Objective— The investigation of the histology of the placental bed spiral arteries in normal pregnancy and in pregnancies complicated by hypertension, with or without proteinura. Design— An observational study, based on women having caesarean sections for clinical reasons. Subjects— 17 normal pregnant women, 43 with gestational hypertension, of whom 39 had proteinuria, 17 with chronic hypertension, of whom 6 had proteinuria, and 5 with unclassified hypertension. Interventions— Placental bed biopsies obtained during caesarean section. Main outcome measures— Histological appearance of sections stained with haematoxylin and eosin PAS and Lendrum's MSB. Results— Biopsies containing spiral arteries were obtained from 6 normotensive and 44 hypertensive women. Trophoblastic invasion was present in 5 of the 6 normotensive biopsies but absent in the majority of those with hypertension. Subintimal proliferation was seen in all the normotensive biopsies but in only 8 of 28 from those with gestational hypertension and proteinuria. Other features seen predominantly or only in the hypertensive biopsies, in order of frequency, were medial hyperplasia, fibrin deposits, acute atherosis, endothelial vacuolation and thrombosis. Conclusion— Absence of physiological changes may not be peculiar to preeclampsia but may be associated or even a result of various forms of hypertension in pregnancy. Spiral arteries show a spectrum of changes in hypertensive pregnancies that do not appear to bear a clear‐cut relation to the clinical signs.

Objective association with placental abruption. Design Prospective descriptive study. Subjects 18 women with clinical evidence of severe placental abruption delivered by caesarean section. Interventions Placental bed biopsies were obtained at caesarean section and studied histologically. Results Six specimens did not include trophoblast in the myometrium and were therefore not representative of the placental bed. Of the 12 representative specimens, seven demonstrated absence of physiological transformation of the utero-placental arteries (four of these were from hypertensive patients). Four biopsies showed abnormal vascular structures deep in the myometrium. One of these abnormal vessels included a fresh plug and extensive surrounding intramyometrial haemorrhage. Conclusions Vascular malformations in association with placental abruption may be the result of trophoblastic invasion and could be the site of vessel rupture. Further descriptive and comparative studies are needed. J Path B0c.t 93, 569-579.

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