Growth & Development

Neonatology Division, Child Health Department,

Medical Faculty of Hasanuddin University
Intra Uterine Growth Restriction

 Intra Uterine Growth Retardation

 Small for gestational age (SGA)

 Foetal growth restriction

 'wasted' and 'stunted'

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 Definitions
 IUGR: Failure of a pregnancy to reach
expected fetal growth and manifest as a
deviation of fetal growth from normal
pattern.
 SGA: Infant with wt < 10 % for GA, or > 2
SDs below mean for GA.
 Low birth weight (LBW) means a baby with a
birth weight of less than 2500 g, which could be
due to IUGR or Prematurity
Easiest way to think about these
terms are

 IUGR: is a term used by OB to describe a

pattern of growth over a period of time.
 SGA: is a term used by Peds to describe a
single point on a growth curve.
Incidence

 5 - 8 % of all pregnancies.
 20 % of stillborns are growth retarded.
 30 % of infants with SIDS were IUGR.
 1/3 of infants with BW < 2800 gms are growth
retarded and not premature.
 9 - 27 % have anatomic and/or genetic
abnormalities.
 Perinatal mortality is 8 - 10 times higher for
these fetuses.
Types of IUGR
 Symmetric IUGR: weight,length and head
circumference are all below the 10 th
percentile. (33 % of IUGR Infants)
 Asymmetric IUGR: weight is below the 10 th
percentile and head circumference and
length are preserved. (55 % of IUGR)
Combined type IUGR: Infant may have
skeletal shortening, some reduction o soft
tissue mass. (12 % of IUGR)
 Symmetrical Asymmetrical

the baby's head and body baby's brain is abnormally

are proportionately small. large when compared to the
may occur when the liver.
foetus experiences a may occur when the foetus
problem during early experiences a problem
development. during later development

In a normal infant, the brain weighs about three times more than the liver. In
asymmetrical IUGR, the brain can weigh five or six times more than the liver.
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 Classification
Newer Classification: -
1. Normal small fetuses- have no structural abnormality,
normal umbilical artery & liquor but wt., is less.They are
not at risk and do not need any special care.
2. Abnormal small fetuses- have chromosomal anomalies
or structural malformations. They are lost cases and
deserve termination as nothing can be done.
3. Growth restricted fetuses- are due to impaired
placental function.Appropriate & timely treatment or
termination can improve prospects.

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 Diagnosis
Intrauterine -
 IUGR can be difficult to diagnose.
 Presence of risk factors.
 Inadequate growth detected by serial
measurement of Wt., abdominal girth and
fundal .
 Ultrasound to evaluate the foetal growth.
 Inadequate foetal growth.
 Placental calcification.

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 Diagnosis,
cont...
Neonatal -
 Low ponderal index (Wt./Fl).
 Decreased subcutaneous fat.
 Presence / appearance of –
 Hypoglycemia,
 Hyperbilirubinemia,
 Narcotizing enterocolitis,
 Hyper viscosity syndrome

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Neonate and Placenta in IUGR

 Normal & IUGR Newborn

babies

 Normal & IUGR Placentas

IUGR - Prof.S.N.Panda 12 October 2002 11

Ponderal Index

 Way of characterizing the relationship of height

to mass for an individual.
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 PI = 1000 x Mass (kgs)
Height (cms)

 Typical values are 20 to 25.

 PI is normal in symmetric IUGR.
 PI is low in asymmetric IUGR.
 Etiology
 Growth inhibition in stage I:
- Undersized fetus with fewer cells.
- Normal cell size.
Result in symmetric IUGR.
Associated conditions:
- Genetic
- Congenital anomalies
- Intrauterine infections
- Substance abuse
- Cigarette smoking
- Therapeutic irradiation
Etiology, cont…

 Growth Inhibition in Stage II/III

-Decrease in cell size and fetal weight
- Less effect on total cell numeric, fetal length,
head circumferance.
Result in asymmetric IUGR.
Associated Conditions:
- Uteroplacental insufficiency.
• Combination above associated mixed type IUGR.
 Normal Intrauterine
Growth pattern

 Stage III ( Hypertrophy)

- 28 to 40 weeks
- Rapid increase in cell size.
- Rapid accumulation of fat, muscle and
connective tissue.
 95% of fetal weight gain occurs during last 20
weeks of gestations.
 Pathophysiology
1) Fetal factors:
 Genetic Factors:
- Race, ethnicity, nationality
- sex ( male weigh 150 -200 gm more than
female )
- parity ( primiparous, weigh less than
subsequent siblings)
-genetic disorders ( Achondroplasia, Russell -
silver syn.)
 Chromosomal anomalies:
- Chromosomal deletions
- trisomies 13,18 & 21
Pathophysiology
 Congenital malformations:
examples:Anencephaly, GI atresia, potter’s
syndrome, and pancreatic agenesis.
 Fetal Cardiovascular anomalies
 Congenital Infections:
mainly TORCH infections.
 Inborn error of metabolism:
- Transient neonatal diabetes
- Galactosemia
- PKU
2) Maternal Factors:
 Decrease Uteroplacental blood flow:
- Pre eclampsia / eclampsia
- chronic renovascular disease
- Chronic hypertension
 Maternal malnutrition
 Multiple pregnancy
 Drugs
- Cigarettes, alcohol, heroin, cocaine
- Teratogens, antimetabolites and
therapeutic agents such as trimethadione,
warfarin, phenytoin
Pathophysiology
 Maternal hypoxemia
- Hemoglobinopathies
- High altitudes
• Others
- Short stature
- Younger or older age (<15 and >45)
- Low socioeconomic class
- Primiparity
- Grand multiparity
- Low pregnancy weight
- Previous h/o preterm IUGR baby
- Chronic illness ( DM, renal failure, cyanotic heart
disease etc.)
Pathophysiology

