Тopic 2. Fetus as a patient. Pharmacotherapy in obstetrics. Placental dysfunction. Fetal hypoxia. Fetal intrauterine growth retardation syndrome.

Etiology, pathogeny of placental dysfunction, retardation, hypotrophy, fetal hypoxia and newborn asphyxia. Fetoplacental dysfunction diagnostics methods and treatment. Fetal hypoxia acute and chronic.

"Placental dysfunction. Intrauterine Growth Retardation Syndrome ." 1. Relevance of the topic.

Many researchers have proven that the health of a newborn is significantly defined by the course of the antenatal period. Today, it is established, that the most frequent reason for fetal disorders during a pregnancy is placental dysfunction.

Placental dysfunction serves as the main cause of disorders of the functional condition of the fetus; it is very important during the pregnancy to correctly evaluate the functions of the placenta and prescribe adequate therapy for its insufficiency so as to prolong the pregnancy to term. Early diagnostics of congenital fetal disorders and disorders of the placenta and also timely therapy of these pathological changes helps provide for the birth of a healthy baby.

The knowledge of modern methods of diagnostics during the antenatal period during a non-complicated pregnancy helps reveal fetal disorders in the early stages of a pregnancy.

2.Goals of the study: Educational:

1.Know the definition, etiology and pathogenesis of placental dysfunction.

2.Know the classification of placental dysfunction.

3.Be able to correctly evaluation the fetal condition during placental dysfunction depending on the degree of compensatory placental mechanisms.

4.Be able to determine the use of medical actions to correct any disorders in the development of the fetus.

5.Be able to accurately predict the course of the pregnancy and the fetal condition depending on the degree of placental dysfunction.

6.Know the definition, etiology and pathogenesis of fetal distress syndrome.

7.Know the definition, etiology and pathogenesis of IUGR (retardation, hypotrophy of the fetus).

3.Contents of the lesson:

Placental dysfunction

Placenta ("child’s place") – is an extremely important organ, which exists only during pregnancy. It connects the functional systems of two organisms – the mother and fetus, providing the fetus with necessary vital substances. During the course of a normal pregnancy, the placenta is located in the corpus of the uterus on the posterior (more often) or anterior wall. It is completely formed by 15-16 weeks of pregnancy, after 20 weeks is when active exchange through the placenta vessels begins. From 22 to 36 weeks, the placenta increases in weight, and by 36 weeks it reaches it full functional maturity.

The placenta is similar to a round flat disk. By the end of the pregnancy, the placenta weighs 500-600 gr., has a diameter of 15-18 cm and a thickness - 2-3 cm. There are two surfaces distinguished on the placenta: maternal, turned toward the uterine wall, and the fetal – turned toward the amnion cavity.

Normally, the placenta together with its membranes (afterbirth) is born 10-15 minutes after the birth of the fetus. It is attentively examined and sent for morphological research. First, it is very important to be convinced that the placenta was born (detached) entirely (i.e. there are no damages on its surface and no lobes or parts of the placenta have remained inside the uterine cavity). Secondly, the condition of the placenta can be judged by the course of the pregnancy (whether there was detachment, infectious processes, etc.).

Placental functions:

First, the placenta participates in the gas exchange: diffusion of oxygen occurs from the mother’s blood to the fetus, and carbonic gas is transported in the opposite direction.

Secondly, the fetus receives vital substances necessary for its growth and development through the placenta. It is necessary to remember that a lot of substances (alcohol, nicotine, narcotics, many medical preparations, viruses) easily penetrate through the placenta and can harm the fetus. Besides, with the help of the placenta, the fetus gets rid of products of metabolism.

Thirdly, the placenta provides immunological protection for the fetus by detaining the cells of the mother’s immune system which, can penetrate to the fetus causing it to be a foreign object and then cause an immune conflict, which could start rejection reactions. At the same time, the placenta passes the maternal antibodies, which protect the fetus from infections.

a)acute – acute disturbances of decidual perfusion and disturbances of the utero-placental blood circulation play a leading role in its development. This kind of placental dysfunction appears as large infarctions of the placenta, preterm detachment of a normally located placenta. As a result, death of the fetus and the termination of the pregnancy can occur quickly.

b)chronic – very frequent pathology (it is observed in approximately every third pregnancy woman in the group of high risk). It can occur in the ІІ trimester and last for a long time.

ІІІ. by the condition of the compensatory-adaptive reactions:

a)relative – when the compensatory reactions in the placenta are preserved. Vital support of the fetus is caused by compensatory reactions, which operate on the tissue (increase the number of reabsorbing villa, capillaries of terminal villa, functioning syncytial nodes), cellular and subcellular levels of the syncytiotrophoblast. Infringements of maturing of the placenta and immune disorders have certain value in the development of this type of PD.

b)absolute - most difficult form of chronic PD. It is characterized by the development of damage to the placenta of involution-dystrophic, circulatory and inflammatory character, which is accompanied by the absence of compensatory-adaptive reactions of the chorion at the tissue level.

Diagnostics of disorders of the functions of the placenta.

1.Determine the degree and character of changes in the placenta. \

a)hormonal researches:

Hormonal methods of diagnostics of PD consist of determining the level of hormones in the amniotic fluid, patient’s blood and urine. But, it cannot be limited to the research of one hormone only one time. It is advisable to use dynamic supervision of a complex of hormones in the placental complex, placental lactogen (PL) and chorionic gonadotropin (CG) – to diagnose the condition of the syncytiotrophoblast of the placenta; estrogen (estradiol-E2 and estriol-E3) – to evaluate the function of the placental complex; progesterone (Pg)-to diagnose the condition of the uterine-placental-fetal system (see table 1).

2.Determine the condition of the fetus and placental system.

a)measure the height of the uterine fundus over the pubis symphysis and the circumference of the abdomen in dynamics.

Special attention should be paid during external measurement in the ІІ and beginning of the ІІІ trimester when the received sizes are comparison to the term of the pregnancy, which shows any fetal growth retardation. It is convenient to use a gravidogram, where normal measurements of the height of the uterus fundus are marked. The lack of 20 mm in the size of the uterus or more at 32-33 weeks is basis for considering the presence of hypotrophy of the fetus.

b)determine the sizes of the fetus with an ultrasound.

c)study the respiratory activity of the fetus with an ultrasound.

d)determine the movement activity of the fetus with an ultrasound.

It is performed at 7-8 weeks of pregnancy, but its evaluation has the greatest value in the ІІІ trimester when the fetus does 5 and more movements in 30 minutes. Thus, an increase in general movement activity of the fetus is considered compensatory reactions, a decrease - an adverse sign.

e) ultrasound of the urinary functions of the kidneys of the fetus by the amount of excreted urine.

The latter is determined by the difference between the volume of the urinary bladder during the first US and the repeated US in 1 hour. The given test is especially valuable when diagnosing hypotrophy of the fetus, during which the excretion of the urine decreases to 15-18 ml (normal – 24-27 ml). Also consider, that a decrease in the speed of urine excretion of the fetus is observed during gestosis of the pregnant women, in those cases there is no growth retardation by data from the US. The degree of decrease in the production of urine is directly dependant on the severity of gestosis, which is connected not only to fetal growth retardation, but also to the infringement in the regulation of the kidney functions.

f)evaluation of the fetal heart activity.

Along with auscultation, the most accessible and widespread method of evaluating the fetal heart activity is cardiotocography, registration of fetal heart rate (HR). Cardiomonitoring shows initial and expressed signs of suffering of the fetus as a result of fetal distress.

