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PubMed2003

Hindlimb glucose and lactate metabolism during umbilical cord compression and acute hypoxemia in the late-gestation ovine fetus.

The metabolic adaptation of the hindlimb in the fetus to a reversible period of adverse intrauterine conditions and, subsequently, to a further episode of acute hypoxemia has been examined. Sixteen sheep fetuses were chronically instrumented with vascular catheters and transit-time flow probes. In nine of these fetuses, umbilical blood flow was reversibly reduced by 30% from baseline for 3 days (umbilical cord compression), while the remaining fetuses acted as sham-operated, age-matched controls. Acute hypoxemia was subsequently induced in all fetuses by reducing maternal fractional inspired oxygen concentration for 1 h. Paired hindlimb arteriovenous blood samples were taken at appropriate intervals during cord compression and acute hypoxemia, and by using femoral blood flow and the Fick principle, substrate delivery, uptake, and output were calculated. Umbilical cord compression reduced blood oxygen content and delivery to the hindlimb and increased hindlimb oxygen extraction and blood glucose and lactate concentration in the fetus. However, hindlimb glucose and oxygen consumption were unaltered during umbilical cord compression. In contrast, hindlimb oxygen delivery and uptake were significantly reduced in all fetuses during subsequent acute hypoxemia, but glucose extraction, oxygen extraction, and hindlimb lactate output significantly increased in sham-operated control fetuses only. Preexposure of the fetus to a temporary period of adverse intrauterine conditions alters the metabolic response of the fetal hindlimb to subsequent acute stress. Additional data suggest that circulating blood lactate may be derived from sources other than the fetal hindlimb under these circumstances. The lack of hindlimb lactate output during acute hypoxemia in umbilical cord-compressed fetuses, despite a significant fall in oxygen delivery to and uptake by the hindlimb, suggests that the fetal hindlimb may not respire anaerobically after exposure to adverse intrauterine conditions. hypoxia

Acid-Base Equilibrium↗
PubMed1981

Developmental aspects of the renal response to hypoxemia in the lamb fetus.

The effects of fetal hypoxemia on renal hemodynamics and renal function were studied in two groups of chronically catheterized young (< 120 days of gestation) and near-term lamb fetuses (> 130 days). Fetal hypoxemia produced, in both groups, a significantly decrease in renal blood flow (RBF) and a significant increase in the filtration fraction. However, the glomerular filtration rate (GFR) did not change significantly suggesting that the renal vasoconstriction associated with fetal hypoxemia was more important at the efferent than at the afferent arteriolar level. In the group of near-term fetuses, the decrease in RBF correlated closely with changes in plasma renin activity (PRA) (r = 0.77). No changes in PRA were observed during hypoxemia in the group of young fetuses. After hypoxemia, reactive hyperemia associated with a significant increase in urinary prostaglandin excretion (PGE and PGF2 alpha) was observed in near-term fetuses but not in young fetuses. It also was demonstrated that fetal hypoxemia produced a significant increase in fetal plasma concentrations of vasopressin associated with an antidiuresis in all but one near-term fetus and in 50% of the young fetuses, suggesting that the ability of the fetal kidney to reabsorb free water is more developed in near-term fetuses. Finally, fetal hypoxemia had no effect on mean arterial pressure and heart rate in young fetuses; however, in near-term fetuses, a significant increase in blood pressure and a decrease in heart rate were observed. In summary, it appears that the response of the fetal kidney to hypoxemia depends on the degree of fetal maturation.

Animals↗
PubMed2005

Biometry of face and brain in fetuses with trisomy 21.

