Fetal growth retardation: causes and consequences

In every tenth case of pregnancy, a diagnosis is made - intrauterine growth retardation (the pathology is also known under the abbreviation IUGR). The doctor determines the deviations, which are characterized by a discrepancy between the size of the child and the normal indicators for a particular week of pregnancy. How dangerous this pathology is and what exactly is to be afraid of, it is useful for every future mother to know, because no one is immune from such a phenomenon.

Intrauterine growth retardation of the fetus is diagnosed at various stages of pregnancy. This happens if the baby does not receive enough nutrients and oxygen, which are actively involved in the formation of a small organism. The reasons for this can be very different:

  • placental pathology: incorrect presentation or detachment;
  • chronic diseases of the mother: high blood pressure, problems with the cardiovascular system, anemia, improper functioning of the respiratory tract;
  • deviations in the chromosome set: Down syndrome;
  • pathologies of intrauterine development: malformation of the abdominal wall or kidneys;
  • mother's bad habits;
  • infectious diseases suffered by a woman during pregnancy: toxoplasmosis, syphilis, cytomegalovirus;
  • inadequate or malnutrition;
  • constant stress;
  • gynecological diseases;
  • self-administration of medications during pregnancy without a doctor's prescription;
  • multiple pregnancy;
  • climatic conditions: living in an area that is located high above sea level.

Smoking and alcoholism during childbearing can lead to such a phenomenon as asymmetric fetal growth retardation, when, according to ultrasound, the child's skeleton and brain correspond to the term, but the internal organs remain undeveloped. It is especially important to supply the fetus with everything necessary in the last weeks of pregnancy so that it successfully adapts to the new environment.

Symptoms of IUGR

The first signs of the IUGR syndrome are detected already in the early stages of pregnancy (at 24–26 weeks), but the woman is not able to determine them on her own. This can only be done by a doctor. Symptoms are considered non-compliance with the norm of the following indicators:

  • abdominal circumference at a certain level, the height of the fundus of the uterus (palpable by hand by a gynecologist);
  • the size of the head, femur, belly of the baby;
  • growth with constant monitoring;
  • the amount of amniotic fluid;
  • violations of the functioning of the placenta (the size or structure may change);
  • blood flow velocity in the placenta and umbilical cord;
  • baby's heart rate.

Even doctors are often mistaken in the diagnosis, because sometimes the discrepancy between these parameters is nothing more than a genetic or hereditary predisposition. To avoid misdiagnosis, a survey of parents is conducted, with what weight they were born. Whereas a delay in fetal development for 2 weeks or more already gives serious reasons to believe that the diagnosis is accurate.

Treatment Methods

Treatment largely depends on the degree of observed abnormalities:

  • intrauterine growth retardation of the 1st degree - a lag of 2 weeks (therapy can be quite successful and negate the negative consequences for the further development of the baby);
  • 2 degrees - a delay of 3-4 weeks (strong treatment will be required, and the results can be completely unpredictable);
  • 3 degrees - a lag of more than a month (even the most intensive therapy will not be able to equalize such a large lag, and the child may be born with serious deviations from the norm).

Treatment includes:

  • therapy for maternal diseases;
  • treatment of pregnancy complications;
  • increasing the resistance of a small organism to;
  • normalization of placental insufficiency (as a rule, drugs are prescribed to dilate blood vessels to improve the blood supply to the fetus and uterus, as well as means to relax the muscles of the uterus).

The treatment is carried out on a stationary basis so that the mother and child are constantly under medical supervision. The timing and methods of delivery depend on the well-being of the mother and the condition of the fetus.

The consequences that the syndrome of fetal growth retardation entails can be very different. Children with this diagnosis after birth can have serious health problems.

In infancy:

  • obstetric complications during childbirth: hypoxia, neurological disorders;
  • poor adaptation to new living conditions;
  • hyperexcitability;
  • increased or decreased muscle tone;
  • poor appetite;
  • small weight gain;
  • psychomotor retardation in development;
  • inability to maintain body temperature constant within the normal range;
  • insufficient degree of development of internal organs;
  • high susceptibility to infectious diseases.

At older age:

  • diabetes;
  • tendency to corpulence;
  • high blood pressure.

In adulthood:

  • cardiovascular diseases;
  • obesity;
  • non-insulin dependent diabetes mellitus;
  • elevated blood lipid levels.

However, many babies diagnosed with intrauterine growth retardation over time may not differ at all from their peers, catching up with them in terms of both height and weight, without any consequences for their health at any age.

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DHA (OMEGA 3) - VITAMINS FOR BRAIN DEVELOPMENT

There are many types of omega-3 fatty acids and vitamins based on them.

Which vitamins should be taken?

For the development of the brain and for health, the answer is very simple: special attention should be paid to the intake of DHA and vitamins for pregnant and lactating mothers, which are produced on their basis. And this is AlvoGenius. Just what you and your baby need.

Omega-3 - vitamins for beauty and health

What is the source of DHA and polyunsaturated fatty acids that provide energy for a fulfilling life? Of course, it's Omega-3. This substance is not synthesized in the human body, and therefore everyone who cares about their health should eat foods rich in Omega-3.

This component is especially important for expectant mothers and for nursing women, since during this difficult period they must provide useful substances not only for themselves, but also for their baby.

Vitamins for nursing mothers

All organs and systems of a newborn develop very quickly, for this they need a full-fledged "building material". And it is contained in sufficient quantities in the Omega-3 complex. It is too early for a baby to drink vitamins, but if the mother consumes nutrients in the right amount, then the child's body will receive everything it needs in full.

Omega-3 is essential for:

  • Development of brain cell membranes;
  • Strengthening the immune system;
  • Development of memory and attention.

Do you want to see your children healthy and happy? Do not forget to take vitamins during lactation!

1 Innis, S. (2005). Essential fatty acid transfer and fetal development. Placenta, S70-S75.
2 Jensen, C. V. (2010). Effects of early maternal docosahexaenoic acid intake on neuropsychological status and visual acuity. The Journal of Pediatrics, 157, 900-905.
3 Smuts, C. H. (2003, March). A randomized trial of docosahexahexathirdenoic acid supplementation during the trimester of pregnancy. Obstetrics & Gynecology, 101(3), 469-479.
4 Brenna, J. L. (2009). Background paper on fat and fatty acid requirements during pregnancy and lactation. Annals of Nutrition & Metabolism, 55, 97-122.
5 Simopoulos, A. (2002). The importance of the ratio of omega6-omega3 essential fatty acids. Biomedicine and pharmacotherapy, 56, 365-379.
6 Simopoulos, A. (2006). Evolutionary aspects of diet, the omega 6- omega3 ratio and genetic variation- nutritional implications for chronic diseases. Biomedicine & Pharmacotherapy, 60, 502-507.
7 Innis, S. (2007). Dietary (n-3) fatty acids and brain development. The Journal of Nutrition, 855-859.
8 Hughes, T. B. (2005). New paradigms for supporting the resilience of marine ecosystems. Trends in ecology and evolution, 380-386.
9 Ramón, R. B. (2009). Fish consumption during pregnancy, prenatal mercury exposure, and anthropometric measures at birth in a prospective mother-infant cohort study in Spain. The American Journal of Clinical Nutrition, 90, 1047-1055.
10 Arterburn, L. H. (2006). Distribution, interconversion, and dose-response of n-3 fatty acids in humans. Am J Clin Nutr, 1467S-1476S

