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Twin Anemia–polycythemia Sequence with Placental Arterio-arterial Anastomoses
Placenta 31 (2010) 652
Contents lists available at ScienceDirect
Placenta journal homepage: www.elsevier.com/locate/placenta
Letter to the Editors
Twin Anemia–polycythemia Sequence with Placental Arterio-arterial Anastomoses
Sirs, We read with great interest the recent report by van Meir et al., showing a case of twin anemia–polycythemia sequence (TAPS) with an arterio-arterial (AA) anastomosis in the placenta [1]. TAPS has been suggested to be mediated through minuscule unidirectional anastomoses such as small arterio-venous (AV) anastomoses, while AA anastomoses have been suggested to carry a protective effect against the development of this complication [2,3]. Their recent case indicated that absence of AA anastomoses do not prevent the development of TAPS with AV anastomoses [1]. Recently, we have encountered a case of TAPS having placental AA anastomoses without AV anastomoses. A 27-year-old gravida 2 para 1 had a Cesarean delivery at 34 weeks’ gestation because of monochorionic–diamniotic twin pairs with late-onset discordant growth. The amniotic pockets of both twins were normal (4.0 and 4.0 cm) and the fetal heart rate tracings showed reassuring patterns in both the twins. At delivery, twin A was a 2436-g male infant with Apgar scores of 6 and 8 at 1 and 5 min, respectively, while twin B was a 1698-g male with Apgar scores of 8 and 9, respectively with no signs of acute hemorrhagic shock (growth differences: 30%). The hemoglobin concentration of twin A was 22.3 g/dL (normal: 13–22 g/dL) with reticulocyte counts of 2.6% (normal: <7%), while it was 11.4 g/dL with reticulocyte counts of 14.7% in twin B. After delivery, twin A required intravenous infusion of 10% glucose and 4.4% human serum albumin for correction of polycythemia, while twin B required a transfusion of red cell concentrate (22 ml). The placenta was confirmed as monochorionic with 2 superficial AA anastomoses by milk injection. However, we could not find any AV anastomoses in the placenta. Unfortunately, we could not take a good photograph of the placenta; however, our case suggests that there may be more
0143-4004/$ – see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.placenta.2010.04.008
various mechanisms leading to the development of TAPS than those suggested previously [1–5]. In our case, the similar collateral flow through the AA anastomoses might have occurred in smaller scale which triggered onset of TAPS. Otherwise, we might not be able to find the presence of anastomoses of the trace degree with our injection technique limitations. The elucidation of the mechanisms leading to TAPS is needed by accumulation of the same case reports.
References [1] van Meir H, Slaghekke F, Lopriore E, van Wijngaarden WJ. Arterio-arterial anastomoses do not prevent the development of twin anemia–polycythemia sequence. Placenta 2010;31:163–5. [2] Lopriore E, Deprest J, Slaghekke F, Oepkes D, Middeldorp JM, Vandenbussche FP, et al. Placental characteristics in monochorionic twins with and without twin anemia–polycythemia sequence. Obstet Gynecol 2008;112:753–8. [3] Lopriore E, Oepkes D. Fetal and neonatal haematological complications in monochorionic twins. Semin Fetal Neonatal Med 2008;13:231–8. [4] Lewi L, Gucciardo L, Huber A, Jani J, Van Mieghem T, Doné E, et al. Clinical outcome and placental characteristics of monochorionic diamniotic twin pairs with early and late-onset discordant growth. Am J Obstet Gynecol 2008;199: 511. e.1–7. [5] Lopriore E, Middeldorp JM, Oepkes D, Kanhai HH, Walther FJ, Vandenbussche FP. Twin anemia–polycythemia sequence in two monochorionic twin pairs without oligo-polyhydramnios sequence. Placenta 2007;28: 47–51.
