o_1977r8vv9vk1ts2ms0kd8pksa.pdf

290 W. J. Ott
Fig. 18.10. Normal inferior vena cava flow at 30 weeks'
gestation. Note the tri-phasic pattern with a small reverse
A wave during atrial contraction
Fig. 18.12. Abnormal inferior vena cava waveform with a
large A wave in a fetus at 22 weeks' gestation who died
from placental abruption
Fig. 18.11. Normal ductus venosus flow at 24 weeks. Note
that there is always forward flow during the entire cardiac
cycle
Fig. 18.13. Markedly abnormal ductus venosus flow with
reverse flow during atrial contractions and transmitted venous
pulsation in the umbilical vein in a severely growthrestricted
fetus at 32 weeks' gestation
formation concerning fetal status [150±156]. Rizzo et
al. evaluated numerous Doppler indices from the inferior
vena cava and ductus venosus in a series of normal
and growth-restricted fetuses prior to cordocentesis
[157]. They found the inferior vena cava preload
index (the peak velocity during atrial contraction
divided by the peak velocity during systole) was
the best index for predicting acidemia. Figures 18.10
and 18.11 show normal venous flow in the inferior
vena cava and ductus venosus, respectively.
During pathological situations, transmission of increased
reverse flow in the inferior vena cava and
ductus venosus may result in venous pulsations in
the umbilical vein. Indik et al. have postulated that it
may be possible to distinguish subgroups of fetuses
with abnormal umbilical artery S/D ratios by evaluating
fetal vena cava flow [156]. Nakai et al. evaluated
209 patients and found 9 (4%) fetuses with umbilical
venous pulsations, 7 of which (78%) had significant
growth restriction [158]. Mitra followed seven singleton
fetuses and two sets of twins with umbilical venous
pulsations [159]. All fetuses showed tricuspid
regurgitation and abnormal right-to-left ventricular
diameter ratios ± suggesting fetal heart failure. All
seven of the singleton fetuses were significantly
growth restricted, while the two twin pregnancies had
twin±twin transfusion syndrome with the donor twin
being growth restricted and the recipient twin being
macrosomic. Studies in the fetal lambhave supported
these clinical findings, suggesting that umbilical venous
pulsations develop as a result of significant fetal
venous pressure elevations [160]. In many clinical situations
umbilical venous pulsations are a significant
pathological event that require careful fetal evaluation,
especially evaluation of the fetal cardiovascular