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Morphological and Morphometric Studies of the Placenta with Doppler Abnormalities of the Fetal Umbilical Arteries
Intravillous blood volume <85 ml (n= 56)
Intravillous blood volume >85 ml (n=104)
SGA
pH<7.15
5–min Apgar<8
Cesarean section
for asphyxia
0
20 40
60
Percent
n=43
n=29
n=6
n=1
n=10
n= 7
n=28
n= 9
80
Fig. 25.3 Perinatal risks as a function of the size of the fetoplacental
vascular tree (n = 160). With a small intravillous blood volume (yellow
Grams
2
cm
600
500
400
300
200
100
300
250
200
150
100
50
Placental weight (g)
0
Placental area of attachment (cm
0
bars), the rates of SGA fetuses (p = 0.000), the incidence of severe
acidosis (pH ⬍ 7.15 ) ( p = 0.004), the number of fetuses with a low 5-
min Apgar score (⬍ 8) (p = 0.029), and therate of cesarean sections for
impending intrauterine asphyxia (p = 0.000) are significantly increased
relative to fetuses whose placentas have an adequate intravillous
25
blood volume (blue bars). Fisher’s exact test.
60
50
Percent
40
30
20
10
0
Relative frequency of infarction
Normal flow Abnormal flow AEDF
End-Diastolic Blood Flow Velocities in the Umbilical Arteries
Fig. 25.4 Placental weight, area of placental attachment, and
A relative reduction or absence of end-diastolic blood flow
velocities in the umbilical arteries reflects an increased impedance in the downstream vascular bed and therefore may
signify abnormal vascularization of the placenta
12, 13, 15
. On the
other hand, a steady rise of end-diastolic blood flow velocities
with advancing gestation occurs in normal pregnancies and reflects a decline of impedance due to placental growth as well as
maturation of the villous and vascular tree
49
. Our study in a
nonselected population showed that as the severity of Doppler
abnormalities increased, there was a decrease in placental
weight and attachment area and an increase in the frequency
of infarctions (Fig. 25.
ment of the villous tree (Fig. 25.
4) and defective maturation and develop-
17, 23
5)
.
frequency of infarction versus Doppler findings in the umbilical arter-
ies. Normal flow: n = 193. Abnormal flow: n = 31. Absent end-diastolic
flow (AEDF): n =9.
Normal flow
24 %
76 %
Abnormal flow
34%
66%
2
44%
)
AEDF
56%
252
Absent end-diastolic flow in the umbilical arteries. We did a
comparative case–control study in a selected group of 37 patients
with absent end-diastolic flow (AEDF) in the umbilical arteries and
in matched controls of equal gestational age (⫾ 3 days) with normal umbilical artery flow
16
. This matched-pair study design enabled
us to compare placental histology and macromorphometric findings independently of gestational age (Table 25.1). For the same
gestational ages in both groups, the mean birthweight of cases
in the matched controls. The rate of intrauterine growth retarda-
tion (IUGR) was approximately 10 times higher with this flow pattern (76% vs. 8 %, McNemer test: p = 0.0000). This supply deficit is
reflected in the macromorphometric placental data.
Predominantly intermediate villi
Predominantly terminal villi
Fig. 25.5 Percentages of villous types in the peripheral villous tree as
a function of umbilical artery Doppler findings. Normal flow:
n = 193. Abnormal flow: n = 31.Absent end-diastolic flow (AEDF): n =9.
Table 25.1 Gestational age, birthweight, and macromorphometric
placental findings in absent or reverse end-diastolic umbilical artery
flow compared with normal matched controls
Delivery
Normal
matched
controls
(n = 37)
231 ⫾ 25 231 ⫾ 25 –
Absent or
reverse enddiastolic flow
(n = 37)
p
(Wilcoxon
test)
(days
gestation)
Birthweight
1801 ⫾ 710 1425 ⫾ 652 0.0001
(g)
SGA ⬍ 10.
n = 3 (8%) n = 26 (76%) 0.0023
percentile
Placental
362 ⫾ 117 273 ⫾ 153 0,0001
weight (g)
Area of
213 ⫾ 78 151 ⫾ 54 0.0001
placental
attachment
2
)
(cm
SGA = Small for gestational age.
