Redistribution pattern of fetal liver circulation in intrauterine growth restriction

Ebbing, Cathrine, Rasmussen, Svein, Godfrey, Keith M., Hanson, Mark A. and Kiserud, Torvid (2009) Redistribution pattern of fetal liver circulation in intrauterine growth restriction. Acta Obstetricia et Gynecologica Scandinavica, 88 (10), 1118-1123. (doi:10.1080/00016340903214924).

Abstract

Objective

Fetal liver blood supply is an important determinant of fetal growth and adaptation. Most fetal liver blood supply is from the umbilical vein, but the portal vein contributes 14-20% and studies of low-risk pregnancies suggest the splanchnic arteries are also involved in the homeostasis of fetal liver perfusion.

Here we determine the circulatory pattern of the fetal liver in intrauterine growth restriction (IUGR). Design. Cross-sectional study. Population. Thirty-one IUGR fetuses (estimated fetal weight <5th centile).

Methods

Pulsatility index (PI) measurements of the umbilical, middle cerebral, splenic, hepatic, and superior mesenteric arteries were compared with a reference population and related to umbilical venous flow, umbilico-caval pressure gradient (assessed by ductus venosus peak velocity) and venous distribution within the liver (assessed by flow velocity in the left portal vein).

Results

Thirteen of 31 IUGR fetuses had umbilical artery PI > 97.5 centile and 13 showed a middle cerebral artery brain-sparing pattern (PI Z-score < - 2). In IUGR, umbilical venous flow was lower and less umbilical blood was distributed to the right liver lobe, while the umbilico-caval pressure gradient was kept normal. The hepatic and splenic arteries, but not the superior mesenteric artery, had low PI compared with the reference population.

Conclusions

IUGR fetuses with increased or normal umbilical artery PI maintained venous perfusion pressure to the liver while distributing less umbilical blood to the right liver lobe. They showed regional splanchnic arterial redistribution with low splenic and hepatic artery PI, implying increased portal venous flow and direct arterial contribution to hepatic perfusion, respectively.

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Contributors

Author: Keith M. Godfrey

Author: Mark A. Hanson

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