This case report describes a 23-year-old primigravida woman admitted at 36 weeks and 3 days gestation for suspected fetal growth restriction based on serial ultrasounds. On examination, fundal height was found to be 32 weeks while ultrasound estimated fetal weight was approximately 2 kg below expected. The patient's history and lab results did not reveal any significant maternal factors that could account for the growth restriction. A diagnosis of probable fetal growth restriction was made pending further evaluation and monitoring of the fetus.

1. Presented by,
Dr. Khan Amreen kausar

2. CASE REPORT :
Patient’s name:- Mrs. Asma sayyad, Age 23yrs
High school passout now household
Residence of JALNA
Married to Feroz sayyed 32Yrs
Working as teacher
Belonging to lower middle socioeconomic class
Unbooked case
Primigravida with 9 month amenohorrea
Admittted with reduced growth of fetus on serial ultrasound since last 4wks

3. History of present illness
• Patient was told to have reduced growth of fetus on
serial ultrasound since last 4wks and was admitted for
close monitoring
• She perceived fetal movement well
• No h/o leaking pv
• No h/o bleeding pv

4. 1ST TRIMESTER
• Spout of conception
• Pregnancy was confirmed after 1-1/2month of missed period by
UPT and she was booked case at Deepak hospital .
• RegularANC visits.
• 2 dose of injection Tt were taken .
• Folic acid tablets were taken .
• First trimester ( dating scan) was done .
• No H/O
• Nausea & vomiting
• bleeding p/v
• pain in abdomen .
• fever with or without rashes .
• Radiation exposure and drug intake .

5. 2ND TRIMESTER:
Quickening was felt at 5 month of gestation
Second trimester (anomaly scan )was done and no anomalies
were found
Iron and calcium tablets were taken.
No h/o fever with rash .
No h/o any drug intake or radiation exposure .
No h/o PV bleeding .
No h/o pedal oedema or headache .
No h/o raised bp recording or raised blood sugar recording

6. 3RD TRIMESTER
• Fetal movement well perceived .
• Iron calcium tablets were taken .
• USG was done at 32 weeks which shows some differences in
growth of the fetus .Arepeat scan after 2 weeks was advised
which shows no significant increase in growth of the fetus .
• She was told that 1st USG taken 2 day back showed mild
changes in blood supply to the fetus and was adviced
hospitalization .
• No h/o high blood pressure or pedal oedema.
• No h /o abdominal pain .
• No h/o PV bleed/leaking per vagina .
• Weight gain in pregnancy is -9kg.

7. MENSTRUAL HISTORY:
Menarche at 14yearsofage
Pastcycle :-2-3days/28days/regular/moderateflow/changing
2-3pad/day
Noh/odysmenorrhea,passageofclot
LMP-13/5/21
EDD-22/2/22
By Dates-36 wks 3 days(dates sure)
By 33 wks scan-32 wks 4 days
No h/o prolonged menstrual cycles.

8. OBSTETRIC HISTORY:
• Married at 20 yr of age and conceived
spontaneously 3 month after marriage
• Primigravida
PASTHISTORY:
No h/o DM,HTN ,Asthma ,tuberculosis , cardiac
disease.
No h/o previous surgeries
No h/o drug allergies
No h/o previous blood transfusion

9. PERSONAL HISTORY
• Diet mixed
• Appetite : Normal
• Sleep-undisturbed
• Bladder/Bowel- Normal and regular
• No h/o of smoking, Alcoholism , drug abuse.
FAMILY HISTORY
No h/o bleeding disorder in family.
No h/o childrens with chromosomal anomaly,birth
defect .

10. DIETORY HISTORY
Consumed mixed diet
Calorie requirement -2500kcal/day
Her intake -2000kcal/day
Deficiency -500kcal/day
Daily protein requirement-65gm(intake 60gm)

11. EXAMINATION
Patient is moderately built and nourished ,she is
conscious cooperative and well oriented to time place
and person
Weight -59kg
Height-150cm
BMI-26.22kg/m2
Pallor ,icterus,clubbing cyanosis
Lymphadenopathy ,edema :- Absent
Breast ,spine,thyroid :- Normal

12. VITALS
Pulse - 94/min, regular Rhythm, good volume, normal
in character
Blood Pressure- 110/70mmHg taken from left hand in
sitting position .
Respiratoy rate- 20 cycles /min.
Temp.- Afebrile.

