ABSTRACT
Although the diagnosis and treatment of twin-twin transfusion syndrome (TTTS) has improved greatly in recent decades, this condition represents one of the greatest challenges in modern fetal medicine. First, two fetuses are involved. Second, the natural history of fetal loss or damage is extremely high compared with other fetal pathologies. Third, because the defect originates in the placenta, these fetuses are structurally normal, and thus potentially completely salvageable. Finally, it is relatively common, occurring in 10-15% of monochorionic (MC) twins, affecting about 1:3200 pregnancies or 1:1600 fetuses1. Significant barriers to developing rational treatments have been the lack of understanding of the underlying vascular pathophysiology as well as the lack of an appropriate animal model.