The basic treatment for placental dysfunction:

1)Improving the uterine-placental blood circulation;

2)Normalizing the gas exchange between the mother and fetus;

3)Improving the metabolic functions of the placenta;

4)Acting on the fetus, through the placenta and using the para-placental way of exchange.

Different methods and different means influence multiple functions of the placenta at once. Normalizing the uterine-placental blood flow, certainly, improves the transport of nutrients and gas exchange, which is an important factor in the synthesis of hormones. Correcting the metabolic changes leads to the improvement of gas exchange and normal function of the placenta which in turn, improves the haemodynamics of the placenta.

Normalizing the uterine-placental blood flow is the basic link in normalizing the function of the placenta; it is achieved by using vasodilating means or preparations which relax the uterus, along with actions directed on normalizing the reocoagulate properties of the blood:

a)physical methods of action (electro-relaxation of the uterus, electrophoresis of magnesium, thermal procedures on the renal area, diathermy, inductothermy, etc.) reflex the biometry and lead to the dilation of vessels;

b)abdominal decompression removes extra muscle work of the uterus by overcoming of the tonus of the abdominal muscles. It leads to an increase in blood flow in the uterus and improves placental perfusion. Besides that, it leads to an increase in the synthesis of estriol and an increase in the transport function of the placenta;

c)hyperbaric oxygenation is applied to improve the function of the placenta and fetal condition, especially in pregnant women heart disorders. It preserves the activity of the respiratory enzymes, assists in normalizing the carbohydrate metabolis;

d)medicament means. Aminophylline or teophylline, vasodilating substances, are used; they can be introduced by i\v by stream or droplet introduction. Complamin, teonicole are used for the same purposes. It should be noted that hypersensibility is possible in pregnant woman and so individual doses of complamin should be selected. Considerable improvement in the uterine-placental blood circulation causes vaso-active preparation trental. It has vasodilating action, decreases the resistance of peripheral vessels, increases the collateral blood circulation. The preparation improves the rheological properties of blood and microcirculation, and it can be used in hospitals and female consultations.

Example of treatment plan:

І. In the hospital:

Treatment of the basic pathology of the pregnancy;

Oxygen therapy - inhalation of mixed oxygen for 30-60 minutes 2 times per day;

Preparations which influence metabolism: glutamic acid 1,0 gr. х 3 times a day, methionine 0,25-0,5 gr х 3 times a day.

Galaxorbin as ferroplex 1 tab. х 3 times a day. Cocarboxilase 50 mg i\m every day.

Vaso-active substances: trental, partusisten, isadrin, aminophylline i\v or per os (i\v with glucose or physiological solution). I\v introduction + 3х per os (in pills). Course of the vaso-active substances is 4-6 weeks, of them 5-7 days – infusion therapy, and the other days – per os. Complamin (teonicole) 0,15 gr. per os with food 3 times a day can be used as vaso-active substances.

Reopolyglucin 10 % solution 400-500мл every day i\v droplets, 3-4 times, or 2-3 times a week (it can be used as a loading liquid before introducing vaso-active substances).

Native plasma – 150 ml i\v droplets for low protein in the blood (below 6%).

When introducing large doses of glucose it is used with insulin - 1 unit for 4 gr. of dry substance.

ІІ. In the female consultation:

Diathermy at the renal area – up to 10 sessions alternating with ultraviolet irradiation (10 sessions). Diet rich in fiber and vitamins (boiled meat, fish, cheese);

I\v introduction of glucose 40% - 20,0 with corglicon 0,06% - 0,5 ml gradually every day or every other day (10 injections);

Cocarboxilase i\m 50 mg every day, for 10-14 days;

Aminophylline 0,15 gr per os 2 times a day and 0,2 gr suppositories at night, for 14 days (or no-shpa, papaverin);

Trental 1 pill 3 times a day or isadrin 0,005 gr (under tongue) 3 times a day in combination with finoptin (isoptin);

Orotate potassium 0,5 gr 3 times a day;

Ferroplex (conferon) 1 dragee (capsule) 3 time a day; Methionine 0,5 gr 3 times a day;

Ascorutin 1 pill 3 times a day.

If not effective during 2 weeks – hospitalization

Prevention of placental dysfunction

1) eliminating the influence of harmful factors during the period before conception and especially during the first days and weeks of pregnancy:

a)eliminating smoking, alcohol, taking of medicines (without prescription from the doctor);

b)before pregnancy (and during pregnancy) sanation of sites of infection, treatment of chronic diseases.

2)after the patient becomes pregnant, it is necessary to explain to her the role of high-grade balanced food, high-grade and extra sleep.

3)finding the group of high risks and registering them for regular medical check-ups.

Fetal distress syndrome

According to order of the Ministry of Health of Ukraine №900 from 27.12.2006 about the statement of the clinical report about obstetrical help for "Fetal distress during pregnancy and during birth ", the terms "chronic hypoxia of the fetus ", "acute hypoxia " are not clinical, because for the diagnostics of these disorders, indicators of oxygen contents in the fetus (metabolic acidosis) are not used in routine medical practice. So, all disorders of the functional condition of the fetus at the present are distinguished as "fetal distress". The concept "chronic fetal hypoxia", "acute fetal hypoxia" are not used.

І. In the conditions of a hospital:

Treatment of the basic pathology of pregnancy;

І. In the hospital:

Treatment of the basic pathology of the pregnancy;

Oxygen therapy - inhalation of mixed oxygen for 30-60 minutes 2 times per day;

Preparations which influence metabolism: glutamic acid 1,0 gr. х 3 times a day, methionine 0,25-0,5 gr х 3 times a day.

Galaxorbin as ferroplex 1 tab. х 3 times a day. Cocarboxilase 50 mg i\m every day.

Vaso-active substances: trental, partusisten, isadrin, aminophylline i\v or per os (i\v with glucose or physiological solution). I\v introduction + 3х per os (in pills). Course of the vaso-active substances is 4-6 weeks, of them 5-7 days – infusion therapy, and the other days – per os. Complamin (teonicole) 0,15 gr. per os with food 3 times a day can be used as vaso-active substances.

Reopolyglucin 10 % solution 400-500мл every day i\v droplets, 3-4 times, or 2-3 times a week (it can be used as a loading liquid before introducing vaso-active substances).

Native plasma – 150 ml i\v droplets for low protein in the blood (below 6%).

When introducing large doses of glucose it is used with insulin - 1 unit for 4 gr. of dry substance.

ІІ. In the female consultation:

Diathermy at the renal area – up to 10 sessions alternating with ultraviolet irradiation (10 sessions). Diet rich in fiber and vitamins (boiled meat, fish, cheese);

I\v introduction of glucose 40% - 20,0 with corglicon 0,06% - 0,5 ml gradually every day or every other day (10 injections);

Cocarboxilase i\m 50 mg every day, for 10-14 days;

Aminophylline 0,15 gr per os 2 times a day and 0,2 gr suppositories at night, for 14 days (or no-shpa, papaverin);

Trental 1 pill 3 times a day or isadrin 0,005 gr (under tongue) 3 times a day in combination with finoptin (isoptin);

Orotate potassium 0,5 gr 3 times a day;

Ferroplex (conferon) 1 dragee (capsule) 3 time a day; Methionine 0,5 gr 3 times a day;

Ascorutin 1 pill 3 times a day.

