Neoreviews
HOME HELP CONTACT US SUBSCRIPTIONS CME ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Take the CME quiz:
 Vol. 7 No. 4, April 2006
Right arrow E-Letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-Letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fouron, J.-C.
Right arrow Articles by Audibert, F.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Fouron, J.-C.
Right arrow Articles by Audibert, F.

NeoReviews Vol.7 No.4 2006 e195
© 2006 American Academy of Pediatrics

Best Timing of Birth in Placental Insufficiency

Jean-Claude Fouron, MD*
François Audibert, MD{dagger}

* Fetal Cardiology Unit, Cardiology Service, Department of Pediatrics, St. Justine Hospital, University of Montreal, Montreal, Canada
{dagger} Division of Maternal-Fetal Medicine, Department of Obstetrics, St. Justine Hospital, University of Montreal, Montreal, Canada

The first 300 words of the full text of this article appear below.


   Objectives
 
After completing this article, readers should be able to:

  1. Explain the pathophysiology of fetal hypoxemia during uteroplacental circulatory insufficiency (UPI).
  2. Describe the effect of UPI on nutritional substrates.
  3. Delineate the potential and limitations of using Doppler flow velocity waveforms to guide delivery decisions in the presence of intrauterine growth restriction.


   Introduction
 
Uteroplacental circulatory insufficiency (UPI) accounts for more than 70% of intrauterine growth restriction (IUGR) (1) and is associated with an increased risk of hypoxemic stress and nutritional deficiency. Both of these threats are concomitant and, to some extent, interrelated, but more importantly, both could lead to the feared complication of UPI—cerebral damage and secondary neurodevelopmental disabilities. To better appreciate the challenge involved in establishing the best time to deliver fetuses that have placental insufficiency, this article is divided in two parts. In the first section, present knowledge of the pathophysiology of fetal hypoxemia and nutritional deficiency in the context of UPI is reviewed briefly. The second section is devoted to a critical appraisal of the criteria currently applied to reach the decision that a fetus that has IUGR should be delivered.


   Fetal Hypoxemia During UPI
 
Fetal arterial oxygen (O2) concentrations are the result of relative proportions of blood that has different O2 saturations from various venous channels (the two venae cavae, the pulmonary veins, the coronary sinus, and the umbilical vein) draining into the cardiac cavities. Final arterial O2 saturation, therefore, predominantly is dictated by the volume of better-oxygenated blood arriving from the umbilical circulation. Normally, because of its low vascular resistance, the placenta accommodates 50% of the fetal combined cardiac output. Any change in this determinant part of venous return necessarily has a significant impact on intrauterine O2 delivery, even if PO2 in the umbilical vein is within normal range. Experimental (2)(3) and clinical (. . . [Full Text of this Article]






HOME HELP CONTACT US SUBSCRIPTIONS CME ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Academy of Pediatrics.