Recommendations for the treatment of cerebrovascular disorders in children and adolescents. Circulatory failure Cerebrovascular accident in newborns: causes and symptoms

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Violations cerebral circulation(NMC) are much less common in children than in adults. In childhood, atherosclerotic lesions of cerebral vessels do not occur, there are no vascular changes characteristic of hypertension, cerebral vessels are elastic, and the outflow of blood from the cranial cavity is not impaired. Thus, the causes of cerebral blood supply disorders in children differ from those in adults.

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Among the causes of vascular disorders in children are the following factors: Blood diseases. Traumatic lesions of blood vessels and their membranes. Pathology of the heart and disruption of its activity. Infectious and allergic vasculitis (rheumatism). Diseases with symptomatic arterial hypertension. Vasomotor dystonia (angiospasms, perverted vascular reactivity). Diseases of the endocrine organs. Hypertonic disease. Children's form of atherosclerosis of cerebral vessels. Toxic damage to the blood vessels of the brain and its membranes. Compression of brain vessels due to changes in the spine and tumors. Congenital anomalies cerebral vessels.

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The nature of damage to cerebral vessels in children can be as follows: Vascular thrombosis Reduced blood flow due to narrowing, bending, compression of a vessel by a tumor Rupture of the vascular wall due to injury, hemorrhagic diathesis, aneurysms. Increased permeability of the vascular wall during inflammatory changes in blood vessels and blood diseases. Embolism

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The basis of most vascular disorders of the brain is hypoxia - a lack of oxygen in the tissues.

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The causes of cerebral obstruction in newborns are birth asphyxia, birth trauma, congenital heart disease, cerebral vascular malformations, intrauterine infection. Asphyxia during childbirth can be caused by premature abruption of the placenta, rupture of the umbilical cord vessels, the baby being entangled in the umbilical cord, massive blood loss, placenta previa, as well as disturbances in the movement of the child along the birth canal, some obstetric manipulations (for example, the application of forceps.) Treatment of hypoxia of the newborn is a difficult task. . Immediately after birth, resuscitation measures are carried out (opening the upper respiratory tract, tactile stimulation and artificial respiration). Further therapy depends on the cause of hypoxia: in case of prematurity, surfactants are administered, in case of traumatic brain injury - decongestant therapy, nootropic treatment, in case of infection - antibacterial therapy.

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Brain hypoxia in a newborn baby is a dangerous condition that can lead to mental and mental impairment. physical development Particularly often susceptible to asphyxia during childbirth is a fetus that has experienced intrauterine hypoxia during a complicated pregnancy: toxicosis, prematurity or postmaturity, maternal diseases during pregnancy - infectious, as well as some others (for example, cardiovascular, drug addiction, smoking, alcohol abuse.)

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Cerebrovascular accidents can be acute or chronic. Acute Chronic Develops gradually, progressing slowly over several weeks, months and even years. 1, 2A 2B, 3 Symptoms that appeared in a short period of time - in a few minutes, hours or 1-2 days. There are 3 degrees of Strokes Crises

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The clinical picture is dominated by general cerebral symptoms: 1. Short-term loss or confusion of consciousness. 2. Headaches. 3. Dizziness. 4. Epileptiform seizures. 5. Autonomic disorders in the form of sweating, cold extremities, paleness or redness of the skin, changes in pulse and breathing. The following focal symptoms may occur: 1. Hemiparesis. 2. Hemihypesthesia. 3. Facial asymmetry. 4. Diplopia. 5. Nystagmus. 6. Speech disorders. Focal symptoms depend on the localization of dyscirculation. It lasts for several hours.

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There are generalized and regional cerebral vascular crises Discirculation in the pool carotid arteries manifested by the following symptoms: Transient hemiparesis and hemiplegia. Hemihypesthesia. Paresthesia. Short-term speech disorders. Visual impairment. Visual field impairment. When there is discirculation in the vertebrobasilar system, the following occurs: Dizziness. Nausea. Vomit. Noise in the ears Unsteadiness when walking. Nystagmus. Loss of vision. Generalized vascular crises often develop against the background of an increase or decrease in blood pressure. In this case, general cerebral and autonomic symptoms. Focal ones are expressed to a much lesser extent. In regional vascular crises, discirculation develops in the carotid artery basin or the vertebrobasilar system.

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In childhood, the cause of paroxysmal cerebrovascular accidents is the syndrome of autonomic dystonia with angiospastic disorders. It occurs more often in girls puberty and manifests itself in the form of periodic attacks of headaches, dizziness, nausea, and fainting. These conditions occur with excitement, overwork, in a stuffy room, or with a sudden change in the position of the body. Noted poor tolerance riding in transport. Such children are characterized by severe vegetative symptoms, emotional lability, and unstable blood pressure.

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Stroke is extremely rare in children. Most often, its cause at this age is thromboembolism due to heart defects, hemorrhage due to blood diseases. There are ischemic and hemorrhagic strokes.

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Ischemic stroke occurs as a result of thrombosis, embolism, or narrowing of blood vessels in the brain. According to the period of origin, childhood strokes are divided into: perinatal or intrauterine; strokes that occurred in the newborn phase; PMC under the age of 18 years. Treatment and diagnosis vary depending on the age group. The most common are considered to be cerebrovascular accidents (cerebral circulatory disorders) of the first two age groups: statistics show the probability of this event is 1 in 4,000 thousand children born. The latter group has a rate of 1 case per 100,000 people. The severity of a childhood stroke is determined by its location in the brain.

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Symptoms of the perinatal period Signs of the disease during this period appear immediately after birth within three days: The child is restless, anxious for no reason; Monotonous constant crying; No sleep, while awake – lethargy, indifferent attitude to the world around you; Any, even weak stimulus (sound, touch) causes a violent reaction; Sucking and swallowing reflexes are impaired, frequent regurgitation; Constant tension in the neck muscles, other muscles are either constantly tense or relaxed, frequent cramps of the limbs; Strabismus suddenly appears and intensifies.

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Possible reasons for the gap blood vessel in the child’s brain: traumatic brain injury, subsequently leading to the destruction of brain vessels; aneurysm (in other words, weakness in the artery wall); vitamin deficiency, intoxication; arterial hypertension; a brain tumor; maternal alcoholism or drug addiction; blood diseases. (hemophilia, leukemia, hemoglobinopathy, aplastic anemia). Hemorrhagic stroke in children occurs due to the rupture of a blood vessel in the brain. In this case, blood flows into the brain, causing damage. This type of cerebrovascular accident occurs less frequently in children.

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Ischemic stroke in children (cerebral infarction) is more common than hemorrhagic stroke. The main causes of this type of stroke are the following: lack of oxygen during childbirth; transferred infectious diseases(chickenpox, meningitis); Congenital heart defect; bacterial endocarditis; heart valve prosthesis; cerebral vasculitis (typical for children with autoimmune diseases); diabetes; anomalies of blood vessels, veins, arteries, capillaries.

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At the same time, there are reasons related to the problems the mother suffered during pregnancy or childbirth: increased blood pressure which can cause swelling of the limbs; premature discharge of amniotic fluid (more than a day before birth); narcotic or alcohol addiction; detachment of the placenta, which is responsible for saturating the baby with oxygen in utero.

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Symptoms of childhood strokes are similar to those seen in adults. Among them are sudden weakness, clouding of consciousness, slurred speech, and sudden temporary deterioration of vision. A baby who has suffered a stroke in the perinatal period often does not show any special symptoms for a long time after birth. The development of such a child may proceed normally, but at a slower pace than in other children. In cases of serious intrauterine strokes, the baby may subsequently experience seizures, the severity of which varies greatly.

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Bleeding in the brain can be parenchymal (into the substance of the brain), subarachnoid, epidural, subdural, intraventricular. Symptoms of hemorrhagic strokes are as follows: Apoplectiform onset with acute development cerebral coma. Cyanosis and purplish-red tint of the skin. High blood pressure. Breathing problems. Leukocytosis in the blood. Reduced blood viscosity. Reduced blood clotting properties. Blood in the cerebrospinal fluid.

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Stroke suffered by young children manifests itself as follows: problems with appetite; spasms of any limb; apnea in a child - breathing problems; developmental delay (young children may, for example, start crawling later than expected). Older children may be prone to seizures - sudden paralysis whole body or limbs. Inability to move, deterioration in concentration, lethargy, slurred speech - these symptoms will allow parents to recognize IUD in a teenager. If one of the the following symptoms, you must immediately consult a doctor or call an ambulance: headaches, possibly with vomiting; slurred speech, problems with the speech apparatus, previously absent seizures; sudden loss of memory, concentration; problems breathing or swallowing; preferential use of one side of the body (this may be due to damage to one part of the brain); paralysis.

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Rules of the “Therapeutic Window” The first three hours after the onset of symptoms similar to a stroke in children is the time when the medical care and treatment provided will give the maximum result. It is necessary to remember this by acting immediately and in a timely manner. A few simple steps that will help identify a stroke: Pay attention to the smile - is it symmetrical, does it look natural. If the baby smiles on only one half of his face, this is the first sign of a possible stroke. Ask the child to raise his arms up: if there is weakness in one of the limbs, the inability to perform this action is the second sign. Say a sentence and ask them to reproduce it. At the same time, pay attention to whether the baby completely repeated what he heard, whether there is a speech disorder or slurredness. If he failed the task or had difficulty pronouncing, this is the third sign of a possible stroke.

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Methods for diagnosing childhood stroke Diagnosis of brain disease is impossible without modern equipment and qualified specialists Computed tomography - will see the area of ​​injury and its intensity; Magnetic resonance imaging clarifies the situation and provides facts for choosing the right treatment; A cerebral arteriogram will give a picture of vascular damage; for this, a dye is injected into the blood; An echocardiogram examines the functioning of the heart, because this is where the causes of blood clots are located; Blood is taken for a clotting test; Puncture spinal cord. If hemorrhage has already been established, then spinal cord puncture to check for blood in the tissues will be unnecessary. It is justified only to determine the nature of the infection of the nervous system.

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statistic:

Brain hypoxia in newborns

Brain hypoxia in newborns is oxygen starvation of the child during pregnancy and childbirth. Among all pathologies of newborns, this condition is recorded most often. Very often, due to hypoxia of a child, a serious threat to his health and life occurs. Severe cerebral hypoxia in newborns often leads to child disability or even death.

Due to hypoxia, both the baby’s entire body as a whole and individual tissues, organs and systems suffer. Hypoxia occurs due to long delay breathing, asphyxia of the fetus, diseases of the newborn, making breathing defective, low oxygen content in the air.

Due to hypoxia, a newborn baby develops irreversible disturbances in the functioning of vital organs and systems. The first to respond to a lack of oxygen are the heart muscle, central nervous system, liver, kidneys, and lungs.

Causes of cerebral hypoxia in newborns

The state of fetal hypoxia can be caused by one of four reasons:

1.Serious illnesses of the mother. pathological course of pregnancy and childbirth, maternal hypoxia. Baby hypoxia can be caused by premature placental abruption, maternal bleeding, maternal leukemia, maternal heart disease, lung disease, severe intoxication.

2. Pathology of umbilical cord blood flow. uteroplacental circulation: umbilical cord collisions, entanglement, breech presentation of the fetus with umbilical cord clamping, rupture of umbilical cord vessels, trophic disorders in the placenta during post-term pregnancy, prolonged labor, rapid labor, instrumental extraction of the child.

