The child is growing every day. In order to assess his physical growth, to understand whether he is developing correctly, there are centile tables. Pediatricians, observing the baby, regularly evaluate its weight and size, advise parents what to do if the child's parameters differ significantly in one direction or another from the average. Proper physical development is important for the subsequent life of a small person.

What are centiles and centile tables in pediatrics

The principle of these tables is that centiles divide the values ​​into 100 intervals, most often used: 3, 10, 25, 50, 75, 90 and 97th. Centiles are data values ​​(height, weight, head circumference and chest), which have a certain number of examined children. They are used in order to quickly assess how the child is developing, whether his data correspond to the norm (the average value characteristic of most children at a particular age). The norm is the number of signs characteristic of half of healthy boys and girls, that is, an interval from 25 to 75 centiles. The standard is considered to be physical development, defined as the 50th centile.

How to use, knowing the height and weight of the child

Using tables is simple and convenient. You need to weigh and measure the baby, find his age and see which corridor his data fell into. The centile corridor is the interval on the centile scale that corresponds to your child's performance. For convenience, the centile corridors are marked with numbers from 1 to 8, and the columns indicating the norm are highlighted in color. The indicators on the left (1–3) and on the right (6–8) are rated as below and above the average. Corridors 2 and 7 are areas of focus that may require further consultation. Corridors 1 (very low) and 8 (very high) - there is a possibility of developmental pathology. Under the corridor numbers, the quantitative boundaries of the trait are indicated for a certain proportion (percentage, centile) of children of a given age and gender.

Example: boy, age 3 months. Determine the level of his physical development from the tables:

• body length - 60 cm, average (corridor 5);
• weight - 5600 g, average (corridor 4);
• chest circumference - 39 cm, average (corridor 5);
• head circumference - 40 cm, average (corridor 4).

The meaning of centiles and compliance with the norms - table

standard deviation

The standard deviation "σ" (usually denoted by the Greek letter sigma) allows you to estimate how much the values ​​from the set can differ from the average value. Estimation of body length/height using "σ" is made by calculating standard deviations from 50% of the values ​​of growth indicators for this age group.

Indicator score:

• within ± 1 σ - average growth;
• from ± 1 σ to ± 2 σ - growth below/above average;
• from ± 2 σ to ± 3 σ - low/high growth;
• going beyond +/- Зσ - growth is very high (gigantism) / very low (dwarfism).

Failure of the child's indicators to return to normal

Very low and highest rates are sometimes found in healthy children. They may be related to weight at birth, parameters of mom and dad, or metabolism.

Centile tables are never diagnosed. Failure to meet the norm of any of the indicators does not mean anything. To assess the physical size of the child, you need to determine the corridor into which his data falls. If they remain within the boundaries of one corridor or differ by one or two, then the child develops proportionally. When the difference in indicators is more than two corridors, this indicates an inharmonious formation. If the pediatrician reveals this difference, there is no need to be afraid, in such cases the baby may be sent for an additional examination or consultation to find out the cause. It is possible that the baby is healthy, he just has such features or hereditary signs.

Breastfed babies often develop unevenly. In one month there may be a lack of weight, and the next vice versa. Parents need to record their child's performance and compare them so as not to worry once again. At the age of one year, children need to be shown to the pediatrician monthly in order to monitor the health of the child and understand whether he is growing properly.

There are different charts for boys and girls, as boys tend to grow, gain weight and develop faster. For children, height is key. Everything else is considered in conjunction with it, that is, with an increase in body length, other indicators (weight, head and chest girths) increase.

WHO centric tables for assessing the physical development of girls - photo gallery

Height and weight of girls Chest and head circumference of girls Proportionality of height and weight of girls

Centile tables for boys

Central tables of physical development of children

When you bring your son to an appointment with a pediatrician who will weigh him and measure his height, chest and head circumference, you hear an assessment of these indicators: a four, or another number from one to eight. What are these points? This centile corridor, which contains the indicators of your boy according to the table. Centile tables are given below.

physical development of the child

An example of assessing the physical development of a newborn boy

Height-length - 50 cm, corresponds to the "average" indicators. Weight - 3800 g, corresponds to the assessment of "above average". Chest circumference - 37 cm, corresponds to the assessment of "wide". Head circumference - 36 cm, corresponds to the "average" values. Correspondence of weight to the length of the child's body - a moderate excess of weight relative to length, "above average".

When you bring your baby to an appointment with a pediatrician who will weigh her and measure her height, chest and head circumference, you hear an assessment of these indicators: a four, or another number from one to eight. What are these points? This centile corridor, which contains the indicators of your girl according to the table.

From the tables, you can find out if your child's height and weight are normal at a given age (from birth to 17 years). Centile tables are given below.

Dental tables for assessing the physical development of a child represent a kind of "mathematical photograph" of the distribution of a large number of children according to increasing indicators of height, weight, chest and head circumference. The practical use of these tables is extremely simple and convenient, combined with a good logical understanding of the evaluation results.

The columns of the centile tables show the quantitative boundaries of the trait in a certain proportion (percentage, centile) of children of a given age and gender. At the same time, the values ​​typical of half of healthy children of a given sex and age are taken as average or strictly normal values, which corresponds to an interval of 25-50-75%. In our tables, this interval is shaded. Intervals that are close to the average are rated as below and above the average (respectively 10-25% and 75-90%). These indicators parents can also be regarded as normal. If the indicator falls into the zone of 3-10 or 90-97%, you should be alert and point this out to the doctor. This is an area of ​​attention that requires additional consultations and examination. If the child's indicator goes beyond 3 or 97%, it is very likely that the child has some kind of pathology that affects the indicators of his physical development.
distribution of children by head circumference

You can understand what a dental scale, for example, growth, is in the following example. Imagine 100 children of the same age and gender, lined up in order from smallest to tallest. The growth of the first three children is assessed as very low, from 3rd to 10th - low, 10-25th - below average, 25-75th - average, 75-90th - above average, 90-97 - tall and the last three guys are very tall.

The indicator of height, weight, etc. of a particular child can be placed in its own “corridor” of the centile scale of the corresponding table. Depending on which "corridors" the child's anthropometric data fell into, a value judgment is formulated and an appropriate tactical medical decision is made.

According to the same principle, the correspondence of body weight to the length-height of the child is assessed, while the distribution is built using the weight indicators of children with the same height.

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To assess the physical development of a newborn, average statistical indicators (M ± st) of the main parameters are used depending on the gestational age or evaluation tables built on the principle of percentiles.

Gestational age is determined by the time of the last menstruation in the mother (the number of weeks from the first day of the last menstruation to the birth of the child), the date of the first movement of the fetus (the number of weeks from the date of the first movement of the fetus to delivery is added to 18-20 weeks in primigravida and to 16-18 weeks in multi-pregnant women), according to objective observation of a pregnant woman in antenatal clinic, including ultrasound examination, as well as on the basis of a clinical assessment of the maturity of the newborn.

According to statistical data, indicators within M ± 2a or P 10 - P9 0 are considered normal for a given gestational age, and those that differ on average (M) by 2 or more st or above P 90 and below P10 are sharply different from the norm.

Indicators of the physical development of newborns depend on the age and anthropometric parameters of the parents, the serial number of pregnancy, the sex of the fetus, nutrition and living conditions of the mother. So, in multiparous women, large and physically strong parents, larger children are born. The average body weight of boys from the 34th week of pregnancy is greater than that of girls. Young and older women, as well as in highland areas, give birth to children with a lower body weight. These factors cause biological fluctuations in the indicators of the physical development of newborns.

Important for the assessment of physical development is the characteristic of the proportionality of the physique and nutritional status of the newborn

Depending on the duration of pregnancy in MaTept, newborns are divided into full-term, premature and post-term.

A full-term newborn is a child born at a gestational age of 38-42 weeks (259-293 days) with an average body weight according to our data (M ± a), 3610 ± 416 g for boys and 3480 ± 484 g for 5 girls, body length 51 .5±1.7 cm and 51±1.9 cm, respectively.

In a full-term newborn, the head makes up 1/4 of the body. Its large size is associated with the prevailing development of the brain.

It is important to determine the shape of the head and the circumference of the skull; at birth. During the first 2-3 days of a child's life, save! the configuration of the skull, due to the passage of the head through the birth canal. Variants of the norm include such forms of the skull as dolichocephalic (elongated in the anteroposterior direction), brachycephalic (elongated in the transverse direction), tower skull. The bones of the skull are distinguished by some elasticity, their location on each other and the course of the sagittal and coronal sutures are observed. The parietal bones can be found in the occipital or frontal.

The circumference of the skull in full-term children is 33-36 cm and may exceed the circumference of the chest by 1-2 cm. (small) fontanel - no more than 0.5 cm.

In a full-term newborn, the subcutaneous fat layer is quite well developed, the skin is pink, velvety, covered with vellus hair (lanugo), mainly in the shoulder girdle, the nipple circle of the mammary gland is well developed (1 cm or more in diameter), the striation of the sole occupies 2 / 3 of its surface, the cartilage of the auricles is elastic, the nails are dense. The umbilical ring is located in the middle of the distance between the bosom and the xiphoid process, in boys the testicles are lowered into the scrotum, in girls the large labia cover the small ones. The cry of a child is loud. Muscle tone and physiological reflexes of the newborn are well expressed, the child takes a flexor posture. His sucking function is well developed.

Premature baby. Until recently, all children born weighing less than 2500 g, regardless of gestational age, were classified as premature. The frequency of birth of these children, according to statistics from different countries, ranges from 6 to 13.6%.

Subsequent studies have shown that body weight, although reflecting the maturity of the fetus, may not be the main criterion for prematurity. It was found that among children with a birth weight of less than 2500 g, about 1/3 are children born at term. In this regard, WHO recommended using the term "low birth weight" (or, in modern terminology, "low birth weight") for all children weighing less than 2500 g, and retaining the term "premature" for those of them who are born at a period of 37 weeks or less (before the 259th day of pregnancy) and have all the signs of immaturity.

Diagnostic signs of premature babies are:

• birth at 28-37 weeks of gestation with body weight in most from 1000 to 2500 g, length 38-47 cm, head circumference 26-34 cm, chest 24-33 cm;
• functional and morphological immaturity of the leading systems of the body: central nervous system, pulmonary, cardiovascular (muscle hypotension, hyporeflexia, hypothermia, primary insufficient expansion of the lungs, etc.);
• decreased lecithin/sphingomyelin ratio in amniotic fluid ah, bronchial and gastric aspirates;
• external signs of immaturity (thin skin with translucent veins, collaterals and capillaries, underdevelopment of the shape and cartilage of the auricles, widespread vellus on the body, weak striation of the feet, etc.);
• functional insufficiency of self-regulation and homeostasis processes;
• high levels of a-fetoprotein;
• late start of maturation of protective morphofunctional structures;
• high incidence of edematous syndrome in the first days of life (40%), SDR (60-70%), intracranial hemorrhages, severe and prolonged conjugative hyperbilirubinemia.

A post-term newborn is a baby born after the 294th day, or 42nd week of pregnancy. The frequency of birth of such children is, according to different authors, from 8 to 12%.

Pregnancy prolongation is characterized by the presence of risk factors in a woman: the first birth after 30 years, ovarian dysfunction, no increase in body weight after the 41st week of pregnancy, a decrease in abdominal circumference by 5-10 cm, oligohydramnios, an admixture of meconium in the amniotic fluid, a decrease in glucose concentration in the amniotic fluid up to 0.55 mmol / l (at a rate of 1.11-2.75 mmol / l) and an increase in the number of fatty non-nuclear cells ("orange") over 50%, a decrease in the excretion of estriol in the urine, a large number of intermediate and the absence of surface cells in a cytological examination of a smear from the vagina. Belated childbirth is accompanied by weakness of labor activity, a long anhydrous interval in childbirth, and intranatal fetal hypoxia. Destructive changes in the placenta, yellow-green staining of the umbilical cord, amniotic membranes and placenta are characteristic.

The child has clinical signs of trophic disorders - thinning and flabby turgor of the subcutaneous fat layer; desquamation of the skin of the palms and feet; dry, parchment-like, flaky skin; lack of cheese-like lubricant; greenish-icteric staining of the umbilical cord, skin of the nails; dense bones of the skull with closed sutures.

Depending on the severity of these symptoms, S. Clifford identified 3 stages, known in the literature as Clifford syndrome I, II or III degree.

Often these children show changes in the state of blood homeostasis! (metabolic acidosis, increased hemoglobin content, hypoglycemia, lability of water-salt metabolism).

Among post-term newborns, there is a high frequency of hypoxic-traumatic lesions of the central nervous system, meconium aspiration syndrome; they are prone to a large loss of body weight in the first days of life, transient fever, infectious lesions of the skin and lungs.

When comparing indicators of physical development and the gestational age at which the child was born (gestational age), the following groups of children are distinguished:

1. Newborns with a large body weight.
2. Newborns with normal physical development for a certain gestational age.
3. Newborns with low weight in relation to gestational age are "small-to-term babies", or newborns with intrauterine growth retardation.
4. Newborns with intrauterine (congenital) malnutrition.

These newborns can be among full-term, premature and post-term children.

Newborns with normal physical development for a given gestational age are characterized by body weight, head and chest circumference within the average values ​​(M ± 20 or P 10 to P 90).

Newborns with low weight for gestational age, "small for term", or newborns with intrauterine growth retardation account for 2 to 10% of all live births, and among children with low birth weight (i.e., weighing less than 2500 d) - about 1/3.

They can be premature, full-term and post-term.

Risk factors for the birth of "small-to-term" newborns are: nephropathy (63%) and chronic infectious and inflammatory diseases in pregnant women (29%), multiple pregnancies (27.8%), aggravated obstetric history in terms of stillbirths and infertility; pathology of the placenta and umbilical cord; low birth weight in the pedigree (especially mother, father, siblings), low rates of physical development of parents.

These newborns have a body weight at birth below the due gestational age by 20 or more, or below the 10th percentile! In most children, it does not exceed 2500 g. These children are also characterized by a decrease in other parameters of physical development and various body disproportions: a significant lag in body weight and length with a relatively large sizes head, a pronounced decrease in length along! compared with body weight and head circumference, a more significant decrease in head size than body weight and length.

They are characterized by dissociation of clinical-functional, neurological and biochemical indicators of maturity, as a result of which they occupy! as if an intermediate position in terms of maturity between the true gestational age and the estimated birth weight.

In such children, selective morphostructural immaturity of organs is revealed - a decrease in the size and cellular composition of such organs as! the thymus gland, the adrenal glands, and in some children the brain, with the relative maturity of the structures of the lung, heart, and thyroid gland. They are characterized by: a slow rate of change of fetal hemoglobin to an adult (especially in full-term children); increase in hematocrit, amount of hemoglobin, red blood cells; hypoglycemia (in 20-40%), hypocalcemia; disimmunoglobulinemia with an increase in the content of IgM and a decrease in IgG; slight initial weight loss (6.33% on average), moderate "physiological" hyperbilirubinemia (absent in 15-20% of children). These children have a high frequency! malnutrition (63%), asphyxia at birth and aspiration syndrome, chromosomal and gene mutations (7.4%), congenital anomalies (10%) of intrauterine infection (rubella, toxoplasmosis, etc.).

