Chapter 6. Placental Abnormalities
BS. Nguyễn Hồng Anh
During pregnancy, the placenta provides the indispensable
interace between mother and etus (Chap. 5, p. 86). However, in part due to inaccessibility throughout gestation, the
placenta’s anatomy, physiology, and molecular structure still
remain some o the most understudied and intriguing topics in
obstetrics. Furthermore, the parallels between placental ormation and cancer aord opportunities to understand tumor biology and pathogenesis (Costanzo, 2018; Guttmacher, 2014).
Visual placental inspection by the obstetrician is recommended, but routine pathological examination is not mandatory. Indeed, specic conditions that merit submission or
detailed inspection are still debated. For example, the College
o American Pathologists recommends placental examination
or an extensive list o indications, however many providers
are not aware (Langston, 1997; Odibo, 2016). Moreover, data
are insucient to support all o these. At minimum, the placenta and cord should be inspected in the delivery room. Te
decision to request pathological examination should be based
on clinical and placental ndings (Table 6-1) (Redline, 2008;
Roberts, 2008).
NORMAL PLACENTA
At term, the typical placenta weighs 470 g, is round to oval
with a 22-cm diameter, and has a central thickness o 2.5 cm
(Benirschke, 2012). It is composed o a placental disc, extraplacental membranes, and three-vessel umbilical cord. Te disc
surace that lies against the uterine wall is the basal plate, which
is divided by clets into portions—termed cotyledons. Te etal
surace is the chorionic plate. Here, the umbilical cord inserts,
typically in the center. Large etal vessels that originate rom
the cord vessels then spread and branch across the chorionic
plate beore entering stem villi o the placenta parenchyma. In
tracing these, etal arteries almost invariably cross over veins.
Te chorionic plate and its vessels are covered by thin amnion,
which can be easily peeled away rom a postdelivery specimen.
During prenatal sonographic examinations, multiple societies, including the American Institute o Ultrasound in Medicine (2018), recommend identiying and recording placental
location and its relationship to the internal cervical os. As seen
sonographically, the normal placenta is homogenous and 2 to
4 cm thick, lies against the myometrium, and indents into the
amnionic sac. Te retroplacental space is a hypoechoic area that
separates the myometrium rom the basal plate and measures
less than 1 to 2 cm. Te umbilical cord is also imaged, its etal
and placental insertion sites examined, and its vessels counted.
Many placental lesions can be identied grossly or sonographically, but other abnormalities require histopathological
examination or clarication. A detailed description o these
is beyond the scope o this chapter, and interested readers
are reerred to textbooks by Benirschke (2012), Fox (2007),
and Faye-Petersen (2006) and their colleagues. Moreover, the
placenta accreta spectrum, placenta previa, and gestational
TABLE 6-1. Some Indications for Placental Pathological
Examinationa
Maternal Indications
Abruption
Antepartum infection with fetal risks
Anti-CDE alloimmunization
Cesarean hysterectomy
Oligohydramnios or hydramnios
Peripartum fever or infection
Preterm (<32 wks) delivery
Postterm (>42 wks) delivery
Severe trauma
Suspected placental injury
Systemic disorders with known placental effects
Thick meconium
Unexplained late pregnancy bleeding
Unexplained or recurrent pregnancy complications
Fetal and Neonatal Indications
Admission to an acute care nursery
Birth weight <10th or >95th percentile
Fetal anemia
Fetal or neonatal compromise
Neonatal seizures
Hydrops fetalis
Infection or sepsis
Major anomalies or abnormal karyotype
Multifetal gestation
Stillbirth or neonatal death
Vanishing twin beyond the first trimester
Placental Indications
Gross lesions
Markedly abnormal placental shape or size
Markedly adhered placenta
Term cord >32 cm or <100 cm
Umbilical cord lesions
Velamentous cord insertion
aIndications are organized alphabetically.
A B
FIGURE 6-1 Succenturiate lobe. A. Vessels extend from the main
placental disc to supply the small round succenturiate lobe located
to the left. (Reproduced with permission from Dr. Rachel Gardner.)
B. Sonographic imaging with color Doppler shows the main placental disc implanted posteriorly (asterisk). The succenturiate lobe
is located on the anterior uterine wall across the amnionic cavity.
Vessels are identified as the long red and blue crossing tubular
structures that travel within the membranes to connect these two
portions of placenta.Placental Abnormalities 109
CHAPTER 6
an actual hole in the placenta. More oten, only villous tissue is
missing, and the chorionic plate remains intact.
During pregnancy, the normal placenta increases its thickness at a rate that approximates 1 mm per week. Although not
measured as a component o routine sonographic evaluation,
this thickness typically does not exceed 40 mm (Hoddick,
1985). Placentomegaly denes those thicker than 40 mm and
commonly results rom striking villous enlargement. Underlying maternal etiologies are diabetes mellitus or severe anemia,
whereas etal sources include hydrops, anemia, syphilis, toxoplasmosis, or inection caused by parvovirus or cytomegalovirus. In these conditions, the placenta is homogeneously
thickened. In other cases placentas are thick but inhomogeneous. Partial mole is a classic example. Te thickened placenta contains edematous villi, which appear as multiple,
small, anechoic placental cysts (Chap. 13, p. 239). Cystic
vesicles also are seen with placental mesenchymal dysplasia. In
this rare condition, vesicles correspond to enlarged stem villi.
