Refining Trauma-Informed Perinatal Care for Urban Prenatal Care Patients with Multiple Lifetime Traumatic Exposures: A Qualitative Study.

INTRODUCTION: Because lifetime trauma exposure has been linked to multiple adverse pregnancy outcomes, there is a need for all perinatal care providers to be versed in trauma-informed care practices. However, there are few data to guide trauma-informed practice during the perinatal period. The objective of this study was to refine ongoing development of a trauma-informed care framework for perinatal care by conducting a qualitative study of all trauma experiences and preferred screening practices of pregnant patients at an urban prenatal clinic. METHODS: In this qualitative study, we conducted semistructured interviews with 30 women receiving prenatal care at an urban clinic. Participants also completed a trauma history questionnaire. Inductive coding was used to generate themes and subthemes. RESULTS: Participants described multiple lifetime traumatic exposures as well as background exposure to community violence. Not all participants desired routine trauma screening; factors limiting disclosure included fear of retraumatization and belief that prior trauma is unrelated to the current pregnancy. Strong therapeutic relationships were identified as critical to any trauma history discussion. DISCUSSION: This study supports a trauma-informed care approach to caring for pregnant women with prior traumatic exposures, including trauma screening without retraumatization and trusting patient-provider relationships.

Extended wakefulness: compromised metabolics in and degeneration of locus ceruleus neurons.

Modern society enables a shortening of sleep times, yet long-term consequences of extended wakefulness on the brain are largely unknown. Essential for optimal alertness, locus ceruleus neurons (LCns) are metabolically active neurons that fire at increased rates across sustained wakefulness. We hypothesized that wakefulness is a metabolic stressor to LCns and that, with extended wakefulness, adaptive mitochondrial metabolic responses fail and injury ensues. The nicotinamide adenine dinucleotide-dependent deacetylase sirtuin type 3 (SirT3) coordinates mitochondrial energy production and redox homeostasis. We find that brief wakefulness upregulates SirT3 and antioxidants in LCns, protecting metabolic homeostasis. Strikingly, mice lacking SirT3 lose the adaptive antioxidant response and incur oxidative injury in LCns across brief wakefulness. When wakefulness is extended for longer durations in wild-type mice, SirT3 protein declines in LCns, while oxidative stress and acetylation of mitochondrial proteins, including electron transport chain complex I proteins, increase. In parallel with metabolic dyshomeostasis, apoptosis is activated and LCns are lost. This work identifies mitochondrial stress in LCns upon wakefulness, highlights an essential role for SirT3 activation in maintaining metabolic homeostasis in LCns across wakefulness, and demonstrates that extended wakefulness results in reduced SirT3 activity and, ultimately, degeneration of LCns.