o_1977r8vv9vk1ts2ms0kd8pksa.pdf

188 P. Arbeille et al.
moglobin content lower than 5 g/100 ml was closely associated
with fetal flow redistribution and abnormal
FHR. On the other hand, the occurrence of abnormal
FHR was associated with C/U 7 days)
70% of the fetuses were premature, 70% had abnormal
FHR at delivery (several weeks later), C/U
decreased by ±14 Ô 6%, and the mean HI was equal to
±187 Ô 54. (Fig. 13.10).
A second similar study performed in 1996 in the
same area and using the same protocol showed only
a short crisis (150% was predictive of abnormal
FHR at delivery with a sensitivity of 80% and specificity
of 85%.
The HI allowed prediction of abnormal FHR at delivery
several weeks in advance. Moreover, the lower
amplitude of the hemodynamic response (lower HI)
in the second group associated with a lower rate of
abnormal FHR was likely related to an improvement
in pregnancy recruitment and management or with
the acquisition of an adapted immunity by the
mother.
C/U Ratio in Non-Reversible Hypoxia
(Pregnancy-Induced Hypertension)
Prediction of Abnormal FHR at Delivery
In a study of fetal cerebral and umbilical flow adaptation
in pregnancies complicated by hypertension,
which included 82% with IUGR, the fetal hemodynamics
were monitored every 2 days by Doppler over
several days from admission until delivery [59]. As
flow redistribution was identified at its early stage
both the intensity and the duration of the flow redistribution
period (hypoxic period) were considered
for predicting the occurrence of abnormal FHR. By
the end of the study the limit for the HI was 160%.
Figure 13.12 shows a graphic representation of HI
(area between the C/U curve and the C/U=1.1 cut-off
line). This area represents the total oxygen deficit
during the period of observation.
A HI higher than 160% was much more powerful
(PPV: 87%; NPV: 88%) than the final URI, CRI, or
C/U value measured for predicting abnormal FHR at
delivery [URI (PPV: 63%; NPV: 74%) ± CRI (PPV:
59%; NPV: 70%) ± C/U (PPV: 57%; NPV: 92%)].
Moreover, as shown on Fig. 13.12, the C/U may
change from one day to another; thus, a single Doppler
measurement is not sufficient to identify the real
hemodynamic stage induced by hypoxia. On the
other hand, the HI increase is associated with an increase
in the degree of fetal growth restriction as expressed
in percentile. This suggests that the HI, by
measuring the cumulated oxygen deficit during the
observation period, also likely expresses the deficit in
the nutrition supply responsible for the fetal growth
restriction.
Finally, it should be noted that this study addressed
high-risk pregnancy but not very poor fetal
outcomes: 22% of all fetuses required intensive care
assistance (but < 2 days and two-thirds of them
< 33 weeks) and all survived in good health; only one
fetus died at delivery. Thus, HI is a very early predictor
of poor fetal outcome. In contrast, absent end-diastolic
flow in the umbilical arteries was found in 9
cases (13% of the whole population), but all delivered
before 33 weeks; all presented abnormal FHR; all
were severely growth restricted (centile: 6+2); 8
(88%) delivered by Cesarean section; and 5 (56%) required
intensive care assistance. These fetuses presented
the lowest C/U ratio (0.7Ô0.1) and umbilical
cord pO 2 value at delivery (16Ô6) and the highest HI
values (387 Ô 173%) in the population.