Sudden Infant Death Syndrome and vaccinations. How high is the risk of developing SIDS? Immune theory of VDS syndrome

Sudden Infant Death Syndrome (SIDS) is a medical diagnosis of a healthy child who has died for no apparent reason. This is an inexplicable tragic case that does not have unambiguous scientific confirmation. According to statistics, today, 0.2% of infants are subject to uncaused death.

Causes

If the doctor could not determine why the child died, he is diagnosed with Sudden Infant Death Syndrome. The reasons why children die are still unknown.

One version of SIDS is considered to be a defect in the centers of respiration and awakening. Such infants cannot adequately respond to non-standard situations. If oxygen supply is cut off during sleep, the baby may not wake up from anxiety and SIDS will occur.

As the child grows older, the risk of sudden death tends to zero. The highest frequency of SIDS cases is observed among children of the second - fourth month of life.

Preschoolers no longer have the concept of Sudden Infant Death Syndrome. Most often, after nine months there is no reason to fear for the condition of the child.

Possible causes of SIDS are:

  1. Prolongation of the QT interval on the ECG. This indicator reflects the time from the moment of contraction of the ventricles of the heart to their complete relaxation. Normally, this indicator is 0.43-0.45 ms. Increasing this value may result in ventricular arrhythmias resulting in neonatal death;
  2. Apnea. The brain temporarily stops stimulating the respiratory muscles. An adult can control this condition, hold the air up to 2-3 minutes. For infants, failure to take in oxygen within 30 seconds will result in death. The intervals between breaths are lengthened mainly in premature babies;
  3. serotonin receptors. At autopsy after SIDS, an insufficient number of these cells was found in the medulla oblongata. A deficiency of nerve endings that respond to serotonin disrupts the cohesive work of the respiratory and cardiovascular centers. There is a theory that this is what causes SIDS;
  4. Errors in thermoregulatory function. The air temperature in the room where the child is located should be in the range of 18-20 ° C. When overheated, immature cells of the medulla oblongata may refuse to perform their functions. Even a short-term cardiac arrest or cessation of breathing will cause the sudden death of an infant;
  5. Infection. The immune system protects the child not only from the negative effects of bacteria and viruses, but also takes part in the work of the heart and lungs. Weakening of the body in utero or during the neonatal period can cause SIDS;
  6. genetic predisposition. If the family has already encountered cases of sudden cardiac arrest or SIDS, then the risk of death of the baby is about 90%. The birth of a healthy child with strong immunity is not a guarantee of his viability.

Predisposing factors

  • cold season;
  • second month of life;
  • mother of a child under 20;
  • smoking during pregnancy;
  • premature baby;
  • low birth weight;
  • intrauterine fetal hypoxia;
  • resuscitation to the child during delivery.

You can reduce the risk of death by observing the following conditions to preserve the health of the child:

  1. Do not put the baby to sleep on the stomach.

Until the baby learns to roll over on his own, sleep should occur while lying on his side. If the child is laid on the stomach, the risk of asphyxia or suffocation increases, as a result - death.

When oxygen is cut off, the baby will be inactive - suffocation will cause sudden infant death syndrome. The age of a child who rolls over from his stomach to his back on his own is more than six months;

  1. Maintain optimum temperature.

Overheating, as well as excessive cooling of the child's body, adversely affects the functioning of the body, leading to the death of the baby. To prevent SIDS, the temperature is adjusted using air conditioners and heaters;

  1. Eliminate smoking.

Nicotine, both during pregnancy and after the birth of a child, is very harmful. The task of a parent is to protect their baby from SIDS, so it is worth limiting not only the active exposure to tobacco smoke, but also the passive one.

The apartment where the child is located should not smell of cigarettes. If one of your relatives has such an addiction, ask them to go outside and keep them away from the baby until all the smell has completely disappeared;

  1. The sleeping surface should be of medium hardness.

Choose mattresses specially adapted for newborns. Do not put a pillow under the child's head (the exception is orthopedic rollers recommended by a pediatrician or orthopedist).

With a disproportionate load on the musculoskeletal system of the infant, deformation of the ribs and spine occurs. Compression of the chest negatively affects respiratory and cardiac activity, death will occur if the work of vital organs stops;

  1. Baby blankets. To minimize the risk of SIDS during sleep, do not cover the child with voluminous and heavy capes;

Note! In the cold season, it is better to dress the child warmer rather than using a blanket. The baby can move it to his face with his hands and cut off access to oxygen.

  1. Leg support. The child is placed mainly in the bottom of the bed. If the legs rest against the side, this will reduce the likelihood of slipping down and covering the head with a blanket, and will prevent death from suffocation.

Features of the child's behavior

SIDS is neither predictable nor preventable. All that parents can do is to show a little more control over the health and behavior of the baby. Give your child more attention if you notice the following:

  • increased body temperature;
  • loss of appetite;
  • motor passivity;
  • the presence of respiratory diseases (read how to protect a child from a cold?>>>);
  • long laying the child to sleep;
  • frequent crying;
  • sleep in unusual conditions for the child.

Sleep with parents

If you feel more comfortable sleeping with your baby, good luck. You don't have to get out of bed to breastfeed your baby.

Feeling the native smell, the baby sleeps more soundly and calmly, he wakes up less often. Mom will immediately calm down if the little one starts to act up. Waking up will be more awake for parents who didn't run half the night to the crib.

Constant contact strengthens the emotional connection. A mother's dream is very sensitive. Even in sleep, you control every movement of your baby and can eliminate the occurrence of SIDS.

Important! When sleeping together, mother and baby should not hide in the same blanket.

The choice is yours. Sleep the way you feel most comfortable. You don't have to change your routine on purpose. Co-sleeping is the best solution for a mother with a baby, and it does not increase the risk of SIDS.

Parents should not sleep in the same bed as their child if:

  • very tired;
  • drank alcohol;
  • are taking sedatives.

Should I give my baby a pacifier?

How does a pacifier affect the occurrence of SIDS? Sucking during sleep actually reduces the risk of infant death. One explanation is that air is constantly drawn in through the pacifier circle, even if the baby is covered up. But don't force it into your child's mouth.

Note! If the child is used to sleeping with a pacifier, then it is worth weaning him gradually. Abruptly stopping the use of a pacifier, on the contrary, can increase the risk of death.

Breath monitor

Continuous monitoring of the newborn's breathing can be ensured by using an electronic device. The sensor is attached to the child's body, and the ultrasonic sensor is attached to the child's bed. In case of interruptions in breathing, the device will signal a rhythm failure.

Does everyone need to use it? Such a device will help prevent SIDS. But it is used if the child has breathing problems or is at increased risk of infant death. No one forbids purchasing a monitor for parental peace of mind.

First aid for respiratory arrest

You notice that the child has stopped breathing. Do not panic, get together, it depends on the accuracy of your actions whether SIDS will come or not. Sharp movements are made with the fingers along the spinal column from the bottom up. The baby is taken in your arms: start to shake him up, massage the arms, legs and earlobes.

These actions are enough to normalize breathing and prevent SIDS. If the condition does not improve, call an ambulance. Start doing chest massage and artificial respiration. The onset of death can only be ascertained by a doctor, until his arrival, continue resuscitation.

Important! The chest of a child is very fragile. The heart area is massaged with the index and middle fingers on the lower third of the sternum.

Predisposition to death in infancy is laid in utero. Bad habits of both parents can seriously affect the health of the baby and provoke SIDS. During pregnancy, you should completely avoid the use of alcohol, drugs and cigarettes. Do not neglect the advice of doctors.

Lack of proper control over the child, lack of attention to him from the parents can lead to death in the cradle. More than half of SIDS cases occur on weekends and holidays, according to a study by British pediatricians.

