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Chapter 42 ■ Fetal Measurements: Normal and Abnormal Fetal Growth 1467
FETAL AND PLACENTAL RISK
FACTORS ASSOCIATED WITH FETAL
GROWTH RESTRICTION
FETAL FACTORS
Chromosomal Abnormalities
Trisomy 13, 18, 21
Monosomy (45,XO)
Deletions
Uniparental disomy
Confined placental mosaicism
Congenital Malformations
Absence of fetal pancreas
Anencephaly
Diaphragmatic hernia
Omphalocele
Gastroschisis
Renal agenesis/dysplasia
Multiple malformations
Multiple Gestations
Monochorionic twins
One fetus with malformations
Twin-to-twin transfusion
Discordant twins
Triplets
PLACENTAL FACTORS
Abnormal trophoblastic invasion
Multiple placental infarctions (chronic abruption)
Umbilical-placental vascular anomalies
Abnormal cord insertion (velamentous cord
insertion)
Placenta previa
Circumvallate placenta
Chorioangiomata
From Lin CC, Santolaya-Forgas J. Current concepts of fetal
growth restriction. Obstet Gynecol 1998;92:1044-1055.
MATERNAL RISK FACTORS
ASSOCIATED WITH FETAL GROWTH
RESTRICTION
Genetic/Constitutional
Nutrition/Starvation
Inflammatory bowel disease
Ileojejunal bypass
Chronic pancreatitis
Low prepregnancy weight
Poor pregnancy weight gain, second and third
trimesters
Hypoxic
Severe lung disease
Cyanotic heart disease
Sickle cell anemia
Vascular
Chronic hypertension
Preeclampsia
Collagen vascular disease
Type 1 diabetes mellitus
Renal
Glomerulonephritis
Lipoid nephritis
Arteriolar nephrosclerosis
Renal transplantation
Antiphospholipid Antibodies
Environment and Drugs
High altitude
Emotional stress
Physical stress
Cigarette smoking
Alcohol abuse
Substance abuse (heroin, cocaine)
Therapeutic drugs
Antimetabolites
Anticonvulsants
Anticoagulants
nourishment and oxygenation, to determine if Doppler
criteria were useful for predicting fetal growth restriction. These criteria, however, were found to be poor
predictors of IUGR.
111,113,114
More recent studies of Doppler ultrasound, however,
have shown that it can play a useful role in determining
the prognosis of fetuses with IUGR.
115-119
In growthrestricted fetuses, reversed diastolic flow in the umbilical artery carries a very poor prognosis, an elevated risk
of fetal demise. They often die if not delivered soon.
An absent diastolic flow or an elevated systolic/
diastolic ratio is associated with poor prognosis,
including increased likelihood of fetal distress in labor,
admission to the intensive care unit, and perinatal
mortality.
116-118,120-125
Although no single criterion permits confident diagnosis of IUGR, the following three key parameters can
be used in combination to establish the diagnosis with
greater certainty
126
:
Poor Obstetric History
Previous stillbirths
Recurrent aborters
Previous birth of growth-restricted fetus
Previous preterm births
From Lin CC, Santolaya-Forgas J. Current concepts of fetal
growth restriction. Obstet Gynecol 1998;92:1044-1055.
• Estimated fetal weight
• Amniotic fluid volume
• Maternal blood pressure status (normal vs.
hypertensive)
Other proposed parameters for diagnosing IUGR
can be safely ignored because they add no significant
information.
127,128
The three key parameters can be combined into an
IUGR score or a table that permits the confident diagnosis or exclusion of growth restriction in most cases
126,127
1468 PART IV ■ Obstetric Sonography
TABLE 42-13. CONVENTIONAL SONOGRAPHIC CRITERIA FOR INTRAUTERINE GROWTH
RESTRICTION (IUGR): PERFORMANCE CHARACTERISTICS
(%) Predictive Values (%)*
CRITERION†
Advanced placental grade 62 64 16 94
Elevated FL/AC 34-49 78-83 18-20 92-93
Low TIUV 57-80 72-76 21-24 92-97
Small BPD 24-88 62-94 21-44 92-98
Small BPD and advanced placental grade 59 86 32 95
Slow rate of BPD growth 75 84 35 97
Low EFW 89 88 45 99
Decreased AFV 24 98 55 92
Elevated HC/AC 82 94 62 98
SENSITIVITY SPECIFICITY POSITIVE (PPV) NEGATIVE (NPV)
From Benson CB, Doubilet PM, Saltzman DH. Intrauterine growth retardation: predictive value of ultrasound criteria for antenatal diagnosis. Radiology 1986;160:415-417.
