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IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
IUGR-New_edited-13-09-10.ppt
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IUGR-New_edited-13-09-10.ppt

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  • 1. Intra Uterine Growth Restriction [IUGR]
  • 2.
    • Definition :
    • Intra uterine growth restriction is said to be present in those babies whose birth weight is below the tenth percentile of the average for the gestational age.
    • Growth restriction can occur in preterm, term or post-term babies.
  • 3.
    • Incidence :
    • Dysmaturity comprises about one-third of low-birth weight babies.
    • In developed countries, its overall incidence is about 2-8%.
    • The incidence among the term babies is about 5% and that among the post-term babies is about 15%.
  • 4.
    • Nomenclature :
    • SGA and IUGR are too often used synonymously although there is a degree of overlap.
    • SGA fetus is not necessarily growth retarded.
    • The baby may be constitutionally small.
    • Similarly late onset of pathological cessation of growth may produce a baby with typical features of IUGR but may not be small for gestation (ie. Appropriate for gestational age).
    • However, both attempt to identify fetuses or neonates that are small for reasons other than being preterm.
  • 5.
    • Normal fetal growth
    • Is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone.
  • 6.
    • Types: Based on the clinical evaluation and ultrasound examination the small fetuses are divided into:
    • 1.   Fetuses that are small and healthy. The birth weight is less than 10 th percentile for their gestational age. They have normal ponderal index, normal subcutaneous fat and usually have uneventful neonatal course.
    • 2. Fetuses where growth is restricted by pathological process (true IUGR). Depending upon the relative size of their head, abdomen and femur, the fetuses are subdivided into:
    • (a) Symmetrical or Type I
    • (b) Asymmetrical or Type II.
  • 7.
    • Symmetrical (20%) –
    • The fetus is affected from the noxious effect very early in the phase of cellular hyperpllasia.
    • The total cell number is less. This form of growth retardation is most often caused by structural or chromosomal abnormalities or congenital infection (TORCH).
    • The pathologic process is intrinsic to the fetus and involves all the organs including the head.
  • 8.
    • Asymmetrical (80%) –
    • The fetus is affected in later months during the phase of cellular hypertrophy.
    • The total cell number remains the same but size is smaller than normal.
    • The pathologic processes that too often result in asymmetric growth retardation are maternal diseases extrinsic to the fetus.
    • These diseases alter the fetal size by reducing utero-placental blood flow or by restricting the oxygen and nutrient transfer or by reducing the placental size.
  • 9.
    • Etiology: The causes of fetal growth retardation can be divided into four types.
    • Maternal –
    • Maternal nutrition before and during pregnancy – Critical substrate requirement for the fetus such as glucose, aminoacids and oxygen are lacking during pregnancy.
    • This is an important cause of small weight of the babies in the developing countries.
    • As most of the fetal weight gain (two-third) occurs beyond 24 th week of pregnancy, malnutrition, anaemia, hypertension, antiphospholipid syndrome in the second half of pregnancy play significant role in the reduction of the birth weight.
  • 10.
    • Fetal –
    • There is enough substrate in the maternal blood and also crosses the placenta but is not utilized by the fetus. The failure of non utilization may be due to
    • (1) Congenital anomalies either cardio vascular, renal or others
    • (2) Chromosomal abnormality is associated with 8-12% of growth retarded infants. The common abnormalities are trisomy 21, trisomy 18 (Edward’s Syndrome), trisomy 16, trisomy 13 and Turner’s syndrome
    • (3) Accelerated fetal metabolism due to TORCH agents (toxoplasmosis, rubella, cytomegalovirus and herpes simplex) and parvo virus B19
    • (4) Multiple pregnancy – There is mechanical hindrance to growth and excessive fetal demand.
  • 11.
    • Placental –
    • The causes include cases of poor uterine blood flow to the placental site for a long time.
    • This leads to chronic placental insufficiency with inadequate substrate transfer.
