Twins account for about 1% of all pregnancies with two-thirds being dizygotic and one-third monozygotic. All dizygotic pregnancies are dichorionic. In monozygotic pregnancies, splitting of the single embryonic mass into two within 3 days of fertilization, which occurs in one-third of cases, results in dichorionic twins. When embryonic splitting occurs after the 3rd day following fertilization, there are vascular communications within the two placental circulations (monochorionic). Embryonic splitting after the 9th day following fertilization results in monoamniotic monochorionic twins, and splitting after the 12th day results in conjoined twins.

Determination of chorionicity can be performed reliably by ultrasound examination at 11–14 weeks of gestation (Figure 1); in dichorionic twins, there is an extension of placental tissue into the base of the intertwin membrane (lambda sign)^1,2.

Figure 1: Ultrasound appearance of monochorionic (left) and dichorionic (right) twin pregnancies at 12 weeks of gestation. In both types, there appears to be a single placental mass but, in the dichorionic type, there is an extension of placental tissue into the base of the intertwin membrane, forming the lambda sign.

In dichorionic twins, the rate of at least one fetal loss between 10 and 24 weeks is about 2.5%, whereas, in monochorionic twins, the rate of fetal loss is about 12%³. This increased loss in monochorionic pregnancies is likely to be the consequence of severe early-onset twin-to-twin transfusion syndrome.

The perinatal mortality rate in twins is around six times higher than in singletons, and is about three to four times higher in monochorionic compared to dichorionic twins, regardless of zygosity^4,5. This increased mortality is mainly due to prematurityrelated complications. In a singleton pregnancy, the chance of delivery between 24 and 32 weeks is 1–2%. In monochorionic twins, the incidence is about 9% and in dichorionic twins it is about 5%³. In monochorionic twins, an additional complication to prematurity is twin-to-twin transfusion syndrome.

In twin pregnancies, the risk of delivering growth-restricted babies is about ten times higher than in singleton pregnancies⁶. In a study of 467 twin pregnancies, the chance of growth restriction (birth weight below the 5th centile for gestation in singletons) of at least one of the fetuses was 34% for monochorionic and 23% for dichorionic twins³. Furthermore, the chance of growth restriction of both twins was about four times as high in monochorionic (7.5%) compared to dichorionic (1.7%) pregnancies³. In monochorionic twins, a disparity in size between the fetuses may be a consequence of the degree of imbalance in fetal nutrition as a result of chronic twin-to-twin transfusion syndrome. In dichorionic twins, disparity in size may also be due to differences in fetal nutrition, but in this case such differences may be a consequence of discordancy in the effectiveness of trophoblastic invasion of the maternal spiral arteries and therefore placental function.

In monochorionic twin pregnancies, there are placental vascular anastamoses which allow communication of the two fetoplacental circulations⁷. In about 25% of pregnancies, imbalance in the net flow of blood across the placental vascular arteriovenous communications from one fetus, the donor, to the other, the recipient, results in twin-to-twin transfusion syndrome; in about half of these cases, there is severe twin-to-twin transfusion syndrome presenting as acute polyhydramnios in the second trimester. The pathognomonic features of severe twin-to-twin transfusion syndrome by ultrasonographic examination are the presence of a large bladder in the polyuric recipient fetus in the polyhydramniotic sac and ‘absent’ bladder in the anuric donor, that is found to be ‘stuck’ and immobile at the edge of the placenta or the uterine wall, where it is held fixed by the collapsed membranes of the anhydramniotic sac (Figure 2)⁸.

Other sonographic findings that may prove to be of prognostic significance include the presence of a hypertrophic, dilated and dyskinetic heart, with absence or reversal of flow in the ductus venosus during atrial contraction (Figure 3)⁹. In the donor, the heart may be dilated, the bowel is hyperechogenic, and there is absent end-diastolic flow in the umbilical artery; these features are commonly seen in hypoxemic fetuses in pregnancies with severe uteroplacental insufficiency. In severe twin-to-twin transfusion syndrome, survival with expectant management is less than 10%⁸.

