Intrauterine hypoxia of the fetus and asphyxia of the newborn. Stages of hypoxic-ischemic brain damage in full-term newborns according to h.B

). Due to the lack of oxygen, under-oxidized metabolic substances accumulate in the fetus's body - pyruvic acid, lactic acid, fat metabolism products - ketone bodies and others (metabolic acidosis).

Causes of asphyxia in newborns and theirs. in newborns in 75-80% of cases it is a continuation of intrauterine fetal hypoxia and is classified as primary, or congenital. In 20-25% of cases, secondary, or acquired, asphyxia is identified, which occurs after birth 30-40 minutes - up to 5 days. Clinically, the secondary is manifested by intermittent, difficult breathing, shortness of breath, increasing cyanosis, and motor restlessness. If help is delayed, he may die. This is a clinical manifestation of the pathology of the fetus itself. The following groups of causes of secondary asphyxia can be distinguished.

1. Violation of central function as a result of the damaging effect on brain tissue of intrauterine hypoxia, acidosis and electrolyte changes that cause swelling of the brain and nerve centers that regulate. It is believed that the reticular formation of the midbrain, involved in the mechanism of the first breath, is the most vulnerable. It is the insufficient maturity of the midbrain or various damaging factors affecting it that can cause asphyxia in a newborn.

5. Hemorrhage into the lung tissue of a newborn, especially in premature infants, is combined with various types of pneumopathy.

Apgar score

Signs		Lethargic. Limbs dangling		Active limb movements
	Prevention of septic and inflammatory diseases is prescribed, mainly semi-synthetic ones (oxacillin sodium salt, metacillin sodium salt). Antihemorrhagic therapy is mandatory (calcium chloride 5% solution orally, Vicasol 0.3% solution 0.1 ml 2 times intramuscularly for 3 days, ascorbic acid, group B). Subsequently, those who have suffered asphyxia should be under the supervision of a neurologist and pediatrician.

Structure of perinatal mortality

Prematurity (50%).

Intrauterine hypoxia:

Stillbirths;

Hypoxia during childbirth.

Developmental defects.

Infection.

Accident or injury not related to childbirth.

Other unclassifiable causes.

In absolute frequency, the most common cause of perinatal mortality is intrauterine asphyxia. The development of placental insufficiency and fetal asphyxia is associated with a complex of both maternal and fetal factors, including the adaptive capabilities of the fetus.

Factors affecting fetal oxygenation

External environment:

Atmospheric oxygen pressure.

Maternal factors:

Hemoglobin concentration and its affinity for oxygen;

Maternal cardiovascular and respiratory adaptation.

Placental factors.

1. Physiological:

Speed ​​of umbilical cord and uterine blood flow.

2. Structural:

The area of ​​the diffusion surface of the villous epithelium;

Thickness of the diffusion membrane of the villi;

Diffusion shunts.

Fruit factors:

Concentration and predominant type of hemoglobin;

Cardiac output and blood flow distribution.

Mechanisms of fetal adaptation to hypoxia

High hemoglobin concentration.

High affinity of fetal hemoglobin (FHb) for oxygen.

High blood flow speed.

The perfusion rate of fetal organs is higher than the physiological oxygen demand.

Anaerobic glycolysis.

Classification of fetal hypoxia by course

Chronic.

Exacerbation of chronic

Classification of hypoxia

Hypoxic:

Maternal hypoxia (extragenital pathology);

Placental insufficiency (placental abruption).

Hemic:

Diseases of the fetus with impaired oxygen binding (hemolytic disease).

Circulatory:

Umbilical cord compression;

Congenital heart defect.

Fabric:

Incomplete utilization of oxygen by tissues due to disruption of enzymatic systems.

The main causes of fetal hypoxia (distress)

Placental insufficiency.

Fetal pathology.

Umbilical cord compression.

Maternal hypoxia.

Placental insufficiency is characterized by a gradual decrease in the transfer of oxygen and nutrients to the fetus.

The passage of nutrients is the first function that is disrupted during FPN with the formation of intrauterine growth retardation, followed by a decrease in the respiratory function of the placenta with the formation of hypoxia. Persistent hypoxia causes anaerobic metabolism and fetal acidosis. Thus, a significant clinical manifestation of chronic placental insufficiency is fetal growth restriction.

