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Clinical Features

• Absence of GI symptoms within 6hr of ingestion excludes significant iron ingestion (exception: enteric coated tablets)
• Significant iron toxicity can result in a severe lactic acidosis from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.

Iron Toxicity Stages

Staging	Clinical Effect	Time Frame
Stage 1	GI irritation: nausea and vomiting, abdominal pain, diarrhea	30 mins-6 hours
Stage 2: Latent	Reduced GI symptoms	6-24 hours
Stage 3: Shock and metabolic acidosis	Metabolic acidosis, lactic acidosis, dehydration	6-72 hours
Stage 4: Hepatotoxicity/ Hepatic necrosis	Hepatic failure	12-96 hours
Stage 5: Bowel obstruction	GI mucosa healing leads to scarring	2-8 weeks

• Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of iron on the gastric and intestinal mucosa
• Stage II: Quiescent phase with resolution of GI symptoms and apparent clinical improvement
  • controversy between toxicologists whether this stage exists in significant poisonings
• Stage III: Systemic toxicity: shock and hypoperfusion
  • Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
  • GI fluid losses, increase capillary permeability, decreased venous tone
  • Severe anion gap acidosis
  • Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
  • Hepatotoxicity from iron delivery via portal blood flow
• Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4
• Stage V: Late onset of gastric and pyloric strictures (2-8 week later)

CDC management guidelines for children with elevated blood levels

Blood lead level (μg/dL)	Treatment
10–14	Education, repeat screening
15–19	Repeat screening, case management to abate sources
20–44	Medical evaluation, case management
45–69	Medical evaluation, chelation, case management
>69	Hospitalization, immediate chelation, case management

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