The twin-to-twin transfusion syndrome poses a major challenge for fetal therapy. Untreated, it results in inordinate perinatal mortality and morbidity. It affects two babies, both of whom are structurally normal. Because the connections mediating intertwin transfusion lie on the placental surface, they should be amenable to therapeutic interruption.Although all monochorionic twins have vascular anastomoses and thus intertwin transfusion, the clinical syndrome develops in only 15 percent. This results in midtrimester discordance in amniotic-fluid levels and growth between the twins, with signs of hypovolemia and uteroplacental insufficiency in the donor and hypervolemia and cardiac dysfunction in the recipient (Figure 1). . . .
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Fisk et al. (2004) studied this question.
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