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Biomedical subjects

R L Naeye

Publications and source records attributed to R L Naeye.

At least 19 recordsLinked to original sources
PubMed2001

Determination of the timing of fetal brain damage from hypoxemia-ischemia.

OBJECTIVE: This study analyzed the cases of 55 children with cerebral palsy to evaluate methods for determination of the time before birth at which antenatal hypoxemia-ischemia damaged the brain. STUDY DESIGN: In primate fetuses persistent fetal bradycardia develops close to the time that hypoxemia-ischemia damages basal ganglia structures in the brain. The same proved true in children in this study, so this time was thereafter used as a baseline to test the values of other proposed timers of hypoxemicischemic brain damage. RESULTS: Basal ganglia lesions predominated when bradycardia lasted <30 minutes before birth. As the bradycardia duration lengthened, white matter and eventually watershed brain lesions predominated. Lymphocytosis appeared 25 minutes after the bradycardia began, and thrombocytopenia appeared at 20 to 28 hours. The lymphocytosis disappeared 14 to 18 hours after it first appeared. CONCLUSIONS: Counting back from the time that lymphocytosis ended and thrombocytopenia began can sometimes identify the time when hypoxemia-ischemia damaged the fetal brain.

Basal Ganglia↗
PubMed1997

Chorioamnionitis, cortisol, and acute lung disease in very low birth weight infants.

OBJECTIVE: To explore the relationship between chorioamnionitis, postnatal cortisol concentrations, and acute respiratory distress in very low birth weight infants. METHODS: Appropriate for gestational age infants weighing between 501 to 1500 g at birth were enrolled into this prospective, observational study, and data regarding respiratory distress on the first day of life were recorded. Serum cortisol concentrations were measured on (a) day 2, (b) day 3 or 4, and (c) day 5, 6, or 7 of life. On day (b) or (c), 3.5 microg/kg of cosyntropin (an adrenocorticotrophic hormone analog) was given, and a repeat specimen was drawn 30 minutes later. Chorioamnionitis was diagnosed by placental examination by one author (R.L.N.). RESULTS: Forty-two infants exposed to chorioamnionitis and 37 infants not exposed were enrolled. Chorioamnionitis correlated inversely with gestational age, and was associated with decreased measures of acute respiratory support (exogenous surfactant, fraction of inspired oxygen, and ventilator support at 12 and 24 hours). Infants with chorioamnionitis had higher cortisol concentrations, both basal and stimulated. Gestational age was not significantly related to basal cortisol, but did correlate positively with stimulated values. Cortisol values from the 16 infants exposed to prenatal glucocorticoid therapy were excluded from these analyses. CONCLUSIONS: These results provide evidence that prenatal inflammation leads to adrenal stimulation, resulting in increased cortisol secretion and accelerated lung maturation. The enhanced response to cosyntropin stimulation seen in these infants may reflect an increased adrenal capacity to respond to postnatal stressors. Because of the apparent magnitude of the effect of chorioamnionitis on cortisol measures, this factor should be included in future investigations of adrenal function in very low birth weight newborns.

Chorioamnionitis↗
PubMed1995

Can meconium in the amniotic fluid injure the fetal brain?

OBJECTIVE: To determine if meconium in the amniotic fluid (AF) can cause cerebral palsy by stimulating umbilical and placental blood vessels to constrict. METHODS: Brain injury patterns were analyzed in 43 children whose exposure to meconium in the AF was their only identified risk for quadriplegic cerebral palsy. The times their injuries occurred were established by following lymphocyte counts in their blood after birth. RESULTS: All 43 had cerebral cortical and subcortical brain damage of the type produced by late gestational ischemia and hypoxemia. The time between the onset of injury and birth ranged from 2-38 hours. The neonates were severely acidotic at birth when birth occurred within 12-14 hours after ischemia and hypoxemia began. Thereafter, the acidosis receded as the time between its start and birth increased, presumably because vasoconstriction had ended. Severe acidosis did not recede in nine children whose cerebral palsy was due to disorders that kept them hypoxemic until birth. CONCLUSION: Meconium in the AF may sometimes initiate vasoconstriction that leads to ischemic, hypoxemic cerebral palsy.

