| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
ORIGINAL RESEARCH |
From the Departments of Obstetrics, Gynecology and Reproductive Medicine, and The Department of Pediatrics, State University of New York at Stony Brook, Stony Brook, New York.
Address reprint requests to: Andrew Elimian, MD, Division of Maternal Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Medicine, State University of New York at Stony Brook, Health Science Center, T9-030, Stony Brook, NY 11794-8091; E-mail: aelimian{at}notes.cc.sunysb.edu.
 |
ABSTRACT |
|---|
TOP
 ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
METHODS: We studied consecutive neonates born at 23–34 weeks’ gestation between January 1, 1998, and July 31, 2002. The study population was divided into a group exposed to one 12-mg dose of betamethasone before delivery and a non–corticosteroid-exposed group, which were compared for various perinatal outcome variables. The Student t test, 
2, Fisher exact tests, and logistic regression were used for analysis.
RESULTS: One hundred twenty-five neonates (55.6%) were exposed to one 12-mg dose of betamethasone before delivery, whereas 104 neonates (45.4%) did not receive antenatal corticosteroids. Mean gestational age at delivery (28.4 ± 3.1 weeks versus 29.7 ± 3.5 weeks, P = .002) and birth weight (1189 ± 409 g versus 1289 ± 441 g, P = .07) were lower among the steroid-exposed group. Adjusting for gestational age, one dose of betamethasone was associated with significant reduction in the need for vasopressors (odds ratio [OR] 0.35; 95% confidence interval [CI] 0.14, 0.85; P = .02), the rate of intraventricular hemorrhage (OR 0.42; 95%CI 0.19, 0.92; P = .03), and neonatal death (OR 0.31; 95% CI 0.11, 0.86; P = .02). There were no differences between groups in the rate of clinical and histological chorioamnionitis, low Apgar scores, postnatal surfactant exposure, respiratory distress syndrome, bronchopulmonary dysplasia, necrotizing enterocolitis, patent ductus arteriosus, retinopathy of prematurity, and neonatal sepsis.
CONCLUSION: An incomplete course of antenatal corticosteroids is associated with reduction in the need for vasopressors, the rate of intraventricular hemorrhage, and neonatal death in preterm neonates.
Antenatal corticosteroids decrease the risk of respiratory distress syndrome (RDS), intraventricular hemorrhage, and neonatal death in preterm neonates.1–8 These benefits are reportedly seen 24 hours after administration of corticosteroids and persist for at least 7 days after treatment.1 However, there are circumstances where delivery becomes inevitable or is undertaken before a 24-hour interval for both maternal and fetal indications. There are few data on the perinatal effects of antenatal corticosteroids in this circumstance.9 Our objective was to assess the effectiveness of an incomplete course of antenatal corticosteroids on perinatal morbidity and mortality.
|
MATERIALS AND METHODS |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Preterm labor with intact membranes was diagnosed in the presence of six to eight contractions per hour or four contractions in 20 minutes associated with cervical changes but with no prelabor rupture of membranes. Premature rupture of membranes was documented by pooling of fluid on sterile speculum examination, the microscopic appearance of ferning on dry smear, and alkaline pH by a phenaphthazine pH indicator paper used with fluid obtained from the posterior vaginal fornix. Gestational age was estimated by using the last menstrual period confirmed by ultrasonography performed in the first 20 weeks of pregnancy.
