Fetal Growth Restriction

1. FETAL GROWTH
RESTRICTION
- RAHUL SUTHAR

2. INTRODUCTION
Fetal growth restriction (FGR) is
• affects about 3% to 7% of all pregnancies
• Birth weight <10th percentile
• Pathologic process that inhibits normal growth potential (intrinsic)
• of short-term and long-term complications
Classification
◦ EFW between3 and 9th percentile – moderate FGR
◦ EFW less than the 3rd percentile - severe FGR
• FGR can be categorized as symmetrical and asymmetrical

3. Normal intrauterine Growth pattern
•Stage I (Hyperplasia)
• 4 to 20 weeks
• Rapid mitosis
• Increase of DNA content
•Stage II (Hyperplasia & Hypertrophy)
• 20 to 28 weeks
• Declining mitosis
• Increase in cell size
•Stage III (Hypertrophy)
• 28 to 40 weeks
• Rapid increase in cell size
• Rapid accumulation of fat, muscle and connective tissue
•95% of fetal weight gain occurs during last 20 weeks of gestations

4. Symmetrical FGR
• 20% to 30% of all FGR cases
• Affected from noxious effect very early in the phase of cellular hyperplasia
• Adverse intrauterine conditions beginning in the early pregnancy (first
trimester)
• Fetal nutrient restriction, such as smoking, cocaine use, chronic hypertension,
anemia, and chronic diabetes mellitus
• Chromosome anomalies, such as aneuploidy
• TORCH infection (Toxoplasma gondii, cytomegalovirus, herpes simplex virus,
varicella-zoster virus, Treponema, and others) contracted prenatally are
present in 5% to 15% of cases
• Severe fetal malnutrition can cause either symmetrical or asymmetrical FGR.

5. Asymmetrical FGR
•70% to 80% of all FGR cases
•Affected in later months during cellular hypertrophy
•The growth restriction is disproportionate, with relative preservation of head circumference (fetal brain) and
reduced abdominal circumference (fetal liver), resulting in an increased brain to the liver ratio (BLR).
• Preeclampsia cause of asymmetrical FGR
• Develops after 20 weeks of gestation and is characterized by hypertension and proteinuria
• Chronic hypertension - placental vascular remodeling, vascular sclerosis, and ischemia
• fetal liver glycogen and body adipose tissues are diminished
• brain continues to grow normally with a preferential blood supply.

6. ETIOLOGY
Fetal causes:
◦ Fetal genetic anomalies- 5% to 20%
◦ Aneuploidy, uniparental disomy, single-gene mutations, partial deletions or
duplications, ring chromosome, and aberrant genomic imprinting
◦ The finding of symmetric FGR prior to 20 weeks of gestation suggests aneuploidy
◦ Fetal infection is responsible for 5% to 10% of FGR cases,
◦ the most common being cytomegalovirus and toxoplasmosis
◦ Other agents are varicella-zoster virus, malaria, syphilis, and herpes simplex.
◦ Fetuses with non-chromosomal congenital anomalies or specific syndromes may
also be growth restricted.

7. ETIOLOGY
•Maternal causes
o Uteroplacental-fetal blood flow and cause FGR
o Chronic hypertension, gestational or pregestational diabetes mellitus, systemic lupus
erythematosus, antiphospholipid syndrome, severe cardiopulmonary or renal diseases, severe
anemia and malnourishment, sickle cell disease
o substance abuse (alcohol, cocaine, nicotine, heroin, marijuana, and others),
o anti-neoplastic drugs or radiation exposure, chronic antepartum hemorrhage, low pre-
pregnancy weight or poor gestational weight gain, extremes of maternal age, short
interpregnancy interval, high altitude residency, multiple gestations, uterine malformations, and
assisted conception
o Maternal nutritional status can be responsible for almost a 10% variance in fetal weight.
Mothers who were growth restricted carry twice the risk for delivering FGR neonates.

8. Placental/umbilical cord causes
•Chromosomal placental mosaicism (CPM), presenting with placental trisomy (most commonly
trisomy 21) and a chromosomally normal fetus, is identified in 10% of idiopathic cases of FGR
and 33% of FGR with placental infarction and decidual vasculopathy.
• Placental anomalies
• umbilical cord anomalies (single artery, velamentous or marginal cord insertion) are other
causes of FGR
• Maternal morbidities impact fetal growth via their adverse effects on the placental functions.

9. PATHOPHYSIOLOGY
• Body fat and muscle mass are reduced in the fetus - resulting in decreased
subcutaneous fat, as well as body nitrogen and protein contents
• The reduction in the maternal-fetal transfer of nutrients due to placental
insufficiency, namely glucose, amino acids, and minerals - leads to lesser
deposition of glycogen in the liver and muscles, and of minerals in the
bones
•As the fetus continues to be under stress, the blood flow is diverted away
from less vital organs and redirected preferentially to the brain, heart,
adrenal glands, and placenta.

10. History
The maternal history of the following may suggest an increased risk of FGR.
 Previous pregnancy with FGR
 Previous pregnancy with preeclampsia
 History of smoking or substance abuse
 Multiple gestations
 Assisted conception
 Chronic illnesses
Extremes of maternal age

11. Physical examination
Maternal Findings
The fundal height that estimates gestational age by measuring the distance
between the pubic symphysis and the top of the uterus might be decreased.
Neonatal Findings
•FGR is less than 10 percentile for weight
•decreased muscle mass and subcutaneous fat at birth
• The head may look proportionately large or small depending upon the
pathogenic factor for intrauterine growth restriction
• The facies may appear thin, and the umbilical cord shrunken
• Due to the lack of proper bone mineralization and bone formation,

12. EVALUATION
•The American College of Obstetricians and
Gynecology (ACOG) recommends performing serial
fundal height during every prenatal visit.
• ultrasonography study is warranted if the fundal
height is less by 3 cm or more than the gestation in
weeks.
•The ultrasound scan also serves to detect the presence
of anatomical abnormalities in the fetus.
•. If FGR is detected, amniotic fluid volume
estimations and umbilical arterial Doppler blood flow
velocimetry (UADV) studies should be performed.

13. Differential Diagnosis
1. Misdated pregnancy: First-trimester ultrasound (either transvaginal or
transabdominal) provides the most accurate dating of pregnancy.
2. Oligohydramnios: The discrepancy between fundal height and gestational age may
be observed in women with low amniotic fluid volume. An ultrasound scan can be
used to reliably predict the estimated fetal weight (EFW).

14. • Short term
 Occur soon after birth and include respiratory distress, perinatal asphyxia,
meconium aspiration syndrome, hypoglycemia, polycythemia, hyperviscosity,
non-physiological hyperbilirubinemia, sepsis, hypocalcemia, poor
thermoregulation, and immunological incompetence
• Long term
 Perinatal mortality is increased
 the occurrence being related directly to the severity of growth restriction and
inversely to the maturational status at birth
 Malnutrition and low IQ, neurological handicaps
 It rises abruptly if the birth weight drops below the 6 percentile

17. Thank you