Scientists have confirmed the fact that preventive vaccinations, air travel or the type of mattress in a baby's crib are not the causes of sudden infant death syndrome.

Roshchina Alena Alexandrovna, pediatrician. Especially for the site Lessons for moms.

Sudden Infant Death Syndrome (SIDS)- a concept applied to the unexpected death of a child of the first year, which occurred in a dream without established causes. They talk about SIDS if the study of the medical record and the place of death, as well as the post-mortem examination, do not give a clear answer about the causes of the death of the infant. To assess the risk of sudden infant death, test algorithms (Magdeburg scoring table) are proposed, ECG and polysomnography are performed. Prevention of SIDS includes optimizing the child's sleep conditions, identifying children at risk, and providing home cardiorespiratory monitoring.

The algorithm proposed by I.A. Kelmanson, contains 6 clinical and 12 morphological features that allow post-mortem differential diagnosis of sudden infant death syndrome and life-threatening diseases and is of interest mainly to pathologists.

Prevention

If an obvious life-threatening episode occurs, it is necessary to take the child in your arms, shake it up, vigorously massage the hands, feet, earlobes, and back along the spine. Usually these actions are enough for the child to breathe again. If breathing is not restored, it is urgent to call an ambulance and start artificial respiration and closed heart massage.

Prevention of SIDS includes primary and secondary measures. The principles of primary prevention are based on antenatal measures (refusal of bad habits before pregnancy, rational nutrition of the mother, sufficient physical activity, prevention of preterm birth, early registration and management of pregnancy under the supervision of an obstetrician-gynecologist, etc.). Primary prevention measures also include optimizing the sleeping conditions of an infant: sleeping on the back, using a sleeping bag that prevents the child from rolling over on his tummy, sleeping on a dense mattress, avoiding overheating, sufficient access to fresh air, maintaining a temperature and humidity regime, the absence of pungent odors and tobacco smoke.

Secondary prevention of SIDS involves identifying high-risk groups and carrying out targeted activities (restorative treatment, massage), home cardiorespiratory monitoring, etc.

Fetal death can occur: before childbirth (in the antenatal period), during childbirth and after them (in the postnatal period), It can be both non-violent and violent.

Nonviolent the death of the fetus and may be due either to underdevelopment (non-viability), or the presence of malformations incompatible with life (anencephaly, eventration of internal organs, etc.). In addition, non-violent death of the fetus and newborn can be caused by various pathological processes or birth trauma.

In more than half of all cases, the cause of death is intrauterine asphyxia (which may be based on changes in both the fetus and the mother) from circulatory disorders, placenta previa and its infarction, true umbilical cord nodes, etc. In other cases, non-violent death can be caused by acute infectious diseases, some chronic diseases (for example, syphilis, etc.).

A common cause of death of a child during childbirth is a birth injury, which occurs more easily in immature fetuses, with a mother, with a large fetus, and with prolonged childbirth. can be expressed in bone fractures, intracranial hemorrhage in the membranes and substance of the brain, in damage to the bones of the skeleton: clavicles, cervical vertebrae; in injuries of internal organs (subcapsular hematomas of the liver, apoplexy of the kidneys and adrenal glands, hemorrhages in the lung tissue, etc.).

violent neonatal death during childbirth is rare.

Here we should note the injuries that occur during self-help during childbirth, which occur outside the obstetric institution and without assistance. Trying to help herself, having no experience, a woman in labor with her hands damages the presenting part of the fetus, more often the head. In this case, abrasions, bruises, wounds, lower dislocations, and bone fractures may occur.

After childbirth, the violent death of newborns can be the result of infanticide, murder and accident.

As already indicated, infanticide can be passive (when a newborn is left without care and help) and active.

With active infanticide (and the murder of a newborn), death often occurs from various types of mechanical asphyxia.

There are cases when a newborn is thrown into reservoirs, cesspools. In these cases, death occurs from hypothermia, etc. There are cases of death from closing the respiratory openings with hands, soft objects. It should be borne in mind that during childbirth outside a hospital, when the woman in labor is alone and cannot provide the necessary assistance to the newborn, he can bury his face in a soft object and suffocate.

As a method of infanticide, strangulation with a noose can be used, which can be used as rags, twine, sometimes parts of the mother's linen or clothes.

It should be borne in mind that sometimes a loop of the umbilical cord is found around the baby's neck. There may be entanglement of the umbilical cord around the neck during childbirth. At the same time, the possibility of killing a newborn by strangulation with the umbilical cord cannot be ruled out.

Mechanical damage as a way of infanticide is less common. There may be damage to vital organs with blunt or sharp objects. Blunt injury must be distinguished from birth trauma and injuries that occur during so-called rapid labor.

test questions
1. What kind of baby is considered a newborn?
2. Define the concept of "infanticide".
3. How to determine if full-term and mature?
4. How to determine the period of intrauterine life of a newborn?
5. What is the difference between "fetus" and "newborn baby"?
6. How can you tell if a baby was born alive or dead?
7. What confirms the viability of a newborn baby?
8. How to determine the duration of extrauterine life?
9. What are the most common causes of infant death:
a) before childbirth;
b) during childbirth;
c) after childbirth.

/ Zubov L.A., Bogdanov Yu.M., Valkov A.Yu. — 2004.

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Syndrome of sudden infant death / Zubov L.A., Bogdanov Yu.M., Valkov A.Yu. — 2004.

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/ Zubov L.A., Bogdanov Yu.M., Valkov A.Yu. — 2004.

In the medical literature, you can find several options for the names of the death of an infant that occurred quite suddenly, in a dream - without previous illnesses, severe injuries, and for no apparent reason at all: sudden infant death syndrome, sudden infant death syndrome in children, sudden infant death syndrome (SIDS). All these terms, similar to each other, basically mean the same thing - the sudden death of a child in the first year of life, which cannot be explained either by a detailed study of the baby's medical history or the results of a pathoanatomical study. Most often, SIDS occurs during sleep, which is why it is also called "death in the cradle."

There are several definitions for SIDS:

Administrative– National Institute for Child Health and Human Development (NICHHD) consensus group definition: “sudden death of any infant or young child that is clinically unexplained and for which a carefully conducted post-mortem examination has failed to demonstrate an adequate cause of death” . In 1989, the same group improved the definition: " SIDS is defined as the sudden death of an infant under one year of age that remains unexplained after a full post-mortem examination, including an autopsy, examination of the place of death, and review of medical records. Cases that do not fall under this standard definition, including those in which no post-mortem examination was performed, should not be diagnosed as SIDS. Cases that do not meet this definition and remain unclear after careful post-mortem examination should be classified as indeterminate, unexplained, etc.» .

Scientific- a narrower working definition for scientific and diagnostic verification of SIDS - proposed by J. Beckwith: " Sudden death of an infant between 3 weeks and 8 months of age, occurring during sleep and not preceded by symptoms or signs of a fatal illness. There were no sudden, unexpected or unexplained infant deaths in close relatives. A complete post-mortem examination, which included a full examination of the medical records and circumstances of death, an autopsy performed by a board-certified pathologist with expertise in pediatrics and forensic medicine, failed to identify an acceptable cause of death.» .

Non-classic or atypical SIDS- this definition applies to those cases that fall under the administrative definition of SIDS, but due to the presence of such circumstances as an age discrepancy, a positive family history, death in an awake state, the absence of petechiae, the presence of a weak inflammatory process, do not fit into the framework of the classical definition.

Research on the problem has been intensively conducted since the second half of the 80s of the XX century. The registration of cases of sudden infant death syndrome over the past two decades has been carried out in all industrialized countries of the world, where at present this syndrome occupies one of the first places among the causes of postneonatal infantile death. of death .

