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INTRA UTERINE GROWTH RETARDATION
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INTRA UTERINE GROWTH RETARDATION

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Care of IUGR babies

Care of IUGR babies

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  • 1. IUGR PRESENTED BY AMRUTHA R 1st yr MSc nsg 18-03-2013 CHILD HEALTH NURSING
  • 2. SGA IUGR
  • 3. NORMAL FOETAL GROWTH • Cellular hyperplasia • Hyperplasia and hypertrophy • hypertrophy
  • 4. Stages • Stage I (Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA content
  • 5. Stages • Stage II (Hyperplasia & Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.
  • 6. Stages • Stage III ( Hypertrophy) - 28 to 40 weeks - Rapid increase in cell size. - Rapid accumulation of fat, muscle and connective tissue. • 95% of fetal weight gain occurs during last 20 weeks of gestations.
  • 7. CAUSES OF IUGR • • • • Maternal factors Fetal factors Placental factors Environmental factors
  • 8. MATERNAL FACTORS • Medical disease • Malnutrition  BMI < 19 twice the risk of IUGR • Multiple pregnancy • Smoking (460 gm < then none smoker)
  • 9. MATERNAL FACTORS • Alcohol  12-fold increase risk of IUGR • Drugs  Beta- Blockers(Atenolol in second trimster, Anticoagulants, Anticonvulsants( phenytoin) • Hypoxemia • Infections  UTI, Malaria, TB, Genital Infections
  • 10. MATERNAL FACTORS • • • • Small stature/ low pre-pregnancy weight Teen pregnancy Primi gravida Grand multiparity
  • 11. FETAL FACTORS • A Chromosome Defect In second trimester 20% SGA fetuses have chromosomal abnormality  Triploid is most common under 26 wks.  Trisomy-18 is common after 26 wks .  Other are 21(Down’s syndrome), 16, 13, xo (turner’s syndrome).
  • 12. FETAL FACTORS • Exposure to an infection• German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus
  • 13. FETAL FACTORS • birth defects • (cardiovascular, renal, anencephally, limb defect, etc). • A primary disorder of bone or cartilage. • A chronic lack of oxygen during development (hypoxia • Placenta or umbilical cord defects.
  • 14. PLACENTAL FACTORS • Uteroplacental Insufficiency Resulting From -. – Improper / inadequate trophoblastic invasion and placentation in the first trimester. – Lateral insertion of placenta. – Reduced maternal blood flow to the placental bed.
  • 15. PLACENTAL FACTORS • Fetoplacetal Insufficiency Due To-. – Vascular anomalies of placenta and cord. – Decreased placental functioning mass-. • Small placenta, abruptio placenta, placenta previa, post term pregnancy
  • 16. Normal & IUGR Newborn babies
  • 17. Normal & IUGR Placentas
  • 18. Environmental Causes of IUGR • High altitude - lower environmental oxygen saturation • Toxins
  • 19. Types of IUGR • Symmetric IUGR: (33 % of IUGR Infants) • Asymmetric IUGR (55 % of IUGR) • Combined type IUGR: (12 % of IUGR)
  • 20. SYMMETRICAL • height, weight, head circ proportional • early pregnancy insult: • commonly due to congenital infection, genetic disorder, or intrinsic factors • Reduced no of cells in fetus • normal ponderal index • low risk of perinatal asphyxia • low risk of hypoglycemia
  • 21. PONDERAL INDEX • The ponderal index is used determine those infants whose soft tissue mass is below normal for their stage of skeletal development. Ponderal Index = birth weight x 100 crown-heel length
  • 22. PONDERAL INDEX • Typical values are 20 to 25. • Those who have a ponderal index below the 10th % can be classified as SGA • PI is normal in symmetric IUGR. • PI is low in asymmetric IUGR
  • 23. ASSYMETRICAL • later in pregnancy: • commonly due to utero placental insufficiency, maternal malnutrition, hypoxia, or extrinsic factors • low ponderal index • Cell number remains same but size is small • increased risk of asphyxia • increased risk of hypoglycemia
  • 24. • Growth restriction in the stage of hypertrophy • Brain sparing effect • Head growth remains normal but abdominal girth slows down