*Computed using Bayes’ theorem,
†A range of values is given for a criterion when different studies apply that criterion in two or more ways.
FL/AC, Femur length/abdominal circumference ratio; TIUV, total intrauterine volume; BPD, biparietal diameter; EFW, estimated fetal weight; AFV, amniotic fluid volume;
HC/AC, head circumference/abdominal circumference ratio.
112
assuming an IUGR prevalence rate of 10%.
TABLE 42-14. CRITICAL VALUES* FOR ESTIMATED FETAL WEIGHT (IN GRAMS) FOR
DIAGNOSING OR EXCLUDING INTRAUTERINE GROWTH RESTRICTION
Status of Maternal Blood Pressure and Amniotic Fluid Volume
GA WK
26 516-660 646-826 743-950 610-780 763-976 878-1123
27 597-761 745-949 855-1090 704-898 878-1119 1009-1285
28 693-877 859-1087 982-1244 813-1030 1008-1276 1153-1460
29 803-1008 988-1239 1124-1410 937-1176 1152-1446 1312-1646
30 931-1155 1132-1405 1281-1589 1078-1337 1311-1627 1483-1840
31 1075-1317 1293-1584 1452-1779 1234-1512 1484-1819 1667-2042
32 1235-1493 1468-1774 1635-1976 1405-1698 1670-2018 1860-2248
33 1411-1682 1656-1973 1830-2180 1590-1895 1865-2223 2061-2456
34 1600-1880 1853-2177 2031-2386 1785-2098 2067-2429 2266-2662
35 1798-2083 2055-2382 2236-2590 1987-2302 2272-2633 2471-2863
36 1997-2285 2257-2583 2437-2789 2189-2504 2474-2830 2671-3056
37 2192-2479 2452-2774 2631-2976 2383-2696 2666-3016 2861-3236
38 2371-2658 2631-2949 2807-3147 2563-2872 2843-3186 3034-3400
39 2526-2812 2785-3101 2961-3296 2717-3025 2996-3335 3185-3545
40 2645-2933 2906-3223 3083-3419 2838-3147 3118-3458 3307-3668
41 2717-3013 2985-3310 3166-3511 2915-3232 3202-3551 3396-3766
42 2736-3045 3016-3356 3205-3567 2942-3274 3243-3609 3447-3836
NL BP
NL/POLY
NL BP
M-M OLIGO
NL BP
SEV OLIGO
HTN
NL/POLY
HTN
M-M OLIGO
HTN
SEV OLIGO
From Benson CB, Belville JS, Lentini JF, et al. Intrauterine growth retardation: diagnosis based on multiple parameters: a prospective study. Radiology 1990;177:499-502.
*For each pair, estimated weight less than the lower value allows confident diagnosis of intrauterine growth restriction (IUGR; positive predictive value, 74%). Estimated
weight greater than the upper value virtually excludes IUGR (negative predictive value, 97%). Estimated weight between the two values is indeterminate for IUGR (likelihood
of IUGR, 13%).
GA, Gestational age; Nl BP, normal blood pressure; Htn, hypertension; Nl, normal fluid; Poly, polyhydramnios; M-M, mild to moderate; Oligo, oligohydramnios; Sev,
severe.
(Table 42-14). For any gestational age, amniotic fluid
volume (subjectively assessed), and maternal blood
pressure status, the table presents two values. When a
fetus has an estimated weight below the smaller value,
IUGR can be diagnosed with confidence. If the estimated weight is above the larger value, growth restriction
can be excluded with near certainty. An estimated weight
between the two values is indeterminate for IUGR.
