Pediatric Iron Toxicity Workup

  • Author: Jennifer S Boyle, MD, PharmD; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Apr 12, 2012
 

Laboratory Studies

  • Iron toxicity is a clinical diagnosis and any studies are simply adjuncts.
  • Toxic effects of iron may occur at doses of 10-20 mg/kg of elemental iron.
  • Little is known about the absorption rate of iron in an overdose, the timing of peak serum iron levels, or the rate at which serum levels fall from their peak levels. Serum iron levels generally correlate with clinical severity and are as follows:
    • Mild - Less than 300 µg/dL
    • Moderate - 300-500 µg/dL
    • Severe - More than 500 µg/dL
  • Difficulties involved with interpretation of serum iron levels include the following:
    • The ideal serum iron level is a peak level at 2-6 hours postingestion, and the time from ingestion is often unknown.
    • Deferoxamine interferes with standard assays and leads to falsely decreased iron levels.
    • Serum iron levels may not be available in a timely fashion. Serum levels obtained more than 8-12 hours postingestion may not be useful because iron redistributes into the tissues and the serum level does not reflect the total body burden of iron.
  • Total iron-binding capacity (TIBC) has traditionally been used to determine toxicity. Previously, a patient with a serum iron level greater than the TIBC was thought to be at risk for developing systemic toxicity. However, determining the TIBC in the presence of large amounts of iron or deferoxamine may yield a falsely elevated number. Hence, a TIBC above the iron level does not indicate sufficient binding capacity, and this test is not useful in determining the likelihood of toxicity.
  • Because iron levels are not always readily available, the predictive value of other laboratory test results has been explored. Previously, a WBC count greater than 15,000/µL and a serum glucose level greater than 150 mg/dL were said to correlate with iron levels greater than 300 µg/dL. However, more recent studies do not support the predictive value of these ancillary tests, and they are not useful in the setting of iron poisoning.
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Imaging Studies

  • Abdominal radiography may offer information on the iron ingestion, both initially and subsequently. Do not delay treatment for radiography.
  • A positive radiographic finding is one that shows radiopaque tablets or particles. This indicates that the ingested iron has not been completely absorbed. Obtaining a radiograph pre–GI decontamination and post–GI decontamination may yield information as to the success of therapy. If the radiographic findings remain positive after decontamination, additional decontamination is required.
  • An initial negative radiographic finding may mean that no iron was ingested or that the ingested iron tablets or solution have dissolved. In addition, liquid preparation and chewable vitamins are not visible on radiographs.
  • If the radiographic findings were initially positive and are negative after GI decontamination, this indicates that GI decontamination was successful, although iron levels should still be monitored because of iron absorption prior to initiation of therapy.
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Other Tests

  • The deferoxamine challenge test consists of administering a single dose of deferoxamine that binds available free iron and is excreted in the urine as the ferrioxamine complex (deferoxamine and iron).
  • This complex changes the urine to a reddish (vin rosé) color, indicating the need for chelation. However, the urine does not change color reliably, even when elevated serum iron levels are present.
  • This test is not reliable and does not alleviate the need for monitoring serum iron levels. Therefore, one should not rely on the deferoxamine challenge test.
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Contributor Information and Disclosures
Author

Jennifer S Boyle, MD, PharmD  Consulting Staff, Emergency Medicine/Medical Toxicology, Salem Veterans Affairs Medical Center

Jennifer S Boyle, MD, PharmD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

David T Lawrence, DO  Assistant Professor, Department of Emergency Medicine, Division of Medical Toxicology, University of Virginia School of Medicine

David T Lawrence, DO is a member of the following medical societies: American College of Emergency Physicians and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Christopher P Holstege, MD  Associate Professor of Emergency Medicine and Pediatrics, University of Virginia School of Medicine; Chief, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Center; Medical Toxicology Fellowship Director, University of Virginia

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, European Association of Poisons Centres and Clinical Toxicologists, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Kathryn Clark Emery, MD  Associate Professor, Department of Pediatrics, University of Colorado Health Sciences Center; Consulting Staff, Department of Emergency Medicine, Children's Hospital of Denver

Kathryn Clark Emery, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Halim Hennes, MD, MS  Division Director, Pediatric Emergency Medicine, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director of Emergency Services, Children's Medical Center

Halim Hennes, MD, MS is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD  Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

Paul D Petry, DO, FACOP, FAAP  Consulting Staff, Freeman Pediatric Care, Freeman Health System

Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD  Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

References
  1. Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatr Emerg Care. Oct 2011;27(10):978-85. [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].

  3. [Best Evidence] Ziegler EE, Nelson SE, Jeter JM. Iron supplementation of breastfed infants from an early age. Am J Clin Nutr. Feb 2009;89(2):525-32. [Medline].

  4. Juurlink DN, Tenenbein M, Koren G, Redelmeier DA. Iron poisoning in young children: association with the birth of a sibling. CMAJ. Jun 10 2003;168(12):1539-42. [Medline].

  5. [Guideline] Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-70. [Medline].

  6. Bryant SM, Leikin JB. Iron. Critical Care Toxicology. 2005;687-693.

  7. Desferal (deferoxamine mesylate) [package insert]. East hanover, NJ: Novartis Pharmaceuticals Corporation; 2007. [Full Text].

  8. Eldridge DL, Holstege CP. Utilizing the laboratory in the poisoned patient. Clin Lab Med. Mar 2006;26(1):13-30, vii. [Medline].

  9. Engle JP, Polin KS, Stile IL. Acute iron intoxication: treatment controversies. Drug Intell Clin Pharm. Feb 1987;21(2):153-9. [Medline].

  10. Fine JS. Iron poisoning. Curr Probl Pediatr. Mar 2000;30(3):71-90. [Medline].

  11. Jacobs J, Greene H, Gendel BR. Acute iron intoxication. N Engl J Med. Nov 18 1965;273(21):1124-7. [Medline].

  12. Madiwale T, Liebelt E. Iron: not a benign therapeutic drug. Curr Opin Pediatr. Apr 2006;18(2):174-9. [Medline].

  13. McGuigan MA. Acute iron poisoning. Pediatr Ann. Jan 1996;25(1):33-8. [Medline].

  14. Perrone J. Iron. Goldfrank's Toxicologic Emergencies. 2006;629-637.

  15. Siff JE, Meldon SW, Tomassoni AJ. Usefulness of the total iron binding capacity in the evaluation and treatment of acute iron overdose. Ann Emerg Med. Jan 1999;33(1):73-6. [Medline].

  16. Tenenbein M. Position statement: whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 1997;35(7):753-62. [Medline].

  17. Tenenbein M. Whole bowel irrigation in iron poisoning. J Pediatr. Jul 1987;111(1):142-5. [Medline].

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The oxidative potential of iron was first proposed by Fenton in 1894. The importance of reduced oxygen species in biological reactions became apparent with the discovery of superoxide dismutase by McCord and Fridovich in 1969. The potential role of metal ion catalysis was reported the following year. Subsequently, a plethora of evidence has accumulated linking chronic excess body iron to cardiovascular disease, carcinogenesis, aging, stroke, Alzheimer disease, and Parkinson disease. The organ damage that occurs in the hereditary iron overloading disorders is well documented and can be averted and improved by decreasing the excess iron. Acute iron overload likewise produces tissue and organ damage due to the presence of free ionic iron.
 
 
 
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