The Fetal Response to Chronic Placental Insufficiency
Section snippets
Oxygenation and Acid-Base Status
With the identification of FGR as a clinical entity by Lubchenco and coworkers1 in 1963 came the observation of an associated risk of perinatal morbidity and mortality. The identification of asphyxia in the neonatal period2 as well as an increased risk of hypoxic insults led to the observation that chronic hypoxemia may be a prenatal finding. These suspicions were supported by the findings of antenatal fetal heart rate monitoring, which also suggested that growth-restricted fetuses may be
Fetal Hematology
The relative hypoxemia to which growth-restricted fetuses are exposed is a stimulus for erythropoiesis, likely as a compensatory response. Growth-restricted fetuses tend to have normal to increased hematocrits and increased nucleated red blood cell counts.4, 21, 22 The severity of fetal hypoxia correlates with the degree of erythoblastosis.4 The elevated nucleated red blood cell count is likely not only a compensatory response to hypoxia, but may also reflect ongoing consumption of red cells.
Protein and Carbohydrate Metabolism
Normal pregnancy advancement brings increased nutrient demands, increased placental nutrient transport capacity, and increased placental perfusion. A knowledge of these physiologic parameters led naturally to nutrient supply, delivery, and metabolism as primary objects of early investigations into the causation of FGR. Maternal amino acid concentrations have a direct influence on placental amino acid transport capacity for both normal and FGR pregnancies.27 Amino acid concentrations are
Fetal Endocrinology
Insulin-like growth factors (IGFs) promote cellular proliferation as well as the uptake of glucose and amino acids.50 IGFs play a prominent role in the regulation of fetal growth. IGF-1 levels increase during the second half of human pregnancy, and umbilical venous IGF-1 levels are correlated with birth weight.51, 52 In growth-restricted fetuses, umbilical venous IGF levels are diminished,52, 53, 54 whereas growth hormone, IGF-II, and IGF-binding protein II are similar to normally grown
Summary
Placental dysfunction results in a fetal environment that is characterized by hypoxemia and acidemia. The fetus attempts to respond to chronic hypoxemia by maximizing red blood cell production. Fetal hematocrits are usually normal to slightly increased. Placental vasculopathy may result in destruction of both platelets and red cells. The maternal–fetal glucose gradient is increased in growth-restricted fetuses proportional to the severity of FGR. This may be an adaptive response to placental
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Cited by (56)
The Proteome Landscape of Human Placentas for Monochorionic Twins with Selective Intrauterine Growth Restriction
2024, Genomics, Proteomics and BioinformaticsCerebroplacental ratio as an indicator of placental functioning and its relationship with early communicative gestures acquisition
2023, Revista de Logopedia, Foniatria y AudiologiaMaternal physical activity significantly alters the placental transcriptome
2020, PlacentaCitation Excerpt :Alterations in expression of placenta transporters, receptors, and signaling pathways involved in nutrient sensing and transport may be a potential mechanism for restricting growth when nutrition is limited and accelerating growth when there is an excess [19–22]. Considering its servitude to the fetus, variations in placenta function can also promote reactions in the fetus, including alterations in circulation, metabolism, and endocrinology [23]. What remains unknown is how maternal PA impacts human placenta.
Assessment of fetal myocardial performance in severe early onset pre-eclampsia (EO-PET) with and without intrauterine growth restriction across deteriorating stages of placental vascular resistance and links to adverse outcomes
2017, European Journal of Obstetrics and Gynecology and Reproductive BiologyCitation Excerpt :As early onset pre-eclampsia and early onset intrauterine growth restriction arise from the same pathophysiological process (with the EO-PET phenotype representing a deterioration in the placental pathology compared to IUGR [15]) these conditions are intertwined, and we would expect a significant proportion of severe EO-PET fetuses to also be growth restricted. IUGR was defined by the following 2 criteria (both needed to be present): AC <10th percentile for gestational age and umbilical artery resistance index 2 standard deviations above mean [22–25] Standard growth charts were used. The study was approved by the Biomedical Research Ethics Committee of the University of Kwa-Zulu Natal, Durban, South Africa (BE228/12)