Abstract
The effect of ethacrynic acid on cerebral edema of the newborn was evaluated in 9 infants who experienced severe hypoxia-ischemia during delivery. Six expired, without clinical or pathological evidence of cerebral edema at autopsy. The 3 surviving infants are normal developmentally. One has a seizure disorder.
Ethacrynic acid has been used effectively in immature animals to prevent cerebral edema. Bourke et al. have used ethacrynic acid in the immature cat to prevent edema that was K+ dependent, HCO3-stimulated and appeared following the stage of brain maturation characterized by glial proliferation.
The human infant has significant glial cell proliferation by 35-36 weeks of gestational age and becomes subject to severe cerebral edema at that time. The infant who experiences anoxia is considered to sustain cellular damage initially from hypoxemiaischemia and secondarily from cerebral edema. The goal of treatment with ethacrynic acid is to change the impact of the secondary cerebral edema. Criteria for initiation of treatment were strict: apgar of 0-1 at 1 minute and less than 3 at 5 minutes, or late or variable deceleration with heart rate under 100 beats per minute for 20 minutes or longer during the delivery. After resuscitation and stabilization, 1 mg/kg per IV was given every 12 hours for a 48 hour period.
Our initial study suggests that ethacrynic acid is a safe and effective drug for treatment of cerebral edema in the newborn.
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Ellison, P., Macdonald, M. & Bourke, R. 1124 ETHACRYNIC ACID THERAPY OF CEREBRAL EDEMA IN THE NEWBORN. Pediatr Res 12 (Suppl 4), 551 (1978). https://doi.org/10.1203/00006450-197804001-01130
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DOI: https://doi.org/10.1203/00006450-197804001-01130