Physiological Rationale

Amnioreduction: Physiological Rationale

Amnioreduction, the percutaneous removal of large volumes of amniotic fluid from the sac of the recipient fetus in TTTS, was the first widely employed intervention to significantly alter the dismal perinatal prognosis of this condition. 

Indeed, this technically simple procedure remains a central component of the therapeutic armamentarium of TTTS, either alone or as an adjunct to placental laser ablation techniques. The hallmark diagnostic feature of TTTS is the oligohydramnios/polyhydramnios sequence.17,18 The donor fetus is characterized by a restrictive oligohydramnios (maximum vertical pocket [MVP] ? 2 cm) secondary to hypovolemia, whereas the recipient fetus displays hypervolemic polyuric polyhydramnios (MVP ?8 cm), creating a unique sonographic portrait (Figure 8.1). 

The polyhydramnios of the recipient fetus may reach extreme levels, with secondary maternal respiratory compromise. Preterm labor or preterm membrane rupture may occur secondary to the excessive amniotic fluid volume, frequently at very preterm gestations. 

Amniotic fluid pressure follows a weakly sigmoid-shaped regression curve, plateauing in the midtrimester, and increasing as gestation advances in both normal singleton and twin gestations. 19 Polyhydramnios is associated with an elevation of intrauterine pressure above the gestation mean, although not always exceeding the upper limit of normal. 

Furthermore, amniotic pressure is positively correlated with the MVP of fluid. In cases where polyhydramnios is associated with an elevated amniotic fluid pressure, drainage of amniotic fluid results in normalization of amniotic fluid pressure.20 Garry et al21 observed an elevated intra-amniotic pressure in all cases of TTTS; this decreased to the normal range following amnioreduction and restoration of normal amniotic fluid volume. 

As amniotic fluid pressure increases, fetal pO2 decreases, an effect independent of gestation.20 There is a significant association between elevated amniotic fluid pressure and abnormal fetal blood gas status.22 Raised amniotic pressure has been associated with an impairment in uteroplacental perfusion in both animal and human studies.23–25 Following therapeutic amnioreduction in 8 pregnancies with polyhydramnios, Bower et al25 observed a 74% median increase of uterine artery volume flow. It is postulated that elevated amniotic fluid pressure compresses the placenta and intervillous space.

These findings were reiterated by Guzman et al,26 who observed significantly improved uterine artery impedance indices and increased flow velocities using Doppler studies prior to and following amnioreduction in severe polyhydramnios. 

Based on the physiological observations outlined above, it has been postulated that the elevated amniotic pressure secondary to the recipient polyhydramnios in TTTS may impair placental perfusion to the donor, contributing to further hypovolemia and oliguria. Decreasing the amniotic fluid pressure with amnioreduction may relieve this abnormality of uteroplacental perfusion, thus providing a potential mechanism for the efficacy of this procedure in TTTS. 

Preterm labor or preterm membrane rupture is also a consequence of polyhydramnios and increased amniotic pressure. Perinatal outcomes for TTTS are greatly influenced by gestation at delivery.27,28 Amnioreduction, by reducing the amniotic pressure, may prolong gestation and improve perinatal outcomes in this indirect manner.