Adolescent Psychological Birth Trauma Following Cesarean Birth.

This study explored associations between depressive symptoms, violence exposure, and psychological birth trauma (PBT) among 44 adolescents experiencing cesarean births. Within 72 hours postpartum, symptoms of PBT were measured via a subjective rating of the birth experience and the Impact of Event Scale (IES). The Edinburgh Postnatal Depression Scale measured depressive symptoms. Single questions assessed violence exposure, including child abuse, partner violence, and traumatic life experiences as attribute variables. Adolescents were typically single with an unplanned first pregnancy. A similar number of adolescents reported a negative or positive birth experience. Correlations between IES scores, parity, depressive symptoms, partner violence, gestational age, and a negative birth appraisal suggested interconnected prenatal vulnerabilities for birth trauma and adverse infant outcomes. Partner violence and depressive symptoms need continuous assessment throughout pregnancy. The potential for continued symptoms and presence of violence beyond discharge requires follow up and education in pediatric settings at well-baby and routine visits.

Transitioning Care Approach for Neonatal Opioid Withdrawal Syndrome and Neonatal Abstinence Syndrome.

The increase in substance use during pregnancy results in a higher incidence of neonatal abstinence syndrome/neonatal opioid withdrawal syndrome (NAS/NOWS), straining health care and social systems and creating an economic burden. There is a paradigm shift in transitioning the care approach for NAS/NOWS from a medical model of care to a family-centered individualized non-pharmacological care approach with non-pharmacological interventions as the first line of treatment. Supporting families after birth with a nurturing environment and providing them with a toolbox of non-pharmacological interventions prepares them for the transition from hospital to home.

Neonatal ICU antibiotic use trends within an integrated delivery network.

BACKGROUND AND OBJECTIVES: There is a need for robust antibiotic stewardship programs (ASPs) in the neonatal population. This study's objectives were to assess neonatal antibiotic use practices over an extended period across an integrated delivery network (IDN), including six Neonatal Intensive Care Units (NICUs), to identify those most successful practices reducing use rates. METHODS: A retrospective cohort study was conducted, including 15,015 NICU admissions from an integrated delivery network, across six hospitals over eight years (50% Level III and 50% Level II) computing antibiotic use rates (AURs) stratified by usage: in the first few days of the stay vs. later in the stay and by gestational age. Several metrics were examined for assumptions of strong correlation with AUR: (1) the percentage of infants given antibiotics early in their stays and (2) durations of courses of antibiotics. RESULTS: Results conclude a wide variation in AURs and trends that these rates followed over time. However, there was a decrease in overall AUR from 15.7-16.6 to 10.1-10.8%, with four of the six NICUs recording statistically significant reductions in AUR vs. their first year of measurement. Specifically, the level III NICUs overall AUR decreases from 15.1-16.22 to 8.6-9.4%, and level II NICUs overall AUR 20.3-24.4 to 14.1-16.1%. A particularly successful level II NICU decreased its AUR from 22.9-30.6 to 5.9-9.4%. CONCLUSION: To our knowledge, this is the first study to utilize data analytics at an IDN level to identify trends in AUR, We have identified practices that allowed an institution to reduce NICU AURs significantly, and which, if done as a standard practice, could be replicated on a broader scale.

Autism, heparan sulfate and potential interventions.

Developmental disabilities are defined as disorders that result in the limitation of function due to impaired development of the nervous system; these disabilities can be present in the form of impairments in learning, language, behavior, or physical abilities. Examples of developmental disorders include attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), cerebral palsy (CP), hearing loss, blindness, intellectual disability, and learning disability. Of these disorders, ASD prevalence was 18.5 per 1000 children (1 in 54) aged 8 in 2016. Current literature suggests that deficient levels of heparan sulfate (HS), an acidic and linear glycosaminoglycan (GAG), is likely causative of ASD. The cascading effect of deficient HS levels can offer compelling evidence for the association of HS with ASD. Deficient levels of HS lead to defective Slit/Robo signaling, which affects axonal guidance and dendritic spine formation. Defective Slit/Robo signaling leads to increased Arp2/3 activity and dendritic spine density, which has been observed in the brains of persons with ASD. Therefore, interventions that target HS and its associated pathways may be viable treatment options for ASD.

The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation.

Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. ASDs are accompanied with substantial economic and emotional cost. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Of particular interest is its role in the Slit/Robo pathway. The Slit/Robo pathway is known to be involved in the regulation of axonal guidance and dendritic spine formation. HS mediates the Slit/Robo interaction; without its presence Slit's repulsive activity is abrogated. Slit/Robo regulates dendritic spine formation through its interaction with srGAPs (slit-robo GTPase Activating Proteins), which leads to downstream signaling, actin cytoskeleton depolymerization and dendritic spine collapse. Through interference with this pathway, HS deficiency can lead to excess spine formation.