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Toxicity, Caustic Ingestions: Treatment & Medication
Updated: Nov 4, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
- Attempt to identify the specific product, concentration of active ingredients, and estimated volume and amount ingested. Obtain MSDS sheets when possible. The product container or labels may be available. Avoid exposure to health care workers.
- Do not induce emesis or attempt to neutralize the substance by using a weak acid or base. This induces an exothermic reaction, which can compound the chemical injury with a thermal injury. It may also induce emesis.
- Small amounts of a diluent, although controversial, may be beneficial if administered as soon as possible after a solid or granular alkaline ingestion, to remove any adhering particles to the oral or esophageal mucosa. Water or milk may be administered in small amounts. It is very unlikely to be of any benefit after more than 30 minutes.
- Some authors discourage the use of diluents because of the concern of inducing emesis.
- Diluents should not be used with any acid ingestion or liquid alkaline ingestion. The risk of vomiting with reexposure of the oral or esophageal mucosa to the offending substance can result in worsening injury or perforation.
Emergency Department Care
- In the treatment area, patients suspected of ingesting a caustic substance should be triaged to a high priority for prompt evaluation and treatment. This includes prompt evaluation of airway and vital signs as well as immediate cardiac monitoring and intravenous access.
- Airway control
- Because of the risk of rapidly developing airway edema, immediate assessment of the patient’s airway and mental status should be performed and carefully monitored. Equipment for endotracheal intubation and cricothyrotomy should be readily available. Gentle orotracheal intubation or fiberoptic-assisted intubation is preferred over blind nasotracheal intubation to avoid the increased risk of soft-tissue perforation.
- If possible, it is best to avoid inducing paralysis for intubation because of the risk of anatomical distortion from bleeding and necrosis.
- Cricothyrotomy or percutaneous needle cricothyrotomy may be necessary in the presence of extreme tissue friability or significant edema.
- Gastric emptying and decontamination
- Do not administer emetics because of risks of reexposure of the vulnerable mucosa to the caustic agent. This may result in further injury or perforation.
- Gastric lavage by traditional methods using large-bore orogastric Ewald tubes are contraindicated in both acidic and alkaline ingestions because of risk of esophageal perforation and tracheal aspiration of stomach contents.
- Large-volume liquid acid ingestions may benefit from nasogastric tube (NGT) suction if performed rapidly after ingestion. Pyloric sphincter spasm may prolong contact time of the agent to the gastric mucosa for up to 90 minutes. NGT suction may prevent small intestine exposure. Esophageal perforation is rare. NGT suction may be of particular value following ingestion of zinc chloride, mercuric chloride, or hydrogen fluoride.
- Activated charcoal is relatively contraindicated in caustic ingestions because of poor adsorption and endoscopic interference.
- Dilution: Dilution may be beneficial for ingestion of solid or granular alkaline material if performed within 30 minutes after ingestion using small volumes of water. Because of the risk of emesis, carefully consider the risks versus benefits of dilution.
- Do not dilute acids with water because of excessive heat production.
- Neutralization: Do not administer a weak acid in alkaline ingestions or a weak alkaline agent in acid ingestions. There is a risk of heat production resulting from this exothermic reaction. In addition, the risk of emesis makes this a hazardous intervention.
- Intravenous fluids and blood products may be required in the event of significant bleeding, vomiting, or third spacing.
Consultations
Airway management can be a multifaceted problem and may be best approached with the availability of a wide array of visualization techniques, and, if time allows, a team of experts. However, the rapid development of airway edema may prompt the need for rapid airway management with the best immediately available visualization approach.
- Obtain a surgical consultation when the following are expected or observed:
- Perforation
- Mediastinitis
- Peritonitis
- Obtain an endoscopic consultation for the following patients:
- Small children
- Symptomatic older children and adults
- Patients with altered mental status
- Patients with intentional ingestions
- Others with a potential for significant injury (eg, ingestion or large volumes or concentrated products)
Once a patient is stabilized, obtain a psychiatric consultation for any patients with a history of an intentional ingestion.
