Causes of twin-to-twin transfusion syndrome

The foetuses in twin-to-twin transfusion syndrome are perfectly normal; the problem lies in the placenta as it contains vascular anastomoses which allow blood to pass from one foetus to the other. For unknown reasons, approximately 15% of monochorionic pregnancies present severe twin-to-twin transfusion. In most cases, 85–90%, it manifests between weeks 16 and 25 of the pregnancy, as twin-to-twin transfusion is less likely to occur in early and late stages of the pregnancy.

In serious cases the blood-giving foetus (donor) develops a loss of volume and the blood-receiving foetus (recipient) accumulates too much blood, leading to volume overload and possibly even heart failure in the worst examples. The donor foetus attempts to reduce the loss of volume by ceasing to urinate; this translates into a decrease in the amount of amniotic fluid (a situation known as oligohydramnios) and therefore the donor becomes “shrink-wrapped” in its amnion, which is why it is also known as the “stuck twin”. Contrastingly, the recipient foetus tries to eliminate the excess volume by producing more urine, thus increasing its amount of amniotic fluid (polyhydramnios). An excess of amniotic fluid increases the risk of premature rupture of membranes and premature delivery due to uterine distention.