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Significance of Donor Anuria Differs between Monoamniotic and Diamniotic Twin–Twin Transfusion Syndrome
Placenta 28 (2007) 523e526
Significance of Donor Anuria Differs between Monoamniotic and Diamniotic TwineTwin Transfusion Syndrome A.H.P. Schaap a,*, J.P.H.M. van den Wijngaard a,b, P.G.J. Nikkels e, A.J.M. van den Broek c, I. Snieders d, M.J.C. van Gemert a,b a
Department of Obstetrics and Gynecology, Academic Medical Centre, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands b Laser Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands c Department of Neonatology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands d Department of Pathology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands e Department of Pathology, University Medical Centre, Utrecht, The Netherlands Accepted 11 September 2006
Abstract Development of severe twinetwin transfusion syndrome (TTTS) in diamnioticemonochorionic twins includes five stages of increasing severity, i.e. recipient polyhydramnios and donor oligohydramnios, donor anuria, abnormal umbilical flow velocities in either twin, hydrops in the recipient, and intrauterine fetal death (IUFD) in either or both twins. In a severe case of TTTS in monoamniotic twins we observed donor anuria to appear after hydrops in the recipient. We conclude that donor anuria is a late and serious symptom in monoamniotic TTTS. Ó 2006 Elsevier Ltd. All rights reserved. Keywords: Monoamniotic twin pregnancy; Twinetwin transfusion syndrome; Amnioreduction; Vascular anastomosis
1. Introduction
2. Case Report
Proven TTTS in monoamniotic twin pregnancy has rarely been reported [1e3]. Several reasons may account for this. First, monoamniotic TTTS has an exceedingly low incidence [2,4]. Second, diagnosis of a stuck donor twin, essential in diamnioticemonochorionic TTTS, obviously is inapplicable in monoamniotic twins. We report a case of monoamniotic TTTS and present evidence that donor anuria in monoamniotic TTTS implies a more severe level of the circulatory imbalance than in diamniotic TTTS.
2.1. Clinical history
* Corresponding author. Tel.: þ31 20 566 9111; fax: þ31 20 696 3489. E-mail address: [email protected] (A.H.P. Schaap). 0143-4004/$ - see front matter Ó 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.placenta.2006.09.003
2.1.1. Obstetrics A 29-year-old nulliparous Caucasian woman reported at 9 weeks gestational age for antenatal care. Ultrasound examination identified a single placental mass, no intertwin membrane, similar distribution of amniotic fluid around both fetuses and free movements of both. Starting at 14 weeks, we examined every two weeks: structural anatomy, biometry to verify the growth of the fetuses, amniotic fluid volume and bladder filling, trunk, limb and thoracic movements, and umbilical artery Doppler. Once signs of TTTS became apparent, the examination frequency increased, starting with twice a week and becoming daily at the end of the pregnancy. Diagnosis of TTTS was based on three criteria (Fig. 1). First, polyhydramnios, defined as the maximal vertical pocket of >8 cm, which increased from 12 cm at 20 weeks to 14.5 cm
A.H.P. Schaap et al. / Placenta 28 (2007) 523e526
524
Deepest Pool [cm]
20 Hydrops
Polyhydramnios
Anuria
15
10
5
Delivery
0 18
20
22
24
26
28
Gestation [weeks] Fig. 1. Deepest pools of amniotic fluid. Onset of polyhydramnios, recipient hydrops and donor anuria, all continuing until the end of pregnancy, are indicated by arrows (top of picture). The gestational ages of amnioreduction are indicated by crosses on the horizontal axis. The removed volumes of amniotic fluid were 2.5, 1.5, 2.0, 1.0 and 1.5 litres, respectively. When coinciding with amnioreduction, the deepest pool was measured prior to the intervention.
at 25 weeks and subsequently decreased to 8.8 cm at 27 weeks. Second, recipient hydrops, which developed at 24 weeks and continued with increasing severity until the end of pregnancy. Third, cessation of donor bladder filling, which was observed at 26 weeks, also continuing until the end of pregnancy. In addition, in the recipient, Doppler flow velocities in the umbilical artery were pathological from 22 weeks until the end of the pregnancy. In the donor, pathological flows in the umbilical artery and fetal redistribution were observed from 26 weeks until the end of the pregnancy. There were no signs of umbilical cord knotting. Five amnioreductions were performed with 1.0e2.5 litres of removed amniotic fluid each time (Fig. 1). In view of the severely hydropic recipient, corticosteroids were administered at 27 3/7 weeks to promote lung maturation, and a Caesarean Section was performed at 27 5/7 weeks because of an abnormal fetal heart rate recording in the donor twin. Two girls were born. The hydropic infant weighed 1580 g, the donor 520 g. Their Apgar scores after 5 min were 3 and 9, respectively.
