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Intrauterine Growth Retardation Restriction

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Long nails. Scaphoid abdomen. Signs of recent wasting - soft tissue wasting ... Signs of long term growth failure - Widened skull sutures, large fontanelles ... – PowerPoint PPT presentation

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Title: Intrauterine Growth Retardation Restriction


1
Intrauterine Growth Retardation (Restriction)
  • Jignesh Patel, MD
  • Texas Tech University HSC
  • Department of Pediatrics

2
Definitions
  • IUGR Failure of normal fetal growth caused by
    multiple adverse effects on the fetus.
  • SGA Infant with wt lt 10 ile for GA, or gt 2
    SDs below mean for GA.

3
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.

4
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 lt 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.

5
Types of IUGR
  • Symmetric IUGR weight,length and head
    circumference are all below the 10 th percentile.
    (33 of IUGR Infants)
  • Asymmetric IUGR weight is below the 10 th
    percentile and head circumference and length are
    preserved. (55 of IUGR)
  • Combined type IUGR Infant may have skeletal
    shortening, some reduction of soft tissue mass.
    (12 of IUGR)

6
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.

3
Mass (kgs) Height (cms)
7
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.

8
Normal Intrauterine Growth pattern
  • Stage III ( Hypertrophy)
  • - 28 to 40 weeks
  • - Rapid increase in cell size.
  • - Rapid accumulation of fat, muscle and
    connective tissue.
  • 95 of fetal weight gain occurs during last 20
    weeks of gestations.

9
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


10
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.

11
Pathophysiology
  • 1) Fetal factors
  • Genetic Factors
  • - Race, ethnicity, nationality
  • - sex ( male weigh 150 -200 gm more than
    female )
  • - parity ( primiparous, weigh less than
    subsequent siblings)
  • -genetic disorders ( Achondroplasia, Russell -
    silver syn.)
  • Chromosomal anomalies
  • - Chromosomal deletions
  • - trisomies 13,18 21

12
Pathophysiology
  • Congenital malformations
  • examplesAnencephaly, GI atresia, potters
    syndrome, and pancreatic agenesis.
  • Fetal Cardiovascular anomalies
  • Congenital Infections
  • mainly TORCH infections.
  • Inborn error of metabolism
  • - Transient neonatal diabetes
  • - Galactosemia
  • - PKU

13
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 therapeutic
    agents such as trimethadione, warfarin, phenytoin

14
Pathophysiology
  • Maternal hypoxemia
  • - Hemoglobinopathies
  • - High altitudes
  • Others
  • - Short stature
  • - Younger or older age (lt15 and gt45)
  • - Low socioeconomic class
  • - Primiparity
  • - Grand multiparity
  • - Low pregnancy weight
  • - Previous h/o preterm IUGR baby
  • - Chronic illness ( DM, renal failure,
    cyanotic heart
    disease etc.)

15
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

16
Postnatal Assessment
  • Growth parameters weight, height, HC
  • Assess GA with Ballard score.
  • Plotted growth parameters in growth chart

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Physical Appearance
20
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

21
  • 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 crown heel length
  • - delayed development of epiphyses
  • Comparison to premature infants,IUGR has brain
    and heart larger in proportion to the body
    weight, in contrast the liver, spleen, adrenals
    and thymus are smaller.

22
Complication
  • Hypoxia
  • - Perinatal asphyxia
  • - Persistent pulmonary hypertension
  • - meconium aspiration
  • Thermoregulation
  • - Hypothermia due to diminished subcutaneous fat
    and elevated surface/volume ratio

23
Complications
  • Metabolic
  • - Hypoglycemia
  • - result from inadequate glycogen stores.
  • - diminished gluconeogenesis.
  • - increased BMR
  • - Hypocalcemia
  • - due to high serum glucagon level, which
    stimulate calcitonin excretion

24
Complications
  • Hematologic
  • - hyperviscosity and polycythemia due to
    increase erythropoietin level sec. to hypoxia
  • Immunologic
  • - IUGR have increased protein catabolism and
    decreased in protein, prealbumin and
    immunoglobulins, which decreased humoral and
    cellular immunity.

25
Management
  • Antenatal diagnosis and management is the key 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 )

26
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

27
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

28
Management
  • Early feeding and caloric intake should be
    100-120 kcal/kg/d
  • Developmental and growth f/u in all IUGR infants

29
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 - handicap
    rate gt 50
  • IUGR has higher rate of learning disability.

30
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