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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5786_Библиотеки_им_академика_М_И_Перельмана.pdf
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Table 11.2 Sensitivity of second-trimester uterine artery Doppler screening studies in
predicting pre-eclampsia and FGR
Sensitivity
Total study group Delivery <34 weeks
Study
Harrington
et al 1996
Albaiges
et al 2000
Papageorghiou
et al 2001
Ultrasound in obstetrics and gynaecology
therefore do not need serial monitoring as suggested for those with abnormal
Doppler results.
Abnormal
test result Screen + Pre-eclampsia
23
1
38
Bilateral
notch (19–21
weeks)
PI 1.45
(23 weeks)
PI 1.63
(23 weeks)
1,23,28,39
9.1% 55% 22% 81% 58%
5.1% 35% 21% 80% 70%
5.1 % 41% 16% 81% 64%
The combination of uterine artery Doppler studies with
FGR
<10th cent.
Preeclampsia
FGR
<10th cent
maternal history and biochemical markers, such as plasma-protein A, inhibin-A,
vascular endothelial growth factor or soluble fms-like tyrosine kinase 1 may further increase the accuracy of risk assessment.
2,40,41,46
A significant negative correlation exists between birthweight and first-trimester uterine Doppler flow patterns.
The value of first-trimester uterine artery Doppler as a prognostic screening tool,
either in isolation or in conjunction with maternal biochemistry, remains to be
determined.
27
In women with increased uterine artery impedance to flow at 20–24 weeks,
follow-up is recommended at 26–28 weeks. If the uterine artery resistance has
normalized at this time, the patient will receive regular antenatal care. However,
even if late normalization occurs, birthweight is significantly lower compared to
those with normal uterine artery Doppler at 20 weeks.13 If high uterine resistance
or notching maintains, 3–4-week monitoring intervals are advised. Increased uterine artery vascular impedance in third-trimester pregnancies is associated with a
higher risk for developing fetal distress and the need for delivery by caesarean
section.
30,44
214
UMBILICAL ARTERY DOPPLER
The umbilical artery was the first vessel studied by obstetric Doppler examination.
Flow velocity waveforms from the umbilical artery represent the downstream or
placental resistance to flow. Umbilical artery resistance decreases progressively
throughout gestation, reflecting the increase and dilation in villous vascularization. In normal pregnancies, end-diastolic blood flow is usually seen in almost
all fetuses from 14 weeks of gestation onwards. Absent or reduced end-diastolic
blood flow in the mid-second or third trimester may be related to incorrect measurement techniques, by too large insonation angle, use of too high high-pass
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filter setting, low transducer frequency, and marked fetal breathing movements.
The location of the Doppler sampling site along the umbilical cord also affects
the Doppler waveform, as resistance progressively declines from the fetal to the
placental end of the cord.
Significant reduction of the villous exchange area due to decreased numbers
and maldevelopment of peripheral villi results in increased fetoplacental resistance, causing a reduction of umbilical artery end-diastolic flow. Local intraplacental stem vessel vasoconstriction and a low cardiac output are additional
mechanisms that may contribute to increased umbilical artery pulsatility. In the
small-for-date fetus, umbilical artery Doppler distinguishes between the fetus
with true growth restriction due to uteroplacental dysfunction and the fetus that
is just constitutionally small. The combination of FGR and increased umbilical
artery resistance should also warrant detailed anatomical examination, as some of
these fetuses will have associated malformations and/or aneuploidy. The latter is
especially true for fetuses with distinct FGR and increased amount of amniotic
fluid in the late second and third trimester and/or structural anomalies and/or
normal uterine Doppler flow velocity waveforms.
Doppler velocimetry of the umbilical artery has been the subject of multiple clinical studies, but results have been inconsistent due to heterogeneity in
methodologies and studied populations. A meta-analysis of 11 studies involving nearly 7000 women reported an improvement in obstetric care in selected
high-risk pregnancies, characterized by suspected impaired fetal growth and/or
pre-eclampsia.35 Compared to pregnancies with no Doppler ultrasound evaluation, the use of Doppler surveillance resulted in fewer admissions to hospital
(odds ratio 0.56, 95% CI 0.43–0.72) and fewer inductions of labour (odds ratio
0.83, 95% CI 0.74–0.93). A promising trend towards reduction in perinatal death
was also noted (odds ratio 0.71, 95% CI 0.5–1.0). No difference was found for
intrapartum fetal distress and caesarean delivery. A separate analysis of umbilical Doppler in low-risk patients concluded that there was no evidence for any
benefit.
