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Arterio-Arterial Anastomoses do not Prevent the Development of Twin Anemia-Polycythemia Sequence
Placenta 31 (2010) 163–165
Contents lists available at ScienceDirect
Placenta journal homepage: www.elsevier.com/locate/placenta
Case report
Arterio-Arterial Anastomoses do not Prevent the Development of Twin Anemia-Polycythemia Sequence H. van Meir a, *, F. Slaghekke b, E. Lopriore c, W.J. van Wijngaarden a a
Division of Gynecology and Obstetrics, Bronovo Hospital, Bronovolaan 5, 2597 AX Den Haag, The Hague, The Netherlands Division of Gynecology and Obstetrics, Leiden University Medical Center, Leiden, The Netherlands c Division of Neonatology, Leiden University Medical Center, Leiden, The Netherlands b
a r t i c l e i n f o
a b s t r a c t
Article history: Accepted 19 November 2009
Monochorionic twin pregnancies are associated with increased perinatal morbidity and mortality. The vascular placental anastomoses in these pregnancies can cause severe complications. We describe a case of twin anemia-polycythemia sequence (TAPS) with an atypical placental angioarchitecture. During pregnancy serial ultrasound examinations of both twins revealed no amniotic fluid discordance and no abnormal Doppler ultrasound measurements (umbilical cord pulsatility index and middle cerebral artery peak systolic velocity). The twins, born at 33 þ 3 weeks gestation after spontaneous onset of labour, were found to be anemic and polycythemic, respectively. Placental examination with colored dye injection showed, apart from small ateriovenous anastomoses, an arterioarterial anastomosis. As arterio-arterial anastomoses have not been described in cases with spontaneous TAPS to date, it was postulated that such anastomoses carried a protective effect against the development of this complication. Ó 2009 Elsevier Ltd. All rights reserved.
Keywords: Twin anemia-polycythemia sequence Placental angioarchitecture Arterio-arterial anastomosis
1. Introduction Placental vascular anastomoses in monochorionic twin gestations may lead to twin-to-twin transfusion syndrome (TTTS). Recently, a variant of TTTS was described: twin anemia-polycythemia sequence (TAPS) [1–3]. TAPS is characterized by the presence of a large inter-twin difference in haemoglobin level and reticulocyte count without any signs of the oligo-polyhydramios sequence as seen in TTTS. TAPS may occur spontaneously (spontaneous form) or after laser surgery in the treatment of TTTS (postlaser form). The spontaneous form of TAPS occurs in approximately 3%–5% of monochorionic twin pregnancies [3,4], whereas the postlaser form of TAPS may occur in up to 13% of TTTS cases treated with laser [5]. TAPS may be suspected antenatally based on abnormal Doppler ultrasound findings in the absence of amniotic fluid discordance. Abnormal Doppler findings in TAPS consist of an increased middle cerebral artery peak systolic velocity (MCA-PSV) suggesting anemia in one fetus, with a simultaneous decrease in the MCA-PSV in the co-twin suggesting polycythemia [3–5]. Postnatal diagnosis of TAPS
* Corresponding author. Tel.: þ31 70 3124141. E-mail address: [email protected] (H. van Meir). 0143-4004/$ – see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.placenta.2009.11.009
is based on the presence of chronic anemia (with reticulocytosis) in the donor and polycythemia in the recipient twin. The pathophysiological mechanism leading to TAPS is not clear. We recently studied the placental angioarchitecture of a small group (N ¼ 11) of monochorionic placentas with TAPS and compared those with a control group of monochorionic placentas from uncomplicated twin pregnancies [4]. We found that TAPS placentas were characterized by the presence of only few and thin arterio-venous (AV) anastomoses, in the absence of arterio-arterial (AA) anastomoses [4], and speculated on the hypothetical link between this particular angioarchitecture and the development of TAPS. We now describe a spontaneous case of TAPS with an atypical placental angioarchitecture. 2. Case presentation A healthy 30-year-old gravida 3 para 0 was referred to our hospital at 12 weeks’ gestation with a spontaneous monochorionicdiamniotic twin pregnancy. The course of the pregnancy was uneventful and serial fetal ultrasound examinations performed every two weeks showed no signs of a twin oligo-polyhydramios sequence. The umbilical artery pulsatile index (PI) was never abnormal in either twin. Until 30 weeks’ gestation, Doppler measurements of the MCA-PSV showed no abnormalities and both
