Faculty of Population Health Sciences, Elizabeth Garrett Anderson Institute for Women's Health, Faculty of Population Health Sciences, London, United Kingdom.
Faculty of Population Health Sciences, Elizabeth Garrett Anderson Institute for Women's Health, Faculty of Population Health Sciences, London, United Kingdom.
Am J Obstet Gynecol. 2022 Sep;227(3):384-391. doi: 10.1016/j.ajog.2022.02.038. Epub 2022 Mar 3.
Placenta accreta has been described as a spectrum of abnormal attachment of villous tissue to the uterine wall, ranging from superficial attachment to the inner myometrium without interposing decidua to transmural invasion through the entire uterine wall and beyond. These descriptions have prevailed for more than 50 years and form the basis for the diagnosis and grading of accreta placentation. Accreta placentation is essentially the consequence of uterine remodeling after surgery, primarily after cesarean delivery. Large cesarean scar defects in the lower uterine segment are associated with failure of normal decidualization and loss of the subdecidual myometrium. These changes allow the placental anchoring villi to implant, and extravillous trophoblast cells to migrate, close to the serosal surface of the uterus. These microscopic features are central to the misconception that the accreta placental villous tissue is excessively invasive and have led to much confusion and heterogeneity in clinical data. Progressive recruitment of large arteries in the uterine wall, that is, helicine, arcuate, and/or radial arteries, results in high-velocity maternal blood entering the intervillous space from the first trimester of pregnancy and subsequent formation of placental lacunae. Recently, guided sampling of accreta areas at delivery has enabled accurate correlation of prenatal imaging data with intraoperative features and histopathologic findings. In more than 70% of samples, there were thick fibrinoid depositions between the tip of most anchoring villi and the underlying uterine wall and around all deeply implanted villi. The distortion of the uteroplacental interface by these dense depositions and the loss of the normal plane of separation are the main factors leading to abnormal placental attachment. These data challenged the classical concept that placenta accreta is simply owing to villous tissue sitting atop the superficial myometrium without interposed decidua. Moreover, there is no evidence in accreta placentation that the extravillous trophoblast is abnormally invasive or that villous tissue can cross the uterine serosa into the pelvis. It is the size of the scar defect, the amount of placental tissue developing inside the scar, and the residual myometrial thickness in the scar area that determine the distance between the placental basal plate and the uterine serosa and thus the risk of accreta placentation.
胎盘植入被描述为绒毛组织与子宫壁异常附着的一种连续谱，范围从绒毛组织仅附着于浅肌层而无蜕膜间插至穿透整个子宫壁并超出子宫壁的全层侵入。这些描述已经存在了 50 多年，是诊断和分级胎盘植入的基础。胎盘植入主要是由于手术后子宫重塑引起的，主要是剖宫产手术后。下段子宫瘢痕缺陷大与正常蜕膜化失败和蜕膜下子宫肌层丧失有关。这些变化允许胎盘附着绒毛植入，并使绒毛外滋养细胞迁移，接近子宫浆膜面。这些微观特征是胎盘植入绒毛组织过度侵袭的误解的核心，导致临床数据的混淆和异质性。子宫壁内大动脉的逐渐募集，即螺旋状、弓形和/或放射状动脉，导致高流速的母体血液从妊娠早期进入绒毛间隙，随后形成胎盘血池。最近，在分娩时对胎盘植入部位进行引导性取样，使得产前影像学数据与术中特征和组织病理学发现能够准确相关。在超过 70%的样本中，在大多数附着绒毛的尖端和其下方的子宫壁之间以及所有深层植入的绒毛周围，都有厚厚的纤维蛋白样沉积物。这些致密沉积物对胎盘-子宫界面的扭曲以及正常分离平面的丧失是导致胎盘异常附着的主要因素。这些数据挑战了胎盘植入仅仅是由于绒毛组织位于无蜕膜间插的浅肌层上的经典概念。此外，在胎盘植入中没有证据表明绒毛外滋养细胞异常侵袭或绒毛组织可以穿过子宫浆膜进入盆腔。决定胎盘基底部与子宫浆膜之间距离以及胎盘植入风险的是瘢痕缺陷的大小、在瘢痕内发育的胎盘组织的量以及瘢痕区域的残余子宫肌层厚度。
