Summary of the Pathophysiology

Summary of the Pathophysiology of Twin–Twin Transfusion Syndrome

TTTS presumably results from an unbalanced exchange of blood between two or more fetuses via placental vascular anastomoses. While this fundamental hypothesis has not been proven, circumstantial evidence suggests that this indeed may be the main operating pathophysiological mechanism. 

The etiology of the unbalanced blood exchange can be traced back to either an abnormal design of the placental vascular anastomoses (obligatory etiology), or, less often, to primary hemodynamic differences between the fetuses. Hypovolemia in the donor twin elicits the RAS and increased ADH, causing local vasoconstriction, oliguria, oligohydramnios, and renal tubular dysgenesis. Hypervolemia in the recipient twin results in increased ANF secretion, polyuria, polyhydramnios, and hypertension. 

Hypertension in the recipient twin may also result from passive transfer of angiotensin II, and lead to cardiac hypertrophy, dysfunction, and eventually failure and or death. The degree of polyuria in the recipient twin seems to be out of proportion to the presumed amount of excessive blood transfer, consistent with an endocrine effect on the recipient’s vascular system. The resulting vicious cycle may lead to death of one or both fetuses, or to miscarriage from polyhydramnios and incompetent cervix in 95% of cases. Therapy is therefore indicated, to avert the natural history of the disease.