IUGR is defined by clinical features of malnutrition and evidence of reduced growth regardless of an infant's birth weight percentile.

[11] In asymmetrical IUGR, there is decreased oxygen or nutrient supply to the fetus during the third trimester of pregnancy due to placental insufficiency.

Specific causes include:[citation needed] Symmetrical IUGR is commonly known as global growth restriction, and indicates that the fetus has developed slowly throughout the duration of the pregnancy and was thus affected from a very early stage.

[17] If the cause of IUGR is intrinsic to the fetus, growth is restricted due to genetic factors or as a sequela of infection.

There is also increased vasoconstriction of the arteries in the periphery, which occurs in response to chronic hypoxia in order to preserve adequate blood flow to the fetus' vital organs.

Therefore, the fetal heart must work harder to contract during each heartbeat, which leads to an increase in wall stress and cardiac hypertrophy.

Preterm infants with IUGR are more likely to have bronchopulmonary dysplasia (BPD), a chronic lung disease that is thought to be associated with prolonged use of mechanical ventilation.

[20] Magnetic resonance imaging (MRI) can detect changes in volume and structural development of infants with IUGR compared with those whose growth is appropriate for gestational age (AGA).

[citation needed] Mothers whose fetus is diagnosed with intrauterine growth restriction can be managed with several monitoring and delivery methods.

Doppler velocimetry is useful in monitoring blood flow through the uterine and umbilical arteries, and may indicate signs of uteroplacental insufficiency.

[25] This method may also detect blood vessels, specifically the ductus venosus and middle cerebral arteries, which are not developing properly or may not adapt well after birth.

[26] Fetuses with an anticipated delivery before 34 weeks gestation are recommended to receive corticosteroids to facilitate fetal maturation.

[29] After correcting for several factors such as low gestational parental weight, it is estimated that only around 3% of pregnancies are affected by true IUGR.

[31] Feeding intolerance, hypothermia, hypoglycemia, and hyperglycemia are all common in infants in the postnatal period, indicating the need to closely manage these patients' temperature and nutrition.

[32] Furthermore, rapid metabolic and physiologic changes in the first few days after birth can yield susceptibility to hypocalcemia, polycythemia, immunologic compromise, and renal dysfunction.

[33][34] According to the theory of thrifty phenotype, intrauterine growth restriction triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage.

If the offspring actually develops in an environment where food is readily accessible, it may be more prone to metabolic disorders, such as obesity and type II diabetes.

Infants who fail to display adequate catch-up growth in the first few years of life may exhibit worse outcomes.

[37][38] Catch-up growth can alter fat distribution in children diagnosed with IUGR as infants and increase risk of metabolic syndrome.

[39] Infants with IUGR may be susceptible to long-term dysfunction of several endocrine processes, including growth hormone signaling, the hypothalamic-pituitary-adrenal axis, and puberty.

Normally, ovine placental mass increases until about day 70 of gestation,[45] but high demand on the placenta for fetal growth occurs later.