I.U.G.R.

1
I.U.G.R. Intrauterine Growth Retardation
(Restriction)
Presented by
DR. NABEEL S. BONDAGJI
2
DEFINITIONS

• Low birth weight (LBW)
• Very low birth weight (VLBW)
• Extremely low birth weight (ELBW)
• Premature
• Small for Gestational Age (SGA)
• Large for Gestational Age (AGA)
• Intrauterine Growth Retardation (IUGR)
• SGA IUGR SFD

3
Incidence of SGA   By definition, babies with BW
lt 10th centile on growth curves are
SGA.   Therefore, 10 of babies are
SGA.   However, not as simple as this.
4
Factors affecting Fetal/Baby size

• Sex Male infants are 150 grams heavier and o.0
  cm. longer than female infants.
• Parity First born infants tend to be smaller
  than infants born subsequently this effect
  dissipates after the third birth.
• Racial and ethnic groups and nationalities have
  differing normal birth weights.

5
4. Altitude In USA for example, growth
curves based on the Denver population located
approximately 5000 feet above sea level tend to
underestimate infants' weights after 32 weeks'
gestation. 5. Maternal size direct
association between maternal height and weight
and the size of the fetus is well established.
Birth weight variation of 750 g between infants
born to mothers of 170 cm in height and 75 kg
weight when compared with infants born to mothers
150 cm tall and weighing 40 kg has been described.
6
6. Number of fetuses mean birth weight
decreases with the number of fetuses.   ?
Need for different growth curves to
take the above into account.
7
Types of SGA

• Symmetrical weight, head and length are all
  below the 10th percentile.
• 20 to 30.
• Asymmetrical weight is below the 10th
  percentile and head and length are preserved.
• 70 to 80. 

8
Why Distinguish?   Symmetric IUGR babies are
more likely to have an underlying
cause.   9-27 of IUGR infants have anatomic
and or genetic abnormalities.  
9

• SGA Correlates
•  
• Perinatal Mortality and Morbidity are greater in
  SGA infants.
•  
• As noted Increased risk of underlying
• abnormalities. 
• Perinatal morbidity is due to asphyxia
• and acidosis hypoglycemia hypocalcemia,
• hypothermia and polycythemia.

10
The overall perinatal mortality in IUGR infants
is increased eight- to ten-fold that of AGA
infants.   Higher risk of developmental problems
in SGA infants.  
11
Causes of SGA

• Fetal growth occurs in 3 phases.
•  
• 4-20 weeks' gestation rapid cellular
  development with mitosis
• 2. 20-28 weeks increase in cellular size
  combined with ongoing mitosis.
•  

12

• 28-40 weeks cells rapidly increasing in size,
  with peak at 33 weeks. In addition, rapid
  accumulation of fat, muscle and connective tissue
  occurs.

13

• Ninety five percent of fetal weight gain occurs
  during the last 20 weeks of gestation.
• Growth inhibition during stage I will
• produce an undersized fetus with fewer
• cells, but normal cell size, causing
• symmetric IUGR.

14

• Growth inhibition during stage II and III will
  cause a decrease of cell size and fetal weight
  with less effect on total cell number and fetal
  length and head circumference, causing asymmetric
  IUGR.

15

• Conditions associated with symmetric IUGR
•  
• Genetic - constitutional, chromosomal and
• single gene defects, and deletion disorders
• and inborn errors of metabolism.
•  
• Congenital anomalies,
•  
• Intrauterine infections
•  
• Others substance abuse, cigarette smoking
• and therapeutic irradiation.

16
Conditions associated with asymmetric IUGR
  Uteroplacental insufficiency       -
chronic hypertension,       - preeclampsia,
      - placental infarcts       - abruptio
placenta       - velamentous insertion of the
umbilical cord and circumvallate
placenta
17
Maternal illnesses        - chronic renal
disease,        - cyanotic heart disease,
       - hemoglobinopathies        -
substance abuse and cigarette
smoking. Other factors         - multiple
gestation        - altitude
18

• Under conditions of stress (eg. Hypoxia)
• fetus mounts response with increased
• Adr and NorAdr (found in amniotic
• fluid) leads to anti-insulin effect.
•  
• In addition, this results in loss of fat,
• muscle and glycogen with changes in
• blood flow distribution to vital organs
• (brain, heart and adrenal) asymmetric.