The aim of this study was to specify the early setting of the particular craniofacial morphology in Down syndrome during the fetal period from data based on postmortem examinations. The study included 1277 fetuses at 15-38 gestational weeks (GW): 922 control fetuses and 355 fetuses with trisomy 21, selected from fetopathology units in Paris. Body weight (BW) and nine dimensions of the face, skull, and brain were recorded: the outer and inner canthal distances (OCD, ICD), biparietal diameter (BPD), head circumference (HC), brain weight (BrW), occipitofrontal diameters of left and right hemispheres (lOFD, rOFD), weight of the infratentorial part of the brain (IBW), and maximal transversal diameter of the cerebellum (CTD). Four ratios were computed: BPD/HC, OCD/BPD, BrW/BW, IBW/BrW. Differences between trisomic fetuses and control fetuses were tested by age interval. Results showed that BW, rOFD, and lOFD were lower in trisomic fetuses as early as 15 GW. Cerebellar hypoplasia included lower IBW and CTD in trisomic fetuses. The IBW/BrW ratio was higher in trisomic fetuses, showing that growth restriction affected the infratentorial part of the brain less than the supratentorial part. Early brachycephaly was found in trisomic fetuses, with higher values of BPD and BPD/HC from 15 GW. ICD and OCD were not significantly different in the two groups, but OCD/DBP ratio was lower in trisomic fetuses. These results confirm the early phenotypical expression of trisomy 21 on craniofacial morphology, associated with a marked restriction of brain growth, especially in the supratentorial part.

Biometry↗
PubMed1984

Differential effects of maternal stress on circulating levels of corticosterone, progesterone, and testosterone in male and female rat fetuses and their mothers.

Testosterone, progesterone, and corticosterone titers were measured by RIA in plasma of stressed and control pregnant rats and their male and female fetuses on days 17, 18, 19, and 21 of gestation and on the day of birth. The regimen of stress used (three 45-min periods of restraint under intense illumination daily from days 14-21 of pregnancy) causes failure of masculinization and defeminization of behavioral potentials in male offspring. In fetuses of both sexes, corticosterone titers increased sharply between days 17 and 18 postconception (pc) to a peak that was maintained through day 19 and then declined. This pattern resembled that obtained for testosterone in control male fetuses in which the levels of testosterone also rose sharply between days 17 and 18 pc. Corticosterone titers were elevated in samples obtained during the middle of the stress session from both the mothers (serum) and their male and female fetuses (plasma). Increased corticosterone levels were no longer evident in samples obtained from fetuses 75-165 min after the end of a stress session. Testosterone titers were altered by stress only in male fetuses. Their testosterone levels were elevated on day 17 pc, and the surge on days 18 and 19 pc, characteristic of control males, was absent in samples obtained 75-165 min after termination of stress. Progesterone titers were not affected by stress in either mothers or their fetuses. In both stressed and control groups, progesterone concentrations were identical in male and female fetuses, were higher in mothers than in fetuses, and declined in both fetuses and mothers between days 19 and 21 pc. Thus, a persistent effect of stress was observed only on testosterone and only in males.

Animals↗
PubMed1989

Hormone ontogeny in the ovine fetus. XXIII. Pulsatile administration of follicle-stimulating hormone stimulates inhibin production and decreases testosterone synthesis in the ovine fetal gonad.

