Acute respiratory infections (ARI) in children 2024-25.pptx

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1. Acute respiratory infections (ARI) in children Croup (acute laryngotracheitis) / Chief of the Children’s Department Bashkir State Medical University PhD, prof. E. I. Etkina

2. Intrauterine development of the respiratory system

3. Respiratory organs are a system that is open to the external environment and feels the constant impact of potentially pathogenic factors. Respiratory diseases remain the leading cause of death in children of the first year of life - 21.8 per 10,000 births, and children from 1 to 4 years - 55.6 per 100,000 children of this age, compared with 2.6 per 100,000 children aged 5 to 9 years. The most common cause of death is pneumonia, a major complication of bronchitis in early childhood. In the last 3 years, there has been an annual increase of 3% in the number of children hospitalized for acute bronchitis, complicated by ARI.

4. Respiratory diseases are the leaders in the morbidity structure of children aged 0-14 years in Russia

5. Prevalence of respiratory diseases

6. The frequency of detection of acute respiratory infections in children

7. Every year, up to 10 billion people are registered in the world with ARI. T here are 27.3-41.2 million people in the Russian Federation, WHO - about 20% of world's population are ill, 90% of them are acute respiratory infections, half of them are children. In adults, the incidence of acute respiratory infections is 18%, in children it is 3.6 times higher and is 69 thousand per 100 thousand children under 14 years of age. On average, each child has 6 episodes of respiratory infections per year (children 2-3 years – no more than 5, 4 years and older than 5 years – no more than 3 episodes of ARI per year).

8. The epidemiological situation in the Russian Federation for ARI is characterized by an increase in all age groups by 12% compared to the previous decade. ARI and its complications cause 4.5 million deaths worldwide every year, including 4 million children under 5 years of age (66% of those who died before 1 year of age). In 75% of cases, the cause of child mortality from ARI is pneumonia. Every adult on average has the flu or other ARI 2 times during the year, a schoolboy - 3 times, a preschooler - 6 times. During our lifetime, we spend 1-2 years as patients with colds. 65% of patients who had been ill for 1 month had post-viral asthenia syndrome. Cases of disability and death of patients from ARVI account for 6%, the death rate from a seemingly harmless disease is 250,000-500,000 people annually. In the US А , about 110,000 ARI patients are hospitalized every year and 2-3 thousand patients die from complications associated with this disease. Colds are the cause of sick leave in 40% of cases, absenteeism in school - in 30%.

9. In the structure of children's morbidity, acute respiratory infections occupy the 1st place and make up 68-72% under 14 years of age, 76-82% under 4 years of age. Often sick children carry ARI more than 6 times a year, and in Russia it is every 4-5 children (15-75%) (with the frequency of ARI more than 6 times a year, the immune system does not have time to recover). During an influenza epidemic, mortality from non-communicable causes increases ("additional" mortality): from acute or recurrent myocardium infarct and chronic cardiosclerosis - by 18-20%, lung diseases and malignancies - by 15-20%, the relative weighted average risk of death in chronic heart diseases increases by 3 times. Among vaccinated UK citizens, the number of hospitalizations for cardio-vascular diseases decreased by 19%, and flu and pneumonia - by 32%.

10. ARI is a polyetiological group of acute non-specific infectious diseases from the respiratory tract of any localization, but having similar epidemiological, pathogenetic, clinical and therapeutic approaches .

11. The term ARI requires decoding - an indication of an organ lesion (rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis, otitis, etc.). Basically, this is a self - limiting disease , but it creates a great economic strain for any country - up to 40% of the total temporary disability of the population, damage of 40 billion rubles/year, accounting for up to 80% of the damage from all infectious diseases. The economic losses of the Russian Federation from respiratory infections are about 3 billion rubles. Direct and indirect financial losses from influenza and ARI are associated with loss of working time - more than 1 billion US dollars are estimated annually, as well as with the cost of purchasing medicines for the population, excluding medical treatment of complications of influenza and ARI, more than 1.25 billion US dollars. The damage from ARI is 86% .

12. The high frequency of occurrence among children is explained by: 1. features of the formation of the immune system 2. a wide variety of pathogens 3. high contagiousness of viral infections 4. unstable immunity to them.

13. Etiological factors – more than 200 pathogens. 25-30 % - mixed infection . Group Pathogens Respiratory viruses Influenza A, B, parainfluenza, adenoviruses, RS virus, rhinoviruses, coronaviruses Intra - and extracellular pathogens Chlamydophila pneumonia, chlamydia trachomatis, Mycoplasma pneumonia and hominis, Pneumotsista Herpesviruses Herpes types 1 and 2, EBV types 4, CMV types 5, herpes types 6 Representatives of endogenous microflora Staphylococci, streptococci, enterococci, etc. Bacterial pathogens of digestive system and respiratory tract infection Pneumococcus, Hemophilus infl., Moraxella catarr ., Staphylococcus aureus, Escherichia coli, Klebsiella Other pathogens Legionella, bocavirus, metapneumovirus  

14. Different positions in Russia and foreign sources regarding the etiology of acute respiratory infections. Etiology of acute respiratory infections in the Russian Federation Etiology of acute respiratory infections in the world Influenza types A and B 10-20% Etiology not established 20-30% Flu C 1-2% Rhinoviruses 30-50% Parainfluenza 8-10% Coronaviruses 10-15% RS-infection 8-10% Influenza viruses 5-15% Adenoviruses 8-10% PC viruses 5% Coronaviruses 4-8% Parainfluenza 5% Rhinoviruses 7-17% Adenovirus 5% Enteroviruses 5-10% Enteroviruses 5% Reoviruses 1-2% Metapneumoviruses <1% Mycoplasma 10-15%    

15. Etiological factor s of ARI ( continued ) 1. 85-90% - respiratory viruses , have epitheliotropy and toxicity. The main groups of viruses: - RNA-containing viruses (orthomyxoviruses: influenza A, B, C and their various antigenic types and variants; paramyxoviruses (parainfluenza type 4, RS viruses, viruses of mumps and measles, human metapneumovirus), coronaviruses - 4 types, picornoviruses , rhinoviruses - 102 serotypes) - DNA-containing viruses (adenoviruses - 32 serotypes, herpes). 2. Bacterial ARI – no more than 5-10%, typical and atypical (intracellular), out-of-hospital (outpatient) and in-hospital (hospital, nosocomial). In children, ARI often occur with additional colonization of the respiratory tract by bacteria or as a superinfection (activation of opportunistic pneumotropic bacterial flora in their obligate habitats, i.e. in upper airways ). 3. Viral-bacterial (+ Mycoplasma) and viral-viral associations . According to British researchers, it is possible to isolate the culture of the virus that causes ARI only in 43% of cases. ARI is characterized by seasonality with a peak in the autumn-winter period.

16. Etiology of respiratory tract infections

17. Influenza virus (orthomyxovirus family, influenza virus genus). There are 3 serotypes that differ in the complement-binding ability of internal nucleocapsid proteins (S-antigen). Serotype A causes disease in humans, wild and domestic mammals, and birds, but the main reservoir – waterfowl - causes pandemics. Serotype B - epidemics, only in humans, S erotype C - sporadic cases, in humans and pigs.

18. The virus subtype is determined by specific hemagglutinin (H) and neuraminidase (N), which are part of the outer glycoprotein envelope (Vi - antigen). Genetic instability is defined as 2 types of antigen variability : * Drift - the change of antigenic determinants due to point mutations occurs gradually over 11-18 years; * Shift (only for type A viruses) – drastic changes in the form of genetic recombination of the virus (there is no specific immunity to shift variants of the virus), leading to pandemics. A feature of modern influenza is the simultaneous circulation of several serotypes. Everyone is susceptible to flu, more often in winter and spring (extremely resistant to low temperatures and freezing). Influenza C virus (less than 1% of ARI) has only one surface antigen - glycoprotein NA-esterase, greater stability of properties, lower reproductive activity in cellular systems. As a rule, it affects newborns and young children, causing persistent immunity. The reservoir of the virus in nature is the birds of the water and near-water region.

