Ultrasound of Placental
Abnormalities
Guy Steinberg, MD
March 5, 2011
Initial examination
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5-7 Weeks - placenta is a diffusely echogenic ring.
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By 8-13 Weeks - focal chorionic thickening and determination of placental site,
umbilical cord inserts in center of the chorionic frondosum.
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R/o implantation on fibroid and succinturiate lobes.
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Implantation in areas with less blood supply, such as a myoma or a uterine
septum, can be associated with later complications such as spontaneous
miscarriage, IUGR, preterm labor, placental abruption and PPH.
Initial examination

Second trimester placenta - More heterogeneous, sonolucencies are common.

Prominent sonolucencies in the second trimester usually result in a normal outcome,
and is more common in women with elevated MSAFP or first trimester bleeding. 218% of placentas have sonolucencies at 15-34 W.

Usually are venous lakes with minimal blood flow , and eventually have fibrin
deposition. May be more than 1 cm in diameter, have swirling blood flow, and
may change in shape during the exam.

More often seen in thick placentas - placenta > 3 cm is 6X more likely to have
sonolucencies. If extensive (>3), large (>2cm), or if present before 20-25 W f/u
and look for signs of placental insufficiency - IUGR, oligo, doppler.

“Swiss cheese” placental variant: patchy placenta from diffuse fibrin deposition,
many sonolucencies, placentomegaly, r/o gestational trophoblastic neoplasia.
DD: chorioangioma, abruption.
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Placenta Previa
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Low lying placenta (<2cm), marginal previa (edge at internal os) and complete previa
(internal os completely covered by placental tissue). Epidemiology: 5% incidence at
15-16 W, 0.5% at term.

Risk factors: AMA, multiparity, smoking, cocaine use, prior previa, previous CS,
uterine transcavitary surgery as well as prior vigorous sharp curettage.

Placenta previa is associated with accreta/perceta spectrum: abnormal placenta may
grow through endometrium. 5% of placenta previa have associated accreta/perceta.
Higher risk if if prior CS and anterior PP, increased risk with increasing prior CS. 67%
risk if previa and >4 CS.

Look for hypoechoic line between bladder and placenta.
Placenta Previa
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Placental migration is the displacement of the placenta from a low or previa
implantation to a higher position in the uterus.
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Likely involves peripheral degeneration secondary to decreased vascularization with
preferential growth in areas assumed to be optimally perfused.
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May involve more rapid growth of the lower uterine segment, as compared to the rest
of the uterine body.
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Trophotropism: atrophy is areas of low blood supply (LUS) and growth in areas of
better blood supply. Placental “migration” is about 5mm/wk.
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Vasa Previa
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Fetal vessels run through the membranes, unprotected by placental tissue or
Wharton's jelly, below the fetal presenting part and close to the internal cervical os.
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It should particularly be suspected when the placental edge covers the os in mid-pregnancy
but recedes later on. Occurs in 1/2500 deliveries.

Risk factors include multiple pregnancy, pregnancy resulting from IVF, presence of
velamentous insertion of the umbilical cord, succenturiate or accessory placental
lobes.

Velamentous insertion of the cord refers to vessels traveling through the fetal
membranes before entering the actual placenta, as opposed to the normal insertion
of the cord directly into the placenta.

This has to be differentiated from marginal insertion of the cord, when the insertion is at the
placental edge, rather than more centrally.
Vasa Previa

It should be distinguished from funic presentation, when loops of a normally
implanted cord are preceding the presenting part at the internal os.

With funic presentation, manual displacement of the presenting part and manipulation
of the lower segment, generally demonstrate movement of the loops of cord.

US Findings: More common: vasa previa from succinturate lobe, or vasa previa from
velamentous cord insertion.

TVS + doppler required for Dx: color doppler shows crossing vessels, pulsed doppler
shows fetal vascularity.
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Most commonly an incidental finding with succinturate lobe. 60-80% fetal mortality if
diagnosis missed.
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Placenta accreta
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Abnormal adherence of the placenta to the uterus, due to an absence or
deficiency of Nitabuch's layer or the spongious layer of the decidua.


Invasion to the myometrium is defined as placenta increta, and invasion through
the myometrium and serosa is called placenta percreta.
The incidence of placenta accreta is rising, primarily because of the rise in
CS deliveries. The risks increase with the number of previous CS: 4-fold
after one previous CS, up to 11.3 RR increase after two.

Patients with a previous CS and previa implantation of the placenta are 5X more
likely to have placenta accreta. Another etiological factor is local tissue alteration,
secondary to curettage.
Placenta accreta

Prenatal diagnosis of placenta accreta by imaging should be based on the
irregularly shaped placental lacunae signs (swiss cheese appearance)
representing vascular spaces rather than only the loss of the normally
obvious retroplacental clear space.

