Placental angioarchitecture in monochorionic twin pregnancies: relationship to fetal growth, fetofetal transfusion syndrome, and pregnancy outcome.

OBJECTIVE We sought to correlate placental vasculature with fetal growth and outcome in monochorionic twins. STUDY DESIGN Eighty-two patients with consecutive monochorionic pregnancies underwent biweekly ultrasonography for determination of fetal growth and well-being. After delivery, blinded placental injection studies delineated vascular anastomoses and territory share. Degree of balance in arteriovenous anastomoses equaled the number of arteriovenous anastomoses in one direction minus the number in the other. RESULTS Pregnancies affected by fetofetal transfusion syndrome (n = 21) had numbers of arteriovenous and venovenous anastomoses that were similar to those in pregnancies without fetofetal transfusion syndrome but fewer arterioarterial anastomoses (P <.0001). Fetofetal transfusion syndrome occurred in 78% of pregnancies with >/=1 arteriovenous and no arterioarterial anastomoses. Birth weight discordancy correlated with placental territory discordancy (P <.0001) and the degree of balance in arteriovenous anastomoses (P =.004). The larger placental share twin had a greater growth velocity than its smaller placental share co-twin (P =.008) for all but one anastomotic pattern. Where arteriovenous anastomoses were aligned with the net venous outflow to the fetus with the smaller territory, co-twins had similar birth weights and growth velocities irrespective of placental share. Fetal survival was higher in pregnancies with an arterioarterial anastomosis (P =.01) but lower with a venovenous anastomosis (P =. 01). Survival of both fetuses was inversely associated with birth weight discordancy (P <.0001). CONCLUSION Although interrelationships among the various types of anastomoses are complex, our data suggest that the placental territory share and the pattern of arteriovenous anastomoses influence fetal growth, that arterioarterial anastomoses protect against fetofetal transfusion syndrome, and that venovenous anastomoses reduce perinatal survival.

[1]  T J Cole,et al.  Cross sectional stature and weight reference curves for the UK, 1990. , 1995, Archives of disease in childhood.

[2]  N. Fisk,et al.  Angioarchitecture of monochorionic placentas in relation to the twin-twin transfusion syndrome. , 1995, American journal of obstetrics and gynecology.

[3]  N. Fisk,et al.  Selective termination by intrahepatic vein alcohol injection of a monochorionic twin pregnancy discordant for fetal abnormality , 1997, British journal of obstetrics and gynaecology.

[4]  N. Fisk,et al.  High failure rate of umbilical vessel occlusion by ultrasound‐guided injection of absolute alcohol or enbucrilate gel , 1999, Prenatal diagnosis.

[5]  N. Fisk,et al.  Colour Doppler energy insonation of placental vasculature in monochorionic twins: absent arterio‐arterial anastomoses in association with twin‐to‐twin transfusion syndrome , 1998 .

[6]  H. Schulman,et al.  Doppler velocimetry and placental disease. , 1989, American journal of obstetrics and gynecology.

[7]  S. Kjos,et al.  Ultrasonographic measurement of amniotic fluid volume in normal diamniotic twin pregnancies. , 1996, American journal of obstetrics and gynecology.

[8]  T. Porter,et al.  Normal Values for Amniotic Fluid Index During Uncomplicated Twin Pregnancy , 1996, Obstetrics and gynecology.

[9]  G. Machin,et al.  Correlations of placental vascular anatomy and clinical outcomes in 69 monochorionic twin pregnancies. , 1996, American journal of medical genetics.

[10]  N. Fisk,et al.  X-chromosome inactivation patterns do not implicate asymmetric splitting of the inner cell mass in the aetiology of twin-twin transfusion syndrome. , 1999, Molecular human reproduction.

[11]  N. Fisk,et al.  First‐trimester cord entanglement in monoamniotic twins , 1999, Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology.

[12]  K. Benirschke,et al.  Pathology of the Human Placenta , 1992, Springer New York.

[13]  K. Elliott,et al.  Size at birth , 1974 .

[14]  N. Fisk,et al.  Medical amnioreduction with sulindac to reduce cord complications in monoamniotic twins. , 1997, American journal of obstetrics and gynecology.

[15]  C. Rodeck,et al.  Maternal-fetal glucose gradient in normal pregnancies and in pregnancies complicated by alloimmunization and fetal growth retardation. , 1989, American journal of obstetrics and gynecology.

[16]  K. Benirschke,et al.  Antenatal origin of neurologic damage in newborn infants. II. Multiple gestations. , 1990, American journal of obstetrics and gynecology.

[17]  K. Benirschke,et al.  Antenatal origin of neurologic damage in newborn infants: I. Preterm infants , 1988 .

[18]  N. Fisk,et al.  Chorionicity and twins , 1996 .

[19]  K. Nicolaides,et al.  The hidden mortality of monochorionic twin pregnancies , 1997, British journal of obstetrics and gynaecology.

[20]  E. G. Robertson,et al.  Placental injection studies in twin gestation. , 1983, American journal of obstetrics and gynecology.

[21]  R. Bajoria Vascular anatomy of monochorionic placenta in relation to discordant growth and amniotic fluid volume. , 1998, Human reproduction.

[22]  V. Baldwin Pathology of Multiple Pregnancy , 1993, Springer US.