Placental Immaturity, Endocardial Fibroelastosis and Fetal Hypoxia

Abstract

We describe a term newborn who, after a normal gestational course, presented at birth with absent cardiac activity and no spontaneous breathing. Death occurred within 30 h. Autopsy revealed placental villous immaturity, multiple acute hypoxic lesions, but also chronic hypoxic lesions like endocardial fibroelastosis. This striking association of endocardial fibroelastosis and placental villous immaturity is reviewed and correlated with 2 other cases of placental villous immaturity that led to in utero death at 39 and 41 weeks of gestation. Placental villous immaturity must be suspected and looked for by both pediatricians and obstetricians in every case of stillbirth or perinatal asphyxia of unclear origin. In order to minimize the risk of recurrence in further pregnancies, elective cesarean section may be considered.

Hypoxic Patterns of Placental Injury: A Review

“…Hypomature placentas (placentas with maturation defect) are pale, normal sized or even larger than normal, with plumper terminal chorionic villi, superficially resembling intermediate villi, 67 and show defective formation of both terminal villous sinusoids (although numerically usually normal) and vasculosyncytial membranes (Figure 2, F), which can be better highlighted with CD34 immunostain (Figure 2, F inset). Although the vasculosyncytial membranes are normally poorly formed in early pregnancy, they are well formed in term pregnancies and are absent in only 5% of chorionic villi at term.…”

‘Knockout-first’ mouse model as a biological tool to study the role of KIAA0182 gene in hypoplastic left heart syndrome

“…Non-infectious etiologies can also play a role in the occurrence of endocardial fibroelastosis, as it was found to be the result of some metabolic abnormalities, such as the absence of lysosomal alphaglucosidase or Carnitine deficiency (Dincsoy et al 1965;Tripp et al 1981). Placental immaturity and myocardial hypoxia in the fetus may also be responsible for this reaction (Perez et al 2009). Immunological problems, such as maternal anti-Ro and anti-La, were reported to be associated with endocardial fibroelastosis together with congenital heart block (Nield et al 2002).…”