Other signs include thinning of the myometrium overlying the placenta,
protrusion of the placenta into the bladder, increased vascularity of the
uterine serosa bladder interface, and turbulent flow through the lacunae
using Doppler studies.
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Placental abruption
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This is a leading cause of vaginal bleeding in the latter half of pregnancy,
complicating about 0.5-1% of pregnancies.
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Risk factors are defined and consist of abruption in a previous pregnancy,
maternal hypertension, AMA, smoking, cocaine use, trauma and some
uterine anomalies.

The diagnosis of abruption is a clinical one, and ultrasonography is of
limited value with a sensitivity of no more than 50%.

On ultrasound one might see placental edge separation, subchorionic and
retroplacental hematomas.

In the acute phase, the area of detachment may appear hyperechoic,
becoming hypoechoic after a few days.
Placental bed infarction

Also known as intervillous thrombosis, this is a vascular lesion caused by
thrombosis in the villous spaces (ischemic necrosis).

Round, mostly anechoic, intraplacental, measuring up to several
centimeters. It is common and, unless massive, of minimal clinical
significance.

Large infarcts or those occurring in early pregnancy may reflect underlying
maternal vascular disease.

It is different from maternal floor infarction (not a true infarct), a recurrent
lesion of unknown etiology, in which fibrin is deposited throughout the
placenta, leading to necrosis of villi, and often accompanied by fetal demise.
Hematomas
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These appear as crescent-shaped, sonolucent fluid. These can be on the
fetal (retrochorionic, subchorionic) or maternal (retroplacental) side.

Retrochorionic hematomas are lesions involving maternal blood separating
the chorionic membrane from the villous chorion.

Minimal clinical significance, unless + vaginal bleeding or uterine
contractions when they can be markers of later complications, such as
abortion, IUGR, PTL, placental abruption and fetal distress.

Commonly confused with chorioangiomas.
Hematomas

Subamniotic hematomas - between the amniotic and chorionic membrane
and result from rupture of chorionic vessels, near the cord insertion.
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Clinically more significant, retroplacental hematomas are typically located
between the placental basal plate and the uterine wall.
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They usually bulge towards the fetal side and result from bleeding from the spiral
arteries.
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Associated with perinatal complications, secondary to the presence of blood.
Management consists of close observation.
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Placental thickness/size (volume)
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Placental size has been shown to be an important factor in abnormal fetal growth. In
daily clinical practice, it is not routine to measure placental thickness.

During examination of the placenta, thickness is grossly evaluated and, if appearing
normal to the eye, is not further delineated.

Only if suspicious, will the maximal vertical thickness be measured.

Increased thickness is non-specific and can be found with maternal diabetes,
maternal anemia, abnormalities of fetal growth, fetal hydrops, and TORCH infections.
Placental thickness/size (volume)

Placenta thickness increases with gestation: 10mm at 10W, 20 mm at 20 W, 30mm at
30 W - >40 mm considered placentomegaly. Mature weight 250-550 gr, 16-20 cm in
diameter.

DD of placental thickening/placentomegaly: placental insufficiency, diabetes, maternal
or fetal anemia, hydrops, intrauterine infection, Beckwith-Wiedemann syndrome,
hydatiform mole, chromosomal abnormalities, placental mosaicism.
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A thickened placenta is usually nonspecific and associated with a normal outcome.

A very thickened placenta n early pregnancy increases risk of IUGR and placental
insufficiency.
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Circumvallate and circummarginal placenta
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When the chorionic plate is smaller than the basal plate of the placenta, the placental
periphery is not covered, leading to some of the placenta to be extrachorial.
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Circumvallate placenta (1-2%) is caused when the fetal surface presents a central
depression surrounded by a thickened ring, composed of a double fold of amnion and
chorion with degenerated decidua and fibrin in between.

This creates an irregular edge with uplifted margins or placental sheet or shelf.

Linked to placental abruption, fetal hemorrhage and accordingly to adverse perinatal
outcome, including increased fetal morbidity and mortality.
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When the ring is flat, rather than and lacks central depression, it is called
circummarginal placenta (15-20%), a condition with questionable clinical significance.
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Accessory lobe: succenturiate placenta
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Succenturiate placenta : one or more small accessory lobes that develop at a
distance from the main placenta.
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A smaller version of a bilobate placenta which occurs when two approximately equal
lobes of placenta are found.
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The recognition of this condition is important since intramembranous vessels
connecting the main placenta with the succenturiate placenta may rupture during
labor with rupture of the membranes (vasa previa) and fetal death may ensue.