Inhibin, a gonadal glycoprotein with selective FSH-suppressing activity, is synthesized by the Sertoli cell of the testis and the granulosa cell of the ovary mediated by the action of FSH. It is not known whether inhibin is produced by the fetal testes and ovaries or if FSH has the capacity to stimulate inhibin production by the fetal gonad. To explore these questions, we examined the bioactive inhibin content of the gonads of 16 chronically catheterized sheep fetuses between 111 and 143 days gestational age (0.7-0.95 gestation) in an ovine pituitary bioassay. Both the fetal testes and ovary contained inhibin activity (testes, 53.5-1,240 U inhibin/g tissue; ovaries, 58.5-2,250 U/g). After pulsatile administration of oFSH (5 micrograms every 3 h) to the fetus for 5 days in 1 fetus and 10 days in 2 fetuses, 10-day gonadal inhibin content of fetal testes increased to 5,080 +/- 3,180 U/testes (n = 3) vs. 165 +/- 50 U/testes in controls (n = 8; P less than 0.02); the concentration of testicular inhibin in these features rose to a mean of 9,100 +/- 6,620 vs. 415 +/- 126 U/g tissue in controls (P less than 0.01). Ovarian inhibin content in female fetuses given ovine FSH for 10 days was 5,220 +/- 4,920 U/ovary (n = 4) compared to 40 +/- 16 U/ovary in controls (n = 4); the inhibin concentration was 41,000 +/- 30,000 U/g in ovaries of FSH-treated fetuses vs. 1,190 +/- 960 U/g in controls. The ovary of 1 female fetus contained several large follicles and the highest inhibin concentration. Unexpectedly, FSH administration was associated with a decrease in testosterone content in the fetal testes and ovaries. The testosterone content was 0.54 +/- 0.42 ng/ovary after FSH treatment (n = 4) vs. 2.11 +/- 0.68 ng/ovary in controls (n = 4; P less than 0.02). The testosterone concentration fell to 5.8 +/- 2.0 ng/g in treated female fetuses vs. 60.3 +/- 14.6 ng/g in controls (P less than 0.0005). The testosterone content in fetal testes decreased to 21.7 +/- 6.9 ng/testes in FSH-treated fetuses (n = 3) vs. 75.1 +/- 24.0 ng/testes in controls (n = 5; P less than 0.04); the testosterone concentration fell to 38.6 +/- 16.1 ng/g tissue compared to 223.0 +/- 88.7 ng/g in untreated controls (P less than 0.03). In male fetuses the concentration of plasma testosterone decreased to 15.5 +/- 2.3 ng/dl after FSH treatment, significantly lower than 39.6 +/- 4.5 ng/dl in controls (P less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Effect of long-term infusion of ovine corticotrophin-releasing factor in the immature ovine fetus.

Synthetic ovine corticotrophin-releasing factor (oCRF) was infused continuously into the jugular veins of six ovine fetuses for 5-11 days. Two fetuses receiving 0.1 and 1.0 microgram oCRF/h from gestational days 134 and 135 respectively, lambed prematurely on days 141 and 140 respectively. Three out of four fetuses receiving oCRF at 2.4 micrograms/h, from 125 days of gestation, delivered spontaneously at 131, 131 and 136 days, whilst one died in utero at 132 days. Two fetuses receiving vehicle only or oCRF intra-amniotically, were born at 148 and 145 days respectively, whilst six fetuses chronically cannulated but not infused were born at 149.8 +/- 2.1 (S.D.) days. In ewes lambing at term, maternal plasma progesterone concentrations were 41.4 +/- 11.4 (S.E.M.; n = 5), 28.8 +/- 7.8 (n = 6), 17.1 +/- 4.8 (n = 5) and 7.9 +/- 1.1 (n = 4) nmol/l on 3, 2, 1 and 0 days respectively before the lambs were born. No such decrease in maternal plasma progesterone concentrations was seen in the oCRF-infused fetuses. Fetal plasma concentrations of immunoreactive ACTH were maintained above normal in oCRF-infused fetuses, but some desensitization to bolus oCRF injections occurred in these fetuses. Four of the five fetuses born prematurely were sufficiently mature to survive, being able to stand, breathe and suckle. It is concluded that continuous oCRF infusions into immature fetuses can accelerate maturation of a number of organs and systems culminating in the premature delivery of viable lambs.

Adrenocorticotropic Hormone↗
PubMed2002

Endocrine pancreas development in growth-retarded human fetuses.