However, unlike molar pregnancy, trophoblast prolieration
is not excessive, and chromosomal complements are diploid
(Woo, 2011).
Rather than villous enlargement, inhomogeneous placentomegaly oten may result rom collections o blood or brin,
which impart heterogeneity to the placenta. Examples o this
are discussed later and include massive perivillous brin deposition, intervillous or subchorionic thromboses, and large retroplacental hematomas (p. 110).
EXTRACHORIAL PLACENTATION
Te chorionic plate normally extends to the periphery o the placental disc and has a diameter similar to that o the basal plate.
With extrachorial placentation, however, the chorionic plate ails to
extend to this periphery and leads to a chorionic plate that is smaller
than the basal plate (Fig. 6-2). Circummarginate and circumvallate
placentas are the two types. In a circummarginate placenta, brin
and old hemorrhage lie between the placental disc and the overlying sheer amniochorion. In contrast, with a circumvallate placenta,
the chorionic plate periphery is a thickened, opaque, gray-white
circular ridge composed o a double old o chorion and amnion.
Sonographically, the circumvallate old can be seen as
a thick, linear band o echoes extending rom one placental
edge to the other. On cross section, however, it appears as two
“shelves,” with each lying above an opposing placental margin
(see Fig. 6-2). Tis anatomy can help dierentiate this shel
rom other bands (Table 6-2).
In small observational studies o circumvallate placenta
diagnosed postpartum, it was associated with increased risk
or antepartum bleeding, abruption, etal demise, and preterm birth (Suzuki, 2008; aniguchi, 2014). In a prospective
sonographic investigation o 17 cases, however, Shen and associates (2007a) ound most circumvallate placentas to be transient. Persistent cases were benign. In general, most otherwise
uncomplicated pregnancies with either type o extrachorial placentation have normal outcomes, and no increased surveillance
is usually required.
CIRCULATORY DISTURBANCES
Functionally, placental perusion disorders can be grouped
into: (1) those in which maternal blood fow to or within the
intervillous space is disrupted, and (2) those with disturbed
etal blood fow through the villi. Tese lesions are requently
identied in the normal, mature placenta. Although they can
limit maximal placental blood fow, unctional reserve within
the placental prevents harm in most cases. Indeed, some estimate that up to 30 percent o placental villi can be lost without
untoward etal eects (Fox, 2007). I extensive, however, these
lesions can prooundly limit etal growth.
Lesions that disrupt perusion are requently seen grossly
or sonographically, whereas smaller lesions are seen only histologically. With sonography, many o these, such as subchorionic brin deposition, perivillous brin deposition, and
intervillous thrombosis, appear as ocal sonolucencies within
the placenta. Greater magnetic resonance (MR) imaging use
in pregnancy has permitted detection and urther characterization o these lesions (Bockoven, 2020; Capuani, 2017).
Importantly, in the absence o maternal or etal complications, small isolated placental sonolucencies are considered
incidental ndings.
A B
FIGURE 6-2 A. In this illustration, circummarginate (left) and circumvallate (right) varieties of extrachorial placentation are shown. A circummarginate placenta is covered by a single layer of amniochorion. B. This transabdominal grayscale sonographic image shows a circumvallate placenta. The double fold of amnion and chorion creates a broad, opaque white ring and ridge on the fetal surface.110 Placentation, Embryogenesis, and Fetal Development
Section 3
■ Maternal Blood Flow Disruption
Subchorionic Fibrin Deposition
Tese collections are caused by slowing o maternal blood fow
within the intervillous space. In the upper portion o this space
near the chorionic plate, blood stasis is prominent and leads
to subsequent brin deposition. In viewing the placental etal
surace, subchorionic lesions are seen as white or yellow, rm,
round, elevated plaques just beneath the chorionic plate.
Perivillous Fibrin Deposition
Stasis o maternal blood fow around an individual villus also
results in brin deposition and can lead to diminished villous
oxygenation and necrosis o syncytiotrophoblast (Fig. 6-3).
Tese small yellow-white placental nodules are grossly visible
within the parenchyma o a sectioned placenta. Within limits,
these refect normal placental aging. Deposition that aects
>25 percent o villi is associated with etal-growth restriction
and adverse neonatal outcomes (Devisme, 2017; Spinillo, 2019).
FIGURE 6-3 Potential sites of maternally and fetally related placental circulatory disturbances.
