Umbilical Blood Samples Research Articles

Alteration in the Low-Frequency Domain in Power Spectral Analysisof Fetal Heart Beat Fluctuations

Objective: Spectral analysis was conducted on fetal heart rate fluctuations for the purpose of investigating the change in gestational age and examining the usefulness as a method of estimating fetal blood gas. Study Design: Five hundred and twenty-nine pregnant women with a single normal fetus and 26 women with intrauterine growth restriction (IUGR) were studied during the 20th to 38th gestational weeks. In cases of IUGR, fetal blood gas levels were evaluated with percutaneous umbilical blood sampling. A time series of fetal heart rate fluctuation was obtained with a 1.15-MHz ultrasonic transducer, and power spectral analysis of 200 consecutive stable beats was performed with an autoregression method. Integrated areas of 0.025–0.125 cycles/beat were defined as low-frequency areas (LFAs) and were examined in normal fetuses. In addition, the relation between LFA and fetal blood gas values was studied. Results: As pregnancy progressed, LFA increased with a cubic regression equation (Y = 6.484 – 0.764X + 0.029X² – 0.00034X³). The correlation coefficient was 0.625 (p < 0.05). In the cases of IUGR, ΔLFA was highly correlated with ΔpO₂ and ΔpH (correlation coefficient, 0.650 and 0.618, respectively). Conclusions: Measurement of LFA provides insight into the development of fetal autonomic function and also may serve as a quantitative index of fetal well-being in mid-pregnancy.

Changes in leptin concentration during the early postnatal period: adjustment to extrauterine life?

There are substantial alterations in fuel homeostasis immediately after birth. Leptin is a putative regulator of energy metabolism. Consequently, the aim of this study was to examine whether there are changes in circulating leptin concentrations during the early postnatal period. Umbilical cord mixed blood samples were taken at delivery, and a venous blood sample was obtained at 3 d of age from 38 healthy newborn infants (20 male, 18 female; gestational age 36.3 to 41.9 wk) for analysis of leptin concentration with radioimmunoassay. Cord plasma leptin concentration was 9.7+/-5.2 microg/L (mean+/-SD), with no gender difference between male (8.6+/-4.6 microg/L) and female (10.9+/-5.6 microg/L) infants. In male newborns, cord plasma leptin concentration correlated with arm circumference (r = 0.48, p < 0.05), and in female newborns with body mass index (r = 0.62, p < 0.01), thickness of the s.c. fat (r = 0.54, p < 0.05), and arm circumference (r = 0.72, p < 0.01). By the third postnatal day, plasma leptin decreased similarly in male (to 1.8+/-0.4 microg/L, p < 0.001) and female (to 2.3+/-0.8 microg/L, p < 0.001) infants, when there was a significant gender difference in leptin levels (p = 0.01). At 3 d of age, plasma leptin correlated with weight (r = 0.49, p < 0.05) and arm circumference (r = 0.49, p < 0.05) in female but not in male newborns. In conclusion, 1) circulating leptin already correlates with adiposity at birth in female but not in male newborn infants and 2) leptin decreases markedly in both genders by the third postnatal day, and the gender difference with higher leptin levels in females develops by that time. Thus, the postnatal decrease in plasma leptin concentration may be a physiologically feasible adaptation to profound alterations in fuel homeostasis during the first days of extrauterine life.

A new exanthematous disease in newborn infants caused by exotoxins producing Staphylococcus aureus; exotoxins production of the isolates and serum levels of antitoxin antibody in the patients and umbilical cord blood