Validation of Doppler Findings by Placental Histology
AEDF
600
500
400
Placental weight (g)
300
200
100
Matched controls
0
160 220
180
200 240 260 280 300
Fig. 25.6 Placental weight as a function of gestational age in a group
with absent orreverse end-diastolic flow (AEDF, n = 37) andin matched
controls of equal gestational age with normal flow (n = 37).
Regression functions for AEDF:
y =–274.76+2.13x; r = 0.568; r
For matched controls: y = – 339.01+ 3.03x; r = 0.637; r
Linear function for AEDF
Linear function for matched controls
Gestational age (days)
2
= 0.322
2
= 0.405
Specific Obstetric Problems
Placental weight. With AEDF in the umbilical arteries, we find that
the mean placental weight at a given gestational age is reduced by
approximately 100 g. The area of placental attachment is also reduced. When placental weight is plotted againstgestational age for
both study groups using a linear regression function (Fig. 25.6), we
find that while the organ weight is decreased in AEDF as described
above, growth of these placentas is still observed with advancing
gestational age. The curve has a flatter slope than in the matched
controls, however. This could indicate an early implantation defect
with a consequent delay in placental growth and maturation as a
pathogenic mechanism for the development of AEDF in the umbilical artery. Accordingly, a relationship is also found between abnormal findings in the placental vascular bed
placental findings
20
and the flow patterns recorded in the uterine
56
and morphological
arteries.
Microscopic findings. The microscopic evaluation of villous maturation in umbilical artery AEDF does not show development appropriate for gestational age. This condition is characterized by severe
increases of flow resistance with absent or reverse end-diastolic
flow in the umbilical arteries in a small placenta, with associated abnormalities of the central and peripheral villous and vascular trees.
The dominant finding is chronic placental infarctions followed by
delayed villous maturation and endarteropathy obliterans. Perhaps
as a result of these changes, the impaired maturation of the peripheral villous tree isoften accompanied by accelerated villous matura-
tion and angiosis of the terminal villous vessels reflecting a compensatory mechanism. Figure 25.7 shows histological examples.
Defective maturation of the peripheral villous tree. The progression of this pathology over time is not yet fully understood.
A number of recent studies suggest that changes in the peripheral villous tree are of major significance with regard to increased impedance in the fetoplacental compartment. Jackson
25
et al.
and Macara et al.34found vascular maldevelopment in
the terminal villous compartment of growth-restricted fetuses
with abnormal flow patterns in the umbilical arteries. The
number and luminal diameters of the stem villous vessels were
unchanged relative to the control group, but their wall thickness was significantly decreased in cases with abnormal flow.
Detailed electron-microscopic studies by Krebs et al.
33
confirmed abnormal maturation of the peripheral villous tree in
pregnancies with AEDF in the umbilical arteries, which validates our histometric studies (Fig. 25.
sults of Nordenvall et al.
38
, whose radiographic studies showed
2). Together with the re-
abnormal dichotomous branching of endplate vessels and few
cotyledons in placentas from fetuses with AEDF, it is reasonable to assume a generalized maldevelopment of the central and peripheral villous tree as the pathogenic principle that
underlies abnormal umbilical artery blood flow. Overall,
however, the capillary compartment in the terminal villi probably does affect fetoplacental impedance and thus the Doppler
velocity waveforms in the umbilical arteries.
253
Morphological and Morphometric Studies of the Placenta with Doppler Abnormalities of the Fetal Umbilical Arteries
Fig. 25.7 Placentas from fetuses with AEDF in the
umbilical arteries.
a AEDF placenta in the 17th
week of gestation. Terminal
villus with microthrombosis
in the sinusoidal vessels
(H & E, ⫻250).
b AEDF placenta in the 35th
week of gestation. Microinfarct with “ghost villi” (H & E,
⫻100).
c AEDF placenta in the 31st
ab
25
cd
week of gestation. Trisomy
18, arrested ramification and
deficient vascularization of
the malformed villi
(H & E,⫻125).
d AEDF placenta in the 35th
week of gestation. Intermediate villi are deficient almost
none are seen between the
mainstem villi and the finely
branched terminal villi (H & E,
⫻100).
e AEDF placenta in the 36th
week of gestation. Endarteropathy obliterans of a
mainstem villous vessel with
intravascular calcium deposition and signs of recanalization (Pearce, ⫻80).
f AEDF placenta in the 40th
week of gestation. Intermediate villi show villositis and a
marked disturbance of vascularization (H & E, ⫻100).