11 Jacobson, J.J.-E. (2008). Beneficial effects of a polyunsaturated fatty acid on infant development: Evidence from the Inuit of Arctic Quebec. J Pediatr, 152, 356-64.
12 Forsyth, J. W. (2003). Long chain polyunsaturated fatty acid supplementation in infant formula and blood pressure in later childhood: follow up of a randomized controlled trial. BMJ, 326, 953-955.
13 Bossart, G. (2006). Marine mammals as sentinel species for oceans and human health. Oceanography, 19(2), 134-137.
14 Charuku, S. M.-D.-K. (2003). Higher maternal plasma docosahexaenoic acid during pregnancy is associated with more mature neonatal sleep-state patterning. Am J Clin Nutr, 608-613.
15 Hanson, L. K. (2002). The role of breastfeeding in prevention of neonatal infection. Semin Neonatol, 275-281.
16 Wagner, C. G. (2008). Prevention of rickets and vitamin D deficiency in infants, children and adolescents. Pediatrics, 1142-1152.
17 Prayer, D. K. (2005). MRI of normal fetal brain development. European Journal of radiology, 199-216.
18 Paolicelli, R. C. (2011). Synaptic pruning by microglia is necessary for normal brain development. Science, 1456-1458.
19 Hepper, P. S. (1994). Development of fetal hearing. Archives of disease in childhood., 71, F81-F87.
20 Hoffman, D. T. (2004). Maturation of visual acuity is accelerated in breast-fed term infants fed baby food containing DHA-enriched egg yolk. The Journal of Nutrition, 134(9), 2307-2313.

IUGR of the fetus and newborn is an important problem in perinatology. The introduction of new technologies into perinatology, such as ultrasound, dopplerometry, amnio- and choriocentesis, cordocentesis, genetic diagnostic methods, have advanced our knowledge of the causes and pathophysiological processes that create this risk for the fetus and newborn.

DEFINITION

IUGR is a syndrome that appears in the prenatal period and is characterized by slowing, stopping or negative dynamics of fetal size and manifests itself in a newborn by a decrease in body weight (as an integral indicator of fetal size) by two or more standard deviations (or below the 10th centile) compared to due to gestational age (i.e., the gestational age at which the child was born). In 80% of children with IUGR, weight loss is combined with a similar deviation in body length (height) and chest circumference, in 64% - head circumference.

EPIDEMIOLOGY

The rate of birth of children with IUGR varies widely and depends largely on the criteria underlying the diagnosis, on the genetic load of the population, on socioeconomic conditions, as well as on geographic factors such as altitude.

According to data obtained on the population of newborns in Moscow, the frequency of children with IUGR is 67.4 per 1000 children born alive at term, and 179.5 per 1000 children born prematurely. According to the literature, in European economically developed countries (Sweden, England), newborns with IUGR make up 2-3% of the general population of newborns. A clear correlation was noted between the frequency of newborns with low birth weight (less than 2500 g) and the presence of IUGR. So, according to J. Villar et al. (1982), in economically developed countries, where low birth weight newborns account for 3-10%, IUGR is observed in 30-40% of such children, while in developing countries with a higher frequency of low birth weight children (10- 40%), the percentage of newborns with IUGR among them is 40-70.

The frequency of IUGR increases with decreasing gestational age. So, with a period of 41 weeks and above, the frequency is 5.7%, with 37-40 weeks - 5.5%, with 34-36 weeks - 7.4%. At 31-33 weeks - 9.4%, at 28-30 weeks - 13.1%.

RISK FACTORS

IUGR is one of the universal reactions of the fetus in response to unfavorable conditions in the period of intrauterine development associated with risk factors in the mother, pathology of the placenta, or pathology of the fetus itself.

maternal factors

Constitutional features associated with short stature.

Age over 40 years.

Unfavorable social conditions (protein-calorie starvation, lack of perinatal care, single-parent family, constant work during pregnancy, etc.).

Aggravated obstetric and gynecological history (previous infertility, stillbirth, non-developing pregnancy, fetal IUGR).

This includes unfavorable factors during this pregnancy that disrupt uteroplacental circulation and oxygenation. Among these factors, preeclampsia, chronic placental insufficiency, and preeclampsia play an important role. A significant role among maternal factors is assigned to diseases during pregnancy, in which hypertension and vascular disorders develop (hypertension, kidney pathology, diabetes classes D, E, F, R); intake or absorption of nutrients is disturbed (chronic eterocolitis, pancreatitis); there is a significant loss of protein (glomerulonephritis, lupus nephritis), severe hypoxemia and anemia develop (cyanotic heart defects, sickle cell anemia). In recent years, attention has been paid to the importance of antiphospholipid syndrome in a pregnant woman in the formation of fetal IUGR. The effect of smoking during pregnancy on impaired uteroplacental blood flow and fetal growth retardation has been convincingly proven. Although the relative risk of having children with IUGR in pregnant women who smoke is low (2.27), the attributable risk is more than 10 times higher and equals 27, which indicates the possibility of reducing the incidence of IUGR in the fetus by 27% if this factor is eliminated. Multiple pregnancies can lead to growth retardation of one of the fetuses in twins or all fetuses in triplets.

Let's add the impact of teratogenic factors during pregnancy, such as alcohol, some drugs, chemicals. Alcohol use during pregnancy is associated with a high risk of developing fetal alcohol syndrome, which is characterized by significant growth retardation, special facial features (flat face, narrow palpebral fissures, deep nose bridge, low-lying ears), congenital heart defects (CHDs) and malformations of other organs, mental backwardness. IUGR in combination with dysmorphic facial features, congenital malformations are observed in cocaine, hydantoin, valproeus syndromes.

Placental factors

Secondary violations of the structure and function of the placenta under the influence of maternal diseases or associated with multiple pregnancy.

Malformations of the placenta and umbilical cord: placental hypoplasia, single umbilical artery, sheath attachment of the umbilical cord, angiomas.

Tumors of the placenta.

Fetal factors

Genetically "small" child.

Chromosomal diseases of the fetus. Trisomy 13,18 is almost always accompanied by a significant delay in the growth and development of the fetus. The significant role of genetic factors in fetal growth retardation is indicated by the high frequency of low birth weight (more than 50%) in the family pedigree. Parental isodysomies (the presence in the child's genome of two allelic chromosomes of one of the parents, more often chromosomes 7,8,16) can manifest as intrauterine malnutrition and growth retardation. There is more and more evidence indicating that Silver-Roussel syndrome (IUGR, "triangular" face, clinodactyly) is due to maternal isodisomy of the 7th or 8th chromosome, the absence of paternal isochromosomes. Duplication of the long arm of chromosome 3 was found in some patients with Cornelia de Lange syndrome (IUGR, microcephaly, hypertrichosis, micromelia). Dubovitz's syndrome (IUGR, narrow palpebral fissures, ptosis, sparse hair) is also genetically determined. Autosomal recessive Szekel syndrome is also characterized by significant IUGR, microcephaly, coracoid nose, and skeletal abnormalities. It has been established that this syndrome is associated with instability or fragility of autosomes.

Congenital malformations, especially of the central nervous system and skeleton.

Congenital infections, especially rubella and cytomegaly, in which children (60% and 40%, respectively) have IUGR.

Multiple pregnancy.

PATHOGENESIS

IUGR - the reaction of the fetus in response to various adverse factors. The pathophysiological mechanisms underlying the formation of this syndrome are different and have not yet been fully elucidated, as well as the factors that control the process of intrauterine growth and fetal development.

