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Chapter 43 ■ Fetal Surveillance: Doppler Assessment of Pregnancy and Biophysical Profile 1497
55. Eik-Nes SH, Marsal K, Brubakk AO, et al. Ultrasonic measurement
of human fetal blood flow. J Biomed Eng 1982;4:28-36.
56. Lingman G, Marsal K. Fetal central blood circulation in the third
trimester of normal pregnancy: a longitudinal study. II. Aortic blood
velocity waveform. Early Hum Dev 1986;13:151-159.
57. Mari G. Arterial blood flow velocity waveforms of the pelvis and
lower extremities in normal and growth-retarded fetuses. Am J
Obstet Gynecol 1991;165:143-151.
58. Abuhamad AZ, Mari G, Bogdan D, Evans 3rd AT. Doppler flow
velocimetry of the splenic artery in the human fetus: is it a marker
of chronic hypoxia? Am J Obstet Gynecol 1995;172:820-825.
59. Finne PH, Halvorsen S. Regulation of erythropoiesis in the fetus and
newborn. Arch Dis Child 1972;47:683-687.
60. Fischer JW. Control of erythropoietin production. Exp Biol Med
1984;173:289-305.
61. Abuhamad AZ, Mari G, Cortina RM, et al. Superior mesenteric
artery Doppler velocimetry and ultrasonographic assessment of fetal
bowel in gastroschisis: a prospective longitudinal study. Am J Obstet
Gynecol 1997;176:985-990.
62. Rhee E, Detti L, Mari G. Superior mesenteric artery flow velocity
waveforms in small for gestational age fetuses. J Matern Fetal Med
1998;7:120-123.
63. Mari G, Uerpairojkit B, Abuhamad AZ, Copel JA. Adrenal artery
velocity waveforms in the appropriate and small-for-gestational-age
fetus. Ultrasound Obstet Gynecol 1996;8:82-86.
64. Mari G, Kirshon B, Abuhamad A. Fetal renal artery flow velocity
waveforms in normal pregnancies and pregnancies complicated by
polyhydramnios and oligohydramnios. Obstet Gynecol 1993;81:
560-564.
65. Vyas S, Nicolaides KH, Campbell S. Renal artery flow-velocity
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1989;161:168-172.
66. Uerpairojkit B, Chan L, Reece AE, et al. Cerebellar Doppler velocimetry in the appropriate- and small-for-gestational-age fetus.
Obstet Gynecol 1996;87:989-993.
67. Gudmundsson S, Tulzer G, Huhta JC, Marsal K. Venous Doppler
in the fetus with absent end-diastolic flow in the umbilical artery.
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68. Nakai Y, Miyazaki Y, Matsuoka Y, et al. Pulsatile umbilical venous
flow and its clinical significance. Br J Obstet Gynaecol 1992;99:
977-980.
69. Edelstone DI, Rudolph AM, Heymann MA. Liver and ductus
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70. Rudolph AM. Distribution and regulation of blood flow in the fetal
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71. Mari G, Uerpairojkit B, Copel JA. Abdominal venous system in the
normal fetus. Obstet Gynecol 1995;86:729-733.
72. Van Splunder IP, Huisman TW, Stijnen T, Wladimiroff JW. Presence of pulsations and reproducibility of waveform recording in the
umbilical and left portal vein in normal pregnancies. Ultrasound
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73. Reed KL, Appleton CP, Anderson CF, et al. Doppler studies of vena
cava flows in human fetuses: insights into normal and abnormal
cardiac physiology. Circulation 1990;81:498-505.
74. Rizzo G, Arduini D, Romanini C. Inferior vena cava flow velocity
waveforms in appropriate- and small-for-gestational-age fetuses. Am
J Obstet Gynecol 1992;166:1271-1280.
75. Kiserud T, Eik-Nes SH, Blaas HG, Hellevik LR. Ultrasonographic
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76. Rizzo G, Arduini D, Romanini C. Umbilical vein pulsations: a
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77. Picconi JL, Hanif F, Drennan K, Mari G. The transitional phase of
ductus venosus reversed flow in severely premature IUGR fetuses.
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78. Picconi JL, Kruger M, Mari G. Ductus venosus S-wave/isovolumetric
A-wave (SIA) index and A-wave reversed flow in severely premature
growth-restricted fetuses. J Ultrasound Med 2008;27:1283-1289.
79. Rizzo G, Arduini D, Romanini C, Mancuso S. Doppler echocardiographic assessment of atrioventricular velocity waveforms in normal
and small-for-gestational-age fetuses. Br J Obstet Gynaecol 1988;
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80. Hecher K, Campbell S, Snijders R, Nicolaides K. Reference ranges
for fetal venous and atrioventricular blood flow parameters. Ultrasound Obstet Gynecol 1994;4:381-390.
81. Carceller-Blanchard AM, Fouron JC. Determinants of the Doppler
flow velocity profile through the mitral valve of the human fetus. Br
Heart J 1993;70:457-460.
82. Hata T, Hata K, Takamiya O, et al. Fetal ventricular relaxation
assessed by Doppler echocardiography. J Cardiovasc Ultrasonogr
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83. Reed KL, Anderson CF, Shenker L. Changes in intracardiac Doppler
blood flow velocities in fetuses with absent umbilical artery diastolic
flow. Am J Obstet Gynecol 1987;157:774-779.