  • 25. Newer Classification: 1. Normal Small Fetuses- Have no structural abnormality, normal umbilical artery & liquor but wt., is less. They are not at risk and do not need any special care.
  • 26. Abnormal Small Fetuses- have chromosomal anomalies or structural malformations. They are lost cases and deserve termination as nothing can be done. Growth Restricted Fetuses- are due to impaired placental function. Appropriate & timely treatment or termination can improve prospects.
  • 27. CLINICAL FEATURES
  • 28. Weight deficit Large head circumference Old man look Cartilaginous ridges on pinna Dry wrinkled skin
  • 29. Length remain unaffected Open eyes Well defined creases Alert and active Normal reflexes Normal cry Thin umbilical
  • 30. • Scaphoid abdomen
  • 31. • Signs of recent wasting - soft tissue wasting - diminished skin fold thickness - decrease breast tissue - reduced thigh circumference • Signs of long term growth failure - Widened skull sutures, large fontanelles - shortened crown – heel length - delayed development of epiphyses
  • 32. PREDICTION OF IUGR • History risk factors last menstrual period - most precise size of uterus time of quickening (detection of fetal movements) • Examination /
  • 33. MATERNAL SERUM SCREENING • AFP • more for gestation in the absence of fetal anomaly, there is a 5-10 fold increase in the risk of FGR
  • 34. • Uterine Artery Doppler Velocimetry - Notching of the waveform /reduce EDF associated 3-fold increase in risk of FGR. • Bright or echogenic fetal bowel in the second trimester is associated with increase risk of FGR.
  • 35. • Combination of un-explain elevated maternal AFP is powerful predictor of adverse perinatal outcome (FGR) • Increase AFP combine with echogenic bowel is strong predictor of FGR
  • 36. • DOPPLER OF THE UMBILICAL ARTERY • Reduced end diastolic flow. • Absent end diastolic flow • Reversed end diastolic flow( severe cases)
  • 37. Problems • Hypoxia - Perinatal asphyxia - Persistent pulmonary hypertension - meconium aspiration • Thermoregulation - Hypothermia due to diminished subcutaneous fat and elevated surface/volume ratio
  • 38. Metabolic - Hypoglycemia - result from inadequate glycogen stores. - diminished gluconeogenesis. - increased BMR - Hypocalcemia - due to high serum glucagon level, which stimulate calcitonin excretion
  • 39. • Hematologic - hyperviscosity and polycythemia due to increase erythropoietin level sec. to hypoxia • Immunologic - IUGR have increased protein catabolism and decreased in protein, prealbumin and immunoglobulins, which decreased humoral and cellular immunity.
  • 40. • Fetal distress, • Hypoxia, Acidosis and Low Apgar Score at birth. Increased perinatal morbidity and mortality • Grade 3-4 intraventricular haemorrhage • Necrotizing enterocolitis
  • 41. • • • • • • BIOPHYSICAL HC:AC Brfore 32 wks more than 1 32—34 wks app 1 FEMUR LENGTH FL:AC IS 22at all gest wks from 21 wks to term • More than 23.5 indicate IUGR
  • 42. • AFI • <2 Suggest IUGR • PI
  • 43. PREVENTION OF HYPOTHERMIA • MUMMIFICATION • KMC • NESTING • DELAY BATH • WARMER
  • 44. MAINTAINING BREATHING • VENTILATOR • C PAP • 02 SUPPLEMENTATION
  • 45. NUTRITION FLUID AND FEEDING • <30– IV FLUIDS, NG ,KATORI, BREAST FEEDS • 30—34 NG ,KATORI, BREAST FEEDS • >34 KATORI, BREAST FEEDS
  • 46. Monitoring • Vital signs • Activity and behaviour. • Color; Pink, pale, grey, blue, yellow. • Tissue perfusion • Fluids, electrolytes and ABG's.
  • 47. • Bronchopulmonary dysplasia Metabolic disturbances and hypoglycemia Polycytemia Hypothermia Impaired cognitive function and cerebral paresis
  • 48. MEDICAL • ASPIRIN THERAPY • Other forms of treatment that have been studied are • nutritional supplementation, • zinc supplementation, • fish oil, • hormones and • oxygen therapy
  • 49. MANAGEMENT • • • • • 3—10 Percentile Skin to skin care Breast feeding Glucose level monitoring Polycythemia
  • 50. <3 percentile • Thermal protection • feeding
  • 51. THANK YOU