164
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twins had a normal growth along their individual percentiles. At 32 þ 5 weeks’ gestation, the last ultrasound examination before delivery (at 33 þ 3 weeks) was performed. Due to deep engagement of the fetal head the MCA-PSV of the first twin could not be measured accurately during the last two weeks before delivery. At 33 þ 3 weeks gestation, preterm uterine contractions started spontaneously and treatment with atosiban and corticosteroids was initiated. There were no signs of a twin oligo-polyhydramios sequence on ultrasound. Analysis of antepartum cardiotocography showed no signs of fetal distress in both fetuses. Spontaneous rupture of the membranes occurred a few hours after admission and was rapidly followed by a normal vaginal delivery of two girls both in cephalic position. The first twin was pale and weighed 1810 g (50th percentile). The second was plethoric and weighed 2355 g (80th percentile). The Apgar scores were 8/9/10 and 8/10/10 respectively and the fetal umbilical cord pH was normal for both girls. The hemoglobin levels at birth were 11.8 g/dL in twin 1 and 22.6 g/dL (normal range 14–20 g/dL) in twin 2. The hematocrit value of the second twin was 67%. The reticulocyte count was 10.6% in twin 1 and 3.8% in twin 2 (normal range: 2–6%). Twin 1 showed no signs of hemodynamic compromise and did not require a red blood cell transfusion. The polycythemic infant had no clinical symptoms associated with hyperviscosity and did not require a partial exchange transfusion. The neonatal hematological differences found at birth (anemia with reticulocytosis in one and polycythemia in the other twin) were diagnostic of chronic intertwin transfusion as seen in TAPS. TTTS was excluded given the absence of twin oligo-polyhydramnios sequence. Acute peripartum transfusion was deemed unlikely as there were no signs of hemorrhagic hypovolemic shock in the donor and the presence of reticulocysis was suggestive of a chronic event. Cranial ultrasound examination of both twins showed no abnormalities and further neonatal course was uneventful. Macroscopic placental examination confirmed a monochorionic-diamniotic placenta. The placental share of the donor and recipient twin was estimated 58% and 42%, respectively (Fig. 1). Colored dye injection of the placental vessels showed 3 small AV anastomoses (diameters from 0.3 to 0.4 mm) from donor to recipient and 2 small AV anastomoses from recipient to donor (diameter 0.3–0.4 mm) (Figs. 1 and 2). A small AA anastomosis (diameter 0.8 mm) was also detected (Figs. 1 and 2). The diameters of the anastomoses and the placental share discordance were measured on the digital picture of the placenta using Image Tool for Windows version 3.0 (Image Tool, San Antonio, TX, USA). Details on the technique used for placental injection and for the measurement of the placental territory and diameter of the vascular anastomoses have been described previously [6].
3. Comment We present a monochorionic-diamniotic twin pregnancy, complicated by a spontaneous form of TAPS with an atypical placental angioarchitecture. Placental injection study showed the atypical presence of an AA anastomosis. AA anastomoses are bi-directional anastomoses and are often referred to as ‘‘superficial’’ anastomoses since they lie on the chorionic plate. Various studies have demonstrated that AA anastomoses occur more frequently in uncomplicated monochorionic placentas than in TTTS placentas, respectively 80% versus 25% [7,8]. AA anastomoses are thus thought to exert a relative protection against the development of TTTS by compensating for the circulatory imbalance caused by the unidirectional AV anastomoses. This protective role of AA anastomoses which was already proposed by
Fig. 1. On top: maternal surface of the placenta showing the placental sharing discordance and the difference in color between the pale placental share of the donor (right side) and the congested placental share of the recipient (left side). Below: Placenta after dye injection (blue or green for arteries and orange for veins). The white arrow indicates the small AA anastomosis. The white stars indicate the small AV anastomoses from donor (right side) to recipient (left side). The blue stars indicate the small AV anastomoses from recipient to donor.