If not effective during 2 weeks – hospitalization

Respiratory distress syndrome in newborns (respiratory disorder syndrome) – non-infectious pathological processes (primary atelectasis, disease of the hyaline membrane, hydropichemorrhagic syndrome) that form in the prenatal and early neonatal periods of development of an infant and breathing; it appears as respiratory disorders. The frequency of development of respiratory distress depends on the degree of immaturity and averages about 60% of children born at the pregnancy term less than 28 weeks, 15-20% -at the term 32-36 weeks and 5% - 37 weeks and more. With rational nursing of such children, the mortality rate is close to 10%.

Fetal distress syndrome means hypoxia.

Hypoxia of the fetus - insufficient supply of oxygen to the tissue and organs or their incomplete digestion of the oxygen. This term was recommended by the World Health Organization, but it is not the only one: the terms fetal distress ("suffering") and asphyxia (without pulse; but has dyspnea, i.e. a lack of oxygen and accumulation of carbonic gas in the organism) also exist. The term hypoxia of the fetus and asphyxia of newborns are not used.

The consequences of oxygen insufficiency for a fetus during different periods of pregnancy are different. In early terms (before 16 weeks), when organs and systems are forming, expressed hypoxia can be accompanied by embryo growth delay and the occurrence of development anomalies. Oxygen starvation in later pregnancy terms can

lead to fetal growth retardation, defects of the central nervous system in the fetus and newborns, infringement of the processes of the infant’s adaptation after birth; in special cases it can be the reason for stillborn deliveries or death in infants.

Depending on the duration, chronic and acute fetal distress is distinguished. Chronic distress develops when there is an insufficient supply of oxygen to the fetus throughout a long period of time due to diseases of the mother’s internal organs (diabetes, chronic diseases of the lungs, kidneys, anemia, etc.), complicated course of the pregnancy (gestosis, risk of miscarriage, over-due pregnancy, immunological incompatibility of the mother and fetus blood by Rhesus factor, pre-natal fetal infection). Chronic distress also can be the result of smoking, use of alcohol, drugs during pregnancy. Acute fetal distress, as a rule, occurs during the delivery (in connection with anomalies of labor activity, entanglement of the umbilical cord, prolapse or compression of loops of the umbilical cord, short umbilical cord). Less often, acute fetal distress is observed during the pregnancy during life-threatening conditions of the mother (premature detachment of the placenta, rupture of the uterus). Sometimes, chronic and acute distress is observed together.

Intrauterine fetal distress - pathological condition connected with oxygen insufficiency during the pregnancy and delivery. It is caused by the reduction or absence of oxygen in the body and the accumulation of metabolism products in the blood. Hypoxia leads to an imbalance in the oxidation-reduction reactions in the fetus’s organism resulting in the development of acidosis, when tissue ceases to receive oxygen. Carbonic acid accumulation causes irritation of the respiratory center. The fetus starts to breathe through an open vocal fissure and aspirates amniotic fluid, mucous, blood.

Many kinds of obstetrical pathologies, different extra-genital diseases, dysfunction of the placenta, pathology of the umbilical cord and fetus are just some of the reasons.

Etiology and pathogenesis

The main pathogenesis for distress of the fetus and newborn is placental dysfunction with obstetrical and extra-genital pathologies. Defects in the structure of the placenta and processes of microcirculation in pregnant women with gestosis, the action of medical preparations and other harmful factors lead to chronic oxygen starvation which is accompanied by a decrease of oxygen in blood, hypercapnia, non-compensated acidosis, imbalance in the water-electrolyte exchange, decrease of the contents of corticosteroids. It, in turn, causes dysfunction of the central nervous and cardiovascular systems, homeostasis regulation, and increase in the permeability of vessels, decrease in the immunological reactance of the fetus’s organism. Conditions of fetal hypoxia are connected with the changes in the complex uterine-placental-fetal system. This testifies that the result of the pregnancy for the fetus and in many respects for the mother depends on the condition of the compensatory-reactive mechanisms of the fetoplacental complex and rational correction of disorders.

Acute and chronic fetal distress is distinguished. The symptoms of acute fetal distress usually appear during delivery. Chronic fetal distress (more than 7-10 days) - the consequence of prolonged obstetrical or extragenital pathologies, which lead to fetal development delay.

The reasons for fetal distress and distress in newborns can be divided into 4 groups: I group - diseases of the mother.

Blood loss during obstetrical bleedings (detachment of the placenta, placental presentation, rupture of the uterus); blood diseases (anemia, leukemia, etc.).

Shock conditions of any origin.

Diseases of the cardiovascular system (congenital and acquired heart disorders with haemodynamic infringement). Diseases of the respiratory system with gas exchange infringement (bronchial asthma, pneumonia).

Any intoxications.

II group - pathology of the uterine-placental and umbilical cord circulation.

Umbilical cord pathology (umbilical cord knots, entanglement of the umbilical cord around the extremities, prolapse of the umbilical cord, compression of the umbilical cord during delivery in pelvic presentation).

Bleedings (detachment of the placenta, placental presentation, rupture of vessels with membrane attachment of the umbilical cord).

Defects in the placental blood circulation in connection with dystrophic changes of the vessels (during gestosis, over-due pregnancy).

Anomalies of the birth activity (very long or fast contractions, discoordination of the birth activity).

III group - reasons connected with the fetus.

Genetic illnesses of newborns.

Hemolytic disease of newborns.

Congenital defects of the cardiovascular system.

Pre-natal infection.

Intracranial trauma.

IV group.

Partial or complete obstruction of the respiratory tract (characteristic only for distress of newborns).

Clinical picture

Main displays of fetal distress: heart rate abnormalities (at first tachycardia, then bradycardia), muffled heart sounds (in the beginning little increase, then muffled); arrhythmia, decrease in the intensity of fetal movements, excretion of meconium, change in the indicators of the acid-base balance of the amniotic fluid and blood.

Diagnostics

Diagnostics of fetal distress can only be complex. Registration of cardiac activity is one of the most simple and widespread methods of monitoring the functional condition of the fetus during pregnancy and delivery. In clinical practice, CTG is used.

Test with functional loads (diagnostics of chronic fetal distress). The pregnant woman for 3-4 min. steps up and down on 2 steps. Before and after the workout register the fetal cardiac activity. During a normal course of pregnancy, the heart rate remains within the physiological borders 116-160 b.p.m. When the fetus is in distress, monotony of the rhythm of the heart is marked, tachycardia or bradycardia.

Test with oxytocin. Under the influence of oxytocin, the blood circulation decreases in the intervillous lacuna, appearing as change in the fetal heart rate. To perform the test, 1 unit of oxytocin is dissolved into 100 ml of 5% glucose. 1 ml of this solution contains 0,01 units of oxytocin. 5 ml of the solution is put into a syringe, and introduced by i\v with a speed of 1 ml per minute. Normally, the fetal heart rate does not change. When the fetus is in distress tachycardia or bradycardia is observed.

Test with holding of breath during inhalation and during exhalation. Normally, when breath is held, the fetal heart rate changes on average 7 b.p.m. Holding of breath during inhalation causes a decrease, and on exhalation - increase in fetal heart rate. When the fetus is in distress, there is no change in fetal heart rate.

Cold test gives a decrease in fetal heart rate by 10 b.p.m. When the fetus is in distress, the rhythm does not

change.

There are tests with the introduction of atropine sulphate, aminophylline, etc. Atropine easily passes through the placenta and causes tachycardia, so it is not recommended.

