In sum, these syndromes can have disastrous outcomes for both mother and fetus. Although the depth of placental invasion does not correspond with perinatal outcome, it is of paramount maternal significance (Seet, 2012). Shown in Table 41-6 are outcomes from reports of women from tertiary-care hospitals and in whom the diagnosis of morbidly adherent placenta was made preoperatively. Despite these advantages, a litany of complications included hemorrhage, urinary tract injury, intensive care unit admission, and secondary surgical procedures. Some of these reports chronicle outcomes in a second cohort of women in whom care was not given at a tertiary-care facility or in whom the diagnosis of percreta was not made until delivery, or both. In these cohorts, morbidity was higher, and there was one maternal death.
The terms consumptive coagulopathy, deibrination syndrome, or disseminated intravascular coagulation (DIC) are often used interchangeably, but there is an important distinction in these terms. An event related to actual consumption of pro coagulants within the intravascular tree results in a consumptive coagulopathy. In contrast, massive loss of procoagulants from hemorrhage results in a dilutional coagulopathy. Semantics aside, the clinicopathological coagulation disturbances with consumptive coagulopathy culminate in a systemic intravascular activation that completely disrupts natural hemostasis. As a result, an inefective balance of natural anticoagulant mechanisms leads to widespread fibrin deposition that can cause multiorgan failure (Levi, 2013).
Because of the many deinitions and variable severity, citing an accurate incidence for consumptive coagulopathy in pregnant women is problematic, but it ranges from 0.03 to 0.35 percent (Erez, 2014; Rattray, 2012). For example, some degree of significant coagulopathy is found in virtually all cases of placental abruption and amnionic fluid embolism. Other instances in which frequently occurring but less recognized degrees of coagulation activation can be found include sepsis, thrombotic microangiopathies, acute kidney injury, acute fatty liver, severe preeclampsia, and hemolysis, elevated liver enzyme levels, low platelet count (HELLP) syndrome (Cunningham, 2015). he overall contribution of each of these obstetrical disorders also varies depending on the population studied (Erez, 2015).
JOutcomes shown as mean ± 1 SO; median (range). hOata from Warshak, 2010. (Data from Eller, 201n1n.
dOata from Walker, 2013.
eOata from AI-Khan, 2014. fData from Erfani, 2017b; Shamshirsaz, 2015.
FFP = fresh-frozen plasma; ICU = intensive care unit; LOS = length of stay; NS = not stated; RBC = red blood cells.