3. Genetic diseases of the child. Rhesus conflict of mother and child, congenital heart defects in a newborn, severe anomalies of fetal development, infectious diseases of a child, intracranial injuries of a newborn.

4. Asphyxia of the newborn. blockage of the airways.

Symptoms of hypoxia in a newborn.

A child who has suffered hypoxia experiences tachycardia, which is then replaced by bradycardia, arrhythmia of heart sounds, and heart murmurs. Meconium is found in the amniotic fluid. At the beginning, the child makes many movements in utero, which then weaken. The child develops hypovolemia, multiple blood clots and small hemorrhages in the tissue form.

In a state of hypoxia, the fetus gradually accumulates critical level carbon dioxide in the blood, which begins to irritate the breathing centers in the brain. The child still performs breathing movements in utero - aspiration of the respiratory tract with amniotic fluid, blood and mucus occurs. At birth, a child who has aspirated may experience pneumothorax during the first breath, which is life-threatening.

At the birth of a child who has suffered hypoxia or received aspiration, a set of resuscitation measures is required aimed at clearing his airways and delivering oxygen to the baby’s airways.

In order to prevent the occurrence of hypoxia in a child and take timely measures, diagnostic methods such as electrocardiography of the child, phonocardiography, amnioscopy, and blood testing of the newborn are used.

Treatment of hypoxia in newborns, preventive measures

If there is a suspicion of fetal hypoxia, doctors make a decision to speed up the process of childbirth, use auxiliary methods of obstetric care (obstetric forceps, C-section etc.). Immediately after birth, the child should receive oxygen and drug therapy against the manifestations of hypoxia.

Immediately after birth, the baby is placed in a chamber with access to oxygen; in severe cases, birth is carried out in a pressure chamber.

During childbirth, drugs are used that improve placental blood circulation and metabolic processes in the child’s body.

The condition of the newborn baby is assessed using the Apgar score. To do this, the heartbeat, breathing, condition of the newborn’s skin, muscle tone and reflex excitability are assessed using a 0-1-2 point system. The norm is 8-10 points, while the ideal score is 10 points. Average hypoxia is 5-6 points, severe hypoxia of a newborn is estimated at 1-4 points. Indicator 0 points – the child is stillborn.

In case of hypoxia of a newborn, a complex of resuscitation measures is used, clearing the child’s respiratory tract from mucus, warming the child’s body and artificial respiration, introducing nutrient solutions of glucose, calcium gluconate, etimizol, sodium bicarbonate into the baby’s umbilical cord vessels, intubation, external cardiac massage. Resuscitation measures are carried out continuously until the child’s condition improves.

Subsequently, a baby who suffered hypoxia at birth should be continuously monitored by pediatricians to monitor the dynamics of development.

Measures to resuscitate the child are stopped if spontaneous breathing does not appear after 10 minutes of intensive resuscitation.

A long-term state of hypoxia threatens severe disability of the child, delaying his mental and physical development.

Prevention of hypoxia in a newborn should begin at the beginning of pregnancy, for this it is necessary to prevent toxicosis of pregnancy in the mother, treat diseases and correct pathological conditions that arise during pregnancy, prevent complications of pregnancy and childbirth in a timely manner, conduct childbirth correctly, and take timely measures to speed up labor activity or take additional measures for obstetric care.

Brain hypoxia in newborns is not a disease, but a pathological condition that can be prevented and measures can be taken to eliminate the consequences for the child’s health, therefore pregnancy and childbirth should be under medical supervision.

Causes of cerebral ischemia in a newborn

Cerebral ischemia in a newborn develops due to oxygen starvation. which occurs with poor cerebral circulation. To be more precise, only a condition in which an insufficient amount of oxygen enters the brain is called hypoxia, and a complete cessation of oxygen supply to the brain is called anoxia.

The development of cerebral ischemia in a newborn is a serious problem, since it leads to irreversible consequences; drugs have not yet been found that can help a little person cope with this serious disease without dangerous consequences for the body. Existing methods of treating this pathology in newborns are not effective enough.

Causes of development of cerebral ischemia

The causes of ischemia in newborns and adults differ. In adults, the cause of cerebral ischemia can be atherosclerosis of cerebral vessels - this is a disease in which fatty deposits build up on the walls of blood vessels, gradually narrowing their lumen. Most often, cerebral vascular ischemia occurs precisely because of atherosclerosis, less often due to other reasons that caused thrombosis of cerebral vessels.

Cerebral ischemia in newborns usually develops as a result of hypoxia, which can occur during pregnancy or childbirth. You should especially be wary of the development of this disease in a child of mothers over 35 years of age.

Causes of cerebral ischemia in premature infants:

• Multiple pregnancy;
• Placenta previa or abruption;
• Late toxicosis in severe form, which is accompanied by the appearance of protein in the urine and increased pressure;
• Various maternal diseases;
• Violation of the uteroplacental circulation, which leads to the necrosis of some areas of the newborn’s brain;
• The birth of a child earlier or later than the due date;
• Defects of the baby's cardiovascular system.

Due to oxygen deficiency, quite complex pathological processes occur in the baby’s brain:

• Metabolic disorders - from mild (the changes are still reversible) to severe (the onset of irreversible changes in the brain substance followed by the death of neurons);
• Death of brain neurons;
• Development of coagulation necrosis in the medulla.

Symptoms of cerebral ischemia in newborns:

• Syndrome of increased neuro-reflex excitability - with this pathology, there is a change in muscle tone (decreased or increased), tremors of the arms, legs and chin, as well as shuddering, increased reflexes, restless sleep and crying for no apparent reason;
• CNS depression syndrome - it is characterized by decreased tone absolutely all muscles of the body, decreased motor activity, weak swallowing and sucking reflexes, sometimes even facial asymmetry and strabismus can be observed;
• Hydrocephalic syndrome – accompanied by an enlarged head; When this syndrome occurs, a liquid called cerebrospinal fluid accumulates in the spaces of the baby’s brain, and this process is also accompanied by an increase intracranial pressure. it is for this reason that the size of the head increases;
• Comatose syndrome is a severe unconscious state of a child, accompanied by a complete lack of coordination, for which the brain is responsible;
• Convulsive syndrome - seizures are observed, accompanied by twitching of the child’s head and limbs, shaking of the body and other manifestations of seizures.

Degrees of cerebral ischemia

In medicine, there are three degrees of this disease:

With mild ischemia this disease the child may experience an excessively depressed or excited state, which persists for 5-7 days of his life.

Moderate disease is accompanied by convulsions that are observed in the baby a long period time.

Newborns with severe cerebral ischemia are placed in the intensive care unit.

It is worth noting that mild to moderate hypoxic brain lesions in newborns are very rarely considered the cause of the development of neurological disorders. But if they do appear, doctors characterize them as functional. In addition, it has been proven that such disorders completely disappear after timely and adequate therapy.

If the brain is significantly damaged, then due to the development of severe ischemic damage to the brain, that is, structural, organic damage to the central nervous system inevitably occurs in the child’s body, which in turn entails the occurrence of ataxia, focal seizures, impaired vision and hearing, and also delayed psychomotor development.

Treatment

Modern pediatrics is making significant progress in the treatment of cerebral ischemia in newborns.

Treatment of chronic cerebral ischemia in newborns includes restoration of blood circulation in the brain and timely creation of all the conditions necessary for the full functioning of areas of the brain undamaged by the disease, which includes the active intake of antioxidant complexes.

To treat the initial stage of this disease, a fairly simple course of treatment is used; most often, doctors do not prescribe any medicines, getting by with regular massages. For moderate and severe stages of the disease, therapy is selected by the doctor individually for each child.

Prognosis and consequences of the disease

The prognosis depends on how severe the infant’s cerebral ischemia is, as well as on the presence of concomitant pathologies and the effectiveness of rehabilitation procedures prescribed by the attending physician.

The consequences of the disease can be quite severe, so treatment should always begin as quickly as possible.

Possible consequences of chronic cerebral ischemia in newborns:

• Headache;
• Constant irritability;
• Mental retardation;
• Attention deficit, learning difficulties;
• Epilepsy;
• Sleep disturbance;
• Silence.

Only the experienced doctor. He will immediately take all necessary measures to minimize losses or completely eliminate brain hypoxia in a newborn.

Cerebral ischemia in newborns

The main steps to establish a diagnosis include:

• Physical examination: assessment of respiratory and cardiac functions, mandatory analysis of the child’s nervous status;
• Duplex ultrasound examination of arteries to analyze blood circulation in vessels;
• Angiography to detect disorders in the functioning of the brain: thrombosis, narrowing of the arteries, aneurysms;
• MR angiography and CT angiography;
• Additionally, ECG, ECHO-CG, X-ray, and blood tests are performed.

Treatment of ischemia in newborns

Despite significant advances in the treatment of ischemia in newborns, there are still no effective means of eliminating the disease.

The main goal of treatment is to restore blood circulation to the blood vessels to ensure normal functioning of the damaged areas of the brain.

In the mild stage of the disease, the treatment method is very simple and accessible to everyone - it is a regular massage without the use of any medications. In the case of more complex stages of the disease, therapy is selected according to individual characteristics and always according to the indications of a medical specialist.

Usually, medications are prescribed to stimulate brain function, normalize the circulatory system, and medications to restore and strengthen protective forces the child's body.

Folk remedies are widely used in the treatment of cerebral ischemia, and they must be combined with basic medications. Traditional methods can relieve the symptoms of the disease well, but only medications and surgery can eliminate the cause.

Traditional methods of treatment are not used for newborn babies.

You can find out Dr. Komarovsky’s opinion on intracranial pressure in infants here.

Possible consequences of the disease for newborns

The prognosis and consequences of ischemia depend entirely on the stage and severity of ischemia. In addition, existing pathologies and the correctness of treatment methods and rehabilitation methods are of great importance.

It is not excluded severe consequences, so treatment should begin as quickly as possible.

Cerebral ischemia in newborns can cause:

• Headaches;
• Restless sleep and irritability;
• Difficulties in communication and learning;
• Mental retardation;
• In difficult cases - epilepsy.

Ischemia can even lead to death. You can avoid death if you seek medical help right away. Only a doctor will make an accurate diagnosis and recommend appropriate treatment.

The most important thing is that it is necessary to engage in prevention, preserving the health of the child for many years.

Disease prevention

You should think about your health from early childhood. After all, the disease can be fatal.

To avoid the development of ischemia, the following actions should be taken:

• Do exercises regularly;
• Walk a lot in the fresh air;
• Eat right, try to stick to your diet;
• Quit smoking and other unhealthy habits;
• Avoid stress and have a positive attitude towards life.

These rules are very simple, and following them will protect anyone from dangerous diseases. In addition, a pregnant woman should regularly visit a gynecologist, treat all diseases in a timely manner, undergo routine ultrasounds, eat right, walk a lot in the fresh air and not be nervous.

Observing simple rules, you can give birth to a healthy baby.

The video discusses one of the main causes of ischemia in newborns - fetal hypoxia during pregnancy:

Disturbances of cerebral circulation and acute disorders of cerebrospinal fluid circulation directly related to vascular changes are in most cases the same type of reaction of the newborn’s body to various causal mechanisms that cause changes in the blood vessels of the brain. The causes of disturbances in cerebral blood and liquor circulation can affect the fetus in utero throughout the entire prenatal period or the newborn in the early neonatal period.