Recently, in Japan newly neonatal exanthematous disease was elucidated to be caused by staphyloccocal supcrantigcnic exotoxins, mainly TSST-1. We studied exotoxins producibility of 43 strains of S. aureus isolated from neonates with exanthematous disease and examined antibody titers to staphylococcal enterotoxin A, B, C (SEA, SEB, SEC) and toxic shock syndrome toxin 1 (TSST-1) of the patients and control (umbilical cord blood from term infants). The results were as follows 1.34 of 43 strains (79%) isolated from the patients were SEC and TSST-1 producing MRSA, 5 strains (12%) were SEB, SEC, and TSST-1 producing MRSA, 1 strain (2%) was SEB and TSST-1 producing MRSA, 2 strains (12%) were SEB producing MSSA and did not produce TSST-1. The 1 strain (2%) was MSSA which produced SEC and TSST-1. 2. 16 neonates with exanthematous disease, who showed typical clinical signs and laboratry findings of thrombocytopenia, with SEC and TSST-1 producing MRSA isolates had significantly low anti-TSST-1 antibody titers at onset (p < 0.05), compared with the control (umbilical cord blood from term infants): TSST-1 appeared to the causative agent for the disease. In two neonates with exanthematous disease, with SEB- and non- TSST-1-producing MSSA isolates, anti-SEB antibody titers were low at onset, so SEB appeared to the causative agent for the disease. 3. In Japan, low anti-TSST-1 antibody titers were found in the umbilical blood samples from about 70% of term infants; and low anti-SEB or anti-SEC antibody titers were found in samples from only about 10% of them, that is, a number of term infants had anti-SEB and anti-SEC antibodies. The majority of S. aureus isolated from neonates with exanthematous disease were enterotoxin- and TSST-1-producing MRSAs. The results of our study by measuring antitoxin antibody titers suggested that SEB and SEC might not be pathogenically responsible, but TSST-1 was considered to be responsible for the majority of exanthematous disease. Prevalence of TSST-1-producing MRSA in the neonatal and premature baby ward is the main cause for the high incidence of this disease in Japan, whereas the low antibody titer to TSST-1 in the mother, in comparison with the anti-enterotoxin antibody titers, may also be a predisposing factor.

False-negative findings in chorionic villus sampling. An experimental approach and review of the literature

61 fetuses/newborns who had an aberrant karyotype in amniocentesis (AC) or percutaneous umbilical blood sampling (PUBS) were followed-up by chorionic villus sampling (CVS) at birth or after interruption. The overall rate of discrepancies is surprisingly high. Among 46 cases with a non-mosaic numerical aberration an AC or PUBS three had a discrepant finding in placental tissue. This was also true in one of seven cases with non-mosaic structural aberrations and in three of five cases with mosaic structural aberrations. All three cases with a mosaic numerical aberration in AC or PUBS were not represented by CVS and/or lymphocytes or fibroblasts, demonstrating the general problem of the unpredictable prognostic value of mosaicism. Our data suggest, that in case of prenatal diagnosis by CVS, using a combined procedure of short-term (STC) and long-term culture (LTC), in our sample we would have missed one case of 45,X (1.6 per cent). When relying only on STC another two cases, one with 47, +21 and one with 46,XX,der(22) would not have been recognized (4.9 per cent, n = 3). All other chromosome aberrations would have been detected by STC alone. On the other hand, one case of 45,X was 'nearly missed' because of low-grade mosaicism in AC (45,X[1]/46,XX[19]), whereas in placental tissues and PUBS only 45,X was represented. This study mimics a false-negative rate of about 1:3000 (STC plus LTC) or about 1:1000 (STC alone) for an a priori risk group of two per cent (e.g., advanced maternal age).

Regulation of hypothalamic arginine vasopressin messenger ribonucleic acid and pituitary arginine vasopressin content in fetal sheep: Effects of acute tonicity alterations and fetal maturation

