Comparison of fetal growth estimates based on birth weight and ultrasound references.

OBJECTIVE: To compare three different methods for modeling fetal weight gain during the third trimester of pregnancy. METHODS: Ultrasound and live birth weight data were used to construct three models for defining fetal growth during the third trimester: longitudinal ultrasound estimates of fetal weight obtained serially at 3-4 week intervals in 50 uncomplicated, well-dated pregnancies between 19 and 40 weeks' gestation; cross-sectional ultrasound estimates of fetal weight obtained from 2018 ultrasound examinations of singleton, non-anomalous fetuses between 24 and 39 weeks' gestation; and cross-sectional birth weight data obtained from 9553 live singleton, non-anomalous neonates between 24 and 43 completed weeks. Analysis was performed by pairwise partial f test to compare regression curves and zeta test for comparison of mean weekly weight gain. A value of p < 0.05 was accepted for significance. RESULTS: Derived regression lines depicting fetal size across gestation were significantly different from each other (f tests, p < 0.05). Estimates of mean fetal weight were significantly different between the three different models at specific gestational ages. Significant weekly variations in fetal weight gain were observed within the raw cross-sectional data sets, both for ultrasound-estimated fetal weight (range 91-278 g/week) and birth weight (65-309 g/week). CONCLUSIONS: Each of the methods used to model normal fetal weight gain in the third trimester defined a distinct pattern of fetal growth. Normal fetal growth, defined longitudinally, was most closely matched by a combination of cross-sectional ultrasound-derived estimated fetal weight in preterm gestation below 34 weeks' gestation and live birth weight at or beyond 34 weeks.

Plasma volume expansion in early pregnancy.

OBJECTIVE: To determine the time course of plasma volume expansion in early pregnancy. METHODS: We prospectively measured plasma volume by Evans blue dye dilution during the menstrual (cycle day 2--3), follicular (cycle day 9--10), and luteal phases (cycle day urinary leutinizing hormone [LH] surge plus 9--10) of the menstrual cycle and at three additional time points (LH surge + 16 days, LH surge + 28 days, and LH surge + 70 days) in women achieving pregnancy. Twenty-one subjects were examined during 38 menstrual cycles to establish baseline menstrual cycle data. Ten subjects conceived within 1 year of menstrual cycle studies. All ten pregnancies were viable and reached the third trimester. Analyses used repeated-measures analysis of variance with P <.05 accepted for significance. RESULTS: Mean plasma volume was found to change significantly across the period of observation (P <.008) in those who conceived. Plasma volume at LH surge + 70 days (12 menstrual weeks, 2320 +/- 280 mL) was greater than either menstrual cycle estimates or early pregnancy estimates of plasma volume. There was no difference in plasma volume at LH surge + 16 days (2077 +/- 288 mL) or LH surge + 28 days (2010 +/- 271 mL) compared with menstrual cycle measurements during the menstrual phase (2156 +/- 292 mL), follicular phase (2036 +/- 280 mL), and luteal phase (2120 +/- 425 mL). There was no significant difference between those who conceived and those who did not in their mean menstrual cycle plasma volume. CONCLUSION: Plasma volume expansion in early human pregnancy cannot be identified until after the sixth menstrual week. By 12 menstrual weeks, plasma volume has expanded by approximately 14% +/- 12% (mean +/- SD) over follicular phase measurements.

Impact of maternal cigarette smoking on fetal growth and body composition.

