title: Modelling the influence of amnionicity on the severity of twin-twin transfusion syndrome in monochorionic twin pregnancies.
abstract: Clinical treatment for diamniotic-monochorionic twin-twin transfusion syndrome (TTTS) may include conversion of diamniotic pregnancies to a monoamniotic-monochorionic state by disrupting the amnion septum. We sought to test the underlying hypothesis, i.e. that a monoamniotic state reduces the severity of TTTS. With use of our previously developed mathematical model of two equal fetoplacental circulatory units connected by various sizes and types of placental anastomoses, we compared the haemodynamic and amniotic fluid dynamics of monoamniotic and diamniotic twins that develop TTTS. We used three anastomotic patterns that produce severe, moderate or mild forms of TTTS, respectively, in our diamniotic-monochorionic twin model. Monoamnionicity was modelled by adding the two amniotic fluid volumes and using the volume-averaged amniotic fluid osmolality. The results were as follows: for severe TTTS, small differences develop between diamniotic and monoamniotic donor twins in fetal urine production, swallowed volume, blood volume, blood pressures, net fetofetal transfusion, and blood and amniotic fluid osmolality. However, the circulatory imbalance between the monoamniotic twins deteriorates similar to that of diamniotic twins. The pathophysiological differences tend to disappear for milder TTTS. In conclusion, our model suggests that the uncommon finding of TTTS in monoamniotic twins is not due to the presence of a single amniotic sac. Rather, clinically significant differences in anastomotic patterns and the delayed or lack of identification of manifestations in monoamniotic twins account for the reduced rate of TTTS diagnosis. Based on these results we expect the clinical disruption of the amnion septum in diamniotic-monochorionic TTTS pregnancies to have only minimal benefits.
authors.affiliation: Laser Center and Department of Obstetrics and Gynecology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Jeroen P H M
authors.initials: JP
authors.lastname: van den Wijngaard
authors.forename: Asli
authors.initials: A
authors.lastname: Umur
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
authors.forename: Martin J C
authors.initials: MJ
authors.lastname: van Gemert
mesh_terms: D000650:Amnion / Q000098:blood supply* / Q000503:physiopathology*; D000653:Amniotic Fluid; D005314:Embryonic and Fetal Development; D005260:Female; D005312:Fetal Blood; D005330:Fetofetal Transfusion / Q000503:physiopathology*; D005865:Gestational Age; D006801:Humans; D008955:Models, Cardiovascular; D010920:Placenta / Q000502:physiology; D011247:Pregnancy; D014427:Twins