The most common cause of cerebrovascular accidents is chronic intrauterine hypoxia, which is based on various factors leading to pathological changes in metabolic and respiratory function placenta. Changes in the placenta often occur under the influence of acute (especially viral) and chronic infections and intoxications. Late toxicoses of pregnancy are of greatest importance (E. Govorka, 1970; S. M. Becker, 1970, etc.).

Directly during childbirth, impaired blood and liquor circulation may result from acute asphyxia(hypoxia) or birth trauma.

Cerebrovascular accident

With birth trauma, mechanical damage to the fetal brain tissue occurs during childbirth. Damage to tissue structures can be in the form of ruptures, crushing, as well as local circulatory disorders with edema, venous stagnation, stasis, thrombosis and bleeding (I. S. Dergachev, 1964; Yu. V. Gulkevich, 1964). The cause of mechanical damage may be an anatomical or clinical discrepancy between the sizes of the fetal head and the mother’s pelvis, incorrect position of the fetus; Damage to the skull is often observed when breech presentation, rapid childbirth. Mechanical damage may be a consequence of complicated obstetric operations - application of obstetric forceps, vacuum extraction of the fetus, etc.

Depending on the severity of the damage, skull trauma results in functional changes or causes irreversible morphological lesions (foci of ischemic necrosis, extensive hemorrhages, etc.).

Morphological picture of vascular changes in the central nervous system with all of the above causal factors most newborns have the same type. Three phases can be observed in the morphological picture. The first phase of reversible vasospasm, caused by excitation of vasoconstrictors, leads to overproduction of cerebrospinal fluid and short-term initial symptoms of cerebral edema.

In the second phase, paralysis of vasoconstrictors and excitation of vasodilators develops. Discirculatory vascular paralysis develops with stasis, symptoms of cerebral edema, pronounced liquorodynamic disturbances and pinpoint diapedetic hemorrhages.

The third phase is characterized by significant cerebral edema and severe vasomotor disturbances with hemorrhages in the membranes and substance of the brain (S. L. Keilin, 1957).

Cerebral hemorrhages in newborns are often of venous origin. Depending on the location, there are: a) epidural hemorrhages (between the inner surface of the skull bones and the dura mater), b) subdural with displacement of bones and stretching of the sinus transversus et sinus sagittalis, often with damage to the venous vessels leading to a tear or rupture of the cerebellar tentorium, c) subarachnoid - the most common (up to 55%), d) in the ventricles and brain matter, and also e) mixed with different localization.

Actually traumatic lesions Radiation trauma to the skull most often results in subdural hemorrhages, ruptures of the sinuses and cerebellar tentorium.

Clinic. Depending on the clinical manifestations and morphological changes There are three degrees of cerebrovascular accident (V.I. Tikheyev, 1953).

In case of cerebrovascular accident of the first degree, clinical manifestations are characterized by mild and unstable neurological symptoms: a moderate decrease or increase in spontaneous motor activity, some revival or suppression of unconditioned reflexes, muscle dystonia, transient Graefe's symptom, small-scale tremor of the limbs. As a rule, these phenomena disappear by the 3-4th day after birth.

An analysis of the dynamics of the condition of children with stage I cerebrovascular accident shows that these conditions are based on liquorodynamic disorders with phenomena of cerebral edema that linger for

3-4 days. Moderate cerebral edema is also observed in healthy newborns during the process of vascular adaptation of the brain, which is revealed by rheoencephalography on the first day after birth. In this case, the symptoms of edema decrease on the 2nd day of life with complete normalization by the 3rd day.

4th day after birth (Yu. A. Yakunin, A. S. Rykina,

In children with cerebrovascular accidents

I degree cerebral edema lingers correspondingly longer, despite the disappearance of clinical symptoms. Although these changes are functional in nature, they can leave behind increased "neuro-reflex excitability" (Yu. Ya. Yakunin, E. O. Yampolskaya,

1974) . In this case, it is expedient to speak of a hypertensive syndrome even with the short duration of intracranial hypertension, which determines the treatment tactics.

In case of violation of cerebral circulation of the II degree, the clinical picture shows marked anxiety, sleep disturbance, increased motor activity, transient hypertonicity, revitalization of tendon reflexes, tremor, spontaneous Moro reflex, Graefe's symptom.

In other cases, general lethargy, adynamia, and a decrease in unconditioned reflexes and muscle tone predominate. Against the background of excitement or depression, short-term clonic convulsions may be observed.

In such children, horizontal and vertical nystagmus often occurs, convergent (less often divergent) strabismus appears, and the hands acquire the position of “seal feet.” The limbs are in an extensor position, as is the head (with a tendency to hyperextension). When trying to bend the head, there is anxiety and a monotonous (hydrocephalic) cry, pulsation, and sometimes bulging of the fontanelles. In addition to Graefe’s symptom, the “setting sun” symptom appears (Fig. 65). Such symptoms suggest hypertensive-hydrocephalic syndrome.

In the central nervous system, in case of cerebral circulation disorder of the second degree, more pronounced cerebral edema, discirculatory vascular paralysis and small-point hemorrhages are noted. There may often be local swelling in the area of ​​the third and fourth ventricles, which in the clinic is accompanied by attacks of secondary asphyxia.

Stage III cerebrovascular accident is characterized by a very serious condition of the patient with pronounced agitation, a high-pitched “brain” scream, “eyes wide open” syndrome, strabismus, anisocoria, tonic or tonic-clonic convulsions. In some patients, increased excitability is replaced by adynamia, areflexia, vertical nystagmus, the symptom of “floating eyes”, and impaired pupillary reactions; convulsions turn into opisthotonus; Frequent respiratory and cardiac disorders.

With a pronounced extensor posture of the limbs, the arms take a vicious pronator position, the hands are in the “seal’s paw” position - open, sometimes with horizontal opposition of the fifth finger; legs with a tendency to cross with a varus position of plantar or dorsiflexed feet.

The severity of the condition is due to severe swelling and hemorrhages in the membranes and substance of the brain, pronounced ischemic changes (Fig. 66). With cerebral circulation disorders of the third degree, children often die due to symptoms of general vascular insufficiency - shock. In survivors, focal disturbances often appear against the background of general symptoms.

In the clinic of cerebral circulatory disorders in newborns in the first days after birth, general symptoms predominate and differentiate cerebral edema from intracranial hematoma very hard.

The presence of symptoms of intracranial hypertension in a child in combination with general lethargy, suppression of newborn reflexes and repeated tonic convulsions, indicating phenomena of irritation of the brain stem structures, makes it possible to suspect subarachnoid hemorrhage (Fig. 68). The appearance of asymmetry in the motor activity of the limbs against this background, even without pronounced hemiparesis, suggests hemorrhage into the brain.

With a subdural hematoma, symptoms appear more often after an apparent “clear interval”. Characterized by attacks of secondary asphyxia, tonic or tonic-clonic convulsions (sometimes local in the limbs of one side), anisocoria, pulse asymmetry with a tendency to bradycardia on the contralateral side. Hemiparesis is detected less frequently and later, after 2-3 days.

In a maternity hospital and especially in a hospital, it is necessary to carry out a differential diagnosis between cerebrovascular accidents that occur during childbirth as a result of asphyxia or mechanical birth trauma (or a combination thereof) in a normally developing child in utero, and the layering of asphyxia on various intrauterine pathologies. Dysraphic stigmas - incorrect relationship between the head and facial skeleton, deformation in structure ears, syndactyly, etc., allow speech to a certain extent

about an unfavorable embryonic period. A large head size at birth with a tendency to rapid growth from the first days after birth, frequent repeated polymorphic convulsions, pronounced manifestations of spasticity in the limbs immediately after birth -■ allow one to think about intrauterine meningoencephalitis or a disorder in the formation of the brain and its cerebrospinal fluid systems due to chronic hypoxia in the fetal period.

Often, intrauterine cerebral insufficiency is detected in children with signs of intrauterine malnutrition.

In newborns with clinical signs of cerebrovascular accident, various additional research methods are currently used for differential diagnosis: spinal tap, transillumination (diaphanoscopy), electroencephalography, rheoencephalography and echoencephalography, examination of the condition of the retina and fundus.

Particular attention should be paid to spinal puncture and changes in the cerebrospinal fluid. Repeated convulsions are a direct indication for puncture in the maternity hospital. When performing a puncture, the fluid pressure is checked, which normally in newborns varies from 80 to 100 mm of water. Art.

In the unchanged cerebrospinal fluid of newborns, the number of cellular elements in 1 mm 3 ranges from 5 to 15-20, protein - from 0.165 to 0.33%, sugar, as a rule, no more than 0.5 g/l with a tendency to decrease. In premature infants, the character of the cerebrospinal fluid does not differ from that of full-term infants (Yu. N. Baryshnev, 1971). With subarachmoidal hemorrhage, fresh and leached red blood cells are found in the cerebrospinal fluid; the number of leukocytes may be increased with a change in their composition (the appearance of neutrophils), which sometimes makes differential diagnosis with the initial symptoms of purulent meningitis difficult. The appearance of the cerebrospinal fluid is characteristic: with massive hemorrhage, the color of meat slop.

Transillumination is simple and available in any maternity hospital. The examination technique involves illuminating the skull bones with a special lamp in a dark room. Normally, the glow around the lamp is in the form of a corolla, in the area of ​​the frontal and parietal bones does not exceed 1.5-2 cm, in the area of ​​the occipital bones it is 1 cm. When edema occurs, the corolla increases, which indicates overproduction of cerebrospinal fluid in the subarachnoid space.

Malformations of the brain (porencephaly, atrophy of various parts of the brain structures, progressive cerebral hydrocele, etc.) are detected by luminescence disturbances in the form of beam penetration into the other hemisphere, luminescence spreading diffusely throughout the skull, etc.

If cerebral circulation is impaired, changes in brain function can be detected using electroencephalography. Depending on the severity of vascular and cerebrospinal fluid changes, the depth of cerebral edema and local damage on the EEG, varying degrees inhibition of bioelectrical activity of the brain with the appearance of slow, high-amplitude waves. The presence of convulsive syndrome is confirmed by paroxysms of generalized both acute and slow high-amplitude waves (Yu. A. Yakunin,

1974) . The appearance of such waves without convulsive syndrome should raise alarm bells regarding intrauterine pathology.

Using rheoencephalography, you can diagnose the state of blood supply to the blood vessels of the brain, their tone, as well as intracranial hemorrhages. A normal rheoencephalogram of a newborn at the end of the neonatal period has a steep anacrotic, moderate roundness of the apex, a rapid descent of the catacrotic and a dicrotic tooth (K-V. Chachava, 1969). The rheographic wave norm is 0.149 Ohm (average amplitude).

Brain edema with increased blood supply to the cerebral vessels is reflected in the rheoencephalogram. The most clear changes are detected in hemorrhages - subarachnoid hemorrhage is characterized by a distinct lengthening of the anacroga, an increase in the convexity or flatness of the catacrota (sometimes with interhemispheric asymmetry). With parenchymal hemorrhage, interhemispheric asymmetries increase - a decrease in blood pressure in one hemisphere. These changes are associated with difficulties in arterial inflow and venous outflow (Yu. A. Yakunin, I. A. Rykina, 1973).

