1. Intracranial birth hemorrhages (ICH).
2. Hypoxic-ischemic encephalopathy.
3. Infectious lesions of the brain and its membranes.
4. Congenital anomalies of brain development.
5. 5 Seizures.

Intracranial birth hemorrhages (ICH). At autopsy, 1/2 - 1/3 of dead newborns are found to have intracranial hemorrhages or damage to the anatomical structures of the brain.
The direct cause of birth trauma of the brain is the discrepancy between the bone pelvis of the mother and the head of the child, rapid (less than 2 hours) or protracted (more than 12 hours) labor, forceps, obstetric aids, traction behind the head, surgical interventions, excessive concern for "perineal protection" .

The most typical symptoms of any ICH in newborns are:

Sudden worsening of the child's condition with the development of a syndrome of depression with periodically appearing signs of hyperexcitability;
- change in the nature of the cry - the cry becomes monotonous, constant, quiet or loud, irritated, piercing, a groan appears;
- tension and bulging of a large fontanel;
- abnormal movements of the eyeballs - "floating eyeball movements", nystagmus;
- violation of thermoregulation - increase or decrease in temperature;
- vegetative-visceral disorders - regurgitation, pathological weight loss, flatulence, unstable stools, increased respiration, tachycardia;
- motor disorders - decrease or lack of motor activity;
- a change in muscle tone - an increase in the tone of certain muscle groups, for example, extensors or flexors of the limbs, due to which the limbs are in an extended or excessively bent position, with a decrease in muscle tone, the limbs are in an extended position, sag, the child may be in the “frog position” »;
- convulsions can be relied upon. The clinical manifestations of ICH in children depend on
from a combination of these symptoms, depending on the gestational age of the child, the localization and massiveness of ICH, concomitant diseases.

The following variants of ICH are distinguished: epidural, subdural, subarachnoid, intraventricular, parenchymal and cerebellar, hemorrhagic cerebral infarction (hemorrhage at the site of softening of the brain after ischemia due to thrombosis or embolism). Supratentorial and subtentorial hemorrhages are also distinguished.
Indirect signs of brain trauma in a newborn are a large birth tumor, cephalohematoma, and skull deformity.

With supratentorial hemorrhage, there may be a light interval from several hours to several days, since hemorrhages are located relatively far from the medulla oblongata, where the life support centers are located - respiratory and vasomotor. Very often, with the first application to the chest, the condition worsens sharply, a pronounced CNS excitation syndrome appears: a piercing cry, a groan, symptoms of hypertensive syndrome - tension of the large fontanel, stiff neck, eye symptoms appear: “floating movements of the eyeballs”, a fixed look, turning of the eye apples in one direction (hematomas), nystagmus, strabismus, dilated pupil on the side of the lesion. A convulsive syndrome may join, attacks of tonic or tonic-clonic convulsions (monotonous contractions of a certain group of muscles or limbs), there may be seizure equivalents: large-scale tremor, symptoms of oral automatism (constant sucking movements or constant protrusion of the tongue).
With subtentorial hemorrhages, the period of excitation is very short and is replaced by a period of CNS depression: there is no reaction to examination or a very weak reaction, crying is quiet or silent, eyes are wide open, gaze is indifferent, muscle hypotension, physiological reflexes are either very reduced or absent (including sucking, swallowing). Sleep apnea, SDR, tachycardia, or bradycardia may occur.
Depending on the localization of the ICH and the period of the disease, there is a significant fluctuation in the general condition from the excitation syndrome, turning into the depression syndrome up to coma with a periodic change of these conditions.

Additional research methods used in the diagnosis of ICH:

1. Spinal puncture. With subarachnoid and intraventricular hemorrhage, a large number of red blood cells are found in the cerebrospinal fluid.
2. Echo-encephaloscopy - ultrasound examination of the brain.
3. Neurosonography is a two-dimensional ultrasound examination of the brain through the large fontanel.
4. Computed tomography provides the greatest amount of information about the nature and location of pathological changes in the brain.

Treatment. With epidural and subdural hemorrhages, the most effective surgical treatment is the removal of a hematoma. Protective mode: reduce the intensity of sounds and visual stimuli, sparing examinations, all manipulations are carried out on the spot (washing, processing, injections), the appointment of minimally traumatic procedures, prevention of cooling and overheating, mother's participation in child care. Feed depending on the condition: parenterally, through a tube or from a bottle. It is necessary to establish monitoring of the main vital parameters: blood pressure, Ps, respiratory rate, temperature, diuresis, body weight, amount of fluid injected, assessment of the content of 02 and CO2 in the blood. Craniocerebral hypothermia is performed - cold to the head. Hemostatic drugs are introduced: vikasol, drugs that strengthen the vascular wall - ascorbic acid, rutin, calcium chloride. Dehydration therapy - magnesia sulfate, lasix, plasma. Anticonvulsants - phenobarbital, GHB, seduxen, drugs that improve cerebral circulation - cavinton, and brain tissue trophism - piracetam.

