HYPERBARIC, CEREBRAL PALSY AND RETROLENTAL FIBROSPLASIA
STARTLING INFORMATION RECENTLY UNCOVERED BY DR. JAMES
SURFACE OXYGEN (80% O2) IN PREMIES IS NOT THE CAUSE OF RETROLENTAL FIBROPLASIA
SLIDE 1
Oxygen treatment of Premature Babies and Cerebral Palsy
1 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 (p<0.02)
Significance for increase in CP without additional oxygen (p<0.05)
Significance of reduction of retrolental fibroplasia without additional oxygen (p<0.02)
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
Szewczyk first suggest that retrolental fibroplasia was produced by habituating a child to an enriched oxygen atmosphere and by too sudden withdrawal.
If Szewczyk'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 Palsy 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 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