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  • Alkali burns cause liquefaction necrosis, a deep penetration injury associated with a pronounced exothermic reaction.
  • Acid burns cause coagulation necrosis with severe injury to superficial tissues; penetration to deeper tissues is limited by the formation of an eschar.
  • Induction of emesis in caustic ingestions is contraindicated.
  • Ophthalmic exposures require urgent and copious irrigation with tap water if necessary; a delay of a few minutes can dramatically alter outcome.
  • Endoscopy helps to define the severity of the injury and aids in determining prognosis.
  • A battery lodged in the esophagus requires urgent removal.
  • In a significant number of caustic exposures, the product is not in the original or appropriate container.


On direct contact with tissues, caustics cause immediate functional and histologic injury. Acids, alkalis, and antiseptics such as iodine, concentrated hydrogen peroxide, phenol, and formaldehyde are all capable of causing injury. Other common exposures include drain cleaners, household ammonia, automatic dishwasher detergents, and hair relaxer products. Although improvements in safety packaging, child-resistant caps, and federal regulations lowering the maximum concentration for many household caustics have decreased the overall incidence of unintentional pediatric caustic exposures, thousands of accidental exposures occur annually.1 Acids are frequently reported, but the severe pain caused on initial contact usually limits the amount swallowed by small children. In contrast, intentional caustic ingestions by adolescents and adults may involve significantly larger quantities, which generally have a worse outcome. Long-term survivors of moderate and severe esophageal caustic injuries have a 1000-fold risk of esophageal carcinoma.2


Regardless of whether the caustic is an acid or an alkali, the severity of injury depends on:


  • the type, concentration, volume, pH, and titratable acid (or alkaline) reserve of the agent
  • duration of contact with tissues
  • presence or absence of contents in the stomach
  • tonicity of the pyloric sphincter
  • esophageal reflux after the ingestion


Solids and liquids have different effects on the nature of the injury. Solids tend to produce intense localized oral pharyngeal or upper esophageal injury, while liquids, especially strong bases, tend to produce circumferential lesions in the distal esophagus. Areas of anatomic narrowing may be subject to longer contact time and suffer greater injury. Theoretically, the presence of stomach contents can decrease tissue injury by exerting a buffering effect. Pylorospasm prevents gastric emptying which increases contact time of the corrosive with the stomach and results in more severe gastric injury. Any reflux of ingested material back into the esophagus reexposes the tissues to further caustic damage. The titratable acid or alkaline reserve (TAR) is the amount of a xenobiotic required to neutralize or raise the pH of a caustic to that of physiologic tissues. This neutralization results in an exothermic reaction, which can produce or worsen injury.2,3 There are three major pathophysiologic phases of both acid and alkali injuries3:


  • Phase 1 is an acute inflammatory stage in which vascular thrombosis occurs. Cellular necrosis peaks on days 1 ...

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