Ventilatory Strategies in Infants with Established Severe Bronchopulmonary Dysplasia: A Multicenter Point Prevalence Study.

We performed a point prevalence study on infants with severe bronchopulmonary dysplasia (BPD), collecting data on type and settings of ventilatory support; 187 infants, 51% of whom were on invasive positive-pressure ventilation (IPPV), from 15 centers were included. We found a significant center-specific variation in ventilator modes.

A Quality Improvement Project to Increase Frequency of Skin-to-Skin Contact for Extreme Low-Birth-Weight Infants in the Neonatal Intensive Care Unit.

Benefits of skin-to-skin contact (SSC) are documented but often delayed in the extremely preterm population due to medical complexity and staff misconceptions about safety. This quality improvement initiative was designed to increase SSC utilization among infants born before 29 weeks' gestation regardless of respiratory support by addressing nursing barriers inhibiting SSC. A pre-/postsurvey evaluated comfort level performing and perceived barriers to SSC utilization. Implementation consisted of an updated unit-specific SSC protocol and tailored education specific to identified barriers. Evaluation included SSC rates and maternal human milk usage in the first 30 days of life. In total, 81 patients (22-28 weeks, 370-1410 g) were included. SSC rates ranged from 3.3% to 17.7% at baseline and increased to 33.2% to 39.1% postintervention. Maternal human milk utilization increased above target (≥75%) postintervention for days 7 and 14, but declined towards baseline on days 21 and 30. A statistically significant increase was observed in nursing comfort level when performing SSC for intubated infants as well as infants with a peripherally inserted central catheter or umbilical venous catheter. SSC rates increased with infants younger than 29 weeks requiring intubation and central line management, possibly as a result of greater nursing comfort surrounding with SSC.

Neonatal abstinence syndrome: an update.

PURPOSE OF REVIEW: The current review provides an update focused on the evolving epidemiology of neonatal abstinence syndrome (NAS), factors influencing disease expression, advances in clinical assessment of withdrawal, novel approaches to NAS treatment, and the emerging role of quality improvement in assessment and management of NAS. RECENT FINDINGS: The rise in the incidence of NAS disproportionately occurred in rural and suburban areas. Polysubstance exposure and genetic polymorphisms have been shown to modify NAS expression and severity. New bedside assessments using a limited number of factors to identify infants with NAS result in fewer infants receiving pharmacotherapy. In addition, buprenorphine may be a promising therapeutic alternative to morphine to treat NAS. Lastly, local, state, and national quality improvement initiatives have emerged as an effective mechanism to advance the care of infants with NAS. SUMMARY: NAS remains a critical public health issue associated with significant medical, economic, and personal burdens. Emerging data on associated risk factors, assessment of and treatment for NAS provide clinicians and hospitals with new knowledge and an urgency to promote standardization of care for infants with NAS.

Developing a Respiratory Quality Improvement Program to Prevent and Treat Bronchopulmonary Dysplasia in the Neonatal Intensive Care Unit.

Improvements in respiratory care have resulted in improved outcomes for preterm infants over the past three decades. To target the multifactorial nature of neonatal lung diseases, neonatal intensive care units (NICUs) should consider developing comprehensive respiratory quality improvement programs that address all drivers of neonatal respiratory disease. This article presents a potential framework for developing a quality improvement program to prevent bronchopulmonary dysplasia in the NICU. Drawing on available research and quality improvement reports, the authors discuss key components, measures, drivers, and interventions that should be considered when building a respiratory quality improvement program devoted to preventing and treating bronchopulmonary dysplasia.

Increased Severity of Neonatal Abstinence Syndrome Associated With Concomitant Antenatal Opioid and Benzodiazepine Exposure.