Objective: Fetal arginine vasopressin contributes to fetal and amniotic fluid homeostasis by increasing water resorption in the kidney and, at higher plasma levels, circulatory homeostasis by vasopressor effects. In utero and neonatal exposure of rat pups to prolonged alterations in plasma osmolality may permanently alter (imprint) pituitary arginine vasopressin content and adult responses to osmotic challenges. Our objective was to investigate fetal developmental changes and the impact of maternal dehydration and maternal hyponatremia on fetal pituitary arginine vasopressin content and hypothalamic arginine vasopressin messenger ribonucleic acid expression. Study Design: Ten pregnant ewes with singleton fetuses (135 ± 1 day) were chronically prepared with maternal vascular catheters. Ewes were assigned to receive water deprivation (n = 4) [desamino, d -Arg8]-arginine vasopressin–induced plasma hyponatremia (n = 3), or 4 days of observation (n = 3). Three additional pregnant ewes with preterm (110 ± 1 day) singleton fetuses were also included for a study of maturational effects. Daily maternal blood samples were analyzed for determination of plasma arginine vasopressin, electrolytes, and osmolality. After the study protocol, fetuses were operatively delivered, umbilical blood samples obtained, and fetuses put to death for pituitary and hypothalamic tissues. Pituitary arginine vasopressin content was determined by radioimmunoassay, and hypothalamus arginine vasopressin messenger ribonucleic acid expression was detected by Northern blotting. Results: Dehydration significantly (P < .05) increased, and hyponatremia significantly decreased maternal plasma sodium concentration compared with controls. Fetal plasma sodium concentration significantly changed in parallel with maternal values (dehydration: 139 ± 1 to 150 ± 1 mEq/L; hyponatremia: 138 ± 1 to 128 ± 5 mEq/L). Fetal hypothalamic arginine vasopressin messenger ribonucleic acid expression and pituitary content did not change in relation to these relatively acute alterations in plasma tonicity. However, among all animals, arginine vasopressin messenger ribonucleic acid expression was significantly negatively correlated with pituitary arginine vasopressin content (r2 = 0.563; P = .02). Arginine vasopressin messenger ribonucleic acid expression was significantly lower in both preterm and near-term fetuses (P < .05) than that in the maternal ewe, although pituitary arginine vasopressin content (in micrograms per milligram of protein) was significantly greater in preterm fetuses (P < .01, vs maternal; P < .05, vs near term). Conclusions: The significant inverse relation between arginine vasopressin content and arginine vasopressin messenger ribonucleic acid suggests a dynamic arginine vasopressin synthesis–content feedback relationship is functional in the near-term fetus. Although relatively acute periods of maternal hypertonicity or hypotonicity do not alter fetal pituitary arginine vasopressin content or hypothalamic arginine vasopressin messenger ribonucleic acid expression, longer-term plasma tonicity alterations may potentially have an impact on the fetal arginine vasopressin hypothalamic-pituitary axis. (Am J Obstet Gynecol 1998;179:899-905.)

Congenital diaphragmatic defects and associated syndromes, malformations, and chromosome anomalies: A retrospective study of 60 patients and literature review

Congenital diaphragmatic defects (CDDs) may occur in malformation syndromes of varied causes. Syndromic cases of CDDs due to chromosomal defects, autosomal recessive, autosomal dominant, or X-linked inheritance have been described. In order to determine the frequency and nature of syndromes, malformations, and chromosome abnormalities associated with CDDs, we reviewed the records of all patients with CDDs evaluated over a 4-year period. During the 4-year interval, a total of 60 patients was evaluated. Of these, 29 had a therapeutic or spontaneous abortion, and 31 received postnatal care. On prenatal ultrasonography, 20 of 60 (33%) of patients with CDDs had additional anomalies. Additional anomalies, besides CDDs, were present in 15 of 31 (48%) of liveborn patients on newborn evaluation. In total, 16 patients with multiple anomalies were evaluated. Of these, 12 of 16 (75%) had additional abnormalities detected by prenatal ultrasonography. The 4 of 16 (25%) without additional anomalies on prenatal sonography had multiple anomalies found neonatally, lethal multiple pterygium syndrome being diagnosed in one case. Prenatal chromosome analysis was performed in 7 of 16 patients, and all had postnatal karyotypes. All initial karyotypes were normal. Tetrasomy 12p was documented on postnatal fibroblast analysis in one case who had percutaneous umbilical blood sampling (PUBS). Syndromes diagnosed postnatally in 7 of 16 patients (44%) include: Fryns syndrome (2), Simpson-Golabi-Behmel syndrome (2), tetrasomy 12p (1), Brachmann-de Lange syndrome (1), and lethal multiple pterygium syndrome (1). We were unable to make a specific diagnosis in 9 of 16 patients (56%) with multiple malformations. In patients with CDDs, a normal prenatal karyotype, especially if obtained by PUBS, and absence of other detected abnormalities by fetal ultrasonography, do not exclude the presence of other major anomalies, including chromosome abnormalities and severe multiple malformation syndromes.