254
ef
Diagnosis of fetal growth restriction. These findings support
Clinical and Diagnostic Value of Doppler Sonography of the Umbilical Arteries
the thesis that it is possible to differentiate a genetically small
and thus noncompromised fetus with normal umbilical artery
waveforms from a growth-restricted fetus with abnormal flow
To investigate the clinical and diagnostic value of umbilical artery
Doppler, we examined morphometrically the placentas of SGA fe-
tuses with abnormal umbilical artery flow patterns, SGA fetuses
with normal umbilical artery flow, and a control group of eutrophic
(AGA, “appropriate for gestational age”) fetuses with normal
19
. The Doppler waveforms were recorded during the final week
flow
before delivery. The data are shown in Table 25.2.
Particularly noteworthy is the fact that there were no significant
differences in any of the tested histometric criteria between the
groups of SGA and AGA fetuses with normal Doppler waveforms.
This means that both groupswere equally well endowed at the level
of the terminal villi and that Doppler sonography of the umbilical
artery can demonstrate this antenatally. By contrast, the placentas
of SGA fetuses with abnormally increased resistance indices in the
umbilical arteries showed a reduction of vascularization and diffusion parameters.
that is threatened by placental insufficiency
not truly growth-restricted but only biometrically small, and
these pregnancies can be followed on an outpatient basis as
there is no increase in perinatal risk. On the other hand, cases
with abnormal umbilical artery waveforms warrant a more
thorough diagnostic workup and may require inpatient monitoring and delivery. This was convincingly demonstrated by
59
Weiss
.
Low resistance indices. Initial studies
abnormally high Doppler resistance indices in the fetal umbilical arteries have major diagnostic implications, but that
markedly low indices below the 10th percentile may also be
associated with increased fetal risk. These cases involve a premature, “accelerated” maturation of the villous and vascular
9, 57
. The former is
22
indicate not only that
Validation of Doppler Findings by Placental Histology
Table 25.2 Macromorphometric and micromorphometric data in SGA fetuses as a function of Doppler findings compared with a control group of
eutrophic fetuses
Weight ⬍ 10t h
percentile,
S/D ratio ⬎ 3
(n =9)
Weight ⬍ 10t h
percentile,
S/D ratio ⬍ 3
(n =7)
Weight appropriate for
gestational age (AGA),
S/D ratio ⬍ 3
(n =14)
Gestational age (days) 247 ⫾ 23** 280 ⫾ 15 NS 276 ⫾ 11
Birthweight (g) 1680 ⫾ 527* 2617 ⫾ 217*** 3503 ⫾ 676
Placental weight (g) 359 ⫾ 12 6 N S 4 21 ⫾ 75** 598 ⫾ 16 4
2
Decidual attachment area (cm
)183⫾ 63 NS 223 ⫾ 57* 293 ⫾ 71
Placental-fetal weight index 0.219 ⫾ 0.063* 0.160 ⫾ 0.030 NS 0.170 ⫾ 0.031
2
µm
Mean villous surface area (
Mean villous circumference (
Diffusion path (
µm) 4.6 ⫾ 1.6 * 3.3 ⫾ 0.4 NS 3.7 ⫾ 0.7
Mean vascular surface area (
) 1997 ⫾ 279 NS 2116 ⫾ 398 NS 2273 ⫾ 361
µm) 158 ⫾ 10 NS 163 ⫾ 15 NS 169 ⫾ 13
2
µm
)476⫾ 213 * * 924 ⫾ 310 N S 88 4 ⫾ 229
Number of vessels per villus (n)4.1⫾ 0.7 NS 3.8 ⫾ 0.7 NS 4.2 ⫾ 0.6
Degree of vascularization (%) 29.2 ⫾ 8.8 ** 42.8 ⫾ 7.5 NS 38.9 ⫾ 8.7
2
µm
Mean surface area of a single vessel (
Mean length of epithelial plates (
µm) 11.2 ⫾ 1.5 ** 14.7 ⫾ 2.9 NS 13.4 ⫾ 2.2
)139⫾ 38 * 252 ⫾ 112 N S 2 13 ⫾ 81
Number of epithelial plates/villus (n)1.8⫾ 0.3 NS 1.8 ⫾ 0.5 NS 1.8 ⫾ 0.4
Percentage of epithelial plates on villous circumference (%) 7.1 ⫾ 0.9* 9.0 ⫾ 1. 5 NS 7. 9 ⫾ 1. 3
Significance was calculated for the adjacent column, i.e., weight ⬍ 10th percentile with normal flow versus weight ⬍ 10th percentile withabnormal flow, and weight
⬍ 10th percentile with normal flow versus AGA weight with normal flow.