35
In terms of monitoring pregnancies with FGR, reduction of umbilical artery
end-diastolic flow is an early sign of fetal impairment. FGR pathologies are
known to follow an abnormal pulsatility in the umbilical artery by many weeks
at an early gestational age.9 Progressively decreasing umbilical artery end-diastolic
blood flow in early growth restriction should alert the obstetrician to the need for
appropriate referral, administration of steroids and detailed maternal evaluation
to exclude associated maternal pathology.
The differentiation of fetal well-being in cases with increased umbilical resistance requires intensified monitoring, using additional Doppler information
from systemic vessels (middle cerebral artery, ductus venosus) and the biophysical profile.22 Progressive increase in placental blood flow resistance is mirrored
by worsened umbilical artery Doppler waveforms, as absent end-diastolic flow
(AEDF) or even reversed end-diastolic flow (REDF) (Fig. 11.3). REDF represents the extreme end of the whole spectrum and the majority of fetuses will
have an estimated weight below the 10th percentile. If this flow pattern occurs,
Evaluation of fetal and uteroplacental blood flow
215
216
A
B
C
D
E
Ultrasound in obstetrics and gynaecology
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Figure 11.3 (A) Umbilical artery: reversed end-diastolic blood flow in a second-trimester growth-restricted fetus. (B) Severe fetal growth restriction at
27 weeks of gestation; absent end-diastolic umbilical artery blood flow. (C) Brain-sparing effect. (D) Increased ductus venosus pulsatility. (E) Tricuspid
regurgitation.
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a significant number of fetuses will additionally have abnormal flow waveforms
in the cerebral and venous circulation. Fetuses with AEDF or REDF constitute a
group with increased perinatal mortality and a high risk for developing fetal distress in labour, with lower Apgar scores and blood gases. In a multicentre study
involving high-risk patients, perinatal mortality in fetuses with AEDF and REDF
compared to fetuses with positive end-diastolic flow was increased 4.0-fold and
10.6-fold, respectively.29 The majority of those fetuses were delivered by caesarean section with variable prematurity and the possible consequences thereof,
such as respiratory distress, intraventricular haemorrhage, necrotizing enterocolitis and subsequently prolonged stay at the neonatal intensive care unit.
5,8,37
However, in recent years a number of research groups have noticed that the
umbilical artery is not the ultimate determinant of adverse outcome, especially
not in the early and most severe forms of FGR. Doppler changes of the cerebral
and venous circulation are more predictive for fetal outcome.
6,8,12,16,25
Therefore,
preterm delivery based on results of umbilical artery Doppler alone seems no
longer appropriate.
Growth restriction in the third-trimester fetus might present differently. Many
fetuses with mild restriction will maintain normal or only slightly altered umbilical blood flow.
30,44
Therefore, increased umbilical artery resistance identifies the
fetus at risk, but a normal umbilical Doppler does not necessarily exclude the
fetus from being at risk. For this group of fetuses, Doppler evaluation of the middle cerebral and uterine arteries will provide more valuable information. When
both vessels have normal waveforms, the chances of distress are small.
30,44
Evaluation of fetal and uteroplacental blood flow
MIDDLE CEREBRAL ARTERY DOPPLER
To perform Doppler studies of the middle cerebral artery (MCA), a transverse
view of the fetal brain at the level of the biparietal diameter is obtained. The
transducer is then moved towards the base of the fetal skull. By colour Doppler
imaging, the circle of Willis is easily visualized. The MCA is a short vessel, running along the sphenoid wing in an anterolateral direction. The sampling site
is the internal third of the vessel with a preferred insonation angle of less than
10°. To measure peak systolic velocities (PSV), the image of the circle of Willis
should be enlarged to 50% of the screen. Measurement is repeated at least three
times, the highest PSV being recorded. Because of its favourable course, measurements taken from this vessel are highly reproducible when performed by experienced sonographers. Impedance to flow decreases and maximum blood velocity
increases with advancing gestation. Close to term, increased end-diastolic blood
flow is recognized in a certain number of fetuses, without being associated with
fetal compromise. Fetal head compression should be generally avoided as it can
artificially lead to decreased diastolic flow in the MCA.
In clinical practice, there are two major applications for Doppler studies of the
MCA. The first is the monitoring of IUGR fetuses, especially those with increased
impedance to flow in the umbilical artery. The second is to evaluate peak systolic
flow in fetuses at risk for anaemia.