19. Replication of Influenza A virus

20. Parainfluenza virus : paramyxoviruses; have a stable antigenic structure, there are 4 types, unstable in the external environment, lose their activity at room temperature in 2-4 hours. Isotropic to the mucosa of the nasopharynx and larynx. February-March (October-April). The most common disease in the interepidemic period. In all age groups, but more often in children 3-4 years old. Rhinoviruses - 102 serotypes, usually rhinitis in children under 5 years of age, oropharyngeal diseases. Year-round, can be infected from 1 to 6 times a year, in adults - every second. Enteroviruses (60 serotypes) - late summer, early autumn. Adenoviruses – more than 30 serotypes of various antigenically, the most stable in the external environment. More pronounced destruction of the epithelium. Typical lesions of the respiratory system, eyes, lymphoid tissue, intestines, and bladder. Patients release the virus into the environment for a long time (up to 25 days, from feces – up to 2 months). All age groups are susceptible, especially in the first 3 years of life.

21. RS virus - paramyxovirus, unstable in the external environment, pronounced epitheliotropy of small bronchi and bronchioles , highly contagious, especially in children under 1 year. The main contingent – children from 6 months to 3 years. Epidemic outbreaks in winter or spring.

22. Formation of syncitium by the Р S - virus

23. Metapneumovirus

24. Coronaviruses ( Coronaviridae ) are a large family of RNA-containing viruses that can infect humans and certain animals. In humans, coronaviruses can cause a range of diseases, from mild forms of acute respiratory infection to severe acute respiratory syndrome (SARS). Currently, four coronaviruses (HCoV-229E,- OC43,- NL63, and HKU1) are known to circulate in the population, which are present year-round in the structure of SARS, and usually cause mild to moderate upper respiratory tract damage. According to serological and phylogenetic analysis, coronaviruses are divided into three generations: Alphacoronavirus, Betacoronavirus , and Gammacoronavirus . The natural hosts of most of the currently known coronaviruses are mammals.

25. Coronaviruses - virion structure diagram

26. S easonal coronaviruses are the causative agents of acute respiratory viral infections

27. Coronavirus got to people from animals (bats), was first detected in the market in the Chinese city of Wuhan. It replicates 2-3 times longer than the seasonal flu virus, so isolation and physical distancing in compliance with sanitary and hygienic requirements are highly effective (proven in China and other countries, primarily in the Asia-Pacific region). Coronaviruses are destroyed when heated for 10 minutes and instantly die under the influence of disinfectants. The virus lives for a relatively long time on different surfaces that surround us in everyday life. For example, on wood and glass – up to 4 days, on paper and plastic – up to 5 days, on aluminum – up to 8 hours, on steel – up to 48 hours, in sewage – up to 4 days.

28. The etiology of ARI is also determined by the location of the lesion of respiratory tract: * Upper respiratory tract: 1. respiratory viruses 2. β -hemolytic Streptococcus 3. Staphylococcus epidermal and aureus. 4. intracellular infections * Lower respiratory tract: 1. Viral-bacterial associations 2. Bacterial infection 3. Respiratory viruses (influenza, RS, AV) 4. Fungi

29. С irculation of respiratory viruses year-round

30. Pathogenesis of ARI An inexhaustible source of infection is a sick person who is most contagious during the acute period of the disease (no more than 4 days, including the day before the onset of symptoms). Asymptomatic chronic virus carriers. Convalescents - less often, with flu - up to 2 weeks, with immunodeficient state - up to 22-25 days after the disease of influenza A and up to 30 days after influenza B. Children, especially preschool and school age, are the main distributors of infection. Infection can occur from birds (H5N1, H7N7, H7N9) and pigs (H3N2v).

31. The route of transmission is airborne, with adenovirus infection - fecal-oral, with rhinovirus infection - through personal hygiene items, handshake (contact and household contact). Immunity - short-lived, unstable, type-specific. The development of ARVI several times a year is promoted: 1. a large number of serotypes of ARVI pathogens, the ability to form mixed infections 2. no cross-immunity 3. quick and easy transfer 4. high contamination, high year-round background 5. rapid mutability of the genome, virus variability 6. rapid development of drug resistance.

32. Pathogenesis of ARI Entrance gate (absorption and insertion): from the nose, pharynx and conjunctiva, where, passing through the mucus layer, it comes into contact with epithelial cells (inoculation in the nasopharynx) with specific cellular receptors (for influenza, these are sialic acids of glycoproteins), adhesion occurs, the virus replicates (at the peak of replication , symptoms appear) and reproduces in the epithelial cells of the mucous membrane of the initial parts of the respiratory tract (hundreds and thousands of new virions appear within a few minutes (hours) after entering the cell). ↓ The yield of virions from epithelial cells is accompanied by cell death → damage epithelial layer → the ability transepithelial migration of bacteria , microbial contamination and bacterial superinfection with formation of nosological -defined diseases. Intensive isolation and resorption of products of virus metabolism and epithelial cell breakdown is accompanied by increased permeability of cell membranes, release of proteolytic enzymes , accumulation of under-oxidized products of carbohydrate metabolism, activation of free radical and peroxide reactions .

33. Pathogenesis of ARI The physical and chemical changes occurring in the focus of inflammation contribute to the violation of vascular permeability of the microcirculatory bed, the appearance of edema of the mucosa. Degeneration, necrosis, rejection of affected cells → drop in drainage system functions of the ciliated epithelium and LOCALLY SYSTEMICALLY mucociliary clearance ↓ ↓ ↓ Foreign antigen (Ag) Virusemia , toxemia "exposure" of sensory ↓ ↓ organs of nerve fibers AP-cells (lasts up to 10-14 days) ↓ ↓ ↓ Toxic and toxic-allergic, cough bronchial Release of reaction from internal organs especially the hyperreactivity c ytokines, vascular system - the leading role in the mediators development of neurological syndromes ↓ (wet brain, damage to the central nervous system and zone of midbrain). Inflammation

34. Pathogenesis of ARI Foreign antigens → activation of antigen-presenting (AP) cells (monocytes, macrophages, endotheliocytes, neutrophils, etc.) → a number of cytokines (mono-and lymphokines) → IL-1,-6, -8. -12, -18, TNFa , ELISA → stimulation of leukocyte adhesion and chemotaxis (phagocytic activity of neutrophils and monocytes) → inflammatory mediators (histamine, serotonin, kinins, leukotriene B4, prostaglandins E2, D2, F2, thromboxanes A2 and B2, platelet activation factor, complement components) → early (vascular exudative) phase of inflammation – increased vascular permeability, hyperemia, mucosa edema of respiratory tract, hypersecretion of the mucous glands, spasm of smooth muscles;

35. Pathogenesis of ARI Inflammation: 1. early phase : increased vascular permeability: rhinorrhea, catarrh, edema, narrowing of the lumen. Inflammation caused by viruses leads to stimulation of a 1 -adrenoreceptors (mucus hyperproduction), H 1 -histaminoreceptors (mucosa edema, bronchoconstriction), M-cholinergic receptors, and suppression of β 2 -adrenoreceptors (bronchial obstruction) with the followed development of bronchial hyperreactivity. All this causes a violation of mucociliary clearance and cough . The main feature of the reparative process of upper respiratory airways is metaplasia of the cylindrical epithelium of mucosa. ↓ The defeat of the submucosal tissue and vascular network with the formation of foci of infiltration.

36. Pathogenesis of ARI 2. late phase : the influx of polymorphonuclear leucocytes in the subepithelial part of the epithelium → edema. Chemotactic factors → late (cellular) phase of inflammation (blood cells migrate to the focus of inflammation→ release of proteolytic enzymes, peroxidases, free radicals , and other BAS) → secondary damage to the respiratory epithelium with its desquamation → products of tissue alteration (tissue growth stimulators) → activation of cell proliferation (3rd component of inflammation), which is manifested by mucosal hyperplasia. In damaged tissues, pro-inflammatory cytokines and inflammatory mediators are released again, as a result of which it becomes a "closed circle". In ARI, hyperreactivity of the airway mucosa naturally occurs as a result (it persists in practically healthy people for 2-4 weeks after the disease, with a genetic predisposition - the manifestation of bronchial asthma): 1. inflammatory changes with the release of mediators → increased bronchial tone 2. desquamation of the ciliated epithelium (+) direct effect of viruses on H 1 -histaminoreceptors, a 1 -adrenergic and M-cholinergic receptors, 3. secretions of neuropeptides (substance P, neurokines A and B, vasoactive intestinal peptide).

