Placental insufficiency and postmaturity

Full placental development and functioning are achieved around the 5th month of gestation. Thereafter, until birth, signs of gradual placental aging are observed which are partly compensated by an increase in trophoblastic surface area to maintain adequate fetal oxygen and nutrient supply (Krantz and Kubli, 1967; Hellegers, 1969). Because during the last trimester intervillous blood circulation levels off, placental exchange processes must better utilize O2 and nutrients offered by maternal uteroplacental circulation. Intensification of placental exchange mechanisms is possible through sprouting of smaller villi which contain microvilli thus augmenting villous surface and resorption area. In addition, transformation of villous capillaries into sinusoids and formation of syncytial knots with increase in vasculosyncytial membrane area facilitate placental exchange mechanisms. Because trophoblastic surface srea increases toward term, it has been concluded that morphologic signs of placental aging or degeneration are not correlated with a functional deficiency, but rather that placental maturation and function reach a peak at term (Becker, 1963). However, there are findings which indicate that a peak of placental function (transport capacity) is reached at 36 weeks of gestation at which time chorionic DNA synthesis ceases (Bernstine, 1960). Near term, placental and fetal growth rate is reduced (Fig. l),