SGA-its etiology and diagnosis

1. IUGR-ETIOLOGY & DIAGNOSIS
Dr.Suman Kumari
MS OBGY
TATA MAIN HOSPITAL

2. Introduction
IUGR/FGR
A fetus that has not reached its growth potential because of
genetic or envoirnmental factors. Results in
 BW < 10%tile as per the customised growth curve.
 Inhibition of normal growth potential
 implies pathology
SGA:
 BW less than population norms < 10th %-tile
 usually physiological or constitutional

3. Cause of concern
• Leading contributor - Perinatal mortality rate(50%) at
preterm and 20% at term.
• 40% of all stillbirths are IUGR.
• Perinatal morbidity as well as delayed effects including
cerebral palsy(CP) .

4. Effect of birth weight on Perinatal morbidity and mortality.

5. The developmental origins of adult disease —
Barker’s hypothesis
Growth retardation
in utero can Cause
hypertension,
diabetes ,
Cardiac problems
in adult life.

6. Why antenatal diagnosis
• Early detection of IUGR categorised the women into high
risk group.
• Early identification, further investigation and intervention
leads to significantly improved outcome.
• Depending upon the severity optimal timing of delivery
could be decided.
• Antenatal detection of IUGR has better outcome.(Molin
J.2005).
• Identification and management lowers this perinatal
mortality and morbidity.

7. Normal Intrauterine Growth

8. IUGR - Types
• Symmetric
Stage I growth inhibition
Fewer cells but normal size
weight, head, length all < 10th percentile
• Asymmetric
Stage II/III growth inhibition
Decrease in cell size, less effect on total cell number
weight below 10th percentile,head and length
preserved

9. Physiology

10. Pathophysiology
• Gas exchange and nutrient delivery to the fetus are not
sufficient - IUGR
maternal disease
 diabetes with vascular disease, hypertension, autoimmune
disease affecting the vessels-- dysfunctional oxygen delivery
system
 cyanotic heart disease, smoking, hemoglobinopathy---
causing decreased oxygen-carrying capacity
 smoking, thrombophilia, various autoimmune diseases--
placental damage

12. Pre-eclampsia/ HELLP

13. Diabetes
• Diabetes-usually macrosomic.
• IUGR-15-20% when preeclampsia associated with diabetes
without nephropathy .
• IUGR-50% when preeclampsia associated diabetic
nephropathy.

14. Etiology- Overlapping
Maternal factor
• Chronic hypertension
• Pregnancy associated hypertension.
• Cyanotic heart disease
• Class F or higher diabetes
• Hemoglobinopathies
• Autoimmune disease
• Protein-calorie malnutrition
• Smoking
• Substance abuse

15. Placenta
• Placental insufficiency
– PIH,Preeclampsia,diabetes mellitus.
– Chronic hypertension
• Anatomic
– abnormal insertion
– hemangiomas
– infarcts
– Abruption
– Twin to twin transfusion syndrome.

16. Fetal factors
• Genetic
• Congenital malformations
• Genetic/ chromosomal (trisomies, syndromes)
• Cardiovascular disease
• Congenital infection
• Inborn errors of metabolism

17. Discordant twins
• Growth standards for
multiple pregnancies
are there
but singleton nomograms are more
used commonly
with good accuracy.
Discordance >20-25% is
significant.

19. Trisomy 13
Turner syndrome

20. Toxoplasmosis
Rubella

21. Uterine factors
• Morphological abnormalities
• Fibromyoma

22. Diagnosis
• History
• Physical examination
• Biochemical screening in ANC
• Ultrasound and Fetal biometry
• USG doppler

23. HISTORY
• Risk factor assessment by history.
• Previous h/o still birth baby have a 50% increase risk of severe
growth restriction in current pregnancy. (Villar J,AJOG 2006)
• h/o dysmorphic feature or chromosomal anomaly .

24. TORCH” Stigmata
– hepatoslpenomegaly
– petechiae/ ecchymoses
– blueberry muffin rash
– vesicles/ mucocutaneous lesions
– chorioretinitis/ cataracts/ salt-pepper retinopathy
– PDA
– microcephaly/ hydrocephaly
• Intracranial calcifications

25. Physical exam.
• Abdominal exam-detection rate-30 to 50%.
• Symphysio fundal height(SFH)-sensitivity is 50%.
 Uterine fundal height corresponds to week of
gestation between 18 to 36 week.
 Serial SFH supplemented with anatomic USG-
increases the accuracy of diagnosis.
 Lag of 3 cm-- prompt USG indicated.
 Unsuitable in case of fibroid uterus,obesity.

26. Clinical examination
• SFH

27. Customised growth curve (CGC)
Customised growth curve (CGC)-design to identify fetus
<10%tile of their genetic growth potential

28. Biochemical test in ANC
• Biochemical screening –for at risk pregnancy.
• First trimester-low pregnancy associated plasma
protein –A(PAPP-A) .
• Decrease PAPP-A with increase AFP,inhibin and hCG
suggest IUGR.(Dugoff L,AJOG 2004)

29. Ultrasound diagnosis
• USG assessment requires three basic steps
1. Accurate dating
2. Biometric evaluation and
3. Assessment of growth.

