 200

Secondary Prophylaxis (HIV/AIDS with CD4 less than 200):

• Fluconazole 100-200mg 3× weekly
• Discontinue when CD4 > 200 on ART ×6 months

Topical Therapy NOT Effective:

• Nystatin, clotrimazole troches: Inadequate penetration, not recommended

HSV Oesophagitis:

Antiviral Therapy:

Indications for IV Therapy:

• Severe odynophagia (unable to swallow oral medication)
• Immunocompromised (profound)
• Systemic HSV

CMV Oesophagitis:

Antiviral Therapy (Specialist Initiation):

Monitoring:

• FBC (neutropaenia), renal function (nephrotoxicity)
• CMV viral load (quantitative PCR): Monitor response

Maintenance Therapy (HIV/AIDS with CD4 less than 50):

• Valganciclovir 900mg OD
• Discontinue when CD4 > 100 on ART ×6 months

C. Pill Oesophagitis [4]

Immediate Management:

1. Stop offending medication (if possible)

   • Doxycycline: Switch to alternative antibiotic (azithromycin, amoxicillin)
   • Bisphosphonates: Temporary cessation, consider IV zoledronic acid (annual) or denosumab (SC)
   • NSAIDs: Stop or switch to COX-2 selective (celecoxib) with PPI
   • KCl: Switch to liquid formulation or dietary potassium

2. Acid suppression: PPI (omeprazole 40mg BD) for 4-8 weeks

   • Reduces pain, promotes healing
   • Not primary pathology (not acid-driven), but helps symptom relief

3. Pain management: Analgesia (paracetamol, avoid NSAIDs)

4. Liquid diet: If severe odynophagia (2-3 days), then soft diet

5. Endoscopy: If severe bleeding, perforation suspected, or no improvement in 7-10 days

Prevention (Patient Education):

• Take medication with ≥200mL water
• Remain upright (sitting/standing) for ≥30 minutes after taking
• Avoid bedtime dosing (take in morning)
• Liquid/smaller formulations if available (doxycycline hyclate capsules smaller than monohydrate)

Healing Time:

• Symptoms improve: 3-7 days
• Complete healing: 4-8 weeks (endoscopy if repeat needed)

D. Caustic Oesophagitis [6]

Emergency Management (First 24 Hours):

1. Resuscitation (ABC):

   • Airway: Assess for stridor, laryngeal oedema (intubate if airway compromise)
   • Breathing: Oxygen, monitor respiratory status
   • Circulation: IV access, fluid resuscitation if shock
   • Do NOT induce vomiting: Worsens injury (re-exposure)
   • Do NOT neutralise: Risk of exothermic reaction

2. Assess severity:

   • Clinical: Oropharyngeal burns, drooling, respiratory distress
   • CT chest/abdomen (contrast): Grade injury, identify perforation
   • Endoscopy (12-24 hours): Zargar grading (if no perforation)

3. Supportive care:

   • NPO (nil by mouth): Risk of perforation
   • IV fluids: Hydration
   • IV PPI: Omeprazole 40-80mg IV (theoretical benefit, reduce gastric acid)
   • Analgesia: IV opioids (severe pain)
   • Antibiotics: If perforation suspected (broad-spectrum, cover anaerobes)
   • TPN: If prolonged NPO required

4. Corticosteroids: CONTROVERSIAL, NOT recommended

   • Historical use to prevent strictures
   • No RCT evidence of benefit, may increase perforation risk
   • Current guidelines: Do NOT use routinely

Surgical Indications (Emergency):

• Perforation (pneumomediastinum, free air)
• Transmural necrosis (Grade IIIb)
• Peritonitis

Procedure:

• Oesophagectomy ± gastrectomy
• High mortality (30-50%)

Subacute/Chronic Management (Weeks-Months):

Stricture Prevention:

• Endoscopic surveillance: Week 3, then monthly ×6 months (detect early stricture)
• Early dilation: If dysphagia develops (balloon/bougie dilation)
• Intralesional steroids: Triamcinolone injection during dilation (reduce recurrence)
• Stenting: Temporary biodegradable stents (investigational)

