Pathophysiology

Pathophysiology. Twin–twin transfusion syndrome (TTTS)

Twin–twin transfusion syndrome (TTTS) is thought to result from an unbalanced sharing of blood between two fetuses via placental vascular anastomoses. The negative corollary is evident from the fact that the disease does not occur in dichorionic pregnancies, as vascular anastomoses do not develop in such placentas. 

As a result of the unbalanced blood exchange, one fetus receives too much blood (the recipient twin, or recipient), and one fetus loses too much blood (the donor twin, or donor). The unbalanced blood sharing triggers a series of pathophysiological changes that characterize the natural history and outcome of the disease. Most monochorionic placentas have vascular anastomoses but only 5–10% of monochorionic pregnancies develop TTTS.

What determines then the development of the disease in these patients? Two theories have evolved over the years in our laboratory regarding the etiology of TTTS and, analogous to the microbiology terminology, we have termed them ‘obligatory’ and ‘facultative.’