FETAL GROWTH RESTRICTION/

INTRAUTERINE GROWTH RETARDATION

• LBW infants were defined in 1961 by the expert committee
on Maternal and child health as those weighing <2500 g.
regardless of the gestational age.

• However these infants should be further divided into 3

categories: -
1- Neonates delivered preterm (before 37 wks) but of
appropriate size for gestational age.
2- Neonates delivered preterm and small for gestational age.
3- Neonates delivered at term or beyond who are small for
gestational age.

Infants in latter two categories constitute the entity of

Intrauterine growth restriction (IUGR)
• Furthur neonates are now classified as
• Very small for G.A(less than 3 centile)
• Small for G.A(less than 10 centile)
• App.for G.A(10th to 90th centile)
• Large for G.A(more than 90th centile)
 INCIDENCE
• 2- 8 % of all pregnancies (developed countries).

• In India incidence rate – 25-30% (UNICEF 2007)

• occurs in 53% of preterm stillbirths & 26% of term stillbirths

• Second most common cause of perinatal mortality , 6 - 10

times higher for these fetuses,
 ETIOLOGY

• Maternal causes-25%
• Fetal causes-25%
• Placental causes-10%
• Idiopathic- 40%
 Maternal risk factors
• Constitutionally small mothers
i.e Low pre-pregnancy Maternal Height/Wt. –
If pre pregnancy wt <100 pounds, the risk increased at least 2 folds.
• less wt gain in pregnancy
• Racial & Ethnic group , low Socio-economic group
• Social deprivation , Nutritional support ie poor nutrition before n during
pegnancy
• High altitude
• Toxins-
Smoking
Tobacco Chewing
Alcohol ingestion
other Addictive drugs ( heroin, morphine, cocaine)
• Therapeutic drugs include warfarin, Anticonvulsant drugs &
antineoplastic drugs
• Prior history of IUGR
• Maternal illnesses –
• Vascular diseases like Pre-eclampsia, chronic renal disease etc.
• Maternal malnutrition, inflammatory bowel disease, pancreatitis,
worm infestation.
• Autoimmune disorders eg SLE
• Long standing diabetes ie diabetes with vasculopathy
• Haemalotogial disease – inherited anemias like sickle cell
diseases
• Cyanotic heart & respiratory diseases
• Thrombophillia
• Antiphospholipid antibody syndrome
• pegnancy in women having prior infertility
 FETAL CAUSES
1- Congenital infection :5-10%
• TORCH,
• varicella,syphilis
• Malaria
• UTI
• Tuberculosis

2- Chromosomal aneuploidies :20% (8-12% dutta)

Trisomy -18 :severe early onset IUGR –first trimester

Trisomy-13 early onset IUGR
Trisomy-21- most common trisomy ,mild IUGR

- deletions, translocation and partial trisomies.

3- Congenital malformations
(20-60% CMF fetus –IUGR,10%IUGR-CMF)

• Neural tube defects e g Anencephaly

• cardiovascular malformations –TOF,VSD,Endocardial cushion defects,
• Achondroplasia.
• Ostegenesis imperfecta
• Abdominal wall defects like gastroschisis, omphalocoele,
• Diaphragmatic hernia
• Pancreatic agenesis
• Single umbilical artery

4- MULIPLE PREGNANCY - causes

• mechanical hinderance
• CMF
• increase incidence of maternal diseases- PET, DM
• competition for substrate
• abnormal placentation
 PLACENTAL CAUSES
• Placenta previa – It is associated with increased risk of IUGR because of
unfavourable site of placental implantation. Complete variety has higher
risk of IUGR than partial variety.

• Placental Infection – It decreases functional exchange area.

• Premature placental separation – When not associated with fetal death or

premature labour it increases the risk of IUGR.

• Malformations of placenta & umbilical cord – Like- single umbilical artery,

--velamentous umbilical cord insertion, circumvallate placenta & battledore
placenta , Placenta implanted outside uterus

• Chronic villitis – is seen more frequently on HPE of placenta in IUGR

pregnancies.

