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IUGR.pptx
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- 5. NORMAL FOETAL GROWTH ā¢Cellular hyperplasia ā¢ Hyperplasia and hypertrophy ā¢ hypertrophy
- 6. Stages ā¢ Stage I(Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA content
- 7. Stages ā¢ Stage II(Hyperplasia & Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.
- 8. Stages ā¢ Stage III( Hypertrophy) - 28 to 40 weeks - Rapid increase in cell size. - Rapid accumulation of fat, muscle and connective tissue. ā¢ 95% of fetal weight gain occurs during last 20 weeks of gestations.
- 9. CAUSES OF IUGR ā¢Maternal factors ā¢ Fetal factors ā¢ Placental factors ā¢ Environmental factors
- 10. MATERNAL FACTORS ā¢Medical disease ā¢MalnutritionļØ BMI < 19 twice the risk of IUGR ā¢Multiple pregnancy ā¢Smoking ļØ(460 gm < then none smoker)
- 11. MATERNAL FACTORS ā¢ AlcoholļØ 12-fold increase risk of IUGR ā¢ Drugs ļØ Beta- Blockers(Atenolol in second trimster, Anticoagulants, Anticonvulsants( phenytoin) ā¢ Hypoxemia ā¢ Infections ļØ UTI, Malaria, TB, Genital Infections
- 12. MATERNAL FACTORS ā¢ Smallstature/ low pre-pregnancy weight ā¢ Teen pregnancy ā¢ Primi gravida ā¢ Grand multiparity
- 13. FETAL FACTORS ā¢ AChromosome Defect- ļ In second trimester 20% SGA fetuses have chromosomal abnormality ļ Triploid is most common under 26 wks. ļ Trisomy-18 is common after 26 wks . ļ Other are 21(Downās syndrome), 16, 13, xo (turnerās syndrome).
- 14. FETAL FACTORS ā¢ Exposureto an infection- ā¢ German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus
- 15. FETAL FACTORS ā¢ birthdefects ā¢ (cardiovascular, renal, anencephally, limb defect, etc). ā¢ A primary disorder of bone or cartilage. ā¢ A chronic lack of oxygen during development (hypoxia ā¢ Placenta or umbilical cord defects.
- 16. PLACENTAL FACTORS ā¢ UteroplacentalInsufficiency Resulting From -. āImproper / inadequate trophoblastic invasion and placentation in the first trimester. āLateral insertion of placenta. āReduced maternal blood flow to the placental bed.
- 17. PLACENTAL FACTORS ā¢ FetoplacetalInsufficiency Due To-. āVascular anomalies of placenta and cord. āDecreased placental functioning mass-. ā¢ Small placenta, abruptio placenta, placenta previa, post term pregnancy
- 18. Normal & IUGRNewborn babies
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- 20. Environmental Causes ofIUGR ā¢ High altitude - lower environmental oxygen saturation ā¢ Toxins
- 21. Types of IUGR ā¢Symmetric IUGR: (33 % of IUGR Infants) ā¢ Asymmetric IUGR (55 % of IUGR) ā¢ Combined type IUGR: (12 % of IUGR)
- 22. SYMMETRICAL ā¢ height, weight,head circ proportional ā¢ early pregnancy insult: ā¢ commonly due to congenital infection, genetic disorder, or intrinsic factors ā¢ Reduced no of cells in fetus ā¢ normal ponderal index ā¢ low risk of perinatal asphyxia ā¢ low risk of hypoglycemia
- 23. PONDERAL INDEX ā¢ Theponderal 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
- 24. PONDERAL INDEX ā¢ Typicalvalues are 20 to 25. ā¢ Those who have a ponderal index below the 10th % can be classified as SGA ā¢ PI is normal in symmetric IUGR. ā¢ PI is low in asymmetric IUGR
- 25. ASSYMETRICAL ā¢ later inpregnancy: ā¢ commonly due to utero placental insufficiency, maternal malnutrition, hypoxia, or extrinsic factors ā¢ low ponderal index ā¢ Cell number remains same but size is small ā¢ increased risk of asphyxia ā¢ increased risk of hypoglycemia
- 26. ā¢ Growth restrictionin the stage of hypertrophy ā¢ Brain sparing effect ā¢ Head growth remains normal but abdominal girth slows down
- 30. 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.
- 31. 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.
