Intrauterine stimulation for fetal respiratory system maturation; benefits and risks
Kinalski, M.; Sledziewski, A.; Kretowski, A.
Wiadomosci Lekarskie 53(9-10): 538-545
2000
ISSN/ISBN: 0043-5147 PMID: 11148922 Document Number: 515460
The use of perinatal steroid therapy, first introduced in 1972 is effective in precocious maturation of human lungs. Antenatal corticosteroid therapy results in reduction of fetal mortality, respiratory distress syndrome, intraventricular hemorrhage in preterm babies. These benefits extend to a broad range of gestational age. They comprise the interval between 24 and 34 weeks of human pregnancy and are not limited by the infant's gender or race. The beneficial effects of corticosteroids are the best pronounced after more than 24 hours from the beginning of the treatment. Noteworthy is that therapy less than 24 hours of duration may also improve outcomes. In the presence of premature rupture of membranes, or better with intact membranes, antenatal corticosteroids reduce frequency of RDS, IVH and finally mortality and morbidity. Review of meta-analyses based on randomized trials supports general option that premature infants whose mothers received corticosteroids before delivery are less likely to develop RDS and its complications. Recent data showed that benefits derived from ANS are additive to those of surfactant therapy, rendering the latter more effective. Followup of children up to 12 years of age indicate that ANS do not impair physical growth or psychomotor development. Short-term adverse effects including maternal infection, maternal pulmonary edema were not clearly demonstrated. Pulmonary edema has not been reported when ANS were used alone (i.e. not in combination with betamimetic tocolytics). No long-term unwanted effects on maternal adrenal function have been observed. There is no serious maternal risk resulting from immunosuppressive effect of corticosteroid therapy on maternal immune system. Although glucocorticoid therapy is likely to provoke insulin resistance, and thereby deterioration in diabetic control, and potentially causes cortisol resistance in the fetal lung, the results of scarce randomized trials are not conclusive. In any rate strict control of maternal diabetes mellitus reduces incidence of RDS. Current available data are not indicative of higher risk of fetal mortality in association with maternal hypertensive disease and ANS. In conclusion, most randomized trials of ANS has provided a positive evidence of efficacy and safety of this highly cost effective therapy in most common clinical situations. However, further trials and more precise estimates are justified on ANS treatment specifically related to blood glucose control and evidence concerning the promotion of fetal lung maturity in babies of women with diabetes mellitus. Although benefits of the corticosteroid therapy are beyond any doubts, more experience is needed to assess the effect of ANS on maternal and/or fetal infection in presence of premature rupture of membranes. And finally, further assessments are required on antenatal corticosteroids with dose regimens in patients with multifetal gestation, more common after wide use of techniques of the assisted human reproduction.