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4672 Postpartum hemorrhage (PPH) is one of the leading causes of maternal mortality and is estimated to occur in 1–10% of all childbirths. Postpartum hemorrhage is defined as a blood loss of >500 ml for vaginal delivery or >1000 ml for cesarean delivery. The etiology of PPH is attributed most often to uterine atony (80%); the etiology of atony is unknown. Studies of rat and human myometrial tissues suggest that an increase of 5-HT2 receptors late in pregnancy might trigger parturition by increasing uterine contractility when presented with 5-HT released by mast cells and platelets. Furthermore, the up-regulated receptors may serve to maintain uterine tone postpartum. The most common cited risk factors for PPH include PPH in a previous pregnancy, chorioamnionitis, use of magnesium sulfate, labor induction and augmentation, increased birth weight, and retention of the placenta. The obstetrics literature discounts bleeding disorders as significant risk factors for PPH for the immediate postpartum period although acknowledging that if diagnosed, such disorders should be considered during management of pregnancy. In essence, bleeding disorders are thought to be rare causes of PPH. A few case reports in the literature suggest that platelet storage pool deficiency (SPD) may be a contributing factor for development of PPH. We report the first investigation of the platelet dense granule storage pool during pregnancy. Our hypotheses include that platelet (PLT) delta (δ) granule storage pool deficiency (δSPD) may be a risk factor for the development of PPH. As the PLT dense (δ) granules (DG) store the majority of 5HT excluding the central nervous system, δSPD would intuitively present less 5-HT at parturition potentially resulting in atony. Our IRB approved study is recruiting women during prenatal check-ups. To assess for potential bleeding tendencies, we are utilizing a modified Vincenza bleeding checklist (Tosetto, et al., 2007), a pictorial blood loss assessment (Jannsen, et al, 1995), and a blood sample for PLT whole mounts and biochemical assays. To date, a total of 32 women have been enrolled in the study having an average age of 24.2 ± 4. Bleeding scores average 0.24 ± 0.21 (normal <5) and the pictorial menorrhagia scores average 170.44 ± 30.94 (normal <185). Four women have scores ranging from 267–522 consistent with a clinical diagnosis of menorrhagia and suggesting that they may have a bleeding tendency although their bleeding scores are all within the normal range. The mean number of DG/PLT is 5.34 ± 0.58 which is significantly different than a vetted control group of women (n=26) who have an average of 4.16 ± 0.08 DG/PLT. These data suggest that the state of pregnancy includes an increase in the average number of DG/PLT. It is known that pregnancy results in a variety of hematologic deviations from normal CBC ranges in non-pregnant women including Hgb and Hct that decrease, related to a dilution effect of increased blood volume. Pregnancy is also related to an increased state of coagulability. The increased number of DG/PLT might suggest a potential for increased coagulability in preparation of parturition as all women studied have significantly increased DG numbers in comparison to control subjects. These results are in direct contradiction to our original hypothesis that δSPD might contribute to PPH. We have yet to analyze 5HT extracts from PLTs however these results will be presented with significantly more data as we continue with our recruitment of test subjects. Disclosures: No relevant conflicts of interest to declare.

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