Echoencephalography is a relatively new method for diagnosing cranial formations. When analyzing echo-encephalograms, the displacement of the M-echo signal reflected from the midline structures of the brain is taken into account; ventricular index; position and shape of the M-echo with the number of additional pulses and hemispheric asymmetry of the pulses; the quantity and quality of echo pulsations (reflected signals) with an estimate of the signal amplitude as a percentage (I. A. Skorunekiy, 1968).

In healthy newborns, M-echo shift is not observed; ventricular index is 1.6-1.8; the amplitude of echo pulsations is 30%, the growth coefficient is 0.18 + 0.01 (N. S. Kare, 1974).

Ultrasound echolocation can diagnose local and generalized cerebral edema, hypertensive-hydrocephalic syndrome, and various types of intracranial hemorrhage. According to N. S. Kare, in children with hemorrhages there is a displacement of the midline structures of the brain (M-echo) by 1-6 mm, most often in the projection zone III ventricle. Subarachnoid-parenchymal hemorrhages practically do not cause displacement (1.5-2 mm); with a subdural hematoma, the M-echo moves by 4-5 mm.

Treatment of cerebrovascular accidents begins along with resuscitation measures in the delivery room - ensuring adequate breathing and preventing secondary asphyxia.

Normalization of cerebral circulation is possible only if blood circulation is normalized in general. At pronounced violations hemodynamics, treatment is carried out according to the principles set out in the general part of this book.

To restore hemo- and liquorodynamics of the brain, dehydration therapy is carried out depending on the indications. In severe cases, craniocerebral hypothermia is indicated, which reduces the brain's need for oxygen, reduces edema, improves blood flow and microcirculation in the vessels of the brain (G. M. Savelyeva, 1973; K. V. Chachava, 1971, etc.). Thus, K.V. Chachava suggests performing craniocerebral hypothermia even before the birth of the child.

For this purpose, a vacuum cup - a suction cup - is placed on the presenting head of the fetus. Cooling is carried out with liquid nitrogen vapor, which enters the space between the outer and inner plates of the calyx, while the temperature of the cerebral cortex drops to 20-30°C. Indications for fetal hypothermia: asphyxia after unsuccessful drug treatment, obstetric situations that exclude the possibility of urgent surgical delivery (high position of the head, insufficient dilatation of the cervix) (K. V. Chachava, 1971).

Craniocerebral hypothermia in a newborn is carried out against the background of the use of neuroplegic and antihistamine drugs, most often sodium hydroxybutyrate with droperidol is used.

To cool the skin of a child’s scalp with running water at a temperature of 8-10°C, the domestic device “Cold-2” can be used (N. S. Baksheev, 1972). A shower installation is also used, from which water is poured onto the scalp, and the length of the stream should not exceed 3-4 cm. During craniocerebral hypothermia, the temperature is constantly monitored ear canal(26-28°C) and in the rectum (from 30 to 32°C). The indicated temperature corresponds to moderate (23-25°C) brain hypothermia (G. M. Savelyeva, 1973).

Diprazine in combination with aminazine is the main agent included in the lytic mixture used for the purpose of hypothermia and reducing the excitability of the nervous system, primarily the reticular formation of the brain (M. D. Mashkovsky, 1972). Doses of aminazine and diprazine in newborns range from 2 to 4 mg/kg per day; when used together, the dose is reduced by half.

When a convulsive syndrome occurs, diazepam (p. 126) and phenobarbital (p. 111) are added.

Diazepam and especially phenobarbital, as sedatives and anticonvulsants, are used in combination with sodium hydroxybutyrate (GHB) and droperidol, and in milder cases, alone.

Simultaneously with this therapy, to improve brain nutrition and reduce tissue oxygen needs, repeated administration of ATP intramuscularly and intravenously in a 1% solution of 10 mg per injection and cocarboxylase 8 mg/kg intramuscularly and intravenously with glucose is indicated.

To improve metabolic processes in the brain, the inclusion of biostimulants is indicated: glutamic acid, gammalon, but their use is possible no earlier than 5-7 days, in cases involving inhibition of the central nervous system, especially in children with prenatal pathology. In the presence of agitation, these drugs are given against the background of phenobarbital, carefully, since if the child has increased convulsive readiness, they can provoke convulsive seizures.

To combat cerebral edema, hypertonic solutions are used, which increase the osmotic pressure of the plasma and promote the entry of fluid into the blood from the brain and other tissues (while increasing the excretion of fluid through the kidneys). A decrease in intracranial pressure under the influence of hypertonic solutions is accompanied by an increase in cerebral blood flow, which leads to the restoration of brain functions. Widely used hypertonic glucose solutions reduce blood pressure by 14% and for a short time (35-40 min), so it is rational to use them only simultaneously with g.lasma, which enhances the anti-edematous effect of glucose (I. Kandel, M. N. Chebotarev, 1972) . In newborns, 8-10 ml/kg of 15-20% glucose solution is used simultaneously with plasma.

For the purpose of dehydration, drugs with a high osmotic gradient to the blood-brain barrier, which have a pronounced diuretic effect, are prescribed. The leading drug in this group of osmodiuretics is mannitol (p. 106).

Glycerol (glycerol) - trihydric alcohol, administered orally in a 50% solution with glucose or sugar syrup and give 1/2 teaspoon 2-3 times a day.

By the end of the first day, in the absence of mannitol, saluretics are prescribed. Furosemide is more often used in newborns.

The independent action of diuretics in cerebral edema is less effective than in combination with hypertonic solutions, therefore it is advisable to combine diuretics with the administration of plasma and glucose.

In milder cases, to relieve cerebral edema, it is advisable to include 0.2 ml/kg of a 25% magnesium sulfate solution. In order to reduce cerebral edema and restore

Relevance of the topic. Among the child population, diseases of the cardiovascular system are very common, which are characterized by a severe course, the presence of complications and an unfavorable prognosis. Often patients need to undergo urgent action, especially with regard to acute heart failure, cardiac arrhythmias, vegetative crises, hypoxic crisis, etc. Practical activities require pediatricians, general practitioners and emergency physicians to have solid knowledge and practical skills in the field of emergency care for cardiovascular diseases in children.

Common goal. Improve knowledge and skills in diagnosing and providing emergency care for heart failure, pulmonary edema, cardiac arrhythmias, fainting, collapse, vegetative crises, hypoxic crisis.

specific target. Based on complaints, medical history, objective examination data, determine the main signs of heart failure, fainting, collapse, hypertensive, hypoxic and vegetative crises, life-threatening cardiac arrhythmias, etc., conduct differential diagnostics, and provide the necessary assistance.

Theoretical questions

1. Etiology and pathophysiology of acute heart failure.

2. Clinical signs of fainting, collapse, hypertensive, hypoxic and vegetative crises, pulmonary edema, life-threatening cardiac arrhythmias.

3. Tactics of emergency care for pulmonary edema.

4. Tactics of emergency care during a hypoxic crisis.

5. Tactics of emergency care for ventricular fibrillation.

6. Tactics of emergency care for atrial fibrillation.

7. Tactics of emergency care for Morgagni-Adams-Stokes syndrome.

8. Tactics of emergency care for paroxysmal tachycardia.

9. Tactics for providing emergency care for fainting.

10. Tactics of emergency care for collapse.

11. Tactics for providing emergency care during vegetative crises.

12. Tactics of emergency care for hypertensive crisis.

Indicative basis of activity

During preparation for the lesson, it is necessary to familiarize yourself with the main theoretical issues through the graphological structure of the topic, treatment algorithms (Fig. 1-7), and literature sources.

Pulmonary edema

Pulmonary edema- this is a manifestation of acute left ventricular cardiac decompensation against the background of a discrepancy between the inflow and outflow of blood from the pulmonary circulation, increased capillary pressure, with increased penetration of fluid into the alveoli.

Observed in cases of heart damage, pneumonia, bronchial asthma, anaphylactic shock, coma, head injuries, kidney diseases, with rapid administration of large amounts of fluid.

Clinical manifestations. In the prodromal period, tachycardia, cardiac arrhythmia, low pulse pressure, attacks of suffocation and coughing, anxiety, shortness of breath, cyanosis, and many different types of moist rales are noted. Blood pressure is elevated or normal.

Detailed clinical picture of pulmonary edema: adynamia, loss of consciousness, cyanosis, shortness of breath, copious discharge pink frothy sputum, tachycardia, muffled heart sounds, rapid pulse weak filling, a lot of moist rales in the lungs, first in lower parts, then over the entire surface. The x-ray shows intense darkening.

1. Calm the child, move him to an elevated position with his legs down.

3. Apply venous tourniquets to the limbs for 20-30 minutes. The pulse in the artery distal to the tourniquet should be detected.

4. To reduce blood volume, diuretics are indicated - lasix 0.1-0.2 ml/kg (1-2 mg/kg) intramuscularly, diacarb.

5. If there is slight congestion in the lungs, prescribe nitroglycerin 1/2-1 table. under the tongue.

6. If pulmonary edema is accompanied by bronchospasm, administer aminophylline 24% IM at a dose of 3-4 mg/kg.

7. Immediately hospitalize the patient.

1. Restore airway patency. Place the child in a position with his head elevated. Remove foam from the respiratory tract. Carry out oxygen inhalation in combination with defoamers (30-50% ethyl alcohol or 10% alcohol or ether solution of antifomsilane).

2. To relieve the pulmonary circulation and reduce the volume of blood volume:

— administer diuretics intravenously: furosemide (Lasix) 2-5 mg/kg;

— administer a 2% solution of aminophylline intravenously (1 ml per year of life, but not more than 5 ml);

— intravenously or intramuscularly administer a 1% solution of promedol 0.1 ml/year of life (in the absence of respiratory depression for children over 2 years of age);

— if blood pressure decreases, administer prednisolone 5-7 mg/kg intravenously;

- for hyperkinetic type of circulatory disorders, prescribe ganglion blockers (pentamine, benzohexonium, arfonade). Apply a 5% solution of pentamine diluted in 20 ml of isotonic sodium chloride solution or 5% glucose IV slowly under blood pressure control: children 1-3 years old - 1-3 mg/kg, over 3 years old - 0.5-1 mg/kg kg. A 2% benzohexonium solution can be prescribed to children 1-3 years old - 0.5-1.5 mg/kg, over 3 years old - 0.25-0.5 mg/kg IM.

3. In order to increase cardiac output in hypokinetic type of circulatory disorders, the use of sympathomimetic amines (dopamine, dobutamine) or cardiac glycosides (strophanthin, digoxin) is indicated. Using the Lineomat infusion pump, administer dopamine 3-6 mcg/kg/min or dobutamine 2.5-8 mcg/kg/min. When hemodynamics are stabilized, you can prescribe a 0.05% solution of strophanthin at a dose of 0.01 mg/kg or digoxin 0.03 mg/kg (at a moderate rate of saturation - within three days) intravenously or enterally. Then switch to a maintenance dose - 1/5 of the saturation dose.

4. To improve metabolic processes in the myocardium and correct acid-base balance, prescribe cardiometabolic agents (polarizing mixture - 10% glucose solution 5 ml/kg and panangin 0.5-1.0 ml/year of life; phosphaden, cocarboxylase, riboxin, mildronate, cardonate and etc.).