Medication
Supportive care, rather than specific antidotes, are the mainstay of management following caustic ingestions. A significant exception to this would be the aggressive administration of intravenous calcium for dysrhythmias precipitated by hypocalcemia from hydrogen fluoride ingestion. Such therapy is best performed with the guidance of the toxicologist at the local poison center.
The use of corticosteroids, previously proposed to be beneficial, should be discouraged. Studies have shown that stricture formation is based on the depth of the tissue damage.
The following agents may be of value in supportive care.
Antibiotic, Cephalosporin (Third Generation)
These agents should be administered if evidence of perforation exists. A third-generation cephalosporin or ampicillin/sulbactam may be considered.
Ceftriaxone (Rocephin)
Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.
Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations <25 mcg/mL to 85% bound at 300 mcg/mL.
Adult
1-2 g IV q24h, or divided bid; not to exceed 4 g/d
Pediatric
Neonates >7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants/children: 50-75 mg/kg/d IV, divided q12-24h , not to exceed 2 g/d
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity; hyperbilirubinemic neonates, particularly those who are premature
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; caution in breastfeeding women; may displace bilirubin from albumin-binding sites, increasing the risk of kernicterus; caution with gallbladder, biliary tract, liver, or pancreatic disease, or in patients with history of colitis or penicillin hypersensitivity
Antibiotic, Penicillin and Beta-lactamase Inhibitor
These agents should be administered if evidence of perforation exists. A third-generation cephalosporin or ampicillin/sulbactam may be considered.
Ampicillin and sulbactam (Unasyn)
Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.
Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.
Adult
1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV/IM q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
Pediatric
Not established
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
Proton Pump Inhibitor
Proton pump inhibitors reduce exposure of injured esophagus to gastric acid, which may result in decreased stricture formation.
Pantoprazole (Protonix)
Indicated for short-term treatment of GERD associated with erosive esophagitis. Also effective in treating gastric ulcers, including those caused by H pylori.
Adult
40 mg PO/IV qd
Pediatric
0.5 -1 mg/kg/d PO/IV; not to exceed 40 mg/d
May decrease effects of ketoconazole and iron salts
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Decrease dose in hepatic impairment, half-life can increase 7- to 9-fold; no dose adjustment required in patients with renal impairment
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| Overview: Toxicity, Caustic Ingestions |
| Differential Diagnoses & Workup: Toxicity, Caustic Ingestions |
 Treatment & Medication: Toxicity, Caustic Ingestions |
| Follow-up: Toxicity, Caustic Ingestions |
| Multimedia: Toxicity, Caustic Ingestions |
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References
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Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W, Oderda GM, Benson B, Litovitz T, et al. Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestions. Am J Emerg Med. May 1992;10(3):189-94. [Medline].
Havanond C, Havanond P. Initial signs and symptoms as prognostic indicators of severe gastrointestinal tract injury due to corrosive ingestion. J Emerg Med. Nov 2007;33(4):349-53. [Medline].
Homan CS, Maitra SR, Lane BP, Thode HC Jr, Finkelshteyn J, Davidson L. Effective treatment for acute alkali injury to the esophagus using weak-acid neutralization therapy: an ex-vivo study. Acad Emerg Med. Nov 1995;2(11):952-8. [Medline].
Homan CS, Maitra SR, Lane BP, Thode HC, Sable M. Therapeutic effects of water and milk for acute alkali injury of the esophagus. Ann Emerg Med. Jul 1994;24(1):14-20. [Medline].
Kamijo Y, Kondo I, Watanabe M, Kan'o T, Ide A, Soma K. Gastric stenosis in severe corrosive gastritis: prognostic evaluation by endoscopic ultrasonography. Clin Toxicol. 2007;45(3):284-6. [Medline].
Kim SJ, Cho SB, Cho JM, et al. CT imaging of gastric and hepatic complications after ingestion of glacial acetic acid. J Comput Assist Tomogr. Jul-Aug 2007;31(4):564-8. [Medline].
Pelclová D, Navrátil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion?. Toxicol Rev. 2005;24(2):125-9. [Medline].
Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, et al. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc. Sep 2004;60(3):372-7. [Medline].
Salzman M, O'Malley RN. Updates on the evaluation and management of caustic exposures. Emerg Med Clin North Am. May 2007;25(2):459-76. [Medline].
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Further Reading
Keywords
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