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a Chapter 12 Intrauterine Blood Flow and Postnatal Development 163
the same variables as in the study by McDonnell et
al. [36] but also for degree of deviation in birth
weight, found no differences in outcome except a
lower prevalence of ventilator requirement for RDS in
infants with AREDF [37]. In a prospective study of
mothers with pregnancy-induced hypertension, Eronen
et al. [38] found AREDF in the umbilical artery
to be associated with a higher incidence of gastro-intestinal
complications, bronchopulmonary dysplasia,
intraventricular hemorrhage, and vascular hypotension
in the newborns. Although the infants with
AREDF were delivered at an earlier gestational age,
AREDF remained as a predictor of poor perinatal
outcome after correction for prematurity. The increased
morbidity of infants who showed AREDF in
utero was confirmed by other authors with regard to
the occurrence of cerebral hemorrhage, anemia, and
hypoglycemia [28], as well as chronic lung disease,
retinopathy of prematurity, and impaired intestinal
motility [39].
Weiss et al. [40] found an increased frequency of
abnormal neurological signs in newborn infants with
AREDF as compared with a control group, matched
for gestational age, with normal umbilical velocity
waveforms in the umbilical artery. They found also in
fetuses with preceding AREDF a significant increase
in the cord blood levels of brain type isoenzyme of
creatine kinase (CK-BB) as a possible indication of
intrauterine brain cell damage [41]. Rizzo et al. [42]
described a decreased fetal cerebrovascular resistance
as determined by a decreased pulsatility index (PI) in
the internal carotid artery to be associated with postasphyxial
encephalopathy, as determined by neurological
signs, in a cohort of high-risk pregnancies. On
the other hand, in a study of 117 infants delivered between
25 and 33 gestational weeks in high-risk pregnancies,
no relationship was observed between the ratio
of PI in the fetal umbilical and cerebral circulation,
and neither cerebral hemorrhage nor neurological
abnormality in the neonatal period [43]; however,
both Ley and MarÉ—l [44], and Scherjon et al. [45]
found a sustained abnormal cerebral blood flow in
growth-restricted neonates and preterm neonates who
showed signs of brain sparing in utero. It was speculated
that this might be due to a different setting of
cerebral autoregulation as a consequence of intrauterine
redistribution of blood flow.
Long-Term Neurodevelopmental
Implications
In comparison with the large body of studies published
on short-term perinatal outcome of abnormal
fetal blood flow [27], relatively few investigations
have attempted to evaluate long-term consequences
(Table 12.1).
Weiss et al. [46] found that the combination of
AREDF in the umbilical artery, severe RDS, and delivery
before 28 gestational weeks was predictive of neurological
abnormality at 6 months of age. A similar
finding of a greater risk of permanent neurological
sequelae at the age of 18 months was reported by Valcamonico
et al. [47] for growth-restricted fetuses with
AREDF in the umbilical artery. Abnormal fetal heart
rate patterns were shown to be more predictive of
poor cognitive outcome at 2 years of age than abnormal
waveforms in the umbilical artery in fetuses of
high-risk pregnancies delivered before 34 gestational
weeks [48]. In a descriptive follow-up study, Wilson
et al. [49] found no association between abnormal
umbilical velocity waveforms and major neurological
abnormality at 5 years of age. Similarly, in a group of
193 infants born to women with severe preeclampsia,
there were no differences between those with and
without AREDF in utero, when their neurodevelopmental
outcome was evaluated at the age of 2 and 4
years [50]. The only exception was the lower Performance
subscale test at 24 months in the infants with
previous AREDF.
The study by Vossbeck et al. [39] demonstrated
that infants with AREDF born before 30 gestational
weeks and followed up for between 1 and 8 years
were more often mentally retarded (44 vs 25%) and
had more often severe motor impairment (38 vs 19%)
than the matched controls. Another 5-year prospective
follow-up of fetuses with AREDF showed 6 of 42
infants to be mentally handicapped [26]. A long-term
impairment of intellectual capacity and partial neurodevelopmental
delay was also observed at school age
in 23 infants who have had severely compromised
blood flow in utero [51].
In the previously referred study by Scherjon et al.
[43], subsequent assessment of neurological signs at 6
and 12 months of age showed no relationship between
the ratio of PI in the fetal umbilical and cerebral
circulation and neurological abnormality. A parallel
study showed that infants at 6 months of age
with a raised umbilical artery/middle cerebral artery
PI ratio had shorter visual evoked potential latencies
as compared to infants with a normal ratio (Fig. 12.1)
[52]. This was interpreted as a sign of accelerated
neurophysiological maturation, being of benefit to the
fetus. At the age of 3 years, the adverse neurodevelopmental
development, as evaluated by Hempel examination
[53] in a subgroup of 96 infants from the original
cohort, was related to neonatal cranial ultrasound
abnormality, rather than to the signs of brain sparing
in utero [54]. The authors interpreted this finding as
confirmation of their interpretation of the brain sparing
as being beneficial. Seventy-three of the children
were examined subsequently at the age of 5 years.
The mean IQ score was significantly lower for chil-