Fig. 2. (A) Overview of the dye injected placenta. Donor chorionic arteries are blue and veins yellow. Recipient chorionic arteries are purple and veins orange. The ‘‘bridge’’ vessel, i.e., a vein but acting as a pseudo-arterioarterial connection is red (white arrow) and crosses over the chorionic artery (asterisk). The main arteriovenous anastomosis is indicated by the white triangle (right upper corner), the opposite arteriovenous anastomosis by the black triangle. (B) Detail of (A), including the connection of the non-dye-filled bridge vessel (white arrow) to the recipient chorionic artery (black arrow). The connection of the opposite arteriovenous anastomosis with the recipient chorionic artery is indicated by the black arrowhead.
2.1.2. Neonatology Recipient haemoglobin was 9.4 mmol/l (15.1 g/dl). Echocardiography showed hypertrophic cardiomyopathy. On the second day she developed acute hypovolaemic shock with an anuric period of 2 days, followed by several days of polyuria. After stabilization she weighed 1000 g. Coagulation disturbances consistent with diffuse intravascular coagulation were corrected. Ultrasound scans of the brain showed no abnormalities. On day 19 she developed a massive necrotizing enterocolitis with bowel perforation, causing her demise. Donor haemoglobin was 5.6 mmol/l (9.0 g/dl). She had temporary renal failure. She received several blood transfusions for anaemia. At a post-conceptional age of 42 weeks she was discharged home. At a corrected age of 1 year she weighed 6900 g and showed no neurodevelopmental abnormalities.
perforations, accompanied by free air in the abdomen. The posterior bladder wall showed extensive necrosis of the mucosa and muscularis mucosae, a well known albeit uncommon complication of necrotizing enterocolitis [5]. The heart demonstrated cardiac hypertrophy (weight 22.8 g, versus 9 g normal weight at 31 weeks). Lungs, liver and kidneys had an increased weight compared to normal. These observations confirm the history of long-standing intrauterine cardiac overfilling in this infant.
2.1.3. Pathological findings The autopsy of the recipient revealed no congenital anomalies. The small intestine showed extensive necrosis with
2.1.4. Placental findings The placenta was monochorionic, monoamniotic. Umbilical cords were centrally inserted, 5 cm apart, and knotting
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525
Fig. 3. (A) The villi from the recipient part of the placenta are small and much smaller than usually seen at this gestational age of 28 weeks. (B) The villi from the donor are large and larger than usually seen at 28 weeks, and show minor hydropic changes (open arrows). (C) In the recipient part of the placenta the accelerated maturation can also be observed by the premature formation of syncytio-vascular membranes (open arrowheads). Small groups of avascular fibrotic villi (arrowheads) could be found, indicative of previous fetal vascular thrombosis. (D) In the donor part of the placenta nucleated red blood cells (arrow) could be found easily, in concordance with anaemia due to blood loss and increased haematopoietic activity.