Hypoxic-ischemic encephalopathy (HIE)- brain damage caused by perinatal hypoxia, leading to motor disorders, convulsions, mental developmental disorders and other signs of cerebral insufficiency.
Any trouble during pregnancy turns into hypoxia for the fetus, asphyxia during childbirth leads to a decrease in cerebral blood flow in certain areas of the brain, resulting in ischemia of this area, leading to a change in cell metabolism, their death. The lesion may spread beyond ischemia, with the condition worsening. Acute period - 1 month, recovery period - up to 1 year and outcome.
In the acute period, there are mild, moderate and severe forms of HIE and 5 clinical syndromes: increased neuro-reflex excitability, convulsive, hypertensive-hydrocephalic, depression syndrome, coma.
With a mild form of brain damage (OSHA 6-7 b), a syndrome of increased neuroreflex excitability is characteristic: increased spontaneous motor activity, restless sleep, difficult falling asleep, unmotivated crying, tremor of the limbs and chin.
Moderate-severe form (OSHA 4-6 b) is manifested by hypertensive-hydrocephalic syndrome and depression syndrome. Characterized by an increase in head size by 1-2 cm, opening of the sagittal suture, enlargement and bulging of the large fontanelle, Graefe's symptom, "setting sun", intermittent nystagmus, convergent strabismus. Syndrome of oppression: lethargy, decreased motor activity, muscle hypotension, hyporeflexia.
In a severe form of HIE, a coma syndrome is characteristic (OSA 1-4 b). There is no reaction to examination, no reaction to painful stimuli, "floating eyeballs", reflexes are depressed, respiratory disorders, seizures, there is no sucking and swallowing. May be associated with convulsive syndrome.
The recovery period begins at the end of an acute process of a very different etiology, its beginning is conditionally attributed to the middle of the 2nd week of life. Syndromes of the early recovery period are designated by the term "encephalopathy", which combines brain diseases characterized by dystrophic changes.
The recovery period of HIE includes the following syndromes: increased neuro-reflex excitability, or cerebrasthenic, hypertensive-hydrocephalic, vegetative-visceral disorders, movement disorders, psychomotor developmental delay, epileptic syndrome.
Cerebrosthenic syndrome manifests itself against the background of normal psychomotor development of children. Emotional lability, irritability, restlessness, innate reflexes, spontaneous Moro reflex, startle, tremor of the chin and extremities, superficial sleep, difficulty falling asleep, poor appetite, poor weight gain are noted.
Syndrome of vegetative-visceral disorders. There are vascular spots, impaired thermoregulation (hypo- and hyperthermia), gastrointestinal dyskinesias (regurgitation, vomiting, unstable stools or constipation, flatulence) with pylorospasm, underweight, tachycardia or bradycardia, a tendency to lower blood pressure, tachypnea, rhythm disturbance breathing on the slightest stimulation. The syndrome of vegetative-visceral disorders is almost always combined with other syndromes of the recovery period, more often with hypertension and hydrocephalus.
The syndrome of movement disorders occurs in 2/3 of children with encephalopathies, manifested by a decrease or increase in muscle tone, paresis or paralysis of the limbs. In this case, the limbs are in an extended or excessively bent state, hang down, there is no physiological support reflex, or the child stands on tiptoe.
Syndrome of muscular hypotension: the limbs are extended, a “frog posture” is possible with the lower limbs turned outwards, the child’s motor activity is reduced. When the child is placed face down in the palm of his hand, the limbs, and often the head, hang down, there is no support on the legs.
Muscular hypertension syndrome: the child's motor activity is reduced due to hypertonicity of the limbs, therefore, stiffness is noted. Pathological postures may appear - the "boxer's position", when there is an increase in the tone of the flexors of the arms and at the same time the arms are bent, the fists are tightly clenched, and the extensor tone is increased in the lower extremities, due to which the legs are unbent and difficult to bend, or bend them at all impossible. In severe cases, the tone of all extensor groups - the neck, back, limbs - is increased, which leads to the appearance of opisthotonus. In this case, the child is curved in the form of a "bridge", can lean on the back of the head and heels. With a high tone of the adductor muscles of the hips and flexors, the “embryo” pose appears - the head is thrown back, the upper limbs are bent and pressed to the body, the legs are crossed.
Children with increased muscle tone, when examining physiological support reflexes and automatic walking, stand on tiptoe, but automatic walking does not appear.
hydrocephalic syndrome. In newborns, there is a disproportionate increase in head circumference (head circumference exceeds chest circumference by more than 3 cm). In the first 3 months of life, the head circumference increases by more than 2 cm monthly, there is a divergence of the cranial sutures by more than 5 mm, the large fontanel increases and bulges, the small and lateral fontanelles open, the brain skull prevails over the facial part, the overhanging forehead, the subcutaneous venous network on the scalp is expanded head, on the forehead, temples become thinner and soften the bones of the cranial vault.
Clinical manifestations depend on the severity of the hypertension syndrome: children are easily excitable, irritable, the cry is loud, shrill, sleep is superficial, children do not fall asleep well. With the predominance of hydrocephalic syndrome, lethargy, drowsiness, and a syndrome of vegetative-visceral disorders are noted. There is a symptom of the "setting sun", converging strabismus, horizontal nystagmus. Muscle tone is reduced, the sucking reflex is pronounced, symptoms of oral automatism may appear - protrusion and chewing of the tongue. There is no support reflex. With the progression of hydrocephalus, muscle tone increases, head tilting, large-scale tremor of the limbs and chin appear, and seizures may occur.
Syndrome of delayed psychomotor development. The child later begins to hold his head, sit, crawl, walk, a smile appears later, there is a delay in visual and auditory reactions, later he begins to recognize his mother, speak, and is less oriented in the environment.
Treatment of HIE in the acute period. It is impossible to treat the brain in isolation.

Main directions:

1. Restoration of normal airway patency and adequate ventilation of the lungs.
2. Correction of hypovolemia: plasma, albumin 5-10 ml/kg, reopoliglyukin 10 ml/kg.
3. Dehydration: magnesium sulfate 0.2 ml/kg, lasix, plasma.
4. Improvement of nervous tissue metabolism: piracetam 50 mg/kg, 10% glucose solution.
5. Anticonvulsants: phenobarbital 5 mg/kg, GHB 50 mg/kg, diazepam 1 mg/kg.

Treatment of HIE in the subacute period.

1. Cerebrasthenic syndrome: mixture with citral, diazepam, tazepam, valerian root, motherwort, nootropil, drugs that improve cerebral circulation (cynarizine, cavinton).
2. Hypertension-hydrocephalic syndrome: dehydration therapy (furosemide, glycerol, diacarb), absorbable therapy (lidase, aloe, cerebrolysin).
3. Movement disorders: vitamins Wb, B1; ATP, prozerin, galantamine.
4. Convulsive syndrome: phenobarbital, benzonal. Nootropic and absorbable drugs are required.

Convulsive syndrome in newborns

Seizures are sudden involuntary violent movements.

Causes of seizures in newborns:

1. The most common cause (65-70%) is perinatal hypoxia and the development of hypoxic-ischemic encephalopathy.
2. The second causal factor in terms of frequency is intracranial hemorrhage.
3. Metabolic disorders: hypoglycemia, hypocalcemia, hypomagnesemia, hypo- and hypernatremia, hyperbilirubinemia.
4. Infections: meningitis, encephalitis, sepsis.
5. Genetic and congenital defects in the development of the brain: family epilepsy, malformations of the brain, chromosomal diseases.
6. Withdrawal syndrome (withdrawal) in children whose mothers had drug or drug addiction during pregnancy (opium-containing substances, barbiturates, etc.).
7. Congenital metabolic anomalies: phenylketonuria, maple syrup disease, etc.