Acidosis↗
PubMed1995

Determining the time before birth when ischemia and hypoxemia initiated cerebral palsy.

OBJECTIVE: To test the hypothesis that lymphocyte and normoblast counts in neonatal blood can be used to identify the time that ischemia and hypoxemia produced cerebral palsy. METHODS: Blood lymphocyte and normoblast counts were analyzed at intervals after birth in 16 neonates for whom we knew the time when antenatal ischemic and hypoxemic brain damage began. These counts were compared with counts from normal newborns, infants with low Apgar scores and no cerebral palsy, and infants with cerebral palsy caused by developmental and other early gestational disorders. RESULTS: Lymphocyte counts increased to more than 10,000/mm3 and normoblast counts to 2000/mm3 or more within 2 hours after the brain-damaging ischemia and hypoxemia began. Lymphocyte counts returned to normal levels 24 hours after the damaging event took place, and normoblast counts in 24-36 hours. Normal neonates had a mean +/- one standard deviation lymphocyte count of 4430 +/- 1418/mm3 and a normoblast count of 560 +/- 771/mm3. CONCLUSION: Following the changing counts of lymphocytes and normoblasts in neonates' blood may accurately identify the time before birth when brain-damaging ischemia and hypoxemia began.

Apgar Score↗
PubMed1990

Maternal body weight and pregnancy outcome.

Pregnancies that produced 56,857 children were analyzed to evaluate the relationship of the mothers' relative pregravid body weight to pregnancy outcome. Perinatal mortality rates progressively increased from 37 of 1000 in offspring of thin subjects to 121 of 1000 in the offspring of obese subjects (p less than 0.001). Nearly half of this mortality increase was due to preterm deliveries, particularly before 31 wk of gestation. More than half of the increase in preterm births was caused by acute chorioamnionitis. Other factors that made major contributions to the overall mortality increase were rises in the frequencies of older gravidas (ages 35-50 y), gravidas who had diabetes mellitus, children who had major congenital malformations, and dizygous twins.

Acute Disease↗
PubMed1990

The clinical significance of absent subchorionic fibrin in the placenta.

Patchy fibrin is normally present beneath the chorionic plate of the placenta. The present study attempted to determine whether it has any clinical significance. In 31,622 placentas the amount of this fibrin was related to markers of fetal activity. Fibrin was often absent when the markers indicated hypoactivity. The markers of fetal hypoactivity were neonatal hypotonia, neonatal lethargy, the presence of Down's syndrome, and a short umbilical cord. Umbilical cord length is strongly influenced by tension applied to it by fetal movements--the fewer the movements, the shorter the cord. Children with no subchorionic fibrin subsequently had increased frequencies of cerebral palsy and low intelligence quotient values. Children who were hyperactive at one year of age had increased levels of subchorionic fibrin, which suggests that they were hyperactive before birth. All of these findings raise the possibility that normal fetal movements sometimes traumatize the placenta, which leads to fibrin deposits beneath its surface.

Biomarkers↗
PubMed1990

Preventing the sudden infant death syndrome.

Current efforts in the US to prevent the sudden infant death syndrome (SIDS) are largely based on pneumocardiogram screening and home apnoea monitoring. This technology does not prevent most SIDS deaths because the screening procedures lack the sensitivity and specificity needed to identify most high risk infants. In the UK the largest efforts to prevent SIDS have been based on infant health surveillance. These efforts appear to have been ineffective and along with the US failures highlight the need for new strategies to prevent SIDS. One strategy might be to develop methods to avoid known risk factors for SIDS. Prominent among these risk factors are cigarette smoking and the use of psychotropic drugs during pregnancy, overheating and infections in infants. Possible approaches to avoid these and other risks are described in the present paper.

