Intrauterine restriction (IUGR)

Perinatal mortality and morbidity is markedly increased in intrauterine growth restricted (IUGR) fetuses. Prenatal identification of IUGR is the first step in clinical management. For that purpose a uniform definition and criteria are required. The etiology of IUGR is multifactorial and whenever possible it should be assessed. When the cause is of placental origin, it is possible to identify the affected fetuses. The major complication is chronic fetal hypoxemia. By monitoring the changes of fetal vital functions it is thus possible to improve both management and outcome. The timing of delivery is crucial but the optimal management scheme has not yet been identified. When IUGR is identified at very early gestational ages, serial assessments of the risk of continuing the in utero fetal life under adverse conditions versus the risks of the prematurity should be performed. Delivery of IUGR fetuses should take place in centers where appropriate neonatal assistance can be provided. Careful monitoring of the IUGR fetus during labor is crucial as the IUGR fetus can quickly decompensate once uterine contractions have started.     

Intrauterine growth restriction (IUGR): biometric and Doppler assessment

Intrauterine growth restriction (IUGR) is a common complication in pregnancy and influences morbidity and mortality at all stages of life. Historically, the management of IUGR has been dependent on antenatal biophysical testing and umbilical artery Doppler studies. With recent Doppler studies of the fetal central circulation, including intracardiac flows and the ductus venosus, better timing of delivery to minimize morbidity may be possible. This review will provide the reader with tools to diagnose IUGR, more accurately date the IUGR pregnancy with poor dating criteria, and better assess the condition of the IUGR fetus. A brief review of animal models of IUGR is presented to demonstrate research directions for answering human clinical questions and potentially carrying therapeutic intervention from the bench to the bedside.     

Intrauterine growth retardation

Fetal growth retardation ranks third after prematurity and malformations as a cause of perinatal deaths. Antenatal fetal monitoring (biochemical testing of fetoplacental function plus cardiotocography) has emerged as the most important means of reduction in the number of stillbirths and improvement in the quality of survival of infants who are born alive. Clinical acumen combined with biochemical and/or ultrasonographic testing will identify no more than 70% of growth retarded fetuses. However, not all small for dates fetuses are at risk, and many doomed to die in utero are not by definition, growth retarded. It should be the obstetrician's aim to identify the fetus at risk of death from hypoxia whether growth retarded or not. Biochemical and ultrasonographic methods of testing are not truly comparable, since some aim to identify the growth retarded fetus, irrespective of his state of health, whereas others aim to detect fetoplacental dysfunction, irrespective of whether or not the fetus is growth retarded. With present methods of antenatal diagnosis and treatment and timing of delivery determined by nonstressed cardiotocography, the physical and intellectual prognosis of growth retarded infants is most satisfactory; follow-up studies have shown that only about 2% of these infants are severely handicapped.     

Intrauterine Growth Restriction (IUGR): Etiology and Diagnosis

Intrauterine growth restriction (IUGR) is associated with perinatal morbidity and mortality. IUGR is defined as fetus that fails to achieve his growth potential. Antenatal small for gestational age (SGA) is defined as fetus with weight <10th percentile. IUGR and SGA are commonly used interchangeably. The identification of IUGR is important. IUGR identification begins with assessment of risk factor(s), and the diagnosis is made by ultrasound using biometry when this confirms an estimated fetal weight (EFW) of <10th percentile. The common risk factors include maternal causes (hypertension, diabetes, cardiopulmonary disease, anemia, malnutrition, smoking, drug use), fetal causes (genetic disease including aneuploidy, congenital malformations, fetal infection, multiple pregnancies), and placental causes (placental insufficiency, placental infarction, placental mosaicism). Intrauterine growth determines the perinatal, postnatal, and adult life development. IUGR is associated with increased risk of development in adult life of metabolic diseases including but not limited to hypertension, diabetes, obesity, dyslipidemia, and the metabolic syndrome.     