TABLE 6-2. Sonographic Bands During Pregnancy
Condition Sonographic Findings
Normal early chorioamnionic
separation
Crescent-shaped amnion mirrors the chorion’s curve; distinct from the fetus; fuses after
16 weeks’ gestation
Subchorionic hematoma Echogenic blood lies between the myometrium and chorioamnion, which appears as a
thin band crossing the cavity. Hemorrhage and band resolve over time
Uterine synechiae (Amnionic
sheet)
2.5- to 4.0-mm-thick, broad-based band crosses the cavity. Appears shelflike on cross
section
Circumvallate placenta Broad-based band extends from one placental edge to the other, just above the
placental surface. Appears shelflike on cross section
Amnionic band Thin strands cross and appear to tether fetal parts
Pseudoamnionic band syndrome Thin strands tether fetal parts and form after fetoscopic surgeries or amniocenteses that
are complicated by membrane laceration
Uterine septum Chorioamnionic sac of an early pregnancy fills one horn of a septate or partial
bicornuate uterus. Thick band of echoes, which may be wedge-shaped, extend from
uterine fundus in midline
Membranes from vanishing twin Depending on chorionicity either a thin amnion or thicker chorioamnion spans the cavity
Placental vessels supported by
membranes: velamentous
insertion, succenturiate lobe
With grayscale imaging, vessels appear as bands. Color Doppler will clarify (see Figs. 6-1
and 6-6)
Modified from Dashe, 2017; Lafitte, 2017.Placental Abnormalities 111
CHAPTER 6
Maternal Floor Infarction. Tis extreme variant o perivillous
brin deposition is a dense brinoid layer within the placental
basal plate and is erroneously termed an inarction. Maternal
oor inarction has a thick, yellow or white, rm corrugated
surace that impedes normal maternal blood fow into the intervillous space. In specic cases that extend up and beyond the
basal plate to entrap villi and obliterate the intervillous space,
the term massive perivillous fbrin deposition is used. Te etiopathogenesis is unclear, but maternal auto- or alloimmunity
appears contributory (Faye-Peterson, 2018; Romero, 2013).
Antiphospholipid antibody syndrome and angiogenic actors
involved with preeclampsia also have been implicated (Sebire,
2002; Whitten, 2013).
Tese lesions are not reliably imaged with prenatal sonography, but they may create a thicker basal plate. Aected pregnancies are associated with miscarriage, etal-growth restriction,
preterm delivery, and stillbirth (Andres, 1990; Mandsager,
1994). Importantly, these adverse outcomes can recur in subsequent pregnancies.
Intervillous Thrombus
Tis is a collection o coagulated maternal blood normally ound
in the intervillous space mixed with etal blood rom a break in
a villus. Grossly, these round or oval collections vary in size up
to several centimeters. Tey appear red i recent or white-yellow
i older, and they develop at any placental depth. Intervillous
thrombi are common and typically not associated with adverse
etal sequelae. Tese refect potential communication between
maternal and etal circulations, and thus large lesions are one
cause o elevated maternal serum alpha-etoprotein (MSAFP)
levels (able 17-5, p. 338). (Salaa, 1988).
Infarction
Chorionic villi themselves receive oxygen solely rom maternal circulation and specically rom blood supplied into the
intervillous space. Any uteroplacental disease that diminishes
or obstructs this supply can result in inarction o an individual
villus. Tese are common lesions in mature placentas and are
benign in limited numbers. I numerous, however, placental insuciency can develop. When they are thick, centrally
located, and randomly distributed, they may be associated with
preeclampsia or lupus anticoagulant.
Hematoma
Te maternal–placental–etal unit can develop several hematoma
types. As depicted in Figure 6-3, these include: (1) retroplacental hematoma—ormed between the placenta and its adjacent
decidua; (2) marginal hematoma—ormed between the chorion
and decidua at the placental periphery—known clinically as subchorionic hemorrhage; (3) subamnionic hematoma—derived o etal
vessel origin and ound beneath the amnion but above the chorionic plate, and (4) subchorial thrombus along the roo o the intervillous space and beneath the chorionic plate. With this last type,
massive subchorionic hematomas are also known as Breus moles.
Sonographically, hematomas evolve with time and appear
hyperechoic to isoechoic in the rst week ater hemorrhage,
hypoechoic at 1 to 2 weeks, and nally, anechoic ater 2 weeks.
Most subchorionic hematomas visible sonographically are airly
small and o no clinical consequence (Naert, 2019). However,
extensive retroplacental, marginal, and subchorial collections
are associated with higher rates o miscarriage, stillbirth, placental abruption, and preterm delivery (uuli, 2011). In essence,
placental abruption is a large, clinically signicant retroplacental hematoma.
■ Fetal Blood Flow Disruption
Fetal Vascular Malperfusion
Placental lesions that arise rom etal circulatory disturbances are
also depicted in Figure 6-3. Normally, deoxygenated etal blood
fows rom the two umbilical arteries into arteries within the
chorionic plate. Tese surace arteries divide and send branches
out across the placental surace. Tese eventually supply individual stem villi. Remember that etal blood is oxygenated
within each villus by passive diusion o oxygen rom maternal
blood contained within the intervillous space. Tus, with etal
vessel thrombosis, portions o the villus distal to the obstruction
become nonunctional. Normally, thrombi in limited numbers
are ound in mature placentas. I many villi are aected, which
can be seen with preeclampsia, the etus may suer growth
restriction, stillbirth, or nonreassuring etal heart rate patterns
(Chisholm, 2015; Lepais, 2014; Saleemuddin, 2010).
Villous Vascular Lesions
Villous capillaries show a spectrum o histological lesions. Chorangiosis describes an increased number o capillaries within terminal
villi. Its denition requires ≥10 capillaries to be present in ≥10
villi in ≥10 elds viewed through a 10× lens (Altshuler, 1984).
