The most common agents responsible for caustic ingestion fall into one of three categories: (a) alkalis, (b) acids, and (c) bleaches. Each of these three categories causes a distinct histologic reaction when it comes into contact with the mucosa of the upper aerodigestive tract. Alkali agents cause liquefaction necrosis, wherein the mucosa disintegrates, allowing the agent to penetrate into the surrounding tissues. This is reflected in the finding of more oral and upper esophageal injury. Alkalis are usually odorless and tasteless, which, in the case of accidental ingestion, may allow for the consumption of large volumes. Ingestion of compounds with a pH between 9 and 11, such as many household detergents, rarely cause serious injury. However, ingestion of even small quantities of an alkali with a pH above 11 may cause severe burns. Specific examples of strong alkali are sodium hydroxides (lye, drain and oven cleaner, and dishwashing detergents) and sodium phosphates (dishwashing detergents and laundry detergents). Granular forms of detergents and cleaners are associated with a higher rate of injury than liquid forms because of their adherence to the mucosa. Another commonly ingested alkaline agent is hair relaxer (2,3,4,5). These agents denature structural proteins, thereby straightening curly hair. Fortunately, the degree of mucosal injury following hairrelaxer ingestion has been found to be mild with little to no adverse clinical effect. Unfortunately, alkaline agents may not be perceived by families to represent a potential hazard because of their ubiquitous nature and lack of childproof packaging.

Acidic agents result in coagulation necrosis, which causes a coagulum to form on the mucosa, thereby limiting deeper absorption until the agent reaches the stomach. In addition, these agents tend to have a low viscosity, which facilitates rapid transit to the stomach. Gastric injury following ingestion may result in gastric outlet obstruction or perforation, which is a potentially life-threatening complication as there can be multiorgan injury and rapid clinical decompensation (6). Fortunately, the bitter taste of acidic compounds may help to lower the volumes of accidental
ingestion. Examples of strong acids that may be found around the home are sulfuric acid (drain cleaner), hydrochloric acid (toilet bowl cleaner), sodium bisulfate (toilet bowl cleaner), and hydrofluoric acid (metal cleaner) (6).

Bleaches, which are essentially of neutral pH, are considered esophageal irritants. Large series of patients with bleach ingestion have shown no significant morbidity or mortality. For this reason, extensive workup of patients following bleach ingestion is not warranted (7).

The amount and type of agent ingested, the presence of food in the stomach, gastrointestinal transit time, and the presence of gastroesophageal reflux will all contribute to the extent and severity of injury following caustic ingestion. Initial contact of the caustic agent with the mucosa produces immediate changes that then progress over the following 2 to 3 days. After this acute phase, a latent period begins, during which stricture formation may occur. This process may proceed as rapidly as within 1 month, or slowly evolve over years. Superficial mucosal burns tend to heal without sequelae. Burns that are deep enough to disrupt the submucosa and muscular layer tend to be complicated by a significant loss of mucosa. In these cases, an intense inflammatory response develops in the burned area, with accompanying esophageal dysmotility. In response to the injury, fibroblasts produce a matrix of newly formed collagen fibers, which begin to contract 3 to 4 weeks after the initial insult. Contraction enables adhesive bands to form, which can then lead to the development of both pseudodiverticula and endoluminal strictures. Stricture formation may evolve to include both the submucosal and muscular layers. In general, only circumferential esophageal injuries lead to strictures severe enough to cause clinically significant morbidity.

Caustic ingestions occur most frequently in children younger than 6 years, with the majority of cases occurring in children between 12 and 48 months of age (6). In general, the child has to be ambulatory and have access to cabinets or other areas where cleaning products are stored. The most common symptoms following a caustic ingestion are dysphagia, drooling, food avoidance, and vomiting. More ominous signs and symptoms, such as severe retrosternal or thoracoabdominal pain or tachycardia with hypotension, may be associated with significant gastrointestinal injury. Dysphonia or stridor may herald progressive airway obstruction. The prognostic significance of the presenting clinical signs and symptoms following caustic ingestion has been widely addressed in the literature (8,9). Although minor symptoms do not rule out the presence of relevant injury, an increased number of symptoms do correlate with a greater likelihood of significant injury. A recent Italian study of 102 children reported that the presence of three or more symptoms was an important predictor of severe esophageal burns (10). In the same series, the absence of signs and symptoms was associated with a very low relative risk of severe lesions. However, it is important to note that in this series, 2 of the 70 patients (2.8%) without symptoms had severe injuries on endoscopy.

Even the presence or absence of oral injuries, such as lip or buccal mucosa burns, does not accurately predict the presence or absence of more distal involvement. In a recent survey by Dogan et al. of 473 pediatric caustic ingestions, 240/389 (61%) patients without oral cavity burns had esophageal lesions found at endoscopy (11). A study by Hawkins et al. showed that 70% of patients with oropharyngeal burns did not manifest associated esophageal injuries (12). Therefore, neither the presence nor absence of visible injury on physical exam should influence further investigation.