Definition/General
Introduction:
Esophageal caustic injury results from ingestion of corrosive substances causing chemical burns to esophageal mucosa
Alkaline substances (drain cleaners, lye) cause deeper liquefactive necrosis
Acidic substances (toilet bowl cleaners, battery acid) cause coagulative necrosis
Represents medical emergency with potential for perforation and long-term complications.
Origin:
Results from direct chemical contact with esophageal mucosa
Alkaline injuries penetrate deeper due to liquefactive necrosis
Acid injuries tend to be more superficial due to coagulative necrosis forming protective eschar
Concentration and contact time determine injury severity
Volume ingested affects extent of injury.
Classification:
Grade I: superficial mucosal edema and erythema
Grade II: mucosal ulceration and pseudomembrane formation
Grade III: deep ulceration with potential perforation
Alkaline vs acidic injury patterns
Acute phase (0-48 hours), latent phase (3-14 days), cicatricial phase (>2 weeks).
Epidemiology:
Bimodal distribution: accidental in children (<5 years) and intentional in adults (suicide attempts)
Alkaline substances more commonly ingested
Higher incidence in low socioeconomic areas
Household cleaning products most common agents
Male predominance in adult intentional cases.
Clinical Features
Presentation:
Immediate severe pain in mouth, throat, and chest
Odynophagia (painful swallowing)
Drooling and hypersalivation
Nausea and vomiting (may contain blood)
Respiratory distress (laryngeal edema)
Abdominal pain
Hoarseness or voice changes
Hematemesis in severe cases.
Symptoms:
Severe retrosternal burning pain
Inability to swallow saliva
Oral burns and mucosal sloughing
Respiratory symptoms (stridor, dyspnea)
Shock in severe cases
Fever and systemic toxicity
Dehydration from inability to drink
Aspiration pneumonia risk.
Risk Factors:
Accidental ingestion in young children
Psychiatric disorders (suicide attempts)
Substance abuse and intoxication
Storage in unmarked containers
Easy access to household chemicals
Cognitive impairment (elderly, developmental delay)
Industrial exposure.
Screening:
Immediate medical evaluation after suspected ingestion
Upper endoscopy within 12-24 hours (avoid if suspected perforation)
CT scan if perforation suspected
Chest X-ray for pneumomediastinum
Laboratory studies (CBC, metabolic panel)
Avoid induced vomiting or neutralization.
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Gross Description
Appearance:
Acute phase: mucosal erythema, edema, and whitish pseudomembranes
Deep ulcerations with black eschar formation
Hemorrhagic areas and mucosal sloughing
Perforation in severe cases
Chronic phase: fibrosis, scarring, and stricture formation
Loss of normal mucosal folds.
Characteristics:
Alkaline injuries: deeper penetration, liquefactive necrosis, soft white pseudomembranes
Acid injuries: superficial coagulative necrosis, hard black eschar
Circumferential involvement common
Geographic pattern of injury
Skip lesions possible.
Size Location:
Anatomical narrowings most severely affected (cricopharyngeal area, aortic arch, LES)
Proximal esophagus commonly involved
Distal esophagus affected with large volume ingestion
Gastric involvement common with alkaline substances
Oropharyngeal burns may be absent despite esophageal injury.
Multifocality:
Multifocal injury pattern typical
Skip areas of normal mucosa
Proximal predominance in most cases
Concurrent gastric injury frequent
Respiratory tract involvement possible
Progressive injury over first 48-72 hours.
Microscopic Description
Histological Features:
Acute phase: coagulative or liquefactive necrosis, acute inflammation, vascular thrombosis
Subacute phase: granulation tissue, fibroblast proliferation, angiogenesis
Chronic phase: dense fibrosis, collagen deposition, smooth muscle atrophy
Ulceration extending into submucosa or deeper layers.
Cellular Characteristics:
Necrotic epithelium with loss of cellular detail
Neutrophilic infiltrate in acute phase
Macrophages and lymphocytes in healing phase
Fibroblasts and myofibroblasts in chronic phase
Giant cells around foreign material
Regenerating epithelium at ulcer edges.
Architectural Patterns:
Complete mucosal loss in severe cases
Pseudomembrane formation with fibrin and debris
Granulation tissue with prominent vascularity
Fibrosis extending into muscularis propria
Smooth muscle necrosis and replacement by fibrous tissue
Vascular changes (thrombosis, necrosis).
