Secondary pneumonia develops in people suffering from chronic diseases of the bronchopulmonary system, as well as somatic or other infectious diseases with the localization of the primary affect outside the lungs. Secondary pneumonia occurs much more often than primary pneumonia and has a diverse etiology. It should be noted that all cases of nosocomial acute pneumonia are classified as secondary.

Among secondary pneumonias, a large share is occupied by aspiration, hypostatic And postoperative pneumonia. All of them develop due to the activation of autoinfection.

In aspiration pneumonia, at the first stage of development, damage to the pulmonary parenchyma by the acid of the gastric contents is important. Hypostatic and postoperative pneumonia develop against the background of impaired mucociliary clearance in the bronchial system and circulatory disorders.

In accordance with nosological principle Acute pneumonia is divided into independent diseases - primary acute pneumonia, as well as acute pneumonia, which are complications of other diseases - secondary.

According to clinical and morphological features, Acute pneumonia is divided into lobar (lobar), bronchopneumonia (focal) and interstitial (alveolitis). Lobar (lobar) pneumonia is a nosological form; it refers to contagious infectious-allergic diseases. Bronchopneumonia in the vast majority of cases develops as a complication of another disease. However, there are special etiological variants of bronchopneumonia, which can be considered as independent diseases (for example, Legionnaires' disease), as well as bronchopneumonia of newborns and the elderly. Acute interstitial pneumonia occurs under the influence of certain pathogens - viruses, chlamydia, mycoplasmas, rickettsia and pneumocystis. They can be secondary in nature (pneumocystis), be a manifestation of a specific disease (viral, psittacosis) or be an independent nosological form (Hamman-Rich disease or idiopathic fibrosing alveolitis).

By prevalence acute pneumonia can be unilateral or bilateral; acinar, miliary, focal-confluent, segmental, polysegmental lobar, total.

By nature of the flow: heavy, moderate, light; sharp and lingering. In the scientific literature of past years, according to the clinical course, so-called atypical pneumonias were distinguished, which are actually represented by acute interstitial pneumonia.

LOUPIC PNEUMONIA

Lobar pneumonia- acute infectious-allergic lung disease.

It has several synonyms: lobar (lobar), since one or more lobes of the lung are affected; pleuropneumonia - due to the involvement of the visceral pleura of the affected lobe and the development of pleurisy; fibrinous, lobar, which reflects the nature of exudative inflammation in the lungs. Caused by pneumococci types 1, 2, 3, less commonly by Klebsiella. Infection usually occurs from a patient or carrier. Anyone gets sick

children aged about 30 years and over 50 who do not have immunity to the named virulent strains of pneumococcus. The route of infection is airborne. The spread of bacteria is favored by intoxication, cooling, anesthesia, and inhalation of toxic poisons and dust. The mortality rate is about 3%, despite antibiotic therapy.

Pathogenesis. The occurrence of lobar pneumonia is explained by the development of an immediate hypersensitivity reaction in the “territories” of the respiratory parts of the lung, including the alveoli and alveolar ducts. There are two points of view about the early stages of the pathogenesis of lobar pneumonia. According to the first, pneumococci enter the upper respiratory tract and cause sensitization of the macroorganism. Under the influence of permissive factors (hypothermia, etc.), aspiration of the pathogen into the alveoli occurs and a hyperergic reaction begins with the development of lobar pneumonia. According to the second theory, the pathogen from the nasopharynx penetrates the pulmonary parenchyma, the organs of the reticuloendothelial system (where immune reactions develop), and then into the bloodstream. The stage of bacteremia begins. When pneumococci re-enter the lungs with blood, they interact with antibodies and complement. Immunocomplex damage to the microvasculature of the alveoli occurs with a characteristic exudative tissue reaction.

In the initial stage of the disease, pronounced exudation develops. An important role in this is played by hemolysins, hyaluronidase and leukocidin, secreted by pneumococci and increasing vascular permeability.

Morphogenesis, pathological anatomy. The morphogenesis of lobar pneumonia in the classical version consists of 4 stages: flushing (inflammatory edema), red hepatitis, gray hepatitis and resolution.

The hot flash stage lasts the first day of the disease and is characterized by a sharp congestion of the alveolar capillaries, edema of the interstitial tissue and the accumulation of liquid exudate, reminiscent of edematous fluid, in the lumens of the alveoli. Exudate is formed extremely quickly and spreads through the alveolar ducts and alveolar pores (Cohn's pores) throughout the entire lobe. The exudate contains a large number of bacteria that actively multiply here, as well as single alveolar macrophages and polymorphonuclear leukocytes. Morphologically, the picture resembles that of pulmonary edema, so methods that can identify pneumococcus (cultures, staining smears) can be of great help in diagnosing this stage of pneumonia. At the same time, swelling and inflammatory changes occur in the pleura, which is clinically manifested by acute pain in the side on the side of the affected lobe of the lung.

