The
Pathogenesis of Cerebral Injury in the Newborn
Phillip B James
Wolfson Hyperbaric Medicine Unit
The University of Dundee,
Scotland, UK.
Birth involves the transfer of the
function of oxygenation, the most critical factor in life
support from the placental circulation to breathing. This
transfer oroxygenation to the lungs of the neonate requires
major changes to the neonatal circulation. During labor,
placental blood flow is inevitably compromised by uterine
contractions, and if oxygenation falls below a critical level,
then brain damage may occur at this time. Prystowsky has
suggested that mothers should breathe 100% oxygen during labor
as a preventative measure, because of the increased gradient for
the delivery of oxygen to tissue. Premature placental separation
may also severely compromise fetal oxygenation and delivery may
also be associated with fetal brain tissue. In the last few
weeks of intrauterine life the cerebral circulation of the fetus
matures in preparation for birth. The changes are most prominent
in the mid-brain with increased vascularisation and maturation
of the blood-brain barrier. If delivery is premature the neonate
is at special risk of damage because these critical changes have
not yet taken place. Ultrasonic imaging through the anterior
fontanelle allowed damage to the mid0brain to be detected.
Global oxygen deprivation may result in brain atrophy leading to
Microcephaly, but lesser degrees of hypoxia cause cerebral
edema, particularly in the midbrain where the nutrition of some
the tissue is dependent on the venous drainage. The increased
tissue water content reduces oxygen transport and if the edema
is not resolved the basal ganlia and the critical areas of the
midbrain can undergo cystic degeneration. The blood-brain
barrier failure may also be associated with hemorrhage. Damage
to the internal capsules in cerebral medulla leads often
involves the internal capsules severing the pyramidal tracts.
However, in many cases the tracts continue to function for some
time but myelination is prevented leaving the axis cylinders
exposed. This is associated with a delay in the development of
spasticity which may be as long as two years. The additional
gradient for the transport of oxygen that is provided by
breathing oxygen under Hyperbaric conditions may be able to
prevent brain damage in many children as Magnetic Resonance
Spectroscopy can detect hypoxia inferred from the presence of
lactate it is possible to screen infants at birth to identify
those at risk. Even after a delay, the use of hyperbaric -oxygen
therapy may be beneficial by resolving the edema. This may allow
the completion of myelination and prevent the development of
spasticity.
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