The highest rates (from 0.8 to 1.4 per 1,000 live births) were registered in New Zealand, Australia, England, and the USA. According to WHO, the proportion of this syndrome in the structure of infant mortality in these countries ranges from 15 to 33%. Despite the fact that rather intensive studies of cases of unexpected death of infants did not lead to an explanation of the causes of this phenomenon, in the course of studying the problem, many "character traits" inherent in this pathology were discovered. After the main factors that increase the risk of SIDS were identified, campaigns to reduce the risk of SIDS began in many countries in the early 1990s. As a result of these campaigns, SIDS rates have declined markedly. Approximately 60% of the dead are boys. Most cases occur between 2 and 4 months of age. The risk of SIDS is higher during the winter months.

PROBLEMS OF CLASSIFICATION AND PATHOLOGY OF SIDS

The absence of pathognomonic changes at autopsy may lead some pathologists to use the diagnosis of SIDS as a "diagnostic rubbish" while others may try to find an explanation for the death. Histopathological diagnosis is highly subjective, and while some pathologists have a high enough threshold to state that histopathological manifestations are lethal, others attach great importance to findings that most other pathologists regard as trivial. Moreover, a general pathologist finds SIDS twice as often as a pediatric pathologist. The proportions of unexplained deaths range from 12.2% to 83.1%.

Pathological findings in SIDS are few and include:

At external examination- normal nutrition of the child, cyanosis of the lips and nail plates, the presence of mucous bloody discharge from the nose and mouth, a soiled anus, no signs of violent death.

At internal study- the liquid state of cadaveric blood, which is usually dark in color; dilated right ventricle of the heart, while the left is empty or almost empty. More than half of the cases show small punctate hemorrhages in the pleura and pericardium. Note the empty rectum and bladder; there is often a large amount of curdled milk in the stomach. There are no macroscopic signs of pneumonia, the thymus is of normal size, but hemorrhages are found under the capsule, especially below the level of the clavicles. All lymphoid organs and structures are normal or hyperplastic. The adrenal glands in terms of volume either correspond to the age norm, or are reduced.

Microscopic findings are variable and may include focal fibrinoid necrosis of the larynx and trachea or focal intraepithelial inflammation of these organs (in about half of cases); in the lungs, focal interstitial lymphoid infiltrates are found, often associated with the bronchi (bronchus-associated lymphoid tissue), focal intraalveolar hemorrhages and focal acute or subacute bronchiolitis, lung arterioles have a thickened wall; around the adrenal glands brown fat persists, and in the liver - foci of hematopoiesis. Signs of gliosis are found in the brain stem. .

The issues of the role of intrathoracic petechiae as a marker of lethal upper airway obstruction in SIDS, markers of tissue hypoxia, cardiac pathology in SIDS, as well as dysmorphias and dysplasias as comorbidities in SIDS are discussed.

The discussion about the role of intrathoracic petechiae (ITP) between J. Beckwith and H. Krous led to the conclusion that:

  • Intrathoracic petechiae are a characteristic finding in most cases of SIDS, and they tend to be more numerous in this condition than in death from other causes, including death from asphyxiation (accidental or malicious) and mechanical asphyxia.
  • The localization and distribution of petechiae suggests that negative intrathoracic pressure plays a role in their origin.
  • A number of studies suggest that petechiae originating in the pulmonary microcirculation differ from petechiae originating in systemic thoracic vessels.
  • Experimental studies suggest that vigorous respiratory attempts play a role in their formation, making respiratory paralysis an unlikely mechanism.
  • These studies support the thesis that upper airway obstruction is the ultimate mechanism in most cases of SIDS.
  • The frequency of ITP in SIDS suggests a common etiology for terminal events in SIDS

Among the markers of tissue hypoxia, R. Naeye describes thickening of the walls of the pulmonary arterioles due to hyperplasia of the muscle layer; right ventricular hypertrophy; persistence of brown fat around the adrenal glands; hyperplasia of the adrenal medulla; pathological carotid bodies; persistent hematopoiesis in the liver; gliosis of the brain. However, the NICHHD Cooperative Epidemiological Study was able to confirm only three significantly frequent findings in SIDS that are likely markers of tissue hypoxia - brown fat persistence around the adrenal glands, persistent hematopoiesis in the liver, and brainstem gliosis.

Considering the growing popularity of "cardiac" mechanisms of death in SIDS, attempts were made to find their morphological substrate using special techniques for studying the conduction system of the heart. Among the findings, cartilaginous changes, fibrosis, stenosis of the penetrating atrioventricular bundle, arterial blood supply disorders of the heart nodes, branching of the atrioventricular bundle, additional pathways of the atrioventricular signal were proposed. However, the researchers were unable to demonstrate any specific findings to shed light on the mechanism of SIDS.

I.A. Kelmanson proposed an algorithm (table No. 1), which can serve as an auxiliary diagnostic method and help the pathologist in the analysis of death cases in children suspected of SIDS. The table, which includes 6 clinical and 12 morphological signs, makes it possible to distinguish between cases of SIDS and sudden death from life-threatening diseases.

The interpretation of the recognition results, depending on the amount of points scored by the subject, is as follows:

  • the sum is less than 5 - the probability of SIDS is very high, the probability of sudden death as a result of a life-threatening disease is very small;
  • sum from 5 to 24 - the probability of SIDS is high, the probability of a life-threatening disease is low;
  • the sum of 25-44 - the probability of SIDS is low, the probability of a life-threatening disease is high;
  • the sum is 45 and above - the probability of SIDS is very small, the probability of a life-threatening disease is very high.

Table No. 1
Calculation table for recognition of cases of SIDS

SIDS recognition

signs

Gradations of signs

Points

Clinical Data

1. Examination by a pediatrician of a child within 2 weeks before death

2 days before death and later

days before death and before

2. Clinical diagnosis 2 weeks before death

exanthemic infections

intestinal infections

pneumonia

3. Urgent call of the pediatrician to the child a day before death

4. Symptoms and signs one day before death

catarrhal phenomena

vomiting and spitting up

unmotivated anxiety

lack of appetite

convulsions

5. Temperature in a child a day before death

normal or no measurement required 0

less than 37.5°C

37.5°C and above

6. Prescribing medication to a child the day before death

antipyretic

antibiotics and/or sulfonamides

anticonvulsants

analeptics

Autopsy data

1. Signs of undernutrition

2. Gray skin tone

3. Weakly expressed cadaveric spots

4. Coagulated blood in the cavities of the heart and large vessels

5. Hemorrhages in the brain

6. Signs of pneumonia

missing

unilateral with involvement of one segment

diffuse or bilateral lesions 8
7. The nature of the pneumonic exudate

is absent

serous

purulent or hemorrhagic

8. Tonsillitis

9. Enteritis / colitis

10. Accidental transformation of the thymus

11. Hemorrhages in the adrenal glands

12. Seeding of pathogenic pathogens from the blood

*for calculations according to this table, you can use the program on our website - SIDS recognition

TO THE HISTORY OF STUDYING THE PROBLEM OF SUDDEN INFANT DEATH

Sudden infant death more than 100 years ago was explained by 3 theories: accidental suffocation, Asthma thymicum and Status thymicolymphaticus.

Accidental suffocation
The oldest description of this theory is given in the Old Testament. It tells the story of two women, one of whom "sleep" her child. That same night, she exchanged her dead child for a living one with another woman, and the next morning both women came to King Solomon, who had to decide which of the women belonged to the living child. This story is taken from the legends of the peoples of India and East Asia.

In the Middle Ages, it was forbidden to take children under 3 years old to their parents' bed at night. So, in church decrees, the unintentional strangulation of children in their sleep was regarded as a crime, which until the 17th-18th centuries was punishable by sanctions from the church (repentance, a fine, excommunication). In Florence in the seventeenth century, a device made of wood and metal was constructed, which was applied to children during sleep to protect them from being sprinkled or accidentally strangled. Its use was promoted in Germany, Great Britain, Sweden and Finland; in Denmark there was a competition by the Royal Academy of Sciences to improve this device. There were still indications in nineteenth-century legislation that accidental strangulation in sleep should be considered a crime.

