Effect of antenatal betamethasone administration on placental vascular resistance.
BACKGROUND
High placental vascular resistance is an important cause of fetal growth restriction and subsequent perinatal mortality. Identification of affected pregnancies allows appropriate fetal surveillance and delivery, but there are no known therapeutic strategies to decrease resistance and improve blood flow. However, placental corticotropin-releasing hormone (CRH) is thought to be a potent fetoplacental vasodilator, and exogenous corticosteroids can increase placental CRH secretion. Therefore, we examined whether corticosteroids could improve fetoplacental blood flow in pregnancies with increased vascular resistance.


METHODS
A retrospective review of umbilical-artery flow-velocity waveforms (FVWs) before and after betamethasone administration was undertaken in pregnancies with increased placental vascular resistance, as shown by umbilical-artery absent end-diastolic flow (AEDF). FVWs were obtained by pulsed-wave doppler ultrasonography. We studied all 28 pregnancies monitored at the maternal-fetal medicine unit of a university teaching hospital since 1995.


RESULTS
The median duration of gestation at presentation with AEDF was 27 weeks (range 23-33). In 19 (68% [95% CI 49-86]) pregnancies, umbilical-artery diastolic flow returned within 24 h after betamethasone administration, consistent with decreased resistance. The median duration of this effect was 3 days (range 2-7). There were no differences in duration of gestation at diagnosis or delivery, or in birthweight between fetuses showing a return of flow after betamethasone and those not showing a return of flow.


CONCLUSIONS
In pregnancies with umbilical-artery AEDF, betamethasone treatment is associated with decreased placental vascular resistance, possibly induced via increased placental CRH secretion. This study does not provide insights into whether this effect would be beneficial or harmful to the fetus.
Wallace
E M
EM
Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria, Australia. Euan.Wallace@med.monash.edu.au
Baker
L S
LS
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001623:Betamethasone / Q000627:therapeutic use*; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology; D006801:Humans; D008431:Maternal-Fetal Exchange / Q000187:drug effects; D010920:Placenta / Q000098:blood supply* / Q000000981:diagnostic imaging; D011247:Pregnancy; D011263:Pregnancy Trimester, Third / Q000187:drug effects; D012189:Retrospective Studies; D016216:Ultrasonography, Prenatal; D014655:Vascular Resistance / Q000187:drug effects*
D000893:Anti-Inflammatory Agents; D001623:Betamethasone