Umbilical venous d-dimer concentrations with and without labor

Objective: To determine if labor activates the fetal fibrinolytic system. Methods: A total of 59 umbilical venous blood samples were collecting following vaginal delivery at term ( n = 20), cesarean delivery following labor at term ( n = 12), vaginal delivery before term ( n = 18), and cesarean delivery without labor ( n = 9). D-dimer concentrations, a sensitive marker of fibrinolysis, were measured by enzyme-linked immunosorbent assay, and compared between groups by Kruskel-Wallis and Mann Whitney U tests, with significance defined as P < .05. Results: There were no significant differences in median D-dimer concentrations between newborns delivered vaginally or by cesarean after term labor or preterm labor. There were significant differences in median umbilical venous D-dimer concentrations in subjects delivered vaginally or by cesarean after term or preterm labor compared with term subjects without labor delivered by cesarean (427, 773, and 326 versus 87 ng/mL, P = .01). Conclusion: Elevation of umbilical plasma D-dimer concentrations in laboring patients suggests activation of fetal fibrinolysis before delivery.

Umbilical Venous D-dimer Concentrations With and Without Labor

In Brief Objective To determine if labor activates the fetal fibrinolytic system. Methods A total of 59 umbilical venous blood samples were collecting following vaginal delivery at term (n = 20), cesarean delivery following labor at term (n = 12), vaginal delivery before term (n = 18), and cesarean delivery without labor (n = 9). D-dimer concentrations, a sensitive marker of fibrinolysis, were measured by enzyme-linked immunosorbent assay, and compared between groups by Kruskel-Wallis and Mann Whitney U tests, with significance defined as P < .05. Results There were no significant differences in median D-dimer concentrations between newborns delivered vaginally or by cesarean after term labor or preterm labor. There were significant differences in median umbilical venous D-dimer concentrations in subjects delivered vaginally or by cesarean after term or preterm labor compared with term subjects without labor delivered by cesarean (427, 773, and 326 versus 87 ng/mL, P = .01) Conclusion Elevation of umbilical plasma D-dimer concentrations in laboring patients suggests activation of fetal fibrinolysis before delivery. Fetal fibrinolysis, as reflected by umbilical venous D-dimer concentrations, is activated at birth following labor but not following elective cesarean delivery.

Reference Intervals for 18 Clinical Chemistry Analytes in Fetal Plasma Samples Between 18 and 40 Weeks of Pregnancy

The intrauterine biochemical assessment of the human fetus is important in fetal medicine, for both prenatal diagnosis and therapy of fetal diseases. Percutaneous umbilical blood sampling (PUBS) performed with ultrasound guidance is reliable for this, and the microvolume specimens obtained by this technique are readily analyzed by modern clinical chemistry analyzers to perform complete biochemical profiles with small blood volumes. The interpretation of fetal biochemical tests requires age-gestational specific reference intervals to reveal possible pathological processes and to minimize the remarkable physiological variability observed with fetal growth and maturation, particularly in the last trimester of gestation. Various cord blood analytes have been investigated as potential indicators of fetal distress (1)(2), but no comprehensive report of reference intervals adjusted to various weeks of gestation has been available. Here, we present reference intervals for 18 analytes in plasma samples obtained by PUBS from 72 healthy fetuses between weeks 18 and 40 of pregnancy. We analyzed plasma from 171 fetuses who underwent PUBS between the 18th and 40th week of gestation for various indications (Rh alloimmunization 79, maternal viral or parasitic infection 42, rapid karyotyping 25, and maternal thrombocytopenia 25). Informed consent was obtained from the parents. Gestational age at the time of sampling was determined from menstrual dates or by ultrasonography when the dates were uncertain. We selected 72 fetuses as “healthy” when the …

Umbilical cord blood acid‐base values in uncomplicated termvaginal breech deliveries

