What Is Intrauterine Growth Retardation?

Intrauterine growth retardation means that the weight of the fetus is less than two standard deviations of the average weight of the same age, or less than the tenth percentile of its expected weight, which is one of the important complications during pregnancy.

Chinese name: Intrauterine growth retardation

Foreign name: intrauterine growth retardation

Causes of intrauterine growth retardation and common diseases

1. Intrauterine growth retardation 1. maternal factors

1.1 General Constitution

Conditions include height, weight, and age during pregnancy, which have varying degrees of impact on the weight of the fetus at birth. Newborn babies born before 20 and after 35 years of age are lighter. Uterine abnormalities such as bicornuate uterus and mediastinal uterus directly affect fetal growth, and the incidence of IUGR accounts for about 1% -3%.

1.2 Nutritional status

Pregnant women are the basic source of fetal nutrients. Maternal malnutrition, especially insufficient protein and energy supply, will affect fetal growth and development. In addition, the combination of essential trace elements with amino acids and proteins can form enzymes and hormones with high biochemical effects and special physiological functions. Deficiency of trace elements and vitamins can affect fetal growth and development. For example, zinc deficiency in pregnant women can affect the synthesis of nucleic acids and proteins, reduce the total area of placental villi, affect fetal development, and cause IUGR and fetal malformations. Aubard et al. Reported that due to the deficiency of enzymes or insufficient supply of vitamin B6, B12 or folic acid, hypercysteineemia can be caused, which affects fetal placental development, which can cause abortion, pregnancy-induced hypertension, IUGR, teratology, and placental abruption. complication.

1.3 Bad living habits such as smoking, alcohol and drug use.

Harmful substances in tobacco, such as tar, nicotine acid, carbon monoxide, and cyanuric acid can reduce placental blood vessel formation, damage the endothelium, increase the collagen content of the villous matrix, and widen the cytotrophoblast and basement membrane under the cell trophoblast . At the same time, nicotine and carbon monoxide can stimulate nerve endings to release catecholamines, promote uterine muscle and blood vessel contraction and cause uterine ischemia. In addition, the combination of carbon monoxide and hemoglobin impedes the delivery of oxygen and causes tissue hypoxia. Therefore, whether the mother actively or passively smokes, it has a great impact on the growth and development of the fetus. Clinical investigations show that the weight of newborns who smoke pregnant women is reduced by an average of 96 g compared to the control group. The incidence of IUGR in passive smokers was 18.09%, which was three times higher than that in the control group. Alcohol and its metabolites can affect pancreatic function, hinder the absorption of fats and fat-soluble vitamins A, D, E, and K, thereby inducing uniformly-typed IUGR. 50% of drug abuse pregnant women are born with low birth weight, of which 40% are IUGR and the rest are due to premature birth.

1.4 Pregnancy complications and complications

Such as heart and lung disease, pregnancy-induced hypertension, chronic hypertension, chronic nephritis, severe anemia, diabetes, and chronic wasting diseases. Some of these diseases can cause circulatory disorders and hypoxemia, and some can cause vascular degeneration, vasoconstriction, decreased plasma volume, or placental circulation disorders, which can cause inadequate supply of fetal nutrients or ischemia and hypoxia to cause IUGR.

2. Intrauterine growth retardation 2. fetal factors

2.1 abnormal fetal growth regulators

The most important factor in promoting fetal growth and development is the acquisition and utilization of nutrients. This process can only be achieved through the regulation of various hormones such as insulin and cytokines. Clinical test results show that IUGR fetal cord blood has a significant decrease in growth hormone and insulin. Animal experiments suggest that when islet secretion is reduced, fetal rabbit body weight and bone length are reduced by 7% -13%. Hypoinsulinemia can affect the use of glucose by the fetus and inhibit the growth and development of the fetus. If low insulin and growth hormone coexist, the basal metabolic rate can be reduced, which significantly affects fetal growth and leads to IUGR. In addition, insulin can also promote the placental villi to take up amino acids to synthesize proteins, and promote the synthesis of insulin-like growth factor (IGF) in the placenta. IGF is also regulated by growth hormone to a certain extent. Decreased maternal placental growth hormone levels in IUGR patients can lead to lower IGF- levels. IGF- has assimilation and cell proliferation effects, can promote nutrients to the fetus through the placenta, and promote growth of the placenta and fetus. IGF- is an important factor that affects the development of placenta. Decreased IGF- can cause the placenta to transfer the nutrients and cause IUGR. Leptin is a coding product of obesity gene ob, which has the functions of regulating fetal growth and development, fetal placental angiogenesis, blood cell production, and fetal placental unit hormone synthesis. Clinical studies have found that there is a positive correlation between placental-derived leptin levels and neonatal weight. For example, insufficient placental leptin synthesis may cause IUGR. The experimental IUGR pregnant sheep proved that the decline of fetal prolactin and its receptor levels was positively related to the reduction of placental, fetal liver and fetal kidney weight, indicating that the reduction of prolactin synthesis and secretion restricted the growth and development of important fetal organs.

