Respiratory Distress In Term Infants Research Articles

Adverse respiratory patterns in near-term spontaneously breathing newborn lambs with elevated airway liquid volumes at birth.

Recent evidence indicates that respiratory distress (RD) in near-term infants is caused by elevated airway liquid (EL) volume at the beginning of air-breathing after birth. While the adverse effects EL volumes on newborn lung function are known, the effects on respiratory control and breathing patterns shortly after birth (<4 h) are unknown. We investigated the effects of EL volumes on cardiorespiratory function and breathing patterns in spontaneously breathing near-term newborn lambs in the first hours after birth. At 137-8 days gestation (2-3 days prior to delivery; term ∼147 days), sterile surgery was performed on fetal sheep (n = 17) to implant catheters and blood flow probes. At 140 days, lambs were delivered via caesarean section under spinal anaesthesia. Airway liquid volumes were adjusted to mimic the level expected following vaginal delivery (∼10 ml/kg; Controls; n = 7), or elective caesarean section (∼30 ml/kg; elevated airway liquid group; EL; n = 10). Spontaneous breathing and cardiorespiratory parameters were recorded over four hours after birth. Non-invasive respiratory support with supplemental oxygen was provided if required. EL lambs required higher inspired oxygen levels (p = 0.0002), were less active (p = 0.026), fed less (p = 0.008) and had higher respiratory morbidity scores than Controls (p < 0.0001). EL lambs also displayed higher rates of breathing patterns associated with RD, such as expiratory braking and tachypnoea. These patterns were particularly evident in male EL lambs who displayed higher levels of severe respiratory morbidity (e.g., expiratory braking) than female EL lambs. The study demonstrates that EL volumes at birth trigger respiratory behaviour and breathing patterns that resemble clinically recognised features of RD in term infants.

Spontaneous Pneumomediastinum in a Term Neonate: A Case Report

Pneumomediastinum is an uncommon cause of respiratory distress in term infants. It could be due to many risk factors; vigorous resuscitation, pneumonia, mechanical ventilation or meconium aspiration syndrome. We present a case of spontaneous pneumomediastinum in a term baby with no identified risk factor.

Incidence, Risk factors and Outcome of Respiratory Distress Syndrome in Term Infants at Academic Centre, Jeddah, Saudi Arabia.

Introduction:Respiratory distress syndrome (RDS) is a respiratory disorder of neonates that manifests itself within few hours after delivery. It is one of the most common causes of admission to neonatal intensive care unit (NICU) and respiratory failure in neonates.Aim:The aim of this study was to determine the incidence, risk factors, and the short-term outcomes of RDS in term infants born in an academic tertiary care center at King Abdul-Aziz University Hospital (KAUH), Jeddah, Saudi Arabia.Methods:Data of all infants admitted to the NICU at the academic center between January 1st 2016 and December 31st 2016 were retrospectively collected. Cases were all term infants who were admitted to NICU with the diagnosis of RDS during the study period. Controls were term infants and 1:1 matched for the date of birth (one or two days from the date of birth of the case) and received routine newborn care.Results:Fifty-nine term infants (59/3601, 1.64%) were admitted to the NICU with RDS and 59 control infants were matched during the study period. Infants with RDS were significantly of lower birth weight and had lower Apgar scores at one and five minutes. Although there was a higher number of cesarean section and PROM in the RDS group, but that didn’t reach statistical significance. Three infants (5.1%) died in the RDS group.Conclusion:Respiratory distress in term infants is still a significant cause of admission to NICU and a predisposing factor for neonatal mortality and morbidity. Preventative and anticipatory measures should be further explored to decrease the burden of this disease.

Advances in the management of meconium aspiration syndrome.

Meconium aspiration syndrome (MAS) is a common cause of severe respiratory distress in term infants, with an associated highly variable morbidity and mortality. MAS results from aspiration of meconium during intrauterine gasping or during the first few breaths. The pathophysiology of MAS is multifactorial and includes acute airway obstruction, surfactant dysfunction or inactivation, chemical pneumonitis with release of vasoconstrictive and inflammatory mediators, and persistent pulmonary hypertension of newborn (PPHN). This disorder can be life threatening, often complicated by respiratory failure, pulmonary air leaks, and PPHN. Approaches to the prevention of MAS have changed over time with collaboration between obstetricians and pediatricians forming the foundations for care. The use of surfactant and inhaled nitric oxide (iNO) has led to the decreased mortality and the need for extracorporeal membrane oxygenation (ECMO) use. In this paper, we review the current understanding of the pathophysiology and management of MAS.

