Breech delivery at term: a critical review of the literature.
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Biomedical subjects
Publications and source records attributed to I M Bernstein.
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Characteristic profiles of the free amino acid concentration in umbilical cord blood of growth retarded newborns have been observed. We hypothesized that the amniotic fluid of growth retarded fetal rats would show an increase in the ratio between glycine and valine which would parallel the pattern observed in the cord blood of growth retarded neonates, thus providing an index for the antepartum identification of the substrate deprived growth retarded fetus. Six test and 6 control dams were tested. Four fetuses per dam, matched for uterine location were examined. Test animals were fasted for 72 hours. Sampling was performed on day 21 under anaesthesia. Fetal size was significantly reduced (P < 0.0001) in the test group. [T = 2.68 gs. +/- 0.28 vs. C = 3.67 gs. +/- 0.25]. Fetal plasma concentrations of glycine showed an increase in test animals (P < 0.01) while valine showed a significant reduction (P < 0.0001). Glycine (pm/microliters) T = 308 +/- 64 vs. C = 269 +/- 47, valine (pm/microliters) T = 424 +/- 79 vs. C = 671 +/- 218]. Amniotic fluid concentrations for both glycine and valine were significantly decreased (P < 0.0001) in test animals. [Glycine (pm/microliters) T = 710 +/- 124 vs. C = 931 +/- 178; valine (pm/microliters) T = 845 +/- 169 vs. C = 1,339 +/- 234]. The glycine/valine ratio was significantly increased (P < 0.01) in both fetal plasma and amniotic fluid in test animals [Plasma T = 0.74 +/- 0.18 vs. C = 0.43 +/- 0.13. Amniotic fluid T = 0.85 +/- 0.08 vs. C = 0.69 +/- 0.09]. Consistent with our hypothesis, the amniotic fluid concentrations generally parallel the observations made in the plasma. This finding could enhance the antepartum identification of the substrate deprived growth retarded fetus.
Elevated maternal serum alpha-fetoprotein (MSAFP) levels have been associated with an increased incidence of both placental sonolucencies and pregnancy complications. We designed a prospective study to test the hypothesis that the presence of these sonolucencies or a positive maternal Kleihauer-Betke stain would be associated with an elevated risk of obstetric complications. We enrolled 95 women with singleton pregnancies, elevated MSAFP, and no evidence of fetal anomalies on second-trimester ultrasound evaluation. Placental sonolucencies were documented at the time of ultrasound examination, and a maternal Kleihauer-Betke stain for fetal cells was obtained on the same day. Complications of pregnancy included fetal growth retardation, preterm delivery, late vaginal bleeding (at or after the 20th week of gestation), and fetal death. Women with elevated MSAFP had an increased incidence of placental sonolucencies, positive maternal Kleihauer-Betke stains, first-trimester vaginal bleeding, late vaginal bleeding, preterm delivery, fetal growth retardation, and fetal death compared with controls. Thirty-nine of 95 women with elevated MSAFP (41.1%) had at least one complication. In women with elevated levels, neither the presence of placental sonolucencies nor a positive Kleihauer-Betke stain correlated with first-trimester vaginal bleeding, the MSAFP level, or an increased risk of pregnancy complications. First-trimester vaginal bleeding was associated with an increased risk of preterm delivery in subjects with elevated MSAFP.
Currently available formulas for the estimation of fetal weight assume uniform density of tissue. Because fat tissue is less dense than lean body mass, we hypothesized that the sonographic overestimation of fetal weight in infants of diabetic mothers is the consequence of an elevated proportion of body fat, resulting in a lower body density. We prospectively examined 52 children of diabetic mothers. Each had ultrasound estimation of fetal weight within 7 days of delivery and estimates of neonatal body composition made from anthropometric evaluation within 48 hours of birth. Ultrasound estimates of fetal weight were considered acceptable if they were within 10% of actual birth weight. There was no difference in mean birth weight between those overestimated (N = 22) and those underestimated (N = 8). The sum of skinfolds from two sites, the ponderal index, and percent body fat were all significantly greater in the neonates with sonographic overestimation of fetal weight. Lean body mass was significantly greater (P less than .05) in infants whose sonograms underestimated birth weight. When all subjects were included, a significant correlation was found between the degree of error in the ultrasound estimation of fetal weight and the ponderal index (r = 0.40, P less than .01), the sum of the skinfold measurements (r = 0.29, P less than .05), and the present body fat (r = 0.28, P less than .05). These data suggest that increased body fat in infants of diabetic mothers is associated with sonographic overestimation of fetal weight.
To determine the incidence and risk factors associated with an abnormal postpartum glucose tolerance in women with gestational diabetes, 103 patients with gestational diabetes had a 2-hour, 75 gm oral glucose tolerance test 6 +/- 2 weeks (mean +/- SD) after delivery. Twenty-two percent (23/103) of results were abnormal: Three showed frank diabetes, four showed impaired glucose tolerance, and 16 were, nondiagnostic. There was a significant difference in gravidity, pregravid weight and body mass index, delivery weight, gestational age at diagnosis, fasting and 2- and 3-hour glucose level at the time of the oral glucose tolerance test during pregnancy, need for insulin therapy during gestation, and neonatal weight greater than 4000 gm in the abnormal group as compared with the normal group. Elevated fasting glucose level (p = 0.0001) and earlier gestational age at time of diagnosis of gestational diabetes (p = 0.013) were found to be most predictive of an abnormal postpartum glucose tolerance test result. These results support the importance of postpartum oral glucose tolerance testing in women with gestational diabetes.
