Caustic Injury of the Esophagus

Each year in the United States, 34,000 people ingest caustic substances ( Fig. 7.1 ), leading to tissue destruction through liquefaction or coagulation reactions. The severity of destruction depends on the type, concentration, and amount of substance; whether it is in solid or liquid form; and the duration of contact with the esophageal mucosa. Ingestion of a caustic substance is the most common toxic exposure in children and is almost always accidental. In all patients, 60% of cases of caustic substance ingestion is suicidal, and in 40% it is accidental. Adults usually ingest caustic substances in attempts at suicide and are likely to have more severe injuries.

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Caustic Injury.

The most commonly ingested substances with suicidal intent are strong alkali composed of lye with sodium or potassium hydroxide. Solid crystal lye was most often used for suicide attempts until 1960, when liquid oven cleaners became most common. Liquid oven cleaners cause more distal esophageal burns that are more severe than those caused by lye. Household products such as drain cleaners and other house cleaning products are also common. Highly concentrated acids such as hydrochloric, sulfuric, and phosphoric acid used in toilet bowl or swimming pool cleaners are less common. Bleach, which is 5% sodium hypochlorite, rarely causes a severe esophageal injury. Batteries containing highly concentrated alkaline solutions can cause burns and perforations and should be removed emergently with endoscopy.

Alkali ingestion is more caustic to the esophagus compared with the more distal stomach and bowel, but acid such as glacial acetic acid results in a worse outcome. Acid victims were more likely to have severe mucosal injury, be in an intensive care unit, have perforation, and suffer higher mortality. Ingestion of alkali such as ammonia or sodium hydroxide results in a full-thickness injury to the esophageal wall, causing liquefactive necrosis at a pH greater than 11; this may result in perforation and mortality. The liquefactive process progresses over 4 days, leading to mucosal inflammation, thrombosis of vessels, and ulceration of the esophageal lumen. Cell death is complete by 4 days, and 80% of scars are formed within 60 days. The natural areas of esophageal approximation include the cricopharyngeus, aortic arch, and lower esophageal sphincter and are most commonly involved.

Over 2 weeks the wall becomes thin; fibrosis and regrowth occur, but this process is not complete for 3 months. The development of strictures depends on the depth of damage and degree of collagen deposition. The ingestion of alkali leads to esophageal stricture formation more often than exposure to acid. Morbidity and mortality result most often from severe second- and third-degree burns. Compared with alkali injury, acid-induced injury creates a superficial coagulation necrosis where the mucosal blood vessels thrombose and the connective tissue forms a protective eschar. Acid injury is also limited as it causes pain on contact, thus limiting intake, and moves quickly into the stomach.