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

Abstract

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.

• Authors: Vittorio Fineschi, Rocco Valerio Viola, Raffaele La Russa, Alessandro Santurro, Paola Frati
• Journal: Mediators of inflammation (Mediators Inflamm) Vol. 2017 Pg. 6024959 ( 2017) ISSN: 1466-1861 [Electronic] United States
• PMID: 28883688 (Publication Type: Journal Article, Review)

Chemical References

• HSP70 Heat-Shock Proteins

Topics

• Animals
• Brain (metabolism)
• Female
• HSP70 Heat-Shock Proteins (metabolism)
• Humans
• Hypoxia-Ischemia, Brain (metabolism)
• Male
• Oxidative Stress (drug effects)