Fetal hypoxia - causes of the development of pathology, types (acute, chronic), signs and symptoms. Degrees of intrauterine hypoxia. Asphyxia of the newborn (hypoxia during childbirth). What is asphyxia in medicine? Types, symptoms and consequences

The term "fetal hypoxia" was proposed by WHO to refer to oxygen deficiency. In some countries, the terms "fetal distress" and "fetal asphyxia" are also used.

Under asphyxia in general clinical practice imply suffocation, i.e. lack of oxygen and accumulation of carbon dioxide in the body (hypercapnia), often leading to cardiac arrest. The term "asphyxia" in relation to the state of the fetus and newborn is conditional, since oxygen deficiency in these cases is not always accompanied by severe cardiac disorders and hypercapnia.

In our country, with oxygen deficiency in the prenatal period, the term "fetal hypoxia" is used. To characterize the condition of newborns born with symptoms of oxygen deficiency, the term "asphyxia" is used.

In various periods of pregnancy and childbirth, oxygen deficiency causes unequal consequences for the embryo, fetus and newborn. During the period of organogenesis, pronounced hypoxia may be accompanied by impaired development of the embryo up to its death. Oxygen starvation during fetogenesis can lead to fetal growth retardation, damage to its central nervous system. Oxygen deficiency, depending on its degree, leads to asphyxia, impaired adaptation of the newborn in the postnatal period, stillbirth and death of newborns in the early neonatal period.

Gfetal hypoxia- insufficient supply of oxygen to tissues and organs of the fetus or inadequate utilization of oxygen. Fetal hypoxia is distinguished by duration, intensity and mechanism of development.

Depending on the duration, chronic and acute fetal hypoxia are distinguished.

Chronic hypoxia the fetus develops with prolonged insufficient supply of oxygen to the fetus due to extragenital diseases of the mother, complicated pregnancy (preeclampsia, prolonged threat of interruption, overmaturity, mother and fetus, infection of the fetus), immune blood incompatibility. Fetal hypoxia can also be the result of smoking, drinking alcohol, drug addiction.

Acute fetal hypoxia, usually occurs during childbirth (anomalies labor activity, entanglement of the umbilical cord, prolapse or pressing of the loops of the umbilical cord, the absolute shortness of the umbilical cord, the true knot of the umbilical cord), is less commonly observed during pregnancy in conditions that threaten the life of the mother (premature detachment of the normally located and placenta previa, uterine rupture). Often there is a combination of acute and chronic hypoxia, which is an extremely unfavorable prognostic factor for the fetus.

Distinguish according to intensity functional hypoxia (mild form), manifested by hemodynamic disorders; metabolic hypoxia - deeper, but with reversible changes in metabolism; destructive(severe form), accompanied by irreversible changes at the cellular level.

Depending on the mechanism of development, hypoxia can be hypoxic, circulatory, hemic, tissue.

hypoxic fetal hypoxia is a consequence of impaired oxygen delivery to the uteroplacental circulation; with difficult passage of oxygen through a morphologically and functionally altered placenta, which is observed much more often; with low pO2 in the mother's blood.

Circulatory fetal hypoxia - a decrease in oxygen delivery to tissues with normal saturation, voltage and oxygen content in arterial blood.

hemic a type of hypoxia can be observed with anemia in the fetus (for example, with fetal hemolytic disease).

tissue hypoxia is the inability of fetal cells to absorb oxygen due to dysfunction of enzyme systems that catalyze oxidative processes in tissues, despite the normal content and saturation of blood with oxygen. The development of primary tissue hypoxia in the fetus is sometimes possible when the mother is poisoned with strong poisons. More often, tissue hypoxia is secondary to severe and prolonged oxygen deficiency of the fetus of any genesis.

In its pure form, one or another type of hypoxia in the fetus is rare, more often in clinical practice their combination is observed.

Pathogenesis. The resistance of the fetus to hypoxia is determined by a large minute volume of the heart, reaching 198 ml / kg (in a newborn 85 ml / kg, in an adult 70 ml / kg); increase in heart rate up to 150-160 per minute; significant oxygen capacity of the fetal blood (average 23%); fetal hemoglobin. Fetal hemoglobin quickly attaches oxygen and easily gives it to the tissues (increased affinity for oxygen), which, at a high blood flow rate, ensures that the tissues of the fetus receive a sufficient amount of oxygen per unit time. Fetal hemoglobin accounts for 70% of the total hemoglobin in fetal red blood cells.

A protective factor against oxygen deficiency is the structural features of the fetal cardiovascular system - three arteriovenous shunts: venous, or arantia, duct; interatrial foramen ovale; arterial, or botall, duct. As a result of arteriovenous communications, almost all organs of the fetus receive mixed blood. The mixing of blood flows in the ventricles of the fetal heart leads to more slow decline pO2 than in an adult in case of hypoxia. The fetus, to a greater extent than the newborn, uses anaerobic glycolysis, which is provided by significant reserves of glycogen, energy and plastic metabolic products in vital organs. The resulting metabolic acidosis increases the resistance of the fetus to oxygen starvation.

Under the influence of oxygen deficiency in the initial stages of hypoxia, the functions of the medulla and cortical layers of the adrenal glands of the fetus, the production of catecholamines and other vasoactive substances that cause tachycardia and an increase in peripheral vascular tone increase. As a result, centralization and redistribution of blood flow occur: the minute volume of the heart increases, blood circulation in the brain, adrenal glands, and placenta increases, and blood flow in the lungs, kidneys, intestines, spleen, and skin decreases, which leads to ischemia of these organs. With intestinal ischemia in the fetus, opening of the anal sphincter and the release of meconium into the amniotic fluid are possible.

In the future, prolonged severe hypoxia leads to a sharp inhibition of most of the functional systems of the fetus, and primarily the adrenal glands, which is accompanied by a decrease in the level of cortisol and catecholamines in the blood. There is an oppression of the vital centers of the fetus, a decrease in heart rate, a decrease in blood pressure.

Simultaneously with changes in macrohemodynamics, pronounced disturbances occur in the microcirculation system. A decrease in the tone of arterioles and precapillaries causes vasodilation and an increase in the volume of the vascular bed, which, combined with a decrease in the cardiac output, leads to a slowdown in blood flow up to stasis. Under conditions of acidosis and a decrease in blood flow velocity, blood viscosity, aggregation of blood cells and coagulation potential increase with the development of DIC, a decrease in gas exchange in fetal tissues. In recent years, in the pathogenesis of these disorders, a large role is given to the universal regulator of vascular tone - nitric oxide, which is produced by endothelial cells (including in the amnion, umbilical cord). Nitric oxide, being a vasodilator, reduces platelet aggregation and prevents their adhesion to the vascular wall.

Violation of the trophism of the vascular wall leads to an increase in its permeability and the release of the liquid part of the blood and formed elements from the vascular bed. The result of these changes are hypovolemia, hemoconcentration, tissue edema, diapedetic, and sometimes massive hemorrhages in the vital important organs fetus.

Under the influence of oxygen deficiency, significant changes in metabolic parameters occur, resulting in increased accumulation of under-oxidized metabolic products in the fetal body, i.e. pathological metabolic or respiratory metabolic acidosis.

With prolonged and severe fetal hypoxia, lipid peroxidation is simultaneously activated with the release of toxic radicals, which, along with incompletely oxidized metabolic products, inhibit enzymatic reactions, reduce the activity of respiratory enzymes, disrupt the structural and functional properties of cell membranes, increasing their permeability. The most significant changes in the balance of potassium ions, which leave the cell space, causing hyperkalemia. Hyperkalemia, together with hypoxia and acidosis, plays important role overstimulation of the parasympathetic nervous system and development of fetal bradycardia.

Due to pronounced changes in macro- and microhemodynamics, metabolism in the tissues of the vital organs of the fetus, ischemia and necrosis can develop, especially in the central nervous system and adrenal glands.

clinical picture. The clinical manifestations of fetal hypoxia include changes in its motor activity felt by a pregnant woman.