FGR of the fetus is understood as the discrepancy between its size and the normal size for a given stage of pregnancy. The initial criterion for the presence of FGR in a child is a decrease in the value of his body weight and (or) height, characteristic of gestational age, by 2 weeks (or more) less than the actual one.

By unifying the terminology in accordance with ICD-10, we consider it appropriate to designate the term “asymmetric form of FGR” as a small fetal weight for a given gestational age (RO.5.0), and the term “symmetrical form of FGR” as a small fetal size for a given gestational age (RO.5.1 ), and the term “hypotrophy” is a pathology associated with malnutrition of the fetus (PO.5.2).

The etiology and pathogenesis of FGR are shown in Fig. 101.

Rice. 101. Etiology and pathogenesis of FGR

When generalizing, the reasons for the development of fetal FGR are as follows.

1. Metabolic disorders due to various complications of pregnancy.

2. Congenital anomalies or intrauterine infection.

3. Insufficiency of production of fetal growth hormones or pathology of their receptors.

The main directions in the treatment of placental dysfunction are as follows.

1. Normalization of uteroplacental circulation.

2. Normalization of gas exchange between the mother and fetus.

3. Increased metabolic activity of the placenta.

4. Impact on the fetus that bypasses the placenta (paraplacental metabolic pathway).

Principles of the theory of placental insufficiency

Infusion therapy.

Anabolic, nootropic therapy (actovegin, carnitine chloride, instenon, potassium orotate, riboxin, etc.).

Dissegregation therapy (chimes, aspirin, low molecular weight heparins, pentoxifylline, xanthinol nicotinate, etc.).

Antioxidant therapy (ascorbic acid, tocopherols).

Tocolytic therapy.

Ozone therapy.

Etiotropic therapy.

1. Anabolic therapy

Actovegin- hemoderivative of low molecular weight peptides and nucleic acids.

Main action- increase in cell energy metabolism. Mechanisms of action.

Increases intracellular glucose consumption and transport fivefold.

Increases oxygen utilization and consumption.

Stimulates lipid biosynthesis.

Carnitine chloride

Main pharmacological effect- increasing the energy metabolism of the cell.

Mechanisms of action.

Carries out intracellular transport of acetyl coenzyme-A in mitochondria during β -oxidation of long-chain fatty acids and pyruvate.

Increases acetylcholine production.

Stimulates the synthesis of protein and phospholipids of cell membranes.

Stimulates cholesterol synthesis.

Instenon- three-component nootropic drug.

Etophylline:

Reduces total peripheral vascular resistance;

Increases cardiac output.

Etamivan:

Gives a nootropic effect, activating the respiratory and vasomotor centers, limbic system and reticular formation.

Hexobendine:

Selectively stimulates intracellular metabolism, increasing the utilization of glucose and oxygen when anaerobic glycolysis is activated under hypoxic conditions.

2. Disaggregation and anticoagulant therapy

Low molecular weight heparins.

Fraxiparine (nadroparine calcium) 0.3 ml (7500 units) per day subcutaneously.

Clexane (enoxaparin sodium) 0.2 ml (20 mg) per day subcutaneously.

Medical ozone has a multifactorial effect on the fetoplacental complex. Local effect of ozone: disinfectant activity against bacteria, viruses and fungi. Systemic effect: improvement of the rheological properties of blood and microcirculation in general; activation of enzyme systems of antioxidant protection; stimulation of oxygen-dependent processes in the body; increased activity of immunocompetent cells.

The course of pregnancy and the functioning of the fetoplacental complex, as well as the course of labor and the condition at birth, have a fundamental influence on the perinatal outcome.

If there is no effect from conservative therapy, surgical delivery is indicated - cesarean section, and in the second stage of labor, with the head in the pelvic cavity - obstetric forceps, in case of breech presentation - extraction of the fetus by the pelvic end.

Prevention of fetal hypoxia during childbirth

Stopping labor stimulation.

Lateral position of the woman in labor.

Infusion therapy.

Oxygen inhalation.

Tocolytic therapy.

Intra-amnial infusion.

Until now, the main criterion for the condition of a newborn is the Apgar score, which determines not only the degree of hypoxia, but also (indirectly) the need for resuscitation measures (Table 22).

Note: 6-7 points - mild hypoxia; 4-5 points - moderate hypoxia; less than 4 points - severe hypoxia.