5. For prophylactic purposes, use broad-spectrum antibiotics.

6. Treatment of the underlying disease.

Acute right ventricular failure

Acute right ventricular failure occurs in pathological conditions accompanied by a sudden decrease in blood flow in the pulmonary circulation (a syndrome of respiratory disorders in newborns, an attack of bronchial asthma, atelectasis, hydrothorax, congenital heart defects with depletion of blood flow in the pulmonary circulation, rapid transfusion of citrate blood without the simultaneous administration of calcium and novocaine, rapid intravenous administration of hypertonic solutions, etc.).

Clinical manifestations. Complaints of a feeling of tightness behind the sternum, cardialgia, suffocation, weakness. There is cyanosis, cold sweat, swelling of the jugular veins, a rapid increase in the liver, in young children - and the spleen. There may be peripheral edema and fainting. The borders of the heart are shifted to the right. Tachycardia. Blood pressure is reduced. Heart sounds are weakened, an accent of the second tone is heard over the pulmonary artery.

Emergency care at the prehospital stage

1. Reassure the child, provide him with an elevated position with his legs down.

2. Provide access to fresh air, if possible, carry out oxygen inhalation.

3. Treatment of the underlying disease leading to heart failure:

- for heart defects with poor pulmonary blood flow - myotropic antispasmodics and beta-blockers (propranolol);

- during an attack of bronchial asthma - bronchospasmolytics, glucocorticoids;

- in case of a foreign body - removal foreign body from the respiratory tract;

- for pulmonary embolism - heparin, fibrinolytic agents.

4. Immediate hospitalization in the intensive care unit and intensive care.

Emergency care at the hospital stage

1. Oxygen therapy. Artificial ventilation.

2. Cardiotonic drugs (dopamine/dobutamine). The drugs are contraindicated in obstructive hypertrophic cardiomyopathy, severe aortic stenosis, severe pericarditis, atrial fibrillation!

3. Administer diuretics intravenously: furosemide (Lasix) 2-5 mg/kg.

4. Correction of acid-base balance.

5. Correction of water-electrolyte balance.

Hypoxic crisis

Hypoxic crisis(dyspneic cyanotic attack) - a significant increase in shortness of breath and cyanosis in children with Fallot's disease, which occurs with an increase in physical activity, psycho-emotional stress, intercurrent infections, in response to manipulation.

Clinical manifestations. During an attack, the child takes a forced position, squats or lies with his legs drawn to his stomach. A short attack does not cause fainting, a prolonged one is accompanied by a coma, impaired cerebral circulation. There is a sharp weakness, cyanosis of the mucous membranes and skin, tachycardia, frequent and deep breathing. The noise of pulmonary artery stenosis disappears, blood pressure drops.

Emergency care at the prehospital stage

1. Ensure free breathing: remove squeezing clothing, ventilate the room.

2. Inhale oxygen.

3. Reassure the child, prescribe sedatives - seduxen, pipolfen, etc.

4. If necessary, administer subcutaneous promedol 1% solution 0.1 ml/year of life.

For frequent and prolonged attacks, hospitalization is indicated.

Emergency care at the hospital stage

1. Prescribe oxygen inhalation.

2. Enter cordiamin or promedol, if they were not introduced at the prehospital stage.

3. To correct polycythemia, prescribe rheopolyglucin 5-10 ml/kg intravenously.

4. Spasm of the pulmonary artery is stopped with a 0.1% solution of obzidan 0.1-0.2 mg / kg IV in 10 ml of 20% glucose solution slowly at a rate of 1 ml / min or 0.005 mg / min.

5. In case of convulsions, inject a 20% solution of sodium oxybutyrate at a dose of 50-100 mg/kg IV slowly.

6. If the attack continues and a hypoxic coma occurs, transfer to mechanical ventilation.

Ventricular fibrillation

Ventricular fibrillation is a type of circulatory arrest. It is observed in the terminal period or for a short time in severe cardiovascular pathology. Under conditions of fibrillation, contractions of the ventricles as a whole stop, only contractions of individual muscle fibers take place.

Clinical manifestations correspond clinical death. As a result of stopping hemodynamics, patients lose consciousness and stop breathing. On the ECG, waves are recorded that constantly change in shape, height, direction and duration.

Urgent Care

1. Resuscitation according to principles A, B, C.

2. Urgently carry out defibrillation using an electric shock. Start with 1000 V and then increase the voltage by 500 V each time, bringing it up to 3500 V.

3. If cardiac activity has not resumed, intravenously inject lidocaine at a dose of 1-2 mg/kg or aymalin 1 mg/kg (not more than 50 mg) for isotonic solution sodium chloride.

4. If there is no effect, repeat electropulse therapy. Along with this, exclude the factors that led to ventricular fibrillation - hypoxemia, hypercapnia, hyperkalemia, bleeding.

Atrial fibrillation

Atrial fibrillation- a complex heart rhythm disorder, characterized by uncoordinated, chaotic contractions of individual atrium muscles, when their frequency reaches 600 per minute.

Occurs in severe myocardial lesions (rheumatism, congenital heart defects, myocarditis). There are tachy- and bradyarrhythmic atrial fibrillation.

Clinical manifestations. During an attack, patients experience a feeling of fear. On auscultation, there are tones of varying sonority and different intervals between them. A “deficit” of pulse is characteristic. Signs of circulatory problems are usually detected. There is no P wave on the ECG, the isoelectric line is wavy due to the appearance of atrial fibrillation waves P waves, RR intervals are unequal in duration, irregular.

Urgent Care

1. Calm the child. Give humidified oxygen. Do an ECG.

2. For tachyarrhythmic form, administer cardiac glycosides (0.06% solution of corglycone or 0.06% solution of strophanthin, 0.05 ml/year of life), can be combined with b-blockers (anaprilin, inderal, obzidan - 1-2 mg /kg/day in 3-4 doses), isoptine (0.1-0.15 mg/kg in 20 ml of 5% glucose solution).

3. Then switch to maintenance doses of cardiac glycosides and potassium salts. If therapy is ineffective in the absence of organic lesions of the heart, to restore the heart rhythm, defibrillation is performed under superficial anesthesia and a voltage of 1000-4000 V for 0.01 s.

Morgagni-Adams-Stokes syndrome

A decrease in heart rate to 20-30 per minute leads to cerebral ischemia and the development of Morgagni-Adams-Stokes syndrome.

Clinical manifestations. During an attack, patients experience dizziness, fainting, and convulsions, which indicates significant brain hypoxia.

Urgent Care

1. Start indirect massage heart with a sharp concussion at the border of the middle and lower third of the sternum.

2. In case of respiratory arrest, perform artificial respiration using the mouth-to-mouth method.

3. Introduce intracardially a 0.1% solution of adrenaline hydrochloride and a 0.1% solution of atropine sulfate (0.05 ml per 1 year of life) in combination with a 10% solution of calcium chloride (0.3-0.5 ml per 1 year of life). year of life).

4. B exceptional cases perform electrical stimulation of the heart.

5. For short attacks of asystole, it is necessary to put 0.5-1 tablets under the tongue. isadrin, intravenously inject a 0.2% solution of norepinephrine 0.5-1 ml or a 0.05% solution of alupent (0.1 ml per 1 year of life, but not more than 1 ml), which are diluted in 200 ml of 5% glucose solution. The rate of administration is 10-12 drops per 1 minute under ECG control.

Patients who have suffered a Morgagni-Adams-Stokes attack need to consult a cardiac surgeon to resolve the issue of implanting an artificial pacemaker.

Paroxysmal tachycardia

Paroxysmal tachycardia characterized by an unexpected attack of a significant increase in heart contractions (160-200 per 1 minute).

There are supraventricular and ventricular paroxysmal tachycardia.

Clinical manifestations. Suddenly there are complaints of discomfort in the heart area, pressure and pain. Dizziness, fainting, vomiting, pale skin, shortness of breath, pulsation of the jugular veins, and sometimes signs of circulatory disorders may occur. Auscultation reveals a significant acceleration of heart contractions, blood pressure is reduced, and the pulse is low in volume.

Emergency care at the prehospital stage

1. Calm the child, give humidified oxygen. Do an ECG.

2. Prescribe sedatives (Seduxen 1/2-1 tablet, Corvalol, valerian tincture 1-2 drops per year of life); Panangin 1/2-1 tablet depending on age.

3. In children over 5 years of age with the supraventricular form of paroxysmal tachycardia, methods are used that reflexively increase the tone of the vagus nerve: mechanical pressure on the carotid sinus area, performing the Valsalva maneuver - straining at maximum inspiration while holding the breath for 30-40 s; artificial vomiting, swallowing hard pieces of food, rubbing the skin with cold, or applying a cold compress to the face. The Danini-Aschner test (pressure on the eyeballs) is not recommended due to the risk of retinal detachment.

4. Hospitalize the patient.

Emergency care at the hospital stage

If, according to ECG data, the QRS complex is narrow or wide due to functional blockade of the bundle branches:

1. Prescribe intravenous phenibut or carbamazepine (50-100 mg once) or 1/2 dose of an antiarrhythmic drug that has been effective in the past. Inject intravenously a 1% solution of triphosadenine (ATP) in a dose of 0.5 ml for children under 6 months, 0.8 ml for 6-12 months, 1 ml for 1-7 years, 1.5 ml for 8- 10 years, 2 ml - over 10 years. If the administration is ineffective, it can be repeated two more times with an interval of several minutes (at least 2 minutes).

2. If there is no effect, a slow (at least 3 minutes) intravenous administration of verapamil at a dose of 0.1-0.15 mg/kg is indicated (for newborns - 0.75 mg, for children infancy- 0.75-2 mg, 1-5 years - 2-3 mg, 6-14 years - 2.5-5 mg, up to clinical effect) in saline solution. Verapamil is contraindicated in Wolff-Parkinson-White syndrome, AV block, sick sinus syndrome. Prescribe potassium and magnesium aspartate intravenously 2-5 ml or orally 1-2 mg/kg.

3. In the presence of atrial paroxysmal tachycardia, it is advisable to prescribe propranolol 110-100 mcg/kg IV in a slow stream over 10 minutes, the maximum single dose is 1 mg, the administration can be repeated after a few minutes, up to 3 injections. The drug is ineffective in Wolff-Parkinson-White syndrome and is contraindicated in bronchial asthma, AV block, sick sinus syndrome, and arterial hypotension.

4. If there is no effect, inject intravenously a 5% solution of amiodarone in a 0.9% sodium chloride solution or a 5% dextrose solution. An initial loading dose of 3-5 mg/kg over 20-40 minutes, then a maintenance dose of 0.5 mg/min over 3-6 hours; total daily dose no more than 10 mg/kg or 5-10 mg/kg orally until clinical effect.

If, according to ECG data, the QRS complex is wide:

1. Prescribe IV slowly (over 3-4 minutes) a 1% solution of lidocaine at a dose of 0.5-1.0 mg/kg in 10 ml of 5% glucose solution or physiological saline. If there is no effect, repeat administration after 5 minutes.

2. If there is no effect, inject a 10% solution of procainamide very slowly into 10 ml of saline at a dose of 0.15-0.2 ml/kg (no more than 10 ml) or up to a year - 0.7 mg/kg, older than 1 year - 15 mg/kg. At the same time, administer a 1% solution of phenylephrine intramuscularly at a dose of 0.1 ml/year of life (no more than 1 ml).