Figure 2: Severe twin-to-twin transfusion syndrome at 20 weeks of gestation. In the polyuric recipient, there is a large bladder and polyhydramnios (left) and the anuric donor is held fixed to the placenta by the collapsed membranes of the anhydramniotic sac (right).
Figure 3: Abnormal waveform of the ductus venosus with reversal of flow during atrial contraction in the recipient fetus of a pregnancy with twin-to-twin transfusion syndrome.

The precise underlying mechanisms by which a select population of those monochorionic pregnancies with vascular communications go on to develop twin-to-twin transfusion syndrome is not fully understood. However, it has been hypothesized that primary maldevelopment of the placenta of the donor twin may cause increased peripheral resistance in the placental circulation, which promotes shunting of blood to the recipient; the donor therefore suffers from both hypovolemia due to blood loss and hypoxia due to placental insufficiency⁸. The recipient fetus compensates for its expanded blood volume with polyuria10, but, since protein and cellular components remain in its circulation, the consequent increase in colloid oncotic pressure draws water from the maternal compartment across the placenta. A vicious cycle of hypervolemia, polyuria, hyperosmolality is established, leading to high-output heart failure and polyhydramnios.

These findings are not surprising, since, in the absence of twin-to-twin transfusion syndrome, the underlying pathophysiology for fetal growth restriction due to placental insufficiency in twins is the same as in singleton pregnancies. Giles et al. reported that the histopathological changes in the placentas from twin pregnancies complicated by the presence of abnormal umbilical Doppler results (reduction in the count of small arterial vessels in placental tertiary stem villi restricted to the placenta of the affected fetus) are similar to those found in singleton pregnancies²⁵.

Neilson et al. reported that there were no significant differences between monochorionic and dichorionic pregnancies in either the pattern of umbilical artery flow velocity waveform or intertwin discordance in fetal growth²⁶. It was concluded that, in the absence of severe twin-to-twin transfusion syndrome, the vascular anastomoses that have been shown to be common in monochorionic placentas do not exert a strong influence on fetal growth or fetoplacental blood flow.

Two randomized trials of Doppler ultrasound, which included twin pregnancies, have been reported^27,28. Although the number of twins in these studies was small (16 and 26, and 18 and 22 in the Doppler assessment and control groups, respectively), there was a combined odds ratio of 0.14 (95% confidence interval (CI) 0.03–0.77) for the reduction in fetal death.

Rizzo et al. reported that impedance to flow in the uterine arteries is lower in twin than in singleton pregnancies²⁹. The diagnostic efficacy of impedance in the uterine artery for predicting the development of gestational hypertension and/or preeclampsia was disappointingly low, compared to findings in singleton pregnancies (see Chapter 5).

Hecher et al. examined the role of color Doppler ultrasonography in the identification of the communicating placental vessels in 18 pregnancies with twin-to-twin transfusion syndrome and two with an acardiac twin³⁰. Color Doppler studies of the placental vasculature were performed before fetoscopy for laser coagulation of the communicating vessels. In six cases of twin-to-twin transfusion syndrome, the placental attachment of the intertwin membrane could be visualized, and pulsatile arterial blood flow was observed from the donor to the recipient twin that disappeared after laser therapy. In both cases of acardiac twins, one communicating vessel with pulsatile and another vessel with non-pulsatile blood flow in the opposite direction could be identified. It was suggested that color Doppler imaging is unlikely to play a major role in assisting endoscopic laser separation of chorioangiopagus in patients with acute polyhydramnios, but it may prove to be useful in the early identification of pregnancies at risk of developing twin-to-twin transfusion syndrome.

Denbow et al. examined 45 monochorionic pregnancies for the presence of arterio–arterial anastomoses by color Doppler energy³¹. Arterio–arterial anastomoses were present in 8% (1 of 12) that developed twin-to-twin transfusion syndrome, compared to 71% (20 of 28) of those that did not have twin-to-twin transfusion syndrome. It was concluded that twin-to-twin transfusion syndrome is associated with an absence of functional arterio–arterial anastomoses.

