2. FETAL GROWTH geneticmaternalplacental

3. FETUS HEALTHY NEWBORN & APPR- SIZE Normal circumstances Inheritance Growth potential Introduction

4. Growth potential Environ- ment Ability to reach optimal birth weight Introduction

5. Slow Growth 0 to 15-16 weeks Less than 10 grams/weeks Accelerating Growth 10-17 to 26-27 weeks 85 grams/weeks Maximum Growth 26-27 to 37-38 weeks 200 grams/week Decelerating Growth 37-38 to 44 weeks More than 70 grams/week The normal rate of fetal growth in an ideal cases is limited by its internal constraints (genetic in nature)

6. Introduction

7. Oxygen Glucose Amino Acids Fetal requirement

8. Simple Diffusion Facilitated Diffusion Active Transport

9. Persistent decrease in availability of any of these substrates  limit the ability of the fetus to reach its growth potential Persistent and severe substrate deficiency  threaten the ability of the fetus to survive So many factors associated with reducing substrates supplies to the fetus

10. Intrauterine Growth Retardation Intrauterine Growth Restriction Abnormal Mental Function Slow Growth or Ceases Fetal weight ≤ 10th percentile for gestational age and sex/SGA Present of pathological process Fetal weight ≤ 10th percentile for gestational age and sex/SGA Present of pathological process

11. SGA is defined as birth weight: At 10th or less percentile, or At 5th or less percentile, or At 3rd or less percentile, or 2 SDs below the mean for gestational age The lower cut-off  incidence  and morbidity and mortality 

12. Cut-off 10th percentile: SGA : 3—7 % IUGR: 3 quarter (failed to achieve its potential growth) Non-IUGR: 1 quarters (constitutionally small)

13. Risk factors IUGR occurs when gas exchange and nutrient delivery to the fetus are not sufficient The process occur primariliy because of: Maternal disease causing decreased oxygen-carrying capacity A dysfunctional oxygen delivery system secondary to maternal vascular desease Placental damage resulting from maternal disease Many factors: fetoplacental fac tors and maternal factors

14. Constitutionally small mother Small women have smaller baby Reduced intrauterine growth of mother  reduced intrauterine growth of her children Environment more important than genetic contribution Poor maternal weight gain and nutrition Lack of weight gain in the second trimester associated with fetal growth restriction Social deprivation Associated to lifestyle factors such as smoking, alcohol or other substances abuse and poor nutrition

15. Fetal infections Viral, bacterial, protozoon, and spirochaetal  implicated on fetal growth restriction CMV  direct cytolysis and loss functional cells Rubella  vascular deficiency Another infection affect fetal growth : hepatitis A and B, Listeriosis, TB, Syphilis, Toxoplasmosis and Congenital Malaria Congenital malformations More severe malformation  more likely fetus to be small Espescially with chromosomal abnormalities or serious cardiovascular malformations

16. Chromosomal abnormalities Autosomal trisomies related togrowth restriction Trisomy 18, 13 and 21 Not seen in Turner or Klinefelter Syndrome Trisomi 16 Patches of trisomy 16  confined placental mosaicism  placental insufficiency  fetal growth restriction Primary disorders of cartilage and bone Osteogenesis imperfecta Various chondrodystrophies

17. Chemical teratogens Anticonvulsants (phenitoin, trimethadione) Cigarette Narcotics Alcohol Cocaine Vascular disease Chronic vascular disease especially when further complicated by superimposed preeclampsia Chronic renal disease Renal disease maybe accompanied by restricted fetal growth

18. Chronic hypoxia Women in high altitude Cyanotic heart disease Maternal anemia Anemia does not cause growth restriction (in most cases) Except : sickle cell disease inherited anemia with serious maternal disease deficient total blood volume early in pregnancy

19. Placental and cord abnormalities Chronic partial placental separation Extensive infarction Chorioangioma Marginal insertion of the cord Velamentous insertion of the cord Multiple fetuses Two or more fetuses more likely complicated by diminished growth of one or both fetuses compared with normal singleton

20. Antiphospholipid antibody syndrome Two classes of antiphospholipid antibodies : Anticardiolipin antibodies Lupus anticoagulant Pathophysiological mechanism  maternal platelet aggregation & placental thrombosis Extrauterine pregnancy Fetus gestated outside uterus is usually growth restricted Also some maternal uterine malformations

21. Pathogenesis & Categories There are standards and averages in weight according to gestational age (weeks) Using a fetal growth curve derived from one population and applyng to another  over- or underestimation of true incidence of SGA A population of smaller individual will have smaller babies  the difference lies in genetic growth potential

22. Normal intrauterine growth pattern: 1st stage: 4—20 weeks gestation,  rapid cell division and multiplication (hyperplasia) 2nd stage: 20—28/32 weeks gestation,  cell division (hyperplasia)  and cells increase in size (hypertrophy) 3rd stage: 28/32—40 weeks gestation,  rapid increase in cell size, rapid accumulation of fat, muscle and connective tissue 95% offetal weight gain occurs during the last 20 weeks If development and weight gain is disturbed or interrupted  restricted growth

23. Fetal weight below tenth percentile Pathological process present

24. IUGR First Stage Hyperplactic Stage Symmetric Stage 2 Hyperplastic and Hypertrophic Stage Stage 3 Hypertrophic Stage Asymmetric

25. Pathogenesis & Categories

26. Symmetrical Growth Restriction Growth inhibition during first stage  undersized fetus with fewer cells but normal size Weight, head and length < 10th percentile  proportionally small Condition associated include genetic (constitutional, chromosomal and single gene defect, deletion disorders and inborn error of metabolism), congenital anomalies, intrauterine infections, and therapeutic iradiation

27. Asymmetrical Growth Restriction Growth inhibition during stage 2 and 3  decreased of cell size and fetal weight with less effect on total cell number fetal length and fetal head circumference Implies fetus who is undernourished and directing most of its energy to maintainaning growth of vital organs such as brain and heart at the expensive of the liver, muscle and fat  role of brain sparing effect (redistribution mechanism)

28. Asymmetrical Growth Restriction Normal head but small abdominal circumference, scrawny limbs and thinned skin Condition associated include uteroplacental insufficiency (chronis hypertension or preeclampsia), chronis renal disease, cyanotic heart disease, hemoglobinopathies, placental infarcs, abruptio placenta, multiple gestation, velamentous insertion, cirmcumvallate placenta and high altitude

29. Antepartum Complications Stillbirth Oligohydramnios Intrapartum fetal acidosis

30. Neonatal Complications Meconium aspiration syndrome Persistent fetal circulation Hypoxic-ischemic encephalopathy Hypoglicemia Hypocalcemia Hyperviscosity syndrome Deficient temperature controle

31. IUGR is a part of SGA with present of pathological process Growth restricted fetus have a great chance to suffer from many prenatal and/or neonatal complications Many factors should be recognized Impaired substrates supply may reduce cellular process resulting in symmetrical or asymmetrical IUGR