The use of Rho(D) immune globulin in Rh-negative pregnant women has become standard of care, but many practicing clinicians do not know the dosing recommendations for this essential medication. In this article, we describe a case of a 15-year-old girl who presented with intrauterine fetal demise and was found to have massive fetomaternal hemorrhage. Kleihauer-Betke testing results indicated nearly 460 mL of fetal blood in the maternal circulation. The patient ultimately received 4800 µg of Rho(D) immune globulin, a dose that required close coordination with the obstetrical service and pharmacy. Although this is an unusual case of large-volume, potentially chronic, fetomaternal hemorrhage, it is also an excellent illustration of the principles for diagnosing this condition, as well as providing dosing guidelines for Rho(D) immunoglobulin to prevent alloimmunization.

Triploidy is a genetic occurrence in which the chromosome count is 3n = 69 with a double (2n) chromosomal contribution to the conceptus from one parent. Such pregnancies are usually nonviable and are estimated to account for approximately 1% of recognized conceptions and 10% of recognized miscarriages. Majority opinion is that fetal losses due to triploidies are caused by the presence of 2 copies of paternal chromosomes. In this study, we present a digynic monoandric triploid miscarriage from a 32-year-old G7P1051 at approximately 13 weeks gestation, in which 2 copies of the maternal chromosomes are present in the fetus. This unusual phenomenon is supported by nonmolar placental histology, chromosomal microarray, and short tandem repeat assays, with the latter 2 being discussed in detail. Furthermore, this study includes discussion of recurrent miscarriage, 
recurrent triploidy, and long-term clinical follow-up of the patient.

OBJECTIVES/GOALS: Identify and stratify clinical presentations of thrombotic pathology in PCOS patients. This will be accomplished by 1) evaluating clinical assays for the detection of hypofibrinolysis, and 2) analyzing clinical symptomology of thrombosis in PCOS via Symptom-Disease Pair Analysis of Diagnostic Error (SPADE). METHODS/STUDY POPULATION: Preliminary study populations include n=3 for each of the following groups PCOS with thrombotic complications, PCOS without thrombotic complications, healthy controls, and healthy control samples treated ex vivo with PAI-1. Coagulation assays include ACL coagulation panel, antiphospholipid antibody assays, viscoelastic testing with TEG and Quantra devices, and global fibrinolytic capacity. Coagulation assays will be performed on three samples taken at 4-week intervals. The SPADE techniques will be used to evaluate symptomology of thrombosis in the study period and patient electronic medical history. Molecular testing will be performed for pro-thrombotic polymorphisms (PAI-1 and Apo E) and mutations (Factor V Leiden and Prothrombin). RESULTS/ANTICIPATED RESULTS: We anticipate PCOS and ex vivo PAI-1 samples to show signs of hypofibrinolysis on TEG and Quantra devices outside of reference ranges and with statistical significance. We also anticipate seeing a statistical significance with ACL coagulation panels, however, these results are expected to still be within the reference ranges, as seen in previous studies. We believe the SPADE method will identify clinical presentations of hypofibrinolysis in PCOS patients coinciding with patterns in laboratory tests that were misdiagnosed due to being within reference ranges. We hope to stratify clinical presentations predictive of thrombosis in PCOS patients with standard clinical assays and with increased precision using viscoelastic assays. DISCUSSION/SIGNIFICANCE: The incidence rate of thrombosis is 40x higher in PCOS compared to healthy populations. However, the mechanisms of thrombosis in PCOS are unknown and are undetectable with current clinical assays. We hypothesize that chronic cellular stress in PCOS disrupts the regulation of interconnected immune pathways, causing hypofibrinolysis.

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Background Double trisomies are rare findings among products of conception and are often lethal to the developing embryo or fetus. Methods Here we describe a double trisomy case with symptoms of threatened miscarriage at 9 weeks gestation. Ultrasound revealed an anembryonic pregnancy. Pregnancy was terminated by dilation and curettage at gestational age 11 weeks and 6 days. Histologic examination and chromosome microarray were performed on a formalin-fixed product of conception (POC) sample to identify the cause of the anembryonic pregnancy. Results Chromosome microarray analysis revealed a female chromosome complement with double trisomies 10 and 20, arr(10,20)x3, consistent with a karyotype of 48,XX,+10,+20. Conclusion To the best of our knowledge, this is the first reported case of double trisomy 10 and 20 in a POC. Due to nonspecific histopathological findings, chromosomal microarray is a powerful tool in identifying and differentiating chromosomal aneuploidies.