Peri- and neonatal mortality and morbidity in full-term newborns "small to term" are 3-8 times higher than those in children born at term with normal body weight.

The development of these children in subsequent years of life proceeds, according to our data, with various deviations: a lag in the pace of physical and psychomotor development (42.1%), neuropathic disorders (33.7%) and neurotic reactions (20%), severe neuropsychic diseases (12.6%).

Newborns with large body weight at birth. Children with a large body weight include newborns with a body weight above the average due to a given period by 2a or more (or above 90% of the percentile curve). Full-term babies have a body weight of 4 kg or more and make up 5-11% of the total number of live births.

Children with a large body weight are often born to mothers with diabetes, with poor nutrition, disorders of fat and carbohydrate metabolism in a pregnant woman.

*1 cm down and lateral to the umbilicus.

** Mid-thigh.

Often, weight gain is the result of a genetic predisposition. Parents of such children are also born with a large body weight and have high rates of physical development in adulthood. In these children, along with a large body weight, there is an increase, but less distinct, in other parameters of physical development (length, head and chest circumference), an excess subcutaneous fat layer, a tendency to swelling of tissues (42.4%), an increase in hematocrit , hypernatremia, metabolic acidosis.

They are characterized by a high incidence of conjugative hyperbilirubinemia, symptomatic hypoglycemia, intracranial birth trauma, and SDR, especially in children of diabetic mothers. The perinatal mortality of these children is 2 times higher than that of children with average birth weight.

Intrauterine malnutrition is an acute or chronic malnutrition of the fetus, characterized by the presence of clinical signs of malnutrition (decrease in the thickness of the subcutaneous fat layer, decrease in tissue turgor, dryness and pallor of the skin, etc.), underweight in relation to its length, changes in the functional state of the central nervous system , metabolic disorders and reduced immunological resistance.

The frequency of this pathology in full-term children ranges from 3 to 18-22, in premature babies - 18-24%.

Intrauterine malnutrition is the result of a variety of disorders in the period of intrauterine development. Among the reasons contributing to: the development of intrauterine malnutrition, it should be noted diseases of mothers during pregnancy (chronic and acute), malnutrition toxicosis of pregnancy (especially nephropathy, preeclampsia and eclampsia) multiple pregnancy, the influence of certain industrial hazards, etc. The presence of malnutrition, along with clinical signs, is evidenced by a decrease in the thickness of the skin fold and the circumference of the thigh in comparison with the average, depending on body weight at birth.

Body weight indicators from P25 to P75 are considered the average norm for a given body length of a child (normotrophy); from P25 to P10 - moderately reduced (initial or mild manifestations of malnutrition); from P10 to P3 - low (distinct signs of malnutrition); below P3 - very low (significant manifestations of malnutrition).

However, in the diagnosis of malnutrition, determining the correspondence of body weight to length should be combined with an assessment of other clinical manifestations of malnutrition and laboratory parameters.

Depending on the severity of clinical manifestations and the indicator of physical development, there are: mild malnutrition (I degree), moderate (II degree) and severe (III degree).

Due to the fact that the severity of the behavioral and neurological signs of the newborn depends on the degree of maturation of his CNS, the determination of gestational age should precede the assessment of the neurological status. Rapid determination of the gestational age of the newborn in the delivery room is important for determining further medical tactics. For this purpose, you can use the method of determining the gestational age according to Petrussa.

Table #1

"gestational age" (weeks) = 30 + total points.

Ballard Maturity Scale

The determination of gestational age includes the Ballard scale. The Ballard Maturity Test is the most widely used test for determining gestational age.

This test allows you to estimate gestational age with an accuracy of up to two weeks. The neurological (6 criteria) and physical (6 criteria) development of the child is assessed in points, the points obtained are summed up, and the gestational age of the child is determined according to the proposed table. Criteria for neurological maturity are based on the fact that passive muscle tone is more important for determining gestational age than active.

For greater accuracy, the determination of the gestational age according to Ballard is carried out twice - independently of each other by two doctors. The test should be carried out in the position of the child on the back on the first day of life (no later than 4-5 days), since in the future some signs may change significantly.

physical maturity

Neuromuscular maturity

Pose of the newborn

observation is carried out at rest, when the child lies on his back.

square window

the doctor bends the newborn's hand towards the forearm, holding it between the thumb and forefinger. The maximum possible flexion should be achieved, after which the angle between the surface and the elevation of the thumb is measured.

Response of the hands

the child lying on his back is first bent at the elbow joint and held in this position for 5 minutes, and then fully unbent by pulling the hands, and then released.

Popliteal angle

in a child lying on his back, whose pelvis is pressed against the surface of the table, the doctor, with the help of the index finger of his left hand, holds the thigh in the knee-chest position, while the doctor’s thumb supports the knees of the newborn. Then the child's leg is unbent by light pressure with the index finger right hand doctor on the back surface of the ankle joint of the newborn, after which the popliteal angle is measured.

Pulling the heel to the ear

in a newborn lying on his back, pull the foot of the foot as close to the head as possible, but without effort. The distance between the child's foot and the head is noted, as well as the degree of leg extension in the knee joint.

Oblique movement symptom

taking the hand of the newborn lying on his back, bring his hand as far as possible behind the neck over the opposite shoulder.

Assessment of the maturity of the newborn by points

Premature baby

A premature baby is a baby born with a gestational age of less than 37 completed weeks, i.e. up to the 260th day of pregnancy.

full-term baby

A full-term baby is a baby born between 37 and 42 weeks of gestation, i.e. between 260-294 days of pregnancy

Postterm baby

A post-term baby is a baby born at 42 weeks or more, i.e. on the 295th day of pregnancy and later.

Neonatology- a section of pediatrics concerning the physiology and pathology of a child's development during the neonatal period - the most important period of a person's life, which largely determines his health in subsequent years.

The neonatal period, or neonatal period, begins at birth and ends 28 completed days after birth. In addition, there is a definition of "perinatal period". According to ICD-X, it starts at 22 completed weeks of gestation (154 days) and ends on the 7th completed day after birth. The perinatal period has been singled out due to the special significance for human health of diseases that occur in this period of life due to the influence of pathogenic factors associated with extragenital and obstetric pathology of the mother. The perinatal period is divided into three periods: antenatal, intranatal and early neonatal. The antenatal period begins with the formation of the zygote and ends with the onset of labor. The intranatal period is calculated from the onset of labor to the birth of a child. Early neonatal period - the first 7 days from the birth of a child.

In neonatology, there are concepts necessary to assess the state of health and the degree of morphofunctional development of the child, his adaptive capabilities.

The gestational age of a child is the duration of its intrauterine development, calculated from the first day of the mother's last normal menstruation in full days or full weeks. A full-term baby is considered to be a baby born at 37-42 weeks gestation. Most full-term babies weigh more than 2500 g and have a length of more than 46 cm. A baby born before the end of the 37th week of pregnancy is considered premature. A post-term is a baby born at a gestational age of 42 weeks or more.

Regardless of gestational age, the following are distinguished among newborns:

With low birth weight (less than 2500 g);

Very low body weight (less than 1500 g);

With extremely low body weight (less than 1000 g).

The definitions of live birth and stillbirth are important. A child is called live-born, regardless of his gestational age, if at the moment of birth at least one of the signs of life is present: breathing, heartbeat, umbilical cord pulsation, or obvious movements of voluntary muscles. Stillbirth is the death of the product of conception before its complete expulsion or removal from the mother's body, regardless of the duration of pregnancy.

Based on the division of the neonatal period, indicators of early neonatal mortality (mortality in the first week of life), late neonatal (mortality in the 2-4th week of life) and neonatal mortality (during the first 28 days of life) are calculated. In the neonatal period in Russia, about half of the children who die before the age of one die.

By the time of the birth of a child, a complex system of adaptive mechanisms is formed, due to which, in a relatively short period of time, the newborn adapts to new living conditions. In accordance with the new conditions of nutrition and respiration, metabolic restructuring takes place, during which the catabolic nature of the exchange takes place and a decrease in body weight is observed in the first days of life. As the metabolic adaptation is completed, the anabolic direction of the exchange is again established and the development inherent in early childhood takes place. In parallel with this, adaptive reactions specific for this period of life appear at the cellular, tissue and system levels, which ensure the restructuring of the functions of all body systems, aimed not only at maintaining its vital activity, but also at further development. In a healthy full-term baby, the process of adaptation is completed by the 7-10th day of life, while in a premature baby it proceeds slowly. The less mature the child is, the longer it takes him to adapt to new conditions of life.

During the period of adaptation of the newborn, certain functional states are observed, which are commonly called transitional

(border).Being physiological, under certain conditions they can take on pathological features and contribute to the development of complications (for example, jaundice in very premature babies). Transient states in newborns are:

1) transient loss of initial body weight, most pronounced on the 3rd-4th day of life and not exceeding 6%;

2) transient hypothermia (in the first 30-60 minutes of life) and hyperthermia (observed in some children at the time of maximum weight loss on the 3rd-4th day of life);

3) transient changes in the skin (physiological erythema, birth tumor, toxic erythema - an allergoic reaction on the 3rd-5th day of life);

4) transient hyperbilirubinemia (jaundice appears on the 2nd day of life and gradually disappears by the 5-7th day);

5) transient features of kidney function (oliguria on the first day of life, proteinuria, uric acid infarction, infarct urine);

6) hormonal crisis (breast engorgement, metrorrhagia, etc.);

7) transient dysbacteriosis and physiological dyspepsia;

8) transient state of the circulatory system due to gradual closure of fetal shunts;

9) transient features of hemostasis and hematopoiesis.

The adaptive capabilities of a newborn depend to a large extent on the conditions in which his intrauterine development proceeded, since they largely determine the state of morphological and functional maturity of various organs and systems of the fetus at the time of his birth. Therefore, these transition states are expressed to varying degrees, in various combinations, and sometimes only some of them are observed. In most cases, transitional states in newborns disappear by the end of the early neonatal period, their persistence in children older than 7 days of age should be regarded as a symptom of pathology and measures should be taken for additional examination of the child.

Children with intrauterine growth retardation (IUGR) Code ICD-X - P05 (slow growth and malnutrition of the fetus).

Retardation of intrauterine development of a child is a syndrome that appears in the prenatal period of life and is characterized by

a decrease in body weight and height of the newborn by two standard deviations or more (or below the 10th centile) compared with due for a given gestational age.

The frequency of birth of children with IUGR varies widely in different countries(from 3 to 30%), since it depends on the criteria underlying the diagnosis, on the genetic load of the population, socio-economic living conditions, the health of women of reproductive age and other factors. The frequency of IUGR in the population of newborns in Moscow is 67.4 per 1000 children born alive at term and 179.5 per 1000 born prematurely.

Causes of intrauterine growth retardation.

1. Endogenous: chromosomal diseases, multiple pregnancies, intrauterine infections, congenital malformations.

2. Exogenous: socio-biological, disrupting the normal course of pregnancy (poor economic situation and malnutrition, occupational hazards, bad habits, etc.), maternal somatic diseases and their exacerbations during pregnancy, pregnancy complications and placental pathology.

The gestational age at the time of exposure to an adverse factor and its duration determine the form of IUGR.

Symmetrical shape (hypoplastic variant) - body weight, height and head circumference lag behind the values ​​due for a given gestational age. It is observed in newborns whose intrauterine development proceeded under adverse conditions from the very early dates pregnancy. Often with this form of IUGR, the child has dysembryogenesis stigmas (dysplastic variant).

Asymmetrical shape (hypotrophic variant) - body weight lags behind due for a given gestational age. Height and head circumference correspond to age. It is observed under adverse conditions of intrauterine development in the second half of pregnancy.

There are three degrees of IUGR:

I) mild degree - malnutrition I - deficiency of 1.5 sigma or from the 25th to the 10th centile;

II) medium degree - malnutrition II - deficiency of 2 sigma or from the 10th to the 3rd centile;

III) severe degree - malnutrition III - deficiency of more than 2 sigma or less than the 3rd centile.

Along with the lag of physical development in newborns, there may be a delay in the formation of CNS functions - a mismatch of postural, passive tone and reflex reactions to gestational age. At the same time, a uniform lag of these functions from the proper development for 2-4 weeks or dissociated development is distinguished, when the formation of unconditioned reflexes is delayed to a greater extent than tonic reactions. These children make up the most difficult contingent, since most of them have a violation of neuroimmuno-endocrine regulation at the cellular and tissue levels, which determines the state of multiple organ failure and instability of homeostasis.

The process of adaptation to new environmental conditions in newborns with IUGR is difficult, proceeds slowly with great stress on all functional systems of the body. At the same time, violations of homeostatic functions that require immediate correction often occur, in the development of which a certain role can be played by the peculiarities of metabolic processes associated with IUGR in the child's body and the lack of an individual approach to feeding him.

The most frequent complications of early neonatal adaptation of children with IUGR.

1. Asphyxia at birth.

2. Hypoglycemia occurs on the first day and may occur within a few days.

3. Polycythemia.

4. Neurological disorders.

5. Aspiration syndrome of amniotic fluid and / or meconium.

6. Pulmonary hemorrhages.

7. Increased plasma volume at birth and extracellular fluid volume. Great tendency to edema.

8. Increased heat transfer and reduced heat production.

9. The number of circulating T-lymphocytes is reduced, while the number of B-cells is normal.

10. Reduced processes of opsonization, chemotaxis, phagocytosis.

11. Low level immunoglobulin G.

12. Hypocalcemia, hyperphosphatemia, hyperbilirubinemia in premature infants with IUGR.

13. Delay of postnatal restructuring of hemodynamics. Nursing and feeding of newborns with IUGR requires an individual approach, taking into account the degree of maturity of the child and

the presence of comorbidities. IUGR of a newborn makes a significant contribution to the development of chronic forms of pathology and childhood disability caused by severe CNS damage (cerebral palsy, epilepsy, progressive hydrocephalus, minimal brain dysfunction).

According to the concept of "fetal programming" (Lucas A., 1991), under conditions of nutrient and oxygen deficiency in the fetus, the rate of cell division, the distribution of cell types and their metabolic activity change, which determines the "programming" of the organ structure and regulation features at the cellular level. This determines the predisposition to cardiovascular, metabolic and endocrine diseases in adulthood. Observed:

1) ischemic heart disease;

2) increased blood pressure;

3) type II diabetes mellitus and insulin resistance;

4) violation of cholesterol metabolism and blood clotting (increased levels of serum LDL and fibrinogen concentration in blood plasma);

5) polycystic ovary syndrome (increased levels of androgens during fetal development);

6) changes in skeletal muscle metabolism (reduced levels of glycolysis and ATP production, increased fat oxidation);

7) increased activity of the sympathetic nervous system. Prevention of IUGR of the fetus is to improve the health of women

of reproductive age and in providing adequate assistance to pregnant women: when registering in a antenatal clinic, identifying risk factors for the development of placental insufficiency and IUGR of the fetus, dynamic monitoring of the health of a pregnant woman and timely hospitalization in a hospital.