Characteristic is the damage to the alveoli of the entire lobe at the same time while maintaining the bronchi intact. This microscopic sign persists in other stages of the disease. Macroscopically, changes in the stage of tide are characterized by plethora and compaction of the affected lobe of the lung.

The red liver stage occurs on the 2nd day of illness, when a large number of red blood cells, single polymorphonuclear leukocytes, macrophages appear in the exudate, and fibrin precipitates. Macroscopically, the affected lobe is airless, dense, red, reminiscent of liver tissue, which is where the name of this stage of the disease comes from. Fibrinous deposits are clearly visible on the thickened pleura.

The gray hepatization stage takes 4 -6th day of illness. At this time, there is a collapse of the pulmonary capillaries, a concentration of living and dead polymorphonuclear leukocytes, macrophages and fibrin in the exudate. Granulocytes mainly carry out phagocytosis of opsonized pneumococci and lysis of fibrin, and macrophages - necrotic detritus. Macroscopically, the affected lobe is enlarged in size, heavy, dense, airless, with a granular surface when cut. The pleura is thickened, cloudy, with fibrinous deposits.

The resolution stage occurs on the 9-11th day of illness. Fibrinous exudate undergoes melting and phagocytosis under the influence of proteolytic enzymes of granulocytes and macrophages. The exudate is eliminated through the lymphatic drainages of the lung and separated with sputum. Fibrinous deposits on the pleura resolve. Morphological changes are usually somewhat delayed compared to the clinical manifestations of the disease and can be detected within several weeks after clinical recovery.

Complications lobar pneumonia are divided into pulmonary and extrapulmonary. Pulmonary complications include lung carnification (from the Latin salu - meat) - the organization of exudate, usually developing as a result of insufficiency of the function of polymorphonuclear leukocytes and/or macrophages; formation of acute abscess or gangrene of the lung with excessive activity of polymorphonuclear leukocytes; empyema of the pleura.

Extrapulmonary complications are caused by the possibility of infection spreading through the lymphatic and circulatory pathways. It should be noted that bacteremia in lobar pneumonia is recorded in 30% of cases. With lymphogenous generalization, purulent mediastinitis and pericarditis occur, with hematogenous generalization - metastatic abscesses in the brain, purulent meningitis, acute ulcerative and polyposis-ulcerative endocarditis, most often of the tricuspid valve, purulent arthritis, peritonitis, etc.

Pathomorphosis lobar pneumonia is manifested by a decrease in mortality, abortive forms of the disease and a decrease in the frequency of pulmonary and extrapulmonary complications.

Death with lobar pneumonia it occurs from acute pulmonary heart failure or purulent complications.

A special form of lobar pneumonia is Lobar Friedlander's pneumonia. It is relatively rare (0.5-0.4% of pneumonia cases). Can be classified as nosocomial infections, since in hospitals it is 8-9.8 % acute pneumonia. Infection occurs by aspiration of Klebsiella pneumoniae (Friedlander's diplobacillus) into the upper respiratory tract. Common among alcoholics and newborns. Men get sick 5-7 times more often than women, older people more often than young people. It is usually localized in the upper lobe, but can also be polylobar. In contrast to lobar pneumonia caused by pneumococcus, Friedlander pneumonia is characterized by necrosis of the alveolar septa with frequent formation of abscesses, foci of carnification and severe interstitial fibrosis as a result.

BRONCHOPNEUMONIA

Bronchopneumonia, or focal pneumonia, is characterized by the development in the pulmonary parenchyma of foci of acute inflammation ranging in size from the acinus to the segment associated with the affected bronchiole. The development of the disease is preceded by inflammatory processes in the bronchi, which can be detected simultaneously with foci of bronchopneumonia. Diagnosed in 2/3 of patients hospitalized for acute pneumonia. In terms of pathogenesis, they are often secondary; the etiology is varied (see earlier).

Pathogenesis. Associated with airborne spread of the pathogen, its aspiration from the upper respiratory tract, as well as spread by hematogenous and, less commonly, contact routes.

A prerequisite for the development of bronchopneumonia is a violation of the drainage function of the bronchi, which can be facilitated by hypothermia, intoxication, anesthesia, etc. Violation of the drainage function of the bronchi promotes the penetration of microorganisms into the respiratory parts of the lung - the alveolar ducts, alveoli. In this case, the bronchi are initially damaged, and then the inflammatory process caused by microorganisms spreads from the small bronchi and bronchioles to the adjacent alveoli. Typically, inflammation spreads to the lung tissue in a descending way, intrabronchially, however, with the development of destructive bronchitis and bronchiolitis, a peribronchial route is also possible. With a generalized infection (septicopyemia), a hematogenous route of penetration of the pathogen into the lungs is observed.

A special group of bronchopneumonia consists of aspiration, hypostatic and postoperative pneumonia, caused by activation of autoinfection.

In recent years, no less interest has been attracted to hospital-acquired, acute pneumonia, including pneumonia in patients with reduced immunity, which in most cases relates to opportunistic infections.