13. OBSTETRICS EXAMINATION:
INSPECTION :
Shape of the abdomen – uniformly distended and appears
longitudinally oval .
Flank –full.
Umbilicus is central and everted .
Linea nigra and stria gravidarum = Present
No scar sinuses or dilated veins can be seen.
Hernial orifices are intact.

14. PALPATION:
No local rise in temperature or tenderness
Abdominal girth :31 inch
Fundal height : 32 weeks
Symphysio-fundal height :31cm
Liquor clinically appears mildly reduced
EFW clinically appears 2 kg.

15. OBSTETRICS GRIPS :
Fundal grip : Soft broad mass felt on s/o fetal breech .
Right lateral grip : Uniform continuous curved resistance s/o spine
Left lateral grip :
Irregular knob like structure s/o Limb buds
1st pelvic grip : Hard non ballotable globular , s/o fetal head
2nd pelvic grip : Fingers are diverging
AUSCULTATION:
Fetal heart sounds in the right spino-umilical line -140 bpm regular.

16. Cardiovascular system:
s1 and s2 sound heard ,no murmur heard
Respiratory system:
Normal vesicular sounds heard
No added sounds
Central nervous system:
No focal neurological deficit
SYSTEMIC EXAMINATION

17. Hb% 8.8
Bld grp A +ve
TLC 7800/cu mm
DLC P70L28M02
Platelets 1.8 lacs/cu mm
Bld Sugar 124 mg/dl
S.Urea 30mg%
S.Creatinine 0.42 mg%
HIV, HBsAg, VDRL- NR
INVESTIGATIONS

18. ULTRASONOGRAPHY + DOPPLER STUDY REPORT

19. PROVISIONAL DIAGNOSIS
A 23 yr old patient primigravida with 36 wks
3days of gestation with single live fetus in
longitudinal lie cephalic presentation probably a
case of fetal growth restriction with moderate
anemia.

20. •
Incidence
• Approximately 3-5% of all
pregnancies.
INTRA UTERINE GROWTH RESTRICTION
Definition:
Failure of fetus to reach its genetic growth potential inutero
putting it at risk of perinatal mortality and morbidity
According to WHO SGA is used when newborn baby’s weight
is below the 10th percentile for its gestational age (ACOG)
or
Two standard deviations below the population
mean are considered growth restricted.
Incidence:
• Approximately 3-5% of all pregnancies.

21. NORMAL
GROWTH

22. Stage 1 Stage 2 Stage 3
Hyperplasia Hyperplasia/
hypertrophy
Hypertrophy
4-20 weeks 20-28 weeks 28-40 weeks
Rapid mitosis Declining mitosis Rapid hypertrophy
Increasing DNA
content
Increasing cell size Rapid increasing cell
size
rapid accumulation
of fat, muscle,
connective tissue
Symmetric Mixed- asymmetric Asymmetric
Normal Intrauterine Growth

23. GENETIC POTENTIAL
• Derived from both parents
• Mediated through factors like insulin like growth
factor
SUBSTRATE SUPPLY
• Derived from placenta
• Depend upon Uterine & Placental vascularity
GROWTH DEPENDS ON

24. FETAL
GROWTH
SUBSTRATE TRANSPORT
GLUCOSE
OXYGEN AMINO ACID

25. • May vary by race, gender, multiple gestation.
Normal Rate of
Fetal Growth
• 15 weeks = 5 grams/day
• 20 weeks = 10 grams/day
• 30 weeks = 25 grams/day
• 35 weeks = 35 grams/day
• 40 weeks = 15 grams/day

26. PATHOLOGICAL (IUGR)
FETAL GROWTH RESTRICTION
(OR)
SMALLFOR GESTATION
AGE(SGA)(3-10%)
CONSTITUTIONAL

27. CLASSIFICATION OF IUGR
TYPE 1 / SYMMETRICAL / INTRINSIC: (20-30%):
• Growth inhibition early in the pregnancy (4-20 wks)
• Affects Hyperplastic stage
• Causes are: Intrauterine infections (TORCH)
• Congenital malformations
• HC,AC, FL & Weight below 10th percentile for GA
• Hence Ponderal Index Wt.(gm)is normal
FL(cm)3
• Causative factor is usually uncorrectable.

