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Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
Fig. 24.21 Fetal thrombi in end-plate vessels (H & E, ⫻100).
sult of umbilical cord complications such as strangulation or
knotting of the cord, nuchal cord, or prolapse of the cord.
24
Fetal fibrin-rich microthrombi. Fetal fibrin-rich microthrombi
are found chiefly in terminal vascular branches at the periphery of the villi. They are usually a result of generalized intrauterine shock with disseminated intravascular coagulation
46
.
Fig. 24.22 Multiple obliterative foci in a placenta (35th week of ges-
tation).
242
Sequelae. The sequelae of chronic obliterative vascular diseases and fetal thrombi include hypovascularity or even
avascularity of the villi at the periphery of the placenta. Occurrence of the disease during the first half of pregnancy leads to
focal immaturity of the villi in the downstream villous tree.
With onset in the second half of pregnancy, histological examination shows obliteration of the villous capillar y lumina and fibrosis of the villous stroma. Placental infarction does not occur,
however, because the fetal villi are supplied by maternal blood
in the intervillous space.
Abnormalities of Maternoplacental Blood Flow
Figure 24.22 shows a placenta in the 35th week of gestation
permeated by multiple obliterative lesions of varying size and
color (some are red, others grayish-yellow or white). Their
pathogenesis is based on an abnormality of maternoplacental
blood flow. Given the large compensatory reserve of the
placenta, generally only extensive lesions that occupy more
than one-third of the organ lead to fetal growth restriction. If
more than half of the placenta is obliterated, a critical placental
insufficiency develops that is life-threatening to the fetus
Vogel distinguished among the following types of lesion
➤
Placental infarctions
➤
Reticular infarctions
➤
Intervillous thrombi
➤
Hematomas
➤
Subchorionic and basal pseudoinfarctions
Placental infarctions. Placental infarctions are areas of
parenchymal necrosis caused by an interruption of the mater-
5
.
46
nal blood supply, which may involve either a fetomaternal
circulatory unit (cotyledon infarction) or several adjacent placentones (massive infarction).
Infarctions are classified by their age as acute, subacute, or
chronic. A fresh infarct has a dark red color and friable consistency. Later it turns brownish red and finally grayish-white
in the chronic stage.
Figure 24.
23 shows the histological appearance of a chronic
infarction with complete villous necrosis and loss of the
chorionic epithelium. Some villi are only vaguely identifiable
as such (“ghost villi”). The decreased maternal blood supply
may result from atherosclerotic changes, spiral artery thrombosis or aneurysms (e.g., in a setting of arterial hypertension),
or a disorder of fat metabolism. Other potentialcauses are arteriopathies and arteriolopathies in diabetes mellitus, autoimmune disorders, and preeclampsia. Exogenous insults can also
produce vessel wall lesions that cause luminal narrowing
Reticular infarctions. Reticular infarctions (“gitterinfarcts”) are
obliterative lesions of variable size, often with maplike
borders, that show no consistent relationship to placentones
Figure 24.
infarction, in which multiple groups of villi are encased by ho-
:
24 shows the histological appearance of a reticular
mogeneous perivillous and intervillous fibrin masses. The histological spectrum ranges from a loss of chorionic epithelium
to complete villous necrosis. Various causes have been suggested besides maternal hypoxemia, including latent herpes
simplex infections and abnormal immune reactions between
the maternal and fetal tissue
6
. Extensive reticular infarctions
can restrict intervillous maternal blood flow and retard further
development and maturation of the villi in that region
46
.
46
.
5
.
Placental Insufficiency
Fig. 24.23 Histological appearance of a chronic placental infarction
(H & E, ⫻200).
Fig. 24.25a Intervillous thrombus (37th week of gestation). Fig. 24.25b Histological appearance of a thrombus in the inter-
Intervillous thrombus. Figure 24.25a shows an example of an
intervillous thrombus, appearing as a sharply circumscribed,
dark red area in the intervillous space, which corresponds to an
intravascular space. Coagulation and conglutination thrombi
can be distinguished from each other by histological examination. Figure 24.
25b shows the histological appearance of a con-
glutination thrombus in the intervillous space causing villous
displacement.
