Intrauterine growth restriction (IUGR) is found in 1-10% of all pregnancies, and among women with risk factors even twice often. It is connected to worse obstetric results, and its complications can arise long time after delivery. In the paper we described etiology, diagnostics and monitoring of IUGR and its consequences for the child and for the course of neonatal periode.

Intrauterine growth restriction

Fetal growth restriction (FGR) is a condition that affects 5–10% of pregnancies and is the second most common cause of perinatal mortality. This review presents the most recent knowledge on FGR and focuses on the etiology, classification, prediction, diagnosis, and management of the condition, as well as on its neurological complications. The Pubmed, SCOPUS, and Embase databases were searched using the term “fetal growth restriction”. Fetal growth restriction (FGR) may be classified as early or late depending on the time of diagnosis. Early FGR (<32 weeks) is associated with substantial alterations in placental implantation with elevated hypoxia, which requires cardiovascular adaptation. Perinatal morbidity and mortality rates are high. Late FGR (≥32 weeks) presents with slight deficiencies in placentation, which leads to mild hypoxia and requires little cardiovascular adaptation. Perinatal morbidity and mortality rates are lower. The diagnosis of FGR may be clinical; however, an arterial and venous Doppler ultrasound examination is essential for diagnosis and follow-up. There are currently no treatments to control FGR; the time at which pregnancy is interrupted is of vital importance for protecting both the mother and fetus. Early diagnosis of FGR is very important, because it enables the identification of the etiology of the condition and adequate monitoring of the fetal status, thereby minimizing risks of premature birth and intrauterine hypoxia.

Fetal growth restriction: current knowledge.

Interferons and Proinflammatory Cytokines in Pregnancy and Fetal Development.

The steroid hormones progestagens, estrogens, androgens, and glucocorticoids as well as their precursor cholesterol are required for successful establishment and maintenance of pregnancy and proper development of the fetus The human placenta forms at the interface of maternal and fetal circulation It participates in biosynthesis and metabolism of steroids as well as their regulated exchange between maternal and fetal compartment This review outlines the mechanisms of human placental handling of steroid compounds Cholesterol is transported from mother to offspring involving lipoprotein receptors such as low-density lipoprotein receptor (LDLR) and scavenger receptor class B type I (SRB1) as well as ATP-binding cassette (ABC)-transporters, ABCA1 and ABCG1 Additionally, cholesterol is also a precursor for placental progesterone and estrogen synthesis Hormone synthesis is predominantly performed by members of the cytochrome P-450 (CYP) enzyme family including CYP11A1 or CYP19A1 and hydroxysteroid dehydrogenases (HSDs) such as 3β-HSD and 17β-HSD Placental estrogen synthesis requires delivery of sulfate-conjugated precursor molecules from fetal and maternal serum Placental uptake of these precursors is mediated by members of the solute carrier (SLC) family including sodium-dependent organic anion transporter (SOAT), organic anion transporter 4 (OAT4), and organic anion transporting polypeptide 2B1 (OATP2B1) Maternal-fetal glucocorticoid transport has to be tightly regulated in order to ensure healthy fetal growth and development For that purpose, the placenta expresses the enzymes 11β-HSD 1 and 2 as well as the transporter ABCB1 This article also summarizes the impact of diverse compounds and diseases on the expression level and activity of the involved transporters, receptors, and metabolizing enzymes and concludes that the regulatory mechanisms changing the physiological to a pathophysiological state are barely explored The structure and the cellular composition of the human placental barrier are introduced While steroid production, metabolism and transport in the placental syncytiotrophoblast have been explored for decades, few information is available for the role of placental-fetal endothelial cells in these processes With regard to placental structure and function, significant differences exist between species To further decipher physiologic pathways and their pathologic alterations in placental steroid handling, proper model systems are mandatory

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Physiology and Pathophysiology of Steroid Biosynthesis, Transport and Metabolism in the Human Placenta