• Uterine developmental anomalies and fibromyomas – Increase the risk of

IUGR by suboptimal uterine blood flow & abnormal placentation
 symmetrical Asymmetrical

Incidence 20-30% 70-80%

Invol ves all biometric measures like Relative sparing of skeletal and head
skeletal, head and abdomen measurement but a decreased abdominal
circumference
Associated with reduction of absolute Asso with reduction of fetal cell growth
number of cells
Cause-genetic disease or cong. Infections Cause- chronic utero placental
( intrinsic to fetus) insufficiency ( extrinsic to fetus)
HC/AC – elevated
FL/AC - normal
Ponderal index ( birth weight / crown – Low
heal length 3) ---normal
neonatal outcome- Greater morbidity Lesser morbidity &mortality
&mortality
 DIAGNOSIS
A)- evaluation of maternal Weight gain:

Decreased maternal weight gain during pregnancy is a

relatively insensitive sign of inadequate fetal growth.

B)- Clinical palpation of uterus for

- fundal height
- liquor volume
- fetal mass
May be used as screening tool , Less sensitive
D)- Symphysio fundal height:
simple, safe, inexpensive
• Recommended at each visit after 24 weeks as this improves
prediction of SGA babies
• Fundal height should correspond to number of weeks with an
allowance of 2cm ( 18 - 30 weeks)
• A lag of 4 cm or more suggest growth restriction
•
• E)- Measurement of abdominal girth:
shows stationary or falling values

AG at term is ???
increases per weekly ( >30 weks) ??
 2- SONOGRAPHIC PARAMETERS-

Numerous sonographic parameters using both conventional

and Doppler ultrasound have been proposed for antenatal
diagnosis of IUGR. To be useful for diagnosis, a criteria

• Should have high sensitivity i.e. must detect a

substantial fraction of cases of growth retardation.
• Should have a high PPV i.e. positive result must be
associated with a high likelihood of IUGR.
A)- Biparietal diameter: -
Fetal skull is defined ultrasonographically from 13th week onwards.
BPD is measured from outer edge of proximal skull to inner edge
of distal skull.
B)- Abdominal circumference: -
It is the single best measurement for the detection of IUGR since it has the
highest sensitivity (98%) and highest negative predictive value (99%) i.e.
finding a normal AC practically rules out IUGR.

• mean abdominal circumference growth rate is at least 10mm in 2 weeks.

• The fetal AC reflects the volume of fetal subcutaneous fat and size of liver
which in turn correlates with fetal nutrition.
C)- Estimated fetal weight: (SEFW)

• Most accurate methods, gives a rough idea about the size of fetus
• Using ultrasonographically measured BPD, HC, AC and Fl, -SEFW can be
estimated by following formula

Hadlock's Formula: -
1.3596 – 0.00386 (AC x Fl) + 0.0064 (HC) + 0.00061 (BPD x
AC) + 0.0425 (AC) + 0.174 (Fl).

Shepard's Formula: -
1.2508 + (0.166 x BPD) + 0.046 x AC – 0.002646 x AC x
BPD.

• EFW<10TH percentile –mc used diagnosis

• It does not differentiate between IUGR babies & babies who are small and
healthy. This method has a sensitivity of 85% for diagnosis of small fetus.
Johnson's formula:
( applicable only in cephalic presentation)

If Vx is at or above the level of ischial spines (Height of uterus in

cm above public symphysis – 12) x 155.

If Vx is below the level of ischial spines, (Height of uterus in cm

above pubic symphysis – 11) x 155

• if women weight more than 90 kg, 1 is subtracted from the

fundal height
D)- Head to abdomen circumference ratio (HC/AC) -
• compares the most preserved organ in the malnourish fetus with the most
compromised i.e. liver.
• Normally HC > AC ie >1 before32 weeks
HC = AC ie=1 32-34 weeks
HC < AC ie<1at >34 weeks POG.
• HC/AC ratio is
– increased in asymmetrical IUGR
– decreased in macrosomia
– unaffected in symmetrical IUGR

• It means
A fetus with normal HC/AC ratio may be symmetric IUGR or small &
healthy.
E)-Femur to abdomen ratio (FL/AC): -
FL is easy to obtain and is not affected by moulding or abnormal fetal
presentations or positions.

• FL/AC = 22 at all POG after 21 wks.

• FL/AC  23.5 suggests asymmetrical IUGR.

• When FL/AC ratio is Normal – the baby may be small & healthy or have
symmetric IUGR.
F)- Amniotic fluid volume: -

• Oligohydramnios is a late sign of fetal malnutrition.

• It is measured with four quadrant technique which consists of measuring
the largest pool of fluid found in each of the four quadrants of uterus. The
sum of the results is amniotic fluid index (AFI).

