The risk of neonatal respiratory morbidity according to the etiology of late preterm delivery

2017 ◽  
Vol 45 (1) ◽  
Author(s):  
Sung Ae Kim ◽  
Seung Mi Lee ◽  
Byoung Jae Kim ◽  
Chan-Wook Park ◽  
Joong Shin Park ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Preterm Delivery ◽  
Fetal Lung ◽  
Late Preterm ◽  
Respiratory Morbidity ◽  
Preterm Neonates ◽  
Lung Maturation ◽  
Study Population ◽  
Fetal Lung Maturation ◽  
Fetal Compromise

AbstractObjective:The risk of neonatal respiratory morbidity between indicated deliveries vs. spontaneous deliveries has not been consistent in previous studies, in spite of the traditional belief that chronic intrauterine stress might have protective effect on fetal lung maturation. We hypothesized that the heterogeneous etiology of indicated preterm delivery may obscure the relationship between the etiologies of preterm birth and neonatal respiratory morbidity. To address this issue, we divided the indicated preterm birth (PTB) into medically-indicated (without fetal compromise) PTB and maternal/fetal-indicated PTB, and compared the neonatal respiratory morbidity according to the etiology of late PTB.Study design:Neonatal respiratory morbidities were examined in neonates who were delivered between 34+0 and 36+6 weeks of gestation according to the etiology of PTB: 1) medically-indicated PTB (but without fetal compromise), 2) maternal/fetal-indicated PTB, or 3) spontaneous PTB such as preterm labor or preterm premature rupture of membranes.Results:A total of 710 late preterm neonates were included in the study population, including 31 cases of medically-indicated PTB, 202 cases of maternal/fetal-indicated PTB, and 477 cases of spontaneous PTB. The rate of composite respiratory morbidity in cases of medically-indicated PTB is higher than both maternal/fetal-indicated PTB and spontaneous PTB (19% in medically-indicated PTB, 6% in maternal/fetal-indicated PTB, and 7% in spontaneous PTB). This difference between medically-indicated PTB and maternal/fetal-indicated PTB remained significant after adjustment for confounding variables.Conclusion:The medically-indicated PTB is associated with highest risk of neonatal respiratory morbidity in late PTB.

Efficacy and Safety of Corticosteroids’ Administration for Pulmonary Immaturity in Anticipated Preterm Delivery

2020 ◽  
Vol 26 ◽  
Author(s):  
Themistoklis Dagklis ◽  
Ioannis Tsakiridis ◽  
Georgios Papazisis ◽  
Apostolos Athanasiadis
Keyword(s):  
Preterm Delivery ◽  
Neonatal Morbidity ◽  
Fetal Lung ◽  
Respiratory Morbidity ◽  
Efficacy And Safety ◽  
Antenatal Corticosteroids ◽  
Lung Maturation ◽  
Early Neonatal Mortality ◽  
Elective Cesarean ◽  
Fetal Lung Maturation

: Preterm delivery represents the major cause of neonatal morbidity and mortality. Respiratory morbidity is the primary cause of early neonatal mortality and disability. The administration of antenatal corticosteroids, in cases of imminent preterm delivery, can enhance fetal lung maturation and reduce the incidence of respiratory distress syndrome, leading to improved neonatal outcomes. Hence, for those cases, a single course of antenatal corticosteroids from 24 up to 34 gestational weeks should be offered. Betamethasone and dexamethasone are the most widely used drugs, with similar effectiveness and a recommended dosage of 24mg in divided doses, over a 24-hour period. However, there is an ongoing debate regarding the gestational age of administration. Some obstetric societies recommend their administration even at 22 weeks of gestation. Conflicting is also their usefulness in late preterm cases (between 34 and 37 weeks) or in cases of elective cesarean delivery at term. The use of repeated courses of corticosteroids may be considered in specific cases, however, concerns on the long-term outcomes of repeated courses beyond 34 gestational weeks have been raised. The scope of this narrative review was to synthesize available evidence on efficacy and safety of corticosteroids administration during the antenatal period for pulmonary immaturity in cases of anticipated preterm delivery.

scholarly journals Antenatal betamethasone augments early rise in pulmonary perfusion at birth in preterm lambs: role of ductal shunting and right ventricular outflow distribution

2019 ◽  
Vol 316 (6) ◽  
pp. R716-R724
Author(s):  
Joseph J. Smolich ◽  
Kelly R. Kenna ◽  
Jonathan P. Mynard
Keyword(s):  
Blood Flow ◽  
Preterm Birth ◽  
Right Ventricular ◽  
Ductus Arteriosus ◽  
Fetal Lung ◽  
Lung Maturation ◽  
Cord Clamping ◽  
Pulmonary Arterial ◽  
Early Rise ◽  
Fetal Lung Maturation

The glucocorticosteroid betamethasone is routinely administered via maternal intramuscular injection to enhance fetal lung maturation before anticipated preterm birth. Although antenatal betamethasone increases fetal pulmonary arterial (PA) blood flow, whether this agent alters the contribution of 1) right ventricular (RV) output or 2) left-to-right shunting across the ductus arteriosus to rises in PA blood flow after preterm birth is unknown. To address this question, anesthetized control ( n = 7) and betamethasone-treated ( n = 7) preterm fetal lambs (gestation 127 ± 1 days, means ± SD) were instrumented with aortic, pulmonary, and left atrial catheters as well as ductus arteriosus and left PA flow probes to calculate RV output, with hemodynamics measured for 30 min after cord clamping and mechanical ventilation. Mean PA blood flow was higher in betamethasone-treated than in control lambs over the initial 10 min after birth ( P < 0.05). This higher PA flow was accompanied by 1) a greater pulmonary vascular conductance ( P ≤ 0.025), 2) a larger proportion of RV output passing to lungs ( P ≤ 0.01), despite a fall in this output, and 3) earlier reversal and a greater magnitude ( P ≤ 0.025) of net ductal shunting, due to the combination of higher left-to-right ( P ≤ 0.025) and lesser right-to-left phasic shunting ( P ≤ 0.025). These results suggest that antenatal betamethasone augments the initial rise in PA blood flow after birth in preterm lambs, with this augmented rise supported by the combination of 1) a greater redistribution of RV output toward the lungs and 2) a faster and larger reversal in net ductal shunting underpinned not only by greater left-to-right, but also by lesser right-to-left phasic shunting.

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