Chronic reduction in fetal blood flow is associated with placental infarction

The placenta receives two arterial blood supplies, i.e. one maternal and one fetal. It has been suggested that placental infarction should occur only if both blood supplies are compromised (Wigglesworth, 1984). This hypothesis has not been tested. Haemosiderosis of the trophoblast basement membrane (TBMH) has recently been identified as a feature of fetal artery thrombosis and suggested as a marker of impaired fetal blood flow which is identifiable in both viable and necrotic tissue. We examined 50 placental infarcts for evidence of TBMH, both grossly and microscopically. These were compared with four types of control tissue. Eleven placentae from cases of prolonged intrauterine death, in which this feature was first described, and 35 fetal artery thromboses were used as positive controls and 20 placentae from uncomplicated pregnancies were available as negative controls. Non-infarcted tissue adjacent to infarcts served as an internal negative control. Non-infarcted tissue adjacent to infarcts served as an internal negative control. Microscopically, 36 per cent of infarcts showed TBMH in at least 5 per cent of villi within the lesion and 60 per cent of infarcts showed at least one cluster of villi with the feature. These findings point to a disturbance in fetal blood flow intimately associated with but pre-dating the placental infarction. These findings represent the first experimental evidence to support Wigglesworth's theory and suggest that reduction in fetal blood flow prior to thrombosis of maternal vessels contributes to the pathophysiology of placental infarction.