Pathological anatomy. It is largely determined by the type of pathogen, but there are stereotypical changes characteristic of all types of bronchopneumonia. These include the formation of a focus of inflammation around the small bronchus, bronchioles with symptoms of bronchitis and/or bronchiolitis, which is represented by various forms of catarrhal inflammation (serous, mucous, purulent, mixed). Violation of the drainage function of the bronchi contributes to the penetration of pathogens into the respiratory sections of the lungs. In this case, inflammation spreads to the respiratory bronchioles and alveoli. The walls of the bronchioles are infiltrated by inflammatory cells. Exudate accumulates in the lumens of the alveoli and bronchioles, as well as the bronchi. The exudate can be serous, purulent, hemorrhagic, or mixed, which is largely determined by the etiology of the disease and the severity of the process. Along the periphery of the lesions there is preserved lung tissue with symptoms of perifocal emphysema.

Macroscopically, dense, airless foci of various sizes are detected, usually forming around the bronchi, the lumen of which is filled with liquid turbid contents of gray-red color and localized, as a rule, in the posterior and posteroinferior segments of the lungs (II, VI, VIII, IX, X). Depending on the size of the lesions, miliary, acinous, lobular, confluent lobular, segmental and polysegmental bronchopneumonia are distinguished.

Morphological features of certain types of bronchopneumonia.Bronchopneumonia caused by pneumococcus. The most common etiological form of pneumonia. It is characterized by the formation of foci associated with bronchioles containing fibrinous exudate. Microbial edema is expressed along the periphery of such foci, where a large number of pathogens are found.

Bronchopneumonia caused by staphylococcus. Occurs extremely rarely, in 5-10 % acute pneumonia. It can develop after pharyngitis, and also as a complication after a viral infection (usually influenza). It has the morphology of typical bronchopneumonia with hemorrhagic and destructive bronchitis with a clear tendency to suppuration and necrosis of the alveolar septa. As a result of necrosis, acute abscesses, purulent pleurisy, pneumatocele, cysts, as well as severe fibrosis as a result of the disease often develop.

Bronchopneumonia caused by streptococcus. Accounts for 11-13% of acute pneumonia. It is usually caused by hemolytic streptococcus of groups A and B, often in combination with viruses, as well as in patients with diabetes. Damage to the lower lobes is typical. Microscopic examination reveals foci of bronchopneumonia with serous-leukocyte exudate with a pronounced interstitial component. In some cases, acute abscesses and bronchiectasis occur. Often complicated by pleurisy.

Bronchopneumonia caused by Pseudomonas aeruginosa. One of the most common nosocomial acute pneumonias. Two options for the penetration of the pathogen into the lungs are described: by aspiration and through the blood. In the first case, bronchopneumonia develops with abscess formation and pleurisy. In the second case, we are talking about patients with malignant tumors or extensive suppurating wounds, when bronchopneumonia occurs with pronounced coagulative necrosis and a hemorrhagic component. The prognosis is bad. The mortality rate is high.

Bronchopneumonia caused by Escherichia coli. Typically, the pathogen enters the lungs hematogenously during infections of the urinary tract, gastrointestinal tract, and after surgical interventions. Pneumonia is often bilateral with hemorrhagic exudate, foci of necrosis and abscess formation.

Bronchopneumonia caused by fungi. Most often caused by fungi of the genus Candida. Foci of pneumonia of various sizes with accumulations of polymorphonuclear leukocytes and eosinophils, a tendency to form decay cavities where threads of the fungus can be found. With hyperergic reactions, interstitial inflammation develops followed by fibrosis.

Bronchopneumonia caused by L.pneumophilia (Legionnaires' disease). The disease was described in 1970, when it first began: an epidemic of a peculiar pneumonia was recorded among American Legionnaires in Philadelphia. Among the 182 cases, 29 people died. The disease begins with a headache, muscle pain, and dry cough. The pathogen does not stain with Gram, antibodies enhance phagocytosis of the bacterium by macrophages, however, due to the ability of endocytobiosis in phagocytes, the infection can persist in the body for a long time. Several lobes of the lung are involved in the inflammatory process. In some cases, macroscopically, the lesion may resemble lobar pneumonia in the gray hepatic stage with the development of fibrinous pleurisy. Microscopic examination usually reveals hemorrhagic edema, infiltration of alveolar septa by macrophages and polymorphonuclear leukocytes.

Complications. They are largely determined by the etiology of the disease and the severity of its course. They can be divided into pulmonary and extrapulmonary and are represented by the same options as with lobar pneumonia. Among the pulmonary complications of bronchopneumonia, pleurisy should also be mentioned, which develops in cases where the source of inflammation is located under the pleura.

Death patients may be caused by pneumonia itself, its purulent complications and pulmonary heart failure.

Pneumonia (P) – an acute infectious disease of predominantly bacterial etiology, characterized by the formation of an inflammatory infiltrate in the lung parenchyma.

The definition of pneumonia emphasizes the acute nature of inflammation, so you don’t need to use the term “acute pneumonia” (in the ICD – 10 revision (1992) there is no heading “acute pneumonia”).

