Betamimetics in fetal distress: randomised controlled trial. Effect of dexamethasone and betamethasone on fetal heart rate variability in preterm labour: a randomised study. Antenatal corticosteroid therapy and fetal behaviour: a randomised study of the effects of betamethasone and dexamethasone. A randomized, placebo-controlled trial of betamethasone for the prevention of respiratory distress syndrome at 24 to 28 weeks' gestation. Results of a double-blind controlled study on the use of betamethasone in the prevention of respiratory distress syndrome. Randomized trial of a single repeat dose of prenatal betamethasone treatment in imminent preterm birth. The effect of betamethasone and dexamethasone on fetal heart rate patterns and biophysical activities. A prospective randomized trial. A randomized, controlled trial of antepartum thyrotropin-releasing hormone and betamethasone in the prevention of respiratory disease in preterm infants. A multicenter controlled trial of fetal pulse oximetry in the intrapartum management of nonreassuring fetal heart rate patterns.
The objective of the study was to investigate if a single dose of Hexoprenaline administered to patients diagnosed as having fetal distress improves neonatal outcome and whether there are any side effects and complications related to hexoprenaline injection. Patients with fetal distress diagnosed by electronic fetal heart rate monitoring with a gestational age of 35 weeks or more in active labor were eligible. Once the decision to deliver the patient by Cesarean section was made, patients were approached and randomised by sealed opaque envelopes to hexoprenaline or control groups. Ten micrograms of hexoprenaline were administered intravenously to study patients. Main outcomes were cord blood gas values, Apgar scores, the need for resuscitation and admission to intensive care. There were no statistically significant differences in the main outcome measures between the two groups. Fewer babies in the hexoprenaline group had a pH of < 7.2 and a base excess of < -10, but this was not statistically significant. The fetal heart rate pattern was improved in significantly more patients after hexoprenaline administration than controls. In conclusion, despite the statistically significant improvement in fetal heart rate tracings, Apgar scores and blood gas values showed only a trend towards improvement in the hexoprenaline group. To compare the effects of betamethasone and dexamethasone on fetal heart rate in appropriately grown fetuses.
                Eighty-two pregnant women (97 fetuses) with preterm labour were randomly allocated to receive betamethasone (n=42) or dexamethasone (n=40) for fetal lung maturation in a nonblinded fashion. Computerised cardiotocogram (CTG) parameters were compared before, during and after treatment.
                A decrease in fetal heart rate variability was found with betamethasone but no significant changes were found with dexamethasone. Fetal heart rate variability returned to pre-treatment values within a week after cessation of treatment with betamethasone. Neonatal outcome was similar in the two groups.
                These findings might prove useful in the management of compromised fetuses with decreased fetal heart rate variability in which the CTG should be used together with other parameters to assess fetal wellbeing during corticosteroid treatment. Dexamethasone may be preferable as the drug of choice since it was associated with significantly less alteration in fetal heart rate variability compared with betamethasone. To compare the effects of maternal betamethasone and dexamethasone administration on fetal behaviour and fetal heart rate variation.
                A prospective randomised study of 60 women at increased risk of preterm delivery.
                Fetal heart rate and its variation, the incidence of fetal body and breathing movements.
                Obstetric unit, University Hospital, Utrecht, The Netherlands.
                Following maternal betamethasone administration (day 2), fetal heart rate variation was reduced by 19% and fetal body and breathing movements by 49% and 85%, respectively. After dexamethasone treatment there was a significant increase in short term fetal heart rate variation (24%) on day 1. All values returned to baseline on day 4, indicating that no fetal deterioration had occurred during the course of the study period.