Doppler evaluation as a predictor of asphyxia in fetuses with intrauterine growth retardation (IUGR)

Many papers showed that the pulsatility index of the fetal middle cerebral artery decreases during gestation. We observed equalization of the PI in MCA and PI in UMB in the perinatal period (after 38 weeks of gestation). We observed the increase the diastolic cerebral flow through the brain in cases of hypoxia. We interpreted that situation as a vasomotor response to fetal hypoxia (for example in IUGR). This phenomenon, is called in the literature as brain sparing effect. The aim of our study was estimation of application Doppler technique in diagnosis of changes in circulatory system in pregnancies complicated by intrauterine growth restriction (IUGR). We included 66 fetuses with IUGR and sonographic signs of the brain sparing effects, without any congenital malformation, oedema and genetic abnormalities to the study group. We included 1730 foetuses from normal, physiological pregnancies to the control group. In all cases time of gestation were calculated from Naegele's rule and were confirmed in sonographic examination before 16 weeks of gestation. SGA fetuses were defined on the basis of ultrasonographic measurements of BPD, HC, AC, FL and weight below 10th percentile of our reference curve. Sonographic examination were performed on Acuson 128 XP/10 with transducers (2.5 MHz-5 MHz). We performed Doppler examinations in MCA and UMB. Redistribution (brain sparing effect) was diagnosed when CPR (cerebroplacental ratio) was less than 1. We analysed the way and time of delivery and neoanatal follow up. Obtained in advance of researches results made possible expression of following conclusions: 1. Use of Doppler techniques in pregnancies complicated by IUGR makes possible diagnosis of hypoxia that helps in settlement of continuing or ending of pregnancy. 2. Changes in Doppler flows in foetus resoluteness outdistance irregular other values of biophysical methods of foetus monitoring.     

Intrauterine weight index in fetal growth retardation]

The intra uterine ponderal index (IPI) estimated by ultrasound examination (US) in 79 patients with intrauterine growth retardation (IUGR) is presented. The IPI was calculated using the following formula: [formula: see text] 13.2 (DFO) + 22 (DAT) + 8.9 (DAP) - 48.4 (LF) - 7469.1, and ETF = 0.55 (LF) + 8.66. Correlation indexes (r) of EPF, ETF and IPI with neonatal weight, length and ponderal index were 0.92, 0.87 and 0.51 (p < 0.001). The IPI revealed a gradual increase with respect to gestational age ranging from 1.63 to 3.08. The p 10 of the IPI was 1.96 for pregnancies of 30 to 34 weeks and 2.35 for pregnancies of 35 to 39 weeks. Those cases of IUGR with IPI < p 10 (n = 7) had a higher incidence of cesarean section (86% vs 30%, p < 0.01), intrapartum fetal distress (71% vs 11%, p < 0.01), Apgar score of < 7 at 5' (29% vs 1.4%, p < 0.05), PBF < 5 points (43% vs 4.7%, p < 0.01), and moderate or severe neonatal morbidity (57% vs 21%, p < 0.05) than those with IPI > or = p 10 (n = 72). No difference were found with respect to the presence of antepartum meconium (29% vs 6%, p = 0.09). In conclusion, ultrasonographic estimation of the IPI is another element of the examination that can help in the diagnosis of fetal condition in cases of IUGR, permitting to distinguish those fetuses that, having and estimated weight below the tenth percentile in a growth curve, are in higher perinatal risk.     

Intrauterine growth retardation: obstetrical aspects.

We have just begun our study of fetal growth retardation. Prenatal influences upon fetal growth are poorly understood and little studied. One may list multiple etiologies, catalogue numerous physiologic processes, and still not know in any given child what went wrong. The questions far exceed our preliminary answers. How does maternal undernutrition significantly effect the fetal "parasite?" Is the syndrome of intrauterine growth retardation a manifestation of a host versus graft phenomenon, with "runting" in the offspring? Are deficits in cell number and size unalterable? Can these deficits be overcome with good postnatal care? How can we better detect the fetus who is undergoing deprivation in utero? What altered biochemical processes exist? Can we reverse such abnormal influences in utero and prevent their consequences to the fetus? Certainly there are numerous additional areas for investigation and thought.     

Intrauterine growth retardation: standards for diagnosis

An intrauterine growth-retarded infant is commonly defined as one weighing less than the 10th percentile in birth weight for its gestational age. However, because there is no standard population from which to derive these percentiles, the birth weights that serve as the cutoff point in various published studies may differ by several hundred grams at any gestational age. For this reason, we examined the studies from which the currently used 10th-percentile standards are derived to determine which factors may be responsible for the variation. In addition to obvious differences in the populations and geographic areas on which they were based, studies differed in how gestational age was determined, whether the gestational age was "rounded" or given in completed weeks, which types of infants were excluded, whether the studies were hospital or population based, and whether they were controlled for sex of the infant and race and parity of the mother. These differences in study methodology may be as or more important than the population differences in defining the 10th percentile cutoffs. A single national standard for intrauterine growth retardation would allow comparison between studies of risk factors, diagnostic tests, management, and long-term follow-up status of fetuses and infants with intrauterine growth retardation.     