217
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MCA IN FETAL GROWTH RESTRICTION
As a consequence of progressing placental insufficiency, the growth-restricted
fetus shifts its blood flow towards the vital organs, namely the brain, the heart
and the adrenal glands. The increase in blood supply for the brain is called brain
sparing and this redistribution can be assessed by MCA Doppler sonography.
In fetuses with brain-sparing effect, hypoxia-induced cerebrovascular dilation
increases end-diastolic blood flow and therefore the impedance decreases (see
Fig 11.3B). This is in contrast to fetuses with normal growth pattern, where the
resistance of the MCA is usually higher than in the umbilical artery.
Within a certain range, changes in the impedance in peripheral arterial vascular beds represent intact autoregulation and normal hormonal and vegetatively mediated vascular response important for nutrition supply, fetal activities,
continued growth and normal pH.6 In FGR fetuses delivered before 32 weeks of
gestation, Hecher et al reported progressively abnormal MCA PI towards delivery. However, in fetuses delivered after 32 weeks of gestation, a trend towards
normalization of MCA resistance was seen. This finding was thought to be attrib-
Ultrasound in obstetrics and gynaecology
uted to the physiological decrease in cerebrovascular resistance with advancing gestational age. Fetal heart rate (FHR) abnormalities were preceded by approximately
3 weeks by the occurrence of abnormal MCA velocity.25 Improved prediction of
outcome in small for gestational age fetuses by incorporating cerebral Doppler
findings, including the cerebroplacental ratio (CPR), was noted by Bahado-Singh
et al. 3 The CPR has the potential advantage of summarizing information regarding redistribution of blood flow of two different vascular beds. Both, increasing
placental resistance as well as decreasing cerebral vascular resistance might affect
the ratio, therefore fetal response to placental insufficiency might be detected
earlier. MCA Doppler is a useful tool to monitor the third-trimester growthrestricted fetus, as redistribution may occur in the presence of normal umbilical Doppler. Abnormal middle cerebral Doppler findings are associated with an
increased risk of caesarean section delivery and need for neonatal admission.
The information conveyed by MCA Doppler investigation of the preterm
growth-restricted fetus allows further specification of clinical management. While
maintenance of normal MCA values is suggestive of fetal circulatory compensation, decreasing MCA resistance indicates the need for tertiary fetal monitoring,
including venous Doppler studies and biophysical profile scoring.22 When growth
restriction becomes terminal, cardiac output might no longer be sufficient to support optimal blood flow to the brain and other vital organs throughout the entire
cardiac cycle. The concomitant drop in the diastolic portion of the flow signal
may then result in so-called ‘pseudo-normalization’ of MCA flow, which represents an ominous sign.
47
26,44
218
MCA IN FETAL ANAEMIA
The use of MCA PSV is nowadays the standard of care in tertiary referral centres in
managing pregnancies at risk for fetal anaemia.32 The discovery of a negative correlation
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272523
Gestational age (weeks)
MCA-PSV (cm/s)
21191715
10
20
30
40
50
60
70
80
90
100
110
120
29 31 33 35 37 39
Figure 11.4 Peak velocity of systolic blood flow in the middle cerebral artery (MCA) with
advancing gestation. The curves indicate the median (below) and 1.5 multiples of the median
(MoM) (above) peak systolic velocity (PSV) in the MCA. (Reprinted from G. Mari et al. N Engl J
Med 2000;342:9–14, with permission. Copyright © 2000 Massachusetts Medical Society.)
between fetal haemoglobin and MCA PSV has led to a more than 70% reduction
in the need for invasive tests, such as amniocentesis or cordocentesis. Normative
data have been published by the group of Mari et al (Fig. 11.4). In this study, all
fetuses with moderate or severe anaemia had peak systolic values above 1.5 times the
median.31 A prospective multicentre study on an intention to treat basis confirmed
MCA PSV as an accurate method of monitoring pregnancies complicated by red cell
antibodies. The overall sensitivity to detect moderate to severe anaemia below
35 weeks was 88% and the negative predictive value was 98%. This study also demonstrated that the false-positive rate increases following 35 weeks' gestation.51 A recent
comprehensive multicentre study by Oepkes et al in which MCA PSV and amniocentesis were performed prior to cordocentesis reported that MCA PSV is superior
to amniocentesis in detecting fetal anaemia in red cell alloimmunization cases and
can be safely used for the timing of cordocentesis and/or intrauterine transfusion.36
Intrauterine transfusion is associated with a significant decrease in the MCA PSV,
which is proportional to the increase in fetal haematocrit (Fig. 11.5). Measurement of
MCA PSV is also applicable in monitoring cases of Kell alloimmunization, parvovirus
infection, fetomaternal haemorrhage or TTTS. Understandably, MCA PSV serves as a
major diagnostic tool in the differential diagnosis of fetal hydrops.