IN initial stage intrauterine hypoxia a woman notes an increase and increased motor activity of the fetus. With progressive or prolonged hypoxia, fetal movements are weakened until they stop. A decrease in the number of fetal movements to 3 or less within 1 hour indicates intrauterine fetal suffering and is an indication for an urgent additional examination.

An indirect sign of chronic fetal hypoxia can be a decrease in the height of the uterine fundus, indicating a fetal growth retardation, and oligohydramnios.

Diagnosis of fetal hypoxia is based on an assessment of its functional state using additional methods (cardiotocography, echography, Doppler blood flow in the mother-placenta-fetus system, determination of the biophysical profile of the fetus, acid-base state of the umbilical cord blood of the fetus obtained by cordocentesis).

At cardiotocography The initial signs of fetal hypoxia include tachycardia (up to 180 per minute) or moderate bradycardia (up to 100 per minute), a decrease in heart rate variability, short-term (up to 50% of the record) rhythm monotony, weakening of the response to functional tests. In this case, the cardiotocogram is estimated at 5-7 points (Fig. 32.1).

Rice. 32.1. Fetal cardiotocogram. Initial signs of hypoxia (tachycardia)

With severe fetal suffering, significant bradycardia (below 100 per minute) or tachycardia (more than 180 per minute), rhythm monotony (more than 50% of the recording), a paradoxical reaction to functional tests (late decelerations in response to fetal movement during a non-stress test) or its absence. Severe fetal hypoxia is evidenced by a cardiotocogram score of 4 points or less (Fig. 32.2).

Rice. 32.2. Fetal cardiotocogram. Pronounced signs of hypoxia. A - persistent monotony of the rhythm; B - areactive non-stress test

In a pathological non-stress test, it is advisable to study biophysical profile. There is a decrease in the respiratory activity of the fetus up to the cessation of its respiratory movements, with progressive hypoxia, movements and fetal tone are absent.

A total assessment of the biophysical profile of 6-7 points indicates a doubtful condition of the fetus, and therefore a re-examination is required. A score of 5 points or less indicates severe hypoxia of the intrauterine fetus.

In the diagnosis of fetal hypoxia, importance is attached to Doppler assessment of blood flow in the mother-placenta-fetus system. Dopplerometry allows diagnosing chronic intrauterine hypoxia earlier than cardiotocography, which is the basis for careful observation for the condition of the fetus and the timely conduct of therapeutic measures.

A decrease in the diastolic blood flow velocity in the umbilical artery (systolic-diastolic ratio of more than 3.0) indicates an increase in placental vascular resistance, which clearly correlates with hypoxemia, hypercapnia, and fetal acidemia.

Hemodynamic disorders fetal blood flow(in the aorta, in the middle cerebral artery, in the renal arteries of the fetus) indicate a violation of the central hemodynamics in response to a decrease in placental perfusion. An increase in the diastolic blood flow velocity in the fetal brain (systolic-diastolic ratio in the fetal middle cerebral artery less than 2.8) during hypoxia indicates the preservation of the fetal cerebral blood flow due to vasodilation. The compensatory mechanism for maintaining normal blood supply to the brain with reduced placental perfusion is called the "protective circle of blood circulation."

An extremely unfavorable prognostic sign for the fetus is the so-called critical state of blood flow, when zero or negative blood flow is detected in the umbilical artery, blood regurgitation through the tricuspid valve, the absence of diastolic blood flow in the fetal aorta, and an increase in diastolic blood flow velocity in the middle cerebral artery. As hypoxia progresses, disturbances in the venous blood flow in the fetus (venous duct, hepatic veins) occur - a decrease in blood flow velocity in the late diastole phase up to zero or negative values ​​(Fig. 32.3).

Rice. 32.3. Blood flow disorders in the mother-placenta-fetus system during fetal hypoxia (A - uterine artery, B - umbilical cord artery, C - venous duct)

Amnioscopy in cephalic presentation often allows to detect staining amniotic fluid meconium, indicating fetal hypoxia.

Noteworthy is the diagnosis of fetal hypoxia by fetal blood obtained by cordocentesis (decrease in pH, increase in BE).

Diagnosis of fetal hypoxia in childbirth is based on an assessment of his cardiac activity, respiratory and motor activity, CBS of blood, taking from the presenting part and data from the assessment of amniotic fluid.

In addition to auscultation of fetal heart sounds, the most accessible and exact method detection of fetal hypoxia during childbirth is cardiotocography.

In the first stage of labor, the initial signs of fetal hypoxia include periodic monotony of the heart rate or bradycardia up to 100 per minute, both with headache and with breech presentation. The reaction to the fight is manifested by short-term late decelerations. In the second stage of labor initial signs hypoxia are bradycardia up to 90 per minute or tachycardia up to 180 per minute, periodic monotony of the rhythm. In response to an attempt, late decelerations up to 60 per minute occur (Fig. 32.4), which are not restored.

Rice. 32.4. Signs of fetal hypoxia during childbirth. Late decelerations

A sign of severe fetal hypoxia in the first stage of labor is bradycardia up to 80 per minute with head presentation, bradycardia below 80 per minute or tachycardia up to 200 per minute with breech presentation. Regardless of the presentation of the fetus between contractions, persistent monotony of the rhythm and / or arrhythmia may be recorded. In response to a contraction, prolonged late W-shaped decelerations in cephalic presentation and a combination of accelerations with decelerations up to 80 per minute in breech presentation often occur.

In the period of exile, the signs of severe fetal hypoxia include the appearance on the cardiotocogram of bradycardia up to 80 per minute or tachycardia more than 190 per minute; persistent monotony of the rhythm and arrhythmia, long-term late decelerations in response to an attempt up to 50 per minute in both cephalic and breech presentations. In cephalic presentation, W-shaped decelerations of up to 50 per minute can be observed outside the contraction.

Respiratory or motor activity of the fetus(on ultrasound) active phase childbirth is additional feature fetal hypoxia. Identification of episodic respiratory movements, which appear, as a rule, in the latent phase of labor, has no prognostic value and requires dynamic monitoring of the fetal condition. Regular pronounced respiratory activity of the fetus both in the first and second stages of labor poses a threat of aspiration of amniotic fluid, which can later lead to the development of aspiration syndrome in the newborn. The most unfavorable are respiratory movements, accompanied by a pronounced amplitude of diaphragm movement and a predominance of inhalation over exhalation - "suffocation" (gasping).

Of great importance in the detection of fetal hypoxia is CBS study blood obtained from the presenting part (Zaling's test). Hypoxia of the fetus in the first stage of labor is indicated by a pH below 7.2, in the second stage of labor - below 7.14.

In recent years, during childbirth, they have been used pulse oximetry. With fetal hypoxia, it allows you to detect a decrease in oxygen saturation in tissues.

Fetal hypoxia during childbirth can be judged by color and density amniotic fluid with cephalic presentation of the fetus. The evaluation scale proposed for this purpose (Table) makes it possible to predict meconium aspiration.

Staining of amniotic fluid with meconium during cephalic presentation always indicates fetal hypoxia. The most unfavorable prognostic value is thick green, yellowish-brown amniotic fluid, as well as an increase in their density during childbirth.

Treatment. During pregnancy, the treatment of chronic fetal hypoxia should be comprehensive, aimed at treating the underlying disease / complication in a woman and normalizing placental circulation. Assign bed rest, which improves the blood supply to the uterus; tocolytics (b-agonists) - brikanil, ginipral; drugs that improve the rheological properties of blood (trental, chimes, actovegin), anticoagulants (heparin, fraxiparin).

In chronic fetal hypoxia, it is advisable to use membrane stabilizers (Essentiale Forte, Lipostabil) and antioxidants (vitamin E, ascorbic acid, glutamic acid).

With the ineffectiveness of complex therapy, decreasing symptoms of severe chronic fetal hypoxia, as well as with acute hypoxia fetus shows emergency delivery - caesarean section.