28. CLASSIFICATION (CONT..)
TYPE 2 / ASYMMETRICAL /EXTRINSIC:(70-80%)
• Occurs later, usually after 28 wks of GA
• Affects hypertrophic stage
• Due to restriction of nutrient supply in utero
• Associated with maternal d/s.- Chronic Hypertension, Renal
d/s, Vasculopathy etc.
• Brain Sparing Effect
• HC & FL- normal,AC- decreased
• Ponderal index- low

29. CLASSIFICATION (CONT..)
TYPE 3 / INTERMEDIATE IUGR(5-10%)
• Combination of Type-1 & type-2
• Affects both Hyperplasia & Hypertrophy
• Associated with Chronic Hypertension, Lupus nephritis,
vascular d/s. in early 2nd trimester.

30. AETIOLOGY OF IUGR

31. PLACENTAL CAUSES
Placenta Previa
Abruptio Placenta
Placental thrombosis or infarction
Deciduitis, Placentitis, Vasculitis, Edema
Chorioamnionitis
Placental Cyst
Chorioangioma
Velamentous insertion of umblical cord

32. FETAL CAUSES
Infections(TORCH,CMV virus)
Malformations
Heart Disease
Chromosomal abnormalities (single gene defect e.g.trisomy 21)
Osteogenesis Imperfecta

33. MATERNAL CAUSES
Race, Weight, Height
Cardiovascular disease
Renal disease,Acidosis
Fever
Drug intake(DES,Anticancer Warfarin Anticonvulsants Beta-blockers Narcotics)
Anemia
Smoking
Alcohol
High altitude

34. OTHER CAUSES (maternal)
Vitamin D deficiency Short inter-pregnancy interval
ART conception Chronic maternal stress
Radiotherapy Extremes of maternal age
Uterine malformations Grand multi parity
Extremes of reproductive life History of IUGR in previous
pregnancy
Low maternal weight gain in
pregnancy

35. UTERINE CAUSES
Decreased uteroplacental blood flow
Atheromatosis orArteriosclerosis of the decidual spiral arteries
Chronic Hypertension
Preeclamsia
Diabetes Mellitus
Connective tissue disorders
Fibromyomas
Morphologic abnormalities

36.  Perinatal mortality and morbidity of IUGR infants
is 3-20 times greater than normal infants.
Complications of IUGR
Antepartum period :-
• Increased incidence of-
-still births
-oligohydramnios
IUGR is found in 52% of unexplained stillbirths
During labour :-
Higher incidence of-
-muconium aspiration
-fetal distress
-intrapartum fetal death

37. Complications of IUGR contd..
Neonatal period:-
Increased incidence of
-Hypoxic ischemic encephalopathy
-Persistent fetal circulation insufficiency.
• They have difficulty in temperature regulation because
of absent brown fat and small body mass relative to
surface area.
• Lack of glycogen stores may predispose to
hypoglycemia
• Chronic intrauterine hypoxia may lead to
polycythemia, necrotizing enterocolitis, other
metabolic abnormalities.

38. Complications of IUGR contd..
Childhood:-
increases mortality from-
-infectious diseases
-congenital anomalies
Incidence of cerebral palsy are 4-6 times higher.
Subtle impairment of cognitive performance and
educational underachievement.
• Long term complications-
Increased risk of coronary heart disease, hypertension,
type II diabetes mellitus, dyslipidaemia and stroke.

39. DIAGNOSIS OF IUGR
History:-
Correct gestational age
History of Previous IUGR baby
• History of disorders affecting placental function
• Obstetric history
Dietary history
Drug / Radiation exposure / Addiction
Family history
Socioeconomic status

40. Examination:
General examination
Systemic examination
Obstetrical examination-SFH /AG
• After 20 wks SFH corresponds to the no. of wks. of
gestation.(JAMES)
• Between 18-30wks. SFH coincides within 2wks of GA & a
lag of 2-3cms. Denotes growth restriction. (WILLIAMS)
• SFH increases by 1cm/wk b/w 14-32wks. A lag of > 4 wks
denotes moderate IUGR & > 6wks denotes severe IUGR.
(IANDONALD’S).

41. INVESTIGATIONS:
Routine ANC investigations
ULTRASOUND: Most useful investigation.
Gestation age determination- prior to 24 wks, but most
accurate at10-12 wks
CRL is the most accurate parameter (WILLIAMS)
There is an error of around:
7days in 1st trimester
10-11 days in 2nd trimester
21 days in 3rd trimester (JAMES)
• Determination of EFW: AC & EFW inc the sensitivity
• Determination of multiple gestation.
• Determination of Fetal wellbeing.