Among the mechanisms underlying IUGR of the fetus, a large role is played by chronic fetoplacental insufficiency, which is manifested by a violation of the uteroplacental and fetal blood flow, as a result of which the diffusion of substances such as oxygen, urea, and carbon dioxide is disrupted.

Violation of the fetoplacental blood flow leads to insufficient supply of oxygen, energy and plastic substances to the fetus, as well as to a violation of hormonal homeostasis.

There is convincing experimental and clinical confirmation of the connection between oxygen starvation and insufficiency of the intake of plastic substances (starvation) with a delay in the growth and development of the fetus.

Scientific studies and clinical observations have shown that there is also a direct relationship between the degree of decrease in placental blood flow, placental weight and fetal IUGR. The growth of the placenta, according to ultrasound, slows down earlier than the growth of the fetus. The development of IUGR in smoking mothers is associated with impaired uteroplacental blood flow and a decrease in the level of oxyhemoglobin in the blood as a result of increased formation of carboxyhemoglobin.

At the same time, information about the significance of hormonal status disorders and hormonal regulation of fetal growth in the implementation of IUGR is extremely insufficient.

A direct relationship has been established between a decrease in the level of estriol in the blood and urine of a pregnant woman and a slowdown in fetal growth. In recent studies, attention has been paid to the role of insulin-like growth factor-1 (somatomedin) in the mechanisms of fetal growth, which is justified by the presence of a clear correlation between its level in a pregnant woman and fetal growth, as well as a decrease in its content in the blood plasma of newborns with IUGR. It is suggested that IUGR may be associated with the loss of the receptor gene for this growth factor.

There is evidence of an association of IUGR with impaired glucose metabolism in the prenatal period. A significant decrease in the content of C-peptide (a marker of the amount of endogenous insulin) secreted by the fetus was found in the amniotic fluid and blood of a fetus with IUGR. It is believed that a flat glucose tolerance test in pregnant women with normal blood pressure may indicate low placental transfusion of glucose and amino acids, low insulin production and, as a result, fetal IUGR.

In the pathogenesis of intrauterine growth and developmental delay, attention is also paid to the significance of the cytopathic action of viruses in congenital infections. A striking example is rubella embryopathy, one of the manifestations of which is always fetal IUGR. Alcoholic embryopathies in children born to women suffering from chronic alcoholism are considered by many authors as the result of the embryotoxic effect of alcohol and its decay products (acetaldehyde, etc.). IUGR of the fetus is also associated with intoxication and impaired liver function caused by the influence of certain drugs (valproic acid, drugs) and chemicals.

CLINICAL CHARACTERISTICS OF IUGR IN NEWBORN

Newborns with IUGR represent a heterogeneous group. In most newborns, IUGR can be an independent pathology (according to ICD-10, code P05.1), and in about one third it can be one of the syndromes of congenital infection, chromosomal pathology, multiple malformations and other diseases. In this regard, among newborns with IUGR, there are:

Children who developed under conditions of chronic hypoxia and fetoplacental insufficiency;

Children with congenital infections;

Children with fetopathy of various etiologies;

Children with chromosomal and hereditary diseases.

With IUGR in newborns, in addition to reduced parameters of physical development, physique disproportions are noted, relatively large head parameters compared to other parts of the body. Often, a pathological setting of the feet (“heel”), shoulders and limbs is found (shoulders raised and pressed to the head with pronator installation of the upper limbs, flexion contractures in the elbow and phalangeal joints). These changes are largely due to reduced motor activity of the fetus in adverse conditions.

In 63.7% of newborns with IUGR, clinical manifestations of intrauterine malnutrition and trophic skin disorders (dryness, peeling), symptoms of immaturity of both external signs and functional systems are observed. These newborns are characterized by a high frequency of dysembryogenesis stigmas (in 32.4%, more than four stigmas are observed simultaneously), especially on the skin (preauricular outgrowths, deep presacral fold, hemangiomas, etc.). The incidence of congenital malformations is 11.2% and is almost twice as high as in low birth weight newborns without IUGR. The most demonstrative IUGR was in one of the newborn twins.

Newborns with IUGR have an increased risk of such island-related conditions as birth asphyxia, pulmonary hemorrhage, hypoglycemia, hypocalcemia, metabolic acidosis, polycythemia.

Taking into account the degree of decrease in the main parameters of physical development, three degrees of IUGR in newborns are distinguished:

I degree, mild, is characterized by a decrease in body weight by two or more standard deviations (or below the 10th centile), with normal or moderately reduced body length (height). In 80% of these children, the size of the head circumference does not go beyond the normal fluctuations for gestational age. All children have clinical manifestations of malnutrition.

With II degree IUGR, a decrease in both body weight and length by 2-3 standard deviations (10-3rd centile) is observed. In 75% of children, a similar decrease in head circumference was noted. These newborns have the appearance of proportionately small children. They do not have clinical manifestations of malnutrition, but stigmas of disembryogenesis are observed much more often.

Grade III IUGR is the most severe, characterized by a significant decrease in all parameters of physical development (by 3 or more standard deviations, or
Taking into account the clinical characteristics, three variants of IUGR are distinguished: hypotrophic (weight lagging behind body length), hypoplastic (proportional decrease in body weight and length) and dysplastic (body disproportions with a significant decrease in body weight).

DIAGNOSTICS

Diagnosis of IUGR of the fetus in the antenatal period is carried out on the basis of the following provisions:

Insufficient increase in body weight in a pregnant woman;

Stopping or insufficient increase in the size of the fetus, according to ultrasound during pregnancy;

Changes in the area and volume of the placenta and a decrease in uteroplacental and fetal blood flow;

The presence of signs of intrauterine fetal suffering: cardiac disturbance, tachy- or bradycardia, monotonous heart rhythm, lack of acceleration in response to general fetal movements, the occurrence of deceleration (periods of heart rate slowdown), often turning into persistent bradycardia, according to cardiotocography with a non-stress test;

Increased or increased fetal respiratory movements, according to ultrasound scanning, which are normally 30-70 / min for a period of 35-40 weeks;

Elevated levels of AFP and hCG in the blood of a woman in the P-III trimesters of pregnancy;

In a newborn, the diagnosis of IUGR is established on the basis of a comparison of the parameters of his physical development at birth with the proper parameters for the gestational age at which the child was born; scorecards are used. Diagnostic is the value of body weight as an integral indicator of the size of the newborn below 2 or more standard deviations (or at the level of the 10th centile and below). Deviations of other parameters of physical development and the presence of such clinical manifestations as malnutrition, body disproportions, dysembryogenesis stigmas make it possible to assess the degree of IUGR and the clinical variant of the pathology.

Early diagnosis of this condition both in the antenatal and postnatal periods is very important due to the fact that its presence leads to an increased risk of intrauterine and intranatal fetal death, impaired adaptation of the child in the neonatal period and various deviations in health in subsequent years of life.

Violations of postnatal adaptation in newborns with IUGR are primarily associated with a high incidence of asphyxia at birth and posthypoxic CNS damage; respiratory disorders in most cases are due to meconium aspiration syndrome (MAS); in the early neonatal period, they are characterized by such disturbances of homeostasis as hypoglycemia, hypocalcemia, polycythemia. In the early neonatal period, a tendency to low blood levels of norepinephrine and dopamine, cortisol, and IgG is noted. In the neonatal period, 40% of these children

Observe the development of infectious-inflammatory and purulent-septic diseases.

OUTCOMES AND FORECAST

IUGR of the fetus and newborn is an important factor in intrauterine fetal death and death in the neonatal period.