Modern methods of evaluating the condition of the fetus include US (fotometry, placentography, "biophysical profile"), Doppler flowmetry, amniocentesis (рH of the amniotic fluid, delta Oe450, level of hormones, phospholipids), chordocentesis (blood indicators), cardiomonitoring with computer evaluation of the received data,

рH of the blood from the skin of the fetus’s head (during labor).

Treatment

Treatment plan for fetal distress.

Treatment of the mother’s basic disease, regulation of tone of the uterus, correction of placental dysfunction. Treatment of the mother’s basic disease (pathology of pregnancy or extragenital pathologies).

Observation in the hospital (mainly on the left side to prevent inferior vena cava syndrome). Oxygen therapy.

I\v introduction of glucose (500 ml - 10% solution) +10 units of insulin + cocarboxilase 100 mg + ascorbic acid (10 ml - 5%). Infusion for 5-8 days.

I\v introduction of preparations improving the uterine – placental circulation: aminophylline (10 ml - 2,4%), sigentin (2 ml -1%), ATP (2 ml-1%) or curants (2 ml-0,5%). Reopolyglucin 200 ml i\v droplet.

Use of tocolytics (especially with preterm pregnancy and increased irritability of the uterus): magnesium (10 ml - 25% in 5% solution of glucose - 100 ml i\v droplet) or alupent (0,5 mg) in 5% solution of glucose for 2-6 days with further use of pills and i\m introduction.

Treatment plan for acute fetal distress.

Position on left side.

Long inhalation of pure humidified O2 by mask.

I\v introduction of 10% solution of 100 ml glucose + 4 units of insulin + 50 mg of cocarboxilase and 5 ml of solution of ascorbic acid 5%.

10 ml of 2,4% solution of aminophylline i\v gradually + 2 ml of 1% sigetin + ATP (2 ml-1%). I\v droplep introduction of sodium hydrocarbonate (60-80 ml - 5%).

I\v introduction of 10% solution of 10 ml of calcium gluconate.

If the fetus suddenly develops bradycardia - introduce 0,3% ml i\v or 0,7 ml under the skin 0,1% solution of atropine sulphate. If the presented fetal part is accessible, introduce atropine sulphate hypodermically (0.1 ml - 0,1%).

If there is no effect from treatment of acute and chronic fetal distress - deliver.

Retardation, hypotrophy of the fetus.

In literature you meet a large quantity of terms: "intrauterine development delay", "intrauterine growth retardation ", "hypotrophy of the fetus", "fetal retardation", "small gestational age", etc. In the ICD-10 all terms specified above are united into one concept "Delay in growth and lack of nutrition for the fetus".

The term " intrauterine growth retardation " - pathology of the fetus resulting from the influence of harmful factors. IUGR is diagnosed in infants who have insufficient body weight at birth in relation to their gestational age, when the body weight is 10% less than for that pregnancy term, and\or the morphological index of maturity of the fetus is behind by 2 or more weeks from the valid gestational age.

Fetal development delay is one of the most frequent reasons for a decrease in the adaptation of newborns in the neonatal period, high disease rate, psychological disorders. Perinatal death rate for IUGR reaches 80-100%.

The mortality rate for low-weight infants is 35-37 times more than in mature infants with physiological body weight. The death rate for many depends on the body weight at birth. So, with a weight of 500-700 gr the death rate is 56%, with a weight of 751-999 gr - 48%, and with a weight of 1000 gr - 40%. The maximum death rate for low-weight infants is evident in the 1st week of life.

According to recommendations of WHO, infants born with a body weight less than 2500 gr are called infants with small weight at birth. Thus, infants with small weight at birth are divided into three groups:

1)Newborns before 37 weeks of gestational age with corresponding gestation growth to the given term – immature newborns with growth and body weight, corresponding to the gestation term;

2)Newborns before 37 weeks of gestational age and small for the given term – immature newborns with

IUGR;

3)Newborns after 37 weeks gestation and small for the given term – mature newborns with IUGR. Prenatal infections also lead to IUGR and make up about 10% of the reasons for this pathology. Rubella

leads to IUGR in 60% of cases.

Retardation (from lat. - delay) (biological), late rudiment of organs and their slow development in descendants in comparison with ancestors. It depends on the beginning of the organ’s functioning and also on the conditions of environment in which individual development of the organism occurs - ontogenesis.

Retardation - delay (in medicine) - delay of sexual development of an organism. In girls – delay of first menstruation, delay in breast development. In boys – delay of first ejaculation.

Retardation (in literature) – delay in literary and art development, lyrical digressions, different mistakes (interior, characteristic).

Hypotrophy of the fetus

This term doctor’s use for delay in the rate of physical growth of a fetus; it includes: the physical parameters of the fetus do not correspond with the size for given term of pregnancy. Today, very often, the term hypotrophy is replaced by intrauterine growth retardation.

Intrauterine growth retardation (IUGR) in infants who have insufficient body weight at birth in relation to their gestational age, when the body weight is 10% less than for that pregnancy term, and\or the morphological index of maturity of the fetus is behind by 2 or more weeks from the valid gestational age. Evaluation is performed during the first hours of life.

There are two forms of this syndrome: symmetrical and asymmetrical. The symmetric form develops at early terms of pregnancy. All the fetus’s organs are evenly small; upon US the size parameters of the fetus are less than what is characteristic for the given term of pregnancy. The reasons for symmetric form of hypotrophy are intrauterine fetal infection, chromosomal pathology, developmental anomalies of the fetus, and also insufficient nutrition of mother and smoking.

The asymmetrical form develops later, after 28 weeks of pregnancy and is characterized by non-uniform development of different organs; the brain, skeleton, extremities are developed according to pregnancy term, but the development of the organs (liver, kidneys) is delayed. In this case, during US, the sizes of the fetal head and extremities correspond to the pregnancy term, but the size of the circumference of the abdomen is smaller.

Hypotrophy of the fetus is divided into three degrees according to the severity level:

First degree - situation when the fetus is delayed in development by two weeks. Second degree – delayed by 2 to 4 weeks.

Third degree – delayed by more than 4 weeks.

The reasons for asymmetrical hypotrophy are. They are divided into the following basic groups:

I.Social factors:

a)the mother’s age (17 years or younger, 30 years or older)

b)professional harm (difficult physical work, emotional overstrain, work with chemicals)

c)bad habits (smoking, alcohol)

ІІ. Condition of the mother’s organism:

a). chronic infections (chronic tonsillitis, chronic tracheobronchitis)

b) general diseases (diseases of the kidneys, cardiovascular system, endocrine system)

ІІІ. Gynecologic diseases of the pregnant woman and features of the course of previous pregnancies: a) hormonal imbalance – menstrual dysfunction, infertility

-an etiology and pathogenesis of a hypoxia and asphyxia;

-stages of newborn reanimation;

To be able :

-to perform methods of diagnostics of fetal hypoxia and newborn asphyxia;

-to carry out a complex method of fetal hypoxia treatment;

-to acquaint students with modern clinical thinking about fetal hypoxia and newborn asphyxia treatment.

3.The study contents.

Features of a fetal gas exchange.

In appreciable number of cases at fetal gas exchange state infringement the ability of its organism to delete excess of acids as CO suffers first of all. The carbon dioxide from the fetal organism is deduced by means of a diffusion through a placenta as molecular CO and in a result leaves by mother’s organism. But as the fetus can not influence intensity of respiration, the maintenance of the acid-basic state (ABS) in its organism depends on mechanisms, which it is not capable to supervise.