This prospective study was conducted to compare the umbilical cord blood acid-base values of uncomplicated, assisted, vaginal-breech-delivery term neonates with those of uncomplicated, cephalic-vaginal delivery term neonates and to determine whether a different metabolic status should be expected in neonates born by way of uncomplicated vaginal breech delivery. Umbilical cord artery and vein blood samples were obtained from 30 term neonates with frank or complete breech presentations who were born by uncomplicated assisted vaginal breech delivery. All these neonates had an Apgar score of >7 at 5 min and an uneventful neonatal course (study group). For each neonate in the study group the two consecutive term neonates who were delivered by uncomplicated cephalic spontaneous vaginal delivery, and had uneventful neonatal courses, served as controls (control group). The umbilical cord artery blood pH and pO2 were significantly lower (p<0.001 and <0.01, respectively) and the pCO2 was significantly higher (p<0.001) in newborns of the study group, compared to the controls. The umbilical cord vein blood pH was significantly lower (p<0.01), and the pCO2 significantly higher (p<0.01) in the study group. The umbilical cord blood acid-base values of uncomplicated, vaginal-breech-delivery term neonates differ significantly from those of uncomplicated, cephalic-vaginal delivery neonates. These differences may represent a greater degree of acute cord compression that reflects the different mechanisms of labor in vaginal breech delivery.

Transplacental distribution of salbutamol enantiomers at Caesarian section

To investigate the transplacental distribution of salbutamol enantiomers after administration of racemate to women prior to Caesarian section. Five women about to undergo elective Caesarian section were administered a single 0.25 mg bolus intravenous dose of (R,S)-salbutamol. The time from drug administration to delivery was different for each woman (27-105 min). Maternal and foetal umbilical cord venous blood samples were collected immediately after delivery and the plasma fraction analysed for salbutamol enantiomer concentrations by enantioselective high pressure liquid chromatography. The concentrations (mean +/- s.d.) of the active (R) enantiomer of salbutamol in cord and maternal plasma were 0.46 +/- 0.35 and 0.89 +/- 0.50 ng ml-1, respectively, and the difference was statistically significant (95% confidence interval (CI) of the difference: 0.12-0.74 ng ml-1). The corresponding concentrations of the (S) enantiomer of 0.92 +/- 0.45 and 1.11 +/- 0.67 ng ml-1, respectively, were not significantly different (95% CI of the difference -0.08-0.48 ng ml-1). The ratio of (R):(S) in cord plasma was significantly less than that in maternal plasma (P=0.016). Transplacental distribution of salbutamol enantiomers at Caesarian section after prior administration of racemate to mothers leads to concentrations in cord plasma that are significantly less for the active (R) enantiomer and not significantly different for the (S) enantiomer than in maternal plasma presumably due to enantioselective placental-foetal metabolism.

Leptin concentration in cord blood correlates with intrauterine growth.

Leptin is an adipocyte-derived peptide hormone regulating energy balance in experimental animals. Although the physiological function of leptin in humans is still unclear, its secretion is closely related to fat mass in adult humans. To examine how fetal growth correlates with leptin levels at birth, an umbilical cord venous blood sample was obtained at the delivery from 50 term newborn infants. Twenty-eight of the newborn infants had birth weights appropriate for gestational age (AGA; mean +/- SEM, 3362 +/- 90 g; relative birth weight, -0.08 +/- 0.2 SD), 9 were large for gestational age (birth weight, 4655 +/- 165 g; relative birth weight, 3.2 +/- 0.3 SD; P < 0.001 vs. AGA newborn infants), and 13 were small for gestational age (SGA; birth weight, 2385 +/- 69 g; relative birth weight, -2.2 +/- 0.08 SD; P < 0.001 vs. AGA newborn infants). Leptin concentrations were higher in large for gestational age (35.7 +/- 8.0 micrograms/L; P < 0.005), but lower in SGA (3.3 +/- 0.5 micrograms/L; P < 0.001) than in AGA infants (14.5 +/- 2.8 micrograms/L). When adjusted for differences in body weight, mean leptin levels were similar in the three newborn groups. Leptin concentration correlated closely with both absolute and relative birth weights (r = 0.71; P < 0.001 in both), with cord blood insulin concentration (r = 0.67; P < 0.001), and with placental weight (r = 0.60; P < 0.001). These data suggest that leptin is synthesized in utero, and that the circulating leptin concentration relates to the intrauterine growth pattern.

