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According to the 2013 annual report of the American Association of Poison Control Centers, there were nearly 60,000 reported U.S. cases of exposure to caustic agents (48,000 to bleach, 7500 to acids, 4000 to alkalis), most of which occurred by ingestion. The true incidence of caustic ingestion and prevalence of lesions such as strictures is likely under-reported worldwide. There are two age groups at risk for this exposure: children ages 2 to 6 years who ingest household cleaning products and account for up to 80% of caustic ingestion but usually sustain mild injuries; and adults ages 30 to 40 years who have ingested strong corrosives with suicidal intent and present with life-threatening injuries. The diagnosis should be suspected in all patients brought to the emergency department for attempted suicide. Tissue injury from caustic ingestion may be fatal and warrants immediate attention from a wide range of specialties including emergency care physicians, surgeons, anesthesiologists, gastroenterologists, radiologists, otolaryngologists, and psychiatrists. Every effort should be made to identify the ingested substance and the details surrounding the ingestion, because the severity and nature of injury are related to chemical and physical properties of the caustic agent (i.e., acid vs. base, solid vs. liquid form) in addition to the concentration and volume ingested. The properties of the ingested substance affect the duration of contact with the esophagus and influence the likelihood of injuries to other organs (e.g., pharynx, stomach, duodenum, colon),1 ranging in severity from first-, second-, or third-degree burns to full-thickness necrosis and perforation.


In chemical burn injuries, the esophageal sites that are most susceptible are the three areas of normal anatomic narrowing (Fig. 50-1). These are the upper esophagus at the cricopharyngeus, the midesophagus where the aortic arch and left mainstem bronchus cross, and the distal esophagus proximal to the lower esophageal sphincter (LES). Passage of the ingested material is delayed through these regions, increasing the duration of exposure and potential for injury. Reflux-associated LES hypotension causes prolonged exposure of the distal esophagus to the caustic agent. This is exacerbated by pylorospasm, particularly associated with alkali ingestion, which propagates the injury by causing regurgitation of caustic contents back into the esophagus.2 Although there may be relative tolerance of the esophageal squamous epithelium to ingested acid, pylorospasm may lead to pooling of acid, severe gastritis, and full-thickness necrosis with perforation.

Figure 50-1

Anatomy of the esophagus showing areas of normal anatomic narrowing.


Acids cause coagulation necrosis, which is characterized by the formation of eschar. This deposition of dead tissue often limits the injury beyond the superficial esophageal lining, but prolonged gastric contact with pylorospasm explains the preferential stomach involvement by acids. Alkaline exposure causes liquefactive necrosis, which allows the caustic agent to penetrate the esophageal wall more deeply, thereby escalating ...

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