The fetal CO diffusion through a placenta is possible in connection with existence of a CO gradient between mother and fetus circulation systems. The fetal blood pressure changes from 38 up to 44 mm Hg, while at mother it makes 18-24 mm Hg. This difference provides CO transition from fetus in mother’s circulation system.

At CO pressure at mother 35-40 mm Hg the acidosis and fetal death develops, and it is necessary to arrange measures, promoting to CO elimination (endotracheal intubation and artificial lung ventilation).

Fetus required for maintenance of normal rate of body height, development and adequate pH size from 5 up to 10 ml of Oxygenium on 1 kg of body weight per one minute. Oxygenium delivered from mother’s organism is used by both placenta and fetus. The delivery of such amount of Oxygenium is provided with intensity of uteroplacental bloodflow, amounting 500-700 ml/min.

Fetal and newborn hypoxic conditions occupy one of the first places among the reasons of perinatal morbidity and mortality. They result in serious consequences from the CNS side and other organs not only in postnatal period, but also in the further life of the child. Therefore prophylaxis and treatment of fetal oxygen failure are extremely important for maintenance of health of the future generation.

On WHO materials for 1991 in perinatal morbidity and the mortality structure asphyxia makes 45,2 %, mechanical traumas - 21,1 %;

The frequency of a hypoxia and newborn asphyxia makes 4-6 % and depends on pregnancy, labors course, operative measures and other factors.

Under influence of oxygen failure irrespective of the reasons of its occurrence the homeostasis and function of various organs and systems changes happen in fetal organism.

"Hypoxia" means the term of insufficient supply by Oxygenium of tissues and organs or inadequate Oxygenium utilization by them.

Fetal hypoxia classify as intensity, duration and course.

I. Types:

a)hypoxic - at the lowered blood saturation by Oxygenium;

b)circulative - at sufficient blood saturation by Oxygenium, but infringement of its delivery to tissues;

c) haemal - caused by infringement of Oxygenium linkage by hemoglobin or blood hemoglobin quantity

decrease;

d)tissue - at tissue ability decrease to acquire Oxygenium.

II.Intensity:

a)functional hypoxia - most mild form of oxygen failure accompanying only by hemodynamic changes (tachycardia, BP decrease etc.).

b) metabolic hypoxia - stronger oxygen failure, at which the supply of tissues by Oxygenium decrease results in infringements of a metabolism and wears convertible character;

c) destructive hypoxia is expression of serious Oxygenium insufficiency and cause changes on cell level - the irreversible character.

III. The important factor for changes development in fetal organism is the duration of intrauterine hypoxia, which not always manages precisely to be established.

IV. Course: distinguish an acute and chronic hypoxia of a fetus, however series of the authors allocate also a subacute fetal hypoxia.

a)the chronic fetal hypoxia develops at the complicated current of pregnancy (toxicosis of the pregnant women, immunological incompatibility, fetus infectioning etc.). This is long insufficient supply of fetal organism by nutritious substances, that results in development and growth retardation;

b)the subacute hypoxia usually arises 1-2 days prior to labors and is characterized by the fetal reserve opportunities attrition;

c)an acute hypoxia - arise in labors (patrimonial activity anomalies, umbilical cord abaissement or prelum, head long prelum in a pelvic cavity), is observed during pregnancy (hysterorrhesis) less often.

A condition of an acute and chronic hypoxia quite often is observed.

The numerous etiological factors of fetal oxygen failure can be divided into three large groups:

1. Complication of pregnancy and labors, extragenital diseases adducting in oxygen failure in mother (an anemia, pneumonia, cardiovascular diseases, bleeding etc.)

2.Infringement of a fetal-maternal circulation during pregnancy and labors (umbilical cord abaissement or

prelum etc.)

3.Fetal disease (isoserological incompatibility of the mother’s and fetus blood, intrauterine infection, birth trauma of CNS).

The influence of a hypoxia and newborn asphyxia in clinical practice is defined by infringements (CNS damage, various neurologic symptomatology) and neomortality. The doctors efforts should be first of all directed on early revealing, prophylaxis and well-timed treatment of fetal oxygen failure.

For state definition of fetal intrauterine hypoxia it is necessary:

1.To make the careful analysis of the anamnestic data allowing to make representation about a previous condition of woman health, pregnancy, labors, puerperal period.

2.To investigate consistently and carefully the pregnant woman and fetus condition at primary survey.

3.To observe systematically and constantly the woman and fetus condition during a childbirth.

4.To imagine precisely a symptomatology of fetal hypoxia.

The basic signs of fetal intrauterine hypoxia are:

-change of cardiac activity;

-change of a motor performance;

- change of amniotic waters staining by Meconium.

Diagnostics of fetal hypoxia should be complex and include both standard, and special methods of inspection.

The special methods of inspection can be divided into the following groups: 1. Concerning fetus:

-electrocardiotocography;

-ultrasound;

-dopplerometry;

-biophysical fetal profile.

2.Amniotic fluid examination: - amnioscopy;

- amniocentesis;

- biochemical examination of amniotic fluid.

3.Diagnostics of placental function:

-ChG (chorionic gonadotropinum);

-PL (placental lactogen);

-alpha-fetoprotein

-Oestradiolum;

-Progesteronum;

4. Mother’s metabolism parameters examination:

- acids and alkalis.

Cardiotocography

The use of external CTG allows to carry out the continuous observation over fetal cardiac activity for a

long time.

At the fetal condition characteristics in labors the following parameters of CTG are estimated:

-basilar rhythm of heart beat rate;

-its variability;

-the character of slow accelerations and retardation (decelerations) of a cardiac rhythm, in comparison with the uterine contractile activity data.

The KTG study begins from the definition of a basilar rhythm. The basal rhythm is a size between instant meaning of fetal heart beat rate in an interval between contractions. Basilar rhythm is counted up for 10 minute interval. The normal basilar rhythm makes 120-160 beats/min (on the average 140-145 beats/min). The basilar rhythm lower than 120 regard as a bradycardia, higher than 160 beats/min - as a tachycardia.

In I labor period the tachycardia is more common: allocate moderate (161-180 beats/min) and serious (above than 181 beats/min) tachycardia.

The expressiveness tachycardia degree corresponds to expressiveness of a fetal hypoxia degree. The bradycardia in a larger degree testifies fetal reserve opportunities drop; it is sectioned for moderate (119-100 beats/min) and expressed (less than 100 beats/min).

It is necessary to note, that the basal rhythm is one of the most inert parameters of fetal cardiac activity, therefore at an CTG estimation it is necessary to take into account and other pathological changes.

At basal rhythm examination its variability is estimated, i.e. frequency and amplitude of fetal heart beat rate instant changes (instant oscillations). Calculation of frequency and the amplitudes of instant oscillations is carried out during everyone subsequent 10 min. Amplitude of an oscillation is determined by size of a deviation from a basal rhythm, frequency - by quantity of oscillations per 1 min.

In clinical practice more common is the following classification of a basal rhythm types variability:

-mutistic (the monotonous rhythm) is characterized by low amplitude 0-5 beats/min.

-slightly undulate 10-25 beats/min;

-saltatory 25-30 beats/min.

At physiological course of labors all types of basal rhythm variability are present, but most frequent are slightly undulate and undulate rhythms.