Evaluation of fetal and uteroplacental blood flow
DUCTUS VENOSUS
The ductus venosus connects the intra-abdominal portion of the umbilical vein
with the inferior vena cava at its inlet to the right atrium. The shunt plays a critical
role in the delivery of well-oxygenated blood predominantly towards the left side
of the fetal heart and thus to the coronary and cerebral circulation. The small vessel can be visualized by the use of colour Doppler imaging in either a midsagittal
longitudinal section or a transverse view through the upper abdomen. Due to the
narrow diameter of the ductus venosus, colour Doppler indicates the presence of
characteristically higher flow velocities compared to other praecordial veins, and
with a low Nyquist limit this produces an aliasing effect that aids its identification.
The preferred sample site is the inlet, where the highest velocities are recorded.
219
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Ultrasound in obstetrics and gynaecology
220
Figure 11.5 Middle cerebral artery Doppler. (A) Fetal anaemia secondary to red blood cell
alloimmunization prior to intrauterine transfusion at 30 weeks, Hb 8.2 g/dL. (B) The same
fetus on day 1 after intrauterine transfusion (50 mL of packed erythrocytes); Hb 13.6 g/dL.
The typical waveform of the ductus venosus is triphasic, reflecting the pressure differences between the venous system and the heart throughout the cardiac cycle.
Blood flow velocities are highest during ventricular systole (S). Early diastole (D)
represents the second peak of forward flow. The nadir is seen with atrial contraction
(a-wave) in late diastole (see Fig. 11.1). In contrast to the inferior vena cava and the
hepatic veins, with absence or reversal of flow during atrial contraction, blood flow
in the ductus venosus is usually forward in physiological conditions. In the first trimester (11–14 weeks), a negative a-wave may be recorded in about 3% of normal
fetuses. The absolute blood flow velocities increase, whereas the pulsatility (PIV,
PVIV) decreases with advancing gestation, reflecting decreasing cardiac afterload
and maturation of diastolic ventricular function. Reference ranges have been established in the past.
24
Pathological conditions which may alter ductus venosus flow pattern include
myocardial failure, increase in cardiac afterload or increase in cardiac preload.
When right atrial and central venous pressure increases progressively, decreasing velocity during atrial contraction results, escalating to reversal of flow during
a-wave in most severe fetal compromise (see Fig. 11.3; Fig. 11.6).
In growth-restricted fetuses, abnormal ductus venosus flows are frequently
associated with fetal acidaemia and the highest perinatal mortality compared
to those where flow abnormalities are confined to the umbilical or middle
ABC
DEF
Figure 11.6 Ductus venosus blood flow in fetal disease. Ductus venosus in a fetus with Uhls anomaly: progressing cardiac dysfunction due to right
ventricular failure at 28 weeks (A) and 31 weeks (B). Recipient in TTTS: marked cardiomegaly and AV valve regurgitation (C), increased ductus venosus
pulsatility (D). Cardiomegaly in Ebstein anomaly (E) and corresponding ductus venosus flow profile with reduced forward flow during systole (F).
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221
Evaluation of fetal and uteroplacental blood flow
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Table 11.3 Outcome parameters in fetal growth restriction (n=328) according to Doppler
assessment
UA abnormal only
pH <7.20 15.4% 21.0% 39.4%*
5 min Apgar score <7 4.7% 1.2% 11.4%*
Intrauterine death 1.8% 2.3% 15.2%*
Neonatal death 2.9% 4.9% 16.5%*
Perinatal mortality 4.6% 6.9% 28.8%*
DV, ductus venosus; MCA, middle cerebral artery; UA, umbilical artery.
* p<0.05 compared to fetuses with abnormal umbilical artery only and to fetuses with brain sparing.
Data from reference 8.
(n=109)
cerebral artery (Table 11.3).
gestation, progressive increase in ductus venosus pulsatility was accompanied by
a mirror-like decrease of short time variation of the fetal heart rate pattern and
Ultrasound in obstetrics and gynaecology
both became abnormal on average only a few days before delivery.
observations have been made for the biophysical scoring index and venous
Doppler signal deterioration; these two parameters were the last to drop.6
A recent review by Baschat summarized eight studies which evaluated relationships between venous Doppler parameters and various perinatal outcomes.