Convulsive syndrome is manifested by various paroxysmal phenomena.
Clonic convulsions - repetitive rhythmic contractions of the muscles of the face, limbs. They can be limited to one floorboard of the face, one or two limbs, and can spread to all limbs, muscles of the face, torso.
Tonic convulsions are a relatively prolonged contraction of all the muscles of the limbs and torso. At the same time, the limbs are unbent, the fists are tightly compressed, the head is thrown back, the gaze is fixed on one point, accompanied by bouts of apnea.
Myoclonic convulsions are sudden, non-rhythmic jerks of various muscle groups of the limbs.
Minimal convulsions or convulsive equivalents - manifest as sudden screams, ocular paroxysmal symptoms (nystagmus, open, unblinking eyes with a fixed gaze, twitching of the eyelids); symptoms of oral automatism - sucking, chewing, protrusion, trembling of the tongue; general fading, paroxysmal movements in the upper limbs (“swimmers' movements”) or in the lower limbs (“cyclists' movements”); sleep apnea (in the absence of bradycardia).
In newborns, symptoms of increased neuro-reflex excitability are also distinguished: tremor of the limbs, spontaneous Moro reflex (enveloping hand movements), clonus of the feet, startling with sharp sounds. Unlike true convulsions, external stimuli (for example, examining a child) are necessary for the onset of symptoms of increased neuro-reflex excitability.
For the correct treatment of seizures in children, it is necessary to find out their cause, for which they study the course of pregnancy and childbirth, family history; conduct a biochemical study of blood - the level of glucose, calcium, sodium, magnesium, bilirubin, urea, etc.
It is necessary to carry out echoencephaloscopy, echoencephalography, lumbar puncture, x-ray of the skull, computed tomography, screening of urine and blood serum for defects in amino acid metabolism, examination for intrauterine infections.
Treatment. The main task is to stop seizures, since during a convulsive attack, oxygen consumption by the brain increases, and neurons inevitably die. To eliminate a convulsive attack, apply: sibazon (seduxen, relanium) 0.5% solution of 0.04 ml / kg, the dose can be increased by 2 times. You can re-introduce this drug after 30 minutes if there is no effect. Side effects - respiratory depression, drowsiness, inhibition of the sucking reflex, muscle hypotension, lowering blood pressure.
Phenobarbital - for convulsions, it is administered intravenously at a dose of 20 mg / kg (introduced very slowly over 15 minutes), if there is no effect, phenobarbital can be re-introduced 2 times with an interval of 30-60 minutes. In the absence of convulsions in the future, phenobarbital is administered orally.
Sodium hydroxybutyrate (GHB) is administered intravenously in a 20% solution very slowly due to possible respiratory arrest. The anticonvulsant effect develops after 10-15 minutes and lasts 2-3 hours or longer.

With intractable convulsions, vitamin B6 is administered. Magnesium sulfate is administered for hypomagnesemia and cerebral edema. Enter intramuscularly 25% solution at a dose of 0.4 ml/kg of body weight.
With poorly controlled convulsions, along with phenobarbital, finlepsin, radedorm, benzonal, diacarb are prescribed.

In order to prevent neurological disorders in a child in time, it is important to know about hypoxic encephalopathy in the perinatal period.

What is encephalopathy in a newborn and where does it come from

The most common injury in the perinatal period is hypoxic encephalopathy in the newborn. The term "encephalopathy" refers to a non-inflammatory lesion of the brain. Lack of oxygen () during the prenatal period leads to the death of cells that are most sensitive to its deficiency - brain neurons. The rapid growth of the tissue of the central nervous system obliges the body to supply enough nutrients for its full development.

There are many reasons for the growing oxygen deficiency in the fetus, and they differ according to the period of his life. Etiological factors of the disease:

1. Prenatal period (throughout pregnancy)

• concomitant diseases of the mother (diabetes mellitus, heart failure);
• toxic effects (smoking, alcohol);
• multiple pregnancy;
• threats of breakdown, postmaturity;
• Rh-conflict of mother and child;

1. Intranatal period (at the time of birth)

• acute massive blood loss of the mother;
• entanglement of the fetus with the umbilical cord;
• mistakes in conducting labor activity;
• atypical position of the fetus;

Perinatal hypoxic encephalopathy can also develop after childbirth - up to and including the seventh day of a child's life. The reason for this may be congenital heart defects, acute respiratory disorders, etc.

How does the disease develop?

The mechanisms for the occurrence of hypoxia can be different - due to insufficient oxygen levels in the blood, anemia, circulatory disorders and metabolic disorders of fetal tissues. The main impetus for the development of pathology is circulatory disorders in the child's brain tissue.

The process of hypoxic ischemic encephalopathy in newborns is based not only on the slowing of blood flow in the central nervous system, but also on metabolic disorders and the development of brain tissue edema. The subsequent increase in intracranial pressure leads to aggravation of the nutrition of nerve cells and their gradual death.

How not to recognize the disease?

The first symptoms of the disease are usually noticed by a neonatologist immediately after the birth of a child. These include:

• lack of normal reflexes of the newborn, especially sucking;
• late or weak cry of the child;
• frequent crying;
• prolonged cyanosis of the skin;

The diagnosis of posthypoxic encephalopathy in newborns can only be made during the first month of a child's life. Signs and are caused by depression of the central nervous system of varying severity and are graded according to severity.

1. mild severity (usually reversible during the neonatal period):

• restless sleep;
• twitching of the chin;
• difficulty falling asleep;

1. moderate degree (regression occurs partially):

• weakening of normal reflexes;
• local neurological lesions (convergent strabismus, drooping of the upper eyelid);
• widespread muscle weakness;
• frequent causeless screams;

1. severe degree:

• convulsive seizures;
• lack of congenital reflexes;
• decreased blood pressure and heart rate;
• atony (lack of muscle tone);

Hypoxic ischemic encephalopathy in older children manifests itself as an outcome of perinatal pathology in the form of various neurological diseases.

Often, the disease is clinically manifested by disorders of other systems, such as transient tachycardia, cardiac arrhythmias, intestinal colic, and vomiting.

Approaches in the treatment of encephalopathy

The point of application of therapy should be not only the cause itself (oxygen deficiency), but also the main trigger of the disease - metabolic disorders. In the acute period, children are placed in neonatal intensive care units for round-the-clock monitoring of their condition. Patients are given:

Important! Early treatment determines the favorable outcome of the disease.

In the recovery period of perinatal posthypoxic encephalopathy, physiotherapy sessions, sessions with a speech therapist, and therapeutic exercises are carried out. It is also necessary to warn

Outcome and prognosis of the disease

Properly selected therapy helps to reduce cerebral manifestations and the frequency of disability in children who have had anoxic encephalopathy.

Mild and moderately severe degrees of severity have a favorable prognosis provided that the treatment is correctly prescribed. Severe cases of encephalopathy often progress to focal neurologic deficits.

Finally, it should be said that the prevention of hypoxic encephalopathy is very important, and should include antenatal protection of the fetus, careful management of labor and pregnancy. It is necessary to pay more attention to the fetus for the sake of its future health.

Perinatal hypoxic-ischemic encephalopathy (HIE) - this is a consequence of insufficient blood supply to the child's brain during pregnancy, childbirth or during the first month of his life. Hypoxia-ischemia of the brain is the main cause of neurological damage in newborns. One of the main parameters characterizing the severity of hypoxic-ischemic brain damage during childbirth and during pregnancy is the Apgar score and the presence of meconium in the amniotic fluid.

The consequences of HIE can be different: from a slight decrease in attention and restlessness of the child to severe forms of cerebral palsy.

Children with moderate brain damage may appear healthy during the first days and even months of life. Pathology in them is detected during an ultrasound of the brain in the first month of life, when examined by a neurologist and other specialists.

Babies with severe HIE and birth asphyxia usually require intensive care and are treated step by step in the maternity hospital and neonatal pathology department.

Perinatal hypoxic-ischemic encephalopathy of moderate and severe degree is one of the main risk factors for the development of cerebral palsy.

The course of HIE is very individual, but, as a rule, it is accompanied by the death of some brain cells and requires timely and correct treatment. Compliance with this principle allows you to achieve significant improvement even with severe brain damage.