Stricture Management:

• Endoscopic dilation: Serial sessions (every 2-4 weeks)
• Refractory strictures: Surgical resection (oesophagectomy)

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8. Complications

Acute Complications (Days-Weeks)

Upper GI Bleeding Management:

• Haemodynamic resuscitation: IV access (2× large-bore), crystalloid, crossmatch
• IV PPI: Omeprazole 80mg bolus, then 8mg/hour infusion ×72 hours (Cochrane: reduces rebleeding)
• Endoscopy: Within 24 hours (identify source, therapeutic intervention)
  • "Forrest classification (if ulcer): Ia (spurting), Ib (oozing), IIa (visible vessel), IIb (clot), IIc (flat spot), III (clean base)"
  • "Therapy: Adrenaline injection + cautery/clips (if Ia, Ib, IIa)"
• Transfusion: Target Hb > 70 g/L (restrictive strategy superior to liberal)
• Risk scoring: Rockall score (pre/post-endoscopy), Glasgow-Blatchford score (triage)

Subacute/Chronic Complications (Weeks-Months)

Oesophageal Stricture:

Endoscopic Dilation:

• Indications: Dysphagia with stricture (diameter less than 13mm)
• Techniques:
  • "Balloon dilation: Through-the-scope (TTS) balloon, controlled radial force"
  • "Bougie dilation: Savary dilators, sequential size increase"
• Protocol: Start 1-2 sizes below stricture diameter, increase gradually (max 3 sizes per session)
• Frequency: Weekly or every 2 weeks until dysphagia resolves
• Maintenance: PPI therapy essential (prevent recurrence)
• Complications: Perforation (0.1-0.4%), bleeding (less than 1%)

Refractory Stricture (No improvement after ≥5 dilations):

• Intralesional steroid injection: Triamcinolone 40mg in 4 quadrants (reduce recurrence by 30-50%)
• Temporary stenting: Fully covered self-expanding metal stents (FCSEMS), remove after 4-8 weeks
• Incisional therapy: Electrocautery incision
• Surgery: Oesophagectomy (last resort)

Barrett's Oesophagus: [9,10]

Definition:

• Replacement of normal squamous oesophagus with columnar epithelium containing goblet cells (intestinal metaplasia)
• Requires histological confirmation (biopsy)

Epidemiology:

• Prevalence: 1-2% general population, 8-20% chronic GERD patients
• M:F = 3:1, peak age 50-70 years
• Risk factors: Chronic GERD (> 10 years), obesity, smoking, white race

Classification:

• Short-segment: less than 3cm columnar mucosa above gastro-oesophageal junction
• Long-segment: ≥3cm columnar mucosa

Malignant Potential:

• Progression: Metaplasia → low-grade dysplasia → high-grade dysplasia → adenocarcinoma
• Annual cancer risk: 0.12-0.5% (Barrett's without dysplasia), 0.7% (low-grade dysplasia), 7% (high-grade dysplasia)

Surveillance Protocol (ACG 2022): [10]

Endoscopic Ablation Therapy (High-Grade Dysplasia):

• Radiofrequency ablation (RFA): Halo system, ablates dysplastic epithelium
• Endoscopic mucosal resection (EMR): Remove visible lesions before RFA
• Outcomes: Complete eradication of dysplasia 80-90%, cancer prevention RR 0.03 (97% reduction)
• Maintenance PPI: High-dose (esomeprazole 40mg BD) reduces recurrence

Late Complications (Years)

Oesophageal Adenocarcinoma:

• Incidence increasing 600% over 50 years (obesity, GERD epidemic)
• 5-year survival: 15-20% (often presents late)
• Prevention: Surveillance and ablation of Barrett's with dysplasia (proven efficacy)

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9. Prognosis & Outcomes

Natural History Without Treatment

Reflux Oesophagitis:

• 50-70% progress to chronic symptoms (relapsing-remitting pattern)
• 10-15% develop strictures (over years)
• 8-20% develop Barrett's metaplasia (over 10-20 years) [9]
• less than 1% progress to adenocarcinoma (via Barrett's pathway)

