Module 28.1 - Acute Iron Toxicity - Introduction

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As clinicians engaged in medical education, we understand the critical nature of toxicologic emergencies. This module provides a comprehensive, essential overview of Acute Iron Toxicity, focusing on effective diagnosis and management.
Clinical Stages and Systemic Effects Acute iron toxicity affects multiple organ systems, including the GI tract (risk of delayed stricture formation), liver (hemorrhagic hepatic periportal necrosis), and the cardiovascular system. Circulatory shock is identified as the most common cause of death, often stemming from hypovolemia, vasodilation, and a direct negative inotropic effect on the myocardium. We review the five classic clinical stages, highlighting the dynamic nature of presentation and the misleading "quiescent" phase (6–24 hours post-ingestion). Metabolic acidosis is a prominent and critical feature, resulting partly from the hydrolysis of unbound ferric iron liberating unbuffered protons.
Diagnosis and Management Accurate diagnosis integrates clinical signs with laboratory markers. The serum iron concentration is the most effective parameter to gauge toxicity, with levels 500 per mu g per dL at 4–6 hours post-ingestion indicating pronounced systemic toxicity. However, note that Total Iron-Binding Capacity is of limited value. The presence of a high anion gap metabolic acidosis accompanied by an elevated lactate concentration is considered a reliable marker of serious cellular toxicity and necessitates chelation.
Management begins with initial stabilization and prompt intravenous volume repletion. Given that activated charcoal is ineffective, Whole-Bowel Irrigation is the mainstay for GI decontamination if radiopaque tablets are visible.
Deferoxamine (DFO) Chelation Therapy Deferoxamine is the parenteral chelator of choice, strongly indicated for moderate-to-severe systemic toxicity. DFO is a hexadentate chelator highly specific for ferric iron, binding it to form the renally excreted complex ferrioxamine. Critically, DFO should not be withheld in seriously poisoned pregnant patients.
Endpoints for DFO therapy are primarily guided by clinical stability and the resolution of metabolic acidosis. Clinicians must be vigilant for associated risks, including Acute Respiratory Distress Syndrome linked to prolonged continuous infusions and the enhanced risk of sepsis from ferrophilic organisms like Yersinia enterocolitica.