Fetal growth restriction (FGR) occurs when a baby in the womb doesn’t reach its expected growth potential due to problems with the mother’s health, the placenta, or the baby itself. It’s broadly defined as an estimated fetal weight or abdominal circumference below the 10th percentile for gestational age on ultrasound. FGR affects both the short-term safety of the pregnancy and the long-term health of the child, making early detection and monitoring essential.
FGR vs. Small for Gestational Age
These two terms are often used interchangeably, but they mean different things. Small for gestational age (SGA) simply describes any newborn whose birth weight falls below the 10th percentile for their gestational age. That group includes babies with FGR, but it also includes babies who are constitutionally small, meaning they’re just genetically smaller and perfectly healthy. About 40% of babies flagged as SGA have no underlying problem at all.
FGR, by contrast, means something is actively preventing the baby from growing the way it should. The distinction matters because a constitutionally small baby typically needs no extra intervention, while a baby with true growth restriction may need closer surveillance and earlier delivery.
What Causes Fetal Growth Restriction
The causes fall into three broad categories: problems originating with the mother, the placenta, or the baby. Placental insufficiency, where the placenta can’t deliver enough blood, oxygen, and nutrients, is the most common cause overall.
Maternal Factors
A range of maternal health conditions can interfere with blood flow to the placenta. These include chronic high blood pressure, pregestational or gestational diabetes, lupus, antiphospholipid syndrome, severe kidney or heart disease, severe anemia, and sickle cell disease. Substance use during pregnancy, including alcohol, cocaine, nicotine, heroin, and marijuana, is also strongly associated with restricted fetal growth. Other contributors include low pre-pregnancy weight, poor weight gain during pregnancy, certain medications (particularly cancer drugs), radiation exposure, high-altitude living, and uterine abnormalities. Notably, mothers who were themselves growth-restricted as babies carry roughly twice the risk of delivering a growth-restricted infant.
Placental and Umbilical Cord Factors
Structural problems with the placenta or umbilical cord can reduce the blood supply reaching the baby. Placental abruption (where the placenta partially separates from the uterine wall), placental infarction, abnormally shaped placentas, and placenta previa are all linked to FGR. Umbilical cord abnormalities, such as having only a single artery instead of two or the cord inserting at the edge of the placenta rather than the center, also impair nutrient delivery.
Fetal Factors
Genetic abnormalities account for about 5% of FGR cases. Chromosomal conditions like trisomy 13 or 18 lead to growth restriction in roughly half of affected pregnancies. When FGR appears symmetrical (the entire body is proportionally small) before 20 weeks, a chromosomal abnormality is more likely. Fetal infections are responsible for another 5% to 10% of cases. Globally, malaria is the leading infectious cause. In other settings, cytomegalovirus, toxoplasmosis, syphilis, chickenpox, and herpes simplex are more common culprits.
Early-Onset vs. Late-Onset FGR
Clinicians divide FGR into two types based on when it’s detected, and the distinction affects both diagnosis and monitoring.
Early-onset FGR is diagnosed before 32 weeks of gestation. It tends to involve more severe placental dysfunction and is associated with more widespread changes in fetal brain development, particularly in the brain’s white matter. To meet the diagnostic threshold before 32 weeks, at least one of the following must be present: the baby’s abdominal circumference or estimated weight falls below the 3rd percentile, blood flow in the umbilical artery is absent or reversed at the end of each heartbeat, or the baby measures below the 10th percentile with abnormal blood flow patterns in the uterine or umbilical arteries.
Late-onset FGR is diagnosed at or after 32 weeks. It’s more common and often subtler. Diagnosis requires either measurements below the 3rd percentile on their own, or a combination of at least two findings: measurements below the 10th percentile, a significant drop in growth trajectory (crossing two quartiles on a growth chart), or abnormal blood flow in the umbilical artery or the ratio of blood flow between the baby’s brain and placenta.
