Pediatric Iron Toxicity Treatment & Management

  • Author: Jennifer S Boyle, MD, PharmD; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jun 24, 2009
 

Medical Care

The first step in treating a case of acute iron toxicity is to provide appropriate supportive care, with particular attention paid to fluid balance and cardiovascular stabilization. Initial treatment should also address the issue of preventing further absorption of iron by the GI tract.

  • Ipecac-induced emesis is not recommended. This is especially true in iron ingestion. GI distress is an early finding in iron poisoning and is present in all potentially serious ingestions. Ipecac-induced vomiting may cloud the clinical picture.
  • Gastric lavage is not recommended because iron tablets are relatively large and become sticky in gastric fluid, making lavage unlikely to be of benefit.
  • Whole bowel irrigation has been used to speed the passage of undissolved iron tablets through the GI tract. A polyethylene glycol electrolyte solution (eg, GoLYTELY) may be administered orally or nasogastrically at a rate of 250-500 mL/h for toddlers and preschoolers and 2 L/h for adolescents. Continue irrigation until the repeat radiographic findings are negative or rectal effluent is clear.
  • Deferoxamine is the iron-chelating agent of choice. Deferoxamine binds absorbed iron, and the iron-deferoxamine complex is excreted in the urine. Deferoxamine does not bind iron in hemoglobin, myoglobin, or other iron-carrying proteins. Base the indications for using deferoxamine on both clinical and laboratory parameters. Indications for treatment include shock, altered mental status, persistent GI symptoms, metabolic acidosis, pills visible on radiographs, serum iron level greater than 500 µg/dL, or estimated dose greater than 60 mg/kg of elemental iron. Initiate chelation if a serum iron level is not available and symptoms are present.
    • The administration of deferoxamine may be intramuscular or intravenous. The intramuscular route is not recommended because it is painful and less iron is excreted compared with the intravenous route. The intravenous route is administered as a continuous infusion. The standard dose is 15 mg/kg/h, with an initial dose administered for 6 hours.
    • No clear end point of therapy is noted; however, indications for cessation include significant resolution of shock and acidosis. Deferoxamine, administered 6-12 hours, has been suggested for moderate toxicity. For severe toxicity, administer deferoxamine for 24 hours. Because these end points are arbitrary, observe the patient for the recurrence of toxicity 2-3 hours after the deferoxamine has been stopped.
    • Adverse effects from deferoxamine are unusual. Pulmonary toxicity (ie, acute respiratory distress syndrome [ARDS], tachypnea) has been described, especially if patients are treated with deferoxamine for more than 24 hours. Rate-related hypotension can occur. Therefore, monitor the patient while titrating the infusion rate upward to a final rate of 15 mg/kg/h.
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Surgical Care

  • If retained iron tablets are evident after GI decontamination, consider endoscopy or surgery for their removal.
  • Failure to remove the iron can result not only in continued iron absorption and exacerbation of systemic symptoms but also in gastric perforation and severe hemorrhage.
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Consultations

  • Regional poison control centers may be contacted for assistance in patient management.
  • In addition, consult an intensivist for help in managing the moderately to severely ill child.
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Contributor Information and Disclosures
Author

Jennifer S Boyle, MD, PharmD  Fellow in Toxicology, University of Virginia Health System

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; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Ctr, Associate Medical Toxicology Fellowship Director, VA Dept of Health

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Association for the Advancement of Science, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, 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, Pediatric Emergency Medicine Research Director, Professor, Departments of Pediatrics and Emergency Medicine, Medical College of Wisconsin

Halim Hennes, MD 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; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD  Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and 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

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

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

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

  14. 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].

  15. 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].

  16. 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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