Acceleration/ejection time ratio in the fetal pulmonary artery predicts fetal lung maturity
Humberto Azpurua, MD; Errol R. Norwitz, MD, PhD; Katherine H. Campbell, MD, MPH; Edmund F. Funai, MD; Christian M. Pettker, MD, MPH; Michael Kleine, RDMS, RVT; Mert O. Bahtiyar, MD; Herbert Malkus, PhD; Joshua A. Copel, MD; Stephen F. Thung, MD
OBJECTIVE: Theaim of this study was to determine whether sonoRESULTS: Twenty-nine subjects met study criteria. The acceleration-time/
graphic fetal pulmonary artery ﬂow velocity waveforms correlate with amniotic ﬂuid biomarkers of fetal lung maturity.
STUDY DESIGN: We studied women with singleton pregnancies un-
dergoing clinically indicated amniocentesis for fetal lung maturity at Yale-New HavenHospital. Fetal pulmonary artery ﬂow velocity measurements, including systolic/diastolic ratio, pulsatility index, resistance index, and acceleration-time/ejection-time ratio were obtained using spectral Doppler ultrasound. Pearson’s correlation coefﬁcient was used to determine the association between fetal pulmonary artery ﬂow velocity parameters and the lecithin/sphingomyelin ratio.
ejection-timeratio was inversely correlated with the lecithin/sphingomyelin ratio (r 0.76; P .001). This relationship was maintained after controlling for potential confounders. Other fetal pulmonary artery ﬂow velocity measurements were not associated with the lecithin/sphingomyelin ratio.
CONCLUSION: There is an inverse correlation between the accelera-
tion-time/ejection-time ratio in the fetalpulmonary artery and the amniotic ﬂuid lecithin/sphingomyelin ratio. This suggests that ultrasound evaluation of fetal pulmonary artery blood ﬂow may be a promising new noninvasive technique to evaluate fetal lung maturity. Key words: fetal lung maturity, fetal pulmonary artery ﬂow velocity, lecithin/sphingomyelin ratio, respiratory distress syndrome
Cite this article as: Azpurua H, Norwitz ER,Campbell KH, et al. Acceleration/ejection time ratio in the fetal pulmonary artery predicts fetal lung maturity. Am J Obstet Gynecol 2010;203:40.e1-8.
eonatal respiratory distress syndrome (RDS) refers to respiratory compromise presenting at or shortly after delivery related to a deﬁciency of pulmonary surfactant, a naturally occurring phospholipid required to decrease surface tensionwithin the alveoli to prevent alveolar collapse. Originally described by Avery and Mead in 1959,1 RDS remains a
From the Departments of Obstetrics, Gynecology, and Reproductive Sciences (Drs Azpurua, Norwitz, Campbell, Funai, Pettker, Bahtiyar, Copel, and Thung and Mr Kleine) and Laboratory Medicine (Dr Malkus), Yale University School of Medicine, New Haven, CT.
Presented orally at the 18th WorldCongress on Ultrasound in Obstetrics and Gynecology of the International Society of Ultrasound in Obstetrics and Gynecology, Chicago, IL, August 24-28, 2008. Received July 25, 2009; revised Nov. 5, 2009; accepted Jan. 24, 2010. Reprints not available from the authors. 0002-9378/$36.00 © 2010 Mosby, Inc. All rights reserved. doi: 10.1016/j.ajog.2010.01.075
major cause of neonatal morbidityand mortality. A recent epidemiologic study in the United States estimates that there are 80,000 cases of neonatal RDS each year, resulting in 8500 deaths and hospital costs in excess of $4.4 billion.2 However, not all infants are at equal risk, as the pulmonary system is among the last of the fetal organ systems to become functionally mature.2-5 As such, RDS is primarily, although notexclusively, a disease of premature infants, with an incidence and severity highly dependent on gestational age (GA).2-6 Given the importance of RDS as a cause of neonatal morbidity and mortality, even in late preterm deliveries,7 a number of biochemical tests have been developed to predict the risk of RDS and assist obstetric care providers in delivery timing. These tests, including, among others, the...