What is hypoxic-ischemic encephalopathy? Diagnosis of PEP - perinatal encephalopathy Ischemic encephalopathy in a newborn
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:
- The first degree is mild - transient disorders of the neurological status, lasting no more than a week.
- 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,.
- 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:
- High neuro-reflex excitability;
- Sleep disorders, anxiety;
- Trembling of the limbs, chin;
- Possible regurgitation;
- 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:
- Favorable with rapid positive dynamics;
- Favorable course with rapid regression of neurological deficit, when by the time of discharge the changes either disappear or remain minimal;
- Unfavorable course with progression of neurological symptoms;
- Disability during the first month of life;
- 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
Perinatal encephalopathy is a brain lesion that has various causes and manifestations. This is a huge variety of symptoms and syndromes, manifestations and characteristics: children with severe perinatal encephalopathy require special attention and mandatory medical supervision. Perinatal injuries of this nature account for about half of the pathologies of the nervous system in children and often become the causes of epilepsy, cerebral palsy, and brain dysfunction.
Perinatal posthypoxic encephalopathy
PPE (transient encephalopathy of newborns) implies the appearance of disorders of the child’s brain that arose before or during childbirth. The most important factors contributing to the occurrence of PPE are birth injuries, neuroinfections, fetal intoxication and oxygen deprivation.
Symptoms also occur in large newborns, premature babies, and if the child was born entwined with the umbilical cord. The diagnosis is indicated by high fetal weakness on the Apgar scale, the absence of a sucking reflex in children, heart rhythm disturbances and constant nervous agitation.
About the diagnosis "hypoxic-ischemic perinatal encephalopathy" we are talking about when multiple disorders are noticed in the prenatal period. This leads to a pathology in the supply of oxygen to the fetal tissues, but the brain is primarily affected.
Perinatal encephalopathy in newborns
Immediately after birth, a child with brain damage attracts attention with restless behavior, frequent spontaneous flinching and regurgitation, excessive lethargy and stiffness, and increased reactions to sound and light.
Throwing back the head with uncontrollable crying, poor thermoregulation, and disturbed sleep often resolve during the first week of life. CNS depression syndrome in newborns manifests itself in the form of lethargy, lethargy, and often different muscle tone, leading to asymmetry of the body and facial features.
If the symptoms do not disappear during the first month of life, but acquire a new color and strength, doctors diagnose perinatal encephalopathy.
Types of encephalopathy in children
- Residual form Brain damage is diagnosed if, in the presence of previous birth injuries, the child suffers infections, inflammation, and also with poor blood supply to the brain. Such children suffer, often with mental problems, decreased intelligence, and learning difficulties.
- Encephalopathy- damage to brain tissue caused by impaired blood supply. The causes are osteochondrosis, hypertension, increased blood pressure, and dystonia.
- Ischemic encephalopathy is expressed in poor blood supply to the brain and destructive processes occurring in certain tissue areas. Excessive smoking, stress and alcohol abuse lead to this diagnosis.
- Toxic encephalopathy becomes a consequence of brain poisoning by toxic substances during infections, poisoning with chemicals and alcohol. Severe poisoning of brain tissue leads to epileptic seizures.
- Radiation encephalopathy appears as a result of exposure to ionizing radiation on the brain of patients.
- Encephalopathy of mixed origin characterized by the presence of extensive complaints and symptoms; only a doctor can make a correct diagnosis based on tests and brain studies.
Severity
During PE it is customary to distinguish several periods.
The period after birth and up to the 1st month of life is considered acute. The recovery period lasts up to a year or two. What follows is the outcome of the disease.
Each period is characterized by a special course and the presence of various syndromes; sometimes combinations of manifestations are noted.
Each syndrome requires appropriate treatment and correctly prescribed medications.
Even mild manifestations of brain disorders should be carefully examined - untreated disorders are fraught with developmental delays and adverse outcomes. When the severity of brain damage is severe or moderate, qualified inpatient treatment is necessary.
Mild disorders can be treated on an outpatient basis under the supervision of a neurologist.
Video of Dr. Komarovsky talking about the difference between perinatal encephalopathy and normal physiological reflexes of newborns:
Causes of perinatal encephalopathy
Risk factors, contributing to the appearance of this group of brain lesions:
- The presence of chronic diseases of the mother;
- Eating disorders;
- Maternal alcohol intake and smoking;
- Autoimmune conflict;
- Previous infectious diseases during pregnancy;
- Borderline age of the woman in labor;
- Stress;
- Pathology during pregnancy and childbirth (toxicosis, rapid labor, trauma during childbirth);
- Prematurity of the fetus;
- Unfavorable environmental conditions.
