Clinical meaning
Acute iron poisoning is one of the leading causes of fatal poisoning in children under 6 years, primarily from accidental ingestion of adult iron supplements or prenatal vitamins. The NP must understand the dose-dependent toxicity: less than 20 mg/kg of elemental iron causes minimal symptoms; 20-60 mg/kg produces moderate GI toxicity; greater than 60 mg/kg causes severe systemic toxicity; and greater than 150-200 mg/kg is potentially lethal. Iron exerts toxicity through two primary mechanisms. First, direct caustic injury: iron is a corrosive agent that causes hemorrhagic necrosis of the GI mucosa (primarily stomach and proximal small intestine) within hours of ingestion, producing vomiting, bloody diarrhea, and potentially GI hemorrhage and perforation. Second, systemic cellular toxicity: once iron is absorbed and exceeds transferrin binding capacity, free (non-transferrin-bound) iron enters cells and generates hydroxyl radicals via the Fenton reaction (Fe2+ + H2O2 → Fe3+ + OH• + OH-), causing mitochondrial dysfunction, lipid peroxidation, and cellular necrosis primarily in the liver, heart, and brain. Additionally, free iron causes direct vasodilation and increased capillary permeability, leading to third-spacing, hypovolemia, and distributive shock. Iron poisoning progresses through five clinical phases. Phase 1 (0-6 hours): GI phase with nausea, vomiting, diarrhea, abdominal pain, and hematemesis from direct mucosal injury. Phase 2 (6-24 hours): apparent recovery or 'quiescent phase' where GI symptoms may temporarily improve, creating a dangerous false reassurance -- ongoing cellular damage and lactic acidosis may be developing. Phase 3 (12-48 hours): systemic toxicity phase with cardiovascular collapse, metabolic acidosis with anion gap, hepatic failure (hepatocellular necrosis from direct iron toxicity to hepatocytes), coagulopathy, renal failure, and potentially death. Phase 4 (2-4 days): hepatotoxicity phase with fulminant hepatic failure, coagulopathy, and encephalopathy if the patient survives phase 3. Phase 5 (2-8 weeks): late complications including GI stricture formation (particularly pyloric stenosis) from scarring of the initial caustic mucosal injury.