At the complicated labors course it is necessary to pay attention to mutistic and saltatory variability type of basal rhythm occurrence, especially in a combination to a tachycardia or bradycardia. Mutistic type is considered to be most favorable, especially at simultaneous amplitude drop (less than 3 beats/min) and oscillation frequency (less than 6 oscillations in 1 min). The complete curve usually testifies about deep hypoxic influence on a fetal CNS and is in effect terminal.

At uncomplicated course of labors mutistic type of basal rhythm variability can be caused by narcotic and sedatives influence. At physiological course of labors the accelerations are observed almost constantly with frequency 4-5 and more for 30 min, the duration makes them 20-60 sec, amplitude more than 15 beats/min. The periodic accelerations arise in the beginning of labors and are connected with uterus contractions or umbilical cord pressing. The sporadic accelerations are more often connected with fetus movements.

The important meaning for fetal condition diagnostics has the basal rhythm slow waves decelerations estimation. The decelerations occurrence specifies the certain pathological changes in fetal-placental system.

Depending on time of decelerations occurrence concerning uterus contractions 4 types are allocated: Dip 0, Dip I, Dip II, Dip III.

In clinical practice the decelerations account is limited to three parameters:

-time from a contraction beginning up to deceleration occurrence;

-decelerations duration;

-decelerations amplitude.

Dip 0 – peak-formed deceleration, arising in reply to uterus contraction, less often sporadic, proceeds 20-30 sec. and has amplitude 30 beats/min and more. In II period of labors it is not important.

Dip I - early deceleration, fetal CVS reaction on a head or umbilical cord prelum in time of contractions. The basal rhythm at Dip I is within the limits of norm.

Dip II - late deceleration, attribute of uteroplacental bloodflow infringement and progressing fetal hypoxia. Is shown through 30-60 sec after contraction beginning, general deceleration duration more than 60 sec, deceleration peak more than 60 sec, the deceleration peak reaches maximum through 30-60 sec.

Dip IIIvariable deceleration, which is connected with umbilical cord pathology and is explained by influence of two factors:

-stimulation of a vagus nerve;

-secondary hypoxia.

The deceleration amplitude changes within the limits of 30-90 beats/min, common duration 30-80 sec and

more.

Ultrasound examination

-placenta biometry - thinning up to 2 cm or the augmentation more than 5 cm speaks about fetus suffering;

-definition of a fetation features: fetus length, fetus mass;

-amount of amniotic fluid;

-number of respiratory movements;

-frequency of cardiac contractions;

-conformity of fetal sizes to the gestational age.

With the diagnostic purpose in labors a rheoencephalography (REG) and electroencephalography (EEG)

are used.

Diagnostics of fetus hypoxia during pregnancy and in labors

During pregnancy the acute hypoxia basically is shown as a bradycardia:

-up to 90-100 - the emergency delivery guarantees child birth in a good and satisfactory condition;

-80-85 - proof hypoxia and children are born in an asphyxia condition

-60 and less - very strong hypoxia form, which does not guarantee birth of the normal child.

At a chronic hypoxia a proof fetal bradycardia not caused by uterus contraction, umbilical cord prelum or vena cava inferior prelum syndrome, is taped only in terminal stage of a hypoxia.

Prophylaxis and treatment of fetal hypoxia.

The prophylaxis fetal intrauterine hypoxia should be carried out in a female advice.

As one of its major tasks it is necessary to consider well-timed revealing and treatment of pregnancy complications:

-late toxicosis of pregnancy;

-late-term pregnancy;

-premature abortion;

-isoserological incompatibility of mother’s and fetal blood;

-extragenital diseases;

-anomalies of patrimonial activity.

Treatment of fetal hypoxia.

At fetal hypoxia its oligotrophy in a consequence of uteroplacental bloodflow failure frequently is marked.

In this connection it is expedient to the order mother’s basic disease therapy and pregnancy complications treatment to carry out measures directed on uteroplacental circulation improvement, fetal oxygenation augmentation, normalization of its metabolism. The preventive and medical measures should be carried out three times: at 8-18 weeks, 18-20 weeks, 28-32 weeks:

-ultra-violet irradiation (15-20 sessions);

-diathermy of pararenal area every other day per 20 min. (15-20 sessions);

-stylostixis;

-estrogens (Folliculinum, Sinestrolum) improve a uteroplacental metabolism and bloodflow, influence on metabolic processes in endometrium. Estrogens raise a permeability of a placenta, enlarge glucose and other nutritious substances transition to a fetus. For struggle with a metabolic acidosis the listed therapy is supplement by an infusion of alkaline solutions (Sodium hydrogenum 150-200 ml). Precise monitoring of AAH parameters for alkalosis preventive development is necessary. Good results are obtained from drugs infusions for brain tissue fastness increase to Oxygenium insufficiency (Seduxenum, sodium hydroxybutyrate ).

-glucose 40 % 20 ml + Sygethinum 2-5 i/v № 10-15;

tocolytics:

-Partusistenum 0,5 mg i/v, Alupentum, Ritodrinum;

-Trentalum (raises bloodflow in intervillous space) 100 mg/5 ml in 500 ml of 5-10 % glucose;

tocolytics are applied simultaneously:

-with Rheopolyglucinum (400-500 ml 10 %);

-with a glucose (200 ml 10 %);

-with Korglykonum (1 ml 0,06 %); With the purpose of side effect decrease:

-Isoptinum on 1 tab. 3 times per day (beta-blocker);

-Euphyllinum 2,4 % 10 ml with 10 ml of 20-40 % glucose i/v;

- Theophyllinum 0,1-0,2 3-4 times per day;

-Komplaminum 0,15 3 times per day during meal;

-Dipiridamolum (Curantylum) 0.5 ml on 1 kg of mass i/v ;

-in 6 hours 5.000 ME of Heparinum i/m, similar treatment will carry out within 10 days;

-inhalation of a Oxygenium-air admixture within 1 hour 2 times per day;

-hyperbaric oxygenation 60-90 min. № 10-15;

For metabolism stimulation :

- Glutaminum acid 0, 2 (1,0 3 times per day);

- methionine 0,25 3 times, Cytochrome C (5-7 ml in 20 ml of 40 % glucose);

-vitamin therapy (C, E, B group, Acidum folicum 0,02 3 times per day);

-Ferroplexum 1 tab. 3 times;

-cocarboxylase 50 mg i/v.

Obstetrical tactics at hypoxia in labors.

Obstetrical tactics at hypoxia in labors changes depending on an obstetrical situation, the high-speed effective drugs (glucose, humidified Oxygenium, cocarboxylase, Acidum ascorbinicum. Sygethinum, Curantylum. The vitamin В2) which introduction is combined with an operative delivery (cesarean section, obstetrical forceps).

The therapy and preparation for a delivery is especially important at premature births, at which the hypoxia is aggravated by a dismaturity of a pulmonary tissue. For intensifying maturing of fetal pulmonary tissue the assignment of glucocorticoids is necessary:

-Dexamethasone 4 times per day within 2-3 day;

-Mucosolvanum (threat of labors up to term from 29th to 34th week, premature rupture of amniotic membranes in term 29-34 weeks at forecasting labors not earlier than in 24 hours); 50 ml of Mucosolvanum + 400 ml of saline solution i/v by drops within 4 hours. A rate of administering 42 drops / min. Repeated introduction through 48 and 72 hours. To repeat a course in 10 days № 3. In labors Dexasonum and Prednisolonum are entered.

Newborn asphyxia, clinic, diagnostics.