Giles et al. examined 11 pregnancies with twin-to-twin transfusion syndrome (diagnosed retrospectively by the presence of monochorionic placentation and umbilical venous blood hemoglobin differences exceeding 5 g/dl at delivery)³². There was no significant difference in the impedance to flow in the umbilical artery between donor and recipient fetuses. In contrast, Pretorius et al. examined eight cases of twin-to-twin transfusion syndrome and reported significant differences in umbilical arterial impedance to flow between the fetuses in all cases³³. However, Doppler studies could not differentiate donor from recipient or provide prognostic data regarding outcome. Yamada et al. examined 31 twin pregnancies, including six with twin-to-twin transfusion syndrome³⁴. In seven cases, the intertwin difference in umbilical arterial pulsatility index was above 0.5, and, in six of these, there was twin-to-twin transfusion syndrome. Ohno et al. reported that, in five pregnancies with twin-to-twin transfusion syndrome, there was intertwin discordancy in umbilical arterial pulsatility index (PI) greater than 0.5 and, in all cases, the PI in the recipient was above the normal range³⁵. In contrast, in 28 pregnancies without twin-to-twin transfusion syndrome, there were no cases with increased impedance or discordancy greater than 0.5.

Gaziano et al. assessed impedance to flow in the umbilical artery and middle cerebral artery in 33 monochorionic diamniotic twin pregnancies and 50 dichorionic pregnancies³⁶. Monochorionic twins demonstrated a significantly greater probability of blood flow redistribution (increased impedance in the umbilical artery and decreased impedance in the middle cerebral artery) than dichorionic twins of similar low birth weights. It was suggested that placental vascular connections and the attendant hemodynamic changes in the fetuses of monochorionic twins may account for this difference.

Hecher et al. investigated the circulatory profile of the donor and recipient fetuses in pregnancies with twin-to-twin transfusion syndrome manifested by acute polyhydramnios during the second trimester of pregnancy³⁷. Doppler investigations of the umbilical arteries and of the fetal descending thoracic aortas and middle cerebral arteries were performed in both fetuses of 27 pregnancies with twin-to-twin transfusion syndrome at 18–25 weeks of gestation. Significant differences from normal values were increased umbilical artery PI and decreased aortic mean velocity in both donor and recipient fetuses, decreased middle cerebral artery PI in recipients and decreased middle cerebral artery mean velocity in donors. Increased umbilical artery PI in some donor and recipient fetuses may be the consequence of abnormal placental development and polyhydramnios-related compression, respectively. Doppler findings in the fetal circulation are compatible with hypovolemia in the donor and hypervolemia with congestive heart failure in the recipient.

Ishimatsu et al. examined 40 twin pregnancies, including six with twin-to-twin transfusion syndrome, and reported that the syndrome was not associated with any distinctive findings in umbilical artery blood flow velocity waveforms³⁸. However, cardiomegaly in five of the recipient fetuses and tricuspid regurgitation and biphasic umbilical vein waveforms in three recipient fetuses constituted characteristic features of twin-to-twin transfusion syndrome.

Rizzo et al. compared Doppler results in 15 dichorionic twin pregnancies (in which the smaller twin subsequently developed antepartum fetal heart rate late decelerations) and ten pregnancies with twin-to-twin transfusion syndrome³⁹. Doppler recordings were obtained from umbilical artery, descending aorta, and middle cerebral artery, and the PI was measured. Furthermore, peak velocity from cardiac outflow tract and the percentage of reverse flow in the inferior vena cava were calculated. For all these index values, the intertwin differences (delta value) were determined by subtracting the values obtained in the larger twin from those of the smaller twin. In the dichorionic pregnancies, there were significant changes of delta values for all the parameters tested. In particular, delta values of PI from the umbilical artery and descending aorta progressively increased, approaching the occurrence of late decelerations, whereas the delta value for the middle cerebral artery reached a nadir 2 weeks before delivery. Similarly, delta values of peak velocity from outflow tracts significantly decreased, whereas those of the percentage reverse flow in the inferior vena cava increased. In the pregnancies with twin-to-twin transfusion syndrome, there were no significant intertwin differences in PI in any of the vessels that were examined, but there was a significant increase in delta of the peak velocity from the outflow tract and a decrease in the percentage of reverse flow in the inferior vena cava. It was concluded that serial Doppler recordings may show hemodynamic changes in the fetal circulation of discordant twins. Different trends occur according to the underlying pathophysiological mechanisms of the growth defect.