37. Factors contributing to the penetration of the pathogen 1. External : - harmful substances contained in the air (prof. harms) - high humidity and low air temperature – socio-economic situation (alcohol, smoking, malnutrition). 2. Internal : - immature immune defense and metabolic disorders - constitutional predisposition - a tendency to relapse of inflammatory processes. - anatomical and physiological features (closed cavities, deep pockets in the region of upper airways) - concomitant disease.

38. Interaction of the virus with respiratory epithelial cells at the initial stages of the disease development is accompanied by activation of local protection factors , in particular: The first barrier: 1. physical ( mucociliary transport) lines of defense - respiratory reflexes (sneezing, coughing) 2. chemical (antimicrobial substances) lines of defense: lysozyme, lactoferrin, secretory IgA S antibodies (prevent pathogen adhesion); specific reactions - antibody production. 3. cell lines of defense - non-specific immune response: phagocytic neutrophils and mononuclears . The second barrier is epithelial cells The third barrier is connective tissue.

39. It should be remembered that the symptoms of ARI are caused more by the host's reaction to a viral infection than by the direct damaging effect of the virus on respiratory mucosa. Therefore, the destruction of the virus is not a necessary condition for the effectiveness of treatment.

40. All factors of immune protection : non-specific (tissue barriers, macrophages, natural killers, lysozyme, complement, acute phase proteins, cytokines: interferons and interleukins 1, 6, 8 (fever, acute phase proteins, leukocytosis), TNFa → systemic manifestations); specific are related and complement each other. The higher the activity of inflammation, the higher the intensity of the protective reaction. Cooling is a direct predisposing factor.

41. The pathogenesis of a new coronavirus infection It is known that the virus enters the body through the mucosa of the upper respiratory tract. After that, it begins to spread rapidly to the bronchi and lungs. The speed and severity of the consequences depends on the immune system, age, the presence of chronic diseases, and other factors. There are a lot of individual physiological features in this issue. The patient's blood produces antibodies, but this does not guarantee that there will be no re-infection. Once inside the cell, coronaviruses multiply in the cytoplasm. They settle on immunocompetent cells, use them as a vehicle, and quickly disperse throughout the body. Coronaviruses suppress the immune system and contribute to the development of cancer pathology. They have a complex antigenic structure and require special cultivation conditions. Antigenic components are located in the outer shell, intermediate membrane, and virion capsid.

42. The pathogenesis of a new coronavirus infection However, it is children of any age who should be the focus of special attention, as they play a huge role in the spread of the disease, including by secreting the pathogen with feces. This again raises the question of the fecal-oral pathway of pathogen transmission, as no less important (compared to airborne and contact) for SARS-CoV-2.

43. Susceptibility to the coronovirus is high, especially in preschool children. After the disease, a type-specific immunity is formed. Antibody synthesis does not protect against re-infection. Seasonality falls on the winter-spring period. Types of coronavirus transmission : airborne (when talking to another person, coughing or sneezing); air-dust (infection enters the body with dust particles); contact-household (through contact with an infected person, for example, when shaking hands, through objects that the infected person came into contact with). fecal-oral

44. Main pathogenetic stages of SARS-CoV-2 disease Inflammation of the nasopharyngeal mucosa, Replication of viruses in epithelial cells, Fullness and puffiness of the mucosa , dilatation of blood vessels, penetration of viruses into the cells of the alveoli , their reproduction in the cytoplasm, exit of viruses into the intercellular space, Accumulation of fluid in the pulmonary interstitium , destruction of surfactant, alveolar Collapse, violation of gas exchange . These viruses have an affinity for the cells that make up human lungs. In the respiratory system, the virus, penetrating into the alveoli - the structural units of the lungs, in which gas exchange and blood oxygen saturation occur, attaches to the cell with the help of "spines" and then – inside. Inside the cell, the virus breaks down to a single strand of RNA, which is embedded in the structural elements and causes the human cell to reproduce similar viral particles. In this way, the virus attacks the cell, destroying it and using everything and all the resources of the cell to reproduce.

45. The pathogenesis of a new coronavirus infection * There are two types of cells in the nose with the highest concentration of ACE 2 and TMRSS 2 proteins that allow the coronavirus to enter the body. * The ACE 2 receptor protein and TMRSS 2 protease are expressed in cells of various organs, including on the inner surface of the nose. From all the cells of the respiratory tract the highest concentrations of these receptors in goblet cells, involved in the development of mucus, and ciliated cells of the upper respiratory tract and in the cells of the cornea, the mucosa of the esophagus, ileum and colon, which indicates the possibility of infection through the eyes and tear ducts, the presence of fecal-oral route of infection.

46. SARS-like viruses use the ACE2 receptor and cellular proteases (TMPRSS2) to enter the cell (for this it is necessary to break down the protein S)

47. According to the latest data, coronaviruses are also able to invade the cells of the bronchial wall, intestines and cause symptoms similar to bronchitis and enteritis. Especially often the manifestation of intestinal symptoms is observed in children. Oxygen exchange at the level of the alveoli ceases to function. There is a violation of microcirculation. Coronavirus provokes increased blood clotting with thrombosis, which in turn further blocks respiratory function, causes symptoms of kidney failure, loss of smell and taste. Therefore, patients with high levels of plasmin, which normally breaks down thrombin, are more difficult to tolerate infection. The virus encodes proteins that affect the innate immune response and further the "cytokine storm". Excess iron in the body: the coronavirus damages the hemoglobin gene, which leads to iron blocking, its overabundance and, consequently, oxygen starvation (the special role of ferritin).

48. Clinic of ARI Depending on the location of the respiratory tract lesion, it is customary to distinguish various variants of infection of the upper (rhinitis, nasopharyngitis, tonsillopharyngitis, etc.) and lower (laryngotracheitis, tracheitis, bronchitis, pneumonia) respiratory tract. Localization is determined by the tropism of viruses to certain parts of the respiratory tract. The incubation period is from 12-48 hours to 5-7 days (2-3 days on average). The clinical picture as a whole is represented by 3 syndromes : - inflammatory syndrome (persistent fever) - intoxication syndrome (involving the central nervous system, autonomous nervous system and internal organs) - catarrhal syndrome (damage to the nasopharynx and respiratory tract at various levels) of varying severity: runny nose, conjunctivitis, cough, sore throat, etc.

49. A typical picture of ARI consists of: 1. typical symptoms of acute respiratory infections of varying severity 2. syndromes of emergency conditions that develop in severe and extremely severe acute respiratory infections 3. manifestations of complicated course. A typical ARI symptom complex includes: * acute rhinitis : difficult nasal breathing (nasal obstruction), copious discharge from the nose of a mucous and mucopurulent nature, violation of the sense of smell. * acute pharyngitis (nasal-nasopharyngitis; oral - oropharyngitis ; tonsillopharyngitis): sore throat, dysphagia * acute laryngitis : hoarseness of the voice, abrasion, scratching, sore throat, which increases with voice loads, rough cough. Edema or accumulations in the larynx of viscous drying sputum, crusts may be accompanied by mechanical obstruction of the airways, shortness of breath. * acute tracheobronchitis : * Inflammation of the paranasal sinuses : swelling from the nasal cavity leads to blocking of the natural sinus constrictions, impaired ventilation, and retention of secretions in the nasal cavity. * Nasopharyngeal inflammation and impaired mucociliary clearance → eustachiitis → aseptic inflammation in the middle ear or edema.

50. Influenza (J 11.1 according to ICD-10) WHO has proposed a diagnosis of "flu-like illness" along with the terms ARI and severe ARI (TORI). The prodromal period lasts from several hours to 1.5 days. The onset is acute, chills, rapid increase in symptoms: hyperthermia, toxicosis (determines the severity of the disease), headache (frontotemporal region, dizziness, myalgia, pain in the eyeballs, photophobia, severe weakness, vomiting, fainting, meningism). Specific influenza intoxication dominates. The febrile period lasts an average of 4.5 days (with influenza B - longer), reduced by accelerated lysis. If more than 5 days, it indicates the presence of complications. Signs of severity : 1 - up to 38.5 degrees, 2 - up to 39 degrees; 3 - up to 40-40,5 degrees (hypertoxic). The main sign of toxicosis is cyanosis, mainly of the lips and soft palate mucosa.

