Search PubMed⌕ Search

Biomedical subjects

R L Naeye

Publications and source records attributed to R L Naeye.

At least 91 records · Page 5Linked to original sources
PubMed1979

Neonatal apnea: underlying disorders.

Data from a prospective study of 50,826 neonates were used to determine the frequency and significance of disorders related to apnea in newborns. Such apnea proved to be a significant prognosticator for neonatal death. Fifty-eight percent of preterm neonates with multiple apneic episodes and 18% with a single episode died, whereas only 6% of those without recorded apnea died. The rates were 44%, 5%, and 1% for full-term infants. Amniotic fluid infection was the underlying disorder in 35% of the preterm and 25% of the term neonates who had multiple episodes of apnea. A third of the preterm and 25% of the term infants who had such apneic episodes had antecedent hypoxia-related disorders, i.e., abruptio placentae, erythromblastosis fetalis, placenta previa, large placental infarcts, and umbilical cord compression. Among the apneic neonates, those who were infected were twice as apt to die as were those who had hypoxia-related disorders. Hypoplasia of the lungs and easily recognized central nervous system malformations were responsible for most of the apnea-related deaths associated with congenital malformations.

Amniotic Fluid↗
PubMed1978

Twins: causes of perinatal death in 12 United States cities and one African city.

The perinatal mortality rate in a large U. S. study was 139 per 1,000 births for twins and 33 per 1,000 for singletons. Sixteen per cent of the twin deaths were due to amniotic fluid infections, 11 per cent to premature rupture of the membranes, 8 per cent to the monovular twin transfusion syndrome, 8 per cent to large placental infarcts, 7 per cent to congenital anomalies, and the rest to over 20 other disorders. The perinatal mortality rate for monozygotic twins was 2.7 times that for dizygotic twins, mainly due to more amniotic fluid infections, congenital anomalies, and the twin transfusion syndrome in the monozygotic pairs. To study the role of poor maternal nutrition on twins, a similar study of perinatal mortality rates was undertaken in Addis Ababa, Ethiopia. Addis Ababa twins had 2.5 times the mortality rate of U. S. twins, mainly due to a higher frequency of amniotic fluid infections, abruptio placentae, cord accidents, obstructed labors, congenital syphillis, and the twin transfusion syndrome in the Ethiopians.

Abruptio Placentae↗
PubMed1978

Causes and consequences of placental growth retardation.

Placental growth retardation caused 84 fetal and neonatal deaths per 100,000 births. Its frequency increased as mothers' diastolic blood pressure levels increased, an effect augmented by proteinuria. The perinatal deaths also increased with advancing maternal age, anemia, and poverty. Maternal weight gains were low in the involved pregnancies, and the fetuses and neonates who died had a pattern of growth retardation characteristic of fetal undernutrition. Microscopic abnormalities in the decidua and placenta were characteristic of inadequate perfusion of the placenta from the uterus. They included fibrinoid changes in the arteries and arterioles of the decidua, villous cytotrophoblastic hyperplasia, and an obliterative endarteritis in fetal stem arteries of the placenta.

Decidua↗
PubMed1978

Causes of perinatal mortality excess in prolonged gestations.

The study sought to determine what proportion of the perinatal mortality excess associated with prolonged gestations was due to placental insufficiency. Using data from a large prospective study of pregnancy, the perinatal mortality rate was 20.9/1000 births for post-term and 11.7/1000 for term infants. Only a quarter of the perinatal mortality rate excess in the post-term pregnancies was due to disorders related to inadequate uteroplacental perfusion, i.e., abruptio placentae, large placental infarcts and marked placental growth retardation. Twenty-six per cent of the mortality excess was due to congenital malformations, 19% to amniotic fluid infections, 8% to Rh erythroblastosis fetalis and the remaining 22% to a variety of other disorders. The post-term mortality excess due to congenital malformations was in infants who had hypoplastic adrenal glands, a well-known cause of prolonged gestation. The 4205 placentas of the post-term infants did not show any significant increases in those microscopic lesions that are characteristic of uteroplacental under-perfusion.

Abruptio Placentae↗
PubMed1978

Effects of maternal cigarette smoking on the fetus and placenta.

In a large, prospective study, mothers who smoked during one pregnancy but not another had smaller infants in the pregnancy in which they smoked, irrespective of birth order and many other factors that affect fetal growth. Light cigarette smokers gained an average 90 g less at term than non-smokers, entirely due to the smaller size of the light smokers' newborn infants. Heavy smokers gained 533 g less than non-smokers, only one-third of which was due to the smaller size of the heavy smokers' newborn infants. As smoking increased, placentas enlarged and developed microscopic lesions characteristic of underperfusion from the uterus. This underperfusion was probably periodic rather than continuous because the smokers' decidua had few of the arterial lesions that are characteristic of chronic low blood flow. Pregnancies were a mean 1.5 days shorter in smokers than in non-smokers, due to more frequent amniotic fluid infections in the smokers.

Birth Weight↗
PubMed1978

Distortions in fetal growth standards.

The study analyzed several errors incorporated in widely used fetal growth standards. Such standards contain measurements from many infants who died as neonates. The present study found many of these nonsurvivors to be growth retarded so new standards were developed which contain only measurements from survivors. The study also found that weights and other body measurements of prematurely born neonates cluster at intervals consistent with maternal vaginal bleeding at monthly intervals in early pregnancy. Such bleeding is often mistaken for the last menstrual period. To avoid this error, the probability plot method was used to separate the clusters of measurements at each gestational age. The cluster with the lowest values at each gestational age was used as the data base for the new growth standards. Standard deviations from most mean values in the new growth standards are much smaller than are such deviations in the older standards.