Schartz in the 19th century [9], has recently also been demonstrated in a mathematical computer model of TTTS [10]. In a recent study on the placental angioarchitecture of 11 individual cases of spontaneous TAPS, we found only small AV anastomoses (diameter < 1 mm), and no superficial AA anastomoses [4]. The AV anastomoses in the 11 TAPS cases were from donor to recipient (AV anastomosis) and from recipient to the donor (VA anastomosis). In analogy with the protective role of AA anastomoses against the development of TTTS, we suggested a link between the development of TAPS and the absence of AA anastomoses [4]. We postulated that this particular angioarchitecture would lead to a slow inter-twin blood transfusion, allowing sufficient time for hemodynamic compensatory mechanisms to take place, thus avoiding the development of a twin oligo-polyhydramnios sequence [2]. In a recent report, we described a post-laser case of TAPS in which a residual AA anastomosis was also detected [1]. The current case is the first described case of spontaneous TAPS in the presence of an AA anastomosis. In analogy with the development of TTTS, the presence of an AA does not always prevent TAPS to
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transfusion between donor and recipient twins. Nevertheless, in most cases these physiological circumstances are probably not sustained and a net blood flow over the AA anastomosis does ensue, thus protecting against the development of TAPS, or for that matter, TTTS. In contrast with the previously reported case [1], filling of the AA anastomosis with colored dye in the current case occurred easily without increased injection pressure or forced manual compression of the colored dye, suggesting that the AA anastomosis was also patent in utero. Interestingly, the diameter of the AA anastomosis in both cases was very small (<1 mm). We hypothesize that the small size of the AA anastomoses in these 2 cases may have played a role in the development of TAPS by preventing adequate inter-twin blood volume equilibration. In conclusion, we describe a new case of a TAPS with an AA anastomosis, showing that the absence of AA anastomoses is not a conditio sine qua non for the development of TAPS. This case report emphasizes the extreme complexity of the pathophysiological mechanisms responsible for the complications seen in monochorionic twin pregnancies and the work that still needs to be done to understand these mechanisms. References
Fig. 2. On top: details of the small AV anastomoses from donor to the recipient (white stars) and from recipient to the donor (blue stars). Below: details of the aterio-arterial anastomosis (white arrow).
develop. Although AA anastomoses appear to be rare in TAPS, the absence of an AA should not be considered as a diagnostic criterion for TAPS. However, the relatively rare occurrence of AA anastomoses in TAPS does not necessarily contradict the postulated pathophysiology of the underlying mechanism. One could argue that under certain sustained physiological circumstances the net blood flow over the AA anastomosis is nil or minimal, allowing the other AV anastomoses to lead to imbalanced blood
[1] Lopriore E, van den Wijngaard JP, Middeldorp JM, Oepkes D, Walther FJ, van Gemert MJ, et al. Assessment of feto-fetal transfusion flow through placental arterio-venous anastomoses in a unique case of twin-to-twin transfusion syndrome. Placenta 2007;28:209–11. [2] Lopriore E, Middeldorp JM, Oepkes D, Kanhai HH, Walther FJ, Vandenbussche FP. Twin anemia-polycysthemia sequence in two monochorionic twin pairs without oligo-polyhydramnios sequence. Placenta 2007; 28:47–51. [3] Lopriore E, Oepkes D. Fetal and neonatal haematological complications in monochorionic twins. Semin Fetal Neonatal Med 2008;13:231–8. [4] 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. [5] Robyr R, Lewi L, Salomon LJ, Yamamoto M, Bernard JP, Deprest J, et al. Prevalence and management of the late fetal complications following successful selective laser coagulation of chorionic plate anastomoses in twin-to-twin transfusion syndrome. Am J Obstet Gynecol 2006;194:790–5. [6] Lopriore E, Sueters M, Middeldorp JM, Oepkes D, Walther FJ, Vandenbussche FP. Velamentous cord insertion and unequal placental territories in monochorionic twins with and without twin-to-twin transfusion syndrome. Am J Obstet Gynecol 2007;196(2):159. [7] Umur A, van Gemert MJ, Nikkels PG. Monoamniotic versus diamniotic-monochorionic twin placentas: anastomoses and twin-twin transfusion syndrome. Am J Obstet Gynecol 2003;189(5):1325–9. [8] Bajoria R, Wigglesworth J, Fisk NM. Angioarchitecture of monochorionic placentas in relation to the twin-twin transfusion syndrome. Am J Obstet Gynecol 1995;172(3):856–63. [9] Schatz F. Eine besondere Art von einsietiger Polyhydramnie mit andersietiger Oligohydramnie bei eineiige Zwillingen. Arch Gynaecol 1882;19:329–69. [10] Umur A, van Gemert MJ, Nikkels PG, Ross MG. Monochorionic twins and twintwin transfusion syndrome: the protective role of arterio-arterial anastomoses. Placenta 2002;23(2–3):201–9.
