Healthy Monochorionic Diamniotic Twin Microvasculature and Placental Imaging

Twin-twin transfusion syndrome (TTTS) is a pathology that can arise in monochorionic, diamniotic (MoDi) identical twins arising from the division of a single fertilized ovum at 4-8 days gestational age (GA), after the chorion has formed but before the amnion's formation. TTTS can also arise in monochorionic, monoamniotic (MoMo) twins when there is a division in the fertilized ovum between day 8-13 GA, also resulting in a single chorion but also a single amnion. The amnion is the tissue layer that will develop into the amniotic sac, while the single chorion in both MoDi and MoMo twins, made up of the cytotrophoblastic and syncytiotrophoblastic layers as well as the extraembryonic mesoderm tissue layers; eventually composing the fetal side of the placenta including the chorionic plate and villi.

The fetal side of the placenta is composed of low-resistance, higher-pressure vascular beds terminating in villous capillaries where deoxygenated blood can be easily exchanged with the lower-pressure, extra-vascular, maternal-side blood supply for oxygenated blood flowing through the chorionic and umbilical vein(s). The maternal and fetal blood supplies are not directly connected.

The placental vasculature is further broken down into 15-28 cotyledons, which are fed originally by each umbilical artery that branch into eight or more terminal chorionic plate arteries/'stem' arteries. These arteries then divide into first-order-branching truncal vessels which in turn divide into 4-8 horizontal cotyledonary vessels of the second-order. These horizontal cotyledonary vessels then branch further into third-order, villous branches of which there are 30-60 main branches per cotyledon, terminating in a vast network of even smaller capillaries.

As mentioned, arterial and venous blood flow should not directly be connected. However, in monochorionic twin pregnancies sharing a single placenta often unevenly, anastomoses [connections] artery to artery (AA), vein to vein (VV), and artery to vein (AV) can occur. AA and VV anastomoses often occur superficially on the placenta, with AA anastomoses being considered protective against TTTS. These AA and VV anastomoses tend to have bi-directional flow and are of less clinical concern.

In contrast, AV anastomoses usually flow in a unilateral manner and often shunt blood unevenly towards one twin and away from the other. This can be further complicated by one twin's vasculature dominating the majority of the placenta's vascular area and thus oxygen-CO2 exchange. These factors can lead to one twin with hypovolemia [lack of blood volume/flow], leading to renal hypoperfusion and stimulating the renin-angiotensin-aldosterone system (RAAS) which then induces potent vasoconstriction, water and sodium retention, increased blood pressure, and vascular resistance within the kidney. These factors, in turn, lead to oligouria, a low urine output by the fetus and oligohydramnios, a low volume of amniotic fluid, with increased collagen synthesis, hypertrophy [increased size] of the vascular media, and smooth-muscle hypertrophy following.