Fetal growth restriction (FGR) continues to be a leading cause of preventable stillbirth and poor neurodevelopmental outcomes in offspring, and furthermore is strongly associated with the obstetrical complications of iatrogenic preterm birth and pre-eclampsia. The terms small for gestational age (SGA) and FGR have, for too long, been considered equivalent and therefore used interchangeably. However, the delivery of improved clinical outcomes requires that clinicians effectively distinguish fetuses that are pathologically growth-restricted from those that are constitutively small. A greater understanding of the multifactorial pathogenesis of both early- and late-onset FGR, especially the role of underlying placental pathologies, may offer insight into targeted treatment strategies that preserve placental function. The new maternal blood biomarker placenta growth factor offers much potential in this context. This review highlights new approaches to effective screening for FGR based on a comprehensive review of: etiology, diagnosis, antenatal surveillance and management. Recent advances in novel imaging methods provide the basis for stepwise multi-parametric testing that may deliver cost-effective screening within existing antenatal care systems.

Screening for fetal growth restriction and placental insufficiency.

OBJECTIVES To assess intracranial structure volumes by 3-dimensional (3D) sonography in fetuses with growth restriction. METHODS We conducted a prospective cross-sectional case-control study involving 59 fetuses with growth restriction (38 fetuses with estimated weight <3rd percentile and 21 fetuses with estimated weight between 3rd and 10th percentiles, according to Hadlock et al [Radiology 1984; 150:535-540]) and 54 controls between 24 and 34 weeks' gestation. The following fetal intracranial structure volumes were assessed: cerebellum, brain, and frontal region. The volume was assessed by 3D sonography using the extended imaging virtual organ computer-aided analysis method with 10 sequential planes. Analysis of variance was used to compare fetal groups. The intraclass correlation coefficient was used to assess intraobserver and interobserver reproducibility. RESULTS Statistical significance between the brain, frontal region, and cerebellar volumes and a relationship between the frontal region and the brain in fetuses with estimated weights below the 3rd percentile and controls were observed (P < .001; P < .001; and P = .002; and P = .008, respectively). Good intraobserver and interobserver reproducibility was observed for the fetal brain, frontal region, and cerebellar volumes, with intraclass correlation coefficients of 0.998, 0.997, 0.997, 0.999, 0.997, and 0.998, respectively. CONCLUSIONS The intracranial structure volumes assessed by 3D sonography using the extended imaging virtual organ computer-aided analysis method were reduced in fetuses with growth restriction (estimated weight <3rd percentile).

https://onlinelibrary.wiley.com/doi/pdf/10.7863/ultra.34.8.1397

Assessment of Intracranial Structure Volumes in Fetuses With Growth Restriction by 3-Dimensional Sonography Using the Extended Imaging Virtual Organ Computer-Aided Analysis Method

Aim: To evaluate the modified myocardial performance index (Mod-MPI) in foetuses with growth restriction and compare this index with appropriate for gestational age foetuses. Material and methods: A prospective cross-sectional case-control study was conducted involving 76 singleton foetuses between 24 and 34 weeks of gestation divided into three groups (24 appropriate growth foetuses, 30 foetuses with estimated weight between the 3 rd and 10 th percentiles and 22 foetuses with estimated weight < 3 rd percentile, according to the Hadlock table). The Mod-MPI was obtained in the plane of the four chamber view, and the spectral Doppler sample volume was placed in the lateral wall of the aorta, close to the mitral valve. Doppler of umbilical artery was normal in all cases. Analysis of variance (ANOVA) was used to compare the groups and the intra-class correlation coefficient (ICC) was used to assess intra- and inter-observer reproducibility. Results: The mean Mod-MPI in the groups of appropriate for gestational age, estimated weight between the 3 rd and 10 th percentiles, and estimated weight < 3 rd percentile was 0.32 ± 0.05, 0.35 ± 0.05 and 0.36 ± 0.06, respectively; there was no statistical difference between the groups (p = 0.072). There was good intra- and inter-observer reproducibility (ICC = 0.726 and 0.760, respectively). Conclusion: Mod-MPI was not significantly different between foetuses appropriate for gestational age and those with growth restriction. Mod-MPI proved to be a feasible and reproducible technique.

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Carolina Pacheco Silva

Papers

Fetal growth restriction: current knowledge.

Assessment of Intracranial Structure Volumes in Fetuses With Growth Restriction by 3-Dimensional Sonography Using the Extended Imaging Virtual Organ Computer-Aided Analysis Method

Assessment of modified myocardial performance index in foetuses with growth restriction.