42. Determination of Congenital anomalies:
at 16-20 wks of gestation (WILLIAMS)
Determination of placenta :
Assessment of fetal growth : Repeat at 32-34 wks
BPD(Bi Parietal Diameter) - Most accurate for
dating in 2ndtrimester (14 - 26wks) (WILLIAMS)
SONOGRAPHIC EVALUATION-is
most useful tool for diagnosis of IUGR
To differentiate between symmetrical and
asymmetrical IUGR
To monitor the fetal condition.

43. FETAL BIOMETRY:
BPD (Biparietal Diameter) :
Determines gestational age and type of IUGR.
When growth rate of BPD is below 5th percentile 82% of
births are below 10th percentile(i.e. IUGR).
MEASURED AT THE LEVEL OF
THALAMUS & CAVUM SEPTUM
PELLUCIDUM.
(WILLIAMS 23rd EDITION)

44. HC(Head circumference): FL(Femur Length):
Better than BPD in predicting IUGR Measured at the level perpendicular to
shaft excluding the Epiphysis Correlates
well with the BPD & Gestational age

45. Transverse cerebellar
diameter(TCD)-
Can be used as a method to
assess gestational age.
Correlates well with the
gestation age.
Relatively spared in mild to
moderate Uteroplacental
dysfunction.
Upto 25 wks TCD in cms. =
GA (IAN DONALD’S)

46. ABDOMINAL CIRCUMFERENCE (AC) :-
Single best parameter for detection of IUGR because it is
related to the liver size which reflects fetal glycogen
storage (JAMES)
Its sensitivity is further inc. by serial measurements atleast
14 days apart (JAMES)
We should not not label as growth restricted fetus unless
AC is far below normal or unless other parameters
correlate. (JAMES)

47. MEASUREMENT RATIOS:-
there are some age
independent ratios to detect IUGR.
HC/AC: decreases linearly from 16 to 20 wks of
gestation.
HC/AC >2 SD above mean is predictive of IUGR. (IAN DONALD’S)
FL/AC: normal value ranges from 22 + 2% in the
second half of pregnancy. Ratio above 23.5% is
considered abnormal. (IAN DONALD’S)
Placental Morphology:
Acceleration of placental maturation may occur with IUGR and PIH.
(Placenta is graded from grade 0 to grade III)
Amniotic fluid volume:
type 2 IUGR is usually
associated with oligohydramnios.
Amniotic fluid index(AFI) between 8cm and 25cm is
normal.
Maximum Liquor Pocket = 2-8 cms.

48. OTHER INVESTIGATION
Amniocentesis
Karyotyping
Colour doppler
TORCH test
Antiphospholipid antibody
Thrombophillia screen
Thyroid function test
Detailed level II ultrasound
Biophysical Profile(BPP)
Cardiotocography

49. MATERNAL
COMPARTMENT
FETAL
COMPARTMENT
•Uterine Artery • Umblical Artery
•Middle Cerebral Artery
•Venous Doppler
COLOUR DOPPLER

50. DOPPLER ULTRASONOGRAPHY:
Doppler flow studies are
important adjuncts to fetal biometry in identifying
the IUGR fetuses at risk of adverse outcome.
Most widely used arterial indices are
Pulsatility index (PI): Systolic end diastolic peak
velocity / time averaged maximum velocity
Resistance Index(RI): Systolic end diastolic peak
velocity/ systolic peak velocity
Systolic to diastolic ratio(S/D): Systolic peak velocity /
diastolic peak velocity.

51. UTERINE ARTERY DOPPLER:
High diastolic flow velocities
Its main use is in screening.
• Early diastolic notch in the uterine artery
at 12-14 wks. suggest delayed trophoblastic
invasion (JAMES)
• Persistence of notch beyond 24 wks confirms &
indicates an increase risk of Pre-eclampsia,
Placental abruption & Early onset IUGR. (JAMES)
• Increase impedence of flow in Uterine artery
at 16-20 wks was predictive of superimposed
pre-eclampsia developing inwomen with chronic
hypertension. (WILLIAMS)

53. UMBLICALARTERY DOPPLER:-
The amount of flow during diastole increases as gestation advances
• Thus the S/D ratio dec. from 4 @ 20 wks to 2 @ 40 wks. (WILLIAMS)
• Umbilical A. S/D ratio is generally < 3 after 30 wks. (WILLIAMS).
• Umbilical A. Doppler indices should be measured
only after 23 wks (STUDD)

