As discussed on page 140, there is a functional diference between hemoglobins A and F. At any given oxygen tension and at identical pH, fetal erythrocytes that contain mostly hemoglobin F bind more oxygen than do those that contain nearly all hemoglobin A (Fig. 47-2, p. 920). his is because hemoglobin A binds 2,3-diphosphoglycerate (2,3-DPG) more avidly than does hemoglobin F, thus lowering the ainity of hemoglobin A for oxygen. During pregnancy, maternal 2,3-DPG levels are greater, and because fetal erythrocytes have lower concentrations of 2,3-DPG, the latter has increased oxygen ainity.
he amount of hemoglobin F in fetal erythrocytes begins to decrease in the last weeks of pregnancy. At term, approximately three fourths oftotal hemoglobin levels are hemoglobin F. During the irst 6 to 12 months of life, the hemoglobin F proportion continues to decline and eventually reaches the low levels found in adult erythrocytes.
With the exception of fibrinogen, there are no embryonic forms of the various hemostatic proteins. he fetus starts producing normal, adult-type procoagulant, ibrinolytic, and anticoagulant proteins by 12 weeks. Because they do not cross the placenta, their concentrations at birth are markedly below the levels that develop within a few weeks of life (Corrigan, 1992). In normal neonates, the levels of factors II, VII, IX, X, XI, and of protein S, protein C, antithrombin, and plasminogen all approximate 50 percent of adult levels. In contrast, levels of factors V, VIII, XIII, and ibrinogen are closer to adult values (Saracco, 2009). Without prophylactic treatment, the levels of vitamin K-dependent coagulation factors usually decrease even further during the irst few days after birth. his decline is ampliied in breastfed infants and may lead to newborn hemorrhage (Chap. 33, p. 626).
Fetal ibrinogen, which appears as early as 5 weeks, has the same amino acid composition as adult ibrinogen, however, it has diferent properties (Klagsbrun, 1988). It forms a less compressible clot, and the ibrin monomer has a lower degree of aggregation (Heimark, 1988). Although plasma ibrinogen levels at birth are less than those in nonpregnant adults, the protein is functionally more active than adult ibrinogen (Ignjatovic, 2011).
Levels of functional fetal factor XIII-ibrin stabilizing factor-are signiicantly reduced compared with those in adults (Henriksson, 1974). Nielsen (1969) described low levels of plasminogen and elevated ibrinolytic activity in cord plasma compared with that of maternal plasma. Platelet counts in cord blood are in the normal range for nonpregnant adults (see Fig. 7-11).
Despite this relative reduction in procoagulants, the fetus appears to be protected from hemorrhage, and fetal bleeding is rare. Even after invasive fetal procedures such as cordocentesis, excessive bleeding is uncommon. Ney and coworkers (1989) have shown that amnionic luid thromboplastins and a factor(s) in Wharton jelly combine to aid coagulation at the umbilical cord puncture site.
Various thrombophilias may cause thromboses and pregnancy complications in adults (Chap. 52, p. 1008). If the fetus inherits one of these mutations, thrombosis and infarction can develop in the placenta or fetal organs. his is usually seen with homozygous inheritance. One example is homozygous protein C mutation, which causes purpura fulminans.