Ductus venosus shunting in growth-restricted fetuses and the effect of umbilical circulatory compromise.
OBJECTIVE
To determine the degree of ductus venosus (DV) shunting in fetuses with intrauterine growth restriction (IUGR) and the effect of various degrees of umbilical circulatory compromise.


METHODS
This was a cross-sectional observational study. Sixty-four fetuses with IUGR (estimated weight < or = 2.5(th) percentile) underwent ultrasound examination. The diameter, velocity, and blood flow were determined in the DV and intra-abdominal umbilical vein (UV), and the fraction of shunting and DV : UV diameter ratios were calculated. Placental compromise was classified according to either normal umbilical artery (UA) pulsatility index (PI), UA-PI > 97.5(th) percentile, or absent or reversed end-diastolic flow velocity (A/REDV). Regression analysis was used to construct mean values, and SD scores were used to determine differences compared with a reference population (n = 212) after ln- or power-transformation.


RESULTS
In the 64 growth-restricted fetuses, the average DV shunting was 39% compared with 25% in the reference group (overall P < 0.0001). The corresponding values in the subgroups with normal UA-PI, UA-PI > 97.5(th) percentile, and A/REDV were 31%, 35%, and 57%, respectively. Fetuses with IUGR and normal UA-PI (SD score: mean, 0.48; 95% CI, 0.04-0.92) did not shunt significantly more than did the reference fetuses (SD score: mean, 0.0; 95% CI, - 0.15 to 0.15), but those with UA-PI > 97.5(th) percentile (SD score: mean, 0.85; 95% CI, 0.41-1.29), and particularly those with A/REDV (SD score: mean, 1.56; 95% CI, 1.0-2.12) did shunt significantly more. With more DV shunting, these fetuses distributed correspondingly less umbilical blood to the liver, one of the mechanisms being a lower perfusion pressure as reflected in the lower DV blood velocity (P < 0.0001).


CONCLUSIONS
DV shunting is higher and the umbilical blood flow to the liver is less in fetuses with IUGR, particularly in those with the most severe umbilical hemodynamic compromise.
Kiserud
T
T
Department of Clinical Medicine, Section of Obstetrics and Gynaecology, University of Bergen, Norway. torvid.kiserud@kk.uib.no
Kessler
J
J
Ebbing
C
C
Rasmussen
S
S
D001783:Blood Flow Velocity / Q000502:physiology; D016022:Case-Control Studies; D003251:Constriction, Pathologic / Q000196:embryology / Q000503:physiopathology; D003430:Cross-Sectional Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000473:pathology / Q000503:physiopathology*; D005865:Gestational Age; D006801:Humans; D008099:Liver / Q000098:blood supply* / Q000196:embryology; D008297:Male; D011169:Portal Vein / Q000196:embryology / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011256:Pregnancy Outcome; D012039:Regional Blood Flow / Q000502:physiology; D014471:Umbilical Veins / Q000196:embryology / Q000473:pathology / Q000503:physiopathology*; D014682:Vena Cava, Inferior / Q000196:embryology / Q000473:pathology / Q000503:physiopathology*