Glucose intolerance in adults born with intrauterine growth retardation (IUGR) may involve peripheral insulin resistance and/or abnormal endocrine pancreas development during fetal life. We quantified insulin-containing cells in deceased human fetuses with IUGR (<10th percentile, n = 21) or normal growth (control fetuses, n = 15). Paraffin-embedded pancreatic tissues from fetuses older than 32 weeks were obtained from two fetopathology departments. Mean gestational age was 36 weeks in both groups. Tissues with lysis and those fetuses with defects, aneuploidy, or genetic abnormalities were excluded. For each subject, six pancreatic sections spaced evenly throughout the organ were immunostained with anti-insulin antibody. Total tissue and insulin-positive areas were measured by computer-assisted quantitative morphometry. Results were expressed in percentages. To evaluate islet morphogenesis, the percentages of beta-cells inside and outside islets were determined. Islet density was similar in the two groups (P = 0.86). The percentage of pancreatic area occupied by beta-cells (beta-cell fraction) was not correlated with gestational age (r = 0.06 and P = 0.97 in IUGR fetuses; r = 0.12 and P = 0.67 in control fetuses) or body weight (r = 0.16 and P = 0.47 in IUGR fetuses; r = 0.24 and P = 0.39 in control fetuses). Mean beta-cell fraction was 2.53% in the IUGR fetuses and 2.86% in the control fetuses (P = 0.47). The percentage of beta-cells located within islets was identical in the two groups (mean 35%). Our data militate against a primary developmental pancreatic abnormality in human IUGR, leaving peripheral insulin resistance as the most likely mechanism of glucose intolerance in adults born with IUGR.

Cohort Studies↗
PubMed1984

Histochemical and cellular aspects of adipose tissue development in decapitated pig fetuses: an ontogeny study.

Adipose tissue from fetuses decapitated at 45 d of gestation was removed and structurally and histochemically analyzed at 65, 85 and 110 d of gestation. Subcutaneous adipose tissue from decapitated and control fetuses at 65 d of gestation was histologically and histochemically similar. A reduced number of fat cell clusters in the outer layer of subcutaneous tissue and a poorly developed dermis was evident in decapitated fetuses at 85 d of gestation. Fat cell size was similar for control and decapitated fetuses at 65 d of gestation, whereas cells in 85 d-old decapitated fetuses were larger than cells in control fetuses. Adipocytes from control and 85 d-old decapitated fetuses were histochemically similar except for an elevated number of esterase positive cells in decapitated fetuses. At 110 d of gestation, adipocytes from decapitated fetuses had higher activities of the following enzymes than did control adipocytes: malate dehydrogenase (NADP dependent) glucose 6-phosphate dehydrogenase NADP dependent), isocitrate dehydrogenase (NADP dependent), alpha-glycerol phosphate dehydrogenase (NADP dependent), NADPH-tetrazoleum reductase and esterase. Levels of succinate dehydrogenase, glutamate dehydrogenase and NADH-tetrazoleum reductase were similar in cells from controls and decapitated fetuses. These data indicate that fetal decapitation probably exerts a positive influence on enzymes involved in lipid synthesis. However, fetal decapitation also exerts a negative influence on fat cell hyperplasia.

Adipose Tissue↗
PubMed1999

Increased fetal DNA concentrations in the plasma of pregnant women carrying fetuses with trisomy 21.