When accurate dating by an ultrasound performed
before 20 weeks’ gestation is available, a simpler rule
applies, using only the lower value in the appropriate
column. IUGR can be diagnosed if the estimated fetal
weight falls below this value and can be excluded if the
weight estimate falls above this same value.
To illustrate the use of this table in the diagnosis of
IUGR, consider a case in which the gestational age is
34 weeks (based on a 24-week ultrasound), there is
moderate oligohydramnios, and the mother is normotensive. On the basis of Table 42-14, if the estimated
fetal weight is below 1853 g, IUGR can be diagnosed
Chapter 42 ■ Fetal Measurements: Normal and Abnormal Fetal Growth 1469
with confidence, and if it is above 2177 g, growth restriction can be ruled out. A weight estimate between these
two values is indeterminate for IUGR. If the age of 34
weeks had been based on a 12-week ultrasound, IUGR
could be diagnosed if the estimated weight was below
1853 g and excluded if the weight estimate was above
1853 g. Table 42-14 provides a rational and reliable
means for prenatal diagnosis of IUGR. When growth
restriction is diagnosed, further evaluation using Doppler
velocimetry can help to determine the prognosis.
129
Once IUGR has been diagnosed, an attempt should
be made to determine its etiology, through evaluation of
both the mother and the fetus. Maternal assessment
should include physical examination and blood tests,
directed toward diagnosis of hypertension, renal
disease, and other maternal conditions that can cause
IUGR. Fetal assessment begins with a careful sonographic examination, looking especially for findings
suggestive of a chromosomal or viral etiology (e.g.,
holoprosencephaly, clenched hands, rocker-bottom feet,
intracranial calcifications). If such a finding is present,
amniocentesis or umbilical blood sampling can confirm
the diagnosis of a chromosomal abnormality. A viral
etiology of IUGR may also be diagnosed by these procedures, in some cases.
128
Growth-restricted fetuses, other than those with a
lethal condition such as trisomy 13 or 18, should be
carefully monitored for the remainder of the pregnancy.
The monitoring is usually performed at weekly or semiweekly intervals. Sonographic features to be followed
include amniotic fluid volume, biophysical profile
score, estimated fetal weight percentile, and umbilical
artery Doppler assessment (see Chapter 43). A worsen-
ing trend in one or more of these features should prompt
consideration of early delivery.
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99. Colman A, Maharaj D, Hutton J, Tuohy J. Reliability of ultrasound
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100. Lugo G, Cassady G. Intrauterine growth retardation: clinicopathologic findings in 233 consecutive infants. Am J Obstet Gynecol
1971;109:615-622.
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1979;133:281-286.
102. Divon MY, Chamberlain PF, Sipos L, et al. Identification of the
small for gestational age fetus with the use of gestational age-independent indices of fetal growth. Am J Obstet Gynecol 1986;155:
1197-1201.
103. Sabbagha RE. Intrauterine growth retardation avenues of future
research in diagnosis and management by ultrasound. Semin Perinatol 1984;8:31-36.
104. Reed K, Droegmueller W. Intrauterine growth retardation. In: Centrullo CL, Sbarra AJ, editors. The problem-oriented medical record.
New York: Plenum; 1984. p. 174-194.
105. Lockwood CJ, Weiner S. Assessment of fetal growth. Clin Perinatol
1986;13:3-35.
106. Lin CC, Santolaya-Forgas J. Current concepts of fetal growth restriction. Part I. Causes, classification, and pathophysiology. Obstet
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107. Seeds JW. Impaired fetal growth: definition and clinical diagnosis.
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109. Benson CB, Doubilet PM. Head-sparing in fetuses with intrauterine
growth retardation: does it really occur? Radiology 1986;161(P):75.
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111. Benson CB, Doubilet PM. Doppler criteria for intrauterine growth
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112. Weinstein MC, Fineberg HV, Elstein AS, et al. Clinical decision
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113. Ott WJ. Diagnosis of intrauterine growth restriction: comparison of
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115. McCowan LM, Erskine LA, Ritchie K. Umbilical artery Doppler
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117. Rochelson BL, Schulman H, Fleischer A, et al. The clinical significance of Doppler umbilical artery velocimetry in the small for gestational age fetus. Am J Obstet Gynecol 1987;156:1223-1226.