84. Shapiro I, Degani S, Leibovitz Z, et al. Fetal cardiac measurements
derived by transvaginal and transabdominal cross-sectional echocardiography from 14 weeks of gestation to term. Ultrasound Obstet
Gynecol 1998;12:404-418.
85. Mari G, Deter RL, Hanif F, et al. Sequence of cardiovascular changes
occurring in severe IUGR fetuses. Part II. Ultrasound Obstet
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86. Kenny JF, Plappert T, Doubilet P, et al. Changes in intracardiac blood
flow velocities and right and left ventricular stroke volumes with
gestational age in the normal human fetus: a prospective Doppler
echocardiographic study. Circulation 1986;74:1208-1216.
87. Machado MV, Chita SC, Allan LD. Acceleration time in the aorta
and pulmonary artery measured by Doppler echocardiography in the
midtrimester normal human fetus. Br Heart J 1987;58:15-18.
88. Kitabatake A, Inoue M, Asao M, et al. Noninvasive evaluation of
pulmonary hypertension by a pulsed Doppler technique. Circulation
1983;68:302-309.
89. Al-Ghazali W, Chita SK, Chapman MG, Allan LD. Evidence of
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Br J Obstet Gynaecol 1989;96:697-704.
90. Allan LD, Chita SK, Al-Ghazali W, et al. Doppler echocardiographic evaluation of the normal human fetal heart. Br Heart J
1987;57:528-533.
91. De Smedt MC, Visser GH, Meijboom EJ. Fetal cardiac output
estimated by Doppler echocardiography during mid- and late gestation. Am J Cardiol 1987;60:338-342.
92. Shiraishi H, Silverman NH, Rudolph AM. Accuracy of right ventricular output estimated by Doppler echocardiography in the sheep
fetus. Am J Obstet Gynecol 1993;168:947-953.
93. Moise Jr KJ, Mari G, Fisher DJ, et al. Acute fetal hemodynamic
alterations after intrauterine transfusion for treatment of severe red
blood cell alloimmunization. Am J Obstet Gynecol 1990;163:776-
784.
94. Rizzo G, Nicolaides KH, Arduini D, Campbell S. Effects of intravascular fetal blood transfusion on fetal intracardiac Doppler velocity
waveforms. Am J Obstet Gynecol 1990;163:1231-1238.
95. Gonzalez R, Medina L, Arriagada P, et al. Transdermal administration of a nitric oxide donor is not associated with changes in major
fetal cardiac and systemic hemodynamic parameters. Am J Obstet
Gynecol 1999;180:S3.
Prediction of Fetal Hematocrit
96. Mari G, Moise Jr KJ, Deter RL, Carpenter Jr RJ. Flow velocity
waveforms of the umbilical and cerebral arteries before and after
intravascular transfusion. Obstet Gynecol 1990;75:584-589.
97. Mari G, Moise Jr KJ, Deter RL, et al. Flow velocity waveforms of
the vascular system in the anemic fetus before and after intravascular
transfusion for severe red blood cell alloimmunization. Am J Obstet
Gynecol 1990;162:1060-1064.
98. Mari G, Moise Jr KJ, Deter RL, Carpenter Jr RJ. Doppler assessment of renal blood flow velocity waveforms in the anemic fetus
before and after intravascular transfusion for severe red cell alloimmunization. J Clin Ultrasound 1991;19:15-19.
99. Mari G, Rahman F, Olofsson P, et al. Increase of fetal hematocrit
decreases the middle cerebral artery peak systolic velocity in pregnancies complicated by rhesus alloimmunization. J Matern Fetal Med
1997;6:206-208.
100. Stefos T, Cosmi E, Detti L, Mari G. Correction of fetal anemia on
the middle cerebral artery peak systolic velocity. Obstet Gynecol
2002;99:211-215.
101. Mari G, Moise KJ, Kirshon B, et al. Middle cerebral artery pulsatility index and maximal velocity as indicators of fetal anemia. 37th
Annual Meeting of Society for Gynecologic Investigation, 1990.
102. Mari G, Adrignolo A, Abuhamad A, et al. Doppler ultrasound in
the management of the pregnancy complicated by fetal anemia. Am
J Obstet Gynecol 1993;168:318.
103. Mari G, Adrignolo A, Abuhamad AZ, et al. Diagnosis of fetal anemia
with Doppler ultrasound in the pregnancy complicated by maternal
1498 PART IV ■ Obstetric Sonography
blood group immunization. Ultrasound Obstet Gynecol
1995;5:400-405.
104. Mari G, Detti L, Oz U, et al. Accurate prediction of fetal hemoglobin by Doppler ultrasonography. Obstet Gynecol 2002;99:589-
593.
105. Pereira L, Jenkins TM, Berghella V. Conventional management of
maternal red cell alloimmunization compared with management by
Doppler assessment of middle cerebral artery peak systolic velocity.
Am J Obstet Gynecol 2003;189:1002-1006.
106. Van Dongen H, Klumper FJ, Sikkel E, et al. Non-invasive tests to
predict fetal anemia in Kell-alloimmunized pregnancies. Ultrasound
Obstet Gynecol 2005;25:341-345.
