INTRA UTERINE GROWTH RETARDATION

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Care of IUGR babies

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INTRA UTERINE GROWTH RETARDATION

  1. 1. IUGR PRESENTED BY AMRUTHA R 1st yr MSc nsg 18-03-2013 CHILD HEALTH NURSING
  2. 2. SGA IUGR
  3. 3. NORMAL FOETAL GROWTH • Cellular hyperplasia • Hyperplasia and hypertrophy • hypertrophy
  4. 4. Stages • Stage I (Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA content
  5. 5. Stages • Stage II (Hyperplasia & Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.
  6. 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. 7. CAUSES OF IUGR • • • • Maternal factors Fetal factors Placental factors Environmental factors
  8. 8. MATERNAL FACTORS • Medical disease • Malnutrition  BMI < 19 twice the risk of IUGR • Multiple pregnancy • Smoking (460 gm < then none smoker)
  9. 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. 10. MATERNAL FACTORS • • • • Small stature/ low pre-pregnancy weight Teen pregnancy Primi gravida Grand multiparity
  11. 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. 12. FETAL FACTORS • Exposure to an infection• German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus
  13. 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. 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. 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. 16. Normal & IUGR Newborn babies
  17. 17. Normal & IUGR Placentas
  18. 18. Environmental Causes of IUGR • High altitude - lower environmental oxygen saturation • Toxins
  19. 19. Types of IUGR • Symmetric IUGR: (33 % of IUGR Infants) • Asymmetric IUGR (55 % of IUGR) • Combined type IUGR: (12 % of IUGR)
  20. 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. 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. 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. 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. 24. • Growth restriction in the stage of hypertrophy • Brain sparing effect • Head growth remains normal but abdominal girth slows down
  25. 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. 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. 27. CLINICAL FEATURES
  28. 28. Weight deficit Large head circumference Old man look Cartilaginous ridges on pinna Dry wrinkled skin
  29. 29. Length remain unaffected Open eyes Well defined creases Alert and active Normal reflexes Normal cry Thin umbilical
  30. 30. • Scaphoid abdomen
  31. 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. 32. PREDICTION OF IUGR • History risk factors last menstrual period - most precise size of uterus time of quickening (detection of fetal movements) • Examination /
  33. 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. 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. 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. 36. • DOPPLER OF THE UMBILICAL ARTERY • Reduced end diastolic flow. • Absent end diastolic flow • Reversed end diastolic flow( severe cases)
  37. 37. Problems • Hypoxia - Perinatal asphyxia - Persistent pulmonary hypertension - meconium aspiration • Thermoregulation - Hypothermia due to diminished subcutaneous fat and elevated surface/volume ratio
  38. 38. Metabolic - Hypoglycemia - result from inadequate glycogen stores. - diminished gluconeogenesis. - increased BMR - Hypocalcemia - due to high serum glucagon level, which stimulate calcitonin excretion
  39. 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. 40. • Fetal distress, • Hypoxia, Acidosis and Low Apgar Score at birth. Increased perinatal morbidity and mortality • Grade 3-4 intraventricular haemorrhage • Necrotizing enterocolitis
  41. 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. 42. • AFI • <2 Suggest IUGR • PI
  43. 43. PREVENTION OF HYPOTHERMIA • MUMMIFICATION • KMC • NESTING • DELAY BATH • WARMER
  44. 44. MAINTAINING BREATHING • VENTILATOR • C PAP • 02 SUPPLEMENTATION
  45. 45. NUTRITION FLUID AND FEEDING • <30– IV FLUIDS, NG ,KATORI, BREAST FEEDS • 30—34 NG ,KATORI, BREAST FEEDS • >34 KATORI, BREAST FEEDS
  46. 46. Monitoring • Vital signs • Activity and behaviour. • Color; Pink, pale, grey, blue, yellow. • Tissue perfusion • Fluids, electrolytes and ABG's.
  47. 47. • Bronchopulmonary dysplasia Metabolic disturbances and hypoglycemia Polycytemia Hypothermia Impaired cognitive function and cerebral paresis
  48. 48. MEDICAL • ASPIRIN THERAPY • Other forms of treatment that have been studied are • nutritional supplementation, • zinc supplementation, • fish oil, • hormones and • oxygen therapy
  49. 49. MANAGEMENT • • • • • 3—10 Percentile Skin to skin care Breast feeding Glucose level monitoring Polycythemia
  50. 50. <3 percentile • Thermal protection • feeding
  51. 51. THANK YOU

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