In fetuses with normal venous Doppler studies, neonatal deaths accounted for
most of the perinatal mortality, while in fetuses with elevated venous Doppler
indices, stillbirth and neonatal mortality were equal contributors to an overall
increased perinatal mortality. With the exception of necrotizing enterocolitis, the frequency of all postpartum complications was significantly increased
in fetuses with abnormal venous Doppler findings.
ductus venosus deterioration correlates well with adverse fetal outcome, the
question remains whether the risk of fetal damage that has already occurred by
the time of detection of pathological venous changes or the risk of prematurity
by timing the delivery before these changes is higher. Randomized management trials are necessary to verify this issue including the impact of gestational
age at delivery.
Assessment of ductus venosus flow velocity waveforms may also provide useful information in fetuses with cardiac disease and non-immune fetal hydrops (see
Fig. 11.6). In the latter, alterations in ductus venosus blood flow may be seen in
fetuses with AV malformations, indicating high cardiac output failure. Persistent
arteriovenous (AV) fetal tachyarrhythmia above a critical frequency of 210–220
bpm causes marked reversal of ductus venosus blood flow during entire diastole,
indicating an abrupt increase in central venous pressure. Although ductus venosus
pulsatility is not reliable in terms of screening for cardiac defects in the third or
second trimester,19 it does characterize the specific haemodynamic situation in certain
groups of heart disease. In a study comprising fetuses with right-sided cardiac lesions
222
5,6,8,12,16,25
MCA abnormal
(n=87)
DV abnormal
(n=132)
In fetal growth restriction <32 weeks of
12,25
Similar
7
While it is evident that
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with obstructions of the inflow or outflow with intact ventricular septum, abnormal high pulsatilities in the ductus venosus were found, without being necessarily associated with cardiac failure or hypoxaemia.11 However, in some cases with
severe AV regurgitation, progressive increase in right atrial and central venous
pressure occurs, resulting in hydrops and poor prognosis.11 Heart compression by
pericardial effusion also increases ductus venosus pulsatility. Impairment of systolic forward flow with subsequent decrease in peak velocity may occasionally
be found in fetuses with severe tricuspid regurgitation (e.g. Ebstein's anomaly)
(see Fig. 11.6C).
45
Recently, ductus venosus Doppler evaluation has been integrated into detailed
first-trimester screening studies in selected high-risk groups. In conjunction
with increased nuchal translucency, reversed velocity during atrial contraction
improves the predictive capacity for an underlying chromosomal abnormality
and/or a major cardiac defect.
15,34
However, the application of ductus venosus
Doppler studies as a reliable screening tool in true low-risk patients has not been
clarified yet. A second critical issue is that accurate examination of the ductus
venosus is more time consuming and requires highly trained operators, as currently available at specialist centres only.
UMBILICAL VEIN
Evaluation of fetal and uteroplacental blood flow
In first-trimester pregnancies, umbilical venous pulsations are frequently seen
but progressively disappear until 14 weeks of gestation. The normal flow profile
of the umbilical vein in the second and third trimester is continuous forward
flow. Mild pulsations or sinusoidal waveforms might be seen during fetal breathing movements. Severe, biphasic or triphasic pulsations, mimicking systemic
venous flow patterns, have been described in fetal compromise, such as terminal
growth restriction and fetal right heart decompensation.4 Umbilical venous pulsations in the context of fetal pathology are considered an ominous sign, associated with intrauterine demise and neonatal complications. An exception to this
rule is fetal tachyarrhythmia, where umbilical venous pulsations are already seen
in the early stage of the disease.
In severe growth-restricted fetuses, Doppler examination of venous blood
flow volume demonstrated a significant increase in the shunting of umbilical vein
blood flow through the ductus venosus, providing preferential blood flow to the
heart and brain at the expense of fetal hepatic perfusion.
10
DOPPLER IN TWIN PREGNANCIES
Compared to singletons, twin pregnancies are at increased risk for a range
of pregnancy complications including preterm delivery, pre-eclampsia, fetal
growth restriction and subsequent birthweight discordance. In monochorionic
pregnancies, the risks of early fetal loss, severe preterm delivery and intrauterine death are even higher, mainly attributed to the complications of TTTS.
223