Prevention of fetal hypoxia should be based on early diagnosis complications of pregnancy and childbirth and their treatment, the choice of an adequate term and method of delivery.

Asphyxia of newborns due to lack of oxygen. Asphyxia is manifested immediately after birth by the absence or inefficiency of breathing, circulatory disorders and depression of the neuro-reflex activity of the central nervous system.

The cause of newborn asphyxia can be acute or chronic fetal hypoxia, which develops both antenatally and during childbirth. Neonatal asphyxia may be due to aspiration of milk during feeding.

The severity of newborn asphyxia is determined by the state of the respiratory, cardiovascular system and central nervous system in accordance with the Apgar scale, applied 1 and 5 minutes after birth (see the chapter "Examination methods in obstetrics and perinatology").

There are mild, moderate and severe asphyxia of newborns. Apgar score of 6-7 points 1 min after birth corresponds to mild asphyxia of the newborn, 4-5 points - asphyxia moderate, 0-3 points - severe asphyxia.

The Apgar score 5 minutes after birth reflects the effectiveness or failure of resuscitation.

While maintaining a low score after 5 minutes, it is advisable to assess the child's condition on the Apgar scale also at the 10th, 15th and 20th minutes of life until the score reaches 7 points or primary resuscitation is terminated due to its ineffectiveness. In resuscitation measures, including mechanical ventilation, the Apgar score takes into account the presence or absence of an attempt to spontaneous breathing (0 or 1 point, respectively).

In addition to assessing the state of the newborn on the Apgar scale, in all children born with asphyxia, it is necessary to determine the acid-base state, which to a large extent reflects the severity of asphyxia.

With mild asphyxia, the pH of the blood from the vein of the umbilical cord is ‹ 7.2;

BE $ - 10 meq / l. In severe asphyxia, the change in the acid-base state of the blood is more pronounced: pH ‹ 7.0 and BE > -15 meq/l.

Treatment. Primary resuscitation of a child born in asphyxia is carried out in the delivery room by a neonatologist-resuscitator. First aid to a child born in asphyxia should be able to provide an obstetrician.

The beginning of therapeutic measures depends on the signs of live birth, which include spontaneous breathing, heartbeat, umbilical cord pulsation, and voluntary muscle movements. In the absence of all these signs of live birth, the fetus is considered stillborn and is not subject to resuscitation. If a child has at least one of the signs of a live birth, the child must be provided with primary medical care.

Newborns born in asphyxia are assisted in accordance with Appendix 1 to the Order of the Ministry of Health of the Russian Federation No. 372 "Primary and resuscitation care for a newborn in the delivery room."

The volume and sequence of resuscitation measures depend on the degree of respiratory failure and cardiac activity of the newborn.

The provision of primary care to a child born in asphyxia begins with the restoration of free airway patency. With aspiration of amniotic fluid, especially with an admixture of meconium, tracheal intubation is necessary, followed by sanitation of the tracheobronchial tree. The diameter of the endotracheal tube is determined by the body weight of the newborn: up to 1000 g - 2.5 mm, from 1000 to 2500 g - 3 mm, more than 2500 kg - 3.5 mm.

With absence spontaneous breathing or its inadequacy (convulsive, irregular, superficial) start mechanical ventilation.

IVL can be carried out with a self-expanding bag (Ambu bag) through a face mask or endotracheal tube. The first 2 breaths with mask ventilation are performed with a maximum pressure at the end of inspiration - 30 cm of water column, and during subsequent breaths, the pressure is maintained within 15 cm of water column. with healthy lungs and 20 cm of water. with meconium aspiration or respiratory distress syndrome.

With a heart rate below 80 per minute and mask ventilation, an indirect heart massage is performed, placing the child on a hard surface. An indirect heart massage can be performed using the II and III fingers of one hand or using the thumbs of both hands, wrapping the brushes around the chest of the newborn. The frequency of massage movements should be 2 per second. If cardiac activity is not restored or bradycardia persists, intravenous (intracardiac) administration of a 0.1% solution of adrenaline at a dose of 0.1 mg / kg is necessary.

Resuscitation in the delivery room is stopped if adequate spontaneous breathing, normal heart rate and skin color are noted. If 20 minutes after birth, with adequate resuscitation, cardiac activity is not restored, death is declared.

Resuscitation in the delivery room is only the first step in helping children born with asphyxia. Further observation and treatment is carried out in the intensive care unit (ward), where the child is transferred immediately after the end of resuscitation. With inadequate spontaneous breathing, shock, convulsions and central cyanosis, the newborn is taken to the intensive care unit (ward) with ongoing mechanical ventilation started in the delivery room. Further complex treatment is carried out according to the general principles of intensive care for newborns, depending on the type of pathology.

Posthypoxic lesions of the CNS. Fetal hypoxia and asphyxia of the newborn can lead to perinatal lesions of the central nervous system, primarily to hypoxic-ischemic and hypoxic-hemorrhagic lesions of the brain.

With mild lesions of the central nervous system, a child has mild and unstable neurological symptoms (increased neuro-reflex excitability).

With lesions of the central nervous system of moderate severity, symptoms of general depression predominate; hypertensive syndrome may develop. With general depression, muscle tone is reduced or increased, its asymmetry in the upper and lower extremities is possible; oppression of many congenital unconditioned reflexes is noted; newborns sluggishly suck, often spit up. Local neurological symptoms are usually absent. With hypertension syndrome, motor anxiety increases with bulging fontanelles, small-amplitude tremor, Graefe's symptom and "setting sun", horizontal nystagmus; short-term attacks of clonic convulsions are possible.

Children with severe CNS damage are born in a state of hypoxemic shock with severe hemodynamic disturbances; Apgar score at birth does not exceed 3 points. After primary resuscitation, the child retains cardiovascular and respiratory disorders, a sharp depression of the central nervous system. Children are in a coma, inactive, moaning weakly, frequent convulsive seizures with a predominance of the tonic component, focal symptomatics are possible. The severity of the clinical picture is due to generalized cerebral edema and / or intracranial hemorrhages.

The most common manifestations of posthypoxic perinatal CNS damage, especially in preterm infants, are peri/intraventricular hemorrhages and periventricular leukomalacia.

Peri/intraventricular hemorrhages. Neonatal hemorrhages first develop in the subependymal germinal matrix (source of cerebral neuroblasts) located ventrolateral to the lateral ventricle. Hemorrhage into the germinal matrix can occur immediately after birth, but more often occurs in the first 4 days of life. A cyst may form at the site of the hemorrhage in the germinal matrix. Hemorrhage can spread throughout the ventricular system of the brain.

Clinical examination of newborns, especially those who are very premature, in the first hours and days does not always reveal a clear picture of a neurological defect.

Neurosonography plays an important role in the diagnosis of perinatal CNS lesions.

According to neurosonography, 4 degrees of peri / intraventricular hemorrhages are distinguished:

I degree - isolated subependymal hemorrhage (Fig. 32.5);

II degree - intraventricular hemorrhages without expansion of the ventricles of the brain;

III degree - intraventricular hemorrhages with the expansion of the ventricles of the brain;

IV degree - intraventricular hemorrhages with ventriculomegaly and parenchymal hemorrhage (Fig. 32.6).

Rice. 32.5. Hemorrhage I degree. neurosonogram
Rice. 32.6. Hemorrhage IV degree. neurosonogram

Under periventricular leukomalacia understand bilateral ischemic infarction of the white matter adjacent to the lateral ventricles of the brain. Priventricular leukomalacia is especially common in preterm infants.

Risk factors for the development of periventricular leukomalacia are acidosis, episodes of hypotension (mean blood pressure below 30 mm Hg), hypovolemia, a sharp decrease in blood pressure, episodes of bradycardia.

In the clinical picture in the neonatal period, the general symptoms of CNS depression, which are manifested by muscle hypotension, mainly in the lower extremities, come to the fore.

The diagnosis is established by neurosonography (Fig. 32.7). The white matter lesion may be focal, with evolution into multiple cystic cavities after 1-2 weeks. The sizes, number and localization of cysts serve as an important prognostic criterion.