Brain↗
PubMed1989

Origins of cerebral palsy.

Analyses were undertaken to determine the causes of cerebral palsy in a prospective study of 43,437 full-term children. Presumed causes were found for about 71% of the 34 quadriplegic and 40% of the 116 nonquadriplegic patients with cerebral palsy. Risk estimates based on predictive models, adjusted for multiple factors, suggest that 53% of the quadriplegic patients with cerebral palsy could be attributed to congenital disorders, 14% to birth asphyxia, and 8% to other identified disorders. Thirty-five percent of the nonquadriplegic patients with cerebral palsy could be attributed to congenital disorders and 6% to other disorders. In the victims of cerebral palsy, characteristic consequences of birth asphyxia were more often the result of nonasphyxial disorders. These included meconium in the amniotic fluid, low 10-minute Apgar scores, neonatal apnea spells, seizures, persisting neurologic abnormalities, and slow head growth after birth.

Aged↗
PubMed1989

Pregnancy hypertension, placental evidences of low uteroplacental blood flow, and spontaneous premature delivery.

This study was undertaken to determine if preeclampsia and low uteroplacental blood flow cause spontaneous preterm births. No non-invasive methods are currently available to accurately measure uteroplacental blood flow, so surrogates that are known to be associated with low uteroplacental flow were used. These are preeclampsia, placental infarcts, abnormally small placental villi, and excessive syncytial knots. Preeclampsia was associated with a frequency of spontaneous preterm births that was 41% greater than expected (P less than .001). Normotensive gestations with placental findings of low uteroplacental blood flow ended preterm 147% more frequently than expected, and when a woman had two such pregnancies in succession, the second had a particularly high frequency of spontaneous preterm delivery (64%). Overall, preeclampsia and placental findings of low uteroplacental blood flow were associated with 26% of the spontaneous preterm deliveries in this study. Preeclampsia and low uteroplacental blood flow may be major causes of preterm birth.

Delivery, Obstetric↗
PubMed1989

New brain stem and bone marrow abnormalities in victims of sudden infant death syndrome.

The study looked for new abnormalities in 31 victims of sudden infant death syndrome (SIDS). The focus was on respiratory control centers in the brain stem, because some SIDS victims have had abnormalities in respiratory control during sleep. A major respiratory control area (lateral reticular nucleus) of the medulla was hypomyelinated in 9 of the 31 SIDS victims. In a second study, the size of the 12th cranial nerve nucleus and its neuronal composition were analyzed because this nucleus regulates tongue movements, and the tongue has been postulated to help obstruct the airway in some SIDS victims. The 12th nucleus was found to have a neuronal deficit in more than two thirds of the SIDS victims. Finally, the SIDS victims were found to have a normoblastic hyperplasia in their bone marrows, a presumed response to chronic hypoxemia during sleep.

Bone Marrow↗
PubMed1987

Antenatal hypoxia and low IQ values.

We undertook analyses to determine if fetal, intrapartum, and neonatal hypoxia are important causes of low IQ values. We analyzed prospectively collected pregnancy, perinatal, and subsequent developmental data for 19,117 children. As expected, sociohereditary and demographic factors had a large influence on IQ scores. Taking these latter influences into consideration, nothing that happened during labor, delivery, or the neonatal period affected subsequent IQ values. The same was true for early pregnancy disorders that can produce acute fetal hypoxia. By contrast, antenatal disorders and conditions that can produce subacute or chronic fetal hypoxia correlated with low IQ values. These antenatal disorders and conditions were maternal gestational anemia, relative gestational hypotension, hypertension, multiple births, and fetal growth retardation. All of these findings were the same whether neurologic abnormalities were absent or present, suggesting that the same factors were sometimes involved in the genesis of cognitive impairments and neurologic abnormalities.

Child↗