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INTRODUCTION:
Fetal growth restriction otherwise known as intra uterine
growth restriction (IUGR) is defined as a pathologic decrease in
rate of fetal growth and ultimately results in a fetus that does
not achieve its inherent growth potential, putting it at risk
for increased perinatal morbidity and mortality. Small for
gestational age is conceptually not the same entity as FGR.
CLASSIFICATION:
* Intrinsic IUGR: Fetuses are small because of fetal condition
such as intrauterine infection or chromosomal abnormality.
* Extrinsic IUGR: Growth failure is caused by an element outside
of fetus such as a) Placental condition or b) Maternal disease
* Combined IUGR: Both extrinsic and intrinsic factors acting in
conjunction to bring about growth failure.
* Idiopathic IUGR: cause of fetal growth failure is unknown.
PATHOPHYSIOLOGY OF PLACENTAL INSUFFICIENCY
Normal Placentation- the number of spiral arteries supplying
the placental bed is fixed relatively early in pregnancy. In
order to accommodate necessary blood flow the spiral arteries
undergo following changes mediated by trophoblastic invasion.
1) In the I- trimester- decidual segments of the arteries
undergo degeneration of internal elastic lamina–denudation of
smooth muscle & elastin in the inner and outer media, which are
replaced by hyaline & fibrin.
2) 2nd Phase (16-18 weeks) -extension of trophoblastic invasion
into the myometrial segment of spiral arteries
Placental insufficiency:
-Reduction in villi & stem capillaries
-Decrease in parenchyma & increase in stroma
-Clumps of syncitial villi forming knots in the intervillous
space
-Trophoblastic invasion restricted to decidual segments
-Myometrial segments remain intact and responsive to
vasoconstrictors
-Acute atherosis of stem villi-- lipid necrosis of myometrium &
smooth muscle cells
-Hyperplastic proliferation of the remaining smooth muscle cells
resulting in narrowing of the lumen.
MATERNAL FACTORS:
1) Constitutionally Small Mothers:
2) Maternal Vascular disease:
3) Maternal Habits:
4) Maternal malnutrition:
5) Maternal Medication:
FOETAL FACTORS INCLUDING GENETIC PERSPECTIVES:
1) Chromosomal abnormalities:
A) Trisomy 21.
B) Trisomy-18:
C) Trisomy –13:
D) Trisomy- 16-
II) CONGENITAL ANOMALIES:
· Potter’s syndrome
· Cardiac anomalies
· Primarily disorders of cartilage and bone
· Osteogenesis imperfecta
· Chondrodystrophies
III) MULTIFETAL GESTATION:
IV) INFECTIONS:
A) Rubella: Causes capillary endothelial
damage, decreases number of normalized cells, reduces cell
division rate.
B) Cytomegalovirus: Decreases cell number because of cytolysis
and localized organ necrosis.
C) Possibly- Toxoplasmosis,
-Varicella zoster
-Tuberculosis
-Malaria
-Syphilis
PRENATAL DIAGNOSIS:
MATERNAL HISTORY:
Age:
Education level:
Family problems
Occupation:
Environmental factors:
Parity:
Personal Habits:
Drugs:
History of maternal vascular disease:
GENERAL EXAMINATION: -
Built & nutrition:
Measurement of fundal height:
1. Inference – If the measurement is 4 cm less than the expected
height inappropriate fetal growth is suspected. (According to
Williams Obstetrics 2 cm less than the expected is worrisome)
Positive Roll Over Test:
· Is predictive of IUGR
AMNIOTIC FLUID VOLUME:
· Oligohydramnios is frequently associated with IUGR especially
asymmetric IUGR and may reflect decreased renal blood flow and
urine output.
· It occurs in about 16% of IUGR pregnancies.
POSITIVE PREDICITIVE VALUES:
· Fundal height 20-60%
· Decreased amniotic fluid volume 55%
DIAGNOSIS OF FGR BY USG
1) ESTIMATED FETAL WEIGHT-
Fetal weight estimation is within 5-10% of the true fetal
weight. Fetal weight estimation is valuable in the diagnosis of
small fetuses but do not differentiate between FGR and small but
healthy babies.
2) FETAL PONDERAL INDEX-
PI=Estimated Fetal Weight/(Femur length) 3 PI value 8.325+/-
2.5 (2SD). Value of 7 or less than 7 strongly suggest fetal
malnutrition
3) ESTIMATED GESTATIONAL AGE-
Estimating the gestational age of the fetus by averaging
routine fetal measurements. The difference between the USG
derived and clinically estimated gestational age (only if the
gestational age is reliable) gives a quantitative idea of fetal
growth impairment
4) BIPARIETAL DIAMETER-
- Serial measurements of BPD demonstrate 2 distinct patterns
of impaired fetal growth.
