Risk factors for perinatal brain pathology include:

• Various chronic diseases of the mother.
• Acute infectious diseases or exacerbations of chronic foci of infection in the mother’s body during pregnancy.
• Eating disorders.
• The pregnant woman is too young.
• Hereditary diseases and metabolic disorders.
• Pathological course of pregnancy (early and late toxicosis, threat of miscarriage, etc.).
• Pathological course of labor (rapid labor, weakness of labor, etc.) and injuries when providing assistance during childbirth.
• Harmful environmental influences, unfavorable environmental conditions (ionizing radiation, toxic effects, including the use of various medicinal substances, environmental pollution with salts of heavy metals and industrial waste, etc.).
• Prematurity and immaturity of the fetus with various disorders of its vital functions in the first days of life.

It should be noted that the most common are hypoxic-ischemic (their cause is oxygen deficiency that occurs during the baby’s intrauterine life) and mixed lesions of the central nervous system, which is explained by the fact that almost any problem during pregnancy and childbirth leads to disruption of the oxygen supply to tissues the fetus and primarily the brain. In many cases, the causes of PEP cannot be determined.

The 10-point Apgar scale helps to form an objective picture of the child’s condition at the time of birth. This takes into account the child’s activity, skin color, the severity of the newborn’s physiological reflexes, and the state of the respiratory and cardiovascular systems. Each indicator is scored from 0 to 2 points.

The Apgar scale allows already in the delivery room to assess the child’s adaptation to extrauterine conditions of existence within the first minutes after birth. A score of 1 to 3 indicates a severe condition, 4 to 6 indicates a moderate condition, and 7 to 10 indicates a satisfactory condition. Low scores are considered risk factors for the child’s life and the development of neurological disorders and dictate the need for emergency intensive care.

Unfortunately, high Apgar scores do not completely exclude the risk of neurological disorders; a number of symptoms appear after the 7th day of life, and it is very important to identify possible manifestations of PEP as early as possible. The plasticity of a child’s brain is unusually high; timely treatment measures help in most cases to avoid the development of neurological deficits and prevent disorders in the emotional-volitional sphere and cognitive activity.

In newborns

The causes of hypoxic ischemic encephalopathy in newborns may be the following:

• asphyxia during childbirth (weak contractions);
• premature and pathological birth (umbilical cord prolapse);
• maternal infectious diseases;
• physical factors (polluted air, radiation).

In adults

In adults, the disease occurs as a result of:

• carbon monoxide poisoning;
• in case of strangulation;
• sharply low blood pressure;
• drug or alcohol overdose;
• consequences after general anesthesia;
• complications after head injuries.

All of the above reasons arise due to a decrease in oxygen supply to the brain.

Severity

For mild severity:

• pupil dilation;
• the patient cannot concentrate;
• body coordination is impaired;
• drowsy state;
• hyperemotionality;
• increased irritability;
• eyelids wide open;
• lack of appetite;
• a wandering phenomenon is observed;
• cerebrovascular accident.

Moderate severity:

• periodic causeless screams of the child;
• reflexes are partially weakened or completely absent (protective, support);
• muscle weakness (muscle tone decreases and then involuntarily increases);
• drooping upper eyelid;
• increased cerebrospinal fluid pressure;
• metabolic acidosis of the blood;
• neurological disorders;
• violation of the swallowing process.

In more severe cases:

• convulsive state;
• cyanosis of the skin;
• loss of consciousness;
• hypertension;
• strabismus;
• lack of response to pain and motor activity;
• precomatose or comatose state;
• the reaction of the pupils to light is practically absent;
• disturbance of the respiratory process, accompanied by arrhythmia;
• rapid heartbeat (tachycardia).

The severity of the disease is determined directly in the maternity hospital by medical specialists. If necessary, appropriate treatment is prescribed.

Lightweight	Average	Heavy
slight increase in muscle tone strengthening deep tendon reflexes poor appetite, tearfulness or drowsiness disappearance of symptoms within the first three days In premature infants, mild ischemia may be manifested not by increased, but by decreased reflexes and muscle tone.	decreased muscle tone decreased tendon reflexes flaccid Moro reflex (spreading of arms when throwing back head), sucking, grasping reflexes (or their complete disappearance) frequent apneas (pauses in breathing) symptoms appear on the first day. Recovery within the first two weeks indicates a favorable prognosis.	stupor or coma (up to lack of response to all stimuli) irregular breathing, need for mechanical ventilation decreased muscle tone and tendon reflexes absence of newborn reflexes (Moro, grasping, sucking) strabismus, nystagmus, uncoordinated eye movements heart rhythm disturbances, blood pressure surges convulsions in a child

How does cerebral ischemia develop in newborns?

Poor circulation in newborns has causes related to the course of pregnancy and childbirth. The health of the mother during pregnancy is of great importance. The main causes of hypoxic-ischemic encephalopathy in newborns and infants:

If there are signs of intrauterine fetal hypoxia, the frequency of movements will be less than 10 times per day. After the 20th week of pregnancy, the expectant mother should count fetal movements daily and record them in a table. If there is less movement, you should immediately consult a doctor.

Etiological causes of HIE in adults:

• stroke;
• myocardial infarction;
• frequent fainting;
• poisoning;
• blockage of the carotid or vertebral artery by a thrombus or embolus.
• chickenpox encephalitis.

Oxygen carried by the blood to every cell of the body is essential for life. When its content is low, blood redistribution in organs begins. The brain and heart begin to receive the maximum possible amount of oxygen and nutrients, while other tissues and organs experience their deficiency.

If asphyxia continues, then these compensatory abilities are not enough for the life of nerve cells. They begin to die one after another. Hypoxic-ischemic encephalopathy of newborns occurs. The more brain tissue is damaged, the worse the prognosis for the baby will be. In some cases, due to hypoxia, cerebral hemorrhages may occur, which increases the risk of an unfavorable outcome.

Cerebral ischemia in full-term and premature infants

The nature of brain damage due to asphyxia differs between children born at term and premature babies. The earlier a child is born, the greater the risk of periventricular leukomalacia (PVL). This term means necrosis of the white matter of the brain located near special cavities (ventricles).

In full-term infants, the cerebral cortex - the gray matter - is more often damaged. The health consequences will depend on the volume and location of damaged neurons. If the asphyxia was severe and acute, the brain stem, which is responsible for breathing and heartbeat, may be damaged. This poses a direct threat to the baby's life.

Signs of prolonged asphyxia and severe ischemia in newborns

• Low Apgar scores (0-3) after the first 5 minutes of life
• Coma, absence of tendon reflexes and muscle tone
• Disorders of internal organs (kidneys, lungs, liver, heart)

The baby's condition is recorded 1 and 5 minutes after birth. After 1 minute, the need for resuscitation is determined by the number of points. Scores at 5 minutes reflect to some extent hypoxic brain damage (if any).

Overdiagnosis and ineffective therapy of ischemic encephalopathy

The diagnosis of perinatal brain damage can be made on the basis of clinical data and knowledge of the characteristics of pregnancy and childbirth.

Data from additional research methods are of an auxiliary nature and help clarify the nature and extent of brain damage, serve to monitor the course of the disease, and evaluate the effectiveness of the therapy.

Neurosonography (NSG) is a safe method of examining the brain, allowing one to assess the condition of brain tissue and cerebrospinal fluid spaces. It reveals intracranial lesions and the nature of brain lesions.

Dopplerography allows you to assess the amount of blood flow in the vessels of the brain.

Electroencephalogram (EEG) is a method for studying the functional activity of the brain, based on recording electrical potentials of the brain. According to EEG data, one can judge the degree of delay in age-related brain development, the presence of interhemispheric asymmetries, the presence of epileptic activity, and its foci in various parts of the brain.

Video monitoring is a method that allows you to assess spontaneous motor activity in a child using video recordings. The combination of video and EEG monitoring makes it possible to accurately identify the nature of seizures (paroxysms) in young children.

Electroneuromyography (ENMG) is an indispensable method in the diagnosis of congenital and acquired neuromuscular diseases.

Computed tomography (CT) and magnetic resonance imaging (MRI) are modern methods that allow a detailed assessment of structural changes in the brain. The widespread use of these methods in early childhood is difficult due to the need for anesthesia.

Positron emission tomography (PET) allows you to determine the intensity of metabolism in tissues and the intensity of cerebral blood flow at various levels and in various structures of the central nervous system.

Neurosonography and electroencephalography are most widely used in PEP.

In case of pathology of the central nervous system, an examination by an ophthalmologist is required. Changes detected in the fundus help diagnose genetic diseases, assess the severity of intracranial hypertension, and the condition of the optic nerves.

Typically, cerebral ischemia manifests itself in the first days after birth. Mild encephalopathy resolves fairly quickly, but severe encephalopathy may have a false “bright spot,” a few hours or days of improvement followed by a sharp deterioration. Therefore, a complete examination is necessary to make a diagnosis.

Pediatric neurology is one of the few areas of Russian medicine in which most doctors do not follow the latest recommendations for the diagnosis and treatment of PEDs. And if newborn babies with brain damage in our country are looked after very well, then the “consequences of PEP” are treated incorrectly and unreasonably.

• Newborn babies and children in the first 3-6 months of life have features that are mistaken for encephalopathy. For example, trembling, increased muscle tone, Graefe's symptom - all this is the norm for babies up to six months. Most pediatricians and neurologists, unfortunately, do not know about this.
• Examination of a frightened or sleepy baby is another reason for overdiagnosis of cerebral ischemia. In such cases, he may be overly excited or lethargic.
• Overdiagnosis usually results in the prescription of unnecessary medications. Such drugs do not help children with the real consequences of hypoxia, and they are not needed at all for healthy children.

How dangerous is the pathology, and how to treat it?

As mentioned above, children with severe and moderate damage to the central nervous system during the acute period of the disease require hospital treatment. In most children with mild manifestations of syndromes of increased neuro-reflex excitability and motor disorders, it is possible to limit ourselves to the selection of an individual regimen, pedagogical correction, massage, physical therapy, and the use of physiotherapeutic methods.

In case of hypertensive-hydrocephalic syndrome, the severity of hypertension and the severity of hydrocephalic syndrome are taken into account. If intracranial pressure is increased, it is recommended to raise the head end of the crib by 20-30°. To do this, you can place something under the legs of the crib or under the mattress. Drug therapy is prescribed only by a doctor, the effectiveness is assessed by clinical manifestations and NSG data.

In mild cases, they are limited to herbal remedies (decoctions of horsetail, bearberry leaf, etc.). In more severe cases, diacarb is used, which reduces the production of cerebrospinal fluid and increases its outflow. If drug treatment is ineffective in especially severe cases, it is necessary to resort to neurosurgical methods of therapy.

In cases of severe movement disorders, the main emphasis is placed on the methods of massage, physical therapy, and physiotherapy. Drug therapy depends on the leading syndrome: for muscle hypotonia and peripheral paresis, drugs that improve neuromuscular transmission (dibazole, sometimes galantamine) are prescribed; for increased tone, agents are used to help reduce it - mydocalm or baclofen. Various options for administering drugs orally and using electrophoresis are used.

The selection of drugs for children with epileptic syndrome depends on the form of the disease. Taking anticonvulsants (anticonvulsants), doses, and time of administration are determined by the doctor. The change of drugs is carried out gradually under EEG control. Abrupt spontaneous withdrawal of drugs can provoke an increase in attacks.

