Intrauterine Growth Retradation

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Intrauterine Growth
Retardation (Restriction)
Jignesh Patel, MD
Texas Tech University HSC
Department of Pediatrics
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.
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.
Incidence





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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.
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)
Ponderal Index

Way of characterizing the relationship of height to
mass for an individual.
3


PI = 1000 x
Mass (kgs)
Height (cms)
Typical values are 20 to 25.
 PI is normal in symmetric IUGR.
 PI is low in asymmetric IUGR.
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.
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.
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
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.
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
Pathophysiology

Congenital malformations:
examples:Anencephaly, GI atresia, potter’s
syndrome, and pancreatic agenesis.
 Fetal Cardiovascular anomalies
 Congenital Infections:
mainly TORCH infections.
 Inborn error of metabolism:
- Transient neonatal diabetes
- Galactosemia
- PKU
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
Pathophysiology

Maternal hypoxemia
- Hemoglobinopathies
- High altitudes
•
Others
- Short stature
- Younger or older age (<15 and >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.)
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

Postnatal Assessment

Growth parameters: weight, height, HC
 Assess GA with Ballard score.
 Plotted growth parameters in growth chart
Physical Appearance
Physical appearance:
•
•
•
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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
•
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.
Complication
 Hypoxia
- Perinatal asphyxia
- Persistent pulmonary hypertension
- meconium aspiration
 Thermoregulation
- Hypothermia due to diminished
subcutaneous fat and elevated
surface/volume ratio
Complications
 Metabolic
- Hypoglycemia
- result from inadequate glycogen stores.
- diminished gluconeogenesis.
- increased BMR
- Hypocalcemia
- due to high serum glucagon level, which
stimulate calcitonin excretion
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.
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 )
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
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
Management

Early feeding and caloric intake should be
100-120 kcal/kg/d
 Developmental and growth f/u in all IUGR
infants
Outcome
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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 > 50%
IUGR has higher rate of learning disability.
Thank You
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