Intrauterine Growth RestrictionIUGR

Dana Rivera, M.D.

October, 2010

SGA vs IUGR

SGA: BW less than population

norms

< 10th %-tile OR

< 2 standard deviations below the mean (~3rd %-tile)

pathologic or non-pathologic causes

IUGR: BW < expected

inhibition of normal growth potential

implies pathology

True or False?

All SGA infants are IUGRFalse

All IUGR infants are SGAFalse

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 inhibitionFewer cells but

normal size

- weight, head, length all < 10th percentile

Perinatal problems?

Higher

Lower

Growth potential?

Higher

Lower

Asymmetric

- Stage II/III growth inhibitionDecrease 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?

Sexterm males 150 gm

heavier and 0.9 cm longer than females

Parity1st born infants smaller

effect loss after 3rd birth

Race, ethnicity, nationality

AltitudeDenver population growth

curves under estimate weights of infants born at sea level

Maternal sizematernal pre-pregnancy

weight and pregnancy weight gain correlate with fetus size

“Maternal constraint”- non-genetic

Number of fetusesReduced 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 factorsMedical disease (US) Malnutrition (world-

wide)Multiple pregnancyDrugsHypoxemia

Small stature/ low pre-pregnancy weight

Teen pregnancyLow SESPrima gravidaGrand multiparity

Maternal, Fetal, Placenta

Fetal

GeneticCongenital malformationsGenetic/ chromosomal (trisomies, syndromes)Cardiovascular diseaseCongenital infection Inborn errors of metabolism

Placenta

placental insufficiencypost dates

anatomicabnormal insertionhemangiomasinfarctsabruption

Case # 1

A baby is delivered at 36 WGA via repeat C- sectionBW- 2 kgHC- < 10th %tileLt- < 10th %tile

CMV

Case #1- What if?

Toxoplasmosis

Rubella

“TORCH” Stigmata

hepatoslpenomegalypetechiae/ ecchymosesblueberry muffin rashvesicles/ mucocutaneous lesionschorioretinitis/ cataracts/ salt-pepper retinopathyPPS/PDAmicrocephaly/ hydrocephaly

Intracranial calcifications

Diagnosis Algorithm

IUGR

yesTORCH stigmata work-up? no

Case # 2

A baby is delivered via NSVD, no prenatal care, EGA 35 weeksBW- 1500 gmHC- < 10thLt- <10th

Trisomy 13

Case #2- What if?

Trisomy 18 Turner syndrome

Diagnosis Algorithm

IUGR

yesTORCH stigmata work-up? no yesDysmorphic features work-up? no

Case # 3

Infant is delivered at 38 weeks to mom who presents with headaches and epigastric painBW: 2.1 kgHC: 50th%tileLt: 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

yesTORCH stigmata work-up? no yesDysmorphic features work-up? no

yesMaternal/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

yesTORCH stigmata work-up? no yesDysmorphic features work-up? no

yesMaternal/placental explanation work-up?

no yes

Maternal drug use tox screenno

Unknown cause

True or False

IUGR infants are prone to asphyxia

True

Why or why not?Perinatal hypoxia

Chronic and acute Increased C/S rate,

decreased Apgar, increased resuscitation need

An IUGR infant is at risk for

Hypothermia?

Hypoglycemia?

Or

Hypocalcemia?

decreased subcutaneous fat, increased surface- volume ratio, decreased heat production

decreased glycogen stores/ glycogenolysis/ gluconeogenesis

increased metabolic rate

deficient catecholamine release

Associated with perinatal stress, asphyxia, prematurity

Which lab result(s) would not be associated with IUGR?WBC 4, S8 & B1H & H 11/ 33Plt 65PT 16PTT 56Direct bilirubin 4.5

NeutropeniaPolycythemia

Elevated erythropoietin

Thrombocytopenia Elevated coagsTORCH

Which CxR is more consistent with IUGR?

Increased meconium aspiration

Decreased surfactant deficiency

Perinatal problems

Perinatal asphyxiaHypothermiaHypoglycemiaHypocalcemiaPolycythemia,

hyperviscosityThrombocytopenia

NeutropeniaElevated coagsDecreased surfactant

deficiencyIncreased meconium

aspiration syndromeDirect

hyperbilirubinemia

Evaluation and Management

Physical examLabs

- 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 growthneeds may exceed

100-120 cal/kg/dcatch- up by 6-12

monthsHypersomatotropism-

accelerated growth velocity

? Safety of aggressive feeding

rapid weight gain may predispose to childhood obesity highest risk for developing type 2 DM

IUGR- Outcome

Neurodevelopmentetiology and adverse event dependentlower intelligence, learning/ behavioral

disorders, neurologic handicapssymmetric, chromosomal disorders, congenital

infections--- poorer outcomeschool performance influenced by social class

World’s smallest…..