Currently, a wide range of anticonvulsants are used. Taking anticonvulsants is not indifferent to the body and is prescribed only if a diagnosis of epilepsy or epileptic syndrome is established under the control of laboratory parameters. However, the lack of timely treatment of epileptic paroxysms leads to impaired mental development. Massage and physiotherapeutic treatment for children with epileptic syndrome are contraindicated.

For psychomotor development delay syndrome, along with non-drug treatment methods and socio-pedagogical correction, drugs are used that activate brain activity, improve cerebral blood flow, and promote the formation of new connections between nerve cells. The choice of drugs is large (Nootropil, Lucetam, Pantogam, Vinpocetine, Actovegin, Cortexin, etc.). In each case, the drug treatment regimen is selected individually depending on the severity of symptoms and individual tolerance.

For almost all PEP syndromes, patients are prescribed preparations of B vitamins, which can be used orally, intramuscularly and in electrophoresis.

By the age of one year, in most mature children, PEP phenomena disappear or minor manifestations of perinatal encephalopathy are detected, which do not have a significant impact on the further development of the child. Frequent consequences of encephalopathy are minimal brain dysfunction (mild behavioral and learning disorders), hydrocephalic syndrome. The most severe outcomes are cerebral palsy and epilepsy.

Treatment of hypoxic ischemic encephalopathy must be carried out in a hospital.

Correct and timely drug treatment will prevent further consequences and complications, and in most cases the prognosis of the disease will be favorable.

Treatment should be aimed at eliminating the underlying problem of lack of oxygen in the body.

Treatment of the disease includes:

1. Taking medications.
2. Physiotherapeutic procedures.

Treatment of this disease requires an integrated approach and immediate prescription of medications.

Adult patients should give up all sorts of bad habits (alcohol, smoking). It is necessary to reconsider your diet and, if necessary, adjust it by including vegetables and fruits. For a full recovery, it is necessary to undergo several courses of treatment throughout the year.

For mild cases, homeopathic medicines are used.

To improve metabolic processes in the brain, use:

• Pantogam;
• Piracetam;
• Cinnarizine;
• Actovegin.

All of the above medications are prescribed by the attending physician. Self-medication is strictly prohibited!

In some cases, if the central nervous system is damaged, anticonvulsant medications are continued for three months or six months. The discontinuation of drug treatment is determined by the attending physician, guided by the clinical picture and electroencephalogram studies.

There are several predisposition factors to the disease:

• early or late pregnancy;
• infectious diseases during pregnancy;
• diseases transmitted by inheritance;
• eating disorder;
• unfavorable environmental conditions;
• pathological pregnancy.

With stage 1 disease, the brain completely recovers on its own within 10 days or a month; stages 2 and 3 of ischemic damage require timely assistance.

There is no specific treatment that can restore brain cells damaged by ischemia. There are no pills, no IVs, no physical procedures that can replace dead areas with viable ones. But there are methods to prevent further hypoxia and help the child to rehabilitate.

Consequences of oxygen deprivation of the brain

The consequences of a mild or moderate form can be favorable and full recovery can be achieved.

If the clinical picture persists for 10 days in newborns who have suffered this disease, then the likelihood of a complete recovery is very low.

In severe cases, death is possible in 30% of cases; treatment must be carried out strictly in the intensive care unit

During the recovery period, the effectiveness of physiotherapeutic procedures and pharmacological agents is great.

Prevention of hypoxic ischemic encephalopathy is very important, because the disease is easier to prevent than to treat.

In young children the disease is much milder than in adults. With the right approach to this disease, the brain is completely restored and the child achieves full recovery. The earlier a diagnosis is made and a course of treatment is prescribed, the greater the likelihood of recovery without pathological consequences. The consequences depend entirely on active treatment and rehabilitation.

• Severe cerebral ischemia in 25-50% of cases it ends in the death of the child in the first days of life, or a little later from pneumonia and other infections. Among surviving children, 80% have severe long-term consequences (dementia, cerebral palsy, autism), 10% suffer from moderate complications and 10% do not have significant consequences of asphyxia.
• Cerebral ischemia 2nd degree severity (moderate) causes severe long-term consequences in 30-50% of surviving children, and moderate complications in 10-20% (see. increased intracranial pressure,frequent regurgitation in a newborn).
• Mild cerebral ischemia in newborns it almost always ends well, without significant consequences for the child (see. hyperactivity in a child,malnutrition in a child).

Prevention of cerebral ischemia in newborns

To prevent the development of hypoxia in a newborn, a woman needs to plan the birth of her child in advance. 1 year before conception, you need to undergo an examination and be tested for sexually transmitted diseases. If sexually transmitted infections are detected, the doctor will prescribe appropriate treatment. This will help avoid intrauterine infection and infection of the child during its passage through the birth canal. If there are chronic diseases, they should also be cured.

During obstetrics today, obstetric forceps and rotation on the leg are not used. In case of breech presentation of the fetus and severe pregnancy (eclampsia), or the presence of heart failure, a cesarean section is performed. Prolonged labor of more than 15 hours is stimulated by the administration of Oxytocin.

In newborns and infants, mild hypoxia can be treated quite successfully. The second degree of hypoxia can affect the development of the child, but with maintenance therapy for the disease, the symptoms of hypoxic brain damage fade away. In adults, the likelihood of a severe outcome from cerebral ischemia depends on the severity of the injury. Early diagnosis of hypoxia also ensures good treatment results.

• Careful pregnancy planning
• Completing all necessary studies (ultrasound, blood and urine tests) during pregnancy
• If necessary, take iron supplements
• Screening for infections before and during pregnancy
• Rejection of bad habits
• In case of complicated pregnancy - timely hospitalization

Course of PEP and possible prognosis

During PEP, three periods are distinguished: acute (1st month of life), recovery (from 1 month to 1 year in full-term infants, up to 2 years in premature infants) and outcome of the disease. In each period of PEP, various syndromes are distinguished. More often there is a combination of several syndromes. This classification is advisable, since it allows us to distinguish syndromes depending on the age of the child.

For each syndrome, appropriate treatment tactics have been developed. The severity of each syndrome and their combination make it possible to determine the severity of the condition, correctly prescribe therapy, and make prognoses. I would like to note that even minimal manifestations of perinatal encephalopathy require appropriate treatment to prevent adverse outcomes.

Let us list the main syndromes of PEP.

Acute period:

• CNS depression syndrome.
• Comatose syndrome.
• Convulsive syndrome.

Recovery period:

• Syndrome of increased neuro-reflex excitability.
• Epileptic syndrome.
• Hypertensive-hydrocephalic syndrome.
• Syndrome of vegetative-visceral dysfunctions.
• Movement impairment syndrome.
• Psychomotor development delay syndrome.

• Full recovery.
• Delayed mental, motor or speech development.
• Attention deficit hyperactivity disorder (minimal brain dysfunction).
• Neurotic reactions.
• Autonomic-visceral dysfunctions.
• Epilepsy.
• Hydrocephalus.
• Cerebral palsy.

All patients with severe and moderate brain damage require hospital treatment. Children with mild impairments are discharged from the maternity hospital under outpatient supervision by a neurologist.

Let us dwell in more detail on the clinical manifestations of individual PEP syndromes, which are most often encountered in outpatient settings.

The syndrome of increased neuro-reflex excitability is manifested by increased spontaneous motor activity, restless shallow sleep, prolongation of the period of active wakefulness, difficulty falling asleep, frequent unmotivated crying, revival of unconditioned innate reflexes, variable muscle tone, tremor (twitching) of the limbs and chin.

In premature infants, this syndrome in most cases reflects a lowering of the threshold for convulsive readiness, that is, it indicates that the baby can easily develop convulsions, for example, when the temperature rises or when exposed to other irritants. With a favorable course, the severity of symptoms gradually decreases and disappears within a period of 4-6 months to 1 year. If the course of the disease is unfavorable and there is no timely treatment, epileptic syndrome may develop.

Convulsive (epileptic) syndrome can manifest itself at any age. In infancy it is characterized by a variety of forms. An imitation of unconditioned motor reflexes is often observed in the form of paroxysmal bending and tilting of the head with tension in the arms and legs, turning the head to the side and straightening the arms and legs of the same name;

Hypertensive-hydrocephalic syndrome is characterized by excess fluid in the spaces of the brain containing cerebrospinal fluid (CSF), which leads to increased intracranial pressure. Doctors often call this disorder to parents exactly this way - they say that the baby has increased intracranial pressure.

The mechanism of occurrence of this syndrome can be different: excessive production of cerebrospinal fluid, impaired absorption of excess cerebrospinal fluid into the bloodstream, or a combination of both. The main symptoms of hypertensive-hydrocephalic syndrome, which doctors focus on and which parents can control, are the rate of increase in the child’s head circumference and the size and condition of the large fontanel.

For most full-term newborns, the normal head circumference at birth is 34 - 35 cm. On average, in the first half of the year, the monthly increase in head circumference is 1.5 cm (in the first month - up to 2.5 cm), reaching about 44 cm by 6 months. In the second half of the year, the growth rate decreases; by one year, head circumference is 47-48 cm.

However, large head sizes often occur in absolutely healthy babies and are determined by constitutional and family characteristics. The large size of the fontanel and the “delay” in its closure are often observed with rickets. The small size of the fontanel at birth increases the risk of intracranial hypertension in various unfavorable situations (overheating, increased body temperature, etc.).

Carrying out a neurosonographic examination of the brain makes it possible to correctly diagnose such patients and determine treatment tactics. In the vast majority of cases, by the end of the first six months of a child’s life, normal growth of head circumference is noted. In some sick children, hydrocephalic syndrome persists by 8-12 months without signs of increased intracranial pressure. In severe cases, the development of hydrocephalus is noted.

Comatose syndrome is a manifestation of the serious condition of the newborn, which is assessed by 1-4 points on the Apgar scale. Sick children exhibit severe lethargy, decreased motor activity up to its complete absence, and all vital functions are depressed: breathing, cardiac activity. Seizures may occur. The severe condition persists for 10-15 days, with no sucking or swallowing reflexes.

The syndrome of vegetative-visceral dysfunctions, as a rule, manifests itself after the first month of life against the background of increased nervous excitability and hypertensive-hydrocephalic syndrome. Frequent regurgitation, delayed weight gain, disturbances in cardiac and respiratory rhythm, thermoregulation, changes in the color and temperature of the skin, marbling of the skin, and dysfunction of the gastrointestinal tract are noted.

The syndrome of movement disorders is detected from the first weeks of life. From birth, a violation of muscle tone can be observed, both in the direction of its decrease and increase, its asymmetry can be detected, and there is a decrease or excessive increase in spontaneous motor activity. Often the syndrome of motor disorders is combined with a delay in psychomotor and speech development, because

With delayed psychomotor development, the child later begins to hold his head up, sit, crawl, and walk. A predominant disorder of mental development can be suspected in the presence of a weak monotonous cry, impaired articulation, poor facial expressions, late appearance of a smile, and delayed visual-auditory reactions.