118. Berkowitz GS, Mehalek KE, Chitkara U, et al. Doppler umbilical
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123. Trudinger BJ, Giles WB, Cook CM. Flow velocity waveforms in the
maternal uteroplacental and fetal umbilical placental circulations.
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124. Baschat AA, Gembruch U, Reiss I, et al. Relationship between arterial and venous Doppler and perinatal outcome in fetal growth
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125. Fong KW, Ohlsson A, Hannah ME, et al. Prediction of perinatal
outcome in fetuses suspected to have intrauterine growth restriction:
Doppler ultrasound study of fetal cerebral, renal, and umbilical
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126. Benson CB, Boswell SB, Brown DL, et al. Improved prediction of
intrauterine growth retardation with use of multiple parameters.
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Radiology 1990;177:499-502.
128. Doubilet PM, Benson CB. Sonographic evaluation of intrauterine
growth retardation. AJR Am J Roentgenol 1995;164:709-717.
129. Hecher K, Bilardo CM, Stigter RH, et al. Monitoring of fetuses with
intrauterine growth restriction: a longitudinal study. Ultrasound
Obstet Gynecol 2001;18:564-570.
CHAPTER 43
Fetal Surveillance: Doppler
Assessment of Pregnancy
and Biophysical Profile
Maryam Rivaz, Norman L. Meyer, Rebecca A. Uhlmann, and
Giancarlo Mari
Chapter Outline
FETAL CIRCULATION
INTRAUTERINE GROWTH
RESTRICTION
Doppler Waveform Analysis
Uterine Artery
Umbilical Artery
Middle Cerebral Artery
Other Arteries
Fetal Venous System
Fetal Cardiac System
Management: Staging and
Classification
RED CELL ALLOIMMUNIZATION
PREDICTION OF FETAL
HEMATOCRIT
MULTIPLE GESTATIONS
Umbilical Artery Doppler Ultrasound
in Discordant Twins
Doppler Ultrasound in Twin-Twin
Transfusion Syndrome
Fetal surveillance by ultrasound is performed by a
combination of assessment of growth (Chapter 42),
Doppler ultrasound waveform analysis, and biophysical
profile.
Studies have shown that Doppler ultrasound, introduced in obstetrics in 1977, represents an important
screening and diagnostic tool in modern obstetrics.
FitzGerald and Drumm
cal artery (UA) waveforms are abnormal in fetuses with
intrauterine growth restriction (IUGR), and that
reversed flow of the UA is associated with poor prog-
nosis. Their breakthrough concept of studying waveforms resulted in several important clinical applications.
For example, the American College of Obstetrics and
Gynecology (ACOG) has endorsed the use of UA
Doppler ultrasound in high-risk pregnancies.
ultrasound assessment of the UA has become a standard
of care for fetuses with IUGR, which helps to decrease
the perinatal mortality in high-risk pregnancies.
ultrasound of the middle cerebral artery has become
the standard care for the diagnosis of fetal anemia, thus
avoiding unnecessary invasive procedures.
Information obtained with Doppler ultrasound helps
manage pregnancies complicated by IUGR, fetal anemia,
and multiple gestations. In addition, Doppler sonography is useful in the assessment of medication effects on
maternal and fetal circulation.
3
first reported that the umbili-
4
1
5-8
FETAL CIRCULATION
The fetal blood circulation consists of parallel blood flow
pathways and two shunts (Fig. 43-1). The oxygen (O
1,2
Doppler
Doppler
)–
2
INDOMETHACIN AND DUCTUS
ARTERIOSUS
DOPPLER ULTRASOUND IN
FETAL MORPHOLOGIC
ABNORMALITIES
BIOPHYSICAL PROFILE SCORING
Modified Profile
Growth-Restricted Fetuses
CONCLUSION
rich and nutrient-enriched blood goes from the placenta
to the umbilical vein, and once it reaches the liver, some
blood flows through it, turns right, and joins the transverse portion of the left portal vein. Some blood bypasses
the liver via the ductus venosus and enters the right
atrium via the inferior vena cava (IVC).