51. Influenza Appearance of the patient : hyperemia, puffiness of the face, injection of sclera, conjunctiva, cyanosis of the lips, the entire skin. From the cardiovascular system : relative bradycardia, hypotension, gentle systolic noise, muted tones, prolongation of the PQ interval, decrease in the T wave - transient nature. Catarrhal syndrome on day 1-2 of the disease - later than toxicosis: nasal congestion, rhinitis, dry cough, sore throat, hyperemia of the palate with a cyanotic tinge. T racheitis (dry rough painful cough that lasts for more than 10 days, pain behind the sternum, intercostal muscles, rectus abdominis muscles) – the most affected area of the respiratory tract in influenza . From the central nervous system on day 3-7 of the disease, there are general cerebral symptoms, vegetative-vascular disorders, symptoms of intracranial hypertension, convulsions, changes in consciousness. In the general blood test - leukopenia for 3-4 days .

52. Criteria for assessing the form and severity of influenza Form of severity Severity assessment Criterion nature of the course Complication Light Less than 38.5, intoxication is weak or absent, rhinitis, pharyngitis, tracheitis, laryngitis. Smooth Missing Moderate- severe 38.5-39.5 degrees , moderate intoxication (chills, weakness, headache, dizziness, myalgia, artalgia , drowsiness or increased excitability, adynamia , vomiting or nausea, tracheitis, laryngitis, bronchitis, acute stenosing laryngotracheitis I and II degree Smooth or non-smooth Pneumonia with 1-2 segments, otitis, sinusitis, pyelonephritis Severe Above 39.5 degrees , encephalitic or meningoencephalitic reactions, infectious toxicosis of the 1st degree, heart, vascular or combined insufficiency, hemorrhagic or disseminative intravascular coagulation (stages I-II) syndromes, acute stenosing laryngotracheitis of the II degree, respiratory insufficiency of the II degree. Smooth (less often), not smooth Pneumonia with more than 2 segments, encephalitis, serous meningitis, neuritis, purulent otitis. Hypertoxic Sudden onset, more than 40 degrees , systemic inflammatory response syndrome, hemorrhage in vital organs, disseminated intravascular coagulation syndrome, multiple organ dysfunction syndrome, acute RDS. Fulminant, high mortality Syndromes Keisha, Ray, Waterhouse- Friderichsen , Gasser, generalization process.  

53. Parainfluenza Incubation period - 1-7 days. The beginning is gradual. The duration of the disease is 2-7 days, mild toxicosis, gradual onset, cough, runny nose, subfebrility . Laryngitis is the most affected area of the respiratory tract in parainfluenza infection : sore throat, "barking" cough, hoarseness of voice. Moderate runny nose, shortness of breath, swelling of the nasal mucosa, cough up to 2 weeks, fever longer than with the flu. RC virus Incubation period – 2-7 days. Subfebrile temperature 2-7 days, gradual onset, possible runny nose, hyperemia with cyanosis. After a short viremia (2-3 days), small bronchi and bronchioles are affected with the development of respiratory failure, an abundance of small-bubble and dry wheezes. Dry cough, turning into wet, expiratory shortness of breath. X-ray: interstitial changes with bronchiolar emphysema, often complicated by obstructive syndrome, pneumonia.

54. Adenovirus The incubation period lasts 4-14 days. The respiratory tract, eyes, and a sharp exudative component are affected. Gradual start. Catarrhal syndrome, general toxic syndrome is moderately expressed. Runny nose is plentiful, enlarged lymph follicles, tonsils (white overlays in the form of dots and threads). The X-ray shows an increase in the pulmonary pattern due to peribronchial infiltration. Possible unilateral membranous conjunctivitis. A separate form is pharyngoconjunctival fever , characterized by fever, intoxication, rhinopharyngitis, conjunctivitis, lymphadenopathy (enlargement of the cervical and mediastinal lymph nodes), diarrhea. Creeping nature of mucosal inflammation: the formation of new foci when the old ones subside. Long-term undulating character of temperature. Those who have been ill for a long time secrete the virus through tears, feces, from the upper airways - up to 40 days. Possible intrauterine infection. Rhinovirus Rhinitis lasts from 7 to 14 days. No intoxication. Profuse runny nose. Complications – acute otitis media and acute sinusitis.

55. Clinic of 2019-nCoV infection Currently, the main source of infection is a sick person, including those who are in the incubation period of the disease. Once in the body, the coronavirus causes symptoms typical of all pneumotropic viruses. The incubation period is from 2 to 14 days. The new coronavirus infection caused by 2019-nCoV is characterized by the presence of clinical symptoms of acute respiratory viral infection: - increased body temperature (>90%); - cough (dry or with a small amount of sputum) in 80 % of cases; - shortness of breath (55%) - myalgia and fatigue (44%); - feeling of stuffiness in the chest (>20%), The most severe shortness of breath develops by the 6th-8th day from the moment of infection. It was also found that the first symptoms may include headaches (8%), hemoptysis (5%), diarrhea (3%), nausea, vomiting, and palpitations. These symptoms at the onset of infection can be observed in the absence of an increase in body temperature.

56. Clinical variants and manifestations of 2019-nCoV infection 1. Acute respiratory viral infection of a light course. 2. Pneumonia without respiratory failure. 3. Pneumonia with acute respiratory failure. 4. Acute respiratory distress syndrome (RDS). 5. Sepsis. 6. Septic (infectious-toxic) shock. Hypoxemia (SpO 2 reduction less than 88%) develops in more than 30% of patients. There are light, medium and severe forms of 2019-nCoV infection. In severe cases, rapidly progressive lower respiratory tract disease, pneumonia, acute respiratory failure, acute RDS, sepsis and septic shock are observed.

57. Children with congenital heart disease, broncho-pulmonary dysplasia, respiratory tract defects, anemia or abnormal hemoglobin levels, severe malnutrition, immunodeficient state, or long-term immunosuppressive therapy, who have come into contact with patients with COVID-19 infection, and who have one of the following symptoms should be considered at risk for developing a severe course of the disease: 1. Shortness of breath: >/ = 60 for children under 2 months, > 50 per min. for children 2-12 months, > 40 per min. for children 1-5 years, > 30 per min. for children over 5 years (regardless of the episode of crying or fever) 2. Decrease saturation </=92% 3. Fever over 3-5 days 4. Impaired consciousness (weak reaction to others, lethargy, etc.) 5. Increased levels of blood enzymes (hepatic, myocardial, lactat-dehydrogenasa , etc.) 6. Unexplained metabolic acidosis 7. Changes in the lung radiograph (in the form of bilateral or multi-lobe infiltrative changes, pleural effusion, or rapid increase in changes) 8. The age of the child younger than 3 months.

58. Diagnosis In all cases of ARI, you must specify: * Respiratory tract syndrome ( from rhinitis to bronchiolitis ) in isolation or in combination * Clinical form : manifest, erased, typical, atypical, asymptomatic, lightning-fast (hypertoxic) * The severity of the syndrome of intoxication * Course : uncomplicated and complicated: Non-specific complications: - toxic shock - in the first days of the disease (acute cardio-vascular failure, pulmonary edema, brain edema, disseminated intravascular coagulation syndrome), - pneumonia (primary - influenza, secondary - bacterial, mixed - viral-bacterial), - aseptic meningitis , meningoencephalitis, - infectious-allergic myocarditis , pericarditis, rhabdomyolysis syndrome with the development of acute renal failure. Specific complications : - laryngeal stenosis, - viral lesions of the central nervous system .

59. Diagnostics of ARI 1 . Clinical and epidemiological data. 2. Laboratory: * non-specific (general blood test, biochemical analysis) * specific : - Immunofluorescence (antigen detection) – Enzyme immunoassay (Ig M-antibodies) – Serological method - an increase in the at titer by 4 or more times to the antibodies of the respiratory virus in the dynamics of the disease. - PCR (viral DNA) and reverse transcription polymerase chain reaction (RT-PCR) for respiratory infections: influenza viruses type A and B, RS-virus, parainfluenza viruses, rhinoviruses, adenoviruses, human metapneumoviruses, MERS- CoV . - Microbiological diagnostics (culture study) and/or PCR diagnostics for Streptococcus pneumoniae, Haemophilus influenzae type B, Legionella pneumophila, as well as other pathogens of bacterial respiratory infections of the lower respiratory tract are mandatory. For rapid diagnostics, rapid tests can be used to detect pneumococcal and Legionella antigen- uria .

