U.G.R.

Retardation (Restriction)

Presented by:

DR. NABEEL S. BONDAGJI

DEFINITIONS:
a) Low birth weight (LBW)
b) Very low birth weight (VLBW)
c) Extremely low birth weight (ELBW)
d) Premature
e) Small for Gestational Age (SGA)
f) Large for Gestational Age (AGA)
g) Intrauterine Growth Retardation (IUGR)

SGA = IUGR = SFD

Incidence of SGA:
By definition, babies with BW < 10th
centile on growth curves are SGA.

Therefore, 10% of babies are SGA.

However, not as simple as this.

Factors affecting Fetal/Baby size:

1. Sex: Male infants are 150 grams heavier

and o.0 cm. longer than female infants.
2. Parity: First born infants tend to be
smaller than infants born subsequently;
this effect dissipates after the third birth.
3. Racial and ethnic groups and
nationalities have differing normal birth
weights.
 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. Number of fetuses: mean birth
weight decreases with the number of
fetuses.

? Need for different growth curves to

take the above into account.
Types of SGA:
•Symmetrical: weight, head and length are a
•20 to 30%.

•Asymmetrical: weight is below the 10th pe

•70 to 80%.
 Why Distinguish?

Symmetric IUGR babies are more likely to h

9-27% of IUGR infants have anatomic and o

SGA Correlates:
Perinatal Mortality and Morbidity are great

- As noted – Increased risk of underlying

abnormalities.
- Perinatal morbidity is due to asphyxia
and acidosis hypoglycemia hypocalcemia,
hypothermia and polycythemia.
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.
Causes of SGA:

Fetal growth occurs in 3 phases.

1. 4-20 weeks' gestation – rapid cellular

development with mitosis

2. 20-28 weeks – increase in cellular size

combined with ongoing mitosis.
3. 28-40 weeks – cells rapidly increasing
in size, with peak at 33 weeks. In
addition, rapid accumulation of fat,
muscle and connective tissue occurs.
Ninety five percent of fetal weight gain o
• Growth inhibition during stage I will
produce an undersized fetus with fewer
cells, but normal cell size, causing
symmetric IUGR.
• 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.
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.
Conditions associated with
asymmetric IUGR:
Uteroplacental insufficiency
- chronic hypertension,
- preeclampsia,
- placental infarcts
- abruptio placenta
- velamentous insertion of the
umbilical cord and circumvallate
placenta
Maternal illnesses
- chronic renal disease,
- cyanotic heart disease,
- hemoglobinopathies
- substance abuse and cigarette
smoking.
Other factors
- multiple gestation
- altitude
• 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.
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.
- 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.
Prenatal Diagnosis:
1. 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.
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.
- Ratio of femoral length to abdominal
circumference (FL/AC) provides also an
accurate prediction of IUGR.
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.
6. Biochemical data:

a. Estriol: low 24 hours urinary estriol

excretion is associated with 21% of
IUGR infants.
b. Human placental lactogen (HPL).
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
- Ongoing close observations, with U/S
(including doppler flows) and CTG’s.

- 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.
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.
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.
- 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.
Physical findings:
- Obviously, < 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
- wisened old man appearance
- lack of subcutaneous fat
- skin is dry cracked and peeling
(especially palms & soles)
- often thin cord due to lack of Wharton’s
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.
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%.
 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.
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.
 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.
 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
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).
If baby jittery, then glucose and calcium
and magnesium must be checked.

Full blood count - 3 reasons

- polycythaemia
- platelet count
- white cells
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
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.
- 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.
DON’T FORGET THE PARENTS!!!
 Parental counselling about diagnosis,
risk for physical and developmental
sequelae, and risk of IUGR in a
subsequent pregnancy, should be
provided
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.
 - 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
- 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.
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.
 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.