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Background Studies have reported prenatal acetaminophen exposure is associated with abnormal neurodevelopment. There is limited and conflicting data on neurodevelopmental outcomes following postnatal acetaminophen exposure. Our objective was to investigate the neurodevelopmental outcomes of preterm infants < 29 weeks gestation postnatally exposed to acetaminophen. Methods Retrospective cohort study of infants born between 2008 and 2017 at a tertiary care perinatal center. Exclusion criteria included chromosomal disorders, major congenital abnormalities, and congenital infections. The primary outcome was a composite score of <85 on the cognitive, language, or motor components of the Bayley Scales of Infant and Toddler Development, 3rd edition, assessed at 18 to 21 months corrected gestational age. Multivariate logistic regression was used to assess confounders. Results Of the 945 infants included in the study, 120 were in the acetaminophen group. There was no difference in any of Bayley-III cognitive, language or motor composite scores of < 85 between the two groups for postnatal acetaminophen exposure, adjusted odds ratios (aORs) 1.03, 95% CI 0.60–1.78, or days of acetaminophen use, aORs 1.10, 95% CI 0.93–1.29. Conclusions There was no difference in neurodevelopmental outcome between the acetaminophen exposed and non-exposed groups. Our results need validation in larger cohorts. Impact Animal research and cohort studies have suggested that prenatal acetaminophen exposure may be associated with an elevated risk of neurobehavioral abnormalities. However, there is limited and conflicting research on the impact of postnatal acetaminophen on neurodevelopment. The results of this study suggest that postnatal acetaminophen does not negatively impact neurodevelopment at 18 to 21 months in preterm infants born at <29 weeks gestational age. While these results need validation in larger and more longitudinal studies, this study provides reassurance for the use of postnatal acetaminophen in extremely preterm infants.

BackgroundHypertensive disorders of pregnancy (HDP) are associated with dysfunctional placentation and are a major cause of maternal and neonatal morbidity and mortality. Twin pregnancies have a larger placental mass and are a risk factor for HDP. The effect of HDP on neonatal outcomes in twin pregnancies is unknown.MethodsRetrospective cohort study using the Canadian Neonatal Network database from 2010–2018 of twin infants <29 weeks gestation born to mothers with HDP and normotensive pregnancies. Using multivariable models, we determined adjusted odds ratios (AORs) and 95% confidence intervals (CI) for mortality, bronchopulmonary dysplasia, severe neurologic injury, severe retinopathy of prematurity (ROP), necrotizing enterocolitis, and nosocomial infection in twin infants of mothers with HDP compared to twin infants of normotensive mothers.ResultsOf the 2414 eligible twin infants <29 weeks gestational age, 164 (6.8%) were born to mothers with HDP and had higher odds of severe ROP (AOR 2.48, 95% CI 1.34–4.59). Preterm twin infants born to mothers with HDP also had higher odds of mortality (AOR 2.02, 95% CI 1.23–3.32). There was no difference in other outcomes.ConclusionPreterm twin infants <29 weeks gestation of HDP mothers have higher odds of severe ROP and mortality.ImpactHypertensive disorders of pregnancy, associated with placental dysfunction, are a major cause of maternal and neonatal morbidity and mortality.Twin pregnancy, associated with a larger placental mass, is a risk factor for hypertensive disorders of pregnancy.The effect of hypertensive disorders of pregnancy on outcomes of preterm twins is unknown.Preterm twins of mothers with hypertensive disorders of pregnancy are at higher risk of severe retinopathy of prematurity and mortality.Our data can be used to counsel parents and identify infants at higher risk of severe retinopathy of prematurity and mortality.

Sudden infant death syndrome (SIDS) is one of the most common causes of postneonatal infant mortality in the developed world. An insufficient cardiorespiratory response to multiple environmental stressors (such as prone sleeping positioning, overwrapping, and infection), during a critical period of development in a vulnerable infant, may result in SIDS. However, the effect of multiple risk factors on cardiorespiratory responses has rarely been tested experimentally. Therefore, this study aimed to quantify the independent and possible interactive effects of infection, hyperthermia, and hypoxia on cardiorespiratory control in rats during the neonatal period. We hypothesized that lipopolysaccharide (LPS) administration will negatively impact cardiorespiratory responses to increased ambient temperature and hypoxia in neonatal rats. Sprague–Dawley neonatal rat pups were studied at postnatal day 6–8. Rats were examined at an ambient temperature of 33°C or 38°C. Within each group, rats were allocated to control, saline, or LPS (200 μg/kg) treatments. Cardiorespiratory and thermal responses were recorded and analyzed before, during, and after a hypoxic exposure (10% O2). Serum samples were taken at the end of each experiment to measure cytokine concentrations. LPS significantly increased cytokine concentrations (such as TNFα, IL‐1β, MCP‐1, and IL‐10) compared to control. Our results do not support a three‐way interaction between experimental factors on cardiorespiratory control. However, independently, heat stress decreased minute ventilation during normoxia and increased the hypoxic ventilatory response. Furthermore, LPS decreased hypoxia‐induced tachycardia. Herein, we provide an extensive serum cytokine profile under various experimental conditions and new evidence that neonatal cardiorespiratory responses are adversely affected by dual interactions of environmental stress factors. An insufficient cardiorespiratory response to multiple environmental stressors during a critical period of development in a vulnerable infant, may result in SIDS. This study provides an extensive serum cytokine profile under various experimental conditions and new evidence that neonatal cardiorespiratory responses are adversely affected by dual interactions of environmental stress factors.