Rice. 32.7. Periventricular leukomalacia. neurosonogram

Long-term consequences of periventricular leukomalacia - spastic diplegia, mainly of the lower extremities. In severe cases, damage to the lower extremities is combined with damage to the upper extremities and mental retardation; visual disturbances may occur.

Neonatal asphyxia is suffocation, manifested by a violation of breathing, or the absence of spontaneous breathing in the presence of a heartbeat and other signs of life. In other words, the baby is not capable, cannot breathe on his own immediately after birth, or he breathes, but his breathing is inefficient.

40% of premature and 10% of full-term babies need medical attention due to impaired spontaneous breathing. Neonatal asphyxia is more common in premature babies. Among all newborns, children born in asphyxia account for 1-1.5% of the total.

A child born in asphyxia is a serious problem for doctors providing care in the delivery room. Around the world, about a million children die every year from asphyxia, and about the same number of children have serious complications later.

Asphyxia of the fetus and newborn proceeds with hypoxia (decrease in oxygen concentration in tissues and blood) and hypercapnia (increase in carbon dioxide in the body), which is manifested by severe respiratory and circulatory disorders and impaired functioning of the child's nervous system.

Causes of asphyxia in newborns

Factors contributing to the development of asphyxia

There are antenatal and intranatal factors.

Antenatal affect the developing fetus in utero and are a consequence of the lifestyle of a pregnant woman. Antenatal factors include:

• maternal diseases (diabetes mellitus, hypertension, diseases and malformations of the heart and blood vessels, kidneys, lungs, anemia);
• Problems previous pregnancies(miscarriages, stillbirths);
• complications during this pregnancy (threat of miscarriage and bleeding, polyhydramnios, oligohydramnios, prematurity or overmaturity, multiple pregnancy);
• taking certain medications by the mother;
• social factors (drug use, lack of medical supervision during pregnancy, pregnant women under the age of 16 and over 35).

Intranatal factors affect the child during childbirth.

Intranatal factors include various complications that occur immediately at the time of birth (rapid or prolonged labor, placenta previa or premature abruption, anomalies of labor activity).

All of them lead to fetal hypoxia - a decrease in oxygen supply to tissues and oxygen starvation, which significantly increases the risk of having a child with asphyxia.

Causes of asphyxia

Among the many causes, there are five main mechanisms that lead to asphyxia.

1. Insufficient clearance of toxins from the maternal part of the placenta as a result of low or high pressure in the mother, excessively active contractions or for other reasons.
2. Decrease in the concentration of oxygen in the blood and organs of the mother, which can be caused by severe anemia, insufficiency of the respiratory or cardiovascular system.
3. Various pathologies from the placenta, as a result of which gas exchange through it is disturbed. Among them are calcifications, placenta previa or premature detachment, inflammation of the placenta and hemorrhages in it.
4. Interruption or disruption of blood flow to the fetus through the umbilical cord. This occurs when the umbilical cord tightly wraps around the baby's neck, when the umbilical cord is compressed during the passage of the child through the birth canal, when the umbilical cord falls out.
5. Insufficient respiratory efforts of the newborn with a depressing effect of drugs on the nervous system (a consequence of the mother's treatment with various drugs), as a result of severe malformations, with prematurity, due to the immaturity of the respiratory organs, due to a violation of the flow of air into the respiratory tract (blockage or compression from the outside), Consequently birth trauma and severe intrauterine infections.

A special risk group for the development of asphyxia are premature babies who have extremely low birth weight, post-term and children who have a delay prenatal development. These children are at the highest risk of developing asphyxia.

The majority of children who are born with asphyxia have a combined effect of ante- and intranatal factors.

Today, among the causes of chronic intrauterine hypoxia, not the last place is occupied by drug addiction, substance abuse and alcoholism of the mother. The number of smoking pregnant women is progressively increasing.

Smoking during pregnancy causes:

• narrowing of the uterine vessels, which continues for another half an hour after a cigarette is smoked;
• suppression of the respiratory activity of the fetus;
• an increase in the fetal blood concentration of carbon dioxide and the appearance of toxins, which increases the risk of prematurity and premature birth;
• hyperexcitability syndrome after birth;
• lung damage and delayed physical and mental development of the fetus.

With short-term and moderate hypoxia (decrease in the level of oxygen in the blood), the fetal body tries to compensate for the lack of oxygen. This is manifested by an increase in blood volume, an increase in heart rate, increased respiration, and an increase in fetal motor activity. Such adaptive reactions compensate for the lack of oxygen.

With prolonged and severe hypoxia, the fetal body cannot compensate for the lack of oxygen, tissues and organs suffer from oxygen starvation, because oxygen is delivered primarily to the brain and heart. The motor activity of the fetus decreases, the heartbeat slows down, breathing becomes less frequent, and its depth increases.

The result of severe hypoxia is an insufficient supply of oxygen to the brain and a violation of its development, which can aggravate respiratory failure at birth.

The lungs of a full-term fetus secrete fluid before birth, which enters the amniotic fluid. The fetal breathing is shallow and the glottis is closed, so when normal development amniotic fluid cannot enter the lungs.

However, severe and prolonged hypoxia of the fetus can cause irritation of the respiratory center, as a result of which the depth of breathing increases, the glottis opens and amniotic fluid enters the lungs. This is how aspiration occurs. Substances present in the amniotic fluid cause inflammation of the lung tissue, make it difficult for the lungs to expand at the first breath, which leads to respiratory failure. Thus, the result of aspiration of amniotic fluid is asphyxia.

Respiratory disorders in newborns can be caused not only by impaired gas exchange in the lungs, but also as a result of damage to the nervous system and other organs.

Non-lung causes of respiratory problems include the following:

1. Nervous system disorders: abnormalities in the development of the brain and spinal cord, the effects of drugs and drugs, infection.
2. Violation of the cardiovascular system. These include malformations of the heart and blood vessels, dropsy of the fetus.
3. Malformations gastrointestinal tract: esophageal atresia (blindly ending esophagus), fistulas between the trachea and esophagus.
4. Metabolic disorders.
5. Adrenal and thyroid dysfunction.
6. Blood disorders such as anemia.
7. Improper development of the airways.
8. Congenital malformations of the skeletal system: malformations of the sternum and ribs, as well as injuries of the ribs.

Types of asphyxia in newborns

1. Acute asphyxia caused by exposure to only intranatal factors, that is, that occurred during childbirth.
2. Asphyxia, which developed against the background of prolonged intrauterine hypoxia. The child developed in conditions of lack of oxygen for a month or more.

According to the severity are distinguished:

• mild asphyxia;
• moderate asphyxia;
• severe asphyxia.

Neonatologists assess the condition of the newborn using the Apgar scale, which includes an assessment of breathing, heart rate, muscle tone, skin color and reflexes of the newborn. Assessment of the condition of the newborn is carried out at the first and fifth minute of life. Healthy children gain 7-10 points on the Apgar scale.

A low score indicates that the child has problems with either breathing or heartbeat and requires immediate medical attention.

Light asphyxia

Manifested by cardiorespiratory depression. This is the depression of breathing or heartbeat as a result of the stress that the child feels during the transition from intrauterine life to the outside world.

Childbirth is a huge stress for a child, especially if there are any complications. At the same time, in the first minute of life, the baby receives an Apgar score of 4-6 points. As a rule, for such children it is enough to create optimal conditions the environment, warmth and temporary support of breathing, and after five minutes the child recovers, he is given 7 points and above.

Asphyxia of moderate severity

The condition of the baby at birth is assessed as moderate. The baby is lethargic, reacts poorly to examination and stimuli, but spontaneous movements of the arms and legs are observed. The child screams weakly, unemotionally and quickly falls silent. The child's skin is bluish, but quickly turns pink after inhaling oxygen through the mask. Palpitation is rapid, reflexes are reduced.

