A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

Abstract

December 7, 2006; doi:10.1152/ajpregu.00534.2006.-The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The "normal" staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS. stage III; quintero staging sequence IN THE UNITED STATES, about 10% of all monochorionic twin pregnancies, resulting in ϳ3,000 fetal twin pairs each year, develop twin-twin transfusion syndrome (TTTS). Caused by uncompensated fetofetal transfusion through a placental arteriovenous (AV) connection from one twin (the donor) to the other (the recipient), TTTS often leads to intrauterine fetal death or premature delivery (24, 49). TTTS severity can be mitigated by other, compensating anastomoses, which return part of the AV transfusion back to the donor twin [i.e., opposite arteriovenous (VA), arterioarterial (AA) (45), and venovenous (VV) anastomoses].TTTS is believed to progress through four worsening stages of severity with both twins alive (36). Stage I TTTS is diagnosed by the oligo-polyhydramnios sequence, where the donor has almost no amniotic fluid and the recipient simultaneously has excess amniotic fluid. More severe stages of TTTS often develop subsequently: stage II includes lack of donor bladder filling; stage III, abnormal umbilical flows in either twin (i.e., reduced or reversed end-diastolic flow) (21); and stage IV, congestive cardiac failure and hydrops in the recipient.The syndrome has a largely inaccessible pathophysiology, because invasive fetal study is unethical and an ani...

Modeling Acardiac Twin Pregnancies

“…That was considered the easiest approach here because in that model we related fetal growth to the placental perfusion, a mechanism that needed very little adaptation in the present model, where we related fetal growth to umbilical blood flow. Our most recent model includes amniotic fluid dynamics and fetal cardiac failure, 25 and was not considered suitable for modeling acardiac growth, basically because it is unknown whether the fluid shifts that are essential in that model occur at all in acardiac bodies. Here, we defined fetal growth from the transplacental fluid flow, that is, from the maternal blood to the fetal blood, which is a problem in acardiac twins because the blood flow that perfuses the acardiac placenta never reaches the acardiac twin directly.…”

“…Furthermore, our recent model also includes other fluid flows (e.g., between fetus and amniotic fluid, by urination, lung secretion, swallowing, and the intramembranous flow), and it is unknown whether, and if so, to what extent, such flows develop at all in the acardiac twin. Nevertheless, our recent model includes development of hydrops due to cardiac failure, and thickening of arteries due to overfilling, 25 thus important pathologies that often occur in pump twins developing complications due to perfusion of the acardiac twin.…”

Twin Anemia-Polycythemia Sequence: Diagnostic Criteria, Classification, Perinatal Management and Outcome

“…Some monochorionic twins may first develop severe Hb discordance followed by amniotic fluid discordance. We were able to reproduce this chain of events in a computerized model in which incomplete laser therapy was simulated and one patent AV anastomosis was left open [14] . In some circumstances, e.g.…”

Computational modelling of amino acid transfer interactions in the placenta

“…For flow, the pulse propagation in arterial placental networks has been modelled to investigate the blood supply in monochorionic twin pregnancies and the effect of the timing of the fetal heart beats (Franke et al 2003). In addition, factors such as viscoelastic arteries, the effect of elastin on blood vessel compliance and blood haematocrit dynamics have been included (van den Wijngaard et al 2007). Furthermore, recently, mathematical modelling was applied to study the effect of the maternal flow configuration in and out of the placenta on generalized nutrient uptake efficiency, with the intervillous space modelled as a homogeneous porous medium (Chernyavsky et al 2010).…”