title: Subtle hemorrhagic brain injury is associated with neurodevelopmental impairment in infants with repaired congenital heart disease.
abstract: OBJECTIVE
  Perioperative stroke and periventricular leukomalacia have been reported to occur commonly in infants with congenital heart disease. We aimed to determine the incidence and type of brain injury in infants undergoing 2-ventricle repair in infancy and to determine risk factors associated with such injury.
  
  
  METHODS
  Forty-eight infants enrolled in a trial comparing 2 different hematocrits during surgical repair of congenital heart disease underwent brain magnetic resonance imaging scans and neurodevelopmental testing at 1 year of age.
  
  
  RESULTS
  Eighteen (38%) of our subjects had tiny foci of hemosiderin by susceptibility imaging, without evidence of abnormalities in corresponding regions on conventional magnetic resonance imaging sequences. Subjects with foci of hemosiderin had a significantly lower Psychomotor Developmental Index at 1 year of age (79.6 +/- 16.5, mean +/- standard deviation) compared with subjects without these foci (89.5 +/- 15.3; P = .04). Older age at surgery and diagnostic group were significantly associated with the presence of hemosiderin foci. Only 1 subject had a small stroke (2%), and 2 subjects had periventricular leukomalacia (4%).
  
  
  CONCLUSIONS
  Foci of hemosiderin without radiologic evidence of ischemic brain injury are an abnormality associated with adverse neurodevelopmental outcome not previously described in magnetic resonance imaging studies of children with surgically repaired congenital heart disease. The association of hemosiderin foci with older age at surgery and cardiac diagnosis, and not with risk factors associated with brain injury, in previous studies suggests that the cause and pathogenesis of this abnormality are different from ischemic brain lesions reported previously.
authors.affiliation: Department of Neurology, Children's Hospital Boston, Boston, MA 02115, USA. janet.soul@childrens.harvard.edu
authors.forename: Janet S
authors.initials: JS
authors.lastname: Soul
authors.forename: Richard L
authors.initials: RL
authors.lastname: Robertson
authors.forename: David
authors.initials: D
authors.lastname: Wypij
authors.forename: David C
authors.initials: DC
authors.lastname: Bellinger
authors.forename: Karen J
authors.initials: KJ
authors.lastname: Visconti
authors.forename: Adré J
authors.initials: AJ
authors.lastname: du Plessis
authors.forename: Barry D
authors.initials: BD
authors.lastname: Kussman
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Scoppettuolo
authors.forename: Frank
authors.initials: F
authors.lastname: Pigula
authors.forename: Richard A
authors.initials: RA
authors.lastname: Jonas
authors.forename: Jane W
authors.initials: JW
authors.lastname: Newburger
mesh_terms: D001921:Brain / Q000378:metabolism / Q000473:pathology*; D002543:Cerebral Hemorrhage / Q000150:complications* / Q000175:diagnosis; D002658:Developmental Disabilities / Q000175:diagnosis / Q000209:etiology*; D005260:Female; D006330:Heart Defects, Congenital / Q000150:complications* / Q000473:pathology / Q000601:surgery; D006485:Hemosiderin / Q000032:analysis; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007969:Leukomalacia, Periventricular / Q000150:complications; D008279:Magnetic Resonance Imaging; D008297:Male; D012307:Risk Factors; D020521:Stroke / Q000150:complications
chemical_list: D006485:Hemosiderin