Cerebral palsy (CP) is a neurological disease that occurs as a result of early damage to the central nervous system. In cerebral palsy, developmental disorders usually have a complex structure, combining motor disorders, speech disorders, and mental retardation. Motor disorders in cerebral palsy are expressed in damage to the upper and lower extremities;

fine motor skills, articulatory muscles, and oculomotor muscles suffer. Speech disorders are detected in most patients: from mild (erased) forms to completely unintelligible speech. 20 - 25% of children have characteristic visual impairments: convergent and divergent strabismus, nystagmus, limitation of visual fields. Most children have mental retardation. Some children have intellectual impairments (mental retardation).

Attention deficit hyperactivity disorder is a behavioral disorder associated with the child's poor control of his attention. It is difficult for such children to concentrate on any task, especially if it is not very interesting: they fidget and cannot sit still calmly, and are constantly distracted even by trifles. Their activity is often too violent and chaotic.

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

Despite the fairly high frequency of the pathology, effective measures to combat it have not yet been developed, and Modern medicine is powerless against irreversible structural damage to the brain. 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 a lack of oxygen in the blood. In a growing fetus and newborn child, the immature structures of the brain 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.

example of hypoxia due to insufficiency of uteroplacental blood flow

Hypoxia can be severe or mild, it lasts for a long time or several minutes during childbirth, but it always provokes disorders of brain function.

In the case of mild damage, the process is completely reversible, and some time after birth the brain will restore its function.

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 a pathological course. However, even after birth, hypoxic-ischemic changes can occur if the baby’s respiratory function is impaired, blood pressure drops, blood clotting disorders, etc.

In the literature you can find two names for the described pathology - hypoxic-ischemic damage to the central nervous system And hypoxic-ischemic encephalopathy (HIE). The first option is more often used when diagnosing severe disorders, the second - for mild forms of brain damage.

Discussions regarding the prognosis for hypoxic brain damage do not subside, but the accumulated experience of neonatologists shows that the child’s nervous system has a number of self-defense mechanisms and is even capable of regeneration. This is also evidenced by the fact that Not all children who have suffered severe hypoxia have severe neurological abnormalities.

In severe hypoxia, the immature structures of the brainstem and subcortical nodes are primarily affected; with prolonged, but not intense hypoxia, diffuse lesions of the cerebral cortex develop. One of the factors protecting the brain 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 suffered from hypoxia of varying severity is to objectively assess the neurological status, exclude adaptive manifestations (tremor, for example), which may be physiological, and identify truly pathological changes in brain activity. When diagnosing hypoxic damage to the central nervous system, foreign specialists are based on the stages of the pathology, while Russian doctors use a syndromic approach, pointing to specific syndromes in a particular part of the brain.

Causes and stages of hypoxic-ischemic damage

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

• Disorders, bleeding in pregnant women, pathology of the placenta (thrombosis), delayed fetal development;
• Smoking, drinking alcohol, taking certain medications during pregnancy;
• Massive bleeding during childbirth, entanglement of the umbilical cord around the fetal neck, severe bradycardia and hypotension in the baby, birth injuries;
• After childbirth - hypotension in the newborn, congenital heart defects, disseminated intravascular coagulation syndrome, episodes of respiratory arrest, pulmonary dysfunction.

example of hypoxic-ischemic brain damage

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

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

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

In full-term infants, post-hypoxic damage is noted mainly in the area of ​​the cortex, subcortical structures, and brain stem; in premature infants, due to the maturation of the nervous tissue and 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 is 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, temporary increase in intracranial pressure,.
3. A severe form of hypoxic-ischemic damage is a disorder of consciousness (stupor, coma), convulsions, manifestations with brainstem symptoms and disruption of the functioning of vital organs.

Symptoms of hypoxic-ischemic damage to the central nervous system

Damage to the central nervous system in newborns is diagnosed in the first minutes of a baby’s life, and the symptoms depend on the severity and depth of the pathology.

I degree

In mild cases of HIE, the condition remains stable; on the Apgar scale, the child is rated 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 the limbs, chin;
4. Possible regurgitation;
5. Reflexes can be either increased or decreased.

The described symptoms usually disappear during the first week of life, the child becomes calmer, begins to gain weight, and severe 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 brain function. Typically, the second degree of HIE accompanies combined forms of hypoxia, which is diagnosed both during the intrauterine growth stage and at the time of birth. In this case, muffled fetal heart sounds, increased rhythm or arrhythmia are recorded; the newborn scores no more than 5 points on the Apgar scale. Neurological symptoms include:

• Suppression of reflex activity, including sucking;
• A decrease or increase in muscle tone, spontaneous motor activity may not appear in the first days of life;
• Severe blueness of the skin;
• Rising ;
• Autonomic dysfunction - respiratory arrest, increased heart rate or bradycardia, disturbances in intestinal motility and thermoregulation, 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 sensitivity of the skin appears, sleep is disturbed, tremor of the chin, arms and legs increases, bulging of the fontanelles becomes noticeable, horizontal nystagmus and oculomotor disorders are characteristic. Signs of intracranial hypertension may include seizures.

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

III degree

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

In 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 birth, a sharp depression of the brain occurs, a coma sets in, accompanied by atony, an almost complete absence of reflexes, dilated pupils with a reduced reaction to a light stimulus or its absence.

The inevitably developing cerebral edema is manifested by generalized convulsions, respiratory and cardiac arrest. Multiple organ failure is manifested by increased pressure in the pulmonary artery system, decreased urine filtration, hypotension, necrosis of the intestinal mucosa, liver failure, electrolyte disturbances, and blood coagulation disorders (DIC).

A manifestation of severe ischemic damage to the central nervous system is the so-called post-asphyxial syndrome - babies are inactive, do not cry, do not respond to pain and touch, their skin is pale bluish, and a general decrease in body temperature is characteristic. Important signs of severe brain hypoxia include swallowing and sucking disorders, which make natural feeding impossible. To save the life of such patients, intensive care in intensive care is necessary, 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 considered to be an increase in neurological deficit over time, even with intensive therapy. 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 occur in different ways:

1. Favorable with rapid 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. Latent course, when after six months motor and cognitive disorders increase.

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

• Acute - first month.
• Restorative - 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, and 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, MRI of the brain, coagulogram, ultrasound with Dopplerography of cerebral blood flow are most often used.

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 nervous tissue. Nevertheless, it is still possible to at least partially restore brain activity in severe forms of pathology.

Drug treatment for HIE depends on the severity of the specific syndrome or symptom.

For mild to moderate degrees of the disease, anticonvulsant therapy is prescribed; severe forms of perinatal encephalopathy require immediate resuscitation measures and intensive care.

With increased excitability of the nervous system without convulsive syndrome, neonatologists and pediatricians usually limit themselves to monitoring the child, without resorting to specific therapy. In rare cases, the use of diazepam is possible, 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). For sleep disorders, the use of nitrazepam and herbal sedatives is allowed - valerian extract, mint, lemon balm, motherwort. Massage and hydrotherapy have a good calming effect.

In case of severe hypoxic lesions, in addition to anticonvulsants, measures to eliminate cerebral edema are necessary:

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

Respiratory and palpitation disorders require immediate resuscitation measures, artificial ventilation, administration of cardiotonic drugs and infusion therapy.

Diuretics occupy the main place in treatment, 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 cavities.

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

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

Delays in mental development and speech development according to the child’s age become noticeable by the end of the first year of life. In such cases, nootropic drugs (nootropil, encephabol) and B vitamins are used. Special classes with teachers and defectologists who specialize in working with developmentally delayed children play a very important role.

Very often, parents of children who have suffered perinatal encephalopathy are faced with the prescription of a large number of different drugs, which is not always justified. Overdiagnosis and “reinsurance” by pediatricians and neurologists lead to the widespread prescription of Diacarb, nootropics, vitamins, Actovegin and other drugs, which are not only ineffective for mild forms of HIE, but are also often contraindicated due to age.

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

Long-term consequences of HIE are epilepsy, cerebral palsy, hydrocephalus, and mental retardation (oligophrenia). Oligophrenia is always persistent and does not regress, and the somewhat delayed development of the psychomotor sphere during the first year of life may pass over time, and the child will be no different from most of his peers.

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

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HYPOXIC-ISCHEMIC ENCEPHALOPATHY OF NEWBORNS

Chapter 5 (The chapter from the book is published in an abbreviated version, without drawings, footnotes, bibliography and tables)

CLINICAL PICTURE OF HYPOXIC-ISCHEMIC BRAIN LESIONS IN NEWBORNS

Ideas about the clinical picture of hypoxic-ischemic brain lesions, despite the obviousness of their main manifestations, are quite contradictory. This inconsistency lies mainly in the difficulty of defining the boundaries between physiological adaptive states of the neonatal period, which can manifest themselves in the same way as NHIE (for example, tremor, stiffness or depression). In addition, there is no unity in ideas about the duration of the course and periods of NGIE. Currently, 2 basic principles have been formed in the approach to the clinical picture of hypoxic brain lesions: staged (phase) and syndromic. The first of these approaches prevails abroad, the second - in Russia.

5.1. Normal and deviant neurological status of a newborn child

Before moving on to the description of the clinical picture of hypoxic lesions of the newborn’s brain, it is necessary to clarify what are the limits of the normal, or optimal according to B. C. L. Touwen, neurological status of the newborn. N. F. R. Prechtl and L. M. S. Dubowitz identified the main stages that should be satisfied by a neurological examination in general, and examination of a newborn in particular (Fig. 6). A neurological examination of a newborn child should begin with the standardization of examination conditions, since inadequate room temperature and the nature of lighting affect the resulting reflexes, reactions, etc. The examination is carried out at the optimal room temperature of about 24-26 ° C after 1-2 minutes of adaptation of the child in the unfolded position. form under a radiant heat source. At low temperatures, it is more likely to get a reaction of increased muscle tone and tremor, at high temperatures - muscle hypotension. Lighting should be symmetrical in relation to the newborn, since light falling from one side causes a narrowing of the pupil and palpebral fissure on the side of the illumination. During examination, it is necessary that the child’s head is in the sagittal plane, since due to the asymmetric cervical-tonic reflex, a decrease in muscle tone is noted on the side of the head rotation, and an increase on the opposite side.

It is also necessary to take into account the time that has passed since the last feeding, since after saturation the child is relaxed, he may have reduced muscle tone and a number of reflexes and reactions, and before feeding he may be in a state of relative hypoglycemia, leading to anxiety, tremor and increased muscle tone .

Next, it is advisable to determine the state in which the newborn is, since the same indicators of reflexes and reactions can be physiological for one state of the child and pathological for another.

According to H. F. R. Prechtl and D. J. Beintema, the following conditions of the newborn are distinguished.

1. Eyes are closed, breathing is uniform, there are no movements.

2. Eyes are closed, breathing is uneven, there are no significant movements.

3. Eyes open, no significant movements.

4. Eyes open, constant noticeable movements, no screaming.

5. Eyes open or closed, screaming or agitated state.

6. Any other condition (including coma, describe).

Condition 4 is optimal for inspection.

T. V. Brazelton identifies the following states

nervous system in a newborn.

1. Deep sleep with regular breathing, eyes closed, no spontaneous activity, no eye movements.

2. Shallow sleep with eyes closed, rapid eye movements, irregular breathing.

3. Drowsy or half-asleep, eyes open or closed, activity varies, movements are usually calm.

4. Attention with clear eyes, minimal physical activity.

5. Eyes open, significant motor activity.

According to this classification, conditions 4 or 5 are optimal for examination.

