Caustic Ingestions Treatment & Management

  • Author: Eric M Kardon, MD, FACEP; Chief Editor: Asim Tarabar, MD   more...
 
Updated: May 21, 2010
 

Prehospital Care

  • Attempt to identify the specific product, concentration of active ingredients, and estimated volume and amount ingested. Obtain MSDS sheets when possible for workplace exposures. 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 re-exposing tissue to the caustic agent.
  • 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 of the literature available on this topic discourages the use of diluents because of the concern of inducing emesis resulting in re-exposure of tissue to caustic agent.
    • Diluents should not be used with any acid ingestion or liquid alkaline ingestion. The risk of vomiting with re-exposure of the oral or esophageal mucosa to the offending substance can result in worsening injury or perforation.
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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 continually monitored. Equipment for endotracheal intubation and cricothyrotomy should be readily available. Gentle orotracheal intubation or fiberoptic-assisted intubation is preferred. Blind nasotracheal intubation should be avoided due to 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. If a difficult airway is anticipated, IV ketamine can be used to provide enough sedation to obtain a direct look at the airway.
    • 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 re-exposure 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, unless signs of perforation are present. This should be done after consulting with a regional poison control center.
    • 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.
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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)

Consultation with the local poison control center may be helpful, particularly if unfamiliar or unique agents are involved. These may include industrial strength detergents, button batteries, zinc chloride, mercuric chloride, hydrogen fluoride, phenol, and Clinitest tablets.

Once a patient is stabilized, obtain a psychiatric consultation for any patients with a history of an intentional ingestion.

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Contributor Information and Disclosures
Author

Eric M Kardon, MD, FACEP  Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Lance W Kreplick, MD, FAAEM, MMM  Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC

Lance W Kreplick, MD, FAAEM, MMM, is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References
  1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol. Dec 2007;45(8):815-917. [Medline].

  2. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline]. [Full Text].

  3. Kay M, Wyllie R. Caustic ingestions in children. Curr Opin Pediatr. Jun 18 2009;[Medline].

  4. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2008 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 26th Annual Report. Clin Toxicol (Phila). Dec 2009;47(10):911-1084. [Medline].

  5. Riffat F, Cheng A. Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus. 2009;22(1):89-94. [Medline].

  6. 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].

  7. 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].

  8. 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].

  9. 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].

  10. 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].

  11. 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].

  12. Pelclová D, Navrátil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion?. Toxicol Rev. 2005;24(2):125-9. [Medline].

  13. 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].

  14. 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].

  15. Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J. May 2005;22(5):359-61. [Medline].

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Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive thrombosis of the esophageal submucosal vessels giving the appearance similar to chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the appearance of the thrombosed esophageal submucosal vessels giving the appearance of chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive burn and thrombosis of the submucosal esophageal vessels, which gives the appearance of chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
 
 
 
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