OBJECTIVE: The aim of this study was to determine the impact of maternal cigarette smoking on the fetal accretion of fat and lean body mass. We hypothesized that maternal smoking would result in a reduction in the deposition of lean body mass. STUDY DESIGN: Longitudinal ultrasonographic examinations on 65 singleton fetuses without anomalies of smoking mothers were compared with 36 singleton fetuses without anomalies of nonsmoking mothers. A total of 214 ultrasonographic examinations were performed between 27 and 37 weeks' gestation. All subjects underwent at least 2 ultrasonographic examinations separated by 4 weeks. We compared the slopes of the growth curves for individual morphometric parameters including head circumference, femur length, abdominal circumference, thigh muscle area, thigh fat area, estimated fetal weight and percentage of thigh fat between groups. Analysis was performed with a repeated measures analysis of covariance. Potential covariates included prepregnancy body mass index (in kilograms per square meter), weight gain during pregnancy, maternal age, parity, and fetal sex recorded at birth. Demographic variables are expressed as mean +/- SD; fetal measurements are expressed as mean +/- SE. Both t tests and chi(2) analyses were used to compare groups with respect to demographic variables. P <.05 was accepted for significance. RESULTS: There were no significant differences between groups in maternal prepregnancy weight, maternal height, maternal prepregnancy body mass index, weight gain in pregnancy, parity, or fetal sex. Smokers were younger than nonsmokers (smokers, 23.7 +/- 6.0 years; nonsmokers, 31.8 +/- 6. 0 years; P <.0001), and neonatal weight was reduced among smokers (smokers, 3269 +/- 507 g; nonsmokers, 3519 +/- 411 g; P <.01). There were no differences in the growth rates of head circumference (P =. 79) and femur length (P =.67). Growth rates of abdominal circumference (smokers, 9.0 +/- 0.3 mm/wk; nonsmokers, 10.3 +/- 0.5 mm/wk; P =.01), estimated fetal weight (smokers, 171 +/- 5.4 g/wk; nonsmokers, 193 +/- 8.0 g/wk; P =.008), and muscle area (smokers, 64. 1 +/- 3.8 mm(2)/wk; nonsmokers, 76.4 +/- 5.6 mm(2)/wk; P =.03) were significantly reduced among smokers. There was a reduction in the rate of fat deposition in the thighs of fetuses of smoking mothers (smokers, 38.7 +/- 3.7 mm(2)/wk; nonsmokers, 54.6 +/- 5.4 mm(2)/wk; P =.004); however there was no absolute difference in the amount of fat measured in the thigh between 33 and 37 weeks' gestation. CONCLUSION: We detected reduced fetal growth that selectively affected abdominal circumference and peripheral muscle mass while not affecting head circumference and femur length in fetuses of smoking mothers. The effect of cigarette smoking on fetal fat deposition was less clear. Cigarette smoking appears to have a selective effect within lean body mass compartments, with affected compartments including peripheral fetal muscle. The findings of a reduction in abdominal circumference growth compared with control subjects in combination with no difference in subcutaneous fat content beyond 33 weeks' gestation are potentially explained by a reduction in fetal liver size that may result from maternal smoking.

Morbidity and mortality among very-low-birth-weight neonates with intrauterine growth restriction. The Vermont Oxford Network.

OBJECTIVE: We sought to determine the associations between intrauterine growth restriction and neonatal morbidity and mortality, as well as the impact of prenatal glucocorticoid administration on the frequency of specific complications of prematurity among neonates with intrauterine growth restriction. STUDY DESIGN: We examined the association between intrauterine growth restriction and adverse neonatal outcomes in a population of 19,759 singleton very-low-birth-weight neonates without major birth defects. We included neonates from 25 to 30 weeks' gestation entered in the Vermont Oxford Network database between 1991 and 1996 by 196 institutions. Intrauterine growth restriction was defined as the 10th percentile for birth weight according to the 1993 US national statistics. Odds ratios were estimated according to stepwise logistic regression for each neonatal outcome. Potential explanatory variables included gestational age, intrauterine growth restriction, race, prenatal care, prenatal glucocorticoid administration, route of delivery, fetal sex, and birth within versus postnatal transfer to a network institution. RESULTS: There was a statistically significant association of intrauterine growth restriction with neonatal death (odds ratio, 2.77; 95% confidence interval, 2.31-3. 33), necrotizing enterocolitis (odds ratio, 1.27; 95% confidence interval, 1.05-1.53), and respiratory distress syndrome (odds ratio, 1.19; 95% confidence interval, 1.03-1.36). There was a trend (P <. 10) toward association of intrauterine growth restriction with increased risks of intraventricular hemorrhage (odds ratio, 1.13; 95% confidence interval, 0.99-1.29) and severe intraventricular hemorrhage (grades III and IV; odds ratio, 1.25; 95% confidence interval, 0.98-1.59). Maternal prenatal glucocorticoid administration was associated with significantly lower risks of respiratory distress syndrome (odds ratio, 0.51; 95% confidence interval, 0.44-0.58), intraventricular hemorrhage (odds ratio, 0.67; 95% confidence interval, 0.61-0.73), severe intraventricular hemorrhage (odds ratio, 0.50; 95% confidence interval, 0.43-0.57), and death (odds ratio, 0.54; 95% confidence interval, 0.48-0.62). The benefits of prenatal glucocorticoid therapy for growth-restricted newborns were similar to those among normally grown infants. CONCLUSIONS: Intrauterine growth restriction within the range of 501 to 1500 g birth weight is associated with increased risks of neonatal death, necrotizing enterocolitis, and respiratory distress syndrome. Prenatal corticosteroid use was associated with decreased risks of all outcomes studied except necrotizing enterocolitis. We found no evidence that this benefit was dependent on fetal size.

