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Letters to the Editor
Figure 1 Ultrasound image of 13-week fetus showing increased nuchal translucency thickness and generalized subcutaneous edema.
Cause of fetal demise in first-trimester parvovirus infection: anemia, placentitis or myocarditis? Increased nuchal translucency and/or the presence of fetal hydrops during first-trimester ultrasound examination has been reported as a sign of congenital infection with parvovirus. Recent reports on parvovirus infection in pregnancy have described altered fetal hemodynamics
Copyright © 2014 ISUOG. Published by John Wiley & Sons Ltd.
resulting from mild cardiomegaly, progressive augmentation of peak systolic velocity in the middle cerebral artery (MCA-PSV), reversed flow in the ductus venosus during atrial contraction and development of hydrops1 – 4 . We report the case of a 35-year-old woman, gravida 3 para 2, with no relevant prior medical history who underwent routine ultrasound examination at 13 weeks’ gestation (according to the date of her last menstrual period as well as measurement of fetal crown–rump length of 69 mm), which revealed a nuchal translucency measurement of 3.6 mm (>99th centile). The fetus was hydropic with generalized subcutaneous edema, pleural and pericardial effusion as well as ascites (Figure 1). Doppler examination showed tricuspid regurgitation, reversed flow in the umbilical artery and an MCA-PSV of 24.06 cm/s (Figure 2). Although reference data for normal values of MCA-PSV do not cover this early gestational age, fetal anemia was suspected. Intrauterine spontaneous fetal demise was diagnosed 2 days later. Complementary investigations were performed and revealed a normal karyotype and maternal immunoglobulin G and immunoglobulin M for parvovirus B19. Virologic analysis of amniocyte culture revealed parvovirus B19 DNA. Maternal parvoviral seroconversion rates vary between 3% and 34% and the risk of vertical transmission is approximately 30%3,4 . Fetal hydrops develops in 0–12.5% of infected fetuses with a peak between 17 and 24 weeks’ gestation, while fetal demise is estimated to occur at a rate of 5–10%, with or without the diagnosis of fetal hydrops in cases of unclear pathophysiology3 – 5 . We consider that there are three hypothetical causes of fetal demise in first-trimester parvovirus fetal infection: 1) primary viral infection of the myocardial cells initially causes myocarditis, leading to hydropic cardiac failure and demise; 2) bone marrow transient aplastic crisis occurs as the primum movens for anemia, leading to the sequence of congestive heart failure/hydrops/death; 3) placentitis without fetal infection causes placental dysfunction and ultimately fetal demise3,4 . Although postmortem examination was not conclusive, this case suggests that B19 parvovirus may cause fetal hydrops in the first trimester, recognition of which is likely
Ultrasound Obstet Gynecol 2014; 44: 617–619.
Letters to the Editor
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Figure 2 Doppler ultrasound images at 13 weeks’ gestation showing reversed flow in the umbilical artery (a) and increased peak systolic velocity in the fetal middle cerebral artery (b).
to contribute to postmortem counseling. It also supports the notion of an early response of middle cerebral artery systolic velocities to anemia. G. E. Chalouhi*†, S. Benedetti†, C. Alby†‡, N. Benzina† and Y. Ville† †Obstetrics and Fetal Medicine Department, Necker-Enfants-Malades Hospital, APHP, Paris V University, Paris, France; ‡Department of Genetics, Pathology, Embryology and Cytogenetics, Necker-Enfants-Malades Hospital, APHP, Paris V University, Paris, France *Correspondence. (e-mail: [email protected]) DOI: 10.1002/uog.13416
Copyright © 2014 ISUOG. Published by John Wiley & Sons Ltd.
References ˜ O, Montenegro N. Early signs of 1. Carraca T, Matias A, Brandao cardiac failure: a clue for parvovirus infection screening in the first trimester? Fetal Diagn Ther 2011; 30: 150–152. ¨ 2. Kempe A, Rosing B, Berg C, Kamil D, Heep A, Gembruch U, Geipel A. First-trimester treatment of fetal anemia secondary to parvovirus B19 infection. Ultrasound Obstet Gynecol 2007; 29: 226–228. 3. Lamont RF, Sobel JD, Vaisbuch E, Kusanovic JP, Mazaki-Tovi S, Kim SK, Uldbjerg N, Romero R. Parvovirus B19 infection in human pregnancy. BJOG 2011; 118: 175–186. 4. Ergaz Z, Ornoy A. Parvovirus B19 in pregnancy. Reprod Toxicol 2006; 21: 421–435. 5. Morel O, Chagnaud S, Laperrelle J, Cl´ement D, Malartic C, Akerman G, Tulpin L, Sitbon M, Barranger E. Parvovirus B19 et grossesse: revue de la litt´erature. Gynecol Obstet Fertil 2007; 35: 1095–1104.
Ultrasound Obstet Gynecol 2014; 44: 617–619.