2.2 chromosomal abnormalities

The whole process of fetal growth and development is controlled by genes, and 40% of the difference in fetal birth weight comes from genetic factors, especially the maternal genetic and environmental factors. About 17% of IUGR fetuses have chromosomal abnormalities. Such as Turner syndrome, abnormal sex chromosomes, chromosomal imbalance, etc., especially those with trisomy 13, 18, 21, IUGR often appears earlier. It is thought that the SHOX gene at the short arm terminal of X chromosome may be related to intrauterine growth in children. Peripheral blood and cord blood sister chromatid exchange frequency measurement found that IUGR patients were significantly higher than normal pregnant women and newborns, indicating that the adverse external environment during pregnancy may also be the cause of IUGR. It can damage the DNA of early embryos or fetuses, reduce or limit the fetus' growth ability and cause IUGR.

2.3 Fetal infections

Such as rubella, giant cells, herpes simplex, toxoplasma, mycoplasma, chlamydia, parvovirus, malaria, syphilis and so on. These pathogens can cause placental chorionitis and chorionic inflammatory disease through blood flow, resulting in impaired villous development and impaired interstitial blood vessel formation, resulting in a decrease in the area of exchange between the mother and the fetus, as well as a decrease in placental villous function.

2.4 Others such as twins, parity, etc. also have a certain impact on fetal weight.

The incidence of IUGR in twins increased significantly, mainly due to an increase in preterm and low birth weight infants. Among them, the incidence of IUGR in twins conceived by assisted pregnancy technology was significantly higher than that of natural pregnancy.

3. Fetal intrauterine growth retardation 3. Placental factors

Among the many causes of IUGR, reduced uterine placental blood flow has an important role. The measurement of placental scintillation technique showed that the uterine placental blood flow of IUGR pregnant women decreased by more than 50% compared with normal pregnant women. Most IUGR fetal umbilical vein blood pH and PO _{2 were} lower than those in the normal control group. Pathological examination found that 68.42% IUGR placenta had obvious pathological changes, mainly villitis and villous development retardation.

3.1 Reduced placental microvilli exchange area

The stereoscopic observation of placenta showed that the placental weight, volume, villus surface area, and villus capillary surface area of IUGR group were significantly reduced, and the microvilli surface area density and interluminal surface area density were also smaller than those of the control group. Microvilli covering the surface of syncytiotrophoblasts are sites of transporter and receptor activity, and play an important role in fetal nutrition and maternal-fetal immunity. Microvilli can not only increase the contact area between trophoblasts and the mother body, but also its ultrastructure can promote the microcytosic effect of the villous space. Therefore, the reduced surface exchange area of the IUGR placental trophoblast reduces the intake and transport of nutrients and is the morphological basis for IUGR placental dysfunction.

3.2 Vascular abnormalities of uterine placenta bed

Pathological studies of blood vessels in the placenta bed show that under normal circumstances, trophoblasts invade the spiral arteriolar wall of the decidual segment 12 weeks ago, destroying their smooth muscle fibers and elastic fibers, progressively expanding their ends, and endogenous angiotensin Does not respond to increase blood flow to the placenta. At 1620 weeks of pregnancy, a second countercurrent migration should also be performed to destroy the muscle fibers and elastic fibers of the superficial spiral blood vessels, while the IUGR placental bed vessels have not been completed or pathological changes such as acute atherosclerosis have thickened the vessel wall Endometrial hyperplasia and narrowing of the lumen severely affect the blood flow of the uterine placenta, and its mechanism may be related to IUGR immune disorders. Other studies have shown that the abnormal angiogenesis of IUGR placenta is related to the imbalanced expression of vascular endothelial growth factor and placental growth factor, which causes damage to placental trophoblasts and villus vascular endothelium, and affects the reduction of trophoblast-derived NO.

3.3 Other placental factors

For example, the function of the placental villus to transport amino acids is reduced, which causes the fetal essential amino acids and branched chain amino acids, including valine, leucine, isoleucine, and lysine, to be significantly reduced, affecting fetal protein synthesis. In addition, abnormal placenta, such as multiple placental infarcts, multi-leaf placenta, contoured placenta, partial placental abruption, placental hemangioma, etc., also affect the uterine placental blood circulation to varying degrees, reduce fetal blood supply, and cause IUGR.

Differential diagnosis of intrauterine growth retardation

1. Whether it is partial to spicy or cold, whether there are feelings of depression or extreme anger.

2. Dynamic measurement of uterine floor height is an important method to understand fetal intrauterine development and can accurately detect fetal development.

3 Pay attention to the increase in weight of pregnant women. Under normal circumstances, the weight in the end of pregnancy increases by 0.5kg per week. If the weight does not increase or decreases, pay attention to the possibility of intrauterine growth retardation.

Fetal intrauterine growth retardation

1. B-ultrasound: If the diameter of the fetal head increases by 2 mm or less every 2 weeks before 36 weeks, it is considered to be intrauterine growth retardation.

2. Inspection of fetal maturity: if more than 36 weeks, amniotic fluid can be drawn through the abdominal wall to determine L / S value, creatinine value, bilirubin content, orange cell count, etc.

3 Examination to diagnose placental dysfunction: Urine estriol measurement, oxytocin irritation test, and amniocentesis can be used to help diagnose placental dysfunction.

Fetal intrauterine growth retardation treatment principles

General treatment : Give a high-protein, high-vitamin diet, lying on the left side, inhaling oxygen twice a day for 30 minutes each time. A course of 4 weeks.

Etiology treatment : Active treatment of primary disease and pregnancy complications.

Increase fetal nutrition : Give intravenous drip of compound amino acid, high sugar, energy mixture to increase fetal nutrition and calories; intravenous drip of compound salvia miltiorrhiza, low-molecular dextran to improve microcirculation and blood viscosity, and increase uterine placental perfusion flow.