Symptoms of the disease
- Prolonged crying;
- Frequent regurgitation;
- Throwing of limbs;
- Restless shallow sleep at night and short sleep during the day;
- Lethargy or hyperactivity;
- Inadequate reaction to light and sound stimuli;
- Lack of sucking reflexes;
- Muscle tone disorders.
These and many other symptoms need to be carefully studied by your doctor.
At a later age, the child experiences frequent bad mood, absent-mindedness, sensitivity to weather changes, and difficulty getting used to child care facilities.
Main syndromes of perinatal encephalopathy
- Hypertensive-hydrocephalic syndrome manifested by the presence of excess fluid inside the brain, this leads to changes in intracranial pressure. The diagnosis is made based on observation of the size of the head and the condition of the large fontanel. Also manifestations of the syndrome are restless sleep, monotonous crying, increased pulsation of the fontanel.
- Hyperexcitability syndrome more often makes itself felt by increased motor activity, problems with falling asleep and staying asleep, frequent crying, a decrease in the threshold of convulsive readiness, and increased muscle tone.
- Convulsive syndrome known as epileptic and has a variety of forms. These are paroxysmal movements of the body, shudders, twitching and spasms of the limbs.
- Comatose syndrome manifests itself as severe lethargy, decreased motor activity, depression of vital functions, and absence of sucking and swallowing reflexes.
- Vegetative-visceral dysfunction syndrome expressed by increased nervous excitability, frequent regurgitation, disorders of the digestive system, enteritis, stool disorder, and abnormal skin condition.
- Movement disorder syndrome manifests itself in the direction of a decrease or increase in muscle tone, which is often combined with developmental disorders, making it difficult to master speech.
- Cerebral palsy has a complex structure: these are disorders of fine motor skills, lesions of the limbs, speech dysfunction, visual impairment, mental retardation and reduced ability to learn and social adaptation.
- Hyperactivity syndrome is expressed in children’s reduced ability to concentrate and attention disorders.
Diagnostics
The diagnosis is made based on clinical data and information about the course of pregnancy and childbirth. The following modern and effective methods are used for diagnosis.
- Neurosonography reveals intracranial brain damage.
- Doppler sonography studies the amount of blood flow in brain tissue.
- An electroencephalogram, by recording the electrical potentials of the brain, makes it possible to determine the presence of epilepsy and delayed age-related development at various stages.
- Video monitoring helps to evaluate the characteristics of children’s motor activity based on video recordings.
- Electroneuromyography allows you to study the sensitivity of peripheral nerve fibers.
- Available types of tomography are used to assess structural changes in the brain.
Most often, objective information about the disease is obtained using neurosonography and electroencephalography. Sometimes an examination is prescribed by an ophthalmologist, who examines the fundus and the condition of the optic nerves, and identifies genetic diseases.
Treatment of encephalopathy in children
If the symptoms are moderate and mild, doctors leave the child for home treatment and give recommendations to parents on how to maintain the condition.
But severe damage to the nervous system and an acute period require hospital treatment. In any case, it is necessary to choose an individual regimen, massage, physical therapy, herbal medicine methods and homeopathic remedies.
Drug treatment
When prescribing treatment, the severity of the diagnosis is taken into account. To improve blood supply to the brain, a newborn is prescribed piracetam, actovegin, and vinpocentine.
Drug therapy is prescribed by a doctor.
- For severe motor dysfunctions, emphasis is placed on the drugs dibazole and galantamine; for increased tone, baclofen or mydocalm are prescribed. To administer drugs, various options for oral administration and the electrophoresis method are used. Massages, physiotherapy, and daily special exercises with the child are also indicated.
- For epileptic syndrome, taking anticonvulsants in doses recommended by a doctor is indicated. Anticonvulsants are prescribed for serious indications and severe epilepsy. Physiotherapy methods are contraindicated for children with this syndrome.
- For disorders of psychomotor development, medications are prescribed that are aimed at stimulating brain activity and improving cerebral blood flow - these are nootropil, actovegin, cortexin, pantogam, vinpocetine and others.
- For hypertensive-hydrocephalic syndromes, appropriate drug therapy is prescribed based on the severity of symptoms. In mild cases, the use of herbal remedies (decoctions of bearberry and horsetail) is indicated; in more complex cases, diacarb is used, which increases the outflow of liquor.
For particularly severe patients, it is rational to prescribe methods of neurosurgical therapy. Hemodialysis, reflexology, ventilation, and parenteral nutrition are also used. Children with PEP syndromes are often prescribed B vitamins.