was absent. Placental weight was 830 g, with a 0.45:0.55 donor/recipient sharing. The donor cord had a diameter of maximally 6 mm and the recipient cord 20 mm diameter; both had three vessels. The placental angioarchitecture was studied by standard umbilical dye injection and revealed a large arteriovenous anastomosis from donor to recipient (Fig. 2A, white triangle), a smaller opposite arteriovenous anastomosis and a third, unusual anastomosis (Fig. 2A,B, white arrow), connecting two chorionic arteries of both twins by two cotyledons, one for each artery, and a ‘‘bridge’’ vessel that could not be filled with dye because it was deprived of venous drainage [6]. Histology of the placental parenchyma showed small recipient villi of accelerated maturation (Fig. 3A,C) and large immature donor villi (Fig. 3B). 2.2. Simulations by the TTTS model We used our computer model for TTTS [7], with the same anastomotic pattern as found in this case, and included the five amnioreductions. In concordance with the clinical findings, recipient hydrops developed earlier than donor anuria. 3. Discussion Our case presents the typical prenatal clinical criteria for severe diamnioticemonochorionic TTTS (polyhydramnios,
lack of donor bladder filling, and recipient polyuria and hydrops). In addition, the old neonatal criteria for TTTS are valid here, i.e. birth weight difference of >20% (here 67%), and >5 g/dl haemoglobin concentration difference (here 6.1 g/dl), which supports our previous hypothesis that these criteria are likely valid in the current anastomotic pattern [8]. Further, it shows the typical postnatal placental histological criteria of TTTS, i.e. large immature donor villi due to anaemia and low colloid osmotic pressure (COP), and small recipient villi of accelerated maturation due to polycythaemia and high COP. In addition, our computer model simulated that donor anuria is a late phenomenon in severe monoamniotic TTTS. When amnioreductions were included, the model correctly simulated the sequence of clinical events. The underlying mechanism is that amnioreduction acutely normalizes the excess amniotic fluid hydrostatic pressure. This causes an acutely increasing maternofetal (transplacental) fluid flow to both twins, which increases their arterial pressures. In addition, monoamniotic donor twins continue to swallow, which positively affects donor arterial pressure. Thus, both these mechanisms increase the donor’s arterial pressure which delays onset of donor anuria. In the recipient, the amnioreductions only slightly affect the moment of onset of hydrops. As a result, our model predicts that recipient hydrops precedes donor anuria in cases of multiple amnioreductions. Nevertheless, if arteriovenous fetofetal transfusion is so large
526
A.H.P. Schaap et al. / Placenta 28 (2007) 523e526
that the donor’s arterial pressure decreases toward levels that are incompatible with urine production, amnioreductions have to be performed more and more frequently and with shorter and shorter time intervals. When urine production finally ceases completely, even following a maternofetal fluid flow in response to amnioreduction, subsequent amnioreductions fail to resolve donor urine production. In our simulations this happened after the fifth amnioreduction (not shown). In a multicentre retrospective cohort analysis of 11 centres over a 10-year period [2] only three TTTS cases were observed. This 3% monoamniotic TTTS incidence, combined with assuming that monochorionic twins constitute 0.3% of pregnancies and monoamnionicity 3% of monochorionicity, results in an estimated monoamniotic TTTS incidence of one per 370,000 pregnancies. This exceedingly low incidence implies that obstetricians, even when frequently involved in TTTS management, will rarely encounter this event. Therefore, careful future documentation and reporting of monoamniotic TTTS cases is called for. In conclusion, amnioreduction in monoamniotic TTTS can be an effective therapy for the donor twin (delayed onset of anuria). However, if donor anuria occurs the obstetrician should be alarmed because this indicates, both clinically and from modeling, a late and severe form of monoamniotic TTTS.
Acknowledgement J.P.H.M.v.d.W. is supported in part by the European Community Eurofoetus programme. References [1] Suzuki S, Kaneko K, Shin S, Araki T. Incidence of intrauterine complications in monoamniotic twin gestation. Arch Gynecol Obstet 2001;265:57e9. [2] Heyborne KD, Porreco RP, Garite TJ, Phair K, Abril D. Improved perinatal survival of monoamniotic twins with intensive inpatient monitoring. Am J Obstet Gynecol 2005;192:96e101. [3] Gallot D, Saulnier J-P, Savary D, Laurichesse-Delmas H, Lemery D. Ultrasonographic signs of twin-twin transfusion syndrome in a monoamniotic twin pregnancy. Ultrasound Obstet Gynecol 2005;25:307e11. [4] Umur A, van Gemert MJC, Nikkels PGJ. Monoamniotic versus diamniotic-monochorionic twin placentas: anastomoses and twin-twin transfusion syndrome. Am J Obstet Gynecol 2003;189:1325e9. [5] Morrison SC. Pneumatosis of the bladder wall associated with necrotizing enterocolitis. J Clin Ultrasound 2000;28:497e9. [6] van Gemert MJC, van den Wijngaard JPHM, de Vries HR, Nikkels PGJ. Invited Comment on the paper by M.J.O. Taylor, D. Talbert and N.M. Fisk. Pseudo-arterio-arterial anastomoses in twin-twin transfusion syndrome. Placenta 25, 742-747, 2004. Placenta 2004;25:748e51. [7] van den Wijngaard JPHM, Umur A, Krediet RT, Ross MG, van Gemert MJC. Modeling a hydropic recipient twin in twinetwin transfusion syndrome. Am J Physiol Regul Integr Comp Physiol 2005;288:R799e814. [8] Nikkels PGJ, van Gemert MJC, Sollie-Szarynska KM, Molendijk H, Timmer B, Machin GA. Rapid onset of severe twinetwin transfusion syndrome caused by placental venous thrombosis. Pediatr Dev Pathol 2002;5:310e4.
