Airway management and recognition of esophageal or gastric perforation are the highest priorities. Fluid resuscitation and supportive care are critical to the treatment of the patient with a caustic exposure. Patient should not be fed until it is deemed safe to do so.
Laboratory and Radiology Studies
In patients with signs of respiratory distress, oxygen saturation or arterial blood gases along with a chest radiograph should be obtained, since many caustics are powerful emetics and, if aspirated, can cause severe pneumonitis or noncardiogenic pulmonary edema.
Laboratory studies should include blood pH, complete blood count, electrolytes, renal function, coagulation profile, and serum lactate. Patients with abdominal pain or tenderness also require radiologic evaluation to exclude the presence of free air. The initial evaluation immediately following a caustic ingestion is esophagoscopy; a contrast esophogram may be useful to identify strictures at a later point.2
Some medical sources and product labels may still advocate neutralization of caustics with acidic substances such as lemon juice or vinegar after an alkali ingestion, or sodium bicarbonate following an acid ingestion. Most authors, however, now advise against neutralization of a caustic due to the concern that attempting to buffer a strong acid or alkali may lead to an exothermic reaction and worsen tissue destruction. There may be a role for diluents, however, in the ingestion of a weak acid since such injuries are usually purely caustic and there is no risk of thermal injury. Studies demonstrate limited effects of diluents and extrapolation of these studies suggests that dilutional therapy is probably most beneficial in the first seconds or minutes after ingestion.2,3 Milk or water dilution may be indicated in an attempt to move particulate material out of the oropharynx and esophagus. The amount given should be easily tolerated by the child; gastric distention from too much fluid can precipitate emesis. Dilutional therapy should be limited only to those patients with no airway compromise, no drooling or vomiting, and no chest or abdominal pain. There is probably no value in administering diluents in liquid alkali ingestions because the injury is likely to be complete in a very short time.3
Induction of emesis in caustic ingestions is absolutely contraindicated, since increased tissue damage can occur as the esophagus is reexposed to the offending agent. Violent episodes of emesis can increase risk of both pulmonary aspiration and esophageal perforation.
In general, there is no role for gastric emptying in accidental caustic ingestions. Risks include induction of emesis, aspiration, or perforation. Cautious placement of a small bore nasogastric tube in a massive intentional ingestion of a potentially lethal acid could potentially be considered if the benefits are judged to greatly outweigh the risks. However, these situations are very rare and should be seriously considered only in massive ingestions where the patient presents within minutes to the hospital.2 The administration of charcoal is not recommended because caustics are poorly adsorbed by charcoal, and charcoal creates a problem with visualization for the endoscopist.
The challenge in managing the child with a caustic ingestion is in identifying the patient who is at risk for a serious injury. Several studies indicate that the clinical manifestations of caustic ingestion injuries are poor predictors of the severity of injuries. There is no correlation between the presence or absence of oral burns and the presence of esophageal or gastric injuries. Crain et al. found that 33% of patients with evidence of oral cavity burns had esophageal burns.4 Dogan et al. found that 61% of 389 patients with no oral burns had esophageal lesions.5 Wijburg et al. found esophageal lesions in 39% of children who were suspected of having ingested a caustic agent.5 In Gandreault's study of 378 children with caustic ingestions, 10 of 80 children who were asymptomatic had grade II lesions on endoscopy. If two of the three symptoms of vomiting, drooling, or stridor are present, the likelihood of gastrointestinal burns is high. Of the three, vomiting is the most powerful predictor of severe esophageal injury.6
Endoscopy should ideally be performed within 12 hours and no later than 24 hours after the ingestion, because the risk of perforation begins a few days and continues for 2 to 3 weeks after the exposure.2 Early endoscopy helps to define the extent of the injury and to establish a prognosis.7 Caustic injury is categorized as first, second, and third degree, based on appearance at endoscopy. Any child with a history of a potentially significant ingestion, with oral lesions, or who is otherwise symptomatic, warrants endoscopy. Most intentional ingestions warrant endoscopy. For asymptomatic patients with accidental ingestions of household bleach, ammonia, or nonphosphate detergents, observation may be acceptable. Evidence of perforation or shock is a clear contraindication to endoscopy.
Immediate surgical involvement is advised if endoscopy demonstrates evidence of perforation. Other signs in which surgical consultation is warranted include severe abdominal tenderness or rigidity, hematemesis or melena, worsening acidemia, hypotension, or shock.
Steroids remain a controversial aspect of management of caustic ingestions. Theoretically, steroids decrease the incidence of esophageal strictures in patients with severe burns; they have been shown to decrease the incidence of strictures in animal models.3 In humans, studies show conflicting results.8 Steroids are not indicated for first-degree burns, because they do not form strictures. Third-degree burns invariably develop strictures, and since steroids may significantly increase complications, they are not recommended. Steroids may be of benefit in second-degree burns. Potential adverse effects of steroids include risk of infection and perforation. The potential benefit of steroids in this setting must be weighed against the risks.
