Acardiac twin pregnancies part VI: Why does acardiac twinning occur only in the first trimester?

Clinical observation suggests that acardiac twinning occurs only in the first trimester. In part, this contradicts our previous analysis (part IV) of Benirschke's concept that unequal embryonic splitting causes unequal embryo/fetal blood volumes and pressures. Our aim is to explain why acardiac onset is restricted to the first trimester.

We applied the vascular resistance scheme of two fetuses connected by arterio-arterial (AA) and veno-venous (VV) anastomoses, the small VV resistance approximated as zero. The smaller twin has volume fraction α < 1 of the assumed normal larger twin, and has only access to fraction X < 1 of its placenta; the larger twin's larger mean arterial pressure accesses the remaining fraction. Before 13 weeks, embryos have a much smaller vascular resistance than placentas. After 13 weeks, when maternal blood provides oxygen, smaller twins can increase their vascular volume by hypoxemia-mediated neovascularization. Estimated AA radii at 40 weeks, r_AA (40), are 0.5-1.3 mm.

Embryos with α < 0.33 unlikely survive 13 weeks and acardiac twinning occurs under appropriate conditions (AA-VV, small placenta). Acardiac body perfusion occurs because of a much smaller vascular resistance than the placenta. When α > 0.33 and r_AA (40)=1.3 mm, modeled survival is >32 weeks.

Before 13 weeks, embryos with α < 0.33 cannot survive and may result in the onset of acardia. Beyond 13 weeks, fetuses with α ≥ 0.33 survive because r_AA (40) is too small for acardiac onset. Following fetal demise, exsanguination from the live twin increases its blood volume and, we assumed also, its vascular resistance. Perfusion then occurs through the lower resistance placenta.