Presence Of Intrauterine Growth Retardation Research Articles

THE ROLE OF CARDIOTOCOGRAPHY IN ASSESSING THE CONDITION OF A FETUS IN PREECLAMPSIA

The role of cardiotocography (CTG) in preeclampsia is still vaguely defined. The aim of this study was to investigate the possible role of CTG in assessing the condition of the fetus in preeclampsia with and without intrauterine growth retardation (IUGR) and to compare the CTG findings with Doppler parameters and perinatal outcome. The prospective study included 30 singleton pregnancies with preeclampsia completed by caesarean section. The study group was divided into subgroups based on the presence of IUGR in relation to the severity of preeclampsia. The control group consisted of 20 healthy women delivered by elective caesarean section. In 53.3% of preeclamptic cases, cardiotocographic findings differed from normal (p<0.001) and they were either warning or pathological. There were no significant differences in the presence of a pattern deviating from normal based on the severity of preeclampsia, and it was significantly more prevalent in preeclampsia with IUGR (p<0.01) than the one without it. The prevalence of CTG pattern types in the study group was significantly altered by presence of olygoamnion (p<0.05) as well as the parameters of the flow through the uterine arteries, umbilical artery and middle cerebral artery (p<0.05). Apgar score significantly depends on the CTG findings and decreases with the unfavourable CTG pattern. CTG and Doppler ultrasonography complement each other in order to improve perinatal outcome in preeclampsia. CTG is irreplaceable as a first measure of rapid assessment of the fetal condition in newly diagnosed cases of preeclampsia, aiming also to and in order to detect complications from umbilical cord during its follow-up.

Prenatal diagnosis of 4p deletion with aortic valve stenosis

Wolf-Hirschhorn syndrome (WHS) is caused by variable sized terminal deletions of the short arm of chromosome 4 (chromosomal region 4p16.3) and usually presents as severe intrauterine growth retardation with characteristic dysmorphic features (hypertelorism, a short philtrum with downturned corners of the mouth and a ‘Greek warrior helmet appearance’ of the face), developmental delay and epilepsy. Often WHS is only diagnosed postnatally but prenatal diagnosis has been reported in the presence of intrauterine growth retardation with facial dysmorphism, cardiac malformations (ventricular septal defect, arrhythmia) or other associated malformations (oesophageal atresia, renal hypoplasia, diaphragmatic hernia, foot deformity, choroid plexus cysts, corpus callosumagenesis, hypospadias), or in the present of a parental balanced translocation. Here we present the prenatal diagnosis of WHS based on the prenatal onset of growth delay and characteristic facial features and aortic valve stenosis.

The Endocrine Phenotype in Silver-Russell Syndrome Is Defined by the Underlying Epigenetic Alteration

Around 50% of children with Silver-Russell syndrome (SRS) carry a hypomethylation of the imprinting control region 1 at the IGF2/H19 locus on 11p15, the functional significance of which is unknown. We aimed to compare the genotype in SRS with the endocrine phenotype. The retrospective study included all SRS children who were treated during the last 18 yr at our hospital and for comparison a cohort of GH treated nonsyndromic short children born small for gestational age (SGA). The 61 patients with SRS included were defined by the presence of intrauterine growth retardation, lack of catch-up growth, and at least two of the criteria: typical face, relative macrocephaly, and skeletal asymmetry. Routine karyotype and GH secretion was normal in all children studied. A subgroup of 53 patients was treated with GH. Genomic DNA was available from 44 children. Multiplex ligation probe-dependent amplification analysis was performed to detect hypomethylation at the imprinting control region 1 on 11p15. Uniparental disomy of chromosome 7 (UPD7) was analyzed by short tandem repeats typing. Serum levels of GH, IGF-I, and IGF-binding protein (IGFBP)-3 were measured by RIA. Epimutations at 11p15 were found in 19 of 44, UPD7 in five of 44, and small structural aberrations of the short arm of chromosome 11 in two of 44 children. Of 44 cases, 18 were negative for any genetic defect known (41%). The most severe phenotype was found in children with 11p15-SRS. Children with UPD7-SRS had a significantly higher birth length (P < 0.004) but lost height sd score (SDS) postpartum, whereas children with 11p15-SRS showed no change in height SDS. IGF-I and IGFBP-3 serum levels were inadequately high in 11p15-SRS at -0.02 SDS (1.07, sd) and +1.38 SDS (1.01), compared with the low levels in UPD7-SRS and in the cohort of 58 nonsyndromic SGA children (P < 0.0009). During GH therapy, IGFBP-3 serum levels increased above normal values in 11p15-SRS (P < 10(-4)), whereas IGF-I increase was moderate. There was a trend toward more height gain in children with UPD7 than in those with 11p15 epimutation under GH therapy (+2.5 vs. +1.9 height SDS after 3 yr) (P = 0.08). Children with SRS and an 11p15 epimutation have IGFBP-3 excess and show endocrine characteristics suggesting IGF-I insensitivity, whereas children with SRS and UPD7 were not different from nonsyndromic short children born SGA. This phenotype-genotype correlation implicates divergent endocrine mechanisms of growth failure in SRS.

