ABSTRACT
Twin-twin transfusion syndrome (TTTS) is a unique complication of monochorionic twin pregnancies, diagnosed by discordant amniotic fluid volume (oligo/anhydramnios-polyhydramnios sequence). Often, but not always, serious cardiovascular sequelae develop, resulting in the assessment of TTTS as having a widely variable and unpredictable clinical presentation. TTTS is a consequence of placental anastomoses, which can be arteriovenous from donor to recipient (AVDR), arteriovenous from recipient to donor (AVRD), arterioarterial (AA), and venovenous (VV). These anastomoses allow a net fetofetal transfusion to develop from one twin (the donor) to the other (the recipient). While about 96% of all monochorionic placentas have anastomoses, only 5-10% of them develop TTTS (see Chapter 3). TTTS severity has been classified.1 Stage I includes the oligo-polyhydramnios sequence without further complications. Stage II also includes lack of donor bladder filling. Stage III includes critically abnormal arterial or umbilical venous flow and/or ductus venosus patterns in either twin. Stage IV includes hydrops, and stage V intrauterine fetal demise in either or both twins. Although ultrasonography can study the fetal and placental anatomy, and Doppler sonography the blood flow of major fetal, umbilical, and placental vessels, other parameters contributing to TTTS presentation and sequelae cannot be studied directly
(i.e. the fluid flows responsible for the amniotic fluid discordance, cardiovascular parameters including fetal blood pressures, and the net fetofetal transfusion). Because an animal model of TTTS is not available, understanding the complex pathophysiology of TTTS to its full extent is problematic. As an alternative, mathematical models of monochorionic twin pregnancies have been developed with the hope that they can aid in identifying and understanding the sequence of events that leads to the various TTTS manifestations and the potential efficacy of therapies.
