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Although comparisons have been made between Doppler
velocimetry and other prevalent modes of fetal
surveillance, no single testing modality should be regarded
as the exclusive choice for fetal surveillance,
as these tests reveal different aspects of fetal pathophysiology,
often in a complementary manner. Obviously,
more work is needed to determine the optimal
integration of the various surveillance methods for
improving the perinatal outcome in a cost-effective
manner: It is important to establish the sequence in
which the various signs of fetal compromise manifest
during surveillance of the fetus at risk. It is known that
not all of these signs appear simultaneously. We have
witnessed a variable chronology of falling cerebral
Doppler indices, rising umbilical arterial Doppler indices,
eventual disappearance of the end-diastolic flow,
and the occurrence of ominous cardiotocographic patterns.
It is also critical to examine the prognostic significance
of the pattern of these occurrences. A few
studies have systematically addressed this issue.
Arduini et al. [31] followed 36 SGA fetuses with an
abnormal elevation of the umbilical and middle cerebral
artery PI ratios (> 95th percentile) until the onset
of antepartum late deceleration of the fetal heart rate.
Comprehensive Doppler evaluation of the fetal circulation
was performed along with fetal cardiotocographic
examination. Statistically significant changes
in PI occurred in all the vessels (umbilical artery, descending
aorta, renal artery, internal carotid artery,
middle cerebral artery). The most significant fall in
the middle cerebral PI occurred 2 weeks before the
onset of late deceleration, indicating the maximum
compensatory vasodilatory response of the cerebral
circulation. In contrast, significant increases in the
peripheral and umbilical PI occurred close to the onset
of abnormal fetal heart rate patterns. James et al.
[32] evaluated the chronology of abnormalities of: (1)
umbilical artery Doppler results; (2) fetal growth as
indicated by ultrasound measurement of the fetal abdominal
circumference; and (3) biophysical profile
score. The retrospective study of 103 fetuses at risk of
chronic fetal asphyxia revealed that the umbilical artery
Doppler result deteriorated first, followed by the
abdominal circumference, and then the biophysical
profile score. Whereas an abnormality of one of these
parameters in isolation did not result in any adverse
consequences, abnormality of all three ultrasonographic
features led to the worst outcome.
A prospective longitudinal investigation was conducted
by Ribbert et al. [33] that included the followa
Chapter 24 Doppler Velocimetry for Fetal Surveillance: Adverse Perinatal Outcome and Fetal Hypoxia 371
cordocentesis for fetal blood sampling, showed a significant
quadratic relation between fetal hypoxemia
and the degree of reduction in the PI. The maximum
fall in PI occurred when the fetal PO 2 was 2±4 SD below
the normal mean for gestation. When the oxygen
deficit increased, the PI tended to rise. The authors
speculated that this increase reflected the development
of fetal brain edema.
The fetal cerebral and umbilical circulatory responses
to hypoxia, hypercapnia, and acidosis were
investigated by Chiba and Murakami [29] in 17 SGA
fetuses. Cordocentesis was performed to determine
umbilical venous blood gases and pH. The fetal circulatory
response was evaluated by gestation-adjusted
RI values from the middle cerebral and umbilical arteries.
The middle cerebral artery demonstrated decreased
impedance in the presence of hypoxia and
acidosis. In contrast, the umbilical artery impedance
increased with acidosis but was insensitive to hypoxia
and hypercapnia. These observations were corroborated
by Akalin-Sel et al. [30], who found a low PO 2
and pH and a high PCO 2 in the umbilical venous
blood sampled by cordocentesis from the SGA fetuses
compared to the gestation-related normal values. The
cerebral circulation was responsive to hypoxia and
hypercapnia, whereas the aortic and umbilical circulations
were responsive to hypercapnia and acidosis
but not to hypoxia. Decreased impedance in the cerebral
arterial system was associated with increased impedance
in the aortic, umbilical, and uteroplacental
arteries.
These findings have significant clinical implications
for managing high-risk pregnancies. Although
some animal studies suggest that fetal Doppler velocimetry
may not be efficacious for identifying fetal
asphyxia, it may not be applicable to the human situation,
as indicated by the results of clinical research
summarized above. Obviously, the fetal cardiovascular
response to chronic and progressive hypoxia and
acidosis is complex. Doppler investigation helps us to
elucidate this phenomenon and may contribute to improving
the perinatal outcome. The differential response
of the umbilical and cerebral hemodynamics
to hypoxia and acidosis may be utilized to sequence
the progression of fetal compromise, which may significantly
enhance the diagnostic efficacy of the Doppler
technique. Moreover, integration of the current
modes of fetal surveillance, such as antepartum
cardiotocography or biophysical profile scoring with
the Doppler mode, offers exciting possibilities for improving
the clinical value of this diagnostic approach.
Sequence of Changes
in Fetal Surveillance Parameters
with Progressive Antepartum
Fetal Compromise