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.

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 require observation alone because these injuries do not cause perforation or strictures. Second- and third-degree burns of the esophagus require ongoing monitoring for perforation or progression to generalized necrosis. Perforation or near-perforation requires immediate surgical intervention (see Chapter 48), whereas the absence of full-thickness necrosis and perforation necessitates frequent reevaluation and investigation over a prolonged time period.

The symptoms of caustic ingestion include oral pain, drooling, inability, or refusal to swallow secondary to pain, and hematemesis. Hoarseness, stridor, or dyspnea suggests a laryngeal or supralaryngeal injury. Airway management is of paramount importance because of possible associated burns to the larynx. Intubation guided by fiberoptic or rigid bronchoscopy should be performed. One should be prepared to perform a surgical airway if required. After the airway is addressed, a thorough history and physical examination is completed. History includes verification of the caustic agent and documentation of the time between exposure and treatment. Symptoms of acute perforation include progressive neck, substernal, back, or abdominal pain. Signs of acute perforation are tachycardia, fever, subcutaneous emphysema, pericardial crunch, and chest dullness to percussion. Absence of symptoms does not entirely exclude significant injury, but the number of signs and symptoms present correlates with severity of injury.

Radiologic evaluation may include chest x-ray and CT scans to rule out pneumomediastinum or free intraperitoneal air. Initial CT scans of the neck, chest, and abdomen may be performed without contrast agents, although the administration of water-soluble contrast material improves the predictive value of the scans. Barium esophagram is of limited utility in the initial evaluation as it carries a 30% to 60% false-negative rate.⁸

All caustic ingestion patients are monitored with telemetry and resuscitated with IV fluids. Patients are kept nothing by mouth and given prophylactic IV H₂-blockers or proton pump inhibitors for both symptom relief and to treat reflux.⁹ Flexible esophagoscopy is used for evaluation in nearly every patient with esophageal caustic injury. There is controversy regarding the optimal timing for initial endoscopic evaluation.¹⁰ In the past, there was a tendency to wait at least 24 hours of injury, after the patient had been medically stabilized. Most agree that flexible esophagogastroduodenoscopy for complete evaluation should be carried out between 12 and 24 hours after injury (see Chapter 14). Endoscopy past 48 hours is discouraged due to the increased risk of perforation attributable to progressive wall weakening. Esophagogastroduodenoscopy may be impossible to complete depending on the severity of the patient’s injury. The flexible scope may be carefully advanced past a site of mild injury but should be stopped at the site of circumferential Grade 2 and 3 injuries. Endoscopy distal to the site of first injury risks iatrogenic perforation.

Patients with first-degree burn are observed for at least 48 hours while their oral diet is advanced cautiously. Patients with second- or third-degree injuries without perforation should be admitted to the ICU and treated with broad-spectrum antibiotics and possibly steroids. While controversial, the administration of antibiotics and steroids may help to lessen gastrointestinal bacterial translocation and to decrease inflammation, respectively.^11–13 This may decrease the frequency and severity of stricture formation, as well as the necessity of multiple subsequent esophageal dilations, although the side effects of steroids with regard to increased susceptibility to infection should be carefully considered. Steroid administration also may relieve airway obstruction owing to mucosal edema and bronchospasm in the acute setting.⁷ Reflux secondary to impaired esophageal function at the LES may also increase the potential for stricture formation. Proton pump inhibitors are employed to reduce reflux. Patients are monitored with serial chest x-rays. NPO status is maintained until the patient is able to swallow saliva without pain. A means for either enteral or parenteral nutrition is established. Rigid endoscopy is recommended for the safe placement of nasogastric tube, which serves both to stent the area of injury as well as to provide enteral nutrition. An initial esophagram with water-soluble contrast material is obtained within 48 hours and may be repeated at intervals as clinically indicated. Consideration may be given to various surgical treatments (discussed below) throughout the patient’s hospital course.

Intermediate-term follow-up at 3 to 4 weeks, 3 months, and 6 months is necessary to monitor for stricture formation, gastric outlet obstruction, and the development of hourglass esophagus or linitis plastica.^1,10,14 After 6 months, long-term follow-up is required to monitor for the development of esophageal dysmotility or esophageal squamous cell carcinoma.

Surgical management of chemical and burn injuries of the esophagus includes several broad categories of procedures and operations. Initial diagnostic procedures include bronchoscopy and esophagogastroduodenoscopy. Exploratory laparotomy, esophageal stenting, and enteral feeding tube insertion or parenteral feeding access are surgical procedures used often during the initial hospitalization of a chemical burn injury patient. Surgical intervention in the acute setting is rare but may be indicated for a full-thickness injury that results in esophageal perforation or diffuse necrosis evidenced by a systemic inflammatory response. Surgical techniques employed in this setting include esophageal resection and diversion, as is applied in severe cases of necrotizing esophageal perforation (see Chapters 48, 51, and 58).

In the subacute phase, esophageal dilation is often required for the treatment of strictures. Surgical resection with reconstruction may be considered in the chronic phase of injury after a severely strictured esophagus has failed repeated dilations. Esophagectomy ultimately may be required to reduce the risk of late carcinoma, which approaches 40% and manifests after a delay of 20 to 50 years.^15,16