The newborn asphyxia depends on a degree of fetal hypoxia, its duration, features of a childbirth, fetus condition before birth. Besides the severity of asphyxia frequently causes a traumatic component (extensive subdural hemorrhages, breaks of cerebellar tent, traumas of a spinal cord). Thus at newborn the vascular shock with the expressed paleness of dermal integuments and hyperexcitability is taped. Newborn are restless, the tremor of extremities is expressed, cry is shrill, flexoral hypertension, tendons hyperreflexia, intensifying of oral automatism reflexes, flaccid reaction to light, strabismus, sign " of the coming sun ", assymetry of palpebral fissures and nasallabial folds . In 4 hours at injured children (each fourth child) occurs a convulsive syndrome.

Newborn asphyxia – syndrome, which is characterized by absence of respiration or separate irregular respiratory movements at the child with presence of cardiac activity.

The asphyxia at birth can be a consequence of a pathology in labors (acute intranatal asphyxia), but quite often is reflection of pathological processes, begun at a fetus even prior to the beginning of patrimonial activity, i.e. antenatal hypoxia.

The frequency of birth of children in asphyxia makes about 5 %. The monitor control of fetus condition in labors promotes well-timed correction of an intranatal hypoxia and decrease of this parameter to 1,5 %.

Clinical picture.

The clinic of moderate (average gravity) asphyxia at birth in the International classification of illnesses (ICI) of IX reconsideration (Geneva 1980) is described as follows: the normal respiration was not established within the 1-st minute after birth, but heart beats frequency is 100 and more in 1 min; has a place an insignificant muscle tone, weak reaction to a boring, an estimation on scale Apgar through 1 min - 4-6 points. " An asphyxia Livida ".

A condition of the child at birth usually regard as average gravity. First minutes of life the child more often flaccid, is observed a spontaneous motor performance, reaction to survey and boring weak. The physiological reflexes of newborn are depressed. Cry short, low emotional. Dermal integuments cyanochroic, however at an additional oxygenation (with the help of a mask, oxygen tent, funnel closing completely the person) fastly become pink.

Quite often thus there is a Crocq's disease. At heart auscultation tap a tachycardia, the cardiac sounds of increased sound or are muffled. The respiration after lingering primary apnoe rhythmical, is possible a interrib space retraction. Are characteristic repeated short-term apnoe. Auscultatively above lungs probably weakened respiration, presence of variegrated wet rhonchuses of changeable localization and sound. The percussion tone is more often with a box shade.

Per the first 2-3 days of life at these newborn hyperexcitability occurs, marked usually from the first hours after birth. The often regurgitations, hyperesthesia, tremor of hands intensified at cry and anxiety, excited cry, infringement of dream, spontaneous reflex Moro are characteristic. The changes of newborn physiological reflexes and muscle tone are individual. The described infringements are overcoming and also wear functional character, being a consequence of metabolic infringements and intracranial hypertension.

The condition of children who have transferred a moderate hypoxia at birth, in case of realization of adequate therapy is quickly improved and becomes satisfactory by 3-5 day of life.

The serious primary asphyxia is described in ICI so: pulse at birth less than 100 beats/min, slowed down or established, the respiration is absent or difficult, the skin acyanotic, muscles atonic An estimation on a Apgar scale 0-3 points, "asphyxia pallida". A condition at birth estimate as serious. A muscle tone, spontaneous motor performance, reaction to survey and pain stimulation are reduced or are absent. Physiological reflexes of newborn at the first hours of life usually is not possible to reveal. The color of dermal integuments cyanotic-acyanotic or acyanotic is restored at an active oxygenation (more often ALV) up to pink slowly, that speaks about the large oxygen debts expressed infringements of a metabolism and microcirculation. The cardiac sounds are muffled or deaf, the occurrence of systolic hum is possible. The physical data above lungs are variable. Meconium usually depart up to or during a childbirth.

At a very serious condition at birth the clinical picture can correspond to a hypoxic shock. Dermal integuments acyanotic or with gray shade. The independent respiration is absent. There is no reaction to survey and pain stimulation, are observed an adynamia, areflexia, muscular atony. The eyes are closed. The reaction of pupils to light flaccid or is absent, is possible as a miosis, and mifiosis, horizontal, vertical nystagmuses. It is possible to listen cardiac sounds deaf, sometimes only in epigastric area. Are characteristic a serious arterial hypotension, rasping

systolic hum of haemodynamic character, expansion of borders of relative cardiac dullness. At occurrence of spontaneous respiratory movements the expressed participation of an auxiliary musculation is observed. Respiratory movements arythmical, often hasps. Above lungs the variegrated wet rhonchuses (consequence of a aspirative syndrome) on a background of the weakened respiration (presence of pathological atelectases) are auscultated.

At a n abdomen palpation augmentation of a liver (haemodynamic frustration, especially characteristic for a chronic hypoxia) is tapped, at auscultation distinguish a flaccid intestine peristalsis (caused by an ischemia and metabolic infringements).

The improvement of child condition who have transferred a serious primary asphyxia, occurs slowly. Per the first 2-3rd day of life, as a rule, remain reduced a muscle tone, reaction to survey. The physiological reflexes of newborn occur, but they are weakened and quickly are exhausted (more often Babkin’s, Moro, Gomant), the absence within several days of sucking and swallowing reflexes at the child born in time is dangerous, as it testifies to a serious defeat of a brain. At presence of intracranial hemorrhages or transferred serious brain edema, clottage of a sinus there is a convulsive readiness, cramps.

The features of the newborn period of acclimatization, transferred a serious hypoxia, are shown also thermostability, deafness of cardiac sounds, apnoe attacks, large transitional loss of body weight up to 8-9 % and its slower restoration, late amputation of the umbilical rest and failure of umbilical wound healing. At a resorption of massive hemorrhages there is an intensive icterus.

Dynamics of children condition, who have transferred a serious asphyxia, depends on gravity of a brain injury, caused duration of a hypoxia, background, on which it developed, expressiveness of aspirative syndrome, connection of an infection, completeness both timeliness of primary reanimation and treatment of a posthypoxic syndrome.

Complications.

At children who have transferred an asphyxia, often early complicationsare aspirative pneumonia, absentminded or polysegmental atelectases, edematic-hemorrhagic syndrome. The neurologic frustration concern to the remote complications of an asphyxia.

Diagnosis.

An asphyxia is diagnosticated on the basis of an estimation on a Apgar scale on 1-st and 5-th minutes of life, clinical-laboratory researches data.

At an asphyxia of average gravity, is especial on a background of intrauterine hypoxia, after realization of primary reanimation or in first 3 hours of life, the definition of the acid-basic condition and gas blood structure, level of glycemia, arterial pressure, clinical analysis of a blood, including definition of thrombocytes amount, time of coagulation and duration of a bleeding is desirable. At a serious hypoxia, besides the hematocrite definition, blood electrolytes (potassium, sodium, Ca and Mg), realization of an electrocardiography, echoencephalography, monitor observation over a condition of the child (frequency of cardiac contractions and respirations, tissue pressure of O2 and CO2 with the help of epicutaneous gauges) is expedient. The repeated analyses are made under the indications.

Differential diagnosis.

Differential diagnostics is carried out with intrauterine infection, intracranial and spinal birth trauma, acute adrenal failure, trauma of parenchymatous organs, diafragmal hernia, inherent defects of heart, posthemorrhagic anemia, pneumopathies.

Treatment.

