a specific biometric or estimated weight threshold by a specific gestational age. > 10 th centile
Abdominal circumference
Estimated fetal weight
severe SGA as an EFW or AC less than the 3rd
IntraUterine Growth Restriction(IUGR) is not synonymous with SGA. Some, but not all, IUGR fetuses/infants are SGA while 5070% of SGA fetuses are constitutionally small, with fetal growth appropriate for maternal size and ethnicity. The likelihood of IUGR is higher in severe SGA infants. Growth restriction implies a pathological restriction. As a result, growth restricted fetuses may manifest evidence of fetal compromise (abnormal Doppler studies, reduced liquor volume). Normal Fetal Growth Normal fetal growth is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone. Indicators
Weight gain Symphysiofundal height Abdominal girth Classifications
1. symmetrical or intrinsic IUGR
2. assymetric IUGR 3. Intermediate IUGR symmetrical IUGR- (20-30%) Occurs as a result of growth inhibition early in pregnancy i.e. the hyperplastic stage. Any pathological insult at this phase leads to reduced no. of cells in fetus and overall decreased growth potential. Causes include- Intrauterine infections (TORCH ) Chromosomal disorders Congenital malformations All parameters(head and abdo circumference, length and weight) are below 10th percentile for gestational age, hence normal ponderal index (birth weight/ht3). asymmetric IUGR (70-80%)
Occurs as a result of restriction of
nutrient supply in utero i.e. uteroplacental insufficiency. It is usually associated with maternal diseases like:- Chronic hypertension Renal disease Vasculopathies The onset of growth restriction occurs usually after 28 wks of gestation i.e. in the stage of hypertrophy. The fetus has near normal total no. of cells but cell size is reduced. There is brain sparing effect so that the head growth remains normal but the abdominal girth slows down. The Ponderal index is low. This asymmetry results from redistribution of fetal cardiac output with increased flow to brain and heart at the expense of reduced splanchnic circulation. Liver size is reduced because of diminished glycogen stores. In case of severe placental insufficiency the head growth may also be affected. This type of growth restriction leads to decreased amniotic fluid, chronic hypoxia and may result in fetal death. Intermediate IUGR
It is a combination of type 1 and
type 2. Fetal growth restriction occurs during intermediate phase of growth affecting both hyperplasia and hypertrophy, resulting in decrease in cell no. as well as size. Causes include Chronic HT Lupus nephritis RFs Complications of IUGR Antepartum period- increased incidence of- -still births -oligohydramnios IUGR is found in 52% of unexplained stillbirths. During labour- higher incidence of- -meconium aspiration -fetal distress -intrapartum fetal death Neonatal period- increased incidence of- -Hypoxic ischemic encephalopathy -Persistent fetal circulation insufficiency They have difficulty in temperature regulation because of absent brown fat and small body mass relative to surface area. Lack of glycogen stores may predispose to hypoglycemia Complications cont.. Childhood- increases mortality from- -infectious diseases -congenital anomalies Incidence of cerebral palsy are 4-6 times higher. Subtle impairment of cognitive performance and educational underachievement. Long term complications- increased risk of coronary heart disease, Diagnosis of IUGR 1. Clinically- Serial measurement of fundal height and abdominal girth. Symphysio-fundal height normally increases by 1cm per wk b/w 14 and 32 wks. A lag in fundal ht. of 4wks is suggestive of moderate IUGR. A lag of >6 wks is suggestive of severe IUGR. 2. Sonographic evaluation- Fetal biometry: i. BPD(Biparietal Diameter)- determines gestational age and type of IUGR. ii. Head circumference- better than BPD in predicting IUGR. iii. Transeverse cerebellar diameter(TCD)- can be used as a method to assess gestational age. iv. Abdominal circumference(AC)- AC and fetal wt are most accurate ultrasound parameters for diagnosis of IUGR. An increase in fetal AC of less than 10 mm in 14 days has sensitivity of 85% and specificity of 74% for identification of IUGR. iv. Measurement ratios- there are some age independent ratios to detect IUGR. HC/AC: decreases linearly from 16 to 20 wks of gestation. HC/AC >2 SD above mean is predictive of IUGR. FL/AC: normal value ranges from 22 + 2% in the second half of pregnancy. Ratio above 23.5% is considered abnormal. Placental Morphology: Acceleration of placental maturation may occur with IUGR and PIH. Amniotic fluid volume: assymetrical IUGR is usually associated with oligohydramnios. 3. Doppler Ultrasonography: doppler flow studies are important adjuncts to fetal biometry in identifying the IUGR fetuses at risk of adverse outcome. Most widely used arterial indices are : Pulsatility index (PI): Systolic end diastolic peak velocity / time averaged maximum velocity , 1.2-0.9 Resistance Index(RI): Systolic end diastolic peak velocity/ systolic peak velocity , 0.7- 0.6 Systolic to diastolic ratio(S/D): Systolic peak Umblical Artery doppler- In IUGR there is increased umblical artery resistance (increased S/D ratio), absent end diastolic flow and finally reversed end diastolic flow. Perinatal mortality rate increases significantly in fetuses with absent end diastolic flow (9-41%) and reversed end diastolic flow (33-73%) in umblical artery. Middle cerebral artery doppler- in a normal fetus has relatively little flow during diastole. Increased resistance to blood flow in placenta results in redistribution of cardiac output to favour cardiac and cerebral circulations leading to increased flow in the diastolic phase with decreased S/D ratio. Cerebral/Placental ratio: ratio between MCA PI and umblical artery PI is more sensiive predictor than either MCA and umblical artery velocimetry alone to detect redistribution of blood flow. Cut off values below 1.0 to 1.1 are considered to be diagnostic of brain spairing effect. MCA peak systolic velocimetry: is good indicator of fetal anaemia and is less Ductus venosus doppler: Perinatal mortality in growth restricted fetuses has been found to be significantly worse when abnormalities in fetal venous circulation are detected. In the normal fetus, flow in the ductus venosus is forwards , moving towards the heart during entire cardiac cycle. When circulatory compensation of the fetus fails, the ductus venosus waveform shows absent or reverse blood flow during atrial conraction. Perinatal mortality being 63- 100%. Therefore it is recommended that fetus