Effect of unbalanced blood exchange in the recipient twin

Effect of unbalanced blood exchange in the recipient twin

The excessive blood volume in the recipient twin presumably results in an increased production of atrial natriuretic factor, or ANF.9 Wieacker et al studied three cases of severe twin transfusion syndrome and demonstrated that the concentration of ANF in the cord blood of recipient twins is significantly elevated compared to that of donor twins. Increased ANF results in increased fetal urine production, bladder distention, and polyhydramnios. 

The discrepancy between recipient and donor concentration correlated with the volume of transfusion. They proposed the following pathophysiological mechanism to explain the development of polyhydramnios in recipient twins: chronic blood volume overload in twins causes enhanced release of ANF from the fetal heart; increased fetal urine production leads to polyhydramnios, which is additionally enhanced by inhibition of antidiuretic hormone (ADH) release. 

Hypertension may also develop in the recipient twin, both as a result of hypervolemia as well as from transfer of angiotensin II and paradoxical activation of the RAS system from the donor twin. Hypertension in the recipient twin results in thickened myocardial walls and potential myocardial dysfunction. Hypertension may be severe enough to cause myocardial infarction in the recipient. Hypertension in the recipient twin may be assessed with pulsed 

Doppler assessment of the tricuspid regurgitant jet using the modified Bernoulli equation: 

?P = 4 ? Vmax 2 

We have noted tricuspid regurgitation in approximately 27% of recipients (138/498). The incidence of tricuspid regurgitation increased with stage (Figure 3.8), but has no prognostic value. 

Transplacental passage of renin and/or angiotensin II from the donor to the recipient may suppress renin synthesis by the recipient kidney. This would result in increased renal blood flow, polyuria, and polyhydramnios. 

Spontaneous demise of the recipient twin may result from hypertension, heart failure with hydrops, hemorrhage, or thrombosis from hyperviscosity.