Chapter 1

premature babies

A newborn is considered premature, born between the 22nd-37th weeks of pregnancy (154-259 days from the first day of the last menstrual cycle) with a weight of 500 to 2500 g and a length of up to 45 cm. (WHO recommendations 1977)

Code ICD-X-P07.

Epidemiology.Statistical indicators regarding the frequency of birth of premature babies have significant differences (4-16%), since in a number of countries those children who were born before the 28th week of pregnancy are not counted as newborns. Is there an order of the Ministry of Health of the Russian Federation in Russia? 318 dated December 4, 2002 “On the transition to the criteria for live birth and stillbirth recommended by the World Health Organization (WHO), according to which the perinatal period is calculated from the 28th week of pregnancy. The frequency of birth of premature babies, whose gestational age is 28-36 weeks, is 5.5-8%. Among premature babies, 80% are children born at a gestational age of 32-36 weeks.

It is customary to distinguish four groups of premature babies depending on body weight at birth:

I degree of prematurity - 2500-2001;

II degree of prematurity - 2000-1501;

III degree of prematurity - 1500-1001 g - very low body weight;

IV degree of prematurity - less than 1000 g - extremely low body weight.

The morbidity and mortality of premature babies, the frequency of disability is higher, the lower the gestational age of the child. Nursing, treatment and rehabilitation of premature babies require significant financial costs, so the prevention of preterm birth is not only the most important medical but also a social problem.

Reasons leading to the birth of a premature baby

1. Socio-economic and demographic factors (family income and housing conditions, nutrition of the pregnant woman, nature of work

women, education, nature of medical care, etc.). IN last years the role of smoking, alcoholism, drug addiction has increased.

2. Socio-biological factors (age of parents, serial number of pregnancy, interval between births, outcome of a previous pregnancy, multiple pregnancy, etc.).

3. Clinical factors: 1) infectious diseases of the mother; 2) complications associated with pregnancy (preeclampsia); 3) traumatic damage to the uterus (previous abortions); 4) isoserological incompatibility of maternal and fetal blood; 5) anomalies in the development of female genital organs; 6) diseases of the mother, including sexually transmitted infections; 7) neuroendocrine pathology of the mother; 8) chromosomal abnormalities of the child.

In most cases, the combination of unfavorable factors that cause premature birth of a child determines its functional maturity and development rates in the postnatal period.

Anatomical and physiological features of a premature baby

Morphological features: body disproportionate, lower limbs and neck are short, the umbilical ring is low, the head is relatively large. The bones of the skull are pliable, the sutures and fontanelles are open. The auricles are soft, tightly pressed to the head. On the skin of the back, in the area of ​​the shoulders, on the forehead, cheeks and thighs - abundant lanugo, the skin is thin, physiological erythema is clearly expressed. The subcutaneous fat layer is thinned or absent, remaining only in the cheek area. Nails often do not reach the fingertips. The genital gap in girls gapes, since the large labia do not cover the small ones. The testicles in boys are not lowered into the scrotum.

Premature babies are characterized by anatomical and functional immaturity of the CNS, which determines their features: lethargy, drowsiness, decreased muscle tone, weak cry, underdevelopment of swallowing and sucking reflexes, imperfection of thermoregulation. The severity of symptoms depends on the gestational age of the baby. Reactions to various stimuli are characterized by generalization, weakness of active inhibition, and irradiation of excitation.

In premature babies, a suppressive orientation of the reactions of the cells of the immune system is observed, which has a great biological meaning: to prevent the development of pathology with a powerful flow of antigenic effects on the body immediately after birth. Features of the nonspecific reaction of the immune system: rapid depletion of the bone marrow granulocytic reserve, low chemotactic activity, insufficiency of activation of the complement system, imperfect phagocytosis, the ability of leukocytes to produce interferon is significantly reduced. There is an immaturity of intercellular interactions that determine both the primary nonspecific defense reaction and the maturation of B-lymphocytes and a specific immune response. The lower the gestational age, the more these indicators are reduced. Humoral protective reactions are provided mainly by maternal antibodies, which (IgG) mainly come to the fetus in the third trimester of pregnancy. "Physiological" immunodeficiency determines the low resistance of premature infants to opportunistic flora, a tendency to generalization of the infectious process, septic conditions, and high sensitivity to viral infections.

The endocrine glands are structurally differentiated by the time of birth, but their functionality during the period of adaptation is limited. The impact of harmful factors leads to overstrain, and then to the depletion of the function.

The respiratory rate of a premature baby is variable (36-82 per minute), the more, the less the body weight of the child. Breathing is characterized by a smaller and uneven depth, lengthening of individual inhalations and exhalations, and the appearance of different durations of respiratory pauses. The diversity of the rhythm of respiratory movements is determined by the large representation (80%) of the activated phase of sleep in preterm infants (the homologue of paradoxical phase sleep in adults). The degree of morphological maturity of the lungs depends on the gestational age of the child and the conditions of its intrauterine development. In those born before the 28-30th week of pregnancy, the alveoli and the capillary network of the lungs are not developed, the extensibility of the lungs is low, and the production of surfactant is insufficient, which leads to the appearance of respiratory disorders during the transition to new environmental conditions.

The heart rate in premature babies, as well as breathing, is variable (130-150 per minute), arterial

nal pressure is lower in the first days and rises by the 3rd-4th day (85/40 mm Hg). The restructuring of hemodynamics after birth, associated with the beginning of the functioning of the pulmonary circulation, occurs the slower, the lower the gestational age of the child and the more pronounced the morphofunctional immaturity of the lung tissue. All this predisposes to the occurrence of hemodynamic disorders with the appearance of concomitant pathology.

A small volume of the stomach, the predominance of the tone of the pyloric sphincter over the cardiac sphincter, weak intestinal motility determine frequent regurgitation and bloating. The volume of gastric juice in premature babies is 3 times less than in full-term ones, pH is 4.4-6.6. Reduced content of gastrin, chymosin, pepsin, motilin, low activity of the enzymes trypsin and chymotrypsin, lactase, enterokinase, leucine aminopeptidase, alkaline phosphatase. In premature babies, the activity of enzymes in the mucous membrane of the small intestine, where lactose is digested under the influence of lactase, is reduced, and therefore incomplete digestion and fermentation are possible. The activity of enzymes is the lower, the greater the degree of prematurity.

Daily diuresis ranges from 60 to 130 ml, the frequency of urination is 8-13 times a day, the volume of urination is from 1.5 to 15 ml. Functional features of the kidneys: low glomerular filtration volume, reduced tubular reabsorption of water, almost complete reabsorption of sodium entering the tubular system, poor renal response to the administration of diuretics. In premature babies, the concentration ability of the kidneys, renal osmoregulation and the ability to maintain the acid-base state are less perfect than in full-term babies.

Water-salt homeostasis

The water content in the body of a newborn baby is high. In premature babies with a body weight of 1500-2000 g, it is 80-85%. As the child grows, the water content in the body decreases, which is explained by an increase in the structural cellular material, primarily protein. Most of the water in newborns is extracellular fluid. In premature babies, it accounts for 42.5% of body weight. However, if we calculate the water content in the body per unit of body surface, it turns out that the excess of water is not so great. This indicates a special

buyu tension of water exchange and makes premature babies especially sensitive to the violation of water balance.

Premature babies have a higher circulating blood volume per kilogram of body weight at birth than full-term babies. From the first minutes after birth, the redistribution of the extracellular fluid begins, the outflow of blood from the vessels into the interstitial space occurs, which, with a low content of protein in the plasma, leads to widespread edema.

The fate of water in the body and its excretion are related to the electrolyte composition of body fluids. The osmotic concentration of plasma varies widely and ranges from 252 to 354 mosm / l, the highest figures are observed in less mature children. Almost half of the osmolar plasma concentration is determined by sodium, the concentration of which is 154-165 mmol / l. The content of potassium in the blood of premature babies ranges from 3.5 to 6.5 mmol / l.

Under normal conditions, a newborn child loses more than 1-1.2 g/kg/hour of water by perspiration. Exsicosis develops especially easily and poses a great danger to a premature baby, since acidosis also deepens at the same time.

Acid-base state (ACS) of the blood

The CBS of blood is an important indicator of the process of adaptation of a premature baby to extrauterine life. The average blood pH value immediately after birth is 7.25, normalization occurs only by the 12th hour of life, but the instability of this indicator remains. With any adverse effect, acidosis easily occurs.

nitrogen homeostasis

In the first days of life, when a newborn does not receive enough dietary protein, catabolism processes predominate, which leads to an increase in the content of nitrogenous products in the blood, especially in very premature babies. Their transition from the catabolic phase of protein metabolism to the anabolic phase is slowed down as a result of the fact that with a lack of fat and glycogen stores in the body, they begin to use protein for energy purposes.

Carbohydrate homeostasis

The energy needs of the intrauterine fetus are covered solely by glucose from the mother's blood, and in

the last terms of intrauterine development in the body of the fetus is a rapid accumulation of glycogen. The less mature the fetus is born, the less glycogen stores it has. From the first hours after birth, the blood sugar content begins to decline rapidly, reaching its minimum values ​​by the end of the 2-4th hour of life. Then glycemia begins to gradually increase towards the end of the first day of life. Premature newborns have low glycogen stores, so there is no increase in glycemia by the end of the first day. On the contrary, hypoglycemia can be observed, often accompanied by clinical symptoms: anxiety, tremor of the limbs, tachycardia, respiratory distress, and even clonic convulsions. Hypoglycemia deepens the state of acidosis, since the lack of glucose inhibits the oxidation of ketone bodies to carbon dioxide and water.

lipid homeostasis

As a source of energy, the newborn body uses its own fat, the reserves of which in premature babies are low. With the rapid depletion of carbohydrate reserves, the oxidation of fatty acids does not occur completely. Therefore, already in the first 12 hours of life in premature babies, there is a significant increase in the blood of ketone bodies, the concentration of which increases up to the 2nd week of life, which enhances and maintains metabolic acidosis. Along with this, they are deficient in polyunsaturated fatty acids, namely linoleic and α-linolenic (ω3 and ω6), as well as long-chain polyunsaturated fatty acids (DLPUFA), especially arachidonic (AA) and docosohexaenoic (DHA). The latter are included in the structural lipids of the cell membranes of the brain, retina and other tissues, ensuring their normal function, and affect the properties of receptors, the activity of ion pumps, the synthesis of specific proteins and enzymes, and the transfer of signaling molecules. DLPUFAs are precursors of eicosanoids that modulate the body's inflammatory and immune responses.

Hyperbilirubinemia

In premature newborns during the period of adaptation, jaundice is observed due to increased hemolysis of erythrocytes and immaturity of the enzymatic system of the liver. The maximum concentration of indirect bilirubin in the blood is reached by the 5-8th day of life, jaundice persists for up to three weeks or more. Indirect bilirubin is not

dissolves in water and is therefore not excreted in the urine. With excessive formation, it accumulates in cell membranes, especially in nerve cells, and disrupts the process of cellular respiration and metabolism. The development of bilirubin intoxication in premature infants can be facilitated by: 1) a reduced ability to bind plasma proteins due to their hypoalbuminemia; 2) severe hypoglycemia, since glucose is involved in the process of transformation of indirect bilirubin in the liver cells; 3) hypoxia, in which the permeability of cell membranes for bilirubin increases. Symptoms of bilirubin intoxication: general lethargy of the child, muscle hypotension, decreased sucking reflex, respiratory failure.

thermoregulation

Premature infants have a reduced ability to generate heat due to low reserves of brown fat, low muscle tone, and malnutrition in the first days of life. At the same time, heat transfer is increased due to the large surface of the body and the weak development of the protective fatty layer, as well as the peculiarities of the blood supply to the skin (superficial location of the vessels) and the prevalence of vasodilating reactions. All this creates the possibility of rapid cooling of the body of a premature baby, while acidotic shifts increase, capillary permeability increases, and edema occurs. Premature babies also have immaturity of the heat-regulating structures of the central nervous system, as a result of which the child may suffer not only from cooling, but also from overheating.

Under the right conditions for caring for a premature baby, his axillary body temperature is kept within 36-37?. In the first days of life, daily temperature fluctuations (up to 1?) can be observed, but over time they become insignificant (0.3-0.5?).

Thus, the degree of morphofunctional maturity of a premature baby determines the ability to implement adaptive reactions and survive in new environmental conditions.

Organization of nursing of premature babies

In Russia, a two-stage system for nursing premature babies is provided. The first stage is a specialized maternity

pre-term birth house or separate rooms for intensive care and therapy for premature babies in a conventional maternity hospital. The second stage is a specialized hospital or department for the treatment and care of premature babies transferred from maternity hospitals. The transfer of premature babies to the second stage of nursing is determined by age in days, body weight, clinical condition and is carried out no earlier than the 8th day of life.

The basic principles of nursing: 1) ensuring optimal temperature and humidity conditions for the child (special conditions of the delivery room and special incubators are provided for this); 2) in the delivery room and at subsequent stages, the principle of caution and care should be strictly observed, the number of manipulations in relation to the child should be minimized; 3) observance of asepsis in care, prevention of infection; 4) timely and adequate correction of homeostasis disorders; 5) individual approach to the choice of the start time and method of feeding the child using for this purpose mother's unpasteurized milk or, in its absence, adapted milk mixtures. Feeding a premature baby is a problem, the successful solution of which depends on the experience and skill of doctors and nursing staff. Therefore, nursing of premature babies (especially those with low and extremely low body weight) should be carried out by highly qualified medical personnel.

Many premature babies need intensive care from the first hours of life. The main therapeutic measures in premature newborns are reduced to the fight against hypoxia, the correction of acidosis, the maintenance of water-salt homeostasis, the function of external respiration, the cardiovascular system, and the replenishment of energy resources. In the presence of infectious processes, the use of antibiotics is required, taking into account the etiological factor and immunocorrective therapy. The task of nursing and treating a premature baby is to save life and prevent adverse consequences caused by the pathology that caused his premature birth and postnatal disease.

Chapter 2

Respiratory distress syndrome (RDS) (hyaline membrane disease)

SDR is a severe violation of the function of external respiration in the early neonatal period in premature babies, due to lung immaturity and primary surfactant deficiency.

ICD-X code - R 22.0.

This pathology is observed in children whose gestational age is less than 34 weeks, as well as in those born to mothers with diabetes mellitus. The frequency of occurrence is higher, the lower the gestational age of the child: 60-80% in those born before the 30th week of pregnancy and 25-35% in those born at the 30-34th week. Prophylactic use of corticosteroids by pregnant women reduces the incidence of SDR by 2 times.

