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Resistance index of uterine artery and placental location in intrauterine growth retardation

BACKGROUND
Our aim was to investigate the relationship between placental location and resistance index (RI) of uterine arteries in cases with intrauterine growth retardation (IUGR).


METHODS
Placental location and flow velocity waveforms of uterine arteries in 86 normal and 20 IUGR cases from 33 to 38 weeks of gestation were examined using a combined real-time scanner and pulsed Doppler ultrasonography. The location of placenta was classified as lateral when most of it was located to either the right or the left side of the uterine midline. Otherwise it was called central. Cases where the placenta was located in the uterine fundus or in the lower segment were not included. RI values were calculated from the uterine arteries on the placental side, on the non-placental side and in case of central placentas as a mean of both uterine arteries. In normal cases, the calculations were done every second week from 33 to 38 weeks of gestation, and the difference in variance among three gestational ages in each artery was tested by a one-way ANOVA. In IUGR cases, a standard deviation score (SDS) was calculated individually in each artery as (RI - normal mean)/normal SD. Differences in SDS between three categories of uterine arteries were examined by non-parametric tests.


RESULTS
In normal cases, there was no significant difference in variance of RIs among three gestational ages in each category of arteries. In IUGR cases, SDSs on the placental side were higher than those on the non-placental side and those in central placenta, (p<0.01, Wilcoxon's and Mann Whitney's tests, respectively). SDSs in five of eight cases with central placentas were below 1.0. Two of 12 cases with lateral placentas had higher SDSs on the non-placental side than on the placental side and resulted in abruptio placentae.


CONCLUSIONS
Deviation of RIs in uterine arteries with IUGR could be affected by the pathologic conditions of the utero-placental blood flow on the placental side of lateral placenta rather than in central placenta and might be done by dramatic increase in resistance to flow of the myometrial vessels on the non-placental side.