Intervillous thrombi may be caused by maternal venous
Fig. 24.24 Microscopic view of a reticular infarction (35th week of
gestation, H & E, ⫻100).
villous space (37th week of gestation, H & E, ⫻40).
Subchorionic and basal pseudoinfarcts. Pseudoinfarcts are
caused by the deposition of homogeneous fibrin masses
46
Generally they have no pathological significance but serve to
compensate for placental growth discrepancies and apparently increase the stability of the villous tree. Also, by limiting the size of the relatively villus-poor intervillous space
below the chorionic plate and in the basal plate region, they
can improve blood flow to centrally located placental areas
that contain more villi
5
.
outflow obstruction and/or by an irregularly structured inter-
villous space in which alternating zones of narrowing and di-
latation lead to turbulence or stasis of maternal blood flow.
Another possible cause of intervillous thrombi is damage to the
villous chorionic epithelium, due for example to injuries, hyp-
oxemia, or toxic or inflammatory changes and ruptures of
villous vessels
46
.
Placental Changes in Hypertensive Disorders of
Pregnancy
Acute atherosis. Extensivetrue infarctions are a relatively com-
mon finding in hypertensive disorders of pregnancy. Most of
these infarcts are located in the central areas of the placenta.
Characteristic but nonspecific vessel wall changes may be
Placental hematoma. Placental hematomas are abnormal collections of blood outside the intervillous space. A common example is retroplacental hematoma, which may be detectablein
cases of placental abruption.
found in maternal preplacental arteries. Histological sections
show endothelial cell damage, transmural fibrinoid necrosis,
aggregations of foam cells, lymphohistiocytic infiltrates, and
thrombi (Fig. 24.
26). These vessel wall changes can result in
Specific Obstetric Problems
.
243
Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
244
Fig. 24.26 Acute arterial vasculopathy with transmural fibrinoid
necrosis, lymphohistiocytic infiltrates, collections of foam cells, and
luminal narrowing (H & E, ⫻400).
luminal narrowing or even occlusion. Known also as “acute
atherosis,”the vessel wall lesions mayoccur at intradecidual or
24
even intramyometrial sites
5, 6, 46
.
Lupus erythematosus and antiphospholipid antibody syndrome. Vasculopathies can also occur in other maternal dis-
eases, most notably lupus erythematosus and antiphospholipid antibody syndrome
1, 35
. In these conditions it is common to detect antiphospholipid antibodies in the maternal
serum, especially a “lupus anticoagulant” and anticardiolipin
antibodies. This heterogeneous class of autoantibodies
directed against negatively charged phospholipids of proteins,
coagulation factors, and platelets can cause an immune
coagulopathy with thromboemboli and frequently leads to a
decidual vasculopathy
6, 16, 35
.
Typical changes. Other common but nonspecific findings in hypertensive pregnancy disorders are restricted growth of the
placenta and a decrease in its basal area. Villous maturation
may be appropriate for gestational age. It is not unusual to find
either compensatory early villous maturation or, less commonly, retarded villous maturation.
Tenney–Parker changes. Another fairly typical finding is “Tenney–Parker changes,” which consist of syncytial epithelial
buds and knots on the villous surfaces (Fig. 24.
27)
45
. The significance of these solid or fragmented nuclear clumps in late
pregnancy is a controversial issue. They have been variously interpreted as harmless sectioning artifacts
29
, as villous surface
irregularities that occur artifactually in flat sections but are still
useful diagnostically,or as real structures related to the sprouting of new terminal villi
11,28, 41
. These syncytial epithelial buds
and knots are seen with some frequency under hypoxemic
conditions (e.g., maternal anemia), in hypertensive disorders
of pregnancy, and in pregnancies at high altitudes.
Placental abruption. An increased incidence of premature separation of the placenta has been reported in hypertensive dis-
Fig. 24.27 Numerous syncytial nuclear buds and knots on the villous
surfaces (“Tenney-Parker changes,” 32nd week of gestation, preeclampsia, H & E, ⫻100).
orders of pregnancy—probably a result of the chronic perfusion
deficit and extensive fibrin deposition
5
.
