A case of intravenous iron administration resulting in cerebral edema expansion

Iron plays an important role in the development of perihematomal edema (PHE) in the setting of intracerebral hemorrhage (ICH). Cerebral iron is increased via direct hemoglobin release in ICH, and several studies have investigated the use of iron-chelating agents to mitigate its toxicity. However, the effect of systemic iron administration, corroborating the reverse concept, has never been investigated or reported clinically. We report the first case of systemic iron administration in the setting of hemorrhagic traumatic brain injury (TBI).

A 46-year-old woman was admitted to the hospital with acute moderate-to-severe TBI. Her head computed tomography (CT) scan showed bifrontal hemorrhagic contusions with mild PHE. She was started on hypertonic saline 3% continuous infusion and her condition remained stable initially. She was found to be anemic and was given intravenous iron sucrose. Shortly after iron administration, her mental status declined, and left pupil became dilated and sluggish. Repeat CT demonstrated significantly worsening PHE. This prompted maximum hyperosmolar therapy and external ventricular drain (EVD) placement which both were weaned off slowly due to liable ICPs. She was discharged home after a 25-day hospital stay.

We believe this is the first report of exacerbating PHE accompanied by clinical decline after intravenous iron administration in the setting of acute hemorrhagic brain contusions. Though the effects of systemic iron administration on brain edema and the treatments targeting cerebral iron are poorly understood, the administration of systemic iron in acute TBI seems to be detrimental. More research is needed to address iron toxicity in TBI. Our case adds to the growing evidence for such a pathway in the treatment of ICH and TBI.