· SLOW GROWTH PROFILE- Fetuses which show continuous BPD growth
during the entire pregnancy but measurements remain at all times
below the 10th percentile for the gestational age.
· LATE FLATTENING PROFILE: Fetuses that exhibit normal BPD
growth during the first two trimesters of pregnancy followed by
arrest of growth during the last trimester.
5) ABDOMINAL CIRCUMFERENCE-
The best single measurement is AC. Serial AC value plotted
over a graph that is linear from 15 weeks of gestation that is 1
cm in 2 weeks correctly identified most FGR babies. Negative
predictive value- 99%. Therefore finding a normal AC practically
rules out that the baby is small
6) HEAD TO ABDOMEN RATIO
The ratio compares the most preserved organ in the
malnourished fetus, the brain with the most compromised, the
liver. AC is measured at the level of bifurcation of hepatic
vein in the center of the liver. HC is measured at the level of
thalami. It is important to diagnose the type of IUGR.
7) FEMUR TO ABDOMEN RATIO-
- When F/A is abnormally high—fetal malnutrition
- When F/A ratio is normal--- small but healthy baby,
symmetrical FGR but it is unlikely that the baby is suffering
from severe malnutrition.
8) OLIGOHYDRAMNIOS-
- Late sign of fetal malnutrition
- The fluid is decreased if AFI<10 and markedly decreased if AFI<5
8) PLACENTAL GRADING
When BPD & FL suggests less gestational age and placental
grading is high S/O FGR
9) CONGENITAL ANOMALIES
FETAL ECHOCARDIOGRAPHY:
- Ultrasonography imaging of fetal heart & blood vessels
started with the Doppler recording of placental blood flow and
some experimental M mode studies.
Timing of Fetal Echo:
- The first study should ideally be done between 20-22 weeks of
gestation to allow a possible decision of termination.
- By current techniques of fetal echo, the best impression
however is found between 23-26 weeks.
- If indicated, the fetus is followed up with serial echo at
intervals of one to two weeks.
DOPPLER FLOW VELOCIMETRY
Deteriorating placental function triggers a sequence of fetal
protective mechanisms resulting in altered fetal cardiac
function. These cardiac vascular alterations are mirrored by
fetal arterial and venous Doppler studies. Doppler velocimetry
–Best fetal surveillance technique for predicting
hypoxemia/academia
- Indices used are:
1) S/D Ratio: Maximal systole flow velocity/ minimal end
diastolic flow velocity.
2) S-D/ S: Resistance index (Pourcelot index)
3) S-D/ Mean: Pulsatility index.
4) Percentage of reverse flow
5) Preload index: - PLI = PVA (Peak velocity in atrial
contraction)/
PVS (Peak velocity in ventricular systole)
N: 0 to 0.37
6) Cerebro-placental Ratio: Cerebral flow/ placental or
umbilical flow Normal:> 1
Doppler Sequencing Of Foetal Jeopardy:
1) Impaired endovascular trophoblastic invasion (secondary
invasion)
2) This is expressed as high resistance in uterine artery fetal
blood flow velocity waveforms (FVW) – systolic or/ and diastolic
notching can be there. Abnormal Doppler Indices need not always
be present in uterine artery in FGR.
3) This altered deicidal circulation leads to impaired
uteroplacental perfusion, which causes decreased oxygen
perfusion.
4) The placental tertiary arteries decrease in number. Until the
reduction is more than 50%, umbilical blood flow can be
maintained. There- fore umbilical artery FVW is not sensitive to
fetal hypoxemia, hypoxia or partly decompensated respiratory
acidosis. It can only determine fetal acidosis with sensitivity
ranging near 100%. It still identifies fetal acidosis well ahead
of gross changes in biophysical profile.
5) There is increased placental vascular resistance and reduced
fetal oxygenation.
6) Resultant fetal hypoxemia causes peripheral vasoconstriction.
Which when worsened is expressed as umbilical artery impedance
(High S/D ratio)
7) The right ventricular after load increase and reduction in
fetal perfusion of substrate and oxygen
8) This fetal hypoxemia causes dilatation of ductus venosus and
vasoconstriction of hepatic microcirculation.
9) Amplitude of flow in microcirculation: A 50% decrease in
umbilical blood flow is associated with 75% decrease in hepatic
blood flow.
10) Streaming of more blood through ductus venous across the
foramen ovale and resultant increase in left ventricular
pre-load.
11) There is cerebral vasodilatation and increase blood flow
(low S/D ratio in middle cerebral artery). Myocardial blood flow
is also similarly increased. Thus, brain and heart are perfused
with oxygenated blood even in fetal hypoxemia. The normal fetal
cerebral circulation is of high impedance low flow. The
cerebroplacental ratio (CPR) compare the resistance to blood
flow in umbilical artery and middle cerebral artery.