Relation between pesticide exposure and intrauterine growth retardation

The increased use of organophosphorus insecticides in agriculture and their widespread existence in the environment poses a potential health hazard. To determine the relationship between exposure to pesticides and intrauterine growth retardation (IUGR), live newborns from singleton pregnancies, with ( n=79) and without ( n=292) IUGR were studied. During the gestational period the mothers were living in agricultural communities in the state of Chihuahua, Mexico. Exposure to agrochemical products was evaluated. A significant association between the history of positive exposure to pesticides (i.e. the women themselves or their newborns who showed acetylcholinesterase activity levels lower than 20%) and the presence of IUGR was found. The proportions of exposure in the cases were 18% and 8% in the control group; the adjusted OR (fat free mass, anti-cytomegalovirus antibodies and placental weight) was 2.33 ( p=0.04).

A Case Series of Gastrointestinal Abnormalities in Fetuses with Echogenic Bowel Detected During the Antenatal Period

Objective: The objective was to evaluate the incidence of gastrointestinal abnormalities amongst those fetuses with antenatally diagnosed echogenic bowel (EB). Materials and Methods: A retrospective review of all cases delivered from April 2002 to March 2003 with antenatally diagnosed EB was conducted. This was defined as bowel that appeared as echogenic as (if not greater than) the iliac bone on a real-time image. The postnatal outcomes with regard to gastrointestinal abnormalities, till their discharge, were noted. Results: Of the 13,941 patients delivered, there were 70 cases with antenatally diagnosed EB, giving an incidence of 70/13,941 or 0.50%. Of these, 6 defaulted follow-up and 1 had a mid-trimester termination of pregnancy at 21 weeks’ gestation for social reasons. Of the remaining 63 cases with EB, 2 were stillbirths at 31 weeks and 35 weeks of gestation, respectively. Three fetuses (3/63 or 4.76%) were diagnosed with gastrointestinal abnormalities. Meconium plug syndrome was diagnosed postnatally in 2 cases, of which, 1 resolved with conservative management while the other required an emergency laparotomy. Intestinal atresia was diagnosed in the postmortem of one of the stillbirths. There was evidence of intrauterine growth retardation (IUGR) in both the stillbirth and the fetus that had required laparotomy. None of the 3 fetuses exhibited clinical features of aneuploidy. Conclusion: As the quoted background risk for gastrointestinal pathology is 0.23%, an increased incidence (4.76%) is observed in those fetuses found to have antenatal EB. It is possible that the presence of IUGR is associated with a worse prognosis. Further prospective studies are needed to verify this association.

Fetal distress

The term ‘fetal distress’ should be replaced by ‘suspected fetal compromise’ because the diagnosis of ‘fetal distress’ is often unproven. Cardiotocography remains the cornerstone of making the diagnosis, but as a test it is renowned for its high sensitivity and low specificity. It has reduced intrapartum fetal mortality but not long-term neonatal morbidity or the incidence of cerebral palsy. There is no doubt that when obvious signs of fetal compromise, such as late decelerations in the presence of intrauterine growth retardation and oligohydramnios, are present, the diagnosis of fetal compromise is relatively simple. Often, however, the subtle signs of fetal compromise are missed; these are a change in the grade of meconium in the amniotic fluid, a rising base-line fetal heart rate, the absence of accelerations, the presence of ‘atypical’ variable decelerations or a combination of the above. To date, there is no test available to replace the cardiotocograph, although fetal pulse oximetry is the most promising adjunctive test. Above all, no test result obtained in isolation must detract from the whole clinical picture.

