intra utrine growth retardation

1. IUGR--Definition
Failure of the fetus to reach genetically
determined growth potential associated with
increased morbidity and mortality

3. IUGRFacts
• IUGRassociated with 3-10 %of all
pregnancies
•
•
•
•
• Perinatal mortality rate is 5-20 times higherfor
growth retarded fetuses.
2ndleading contributor to the Perinatalmortality
rate
20%of all stillbirths areIUGR
Incidence of intrapartum asphyxia in casesof
IUGRhasbeen reported to be 50%.
Early and proper identification andmanagement
lowers this perinatal mortality andmorbidity

4. Weight gain
• Fetal growth accelerates from about 5gper
day at 14 -15 wks of gestationto
• 10g per day at 20wks
• Peaksat 30 -35g per day at 32-34wks
• After which growth ratedecreases.
Fetal Growth Indices

5. • Symphysiofundal height increases by about
1cm per wk between 14 and 32wks.
• Abdominal girth increasesby 1 inch per wk
after 30 wks. Itis about 30 inches at 30wks in
an average built woman.

6. Classificationof Inrauterine GrowthRestriction
1. Symmetrical IUGR
2. Asymmetrical IUGR

7. SymmetricalIUGR
Headcircumference, length, and weight are all proportionally
reduced for grstational age(below 10thpercentile).
It is due to either decreased growth potential of the fetus or
extrinsic conditions that are active inpregnancy .
AsymmetricalIUGR
Fetal weight is reduced out of proportion to length and head
circumference .
Theusual causesare uteroplacental insufficiency, maternal
malnutrition, or extrinsic conditions appearing late in pregnancy.

8. Aetiology
• IUGRis amanifestation of fetal, maternaland
placental disorders that affect fetalgrowth.
A.Fetal Causes
1. Chromosomal Disorders-
usually result in early onsetIUGR.
Trisomies 13, 18, 21 contribute to 5%of IUGRcases
Sexchromosome disorders are frequently lethal,
fetuses that survive may have growth restriction
(Turner Syndrome)

9. Fetal causescontd..
2. Congenital Infections:
•
•
• Thegrowth potential of fetus may beseverely
impaired by intrauterine infections.
Thetiming of infection is crucial astheresultant
effects depends on the phase of organogenesis.
Viruses- rubella, CMV,varicella and HIV
rubella is the most embryotoxic virus, it causecapillary
endothelial damageduring organogenesis and impairs fetal
growth.
CMVcausescytolysis and localized necrosis in fetus.
• Protozoa- like malaria, toxoplasma, trypanosoma
have also been associated with growthrestriction.

10. Fetal causescontd..
3. StructuralAnomalies-
All major structural defects involving
CNS,CVS,GIT
,Genitourinary and musculoskeletal
system are associated with increased risk offetal
growth restriction.
4. Genetic Causes-
Maternal geneshave greater influenceon
fetal growth.

11. B.Placental causes
• Placenta is the sole channel for nutritionand
oxygen supply to thefetus.
Singleumblical artery
abnormal placental implantation
velamentous umblical cord insertion
bilobed placenta
placental haemangiomas have all beenassociated
with fetal growthrestriction

12. C. Maternal Causes
1. Maternal Characteristics:
those contributing to IUGRare-
Extremes of maternalage
Grandmultiparity
History of IUGRin previous pregnancy
Low maternal weight gain in pregnancy

13. 2. Maternal diseases:
Uteroplacental insufficiency resulting from
medical complications like
Hypertension
Renaldisease
Autoimmune disease
Hyperthyroidism
Longterm insulin dependentdiabetes

14. Maternal causescontd..
• Smoking-active or passive,especially during third
trimester is important causeof IUGR. Nicotine has
vasoconstrctive effect on the maternal circulation
and leads to formatonof toxic metabolites infetus.
• Alchohol and Drugs- Alchohol crosses the
placenta freely. It acts as a cellular poison
reducing fetal growthpotential.
• Cocaine and opiates are potent vasoconstrictors.
• Warfarin, anticonvulsants and antineoplastic
agents are also implicated in growth restriction

15. • Thrombophilias- antiphospholipid antibody
syndrome and other thrombophilias leading to
placental thrombosis and impairedtrophoblastic
function.
• Nutritional Deficiency- leads to deficientsubstrate
supply to thefetus

16. Diagnosis of IUGR
Identifying mothers at risk:
Poormaternal nutrition
PoorBMI at conception
Pre-eclampsia
Renaldisorders
Diseasescausesvascular insufficiency
Infections (TORCH)
Poormaternal wt. gain duringpregnancy

17. • Determination of gestational ageis ofutmost
importance-
– Canbe calculated from the date of LMP-not
reliable
– Ultrasound dating before 21 wks ofpregnancy
provides more accurateestimate.