Clinically, long-standing hypoperusion or hypoxia is thought to
be causative (Stanek, 2016). Focal chorangiosis is increased capillary
vascularity in a signicant portion o the placenta but not diusely.
In one small study, lower Apgar scores and etal vascular malperusion were associated outcomes (Sung, 2019). Prenatal detection o
chorangiosis has been reported (Inubashiri, 2017). Chorangiomatosis describes increased capillary number in stem villi, but terminal villi are spared. Tis nding has been linked with etal-growth
restriction and anomalies (Bagby, 2011). Despite these associations, the clinical signicance o both vascular conditions remains
unclear. Chorioangiomas are described subsequently.
Subamnionic Hematoma
As noted earlier, these hematomas lie between the chorionic
plate and amnion. Tey most oten are acute iatrogenic events
o no clinical consequence during third-stage labor when cord
traction ruptures a vessel near the cord insertion.
Large, chronic antepartum lesions may cause etomaternal
hemorrhage or etal-growth restriction (Deans, 1998). Tey
also may be conused with other placental masses such as chorioangioma. In most cases, color Doppler interrogation will
show absent internal blood fow within a hematoma and permit
dierentiation (Sepulveda, 2000).
PLACENTAL CALCIFICATION
Calcium salts can be deposited throughout the placenta but
are most common on the basal plate. Calcication accrues112 Placentation, Embryogenesis, and Fetal Development
Section 3
with advancing gestation, and greater degrees are associated
with smoking and higher maternal serum calcium levels (Bedir
Findik, 2015). Tese hyperechoic deposits can easily be seen
sonographically, and a grading scale rom 0 to 3 refects increasing calcication with increasing numerical grade (Grannum,
1979). Following this scheme, a grade 0 placenta is homogeneous, lacks calcication, and displays a smooth, fat chorionic
plate. A grade 1 placenta has scattered echogenicities and subtle
chorionic plate undulations. Grade 2 shows echogenic stippling
at the basal plate. Large, echogenic comma shapes originate
rom an indented chorionic plate, but their curve alls short o
the basal plate. Last, a grade 3 placenta has echogenic indentations extending rom the chorionic plate to the basal plate,
which create discrete components that resemble cotyledons.
Basal plate densities also increase.
Tis grading scale poorly predicts neonatal outcome near
term (McKenna, 2005; Mirza, 2018). However, data rom
two small studies link grade 3 placenta prior to 32 weeks with
stillbirth and some other adverse pregnancy outcomes (Chen,
2011, 2015; Mirza, 2018).
PLACENTAL TUMORS
■ Chorioangioma
Tese benign tumors have components similar to the blood
vessels and stroma o the chorionic villus. Also called chorangiomas, these placental tumors have an incidence that
approximates 1 percent (Guschmann, 2003). In some cases,
etal-to-maternal hemorrhage across tumor capillaries leads to
elevated levels o MSAFP. Tis typically prompts sonographic
evaluation to exclude a neural-tube deect, which also shows
high MSAFP levels. Sonographically, chorangiomas appear
as a well-circumscribed, rounded, predominantly hypoechoic
lesion lying near the chorionic plate and protruding into the
amnionic cavity (Fig. 6-4). Documenting increased blood fow
by color Doppler helps to distinguish these lesions rom other
placental masses such as hematoma, partial hydatidiorm mole,
teratoma, metastases, and leiomyoma (Prapas, 2000). Although
rare, chorangiocarcinoma tumors mirror chorioangiomas clinically (Huang, 2015).
Small chorioangiomas are usually asymptomatic. Large
tumors, typically those measuring >4 cm, can create signicant
arteriovenous shunting within the placenta to cause high- output
heart ailure, hydrops, and etal death (Al Wattar, 2014). Compression or shearing o etal erythrocytes within tumor vessels
can lead to hemolysis and microangiopathic anemia (Bauer,
1978). Hydramnios, preterm delivery, and etal-growth restriction are other sequelae (Dong, 2020). Large tumor size and
etal hydrops are the primary determinants and signal a potential adverse perinatal outcome (Buca, 2020).
Grayscale and color Doppler interrogation o the placenta
and amnionic fuid volume are used to identiy these tumors.
Diagnostic tools that can arm associated etomaternal hemorrhage include MSAFP level and Kleihauer-Betke stain (Chap.
18, p. 358). With etal concern, echocardiography assesses cardiac unction, whereas middle cerebral artery interrogation is
used to identiy etal anemia.
Several etal therapies interere with the vascular supply to
the tumor and reverse etal heart ailure. At specialized perinatal centers, endoscopic laser ablation o eeder vessels to the
tumor is most requently used and is associated with avorable
etal outcomes (Hosseinzadeh, 2015). Discussed in Chapter
16, etal transusion can treat serious anemia, amnioreduction
can temporize hydramnios, and digoxin therapy can assist etal
heart ailure.
■ Metastatic Tumors
Maternal malignant tumors rarely metastasize to the placenta.
O those that do, melanomas, leukemias and lymphomas,
A B
FIGURE 6-4 Placental chorioangioma. A. Color Doppler imaging
displays blood flow through a large chorioangioma with its border
outlined by white arrows. B. Grossly, the chorioangioma is a round,
well-circumcised mass protruding from the fetal surface.Placental Abnormalities 113
CHAPTER 6
and breast cancer are the most common (Al-Adnani, 2007).
umor cells usually are conned within the intervillous space.