54. • It is useful adjunct in the management of pregnancies complicated by
fetal-growth restriction.(ACOG-2008)
• It is not recommended for screening of low-risk pregnancies or for
complications other than growth restriction. (WILLIAMS)
• Umbilical artery Doppler becomes abnormal when at least 30% of the
fetal villous structure is abnormal. (JAMES)
•In extreme cases of growth restriction, end-diastolic flow may become
absent or even reversed (AREDF).
•AREDF occurs when 60-70% of the fetal villous
structure is abnormal.
•About ½ of the cases of AREDF are associated with
aneuploidy or a major anomaly (WILLIAMS)
•Fetuses of preeclamptic women who had AREDF
were more likely to have hypoglycemia &
polycythemia. (WILLIAMS)

55. RESISTANCE INDEX & S/D RATIO IS INCREASING

56. Perinatal mortality rate in AEDF- 9-41% (IAN DONALD’S)
ABNORMAL UMBILICAL ARTERY
WAVEFORM

57. Reversal of the End Diastolic Flow
Perinatal mortality rate of REDF- 33-73% (IAN DONALD’S)

58.  Abnormal Umbilical artery flow pattern indicate an increased
risk of hypoxemia & acidemia proportionate to severity of
Doppler abnormality. (JAMES)
 Umbilical artery Doppler can also be used to distinguish b/w
the high risk small fetus that is truly growth restricted that
needs inc. monitoring & the low risk small fetus. (IAN DONALD’S)
 When Umbilical artery Doppler are incorporated into
management algorithm of growth restricted fetus, perinatal
death is reduced as much as 29%. (STUDD)
 In summary UA Doppler in suspected IUGR pregnancies
improves perinatal outcome & should be used to monitor these
fetuses

59. DUCTUS ARTERIOSUS DOPPLER
• Primarily used to monitor fetuses exposed to
indomethacin and other NSAIDs.
• Indomethacin was used for tocolysis.
• They causes Premature closure of Ductus
Arteriosus Increased pulmonary flow
Reactive hypertrophy of pulmonary arterioles
Pulmonary Hypertension.
WILLIAMS 23rd EDITION

60. MIDDLE CEREBRALARTERY DOPPLER
It was used for assessment of-
Fetal Anemia
Growth restriction
FETAL ANEMIA: (In Rh isoimmunisation)
With increasing anemia cardiac output increases
& blood viscosity decreases increase flow to
brain Elevated peak systolic velocity
WILLIAMS 23rd EDITION

61. MCA DOPPLER IN FETAL ANEMIA
INCREASED PEAK SYSTOLIC VELOCITY

62. MCA WAVEFORM IN IUGR
MCA WAVEFORM IN IUGR
INCREASED FLOW DURING DIASTOLE

63. GROWTH RESTRICTION:
•It is involved in severely growth restricted fetus
after involvement of Umbilical artery.
•It is the progression of the Doppler finding & is
due to the adaptive compensatory mechanism
in the fetus against increasing hypoxia (Brain
sparing effect)

64. Umbilical artery involved
Inc. blood flow to Vital
Organs(Brain, Heart&
Adrenals)
BRAIN SPARING EFFECT
Or
CEPHALISATION
Increasing hypoxia
OLIGOHYDRAMINOS
Dec. blood flow to
Abdominal Organs(Liver &
Kidneys)
MCA DOPPLER- Inc.
OLIGOHYDRAMINOS
Diastolic Flow
Dec. RI/PI/SD ratio & abn
MCAPSV

65. DUCTUS VENOSUS DOPPLER
PERINATAL MORTALITY IN ABSENT OR REVERSE FLOW OF DV IS
63-100% (IAN DONALD’S)

66. HYPOXIA
INC BLOOD SHUNTING THROUGH
DV B/W UMBILICALVEIN & IVC PSV-ATRIAL CONTRACTION
VELOCITY
Avg. Vel. Drng cardiac cycle
INC. PULSATILITY
INDEX FOR VEINS (PIV)
REVERSED a WAVE
IN
DV PULSATION
PULSATIONS IN THE
UMBILICAL VEIN
REVERSALOF FLOW IN
IVC DURING ATRIAL
CONTRACTION

67. ABNORMAL WAVEFORM IN
UMBILICAL VEIN

68. Important points on venous
Doppler
Especially useful in early onset IUGR
Reason: In Term /near term fetuses
there is shorter interval & delivery is often
indicated
With advancing GA cardiac
activity becomes more efficient slow Steady
decline in Doppler indices
• When DV & Umbilical vein Doppler- Sensitivity
inc to 70-80%.

