pulmicort and Chorioamnionitis

Despite advances in neonatal intensive care in the recent decade, a large number of very preterm infants (VPIs) remain at risk for significant neurodevelopmental impairment (NDI). Given that there are many interventions need to be implemented during the critical perinatal period so that complications of these vulnerable VPIs could be minimized, it is urgent to develop multi-discipline strategies based on evidence to be carried out. The objective of this new term evidence-based perinatal critical strategies (EBPCS), is to provide beneficial intervention towards better neurodevelopmental outcomes, specifically for preterm infants below 28 weeks gestational age. EBPCS is defined as the management of the VPIs during the perinatal period which would include antenatal counseling with team briefing and share decision making, treat the chorioamnionitis, antenatal MgS04, antenatal steroid, delayed cord clamping/milking, neonatal resuscitation team preparation, prevention of hypothermia, immediate respiratory support with continuous positive airway pressure at delivery room, less invasive surfactant administration, early surfactant with budesonide therapy, support of cardiovascular system, early initiate of probiotics administration, early caffeine, early parenteral and enteral nutrition, promptly initiating antibiotics. These critical strategies will be discussed detail in the text; nonetheless, standardized protocols, technical skills and repeated training are the cornerstones of successful of EBPCS. Further experience from different NICU is needed to prove whether these very complicate and comprehensive perinatal critical strategies could translate into daily practice to mitigate the incidence of NDI in high-risk VPIs.

Topics: Anti-Bacterial Agents; Bronchopulmonary Dysplasia; Budesonide; Caffeine; Central Nervous System Stimulants; Chorioamnionitis; Continuous Positive Airway Pressure; Counseling; Decision Making, Shared; Enteral Nutrition; Evidence-Based Practice; Female; Glucocorticoids; Humans; Hypotension; Hypothermia; Infant; Infant, Extremely Premature; Infant, Newborn; Magnesium Sulfate; Neurodevelopmental Disorders; Parenteral Nutrition; Patient Care Team; Pregnancy; Premature Birth; Prenatal Care; Probiotics; Pulmonary Surfactants; Resuscitation; Tocolytic Agents

Chorioamnionitis is associated with increased rates of bronchopulmonary dysplasia (BPD) in ventilated preterm infants. Budesonide when added to surfactant decreased lung and systemic inflammation from mechanical ventilation in preterm lambs and decreased the rates and severity of BPD in preterm infants. We hypothesized that the addition of budesonide to surfactant will decrease the injury from mechanical ventilation in preterm lambs exposed to intra-amniotic (IA) lipopolysaccharide (LPS).. Lambs at 126 ± 1 day GA received LPS 10 mg IA 48 h prior to injurious mechanical ventilation. After 15 min, lambs received either surfactant mixed with: (1) saline or (2) Budesonide 0.25 mg/kg, then ventilated with normal tidal volumes for 4 h. Injury markers in the lung, liver, and brain were compared.. Compared with surfactant alone, the addition of budesonide improved blood pressures, dynamic compliance, and ventilation, while decreasing mRNA for pro-inflammatory cytokines in the lung, liver, and multiple areas of the brain. LPS caused neuronal activation and structural changes in the brain that were not altered by budesonide. Budesonide was not retained within the lung beyond 4 h.. In preterm lambs exposed to IA LPS, the addition of budesonide to surfactant improved physiology and markers of lung and systemic inflammation.. The addition of budesonide to surfactant decreases the lung and systemic responses to injurious mechanical ventilation preterm lambs exposed to fetal LPS. Budesonide was present in the plasma by 15 min and the majority of the budesonide is no longer in the lung at 4 h of ventilation. IA LPS and mechanical ventilation caused structural changes in the brain that were not altered by short-term exposure to budesonide. The budesonide dose of 0.25 mg/kg being used clinically seems likely to decrease lung inflammation in preterm infants with chorioamnionitis.

Topics: Animals; Biological Products; Brain; Bronchopulmonary Dysplasia; Budesonide; Chorioamnionitis; Cytokines; Disease Models, Animal; Drug Therapy, Combination; Female; Fetal Diseases; Gestational Age; Glucocorticoids; Inflammation Mediators; Lipopolysaccharides; Lung; Phospholipids; Pneumonia; Pregnancy; Pulmonary Surfactants; Respiration, Artificial; Sheep, Domestic; Systemic Inflammatory Response Syndrome

In preterm infants on moderately high ventilator support, the addition of budesonide to surfactant lowered bronchopulmonary dysplasia (BPD) rates by 20% without increased morbidity or mortality. The aim of this cohort comparison was to determine the safety and efficacy of the combination in infants with milder respiratory distress syndrome (RDS).. In August 2016 we began administering budesonide (0.25 mg/kg) mixed with surfactant (Survanta 4 mL/kg) to all infants ≤ 1250 g who failed CPAP and required intubation. Infants were compared to a historical cohort (2013-2016) who received surfactant alone.. BPD or death did not change between the historical surfactant cohort (71%, n = 294) and the budesonide cohort (69%, n = 173). Budesonide was associated with a decrease in the need for continued mechanical ventilation, severe BPD type II or death (19-12%), grade III BPD or death (31-21%), and the median gestational age at discharge was 1 week earlier. Histologic chorioamnionitis was associated with decreased budesonide effects. Secondary morbidities (NEC, IVH, ROP, Sepsis) were similar.. Overall BPD rates remained unchanged with the addition of budesonide. Budesonide was associated with decreased severity of BPD, decreased mechanical ventilation use, earlier discharge, and similar short-term outcomes.

Topics: Bronchopulmonary Dysplasia; Budesonide; Chorioamnionitis; Female; Humans; Infant, Newborn; Male; Patient Discharge; Patient Safety; Pregnancy; Pulmonary Surfactants; Respiration, Artificial; Respiratory Distress Syndrome, Newborn; Surface-Active Agents; Treatment Outcome