BACKGROUND: The recent discovery of the presence of circulating cell-free fetal DNA in maternal plasma opens up new prenatal diagnostic applications and provides new avenues for clinical investigation. It is of research and potential diagnostic interest to determine whether fetal trisomy 21 may be associated with quantitative abnormalities of circulating fetal DNA in maternal plasma. METHODS: Maternal plasma samples were prospectively collected from two centers situated in Hong Kong and Boston. Samples collected from Boston consisted of 7 women carrying male trisomy 21 fetuses, 19 carrying euploid male fetuses, and 13 carrying female fetuses. Samples collected from Hong Kong consisted of 6 women carrying male trisomy 21 fetuses, 18 carrying euploid male fetuses, and 10 carrying female fetuses. Male fetal DNA in maternal plasma was measured using real-time quantitative Y-chromosomal PCR. RESULTS: For patients recruited from Boston, the median circulating fetal DNA concentrations in women carrying trisomy 21 and euploid male fetuses were 46.0 genome-equivalents/mL and 23.3 genome-equivalents/mL, respectively (P = 0.028). For patients recruited from Hong Kong, the median circulating fetal DNA concentrations in women carrying trisomy 21 and euploid male fetuses were 48.2 genome-equivalents/mL and 16.3 genome-equivalents/mL, respectively (P = 0.026). None of the samples from women carrying female fetuses had detectable Y-chromosomal signals. CONCLUSIONS: Abnormally high concentrations of circulating fetal DNA are found in a proportion of women carrying fetuses with trisomy 21. The robustness and reproducibility of real-time PCR analysis of maternal plasma makes it a valuable tool for cross-institutional collaboration involving centers located in different parts of the world.

Biomarkers↗
PubMed2002

Longitudinal umbilical vein blood flow changes in normal and growth-retarded fetuses.

OBJECTIVE: To explore whether the umbilical vein blood flow of growth-retarded fetuses with normal Doppler parameters changes over time differently to that of normally grown fetuses. METHODS: Fifteen consecutive women whose fetus was diagnosed to be growth restricted were compared with 30 women whose fetus was normally grown. Two ultrasonographic evaluations were conducted at 2-weekly intervals (+/- 2 days) in all cases. At each sonographic evaluation, umbilical vein blood flow parameters were obtained by digital color Doppler velocity profile integration. To allow comparisons among fetuses, the umbilical vein blood flow per minute was normalized for abdominal circumference. RESULTS: The absolute vein blood flow was lower in growth-retarded than in normally grown fetuses (209 ml/min +/- 73 vs. 313 ml/min +/- 72, p < 0.01). The median (range) umbilical vein blood flow normalized for abdominal circumference was significantly lower in growth-retarded than in normally grown fetuses at the first [0.70 (0.32; 1.15) vs. 1.11 (0.65; 2.07), p < 0.05] and at the second [0.71(0.30; 1.09) vs. 1.14 (0.69; 2.05), p < 0.05] sonographic evaluation. The difference in umbilical vein blood flow normalized for abdominal circumference between the second and the first examination was significantly lower in growth-retarded than in appropriate for gestational age fetuses [-0.005 (- 0.08; 0.06) vs. 0.02 (- 0.08; 0.1), p < 0.05]. CONCLUSION: This study demonstrates that umbilical vein blood flow normalized for biometric parameters is lower in growth-retarded fetuses than in healthy fetuses even in the absence of umbilical artery Doppler abnormalities.

Adult↗
PubMed1998

Is maternal serum triple screening a better predictor of Down syndrome in female than in male fetuses?

Among euploid gestations, female fetuses have been reported to have significantly lower maternal serum alpha-fetoprotein (MSAFP) and higher human chorionic gonadotropin (hCG) levels than male fetuses. Since in maternal serum triple screening, low MSAFP and high hCG MOM independently confer greater risk of a Down syndrome fetus, we investigated the hypothesis that maternal serum triple screening is more efficacious at detecting female than male Down syndrome fetuses. A database containing all karyotypes from amniocentesis performed between August 1994 and August 1996 was accessed. All trisomy 21 cases were identified. The male-to-female ratio among trisomy 21 fetuses detected at amniocentesis after abnormal maternal serum triple screening was compared with that among trisomy 21 fetuses detected at amniocentesis for advanced maternal age (AMA), which served as the control group. Statistical analysis utilized chi-square, Fisher's exact test, and Student's t-test. A P value of less than 0.05 was considered statistically significant. Forty-nine trisomy 21 fetuses were detected in the women who underwent amniocentesis because of abnormal triple screening and 311 were detected in the control group. The proportion of male fetuses among the triple screening group was not significantly different from that of the AMA group (55 per cent vs. 57 per cent; P=0.9). Our study had a power of 80 per cent to detect a difference of 25 per cent in the male-to-female ratio (alpha=0.05, beta=0.20). The reported differences in MSAFP and hCG levels between male and female euploid fetuses do not appear to affect the sex ratio among Down syndrome fetuses detected because of an abnormal maternal serum triple screening.