At the beginning of the last century, when children began to sleep more and more alone in cribs, some of them, after sleeping, were still found dead in cribs. Then more often began to suggest suffocation with bed linen or blankets during sleep. In the early 1940s, the concept of mechanical strangulation of infants was subjected to extensive testing and scrutiny. P. Wooley discovered in 1945 that infants are able to change position to ensure the process of breathing during sleep, regardless of the position in which they sleep or the bed linen used and other breathing obstructions.

His findings gave impetus to the development of a new understanding of sudden unexplained death of infants. In the analysis of air under various blankets, a decrease in oxygen content or an increase in carbon dioxide content was determined only when blankets were used with a rubber lining tightly fitting on the sides. Children covered with non-rubber blankets did not show any abnormalities for a long time, until there was an increase in temperature under the covers and the children began to sweat. Attempts were made to put the children tightly with their nose or mouth to the mattress than to cause a lack of oxygen. However, even the smallest child was able to turn so that the airway remained free.

So far, there is no study that would give criteria for distinguishing death as a result of soft covering, for example, when lying on soft pillows, from sudden infant death. In addition, studies in recent years have shown that the discussion about accidental strangulation is not yet over.

Asthma thymicum

The theory of Asthma thymicum, according to which the trachea is compressed by an enlarged thymus, which causes the child to suffocate, is associated with the report of the Basel physician Felix Platter, who in 1614 described an autopsy of a 5-month-old child who died suddenly with symptoms of stridor and shortness of breath. However, Platter was probably not describing an enlarged thymus, but struma (goiter), which at that time was a fairly common disease in the Alps [op. according to 19].

The notion of a painfully enlarged thymus existed until the last century. The final answer to the question about Asthma thymicum was received only after the publication of the study by Friedle-ben, who, on the basis of the anatomical, physiological and experimental studies carried out, came to the following conclusion: “The thymus cannot cause laryngism either in a normal or in a hypertrophied state; Asthma thymicum does not exist!” .

Status thymico-lymphaticus

In 1889-90, Paltauf abandoned the mentioned hypothesis of compression of the trachea or neck vessels by an enlarged thymus; instead, he explained the sudden death of infants without morphologically detectable causes of death as a lymphatic-hypoplastic anomaly of the constitution, manifested by an enlarged thymus, hyperplasia of the lymph nodes and a narrow aorta. He pointed out that "in a hypoplastic or pathologically persistent thymic gland, not one cause of death is recognized, but only a partial symptom of a general malnutrition." In the presence of such an anomaly of the constitution and additional loads (excitation, pathological irritation, for example, immersion in water), sudden cardiac arrest may occur. The anomaly of the constitution postulated by him later became known under the name "Status thymico-lymphaticus" and in subsequent years was issued as the cause of death of many suddenly deceased children, as well as in other sudden deaths.

The theory of Status thymico-lymaphaticus also proved to be very attractive scientifically: between 1890 and 1922, many publications appeared on this topic. At the same time, even then, many authors showed that this theory is untenable. In England there was even a "Status Lymphaticus Investigation Committee" which, after reviewing more than 600 autopsy results, concluded that there was no evidence "that there is a so-called status thymico-lymphaticus as a pathological unit." After this explanation, there was a sharp decrease in the frequency of this diagnosis in death certificates. As such, the diagnosis of suffocation under the covers has increased again [op. according to 19].

Thus, the history of the study of sudden infant death in many ways represents a paradigm of possible misconceptions in medicine. The misconceptions shown here may serve as a warning to us that new theories of the occurrence of hitherto incomprehensible diseases should at least be critically examined as to whether they correspond to the already known epidemiological and morphological characteristics of these diseases, and not allow, so impressively well-founded plausibility of the new theory mislead yourself.

MODERN PATHOPHYSIOLOGICAL MODELS TRYING TO EXPLAIN SUDDEN INFANT DEATH

Despite the significant increase in knowledge about sudden infant death, we must state with dissatisfaction that in our study of causes and pathogenesis we are still far from a causal explanation of it. From the variety of hypotheses of the pathogenesis of SIDS, we will try to critically discuss some of them, including those that have already influenced practical activities.

Apnea hypothesis

The apnea hypothesis is based on a 1972 report describing sleep apnea of ​​more than 20 seconds in 5 infants. Two of these children later died with a diagnosis of SIDS. They were brothers and came from the same family with a history of 3 other cases of SIDS. It was concluded that prolonged sleep apnea is an important element in the pathogenesis of SIDS and therefore, with timely recognition, opens the way for targeted prevention of SIDS. This hypothesis was quickly accepted and led to the introduction of respiratory monitoring as a screening method.

Only 20 years later it turned out that both patients, on which the hypothesis was based, were killed by their mother, and the described apneas in these children have never been objectively confirmed. At the same time, the apnea hypothesis has significantly lost its plausibility with its practical consequences, primarily related to the use of polysomnographic monitoring for the prevention of SIDS. In addition, the apnea hypothesis was not consistent with the autopsy data of SIDS victims: more than 90% of these children had petechiae on the thymus, pericardium, and/or pleura. In an animal experiment, petechiae never occurred with drug-induced respiratory paralysis, but appeared only after strong intra-alveolar pressure fluctuations in combination with hypoxia, as usually develops as part of upper airway obstruction.

In the International Classification of Diseases X revision in the section under the code G 47.3 is "Children's sleep apnea". This term refers to central or obstructive sleep apnea observed in children during sleep. There are 4 variants of this syndrome: apnea in premature babies (due to severe immaturity of the respiratory system), an obvious life-threatening episode, which will be discussed in detail in a separate section of this review, early childhood apnea, obstructive sleep apnea syndrome.

Apnea syndrome is represented by respiratory arrests beyond the physiological norm (sleep apnea lasting 9-12 seconds is considered pathological). Also considered pathological:

  • frequent physiological apnea;
  • a combination of apnea (physiological and pathological) with periodic breathing (3 or more episodes of respiratory arrest lasting 3 or more seconds, alternating with periods of normal breathing, lasting 20 seconds or less);
  • combination of apnea with shallow breathing (hypoventilation combined with bradycardia); apnea with rapid breathing (hyperventilation);
  • apnea with prolonged periodic breathing (more than 12-15% of sleep time in preterm infants and more than 2-3% in full-term infants).

Long QT Syndrome

World experience in clinical cardiology shows that cardiac arrhythmias occupy a special place among the risk factors for "sudden cardiogenic death". Among them, priority is given to arrhythmias in long QT syndrome.

For the first time in 1957, Jervell A., Lange-Nielsen F. described cases of a combination of congenital deaf-mutism with functional disorders of the heart, prolongation of the QT interval on the ECG and episodes of loss of consciousness, often ending in sudden death in children in the first decade of life. Romano C. et al. (1963) and Ward O. (1964), independently of each other, described a similar clinical picture of the combination of ECG QT interval prolongation with cardiac arrhythmias and episodes of syncope in children without hearing loss. For the diagnosis of congenital forms of long QT syndrome in the case of borderline lengthening of the QT interval and (or) the absence of symptoms, Schwartz in 1985 proposed a set of diagnostic criteria. Major criteria are corrected QT interval prolongation (QT>440 ms), a history of syncope, and long QT syndrome in family members. "Small" criteria are congenital sensorineural deafness, episodes of T-wave alternation, slow heart rate (in children), and pathological ventricular repolarization. In 1993, these criteria were revised to take into account the dependence of the duration of the QT interval on the sex of patients. Significant prolongation of the QT interval, paroxysms of ventricular tachycardia torsade de pointes and episodes of syncope are of the greatest diagnostic value.

