Infection and fetal neurologic injury.
OBJECTIVE
Antepartum fetal exposure to infection/inflammation is a more important risk factor for brain injury than intrapartum hypoxia in both the term and preterm neonate. Such preexisting infection/inflammation might also provide the platform for subsequent intrapartum hypoxic-ischaemic damage. This review will discuss the complex interaction between fetal inflammatory response and neurotoxicity, and focus on the clinical implications of the synergistic interaction between infection/inflammation and hypoxia-ischaemia.


RESULTS
Current evidence indicates that inflammatory mediators are directly neurotoxic, and also sensitize the fetal brain tissue to a greater magnitude of damage by subsequent hypoxia-ischaemia by lowering the threshold at which hypoxia initiates neuronal cell apoptosis/cell death.


CONCLUSIONS
Further studies are urgently needed to characterize the fetuses at risk of damage, the duration of exposure required to cause injury, the influence of gestational age and whether Caesarean section may be protective. Until then clinicians should maintain a high level of surveillance in labours complicated by infection and avoid additional exposure to hypoxic-ischaemic insults.
Ugwumadu
Austin
A
Department of Obstetrics & Gynecology, St George's Hospital, London, UK. augwumad@sgul.ac.uk
D002821:Chorioamnionitis / Q000503:physiopathology*; D005260:Female; D005311:Fetal Hypoxia / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000503:physiopathology*; D007231:Infant, Newborn; D007249:Inflammation; D007969:Leukomalacia, Periventricular / Q000503:physiopathology*; D011247:Pregnancy