Intrauterine growth retardation and fetal cardiac function

Intrauterine growth retardation is a pathology which is found in 3-10% of all pregnancies and it is associated with around 20-25% of all fetal intrauterine deaths and with long-term neurologic sequelae. It presents an increased risk of distress during labor and delivery and a greater risk of perinatal mortality. The causes of IUGR and the cardiac and venous Doppler in normal fetuses are analyzed, and the hemodynamic cardiac modifications in IUGR fetus are discussed. The fetal cardiac function in intrauterine growth retardation shows a redistribution of the fetal cardiac output, which tends to favor the left ventricle as the mechanism to compensate for the uteroplacental insufficiency. The Doppler velocity indices are modified as the fetal condition progressively deteriorates and they represent an important tool for the management of the complicated pregnancy.     

Prediction of extrauterine growth retardation (EUGR) in VVLBW infants.

BACKGROUND: Long-term growth failure in very very low birth weight (VVLBW) infants is a common complication of extreme prematurity. Critical illnesses create challenges to adequate nutriture. PURPOSE: To identify predictors of extrauterine growth retardation (EUGR) in VVLBW infants and to evaluate their nutritional intake and subsequent growth. STUDY DESIGN: A 4-year retrospective chart review of 221 infants 相似文献   

Intrauterine growth retardation and urinary elimination of estriol

33 measurements of urinary estriol from 30-40 weeks' gestation in 22 pregnancies where dysmaturity was diagnosed in utero are shown graphically. The mean estriol excretion was about 2-3 mg below the lower limit of normal; it increased more slowly with gestational age: and it declined precipitously from 34-38 weeks. 1/3 of the women delivered at 38 weeks, either spontaneously or by induction. The mean estriol curve in the remaining women rose during treatment until delivery at 40 weeks. No correlation could be discerned in individual cases between the estriol excretion curve (or especially between an individual estriol value) and fetal weight, maturity, fetal distress in labor, or fetal death (1 case).     

Intrauterine growth retardation of newborns with congenital anomalies

The authors examined 11,799 newborns whose intrauterine life lasted from 28 to 42 weeks. In the group of dysmature infants (443) malformations were present in 11% and in the group of prematures (841) in 4.3%. Malformations were divided according to localization. The most significant difference was observed in the occurrence of malformations of the extremities (dysmature infants 27.17% and prematures 15.79%). It is concluded that malformations appear to be considerably more frequent in dismature infants than in prematures and that by their presence they affect the child's intrauterine growth.     

Intrauterine growth retardation. Antenatal diagnosis by ultrasound

Serial cephalometry is useful not only in defining the risk for intrauterine growth retardation (IUGR) in relation to each fetus' growth potential but also in identifying symmetric versus asymmetric undergrown fetuses. It is suggested that all fetuses with biparietal diameters falling below the 25th percentile or dropping to a lower percentile division undergo biophysical and biochemical monitoring for detection of the affected fetus. The value of the head-to-abdomen circumference ratio close to term in delineating asymmetric undergrown fetuses is discussed.     

Intrauterine growth retardation: a neonatologist's approach.

Early recognition of intrauterine growth retardation, and recognition of these compromised infants at birth, is essential, to correct, if possible, any adverse intrauterine influence; then, to provide proper nursery care, screening for abnormalities, and proper post-natal nutrition. Improved management of both the in-utero and the ex-utero environment may offer these neonates a more favorable prognosis for their physical, neurological, and intellectual development.     

Intrauterine growth retardation: A preliminary behavioural intervention study

Abstract

A simple exploratory intervention was undertaken with a group of mothers whose infants had been born small-for-gestational-age (SGA). Information derived from an earlier study of SGA infant behaviour was given to half the subjects while the other half were given general information about infants. A group of mothers of appropriately-grown (AGA) infants was given the same information. Observations of infant-mother interaction patterns at two months of age indicated state and behavioural differences between SGA and AGA groups. However, differences were also found between the intervention SGA and control SGA dyads in state stability, infant and mother signalling, and levels of interaction, all in the direction of more optimal patterns of interaction for the intervention group.