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INTRODUCTION

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In some pregnancies, the placenta may develop at an abnormal location or may extensively invade the adjacent myometrium. Clinical entities include placenta previa, in which trophoblastic cells implant over or near the internal cervical os (Fig. 27-1). In other cases, trophoblast aggressively burrows into the myometrium. Depending on the invasion depth, placenta accreta, placenta increta, or placenta percreta is diagnosed (Fig. 27-2). The term placenta accrete syndromes is clinically useful to summarize these three types and is used here and throughout the text. Another interchangeable phrase also often used is morbidly adherent placenta (Bailit, 2015; Silver, 2015a).

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FIGURE 27-1

Placenta previa showing that copious hemorrhage could be anticipated with any cervical dilatation. (Reproduced with permission from Cunningham FG, Leveno KJ, Bloom SL, et al (eds): Obstetrical hemorrhage. In Williams Obstetrics, 24th ed. New York, McGraw-Hill Education, 2014.)

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FIGURE 27-2

Placenta accrete syndromes. A. Placenta accreta: villi are attached to myometrium. B. Placenta increta: villi have invaded the myometrium. C. Placenta percreta: villi have penetrated through the myometrium and serosa. (Reproduced with permission from Cunningham FG, Leveno KJ, Bloom SL, et al (eds): Obstetrical hemorrhage. In Williams Obstetrics, 24th ed. New York, McGraw-Hill Education, 2014.)

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For the gravida and her newborn, catastrophic sequelae can result from abnormal placental implantation. Of these, obstetric hemorrhage, cesarean hysterectomy, preterm delivery, and their attendant complications are prominent. Worryingly, rates of both placenta previa and accrete syndromes are rising. Most of this trend in the United States derives from the current substantial cesarean delivery rate, which is a known risk factor for both (Chap. 25, p. 404). Early identification and preparation can mitigate several of the associated complications. This chapter emphasizes many of these preventive steps.

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PLACENTAL PHYSIOLOGY

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In understanding the pathophysiology and management of placental disorders, one key concept is the mechanism by which hemostasis is achieved after normal delivery. First, recall that an incredible volume of blood flows through the intervillous space near term. Accurately measuring uteroplacental blood flow is challenging, and simultaneous calculation of uterine, ovarian, and collateral vessel contributions is currently not technically possible. This limitation stands even if the orthogonal capabilities of magnetic resonance angiography are used (Pates, 2010). With indirect methods that include clearance rates of androstenedione and xenon-133, uteroplacental blood flow has been calculated to increase progressively throughout pregnancy. Estimates at term range from 450 to 600 mL/min (Edman, 1981; Kauppila, 1980). These values are similar to those obtained with invasive methods—500 to 750 mL/min (Assali, 1953; Browne, 1953; Metcalfe, 1955). To put this remarkable rate of blood flow into context, remember that the entire cardiac output of a nonpregnant woman approximates only 3500 mL/min.

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This prodigious flow ...

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