Pathogenesis

The development of SDR is based on: 1) morphological immaturity of the lung tissue (insufficient development of the alveoli and vascular system); 2) immaturity and / or hypoxia-induced dysfunction of cells that produce a surfactant - surfactant; 3) disorder of microcirculation in the lungs due to vasospasm and / or violation of the rheological properties of blood; 4) immaturity of the central nervous system and mechanisms for regulating the rhythm and depth of respiratory movements. Ultimately, the leading pathophysiological mechanism for the development of SDR and its severity depend on the degree of impairment of the listed functions and their combinations.

Surfactant - a substance consisting of phospholipids, neutral lipids and proteins, is produced by type II alveolocytes from the 20-24th week of intrauterine development and provides, from the beginning of the first breath of the child, a decrease in the surface tension force in the alveoli and maintaining their stability during breathing. In addition, surfactant has bactericidal activity and stimulates the function of macrophages in the lungs.

Insufficiency of surfactant against the background of morphological immaturity of the lung tissue and blood vessels leads to the collapse of the alveoli on exhalation,

which contributes to the formation of widespread atelectasis. At the same time, gas exchange is disturbed, anaerobic glycolysis is activated, and metabolic acidosis develops. Under the influence of acidosis, spasm of the pulmonary arterioles increases, which leads to impaired lung perfusion and to intrapulmonary blood shunting, which increases hypoxemia. At the same time, under these conditions, the permeability of the pulmonary vessels increases, the penetration of plasma proteins into the interstitial space and into the lumen of the alveoli, which leads to the formation of hyaline membranes.

Changes in the function of external respiration in SDR are manifested by a decrease in lung compliance, functional residual capacity, tidal volume of alveolar ventilation and perfusion, and an increase in resistance respiratory tract on the inhale.

Clinical characteristics of SDR

SDR develops in the first minutes and hours of a child's life. There is a persistence of pronounced local or general cyanosis, despite the presence of breathing. In this case, breathing is superficial difficult. Auxiliary muscles are involved in the act of breathing (drawing in of the compliant places of the chest), shortness of breath (more than 60 breaths per minute) and expiratory moan ("grunting" exhalation) are observed. The severity of clinical symptoms, the rate of their increase correlate with auscultatory data: the weakening of respiratory sounds up to their complete absence in certain areas of the chest and the appearance of fine bubbling rales in the lungs. Evaluation of several clinical parameters over time allows obtaining an objective idea of ​​the rate of development and severity of respiratory disorders (modified Downes scale) (Table).

The radiographic picture depends on the time elapsed after birth and the severity of the disease: from a slight decrease in pneumatization to its almost complete absence (“white lungs”). A characteristic picture of the disease of hyaline membranes of the lungs: a diffuse decrease in the transparency of the lung fields, a mesh pattern, areas of enlightenment in the region of the lung root (air bronchogram).

The study of CBS of blood reveals the presence of uncompensated respiratory or respiratory metabolic acidosis and a decrease in oxygen tension (hypoxemia). A clinical blood test in the first hours of life has no characteristic features.

Differential diagnosis: transient tachypnea of ​​newborns, pneumonia, amniotic fluid aspiration syndrome.

SDR Severity Assessment

Note. A score of 3-4 points corresponds to a mild severity of SDR; 5-6 points - moderate; more than 6 points - severe SDR.

Treatment

1. Ensuring an adequate temperature regime, humidity and protective regime.

2. Monitoring the state of vital functions (registration of heart rate, respiration, blood pressure, blood oxygen saturation).

3. Elimination of surfactant deficiency by introducing surfactant preparations: "Surfactant HL", (Russia); Surfactant BL (Biosurf, Russia); Curosurf (Chiesi Farmactutici Parma, Italy); Exosurf neonatal (Glaxo Wellcome, UK).

4. Oxygen therapy to maintain arterial blood pO 2 at 50-80 mm Hg. Art. by creating a constant positive pressure in the airways during spontaneous breathing through nasal cannulas or an endotracheal tube during mechanical ventilation.

5. Therapy aimed at maintaining water and electrolyte balance, correcting acidosis, replenishing the energy costs of the body. In the presence of hypovolemia and arterial hypotension, along with the replenishment of fluid volume, cardiotonic drugs (dopamine, dobutamine) are prescribed.

6. Antibacterial therapy.

7. As the child's condition improves, start enteral nutrition early.

Complications of SDR

In the acute period: interstitial pulmonary emphysema, pneumothorax, pneumomediastinum, functioning open ductus arteriosus, intraventricular hemorrhage, bacterial infection. Long-term effects: bronchopulmonary dysplasia (5-30% of survivors), retinopathy of prematurity, psychomotor retardation.

Mortality in SDR is 10-15% in Russia.

HEMOLYTIC DISEASE OF THE NEWBORN

Hemolytic disease of the fetus and newborn (HFN) is a form of pathology caused by the immunological incompatibility of the blood of the mother and fetus for various erythrocyte antigens.

ICD-X code.

P55 Hemolytic disease of the fetus and newborn. P55.0 Rh isoimmunization of the fetus and newborn. P55.1 ABO - isoimmunization of the fetus and newborn. P56 Fetal dropsy due to isoimmunization. P57.0 Kernic jaundice due to isoimmunization.

Epidemiology

In Russia, HDN is diagnosed in 0.6% of newborns.

Classification

Depending on the form of the conflict, the incompatibility of the blood of the mother and child is distinguished by the Rh factor, by the AB0 system and by rare blood factors.

Clinical forms of HDN: anemic, icteric, edematous. According to the severity of jaundice and anemia, there are mild, moderate and severe degrees of the disease. Complications of HDN: kernicterus, bile thickening syndrome.

Etiology

A conflict is possible in the case of an Rh-positive (Rh +) fetus from an Rh-negative mother. With group incompatibility, the mother has predominantly O (I) blood type, and the fetus has A (II) or B (III). Much less often, HDN occurs when there is incompatibility of blood

mother and fetus for other erythrocyte antigens. Currently, more than 10 isoserological systems of erythrocyte antigens are known.

The frequency of HDN due to incompatibility according to the ABO system is 1:200-256 births, occurs when the barrier function of the placenta is impaired already during the first pregnancy.

The Rh factor is represented by a system of antigens (D, C, E, c, e), among which the D antigen is the most immunogenic. 85% of people of the European race are Rh-positive. If an Rh-negative woman is pregnant by an Rh-positive man, then the fetus has a 50% chance of being Rh-positive like the father.

Group antigens of the ABO system are found in the erythrocytes of the embryo from the 5-6th week, and the Rh factor - at 8 weeks of pregnancy. Fetal erythrocytes are detected in the maternal circulation in the third trimester of pregnancy, but immunization during the first pregnancy is rare (in about 1% of Rh-negative women), which is facilitated by a complicated pregnancy. Most often, the primary stimulus for the development of isoimmunization occurs during childbirth, especially in the presence of surgical interventions that increase the transplacental transfer of fetal erythrocytes into the mother's bloodstream. After the first pregnancy with an Rh-positive fetus, 10% of Rh-negative women are sensitized.

In response to the antigen entering the mother's body, antibodies are formed that belong to the class of immunoglobulins M, G, A. Based on the difference in serological properties, they are divided into "complete" (IgM), agglutinins and "incomplete" (IgG and IgA). IgG antibodies have a lower molecular weight than "full" antibodies, and therefore easily cross the placenta, being the main cause of development in the fetus hemolytic disease.

Pathogenesis

When maternal antibodies enter the fetus, they bind to antigen-containing erythrocytes, which leads to their hemolysis. As a result of developing anemia, compensatory mechanisms are activated, aimed at increasing the production of red blood cells. The formation of young forms of erythrocytes in the bone marrow is stimulated, foci of extramedullary hematopoiesis appear in the liver and spleen, and hepatosplenomegaly is formed. The predominance of the process of hemolysis of erythrocytes

over hematopoiesis leads to the development of anemia and hypoxia in the fetus. As a result of hemolysis of erythrocytes, an excessive formation of indirect bilirubin occurs, the release of which, to a certain limit, is carried out through the mother's body. With excessive accumulation of bilirubin, its toxicity is manifested, which leads to a violation of tissue metabolism, liver function, especially protein synthesis. Hypoproteinemia, hypoalbuminemia, hypertension in the portal and umbilical veins develop, and the permeability of the vascular wall increases. As a result of stagnation in the systemic circulation, fluid sweats out in the tissues and cavities, and anasarca develops.

Clinical picture

Hemolytic anemia without jaundice and dropsy - the least common and most mild form of the disease. Pallor of the skin, muffled heart sounds, systolic murmur, tachycardia are noted. In the blood, the number of red blood cells and hemoglobin is reduced.

Hemolytic anemia with jaundice - the most common and severe form of the disease. Jaundice can be observed already at birth or appears in the first 24 hours of life. Characterized by an increase in the size of the liver and spleen, some pallor of the skin. In severe cases, icteric staining of amniotic fluid, primordial lubrication, and umbilical cord membranes can be observed. In case of a conflict according to the ABO system, jaundice of the skin appears later - on the 2nd day, but its intensity rapidly increases by the 3rd-4th day of life. In the blood, there is a moderately pronounced anemia of a normochromic or hyperchromic nature, reticulocytosis, normoblastosis, and the level of indirect bilirubin exceeds 51 μmol / l. The severity of the developing disease depends on the rate of erythrocyte hemolysis, the accumulation of bilirubin, the rate of its conjugation in the liver, excretion through the kidneys and the gastrointestinal tract. The intensity of the hourly increase in bilirubin exceeds 5.1 µmol/l/h.

Hemolytic anemia with jaundice and dropsy - the most severe form of hemolytic disease, in which children are born dead or die shortly after birth. There is a sharp pallor of the skin with an icteric tint, general edema, ascites, enlargement of the liver and spleen, hemodynamic disturbances. Respiratory disorders and hemorrhages often develop

chesky syndrome. In the blood, severe anemia, normoblastosis, erythroblastosis, hypoproteinemia, hyperbilirubinemia are detected.

The severity of hemolytic disease is determined by the severity of the main symptoms at birth (jaundice, anemia, enlargement of the liver and spleen, edema) and the rate of their increase in the subsequent hours of the child's life. The severity of HDN is determined by the degree of prematurity of the child, which determines the prognosis for life and the development of complications. The most severe complication - kernicterus - occurs as a result of damage to the nuclear formations of the brain stem, cerebellum with indirect bilirubin, which is highly soluble in lipids of cell membranes. The first symptoms of bilirubin intoxication: a decrease in sucking activity up to the complete disappearance of the sucking reflex, the appearance of apnea attacks, fever, lethargy, and the development of convulsive syndrome.

Diagnosis of hemolytic disease

1. Evaluation of the mother's medical history (Rh-negative blood, blood type O (I), presence of antibodies in the blood, indications of hemolytic disease in previously born children, miscarriages, stillbirths).

2. During the physical examination of the newborn, the identification of clinical signs of hemolytic disease and monitoring the dynamics of their increase.

3. Determination of the child's blood type and Rh factor, as well as the level of bilirubin in the cord blood. Statement of direct and indirect Coombs reaction. If necessary, conduct additional studies to identify the incompatibility of the blood of the mother and child for rare factors.

4. Determination of the hourly increase in bilirubin.

5. Evaluation of a clinical blood test (erythrocyte count, hemoglobin, hematocrit, the presence of normoblastosis and erythroblastosis).

Treatment of hemolytic disease

In the antenatal period of a child's life, therapeutic measures are aimed at reducing the degree of erythrocyte hemolysis and preventing the development of severe anemia. They use therapeutic and prophylactic non-invasive methods of treatment (desensitizing therapy with antigens, plasmapheresis, lymphocytoimmunotherapy, pro-

prevention of placental insufficiency). With severe sensitization of a pregnant woman and when a severe form of hemolytic disease is detected in the fetus, an invasive method of therapy is used - an intravascular blood transfusion is performed on the fetus.

After the birth of a child, the main goal is to prevent toxic concentrations of indirect bilirubin in the blood in order to avoid disabling kernicterus. The following methods of treatment of indirect hyperbilirubinemia are used: 1) exchange transfusion, in which bilirubin and antibodies are removed; 2) phototherapy aimed at converting indirect bilirubin into a water-soluble photoisomer of lumirubin that does not have a neurotoxic effect; 3) intravenous administration of standard immunoglobulins, which contributes to the blocking of Fc-receptors of cells of the reticuloendothelial system and inhibition of further hemolysis of erythrocytes; 4) the use of sorbents to bind bilirubin in the gastrointestinal tract.

Forecast

The prognosis is favorable with timely effective treatment. With the development of nuclear jaundice, the death of a child or the formation of cerebral palsy is possible. In severe edematous form, the prognosis is unfavorable for the life and subsequent development of the child.

Prevention of Rh sensitization

In the antenatal clinic, when registering pregnant women, it is necessary to determine the blood type and Rh-affiliation. With Rh-negative blood in a pregnant woman and Rh-positive blood in her husband, it is necessary to determine the presence of antibodies in her. In the absence of antibodies, re-screening is performed at 24 and 28 weeks of gestation. In the absence of antibodies at 28 weeks, prophylaxis of Rh sensitization is carried out with the appointment of anti-D immunoglobulin. After childbirth (no later than 72 hours), anti-D immunoglobulin is administered in the event of the birth of a Rh-positive child. It is necessary to administer anti-D immunoglobulin to all Rh-negative non-sensitized women after abortions and miscarriages at a short term of pregnancy, with invasive procedures during pregnancy, with placental abruptions.

Chapter 3

Intrauterine infections

Intrauterine infections are infectious diseases of newborns, the infection of which occurred before birth as a result of the penetration of the pathogen from the mother's body. The gestational age at which this happened largely determines the nature of the infectious process. So, when infected in the embryonic period, malformations are formed or the death of the embryo occurs. Infectious processes in the early fetal period (4-6 months of pregnancy) can be expressed in a violation of the normal development of the body's functional systems, mainly the central nervous system. When infected after the 27th week of pregnancy, the infectious disease of the fetus is accompanied by the same inflammatory reactions and clinical symptoms that are observed in newborns. The outcome of infectious diseases in the antenatal period may be different: the fetus may die before birth, be born sick, or have residual effects of the disease at birth. Infection of the fetus can also occur during birth by contact, as well as by aspiration and ingestion of infected mucus from the birth canal or infected amniotic fluid. With intranatal infection, the first signs of the disease may appear in a child in different dates after birth (from several hours to several days), which depends on the virulence of the pathogen, the severity of infection and the condition of the fetus at the time of birth.

Ways of transmission of infection to the fetus

1. Transplacental route - the direct entry of the pathogen from the mother's blood into the blood of the fetus or the primary lesion of the placenta, followed by infection of the amniotic membranes, umbilical cord and amniotic fluid.

2. Ascending way - the infectious agent comes from the vaginal canal or cervix, then inflammatory foci in the fetus are found most often in the lungs and in the gastrointestinal tract as a result of aspiration and ingestion of infected amniotic fluid.

