Hydrostatic and osmotic pressure gradients produce manifestations of fetofetal transfusion syndrome in a computerized model of monochorial twin pregnancy.
OBJECTIVE
In spite of recent advances in the assessment and treatment of fetofetal transfusion syndrome, its underlying mechanism remains controversial. We aimed to determine whether the clinical features of fetofetal transfusion syndrome could be explained by unidirectional or bidirectional intertwin transfusion along placental vascular anastomoses.


METHODS
We constructed a dynamic computerized model of monochorial twin fetoplacental units on the basis of numerous interrelated hemodynamic, osmotic, and metabolic physiologic variables. The circulations were then linked by various combinations of direction and number of arteriovenous anastomoses.


RESULTS
With unidirectional anastomoses disease severity, characterized by disparity in blood solids, depended on donor arterial pressure but not on the number of anastomoses. In the chronic state water movement resulting from raised osmotic pressure in the recipient and reduction in the donor produced hydroosmotic pressure equilibrium, reducing anastomotic flow to near zero. Atrial natriuretic peptide-driven urine production was markedly increased in the recipient because of the raised vascular hydrostatic pressure component. With bidirectional anastomoses recirculation between twins reduced discordancy in colloids and hematocrit, and the clinical picture was determined by the degree of asymmetry in the number of connections.


CONCLUSIONS
Severe manifestations of fetofetal transfusion syndrome can be explained by unidirectional intertwin transfusion and lesser degrees by asymmetric bidirectional transfusion.
Talbert
D G
DG
Institute of Obstetrics and Gynaecology, Queen Charlotte's and Chelsea Hospital, London, United Kingdom.
Bajoria
R
R
Sepulveda
W
W
Bower
S
S
Fisk
N M
NM
D001163:Arteriovenous Anastomosis; D009320:Atrial Natriuretic Factor / Q000502:physiology; D001794:Blood Pressure; D003198:Computer Simulation; D004231:Diuresis; D005260:Female; D005330:Fetofetal Transfusion / Q000503:physiopathology*; D006801:Humans; D006874:Hydrostatic Pressure; D008954:Models, Biological; D009997:Osmotic Pressure; D011247:Pregnancy; D014430:Twins, Monozygotic; D014655:Vascular Resistance
D009320:Atrial Natriuretic Factor