PG Classroom - Seminar - IUGR

1. Definition -Ankita
2. Etiology:

a. Placental factors -Rimpi
b. Maternal factors -Maitri
c. Fetal factors (including genetic perspectives) -Chetali

3. Clinical diagnosis of IUGR -Ankita

4. Non-clinical diagnosis of IUGR

• Non-invasive
a. USG for fetal growth parameter -Rimpi
b. Fetal echocardiography -Maitri
c. Doppler – colour-Velocimetry -Chetali
• Invasive:
a) Cordocentesis -Ankita
b) Placental biopsy -Rimpi
c) Chorion-villus sampling -Maitri

5. Fetal Therapy

a. Bed rest, Maternal nutrition -Ankita
b. Oxygen/Aspirin -Rimpi
c. β mimetic, IGF, A.N.P -Maitri
d. Fetal Nutrition & Supplement
e. Mechanical Treatment
f. Status of induction of pulmonary maturity -Chetali

6. Issues regarding decision making

a. Early onset IUGR (Timing & method of delivery) -Maitri
b. Late onset IUGR (Timing & method of delivery) -Chetali

7. SFD Baby - Rimpi



The growth of fetus in utero reflects a delicate equilibrium between the mother, the placenta, and the fetus. Fetal growth restriction is not a single disease entity, but rather a physical sign that may result from a broad variety of pathogenic mechanisms. 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. It is defined as a fetus that has failed to achieve a specific and arbitrary anthropometric or weight threshold by a specific gestational age. SGA: New born with birth weight less than the 10th percentile for their gestational age and less than 2500 gms. Both terminologies attempt to identify fetus that are small for reasons other than being preterm.
Fallacy: Is the variation in birth weight for gestational age standards. SGA and IUGR do not separate normal and healthy fetuses that have a weight below the 10th percentile from those who are small because of intrauterine malnutrition.


* 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.


Symmetric (33%) Asymmetric (55%)
Growth of both fetal abdomen and head are proportionally decreased There is disproportionate decrease in size of fetal abdomen with respect to fetal head. Also called head sparing type.
Normal HC/AC Increased HC/AC
Etiology: Early insult Late insult
Genetic, infective pathology, substance abuse, cigarette smoking (impairs cellular hyperplasia leading to long periods of subnormal growth) Placental vascular insufficiency
(Impairs cellular hypertrophy with increased risk of perinatal hypoxia and hypoglycemia)

Risk for long-term neuro-developmental dysfunction resulting from a deficit in total number of brain cells. Long term prognosis good
Normal Ponderal Index Low PI
Although this division is conceptually attractive whether this classification is useful in defining etiology or in predicting outcome is less clear


• Stage-I (hyperplasia): 4-20 weeks gestation rapid mitosis & increase of DNA content.
• Stage-II (hyperplasia & hypertrophy): 20-28 weeks declining mitosis & increase in cell size.
• Stage-III (hypertrophy): 28-40 weeks rapid increase in cell size with peak velocity at 33 weeks gestation, rapid accumulation of fat, muscle & connective tissue. 95% of fetal weight gain occurs during last 20 weeks of gestation.


1) Small Placenta
2) Premature aging of placenta
3) Abruptio placenta
4) Placenta previa
5) Chronic villitis, vasculitis
6) Chorioamnionitis
7) Chorioangioma, hemangioma, placental cysts
8) Circumvallate placenta
9) Twin to twin transfusion (Placental Anastomosis)
10) Umbilical cord complications- single umbilical artery – true knots, velamentous cord insertion
11) Amniotic bands
12) Repeated first trimester bleeding


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.


1) Constitutionally Small Mothers:
a) Small women typically have small babies.
b) If woman begins pregnant weighing less than 100 pounds, the risk of delivering a small for gestational age infant is increased at least 2 fold.
c) Reduced intrauterine growth of the mother is a risk factor for reduced intrauterine growth of her children.

