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Figure 1A: Endoscopic view of the posterior pharyngeal wall at the level of the epiglottis (denoted with **). Note early eschar formation. Figure 1B: Endoscopic view of the pyriform sinus with extensive eschar formation.

Despite educational campaigns, improved warning labels and child-resistant packaging, accidental ingestion of caustic substances by children still occurs. It is estimated that in the United States in 2008, more than 200,000 cases of caustic substance ingestion (CSI) were reported. CSI occurs more commonly in boys and during the spring and summer months. Children around the age of three are most commonly affected, and most injuries occur in the home. Liquids stored in non-original containers, usually improperly labeled water bottles, are a frequent source of exposure. These containers often lack child-proof caps and are mistaken by children for beverages.  

CSI can inflict a broad range of damage, dependent primarily on the form and the pH of the material ingested. Strong acids tend to have a powerful taste that may limit the amount swallowed. Furthermore, most acids have a rapid transit time through the pharynx and esophagus and tend to cause most of their damage in the stomach. Alkaline agents can be more palatable and tend to cause damage to the pharynx, airway and esophagus. Mucosal damage occurs within seconds of exposure to a strong acid or alkaline substance, however the damage caused by these two types of agents varies greatly (a 30% solution of sodium hydroxide can induce full thickness injury with only 1 second of tissue exposure). Acid initiates a coagulation necrosis within the mucosa with limited depth of penetration in most instances. Alkaline agents, in contrast, penetrate more deeply into tissue and induce a liquefactive necrosis that is followed by tissue ischemia and thrombosis. An eschar forms but tissue damage continues deep to this until the agent can be neutralized. Within the first 24 hours after exposure, an intense inflammatory response begins. If the damage is transmural, this can lead to perforation. Bacterial contamination occurs and small abscesses can develop within the injured tissue, furthering the inflammatory response and increasing the potential for serious complications. The involved tissue will begin to slough several days later and the inflammatory response resolves. Gastroesophageal reflux can develop from dysfunction of the lower esophageal sphincter and contribute to stricture/scar formation. Around the third week after caustic ingestion, scar formation sets in, and this is when stricture formation is likely to occur. If enough muscle is replaced by scar in the esophagus, long term motility issues may also develop.

The clinical presentation of a child with CSI can vary depending on a number of factors. Most commonly children present with drooling, odynophagia, obvious oral mucosal burns, chest/abdominal pain and a reluctance to swallow/eat. Stridor, dysphonia, and retractions can herald airway compromise, which may necessitate acute airway management.

Studies have sought to determine which presenting symptoms would warrant further evaluation via EGD and possibly microlaryngoscopy and bronchoscopy to assess the degree of mucosal damage.   Strong relationships between certain presenting signs/symptoms and endoscopic grades of injury have concluded that examination of the aerodigestive tract is not indicated in all cases of CSI. The DROOL system put forth by Uygun and colleagues is a noninvasive scoring method that takes into account the duration and severity of several presenting signs and symptoms. These include: "D" - drooling of saliva, "R" - reluctance to eat or food intolerance, "O" - oral or oropharyngeal burns, "O" - other symptoms (fever, hematemesis, abdominal pain, dyspnea, chest pain) and "L" - leukocytosis > 20,000. Unfavorable DROOL scores are highly correlated with eventual stricture formation.

The primary assessment of a child who has sustained a CSI must include an assessment of impending airway issues. If the airway is stable, focus can turn to the nature of the injury, timing, substance ingested and whether or not other toxic side-effects are occurring. It is not recommended to induce vomiting (repeated exposure to chemical), administer charcoal (does not absorb caustic agents) or dilute the agent with water/milk (no human studies have shown benefit to this). The poison control center should be notified to provide any additional information about other possible chemicals within the ingested substance. A chest xray should be performed within the emergency room to evaluate for mediastinal or peritoneal air. A complete blood count should also be obtained. The possibility of intentional ingestion must be entertained, especially in older children. These cases tend to have much higher exposure levels and patients may not admit to symptoms. Some authors recommend formal mucosal examination for all intentional ingestions.

The management of children with accidental CSI remains somewhat controversial. Many different specialties (emergency medicine, pediatrics, pediatric GI, pediatric surgery and otolaryngology) may all be involved and this can complicate management strategies.   Most would agree that early examination of the involved mucosa within 48 hours of the injury is the safest and most effective way to assess the extent of the injury, however, identifying which patients should undergo early examination is not clearly defined in the literature. Some authors feel that it is safe to perform EGD up to 96 hours after exposure. We prefer to examine within the first 48 hours if possible given the possible increased risk of perforation with prolonged waiting times. Examination can reveal pharyngeal injury not seen on initial physical exam (Figure 1), demonstrate injury to the larynx, and also evaluate the extent of any esophageal injury.

Multiple medications have been used in the management of CSI (antacids, neutralizing agents, corticosteroids, antibiotics and others), however no consensus exists as to their exact role. A recent meta-analysis concluded that corticosteroids did not reduce the incidence of esophageal stricture formation. They may play some role in the management of airway symptoms should they be present. The role of antibiotics in the routine management of CSI patients is controversial. Many would argue that antibiotic use is warranted in patients with extensive necrosis of the pharyngeal or esophageal mucosa, evidence of sepsis or perforation of the esophagus.        

1. Uygun, I. Caustic oesophagitis in children: prevalence, the corrosive agents involved, and management from primary care through to surgery. Curr Opin Otolaryngol Head Neck Surg. 2015;23:423-432.
2. Miller AJ, Cox SG. Caustic injury of the oesophagus. Pediatr Surg Int. 2015;31:111-121.
3. Park KS. Evaluation and management of caustic injuries from ingestion of acid or alkaline substances. Clin Endosc. 2014;47:301-307.
4. Uygun I, Aydogdu B, Okur MH, et al. Clinico-epidemiological study of caustic substance ingestion accidents in children in Anatolia: the DROOL score a new prognostic tool. Acta Chir Belg. 2012;112:346-354.