Significance of Donor Anuria Differs between Monoamniotic and Diamniotic TwineTwin Transfusion Syndrome A.H.P. Schaap a,*, J.P.H.M. van den Wijngaard a,b, P.G.J. Nikkels e, A.J.M. van den Broek c, I. Snieders d, M.J.C. van Gemert a,b a
Department of Obstetrics and Gynecology, Academic Medical Centre, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands b Laser Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands c Department of Neonatology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands d Department of Pathology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands e Department of Pathology, University Medical Centre, Utrecht, The Netherlands Accepted 11 September 2006
Abstract Development of severe twinetwin transfusion syndrome (TTTS) in diamnioticemonochorionic twins includes five stages of increasing severity, i.e. recipient polyhydramnios and donor oligohydramnios, donor anuria, abnormal umbilical flow velocities in either twin, hydrops in the recipient, and intrauterine fetal death (IUFD) in either or both twins. In a severe case of TTTS in monoamniotic twins we observed donor anuria to appear after hydrops in the recipient. We conclude that donor anuria is a late and serious symptom in monoamniotic TTTS. Ó 2006 Elsevier Ltd. All rights reserved. Keywords: Monoamniotic twin pregnancy; Twinetwin transfusion syndrome; Amnioreduction; Vascular anastomosis
1. Introduction
2. Case Report
Proven TTTS in monoamniotic twin pregnancy has rarely been reported [1e3]. Several reasons may account for this. First, monoamniotic TTTS has an exceedingly low incidence [2,4]. Second, diagnosis of a stuck donor twin, essential in diamnioticemonochorionic TTTS, obviously is inapplicable in monoamniotic twins. We report a case of monoamniotic TTTS and present evidence that donor anuria in monoamniotic TTTS implies a more severe level of the circulatory imbalance than in diamniotic TTTS.
2.1. Clinical history
* Corresponding author. Tel.: þ31 20 566 9111; fax: þ31 20 696 3489. E-mail address: [email protected] (A.H.P. Schaap). 0143-4004/$ - see front matter Ó 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.placenta.2006.09.003
2.1.1. Obstetrics A 29-year-old nulliparous Caucasian woman reported at 9 weeks gestational age for antenatal care. Ultrasound examination identified a single placental mass, no intertwin membrane, similar distribution of amniotic fluid around both fetuses and free movements of both. Starting at 14 weeks, we examined every two weeks: structural anatomy, biometry to verify the growth of the fetuses, amniotic fluid volume and bladder filling, trunk, limb and thoracic movements, and umbilical artery Doppler. Once signs of TTTS became apparent, the examination frequency increased, starting with twice a week and becoming daily at the end of the pregnancy. Diagnosis of TTTS was based on three criteria (Fig. 1). First, polyhydramnios, defined as the maximal vertical pocket of >8 cm, which increased from 12 cm at 20 weeks to 14.5 cm
A.H.P. Schaap et al. / Placenta 28 (2007) 523e526
524
Deepest Pool [cm]
20 Hydrops
Polyhydramnios
Anuria
15
10
5
Delivery
0 18
20
22
24
26
28
Gestation [weeks] Fig. 1. Deepest pools of amniotic fluid. Onset of polyhydramnios, recipient hydrops and donor anuria, all continuing until the end of pregnancy, are indicated by arrows (top of picture). The gestational ages of amnioreduction are indicated by crosses on the horizontal axis. The removed volumes of amniotic fluid were 2.5, 1.5, 2.0, 1.0 and 1.5 litres, respectively. When coinciding with amnioreduction, the deepest pool was measured prior to the intervention.
at 25 weeks and subsequently decreased to 8.8 cm at 27 weeks. Second, recipient hydrops, which developed at 24 weeks and continued with increasing severity until the end of pregnancy. Third, cessation of donor bladder filling, which was observed at 26 weeks, also continuing until the end of pregnancy. In addition, in the recipient, Doppler flow velocities in the umbilical artery were pathological from 22 weeks until the end of the pregnancy. In the donor, pathological flows in the umbilical artery and fetal redistribution were observed from 26 weeks until the end of the pregnancy. There were no signs of umbilical cord knotting. Five amnioreductions were performed with 1.0e2.5 litres of removed amniotic fluid each time (Fig. 1). In view of the severely hydropic recipient, corticosteroids were administered at 27 3/7 weeks to promote lung maturation, and a Caesarean Section was performed at 27 5/7 weeks because of an abnormal fetal heart rate recording in the donor twin. Two girls were born. The hydropic infant weighed 1580 g, the donor 520 g. Their Apgar scores after 5 min were 3 and 9, respectively.