• Single deepest vertical pocket (SVDP) , between 2-8 cm is normal

• Pocket < 2cm (1cm, dutta) suggests oligohydrommios In up to 96% cases.
• Normal AFI is between 5-25 cm ( 5-24, dutta)
• AFI < 5cm suggests oligohydramnios.
• we should also perform fetal ECHO to rule out heart lesions
especially cyanotic heart lesion
• Done at 22- 24 weeks
 3- Diagnosis by Doppler waveform analysis:
-
• Doppler is used to determine the volume and rate of blood flow through
maternal and fetal vessels.
• Some quantitative indices used to characterize the Doppler flow velocity
waveform are: -

systolic peak velocity

S/D ratio = diastolic peak velocity
 
• Pulsatility index = S-D/Mean

• Resistance index = S-D/S

Resistance index is the most discriminatory for predicting poor outcome.

• Where the fetal AC or EFW is < 10th centile or there is evidence of
reduced growth velocity

• women should be offered serial assessment of fetal size

(3 WEEKLY) • and umbilical artery Doppler. (weekly)
RCOG 2013

• ACOG 2002 IN IUGR recommends biometry 2-4 weekly Doppler

(weekly) Abnormal doppler (raised S/D RATIO,AEDF):biometry
weekly
 BIOPHYSICAL PROFILE
• ➢ If UA doppler is abnormal,BPP useful as it gives
good NPV in high risk pregnancies (RCOG2002)
• ➢ Used as back up test for non reassuring NST

• ➢ Fetal death in 1 week of a normal BPP is extremely

rare (AJOG1999) ◦ Do once or twice per week

• ➢ Daily in severe FGR, severe oligohydramnios, AEDF,

REDF
 3- ROLE OF BIOCHEMICAL MARKERS

• VARIOUS BIOCHEMICAL MARKERS FOR

IUGR ??
In 1st trimester –

Decrease in the PAPP-A below 0.4 multiples of the median (MOM)

(RCOG 2013) is a predictor of iugr

In 2nd trimester-

• Elevated MSAFP or hCH (markers of abnormal placentation )

• decrease unconjugated serum estriol
• increased inhibin A

(less sensitive)
 COMPLICATIONS

• VARIOUS COMPLICATIONS IN IUGR FETUS?

• ANTEPARTUM COMPLICATIONS (ANTENATAL)-
1- chronic fetal distress
2- fetal death---
- 20% of fetuses with unexplained stillbirth have evidence of IUGR.
( IUD more frequent after 35 weeks).

3-Oligohydramnios: -
The incidence of IUGR when AFV is normal is 5%.
When oligohydramnios is present, it is app. 40%.

• INTRAPARTUM COMPLICATIONS (INTRANATAL)-

hypoxia &
acidosis
in about 40% of IUGR fetus manifested by late decelerations, severe variable
decelerations, and episodes of bradycardia.
• POST PARTUM (AFTER BIRTH)
imediate
-asphyxia
- bronchopulmonary dysplasia n RDS
- hypoglycemia (shortage of glycogen reserve)
- hypothermia
- meconium aspiration syndrome
- polycythemia , anemia, thrombocytopenia

-necrotising enterocolitis ( decreased intestinal blood flow)

- electrolyte imbalance ( due to impaired renal function)
- multiorgan failure
late-
• retarded neurological and intellectual development especially in IUGR
babies caused by chromosomal defects, CMF, infections

• Increased risk of metabolic syndrome in adult life (obesity,HTN, CHD)

• Altered orexigenic mechanism ( causes increased appetite and reduced

satiety

• reduced no of nephrons- causes renal vascular HTN

• On gross examination IUGR infants shows

– Signs of soft tissue wasting.

– The skin is loose and thin.
– There is little subcutaneous fat.
– The abdomen is scaphoid.
– The ribs are protuberant.
– The muscle mass of arms, buttocks & thighs is reduced.
– The umbilical cord is limp, thin & frequently meconium stained.
– HC is larger than AC in most cases.
– The birth weight & placental weight are below the 10 th percentile.
 MORTALITY
• Neonatal mortality is about 6 times more than the normal
newborns.
• It is lower than premature AGA of the same birth weight
• Most babies dies within 24 hrs.

MORBIDITY
• Morbidity rate rises to about 50 %, they are at high risk for
poor post natal growth and cognitive outcome.
• THANK U
  
MANAGEMENT: -

• The first step in managing suboptimal fetal growth is to

identify patients at high risk for small infants.

• The second step is to differentiate IUGR fetus from fetus that

is small and healthy.

