Article

Brain injury in preterm newborn infants is often attributed to hypoxia-ischemia
even when neither hypoxia nor ischemia is documented,
and many causative
speculations are based on the same assumption. We review human and animal study
contributions with their strengths and limitations, and conclude that - despite
all the work done in human fetal neuropathology and developmental models in
animals - the evidence remains unconvincing that hypoxemia, in the fetus or
newborn infant, contributes appreciably to any encephalopathy of prematurity.
Giving an inappropriate causal name to a disorder potentially limits the options
for change, should our understanding of the etiologies advance. The only
observationally-based title we think appropriate is 'encephalopathy of
prematurity'. Future pathophysiological research should probably include
appropriately designed epidemiology studies, highly active developmental
processes, infection and other inflammatory stimuli, the immature immune system,
long chain fatty acids and their transporters, and growth (neurotrophic) factors.
WHAT THIS PAPER ADDS: Fetal hypoxemia is rarely documented in brain injury
studies. Animal studies fail to consider human-animal fetal anatomical
differences. Putative treatments from animal models have not found clinical use.
Observational studies constitute the only approach to etiological understanding.
No convincing evidence yet that hypoxemia injures preterm brain. Encephalopathy
of prematurity is preferable to hypoxia-ischemia as a term for this disorder.
Encephalopathy of prematurity is preferable to hypoxia-ischemia as a term for
this disorder.
CI - (c) 2017 The Authors. Developmental Medicine and Child Neurology published by Mac
Keith Press.

Langue : ANGLAIS