107. Cosmi E, Mari G, Delle Chiaie L, et al. Noninvasive diagnosis by
Doppler ultrasonography of fetal anemia resulting from parvovirus
infection. Am J Obstet Gynecol 2002;187:1290-1293.
108. Delle Chiaie L, Buck G, Grab D, Terinde R. Prediction of fetal
anemia with Doppler measurement of the middle cerebral artery
peak systolic velocity in pregnancies complicated by maternal blood
group alloimmunization or parvovirus B19 infection. Ultrasound
Obstet Gynecol 2001;18:232-236.
109. Senat MV, Loizeau S, Couderc S, et al. The value of middle cerebral
artery peak systolic velocity in the diagnosis of fetal anemia after
intrauterine death of one monochorionic twin. Am J Obstet Gynecol
2003;189:1320-1324.
110. 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 practice. New
York: McGraw-Hill; 2001. p. 247-283.
111. Sueters M, Arabin B, Oepkes D. Doppler sonography for predicting
fetal anemia caused by massive fetomaternal hemorrhage. Ultrasound Obstet Gynecol 2003;22:186-189.
112. Cosmi E, Dessole S, Uras L, et al. Middle cerebral artery peak systolic and ductus venosus velocity waveforms in the hydropic fetus.
J Ultrasound Med 2005;24:209-213.
113. Hernandez-Andrade E, Scheier M, Dezerega V, et al. Fetal middle
cerebral artery peak systolic velocity in the investigation of nonimmune hydrops. Ultrasound Obstet Gynecol 2004;23:442-445.
Multiple Gestations
114. Gaziano EP, Knox H, Ferrera B, et al. Is it time to reassess the risk
for the growth-retarded fetus with normal Doppler velocimetry of
the umbilical artery? Am J Obstet Gynecol 1994;170:1734-1741;
discussion 1741-1743.
115. Giles WB, Trudinger BJ, Cook CM, Connelly A. Umbilical artery
flow velocity waveforms and twin pregnancy outcome. Obstet
Gynecol 1988;72:894-897.
116. Divon MY, Girz BA, Sklar A, et al. Discordant twins: a prospective
study of the diagnostic value of real-time ultrasonography combined
with umbilical artery velocimetry. Am J Obstet Gynecol 1989;161:
757-760.
117. Degani S, Gonen R, Shapiro I, et al. Doppler flow velocity waveforms in fetal surveillance of twins: a prospective longitudinal study.
J Ultrasound Med 1992;11:537-541.
118. Hecher K, Ville Y, Nicolaides KH. Fetal arterial Doppler studies in
twin-twin transfusion syndrome. J Ultrasound Med 1995;14:101-
108.
119. Kontopoulos EV, Quintero RA, Chmait RH, et al. Percent absent
end-diastolic velocity in the umbilical artery waveform as a predictor
of intrauterine fetal demise of the donor twin after selective laser
photocoagulation of communicating vessels in twin-twin transfusion
syndrome. Ultrasound Obstet Gynecol 2007;30:35-39.
120. Quintero RA, Morales WJ, Allen MH, et al. Staging of twin-twin
transfusion syndrome. J Perinatol 1999;19:550-555.
121. Mari G, Roberts A, Detti L, et al. Perinatal morbidity and mortality
rates in severe twin-twin transfusion syndrome: results of the International Amnioreduction Registry. Am J Obstet Gynecol 2001;
185:708-715.
122. Huhta JC, Moise KJ, Fisher DJ, et al. Detection and quantitation
of constriction of the fetal ductus arteriosus by Doppler echocardiography. Circulation 1987;75:406-412.
123. Robyr R, Lewi L, Salomon LJ, et al. Prevalence and management of
late fetal complications following successful selective laser coagulation of chorionic plate anastomoses in twin-to-twin transfusion syndrome. Am J Obstet Gynecol 2006;194:796-803.
Indomethacin and Ductus Arteriosus
124. Rasanen J, Debbs RH, Wood DC, et al. The effects of maternal
indomethacin therapy on human fetal branch pulmonary arterial
vascular impedance. Ultrasound Obstet Gynecol 1999;13:112-
116.
125. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin. Antepartum fetal surveillance. (No 9, Oct 1999;
replaces Tech Bull No 188, Jan 1994.) Clinical management guidelines for obstetrician-gynecologists. Int J Gynaecol Obstet 2000;
68:175-185.
Biophysical Profile Scoring
126. Manning FA, Platt LD, Sipos L. Antepartum fetal evaluation: development of a fetal biophysical profile. Am J Obstet Gynecol 1980;
136:787-795.
127. Morrison I. Perinatal mortality: basic considerations. Semin Perinatol 1985;9:144-150.
128. Manning FA, Morrison I, Lange IR, et al. Fetal biophysical profile
scoring: selective use of the nonstress test. Am J Obstet Gynecol
1987;156:709-712.
129. Chamberlain PF, Manning FA, Morrison I, et al. Ultrasound evaluation of amniotic fluid volume. I. The relationship of marginal and
decreased amniotic fluid volumes to perinatal outcome. Am J Obstet
Gynecol 1984;150:245-249.
130. Patrick JE, Dalton KJ, Dawes GS. Breathing patterns before death
in fetal lambs. Am J Obstet Gynecol 1976;125:73-78.
