Fetal growth restriction (FGR) is a complication of pregnancy where the developing fetus fails to achieve its genetically determined growth potential. The condition is defined when the estimated fetal weight or abdominal circumference is below the 10th percentile for the current gestational age. This reduced growth rate indicates the fetus is not receiving adequate nutrients or oxygen, or that an intrinsic issue prevents normal development. FGR is a serious diagnosis requiring close prenatal monitoring, as it is associated with increased risks of stillbirth and neonatal complications.
Placental Issues
Placental dysfunction is the most common cause of FGR, as the placenta serves as the interface for nutrient and gas exchange between the mother and the fetus. This dysfunction, often termed placental insufficiency, means the organ cannot transfer the necessary substrates to sustain expected fetal growth. The problem frequently originates early in pregnancy with defective trophoblast invasion, where placental cells fail to remodel the maternal spiral arteries. Instead of becoming wide, low-resistance vessels, the arteries remain narrow and sensitive to maternal blood pressure changes.
This incomplete remodeling results in high vascular resistance and reduced blood flow into the intervillous space of the placenta. The diminished flow starves the placenta itself, leading to areas of damage known as placental infarctions. As the pregnancy progresses, the reduced cross-sectional area of the placental blood vessels means an inadequate supply of oxygen and glucose reaches the fetus. The fetus adapts by redirecting blood flow, prioritizing the brain over other organs, a phenomenon observable via Doppler ultrasound.
The severity of placental insufficiency often correlates with the timing of FGR onset. Earlier onset, typically before 32 weeks, indicates more severe placental damage and a higher degree of growth restriction. Later onset FGR, occurring after 32 weeks, may be less severe but still represents the placenta failing to meet the rapidly increasing demands of the third-trimester fetus.
Maternal Health Conditions
Systemic maternal diseases or pre-existing chronic conditions can profoundly compromise the intrauterine environment and the function of the placenta. Preeclampsia, a disorder characterized by new-onset hypertension and often protein in the urine after 20 weeks of gestation, is a major contributor to FGR. This condition shares a common pathology with placental insufficiency, where the maternal blood vessels feeding the placenta are constricted, severely limiting blood flow. The resulting poor perfusion restricts nutrient delivery, causing the growth restriction.
Chronic hypertension, even when controlled, increases vascular resistance in the vessels supplying the uterus and placenta. Similarly, pre-existing kidney disease impairs the mother’s ability to maintain blood volume and can trigger placental under-perfusion. Autoimmune conditions such as systemic lupus erythematosus (Lupus) or antiphospholipid antibody syndrome promote blood clotting. These disorders increase the risk of microscopic clots forming within the small placental blood vessels, physically blocking blood flow to the fetus.
Uncontrolled or advanced diabetes, particularly with existing vascular complications, can lead to placental compromise and restricted growth. Severe maternal anemia, which reduces the oxygen-carrying capacity of the blood, directly impacts the oxygen available for transfer across the placenta. Chronic malnutrition or a very low pre-pregnancy body mass index (BMI) means the mother lacks the nutritional reserves required for fetal development.
Fetal and Genetic Factors
In some cases, the cause of FGR originates not with the placenta or the mother’s health, but with an intrinsic issue within the fetus itself. Chromosomal abnormalities, which are structural or numerical errors in the fetal genetic material, are a known cause of growth restriction. Conditions like Trisomy 18 (Edwards syndrome) or Trisomy 13 (Patau syndrome) frequently result in severe, early-onset FGR because the genetic anomaly inherently limits the fetus’s ability to grow normally.
Genetic syndromes, which are caused by single-gene mutations or smaller structural variations, can also impair growth potential. These conditions disrupt the complex signaling pathways necessary for cell division and organ development, leading to a fetus whose growth trajectory is intrinsically restricted, regardless of optimal nutrient supply. Congenital structural anomalies, such as severe cardiac defects or major kidney malformations, place an extraordinary metabolic burden on the fetus. The energy required to compensate for the malfunction of a major organ system can divert resources away from general growth, resulting in a measurable restriction.
Specific infectious agents that cross the placenta and infect the fetus directly can also cause FGR. The group of infections known as TORCH are particularly implicated:
- Toxoplasmosis
- Rubella
- Cytomegalovirus (CMV)
- Herpes Simplex Virus (HSV)
These pathogens damage fetal cells and organs, causing inflammation and disrupting cellular proliferation and differentiation, which limits the fetus’s overall size.
Environmental and Lifestyle Influences
External factors related to the mother’s environment and lifestyle represent highly modifiable risks that can contribute significantly to FGR. Cigarette smoking is one of the most recognized and preventable causes, as nicotine and carbon monoxide from smoke constrict the uterine and placental blood vessels. Carbon monoxide also binds to the mother’s hemoglobin, effectively reducing the oxygen available to be delivered across the placenta.
The use of alcohol and illicit drugs, such as cocaine and heroin, can similarly restrict fetal growth through mechanisms of vasoconstriction and placental hypoperfusion. Cocaine, for instance, is a potent vasoconstrictor that can acutely reduce blood flow to the uterus, causing an immediate and severe drop in oxygen and nutrient supply. Exposure to certain prescription medications, such as some anti-epileptic drugs, can also be associated with reduced fetal growth trajectories.
Even the physical environment plays a role, as living at high altitudes reduces the partial pressure of oxygen in the atmosphere. This chronic low-oxygen environment can lead to a measurable restriction in fetal growth due to the reduced oxygen gradient available for transfer across the placenta. Poor maternal weight gain throughout the pregnancy, often linked to inadequate caloric and protein intake, can also place the fetus at risk. A failure to gain the necessary weight reflects insufficient nutrient availability, which directly limits the substrates required for optimal fetal growth.