Fetal growth retardation: physiopathology. Review of the literature
Boulot, P.; Giacalone, P.L.; Hedon, B.; Laffargue, F.; Viala, J.L.
Journal de Gynecologie Obstetrique et Biologie de la Reproduction 21(8): 851-856
1992
ISSN/ISBN: 0368-2315 PMID: 1491129 Document Number: 402752
Fetal hypotrophy or intrauterine growth retardation is an important cause of fetal and neonatal mortality and a real cause of iatrogenic prematurity. When pregnancy is progressing normally there are histological changes in the spiral arteries with an equilibrium between the endothelial prostacyclin and platelet thromboxane on the one part and peroxides and Vitamin E on the other part. This allows uteroplacental circulation to flow rapidly and at a low pressure. Furthermore immunological tolerance of the mother's system in the relationship to her embryo plays a part in bringing about this special haemodynamic state. The physiopathology of retarded growth stemming from the blood vessels brings into play multiple mechanisms. The first cause is a defect in placentation which is shown up as insufficient trophoblastic invasion in the second stage. This brings about endothelial dysfunction with disappearance of the normal equilibrium of the prostaglandins and an alteration in the physiological equilibrium between the peroxides and a natural antagonist, which is vitamin E. Immunological disturbances have also been considered following studies on the immunohistochemistry and with the frequent association of obstetrical vascular complications together with phospholipid specific autoantibodies.