A Controversial Medicolegal Issue: Timing the Onset of Perinatal Hypoxic-Ischemic Brain Injury

Perinatal hypoxic-ischemic brain injury, as a result of chronic, subacute, and acute insults, represents the pathological consequence of fetal distress and birth or perinatal asphyxia, that is, “nonreassuring fetal status.” Hypoxic-ischemic injury (HII) is typically characterized by an early phase o...

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Bibliographic Details
Published in:Mediators of inflammation 2017-01, Vol.2017 (2017), p.1-11
Main Authors: Santurro, Alessandro, La Russa, Raffaele, Viola, Rocco Valerio, Fineschi, Vittorio, Frati, Paola
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Asphyxia
Asphyxia neonatorum
Autophagy
Biomarkers
Births
Brain
Brain - metabolism
Brain injury
Brain research
Chaperonins
Complications and side effects
Cytotoxicity
Edema
Excitotoxicity
Female
Fetal distress
Fetuses
Health aspects
HSP70 Heat-Shock Proteins - metabolism
Humans
Hypoxia
Hypoxia-Ischemia, Brain - metabolism
Infants (Newborn)
Inflammation
Injuries
Ischemia
Lysis
Male
Mitochondria
Neonates
Neurosciences
Oxidative stress
Oxidative Stress - drug effects
Pathology
Pediatrics
Phagocytosis
Proteins
Reperfusion
Review
Stillbirth
Traumatic brain injury
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Summary:Perinatal hypoxic-ischemic brain injury, as a result of chronic, subacute, and acute insults, represents the pathological consequence of fetal distress and birth or perinatal asphyxia, that is, “nonreassuring fetal status.” Hypoxic-ischemic injury (HII) is typically characterized by an early phase of damage, followed by a delayed inflammatory local response, in an apoptosis-necrosis continuum. In the early phase, the cytotoxic edema and eventual acute lysis take place; with reperfusion, additional damage should be assigned to excitotoxicity and oxidative stress. Finally, a later phase involves all the inflammatory activity and long-term neural tissue repairing and remodeling. In this model mechanism, loss of mitochondrial function is supposed to be the hallmark of secondary injury progression, and autophagy which is lysosome-mediated play a role in enhancing brain injury. Early-induced molecules driven by hypoxia, as chaperonins HSPs and ORP150, besides common markers for inflammatory responses, have predictive value in timing the onset of neonatal HII; on the other hand, clinical biomarkers for HII diagnosis, as CK-BB, LDH, S-100beta, and NSE, could be useful to predict outcomes.
ISSN:0962-9351
1466-1861
DOI:10.1155/2017/6024959