Treatment at home
It is important to pay special attention to children with perinatal encephalopathy from the first days of life. Parents should tune in to the need to introduce hardening, massage, swimming, and air baths.
Therapeutic massage and special gymnastics complexes help improve body tone, develop motor functions of the hands, train and strengthen the baby’s health. If a child has been diagnosed with asymmetry of muscle tone, therapeutic massage is indispensable.
Parents should be prepared for the fact that at times of increased stress, all syndromes may worsen. This happens when children go to kindergarten or school, when the weather and climate change, during a period of intensive growth of the child. Childhood infections may also influence symptoms.
It is mandatory to take vitamin complexes, you should allocate enough time for walks in the fresh air, activities and exercises. You also need a balanced diet and a calm, balanced environment in the home, absence of stress and sudden changes in daily routine.
The better the quality of treatment a child receives, the more attention is paid to such children from birth and in the first years of life, the lower the risk of severe consequences of brain damage.
Consequences and possible prognosis of the disease
The most common consequences of perinatal encephalopathy can be: delayed development of the child, brain dysfunction (expressed in lack of attention, poor learning ability), various dysfunctions of internal organs, epilepsy and hydrocephalus. Vegetative-vascular dystonia may occur.
About a third of children recover completely.
A woman's adherence to a daily routine, rules of conduct during pregnancy and personal hygiene, and abstinence from smoking and alcohol can reduce the risk of brain damage in newborns.
Adequately conducted childbirth, qualified medical care and observation by a neurologist, timely diagnosis and treatment reduce the risk of the consequences of perinatal encephalopathy.
Perinatal encephalopathy and can it be cured:
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 appropriate, 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.
This is not an inflammatory disease of the brain; it is associated with impaired blood supply, reduction and destruction of brain cells. It can be an acquired disease, as a result of birth trauma, hypoxia, which leads to serious brain disorders, but most often it is a congenital pathology. This disease is diagnosed in approximately 50% of infants. More severe forms of PPCNS occur in only 10% of newborns. More vulnerable are congenital encephalopathy in infants, complicated during childbirth (birth trauma, placental abruption, abnormal fetal position, large head in a child, narrow pelvis in a woman). It can be suspected for the first time immediately after the birth of a child. At birth, the internal organs, including the central nervous system, are not fully developed; the development of all systems requires a period of time. There are several forms of encephalopathy.
Perinatal encephalopathy in newborns.
It is considered from the 28th week of pregnancy to the 8th day of the child’s life. It can occur if (causes of encephalopathy):
- The child's mother is too young or old.
- Abortion.
- Miscarriages.
- Infertility treatment.
- Mom's diabetes.
- Mother's heart defects.
- Mom's flu.
- Smoking, alcohol.
- Risk of miscarriage.
- Work in hazardous production.
- Taking medications.
- Fast (less than 6 hours, slow more than 24 hours) labor.
- C-section.
- Premature placental abruption.
- Umbilical cord entanglement, umbilical cord prolapse.
- Multiple birth.
Periods of perinatal encephalopathy in newborns.
- The acute period is 7-10 days to a month.
- Early recovery period up to 4 – 6 months.
- Late recovery period up to 1 – 2 years.
In the acute period observed: lethargy, muscle hypotonia, decreased reflexes (sluggish sucking) or, conversely, hyperexcitability of the nervous system (shallow sleep, trembling of the chin and limbs), throwing the head back.
Early period of perinatal encephalopathy in newborns, when general cerebral symptoms decrease, and focal brain lesions appear. Muscle hypotonicity or hypertonicity appears. Possible paresis and paralysis, hyperkinesis (enlargement of the head, expansion of the venous network on the forehead, temples, enlargement and bulging of the fontanelle. Marbling and pallor of the skin, cold hands and feet, changes in the gastrointestinal tract (constipation, increased gas production), heart rhythm disturbances and breathing.
Late period of perinatal encephalopathy in newborns, muscle tone and other functions gradually normalize. Dynamic development occurs in the central nervous system and psyche of the child. Pre-speech and speech development is being formed. At this age, you can already notice that the child is lagging behind; those reflexes and skills that should be there, or they are not there, or they are very weak, are sharply delayed. There may be persistent spastic syndrome or, conversely, muscle hypotension.
Hypoxic-ischemic damage to the nervous system.
One of the forms of encephalopathy caused by fetal hypoxia (oxygen starvation of brain cells). With chronic intrauterine hypoxia they suffer, the capillaries of the brain grow slowly and become more penetrating. During childbirth, this leads to asphyxia (severe respiratory and circulatory disorders). Therefore, asphyxia of a newborn at birth is a consequence of fetal hypoxia. Several degrees of hypoxic-ischemic form can be distinguished infant encephalopathy:
- Depression and excitation of the central nervous system, which lasts up to 7 days after birth.