3. Penetration of the infectious agent from the mother's abdominal cavity through the fallopian tubes with damage to the adjacent areas of the amniotic membranes and subsequent infection of the amniotic fluid.

On the way of penetration of an infectious agent from the mother's body to the fetus, there are protective barriers: the placenta and the fetal immune system, the effective protection of which depends on the gestational age of the child.

Any pathogens of acute or chronic infection of the mother can cause intrauterine infection in the child - these are viruses, bacteria, mycoplasmas, chlamydia, protozoa, fungi, etc.

In the ICD-X, intrauterine infections are presented according to the etiological principle in class XVI "Certain conditions that occur in the perinatal period" in blocks P35-P39 "Infectious diseases specific to perinatal period».

Infectious diseases specific to the perinatal period (P35 - P39).

P35 Congenital viral diseases. P35.0 Congenital rubella syndrome. P35.1 Congenital cytomegalovirus infection. P35.2 Congenital herpes simplex virus infection (Herpes simplex).

P35.8 Other congenital viral infections.

P35.9 Congenital viral disease, unspecified.

P37.0 Congenital tuberculosis.

P37.1 Congenital toxoplasmosis.

P37.2 Neonatal (disseminated) listeriosis. P37.3 Congenital malaria due to Plasmodium falciparum. P37.4 Other congenital malaria.

P39 Other infectious diseases specific to the perinatal period.

INTRAuterine VIRAL INFECTIONS

Congenital rubella - P35.0

Infection of the fetus occurs during a primary infection during pregnancy, since a previously transferred disease leaves a strong immunity. The risk of intrauterine infection with the rubella virus in the first 2 weeks of pregnancy approaches 100%, but as the gestational age increases, it decreases and is 30% at 16-20 weeks.

The classic triad in case of infection of the fetus in the first trimester of pregnancy: congenital heart disease, eye damage (cataract, glaucoma, chorioretinitis), hearing loss due to damage to the auditory nerve. With later infection: IUGR, neurological disorders due to CNS damage (meningoencephalitis), anemia, thrombocytopenia, jaundice, multiple hemorrhages.

Diagnosis consists in isolating the virus from urine and pharyngeal secretions and detecting low-avid anti-rube IgG antibodies in the blood. Treatment is symptomatic, as there is no specific antiviral chemotherapy. Sick children need isolation because they shed the virus for a long time. Prevention consists in the use of prophylactic vaccinations against rubella. Pregnant women are advised to avoid contact with children with rubella and persons communicating with them.

Herpetic infection - P35.2

The disease of newborns is usually caused by herpes simplex viruses (HSV) types 1 and 2, belonging to the subfamily Alphaherpesvirinae. The herpes virus is highly neurotropic.

The frequency of neonatal herpes is 1 case per 7500 births. Infection of the fetus occurs as a result of an infection that first occurred in a pregnant woman, less often during an exacerbation of a chronic infection. 30-40% of children become infected when passing through the birth canal if the mother has manifestations of genital herpes. With a primary disease of the mother in the first trimester of pregnancy, the virus, penetrating to the fetus by the hematogenous route, can lead to the formation of malformations (microcephaly, microphthalmia, calcifications in the brain tissue). Herpetic infection in more late dates pregnancy leads to stillbirth, and when infected immediately before childbirth or during childbirth, children experience an acute (generalized or local form) or latent course of infection.

The first symptoms of a herpes infection are already present at birth or appear in the first week of life. The child becomes lethargic, sucks badly. His body temperature rises, shortness of breath, tachycardia, jaundice appear. Vomiting and loose stools mixed with blood are sometimes observed. There are symptoms of CNS damage (convulsions, opisthotonus) - meningoencephalitis, encephalitis. Lethality is 80%. Children who survive develop microcephaly, hydrocephalus, mental retardation, and eye damage (chorioretinitis, cataracts, blindness).

With localized forms of herpetic infection, skin lesions in the form of vesicular erythema and eye diseases in the form of conjunctivitis, keratoconjunctivitis, chorioretinitis, and keratitis are possible.

The latent course of infection in the early neonatal period is possible in full-term children, which poses a risk of developing a chronic sluggish infection with the gradual development of neurological disorders.

Diagnosis of intrauterine herpetic infection is carried out on the basis of the clinical picture of the disease, the mother's medical history and the results of laboratory tests. The following methods are used: 1) examination of the contents of vesicles or scrapings from eroded skin areas by direct immunofluorescent method to detect the herpes simplex virus antigen; 2) detection of the virus genome in blood and cerebrospinal fluid by polymerase chain reaction (PCR).

Antiviral treatment is carried out with acyclovir. According to the recommendations of the Russian Association of Perinatal Medicine Specialists (2002), with isolated skin lesions, acyclovir is used at a dose of 45 mg/kg/day for 10 days. With a generalized form of infection, the dose of acyclovir is increased to 60 mg / kg / day. The duration of treatment is 14-21 days. With ophthalmic herpes, an eye ointment containing acyclovir is used.

Prevention is carried out by identifying pregnant women at high risk of vertical transmission of infection, treating them and choosing the most optimal method of delivery.

Cytomegalovirus infection (CMVI) - P35.1

Pathogen Cytomegalovirus hominis- DNA-containing virus of the family herpesviridae, subfamilies Betaherpesviriaae.

Cytomegaly virus is widespread among people, so the number of seropositive women of childbearing age reaches 90%. Changes in the immune system characteristic of pregnancy can contribute to the reactivation of persistent infection and atenatal or intranatal infection of the fetus. However, the greatest risk of intrauterine infection of the fetus and the development of severe forms of the disease is noted in the case of a primary disease of a pregnant woman with CMVI. The frequency of CMVI in newborns is 0.2-2.5%.

Penetrating into the cell, into its nucleus, the cytomegalovirus begins to actively replicate. At the same time, the nucleus increases in size, inclusions are determined in it, the cell hypertrophies and acquires a feature typical for cytomegaly - “owl's eye”. Peculiar giant cells are localized mainly in the epithelial tissue of various organs, primarily in the ducts of the parotid and other salivary glands, and in severe cases in the liver, spleen, lungs, kidneys, pancreas, and brain.

When the fetus is infected with cytomegalovirus, as well as with other viral infections, the manifestations of CMVI depend on the duration of pregnancy - infectious blastopathy, embryopathy, fetopathy.

In newborns, a generalized form of infection or its asymptomatic course is observed. Clinical signs of CMVI: IUGR, microcephaly, hepatosplenomegaly, jaundice, petechial rash and thrombocytopenia, chorioretinitis, symptoms of CNS damage (anxiety, tremor, convulsions or, on the contrary, deep depression of functions), according to ultrasound of the brain, hyperechogenicity of the periventricular zones is detected, a picture is often observed interstitial pneumonia.

Asymptomatic CMVI occurring in the early neonatal period in some children (5-17%) can lead to the formation of an inflammatory-degenerative process in the brain in the future and be one of the causes of cerebral pathology in childhood(sensory deafness, psychomotor retardation, minimal brain dysfunction, etc.).

Diagnosis of intrauterine CMVI is carried out on the basis of the mother's history, the clinical picture of the disease and the results of laboratory tests. The following methods are used: 1) detection of the virus genome in blood and cerebrospinal fluid using DNA hybridization and polymerase chain reaction (PCR), which reliably indicates a clinically significant activity of CMV replication;

2) serological examination - detection in the blood using enzyme immunoassay of specific IgG antibodies, the low avidity of which indicates the activity of the process. This is also indicated by the detection of specific IgM antibodies or a 4-fold increase in titers of anti-CMV-IgG antibodies in paired sera during examination of the child in dynamics after 3-4 weeks. However, if the titers of anti-CMV-IgG antibodies at birth are equal to the maternal ones, and upon re-examination they decrease by 1.5-2 times, then the antibodies detected in the child are maternal and therefore cannot serve as a diagnostically significant sign of CMVI in the child.

Treatment of CMVI in newborns is carried out with a specific hyperimmune anticytomegalovirus immunoglobulin - NeoCytotect. The action of the drug is based on the neutralization of extracellularly located viruses by the anti-CMV-IgG antibodies contained in the drug, which prevents the virus from infecting unaffected cells and thereby inhibits the spread of CMV in the body. Studies are being conducted on the effectiveness of treatment of intrauterine CMVI with α-interferons. Feeding a sick child with mother's unpasteurized milk containing anti-CMV antibodies prevents the active replication of the virus and contributes to the development of an asymptomatic form of the disease.

Children with intrauterine CMVI can be a source of infection for others, so it is not recommended to allow pregnant women to care for them.

adenovirus infection

Adenoviruses, DNA-containing viruses, constitute a large group, including 32 serological types, of which intrauterine infection of the fetus is most often caused by viruses of types 3 and 7. Adenovirus infection in humans can occur in a latent form, with prolonged persistence of the virus in the tonsils and adenoids. If during pregnancy there is an exacerbation of the infection, infection of the fetus may occur. Since adenoviruses have a cytopathic effect, contributing to the formation of intranuclear inclusions, changes in the chromosomal apparatus of the cell and inhibition of the process of cell division, they can cause developmental abnormalities in the embryo.

In pregnant women, the infection most often occurs in the form of catarrh of the upper respiratory tract. The course of the pathological process in the fetus

depends on the time of intrauterine infection, the degree of infection and the condition of the fetus. In severe illness, the fetus dies before birth or is born in a state of asphyxia. Adenovirus infection in a newborn manifests itself in the form of pneumonia, which is diagnosed already at birth or develops rapidly in the first hours of life, usually proceeds severely with severe symptoms of intoxication and fever. Adenovirus infection is characterized by damage to the conjunctiva of the eyes. In a severe generalized infection, membranous conjunctivitis, symptoms of CNS lesions such as encephalitis, and dyspeptic disorders may appear. In surviving children, the persistence of the virus persists for a long time.

Diagnosis is based on the data of the clinical picture of the disease (pneumonia with eye damage) in comparison with the history of the mother and the results of a blood and cerebrospinal fluid test to detect viral DNA.

influenza infection

Influenza viruses (A, B, C) contain RNA and have a short reproduction cycle. They are not characterized by cytopathic action.

During periods of influenza epidemic among the population, there was no clear correlation between the frequency of this infection in pregnant women and the frequency of intrauterine infection in fetuses and newborns. Intrauterine infection of the fetus with the influenza virus shortly before birth most often causes the development of pneumonia, which can be hemorrhagic in nature and be complicated by pulmonary edema. In premature infants, the infection is generalized with CNS involvement and hemorrhagic syndrome. A characteristic morphological sign of influenza pneumonia in newborns is a pronounced proliferation of the bronchial epithelium.

There is no etiotropic treatment, symptomatic therapy and prevention of secondary infection are carried out.

Enteroviral infections

The group of enteroviruses combines Coxsackie, ECHO viruses (each group contains more than 30 serological types) and poliomyelitis.

More often, the fetus is affected by Coxsackie B 2 , B 3 , B 4 and A 6 viruses, which have a cytopathic effect and a teratogenic effect.

Intrauterine infection caused by Coxsackie viruses in newborns occurs in the form of myocarditis, meningoencephalitis and hepatitis. Signs of the disease can be at birth or appear in the first days of life.

Along with severe generalized forms of infection, which give high mortality, a subclinical course of the disease is observed, which in most cases is diagnosed as a difficult postnatal adaptation. Clinically significant infection caused by ECHO viruses is not observed in newborns.

There is no etiotropic treatment, symptomatic therapy and prevention of secondary infection are carried out.

Viral hepatitis

HB infection in newborns g Ag-positive mothers occur in the same way as with other viral infections. Therefore, all pregnant women are screened for HB S Ag, with early onset and persistently progressive jaundice in newborns. If its immunological genesis is excluded, one should think about congenital hepatitis, which is characterized by an increase in the activity of ALT and AST, the appearance of a high fraction of direct bilirubin in the blood, and moderate discoloration of the stool. The size of the liver and spleen increases, the general condition of the child worsens, regurgitation appears, and in severe cases of the disease - hemorrhagic syndrome. Most children with congenital hepatitis survive, but the carriage of HB S Ag remains, which poses a risk of developing hepatocellular cancer. In the early neonatal period of a child's life, an asymptomatic course of the disease is also possible.

Diagnosis is based on the detection of specific antigen and antibodies.

Treatment of congenital viral hepatitis is symptomatic, it is possible to use a specific immunoglobulin against hepatitis B.

Prevention of hepatitis B. According to the recommendations of the Russian Association of Perinatal Medicine, newborns whose mothers are carriers of the hepatitis B virus are vaccinated in the first 12 hours of life. In cases where

a newborn due to the severity of the condition cannot be vaccinated in a timely manner, a single administration of specific immunoglobulin against hepatitis B is indicated with mandatory active immunization immediately after stabilization of the condition.

Newborns who have received a specific immunoglobulin against hepatitis B or a vaccine should be observed by a pediatrician and an infectious disease specialist for 1.5 years.

Intrauterine bacterial infections

Fetal diseases can be caused by various pathogenic and opportunistic bacteria, among which the leading place is occupied by streptococci, listeria and E. coli, causing acute and chronic inflammatory processes in a pregnant woman (tonsillitis, cholecystitis, pyelonephritis, cystitis, endocervicitis).

streptococcal infection

The frequency of intrauterine streptococcal infection is 1 case per 1500-2000 live births.

Group A streptococci often cause various acute and chronic inflammatory processes in the upper respiratory tract in humans. Group B streptococci are found in the vaginal flora, in the urine, and they can be the cause of postpartum diseases. Group D streptococci are common saprophytes of the human intestinal tract, but can cause inflammation in the biliary and urinary tracts. Therefore, infection of a child can occur with an exacerbation of a chronic infection of the mother, persistent bacteriuria, a long anhydrous interval in childbirth.

Generalized infection occurs with damage to the lungs (pneumonia), brain (meningitis, meningoencephalitis), urinary tract (pyelonephritis), heart (myocarditis), gastrointestinal tract (gastropathy). The clinical picture of the disease caused by streptococcus B often follows the pattern of persistent fetal hypertension or hyaline membrane disease of the lung, since streptococcus B affects alveolar pneumocytes and capillary endothelial cells and thereby suppresses the formation of pulmonary surfactant. Characterized by an increase in the size of the liver and spleen, hemorrhagic manifestations, in the study of blood - leukocytosis of a neutrophilic nature, a shift of the leukocyte formula to the left, thrombocytopenia.

Etiotropic treatment begins with antibiotics of the penicillin series, and then taking into account the sensitivity to antibiotics of the isolated pathogen. Immunocorrective and symptomatic therapy is carried out.

Prevention consists in the rehabilitation of chronic foci of infection in a woman at the stage of family planning and during pregnancy.

coli bacterial infection

Infection of the fetus with Escherichia coli occurs mainly in an ascending way, which is associated with the frequent presence of the microbe in the vaginal flora in pregnant women, the excretion of the microbe in the urine during pyelonephritis. In acute pyelitis and pyelocystitis, bacteremia sometimes occurs in pregnant women, and then E. coli can cause the formation of foci of inflammation in the placenta and infection of the amniotic fluid.