A subdiaphragmatic venous vestibulum is formed by
the confluence of the three hepatic veins, the ductus
venosus, and the IVC just below the level of the right
atrium. The right atrium receives venous return from
the upper part of the body through the superior vena
cava (SVC) and from the myocardium via the coronary
sinus. The largest amount of the blood from the right
atrium flows through the foramen ovale into the left
atrium and through the mitral valve into the left ven-
tricle. From there, blood empties into the aorta, passes
through the aortic arch over the bifurcation in the right
and left pulmonary artery, and enters the descending
part of the aorta.
In contrast, carbon dioxide (CO
blood flows from the SVC into the right atrium, is partially
mixed with the O
enters the right ventricle via the tricuspid valve. A small
portion of the blood passes through the pulmonary circulation via the pulmonary trunk and the pulmonary
arteries and reaches the left atrium through the pulmonary
veins, followed by entrance into the systemic circulation
system. Because of the high pulmonary arterial pressure
in the lungs, however, a substantially larger part flows
through the ductus arteriosus and goes into the descend-
ing aorta and directly into the systemic circulation.
The blood streams to the right atrium carry blood
with different concentrations of nutrients and oxygen,
-rich blood from the placenta, and
2
)–rich, nutrient-poor
2
1472
Chapter 43 ■ Fetal Surveillance: Doppler Assessment of Pregnancy and Biophysical Profile 1473
Right ventricle
~65% of venous return
IVC, SVC and coronary sinus
Main pulmonary
Pulmonary artery
Lung
8% CCO
trunk
pulmonary vein and ductus venosus
Coronary artery
Heart
3% CCO
Ductus arteriosus
57% CCO
Left ventricle
~35% of venous return
Brain
21% CCO
Descending aorta
67% CCO
Placenta
41% CCO
Ascending aorta
Aortic isthmus
10% CCO
FIGURE 43-1. Diagram of fetal
heart. Percentages of combined ventricular
output ejected by each ventricle in the circulation of the fetal lamb. Well-oxygenated left
ventricular blood supplies the brain and
heart while right ventricular blood with
lower oxygen content is predominantly
distributed to the placenta. The largest proportion of the combined cardiac output
(CCO) is distributed to the placenta for
oxygenation.
so appropriate channeling is necessary to ensure that
sufficient nutrient and oxygen is delivered to the vital
organs. This is accomplished by several unique features
of the ductus venosus foramen ovale, aortic isthmus, and
origin of the UA that result in different velocities and
directions in venous bloodstreams. The umbilical vein
transports nutrient-rich blood from the placenta, and a
large part of it is channeled through the bed of capillaries
in the liver.
A functional sphincter regulates the flow of blood
through the ductus venosus (DV). The DV develops at
approximately 7 weeks’ gestation and shows relatively
little increase in size, in contrast to the other precordial
veins, which grow proportionally with the embryo.
After the first trimester, diameter of the DV measures
approximately one-third the umbilical vein diameter. As
a result, blood from the umbilical vein accelerates on
entering the DV.
10
This accelerated blood flow enters the
IVC with the left hepatic venous return, and the combined flow is directed through the foramen ovale into
the left atrium. By comparison, the venous returns from
the right and middle hepatic veins and IVC have slower
blood flow velocities and are directed toward the right
atrium. There is relatively little mixing of the venous
returns from the DV/left hepatic vein and the right and
middle hepatic veins/IVC because of the differences in
velocity and direction of the incoming bloodstreams. As
a result, O
-rich blood reaches the left ventricle through
2
the foramen ovale, whereas O2-poor blood enters the
right ventricle through the tricuspid valve.
Blood from the left ventricular output is circulated
through the brachiocephalic vessels to the brain and
upper body and through the coronary vessels to the
myocardium. Right ventricular output largely bypasses
the lungs and reaches the aorta through the ductus arteriosus. The blood from both ventricles is mixed and
eventually reaches the placenta through the umbilical
arteries.
