IUGR
PRESENTED BY
AMRUTHA R
1st yr MSc nsg
18-03-2013
CHILD HEALTH NURSING
SGA
IUGR
NORMAL FOETAL GROWTH
• Cellular hyperplasia
• Hyperplasia and hypertrophy
• hypertrophy
Stages
• Stage I (Hyperplasia)
- 4 to 20 weeks
- Rapid mitosis
- Increase of DNA content
Stages
• Stage II (Hyperplasia & Hypertrophy)
- 20 to 28 weeks
- Declining mitosis.
- Increase in cell size.
Stages
• 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.
CAUSES OF IUGR
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•
•
•
Maternal factors
Fetal factors
Placental factors
Environmental factors
MATERNAL FACTORS
• Medical disease
• Malnutrition  BMI < 19 twice the risk
of IUGR
• Multiple pregnancy
• Smoking (460 gm < then none
smoker)
MATERNAL FACTORS
• Alcohol
 12-fold increase risk of IUGR
• Drugs
 Beta- Blockers(Atenolol in second
trimster,
Anticoagulants, Anticonvulsants(
phenytoin)
• Hypoxemia
• Infections  UTI, Malaria, TB, Genital Infections
MATERNAL FACTORS
•
•
•
•
Small stature/ low pre-pregnancy weight
Teen pregnancy
Primi gravida
Grand multiparity
FETAL FACTORS
• A Chromosome Defect In second trimester 20% SGA fetuses have
chromosomal abnormality
 Triploid is most common under 26 wks.
 Trisomy-18 is common after 26 wks .
 Other are 21(Down’s syndrome), 16, 13, xo
(turner’s syndrome).
FETAL FACTORS
• Exposure to an infection• German measles (rubella),
cytomegalovirus, herpes simplex,
tuberculosis, syphilis, or toxoplasmosis,
TB, Malaria, Parvo virus
FETAL FACTORS
• birth defects
•
(cardiovascular, renal, anencephally, limb
defect, etc).
• A primary disorder of bone or cartilage.
• A chronic lack of oxygen during
development (hypoxia
• Placenta or umbilical cord defects.
PLACENTAL FACTORS
• Uteroplacental Insufficiency
Resulting From -.
– Improper / inadequate trophoblastic
invasion and placentation in the first
trimester.
– Lateral insertion of placenta.
– Reduced maternal blood flow to the
placental bed.
PLACENTAL FACTORS
• Fetoplacetal Insufficiency Due To-.
– Vascular anomalies of placenta and
cord.
– Decreased placental functioning mass-.
• Small placenta, abruptio placenta,
placenta previa, post term pregnancy
Normal & IUGR Newborn babies
Normal & IUGR
Placentas
Environmental Causes of IUGR
• High altitude - lower environmental oxygen
saturation
• Toxins
Types of IUGR
• Symmetric IUGR:
(33 % of IUGR Infants)
• Asymmetric IUGR
(55 % of IUGR)
• Combined type IUGR:
(12 % of IUGR)
SYMMETRICAL
• height, weight, head circ proportional
• early pregnancy insult:
• commonly due to congenital infection,
genetic disorder, or intrinsic factors
• Reduced no of cells in fetus
• normal ponderal index
• low risk of perinatal asphyxia
• low risk of hypoglycemia
PONDERAL INDEX
• The ponderal index is used determine
those infants whose soft tissue mass is
below normal for their stage of skeletal
development.
Ponderal Index =
birth weight x 100
crown-heel length
PONDERAL INDEX
• Typical values are 20 to 25.
• Those who have a ponderal index below
the 10th % can be classified as SGA
• PI is normal in symmetric IUGR.
• PI is low in asymmetric IUGR
ASSYMETRICAL
• later in pregnancy:
• commonly due to utero placental
insufficiency, maternal malnutrition,
hypoxia, or extrinsic factors
• low ponderal index
• Cell number remains same but size is
small
• increased risk of asphyxia
• increased risk of hypoglycemia
• Growth restriction in the stage of
hypertrophy
• Brain sparing effect
• Head growth remains normal but
abdominal girth slows down
Newer Classification: 1. Normal Small FetusesHave no structural abnormality,
normal umbilical artery & liquor but
wt., is less.
