Why does second trimester demise of a monochorionic twin not result in acardiac twinning?

Abstract

Background We previously explained why acardiac twinning occurs in the first trimester. We raised the question why a sudden demised monochorionic twin beyond the first trimester does not lead to acardiac twinning. We argued that exsanguinated blood from the live twin would strongly increase the demised twins' vascular resistance, preventing its perfusion and acardiac onset. However, our current hypothesis is that perfusion of the demised twin does occur but that it is insufficient for onset of acardiac twinning. Methods We analyzed blood pressures and flows in a vascular resistance model of a monochorionic twin pregnancy where one of the fetuses demised. The resistance model consists of a demised twin with a (former) placenta, a live twin and its placenta, and arterioarterial (AA) and venovenous placental anastomoses. We assumed that only twins with a weight of at least 33% of normal survived the first trimester and that exsanguination of more than 50% of its blood volume is fatal for the live twin. Results At 20 weeks, only AA anastomoses with radii ≲1 mm keep the exsanguinated blood volume below 50%. Then, perfusion of the deceased body with arterial blood from the live fetus is about 5–40 times smaller than when that body was alive. Beyond 20 weeks, this factor is even smaller. At 14 weeks, this factor is at most 2. Conclusion We hypothesize that this small perfusion flow of arterial blood prevents further growth of the deceased body and hence precludes onset of acardiac twinning.

Hypothesized pathogenesis of acardius acephalus, acormus, amorphus, anceps, acardiac edema, single umbilical artery, and pump twin risk prediction

“…Acardiac twinning develops in about 2.6% of monochorionic twins and, depending upon frequency and method of assisted reproduction, happens about once per 9,500–12,000 pregnancies (van Gemert, van den Wijngaard, & Vandenbussche, 2015 ). Acardiac onset occurs in the first trimester only (van Gemert, Ross, van den Wijngaard, & Nikkels, 2021 ; van Gemert, van der Geld, Ross, Nikkels, & van den Wijngaard, 2021 ), and requires a set of AA and VV anastomoses. It was demonstrated by ultrasound that during acardiac development a reverse flow in the arteries and aorta occurs (hence the name twin reverse arterial perfusion [TRAP] sequence; Van Allen, Smith, & Shepard, 1983 ).…”