Intrauterine Growth Restriction IUGR Dana Rivera, M.D. October, 2010

SGA vs IUGR SGA: BW less than population norms < 10 th %-tile OR < 2 standard deviations below the mean (~3 rd %-tile) pathologic or non- pathologic causes IUGR: 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 1Stage 2Stage 3 HyperplasiaHyperplasia/ hypertrophyHypertrophy 4-20 weeks20-28 weeks28-40 weeks Rapid mitosisDeclining mitosisRapid hypertrophy Increasing DNA contentIncreasing cell sizeRapid increasing cell size rapid accumulation of fat, muscle, connective tissue SymmetricMixed- asymmetricAsymmetric

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 factors  Medical disease (US)  Malnutrition (world- wide)  Multiple pregnancy  Drugs  Hypoxemia Small stature/ low pre- pregnancy weight Teen pregnancy Low SES Prima gravida Grand multiparity Maternal, Fetal, Placenta

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- < 10 th %tile  Lt- < 10 th %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 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: 50 th %tile  Lt: 30 th %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 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 & 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? Increased meconium aspiration Decreased surfactant deficiency

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 cal/kg/d  catch- up by 6-12 months Hypersomatotropism- accelerated 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

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