30. USG
1. Accurate assessment of the gestational age is most
important before diagnosing IUGR.
• 1ST trimester USG can confirm the date with margin of 1 wk.
• TCD-most effective ,for dating in second and third trimester
and being normal in 75% of 73 previously dated IUGR fetuses.
• serial measurement are nessessary to depict actual growth
lag.
• Interval between growth scan should be atleast 2 wk.

31. Parameters
2.Parameters to assess biometric growth are-
 Biparietal diameter(BPD)
 Head circumference(HC)
 Abdominal circumference(AC)
 Femur length.(FL)
To estimate fetal weight(EFW)-sensitivity
89%,specificity-91%
 HC/AC ratio,FL/AC ratio

32. Abdominal circumference(AC)
 Most accurate measurement to predict IUGR.
 Cut off-below the 10TH %tile.
 Sensitivity 74-94% ,specificity-50%
 Should increase by atleast 10mm / 2 week.
 So SFH measurment and biometry scan are basically
surveillance test,require serial monitoring.

33. USG
• For fetal anatomy (anomaly scan)
 At 18 -20 wk gestation.
 Risk factors are-
 Asymmetry of parameters
 Short femur
 Bowel echogenisity
 Oligohydraminous
• Placental mlorphology
• Amniotic fluid volume.(AFI)-when oligohydraminous
AFI<5cm at 37 wk-suspected IUGR.
• Polyhydraminous with suspected IUGR s/o fetal cause.

34. Doppler velocimetry.
• Purpose to dectect IUGR fetus at risk of hypoxia
• Not to be used as routine screening method.
• Used only when USG picks up IUGR.

35. Umbilical artery doppler
• Umblical artey doppler is the standard test ,to detect
Placental insufficiency(m.c cause of IUGR)
• Diffrentiate between SGA and IUGR.
• Progression is from normal end-diastolic velocity
(EDV)---- to decreased,---- to absent to ------reverse
EDV.
• Absent or reversed end-diastolic velocities are mostly
S/O early-onset IUGR.
• These patterns seen to be present approx. 1 week
before the acute deterioration.(Ferrazzi E,2002)

36. • The normal umbilical artery flow --marked positive end-diastolic velocity (A).
• Moderate abnormalities in the villous vascular structure raise the blood flow
resistance and are associated with a decline in end-diastolic velocities (B).
• When a significant proportion of the villous vascular tree is abnormal (50-70%),
end-diastolic velocities may be absent (C) or even reversed (D).
• Depending on the magnitude of placental blood flow resistance and the fetal
cardiac function, reversal of end-diastolic velocities may be minimal (D),
moderate (E), or severe (F).

37. Uterine artery doppler
• By 20 weeks, low-impedance waveform and no diastolic
notch.
• If still high impedance and diastolic notch, high risk of
IUGR and/or preeclampsia.
• As screening test, 82% sensitivity, 38% specificity
(Bewley, 1991)
• Value in high-risk patients only

38. Flow velocity waveforms
obtained from the uterine
artery
• (A) high-volume diastolic
flow –normal
• placental vascular
resistance is associated
with a decline in diastolic
velocities and a subsequent
rise in the Dopplerindex
(B).
• Persistence of an early
diastolic notch is evidence
of increased spiral artery
blood flow resistance. (C)
“notching” (D).

39. Ductus venosus doppler
• Normal is forward flow during atrial contraction.
• IUGR causes  peripheral resistance and eventually heart
failure with no forward flow.
• When back pressure reaches umbilical vein, normally
minimally pulsatile waveform becomes pulsatile as sign of
imminent demise.

40. In the ductus venosus blood flow is always antegrade throughout the cardiac cycle under
normal circumstances. Pulsatility is less pronounced in waveform patterns obtained at the
inlet (A) versus the outlet (B). With impaired cardiac forward function there is a decline in
forward flow during atrial systole (C). If progressive atrial forward flow may be lost (D) or
reversed (E, F).

41. Middle cerebral artery doppler
• In normal fetus –increase in middle cerebral artery resistance
as shown by resistance indices.
• When there is hypoxia,or stress,fetus show redistribution of
blood flow preferentially to brain and heart(brain sparing).
• doppler showing decrease in middle cerebral artery
resistance.

42. MCA doppler cont....
• Up to 20% of SGA fetuses have reduced resistance in the
middle cerebral artery (MCA),
• This sign is associated with poorer perinatal outcome
• suboptimal neurodevelopmental development at 2 years of
age.

43. A, Color Doppler assessment of the MCA at the level of the circle of Willis. B,
Normal and abnormal(high diastolic velocities and decreased pulsatility index) C,

44. Diagnostic algorythm
History s/o –IUGR
Usg for dating
Biochemical markers
serial SFH and biometric assessment
Umblical artery doppler Ut. artery doppler
MCA/DV doppler