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Toxicity, Iron: Treatment & Medication

Author: Clifford S Spanierman, MD, Consulting Staff, Departments of Emergency Medicine and Pediatrics, Lutheran General Hospital of Oak Brook, Advocate Health System
Contributor Information and Disclosures

Updated: Mar 26, 2009

Treatment

Prehospital Care

  • This section only refers to the acute overdose.
  • IV access should be established immediately.
  • For patients who are hypovolemic, administer fluid boluses of 20 mL/kg of 0.9 isotonic sodium chloride solution or lactated Ringer (LR) solution.
  • Provide oxygen to patients in shock.

Emergency Department Care

  • Assume that symptomatic patients are hypovolemic. Administer vigorous isotonic crystalloid therapy (eg, 0.9 isotonic sodium chloride solution, LR solution) in 20 mL/kg boluses to attain and maintain hemodynamic stability.
  • Gastric lavage with a large-bore orogastric tube or administration of ipecac syrup may remove iron from the stomach. However, ipecac is not used routinely for iron removal because it can mask clinical signs of iron toxicity (vomiting). Due to local caustic effect of iron, poisoned patients routinely are vomiting on their own performing self-decontamination even without ipecac.
  • Ideally, these treatments should be performed 1-2 hours postingestion or even later if evidence of iron products in the stomach are observed on a radiograph. Each modality has its disadvantages.
    • Iron has a gelatinous texture and may be difficult to remove by lavage. Bezoar formation may occur.
    • Ipecac is not routinely indicated. Significant ingestions of iron may cause hypotension and unstable vital signs, and ipecac may endanger the patient's airway as an aspiration risk. The only exception to the rule might be the patient who presents very early and with a very large amount of ingested iron where ipecac can expedite evacuation. Prolonged vomiting (more than one hour) should be attributed to iron toxicity rather than to the effects of ipecac.
  • Perform whole-bowel irrigation in patients with a radiopacity on KUB until the radiopacity clears. Activated charcoal does not bind iron but should be utilized if co-ingestants are suspected.
  • Oxygen should be supplemented.

Consultations

  • Consultation with a toxicologist is recommended.
  • Obtain a gastroenterology consultation for patients who have large iron bezoars.

Medication

The goals of pharmacotherapy are to reduce iron levels, prevent complications, and reduce morbidity.

Chelating agents

Chelation is the mainstay of therapy. It is indicated for serum iron levels >350 mcg/dL with evidence of toxicity or >500 mcg/dL regardless of signs or symptoms.


Deferoxamine (Desferal)

DOC for iron intoxication. Freely soluble in water. Approximately 8 mg of iron is bound by 100 mg of deferoxamine. Excreted in urine and bile and gives urine a red discoloration. Readily chelates iron from ferritin and hemosiderin but not transferrin. Most effective when administered continuously by infusion. May be administered by IM injection or slow IV infusion. Does not effectively chelate other trace metals of nutritional importance. Provided in vials containing 500 mg of lyophilized sterile drug. Add 2 mL of sterile water to each vial for injection, bringing the concentration to 250 mg/mL. For IV use, may be diluted in 0.9% sterile saline, 5% dextrose solution, or Ringer solution. IM is preferred route of administration, except in hypotension and cardiovascular collapse when the IV route should be considered.

Adult

1000-2000 mg IM, followed by 500 mg q4h for 2 doses; not to exceed 6000 mg/24 h
Alternatively, 1000 mg IV may be administered at initial rate of 5 mg/kg/h and not to exceed 15 mg/kg/h to avoid hypotension; followed by 500 mg q4h for 2 doses; administer additional IV infusion slowly over 24 h; not to exceed 6000 mg/24 h to reduce the hypotensive effects of deferoxamine

Pediatric

<3 years: Not established
>3 years: Start at 5 mg/kg/h and titrate up to 15 mg/kg/h IV, not to exceed 6 g/d (acute) or 12 g/d (chronic)