18. Diagnosis of IUGR
1. Clinically- Serial measurement of fundal
height and abdominalgirth.
Symphysio-fundal height normally increasesby
1cm per wk b/w 14 and 32wks.
Alag in fundal ht. of 4wksissuggestiveof
moderate IUGR.
Alag of >6wksissuggestiveof severe IUGR.

19. Sonographic evaluation-
Fetal biometry:
i. BPD(Biparietal Diameter)- When growth rate
of BPDis below 5thpercentile.
ii.Abdominal circumferenceACand fetal wtare
most accurate ultrasound parameters for
diagnosis of IUGR.
AC<5mm/wk reduction is suggestiveofIUGR

20. iii. Measurement ratios- there are someage
independent ratios to detectIUGR
HC/AC:Persistence of ahead to abdomen ratio <1
late in gestation is predictive ofasymmetric IUGR.
Femurlength : serial measurements of femurlength
are effective for detecting symmetricIUGR

21. Placental Morphology: Acceleration of
placental maturation may occur with IUGR.
Placental volume: helpful in predicting
subsequent fetal growth.
Amniotic fluidvolume:
Amniotic fluid index(AFI) between 8 and 25is
normal.

22. Neonatal Assessment
• Reducedbirth weight for gestationalage
• Physicalappearance: thin loose, peelingskin,
scaphoid abdomen, dispropotionately large head
• Appropriate growth charts should beused
• Ponderal index lessthan 10thcentile.
(used to identify infants whose soft tissue massis bellow normal for the
stsgeof skeletal development)
Birthweight x
100 Ponderal index = Crown –heel
length³
• Ballard score

23. MANAGEMENT
Principles:
1. Identify the causeof growthrestriction.
2. Treat the causeif found.
3. General management

24. MANAGEMENT
Firststepisto identify the aetiology of IUGR:-
Maternal history pertaining tothe risk factors of
IUGR.
Clinical examination- maternal habitus, height,
weight, BPetc.

25. Treatment of underlyingcause
Hypertension,
Cessation of smoking,
Protein energy supplementation inpoorly
nourished and underweight women.

26. GeneralManagement
Bedrest in left lateral position to increase
uteroplacental blood flow
Maternal nutritional supplementation withhigh
caloric and protein diets, antioxidents,
haematinics and omega 3 fatty acids, arginine.
Maternal oxygen therapy: Adminitration of55%
oxygen at arate of 8L/min round the clock has
shown decreased perinatal mortality rate.

27. Pharmacological therapy
Aspirin in low doses(1-2 mg/kg body wt.) have
been tried but all have failed to show any
significant difference in incidence ofIUGR.
Thusthere is no form of therapy currently
available which can reverse IUGR,the only
intervention possible in most casesisdelivery.

28. Delivery
• Since IUGR fetus is at increased risk of
intrauterine hypoxia and intrauterine demise,
the decision needs to delicately balance the
risk to the fetus in utero with continuation of
pregnancy and that of prematurity if delivered
before term.

29. The optimum timing of deliveryis
determined by
• Gestational age,
• Underlying etiology,
• Possibility of extrauterine survivaland
• Fetal condition.
• Strict fetal surveillance is needed tomonitor
fetal well being and to detect signs of fetal
compromise

30. Roleof steroids
Antenatal glucocorticoid administration
reduces the incidence of respiratorydistress
syndrome, intraventricular hemorrhage and
death in IUGRfetuses weighing lessthan
1500gm.

31. Mode of Delivery
Fetuses with significant IUGR should be
preferably delivered in well equiped
centres which can provide intrapartum
continuous fetal heart monitoring , fetal
blood sampling and expert neonatalcare.

32. Vaginaldelivery:
can be allowed as long as there is no obstetric
indication for caesarian section and fetal heart
rate isnormal.
• Fetuses with major anomaly incompatible
with life should also be deliveredvaginally.
Caesariansection

33. Management of new born
Delivery
Resuscitation
Prevention of heatloss
Hypoglycemia
Hematologic disorders
Congenital infections
Genetic anomalies

34. Complicationsof IUGR
Perinatal mortality and morbidity of IUGRinfants
is 3-20 times greater than normalinfants.
• Antepartum period- increased incidenceof-
-stillbirths
-oligohydramnios
IUGRis found in 20%of unexplainedstillbirths.
• During labour- higher incidenceof-
-meconium aspiration
-fetal distress
-intrapartum fetal death

35. Complicationscont..
• Childhood- increases mortality from-
-infectious diseases
-congenital anomalies
Incidence of cerebral palsy are 4-6 timeshigher.
Subtleimpairment of cognitive performanceand
educational underachievement.
• Longterm complications- increased risk of
coronary heart disease, hypertension, typeII
diabetes mellitus, dyslipidaemia andstroke.

36. Complicationsof IUGRcontd..
• Neonatal period-
• increased incidence of-
-Hypoxic ischemic encephalopathy
-Persistent fetal circulationinsufficiency

37. Prognosis
• Mortality increases with prematurity.
• Neurodevelopmental morbidities are seen5-
10 times more often in IUGRinfants.