Intrauterine Growth Restriction

IUGR
Dana Rivera, M.D.
October, 2010
SGA vs IUGR
SGA: IUGR:
BW less than population BW < expected
norms inhibition of normal
< 10th %-tile OR growth potential
< 2 standard deviations
below the mean (~3rd implies pathology
%-tile)
pathologic or non-
pathologic causes
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 Perinatal problems?

inhibition Higher
Fewer cells but Lower
normal size
- weight, head, length Growth potential?
all < 10th percentile Higher
Lower
Asymmetric

- Stage II/III growth Perinatal problems?

inhibition Higher
Decrease in cell Lower
size, less effect on
total cell number
Growth potential?
- weight below 10th Higher
percentile,head and
Lower
length preserved
What factors affect fetal weight?
Sex Altitude
term males 150 gm Denver population growth
heavier and 0.9 cm curves under estimate
longer than females weights of infants born
Parity at sea level

1st born infants smaller Maternal size

effect loss after 3rd birth maternal pre-pregnancy
weight and pregnancy
Race, ethnicity, weight gain correlate
nationality with fetus size
Maternal constraint- non-genetic
Number of fetuses Small breed embryo
Reduced rate of fetal transplanted into
growth of multiples 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) Small stature/ low pre-
Malnutrition (world- pregnancy weight
wide) Teen pregnancy
Multiple pregnancy Low SES
Drugs Prima gravida
Hypoxemia 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 C-
section
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 c-
section 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 Why or why not?
prone to asphyxia Perinatal hypoxia
Chronic and acute
Increased C/S rate,
True 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
Or
deficient catecholamine release

Associated with perinatal stress,

Hypocalcemia? asphyxia, prematurity
Which lab result(s) would not be
associated with IUGR?
WBC 4, S8 & B1 Neutropenia
H & H 11/ 33 Polycythemia
Plt 65 Elevated
erythropoietin
PT 16
Thrombocytopenia
PTT 56
Elevated coags
Direct bilirubin 4.5
TORCH
Which CxR is more consistent with
IUGR?

Increased meconium aspiration

Decreased surfactant deficiency
Perinatal problems
Perinatal asphyxia Neutropenia
Hypothermia Elevated coags
Hypoglycemia Decreased surfactant
Hypocalcemia deficiency
Polycythemia, Increased meconium
hyperviscosity aspiration syndrome
Thrombocytopenia 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 ? Safety of aggressive
gain/ head growth feeding
rapid weight gain may
needs may exceed predispose to childhood
100-120 cal/kg/d obesity highest risk for
developing type 2 DM
catch- up by 6-12
months
Hypersomatotropism-
accelerated growth
velocity
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
Worlds smallest..