11
In the human fetus, 60% to 70% of umbilical venous
blood is circulated to the liver and the remainder to the
heart. With chronic hypoxemia, this proportion may be
9
adjusted so that a larger proportion of umbilical venous
blood can bypass the liver to reach the heart.
INTRAUTERINE GROWTH
RESTRICTION
The fetus with IUGR is a fetus that does not reach its
potential growth. However, most of the studies that
report on IUGR have not differentiated between “constitutionally” small and “pathologically” small fetuses.
Additionally, studies on the pathogenesis of IUGR have
been limited by the concept that IUGR fetuses represent
a homogeneous group. This has created some confusion
about the mechanisms of IUGR. We use the term small
12
1474 PART IV ■ Obstetric Sonography
for gestational age (SGA) for those small fetuses with
no maternal pathology and with normal UA and middle
cerebral artery (MCA) Doppler ultrasound results. In
contrast, growth-restricted fetuses are small fetuses with
a recognizable maternal pathology or an abnormal UA
or MCA Doppler ultrasound. In many IUGR fetuses,
there is an underlying maternal pathology, such as
chronic hypertension or advanced-stage diabetes mel-
litus, as the basis of placental insufficiency. In other
fetuses with IUGR, placental insufficiency has no identifiable cause, but there is an abnormal fetal Doppler
ultrasound, defined as “idiopathic” IUGR.
13,14
The concept that placental insufficiency is “the” cause
of IUGR is a source of confusion. Placental insufficiency
is not the “cause” of the problem, but rather is the con-
sequence of a poorly understood disease process.
14,15
Placental insufficiency is a “symptom” with many potential
underlying causes. With IUGR, we often view the
problem from the wrong direction—as a consequence
of placental insufficiency—and we therefore believe that
we should treat the placental insufficiency. In reality,
we should find and treat the specific cause of placental
insufficiency.
Optimal management, however, would be the prevention of IUGR entirely. Growth-restricted fetuses undergo
a different series of cardiovascular changes that in patients
with preeclampsia, or other maternal pathology, and
fetuses with idiopathic IUGR. In idiopathic IUGR,
Doppler ultrasound changes can be predicted on almost
a day-by-day basis. If no sudden adverse event occurs,
such as a placental abruption, these fetuses can be followed until fetal cardiac failure occurs. This is not the
case in patients with preeclampsia, in whom Doppler
ultrasound changes of IUGR are unpredictable.
16
The
importance of this concept is that in cases of idiopathic
IUGR, delivery has the potential of being timed. It is
important to emphasize that not all IUGR fetuses are
the same, and that they must be categorized into appropriate groups according to severity and etiology.
14-24
Doppler ultrasound plays a fundamental role in the
diagnosis of IUGR and also has the potential to play an
important role in timing the delivery of some growthrestricted fetuses. Doppler sonography of the UA and
MCA, in combination with biometry, provides the best
tool to identify small fetuses at risk for an adverse
outcome.
the fetal cardiovascular system allow assessment of the
blood flow redistribution observed in IUGR.
25,26
In addition, Doppler ultrasound studies of
26
This
process is mainly characterized by an increased UA and
a decreased MCA pulsatility index, which suggests
increased vascular resistance of the UA and cerebral
vasodilation.
Doppler Waveform Analysis
Doppler ultrasound waveforms reflect blood velocity.
However, Doppler waveforms also may provide
S
Frequency velocity (cm/sec)
FIGURE 43-2. Typical Doppler waveform of a fetal
artery. The beginning of the waveform coincides with the
beginning of the cardiac systole; S, peak systolic velocity (PSV);
D, end diastolic velocity (EDV); M, mean velocity (MV). Velocity
is shown on the Y axis. Note that the velocity is the true velocity
if the angle between the ultrasound beam and the blood flow is
close to 0 degrees.
M
D
Time (sec)
information on various aspects of blood flow in circulation, including the presence and direction of flow, velocity profile, volume of flow, and impedance to flow.
