Twin-twin transfusion syndrome. Three possible pathophysiologic mechanisms.

OBJECTIVE

To propose a classification of twin-twin transfusion syndrome based upon three categories of placental anastomotic patterns.

STUDY

DESIGN

A mathematical model developed to compute fetal blood volume in monochorionic twins combines fetoplacental circulation with net fetofetal transfusion along placental anastomoses. We included (1) unequal cotyledonic sharing, assuming that smaller fractions cause smaller twins with lower blood pressure, and (2) significantly decreasing anastomotic resistance, combining Poiseuille's law with placental anastomotic growth. Fetoplacental compensatory mechanisms were not studied.

RESULTS

First, unidirectional arteriovenous anastomoses produce steadily increasing fetal discordance by small anastomotic blood flow. Second, arteriovenous plus compensating anastomoses (venoarterial, arterioarterial, venovenous) produce fetal discordance followed by a dynamic steady state of minimal net fetofetal transfusion and large anastomotic flow. This circumstance mitigates further discordant growth. Third, unequal cotyledonic sharing plus superficial compensating anastomoses (arterioarterial, venovenous) produce fetal discordance followed by a steady state of equal fetal growth and small anastomotic flow. The model predictions include spontaneous disappearance and reversal of discordance. Serial measurement of fetal growth patterns and anastomotic flow could identify the syndrome's underlying pathophysiology.

CONCLUSION

Testing the model predictions by relating clinical presentation with placental anatomy could increase our understanding and direct diagnostic and therapeutic strategies to match the underlying placental anatomy.