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CLINICAL LETTERS
Rapid Evolution of Placental Chorioangioma:
Natural Progression and Outcome
Placental chorioangioma is a benign vascular tumor most
frequently diagnosed in the second trimester of pregnancy
by sonographic and Doppler evaluation. The course of the
tumor may be totally indolent, with minimal to no maternal and fetal consequences, or it may also lead to premature
labor, intrauterine growth restriction, hydrops fetalis, and
high-output fetal heart failure, which may be due to arteriovenous anastomoses between the tumor and the placenta.
We present the case of a rapidly growing chorioangioma,
which culminated in premature labor, neonatal anemia,
and heart failure, eventually leading to neonatal death. The
uniqueness of our case resides in its sudden and brisk temporal evolution, which led to critical consequences.
The patient was a 32-year-old woman, gravida 3, para
2, with a history of 2 cesarean deliveries, 1 of which resulted
in a live birth and the other in neonatal death due to sepsis.
First-trimester screening for major abnormalities and aneuploidy yielded negative findings.
On a second trimester scan at 18 weeks, a chorioangioma was discovered, and close surveillance was initiated.
At 22 weeks, the tumor measured 58 × 43 mm (Figure
1A). No single vascular pedicle was identified, and the
fetus was growing appropriately without any signs of
impairment. At 27 weeks 3 days, the tumor nearly doubled in size and measured 96.7 mm; this rapid increase
motivated close surveillance, despite the normal fetal
growth, the normal amniotic fluid index, and the normal
umbilical and middle cerebral artery Doppler findings
(1.29 multiples of the median). Prenatal treatment was
discussed at that time. Eight days later, the sonographic
evaluation showed further tumor growth, which now
measured 15 cm. In addition, the fetus now manifested
signs of hydrops, with scalp edema, ascites, and polyhydramnios present as well. She was thus admitted at 28
weeks 4 days for close surveillance, and cortisone was
administered in anticipation of imminent delivery. Blood
work values were within the normal range except for
maternal anemia. She received 12 mg of betamethasone
twice over 24 hours. Nonstress fetal heart testing maintained reactivity and was performed repeatedly. She
underwent a cesarean delivery 24 hours after admission
because of the fetal hydrops. We noticed an excess of fluid,
and the placenta and cord were hydropic. Surgery was
complicated by transient uterine atony, which responded
to medical treatment.
The female neonate had considerable edema, weighed
2100 g, and had an Apgar score of 7 at 1 minute but rapidly
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became cyanotic. No heart murmur was heard. She had
substantial ascites, and the presence of ecchymosis was
noted on several areas of her body. She later had spontaneous bleeding from her mouth. The neonate’s hemodynamic status was critical, with substantial desaturation,
which necessitated mechanical ventilation. Fetal bradycardia ensued as well and partially responded to dobutamine, a continuous adrenaline infusion, as well as cardiac
massage. Neonatal echocardiography revealed a structurally normal heart that was, however, in severe heart failure. The neonate then went into a cardiac arrest, and
resuscitation for 20 minutes was unsuccessful, leading to
neonatal death. Postmortem blood work revealed severe
anemia (hemoglobin level, 5.6 g/dL) and disseminated
intravascular coagulation.
The mother had an uncomplicated postoperative
medical course and was discharged home on postoperative day 2 in good physical condition and without complications. Our medical team provided her with ongoing
psychological support and follow-up. The pathology report
showed a hypertrophic 1130-g placenta with a 15-cm
chorioangioma. Vascularization of the chorioangioma was
seen (Figure 1B).
Placental chorioangioma is the most common placental tumor, with an estimated prevalence of 1% in systematic placental histologic studies.1 The first case of a
prenatal sonographically diagnosed chorioangioma was
reported by Asokan et al2 in 1978. Small chorioangiomas
tend to remain asymptomatic during pregnancy. Large or
giant chorioangiomas (>4–5 cm in diameter) are more
often diagnosed prenatally by sonography during the second trimester.