The sociability of a newborn as the main indicator of general activity is assessed by the reaction of displeasure in the presence of discomfort (forced awakening, hunger, wet diapers, etc.) and the speed of calming when eliminating irritating factors, as well as by the response to positive stimuli (response to affectionate speech, stroking, picking up).

The interaction between the child and the researcher is essential in determining the communication skills and behavior of a newborn, and therefore the role of not only the reactions of the newborn described below is important, but also the persistence of the researcher in obtaining them, his positivity towards the child during examination. In response to a light stimulus, the child closes his eyelids (if his eyes are closed) or squints his eyes (if his eyes are open). Some newborns experience fixation of gaze on a bright object, and sometimes even tracking in the first days of life. When auditory stimulation occurs, a newborn may close the eyes (cochleopalpebral reflex) or constrict the pupil (cochleopupillary reflex). In some cases, a generalized startle reaction occurs (see below), an element of which may be the Moro reflex. To assess a child’s sociability, the difference in auditory and visual reactions to animate (the face and voice of the researcher) and inanimate (artificial and natural light sources, rattle, bell, clap) stimuli is important. The presence of search, palm-oral, grasping reflexes and the Babinsky reflex (see below) indicates the presence of tactile sensitivity. Pricking a child with a needle causes frowning of the eyebrows, clenching of the eyes, wrinkling of the nasolabial furrow, opening of the mouth, pouting of the lips, stretching of the mouth, tension of the tongue, trembling of the chin, screaming, as well as a motor reaction: flexion with adduction of the limbs. A painful reaction occurs a few seconds after the application of irritation, which is due to slow conduction through the nerves of the newborn due to insufficient myelination.

A decrease in the listed reactions may be either a sign of depression of the central nervous system as a result of a number of somatic and neurological diseases, or damage to the corresponding analyzer. Thus, lack of response to pain may be a consequence of hereditary sensory polyneuropathy.

Among the signs of the child’s general activity, spontaneous motor activity should be noted. Its assessment is quite subjective and depends on the doctor’s experience, but objectification is possible only by analyzing a video recording of activity for 1 hour. Typically, spontaneous movements consist of periodic flexion and extension of the legs, their crossing, pushing away from the support; movements of the hands at chest level in the elbow and wrist joints with clenching of fists. The presence of a choreoathetoid component in movements, which is physiological for, indicates the predominance of extrapyramidal (striatal) motility and consists in restlessness of the tongue, spreading and independent movements of the fingers.

The facial expressions of a newborn are quite rich and, as a rule, symmetrical and consist of squeezing the eyes, frowning the forehead, deepening the nasolabial folds, tense the tongue, and open the mouth. Facial asymmetry is possible on the first day due to the peculiarities of the passage of the baby’s head through the birth canal. On the other hand, facial asymmetry may be due to damage to the cranial innervation.

The study of the eyes must begin with an examination of the sclera, hemorrhages in which may indicate hypoxia or trauma during childbirth.

The movements of the eyeballs in a newborn are not sufficiently coordinated and jerky; a number of children may experience horizontal nystagmus at rest, and its presence when the child rotates is a sign of the preservation of the vestibular apparatus. Constant or prolonged (more than 20 s) nystagmus (horizontal, vertical, rotatory) indicates irritation of the vestibular apparatus due to hypoxic-ischemic encephalopathy (stage II), intracranial hemorrhage, vertebrobasilar insufficiency due to spinal injury at the level of the fifth and (or) sixth cervical segment of the spinal cord. The presence of transient convergent strabismus may be a physiological feature of a healthy newborn, but requires dynamic monitoring. Persistent convergent strabismus with adduction of one eyeball indicates damage to the abducens nerve; divergent strabismus indicates damage to the oculomotor nerve and is usually associated with ptosis on the affected side and pupil dilation (mydriasis).

Normally, the pupils are round, symmetrical and have a diameter of 2-3 mm. Symmetrical constriction of the pupils (miosis) is observed in stage II of hypoxic-ischemic encephalopathy; unilateral miosis, associated with ptosis and enophthalmos, is a sign of damage to the spinal cord at the level of the seventh cervical segment on the side of the constriction of the pupil (Bernard-Horner syndrome); in the presence of ataxia, tremor and myoclonus on the side of miosis, damage to the tegmentum of the brain can be assumed. Symmetrical mydriasis is observed in stage I of hypoxic-ischemic encephalopathy; unilateral mydriasis, along with the above-mentioned damage to the oculomotor nerve, may indicate damage to the midbrain and, when associated with ptosis on the side of mydriasis and hemiparesis on the opposite side, forms Weber syndrome.

Conditions leading to narrowing of the palpebral fissure are described above. When the palpebral fissure is widened with the inability to close the eyelids (lagophthalmos), upward movement of the eyeball (Bell's phenomenon), increased lacrimation or, conversely, dry eye, we can talk about peripheral damage to the facial nerve or its nucleus. The presence of similar symptoms with increased muscle tone, periosteal reflexes and hypokinesia on the opposite side indicates damage to the midbrain (Millard-Hubler syndrome); the combination of signs of peripheral paresis of the facial nerve with impaired sucking, swallowing, atrophy of the tongue muscles, as well as in some cases with deformation of the ear cartilage and underdevelopment of the lower jaw indicates congenital (usually autosomal dominant) underdevelopment of the nuclei of the facial nerves (Mobius syndrome).

With spontaneous downward movements of the eyeballs or with rapid movement of the head, a white stripe of sclera appears in the space between the eyelid and the iris (Graefe's symptom). Graefe's symptom can occur in healthy premature and immature children, as well as full-term children in the first days of life. This symptom can occur with hydrocephalus, intracranial hypertension syndrome, and bilirubin encephalopathy.

Asymmetrical opening of the mouth when yawning and crying in a child may be a sign of unilateral damage to the motor portion of the trigeminal nerve. Impaired swallowing, crying, and atrophy of the tongue muscles in a newborn may be associated with damage to the caudal group of cranial nerves (glossopharyngeal, vagus and hypoglossal), while a decrease in the swallowing reflex indicates peripheral damage to the caudal group of nerves (bulbar palsy), an increase indicates damage to the supranuclear formations (pseudobulbar palsy).

It is one of the most important indicators of its overall activity and is assessed by intensity and character. A healthy newborn is characterized by a loud, well-modulated, emotional cry. A weak cry is observed in all diseases, both neurological (intracranial hemorrhage, neuroinfections, stage II hypoxic-ischemic encephalopathy) and somatic (sepsis, pneumonia, etc.), accompanied by depression of the central nervous system. An irritated cry is characteristic of all conditions, both neurological (stage I hypoxic-ischemic, intracranial hemorrhages) and metabolic (hypoglycemia, hypocalcemia, hypomagnesemia, etc.), which are accompanied by increased neuro-reflex excitability or increased intracranial pressure. A monotonous cry may indicate congenital hydrocephalus and bilirubin encephalopathy. A “nasal” cry occurs when the caudal group of cranial nerves or supranuclear fibers supplying these nuclei is damaged.

The frequency response of a newborn's cry corresponds to 400-650 Hz. The appearance of a cry with a frequency of 800-1200 Hz with an increasing-decreasing melody indicates that the child is in pain.

Tremor as a periodic oscillation around a fixed axis of a certain amplitude and frequency occurs in almost half of newborns. Low-amplitude, high-frequency tremor when a newborn is crying or excited, as well as in some stages of sleep, is a physiological phenomenon. In terms of prevalence, tremor can affect the chin, tongue, and limbs.

Muscle tone is the most important characteristic of motor activity. We can talk about the child’s active muscle tone (posture) and passive, the value of which is determined by checking mobility in the joints. A healthy full-term baby has a so-called fetal position due to a flexor increase in tone (arms are bent in all joints, brought to the body and pressed to the chest, hands are clenched into fists, the thumbs of the hands lie under the other four; legs are bent at the joints and abducted in hips, dorsiflexion predominates in the feet). In some cases, a predominant physiological increase in muscle tone in the arms compared to the legs and neck extension are noted. The active muscle tone of the newborn can also be judged by holding the baby in the air face down, with the baby's head in line with the body, the baby's arms slightly bent and legs extended. “Sinking” of the child’s head when he is pulled up by the shoulder girdle (symptom of “flaccid shoulders”) in full-term newborns occurs both with hypoxic parasagittal lesions of the brain and with injury to the cervical spinal cord.

Approximate indicators of normal passive muscle tone are: when moving the head to the side, the chin touches the acromion process; extension of the arms at the elbow joints is possible up to 180°, flexion at the wrist joints - up to 150°, abduction towards the bent hips - 75° in each direction; extension of the leg at the knee joint with the hip bent at an angle of 90° is possible up to 150°; dorsal flexion of the feet is 120°. When performing traction on the newborn (pulling) by the wrists and normal muscle tone, slight extension occurs in the elbow joints. After this, the tone in the flexors increases again with the child being pulled towards the hands of the researcher.

Muscle tone can vary depending on the constitution and physiological state of the child. Therefore, unstable and minor changes in muscle tone should not be considered as obviously pathological. Changing tone in the same muscle group is called muscular dystonia.

An increase in muscle tone is manifested by an increase in flexor hypertension (in a state of suspension, the child’s arms and legs are sharply bent, with traction there is no extension phase), the angular indicators indicated above are significantly reduced. Such an increase in muscle tone is characteristic of the initial stages of hypoxic-ischemic encephalopathy and intracranial hemorrhage. In some cases, there is an increase in the tone of the extensor muscle group, which is manifested by the disappearance of flexor hypertension, and in a state of hanging face down, the child’s head is thrown back and his arms are extended. Extensor hypertension is most expressed in the form of opisthotonus: the head is thrown back, the legs are extended and often crossed. An extensor increase in muscle tone is characteristic of stage III hypoxic-ischemic encephalopathy, meningitis, encephalitis, intracranial hemorrhages (especially in the posterior cranial fossa). Bilirubin encephalopathy is also characterized by a specific posture of the child with “extended” limbs and hands clenched into fists.

A decrease in muscle tone can be local and generalized.

With a generalized decrease in muscle tone, a specific posture of the newborn is noted - the “frog” pose (limbs extended in all joints, hips abducted and externally rotated, abdomen wide and flattened). The range of passive movements is increased; when hanging face down, the head and limbs hang down; during traction, there is no flexion phase and the head is thrown back. Generalized hypotension can be a sign of most somatic and neurological diseases of the newborn period (sepsis, pneumonia, respiratory distress syndrome, intrauterine infections of various etiologies, metabolic disorders, stage II-III hypoxic-ischemic encephalopathy, intracranial hemorrhage, spinal birth injury, neuromuscular diseases, including Werdnig-Hoffmann disease). It should be noted that muscle hypotonia may be a sign of individual characteristics of the evolution of the spinal cord (benign muscular hypotonia of Walton) or the cerebellum.

Local hypotension may be caused by neural innervation (traumatic neuropathy, plexopathy) or segmental disorders (birth spinal injury).

