Martin J C van Gemert1, Jeroen P H M van den Wijngaard1,2, K Marieke Paarlberg3, Helena M Gardiner4, Peter G J Nikkels5. 1. Department of Biomedical Engineering & Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. 2. Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, The Netherlands. 3. Department of Obstetrics and Gynecology, Gelre Hospitals, location Apeldoorn, The Netherlands. 4. The Fetal Center, McGovern Medical School at UTHealth, University of Texas, Houston, TX, USA. 5. Department of Pathology, Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands.
Abstract
BACKGROUND: Benirschke postulated that acardiac twinning occurs when markedly unequal embryonic splitting combines with arterioarterial (AA) and venovenous placental anastomoses. We tested this hypothesis by model simulations and by comparison of outcomes with 18 "pseudo-" (twin fetus with beating heart but otherwise with clear signs of an acardiac) and 3 "normal" acardiac cases. METHODS: The smaller/larger cell volume ratio at embryonic splitting becomes the smaller/larger embryonic/fetal blood volume ratio (a). From a, we derived nonpulsating blood pressures using normal values (larger twin) and normal values at an appropriate earlier gestational age (smaller twin). These unequal pressure sources were used in a linear resistance fetoplacental network to calculate umbilical venous diameter ratios. Acardiac onset occurs when the smaller twin has 50% left of its normal, singleton placenta. Comparison with clinical cases approximated a by crown-rump-length-ratio to the 3rd power. Input parameters are a and the AA-radius at 40 weeks. RESULTS: Acardiacs can be small or large, can occur early or late, earlier at smaller a and larger AA, with larger umbilical venous diameter ratios at smaller a and smaller AA. Comparison with the 21 clinical cases was good, except for 2. CONCLUSION: Our analysis supports Benirschke's hypothesis. The smaller twin has to share its placental perfusion with the larger twin, which is a novel finding. The AA size is essential for the future of both fetuses but complicates easy understanding of (pseudo-)acardiac clinical presentations. Late acardiac onset occurs infrequently. Using nonpulsating circulations may have caused our extensive predictions of late onset. An improved model requires including hypoxemia in the smaller twin from chronic placental hypoperfusion. Birth Defects Research 109:211-223, 2017.
BACKGROUND: Benirschke postulated that acardiac twinning occurs when markedly unequal embryonic splitting combines with arterioarterial (AA) and venovenous placental anastomoses. We tested this hypothesis by model simulations and by comparison of outcomes with 18 "pseudo-" (twin fetus with beating heart but otherwise with clear signs of an acardiac) and 3 "normal" acardiac cases. METHODS: The smaller/larger cell volume ratio at embryonic splitting becomes the smaller/larger embryonic/fetal blood volume ratio (a). From a, we derived nonpulsating blood pressures using normal values (larger twin) and normal values at an appropriate earlier gestational age (smaller twin). These unequal pressure sources were used in a linear resistance fetoplacental network to calculate umbilical venous diameter ratios. Acardiac onset occurs when the smaller twin has 50% left of its normal, singleton placenta. Comparison with clinical cases approximated a by crown-rump-length-ratio to the 3rd power. Input parameters are a and the AA-radius at 40 weeks. RESULTS: Acardiacs can be small or large, can occur early or late, earlier at smaller a and larger AA, with larger umbilical venous diameter ratios at smaller a and smaller AA. Comparison with the 21 clinical cases was good, except for 2. CONCLUSION: Our analysis supports Benirschke's hypothesis. The smaller twin has to share its placental perfusion with the larger twin, which is a novel finding. The AA size is essential for the future of both fetuses but complicates easy understanding of (pseudo-)acardiac clinical presentations. Late acardiac onset occurs infrequently. Using nonpulsating circulations may have caused our extensive predictions of late onset. An improved model requires including hypoxemia in the smaller twin from chronic placental hypoperfusion. Birth Defects Research 109:211-223, 2017.
Authors: Martin J C van Gemert; Michael G Ross; Jeroen P H M van den Wijngaard; Peter G J Nikkels Journal: Birth Defects Res Date: 2021-12-20 Impact factor: 2.661
Authors: Martin J C van Gemert; Cees W M van der Geld; Michael G Ross; Peter G J Nikkels; Jeroen P H M van den Wijngaard Journal: Birth Defects Res Date: 2021-05-17 Impact factor: 2.344