What is the treatment for HIE?

The best treatment for HIE is prevention and early treatment of intrauterine hypoxia and neonatal asphyxia. But, despite significant progress in the prevention of complications of childbirth, moderate and severe hypoxic-ischemic encephalopathy still occurs with a frequency of 1-2 per 1000 children born. Until recently, medicine could offer such children only supportive therapy for organ dysfunction.

Since 2010, induced hypothermia has become the standard of care for HIE. This method consists in the fact that starting from 6 hours after birth, the child's body temperature is maintained at 33.5 ° C for 72 hours. Unfortunately, even after the use of induced hypothermia, a significant number of infants with HIE retain neurological disorders of varying severity.

Today, for the treatment of newborns with HIE, scientists offer a new method - regenerative therapy with cord blood stem cells.

New treatment for HIE

In HIE, cord blood mononuclear fraction containing stem cells is used. When it is administered intravenously to a child, brain cells are restored and regenerated, and the immune system is regulated. If the therapy was started at an early stage of the disease, then encephalopathy can be cured due to the powerful regenerative potential of the umbilical cord blood and the restoration of the population of nerve cells. The uniqueness of cell therapy in encephalopathy lies in the achievement of high treatment results in each case. To date, more than 330 children suffering from cerebral palsy have already been saved in Russia with the help of harvested cord blood.

Treatment of hypoxic-ischemic encephalopathy with cord blood mononuclear fraction in the early stages is the most important factor in a favorable prognosis, reducing the risk of developing cerebral palsy, as well as the correct development of the child and improving his quality of life in subsequent years.

Thus, having decided to preserve cord blood, parents give their baby a wonderful "biological insurance" against cerebral palsy: if necessary, treatment can be started from the first day of a newborn's life, using his own cord blood cells, right in the maternity hospital.

Parents - be vigilant: prepare your child's umbilical cord blood and thus you will save him from many diseases.

Hypoxic-ischemic damage to the central nervous system in newborns is a significant problem of modern neonatology, because according to statistics, almost every tenth newborn baby has certain signs of impaired brain activity in connection with. Among all the pathological conditions of the neonatal period, hypoxic brain damage occupies the first place. Especially often the disease is diagnosed in premature babies.

Despite the rather high incidence of pathology, effective measures to combat it have not yet been developed, and against irreversible structural damage to the brain, modern medicine is powerless. None of the known drugs can restore dead nerve cells in the brain, but research in this area continues, and the latest generation of drugs are undergoing clinical trials.

The CNS (central nervous system) is very sensitive to lack of oxygen in the blood.. In a growing fetus and a newborn child, immature brain structures need nutrition even more than in an adult, so any adverse effects on the expectant mother or the fetus itself during pregnancy and childbirth can be detrimental to the nervous tissue, which will subsequently manifest itself as neurological disorders.

an example of hypoxia due to insufficiency of uteroplacental blood flow

Hypoxia can be severe or mild, and it lasts for a long time or a few minutes during labor, but always provokes brain function disorders.

In the case of minor injuries, the process is completely reversible, and some time after birth, the brain will restore its work.

With deep hypoxia and asphyxia (complete cessation of oxygen supply to the brain), organic damage develops, often causing disability in young patients.

Most often, brain hypoxia occurs in the prenatal period or during childbirth with their pathological course. However, even after birth, hypoxic-ischemic changes can occur in case of a violation of the respiratory function in the baby, a drop in blood pressure, blood clotting disorders, etc.

In the literature, two names of the described pathology can be found - hypoxic-ischemic CNS injury and hypoxic-ischemic encephalopathy (HIE). The first option is more often used in the diagnosis of severe disorders, the second - in mild forms of brain damage.

Discussions regarding prognosis in hypoxic brain damage do not subside, however, the accumulated experience of neonatologists shows that the child's nervous system has a number of self-protection mechanisms and is even capable of regeneration. This is also evidenced by the fact that far from all children who have undergone severe hypoxia have gross neurological abnormalities.

In severe hypoxia, the immature structures of the brainstem and subcortical nodes primarily suffer; with prolonged, but not intense hypoxia, diffuse lesions of the cerebral cortex develop. One of the brain protection factors in a fetus or newborn is the redistribution of blood flow in favor of stem structures, therefore with prolonged hypoxia, the gray matter of the brain suffers to a greater extent.

The task of neurologists when examining newborns who have undergone hypoxia of varying severity is to objectively assess the neurological status, exclude adaptive manifestations (tremor, for example), which can be physiological, and identify truly pathological changes in brain activity. When diagnosing hypoxic lesions of the central nervous system, foreign experts are based on the staging of pathology, Russian doctors use a syndromic approach, pointing to specific syndromes from one or another part of the brain.

Causes and stages of hypoxic-ischemic injury

Perinatal damage to the central nervous system in newborns is formed under the influence of adverse factors in utero, in childbirth or during the newborn. The reasons for these changes can be:

• Disorders, bleeding in pregnant women, pathology of the placenta (thrombosis), retardation of fetal development;
• Smoking, drinking alcohol, taking certain medications during pregnancy;
• Massive bleeding during childbirth, entanglement of the umbilical cord around the neck of the fetus, severe bradycardia and hypotension in the infant, birth trauma;
• After childbirth - hypotension in the newborn, congenital heart defects, DIC, episodes of respiratory arrest, impaired lung function.

example of hypoxic-ischemic brain injury

The initial moment of development of HIE is oxygen deficiency in arterial blood, which provokes the pathology of metabolism in the nervous tissue, the death of individual neurons or their entire groups. The brain becomes extremely sensitive to fluctuations in blood pressure, and hypotension only exacerbates existing lesions.

Against the background of metabolic disorders, “acidification” of the tissue (acidosis) occurs, edema and swelling of the brain increase, and intracranial pressure increases. These processes provoke widespread necrosis of neurons.

Severe asphyxia is also reflected in the work of other internal organs. Thus, systemic hypoxia causes acute renal failure due to necrosis of the epithelium of the tubules, necrotic changes in the intestinal mucosa, and liver damage.

In full-term children, post-hypoxic lesions are noted mainly in the region of the cortex, subcortical structures, and the brain stem; in premature infants, due to the peculiarities of the maturation of the nervous tissue and the vascular component, periventricular leukomalacia is diagnosed, when necrosis is concentrated mainly around the lateral ventricles of the brain.

Depending on the depth of cerebral ischemia, several degrees of severity of hypoxic encephalopathy are distinguished:

1. The first degree - mild - transient disorders of the neurological status, lasting no more than a week.
2. HIE of the second degree - lasts longer than 7 days and is manifested by depression or excitation of the central nervous system, convulsive syndrome, a temporary increase in intracranial pressure,.
3. A severe form of hypoxic-ischemic injury is a disorder of consciousness (stupor, coma), convulsions, manifestations with stem symptoms and impaired activity of vital organs.