As a result, metastasis to the etus is uncommon but is most
oten seen with melanoma (Alexander, 2003).
Similarly, cases in which etal malignancy metastasizes to
the placenta are rare (Rei, 2014). Tese are predominantly
etal neuroectodermal tumors, and only one case in the literature describes transplantation o tumor to the maternal uterus
(Nath, 1995).
AMNIOCHORION
■ Chorioamnionitis
Normal genital-tract fora can colonize and inect the membranes, umbilical cord, and eventually the etus. Bacteria most
commonly ascend ater prolonged membrane rupture and during labor to cause inection. Organisms initially inect the chorion and adjacent decidua in the area overlying the internal os.
Subsequently, progression leads to ull-thickness involvement
o the membranes—chorioamnionitis. Organisms oten then
spread along the chorioamnionic surace to colonize and replicate in amnionic fuid. Infammation o the chorionic plate
and o the umbilical cord—unisitis—may ollow (Kim, 2015;
Redline, 2012).
Most commonly, chorioamnionitis is microscopic or
occult and caused by a wide variety o microorganisms. Tis
is requently cited as a possible explanation or many otherwise unexplained cases o ruptured membranes, preterm
labor, or both (Chap. 45, p. 789). In some cases, gross inection is characterized by visible membrane clouding and is
sometimes accompanied by a oul odor that depends on bacterial species.
■ Other Membrane Abnormalities
Amnion nodosum is a condition characterized by numerous
small, light-tan nodules axed to the amnion that overlies the
chorionic plate. Tese may be scraped o the etal surace and
contain deposits o etal squames and brin that refect prolonged and severe oligohydramnios (Adeniran, 2007).
wo notable bands can be ormed by the etal membranes.
First, amnionic band sequence is an anatomical disruption
sequence in which amnion bands tether, constrict, or amputate etal parts. Bands may orm spontaneously or ollow etal
surgery procedures (see able 6-2) (Latte, 2017). Amnionic
bands commonly cause limb-reduction deects, acial clets,
or encephalocele (Barzilay, 2015; Guzmán-Huerta, 2013).
Umbilical cord compromise is another sequela (Barros, 2014).
Severe deects o the spine or ventral wall that accompany
amnionic bands suggest a limb-body wall complex, described in
Chapter 15 (p. 297).
Sonography oten rst identies the sequelae o this
sequence rather than the bands themselves. As with any etal
anomaly, targeted sonography is indicated. Identication o a
limb-reduction deect, an encephalocele in an atypical location,
or an extremity with edema or positional deormity should
prompt careul evaluation or amnionic bands.
Management depends on the degree o anatomic deormity
(Society o Maternal–Fetal Medicine, 2019). Fetoscopic laser
interruption o the band may be suitable in highly selected
antepartum cases (Gueneuc, 2019; Javadian, 2013).
Second, an amnionic sheet in contrast is ormed by normal
amniochorion draped over a preexisting uterine synechia. Generally, these sheets pose little etal risk, although slightly higher
rates o preterm membrane rupture and placental abruption
have been described (Nelson, 2010; uuli, 2012).
UMBILICAL CORD
■ Length
Most umbilical cords at delivery measure 40 to 70 cm long, and
very ew measure <30 cm or >100 cm. Cord length is infuenced positively by both maternal parity and body mass index
(Linde, 2018). In retrospective studies, short cords have been
linked with congenital malormations and intrapartum distress
(Krakowiak, 2004; Linde, 2018; Yamamoto, 2016). Excessively
long cords are linked with cord entanglement or prolapse and
with etal anomalies (Olaya-C, 2015; Rayburn, 1981).
Because antenatal determination o cord length is technically limited, cord diameter has been evaluated as a predictive
marker or etal outcomes. Some have linked lean cords with
poor etal growth and large-diameter cords with macrosomia
(Proctor, 2013). However, the clinical utility o this parameter
is still unclear (Cromi, 2007; Raio, 2003).
■ Coiling
Cord coiling characteristics are not currently part o standard
sonographic evaluation. Usually the umbilical vessels spiral
through the cord in a sinistral, that is, let-twisting direction
(Fletcher, 1993; Lacro, 1987). Te number o complete coils
per centimeter o cord length is termed the umbilical coiling
index—UCI (Strong, 1994). A normal, antepartum, sonographically derived UCI is 0.4, and this contrasts with a normal, postpartum, physically measured value o 0.2 (Sebire,
2007). UCIs <10th percentile are considered hypocoiled, and
those >90th percentile are hypercoiled.
Clinically, the signicance o coiling extremes is controversial. Some studies evaluating large, unselected cohorts nd no
associations between UCI values and poor neonatal outcome
(Jessop, 2014; Pathak, 2010). In others, extremes are linked
with various adverse outcomes but most consistently with
intrapartum etal heart rate abnormalities, preterm labor, or
etal-growth restriction (Chitra, 2012; de Laat, 2006; Pergialiotis, 2019).