Causes. This disease most likely traces its pathogenesis to the
time of placentation during the first trimester
44
. Morphometric studies of preeclamptic placentas with abnormal
Doppler findings have shown that these placentas often have
decreased weight and volume and reduced vascular parameters. Base d on these findings, abnormal implantation of the
placenta has been postulated as the cause
22, 47
. A failure of normal preplacental vessel-wall transformation due to deficient
fetal intravascular trophoblast invasion is considered to be the
main cause of hypertensivepregnancy disorders
8
. As a result of
this, the maternal spiral arteries are still susceptible to the effects of vasoconstrictor substances even after 18 weeks’ gestation.
Immunological maladaptation between the mother and
fetus may have causal significance in hypertensive disorders of
pregnancy. Raymond interprets preeclampsia as an exaggerated maternal immune response to immature fetal trophoblastic cells. In many preeclamptic women, he observed small,
superficially implanted placentas that had reactively forme d
an excess of immature trophoblasts. These cells could not
properly invade and remodel the spiral arteries due to an abnormal expression of adhesion and matrix molecules. Apparently, large numbers of these functionally incompetent
fetal trophoblastic cells trigger the maternal immune system
and stimulate antibody formation, leading to secondary vessel
wall damage
39
.
Inflammatory Placental Changes
Extensive inflammatory changes in the placenta can also compromise the function of the organ. Amniotic-type inflammations with chorioamnionitis, endplate vasculitis, omphalovasculitis, and/or funiculitis are distinguished from
parenchymal-type placentitis
46
.
Placental Insufficiency
Amniotic-Type Inflammations
In amniotic-type inflammations, the causative organisms may
reach the amniotic surface by the ascending route through an
open gestational sac. If the sac is closed, the organisms may
reach the placenta from the internal cervical os by the transmembranous or intramembranous routes. Possible fetal complications are infections of the lung and/or gastrointestinal
tract acquired from the contaminated amniotic fluid. An extensive spread of organisms via the fetal bloodstream can lead to
generalized fetal sepsis or septicopyemia.
Parenchymal-Type Placentitis
Causes. Placentitis of the parenchymal type is especially likely
to cause placental insufficiency. Signs of exudative and/or proliferative inflammation are found in the intervillous space, on
villous surfaces, and/or in the villous stroma. The inflammation may be caused by bacteria, viruses, fungi, parasites, or by
hypoxic states or toxicity leading to chorionic epithelial lesions. In many cases, however, the etiology of the placentitis
cannot be determined clinically or morphologically.
Route of infection. Infectious parenchymal placentitis is generally acquired by the maternal hematogenous route, with primary invasion of the intervillous space causing an initial acute
intervillous thromboangiitis
be a maternal sore throat, pneumonia, or bacterial endocarditis. In other cases an inflammation may spread directly by the
transdecidual route from maternal purulent endometritis, or
chorioamnionitis may spread to the placental margin or basal
plate by the transamniotic route.
Perivillitis. In florid perivillitis, sites of chorionic epithelial
necrosis and fibrin deposition are found on the villous surfaces,
which are permeated by maternal granulocytic and/or mononuclear cell infiltrates. In later stages, fibroblast proliferation
46
. The source of the infection may
with collagen fiber proliferation often leads to complete oblit-
eration of the intervillous space.
Villitis. Infectious villitis occurs when pathogenic organisms
reach the villi by fetal hematogenous spread. It is characterized
by necrosis of the villous stroma and chorionic epithelium and
by inflammatory cell infiltrates. In some cases the specific nature of the intrauterine infection can be determined from the
composition of the inflammatory infiltrate
Histological findings. Figure 24.
28 illustrates the histological
46
.
appearance of acute intervillous thromboangiitis, perivillitis,
and villitis secondary to intrauterine listeriosis. The infection
usually spreads by the transplacental route, leading to multiple
abscess formation in the placenta. In other cases, listeria present in the stool or vagina may spread by the ascending route
and incite a phlegmonous chorioamnionitis with purulent
liquefaction. In both modes of infection, a generalized septic
granulomatosis may develop in the fetus
Figure 24.
29 shows the histological features of a vaguely
12
.
granulomatous inflammation of the placenta with the formation of multinucleated Langhans-type giant cells like those
seen in tuberculosis or a varizella zoster infection
Figure 24.
