Chang Kenneth T E, Keating Sarah, Costa Stacy, Machin Geoffrey, Kingdom John, Shannon Patrick
Department of Pathology and Laboratory Medicine, KK Women's and Children's Hospital, Republic of Singapore.
Pediatr Dev Pathol. 2011 Sep-Oct;14(5):345-52. doi: 10.2350/10-07-0882-OA.1. Epub 2011 Feb 23.
Although in recent years placental pathology has been the subject of a wealth of detailed descriptions and diagnostic categorization, systematic correlation of these conditions with the pathology of stillbirth has not been attempted. We examine the relationship between specific inflammatory, maternal, and fetal vascular pathologies and the central nervous system pathology and histological indicators of fetal compromise. Our design was a retrospective case series of 37 3rd-trimester intrauterine fetal deaths. In general, mixed placental pathologies were the rule, with three quarters of the placentas demonstrating combinations of maternal vascular pathology, fetal vascular pathologies, umbilical cord abnormalities, or inflammatory lesions. The range of brain pathology was limited to acute, severe congestion, white matter edema, and neuronal karyorrhexis (pontosubicular necrosis with or without neuronal karyorrhexis at other sites). Established periventricular leukomalacia was present in only 2 cases. The presence of neuronal karyorrhexis or white matter gliosis was correlated with the presence of a high-grade inflammatory lesion and with fetal thymic involution. Neuronal karyorrhexis, but not white matter gliosis, correlated as well with histologically established fetal vascular lesions in the placenta, even once the effect of inflammation was accounted for. Gliosis also correlated with inflammation, meconium staining, and thymic involution. Central nervous system injury may be the end result of complex placental pathologies, and neuronal injury may be a consequence of the fetal inflammatory response. The correspondence between the time courses of histological features of chorioamnionitis, neuronal karyorrhexis, and thymic involution points to irreversible central nervous system injury being common 12-48 hours prior to in utero demise.
尽管近年来胎盘病理学已成为大量详细描述和诊断分类的主题，但尚未尝试将这些情况与死产病理学进行系统关联。我们研究了特定的炎症、母体和胎儿血管病理学与中枢神经系统病理学以及胎儿窘迫的组织学指标之间的关系。我们的设计是对37例孕晚期宫内胎儿死亡病例进行回顾性系列研究。一般来说，混合性胎盘病理学是常见情况，四分之三的胎盘表现出母体血管病理学、胎儿血管病理学、脐带异常或炎症性病变的组合。脑病理学范围限于急性、严重充血、白质水肿和神经元核溶解（脑桥亚皮质坏死，其他部位有或无神经元核溶解）。仅2例出现既定的脑室周围白质软化。神经元核溶解或白质胶质增生的存在与高级别炎症性病变的存在以及胎儿胸腺退化相关。即使考虑到炎症的影响，神经元核溶解而非白质胶质增生也与胎盘中组织学确定的胎儿血管病变相关。胶质增生也与炎症、胎粪染色和胸腺退化相关。中枢神经系统损伤可能是复杂胎盘病理学的最终结果，而神经元损伤可能是胎儿炎症反应的后果。绒毛膜羊膜炎的组织学特征、神经元核溶解和胸腺退化的时间进程之间的对应关系表明，在宫内死亡前12 - 48小时，不可逆的中枢神经系统损伤很常见。