69. Presumptive diagnosis of IUGR
• SFH not increasing at a normal rate
• Fetuses with small AC
• Flattening of growth curve on two consecutive occasion
14 days apart.
• Beyond 24 wks, an elevated umbilical artery Doppler
index
• After 34 wks umbilical artery Doppler index may be
normal & a dec. CPR or MCA Doppler index may be the
only supporting evidence of placental-based IUGR

70. Diagnostic work-up
It is important to decide the cause
of IUGR before delivering the
fetus.

71. MANAGEMENT
Principles:
1. Identify the cause of growth restriction.
2. Treat the cause if found.
3. General management.
First step is to identify the aetiology of IUGR
 Maternal history pertaining to the risk factors of IUGR.
 Correct dating
 Clinical examination-, measurement of fundal height, maternal habitus,
height, weight, BP etc.
 Laboratory investigations- Hb, blood sugar, renal function tests, serology for
TORCH.
 Specific investigations for thrombophilias in pts with history suggestive of early
onset growth restriction.
•Fetal evaluation: through ultrasound for growth restriction, congenital anomalies
and doppler evaluation,biometry (HC and AC) ,estimation of fetal weight (BPD,
HC, AC, FL),measurement of amniotic fluid (AFI or MVP)

72. CORRECT DATING :
 Pregnant women should be offered an early US scan between 10
weeks 0 days and 13 weeks 6 days to determine gestational age.
 CRL measurement appears to be the most precise, allowing an
accurate determination of the day of conception, to within 5 days
either way in 95% of cases
ISUOG Practice Guidelines: performance of first-trimester fetal ultrasound scan.

73. CORRECT TOOLS TO ASSESS
BIOMETRY
 Biometric assessment - central role in the
identification of fetuses at risk of FGR and related
adverse outcomes
 Multiple tools to assess the likelihood of FGR
prenatally, using biometric measurements:
 Biometry charts
 Etimated fetal weight (EFW) and related charts

74. ESTIMATED FETAL WEIGHT (EFW)
• ultrasound superior to clinical estimate before 37 weeks.
• clinical estimate has accuracy similar to that of ultrasound
at term.
• 80% of EFW are within 10% of actual birthweight,
remainder are within 20% actual BW (Chauhan AJOG 1998)
 Hadlock (AJOG 1985) - EFW calculated from HC, AC, and FL
(log EFW = 1.326 + 0.0107 HC + 0.0438 AC + 0.158 FL – 0.00326 AC x FL)
 Intergrowth estimated fetal weight standards (Stirnemann et al, Ultrasound
Obstet Gynecol 2017;49:478-486)

75. most reliable formula – Hadlock 3
Estimated fetal weight

76. Appropriate diagnosis of FGR in SGA fetuses
 Diagnosis of FGR currently performed by means of combination of
biometric measurements and other parameters:
o Umbilical artery (UA) Doppler historically used to distinguish FGR
from SGA - identifies severe placental disease but fails to pick up
mild placental disease, i.e. majority of FGR.
o UA should always be used in combination with cerebroplacental ratio
(CPR)
o Uterine artery Doppler PI (Ut.A PI) and very low estimated fetal
weight (<p3) independently predict poorer outcome in small fetuses.
o maternal symptoms
o crossing centiles
 Abnormal biometry (EFW and/or AC <10th centile)
o  UA, CPR, UtA PI, amniotic fluid etc

77. Early FGR and late FGR
Early FGR
• easy to diagnose, difficult to treat
Late FGR
• difficult to diagnose, easy to treat

78. EARLY AND LATE ONSET FGR – MAIN
DIFFERENCES

79. STAGE BASED CLASSIFICATION AND MANAGEMENT
OF FGR:

80. TREATMENT OF UNDERLYING CAUSE:
such as hypertension, cessation of smoking, protein energy
supplementation in poorly nourished and underweight women.
GENERAL MANAGEMENT:
▪ Bed rest in left lateral position to increase
uteroplacental blood flow
▪ Maternal nutritional supplementation with high caloric and
protein diets, antioxidents, haematinics and omega 3 fatty
acids, arginine .
▪ Maternal oxygen therapy: Adminitration of 55% oxygen at
a rate of 8L/min round the clock has shown decreased
perinatal mortality rate.

81. PHARMACOLOGICAL THERAPY:
•Aspirin in low doses(1-2 mg/kg body wt.),
betamimetics etc have been tried but all have failed
to show any significant difference in incidence of
IUGR.
• Thus there is no form of therapy currently available
which can reverse IUGR, the only intervention possible
in most cases is delivery.