Currently, numerous studies confirm that congenital long QT syndrome is a genetically heterogeneous disease; About 180 mutations are described in the literature, which are localized in six genes located mainly on three chromosomes 7, 11 and 3. One gene encodes the sodium channel (SCN5A), two genes encode potassium channels (HERG and KvLQT1) and two are a modulator of the work potassium channel minK (KCNE1, KCNE2). Knowledge of specific genes and gene defects has clinical implications: gene defects lead to increased function (SCN5A) or decreased function (HERG, KvLQT1) of channels and therefore may determine appropriate therapy.

There are three main types of mutations in the LQTS1, LQTS2 and LQTS3 genes. Two of them, LQTS1 and LQTS2, are associated with a mutation in the genes encoding protein subunits of potassium channels. The third variant LQTS3 is associated with impaired sodium channel function. Due to the fact that mutations occur in genes encoding ion channel proteins, long QT syndrome is referred to as ion channel disorders. There is evidence of the most frequent occurrence of clinical symptoms of QT-long interval syndrome (syncope, cardiac arrest, sudden death) during exercise - with LQT1 forms, during sleep - with LQT2 and LQT3 forms. Carriers of the LQTS2 genes in 46% of cases have tachycardia induced by sharp sounds. Sudden death during sleep is more common in LQT3 forms of long QT syndrome.

The suggestion that at least some of the cases of SIDS were associated with intracardiac disturbances in the conduction of excitation was made about 30 years ago. This hypothesis received decisive confirmation in 1998, when the results of a prospective (almost 20 years) ECG study of 34,442 newborns were published. Of the 24 subsequent cases of SIDS in this population, 12 had a prolonged QT interval. From here, a 41-fold increase in risk was calculated for this syndrome.

As a practical consequence of the above study, ECG screening of all newborns has been introduced in some countries; children with a prolonged QT interval during the first year of life received a beta-blocker. The question remains, what side effects are associated with the risk of overdose with this method of prevention. A significant argument against this approach is the pathomechanism associated with the QT hypothesis, that is, Tor-sades-de-point ventricular tachycardia followed by ventricular flutter, which was not observed in any case among those who died from SIDS under monitoring. It cannot be ruled out that this cause of death occurs in some cases of SIDS.

Decreased brain stem perfusion

Saternus in 1985 hypothesized that the prone position and the associated turning of the head to the side may cause compression of the a. vertebralis with subsequent reduction in brainstem perfusion, resulting in central apnea with a fatal outcome. However, the introduction of Doppler sonography as a screening method in identifying children at risk of SIDS seems premature. Against this hypothesis, however, is the fact that in a recent analysis of 246 cases of SIDS and 56 control cases with other causes of death in both groups, an equally high proportion (40% vs. 41%) of children were found with a rotated or elongated head. .

Thus, this hypothesis is not yet sufficiently well substantiated to proceed on its basis to any practical actions such as ultrasound screening (with possibly significant parental concern if the result is abnormal).

Violation of the awakening reaction and "grasping" breathing

When analyzing monitoring of cardiac activity and respiration recorded during the death of an infant, it turned out that in 7 out of 9 cases, the primary alarm signal was caused by slowly progressive bradycardia. Almost at the same time, there was a gasping breath.

Prolonged apnea appeared, on the contrary, most often a few minutes later. Since "grasping" breathing occurs only at arterial pO2 New data call into question the use of cardio-respiratory monitors. If these devices in some children give an alarm when they already have grasping breath, then it is quite possible to imagine that it may be difficult to resuscitate these children. The data, however, do not answer how this hypoxia came about.

Before we can unequivocally prove that SIDS is the result of endogenous or exogenous upper airway obstruction, the question arises why children in this life-threatening situation do not awaken and release from it and why their "grasping" breathing is not effective.

While the regulation of breathing during sleep and the response to hypoxia and hypercapnia have been known for over 100 years, relatively little attention has been given to the awakening response. Awakening is given an important function: when in a dream, for example, a pillow covers the mouth and nose, it is unlikely that increased breathing will help; waking up and removing the pillow can play a life-saving role.

Delayed awakening has been found to be associated with numerous known risk factors for SIDS. For example, exposure to smoking, prone positioning, covering the face with a diaper, respiratory tract infections, and elevated room temperature are associated with an increased awakening threshold. The use of a pacifier and breastfeeding, which in epidemiological studies have been associated with a reduced risk of SIDS, on the contrary, lead to a decrease in the awakening threshold. These data represent a link between epidemiology and pathophysiology and are indicative of the significance of impaired arousal in the pathogenesis of SIDS.

An important factor in mediating the awakening response is serotonin, which, as a neurotransmitter, plays a central role in the regulation of sleep, respiration, chemoreception, and temperature homeostasis. In studies of the binding of various receptors to a neurotransmitter in children who died of SIDS, the most distinct changes were revealed on serotonin receptors. Since serotonin is involved in the regulation of almost all mechanisms associated with SIDS (upper airway control, respiratory mechanics, awakening, "grasping breath"), it is possible that this neurotransmitter actually plays a key role in the pathogenesis of SIDS.

Along with awakening, "grasping" breathing is the second self-survival mechanism that must fail in order for SIDS to occur. "Hatching" breathing has clearly occurred in many victims of SIDS, however, it has proven to be ineffective.

Severe hypotension develops early in SIDS. This could explain why "grasping" breathing does not lead to the restoration of vital functions. Since the blood pressure of an infant during sudden death has not yet been measured, this hypothesis looks speculative (controversial); in addition, there are indications that the petechiae mentioned above appear primarily after an increase in systemic circulatory resistance, but not after induction of hypotension by blockade of alpha-adrenergic receptors, so this hypothesis is not consistent with the pathology of SIDS.

Other hypotheses

In the very late 80s - early 90s, it was found that a number of children who died from SIDS had a low concentration of the substance P - an antagonist of endogenous endorphins, that is, respiratory arrest occurs from an excess of endogenous narcotic substances - endorphins.

Another hypothesis for the genesis of SIDS is associated with a defect in the beta-oxidation of long-chain fatty acids, which during hypoglycemia provide the synthesis of ketone bodies. The brain during hypoglycemia uses ketone bodies as an energy substrate, and during hypoglycemia provoked by starvation, fever, banal infections, due to a deficiency in the formation of ketone bodies, the brain can be affected. The defect is localized - the 985th position of the medium-chain fatty acid dehydrogenase gene. It is believed that such a defect is responsible for 15-20% of SIDS cases.

Recently, a hypothesis has been discussed, according to which children with SIDS have a delay in the maturation of cardiorespiratory control from the central nervous system. Pathological examination of the brain reveals underdevelopment and a decrease in interneuronal connections in the region of the arcuate nucleus, which is responsible for controlling respiration and cardiac activity. In situations that cause a violation of the homeostasis of the body (hypoxia, hypercapnia, acidosis), more often occurring in a state of sleep, the centers for regulating the vital functions of the body in the brain stem are unable to adequately change breathing and cardiac activity, resulting in death.

I. M. Vorontsov et al. consider SIDS to be a kind of borderline condition caused by the intensive process of the child's growth and active differentiation of its tissue structures, characterized by a pronounced maladaptation of the child in the first year of life, the extreme variant of which can be a lethal outcome against the background of exposure to a non-specific factor that is minimal in its severity. Markers of this borderline state can be phenotypic features that characterize the pace and harmony of the biological maturation of the child.