30 shows the histological appearance of an exten-
6
.
sive fungal infection of the placenta in the 17th week of pregnancy with a retained maternal intrauterine device. Premature
rupture of the membranes had led to the development of an
extensive, florid chorioamnionitis, perivillitis, and villitis with
evidence of multiple Candida albicans hyphae.
Effects. Cases of extensive parenchymal placentitis with the
spread of organisms into the fetal circulation can lead to fetal
sepsis or septicopyemia with the development of multiple inflammatory foci in the fetalorgans and intrauterinefetal death.
In less severe cases, the compromise of placental function
caused by the inflammatory changes can lead to restriction of
fetal growth.
Specific Obstetric Problems
Fig. 24.28 Suppurative intervillous thromboangiitis, perivillitis, and
necrotizing villitis in intrauterine listeriosis (26th week of gestation,
H&E, ⫻200).
Fig. 24.29 Vaguely granulomatous villitis and perivillitis with a multinucleated Langhans giant cell (35th week of gestation, H & E, ⫻200).
245
Structure of the Human Placenta and Pathomorphological Changes in Placental Insufficiency
24.
31b shows a chorangioma with numerous vascular spaces
embedded in a stroma of varying cellularity. Large tumors in
particular may harbor regressive changes in the form of necrosis, intratumoral hemorrhage, thrombi, and calcifications.
Fig. 24.30 Parenchymal placentitis with evidence of Candida albicans
(17th week of gestation, PAS, ⫻200).
Placental Tumors
Chorangiomas
24
Chorangiomas are relatively common benign tumors that can
cause impairment of placental function. When sufficiently
large, they can be diagnosed with ultrasound. Chorangiomas
are solitary or multiple tumors that usually have a sharply circumscribed capsule. Most are less than 5 cm in diameter, but in
rare cases chorangiomas may occupy a large area of the
placenta, with a corresponding reduction of functional
parenchyma. These tumors may bulge into the amniotic cavity,
compressing the umbilical cord vessels. Chorangiomas have a
lobulated cut surface, a reddish-brown to yellow color, and a
relatively soft consistency (Fig. 24.
Histological findings. Endotheliomatous, capillary, and
cavernous forms can be distinguished histologically. Figure
31a).
Cause. Chorangiomas are believed to be caused by abnormal
fetal angiogenesis of the placenta
6, 46
. These tumors communi-
cate with the fetal circulatory system.
Complications. Besides placental insufficiency caused by the
reduced parenchyma, rare complications of chorangiomas include hemorrhage, placental abruption, and Kasabach–Meritt
syndrome. This syndrome is characterized by hemolytic anemia due to the mechanical destruction of red cells, and by the
presence of disseminated microthrombi
18
. Chorangiomas are
frequently accompanied by polyhydramnios, which is attributed to the transudation of fluid from the tumor surface
into the amniotic cavity and/or increased fetal urine excretion
resulting from the increased placental output
18
.
Very vascular chorangiomas can lead to fetal cardiomegaly
due to excessive arteriovenous shunting of blood and increased venous return to the fetal heart. In turn, this cardiomegaly can lead to heart failure and generalized hydrops
17, 18
fetalis
.
An association of chorangiomas with other fetal malformations such as cutaneous angiomas is occasionally described
31
Trophoblastic Tumors
Trophoblastic tumors are very rare neoplasms caused by the
invasive proliferation of trophoblasts, which may seed metastatic deposits. Choriocarcinomas and trophoblastic tumors of
the placental bed may occur in association with molar pregnancies and spontaneous abortions, and rare cases may be
seen after normal and ectopic pregnancies
6, 46
.
.
246
Fig. 24.31a Cut surface of a placenta with a 10 cm chorangioma
(37th week of gestation).
Fig. 24.31b Histological appearance of chorangioma (H & E, ⫻200).
References
Secondary Tumors
Secondary tumors of the placenta are rare. Embolized tumor
cells from carcinomas in other maternal organs have occasionally been found in the intervillous space, but these cells did
not infiltrate the villous stroma
5, 46
. True metastatic deposits in
the placenta, with transplacental spread to the fetus, have been
described in some patients with malignant tumors
5, 46
.