Severe respiratory distress in term infants born electively at high altitude

BackgroundWe studied the contribution of elective delivery to severe respiratory distress syndrome (RDS) in term babies born at high altitude.MethodsWe prospectively studied the charts of term babies born in Taif Maternity Hospital (1640 m above sea level) between 1/1/2004 and 31/10/2004 who developed RDS and required mechanical ventilation.Results8634 deliveries occurred from 37–<41 weeks; 13 (0.15%) had RDS requiring mechanical ventilation. Seven infants delivered at 37–<38 weeks, (OR for RDS = 26 95%CI -4.6 to 5.8), five delivered at 38–<39 weeks, (OR for RDS = 10 95%CI -4.9 to 5.4) and one delivered at >39 weeks. Six of 13 infants were electively delivered without documented lung maturity.ConclusionInfants born at 37 and 38 weeks' gestation remain at significantly increased risk for severe RDS. Elective delivery is responsible for 50% of the potentially avoidable cases. Our data suggest that the altitude does not seem to influence the incidence of severe RDS in term infants born electively.

Respiratory Distress in the Term and Near-term Infant

After completing this article, readers should be able to: 1. Differentiate between cardiac and respiratory causes of cyanosis. 2. Describe the primary parenchymal diseases that can cause respiratory distress in the neonate. 3. Describe the primary developmental lung abnormalities that can cause respiratory distress in the neonate. One of the most common reasons for admission of term neonates to a neonatal intensive care unit (NICU) is respiratory distress. (1) The cause may be of pulmonary or nonpulmonary origin. The nonpulmonary causes include cardiac, infectious, metabolic, central nervous system, and miscellaneous conditions. This review focuses on the major pulmonary causes for respiratory distress in term infants, in particular, the first two of the four groups that appear in Table 1. (2) | Parenchymal conditions | || | Developmental abnormalities | | Airway abnormalities | | Mechanical abnormalities | Table 1. Potential Pulmonary Causes for Respiratory Distress in Neonates Differentiating cardiac and respiratory causes of cyanosis is a common clinical problem, particularly in cases in which there is little or no tachypnea or respiratory distress. The major signs of neonatal respiratory distress are tachypnea and cyanosis, in which tachypnea is defined as a respiratory rate consistently greater than 60 breaths/min. A hyperoxia test may assist in differentiating between the two. Pulse oximetry may help to decide whether a formal hyperoxic test is useful. A neonate who exhibits cyanosis without marked respiratory distress and has an O2 saturation of less than 85% in both room air and 100% oxygen likely has an intracardiac shunt. If the O2 saturation increases to more than 85% on 100% oxygen, …

Mechanism of SPB gene regulation by cortisol and retinoic acid in a human pulmonary epithelial cell line. † 280

Surfactant protein B (SPB) is required for the normal function of pulmonary surfactant. A deficiency in SPB at birth has been associated with lethal respiratory distress in term infants. H441 cells are a human pulmonary epithelial adenocarcinoma cell line that produces SPB mRNA and protein. We have shown that both cortisol and alltrans retinoic acid (RA) increase the content of SPB mRNA in a dosedependent manner in H441 cells when compared to untreated controls. We have also shown that the combination of cortisol plus RA causes a further stimulation of SPB mRNA content over the levels in cells treated with either hormone alone. We investigated the mechanisms of action of cortisol, RA and the combination of cortisol plus RA by studying their transcriptional and posttranscriptional effects on SPB gene expression. In the first series of experiments, H441 cells were treated for 24 hours in serumfree media with either no additions (control), cortisol (106M), RA(106M), or a combination of cortisol (106M) plus RA(106M). Nuclear runon transcription assays were performed to determine the rate of SPB gene transcription. When compared to controls, the rate of SPB gene transcription was increased 4.2 ± 0.8 times by cortisol, 1.7± 0.3 times by RA and 4.6 ± 1.2 times by the combination of cortisol and RA (all values are mean ± SEM, n=5). We then examined the effects of these hormones and hormone combinations on SPB mRNA stability. H441 cells were treated for 12 hours with cortisol and/or RA, at the concentrations listed above, and then with the same hormones in the presence of actinomycin D(10 μg/ml), a RNA synthesis inhibitor, for up to an additional 24 hours. Northern blot analysis was performed on RNA harvested from the control and treated cells after 0, 4, 8, 12 and 24 hours of incubation in hormone plus actinomycin D. The halflife of SPB mRNA was 21 hours in control cells, 29 hours in cortisoltreated cells, 22 hours in RA treated cells, and 44 hours in cells treated with cortisol plus RA (n = 3). We conclude that cortisol regulates SPB mRNA via increased gene transcription and increased mRNA stability. RA, in contrast, increases SPB gene transcription but has no effect on SPB mRNA stability. We conclude further that the combination of cortisol plus RA increases SPB mRNA levels primarily via an effect on mRNA stability.