Antenatal corticosteroid therapy in premature infants

Smrcek, J.; Schwartau, N.; Kohl, M.; Berg, Christoph; Geipel, A.; Krapp, M.; Diedrich, K.; Ludwig, Michael

doi:10.1007/s00404-004-0664-4

Cited by 29 publications

(36 citation statements)

References 19 publications

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“…Antenatal corticosteroid therapy has associated with improved neonatal outcomes, including a lower incidence of RDS in women at risk for preterm delivery [1][2]. Corticosteroids (such as betamethasone) administered antenatally increase production of surfactant in the lining of the fetal lungs, leading to reduced morbidity [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Does corticosteroid therapy impact fetal pulmonary artery blood flow in women at risk for preterm birth?

et al. 2015

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Aim: Maternal corticosteroid administration in pregnancy is known to enhance fetal lung maturity in at risk fetuses. The aim of this study was to test the hypothesis that corticosteroid therapy alters fetal pulmonary blood flow in pregnancies at risk for preterm birth (PTB). Material and methods: We prospectively evaluated main fetal pulmonary artery (MPA) blood flow in pregnant women at risk for PTB and treated with corticosteroids (betamethasone), compared to an uncomplicated cohort without steroid therapy. The Doppler indices of interest included Peak Systolic Velocity (PSV), Resistive Index (RI), Pulsatility Index (PI), Systolic/Diastolic ratio (S/D ratio), Acceleration Time (AT), and Acceleration Time/Ejection Time Ratio (AT/ ET ratio), with the latter serving as the primary outcomes due to its stability irrespective of gestational age. Results: When compared with controls, fetuses treated with corticosteroids demonstrated significantly decreased pulmonary artery acceleration time (median: 28.89 (22.22-51.11) vs. 33.33 (22.20-57.00), p=0.006), while all other indices remained similar. We found no difference in pulmonary blood flow between fetuses who developed respiratory distress syndrome (RDS) and those that did not (31.56 ± 6.842 vs. 32.36 ± 7.265, p= 0.76). Conclusion: Our data demonstrate altered fetal pulmonary blood flow with corticosteroid therapy, possibly due to increased arterial elastance brought on by medication effect, which leads to the decreased acceleration time or possible gestational age affect. Contrary to a recent report, we did not observe any Doppler differences in fetuses with RDS, which underscores the need for further examination of this proposed association.

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Section: Introductionmentioning

confidence: 99%

Does corticosteroid therapy impact fetal pulmonary artery blood flow in women at risk for preterm birth?

et al. 2015

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“…Prenatal steroid administration to humans will reduce the incidence of respiratory distress syndrome Fig. 1 Electron micrograph showing the lamellar bodies (arrows) of Type II pneumocytes in the lung of a non-shunted rabbit that received dexamethasone (3,000·) where surfactant deficiency is involved in the pathophysiology [1][2][3][4]22]. However, the exact mechanisms for the modulation of the surfactant apoproteins' expression in the fetal lungs via maternal corticosteroid administration remain debatable, because the responses are dependent on dosage, gender, specimens, route of administration, time of gestation when corticosteroids are administered, and the length of exposure to corticosteroids [22].…”

Section: Discussionmentioning

confidence: 99%

“…Clinical [1][2][3][4] and experimental [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] analyses have demonstrated that the antenatal administration of corticosteroid results in an acceleration of fetal lung development. Antenatal corticosteroid treatment has been shown to influence surfactant synthesis, the formation of connective tissue, and the antioxidant enzymes in fetal lungs .…”

Section: Introductionmentioning

confidence: 99%

Effect of maternal dexamethasone treatment on the type II pneumocytes in hypoplastic lung by oligohydramnios: an ultrastructural study

et al. 2007

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A previous study documented the effects of maternal corticosteroid treatment on structural growth and functional development in fetal lungs associated with pathogenic conditions such as oligohydramnios using immunohistochemical and morphometric analyses. The purpose of the present study was to examine the effect of maternal dexamethasone treatment the expression of lamellar body in type II pneumocytes of the fetal rabbit lungs with hypoplasia induced by oligohydramnios using electron microscopy. Using an amniotic shunting rabbit model, pregnant rabbits were injected intravenously with either 0.1 ml of saline or 0.25 mg/kg/day of dexamethasone in 0.1 ml of saline 48 and 24 h before the delivery of fetuses, at day 30 of gestation. The number of lamellar bodies per type II pneumocyte was counted in each group using electron micrographs. The number of lamellar bodies per type II pneumocyte in the lungs of the shunted group that received saline was consistently and significantly less than that of the other three groups (5.49 +/- 2.07 vs. 7.34 +/- 2.27: shunted group that received dexamethasone, 7.58 +/- 2.08: non-shunted group that received saline, 7.79 +/- 1.90: non-shunted group that received dexamethasone; P < 0.01). These results suggest that maternal dexamethasone treatment accelerates the maturation of the surfactant system, especially the expression of lamellar bodies in type II pneumocytes, even in hypoplastic lungs induced by oligohydramnios.

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“…Nevertheless, such a risk dramatically increases when this preventive administration cannot be performed at the due time when an emergency delivery procedure is already in progress (1,2). Indeed, very low birth weight (VLBW) newborns, whose mothers were not antenatally supplemented with GC, are at the highest risk of early intubation in the delivery room, prolonged mechanical ventilation support, chronic lung disease (CLD), protracted stay in the neonatal intensive care unit (NICU) and hospital, and constitute the majority of the cases at higher risk of neurologic handicap and of ominous neonatal outcome (1)(2)(3)(4)(5).…”

mentioning

confidence: 99%

First intention high-frequency oscillatory and conventional mechanical ventilation in premature infants without antenatal glucocorticoid prophylaxis*

Salvo

Zimmermann

Gavilanes

et al. 2012

Pediatric Critical Care Medicine

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We found that high-frequency oscillatory ventilation in very low birth weight infants without antenatal glucocorticoid prophylaxis reduced the need of ventilatory support, surfactant therapy, and reintubation, and shortened neonatal intensive care unit and hospital stay, thus reducing unit and hospital costs. These data would support the usefulness of first intention high-frequency oscillatory ventilation strategy in managing in a selected population, such as very low birth weight newborns complicated by severe respiratory distress syndrome not antenatally treated with glucocorticoids.

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Antenatal corticosteroid therapy in premature infants

Cited by 29 publications

References 19 publications

Does corticosteroid therapy impact fetal pulmonary artery blood flow in women at risk for preterm birth?

Does corticosteroid therapy impact fetal pulmonary artery blood flow in women at risk for preterm birth?

Effect of maternal dexamethasone treatment on the type II pneumocytes in hypoplastic lung by oligohydramnios: an ultrastructural study

First intention high-frequency oscillatory and conventional mechanical ventilation in premature infants without antenatal glucocorticoid prophylaxis*

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