Grading Criteria:
Grade I: mucosal erythema and edema only
Grade II: mucosal ulceration, no muscle involvement
Grade III: transmural necrosis, potential perforation
Grading based on depth of injury and extent of involvement.
Immunohistochemistry
Positive Markers:
Cytokeratins highlight regenerating epithelium
Smooth muscle actin shows muscle layer damage and myofibroblasts
CD68 highlights macrophages
CD34 shows vascular damage and angiogenesis
Collagen stains demonstrate fibrosis
Ki-67 shows proliferative activity in healing areas.
Negative Markers:
Neuroendocrine markers typically negative
Malignancy markers negative (rule out carcinoma)
Infectious agents typically absent unless secondary infection
Specific chemical markers generally not available.
Diagnostic Utility:
Epithelial markers assess regenerative capacity
Smooth muscle markers evaluate muscle layer integrity
Fibrosis markers assess healing and scarring potential
Proliferation markers indicate healing activity
Vascular markers assess perfusion status.
Molecular Subtypes:
Classification based on causative agent (alkaline vs acidic)
Severity grading (superficial vs transmural)
Healing pattern (normal vs hypertrophic scarring)
Complications (stricture, malignancy risk)
Time phase (acute, subacute, chronic).
Molecular/Genetic
Genetic Mutations:
p53 mutations may occur in chronic injury with malignant transformation risk
Inflammatory gene activation (IL-1β, TNF-α, TGF-β)
Fibrosis-related genes (COL1A1, ACTA2)
Angiogenesis factors (VEGF, FGF)
Apoptosis pathways activated in acute injury.
Molecular Markers:
Inflammatory cytokines elevated in acute phase
Growth factors (TGF-β, PDGF) in healing phase
Matrix metalloproteinases in remodeling phase
Collagen synthesis markers in fibrotic phase
Oxidative stress markers in acute injury.
Prognostic Significance:
Depth of injury most important prognostic factor
Alkaline substances generally worse prognosis
Large volume ingestion indicates worse outcome
Age <5 years or >65 years worse prognosis
Delayed presentation associated with complications.
Therapeutic Targets:
Corticosteroids controversial in acute phase
Proton pump inhibitors for acid suppression
Antibiotics for secondary infection prevention
Nutritional support during healing
Endoscopic dilation for strictures
Surgical intervention for severe complications.
Differential Diagnosis
Similar Entities:
Infectious esophagitis
Reflux esophagitis
Pill esophagitis
Radiation esophagitis
Eosinophilic esophagitis
Autoimmune conditions (pemphigoid, pemphigus)
Malignancy
Thermal injury.
Distinguishing Features:
Caustic injury: history of ingestion crucial
Caustic: acute onset with immediate symptoms
Caustic: geographic pattern of injury
Infectious: immunocompromised host, pathogens present
Reflux: chronic symptoms, distal location
Pill: medication history, focal injury
Radiation: treatment history.
Diagnostic Challenges:
Obtaining accurate history in acute setting
Child abuse considerations in pediatric cases
Substance identification may be unclear
Extent assessment difficult in acute phase
Perforation risk limits diagnostic procedures.
Rare Variants:
Chronic caustic esophagitis with malignant transformation
Thermal injury from hot liquids
Industrial chemical exposure
Medication-induced injury (chemotherapy, bisphosphonates)
Mixed caustic and thermal injury
Chronic stricture with secondary changes.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
Esophageal biopsies [time] after caustic ingestion, showing [endoscopic findings]
Clinical History
Ingestion of [caustic agent] [time] prior to biopsy with [clinical symptoms]
Injury Grade
Grade [I/II/III] caustic injury based on depth and extent
Microscopic Findings
Shows [coagulative/liquefactive] necrosis with [depth] of involvement
Healing Phase
[Acute/Subacute/Chronic] phase with [inflammatory/granulation/fibrotic] tissue
Complications
[Present/Absent]: [perforation/stricture/other complications]
Regenerative Changes
Epithelial regeneration: [present/absent]. Quality: [normal/abnormal]
Prognostic Assessment
Prognosis: [good/guarded/poor] based on injury severity and healing response
Recommendations
[Supportive care/surgical intervention/endoscopic surveillance] recommended
Final Diagnosis
Caustic esophageal injury, Grade [I/II/III], [acute/subacute/chronic] phase