Indomethacin modifies the fetal hemodynamic response induced by percutaneous umbilical blood sampling

OBJECTIVE: Percutaneous umbilical blood sampling induces a marked decrease of impedance to flow in the umbilical artery. Because these changes are believed to be the result of the release of prostanoids, we conducted a study to determine whether indomethacin administration before percutaneous umbilical blood sampling affects the hemodynamic response induced by this procedure. STUDY DESIGN: Percutaneous umbilical blood sampling was performed in 20 singleton pregnancies that were treated for 3 days before the procedure with indomethacin (25 mg orally 6 hours apart) as tocolytic agent and in 22 untreated pregnancies. All the procedures were uncomplicated, and sampling of the umbilical vein was confirmed by blood pressure measurement at the time of the procedure. The umbilical artery pulsatility index and the fetal heart rate were measured immediately before and after the procedure. The first and last aliquots of umbilical vein plasma obtained at the beginning and closing of the procedure were assayed for endothelin-1, 6-keto-prostaglandin F 1α and thromboxane B 2. RESULTS: In untreated pregnancies percutaneous umbilical blood sampling induced a decrease of the umbilical artery pulsatility index ( p < 0.0001) and an increase in 6-keto-prostaglandin F 1α ( p < 0.001) and endothelin-1 levels ( p = 0.001), whereas no significant changes were present in fetal heart rate and thromboxane B 2 levels. In pregnancies treated with indomethacin, 6-keto-prostaglandin F 1α, and thromboxane B 2, concentrations at the beginning of the procedure were both significantly less ( p < 0.0001) than those found in untreated pregnancies. In pregnancies treated with indomethacin percutaneous umbilical blood sampling did not affect umbilical artery pulsatility index, and 6-keto-prostaglandin F 1α and thromboxane B 2 levels did not vary during the procedure. However, endothelin-1 ( p < 0.001) and fetal heart rate ( p < 0.0001) increased after the procedure. CONCLUSION: Indomethacin affects the fetal hemodynamic response to percutaneous umbilical blood sampling by inhibiting the release of prostanoids and the fall in umbilical artery pulsatility index. Under this condition the fetus adapts to the procedure by increasing the heart rate. (Am J Obstet Gynecol 1997;177:758-64.)

Serum concentrations of insulin-like growth factors and placental lactogen during gestation in cattle I. Fetal profiles

Sixty crossbred beef heifers pregnant with fetuses of either high (H; n = 30) or low (L; n = 30) genetic potential for growth were used to establish fetal serum profiles of insulin-like growth factor (IGF)-I, IGF-II, and placental lactogen (PL), and to examine relationships between serum hormone concentrations and fetal growth parameters. Three H and three L fetuses were collected by caesarean section at 21-d intervals from Day 85 through Day 274 of gestation. Arterial, venous, and mixed umbilical blood samples were collected during surgery. Fetal body weight, crown-rump length, hip height, and heart girth were measured. Serum concentrations of IGF-I and IGF-II increased (P < 0.0001) with advancing gestational age, whereas serum PL declined (P < 0.0001) linearly (P < 0.01) throughout gestation. Serum concentrations were greater in the umbilical vein compared with the umbilical artery for IGF-11 (P < 0.0001) and PL (P < 0.05), but not IGF-1. Fetal IGF-I, IGF-II, and PL serum concentrations were not correlated with serum concentrations of the respective maternal hormones. Fetal serum IGF-I concentrations were correlated to fetal body weight (r = 0.66), growth rate (r = 0.72), crown-rump length (r = 0.20), hip height (r = 0.17), and heart girth (r = 0.20). Correlations between fetal serum IGF-11 concentrations and the same parameters were 0.60, 0.62, 0.39, 0.34, and 0.37, respectively. Fetal serum PL concentrations were negatively correlated to body weight (r = −0.40) and growth rate (r = −0.40) and not correlated with any fetal linear measure. Fetal genotype (L vs. H) differences were detected for IGF-I (P < 0.05) and PL (P = 0.09) concentrations. Fetal sex effects were not observed for any hormone. Maternal sire breed, hip height, and body condition score did not influence fetal serum hormone concentrations.