82. RISK OF PREMATURITY
❖ DIFFICULT EXTRA
UTERINE EXISTENCE
RISK OF IUD
• HOSTILE INTRA UTERINE
ENVIRONMENT
Judge Optimum Time Of Delivery
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.

83. The optimum timing of delivery is determined by gestational age,
underlying aetiology, possibility of extrauterine survival and fetal
condition.
Strict fetal surveillance is needed to monitor fetal well being and to
detect signs of fetal compromise
Fetal Surveillance
1. Daily fetal movement score
2. Non stress test(NST)
3. Biophysical profile(BPP)
4. Amniotic fluid index(AFI)
5. Growth parameters
6. Doppler studies
Sonography is usually repeated every 2 wks.

84. ROLE OF STEROIDS:
Antenatal glucocorticoid administration reduces the incidence of
respiratory distress syndrome, intraventricular hemorrhage and death in
IUGR fetusus weighing less than 1500gm
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 neonatal
care.
➢Vaginal delivery: can be allowed as long as there is no
obstetric indication for caesarian section and fetal heart rate is
normal.
• Fetuses with major anomaly incompatible with life should also be

85. BIOPHYSICAL PROFILE
Biophysical profile
variable
Normal score (2) Abnormal score (1)
fetal breathing
movement
one episode fetal breathing 30 s absent or < 30 s
gross fetal movement three discrete body/limb
movements
two or less
fetal tone one episode active extension with
return to flexion of fetal limbs /
trunk
slow extension with partial
flexion or limb movement
without flexion or none
fetal heart rate
reactivity
• < 26wks: two accelerations of ≥
10 beats, two of ≥10 s
• 26–36wks: two accelerations of
≥10 beats, ≥15 s
• ≥ 36wks: two accelerations of
≥20 beats, ≥20 s
less than two episodes of
accelerations and durations
as specified
amniotic fluid volume pocket 2 x 2 cm pocket < 2 x 2 cm

86. CAESARIAN SECTION
❖ In all cases of IUGR with features of acidosis caesarian
section should be done without trial of labour. These
include:
➢Repetitive late decelerations
➢poor biophysical profile
➢reversal of end diastolic flow in umblical artery
➢abnormal venous doppler
➢blood gas analysis showing acidic pH on
cordocentesis.

87. Clinical suspicion of
IUGR
AC/EFW<10 th
PERCENTILE
Anatomical survey &
AFI
•Aneuploidy
•Syndromes
•Viral infections
Normal /
oligohydraminos
Anomaly/
polyhydrami nos
Umbilical Artery Doppler
/ MCADoppler
Dec./AREDF/
brain sparing
effect
Placental
insufficiency
NORMAL
Cerebro-Placental ratio
Repeat USG after 14 days
C O N S T I T U T I O N
A l
Norma l
Abnormal

88. IUGR > 24 WKS
UMBILICALA.DOPPLER
•NST twice weekly
•BPP weekly
•AFI Weekly
•Umbilical A. Doppler wkly
•Fetal growth 3 wkly
Deliver @ 37-39wks
Deliver @34-36 wks
Normal /
mildly
elevated
AREDF
ABNOR MAL
NOR MAL
•Hospitalise the pt.
•Continuous /frequent fetal
monitoring
•Corticosteroids
•MCA Doppler wkly
•DV Doppler every 3-4days
•BPP daily
•Fetal growth every 3wk
NORMAL
STUDD
RCOG2013- 37wks RCOG2013- 32wks

89. 1
Intervention Mechanism of Action Recommendation
Bedrest  Reduces the
catecholamine
release
 Improves
central
intravascular
volume
 Improves
uterine
perfusion
Unproven bene t
MEDICAL MANAGEMENT OF FGRFGR(summary)
Summary of treatment with unproven benefit

90. 1
Intervention Mechanism of Action Recommendation
Low Dose Aspirin  Suppress production
of prostaglandins and
thromboxane through its
irreversible inactivation
of the cyclooxygenase
enzyme.
 Cytoprotective
mechanisms.
 Antioxidant mechanisms
 Low-dose aspirin
prophylaxis is not
recommended for
prevention of fetal
growth restriction,
in the absence of
risk factors for
preeclampsia.
(ACOG 2018)
No role in treatment
once FGR sets in.

