1. Intra Uterine Growth Retardation

2. What is the definition of IUGR? < 10th centile for age  include normal fetuses at the lower ends of the growth curve + fetuses with IUGR This definition is not helpful clinically < 5th centile for age  < 3rd centile for age  the most appropriate definition but associated with adverse perinatal outcome

3. IUGR  Failure of the fetus to chieve the expected weight for a given gestation What is the deference between IUGR & SGA? SGA  < 10th centile for the population, which means it is at the lower end of the normal distribution ie. Constitutionally small but have reached their full growth potential

4. Small for Gestational Age SGA infants are those with weights below the 10 percentile for their gestational age

5. The neonatal mortality rate of a SGA infant born at 38 weeks 1% compared 0.2% in those with AGA * AGA -appropriate for gestational age

6. Incidence 3 -10 % of infants are growth restricted

7. 25 -60 % of infants conventionally diagnosed to be SGA were in fact AGA when Determinant of birth weight such as maternal * Ethnic group * Parity * Weight * Height

8. MORTALITY & MORBIDITY Fetal demise Birth asphyxia Meconium aspiration Neonatal hypoglycemia Hypothermia Abnormal neurological development

9. ACCELERATED MATURATION

10. Accelerated maturation The fetus resoponses to stressed envirorment by adrenal glucocorticoid Earlier or accelerated maturation

11. SYMMETRICAL VERSUS ASYMMETRICAL GR..

12. Fetal growth has been divided into three phases. 1-cellular hyperplasia 2- hyperplasy & hypertrophy 3- hypertrophy  cell size  fat deposition  fetal weight as much as 200 G.r. per week.

13. symmetrical An early insult due to : chemical viral aneuploidy  Cell size  Cell num. Proportionate reduction in head & body

14. A late pregnancy insult such as placental insufficiency would affect cell size. Asymmetrical

15. The ratio of brain weight to liver weight over in the last 12 wk of pregnancy is increased to 5/1 or more

16. Growth pattern may potentially reveal the cause

17. In practice accurate identification of symmetrical versus asymmetrical fetus has proved difficult.

18. *Maternal *fetal *placental and cord abn. Risk factors for FGR * FGR - fetal growth retardation

19. *Constitutionally small mother *Poor maternal weight gain & nutrition *Social deprivation Maternal causes

20. *vascular disease *maternal anemia *anti phospholipid Ab syn. *Extra uterine pregnancy *chronic renal disease

21. *fetal infections *congenital malformations *chromosomal abnormalities *trisomy 16 *multiple fetus FETAL CAUSES

22. Placental and cord abnormalities chromic partial placental sep. extensive infarct. Chorioangioma placenta previa

23. ADDITIONAL INSIGHT OF FGR

24. These fetus also had Ê Hypoglycemia Ë hypoinsulinemia Ì glycin/valin Í hypertriglycemia Î thrombocytemia

25. *Early establishment of G.A *Attention to maternal weight gain *Measurement of uterine height throughout pregnancy Screening and identification of F.G.R

26. Identification of risk factors A previously GR fetus in women with significant risk factors Serial sonography

27. Definitive diagnosis usually can not be made until delivery.

28. MANAGEMENT Once a SGA is suspected, intensive effort should be made to determine if GR is present and if so, its type and etiology.

29. In the presence of sonographically detectable anomalies, cordocentesis may be performed for kariotyping.

30. Prompt delivery is likely to afford the best outcome for the GR fetus GR. NEAR TERM

31. In the presence of significant oligohydraminos most fetus will be delivered if G.A has reached>34 wk.

32. Such often tolerate labor less than AGA and C/S is indicated for intrapartum fetal compromise. Unfortunately

33. Importantly Uncertainly about the diagnosis of GR should preclude intervention until fetal lung maturity is assured.

34. GR. REMOTE FROM TERM before 34 wk Normal Amniotic volume Normal fetal surveillance Observation Sono is repeated at interval 2-3 wk

35. Pregnancy is allowed to continue until fetal maturity is achieved.

36. At times amniocentesis for assessment of pulmonary maturity may be helpful in clinical decision making.

37. There is no specific treatment that will ameliorate the condition

38. Many clinicians advised a program of modified rest in the lateral recumbent position in which c.o.p and placental perfusion is maximized. Many clinicians advised a program of modified rest in the lateral recumbent position in which c.o.p and placental perfusion is maximized.

39. Optimal management of the preterm GR fetus remain undefined.

40. Mortality and morbidity in GR fetuses were determined by GA and birth weight and not by abnormal fetal testing.

41. Early anti platelet therapy with low dose aspirin may prevent *uretroplacental thrombosis *placental infarction *idiopathic GR in women with a Hx of recurrent sever GR

42. LABOR AND DELIVERY

43. FHR MONITORING

44. GR is the result of insufficient placental function  A.f cord compression breech presentation  c/s

45. Expert assistance *In making a successful transition to air breathing *clear the airway below the vocal cord *ventilate the infant as needed

46. The severely GR newborn is susceptible to *Hypothermia *serious hypoglycemia *polycytemia *hyper viscosity

47. Prolonged symmetrical FGR is likely to be followed by slow growth after birth. Subsequent development of the GR

48. The asymmetrically GR is more likely to catch up after birth.

49. NEUROLOGICAL AND INTELLECTUAL CAPABILITY

50. A LONG TERM FABORABLE OUT COME MAY BE EXPECTED.

51. In a 9-11 year follow up study learning deficit in almost half of GRF

52. A significant association between fetal growth restriction and cerebral palsy.

53. The risk of recurrent FGR is increased in women *Who have previously had this complication *With Hx of FGR &A continuing medical complication