Injection of corticosteroids into mother to prevent neonatal respiratory distress syndrome

Morrison, John C.; Whybrew, W.D.; Bucovaz, E.T.; Schneider, Jack

doi:10.1016/0002-9378(78)90408-8

Cited by 81 publications

(21 citation statements)

References 24 publications

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“…Block et al (3) and Morrison et al (14) have recently partly confirmed the results of Liggins and Howie (13). Block er al.…”

Section: Speculationmentioning

confidence: 56%

“…The incidence of RDS was significantly reduced in the study of Block et al (3) only when all premature infants were grouped together (including infants up to 37 wk of gestation), whereas Liggins and Howie observed a beneficial effect of betamethasone only in pregnancies lasting 32 wks or less. Morrison et al (14) injected 500 mg hydrocortisone or placebo IV every 12 hr for 48 hr to mothers at risk for premature delivery. They observed a significant reduction of RDS in patients treated with hydrocortisone (at least two injections) when gestation was less than 32 wk.…”

Section: Speculationmentioning

confidence: 99%

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Maternal Glucocorticoid in Unplanned Premature Labor. Controlled Study on the Effects of Betamethasone Phosphate on the Phospholipids of the Gastric Aspirate and on the Adrenal Cortical Function of the Newborn Infant

1980

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SummaryThe effects of betamethasone on surfactant composition and neonatal adrenal function were compared with placebo in a doubleblid study, which included 74 patients at risk for premature delivery. The overall incidence of respiratory distress syndrome was low, and no difference was observed between the betamethasone and placebo groups. The phospholipid pattern (lecithin/sphingomyellin ratio, acetone precipitated lecithin, pbosphatidylinositol/sphingomyelin ratio, and phosphatidylglycerol/sphingomyelin ratio) from gastric aspirates of newborn infants was similru in the betamethasone and placebo groups, suggesting a similarity in lung surfactant. The responsiveness of the adrenal cortex of the newborn infants, evaluated by a 2-hr adrenocorticotropic hormone test at the age of 24 hr, did not differ between infants whose mothers had received either betamethasone or placebo. The low incidence of respiratory distress syndrome in the betamethasone and placebo groups was ascribed in part to a high incidence of prolonged rupture of fetal membranes. Our results do not exclude the possibility that antenatal maternal administration of betamethasone could prevent respiratory distress syndrome in other defined high-risk infants. SpeculationMaternal betamethasone administration does not enhance the acceleration of the fetal lung maturation in "fetal stress" due to rupture of fetal membranes, even if the phospholipids of the lung effluent are somewhat immature. Betamethasone phosphate only transiently suppresses fetal adrenal function. Due to the potential long-term side effects, the use of glucocorticoids should be limited to cases in which the risk to develop respiratory distress syndrome is high and spontaneous acceleration of lung maturation is not expected.Liggins and Howie (13) showed in 1972 that betamethasone administered to the mother prevented respiratory distress syndrome (RDS) in premature infants born before the end of the 32nd pregnancy wk. Block et al. ) injected 500 mg hydrocortisone or placebo IV every 12 hr for 48 hr to mothers at risk for premature delivery. They observed a significant reduction of RDS in patients treated with hydrocortisone (at least two injections) when gestation was less than 32 wk.Potential side effects of glucocorticoid treatment in the perinatal period have been reported in experimental animals and humans [see review by Taeusch (22)). There is suggestive evidence that large doses of glucocorticoids given in the perinatal period to rodents decrease the rate of mitosis and myelinization of the brain, with subsequently impaired motor performance (10, 19). There is also suggestive evidence that mothers with preeclampsia treated with betamethasone may have increased fetal deaths compared with controls (13). It has been shown in the rabbit that glucocorticoids may compromise placental function (25). Whether the dose of glucocorticoids given antenatally for the prevention of RDS has any effect on the development of the human infant is unknown. As long as this information is lacking, it is...

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“…Block et al (3) and Morrison et al (14) have recently partly confirmed the results of Liggins and Howie (13). Block er al.…”

Section: Speculationmentioning

confidence: 56%

Section: Speculationmentioning

confidence: 99%

Maternal Glucocorticoid in Unplanned Premature Labor. Controlled Study on the Effects of Betamethasone Phosphate on the Phospholipids of the Gastric Aspirate and on the Adrenal Cortical Function of the Newborn Infant

1980

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“…LIGGINS and HOWIE [14] first reported the beneficial effect of the maternal administration of antepartum glucocorticoid on the incidence of RDS in premature infants. This has since been confirmed by others [3,5,8,18]. However, attention must be drawn to the possibility of an adverse effect of corticosteroid treatment in cases with hypertensionedema-proteinuria syndromes.…”

Section: Introductionmentioning

confidence: 57%

Intraamniotic Triidothyronine instillation for prevention of respiratory distress syndrome in pregnancies complicated by hypertension

Schreyer¹,

Caspi²,

Letko³

et al. 1982

Journal of Perinatal Medicine

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“…Another group of women in whom corticosteroids is contraindicated comprises those with any kind of infec tion, which might be reactivated or aggravated by cortico steroid therapy [7], A decreased inflammatory response, diminished febrile response, increased risk of infection, enhanced dissemination of infection, and decreased anti body response have all been documented following gluco corticoid administration [8]. Women with premature rup ture of the membranes treated with steroids can acquire an intrauterine infection without a fever or other clinical sign of infection [9], Suidan and Baassiri [10] found that between 28 and 32 weeks gestation, the protective effect against RDS af forded by prenatal treatment with betamethasone is no better than that provided by prolonged rupture of the membranes alone.…”

Section: Discussionmentioning

confidence: 99%

Betamethasone and Intrauterine Fetal Death

Sharony

Oettinger²

1994

Gynecol Obstet Invest

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Three cases of intrauterine fetal death occurring shortly (within 24 h) after betamethasone administration are described. Two of the women were diabetic, and the third had secondary infertility due to hyperprolactinemia. None of the stillborns had evidence of gross malformations. In view of the fact that infants born prematurely now have a better chance of survival in intensive care units than in previous years, we believe that for certain high-risk mothers, the policy of betamethasone administration for preventing respiratory distress syndrome in premature babies must be revised.

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Injection of corticosteroids into mother to prevent neonatal respiratory distress syndrome

Cited by 81 publications

References 24 publications

Maternal Glucocorticoid in Unplanned Premature Labor. Controlled Study on the Effects of Betamethasone Phosphate on the Phospholipids of the Gastric Aspirate and on the Adrenal Cortical Function of the Newborn Infant

Maternal Glucocorticoid in Unplanned Premature Labor. Controlled Study on the Effects of Betamethasone Phosphate on the Phospholipids of the Gastric Aspirate and on the Adrenal Cortical Function of the Newborn Infant

Intraamniotic Triidothyronine instillation for prevention of respiratory distress syndrome in pregnancies complicated by hypertension

Betamethasone and Intrauterine Fetal Death

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