Abstract
Background and PurposeMaternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; however, its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the preterm brain.MethodsChronically instrumented singleton fetal sheep at 0.7 of gestation received asphyxia induced by complete umbilical cord occlusion for 25 minutes. 15 minutes after release of occlusion, ewes received a 3 ml i.m. injection of either dexamethasone (12 mg, n = 10) or saline (n = 10). Sheep were killed after 7 days recovery; survival of neurons in the hippocampus and basal ganglia, and oligodendrocytes in periventricular white matter were assessed using an unbiased stereological approach.ResultsMaternal dexamethasone after asphyxia was associated with more severe loss of neurons in the hippocampus (CA3 regions, 290±76 vs 484±98 neurons/mm2, mean±SEM, P<0.05) and basal ganglia (putamen, 538±112 vs 814±34 neurons/mm2, P<0.05) compared to asphyxia-saline, and with greater loss of both total (913±77 vs 1201±75/mm2, P<0.05) and immature/mature myelinating oligodendrocytes in periventricular white matter (66±8 vs 114±12/mm2, P<0.05, vs sham controls 165±10/mm2, P<0.001). This was associated with transient hyperglycemia (peak 3.5±0.2 vs. 1.4±0.2 mmol/L at 6 h, P<0.05) and reduced suppression of EEG power in the first 24 h after occlusion (maximum −1.5±1.2 dB vs. −5.0±1.4 dB in saline controls, P<0.01), but later onset and fewer overt seizures.ConclusionsIn preterm fetal sheep, exposure to maternal dexamethasone during recovery from asphyxia exacerbated brain damage.
Highlights
Fetuses at risk of premature delivery are routinely exposed to maternal treatment with synthetic glucocorticoids
In near-term fetal sheep, at an age when brain maturity is broadly equivalent to term infants, maternal dexamethasone treatment 48 hours before cerebral ischemia did not modify the pattern of injury [12]
DEX was associated with higher fetal PaO2 at 1 and 2 days after occlusion, greater fetal plasma glucose from 4 to 48 h and higher plasma lactate at 4 and 6 h compared to asphyxia-saline. 4 asphyxia-DEX fetuses, but no asphyxia-saline or sham controls, went into labor within 48 h after asphyxia
Summary
Fetuses at risk of premature delivery are routinely exposed to maternal treatment with synthetic glucocorticoids. Maternal glucocorticoids substantially reduce acute neonatal morbidity and mortality and reduce intraventricular hemorrhage [3]. They reduce the risk of white matter injury [4,5], the effect on later neurodevelopmental outcome is still unclear [6], and some studies report reduced head size [7]. Maternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the preterm brain
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