Hecher et al. investigated the circulatory profile of the donor and recipient fetuses in 20 pregnancies with twin-to-twin transfusion syndrome presenting with acute polyhydramnios at 17–27 weeks of gestation⁹. Doppler investigations of the arterial vessels and ductus venosus, inferior vena cava, right hepatic vein, tricuspid and mitral ventricular inflow were performed in both fetuses. Mean values of most blood flow velocities on the venous side showed a significant decrease in both groups of fetuses, and a significant increase in mean values for indices describing waveform pulsatility was found in all three venous vessels in the group of recipients, whereas, in the donor group, this was only the case in the ductus venosus. Mean values of atrioventricular flow velocities showed a significant decrease in the donor group. The most significant findings on the arterial side were an increased mean umbilical artery PI and a decreased mean value for aortic blood flow velocity in both groups of fetuses. Five recipients and four donors had absence or reversal of blood flow during atrial contraction in the ductus venosus. All these fetuses showed pulsations in the umbilical vein (Figure 4). Tricuspid regurgitation was present in eight recipients (Figure 5). Absence or reversal of end-diastolic velocities in the umbilical artery was found in four donors. The circulation of the recipient showed the characteristics of congestive heart failure due to hypovolemia. The significant decrease of diastolic venous blood flow velocities is compatible with increased end-diastolic ventricular pressure. Alterations in the circulation of the donor are consistent with decreased venous return due to hypovolemia and increased cardiac afterload due to increased placental resistance.

Zosmer et al. examined five pregnancies with twin-to-twin transfusion syndrome and reported increased cardiothoracic ratio and tricuspid regurgitation in all recipient twins⁴⁰. High pulmonary artery velocities developed in three. One recipient twin died a week after delivery of endocardial fibroelastosis and infundibular pulmonary stenosis. Two others had balloon dilatation for pulmonary stenosis, one shortly after birth and one at 4 months. A further twin had apical thickening of the right ventricle at 6 months. The remaining recipient twin had normal echocardiographic findings at follow-up.

Figure 4: Pulsations in the umbilical vein with reversal of flow at the end of diastole in the recipient fetus of a pregnancy with twin-to-twin transfusion syndrome

Figure 5: Holosystolic tricuspid regurgitation in the recipient fetus of a pregnancy with twin-to-twin transfusion syndrome

Hecher et al. described the sequence of events in the development and  subsequent spontaneous resolution of functional tricuspid valve atresia in the donor fetus in a case of twin-to-twin transfusion syndrome⁴¹. Fetoscopic laser coagulation of the placental anastomoses was performed at 20 weeks of gestation. Subsequently, there was evidence of increased placental vascular resistance in the donor twin and major impairment of right ventricular function, with no forward flow through the tricuspid valve. During the next 4 weeks, however, there was spontaneous and complete recovery of ventricular function and resolution of the functional tricuspid valve atresia. These findings suggest that alterations in fetal hemodynamics may result in structural cardiac abnormality and may be the precursors of some forms of congenital heart disease.

Lachapelle et al. examined whether index values of cardiac performance could discriminate between the twin-to-twin transfusion syndrome and placental insufficiency as the etiology of the polyhydramnios–oligohydramnios sequence in monochorionic diamniotic twins, by comparing findings in eight cases with placental insufficiency and five with twin-to-twin transfusion syndrome⁴². Intertwin comparisons were made for the following cardiac parameters: cardiothoracic index, end-diastolic thickness of the ventricular walls and septum, aortic and pulmonary artery Doppler peak velocities, ejection and acceleration times, left ventricular shortening fraction, and combined cardiac output and output indexed to fetal weight. All five recipient twins had thickened ventricular walls. The left ventricular shortening fractions and outputs were significantly increased in the donor twin with twin-to-twin transfusion syndrome and normal in placental insufficiency. It was concluded that, in twin-to-twin transfusion syndrome, the donor twin shows evidence of a hyperdynamic cardiac state. Intertwin comparison of cardiac parameters, especially the left ventricular shortening fraction, can be considered a useful tool in diagnosing the different etiologies of the polyhydramnios–oligohydraminos sequence.