Effects of intrauterine growth retardation in premature infants on early childhood growth

Objective: To evaluate in preterm infants the role of intrauterine growth retardation and infant body proportionality on subsequent childhood growth. Methods: Preterm infants (818) prospectively enrolled in the Infant Health and Development Program were studied from birth to 36 months of corrected age. Weights and lengths were recorded at eight intervals. Growth parameters were compared in preterm infants with differing body symmetry at birth, defined by length-for-age and weight-for-age. Infants with both low length-for-age and low weight-for-age at birth were categorized as symmetrically growth retarded, and infants with normal length-for-age and low weight-for-age were categorized as asymmetrically growth retarded. Results: Infants born with low length-for-age demonstrated increased growth velocity until 8 months of corrected age ( p <0.001). However, infants born with low weight-for-age demonstrated decreased weight-gain velocity compared with preterm infants with appropriate weight for gestational age (AGA) until 40 weeks of corrected age ( p <0.001). Heights and weights of infants with either symmetric or asymmetric intrauterine growth retardation remained significantly retarded compared with AGA preterm patients and the National Child Health Survey (NCHS) reference population ( p <0.001). Infants born short but with normal weight did not significantly differ from AGA preterm infants in either weight or length at 36 months of corrected age. Preterm infants with both symmetric and asymmetric growth retardation demonstrated limited catch-up growth in weight until age 4 months and then paralleled the AGA preterm patients and the NCHS reference population. Very low birth weight (≤1250 gm), gestational age, and a broad-based day-care intervention did not influence growth outcome after control for the presence of intrauterine growth retardation. Conclusions: Preterm infants with both symmetric and asymmetric intrauterine growth retardation demonstrate limited catch-up growth. Intrauterine growth deficits persist into early childhood. (J Pediatr 1997;130:95-102)

Color Doppler flow patterns and flow velocity waveforms of the intraplacental fetal circulation in growth-retarded fetuses

We examined intraplacental color Doppler flow patterns and spectral Doppler flow velocity waveforms of villous arteries in pregnancies with intrauterine growth retardation. A total of 192 uncomplicated pregnancies and 29 pregnancies with intrauterine growth retardation between 26 and 41 weeks' gestation were examined in this cross-sectional study. Intraplacental color Doppler flow findings and pulsatility indexes of umbilical and villous arteries were correlated with the presence of intrauterine growth retardation and multiple outcome variables. Villous arteries were identified by their intraplacental color Doppler flow image, and flow velocity waveforms were obtained by superimposition of pulse-wave Doppler. (1) Intraplacental color Doppler flow signals from two or more villous arteries were detected in all 192 normal pregnancies but were undetectable in 8 of 29 fetuses with intrauterine growth retardation (27.6%, p < 0.0001). Absence of intraplacental color Doppler flow signals was associated with fetal distress in 6 of 8 cases (87.5%) and perinatal death in two cases (25.0%), compared with 3 of 21 (14.2%, p < 0.005) and 0 of 21 (not significant) cases of intrauterine growth retardation with detectable intraplacental color Doppler flow. Median Apgar scores at 1 minute were 5 and 8 (p < 0.05), respectively, and at 5 minutes were 8 and 8 (not significant), respectively. (2) Umbilical artery flow velocity waveforms were abnormal (> 95th percentile) in 8 of 21 cases of intrauterine growth retardation (38.0%) with detectable intraplacental color Doppler flow, including two cases with reversed end-diastolic flow. In contrast, the corresponding villous artery flow velocity waveforms were abnormal in only 1 of 21 cases (p < 0.04). (1) Failure to detect intraplacental color Doppler flow signals is associated with intrauterine growth retardation and fetal distress. (2) Flow velocity waveforms of detectable villous arteries are usually normal in intrauterine growth retardation, even in the presence of extremely abnormal umbilical artery flow velocity waveforms.