- After 7 days, convulsions, increased intracranial pressure, and disturbances in heart and respiratory rhythm are added.
- Severe convulsive condition, high intracranial pressure.
Mixed lesion disease.
In addition to hypoxic-ischemic damage to the central nervous system, intracranial hemorrhages (not traumatic) are added; the severity depends on where the hemorrhage occurred.
Traumatic damage to the central nervous system.
Damage to the spinal cord during childbirth, this can happen if the fetus is large or incorrectly positioned. When it is easier to remove the head and shoulders, when the head is diligently turned when it is removed, or when it is pulled behind the head, the obstetrician performs these manipulations to reduce the child’s hypoxia. It all depends on the experience of the doctor. Damage can also occur during a caesarean section with a “cosmetic incision” that is not sufficient to remove the child’s head. Artificial ventilation of the lungs in the first 2 days can lead to damage, especially in children and those with low weight.
Metabolic disorders.
Alcohol syndrome, nicotine, drug disorders occur as a result of the cessation of the intake of alcohol, nicotine, and drugs.
Intrauterine infection.
Depends on the type and severity of the disease. Such children are often born in a state of asphyxia, with low weight, an enlarged liver, developmental defects, and there may be a convulsive syndrome.
In the maternity hospital, neonatologists examine newborns and identify perinatal damage to the central nervous system and prescribe treatment. But this treatment must be continued at home. What should alert the mother: frequent restlessness of the child, regurgitation, trembling of the chin, arms and legs, freezing of the child in one position, unusual eye movements, rapid head growth of more than 1 cm per week, enlargement of the edges of the fontanel and its bulging.
If your baby has something, you need to consult a neurologist, the sooner the better, and begin treatment to fully restore your baby’s health.
Treatment of encephalopathy in infants.
Treatment is usually complex, it begins after a complete examination of the baby, for this you need to pass tests:
Take examinations:
- NSG (neurosonography)
- EEG (encephaloelectrography)
- MRI (magnetic resonance imaging)
- Cerebrospinal fluid
- Neurologist
- Oculist
With proper treatment and timely diagnosis infant encephalopathy It is well treated, treatment is carried out both at home and in the hospital, it all depends on the severity of the disease, but treatment is carried out over a long period of time and in courses. Drugs are prescribed to restore the structure of the brain, improve blood supply to the brain, B vitamins (Magne B6, Magnelis), sedatives, drugs that treat symptoms: for seizures, anticonvulsants (Konvulex, Finlepsin, Depakine), drugs that relieve muscle hypertonicity, as well as drugs that treat movement disorders. Other drugs can be prescribed intramuscularly and intravenously. Electrophoresis is well used for the treatment of encephalopathy (if there is no history of seizures), neurologists like to prescribe physical therapy, massage, and herbal medicine. One of the important principles of treatment is: alternating sleep and wakefulness, mandatory walks in the fresh air, and proper balanced nutrition. If you follow all the principles of treatment and regularly visit a neurologist, pediatrician, or physiotherapist, most children have a chance of a full recovery, without consequences in adulthood.
With a diagnosis of encephalopathy, children are registered at a dispensary for further observation at least twice a year.
Consequences of encephalopathy in a newborn.
With severe damage to brain cells, poor or untimely treatment, complications arise:
- Neuroses.
- Epilepsy.
- Possible depression.
- Strabismus.
- Migraine.
- Hydrocephalus.
- Schizophrenia in adolescence.
- Fainting.
- Dizziness.
Hypoxic-ischemic encephalopathy combines brain lesions of different etiology or unspecified origin that occur before and during childbirth.
The causes of hypoxic-ischemic encephalopathy of the newborn are varied (hypoxic, traumatic, toxic, metabolic, stress effects, radiation, immunological abnormalities in the mother-placenta-fetus system), but they all lead to intrauterine hypoxia or asphyxia of the fetus and newborn.
