The Fetal Response to Chronic Placental Insufficiency

https://doi.org/10.1053/j.semperi.2007.11.002Get rights and content

Fetal growth restriction is most commonly caused by failure of the placenta to meet the increasing demands for oxygen and substrate of the developing fetus, resulting in common fetal compensatory responses. Understanding these responses is helpful in developing a management strategy that will optimize pregnancy outcome.

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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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