■ Vessel Number
Counting cord vessel number is a standard component o anatomical evaluation during etal sonographic examination and
immediately ater delivery (Fig. 6-5). Embryos initially have
two umbilical veins. In the rst trimester, the right vein typically atrophies to leave one large vein to accompany the two,
thick-walled umbilical arteries. Four-vessel cords are rare and
oten associated with congenital anomalies (Puvabanditsin,114 Placentation, Embryogenesis, and Fetal Development
Section 3
2011). I it is an isolated nding, however, prognosis can be
good (Avnet, 2011).
Te most common aberration is that o a single umbilical
artery (SUA). Its cited incidence is 0.63 percent in liveborn neonates, 1.92 percent in perinatal deaths, and 3 percent in twins
(Heietz, 1984). Fetuses with major malormations requently
have an SUA. Tus, its identication oten prompts consideration
or targeted sonography and possibly etal echocardiography. Te
most requent anomalies are cardiovascular and genitourinary
(Hua, 2010; Murphy-Kaulbeck, 2010). In an anomalous etus,
an SUA greatly increases the aneuploidy risk, and amniocentesis
is recommended or karyotype assessment (Dagklis, 2010).
I targeted sonography nds otherwise normal anatomy, an
isolated SUA in an otherwise low-risk pregnancy does not signicantly raise the etal aneuploidy risk. However, as an isolated
nding, it has been associated with etal-growth restriction and
perinatal death in some but not all studies (Chetty-John, 2010;
Ebbing, 2019; Voskamp, 2013). Tus, clinical monitoring o
growth is reasonable, but the value o sonographic surveillance
is unclear.
In contrast, a used umbilical artery with a shared lumen
is rare. It arises rom ailure o the two arteries to split during
embryological development. Te common lumen may extend
through the entire cord, but, i partial, it is typically ound
near the placental insertion site (Yamada, 2005). In one report,
these malormations were associated with a higher incidence o
marginal or velamentous cord insertion but not o congenital
etal anomalies (Fujikura, 2003).
Found in most placentas, the Hyrtl anastomosis is a connection between the two umbilical arteries, and it lies near the
cord’s insertion into the placenta. Tis anastomosis acts physiologically to equalize pressures between the arteries (Gordon,
2007). Te resulting redistribution o pressure gradients and
blood fow improves placental perusion, especially during uterine contractions or during compression o one umbilical artery.
Fetuses with an SUA lack this saety valve (Raio, 1999, 2001).
■ Remnants and Cysts
Several structures are housed in the umbilical cord during
etal development, and their remnants may be seen when the
mature cord is inspected transversely. Indeed, in grossly sectioned cords, remnants o the allantoic duct, vitelline duct, and
embryonic vessels are ound in 25 to 50 percent (Grottling,
2019; Jauniaux, 1989). Tese are not associated with congenital malormations or perinatal complications.
Cysts occasionally are ound along the course o the cord.
Tey are designated according to their origin. True cysts are
epithelium-lined remnants o the allantoic or vitelline ducts
and tend to be located closer to the etal insertion site. In contrast, the more common pseudocysts orm rom local degeneration o Wharton jelly and occur anywhere along the cord. Both
have a similar sonographic appearance. Single umbilical cord
cysts identied in the rst trimester tend to resolve completely,
however, multiple cysts may portend miscarriage or aneuploidy
(Ghezzi, 2003; Hannaord, 2013). Cysts persisting beyond this
time are associated with a risk or structural deects and chromosomal anomalies (Bonilla, 2010; Zangen, 2010).
■ Insertion
Te cord normally inserts centrally into the placental disc, but
eccentric, marginal, or velamentous insertions are variants.
O these, eccentric insertions in general pose no identiable
etal risk. Marginal insertion is a common variant—sometimes
reerred to as a battledore placenta—in which the cord anchors
at the placental margin. In one population-based study, the
rate was 6 percent in singleton gestations and 11 percent in
twins (Ebbing, 2013). Tis common insertion variant rarely
causes problems, but it and velamentous insertion occasionally result in the cord being pulled o during delivery o the
placenta (Ebbing, 2015; Luo, 2013). In monochorionic twins,
marginal insertion may be associated with weight discordance
(Kent, 2011).
A B
FIGURE 6-5 Two umbilical arteries are typically documented sonographically in the second trimester. They encircle the fetal bladder
(asterisk) as extensions of the superior vesical arteries. A. In this color Doppler sonographic image, a single umbilical artery, shown in red,
runs along the bladder wall before joining the umbilical vein (blue) in the cord. Remember with color Doppler that color signifies only
blood flow direction relative to the transducer. B. A cross section of a floating cord segment shows the two vessels of the cord. The smaller
circle is the single umbilical artery and the larger circle, the umbilical vein.Placental Abnormalities 115
CHAPTER 6
With velamentous insertion, the umbilical vessels characteristically travel within the membranes beore reaching the
placental margin (Fig. 6-6). Te incidence o velamentous
insertion approximates 1 percent but is 6 percent with twins
(Ebbing, 2013). It is more commonly seen with placenta previa (Papinniemi, 2007; Räisänen, 2012). Antenatal diagnosis
is possible sonographically, and cord vessels are seen traveling
along the uterine wall beore entering the placental disc. Clinically, vessels are vulnerable to compression, which may lead
to etal hypoperusion and acidemia. Higher associated rates
o low Apgar scores, stillbirth, preterm delivery, and small or
gestational age have been noted (de Los Reyes, 2018; Ebbing,
2017; Esako, 2015; Vahanian, 2015). Accordingly, monitoring o etal growth is reasonable either clinically or sonographically (Vintzileos, 2015).