19

• Smoking, substance abuse and SGA.
•  
• The mean birth weight is reduced by 175-
• 200 g in infants born to cigarette smokers
•  
• Cotinine decreases uteroplacental blood
• flow in a dose-related way by stimulating
• sympathetic neurons.
•  
• Carboxyhemoglobin levels are elevated in
• mothers who smoke and in their fetuses, and
• the avidity of fetal hemoglobin to carbon
• monoxide may exacerbate fetal hypoxia.

20

• Nicotine has a demonstrated teratogenic
• effect in animals.
•  
• Marijuana, cocaine, heroin, amphetamines
• and alcohol can all cause IUGR, with the
• head circumference affected in many
• studies, suggesting a symmetrical form of
• growth retardation and an insult during the
• cell mitotic phase in early pregnancy.

21

• Prenatal Diagnosis
•  
• Maternal history e.g. pregnancy-
• induced-hypertension.
•  
• 2. Maternal examination - measurement of fundal
  height is an excellent screening tool for IUGR.
  95 sensitivity.
• - If fundal height is 4 cm less than expected -
  ?SGA. Fundal height in cms should equal gestation
  at 20 to 25 weeks.

22
3. Fetal ultrasound BPD and AC measured.
- BPD (biparietal diam) 43-100 accurate
but inaccuracy due to head-sparing in
asymmetric IUGR. - AC (Abdominal
circumference better sensitivity than that
of cephalometry for IUGR detection.  -
HC/AC (Head circumference/abdominal
circumference ratio) is an important
measurement for detection of asymmetric
IUGR infants.       
23

• Ratio of femoral length to abdominal
  circumference (FL/AC) provides also an accurate
  prediction of IUGR.

24
4. Amniotic fluid volume oligohydramnios due
to decreased renal blood flow and urine
output. 5. Blood flow measurements by Doppler
flow studies, fetal and uterine blood flow
can be measured and therefore
uteroplacental circulation dysfunctions can
be assessed.    
25

• Biochemical data
• a. Estriol low 24 hours urinary estriol
• excretion is associated with 21 of
• IUGR infants.
• b. Human placental lactogen (HPL).

26
Prenatal Management   - Symmetric IUGR need to
consider amniocentesis and TORCH analysis, along
with Maternal TORCH antibody titres.   - Also
need to look at Maternal Health e.g. illness
such as chronic renal disease need to be
considered. This includes discouraging tobacco
use, and substance abuse as well as regular
checks through pregnancy
27
- Ongoing close observations, with U/S
(including doppler flows) and CTGs.   - Early
delivery has to be considered based upon the
relative chance of fetal morbidity and mortality
in-utero to the chance of morbidity and mortality
of prematurity. Can often be a difficult choice.
28

• Postnatal Management of SGA baby
•  
• These babies handle stress of birth and
  post-natal life poorly.
• Greater risk of stillbirth (4x)
• Greater risk of asphyxia (2x)
• Likely to have lower APGAR scores
• Higher incidence of meconium at delivery
• Risk of hypoglycaemia
• Risk of hypocalcaemia and hypomagnesaemia
• Risk of hypothermia
• Note, risk of lung disease is less than
  with AGA
• babies as long as they get through birth
  OK.

29
At delivery   - IUGR infants are more prone to
hypoxemia during labor and delivery because of
uteroplacental insufficiency, and more prone to
cord compression due to lack of amniotic fluid
and a thin cord.
30
- A neonatal team capable of managing asphyxia
and meconium aspiration syndrome should be
available at the time of delivery.   - Special
attention should be addressed to prevention of
hypothermia and hypoglycemia.
31

• Physical findings
•  
• Obviously, lt 10th centile for gestation.
• Look at baby carefully especially if
• symmetrically growth retarded.
• Need to be wary of genetic/infective
• causes look for dysmorphic features, for
• skin rashes (blueberry muffin and
• patechiae) and for hepatosplenomegaly

