Parkland Hospital, 44 percent of cesarean hysterectomies were placenta (Wortman, 2015). The technique for peripartum hys terectomy is described in Chapter 30 (p. 580).
ute substantively to maternal morbidity and mortality rates. he maternal mortality ratio is increased approximately threefold for women with a placenta previa (Gibbins, 2018; Oyelese, 2006).
In another report of 5367 maternal deaths in the United States from 2006 to 2013, placenta previa alone accounted for nearly 3 percent of deaths from hemorrhage (Creanga, 2015, 2017).
The report from the Consortium on Safe Labor emphasizes the ongoing perinatal morbidity with placenta previa (Lai, 2012). Preterm delivery continues to be a major cause of perinatal death (N0rgaard, 2012). In deliveries with placenta previa in the United States in 1997, the neonatal mortality rate was threefold higher than that in unafected pregnancies and stemmed primarily from preterm delivery (Salihu, 2003). Ananth and colleagues (2003) reported a comparably elevated risk of neonatal death even for fetuses who delivered at term. This is at least partially related to the fetal anomaly rate, which is two-to threefold higher in pregnancies with placenta previa (Crane, 1999).
The association of fetal-growth restriction with placenta previa is likely minimal ter controlling for gestational age. In a populationbased cohort of more than 500,000 singleton births, Ananth and associates (2001) found that most low-birthweight newborns associated with placenta previa resulted from preterm birth. Harper and coworkers (2010) reported similar indings from a cohort of nearly 58,000 women. In contrast, at least two studies reported a greater risk for fetal-growth restriction (iisanen, 2014; Weiner, 2016).
The term morbidy adherent placenta describes aberrant placentation characterized by abnormally implanted, invasive, or adhered placenta. We also refer to these disorders collectively as accrete syndromes and use these terms interchangeably. Derivation of accrete comes from the Latin ac-+ crescere-to adhere or become attached to (Benirschke, 2012).
In the accrete syndromes, abnormal placental adherence to the myometrium stems in part from partial or total absence of the decidua basalis and imperfect development of the ibrinoid or Nitabuch layer, described in Chapter 5 (p. 86). If the decidual spongy layer is lacking either partially or totally, then the physiological line of cleavage is absent, and some or all cotyledons are densely anchored. Microscopically, placental villi attach to smooth muscle ibers rather than to decidual cells. This decidual deiciency then prevents normal placental separation after delivery. he surface area of the implantation site involved and the depth of trophoblastic tissue ingrowth are variable between women, but all afected placentas can potentially cause signiicant hemorrhage.
Substantiated data now suggest that accrete syndromes are not solely caused by this anatomical layer deficiency (Duzyj, 2017; T antbirojn, 2008). Indeed, the cytotrophoblasts may control decidual invasion through factors such as angiogenesis (Duzyj, 2015; Goh, 2016; Wehrum, 2011). Also, accrete syndrome tissue specimens show "hyperinvasiveness" (Pri-Paz, 2012) . Myometrial ibers attached to the basal plate in an antecedent pregnancy are predictive markers for a subsequent