60. The diagnosis of 2019-nCoV infection is based on a clinical examination, epidemiological history, and laboratory results. 1. Detailed assessment of all complaints, medical history, and epidemiological history . When collecting an epidemiological history, attention is drawn to visits within 14 days before the first symptoms to countries and regions that are epidemically unfavorable for 2019-nCoV, and close contacts over the past 14 days with persons suspected of being infected with 2019-nCoV, or persons whose diagnosis has been confirmed by laboratory. 2. Physical examination , which must include: - assessment of the visible mucous membranes of the upper respiratory tract, - auscultation and percussion of the lungs, - palpation of the lymph nodes, - examination of the abdominal organs to determine the size of the liver and spleen, - thermometry, to determine the severity of the patient's condition. 3. General laboratory diagnostics : - performing a general (clinical) blood test to determine the level of red blood cells, hematocrit, white blood cells, platelets, and leukocyte formula;

61. The diagnosis of 2019-nCoV infection ( continued ) - biochemical blood analysis (urea, creatinine, electrolytes, liver enzymes, bilirubin, glucose, albumin) does not provide any specific information , but the detected deviations may indicate the presence of organ dysfunction, decompensation of concomitant diseases and the development of complications, have a certain prognostic value, and influence the choice of medications and/or their dosage regimen. - study of the level of C-reactive protein (CRP) in the blood serum. The level of CRP correlates with the severity of the course, the prevalence of inflammatory infiltration, and the prognosis for pneumonia; - pulse oximetry with SatO 2 measurement to detect respiratory failure and assess the severity of hypoxemia. Pulse oximetry is a simple and reliable screening method, to identify patients with hypoxemia who need respiratory support and evaluate its effectiveness; - patients with signs of acute respiratory failure (SatO 2 less than 90% according to pulse oximetry) are recommended to study arterial blood gases with the determination of PaO 2 , PaCO 2 , pH, bicarbonates, lactate; - patients with signs of acute respiratory failure are recommended to perform a coagulation test with determination of prothrombin time, international normalized ratio (INR), and activated partial thromboplastin time.

62. The diagnosis of 2019-nCoV infection ( continued ) 4. Laboratory diagnostics specific: - detection of 2019-nCoV RNA by PCR is performed in patients with clinical symptoms of respiratory disease suspected of infection caused by 2019-nCoV, especially those arriving from epidemiologically disadvantaged regions immediately after the initial examination, as well as contact persons. 5. Instrumental diagnostics: - overview radiography of the chest organs in the anterior and lateral projections is recommended for all patients with suspected pneumonia (if the location of the inflammatory process is unknown, it is advisable to take a picture in the right side projection). Chest radiography reveals bilateral drain infiltrative darkening. Most often, the most pronounced changes are localized in the basal parts of the lungs. A small pleural effusion may also be present; - computed tomography (CT) of the lungs is a more sensitive method for diagnosing viral pneumonia. The main findings in pneumonia are bilateral infiltrates in the form of "frosted glass" or consolidation, which have a predominant distribution in the lower and middle zones of the lungs; - electrocardiography (ECG) in standard leads is recommended for all hospitalized patients. This study does not contain any specific information, but it is currently known that viral infection and pneumonia, in addition to decompensating chronic comorbidities, increase the risk of developing rhythm disorders and acute coronary syndrome, the timely detection of which significantly affects the prognosis. In addition, certain changes in the ECG (for example, prolongation of the QT interval) require attention when evaluating the cardiotoxicity of a number of antibacterial drugs.

63. Biological sample collection kit

64. Laboratory diagnostics of ARI in children: - at the beginning of the disease , normal leukocyte counts are recorded in children or leukopenia with signs of lymphopenia (some infected children may have increased levels of transaminases, CRP and myoglobin); - the level of CRP is elevated in most patients, and prothrombin test remains normal (but in severe patients it is increased more often than in adults); - more severe cases are accompanied by an increase in D-dimer levels and ongoing lymphopenia/eosinopenia; - biological samples of sick children (nasopharyngeal swabs, sputum, broncho-alveolar lavage, blood and stool samples (not urine!) contain RNA of the virus.

65. The diagnosis of coronavirus infection in children is established with a positive epidemiological history and in the presence of any 2 of the clinical symptoms.

66. Differential diagnosis of ARI is made with the following infections: - Flu - Parainfluenza - Adenovirus infection - RSV infection - RV (rhino) infection - infection caused by human metapneumovirus - SARS-coronavirus infection - other viral infections - infections caused by Mycoplasma pneumoniae and Chlamydia pneumoniae - bacterial pneumonia

67. Treatment of ARI - g eneral measures (maximum isolation, bed rest for at least 3-5 days, heavy drinking, dairy-plant diet, then - by age). Form of ARI Therapy Medications and activities Mild Specific (antiviral) from 1 year- Oseltamivir, from 3 years – Arbidol, from 5 years – Zanamivir, from 7 years - Remantadine, from 18 years – Ingavirin. Interferons and their stimulants Grippferon , Viferon , Anaferon for children, Derinat ; from 6 months Genferon -light, from 3 years -Isoprinosine, Kagocel , Reaferon-lipint , from 4 years – Cycloferon , from 6 years – Cytovir , from 7 years – Ingaron , Amixin . Pathogenic diaphoretic herbs, copious drinking, Vit. A, C, E, rutin . Aflubin , Influcid ®, and other means (baby),vasoconstrictive preparations. Irrigation of the pharynx, expectorant reflex action (with pharyngitis and tracheitis). Moderate Etiotropic the same as in the light form + antioxidants Pathogenetic the same as in mild form + antipyretics, with a painful cough – drugs that suppress cough Immunostimulating in frequently ill children and prolonged course-adaptogens Antibacterial In the presence of bacterial infection: Penicillins , Macrolides Heavy Etiotropic is the same as for light and medium-heavy forms Antibacterial is the same as for moderate, broad-spectrum AB for hyperthermia lytic mixtures + antispasmodics, ganglioblockers, physical cooling measures for hemodynamic disorders the same + antispasmodics, neuroleptics, oxygen therapy, ganglioblockers for convulsive syndrome neuroleptics, tranquilizers, barbiturates, hormones, diuretics in hemorrhagic syndrome GCS, proteolysis inhibitors, Dicinone , Vit. C, K, Rutin at the threat of edema of the brain and lungs, oxygen therapy, GCS, ganglioblockers, neuroleptics, diuretics in heart failure the same + glycosides without calcium and aminazine , antiaggregants , angioprotectors . when the collapse adrenomimetics ( mezaton , epinephrine), dopamine, GCS, calcium preparations Immunostimulating the same as in the moderate form + pre-and probiotics.

68. Chemopreparations in the treatment of ARI – selective suppression of individual parts of virus reproduction: M 2 -channel blockers (Amantadine, Algirem syrup for children) and neuraminidase inhibitors (against influenza A and B: Oseltamivir (Tamiflu) orally from 1 year and Zanamivir ( relenza ) - intranasally inhaled from 5 years); and Ribavirin ( V irazol – inhaled through a nebulizer only in a hospital), also active against the RS virus (RNA and DNA-containing).

69. I mmunocorrective therapy in the treatment of ARI : A. N atural (immunomodulatory activity: human dry leukocyte interferon, Laferon ) and recombinant (antiviral and antitumor activity: Reaferon , Betaferon , Roferon A, Intron A, Wellferon , etc.). B. Monovalent and combined ( Viferon I, II with the addition of Tocopherol and ascorbic acid, Leukinferon , Grippferon ). IFNa and β inhibit the synthesis of virus proteins and block the output virions from the cell. IFNỵ affects immune cells (an immunomodulator). 2. Inducers of endogenous interferon production : Synthetic: Cycloferon , Poludan , N eovir , Amixin Natural: Kagocel , R idostin , M egasel , S abrac . 3. Bacterial lysates : Imudon , IRS-19, Ismigen , Licopid 4. Bacterial vaccines : Bronchomunil , R ibomunil . 5. Aflubin - a complex homeopathic medicine with anti-inflammatory and immunomodulatory activity (in drops) . Immunoglobulins : anti-influenza, anti-herpetic, anti-cytomegalovirus.