131. Romero R, Chervenak FA, Berkowitz RL, Hobbins JC. Intrauterine
fetal tachypnea. Am J Obstet Gynecol 1982;144:356-357.
132. Manning FA, Baskett TF, Morrison I, Lange I. Fetal biophysical
profile scoring: a prospective study in 1,184 high-risk patients. Am
J Obstet Gynecol 1981;140:289-294.
133. Phelan JP, Ahn MO, Smith CV, et al. Amniotic fluid index measurements during pregnancy. J Reprod Med 1987;32:601-604.
134. Manning FA, Harman CR, Morrison I, et al. Fetal assessment based
on fetal biophysical profile scoring. IV. An analysis of perinatal
morbidity and mortality. Am J Obstet Gynecol 1990;162:703-709.
135. Magann EF, Doherty DA, Field K, et al. Biophysical profile with
amniotic fluid volume assessments. Obstet Gynecol 2004;104:5-
10.
136. Jansen AH, Chernick V. Fetal breathing and development of control
of breathing. J Appl Physiol 1991;70:1431-1446.
137. Kurjak A, Andonotopo W, Hafner T, et al. Normal standards for
fetal neurobehavioral developments: longitudinal quantification by
four-dimensional sonography. J Perinat Med 2006;34:56-65.
138. Kim SY, Khandelwal M, Gaughan JP, et al. Is the intrapartum
biophysical profile useful? Obstet Gynecol 2003;102:471-476.
139. Odibo AO, Quinones JN, Lawrence-Cleary K, et al. What antepartum fetal test should guide the timing of delivery of the preterm
growth-restricted fetus? A decision-analysis. Am J Obstet Gynecol
2004;191:1477-1482.
140. Clark SL, Sabey P, Jolley K. Nonstress testing with acoustic stimulation and amniotic fluid volume assessment: 5973 tests without unexpected fetal death. Am J Obstet Gynecol 1989;160:694-697.
141. Nageotte MP, Towers CV, Asrat T, Freeman RK. Perinatal outcome
with the modified biophysical profile. Am J Obstet Gynecol 1994;
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142. Seeds AE. Current concepts of amniotic fluid dynamics. Am J Obstet
Gynecol 1980;138:575-586.
143. Rutherford SE, Phelan JP, Smith CV, Jacobs N. The four-quadrant
assessment of amniotic fluid volume: an adjunct to antepartum fetal
heart rate testing. Obstet Gynecol 1987;70:353-356.
144. Miller DA, Rabello YA, Paul RH. The modified biophysical profile:
antepartum testing in the 1990s. Am J Obstet Gynecol 1996;174:
812-817.
145. Baschat AA, Gembruch U, Harman CR. The sequence of changes
in Doppler and biophysical parameters as severe fetal growth restriction worsens. Ultrasound Obstet Gynecol 2001;18:571-577.
146. Mari G, Hanif F, Treadwell MC, Kruger M. Gestational age at
delivery and Doppler waveforms in very preterm intrauterine
growth-restricted fetuses as predictors of perinatal mortality. J Ultrasound Med 2007;26:555-559; quiz 560-562.
147. Manning FA, Martin Jr CB, Murata Y, et al. Breathing movements
before death in the primate fetus (Macaca mulatta). Am J Obstet
Gynecol 1979;135:71-76.
CHAPTER 44
Sonographic Evaluation of
the Placenta
Thomas D. Shipp
Chapter Outline
PLACENTAL DEVELOPMENT
Placental Appearance
Placental Size
Placental Vascularity and Doppler
Ultrasound
Amnion-Chorion Separation
PLACENTA PREVIA
PLACENTA ACCRETA
PLACENTAL ABRUPTION
PLACENTAL INFARCTION
PLACENTAL MASSES
MESENCHYMAL DYSPLASIA OF
THE PLACENTA
MOLAR GESTATIONS
MORPHOLOGIC PLACENTAL
ABNORMALITIES
Circumvallate Placenta
Succenturiate Lobe
Bilobed Placenta
UMBILICAL CORD
The use of ultrasound to evaluate the placenta is
routine among the majority of pregnant American
women because they have at least one ultrasound examination during pregnancy. A wide range of pregnancy
complications result from abnormal placental development, including preeclampsia, intrauterine growth
restriction (IUGR), and abruption. Other placental
abnormalities, such as placenta previa, percreta, or vasa
previa, may cause major maternal and fetal complications. Timely recognition of these abnormalities can lead
to improved management of pregnancy and delivery.
Thus, careful examinations of the placenta by ultrasound
can contribute directly to enhanced patient care and
improved outcomes.
PLACENTAL DEVELOPMENT
The early developing embryo is surrounded by amnion
and chorion. Villi cover the entire surface of the chorion
up to about 8 weeks of gestation (Fig. 44-1). The villi,
which are the basic structures of the placenta, initially
form by 4 or 5 weeks’ gestation. The villi next to the
decidua capsularis degenerate, forming the chorion
laeve. The villi contiguous with the decidua basalis
become the chorion frondosum and later the placenta.
The fetal side of the placenta consists of the chorionic
plate and chorionic villi. The maternal side consists of
the decidua basalis, which open up into large cisterns,
the intervillous spaces. The fetal villi are immersed in
maternal blood located in the intervillous spaces. Anchoring villi develop from the chorionic plate.