Population Study of the Risk of Fetal Death and Its Relationship to Birthweight, Gestational Age, and Race

With more than 20,000 fetal deaths occurring annually in the United States, accurate epidemiological data concerning fetal death offer the potential to develop interventions aimed at saving a considerable number of fetuses. Currently, fetal death rates are determined by dividing the number of deaths by total births. These raw death rates do not focus on cause or preventability, nor do they delineate the risk for a individual pregnancy or any specific gestational age. Using data from 747,033 births in Illinois from 1984 to 1988, we estimated the fetal death risk (FDR) according to fetal weight and gestational age expressed as a function of the number of remaining fetuses. This procedure permits the comparison of FDR across all weights (including fetuses with growth retardation and macrosomia) and gestational ages. In addition, we examined the effect of race on this analysis. Between 28 and 36 weeks' gestational age, white fetuses with mean weights have a constant risk of fetal death at 0.1/1000 remaining fetuses. The risk is two to three times greater for black fetuses. If the fetus has growth retardation or is appropriately grown beyond 37 weeks' gestational age, the FDR increases further, with black fetuses remaining at higher risk. These data attempt to quantify the risk of fetal death. They support the widely held belief that the risk of fetal death increases in the presence of intrauterine growth retardation, but they also demonstrate that the risk of fetal death for all fetuses, including those appropriately grown, increases exponentially after 37 weeks' gestational age.(ABSTRACT TRUNCATED AT 250 WORDS)

Confirmation of CVS mosaicism in term placentae and high frequency of intrauterine growth retardation association with confined placental mosaicism

About 2 per cent of specimens from chorionic villus sampling (CVS) analysed either on direct preparation of cytotrophoblast cells or after culture of mesenchymal stroma reveal confined placental mosaicism (CPM), most commonly involving chromosomal trisomy. A significantly higher rate of prenatal loss (22 per cent) as well as the presence of intrauterine growth retardation (IUGR) has been reported among pregnancies with CPM. To evaluate more precisely the effect of these aneuploid cell lines confined to the placenta on intrauterine fetal growth and fetal survival, we have studied 34 term placentae from pregnancies with CPM diagnosed on CVS and confirmed identical mosaicism in 17 of these placentae. There was a direct correlation between a high number of aneuploid cells present at CVS and a high likelihood of their detection in term placenta. Also, the proportion of aneuploid cells in the mosaic term placentae correlated with that observed in CVS specimens. Among 17 gestations with confirmed CPM at delivery, there were six cases of IUGR identified, five in liveborns and one associated with intrauterine death.

Congenital Anomalies: An Increasingly Important Cause of Mortality and Workload in a Neonatal intensive Care Unit

With improvement in perinatal management and advances in neonatal intensive care, congenital anomalies have emerged as a major cause of neonatal mortality and morbidity. A 1 year review (1985) of all the admissions to our neonatal intensive care unit (NICU) showed that 78 of 790 (10%) had one or more congenital anomalies. Of these, 26% died in the NICU; another 10% died during the first year; therefore the total mortality of infants with congenital anomalies in the first year of life was 36%. Even though they accounted for only 10% of the total admissions, the infants with congenital anomalies were responsible for 13% of the total NICU patient-days, 26% of the total NICU mortality, 32% of all deaths within the first year, and 35% of all NICU infants with intrauterine growth retardation (IUGR). Of interest, 67% of the infants with anomalies were suspected or diagnosed prenatally. Of these, 54% were delivered by cesarean section, done for fetal reasons in the majority of cases. The highest mortality was associated with (1) multiple abnormal prenatal ultrasound findings; (2) extreme prematurity (less than 30 weeks gestation); and (3) the presence of IUGR. These findings raise concerns about the use of resources in the management of the pregnancy and the delivery of infants with congenital anomalies, particularly when diagnosed prenatally.

Pränatale Chromosomenbefunde bei sonographisch auffälligen Feten

A retrospective evaluation of 463 prenatal chromosome analyses in a total of 375 patients with suspicious ultrasound findings, revealed a high rate of severe chromosomal abnormalities (16%). The highest risk for an abnormal karyotype was found after sonographic detection of hygroma colli. Abnormal chromosome counts were also frequently found in fetuses with omphaloceles, duodenal atresia and hydrops fetalis, as well as in presence of intrauterine growth retardation and/or anomalies of the amniotic fluid volume. The anomalies mentioned above are, therefore, an urgent indication for a prenatal chromosome analysis. The technical improvements of ultrasound machines and growing experience of operators will lead to an increasing importance of sonography as a method for the identification of pregnancies, that are at high risk for chromosomal abnormalities.