Umbilical artery blood gases in healthy term newborn infants

Objective: To study the distributions of pH and gas values in umbilical arterial (UA) blood of normal newborns following uncomplicated pregnancies and vaginal births. Methods: In 681 consecutive normal term infants who were born during 1990, we examined the UA pH and blood gas values obtained immediately following delivery. Maternal inclusion criteria were defined as an uncomplicated pregnancy and a normal spontaneous vaginal delivery. Umbilical artery blood samples were collected at each birth and were evaluated for pH, carbon dioxide pressure (PaCO 2), oxygen pressure (PaO 2), bicarbonate, and base excess. All newborns in this study had the following inclusion criteria: singletons, no malformations, growth appropriate for gestational age (AGA), and Apgar scores of 7 or more at 1, 5 and 10 min of life. Results: The lowest UA pH was 7.04 and the 10th percentile value was 7.21. The lowest UA PaO 2 was 4.6 mmHg and the 10th percentile value was 10.1 mmHg. The highest UA PaCO 2 was 75.4 mmHg and the 90th percentile 62 mmHg. The 10th percentile of the base deficit in the extracellular fluid was 5.9 mmol/l. Conclusions: The distributions of the UA pH and gas values of a collective of normal newborns were illustrated.

Changes in umbilical artery, middle cerebral artery, and aorta blood flow Doppler waveform pulsatility indices after funisocentesis

This study evaluates the effect of funisocentesis on umbilical artery, fetal cerebral artery, and aortic circulation. The pulsatility index in the umbilical artery, fetal middle cerebral artery, and descending aorta was measured by pulsed Doppler ultrasonography before and after 41 diagnostic funisocenteses. Percutaneous umbilical artery blood sampling was associated with a significant decrease in umbilical artery pulsatility index (mean -0.132, standard deviation 0.259, P = 0.002) and in middle cerebral artery pulsatility index (mean -0.143, standard deviation 0.260, P = 0.001). The decline in resistance to flow of the umbilical artery (r = 0.340, P = 0.029) and middle cerebral artery (r = 0.457, P = 0.002) was correlated with gestational age at sampling. These findings suggest that alterations in the waveforms from both the umbilical and the fetal cerebral circulations can be induced by fetal blood sampling.

Remote umbilical arterial blood pH analysis: accuracy, utility, and limitations.

It is not always possible or feasible to perform routine umbilical artery blood sampling at birth. This study was undertaken to assess the accuracy of selective remote umbilical arterial blood analysis to retrospectively predict the original birth pH of any newborn. Umbilical arterial blood samples were obtained in two preheparinized syringes immediately following 1007 deliveries. One sample was analyzed within 60 minutes of delivery. The other was placed on ice and later analyzed at variable time intervals up to 180 hours postpartum. The results of each remote analysis were adjusted using a previously published regression equation to accurately identify which newborns had pH values < 7.00, < or = 7.10, or < 7.20 at birth. Among the 1007 newborns, there were 14 (1.3%), 44 (4.3%), and 187 (18.5%) who had pH values < 7.00, < or = 7.10, and < 7.20, respectively, at birth. Remote umbilical arterial samples analyzed within 72 hours of delivery correctly identified newborns with an original pH < 7.00, < or = 7.10, or < 7.20 with: (1) a sensitivity of 100, 82, and 84%, respectively; (2) positive predictive values of 100, 93, and 66%, respectively; and (3) a test efficiency of 100, 99, and 89%, respectively. Up to 72 hours after delivery, remote umbilical arterial blood pH analysis can be reliably used to accurately identify the newborn that was acidotic at birth.

Non-mosaic trisomy 16 in a third-trimester fetus: Yancey M.K.; Hardin E.L.; Pacheco C.; Kuslich C.D.; Donlon T.A. USA Obstet Gynecol 1996 87/5 II Suppl (856–860)

Trisomy 16 in the most common trisomy first-trimester spontaneous abortions, suggesting a high rate of non-disjunction of this chromosome. Deoxyribonucleic acid studies in aborted conceptuses with trisomy 16 have demonstrated a maternal origin in all cases. There have been cases of confined placental mosaicism, fetal mosaicism, and partial trisomy involving chromosome 16 reported in term fetuses. However, to our knowledge, there have been no previous reports of a near-term fetus with full trisomy 16 since the advent of modern chromosomal banding techniques.A 25-year-old Filipino woman underwent obstetric sonographic evaluation at 32 weeks' gestation; results were remarkable for oligohydramnios, severe growth restriction, and multiple dysmorphic features. Percutaneous umbilical blood sampling was performed for rapid karyotyping, viral serology, and blood profiles. The fetal karyotype was 47, XY+16; the remainder of the laboratory analysis was unremarkable. The patient went into spontaneous labor at 35 weeks' gestation and delivered a stillborn female fetus (birth weight 783 g). Chromosomes from skin, brain, and chorionic villi were examined and all demonstrated trisomy 16 (47, XX,+16). Deoxyribonucleic acid primers for known polymorphic regions of chromosome 16 were used and determined the origin of the extra chromosome to be non-disjunction during paternal meiosis.Previously, full trisomy 16 has been thought to be incompatible with fetal survival past the early second trimester. This case also contrasts with previously reported experience with trisomy 16 in that parental origin studies determined that the extra chromosome 16 originated from the father, suggesting that paternal derivation of the additional chromosome may play a role in the ultimate phenotypic expression.

