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Placenta accreta spectrum (PAS) has been classically defined by trophoblastic attachment to the myometrium without intervening decidua. It occurs as a consequence of partial or complete absence of the decidua basalis and defective formation of the Nitabuch (fibrinoid) layer.Table 4.9.1 General Classification of Placenta Accreta Spectruma
Grade 1: Abnormally Adherent Placenta (Placenta Adherenta or Creta)
Clinical Criteria
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At vaginal delivery
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No separation with synthetic oxytocin and gentle controlled cord traction
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Attempts at manual removal of the placenta result in heavy bleeding from the placenta implantation site requiring mechanical or surgical procedures
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If laparotomy is required (including for cesarean delivery)
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Same as above
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Macroscopically, the uterus shows no obvious distension over the placental bed (placental “bulge”), no placental tissue is seen invading through the surface of the uterus, and there is no or minimal neovascularity.
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Histologic Criteria
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Microscopic examination of the placental bed samples from hysterectomy specimen shows extended areas of absent decidua between villous tissue and myometrium with placental villi attached directly to the superficial myometrium.
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The diagnosis cannot be made on just delivered placental tissue nor on random biopsies of the placental bed.
Grade 2: Abnormally Invasive Placenta (Increta)
Clinical Criteria
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At laparotomy
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Abnormal macroscopic findings over the placental bed: Bluish/purple coloring, distension (placental “bulge”)
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Significant amounts of hypervascularity (dense tangled bed of vessels or multiple vessels running parallel craniocaudally in the uterine serosa)
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No placental tissue seen to be invading through the uterine serosa
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Gentle cord traction results in the uterus being pulled inward without separation of the placenta (so-called dimple sign)
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Histologic Criteria
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Hysterectomy specimen or partial myometrial resection of the increta area shows placental villi within the muscular fibers and sometimes in the lumen of the deep uterine vasculature (radial or arcuate arteries)
Grade 3: Abnormally Invasive Placenta (Percreta)
Grade 3a: Limited to the Uterine Serosa
Clinical Criteria
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At laparotomy
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Abnormal macroscopic findings on uterine serosal surface (as above) and placental tissue seen to be invading through the surface of the uterus
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No invasion into any other organ, including the posterior wall of the bladder (a clear surgical plane can be identified between the bladder and uterus)
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Histologic Criteria
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Hysterectomy specimen showing villous tissue within or breaching the uterine serosa
Grade 3b: With Urinary Bladder Invasion
Clinical Criteria
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At laparotomy
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Placental villi are seen to be invading the bladder but no other organs.
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Clear surgical plane cannot be identified between the bladder and uterus.
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Histologic Criteria
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Hysterectomy specimen showing villous tissue breaching the uterine serosa and invading the bladder wall tissue or urothelium
Grade 3c: With Invasion of Other Pelvic Tissue/Organs
Clinical Criteria
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At laparotomy
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Placental villi are seen to be invading into the broad ligament, vaginal wall, pelvic sidewall, or any other pelvic organ (with or without invasion of the bladder).
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Histologic Criteria
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Hysterectomy specimen showing villous tissue breaching the uterine serosa and invading pelvic tissues/organs (with or without invasion of the bladder)
aFor the purposes of this classification, “uterus” includes the uterine body and uterine cervix.
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PAS is now classified and graded clinically according to the International Federation of Gynecology and Obstetrics (FIGO) (Table 4.9.1 and Figure 4.9.1A and B) (1).
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The incidence of PAS appears to be rising dramatically worldwide and is thought to be associated with the increase in the rate of cesarean delivery, conservative gynecologic surgery and in vitro fertilization. Because of the relative rarity of PAS before the 1970s, the reported incidence varied, but Breen et al. looked at the average rate in reports from 1871 to 1972 and found it to be 1 in 7,000 deliveries (2). In the United States, the incidence increased from 1 in 30,000 pregnancies in the 1960s to ˜1 in 2,500 pregnancies in a cohort from 1985 to 1994 (3). This further increased to 1 in 533 pregnancies in a cohort from 1982 to 2002 (4). There are reports of a rate as high as 1 in 300 pregnancies (5). It is important to note that these figures likely represent a high-risk cohort of women identified in tertiary centers, rather than a population that includes low-risk pregnancies. A population-based study in the United Kingdom and a review of a large, multicenter database that included deliveries from both tertiary referral hospitals and community hospitals in the United States independently reported a rate of PAS of 1 in 713 to 1.7 in 10,000 (6,7).