These waveforms have been used extensively for assessing
downstream circulatory impedance. The essential condition for the assessment of true velocity depends on the
angle between the ultrasound beam and the direction of
the blood flow, which needs to be as close as possible to
0 degrees (Fig. 43-2). As the incident angle increases,
blood velocity is progressively underestimated; therefore
the following angle-independent indices are used:
1. Systolic-to-diastolic (S/D) ratio = Peak systolic
velocity/End diastolic velocity (PSV/EDV)
2. Resistive index (RI) = (PSV − EDV)/PSV
3. Pulsatility index (PI) = (PSV − EDV)/Mean
velocity
Blood flow velocity of the fetal vascular system can be
either pulsatile or continuous. The arteries always have
a pulsatile pattern, whereas the veins have either a pulsatile or a continuous pattern (Fig. 43-3). The S/D ratio
and RI are easy to calculate. The PI is more complex
because it requires the calculation of the mean velocity
(MV), but modern Doppler ultrasound equipment provides those values in real time. In practice, for the UA,
the MCA, and the uterine arteries, no one index is superior to the others, and any of the indices may be used.
These three indices provide information on vascular
impedance, which is not the same as vascular resistance.
In fact, impedance has a more extensive meaning than
resistance, because it depends on vascular resistance,
preload, heart rate, and cardiac contractility. The term
vascular resistance, however, has been extensively used
in the literature and is commonly accepted. By calculating one of these indices and therefore estimating the
vascular resistance, we can obtain information on the
amount of blood flow. For example, if we assess the PI
Chapter 43 ■ Fetal Surveillance: Doppler Assessment of Pregnancy and Biophysical Profile 1475
A
C
(or the RI or S/D ratio) at the level of the MCA in fetuses
appropriate for gestational age (AGA) and in growthrestricted fetuses at the same gestational age, the IUGR
fetuses will have a lower PI value at the MCA than the
AGA fetuses. Our interpretation is that in IUGR fetuses,
there is a lower vascular resistance at the MCA than in
AGA fetuses. This suggests an increased blood flow to
the brain. However, we do not know the true value of
the vascular resistance or the true amount of cerebral
blood flow.
Uterine Artery
In the first half of pregnancy, trophoblasts invade the
uterine vessels and result in dilated spiral arteries, which
increase the uterine perfusion 10-fold to 12-fold. These
arteries provide nutrient supply and gas exchange for the
fetus. Each uterine artery should be sampled soon after
the crossing of the iliac vessels (Fig. 43-4).
The uterine arterial blood flow in nonpregnant women
is 50 mL per minute and increases to over 700 mL/min
B
FIGURE 43-3. Umbilical artery and umbilical vein. A,
The umbilical vein has a constant velocity, whereas the umbilical artery
(UA) is pulsatile because it reflects the systole and diastole of the cardiac
cycle. In this case, the umbilical vein blood flow was toward the transducer, and therefore the waveform is represented above the baseline.
The UA blood flow was directed away from the transducer, and therefore arterial flow is represented below the baseline. B, “Chasing” the
cord in gray scale will lead to inadvertently large angles of insonation
and the erroneous impression of reduced or even absent end diastolic
flow. Magnification of a cord segment followed by use of color flow
Doppler ultrasound, detecting blood flow velocity in the vertical plane,
allows the pulsed Doppler gate to be placed in each artery with a
minimal angle of insonation. C, Normal arterial waveform in the same
patient as B. (A from Mari G, Detti L. Doppler ultrasound: application
to fetal medicine. In Fleischer AC, Manning FA, Jeanty P, Romero R,
editors. Sonography in obstetrics and gynecology: principles and prac-
tice. New York, 2001, McGraw-Hill, pp 247-283.)
in the third trimester of pregnancy. Thus the diastolic
component of the uterine artery Doppler waveform is
transformed during normal pregnancy from one of low
peak flow velocity and an early diastolic notch, to one
of high flow velocity and an early diastolic notch by 18
to 22 weeks.
27
The uterine artery waveform by the mid–
second trimester is therefore characterized by high end
diastolic velocities (EDVs) with continuous forward
blood flow throughout diastole. With advancing gestation, the degree of end diastolic flow typically increases.
Indices used to quantify these waveforms include PI, RI,
and notching of one or both uterine arteries.