Thus, from the presented data it becomes clear that at present, even with the most diverse assumptions of pathogenesis, no single hypothesis can explain the phenomenon of SIDS. Rather, it can be assumed that many factors must overlap to cause sudden infant death. Thus, it is conceivable that an exogenous load (eg, prone position) can cause SIDS when it falls on a susceptible child (eg, with a mutation in the serotonin transporter gene) who is in a critical phase of his development.

OBVIOUS LIFE-THREATING EPISODE IN INFANTITY

In 1986, for the first time at a conference of the American Institute of Health, the concept of "apparent life-threatening episode" (apparent life-threatening events - ALTE) for infancy was introduced. It has a number of synonyms (near-miss SIDS, abortive SIDS, etc.) and refers to infants who have experienced life-threatening episodes and survived. At the same time, ALTE should not be understood as a diagnosis, because it only gives a description of the situation, the cause of which is currently not understood.

The following characteristic signs should be looked for according to the ALTE definition: sudden cessation of breathing (central sometimes obstructive apnea), acute discoloration of the skin (cyanotic or pale, often plethoric) and extremely pronounced violations of muscle tone (muscle hypo- or hypertension). Such a change in the state of the child most often occurs in complete well-being, having a particularly dramatic effect on those present and often gives the impression that the child has died. This explains the terminological proximity of the above synonyms related to the issue of sudden infant death. First of all, emergency physicians, pediatricians and rescue workers are most often encountered with a description of an apparent life-threatening episode. Since, with the help of resuscitation and stimulation measures, an acute condition, as a rule, already passes before the arrival of a doctor, the first person conducting the study faces the difficult question of what further diagnostic and therapeutic actions to take.

The frequency of ALTE is estimated to be about 0.6%. Obvious life-threatening episodes occur from the first week of life with increasing frequency and peak in the first month of life. In principle, it can be assumed that during the first 4 months 60% of all cases of ALTE are registered, which can be expected during the first year of life.

Despite the relationship between the phenomenon of an acute threatening episode and the actual onset of sudden infant death, the assumption of an identical pathophysiological cause has not been confirmed to date. In numerous studies on ALTE, the identified pathological findings point to a trigger due to the disease, which in fact can pose a serious threat to vital regulatory mechanisms. Some of the possible triggers for life-threatening manifestations are: central obstructive or mixed sleep apnea on polysomnographic studies; seizures; infections of the upper and / or lower respiratory tract; gastroesophageal reflux; metabolic diseases or circadian rhythm disorders.

Table No. 2 presents the differential diagnosis and the corresponding diagnostic measures for the verification of ALTE.

Table number 2
Conducting differential diagnosis in ALTE

Differential Diagnosis

Congenital malformations

Whole body status, cranial, abdominal sonography

Diseases of the upper and lower respiratory tract

Infectious diagnosis, serology (eg, whooping cough, RS virus infection, etc.), microbiology, chest x-ray, cardiorespiratory monitoring, and, when available, polysomnography

CNS diseases (including cardiorespiratory dysregulation and circadian rhythm disorders)

Neurological status (corresponding to gestational age), EEG, cranial sonography, sometimes MRT, polysomnography

Gastroenterological and/or metabolic diseases

Newborn screening
Amino acid metabolism disorders
Acid-base state, differential blood picture, glucose, ammonia, magnesium, calcium, carnitine, lactate, pyruvate, etc.
Continuous pH-metry, abdominal sonography

Diseases of the heart, circulation

ECG, Holter monitoring
echocardiography
Heart rate variability
Doppler sonographic examination of blood vessels

Myopathies

Neurological status
EMG
Polysomnography

Rare emergency causes (eg, child abuse, Munchausen-by proxy syndrome)

Whole body status
Ophthalmic diagnostics
Videometry

If it is possible to identify a pathological correlation that most likely explains the life-threatening situation, then treatment can be carried out causally. And if, on the contrary, diagnostic efforts remain ineffective, home monitoring with the option of collecting information can be offered. This seems logical as in a high percentage of cases (>30%) the next ALTE should be expected within a few weeks.

However, for the use of home monitors in infants, there are still no evidence-based recommendations for the prevention of SIDS. At the very least, we can expect improvements in home monitoring with the latest generation of devices still in clinical trials. After detailed consultation on the use of the monitor, parents should be trained in resuscitation.

The duration of home monitoring mainly depends on the capabilities of the parents. Since already a few weeks after the development of a threatening situation, the probability of recurrence becomes very small, it seems rational to carry out home monitoring within 3 months after the last actually life-threatening event.

Seemingly life-threatening episodes in infancy are not uncommon and should be taken seriously. In many cases, it is recommended to carry out differential diagnostics in stationary conditions. In 50-70% of children with such episodes, it is possible to find the cause and carry out appropriate therapy.

Since the concept of "sudden infant death" is not monocausal, the development of preventive concepts is a rather difficult task. Primary prevention of sudden infant death aims at the healthy behavior of the entire population, while secondary prevention, through appropriate interventions, identifies particularly susceptible individuals and is limited to remedial measures in this group. The concept of tertiary prevention should also be mentioned: in this case, the patient is already being treated in order to prevent the development of complications of his disease. Such falls in sudden infantile death because of its finality.

Primary prevention

Antenatal activities

Optimizing sleep conditions

  • no pillows
  • Position on the back
  • Fresh air
  • No tobacco smoke
  • No duvets or sheepskins
  • Sleeping bag
  • Room temperature 18 o C

Smoking

Breast-feeding

Secondary prevention

Identification of risk groups

Signs of risk

>2 deliveries and/or body weight 2500 g

1st or 2nd delivery and body weight >2500 g

The position of the child in a dream

On the stomach

Bed dress

Pillows and/or sheepskin

mother smoking

>10 cigarettes a day

non smoking

>4 months

CONCLUSION

Since the concept of "sudden infant death" is not monocausal, the development of preventive concepts is a rather difficult task. Primary prevention of sudden infant death aims at the healthy behavior of the entire population, while secondary prevention, through appropriate interventions, identifies particularly susceptible individuals and is limited to remedial measures in this group. The concept of tertiary prevention should also be mentioned: in this case, the patient is already being treated in order to prevent the development of complications of his disease. Such falls in sudden infantile death because of its finality.
The history of pediatrics is characterized by the fact that it, more than in other disciplines, follows the strategy of primary and secondary prevention.

Principles for the prevention of sudden infant death

The principle of primary prevention is to break the causal constellation of possible factors in sudden infant death. Due to the existing ambiguities in the pathophysiological process, the rupture sites can currently only be determined on the basis of epidemiological studies, that is, empirically. This principle - prevention without precise knowledge of pathogenesis - is not new in medicine.

Over the past 15 years, a number of risk factors for sudden infant death have been identified. Only those risk factors that satisfy at least 3 conditions are suitable for the application of the preventive concept:

  1. it must be probable that the relevant risk factor, by virtue of its severity, its resistance to influencing factors, its biological plausibility and sometimes dose-dependence, and its confirmation by numerous studies, is in close proximity to causality.
  2. the risk factor must have a high prevalence (frequency) as a prerequisite for the effect of the intervention, which is in a reasonable ratio to the costs of the intervention.
  3. the risk factor should in principle be modifiable and practically acceptable.

In addition, it must be taken into account that recommendations aimed at reducing sudden infant death are not harmful to the child (have no side effects in relation to other health disorders). Little research has been done in this direction so far, since in previous studies the health goal of "eliminating sudden infant death" came to the fore in its significance. However, in the future it is necessary to require that the possible side effects of the recommendations given be traced.

Primary prevention

Antenatal activities

The primary prevention of SHS is reduced to medical education of the population and improvement of the work of family planning centers, so that a woman, already at the time of pregnancy planning, gives up bad habits (smoking, drinking alcohol, drugs), observes the principles of rational nutrition, physical activity, and lifestyle.