Epidemiology. The incidence of pneumonia is on average 1%, that is, every year one out of 100 people gets sick. This rate is significantly higher in children and people over 60 years of age. Men get sick more often than women. In a number of patients (up to 20%), pneumonia is not diagnosed, occurring under the guise of bronchitis or other diseases.

The average mortality rate from pneumonia is 1 – 5%, in severe forms of the disease reaches 40 – 50%. Among all causes of human death, pneumonia ranks 4th after cardiovascular diseases, malignant neoplasms, injuries and poisoning, and among all infectious diseases it ranks 1st.

Etiology. The causative agents of pneumonia can be almost all known infectious agents: more often - gram-positive and gram-negative bacteria, less often - mycoplasma, chlamydia, legionella, viruses, etc. Associations of two or more microorganisms are possible. The etiological structure of pneumonia depends on the conditions under which the disease occurs.

According to the International Consensus and Standards (protocols) for the diagnosis and treatment of patients with nonspecific lung diseases, the Ministry of Health of the Russian Federation (1998), based on epidemiological and clinical-pathogenetic features, all pneumonia is divided into 4 groups:

Community-acquired (out-of-hospital) pneumonia that developed in community-acquired conditions, including “atypical” pneumonia caused by “atypical” intracellular microorganisms.

Intrahospital (hospital or nosocomial) pneumonia that developed within 48–72 hours or more after the patient was admitted to the hospital for another disease.

Pneumonia in immunodeficiency states ( congenital immunodeficiency , HIV infection, drug (iatrogenic) immunosuppression).

Aspiration pneumonia.

Each group of pneumonia is characterized by its own spectrum of infectious pathogens, which allows for more targeted prescribing of antibacterial therapy at the initial stage of treatment before verification of the pathogens.

I. When community-acquired pneumonia the most common pathogens are: pneumococcus (40–60%), mycoplasma (15–20%), Haemophilus influenzae (15–25%), Staphylococcus aureus (3–5%), Klebsiella pneumoniae (3–7%), Legionella ( 2–10%), respiratory viruses (2–15%), chlamydia.

II. For nosocomial pneumonia The most common gram-negative infectious agents are: Klebsiella pneumoniae (Friedlander's bacillus), Pseudomonas aeruginosa, Escherichia coli, Proteus, as well as Staphylococcus aureus and anaerobes. They highlight.

III. Pathogens of pneumonia in patients with immunodeficiency conditions in addition to the usual gram-positive and gram-negative bacteria, there are cytomegaloviruses, which are considered markers of HIV infection, pneumocystis, pathogenic fungi, and atypical mycobacteria.

IV. Aaspiration pneumonia most often caused by associations of Staphylococcus aureus and gram-negative bacteria with anaerobic microorganisms, always present in the oral cavity and nasopharynx.

During periods of influenza epidemics, the etiological role of viral-bacterial associations, as well as opportunistic microorganisms, increases. By damaging the mucous membranes of the respiratory tract, respiratory viruses (influenza viruses, adenoviruses, respiratory syncytial viruses, etc.) open the “gate” for bacterial flora, most often staphylococci.

Determining the etiology of pneumonia is difficult. At the initial stage, the etiological diagnosis is empirical (presumptive) and is made taking into account clinical and epidemiological data. Thus, with the development of nosocomial pneumonia in a patient in a purulent surgical department, staphylococcal etiology is most likely. Community-acquired lobar pneumonia is most often pneumococcal. A group outbreak is characteristic of mycoplasma pneumonia. In order to identify pathogens, the patient’s sputum and bronchial washings are examined. In the diagnosis of mycoplasma and viral pneumonia, the complement fixation reaction (CFR) is used with the patient’s blood serum and antigens of viruses or mycoplasma. Even with a well-equipped microbiological laboratory, the etiology of pneumonia can only be determined in 50-60% of cases.

Pathogenesis. Risk factors pneumonia are hypothermia, childhood and old age, smoking, stress and overwork, smoking and alcohol abuse, exposure to adverse environmental and occupational factors on the respiratory system, influenza epidemics, chronic bronchitis, congestion in the pulmonary circulation, immunodeficiency states, contact with birds and rodents, staying in air-conditioned rooms, prolonged bed rest, bronchoscopic examinations, mechanical ventilation, tracheostomy, anesthesia, septic conditions, etc.

In pathogenesis pneumonia, the pathogenic properties of infectious microorganisms and the patient’s defense mechanisms interact.

The lower respiratory tract is normally sterile thanks to the system of local bronchopulmonary protection: mucociliary clearance (mucociliary lifting cleansing of the bronchi), production in the bronchi and alveoli of humoral protective factors (Ig A, lysozyme, complement, interferons, fibronectin), alveolar surfactant and phagocytic activity of alveolar macrophages, the protective function of broncho-associated lymphoid tissue.