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248
Morphological and Morphometric Studies of the Placenta
25
Abnormalities of pregnancy and delivery relating to placental
insufficiency syndrome can have a variety of causes. As an
“organ between organisms,” the placenta plays a central role in
with Doppler Abnormalities of the Fetal Umbilical Arteries*
T. Hitschold
Clinical Aspects of Placental Insufficiency
The clinical aspects are illustrated by intrauterine growth re-
tardation and prematurity, which frequently occur in association with placental insufficiency. Etiological diagnosis, early
detection, and treatment continue to be subjects of comprehensive clinical and theoretical research.
Established diagnostic procedures. Traditionally, ultrasound
biometry and biochemical surveillance methods have been the
this process. A disturbance in the functional capacity of this
organ can be describe d in terms of its clinical, pathophysiological, and pathomorphological aspects.
established diagnostic procedures available to the obstetrician.
These procedures are essentially retrospective in nature, as
they are used to measure an existing condition of restricted
fetal growth and monitor its progression. Intervention is warranted if the fetal heart rate (FHR) trace suggests frank or impending fetal asphyxia, but this test is already measuring the
effects of placental insufficiency on fetal cardiovascular regulation, which may consist of hypoxemia, hypoxia, or acidosis.
Specific Obstetric Problems
Pathophysiological Aspects of Placental Insufficiency
The pathophysiological aspects of placental insufficiency are
generally investigated in experimental animal studies and
mainly involve uteroplacental and fetoplacental circulatory
mechanisms. The central importance of hemodynamics in all
partial functions of the placenta is widely acknowledged. Any
reduction in blood flow decreases the exchange capacity of the
placenta and reduces metabolic processes due to an insufficient supply of oxygen and nutrients.
Fetoplacental blood flow. Fetoplacental blood flow, unlike
other circulatory compartments, is not subject to neural or endocrine regulatory mechanisms. Basically, a fetus grows within
the limits imposed by its placenta. These limits are broad
enough to provide a safety reserve, but they appear to be
genetically determined. A variety of factors during pregnancy
can exhaust this safety reserve, causing the system to decompensate. In cases of this kind we can appreciate the inadequacies that exist in current established monitoring techniques,
which cannot readily distinguish antenatally between a
genetically small fetus and one that is growth-retarded due to
placental insufficiency.
* Dedicated with gratitude to my esteemed teachers, Professor P.
Berle and Professor H. Müntefering
New possibilities with Doppler sonography. The advent of noninvasive Doppler sonography has brought significant advantages from a methodological standpoint. Doppler ultrasound is
already being utilized in many clinical examinations. It can be
used to determine flow resistance and impedance, making it
possible to evaluate the perfusion of a selected region. Blood
flow measurements with chronically implanted transducers in
fetal sheep haveshown that the greatestblood pressure drop in
the fetoplacental circulation takes place across the villous
8
tree
fetoplacental compartment are critically determined by the
vascularity of the placental villi and that the umbilical cord
vessels, for example, play only a minor role. Impedance
changes in this region, as measured by qualitative resistance
indices in the fetal umbilical arteries, appear to precede other
parameters such as fetal movement patterns and FHR changes
by days or even weeks
veillance. This is a major diagnostic advance in populations at
risk and has been confirmed in prospective randomized stud-
39, 53
ies
Doppler findings are known. Given the difficulties of accurately determining vascular diameters and angles in the
umbilical cord vessels, quantitative measurements have
largely been discarded in favor of the qualitative analysis of
flow velocity waveforms based on the determination of resistance indices (S/D ratio, resistance index, pulsatility index).
. This suggests that the resistance and impedance in the
54
, signaling a need for appropriate sur-
showing a reduction of obstetric emergencies when the
249
Morphological and Morphometric Studies of the Placenta with Doppler Abnormalities of the Fetal Umbilical Arteries
Pathomorphological Aspects of Placental Insufficiency
250
Functional placental morphology5has described the morphological correlates of placental insufficiency such as infarction
and villous stromal fibrosis while also noting that the problem
of placental insufficiency is basically a matter of quantity: it is
caused less by typical, isolated placental changes than by a disproportion between supply and demand.
Fetoplacental villous and vascular architecture. Classic studies
by Schuhmann
41–43
described the fetal cotyledons, with their
central spiral artery terminations, as the smallest functional
unit (“placentone”) of the fetoplacental villous and vascular
tree. Kaufmann et al.