Mortality among full-term children with IUGR is 3-10 times higher than in newborns with normal physical development. About 40% of newborns with IUGR are susceptible to infectious and inflammatory diseases, and mortality in them is directly dependent on the degree of IUGR.

For stillborn premature infants with IUGR is 62.8%, and among those who died in the perinatal period - 41.9%.

IUGR of the fetus and newborn makes a significant contribution to the development of chronic forms of pathology and childhood disability. More than half of children with IUGR have a lag in physical development in early and adolescence, one third retains stable hypotrophy, and 20-40% of children develop neurotic reactions. Disability caused by severe CNS injuries - cerebral palsy (ICP), epilepsy, progressive hydrocephalus - occurs by the age of 6 years in 12.6% of children with IUGR.

PREVENTION AND TREATMENT

Prevention and treatment begin with the provision of adequate perinatal care for pregnant women: identification of risk factors for IUGR of the fetus and dynamic monitoring of the state of health of the pregnant woman; dynamic ultrasound with assessment of fetal growth; determination of the condition of the fetus using special tests; identifying the cause of fetal growth retardation and taking therapeutic measures; making a decision on the timing and methods of delivery, taking into account the condition of the fetus and the pregnant woman.

Given the possible perinatal problems in newborns with IUGR (asphyxia during childbirth, meconium aspiration, pulmonary hypertension, etc.), which require resuscitation, delivery should be carried out in well-equipped specialized institutions (Perinatal Center, obstetric departments of large clinical hospitals). The rate of deliveries by caesarean section in pregnancy complicated by fetal growth retardation is significantly higher than the average, exceeding 20% ​​in some institutions.

Due to the fact that newborns with IUGR represent a heterogeneous group, treatment is carried out depending on the diagnosed pathology.

In the early neonatal period, the definition and correction of adaptation disorders, hypoglycemia, hypocalcemia, and polycythemia characteristic of such children, is important. Newborns with IUGR are shown to start breastfeeding early (from the 1st hour of life), provided that the clinical condition is stable. In an unstable state, the introduction of a 5% glucose solution is recommended, followed by a change to milk. If EP is not possible due to the condition of the child, then PP is prescribed. For newborns with IUGR, nutrition is calculated taking into account a higher calorie content (by 1020%) than that corresponding to their body weight at birth.

An important place in the complex therapy in the neonatal period is occupied by measures aimed at the treatment of malnutrition and cerebral disorders, the correction of orthopedic disorders (massage, therapeutic swimming, special styling), and the prevention of infectious and inflammatory diseases.

In the children's clinic, children born with IUGR should be under dispensary observation. The high frequency of violations of the pace and disharmonious physical development, changes in the state of the central nervous system serve as the basis for special rehabilitation measures with the participation of a neuropathologist, psychologist, speech therapist and teacher in children's clinics and preschool institutions. Most children need individual regimens that provide for a longer stay in the fresh air, dosed physical activity, and therapeutic nutrition.

It happens that expectant mothers hear at the appointment with the attending physician or in the ultrasound room a frighteningly incomprehensible abbreviation - IUGR. Its decoding is even more frightening - "delayed intrauterine development of the fetus." A pregnant woman faced with a similar diagnosis is tormented by many questions. How dangerous is this condition? How will it affect the health of the baby? Will he be able to catch up?

What is FPI and IUGR?

Nutrition and respiration of the fetus is provided by a temporary ("provisional") organ - the placenta, which supplies the fetus with the substances necessary for life, receiving them from the mother's circulating blood. A condition in which the placenta does not adequately cope with its duties is called (FPN). Fetoplacental insufficiency over time leads to the fact that the fetus, not receiving the required amount of nutrients, weighs less than normal. This condition is called intrauterine growth retardation (IUGR), or intrauterine growth retardation (IUGR), or fetal malnutrition.

The causes of FPI are manifold. These include: late (nephropathy) - increased blood pressure, the appearance of protein in the urine, edema, long-term increased with the threat of premature birth, anomalies in the development of the uterus, anomalies in the development of the placenta and umbilical cord (for example, a short umbilical cord), general maternal diseases (heart defects, hypertension), common infections (from to influenza), . Factors predisposing to the development of FPI are rightly considered bad habits - smoking, addiction to alcohol and any drugs. Quite often, one or both fetuses with twins are affected by developmental delay.

Sick or just small?

Of course, not always a child is born small due to FPI. There is the concept of "constitutionally small fetus." It is logical when a small child is born to parents of short stature. In this case, the child is born with a low body weight, but absolutely healthy, not experiencing additional difficulties in the period of adaptation to extrauterine life, like children prone to true IUGR. Hypotrophic children differ from low-weight children in insufficient functioning of organs. It is important to understand that IUGR is not just underweight, but an important symptom of advanced FPI. And most importantly, FPI can cause intrauterine death of the fetus, since in case of circulatory disorders in the "mother-placenta-fetus" system, in extreme cases, the delivery of oxygen and nutrients to the fetus can be stopped.

Diagnosis of FPI

The simplest method of monitoring the growth of the fetus is to measure the height of the uterine fundus above the womb and compare the results with the standards for a given period. Along with this, newer methods are also used - determining the content of placental hormones in the mother's blood - placental lactogen, alkaline phosphatase, and some others. Obviously, a healthy placenta produces hormones in sufficient quantities, and the affected by a pathological process, on the contrary. These parameters are determined as part of a maternal blood test. An important role in the diagnosis of FPI is also played by cardiotocography (CTG), during which the cardiac activity of the fetus is recorded on a special tape and on the screen. During this study, a special sensor is attached to the belly of the expectant mother, with the help of which the vibrations created by the baby's heartbeat are transmitted to the device, where the signal is transformed into a certain curve, which reflects the number of heartbeats of the fetus. The purpose of this study is to make sure that the fetus does not lack oxygen. If the normal number of fetal heartbeats is 120-160 beats per minute, then with a lack of oxygen, it decreases or increases. Other indicators also change - the reaction to movements, etc.

The most common and accurate method for diagnosing intrauterine growth retardation is ultrasound. With the help of ultrasound, it is possible to accurately establish not only the discrepancy between the fetal weight and normal for a given period of pregnancy, but also find out how the development of the fetus is proportional and harmonious, how the internal organs of the fetus function, whether the placenta and umbilical cord have a normal structure. With the help of a variety of ultrasound - Doppler study - you can get information about the speed and direction of blood flow through the vessels of the umbilical cord and large arteries of the fetus.

Treat or feed?

Fetal growth retardation detected by ultrasound should be treated. The goal of treatment in this case is not to “fatten the baby”, but to normalize metabolic processes and support the vital functions of the fetus.

A large arsenal of medicines is used to treat fetal hypotrophy. Treatment should be individualized, taking into account the cause that caused FPI in this particular case. The success of treatment largely depends on how timely it is started.

In the treatment of FPI, tocolytic (i.e., relaxing the uterus) and vasodilators are widely used. Their use allows you to expand small vessels and increase the volume of uteroplacental blood flow. A similar goal is pursued by the appointment of infusion therapy - intravenous drip of blood substitute solutions that reduce blood viscosity and facilitate its passage through the capillaries. Of great importance in the treatment of placental insufficiency is also the use of vitamins (especially vitamin C and E) and amino acids, which allows you to normalize the composition of circulating blood and enrich it with substances necessary for the construction of organs and tissues of the fetus, as well as the synthesis of its enzymes and hormones.

