Placental Tissue Destruction and Insufficiency From COVID-19 Causes Stillbirth and Neonatal Death From Hypoxic-Ischemic Injury
Placental Tissue Destruction and Insufficiency From COVID-19 Causes Stillbirth and Neonatal Death From Hypoxic-Ischemic Injury
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DOI：
10.5858/arpa.2022-0029-sa
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发表时间：
2022-06-01
影响因子：
4.6
通讯作者：
Zaigham, Mehreen
中科院分区：
文献类型：
--
作者：
Schwartz, David A.;Avvad-Portari, Elyzabeth;Zaigham, Mehreen
背景。随着2019冠状病毒病（COVID-19）大流行的持续，围产期死亡是一个日益重要的问题，但死亡机制尚不清楚。客观。-评估母体感染COVID-19并证实胎盘呈严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）阳性后，胎盘在导致死产和新生儿死亡中的作用。设计。-由来自12个国家的44名围产期专家组成的跨国小组对64名死胎和4名新生儿死亡的胎盘和尸检病理学结果进行了基于病例的回顾性临床病理学分析，这些死胎和新生儿死亡的胎盘在COVID-19母亲分娩后检测为SARS-CoV-2阳性。结果。在构成SARS-CoV-2胎盘炎的3个发现中，所有68个胎盘都有纤维蛋白沉积增加和绒毛滋养层坏死，66个有慢性组织细胞绒毛间炎。63个胎盘有大量的绒毛周围纤维蛋白沉积。SARS-CoV-2胎盘炎的严重破坏性胎盘疾病平均有77.7%的组织受累。其他发现包括多发性绒毛间血栓（37%; 25/68）和慢性绒毛炎（32%; 22/68）。30例尸检中的大多数（19例; 63%）显示，除宫内缺氧和窒息外，无明显胎儿异常。在所有68例病例中，28例检测病例中有16例从身体标本中检测到SARS-CoV-2，最常见的是从鼻咽拭子中检测到。四具尸体的内脏器官中发现了SARS-CoV-2。结论。构成SARS-CoV-2胎盘炎的病理学异常引起广泛和严重的胎盘破坏，导致胎盘灌注不良和功能不全。在这些情况下，宫内和围产期死亡可能直接由胎盘功能不全和胎儿缺氧缺血性损伤引起。没有证据表明SARS-CoV-2对胎儿的影响在导致这些死亡中起作用。(Arch Pathol Lab Med.2022;146：660-676; doi：10.5858/ arpa.2022-0029-SA）
Context.-Perinatal death is an increasingly important problem as the coronavirus disease 2019 (COVID-19) pandemic continues, but the mechanism of death has been unclear. Objective.-To evaluate the role of the placenta in causing stillbirth and neonatal death following maternal infection with COVID-19 and confirmed placental positivity for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Design.-Case-based retrospective clinicopathologic analysis by a multinational group of 44 perinatal specialists from 12 countries of placental and autopsy pathology findings from 64 stillborns and 4 neonatal deaths having placentas testing positive for SARS-CoV-2 following delivery to mothers with COVID-19. Results.-Of the 3 findings constituting SARS-CoV-2 placentitis, all 68 placentas had increased fibrin deposition and villous trophoblast necrosis and 66 had chronic histiocytic intervillositis. Sixty-three placentas had massive perivillous fibrin deposition. Severe destructive placental disease from SARS-CoV-2 placentitis averaged 77.7% tissue involvement. Other findings included multiple intervillous thrombi (37%; 25 of 68) and chronic villitis (32%; 22 of 68). The majority (19; 63%) of the 30 autopsies revealed no significant fetal abnormalities except for intrauterine hypoxia and asphyxia. Among all 68 cases, SARS-CoV-2 was detected from a body specimen in 16 of 28 cases tested, most frequently from nasopharyngeal swabs. Four autopsied stillborns had SARS-CoV-2 identified in internal organs. Conclusions.-The pathology abnormalities composing SARS-CoV-2 placentitis cause widespread and severe placental destruction resulting in placental malperfusion and insufficiency. In these cases, intrauterine and perinatal death likely results directly from placental insufficiency and fetal hypoxic-ischemic injury. There was no evidence that SARS-CoV-2 involvement of the fetus had a role in causing these deaths. (Arch Pathol Lab Med. 2022;146:660-676; doi: 10.5858/ arpa.2022-0029-SA)