No abstract

Context.—In utero hypoxia is an important cause of perinatal morbidity and mortality and can be evaluated retrospectively to explain perinatal outcomes, to assess recurrence risk in subsequent pregnancies, and to investigate for medicolegal purposes by identification of many hypoxic placental lesions. Definitions of some placental hypoxic lesions have been applied relatively liberally, and many of them are frequently underreported. Objectives.—To present a comprehensive assessment of the criteria for diagnosing acute and chronic histologic features, patterns, and lesions of placental and fetal hypoxia and to discuss clinicopathologic associations and limitations of the use thereof. The significance of lesions that have been described relatively recently and are not yet widely used, such as laminar necrosis; excessive, extravillous trophoblasts; decidual multinucleate extravillous trophoblasts; and, most important, the patterns of diffuse chronic hypoxic preuterine, uterine, and postuterine placental injury and placental maturation defect, will be discussed. Data Sources.—Literature review. Conclusions.—The placenta does not respond in a single way to hypoxia, and various placental hypoxic features should be explained within a clinical context. Because the placenta has a large reserve capacity, hypoxic lesions may not result in poor fetal condition or outcome. On the other hand, very acute, in utero, hypoxic events, followed by prompt delivery, may not be associated with placental pathology, and many poor perinatal outcomes can be explained by an etiology other than hypoxia. Nevertheless, assessment of placental hypoxic lesions is helpful for retrospective explanations of complications in pregnancy and in medicolegal investigation.

Molar ultrasonographic appearances associated with increased maternal serum alpha-fetoprotein but normal, or slightly elevated, levels of ss human Chorionic Gonadotrophin should raise the clinical suspicion of PMD. The diagnosis of this condition should not be disregarded when an abnormal fetus and/or an abnormal karyotype are demonstrated.

Placenta creta (accreta, increta, or percreta) is a clinically symptomatic condition, usually diagnosed histologically on hysterectomy specimens. At a minimum, focal absence of decidua is the histological finding for this condition; however, excessive amounts of extravillous trophoblasts were recently documented on hysterectomy specimens. The histological finding of basal plate myometrial fibers (BPMF) without intervening decidua in spontaneously delivered placentas, which we term occult placenta accreta (OPA), is not infrequent, even in clinically asymptomatic cases. To prove that OPA is a missing link between normal placental implantation and clinical placenta accreta, CD146 immunohistochemical stains were performed on 25 sections of OPA (study group) and 25 placental sections without BPMF (control group). Implantation-site intermediate trophoblast (ISIT) cell number, thickness, and density were compared between the study and control groups. The ISIT micrometry thickness and cell number at BPMF sites were statistically significantly higher in OPA than in control group and same OPA placentas away from BPMF. There were no statistically significant differences in ISIT density. Therefore, although asymptomatic, OPA features the same histopathology as clinical placenta accreta and may share same pathogenesis, which may include decidual deficiency, abnormal trophoblast/decidua interaction, and/or hypoxia.