Congenital Malformations and Intrauterine Growth Retardation: A Population Study

The relationship between congenital malformations and intrauterine growth retardation was investigated using data from the population-based Metropolitan Atlanta Congenital Defects Program. Between 1970 and 1984, the system ascertained 13,074 infants with major structural malformations diagnosed in the first year of life and born to metropolitan Atlanta residents. These infants were classified as having intrauterine growth retardation if their birth weight was below the race-, sex-, and gestational age-specific tenth percentile limits for all Atlanta births. Overall, the frequency of intrauterine growth retardation among malformed infants was 22.3% (relative risk 2.6). Of 48 defect categories evaluated, 46 were associated with excess intrauterine growth retardation, most notably chromosomal anomalies (eg, 83.7% for infants with trisomy 18, relative risk 46) and anencephaly (73.3%, relative risk 25). Only a few isolated defects (such as isolated polydactyly, pyloric stenosis, and congenital hip dislocation) were not associated with excess intrauterine growth retardation. Among infants with multiple malformations, the frequency of intrauterine growth retardation increased markedly with increasing number of defects--from 20% for infants with two defects to 60% for infants with nine or more defects. The relationship between malformations and intrauterine growth retardation can be explained by one or more of three mechanisms: (1) intrauterine growth retardation can be a secondary disturbance to the presence of malformations; (2) intrauterine growth retardation can predispose the fetus to malformations; and (3) intrauterine growth retardation can coexist with malformations because of common etiologic factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Simultaneous assessment of fetal lung maturity and sebaceous gland function by gas chromatography

Lipid profiles were analysed by gas chromatography of underivatised extracts from pellets and supernatant fractions of amniotic fluid (AFP and AFS). Peaks, identified as diglycerides resulting from on column decomposition of phosphoglycerides at high temperature, were obvious in gas chromatograms of AFS. The C 32 diglyceride, mainly derived from dipalmityl lecithin, was not a prominent peak in AFS from pregnancies from which babies subsequently developed respiratory distress syndrome. There was evidence of a moderate increase of squalene in AFS and AFP for 10 pregnancies of 36–38 weeks gestation resulting in the birth of small for gestational age babies. The increase was not obvious for 21 out of 22 control pregnancies delivering appropriate for gestational age babies. This demonstrated that we had an assessment of two fetal functions in one chromatographic run, the ratio of C 32/C 34 diglycerides providing a measure of lung maturity and squalene providing an index of proximity to term or of the presence of intrauterine growth retardation.

Use of laboratory and clinical factors in the management of pregnancies complicated by maternal disease

Data are presented on 300 cases from the Obstetric Service of the Medical College of Virginia Hospitals where the combination of clinical and laboratory data were utilized in the management of a variety of obstetric complications. The results indicated a high degree of reliability with the mature LSratio in patients with premature rupture of membranes. The LSratio distinguished those patients who would benefit from immediate delivery from those who would benefit from expectant management. The LSratio was utilized in the evaluation of 47 elective repeat cesarean sections resulting in postponement of surgery in many and an apparent reduction of neonatal deaths from this procedure. The combination of good clinical management, frequent urinary estriols, and amniotic fluid LSratio was used in 14 pregnancies of 12 Class B to R diabetics. There were no fetal losses. The interplay of the various tests is demonstrated and discussed. Twenty-one pregnancies in hypertensive patients show the reduction in urinary estriol excretion and the presence of intrauterine growth retardation. The possible use of urinary estriol and amniotic fluid LSto identify the fetus who may benefit from early delivery is discussed.

Hypercoagulability in the dysmature syndrome

A discordance between gestational age and fetal weight has been recognized clinically since the turn of the century. The failure to maintain a normal growth rate in utero is referred to as the “dysmature syndrome” or intrauterine growth retardation. Several etiologies, notably hypertensive pregnancy and renal disease, have been assigned to this syndrome, but in many of the cases there has been no demonstrable associated cause. It is proposed that an aberration of the clotting mechanism may play a role in some cases of intrauterine growth retardation. Cases are presented where a subclinical state of hypercoagulability has been encountered in the presence of intrauterine growth retardation, as measured by the presence of fibrin monomers, platelet function, and other factors related to the preconsumptive phase of the clotting mechanism.