The assessment of reflex activity is carried out on the basis of at least three tests of this reflex. If the reflex amplitude is maintained in all three tests or the amplitude decreases slightly in the third, the reflex is considered normal; if the initial amplitude value is low, persists in three tests or progressively decreases with repeated testing of the reflex, and also if repeated stimulation is necessary to obtain the reflex, it is considered reduced. The normal amplitude of the reflex during the first testing and its subsequent decrease or disappearance of the reflex indicate its depletion. A high amplitude of the reflex or its increase as testing progresses indicates an increase in the reflex. The exaltation of a reflex is understood as its spontaneous occurrence or occurrence in response to inadequate stimulation, the absence of extinction and the activation of protective mechanisms. The study can be shortened in time by combining in one technique (maneuver) testing several reflexes (Moro and upper grasping; support and stepping).

The periosteal (tendon, deep) muscles of a child are quite labile and their assessment, isolated from other indicators, is not very informative. The knee reflexes are most regularly evoked; the minimum scope of examination of a newborn can include the study of the Achilles, bicipital and carporadial reflexes. A symmetrical decrease or inhibition of periosteal reflexes can be observed with general depression of the central nervous system due to somatic and metabolic diseases of newborns, as well as with stages II and III of hypoxic-ischemic encephalopathy, birth spinal injury, and hereditary neuromuscular diseases. An asymmetric decrease or suppression of reflexes may indicate a neural or segmental spinal lesion in accordance with the zones of innervation.

A symmetrical increase or exaltation of periosteal reflexes is characteristic of a number of somatic and metabolic diseases (for example, hypoglycemia, hypocalcemia, etc.), as well as with the phenomenon of jitteriness described below, stage I hypoxic-ischemic encephalopathy, intracranial hemorrhage and other conditions accompanied by intracranial hypertension. An asymmetric increase in periosteal reflexes, together with hypokinesia, increased muscle tone and disturbances of cranial innervation, may be evidence of damage to the precentral gyrus of the opposite hemisphere of the brain or the descending pyramidal tracts.

Testing of abdominal and cremasteric reflexes is of limited value in neonatology due to their variability in detection and severity.

Of particular importance is checking (“primary”, “unconditioned” reflexes). Most of the reflexes of newborns reflect the evolutionary maturity of the child, his functional state, and only some of them have a specific topical significance. Due to their large number, it is necessary to focus on the most informative ones. When stroking the baby's skin in the area of ​​the corner of the mouth, the head turns towards the stimulus (search reflex), when a finger lightly touches the newborn's lips, the lips stretch (proboscis reflex), and when a pacifier is placed in the mouth, sucking movements occur (sucking reflex). When pressing on the thenar area, the child opens his mouth, tilts his head, bends his shoulders and forearms (Babkin's palmo-oral reflex), when placing fingers in the newborn's hand, the researcher's fingers are grasped (upper grasp reflex), and if the child can be lifted, the Robinson reflex occurs.

The Moro reflex is multimodal in the way it is evoked, which is due to its belonging to the so-called startle reaction (startle reaction) or arousal reaction (awakening reaction), i.e. a rather complex behavioral act. The Moro reflex can occur in response to auditory stimuli (clap), tactile and vestibular stimuli (patting on the changing pad, moving the position of the child's torso, etc.). In response to irritation, the newborn’s arms move to the sides and the hands unclench (phase I), after which the arms return to their original position (phase II).

When the skin of the back along the spine is irritated, the newborn bends the torso in an arc open towards the irritation (Galant reflex).

A child raised under the armpits bends his legs in all joints, and when placed on a support, he stands on half-bent legs (support reflex); when bending forward, the child makes stepping movements (stepping reflex), while crossing his legs in the lower third of the lower leg is possible. In the position of the child on his stomach, when the researcher’s palms are applied to his feet, a reflex repulsion and crawling occurs (Bauer reflex). When pressing on the ball of the foot in the area of ​​the II-III toe, plantar flexion occurs (inferior grasping reflex of Verkom), and when the sole is irritated by strokes, its extension and fan-shaped divergence of the toes occurs (Babinsky reflex).

May be caused by the same conditions as changes in periosteal reflexes. A decrease in the palmar-oral and superior grasp reflex, as well as the Robinson reflex, may indicate damage to the corresponding cervical segments of the spinal cord. The same applies to the Moro reflex, but its decrease may also be due to brainstem lesions. The state of the Moro reflex is one of the main indicators of the general functional state of the newborn. Other important indicators of general functional are the inferior plantar reflex and the Babinski reflex, the disappearance of which occurs with severe depression of the nervous system. It should be noted that the step reflex and support reflex are often absent in large children; the Galant reflex sometimes appears after the 5th day of life.

The uniqueness of the reflex activity of a newborn child is the presence of specific vestibular reflexes. When the head of a newborn lying on his back is tilted, the flexor tone in the arms increases, and the extensor tone in the legs; when the head is extended, the opposite reaction occurs (symmetrical cervical-tonic reflex). When the child's head turns to the side, extension occurs in the arm and leg on the side of rotation and flexion on the opposite side. The most pronounced cervical-tonic reflexes are in children 36-37 weeks of gestation, and their excessive severity in a full-term newborn occurs in stage II hypoxic-ischemic encephalopathy, bilirubin encephalopathy, and intracranial hemorrhage.

The function of the autonomic nervous system in a newborn can be assessed by the balance of influences of the sympathetic and parasympathetic structures of the autonomic nervous system. Among the indicators of autonomic function in a newborn child, it is necessary to highlight the condition of the pupils, skin, blood pressure level, heart rate and breathing rate, rhythm and independence of breathing, intestinal motility, salivary and bronchial secretions.

With sympathicotonia, mydriasis, arterial hypertension, tachycardia, tachypnea, “convulsive” breathing, decreased intestinal motility, scanty salivary and bronchial secretions are noted. On the part of the skin, pallor and a predominance of white dermographism are noted.

The predominance of sympathicotonia is observed in the acute phase of a number of somatic diseases of newborns (sepsis, pneumonia), and is also characteristic of stage I of hypoxic-ischemic encephalopathy, the onset of meningoencephalitis. Due to hypernoradrenalemia, sympathicotonic states are accompanied by tremor.

The dominance of parasympathetic (and its associated serotonergic) tone is manifested by miosis, arterial hypotension, bradycardia and bradypnea, arthymic breathing with episodes of apnea, abundant salivary and bronchial secretions. The skin is hyperemic, dermographism is usually red. The predominance of parasympathicotonia is characteristic of severe (sometimes terminal) forms of somatic and neurological diseases (sepsis, respiratory distress syndrome, meningoencephalitis, stage II hypoxic-ischemic encephalopathy, subtentorial hemorrhages). More often in neonatological practice, instability of autonomic tone is noted (vegetative dystonia syndrome or autonomic-visceral dysfunction syndrome), which is manifested by lability of pupil diameter, frequency and rhythm of heartbeat and breathing, changing bronchial and salivary secretion. The skin takes on a spotted (“marble”) hue. If, when a newborn is turned on its side, the lower half of the body becomes hyperemic and the upper half becomes pale (the “harlequin” symptom), we can assume immaturity of autonomic regulation in premature infants and children with intrauterine growth retardation, as well as autonomic dystonia syndrome in full-term infants, which is more common in intracranial hemorrhages.

It should be noted that a dynamic study of the state of the nervous system of healthy newborns indicates the presence of transient physiological changes in the neurological status of the child in almost half of the children (see below). Therefore, to classify a particular deviation in the neurological status of a newborn as physiological or pathological, it is necessary to evaluate it in connection with other phenomena, dynamic observation, and in some cases the use of adequate additional research methods.

5.2. Classifications of hypoxic encephalopathy (phase principle)

The first and most popular classification of hypoxic encephalopathy among neonatologists was proposed by H. B. Sarnat and M. S. Sarnat in 1976.

The classification of “postanoxic encephalopathy,” as this condition is formulated by the authors, is the most used classification abroad (Table 7).

It is necessary to emphasize the following features of this classification.

1. A number of basic indicators of a newborn are considered (level of consciousness, neuromuscular control, complex reflexes, autonomic function, presence of seizures, EEG data), which undergoes certain dynamics over time.

3. Within each stage of encephalopathy, a combination of phenomena is noted that emphasize the multidirectionality and inconsistency of the clinical picture of postanoxic encephalopathy (for example, in stage I, an increase in periosteal reflexes, the Moro reflex is combined with a decrease in the sucking reflex; in stage II - lethargy, muscle hypotonia, decreased sucking reflex and Moro reflex are combined with distal flexion, increased periosteal, oculovestibular and cervical-tonic reflexes, convulsions, etc.).

4. A significant place in the clinical picture is given to autonomic dysfunction, namely, its “big” signs (the state of the pupils, heartbeat, bronchial and salivary secretion, intestinal motility).

5. EEG is an integral part of the diagnosis.

Later, Canadian neonatologists N. N. Finer et al. proposed a modification of this classification (Table 8).

Retaining the features of the classification of H. B. Sarnat et al. , this classification is even simpler, it includes thermoregulation disorders, the number of indicators considered is reduced, EEG and temporary indicators of the course of the disease are excluded.

In the UK, the classification of hypoxic-ischemic encephalopathy by L. M. S. Dubowitz et al. is widely used. (Table 9).

The classification scheme below differs from the previous ones in the following features.

1. This classification is four-stage.

2. It lacks the concept of consciousness of a newborn, the existence of which is denied by British neonatologists, and the concept of habituation appears, meaning a change in the child’s reaction to repeated homogeneous stimuli of the same intensity.

3. There is no universal classification in the various stages of encephalopathy and these stages have a different number of clinical signs.

4. Particular importance is attached to individual clinical phenomena, in particular, the dynamics of the position of the thumb.

J. J. Volpe classifies hypoxic-ischemic encephalopathy depending on the time elapsed since birth. In the first 12 hours after birth, there is deep stupor or coma, periodic breathing, preservation of pupillary reactions and eye movements, muscle hypotonia and minimal movements, convulsions; in the period from 12 to 24 hours, an obvious restoration of the level of consciousness is revealed, convulsions are more common, attacks of apnea occur, increased excitability and tremor with stiffness (jitteriness), muscle weakness, mainly proximal and in the upper extremities, hemiparesis (in full-term children) or lower extremities (in premature babies). From 24 to 72 hours, the child again experiences stupor or coma, respiratory arrest, brainstem oculomotor and pupillary disturbances occur, and in premature infants there is a catastrophic deterioration in condition due to intraventricular hemorrhage. After 72 hours, constant or even decreasing stupor, impaired sucking, swallowing, tongue movements, absence of screaming, the predominance of muscle hypotonia over hypertension, muscle weakness with a distribution characteristic of the period of 12-24 hours occur. According to the author of this periodization, the rate of recovery from the described conditions are extremely variable and difficult to predict. G. M. Fenichel compares the stages of the first classification and the time frame of the course of encephalopathy, distinguishing mild, moderate and severe encephalopathy. Along with the above-described EEG signs of the severity of NGIE, G. M. Fenichel includes in the diagnostic scheme evoked potentials of the brain, the diagnostic and prognostic significance of which becomes crucial in moderate encephalopathy. The author emphasizes that the phenomenon of jitteriness, characteristic of mild encephalopathy, has no connection with the phenomena of hyperactivity and learning problems in older children. J.-L. Wayenberg et al. assess the neurological status of the newborn after asphyxia according to the level of consciousness (normal or agitation - 2 points, lethargy - 1, stupor - 0), respiratory pattern (regular breathing - 2, irregular - 1, absent - 0), the state of the Moro reflex and grasping (normal or elevated - 2, depressed - 1, absent - 0).