Fesslova et al. examined 17 pairs of monochorionic diamniotic twin fetuses with twin-to-twin transfusion syndrome treated by decompressive amniocenteses⁴³. Serial Doppler echocardiographic sudies showed no specific cardiac involvement in the donor twins, either in uteroor after birth. In contrast, all recipient twin fetuses showed variable degrees of biventricular hypertrophy and dilatation with tricuspid regurgitation. These features were evident postnatally but they resolved 1–6 months after birth.

• In twin pregnancies, impedance to flow in the uterine arteries is lower than in singleton pregnancies.

• In twin pregnancies, impedance to flow in the uterine arteries is not as predictive as in singleton pregnancies of the subsequent development of pre-eclampsia.

• In twin pregnancies, increased impedance to flow in the umbilical arteries provides a useful prediction of the subsequent development of fetal growth restriction and adverse perinatal outcome.

• In twin pregnancies with fetal growth restriction due to placental insufficiency, the growth-restricted fetus demonstrates the same circulatory changes as observed in singleton pregnancies with the same complication. Thus, increased impedance to flow in the umbilical artery is usually associated with arterial redistribution in the fetal circulation, demonstrated by decreased PI in the middle cerebral artery and preferential shift of cardiac output in favor of the left ventricle. Deterioration in the fetal condition is associated with a breakdown of hemodynamic compensatory mechanisms, with a decline in cardiac output and the development of abnormal venous flow with increase in pulsatility of ductus venosus waveforms and loss of forward flow velocity during atrial contraction.

• In pregnancies with twin-to-twin transfusion syndrome, placental vascular anastomoses can be identified by Doppler only in a minority of cases. In monochorionic twins with no twin-to-twin transfusion syndrome, the incidence of vascular anastomoses is much higher than in those with the syndrome.

• In pregnancies with severe twin-to-twin transfusion syndrome, there is increased umbilical artery PI in both the donor and recipient fetuses, which may be the consequence of abnormal placental development and polyhydramnios-related compression, respectively.

• In pregnancies with severe twin-to-twin transfusion syndrome, there is decreased middle cerebral artery PI in recipients and decreased middle cerebral artery mean velocity in donors. Additionally, there is decreased blood flow velocity and increased impedance to flow in the ductus venosus of both the donor and recipient fetuses. In donor fetuses, flow velocities across the atrioventricular valves are decreased. In a high proportion of recipient fetuses, there is tricuspid regurgitation.

• In pregnancies with severe twin-to-twin transfusion syndrome, Doppler findings in the fetal circulation of the donor are consistent with decreased venous return due to hypovolemia and increased cardiac afterload due to increased placental resistance. In the recipient, there is evidence of hypervolemia with congestive heart failure; hypervolemia may cause compensatory cardiac hypertrophy, but eventually the pumping capabilities ofthe enlarged heart are exceeded and cardiac failure occurs.

1. Bessis R, Papiernik E. Echographic imagery of amniotic membranes in twin pregnancies. In Gedda L, Parisi P, eds. Twin Research 3: Twin Biology and Multiple Pregnancy. New York: Alan R Liss, 1981:183–7

2. SepulvedaW, Sebire NJ, Hughes K, Odibo A, Nicolaides KH. The lambda sign at 10–14 weeks of gestation as a predictor of chorionicity in twin pregnancies. Ultrasound Obstet Gynecol 1996;7:421–3

3. Sebire NJ, Snijders RJM, Hughes K, Sepulveda W, Nicolaides KH. The hidden mortality of monochorionic twin pregnancies. Br J Obstet Gynaecol 1997;104:1203–7

4. Derom R, Vlietnick R, Derom C, ThieryM, Van Maele G, Van den Berghe H. Perinatal mortality in the East Flanders prospective twin survey. Eur J Obstet Gynecol 1991;41:25–6

