Occult Placenta Accreta: The Missing Link in the Diagnosis of Abnormal Placentation

Abstract

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.

Sensitivity and specificity of finding of multinucleate trophoblastic giant cells in decidua in placentas from high-risk pregnancies

“…Different patterns of interstitial trophoblast clustering and fusion occur in different types of hypertensive complications of pregnancy [18] and also in nonhypertensive but otherwise high risk for in utero hypoxic conditions (Table 1). Another clinical condition associated with shallow implantation, extravillous trophoblast dysfunction, and its placental accumulation is the placenta creta [5][6][7]. In most cases of the adherent placenta, MTGC were seen in the decidua basalis and in none of the control placentas [32].…”

“…MTGC are decreased in placentas cretas [5][6][7] but are increased and regarded as a feature of maternal vascular underperfusion in preeclampsia [8]. Together with the immature intermediate trophoblast at the implantation site, MTGC were found to be more sensitive and efficient predictors of preeclampsia than atherosis and muscularized basal plate arteries that, however, were more specific in a series of 20 placentas, including 14 cases of preeclampsia [9].…”

Hypoxic Patterns of Placental Injury: A Review

“…22 The UH pattern is frequently associated with other placental features of uteroplacental malperfusion related to shallow, trophoblastic invasion, such as an accumulation of extra- and basal-plate myometrial fibers, and occult placenta accreta (Figure 3, F). 27,38,[48][49][50][51][52][53][54] Excessive amounts of extravillous trophoblasts must be distinguished from massive perivillous fibrin deposition/maternal floor infarction, 49 which is associated with FGR, impaired neurologic development, recurrent fetal loss, and stillbirth, 9,12,55 but not necessarily with UH. Pathogenesis of the massive, perivillous fibrin deposition is different, 9 but it can evoke fetal hypoxia by virtue of eliminating a substantial amount of functional placental parenchyma.…”

Relaxin, Its Receptor (RXFP1), and Insulin-Like Peptide 4 Expression Through Gestation and in Placenta Accreta

“…In the latter, there can be an area of abnormal adherence with no decidua next to an area of normal decidua and BP. 9 This suggests a focal TR/decidual antagonism existing at the molecular level, with the decidua having an impact on trophoblastic differentiation and invasion. Abnormal vascular remodeling and neovascularization is certainly a key feature in accreta development.…”