Pregnancy-related mortality in the United States, 2003-2016: age, race, and place of death.

BACKGROUND: Pregnancy-related deaths in the United States are increasing. Medical, social, economic, and cultural issues have all been implicated in this trend, but few data exist to differentiate the relative contributions of these various factors. OBJECTIVE: The objective of the study was to examine trends in US pregnancy-related mortality by place of death and maternal race and age. We hypothesized that such an analysis may allow some distinction between deaths related to medical performance and those more closely related to social, cultural, or environmental issues. STUDY DESIGN: We conducted a retrospective, cross-sectional study for the years 2003-2016 using multiple cause-of-death mortality data provided by the Centers for Disease Control and Natality Data provided by National Vital Statistics System of the National Center for Health Statistics. Temporal trends analyses for the place of death, race/ethnicity, and age at the time of death were performed using joinpoint regression over the study period. RESULTS: Approximately one third of pregnancy-related deaths occurred outside a medical facility. The fraction of maternal deaths occurring in inpatient facilities fell by 20% over the study period, from 53% to 44% of all maternal deaths (P < .0001). Maternal deaths in an outpatient facility or emergency room demonstrated a similar decline (24%) in relative frequency (P < .0001). In contrast, there was a significant increase in the relative frequency of maternal mortality in other settings, particularly within the descendant's home, with a doubling over this time period. However, overall pregnancy-related deaths continued to increase in all settings. These increases were particularly striking in non-Hispanic black and white women and among women in the youngest and oldest age groups. CONCLUSION: Against a background of rising US pregnancy-related mortality, stratification of such deaths by place of death and maternal age and race highlights both the need for ongoing improvements in the quality of medical care and the potential contribution of events occurring outside a medical facility to the overall morality ratio. Current trends in pregnancy-related mortality in the United States are, in part, driven by social, cultural, and financial issues beyond the direct control of the medical community.

Opportunities for hospitals, hospital systems and leadership to improve VTE prophylaxis.

A sustained increase in the maternal death rate in the U.S. remains one of the most challenging issues of the twenty-first century. Ten years ago, we investigated the major conditions contributing to the maternal death rate between the years 2000 and 2006. The leading causes of death in the U.S. at that time were complications of preeclampsia, pulmonary thromboembolism, amniotic fluid embolism, obstetric hemorrhage and cardiac disease. Venous thromboembolism accounted for 9% of all maternal death, and an overall pregnancy-related mortality risk of 0.9 maternal deaths per 100,000 live births. VTE was the most common preventable cause of maternal death noted during that time period. In this paper, we will review and summarize changes in obstetric health care over the last ten years implemented to prevent VTE and its related morbidity. We will then examine opportunities for hospitals and hospital systems to improve VTE prophylaxis.

Characterization of Placental Microvasculature Using Superb Microvascular Imaging.

Superb Microvascular Imaging (SMI; Canon Medical Systems, Tustin, CA) uses clutter suppression to extract flow signals at rapid frame rates, which provides high-resolution vessel-branching details without the need for contrast agents. The potential diagnostic benefits of SMI, as described in other areas of medicine, requires further exploration during pregnancy. In this pictorial essay, we demonstrate the complementary use of SMI compared to conventional Doppler ultrasound and how it may improve our ability to characterize placental microvascular patterns without the need for ultrasound contrast agents.

Risk Factors for Intrapartum Fever in Term Gestations and Associated Maternal and Neonatal Sequelae.

AIM: To determine factors associated with intrapartum fever and to examine associated maternal and neonatal outcomes. METHODS: Retrospective study of patients between 360/7 and 420/7 gestational weeks who entered spontaneous or induced active labor and developed temperature ≥38°C; a similar group that did not develop fever were controls. Univariate and multivariate analyses were performed with p < 0.05 as significant. RESULTS: Fifty-four febrile patients and 306 nonfebrile controls met inclusion criteria. Nulligravidity (45.8 vs. 77.8%, p < 0.001), length of first stage ≥720 min (OR 3.59, 95% CI 1.97-6.55, p < 0.001), length of second stage ≥120 min (OR 4.76, 95% CI 2.29-9.89, p < 0.001), membrane rupture ≥240 min (46.4 vs. 79.6%, p < 0.001), increasing number of vaginal exams (4 vs. 6, p < 0.001), oxytocin (44.8 vs. 63.0%, p = 0.014), and meperidine (14.7 vs. 35.2%, p < 0.001) were all associated with intrapartum fever. Associated morbidity included cesarean delivery (22.5 vs. 44.4%, p = 0.001), Apgar score <7 at 5 min (0.7 vs. 5.6%, p = 0.011), and neonatal intensive care unit admission (9.5 vs. 51.9%, p < 0.001). CONCLUSION: We have identified several noninfectious factors that are associated with intrapartum fever. Modification of risk factors may improve both maternal and neonatal outcomes.