70. Symptomatic therapy in the treatment of ARI : Runny nose. • Irrigation treatment of the upper airways. * a- adrenomimetics , sympathomimetics (derivatives of Oxymetazoline - Nasol , Nasivin ) in the form of drops, sprays (older than 6 years) in the first 1-3 days 2-4 times/day. Vibrocil (a- adrenomimetic + antihistamines). * Systemic medications - pseudoephedrine (for children over 12 years of age). * Antihistamines - WHO does not recommend.

71. The pathways involved in the formation of a cough reaction.

72. Symptomatic therapy in the treatment of ARI ( continued ) : Cough - a protective reaction when mucociliary clearance is ineffective!!! Dry, painful, paroxysmal, wet including after surgery - antitussive medications. Central action drugs: Narcotic – do not recommended in children Non-narcotic- not cause addiction: Sinekod - from 2 months Peripheral action drugs : reduce intensity of cough, but increase bronchial hyperreactivity – be careful in patients with bronchial asthma. Mucolytics ( Acethylcisteine ): only for viscous sputum, short course of using, reduces IgA and lysozyme, stimulate gastropulmonary reflex. Combined Mucolytics (+Expectorants – Alkaloids or Saponins) Drugs with mucoregulyatory activity : Carbocisteine (Bromhexine, Ambroxol )

73. Symptomatic therapy in the treatment of ARI : Fever : indications for temperature decreasing: 1. above 38.5 degrees 2. above 38 degrees in people with cardiopulmonary pathology 3. above 38 degrees in children under 5 years of age. A . Paracetamol 10-15 mg/kg/day. B . Ibuprofen 5-10 mg/kg/day. (repeat after 4-6 hours) C . Methamizola Natrii ( Analgin ) 50% in/m 0.1 ml/year of life – only in difficult cases + physical cooling + vasodilators methods of preparation. Body temperature above 38.5 does not require intervention in a healthy child and with antibacterial therapy.

74. Symptomatic therapy in the treatment of ARI Pain in the throat Local anesthetics with antiseptic activity: Strepsils and Septolete . Severe forms of acute respiratory infections - hospitalization with detoxification therapy. AB-therapy – only when bacterial complications are layered, severe forms, clinical signs of immunodeficient state, and an unfavorable premorbid background.

75. Treatment of COVID-19 infection Place of treatment: 1. Depending on the condition, patients with suspected COVID-19 are isolated or self-isolated at home; 2. Confirmed hospital case can stay in the same branch; 3. Severe patients should be immediately transferred to the intensive care department. General principles of treatment Bed rest, sufficient caloric intake and adequate hydration, monitoring of electrolyte balance and homeostasis, vital functions and oxygen saturation, monitoring of respiratory tract patency and according to indications - oxygen therapy, control blood and urine tests (CRP, electrolytes, hepatic and myocardial enzymes, renal parameters, coagulation test). Analysis of the gas composition of the blood and repeated X-ray observation of the lungs according to indications.

76. Treatment of COVID-19 infection Symptomatic therapy Patients with fever > 38.5, bringing discomfort-physical cooling methods, paracetamol in age-related dosages. For convulsions - anticonvulsants. Oxygenotherapy If there are signs of hypoxia, immediately start oxygen therapy through a nasal probe or mask. High-flow oxygen therapy, non-invasive or invasive mechanical ventilation – as indicated. Antiviral therapy IFN-a can reduce the viral load in the initial stages of the disease, relieve symptoms, and reduce the duration of the disease. I n the Russian Federation, forms of interferon-alpha for nebulizer are not registered. Nebulizers are generally not recommended to use because of the high risk of infection of others! Lopinavir / ritonavir for adults in tablets of 200/50 mg – 2 tablets per reception 2 times a day, no more than 10 days.

77. Treatment of COVID-19 infection The recommendation for glucocorticosteroids ( GCS) appeared due to the fact that many patients had high levels of pro-inflammatory cytokines in the blood (IL-6, TNF-alfa, etc.). The idea of using biological agents , such as tocilizumab , was based on this fact. Another possible option may be the use of zinc pyrithione , which has been proven to inhibit the activity of coronavirus in in vitro studies. Unnecessary use of antibiotics , especially broad-spectrum ones, should be avoided. It is necessary to monitor the condition of a child with co-infection, signs of bacterial or fungal infection. If the pathogen is confirmed, antibacterial or antifungal therapy is prescribed. Respiratory support : non-invasive or invasive (only if life-saving) ventilation, if ineffective - ESMO. There is a lot of work that fatalities are more often observed in those who were transferred to a ventilator.

78. Treatment of COVID-19 infection There were works on the high effectiveness of hydroxychloroquine (including in combination with azithromycin) in patients with COVID-19, as well as reviews on the possibilities of its use, taking into account antiviral activity in vitro and in vivo studies. Circulation support: to monitor the volumes of injected fluids, the improvement of microcirculation, vasoactive drugs and hemodynamic monitoring when required. Psychotherapy : psychological counseling is necessary for a quick recovery. Active psychological support and treatment is indicated for older children, especially those with phobias, anxiety, and psychological disorders. In general, children and adolescents are vulnerable to developing the syndrome post-traumatic stress disorder

79. Prevention ARI Non-specific prevention by type of use is divided into: Post-contact (emergency) intra-focal in the focus of ARVI; Post-contact (emergency) out-of-focus prevention in public places after detection of a patient with influenza and ARI in the team, in the region; Seasonal (planned) – during the entire epidemic season or during the rise of ARI in the territory; Post-vaccination - prevention for 2-4 weeks after vaccination against influenza. Planned seasonal non-specific prevention among the population is carried out with immunocorrecting drugs of various origins in courses in accordance with the recommendations for their use. The timing of seasonal immunocorrection in each territory is determined in accordance with the long-term forecast and based on a retrospective analysis of the incidence of ARI and influenza for a number of previous years

80. Prevention ARI ( continued ) 2. Specific (vaccination) - only for flu. Individuals at high risk of complications and those in close contact with them. • Live ( allantoine ) vaccine: 1. as an aerosol in the nose of children from 3 years of age 2. from the age of 7 • inactivated vaccines- In/m: 1. whole ( Begrivac , Vaksigripp , Flyuaryks ) 2. subunit ( Influvak , Agricol , Grippol ). Immediately after the introduction of the vaccine, an immunosuppressive period (from 1 to 2 weeks) occurs - an exacerbation of chronic foci of infection (herpes). The protective antibody titer is formed by the end of the 3rd week and persists for up to 6 months. * specific immunization with Palivizumab ( Synagis ) i /m - humanized monoclonal antibodies, specific to the RS-virus f usion protein, for children at risk.

81. Acute stenosing laryngotracheitis (CROUP) (Scottish - CAW or croak ) This is a clinical syndrome of an infectious disease, always implying the presence of acute stenosing laryngitis or laryngotracheitis (ICD-10 acute obstructive laryngitis) or less often - laryngotracheobronchitis, characterized by a triad of symptoms: 1. stridor (stenotic breathing) - noisy breathing on inspiration (inspiratory shortness of breath) 2. rough "barking" cough -irritation of the nervous endings with inflammatory edema, exudate 3. change in the timbre of the voice - hoarseness of the voice up to aphonia as a result of restriction of the mobility of the true vocal cords due to inflammation.

82. Acute stenosing laryngotracheitis (CROUP) ( continued ) There are primary , repeated (up to 3 times) and recurrent (more than 3 times). By the nature of the inflammatory process: catarrhal , fibrous-purulent and ulcerative-necrotic . False croup includes all stenosing laryngitis of a non-diphtheria nature, in which the inflammatory process is localized mainly on the mucous membrane of the space under true vocal cord of the larynx . True croup develops as a result of damage to the true vocal cords. In any case, acute obstruction of the upper airways (narrowing of the laryngeal lumen with respiratory disorders and the development of acute respiratory failure - violation of the patency of the main airways) is primarily an emergency condition that requires emergency diagnosis and therapy at the pre-hospital stage. Increasing the mucosa thickness by 1 mm reduces the laryngeal lumen by half. Age 6 months -3 years (1-6 years, at the 2nd year of life -up to 5% of children). Boys are 1.5 times more likely. Summer, mid-autumn .