Symptoms of hypoxic-ischemic damage to the central nervous system

The defeat of the central nervous system in newborns is diagnosed in the first minutes of a baby's life, while the symptoms depend on the severity and depth of the pathology.

I degree

With a mild course of HIE, the condition remains stable, according to the Apgar scale, the child is assessed at least 6-7 points, a decrease in muscle tone is noticeable. Neurological manifestations of the first degree of hypoxic damage to the central nervous system:

1. High neuro-reflex excitability;
2. sleep disorders, anxiety;
3. Trembling of limbs, chin;
4. Possible regurgitation;
5. Reflexes can be both enhanced and reduced.

The described symptoms usually disappear during the first week of life, the child becomes calmer, begins to gain weight, gross neurological disorders do not develop.

II degree

With moderate brain hypoxia, signs of brain depression are more obvious, which is expressed in deeper disorders of the brain. Usually, the second degree of HIE accompanies combined forms of hypoxia, which is diagnosed both during the intrauterine growth stage and at the time of delivery. At the same time, muffled fetal heart sounds, increased rhythm or arrhythmia are recorded, according to the Apgar scale, the newborn gains no more than 5 points. Neurological symptoms are:

• Inhibition of reflex activity, including sucking;
• A decrease or increase in muscle tone, spontaneous motor activity may not manifest itself in the first days of life;
• Severe cyanosis of the skin;
• Rising ;
• Vegetative dysfunction - respiratory arrest, accelerated heart rate or bradycardia, impaired intestinal motility and thermoregulation, a tendency to constipation or diarrhea, regurgitation, slow weight gain.

intracranial hypertension accompanying severe forms of HIE

As intracranial pressure increases, the baby's anxiety increases, excessive skin sensitivity appears, sleep is disturbed, the tremor of the chin, arms and legs increases, bulging of the fontanelles becomes noticeable, horizontal nystagmus and oculomotor disorders are characteristic. Seizures can be signs of intracranial hypertension.

By the end of the first week of life, the condition of a newborn with a second degree of HIE gradually stabilizes against the background of intensive treatment, but neurological changes do not disappear completely. In an unfavorable combination of circumstances, the condition may worsen with depression of the brain, a decrease in muscle tone and motor activity, depletion of reflexes, and coma.

III degree

Perinatal damage to the central nervous system of hypoxic-ischemic genesis of a severe degree usually develops during severe second half of pregnancy, accompanied by high hypertension in a pregnant woman, impaired renal function, and edema. Against this background, a newborn is already born with signs of malnutrition, intrauterine hypoxia, developmental delay. The abnormal course of labor only exacerbates the existing hypoxic damage to the central nervous system.

With the third degree of HIE, the newborn has signs of severe circulatory disorders, there is no breathing, tone and reflexes are sharply reduced. Without urgent cardiopulmonary resuscitation and restoration of vital functions, such an infant will not survive.

During the first hours after childbirth, a sharp depression of the brain occurs, a coma occurs, accompanied by atony, an almost complete absence of reflexes, dilated pupils with a reduced response to a light stimulus or its absence.

Inevitably developing cerebral edema is manifested by convulsions of a generalized type, respiratory and cardiac arrest. Multiple organ failure is manifested by an increase in pressure in the pulmonary artery system, a decrease in urine filtration, hypotension, necrosis of the intestinal mucosa, liver failure, electrolyte disturbances, and blood clotting disorders (DIC).

A manifestation of severe ischemic damage to the central nervous system is the so-called postasphyxial syndrome - babies are inactive, do not scream, do not respond to pain and touch, their skin is pale cyanotic, and a general decrease in body temperature is characteristic. Swallowing and sucking disorders are considered important signs of severe cerebral hypoxia, which makes natural feeding impossible. To save their lives, such patients require intensive care in intensive care, but the unstable condition still persists until the 10th day of life, and the prognosis often remains poor.

A feature of the course of all forms of HIE is the increase in neurological deficit over time, even under conditions of intensive care. This phenomenon reflects the progressive death of neurons that have already been damaged during a lack of oxygen, and also determines the further development of the baby.

In general, ischemic-hypoxic damage to the central nervous system can proceed in different ways:

1. Favorable with fast positive dynamics;
2. Favorable course with rapid regression of neurological deficit, when by the time of discharge the changes either disappear or remain minimal;
3. Unfavorable course with progression of neurological symptoms;
4. Disability during the first month of life;
5. A latent course, when after six months motor and cognitive disorders increase.

In the clinic, it is customary to distinguish between several periods of ischemic encephalopathy in newborns:

• Acute - the first month.
• Recovery - within one year.
• period of long-term consequences.

The acute period is manifested by the whole gamut of neurological disorders from barely noticeable to coma, atony, areflexia, etc. During the recovery period, the syndrome of excessive neuro-reflex excitability, convulsive syndrome, possibly delayed intellectual and physical development come to the fore. As the child grows, the symptoms change, some symptoms disappear, others become more noticeable (speech disorders, for example).

Treatment and prognosis for HIE

Diagnosis of HIE is established on the basis of symptoms, data on the course of pregnancy and childbirth, as well as special research methods, among which neurosonography, echocardiography, CT, brain MRI, coagulogram, ultrasound with dopplerography of cerebral blood flow are most often used.

The treatment of ischemic lesions of the central nervous system in newborns is a big problem for neonatologists, since no drug can achieve regression of irreversible changes in the nervous tissue. Nevertheless, it is still possible to at least partially restore brain activity in severe forms of pathology.

Drug treatment of HIE is carried out depending on the severity of a particular syndrome or symptom.

With a mild and moderate degree of the disease, anticonvulsant therapy is prescribed, a severe form of perinatal encephalopathy requires immediate resuscitation and intensive care.

With increased excitability of the nervous system without a convulsive syndrome, neonatologists and pediatricians are usually limited to monitoring the child, without resorting to specific therapy. In rare cases, it is possible to use diazepam, but not for a long time, since the use of such drugs in pediatrics is fraught with a delay in further development.

It is possible to prescribe pharmacological agents that have a combined nootropic and inhibitory effect on the central nervous system (pantogam, phenibut). In case of sleep disorders, the use of nitrazepam and herbal sedatives is allowed - valerian extract, mint, lemon balm, motherwort. Massage and hydrotherapy have a good sedative effect.

In severe hypoxic lesions, in addition to anticonvulsants, measures are needed to eliminate cerebral edema:

• - furosemide, mannitol, diacarb;
• Magnesium sulfate.

Respiratory and palpitation disorders require immediate resuscitation, the establishment of artificial lung ventilation, the introduction of cardiotonic drugs and infusion therapy.

With the main place in the treatment is occupied by diuretics, and diacarb is considered the drug of choice for children of all ages. If drug therapy does not lead to the desired result, then surgical treatment of hydrocephalus is indicated - shunt operations aimed at dumping cerebrospinal fluid into the abdominal or pericardial cavity.

With convulsive syndrome and increased excitability of the central nervous system, anticonvulsants - phenobarbital, diazepam, clonazepam, phenytoin can be prescribed. Newborns are usually given barbiturates (phenobarbital), infants are usually given carbamazepine.

