Chronic Fetal Stress and the Risk of Infant Respiratory Distress Syndrome

The relationship between five conditions of chronic fetal stress and the incidence of infant respiratory distress syndrome (RDS) was investigated among 614 premature (less than or equal to 36 weeks) infants delivered at the University of Washington Hospital from 1977 to 1980. The strongest associati...

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Veröffentlicht in:Obstetrics and gynecology (New York. 1953) 1986-01, Vol.67 (1), p.57-62
Hauptverfasser: WHITE, EMILY, SHY, KIRK K., BENEDETTI, THOMAS J.
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Sprache:eng
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Zusammenfassung:The relationship between five conditions of chronic fetal stress and the incidence of infant respiratory distress syndrome (RDS) was investigated among 614 premature (less than or equal to 36 weeks) infants delivered at the University of Washington Hospital from 1977 to 1980. The strongest association found was a protective effect of abnormal antepartum testing (nonreactive nonstress test, positive contraction stress test, or low or falling maternal urinary estriols). Among the 45 infants with abnormal antepartum testing, the probability of RDS was 15.0 versus 33.8% for the infants without the complication (odds ratio = 0.35, P ≤ .01, adjusted for gestational age and mode of delivery). Rupture of the membranes for greater than 24 hours (N = 151), amnionitis (N = 63), and vaginal bleeding beginning more than 24 hours before delivery (N = 108) were each associated with a reduced risk of RDS (adjusted odds ratios = 0.63, 0.51, and 0.58, respectively, P ≤ .05). Hypertensive disease of pregnancy was not associated with a decreased risk of RDS; in fact, the opposite trend occurred (N = 96, odds ratio = 1.67, P = .07). The associations with RDS were not explained by differences between births with and without each complication in terms of gestational age, mode of delivery, absence of labor, administration of antenatal steroids, and other complications of pregnancy. This study adds support to the hypothesis that certain conditions associated with chronic fetal stress lead to an acceleration in pulmonary maturity.
ISSN:0029-7844
1873-233X