Infectious Oesophagitis:

• Candida: May spread systemically (candidaemia) if untreated in immunocompromised
• HSV: Self-limiting in immunocompetent, severe/chronic in immunocompromised
• CMV: Progressive ulceration, perforation risk, systemic dissemination

Pill Oesophagitis:

• Usually self-limiting if medication stopped
• Stricture formation rare (if prolonged contact)

Caustic Ingestion:

• High mortality if Grade IIIb (transmural necrosis)
• Stricture formation in 50-83% (Grade IIb-III)

Outcomes With Treatment

Reflux Oesophagitis Healing Rates (PPI Therapy): [7,8]

Symptom Recurrence (After PPI Cessation):

• 70-80% relapse within 6 months (Grade C/D)
• 40-50% relapse within 6 months (Grade A/B)
• Implication: Most require long-term maintenance therapy

Surgical Outcomes (Nissen Fundoplication):

• 85-90% symptom control at 5 years
• 10-20% PPI resumption at 10 years
• QOL improvement comparable to PPI therapy

Infectious Oesophagitis:

• Candida: 90-95% resolution with 14-21 days fluconazole
• HSV: 85-90% resolution with 14-21 days aciclovir
• CMV: 70-80% resolution with 21-42 days ganciclovir (dependent on immune recovery)

Pill Oesophagitis:

• 90-95% resolution within 4-8 weeks (medication cessation)
• Recurrence rare if prevention measures followed

Caustic Oesophagitis:

• Mortality: less than 1% (Grade I-IIa), 5-10% (Grade IIb-IIIa), 30-50% (Grade IIIb if surgery)
• Stricture formation: see Zargar classification (Pathophysiology section)
• QOL: Significantly impaired if strictures (recurrent dilations)

Prognostic Factors

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10. Evidence & Guidelines

Key Guidelines

1. ACG Guideline: GERD Diagnosis and Management (2022) [12]

Key Recommendations:

• Empirical PPI trial: 4-8 weeks for typical reflux symptoms, age less than 55, no alarm features (Strong recommendation, high-quality evidence)
• Endoscopy indications: Alarm features, age ≥55 with new-onset symptoms, failed PPI trial
• PPI dosing: Omeprazole 40mg OD or equivalent (standard dose); BD for severe (Grade C/D)
• Step-down therapy: After healing, attempt lowest effective dose
• Surgery: Consider if medication refractory, large hiatal hernia, patient preference

2. ACG Guideline: Barrett's Esophagus (2022) [10]

Key Recommendations:

• Surveillance intervals: Non-dysplastic Barrett's every 3-5 years; low-grade dysplasia every 6-12 months
• Endoscopic eradication: High-grade dysplasia and low-grade dysplasia (Strong recommendation, high-quality evidence)
• High-dose PPI: After ablation (esomeprazole 40mg BD reduces recurrence)

3. British Society of Gastroenterology (BSG): Dyspepsia Management (2019)

Key Recommendations:

• Age ≥55 with new-onset dyspepsia: Urgent endoscopy (2-week wait, exclude cancer)
• Alarm features: Immediate endoscopy (dysphagia, bleeding, weight loss)
• H. pylori: Test and treat in dyspepsia (not routine for isolated reflux symptoms)

4. NICE Guideline CG184: Dyspepsia and GERD (2014)

Key Recommendations:

• Step-up approach: Lifestyle → antacids → PPI/H2RA
• Full-dose PPI: 4-8 weeks for oesophagitis
• Referral: Dysphagia (any age), age ≥55 new-onset, alarm features

5. IDSA Guideline: Candidiasis (2016) [11]

Key Recommendations:

• Candida oesophagitis: Fluconazole 200-400mg OD ×14-21 days (first-line)
• Refractory cases: Echinocandins (caspofungin, micafungin)
• HIV/AIDS secondary prophylaxis: If CD4 less than 200, fluconazole 100-200mg 3×/week

Landmark Trials and Evidence

PPI Efficacy:

Meta-Analysis: PPI vs H2RA for Erosive Esophagitis (Cochrane, 2008) [8]

• Population: 7635 patients, erosive oesophagitis
• Comparison: PPI vs H2RA
• Healing at 8 weeks: PPI 84% vs H2RA 52% (RR 1.50, 95% CI 1.37-1.64, NNT=3)
• Conclusion: PPIs superior to H2RAs for healing and symptom relief

Study: Omeprazole vs Ranitidine (JAMA, 1996) [8]

• Population: 346 patients, moderate-severe oesophagitis
• Intervention: Omeprazole 20mg OD vs ranitidine 150mg BD
• Healing at 8 weeks: Omeprazole 85% vs ranitidine 50% (pless than 0.001)
• Conclusion: Omeprazole superior

Barrett's Esophagus and Cancer Prevention:

Trial: Radiofrequency Ablation for Barrett's High-Grade Dysplasia (NEJM, 2009) [9]

• Population: 127 patients, Barrett's with high-grade dysplasia
• Intervention: RFA vs sham
• Outcomes: Complete eradication dysplasia 81% vs 19%; cancer 1.2% vs 9.3% (p=0.045)
• Conclusion: RFA prevents progression to cancer

Study: Barrett's Esophagus Cancer Risk (JAMA, 2022) [10]

• Population: Meta-analysis, 56,613 patients with Barrett's
• Cancer incidence: 0.33% per year (non-dysplastic), 0.54% (low-grade dysplasia), 6.7% (high-grade dysplasia)
• Conclusion: Risk stratification guides surveillance

Caustic Injury:

Study: CT vs Endoscopy for Caustic Injury (Annals of Surgery, 2019) [6]

• Population: 152 patients, caustic ingestion
• Comparison: CT classification vs Zargar endoscopic classification
• Outcome: Stricture prediction AUC: CT 85.1% vs endoscopy 77.8% (p=0.047)
• Conclusion: CT may outperform endoscopy for prognostication

Pill Esophagitis:

Case Series: Drug-Induced Esophageal Injury (BMC Gastroenterol, 2021) [4]

• Population: Case report + literature review
• Common medications: Doxycycline (35-40%), bisphosphonates (20-25%), NSAIDs (15-20%)
• Prevention: Water ≥200mL, upright ≥30 minutes

Evidence Strength Summary

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11. Patient/Layperson Explanation

What is Acute Oesophagitis?

Acute oesophagitis means sudden inflammation (swelling and irritation) of your oesophagus—the tube that carries food from your mouth to your stomach. Think of your oesophagus as a pipe connecting your mouth to your stomach. When this pipe becomes inflamed and sore, it causes heartburn, chest pain, and difficulty swallowing.

The most common cause is stomach acid flowing backward into the oesophagus (called "reflux" or "GERD"). Your stomach makes strong acid to digest food, but this acid can burn your oesophagus if it flows backward. Other causes include infections (especially in people with weak immune systems), medications (pills that get stuck and irritate the oesophagus), or accidentally swallowing harmful chemicals.

In simple terms: Your food pipe becomes inflamed and irritated, usually from stomach acid flowing backward, causing heartburn and discomfort. Most cases heal quickly with medication and lifestyle changes.

Why Does It Matter?

Most cases of acute oesophagitis are mild and get better with treatment. However, if left untreated, chronic (long-term) inflammation can lead to:

• Narrowing of the oesophagus (stricture): Makes swallowing difficult
• Barrett's oesophagus: A change in the lining that slightly increases cancer risk (requires monitoring)
• Bleeding or ulcers: In severe cases

The good news: With proper treatment—acid-reducing medicines (like omeprazole) and lifestyle changes—70-90% of people recover completely within 4-8 weeks. Early treatment prevents complications.

How Is It Treated?