The causes of asphyxia in newborns are reflected in table. 23.

The procedure for resuscitation measures

Heating (t = 32-33 °C).

Restoring airway patency:

Suction of mucus;

Intubation and sanitation of the trachea and bronchi.

Breathing support:

Ambu bag;

Hardware ventilation;

Naloxone.

Circulatory support:

Infusion therapy;

Cadiotonics: dopamine, dobutrex.

Indirect cardiac massage is performed with persistent bradycardia lasting more than 15-30 s and heart rate below 60 beats/min at

background of mechanical ventilation.

Table 23

Causes of newborn asphyxia

Group of reasons	Etiological factors	Clinical manifestations
	Umbilical cord prolapse Breech birth Abnormal positions Obstetric forceps	Circulatory disorders Hypovolemia Shock
Medicines	Narcotic analgesics Sedatives	Respiratory depression
Congenital pathology	Intrauterine infection	Cardiopulmonary failure
Maternal diseases and pregnancy complications	Diabetes mellitus Eclampsia Postmaturity Rh conflict	Hypoglycemia Anemia Meconium aspiration
Exogenous and iatrogenic	Childbirth in the cold Pneumothorax, mediastinum due to mechanical ventilation	Hypothermia Compression of the heart and lungs

Infant mortality from congenital malformation is caused in: 45.9% of cases - congenital heart defects and circulatory system defects; in 32.9% - multiple malformations; in 18.4% - spina bifida and other defects of the nervous system. Thus, a significant reserve for reducing infant mortality is improving the organization and improving the quality of prenatal diagnostics.

Ways to reduce perinatal morbidity and mortality

Competent management of the prenatal period.

Widespread prenatal screening.

Training of specialists in prenatal diagnostic methods and data interpretation.

Involvement of experienced specialists and consultants in the management of high perinatal risk births.

Expert assessment of perinatal mortality cases.

Staffing with full-time specialized specialists.

Fetal hypoxia is a pathological condition based on intrauterine oxygen deficiency.
Risk factors for the development of antenatal hypoxia fetus are: post-term pregnancy, long-term (more than 4 weeks) gestosis in pregnant women, multiple pregnancy, threat of miscarriage, diabetes mellitus in pregnant women, bleeding, somatic and infectious diseases in the first trimester of pregnancy, smoking and other types of drug addiction in pregnant women.

Under acute asphyxia newborn refers to the absence of gas exchange in the lungs after the birth of the child, i.e. suffocation in the presence of other signs of live birth as a result of exposure to intrapartum factors (oxygen deficiency, accumulation of carbon dioxide and under-oxidized products of cellular metabolism). Asphyxia, which developed against the background of chronic intrauterine hypoxia, is asphyxia of the newborn, which developed antenatally in conditions of placental insufficiency.

The main factors of high risk of developing intrapartum fetal asphyxia:

C-section; pelvic, breech and other abnormal presentations of the fetus;

Premature and late birth;

Anhydrous interval 10 hours;

Rapid labor - less than 4 hours for primiparous women and less than 2 hours for multiparous women;

Previa or premature placental abruption, uterine rupture;

Use of obstetric forceps 11 other aids during childbirth (shock, etc.);

Disorders of the placental-fetal (umbilical cord) blood circulation due to tight entanglement, true nodes, etc.;

Diseases of the heart, lungs and brain in the fetus, abnormal heart rate in the fetus;

Meconium in amniotic fluid and its aspiration;

narcotic analgesics administered 4 hours or less before the birth of the child.

Summarizing the above, we can identify five leading mechanisms leading to acute asphyxia of newborns:

1. Interruption of blood flow through the umbilical cord (true knots of the umbilical cord, compression of it, tight entanglement of the umbilical cord around the neck)

2. Impaired exchange of gases through the placenta (premature complete or incomplete placental abruption, etc.)

3. Inadequate hemoperfusion of the maternal part of the placenta (excessively active contractions, arterial hypotension and maternal hypertension)

4. Deterioration of maternal blood oxygenation (anemia, cardiovascular and respiratory failure)

5. Insufficient respiratory efforts of the newborn (damage to the fetal brain, congenital malformations of the lungs, etc.).