5.3. Classifications of perinatal lesions of the nervous system (syndromological principle)

B. C. L. Touwen notes that neurological can be normal or deviant, and among the variants of the latter he notes one of the following neurological syndromes: increased excitability, muscle hypertension or hypotension, apathy, hemisyndrome; or their combinations. In Russia, the most common classification of lesions of the nervous system in newborns and young children is Yu. A. Yakunina et al. . Within the framework of this classification, hypoxic encephalopathy is considered as a particular manifestation of the pathology of the nervous system of this period. In the classification of Yu. A. Yakunin et al. consider the periods of action of the harmful factor: prenatal (embryonic, early fetal) and perinatal (antenatal or late fetal, intranatal and neonatal). The next category of this classification is etiology (dominant factor), which, in addition to hypoxia, mentions trauma, infection, intoxication, inborn errors of metabolism, chromosomal aberrations, unspecified and unclassified conditions. Next, the form of encephalopathy is assessed according to severity (mild, moderate, severe) with a deciphering of the pathomorphological and pathogenetic mechanisms underlying these disorders. Then the periodization of the disease is considered, starting with the acute period (from 7-10 days to 1 month), the subacute period, or early recovery period (up to 3 months), and, finally, the late recovery period (from 4 months to 1 year, sometimes up to 2 years). Among the levels of damage are the meninges, cerebral cortex, subcortical structures, trunk, spinal cord, peripheral nerves, combined forms.

The last section evaluates the clinical syndromes of the main periods of encephalopathy: acute period syndromes include increased neuroreflex excitability, syndromes of general depression of the central nervous system, autonomic-visceral dysfunction, hydrocephalic-hypertensive, convulsive, coma.

Among the syndromes of the recovery period, delays in mental, motor, speech development, as well as syndromes of autonomic-visceral dysfunction, hyperkinetic, epileptic, hydrocephalic and cerebrasthenic are considered. Possible outcomes of the disease are presented in the form of recovery, delays in the rate of psychophysical and speech development, encephalopathy with focal microsymptoms, moderate intracranial hypertension, compensated hydrocephalus, cerebrasthenic syndrome and neurosis-like conditions, as well as in the form of gross organic forms of damage to the central nervous system with pronounced motor, mental disorders, epilepsy, progressive hydrocephalus.

Perinatal encephalopathy (PEP) (peri- + Lat. natus - “birth” + Greek encephalon - “brain” + Greek patia - “disturbance”) is a term that unites a large group of brain lesions that are different in cause and not specified in origin brain problems that occur during pregnancy and childbirth. PEP can manifest itself in different ways, for example, hyperexcitability syndrome, when the child’s irritability is increased, appetite is decreased, the baby often spits up during feeding and refuses to breastfeed, sleeps less, has difficulty falling asleep, etc. A rarer, but also more severe manifestation of perinatal encephalopathy is central nervous system depression syndrome. In such children, motor activity is significantly reduced. The baby looks lethargic, the cry is quiet and weak. He gets tired quickly during feeding, and in the most severe cases the sucking reflex is absent. Often the manifestations of perinatal encephalopathy are mild, but children who have suffered this condition still require increased attention and sometimes special treatment.

Causes of perinatal pathology

Risk factors for perinatal brain pathology include:

• Various chronic diseases of the mother.
• Acute infectious diseases or exacerbations of chronic foci of infection in the mother’s body during pregnancy.
• Eating disorders.
• The pregnant woman is too young.
• Hereditary diseases and metabolic disorders.
• Pathological course of pregnancy (early and late toxicosis, threat of miscarriage, etc.).
• Pathological course of labor (rapid labor, weakness of labor, etc.) and injuries when providing assistance during childbirth.
• Harmful environmental influences, unfavorable environmental conditions (ionizing radiation, toxic effects, including the use of various medicinal substances, environmental pollution with salts of heavy metals and industrial waste, etc.).
• Prematurity and immaturity of the fetus with various disorders of its vital functions in the first days of life.

It should be noted that the most common are hypoxic-ischemic (their cause is oxygen deficiency that occurs during the baby’s intrauterine life) and mixed lesions of the central nervous system, which is explained by the fact that almost any problem during pregnancy and childbirth leads to disruption of the oxygen supply to tissues the fetus and primarily the brain. In many cases, the causes of PEP cannot be determined.

The 10-point Apgar scale helps to form an objective picture of the child’s condition at the time of birth. This takes into account the child’s activity, skin color, the severity of the newborn’s physiological reflexes, and the state of the respiratory and cardiovascular systems. Each indicator is scored from 0 to 2 points. The Apgar scale allows already in the delivery room to assess the child’s adaptation to extrauterine conditions of existence within the first minutes after birth. A score of 1 to 3 indicates a severe condition, 4 to 6 indicates a moderate condition, and 7 to 10 indicates a satisfactory condition. Low scores are considered risk factors for the child’s life and the development of neurological disorders and dictate the need for emergency intensive care.

Unfortunately, high Apgar scores do not completely exclude the risk of neurological disorders; a number of symptoms appear after the 7th day of life, and it is very important to identify possible manifestations of PEP as early as possible. The plasticity of a child’s brain is unusually high; timely treatment measures help in most cases to avoid the development of neurological deficits and prevent disorders in the emotional-volitional sphere and cognitive activity.

Course of PEP and possible prognosis

During PEP, three periods are distinguished: acute (1st month of life), recovery (from 1 month to 1 year in full-term infants, up to 2 years in premature infants) and outcome of the disease. In each period of PEP, various syndromes are distinguished. More often there is a combination of several syndromes. This classification is advisable, since it allows us to distinguish syndromes depending on the age of the child. For each syndrome, appropriate treatment tactics have been developed. The severity of each syndrome and their combination make it possible to determine the severity of the condition, correctly prescribe therapy, and make prognoses. I would like to note that even minimal manifestations of perinatal encephalopathy require appropriate treatment to prevent adverse outcomes.

Let us list the main syndromes of PEP.

Acute period:

• CNS depression syndrome.
• Comatose syndrome.
• Convulsive syndrome.

Recovery period:

• Syndrome of increased neuro-reflex excitability.
• Epileptic syndrome.
• Hypertensive-hydrocephalic syndrome.
• Syndrome of vegetative-visceral dysfunctions.
• Movement impairment syndrome.
• Psychomotor development delay syndrome.

Outcomes:

• Full recovery.
• Delayed mental, motor or speech development.
• Attention deficit hyperactivity disorder (minimal brain dysfunction).
• Neurotic reactions.
• Autonomic-visceral dysfunctions.
• Epilepsy.
• Hydrocephalus.

All patients with severe and moderate brain damage require hospital treatment. Children with mild impairments are discharged from the maternity hospital under outpatient supervision by a neurologist.

Let us dwell in more detail on the clinical manifestations of individual PEP syndromes, which are most often encountered in outpatient settings.

Syndrome of increased neuro-reflex excitability manifested by increased spontaneous motor activity, restless shallow sleep, prolongation of the period of active wakefulness, difficulty falling asleep, frequent unmotivated crying, revitalization of unconditioned innate reflexes, variable muscle tone, tremor (twitching) of the limbs and chin. In premature infants, this syndrome in most cases reflects a lowering of the threshold for convulsive readiness, that is, it indicates that the baby can easily develop convulsions, for example, when the temperature rises or when exposed to other irritants. With a favorable course, the severity of symptoms gradually decreases and disappears within a period of 4-6 months to 1 year. If the course of the disease is unfavorable and there is no timely treatment, epileptic syndrome may develop.

Convulsive (epileptic) syndrome can appear at any age. In infancy it is characterized by a variety of forms. An imitation of unconditioned motor reflexes is often observed in the form of paroxysmal bending and tilting of the head with tension in the arms and legs, turning the head to the side and straightening the arms and legs of the same name; episodes of shuddering, paroxysmal twitching of the limbs, imitations of sucking movements, etc. Sometimes it is difficult even for a specialist to determine the nature of the convulsive conditions that arise without additional research methods.

Hypertensive-hydrocephalic syndrome characterized by excess fluid in the spaces of the brain containing cerebrospinal fluid (CSF), which leads to increased intracranial pressure. Doctors often call this disorder to parents exactly this way - they say that the baby has increased intracranial pressure. The mechanism of occurrence of this syndrome can be different: excessive production of cerebrospinal fluid, impaired absorption of excess cerebrospinal fluid into the bloodstream, or a combination of both. The main symptoms of hypertensive-hydrocephalic syndrome, which doctors focus on and which parents can control, are the rate of increase in the child’s head circumference and the size and condition of the child’s head. For most full-term newborns, the normal head circumference at birth is 34 - 35 cm. On average, in the first half of the year, the monthly increase in head circumference is 1.5 cm (in the first month - up to 2.5 cm), reaching about 44 cm by 6 months. In the second half of the year, the growth rate decreases; by one year, head circumference is 47-48 cm. Restless sleep, frequent profuse regurgitation, monotonous crying combined with bulging, increased pulsation of the large fontanel and throwing the head back are the most typical manifestations of this syndrome.

However, large head sizes often occur in absolutes and are determined by constitutional and family characteristics. The large size of the fontanel and the “delay” in its closure are often observed with rickets. The small size of the fontanel at birth increases the risk of intracranial hypertension in various unfavorable situations (overheating, increased body temperature, etc.). Carrying out a neurosonographic examination of the brain makes it possible to correctly diagnose such patients and determine treatment tactics. In the vast majority of cases, by the end of the first six months of a child’s life, normal growth of head circumference is noted. In some sick children, hydrocephalic syndrome persists by 8-12 months without signs of increased intracranial pressure. In severe cases, development is noted.

Comatose syndrome is a manifestation of the serious condition of the newborn, which is assessed by 1-4 points on the Apgar scale. Sick children exhibit severe lethargy, decreased motor activity up to its complete absence, and all vital functions are depressed: breathing, cardiac activity. Seizures may occur. The severe condition persists for 10-15 days, with no sucking or swallowing reflexes.

Syndrome of vegetative-visceral dysfunctions, as a rule, manifests itself after the first month of life against the background of increased nervous excitability and hypertensive-hydrocephalic syndrome. Frequent regurgitation, delayed weight gain, disturbances in cardiac and respiratory rhythm, thermoregulation, changes in the color and temperature of the skin, marbling of the skin, and dysfunction of the gastrointestinal tract are noted. Often this syndrome can be combined with enteritis, enterocolitis (inflammation of the small and large intestines, manifested by stool upset, impaired weight gain), caused by pathogenic microorganisms, with rickets, aggravating their course.

Movement disorder syndrome is detected from the first weeks of life. From birth, a violation of muscle tone can be observed, both in the direction of its decrease and increase, its asymmetry can be detected, and there is a decrease or excessive increase in spontaneous motor activity. Often the syndrome of motor disorders is combined with a delay in psychomotor and speech development, because disturbances in muscle tone and the presence of pathological motor activity (hyperkinesis) interfere with purposeful movements, the formation of normal motor functions, and mastery of speech.

With delayed psychomotor development, the child later begins to hold his head up, sit, crawl, and walk. A predominant disorder of mental development can be suspected in the presence of a weak monotonous cry, impaired articulation, poor facial expressions, late appearance of a smile, and delayed visual-auditory reactions.