Respiratory distress syndrome was diagnosed clinically by the need for mechanical ventilation and oxygen for at least 48 hours in the presence of radiographic chest findings (air bronchograms and reticulogranular appearance of the pulmonary parenchyma). Bronchopulmonary dysplasia was defined as oxygen dependency at 28 days of life or more. Each neonate had transfontanelle head ultrasonographic scans on days 3 and 7 of life and subsequent head ultrasonograms as indicated. Neurosonograms were evaluated by an experienced sonographer unaware of the antenatal steroid exposure status of the parturient. Intraventricular hemorrhage was graded as described by Papile et al.10 Necrotizing enterocolitis was diagnosed clinically and radiographically and was confirmed at surgery or autopsy. Neonatal sepsis was defined by positive blood or cerebrospinal fluid cultures. A low Apgar score was defined as a score of less than 7 at 5 minutes of life. Histological chorioamnionitis was diagnosed using criteria described by Salafia et al.11 Tissue samples included sections of umbilical cord, chorionic plate, and a roll of membranes that extended from an area of membrane rupture to the margin of the placenta. Tissue blocks were fixed with 10% formalin and embedded in paraffin. Sections of tissue blocks were stained with hematoxylin–eosin and read by a perinatal pathologist who was masked to clinical courses of patients. The presence of five or more polymorphonuclear leukocytes in any tissue qualified as positive for histological chorioamnionitis. Clinical chorioamnionitis was diagnosed in the presence of a maternal temperature of at least 37.8C plus at least two of the following criteria: 1) uterine tenderness, 2) malodorous vaginal discharge, 3) maternal leukocytosis (white blood cell count of more than 15,000 cells/mm3, and 4) fetal tachycardia (more than 160 beats per minute).
The distributional characteristics of the variables were examined. Continuous data were normally distributed (Kolmogorov–Smirnov goodness of fit). As such, differences between groups defined by exposure to an incomplete course of antenatal corticosteroids were examined using the Student t test for continuous variables. The 2 test was used to examine categoric data. The Fisher exact test was used when expected cell frequencies were five or less. Logistic regression was used to examine the influence of an incomplete course of antenatal corticosteroids on selected outcomes, adjusting for gestational age. All tests of significance were two sided at a critical level of P < .05.
|
RESULTS |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
On univariate analysis, there were no differences between groups in the rate of clinical and histological chorioamnionitis, low Apgar scores, postnatal surfactant exposure, and the need for vasopressor therapy in the immediate neonatal period. In addition, there were no differences between groups in the rate of RDS, intraventricular hemorrhage, necrotizing enterocolitis, patent ductus arteriosus, retinopathy of prematurity, neonatal sepsis, and neonatal death. However, the rate of bronchopulmonary dysplasia was significantly higher in the steroid-exposed group (46 of 125, 36.8%) relative to the non–corticosteroid-exposed group (17 of 104, 16.3%) (P = .001) (Table 1
).
|
), exposure to one dose of betamethasone before delivery was significantly associated with reductions in the need for vasopressors (odds ratio [OR] 0.35; 95% CI 0.14, 0.85; P = .02), in the rate of intraventricular hemorrhage (OR 0.42; 95% CI 0.19, 0.92; P = .03), and in the rate of neonatal death (OR 0.31; 95% CI 0.11, 0.86; P = .02) relative to the non–steroid-exposed group. There were no differences between groups in the rate of clinical and histological chorioamnionitis, low Apgar scores, postnatal surfactant exposure, RDS, bronchopulmonary dysplasia, necrotizing enterocolitis, patent ductus arteriosus, retinopathy of prematurity, and neonatal sepsis.
|
|
DISCUSSION |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
One interesting finding in the incompletely treated group was the appearance of a higher rate of bronchopulmonary dysplasia relative to the untreated group on univariate analysis. This probably reflects the greater degree of lung immaturity in the group exposed to one dose of steroid. There was an approximately 1.5-week average gestational age difference that may have affected bronchopulmonary dysplasia outcome. This was confirmed by controlling for gestational age with logistic regression. Also, by defining bronchopulmonary dysplasia as an oxygen requirement at 28 days of life, the greater immaturity of the incompletely treated group may have artificially increased the rate of bronchopulmonary dysplasia.
Overall, the results of this study indicate that even an incomplete course of antenatal glucocorticoids appears to favorably influence neonatal outcome with respect to several of the most critical complications of neonatal intensive care. The clinician should strongly consider the administration of even a single dose of betamethasone to a mother in danger of imminent delivery.
|
Footnotes |
|---|
Received January 17, 2003. Received in revised form March 4, 2003. Accepted March 13, 2003.
|
REFERENCES |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
2. Block MF, Kling OR, Crosby WM. Antenatal glucocorticoid therapy for the prevention of respiratory distress syndrome in the premature infant. Obstet Gynecol 1977; 50:186–90.
