CHRONIC REDUCTION IN FETAL BLOOD-FLOW IS ASSOCIATED WITH PLACENTAL INFARCTION

The placenta receives two arterial blood supplies, i.e. one maternal a nd one fetal. It has been suggested that placental infarction should o ccur only if both blood supplies are compromised (Wigglesworth, 1984). This hypothesis has not been tested. Haemosiderosis of the trophoblas t basement membrane (TBMH) has recently been identified as a feature o f 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 a nd microscopically. These were compared with four types of control tis sue. Eleven placentae from cases of prolonged intrauterine death, in w hich this feature was first described and 35 fetal artery thromboses w ere used as positive controls and 20 placentae from uncomplicated preg nancies mere available as negative controls. Non-infarcted tissue adja cent to infarcts served as an internal negative control. Microscopical ly, 36 per cent of infarcts showed TBMH in at least 5 per cent of vill i within the lesion and 60 per cent of infarcts showed at least one cl uster of villi with the feature. These findings paint to a disturbance in fetal blood flow intimately associated with but pre-dating the pla cental infarction. These findings represent the first experimental evi dence to support Wigglesworth's theory and suggest that reduction in f etal blood flow prior to thrombosis of maternal vessels contributes to the pathophysiology of placental infarction.