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Updated: May 18, 2026

Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
Published on: June 29, 2013
Placental insufficiency and fetal growth restriction
Usha Krishna1, Sarita Bhalerao
1AjitVilla, Laburnum Road, Gamdevi., Mumbai, 400007 India ; Breach Candy, Bhatia and St. Elizabeth's Hospitals, Mumbai, India.
Insights
Fetal growth restriction, often caused by uteroplacental dysfunction, signifies a slowed fetal growth rate. Diagnosis involves Doppler assessment of fetal blood vessels, with severe cases necessitating timely delivery.
Area of Science:
- Perinatology
- Fetal Medicine
- Obstetrics
Background:
- Fetal growth restriction (FGR) is a pathological condition characterized by a reduced rate of fetal growth.
- Uteroplacental dysfunction is the most common cause of late-onset FGR, stemming from insufficient nutrient and oxygen supply.
- Symmetrical FGR requires careful exclusion of fetal chromosomal anomalies, structural abnormalities, and infections.
Purpose of the Study:
- To elucidate the pathophysiology of uteroplacental dysfunction in fetal growth restriction.
- To highlight diagnostic methods for identifying placental compromise.
- To outline management strategies for severe cases of FGR.
Main Methods:
- Review of the pathophysiology of uteroplacental vascular maladaptation.
- Description of diagnostic utility of Doppler ultrasound in assessing fetal and placental circulation.
- Discussion of clinical management based on fetal and placental status.
Main Results:
- Uteroplacental dysfunction leads to increased vascular resistance and reduced placental blood flow.
- Placental underperfusion results in villous damage and decreased capillary bed, increasing placental resistance.
- Doppler assessment of uterine, umbilical, middle cerebral arteries, and ductus venosus reveals characteristic changes.
Conclusions:
- Doppler velocimetry is crucial for diagnosing placental changes associated with FGR.
- Severe FGR cases require careful intrapartum surveillance and may necessitate preterm delivery via Cesarean section.
Objectives:
Fetal growth restriction is defined as a pathologic decrease in the rate of fetal growth. The most frequent etiology for late onset fetal growth restriction is uteroplacental dysfunction which is due to inadequate supply of nutrients and oxygen to support normal aerobic growth of the fetus. However, for symmetrical IUGR, fetal chromosomal anomalies, structural anomalies and fetal infections should be carefully excluded. Consequent to the uteroplacental vascular maladaptation of endovascular trophoblastic invasion, there is increased vascular resistance and decreased blood flow to the placenta in the choriodecidual compartment.
Conclusions:
This under perfusion of the placenta causes villous damage; that is, total tertiary villous capillary bed is reduced leading to increased placental resistance. These changes can be diagnosed by Doppler and characteristic changes are seen in the uterine, umbilical, middle cerebral arteries and ductus venosus vessels. In severe cases, delivery of the fetus with optimum intrapartum surveillance, or caesarean section, is essential.
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