Alternative: administer a single iv slowly 2.5% solution of ajmaline 1 mg/kg (not more than 50 mg) in 10 ml of saline or 5% glucose solution or prescribe ajmaline 1-3 mg/kg/day orally in 3 divided doses before clinical effect or orally propafenone 5-15 mg/kg/day in 3 doses until clinical effect.

3. Lack of effect requires cardioversion of 2 J/kg, if paroxysm persists - 4 J/kg. If there is no effect, repeat the scheme: cardiopulmonary resuscitation - drug therapy- cardioversion.

Fainting

Fainting- short-term loss of consciousness caused by cerebral hypoxia with a violation of the central mechanism of regulation of vascular tone (organic damage to the central nervous system, autonomic dysfunction), changes in muscle tone (myopathy), a sharp limitation of blood flow to the heart (acute blood loss, convulsions, constrictive pericarditis), heart damage (aortic insufficiency, significant bradycardia, myocarditis), etc.

Clinical manifestations. Dizziness, ringing in the ears, nausea, short-term loss of consciousness. The patient is pale, the skin becomes covered with sweat, the pulse slows down.

Emergency care at the prehospital stage

1. Provide the patient with a horizontal position, raise the lower limbs at an angle of 30-45°.

2. Ensure free breathing - unfasten the collar, belt, remove constrictive clothing, ventilate the room.

3. Wipe your face with cold water. Allow to inhale a liquid that irritates the upper respiratory tract (ammonia, ether, vinegar). If fainting persists, hospitalization is indicated.

Emergency care at the hospital stage

1. In case of prolonged fainting, administer intramuscularly a 10% solution of caffeine sodium benzoate 0.1 ml/year of life or cordiamine 0.1 ml/year of life, 1% solution of mezatone 0.1 ml/year of life (no more than 1 ml). In case of significant hypotension and bradycardia, a 0.1% solution of atropine 0.1 ml/year of life (no more than 1 ml) subcutaneously or intramuscularly is effective.

2. If there is no effect, hospitalization in the intensive care unit or intensive care unit is indicated.

3. After regaining consciousness, give the patient hot tea, calm him down, rub his limbs, and cover him with heating pads.

Collapse

Collapse- acute vascular insufficiency, accompanied by a drop in vascular tone and a decrease in circulating blood volume, manifested by a sharp decrease in arterial and venous pressure, signs of cerebral hypoxia and depression of vital functions.

Sympathotonic, vagotonic and paralytic forms are determined.

Clinical manifestations. The sympathotonic form occurs against the background of pneumonia, neurotoxicosis, blood loss or dehydration as a result of spasm of arterioles and accumulation of blood in the cavities of the heart and great vessels. Systolic blood pressure is increased, pulse is decreased, tachycardia, centralization of blood circulation.

Vagotonic form caused by a sharp drop in blood pressure as a result of expansion of arteriovenous anastomoses, impaired microcirculation, decreased blood supply to tissues, and hypoxia. Accompanied by bradycardia.

Paralytic form causes passive expansion of capillaries. Consciousness is confused, tachycardia, blood pressure is significantly reduced, the pulse is thready, the skin is cold, covered with sticky sweat.

The severity of the condition is determined by the degree of blood pressure reduction.

Emergency care at the prehospital stage

1. Give the patient a comfortable horizontal position, raise the lower limbs at an angle of 30-45°.

2. Ensure free breathing - remove constrictive clothing, ventilate the room.

3. Inhale liquid that irritates the upper respiratory tract.

4. Rub or massage the limbs. Cover the patient with heating pads and a blanket.

5. Inject subcutaneously a 10% solution of caffeine sodium benzoate 0.1 ml/year of life (no more than 1.0 ml).

Emergency care at the hospital stage

1. Simultaneously prescribe glucocorticosteroids in a single dose: with sympathotonic form, prednisolone 3-5 mg/kg IV or IM or dexamethasone 0.5-1 mg/kg IV is better, with vagotonic and paralytic - hydrocortisone 10- 15 mg/kg.

2. Restore the volume of circulating blood by intravenous administration of rheopolyglucin (10-20 ml/kg) or plasma (5-10 ml/kg), glucose-salt solutions. The infusion rate is determined depending on the child’s condition - 5-20 ml/kg/hour.

3. If there is no effect, 0.2% solution of noradrenaline is injected intravenously (children under one year old - 0.1-0.15 ml, 1-5 years old - 0.3 ml, 6-10 years old - 0.5 ml, 11-15 years - 0.75 ml) in 50 ml of 5% glucose solution at a rate of 10-20 drops / min, in the most severe cases - 20-30 drops / min under the control of blood pressure. You can prescribe a 1% solution of mezaton 0.1 ml / year of life, but not more than 1.0 ml intravenously.

4. If there is no effect, prescribe dopamine 8-10 mcg / kg / min under the control of blood pressure and heart rate. Transfer to the intensive care unit.

5. To improve microcirculation, prescribe antiplatelet agents (chimes - 3-5 mg/kg), complamin (10-20 mg/kg/day).

6. Constantly carry out oxygen therapy, correct water and electrolyte disorders, acid-base balance.

Vegetative crises

Vegetative crises- these are the most striking and dramatic manifestations of the autonomic dysfunction syndrome. They are characterized by: paroxysmal nature, polysystemic autonomic disorders, emotional and affective manifestations. There are sympathoadrenal, vagoinsular and mixed crises.

Sympathoadrenal crisis characterized by a feeling of anxiety, in some patients - fear, fever and blood pressure, palpitations, tachycardia, mydriasis, hyperglycemia, cold extremities, dry mouth. Possible headache, cardialgia, slowed intestinal motility. The attack is accompanied movement disorders, ends with polyuria. Panic attack often predetermines constant fear occurrence of another attack.

Vagoinsular crisis begins with precursors in the form of lethargy, weakness, anxious mood, and is accompanied by a decrease in blood pressure, sometimes even to the point of loss of consciousness. Characteristic: bradycardia, dizziness, hyperhidrosis, gastrointestinal dyskinesia, nausea, discomfort in the epigastrium, profuse diarrhea is possible. There may also be laryngeal spasm, shortness of breath with difficulty breathing, migraine-like headache, allergic rashes and Quincke's edema, flushes of heat to the face.

Flow mixed generalized crisis accompanied by sympathoadrenal and vagoinsular manifestations.

In most cases, the nature of the crises corresponds to the initial vegetative tone of the child. The duration of the crisis ranges from several minutes to several hours.

Emergency care at the prehospital stage

1. Calm the child, give him a comfortable position, provide access to fresh air.

2. Apply phytotherapeutic agents with a sedative effect (valerian, lemon balm, motherwort, astragalus, wild rosemary, peony, viburnum leaves and flowers, dill seeds and leaves, mint, sage, saffron, oregano, etc.) or Corvalol, Corvaldin 1-2 drops for 1 year of life.

During sympathoadrenal crisis

1. If the attack continues, prescribe one of the tranquilizers in a single dose: Seduxen 0.1 ml/year of life IM or 0.4 mg/kg orally; tazepam 10-20 mg per day orally; sibazon for children 1-3 years old - 0.001 g, 3-7 years old - 0.002 g, over 7 years old - 0.003-0.005 g 2 times a day; Rudotel for children 1-2 years old - 0.001 g, 3-6 years old - 0.001-0.002 g, 7-8 years old - 0.002-0.008 g 2-3 times a day.

2. During severe tachycardia, prescribe beta-blockers: propranolol (Inderal) 0.5-1 mg/kg orally. Potassium preparations (panangin, asparkam) are indicated.

3. For diencephalic paroxysms, prescribe pyroxan (a beta-blocker) 1-2 tablets. per day.

4. If a crisis occurs against the background of increased hydrolability of the patient or disorders of water-salt balance, emergency therapy should begin with the use of furosemide 20-40 mg orally once and nifedipine 2.5-5 mg sublingually or in drops. If there is no effect, repeat the administration of Lasix or furosemide after 30 minutes.

5. In the presence of high blood pressure, vasodilators: 1-2% solution of papaverine, 0.5-1% solution of dibazole or noshpa, 0.1 ml/year of life IM. If there is no effect, it is impossible to carry out injections, prescribe nifedipine (Corinfar) 2.5-5 mg sublingually. In the absence of a rapid effect, it is possible to combine these drugs with diuretics (Lasix 1 mg/kg IM or IV).

6. If there is convulsive readiness, emergency therapy should begin with the administration of seduxen 1-2 ml of a 0.5% solution (5-10 ml) IV in a slow stream or magnesium sulfate 25% solution 0.2 ml/kg IV ( 10-20 ml).

7. In difficult situations, older children with layers of hysteria, in the presence of tachypnea, diffuse cyanosis, can be administered morphine - 0.05 ml/year of life s.c.

During vagoinsular crisis

1. Cover with heating pads and give a warm, sweet drink.

2. If there is a significant decrease in blood pressure, prescribe cordiamine 0.05-0.1 ml/year of life subcutaneously or 1% mezatone solution 0.05-0.1 ml/year, no more than 1 ml per 1 administration.

3. Adaptogens of plant origin with the greatest stimulating effect (ginseng, Chinese magnolia vine, leuzea, eleutherococcus, zamaniha, Rhodiola rosea) are shown in a single dose of 1 cap/year of life 30 minutes before meals 1-2 times a day; vegetotropic drugs: bellataminal (bellaspon) or belloid.

4. In the absence of effect and the presence of bradycardia, prescribe atropine in a single dose (per 1 kg of weight): children under 1 year old - 0.018 mg (0.018 ml of a 0.1% solution); 1-5 years - 0.016 mg (0.016 ml); 6-10 years - 0.014 mg (0.014 ml); 11-14 years - 0.012 mg (0.012 ml).

In a mixed crisis

Doses of antihypertensive drugs should be 2 times lower. It is possible to use belloid, bellaspon, bellataminal.

If the vegetative crisis continues, hospitalization is indicated.

Hypertensive crisis

Hypertensive crisis - sharp increase Blood pressure accompanied by symptoms of cerebrovascular accident, left ventricular heart failure, and autonomic reactions. Occurs with symptomatic arterial hypertension (renal, cardiovascular, endocrine, neurogenic), extremely rarely with primary hypertension.

Clinical manifestations. Sharp, piercing headache, lethargy, nausea, vomiting, dizziness, tachycardia, paresthesia, tremors of the limbs, convulsions, blurred vision and hearing. The ECG may show a decrease in the ST segment below the isoelectric line, a biphasic negative T wave.

Emergency care at the prehospital stage

1. Give the child a semi-sitting position. Take a hot foot bath and place mustard plasters along the spine. Calm the child.

2. Inject intramuscularly a 1% dibazole solution 0.1-0.2 ml/year of life and Lasix 0.1 ml/year of life or prescribe sublingual nifedipine 0.25-0.5 mg/kg/day at 3-4 administration (adolescents 10 mg/day).

If there is no effect, hospitalize the patient.

Emergency care at the hospital stage

1. If not prescribed at the prehospital stage, administer 1% Dibazol 0.1-0.2 ml/year of life IM or IV in combination with diuretics (Lasix 0.1 ml/year of life).

