Prognostic Value of Fetoplacental Function Tests: A Review1

The placenta is the life-support system of the fetus and has two functions: transport and synthesis. Its villous structure provides an enormous surface area for bringing the fetal circulation via the capillaries of the villi into close relationship with the maternal circulation of the intervillous or choriodecidual space. During normal pregnancy at term, the mean maternal blood flow through the intervillous space is 600 ml per minute (Browne & Veall 1953), and at the functional level of the terminal villi the maternal blood is separated from the fetal blood by only the endothelium of the villous capillaries juxtaposed to the very attenuated syncytiotrophoblast. In certain complications of pregnancy, principally those associated with hypertension and postmaturity, placental function may become impaired. In the hypertensive disorders of pregnancy this is due to pathological narrowing of the spiral arterioles which supply the intervillous space (Robertson et al. 1967) and may result in reduced placental perfusion by maternal blood. In postmaturity the reason for impaired placental function is less clear, but it may be related to intrinsic ageing changes in the placenta. When there is impaired placental function, the main clinical consequences are due to interference with transport of substances between the maternal and fetal circulations. Reduced active transport of amino acids will tend to occur first when there is chronic placental insufficiency, and will be associated with intrauterine growth retardation of the fetus. The baby is born dysmature, which means not only that it is too small in relation to weight distribution curves standardized for parity, gestation age, and sex of the infant, but also that it shows functional signs of inadequate development. These babies are at increased risk during the neonatal period and have also been shown to remain at a disadvantage into childhood, being less well developed both physically and intellectually when compared with preterm babies whose birth weights fell into the normal range for gestation age (Neligan et al. 1976). Reduced passive transport of oxygen occurs when there is acute placental insufficiency, either as an end stage of the chronic form, or when it arises de novo in relation to severe hypertension of sudden onset, or when there has been an abruptio placentae. The resulting fetal hypoxia commonly presents as fetal distress in labour but may cause the death of the fetus then, or during pregnancy. Fetal hypoxia and dysmaturity remain among the most important causes not only of perinatal mortality and morbidity but also of subsequent abnormal development during childhood. Since they are commonly but not exclusively the result of impaired placental transport, the early recognition of what is still rather loosely termed 'placental insufficiency' continues to be one of the main objectives of antenatal care. However, since the main concern is with fetal prognosis, the aims should be to diagnose intrauterine growth retardation in order to predict the risk of dysmaturity, and to accurately predict the fetus which will be at risk from fetal distress in labour or from intrauterine death due to hypoxia. The routine clinical screening procedures performed during pregnancy will identify many but not all those women whose fetuses are at risk from hypoxia or dysmaturity. Moreover, these clinical screening procedures will identify some pregnancies as being at risk, although the fetal outcome turns out to be entirely normal. Some of the important features associated with increased fetal risk are: maternal age, with increased risk at both extremes of the reproductive epoch; low socioeconomic class of the mother; a previous pregnancy which resulted in a