TTTS. Partitioning of Placental Mass
In addition to the vascular anatomy, it is important to consider the division of the placental mass of monochorionic placentas. Monochorionic twins may not share equal masses of villous tissue; one twin may have more placental tissue for development (Figure 5.10).
This finding has several important implications regarding monochorionic twin gestations, particularly if they are complicated by TTTS. What is the role of the individual placental mass in the pathogenesis of TTTS? Is the relatively high rate of intrauterine growth restriction noted in TTTS due the unequal partitioning of the placental mass? To help answer these questions,
Quintero et al36 studied the individual placental mass (IPM) of the donor and recipient twins after selective laser photocoagulation of communicating vessels and compared that to the IPMs of uncomplicated monochorionic twins. Because of fibrosis and degeneration of the placenta associated with fetal demise, all such cases were excluded from the analysis. Thus, placentas from 75 TTTS cases treated with laser surgery and 61 uncomplicated monochorionic twins were analyzed. The fresh placentas were cut along the vascular equator and individually weighed, thereby obtaining the IPM. The individual placental territory (IPT) for each fetus was calculated by dividing its IPM by the total placental mass and multiplying by 100.
The donor fetuses were noted to weigh less than smaller control fetuses, whereas there was no significant difference in weight between the recipients and the larger controls. Corrected for gestational age, the IPT was not different between TTTS and control fetuses. This finding has two important ramifications: first, the partitioning of placental mass does not seem to be a primary cause for the development of TTTS; secondly, if placental territories were no different between the donors and smaller controls, why were the donor fetuses more growth restricted? This finding suggests that placental mass alone does not explain the growth restriction that may occur in the donor fetus. Other factors that are present in the TTTS cases but not the uncomplicated monochorionic cases may explain this, such as the imbalanced blood flow via the vascular communications or the poor nutrient exchange due to the histological changes noted in donor villus.
Another interesting finding of this study was that as little as 10–14% of the placental territory was able to sustain fetal life and result in perinatal survival. This finding demonstrates the ability of the fetus to adapt to chronic placental insufficiency. Why some donor fetuses with diminutive placental territory survive while others with more equable placental mass succumb is unknown. At this time, there is no accurate means of predicting placental territory prenatally.
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