Pneumonia pathogens enter the respiratory tracts of the lungs from the environment most often bronchogenic through inhaled air or aspiration from the oral cavity and nasopharynx. Hematogenous And lymphogenous routes of infection into the lungs are observed in sepsis, general infectious diseases, thromboembolism, and chest injuries. Inflammation of the lung tissue can develop without exposure to external infectious agents - with the activation of opportunistic microflora located in the patient’s respiratory tract, which occurs when the general reactivity of the body decreases.

When infectious microorganisms enter the respiratory tract, they adhere to the surface of the bronchial and alveolar epithelium, leading to damage to cell membranes and colonization of pathogens in epithelial cells. This is facilitated by previous damage to the epithelium by viruses, chemicals, weakening of general and local protective mechanisms as a result of exposure to infectious and other unfavorable factors of the external and internal environment.

Further development of the inflammatory process is associated with the production of endo- or exotoxins by infectious agents, the release of humoral and cellular inflammatory mediators in the process of damage to lung tissue by the influence of infectious microorganisms, neutrophils and other cellular elements. Humoral mediators of inflammation include complement derivatives, kinins (bradykinin). Cellular mediators of inflammation are represented by histamine, arachidonic acid metabolites (prostaglandins, thromboxane), cytokines (interleukins, interferons, tumor necrosis factor), lysosomal enzymes, reactive oxygen metabolites, neuropeptides, etc.

Pneumococci, Haemophilus influenzae, Klebsiella pneumoniae produce endotoxins(hemolysins, hyaluronidase, etc.), which sharply increase vascular permeability and contribute to pronounced swelling of the lung tissue.

Pneumococcal(lobar or lobar) pneumonia begins in the form of a small focus of inflammation in the lung parenchyma, which, due to the formation of excess edematous fluid, spreads “like an oil slick” from alveoli to alveoli through Cohn’s pores until it covers the entire lobe or several lobes. With early treatment, the inflammatory process can be limited to a segment of the lung. Pneumococci are located on the periphery of the inflammatory focus, and in its center a germ-free zone of fibrinous exudate is formed. The term “lobar pneumonia,” common in Russian pulmonology, comes from the word “croup,” which means a certain type of fibrinous inflammation.

Friedlander's pneumonia, caused by Klebsiella and similar in development to pneumococcal pneumonia, is characterized by thrombosis of small vessels with the formation of necrosis of the lung tissue.

Streptococci, staphylococci and Pseudomonas aeruginosa allocate exotoxins, destroying lung tissue and forming foci of necrosis. Microorganisms are located in the center of the inflammatory-necrotic focus, and inflammatory edema is observed along its periphery.

Micoplasma, chlamydia and legionella are characterized by long-term persistence and replication within the cells of the macroorganism, which determines their high resistance to antibacterial drugs.

In the pathogenesis of pneumonia, sensitization of the body to infectious microorganisms is of particular importance, the severity of which determines the characteristics of the clinical course of the disease. The body's response in the form of the formation of antimicrobial antibodies and immune complexes (antigen-antibody-complement) contributes to the destruction of pathogens, but at the same time leads to the development of immunoinflammatory processes in the lung tissue. When the pulmonary parenchyma is damaged by infectious microorganisms, autoallergic reactions of the cellular type may develop, contributing to the protracted course of the disease.

A hyperergic inflammatory reaction in the alveolar zone is especially characteristic of pneumococcal (lobar) pneumonia, which is associated with sensitization of the body to pneumococcus, which is present in the normal microflora of the upper respiratory tract in 40–50% of healthy individuals. Focal pneumonia often manifests itself as a normo- or hypergic inflammatory reaction.

Taking into account pathogenetic factors, pneumonia is divided into primary and secondary. Primary pneumonia develops as an acute infectious-inflammatory process in a previously healthy person, secondary pneumonia occurs against the background of chronic respiratory diseases or pathologies of other organs and systems.

According to the mechanism of development, secondary pneumonia is often bronchopneumonia – First, local bronchitis develops, and then the inflammatory process spreads to the alveolar tissue.

Pathological picture most typical for pneumococcal (lobar) pneumonia, which has a cyclic course. Highlight high tide stage(from 12 hours to 3 days), which is characterized by hyperemia and inflammatory edema of the lung tissue. In the next stage, lesions appear red and gray hepatization of lung tissue(from 3 to 6 days) as a result of diapedesis of erythrocytes, leukocytes and effusion of plasma proteins, primarily fibrinogen, into the alveoli. Stage permissions(duration varies individually) is characterized by gradual dissolution of fibrin, filling of the alveoli with macrophages and restoration of airiness in the affected parts of the lungs. Against the background of the separation of purulent sputum through the respiratory tract (in the resolution stage), local bronchitis is usually associated with pneumonia. Pneumococcal pneumonia is characterized by fibrinous pleurisy.

With focal pneumonia, a mosaic pathological picture is observed within one or several segments. The inflammatory process involves lobules or groups of lobules, alternating with areas of atelectasis and emphysema or normal lung tissue. The exudate is most often serous, but can be purulent or hemorrhagic. Focal confluent pneumonia often develops. The pleura is usually not affected.

