Although precise measurements of human fetoplacental blood volume are lacking, Usher and associates (1963) reported values in term normal newborns to average 78 mLlkg when immediate cord clamping was conducted. Gruenwald (1967) found the fetal blood volume contained in the placenta after prompt cord clamping to average 45 mLlkg of fetal weight. Thus, fetoplacental blood volume at term is approximately 125 mLlkg of fetal weight. This is important when assessing the magnitude of fetomaternal hemorrhage as discussed in Chapter 15 (p. 307).
In the early embryo, hemopoiesis is demonstrable first in the yolk sac, followed by the liver, and inally spleen and bone marrow. Both myeloid and erythroid cells are continually pro duced by progenitors that are from hematopoietic stem cells (Golub, 2013; Heinig, 2015). The first erythrocytes released into the fetal circulation are nucleated and macrocytic. The mean cell volume is at least 180 L in the embryo and decreases to 105 to 115 L at term. The erythrocytes of aneuploid fetuses mean cell volumes-130 L on average (Sipes, 1991). As fetal development progresses, more and more of the circulating erythrocytes are smaller and nonnucleated. With fetal growth, both the blood volume in the common fetoplacental circu lation and hemoglobin concentration increase. As shown in
Figure 7-10, fetal hemoglobin concentrations rise across preg nancy. The Society for Maternal-Fetal Medicine (2015) rec ommends a cutof hematocrit value of 30 percent to define anemia.
Because of their large size, fetal erythrocytes have a short life span, which progressively lengthens to approximately 90 days at term (Pearson, 1966). As a consequence, red blood cell production rises. Reticulocytes are initially present at high levels, but decrease to 4 to 5 percent of the total at term. Fetal erythrocytes difer structurally and metabolically from those in the adult (Baron, 2012). They are more deformable, which serves to ofset their higher viscosity. They also contain several enzymes with appreciably diferent activities.
Erythropoiesis is controlled primarily by fetal erythropoietin because maternal erythropoietin does not cross the placenta. Fetal hormone production is influenced by testosterone, estrogen, prostaglandins, thyroid hormone, and lipoproteins (Stockman, 1992). Serum erythropoietin levels rise with fetal maturity. Although the exact production site is disputed, the fetal liver appears to be an important source until renal production begins. There is a close correlation between the erythropoietin concentration in amnionic fluid and that in umbilical venous blood obtained by cordocentesis. After birth, erythropoietin normally may not be detectable for up to 3 months.
In contrast, platelet production reaches stable levels by midpregnancy, although there is some variation across gestation (Fig.
The fetal and neonatal platelet count is subject to various agents as discussed in Chapter 15 (p. 307).
This tetrameric protein is composed of two copies of two diferent peptide chains, which determine the type of hemoglobin produced. Normal adult hemoglobin A is made of a and 3 chains. During embryonic and fetal life, various a and 3 chain precursors are produced. This results in the serial production of several diferent embryonic hemoglobins. Genes for 3-type chains are on chromosome 11, and those for a-type chains on chromosome 16. Each of these genes is turned on and then of during fetal life, until a and 3 genes, which direct the production of adult hemoglobin A, are permanentlyiactivated.