etiology of TTTS appears to result from a net unbalanced flow of blood between two MC fetuses through placental vascular communications, which results in a donor twin and a recipient twin. Although actual documentation of the unbalanced blood flow remains elusive [5], vascular anastomoses might be responsible for the development of TTTS if the vas- cular design is such that it forces a net flow from donor to recipient [5]. Alternatively, vascular anas- tomoses might play a passive role in the develop- ment of the syndrome, but nonetheless allow its development. This is the case with MC twins who are discordant for congenital heart disease, cardio- myopathies, cord anomalies, or other conditions associated with uneven hemodynamic competence [6]. When the onset of this condition occurs before 26 weeks of gestation, there is a significant associ- ated risk of fetal loss, perinatal death, and subse- quent handicap in survivors [7]. If untreated at its early onset, severe TTTS has a dismal prognosis, with perinatal mortality rates > 90% [8], and > 30% of survivors suffering from associated neurodevel- opmental anomalies [8].