3. Taeusch HW, Frigoletto F, Kitzmiller J, Avery ME, Hehre A, Fromm B, et al. Risk of respiratory distress syndrome after prenatal dexamethasone treatment. Pediatrics 1979; 63:64–72.
4. Doran TA, Swyer P, MacMurray B, Mahon W, Enhorhing G, Bernstein A, et al. Results of a double-blind controlled study on the use of betamethasone in the prevention of respiratory distress syndrome. Am J Obstet Gynecol 1980;136:313–20.[Medline]
5. Collaborative Group on Antenatal Steroid Therapy. Effect of antenatal dexamethasone administration on prevention of respiratory distress syndrome. Am J Obstet Gynecol 1981;141:276–87.[Medline]
6. Gamsu HR, Mullinger BM, Donnai P, Dash CH. Antenatal administration of betamethasone to prevent respiratory distress syndrome in preterm infants: Report of a UK multicentre trial. Br J Obstet Gynaecol 1989;96:401–10.[Medline]
7. National Institutes of Health. Report of the Consensus Development Conference on the effect of corticosteroids for fetal maturation on perinatal outcomes. National Institute of Child Health and Human Development. NIH publication no. 95-3784. Bethesda, Maryland: National Institutes of Health, 1994.
8. Gardner MO, Papile LA, Wright LL. Antenatal corticosteroids in pregnancies complicated by preterm premature rupture of membranes. Obstet Gynecol 1997;90:851–3.[Abstract]
9. Crowley P, Chalmers I, Keirse MJ. The effects of corticosteroid administration before preterm delivery: An overview of the evidence from controlled trials. Br J Obstet Gynaecol 1990;97:11–25.[Medline]
10. Papile LA, Burstein J, Koffier H. Incidence and evolution of subependymal and intraventricular hemorrhage: A study of infants with birthweights less than 1500 gm. J Pediatr 1978;92:529–34.[Medline]
11. Salafia CM, Weigl C, Silberman L. The prevalence and distribution of acute placental inflammation in uncomplicated term pregnancies. Obstet Gynecol 1989;73:383–9.
12. Demarini S, Dollberg S, Hoath SB, Ho M, Donovan EF. Effects of antenatal corticosteroids on blood pressure in the very low birth weight infants during the first 24 hours of life. J Perinatol 1999;19:419–25.[Medline]
13. Canterino JC, Verma U, Visintainer PF, Elimian A, Klein SA, Tejani N. Antenatal steroids and neonatal periventricular leukomalacia. Obstet Gynecol 2001;97:135–9.
This article has been cited by other articles:
|
|
 |
|
  X. Qiu, S. K. Lee, K. Tan, B. Piedboeuf, R. Canning, and for the Canadian Neonatal Network Comparison of Singleton and Multiple-Birth Outcomes of Infants Born at or Before 32 Weeks of Gestation Obstet. Gynecol., February 1, 2008; 111(2): 365 - 371. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Holzman, X. Lin, P. Senagore, and H. Chung Histologic Chorioamnionitis and Preterm Delivery Am. J. Epidemiol., October 1, 2007; 166(7): 786 - 794. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. M. Peltoniemi, M. A. Kari, O. Tammela, L. Lehtonen, R. Marttila, E. Halmesmaki, P. Jouppila, M. Hallman, and for the Repeat Antenatal Betamethasone Study Group Randomized Trial of a Single Repeat Dose of Prenatal Betamethasone Treatment in Imminent Preterm Birth Pediatrics, February 1, 2007; 119(2): 290 - 298. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L F J Mildenhall, M R Battin, S M B Morton, C Bevan, C A Kuschel, and J E Harding Exposure to repeat doses of antenatal glucocorticoids is associated with altered cardiovascular status after birth Arch. Dis. Child. Fetal Neonatal Ed., January 1, 2006; 91(1): F56 - F60. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