Wilcoxon test: * p ⬍ 0.05; ** p ⬍ 0.01; *** p ⬍ 0.001; NS, not significant.
Specific Obstetric Problems
tree, which accounts for the low resistance. These placentas
reach the limits of their performance reserve too early. As a result, we find a high incidence of prematurity, growth retardation, and infants with low Apgar scores and pH values. These
cases reaffirm the correlation between Doppler findings and
placental morphology.
Comments. It appears that the morphological correlates described above can be detected antenatally by Doppler scanning
of the umbilical arteries to assess the impedance of the fetoplacental compartment. Doppler sonography thus provides an
important new tool for the evaluation of individual fetal risk.
Based on these considerations, it is at least conceivable that
this modality can further reduce perinatal mortality and particularly the rate of intrauterine fetal deaths.
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257
Gynecological Ultrasound
Sonographic and Doppler Sonographic Examination of
26
Uterine Anomalies
S. Kupesic and A. Kurjak
Classification of Uterine Anomalies
Congenital uterine malformations have a variable incidence
that is usually estimated at 3–4 %. Less than half of these
anomalies have clinical manifestations
can be classified into the following main types:
➤
Unicornuate uterus
➤
Uterus didelphys
➤
Bicornuate uterus
➤
Septate uterus
Unicornuate uterus. Unicornuate uterus results from a
26
developmental error in one of the müllerian ducts. One rudimentary horn may be present, and implantation in this horn
creates a very high likelihood of an abnormal pregnancy or
tubal gestation. This anomaly can be diagnosed very accurately
with three-dimensional (3 D) ultrasound (Fig. 26.
1, 8, 24
. Uterine anomalies
1).
Uterus didelphys. The didelphic uterus is based on a failure of
fusion of the paired müllerian ducts, resulting in duplication of
the uterine corpus and cervix. These patients generally have no
difficulties with menstruation or with coitus. Pregnancy,
however, is associated with an increased risk of abnormal fetal
presentations and prematurity.
Bicornuate uterus. If the müllerian ducts undergo only partial
fusion, a bicornuate uterus develops with a single cervix and
variable separation of the uterine horns. This anomaly is associated with high rates of early pregnancy loss, prematurity,
and breech presentation (Fig. 26.
Septate uterus. Incomplete absorption of the septum between
the müllerian ducts leads to defects ranging from a partial septum to significant separation of the endometrial uterine cavity.
A complete failure of absorption leads to a longitudinal vaginal
septum, called a “double vagina.”
2).
Fig. 26.1 Three-dimensional ultrasound image of a unicornuate
uterus. Absence of the left uterine horn is clearly demonstrated.
Fig. 26.2 Three-dimensional ultrasound image of a bicornuate
uterus. Note the separation of the two horns and the concave shape of
the fundus.
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Ultrasound in the Diagnosis and Treatment of Septate Uterus—Authors’ Results
Diagnosis and Complications of Septate Uterus
The septate uterus accounts for up to 50% of symptomatic
uterine anomalies
6, 8
.