Cerebral palsy (CP)- a neurological disease that occurs as a result of early damage to the central nervous system. In cerebral palsy, developmental disorders usually have a complex structure, combining motor disorders, speech disorders, and mental retardation. Motor disorders in cerebral palsy are expressed in damage to the upper and lower extremities; fine motor skills, articulatory muscles, and oculomotor muscles suffer. Speech disorders are detected in most patients: from mild (erased) forms to completely unintelligible speech. 20 - 25% of children have characteristic visual impairments: convergent and divergent, nystagmus, limitation of visual fields. Most children have mental retardation. Some children have intellectual impairments (mental retardation).

Attention deficit hyperactivity disorder- behavioral disorder associated with the fact that the child has poor control of his attention. It is difficult for such children to concentrate on any task, especially if it is not very interesting: they fidget and cannot sit still calmly, and are constantly distracted even by trifles. Their activity is often too violent and chaotic.

Diagnosis of perinatal brain damage

Treatment with AEDs

As mentioned above, children with severe and moderate damage to the central nervous system during the acute period of the disease require hospital treatment. In most children with mild manifestations of syndromes of increased neuro-reflex excitability and motor disorders, it is possible to limit ourselves to the selection of an individual regimen, pedagogical correction, massage, physical therapy, and the use of physiotherapeutic methods. Of the medicinal methods for such patients, herbal medicine (infusions and decoctions of sedative and diuretic herbs) and homeopathic drugs are most often used.

In case of hypertensive-hydrocephalic syndrome, the severity of hypertension and the severity of hydrocephalic syndrome are taken into account. If intracranial pressure is increased, it is recommended to raise the head end of the crib by 20-30°. To do this, you can place something under the legs of the crib or under the mattress. Drug therapy is prescribed only by a doctor, the effectiveness is assessed by clinical manifestations and NSG data. In mild cases, they are limited to herbal remedies (decoctions of horsetail, bearberry leaf, etc.). For more severe cases use diacarb, reducing the production of cerebrospinal fluid and increasing its outflow. If drug treatment is ineffective in especially severe cases, it is necessary to resort to neurosurgical methods of therapy.

In cases of severe movement disorders, the main emphasis is placed on the methods of massage, physical therapy, and physiotherapy. Drug therapy depends on the leading syndrome: for muscle hypotonia and peripheral paresis, drugs that improve neuromuscular transmission are prescribed ( dibazole, Sometimes galantamine), with increased tone, means are used to help reduce it - mydocalm or baclofen. Various options for administering drugs orally and using electrophoresis are used.

The selection of drugs for children with epileptic syndrome depends on the form of the disease. Taking anticonvulsants (anticonvulsants), doses, and time of administration are determined by the doctor. The change of drugs is carried out gradually under EEG control. Abrupt spontaneous withdrawal of drugs can provoke an increase in attacks. Currently, a wide range of anticonvulsants are used. Taking anticonvulsants is not indifferent to the body and is prescribed only if a diagnosis of epilepsy or epileptic syndrome is established under the control of laboratory parameters. However, the lack of timely treatment of epileptic paroxysms leads to impaired mental development. Massage and physiotherapeutic treatment for children with epileptic syndrome are contraindicated.

For psychomotor development delay syndrome, along with non-drug treatment methods and socio-pedagogical correction, drugs are used that activate brain activity, improve cerebral blood flow, and promote the formation of new connections between nerve cells. The choice of drugs is large ( nootropil, lucetam, pantogam, vinpocetine, actovegin, cortexin etc.). In each case, the drug treatment regimen is selected individually depending on the severity of symptoms and individual tolerance.

For almost all PEP syndromes, patients are prescribed preparations of B vitamins, which can be used orally, intramuscularly and in electrophoresis.

By the age of one year, in most mature children, PEP phenomena disappear or minor manifestations of perinatal encephalopathy are detected, which do not have a significant impact on the further development of the child. Frequent consequences of encephalopathy are minimal brain dysfunction (mild behavioral and learning disorders), hydrocephalic syndrome. The most severe outcomes are cerebral palsy and epilepsy.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2014

Other specified cerebral disorders of the newborn (P91.8), Cerebral ischemia (P91.0), cerebral disorders of the newborn, unspecified (P91.9), Neonatal coma (P91.5), Cerebral irritability of the newborn (P91. 3), Cerebral depression in the newborn (P91.4)

Neurology

general information

Short description

Approved by the Expert Commission

On health development issues

Ministry of Health of the Republic of Kazakhstan

HIE- acquired syndrome, characterized by clinical and laboratory signs of acute brain damage after perinatal hypoxia and asphyxia during childbirth and manifested by respiratory disorders, suppression of physiological reflexes, decreased muscle tone, impaired consciousness with frequent occurrence of seizures.

The mechanism of injury is hypoxic/ischemic in nature, due to both insufficient oxygen supply to the brain tissue with its reduced content in arterial blood (hypoxemia) and a decrease in cerebral blood flow (ischemia). The final severity of neurological damage primarily depends on the duration of action of the primary factor that caused hypoxia.

I. INTRODUCTORY PART

Protocol name: Hypoxic-ischemic encephalopathy

Protocol code:

ICD-10 code(s):

P91 Other disorders of cerebral status in the newborn

P91.0 Cerebral ischemia

P91.3 Cerebral excitability of the newborn

P91.4 Cerebral depression of the newborn

P91.5 Neonatal coma

P91.8 Other specified brain disorders in a newborn

P91.9 Brain disorders in newborns, unspecified

Abbreviations used in the protocol:

HIE - hypoxic-ischemic encephalopathy,

EN - encephalopathy of the newborn,

RDS - respiratory distress syndrome,

CHD is a congenital heart defect.

PDA - hemodynamically significant patent aortic duct

PFC - persistent fetal communications,

EEG - electroencephalogram,

IVL - artificial lung ventilation

MCA - middle cerebral artery,

ACA - anterior cerebral artery,

Ultrasound - ultrasound examination.

MRI - magnetic resonance imaging,

SaO2 - oxygen saturation.

Date of development of the protocol: year 2013.

Protocol users: neonatologists, neurologists, pediatricians.

Classification

Clinical classification:

There are 3 degrees of severity of HIE (according to Amiel-Tyson & Ellison and Sarnat & Sarnat):

Lightweight;

Moderate;

Heavy.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

Basic diagnostic measures

A. Analysis of risk factors contributing to the development of HIE:

. antenatal:

Severe somatic diseases of the mother, especially in the stage of decompensation: pathology of pregnancy (long-term toxicosis, threat of miscarriage, postmaturity, etc.);

Endocrine diseases (diabetes mellitus);

Infections of various etiologies, especially in the 2-3 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;

. intrapartum:

Abnormal presentation of the fetus;

Use of aids during childbirth (obstetric forceps, vacuum extractor);

Acute hypoxia during childbirth in the mother (shock, decompensation, somatic pathology);

Disorders of the placental-fetal circulation (eclampsia, tight entanglement of the umbilical cord, true umbilical cord knots, prolapse of umbilical cord loops, tension in a short umbilical cord, etc.);

Rapid, fast, protracted labor;

Placenta previa or premature abruption of the placenta;

Discoordination of labor;

Uterine rupture;

Caesarean section (especially emergency).

B. Clinical manifestations (according to Amiel-Tyson & Ellison and Sarnat & Sarnat):

Light HIE:

Muscle tone is slightly increased and tendon reflexes are active during the first few days after birth.

Transient behavioral disturbances such as poor sucking, irritability, restlessness, or drowsiness may occur.

After 3-4 days, the neurological status returns to normal.

Moderate HIE:

The newborn is in a state of lethargy: lethargic, drowsy, with symptoms of muscle hypotonia and a significant decrease in tendon reflexes.

The newborn's reflexes, such as grasping, sucking and Moro, may be severely reduced or absent.

The newborn may experience periods of brief apnea.

Seizures may appear on the first day of life.

Complete neurological recovery is possible within 1-2 weeks, which is associated with a good long-term prognosis.

An initial period of well-being may be followed by sudden deterioration, usually indicative of reperfusion disorders.

During this period, the intensity of the seizures may increase.

Severe HIE:

Stupor or coma is typical. The newborn may not respond to physical stimuli.

Breathing may be irregular, and such a child usually requires breathing support.

In all cases, diffuse muscle hypotonia and a pronounced decrease in tendon reflexes are noted.

The newborn's reflexes (sucking, swallowing, grasping, Moro) are absent.

Examination of cranial nerve function may reveal oculomotor abnormalities such as nystagmus, exophthalmos, and absence of doll's eyes (i.e., absence of cooperative movements of the eyeballs).

The pupils may be wide, unresponsive or poorly responsive to light.

Early and frequent seizures may initially be resistant to standard therapy. Seizures are usually generalized and their frequency may increase over the next 2-3 days, correlating with the phase of reperfusion injury.

As the damage progresses, seizures subside and the EEG may become isoelectric or exhibit suppression of the pattern. At the same time, depression of consciousness may increase, and tension in the fontanelle may appear, indicating an increase in cerebral edema.

Typical for the period of reperfusion damage is instability of heart rate and blood pressure, and the onset of death from cardiorespiratory disorders.

Additional diagnostic measures

To confirm the severity of hypoxia suffered during the first 30 minutes after birth, arterial blood is collected from a mother with the above risk factors from the clamped umbilical cord to determine its gas composition (the stability of the gas composition of the collected blood is maintained in a plastic syringe for 30 minutes!).

Markers of severe perinatal hypoxia (asphyxia) are:

Severe metabolic acidosis (in arterial blood of the umbilical cord pH<7,0 и дефицит оснований ВЕ ≥ 12 ммоль/л);

Apgar score 0-3 points at 5 minutes;

Clinical neurological disorders manifesting in the early stages after birth (convulsions, hypotension, coma - neonatal encephalopathy (NE);

Signs of multiple organ damage in the early stages after birth.

Diagnostic criteria

Complaints and medical history of the mother:

Analysis of data on the characteristics of pregnancy and childbirth, their complications, allowing us to establish the cause of neurological disorders in the newborn.

Physical examination(children with perinatal hypoxia have a high risk of multiple organ damage, which determines the need for careful monitoring of the function of vital systems and neurological status for timely diagnosis and adequate treatment):

Analysis of the condition of the newborn at birth, the need for resuscitation measures and their effectiveness;

Monitor the clinical and neurological status of the newborn, paying particular attention to:

Instability of body temperature

Frequency and pattern of breathing

Frequency and pattern of heart contractions

Color of skin and mucous membranes

Activity (convulsions, depression, neurological status)

Diuresis.

Laboratory research(in the dynamics of the child’s stay in the hospital):

Blood gases;

Glycemic level;

Electrolyte composition of blood serum;

Levels of urea, creatinine;

Liver enzymes;

Assessment of hematological parameters and blood coagulation system (according to indications)

Blood oxygen saturation (if possible)

Blood pressure (if possible).

Instrumental studies:

Ultrasound of the brain;

Dopplerography of the middle cerebral (MCA) and anterior cerebral arteries (ACA) in the first 48 hours; persistent changes in the basal ganglia or disturbance in the territory of the middle cerebral artery are characteristic signs of an unfavorable neuromotor outcome;

MRI in children with moderate to severe HIE at one week of age; symmetrical lesions of the basal ganglia and thalamus, as well as pathological changes in the posterior limb of the internal capsule are predictors of unfavorable outcome;

Standard EEG for moderate to severe encephalopathy or seizures;

Amplitude-integrated EEG (when available) can be used to monitor cerebral activity, detect seizures, and predict outcome.

