Neonatal nucleated red blood cell (nrbc) counts in small for gestational age (sga) fetuses with abnormal umbilical artery (UA) doppler studies

OBJECTIVE: The presence of elevated NRBC counts in neonatal blood has been associated with fetal hypoxia. We sought to determine whether SGA fetuses with abnormal UA Doppler flow velocity waveforms have elevated NRBC counts. STUDY DESIGN: Hospital charts of neonates with the discharge diagnosis of SGA (birthweight <10th %ile) who were delivered between 10/88 - 6/95 were reviewed for antepartum testing, delivery conditions and neonatal outcome. We studied fetuses who had an UA systolic/diastolic (S/D) ratio within three days of delivery and a complete blood count (CRC) on the first day of life. Multiple gestations, anomalous fetuses and infants of diabetic mothers were excluded. Statistical analysis included Chi-square, ANOVA, simple and stepwise regression. RESULTS: Fifty-two infants met the inclusion criteria. Univariate analysis demonstrated that abnormal UA S/D ratios were associated with significantly higher NRBC counts (p = 0.0001). Those with absent or reverse end diastolic How (AEDF/REDF; n= 19) had significantly greater NRBC counts than those with end diastolic flow present (n = 33) (NRBC/100 nucleated cells ±S.D.: 135-5 ±138 vs. 17.4 ±23.7; p<0.0001). These infants exhibited significantly longer time intervals for clearance of NRBCs from their circulation (p<0.0001). They also had lower birth weight (p=0,002), lower initial platelet count (p=0.0006), lower arterial cord blood pH (p = 0.04), higher cord blood base deficit (p=0.003) and an increased likelihood of cesarean section for fetal distress (p = 0.0005). Multivariate analysis demonstrated that AEDF/REDF (p<0.0001, r=0.522) and low birthweight (p=0.0001, r² = 0.364) contributed to elevation of NRBC count while gestational age at delivery was not a significant contributor. CONCLUSION: Surprisingly, we observed significantly lower platelet counts in SGA fetuses with abnormal UA Doppler studies. This may suggest that antenatal thrombotic events lead to an increased placental impedance. Fetal response to this chronic condition results in an increased NRBC count.