How FGR Is Detected and Monitored
Ultrasound is the primary tool for identifying and tracking FGR. Technicians measure the baby’s head circumference, abdominal circumference, and thigh bone length, then plug those numbers into a formula to estimate fetal weight. That estimate is plotted on a growth chart derived from uncomplicated pregnancies to see where the baby falls.
Once FGR is suspected, Doppler ultrasound becomes central to monitoring. This technique measures blood flow through the umbilical artery, which reflects how well the placenta is functioning. Rising resistance in the umbilical artery suggests the placenta is struggling. In severe cases, blood flow can stop or even reverse direction at the end of each heartbeat, which signals serious compromise. One important nuance: blood flow measurements can differ between the baby’s two umbilical arteries by an average of about 12%, and in roughly 1 in 6 cases, one artery reads as normal while the other reads as abnormal. This variability means repeated measurements and careful interpretation matter.
Monitoring frequency depends on severity. Babies with mildly reduced growth might be assessed every two to four weeks, while those with abnormal blood flow patterns need much more frequent checks, sometimes multiple times per week.
Risks to the Baby After Birth
Growth-restricted babies face a distinct set of challenges in the newborn period, especially if they’re also born preterm. A 2025 study in the Journal of Perinatology compared preterm SGA infants to preterm babies of normal size and found significantly higher rates of three key problems.
Hypothermia is the most immediate concern. Nearly 45% of preterm SGA infants had low body temperature on admission to the nursery, compared to about 15% to 17% of normally grown preterm infants. This happens because growth-restricted babies have less body fat and a higher surface-area-to-weight ratio, making it harder to retain heat. Low body temperature after birth is directly linked to higher rates of complications and mortality.
Low blood sugar is also more common. SGA infants had significantly lower blood sugar levels both at birth and throughout the first week of life compared to weight-matched controls. This matters because the newborn brain depends heavily on a steady glucose supply, and repeated low blood sugar episodes can cause lasting harm.
The third elevated risk is necrotizing enterocolitis, a serious intestinal condition where portions of the bowel become inflamed and can die. Reduced blood flow to the gut during fetal life appears to prime the intestines for this complication after birth.
Long-Term Health Consequences
The effects of fetal growth restriction don’t end at birth. Being growth-restricted in the womb reprograms how certain organs develop and function, with consequences that can emerge decades later.
Cardiovascular disease is the most well-documented long-term risk. Adults born after FGR have higher rates of hypertension, coronary artery disease, heart failure, and arterial stiffness. These changes are detectable even in young adults, who show elevated systolic blood pressure and stiffer blood vessels compared to peers who grew normally in utero.
Metabolic problems are closely linked. Growth restriction triggers changes in the liver and in how the body responds to insulin, setting the stage for metabolic syndrome: a cluster that includes abnormal cholesterol levels, fatty liver, high blood pressure, and type 2 diabetes. The body essentially adapts to a low-nutrient environment before birth, then struggles to handle normal or excess nutrition after birth.
Kidney function is also affected. Growth-restricted babies are born with fewer filtering units in their kidneys, which reduces their renal reserve over time. Impaired lung development and reduced lung function in adulthood have been documented as well. Together, these findings suggest that FGR doesn’t just affect size at birth. It shapes the trajectory of health across an entire lifetime.
Prevention With Low-Dose Aspirin
For most pregnancies, there’s no proven way to prevent FGR directly. However, because preeclampsia (a dangerous blood pressure condition in pregnancy) is one of the leading causes of placental insufficiency, preventing preeclampsia can indirectly reduce the risk of growth restriction in some cases.
Low-dose aspirin (81 mg daily) is recommended for pregnant women at high risk of preeclampsia. High-risk factors include a history of preeclampsia, carrying multiples, kidney disease, autoimmune conditions, type 1 or type 2 diabetes, and chronic high blood pressure. Women with more than one moderate risk factor, such as being over 35, having a BMI above 30, or being pregnant for the first time with a family history of preeclampsia, are also candidates. Aspirin should ideally be started before 16 weeks of pregnancy and continued until delivery. For women without these preeclampsia risk factors, current evidence does not support using aspirin to prevent FGR on its own.