2. To prevent cerebral edema and seizures, administer a 25% solution of magnesium sulfate 5-10 ml intravenously.

3. Prescribe pathogenetic therapy. To relieve renal hypertension, prescribe captopril orally for children under 6 months. 0.05-0.5 mg / kg / day, older than 6 months. 0.5-2.0 mg / kg / day in combination with obzidan (1 mg / kg) or furosemide (1-3 mg / kg) orally. You can prescribe nifedipine 0.25-0.5 mg/kg/day or prazosin 0.05-0.1 mg/kg/day (maximum 0.5 mg/kg/day).

For crises caused by pheochromocytoma, prescribe beta-blockers: phentolamine 0.1-0.2 mg/kg IV, tropafen 10-30 mg IM or 5-15 mg IV, phenoxybenzamine hydrochloride 10 mg/day .

Literature

Main

1. Selected nutrition for pediatric cardio-rheumatology / Volosovets O.P., Savvo V.M., Krivopustov S.P. ta inshi / Ed. O.P. Volosovtsia, V.M. Savvo, S.P. Krivopustova. - Kyiv; Kharkiv, 2006. - 246 p.

2. Primary arterial hypertension in children and children / Maidannik V.G., Moskalenko V.F., Korenev M.M. ta inshi / Ed. V.G. Maidannik and V.F. Moskalenka. - K., 2006. - 389 p.

3. Order of the Ministry of Health of Ukraine No. 437 dated 30.08.2004. About the confirmation of clinical protocols for the provision of medical assistance for difficult conditions in children at the hospital and pre-hospital stages.

4. Order of the Ministry of Health of Ukraine No. 362 dated 19.07.2005. About the confirmation of diagnostic protocols and treatment of cardio-rheumatological diseases in children.

5. Inconsistencies in Pediatrics: Navch. pos_b. / Volosovets O.P., Marushko Yu.V., Tyazhka O.V. ta inshi / Ed. O.P. Volosovtsia and Yu.V. Marushko. - Kh.: Prapor, 2008. - 200 p.

6. Emergency conditions in children / Petrushina A.D., Malchenko L.A., Kretinina L.N. and others / Ed. HELL. Petrushina. - M .: LLC "Medical Information Agency", 2007. - 216 p.

7. Peshiy M.M., Kryuchko T.O., Smyan O.I. Nevidkladna dopomoga in pediatric practice. - Poltava; Sumi, 2004. - 234 p.

8. Emergency medical care for children at the prehospital stage / G.I. Posternak, M.Yu. Tkacheva, L.M. Beletskaya, I.F. Volny / Ed. G.I. Belebezeva. - Lvov: Medicine for the World, 2004. - 186 p.

Additional

1. Veltishchev Yu.E., Sharobaro V.E., Stepina T.G. Emergency conditions in children. - M.: Medicine, 2004. - 349 p.

2. Dyadyk A.I., Bagriy A.E. Arterial hypertension in modern times clinical practice. - Donetsk: Nord-Computer, 2006. - 322 p.

3. Kislyak O.A. Arterial hypertension in adolescence. - M.: Miklos, 2007. - 288 p.

4. Mazur N.A. Paroxysmal tachycardia. - M.: ID MEDPRACTIKA-M, 2005. - 252 p.

5. Mutafyan O.A. Cardiac arrhythmias in children and adolescents (clinic, diagnosis, treatment). - St. Petersburg: Nevsky Dialect, 2003. - 224 p.

7. Cardiac deficiency in pediatric practice: Materials of Science. symposium. — Kharkiv, April 18, 2007 — 168 p.

8. Shkolnikova M.A. Life-threatening arrhythmias in children. - Moscow. — 230 s.

9. Yakovlev V.B., Makarenko A.S., Kapitonov K.I. Diagnosis and treatment of cardiac arrhythmias: A manual for doctors. - M.: BINOM. Knowledge Laboratory, 2003. - 168 p.

A wide variety of risk factors and the lack of regulated approaches to the treatment of vascular accidents in pediatric practice greatly complicates the problem of treating cerebrovascular accidents (CVD) in children. Significant differences from the adult contingent relate to both the predominance of one or another pathogenetic type of stroke, and the characteristics of the clinical manifestations, course and outcomes of stroke.

So, according to statistics, in Western Europe, the share of hemorrhagic stroke (HI) in adults accounts for no more than 5% of cases. In children, cerebrovascular accidents of the ischemic type account for about 55%, in other cases GI is diagnosed.

Often, the clinical manifestations of cerebrovascular accidents in children and adolescents contradict the very definition of stroke recommended by the World Health Organization. This is demonstrated by the frequent presence of an ischemic focus clearly defined by neuroimaging methods in children with clinical manifestations that meet the criteria for transient ischemic attacks (TIA).

Children with sinus venous thrombosis (SVT) often have headaches or seizures. A symptom complex similar to stroke can be observed in many conditions associated with metabolic disorders, with migraine paroxysms, and, of course, requires specific therapy. In addition, the presence of a previous infectious process or an indication of a recent injury should not exclude suspicion about the possible development of cerebrovascular accident.

Epidemiology of stroke in children

The data of American researchers of the epidemiology of stroke in children generally indicate the predominance of the hemorrhagic type of stroke over the ischemic one. So, according to the data presented by a number of authors, the number of cases of NCC) by ischemic and hemorrhagic types in children under the age of 15 years averaged 0.63 and 1.89 per 100 thousand people per year, respectively. Approximately the same ratio was revealed in studies of recent years: about 1.5 and 1.2 per 100 thousand people per year with hemorrhagic and ischemic cerebrovascular accidents, respectively.

In boys, the risk of developing cerebrovascular accident was significantly higher. When controlling for racial differences, the highest risk for vascular disease was found in African Americans. It is interesting that the more frequent presence of sickle cell anemia (SCA) in this group of children does not fully explain such selectivity. In the Chinese population, the frequency of detected ischemic-type NMCs was comparable to the data of American researchers, but the HI was only 28%. About a third of strokes were observed in the first year of life (one in 4 thousand cases; mainly ischemic strokes and parenchymal hemorrhages). In adolescence, subarachnoid hemorrhages predominated. Data on the incidence of TVS in children are estimated at approximately 0.3 cases per 100 thousand people, however, these studies do not fully reflect reality due to the insufficient use of highly sensitive examination methods (computed and nuclear magnetic resonance imaging [MRI], Doppler ultrasound) .

The causes of stroke in children vary. More than 50% of children with focal neurological symptoms of vascular origin had an identified primary risk factor for vascular disease and one additional or more.

A risk factor for the development of cerebrovascular accidents is the presence of traumatic brain injury, SCA, thalassemia, coagulopathies, congenital or acquired heart defects, infectious processes (varicella, meningitis, otitis media, tonsillitis). The same etiological factors can contribute to the development of cerebral venous thrombosis, but the list of possible causes is often supplemented by the presence inflammatory process in the head and neck area, conditions accompanied by dehydration, less often - autoimmune diseases, including inflammatory diseases intestines.

About 80% of cerebrovascular accidents in the perinatal period (from the 28th week of pregnancy to the first week of life) are ischemic, 20% are cerebral venous thrombosis (including TVS) and GI. Risk factors for cerebrovascular disorders in the perinatal period include: cardiopathy, pathology of the blood coagulation and anticoagulation systems, neuroinfections, perinatal injuries (craniocerebral, cervical spine injuries), gestosis, perinatal asphyxia. A number of authors suggest that the presence of chorioamnionitis in pregnant women and premature rupture of amniotic fluid may have an adverse effect. As a result of a large number of multicenter studies concerning the prevalence and causes of cerebrovascular pathology in the pediatric population, it is reliably known that the presence of several risk factors for cerebrovascular accidents greatly increases the likelihood of their development.

Treatment of cerebral circulation pediatrics stroke

To optimize the treatment of stroke in children, the American Heart Association Stroke Council guidelines specify classes of predicted effectiveness and levels of evidence.

Class I includes conditions for which the therapeutic regimen has a high likelihood of effectiveness (strong evidence base).

Class II involves conditions that require therapeutic measures, the effectiveness of which in this case there is conflicting data (IIa - less doubtful, IIb - more doubtful).

Class III summarizes conditions for which current treatment strategies may not be sufficiently effective or may have adverse effects.

According to these recommendations, levels of evidence indicate the strength and breadth of the evidence base (level A is data from multiple randomized clinical trials, level B is from a single study, level C is a consensus of expert opinion).

• 1. Mandatory correction of thrombocytopenia in children with HI (class I, level of evidence B).
• 2. Newborns with HI due to a deficiency of blood coagulation factors require the administration of procoagulants (class I, level of evidence B).
• 3. Administration of Vikasol for vitamin K-dependent coagulopathies (class I, level of evidence B). Higher doses are recommended for drug-induced coagulopathies.
• 4. Neonates with hydrocephalus due to intracerebral hemorrhage should receive ventricular drainage followed by shunting (if signs of severe hydrocephalus persist) (Class I, Level of Evidence B).

• 1. Correction of dehydration and treatment of anemia are appropriate measures (Class IIa, Level of Evidence C).
• 2. Use of neurorehabilitation methods to reduce neurological deficits (class IIa, level of evidence B).
• 3. Administration of folates and vikasol to patients with an MTHFR mutation to normalize homocysteine ​​levels (class IIa, level of evidence C).
• 4. Removal of intracerebral hematomas to reduce intracranial pressure (class IIa, level of evidence C).
• 5. The use of anticoagulants, including low molecular weight heparinoids and unfractionated heparin, is possible only in newborns with severe thrombotic complications, multiple cerebral or systemic emboli, clinical or magnetic resonance signs of progressive cavernous sinus thrombosis (if therapy is ineffective) (class IIb, level evidence C). The prescription of anticoagulants in other cases is unacceptable due to insufficiency clinical trials regarding the safety of their use in newborns.

Class III

1. Thrombolytic therapy in newborns is not recommended without sufficient criteria for its safety and effectiveness in this category of patients (class III, level of evidence C).

• 1. Urgent Care for ischemic stroke (IS) against the background of SCA should include optimization of water-electrolyte and acid-base balance, combating hypotension (class I, level of evidence C).
• 2. Fractional blood transfusions in children 2-16 years of age (in the presence of unfavorable Doppler indicators) are advisable in order to prevent the development of stroke (class I, level of evidence A).
• 3. Children with SCD and confirmed IS should be given an adequate blood transfusion regimen and serum iron levels monitored (Class I, Level of Evidence B).
• 4. Reducing the percentage of pathologically altered hemoglobin by blood transfusion before cerebral angiography in children with SCD (Class I, Level of Evidence C).

• 1. Using exchange blood transfusion, the concentration of pathologically altered hemoglobin should be reduced to a level of less than 30% of its total content (class IIa, level of evidence C).
• 2. In children with SCD and HI, an assessment of the possibility of structural vascular lesions is necessary (class IIa, level of evidence B).
• 3. In children with SCD, annual transcranial Doppler ultrasound (TCDG) is necessary, and if detected pathological changes- at least once a month. Carrying out TCD when identifying borderline pathology is recommended once every 3 or 6 months (class IIa, level of evidence B).
• 4. Long-term blood transfusions are not recommended for children and adolescents with cervical urinary tract secondary to SCD taking hydroxyurea (hydroxyurea) (class IIb, level of evidence B).
• 5. Children with SCD may be candidates for transplantation bone marrow(Class IIb, Level of Evidence C).
• 6. Surgical methods of revascularization can be recommended for children with SCA and cervical vascular disease if vascular therapy is ineffective (class IIb, level of evidence C).