Spontaneous abortion. The risk of spontaneous abortion in this
group during the first trimester is between 28 % and 45%, while
the risk of second-trimester abortion is approximately 5%
Premature births, abnormal fetal presentations, preterm labor,
and dystocia are typical complications of septate uterus
10
. Deficient blood flow to the septum is the presumed cause of the
pregnancy loss
6
. Electron-microscopic studies by Fedele et al.
showed that the endometrium covering the septum of the malformed uterus undergoes few if any preovulatory changes. This
may play a role in the pathogenesis of primary infertility in
women with a septate uterus.
Surgical intervention. Unfavorable obstetric conditions can be
eliminated by surgical cor rection of the intrauterine septum.
Formerly the septum was removed by transabdominal metro-
6
plasty
, but hysteroscopic treatment has now become the
method of choice. The advantage of this simple and effective
treatment is that it does not leave a scar in the myometrium.
Cararachet al.
2
and Goldenberg et al.9report pregnancyrates of
75% and 88.7% following hysteroscopic surgery.
Transvaginal sonography. The technical simplicity and effectiveness of hysteroscopy have compelled the clinician to make
an early, reliable diagnosis of uterine anomalies. Transvaginal
ultrasound has a sensitivity of almost 100% in screening for
congenital uterine anomalies
distinguish between different types of anomalies
19, 26
, although it cannot positively
20, 21
.
Hysterosalpingography. Hysterosalpingography(HSG) is an in-
vasive diagnostic procedure that involves the use of contrast
medium and x-rays. Although the uterine cavity is clearly delineated by HSG, it is not always possible to detect smaller
8
.
6
Fig. 26.3 Hysterosonographic image of a septate uterus demonstrates two endometrial echoes separated by a thick septum.
anomalies or distinguish among different types of lateral fusion defects.
Hysterosonography. Hysterosonography
22
is a technique in
Gynecological Ultrasound
which the uterine cavity is distended with saline solution and
then examined with transvaginal ultrasound. This simple and
minimally invasive procedure supplies anatomical images of
the endometrium and myometrium, clearly defines the septate
uterus, and even allows the thickness and length of the septum
to be measured
23
(Fig. 26.3).
Other diagnostic procedures. Although several reports note
the high accuracy of magnetic resonance imaging
three-dimensional ultrasound
11
in the diagnosis of uterine
3, 17
and
anomalies, so far these techniques have rarely been used in the
routine investigationof these conditions. In patients scheduled
for corrective surgery, the examination is usually supplemented by another invasive procedure, CO
hysteroscopy25.
2
Ultrasound in the Diagnosis and Treatment of Septate Uterus—Authors’ Results
Our study is an attempt to evaluate the combined use of trans-
vaginal ultrasound, transvaginal color and pulsed Doppler
sonography, hysterosonography, and three-dimensional ultrasound in the preoperative evaluation of the septate uterus
15
.In
the second part of the study, we analyzed the obstetric and
perinatal complications of septate uterus and assessed the
reproductive outcome after hysteroscopic treatment.
Patients and Methods
Study patients. A total of 420 infertile women undergoing hys-
teroscopic surgery were included in the study. Table 26.
marizes the intraoperative findings in the 420 patients. An intrauterine septum was present in 278 patients and was surgically corrected. Forty-three of the women with a septate uterus
had a prior history of recurrent spontaneous abortions, 71
1 sum-
women had a history of one spontaneous abortion (56 in the
first trimester, 15 in the second trimester), 82 had primary infertility, and 20 had had premature deliveries, including six
breech presentations and two transverse presentations.
Seventy-six patients had a prior history of ectopic pregnancy.
B-mode imaging and Doppler sonography. All of the patients
underwent transvaginal B-mode and Doppler ultrasound examinations during the luteal phase of their cycle. First the
uterus was systematically examined to assess its position, size,
and morphology. Uterine morphology was carefully defined in
the B-mode image, giving special attention to the endometrium in the sagittal and transverse planes. The septum
could be recognized as an echogenic structure dividing the
uterus into two cavities. Next, transvaginal color Doppler scanning was performed by a different examiner who did not know
the results of the B-mode examination.
261