Abstract

Objective: Monochorionic twins with circulatory sharing have an incompletely understood response to acute hemodynamic events. We relate placental vascular anatomy with, first, the response to (a) acute fetal demise and (b) laser interrupted placental anastomoses and, second, the efficacy of current and possibly future therapeutic interventions in twin-twin transfusion syndrome. Design: Hemodynamic response to acute fetal demise and laser interrupted anastomoses is analysed using the model previously developed for monochorionic twins. Efficacy of therapeutic interventions in twin-twin transfusion syndrome is analysed by combining the estimated incidence of placental anastomotic patterns with three previously proposed pathophysiologic mechanisms. Results: Fetal demise may cause sequelae for the co-twin in all anastomotic patterns except unidirectional arteriovenous and single venovenous anastomoses which are predicted to be hemodynamically harmless. In twin-twin transfusion syndrome, laser interruption of all anastomoses mitigates further transfusion. This is of benefit for the twins in equally but not in unequally shared placentas. Analysis predicts that ≈75% fetal survival could be achieved interrupting only arteriovenous anastomoses. Amniocentesis may only prolong pregnancies that lack progressively increasing discordance, assuming that placental anastomoses remain patent following polyhydramnios. This proposed mechanism of action predicts current therapeutic efficacy accurately and could explain the significantly higher reported serious morbidity compared with laser (15/81=19±5% versus 4/146=3%, P=0.00004). However, if therapeutic interventions could match the syndrome's individual placental anatomy, the analysis suggests ≈10-15% laser related mortality (premature rupture of membranes) and <3% severe morbidity could possibly become achievable goals. Conclusion: Our predictions allow clinical testing. This information may contribute to an improved management of monochorionic twins.

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