Among the causes of perinatal brain damage, the leading place is occupied by intrauterine and intrapartum fetal hypoxia. Intrauterine fetal hypoxia May be hypoxic occurs when there is insufficient oxygen saturation of the blood, hemic, due to a drop in hemoglobin levels in the blood, circulatory– disruption of blood flow and tissue– as a result of disruption of oxidative processes in fetal tissues. Currently, instead of the term perinatal encephalopathy, the term hypoxic-ischemic encephalopathy (HIE) of the newborn is used. For unfavorable reasons antenatal period, contributing to fetal hypoxia include: severe somatic diseases of the mother, especially in the stage of decompensation: pathology of pregnancy (long-term toxicosis, threat of miscarriage, postmaturity, etc.); endocrine diseases (diabetes mellitus); infections of various etiologies, especially in the 2nd - 3rd trimesters of pregnancy; bad habits of the mother (smoking, alcoholism, drug addiction); genetic, chromosomal pathology; immunological abnormalities in the mother-placenta-fetus system; multiple pregnancy. IN intranatal period: 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 (preeclampsia, from the umbilical cord: tight entanglement, true nodes, loss of loops, tension in the umbilical cord, which is short in length, etc.); rapid, fast, protracted labor; placenta previa or premature placental abruption; discoordination of labor; uterine rupture; caesarean section (especially emergency).
The second most important factor in the development of newborn encephalopathy belongs to the factor mechanical trauma to the central nervous system child during childbirth, usually in combination with previous intrauterine hypoxia: intracranial hemorrhages of hypoxic origin (IVH, subarachnoid) and traumatic injuries of the nervous system (RFI, spinal cord, peripheral nervous system).
In recent years, the structure of etiopathogenetic factors of perinatal CNS damage has included toxic-metabolic(transient metabolic disorders - kernicterus, hypoglycemia, hypo-, hypermagnesemia, hypocalcemia, hypo-, hypernatremia; with dysfunction of the central nervous system due to the use of alcohol, drugs during pregnancy, smoking, medications, exposure to viral and bacterial toxins), infectious(intrauterine infections, neonatal sepsis), hereditary And combined brain damage.
The polyetiology of newborn encephalopathy predetermines various mechanisms of brain damage.
One of them is decreased cerebral blood flow , which may be caused by antenatal hypoxia, accompanied by slower growth of brain capillaries, increasing their permeability and vulnerability, in addition, increasing the permeability of cell membranes. Against the background of increasing metabolic acidosis, cerebral ischemia occurs with the development of intracellular lactic acidosis and neuronal death.
The decrease in cerebral blood flow is affected by violations of the mechanisms of autoregulation of cerebral blood flow. In healthy children, cerebral blood flow and intracranial pressure are relatively stable and do not depend on fluctuations in blood pressure (BP). In children who have suffered hypoxia, the mechanisms of autoregulation of cerebral blood flow are either reduced (moderate hypoxia) or absent (severe hypoxia) and cerebral blood flow depends on blood pressure fluctuations. In addition, in children who have suffered hypoxia, cardiac output is reduced (hemodynamic disturbances and hypoxic damage to the myocardium), blood pressure is reduced, venous outflow from the brain is impaired, and vascular resistance in the brain itself is increased due to hypoxic damage to the endothelium, which leads to a sharp decrease in the lumen of the capillaries .
Against the background of decreased cerebral blood flow and impaired ADH production (asphyxia - excess production, hypoxia - insufficient secretion syndrome) develops vasogenic cerebral edema .
Due to disturbances in cerebral blood flow, the development of vasogenic cerebral edema, cytotoxic edema , caused by the release of “exciting” amino acids, primarily glutamate. Hypoxia reduces the delivery of energy (glucose) to neurons → the synthesis of ATP and creatine phosphates is inhibited → the functioning of cell membrane pumps is disrupted → depolarization of the outer membranes occurs → excessive release of glutamate into the interstitium and insufficient absorption of it by neurons affects neuron receptors, opening channels through which into the cell includes sodium and calcium. Sodium pulls water with it, which leads to the development of cellular edema, and excessive calcium intake leads to the development of cellular calcium necrosis.
J.J. Volpe presents several chains of pathogenesis of perinatal hypoxic-ischemic encephalopathy as a result of intrauterine hypoxia: intrauterine hypoxia → decreased oxygen saturation and increased carbon dioxide saturation, fetal acidosis → intracellular edema → swelling of brain tissue → local decrease in cerebral blood flow → generalized cerebral edema → increased intracranial pressure → generalized decreased cerebral blood flow → necrosis of the medulla.
In case of acute hypoxic changes in the brain, the following stages are morphologically distinguished: Stage I – edematous-hemorrhagic; Stage II – encephalic edema; Stage III – leukomalacia (necrosis); Stage IV – leukomalacia with hemorrhage. The first two stages are curable, the next two lead to irreversible death of neurons. With antenatal (chronic) hypoxia, neuronal degeneration, glial proliferation, sclerosis phenomena, and the formation of cystic cavities at the sites of small foci of necrosis are observed.
Thus, the main links in the pathogenesis of perinatal hypoxic-ischemic encephalopathy are metabolic disorders, the trigger of which is oxygen deficiency, and the directly damaging factors to the brain are products of impaired metabolism.