• 1. The use of revascularization techniques reduces the risk of vascular complications in children with moyamoya syndrome (Class I, Level of Evidence B). The lack of sufficient large-scale clinical trials in this area significantly limits the therapeutic spectrum.
• 2. Surgical revascularization has a beneficial effect on the course of cerebrovascular accident in moyamoya syndrome (class I, level of evidence B).
• 3. Indirect revascularization is preferred in children due to the small diameter of the vessels, which makes direct anastomosis difficult, while direct anastomosis is advisable in older age groups (Class I, Level of Evidence C).
• 4. Indications for revascularization include: progression of symptoms of cerebral ischemia, inadequate cerebral blood flow/perfusion reserve (Class I, Level of Evidence B).

• 1. TCD is a necessary diagnostic method in children with moyamoya syndrome (class IIb, level of evidence C).
• 2. During hospitalization of children with Moyamoya syndrome, it is necessary to minimize stress reactions in order to prevent the development of stroke associated with hyperventilatory vasoconstriction (class IIb, level of evidence C).
• 3. Effective measures to prevent systemic hypotension, hypovolemia, hyperthermia and hypocapnia during surgery and in the early postoperative period can reduce the risk of vascular complications in this category of children (class IIb, level of evidence C).
• 4. For children with moyamoya syndrome, it is advisable to prescribe aspirin for the prevention of cervical cerebrovascular accidents, especially after surgical revascularization (class IIb, level of evidence C).
• 5. The diagnostic spectrum for moyamoya syndrome should include methods that allow the assessment of hemodynamic parameters (cerebral perfusion, blood flow reserve) (class IIb, level of evidence C).

• 1. Anticoagulant therapy is not indicated for patients with moyamoya syndrome, with the exception of children with frequent TIAs, multiple cerebral infarctions (against the background of ineffective antiplatelet therapy and surgical interventions) due to the high risk of hemorrhagic complications (class III, level of evidence C).
• 2. Only the combination of clinical signs and family history of moyamoya syndrome warrants screening studies (Class III, Level of Evidence C).

• 1. In children with extracranial arterial dissection, it is advisable to begin therapy with unfractionated or low molecular weight heparin followed by transition to oral anticoagulants (Class IIa, Level of Evidence C).
• 2. The duration of taking anticoagulants (low molecular weight heparin, warfarin) should be 3-6 months (class IIa, level of evidence C).
• 3. Low molecular weight heparin or warfarin can be used as an alternative to antiplatelet therapy. In children with episodes of recurrent cerebrovascular accidents, it is advisable to extend the course of anticoagulant therapy to 6 months (Class IIa, Level of Evidence C).
• 4. It is advisable to continue antiplatelet therapy for up to 6 months in cases where there are imaging signs of gross residual changes in the dissected artery (Class IIa, Level of Evidence C).
• 5. With increasing symptoms of RCCA and the ineffectiveness of conservative therapy, surgical treatment should be considered (class IIb, level of evidence C).

• 1. Children and adolescents with IS and migraine symptoms should undergo a comprehensive evaluation to identify other possible risk factors for cerebrovascular accidents (Class IIb, Level of Evidence C).
• 2. Adolescents with IS and migraine symptoms taking oral contraception, alternative methods of contraception should be recommended (Class IIa, Level of Evidence C).
• 3. It is advisable to avoid prescribing drugs containing triptans in children with hemiplegic and basilar forms of migraine, in the presence of risk factors for vascular accidents, previous cardiac or cerebral ischemia (class IIa, level of evidence C).

• 1. Adequate and timely treatment of congestive heart failure significantly reduces the risk of developing cardiogenic embolism (Class I, Level of Evidence C).
• 2. In case of congenital heart defects, especially combined ones (with the exception of patent foramen ovale), surgical intervention is necessary, as this will help to significantly improve hemodynamic parameters and reduce the risk of developing cerebrovascular accident (class I, level of evidence C).
• 3. Resection of atrial myxoma reduces the risk of cerebrovascular complications (Class I, Level of Evidence C).

• 1. For children with cardioembolic cerebrovascular accidents (not associated with patent foramen ovale), who have a high risk of recurrent cerebral dysgemia, it is advisable to prescribe unfractionated or low molecular weight heparin against the background of an optimized warfarin administration regimen (class IIa, level of evidence B). This regimen can also be used followed by switching to warfarin (Class IIa, Level of Evidence C).
• 2. For children with risk factors for cardioembolism, low molecular weight heprin or warfarin is recommended for at least a year (or until surgery) (Class IIa, Level of Evidence C). If the risk of cardioembolism is high, long-term anticoagulant therapy is prescribed (provided that it is well tolerated) (Class IIa, Level of Evidence C).
• 3. When assessing the risk of cardioembolism (not associated with patent foramen ovale), in the case of a low or doubtful likelihood of developing cerebrovascular accident, it is advisable to prescribe aspirin for at least one year (class IIa, level of evidence C).
• 4. Surgical repair, including using catheter technology, reduces the risk of developing cerebrovascular accident and cardiac complications in children and adolescents with atrial septal defect (class IIa, level of evidence C).
• 5. In case of development of endocarditis after cardiac valve replacement, it is recommended to continue anticoagulant therapy if it was previously prescribed (Class IIb, Level of Evidence C).

• 1. Anticoagulation therapy is not recommended in patients with congenital valvular endocarditis (Class III, Level of Evidence C).
• 2. In the absence of symptoms suggestive of cerebrovascular disease, there is no need to remove rhabdomyoma in children (Class III, Level of Evidence C).

• 1. The likelihood of developing a stroke in children with coagulopathies increases significantly in the presence of additional risk factors. Assessing the state of the coagulation and anticoagulation systems requires special attention even in the presence of other risk factors (Class IIa, Level of Evidence C).
• 2. Adolescents with IS or SVT should stop taking oral contraceptives (Class IIa, Level of Evidence C).
• 3. It is advisable to determine the serum concentration of homocysteine ​​in children with IS or TVS (class IIa, level of evidence B). If its level increases, therapy (diet, folate, vitamin B6 or B12) should be prescribed (class IIa, level of evidence B).

• 1. Children with Fabry disease should receive adequate b-galactosidase replacement therapy (Class I, Level of Evidence B).
• 2. Children or adolescents who have had a stroke and have a drug-correctable risk factor for stroke should receive pathogenetic therapy (Class I, Level of Evidence C).
• 3. Early identification of iron deficiency conditions, especially in individuals with additional risk factors for stroke, will help minimize the possibility of their development (Class IIa, Level of Evidence C).
• 4. If iron deficiency is detected in children, it is necessary to limit the consumption of cow's milk (Class IIb, Level of Evidence C).
• 5. Children, adolescents who have suffered cervical cerebrovascular accidents, and members of their families should be informed about the positive impact of a healthy lifestyle (diet, dosed physical activity, smoking cessation) on the duration and course of the residual period (class IIa, level of evidence C).
• 6. Adolescents who have had cervical urinary infarction using oral contraceptives should be advised to use alternative methods of contraception, especially if coagulopathy is detected (Class IIa, Level of Evidence C).

• 1. For children who have had a stroke, it is necessary to develop an age-appropriate rehabilitation therapy program (Class I, Level of Evidence C).
• 2. When planning therapy, the results of an assessment of cognitive functions and identified speech disorders and the recommendations of educational rehabilitation programs for children who have suffered a stroke should be taken into account (class I, level of evidence C).

• 1. Children with non-traumatic GI should undergo the fullest possible range of examinations to identify existing risk factors. Cerebral angiography is recommended for patients with low information content of non-invasive methods (class I, level of evidence C).
• 2. Children with severe coagulation factor deficiency should receive adequate replacement therapy. Less severely deficient children need replacement if there is a previous traumatic brain injury (Class I, Level of Evidence A).
• 3. Taking into account the risk of repeated GI in the presence of cerebral vascular anomalies (as well as other risk factors), their early detection is necessary, and if appropriate and there are no contraindications - surgical treatment(Class I, Level of Evidence C).
• 4. Treatment of GI in children should include stabilization of respiratory function, reduction of arterial and intracranial hypertension, effective relief of seizures (class I, level of evidence C).

• 1. In the presence of factors contributing to the development of cerebral vessel aneurysms, it is advisable to perform an MRI of the brain once every 1-5 years (depending on the degree of perceived risk) (class IIa, level of evidence C).
• 2. In the presence of clinical symptoms of an aneurysm, cerebral or computed tomography angiography is recommended, even in the absence of its signs according to MRI (class IIb, level of evidence C).
• 3. Given the need for long-term neuroimaging follow-up in children with clinical symptoms of an aneurysm, the preferred research method in this case is computed tomography angiography (class IIb, level of evidence C).
• 4. Treatment of SCD in children should include active control of vasospasm (Class IIb, Level of Evidence C).

• 1. The decision on the removal of hematomas should be strictly individual. Conservative treatment is preferred for patients with supratentorial intracerebral hematomas (Class III, Level of Evidence C). Some studies indicate a positive effect of surgical intervention, especially in cases of severe intracranial hypertension and the formation of tentorial cerebral hernias.
• 2. Despite the proven benefits of using blood transfusions in children with SCD, there is currently no reliable data on reducing the risk of developing IS in this category of patients (class III, level of evidence B).

• 1. Treatment of TVS should include several areas: adequate hydration, relief of seizures, reduction of intracranial hypertension (Class I, Level of Evidence C).
• 2. Children with TVS need to study the entire range of hematological parameters with their careful monitoring (class I, level of evidence C).
• 3. In the presence of bacterial infections in children with TVS, adequate antibiotic therapy is necessary (Class I, Level of Evidence C).
• 4. Considering possible complications, children with TVS require periodic testing of visual acuity and visual fields along with the use of therapeutic measures aimed at reducing intracranial hypertension (Class I, Level of Evidence C).

• 1. Children with TVS require hematological monitoring (especially in relation to the platelet component) to identify coagulopathies that are a risk factor for recurrent thrombosis (class IIb, level of evidence B).
• 2. It is advisable to include in the examination plan for children with TVS bacteriological examination blood and radiography (class IIb, level of evidence B).
• 3. In the acute stage of TVS, monitoring of intracranial pressure is advisable (class IIb, level of evidence C).
• 4. For children with TVS, it is advisable to undergo repeated neuroimaging to assess the effectiveness of the therapy (class IIb, level of evidence C).
• 5. Considering the frequency of development of generalized convulsive seizures in children with TVS, with impaired consciousness (or artificial ventilation), continuous electroencephalographic monitoring is necessary (class IIb, level of evidence C).
• 6. In children with TVS, administration of unfractionated or low molecular weight heparin (followed by warfarin for 3-6 months) is appropriate (Class IIa, Level of Evidence C).
• 7. In some cases, in the presence of TVS, it is possible to justify the prescription of thrombolytic therapy (class IIb, level of evidence C).

1. Anticoagulants are not the treatment of choice in newborns with SVT, given the questionable safety and effectiveness profile in this age category. To date, there is no solid evidence base (Class III, Level of Evidence C). The exceptions are cases of severe coagulopathies, the presence of multiple cerebral or systemic embolism, and confirmed progression of TVS.