2) Maternal Vascular disease:
a) E.g. Chronic hypertension, preeclampsia, renal disease, diabetes, collagen vascular disease like SLE, cyanotic heart disease, severe anemia as can be seen with sickle cell anemia, chronic pulmonary disease such as asthma.
b) In case of preeclampsia, there is a deficient trophoblastic invasion.
c) Incidence of fetal growth retardation is increased 2 to 3 fold in hypertensives disorders of pregnancy.
d) In case of pregestational diabetes, the risk of fetal growth restriction increases with increasing severity & duration of the disease.
e) This may be due to damage in the microcirculation that is associated with diabetes.
f) Affection of microcirculation could risk the development of PIH & cause severe IUGR.
g) Collagen vascular disease such as SLE is frequently associated with fetal growth restriction with an increase of more than 8 folds that of general incidence of IUGR.

3) Maternal Habits:
a) Cigarette smoking is the most important preventable cause. The reduction in foetal growth is between 150 to 400 gm at term. Carbon monoxide exposure causes decrease in foetal hemoglobin oxygen carrying capacity. Nicotine releases catecholamines. This could cause repetitive episodes of reduced maternal perfusion of the placenta. Placental abruption also has been reported to occur more frequently among them.
a) Tobaccos chewing gravidas & passive smoker also have reduced foetal weight. This is because decreased intervillous blood flow, the effect of carbon monoxide & thiocyanate on the fetus, decreased prostacyclin production.
b) Maternal alcohol ingestion is another well recognized cause of IUGR & it has synergistic effect with smoking.
c) The chronic ingestion of heroin, morphine, Cocaine & other additive substances is frequently associated with IUGR.

4) Maternal malnutrition:
a) Major cause of IUGR
b) Lack of weight gain in the 2nd trimester is strongly correlated with decreased birth weight.
c) The human foetus behaves as a parasite & its growth rate is not affected except in extreme states of severe dietary deprivation.

5) Maternal Medication:
a) The use of certain medication during pregnancy is associated with IUGR babies. E.g.
• Cancer chemotherapeutic agents, warfarin
• Anticonvulsants like phenytoin
• Folic acid antagonists.

1) Chromosomal abnormalities:
• Frequency 10% may be as high as 38%
• Majority have symmetric measurements
• Most common are karyotype abnormalities

A) Trisomy 21.
• Foetal growth restriction generally mild
• After first trimester growth of all long bones lag behind.
• Shortened femur length and hypoplasia of middle phalanx documented with increased frequency.

B) Trisomy-18:
• Significant restriction of growth
• As early as first trimester
• Upper extremity more severely affected than lower.
• Visceral organs growth may be abnormal.

C) Trisomy –13:
• Mild growth restriction

D) Trisomy- 16-

• Usually lead to spontaneous abortions.
• Affect the placenta called confined placental mosaicism lead to placental insufficiency.
• Placentas of foetal autosomal trisomies have reduced number of small muscular arteries in tertiary stem villi.

• Potter’s syndrome
• Cardiac anomalies
• Primarily disorders of cartilage and bone
• Osteogenesis imperfecta
• Chondrodystrophies

• Up to 21% affected
• More common with monochorionic placentation
• Causes
- Abnormal placentation
- Decreased placental size
- Abnormal placental vascular Anastomosis

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


Personal history
Past history
Weight gain
Uterine fundal height
Abdominal circumference
Non stress test
Fluid volume


Age: < 17 Yrs Or > 35 Yrs.
Marital status: Single mothers / unwanted pregnancies
Education level: Low educational level.
Family problems
Occupation: Strong physical work and intellectual stress.
Environmental factors: Urban environment, economic depression, migration, culture.
Parity: Mainly when the intergenesic period is less than 2 years & in precocious primigravida, history of IUGR baby in previous pregnancy.
Personal Habits: Smoking as in active and/or passive smoking.
Alcohol, which provokes irreversible damage, mental deficiency & malformations have been reported.
Drugs: Cytostatic medications, propylthiouracil, heroine,
propranolol, anticonvulsants, prednisone.
History of maternal vascular disease: Chronic hypertension
Renal disease
Collagen vascular disease
Cyanotic heart diseases
Sickle cell disease

Built & nutrition: Height: low (< 1.50m)
Weight: starting pregnancy underweight and with inadequate gain during the same.

