PC3081: Lethal Pediatric Iron Ingestion Refractory to Extracorporeal Support

Introduction: We report the case of a 23-month-old male with a high serum iron level refractory to deferoxamine chelation therapy and continuous venovenous hemodialysis (CVVHD). Extracorporeal membrane oxygenation (ECMO) support was required due to cardiopulmonary collapse. Extracorporeal therapies may be beneficial in cases of severe, refractory iron poisoning, if initiated early.

Case Description: A previously-healthy 23-month-old boy presented to the emergency department with vomiting and altered mentation, following ingestion of an unknown amount of ferrous sulfate tablets. He was lethargic, tachycardic and poorly perfused. Initial bloodwork revealed high anion gap metabolic acidosis. Serum iron concentration was 23,300 µg/dL. His clinical status quickly deteriorated, prompting tracheal intubation and initiation of vasoactive infusions for worsening hemodynamics. Additionally, he was started on a deferoxamine infusion. Continuous renal replacement therapy in the form of CVVHD was initiated to expedite iron removal, as his hemodynamics worsened. Unfortunately, within 24 hours of ingestion, he progressed to multi-organ system failure, including acute hepatic failure with severe coagulopathy and refractory cardiogenic shock. ECMO for cardiopulmonary support was initiated. During venoarterial ECMO cannulation, the patient’s clinical bleeding acutely worsened. Ultimately, even rapid blood product administration was unable to stabilize and maintain ECMO support. The patient’s family and care team transitioned to comfort care measures, and he died quickly after ECMO discontinuation.

Discussion: Intravenous deferoxamine is the antidote for serious iron toxicity. Deferoxamine acts as a chelating agent, binding ferric iron in the blood, to form water soluble ferrioxamine, a byproduct excreted by the kidneys. Hypotension secondary to histamine release may occur with administration of deferoxamine. In this case, the deferoxamine infusion dose was limited secondary to refractory shock and cardiopulmonary collapse. Extracorporeal methods of iron removal are only capable of eliminating free-circulating iron, so these methods are not useful once intracellular iron transport has occurred. It is imperative that these procedures are initiated early following the ingestion, before refractory shock ensues. There is a paucity of literature to support management of severe iron overdose, efficacy of exchange transfusion, or CVVHD.

Conclusion: Our patient’s case is unique, given the exceptionally high serum iron concentration. In our literature review, we were unable to find previously reported serum iron concentrations near that of our patient. Despite aggressive therapies and resuscitation, this patient could not be stabilized. We propose early initiation of ECMO for life-threatening iron ingestions to allow for more aggressive deferoxamine titration and hemodialysis sooner in the clinical course, despite limitations of current literature. The risks of worsening coagulopathy must be weighed with potential ECMO bleeding complications. In addition to ECMO, CVVHD should be considered in cases with high levels of iron toxicity. Literature is lacking in iron toxicity reports and management experience.