5. Machin G, Bamforth F, Innes M, Minichul K. Some perinatal characteristics of monozygotic twins who are dichorionic. Am J Med Genet 1995;55:71–6

6. Luke B, Keith LG. The contribution of singletons, twins and triplets to low birth weight, infant mortality and handicap in the United States. J Reprod Med 1992;37:661–6

7. Benirschke K. Twin placenta in perinatal mortality. N Y St J Med 1961;61:1499–508 8. Saunders NJ, Snijders RJM, Nicolaides KH. Therapeutic amniocentesis in twin–twin transfusion syndrome appearing in the second trimester of pregnancy. Am J Obstet Gynecol 1992;166:820–4

9. Hecher K, Ville Y, Snijders R, Nicolaides KH. Doppler studies of the fetal circulation in twin–twin transfusion syndrome. Ultrasound Obstet Gynecol 1995 5:318–24

10. Rosen D, Rabinowitz R, Beyth Y, Feijgin MD, Nicolaides KH. Fetal urine production in normal twins and in twins with acute polyhydramnios. Fetal Diagn Ther 1990;5:57–60

11. Rodis JF, McIlveen PF, Egan JF, Borgida AF, Turner GW, Campbell WA. Monoamniotic twins: improved perinatal survival with accurate prenatal diagnosis and antenatal fetal surveillance. Am J Obstet Gynecol 1997;177:1046–9

12. Overton TG, Denbow ML, Duncan KR, Fisk NM. First-trimester cord entanglement in monoamniotic twins. Ultrasound Obstet Gynecol 1999;13:140–2

13. Arabin B, Laurini RN, Van Eyck J. Early prenatal diagnosis of cord entanglement in monoamniotic multiple pregnancies. Ultrasound Obstet Gynecol 1999;13:181–6

14. Bajoria R. Abundant vascular anastamoses in monoamniotic versus diamniotic monochorionic placentas. Am J Obstet Gynecol 1998;179:788–93

15. Giles WB, Trudinger BJ, Cook CM. Fetal umbilical artery flow velocity-time waveforms in twin pregnancies. Br J Obstet Gynaecol 1985;92:490–7

16. Farmakides G, Schulman H, Saldana LR, Bracero LA, Fleischer A, Rochelson B. Surveillance of twin pregnancy with umbilical arterial velocimetry. Am J Obstet Gynecol 1985;153:789–92

17. Gerson AG,Wallace DM, Bridgens NK, Ashmead GG,Weiner S, Bolognese RJ. Duplex Doppler ultrasound in the evaluation of growth in twin pregnancies. Obstet Gynecol 1987;70:419–23

18. Nimrod C, Davies D, Harder J, Dempster C, Dodd G, McDicken N, Nicholson S. Doppler ultrasound prediction of fetal outcome in twin pregnancies. Am J Obstet Gynecol 1987;156:402–6

19. DivonMY, Girz BA, Sklar A, Guidetti DA, Langer O. Discordant twins – a prospective study of the diagnostic value of real-time ultrasonography combined with umbilical artery velocimetry. Am J Obstet Gynecol 1989;161:757–60

20. Hastie SJ, Danskin F, Neilson JP, Whittle MJ. Prediction of the small for gestational age twin fetus by Doppler umbilical artery waveform analysis. Obstet Gynecol 1989;74:730–3

21. Gaziano EP, Knox GE, Bendel RP, Calvin S, Brandt D. Is pulsed Doppler velocimetry useful in the management of multiple-gestation pregnancies? Am J Obstet Gynecol 1991;164:1426–33

22. Degani S, Gonen R, Shapiro I, Paltiely Y, Sharf M. Doppler flow velocity waveforms in fetal surveillance of twins: a prospective longitudinal study. J Ultrasound Med 1992;11:537–41

23. Kurmanavicius J, Hebisch G, Huch R, Huch A. Umbilical artery blood flow velocity waveforms in twin pregnancies. J Perinat Med 1992;20:307–12

24. Jensen OH. Doppler velocimetry in twin pregnancy. Eur J Obstet Gynecol Reprod Biol 1992;45:9–12 25. GilesW, Trudinger B, Cook C, Connelly A. Placental microvascular changes in twin pregnancies with abnormal umbilical artery waveforms. Obstet Gynecol 1993;81:556–9

