Neonatal hypoxia ischemia Flashcards
What is the effect of hypoxic ischaemia on the developing brain
cerebral metabolism
what causes hypoxic ischemic brain injurt
maternal factors- hypotension cord factors - prolapse, occlusion placental - abruption uternine - rupture neonatal postnatal e.g. shock cardiac arrest
what can influence injury outcome
maturational stages of brain regional changes in cbf general health of infant how long/deep was injury etiology
what can happen in neonatal encephalopathy
difficulty with respiration
depression of tone/reflexes
seizures
subnormal level of consciousness
one of highest no. of DALYs
85% in se Asia, SS africa
what is outcome following perinatal HI
HI injury at birth is a catastrophic end to a normal
pregnancy of a healthy fetus
– 10-15% of affected infants die in the first few days
– 15% of survivors develop cerebral palsy
– 40% of survivors other significant problems including deafness,
blindness, epilepsy, global developmental delay, autism, problems
with cognition, memory and fine motor skills
what happens inside during brain HI injury - cerebral metabolism
sugar becomes pyruvate by glycolysis if oxygen then lactate otherwise acetyl which goes to TCA cycle to NADH (mitochondria helps to produce this which goes into chain and produces energy in form of ATP)
what modalities are there to see cerebral metabolism
H MRS - lactate
P MRS - ATP, PCr, Pi
broadband NIRS - oxidative phosphorylation
using MRS/ NIRS - probe energy metabolism in the brain at different points
what can P MRS measure
brain intracellular pH
what happens during primary secondary injury between HI and resus, latent phase, secondary phase, tertiary phase
energy status drops so resuscitate baby. in latent phase significant energy happening in brain
in secondary phase, energy can drop again
in H MRS what are choline, cr, NAA, lactate markers of
choline - cell membranes
creatine - energetics
NAA - neuronal/axonal density and viability
lactate - marker of failed oxidative phosphorylation
what happens during the phases after HI
primary- minutes - cerebral hypoxia ischemia of sufficient severity to deplete tissue energy reserves
latent - hours - reperfusion and rexoygenation and restoration of glucose use and high energy phosphates
secondary - days - decrease in high energy phosphate in parallel with cell injury
tertiary - weeks/years 0 long term cell regeneration and repair
what treatments can we do for HI
therapeutic hypothermia- bring temp down - 7 trials showed cooling reduced risk of death or major neurodevelopmental disability
what is the effect of cooling on infants as seen in MRI
normals scans
reduced incidence of lesions in basal ganglia, WM, abnormal posterior limb of the internal capsule