Specialist consultations:

Neurologist,

Neurosurgeon,

Oculist,

Cardiologist.

Differential diagnosis

Differential diagnosis:

Exposure to drugs, abstinence syndrome.

Acute cerebrovascular accident (ACVA).

Neuromuscular diseases, including neonatal myopathies.

Brain tumors.

Infections.

Perinatal stroke.

Intracranial hemorrhage.

Congenital malformations of the brain.

Congenital metabolic disorders.

Genetic syndromes.

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Treatment

Treatment goals: Provide optimal nursing conditions and interventions that will minimize adverse outcomes and quality of life.

Treatment tactics:

Carrying out adequate treatment of respiratory disorders.

Maintaining a stable level of systemic and cerebral hemodynamics.

Constant monitoring and correction of biochemical abnormalities.

Prevention and treatment of seizures.

Principles of care and treatment of newborns with HIE:

Optimal air temperature in the room (not lower than 25°C).

Comfortable position of the child in the incubator; create a “nest” with free placement of arms and legs (do not use tight swaddling).

Avoid excessive lighting in the room (cover incubators, use concentrated light sources).

Maintain silence (talk quietly; do not slam doors or incubator doors, etc.).

If frequent blood sampling is necessary, install a venous catheter (but do not constantly install an umbilical catheter into the umbilical cord vein).

Ensure adequate pain relief: skin-to-skin contact with the mother (if the child’s condition allows).

Encourage the mother or family to stay with the baby and participate in the baby's care (talking to the baby, touching the baby, helping to change and feed the baby).

If respiratory distress occurs, provide assisted ventilation or oxygenation.

Provide adequate nutrition and/or IV fluids to prevent or treat hypoglycemia or other metabolic disorders.

As soon as the baby's condition improves, start enteral feeding: expressed breast milk using an alternative method. If the child is digesting well and has no problems, continue to increase the amount of milk while reducing the amount of intravenous fluid, maintaining the total daily volume in accordance with the child's daily needs. Feed your baby every three hours or more often.

Discontinue IV fluids if the child receives more than two-thirds of the daily fluid intake orally and is not vomiting or having abdominal distension.

Oxygen therapy for respiratory disorders:

Determine the method of oxygen supply, assessing all the advantages and disadvantages of each method. To use the required oxygen concentration, a source of compressed air and a gas mixer are required.

Use a pulse oximeter to ensure that the child is receiving the appropriate concentration of oxygen. If a pulse oximeter is not available, monitor for signs of oxygenation, assessing the child for respiratory distress or central cyanosis (blue tongue and lips).

Infusion therapy:

Determine the required volume of infusion according to the body weight and age of the child.

In the first three days of a child's life, a 10% glucose solution is used. If diuresis is sufficient, from the 4th day of life, if indicated, add sodium to a 10% glucose solution at the rate of 3 mmol/kg body weight and potassium at the rate of 2 mmol/kg body weight.

Hemodynamic support:

Heart rate and blood pressure must be monitored.

If the child has low blood pressure or shows signs of shock (skin cool to the touch, positive white spot sign, heart rate greater than 180 beats per minute, lack of consciousness, etc.) but no signs of bleeding, saline should be administered ( 0.9% sodium chloride solution) intravenously at 10-20 ml/kg, if myocardial dysfunction is excluded.

If after administration of saline it is not possible to satisfactorily increase blood pressure, dopamine (2-20 mcg/kg/min) must be administered.

If low systemic blood flow persists or myocardial dysfunction needs to be treated, dobutamine (5-20 mcg/kg/min) should be used as a 1st line drug and epinephrine as a 2nd line drug (0.01-1.0 g/kg /min).

In cases of refractory hypotension, when traditional therapy is ineffective, hydrocortisone (1 mg/kg every 8 hours) should be used.

Treatment of seizures

If a child has seizures, it is necessary to determine the blood glucose level:

If its level is less than 2.6 mmol/l, a 10% glucose solution should be administered at a rate of 2 ml/kg body weight IV slowly over 5 minutes (bolus) and continued intravenous drip administration of a 10% glucose solution in a maintenance volume according to the age-related physiological need for fluid;

If, 30 minutes after the bolus administration of glucose, its level in the blood has not increased and even dropped below 1.4 mmol/l, the bolus should be repeated.

Inject glucose at the same dose intravenously over 5 minutes and continue the infusion;

Continue measuring your blood glucose level until it reaches 1.4 mmol/L in two repeat measurements;

If the blood glucose level is 1.4 mmol/L, continue the infusion and repeat the blood glucose level every three hours until it reaches 2.6 mmol/L or higher in two subsequent measurements;

Over the next few days, blood glucose levels are measured every 12 hours;

The frequency of measurements should be increased if clinical signs of hypoglycemia persist.

If the glucose level is within the normal range or the convulsions do not stop after intravenous administration of a glucose solution, the administration of phenobarbital is indicated:

Phenobarbital is administered intravenously slowly over 5 minutes at the rate of 20 mg/kg body weight;

If intravenous administration is not possible, a single intramuscular injection is possible slowly at a dose of 20 mg/kg;

If convulsions have not stopped 30 minutes after the administration of phenobarbital, its slow intravenous administration should be repeated over 5 minutes at the rate of 10 mg/kg body weight;

If necessary, repeat again.

If seizures continue or recur within 6 hours, give phenytoin:

Phenytoin is administered at a dose of 20 mg/kg body weight only intravenously after diluting the calculated dose of the drug in 15 ml of physiological sodium bicarbonate solution at a rate of 0.5 ml/min for 30 minutes.

Induced therapeutic hypothermia is carried out in newborns with moderate to severe HIE strictly in accordance with the protocol:

A. Indications for hypothermia(all criteria must be met):

Gestational age ≥ 36 weeks;

Postnatal age ≤ 6 hours;

PH< 7,00 и дефицит оснований ВЕ ≥12 ммоль/л (на 1-й минуте жизни);

Apgar score< 5 через 10 мин.,

Or the need for positive pressure ventilation 10 minutes after birth;

Clinical signs of encephalopathy.

B. Contraindications to hypothermia:

Gestational age< 36 недель;

Postnatal age > 6 hours;

Serious congenital malformations;

Hemorrhages.

B. Onset of hypothermia

It is most advisable to start hypothermia as early as possible:

Turn off the heater in the delivery room;

Maintain the child's temperature at 33.5-34.5 ° C for 72 hours, covering it with dry ice packs, or use special equipment for hypothermia;

Conduct continuous monitoring of rectal temperature;

After 72 hours (three days), begin slowly warming the child (0.5°C per hour).

D. Potential side effects and their solutions:

Sinus bradycardia;

Pulmonary hypertension;

Thrombocytopenia;

In most cases, a temporary increase in body temperature by 0.5-1°C eliminates these disorders.

D. Nutrition for hypothermia

During hypothermia, newborns receive parenteral nutrition due to poor intestinal perfusion. You should not allow your baby to tremble, as this can stimulate brain activity and metabolism. If tremors occur, a continuous infusion of morphine is recommended.

Prevention: ensuring the health of a woman before and during pregnancy, differentiated antenatal and intranatal care (according to the identified pathology), adequate stabilization of the condition of the newborn in the maternity ward and the postnatal period.

Forecast:

The presence of seizures is a threatening symptom; the risk of neurological retardation in such children is noticeably higher, especially if seizures are frequent and poorly controlled;

Pathological neurological symptoms (muscle hypotonia, hypertonicity, decreased reflexes) that persist after two weeks usually indicate a poor prognosis.

Indicators of treatment effectiveness:

Newborns whose neurological disorders disappear after 1-2 weeks develop normally in the future.

Drugs (active ingredients) used in treatment

Hospitalization

Indications for hospitalization

Newborns with moderate and severe encephalopathy are hospitalized in level 3 obstetric organizations.

Information

Sources and literature

1. Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2014
   1. 1) Amiel-Tison C, Gosselin J. Clinical assessment of the infant nervous system. In: Levene MI and Chervenak FA. Fetal and neonatal neurology and neurosurgery, 4th ed. Philadelphia, Churchill Livingstone Elsevier, 2009:128–154. 2) Barnett A et al. Neurological and perceptual-motor outcome at 5-6 years of age in children with neonatal encephalopathy: relationship with neonatal brain MRI. Neuropediatrics, 2002, 33(5):242–248. 3) Cowan F et al. Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet, 2003, 361(9359):736–742. 4) Edwards AD et al. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal hypoxic ischemic encephalopathy: synthesis and meta-analysis of trial data. British Medical Journal, 2010, 340:1–7. 5) Ellis M et al. Outcome at 1 year of neonatal encephalopathy in Kathmandu, Nepal. Developmental Medicine and Child Neurology 1999, 41:689. 6) Finer NN et al. Hypoxic-ischaemic encephalopathy in term neonates: perinatal factors and outcome. Journal of Pediatrics, 1981, 98:112. 7) Guidelines for Perinatal Care. American Academy of Pediatrics and American College of Obstetricians and Gynecologists, 1997. 8) Levene M.I. and de Vries L.S. Hypoxic-ischaemic encephalopathy. In: Martin RJ, Fanaroff AA, Walsh MC, eds. Neonatal-perinatal medicine: diseases of the fetus and infant, 9th ed. St Louis, Elsevier Mosby, 2011:952–976. 9) Low JA et al. The relationship between perinatal hypoxia and newborn encephalopathy. American Journal of Obstetrics and Gynecology 1985, 152:256. 10) Marlow N et al. Neuropsychological and educational problems at school age associated with neonatal encephalopathy. Archives of Disease in Childhood. Fetal and Neonatal Edition, 2005, 90:F380. 11) Miller SP et al. Clinical signs predict 30-month neurodevelopmental outcome after neonatal encephalopathy. American Journal of Obstetrics and Gynecology, 2004, 190:93. 12) Moster D et al. Joint association of APGAR scores and early neonatal symptoms with minor disabilities at school age. Archives of Disease in Childhood. Fetal and Neonatal Edition, 2002, 86:F16. 13) Murray DM et al. The predictive value of early neurological examination in neonatal ischemic encephalopathy and neurodevelopmental outcome at 24 months, Developmental Medicine and Child Neurology, 2010, 52(2):e55–e59. 14) Robertson C and Finer NN. Term infants with hypoxic-ischaemic encephalopathy: outcome at 3.5 years. Developmental Medicine and Child Neurology 1985, 27:473. 15) Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress: a clinical and electroencephalographic study. Archives of Neurology 1976, 33:696–705. 16) Thompson CM et al. The value of a scoring system for hypoxic-ischaemic encephalopathy in predicting neuro-developmental outcome. Acta Paediatrica 1997, 86:757. 17) Volpe JJ. Neurology of the newborn, 3rd ed. Philadelphia, WB Saunders, 1995. 18) Volpe JJ. Neurology of the newborn, 5th ed. Philadelphia, Saunders Elsevier, 2008. 19) de Vries LS, Toet MC. Amplitude integrated electroencephalography in the full-term newborn. Clinics in Perinatology 2006, 33:619–632. 20) Wall SN et al. Reducing intrapartum-related neonatal deaths in low- and middle-income countries – what works? Seminars in Perinatology, 2010, 34:395–407.
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