However, failure of normal endovascular trophoblastic invasion of the spiral arteries results in increased
uterine artery vascular resistance and decreased perfusion
of the placenta.
28,29
If the end diastolic flow does not
increase throughout pregnancy, or if a small notch is
detected at the beginning of diastole, the fetus is at high
risk for developing IUGR.
30
Diastolic blood flow may be
absent or even reversed with extreme degrees of placental
dysfunction. Such findings are ominous and may precede
1476 PART IV ■ Obstetric Sonography
UTA
EIA
EIV
A
B
C
FIGURE 43-4. Uterine artery as it crosses iliac vessels. A, When it appears to originate from the external iliac artery, this
is an artifact. The uterine artery (UTA) is sampled on color Doppler ultrasound soon after it crosses the iliac vessels. EIA, External iliac
artery; EIV, external iliac vein. B, Normal UTA waveform with high diastolic flow. C, Abnormal UTA waveform with obvious early
diastolic notch. (From Mari G. Doppler ultrasonography in obstetrics: from the diagnosis of fetal anemia to the treatment of intrauterine growth-
restricted fetuses. Am J Obstet Gynecol 2009;200:613 e1-e9.)
fetal death or signal a high risk of abnormal fetal neurologic outcome.
31
The PI of each uterine artery should be
obtained independently, using a PI value of 1.41 to differentiate between normal and abnormal values. Doppler
ultrasound studies of the uterine artery in early pregnancy have been evaluated as a screening tool for pregnancies destined to develop preeclampsia or IUGR.
31
A recent literature review reported that abnormal
uterine artery waveforms are a better predictor of preeclampsia than of IUGR when performed after 16 weeks’
gestation.
32
However, different indices best predicted
preeclampsia or IUGR based on the a priori risk. Thus,
an abnormal PI and uterine artery notching in the second
trimester best predicted preeclampsia, whereas the best
predictor of IUGR in high-risk patients was an increased
33
The following issues, however, remain unclear:
RI.
1. When the assessment of uterine arteries should be
carried out: at 16, 20, or 24 weeks of gestation.
2. Whether assessment of the maternal uterine arteries
notching is useful.
3. If the PI or RI is the most useful parameter.
4. Whether the addition of the PI or RI of both
maternal uterine arteries is necessary.
Future studies will have to clarify when to assess the
uterine arteries, what cutoff value to use for the uterine
artery Doppler RI and PI, and whether biochemical
markers need to be added to the Doppler ultrasound
assessment for better predictive information.
It is also important to minimize subjective interpretation of the waveforms, especially characterization if
a notch is present, which can depend on the speed
of recording the Doppler ultrasound tracing. The
indications for the assessment of the uterine artery
Doppler ultrasound are (1) previous history of preeclampsia, (2) previous child with IUGR, (3) unexplained high maternal serum alpha-fetoprotein levels,
and (4) high human chorionic gonadotropin levels. If
the PI values of both uterine arteries are normal, the
patient can be informed that she most likely will not
develop preeclampsia or have an IUGR fetus. This is
because of the high negative predictive value (>99%) of
the test. If one of the uterine arteries is abnormal, patients
are followed with more frequent clinic visits and ultrasounds for growth because the positive predictive value
in populations at risk ranges from 50% to 75%.
Umbilical Artery
Placental blood is assessed by studying the umbilical
artery. UA waveforms are slightly different at the fetal
abdominal wall and at the placental insertion,
34
with
indices higher at the wall than the insertion (Fig. 43-5).
However, the difference is minimal, so it is not important to obtain the waveforms always at the same level. In
practice, the UA is best examined in a segment of free-
floating umbilical cord. Waveforms are optimized by
selecting the vessel to be interrogated, zooming in on the
region, and placing the Doppler ultrasound gate in a
segment of cord flowing at close to 0 degrees to the
transducer. If there is reversed flow, the UA is reexamined close to the placental insertion, because this segment
of the UA is the last part to develop reversed flow
43-6). UA waveforms change with advancing gesta-
3,35
End diastolic flow is often absent in the first
tion.
16
(Fig.
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