Measurement of fundal height:
1. Measurement of fundal height is an excellent screening tool for IUGR.
2. Sensitivity may reach 95% when precise gestational dates are available.
3. Measured from symphysis pubis to superior aspect of uterine fundus.
4. Between 20-34 weeks the uterine fundal height in cms. roughly coincides with weeks of gestation.
5. While this measurement is useful it is fraught with potential measurement problems in women who are overweight and the inability of the physician to identify the top of uterus for proper measurement.
6. Patients’ bladder should be evacuated prior to the examination.
7. 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)
8. Difficulty:
• If uterine fundus is deviated to one side measurement taken in middle will be inaccurate
• Maternal obesity
• Breech / transverse presentation
• Uncertain dates
• Uterine anomalies such as fibroids / twins / hydramnios
• This screening method can identify < 50% of fetus with IUGR.

Positive Roll Over Test:
• Is predictive of IUGR
• Is defined as a rise in diastolic blood pressure of 20 mm Hg or more with a position change from the left lateral recumbent to supine.

• 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.

• Fundal height 20-60%
• Roll over test 22%
• Decreased amniotic fluid volume 55%


It is very important, non-invasive, easily available accurate method for the diagnosis and confirmation of FGR.

Fetal weight estimation is within 5-10% of the true fetal weight. Also the method requires precise knowledge of the gestational age. Fetal weight estimation is valuable in the diagnosis of small fetuses but do not differentiate between FGR and small but healthy babies. This method has sensitivity of 87% and specificity of 87% when the estimated fetal weight is below the 10th percentile for the gestational age.


It is gestational age independent and gives a constant value throughout the second part of pregnancy. 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


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


- 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. These are the true FGR.

But sensitivity & specificity is too low since
- Head is one of the last organ to be affected by fetal malnutrition
- Late in pregnancy fetal head enters the pelvis and undergo moulding process.


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


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 thalamii. It is important to diagnose the type of IUGR.

- SYMMETRIC FGR - refers to a growth pattern in which the growth of both fetal head & abdomen are decreased proportionately. It results from an early insult and is characterized by a long period of subnormal growth. These infants do not have perinatal asphyxia but are at a risk of neuro-developmental dysfunction resulting from a deficit of total number of brain cells. It is associated with infective /genetic pathology

- ASYMMETRIC FGR- refers to the growth-retarded fetus in whom, a disproportionate decrease in the size of the fetal abdomen with respect to fetal head is seen. This pattern is also known as head sparing type. It is caused by a late insult that impairs cellular hypertrophy. It is usually associated with progressive uteroplacental insufficiency. Greater risk of perinatal hypoxia and neonatal hypoglycemia, their long-term prognosis by appropriate management is good.

There is a substantial overlap between the two patterns. Although this differentiation is conceptually attractive the usefulness in defining etiology and predicting outcome is less clear.


- This method compares femur length that is minimally affected by fetal growth impairment with the abdominal circumference, which is the most affected.
- Advantage: FL is easy to obtain, Not affected by moulding/abnormal presentation and position
- FL remains constant after 20 weeks
- Normal value of FL/AC= 22+/-2 (upper limit 23.5)
- 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.


- Late sign of fetal malnutrition
- Amniotic fluid volume is measured by four quadrant technique (AFI)
- The fluid is decreased if AFI<10 and markedly decreased if AFI<5


- When BPD & FL suggests less gestational age and placental grading is high S/O FGR


- Important etiological factors for FGR
- USG done to rule out congenital anomalies


- Ultrasonography imaging of foetal heart & blood vessels started with the Doppler recording of placental blood flow and some experimental M mode studies. The most important application of foetal echo remains in determining cardiac structural & functional status in a pre-viable foetus.

