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Prenatal Cardiology
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Case report

Placental cyst – case study

Julia Murlewska
Maria Respondek-Liberska
1, 2
Agata Lusińska
Przemysław Poszwa
Stefan Sajdak

  1. Department of Prenatal Cardiology, Polish Mother’s Memorial Hospital Research Centre, Lodz, Poland
  2. Fetal Malformations Department, Medical University in Lodz, Poland
  3. Division of Gynaecological Surgery, Poznan University of Medical Sciences, Poland
  4. Institute of Materials Technology, Poznan University of Technology, Poland
Prenat Cardio 2019; 9(1): 51-55
Online publish date: 2020/01/16
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Subchorionic/chorionic or membranous placental cysts are echo-free cavities with no blood flow within, and they have a prevalence of approximately 2–7%. A large placental cyst located near the umbilical cord insertion or multiple cysts (with more than three cysts) could induce partial occlusion of umbilical cord blood flow and possible haematomas formation, infarction, fetal growth restriction, preterm birth, and/or neonatal morbidity [1–20].

Case study

A G2P0 30-year-old pregnant woman was referred at 26 w 5 d to our Institution for fetal echocardiography due to a diagnosis of a placental cyst at a routine second-trimester scan performed elsewhere. She had gynaecological history of PCOS and had been under gynaecological oncologist observation for two years due to a simple left ovarian cyst: 53.5 × 27.7 mm (width × height) with no growth progression nor higher risk of malignancy algorithms, and she had had hormonal therapy before pregnancy, without any ovulation induction nor in vitro fertilisation.
The first trimester combined test for common trisomy was negative. The second trimester routine anomaly-scan was negative for congenital anomalies. The patient had recurrent infections in her pregnancy: bronchitis and persistent vaginal infections, treated with antibiotics, so she had a very tight obstetric schedule.
The first ultrasound anomaly was detected at 25.6 weeks when we saw a single cyst at the fetal side of the placenta with the size of 38.4 × 37.4 × 29.9 mm and volume of 22.484 cm3, the placenta was positioned at the posterior wall, and the cyst was located near the placental marginal cord insertion. The cyst was anechoic with no masses, with very thin wall, and no c-Doppler flow within it. The enlargement of the cyst in the pregnancy was as follows: cyst size ranged from 43.2 × 41.3 × 39.5 mm, volume of 36.9 cm3 at 27.5 weeks to, finally: 72.8 × 68.1 × 55.2 mm, volume of 143.29 cm3 at 37.5 weeks (Figures 1–5).
The placenta was growing adequately until 34.5 weeks of gestation, when infection and oedema of the placenta was suspected: the thickness/length/width of the placenta ranged from 47.1 × 16.17 × 13.56 mm, with volume of 540.741 cm3 at 34.5 weeks to 83.5 × 15.28 × 12.01 mm, volume of 802.327 cm3 at 38.2 weeks (Figures 4, 5).
Figure 4 shows the chart of growth of the placental cyst volume and placental plate volume in gestation (25.6–37.5 weeks). Figure 5 shows the ratio of the placental cyst volume to the placental plate volume in the pregnancy (36.5–38.2 weeks). Apart from the placental abnormalities, the fetal growth charts were adequate throughout the time of gestation.
The echocardiographic evaluation was performed three times, at 20 weeks, 27.5 weeks, and 29.6 weeks, and apart from the reduced contractility of the ventricles, with the 18% of shortening fraction for RV and 25% for LV, the fetus was cardiovascularly stable with a 9/10 CVP score (cardio-vascular profile).
The prenatal course, except of the placental enlargement and growing of the placental cyst, was uneventful up to 36.5 weeks. Then we discovered evidence of progressive and persistent biweekly repeated reduction of fetal cerebral-placental blood flow with the CPR (cerebroplacental ratio): 0.67 at 36.5 weeks (PIUMBA = 0.69; PSUMBA = 42 cm/s; PIMCA = 1.02; PSMCA = 28 cm/s) and 0.62 (PIUMBA = 0.64; PSUMBA = 53 cm/s; PIMCA = 1.03; PSMCA = 21 cm/s) at 38.2 weeks (Table 1) with fetal tachycardia of 180 bpm and a probable false umbilical knot near the fetal face documented by ultrasound (Figure 6).
A scheduled caesarean section was performed at 38.5 weeks because of these findings and with the intention to remove the left ovarian cyst during the same operating cycle. A 3300 γ baby girl was delivered; Apgar scores were 10, 10, and gasometry: pH: 3, 7.31; pH: 7,35; BE = –0.7; BE = –1.2. The baby girl had a neonatal erythema with good reaction to the potassium permanganate and jaundice with a bilirubin value at the third day of life, on the day of discharge, of about 9.6 mg/dl.
Pathologic postnatal evaluation revealed that the placenta weighted 600 g, measured 15 × 118 × 2 cm, and with an umbilical cord length of 40 mm of the marginal cord insertion. The microscopic examination showed wide limiting of the exchange placental surface: wide placental infarction, fibrin exudation, decalcifications, severe disturbances in fetal and maternal circulation, and a sole membranous cyst located near the marginal placental cord insertion (Figure 7). The left ovarian cyst was reported by pathologists as cystadenoma mucinosum.


The thickness of the anterior placenta greater than 33 mm and 40 mm for the posterior placenta should be considered as abnormally thick placenta, based on the pilot study of Lee et al. [21]. In our case, we observed a posterior positioned thickened placenta with a placental cyst. Many studies show the correlations between abnormally thick placenta and poor outcome, with higher risk of perinatal mortality and growth restriction. Placental alterations have been associated with a wide variety of maternal and fetal conditions, including infections, diabetes, PCOS, and hydrops [21–33].
Placental chorionic plate cysts are usually benign, but such large and growing placental cysts, as presented in our study, are reported very rarely. They are often associated with progressive reduction in fetal blood flow and placental-maternal floor infarction [2, 4, 11, 31, 32].
In pregnant women with PCOS gestational androgen excess and insulin resistance might alter and contribute to endovascular trophoblast invasion. Adipokines produced by placenta and ovaries have a significant effect on fetal and placental growth, and programming of insulin sensitivity. Placental growth factor is increased in women with PCOS and might play a role in placental cyst pathogenesis and the angiogenic placental dysregulation mentioned in our case [33–37].
Recurrent symptomatic infections observed in our case supported the evidence of the presence of chronic low-grade inflammation in women with polycystic ovarian syndrome [38]. If any recurrent infections occur in pregnancy, we recommend a schedule of prenatal visits: every two weeks after 26 weeks, to monitor fetal growth, repeated, detailed fetal echocardiography, and ultrasound placental evaluation for the continuation of a safe pregnancy and avoidance of prematurity.

Conflict of interest

The authors declare no conflict of interest.


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Division of work:
Julia Murlewska (ORCID: 0000-0002-8266-4585): research concept and design, collection and/or assembly of data, data analysis and interpretation, writing of the article
Maria Respondek-Liberska (ORCID: 0000-0003-0238-2172): data analysis and interpretation, critical revision, final approval of the article
Agata Lusińska (ORCID: 0000-0002-9166-8238): collection and/or assembly of data, critical revision of the article, final approval of the article
Przemysław Poszwa (ORCID: 0000-0001-6004-5401): data analysis and interpretation
Stefan Sajdak (ORCID: 0000-0002-8641-4188): final approval of the article
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