12) Increased cerebral flow decrease the left ventricular after
load.
13) Superior vena cava venous return greatly increases cerebral
flow. This deoxygenated blood from the cerebral region in large
volume reaches the right atrium and ejected into right
ventricle, increasing right ventricular preload. At this stage
ductus venosus may reveal decreased amplitude and absent or
reverse flow during arterial contraction. Concurrently AEDV or
reversed flow develops in umbilical artery. Reduced oxygenation
causes vasoconstriction of ductus arteriosus and pulmonary
trunk. Hence the right ventricular blood cannot be properly
pumped into descending aorta and placenta for oxygenation. This
stagnation leads to recirculation of deoxygenated blood into
cerebral circulation. Increased flow of this deoxygenated blood
causes cerebral congestion and edema leading to vascular
impendence in middle cerebral artery (high S/D ratio)
14) This deoxygenated blood recirculated in vasorum causes
myocardial ischemia
15) Combined with increase right ventricular load the myocardial
ischemia leads to cardiac failure and poor contractile force.
16) This is evidenced by absent or reverse flow in ductus venous
and IVC and appearance of pulsations in umbilical vein.
17) Cardiac dilatation and tricuspid regurgitation are other
signs of failure.
TREATMENT:
MATERNAL NUTRITION
Adequate perfusion of uteroplacental bed and adequate delivery
of amino acids, lipids and carbohydrates are necessary for
normal fetal growth.
· Weight gain in women with normal pre pregnancy body mass index
should be at least 11.29 kg to prevent preterm births & fetal
growth restriction.
Energy Needs: -
· 36 k cal /kg
· Increase 10-15% over pre-pregnant state
· Proteins: Additional 10-12 gm for fetal growth.
· Minerals: Calcium: 1000gm –fetal skeletal tissue, muscle
action, blood coagulation, Iron: 30mg
· Vitamins: Folic acid: 1mg, Vitamin C: 70 mg, Vitamin A: 6000
IU
BED REST:
Results in decreased blood flow to the periphery and increase in
blood flow to uteroplacental circulation that contributes to
improved fetal growth.
MATERNAL HYPEROXYGENATION THERAPY:
Maternal hyper-oxygenation with 55% oxygen administered at a
rate of 8L/min around the clock in gestational age of 26-34
weeks in FGR fetuses with oligohydramnios and abnormal umbilical
artery Doppler studies. pH is increased from 7.31—7.34.
ASPIRIN
ATRIAL NATRIURETIC PEPTIDE (ANP):
Recent studies support the administration of ANP as a novel
measure for treatment of IUGR. Infusion of ANP has resulted in
26% increase in blood flow to the placenta.
INSULIN LIKE GROWTH FACTOR (IGF):
It has a direct effect on placental carbohydrate metabolism
thereby facilitating transfer of substrate to the fetus & foetal
growth. This may explain how maternal IGF-1administration
reverses maternal constraint of foetal growth in FGR. Short-term
IGF-1 infusions improved the placental carbohydrate metabolism,
but have no effect on foetal oxygenation.
FOETAL THERAPY-
I) FOETAL NUTRITIONAL SUPPLEMETNATION
II) MECHANICAL THERPAY
III) STATUS OF INDUCTION OF PULMONARY MATURITY:
ISSUES REGARDING DECISION MAKING MANAGEMENT
EARLY ONSET IUGR- (before 32 weeks)
- Classify IUGR by etiology.
- Determine IUGR type
- Treat maternal condition-- improve nutrition, reduce stress
- Encourage maternal rest
- Evaluate growth scans & umbilical artery Doppler velocity
every 3 weeks unless 36 weeks or severe oligohydramnios develops
- Consider hospitalization if AFI less than 2.5 percentile with
normal umbilical Doppler velocity (UAD)
- Absent umbilical end diastolic flow (AEDF) or reversed
umbilical artery end-diastolic flow.
- Determine IUGR type: symmetric vs. asymmetric
Consider delivery of:
- Anhydramnios (no pockets of fluid that are clear of cord loops
at 30 weeks gestation or beyond.
- Repetitive fetal heart rate decelerations
- Lack of growth over 3 week period and mature lung studies
- Abnormal UAD (AEDF OR REDF)
LATE ONSET IUGR- (32 WEEKS OR GREATER)
- Classify IUGR
- Determine IUGR type
- Treat maternal condition reduce stress improve nutrition
- Encourage maternal rest in lateral position
- Growth scans and UAD every 3 weeks
- Each week do full biophysical profile & non stress test
DECISION MAKING:
The ideal strategy of management of FGR with depend on:
1) Gestational age
2) Underlying etiology
3) Probability of intact extra uterine survival
4) Level of expertise
5) Available technology
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