Primary reanimation. At the moment of a child head birth pump out slime from an oral cavity and nasal courses (just in such sequence). This procedure repeat at once after birth of the child before separating from the mother. Then cut the umbilical cord and, by drying a skin of the child by sterile linen, it is stacked on reanimation table (on dry linen) under light source of heat. Further at absence of respiration pump out slime from the top respiratory ways and trachea under the control of a direct laryngoscope. This procedure is especially necessary for children, born in an asphyxia, at which Meconium has departed intrauterine. At average gravity of an asphyxia after restoration of permeability of respiratory ways an oxygenation is carried out, using an oxygen mask. At absence of effect within several minutes, the child is treated, as at a serious asphyxia. The serious asphyxia at birth is the absolute indication for an intubation of a trachea, drainage of a tracheobronchical tree through an endotracheal tube and artificial ventilation of lungs.

Lung artificial ventilation is carried out with the help of system Aira or devices intended for newborn and children of younger age "Mlada", "Vita-1", "Batlog", "Angstreme" etc. First minutes for artificial ventilation use 100 % Oxygenium, and then (depending on dynamics of child condition) 50-60 % a Oxygenium-air admixture. The compulsory pressure of the first inspirations makes 30-40 mm Hg (3,9-5,2 kPa), and further - no more than 20 mm Hg (2,6 kPa). Respiratory volume establish usually within the limits of 15-25 cubic cm (6 cm/kg), ratio of an inspiration and exhalation 1:2 frequency of respirations 40-50 in 1 min.

In case of absence of independent inspirations during 15-20 mines from a ALV beginning the reanimation measures should be stopped, as it testifies to serious irreversible changes of a brain. Exception are children, born in a condition of medicamental dream (cesarean section, labors under a narcosis etc.).

After the ALV termination in the event that it proceeded more than 10 min, the child is expedient to transfer to spontaneous respiration with constant positive pressure in pneumatic ways - by a Gregory or Martin-Buer method. Superfluous concentration of Oxygenium in an inhaled admixture select individually depending on a condition of the child and parameters of gas structure of a blood (the О2 pressure should not exceed 10,4 kPa, or 80 mm Hg).

At primary newborn reanimation newborn orotracheal intubation by elastic endotracheal tubes, which outside diameter for children makes 3-3,5 mm, and for premature (depending on body mass at birth) - from 2 up to 3,5 mm

An endotracheal tube enter on depth about 2 cm (length of a trachea at normal children about 4 , and at premature about 2 cm). After an intubation check correctness of a position of an endotracheal tube (auscultation of symmetric pulmonary fields in supraclavicular area), then it is fixed by an adhesive plaster. Lavage of a bronchial tree is carried out in case of massive aspirative syndrome by a sterile isotonic solution of a Sodium chloridum in quantity several ml with subsequent its careful erasion by electropump through a thin catheter entered in an endotracheal tube on depth no more 5 cm. The outside diameter of a catheter makes no more 2/3 internal sections of an endotracheal tube. The negative pressure on the electropump monitor should not exceed 3,05 kPa. It is necessary to limit duration of procedure 20 sec, combining it with vibratory massage of a thorax.

After restoration of independent respiration it is necessary to remove the stomach content through a probe. At heart beats absence or expressed bradycardia (less than 60-70 impacts in 1 min) the closed cardiac

massage with frequency about 100 in 1 min must be carried out with amplitude of shift of a breast bone 1,5-2,0 cm. The closed cardiac massage is carried out by the first fingers of both arms, by establishing them in the field of a newborn xiphoid processus, thus the brushes of arms cover its thorax. Absence of cardiac reductions is also indication for internal introduction of a Adrenalinum solution.

After clearing of respiratory ways and the adjustments of an oxygenation by that or different way the correction of metabolic infringements is carried out. In case of average gravity of an asphyxia the umbilical vein is punctured and slowly with rate 2-3 ml in 1 min is entered 20 % solution glucose from account of 5 ml/kg, and also 8-10 ml/kg of a cocarboxylase.

To children transferred weak hypoxia it is expedient with the first minutes of life to carry out infusive therapy through constant catheter, entered in umbilical vein (in aseptic conditions, processing of arms as for surgical operation), the outside diameter of a catheter usually makes 2-3,5 mm, depends on mass of the child at birth and should densely close a lumen of a vessel (in order to prevent bleeding). Umbilical wound is closed by a sterile napkin, and a catheter fixed by an adhesive plaster to a skin of the abdomen. Through a constant catheter slowly (20 drops in 1 min) 2,5 ml/kg 4 % solution of a sodium hydrocarbonate, 1-2 ml/kg of Prednisolonum (or 4-5 ml/kg of Hidrocortizonum), 5 ml/kg 20 % of a glucose solution, 10 ml/kg of a cocarboxylase are infused.

Once again we emphasize that a hydrocarbonate of a sodium pour in only after adjustment of an adequate oxygenation.

Repeated introduction of a solution of a sodium of a hydrocarbonate can be carried out only at presence of a decompensated acidosis (pH 7,2 and less), however at adequate respiratory and the necessity for it is intimate more often vascular reanimation disappears.

At a respiratory depression of newborn, connected with application at the mother barbiturates, Aether aethylicus, Promedolum, Omnoponum, expediently, unitary introduction of an analeptic Kudrin admixture (0,5-1 ml) or ethimisolum (1 ml/kg).

At a shock resort to infusion of hyperosmolar solutions for struggle with a brain edema and also intravenous introduction of glucocorticoids, Dopaminum, Euphyllinum, Curantylum, Pyracetamum), Heparinum (20 ME/kg everyone 6 hours). The expediency of desagregants assignments at a serious asphyxia is caused by a pachemia, tendency to trombotic complications at the first hours and days of life. More preferable with this purpose to enter Pyracetamum (50-100 mg/kg 2 times into day), which worsening the aggregating ability of thrombocytes, at the same time improves metabolic processes and circulation of a brain, if necessary (vomiting, abdominal distention, the diarrhea, extreme gravity of a condition, shock etc.) at account to a daily liquid load is necessary to proceed from the clinical and laboratory data of the child, its diuresis, age, needs for water and electrolytes.

Taking into account that at a serious asphyxia the oligemia and brain hypoperfusion is typical, such children (is especial at an asphyxia after chronic intrauterine hypoxia) general daily load of a liquid per the 1-st day of life usually makes 50-65 ml/kg with the further its augmentation till 20 ml/kg each day. Daily amount of a liquid divide into 4 parts and enter each part (2-4 drops in 1 min) with an interval at 6 hours. A basis of an entered liquid - 10 % add a solution of a glucose, to which since the 2-nd day electrolytes in the specified quantities. In 1-st and the 3-rd days of life pour plasma, and other days - 10 % a solution of Albuminum (10-15 ml/kg) or Alvesinum, Anionum (0,5 g/kg 2 times per day). The assignment of diuretic (Lasix till 1-2 mg/kg 3 times per day) is necessary.

At absence of the indications to parenteral feeding to children, born in a serious asphyxia, first 2-4 days of life daily pour in intravenously vitamine-glucose-energetic complex (10 % glucose solution 15-20 ml/kg, cocarboxylase 8-10 mg/kg, Acidum ascorbinicum 25 mg/kg), intramuscularly nominate 0,2 ml/kg 25 % solution of Mg sulfas 1 time per day, vitamin K2 (0.3-0,5 ml 1 % solution 1 time per day at birth). In case of an asphyxia of average gravity injection of a vitamine-glucose-energetic complex is done under the indications.

The antibiotics nominate under the strict indications, but is especial to all children transferred a serious hypoxia and who are taking place on ALV.