Anthropometry↗
PubMed1978

Relationship of cigarette smoking to congenital anomalies and perinatal death. A prospective study.

Congenital anomalies caused 3.43 perinatal deaths/1000 births, as reported in a large prospective study. At all gestational ages the mortality rates progressively increased when gravidas smoked more than 10 cigarettes/day. An excessive death rate was also found in males, in offspring of mothers over 39 years of age, and in women of low socioeconomic status. Placentas associated with the malformed infants had an increased frequency of single umbilical arteries and abnormal insertions of fetal membranes and umbilical cords into the placenta.

Abnormalities, Drug-Induced↗
PubMed1978

Amniotic fluid infections with intact membranes leading to perinatal death: a prospective study.

The pathogenesis of fatal amniotic fluid infections was analyzed in a large prospective study that included more than 1,000 medical, demographic, hereditary, and postmortem variables. The disorder was the most frequent cause of death in the study, with an overall perinatal mortality of 6.17 per 1,000 births. The mortality progressively declined after mid-gestation when antimicrobial activity normally appears in the amniotic fluid. A second peak of the fatal infections, after 37 weeks' gestation, was found mainly in the poor and undernourished. Maternal gestational weight gains were suboptimal and the involved neonates had a pattern of growth retardation characteristic of undernutrition. Maternal pregnancy weight gains were positively correlated with the number of prenatal clinic visits. Mother's race, socioeconomic status, age, short stature, and number of prior unsuccessful pregnancies lost their positive association with the fatal infections when mothers made more than nine clinic visits.

Amniotic Fluid↗
PubMed1978

Amniotic fluid infections, neonatal hyperbilirubinemia, and psychomotor impairment.

A large prospective study found that infants born with evidence of recent amniotic fluid infections subsequently had an increased frequency of mental, motor, visual, and hearing impairment. These infections also potentiated the neurotoxicity of neonatla hyperbilirubinemia. This potentiation of bilirubin neurotoxicity of neonatal hyperbilirubinemia. This potentiation of bilirububin neurotoxicity increases with the severity of the amniotic fluid infections. With or without such infections, an increased frequency of long-term mild mental retardation started at peak neonatal bilirubin levels of only 7 mg/dl in both term and preterm infants. Significant neurologic abnormalities began at peak bilirubin levels of 12 to 13 mg/dl.

Amniotic Fluid↗
PubMed1978

Placenta previa. Predisposing factors and effects on the fetus and surviving infants.

The pathogenesis of placenta previa was analyzed in a large prospective study that included more than 1000 medical, demographic, hereditary, and postmortem variables. It caused 73 perinatal deaths per 100,000 births. The frequency of the deaths increased with short maternal stature, increasing parity, prior preterm deliveries, and prior perinatal deaths. More male infants died than females. Placentas showed diffuse hyperplastic enlargement of terminal villi, marginal decidual necrosis, and marginal thrombi. These abnormalities were likely related to blood loss and abruption. Both the infants who died and those who survived had a pattern of fetal growth retardation characteristic of undernutrition. Long-term physical growth and psychomotor development were normal in the surviving infants except for a small excess of neurologic abnormalities.

Child Development↗
PubMed1977

Abruptio placentae and perinatal death: a prospective study.

Abruptio placentae caused 3.96 perinatal deaths per 1,000 births in a large prospective study. Intrapartum but not prepartum maternal hypertension was observed in the fatal cases. Decidual necrosis at the placental margin and large placental infarcts were the most characteristic placental abnormalities. The decidual necrosis was correlated with maternal cigarette smoking and low pregnancy weight gains in the abruption placentae cases. The fetuses and neonates who died had a pattern of growth retardation characteristic of antenatal undernutrition, indicating that poor maternal nutrition during pregnancy may have contributed to the genesis of the abruptio placentae.

Abruptio Placentae↗
PubMed1977

Causes of perinatal mortality in the US Collaborative Perinatal Project.

The underlying causes of 80% of perinatal deaths were identified in a study of 53,518 pregnacies in the United States: 17% of the deaths were due to amniotic fluid infections, 11% to abruptio placentae, 10% to premature rupture of the membranes, 9% to congenital anomalies, 6% to large placental infarcts, and the rest to more than 20 other specific disorders.

Abruptio Placentae↗
PubMed1977

Failure of bacterial growth inhibition by amniotic fluid.

The bactericidal properties of amniotic fluid normally protect fetuses from late gestational infections by bacteria. Recently, such infections were found responsible for nearly a third of the perinatal deaths in Addis Ababa, Ethiopia. This prompted an analysis of the antimicrobial activity of amniotic fluid in patients in that city. The antimicrobial activity of fluid from 53 women, collected at term, was measured by a semiquantitative plate-count technique. Only one of the fluid samples was bactericidal, 12 were bacteriostatic, and 40 were noninhibitory to bacterial growth.

Amniotic Fluid↗
PubMed1977

Amniotic fluid infections in an African city.

Amniotic fluid infections were the most common cause of perinatal death in Addis Ababa, Ethiopia (21.8/1,000 live births). Most such infections appear to originate in the fetal membranes near the cervical os. The high rate of spread of these local infections into the amniotic fluid in Addis Ababa appears related to a lack of antimicrobial activity in amniotic fluids. Factors that adversely affected nutrition in the gravid woman, lack of prenatal medical care, and low water usage were associated with the high rate of fatal infections.

Amniotic Fluid↗