83. Anatomical and physiological features of larynx in children: 1. absolutely small size of the larynx: narrowness of the space under true vocal cord (short narrow vestibule and funnel-shaped chest instead of cylindrical), the smallest diameter of the airways at the level of the cricoid cartilage. High-pitched and disproportionately short vocal folds. 2. the tendency of mucosa layer and loose (abundant layer) connective tissue of the space under true vocal cord to develop edema 3. relative weakness of the respiratory muscles, soft and narrow epiglottis narrows the transverse size of the entrance to the larynx, soft and pliable cartilage skeleton - increased aerodynamic drag. 4. well-innervated laryngeal vascular network and laryngeal innervation feature contribute to the occurrence of reflex laryngospasm (hyperexcitability of adductor muscles closing the glottis), hyperparasympathicotonia , functional immaturity of reflexogenic zones. 5. the specific oxygen demand per 1 kg of body weight is higher than in adults. 6. there is an abundance of lymphoid tissue with a large number of mast cells and vessels with weak development of elastic fibers in the mucus and mucosal base. The younger the child, the greater the relative area occupied by loose connective tissue is .

84. Adverse background factors include: * drug * allergy * congenital stridor • parathophy • birth trauma * type of constitution (different diathesis , atopy, allergy). * delivery by caesarean section • post-vaccination period * sensitization by previous frequent ARI.

85. Acute obstruction of the upper respiratory tract ↓ ↓ infectious non-infectious 1. Viral – 36%: 1. Aspiration of foreign bodies * flu and parainfluenza types 1, 2 and 3 2. Trauma of the larynx * RS 3. Allergic edema * adenovirus 4. Laryngospasm in spasmophilia * Measles, herpes 5. Neoplasms 2. Bacterial (Streptococcus, 6. Trauma Staphylococcus, gram (-) microbes) 7. Malformations (congenital (heavy forms): membranes and cysts) * With the development of epiglottitis 8. Violation of laryngeal innervation * Pharyngeal and peritonsillar abscess (peripheral and central, yatrogenic , • Diphtheria, scarlet fever myasthenia gravis, compression 3. Mixed infection (viral-viral and viral-bacterial) 4. Infectious granulomas (tuberculosis, syphilis, scleroma )

86. In the genesis of acute airway obstruction , 3 mechanisms play a role, but one of them becomes the leading one: 1. inflammatory , including allergic, edema in the area of the space under true vocal cord and vocal cords themselves; edema is secondary to infection, usually viral; cellular infiltration from the larynx and trachea. 2. reflex (neurogenic) spasm of the larynx and trachea muscles, leading to closing of the glottis. 3. blockage of the laryngeal lumen with mucus, inflammatory secretions as a result of hypersecretion of the mucous glands, accumulation of thick sputum, crusts, fibrinous or necrotic overlays, aspiration by food or vomit.

87. Clinical manifestations of acute stenosing laryngitis Respiratory failure due to narrowing of the laryngeal lumen without obvious intoxication occurs more often acutely at night in a dream against the background of ARI symptoms on day 1-2 of the disease as a result of: * changes in the conditions of lymph and blood circulation of the larynx, * reducing the activity of airway drainage mechanisms, * frequency and depth of breathing movements. The obstruction can go lower or higher.

88. During the survey, the following features are most important : 1. degree of airway obstruction, including stridor 2. intercostal retraction 3. inflating the nose wings 4. intensity of air intake 5. colour of the skin 6. the degree of preservation of consciousness. When a bacterial infection is layered, the flow takes on a wave-like character.

89. Laryngeal stenosis differs in the rate of development and the degree of compensation. According to the rate of development of laryngeal stenosis are divided into: 1. Lightning - fast (blockage by a large foreign body or laryngospasm), developing within a few minutes 2. Acute – developing within a few hours (days) The severity of the clinical picture is determined by the degree of narrowing of the larynx and associated violations of the mechanics of breathing and the development of acute respiratory failure.

90. The severity of the clinical picture Compensated - clear consciousness, periodically arousal, pulse corresponds to an increase in body temperature, "barking" cough, tachypnea and light cyanosis around the mouth with anxiety, without the participation of respiratory muscles, duration does not exceed 1 day. Inhaling is difficult, breathing becomes noisy (stridor) - due to the intense turbulent passage of air through the narrowed airways. When the laryngeal tissue edema dominates, a sibilant tone of sound will appear, with an increase in hypersecretion - a hoarse, bubbling component of noisy breathing, with a pronounced spastic component-instability of sound characteristics. With the increase in stenosis due to a decrease in the respiratory volume, the sonority of breathing will decrease!

91. The severity of the clinical picture ( continued ) 2. Subcompensated - clear consciousness, constant arousal, tachypnea, stenosis at rest, has a constant, wave-like or paroxysmal character, persists for up to 2-3 days, symptoms of respiratory insufficiency are present at rest, and with anxiety – increase, retraction of compliant places ( inspiratory stridor ), especially the upper floor of the chest (+) tachycardia, loss on inspiration (+) moderate cyanosis of the nasolabial triangle. Breathing is performed well. Stenosis below the level of the vocal cords is characterized by expiratory stridor with the participation of auxiliary and reserve respiratory muscles in breathing. Laryngeal stenosis in the sub-ligamentous space is usually manifested by a mixed stridor. The absence of voice changes (hoarseness, aphonia) indicates the localization of the pathological process above or below the vocal cords. A hoarse " barking " cough is typical of laryngitis .

92. The severity of the clinical picture ( continued ) 3. Decompensated : confused consciousness, constant sharp arousal, signs of acute respiratory failure are constant, sharp retractions of the compliant areas of the chest with shallow and significantly rapid breathing, pronounced cyanosis of the face, acrocyanosis and marbling of the skin, a constant sense of fear. In the lungs, breathing is weakened, heart tones are muted, rapid (+) “ parodox ” pulse (loss of a wave on inspiration), periodically impaired consciousness. 4. Asphyxia (terminal stage): no consciousness, cyanosis of the whole body, shallow breathing without retractions of the compliant areas of the chest, reduction or absence of respiratory noises, blood pressure drops, pulse is barely defined, threadlike, in some cases – slow, heart tones are deaf, hypoxic brain edema. Rapid breathing and increased body temperature during croup can contribute to significant fluid loss and the development of respiratory exicosis .

93. Based on clinical data, there are 3 main forms of acute laryngeal stenosis: 1. the edematous form - stenotic breathing on the background of moderate hoarseness of the voice, "barking" unproductive cough in high tones - rapid effect of inhalation therapy (0.025% adrenomimetic - naphthysine ) 2. the infiltrative form is the same, but the effectiveness of treatment with adrenomimetics is weak, it lasts more than 2 days. 3. obturation form - pronounced hoarseness of the voice up to aphonia, rare unproductive and painful cough in low tones, the effect of adrenomimetics is absent. Sputum evacuation is effective. Duration-1-1. 5 days.

94. Differential diagnostic criteria for forms of laryngeal stenosis Form of stenosis Edematous Obturation Mechanism of development Edema, spasm Obturation of the laryngeal lumen with mucus content, white blood cell accumulation, edema The onset of symptoms of stenosis Sudden Gradual The temperature Depends on the etiology of ARI Febrile Speed of stenosis relief From several hours to 1-2 days 3-5 days Age 2-3 years Older than 3 years Hoarseness of voice Moderate Pronounced, aphonia Cough Barking at the high notes Silent Degree of stenosis 1-2 2-4 Sputum Mucous Purulent Foci of bacterial infection No Adenoiditis, sinusitis, sinusitis The effect of starting therapy (0.025% Naftizin) Fast Delayed, depends on the nature of the infection and etiotropic therapy General analysis of blood Lymphocytosis Neutrophilia with left shift

95. Westley croup severity rating scale (in points): 1. noisy breathing 2. retraction of the compliant areas of the chest (retraction): no = 0, mild = 1, moderate = 2, severe = 3. 3. airway patency: normal = 0, reduced = 1, noticeably reduced = 2 4. shortness of breath: no = 0, when agitated = 1; at rest = 2 5. cyanosis: no = 0, when agitated = 1, at rest = 5 6. level of consciousness, including sleep = 0, disoriented = 5. The total score ranges from 0 to 17 points. Mild croup - ≤2 (no shortness of breath at rest, only when crying). Moderate severity from 3 to 7 points (shortness of breath at rest). Heavy croup - ≥8.