Intolerance to volume expansion: a theorized mechanism for the development of preeclampsia.

We present a theorized mechanism for the development of preeclampsia, suggesting that one important underlying pathophysiologic mechanism is intolerance to volume expansion. The stage is set for this intolerance by chronic volume constriction, which leads to a requirement for increased basal peripheral vasoconstrictor tone to maintain blood pressure and allow for continued perfusion of the upright hominid head. In pregnancy, volume expansion signaled by the placenta cannot be accommodated by the constricted vascular system. The inability of the normally adaptive endothelial vasodilatory mechanisms to overcome the chronic vasoconstrictor tone leads to endothelial damage, exacerbation of vasoconstriction, and clinical hypertension. Disease resolution, characterized by diuresis, occurs with the elimination of the placenta-derived drive to retain volume. The reason preeclampsia does not recur uniformly with subsequent pregnancy is permanent restructuring of the maternal cardiovascular system with pregnancy that allows for greater plasma volume expansion in future gestations.

Angiotensinogen genotype and plasma volume in nulligravid women.

OBJECTIVE: To determine if nonpregnant plasma volume is altered in women who are homozygous for the T 235 coding angiotensinogen allele, which predisposes women to an increased risk of preeclampsia. METHODS: We measured plasma volume by Evans blue dilution and analyzed it as a function of angiotensinogen genotype in 15 nulligravid women during midfollicular phase of 26 menstrual cycles. Eleven women were evaluated during two cycles, and four women were evaluated in one cycle. Fourteen women were white, and one was Asian. No subjects had illnesses or were taking medication. The range of body mass index (BMI [kg/m2]) was 20.2-31.0. Plasma volume (mL) was reported as plasma volume divided by BMI to control for variations in body sizes. Statistical analysis was performed by analysis of variance with post hoc testing using Fisher least significant difference test for multiple comparisons (P < .05 accepted for significance). RESULTS: Angiotensinogen genotype analysis showed five women homozygous for M 235, three women homozygous for T 235, and seven women who were heterozygous (MT 235). T 235 homozygotes had significantly lower plasma volume divided by BMI compared with women who were homozygous for M 235 and women who were heterozygous for MT 235 (mean + standard deviation [SD] [71.2 + 8.8, 86.6 + 5.2, 95.8 + 15.6, respectively, P < .05]). There was a tendency toward higher plasma volume in heterozygote MT 235 compared with homozygote M 235 carriers, but it was not statistically significant. CONCLUSION: We conclude that the homozygous T 235 coding angiotensinogen genotype is associated with reduced plasma volume in nulligravid women during the follicular phase of the menstrual cycle compared with M 235 homozygotes and heterozygotes. This association of the T 235 coding genotype might contribute to fetal growth restriction in preeclampsia.

Amniotic fluid glycine-valine ratio and neonatal morbidity in fetal growth restriction.

OBJECTIVE: To test the hypothesis that an elevated amniotic fluid glycine-valine ratio predicts neonatal morbidity in growth-restricted newborns. METHODS: Amniotic fluid (AF) was collected from 122 third-trimester pregnancies (range 31-39 weeks), 49 of which were complicated by fetal growth restriction. Amino acid analysis was performed by high-pressure liquid chromatography. Glycine-valine ratios were compared between normal and growth-restricted fetuses. Neonatal morbidity within the group of growth-restricted fetuses was characterized by evaluation of neonatal hypoglycemia, arterial cord blood gas analysis, and birth weight percentile. We also examined the correlation of AF glycine-valine ratio to the umbilical artery resistance index. The median interval between AF sampling and delivery was 1 day (range 0-8 days). Analyses were performed by Student t test, chi 2 with Yates correction, or simple correlation when appropriate. P < .05 was considered significant. RESULTS: Growth-restricted fetuses have a significantly elevated AF glycine-valine ratio compared with control subjects (3.31 +/- 1.06 versus 2.61 +/- 0.77, respectively, P < .001). There was no association of the glycine-valine ratio with gestational age for either group. An elevated glycine-valine ratio was not associated with neonatal hypoglycemia within the growth-restricted group (hypoglycemia: [n = 16] 3.19 +/- 1.07; no hypoglycemia: (n = 30) 3.44 +/- 1.09). There were no significant correlations of glycine-valine ratio with arterial cord blood pH (r = -0.10), oxygen pressure (r = 0.04), or base deficit (r = 0.12). There were no significant correlations of glycine-valine ratio and birth weight percentile (r = -.24) or umbilical artery resistance index (r = -.14). CONCLUSION: Amniotic fluid glycine-valine ratio is elevated in growth-restricted fetuses compared with control fetuses. However, the level of glycine-valine elevation is not associated with neonatal morbidity related to hypoglycemia, arterial cord blood gas abnormalities, or birth weight percentile.