Currently, many non-drug remedies are also used to treat intrauterine growth retardation, such as medical ozone, hyperbaric oxygenation (a medical procedure is breathing oxygen-enriched air under conditions of high barometric pressure) and some others. It is highly desirable to comply with the regime, which in English-speaking countries is called "bed rest" - during the day it is necessary to spend in bed in the side position for at least 6 hours. Well, the original Russian "quiet hour" - daytime sleep in the afternoon.

For expectant mothers who are carrying a small child, it is very important to have a good diet rich in vitamins and animal proteins, as well as a regimen with limited physical activity. Although you should not overeat, remembering that excesses in the diet do not at all lead to a proportional increase in the amount of nutrients taken by the placenta for the fetus. It is a historical fact that even during the blockade, mostly full-weight children were born to Leningrad women.

The effect of therapeutic measures must be constantly monitored using ultrasound and CTG, which are usually prescribed at intervals of 2 weeks (CTG - if necessary and more often). Treatment of IUGR almost always gives good results, although only in 10-20% of cases, the weight of the fetus can be brought to normal. In most cases, it is possible to observe adequate fetal growth, for example, in 7-10 days, the size of the fetus increases accordingly, but does not lag behind even more, which is considered a completely satisfactory result of treatment. In rare cases, when the efforts of doctors are in vain, the ultrasound shows a lack of fetal growth, accession, Doppler indicators worsen, and CTG shows signs of oxygen deficiency. In this case, you need to think about emergency delivery. The choice of method of delivery (delivery or caesarean section) depends on the readiness of the body and the cervix for childbirth and the severity of the fetal condition. If there is no certainty that a weakened child will endure birth stress, a caesarean section is preferred.

Prevention of FPI

It is necessary to think about the well-being of the unborn child even before pregnancy. It must be remembered that abortions, injuring the uterus, can later lead to violations of the uteroplacental circulation. During pregnancy, it is better to strongly refrain from smoking and drinking alcohol, contact with toxic substances and radiation sources - especially in early pregnancy, when the placenta is forming. It is necessary to timely (and better - in advance) treat infectious diseases and possible foci of infection, such as carious teeth or chronic tonsillitis. All expectant mothers, without exception, are advised to take multivitamin preparations for pregnant women.

Sometimes high-risk pregnant women (too young; women over 30 expecting their first child; suffering from chronic diseases; who have given birth to small children in the past; with long intervals between pregnancies) are recommended courses of drug prevention of FPI for up to 12 weeks, 20-23 weeks and 30-32 weeks, which include vasodilators and vitamins.

Detached consequences

As a rule, children who have had IUGR in utero require more careful care after birth. In height and weight, such children usually catch up with their peers by one and a half to two years, although due to reduced immunity, they get sick more often than other children. In addition, these children sometimes have problems with concentration and perseverance. However, medical rehabilitation helps young children overcome all difficulties and have good health in adulthood.

Discussion

Very informative. They did CTG for me, but we were told the scores (from 0 to 10), and not the heart rate of the child.
Also: there are rare cases when the cycle lasts not the "usual" 28-36 days, but more, then you have to prove that you are "not a camel". My two babies were given IUGR 2 weeks behind. And according to ultrasound in dynamics and according to CTG, everything was also in dynamics, but ultrasound showed a delay just for my two weeks and for some reason the doctor did not want to hear about my native even 43 day cycle. In general, the babies were born on their due date, and not set for a 28-day cycle (I don’t remember what this lag is called, but in general, this is an imaginary lag). And although the babies were born with a weight of exactly 3.0 kg each, there was no IUGR. But, my case is an exception :).

Comment on the article "Intrauterine growth retardation"

Cytomegalovirus infection (CMVI) is the most common intrauterine infection, one of the causes of miscarriage and the occurrence of congenital pathologies. In Russia, 90%-95% of expectant mothers are carriers of the virus, many of whom have almost asymptomatic disease. Vasily Shakhgildyan, Candidate of Medical Sciences, Senior Researcher, Federal Scientific and Methodological Center for the Prevention and Control of AIDS FBSI "Central Research Institute of Epidemiology" of Rospotrebnadzor: "Cytomegalovirus...

Anemia is the most common problem during pregnancy, in which the amount of hemoglobin in the blood decreases. Among pregnant women, in the vast majority of cases, anemia occurs from a lack (deficiency) of iron in the body. First, the level of iron in the depot decreases, due to this, at first, the hemoglobin level may still be within the normal range. However, in the future, without adequate therapy, the level of hemoglobin begins to decline sharply and iron deficiency anemia develops ...

Why treat anemia? Iron is an indispensable trace element that is involved in the construction of proteins, enzyme systems, cellular metabolism and redox processes, in the transport of oxygen, electrons and some enzymes, in the formation of immunity. With anemia, there is a violation of the nutrition of tissues and organs, which can lead to a slowdown in the growth and development of a number of organs, including the brain, which can be manifested by memory loss and speech delay, psychomotor and ...

The absence of a testicle in the scrotum can have several "options": cryptorchidism - "delay" of the testicle along the route from the abdominal cavity to the scrotum; testicular ectopia - characterized by a deviation from the normal route; retraction of the testicle - a condition when the testicle is "pulled" into the inguinal canal, however, it can be brought down into the scrotum, where it remains for quite a long time, no operation is required. Such mobility of the testicles may be associated with a powerful cremaster reflex ...

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Amniotic fluid, or amniotic fluid, is the biologically active medium that surrounds the fetus. Throughout pregnancy, amniotic fluid performs a wide variety of functions, ensuring the normal functioning of the mother-placenta-fetus system. The amniotic sac appears at 8 weeks of gestation as a derivative of the embryoblast. Amniotic fluid is a filtrate of blood plasma. In its formation, an important role also belongs to the secret of the amniotic epithelium ...

The most common complications associated with twin/twin/triple pregnancy are: Premature birth. Low birth weight. Retardation of intrauterine development of the fetus. Preeclampsia. Gestational diabetes. Placental abruption. C-section. premature birth. Births that occur before the 37th week of pregnancy are considered premature. The duration of a multiple pregnancy decreases with each additional child. On average, a pregnancy with one baby lasts 39 weeks ...

Discussion

While the violations are minimal, Actovegin and a mixture of vitamins can be dripped. Do 10 droppers and see if there is an effect or not. You shouldn't joke about it. Consult with your doctor and do not be nervous, especially since nothing will change in 3 days and you can calmly relax and live. According to Doppler, these are not strong violations)

I don't quite understand why you were given FPN?
according to your figures, you have a slight degree of impaired uteroplacental blood flow (yes, this is degree 1a) in the left uterine artery (0.63 for you, the norm is 0.59, for me, by the way, this figure is worse - 0.77) . As 2 ultrasound specialists have already explained to me, the child does not suffer with such indicators.
The rest of the indicators - the umbilical artery and the fetal aorta - are normal.
What they told me on the last doppler: track. Do it every 2-3 weeks (after 30 weeks - CTG), such indicators can persist throughout B., the main thing is not to worsen. But what to do if it gets worse - they didn’t tell me, I’m worried myself ... :(

Retardation of intrauterine development of the fetus. With the help of a variety of ultrasound - Doppler study - you can get information about the speed and direction of blood flow through the vessels of the umbilical cord and large arteries of the fetus.