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Several risk factors are associated with PAS including:
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Clinical implications
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Maternal complications: The most common morbidity with PAS is massive hemorrhage. Median estimated blood loss in the setting of PAS ranges from 1,500 to 8,000 mL. Many women require multiple units of red cells and other blood products. The reported median number of units of blood required ranges between 5 and 6 (6,19,20,21); however, in our series of 300 PAS patients managed with a multidisciplinary team approach, the median was 2 units (10,22,23). Complications from transfusion of large volumes of crystalloid, blood products, and other volume expanders may occur and include dilutional coagulopathy, consumptive coagulopathy, immediate transfusion reactions, transfusion-related acute lung injury (TRALI), transfusion-associated cardiopulmonary overload (TACO), acute respiratory distress syndrome, postoperative mechanical ventilation for >4 hours, and electrolyte abnormalities (24). In one patient cohort of 123 singleton patients with PAS, 37 (30.1%; 95% confidence interval [CI] 22.1-39.0) developed coagulopathy, and close to 10% developed severe hypocalcemia (panic level) (25,26). Intraoperative transfusion of ≥4 units red blood cells (RBCs) is predictive of the development of both coagulopathy and severe hypocalcemia in PAS patients who are experiencing active bleeding. Because of this, empiric replacement of 1 g CaCl2 is recommended for every 4 units RBCs transfused.
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Surgical complications also are common, owing to the frequent need for hysterectomy, which can be technically challenging. The most frequently encountered problem is an injury to the bladder. However, it is difficult to assess the true rate of incidental cystotomy because cystotomy is often performed intentionally to facilitate the surgery and to avoid hemorrhage from invasive placental tissue (Figure 4.9.2). In our cohort, intentional cystostomy was performed in 35% of placenta percreta cases, and only 5% of patients had unintentional cystostomy (Figure 4.9.3) (22,23). Ureteral injury is much less common, and in our opinion, the risk may be significantly decreased by preoperatively placing ureteral stents. This helps in the identification of the ureters, especially in the face of heavy intra-abdominal bleeding obscuring the operative field, or in cases of lateral invasion of the placenta percreta into the pelvic sidewall. Other less common surgical complications include injury to the bowel, large vessels, and pelvic nerves, which mostly occur in placenta percreta cases (PAS 3c). Close clinical monitoring of vital signs, urine output, and intraperitoneal drain volume (when placed) is crucial to the early detection of intraperitoneal hemorrhage or hemorrhagic shock. Intraperitoneal drains may be placed in the event of cystotomy and repair or ureteral injury to monitor for early signs of urine leak.
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PAS should be considered in all pregnant women with a history of prior cesarean delivery and placenta previa.
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Digital cervical examination should be avoided until placenta previa is ruled out in PAS cases.
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Cautious sterile speculum vaginal examination should only be performed in a patient with PAS if there is important information that can be gained. The same precautions should be taken as with placenta previa patients.
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Fetal evaluation is unaltered from that in normal pregnancy although oxytocin challenge test is usually contraindicated.
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Definitive diagnosis is via imaging (see the section for Imaging and Other Diagnostics).
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An accurate obstetrical and surgical history is essential because placenta previa significantly increases the risk of PAS in case of prior cesarean delivery or uterine surgeries.
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Placenta previa
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Uterine rupture/dehiscence
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Serial ultrasound monitoring of placental location before delivery as described in the section for imaging.
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Vaginal bleeding should be monitored, and patient precaution should be given regarding pelvic rest.
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Universal screening for placental location during the midtrimester anatomy scan.
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First-trimester ultrasound markers: Several PAS ultrasound markers have been described in the first trimester. In a patient with a previous cesarean delivery, implantation of the gestational sac in the lower uterine segment is one of the most common markers for PAS in the first trimester. A cesarean scar pregnancy (CSP), defined as a gestational sac implanted in the lower uterine segment within or in close proximity to the cesarean scar, markedly increases the risk of PAS (27,28). CSP has been covered in Chapter 1.6. In the late first trimester, low implantation of the gestational sac is identified in ˜28% of patients with PAS (27). Other markers that have traditionally been described in second and third-trimester scans have also been identified in the late first trimester and are variably associated with PAS, as explained below (29).
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Second- and third-trimester ultrasound markers (30):
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Placental lacunae (Figure 4.9.4):
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Irregular, hypo-, or anechoic spaces within the placenta showing vascular flow (seen on grayscale and color Doppler imaging). The following lacunae findings are associated with a high risk of PAS:
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Multiple (often defined as >3)
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Large size
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Irregular borders
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High velocity and/or turbulent flow within
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Abnormal uteroplacental interface:
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Loss of the retroplacental hypoechoic zone between the placenta and myometrium, often noted between the uterus and posterior bladder wall, resulting in partial or complete interruption of the uterovesical interface (Figure 4.9.4)
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Thinning of the retroplacental myometrium (thickness of <1 mm). This marker can be simulated by undue transducer pressure; therefore, during imaging of the placenta, transducer pressure on the abdomen should be minimized (33).
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Abnormal uterine contour (placental bulge): Placental tissue distorting the outer uterine contour resulting in a bulge-like appearance (Figures 4.9.4 and 4.9.5A)
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