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- 33. Weight deficit Large head circumference Oldman look Cartilaginous ridges on pinna Dry wrinkled skin
- 34. Length remain unaffected Open eyes Welldefined creases Normal reflexes Alert and active Normal cry Thin umbilical
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- 36. ā¢ Signs ofrecent wasting - soft tissue wasting - diminished skin fold thickness - decrease breast tissue - reduced thigh circumference ā¢ Signs of long term growth failure - Widened skull sutures, large fontanelles - shortened crown ā heel length - delayed development of epiphyses
- 37. PREDICTION OF IUGR ā¢History risk factors last menstrual period - most precise size of uterus time of quickening (detection of fetal movements) ā¢ Examination /
- 38. MATERNAL SERUM SCREENING ā¢ AFP ā¢more for gestation in the absence of fetal anomaly, there is a 5-10 fold increase in the risk of FGR
- 39. ā¢ Uterine ArteryDoppler Velocimetry - Notching of the waveform /reduce EDF associated 3-fold increase in risk of FGR. ā¢ Bright or echogenic fetal bowel in the second trimester is associated with increase risk of FGR.
- 40. ā¢ Combination ofun-explain elevated maternal AFP is powerful predictor of adverse perinatal outcome (FGR) ā¢ Increase AFP combine with echogenic bowel is strong predictor of FGR
- 42. ā¢ DOPPLER OFTHE UMBILICAL ARTERY ā¢ Reduced end diastolic flow. ā¢ Absent end diastolic flow ā¢ Reversed end diastolic flow( severe cases)
- 44. Problems ā¢ Hypoxia - Perinatalasphyxia - Persistent pulmonary hypertension - meconium aspiration ā¢ Thermoregulation -Hypothermia due to diminished subcutaneous fat and elevated surface/volume ratio
- 45. Metabolic - Hypoglycemia - resultfrom inadequate glycogen stores. - diminished gluconeogenesis. - increased BMR - Hypocalcemia - due to high serum glucagon level, which stimulate calcitonin excretion
- 46. ā¢ Hematologic -hyperviscosity andpolycythemia due to increase erythropoietin level sec. to hypoxia ā¢ Immunologic -IUGR have increased protein catabolism and decreased in protein, prealbumin and immunoglobulins, which decreased humoral and cellular immunity.
- 47. ā¢ Fetal distress, ā¢Hypoxia, Acidosis and Low Apgar Score at birth. Increased perinatal morbidity and mortality ā¢ Grade 3-4 intraventricular haemorrhage ā¢ Necrotizing enterocolitis
- 48. ā¢ BIOPHYSICAL ā¢ HC:AC ā¢Brfore 32 wks ā¢ 32ā34 wks more than 1 app 1 ā¢ FEMUR LENGTH ā¢ FL:AC IS 22at all gest wks from 21 wks to term ā¢ More than 23.5 indicate IUGR
- 49. ā¢ AFI ā¢ <2Suggest IUGR ā¢ PI
- 50. PREVENTION OF HYPOTHERMIA ā¢MUMMIFICATION ā¢ KMC ā¢ NESTING ā¢ DELAY BATH ā¢ WARMER
- 51. MAINTAINING BREATHING ā¢ VENTILATOR ā¢C PAP ā¢ 02 SUPPLEMENTATION
- 52. NUTRITION FLUID ANDFEEDING ā¢ <30ā IV FLUIDS, NG ,KATORI, BREAST FEEDS ā¢ 30ā34 NG ,KATORI, BREAST FEEDS ā¢ >34 KATORI, BREAST FEEDS
- 53. Monitoring ā¢ Vital signs ā¢Activity and behaviour. ā¢ Color; Pink, pale, grey, blue, yellow. ā¢ Tissue perfusion ā¢ Fluids, electrolytes and ABG's.
- 56. ā¢ Bronchopulmonary dysplasia Metabolicdisturbances and hypoglycemia Polycytemia Hypothermia Impaired cognitive function and cerebral paresis
- 57. MEDICAL ā¢ ASPIRIN THERAPY ā¢Other forms of treatment that have been studied are ā¢ nutritional supplementation, ā¢ zinc supplementation, ā¢ fish oil, ā¢ hormones and ā¢ oxygen therapy
- 58. MANAGEMENT ā¢ 3ā10 Percentile ā¢Skin to skin care ā¢ Breast feeding ā¢ Glucose level monitoring ā¢ Polycythemia
- 59. <3 percentile ā¢ Thermalprotection ā¢ feeding
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