Amniocentesis↗
PubMedDate not supplied

Routine obstetrical ultrasound at 18-22 weeks: our experience on 7,236 fetuses.

OBJECTIVE: This study aimed at examining the detection rate of congenital abnormalities by using routine ultrasonography at 18-22 weeks of gestation. METHODS: The sample included 7,236 fetuses. A detailed sonographic examination was performed in each fetus and a neonatal evaluation or pathology examination was made to confirm the prenatal findings. RESULTS: The total prevalence of fetal abnormalities in our sample was 2.24% (162/7,236). There were 29/162 (17.9%) fetuses with CNS abnormalities, 27/162 (16.7%) fetuses with gastrointestinal abnormalities, and 28/162 (17.3%) fetuses with urinary tract abnormalities. There were also 31/162 (19.1%) fetuses with cardiovascular abnormalities, 26/162 (16.0%) with malformation of the limbs and musculoskeletal system, and 21/162 (13%) fetuses with other various abnormalities. The overall sensitivity in detecting fetuses with congenital abnormalities was 80.25% (130/162). The sensitivity per system was 93.1% (27/29) for CNS, 45.2% (14/31) for cardiovascular system, 85.2% (23/27) for gastrointestinal system, 85.7% (24/28) for urinary system, 84.6% (22/26) for musculoskeletal system, and 95.2% (20/21) for the rest of the abnormalities detected. We performed 40 pregnancy terminations in the group of malformed fetuses. Among the fetuses considered as normal, 1.7% had chromosomal abnormalities. CONCLUSIONS: The results indicate that routine sonographic examination at 18-22 weeks of gestation can detect the majority of congenital abnormalities. More experience is needed for the examination of the cardiovascular system, where the sensitivity was particularly low (14/31 or 45.2%).

Central Nervous System↗
PubMed1990

Umbilical cord growth in human and rat fetuses: evidence against the "stretch hypothesis".

A total of 103 human fetuses between the 7th and 30th week of gestation were obtained from induced abortion (40 fetuses were normal and 63 were abnormal), and the umbilical cord length (UCL) was measured. The UCL increased almost linearly with gestational age among normal fetuses, contrary to the commonly held tenet that the UCL increases exponentially during the second trimester. When UCLs from the 63 abnormal fetuses were compared with those of normal fetuses, 15 fetuses were found to have short UCL and 10 fetuses to have long UCL. Among the 15 fetuses with short UCL, 6 had early amnion rupture syndrome. An unexpected finding among the 10 with long UCL was that 8 of them had oligohydramnios. It has been suggested that the UCL increases in response to tensile forces placed upon it ("stretch hypothesis"); however, our results are inconsistent with this hypothesis because fetuses with oligohydramnios should be less active and their umbilical cords be subject to less stress. In a separate experiment, we studied the normal development of the UCL in rat fetuses and observed an almost linear increase during the whole gestation similar to that seen in humans. This finding is also inconsistent with the "stretch hypothesis" because amniotic fluid volume decreases significantly from day 19 of gestation to term in rats.

Animals↗
PubMed2005

Impact of congenital heart disease on cerebrovascular blood flow dynamics in the fetus.

