STARTLING
INFORMATION RECENTLY UNCOVERED BY DR. JAMES:
SURFACE OXYGEN (80% 02) IN PREMIES IS NOT THE CAUSE OF
RETROLENTAL FIBROPLASIA.
SLIDE I
Oxygen Treatment of Premature Babies and Cerebral Palsy
I of 16 children in 1950 to 1952 had cerebral palsy and 4 had
retrolental fibroplasia.
10 of 25 born in 1953-1955 had cerebral palsy and None had
retrolental fibroplasia
(P0.02)
Significance for increase in CP without additional oxygen
(p0.05)
significance of reduction of retrolental fibroplasia without
additional oxygen
(p0.02)
Alison D McDonald
Dev,, Med Child Neurol 1964-.6:313-314.
SLIDE 2
Oxygen Treatment of Premature Babies and Cerebral Palsy
Unfortunately it may prove impossible to prevent spastic
diplegia by increasing the ambient oxygen Concentration without
causing retrolental fibroplasia, and in that case some way of
improving the blood flow to vulnerable areas of the brain may
have to be considered.
Alison D McDonald
Dev Med Child Neurol 1964-.6:313-314.
SLIDE 3
Oxygen Cerebral Palsy and Retrolental Fibroplasia
Szewczvk first suggest that retrolental fibroplasia was produced
by habituating a child to an enriched oxygen atmosphere and by
too sudden withdrawal.
If Szewczvk's theory was correct the disease in the early stage
should appear after the child's removal from a high oxygen
environment: this is. almost without exception, true.
Forrester RM
Dev Med Child Neurol 1964;6:648-650
SLIDE 4
Oxygen Cerebral Palsv and Retrolental Fibroplasia
The next logical step was to say, that if the retinopathy
developed when the child came out of oxygen the safest thing to
do would be to put him back in again. We used this technique in
17 cases.
The results were spectacular: in each individual case the
retinal vascular pattern having shown gross abnormalities.
returned to normal.
Forrester RM
Dev, Med Child Neurol 1964:6:648-650
SLIDE 5
oxygen Cerebral Palsy and Retrolental Fibroplasia
In most cases a slow, reduction of oxygen and final return to
atmospheric concentration over a period of weeks was all that
was necessary, but two infants needed a third period of oxygen
exposure because the disease again became active.
Many of the infants were exposed to high oxygen tensions for
very long periods
(the longest were 93,88,85 and 83 days).
Twelve of these infants recovered with normal eyes and five had
minor permanent changes not causing blindness.
Forrester RM
Dev, Med Child Neurol 1964:6:648-650
SLIDE 6
oxygen Cerebral Palsy and Retrolental Fibroplasia
If one believes that oxygen has a direct toxic effect on the
infant's retina these surely would have been the infants who
became blind for they were all of very low birth weight, all had
the early retinopathy and they were all subjected to intensive
and prolonged therapy.
Forrester RM
Dev, Med Child Neurol 1964-.6:648-650
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