The authors hypothesized that ultrasound-generated measurements of the fetus could be used to predict body composition for children of diabetic mothers. Seven ultrasonically identifiable fetal morphometric parameters were measured on 21 fetuses of diabetic mothers within 7 days of delivery. These seven individual measurements were then matched to neonatal morphometric estimations of body composition by means of stepwise regression analysis. Ultrasound variables which were found to show significant correlation to the newborn estimates of body composition were combined to generate an equation that could predict neonatal lean body mass and fat mass. Neonatal lean body mass could be predicted with R = .93 (P less than .001, 95% confidence limits .80-.98). Neonatal fat mass could be predicted with R = .81 (P less than .001, 95% confidence limits .55-.92). Prospective evaluation of the regression equations in an additional 18 patients showed no significant difference between ultrasound-predicted body composition and newborn morphometric estimation of body composition. The authors conclude that estimations of fetal body composition are possible, and may provide a valuable tool in the identification of fetal growth abnormalities.
Plasma, amniotic fluid, and tissue concentrations of IGF-I were examined in nutritionally deprived, growth-retarded fetal rats to determine whether IGF-I concentration serves as a marker for nutritional status. Growth retardation was induced by 72 h of maternal fasting. Twenty-three control and 17 growth-retarded fetuses were individually analyzed and compared. Plasma IGF-I concentrations were significantly lower in test compared with control animals (test 56.8 +/- 14.9, control 87.4 +/- 17.5 ng/mL, p less than 0.01). Amniotic fluid IGF-I concentrations were not different (test 14.0 +/- 8.7, control 12.2 +/- 2.6 ng/mL). IGF-I concentrations obtained from both placental and hepatic tissues were lower in test compared with control animals [placenta: test 293 +/- 25 versus control 655 +/- 114 ng/g (p less than 0.001); hepatic: test 173 +/- 38 versus control 230 +/- 51 ng/g (p less than 0.01)]. Reductions in fetal, placental, and hepatic weights in test animals were more closely related to changes in placental IGF-I concentration than to either plasma or hepatic IGF-I concentrations. We conclude that fetal plasma IGF-I is a valuable marker for intrauterine substrate deprivation and that the growth-retarded rat fetus is accurately identified and specifically characterized by a low placental concentration of extractable IGF-I.
Diabetic ketoacidosis occurred in a woman without a prior history of glucose intolerance. The condition was associated with the combined administration of terbutaline and betamethasone. The patient required insulin therapy for the remainder of her pregnancy but had no further insulin requirements postpartum.
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A woman was referred at 19 weeks' gestation for genetic counseling regarding elevated maternal serum alpha-fetoprotein levels. Sonography identified fetal hydrops and fetal death. Fetal tissue specimens showed evidence of human parvovirus infection by DNA probe analysis.
A 30-year-old woman suffered massive brain injuries after a motor vehicle accident at 15 weeks' gestation. The patient was diagnosed as brain-dead on her tenth hospital day. She was supported with intensive care for 107 days after this diagnosis, and a normal 1555-g male infant was delivered at approximately 32 weeks' gestation by repeat cesarean section. The child is developing normally at 11 months of age. This represents the longest reported case of prolongation of pregnancy after brain death.
To investigate whether there are subclinical abnormalities of glucose metabolism in women with previous gestational diabetes that are consistent with a high incidence of diabetes mellitus in later life, eight patients with previous gestational diabetes and normal oral glucose tolerance were evaluated by means of body composition studies, intravenous glucose tolerance tests, and the hyperinsulinemic-euglycemic clamp coupled with 6-6 dideuterated glucose infusion, indirect calorimetry, and measurement of islet cell antibodies. Eight control subjects were matched for percent body fat and diet and studied in a similar fashion. Abnormalities of insulin response and insulin resistance were present in four (50%) of patients with previous gestational diabetes. Insulin resistance was significantly greater in the patients than in the control subjects. When compared with lean patients, obese patients with previous gestational diabetes had significantly greater insulin response to the intravenous glucose tolerance test and insulin resistance. These changes are consistent with reported findings of an early and progressive development of overt diabetes in patients who had gestational diabetes.
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We hypothesized that normal fetal size would be most appropriately characterized by a hybrid cross-sectional growth chart combining preterm (< 37 weeks) ultrasound-estimated fetal weights and full-term (> or = 37 weeks) birthweights. Concurrent cross-sectional charts defining fetal size were constructed from 1,331 ultrasound-estimated fetal weights (US) (24-40 weeks) and 9,553 birthweights (BW) (24-43 weeks) from a population of singleton offspring without anomalies. Percentile ranks (10th-90th) were established for both charts. Best-fit third-order equations generated by least-squares regression analysis were compared between the two growth charts. Weight distributions (percentile ranks) were compared separately across gestational age, and for preterm and term gestation. Statistical analysis was performed by chi-square analysis where appropriate with P < .05 accepted for significance. The BW standard failed to appropriately characterize ultrasound-estimated fetal weight across gestational age. (US: < 10th%, n = 42 [3.1%]; 10-90th%, n = 978 [73.5%]; > 90th%, n = 311 [23.4%], P < .001). The characterization of both preterm and term weights was significantly different between fetal size curves. The birthweight growth curve limited the designation of fetal growth restriction (< 10th%) in the preterm ultrasound group to 1.6% of subjects examined (n = 17, P < .001). In contrast, at term the ultrasound estimation of normal fetal weight (between the 10th and 90th percentiles) included 84% of the term birthweights (P < .05). Cross-sectional sonographically defined fetal size curves provide optimal characterization of preterm fetal weight as estimated by ultrasound. In term gestation, a normative size chart derived from ultrasound estimated fetal weight appears to broaden or overrepresent the tails of the distribution. Hybrid size curves, combining preterm ultrasound estimated fetal weight and term birthweight, provide the best estimate of the normal range of fetal weight across gestational age.