26. Neilson JP, Danskin F, Hastie SJ. Monozygotic twin pregnancy: diagnostic and Doppler ultrasound studies. Br J Obstet Gynaecol 1989;96:1413–18

27. Omtzigt AWJ. Clinical value of umbilical Doppler velocimetry; randomized controlled trial. Doctoral thesis, University of Utrecht, 1990

28. Johnstone FD, Prescott R, Hoskins, Greer IA, McGlew T, Compton M. The effect of introduction of umbilical Doppler recordings to obstetric practice. Br J Obstet Gynaecol 1993;100:733–41

29. Rizzo G, Arduini D, Romanini C. Uterine artery Doppler velocity waveforms in twin pregnancies. Obstet Gynecol 1993;82:978–83

30. Hecher K, VilleY, Nicolaides KH. Color Doppler ultrasonography in the identification of communicating vessels in twin–twin transfusion syndrome and acardiac twins. J Ultrasound Med 1995;14: 37–40

31. Denbow ML, Cox P, Talbert D, Fisk NM. Colour Doppler energy insonation of placental vasculature in monochorionic twins: absent arterio–arterial anastomoses in association with twin-to-twin transfusion syndrome. Br J Obstet Gynaecol 1998;105:760–5

32. Giles WB, Trudinger BJ, Cook CM, Connelly AJ. Doppler umbilical artery studies in the twin–twin transfusion syndrome. Obstet Gynecol 1990;76:1097–9

33. Pretorius DH, Manchester D, Barkin S, Parker S, Nelson TR. Doppler ultrasound of twin transfusion syndrome. J Ultrasound Med 1988;7:117–24

34. Yamada A, Kasugai M, Ohno Y, Ishizuka T, Mizutani S, Tomoda Y. Antenatal diagnosis of twin–twin transfusion syndrome by Doppler ultrasound. Obstet Gynecol 1991;78:1058–61

35. Ohno Y, Ando H, Tanamura A, Kurauchi O, Mizutani S, Tomoda Y. The value of Doppler ultrasound in the diagnosis and management of twin-to-twin transfusion syndrome. Arch Gynecol Obstet 1994;255:37–42

36. Gaziano E, Gaziano C, Brandt D. Doppler velocimetry determined redistribution of fetal blood flow: correlation with growth restriction in diamniotic monochorionic and dizygotic twins. Am J Obstet Gynecol 1998;178:1359–67

37. Hecher K, Ville Y, Nicolaides KH. Fetal arterial Doppler studies in twin–twin transfusion syndrome. J Ultrasound Med 1995;14:101–8

38. Ishimatsu J, Yoshimura O, Manabe A, Matsuzaki T, Tanabe R, Hamada T. Ultrasonography and Doppler studies in twin-to-twin transfusion syndrome. Asia Oceania J Obstet Gynaecol 1992;18: 325–31

39. Rizzo G, Arduini D, Romanini C. Cardiac and extracardiac flows in discordant twins. Am J Obstet Gynecol 1994;170:1321–7

40. Zosmer N, Bajoria R,Weiner E, Rigby M, Vaughan J, Fisk NM. Clinical and echographic features of in utero cardiac dysfunction in the recipient twin in twin–twin transfusion syndrome. Br Heart J 1994;72:74–9

41. Hecher K, Sullivan ID, Nicolaides KH. Temporary iatrogenic fetal tricuspid valve atresia in a case of twin to twin transfusion syndrome. Br Heart J 1994;72:457–60

42. Lachapelle MF, Leduc L, Cote JM, Grignon A, Fouron JC. Potential value of fetal echocardiography in the differential diagnosis of twin pregnancy with presence of polyhydramnios– oligohydramnios syndrome. Am J Obstet Gynecol 1997;177:388–94

43. Fesslova V, Villa L, Nava S, Mosca F, Nicolini U. Fetal and neonatal echocardiographic findings in twin–twin transfusion syndrome. Am J Obstet Gynecol 1998;179:1056–62