title: Modeling a hydropic recipient twin in twin-twin transfusion syndrome.
abstract: We developed a mathematical model of twin-twin transfusion syndrome (TTTS) that includes a hydropic recipient twin, adding interstitial and intracellular fluid compartments, fetal congestive cardiac failure, and the dynamics of renin-angiotensin system (RAS) mediators to our previous TTTS model. Ten differential equations for each twin, coupled by the net fetofetal transfusion of blood and blood components, i.e., colloids, osmoles, and RAS mediators, describe the development of fetal arterial and venous blood volumes, blood osmolality and colloid osmotic pressure (COP), interstitial fluid volume and COP, intracellular fluid volume, amniotic fluid volume and osmolality, and RAS mediator concentration. We included varying placental anastomoses, placental sharing, and amnionicity. The 20 differential equations were solved numerically from 0 to 40 wk with a 0.6-s time step. Consistent with clinical experience, model predictions are as follows. Unidirectional arteriovenous anastomoses and arteriovenous anastomoses inadequately compensated by oppositely directed anastomoses cause severe TTTS that includes a hydropic recipient. Adequately compensated arteriovenous anastomoses simulated TTTS without hydrops. The probability that oppositely directed anastomoses prevent onset of a hydropic recipient after TTTS onset, i.e., the largest interval between onset of TTTS and onset of hydrops in the recipient, was best for a venovenous anastomosis, closely followed by an arterioarterial and finally an oppositely directed arteriovenous anastomosis. Hydropic recipients have decreased amniotic fluid volume. Unequal placental sharing and amnionicity modify hydrops onset. In conclusion, our model simulates a sequence of events that results in a hydropic recipient twin in severe TTTS. The model may allow an assessment of the efficacy of current therapeutic interventions for TTTS cases that include a hydropic recipient twin.
authors.affiliation: Laser Center, Academic Medical Center, Univ. of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. m.j.vangemert@amc.uva.nl.
authors.forename: Jeroen P H M
authors.initials: JP
authors.lastname: van den Wijngaard
authors.forename: Asli
authors.initials: A
authors.lastname: Umur
authors.forename: Raymond T
authors.initials: RT
authors.lastname: Krediet
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
authors.forename: Martin J C
authors.initials: MJ
authors.lastname: van Gemert
mesh_terms: D000328:Adult; D000465:Algorithms; D000653:Amniotic Fluid / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D004487:Edema / Q000503:physiopathology*; D045604:Extracellular Fluid / Q000502:physiology; D005260:Female; D005312:Fetal Blood / Q000502:physiology; D005330:Fetofetal Transfusion / Q000503:physiopathology*; D005865:Gestational Age; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D007231:Infant, Newborn; D008208:Lymphatic System / Q000502:physiology; D015233:Models, Statistical; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D012039:Regional Blood Flow / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D014563:Urodynamics / Q000502:physiology