Oxygen Saturation Profiles in Healthy Term Infants in Early Postnatal Life.

OBJECTIVE: Oxygen saturation profiles generated by pulse oximetry are used as a clinical tool in the neonatal intensive care unit (NICU). There is limited evidence on normal oxygen saturation profile values in term infants. This study aimed to determine oxygen saturation profiles over an 8-hour monitoring period among healthy term neonates between 24 and 48 hours after birth. STUDY DESIGN: A prospective cohort study of healthy term neonates born at 37 to 41 weeks of gestation. Preductal oxygen saturations were continuously monitored for an 8-hour period between 24 and 48 hours of life using pulse oximetry. Oxygen profile histograms were recorded for analysis. The average percent oxygen saturation (SpO2) was measured over the entire study duration for each neonate and was characterized as the fraction of time of their SpO2 reading was in each of five intervals: ≤80, 81 to 84, 85 to 89, 90 to 94, and 95 to 100%. RESULTS: Seventy-five neonates were included in the study. Median SpO2 was 95.4%. Percentage time spent in each of the five SpO2 intervals was as follows: 0.07 (≤80), 0.15 (81-84), 0.88 (85-89), 26.9 (90-94), and 67.3% (95-100%). Eighteen infants (24%) spent the highest percentage of time in SpO2 of 90 to 94%. CONCLUSION: This study provides reference ranges for oxygen profiles in healthy term neonates during 24 to 48 hours of life. Nearly one-quarter of newborns spent the highest percentage of time in SpO2 of 90 to 94%. This data is important when interpreting oxygen saturation profiles of term neonates admitted to the NICU. KEY POINTS: · This study provide reference ranges for oxygen profiles in healthy term neonates during 24 to 48 hours.. · Median SpO2 was 95.4%.. · Nearly one quarter of newborns spent the highest percentage of time in SpO2 of 90 to 94%..

Are Experiences of Racial Discrimination Associated with Postpartum Depressive Symptoms? A Multistate Analysis of Pregnancy Risk Assessment Monitoring System Data.

Background: Postpartum depression (PPD) is a serious public health crisis disproportionately affecting women of color. We examine whether interpersonal racial discrimination is associated with higher odds of postpartum depressive symptoms (PPDS) among women of color and how it may vary by race/ethnicity and maternal educational attainment. Materials and Methods: We present a secondary analysis of cross-sectional data from Pregnancy Risk Assessment Monitoring System (PRAMS) postnatal surveys conducted in nine jurisdictions between 2012 and 2015 that included a question about being upset by experiences of racial discrimination within 12 months before giving birth. Results: Being upset by racial discrimination was associated with nearly three times higher odds of PPDS. Among women of color with at least some college education, the higher odds of PPDS associated with racial discrimination were greater than threefold, and for women with less than a high school education were less than twofold. Conclusion: Addressing risk factors for PPD, including racial discrimination, may inform strategies to reduce racial disparities in maternal mental health.

Rethinking Bias to Achieve Maternal Health Equity: Changing Organizations, Not Just Individuals.

In this article, we address the limitations of existing implicit bias interventions as a strategy for achieving maternal health equity. We then focus on how institutionally sanctioned racial stereotyping harms Black maternal health and marginalizes a key group in the fight for health equity-Black physicians. Finally, we provide strategies to address racial bias in perinatal health care and structural barriers impeding Black physicians' success.

High Black infant mortality in Wisconsin: factors associated with the ongoing racial inequity.

BACKGROUND: Wisconsin has the highest Black infant mortality rate (IMR) in the nation. OBJECTIVE: Evaluate factors associated with racial inequity in IMR in Wisconsin. STUDY DESIGN: Births/deaths/IMR for Black and White infants from 2011 to 2016 were obtained from the Wisconsin Interactive Statistics on Health system, stratified by gestational age (GA), and compared using direct adjustment method. IMR were compared based on cause of death, maternal age, and education. RESULTS: Crude and adjusted IMR was 13.7 and 9.1 for black infants. Respective IMR for white infants was 4.8 and 5.3. Crude IMR was 180% higher in Black infants. After controlling for GA, IMR among Black infants was 70% higher. In term Black infants, deaths due to sudden infant death syndrome (SIDS), accidents, and assaults were markedly high. CONCLUSIONS: Higher IMR in Black infants was due to increased premature births and increased mortality among term infants. Potentially modifiable causes of death were SIDS, accidents, and assaults.

More Than a "Number": Perspectives of Prenatal Care Quality from Mothers of Color and Providers.

INTRODUCTION: African American mothers and other mothers of historically underserved populations consistently have higher rates of adverse birth outcomes than White mothers. Increasing prenatal care use among these mothers may reduce these disparities. Most prenatal care research focuses on prenatal care adequacy rather than concepts of quality. Even less research examines the dual perspectives of African American mothers and prenatal care providers. In this qualitative study, we compared perceptions of prenatal care quality between African American and mixed race mothers and prenatal care providers. METHODS: Prenatal care providers (n = 20) and mothers who recently gave birth (n = 19) completed semistructured interviews. Using a thematic analysis approach and Donabedian's conceptual model of health care quality, interviews were analyzed to identify key themes and summarize differences in perspectives between providers and mothers. FINDINGS: Mothers and providers valued the tailoring of care based on individual needs and functional patient-provider relationships as key elements of prenatal care quality. Providers acknowledged the need for knowing the social context of patients, but mothers and providers differed in perspectives of "culturally sensitive" prenatal care. Although most mothers had positive prenatal care experiences, mothers also recalled multiple complications with providers' negative assumptions and disregard for mothers' options in care. CONCLUSIONS: Exploring strategies to strengthen patient-provider interactions and communication during prenatal care visits remains critical to address for facilitating continuity of care for mothers of color. These findings warrant further investigation of dual patient and provider perspectives of culturally sensitive prenatal care to address the service needs of African American and mixed race mothers.

beta-N-methylamino-l-alanine induces oxidative stress and glutamate release through action on system Xc(-).

beta-N-methylamino-l-alanine (BMAA) is a non-protein amino acid implicated in the neurodegenerative disease amyotrophic lateral sclerosis/Parkinson-dementia complex (ALS/PDC) on Guam. BMAA has recently been discovered in the brains of Alzheimer's patients in Canada and is produced by various species of cyanobacteria around the world. These findings suggest the possibility that BMAA may be of concern not only for specific groups of Pacific Islanders, but for a much larger population. Previous studies have indicated that BMAA can act as an excitotoxin by acting on the NMDA receptor. We have shown that the mechanism of neurotoxicity is actually three-fold; it involves not only direct action on the NMDA receptor, but also activation of metabotropic glutamate receptor 5 (mGluR5) and induction of oxidative stress. We now explore the mechanism by which BMAA activates the mGluR5 receptor and induces oxidative stress. We found that BMAA inhibits the cystine/glutamate antiporter (system Xc(-)) mediated cystine uptake, which in turn leads to glutathione depletion and increased oxidative stress. BMAA also appears to drive glutamate release via system Xc(-) and this glutamate induces toxicity through activation of the mGluR5 receptor. Therefore, the oxidative stress and mGluR5 activation induced by BMAA are both mediated through action at system Xc(-). The multiple mechanisms of BMAA toxicity, particularly the depletion of glutathione and enhanced oxidative stress, may account for its ability to induce complex neurodegenerative diseases.