Fetal Growth by Dr M. H. L. Snow (auth.), F. Sharp MD, FRCOG, R. B. Fraser

By Dr M. H. L. Snow (auth.), F. Sharp MD, FRCOG, R. B. Fraser MD, FRCOG, DCH, R. D. B. Milner MA, ScD (Cantab), MD (Lond), FRCP (Lond) (eds.)

This publication relies at the twentieth examine crew of the Royal collage of Obstetricians and Gynaecologists, which involved the real subject of fetal development. uncomplicated clinical, and either obstetric and paediatric features of the topic have been addressed in contributions from many various disciplines, and we're enormously indebted to all of the overseas specialists who took half during this workshop on the RCOG in London in November 1988. The deliberations lined the large themes of standard fetal development, fetal over­ progress and undergrowth. medical implications of those entities, specially fetal undergrowth, performed a wide half within the court cases as dictated through c.1inical con­ cerns. Definitions, epidemiology, aetiology and screening have been lined, as have been technological advancements, with particular connection with blood movement and quantity circulation measurements, either fetal and placental. different facets of medical fetal tracking, together with fetal job size, and biophysical evaluate have been rationalised and put in context, and the $64000 newly rising parts of cordocentesis and treatment in IUGR addressed. ultimately, neonatal administration of the SGA child, mortality and long term morbidity have been considered.

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Placental control of fetal metabolism Professor W. W. Hay, Jr. INTRODUCTION The placenta is an organ that exchanges heat and matter between the fetal and maternal circulations. This exchange is the principal means by which the placenta controls fetal metabolism. This review will focus on the placental exchanges of nutrient substrates and how these affect fetal energy and protein metabolism. g. g. progesterone, oestrogen, placental lactogen) are equally important but beyond the scope of this review.

_"____~ 20 40 60 80 100 120 140 160 MATERNAL ARTERIAL BLOOD GLUCOSE (mg/dl) Figure II. (5) Transplacental glucose gradient Widdas first proposed that maternal-to-fetal placental glucose transfer was carrier mediated according to a Michaelis-Menton model:(6) Qf = Vmax {[GA/ (GA + Km)] - [Ga / (Ga + Km)]} where Vmax represents the maximal flux of glucose, Km is the concentration of glucose at which the carriers are 50% saturated and Qf = Vmax/2, and GA and Ga represent the glucose concentrations in maternal and fetal arterial plasmas, respectively.

Thompson HE. Holmes JH. Gottesfeld KR. Taylor ES. Fetal development as determined by pulsed echo techniques. Arner J Obstet Gynec 1965; 92:44-49. 10. Campbell S. Warsof SL. Little D. Cooper DJ. Routine ultrasound screening for the prediction of gestational age. Obstet Gynecol1985; 65:613-620. II. Persson PH. Weidner BM. Reliability of ultrasound fetometry in estimating gestational age in the second trimester. Acta Obstet Gynecol Scand 1986; 65:481-483. Fctal growth ClIITCS 25 12. Persson PH, Weidner 8M.

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