It must be remembered that the nature of morphological changes in the brain during encephalopathy is influenced not only by the etiological factor and its duration, but also largely by the degree of brain maturity at the time of exposure to unfavorable factors.
In the acute period there are light, medium-heavy And severe severity of the disease.
At mild degree brain lesions, minimal changes are observed in the motor and reflex spheres in the form of a syndrome of neuroreflex excitability, excitation or depression, lasting no more than 7 days. They are characterized by transient moderate or mild changes in the nervous system in the form of emotional and motor anxiety. Changes in motor activity are clearly expressed: against the background of normal or changing muscle tone, spontaneous activity and tremor of the limbs increase, knee and unconditioned reflexes are quickened, and there is a decrease in the main reflexes of the newborn period (protective, support and automatic gait, Moreau, Babkin, Robinson, Bauer). In some cases, horizontal nystagmus, transient strabismus, and occasional floating movements of the eyeballs occur.
It should be taken into account that the presence of neuroreflex excitability or its suppression during the first 5–7 days of life may represent a form of transient adaptation of the newborn’s body in the early neonatal period and this condition should not be considered a pathology. This is due to the fact that during childbirth the fetus experiences increasing transient hypoxia at the time of contractions and greater physical exertion when expelled from the mother’s womb and passing through her birth canal. As a result, there is a long-term excitation of the stress adrenergic and pituitary-adrenal systems, on the one hand, and the stress of the limiting system, the modulation of which is carried out by inhibitory mediators, amino acids and neuropeptides (GABA, serotonin, glycine, opioids). Such tension causes minor transient deviations from the optimal neurological status
Moderate degree The disease is manifested by the following main clinical and neurological syndromes: depression or agitation for more than 7 days, hypertensive, hypertensive-hydrocephalic, convulsive. Children experience a decrease in spontaneous motor activity (lethargy, immobility), persistent changes in muscle tone, which is usually reduced and then selectively increases, often in the flexor muscle group. During the first days of life, spontaneous twitching is often observed, and then generalized convulsive twitching joins them. Basic unconditioned reflexes are reduced or suppressed. The manifestation of focal neurological symptoms is possible: anisocoria, ptosis, convergent strabismus, nystagmus, the “setting sun” symptom.
With hypertension syndrome, general hyperesthesia, “brain scream” are observed, sleep is disturbed, swelling and tension of the large fontanel, and a positive Graefe’s symptom are observed. Hypertensive-hydrocephalic syndrome is accompanied by an increase in head circumference, opening of the sagittal suture by more than 0.5 cm, opening of other cranial sutures, and an increase in the size of the fontanelles. The severity of Graefe's symptom increases, nystagmus and convergent strabismus appear. Muscle dystonia is noted, spontaneous shudders and spontaneous Moro reflex occur.
Somatic disorders are possible in the form of regurgitation, vomiting, marbling and cyanosis of the skin, cardiac arrhythmia, tachypnea, etc.
Neurological disorders in moderate forms usually last for 2–4 months.
Severe degree perinatal hypoxic-ischemic damage to the central nervous system manifests itself as a comatose syndrome and is observed only in cases of severe brain damage. Clinically, cerebral coma is diagnosed: apathy, adynamia, areflexia, muscle hypotonia up to atony, eyes and mouth are often open, rare blinking, orbital nystagmus, absence of sucking and swallowing. At the same time, vegetative-visceral disorders are noted: respiratory arrhythmia, apnea, bradycardia, arterial hypotension, sluggish peristalsis, bloating, urinary retention, severe metabolic disorders. Sometimes progressive intracranial hypertension and convulsions develop. The severity of neurological disorders depends on the depth of the coma.
The serious condition lasts up to 1.5 – 2 months. Serious CNS disorders often remain.
Thus, the acute period of central nervous system damage is characterized by the following leading syndromes: increased neuro-reflex excitability; oppression; excitement; hypertensive; hypertensive-hydrocephalic; convulsive; comatose state.
The recovery period for damage to the central nervous system is characterized by the following syndromes: asthenoneurotic; autonomic-visceral dysfunctions; motor disorders; convulsive (epileptic); hydrocephalic; delayed psychomotor and pre-speech development.
The diagnosis of encephalopathy of newborns and birth traumatic brain injury according to Instruction No. 192-1203 of the Ministry of Health of the Republic of Belarus of 2003 can be used only in the neonatal period, i.e. during the first month of life.
