Asymptomatic children with a history of alkali or acid ingestion should be observed for a few hours and may be discharged from the emergency department if oral intake without discomfort is demonstrated.
All symptomatic children should be admitted to hospital.
Eye exposures require urgent and copious irrigation and referral to an ophthalmologist if injury is present.
Alkalis and acids damage or destroy living tissue on direct contact. This process is generically referred to as corrosion. A caustic is an alkali. Consumer product examples of alkalis and acids include drain cleaners, automatic dishwasher detergents, hair relaxer products, toilet bowl cleaners, and bathroom tile cleaners. Of recent concern has been the formulation of laundry detergent into unit-dose capsules. There have been several cases of significant ocular, oral, esophageal, and neurological clinical effects reported with exposures to these products.1,2 Improvements in safety packaging, child-resistant closures, and federal regulations lowering the maximum concentration for many household alkalis and acids have decreased the overall incidence of unintentional corrosive exposures in children. Despite this success, thousands of accidental and intentional exposures occur annually3 and continue to result in a significant burden on health care resources.4
Exposures in small children are usually limited by pain on contact and generally involve small amounts. Most exposures occur in children younger than 6 years, but this group accounts for only 1.9% of the fatalities.3 In contrast, intentional ingestion by adolescents and adults may involve larger quantities, which generally have a worse outcome. Long-term survivors of moderate and severe esophageal caustic injuries have a 1000-fold increased risk of esophageal carcinomas.5
Alkalis and acids cause tissue damage by different mechanisms. Alkalis cause liquefaction necrosis by a process involving saponification of fatty acids within cell membranes and protein disruption. This produces a rapid, penetrating injury associated with a pronounced exothermic reaction, which can occur in seconds. Ingestions of household bleach containing dilute sodium hypochlorite rarely cause serious injury.6 Higher concentrations found in industrial strength products and lye products containing sodium or potassium hydroxide can cause severe esophageal injuries.7
Acids cause tissue damage by a process known as coagulation necrosis. Hydrogen ions are released when acids come in contact with water and cause tissue damage. A coagulum or eschar may form in some cases and limits the extent and depth of injury. Toilet bowl cleaners and anticorrosive cleaners containing higher concentrations of hydrochloric or other acids can cause serious injuries.
Acids and alkalis can cause both esophageal and gastric injuries. Clinical experience has demonstrated that multiple sites are often affected.8 Following the initial tissue contact, the acid or alkali undergoes a process of neutralization resulting in an exothermic reaction, which may worsen the injury.9
The initial acute inflammatory reaction proceeds on to necrosis. The necrotic tissue is sloughed resulting in ulceration or perforation. After a few days and during the next few weeks granulation tissue develops. Because this tissue is weak, perforation may occur during this period. This is followed by cicatrization producing variable degrees of scarring contracture and stricture formation.
The severity of injury is modulated by several factors (Table 126-1). Solids such as crystals or granules can produce intense localized oral, pharyngeal, or upper esophageal injury while liquids, especially strong bases, tend to produce circumferential lesions in the esophagus, which often form strictures. Products with a pH less than 2 or with a pH of 12.5 or greater are likely to cause significant esophageal injury.10 Increasing volume, concentration, and the titratable alkaline or acidic reserve of the agent correlates with esophageal injury.11
The presence of stomach contents may decrease tissue injury by exerting a buffering effect. Pylorospasm prevents gastric emptying, which increases contact time of the corrosive within the stomach and results in more severe gastric injury. Any reflux of ingested material back into the esophagus re-exposes the tissue to further corrosive damage.
Caustic burns are graded first, second, and third degree based on their endoscopic appearance.12 Grade I injuries are superficial, involve the mucosa, and resemble a sunburn. Strictures would not be expected to develop following this type of injury.