Pathogenesis. Main links: intrauterine hypoxia causes the activation of compensation mechanisms aimed at maintaining adequate oxygenation of fetal tissues, increasing the release of glucocorticoids, the number of circulating red blood cells and the volume of circulating blood, enhancing the motor activity of the fetus and the frequency of “respiratory” movements of the chest with a closed glottis, etc.;

Ongoing hypoxia stimulates anaerobic glycolysis, and increasing oxygen deficiency causes the body to reduce oxygenation of the intestines, skin, liver, and kidneys;
a redistribution of blood circulation occurs with predominant blood supply to vital organs (brain, heart, adrenal glands), i.e. the fetus adapts to increasing hypoxia;

Severe and/or prolonged hypoxia entails a breakdown of compensation mechanisms, which is manifested by depletion of the sympathetic-adrenal system and adrenal cortex, arterial hypotension, bradycardia, and collapse;

Developing hypoxic encephalopathy due to ischemia of brain tissue, dyselectrolythemia and minor hemorrhages in brain tissue;

Hemorheological and tissue disorders accompanying hypoxia lead to cardiac hypoperfusion, ischemic necrosis of the endocardium and papillary muscles, and aggravate arterial hypotension;

Hypoxia also maintains high resistance in the pulmonary vessels, resulting in pulmonary hypertension.

So it's heavy perinatal hypoxia can cause multiple organ dysfunctions that manifest themselves in the central nervous system hypoxic-ischemic encephalopathy, cerebral edema, intracranial hemorrhage, convulsions; lungs - pulmonary hypertension, meconium aspiration syndrome, surfactant destruction, post-hypoxic pneumopathy; cardiovascular system - pathological shunting, hyper- or hypovolemia, shock, ischemic necrosis of the endocardium, tricuspid insufficiency; kidneys - oliguria, acute renal failure with or without vascular thrombosis; gastrointestinal tract - necrotizing enterocolitis, vomiting, regurgitation, functional failure; metabolism - pathological acidosis, hypoglycemia, hypocalcemia, hypomagnesemia; vitamin K deficiency, disseminated intravascular coagulation syndrome, secondary immunodeficiency, etc.

Classification of newborn asphyxia. According to the International Classification of Diseases (ICD) IX revision (Geneva, 1980), depending on the severity of the child’s condition at birth, there are:
1. Asphyxia of moderate severity (moderate) - 4-6 points in the first minute, by the fifth - 8-10 points
2. Severe asphyxia - 0-3 points on the Apgar scale at the 1st minute, by the 5th - less than 7 points

Apgar score

Symptoms	Score in points
H SS (in 1 min.)	Absent	Less than 100	100and more
Breath	Absent	Bradypyoe, irregular	Normal, loud scream
Muscle tone	Limbs dangling	Some limb flexion	Active movements
Reflex excitability (reaction to nasal catheter, irritation of soles)	Does not react	Grimace	Cough, sneeze, scream
Skin coloring	Generalized pallor or cyanosis	Pink coloration of the body and bluish extremities (acrocyanosis)	Pink coloring of the whole body and limbs

Clinic of moderate asphyxia: the child’s condition at birth is moderate, the child is lethargic, but spontaneous motor activity is observed, the reaction to examination and irritation is weak. The physiological reflexes of a newborn are depressed. The cry is short, unemotional. The skin is anotic, but with oxygenation it quickly turns pink, often leaving acrocyanosis. During augcultation, tachycardia, muffled heart sounds or increased sonority are heard. Breathing after prolonged apnea is rhythmic, with sighs. Repeated apnea is characteristic. Over the lungs, weakened breathing, moist rales of various sizes, and a boxy percussion tone are possible. Hyperexcitability, small-scale tremor of the hands, impaired “g”, frequent regurgitation, hyperesthesia, and a positive spontaneous Moro reflex are noted. and have a functional character, being a consequence of metabolic disorders and intracranial hypertension. With adequate therapy, the condition of children quickly improves and becomes satisfactory by the 5th-5th day of life.