• To establish adequate method of fetal surveillance for

patients with IUGR fetuses and deliver them under optimal
conditions.
Identification of patients carrying small fetuses: -
• A careful medical & obstetric history and physical examination to recognize
high risk factors like chronic HTN, connective tissue diseases, long standing
diseases, smoking, malnutrition, history of small baby in a prior pregnancy
& substance abuse, and issues identified in this pregnancy like early
pregnancy bleeding, APH, pre-eclampsia etc.

• However app. 40% of all small newborns are born to mothers who have no
high risk factors.

• To identify these patients it is necessary

1- To determine the reliability of dates in all obstetric patients & to

consider at high risk all patients with unreliable dates.

2-To perform serial measurements of uterine fundal height, in all obstetric

patients and to consider at high risk all patients with inadequate fundal
growth.
• All these patients should have baseline ultrasound
examination early in pregnancy for accurate determination of
gestational age.

• In case baseline scan is not available when patient comes in

late pregnancy & history & physical examination suggests
IUGR serial measurements of AC or EFW are better for
demonstrating IUGR.

• In addition umbilical artery doppler and preferably MCA

doppler should also be done

• Normal fetal growth and normal measurements of AC indicate

that the fetus is growing normally & will have normal weight
at birth
IUGR is more likely if: -

• Risk factors for IUGR are present.

• Fetal growth restriction occurs early in pregnancy esp. before 32 weeks.

• The smaller the fetal size, the greater the chance of true growth restriction.
• If structural abnormality is present, it may explain fetal size.
• AC<5th percentile & growth rate of AC is <11mm in 2 weeks.

• When ultrasonographically determined FL/AC ratio, HC/AC ratio suggest

asymmetrical IUGR it is more likely to true IUGR.

• Elevated umbilical artery S/D ratio indicates true IUGR.

• Cerebroplacental ratio is decreased. MCA dopple index is decreased even if

uterine artery doppler is normal (esp. after 34 weeks).
Prevention of IUGR: -
1- Early diagnosis and treatment of any underlying maternal disease
like hypertension, anemia, renal disease, heart disease & control of
diabetes.

2- Patient t education & Avoidance of maternal smoking, tobacco ,

alcohol etc.

3- Treatment of infections: -
- Malaria in endemic areas.
- Though viral infections associated with IUGR like Rubella, CMV or
varicella have no in utero treatment, however if Toxoplasmosis is
identified medication taken by the mother may prevent the spread
of infection to fetus.

4-ED REST in lateral position. Antioxidants and EFA, All vitamins esp.
Folic Acid should be taken
 5- Improving maternal nutrition by balanced diet,
a- 300 extra calories to be taken
b- Antioxidants and EFA should be given
Lycopene, DHA etc. (tablet or dietary)
c- Vegetable Oils, fish, Fish Oil
d- Green Leafy Vegetables

6- low dose aspirin (75 mg od) in selected cases

Rationale:
Inhibits production of TXA2 by platelets

Thromboxane/Prostacyclin ratio decreased

Vasodilatation of Uteroplacental circulation

7-Maternal hyperalimentation by amino acids can improve fetal growth if it
was due to maternal malnutrition only.

Rationale:

Patient with PIH & IUGR have low levels of L-arginine

L-arginine supplementation

↑Endothelial NO synthetase activity hence NO bioavailability

Improves uteroplacental flow of O2 & nutrients to fetus

8-Maternal hyperoxygenation –
though not a long term solution is thought to improve the
intrauterine environment.
technique-55% oxygen by face mask 0r 2.5 L/ min by nasal
prong

9- Maternal Hydration/volumeExpanders-
Adequate Hydration must ,Oral water 2L/day.
May be helpful in improving placental perfusion

the role of above all measures are controversial. Till date

there is no cure for IUGR. Only definitive treatment of IUGR is
delivery
• The strongest determinant of postnatal outcome is gestational
age.
• Timing of delivery is complex because it requires balancing
the risk of continuing intrauterine life due to hypoxaemia
against the risk of preterm delivery.

• The aim in every preterm fetus is to allow the pregnancy to

continue to the point just before damage occurs.

• This is done by antepartum surveillance of IUGR fetus for an

assessment of fetal health.
This can be done by
Clinical methods which include
– Maintenance of gravidogram
– FHR auscultation
– DFMC
-Clinical assessment of appropriate amniotic fluid volume

SUPPLEMENTED BY ADDITIONAL TESTS-

1- Non stress test - It is used in the follow up of a preterm IUGR fetus.
Expectant management is possible as long as NST shows adequate
variability and accelerations & no decelerations.
 
