Fetal growth restriction due to placental disease (original) (raw)
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Pathophysiology of intrauterine growth retardation: role of the placenta
Acta Paediatrica, 1997
The placenta is essential for normal fetal development. Failure of the placenta can result in many fetal conditions, for example, intrauterine growth retardation (IUGR). Placentas from pregnancies complicated by IUGR show vascular damage, which may lead to the onset of pregnancy-induced maternal hypertension. Accurate placental assessment may, therefore, indicate which fetuses are at risk of IUGR and so improve clinical evaluation and management of both the fetus and the mother. Placental development and function can be assessed by a number of methods, including measurement of placental weight at mid-gestation (placental growth in the second trimester correlates strongly with placental weight at birth), assessment of fetal and placental circulation (an association between perinatal morbidity and abnormal blood velocity profiles has been established) and assessment of placental metabolism and nutritional transfer (a reduction in transfer of nutrients may be an early indicator of IUGR). Intrauterine growth retardation, placenta, placental growth, placental transport, placental metabolism
The Relationship of Intrauterine Growth Restriction with Placental Pathologic Changes in Newborns
World Journal of Peri & Neonatology, 2020
Introduction: Intrauterine growth restriction is a multifaceted problem and is associated with a significant increase in the level of morbidity and perinatal mortality. According to some studies, failure of the placenta is responsible for the most cases of intrauterine growth restriction. The aim of this study was to evaluate the placental pathologic changes in the intrauterine growth restriction (IUGR) samples and compare them with normal cases. Methods: A study population consisted of 60 intrauterine growth restriction neonates and 60 normalized neonates born at Tehran Imam Khomeini Hospital between June 2016 and July 2017. The placenta was weighed, immediately after delivery, and the umbilical cord was separated, then stored in 10% formalin and sent for pathological examination as soon as possible. Data collection was performed according to the following items: the pathologist's report, the results of the infants' examination, and the data in the neonatal cases. Resul...
Anales De Pediatria, 2015
Introduction: Intrauterine growth restriction (IUGR) and prematurity have been associated with increased perinatal morbidity and mortality and also with cardiovascular foetal programming. However, there are few studies on the impact of placenta-related IUGR on perinatal outcomes and cardiovascular biomarkers in pre-term infants. Objectives: To determine differences in neonatal morbidity, mortality and cord blood biomarkers of cardiovascular dysfunction between pre-term placenta-related IUGR and non-IUGR new-borns, and to analyse their relationship with the severity of IUGR according to foetal Doppler evaluation. Material and methods: Prospective cohort study: pre-term infants with placenta-related IUGR and matched pre-term infants without IUGR. A Doppler scan was performed, and placenta-IUGR was classified according to severity. Comparative analysis of perinatal outcomes, neonatal morbidity and mortality, and cord blood levels of biomarkers of cardiovascular dysfunction was performed. Results: IUGR new-borns present lower weight, length, head circumference, and Apgar score at birth, as well as increased neonatal and cardiovascular dysfunction biomarker levels, compared with pre-term new-borns without IUGR. These differences increase with the severity of IUGR determined by prenatal umbilical artery Doppler scan. Conclusions: Placenta-related-IUGR pre-term infants, irrespective of gestational age, present increased neonatal morbidity and mortality that is significantly proportional to the severity of IUGR. Placental impairment and severity also determine levels of cardiovascular dysfunction biomarkers at birth.
International Journal of Medical Arts, 2020
Background: Placental thickness appears to be a promising parameter for estimation of gestational age of the fetus due to steady increase in placental thickness with gestational age. Aim of the work: To investigate the relationship between placental thickness and fetal outcome in patients with intrauterine growth restriction [IUGR]. Patients and Methods: This study included patients with fetuses diagnosed clinically and by ultrasound as IUGR [estimated fetal weight <10 th percentile for gestational age], singleton pregnancy, gestational age between 28-40 weeks of gestation, maternal age between 20-40 years old and body mass index between 18-30 kg/m 2. The placental thickness was measured at the second and third trimesters and correlated with the fetal outcome. Results: Results revealed that, estimated fetal weight significantly increased in normal placenta when compared to either thin or thick placentae. In addition, thin placentae had significantly low fetal birth weight [1936.4±409.2] when compared to thick placentae [2236.4±410.1] or normal placentae [2636.4±421.4]. Also, Apgar score was significantly higher and need for NICU admission were significantly lower with normal placentae. In addition, there is significant positive correlation between 3rd trimester placental thickness and fetal birth weight, placental weight and APGAR score. Conclusion: Placental thickness could predict deviations from norms of birth weight in late pregnancy. It seems to be promising for estimation of gestational age of the fetus and predicting fetal outcome.
