twin twin transfusion

description

twin to twin transfusion complicates about 15% of monochorionic twin gestations and is responsible for 17% of the perinatal mortality in multiple pregnancies.

timing of division:

• if embryonic splitting occurs before day three post conception, two independent fetuses with separate placentas will result (dichorionic diamniotic).
• if splitting takes place between days four and seven, a single placenta with two amniotic cavities occurs (monochorionic diamniotic).
• if division of the embryoblast occurs after eight days, the twins share a single placenta and amniotic cavity (monochorionic monoamniotic).
• division beyond day 12 results in conjoined twins.

when two fetuses share the same placenta (monochorionic), vascular anastomoses develop between their circulations. these anastomoses can be of three types:

1. vein-to-vein
2. artery-to-artery
3. artery-to-vein.

even when there are multiple vascular connections within a single placenta, no transfusion should occur provided the anastomoses are balanced. placentas from pregnancies with twin-twin transfusion have fewer anastomoses, which are more likely to be solitary and of deep arteriovenous type than those without twin-twin transfusion.

if transfusion occurs, the donor or ‘pump’ twin becomes hypovolemic due to blood loss. hypoxia develops because of placental insufficiency, which is also responsible for the associated growth restriction. poor renal perfusion leads to oligohydramnios. this latter feature, when severe, is responsible for the classical appearance of the ‘stuck twin’: the amniotic sac becomes too small, the amniotic membrane comes in close contact with the body of the fetus which then appears closely apposed to the uterine wall. hypervolemia with increased renal perfusion leads to polyhydramnios in the sac of the recipient twin. since there is no loss of protein or cellular components from its circulation, colloid osmotic pressure draws water from the maternal compartment across the placenta, establishing a vicious cycle of hypervolemia, polyuria and hyperosmolarity leading to high output cardiac failure, hydrops and polyhydramnios. when the disease manifests during the second trimester there is a high risk of perinatal morbidity and mortality. intrauterine hypoxia, preterm delivery and death of one fetus (usually the donor) with subsequent death or hypoxic-ischemic sequelae (twin embolisation syndrome) in the surviving twin are the most common complications to watch for in these pregnancies.