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Toxicity, Iron: Differential Diagnoses & Workup

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

Differential Diagnoses

Diabetic Ketoacidosis
Toxicity, Mushroom - Gyromitra Toxin
Gastroenteritis
Toxicity, Mushroom - Hallucinogens
Toxicity, Acetaminophen
Toxicity, Mushroom - Orellanine
Toxicity, Alcohols
Toxicity, Organophosphate and Carbamate
Toxicity, Arsenic
Toxicity, Salicylate
Toxicity, Mercury
Toxicity, Theophylline
Toxicity, Mushroom - Amatoxin
Toxicity, Mushroom - Disulfiramlike Toxins

Other Problems to Be Considered

Sepsis

Workup

Laboratory Studies

  • Measure steady-state serum iron levels at least 4 hours postingestion. levels drawn more than 6 hours after ingestion may underestimate toxicity caused by ferritin binding and redistribution of iron.
    • Mild-to-moderate toxicity generally manifests at levels of 350-500 mcg/dL.
    • Hepatotoxicity usually is observed at levels higher than 500 mcg/dL.
    • levels higher than 800 mcg/dL are associated with severe toxicity.
    • Samples drawn too early or too late postingestion may be unreliable.
    • In adults, hyperglycemia, leukocytosis, abdominal pain, and vomiting may be absent.
  • Glucose levels
    • Glucose levels exceeding 150 mg/dL are common with severe iron toxicity.
    • Following glucose levels is important because hepatic dysfunction may cause hypoglycemia.
  • Complete blood count
    • A white blood cell (WBC) count more than 15,000/mm3 is associated with severe iron poisoning.
    • A CBC is also helpful because anemia from blood loss may develop.
  • In addition to serum lactic acid levels (lactate), the arterial blood gas (ABG) measurements are useful in determining the existence and severity of a metabolic acidosis.
  • Coagulation studies are essential. Following the prothrombin time may be helpful.
  • Perform liver function tests (LFTs). Hepatic dysfunction is common in severe iron poisoning because the liver is the first organ outside of the GI tract to encounter large iron load through the portal blood supply.
  • Electrolyte measurements and renal function tests assist in calculation of the anion gap and detection of electrolyte abnormalities and the presence of prerenal azotemia.
  • Lipase and amylase levels may document occasional pancreatic injury.
  • Obtain a pregnancy test in women of childbearing age.
  • Determine type and cross-matching.
  • Ferritin levels are helpful for chronic toxicity >1000 mcg/L.
  • Iron toxicity is one of the MUDPILES (M-methanol; U-uremia; D-DKA, AKA; P-paraldehyde, phenformin; I-iron, isoniazid; L-lactic [ie, CO, cyanide]; E-ethylene glycol; S-salicylates) that causes an acidosis with an increased anion gap.

Imaging Studies

  • A kidneys, ureters, bladder (KUB) film can determine if radiopacities are present; iron tablets are radiopaque for a few hours postingestion. However, the absence of radiopacities does not rule out a significant or lethal ingestion.

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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