The syndrome of movement disorders is treated with drugs that reduce hypertonicity (mydocalm, baclofen), with hypotonicity, dibazol, galantamine in low doses are indicated. To improve the patient's motor activity, massage, therapeutic exercises, physiotherapy, water and reflexotherapy are used.

The delay in mental development and the formation of speech, according to the age of the child, becomes noticeable by the end of the first year of life. In such cases, nootropic drugs (nootropil, encephabol), vitamins of group B are used. Special classes with teachers and defectologists who specialize in working with children who are lagging behind in development play a very important role.

Very often, parents of children who have had perinatal encephalopathy are faced with the appointment of a large number of various drugs, which is far from always justified. Overdiagnosis, "reinsurance" of pediatricians and neurologists lead to the widespread use of diacarb, nootropics, vitamins, actovegin and other drugs that are not only ineffective in mild HIE, but are often contraindicated due to age.

The prognosis for hypoxic-ischemic lesions of the central nervous system is variable: regression of brain disorders with recovery, and progression with disability, and an asymptomatic form of neurological disorders - minimal brain dysfunction are possible.

Epilepsy, cerebral palsy, hydrocephalus, mental retardation (mental retardation) are considered to be long-term consequences of HIE. Oligophrenia always has a persistent character, does not regress, and a somewhat belated development of the psychomotor sphere during the first year of life may pass over time, and the child will not be any different from most of his peers.

Video: about hypoxic-ischemic damage to the central nervous system and the importance of timely treatment

Hypoxic-ischemic encephalopathy combines brain lesions of various etiologies or unspecified origins that occur before and during childbirth.

The causes of hypoxic-ischemic encephalopathy of the newborn are diverse (hypoxic, traumatic, toxic, metabolic, stressful effects, radiation, immunological abnormalities in the mother-placenta-fetus system), but they all lead to intrauterine hypoxia or asphyxia of the fetus and newborn.

Among the causes of perinatal brain damage, the leading place is occupied by intrauterine and intranatal fetal hypoxia. Intrauterine fetal hypoxia may be hypoxic, which occurs when there is insufficient oxygen saturation in the blood, hemic due to a drop in the level of hemoglobin in the blood, circulatory- violation of blood flow and tissue- as a result of a violation of oxidative processes in the tissues of the fetus. Currently, instead of the term perinatal encephalopathy, the term hypoxic-ischemic encephalopathy (HIE) of the newborn is used. For unfavorable reasons antenatal period contributing to fetal hypoxia include: severe somatic diseases of the mother, especially in the stage of decompensation: pathology of pregnancy (prolonged toxicosis, the threat of interruption, postmaturity, etc.); endocrine diseases (diabetes); infections of various etiologies, especially in the 2nd - 3rd trimesters of pregnancy; bad habits of the mother (smoking, alcoholism, drug addiction); genetic, chromosomal pathology; immunological abnormalities in the mother-placenta-fetus system; multiple pregnancy. AT intranatal period: abnormal presentation of the fetus; the use of aids in childbirth (obstetric forceps, vacuum extractor); acute hypoxia in childbirth in the mother (shock, decompensation, somatic pathology); disorders of the placental-fetal circulation (preeclampsia, from the side of the umbilical cord: tight entanglement, true knots, prolapse of loops, tension of the umbilical cord, which is short in length, etc.); rapid, rapid, protracted labor; placenta previa or premature detachment; discoordination of labor activity; uterine rupture; caesarean section (especially emergency).

The second most important place in the development of newborn encephalopathy belongs to the factor mechanical trauma to the central nervous system a child during childbirth, as a rule, in combination with previous intrauterine hypoxia: intracranial hemorrhages of hypoxic origin (IVH, subarachnoid) and traumatic injuries of the nervous system (RTBI, spinal cord, peripheral nervous system).

In recent years, the structure of etiopathogenetic factors of perinatal damage to the CNS includes toxic-metabolic(transient metabolic disorders - kernicterus, hypoglycemia, hypo-, hypermagnesemia, hypocalcemia, hypo-, hypernatremia; with impaired CNS functions due to alcohol, drugs, smoking, drugs, exposure to viral and bacterial toxins during pregnancy), infectious(intrauterine infections, neonatal sepsis), hereditary and combined brain damage.

The polyetiology of newborn encephalopathy predetermines various mechanisms of brain damage.

One of them is decreased cerebral blood flow , which may be due to antenatal hypoxia, accompanied by slowing down the growth of capillaries in the brain, increasing their permeability and vulnerability, in addition, increasing the permeability and cell membranes. Against the background of an increase in metabolic acidosis, cerebral ischemia occurs with the development of intracellular lactate acidosis and the death of neurons.

Decrease in cerebral blood flow violations of the mechanisms of autoregulation of cerebral blood flow. In healthy children, cerebral blood flow and intracranial pressure are relatively stable and do not depend on fluctuations in blood pressure (BP). In children who have undergone hypoxia, the mechanisms of autoregulation of cerebral blood flow are either reduced (moderate hypoxia) or absent (severe hypoxia) and cerebral blood flow is dependent on fluctuations in blood pressure. In addition, in children who have undergone hypoxia, cardiac output is reduced (hemodynamic disturbances and hypoxic myocardial damage), blood pressure is reduced, venous outflow from the brain is impaired, vascular resistance in the brain itself is increased due to hypoxic damage to the endothelium, which leads to a sharp decrease in the lumen of capillaries. .

Against the background of a decrease in cerebral blood flow and a violation of the production of ADH (asphyxia - excessive production, hypoxia - a syndrome of insufficient secretion) develops vasogenic cerebral edema .

Due to a violation of cerebral blood flow, the development of vasogenic cerebral edema, develops cytotoxic edema , due to the release of "exciting" amino acids, primarily glutamate. Hypoxia reduces the delivery of energy (glucose) to neurons → the synthesis of ATP and creatine phosphate is inhibited → the functioning of cell membrane pumps is disrupted → depolarization of the outer membranes occurs → excessive release of glutamate into the interstitium and insufficient absorption of it by neurons affects neuronal receptors, opening channels through which into the cell includes sodium and calcium. Sodium pulls water with it, which leads to the development of cellular edema, and excess calcium intake leads to the development of cellular calcium necrosis.

J.J. Volpe presents several chains of pathogenesis of perinatal hypoxic-ischemic encephalopathy due to intrauterine hypoxia: intrauterine hypoxia → decreased oxygen saturation and increased carbon dioxide saturation, fetal acidosis → intracellular edema → swelling of brain tissue → local decrease in cerebral blood flow → generalized cerebral edema → increased intracranial pressure → generalized decrease in cerebral blood flow → necrosis of the medulla.