Retention of an accessory lobe may lead to PPH.
Placental grading
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Premature aging (grade 3 before 37 W) is associated with perinatal complications,
such as IUGR and fetal distress.
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Grade 3, early in pregnancy is associated with IUGR and/or smoking, chronic
hypertension, SLE, diabetes and other vascular disease.
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Its value in low-risk pregnancies is limited, but some studies have suggested that
ultrasound detection of a grade 3 placenta at 36 W might help to identify a high risk
pregnancy, in terms of subsequent development of gestational hypertension and
IUGR.
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Placental calcifications
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Increases with gestational age and is recognized as a normal part of maturation and
aging. Also described in several infectious processes.
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Numerous small, echogenic nodules on the fetal surface may be consistent with
amnion nodosum or squamous metaplasia.
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Amnion nodosum is a localized, diffuse accumulation of amorphous material (vernix,
desquamated fetal skin cells, epithelial cells, and hair) producing small nodules on
the placental surface. It is typically associated with fetal renal agenesis,
oligohydramnios and poor fetal outcome.
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Squamous metaplasia is similar, localized more around the umbilical cord insertion. It
has no clinical significance, and has been not been described by US.
Gestational trophoblastic disease (GTD)
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Proliferative disorders of the placental trophoblast -benign (80%) and malignant
(20%). Increased β-hCG secretion characterizes this condition which is highly curable
even in the presence of metastases.
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The major risk factors for gestational trophoblastic disease are Asian ethnicity, AMA,
and a past history of GTD.
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Common US presentations include enlarged uterus and absence of fetal parts and a
“snowstorm” appearance without embryonic structure.

Maternal lakes resulting from stasis of blood between the molar villi are common as
well. Large ovarian theca lutein cysts, secondary to the elevated β-hCG levels may
also occur.
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Complete moles: secondary to sperm fertilizing ovum with inactive nucleus, haploid
sperm duplicates to diploid - 47XY karyotype.
Gestational trophoblastic disease (GTD)
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The partial mole: focal trophoblastic hyperplasia with villous hydrops together with
identifiable fetal tissue.
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Fertilization of a normal oocyte by more than a single sperm or a diploic sperm or
fertilization of a diploic oocyte by a normal haploid sperm, all resulting in a conceptus
with 3 sets of chromosomes (69XXX or 69XXY).

> 90% of triploid fetuses show severe, symmetrical IUGR and multiple anomalies,
commonly accompanied by oligohydramnios and abnormal placental Doppler indices.

The typical placental molar features are not always present in triploid partial moles
and are less likely to be apparent on US in early pregnancy.

Malignant trophoblastic disease occurs in 15-20% of patients with hydatidiform mole
but rarely in partial mole - described as irregular echogenic lesions within the
myometrium, often surrounded by echofree areas, corresponding to local
hemorrhage.
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Chorioangioma
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Chorioangioma : most common benign nontrophoblastic placental neoplasm - a
hypervascular cystic lesion, single or multiple, with arterial and venous flow that
produces color signals.
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US: well-circumscribed, rounded, hypoechoic lesion next to the chorionic surface,
often close to the cord insertion.

Small lesions are often present when examining the placentas of completely
asymptomatic, normal pregnancies.
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Larger lesions (>5 cm) are rare, can be associated with non-immune hydrops, IUGR,
neonatal cardiomegaly, anemia and thrombocytopenia) and mortality, as well as
maternal morbidity such as polyhydramnios and pre-eclampsia.

Color Doppler US is useful in the early diagnosis and differentiation from hematomas
as well as evaluation of response to treatment.
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Placental cyst
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Placental cyst is a rare, mostly benign, subchorionic lesion, filled with mucoid
material.
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It is a single finding in most cases, but, occasionally, multiple cysts are present.
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Only if large (>4.5 cm) have they been associated with fetal complications, such as
IUGR or fetal demise.
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Placenta in multiple gestations
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Monochorionic twins are at risk for type-specific perinatal complications, for example,
twin twin transfusion syndrome (TTTS).
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There is a higher frequency of velamentous and marginal cord insertion in twins,
potentially leading to IUGR as a result of unequal sharing of placental tissue.

It is estimated that 95% of MC twin placentas contain interfetal vascular connections.

These connections may be indirect artery-to-vein (A-V), found in up to 80% cases
(within the placental villi), direct artery-to-artery (A-A), in 75% (at the fetal surface), or
direct vein-to-vein (V-V) in 20% (at the fetal surface).
Placenta in multiple gestations

The A-V connections are responsible for TTTS, while A-A may protect against it but
lead to twin reversed arterial perfusion (TRAP), together with V-V connections.

In TRAP sequence, one twin (pump twin) forces blood to the entire placenta and the
acardiac twin who acts as an additional cotyledon but without reoxygenating that
amount of blood that passed through it.
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Sluggish flow increases risk of thrombosis and thromboembolic phenomena in the
pump twin.
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Cord entanglement is another risk specific to monoamniotic twins.
Placenta in multiple gestations

Membranes in a monochorionic pregnancy has been described with the T sign:
membrane inserts the placenta at a 90 degree angle.

The presence of a thick (>2 mm) dividing membrane, from 10 - 14 weeks, supports
the diagnosis of dichorionicity.

The presence of the lambda sign or T sign in the presence of a single placenta, in the
first trimester, is the most reliable indicator of chorionicity.
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This analysis of the membranes should be performed in higher rate multiple
gestations in a similar fashion.
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Thank you