Version May 2024
| Causes of and risk factors for FGR | Comments |
| Fetal genetic abnormalities | Account for 5 to 20% of FGR. Genetic abnormalities include: aneuploidy (including triploidy), uniparental disomy, single gene mutations, partial deletions or duplications. At least 50% of fetuses with trisomy 13 or 18 are FGR. The finding of symmetric FGR (ie, abdomen and head both small) prior to 20 weeks of gestation suggests aneuploidy as the cause, most commonly trisomy 18. Syndromes with asymmetric FGR (abdomen small, head not small) include Russell-Silver, Temple, Smith-Lemli-Opitz, and Prader-Willi. |
| Fetal infection | Accounts for 5 to 10% of FGR. Cytomegalovirus and toxoplasmosis are the most common infectious etiologies of FGR in high income countries. Malaria is a common infectious cause of FGR where the infection is endemic. |
| Fetal structural anomaly | Fetuses with congenital anomalies can have impaired growth, which is often related to coexistent cytogenetic disorders. |
| Multiple gestation | Fetal growth in multiple gestations is directly related to the number of fetuses. The lower weight of fetuses from multiple gestations is thought to be due to an inability of the uteroplacental environment to meet the nutritional needs of multiple fetuses and to pregnancy complications (eg, preeclampsia, twin-twin transfusion syndrome, selective FGR). Placental and umbilical cord anomalies potentially associated with underperfusion are also more common in multiple gestations (eg, velamentous cord insertion). |
| Chromosomal mosaicism in the placenta (CPM), not involving the fetus | CPM usually involves a trisomy and is strongly associated with FGR. CPM has been identified after birth in approximately 10% of otherwise idiopathic FGR and in one-third of FGR associated with placental infarction and decidual vasculopathy. The severity of FGR associated with CPM depends upon the chromosomes involved, the proportion of mosaic cells, and the presence of uniparental disomy. |
| Ischemic placental disease | Ischemic placental disease can manifest clinically as FGR, preeclampsia, placental abruption, stillbirth, or a combination of these disorders, and is often recurrent. Massive perivillous fibrin deposition/maternal floor infarction is an idiopathic rare placental lesion that appears to be associated with a high risk of FGR, as well as miscarriage, preterm birth, and stillbirth. It also has a high recurrence rate. |
| Gross cord and placental abnormalities | Examples include single umbilical artery, velamentous umbilical cord insertion, marginal cord insertion, bilobe placenta, circumvallate placenta, and placental hemangioma. If an association between these entities and FGR exists, it is at most weak. Placental mesenchymal dysplasia is a rare placental abnormality characterized by placentomegaly and grape-like vesicles resembling a partial mole. The euploid fetus with these findings is at increased risk for FGR, perinatal death, and Beckwith-Wiedemann syndrome. |
| Maternal genetic factors | Mothers who were growth-restricted at birth have a twofold increase in risk for FGR in their offspring. Mothers who give birth to an FGR newborn are at high risk of recurrence, and the risk increases with increasing numbers of FGR births. |
| Maternal medical and obstetric conditions | Maternal conditions that can be associated with diminished utero-placental-fetal blood flow and/or oxygen delivery have been associated with FGR. These conditions include, but are not limited to:
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| Teratogens and other environmental factors | Examples include medications such as warfarin, antiseizure medications (eg, valproic acid), antineoplastic agents, and folic acid antagonists. Exposure to alcohol, tobacco, marijuana, and air pollution can also impair fetal growth. Exposure to therapeutic, but not diagnostic, doses of radiation can cause permanent restriction of growth. |
| Assisted reproductive technologies | Singleton pregnancies conceived via assisted reproductive technologies have a higher prevalence of small for gestational age infants compared with naturally conceived pregnancies. |
| Low prepregnancy weight, poor gestational weight gain, malabsorption, poor nutritional status | Maternal weight at birth, prepregnancy weight, and gestational weight gain can affect the risk of FGR as these factors are responsible for approximately 10% of the variance in fetal weight. Macro- and micronutrients in the maternal diet also appear to play a role. |
| Residing at high altitude | A direct relationship between increasing altitude and lower birth weight has been demonstrated in studies performed in Denver and Leadville, Colorado (altitude 1600 and 3100 m, respectively), Tibet (altitude ranging from to 1800 almost 9000 m), and Peru (altitude ranging from sea level to up to 4575 m). |
| Short interpregnancy interval | |
| Extremes of maternal age | |
| Abnormal maternal biochemical markers for Down syndrome screening | Examples include: Low pregnancy-associated plasma protein A (PAPP-A), low beta-human chorionic gonadotropin (hCG), high alpha-fetoprotein (AFP) |
| Discrepancy between crown-rump length measurements and accurate menstrual history by 2 to 6 days |
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