Maternal insulin sensitivity and cord blood peptides: relationships to neonatal size at birth.

OBJECTIVE: To examine the relationship of multiple maternal and cord blood correlates of newborn size to determine the relative strength of the insulin-like growth factor-I association. METHODS: Thirty-seven venous cord blood specimens were obtained at the time of delivery. Ponderal index and birth weight percentile were calculated at birth. Neonatal length estimates were performed with a measuring board. All mothers were nonsmokers and had normal glucose tolerance. There was a wide range of maternal prepregnancy body mass indexes (BMI) (19.6-43.4). Neonates had a wide range of ponderal indexes (2.12-2.75) and birth weight percentiles (7-99th percentile). Univariate correlation coefficients were calculated to determine simple relationships. Stepwise linear regression analyses were performed to determine the relative contribution of potential explanatory variables to both ponderal index and birth weight percentile. Potentially explanatory independent variables included maternal prepregnancy BMI, weight gain in pregnancy, and maternal insulin sensitivity at 32 weeks' gestation. Maternal insulin sensitivity was estimated using the minimal model technique. Neonatal variables included sex, cord blood albumin, insulin, insulin-like growth factor-I, insulin-like growth factor-binding protein-1, and insulin-like growth factor-binding protein-3. RESULTS: Significant positive univariate correlations were identified between cord blood insulin-like growth factor-I and insulin-like growth factor-binding protein-3 with neonatal ponderal index and birth weight percentile. Maternal insulin sensitivity demonstrated a negative correlation with birth weight percentile (r = -.35, P < .05). Cord blood insulin correlated positively with birth weight percentile (r = .32, P < .05). There were no significant associations of cord blood insulin-like growth factor-binding protein-1 or albumin with either index of newborn size. Stepwise logistic regression analysis demonstrated an independent association of insulin-like growth factor-I with ponderal index (r2 = .41, P < .001). Both insulin-like growth factor-I and male sex were associated independently with birth weight percentile (r2 = .38, P < .001). No additional independent variables contributed to the prediction of ponderal index or birth weight percentile. CONCLUSION: These data support a unique relationship between cord blood insulin-like growth factor-I and newborn size under normal growth conditions. This is manifest by the strength and independence of the association between insulin-like growth factor-I and neonatal birth weight percentile ponderal index.

Placenta previa percreta with bladder invasion.

BACKGROUND: Although the clinical presentation and imaging techniques can raise suspicion for placenta previa percreta, this potentially catastrophic condition may remain undiagnosed or its extent underappreciated until delivery. The decision to proceed with definitive surgery in cases of placenta previa percreta should be carefully considered. CASE: A case of placenta previa percreta with bladder invasion was diagnosed prenatally. This case illustrates the magnitude of complications that can arise despite aggressive multidisciplinary perioperative management. CONCLUSION: When possible, hysterectomy performed for placenta previa percreta is best avoided under anything other than ideal conditions. A multidisciplinary approach for preoperative, intraoperative, and postoperative management of placenta previa percreta optimizes maternal outcome.

Differential growth of fetal tissues during the second half of pregnancy.