For severe asphyxia: the general condition at birth is severe or very severe. Physiological reflexes are not evoked in the sand. With active oxygenation (usually with the help of mechanical ventilation), it is possible to restore the skin color to a pink color. The heartbeats are often dull, and systolic murmur may appear. In case of a very serious condition, the clinic may comply hypoxic shock - pale skin with an earthy tint, a “white spot” symptom of 3 seconds or more, low blood pressure, no spontaneous breathing, no reaction to visual inspection and pain stimulation, areflexia, muscle atonia, closed eyes, sluggish reaction of the pupils to light or lack of reaction/ miosis or mydriasis, nystagmus, dysfunction of many other organs and systems are possible.

Complications: early (in the first hours and days of life): brain damage - edema, intracranial hemorrhage, periventricular lesions, necrosis; pulmonary hypertension. polycythemia, shock, myocardial ischemia, acute tubular renal necrosis, renal vascular thrombosis, deficiency of surfactant synthesis, etc.; late complications are dominated by meningitis, sepsis, pneumonia, hydrocephalic syndrome, bronchopulmonary dysplasia of the entero-league
Diagnosis. Asphyxia is diagnosed on the basis of clinical data, in particular, about. Apgar scores at the 1st and 5th minutes of life, as well as indicators of the main clinical and laboratory parameters determined by clinical, hardware and clinical monitoring. Taken into account: heat mass dynamics. registration of temperature, dyspepsia, oxygen concentration in the inhaled mixture, dynamics of characteristic symptoms
clinical symptoms, heart rate, blood pressure, hematocrit, hemoglobin, leukocyte formula, CBS, etc.

Differential diagnosis carried out with conditions causing cardiorespiratory depression, as well as with acute blood loss, intracranial hemorrhage, and in premature infants - RDS (Respiratory Disorder Syndrome).

Treatment. The system of primary neonatal resuscitation was developed by the American Heart Association and the American Academy of Pediatrics. The main stages of resuscitation are called “ABC steps”.

Main stages:

A. ensuring airway patency (Airways);

B. stimulation or restoration of breathing (Breathing);

C. maintaining blood circulation (Circulation).

After the birth of the child, it is necessary to establish the presence or absence of meconium in the amniotic fluid and, depending on this, resuscitation measures are determined.

A. When excluding meconium in the amniotic fluid:
- transfer the newborn from the mother under the source of an infrared heater;

Quickly dry the skin using blotting movements through the diaper (throw away the wet diaper);

Ensure maximum airway patency by correctly positioning the child on his back with his head moderately extended and a cushion under his shoulders.

The cavity of the mouth, nose and pharynx is cleared of contents, while avoiding irritation of the back wall of the pharynx, because this excites the parasympathetic nervous system and provokes bradycardia and apnea;
In the absence of spontaneous breathing, carry out tactile stimulation using one of three techniques, which is repeated no more than 2 times: patting the sole, light blows to the heel, irritation (such as rubbing) of the skin along the spine with the palm of the hand. In most cases, drying, suctioning, and tactile stimulation are sufficient to induce effective spontaneous breathing. The duration of this stage should not exceed 15-20 seconds.

Prohibited:
o Irrigate the child with cold or hot water;
Use a stream of oxygen on your face;
Compress the chest;
Patting the buttocks.

B If meconium is detected in the amniotic fluid, i.e. When meconium aspiration occurs:
- after the birth of the head, the midwife sucks out the contents from the upper respiratory tract
paths:
- the newborn is placed under a source of radiant heat;
and without wasting time on drying, place the child on his back with a slightly thrown back
head and cushion under the shoulders;
- perform tracheal intubation:
- re-suction the contents from the upper respiratory tract:

The contents are sucked out from the tracheobronchial tree directly through the endotracheal tube (without using a catheter). If there are residual meconium in the endotracheal tube after suctioning, intubation and suctioning are repeated. Lavage of the tracheobronchial tree is not performed due to possible damage to the surfactant. All of the above measures must be completed within 20 seconds. After this, the child’s condition is sequentially assessed according to three criteria:

breath,
heart rate,
color of the skin.

In the absence or ineffectiveness of spontaneous breathing, artificial ventilation of the lungs with 90-100% oxygen is immediately started using a mask and an Ambu bag. Respiratory rate 40 per minute, pressure 20-40 cm water column. Carrying out mechanical ventilation for longer than 2 minutes. requires insertion of a tube into the stomach to decompress and prevent regurgitation. The ineffectiveness of mask ventilation dictates the need for endotracheal intubation and continued mechanical ventilation. The effectiveness of ventilation is determined by the presence of chest movements and auscultation data.

