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While accidental ingestion of caustic materials is more common in children, intentional ingestion is the leading cause of caustic esophageal injury in adults. The diagnosis should be suspected in all patients brought to the emergency ward for attempted suicide. The injury may be fatal and warrants immediate treatment. Identifying the nature of the ingested substance is paramount to proper management because the severity and nature of the injury are related to the chemical and physical properties of the caustic agent (i.e., acid vs. base, solid vs. liquid, concentration, quantity, and duration of contact with esophageal tissues).1 These exposures cause injuries ranging in severity from first-, second-, or third-degree burn to full-thickness necrosis and frank perforation, often requiring surgical treatment.


In chemical burn injuries, the esophageal sites 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 black tissue often limits the injury to the superficial esophageal lining. Alkaline exposure causes liquefactive necrosis, which allows the caustic agent to penetrate the esophageal wall more deeply, thereby escalating the severity of the injury.3 Since the degree of injury is also associated with duration of exposure, it is important to determine whether the ingested material is a solid or a liquid. Solid alkali tends to adhere to the oropharyngeal region, whereas liquid alkali passes more quickly, causing greater esophageal and gastric injury.4,5 The three phases of chemical injury are (1) inflammation/necrosis, (2) sloughing and ulceration, and (3) fibrosis with stricture formation. Management is guided by early flexible esophagoscopy to grade the degree and location of injury. Chemical burns are graded according to Zargar's 6-point classification of caustic mucosal injury as assessed from endoscopy.6 First-degree burn (Grade 1) is characterized by hyperemia and edema; second-degree burn (Grade 2A, 2B), by ulceration; and third-degree burn (Grade 3A, 3B), by black or gray discoloration indicative of necrosis.7 First-degree esophageal burns generally ...

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