Cause versus effect

Cause versus effect

The endocrine findings in TTTS are commonly viewed as the effect of the uneven blood exchange. Increased renin in the donor and increased ANF in the recipient, with their hemodynamic and renal consequences, follow the uneven exchange of blood. This view would be in accordance with the obligatory etiology as described above. 

Alternatively, increased renin, increased ADH, and a tendency to raise the blood pressure in the donor could result from placental insufficiency. The increased blood pressure in the donor would in turn force more blood through placental vascular anastomoses into the recipient twin, setting off the vicious cycle. 

This alternative pathophysiological mechanism could operate in the facultative etiology theory discussed above. Potential circumstantial evidence of this mechanism could be seen in post-laser donors that develop hypertension. Baud et al recently reported on a hypertensive ex-donor after laser therapy, with right ventricular pressures of 60 mmHg.10 The authors speculated that the development of hypertension in this fetus may have been due to increased placental resistance or reverse TTTS. In our series, eight donors out of 438 (1.8%) surgeries showed new onset of postoperative TR. 

Pulmonic stenosis has also been viewed as an acquired disease in patients with TTTS.11 As shown in Table 3.3, pulmonic stenosis is a rather rare event (4/615, 0.6%). The low incidence of this complication would suggest it as a cause rather than a consequence of TTTS (facultative etiology). At least two of these fetuses underwent postnatal balloon valvuloplasty, suggesting a permanent rather than a circumstantial change to the pulmonic valve. The issue is not clear, however, and will need further investigation.