The stages of diagnosing and forming a diagnosis of encephalopathy according to Instruction of the Ministry of Health of the Republic of Belarus No. 192-1203 are presented as follows:
During the neonatal period– indication of cerebral dysfunction: encephalopathy of the newborn, indicating the main cause and nature of brain changes, severity and leading clinical disorders (syndromes).
Example of diagnosis: Neonatal encephalopathy of hypoxic-ischemic origin, moderate severity, hypertensive syndrome.
In infancy(from the 2nd month of life):
Prenosological (syndromic) diagnosis: a list of the main clinical syndromes is provided (delayed motor development; mental retardation; autonomic dysfunction syndrome; benign intracranial hypertension; epilepsy and epileptic syndromes not defined as focal or generalized; convulsive syndrome NOS; other syndromes) indicating the cause of their occurrence - encephalopathy or traumatic brain injury.
Example of diagnosis: Delayed psychomotor development due to encephalopathy (traumatic brain birth injury) of a newborn of hypoxic-ischemic origin.
Nosological diagnosis: the main diseases of ICD - X (cerebral palsy; epilepsy; hydrocephalus; mental retardation, other diseases) resulting from neonatal encephalopathy or intracranial birth injury are given without indicating the cause of their occurrence.
Example of diagnosis: Cerebral palsy due to neonatal encephalopathy.
Diagnosis of perinatal lesions of the fetus and newborn brain is possible by taking into account a complex of anamnestic data (the nature of the course of pregnancy and childbirth, Apgar scores), analysis of the dynamics of the clinical picture and modern instrumental methods for diagnosing the nervous system: cranial transillumination, neurosonography (NSG), Doppler encephalography ( DEG), computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), cerebral scintigraphy (CSG), electroneuromyography (ENMG), electroencephalography (EEG), neuroimmunochemical identification of cerebral proteins (neurospecific proteins - NSP ).
The use of modern advanced technologies in perinatal practice makes it possible to clarify the etiology, pathogenetic mechanisms, clinical and morphological structure of cerebral disorders.
This educational manual outlines syndromes that fairly fully reflect the condition of newborns and on the basis of which one can judge their further prognosis.
The best treatment for perinatal brain damage is prevention and early treatment of intrauterine hypoxia of the fetus and newborn. The main therapeutic measures aimed at the main pathogenetic mechanisms of brain damage are:
prenatal prevention of cerebral hypoxia-ischemia,
creating optimal (comfortable) conditions for nursing with and limiting unnecessary traumatic and irritating influences of the external environment
prevention of infection,
rapid restoration of normal airway patency and adequate breathing,
elimination of possible hypovolemia,
restoration and normalization of systemic and cerebral hemodynamics, by preventing hypotension or hypertension, polycythemia and blood hyperviscosity, hypervolemia,
prevention and treatment of cerebral edema and seizure syndrome,
ensuring carbohydrate homeostasis,
correction of acidosis, hypocalcemia, hypomagnesemia, etc.
Treatment of patients with hypoxic-ischemic encephalopathy in the acute period is carried out in the intensive care ward or in the intensive care unit, followed by transfer, if necessary, to a specialized psychoneurological department.
In the acute period, timely correction of RDS and adequate oxygenation are necessary. The head of a newborn with perinatal damage to the central nervous system should be given an elevated position. In the first 3-5 days they carry out:
1. Antihemorrhagic therapy: 1% solution of Vikasol 1 mg/kg/day (0.1 ml/kg), 12.5% dicinone, etamzilate 10-15 mg/kg/day (0.1-0.2 ml/kg) intravenously or intramuscularly.
2. Dehydration therapy: 1% solution of Lasix 1-2 mg/kg, veroshpiron 2-4 mg/kg/day intramuscularly or intravenously, Manitol 0.25-0.5 g/kg once intravenously in slow drips , in case of hypertensive-hydrocephalic or hydrocephalic syndromes from the 5-7th day of life with normal CBS values, the prescription of diacarb according to the regimen of 15-80 mg/kg/day is indicated. with potassium supplements and alkaline drinking. Depending on the severity of hypertensive-hydrocephalic syndrome, glucocorticoid hormones are used in treatment, taking into account their pronounced membrane-stabilizing and anti-edematous effect - dexamethasone 0.1-0.3 mg/kg/day - 7 days, followed by a dose reduction every 3-5 days by 1 /3.
3. Antioxidant and metabolic therapy: aevit 0.1 ml/kg/day intramuscularly or an oily solution of 5% (0.2 ml/kg/day) or 10% (0.1 ml/kg/day) vitamin E solution ; cytochrome “C” 1 ml/kg intravenously; cerebral angioprotectors - actovegin 0.5-1.0 ml intravenously or intramuscularly, mildronate 10% solution 0.1-0.2 ml/kg/day intravenously or intramuscularly, emoxypine (Mexidol) 1% 0.1 ml/kg/day intramuscularly, 20% solution of Elkar (levocarnitine) 4 – 8 (10) drops. 3 times a day.
