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

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I.U.G.R. Intrauterine Growth Retardation (Restriction)

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Intrauterine Growth Retardation (Restriction)

Presented by:




  • 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

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:

  • 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.

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


? Need for different growth curves to

take the above into account.


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%.

Why Distinguish?

Symmetric IUGR babies are more likely to have an underlying “cause”.

9-27% of IUGR infants have anatomic and or genetic abnormalities.


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.

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.
  • 4-20 weeks' gestation – rapid cellular development with mitosis
  • 2. 20-28 weeks – increase in cellular size combined with ongoing mitosis.

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 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.

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



Maternal illnesses

       - chronic renal disease,

       - cyanotic heart disease,

       - hemoglobinopathies

       - substance abuse and cigarette


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:

  • 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.


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


- 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:


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. Hypoglycaemiadue to low sugar reserves and higher energy consumption – esp. with cold stress.


3. Hypothermiadue to lack of subcutaneous

fat and relatively high S.A to body weight


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 glucoseshould 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



  • 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.


  • Parental counselling about diagnosis,

risk for physical and developmental

sequelae, and risk of IUGR in a

subsequent pregnancy, should be



Outcome for SGA babies:

Increased mortality and morbidity as noted.

Long term outlook:


- 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


- Preterm IUGR infants have similar outcomes at

18-24 months of age, compared to AGA preterm


- 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.


- Overall, IUGR infants have an increased

incidence of lower intelligence, learning

and behavioral disorders and neurologic


- 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




- 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.



-Delayed eruption of teeth and enamel


- 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.