Breathing after its restoration is rhythmic, but weakened, intercostal spaces may sink. After medical care in the delivery room, children still need oxygen therapy for some time. With timely and adequate medical care, the condition of children improves quite quickly and they recover on 4-5 days of life.

The condition of the baby at birth is severe or extremely severe.

In severe asphyxia, the child reacts poorly to examination or does not react at all, while the muscle tone and movements of the child are weak or absent at all. The skin color is bluish-pale or just pale. It turns pink after breathing oxygen slowly, the skin restores its color for a long time. The heartbeat is muffled. Breathing irregular, irregular.

In very severe asphyxia, the skin is pale or sallow. The pressure is low. The child does not breathe, does not respond to examination, eyes are closed, no movements, no reflexes.

How asphyxia of any severity will proceed depends directly on the knowledge and skills of medical personnel and good nursing, as well as on how the child developed in utero and on existing concomitant diseases.

Asphyxia and hypoxia. Differences in manifestations in newborns

The picture of acute asphyxia and asphyxia in children who have undergone hypoxia in utero has some differences.

Features of children born in asphyxia who suffered prolonged hypoxia in utero are presented below.

1. Significantly pronounced and long-lasting metabolic and hemodynamic disorders (blood movement in the vessels of the body).
2. Often there are various bleeding as a result of inhibition of hematopoiesis and a decrease in the content of microelements in the blood, which are responsible for stopping bleeding.
3. More often, severe lung damage develops as a result of aspiration, surfactant deficiency (this substance prevents the lungs from collapsing), and inflammation of the lung tissue.
4. Often there are metabolic disorders, which is manifested by a decrease in blood sugar and important trace elements(calcium, magnesium).
5. Neurological disorders resulting from hypoxia and due to cerebral edema, hydrocephalus (dropsy), and hemorrhages are characteristic.
6. Often combined with intrauterine infections, often associated with bacterial complications.
7. After asphyxia, long-term consequences remain.

Among the complications, early ones are distinguished, the development of which occurs in the first hours and days of the baby's life, and late ones, which occur after the first week of life.

TO early complications include the following states:

1. Damage to the brain, which is manifested by edema, intracranial hemorrhage, death of parts of the brain due to lack of oxygen.
2. Violation of blood flow through the vessels of the body, which is manifested by shock, pulmonary and heart failure.
3. Kidney damage, manifested by renal failure.
4. Pulmonary involvement, manifested by pulmonary edema, pulmonary hemorrhage, aspiration, and pneumonia.
5. Damage to the digestive organs. The intestine suffers the most, its motility is disturbed, as a result of insufficient blood supply, some parts of the intestine die off, inflammation develops.
6. The defeat of the blood system, which is manifested by anemia, a decrease in the number of platelets and bleeding from various organs.

Late complications include the following conditions:

1. Attachment of infections, meningitis (inflammation of the brain), pneumonia (inflammation of the lungs), enterocolitis (inflammation of the intestines) develops.
2. Neurological disorders (hydrocephalus, encephalopathy). The most serious neurological complication is leukomalacia - damage (melting) and death of parts of the brain.
3. Consequences of excessive oxygen therapy: bronchopulmonary dysplasia, damage to the vessels of the retina.

Resuscitation of newborns with asphyxia

The condition of children born in asphyxia requires resuscitation. Resuscitation is a complex of medical measures aimed at reviving, resuming breathing and heart contractions.

Resuscitation is carried out according to the ABC system, developed back in 1980:

• "A" means establishing and maintaining a patent airway;
• "B" means breath. It is necessary to restore breathing with the help of artificial or assisted ventilation of the lungs;
• "C" means to restore and maintain heart contractions and blood flow through the vessels.

Resuscitation measures for newborns have their own characteristics, their success largely depends on the readiness of medical personnel and correct assessment child's condition.

1. The readiness of medical personnel. Ideally, care should be provided by two people who have the appropriate skills and know how the pregnancy and childbirth proceeded. Before the birth begins, the medical staff should check that the equipment and medicines are ready to assist.
2. The readiness of the place where the child will be assisted. It should be specially equipped and located directly in the delivery room or in close proximity to it.
3. Providing resuscitation in the first minute of life.
4. Staged resuscitation according to the "ABC" system with an assessment of the effectiveness of each stage.
5. Caution in carrying out infusion therapy.
6. Observation after relief of asphyxia.

Restoration of breathing begins as soon as the head appears from the birth canal, with the suction of mucus from the nose and mouth. Once the baby is fully born, it needs to be warmed up. To do this, it is wiped, wrapped in heated diapers and placed under radiant heat. In the delivery room should not be drafty, the air temperature should not fall below 25 ºС.

Both hypothermia and overheating depress breathing, so they should not be allowed.

If the child screamed, they put it on mother's belly. If the baby is not breathing, breathing is stimulated by rubbing the back and patting the baby's soles. With moderate and severe asphyxia, respiratory stimulation is ineffective, so the child is quickly transferred to radiant heat and begins artificial ventilation lungs (IVL). After 20 - 25 seconds, they look to see if breathing has appeared. If the child's breathing is restored and the heart rate is above 100 per minute, resuscitation is stopped and the child's condition is monitored, trying to feed the child with mother's milk as soon as possible.

If there is no effect from mechanical ventilation, the contents of the oral cavity are sucked off again and mechanical ventilation is resumed. In the absence of breathing on the background of mechanical ventilation for two minutes, tracheal intubation is performed. A hollow tube is inserted into the trachea, which ensures the flow of air to the lungs, the child is connected to an artificial respiration apparatus.

In the absence of a heartbeat or a decrease in the frequency of contractions less than 60 per minute, an indirect heart massage is started, continuing mechanical ventilation. Massage is stopped if the heart begins to beat on its own. In the absence of a heartbeat lasting more than 30 seconds, the heart is stimulated with drugs.

Prevention of asphyxia in newborns

All measures for the prevention of asphyxia are reduced to the timely identification and elimination of causes in a pregnant woman that cause fetal hypoxia.

Every pregnant woman should be observed by a gynecologist throughout her pregnancy. It is necessary to register on time, take tests, consult doctors and receive treatment, which is prescribed if necessary.

The lifestyle of the mother has a significant impact on the development of the fetus.

Conclusion

Treatment of children who have suffered asphyxia, before full recovery- pretty long.

After the activities carried out in the delivery room, the children are transferred to the pediatric intensive care unit or to the neonatal pathology department. In the future, if required, rehabilitation therapy is prescribed in specialized departments.

The prognosis largely depends on the severity of brain damage caused by hypoxia. The more the brain suffers, the greater the likelihood of death, the risk of complications and longer period full recovery. Premature babies have a worse prognosis than babies born at term.

Fetal hypoxia- This pathological condition, which is based on intrauterine oxygen deficiency.
risk factors for the development of antenatal hypoxia of the fetus are: post-term pregnancy, prolonged (more than 4 weeks) gestosis of pregnant women, multiple pregnancy, threatened miscarriage, diabetes mellitus in pregnant women, bleeding, somatic and infectious diseases in the 1st trimester of pregnancy, smoking and other types of drug addiction in pregnant women.

Under acute asphyxia newborn implies 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 intranatal factors (oxygen deficiency, accumulation of carbon dioxide and underoxidized products of cellular metabolism). Asphyxia, which developed against the background of chronic intrauterine hypoxia, is asphyxia of the newborn, which developed antenatal in conditions of placental insufficiency.

The main risk factors for the development of intrapartum fetal asphyxia:

C-section; pelvic, gluteal and other abnormal presentation of the fetus;

Premature and delayed childbirth;

Anhydrous span 10 hours;

Rapid labor - less than 4 hours in nulliparous and less than 2 hours in multiparous;

Previa or premature detachment of the placenta, uterine ruptures;

The use of obstetric forceps 11 other benefits in childbirth in the mother (shock, etc.);

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

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

Meconium in the amniotic fluid and its aspiration;

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

Summarizing the above, five leading mechanisms leading to acute asphyxia of newborns can be distinguished:

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

2. Violation of the exchange of gases through the placenta (premature complete or incomplete detachment of the placenta, etc.)