1
These attach
Size and Appearance
Insertion into the Placenta
Velamentous and Marginal Cord
Insertions
Vasa Previa
PLACENTA DURING LABOR AND
POSTPARTUM
Third Stage of Labor
Retained Products of Conception
CONCLUSION
to the decidua basalis, holding the placenta in place.
By the end of pregnancy, the villi have a surface area of
12 to 14 square meters.
4
2,3
Placental Appearance
The placenta in the first and second trimesters is slightly
more echogenic than the surrounding myometrium (Fig.
44-2, A). The attachment site, or base of the placenta,
should be clearly delineated from the underlying myometrium. The edges of the placenta usually have a small
sinus, the marginal sinus of the placenta (Fig. 44-2,
B), where intervillous blood drains into the maternal
venous circulation. This structure should not be confused with placental separation. As the placenta matures,
areas of echogenicity within the placenta are visualized
(Fig. 44-2, D and E ). In cases of placental infarction,
there may be hypoechoic lesions with echogenic borders.
Placental lakes (venous lakes) occur in up to 5% of
pregnancies
5-9
(Fig. 44-2, C; Video 44-1). They repre-
sent areas of intervillous spaces devoid of placental villous
trees. They can be seen as hypoechoic structures in the
placenta. Moving blood flow can be seen in these areas.
They may have irregular shapes or a narrow, cleftlike
appearance and may change in appearance over time.
Placental Size
Placental length is approximately six times its maximal
width at 18 to 20 weeks’ gestation. The mean thickness
of the placenta in millimeters in the first half of pregnancy closely approximates the gestational age in weeks.
10
1499
Decidual vessel
Maternal
decidua
ET
Floating
villus
Anchoring
villus
Fetal vessels
EVT
Intervillus space
CT
ST
FIGURE 44-1. Human placenta microarchitecture. Fetal derivatives in the placenta consist of fetal vessels and placental coty-
ledons (villi). Villi consist of fetal vessels surrounded by cytotrophoblast cells (CT). Covering the cytotrophoblast cells is a multinucleated
cellular layer called the syncytiotrophoblast (ST). Anchoring villi are in direct contact with the maternal uterine lining, called the decidua.
The decidua is traversed by maternal vasculature. Blood from these vessels empties into the intervillous space and bathes the placental
villi. Note that maternal and fetal blood vessels are separated by trophoblast, villous stroma, and fetal vascular endothelium. Cytotrophoblast cells from anchoring villae can change into an invasive phenotype called extravillous cytotrophoblast cells (EVT). EVT invade deeply
into the maternal decidua. Some EVT, called endovascular trophoblast cells (ET), embed within the walls of the maternal vasculature.
(From Comiskey M, Warner CM, Schust DJ: MHC molecules of the preimplantation embryo and trophoblast. In: Mor G, ed. Immunology of Pregnancy. Austin/New York: Landes Bioscience, 2006.)
Marginal
sinus
FIGURE 44-2. Normal ap-
pearance of placenta. A, At
18 weeks, note the uniformly
echogenic appearance of the placenta and a uterine contraction
deviating the placenta. B, Note
marginal sinus of placenta
(arrow), a circumferential venous
drainage point into the maternal
uterine veins that should not be
mistaken for placental separation.
C, Placental lake (arrow) at 20
weeks. Calipers denote length of
placenta. D and E, Note the
increasing echogenicity in the
placenta as it matures. (D and E
from Burton GJ, Jauniaux E. Sonographic, stereological and Doppler
flow velocimetric assessments of placental maturity. Br J Obstet Gynaecol 1995;102:818-825.)
A B
C
E
D
Chapter 44 ■ Sonographic Evaluation of the Placenta 1501
If the placenta thickness is greater than 4 cm (40 mm)
before 24 weeks, an abnormality should be suspected.
These abnormalities include ischemic-thrombotic
damage, intraplacental hemorrhage, chorioangioma,
and fetal hydrops (Fig. 44-3).
Given the variable shape of the placenta, calculating
a volume from two-dimensional (2-D) imaging can be
complicated. Multiplanar volume calculation involves
FIGURE 44-3. Thick placenta in fetal hydrops. Note
the ascites (arrow).
sequential sections of the placenta at intervals such as
1.0 mm. The margins are manually traced, and a volume
is calculated.11 Most current studies appraising the use
of three-dimensional (3-D) sonography have used the
VOCAL (Virtual Organ Computer-aided AnaLysis)
method,
11
in which the 3-D volume in question is
rotated and the area of interest traced at its margin, after
which a volume is calculated (Fig. 44-4).
Placental volume approximation in the first trimester
holds promise as an important part of early pregnancy
evaluation. Uterine artery Doppler analysis can provide
some information regarding IUGR and maternal hypertension, but it is insufficient as a sole indicator of trophoblast invasion, in part because it is typically performed
late in the second trimester. Small placental volumes in
the first trimester presage abnormal uterine artery perfu-
12
Uterine artery Doppler ultrasound combined
sion.
with assessment of placental volume may identify pregnant women at risk for hypertension, abruption, or
13,14
IUGR.
