Fetal Growth Restriction Is Associated With Prioritization of Umbilical Blood Flow to the Left Hepatic Lobe at the Expense of the Right Lobe

Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Pediatric Research (Impact Factor: 2.31). 04/2009; 66(1):113-7. DOI: 10.1203/PDR.0b013e3181a29077
Source: PubMed


Eighty to 85% of the venous perfusion to the fetal liver is from the umbilical vein, the rest from the portal vein. Umbilical venous flow to the liver is essential for intrauterine growth, and is impaired in placental insufficiency. We hypothesized that in growth-restricted fetuses portal blood flow compensates for insufficient umbilical blood flow to the liver. In 29 fetuses with fetal growth restriction (estimated fetal weight < or =5th percentile), we used ultrasound to measure blood flows in the umbilical vein, ductus venosus, left portal vein, and main portal stem. Compared with normal fetuses, both absolute and normalized total venous liver blood flows were reduced in growth-restricted fetuses, related to the degree of placental compromise and equally affecting both liver lobes. However, portal replaced umbilical flow to the right lobe, in a manner graded according to placental vascular resistance; in extreme cases, the right lobe received no umbilical perfusion. In fetal growth restriction, the liver suffers from venous hypoperfusion, and portal blood partially replaces umbilical flow to the right lobe; this will result in right liver lobe hypoxemia. This striking prioritization in nutrient delivery of left over right lobes suggests an adaptive response to poor placental perfusion that may have functional consequences.

Download full-text


Available from: Jörg Kessler, Sep 29, 2015
28 Reads
  • Source
    • "There is a finely tuned distribution between these sources with 85% umbilical blood as the main venous supply [4]. In cases of reduced umbilical circulation and fetal growth restriction, the portal contribution [5] and hepatic artery hemodynamics [6] suggest operation of a buffer response in the human fetus [7] which partially compensate the low umbilical flow, but with a reduced oxygenation of the right liver lobe as a consequence . Assuming that the fetal liver in such conditions is at increased risk of hypoxic injury, we hypothesize that alanine (ALT) and aspartate (AST) aminotransferases are increased in fetuses with IUGR. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The accepted standard for assessing the wellbeing of the newborn is the Apgar score and blood gas analysis. However, the prediction of neonatal morbidity or mortality is limited. In small-for-gestation (SGA) fetuses at 18-38 weeks of gestation, pO(2) is <5th centile both in the umbilical artery and vein in 30%. In a previous study in singleton term neonates cardiac specific enzymes (B-type natriuretic peptide, BNP and cardiac troponin T, cTnT) are increased in growth-restricted fetuses compared with normals. To test the hypothesis, that fetuses with intra uterine growth restriction (IUGR) have elevated AST (GOT) and ALT (GPT) aminotransferases as a result of hypoxic liver cell injury, and to establish references ranges. Prospective cohort study, serum of umbilical artery (n=156) and vein (n=180), 599 normal singletons at 37(+0)-42(+0)weeks, neonates with IUGR (n=41), analysis for pH, birthweight and maternal weight, spontaneous vs cesarean section, vein vs artery and for the sex. Aspartate aminotransferase (AST, GOT) and Alanine aminotransferase (ALT, GPT) were measured in normals and IUGR neonates. Neonates with IUGR (n=41) had AST values that were not different from the reference group, but had significantly lower ALT (-1.49, 95% CI -1.98 to -1.00 vs 0.14, 95% CI -0.42-0.13), (p<0.001), (Fig. 3). In neonates with IUGR, hypoxic hepatic injury markers in cord blood were not elevated. Rather, a substantially reduced ALT suggests a down-regulated hepatic activity.
    Early human development 12/2011; 88(7):461-5. DOI:10.1016/j.earlhumdev.2011.11.001 · 1.79 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Fetal growth restriction (FGR) due to placental dysfunction has important short- and long-term impacts that may reach into adulthood. Early-onset FGR before 34 weeks' gestation shows a characteristic sequence of responses to placental dysfunction that evolves from the arterial circulation to the venous system and finally to biophysical abnormalities. In this form of FGR safe prolongation of pregnancy is a primary management goal, as gestational age at delivery, birth weight and iatrogenic premature delivery have an important impact on short-term outcome and neurodevelopment. Surveillance intervals should be adjusted based on umbilical artery and venous Doppler studies. Intervention thresholds need to be based on the balance of fetal vs. neonatal risks and therefore critically depend on gestational age. Late-onset FGR presents with subtle Doppler and biophysical abnormalities and therefore poses a diagnostic dilemma. Often unrecognized, term FGR contributes to a large proportion of adverse perinatal outcome. Monitoring intervals should be adjusted based on middle cerebral artery Doppler and fetal heart rate parameters. Delivery timing thresholds can be low. In both forms of FGR neurodevelopmental impacts of placental disease occur before clinical decisions regarding delivery timing arise. This places special emphasis on future preventative studies.
    Journal of Perinatal Medicine 03/2010; 38(3):239-46. DOI:10.1515/JPM.2010.041 · 1.36 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The human fetal venous system is well-recognized as a target for investigation in cases of circulatory compromise, and a broad spectrum of malformations affecting this system has been described. In Part I of this review, we described the normal embryology, anatomy and physiology of this system, essential to the understanding of structural anomalies and the sequential changes encountered in intrauterine growth restriction and other developmental disorders. In Part II we review the etiology and sonographic appearance of malformations of the human fetal venous system, discuss the pathophysiology of the system and describe venous Doppler investigation in the fetus with circulatory compromise.
    Ultrasound in Obstetrics and Gynecology 07/2010; 36(1):93-111. DOI:10.1002/uog.7622 · 3.85 Impact Factor
Show more