Method of probe insertion: It is injected to a depth equal to the distance from the bridge of the nose to the earlobe and from the earlobe to the epigastric region. After inserting the probe, the gas from the stomach is sucked out with a syringe, the probe is left open and fixed with an adhesive plaster to the cheek. Artificial ventilation is continued over the probe. After 15-30 seconds of artificial ventilation, the child’s condition is assessed and the heart rate (HR) is determined. Heart rate is calculated over 6 seconds and multiplied by 10. Ventilation is stopped during the calculation. Heart rate estimate (per 1 min):
and more than 100
O from 60 to 100 and the frequency increases O from 60 to 100 and the frequency does not increase O less than 60

1. Heart rate more than 100: If spontaneous breathing is present, artificial ventilation is suspended and skin color is assessed; in the absence of spontaneous breathing, continue artificial ventilation until it appears;
If the heart rate is less than 100, artificial ventilation is performed regardless of the presence of spontaneous breathing.

2 Heart rate from 60 to 100 and the frequency increases: artificial ventilation continues.

3. Heart rate from 60 to 100 and the frequency does not increase: Artificial ventilation is continued, closed chest compressions are indicated when the heart rate is less than 80.

4. Heart rate less than 60: Artificial ventilation and closed cardiac massage.
Heart rate control is carried out every 10-15 seconds until the frequency exceeds 100 and spontaneous breathing is restored. In this situation, a final assessment of the condition is made.
Skin color is assessed. With effective ventilation and blood circulation, the skin color is pink, the child requires observation.
Acrocyanosis in the first hours after birth is a vascular reaction to the external temperature and is not associated with hypoxia. A sign of hypoxia is general cyanosis. In this case, the child needs an increased concentration of oxygen in the inhaled mixture (up to 80% oxygen during inhalation). The disappearance of cyanosis indicates the elimination of hypoxia, and the administration of the mixture stops.

Closed heart massage. Indications: after 15-30 seconds. artificial ventilation heart rate less than 60 per minute. or 60-80 in 1 minute. and does not increase. Method: pressing on the lower third of the sternum with the thumbs of both hands or 2-3 fingers of the right hand with a frequency of 120 per minute, depth of pressing 1.0-1.5 cm. Synchronization with mechanical ventilation: after 1 breath, 3 compressions on the sternum. The other hand supports the backrest.

Tracheal intubation. Indications: need for prolonged artificial ventilation; meconium aspiration; diaphragmatic hernia; unsuccessful ventilation through bag and mask.

Medicines used in the maternity room for neonatal resuscitation:

A drug	Dosage form	Dose	Pool and administration method
Adrenalin	0.01%dissolution	0.1-0.3 mg/kg	IV or endotracheal, administer quickly
Restoring the volume deficit	0, 9% sodium solution Chloride, 5% albumin. blood, Ringer's solution	10 ml/kg	V/ V administer over 5-10 minutes
Sodium bicarbonate	0.5mmol/l (4.2% solution)	2-4 ml/kg	V/ V slowly (2 ml/kg) only for a child with effective valiyacisn
Nalorphine	0.05% solution	(),1-0.2ml/kg	V/ V quickly or subcutaneously, endotracheally.
Remember	0.5%solution	5-20mkt/kg/min IV under control of pulse and blood pressure, starting with a starting dose of 5 mg/kg/min and increasing it to 10-15-20 mg/kg/min.

Start planned infusion therapy if necessary after 40-50 minutes. after birth. The volume on the first day is about 60-65 ml/kg/day in the form of isotonic sodium chloride solution, Ringer's solution, rheopolyglucin.
Forecast. Full-term babies born in severe asphyxia have a high mortality rate (10-20%) and a frequency of psychoneurological abnormalities. The following are considered prognostically unfavorable: maintaining very low (3 points or less) Apgar scores 15 and 20 minutes after birth; the presence of post-hypoxic encephalopathy of 1st and 2nd degrees and other complications.

Fetal hypoxia- this is an insufficient supply of oxygen to him through the placenta (oxygen deficiency) and the accumulation of under-oxidized metabolic products in his body.

There are chronic and acute fetal hypoxia. Chronic is most often caused by changes in the placenta due to such pathological malfunctions of the mother as late pregnancy, extragenital diseases (heart defects, etc.)