BACKGROUND: Polysubstance use is common among opioid-using women, yet its association with pharmacotherapy for neonatal abstinence syndrome (NAS) remains unclear. We hypothesized that benzodiazepine exposure would increase risk of an infant developing pharmacologically treated NAS. METHODS: We conducted a retrospective cohort study of maternal-infant dyads enrolled in Tennessee Medicaid, using individual-level data linkage of vital records and administrative (ie, outpatient, inpatient, and prescription) data from 2009 to 2011. These data underwent chart review from 2013 to 2016 to obtain clinically relevant exposure data (eg, toxicology testing). The association of antenatal exposures with pharmacologically treated NAS was evaluated by using multivariable logistic regression, controlling for maternal and infant factors and clustered by hospital. RESULTS: Among 112 029 maternal-infant dyads, we confirmed 822 cases of NAS, of which 598 (72.7%) were cases of pharmacologically treated NAS. Infants who developed pharmacologically treated NAS were more likely to have been exposed to antenatal benzodiazepines compared with infants with confirmed NAS not treated pharmacologically (40.9% vs 30.8%; P = .008). In adjusted analyses, benzodiazepine exposure was associated with greater risk of developing pharmacologically treated NAS (odds ratio: 1.51; 95% confidence interval: 1.04-2.21). Alternatively, exposure to tobacco, marijuana, cocaine, gabapentin, and selective serotonin reuptake inhibitors were not associated with increased risk of developing pharmacologically treated NAS. CONCLUSIONS: Among a population of infants with intrauterine polysubstance exposure, benzodiazepine exposure was an independent predictor of an infant developing pharmacologically treated NAS. Obtaining history of antenatal benzodiazepine exposure among opioid-exposed infants may allow for risk stratification and development of personalized care plans.

Heat shock inhibition of lipopolysaccharide-mediated tumor necrosis factor expression is associated with nuclear induction of MKP-1 and inhibition of mitogen-activated protein kinase activation.

OBJECTIVE: Application of heat shock before an inflammatory stimulus often results in an attenuated response to that stimulus. As a result, it has become increasingly appreciated that heat shock may induce cross-tolerance to a variety of stimuli based on in vitro and in vivo models. Circulating peripheral blood monocytes are key mediators of cytokine release following endotoxin challenge. The mitogen-activated protein kinases play a key role in the transcriptional regulation of this response including expression of tumor necrosis factor. As such, counterregulatory phosphatases that target mitogen-activated protein kinase may play a role in this heat shock-mediated effect. We hypothesized that prior heat shock to monocytes would induce a phosphatase, MKP-1, that regulated mitogen-activated protein kinase activity and subsequently conferred cross-tolerance to lipopolysaccharide stimulation. DESIGN: Experimental. SETTING: University research foundation laboratory. SUBJECTS: THP-1 human monocyte cell line. INTERVENTIONS: THP-1 cells were exposed to either heat shock (43 degrees C, 1 hr) or normothermia (37 degrees C, 1 hr) and allowed to recover before stimulation with endotoxin (lipopolysaccharide). MEASUREMENTS AND MAIN RESULTS: Induction of a heat shock response was determined by heat shock protein-70 expression. Tumor necrosis factor and interleukin-10 were measured by enzyme-linked immunosorbent assay to assess heat shock inhibition of lipopolysaccharide-induced gene expression. The effect of heat shock on lipopolysaccharide-mediated activation of the p38 and ERK kinases was examined by measuring phospho-specific isoforms of p38 and ERK1/2 and correlated to in vitro kinase activity. Confirmatory data were generated from experiments employing either pharmacologic inhibition or genetic deletion of MKP-1. Heat shock induced the nuclear localized phosphatase, MKP-1, that attenuated p38 and ERK kinase activity resulting in significantly diminished tumor necrosis factor expression in response to lipopolysaccharide. CONCLUSIONS: The effect of heat shock on decreasing the tumor necrosis factor response to lipopolysaccharide is conferred by induction of MKP-1, which negatively regulates p38 and ERK kinases. Modulation of phosphatase activity may be a potential strategy for attenuating acute inflammatory responses.