Elizabeth Garrett Anderson Institute for Women's Health, Faculty of Population Health Sciences, University College London, London, United Kingdom.
Nuffield Department of Obstetrics and Gynecology, University of Oxford, and the Fetal Medicine Unit, John Radcliffe Hospital, Oxford, United Kingdom.
Am J Obstet Gynecol. 2018 Jan;218(1):75-87. doi: 10.1016/j.ajog.2017.05.067. Epub 2017 Jun 24.
Placenta accreta spectrum is a complex obstetric complication associated with high maternal morbidity. It is a relatively new disorder of placentation, and is the consequence of damage to the endometrium-myometrial interface of the uterine wall. When first described 80 years ago, it mainly occurred after manual removal of the placenta, uterine curettage, or endometritis. Superficial damage leads primarily to an abnormally adherent placenta, and is diagnosed as the complete or partial absence of the decidua on histology. Today, the main cause of placenta accreta spectrum is uterine surgery and, in particular, uterine scar secondary to cesarean delivery. In the absence of endometrial reepithelialization of the scar area the trophoblast and villous tissue can invade deeply within the myometrium, including its circulation, and reach the surrounding pelvic organs. The cellular changes in the trophoblast observed in placenta accreta spectrum are probably secondary to the unusual myometrial environment in which it develops, and not a primary defect of trophoblast biology leading to excessive invasion of the myometrium. Placenta accreta spectrum was separated by pathologists into 3 categories: placenta creta when the villi simply adhere to the myometrium, placenta increta when the villi invade the myometrium, and placenta percreta where the villi invade the full thickness of the myometrium. Several prenatal ultrasound signs of placenta accreta spectrum were reported over the last 35 years, principally the disappearance of the normal uteroplacental interface (clear zone), extreme thinning of the underlying myometrium, and vascular changes within the placenta (lacunae) and placental bed (hypervascularity). The pathophysiological basis of these signs is due to permanent damage of the uterine wall as far as the serosa, with placental tissue reaching the deep uterine circulation. Adherent and invasive placentation may coexist in the same placental bed and evolve with advancing gestation. This may explain why no single, or set combination of, ultrasound sign(s) was found to be specific for the depth of abnormal placentation, and accurate for the differential diagnosis between adherent and invasive placentation. Correlation of pathological and clinical findings with prenatal imaging is essential to improve screening, diagnosis, and management of placenta accreta spectrum, and standardized protocols need to be developed.
胎盘植入谱系是一种与高产妇发病率相关的复杂产科并发症。它是一种相对较新的胎盘功能障碍，是子宫壁子宫内膜-子宫肌层界面损伤的结果。80 年前首次描述时，它主要发生在人工胎盘取出、刮宫术或子宫内膜炎后。轻度损伤主要导致异常粘连胎盘，并在组织学上诊断为完全或部分蜕膜缺失。如今，胎盘植入谱系的主要原因是子宫手术，特别是剖宫产引起的子宫瘢痕。在瘢痕区域的子宫内膜未重新上皮化的情况下，滋养层和绒毛组织可深入子宫肌层，包括其循环系统，并到达周围的盆腔器官。胎盘植入谱系中观察到的滋养层细胞变化可能继发于其发育的异常子宫环境，而不是滋养层生物学的主要缺陷导致子宫肌层过度侵袭。病理学家将胎盘植入谱系分为 3 类：绒毛简单附着于子宫肌层时为胎盘石灰化；绒毛侵入子宫肌层时为胎盘植入；绒毛侵入子宫全层时为胎盘穿透。过去 35 年来，报道了几种产前超声征象与胎盘植入谱系有关，主要是正常胎盘-子宫界面（透明带）消失、子宫肌层明显变薄，以及胎盘内（腔隙）和胎盘床（高血管化）的血管变化。这些征象的病理生理基础是由于子宫壁直至浆膜层的永久性损伤，胎盘组织到达深子宫循环。附着和侵袭性胎盘植可能同时存在于同一胎盘床，并随着妊娠的进展而演变。这可能解释了为什么没有单一或特定组合的超声征象被发现对异常胎盘植入的深度具有特异性，也不能准确区分粘连性和侵袭性胎盘植。病理和临床发现与产前影像学的相关性对于改善胎盘植入谱系的筛查、诊断和管理至关重要，需要制定标准化方案。