4. Antihypoxic (anticonvulsant) therapy: 20% GHB solution 100-150 mg/kg (0.5-0.75 ml/kg) intravenously or intramuscularly, 0.5% seduxen solution 0.2-0, 4 mg/kg (0.04-0.08 ml/kg) intravenously or intramuscularly, phenobarbital 20 mg/kg/day with a transition to 3-4 mg/kg/day intravenously or orally,
5. Correction of central and peripheral hemodynamics: titration of 0.5% dopamine solution, 4% dopamine solution 0.5-10 mcg/kg/min, or dobutamine, Dobutrex 2-10 mcg/kg/min. Patients with low blood pressure, which may be one of the early signs of adrenal insufficiency, should be given intramuscular or intravenous dexomethasone at a dose of 0.5 mg/kg or hydrocotisone 5-10 mg/kg once.
6. Syndromic and symptomatic therapy.
By the end of the early neonatal period, in order to improve the function of the central nervous system, the complex of treatment measures includes nootropic drugs that have both a sedative effect: phenibut (Noofen), Pantogam 20 - 40 mg/kg/day, but not more than 100 mg/day. in 2 doses, and with a stimulating component: piracetam 50-100 mg/kg/day, picamilon 1.5-2.0 mg/kg/day, encephabol 20-40 mg/kg/day in 2 doses, aminalon 0.125 mg 2 times a day day. Cerebrolysate 0.5-1.0 ml IM for 10-15 days (contraindicated in case of convulsive readiness, agitation syndrome), glycine 40 mg/kg/day orally in 2 doses, gliatilin 40 mg/kg have a good neuroprotective-antihypoxic effect. /day intravenously, intramuscularly. In order to improve cerebral circulation in the absence of hemorrhages, the administration of trental, cavinton, vinpocetine 1 mg/kg/day intravenously, tanakan 1 drop/kg 2 times a day, sirmeon 0.5-1.0 mg/kg/day orally is indicated in 2 doses. For disorders accompanied by increased muscle tone with signs of spasticity, muscle relaxant drugs are prescribed - mydocalm 5 mg/kg/day, baclofen, trapofen 1 mg/kg/day 2-3 times a day. To improve the conduction of excitation at neuromuscular synapses and restore neuromuscular conduction, treatment includes vitamins B1.6 0.5-1.0 ml intramuscularly for 10-15 days, galantamine 0.5% 0.18 mg/kg /day, proserin 0.05% 0.04-0.08 mg/kg/day intramuscularly 2-3 times a day, sometimes dibazol is prescribed 0.5 - 1.0 mg orally 1 time a day.
Treatment of neonatal encephalopathy should be comprehensive and staged. An integrated approach involves early (from 3 weeks of the child’s life) prescription of exercise therapy and therapeutic massage (stimulating, relaxing), physiotherapeutic procedures, the choice of which depends on clinical manifestations (with high muscle tone - sinusoidal simulated currents, thermal procedures, such as paraffin and ozokerite applications), if low - electropharesis with calcium on the spine area, etc. To stimulate pre-speech development and fine motor skills, speech therapy classes are conducted from the end of the neonatal period.
Treatment of newborns with hypoxic-ischemic encephalopathy should not be polyprogrammatic. Early protection of the newborn's brain and properly selected drug therapy, taking into account modern neuroimaging research methods, help reduce the severity of cerebral consequences and the degree of disability in children who have suffered from hypoxic-ischemic encephalopathy of newborns.
Prevention of newborn encephalopathy includes a set of measures for antenatal protection of the fetus, careful management of childbirth, early diagnosis and rational treatment of hypoxic, traumatic conditions of the fetus and newborn.
Applications 1
INDICATORS OF QUALITY IN HEALTHY CHILDREN
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Index |
Characteristics of the indicator | |
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Acidity index |
7,35-7,45 |
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Reflects the concentration of carbon dioxide dissolved in blood plasma |
(4.3-6 kPa) |
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Reflects the concentration of dissolved oxygen in the blood |
6 0-80 mmHg |
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Concentration of total CO in blood (plasma) 2 |
22.7-28.6 mmol/l |
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True plasma bicarbonate - HCO concentration 3 in plasma |
19-25 mmol/l |
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Standard plasma bicarbonate |
20-27 mmol/l |
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Buffer base concentration |
40-60 mmol/l |
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Base excess or deficiency |
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