Determination of antepartum and intrapartum risk factors associated with neonatal intensive care unit admission.

OBJECTIVE: To determine antepartum and intrapartum factors that are associated with admission to neonatal intensive care unit (NICU) among infants delivered between 36.0 and 42.0 weeks at our institution. METHODS: The retrospective cohort study included 73 consecutive NICU admissions and 375 consecutive non-NICU admissions. Data on demographic, antepartum, intrapartum and neonatal factors were collected. The primary endpoint defined was admission to NICU. Univariate analyses using the Student's t-test, Mann-Whitney U-test, χ2 Fisher's exact test was performed along with multivariate analysis of significant non-redundant variables. RESULTS: Those with a significantly higher risk of NICU admission underwent induction of labor with prostaglandin analogs (12.5% vs. 24.7%, P=0.007). Length of first stage ≥720 min (33.5% vs. 51.9%, P=0.011), length of second stage of labor ≥240 min (10.6% vs. 31.6%, P<0.001) and prolonged rupture of membranes ≥120 min (54.0% vs. 80.0%, P=0.001) were all associated with an increased chance of NICU admission. Intrapartum factors predictive of NICU admission included administration of meperidine (11.7% vs. 27.4%, P<0.001), presence of preeclampsia (5.5% vs. 0.8%, P=0.015), use of intrapartum IV antihypertensives (1.1% vs. 13.7%, P<0.001), maternal fever (5.3% vs. 31.5%, P<0.001), fetal tachycardia (1.9% vs. 12.3%, P<0.001), and presence of meconium (30% vs. 8%, P<0.001). CONCLUSION: Identification of modifiable risk factors may reduce neonatal morbidity and mortality. Results from this study can be used to develop and validate a risk model based on combined antepartum and intrapartum risk factors.

Heme oxygenase (HO-1) rescue of adipocyte dysfunction in HO-2 deficient mice via recruitment of epoxyeicosatrienoic acids (EETs) and adiponectin.

BACKGROUND/AIMS: HO-1 and EETs are functionally linked and their interactions influence body weight, insulin sensitivity, and serum levels of inflammatory cytokines in metabolic syndrome phenotype of HO-2 null mice. The HO-2 isozyme is essential for regulating physiological levels of ROS. Recent studies have suggested a potential role of EET in modifying adipocyte differentiation through up-regulation of HO-1-adiponectin-AkT signaling in human mesenchymal stem cells (MSCs). Our aim was to examine the consequences of HO deficiency on MSC-derived adipogenesis in vitro using MSC derived from HO-2 null and WT mice in vivo. METHODS: Four-month-old HO-2 null (HO-2(-/-)) and B6/129SF2/J (WT) mice were divided into three groups (four mice/group): WT, HO-2(-/-), and HO-2(-/-) +CoPP. Adipogenesis was performed on purified MSC-derived adipocytes cultured in adipogenic differentiation media and an EET-agonist was added every 3 days. RESULTS: HO-2 depletion of MSC adipocytes resulted in increased adipogenesis (p<0.01) and increased levels of inflammatory cytokines including (TNF)-alpha (p<0.05), (MCP)-1 (p<0.05), and (IL-1)-beta (p<0.05). These results were accompanied by decreases in HO-1 (p<0.05) and subsequently EET and HO activity (p<0.05). Up-regulation of HO-1 resulted in decreased MSC-derived adipocyte differentiation, decreased production of TNF-alpha and MCP-1 and increased levels of adiponectin (p<0.05). Cyp2J5 (p<0.05), HO-1 (p<0.05), and adiponectin mRNA levels (p<0.05) were also decreased in visceral adipose tissue isolated from HO-2 null compared to WT mice. EET agonist stimulation of MSC adipocytes derived from HO-2 null mice yielded similar results. CONCLUSION: Increased levels of EET and HO-1 are essential for protection against the adverse effects of adipocyte hypertrophy and the ensuing metabolic syndrome. These results offer a portal into therapeutic approaches for the prevention of the metabolic syndrome.