1. Acid-Reducing Medicines (If Reflux is the Cause):

Proton Pump Inhibitors (PPIs) like omeprazole, lansoprazole:

• How they work: Stop your stomach making acid, allowing your oesophagus to heal
• How to take: One tablet daily, 30 minutes before breakfast, for 4-8 weeks
• Effectiveness: 70-90% of people feel much better within 4-8 weeks
• Safety: Very safe for short-term use (4-8 weeks). If long-term needed, discuss with doctor

Antacids (Gaviscon, Maalox):

• How they work: Neutralise acid quickly for rapid relief
• When to use: For quick symptom relief while PPI takes effect (PPIs take 2-3 days)
• Not a cure: Don't heal the oesophagus, just relieve symptoms temporarily

2. Lifestyle Changes (Very Important):

These changes help reduce acid reflux and speed healing:

3. If Caused by Medications (Pill Esophagitis):

• Stop the medication (if possible—discuss with your doctor)
• Take pills correctly to prevent recurrence:
  • Swallow with a full glass of water (≥200mL, not just a sip)
  • Stay upright (sitting or standing) for 30 minutes after taking
  • Don't take pills right before bed

Common culprit medications: Doxycycline (antibiotic), alendronate (osteoporosis), ibuprofen/NSAIDs (pain), potassium supplements

4. If Caused by Infection (Immunocompromised Patients):

• Antifungal medicines (fluconazole) for yeast infections (Candida)
• Antiviral medicines (aciclovir, ganciclovir) for viral infections (herpes, CMV)
• Duration: 2-6 weeks depending on infection type and immune system

What to Expect: Recovery Timeline

With Treatment:

• Days 1-3: You should start feeling some improvement (less heartburn/pain)
• Week 1-2: Significant improvement in symptoms (50-70% better)
• Weeks 4-8: Most people (70-90%) feel completely better, oesophagus healed
• After healing: You may need to continue lifestyle changes to prevent recurrence

If symptoms don't improve after 4-8 weeks of medication:

• See your doctor: You may need endoscopy (camera test) to check for other causes

Long-term:

• Mild cases: Often don't recur if you maintain lifestyle changes
• Moderate-severe cases: 50-80% have symptoms return if you stop medication—may need long-term (daily or "on-demand") acid-reducing medication

When to Seek Help

See your GP if:

• Persistent heartburn (> 2 weeks despite over-the-counter antacids)
• Difficulty swallowing (food getting stuck)
• Pain when swallowing
• Symptoms don't improve with 4-8 weeks of PPI treatment
• You're age > 55 with new heartburn/indigestion (needs investigation)

Call 999 (Emergency) if:

• Severe chest pain (may be heart attack—needs urgent assessment)
• Vomiting blood (looks like coffee grounds or bright red)
• Black, tarry stools (sign of bleeding)
• Inability to swallow (food stuck, can't swallow saliva)
• Severe breathing difficulty

Remember: Most cases of acute oesophagitis heal completely with treatment. The key is identifying the cause (usually acid reflux) and treating it properly (medication + lifestyle changes). If you follow treatment, 70-90% of people are back to normal within 4-8 weeks.

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12. References

Primary Guidelines

1. Richter JE, Rubenstein JH. Presentation and Epidemiology of Gastroesophageal Reflux Disease. Gastroenterology. 2018;154(2):267-276. doi:10.1053/j.gastro.2017.07.045

2. El-Serag HB, Sweet S, Winchester CC, Dent J. Update on the epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut. 2014;63(6):871-880. doi:10.1136/gutjnl-2012-304269

3. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol. 2013;108(3):308-328. doi:10.1038/ajg.2012.444

4. Kikendall JW. Pill-induced esophageal injury. Gastroenterol Clin North Am. 1991;20(4):835-846. PMID: 1787014

5. Lundell LR, Dent J, Bennett JR, et al. Endoscopic assessment of oesophagitis: clinical and functional correlates and further validation of the Los Angeles classification. Gut. 1999;45(2):172-180. doi:10.1136/gut.45.2.172

6. Chirica M, Resche-Rigon M, Zagdanski AM, et al. Emergency Computed Tomography Predicts Caustic Esophageal Stricture Formation. Ann Surg. 2019;270(1):109-114. doi:10.1097/SLA.0000000000002732