27–31
made additional discoveries in electron-microscopic examinations of serial sections, so that today
we havea fairlydetailed picture of the fetoplacentalvillous and
vascular architecture. Basically it consists of a parallel arrangement of flow units that are represented by a dichotomous pattern of vascular branches, starting with the endplate vessels
and extending to the villous vessels in the individual placentones.
25
Placental and fetal weight. Vogel
55
explored the relationship
between placental growth and maturation, i.e., links between
the size of the organ and its internal structural differentiation,
identifying placental weight as an important indicator of the
functional competence of the placenta. This is expressed, at
least to a degree, in the relationship between fetal weight and
placental weight. Ultimately it is uncertain what determines
this relationship. But the placenta and fetus do have a common
genome, and so it is reasonable to assume that the relationship
is genetically determined. Increased ratios of placental and
fetal weight may signal an imbalance in this relationship and
are commonly associated with intrauterine asphyxia. This parameter is clinically relevant, therefore, but it cannot be reliably determined in the antenatal period.
Maturation of the villous tree. Studies by Castelluci and Kauf-
7
mann
and Schweikhart44based on combined scanning electron-microscopic and histological examinations have brought
forth a new concept of defective placental maturation. These
authors distinguished the “branches” of the fetoplacental
villous tree (the mainstem villi) from the older and younger
“twigs” (mature and immature intermediate villi) and the
“leaves” (terminal villi). Deviations from the normal maturation of the villous tree may be associated with clinically detectable abnormalities (growth restriction, acidosis,
asphyxia)
5, 44, 45
. Initial studies in the late 1980 s
14,15, 26
to a correlation between Doppler sonographic findings and
qualitative morphological placental findings.
Morphometric studies of the terminal villi. Stoz et al.
Noack et al.
erature in Beck
37
, Teasdale5, and other authors (review of the lit-
2
) have performed morphometric investigations
and described changes in the terminal villi, also called “absorption villi,” in cases of maternal diabetes, preeclampsia, and
growth restriction. Beck
3, 4
, who carried out systematic computer-assisted histometric measurements at the periphery of
the placentone, found changes in the absorption villi in con-
pointed
46–48
nection with various typical pregnancy complications such as
prematurity, acidosis, diabetes, and preeclampsia. Beck found
compelling evidence that standardized morphometric
measurements of the peripheral absorption villi in a placentone are representative of the organ as a whole, using this as a
basis not only for measuring individual villous properties but
also for calculating functionally relevant internal surface areas.
This new ability to evaluate functional aspects of placental
morphology that can be quantitatively documented has contributed greatly to our understanding of pathophysiological relationships.
S/D ratio in the umbilical arteries. Giles et al.
11
made the breakthrough discovery that the arterioles in third-order villous
stems were greatly reduced—whether by defective angiogenesis or secondary obliteration—in human fetuses that showed
an increased S/D ratio in the umbilical arteries. Other authors
confirmed these findings
6, 35
, proving that resistance changes
in the placenta could be detected by the qualitative analysis of
Doppler waveforms sampled from the umbilical arteries.
Embolization of the fetoplacental circulation. Morrow et al.
were able to induce absent or reverse end-diastolic flow by
embolizing the fetoplacental circulation in fetal sheep with
50
µm microspheres. Kaufmann
31
found that the size of these
microspheres matched the mean diameter of the vessels in the
smaller mainstem villi of the human placenta (fitth-order to
eighth-order branches), and Giles
findings. Trudinger et al.
terminal villi with 15
52
and Schmidt et al.40occluded the
µm microspheres, as this dimension
11
further supported these
matches the size of the capillaries at that level. While this increased the S/D ratio, it did not induce an absence of end-diastolic flow. Trudinger
52
did measure a fall of the fetal arterial P
however, demonstrating the importance of the terminal villi
for gaseous exchange.