Classification. When making a diagnosis, be sure to indicate epidemiological group of pneumonia(according to the International Consensus and Standards (protocols) for the diagnosis and treatment of patients with nonspecific lung diseases, Ministry of Health of the Russian Federation, 1998), updated etiology(according to ICD-10 revision) and basic clinical and morphological signs taking into account the widespread classification of pneumonia in Russia, developed by N.S. Molchanov (1962) in a later modification by E.V. Gembitsky (1983).

Pneumonia is an acute inflammatory disease of the respiratory parts of the lungs, predominantly of bacterial etiology, characterized by intra-alveolar exudation.

The occurrence of the disease is caused by the penetration of saprophytic microbes from the oropharynx into the lower respiratory tract - alveoli and bronchioles. Less commonly, pathogens spread through lymphatic capillaries or blood vessels from foci of infection in neighboring organs. The causative agents of pneumonia are most often pneumococci (lobar pneumonia), staphylococci, streptococci and other microbes.

The clinical (external) manifestations of the disease are influenced by many factors:

properties of the pathogen microbe;

the nature of the course and stage of the disease;

structural (morphological) basis of the disease;

prevalence of the process in the lungs;

the presence of complications - pulmonary suppuration, pleurisy or empyema.

Modern classification of pneumonia

Classification according to ICD-10 (by forms and timing of occurrence):

Out-of-hospital - occurs at home or in the first 48 hours of stay in a medical institution. The course is relatively favorable, the mortality rate is 10-12%.

Hospital (nosocomial) - occurs after 48 hours of the patient’s stay in the hospital or if the patient has been treated in any medical institution for 2 or more days over the previous 3 months. In modern protocols, the World Health Organization (WHO) includes in this category patients with ventilator-associated pneumonia (who are on mechanical ventilation for a long time), as well as patients with pneumonia who are kept in nursing homes. It is characterized by a high degree of severity and mortality up to 40%.

Aspiration pneumonia - occurs when a large amount of oropharyngeal contents is swallowed by unconscious patients with impaired swallowing and a weakened cough reflex (alcohol intoxication, epilepsy, traumatic brain injury, ischemic and hemorrhagic strokes, etc.). Aspiration of gastric contents may cause a chemical burn of the mucous membrane of the respiratory tract with hydrochloric acid. This condition is called chemical pneumonitis.

Pneumonia developing against the background of immunodeficiencies, both primary (thymic aplasia, Bruton's syndrome) and secondary (HIV infection, oncohematological diseases).

Community-acquired pneumonia (domestic, home, outpatient), that is, acquired outside a medical institution, usually develops when the protective mechanisms of the respiratory system are impaired. Pneumonia often complicates the course of a respiratory viral infection, such as influenza. The main causative agent of community-acquired pneumonia is pneumococcus. It can also be caused by streptococci or Haemophilus influenzae.

Depending on the extent of organ damage:

lobar pneumonia (pleuropneumonia) - affecting the lobe of the lung;

focal pneumonia (bronchopneumonia) with damage to the group of alveoli adjacent to the inflamed bronchus;

Interstitial pneumonia is inflammation of lung tissue along the bronchi and pulmonary blood vessels.

Lobar pneumonia is only one of the forms of pneumococcal pneumonia, and does not occur with pneumonia caused by other pathogenic microbes.

Classification by pathogen:

Bacterial - the main pathogens are Streptococcus pneumonia, Staphylococcus aureus, Mycoplasmapneumonia, Haemophilus influenza, Chlamydiapneumonia.

Viral - often caused by influenza viruses, parainfluenza, rhinoviruses, adenoviruses, respiratory syncytial virus. In more rare cases, these may be measles, rubella, whooping cough viruses, cytomegalovirus infection, and Epstein-Barr virus.

Fungal - the main representatives in this category are Candida albicans, fungi of the genus Aspergillus, Pneumocystisjiroveci.

Pneumonia caused by protozoa.

Pneumonia caused by helminths.

Mixed - this diagnosis occurs most often with a bacterial-viral association.

Forms of pneumonia by severity:

extremely heavy.

The inflammatory process occurs:

one-sided;

bilateral.

Etiology

Lobar pneumonia most often develops against the background of overwork, hypothermia, lack of vitamins and minerals, and disruption of the immune system. The causes of this lung disease include the following factors:

• 1. Diseases suffered the day before (colds or infections).
• 2. Intoxication of the body.
• 3. Harmful working conditions.
• 4. Living in premises with an unfavorable microclimate and severe dampness.
• 5. Penetration of pathogens of lobar pneumonia (streptococci, pneumococci, staphylococci, Friendler's bacillus) into the patient's body, which, entering the pulmonary parenchyma, provoke the development of an acute inflammatory process and the appearance of the first symptoms of the disease.

The respiratory tract of adults and children is constantly attacked by pathogens, but local defense mechanisms in the form of immunoglobulin A, lysozyme and macrophages in healthy people prevent diseases from developing.