First-trimester placental volumes correlate
with pregnancy-associated plasma protein A (PAPP-A)
and free beta-human chorionic gonadotropin (f-β-hCG)
15
levels,
tal volumes in the first trimester with maternal serum
screening for aneuploidy.
suggesting the potential introduction of placen-
15
The first-trimester placental
volume quotient (placental volume/crown-rump length)
is low for aneuploid fetuses, with 53% having a quotient
less than 10th centile.
is 83%, and for triplets, 76%, that of singletons, for a
given gestational age.
16
For twins, the placental volume
17
The placenta dramatically increases in size until
approximately 15 to 17 weeks’ gestation. From this
FIGURE 44-4. Three-dimensional assessment of placental volume in second trimester.
1502 PART IV ■ Obstetric Sonography
Decidua
Umbilical
Fetal
Umbilical
Amniochorionic
membrane
Decidua
basalis
FIGURE 44-5. Schematic drawing of placental vasculature.
vein
Chorionic
plate
Myometrium
circulation
Endometrial
veins
point, there is a fourfold increase in placental size until
delivery, whereas the fetus has a 50-fold increase in size
until delivery.
ated with maternal nutritional status, birth weight, and
pregnancy outcome.
18
Midtrimester placental volume is associ-
19-23
arteries
Intervillous
space
Maternal circulation
Main stem
Endometrial
arteries
villus
parietalis
Chorion
Amnion
Anchoring villus
ogy by assessing placental flow and documenting the
amount of flow in a given area. Because of its low variability between sampling sites in varied parts of the placenta, 3-D imaging may have a future role in assessing
flow in high-risk pregnancies (e.g., hypertension,
IUGR).
33
Placental Vascularity and Doppler
Ultrasound
The human placenta is a discoidal, villous, hemochorial
structure. Nutrients are exchanged over many villi. Surrounding the villi are the intervillous spaces, which are
bathed in maternal blood. The villi are sproutlike projections from the chorionic plate into the intervillous space.
The villi are directly connected to the fetal vascular
system, whereas the maternal blood emanates from the
developing spiral arteries to the intervillous spaces to
contact directly the trophoblasts of the villi
24
(Fig. 44-5).
Maternal blood flow of the intervillous space depends on
flow from the spiral arteries. Maternal vascular disease
(e.g., hypertension) can directly affect the pregnancy by
limiting this blood flow.
Intervillous blood flow begins early in the first trimes-
26-28
Color Doppler ultrasound has been used to
ter.
25
detect this intervillous and spiral artery flow by 12 weeks’
gestation, but the flow, if any, that occurs before this
time is not well understood.
ence of intervillous blood flow by gray-scale imaging may
indicate failed pregnancy.
Color and power Doppler sonography have been used
to identify blood flow in intraplacental villous arteries.
A decrease in the number of detectable intraplacental
villous arteries is associated with IUGR.
29
Before 12 weeks, the pres-
30
32
31
Threedimensional power Doppler ultrasound provides a better
appreciation of placental vascularity and pathophysiol-
Amnion-Chorion Separation
The amnion normally “fuses” with the chorion early in
the second trimester. Failure of the amnion and chorion
to fuse after 17 weeks is a rare complication of pregnancy, associated with multiple abnormalities. Previous
amniocentesis is a risk factor for amnion-chorion separa-
34
Associated factors may include IUGR, preterm
tion.
delivery, oligohydramnios, placental abruption, and
Down syndrome
35
(Fig. 44-6).
PLACENTA PREVIA
The term “placenta previa” refers to a placenta that is
“previous” to the fetus in the birth canal. The incidence
at delivery is approximately 0.5% of all pregnancies.
Bleeding in the second and third trimesters is the
hallmark of placenta previa. This bleeding can be life
threatening to the mother and fetus. With expectant
management and cesarean delivery, both maternal and
perinatal mortality have decreased over the past 40
37,38
years.
improve the outcome for mother and neonate.
torically been performed by digital assessment of the
lower uterine segment and placenta through the cervix.
Using this potentially hazardous method of evaluation,
Accurate diagnosis of placenta previa is vital to
The differentiation of placental positions has his-
36
Chapter 44 ■ Sonographic Evaluation of the Placenta 1503
FIGURE 44-6. Chorioamniotic separation in second
trimester. Amnion (short arrow) is separated from the chorion
(long arrow).
1
A B C
1
1
1 D 1.62cm
D E F
FIGURE 44-7. Placental position. Transabdominal sonography (A-C) and transvaginal sonography (C-E) can be used to determine
placental position. If the position is unclear transabdominally, vaginal sonography should be used. A, Complete placenta previa (arrow).
The maternal cervix is demarcated by the calipers. B, Marginal placenta previa. The internal cervical os is indicated by the arrow. C, Low
placenta. The long arrow indicates the placental edge and the short arrow indicates the internal cervical os. D, Complete placenta previa.
E, Complete placenta previa. The placental tip (long arrow) crosses the os (short arrow). F,
from the internal os.
placental position was classified as complete placenta
previa, partial placenta previa, incomplete placenta
previa, marginal placenta previa, low-lying placenta, and
placenta distant from the internal cervical os. These classifications do not directly apply to the ultrasound examination of placental position relative to the cervix. The
use of ultrasound to evaluate the position of the placenta
in the uterus has both improved knowledge of the placenta within the uterus and simplified terminology with
respect to placental position (Fig. 44-7). Complete pla-
centa previa describes the situation in which the internal
cervical os is totally covered by the placenta. Marginal
placenta previa denotes placental tissue at the edge of
or encroaching on the internal cervical os. A low pla-
is one in which the placental edge is within 2 cm,
centa
but not covering any portion, of the internal cervical os.