Contents lists available at ScienceDirect
Placenta journal homepage: www.elsevier.com/locate/placenta
Case report
Arterio-Arterial Anastomoses do not Prevent the Development of Twin Anemia-Polycythemia Sequence H. van Meir a, *, F. Slaghekke b, E. Lopriore c, W.J. van Wijngaarden a a
Division of Gynecology and Obstetrics, Bronovo Hospital, Bronovolaan 5, 2597 AX Den Haag, The Hague, The Netherlands Division of Gynecology and Obstetrics, Leiden University Medical Center, Leiden, The Netherlands c Division of Neonatology, Leiden University Medical Center, Leiden, The Netherlands b
a r t i c l e i n f o
a b s t r a c t
Article history: Accepted 19 November 2009
Monochorionic twin pregnancies are associated with increased perinatal morbidity and mortality. The vascular placental anastomoses in these pregnancies can cause severe complications. We describe a case of twin anemia-polycythemia sequence (TAPS) with an atypical placental angioarchitecture. During pregnancy serial ultrasound examinations of both twins revealed no amniotic fluid discordance and no abnormal Doppler ultrasound measurements (umbilical cord pulsatility index and middle cerebral artery peak systolic velocity). The twins, born at 33 þ 3 weeks gestation after spontaneous onset of labour, were found to be anemic and polycythemic, respectively. Placental examination with colored dye injection showed, apart from small ateriovenous anastomoses, an arterioarterial anastomosis. As arterio-arterial anastomoses have not been described in cases with spontaneous TAPS to date, it was postulated that such anastomoses carried a protective effect against the development of this complication. Ó 2009 Elsevier Ltd. All rights reserved.
Keywords: Twin anemia-polycythemia sequence Placental angioarchitecture Arterio-arterial anastomosis
1. Introduction Placental vascular anastomoses in monochorionic twin gestations may lead to twin-to-twin transfusion syndrome (TTTS). Recently, a variant of TTTS was described: twin anemia-polycythemia sequence (TAPS) [1–3]. TAPS is characterized by the presence of a large inter-twin difference in haemoglobin level and reticulocyte count without any signs of the oligo-polyhydramios sequence as seen in TTTS. TAPS may occur spontaneously (spontaneous form) or after laser surgery in the treatment of TTTS (postlaser form). The spontaneous form of TAPS occurs in approximately 3%–5% of monochorionic twin pregnancies [3,4], whereas the postlaser form of TAPS may occur in up to 13% of TTTS cases treated with laser [5]. TAPS may be suspected antenatally based on abnormal Doppler ultrasound findings in the absence of amniotic fluid discordance. Abnormal Doppler findings in TAPS consist of an increased middle cerebral artery peak systolic velocity (MCA-PSV) suggesting anemia in one fetus, with a simultaneous decrease in the MCA-PSV in the co-twin suggesting polycythemia [3–5]. Postnatal diagnosis of TAPS
* Corresponding author. Tel.: þ31 70 3124141. E-mail address: [email protected] (H. van Meir). 0143-4004/$ – see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.placenta.2009.11.009
is based on the presence of chronic anemia (with reticulocytosis) in the donor and polycythemia in the recipient twin. The pathophysiological mechanism leading to TAPS is not clear. We recently studied the placental angioarchitecture of a small group (N ¼ 11) of monochorionic placentas with TAPS and compared those with a control group of monochorionic placentas from uncomplicated twin pregnancies [4]. We found that TAPS placentas were characterized by the presence of only few and thin arterio-venous (AV) anastomoses, in the absence of arterio-arterial (AA) anastomoses [4], and speculated on the hypothetical link between this particular angioarchitecture and the development of TAPS. We now describe a spontaneous case of TAPS with an atypical placental angioarchitecture. 2. Case presentation A healthy 30-year-old gravida 3 para 0 was referred to our hospital at 12 weeks’ gestation with a spontaneous monochorionicdiamniotic twin pregnancy. The course of the pregnancy was uneventful and serial fetal ultrasound examinations performed every two weeks showed no signs of a twin oligo-polyhydramios sequence. The umbilical artery pulsatile index (PI) was never abnormal in either twin. Until 30 weeks’ gestation, Doppler measurements of the MCA-PSV showed no abnormalities and both