                Betamethasone, with probably the greater beneficial effect, has more effects on fetal behaviour and fetal heart rate variation than dexamethasone. When assessing fetal condition, due account needs to be taken of these effects. Previous randomized controlled studies of corticosteroids for the reduction of respiratory distress syndrome have failed to demonstrate benefit in very early premature gestational age groups. A randomized, double-blind, placebo-controlled clinical trial of betamethasone given to mothers with intact membranes and threatened premature delivery between 24 and 28 weeks of pregnancy was conducted. Thirty-six patients were randomized to receive betamethasone, two doses of 12 mg, 24 hours apart, and 41 received placebo. No difference was found in the overall incidence of respiratory distress syndrome between the two groups (betamethasone vs placebo 0.55 vs 0.66) or in the incidence of respiratory distress syndrome in babies delivered between 1 and 7 days after the first dose of drug (betamethasone vs placebo 0.78 vs 0.88). Nor were there any differences observed in any measure of severity of respiratory distress syndrome between the groups. The neonatal death rates were also similar (betamethasone vs placebo 0.25 vs 0.24). The only difference seen was an unexpected reduction in the betamethasone group in the incidence of grades 3 and 4 intraventricular hemorrhage (betamethasone vs placebo 1/31 vs 9/36, p = 0.01). Therefore this study was unable to demonstrate any beneficial effect of corticosteroids in reducing respiratory distress syndrome at less than 28 weeks' gestation in spite of a sample size that had an 80% likelihood of detecting a 50% reduction in the incidence of respiratory distress syndrome with p = 0.05, which is the minimum reduction seen in virtually all randomized trials in other gestational age groups. A double-blind controlled study on the prenatal use of betamethasone in the prevention of respiratory distress syndrome (RDS) was carried out on 137 patients from 24 to 34 weeks' gestation. The incidence of RDS was less in the treated group (5%) than in control group (17%). The neonatal mortality rate was lower in the treated group (5%) than in the control group (18%) due to an excess of neonatal deaths in the placebo group. A single dose of prenatal betamethasone treatment decreases neonatal morbidity rates when administered within 7 days before preterm delivery. A single repeat dose or booster dose of betamethasone before delivery has been proposed to be effective, but its efficacy has not been subjected to a randomized, blinded trial.
                Women with imminent delivery before 34.0 gestational weeks were eligible if they remained without delivery for >7 days after a single course of betamethasone. After stratification, a single repeat dose of betamethasone (12 mg) or placebo was administered. The primary outcome was survival without respiratory distress syndrome or severe intraventricular hemorrhage (grade 3 or 4).
                A total of 249 mothers had been enrolled by the time the study was discontinued. All of the 159 infants in the betamethasone group and 167 in the placebo group were born before 36 weeks of gestation. The intact survival rate was unaffected and was lower than anticipated, because the gestational age-adjusted incidence of respiratory distress syndrome was higher than the population incidence. The requirement for surfactant therapy in respiratory distress syndrome was increased in the betamethasone group. According to posthoc analysis of the data for 206 infants who were delivered within 1 to 24 hours, the betamethasone booster tended to increase the risk of respiratory distress syndrome and to decrease intact survival rates.
                According to this study, a single booster dose of betamethasone just before preterm birth may perturb respiratory adaptation. These results caution against uncontrolled use of a repeat dose of glucocorticoid in high-risk pregnancies. BACKGROUND; Contradictory findings on the effect of betamethasone versus dexamethasone on antenatal tests of fetal well-being have been reported. The purpose of this study was to compare the effects of these steroid compounds on fetal heart rate patterns and biophysical activities in a prospective. randomized trial.
                Forty-six pregnant women (gestational age range 27-34 weeks) at risk for preterm delivery were randomized to receive betamethasone or dexamethasone for enhancement of fetal lung maturity. Fetal heart rate was recorded for 60 minutes and analyzed with the Sonicaid System 8000 before (0 hours), and 48 hours and 96 hours after steroid administration. Subsequently, fetal limb, body and breathing movements were sonographically observed and quantified for 30 minutes. To account for fetal circadian rhythms, all examinations were performed between 1 p.m. and 5 p.m., at least one hour after maternal meals.
                Fetal heart rate accelerations (p<0.001; p<0.01), short-term variation (p<0.0001; p<0.05), long-term variation (p<0.01; p=NS), duration of high episodes (p<0.001; p<0.05), total movement count (p<0.001; p<0.05), and duration of breathing time (p<0.0001; p<0.0001) were substantially reduced 48 h after betamethasone and dexamethasone administration, respectively, with percent reduction being larger for the betamethasone group, except for breathing movements (p<0.05; p<0.001; p<0.001; p<0.005; p<0.05; p=NS; respectively). In 68.2%( and 45.5% of fetuses, less than 30 seconds of continuous breathing movements were found in the betamethasone and dexamethasone groups, respectively. In 71.8% and 12.5%, of fetuses, respectively, less than 2 body/limb movements were observed. Therefore five and two fetuses in the betamethasone and dexamethasone study group, respectively, had both nonreactive fetal heart rate monitors for 60 minutes and biophysical profiles of < or =4/10. All parameters returned to baseline values at 96 h. Baseline fetal heart rate and numbers of decelerations remained unchanged (p=NS).
