Iron Poisoning

Description

• Peak concentrations are 2–4 hr postingestion
• Serum concentrations not reliable if obtained >4–6 hr after ingestion:
  • Enteric coated or sustained release – warrants serial levels
• Postabsorption: Iron redistributes into tissues, and fall in serum iron occurs as free iron shifts intracellularly resulting in cellular injury
• Injury patterns:
  • Corrosive injury to intestinal mucosa may result in profound fluid loss (shock), hemorrhage, and perforation
  • Liver receives largest load of iron because of portal venous circulation – (hemorrhagic periportal necrosis)
• Free iron:
  • Concentrates in mitochondria, disrupting oxidative phosphorylation; catalyzes lipid peroxidation and free radical formation, resulting in cell death; increases anaerobic metabolism and acidosis
  • Causes myocardial depression, venodilation, and cerebral edema
• Hydration of ferric form liberates 3 protons, resulting in acidemia

Etiology

• Nontoxic <20 mg/kg
• Moderate to severe >40 mg/kg
• Lethality possible >60 mg/kg
• Elemental iron equivalents:
  • Ferrous sulfate, 20% (325 mg = 65 mg Fe)
  • Ferrous gluconate, 12%
  • Ferrous fumarate, 33%
• Prenatal vitamins vary from 60–90 mg elemental iron per tablet
• Children's vitamins may contain 5–18 mg elemental iron per tablet

• Historically notorious for the highest mortality rate among pediatric accidental exposures (adult iron products)
• Children's chewable iron products have been shown to be safe