- A careful delineation of the cardiac status may lead to one of the three situations:
- 1) For a potentially irremediable condition such as hypoplastic left heart syndrome (HLHS), one is likely to take a decision for medical termination of pregnancy.
- 2) For a structural problem that is amenable to surgical or trans-catheter intervention treatment, by & large the decision will be to continue the pregnancy. The time & place of delivery will be carefully planned to optimize the neonatal outcome.
- 3) In an otherwise high-risk state, a normal foetal echo always helps to ease the burden of the pregnancy.

- Cardiac arrhythmia is getting more & more frequently diagnosed & assessed by fetal echo, thereby helping medical management of this condition. Fetal echo is emerging as a strong tool and is helping to clarify the pathogenesis of many cardiac abnormalities.

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.

In an ideal world each pregnancy should undergo a fetal cardiac scan to rule out the possibility of congenital heart defects. The following are the situations where a fetal echo is strongly indicated:
- F/h/o congenital heart defects especially previous sib or parents.
- Hydrops fetalis esp. the nonimmune
- Fetal cardiac arrhythmia &/or maternal collagen vascular disease.
- Fetal somatic anomaly on USG
- Suggestion of abnormal genetic, chromosomal or syndromatic pattern in fetus or in the family.
- Maternal condition this associated with fetal abnormalities e.g. diabetes mellitus, polyhydroamnios, oligohydramnios, Rh sensitization, drug exposure esp. alcohol, narcotics, anticonvulsants.
- Any condition that indicates that the fetus is not doing well should preferably be looked into with a fetal echo. E.g. IUGR & unexplained diminished fetal movements.


- 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.
- 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: Amplitude of flow in ductus venous is increased and is the earliest and most sensitive sign of fetal hypoxemia. Normally ductus venosus distributes 50% of umbilical blood directly into inferior vena cava (IVC). Such blood flow ensures the supply of oxygenated blood to coronary and cerebral circulation. During hypoxemia this fraction increases up to 70% and less blood is circulated in liver through portal system. Hence less hepatic glycogen deposition lead to reduced abdominal circumference of FGR fetus. A 50% decrease in umbilical blood flow is associated with 75% decrease in hepatic blood flow. The mechanism responsible could be accounted by active relaxation of ductus venosus or vasoconstriction in hepatic circulation.
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. Even in second hall of pregnancy normal S/D of middle cerebral artery is very high in the range of 2.8 to 3. The cerebroplacental ratio (CPR) compare the resistance to blood flow in umbilical artery and middle cerebral artery. It is the most powerful parameter of assessment of FGR and hypoxemia. It takes into account the placental disturbances due to vascular disease and cerebral response to placental resistance. CPR value is heart rate independent and has significant cut off value of 1. (CPR is normal if it is > 1
12) Increased cerebral flow decrease the left ventricular after load. Fetus even though hypoxemic, is maintained in the compensated phase by the ventricular contractile force.
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.



• To make rapid determination of fetal karyotype when chromosomal defect is suspected.
• To assess degree of fetal hypoxia & acidosis.
• To assess Cytogenetic, Biochemical, Metabolic, Endocrine and Hematological status


- In most series of FGR fetuses, incidence of chromosomal anomalies has been <10% (which can be detected by targeted ultrasound)
- Doppler velocimetry results are found to correlate better with the level of fetal acidosis precluding the need for cord blood study.
- Fetal loss rates within 2 weeks of sampling were 1,7, 14 & 25% in groups: Normal /Abnormal / Growth retarded / hydropic fetus respectively.
- Babies frequently develop prolonged, severe bradycardias requiring emergency caesarean delivery.

