Redistribution pattern of fetal liver circulation in intrauterine growth restriction

Cathrine Ebbing1, Svein Rasmussen, Keith M Godfrey

  • 1Department of Obstetrics and Gynecology, Haukeland University Hospital, Bergen, Norway. cathrine.ebbing@helse-bergen.no

Insights

Intrauterine growth restriction (IUGR) alters fetal liver blood flow. In IUGR, fetuses redistribute blood, increasing portal venous flow and direct arterial supply to the liver, despite reduced umbilical flow.

Area of Science:

  • Fetal Medicine
  • Cardiovascular Physiology
  • Perinatology

Background:

  • Fetal liver blood supply is crucial for growth and adaptation.
  • The umbilical vein is the primary source, with portal vein and splanchnic arteries contributing to liver perfusion homeostasis.
  • Intrauterine growth restriction (IUGR) may alter this circulatory pattern.

Purpose of the Study:

  • To investigate the fetal liver circulatory pattern in intrauterine growth restriction (IUGR).
  • To understand how blood flow is redistributed within the fetal liver in IUGR.
  • To assess the role of splanchnic arteries in maintaining liver perfusion during IUGR.

Main Methods:

  • Cross-sectional study of 31 IUGR fetuses (estimated fetal weight <5th centile).
  • Pulsatility index (PI) measurements of umbilical, middle cerebral, splenic, hepatic, and superior mesenteric arteries.
  • Assessment of umbilical venous flow, umbilico-caval pressure gradient, and intrahepatic venous distribution.

Main Results:

  • IUGR fetuses showed reduced umbilical venous flow and altered distribution to the right liver lobe.
  • A normal umbilico-caval pressure gradient was maintained.
  • Hepatic and splenic arteries exhibited low PI in IUGR fetuses, suggesting increased portal venous flow and direct arterial hepatic perfusion.

Conclusions:

  • IUGR fetuses adapt liver perfusion by maintaining venous pressure despite reduced umbilical flow.
  • Regional splanchnic arterial redistribution occurs, with low splenic and hepatic artery PI.
  • This implies increased portal venous flow and a direct arterial contribution to hepatic perfusion in IUGR.