Join now to get access to this content and more.
Become a SOAP member and have access to our benefits.
- For Review: SOAP Consensus Statement on Neuraxial Procedures in Thrombocytopenic Parturients
- Sample Centers of Excellence Applications
- ASA Corner
- SOAP Policy and Procedure Manual (P&P Manual)
- SOAP Expert Opinions
- SOAP's Learning Modules
- 2019 Annual Meeting Lecture Videos
- December 2018 - SOAP Unofficial Guide to ASA Committees Webinar
- Submit a Position
- View Job Postings
- Previous Meeting Archives
- Previous Meeting Abstract Search
- CMS Guidelines
- Member Benefits
- Newsletter Clinical Articles
- ACOG Documents
- Search our Patient Safety Archive
- Ask SOAP a Question
- Global Health Opportunities
- And more…
Familial clustering of postpartum hemorrhage in the Swedish population
Abstract Number: O1 1
Abstract Type: Original Research
Introduction: Postpartum hemorrhage (PPH) is the leading cause of maternal mortality worldwide. Whether there is an inherited predisposition to PPH has not, to our knowledge, been previously investigated.
Making use of national registers of birth and family relations, we explored familial clustering of PPH in the Swedish population. We also assessed whether clustering could be explained by familial sharing of known PPH risk factors.
Methods: We considered the deliveries of all full and half-siblings born in Sweden between 1997 and 2009. PPH was defined using diagnostic codes based on >1000 mL of estimated blood loss. Familial clustering of PPH was modeled using Alternating Logistic Regression, allowing pair-wise odds ratios to describe the within cluster correlations while at the same time estimating the effect of covariates on the outcome.
Results: In the eligible 466 580 deliveries, the overall risk of PPH was 4.4%. Odds of PPH were increased in women with a previous postpartum hemorrhage, both with the same partner (Odds ratio (OR)=4.0, 95% confidence interval (CI): 3.7, 4.3) and after partner change (OR=3.4, 95% CI: 2.8, 4.2). An affected sibling conferred higher odds of PPH in sisters (OR=1.5, 95% CI: 1.3, 1.8) as well as partners of brothers (OR=1.2, 95% CI: 1.1, 1.5).
Potential familial sharing of risk factors for PPH, including pre-pregnancy BMI, prolonged labor, induction of labor, postterm birth, and fetal size, did not substantially change these estimates of familial clustering.
Conclusion: There is a strong maternal influence on the predisposition to PPH, illustrated by recurrence in women irrespective of partner and by significant clustering in sisters. Lower odds of recurrence in women who change partners compared to those who don’t and clustering in brothers also indicates some paternal influence.
These patterns suggest that the maternal influence on the risk of PPH is genetic and/or due to maternal specific environment shared, at least in part, by sisters. The paternal influence could be through a fetal genetic effect or environment shared by couples and brothers. Known risk factors for PPH did not influence estimates of familial clustering.
Clinically, these findings suggest that practitioners should assess family history when determining a woman’s risk for PPH. Future research is needed to define the basis for the genetic predisposition to PPH.