Module 25.3 - Caustic Ingestions - Lecture

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Welcome to this vital toxicology curriculum focusing on Caustic Ingestions. This module provides a comprehensive overview of corrosive exposures, which carry the risk of severe, life-threatening injury and debilitating long-term complications.
Key Learning Objectives:
Pathophysiology: Understand the difference between alkaline injury (liquefaction necrosis, permitting deeper penetration) and acidic injury (coagulation necrosis, forming an eschar). Injury severity is critically influenced by pH, concentration, and the physical state of the agent.
Clinical Assessment: Clinicians must remember that initial symptoms are highly unreliable predictors of internal injury severity. Signs of airway compromise, such as stridor or hoarseness, constitute an immediate emergency.
Diagnosis: Esophagogastroduodenoscopy (EGD) is the diagnostic gold standard, ideally performed within 12–24 hours post-ingestion to grade the injury using the Zargar classification. Contrast-enhanced CT serves as a crucial adjunct for detecting perforation or assessing transmural damage.
Acute Management: Immediate priority is airway protection and hemodynamic stabilization. Induced emesis, activated charcoal (except for specific cationic metal toxins like ZnCl2/HgCl2), and neutralization are generally contraindicated. Corticosteroids remain highly debated, but evidence suggests a potential role in reducing stricture risk for patients with Grade IIb circumferential esophageal burns. Emergency surgery is required for perforation or extensive necrosis (Grade III).
Long-Term Follow-up: Long-term management involves treating strictures (primarily via endoscopic dilation) and maintaining lifelong surveillance for esophageal squamous cell carcinoma, a risk that is substantially increased (up to 1000-fold) following severe caustic injury.
Effective management requires a comprehensive, multidisciplinary team approach for optimal patient outcomes.