A high risk of SIDS is associated with prematurity and low birth weight. That is why the prevention of preterm birth and the birth of a small child is important. Modern programs for the prevention of preterm birth include the following recommendations: more frequent medical examinations of pregnant women, reduced physical activity, the need to avoid stress, reduced travel and some restriction of mobility, cessation of sexual activity, self-control.

Optimizing sleep conditions

Numerous studies have unequivocally indicated that the risk of death in a child sleeping on his stomach is 5-10 times higher than that of a child who usually sleeps on his back.

Physiological studies have determined that this is due, among other things, to easier awakening in the supine position. The lateral position also carries more risk than the supine position and, as an alternative, the supine position appears to be associated with more SIDS deaths than the prone position. The reason given for the danger of aspiration in infants as a cause of death is extremely rare and the risk does not increase with the supine position.

The supine position is the safest position. This may be due to the fact that in the supine position, gastric reflux through the lower esophagus is more easily returned to the stomach or excreted more efficiently.

At 4-8 months, babies begin to roll over on their own from a supine position to a prone position. There is no certainty regarding the safety of this. Since observing a change in position of a child during a night's sleep is absolutely unrealistic, recommendations can be either the use of a sleeping bag, which is attached to the bed from the sides and at the same time makes it impossible to roll over, or arranging a bed in such a way that the position on stomach risk of sudden death to minimize. The latter is the only option for a very small number of infants who cannot get used to sleeping on their backs at all.

Little is known about the possible side effects of the exceptional supine position during sleep. Perhaps this contributes to the flattening of the nape and some delay in the development of gross motor skills, which is facilitated by the prone position. In addition, in many children, the depth of sleep in the supine position is less.

There is a reassuring circumstance that the supine position is the traditional sleeping position of the human infant, which only in the western part of the world was disrupted in the 1970-1990s by the "prone position" fashion.

For prevention, it is also recommended to observe such sleep conditions to avoid overheating, suffocation, airway obstruction and reverse breathing. This includes having a less soft, firm but breathable mattress, a ventilated railed crib, expanding pillow avoidance, wrapping around the edges including so-called nests, and using only light bedding. Heavy feather beds, fluffy wool sheepskins and multiple layers of blankets are considered inauspicious.

Healthy sleeping conditions for babies

  • Safe baby crib with fence
  • Thick, smooth and breathable mattress
  • no pillows
  • Position on the back
  • Fresh air
  • No tobacco smoke
  • No duvets or sheepskins
  • Sleeping bag
  • Room temperature 18 o C

The use of so-called "Dutch sleeping bags" seems ideal. This is a sleeping bag that leaves the neck, head and arms free, and in the leg area provides sufficient freedom of movement. And if it is attached to the edge of the bed with the help of straps, then active turning becomes impossible without the child being too limited in his freedom of movement. Overheating as well as hypothermia is prevented by adequate clothing.

Room temperature should not, if possible, exceed 18°C, although this is often unrealistic in modern conditions of living in apartments with central heating and multifunctionality of rooms in small apartments.

Co-sleeping in the parent's bed has been considered a risk factor in many studies. The risk is especially increased when there is a danger of overheating and over-covering. Thus, higher risks have been identified in situations where the child spends the whole night in the parents' bed, when the bed area is small, and when alcohol and nicotine play a role.

Especially favorable is the sleep of a small infant in his own bed in the bedroom of his parents. Unfavorable places to sleep are: pockets for carrying children, a seat in a car, a deployable place to sleep in a car, strollers, rocking chairs suspended in the form of a hammock, sofas.

Back in 1992, the American Academy of Pediatrics, as one of the most important measures for the prevention of SIDS, recommended avoiding laying children in the first year of life on their stomach during sleep. Based on this recommendation, a national "Back to Sleep" campaign has been launched in the United States since 1994, designed to convince parents that their babies should sleep on their backs, on their sides, but not on their stomachs. The desired effect was not achieved immediately - habits and family traditions turned out to be very persistent. However, over 4 years of a large-scale educational campaign, the number of little Americans sleeping on their stomachs has almost halved, and the number of cases of "death in the cradle" has been reduced by a factor of three.

Smoking

This risk factor is also of great importance. It is extremely dose dependent. Because of 10 cigarettes smoked a day, the risk for a pregnant woman to lose her child at 1 year of life increases by 5-6 times. The risk is greater, the stronger smoking has had an impact on placental insufficiency and prenatal dystrophy. Maternal smoking postpartum and paternal smoking also have a comparable risk effect. Although nicotine can be transmitted through breast milk during breastfeeding, breastfeeding by smoking mothers is not associated with a high risk.

Therefore, breastfeeding is recommended for at least the first four months of life, even when the mother is unable to stop smoking. Nevertheless, it is not recommended for her to smoke an hour before feeding and during feeding. This is the only way to achieve at least a dose reduction in maternal smoking.

Compared to the risk factor for prone positioning, smoking cessation advice is much less well received. Anti-nicotine programs should start at the elementary school level and take into account the influence of peers on affected children. In addition, the availability of cigarettes should be limited.

Breast-feeding

Infants who are formula-fed early have an increased risk of sudden death. This risk, however, is partly due to the significantly higher proportion of non-breastfeeding mothers who smoke. Since breastfeeding for at least 4–6 months has other benefits and no identified disadvantages, recommendations for breastfeeding and for the prevention of sudden infant death are particularly relevant.

So, in order to minimize the risk of SIDS, the mother should be very attentive to herself and her child during pregnancy. Smoking, drugs, excessive alcohol consumption by a pregnant mother triples the chances of sudden death of a child in the first year of life. In addition, regular medical supervision during pregnancy is very important for the prevention of SIDS.

In the first year of life, at least until the moment when the child himself begins to actively roll over, he should not sleep on his stomach. The crib should have a hard mattress and should not have a large and soft pillow. It is unlikely that a child will need toys in a dream, so they need to be removed from the crib.

During sleep, the baby should not be too warmly dressed. In the room where he sleeps, the air temperature should be comfortable for an adult wearing a short-sleeved shirt. The child during sleep should be covered with a light blanket to shoulder level. You can't swaddle him too tight.

Avoid exposure of the child to pungent odors, sounds and light stimuli, especially during his sleep, including daytime.

It is necessary to strive to ensure that the child sleeps in his own crib, but in the same room with his parents.

Do not smoke in the presence of an infant. Moreover, if for some reason the baby sleeps next to the father or mother, then the latter should not exude pungent odors of tobacco, alcohol, perfumes, etc.

Mother's milk is good protection against SIDS, as well as many other problems. Therefore, natural feeding should be continued as long as possible.

Contrary to common misconceptions, vaccination in no way causes SIDS and, on the contrary, protects the baby from many serious problems. In the absence of medical contraindications, the child must be vaccinated.

Secondary prevention

Secondary prevention of sudden infant death is about identifying high-risk groups and implementing targeted interventions.

Identification of risk groups

Since the cause of SIDS has not been elucidated, the risk factors are determined exclusively by statistical methods. For some of them, the mechanism of influence is more or less clear (if it is known that weaker children are more likely to be susceptible to SIDS, then it is clear why premature babies, multiple pregnancies, etc. are among the risk factors). The list of major factors that increase the risk of SIDS is constantly changing as new studies are carried out, but the main patterns were identified in the early 90s.

An attempt to identify subgroups of infants at greater risk is presented by the Magdeburg SIDS score table. This is an example of a table that can be used to calculate individual statistical risk. However, it should be pointed out that this and other similar tables, as a rule, are valid for a particular region and a certain period of time.
Magdeburg SIDS score table

Signs of risk

>2 deliveries and/or body weight 2500 g

1st or 2nd delivery and body weight >2500 g

The position of the child in a dream

On the stomach

Bed dress

Soft mattress and/or heavy down comforter

Pillows and/or sheepskin

Barred bed and sleeping bag

mother smoking

>10 cigarettes a day

non smoking

Duration of breastfeeding

>4 months

With a score of 0-3, the risk of SIDS is 1:100, with a score of 10 it is well below 1:1000.