164
H. van Meir et al. / Placenta 31 (2010) 163–165
twins had a normal growth along their individual percentiles. At 32 þ 5 weeks’ gestation, the last ultrasound examination before delivery (at 33 þ 3 weeks) was performed. Due to deep engagement of the fetal head the MCA-PSV of the first twin could not be measured accurately during the last two weeks before delivery. At 33 þ 3 weeks gestation, preterm uterine contractions started spontaneously and treatment with atosiban and corticosteroids was initiated. There were no signs of a twin oligo-polyhydramios sequence on ultrasound. Analysis of antepartum cardiotocography showed no signs of fetal distress in both fetuses. Spontaneous rupture of the membranes occurred a few hours after admission and was rapidly followed by a normal vaginal delivery of two girls both in cephalic position. The first twin was pale and weighed 1810 g (50th percentile). The second was plethoric and weighed 2355 g (80th percentile). The Apgar scores were 8/9/10 and 8/10/10 respectively and the fetal umbilical cord pH was normal for both girls. The hemoglobin levels at birth were 11.8 g/dL in twin 1 and 22.6 g/dL (normal range 14–20 g/dL) in twin 2. The hematocrit value of the second twin was 67%. The reticulocyte count was 10.6% in twin 1 and 3.8% in twin 2 (normal range: 2–6%). Twin 1 showed no signs of hemodynamic compromise and did not require a red blood cell transfusion. The polycythemic infant had no clinical symptoms associated with hyperviscosity and did not require a partial exchange transfusion. The neonatal hematological differences found at birth (anemia with reticulocytosis in one and polycythemia in the other twin) were diagnostic of chronic intertwin transfusion as seen in TAPS. TTTS was excluded given the absence of twin oligo-polyhydramnios sequence. Acute peripartum transfusion was deemed unlikely as there were no signs of hemorrhagic hypovolemic shock in the donor and the presence of reticulocysis was suggestive of a chronic event. Cranial ultrasound examination of both twins showed no abnormalities and further neonatal course was uneventful. Macroscopic placental examination confirmed a monochorionic-diamniotic placenta. The placental share of the donor and recipient twin was estimated 58% and 42%, respectively (Fig. 1). Colored dye injection of the placental vessels showed 3 small AV anastomoses (diameters from 0.3 to 0.4 mm) from donor to recipient and 2 small AV anastomoses from recipient to donor (diameter 0.3–0.4 mm) (Figs. 1 and 2). A small AA anastomosis (diameter 0.8 mm) was also detected (Figs. 1 and 2). The diameters of the anastomoses and the placental share discordance were measured on the digital picture of the placenta using Image Tool for Windows version 3.0 (Image Tool, San Antonio, TX, USA). Details on the technique used for placental injection and for the measurement of the placental territory and diameter of the vascular anastomoses have been described previously [6].
3. Comment We present a monochorionic-diamniotic twin pregnancy, complicated by a spontaneous form of TAPS with an atypical placental angioarchitecture. Placental injection study showed the atypical presence of an AA anastomosis. AA anastomoses are bi-directional anastomoses and are often referred to as ‘‘superficial’’ anastomoses since they lie on the chorionic plate. Various studies have demonstrated that AA anastomoses occur more frequently in uncomplicated monochorionic placentas than in TTTS placentas, respectively 80% versus 25% [7,8]. AA anastomoses are thus thought to exert a relative protection against the development of TTTS by compensating for the circulatory imbalance caused by the unidirectional AV anastomoses. This protective role of AA anastomoses which was already proposed by
Fig. 1. On top: maternal surface of the placenta showing the placental sharing discordance and the difference in color between the pale placental share of the donor (right side) and the congested placental share of the recipient (left side). Below: Placenta after dye injection (blue or green for arteries and orange for veins). The white arrow indicates the small AA anastomosis. The white stars indicate the small AV anastomoses from donor (right side) to recipient (left side). The blue stars indicate the small AV anastomoses from recipient to donor.
