Anastomoses

TTTS. Anastomoses

An AVDR anastomosis connects the umbilical artery of the donor with the umbilical vein of the recipient. The AV connections occur at the capillary level within a cotyledon that receives its blood from a donor chorionic artery and drains it by a recipient chorionic vein. AVRD anastomoses, from recipient to donor, often exist next to primary AVDRs, where the AVRDs are defined as having the smaller diameter (higher resistance) compared to the primary AVDR with the largest diameter. Further, 

AA or VV anastomoses directly connect chorionic arteries or veins of the two twins. In our models, the AVDR, AVRD, AA, and VV anastomoses are represented by tubes, which directly connect with the two umbilical circulations, without branches to the normal placental chorionic vessels. This is a simplification, because it is known that most if not all anastomoses have branches to the normal placental circulation of the fetuses. 

Placental anastomoses cause a fetofetal transfusion of blood and its constituents between combinations of arterial and venous blood compartments of the twins. The amount of transfusion results from the driving pressure gradient divided by the anastomotic resistance to blood flow (Ohm’s law). Obviously, AVDR transfusion is the principal flow here and the combined AVRD, AA, and VV transfusions return part of the AVDR flow back to the donor, driven by gradients between recipient and donor vascular pressures. The resulting net fetofetal transfusion is from donor to recipient and is defined as:  

When TTTS develops in the model, recipient arterial and venous pressures exceed those of the donor, so the resulting directions of blood flow through AA and VV anastomoses are from recipient to donor, explaining their negative sign in eqn (1). However, we acknowledge that clinical cases have been described where flow through an AA was found to be from donor to recipient.11 We hypothesize that this unusual phenomenon may occur when the AA connects a short donor chorionic arterial segment with a long, high resistance, recipient segment. 

Then, due to the hydrostatic pressure loss in the recipient, the driving AA pressure gradient is from donor to recipient. However, because fetofetal transfusion reduces the donor’s arterial pressure and increases the recipient’s pressure, we also hypothesize that this can only occur temporarily. In our model, AA anstomoses connect directly with the umbilical arteries of both twins, so we cannot simulate this phenomenon. Furthermore, TTTS in the absence of an AVDR is another remarkable presentation. 12 We confirm this observation, as it also occurred in two of our TTTS cases (unpublished). 

Again, our model cannot simulate this intriguing TTTS presentation. We use Poiseuille’s law of laminar blood flow to define the vascular resistance (Resist) of the anastomoses, which depends on blood viscosity, length, and radius of the tube:  

Note that the radius is included to the 4th power, implying radius has an exceedingly strong influence on resistance, e.g. a radius increase by a factor of 2 decreases the resistance by a factor of 24 (= 16), at constant viscosity and length. 

Although a joint cotyledon (AVDR and AVRD anastomoses) is anatomically not a tube, their resistances nevertheless are equivalent in our model, because of their assumed identical growth behavior.4 Briefly, anastomoses increase their length and radius linearly (see section on ‘Proposed TTTS etiology and pathophysiology’). As eqn (2) includes length divided by radius to the 4th power, the anastomotic resistances decrease proportional to gestational age to the 3rd power. In a cotyledon, the radius of the capillaries does not vary with gestational age. 

Instead, the number of capillaries grows commensurate with the placental volume, assumed proportional to gestational age to the 3rd power.4 Thus, approximating the vascular resistance of a cotyledon by the parallel circuit of identical capillary resistances, overall cotyledonic resistance is inversely proportional to the number of capillaries, and, hence, inversely proportional to the 3rd power of gestation, identical to AVDR and AVRD resistances. In previous work,13 we used a fractal geometry model for the vascular tree to simulate how AVDR and AVRD resistances relate to the diameter of their feeding and draining vessels. In this model, the cotyledon has a 20–24 times higher resistance than the feeding artery plus draining vein. 

Thus, the tube used in our models to represent AVDR or AVRD resistances also has a 20–24 times higher resistance than the feeding artery plus draining vein, implying the AVDR and AVRD anastomotic tube radii in the model cannot represent their actual radii, which are about to times larger than the radii used in the model. Furthermore, because the fetal arterial pressure is much higher than the venous pressure, pressure deviations from normal likely produce much larger intertwin arterial than venous pressure gradients. 

This implies that an AA has a much greater efficacy than a VV of identical dimensions to reduce the net fetofetal transfusion compared with the AVDR alone. We estimated that a VV anastomosis of identical length requires an 8 times smaller resistance (eqn A5 of previous work4), or a 1.7 times larger diameter than an AA for equal reduction of the AVDR transfusion. However, in cases of a hydropic recipient twin, the simulated recipient venous pressure is significantly enlarged, implying a VV is more effective in reducing the AVDR flow than without a hydropic twin (see ‘Results’ section).6 Several unidirectional AV anastomoses are equivalent to a circuit of parallel AV tube resistances and, hence, equivalent to one overall AV tube resistance using the law of parallel resistances, i.e. (RAVoverall)?1 = (RAV1)?1 + (RAV2)?1 + (RAV3)?1 + …. This holds for AVRD, AA, and VV resistances too. So, multiple AVDR, AVRD, AA, and VV anastomoses are equivalent to a set of overall single AVDR, AVRD, AA, and VV resistances. 

We recall that in real monochorionic twin placentas, the anastomotic pattern is not exactly a set of tubes connecting the umbilical cords. Nevertheless, we found that multiple placental anastomoses of certain types are approximately equivalent to a set of overall single anastomotic resistances of the same types.