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Causal effects of competing obstetrical interventions: mediators of placental abruption and perinatal mortality
Cande V Ananth1,2,3,4,5, Wen Wei Loh6,7
1Division of Epidemiology and Biostatistics, Department of Obstetrics, Gynecology, and Reproductive Sciences, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ 08901, United States.
Placental abruption, the premature placental separation, confers increased perinatal mortality risk with preterm delivery as an important pathway through which the risk appears mediated. Although pregnancies complicated by abruption are often delivered through an obstetrical intervention, many deliver spontaneously. We examined the contributions of clinician-initiated (PTDIND) and spontaneous (PTDSPT) preterm delivery at < 37 weeks as competing causal mediators of the abruption-perinatal mortality association. Using the Consortium for Safe Labor (2002-2008) data (n = 203 990; 1.6% with abruption), we applied a potential outcomes-based mediation analysis to decompose the total effect into direct and mediator-specific indirect effects through PTDIND and PTDSPT. Each mediated effect describes the reduction in the counterfactual mortality risk if that preterm delivery subtype was shifted from its distribution under abruption to without abruption. The total effect risk ratio (RR) of abruption on perinatal mortality was 5.4 (95% CI, 4.6-6.3). The indirect effect RRs for PTDIND and PTDSPT were 1.5 (95% CI, 1.4-1.6) and 1.5 (95% CI, 1.5-1.6), respectively; these corresponded to mediated proportions of 25% each. These findings underscore that PTDIND and PTDSPT each play essential roles in shaping perinatal mortality risks associated with placental abruption.
Placental abruption, the premature placental separation, confers increased perinatal mortality risk with preterm delivery as an important pathway through which the risk appears mediated. Although pregnancies complicated by abruption are often delivered through an obstetrical intervention, many deliver spontaneously. We examined the contributions of clinician-initiated (PTDIND) and spontaneous (PTDSPT) preterm delivery at < 37 weeks as competing causal mediators of the abruption-perinatal mortality association. Using the Consortium for Safe Labor (2002-2008) data (n = 203 990; 1.6% with abruption), we applied a potential outcomes-based mediation analysis to decompose the total effect into direct and mediator-specific indirect effects through PTDIND and PTDSPT. Each mediated effect describes the reduction in the counterfactual mortality risk if that preterm delivery subtype was shifted from its distribution under abruption to without abruption. The total effect risk ratio (RR) of abruption on perinatal mortality was 5.4 (95% CI, 4.6-6.3). The indirect effect RRs for PTDIND and PTDSPT were 1.5 (95% CI, 1.4-1.6) and 1.5 (95% CI, 1.5-1.6), respectively; these corresponded to mediated proportions of 25% each. These findings underscore that PTDIND and PTDSPT each play essential roles in shaping perinatal mortality risks associated with placental abruption.
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