Fetal disease is more often caused by hemolytic strains Escherichia coli. The severity of the course of intrauterine infection depends on the massiveness of infection of the child and his gestational age. Premature babies may experience meningitis and meningoencephalitis, severe pneumonia. In full-term children, milder forms of the disease are observed: subfebrile condition, slow scarring of the umbilical wound, lethargy, jaundice.

Diagnosis is carried out taking into account the history of the mother and the results of microbiological examination of the mother-child pair.

Etiotropic treatment begins with the use of aminoglycosides, and then taking into account the sensitivity to antibiotics of the isolated pathogen. Immunocorrective and symptomatic therapy is carried out.

Prevention consists in the rehabilitation of chronic foci of infection in a woman at the stage of family planning.

Listeriosis

The disease is caused by a gram-positive bacillus from the Corynobacterium family, 4 serotypes of Listeria have been identified. Humans become infected through contact with infected animals or through ingestion of contaminated food or water. Listeriosis in pregnancy and

newborns - the most common form of infection in humans (75% of all cases of the disease). Listeriosis infection in women can occur without manifestation or with a picture of chronic pyelocystitis, endocervicitis. An exacerbation that occurs during pregnancy occurs with fever, chills, headache, pain in the lumbar region and catarrhal phenomena, therefore it is often regarded as a viral infection. Infection of the fetus occurs by hematogenous, transplacental or ascending routes. In this case, the intrauterine fetus becomes a source of massive intake of listeria in the mother's body. The result is premature termination of pregnancy, fetal death before birth, or birth in a state of severe asphyxia. After the birth of the fetus, the mother's temperature drops rapidly. After bacteremia, a septic process occurs in a child, ending with the appearance of miliary bacterial toxic necrosis and proliferative cell granulomas in various organs and tissues, the presence of which in the organs of a deceased child becomes a reliable confirmation of the diagnosis of the disease.

The clinical picture of severe listeriosis infection in newborns does not have specific features. There are respiratory and cardiovascular disorders, regurgitation, neurological symptoms (hyperexcitability or CNS depression syndrome), an increase in the size of the liver and especially the spleen. In full-term infants, there may be an increase in body temperature, and in premature infants, hypothermia. Anemia and the appearance of a small-nodular or small-roseolous rash on the skin of the abdomen, back, limbs, and less often on the face attract attention. The rash sometimes takes on a hemorrhagic character. Mortality in a generalized form of infection is 80%, a more favorable prognosis may be with localized forms of listeriosis infection.

The diagnosis of listeriosis is confirmed by the detection of the pathogen in the blood, urine, meconium, cerebrospinal fluid (inoculation on nutrient media).

Treatment includes antibiotics of the penicillin series in combination with symptomatic agents and immunomodulatory therapy.

Prevention consists in carrying out veterinary and sanitary and hygienic control in case of suspected listeriosis infection, as well as in the preventive treatment of pregnant women with suspected listeriosis.

Toxoplasmosis

Toxoplasmosis in newborns occurs only when a woman becomes ill during pregnancy or less than a week before its onset. The risk of transplacental transmission of infection increases from 17% in the first third of pregnancy to 75% in the last third. 1 out of 1000 fetuses is infected.

Clinical manifestations of intrauterine toxoplasmosis are largely determined by the period of infection of the fetus. If the infection occurred in the last third of pregnancy, the child is born in the stage of generalization of the process, and the disease proceeds with the clinical picture of sepsis. With earlier infection, the period of generalization of infection in the fetus ends in utero, and after birth, symptoms of encephalitis predominate or there are already irreversible changes in the central nervous system.

With toxoplasmosis, the fetus develops necrotic meningoencephalitis: there are miliary granules in the brain and spinal cord, necrosis of brain tissue, periventricular vasculitis and ulcers on the walls of the ventricles, cell infiltration of the pia mater and obstruction of the Sylvian aqueduct, cerebral calcifications. Clinical manifestations: convulsions, atony, areflexia, violations of thermoregulation and respiratory rhythm, paresis, in the later stages of the process - microcephaly, a significant delay in psychomotor development.

On the part of the eyes, necrotizing retinochoroiditis is noted, followed by the development of optic nerve atrophy, pseudocoloboma, cataracts, paresis of the eye muscles and microphthalmia.

Sometimes there is hepatosplenomegaly, loose stools, on the skin - maculopapular and petechial rash, less often - jaundice with erythroblastosis, interstitial pneumonia, myocarditis.

Diagnosis is based on clinical signs and laboratory findings. The presence of xanthochromic cerebrospinal fluid with protein-cell dissociation, intracerebral calcifications, leukocytosis with atypical lymphocytes, and peripheral blood eosinophilia greatly facilitate the diagnosis.

For the diagnosis of toxoplasmosis, ELISA is used, with the help of which specific IgM are detected.

Etiotropic treatment of toxoplasmosis is carried out not only in the presence of clinical manifestations of infection, but also in their absence, while an acute infection in the mother should be established. The use of pyrimethamine preparations (tindurin, daraprim, chloridine) in combination with sulfonamides is recommended. Macrolides are in second place in terms of effectiveness, but their advantage lies in less toxicity for newborns (sumamed, vilprafen).

Prevention of congenital toxoplasmosis is reduced to the treatment of a pregnant woman when acute toxoplasmosis is detected in her.

Chlamydia

Chlamydia are obligate intracellular microorganisms of the order chlamydiales, are widely distributed in nature and practically found in all surveyed species of mammals and birds. Among the numerous species of chlamydia belonging to the family Chlamydiaceae and members of the genus Chlamydia and genus chlamydophila, The primary human pathogens are Ch. trachomatis And Ch. pneumoniae

The incidence of chlamydial infection in children is closely related to that in the adult population with chlamydia caused by Ch. trachomatis, is the most common among sexually transmitted diseases. The frequency of infection in pregnant women ranges from 10 to 40%, depending on the contingent of the examined. All this determines the high risk of infection in newborns, the frequency of which is 70% if the infection is not treated during pregnancy and 12-14% when it is treated with macrolides. Chlamydial infection caused by Ch. fneumoniae, is the cause of outbreaks of respiratory diseases in adults in autumn and winter.

Chlamydia multiply only inside the cells of the host organism, so their presence in clinical samples is always evaluated as the presence of an infectious process. infectious form

chlamydia is an elementary body (EB), adapted to extracellular existence, metabolically inactive. The cell captures more than one ET by endocytosis, as a result of which several microcolonies of chlamydia may appear in its cytoplasm. 4-6 hours after infection, chlamydia reorganize through intermediate bodies into vegetative reproducing non-infectious forms - reticular bodies (RT). The latter enter the cell cycle, divide binaryly (only 8-12 cycles), daughter RTs are transformed into intermediate bodies and then again into elementary bodies - infectious forms of a new generation. The full cycle of development takes 48-72 hours, usually ends with rupture of the inclusion membrane, release of new EBs into the extracellular environment, and infection of other host cells.

The cycle can be inhibited under the influence of traditional transforming agents (for example, when using antibiotics - penicillins or cephalosporins), as well as under unfavorable conditions at the stage of functioning of the RT. As a result, L-like and abnormal forms of chlamydia with cell wall defects are formed, which can be transmitted to daughter cells during cell division, which leads to the persistence of the pathogen and the chronic course of the infection. When environmental conditions change (immune factors, hormonal changes in the host's body, exposure to occupational hazards), the normal structure of chlamydia is restored, which leads to the continuation of the cycle of their development and activation of the infectious process. Thus, entering the body and multiplying, chlamydia can simultaneously exist at various stages of development, including in the form of persistent forms that can turn into normal forms of the reproductive cycle at any time.

The source of intrauterine chlamydia caused by Ch. trachomatis and Ch. pneumoniae, is a mother who has had an acute infection during pregnancy or has a chronic persistent chlamydial infection. Infection of the child occurs antenatally or during childbirth, which depends on the localization and severity of the chlamydial inflammatory process. In most cases, vertical transmission of the pathogen is observed, which enters the mucous membranes of the conjunctiva, vulva or urethra, as well as the upper respiratory tract, gastrointestinal tract, by ingestion and / or aspiration of infected amniotic fluid. Except

In addition, infection of the child can occur by the transplacental route, as a result of which there is a generalization of the process with damage to the vascular system of the fetus. The lungs are affected less frequently and to a lesser extent than the brain and heart. However, if this happens, then the child is not viable, dies in childbirth or in the first hours and days of life. During ingestion and aspiration of amniotic fluid, the pharynx, trachea, bronchi, and alveoli are most often infected.

Intrauterine chlamydial infection in newborns has an acute or latent course, which depends on the gestational age at which infection occurred, its massiveness, the degree of morphofunctional maturity of the child and the presence of concomitant pathology associated with adverse conditions of intrauterine development. Acute chlamydial infection in the early neonatal period may have the following clinical forms.

1. Generalized infection with severe damage to the brain, lungs, heart, gastrointestinal tract, liver and other organs, leading to a violation of their function, the birth of a child in severe asphyxia and death in the first hours and days of life.

2. Meningoencephalitis with repeated attacks of clonic-tonic convulsions and apnea.

3. Intrauterine pneumonia.

4. Syndrome of respiratory disorders (in premature babies).

5. Gastroenteropathy.

6. Lymphadenitis.

7. Conjunctivitis.

It should be emphasized that 10-15% of children infected with chlamydia have an asymmetric form of intrauterine growth retardation (IUGR). The frequency of intranatal hypoxia is 30-40%, and the frequency of birth in asphyxia is 2-3 times higher than that in the population of full-term and premature babies.

In children infected with chlamydia, from the first hours of life, nonspecific signs of the disease are observed, indicating a violation of hemodynamics. First of all, symptoms of CNS damage appear not only in children who have undergone asphyxia, but also in those born in a satisfactory condition. There are increased anxiety and reactivity, sleep disturbance, changes in muscle tone, inhibition of physiological reflexes, tremor of the extremities, hyperesthesia of the skin, and regurgitation. Children are prone to rapid cooling. Long-lasting

local cyanosis, "marbling" of the skin. In the following days of life, despite the ongoing therapy, violations of the functional state of the central nervous system become stable, and in some cases an increase in neurological symptoms is observed. At the same time, in full-term children, the syndrome of CNS hyperexcitability most often predominates, short-term tonic-clonic convulsions may occur, while for premature children, the syndrome of depression of the CNS functions, the disappearance of the sucking reflex and the appearance of apnea attacks are more characteristic. The results of neurosonographic examination of the brain indicate the presence of long-term hyperechogenicity of the periventricular zones. In premature infants, echographic signs of intraventricular hemorrhage and moderately severe ventriculomegaly may appear.

The second manifestation of intrauterine chlamydial infection, running in parallel with the symptoms of the central nervous system or somewhat delayed, is a violation of the central hemodynamics. This is expressed in the muffled heart tones and the appearance of systolic murmur, the most intense closer to the base of the heart. According to the ECG data, there is an incomplete blockade of the right leg of the His bundle, a violation of metabolic processes in the myocardium, signs of overload of the right parts of the heart, and on an x-ray of the chest organs - an increase in the basal vascular pattern, "wet" lungs, bloating, an increase in the size of the heart due to its right departments ("spherical heart"). An echocardiographic study also reveals hemodynamic disturbances, increased pressure in the pulmonary circulation, signs of a change in the state of the endocardium and valvular apparatus of the heart in the form of an increase in the acoustic density of the leaflets, prolapse of the mitral and tricuspid valves.

Premature infants with intrauterine chlamydial infection have earlier clinical manifestations of the syndrome of respiratory disorders (already from the first hours of life), and, as a rule, there is a violation of the ventilation-perfusion relationship in the lungs, which requires the supply of ever-increasing oxygen concentrations in order to maintain tissue oxygenation at least for the lowest acceptable limits. The course of the disease is complicated by the long-term preservation of fetal shunts and often by an increase in cardiopulmonary insufficiency. In the most severe cases, hemorrhagic phenomena like melena or dis-

seminal intravascular coagulation. Surviving very preterm infants develop bronchopulmonary dysplasia in the future.

In the majority of full-term infants infected with chlamydia, respiratory disturbances during the first week of life are absent or mild, mainly in the form of difficulty in nasal breathing, slight shortness of breath and weakening of respiratory sounds. Only in children who have aspirated amniotic fluid, and in premature newborns, respiratory disorders in the clinical picture of the disease come to the fore: shortness of breath, participation of auxiliary muscles in the act of breathing, fine bubbling rales in the lungs. Inflammatory infiltration in the lungs, more often on the right, is detected in 60% of sick children by the end of the first, and in the rest - at the 2-3rd week of life.

Severe jaundice, which is a characteristic symptom of most intrauterine infections, occurs mainly in premature infants, in whom hyperbilirubinemia often requires an exchange transfusion.

With the defeat of chlamydia of the gastrointestinal tract, regurgitation, bloating, early appearance of diaper rash with a normal stool are observed. An increase in the size of the liver and spleen is detected in every third child.

Conjunctivitis manifests itself 3-4 days after birth, first with lacrimation, slight redness and swelling of the conjunctiva, then with the appearance of a mucopurulent discharge and an increase in the inflammatory reaction of the eyes.

Changes in the blood during chlamydial infection are expressed in moderate anemia, long-term preservation of relative neutrophilia, an increase in the number of eosinophils (> 7%) and monocytes (> 10%) by the 7-10th day of life. In full-term children in the first week of life, an increase in body temperature up to 38-39º can be observed, which is not associated with a maximum loss of body weight.

In cases where the infection of the fetus occurs in a vertical way shortly before delivery or during childbirth, the disease in full-term children in the early neonatal period of life has a latent course. Clinical symptoms appear later, most often children begin to get sick 3-6 months after birth, when passively acquired immunity is lost.

The infection caused Chl. fneumoniae, may occur during pregnancy. Its most frequent manifestations: weakness, fatigue, rhinitis or pharyngitis, subfebrile temperature, unproductive persistent cough. When a pregnant woman becomes ill, transplacental infection of the fetus can occur. In newborns, the development of intrauterine pneumonia is observed. X-ray examination reveals an increase in the pulmonary pattern and basal infiltration. There is a slow postnatal restructuring of hemodynamics (open foramen ovale) and overload of the right heart. Hyperechogenicity of the periventricular areas of the brain persists for a long time. Increasing thrombocytosis (>500x10 3 /mm 3), monocytosis (10-14%), eosinophilia (12-18%) is noted in the blood.

Diagnostics

The diagnosis of intrauterine chlamydial infection is established on the basis of clinical symptoms, serological studies, and epidemiological data.