OBJECTIVES: Neurological abnormalities are present in some children after repair of congenital heart disease (CHD). Recently, structural brain abnormalities have been identified in infants prior to cardiac surgery. By altering in utero blood flow patterns, the type of CHD may impact upon cerebrovascular flow dynamics prior to birth. We sought to determine whether left- and right-sided obstructive congenital heart lesions modify cerebrovascular flow dynamics in the fetus. METHODS: Pulsed Doppler was used to measure blood flow velocities in the umbilical (UA) and middle cerebral (MCA) arteries in 172 fetuses from 20 to 39 weeks' gestational age referred for fetal echocardiography. Pulsatility index (PI), an indicator of downstream vascular resistance, was determined by (peak systolic velocity--end-diastolic velocity)/mean velocity. RESULTS: Fetuses with hypoplastic left heart syndrome (HLHS; n = 28) had decreased MCA-PI (P = 0.009) compared to normal fetuses (n = 114). Fetuses with right-sided obstructive lesions (RSOL; n = 17) had increased MCA-PI (P = 0.001) when compared to fetuses with HLHS. The UA-PI was elevated in fetuses with RSOLs (P = 0.045). CONCLUSIONS: Cerebrovascular resistance is lower than normal in fetuses with HLHS, a condition in which cerebral perfusion occurs retrograde via the ductus arteriosus. Fetuses with RSOL had significantly higher cerebrovascular resistance compared to fetuses with HLHS. The type of CHD impacts upon fetal cerebrovascular blood flow distribution and this may have implications for later development of neurological sequelae.

Blood Flow Velocity↗
PubMed2006

Left and right lung volumes in fetuses with diaphragmatic hernia.

OBJECTIVE: To compare the volume of the ipsilateral and contralateral lungs in fetuses with congenital diaphragmatic hernia (CDH). METHODS: Left and right lung volumes were measured using three-dimensional (3D) ultrasonography in 42 fetuses with CDH at median 26 (range, 20-32) weeks of gestation. Each value was then expressed as a difference, in standard deviations, from the normal mean for gestation, previously established from the study of 650 normal fetuses at 12-32 weeks (Z-score). The Mann-Whitney U-test was used to determine the significance of the differences between the measurements in fetuses with CDH and normal fetuses and between the ipsilateral and contralateral lungs in fetuses with left- and right-sided CDH. RESULTS: There were 34 fetuses with left-sided CDH and eight with right-sided CDH. In CDH both the ipsilateral and contralateral lung volumes were substantially lower than in normal fetuses. In left CDH the left lung volume was 4.03 (median; range, 3.11-4.78) SDs below the normal mean for gestation, and the respective values for the right lung were 3.04 (median; range, 1.78-4.31) SDs (P < 0.001 for both). In right CDH, the left lung volume was 2.91 (median; range, 1.62-4.07) SDs below the normal mean for gestation and the respective values for the right lung were 4.35 (median; range, 3.07-4.99) SDs (P < 0.001 for both). In both left and right diaphragmatic hernia the deficit in the volume of the ipsilateral lung was significantly greater than the deficit in the contralateral lung. CONCLUSIONS: In fetuses with CDH both the ipsilateral and contralateral lung volumes are substantially lower than in normal fetuses.

Female↗
PubMed2004

Chromosomal abnormalities in fetuses with open neural tube defects: prenatal identification with ultrasound.

