369: Portal vein Doppler in IUGR fetuses delivered at 32 weeks


      Animal studies have shown increased blood flow through the ductus venosus proportionate to the severity of fetal hypoxia. Although data suggest this also occurs in the human fetus, it has never been demonstrated. The aim of this study was to characterize the portal vein (PV) Doppler, which has a monophasic pattern in normal fetuses, from the time of diagnosis of IUGR to delivery of the fetus.

      Study Design

      Initial assessment with PV Doppler occurred at the time of diganosis of IUGR (EFW<10th percentile and abnormal umbilical artery pulsatility index); the final study occurred within 24 hours of delivery. PV waveforms were correlated to perinatal death or acidemia at birth. Umbilical artery cord pH was evaluated at birth [considered abnormal if the value was <7.10 and/or the base deficit was <-9.0 (2 SD below the mean for preterm neonates)]. Fisher's exact test was used for statistical analysis.


      PV Doppler waveforms were assessed on 69 occasions in 14 IUGR fetuses (median: 4 studies; range: 2-10). The median gestational age (GA) at the time of the first study was 26.6 weeks (range: 21.6-30.1 weeks) and at the last study was 28.4 weeks (range: 25-31.6 weeks). Three distinct and progressive Doppler patterns were observed: a) monophasic; b) biphasic; and, c) reversed flow. 86% of the PV Dopplers were monophasic and 14% were biphasic at the 1st examination. Of those that were biphasic, 100% progressed to reversed flow. 50% of those that were monophasic progressed to biphasic and 33% of those progressed to reversed flow. Five fetuses had an adverse perinatal outcome: 3 IUFDs and 2 fetuses who were acidemic at birth. All 5 fetuses had either biphasic (n=2) or reversed flow (n=3) patterns. Among the other 9 fetuses, 7 had monophasic and 2 had biphasic patterns (p<0.05).


      Our study indicates that in IUGR fetuses, PV biphasic or reversed flow patterns are ominous Doppler findings. The data suggest that in IUGR fetuses there is an increased liver vascular resistance with a decreased amount of blood flow rich in oxygen to the liver.