When selecting children at risk of intrauterine infection Chl. trachomatis the mother's history should be reviewed. Consider previously diagnosed urogenital chlamydia, autoimmune diseases, chronic diseases of the respiratory system, gastrointestinal tract, urinary system, as well as indications of chronic adnexitis, ectopic pregnancy, inflammatory changes after abortion or previous births, the threat of termination of a real pregnancy, premature rupture of amniotic fluid, placental abruption. The presence in the anamnesis of indications of chronic diseases of the upper respiratory tract (sinusitis, tonsillitis), infection-dependent and aspirin bronchial asthma, as well as acute respiratory diseases suffered during pregnancy, makes it possible to suspect the possibility of infection Chl. pneumonia. Multiple stigmas of dysembryogenesis in a newborn, intrauterine growth retardation, symptoms of hypoxia and delayed hemodynamic restructuring, together with the data of the mother's history, are the basis for laboratory diagnosis of chlamydial infection

Materials for the study are scrapings from the conjunctiva of the lower eyelid, posterior pharyngeal wall and vulva, urine and blood. Washing waters of the tracheobronchial tree, stomach can be used.

Chlamydia detection methods: 1) "gold standard" - detection of chlamydia in L-929, McCoy, HeLa-920 cell culture; 2) detection of chlamydia antigen in the test material using specific antibodies connected to any label: direct or indirect immunofluorescent methods (PIF, NIF), immunoperoxidase and enzyme immunoassay methods (ELISA - detection of genus-specific lipopolysaccharide), direct and indirect immunofluorescence; 3) the method of polymerase chain reaction (PCR) - detection of the pathogen by repeated copying (amplification) of DNA sequences specific for chlamydia - highly sensitive (80-95%) and specific (about 92%); 4) serological methods that detect the presence of anti-chlamydial antibodies (ELISA with the determination of IgA, IgM, IgG).

Etiotropic treatment in the acute phase of the disease is carried out with macrolides (sumamed, vilprafen). For the treatment of a latent infection, a combination of Viferon-1 with Azithromycin (Sumamed, Pliva) is used.

Prevention of intrauterine infection of a child with chlamydia includes: 1) examination of all women when registering for pregnancy, as well as couples who apply to family planning clinics for infertile marriages; 2) if chlamydial infection is detected during pregnancy, mandatory treatment of married couples; 3) prevention of conjunctivitis by placing a child in the conjunctival sac of each eye with 1% tetracycline or 0.5% erythromycin ophthalmic ointment immediately at birth and again after 2 hours.

Early complex etiopathogenetic therapy of intrauterine chlamydial infection is the prevention of the formation of chronic persistent infection and related diseases in older children.

Mycoplasma infection

Mycoplasmas are the smallest free-living microorganisms, devoid of a cell wall and isolated in a separate class of bacteria. Mollicutes("soft-skinned"). Man is the natural host for at least 10 mycoplasma species, but highest value have Alycoplasma pneumoniae, Alycoplasma hominis, Ureaplasma urealyticum, Alycoplasma genitalium, Alycoplasma fermentans, Alycoplasma incognitis.

The source of infection is a person with mycoplasmosis, or a carrier of mycoplasmas. Transmission of infection can be carried out by airborne droplets, sexual contact, from mother to fetus (intrauterine or during childbirth). Mycoplasmas are able to persist, causing chronic infections. Role A.hominis in diseases of the genitourinary tract, septic abortion, puerperal fever is generally recognized. Connection established A.hominis And A. genitalium with the pathology of pregnancy, ending in miscarriages and premature births with a dead fetus and malformations in children. They also note a significant frequency of detection of lesions of the respiratory tract of the fetus and newborns infected with A.hominis.

Mycoplasmas occupy a special place among the sexually transmitted pathogens of the human urogenital tract. In recent years, there has been an increase in the number of pregnant women (up to 15%), in which mycoplasmas and ureaplasmas are detected during the study. The frequency of infection in children born to mothers whose genital tract was colonized by mycoplasmas and / or ureaplasmas is 18-30%. There are hematogenous and contact ways of transmission of infection to the fetus. The entrance gate of infection is most often the mucous membrane of the eyes, genitals (in girls) and the respiratory tract. Mycoplasma infection in a child can occur at various stages of intrauterine development and is often the cause of spontaneous abortions and premature births.

Intrauterine mycoplasmal infection does not have a characteristic clinical picture. Infection of a child during childbirth can cause conjunctivitis (in 1-2% of cases), skin lesions. Much less often, intrauterine pneumonia is observed, which is interstitial in nature and occurs with severe respiratory failure (rapid breathing difficulty, cyanosis). At the same time, there are no distinct physical phenomena from the lungs. Only later, with the development of the alveolar process, fine bubbling rales are heard in the lungs. In premature babies, mycoplasma pneumonia can develop against the background of hyaline membranes of the lungs. Sometimes intrauterine mycoplasmal infection takes on a generalized character with the defeat of all internal organs and CNS (meningoencephalitis). The temperature reaction in mycoplasmal infection is not typical, sometimes there is a high leukocytosis.

The combination of ureaplasma infection with bacterial infection leads to death in children with low birth weight (< 1500 г).

The presence of intrauterine infection with mycoplasmas or ureaplasmas in 83% of cases leads to early onset (up to 3 years) of pyelonephritis, more frequent relapses of the disease with high leukocyturia, microhematuria and crystalluria. The association of mycoplasmas contributes to the early onset of allergies.

The diagnosis of mycoplasmal infection is confirmed by the detection of the pathogen in scrapings from the conjunctiva, posterior pharyngeal wall, in the urine using polymerase chain reaction (PCR), the sensitivity and specificity of which is 92-98%.

For the treatment of mycoplasmal infection, macrolides are used: azithromycin (Sumamed), roxithromycin (Rulid).

After an acute infection, persistence of mycoplasmas may persist. Children infected with mycoplasma often have iron deficiency anemia, exudative diathesis, early pyelonephritis, and a tendency to frequent respiratory infections.

Candidiasis

Candidiasis is an infectious and inflammatory disease caused by yeast-like fungi of the genus Candida of which during intrauterine infection of children are most often detected candida albicans.

The frequency of intrauterine candidal infection in newborns has recently tended to increase (up to 1% of all cases of candidal infection in children early age) due to an increase in genital candidiasis in pregnant women, which is due to the widespread use of antibiotics and the characteristics of the state of immunity.

Infection of the fetus with fungi of the genus Candida occurs in the transplacental or ascending route. By hematogenous way, fungi enter the body of the fetus in the presence of candidal placentitis or in case of generalized mycotic disease of a pregnant woman, which is extremely rare. Most often, the child becomes infected by swallowing and / or aspiration of infected amniotic fluid, as well as by contact when passing through the birth canal if the mother has genital candidiasis.

Adhesive properties of fungi, their ability to proliferate and toxicity under conditions of imperfection of protective reactions in newborns.

born with physiological characteristics the structures of the skin and mucous membranes lead to the rapid development of an invasive mycotic process.

There are the following forms of intrauterine candidal infection: 1) candidiasis of the skin and mucous membranes; 2) visceral candidiasis; 3) generalized candidiasis. Skin candidiasis is characterized by the presence of infiltration of skin tissues, merging multiple papular elements with jagged edges, framed by a white rim of exfoliated epidermis. Typical localization is the skin around the anus, inner thighs and inguinal region. With mucosal candidiasis, easily removable white cheesy plaques are visible against the background of moderate hyperemia.

With visceral candidiasis in newborns, pneumonia, gastritis, enterocolitis, cystitis, pyelonephritis are diagnosed, the clinical manifestations of which are not characterized by the presence of severe infectious toxicosis. The generalized form of candidiasis proceeds with the involvement in the infectious process of several functional systems of the body, including the central nervous system (meningitis, meningoencephalitis). In blood tests, neutrophilic leukocytosis is noted with a shift of the leukocyte formula to the left, eosinophilia. In the study of cerebrospinal fluid, protein-cell dissociation is detected (a sharp increase in protein content with a slight increase in cellularity), cytosis (no more than 300-500 cells in 3 μl) of a neutrophil-lymphocytic nature.

Diagnosis of intrauterine candidal infection, especially in the presence of visceral and generalized forms, presents significant difficulties. It is based primarily on the data of the anamnesis of the mother and the results of bacteriological examination of the mother-child pair. The materials for the study are scrapings from the sites of skin lesions, mucous membranes, urine, gastric lavage, cerebrospinal fluid. Use the isolation of fungi of the genus Candida in the active state during microscopic examination and in cultures of material from the pathological focus, as well as by PCR.

For the treatment of intrauterine candidiasis, antimycotic drugs of local and systemic action are used, depending on the sensitivity established to them.

Diflucan, a representative of a new class of triazole compounds, has the least side effects in newborns, the fungicidal activity of which has been established when administered intravenously and orally, primarily in diseases caused by fungi of the genus Candida. For local treatment, preparations of 1% clotrimazole, which belongs to imidazole antifungal drugs (Clotrimazole, Kanesten, Candide, Microsporin, Nizoral), are effective. In severe cases of intrauterine fungal infection, immunocorrective and symptomatic therapy is used.

Prevention of intrauterine candidiasis in newborns is based on: 1) treatment of genital candidiasis in women of childbearing age; 2) active detection and treatment of dysbiocenosis of the birth canal in a pregnant woman; 3) treatment of the oral mucosa 2-4 times a day with nystatin in children at high risk of intrauterine infection with fungi of the genus Candida.

Asphyxia of the newborn

The ICD-X code is P21.

Asphyxia of the newborn - a pathological terminal state associated with a violation of the mechanisms of adaptation during the transition from the intrauterine existence of the fetus to the extrauterine.

At the heart of the pathogenesis of asphyxia of the newborn is a violation of hemodynamics in the fetus, resulting from a disorder of the uteroplacental circulation. Normally, immediately after birth, the child takes an intense first breath, which leads to the filling of the alveolar space with air, a decrease in the resistance of the vessels of the pulmonary circulation, an increase in blood flow in the lungs and an increase in systemic arterial pressure. Perfusion of oxygenated blood through the arterial circulation leads to closure of fetal shunts and accelerates postnatal circulation remodeling. In addition, the synthesis of surfactant is activated, which is necessary for the expansion of the lungs and their normal functioning.

According to the international classification of diseases of the X revision, two degrees of severity of asphyxia of newborns should be distinguished: severe and mild or moderate. To this end, all newborns are assessed on the Apgar scale.

Apgar assessment chart for newborns

Severe asphyxia: Apgar score in the first minute of life 0-3 points, by the fifth minute does not become higher than 6-7 points.

Mild or moderate asphyxia: Apgar score in the first minute of life 4-6 points, after 5 minutes 8-10 points.

Asphyxia of the newborn, as a rule, is preceded by fetal hypoxia, which occurs as a result of impaired oxygen delivery to tissues and / or its use in them. Accordingly, there are:

1) hypoxic hypoxia, when the saturation of hemoglobin with oxygen is below the normal level;

2) circulatory hypoxia, when oxygen does not reach the tissues in sufficient quantities, despite its normal tension in the arterial blood;

3) hemic (anemic) hypoxia with a significant decrease in the number of erythrocytes or a low content of hemoglobin in erythrocytes, as well as with a decrease in the ability of hemoglobin to bind oxygen;

4) tissue hypoxia in violation of cellular homeostasis, when cells are not able to fully use oxygen.

The fetus may experience long-term (chronic) or short-term (acute) hypoxia. Causes of chronic hypoxia: 1) mother's disease and unfavorable working conditions (occupational hazards), leading to the development of hypoxia in her; 2) complications of pregnancy and associated disorders of the development of the placenta and disorders of the uteroplacental circulation; 3) diseases of the fetus.

Causes of acute hypoxia: 1) inadequate blood perfusion to the fetus from the maternal part of the placenta (low pressure in the mother, etc.); 2) placental abruption; 3) clamping of the umbilical cord; 4) depletion of the compensatory-adaptive reactions of the fetus and the inability to tolerate changes in oxygenation associated with the contractile activity of the uterus, even under conditions of a normal birth act.

Factors contributing to the birth of a child in asphyxia

Mother's condition: 1) age of the primipara >30 years; 2) hypertension; 3) diabetes mellitus; 4) anemia (hemoglobin less than 100g/l); 5) chronic diseases of the kidneys, urogenital tract; 6) preeclampsia; 7) anomalies of attachment of the placenta; 8) polyhydramnios; 9) isoimmunization; 10) multiple pregnancy; 11) placental abruption and bleeding; 12) alcohol intoxication; 13) the use of drugs and psychotropic drugs; 14) infectious diseases; 15) chronic infections.

Conditions of birth and condition of the fetus: 1) anomaly in the position of the fetus; 2) breech presentation of the fetus; 3) premature rupture of fruit membranes; 4) prolonged or rapid childbirth; 5) complications from the umbilical cord; 6) the imposition of forceps or a vacuum extractor on the head of the fetus; 7) the introduction of sedatives intravenously one hour before birth or intramuscularly 2 hours before birth; 8) intrauterine growth retardation, macrosomia, postmaturity, prematurity, fetal deformities; 9) fetal hypoxia before and during childbirth.

Pathogenesis of fetal hypoxia and neonatal asphyxia

Hypoxia causes the fetus to turn on compensation mechanisms aimed at maintaining adequate tissue oxygenation: erythropoiesis is stimulated (activation of erythropoietin), the production of heme-containing proteins (hemoglobin, myoglobin, neuroglobin, cytoglobin) increases, the level of fetal hemoglobin, which has the highest affinity for oxygen, increases.

the formation of nitric oxide (NO) due to the activation of NO-synthase enzymes increases, the production of catecholamines, glucocorticosteroids, vasopressin, serotonin, melatonin and other neuropeptides increases.

Under conditions of ongoing hypoxia, the following occurs: 1) an increase in the intensity of uteroplacental blood flow; 2) an increase in vascular tone in the fetal body and, due to this, a reduction in a significant part of the vascular bed; 3) deposition of blood in the liver, which facilitates the systemic circulation of the fetus; 4) increase in systolic blood pressure and central venous pressure; 5) increase in cardiac output; 6) redistribution of blood with a predominant supply of the brain, heart, adrenal glands and a decrease in blood flow in the lungs, kidneys, gastrointestinal tract and muscles of the fetus. The inclusion of these processes ensures the maintenance of normal oxygenation of the brain, while the tension of carbon dioxide and pH of the blood remain within the normal range (pH> 7.25).

With prolonged hypoxia of the fetus or with an additional sharp decrease in the supply of oxygen to its bloodstream, the second stage of the reaction occurs: 1) anaerobic glycolysis increases; 2) glycogen is mobilized from the depot (liver, heart, kidneys); 3) phospholipases are activated. These processes contribute to the maintenance of energy processes in tissues, especially in the brain. In addition, the production of prostaglandins, which contribute to the expansion of small capillaries and improve microcirculation, is enhanced. The lengthening of this period leads to the accumulation of acidic metabolic products, peroxynitrite, CO 2 , which contribute to the development of tissue hypoxia and a decrease in oxygen consumption by fetal tissues. A characteristic feature of this stage is respiratory acidosis of the blood (pH = 7.2-7.24).