OBJECTIVE: Our purpose was to examine the pattern of growth of both fetal lean body mass incorporating bone, brain, and muscle and subcutaneous fat mass during the course of normal pregnancy. We hypothesized that there are detectable differences in the accretion of fat versus lean body mass. STUDY DESIGN: To establish our method we correlated standardized cross-sectional ultrasonographic images of the fetal extremities with anthropometric assessment of neonatal body composition in 25 subjects. Subsequently 36 nonsmoking women with normal prepregnancy body mass index, normal glucose screening results, and no medical or obstetric complications were recruited. We performed 135 ultrasonographic examinations between 19 and 40 weeks' gestation (mean 3.8 scans per fetus, range 2 to 6) at 4-week intervals. Lean body mass measures included biparietal diameter, head circumference, and femur length. Fetal subcutaneous fat and lean body mass were examined both in the mid upper arm and midthigh by standardized cross-sectional images. All neonates were born between 37 and 42 weeks' gestation and had normal birth weight distribution. Stepwise regression analysis established best-fit equations for fetal measurements obtained ultrasonographically. Independent variables included gestational age, maternal age, weight gain in pregnancy, parity, fetal gender, and maternal prepregnancy weight. RESULTS: Fetal bone growth was best described by a second-order quadratic equation demonstrating deceleration with advancing gestational age (p < 0.0001, R2 0.92 to 0.96). A quadratic equation that accelerates with advancing gestation best described lean body mass accretion in the extremities (p < 0.0001, R2 = 0.85 to 0.86). Fetal fat deposition in the extremities was characterized by an accelerating quadratic equation when plotted against gestational age with maternal age and prepregnancy weight contributing significantly (p < 0.0001, R2 = 0.80 to 0.81). CONCLUSION: Consistent with our hypothesis, fetal fat and lean body mass demonstrate unique growth profiles. We speculate that, as a result of an accelerated rate of growth in late gestation, the measurement of fetal fat will provide a more sensitive and specific marker of abnormal fetal growth when compared with index values of lean body mass.

Increase in fetal breech presentation in female carriers of Duchenne muscular dystrophy.

Female carriers of Duchenne muscular dystrophy (DMD) may demonstrate elevated serum creatine kinase (CK) and reduction of muscle dystrophin in all muscle types. We hypothesized that decreased dystrophin in uterine or pelvic girdle musculature might affect the obstetrical performance of females heterozygous for a dystrophin mutation. We reviewed the outcome of 34 deliveries resulting in 35 children from 13 women who were mothers of males attending a muscular dystrophy clinic. Obstetrical performance was examined retrospectively by chart review and patient contact. Of 35 children, 6 (17%) were delivered in the breech position, which is a fivefold increase above the national standards for term pregnancies. Of the six infants with breech presentation, two were males affected with DMD, one was a female heterozygote, one was a male who died perinatally, and the carrier status of the other two females is unknown. Most DMD affected males (12/14) were delivered in the vertex position. Thus, it is likely that maternal, rather than fetal, muscle weakness was the significant factor in determination of fetal position at term. We speculate that subtle changes in uterine or pelvic girdle muscle tone may contribute to a higher rate of fetal breech position in carriers of the DMD gene.

Rapid molecular determination of fetal rhesus E type.

The successful prophylaxis of RhD disease has brought attention to other Rh antigens, such as RhE antigen, that can cause hydrops fetalis. Our purpose was to develop simple molecular techniques to permit fetal RhE genotyping. We obtained amniotic fluid, villi, and fetal blood from two RhE-sensitized pregnancies, performed the Polymerase Chain Reaction (PCR), and made a presumptive fetal genotype diagnosis. The restriction enzyme MnlI was used to determine the E/e subtypes. DNA sequencing was used to demonstrate base-pair differences between the mother and fetus in one case. Conventional serology was used to confirm the fetal blood type. Maternal, paternal, and fetal genotypes were identified using molecular techniques. The presence of the fetal E allele was correctly predicted in both cases. Sequencing of maternal and fetal PCR products in one case demonstrated one base-pair substitution associated with the E/e polymorphism. Prenatal diagnosis of the fetal RhE genotype is now possible by PCR. The use of amniocytes obtained in one procedure of amniocentesis for RhE genotyping in sensitized pregnancies is less invasive than currently accepted techniques of cordocentesis, or serial amniocenteses done for delta OD450 measurement.

Case for hybrid "fetal growth curves": a population-based estimation of normal fetal size across gestational age.

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.

Fetal RhD genotyping in fetal cells flow sorted from maternal blood.

