P02.16: Cause of fetal demise in first trimester parvovirus fetal infection: anemia or myocarditis?

14–17 September 2014, Barcelona, Spain Electronic poster abstracts

P02.14: Table 1.

CasesWeeks atdiagnosis Ultrasound findings

Cyst(number) Karyotype

Fetalsex Type of delivery

Weight atbirth

(grams)Apgar 1/5(minutes) pH

1 12 + 4 None 2 46XY Male Normal(Suctionpad)

2830 9/10

2 12 None 1 46XY Male Pending delivery3 12 None 1 Female Normal 2640 9/10 7,334 16 4 None None

2 Male Normal3440 9/10 7,35

2 Male Normal 3440 9/10 7,35

5 33 + 6 None 1 46XY Female Normal 3760 9/10 7,456 16 None 1 46XY 46XY

MalePendingdelivery

Male PendingDelivery 37609/10 7,45 6Pendingdelivery

7 32 None 1 Female Normal 3760 9/108 32 Triplet 1 3 Males Cesarean section 1571,

1400,1100

9/10; 9/10;6/9

9 12 Omphalocele Multiple Pending delivery10 20 Choroid plexus cyst 1 Pending delivery11 12 ISUA + bilateral

pyelic ectasia +oligohydramnios

1 1 46XY TOP 46XY TOP

12 12 Hidropsfetalis + partialmolar pregnancy

Multiple TOP

13 11 + 6 Omphalocele + clawhands + choroidplexus cyst +EIUGR

1 18 TRISOMY Stillbirth

14 12 Mega-cysticbladder +holoprosencephaly+ extremitymalposition

Multiple 18 TRISOMY TOP

15 12 Body wall complex/body stalk anomaly

1 45X0 TOP

16 14 Oligohydramnios +partial molarpregnancy

1 TRIPLOIDY TOP

TOP: termination of pregnancy.ISUA: Isolated single umbilical artery.EIUGR: Early intrauterine growth restriction.

P02.16Cause of fetal demise in first trimester parvovirus fetalinfection: anemia or myocarditis?

G.E. Chalouhi1, S. Benedetti1, C. Alby1,2, N. Benzina1,Y. Ville1

1Department of Obstetrics and Fetal Medicine,Necker-Enfants-Malades Hospital, APHP, Paris V University,Paris, France; 2Department ofGenetics-Pathology-Embryology and Cytogenetics,Necker-Enfants-Malades Hospital, APHP, Paris V University,Paris, France

Increased nuchal translucency and/or fetal hydrops during firsttrimester ultrasound examination have been reported as signs ofcongenital infection with parvovirus infection.

We report the case of a 35-year-old woman, gravida 3 para2 with no prior relevant history who underwent routine US

examination at 13 weeks’ by both dates and CRL (69 mm) anda nuchal translucency (NT) of 3.6 mm (>99th centile). The fetuswas hydropic with generalized subcutaneous edema, pleural, andpericardial effusion as well as ascites. Hemodynamics assessmentshowed tricuspid regurgitation, and reverse flow in the umbilicalartery. The MCA-PSV was 24.06 cm/s.

Although the reference table of MCA-PSV doesn’t cover thisearly gestational age, fetal anemia was suspected. An intra-uterinespontaneous fetal demise was diagnosed 2 days later. Complemen-tary investigations were performed showing a normal karyotype,positive maternal IgG and IgM for Parvovirus B19, the virologyanalysis on amniocytes culture showed positive Parvovirus B19DNA.

Maternal Parvoviral seroconversion rate varies between 3-34%and the risk of vertical transmission is approximately 30%. Fetalhydrops develops in 0 to 12.5% of infected fetus with a peak atbetween between 17 and 24 weeks, while fetal demise is estimatedto occur in 5-10%, with or without the diagnosis of fetal hydropsfollowing an unclear physiopathology.

Ultrasound in Obstetrics & Gynecology 2014; 44 (Suppl. 1): 181–369. 193