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

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

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

Pathogenesis. Main links: intrauterine hypoxia causes the inclusion of compensation mechanisms aimed at maintaining adequate oxygenation of fetal tissues, an increase in the release of glucocorticoids, the number of circulating erythrocytes and circulating blood volume, activation of fetal motor activity and the frequency of "respiratory" movements chest with a closed glottis, etc .;

Ongoing hypoxia stimulates anaerobic glycolysis, and the growing oxygen deficiency causes the body to reduce the oxygenation of the intestines, skin, liver, kidneys;
there is a redistribution of blood circulation with a 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 in 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 the brain tissue, dyselectrolytemia and small hemorrhages in the brain tissue;

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

Hypoxia also maintains high pulmonary vascular resistance, resulting in pulmonary hypertension.

So heavy perinatal hypoxia can cause multiple organ dysfunctions that are manifested by the central nervous system hypoxically-ischemic encephalopathy, cerebral edema, intracranial hemorrhage, convulsions; lungs - pulmonary hypertension, meconium aspiration syndrome, surfactant destruction, posthypoxic 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 insufficiency; metabolism - pathological acidosis, hypoglycemia, hypocalcemia, hypomagnesemia; vitamin K deficiency, DIC, secondary immunodeficiency, etc.

Classification of asphyxia of the newborn. 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 cry
Muscle tone	Limbs hanging down	Some limb flexion	active movements
Reflex excitability (reaction to nasal catheter, sole irritation)	Does not react	Grimace	Cough, sneeze, cry
Skin coloration	Generalized pallor or cyanosis	Pink coloration of the body and cyanotic limbs (acrocyanosis)	Pink coloration of the whole body and limbs

Clinic of moderate asphyxia: the condition of the child at birth is moderate, the child is lethargic, however, spontaneous motor activity is observed, the reaction to examination and irritation is weak. Physiological reflexes The cry is short, unemotional. The skin is iianotic, but quickly turns pink during oxygenation, often with acrocyanosis remaining. Tachycardia, muffled heart tones or increased sonority are heard after augculation. Breathing after prolonged apnea is rhythmic, with sighs. Repeated apnea. Over the lungs, weakened breathing is possible, of various sizes; moist rales, boxed percussion tone. Hyperexcitability, small-scale tremor of the hands are noted, "g" is disturbed., frequent regurgitation, hyperesthesia, positive symptom of Ilpo. spontaneous Moro reflex The described disturbances are transient and functional in nature, being the result of metabolic disturbances and intracranial hypertension. With adequate therapy, the condition of children quickly improves and becomes satisfactory by the 5-5th day of life.

For severe asphyxia: the general condition at birth is severe or very severe. Physiological reflexes of practical sand are not evoked. With active oxygenation (more often with the help of mechanical ventilation), it remains possible to restore the skin color to a pink color. The gonads of the heart are often deaf, systolic murmur may appear. In a very serious condition, the clinic may correspond hypoxic shock - pale skin with an earthy tint, symptom of "white spot" 3 seconds or more, low blood pressure, no spontaneous breathing, no reaction to examination and pain irritation, areflexia, muscle atony, closed eyes, sluggish pupil reaction to light or no reaction / possible miosis or mydriasis, nystagmus, dysfunction of many other organs and systems.

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.; among late complications dominated by meningitis, sepsis, pneumonia, hydrocephalic syndrome, bronchopulmonary dysplasia entero-o-liga
Diagnosis. Asphyxia is diagnosed on the basis of clinical data, in particular, about. | renki on the Apgar scale at the 1st and 5th minutes of life, as well as indicators of the main clinical and laboratory parameters determined by clinical, hardware and visual monitoring control. Taken into account: heat mass dynamics. temperature registration, dyspeptic phenomena, oxygen concentration in the inhaled mixture, dynamics of severe cli-
nic symptoms, heart rate, blood pressure, hematocrit, hemoglobin, leukocyte formula, CBS, etc.

Differential Diagnosis carried out with conditions that cause cardiorespiratory depression, as well as with acute blood loss, intracranial hemorrhage, in premature infants - SDR (Respiratory Disorder Syndrome).

Treatment. The Neonatal Primary Resuscitation System was developed by the American Heart Association and the American Academy of Pediatrics. The main stages of resuscitation are called "ABC - crocks".

Main stages:

A. ensuring the patency of the respiratory tract (Airways);

B. stimulation or restoration of breathing (Breathing);

C. maintenance of blood circulation (Circulation).

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

A. With the exclusion of meconium in the amniotic fluid:
- transfer the newborn from the mother to the source of the infrared heater;

Quickly dry the skin with wetting movements through the diaper (discard the wet diaper);

Ensure maximum airway patency by right position the child on the back with a moderately unbent head and a roller under the shoulders.

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

It is forbidden:
o irrigate the child with cold or hot water;
Use a jet of oxygen on the face;
Compress the chest;
Patting on the buttocks.

B If meconium is found in the amniotic fluid, i.e. when meconium aspiration occurs:
- after the birth of the head, the midwife aspirates the contents from the upper respiratory
ways:
- the newborn is placed under a source of radiant heat;
and without wasting time on drying, lay the child on his back with a slightly thrown back
head and roller under the shoulders;
- Perform tracheal intubation
- re-aspirate the contents from the upper respiratory tract:

O aspirate the contents of the tracheobronchial tree directly through the endotracheal tube (without using a catheter). If there is meconium residue in the intubation tube after suction, intubation and suction are repeated. Lavage of the tracheobronchial tree is not carried out due to possible damage to the surfactant. All of the above activities must be completed within 20 seconds. After that, the child's condition is consistently assessed according to three criteria:

breath,
heart rate,
color of the skin.

In the absence or inefficiency 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 of water column. IVL for longer than 2 min. requires the introduction of a probe into the stomach for decompression and prevention of regurgitation. The inefficiency 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.

Probe insertion technique: 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 insertion of the probe, gas is sucked out of the stomach with a syringe, the probe is left open and fixed with adhesive tape to the cheek. Artificial ventilation continues over the probe. After 15-30 seconds of artificial ventilation, the child's condition is assessed, the heart rate (HR) is determined. The heart rate calculation is carried out for 6 seconds and multiplied by 10. Ventilation is stopped during the calculation. Heart rate assessment (for 1 min):
and more than 100
o 60 to 100 and the frequency increases o 60 to 100 and the frequency does not increase o less than 60

1. Heart rate over 100: In the presence of spontaneous breathing, artificial ventilation is suspended and skin color is assessed; in the absence of spontaneous breathing, continue artificial ventilation until it occurs;
O at heart rate less than 100, artificial ventilation is carried out, 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 of the lungs continues, closed indirect heart massage is indicated with a heart rate of less than 80.

4. Heart rate less than 60: Artificial lung ventilation and closed heart massage.
Heart rate control is carried out after 10-15 seconds until the frequency is more than 100 and spontaneous breathing is restored. In this situation, a final assessment of the state is made.
Assess skin color. With effective ventilation and circulation, the skin color is pink, the child requires observation.
Acrocyanosis in the first hours after birth is a vascular reaction to the ambient temperature and is not associated with hypoxia. A sign of hypoxia is general cyanosis. In this case, the child needs increased concentration oxygen in the inhaled mixture (on inspiration up to 80% oxygen). The disappearance of cyanosis indicates the elimination of hypoxia, giving the mixture is stopped.

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

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

Medications used in the delivery room for neonatal resuscitation:

A drug	Dosage form	Dose	Pool, and method of introduction
Adrenalin	0.01% solution	0.1-0.3mg/kg	IV or endotracheal, inject rapidly
Recovery of volume deficit	0, 9% sodium solution Chloride, 5% albumin. blood, Ringer's solution	10 ml/kg	V/ V enter in 5-10 minutes
sodium bicarbonate	0.5mmol/l (4.2% solution)	2-4 ml/kg	V/ V slowly (2 ml/kg) only to a child with effective valency
Nalorfin	0.05% solution	(),1-0.2ml/kg	V/ V quickly or subcutaneously, endotracheally.
D remember	0.5%solution	5-20mct / kg / min IV under the 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.

