Causes of acute pneumonia in children

Risk factors for acute pneumonia. Intrauterine infections and IUGR, perinatal pathology, congenital defects of the lungs and heart, prematurity, immunodeficiencies, rickets and dystrophy, polyhypovitaminosis, the presence of chronic foci of infection, allergic and lymphaticohypoplastic diathesis, unfavorable social and living conditions, contacts when visiting preschool institutions, especially in children under 3 years of age.

Etiology of acute pneumonia .Typical bacterial pathogens of community-acquired pneumonia in children are Streptococcus pneumoniae, Haemophilus influenzae, and less frequently Staphylococcus aureus; the so-called atypical pathogens, Mycoplasma pneumoniae and Legionella pneumophila, are of some importance. In children in the first months of life, pneumonia is most often caused by Haemophilus influenzae, Staphylococcus, Proteus, and less frequently by Streptococcus pneumoniae. Viral pneumonias are much less common; respiratory syncytial viruses, influenza viruses, and adenoviruses may play a role in the etiology. The respiratory virus causes destruction of cilia and ciliated epithelium, disruption of mucociliary clearance, edema of the interstitium and interalveolar septa, desquamation of the alveoli, disorders of hemodynamics and lymph circulation, disruption of vascular permeability, i.e. it has a "pickling" effect on the mucous membranes of the lower respiratory tract. The immunosuppressive effect of viruses is also known. In such cases, microbial colonization of the lower respiratory tract and respiratory department occurs due to autoflora. The danger of endogenous infection in children with acute respiratory viral infections with unjustified use of antibiotics increases significantly, since antibiotics, without affecting viruses, suppress the saprophytic autoflora of the oropharynx, which plays an important role in the natural resistance of the respiratory system to opportunistic microbes.

In children of the first half of life, 50% of all pneumonias are hospital-acquired, gram-negative microbes predominate in the bacterial flora. Starting from the second half of life and up to 4-5 years, pneumococci, Haemophilus influenzae, and less often staphylococci predominate in the etiology of community-acquired pneumonia. At an older age, along with pneumococci, a significant proportion belongs to mycoplasma infection (more often in the autumn-winter period). In recent years, the role of chlamydial infection as a causative agent of pneumonia in schoolchildren has increased, in whom pneumonia often occurs with concomitant lymphadenitis.

Pathogenesis of acute pneumonia .

The main route of infection penetration into the lungs is bronchogenic with the spread of the infection along the respiratory tract to the respiratory section. The hematogenous route is possible with septic (metastatic) and intrauterine pneumonia. The lymphogenous route is rare, but the process passes from the pulmonary focus to the pleura through the lymphatic pathways.

ARIs play an important role in the pathogenesis of bacterial pneumonia. Viral infection increases mucus production in the upper respiratory tract and reduces its bactericidal properties; disrupts the mucociliary apparatus, destroys epithelial cells, reduces local immunological protection, which facilitates the penetration of bacterial flora into the lower respiratory tract and promotes the development of inflammatory changes in the lungs.

By penetrating the respiratory tract, the infectious agent with its toxins, metabolic products, irritating interoreceptors, leads to reflex reactions of both local and general nature, causing; disorders of the external respiratory function, functions of the central nervous system and other organs and systems. In the clinic, this is manifested by symptoms of intoxication and respiratory disorders.

With the bronchogenic route of infection, inflammatory changes are found in the respiratory bronchioles and in the lung parenchyma. The resulting inflammation leads to a decrease in the respiratory surface of the lungs, to a violation of the permeability of the pulmonary membranes, to a decrease in the partial pressure and diffusion of oxygen, which causes hypoxemia. Oxygen starvation is the central link in the pathogenesis of pneumonia. The body includes compensatory reactions from the cardiovascular system and hematopoietic organs. There is an increase in pulse rate, an increase in stroke and minute volume of blood. An increase in cardiac output, aimed at reducing hypoxia, ultimately does not give an effect, since with plethora of the lungs, the power of forced exhalation decreases and circulatory disorders deepen. In addition, as a result of hypoxia and enzymatic shifts, depletion of energetically active substances is observed (decrease in the level of glycogen, ATP, creatine phosphate, etc.), which leads to the occurrence of insufficiency of this compensatory link, and circulatory hypoxemia joins respiratory hypoxemia . One of the compensatory links is the release of erythrocytes, but their function as oxygen carriers is altered due to enzymatic and histotoxic disorders, and hypoxic hypoxia joins. Intensification of lipid peroxidation processes and disruption of antioxidant protection occur.

Oxygen deficiency affects metabolism, inhibits oxidative processes, underoxidized metabolic products accumulate in the blood, and the acid-base balance shifts toward acidosis. Acidosis is also a key link in the pathogenesis of pneumonia, playing a role in the dysfunction of various organs and systems, especially the liver. Impaired liver function, in turn, aggravates metabolic disorders, especially vitamin metabolism, which leads to clinical manifestations of polyhypovitaminosis. In addition, trophic disorders increase, especially in young children, posing a threat of hypotrophy.

In children with pneumonia, metabolic processes are naturally disrupted:

• acid-base balance - metabolic or respiratory-metabolic acidosis with a decrease in the power of buffer bases, accumulation of under-oxidized products;
• water-salt - fluid retention, chlorides, hypokalemia; dehydration is possible in newborns and infants;
• protein - dysproteinemia with a decrease in albumin levels, an increase in a1- and y-globulins, an increase in the content of ammonia, amino acids, urea, etc.;
• carbohydrate - pathological sugar curves, in severe pneumonia - hypoglycemia;
• lipid - hypocholesterolemia, an increase in the level of total lipids against the background of a decrease in the content of phospholipids.

Respiratory failure is a condition in which either the lungs do not maintain normal gas composition of the blood, or the latter is achieved due to abnormal functioning of the external respiratory system, leading to a decrease in the functional capabilities of the body.

According to morphological forms, focal, segmental, focal-confluent, croupous and interstitial pneumonia are distinguished. Interstitial pneumonia in children is a rare form in pneumocystosis, sepsis and some other diseases. The morphological form of pneumonia is determined by the clinical picture and radiological data. The allocation of morphological forms has a certain prognostic value and can influence the choice of initial therapy.

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