Fig. 2. (A) Overview of the dye injected placenta. Donor chorionic arteries are blue and veins yellow. Recipient chorionic arteries are purple and veins orange. The ‘‘bridge’’ vessel, i.e., a vein but acting as a pseudo-arterioarterial connection is red (white arrow) and crosses over the chorionic artery (asterisk). The main arteriovenous anastomosis is indicated by the white triangle (right upper corner), the opposite arteriovenous anastomosis by the black triangle. (B) Detail of (A), including the connection of the non-dye-filled bridge vessel (white arrow) to the recipient chorionic artery (black arrow). The connection of the opposite arteriovenous anastomosis with the recipient chorionic artery is indicated by the black arrowhead.
2.1.2. Neonatology Recipient haemoglobin was 9.4 mmol/l (15.1 g/dl). Echocardiography showed hypertrophic cardiomyopathy. On the second day she developed acute hypovolaemic shock with an anuric period of 2 days, followed by several days of polyuria. After stabilization she weighed 1000 g. Coagulation disturbances consistent with diffuse intravascular coagulation were corrected. Ultrasound scans of the brain showed no abnormalities. On day 19 she developed a massive necrotizing enterocolitis with bowel perforation, causing her demise. Donor haemoglobin was 5.6 mmol/l (9.0 g/dl). She had temporary renal failure. She received several blood transfusions for anaemia. At a post-conceptional age of 42 weeks she was discharged home. At a corrected age of 1 year she weighed 6900 g and showed no neurodevelopmental abnormalities.
perforations, accompanied by free air in the abdomen. The posterior bladder wall showed extensive necrosis of the mucosa and muscularis mucosae, a well known albeit uncommon complication of necrotizing enterocolitis [5]. The heart demonstrated cardiac hypertrophy (weight 22.8 g, versus 9 g normal weight at 31 weeks). Lungs, liver and kidneys had an increased weight compared to normal. These observations confirm the history of long-standing intrauterine cardiac overfilling in this infant.
2.1.3. Pathological findings The autopsy of the recipient revealed no congenital anomalies. The small intestine showed extensive necrosis with
2.1.4. Placental findings The placenta was monochorionic, monoamniotic. Umbilical cords were centrally inserted, 5 cm apart, and knotting
A.H.P. Schaap et al. / Placenta 28 (2007) 523e526
525
Fig. 3. (A) The villi from the recipient part of the placenta are small and much smaller than usually seen at this gestational age of 28 weeks. (B) The villi from the donor are large and larger than usually seen at 28 weeks, and show minor hydropic changes (open arrows). (C) In the recipient part of the placenta the accelerated maturation can also be observed by the premature formation of syncytio-vascular membranes (open arrowheads). Small groups of avascular fibrotic villi (arrowheads) could be found, indicative of previous fetal vascular thrombosis. (D) In the donor part of the placenta nucleated red blood cells (arrow) could be found easily, in concordance with anaemia due to blood loss and increased haematopoietic activity.