S. Suzuki* Department of Obstetrics and Gynecology, Japanese Red Cross Katsushika Maternity Hospital, 5-11-12 Tateishi, Katsushika-ku, Tokyo 124-0012, Japan * Tel.: þ81 3 3693 5211; fax: þ81 3 3694 8725. E-mail address: [email protected] Accepted 11 April 2010
Contents lists available at ScienceDirect
Placenta journal homepage: www.elsevier.com/locate/placenta
Letter to the Editors
Twin Anemia–polycythemia Sequence with Placental Arterio-arterial Anastomoses
Sirs, We read with great interest the recent report by van Meir et al., showing a case of twin anemia–polycythemia sequence (TAPS) with an arterio-arterial (AA) anastomosis in the placenta [1]. TAPS has been suggested to be mediated through minuscule unidirectional anastomoses such as small arterio-venous (AV) anastomoses, while AA anastomoses have been suggested to carry a protective effect against the development of this complication [2,3]. Their recent case indicated that absence of AA anastomoses do not prevent the development of TAPS with AV anastomoses [1]. Recently, we have encountered a case of TAPS having placental AA anastomoses without AV anastomoses. A 27-year-old gravida 2 para 1 had a Cesarean delivery at 34 weeks’ gestation because of monochorionic–diamniotic twin pairs with late-onset discordant growth. The amniotic pockets of both twins were normal (4.0 and 4.0 cm) and the fetal heart rate tracings showed reassuring patterns in both the twins. At delivery, twin A was a 2436-g male infant with Apgar scores of 6 and 8 at 1 and 5 min, respectively, while twin B was a 1698-g male with Apgar scores of 8 and 9, respectively with no signs of acute hemorrhagic shock (growth differences: 30%). The hemoglobin concentration of twin A was 22.3 g/dL (normal: 13–22 g/dL) with reticulocyte counts of 2.6% (normal: <7%), while it was 11.4 g/dL with reticulocyte counts of 14.7% in twin B. After delivery, twin A required intravenous infusion of 10% glucose and 4.4% human serum albumin for correction of polycythemia, while twin B required a transfusion of red cell concentrate (22 ml). The placenta was confirmed as monochorionic with 2 superficial AA anastomoses by milk injection. However, we could not find any AV anastomoses in the placenta. Unfortunately, we could not take a good photograph of the placenta; however, our case suggests that there may be more
0143-4004/$ – see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.placenta.2010.04.008
various mechanisms leading to the development of TAPS than those suggested previously [1–5]. In our case, the similar collateral flow through the AA anastomoses might have occurred in smaller scale which triggered onset of TAPS. Otherwise, we might not be able to find the presence of anastomoses of the trace degree with our injection technique limitations. The elucidation of the mechanisms leading to TAPS is needed by accumulation of the same case reports.
References [1] van Meir H, Slaghekke F, Lopriore E, van Wijngaarden WJ. Arterio-arterial anastomoses do not prevent the development of twin anemia–polycythemia sequence. Placenta 2010;31:163–5. [2] Lopriore E, Deprest J, Slaghekke F, Oepkes D, Middeldorp JM, Vandenbussche FP, et al. Placental characteristics in monochorionic twins with and without twin anemia–polycythemia sequence. Obstet Gynecol 2008;112:753–8. [3] Lopriore E, Oepkes D. Fetal and neonatal haematological complications in monochorionic twins. Semin Fetal Neonatal Med 2008;13:231–8. [4] Lewi L, Gucciardo L, Huber A, Jani J, Van Mieghem T, Doné E, et al. Clinical outcome and placental characteristics of monochorionic diamniotic twin pairs with early and late-onset discordant growth. Am J Obstet Gynecol 2008;199: 511. e.1–7. [5] Lopriore E, Middeldorp JM, Oepkes D, Kanhai HH, Walther FJ, Vandenbussche FP. Twin anemia–polycythemia sequence in two monochorionic twin pairs without oligo-polyhydramnios sequence. Placenta 2007;28: 47–51.
S. Suzuki* Department of Obstetrics and Gynecology, Japanese Red Cross Katsushika Maternity Hospital, 5-11-12 Tateishi, Katsushika-ku, Tokyo 124-0012, Japan * Tel.: þ81 3 3693 5211; fax: þ81 3 3694 8725. E-mail address: [email protected] Accepted 11 April 2010