Related Experiment Video
Updated: Feb 18, 2026

Intratracheal Instillation of Stem Cells in Term Neonatal Rats
Published on: May 4, 2020
Mortality and pulmonary outcomes of extremely preterm infants exposed to antenatal corticosteroids
Colm P Travers1, Waldemar A Carlo2, Scott A McDonald1
1Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network, Bethesda, MD.
Insights
Antenatal corticosteroid exposure in extremely preterm infants (22-28 weeks gestation) is linked to reduced mortality rates. However, this exposure did not impact the incidence of bronchopulmonary dysplasia in survivors.
Area of Science:
- Neonatal Medicine
- Perinatology
- Obstetrics
Background:
- Antenatal corticosteroids are administered to promote fetal lung maturation.
- Previous meta-analyses of randomized controlled trials have not demonstrated significant mortality or pulmonary benefits for extremely preterm infants.
- Extremely preterm infants face the highest risks of mortality and pulmonary complications.
Purpose of the Study:
- To investigate the association between antenatal corticosteroid exposure and the rates of death and pulmonary morbidities by 36 weeks' postmenstrual age in extremely preterm infants.
- To evaluate the impact of varying levels of antenatal corticosteroid exposure.
Main Methods:
- Analysis of prospectively collected data from 11,022 infants born between 22 0/7 and 28 6/7 weeks' gestational age (January 2006 - December 2014).
- Outcomes assessed included death and physiologic bronchopulmonary dysplasia by 36 weeks' postmenstrual age.
- Statistical models were adjusted for maternal, infant, center, and epoch variables.
Main Results:
- Infants exposed to any antenatal corticosteroids showed a significantly lower death rate (22.7%) compared to unexposed infants (41.5%) (aRR, 0.71; P < .0001).
- Partial exposure also resulted in a lower death rate (26.0%) versus no exposure (41.5%) (aRR, 0.77; P < .0001).
- Rates of bronchopulmonary dysplasia in survivors were similar across exposure groups; however, death from respiratory distress syndrome, surfactant use, and mechanical ventilation were lower with any antenatal corticosteroid exposure.
Conclusions:
- In extremely preterm infants (22-28 weeks' gestation), antenatal corticosteroid exposure (any or partial) is associated with a reduced rate of mortality.
- The rate of bronchopulmonary dysplasia in surviving infants did not differ based on antenatal corticosteroid exposure.
Background:
Antenatal corticosteroids are given primarily to induce fetal lung maturation but results from meta-analyses of randomized controlled trials have not shown mortality or pulmonary benefits for extremely preterm infants although these are the infants most at risk of mortality and pulmonary disease.
Objective:
We sought to determine if exposure to antenatal corticosteroids is associated with a lower rate of death and pulmonary morbidities by 36 weeks' postmenstrual age.
Study Design:
Prospectively collected data on 11,022 infants 22 0/7 to 28 6/7 weeks' gestational age with a birthweight of ≥401 g born from Jan. 1, 2006, through Dec. 31, 2014, were analyzed. The rate of death and the rate of physiologic bronchopulmonary dysplasia by 36 weeks' postmenstrual age were analyzed by level of exposure to antenatal corticosteroids using models adjusted for maternal variables, infant variables, center, and epoch.
Results:
Infants exposed to any antenatal corticosteroids had a lower rate of death (2193/9670 [22.7%]) compared to infants without exposure (540/1302 [41.5%]) (adjusted relative risk, 0.71; 95% confidence interval, 0.65-0.76; P < .0001). Infants exposed to a partial course of antenatal corticosteroids also had a lower rate of death (654/2520 [26.0%]) compared to infants without exposure (540/1302 [41.5%]); (adjusted relative risk, 0.77; 95% confidence interval, 0.70-0.85; P < .0001). In an analysis by each week of gestation, infants exposed to a complete course of antenatal corticosteroids had lower mortality before discharge compared to infants without exposure at each week from 23-27 weeks' gestation and infants exposed to a partial course of antenatal corticosteroids had lower mortality at 23, 24, and 26 weeks' gestation. Rates of bronchopulmonary dysplasia in survivors did not differ by antenatal corticosteroid exposure. The rate of death due to respiratory distress syndrome, the rate of surfactant use, and the rate of mechanical ventilation were lower in infants exposed to any antenatal corticosteroids compared to infants without exposure.
Conclusion:
Among infants 22-28 weeks' gestational age, any or partial antenatal exposure to corticosteroids compared to no exposure is associated with a lower rate of death while the rate of bronchopulmonary dysplasia in survivors did not differ.
Related Concept Videos
COPD: Management Using Bronchodilators and Corticosteroids
Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids
ICS work through a multifaceted mechanism of action. They suppress the inflammatory response caused by the proliferation of TH cells. They also reduce the transcription of the IL-2 gene, which is involved in the...
Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
Upper Respiratory Drugs: Antitussives, Expectorants, and Mucolytics
Antitussives include codeine, dextromethorphan (Robitussin), and benzonatate (Tessalon). Codeine and dextromethorphan exert their effects centrally by suppressing the cough reflex center in the medulla. Benzonatate operates peripherally within the respiratory tract by...
COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
Teratogenicity

