Dr. Madhavi Karki
SYMMETRICAL IUGR ASYMMETRICAL IUGR EARLY ONSET. SEEN IN 20% CASES LATE ONSET. SEEN IN 80% CASES ETIOLOGY: GENETIC DISEASE/ INFECTION (INTRINSIC TO FETUS) ETIOLOGY: CHRONIC PLACENTAL INSUFFICIENCY(EXTRINSIC TO FETUS) TOTAL CELL NUMBER : LESS, CELL SIZE : NORMAL TOTAL CELL NUMBER : NORMAL, CELL SIZE : SMALLER USG : ALL PARAMETERS (HC, BPD, AC, FL) SMALLER THAN EXPECTED USG : HEAD SPARING EFFECT, BUT ABDOMEN IS SMALL NEONATAL COURSE: COMPLICATED WITH POOR Px USUALLY UNCOMPLICATED HAVING GOOD Px
BIOPHYSICAL TEST : THE FIRST EXAM SHOULD CONFIRM THE CLINICAL ESTIMATION OF THE GESTATIONAL AGE
Fetal distress / death. Asphyxia & RDS. Hypoglycemia. Meconium aspiration syndrome. Hypothermia. Pulmonary hemorrhage. May have retarded growth . May have cardiac disease, diabetes, in adulthood, if survives. Long term complications Lower IQ, learning & behavior problems, major neurological handicap seizures, cerebral palsy, mental retardation
Adequate bed rest. Nutritional diet / iron, vitamins, calcium. No smoking / alcohol allowed. Aspirin in low dose (50 mg daily). Ultrasound monitoring of fetus should be done every 4th wks. Termination of pregnancy – beyond 37 week. Before 37 week – conservative t/t to increase placental function till fetus becomes viable.
Severe degree of IUGR – termination is to be done if lung maturation is achieved. - If lung maturation has not been achieved corticosteroid therapy (betnasol 12 mg i.m. 24 hrs apart – 2 doses given to reduce the risk of neonatal RDS) 9. CS – to be done in the case of preterm delivery & unfavorable cervix. 10. Baby should be shifted to intensive neonatal care unit.
ETIOLOGY 1. Preeclampsia/ eclampsia 2. A.P.H. 3. Diabetes 4. Severe anemia 5. Hyperpyrexia/Malaria 6. TORCH infections 8. Fetal malformations 9. Rh-incompatibility 10.Iatrogenic