| Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Caustic Ingestion in Children Caustic ingestion became a significant concern in the late 1800s and 1900s when lye products became available as household cleaners. Accidental ingestion of these products led to serious upper aerodigestive and esophageal injuries in children. Because of this growing problem, Chevalier Jackson became a pioneer against caustic ingestion, and his efforts resulted in the Federal Caustic Act of 1929 which mandated basic labelling of toxic substances. Further advances in the campaign against caustic ingestion included the creation of the Poison Control Center (1953) which provided a central source of information about product contents, toxicity, and treatment of poisoning. Also, the Poison Prevention Packaging Act (PPPA) was passed in 1970 which required toxic products to be packaged in "child-proof" containers. The effects of these legislative efforts were dramatic as the incidence of caustic ingestion dropped from 500,000 to 2,000,000 prior to 1970, to 95,000 in 1973. A recent survey in 1990 revealed only 26,000 cases, with 17,000 of these occurring in children. In all reported series, the substances causing burns most frequently were alkalis, estimated at 60 to 80% of the cases. The remainder of cases of caustic ingestion were due to acids and substances such a Lysol (phenol based) and bleach (sodium hypochlorite). Alkalis include sodium, potassium, and ammonium hydroxide and are bases that dissolve in water. They all contain a positive radical and a hydroxyl group. Alkalis produce a liquefactive necrosis when they come in contact with mucosa and penetrate deeply with full thickness burns common. Acids are compounds that contain hydrogen and one or more nonmetals. Most are soluble in water and create a pH environment of less than 7.0 which causes coagulative necrosis when contacting mucosal surfaces. This coagulum tends to limit the penetration of the acid substance, thus helping to prevent full thickness burns. Phenol (hydroxybenzene) is an acidic compound found in Lysol, and bleach contains 5.25% sodium hypochlorite which has an acidic effect when contacting moist substances. In general, these weaker acidic compounds mainly result in mucosal erosion with greater quantities required to cause serious mucosal injury. It is important to ascertain the type and quantity of substance that a patient is suspected of ingesting. Frequently, parents can provide only the name of the substance, and if they did not bring the container, the composition can be found by contacting the Poison Control Center. A careful history should include questions on the amount ingested and whether the child has vomited. Emesis may result in repeated esophageal/hypopharyngeal exposure to the caustic substance with increased severity of burns. Physical examination may reveal the presence of burns on the lips, chin, hands, and chest due to manipulation of the substance or regurgitation. The most common presenting complaints are dysphagia, odynophagia, and drooling with 40% of children describing severe pain. Edema and erythema of the lips, tongue, and palate are found in 75% of children. It is important to note, however, that the extent of signs and symptoms do not predict the presence or severity of hypopharyngeal or esophageal symptoms. Acute management involves stabilizing the airway and maintaining the circulatory system (ABC's). After a complete head and neck examination, a chest radiograph should be obtained to view the mediastinum and subdiaphragmatic regions to look for free air as an indication of viscous perforation. The majority of clinical experts recommend esophagoscopy within the first 24 to 48 hours after caustic ingestion. It is generally held that after two days esophagoscopy has an increased risk of iatrogenic injury (perforation) because the esophagus is weakest at this point. One should not advance the rigid scope beyond circumferential burns or the first significant ulcer. For children that present beyond 48 hours after caustic ingestion, a barium swallow should be obtained to evaluate esophageal injury. Emetics and gastric lavage are not indicated as they only increase the exposure of caustic substance or risk of perforation. Patients should be maintained NPO until they can swallow their own secretions or until a barium swallow reveals adequate esophageal transit and mucosal surface. Controversy exists as to whether a nasogastric tube should be placed at the time of esophagoscopy, and total parenteral nutrition should be considered for extended periods of NPO when no NG tube is used. Although the use of antibiotics and steroids are also controversial, the majority of authors recommend an antibiotic such as ampicillin and steroids for moderate to severe aerodigestive mucosal injury. Esophageal strictures are not uncommon with moderate to severe mucosal injury and typically become evident within the first 4 to 6 weeks. These strictures can usually be managed by antegrade or retrograde dilation; however, refractory strictures that result in malnourishment may require partial or complete esophagectomy or even gastrectomy in the most severe of cases. The severity of injury from caustic ingestion depends on the type, quantity, concentration, and time of exposure to the toxic substance. Evaluation begins with a thorough history and physical and diagnostic studies should include a chest x-ray and exam under anesthesia with esophagoscopy or barium swallow if presentation is beyond 48 hours. Efforts to reduce granulation and inflammation and reduce stricture formation include maintaining the child NPO and adding steroids and antibiotics for moderate to severe mucosal injury. Treatment for stricture formation involves antegrade or retrograde dilation which controls the majority of cases, with more radical surgery reserved for only the most severe strictures that result in malnutrition. Case Presentation: A 6-year-old African-American, female child with a history of chronic bronchopulmonary dysplasia and developmental delay, presented to the emergency room with complaints of low grade fever and reluctance to drink for two days. The patient had a negative physical exam and a CXR was designated "no pneumonia" by the ER pediatrician. She was given Bactrim for a urinary tract infection and discharged home. The following morning a radiologist's review of the CXR noted a foreign body in the esophagus and the patient was called back into the emergency room and an otolaryngology consultation was obtained. Physical examination revealed a child with mild drooling, a temperature of 100.5, and otherwise no distress. Oral cavity exam was normal, neck exam revealed a mature tracheostomy present since infancy, and the remainder of the exam was negative. Laboratory evaluation was significant only for a WBC of 15.The patient was taken to the operating room where laryngoscopy was normal and esophagoscopy revealed a corroded battery lodged in the upper esophagus. There was circumferential mucosal ulceration at the level of the battery with extension to the muscularis layer anteriorly and no evidence of perforation. After removal of the battery, the esophagus was irrigated with saline and the patient was started on IV antibiotics and steroids. The patient was maintained NPO for three days and remained afebrile. A barium swallow on hospital day four revealed some irregularity in the upper esophagus with overall good passage of barium and no extravasation. The patient tolerated a full liquid diet and was subsequently discharged home with a three week taper of oral prednisone.
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