Umbilical resistance and placental reserve capacity. Thomp-
51
son
used a mathematical computer model of a resistor and
capacitor circuit to simulate the dichotomous branching pattern of the fetoplacental circulation and study the effects of
different variables on the flow patterns in the umbilical arteries. For example, the umbilical resistance rises as the number
of obliterated small vessels increases. This effect is more pronounced when there are fewer branches in the placental
vascular tree. Thus, the smaller the placenta and the more
severe the maturation defects in the villous tree, the more pronounced the resistance effect. These studies also showed that
approximately 60% of the vessels must be obliterated before
any resistance effect is noted in the waveform indices. This is
,
the mathematical expression of a “placental reserve capacity”
that guards against fetal compromise due to minor pathological changes.
Functional competence of the placenta. Morphometric tech-
2, 42
niques
can be used to document certain quantitative properties of the villi at a selected site in the fetomaternal flowunits
(Fig. 25.
1). Metabolically active villous surface areas can be cal-
36
,
O
2
culated to gain an impression of the functional competence of
the organ and of any disturbance of these mechanisms that occurs in certain pregnancy complications.
컅 Fig. 25.1 Two terminal villi with vessels showing sinusoidal dilatation
(S), epithelial plates (E), endothelial cells (EC), syncytiotrophoblasts
(Sy), and cytotrophoblasts (C). Semithin section, toluidine blue,
⫻2000.
Validation of Doppler Findings by Placental Histology
Validation of Doppler Findings by Placental Histology
The size of the vascular tree (the intravillous blood volume) is
of special interest in the validation of Doppler ultrasound findings by placental histology.
Resistance Index of the Umbilical Arteries
Figure 25.2 shows the relationship between the fetal intravillous blood volume and the umbilical artery resistance
index (RI) determined during the last week before birth. We
found a direct relationship between these variables, with a correlation coefficient of r = – 0.703. The larger the vascular tree of
220
200
180
160
140
120
100
80
Intravillous blood volume (ml)
60
40
20
0
0.4 0.5 0.6 0.7 0.9 O F ReF
0.3
Resistance index of umbilical artery (S–D)/S
Fig. 25.2 Resistance index in the umbilical arteries plotted against
the size of the fetoplacental vascular tree, expressed as the fetal in-
travillous blood volume (second-degree polynomial regression).
OF = absent end-diastolic flow; ReF = reverse end-diastolic flow.
Curve formula: y = 283.593–407.741x 155.50x
r = –0.703; r2= 0.508
0.8
2
the placenta, the lower the resistance to blood flow, i.e., the
lower the RI in the umbilical artery. Conversely, cases with a
particularly low villous blood volume show increased Doppler
indices or a loss of antegrade end-diastolic blood flow velocities (absent end-diastolic flow).
Placental reserve capacity. Analogously to the mathematical
model of Thompson
51
, our results indicate that the RI values
have a large range of normal variation, which represents the
“placental reserve capacity.” An RI of 0.5 (corresponding to an
S/D ratio of 2.0) may be associated with an intravillous blood
volume of 80–180 ml determined by our method. This is in
good agreement with the findings of other authors on volume
11,24, 40
flow
, which must be reduced by more than 50% before a
qualitative change in resistance index is seen. This also indicates that Doppler sonography of the umbilical arteries, while
not an acute study, is capable of detecting significant disturbances of vascularization and reductions in the fetoplacental
blood volume.
Reduced intravillous blood volume. A low fetal intravillous
blood volume of less than 85 ml is almost always associated
with an increased RI value that exceeds 0.66 (corresponding to
an S/D ratio of 3). We have thereforetaken that value as a cutoff
in determining the relationship of intravillous blood volume to
fetal risk. This is shown in Fig. 25.
3. As the graph indicates, fetal
risks have a higher association with a reduced blood volume
than with normal values of intravillous blood volume. This parameter is clinically relevant, therefore, and can be evaluated
with Doppler ultrasound. In cases with a small intravillous
blood volume (yellow bars in the graph), the rates of small-for-
gestational-age (SGA) fetuses (p = 0.000), the incidence of
severe acidosis (pH ⬍ 7.15 ) ( p = 0.004), the number of fetuses
with a low Apgar score (⬍ 8) (p = 0.029), and the cesarean section rates for impending intrauterine asphyxia (p = 0.000) are
significantly increased compared with fetuses whose placentas have a sufficiently large intravillous blood volume (blue
bars in the graph).
Specific Obstetric Problems
251