3) Placental Factors:
 Placental insufficiency ( most imp in 3rd trimester)
 Anatomic problems:
 Multiple infarcts
 Aberrant cord insertions
 Umbilical vascular thrombosis & hemangiomas
 Premature placental separation
 Small Placenta
Postnatal Assessment

 Growth parameters: weight, height, HC

 Assess GA with Ballard score.
 Plotted growth parameters in growth chart
Physical
Appearance
 Physical appearance:
• Heads are disproportionately large for their trunks and
extremities
• Facial appearance has been likened to that of a
“wizened old man”.
• Long nails.
• Scaphoid abdomen
• Signs of recent wasting
- soft tissue wasting
- diminished skin fold thickness
- decrease breast tissue
- reduced thigh circumference
• Signs of long term growth failure
- Widened skull sutures, large fontanelles
- shortened crown – heel length
- delayed development of epiphyses
• Comparison to premature infants,IUGR
has brain and heart larger in proportion to
the body weight, in contrast the liver,
spleen, adrenals and thymus are smaller.
Complication

 Hypoxia
- Perinatal asphyxia
- Persistent pulmonary hypertension
- meconium aspiration

 Thermoregulation
- Hypothermia due to diminished subcutaneous
fat and elevated surface/volume ratio
Complications

 Metabolic
- Hypoglycemia
- result from inadequate glycogen stores.
- diminished gluconeogenesis.
- increased BMR
- Hypocalcemia
- due to high serum glucagon level, which
stimulate calcitonin excretion
Complications

 Hematologic
- hyperviscosity and polycythemia due to
increase erythropoietin level sec. to hypoxia
 Immunologic
- IUGR have increased protein catabolism and
decreased in protein, prealbumin and
immunoglobulins, which decreased
humoral and cellular immunity.
Management

 Antenatal diagnosis and management is the

key to proper management of IUGR
 Delivery and Resuscitation
- appropriate timing of delivery
- skilled resuscitation should be available
- prevention of heat loss
 Hypoglycemia
- close monitoring of blood glucose
- early treatment ( IV dextrose, early feeding )
 Management

 Hypothermia : Incubator, Kangaroo Mother Care

 Hematological Disorder
- central Hct to detect polycythemia
- CBC with diff to r/o leukopenia or thrombocytopenia
 Congenital infection
- infant should be examined for signs of congenital
infection (eg.rash, microcephaly hepatosplenomegaly,
lymphadenopathy, cardiac anomalies etc….)
- TORCH titer screening
- Viral cx of urine, nasopharynx
- Head CT to r/o calcification
Management
 Genetic anomalies
- screening as indicated by physical exam
- chromosomal analysis (infant with
dysmorphic features)
 Others
- serum calcium to r/o hypocalcemia
- fractionated bilirubin sec to polycythmia,
congenital infection
- urine, meconium tox for substance abuse
Management

 Early feeding and caloric intake should be

100-120 kcal/kg/d
 Developmental and growth follow up in all
IUGR infants
Outcome

 Symmetric vs. Asymmetric IUGR

- symmetric has poor outcome compare to asymmetric
 Preterm IUGR has high incidence of
abnormalities
 IUGR with chromosomal disease has 100%
incidence of handicap
 Congenital infection has poor outcome -
handicap rate > 50%
 IUGR has higher rate of learning disability.
Short Term Risks of IUGR
 Increased perinatal morbidity and mortality.
 Intra uterine / Intrapartum death.
 Intrapartuum foetal acidosis characterized
by-.
 Late deceleration.
 Severe variable deceleration.
 Beat to beat variability.
 Episodes of bradicardia.

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Short Term Risks of IUGR

 Intrapartum foetal acidosis may occur in as

many as 40 % of IUGR, leading to a high
incidence of LSCS.
 IUGR infants are at greater risk of dying
because of neonatal complications- asphyxia,
acidosis, meconium aspiration syndrome,
infection, hypoglycemia, hypothermia,
sudden infant death syndrome.
 IUGR infants are likely to be susceptible to
infections because of impaired immunity
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Long term Prognosis
.
 The growth that occurs after birth cannot be predicted with
certainty based on the size of the baby when it is born.
 Infants with asymmetrical IUGR are more likely to catch up in
growth after birth than are infants who suffer from prolonged
symmetrical IUGR.
 If IUGR is related to a disease or a genetic defect, the future of
the infant is related to the severity and the nature of that
disorder.

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Long term Prognosis
 IUGR infants are more likely to remain small
than those of normal birth weight. They will
need the special attention of primary health,
nutrition and social services during infancy and
early childhood.
 Implication of IUGR can be life long affecting:
 Body size growth, composition and physical
performance.
 Immunocompetence.

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Long term Prognosis
 It appears to predispose to adult adult-onset,
degenerative diseases like maturity onset
diabetes , obesity, and cardiovascular diseases.
 Impaired Neurodevelopment
 Long term neuromotor dysfunction
 Poor school performance
 Deficits in academic achievements

 Each case is unique. Can not reliably predict an

infant's future progress.
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Asfiksia
Asfiksia :

 Bayi tidak mampu bernapas secara spontan,

teratur dan adekuat segera setelah lahir
- perinatal asfiksia
- Hipoxic ischemic encephalopaty (HIE)
HIE :

 Kumpulan gejala : kejang, gangguan pada

kesadaran, tonus otot, refleks primitif, pernafasan
dan intake
 belajar (spesifik), masalah sekolah
 Berat : kematian atau kecacatan (mikrosefal,
lumpuh) dll