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2010-12-09-12 Partial mole in the second trimester © Cerekja
Partial mole in the second trimester

Albana Cerekja MD.,PhD.*, Carlo Figliolini MD., PhD.**, Francesco Cecinato MD PhD***, Juan Piazze MD.,PhD.****.

*     Pediatric Cardiology. Policlinico Umberto I. University “La Sapienza” Rome, Italy
**   Reparto di ostetricia e ginecologia, Ospedale Fatebenefratelli San Pietro Rome, Italy .
***  Obstetrics Department. Policlinico Umberto I. University “La Sapienza” Rome, Italy.
**** Ultrasound Division, Ceprano Hospital, Ceprano, Italy.


A partial molar pregnancy is a genetic condition characterized by triploidy, 69 chromosomes. The normal egg either receives two sets of chromosomes from the father (diandric triploidy), two haploid sperms or one diploid sperm fertilize a normal ovum. Or the diploid ovum is fertilized by a single normal sperm (digynic triploidy). This results in a triploid conceptus with 69 chromosomes. Partial hydatidiform mole refers to the fetus with triploidy with placental molar degeneration.

On ultrasound, partial
hydatidiform mole presents as an enlarged placenta containing multicystic, avascular, anechoic areas. Since triploidy is a lethal chromosomal abnormality, most affected embryos die within a first few weeks after conception. Diandric triploidies are associated with a higher miscarriage rate and early spontaneous abortion than digynic triploidies. The excess of the paternal contribution to the zygote has an adverse deleterious effect on the placental implantation and development [1]. The partial hydatidiform mole before 12-weeks of gestation can present as an enlarged placenta without obvious macroscopic changes. This suggests that molar transformation becomes more pronounced as the pregnancy advances. In early pregnancy, molar changes are often identified only by histopathological examination. This may escape to the clinical detection, especially in case of first trimester miscarriage [1].

The ultrasound findings of diandric triploidies include:

  • Well-grown or symmetrical growth restricted fetus
  • Changes of the placenta, placentomegaly *
  • Increased nuchal translucency
  • Decreased amount of the amniotic fluid

*There are several studies on placental thickness during the pregnancy [2,3]. Tongsong et al. [2] found a linear equation of the placental thickness to the gestational age in the first half of pregnancy; placental thickness (mm) = gestational age (weeks) x 1.4 - 5.6 (r = 0.82). Chukwuemeka et al. [3] studied placental thickness during the whole pregnancy and found that it's mean value in the first trimester is 12.5 ± 3.7 mm. However, as a simple rule, the placental thickness (in millimeters) should be approximately equal to the gestational age in weeks +/- 10 mm [4]. 

Case report

This is the case of a 43-year-old G5 P4 with non-contributive family or personal history. Beta HCG at 5 weeks was 2, 956 mIU/ml and 10 days later 19, 600 mIU/ml which was consistent with the gestational age. Patient refused the invasive prenatal diagnostic suggested due to a maternal age. 
The first trimester scan at 12 weeks of gestation showed NT=2.5 mm, present nasal bone and reverse flow in the ductus venosus. Placenta appeared normal.

The follow-up ultrasound at 17 weeks showed a female fetus with a symmetrical growth restriction, biometry corresponded to 15 weeks of gestation and a decreased amount of the amniotic fluid. No apparent fetal anomalies were detected.
The only findings were hyperechoic bowel, a small thorax with relative cardiomegaly and dilated right atrium. Placenta occupied a large part of the uterine cavity, placental thickness was 53 mm. There were multiple cystic areas in the placenta of 15 mm in diameter. Placenta did not show any increased vascularization. Multiple theca-lutein cysts were observed on both ovaries.

Beta HCG in the maternal serum was
990, 000 mIU/m alpha-fetoprotein was 548 ng/ml (normal values 0-12 ng/ml). The patient was informed about the maternal risks and poor fetal prognosis. The pregnancy termination was suggested but the patient refused. She presented again in a week for the intense nausea. She had no bleeding and her blood pressure was normal. The ultrasound showed the intrauterine fetal demise and fetal hydrops.

We evaluated retrospectively the images from the examination at 12 weeks. The placenta looked hyperechoic and its thickness was 25 mm which resulted superior to the upper limit for 12 weeks [2,3,4]. The patient was hospitalized and coagulation values were monitored. Considering a very high beta HCG values, the chest X-ray was performed to exclude a metastatic invasion of the gestational trophoblastic disease. A dilatation and curettage was performed the next day. The fetus looked macroscopically normal. Placenta had a classical appearance of a molar degeneration.

Images 1,2
: 12 weeks, image 1 shows fetal profile and image 2 shows placenta.


Images 3,4: 17 weeks, fetus was growth restricted (growth corresponded to 15 week), see normal profile, face and axial view of the brain. The bowel is hyperechoic.

Images 5,6: 18 weeks, intrauterine fetal demise with fetal hydrops.

Images 7,8: Image 7 shows reverse flow in ductus venosus at 12 weeks and normal flow at 17 weeks. Image 8 shows theca-lutein ovarian cysts

Images 9,10:  Placenta with molar degenerations, multiple anechoic cysts, high placenta.

Videos 1,2: Videos show placentomegaly with multiple, avascular cystic areas.

Video 3: 4-chamber view, a color Doppler shows a pulmonary regurgitation.



1. Jauniaux E. Trophoblastic diseases and pregnancy. Review. The Obstetrician & Gynaecologist 2003;5:130-5
2. Tongsong, T. and Boonyanurak, P. Placental thickness in the first half of pregnancy. J Clin Ultrasound 2004;32: 231–234.
3. Chukwuemeka Ohagwu Ch, Oshiotse Abu P, Effiong Udoh B. Placental thickness: A sonographic indicator of gestational age in normal singleton pregnancies in Nigerian women. Internet Journal of Medical Update 2009 July;4(2):9-14
4. Harris RD, Alexander RD. Ultrasound of the placenta and umbilical cord. In: Callen PW, eds. Ultrasonography in obstetrics and gynecology. Philadelphia, Pa: Saunders, 2000;597-625.

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