The effects of prenatal cigarette smoke (CS) exposure and hypoxemia on cardiorespiratory control have been investigated in full-term infants. However, few data are available in preterm infants, who form a particularly vulnerable population, with developmentally immature cardiorespiratory control. To investigate the effects of prenatal CS exposure on the duration and recovery of breathing pauses and oxygen saturation levels under baseline and hypoxemic conditions in preterm infants. The study was performed on 22 (12 born to smoking and 10 to nonsmoking mothers) spontaneously breathing preterm infants between 28 and 36 weeks' gestation. Cardiorespiratory variables were recorded under baseline normoxemic and hypoxemic conditions. Breathing pauses, pause indices, time to recovery, percent pause recovery, oxygen saturation (Sp(O2)), periods of wakefulness, and cardiorespiratory rates were compared between the two groups. Spontaneous recovery of breathing pauses (P = 0.03) and Sp(O(2)) levels (P = 0.017) were attenuated in CS-exposed infants as compared with the control group during the hypoxemic and posthypoxemic periods, respectively. The episodes of wakefulness during the hypoxemic challenge were similar between the two groups. Furthermore, CS-exposed infants showed a greater increase in heart rate (P < 0.001) during the hypoxemic challenge when compared with control infants. We provide evidence of how prenatal CS exposure and hypoxemic episodes affect the duration and recovery of breathing pauses in preterm infants. These observations could help explain why these infants are at a particularly high risk for sudden infant death syndrome.

We describe an unusually severe case of medium chain acyl-CoA dehydrogenase (MCAD) deficiency in a term female neonate, who presented at 12 h of age with lethargy, poor feeding, hypoglycemia and ventricular tachyarrhythmias. While arrhythmias are common in other disorders of fatty acid beta-oxidation, ventricular tachyarrhythmias have rarely been reported with MCAD deficiency in childhood. Since the results of newborn metabolic screening are usually not available within the first 3 days of life, our case highlights the need for health care professionals to be made aware of this early and uncommon but potentially fatal presentation of MCAD deficiency.

Prenatal cigarette smoke (CS) exposure, increased environmental temperature, and hypoxic episodes have been postulated as major risk factors for sudden infant death syndrome. To test the hypothesis that maternal CS exposure disrupts eupneic breathing and depresses breathing responses of neonatal rats to thermal and hypoxic challenges. Experiments were performed on 1-week-old rat pups exposed prenatally to CS (n = 39) or room air (sham; n = 30). Breathing patterns were recorded by whole-body plethysmography during thermoneutral or hyperthermic states under normoxic and hypoxic conditions. Mean pup weight, breaths per minute, and gasping respiratory patterns were measured for both smoke- and sham-exposed groups during thermoneutral and hyperthermic states under normoxic and hypoxic conditions. Under thermoneutral conditions, hypoxia caused gasping in CS-exposed animals but not in sham-exposed animals. Furthermore, under hyperthermic conditions, whereas hypoxia induced gasping in both groups, only CS-exposed animals exhibited a pronounced and longer lasting respiratory depression after the termination of hypoxia. We show that prenatal CS exposure increases the likelihood of gasplike respiration and provide the first experimental evidence that the combined effects of prenatal CS exposure and hyperthermia dramatically prolong the time required for neonates to return to eupneic breathing after hypoxia. These observations provide important evidence of how prenatal CS exposure, hypoxic episodes, and hyperthermia might place infants at higher risk for sudden infant death syndrome.

To the Editor: In the article by Van Meurs et al. (July 7 issue) 1 on the use of inhaled nitric oxide for preterm infants with severe respiratory failure, the authors suggest that inhaled nitric oxide is ineffective in infants weighing less than 1500 g. Other studies of the effects of treatment with inhaled nitric oxide in preterm infants have shown contradictory results. 2 – 5 These differences might be due to an inability to select patients who are especially likely to respond to this therapy. We suggest that it is essential to compare the clinical characteristics of infants who do not respond . . .

ObjectiveTo compare neurodevelopmental outcomes of preterm infants at 18–21 months corrected age (CA) whose mothers smoked during pregnancy to those whose mothers did not smoke.Study designPreterm infants born at <29 weeks of gestation and evaluated at 18–21 months CA were included. Primary outcome was a composite outcome of death or neurodevelopmental impairment (NDI).ResultsOf a total of 2760 infants, 699 met exclusion criteria. Of the remaining 2061 infants, 280 (13.6%) were exposed to maternal smoking and 1781 (86.4%) were not. The odds of the composite outcome of death or NDI (aOR 1.40; 95% CI: 1.03–1.91), NDI alone (aOR 1.43; 95% CI: 1.01–2.03), and Bayley-III motor score <85 (aOR 1.91; 95% CI: 1.31–2.81) were higher in exposed infants.ConclusionsExposure to maternal smoking was associated with adverse composite outcome of death or NDI, NDI alone and lower motor scores at 18–21 months CA.