In acute hypoxic changes in the brain, the following stages are morphologically distinguished: stage I - edematous-hemorrhagic; Stage II - encephalic edema; Stage III - leukomalacia (necrosis); Stage IV - leukomalacia with hemorrhage. The first two stages are curable, the next two lead to irreversible death of neurons. With antenatal (chronic) hypoxia, neuronal dystrophy, glial proliferation, sclerosis phenomena, and the formation of cystic cavities at the sites of small foci of necrosis are observed.

Thus, the main links in the pathogenesis of perinatal hypoxic-ischemic encephalopathy are metabolic disorders, the trigger of which is oxygen deficiency, and the directly damaging factors for the brain are the products of impaired metabolism.

It must be remembered that the nature of morphological changes in the brain in encephalopathy is influenced not only by the etiological factor and its duration, but also in many ways by the degree of brain maturity at the time of exposure to adverse factors.

In the acute period, allocate light, medium and severe degree the severity of the disease.

At mild degree brain lesions, minimal changes are observed in the motor and reflex areas in the form of a syndrome of neuroreflex excitability, excitation or depression, which persist for no more than 7 days. They are characterized by transient moderate or mild changes in the nervous system in the form of emotional and motor anxiety. Changes in motor activity are clearly expressed: against the background of normal or changing muscle tone, spontaneous activity increases, tremor of the limbs, knee and unconditioned reflexes are revived, a decrease in the main reflexes of the neonatal period (protective, support and automatic gait, Moreau, Babkin, Robinson, Bauer) is noted. In some cases, there is a horizontal nystagmus, transient strabismus, episodically floating movements of the eyeballs.

At the same time, it should be taken into account that the presence of neuroreflex excitability or its suppression during the first 5-7 days of life can be a form of transient adaptation of the newborn organism in the early neonatal period and this condition should not be considered as a pathology. This is due to the fact that during childbirth the fetus experiences increasing transient hypoxia at the time of contractions, great physical exertion when it is expelled from the womb and passes through the birth canal. As a result, there is a long-term excitation of the stress adrenergic and pituitary-adrenal systems, on the one hand, and the stress-limiting system, the modulation of which is carried out by inhibitory mediators, amino acids and neuropeptides (GABA, serotonin, glycine, opioids). Such tension causes minor transient deviations from optimal neurological status.

Moderate degree The disease is manifested by the following main clinical and neurological syndromes: depression or excitation for more than 7 days, hypertensive, hypertensive-hydrocephalic, convulsive. In children, there is a decrease in spontaneous motor activity (lethargy, immobility), persistent changes in muscle tone, which is usually reduced, and then selectively increases, more often in the flexor muscle group. During the first days of life, spontaneous shudders are often noted, and then generalized convulsive twitches join them. The main unconditioned reflexes are reduced or inhibited. Possible manifestation of focal neurological symptoms: anisocoria, ptosis, converging strabismus, nystagmus, a symptom of the "setting sun".

With hypertension syndrome, general hyperesthesia, "brain scream" are observed, sleep is disturbed, swelling and tension of the large fontanel are noted, and a positive symptom of Graefe. Hypertensive-hydrocephalic syndrome is accompanied by an increase in head circumference, opening of the sagittal suture by more than 0.5 cm, opening of other cranial sutures, and an increase in the size of the fontanelles. The severity of Graefe's symptom increases, nystagmus and converging strabismus appear. Muscular dystonia is noted, spontaneous shudders, spontaneous Moro reflex occur.

Somatic disorders are possible in the form of regurgitation, vomiting, "marbling" and cyanosis of the skin, cardiac arrhythmia, tachypnea, etc.

Neurological disorders in the moderate form usually last 2 to 4 months.

Severe degree Perinatal hypoxic-ischemic damage to the central nervous system is manifested by a coma syndrome and is observed only with severe brain damage. A cerebral coma is clinically diagnosed: apathy, adynamia, areflexia, muscular hypotension up to atony, eyes and mouth are often open, rare blinking, orbital nystagmus, absence of the act of sucking and swallowing. At the same time, vegetative-visceral disorders are noted: respiratory arrhythmia, apnea, bradycardia, arterial hypotension, sluggish peristalsis, bloating, urinary retention, severe metabolic disorders. Sometimes progressive intracranial hypertension, convulsions develop. The severity of neurological disorders of envy from the depth of coma.

A serious condition lasts up to 1.5 - 2 months. Often there are serious violations of the central nervous system.

Thus, the following leading syndromes are characteristic of the acute period of CNS damage: increased neuro-reflex excitability; oppression; arousal; hypertensive; hypertensive-hydrocephalic; convulsive; coma.

The recovery period in case of damage to the central nervous system is characterized by the following syndromes: asthenoneurotic; vegetative-visceral dysfunctions; movement disorders; convulsive (epileptic); hydrocephalic; delays in psychomotor and preverbal development.

The diagnosis of neonatal encephalopathy and birth traumatic brain injury according to Instruction No. 192-1203 of the Ministry of Health of the Republic of Belarus of 2003 can only be used in the neonatal period, i.e. during the first month of life.

The stages of diagnosis and formation of the diagnosis of encephalopathy according to the Instructions of the Ministry of Health of the Republic of Belarus No. 192-1203 are presented as follows:

During the neonatal period- an indication of cerebral dysfunction: encephalopathy of the newborn, indicating the main cause and nature of brain changes, the severity and leading clinical disorders (syndromes).

An example of a diagnosis: Encephalopathy of the newborn of hypoxic-ischemic genesis, moderate severity, hypertension syndrome.

In infancy(from the 2nd month of life):

Donosological (syndromal) diagnosis: a list of the main clinical syndromes (motor retardation; mental retardation; syndrome of autonomic dysfunctions; benign intracranial hypertension; epilepsy and epileptic syndromes not defined as focal or generalized; convulsive syndrome NOS; other syndromes) is given, indicating the cause of their occurrence - encephalopathy or traumatic brain injury.

An example of a diagnosis: Delayed psychomotor development due to encephalopathy (craniocerebral birth injury) of a newborn of hypoxic-ischemic genesis.

Nosological diagnosis: the main diseases of ICD-X (infantile cerebral palsy; epilepsy; hydrocephalus; oligophrenia, other diseases) resulting from neonatal encephalopathy or intracranial birth trauma are given without indicating the cause of their occurrence.

Diagnosis example: Cerebral palsy due to neonatal encephalopathy.

Diagnosis of perinatal lesions of the brain of the fetus and newborn is possible by taking into account a complex of anamnestic data (the nature of the course of pregnancy and childbirth, Apgar scores), analysis of the dynamics of the clinical picture and modern instrumental methods for diagnosing the nervous system: transillumination of the skull, neurosonography (NSG), Doppler encephalography ( DEG), computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), cerebral scintigraphy (CSG), electroneuromyography (ENMG), electroencephalography (EEG), neuroimmunochemical identification of cerebral proteins (neurospecific proteins - NSP ).

The use of modern advanced technologies in perinatal practice makes it possible to clarify the etiology, pathogenetic mechanisms, clinical and morphological structure of cerebral disorders.

This teaching aid describes syndromes that quite fully reflect the condition of newborns and on the basis of which one can judge their further prognosis.