was absent. Placental weight was 830 g, with a 0.45:0.55 donor/recipient sharing. The donor cord had a diameter of maximally 6 mm and the recipient cord 20 mm diameter; both had three vessels. The placental angioarchitecture was studied by standard umbilical dye injection and revealed a large arteriovenous anastomosis from donor to recipient (Fig. 2A, white triangle), a smaller opposite arteriovenous anastomosis and a third, unusual anastomosis (Fig. 2A,B, white arrow), connecting two chorionic arteries of both twins by two cotyledons, one for each artery, and a ‘‘bridge’’ vessel that could not be filled with dye because it was deprived of venous drainage [6]. Histology of the placental parenchyma showed small recipient villi of accelerated maturation (Fig. 3A,C) and large immature donor villi (Fig. 3B). 2.2. Simulations by the TTTS model We used our computer model for TTTS [7], with the same anastomotic pattern as found in this case, and included the five amnioreductions. In concordance with the clinical findings, recipient hydrops developed earlier than donor anuria. 3. Discussion Our case presents the typical prenatal clinical criteria for severe diamnioticemonochorionic TTTS (polyhydramnios,
lack of donor bladder filling, and recipient polyuria and hydrops). In addition, the old neonatal criteria for TTTS are valid here, i.e. birth weight difference of >20% (here 67%), and >5 g/dl haemoglobin concentration difference (here 6.1 g/dl), which supports our previous hypothesis that these criteria are likely valid in the current anastomotic pattern [8]. Further, it shows the typical postnatal placental histological criteria of TTTS, i.e. large immature donor villi due to anaemia and low colloid osmotic pressure (COP), and small recipient villi of accelerated maturation due to polycythaemia and high COP. In addition, our computer model simulated that donor anuria is a late phenomenon in severe monoamniotic TTTS. When amnioreductions were included, the model correctly simulated the sequence of clinical events. The underlying mechanism is that amnioreduction acutely normalizes the excess amniotic fluid hydrostatic pressure. This causes an acutely increasing maternofetal (transplacental) fluid flow to both twins, which increases their arterial pressures. In addition, monoamniotic donor twins continue to swallow, which positively affects donor arterial pressure. Thus, both these mechanisms increase the donor’s arterial pressure which delays onset of donor anuria. In the recipient, the amnioreductions only slightly affect the moment of onset of hydrops. As a result, our model predicts that recipient hydrops precedes donor anuria in cases of multiple amnioreductions. Nevertheless, if arteriovenous fetofetal transfusion is so large
526
A.H.P. Schaap et al. / Placenta 28 (2007) 523e526
that the donor’s arterial pressure decreases toward levels that are incompatible with urine production, amnioreductions have to be performed more and more frequently and with shorter and shorter time intervals. When urine production finally ceases completely, even following a maternofetal fluid flow in response to amnioreduction, subsequent amnioreductions fail to resolve donor urine production. In our simulations this happened after the fifth amnioreduction (not shown). In a multicentre retrospective cohort analysis of 11 centres over a 10-year period [2] only three TTTS cases were observed. This 3% monoamniotic TTTS incidence, combined with assuming that monochorionic twins constitute 0.3% of pregnancies and monoamnionicity 3% of monochorionicity, results in an estimated monoamniotic TTTS incidence of one per 370,000 pregnancies. This exceedingly low incidence implies that obstetricians, even when frequently involved in TTTS management, will rarely encounter this event. Therefore, careful future documentation and reporting of monoamniotic TTTS cases is called for. In conclusion, amnioreduction in monoamniotic TTTS can be an effective therapy for the donor twin (delayed onset of anuria). However, if donor anuria occurs the obstetrician should be alarmed because this indicates, both clinically and from modeling, a late and severe form of monoamniotic TTTS.
Acknowledgement J.P.H.M.v.d.W. is supported in part by the European Community Eurofoetus programme. References [1] Suzuki S, Kaneko K, Shin S, Araki T. Incidence of intrauterine complications in monoamniotic twin gestation. Arch Gynecol Obstet 2001;265:57e9. [2] Heyborne KD, Porreco RP, Garite TJ, Phair K, Abril D. Improved perinatal survival of monoamniotic twins with intensive inpatient monitoring. Am J Obstet Gynecol 2005;192:96e101. [3] Gallot D, Saulnier J-P, Savary D, Laurichesse-Delmas H, Lemery D. Ultrasonographic signs of twin-twin transfusion syndrome in a monoamniotic twin pregnancy. Ultrasound Obstet Gynecol 2005;25:307e11. [4] Umur A, van Gemert MJC, Nikkels PGJ. Monoamniotic versus diamniotic-monochorionic twin placentas: anastomoses and twin-twin transfusion syndrome. Am J Obstet Gynecol 2003;189:1325e9. [5] Morrison SC. Pneumatosis of the bladder wall associated with necrotizing enterocolitis. J Clin Ultrasound 2000;28:497e9. [6] van Gemert MJC, van den Wijngaard JPHM, de Vries HR, Nikkels PGJ. Invited Comment on the paper by M.J.O. Taylor, D. Talbert and N.M. Fisk. Pseudo-arterio-arterial anastomoses in twin-twin transfusion syndrome. Placenta 25, 742-747, 2004. Placenta 2004;25:748e51. [7] van den Wijngaard JPHM, Umur A, Krediet RT, Ross MG, van Gemert MJC. Modeling a hydropic recipient twin in twinetwin transfusion syndrome. Am J Physiol Regul Integr Comp Physiol 2005;288:R799e814. [8] Nikkels PGJ, van Gemert MJC, Sollie-Szarynska KM, Molendijk H, Timmer B, Machin GA. Rapid onset of severe twinetwin transfusion syndrome caused by placental venous thrombosis. Pediatr Dev Pathol 2002;5:310e4.