Why does second trimester demise of a monochorionic twin not result in acardiac twinning?
| Autor: | Peter G. J. Nikkels, Michael G. Ross, Cees W. M. van der Geld, Martin J. C. van Gemert, Jeroen P. H. M. van den Wijngaard |
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| Přispěvatelé: | Process and Product Design |
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Embryology medicine.medical_specialty Health Toxicology and Mutagenesis Placenta vascular resistance model Blood volume 030105 genetics & heredity Anastomosis Toxicology blood perfusion 03 medical and health sciences monochorionic twin pregnancy Pregnancy AA and VV placental anastomoses Internal medicine medicine Diseases in Twins Humans Fetal Death deceased twin Fetus business.industry modeling venous compliance Fetofetal Transfusion Twins Monozygotic Hypothesis 030104 developmental biology medicine.anatomical_structure Pregnancy Trimester Second Pediatrics Perinatology and Child Health Vascular resistance Cardiology Arterial blood Female second trimester exsanguination Crystal twinning business Perfusion Developmental Biology |
| Zdroj: | Birth Defects Research Birth Defects Research, 113(15), 1103-1111. Wiley |
| ISSN: | 2472-1727 |
| Popis: | Background: We previously explained why acardiac twinning occurs in the first trimester. We raised the question why a sudden demised monochorionic twin beyond the first trimester does not lead to acardiac twinning. We argued that exsanguinated blood from the live twin would strongly increase the demised twins' vascular resistance, preventing its perfusion and acardiac onset. However, our current hypothesis is that perfusion of the demised twin does occur but that it is insufficient for onset of acardiac twinning. Methods: We analyzed blood pressures and flows in a vascular resistance model of a monochorionic twin pregnancy where one of the fetuses demised. The resistance model consists of a demised twin with a (former) placenta, a live twin and its placenta, and arterioarterial (AA) and venovenous placental anastomoses. We assumed that only twins with a weight of at least 33% of normal survived the first trimester and that exsanguination of more than 50% of its blood volume is fatal for the live twin. Results: At 20 weeks, only AA anastomoses with radii ≲1 mm keep the exsanguinated blood volume below 50%. Then, perfusion of the deceased body with arterial blood from the live fetus is about 5–40 times smaller than when that body was alive. Beyond 20 weeks, this factor is even smaller. At 14 weeks, this factor is at most 2. Conclusion: We hypothesize that this small perfusion flow of arterial blood prevents further growth of the deceased body and hence precludes onset of acardiac twinning. |
| Databáze: | OpenAIRE |
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