                Both betamethasone and dexamethasone induce a profound, albeit transient, suppression of fetal heart rate characteristics and biophysical activities in the preterm fetus. However, the effect of betamethasone is more pronounced. Awareness of these phenomena might prevent unwarranted iatrogenic delivery of preterm fetuses. The objective was to investigate whether the addition of thyrotropin-releasing hormone to antepartum betamethasone further reduces the incidence of respiratory disease in preterm infants.
                A randomized, placebo-controlled, double-blind trial of antepartum thyrotropin-releasing hormone (400 micrograms given intravenously four times) and betamethasone (5 mg given intramuscularly four times) was conducted in 378 mothers likely to be delivered between 24 and 32.6 weeks' gestation. Statistical analysis was by relative risk, chi 2, t tests, and multiple logistic regression analysis.
                Four hundred five live-born infants were delivered. In infants without lethal abnormalities delivered between 24 hours and 10 days from entry (n = 175) the incidence of respiratory distress syndrome was reduced from 52% to 31% (relative risk 0.61, 95% confidence interval 0.41 to 0.89) and that of severe respiratory distress syndrome from 42% to 20% (relative risk 0.48, 95% confidence interval 0.29 to 0.78) in the placebo and thyrotropin-releasing hormone groups, respectively. The number of deaths fell from 14 to one (relative risk 0.08, 95% confidence interval 0.01 to 0.63). The incidence of chronic lung disease was not significantly different, but that of an adverse outcome (chronic lung disease or death by 36 weeks' gestation) fell from 29% in the placebo group to 16% with thyrotropin-releasing hormone (relative risk 0.55, 95% confidence interval 0.31 to 0.99).
                The addition of thyrotropin-releasing hormone to antepartum glucocorticoid treatment reduces the incidence of respiratory distress syndrome and improves survival in preterm infants. Recent developments permit the use of pulse oximetry to evaluate fetal oxygenation in labor. We tested the hypothesis that the addition of fetal pulse oximetry in the evaluation of abnormal fetal heart rate patterns in labor improves the accuracy of fetal assessment and allows safe reduction of cesarean deliveries performed because of nonreassuring fetal status.
                A randomized, controlled trial was conducted concurrently in 9 centers. The patients had term pregnancies and were in active labor when abnormal fetal heart rate patterns developed. The patients were randomized to electronic fetal heart rate monitoring alone (control group) or to the combination of electronic fetal monitoring and continuous fetal pulse oximetry (study group). The primary outcome was a reduction in cesarean deliveries for nonreassuring fetal status as a measure of improved accuracy of assessment of fetal oxygenation.
                A total of 1010 patients were randomized, 502 to the control group and 508 to the study group. There was a reduction of >50% in the number of cesarean deliveries performed because of nonreassuring fetal status in the study group (study, 4. 5%; vs. control, 10.2%; P =.007). However, there was no net difference in overall cesarean delivery rates (study, n = 147 [29%]; vs. control, 130 [26%]; P = .49) because of an increase in cesarean deliveries performed because of dystocia in the study group. In a blinded partogram analysis 89% of the study patients and 91% of the control patients who had a cesarean delivery because of dystocia met defined criteria for actual dystocia. There was no difference between the 2 groups in adverse maternal or neonatal outcomes. In terms of the operative intervention for nonreassuring fetal status, there was an improvement in both the sensitivity and the specificity for the study group compared with the control group for the end points of metabolic acidosis and need for resuscitation.
                The study confirmed its primary hypothesis of a safe reduction in cesarean deliveries performed because of nonreassuring fetal status. However, the addition of fetal pulse oximetry did not result in an overall reduction in cesarean deliveries. The increase in cesarean deliveries because of dystocia in the study group did appear to result from a well-documented arrest of labor. Fetal pulse oximetry improved the obstetrician's ability to more appropriately intervene by cesarean or operative vaginal delivery for fetuses who were actually depressed and acidotic. The unexpected increase in operative delivery for dystocia in the study group is of concern and remains to be explained.
Betamimetic therapy appears to be able to reduce the number of fetal heart rate abnormalities and perhaps reduce uterine activity. However, there is not enough evidence based on clinically important outcomes to evaluate the use of betamimetics for suspected fetal distress.