Acute hypoxia, unlike chronic hypoxia, rarely occurs during childbirth and quite often during childbirth. It may be caused by labor abnormalities, premature placental abruption, uterine rupture, etc.
Acute fetal hypoxia in the second stage of labor can develop as a result of the occurrence of reasons that impede blood circulation in the umbilical vessels: pressing of the umbilical cord or entwining it around the neck and other parts of the fetus, the formation of a true umbilical cord knot. Diseases of the fetus itself can cause its hypoxia. Prolonged fetal hypoxia causes circulatory disorders and multiple hemorrhages in various organs, incl. intracranial.

If the phenomenon of hypoxia increases and the supply of oxygen from mother to fetus rarely decreases, the fetus may die in utero.

When diagnosing fetal hypoxia, the following clinical indicators are taken into account:
1. Change in fetal heart rate, increase to 160 beats. per minute or more, and then a persistent slowdown to 110-100 beats. in min or less. Changes in the rhythm and sonority of heart sounds are of particular importance for diagnosis.
2. Detection of meconium (original feces) in the amniotic fluid.
3. Change in fetal motor activity.

To record the existing activity of the fetus, use:
Ultrasound
Phonography
Electro-monitor surveillance

Treatment of fetal hypoxia:
1. Intermittent inhalation of increased oxygen by the mother in labor (or pregnant woman) for 10 minutes, repeated at intervals of up to 2-3
2. IV 40-50 mg 40% glucose
3. i\m 1 mg
4. Sigetin - 2-4 mg of 1% solution dilates the vessels of the uterus, improves uteroplacental circulation and oxygen supply to the fetus.
5. Drugs that improve placental function: (aminophylline, pentoxifylline, chimes, reopolyuglyukin).
6. Severe forms of hypoxia leading to disruption of metabolic processes in the fetus and the development of acidosis, in order to eliminate acidosis of the pregnant or parturient woman, 150-200 ml of a 5% solution of Na hydrocarbonate is administered.
7. If measures to combat fetal hypoxia are not effective, then rapid delivery is necessary because hypoxia can lead to fetal death; often the abdominal method (cesarean section) is used for delivery.

Asphyxia of newborns

Newborn asphyxia is a condition when, after birth, the baby’s breathing is absent or irregular in the presence of cardiac activity.

In a newborn, suppression of all vital functions of the body is observed. In addition to intrauterine hypoxia, asphyxia of a newborn can be caused by congenital defects, development of the central nervous system, heart, lungs and others.

To determine the condition of newborns, the Apgar scale is used, which is based on a 10-point assessment of 5 clinical signs: heartbeat, breathing, muscle tone, reflex excitability and skin color. The maximum score for each of the characteristics is 2 points. If a child receives 5-6 points during the assessment, then it should be considered that he is in a state of mild asphyxia. Children who receive 1-4 points on the Apgar scale are considered to be born with severe asphyxia. In case of clinical death, the Apgar score is 0 points. For low scores, a re-assessment is necessary after 5-10 minutes.

Treatment of newborn asphyxia:
1. Is emergency (resuscitation, resuscitation).
2. Immediately after birth, the airways are cleared of mucus, blood, and amniotic fluid using a rubber catheter connected to a vacuum apparatus or rubber balloon.
3. If the newborn is not breathing, he must be separated from the mother, transferred to a dressing table heated at 37 C and artificial respiration must be started immediately.
4. A 20% solution of glucose cocarboxylase, ascorbic acid, prednisolone, and a 5% solution of sodium bicarbonate are injected into the umbilical vein.
5. In case of cardiac arrest, external massage.
6. If there is no effect from external massage, adrenaline is injected intracardially.

If resuscitation measures carried out within 15-20 minutes do not restore spontaneous breathing in the newborn, then the attempt to revive the child should be abandoned, because with later revival, the child experiences severe neurological disorders

Among other pathologies that can threaten the health and life of a child, a significant place is occupied by fetal hypoxia And asphyxia of the newborn. Fetal hypoxia occurs during intrauterine development, while asphyxia of the newborn can occur shortly before birth and even during it.