Discussion

a friend's daughter had a 100% healthy girl

my second daughter had one artery. my daughter is almost 3 months old, I gave birth myself, this was not an indication for a cop. voevodin on ultrasound was the first to see this and said that I should not think about it at all. I gave birth in the PMC, they also didn’t care at all about this one artery, they cut it off and forgot about it. I was also very worried about this during pregnancy, now I think what a fool I was, I just shook my nerves.

Discussion

I canceled at 16-18 weeks

Canceled after 14 weeks. The medicine is needed to support pregnancy from the 8th to the 12th week, this is a critical period (there are only 3 such terms for pregnancy, IVF women for these periods are generally kept for preservation, regardless of well-being) - if there is not enough own progesterone, then it is during this period that the probability of miscarriage is high or frozen. After 12 weeks, there is no such threat, so they slowly begin to reduce the dose, and at 14 weeks they cancel it altogether. The placenta still continues to form until 14 weeks, and then it is completely ready to take care of the baby.
My own hormones fail, the third pregnancy in the morning in the first trimester - after the abolition, no problems.

Retardation of intrauterine development of the fetus. During pregnancy, it is better to strongly refrain from smoking and drinking alcohol, contact with toxic substances and radiation sources - especially in the early stages of pregnancy ...

True, the ultrasound showed placental hypertrophy and IUGR of the 1st degree, and a small fetus. The local doctors took me to the day hospital. Retardation of intrauterine development of the fetus.

malnutrition is ... there is no such diagnosis of hypertrophy ... malnutrition (intrauterine growth retardation) is put on the basis of a combination of signs, one of which is a low abdominal volume compared to other ultrasound measurements ... malnutrition ...

Discussion

malnutrition is ... there is no such diagnosis of hypertrophy ... malnutrition (intrauterine growth retardation) is put on a combination of signs, one of which is a low abdominal volume compared to other ultrasound measurements ... malnutrition is a consequence of problems with the placenta (premature aging, placental insufficiency, etc.) or (less often) with the umbilical cord (impaired blood flow). In this case, it doesn't matter how much and what you eat, what matters is how much and what reaches the fetus.
It is necessary to do a Doppler (measure the blood flow), and once again see if everything is in order with the placenta ... In general, in my opinion, the baby is normal by the due date ... think the belly is smaller ... not everyone can be short-legged and pot-bellied ...

Hypoxia inhibits intrauterine development of the fetus and can even cause its death. Retardation of intrauterine development of the fetus. A large arsenal of medicines is used to treat fetal hypotrophy.

Discussion

All links to English sites. I could translate some articles, but I need to know which ones are important to you.
And I also gave emails to Russian doctors. They work in the US with adapted children and invite doctors from Russia and Ukraine. I thought that maybe they would advise you on a FAS specialist in Russia. I do not want to give their emails openly, if you need, I will send you in private.

articles for parents of children with FAS
http://www.faslink.org/katoc.htm#PArenting

strategy of behavior with a child with FAS
http://www.come-over.to/FAS/BEAM.htm

Features of infants with FAS
http://come-over.to/FASCRC/ 24.11.2016 01:26:49, Anna1988

Retardation of intrauterine development of the fetus. Nutrition and respiration of the fetus is provided by a temporary ("provisional") organ - the placenta, which supplies the fetus with the necessary pregnancies) ...

Discussion

Yesterday I wrote to you, today I will write more: for a period of 32-33 weeks, the 2nd degree of maturity of the placenta is normal. 3 degree of maturity of the placenta from 35 weeks. If there is a suspicion that the child does not receive the required amount of substances, CTG and Doppler should be done, where everything will become clear. If blood circulation is disturbed, then it really makes sense to go into pathology, they will feed the child.
At 32 weeks, my placenta was 38-40 thick, the doctor in the LC gave me a referral to pathology and after some time persuaded me, I went to the hospital, where I was going to give birth later, I lay there for a week exactly, they didn’t do ANYTHING to me there - someone was put on a dropper or fed with pills, but I just lay there and regretted that I had gone for it.

METHODOLOGICAL INSTRUCTIONS FOR TEACHERS

Department of Pediatrics, Medical and Dental Faculties

    Learning theme number 2.

    Name of the topic: Diseases of the newborn. Retardation of intrauterine development. Modern ideas about the causes of intrauterine growth retardation. Formation mechanisms. Forms of developmental delay. Problems of diagnostics. Approaches to therapy and nursing of children with intrauterine growth retardation.

    The purpose of studying the educational topic. To acquaint students with diseases of newborn children. To study modern ideas about intrauterine growth retardation. To give students an understanding of approaches to therapy and nursing of children with intrauterine growth retardation

Chronocard, calculation of organizational potential

The name of the stage of the lesson

Duration of the stage of the lesson in minutes

Monodidactic systems

Attendance accounting

Introductory speech of the teacher on the relevance and significance of the topic under study

Programmed control of the initial level of knowledge

Demonstration of the patient with a group discussion

Work of students with teaching materials

Independent work with supervised children, mothers

Analysis of tasks on the topic of the lesson

Control of the final level of knowledge

    Topic study plan:

      1. Definition of IUGR

        Clinical manifestations of IUGR

        IUGR forms

        Differential Diagnosis

        Approaches to therapy

        IUGR forecast

    Presentation of educational material.

Growth Retardation(IUGR) is a synonym for the obstetric diagnosis of "intrauterine growth retardation of the fetus", which is established when there are lags in the parameters of the hearth from the average size corresponding to its gestational age.

Epidemiology. In the Russian Federation, the incidence of IUGR varies from 3.5 to 17%, in the USA - from 3 to 7%, in Western Europe - about 4%. According to perinatal diagnostics, the incidence of IUGR in premature babies is 15.7-22%. This is due to the presence of common pathogenetic mechanisms of intrauterine growth retardation and miscarriage.

Risk factors for IUGR include:

Unfavorable socio-economic conditions - low socio-economic status of parents; unavailability of medical care; professional hazards of parents; bad habits (smoking, alcohol, drugs); maternal malnutrition during pregnancy; insufficient weight gain of the mother during pregnancy; low maternal body weight;

Chronic diseases of the mother - chronic arterial hypertension; diabetes; chronic diseases; autoimmune diseases; severe anemia; congenital heart defects with signs of circulatory failure;

Congenital infections - viral (rubella, cytomegaly); bacterial (listeriosis, tuberculosis, syphilis); protozoan (toxoplasmosis, malaria);

Burdened obstetric history - the birth of children with signs of IUGR; stillbirth; mother's age is less than 16 and older than 35;

Complications of this pregnancy - preeclampsia (preeclampsia); bleeding in the second and third trimesters; delayed pregnancy; anomaly of the umbilical cord and placentation; multiple pregnancy;

Congenital malformations of the fetus - trisomy on the 13th, 18th, 21st chromosomes; Turner syndrome; neural tube defects; congenital heart defects.

Etiology and pathogenesis. In the development of the embryo and fetus, three phases are conditionally distinguished:

1) first 16 weeks pregnancy - processes occurring in tissues are mainly associated with cell hyperplasia;

2) second 16 weeks (weeks 16 to 32)- along with cell hyperplasia, there is an increase in their size (cellular hypertrophy);

3) last 8 weeks of pregnancy- hypertrophic processes dominate over hyperplastic ones.

At early onset IUGR decreases the relative number of cells, which is clinically manifested by a symmetrical lag of fetometric parameters from the normative indicators.

Later development IUGR is typical for an asymmetric form and is characterized by a lower rate of cell hypertrophy, which leads to a relative decrease in the size of those organs, the mass of which increases mainly in late pregnancy (for example, the liver).