- 19% Chromosomal defects were detected.
They included:
Trisomy 21
Trisomy 18
Trisomy 13
Deletions or translocations

- Triploidies encountered in second trimester & Aneuploidus, deletions and translocations found in third trimester group.
- Triploidy is associated with the most severe from of early onset growth retardation and that majority of fetuses die before third trimester of pregnancy.
- 2nd trimester most severely asymmetrically small fetuses are chromosomally abnormal.
- Growth retarded fetuses are hyperlacticaemic
- In SGA erythropoetin concentration increased in response to tissue hypoxia & is associated with macrocytosis and erythroblastosis
- Severely growth retarded fetuses are thrombocytopenic & leukopenic as a result of tissue hypoxia & deficiency of essential nutrients.


- It is a procedure for prenatal genetic diagnosis.
- It is performed between 9 & 12 weeks.
- Chorionic villi for antenatal diagnosis can be obtained by:

I) Trans cervical catheter aspiration
II) Trans abdominal needle aspiration
III) Trans vaginal aspiration

I) Trans-cervical catheter aspiration:
- CVS starts with a real-time ultrasound examination.
- The position of uterus, number of gestational sacs, gestational age of foetus, presence of foetal heart activity, localization of the chorion frundosum are determined.
1) Genetic diagnosis is achieved at an early gestational age.
2) Comfortable for the patient.
3) Technically simple.
1) It has a slightly higher risk of foetal loss
2) Chromosome composition of the chorionic villous is occasionally different from the chromosome composition of foetal cells.
3) Enzyme composition of chorionic villous cells may be different from the fetal cells.
4) It is difficult if placenta is fundal.
1. Positive N. gonorrhea culture of cervix
2. Active genital herpes
3. Active bleeding
4. Maternal coagulopathy
5. Cervical stenosis
6. Severe cervicitis
7. Uterine myomata
8. IUD inside the pregnant uterus.
II) Trans-abdominal CVS:
The need to obtain chorionic villi from patients who had contraindications to the performance of Tran cervical CVS & the need to reduce the potential risk of infection associated with the vaginal procedure.
- 1) Minimal risk of infection
- 2) Does not cause vaginal bleeding
- 3) Can be performed in 2nd & 3rd trimester
- The amount of tissue obtained is less
- Greater discomfort
- Difficult to performs if placenta is posterior
- Technically more difficult.

III) Trans Vaginal CVS:
- There are some patients in whom trans abdominal & trans-cervical CVS are difficult to perform because of extreme uterine retroversion, presence of myomas, or placental localization.


- The most common cause of FGR is impaired nutrient supply to the fetus.
- Fetal growth depends on adequate maternal fuel supply and a maternal vascular tree that can deliver these fuels to the fetoplacental unit.
- 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
• Minerals: Calcium: 1000gm –fetal skeletal
Tissue, muscle action, blood
Iron: 30mg
• Vitamins: Folic acid: 1mg, Vitamin C: 70 mg, Vitamin A: 6000 IU


Results in decreased blood flow to the periphery and increase in blood flow to uteroplacental circulation that contributes to improved fetal growth. However there is no striking paucity of data validating these assumptions. Hard and strenuous work should be avoided specially in first trimester and last 6 weeks. On an average patient should be in bed for about 10 hours.


It has been proved that in IUGR baby’s acidosis and decreased oxygen saturation is found in umbilical artery. 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. Po2 is increased from 21.2 mm Hg –27.7mm Hg. PCo2 decreased from 43.7 mm Hg - 38 mm Hg. O2 saturation is increased from 57% to 71.8%. pH is increased from 7.31—7.34. Although there is not much difference in birth weight the mortality significantly decreased from 68-85% to 20-29 %


Role of aspirin is yet to be proven. The dose recommended is low dose aspirin 1-2mg/kg/day. It inhibits the cyclooxygenase pathway, decreases TXA2 but does not alter PGI2 in low dose. TXA2 & PGI2 ratio is altered in favour of PGI2. This leads to vasodilatation in uteroplacental bed. There is insufficient evidence to recommend for or against the routine use of aspirin.
Side effects include Congenital Heart disease (associated with aspirin) use in 1st trimester. However no causal links has been established between aspirin & birth defects. An occasional increased risk of maternal bleeding, abruption, and post partum hemorrhage has been reported. Aspirin use needs very careful proper counseling.


