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ORIGINAL RESEARCH |
From Pediatric Pathology, the Department of Pathology, and the Department of Obstetrics, University Hospital, Zurich, Switzerland, and the Department of Obstetrics, and the Institute of Pediatric Pathology and Placentology, Charite, Campus Virchow-Klinikum, Humboldt University, Berlin, Germany.
Address reprint requests to: Thomas Stallmach, MD, Pediatric Pathology/Department of Pathology University Hospital Schmelzbergstr. 12 Zurich, CH-8091 Switzerland E-mail: thomas.stallmach{at}pty.usz.ch
Objective: To estimate the incidence and lethality of placental maturation defect, and to determine the impact of the pattern of placental dysfunction on the risk of recurrent stillbirth or maternal disease in later life.
Methods: Questionnaire and archival analysis of fetal deaths from placental dysfunction at 3242 weeks (19751995 in Zurich), classified as chronic (parenchyma loss) or acute (maturation defect of the terminal chorionic villi). Population survey of 17,415 consecutive unselected singleton placentas (19941998 in Berlin).
Results: Of the 71 stillbirths, 34 were due to parenchyma loss and 37 to maturation defect. Parenchyma loss predominated in the first pregnancy (73.5% compared with 43.2%; P < .05). The risks of recurrent stillbirth and subsequent childlessness did not differ between the two groups. Eleven percent of mothers whose placenta had maturation defect had diabetes in the index pregnancy; none of the other women in the group developed diabetes over the 520-year observation period. In the population survey, incidence of maturation defect was 5.7%, and was associated with fetal death in 2.3% of cases. Normal placentas were associated with fetal death in 0.033%.
Conclusion: Placental maturation defect can be a cause of fetal hypoxia. Although the risk of stillbirth is 70-fold that of a normal placenta, few affected fetuses actually die. The risk of recurrent stillbirth is tenfold above baseline and occurs mostly after 35 weeks gestation.
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