Documented hypersensitivity; patients who do not have acute iron poisoning; severe renal disease and anuria (consider dose reduction after the loading dose in these circumstances)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Tachycardia, hypotension, and shock may occur in patients receiving chronic therapy and could add to the cardiovascular collapse caused by iron toxicity; GI adverse effects of the drug include abdominal discomfort, nausea, vomiting, and diarrhea, which may add to symptoms of acute iron toxicity; flushing and fever are reported

GI decontaminants

Because adsorption to activated charcoal is minimal, whole bowel irrigation is the GI decontamination method of choice.


Polyethylene glycol bowel prep (GoLYTELY, Colyte)

Laxative with strong electrolytic and osmotic effects that has cathartic actions in the GI tract.

Adult

1000-2000 mL PO or NG tube, until rectal effluent is clear

Pediatric

25 mL/kg/h (not to exceed 500 mL) PO or NG tube, until rectal effluent is clear

Reduces effectiveness and absorption of oral medications

Documented hypersensitivity; colitis, megacolon, bowel perforation, gastric retention, or GI obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in ulcerative colitis and hot loop polypectomy

More on Toxicity, Iron

Overview: Toxicity, Iron
Differential Diagnoses & Workup: Toxicity, Iron
Treatment & Medication: Toxicity, Iron
Follow-up: Toxicity, Iron
References

References

  1. Morse SB, Hardwick WE Jr, King WD. Fatal iron intoxication in an infant. South Med J. Oct 1997;90(10):1043-7. [Medline].

  2. Carlsson M, Cortes D, Jepson S, Kansstrup T. Severe iron intoxication treated with exchange transfusion. Arch Dis Child. April 2008;93(4):321-2. [Medline].

  3. Alymara V, Bourantas D, Chaidos A. Effectiveness and safety of combined iron-chelation therapy with deferoxamine and deferiprone. Hematol J. 2004;5(6):475-9. [Medline].

  4. Bosse GM. Conservative management of patients with moderately elevated serum iron levels. J Toxicol Clin Toxicol. 1995;33(2):135-40. [Medline].

  5. Cheney K, Gumbiner C, Benson B, Tenenbein M. Survival after a severe iron poisoning treated with intermittent infusions of deferoxamine. J Toxicol Clin Toxicol. 1995;33(1):61-6. [Medline].

  6. Goldberg sl. Novel treatment options for transfusional iron overload in patients with myleodysplatic syndromes. Leuk Res. Dec 2007;31:s16-22. [Medline].

  7. Hershko CM, Link GM, Konijn AM. Iron chelation therapy. Curr Hematol Rep. Mar 2005;4(2):110-6. [Medline].

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

  9. Mills KC, Curry SC. Acute iron poisoning. Emerg Med Clin North Am. May 1994;12(2):397-413. [Medline].

  10. Palatnick W, Tenenbein M. Leukocytosis, hyperglycemia, vomiting, and positive X-rays are not indicators of severity of iron overdose in adults. Am J Emerg Med. Sep 1996;14(5):454-5. [Medline].

  11. Tenenbein M. Benefits of parenteral deferoxamine for acute iron poisoning. J Toxicol Clin Toxicol. 1996;34(5):485-9. [Medline].

Further Reading

Keywords

iron, iron poisoning, iron overdose, iron toxicity, Fe, vitamins, symptoms, treatment, causes, iron supplements, corrosive iron toxicity, cellular iron toxicity, iron ingestion, high iron levels, prenatal vitamins, elemental iron, chronic iron toxicity

Contributor Information and Disclosures

Author

Clifford S Spanierman, MD, Consulting Staff, Departments of Emergency Medicine and Pediatrics, Lutheran General Hospital of Oak Brook, Advocate Health System
Disclosure: Nothing to disclose.

Medical Editor

David C Lee, MD, Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School
David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

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.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

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, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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