Risk of placental abruption in relation to maternal depressive, anxiety and stress symptoms

Abstract

Background

Little is known about the influence of psychiatric factors on the etiology of placental abruption (PA), an obstetrical condition that complicates 1–2% of pregnancies. We examined the risk of PA in relation to maternal psychiatric symptoms during pregnancy.

Methods

This case–control study included 373 PA cases and 368 controls delivered at five medical centers in Lima, Peru. Depressive, anxiety and stress symptoms were assessed using the Patient Health Questionnaire (PHQ-9) and the Depression Anxiety Stress Scales (DASS-21). Multivariable logistic regression models were fit to calculate odds ratios (aOR) and 95% confidence intervals (CI) adjusted for confounders.

Results

Depressive symptoms of increasing severity (using the DASS depression subscale) was associated with PA (p for trend = 0.02). Compared with women with no depressive symptoms, the aOR (95%CI) for PA associated with each level of severity of depression symptoms based on the DASS assessment were as follows: mild 1.84 (0.91–3.74); moderate 1.25 (0.67–2.33); and severe 4.68 (0.98–22.4). The corresponding ORs for mild, moderate, and moderately severe depressive symptoms based on the PHQ assessment were 1.10 (0.79–1.54), 3.31 (1.45–7.57), and 5.01 (1.06–23.6), respectively. A positive gradient was observed for the odds of PA with severity of anxiety (p for trend = 0.002) and stress symptoms (p for trend = 0.002).

Limitations

These cross-sectionally collected data may be subject to recall bias.

Conclusions

Maternal psychiatric disorders may be associated with an increased occurrence of AP. Larger studies that allow for more precise evaluations of maternal psychiatric health in relation to PA risk are warranted.

Introduction

Placental abruption (PA), the premature separation of the placenta, is a life threatening obstetrical condition that complicates 1–2% of pregnancies (Macdonald et al., 1989, Younis and Samueloff, 2003, Oyelese and Ananth, 2006). The condition occurs in much higher frequencies among women with multi-fetal gestation, coagulopathies, acquired forms of thrombophilia, uterine anomalies, abdominal trauma, hypertension, premature rupture of membranes, and intrauterine infections (Ananth et al., 2004, Ananth and Wilcox, 2001, Williams et al., 1992, Williams et al., 1991, Kramer et al., 1997, Sanchez et al., 2006). Young and advanced maternal age, grand-multiparity, and maternal cigarette smoking are PA risk factors (Williams et al., 1991, Sanchez et al., 2006, Ananth et al., 1996). Pathophysiologic mechanisms involved in PA, and related perinatal disorders include uteroplacental ischemia, underperfusion, chronic hypoxia, and infarctions. Investigators have begun to conceptualize PA as an “ischemic placental disorder” characterized by acute and chronic pathophysiological features (Younis and Samueloff, 2003, Ananth et al., 2007); and data suggests that transient activation of the sympathetic nervous system might trigger PA (Jablensky et al., 2005). Little is known about the influence of psychosocial and psychiatric factors on the etiology of PA. Over 2 decades ago, panic disorders as a potential trigger of PA was reported in a case (Cohen et al., 1989). More recently, Jablensky et al. (2005) reported that PA was more strongly associated with schizophrenia (OR = 3.17; 95% CI 1.55–6.49) than with depression (OR = 1.36; 95% CI 0.17–2.60). Given the paucity of research in this area, we hypothesized that maternal depressive, anxiety and stress symptoms during pregnancy may be associated with increased risk of PA. We tested this hypothesis in a large case–control study of Peruvian women.