Fetal Growth Restriction (FGR) is a condition diagnosed when an unborn baby fails to reach its inherent growth potential within the womb. This failure is clinically defined as an estimated fetal weight that falls below the 10th percentile for the specific gestational age. The diagnosis indicates a pathological restriction of growth, not merely that the fetus is constitutionally small. Understanding the causes of FGR is important, as the condition increases the risk of complications during and after pregnancy.
The Central Failure: Placental Insufficiency
The most frequent mechanism leading to FGR is placental dysfunction, often termed uteroplacental insufficiency. The placenta transfers oxygen and nutrients from the mother’s bloodstream to the fetus. When its function is compromised, the fetus receives inadequate resources to sustain normal growth.
This failure often begins early in pregnancy with abnormal development of the placental interface. Normally, specialized trophoblasts invade the mother’s spiral arteries, transforming these narrow vessels into wide, low-resistance conduits. In many FGR cases, this process (shallow trophoblast invasion) is incomplete, causing the arteries to remain narrow and restrict blood flow.
The resulting high-resistance, low-flow circulation restricts the volume of maternal blood reaching the placenta. This reduced perfusion can damage placental tissue, leading to lesions or areas of tissue death called placental infarcts. These damaged areas further reduce the surface area available for gas and nutrient exchange.
The limited blood supply causes chronic under-nourishment and hypoxia, forcing the fetus to adapt by redistributing blood flow. This adaptive response, detectable via Doppler ultrasound, shows increased vascular resistance in the fetal circulation. The fetus shunts oxygenated blood primarily to the brain, heart, and adrenal glands, often at the expense of abdominal organs and subcutaneous fat.
This physiological failure results in the fetus not receiving the necessary building blocks for growth, regardless of the mother’s nutrient intake. Severe or early-onset placental insufficiency typically results in the most pronounced cases of FGR. The degree of restriction is directly related to the severity of this placental malfunction.
Contributing Maternal Health and Lifestyle Factors
Various systemic conditions and environmental exposures can compromise the uterine environment and contribute to placental insufficiency. Chronic health conditions affecting the mother’s vascular system are significant contributors. For instance, preeclampsia and chronic hypertension cause widespread blood vessel constriction, reducing blood flow to the uterus and placenta.
Disorders that affect the blood’s ability to clot, such as inherited thrombophilias, can increase the risk of microscopic clots forming in the placental circulation. These small blockages, known as microthrombi, damage the delicate placental vessels and reduce the nutrient transfer capacity. Chronic kidney disease or severe anemia can decrease the mother’s ability to maintain healthy blood volume and oxygen-carrying capacity, thereby limiting fetal supply.
Maternal lifestyle choices also negatively affect fetal growth. Smoking tobacco is a well-established risk factor, as nicotine causes vasoconstriction and carbon monoxide reduces the oxygen-carrying capacity of the blood. Heavy alcohol consumption and the use of illicit drugs, such as cocaine, also cause significant vascular constriction and are independently associated with FGR.
Inadequate maternal weight gain or severe malnutrition, particularly in the third trimester when fetal growth is rapid, can limit the availability of substrates for the placenta to transfer. Even environmental factors, such as living at high altitudes, can induce chronic maternal hypoxia that translates into a reduced oxygen supply for the growing fetus. These maternal factors ultimately operate by hindering the placenta’s ability to function optimally.
Intrinsic Fetal and Genetic Causes
In some instances, FGR originates within the fetus itself, meaning the inherent capacity for growth is limited even if placental supply is adequate. This group is often associated with a symmetrical pattern of growth restriction, where all fetal measurements are proportionally small. Genetic and chromosomal abnormalities represent a substantial portion of these intrinsic issues.
Conditions like Trisomy 18 (Edwards syndrome) or Triploidy involve an incorrect number of chromosomes, directly impairing the cellular processes necessary for normal growth. These genetic anomalies intrinsically constrain the potential size a fetus can attain, regardless of the environment. Chromosomal aberrations are found in a percentage of FGR cases, particularly those presenting early in pregnancy.
Congenital infections acquired during pregnancy can directly damage fetal cells and impede growth. The TORCH group of infections (Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes) cross the placenta and cause inflammatory damage to fetal organs. This direct assault restricts the ability of cells to proliferate, leading to an overall reduction in fetal size.
Structural defects in the fetus, such as severe congenital heart disease, can limit growth by imposing a significant metabolic burden on the developing body. The energy required to compensate for the defect is diverted away from growth processes. Furthermore, in multifetal gestations, FGR may occur due to competition for shared or limited placental resources, even when the placenta is structurally healthy.