Intrauterine Growth Restriction
IUGR
Dana Rivera, M.D.
October, 2010
SGA vs IUGR
SGA:
IUGR:
BW less than population
norms
< 10th %-tile OR
< 2 standard deviations
below the mean (~3rd
%-tile)
pathologic or nonpathologic causes
BW < expected
inhibition of normal
growth potential
implies pathology
True or False?
All SGA infants are IUGR
False
All IUGR infants are SGA
False
Normal Intrauterine Growth
Stage 1
Stage 2
Stage 3
Hyperplasia
Hyperplasia/ hypertrophy Hypertrophy
4-20 weeks
20-28 weeks
28-40 weeks
Rapid mitosis
Declining mitosis
Rapid hypertrophy
Increasing DNA content
Increasing cell size
Rapid increasing cell
size
rapid accumulation of fat,
muscle, connective
tissue
Symmetric
Mixed- asymmetric
Asymmetric
Symmetric
- Stage I growth
inhibition
Fewer cells but
normal size
- weight, head, length
all < 10th percentile
Perinatal problems?
Higher
Lower
Growth potential?
Higher
Lower
Asymmetric
- Stage II/III growth
inhibition
Decrease in cell
size, less effect on
total cell number
- weight below 10th
percentile,head and
length preserved
Perinatal problems?
Higher
Lower
Growth potential?
Higher
Lower
What factors affect fetal weight?
 Sex
term males 150 gm
heavier and 0.9 cm
longer than females
 Parity
1st born infants smaller
effect loss after 3rd birth
 Race, ethnicity,
nationality
 Altitude
Denver population growth
curves under estimate
weights of infants born
at sea level
 Maternal size
maternal pre-pregnancy
weight and pregnancy
weight gain correlate
with fetus size
“Maternal constraint”- non-genetic
 Number of fetuses
Reduced rate of fetal
growth of multiples
 Small breed embryo
transplanted into
large breed uterus will
grow larger
Hormonal Factors
 Insulin
Major hormone for in
utero growth
Produced by fetus
Promotes fetal adipose
deposition, glycogen
stores
Etiology- Overlapping
Maternal, Fetal, Placenta
 Maternal factors
Medical disease (US)
Malnutrition (worldwide)
Multiple pregnancy
Drugs
Hypoxemia
 Small stature/ low prepregnancy weight
 Teen pregnancy
 Low SES
 Prima gravida
 Grand multiparity
Fetal






Genetic
Congenital malformations
Genetic/ chromosomal (trisomies, syndromes)
Cardiovascular disease
Congenital infection
Inborn errors of metabolism
Placenta
placental insufficiency
post dates
anatomic
abnormal insertion
hemangiomas
infarcts
abruption
Case # 1
 A baby is delivered at
36 WGA via repeat Csection
BW- 2 kg
HC- < 10th %tile
Lt- < 10th %tile
CMV
Case #1- What if?
Toxoplasmosis
Rubella
“TORCH” Stigmata
hepatoslpenomegaly
petechiae/ ecchymoses
blueberry muffin rash
vesicles/ mucocutaneous lesions
chorioretinitis/ cataracts/ salt-pepper
retinopathy
PPS/PDA
microcephaly/ hydrocephaly
Intracranial calcifications
Diagnosis Algorithm
IUGR
yes
TORCH stigmata  work-up?
no
Case # 2
 A baby is delivered
via NSVD, no
prenatal care, EGA
35 weeks
BW- 1500 gm
HC- < 10th
Lt- <10th
Trisomy 13
Case #2- What if?
Trisomy 18
Turner syndrome
Diagnosis Algorithm
IUGR
yes
TORCH stigmata  work-up?
no
yes
Dysmorphic features  work-up?
no
Case # 3
 Infant is delivered at
38 weeks to mom
who presents with
headaches and
epigastric pain
BW: 2.1 kg
HC: 50th%tile
Lt: 30th%tile
Pre-eclampsia/ HELLP
Case # 3- What if?
 Mom with no prenatal
care delivers
undiagnosed twins at
EGA 34 weeks
Discordant twins
Case # 3- What if?
 An infant is delivered
at 42 weeks via csection due to NRHTs
after induction
Post dates
- decreased subcutaneous fat
- skin desquamation
- wizened facies
- large AF(diminished
membranous bone formation)
- meconium staining
Diagnosis Algorithm
IUGR
yes
TORCH stigmata  work-up?
no
yes
Dysmorphic features  work-up?
no
yes
Maternal/placental explanation work-up?
no
Case # 3- What if?
 Infant delivered at
EGA 34 weeks to
mom with no prenatal
care and positive tox
screen
Diagnosis Algorithm
IUGR
yes
TORCH stigmata  work-up?
no
yes
Dysmorphic features  work-up?
no
yes
Maternal/placental explanation work-up?
no
yes
Maternal drug use tox screen
no
Unknown cause
True or False
 IUGR infants are
prone to asphyxia
 Why or why not?
Perinatal hypoxia
 Chronic and acute
True
Increased C/S rate,
decreased Apgar,
increased resuscitation
need
An IUGR infant is at risk for
Hypothermia?
decreased subcutaneous fat,
increased surface- volume
ratio, decreased heat
production
Hypoglycemia?
decreased glycogen stores/
glycogenolysis/
gluconeogenesis
increased metabolic rate
deficient catecholamine
release
Or
Hypocalcemia?
Associated with perinatal
stress, asphyxia, prematurity
Which lab result(s) would not be
associated with IUGR?
 WBC 4, S8 & B1
 H & H 11/ 33
 Plt 65
 PT 16
 PTT 56
 Direct bilirubin 4.5
 Neutropenia
 Polycythemia
Elevated
erythropoietin
 Thrombocytopenia
 Elevated coags
 TORCH
Which CxR is more consistent with
IUGR?
Decreased surfactant deficiency
Increased meconium aspiration
Perinatal problems
 Perinatal asphyxia
 Hypothermia
 Hypoglycemia
 Hypocalcemia
 Polycythemia,
hyperviscosity
 Thrombocytopenia
 Neutropenia
 Elevated coags
 Decreased surfactant
deficiency
 Increased meconium
aspiration syndrome
 Direct
hyperbilirubinemia
Evaluation and Management
Physical exam
Labs
- blood sugar
- urine shell vial (CMV)
- calcium
- viral cultures (HSV)
- CBC diff/plt
- syphilis w/u
- bilirubin
- tox screen
- head ultrasound
- chromosomes
- total IgM vs specific
Quick algorithm
Evaluation and Management
 Monitor postnatal weight
gain/ head growth
needs may exceed
100-120 cal/kg/d
catch- up by 6-12
months
 Hypersomatotropismaccelerated growth
velocity
 ? Safety of aggressive
feeding
 rapid weight gain may
predispose to childhood
obesity highest risk for
developing type 2 DM
IUGR- Outcome
Neurodevelopment
etiology and adverse event dependent
lower intelligence, learning/ behavioral
disorders, neurologic handicaps
symmetric, chromosomal disorders, congenital
infections--- poorer outcome
school performance influenced by social class
World’s smallest…..