About 10% of IUGR cases are associated with a pathological karyotype, another 10% with congenital infection (cytomegalovirus infection, rubella, toxoplasmosis, syphilis).

In other cases, the cause of IUGR is uteroplacental insufficiency associated with somatic or obstetric pathology of the mother.

IUGR - the reaction of the fetus to the impact of adverse factors. Among the mechanisms underlying the formation of IUGR, a large role is played by chronic fetoplacental insufficiency, which is manifested by a violation of the uteroplacental and fetal blood flow, as a result of which the diffusion of oxygen, urea and carbon dioxide is disrupted. Violation of the fetoplacental blood flow leads to insufficient supply of oxygen, energy and plastic substances to the fetus, to a violation of hormonal homeostasis. There is a direct relationship between the degree of decrease in placental blood flow, placental weight and fetal IUGR. The development of the placenta slows down before the growth of the fetus. In smoking mothers, the formation of IUGR is also associated with a decrease in the level of oxyhemoglobin in the blood as a result of increased formation of carboxyhemoglobin.

A direct relationship has been established between a decrease in the level of estriol in the blood and urine of a pregnant woman and a slowdown in fetal growth. In the development of IUGR, insulin-like growth factor -1 (somatomedin) also plays a role. In newborns with IUGR, its plasma content is reduced. There is evidence of a relationship between antiphospholipid syndrome in a pregnant woman and the formation of fetal IUGR.

Adverse effects on the fetus are caused by intrauterine infections, the use of pregnant alcohol, drugs, certain medications (valproic acid) and chemicals.

Classification

According to the nature of changes in fetometric parameters in obstetric practice, they distinguish symmetrical and asymmetrical forms of IUGR, and by the time of occurrence - early and late forms.

In neonatological practice, there are: hypotrophic, hypoplastic and dysplastic variants of IUGR.

By severity: mild, moderate, severe.

Research. General analysis of blood and urine, hematocrit, CBS, blood glucose, bilirubin and its fractions, proteinogram, blood electrolytes (potassium, sodium, calcium, magnesium), ultrasound, consultations of an ophthalmologist, neurologist, orthopedist.

Anamnesis, clinic. IUGR can be diagnosed in children of any gestational age. In anamnesis in children with IUGR, it is necessary to identify causative factors (see above).

When examining such children, there are clinical signs of malnutrition, a lag in the score of morphofunctional maturity from gestational age by approximately 2 weeks. Usually these children are prone to a large loss of the initial weight and to its slower recovery, however, with severe IUGR, the transient loss of the initial body weight is small (1-3%) and may even be completely absent. Children with IUGR are characterized by a protracted course and severity of physiological jaundice, slow healing of the umbilical wound, and the absence of manifestations of a hormonal crisis. After a period of hyperexcitability, these infants often have a symptom complex of "energy deficiency", manifested by a decrease in blood levels of glucose, calcium, magnesium. Even the normal course of childbirth in the presence of IUGR in the fetus is often traumatic for the child, so they often develop asphyxia, birth trauma of the brain and spinal cord.

Children with IUGR may experience polycythemia, hypocalcemia, hyperbilirubinemia, as well as hypomagnesemia, hyponatremia, and hypoglycemia. In the early neonatal period, respiratory disorders, manifestations of vitamin K deficiency (hemorrhagic disease of the newborn) and infection are possible.

Hypotrophic variantIUGR (asymmetric shape, prenatal malnutrition) are established at the birth of children with low weight and normal indicators of body length and head circumference. In this case, the mass-height indicator will be reduced, and body weight will be below the 10th percentile in relation to the child's body length. Normally, the mass-height index in full-term children is 60-80. With malnutrition of the first degree - 59-55; II degree - 54-50; III degree - less than 50. The assessment of the severity of this option is carried out according to the degree of body weight deficiency, the thickness of the subcutaneous fat layer, tissue turgor, head circumference and the presence of trophic skin disorders. The asymmetric form often develops in late pregnancy.

The vast majority of children with this form of IUGR do not have antenatal brain lesions, its mass and structure correspond to gestational age. This variant in the English-language literature is also called asymmetric IUGR or the phenomenon of "economical brain" (brain-sparing), since body weight is reduced disproportionately with respect to body length and head circumference. These children appear lean and have a smaller belly circumference than their head due to shrinking livers and depleted glycogen stores.

Hypoplastic variant (symmetrical shape) IUGR. It is detected in newborns with a uniform lag in weight, body length and head circumference from the normative ones for a given gestational age. All parameters of physical development in these children are reduced by 1.5 or more sigma (below the 10th percentile), the weight-height index is within the normal range. Such children look proportionately built, but small. The ratio between the circumferences of the head and chest is not disturbed, the edges of the sutures and fontanelles are soft, supple, the sutures are not closed, often there is no ossification point in the femoral head.

Dysplastic variant of IUGR diagnosed in children who, in addition to weight lag, also have a violation of body proportions, therefore, typical manifestations for this variant of IUGR are the presence of malformations, physique disorders, dysembryogenetic stigmas (detection of five or more stigmas in a patient has a diagnostic value). These children are characterized by severe neurological disorders, metabolic disorders, a tendency to develop anemia and infection.

Diagnosis. Prenatal diagnosis of IUGR is based on a comparison of individual fetometric parameters obtained as a result of ultrasound examination of the fetus with standard values.

In the antenatal period, the following is taken into account:

Insufficient increase in body weight in a pregnant woman;

Stop or insufficient increase in the size of the fetus (according to ultrasound);

Changes in the area and volume of the placenta and a decrease in uteroplacental and fetal blood flow;

Presence of signs of intrauterine suffering of the fetus: changes in heart rate, absence of accelerations, occurrence of deceleration, persistent bradycardia - according to cardiotocography with a non-stress test;

Increased or increased respiratory movements of the fetus (according to ultrasound scanning) (normal 30-70 / min. for a period of 36-40 weeks);

Elevated levels of AFP and hCG in the blood of a woman in the II-III trimesters of pregnancy;

In newborns, IUGR set on the basis of a comparison of the parameters of his physical development at birth with the proper parameters for the gestational age at which the child was born, the assessment of the morphological index of maturity

In many Western countries, for the diagnosis of IUGR, specialists use Lyubchenko's percentile curves (L.O. Lubchenko).

The diagnosis of IUGR is established on the basis of anthropometric data in children with insufficient body weight at the first weighing in relation to the norm for a given gestational age. The diagnosis of IUGR is considered valid if the birth weight of the child is more than 1.5 standard deviations below the mean for the given gestational age (or below the 10th percentile).

Taking into account the degree of decrease in the main parameters of physical development, there are three degrees of IUGR in newborns:

- Idegree, light, a decrease in body weight by 1.5-2 standard deviations (or below the 10th centile), with normal or moderately reduced body length (height). In 80% of these children, the size of the head circumference does not go beyond the normal fluctuations for gestational age. All of these children have clinical signs of malnutrition.

- IIdegree - a decrease in both body weight and length of more than 2 standard deviations (below the 3rd centile). 75% of these children have reduced head circumference. These children have the appearance of proportionately small children. There are no clinical signs of malnutrition, but more often there is an increase in the stigma of dysembryogenesis.

- IIIdegree, severe, - a decrease in all parameters of physical development (by 3 or more standard deviations or ≤ 1st centile), the presence of body disproportion, trophic disorders of the skin, a lot of dysembryogenesis stigmas.

The greater the deviation of the child's body weight from the normative values, the worse both the perinatal and long-term prognosis.