Risk factors for developing pneumonia, as defined by WHO in 1995, include:

old age - people over 60 years of age (due to suppression of the cough reflex, the reflex responsible for spasm of the glottis);

the period of newbornhood and infancy (the reason is the incomplete development of the immune system);

conditions accompanied by loss of consciousness (epilepsy, traumatic brain injury, anesthetized sleep, suicide attempts with sleeping pills or drugs, alcohol intoxication);

respiratory diseases (chronic bronchitis, emphysema, acute respiratory distress syndrome), smoking;

concomitant diseases that reduce the activity of the immune system (oncological diseases, systemic connective tissue diseases, HIV infection, etc.);

negative social and living conditions, malnutrition;

keeping the patient in a lying position for a long time.

(N.S.Molchanov, 1965; E.V.Gembitsky, 1983)

By etiology:

Bacterial (indicating the pathogen)

Viral (indicating the pathogen)

Mycoplasma

Rickettsial (pulmonary form of Q fever)

Ornithosis

Fungal

Mixed (viral-bacterial)

Unknown etiology

By pathogenesis:

Primary

Secondary (stagnant-hypostatic, infarction-pneumonia, postoperative, burn, septic-metastatic, etc.)

With the flow:

Protracted (more than 4 weeks)

By localization:

One- and two-sided

According to clinical and morphological characteristics:

Parenchymatous:

a) lobar, segmental (lobar)

b) focal (bronchopneumonia)

Interstitial

By severity:

Mild degree

According to the state of external respiration function:

No functional impairment

Respiratory failure I, II, III degrees.

Sample formulation of the diagnosis of pneumonia:

Basic: Community-acquired pneumococcal pneumonia of the lower lobe of the right lung, moderate severity

Complication: DN – II Art. Exudative pleurisy on the right

Many authors dispute the validity of the independent diagnosis of “interstitial pneumonia,” since reactive changes in the interstitial tissue are observed in many pulmonary and extrapulmonary diseases. This form of pneumonia is diagnosed more often with a viral or psittacosis infection.

Clinical picture. Clinical manifestations of pneumonia depend on epidemiological conditions, the clinical and morphological form of the disease, the type of pathogen and the state of the macroorganism.

In all cases it is possible to distinguish main clinical syndromes:

1) intoxicating(weakness, weakness, headaches and muscle pain, pallor);

2) general inflammatory changes(chills, increased body temperature, neutrophilic leukocytosis with a shift in the leukocyte formula to the left, increased ESR, levels of seromucoids, fibrinogen, appearance of C-reactive protein);

3) inflammatory changes in lung tissue(cough with sputum, chest pain, increased vocal tremors, dullness of percussion sound, changes in breathing patterns, the appearance of crepitus or moist fine rales, radiological signs of infiltration of the lung tissue);

4) involvement of other organs and systems(cardiovascular system, nervous, digestive, kidney, blood system).

The most typical clinical picture is community-acquired pneumococcal (lobar) pneumonia, which develops more often in young and middle-aged men.

It begins acutely against the background of complete health, usually after hypothermia. The patient develops severe chills, severe weakness, headache and muscle pain, and an increase in body temperature to 39-40°. Shortness of breath is a concern with light exertion or even at rest. There is pain in the chest on the affected side, which intensifies with deep breathing or coughing and is associated with the involvement of the pleura in the pathological process. With lower lobe localization of pneumonia due to damage to the diaphragmatic pleura, pain radiates to the abdominal wall, simulating the picture of an acute abdomen. The cough appears at first dry, and from the 2-3rd day - with the discharge of a small amount of viscous sputum streaked with blood - “rusty”. Subsequently, the sputum becomes purulent or mucopurulent in nature.

When examining the patient, pale skin, cyanosis of the nasolabial triangle, and herpetic rashes on the lips and wings of the nose (due to an exacerbation of persistent herpetic infection) are noted. In severe cases of the disease, disturbances of consciousness and delirium are possible. The body position is often forced - lying on the affected side - to reduce respiratory excursions of the affected lung. Breathing is shallow, increased to 30-40 per minute. Participation in breathing of the wings of the nose and other auxiliary respiratory muscles, and lag of the diseased half of the chest are observed. Palpation of the intercostal spaces in the area of ​​the affected lobe of the lung is painful. Voice tremors increased. Percussion of the lungs reveals shortening and then a pronounced dullness of the percussion sound.

During auscultation in the initial stage of pneumonia, somewhat weakened vesicular breathing is heard, which, with inflammatory compaction of the lung tissue (on the 2-3rd day of illness), is replaced by bronchial breathing. From the first days of the disease (in the flushing stage) it is heard crepitus– characteristic crackling sound when swollen alveoli dissolve at the height of inspiration (crepitatio indux). It is a pathognomonic sign of lobar pneumonia. At the peak of pulmonary inflammation, when the alveoli are filled with inflammatory exudate (red and gray liver stage), crepitus disappears. Pleural friction rub is often detected. With the discharge of sputum, scattered dry and sonorous fine-bubbly, moist rales appear, caused by local bronchitis.

