title: Increasing cardiac output and decreasing oxygenation sequence in pump twins of acardiac twin pregnancies.
abstract: An acardiac twin pregnancy is a rare but serious complication of monochorionic twinning and consists of an acardiac twin and a pump twin. The acardiac twin is a severely malformed fetus that lacks most organs, particularly a heart, but grows during pregnancy because it is perfused by the developmentally normal pump twin via a set of arterioarterial and venovenous placental anastomoses. Pump twins die intrauterine or neonatally in about 50% of the cases. Because the effects of an acardiac mass on the pump twin's development are incompletely known, methods for outcome prognosis are currently not available. We sought to derive simple relations for the pump twin's excess cardiac output and decreased oxygenation and to use available clinical cases for a preliminary test of the model. As a method, we used a theoretical flow model to represent the fetoplacental circulation of an acardiac twin pregnancy and estimated blood deoxygenation and reoxygenation following perfusion of the two bodies and placentas, respectively. The results show the pump twin's excess cardiac output and decrease of venous oxygen saturation to depend on the ratio of pump twin to acardiac twin umbilical blood flow, whose ratio can be measured by ultrasonography. The clinical cases show a decreasing umbilical flow ratio with gestation. In conclusion, prospective serial study is necessary to test whether measurement of umbilical flow ratios allows monitoring the pump twin's pathophysiologic development, possibly resulting in a guideline for prognosis of pump twin survival.
authors.affiliation: Laser Center and Department of Obstetrics and Gynecology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. m.j.vangemert@amc.uva.nl
authors.forename: Martin J C
authors.initials: MJ
authors.lastname: van Gemert
authors.forename: Asli
authors.initials: A
authors.lastname: Umur
authors.forename: Jeroen P H M
authors.initials: JP
authors.lastname: van den Wijngaard
authors.forename: Ed
authors.initials: E
authors.lastname: VanBavel
authors.forename: Frank P H A
authors.initials: FP
authors.lastname: Vandenbussche
authors.forename: Peter G J
authors.initials: PG
authors.lastname: Nikkels
mesh_terms: D009008:Abnormalities, Severe Teratoid; D001703:Biophysics / Q000379:methods*; D001783:Blood Flow Velocity; D002302:Cardiac Output; D018376:Cardiovascular Abnormalities / Q000175:diagnosis*; D004200:Diseases in Twins; D005260:Female; D005313:Fetal Death; D005315:Fetal Diseases; D005318:Fetal Heart / Q000002:abnormalities; D005330:Fetofetal Transfusion; D005333:Fetus / Q000098:blood supply*; D005865:Gestational Age; D006330:Heart Defects, Congenital / Q000175:diagnosis*; D006439:Hemodynamics; D006801:Humans; D008962:Models, Theoretical; D010100:Oxygen / Q000737:chemistry* / Q000378:metabolism; D021041:Placental Circulation; D011247:Pregnancy; D011256:Pregnancy Outcome; D013997:Time Factors; D014427:Twins; D016216:Ultrasonography, Prenatal; D014469:Umbilical Arteries
chemical_list: D010100:Oxygen