OBJECTIVES: To determine the prevalence of chromosomal abnormalities in fetuses with open neural tube defects (NTD) undergoing prenatal chromosome analysis. The role of prenatal ultrasound in detecting those with an underlying chromosomal abnormality was also investigated. METHODS: Over a 6-year period, 144 fetuses with open NTD underwent prenatal chromosome analysis between 12 and 37 weeks of gestation, as part of a prospective, multicenter prenatal diagnosis and counseling program in Chile. This population included 66 fetuses with spina bifida, 46 with acrania/anencephaly, 21 with cephalocele and 11 with iniencephaly. A confident prenatal diagnosis was made in 143 fetuses (99%) and confirmed postnatally in all cases. RESULTS: An underlying chromosomal abnormality was diagnosed in 10 fetuses (7%), six with spina bifida, three with cephalocele and one with craniorachischisis. The prevalence of chromosomal abnormality varied according to the defect present in the fetus, with a 14% (3/21) prevalence among those with cephalocele, 9% (6/66) among those with spina bifida and 2% (1/57) among those with lethal defects such as acrania, anencephaly or iniencephaly. Karyotype results revealed trisomy 18 in seven cases, trisomy 13 in two and mosaicism for a marker chromosome in one. Prenatal ultrasound before the procedure showed that all chromosomally abnormal fetuses had additional findings. The prevalence of chromosomal abnormality in fetuses with spina bifida and cephalocele was higher when chromosome analysis was performed at or before 24 weeks of gestation in comparison to those performed after 24 weeks (5/31 (16%) vs. 4/56 (7%), respectively). However, this difference did not reach statistical significance, probably due to the small number of cases. CONCLUSIONS: A significant number of fetuses with open NTD are chromosomally abnormal. Although prenatal chromosome analysis should be considered in all cases, prenatal ultrasound seems effective in identifying those fetuses with an underlying chromosomal abnormality.

Adult↗
PubMed1989

Fetal heart rate patterns in the small-for-gestational-age human fetus.

A total of 24 pregnant women with growth-retarded fetuses were studied to examine the distribution of fetal heart rate accelerations between 30 and 40 weeks' gestation, as compared with those of fetuses of normal growth that were matched for gestational age and length of fetal heart rate tracings. Growth-retarded fetuses had significantly lower PO2 levels in the umbilical artery at birth (3 mm Hg less) than did healthy fetuses (p less than 0.05), but without metabolic acidosis. There was a larger proportion of small amplitude (less than 10 beats/min) and a smaller proportion of large amplitude (greater than 20 beats/min) fetal heart rate accelerations in the small-for-gestational-age fetuses than in the fetuses of normal growth. Although the number of accelerations was significantly reduced (50% less) in growth-retarded fetuses compared with healthy fetuses, there was no significant difference in the mean basal fetal heart rate and the mean number of decelerations between the two groups. Currently used definition of an acceleration as greater than or equal to 15 beats/min for greater than or equal to 15 seconds was applicable only in fetuses of normal growth. We hypothesized that a decrease in absolute acceleration frequency might be a useful index to detect the chronically hypoxemic fetus before severe metabolic acidosis and irreversible damage occurred.

Blood Gas Analysis↗
PubMed1995

Doppler flow velocimetry of the splenic artery in the human fetus: is it a marker of chronic hypoxia?

OBJECTIVE: The aim of this investigation was to describe splenic artery flow velocity waveforms in the appropriate- and small-for-gestational-age human fetus. STUDY DESIGN: Splenic artery flow velocity waveforms were prospectively obtained from 95 appropriate- and 15 small-for-gestational-age fetuses with pulsed Doppler ultrasonography. The resistance index was used to quantify the Doppler waveform. RESULTS: A second-degree polynomial model expressed the changes of the resistance index in appropriate-for-gestational-age fetuses with advancing gestation (y = 0.057x [Weeks] - 0.001x2, r = 0.53, p < 0.001). In 14 of 15 (93%) small-for-gestational-age fetuses the splenic artery resistance index was below the mean for gestational age. In five of 15 (33%) small-for-gestational-age fetuses the resistance index of the splenic artery was < 2 SEMs. A trend toward a higher hematocrit was noted in the five fetuses with splenic artery resistance index values < 2 SEMs (50.2%) compared with other small-for-gestational-age fetuses (43.0%). CONCLUSION: Our results suggest that some small-for-gestational-age fetuses have decreased resistance at the level of the splenic artery. We postulate that the increased erythropoietin level, stimulated by hypoxia, results in decreased resistance at the level of the splenic artery in small-for-gestational-age fetuses. Finally, management of the small-for-gestational-age fetus may be aided by the study of the splenic artery waveforms.

Blood Flow Velocity↗