Intrauterine growth restriction: Recent developments, definitions and future research
Clinical obstetrics, gynecology and reproductive medicine, 2019
The subject of intrauterine growth restriction has and continues to be in confusion because academic journals continue to publish articles that define the outcome of this disease as low birthweight or small for gestational age. This fault has been recently addressed with the recent publication of Fetal-Placental Growth Restriction: a series of 28 articles in 7 sections by 56 recognised authors. But even in this publication no alternative to low birthweight is clearly defined as an alternative to describe the outcome of this disease. As the name of this publication implies, this aberrant fetal growth has its origin in the maldevelopment of a normal, low resistance, uteroplacental circulation. It is therefore not surprising the many these cases have been detected preclinically using in mid-pregnancy uteroplacental Doppler flow studies. Previous studies have shown that an improvement in outcome definition is achieved when it address the asymmetry of growth these infant have. This review concludes that a ratio of birthweight to head circumference would be the simplest and most appropriate definition.
Pathophysiology of placental-derived fetal growth restriction
American journal of obstetrics and gynecology, 2018
Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular le...
Acta Obstetricia et Gynecologica Scandinavica, 2016
Introduction. Fetal growth restriction (FGR) is associated with poor perinatal outcomes. Screening and prevention tools for FGR, such as uterine artery Doppler imaging and aspirin, underperform in high-risk groups, compared with general antenatal populations. There is a paucity of sensitive screening tests for the early prediction of FGR in high-risk pregnancies. Materials and Methods. This was a prospective observational study based in a dedicated antenatal hypertension clinic at a tertiary UK hospital. We assessed maternal demographic and central hemodynamic variables as predictors for FGR in a group of women at high risk for placental insufficiency due to chronic hypertension (n = 55) or a history of hypertension in a previous pregnancy (n = 71). Outcome variables were birthweight z-score as well as development of FGR (defined as birthweight below the 5th or 3rd centile). Maternal hemodynamics were assessed using a noninvasive transthoracic bioreactance monitor (Cheetah NICOM). Results. The mean gestation at presentation was 13.6 (range: 8.5-19.5) weeks. Sixteen women delivered babies below the 5th centile. Ten of these were below the 3rd centile. Independent predictors of birthweight z-score were body surface area, peripheral vascular resistance and white ethnicity (R 2 = 0.26, p < 0.0001). Independent predictors of FGR were maternal height and cardiac output. The area under the receiver operator characteristic curve for prediction of FGR was 0.915 (95% CI 0.859-0.972) and 0.9079 (95% CI 0.823-0.990) for FGR below the 5th and 3rd centiles, respectively. Conclusion. In women with chronic hypertension or a history of hypertension in a previous pregnancy, maternal size and cardiac output at booking provide a sensitive screening tool for FGR.
Reduced placental volume and flow in severe growth restricted fetuses
Clinics, 2016
OBJECTIVES: To evaluate placental volume and vascular indices in pregnancies with severe fetal growth restriction and determine their correlations to normal reference ranges and Doppler velocimetry results of uterine and umbilical arteries. METHODS: Twenty-seven fetuses with estimated weights below the 3 rd percentile for gestational age were evaluated. Placental volume and vascular indices, including vascularization, flow, and vascularization flow indices, were measured by three-dimensional ultrasound using a rotational technique and compared to a previously described nomogram. The observed-to-expected placental volume ratio for gestational age and observed-to-expected placental volume ratio for fetal weight were calculated. Placental parameters correlated with the Doppler velocimetry results of uterine and umbilical arteries. RESULTS: The mean uterine artery pulsatility index was negatively correlated with the observed-to-expected placental volume ratio for gestational age, vascularization index and vascularization flow index. The observedto-expected placental volume ratio for gestational age and observed-to-expected placental volume ratio for fetal weight and vascularization index were significantly lower in the group with a bilateral protodiastolic notch. No placental parameter correlated with the umbilical artery pulsatility index. CONCLUSIONS: Pregnancies complicated by severe fetal growth restriction are associated with reduced placental volume and vascularization. These findings are related to changes in uterine artery Doppler velocimetry. Future studies on managing severe fetal growth restriction should focus on combined results of placental three-dimensional ultrasound and Doppler studies of uterine arteries.