Antibiotics should be reserved for suspected or documented infections. If systemic steroids are administered, prophylatic antibiotics are often given concurrently.3
Dermatologic burns are treated with debridement, topical antibiotic ointments, and sterile nonadherent dressings. Silver sulfadiazine can be used for second-degree burns. Deep second- or third-degree burns, especially to the face or hands, should be evaluated by a burn specialist.
Caustic eye injuries can have devastating consequences, including blindness. The alkaline by-products of sodium azide released in automobile air bags can cause ophthalmic injury. The cornerstone of management of ophthalmologic exposure is immediate irrigation of the eye for a minimum of 15 to 20 minutes with 0.9% saline, lactated Ringer's solution, or tap water. Irrigation is intended to dilute the offending xenobiotic, remove the xenobiotics, remove any foreign bodies, and normalize the pH. Delays of just a few minutes can affect outcome dramatically. After exposure to acids or alkalis, normalization of the conjunctival pH is often suggested as a useful end point. Full extent of injury may not be evident for 48 to 72 hours. Ophthalmologist evaluation is recommended for all ophthalmic caustic injuries.
Button batteries are frequently swallowed by children. The batteries contain a metallic salt in a concentrated alkaline medium. Although the vast majority of patients do well, this ingestion poses a unique injury, and rare deaths have occurred. In Litovitz's study of 2382 cases of battery ingestion, 2 patients had life-threatening symptoms; both had batteries lodged in the esophagus. The study also showed that 61% of the batteries passed spontaneously within 48 hours and 86% within 96 hours.9 Historically, leakage of battery contents was a legitimate concern; new production techniques are much more effective at preventing leakage of battery contents.
Pressure necrosis at the site where the battery becomes lodged can occur. Lodging is most likely to occur at regions of anatomic narrowing, such as the cricopharyngeus, where the aorta or carina cross the esophagus, or in gut malformations such as Meckel's diverticulum. Rarely, if the battery does break open, the caustic contents may cause ulceration, perforation, or rarely fistula formation. Heavy metal absorption may occur, although clinical toxicity from battery ingestion has not been reported. Finally, injury from electrical current can also occur.
A battery lodged in the esophagus or airway requires urgent removal. Burns have been reported as early as 4 hours after ingestion, and perforation in as early as 6 hours.9 The preferred method of extraction is endoscopy, which allows direct visualization of any esophageal injury. Buttons lodged in nasal passages should also be removed immediately.
If a swallowed battery has passed through the esophagus, as apparent from radiographs, watchful waiting is acceptable, unless there are signs and symptoms of intra-abdominal injury. A large battery ingested by a small child may also require removal. If a battery greater than 15 mm in diameter ingested by a child younger than 6 years of age has not passed the pylorus within 48 hours, it is unlikely to do so.
An asymptomatic patient with a battery that has passed the esophagus can be discharged and followed as an outpatient with serial radiographs to document passage of the battery. Daily radiographs are also recommended. Passage of the battery can be followed by straining the stool. Whole bowel irrigation is an option.
Hydrofluoric acid (HF) is a weak acid found in some cleaning and rust-removing products. External contact can result in severe dermal or ocular injury. Death has been reported with exposures affecting as little as 2.5% of the body surface area. Severe pain and deep penetration despite minimal skin findings is the hallmark of a hydrofluoric acid burn. The mechanism of injury involves liquefaction necrosis and the formation of insoluble calcium and magnesium salts. Oral ingestions are frequently fatal. In cases of significant burns, systemic acidosis, hypocalcemia, hypomagnesemia, and hyperkalemia are common. Renal failure and hemolysis have also been reported to occur.10
En route to the emergency department, decontamination of all burned areas with copious irrigation is indicated. Calcium gluconate gel (2.5%) can be applied topically to HF burns. If unavailable, it can be prepared using 3.5 g of calcium gluconate powder and 150 mL of a sterile water-soluble lubricant (K-Y Jelly), or 25 mL of 10% calcium gluconate in 75 mL of sterile water lubricant. Persistent pain may be alleviated by intradermal injection of calcium gluconate. Calcium chloride or calcium carbonate can be substituted for calcium gluconate. Intra-arterial infusion of calcium gluconate can be considered for refractory cases or cases involving HF burns to arms or legs. Hypocalcemia from ingestions of HF are often refractory to treatment and may require large amounts of calcium (Table 113–2). Ocular HF exposures require immediate copious irrigation with 0.9% normal saline or tap water, if available. One percent calcium gluconate ophthalmic drops have been suggested, although calcium salts may be very irritating to the eye.
Table 113-2. Replacement Therapy for Hypocalcemia* |Favorite Table|Download (.pdf)
Table 113-2. Replacement Therapy for Hypocalcemia*
(Repeat q 10 min as needed; follow QTc, labs, and clinical condition)
(Repeat q 10 min as needed; follow QTc, labs, and clinical condition)
1 amp (10 mL of 10%) over 5 min
10–30 mL of 10% IV over 5 min
10–25 mg/kg up to 1 amp per dose
30–75 mg/kg over 5 min, up to 1 g/dose