Last, with the rare urcate insertion, umbilical vessels lose
their protective Wharton jelly shortly beore they insert. As a
result, they are covered only by an amnion sheath and prone to
compression, twisting, and thrombosis.
Vasa Previa
With this condition, vessels travel within the membranes and
overlie the cervical os. Tere, they can be torn with cervical dilation or membrane rupture, and laceration can lead to
rapid etal exsanguination. Over the cervix, vessels can also be
compressed by a presenting etal part (Matsuzaki, 2019). Vasa
previa may be more common than previously estimated, and
rates are 1 case in 338 to 365 pregnancies (Hasegawa, 2012;
Klahr, 2019). Vasa previa is classied as type 1, in which vessels are part o a velamentous cord insertion, and type 2, in
which involved vessels span between portions o a bilobate or
a succenturiate placenta (Catanzarite, 2001). wo other risks
are conception with in vitro ertilization and second-trimester
placenta previa, with or without later migration (Baulies, 2007;
Schachter, 2003).
Compared with intrapartum diagnosis, antepartum diagnosis greatly improves the perinatal survival rate, which ranges
rom 97 to 100 percent (Oyelese, 2004; Swank, 2016; Zhang,
2021). Tus, vasa previa is ideally identied early, although this
is not always possible. Eective screening or vasa previa begins
during scheduled midtrimester sonographic examination. In
suspicious cases, transvaginal sonography is added and shows
cord vessels inserting into the membranes and vessels running
above the cervical internal os (Fig. 6-7). Routine color Doppler
interrogation o the placental cord insertion site, particularly
in cases o placenta previa or low-lying placenta, may aid its
detection. With this, the vessel waveorm refects the etal heart
rate. In one systematic review, the median prenatal detection
rate was 93 percent (Ruiter, 2015).
Once vasa previa is identied, subsequent imaging is reasonable because up to 39 percent o cases ultimately resolve (Erani,
2019; Klahr, 2019). Bed rest apparently has no added advantage. Antenatal corticosteroids can be provided as indicated or
given prophylactically at 28 to 32 weeks’ gestation to cover possible urgent preterm delivery. Antenatal hospitalization may be
considered at 30 to 34 weeks to permit surveillance and expedited delivery or labor, bleeding, or rupture o membranes.
Data supporting this are limited, and admission may best serve
women with risk actors that portend early delivery (Society
or Maternal-Fetal Medicine, 2015). A ew cases o antepartum etoscopic surgery with vessel laser ablation are described
(Hosseinzadeh, 2015; Johnston, 2014). However, current practice is early scheduled cesarean delivery. Te American College
o Obstetricians and Gynecologists (2021) recommends cesarean delivery at 34 to 36 weeks’ gestation.
At delivery, the etus is expeditiously delivered ater the hysterotomy incision in case a vessel is lacerated during uterine
entry. Delayed cord clamping is not encouraged.
In all pregnancies, otherwise unexplained vaginal bleeding
either antepartum or intrapartum should prompt consideration
o vasa previa and a lacerated etal vessel. In many cases, bleeding is rapidly atal, and neonatal salvage is not possible. With
less hemorrhage, however, it may be possible to distinguish
etal versus maternal bleeding. Various tests can be used, and
A B
FIGURE 6-6 Velamentous cord insertion. A. The umbilical cord inserts into the membranes (arrow). From here, the cord vessels branch
and are supported only by membrane until they reach the placental disc. B. When viewed sonographically and using color Doppler, the
cord vessels appear to lie against the myometrium as they travel to insert into the margin of the placental disc (P).116 Placentation, Embryogenesis, and Fetal Development
Section 3
each relies on the increased resistance o etal hemoglobin to
denaturing by alkaline or acid reagents (Odunsi, 1996).
■ Knots, Strictures, and Loops
Various mechanical abnormalities in the cord can impede
blood fow and sometimes cause etal harm. O these, true knots
are ound in approximately 1 percent o births. Tese orm
rom etal movement, and associated risks include hydramnios
and diabetes mellitus (Hershkovitz, 2001; Räisänen, 2013).
Knots are especially common and dangerous in monoamnionic
twins, which are discussed in Chapter 48 (p. 845). In singleton
etuses, the stillbirth risk is increased our- to tenold compared
with those without knots (Airas, 2002; Sørnes, 2000).
Knots can be ound incidentally during antepartum sonography, and a “hanging noose” sign is suggestive (Ramon y
Cajal, 2006). Tree-dimensional and color Doppler aid diagnostic accuracy (Hasbun, 2007). With these knots, optimal
etal surveillance is unclear but may include umbilical artery
Doppler velocimetry, nonstress testing, or subjective etal
movement monitoring (Rodriguez, 2012). Allowing vaginal
delivery is suitable, and intrapartum etal heart rate tracings do
not dier rom unaected pregnancies (Carter, 2018). In these
cases, cesarean delivery rates are not increased and cord blood
acid-base values are usually normal (Airas, 2002; Maher, 1996).