    • This occurs in conditions such as preeclampsia, essential hypertension, chronic nephritis, organic heart disease, placental and cord abnormalities such as chronic placental abruption, infarction, small placenta, circumvallate placenta, vellamentous insertion of cord etc.
    • Unknown –
    • The cause remains unknown in about 40%
  • 12. Diagnosis
  • 13.
    • The ‘at risk’ mothers are teenaged in present pregnancy with reduced uteroplacental blood flow. This can be achieved as early as 12 weeks by a thorough and meticulous exam.
    • Maternal weight gain remains stationary or at times falling (less than 2 kg/month during second half of pregnancy).
    • If there is reduction of symphysis fundal height by 2 cm before 36 weeks or 3 cm thereafter or the measurement falls below the 10th percentile.
  • 14.
    • Measurement of the abdominal girth showing stationary or falling values.
    • Serial clinical examination by abdominal palpation to measure the relative growth of the uterus and its contents is the commonly used method. The diminishing amniotic fluid volume can also be assessed with fair degree of accuracy.
  • 15.
    • Reduced or absent diastolic flow in umbilical artery as evidenced by Doppler blood flow velocimetry.
    • Normally, the diastolic flow increases as pregnancy progresses.
    • Presence of ‘notch’ in the early diastole waveform, especially in the uterine arteries, suggests incomplete invasion of trophoblasts of the spiral arteries.
    • This ‘notch’ if confirmed at 24 weeks, predicts possible development of IUGR and pre-eclampsia.
  • 16.  
  • 17. Physical features at birth
    • Weight deficit at birth is about 600 gm below the minimum in percentile standard.
    • Length is unaffected.
    • Head circumference is relatively larger than the body.
  • 18. Physical features at birth
    • Physical features show dry and wrinkled skin because of less subcutaneous fat, scaphoid abdomen, thin meconium stained vernix caseosa and thin umbilical cord. All these give the baby an ‘old man look’. Pinna of ear has cartilaginous ridges. Plantar creases are well defined.
    • The baby is alert and having normal cry. Eyes are open.
    • Reflexes are normal including Moro-reflex.
  • 19.  
  • 20.  
  • 21. Complications
    • Fetal:
    • (A) Antenatal – Chronic fetal distress, fetal death,
    • (B) Intranatal – Hypoxia and acidosis
    • (C) After birth:
    • Immediate:
    • Asphyxia (intrauterine and neonatal),
    • Hypoglycemia due to shortage of glycogen reserve in the liver as a result of chronic hypoxia
    • Meconium aspiration pneumonia
    • Microcoagulation leading to DIC during first day of life.
    • Hypothermia
    • Pulmonary hemorrhage
    • Polycythaemia
    • Hyperviscosity syndrome
    • Necrotizing enterocolitis due to reduced intestinal blood flow.
  • 22.
    • Late:
    • Symmetrical growth retarded baby is likely to grow slowly after birth.
    • Whereas the asymmetrical one is more likely to grow faster after birth.
    • The fetuses have retardation of growth evidenced before third trimester are likely to have retarded neurologic and intellectual development in infancy.
    • The worst prognosis is for IUGR caused by congenital infection, congenital abnormalities and chromosomal defects.
  • 23.
    • Mortality
    • The immediate neonatal mortality is about 6 times more than the normal newborn or even similar weight appropriate to the shorter gestational age.
    • Most of the babies die within 24 hours.
    • The morbidity rate rises to about 50%.
  • 24.
    • Management during pregnancy
    • Adequate bed rest specially in left lateral position (2 hours following lunch and 8 hours at night).
    • To correct malnutrition by adequately balanced diet, 300 extra calories per day are to be taken.
    • To institute appropriate therapy for the associated complicating factors likely to produce growth retardation.
    • Avoidance of smoking and alcohol.
    • Low dose aspirin (50 mg daily) may be helpful.
    • Detect fetal anomalies.
  • 25. Yoga practices have helped to prevent IUGR
  • 26. T h a n k Y o u

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