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a Chapter 25 Absent End-Diastolic Velocity in the Umbilical Artery and Its Clinical Significance 379
waveforms correlated closely with reduced small muscular
artery counts. It is apparent that aneuploidy adversely
affects fetoplacental vascularization, which results
in increased fetoplacental circulatory impedance
and may contribute to fetal growth restriction.
Recently, Doppler flow studies in the umbilical artery
were performed in first trimester fetuses. Borrell
and colleagues [30] screened 2,970 pregnancies at 10±
14 weeks' gestation and observed 11 cases of reversed
end-diastolic flow for an incidence of 0.4%. Seven of
the 11 fetuses had an autosomal trisomy and two
other fetuses had a congenital heart defect.
Earlier, Martinez and associates [31] had prospectively
recorded the umbilical artery pulsatility index
(PI) in 1,785 pregnancies before undergoing chorionic
villus sampling or genetic amniocentesis. They
had shown that fetuses with trisomy 18 had an elevated
PI. The PI was measured transvaginally for
pregnancies from 10 to 13 weeks and transabdominally
for pregnancies from 14 to 18 weeks. Seven of
the ten fetuses with trisomy 18 had an elevated PI
above the 95th percentile; nine fetuses had an elevated
PI above the 90th percentile. PI as a marker for
trisomy 18 had good sensitivity (70%±90%), specificity
(> 90%), and negative predictive value (99%) but a
poor positive predictive value (5%±7%). Reversed
end-diastolic flow was detected in two cases, both of
which had trisomy 18.
Intrauterine Growth Restriction
The strength of the relation between AREDV and fetal
growth compromise depends on the stringency of the
definition of growth restriction. A small-for-gestational-age
(SGA) fetus is not necessarily growth-restricted,
as fetal ªsmallnessº may also be constitutional
in nature. It is also probable that a fetus who
fails to realize its full growth potential may not necessarily
be SGA. Indeed, the terms IUGR and SGA
demonstrate diagnostic uncertainty and lack prognostic
reliability. Being SGA does not necessarily indicate
a compromised outcome. Despite these ambiguities,
fetuses experiencing a substantial defined
growth failure often suffer from in utero asphyxia
and its adverse consequences. These fetuses also have
Doppler evidence of increasing fetoplacental arterial
impedance. Thus 50% or more of the fetuses with
AREDV demonstrate a growth disturbance (Table
25.2). A similar proportion of fetuses with sonographic
evidence of growth restriction develop
AREDV. Thus Battaglia and associates [23] noted that
57% of the fetuses identified as being growth restricted
by serial ultrasound measurements developed
AEDV. Similarly, Pattinson and colleagues [22] observed
that 48% of the fetuses suspected of severe
growth restriction in their series developed umbilical
arterial AREDV. It is noteworthy that pregnancies
complicated by both growth restriction and hypertension
demonstrate a greater propensity for developing
AREDV than those with either growth restriction or
hypertension [24].
Fetal Asphyxia and Hypoxia
Fetal asphyxia and hypoxia can largely be attributed
to fetal exposure to chronic hypoxic and asphyxial insult.
The significant association between abnormal
umbilical arterial Doppler indices and fetal hypoxia
and acidosis is discussed in Chap. 24. It is apparent
that the umbilical hemodynamics are affected more
by asphyxia or acidosis and less by hypoxia. One of
the most impressive pieces of evidence has been provided
by Nicolaides and associates [32], who measured
umbilical venous blood gases by cordocentesis
in 59 fetuses suspected of growth restriction (abdominal
circumference below the 5th percentile for gestational
age). These fetuses also demonstrated absent
umbilical arterial end-diastolic flow. In 88% of the
cases the blood gases were abnormal; 42% of the fetuses
were hypoxic, 37% asphyxiated, and 9% acidotic.
Futhermore, there was a poor correlation between
the degree of fetal smallness and acidosis or severity
of hypoxia. Other investigators [33] have also observed
this efficacy of absent end-diastolic flow and fetal
acidosis. The AEDV identified acidosis with a sensitivity
of 90%, specificity 92%, positive predictive value
(PPV) 53%, and negative predictive value (NPV) 100%.
It is important to note that not all fetuses with
AREDV are hypoxic or acidotic. Normal fetal blood
gas values, however, do not ensure fetal well-being.
Several investigators have noted progressive fetal deterioration
and adverse perinatal outcome in fetuses
with AREDV despite normal fetal acid-base status as
determined by cordocentesis [34, 35]. It appears that
progressive fetal hemodynamic decline, as manifested
by umbilical arterial AREDV, is not necessarily related
to fetal asphyxia and presents a serious threat to
the fetus independent of fetal hypoxia or acidosis.
Cerebral Hemorrhage
One of the major concerns regarding chronic intrauterine
asphyxia is its effect on the fetal brain.
Although the risk of fetal brain damage due to prematurity
and birth asphyxia has been well investigated,
the role of antepartum asphyxia in fetal neurologic
damage due to hypoxemic ischemic injury requires
elucidation. One of the gross lesions from such
injury is cerebral hemorrhage, which has been reported
in association with AREDV. The main question
is whether this association is independent of the
preterm birth of these infants.