The best treatment for perinatal brain damage is the prevention and early treatment of intrauterine hypoxia of the fetus and newborn. The main therapeutic measures aimed at the main pathogenetic mechanisms of brain damage are:

prenatal prevention of cerebral hypoxia-ischemia,

creation of optimal (comfortable) conditions for nursing with and limitation of excessive traumatic and irritating environmental influences

infection prevention,

prompt restoration of normal airway patency and adequate breathing,

elimination of possible hypovolemia,

restoration and normalization of systemic and cerebral hemodynamics, by preventing hypotension or hypertension, polycythemia and blood hyperviscosity, hypervolemia,

prevention and treatment of cerebral edema and convulsive syndrome,

maintenance of carbohydrate homeostasis,

correction of acidosis, hypocalcemia, hypomagnesemia, etc.

Treatment of patients with hypoxic-ischemic encephalopathy in the acute period is carried out in the intensive care unit or in the intensive care unit with subsequent transfer, if necessary, to a specialized neuropsychiatric unit.

In the acute period, timely correction of RDS and adequate oxygenation are necessary. The head of a newborn with perinatal CNS damage should be given an elevated position. In the first 3-5 days spend:

1. Antihemorrhagic therapy: 1% solution of vikasol 1 mg/kg/day (0.1 ml/kg), 12.5% ​​dicynone, etamsylate 10-15 mg/kg/day (0.1-0.2 ml/kg) in/venously or in/muscularly.

2. Dehydration therapy: 1% solution of Lasix 1-2 mg/kg, veroshpiron 2-4 mg/kg/day intramuscularly or intravenously, manitol 0.25-0.5 g/kg once intravenously drip slowly , with hypotension-hydrocephalic or hydrocephalic syndromes from the 5th-7th day of life with normal KOS indicators, the appointment of diacarb according to the scheme of 15-80 mg / kg / day is indicated. with potassium supplements and alkaline drink. Depending on the severity of the hypertensive-hydrocephalic syndrome, glucocorticoid hormones are used in the treatment, taking into account their pronounced membrane-stabilizing and anti-edema action - dexamethasone 0.1-0.3 mg / kg / day - 7 days, followed by a dose reduction every 3-5 days by 1 /3.

3. Antioxidant and metabolic therapy: aevit 0.1 ml/kg/day intramuscularly or an oily solution of 5% (0.2 ml/kg/day) or 10% (0.1 ml/kg/day) vitamin E solution ; cytochrome "C" 1 ml/kg intravenously; cerebral angioprotectors - actovegin 0.5-1.0 ml intravenously or intramuscularly, mildronate 10% solution 0.1-0.2 ml / kg / day intravenously or intramuscularly, emoxipin (mexidol) 1% 0.1 ml / kg / day intramuscularly, 20% solution of Elcar (levocarnitine) 4 - 8 (10) drops. 3 times a day.

4. Antihypoxant (anticonvulsant) therapy: 20% GHB solution 100-150 mg/kg (0.5-0.75 ml/kg) intravenously drip or intramuscularly, 0.5% seduxen solution 0.2-0, 4 mg/kg (0.04-0.08 ml/kg) i.v. or i.m.

5. Correction of central and peripheral hemodynamics: titration of 0.5% dopamine solution, 4% dopmin solution 0.5-10 mcg/kg/min, or dobutamine, dobutrex 2-10 mcg/kg/min. Patients with low blood pressure, which may be one of the early signs of adrenal insufficiency, should be injected intramuscularly or intravenously with dexomethasone at a dose of 0.5 mg/kg or hydrocotison 5-10 mg/kg once.

6. Posyndromic and symptomatic therapy.

By the end of the early neonatal period, in order to improve the function of the central nervous system, the complex of therapeutic measures includes nootropic drugs that have both a sedative effect: phenibut (noofen), pantogam 20–40 mg/kg/day, but not more than 100 mg/day. in 2 doses, and a stimulating component: piracetam 50-100 mg / kg / day, picamilon 1.5-2.0 mg / kg / day, encephabol 20-40 mg / kg / day in 2 doses, aminalon 0.125 mg 2 times a day day. Cerebrolysate 0.5-1.0 ml intramuscularly for 10-15 days (contraindicated in convulsive readiness, arousal syndrome), glycine 40 mg / kg / day orally in 2 doses, gliatilin 40 mg / kg / day in / vein, in / muscle. In order to improve cerebral circulation in the absence of hemorrhages, the appointment of trental, cavinton, vinpocetine 1 mg / kg / day intravenously, tanakan 1 cap. / kg 2 times a day, sirmeon 0.5-1.0 mg / kg / day orally in 2 doses. In disorders accompanied by an increase in muscle tone with signs of spasticity, muscle relaxant drugs are prescribed - mydocalm 5 mg / kg / day, baclofen, trapofen 1 mg / kg / day 2-3 times a day. To improve the conduction of excitation in the neuromuscular synapses and restore neuromuscular conduction, the treatment includes B1.6 vitamins 0.5-1.0 ml intramuscularly for 10-15 days, galantamine 0.5% 0.18 mg/kg / day, prozerin 0.05% 0.04-0.08 mg / kg / day intramuscularly 2-3 times a day, sometimes dibazol is prescribed at 0.5 - 1.0 mg orally 1 time per day.

Treatment of encephalopathy of the newborn should be complex and staged. An integrated approach implies early (from 3 weeks of a child's life) appointment of exercise therapy and therapeutic massage (stimulating, relaxing), physiotherapy procedures, the choice of which depends on clinical manifestations (with high muscle tone - sinusoidal simulated currents, thermal procedures, such as paraffin and ozokerite applications), with low - electrophoresis with calcium on the spine, etc. To stimulate pre-speech development and fine motor skills, speech therapy classes are conducted from the end of the neonatal period.

Treatment of newborns with hypoxic-ischemic encephalopathy should not be polypharmacy. Early protection of the brain of a newborn and properly selected drug therapy, taking into account the conducted modern neuroimaging research methods, helps to reduce the severity of cerebral consequences and the degree of disability in children who have undergone hypoxic-ischemic encephalopathy of the newborn.

Prevention of newborn encephalopathy includes a set of measures for antenatal protection of the fetus, careful management of childbirth, early diagnosis and rational treatment of hypoxic, traumatic conditions of the fetus and newborn.

Apps 1

INDICATORS OF THE KOSU OF HEALTHY CHILDREN

Indicator	Characteristics of the indicator
	Medium acidity index	7,35-7,45
	Reflects the concentration of carbon dioxide dissolved in blood plasma	(4.3-6 kPa)
	Reflects the concentration of oxygen dissolved in the blood	6 0-80 mmHg
	The concentration in the blood (plasma) of total CO 2	22.7-28.6 mmol/l
	True plasma bicarbonate - HCO concentration 3 in plasma	19-25 mmol/l
	Standard plasma bicarbonate	20-27 mmol/l
	Buffer Base Concentration	40-60 mmol/l
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