Iron is a direct GI irritant and causes vomiting, diarrhea, and abdominal pain soon after a significant ingestion. Mucosal ulceration and bleeding, as well as intestinal perforation, may also occur. Hypovolemia from GI losses may produce hypotension, tissue hypoperfusion, and metabolic acidosis (based on tissue ischemia). As the mucosal surface is injured, iron passes unimpeded into the blood. When the ability of transferrin to combine with iron is exhausted, free iron becomes available. Free iron enters the mitochondria and inhibits oxidative phosphorylation to produce metabolic acidosis. Iron also participates in the production of toxic hydroxyl free radicals and subsequent membrane lipid peroxidation. Other systemic findings of iron poisoning include coagulopathy through inhibition of serum proteases, 2 myocardial dysfunction,3 and encephalopathy. Coagulopathy may be biphasic, with prolonged prothrombin time and partial thromboplastin time within the first 24 h 2 that appear reversible with chelation therapy as free iron initially interferes with the activity of factors in the coagulation cascade. Later, as iron poisoning causes hepatic injury, factor production decreases, potentially worsening the coagulopathy.

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