Patterns of Fetal Growth ormai fetal growth is characterized by a gontinuous progression throughout pregnancy. From the normal fetal weight growth curves one can discern several features, A maximum rate of growth at around 30 to 32 weeks (and derivative = (0) and a relative slowing in the last. few weeks of gestation. If length is used es Parameter peak growth occurs earlier at around 20 weeks “(2nd derivative = 0) although a Similar lowing is also observed later in the Pregnancy. Intrauterine growth restriction (0GR) ‘can manifest in two ways: as symmetric IUGR and asymmetric IUGR.” symmetric IUGR Since it affects both length and weight Figure Symmeric UR Measurements reflects a factor that operates in the first trimester. Asymmetric IUGR on the other hand usually involves a process that affects growth after 27 weeks. The result will be “a disproporticnately low weight in relation to weight. Both of these patterns ‘Cowan sty amt i are depicted on the right. Generally To] Simettle Tock nes ‘terse prognosis than thy ee , Mimeceic variety.” Te bode dacea® ene" She weusctoepuny Of. Growth support may benefit from” early a delivery. Treatable causes of IUGR must first wre NomalPatensot be identified, if possible and addressed. Gow Etiology anatomically speaking there are ogee ieee three possibilities for the etiology of TUGR: causes attributable to the fetus, causes attributable to the placenta and maternal causes. The work-up for IUGR is guided by these considerations which are detailed in table form below ( tateriat couses |” “Fiacentell Causes” ‘Fetal Cause: Nutritional (fanine, 180, post-op + Abnormal Cord Insertion Chromosomal abnornalitie Pancreatitis! + multiple infarcts + Inborn arrore of Metabolien + myporie (asthna, cystic sbrosis Cee = ee cyanotic heart disease, bronchiectasis, Mis = 7 Spnoscoifosiay + abruptio Placenta Viren ice, mubetia, Herpes, * Vascular (preeclampsia, chronic HIN, ¢-—CArcumvalate Placenta Varicella} collagen vascular sisease, st) + multiple ostation ¢ Bacterial (oyphilia, Listeria + Renat (glonerutonephritis, lipid 3 ees + Protoroal (Toxo, Maleria, Rephrosis, arteriolar nephroscierosis) Chortoenat Chases) + Menstologic (SCD) + Malformations (Microcepnaly, ‘dnencephaly, cV/c1/GU defects, + maviromental (nigh altitude, anoking Anencen a i Eigoholy nerain” aechadone, oteine sqeleces dyeplacias, ventral sreinecinofites, Satlccagslante, antieonvvleanes! Work-up tne work-up progresses from maternal to placental to fetal es shown in figure 4. As the desree of being IUGR is being assessed one continues to cycle through the Doppler, FHR, FM, USG, AFI and BPP studies. Management invoives first addressing any treatable causes (euch as intercurrent systenic disease or Sntection) and secondly edifying the extrauterine enviroment with Reasures such a2 bed Test ang iV hydration. Figure 5 shows 10ch due co severe mavernal inflammatory bowel disease “which wes Feversed with total parenteral mitrivion YF FigureS Severe 1UGR and mater igre 4 Workup of1UGR with TPN a 26 weeks References moore 7, (1999), Gynecology & obstetrics, churchill Livingstone, view York. Source for figure 1 Greasy, AK ang Resnik R, (13941, Maternal-Fetal Medicine, 3rd e0., MB Saunders, Philadelphia, Soures for figure $ See the articles in Clin. cbse & Gmnecclogy, (1992), Vol. 38, Ne i, particularly Clerk Si “Fatterse ef inerauterine Growth