The terms “incomplete placenta previa” and “partial placenta previa” have no place in the current sonographic
Low placenta. The tip of the placenta is 1.6 cm
1504 PART IV ■ Obstetric Sonography
assessment of placental position and should be used only
by a clinician performing a digital examination when a
“double setup” is necessary to determine where the
leading edge of the placenta lies.
Transabdominal scanning can be used to visualize the
internal cervical os and to determine the relation of the
placenta to the cervix in most cases. Factors that can
adversely affect the visualization of the cervix include
prior abdominal surgery, obesity, deep or low position of
the fetal head or presenting part, overfilled or underfilled
maternal bladder, or uterine contractions. Transvaginal
sonography is safe
39
and accurate in depicting the internal
cervical os. The proximity of the cervix to the vaginal
probe allows higher-frequency probes to be used, with
better resolution and thus better visualization of the internal cervical os. With improved resolution, clinicians can
accurately determine the position of the leading placental
edge to the internal cervical os. The use of transvaginal
sonography has been shown to change the assessment of
the placental location in 25% of cases when the placenta
is within 2 cm of the internal cervical os, as identified
transabdominally.40 A leading placental edge greater than
2 cm from the internal cervical os is associated with
vaginal delivery, and distances less than 2 cm are associated with bleeding, leading to cesarean delivery.
41,42
Although placenta previa can occur in nulliparas, risk
factors include number of prior cesarean deliveries (odds
ratio: 4.5 for one; 44.9 for four
independent of number of prior cesarean deliveries,
and increasing maternal age.
43
), increasing parity
45
44
Early in the second trimester, the placenta occupies a
relatively large portion of the uterine cavity and often is
positioned near the cervix. As the uterus grows, a lesser
proportion of placentas are located near the internal
cervical os. This relative change in placental position is
best understood by the placental migration theory.
46
This theory of “dynamic placentation” suggests that as
the uterus develops, the placenta is “drawn away” from
the internal cervical os. It is unclear whether the primary
mechanism is disproportionate development of the lower
uterine segment so that the placenta, although it does
not detach from the uterine wall, comes to lie more
distant from the internal cervical os. This theory would
also be consistent with complete central placenta previas
that do not resolve at a rate approaching that of other
low-lying placentas, because the expansion of the lower
uterine segment would not lead to the resolution of this
type of placenta previa.
If the placenta overlaps the cervix by less than 2 cm,
more than 88% of patients deliver vaginally.47 A rate of
migration (in the second and third trimesters) away from
the internal os of 3.0 to 5.4 mm per week is also associated with vaginal delivery, whereas a placental-internal
os distance of less than 2 cm or a pattern of migration
of 0.3 to 0.6 mm weekly are associated with interventional cesarean delivery and a higher rate of peripartum
complications.
47,48
The prediction of a placenta previa at delivery is best
when the placenta overlaps the internal cervical os by
1.4 cm at 10 to 16 weeks’ gestation,49 or 2 cm at 20 to
23 weeks.50 Mustafa et al.51 demonstrated that if the
placenta overlaps by 2.3 cm at 11 to 14 weeks, the probability of a placenta previa at term is 8%, with a sensitivity
of 83% and a specificity of 86%.
51
Aside from a complete
central placenta previa, given the current data, it is still
difficult to predict precisely which patients will have
resolution of their low placenta; therefore, further ultrasound examinations are required to assess placental position if a low placenta is identified early in gestation.
For women with a low placenta, the description of the
leading edge of the placenta in the early third trimester
as “thin” (≤
1 cm in thickness and/or angle of placental
edge <45 degrees) or “thick” (any other type of placenta)
can be predictive of delivery complications. Antepartum
hemorrhage is more common with thick-edged placentas, as is the rate of cesarean delivery, placenta accreta,
low birth weight, and earlier gestational age at delivery.
Interestingly, a more recent study performed in the
first and second trimesters suggested that a thin-edged
placenta with a smaller angle was more predictive of
placenta previa.
53
Although not ready for clinical implementation, this parameter may help identify patients
who can be reassured early in pregnancy that they will
not have a placenta previa at delivery.
PLACENTA ACCRETA
The normal placenta invades the inner third of the myometrium. At delivery, the placenta separates at the decidual plane, with an abrupt cessation of intraplacental
flow as the myometrium contracts.
abnormally adherent to the uterine wall after delivery is
termed placenta accreta. Placenta increta occurs if
the placenta invades the myometrium more deeply, and
placenta percreta refers to a placenta that at least in part
protrudes through the uterine serosa. Placenta accreta,
increta, and percreta are serious complications of pregnancy associated with maternal blood loss, need for hysterectomy, and retained products of conception. With
ultrasound, placenta accreta can be identified antenatally
so that delivery plans can be made prospectively, improving the outcome for mother and child.
Although placenta accreta (or increta or percreta) can
occur in any pregnancy, important risk factors include
prior uterine surgery (with risk increasing with increasing
number of prior cesarean deliveries), placenta previa,
unexplained elevated maternal serum alpha-fetoprotein
(MS-AFP), increased maternal cell-free placental lactogen, and advancing maternal age.
placenta previa and no prior history of cesarean section
has a baseline risk of 0.26% for placenta accreta. This
increases almost linearly with number of prior cesarean
sections, to 10% in patients with four or more.