In contrast, alse knots orm rom ocal redundancy and olding o an umbilical cord vessel rather than knotting. Tese lack
clinical signicance.
A cord stricture is a ocal narrowing o the diameter that usually develops near the etal cord insertion site (Peng, 2006).
Pathological eatures typically include absent Wharton jelly at
the narrowed segment and obliteration o cord vessels (Sun,
1995). In most instances, the etus is stillborn (French, 2005).
Even less common is a cord stricture caused by an amnionic
band.
Cord loops are requently encountered and are caused by coiling around various etal parts during movement. A cord around
the neck—a nuchal cord—is common, and vaginal delivery is
suitable. One loop is reported in 20 to 34 percent o deliveries;
two loops in 2.5 to 5 percent; and three loops in 0.2 to 0.5 percent (Kan, 1957; Sørnes, 1995; Spellacy, 1966). During labor,
up to 20 percent o etuses with a nuchal cord have moderate to
severe variable heart rate decelerations, and these are associated
with a lower umbilical artery pH (Hankins, 1987). Decelerations are not relieved by amnioinusion (Spong, 1996). Cords
wrapped around the body can have similar eects (Kobayashi,
2015). Despite their requency, nuchal cords are not associated
with greater rates o adverse perinatal outcome (Henry, 2013;
Masad, 2019).
Last, in a unic presentation, the umbilical cord is the presenting part. Tese are uncommon and most oten are associated
with etal malpresentation (Kinugasa, 2007). A unic presentation in some cases is identied with placental sonography and
color fow Doppler (Ezra, 2003). Overt or occult cord prolapse
can complicate labor. Tus, once identied at term, cesarean
delivery is typically recommended.
■ Vascular
Cord hematomas are rare and generally ollow rupture o an
umbilical vessel, usually the vein, and hemorrhage into the
Wharton jelly. Hematomas have been associated with abnormal
cord length, umbilical vessel aneurysm, trauma, entanglement,
umbilical vessel venipuncture, and unisitis (Gualandri, 2008).
Most are identied postpartum, but hematomas are recognized
A B
FIGURE 6-7 Vasa previa. A. Using color Doppler, an umbilical
vessel (red linear structure) is seen overlying the internal os and cervical canal (arrows). At the bottom, the Doppler waveform seen with
this vasa previa has the typical appearance of an umbilical artery.
B. The amniotomy site (held open by hemostat), which was created
at the time of cesarean hysterotomy, illustrates how fetal vessels
may be lacerated and why fetal delivery should be prompt (Reproduced with permission from Dr. Julie Lo.)Placental Abnormalities 117
CHAPTER 6
sonographically as hypoechoic masses that lack blood fow
(Chou, 2003). Sequelae include stillbirth or intrapartum abnormal etal heart rate pattern (Abraham, 2015; Barbati, 2009;
Sepulveda, 2005; owers, 2009). However, case reports have
described normal outcomes (Sanchex-Codez, 2018).
Umbilical cord vessel thromboses are rare in utero events and
seldom diagnosed antepartum. Approximately 70 percent are
venous, 20 percent are venous and arterial, and 10 percent are
arterial thromboses (Heietz, 1988). Tese all have high associated rates o stillbirth, etal-growth restriction, and intrapartum
etal distress (Minakami, 2001; Sato, 2006; Shilling, 2014). I
these are identied antepartum as hypoechoic masses without
blood fow, data rom case reports support consideration o
prompt delivery o viable-aged etuses (Kanenishi, 2013).
An umbilical vein varix can complicate either the intraamnionic or etal intraabdominal portion o the umbilical vein.
Sonographically and complemented by color Doppler, rare
intraamnionic varices show cystic dilation o the umbilical vein
that is contiguous with a normal-caliber portion. O complications, an intraamnionic varix may compress an adjacent umbilical artery or can rupture or thrombose. A systematic review
o 250 cases ound that approximately one th is associated
with other anomalies. Isolated cases had reassuring outcomes
but typically required antenatal surveillance (di Pasquo, 2018).
Te rare umbilical artery aneurysm is caused by congenital thinning o the vessel wall with diminished support rom
Wharton jelly. Indeed, most orm at or near the cord’s placental insertion site, where this support is absent. Tese are associated with SUA, trisomy 18, amnionic fuid volume extremes,
etal-growth restriction, and stillbirth (Hill, 2010; Vyas, 2016).
At least theoretically, these aneurysms could cause etal compromise and death by compression o the umbilical vein.
With aneurysms measuring >5 cm, the blood reservoir within
the aneurysm may pose a risk or high-output heart ailure
(Matsuki, 2017). Tese aneurysms may appear sonographically
as a cyst with a hyperechoic rim. Within the aneurysm, color
fow and spectral Doppler interrogation demonstrate either
low-velocity or turbulent nonpulsatile fow (Olog, 2011; Shen,
2007b). Although not codied, management may include etal
karyotyping, antenatal etal surveillance, and early delivery to
prevent stillbirth (Doehrman, 2014). Some recommend delivery by cesarean to avoid aneurysm rupture
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