Letters to the Editor
Figure 1 Ultrasound image of 13-week fetus showing increased nuchal translucency thickness and generalized subcutaneous edema.
Cause of fetal demise in first-trimester parvovirus infection: anemia, placentitis or myocarditis? Increased nuchal translucency and/or the presence of fetal hydrops during first-trimester ultrasound examination has been reported as a sign of congenital infection with parvovirus. Recent reports on parvovirus infection in pregnancy have described altered fetal hemodynamics
Copyright © 2014 ISUOG. Published by John Wiley & Sons Ltd.
resulting from mild cardiomegaly, progressive augmentation of peak systolic velocity in the middle cerebral artery (MCA-PSV), reversed flow in the ductus venosus during atrial contraction and development of hydrops1 – 4 . We report the case of a 35-year-old woman, gravida 3 para 2, with no relevant prior medical history who underwent routine ultrasound examination at 13 weeks’ gestation (according to the date of her last menstrual period as well as measurement of fetal crown–rump length of 69 mm), which revealed a nuchal translucency measurement of 3.6 mm (>99th centile). The fetus was hydropic with generalized subcutaneous edema, pleural and pericardial effusion as well as ascites (Figure 1). Doppler examination showed tricuspid regurgitation, reversed flow in the umbilical artery and an MCA-PSV of 24.06 cm/s (Figure 2). Although reference data for normal values of MCA-PSV do not cover this early gestational age, fetal anemia was suspected. Intrauterine spontaneous fetal demise was diagnosed 2 days later. Complementary investigations were performed and revealed a normal karyotype and maternal immunoglobulin G and immunoglobulin M for parvovirus B19. Virologic analysis of amniocyte culture revealed parvovirus B19 DNA. Maternal parvoviral seroconversion rates vary between 3% and 34% and the risk of vertical transmission is approximately 30%3,4 . Fetal hydrops develops in 0–12.5% of infected fetuses with a peak between 17 and 24 weeks’ gestation, while fetal demise is estimated to occur at a rate of 5–10%, with or without the diagnosis of fetal hydrops in cases of unclear pathophysiology3 – 5 . We consider that there are three hypothetical causes of fetal demise in first-trimester parvovirus fetal infection: 1) primary viral infection of the myocardial cells initially causes myocarditis, leading to hydropic cardiac failure and demise; 2) bone marrow transient aplastic crisis occurs as the primum movens for anemia, leading to the sequence of congestive heart failure/hydrops/death; 3) placentitis without fetal infection causes placental dysfunction and ultimately fetal demise3,4 . Although postmortem examination was not conclusive, this case suggests that B19 parvovirus may cause fetal hydrops in the first trimester, recognition of which is likely
Ultrasound Obstet Gynecol 2014; 44: 617–619.
Letters to the Editor
619
Figure 2 Doppler ultrasound images at 13 weeks’ gestation showing reversed flow in the umbilical artery (a) and increased peak systolic velocity in the fetal middle cerebral artery (b).
to contribute to postmortem counseling. It also supports the notion of an early response of middle cerebral artery systolic velocities to anemia. G. E. Chalouhi*†, S. Benedetti†, C. Alby†‡, N. Benzina† and Y. Ville† †Obstetrics and Fetal Medicine Department, Necker-Enfants-Malades Hospital, APHP, Paris V University, Paris, France; ‡Department of Genetics, Pathology, Embryology and Cytogenetics, Necker-Enfants-Malades Hospital, APHP, Paris V University, Paris, France *Correspondence. (e-mail: [email protected]) DOI: 10.1002/uog.13416
Copyright © 2014 ISUOG. Published by John Wiley & Sons Ltd.
References ˜ O, Montenegro N. Early signs of 1. Carraca T, Matias A, Brandao cardiac failure: a clue for parvovirus infection screening in the first trimester? Fetal Diagn Ther 2011; 30: 150–152. ¨ 2. Kempe A, Rosing B, Berg C, Kamil D, Heep A, Gembruch U, Geipel A. First-trimester treatment of fetal anemia secondary to parvovirus B19 infection. Ultrasound Obstet Gynecol 2007; 29: 226–228. 3. Lamont RF, Sobel JD, Vaisbuch E, Kusanovic JP, Mazaki-Tovi S, Kim SK, Uldbjerg N, Romero R. Parvovirus B19 infection in human pregnancy. BJOG 2011; 118: 175–186. 4. Ergaz Z, Ornoy A. Parvovirus B19 in pregnancy. Reprod Toxicol 2006; 21: 421–435. 5. Morel O, Chagnaud S, Laperrelle J, Cl´ement D, Malartic C, Akerman G, Tulpin L, Sitbon M, Barranger E. Parvovirus B19 et grossesse: revue de la litt´erature. Gynecol Obstet Fertil 2007; 35: 1095–1104.
Ultrasound Obstet Gynecol 2014; 44: 617–619.