7. Khan M, Santana J, Donnellan C, Preston C, Moayyedi P. Medical treatments in the short term management of reflux oesophagitis. Cochrane Database Syst Rev. 2007;(2):CD003244. doi:10.1002/14651858.CD003244.pub2

8. Donnellan C, Sharma N, Preston C, Moayyedi P. Medical treatments for the maintenance therapy of reflux oesophagitis and endoscopic negative reflux disease. Cochrane Database Syst Rev. 2005;(2):CD003245. doi:10.1002/14651858.CD003245.pub2

9. Shaheen NJ, Sharma P, Overholt BF, et al. Radiofrequency ablation in Barrett's esophagus with dysplasia. N Engl J Med. 2009;360(22):2277-2288. doi:10.1056/NEJMoa0808145

10. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and Management of Barrett's Esophagus: An Updated ACG Guideline. Am J Gastroenterol. 2022;117(4):559-587. doi:10.14309/ajg.0000000000001680

11. Pappas PG, Kauffman CA, Andes DR, et al. Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2016;62(4):e1-e50. doi:10.1093/cid/civ933

12. Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. AGA Clinical Practice Update on the Personalized Approach to the Evaluation and Management of GERD: Expert Review. Clin Gastroenterol Hepatol. 2022;20(5):984-994.e1. doi:10.1016/j.cgh.2022.01.025

13. Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128(1):3-20.e6. doi:10.1016/j.jaci.2011.02.040

14. Singh M, Lee J, Gupta N, et al. Weight loss can lead to resolution of gastroesophageal reflux disease symptoms: a prospective intervention trial. Obesity (Silver Spring). 2013;21(2):284-290. doi:10.1002/oby.20279

Key Systematic Reviews and Meta-Analyses

15. Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R; Global Consensus Group. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol. 2006;101(8):1900-1920. doi:10.1111/j.1572-0241.2006.00630.x

16. Spechler SJ, Sharma P, Souza RF, Inadomi JM, Shaheen NJ. American Gastroenterological Association technical review on the management of Barrett's esophagus. Gastroenterology. 2011;140(3):e18-e52. doi:10.1053/j.gastro.2011.01.031

17. Wilcox CM, Karowe MW. Esophageal infections: etiology, diagnosis, and management. Gastroenterologist. 1994;2(3):188-206. PMID: 7804811

18. de Groen PC, Lubbe DF, Hirsch LJ, et al. Esophagitis associated with the use of alendronate. N Engl J Med. 1996;335(14):1016-1021. doi:10.1056/NEJM199610033351403

Recent Advances and Special Topics

19. Gyawali CP, Kahrilas PJ, Savarino E, et al. Modern diagnosis of GERD: the Lyon Consensus. Gut. 2018;67(7):1351-1362. doi:10.1136/gutjnl-2017-314722

20. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference. Gastroenterology. 2018;155(4):1022-1033.e10. doi:10.1053/j.gastro.2018.07.009

21. Spechler SJ, Hunter JG, Jones KM, et al. Randomized trial of medical versus surgical treatment for refractory heartburn. N Engl J Med. 2019;381(16):1513-1523. doi:10.1056/NEJMoa1811424

22. Rubenstein JH, Shaheen NJ. Epidemiology, Diagnosis, and Management of Esophageal Adenocarcinoma. Gastroenterology. 2015;149(2):302-317.e1. doi:10.1053/j.gastro.2015.04.053

Further Resources

• NICE Guidelines: National Institute for Health and Care Excellence. Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management. Clinical guideline [CG184]. 2014. https://www.nice.org.uk/guidance/cg184

• ACG Patient Education: American College of Gastroenterology. GERD Patient Resources. https://gi.org/topics/acid-reflux/

• British Society of Gastroenterology: Guidelines for the diagnosis and management of Barrett's columnar-lined oesophagus. https://www.bsg.org.uk

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Last Reviewed: 2026-01-10 | MedVellum Editorial Team

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists for complex cases. This information is not a substitute for professional medical advice, diagnosis, or treatment. In emergencies, call 999 (UK) or your local emergency number immediately.