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    Intrauterine GrowthRetardation (Restriction)

    Jignesh Patel, MD

    Texas Tech University HSC

    Department of Pediatrics

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    Definitions

    IUGR: Failure of normal fetal growth

    caused by multiple adverse effects on the

    fetus.

    SGA: Infant with wt < 10% ile for GA, or

    > 2 SDs below mean for GA.

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    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.

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    Incidence

    3 - 10 % 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.

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    Types of IUGR

    Symmetric IUGR: weight,length and headcircumference are all below the 10 thpercentile. (33 % of IUGR Infants)

    Asymmetric IUGR: weight is below the10 th percentile and head circumference andlength are preserved. (55 % of IUGR)

    Combined type IUGR: Infant may haveskeletal shortening, some reduction of softtissue mass. (12 % of IUGR)

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    Ponderal Index

    Way of characterizing the relationship of height to

    mass for an individual.

    PI = 1000 x

    Typical values are 20 to 25. PI is normal in symmetric IUGR.

    PI is low in asymmetric IUGR.

    Mass (kgs)

    Height (cms)

    3

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    Normal Intrauterine Growth pattern

    Stage I (Hyperplasia)

    - 4 to 20 weeks

    - Rapid mitosis

    - Increase of DNA content

    Stage II (Hyperplasia & Hypertrophy)

    - 20 to 28 weeks- Declining mitosis.

    - Increase in cell size.

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    Normal Intrauterine Growth pattern

    Stage III ( Hypertrophy)

    - 28 to 40 weeks

    - Rapid increase in cell size.

    - Rapid accumulation of fat, muscle andconnective tissue.

    95% of fetal weight gain occurs during last20 weeks of gestations.

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    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

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    Etiology

    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.

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    Pathophysiology

    1) Fetal factors: Genetic Factors:

    - Race, ethnicity, nationality

    - sex ( male weigh 150 -200 gm more thanfemale )

    - parity ( primiparous, weigh less thansubsequent siblings)

    -genetic disorders ( Achondroplasia, Russell -silver syn.)

    Chromosomal anomalies:

    - Chromosomal deletions

    - trisomies 13,18 & 21

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    Pathophysiology

    Congenital malformations:

    examples:Anencephaly, GI atresia, potterssyndrome, and pancreatic agenesis.

    Fetal Cardiovascular anomalies Congenital Infections:

    mainly TORCH infections.

    Inborn error of metabolism:

    - Transient neonatal diabetes

    - Galactosemia

    - PKU

    P th h i l

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    Pathophysiology

    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 therapeuticagents such as trimethadione, warfarin, phenytoin

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    Pathophysiology

    Maternal hypoxemia- Hemoglobinopathies

    - High altitudes

    Others

    - Short stature- Younger or older age (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.)

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    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

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    Postnatal Assessment

    Growth parameters: weight, height, HC

    Assess GA with Ballard score.

    Plotted growth parameters in growth chart

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    Physical Appearance

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    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

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    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 crownheel length

    - delayed development of epiphyses

    Comparison to premature infants,IUGR has brainand heart larger in proportion to the body weight,in contrast the liver, spleen, adrenals and thymusare smaller.

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    Complication

    Hypoxia

    - Perinatal asphyxia

    - Persistent pulmonary hypertension- meconium aspiration

    Thermoregulation

    - Hypothermia due to diminishedsubcutaneous fat and elevatedsurface/volume ratio

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    Complications

    Metabolic

    - Hypoglycemia

    - result from inadequate glycogen stores.

    - diminished gluconeogenesis.

    - increased BMR

    - Hypocalcemia

    - due to high serum glucagon level, whichstimulate calcitonin excretion

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    Complications

    Hematologic

    - hyperviscosity and polycythemia due to

    increase erythropoietin level sec. to hypoxia Immunologic

    - IUGR have increased protein catabolism

    and decreased in protein, prealbumin andimmunoglobulins, which decreased humoraland cellular immunity.

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    Management

    Antenatal diagnosis and management is thekey 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 )

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    Management

    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

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    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

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    Management

    Early feeding and caloric intake should be

    100-120 kcal/kg/d

    Developmental and growth f/u in all IUGRinfants

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    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 - handicaprate > 50%

    IUGR has higher rate of learning disability.

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    Thank You