These agents have been employed for tocolysis. One of the effects is stimulation of myometrium adenylate cyclase, which results in myometrial relaxation. These consequently results in decreased resistance to uterine blood flow & increase uterine perfusion. Similarly, a direct vasodilator effect on the uterine arteries may results in increased uterine perfusion. This may theoretically benefit in treatment of IUGR. However, recent studies could not demonstrate enhanced foetal growth associated with Beta-agonist administration.


It is an endogenous peptide synthesized in the right atrium that has diuretic, natriuretic & vasodilator effects. The biologic effects of ANP are thought to be mediated through the stimulation of guanylate cyclase, resulting in increased intracellular concentration of cyclic guanosine monophosphate. This peptide has been reported to dilate the placental vasculature in late pregnancy. 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. An 80% reduction in number of ANP receptors in IUGR has been observed; suggesting that pertubation of ANP receptor physiology may be associated with IUGR.


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.



Nutrients like sugar proteins, amino acids and lactate in amniotic fluid are swallowed, digested and absorbed by the fetus which provides 10-30 calories per day and 0.2-0.3 gm proteins per kg per day in the third trimester. Absorption of nutrients may occur through placenta, foetal membranes and umbilical cord. Trans amniotic foetal feeding (TAFF) with a 10% dextrose solution, amino acids and lipids has been tried. It has been observed that when fetal oxygenation is impaired TAFF might not be of any use in treatment of FGR. The trophic factors on the gastro-intestinal tract present in amniotic fluid are gastrin and epidermal growth factor (EGF). It has been suggested that EGF must be an important constituent of TAFF. The relevance of these data to clinical practice remains to be determined.


A novel approach is intermittent abdominal decompression. A negative pressure of 70mm Hg is applied for 30 seconds every minute for 30 minutes twice daily. This is thought to increase blood flow to placental intervillous space.


The growth-retarded foetus is thought to be stressed and responds to this stress by secreting endogenous corticosteroids that enhance pulmonary maturity. But recently the validity of these data is questioned.


The usual causes for early onset FGR before 32 weeks of gestation are:
- Chromosomal anomalies
- Congenital anomalies
- Intrauterine infection
- Only when these are excluded the probability of: Uteroplacental dysfunction

Nearly 20% fetuses with early onset FGR have a chromosomal abnormality. Using serology, a viral agent can be identified in nearly 5% cases. Foetal infection is most suspected when a severely FGR foetus has normal blood gas levels, normal karyotype & abnormal platelet or WBC count. Screening for toxoplasmosis, rubella, cytomegalovirus, herpes & other viral agents is recommended. Since USG & color Doppler studies can identify nearly 90% of chromosomal anomalies & 65% of all structural anomalies. Major causes of early onset FGR can be sorted out at ultrasound study itself. The normal fetuses otherwise showing early onset FGR should be considered to suffer from uteroplacental dysfunction. They are to be managed conservatively with regular Doppler studies or BPP. The pregnancy could be continued at least until 36 weeks if Doppler is normal. Development of AEDV with venous Doppler abnormality, REDF or severe oligohydramnios will be an indication for delivery. Fetal response to maternal hyper oxygenation may be predictive of which fetus may develop hypoxia

