The first priority is airway maintenance. Patients with respiratory distress may have significant oral, pharyngeal, and/or laryngotracheal injuries that require emergent airway management. If emergency airway management precedes patient decontamination, prevent exposure to the ED staff. Caustic airway injuries are difficult airways. Ideally, patients with potential airway injuries should have fiberoptic evaluation of the airway before intubation to determine the extent of the damage, but this may not always be possible. Blind nasotracheal intubation is contraindicated due to the potential for exacerbating airway injuries. Oral intubation with direct visualization is the first choice for definitive airway management. For potential airway compromise, establish a secure endotracheal airway early rather than risk greater difficulty later when secondary effects of injury, such as edema, complicate the situation. Cricothyrotomy may be needed if oropharyngeal edema, tissue friability, and bleeding make intubation difficult or impossible.
Avoid laryngeal mask airways, combination tubes with pharyngeal and tracheal balloons, retrograde intubation, and bougies because these devices/techniques can increase tissue damage or cause perforation.
DECONTAMINATION, NEUTRALIZATION, AND DILUTION
The ED staff should take precautions to prevent ongoing injury to the patient and staff from continued caustic exposure. ED staff involved should wear protective gowns, gloves, and masks with face shields. Standard decontamination, with removal of soiled or soaked clothing and copious irrigation with towels and soap (as needed), is adequate in most cases. Vomiting may re-expose patient and staff to the caustic agent.
Gastric decontamination with activated charcoal is contraindicated if a caustic is the only ingestion. Charcoal does not adhere well to most caustics and will impede visualization when endoscopy is performed. However, activated charcoal may be considered when coingestants pose a risk for severe systemic toxicity.48 Ipecac syrup is contraindicated, because vomiting will result in repeat exposure of the airway and GI mucosa to the caustic agent and could precipitate perforation.49
In general, do not insert nasogastric tubes until after endoscopic evaluation. With high-grade esophageal burns, feeding tubes may be inserted under endoscopic guidance if clinically indicated.
Dilution and neutralization therapy are not recommended in the prehospital setting or ED because there is no proven human benefit and potential risk of gastric distension, vomiting, and perforation.50,51,52,53
Establish large-bore IV access and resuscitate with crystalloids. Coingestants, bleeding, and third spacing, as well as metabolic disarray from acid-base derangements, can lead to shock. Central venous access may be required for monitoring of resuscitation.
SYSTEMIC STEROIDS AND PROPHYLACTIC ANTIBIOTICS
There is currently no evidence of consistent benefit from systemic steroids, so steroids are not recommended as part of ED treatment.54,55,56,57,58,59,60
The ability of steroids to inhibit the inflammatory response led to the hypothesis that steroids may decrease stricture formation after caustic ingestion, and animal models have suggested benefit. However, individual human trials and pooled meta-analysis have not shown benefit for injury,54,55,56,57,58,59,60 and steroids may increase the risk of infection, perforation, and hemorrhage.56
One criticism of pooled meta-analysis data is that the individual studies did not clearly distinguish between grade 1 and 2A lesions, which do not typically lead to strictures, and grade 2B and 3 injuries, which might theoretically benefit from steroids.59
There is no current evidence to support the ED administration of prophylactic antibiotics after caustic ingestions in humans. However, in protocols in which steroids are used or in grade 2B or 3 injury, addition of penicillin or another antibiotic that covers oral flora has been part of treatment regimen.56,61 Because steroids have largely fallen out of favor, the need for antibiotics in the ED is rare.
SURGERY AND ESOPHAGEAL STENTING AND DILATION
Major ingestions of caustic agents may result in perforation of the GI tract or extensive tissue necrosis requiring emergency surgery.62,63,64,65,66,67 Laparotomy is generally preferred over laparoscopic evaluation for posterior gastric visualization. The indications for emergency laparotomy include esophageal perforation, peritoneal signs, or free intraperitoneal air. Large-volume ingestions (>150 mL), signs of shock, respiratory distress, persistent lactic acidosis, ascites, and pleural fluid may be other indications for surgical exploration.62
For grade 2B and 3 injuries without obvious perforation, recommendations include a period of esophageal rest,68 early gastrostomy for enteral feeding,38,69 and dilation therapy (in the first 3 weeks) with or without stenting.70,71,72,73 Once strictures form, they may be difficult to treat and require stenting and/or multiple balloon dilatations or bouginage.9 Controversy exists about the most appropriate treatment for esophageal stricture (i.e., long-term repetitive dilation therapy versus surgery).9,72,73,74
TREATMENT OF SYSTEMIC TOXICITY
Morbidity or death from alkali injuries usually results from the complications of direct tissue necrosis, but acid ingestions may result in additional systemic toxicity from absorption of the acid.18 Acid-base disorders (increased anion gap or normal anion gap acidosis depending on acid ingested), hemolysis, coagulopathy, and renal failure may result. In cases of systemic toxicity, traditional critical-care principles should be applied to optimize the patient's hemodynamics. Acute lung injury (noncardiogenic pulmonary edema) may follow caustic ingestions as a complication of local or systemic effects.
Nutritional support is often necessary following a severe caustic injury to the esophagus or stomach. Support can be achieved by percutaneous (usually jejunostomy) feeding, nasoenteral feeding, or total parenteral nutrition.61,75
Animal experiments have found that drugs affecting collagen deposition, including interferon-α-2b, octreotide, β-aminopropionitrile, colchicine, N-acetylcysteine, and d-penicillamine,9,76 can prevent esophageal strictures after caustic alkali ingestion. Pentoxifylline, a local inflammatory and microcirculation mediator, has experimental benefit. Mitomycin C, a fibroblast proliferation inhibitor, has been used topically on strictures with some success.9 Oral agents to coat and protect the GI tract from insult, including sucralfate, bismuth subsalicylate, and sodium polyacrylate, are beneficial in animal experiments. None of these agents have been evaluated in controlled human clinical trials, and no specific recommendation can be made regarding their use. H2 blockers and proton pump inhibitors are often used in the treatment protocol,61 but no evidence supports or refutes their use.