96. The degree of the laryngeal stenosis in children Degree of stenosis Symptoms Objective data 1st Barking" cough, hoarse voice. When excited, moving, crying, breathing becomes more noisy General state of moderate severity, deep and more rare breathing, no pause between inhalation and exhalation 2nd Worry, excitement of the child. Sleep disturbance, sweating, expression of fright on the face, feeling of lack of air, "barking" cough that becomes painful General condition of moderate severity or severe. Stenotic breathing at rest, increases with physical exertion. Retraction of the compliant areas of the chest and epigastrium, signs of respiratory failure (cyanosis of the nasolabial triangle, which turns into acrocyanosis with anxiety, shortness of breath, tachycardia) 3rd Expressed anxiety, fear, lack of air, sweating. Dysphonia, rough "barking" cough, stenotic breathing, heard at a distance, Condition is severe or extremely severe. Respiratory failure is severe. Inspiratory dyspnea, cyanosis, participation of the entire respiratory muscles in the act of breathing, epigastrium retraction, frequent thread-like pulse that falls out when inhaling," marbling " of the skin, cold limbs. 4th Convulsions, loss of consciousness, involuntary urination, defecation. The condition is extremely severe or agonal. Violation of the breathing rhythm, sharp deafness of heart tones, bradycardia, blood pressure drops or is not detected. Asphyxia develops .

97. The differential diagnosis is based on the main symptom of acute laryngotracheitis: stenotic breathing . 1. diphtheria 2. foreign body of the larynx 3. pharyngeal abscess 4. laryngospasm 5. bronchial asthma

98. Treatment of laryngeal stenosis Diagnosis at the pre-hospital stage collection of complaints and anamnesis of the disease (stage of compensation or subcompensation ) mandatory questions that need to be clarified during the examination of the patient: • How are you feeling? * Which is more difficult – to inhale or exhale? • Has the voice changed? • Against the background of what appeared shortness of breath? * Was there a cough, vomiting, or skin discoloration? * Is it difficult to swallow? • What is your body temperature? • What causes a sore throat and how long has your throat been sore? * What kind of pain is felt: when an empty throat or when swallowing solid and / or liquid food? • Is it difficult to eat? • Are there functional disorders of the jaw system (opening the mouth, talking, etc.)? • Are there any soft tissue swellings or infiltrates in the submandibular area? • Did the patient take any medications and what was the effect? • How did the condition change when the ambulance team arrived?

99. Examination of the patient * External examination (facial expression, skin color, forced position, type of shortness of breath) • * Voice function status * Inspection of the oral cavity * Palpation of soft tissues of the maxillofacial region, regional submandibular and sub-chin lymph nodes, as well as lymph nodes of the neck and supraclavicular areas * Measurement of blood pressure, the study of the pulse * Auscultation of the lungs * ECG and its transcript (optional) * Pulse oximetry * Thermometry

100. First medical assistance Create emotional and mental peace ( "in the hands of the mother" mode, fresh air, warm alkaline drink ) Respiratory support with oxygen Monitoring of vital functions Try to establish the etiology of laryngeal stenosis For hyperthermia - antipyretics Solving the issue of delivery to a specialized hospital, transportation in a sitting or lying position with the head end raised Readiness for emergency tracheal intubation or an alternative method of restoring airway patency, including upper airway sanitation.

101. Indications for hospitalization 1. All children in 2nd and higher degree of stenosis of the larynx 2. At the 1st degree: * Children under 1 year of age * Lack of effect from the therapy * Previous use of systemic corticosteroids * Prematurity * Accompanying pathology * Congenital malformations of the larynx * Epidemiological indications * Social indications Release of the airway lumen from pathological secretions, The basis is inhalation therapy. Time to provide assistance - no more than 60 minutes (!!!) .

102. First line of treatment Inhalation via nebulizer of an inhaled glucocorticoid – budesonide suspension at a dose of 2 mg once or 1 mg twice after 30 minutes. Budesonide has a pronounced antiinflammatory activity. From 85 to 90% of budesonide in the blood binds to plasma proteins and undergoes intensive metabolism in the liver. In children, this process is 40% faster than in adults, and about 6% of the prescribed dose of budesonide enters the circulatory system, which is about 2 times less than in adults. In this case, inactive metabolites are formed, which are excreted from the body mainly in the urine. The bioavailability of budesonide is 10% of the intestinal fraction; about 28% is absorbed from the lungs. The low level of budesonide detected in the bloodstream, combined with a high clearance per 1 kg of weight and a short half-life, allows the use of identical doses of budesonide through a nebulizer (jet or membrane) in children of early and school age without increasing the risk of development undesirable side reactions. The effect of budesonide occurs in 15-30 minutes with a maximum improvement in 3-6 hours. For drug delivery, we recommend using nebulizers certified in accordance with the European standard for nebulizer therapy EN135544-1.

103. Algorithm for providing medical care to children with acute stenotic laryngotracheitis depending on the degree of stenosis 1 degree <2 points 2 degree 3-7 points 3 degree >8 Emotional peace Fresh air access Comfortable position for the child Distracting treatments: humidified air According to indications – antipyretic therapy Monitoring of respiratory rate, heart rate, pulse oximetry Hospitalization in the intensive care unit or intensive care unit At pulse oximetry SatO2<92% moistened oxygen Dexamethasone 0.6 mg/ kg or prednisone 2-5 mg/ kg in/m Budesonide suspension 2 mg inhaled via nebulizer or 1 mg twice 30 minutes before relief of laryngeal stenosis Reassess symptoms in 20 minutes I f indicated, intubation/tracheostomy Budesonide suspension 1 mg inhaled through a nebulizer with 2 ml of saline solution, if necessary, repeat the inhalation budesonide suspension 1 mg after 30 minutes Reassessment of symptoms after 15-20 minutes, Call emergency medical help, urgent hospitalization Budesonide suspension 2 mg inhaled via nebulizer or 1 mg twice 30 minutes before relief of laryngeal stenosis   If there is no effect from inhalation: Dexamethasone 0.15-0.6 mg/kg or prednisone 2-5 mg/ kg in/m Hospitalization With no effect and/ or reduced SatO2<92% transfer to the intensive care unit or intensive care unit   In 2-3 degree of stenosis - inhalation of 0.1

104. * In 2-3 degree of stenosis - inhalation of 0.1% L-epinephrine at 0.15 mg/kg for 1 dose (no more than 5 mg!) diluted in 3 ml 0.9% physiologic solution through a nebulizer for no more than 15 minutes. You can repeat it in 15-20 minutes. Administration of 3 or more doses over a 2-3-hour period requires immediate installation of heart monitor clips, if this has not been done before. * Sedation is not recommended , as it eliminates the possibility of assessing the severity of the child's condition, and therefore does not allow you to prescribe adequate therapy. * The use of AB is justified only for croup complicated by bacterial infection. If conservative measures are ineffective for 48 hours, the progression of stenosis and respiratory insufficiency and the 4th degree of stenosis – nasotracheal intubation with a thermoplastic tube of a much smaller diameter than the child needs by age (0.5-1.0 mm less) or tracheotomy. * For clinical symptoms of lower respiratory tract obstruction - inhalation through a nebulizer of solutions of bronchodilators (combined preparation of ipratropium bromide and fenoterol , salbutamol, inhaled glucocorticosteroids -budesonide suspension) In children with atopy, the inclusion of 2nd-generation antihistamines in the complex therapy of laryngeal stenosis of 1-2 degrees is justified. After the elimination of acute manifestations of laryngeal stenosis and stabilization of the condition in order to dilute and remove sputum from the respiratory tract with a persistent cough, broncholytic and mucolytic drugs are prescribed inside or by inhalation (acetylcysteine, carbocysteine ) or combined drugs (salbutamol + Bromhexine + guaifenizine ).

105. Thank you for your attention!