Planned infusion therapy is started, 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 an isotonic solution of sodium chloride, Ringer's solution, rheopolyglucin.
Forecast. Full-term babies born with severe asphyxia have a high mortality (10-20%) and the frequency of neuropsychiatric abnormalities. Prognostically unfavorable are: maintaining very low (3 points or less) Apgar scores 15 and 20 minutes after birth; the presence of posthypoxic encephalopathy" 1 and 2 degrees and other complications.

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

Concerning fetal asphyxia, its causes often lie in the state of health of the mother, circulatory disorders in the uterus and placenta, as well as malformations of the fetus. Regardless of the causes of occurrence, the bottom line is that a sufficient amount of oxygen ceases to enter the body of the fetus. In tissues and blood is disturbed normal course redox processes, accumulates abnormally a large number of organic acids. Because of this, the fetus may experience depression of the central nervous system, the functions of the cardiovascular system and excretory organs worsen. 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 an unborn child.

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

Of course, if a woman, for some reason, has impaired hemodynamic or lung function, then not only she, but also the fetus will suffer from a lack of oxygen. There is also an increased risk of fetal hypoxia and with gestosis, i.e. when the functions of vital organs are upset from the additional load on the mother's body. Especially if a woman bears more than one child, or she overdoes the pregnancy. It is in order to reduce this danger to the expectant mother that it is useful to examine the state of health and treat existing diseases before the start of pregnancy.

Placental circulation disorders and fetal hypoxia

As for circulatory disorders, it can be negatively affected by:

• incorrect position of the fetus and umbilical cord, due to which the umbilical cord will be transferred.
• violations of the function of blood circulation in the placenta due to pathology in the development of pregnancy, as well as during prolonged labor, when placental abruption is already occurring, and the child has not yet been able to breathe on its 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 until now, becomes less active, does not respond to external stimuli, or, on the contrary, bothers the mother for a long time with continuous shocks, 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 a newborn, it is customary to distinguish between primary and secondary asphyxia. Primary occurs at the time of birth, and secondary - 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 reasons for the emergence of primary asphyxia of a newborn can be:

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

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

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

Degrees of asphyxia of the newborn

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

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

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

Secondary asphyxia of the newborn

Secondary asphyxia of the newborn sometimes manifests itself in a few hours, even a day after birth. It can be caused by pathologies of the respiratory tract of the newborn, circulatory disorders of the brain, or other causes that have to be established for the appointment of the most proper treatment. But measures to maintain breathing and oxygen content in the blood should be carried out in any case.

Danger warning

Many cases of asphyxia are accompanied by the risk of complications - pneumonia, intracranial hemorrhage, impaired cerebral circulation, and as a result - irreversible dysfunctions of the nervous system. Therefore, it is extremely important to conduct a medical examination of the expectant mother in advance for the occurrence of complications, both during pregnancy and childbirth, it is imperative to carry out treatment in the event of a possible occurrence of fetal hypoxia, and in the event of asphyxia of the newborn, as soon as possible, it is advisable to ensure blood saturation even before the end of the birth process. oxygen and the normalization of other body functions.

Fetal hypoxia is a pathological condition associated with oxygen deficiency during pregnancy and childbirth. This pathology is one of the most common among perinatal pathologies and is one of the most common causes perinatal morbidity (21-45% in the structure of all perinatal pathology).

The term "perinatal" refers to the period of intrauterine development from 28 weeks, the period of childbirth and 7 days after the birth of a child (the neonatal period).

Causes of fetal hypoxia in childbirth

The causes of fetal hypoxia and asphyxia of the newborn are common and are divided into 4 groups:

- the first three are common for fetal hypoxia and neonatal asphyxia;

- Group 4 is inherent only in asphyxia of newborns.

Stages where oxygen transport can suffer:

Mother's condition.

Uteroplacental circulation.

The state of the fetus.

Causes of hypoxia: group 1 - diseases of the mother

Blood loss - obstetric bleeding - with placental abruption, placenta previa, uterine rupture;

Blood diseases (anemia, leukemia, etc.).

Shock states of any origin.

Congenital and acquired heart defects with hemodynamic disorders.

Diseases of the broncho-pulmonary system with impaired gas exchange.

Intoxication of any kind - household, industrial, bad habits.

Causes of hypoxia: group 2 - pathology of uteroplacental and umbilical blood flow

Pathology of the umbilical cord (collisions):

umbilical cord nodes

entanglement of the umbilical cord around the limbs

prolapse of the umbilical cord (threatens with instant asphyxia of the fetus during childbirth, requires immediate surgical intervention)

pressing the umbilical cord during childbirth with breech presentation (therefore, childbirth with breech presentation is a borderline pathology, since in some cases childbirth can take place without complications, and in others - with a slight delay in the progress of the fetus, the head, leaving the last one, compresses the umbilical cord for a long time).

bleeding:

- With placental abruption

- With placenta previa. In this case, blood circulation slows down or stops.

- Rupture of vessels with sheath attachment of the umbilical cord - pathology of the attachment of the umbilical cord (to the membranes, the edge of the placenta). Vessel growth can lead to rupture, most likely during amniotomy.

- Violation of placental circulation due to dystrophic changes in blood vessels:

With gestosis

With a delayed pregnancy. There are processes of aging of the placenta - dystrophic disorders.
Anomalies of labor activity - very protracted or rapid labor, discoordination of labor activity.

Causes of hypoxia: group 3 - causes associated with the fetus

Genetic diseases of newborns.

Hemolytic disease of the newborn is associated with an immunological conflict between mother and child, begins in utero.

Heart defects.

Other developmental anomalies.

intrauterine infection.

Intracranial trauma to the fetus.

Causes of hypoxia: group 4 - blockage of the respiratory tract of the fetus

This is the only cause that is characteristic only for asphyxia of newborns - partial or complete blockage of the airways.

The pathogenesis of fetal hypoxia

Consists of a variety of pathophysiological and biochemical processes.

In the fetal body, in response to a hypoxic state, the release of corticosteroids increases, the number of circulating erythrocytes and BCC increases. At this stage: tachycardia, increased motor activity of the fetus, increased respiratory movements of the fetus, closure of the glottis. Intrauterine breathing is just chest excursions - like training breathing movements.

With increasing acute or ongoing chronic hypoxia, we see the activation of anaerobic glycolysis. Centralization of blood circulation leads to deterioration of peripheral circulation. That is, the fetus seeks to provide blood to vital organs (heart, brain), while hypoxia occurs in the intestines, kidneys, legs, and therefore meconium excretion.

Then there is a breakdown of adaptation - the adrenal cortex is depleted, clinically this is expressed by bradycardia, arrhythmia, muffled heart tones. Fetal movements slow down and eventually stop.

Therefore, the cause of hemorrhages is always a hypoxic background (and when applying forceps, or prolonged standing of the head in one plane).

The accumulation of carbon dioxide causes irritation of the respiratory center. The fetus begins to breathe through the open glottis, that is, it aspirates everything that gets in its way: amniotic fluid, mucus, blood, and newborns are born with ready-made atelectasis. The first breath of such a child can lead to spontaneous pneumothorax even without any external influences.

Classification of fetal hypoxia according to clinical manifestations

Hypoxia of the intrauterine fetus (HWP), depending on the severity: acute and chronic. Depending on whether there Clinical signs GWP, or not GWP is classified into:

threatening GWP

launched GWP

Threatening GWP is a condition when there are no clinical manifestations yet, but there is a condition of the mother or fetus that can lead to GWP (post-term pregnancy, labor anomalies, etc.).

Started hypoxia

The onset of hypoxia is a condition with clinical manifestations of HVP.

Clinical manifestations

With hypoxia, tachycardia, bradycardia (with a deeper GWP), arrhythmia, and muffled tones occur. Normal heart rate is 120-160 beats per minute.