Indications for prompt delivery (if fetus is mature)
• Non reactive NST
• Decrease in beat to beat variability
• Lack of accelerations
• Occurrence of variable decelerations.
• If fetus is preterm & there is non reassuring NST it should be
further evaluated by BPP

2- Biophysical profile: -
The fetal BPP can be used to reduce the number of false
positive NSTs obtained
• It is interpreted as follows -
A score of 8-10 is considered normal.
A score of < 4 is considered abnormal.
A score of 6 is equivocal and should be further evaluated with
Doppler velocimetry.
 NST
 

Non Reactive Reactive

+ Continued growth
 
Continue monitoring
BPP and allow the
Fetal CTG patient to go to term
 

normal If any abnormal

indicates fetal compromise
 
Continue pregnancy
Till 38 week gestation
 
 Fetal Compromise

Management depends on gestational age

If >37 weeks If <37 weeks

Assess fetal Delivery pulmonary maturity

Immature If mature

Consider corticosteroid Continue monitoring Delivery

therapy & deliver

within 24-48 hrs. Doppler shows reversal of

diastolic flow

Only option is delivery

3-Amniotic fluid volume: - The most important ultrasound criteria indicating
a severely compromised IUGR fetus is the presence of oligohydramnios.
It should be performed every week alone or as a component of BPP and
frequency of testing should be increased if AF decreases.

4-Doppler assessment: -
• Umbilical artery doppler: - The use of UA doppler causes a statistically
significant decrease in perinatal mortality. (ACOG 2013a)
Delivery is recommended in presence of REDF beyond 28 weeks POG &
AEDF beyond 34 weeks POG.

• Middle cerebral artery doppler: - An increase in cerebroplacental ratio i.e.

brain sparing effect signifies hypoxic fetus with redistribution of blood to
increase cerebral circulation.

• Venous doppler: - Characteristic patterns of reversal of flow in IVC, Ductus

venous and pulsations in umbilical vein are late changes & are associated
with deteriorating acid base balance & poor perinatal outcome.
 Timing of delivery
• • when risk of IUD is more than the risk of neonatal death
• Between 24-28 wks: each day in utero
improves neonatal survival by 1-2%
• Immediate delivery
◦ ≥32 weeks with REDF
◦ ≥34 weeks with AEDF
◦Changes in venous circulation regardless of gestation ◦Mild
IUGR, raised s/D ratio UA Doppler, no other factors, delivery >37
week • Mild
IUGR, normal UA Doppler, no other factors, delivery delayed till 38-
39 wks but not beyond 40 wks ( AJOG 2012)
• ROLE OF C/S •
prelabour fetal acidemia • CTG
becomes pathological ( spon late decelerations with reduced
variability), • Reversal of
Doppler velocities in ductus venosus during atrial contraction
• Umbilical vein pulsations
• REDF
• ADEF(RCOG clinical experts)
• Biophysical profile becomes
abnormal (≤ 4) (ACOG 2006)
 Intrapartum Management
• Excluding congenital defects, intrapartum asphyxia is the
major cause of perinatal morbidity and mortality.( IUGR baby
tolerate the stress of labour poorly)

• for OPTIMUM OUTCOME-

1-Delivery should take place in a hospital with specialized
facilities both obstetrical and pediatric.

2-Continuous electronic fetal heart monitoring is ideal.

3-The best choice for pain relief is epidual analgesia.

4- Cesarean section is indicated for obstetrical indications or if

prompt delivery is needed as in fetal distress.
5-Early ARM is indicated.

6- Patient should be instructed adequate technique for bearing

down and prophylactic forceps should be used if required.

7- Delivery should be atraumatic.

8-Early clamping of cord is indicated

9-Placenta should be sent for HPE.

 LONG TERM PROGNOSIS: -

• IUGR babies remain smaller than their AGA cohorts despite

they catch up growth during first 6 months of post natal life.

• Chronic intrauterine malnutrition and intra-partum asphyxia

results in permanent decrease in the number of brain cells.

• Some amount of minimal brain dysfunction exists in these

babies.

• Worst prognosis is for babies with IUGR causes by congenital

infections or abnormalities or chromosomal defects.
- management of the pregnant patient with
IUGR fetus requires a high degree of clinical
skill & experience and an appropriately timed
intervention

THANK YOU