Objective. Abnormal umbilical artery Doppler (UAD) studies are associated with poor neonatal outcomes. We sought to determine if postnatal measures of systemic blood flow (SBF), as measured by functional echocardiography (fECHO), could identify which fetuses with abnormal UAD were at the highest risk of adverse outcomes. Study Design. This is a retrospective review of fetuses with abnormal UAD who received fECHO in the first 72 hours of life. Measures of SBF (right ventricular output (RVO) and superior vena cava (SVC) flow) were performed and compared with prenatal variables and postnatal outcomes. Result. 63 subjects had abnormal UAD, 20 of which also had fECHO. Six subjects had abnormal flow. Gestational age at delivery was similar between the two groups. Those with abnormal SBF had fewer days of abnormal UAD prior to delivery and developed RDS ( ). Conclusion. Postnatal measures of SBF were associated with poor postnatal outcomes in fetuses with abnormal UAD. Future studies incorporating antenatal measures of SBF may help obstetricians determine which pregnancies complicated by UAD are likely to have postnatal morbidity. 1. Introduction Abnormal fetal umbilical artery Doppler (UAD) studies represent a problem that is complex in both antenatal prevention and management and postnatal management [1]. In particular, absent and reversed end-diastolic flow of the fetal umbilical arteries are associated with poor neonatal outcomes, ranging from premature delivery and stillbirth to postnatal neurodevelopmental impairment [2] and diseases such as obesity and hypertension later in life [2]. Reversed end-diastolic flow (REDF) is the most advanced stage of abnormal umbilical artery Doppler flow and represents obliteration of nearly 70% of the placental function [3]. REDF also represents a higher risk of NICU admission, need for respiratory support, and perinatal mortality, regardless of age at delivery [4]. As placental function declines, the changes noted in fetal venous Doppler studies represent major changes in the fetal circulation in response to hypoxia. The increase in placental resistance leads to an obliteration of small muscular placental arteries, which leads to a decrease in the diastolic flow in the umbilical artery Doppler. The fetus responds with an increase in red blood cell mass and shunting of blood to nonessential vascular beds in order to increase oxygen utilization [5, 6]. This results in preferential cardiac and cerebral blood flow, with reduced blood flow to the rest of the body [7, 8]. As this process continues, the fetal right ventricular
References
[1]
American College of Obstetricians and Gynecologists, “Fetal growth restriction,” Obstetrics & Gynecology, vol. 121, pp. 1122–1133, 2013.
[2]
A. K. Ertan, H. A. Tanriverdi, A. Stamm, W. Jost, J. Endrikat, and W. Schmidt, “Postnatal neuro-development of fetuses with absent end-diastolic flow in the umbilical artery and/or fetal descending aorta,” Archives of Gynecology and Obstetrics, vol. 285, pp. 1547–1552, 2012.
[3]
J. C. P. Kingdom, S. J. Burrell, and P. Kaufmann, “Pathology and clinical implications of abnormal umbilical artery Doppler waveforms,” Ultrasound in Obstetrics and Gynecology, vol. 9, no. 4, pp. 271–286, 1997.
[4]
R. P. Vasconcelos, J. R. Brazil Frota Arag？o, F. H. Costa Carvalho, R. M. Salani Mota, F. E. De Lucena Feitosa, and C. A. Alencar Júnior, “Differences in neonatal outcome in fetuses with absent versus reverse end-diastolic flow in umbilical artery doppler,” Fetal Diagnosis and Therapy, vol. 28, no. 3, pp. 160–166, 2010.
[5]
K. M. Chalubinski, A. Repa, M. Stammler-Safar, and J. Ott, “Impact of Doppler sonography on intrauterine management and neonatal outcome in preterm fetuses with intrauterine growth restriction,” Ultrasound in Obstetrics and Gynecology, vol. 39, no. 3, pp. 293–298, 2012.
[6]
A. A. Baschat, U. Gembruch, and C. R. Harman, “The sequence of changes in Doppler and biophysical parameters as severe fetal growth restriction worsens,” Ultrasound in Obstetrics and Gynecology, vol. 18, no. 6, pp. 571–577, 2001.
[7]
K. Hecher and B.-J. Hackel？er, “Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations,” Ultrasound in Obstetrics and Gynecology, vol. 9, no. 3, pp. 152–161, 1997.
[8]
E. Ferrazzi, M. Bozzo, S. Rigano et al., “Temporal sequence of abnormal Doppler changes in the peripheral and central circulatory systems of the severely growth-restricted fetus,” Ultrasound in Obstetrics and Gynecology, vol. 19, no. 2, pp. 140–146, 2002.
[9]
A. A. Baschat, “Fetal responses to placental insufficiency: an update,” BJOG: An International Journal of Obstetrics and Gynaecology, vol. 111, no. 10, pp. 1031–1041, 2004.
[10]
A. A. Baschat, “Fetal growth restriction—from observation to intervention,” Journal of Perinatal Medicine, vol. 38, no. 3, pp. 239–246, 2010.
[11]
M. Kluckow and N. Evans, “Low superior vena cava flow and intraventricular haemorrhage in preterm infants,” Archives of Disease in Childhood, vol. 82, no. 3, pp. F188–F194, 2000.
[12]
R. W. Hunt, N. Evans, I. Rieger, and M. Kluckow, “Low superior vena cava flow and neurodevelopment at 3 years in very preterm infants,” Journal of Pediatrics, vol. 145, no. 5, pp. 588–592, 2004.
[13]
D. A. Osborn, N. Evans, M. Kluckow, J. R. Bowen, and I. Rieger, “Low superior vena cava flow and effect of inotropes on neurodevelopment to 3 years in preterm infants,” Pediatrics, vol. 120, no. 2, pp. 372–380, 2007.
[14]
N. Evans and M. Kluckow, “Superior vena cava flow in newborn infants: a novel marker of systemic blood flow,” Archives of Disease in Childhood, vol. 82, no. 3, pp. F182–F187, 2000.
