Evidence of placental abruption as a chronic process: Associations with vaginal bleeding early in pregnancy and placental lesions

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Abstract

Background

Clinicians widely regard placental abruption as an acute event, though accumulating data point towards abruption being the end-result of chronic processes early in pregnancy, and perhaps even extending to conception. The Collaborative Perinatal Project was a prospective cohort study performed from 1959 to 1966 in the United States. Since enrolled pregnancies were managed without the biases created by modern perinatal surveillance and interventions, the natural history of disease in these data is ideal to study obstetrical complications such as placental abruption.

Objective

We assessed the associations versus contributions of the clinical feature of early gestational vaginal bleeding and histologic lesions (chronic and acute) with placental abruption.

Study design

Women enrolled in the Collaborative Perinatal Project (1959–1966) were used, restricting the analysis to those that delivered singleton births (n = 46,364). Risks of placental abruption were compared between women with and without vaginal bleeding at <20 weeks gestation. We also examined the relationships between placental abruption and chronic and acute histologic lesions, including infarcts, decidual necrosis, presence of macrophages in the decidua, amnion or chorion, and neutrophil infiltration in the amnion, chorion, placental surface, and umbilical vein.

Results

Any episode of vaginal bleeding at <20 weeks in pregnancy conferred an increased risk of placental abruption (adjusted relative risk (RR) 1.6, 95% confidence interval (CI) 1.3, 1.8). The greatest risk occurred with bleeding in both the first two trimesters (RR 3.1, 95% CI 2.3, 4.1). The presence of histologic lesions in the placenta, cord and membranes similarly carried an increased risk of placental abruption, even in the absence of vaginal bleeding. The risk of abruption was, however, highest in the presence of both histologic lesions and vaginal bleeding early in pregnancy.

Conclusion

Vaginal bleeding early in pregnancy and histologic lesions of the placenta, umbilical cord, and membranes are associated with increased risk of placental abruption in later pregnancy. However, the increased risk associated with placental lesions, especially chronic inflammatory lesions, even in the absence of early vaginal bleeding, suggests that prolonged inflammation may be implicated in placental abruption.

Introduction

Placental abruption, defined as the premature separation of the placenta prior to the delivery of the fetus, occurs in approximately 1% of pregnancies [1], [2]. The classic clinical hallmarks of placental abruption include vaginal bleeding accompanied by painful tetanic contractions and uterine tenderness [3]. The condition is associated with a high perinatal mortality and severe maternal morbidity [1]. The etiology of placental abruption is poorly understood, but advanced maternal age, grand multiparity, multiple pregnancies, smoking and cocaine use during pregnancy, hypertensive disorders, preterm premature rupture of membranes, oligohydramnios, and intrauterine infections have been implicated as risk factors for the condition [1], [2], [3], [4], [5], [6], [7], [8]. The strongest risk factor for placental abruption is a history of abruption in a prior pregnancy [2], [6], [7]. Despite a priori knowledge of these risk factors, however, prediction of placental abruption is seldom feasible [4].

We hypothesized that vaginal bleeding early in pregnancy—an indicator of early disrupted placental attachment—would be a strong predictor of abruption risk. We further hypothesized that if placental abruption is a chronic process with origins early in pregnancy, then in cases of abruption there should be histologic evidence of chronic pathologic lesions in the placenta, cord, membranes and decidua. If our hypothesis is indeed true, then these lesions should be found more frequently in women diagnosed with placental abruption.

We therefore carried out a study evaluating the role of vaginal bleeding in early pregnancy in determining whether or not women with bleeding subsequently developed placental abruption. We further examined if cases of placental abruption had evidence of histologic lesions in the placenta, membranes, decidua and umbilical cord, and if so, whether such lesions largely represented underlying chronic or acute processes.

Section snippets

United States National Collaborative Perinatal Project, 1959–1966

Data from the United States National Collaborative Perinatal Project (CPP) were utilized to examine the association between vaginal bleeding in the first two trimesters of pregnancy and the risk of placental abruption. The CPP was a large, multi-center, prospective cohort study of pregnant women conducted between 1959 and 1966 in 12 university-based centers across the United States [9]. Sampling of patients for inclusion to the CPP cohort varied across the 12 centers, with some centers

Results

The risk of vaginal bleeding early in pregnancy in relation to maternal and infant characteristics is shown in Table 2. Vaginal bleeding was associated with higher maternal age, and multiparity. Similarly, the proportion of African-American women that bled in early pregnancy was slightly higher when compared to Caucasian women or women of other race/ethnicity.

The overall incidence of vaginal bleeding in the first or second trimesters in pregnancy was 16.6% (n = 7688) (Table 3). Of these women,

Discussion

Our study reveals several new and interesting findings: (i) vaginal bleeding early in pregnancy is strongly associated with placental abruption, with the risk being greatest when bleeding occurs in both the first and second trimesters; (ii) lesions of the placenta, cord, membranes, and decidua are often associated with increased risk of abruption. Interestingly, the relative risk of placental abruption is increased in women who have lesions of the placenta, cord, membranes or decidua, even in

Acknowledgments

Drs. Ananth, Getahun, and Smulian are partially supported through a grant (R01-HD038902) from the National Institutes of Health awarded to Dr. Ananth. The authors thank Susan Fosbre for her help during the preparation of the manuscript.

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