Timing & Method Of Delivery: Chromosomally normal FGR foetus with a gestational age of > 36 weeks should be delivered electively. There is no need for prior documentation of foetal pulmonary maturity. Oligohydramnios at >36weeks is an indication for immediate delivery because of the risk of a cord accident. Failure of growth is also an indication for delivery. As age advances, delivery in the absence of frank fetal distress becomes a more desirable option. The mode of delivery is governed by the underlying etiology, evidence of acidemia & gestational age. As long as ductus venosus flow velocity is normal, vaginal delivery under intrapartum monitoring is quite acceptable. Unless there is an abnormal CTG or a malpresentation, normal but small fetuses should be allowed to go into labour. Growth restricted fetuses without evidence of hypoxemia can be also managed in same way. In case of acidemia, LSCS is ideal. Acidemia is presumed when there is REDF, reverse flow in ductus venosus, significant reverse flow in inferior vena cava, cerebral dilatation or repetitive late deceleration & these fetuses are not suited for vaginal delivery. A trial of labour should be considered first with continuous fetal heart rate monitoring. Thick meconium is an indication for LSCS as lethal meconium aspiration can occur before delivery.


Most frequent etiology is mild to moderate uteroplacental dysfunction which is defined as inadequate supply of nutrient and oxygen to support normal aerobic growth of foetus. Foetal chromosomal and structural anomalies should be ruled out. Indications for delivery are 1) Oligohydramnios at less than 36 weeks. 2) REDF after 32 weeks of gestation 3) AEDF after 34 weeks. 4) Abnormal venous Doppler: Low flow during arterial contraction, absent or reverse flow in ductus venosus, High diastolic flow in middle cerebral artery. With AEDF at less than 34 weeks the fetus should be followed preferably by venous Doppler study or by BPP. Any abnormality in either is an indication for delivery. Sonographic assessment of growth rate is done. Absent growth is an indication for delivery. Hospitalization for bed rest and prophylactic or therapeutic administration of aspirin to women at risk is controversial. Conservative management is recommended for otherwise normal but small fetuses with Doppler profile and BPP normal. They usually demonstrate a slow but fixed velocity of growth. Spontaneous onset of labour at term and vaginal delivery is preferred. Even induction of labour at or near term has not been proved advantageous.
Timing Of Delivery: Chromosomally normal FGR foetus with gestational age > 36 weeks should be delivered electively. Oligohydramnios at > 36 weeks.
Mode Of Delivery: this is governed by underlying etiology, evidence of acidemia and gestational age. If ductus venosus flow velocity is normal, vaginal delivery under intrapartum monitoring is acceptable. A FGR foetus is allowed to labour as long as complicating factors like abnormal CTG or malpresentation are not present. Whenever termination is indicated LSCS is ideal whenever there is good evidence of acidemia. Acidemia is presumed with REDF, reverse flow in ductus venosus or inferior vena cava, cerebral dilatation, repetitive late deceleration


Upon suspicion of IUGR, it is recommended for mother to do daily fetal movement counts. Obtain twice weekly non stress tests. Obtain fetal ultrasound every 2-3 weeks to assess: Fetal growth, Amount of amniotic fluid, Biophysical profile. Make a diagnosis then begin regular antepartum fetal surveillance. 34 weeks gestation is appropriate for most at risk patient. 26-28 weeks is appropriate for high-risk maternal conditions such as chronic hypertension.

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)


- 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

Consider hospitalization if AFI less than or equal to 5 cm

Consider delivery if Oligohydramnios (AFI < 5 cm) at 36 weeks or greater, Oligohydramnios at less than 36 weeks gestation should be combined with other indication of fetal status such as UAD, Abnormal UAD at 36 weeks or greater, REDF after 32 weeks, AEDF after 34 weeks,

If AEDF at less than 34 weeks BPP twice weekly.
- ADEF+ Abnormal NST
- Abnormal BPP-
- Poor fetal growth: If no growth on three week serial growth scans,
- Anhydramnios
- Repetitive fetal heart rate deceleration


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

Doppler velocimetry –Best fetal surveillance technique for predicting hypoxemia/academia


Related to perinatal asphyxia and acidosis
1) Persistent fetal circulation
2) Meconium aspiration syndrome
3) Hypoxic insults including ischemic encephalopathy

Related to metabolic alterations
1) Hypoglycemia
2) Hypocalcaemia
3) Hyperviscosity
4) Hyperglycemia
5) Hypothermia



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