Schartz in the 19th century [9], has recently also been demonstrated in a mathematical computer model of TTTS [10]. In a recent study on the placental angioarchitecture of 11 individual cases of spontaneous TAPS, we found only small AV anastomoses (diameter < 1 mm), and no superficial AA anastomoses [4]. The AV anastomoses in the 11 TAPS cases were from donor to recipient (AV anastomosis) and from recipient to the donor (VA anastomosis). In analogy with the protective role of AA anastomoses against the development of TTTS, we suggested a link between the development of TAPS and the absence of AA anastomoses [4]. We postulated that this particular angioarchitecture would lead to a slow inter-twin blood transfusion, allowing sufficient time for hemodynamic compensatory mechanisms to take place, thus avoiding the development of a twin oligo-polyhydramnios sequence [2]. In a recent report, we described a post-laser case of TAPS in which a residual AA anastomosis was also detected [1]. The current case is the first described case of spontaneous TAPS in the presence of an AA anastomosis. In analogy with the development of TTTS, the presence of an AA does not always prevent TAPS to
H. van Meir et al. / Placenta 31 (2010) 163–165
165
transfusion between donor and recipient twins. Nevertheless, in most cases these physiological circumstances are probably not sustained and a net blood flow over the AA anastomosis does ensue, thus protecting against the development of TAPS, or for that matter, TTTS. In contrast with the previously reported case [1], filling of the AA anastomosis with colored dye in the current case occurred easily without increased injection pressure or forced manual compression of the colored dye, suggesting that the AA anastomosis was also patent in utero. Interestingly, the diameter of the AA anastomosis in both cases was very small (<1 mm). We hypothesize that the small size of the AA anastomoses in these 2 cases may have played a role in the development of TAPS by preventing adequate inter-twin blood volume equilibration. In conclusion, we describe a new case of a TAPS with an AA anastomosis, showing that the absence of AA anastomoses is not a conditio sine qua non for the development of TAPS. This case report emphasizes the extreme complexity of the pathophysiological mechanisms responsible for the complications seen in monochorionic twin pregnancies and the work that still needs to be done to understand these mechanisms. References
Fig. 2. On top: details of the small AV anastomoses from donor to the recipient (white stars) and from recipient to the donor (blue stars). Below: details of the aterio-arterial anastomosis (white arrow).
develop. Although AA anastomoses appear to be rare in TAPS, the absence of an AA should not be considered as a diagnostic criterion for TAPS. However, the relatively rare occurrence of AA anastomoses in TAPS does not necessarily contradict the postulated pathophysiology of the underlying mechanism. One could argue that under certain sustained physiological circumstances the net blood flow over the AA anastomosis is nil or minimal, allowing the other AV anastomoses to lead to imbalanced blood
[1] Lopriore E, van den Wijngaard JP, Middeldorp JM, Oepkes D, Walther FJ, van Gemert MJ, et al. Assessment of feto-fetal transfusion flow through placental arterio-venous anastomoses in a unique case of twin-to-twin transfusion syndrome. Placenta 2007;28:209–11. [2] Lopriore E, Middeldorp JM, Oepkes D, Kanhai HH, Walther FJ, Vandenbussche FP. Twin anemia-polycysthemia sequence in two monochorionic twin pairs without oligo-polyhydramnios sequence. Placenta 2007; 28:47–51. [3] Lopriore E, Oepkes D. Fetal and neonatal haematological complications in monochorionic twins. Semin Fetal Neonatal Med 2008;13:231–8. [4] 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. [5] Robyr R, Lewi L, Salomon LJ, Yamamoto M, Bernard JP, Deprest J, et al. Prevalence and management of the late fetal complications following successful selective laser coagulation of chorionic plate anastomoses in twin-to-twin transfusion syndrome. Am J Obstet Gynecol 2006;194:790–5. [6] Lopriore E, Sueters M, Middeldorp JM, Oepkes D, Walther FJ, Vandenbussche FP. Velamentous cord insertion and unequal placental territories in monochorionic twins with and without twin-to-twin transfusion syndrome. Am J Obstet Gynecol 2007;196(2):159. [7] Umur A, van Gemert MJ, Nikkels PG. Monoamniotic versus diamniotic-monochorionic twin placentas: anastomoses and twin-twin transfusion syndrome. Am J Obstet Gynecol 2003;189(5):1325–9. [8] Bajoria R, Wigglesworth J, Fisk NM. Angioarchitecture of monochorionic placentas in relation to the twin-twin transfusion syndrome. Am J Obstet Gynecol 1995;172(3):856–63. [9] Schatz F. Eine besondere Art von einsietiger Polyhydramnie mit andersietiger Oligohydramnie bei eineiige Zwillingen. Arch Gynaecol 1882;19:329–69. [10] Umur A, van Gemert MJ, Nikkels PG, Ross MG. Monochorionic twins and twintwin transfusion syndrome: the protective role of arterio-arterial anastomoses. Placenta 2002;23(2–3):201–9.