Placental abruption is initiated by hemorrhage into the decidua basalis. he decidua then splits, leaving a thin layer adhered to the myometrium. Consequently, the process begins as a decidual hematoma and expands to cause separation and compression of the adjacent placenta. Inciting causes of many cases have been posited. he phenomenon of impaired tropho blastic invasion with subsequent atherosis is related in some cases of preeclampsia complicated by abruption (Brosens, 2011).
Inflammation or infection may be contributory (Mhatre, 2016;
Nath, 2007). Histological findings cannot be used to determine timing of the abruption (Chen, 2017).
Abruption likely begins with rupture of a decidual spi ral artery and then an expanding retroplacental hematoma.
In the early stages of placental abruption, clinical symptoms may be absent. Even with continued bleeding and placen tal separation, placental abruption can still be either total or partial (Fig. 41-14). With either, bleeding typically insinuates itself between the membranes and uterus, ultimately escaping through the cervix to cause external hemorrhage. Less often, the blood is retained between the detached placenta and the uterus, leading to concealed hemorrhage and delayed diagnosis. The delay translates into greater maternal and fetal hazards. Also with concealed hemorrhage, the likelihood of consumptive coagulopathy is elevated. This is because increased pressure within the intervillous space, caused by the expanding retroplacental clot, forces more placental thromboplastin into the maternal circulation (p. 784).
Nfost blood in the retroplacental hematoma in a nontraumatic placental abruption is maternal. his is because hemorrhage derives from separation within the maternal decidua, and placental villi are usually initially intact. In 78 women at Parkland Hospital with a nontraumatic placental abruption, fetal-tomaternal hemorrhage was documented in only 20 percent-and all of these had < 10 mL fetal blood loss (Stettler, 1992). Atkinson and colleagues (2015) identiied fetal cells in peripheral blood in only 4 percent of 68 women with a placental abruption.
When clinically suspected, an abruption is seen on a freshly delivered placenta as a circumscribed depression on the maternal surface. hese usually measure a few centimeters in diameter and are covered by dark, clotted blood. Because several minutes are required for these anatomical changes to materialize, a very recently separated placenta may appear totally normal at delivery. Our experiences are like those of fetal complications such as nonreassuring fetal status, growth restriction, or death; or neonatal outcomes that include death, preterm delivery, or growth restriction.
External trauma-usually from motor vehicle accidents or aggravated assault-can cause placental separation. he frequency of abruption originating from trauma varies. Kettel (1988) and Staford (1988) and their associates have appropriately stressed that abruption can stem from relatively minor trauma. he clinical presentation and consequences of these abruptions difer somewhat from spontaneous cases. For example, associated fetomaternal hemorrhage, while seldom clinically signiicant with most spontaneous abruptions, is more common with trauma because of concomitant placental tears or "fractures" (Chap. 47, p. 928). Fetal abruption with concealed hemorrhage. To the right is a partial abruption with blood a third of women with a traumatic abrup and clots dissecting between membranes and decidua to the internal cervical os and tion reported by Pearlman (1990). In eight
FIGURE 41-14 Schematic of placental abruption. Shown to left is a total placental bleeding that averaged 12 mL was noted in then externally into the vagina.