32
- wisened old man appearance - lack of
subcutaneous fat - skin is dry cracked and
peeling (especially palms soles) -
often thin cord due to lack of Whartons
jelly - may be meconium stained - ruddy
appearance due to polycythaemia - may be
jittery due to low sugar or calcium - may also
be irritable and show signs of asphyxia,
including fitting.
33
Attempt to identify the cause of IUGR  
Aetiologies a. Vascular diseases of the
mother (hypertension, renal disease,
diabetes, etc.) - 35. b. Chromosomal and
other congenital anomalies of the infant -
10. c. Normal variations (low maternal
weight/height, high altitude, multiple
gestation) - 10.
34
d. Congenital infection - 5. e. Alcohol,
smoking, substance abuse, and
medications (antimetabolites for cancer
therapy, hydantoin and trimethadion for
anticonvulsant therapy) - 5. f. Placenta
and cord defects - 2. g. Uterine
abnormalities - 1. h. Other Therapeutic
radiation, low socioeconomic level and
unknown causes - 32. Careful
history and examination can identify most
causations.
35
Management after birth   SGA babies are at risk
as noted. Therefore attention to WARM, PINK,
SWEET INFECTION needed.   Need to attend to
basics of care in particular 1. Respiratory
care esp. with meconium 2. Hypoglycaemia due
to low sugar reserves and higher energy
consumption esp. with cold stress.
36
3. Hypothermia due to lack of subcutaneous
fat and relatively high S.A to body weight
ratio 4. Beware infection at risk as
immune system of babies is immature
being SGA worsens this.
37
5. Polycythaemia due to in-utero hypoxia.
Can cause venous thrombo-emboli and
can also worsen cerebral ischaemia and
perpetuate hypoglycaemia. 6. Haemorrhage can
develop due to lack of liver coag factor
production, and also may have low
platelets if TORCH 7. Management of asphyxia
38
Investigations of SGA baby   Initially, babies
need to be examined in a warm environment.   True
blood glucose should be assessed at ½ to 1 hour
of age, and pre-feeds for at least the next 2
feeds. Feeds should be frequent (2-3 hourly
initially).  
39
If baby jittery, then glucose and calcium
and magnesium must be checked.   Full blood
count - 3 reasons - polycythaemia - platelet
count - white cells
40
Other investigations done on merit -
chromosomes - TORCH screen - CXR if
respiratory distress - Sepsis workup if
possibility of infection - - Urine drug
screen, etc., if suspect maternal
substance abuse - Cranial US esp. if
concerned about in-utero hypoxia
41

• Nutrition
•  
• Important to establish nutrition as early as
• possible but be wary as hypoxia and
• polycythaemia may have resulted in
• diminished gut blood flow risk of NEC.
•  
• - If delay in establishing enteral feeds, must
• use TPN.
•  
• Weight gain monitoring needed to ensure
• sufficiency of caloric intake.

42

• It is common that caloric intake in IUGR
• infants will exceed the usual intake of 100-
• 120 Kcal/kg/day, and daily weight gain will
• exceed 25 g/day.
•  
• Neurologic prognosis may relate directly to
• restoring good nutrition. Poor subsequent
• head growth bodes poorly for intellectual
• development.
•  

43

• DONT FORGET THE PARENTS!!!
•  
• Parental counselling about diagnosis,
• risk for physical and developmental
• sequelae, and risk of IUGR in a
• subsequent pregnancy, should be
• provided

44
Outcome for SGA babies   Increased
mortality and morbidity as noted.   Long term
outlook   Neurological.   - IUGR infants
have an increased risk of long-term
neurologic and behavioral handicaps.
Infants with ultrasonographic evidence of
delayed head growth before the third
trimester also have delayed neurologic and
intellectual development.
45
- If congenital anomalies and clinically
detected prenatal infections are excluded,
studies show normal IQ/DQ in most SGA
infants. - Preterm IUGR infants have similar
outcomes at 18-24 months of age, compared to
AGA preterm infants. - Severe
malnutrition in utero can decrease the
number of brain cells. Normally in the first 2
years of life there occurs a "spurt in brain
growth" during which the predominant change is
increase in myelinization.
46
- Overall, IUGR infants have an increased
incidence of lower intelligence, learning and
behavioral disorders and neurologic
handicaps. - The long-term neurologic outcome
in SGA infants is related to the type of
SGA, severity and concomitant asphyxial
insult. - Future handicap is dependent also on
the existence of perinatal complications
such as asphyxia, meconium aspiration
syndrome, hypothermia, hypoglycemia and
polycythemia.
47
Growth. - Asymmetric IUGR infants have better
growth potential than symmetric IUGR infants
who typically have suffered a genetic,
infectious or teratogenic insult early in
life. - Asymmetric SGA infants capable of
achieving normal weight and proportions
within 6-12 months of birth. - Symmetric SGA
infants born often remain shorter, lighter
and have a smaller head circumference
throughout life.
48
Other. - Delayed eruption of teeth and enamel
hypoplasia. - Increased incidence of
postnatal infections possibly due to
delayed humoral and cellular immunity found
. - Risk of SIDS considerably greater (30
of SIDS cases occur in SGA infants)
reasons behind SGA may account for this
however.
49
Thank you ...