Umbilical cord blood gas analysis at delivery

Fetal acid-base status is the end point that all antepartum and intrapartum surveillance tools are designed to assess, either directly or indirectly. Umbilical arterial blood pH is normal in 80% of depressed newborns, thereby proving the absence of birth asphyxia both in the delivery room and in the courtroom. The technique, normal ranges, and risks, benefits and cost analysis of routine versus selected umbilical blood sampling are considered. The American College of Obstetricians and Gynecologists recommends performing umbilical blood sampling for acid-base analysis in selected deliveries. However, in our opinion routine umbilical blood sampling at all deliveries has merit. (Am J Obstet Gynecol 1996;175:517-22.)

Developmental regulation of corticosteroid-binding globulin biosynthesis in the baboon fetus.

The present study determined the roles of estrogen and cortisol in maternal and fetal corticosteroid-binding globulin (CBG) levels and fetal hepatic messenger RNA (mRNA) expression in the baboon. Samples of fetal liver, kidney, and brain were obtained from untreated control animals at early (day 60; n = 4), mid (day 100; n = 8), and late (day 165; n = 5) gestation (term = day 184). Maternal and umbilical blood samples were collected on day 100 from baboons in which betamethasone was administered sc to the mother (n = 6) on days 60-99 of gestation and on day 165 from animals (n = 4) in which the fetus was administered betamethasone on days 150-164 of gestation. Maternal serum cortisol concentrations were similar at mid (43 +/- 2 micrograms/dl) and late (42 +/- 3 micrograms/dl) gestation and decreased (P < 0.05) at midgestation (1 +/- 1 micrograms/dl) and term (31 +/- 4 micrograms/dl) after betamethasone treatment. Umbilical serum cortisol levels were also reduced (P < 0.05) at both mid (1 +/- 1 micrograms/dl) and late (14 +/- 5 micrograms/dl) gestation by betamethasone treatment. Fetal serum CBG levels in untreated animals were lower (P < 0.05) on day 165 (444 +/- 29 pmol/ml) than on day 100 (844 +/- 35 pmol/ml) and increased (P < 0.05) at midgestation (1098 +/- 64 pmol/ml), but not at term (551 +/- 24 pmol/ml), after betamethasone treatment. In contrast, maternal serum CBG levels (range, 528-770 pmol/ml) were not altered by gestational age or betamethasone. The human CBG complementary DNA hybridized to a single mRNA species of 1.8 kilobases in baboon fetal liver; however, CBG was not expressed in fetal kidney and was detectable in fetal brain and pancreas only by reverse transcription-PCR. In untreated baboon fetuses, the mRNA levels of hepatic CBG, expressed as a ratio of 18S RNA, progressively decreased (P < 0.05) in early (1.83 +/- 0.17), mid (0.97 +/- 0.12), and late (0.51 +/- 0.04) gestation. These results demonstrate that fetal hepatic CBG mRNA expression and serum CBG concentrations were elevated early in baboon gestation and exhibited a progressive decline during the course of advancing pregnancy. We suggest that the increased levels of fetal CBG in the early stages of gestation reflect stimulation of hepatic CBG synthesis by maternal cortisol, which we previously demonstrated to occur in the fetus as a result of preferential 11 beta-hydroxysteroid dehydrogenase-catalyzed glucocorticoid reduction across the placenta. The decline in fetal CBG may reflect the developmental increase in catabolism of cortisol to bioinactive cortisone in target tissues of the fetus such as the liver.