54
A placenta that is
55-58
A woman with no
59
Women
52
Chapter 44 ■ Sonographic Evaluation of the Placenta 1505
with a placenta previa and an unscarred uterus have a 5%
risk of clinical placenta accreta. With a placenta previa
and one previous cesarean section, the risk of placenta
accreta is 24%; this risk increases to 67% with a placenta
previa and four or more cesarean deliveries.
59
Several sonographic signs are associated with placenta
accreta. The presence of a coexisting placenta previa in
the majority of cases makes it particularly likely that the
adherent portion of the placenta will be low in the
uterus, in the region of a prior cesarean section scar. This
simple fact makes the evaluation of these placentas much
more straightforward with the transvaginal ultrasound
probe. Sonographic findings of placenta accreta include
loss of the normal hypoechoic retroplacental-myometrial
interface, thinning or disruption of the hyperechoic
subvesicular uterine serosa, presence of focal exophytic
masses, and numerous placental lakes
60-63
(Fig. 44-8).
The color Doppler ultrasound findings suggestive
of placenta previa accreta include diffuse lacunar blood
flow throughout the placenta, dilated vascular channels
between the placenta and bladder or cervix, absence of
the normal subplacental venous flow, and the demonstration of vessels crossing the placental-myometrial disruption site.
be helpful for evaluation of vascular anatomy in the
setting of a placenta accreta.
64,65
Three-dimensional sonography may also
66,67
The gray-scale and color
Doppler sonographic findings described for placenta
accreta are also present, but more exaggerated, in placenta
increta/percreta (Fig. 44-9; Videos 44-2 and 44-3).
Three-dimensional color and power Doppler ultrasound
is helpful to demonstrate the extensive torturous vascularity seen with such placentas. Greatly increased vascular
lacunae with turbulent or “tornado” blood flow increases
the likelihood of placenta increta/percreta.
68
As in many aspects of obstetric sonography, early diagnosis is preferable. In women with a history of cesarean
delivery, a gestational sac in the lower half of the uterus,
at or before 10 weeks’ gestation, is associated with
A B
C D
FIGURE 44-8. Placenta accreta with placental lakes. A, Transabdominal sonogram of a third-trimester placenta shows a
placental (venous) lake (arrow). B, In a different patient, transabdominal sonogram of second-trimester placenta shows multiple placental
lakes (long arrow); short arrow, fetal head. C, In another patient, transvaginal sonogram of second-trimester placenta shows intense color
flow within and below the placenta; long arrow, fetal head; short arrow, maternal bladder. D, In the same patient as C, multiple placental
lakes are visualized (arrowheads).
1506 PART IV ■ Obstetric Sonography
FIGURE 44-9. Placenta percreta. Transvaginal sonogram
of a third-trimester placenta shows loss of the hypoechoic border
between the placenta and the myometrium, with protrusion of the
placenta (long arrow) into the maternal bladder (arrowhead); short
arrow, placental lake.
FIGURE 44-10. First-trimester placenta accreta.
The umbilical cord insertion is low in the uterus; arrowheads
indicate multiple small placental lakes. This patient had a prior
cesarean delivery and subsequently was shown to have a placental
previa accreta.
placenta accreta,69 as are first-trimester placental
70,71
lacunae
or nonspecific findings are present, magnetic resonance
imaging (MRI) may be helpful,
(Fig. 44-10). When the diagnosis is unclear
72-76
particularly when the
placenta is posterior over an area of prior uterine scar,
such as from myomectomy (Fig. 44-11).
Information about placenta accreta and its variants is
indispensable for delivery management. Accurate prenatal diagnosis allows uterine conservation and avoidance
of massive blood loss at delivery. Strategies include
preoperative placement of internal iliac artery balloon
catheters and ultrasound-guided fundal classic cesarean
section to deliver the fetus above the upper margin of
the placenta.
PLACENTAL ABRUPTION
Placental abruption is one of the worrisome causes
of vaginal bleeding in the latter part of pregnancy
because it contributes to perinatal mortality. Patients
typically present with third-trimester vaginal bleeding
associated with abdominal or uterine pain and labor. The
incidence is approximately 0.5% of pregnancies. History
of prior abruption, hypertension, prolonged rupture
of membranes, IUGR, chorioamnionitis, polyhydramnios, maternal thrombophilias, maternal substance
use (tobacco, alcohol, cocaine), maternal trauma, and
advanced maternal age are all risk factors for placental
abruption.
77-79
The diagnosis of placental abruption is
typically made based on clinical findings; the retroplacental clot is frequently isoechoic to the placenta or myometrium and cannot always be identified sonographically.
A subplacental hematoma between the placenta and
uterine wall is a placental abruption (Fig. 44-12). This
should be differentiated from a subchorionic hema-
toma, in which the hematoma is underneath the chorion,
not the placenta. Although a subchorionic hematoma
can occur anytime during pregnancy, it is more common
in the first half of pregnancy, and its appearance will
change as the hematoma organizes (Fig. 44-13, A). A
preplacental hematoma is a rare condition likely caused
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