91. 1
Intervention Mechanism of
Action
Recommendation
Heparin and LMWH  Anticoagulant
properties and
ability to
prevent
placental
thrombosis and
subsequent
infarction
 Anti-
inflaammatory
Currently LMWH
therapy for the
prevention of FGR
should be limited to
the research setting.
No role in treatment
once FGR sets in.

92. Summary of treatment for FGR under investigation
Intervention Mechanism of action Current stage of
investigation
Phosphodiesterase type -5
inhibitors
Selective vascular smooth
muscle relaxation and
vasodilatation
Phase II/III clinical trials,
however neonatal
pulmonary hypertension
has been reported as an
adverse effect and caution
has been advised.
Statins Anti-inflammatory,
antioxidant, and
angiogenesis
Phase II/III clinical trials
Nitric Oxide donors Selective vascular smooth
muscle relaxation and
vasodilatation
Phase II nonrandomized
trials
Proton pump inhibitors Angiogenesis Phase II/III clinical trials

93. Intervention Mechanism of action Current stage of
investigation
Maternal VEGF gene
therapy
Local vasodilatation and
angiogenesis
Phase I/IIa clinical trial
Nanoparticles Uterine blood ow,
placental
function
Preclinical
microRNAs Uterine blood ow,
placental
function
Preclinical
Hydrogen sulphide Selective vascular
smooth muscle
relaxation and
vasodilatation
Preclinical
Melatonin Antioxidant Phase II nonrandomized trial
Creatine Cellular energy
homeostasis
Preclinical
N- acetlycysteine Selective vascular
smooth muscle
relaxation and
vasodilatation
Phase II randomized trial

94. MANAGEMENT OF FGR: TIMING OF DELIVERY
2
Timing of delivery
Severity of FGR
and findings of
fetal monitoring
tests
Gestational Age Maternal factors
Key Recommendations:
1.Fetal movement counting is a simple and inexpensive tool monitoring in pregnancies with FGR
in both high- and low-resource settings.
2.Surveillance in pregnancies with FGR should follow a uniform protocol that is based on a
combination of biophysical pro le, fetal heart rate monitoring by NST and Doppler assessment
(umbilical artery and middle cerebral artery, with or without ductus venosus Doppler)

95. Timing and mode of delivery based on ultrasound Findings
Findings Timing and mode of delivery
SGA (EFW at 3rd –9th
percentile, normal
uid and Doppler studies)
 37–39 weeks
 Mode of delivery: Induction
Uncomplicated FGR at <3rd
percentile (normal uid and Doppler studies)
 37–38 weeks
 Mode of delivery: Induction
FGR with mild abnormalities:
•Early Doppler changes:
a.UA PI > 95th percentile, or
b.MCA PI < 5th percentile, or
c.CPR < 5th percentile, or
d.UtA PI > 95th percentile
•Oligohydramnios
•Suboptimal interval growth
 34 –37 weeks
 Mode of delivery: Caesarean section or
induction

96. Baby with growth restriction in-utero
Increased risk of immediate complications Increased risk of long-term complications
● Complications related to prematurity
● Neonatal mortality (5-fold increase): Independently
related to birth weight, irrespective of gestation.
● Affect postnatal growth, can affect height later on.
● Increased risk of adverse long-term
neurodevelopmental outcomes.
● Increased risk of future noncommunicable diseases
including obesity, diabetes, hypertension, and
cardiovascular disease.
Closer follow-up than normally grown infants in the first year
of life
Maternal Follow-up
Women with a history of
pregnancy complicated by
FGR or other placenta-
mediated complications such
as pre- eclampsia
● Maternal CVD and CVD- related morbidities
Cerebrovascular events
● Heart failure
● Hypertensive renal disease
● Chronic renal failure and need for renal
transplantation
Increased
risk
3
Causal pathway is not clear, however, considerable evidence on the association
between birthweight and maternal CVD has been accumulated. It is probable that
the association between neonatal birthweight and maternal cardiovascular risk
re ects both environmental and genetic in uences.
POSTPARTUM FOLLOW-UPAND COUNSELLING
FOR FUTURE PREGNANCIES

97. 3
POSTPARTUM FOLLOW UPAND PRECONCEPTION
COUNSELLING FOR FUTURE PREGNANCY
● Infant follow up.
●Identify modfiable risk factors and educate regarding the same with
an aim to optimize the medical condition before next pregnancy.
● Assess regarding risk of recurrence and stratify risk.
● Educate about long term maternal and fetal consequences.