Many tests performed to diagnose inlammation cannot be used reliably during pregnancy. For example, leukocyte alkaline phosphatase levels-used to evaluate myeloproliferative disorders-are elevated beginning early in pregnancy. he concentration of C-reactive protein, an acute-phase serum reactant, rises rapidly in response to tissue trauma or inflammation. Median C-reactive protein levels in pregnancy and labor are higher than for nonpregnant women (Anderson, 2013; Watts, 1991). Of nonlaboring gravidas, 95 percent had levels of 1.5 mg/ dL or less, and gestational age did not afect serum levels. Another marker of inlammation, the erythrocyte sedimentation rate (ESR), is increased in normal pregnancy because of elevated plasma globulins and ibrinogen levels. Complement actors C3 and C4 levels also significantly rise during the second and third trimesters (Gallery, 1981; Richani, 2005). Last, concentrations ofprocalcitonin, a normal precursor of calcitonin, increase at the end of the third trimester and through the irst few postpartum days. Procalcitonin levels rise with severe bacterial infections but remain low in viral infections and nonspecific inlammatory disease. However, measured levels poorly predict development of overt or subclinical chorioamnionitis after premature rupture of membranes (Thornburg, 2016).
During normal pregnancy, both coagulation and fibrinolysis are augmented but remain balanced to maintain hemostasis (Kenny, 2014). Evidence of activation includes increased concentrations of all clotting factors except factors I and III (Table 4-3).
Of procoagulants, the level and rate of thrombin generation throughout gestation progressively increase (McLean, 2012). In normal nonpregnant women, plasma ibrinogen (factor 1) averages 300 mg/dL and ranges from 200 to 400 mg/dL. During normal pregnancy, the fibrinogen concentration rises approximately 50 percent. In late pregnancy, it averages 450 mg/dL, with a range from 300 to 600 mg/dL. his contributes greatly to ap <.05.
Data shown as mean ± standard deviation.
PlT = partial thromboplastin time; tPA = tissue activator.
Data from Uchikova, 2005.
the striking increase in the ESR. Also, levels of factor XIIIibrin stabilizing oetor-signiicantly drop as normal pregnancy advances (Sharief, 2014).
The end product of the coagulation cascade is ibrin formation, and the main function of the fibrinolytic system is to remove excess ibrin (Fig. 41-29, p. 784). Tissue plasminogen activator (tP A) converts plasminogen into plasmin, which causes ibrinolysis and produces ibrin-degradation products such as D-dimers. Although somewhat conlicting, most evidence suggests that fibrinolytic activity is reduced in normal pregnancy (Kenny, 2014). As reviewed by Cunningham and Nelson (2015), these changes favor ibrin formation. Although this is countered by increased levels of plasminogen, the net result is that pregnancy is a procoagulant state. Such changes serve to ensure hemostatic control during normal pregnancy, particularly during delivery when a certain amount of blood loss is expected.
Several proteins are natural inhibitors of coagulation, including proteins C and S and antithrombin (Fig. 52-I, p. 1005). Inherited or acquired deficiencies of these and other natural regulatory proteins-collectively referred to as thrombophiliasaccount for many thromboembolic episodes during pregnancy. hey are discussed in Chapter 52 (p. 1006).