While accidental ingestion of caustic materials is 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 versus base, solid versus 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. 42-1). These are the upper esophagus at the cricopharyngeus, the midesophagus where the aorta and left main stem bronchus impinge, and the distal esophagus proximal to the lower esophageal sphincter. Passage of the ingested material may be delayed through these regions, increasing the duration of exposure and potential for injury. Lower esophageal sphincter hypotension associated with reflux 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 While there may be relative tolerance of the esophageal squamous epithelium to ingested acid, pylorospasm still may lead to pooling of acid, severe gastritis, and full-thickness necrosis with perforation.
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 of injury, usually within 24 hours of injury, after the patient has been stabilized. First-degree burn is characterized by hyperemia and edema; second-degree burn, by ulceration; and third-degree burn, by massive edema often with eschar formation with or without full-thickness necrosis, which may depend on the acid or basic nature of the ingestion.6 First-degree esophageal burns generally require observation alone because these injuries do not cause ...