Under conditions of progressive hypoxia, meconium is discharged into the amniotic fluid, fetal bradycardia occurs, due to which the duration of diastole increases, which, in turn, improves the filling of the left ventricle and maintains the strength of heart contractions. This allows you to temporarily maintain normal cardiac output and systolic blood pressure. Under such conditions, cerebral blood flow is still sufficient for brain function, although there is already a redistribution of blood in the brain with a predominant supply of subcortical regions. At

This powerful factor in the regulation of local blood flow and microcirculation is the increased production of nitric oxide.

At the last stage of adaptation to hypoxia, compensatory-adaptive reactions are depleted, which leads to a significant decrease in oxygen tension and an increase in carbon dioxide tension and to the development of metabolic acidosis (pH< 7,2). Происходит: 1) падение сосудистого тонуса; 2) снижение системного артериального давления; 3) повышение центрального венозного давления; 4) развитие сердечной недостаточности; 5) снижение мозгового кровотока и гипоперфузия мозга; 6) нарушение метаболизма в нервной ткани.

In case of metabolic disorders in the nervous tissue, the following processes occur:

1) a violation of the synthesis of prostaglandins, accompanied by an increase in the content of thromboxane and prostaglandin F2a, which leads to narrowing of the capillaries, increased platelet aggregation and, as a result, to impaired microcirculation, thrombosis and ischemia of the brain tissue;

2) under conditions of cerebral ischemia, the extracellular concentration of excitatory amino acids (glutamate, aspartate) increases, which contributes to the depolarization of the cytoplasm of neurons and an increase in the permeability of cell membranes;

3) the functional activity of ATPases changes, as a result, the output of potassium from the cell increases and the intracellular sodium content increases, resulting in edema;

4) the concentration of intracellular calcium increases, the activation of phospholipases, lipid peroxidation increases;

5) hyperproduction of nitric oxide and excessive formation of peroxynitrite contribute to the development of apoptosis of nerve cells.

Severe irreversible metabolic acidosis develops (pH< 7,0), повышение проницаемости сосудистой стенки с выходом форменных элементов в межклеточное пространство (диапедезные кровоизлияния на вскрытии), необратимые изменения нервных клеток и их гибель.

Primary resuscitation is carried out for all liveborn children, regardless of their gestational age and body weight (> 500 g), according to the order of the Russian Ministry of Health of 28.12.95? 372 "On the transition to the recommended criteria of the World Health Organization criteria for live birth and stillbirth".

Immediately after the birth of the child, the midwife, using a balloon or catheter connected through a tee to an electric suction (a vacuum of not more than 100 mm Hg), sucks the contents of the upper part of the pharynx and nasal passages, applies clamps and cuts the umbilical cord.

After cutting off the umbilical cord, the newborn is quickly transferred to a warm table heated by a source of radiant heat, laid with his head slightly thrown back, with a folded diaper under his shoulders and back.

The child must be quickly wiped, since the loss of heat by evaporation is very large, and the mechanism of heat generation under hypoxia is broken. In children exposed to hypothermia, metabolic acidosis, hypoxia are aggravated, and hypoglycemia may develop.

The first stage of resuscitation is the rapid restoration of ventilation, lung perfusion and cardiac output.

At the birth of a child, the doctor should note: did spontaneous breathing appear, and if not, is there a heartbeat? Taking into account three signs (heartbeat, breathing patterns and skin color), he must immediately decide on the need for resuscitation and begin them no later than 15-20 seconds from the moment the child is born. The Apgar score should be used to evaluate their effectiveness at the end of the 1st and 5th minutes. The assessment should be repeated (only if spontaneous breathing occurs) every 5 minutes until the 20th minute of life.

If independent, but inadequate respiratory movements appear (convulsive gasping breaths or irregular, labored, shallow breathing), you should immediately start mechanical ventilation using a self-expanding bag (Ambu, Penlon, etc.) or Aira system through a face mask. The respiratory rate is 40 per minute, the oxygen concentration is 90-100%, the O 2 flow is not more than 10 liters per minute, the duration of the initial stage of ventilation is 15-30 s. In case of anomalies in the development of the upper respiratory tract and the inability to ensure their free patency, an oral airway should be used. It should fit freely over the tongue and reach the back of the throat, with the cuff remaining on the child's lips. Next, a minute after birth, the child's condition and the effectiveness of mask ventilation are assessed. If mechanical ventilation is continued through a mask (more than 1.5-2 minutes), a probe (? 8 Fr) is inserted into the child's stomach.

Ventilation with 100% oxygen through a mask using the Penlon apparatus or the Aira system appears to be quite effective.

at the birth of a child in moderate and mild asphyxia. In this case, the correction of acidosis occurs due to oxygenation and a decrease in RCO 2, which contributes to the expansion of the vascular bed of the lungs.

Tracheal intubation should be carried out immediately: 1) in the absence of respiratory movements and the presence of diffuse cyanosis; 2) with massive aspiration of meconium-stained amniotic fluid, requiring tracheal sanitation; 3) newborns whose gestational age is less than 28 weeks, even if they have superficial respiratory movements; 4) if a diaphragmatic hernia is suspected; 5) with ineffective mask ventilation for 1-2 minutes.

The intubation attempt should not exceed 30 seconds. If it is unsuccessful, then it is necessary to carry out ventilation through the mask using the AIRA system for 1 minute and only then make a 2nd attempt at intubation. Start artificial lung ventilation using the Aira system with 100% oxygen at a frequency of 40-50 per 1 minute and pressure at the first 3-6 breaths - 30-35, and then 20-25 cm of water. Art. with an oxygen flow of 8-10 liters per minute. In case of massive aspiration syndrome, before mechanical ventilation, it is necessary to sanitize the tracheobronchial tree with a 2% solution of sodium bicarbonate and suck out the contents of the stomach.

Intubation and ventilation of the lungs should be carried out by a specialist who knows best the methods of resuscitation. At the same time, a second physician (or an experienced nurse) should listen to breath sounds to make sure the endotracheal tube is in the correct position and good gas exchange, and to assess the heart rate. If the heart rate exceeds 80 beats per minute, ventilation should be continued until adequate spontaneous breathing is restored, after which the color of the skin should be assessed. In case of bradycardia (80 beats / min or less), the assistant conducts a heart massage at a frequency of 100-120 per minute, coordinating it with IVL-100% oxygen: 3 pressure on the sternum - 1 breath. Cardiac massage continues until the child's own heart rate reaches 100 beats per minute. If after 30 seconds the heart rate continues to be less than 100 beats per minute, drug therapy should be started. To do this, the second assistant catheterizes the umbilical vein and injects 0.1-0.3 ml / kg of a 0.1% adrenaline solution prepared in advance. The latter can be injected directly into the endotracheal tube. (For dosing accuracy, 1 ml of the drug is diluted to 10 ml with isotonic sodium chloride solution and 0.5-1 ml is injected). Adrenaline increases the rate and force of heart contractions and

promotes an increase in blood pressure, causing vasoconstriction of peripheral vessels.

If after 30 seconds the heart rate is restored and exceeds 80 beats per minute, chest compressions are stopped, but ventilation is continued until spontaneous adequate breathing is restored. If the heart rate remains below 80 beats per minute, adrenaline should be reintroduced. In the presence of persistent pallor of the skin (despite adequate oxygenation) and a weak pulse (which is a sign of hypovolemia or acute blood loss), a 5% albumin solution or saline solution (10 ml / kg) should be administered to replenish the BCC.

In cases where asphyxia of a newborn has occurred against the background of prolonged chronic intrauterine hypoxia (as indicated by severe extragenital pathology of the mother, pregnancy complication by preeclampsia, postmaturity), to eliminate possible metabolic acidosis, the child should be injected into a vein after restoration of adequate pulmonary respiration 4% solution sodium bicarbonate at the rate of 2 meq/kg or 4 ml per kg of body weight. The rate of administration is 1 meq/kg/min. However, it should be remembered that the infusion of sodium bicarbonate at a dose of 3 meq/kg leads to the formation of such an amount of CO 2 that is formed in the body in 1.5 minutes. Therefore, for the removal of CO 2, a good ventilation-perfusion relationship is required, i.e., the restoration of adequate breathing. Since the osmolarity of a 4% sodium bicarbonate solution is 952 mosm/l, the rapid jet administration of this drug can contribute to hypernatremia, which, against the background of hypoxic hemodynamic changes, can lead to the appearance of intraventricular hemorrhages, especially in premature infants.

If 5 minutes after the start of resuscitation, the Apgar score of the newborn remains no higher than 4-5 points, it is recommended to administer an intravenous solution of prednisolone (1 mg/kg) or hydrocortisone (5 mg/kg).

Breathing stimulants are used only if the mother is known to have taken drugs one hour before the birth of the child. In order to combat drug depression, 0.01 ml/kg of naloxone is administered intravenously or endotracheally.

In the process of mechanical ventilation, complications may occur: - hyperoxia (it is necessary to reduce the concentration of O 2 in the inhaled air);

Hypocarbia, leading to a decrease in cerebral blood flow (it is necessary to reduce the respiratory rate);

As pulmonary compliance improves, expiratory pressure may become excessive and then tamponade of the pulmonary circulation, an increase in pulmonary artery pressure, and a right-to-left shunt may occur. This is manifested clinically in a decrease in systemic blood pressure, an increase in blood pressure fluctuations during mechanical ventilation with increased expiratory pressure. In this case, it is necessary to quickly disconnect the endotracheal tube from the airway and a sharp increase in blood pressure will immediately become visible. In this case, it is necessary to reduce the expiratory pressure in order to reduce the size of the shunt;

Pneumothorax can occur as a complication of mechanical ventilation, most often in children with meconium aspiration; tension pneumothorax requires prompt treatment (thoracocentesis).

If the measures taken are effective, the heart rate and blood pressure increase, the pulse pressure increases, the central venous pressure drops, and the child turns pink.

As soon as RO 2 , RCO 2 , blood pH and hemodynamics are normalized, spontaneous respiratory movements occur. The period of time preceding them is directly proportional to the degree of brain damage. So, in children who were born in severe asphyxia (pH = 6.95-7.0), with the appearance of spontaneous breathing at the 10-20th minute of resuscitation, no severe brain damage was subsequently detected. If independent regular breathing was restored later than the 20th minute (Apgar 0-3 points), then the mortality rate of newborns was 53%, and cerebral palsy was noted in 57% of surviving children.

If after 20 minutes spontaneous breathing is not restored, there is no heartbeat, the resuscitation of the child should be stopped. It is more difficult to come to such a conclusion in the absence of spontaneous breathing, but the presence of a heartbeat. Then the issue should be resolved individually, taking into account the degree of maturity of the child, the conditions of its intrauterine development, the presence of congenital malformations.

The next stage of resuscitation includes the transition to spontaneous breathing, the prevention of secondary hypoxia, and the correction of metabolic disorders.

Premature babies weighing less than 1500 g represent a special group that needs resuscitation. Ventilation should be performed in almost all children with an Apgar score.<6 баллов в связи с поверхностным неэффективным дыханием. Вопрос о продолжительности ИВЛ в каждом случае решается индивидуально с учетом жизнеспособности плода. Переводить ребенка с ИВЛ на самостоятельное дыхание надо постепенно, вначале снижая частоту дыхания, затем концентрацию О 2 . Показан переход на дыхание с положительным давлением на выдохе.

At birth in asphyxia of very premature babies (gestational age less than 30 weeks, body weight less than 1350 g), who have a particularly high risk of developing respiratory distress syndrome, prophylactic use of surfactant is possible. It has been shown that the administration of the drug does not prevent the development of respiratory disorders, but reduces by 2 times the mortality from SDR and the frequency of such a formidable complication as bronchopulmonary dysplasia.

The use of a surfactant contributes to an increase in lung compliance at normal values ​​of transpulmonary pressure, increases the stability of the alveoli on expiration and prevents the formation of atelectasis, and reduces the leakage of proteins and water from the vessels of the lungs.

For prophylactic purposes, surfactant preparations (exosurf neonatal, surfactant-bl, curosurf) should be administered in the first 2 hours of life, and the child should be mechanically ventilated.

After resuscitation, the child is placed in an incubator and immediately transferred to the intensive care unit, where 30-60 minutes after the relative stabilization of his condition, the midwife treats the umbilical cord and skin.

After the completion of resuscitation, the doctor must fill out the "Card of primary and resuscitation care for the newborn in the delivery room" - registration form 097-1 / y-95. It should be emphasized that in the organization of resuscitation care, it is important to train personnel in advance and equip the maternity unit with the necessary equipment.

Circulatory disturbances and deep metabolic shifts that occur in the body as a result of hypoxia determine neurological symptoms that resemble the clinical picture of post-resuscitation illness in adults: the initial stage of inhibition of functions is replaced by the stage of general arousal,

which is characterized by a sleep disorder, the appearance of extensor hypertension and various motor automatisms. Prolonged sleep disturbance and convulsive syndrome in themselves significantly exacerbate metabolic disorders in the brain, lead to the accumulation of toxic products, which to a certain extent determines the unfavorable outcome of the disease. Therefore, it is necessary to use pharmacological agents that relieve convulsive readiness and promote the onset of sleep (seduxen intravenously or intramuscularly at 1 mg until a clinical effect is achieved, GHB at 100 mg / kg / 24 hours).

In complex medical measures An important role belongs to infusion therapy, the main tasks of which are: normalization of hemodynamics, water-electrolyte balance and acid-base state of the blood, provision of diuresis and delivery of energy and plastic material to the child. When determining the amount of fluid to be administered, one should proceed from the minimum needs of the body of newborns to cover the needs of basal metabolism and moisture loss through the skin, lungs, intestines and kidneys. These requirements are met by drip administration on the first day of 30-40 ml / kg of liquid. The volume of the infusate on the 3rd day of life is 80-90 ml/kg, on the 4th day - 100-110 ml. The basis of the infusate is 10% glucose solution.

For the purpose of dehydration, plasma (10-15 mg / kg), albumin (10% solution at the rate of 7-10 ml / kg), mannitol (10% solution of 10 ml / kg), lasix (0.2 ml of 1% solution ).

To replenish the volume of circulating blood and improve its rheological properties and microcirculation, trental is prescribed. In addition to infusion therapy, antioxidants (vitamins A, E, C), glutamic acid should be used. In the presence of metabolic acidosis, cocarboxylase and / or 4% sodium bicarbonate solution are used to alkalize the blood.

Correction of the content of sodium, potassium, calcium is carried out in the presence of laboratory data on the composition of blood electrolytes. To do this, use a 10% sodium chloride solution, 7.5% potassium chloride solution, 10% calcium gluconate solution.

In order to improve myocardial contractility, eliminate pulmonary hypertension, hypovolemia and hyperhydration, cardiac glycosides are recommended. Dopamine is used to treat hypotension, improve cardiac output and improve renal function.

Prevention of hypoxia fetus and neonatal asphyxia should be based on prenatal diagnosis and consist of the following components:

Timely hospitalization of pregnant groups with an increased risk of developing fetal hypoxia;

Intensive care of obstetric and extragenital pathology of pregnant women;

Early delivery in the absence of effect from the therapy of fetal hypoxia.