A case of intravenous iron administration resulting in cerebral edema expansion

Abstract Background 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 t...

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Main Authors: Jonathan Espinosa, Umair Rehman, Firas Kaddouh
Format: Article
Language:English
Published: BMC 2023-05-01
Series:BMC Neurology
Subjects:
Online Access:https://doi.org/10.1186/s12883-023-03258-8
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author Jonathan Espinosa
Umair Rehman
Firas Kaddouh
author_facet Jonathan Espinosa
Umair Rehman
Firas Kaddouh
author_sort Jonathan Espinosa
collection DOAJ
description Abstract Background 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). Case presentation 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. Conclusions 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.
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spelling doaj.art-1c2d71c87f3e4150a28210125bf96cd22023-06-04T11:31:57ZengBMCBMC Neurology1471-23772023-05-012311410.1186/s12883-023-03258-8A case of intravenous iron administration resulting in cerebral edema expansionJonathan Espinosa0Umair Rehman1Firas Kaddouh2Department of Neurosurgery, University of Texas Health Science Center San AntonioDepartment of Neurosurgery, University of Texas Health Science Center San AntonioDepartment of Neurology, University of Arizona College of MedicineAbstract Background 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). Case presentation 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. Conclusions 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.https://doi.org/10.1186/s12883-023-03258-8Cerebral edemaIntracerebral hemorrhageTraumatic brain injuryIntravenous ironPerihematomal edemaCase report
spellingShingle Jonathan Espinosa
Umair Rehman
Firas Kaddouh
A case of intravenous iron administration resulting in cerebral edema expansion
BMC Neurology
Cerebral edema
Intracerebral hemorrhage
Traumatic brain injury
Intravenous iron
Perihematomal edema
Case report
title A case of intravenous iron administration resulting in cerebral edema expansion
title_full A case of intravenous iron administration resulting in cerebral edema expansion
title_fullStr A case of intravenous iron administration resulting in cerebral edema expansion
title_full_unstemmed A case of intravenous iron administration resulting in cerebral edema expansion
title_short A case of intravenous iron administration resulting in cerebral edema expansion
title_sort case of intravenous iron administration resulting in cerebral edema expansion
topic Cerebral edema
Intracerebral hemorrhage
Traumatic brain injury
Intravenous iron
Perihematomal edema
Case report
url https://doi.org/10.1186/s12883-023-03258-8
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