Concerning fetal asphyxia, its causes often lie in the state of the mother’s health, circulatory disorders in the uterus and placenta, as well as malformations of the fetus. Regardless of the reasons for the occurrence, the essence is that a sufficient amount of oxygen ceases to enter the fetal body. In tissues and blood, the normal course of redox processes is disrupted, and an abnormally large amount of organic acids accumulates. Because of this, the fetus may experience depression of the central nervous system, and the functions of the cardiovascular system and excretory organs may deteriorate. A kind of self-poisoning of the body occurs, which can affect the course of its development, and in severe cases, lead to the death of the unborn child.

• metabolic disorders in the mother due to diabetes mellitus, infectious diseases, as a result of which oxygen metabolism in the placenta has worsened,
• smoking or drug use,
• the mother's own anemia due to insufficient (improper) nutrition or problems with hematopoiesis.

Of course, if for some reason a woman has impaired hemodynamic or lung function, then not only she, but also the fetus will suffer from a lack of oxygen. The risk of occurrence also increases fetal hypoxia and with gestosis, i.e. when the functions of vital organs are disrupted due to the additional load on the mother’s body. Especially if a woman is carrying more than one child, or post-term pregnancy. Precisely in order to reduce this danger, it is useful for the expectant mother to examine her health status and treat existing diseases before the start of pregnancy.

Placental circulatory disorders and fetal hypoxia

As for circulatory disorders, the following can negatively affect it:

• incorrect position of the fetus and the umbilical cord, due to which the umbilical cord will be compressed.
• impaired circulatory function in the placenta due to pathology in the development of pregnancy, as well as during prolonged labor, when placental abruption has already occurred and the child has not yet received the opportunity to breathe on his own.

Of course, only a specialist can correctly assess the severity of oxygen deficiency for the fetus. But if the fetus, which has been moving normally and regularly, becomes less active, does not respond to external stimuli, or, on the contrary, bothers the mother for a long time with continuous tremors, this is noticeable even without medical knowledge and should be a reason for examination by a doctor.

Asphyxia of the newborn

As for asphyxia of the newborn, then it is customary to distinguish between primary and secondary asphyxia. Primary occurs at the time of birth, and secondary occurs in the first few hours or days after birth. Breathing in a newborn may either be absent altogether or be weak and irregular.

So, the causes of the primary asphyxia of the newborn can be:

• prolonged labor
• blockage of the airways with mucus or inhalation of amniotic fluid.

In such cases, they try to clear the child’s airways as quickly as possible and, if necessary, apply artificial ventilation, possibly with oxygen. If the child is normally developed and healthy, and the period of oxygen starvation was short, then independent breathing should soon occur.

But more often the reason lies in the child’s prolonged oxygen starvation before birth, infection, injury, or even developmental pathology. There is no tone of the respiratory muscles, and the lack of oxygen disrupts the activity of the heart and nervous system, which, in turn, creates additional obstacles to the restoration of normal functioning of the body.

Degrees of newborn asphyxia

Depending on whether intrauterine hypoxia occurred and how severe it was, so-called blue and white asphyxia may occur.

• When blue, the baby's skin may have a bluish or purple tint, muscle tone is present, and the heartbeat may be slow.
• When white, the skin is pale and cold, the muscles are relaxed, and the heartbeat is difficult to hear.

Such a child, even with a cleared airway, will not be able to breathe on his own and needs to use all available methods of revival - artificial respiration, irritation of the respiratory center, injections of appropriate drugs. During the first steps, the umbilical cord is not cut so that the baby can receive oxygen from the mother’s body.

Secondary asphyxia of the newborn

Secondary asphyxia of the newborn sometimes it manifests itself several hours, even a day after birth. It can be caused by pathologies of the newborn’s respiratory tract, cerebral circulatory disorders, or other reasons that have to be determined in order to prescribe the most appropriate treatment. But measures to maintain breathing and oxygen levels in the blood should be carried out in any case.

Hazard warning

Many cases of asphyxia are accompanied by the risk of complications - pneumonia, intracranial hemorrhages, cerebrovascular accidents, and, as a consequence, irreversible dysfunction of the nervous system. Therefore, it is extremely important to conduct a medical examination of the expectant mother in advance for complications, both during pregnancy and childbirth, be sure to carry out treatment in case of possible fetal hypoxia, and if asphyxia of the newborn occurs as quickly as possible, it is advisable to ensure blood saturation even before the end of the birth process oxygen and normalization of other body functions.