Maternal floor infarction.
In an attempt to determine the frequency, course, and outcome of maternal floor infarcts, 39,215 placentas and pregnancies were reviewed. The disorder is somewhat misnamed, because it is characterized by heavy deposition of fibrin in the decidua beneath the placenta rather than by arterial occlusion and ischemic necrosis of villi. The fibrin in floor infarcts often extends into the intervillous space, where it envelops villi, causing them to become atrophic. The disorder was relatively frequent in the present study, being present in nearly one of every 200 placentas. Mortality was high, with 17 per cent of the fetuses being stillborn. It may be a recurrent disorder, because 50 per cent of the gravidas with floor infarcts, compared with 27 per cent of control subjects (P less than 0.001), had had prior abortions and stillbirths. Damage to the decidua basalis by ischemia or infection may initiate many floor infarcts. Atheroma in the decidual arteries, foci of decidual necrosis, and histologic evidence of low uteroplacental blood flow were more frequent in patients with floor infarcts. Low maternal blood volume may contribute to the low blood flow because maternal hemoglobin values were often abnormally high in gravidas in whom floor infarcts developed. Acute chorioamnionitis, which can damage the decidua, had twice the expected frequency in gravidas with floor infarcts.
D003656:Decidua / Q000098:blood supply / Q000473:pathology*; D005260:Female; D005313:Fetal Death / Q000473:pathology; D005317:Fetal Growth Retardation / Q000473:pathology; D005337:Fibrin / Q000378:metabolism; D006801:Humans; D007238:Infarction / Q000473:pathology*; D008599:Menstruation Disturbances / Q000150:complications; D010920:Placenta / Q000473:pathology*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000473:pathology*
D005337:Fibrin