Chorioangioma presents as a well-circumscribed
hypoechoic placental tumor located in most cases at the
chorionic plate, adjacent to the cord insertion. The vascular nature of the tumor can be confirmed by a Doppler
study.3 Signs of shunting with the umbilical vein may also
be shown. In our case, after the rapid growth of the tumor,
several abnormal flow velocity signals were shown, thus
possibly indicating the formation of a vascular communication between the fetal circulation and the tumor.
Complications are due to anastomosis of the arteriovenous system within the placenta, by means of a “stealing” phenomenon, which short circuits blood from a highto a low-resistance vascular bed, leading to heart failure;
this condition can be suspected by the presence of hydrops,
serous effusions, subcutaneous edema, cardiomegaly and
increased tricuspid regurgitation, an enlarged a wave in the
inferior vena cava, and pulsations in the umbilical vein, with
reduced or no diastolic flow.4
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On the other hand, polyhydramnios by itself is associated with a worse prognosis and a 6-fold increase in the
fetal mortality risk.5 Anemia and thrombocytopenia are
frequently reported complications. These can be explained
by tumor cell sequestration as well as by thrombotic
microangiopathy.1
Spontaneous regression of chorioangiomas as a result
of infarction, with resolution of the associated hydrops
fetalis, has been reported.6 In most cases, the size of the
tumor stabilizes, and thus it stays asymptomatic, or else it
grows and causes maternal and fetal consequences. Maternal complications include bleeding, preeclampsia, retroplacental hematoma, hemolytic anemia, and disseminated
intravascular coagulation,7 but the main complications are
mostly fetal and usually manifest as heart failure, polyhydramnios (14%–28%), intrauterine growth restriction
(30%), and prematurity (40%), in addition to the risks of
anemia, thrombocytopenia, and in utero death.8
Several novel interventions have been proposed to
block the vascular supply to the tumor as part of a curative
approach and include endoscopic laser coagulation,9 fetoscopic ligation of the vascular pedicle of the tumor with
bipolar electrocautery, and microcoil embolization.10–13
The use of interstitial laser therapy to devascularize the
tumor has been reported in 3 cases, and they all resulted in
a successful pregnancy outcome.14
Prenatal management of chorioangioma cases has to
be tailored to each case depending on the extent of tumor
involvement with the fetal circulation and relies primarily
on Doppler examination of the umbilical circulation.15
If the umbilical flow velocity waveform is abnormal (eg,
reduced or no diastolic flow), a thorough evaluation of the
functional state of the fetal circulation by means of evaluating fetal cardiac function and flow indices in the aorta, middle cerebral artery, and vena cava is warranted. Hydrops and
fetal heart failure are medical emergencies. A rapid increase
A
B
Figure 1. Placental chorioangioma. A, Vascularization of the chorioangioma at 22 weeks. B, Macroscopic view of the vascular pedicle of the
chorioangioma after delivery.
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in the size of the chorioangioma may be a critical sign signaling the need for aggressive therapy and close surveillance to properly time fetal delivery. These cases should be
managed in tertiary referral centers.
Assaad K. Kesrouani, MD, Joelle Safi, MD,
Mohamad A. El Hajj, MD
13. Lau TK, Leung TY, Yu SC, To KF, Leung TN. Prenatal treatment of
chorioangioma by microcoil embolisation. BJOG 2003; 110:70–73.
14. Zanardini C, Papageorghiou A, Bhide A, Thilaganathan B. Giant placental chorioangioma: natural history and pregnancy outcome. Ultrasound
Obstet Gynecol 2010; 35:332–336.
15. Jauniaux E, Ogle R. Color Doppler imaging in the diagnosis and management of chorioangiomas. Ultrasound Obstet Gynecol 2000; 15:463–467.
Department of Obstetrics and Gynecology
Saint Joseph University
Hotel Dieu de France Hospital
Beirut, Lebanon
We thank Reem S. Abu-Rustum, MD, for assistance with writing this letter.
References
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