They are not at risk and do not need any
special care.
Abnormal Small Fetuses- have
chromosomal anomalies or structural
malformations. They are lost cases and
deserve termination as nothing can be
done.
Growth Restricted Fetuses- are due to
impaired placental function. Appropriate &
timely treatment or termination can
improve prospects.
CLINICAL
FEATURES
Weight deficit
Large head
circumference
Old man look
Cartilaginous
ridges on pinna
Dry wrinkled
skin
Length remain
unaffected
Open eyes
Well defined
creases
Alert and
active
Normal
reflexes
Normal cry
Thin
umbilical
• 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
PREDICTION OF IUGR
• History
risk factors
last menstrual period - most precise
size of uterus
time of quickening (detection of
fetal movements)
• Examination /
MATERNAL SERUM
SCREENING
• AFP
• more for gestation in the absence of fetal
anomaly, there is a 5-10 fold increase in
the risk of FGR
• Uterine Artery Doppler Velocimetry
- Notching of the waveform /reduce
EDF
associated 3-fold increase in risk of
FGR.
•
Bright or echogenic fetal bowel in the
second trimester is associated with
increase risk of FGR.
• Combination of un-explain elevated
maternal AFP is powerful predictor of
adverse perinatal outcome (FGR)
• Increase AFP combine with echogenic
bowel is strong predictor of FGR
• DOPPLER OF THE UMBILICAL ARTERY
• Reduced end diastolic flow.
•
Absent end diastolic flow
•
Reversed end diastolic flow( severe
cases)
Problems
• Hypoxia
- Perinatal asphyxia
- Persistent pulmonary hypertension
- meconium aspiration
• Thermoregulation
-Hypothermia due to diminished
subcutaneous fat and elevated
surface/volume ratio
Metabolic
- Hypoglycemia
- result from inadequate glycogen
stores.
- diminished gluconeogenesis.
- increased BMR
- Hypocalcemia
- due to high serum glucagon level,
which stimulate calcitonin excretion
• 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.
• Fetal distress,
•
Hypoxia, Acidosis and Low Apgar Score
at birth.
Increased perinatal morbidity and mortality
•
Grade 3-4 intraventricular haemorrhage
•
Necrotizing enterocolitis
•
•
•
•
•
•
BIOPHYSICAL
HC:AC
more than 1
Brfore 32 wks
app 1
32—34 wks
FEMUR LENGTH
FL:AC IS 22at all gest wks from 21 wks to
term
• More than 23.5 indicate IUGR
• AFI
• <2 Suggest IUGR
• PI
PREVENTION OF HYPOTHERMIA
• MUMMIFICATION
• KMC
• NESTING
• DELAY BATH
• WARMER
MAINTAINING BREATHING
• VENTILATOR
• C PAP
• 02 SUPPLEMENTATIO N
NUTRITION FLUID AND FEEDING
• <30– IV FLUIDS, NG ,KATORI, BREAST
FEEDS
• 30—34 NG ,KATORI, BREAST FEEDS
• >34
KATORI, BREAST FEEDS
Monitoring
• Vital signs
• Activity and behaviour.
• Color; Pink, pale, grey, blue, yellow.
• Tissue perfusion
• Fluids, electrolytes and ABG's.
• Bronchopulmonary dysplasia
Metabolic disturbances and hypoglycemia
Polycytemia
Hypothermia
Impaired cognitive function and cerebral
paresis
MEDICAL
• ASPIRIN THERAPY
• Other forms of treatment that have been
studied are
• nutritional supplementation,
• zinc supplementation,
• fish oil,
• hormones and
• oxygen therapy
MANAGEMENT
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•
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•
3—10 Percentile
Skin to skin care
Breast feeding
Glucose level monitoring
Polycythemia
<3 percentile
• Thermal protection
• feeding
THANK YOU