Placental abruption is the most common cause of severe consumptive coagulopathy in obstetrics and is discussed more fully on page 767. Typical quantiied levels of ibrin-split products with abruption are shown in Figure 41-30. With preeclampsia, eclampsia, and HELLP syndrome, endothelial activation is a hallmark and is discussed in Chapter 40 (p. 715). In general, the clinical severity of preeclampsia is directly correlated with thrombocytopenia and ibrinogen-ibrin degradation products (Kenny, 2015; Levi, 2010b). As shown in Figure 41-30, intravascular coagulation is seldom severe enough to be clinically worrisome (Pritchard, 1976).
Consumptive coagulopathy associated with prolonged reten tion of a dead fetus is unusual today because fetal death can be easily conirmed and there are highly efective methods for labor induction. With singleton pregnancies, if the dead fetus is unde livered, most women enter spontaneous labor within 2 weeks.
Gross disruption of maternal coagulation rarely develops before 4 weeks (Pritchard, 1959, 1973). After 1 month, however, almost a fourth will develop consumptive coagulopathy.
in a multifetal pregnancy in which one fetus dies while the other survives (Chescheir, 1988; Landy, 1989). his situation is uncommon, and in one study of 22 such pregnancies, none developed a coagulopathy (Petersen, 1999). Most cases are seen in monochorionic twins with shared circulations, which are described in Chapter 45 (p. 877).
he classic triad of abrupt hemodynamic and respiratory compromise along with DIC underpins its diagnosis (Clark, 2016). Most reports describe a frequency of 1 in 40,000 to 1 in 50,000 (Clark, 2014; Knight, 2010; Kramer, 2012). The case-fatality rate in all of these studies ranges from 11 to 43 percent. From another perspective, amnionic fluid embolism was the cause of 5 to 15 percent of all pregnancy-related deaths in the United States and Canada (Berg, 2003, 2010; Creanga, 2015; Kramer, 2012).
Predisposing conditions are rapid labor, meconium-stained luid, and tears into uterine and other large pelvic veins that permit an exchange of luids between the maternal and fetal compartment (Society for Maternal-Fetal Medicine, 2016). Other commonly cited risks include older maternal age; postterm pregnancy; labor induction or augmentation; eclampsia; cesarean, forceps, or vacuum delivery; placental abruption or previa; and hydramnios (Knight, 2010, 2012; Kramer, 2012). The association of uterine hypertonus appears to be the fectrather than the cause because uterine blood low ceases when intrauterine pressures exceed 35 to 40 mm Hg. Thus, a hypertonic contraction would be the least likely circumstance for amnionic luid and other debris to enter uterine veins (Clark, 1985). For this reason, hypertonus from oxytocin is not implicated.