The placenta is a fetomaternal organ. The functional unit of the fetal placenta is the fetal cotyledon. The mature human placenta has about 120 fetal cotyledons grouped into visible lobes (frequently and somewhat confusingly termed ‘maternal cotyledons’). Each cotyledon contains a primary villus stem arising from the chorionic plate and supplied by primary branches of fetal vessels. The primary stems divide to form secondary and tertiary stems from which arise the terminal villi, where maternal–fetal exchange takes place.
The fetal cotyledons appear to develop around the entries of the maternal spiral arteries from the decidual plate. The centre of each cotyledon is hollow and during maternal systole, blood spurts from the spiral arteries and enters the intercotyledon space. Blood rises high to the chorionic plate then disperses laterally between and over the surface of the terminal villi, becoming increasingly desaturated of oxygen and nutrients and picking up carbon dioxide and waste products. The blood then filters into narrow venous channels between the cotyledons, before falling back to the maternal decidual plate, where the maternal veins return the desaturated blood to the maternal circulation. Maternal and fetal blood is separated by three microscopic tissue layers: trophoblastic tissue, connective tissue and the endothelium of the fetal capillaries. However, microscopic examination of the terminal villi surrounding the intracotyledon space shows numerous vasculosyncytial membranes where the fetal capillaries and trophoblast fuse to form a very thin membrane, where most of the transfer of nutrients and blood gases takes place.
The maternal blood fl ow to the fetal placenta increases throughout pregnancy from 50 mL/min in the first trimester to 500–750 mL/min at terms. This increase inperfusion is accomplished by anatomical conversion of the maternal spiral arteries by trophoblast. Trophoblast cells invade the spiral arterioles within the first 12 weeks of pregnancy and replace the smooth muscle of the wall of the vessels, thus converting them to wide bore, low resistance, large capacitance vessels. This process is normally complete by 20 weeks gestation.
In pregnancies destined to be complicated by preeclampsia, FGR and/or abruptio placentae, there is a complete or partial failure of trophoblast invasion of the myometrial segments of the spiral arteries. Hence, spiral arteries retain some of their pre pregnancy characteristics being relatively narrow bore and of low capacitance and high resistance and resulting in impaired perfusion of the fetoplacental unit. The mechanism underlying decreased trophoblast invasion in complicated pregnancies is poorly understood but it may reflect an ‘immune intolerance’ of the mother to the invading trophoblast. Affected placentae have gross morphological changes, which include infarcts and basal haematomas. An infarct represents an area of ischaemic necrosis of a cotyledon resulting from a spiral artery occlusion, usually by thrombosis. A placenta with multiple infarcts is significantly associated with intrauterine fetal death and growth restriction. Basal haematomas consist of a mass of blood in the centre of the fetal cotyledon due to the rupture of a damaged spiral artery. This lesion is associated with maternal hypertension and increased perinatal mortality.
(Reference : Obstetrics by Ten Teachers, 19E – Kenny, Louise, Baker, Philip N)