Along with anamnestic scores, a range of diagnostic measures are offered to identify affected children.

Polysomnography comes to the fore. However, it must be said with all certainty that this costly method, for various reasons, is not suitable as a screening study for recognizing SIDS risks in an unselected group of infants. Its value lies mainly in checking after life-threatening conditions or with certain symptoms of impaired sleep architecture or cardiorespiratory regulation.

Interventions for infants at risk of SIDS

An important principle of monitoring children at high risk of SIDS should be considered increased attention to families where there is such a child. This can give a very real result: with the introduction of dispensary care for children in the UK, based on the identification of a high risk of SIDS, the so-called preventable infant mortality has almost tripled in 4 years, with about 18% of this decrease due solely to the factor of increased surveillance and more thorough care for children. children at risk for SIDS and health education.

A child requires increased attention to himself if he develops even a minimally pronounced ARVI. Against the background of the disease, it is advisable to strengthen the monitoring of the child during the hours of maximum risk of SIDS, and with minimal signs of impaired breathing regulation, such children are shown immediate hospitalization.

In some children with a high risk of developing SIDS associated with hereditary long QT interval syndrome (QT SUI), the use of beta-adrenergic receptor blockers to prevent life-threatening heart rhythm disturbances is justified. This recommendation finds numerous supporters, who were convinced by the results of a large-scale 19-year follow-up of more than 34,000 newborns who underwent an ECG study on the third or fourth day of life to detect SUI QT. The QT interval measured in the first week of life was longer in infants who subsequently died of SIDS compared with infants who lived to at least one year of age, and also compared with infants who died in the first year of life from other causes. .

During the first year of life, 24 children died, the cause of death was SIDS. Half of the children who died as a result of SIDS were diagnosed with SUI QT in the first week of life. The relative risk of SIDS in children with QT SUI was 41.6. This highlights the potential value of neonatal ECG screening. The results of monitoring almost 1000 families showed that the prophylactic administration of beta-blockers to children with SUI QT for several months reduced mortality in this group to 3 percent. At the same time, the question is being discussed: is the risk of such treatment (with possible side effects) in 98 or 99 infants justified in order to save only one child with a real threat of arrhythmogenic death. Potentially huge emotional experiences in the families of infants who will be subjected to such treatment in vain are also discussed. Genetic research would help to solve the problem more radically. Prescription of beta-blockers is much more effective in patients with the LQT1 or LQT2 genotype than in those with the LQT3 subtype.

When a risk group is identified, the question arises of carrying out rational measures. In this case, we can talk about particularly intensive individual consultations regarding the elimination of risk factors.

First of all, this is enhanced control by the pediatrician, who can prescribe vitamins, microelements, stimulants of respiratory and cardiac activity, adaptogens (eleutherococcus, ginseng, etc.).

A further measure for the prevention of SIDS is the appointment and conduct of home monitoring using a cardiorespiratory monitor.

The effectiveness of general home monitoring in reducing mortality from SIDS, however, has not yet been proven in any controlled study. This does not mean that home monitoring cannot be life-saving in some cases, as rescue in individual cases is also unlikely to be studied in large controlled trials or that this possibility can be ruled out. Monitoring allows you to recognize both acute danger and timely detection of cardiorespiratory pathology. At the very least, with the help of it, the heart rate can be recorded. Recording monitoring with automatic collection and storage of received data should be aimed at. Continued home monitoring after 10-12 months of age is recommended only in rare cases. Given the inestimable effectiveness of home monitoring and the cost of conducting it, parental consent, along with the magnitude of the individual risk and the practical possibility of its implementation, are an essential criterion for its appointment.

The undoubted advantage of using monitors is that they have a calming effect on mothers. The appointment of home monitoring for a child born after a previous case of sudden death of a child in the family is fully justified taking into account the experience of the parents, while for a prenatally dystrophic child born to a heavily smoking mother, due to the dubious cooperation of parents, such an appointment, despite a higher risk turns out to be meaningless.

CONCLUSION

Although a lot of epidemiological data on sudden infant death has been accumulated in the world in recent years, they do not provide any explanation for the etiology and pathogenesis of sudden infant death. Sudden infant death is seen as "multifactorial"; this notion, however, is as little help as the term "idiopathic," which we use as a stand-alone term for many other diseases. As our knowledge of the pathophysiology of SIDS expands, it will be possible to recognize and classify the pathological conditions that underlie the sudden death of a child.

Prevention strategies that allow some reduction in the frequency of this tragedy today are based on epidemiological data. Pediatricians in Russia need to adopt a number of rules that have already become mandatory for most countries. Among them - questioning and establishing the degree of risk of the syndrome for each child, familiarizing parents (including future ones) with this syndrome, and introducing measures to prevent it. Just as important as learning about the causes of SIDS is the skillful handling of bereaved parents.

According to I.M. Vorontsov, the system of preventive measures in relation to children at high risk of SIDS needs further adjustment. The real prevention of this syndrome can be the creation of a set of measures aimed at eliminating potential provoking factors for SIDS, increasing the child's resistance to these factors and creating the possibility of monitoring the child's vital functions during critical periods. The development of specific specific measures in certain children, suggesting the possibility of identifying in a particular case the most likely mechanisms that are critical for a given child, is a task for the future.

The full text of this review with bibliography was published in the journal Human Ecology, 2004, No. 2.

What mother doesn't listen to her baby's breathing while he sleeps in his crib? Indeed, from the mere thought that in the morning the baby may not wake up, her heart shrinks from fear. What is the reason? It's all about the syndrome of infantile sudden death, which almost every mother has heard about. Lack of information and little knowledge of this condition give rise to misconceptions. Let's see what it is - "death in the cradle."

The sudden and unexpected death of a child for no apparent reason is given a terrifying name - "death in the cradle." In this case, the child's body is necessarily subjected to a pathoanatomical examination. If the autopsy does not reveal any objective causes of death, then they talk about sudden infant death syndrome (SIDS).

Sudden death can occur in absolutely any child and in any place. No matter how scary it may sound, it happens that a child dies in a stroller during a walk, in a car, or even in the arms of his mother. However, most often they are found dead in the crib.

How to reduce the risk?

Although the causes of "cradle death" remain a mystery, there are certain rules that parents can follow to reduce the risk.

  1. The position of the child in a dream. It is necessary from the very beginning to put the child to sleep on his back, since sleeping on his side is not safe for him. Studies by scientists have shown that for children sleeping on their stomachs, the risk of sudden death is 9 times higher than for those who sleep on their backs.
  2. Smoking during pregnancy increases the risk of sudden death in the baby. Ideally, if neither parent smokes. In no case should you smoke in any apartment, and even more so in the same room with a child! Parents who smoke should not take their children to bed.
  3. Temperature regime. A child wrapped in blankets and warm clothes overheats very easily. It is considered normal if the hands and feet of a child (as well as an adult) are slightly cool. It is not at all necessary to create warmer conditions for it; it is enough to maintain a temperature of 18 0 C in the room where the child plays and sleeps.
  4. Covering the baby's head. Lying in the crib, the child should almost touch the legs of her back. Before the child reaches the age of 12 months, the use of a pillow is not recommended. The crib should be covered with a sheet, and the child, if necessary, covered with blankets in several layers.
  5. Seek medical attention if the child's condition worsens. Weakened children need to be given more fluids and constantly monitor their temperature so that they do not overheat. Children's health needs to be monitored very carefully, because it can be difficult to immediately determine that a child has a serious illness.