Caustic Ingestions Workup

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

Laboratory Studies

  • pH testing of product
    • A pH less than 2 or greater than 12.5 indicates greater potential for severe tissue damage.[5]
    • A pH outside of this range does not preclude significant injury.
  • pH testing of saliva: Unexpected high or low values may confirm ingestion in questionable cases; however, a neutral pH cannot rule out a caustic ingestion.
  • Complete blood count (CBC), electrolyte levels, BUN levels, creatinine level, and ABG levels may all be helpful as baseline values and as indications of systemic toxicity.
  • Liver function tests and DIC panel may also be helpful to establish baselines or, if abnormal, confirm severe injury following acid ingestions.
  • Urinalysis and urine output may help guide fluid replacement.
  • Type and cross are indicated for any potential surgical candidates or those with the potential for gastrointestinal bleeding.
  • Obtain aspirin and acetaminophen levels as well as an ECG in any patient whose intent may have been suicidal.
  • In cases of hydrofluoric acid (HF) ingestion, precipitous falls in calcium level may lead to sudden cardiac arrest. Although ionized calcium levels are likely to have too long a turnaround to be clinically useful, cardiac monitoring and serial ECGs may help anticipate this event.
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Imaging Studies

  • Chest radiography: Obtain an upright chest radiograph in all cases of caustic ingestion. Findings may include pneumomediastinum or other findings suggestive of mediastinitis, pleural effusions, pneumoperitoneum, aspiration pneumonitis, or a button battery (metallic foreign body). However, the absence of findings does not preclude perforation or other significant injury.
  • Abdominal radiography: Findings may include pneumoperitoneum, ascites, or an ingested button battery (metallic foreign body).
  • If contrast studies are obtained, water-soluble contrast agents are recommended because they are less irritating to the tissues in cases of perforation.
  • CT will often be able to delineate small amounts of extraluminal air, not seen on plain radiographs.
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Procedures

  • Airway protection is critical following caustic ingestion if there is any indication of airway compromise. This can develop rapidly and be complicated by multiple factors. See Emergency Department Care.
  • Cardiac monitoring is indicated for any patient with a caustic ingestion.
  • Large-bore intravenous access allows administration of fluids and medications as needed.
  • Endoscopy is generally indicated for the following patients:
    • Small children
    • Symptomatic older children and adults
    • Patients with abnormal mental status
    • Those with intentional ingestions
    • Patients in whom injury is suspected for other reasons (eg, ingestion of large volumes or concentrated products)
  • However, because of the risk of increased injury, esophagoscopy should not be performed in patients with evidence of esophageal or gastrointestinal perforation, significant airway edema, or necrosis and in those who are hemodynamically unstable.
  • Obtaining meaningful information from endoscopy after treatment with activated charcoal is very difficult. Routine use of activated charcoal is not recommended in caustic ingestions.
  • Endoscopic ultrasonography has been shown to more accurately show the depth of lesions than endoscopy alone.[6] Further studies will be necessary to determine the utility of this procedure in aiding in diagnosis and treatment.
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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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