The appearance of meconium in the amniotic fluid.

At the beginning of the GWP - increased frequency and intensification of movements. With developed GWP - slowing down and slowing down movements.

Threatening HWP requires prevention, and treatment that has begun.

Early diagnosis

Various tests (biochemical, functional, hardware). Clinical findings - especially heartbeat.

Functional trials:

The exercise test consists in changing the gas composition of the blood and air.

Heat tests: hot compress or cold to the abdomen.

Introduction of atropine or oxytocin.

These tests make it possible to identify the compensatory capabilities of the fetus until hypoxia has developed.

A stress-free test is the reaction of the fetal heartbeat to its own movements. Normally, the fetus should increase the heart rate by 10-12 beats per minute. If the fetus does not give a reaction, therefore, it is hypoxia. The heartbeat must also respond to the contraction, which can be examined using a cardiotocograph: an ultrasonic effect is used (records heartbeats and contractions), sums up the heartbeat and gives out a tape. Also, the contractile activity of the uterus (tokogram) is recorded. Deceleration is the slowing down of the heartbeat during a contraction. Early bradycardia coincides with the time of the contraction, as a rule, appears in the second stage of labor, when the head passes through the narrow part. Late deceleration - bradycardia after a contraction - a sign of late hypoxia.

Electrocardio- and phonography of the fetal heartbeat: very difficult decoding, that is, a computer is needed for processing.

In the first stage of labor, the heartbeat increases in response to a contraction, in the second period, a short-term decrease in heartbeat is possible, associated with pressing the head. With cephalic presentation up to 80 beats per minute, with breech presentation, even tachycardia up to 180 beats per minute can be considered normal, which is associated with the location of the head in the bottom area.

Motor activity: 5 movements in 30 minutes - the norm, in the 1st period - 1-3 movements, in the second period the fetus normally does not move. Examination of amniotic fluid for meconium - amnioscopy (you can tell if there is or is not meconium), or evaluate leaking water (if there is no fetal bladder).

Amniocentesis is usually used for maternal or fetal indications: genetic pathology, hemolytic disease newborn. The bladder is punctured. The most commonly performed transabdominal amniocentesis with the introduction of a needle into the amniotic cavity. For amniocentesis, the location of the placenta along the anterior wall should be excluded. Transvaginal, suprapubic amniocentesis is used mainly in the early stages.

Determination of acid-base balance. It can be done when examining amniotic fluid, or examining blood from the presenting part of the fetus (therefore, it is done only in childbirth, when there is no bubble).

Study of uteroplacental circulation.

Determination of the level of placental hormones in the urine: one can judge the state of the matcho-placental circulation, and indirectly - the state of the fetus. Determine estriol, pregnandiol (progesterone metabolite), thermostable alkaline phosphatase in the mother's blood.

Isotopic methods (more scientific method).

Ultrasound: determine the size, structure of the placenta, malnutrition in chronic hypoxia.

Prevention and treatment are carried out by the same methods.

Treatment

Treatment should consist in eliminating the cause of hypoxia, as well as treating hypoxia directly (drug pathogenetic therapy and early delivery).

Pathogenetic drug therapy:

1 gr. Oxygen therapy is carried out using pure oxygen, oxygen-air mixture (oxygen is 60%), inhalation for 10-15 minutes.

Hyperbaric oxygenation. You can even give birth in the HBO chamber.

2 gr. Drugs aimed at improving placental circulation:

Vasodilators: eufillin, trental, chimes (the last 2 improve the rheological properties of blood being deaggregants), rheopolyglucin can also be prescribed. Estrogens - increase uteroplacental circulation: natural estrogens - folliculin, artificial - sinestrol. Sigetin is an estrogen-like drug. Tocolytics - beta-agonists: partusisten, brikanil, salbutamol, ritodrine, alupent.

3 gr. Means that increase the resistance of the fetus to oxygen deficiency:

antihypoxants - seduxen, etimizole, sodium hydroxybutyrate, bufenin, piracetam, droperidol.

4 gr. Drugs to enhance metabolic processes in the fetus: glucose, vitamin C, group B, calcium gluconate, calcium chloride, unithiol, cocarboxylase, cytochrome C, etc.

5 gr. Means for combating metabolic acidosis. Sodium bicarbonate is under control of acid-base balance, as it can easily lead to imbalance. There are women of small, medium, large body mass. Depending on this, a different amount of soda is administered: 100-150-200 ml intravenously drip and then intravenously 40 ml of 40% glucose.

Early delivery. Methods depend on the state of the mother's body.

During pregnancy and in the first stage of labor, a caesarean section is used, in the second period - obstetric forceps with head presentation, with breech presentation - extraction of the fetus by the pelvic end.

Asphyxia of the fetus and newborn

Asphyxia of the newborn is a syndrome characterized by a lack of breathing or a separate irregular, ineffective in the presence of cardiac activity.

Asphyxia is not a very appropriate term, since in Latin it means “without a pulse”. Therefore, the modern name for asphyxia of newborns is depression of the newborn (WHO term).

The etiology and pathogenesis are the same as in GWP, since asphyxia begins with GWP (in 70-80% of cases).

Diagnosis of fetal asphyxia

Assessment of the state of the newborn on a number of parameters: the Apgar scale (1910, Virginia Apgar). Signs on a 0-1-2 point system: the state of the heartbeat, respiration, skin, muscle tone, reflex excitability. The ideal score is 10, the norm is 8-10. There are moderate (6-5 points) and severe (4-1 points) degrees of asphyxia. 0 points is a stillbirth. It is possible to characterize asphyxia of a newborn visually: blue asphyxia (6-5 points), white asphyxia (1-4 points).

Treatment of asphyxia of the fetus and newborn

First of all, these are resuscitation measures.

Principles:

restoration of independent adequate breathing and elimination of hypoxia

elimination of disorders of central and peripheral hemodynamics

correction of metabolic disorders

energy balance correction

The sequence of resuscitation measures for asphyxia of moderate severity

Respiratory resuscitation:

the release of the respiratory tract (suction pear, electric suction). Normally, in the bronchi, the embryonic fluid, which is pushed out during childbirth.

respiratory resuscitation in a special room - at the same time it is done: warming the child, mechanical ventilation (mask oxygen), since breathing with this degree of severity is superficial, but there are 30-40 breaths per minute.

resuscitation solutions are introduced into the vessels of the umbilical cord: glucose 10% 5 ml per 1 kg of body weight, cocarboxylase 8 mg/kg; vitamin C 5% 1-2 ml depending on the mass; calcium gluconate 1 ml/kg; sodium bicarbonate under the control of ASC 2-4 ml / kg, etimizole 1.5% 0.3 ml. If interventions are ineffective, we expand them to the scope of treatment of severe neonatal asphyxia.

The sequence of measures for severe asphyxia of a newborn

Restoration of patency of the upper respiratory tract.

Warming up the child.

Intubation, as breathing is very shallow or not at all. IVL with the help of breathing apparatus — VITA, VLADA, Johnson&Johnson.

Intravenously drugs (see above), add to this hydrocortisone - 5 mg per kg of body weight, or prednisone - 1 mg per kg.

If the measures are ineffective, and in the presence of bradycardia, arrhythmia, cardiac arrest, an external heart massage should be performed: rhythmic pressure with the index and middle fingers of the right hand on the sternum in the middle third (at the level of the nipples) with a frequency of 100-140 times per minute, to a depth of 1 -2 cm. If this is ineffective - the introduction of adrenaline hydrochloride intravenously 0.1 ml per kg of body weight. If there is no effect - adrenaline intracardiac.

Resuscitation of the newborn is terminated:

If cardiac activity is not restored within 8-10 minutes.

If the heartbeat is effective, but breathing is not restored after 15-20 minutes on a ventilator (since if breathing is not restored, then there is a severe brain lesion).

The issue is resolved legally. All resuscitation measures do not guarantee against the development of posthypoxic conditions: mental, physical retardation, childhood disability.