Early diagnosis of IUGR, both in the antenatal and postnatal periods, is very important, due to the fact that its presence leads to an increased risk of intrauterine and intranatal death of the fetus, impaired adaptation of the child in the neonatal period and various deviations in health in subsequent years of life .

Treatment,treatment goals: prevention of cold stress, hemorrhagic disease of the newborn, polycythemia, hypoglycemia, hypocalcemia, infectious complications.

Treatment regimen: Mandatory treatment: administration of vitamin K, stay in an incubator, enteral nutrition if possible.

Auxiliary treatment: relief of electrolyte disturbances, hypoglycemia, polycythemia.

Indications for hospitalization in the OPN: the presence of II-III degree IUGR, dysplastic variant of IUGR.

Methods of treatment for IUGR depend on the stage of development of the fetus and newborn.

prenatal period. In modern obstetrics, there are two main approaches to the prevention and treatment of IUGR in the prenatal period:

1) improvement of blood flow in the mother-placenta-fetus system (impact on peripheral and organ hemodynamics, correction of vascular tone, rheological and hemostasiological disorders);

2) pathogenetic treatment of concomitant diseases of the mother, exacerbating placental insufficiency.

The scheme for the treatment of placental insufficiency and IUGR, developed by G. M. Savelyeva, has become widespread in our country. The treatment regimen provides for complex therapy of pregnant women both in the conditions of the antenatal clinic and in the obstetric hospital.

Among the methods of pharmacological treatment of placental insufficiency of IUGR, the following drugs are currently used in obstetric clinics: beta-adrenomimetics, blood substitutes, heparin, trental, hormones, aspirin, solcoseryl / actovegin.

At the same time, from the point of view of evidence-based medicine, none of the proposed methods of prenatal prevention and treatment of IUGR is sufficiently effective.

Among the activities for prenatal prevention of IUVR, much attention is paid to the full nutrition of the pregnant woman. However, malnutrition is rarely the sole cause of IUGR, and the use of various biological and nutritional supplements does not significantly affect perinatal outcomes. However, if a pregnant woman has nutritional deficiencies and hypovitaminosis, then they certainly need to be corrected in a timely manner.

The timing and methods of delivery of a pregnant woman with IUGR are determined taking into account the biophysical profile of the fetus and the dynamics of fetometric parameters against the background of ongoing therapy.

early neonatal period. At the first stage, the treatment of children with IUGR is in many ways similar to the treatment of premature babies. Immediately after birth, such children should be placed under a source of radiant heat, given their tendency to rapidly cool. The need for primary resuscitation and the volume of intensive care are determined by assessing the severity of the condition at birth and based on dynamic observation data in the first hours of life.

In a satisfactory condition (the presence of a sucking reflex, the absence of pronounced neurological changes, normal motor function of the gastrointestinal tract), a child weighing over 2000 g is applied to the chest in the delivery room, children weighing over 1800 g begin to be fed with expressed breast milk from a bottle, in the rest cases, tube feeding with expressed breast milk is started no later than two hours after birth. The required amount of milk is determined according to the same rules as for premature babies. For children weighing over 2 kg, the calculation of nutrition can be carried out according to the formula: V times \u003d 3 x m (kg) x n, where n is the number of days of life. From the 11th day of life, the calculation can be carried out by the volumetric method - 1/5 of the body weight. In the future, the feeding regimen (exclusively breastfeeding, breastfeeding + bottle feeding, bottle feeding, tube and parenteral nutrition), as well as the timing of breastfeeding in newborns who are not attached in the delivery room, depend on the ability of the infant to suck out and retain the required amount of nutrition, from birth weight, neonatal condition, comorbidities and complications.

All children with IUGR, regardless of the severity of the condition at birth, receive 1-2 mg of vitamin K parenterally in the first hours of life.

Further volume of therapy depends on the presence of complications and concomitant diseases.

In children with IUGR in the early neonatal period, hypoglycemia, hypocalcemia, and blood clotting syndrome are often detected.

The complex of treatment also includes the treatment of trophic, cerebral disorders, correction of orthopedic disorders.

Forecast depends on the clinical variant of IUGR and its severity.

At hypotrophic and hypoplastic variants IUGR of the 1st degree, children, as a rule, catch up with their peers in physical development by the end of the first or the beginning of the second half of the year. Their psychomotor development may lag behind. Infectious morbidity does not exceed the morbidity of peers without IUGR.

At IUGRIIdegree most children catch up with the physical development of their peers by the year, some have an increased infectious morbidity and a lag in psychomotor development in terms of pace in the first 2 years of life. In the future, iron deficiency anemia, rickets, mild brain dysfunction (neurotic reactions, mental infantilism, neuropathic disorders) may develop.

In children with IUGRIIIdegree, and also with its dysplastic variant, the prognosis is often unfavorable. In the first 3 years, there is a lag in physical and psychomotor development. In 10-15% of these children, signs of organic damage to the central nervous system develop (cerebral palsy, epilepsy, progressive hydrocephalus, mental retardation). These children already in the neonatal period have a very high infectious morbidity, every 3-4th child develops a bacterial infection.

Mortality among term infants with IUGR exceeds that of infants with normal physical development. Newborns with IUGR are susceptible to infectious and inflammatory diseases. IUGR of the fetus and newborn makes a significant contribution to the development of critical forms of pathology and childhood disability. The main causes of disability are due to severe damage to the central nervous system - cerebral palsy, epilepsy, progressive hydrocephalus.

In children with IUGR, there was a lag in physical development in early and adolescence, sometimes persistent malnutrition persists.

Prevention IUGR provides for the treatment of genital and extragenital pathology in pregnant women, the elimination of bad habits (smoking, alcohol, drugs), the timely treatment of pregnancy complications, genetic counseling, the normalization of pregnant women's nutrition, and the reduction of the harmful effects of environmental factors.

    Educational and methodical material:

Tab. 2.4.Estimation of the gestational age of the child according to the totality of morphological criteria(Bollard J. et al., 1991)

sign

Points

Maximum score

Leather

Sticky, loose, transparent

Transparent, red, impregnated

Thin, pink, pronounced venous network

With superficial "scaly" or rash, mild venous network

Cracking, venous network is almost not expressed

Parchment-like, cracking, venous network is not expressed

Rough, cracked, wrinkled

Lanugo

Absent

Abundant

Bare areas

Mostly missing

Plantar folds

Heel toe

40-50 mm: -1

< 40 мм: –2

No folds

Weak, red

Only on the front third of the sole

On the front two-thirds of the sole

Numerous throughout the sole

Thoracic gland

imperceptible

Barely noticeable

flat areola without nipple

"Grainy" areola, nipple 1 - 2 mm

Protruding areola, nipple 3 - 4 mm

Fully formed areola, nipple 5–10 mm

Eye/Auricle

Eyelids closed

Loose -1

Tight -2

Flat, inelastic

Begins to bend, slight elasticity

Partially curved, good elasticity

Fully curved, fairly tight, very good elasticity

With strong cartilage, the ear is tight

Genitals

The scrotum is flat, smooth

The scrotum is empty, no wrinkles

The testicle descends, the furrows on the scrotum are weakly expressed

The testicle is lowered, the furrows are well defined

Testicles "hung", deep folding of the scrotum

Genitals ♀

The clitoris protrudes, the labia is even

The clitoris and small lips protrude

Large and small lips protrude equally

Big lips protrude more

The clitoris and small lips are completely covered

Overall assessment of morphological maturity