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Clinical Summary

Caustics are a diverse group of household and industrial products and pharmaceutical agents that cause functional and histologic tissue damage through direct contact. They represent the 2nd most common toxic exposure for children 5 years of age or under. These agents are frequently described in terms of pH, with acids typically having a pH less than 3 and alkali (bases) typically having a pH greater than 11. Despite a near-physiologic pH, phenol may produce severe burns due to a high titratable acid reserve.

Alkali exposure results in a liquefactive necrosis, with deep and progressive tissue damage, predominantly to the esophagus. Endoscopic grading of esophageal burns is similar to thermal burns, ranging from mucosal hyperemia and edema (grade I) to full-thickness burns (grade III). Acid ingestion results in coagulative necrosis, which limits the depth of penetration. Damage is predominantly localized to the gastric mucosa, with pooling of the caustic agent in the antrum.

Management and Disposition

The primary goal of management is airway assessment and stabilization. Hypotension is a grave finding. A serum pH less than 7.20 may indicate the need for surgical exploration. Activated charcoal decontamination is relatively contraindicated. Endoscopy is recommended after large or deliberate caustic ingestion, presence of oral burns, or persistent refusal to take oral liquids. Steroids are occasionally used as an effort to prevent esophageal strictures in selected patients, but the decision to administer is made based on endoscopic grading in conjunction with the gastroenterologist.

FIGURE 17.70

Caustic Oropharyngeal Burns. This patient suffered caustic burns by accidentally drinking a highly alkali solution that was stored in a soda can. (Photo contributor: Lawrence B. Stack, MD.)


  1. The absence of oropharyngeal burns is a poor predictor of distal esophageal injury. The presence of vomiting, drooling, or stridor is more predictive of significant esophageal injury on endoscopy.

  2. Analogous to thermal burns after smoke inhalation, upper airway edema and airway obstruction may occur abruptly.

  3. Ingestion of muriatic acid (HCl) results in an initial non-anion gap metabolic acidosis.

FIGURE 17.71

Caustic Esophageal Burns. Close-up image of the alkali burns on the tongue of the patient in Fig. 17.70. (Photo contributor: Lawrence B. Stack, MD.)

FIGURE 17.72

Caustic Esophageal Burns. These esophageal burns were caused by an accidental ingestion of lye in a pediatric patient. (Photo contributor: Philip E. Stack, MD.)

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