OBJECTIVE: The aim of this study was to determine the accuracy of noninvasive fetal RhD genotyping by fetal cell isolation from maternal blood. STUDY DESIGN: Candidate fetal cells from 18 pregnant women (one twin gestation) were flow-sorted. Polymerase chain reaction amplification of a 261 bp fragment of the RhD gene was performed on sorted fetal cells. The presence of amplified product was considered predictive of the Rhd-positive genotype in the fetus. RESULTS: Sixteen of the 19 fetal RhD genotypes were correctly predicted in fetal cells isolated from maternal blood (10 were Rh positive, 6 were Rh negative). In 3 cases no amplification products were detected in RhD-positive fetuses. The association between presence of the fragment and RhD-positive genotype was significant (p=0.003, Fisher's exact test). CONCLUSIONS: Noninvasive prenatal diagnosis of the fetal RhD genotype is feasible. Absence of amplification products in the reaction requires confirmation that fetal material is present. Improvements in fetal cell purity and yield should increase diagnostic accuracy, although the current protocol has a positive predictive value of 100% and a negative predictive value of 67%.

Uterine artery Doppler velocimetry in the detection of adverse obstetric outcomes in women with unexplained elevated maternal serum alpha-fetoprotein levels.

OBJECTIVE: We hypothesized that in pregnancies complicated by unexplained elevations of maternal serum alpha-fetoprotein, second-trimester uterine artery Doppler findings would detect adverse obstetric outcomes. STUDY DESIGN: One hundred three subjects with unexplained elevations of maternal serum alpha-fetoprotein had uterine artery Doppler velocimetry studies performed at the time of targeted ultrasonographic examination (17 to 22 weeks). A resistance index > 95th percentile or the presence of a uterine notch was considered abnormal. Adverse outcomes included preeclampsia, preterm birth, low birth weight, intrauterine growth restriction, abruptio placentae, and fetal death. Statistical analysis was performed by Student t test, chi 2 analysis, and stepwise logistic regression analysis. RESULTS: An elevated uterine resistance index was associated with an increased relative risk for both preeclampsia (relative risk 41.82, 95% confidence interval 5.36 to 326.13) and low birth weight (relative risk 4.65, 95% confidence interval 1.90 to 11.39). A uterine artery notch was associated with an increased risk of preeclampsia (relative risk 52.22, 95% confidence interval 6.82 to 399.70), preterm birth (relative risk 3.21, 95% confidence interval 1.32 to 7.81), and low birth weight (relative risk 4.18, 95% confidence interval 1.64 to 10.66). When the presence of a uterine notch, vaginal bleeding, and level of maternal serum AFP were analyzed by stepwise logistic regression, the presence of a notch was found to be the only significant factor (odds ratio 6.95, 95% confidence interval 1.24 to 39.10) for the development of an adverse outcome. CONCLUSIONS: Abnormal uterine artery Doppler findings are associated with an increased frequency of adverse obstetric outcomes in women with unexplained elevated maternal serum AFP levels. Abnormal Doppler findings demonstrated high sensitivity for the development of preeclampsia but were less sensitive in predicting other outcomes. The presence of a uterine artery notch is a better independent predictor of adverse outcome than are early vaginal bleeding or maternal serum AFP level.

Examination of factors contributing to the risk of cesarean delivery in women with gestational diabetes.

OBJECTIVE: To determine whether increased neonatal fat is associated with an elevated risk of cesarean delivery in infants born to mothers with gestational diabetes mellitus. METHODS: Of 166 infants born to mothers with gestational diabetes, 110 were born vaginally (91 spontaneous, 19 instrumental) and 56 by cesarean. Data were collected on maternal demographics, maternal anthropometrics, delivery variables, and neonatal anthropometrics. We compared all characteristics between women who delivered vaginally and the 29 delivered by cesarean in labor. RESULTS: The difference in birth weight between infants delivered by cesarean and vaginally was not statistically significant (3520 +/- 456 and 3374 +/- 559 g, respectively [mean +/- standard deviation]). There were significant differences between the cesarean and vaginal delivery groups in the rate of nulliparity (80 versus 48%, respectively), maternal pregravid body mass index (28.6 +/- 7.7 versus 25.2 +/- 5.8 kg/m2), fetal position at delivery (23.8 versus 96.2% occiput anterior), and all estimates of neonatal body fat (ponderal index: 2.77 +/- 0.20 versus 2.67 +/- 0.26 kg/m3; sum of two-site skinfold measurements: 11.7 +/- 2.8 versus 10.5 +/- 1.8 mm; and percent body fat: 15.1 +/- 4.9 versus 13.0 +/- 3.3). Stepwise logistic regression analysis demonstrated that fetal position, maternal nulliparity, and fetal fat contributed independently to the cesarean risk. CONCLUSION: Increased newborn fat is associated independently with an increased risk for cesarean in labor.