From the cardiovascular system, tachycardia and hypotension are usually detected, up to collapse.

When adequate treatment of pneumonia is started in a timely manner, the patient’s body temperature quickly decreases and signs of intoxication decrease. As the source of inflammation resolves, percussion dullness is limited, breathing becomes vesicular and harsh. The amount of moist rales decreases, and crepitatio redux reappears. Uncomplicated lobar pneumonia resolves by the end of the 2-3rd week.

Community-acquired focal pneumococcal pneumonia is diagnosed in 80-85% of all cases of pneumonia. In terms of pathogenesis, it is usually secondary - it develops against the background of an acute respiratory infection, exacerbation of chronic bronchitis or other somatic pathology. It is more common in children and the elderly, weakened by frequent colds or other factors predisposing to pneumonia. The clinical picture of the disease is variable due to the variety of its pathogens (bacteria, including pneumococci, mycoplasma pneumoniae, viruses, rickettsia). The cyclical nature of the disease, characteristic of lobar pneumonia, is absent. The severity of the condition and physical findings depend on the extent of the process.

The disease can begin acutely, after hypothermia, with an increase in body temperature to 38-39 o, or gradually against the background of prodromal phenomena. In weakened patients, the body temperature may be low-grade. A dry cough or with mucopurulent sputum, shortness of breath, general weakness, sweating, and headache appear. If pneumonia is associated with an exacerbation of chronic bronchitis, an increase in “bronchitis” cough or an increase in the amount of mucopurulent sputum discharge is noted. Chest pain with focal pneumonia is usually absent, since the inflammatory process does not involve the pleura. Sweating is common with little physical activity.

Objective data are more scarce than for lobar pneumonia. On examination, pallor of the skin is observed, and with concomitant chronic diseases of the respiratory system or cardiovascular system - cyanosis, increased breathing. There is some lag in the diseased half of the chest when breathing. Above the areas of infiltration, an increase in vocal tremors and a shortening of the percussion sound are determined. On auscultation, against the background of hard vesicular breathing, dry and sonorous fine-bubbly, moist rales are heard. Large-focal (confluent) infiltration of lung tissue, according to physical data, resembles lobar pneumonia, but crepitus is not typical for focal pneumonia. With small inflammatory foci, a “mosaic” picture is possible - alternating areas of dullness of percussion sound with areas of normal or boxy, hard breathing with weakened breathing.

Pneumococcal pneumonia, both lobar and focal, is not characterized by destruction of lung tissue, since pneumococci do not produce exotoxins. This also explains the almost complete restoration of the structure of the lung tissue and the function of external respiration.

Community-acquired pneumonia caused by other infectious agents has its own clinical characteristics.

Mycoplasma pneumonia is caused by an “atypical” intracellular pathogen, devoid of a cell membrane and approaching the size of viruses. It most often affects young people and is characterized by epidemic outbreaks in organized groups, reaching a frequency of 30%. It usually begins with a picture of an acute respiratory infection, then a painful, often paroxysmal cough appears with scanty mucopurulent sputum, and a disturbing feeling of “soreness” in the throat. Physical data are scarce due to the predominantly interstitial localization of inflammation. Against the background of hard breathing, a few dry rales are heard in the lower parts of the lungs. It is possible that focal infiltration of the lung tissue may occur with the appearance of dullness of percussion sound and moist fine rales over the affected area. Characteristic is the dissociation of clinical manifestations of the disease (severe intoxication, prolonged low-grade fever, heavy sweats), X-ray picture (only increased pulmonary pattern and interstitial changes) and laboratory data (absence of leukocytosis and neutrophilic shift). Extrapulmonary manifestations of mycoplasma infection are often detected - myalgia, arthralgia, myocarditis. The resolution of mycoplasma pneumonia is delayed, and the asthenic syndrome persists for a long time.

Rickettsial pneumonia (Q fever) has an acute onset, with a temperature of 39-40 o and repeated chills for 10-12 days. Severe intoxication, muscle pain, especially lumbar and calf pain, insomnia, and dyspeptic symptoms are observed. Worried about a cough with a small amount of sputum, chest pain. The cervical lymph nodes are often enlarged. Characterized by slight jaundice and hepatolienal syndrome. Physical data are scarce. Diagnosis is helped by a positive epidemiological history (contact with farm animals) and the complement fixation reaction with Qui-rickettsia antigens.

Legionella pneumonia(legionnaires' disease ) usually develops in epidemic individuals , staying in rooms with air conditioning, in the water systems of which favorable conditions are created for the life of the virulent gram-negative bacillus - Legionella. It is characterized by the fusion of foci of inflammation and high mortality of patients (15-30%). The clinical picture of the disease is characterized by prolonged fever (15 days or more), frequent extrapulmonary lesions, prolonged course, leukocytosis in combination with lymphopenia.

Ornithosis pneumonia caused by chlamydia psittacosis due to contact with infected birds. More often it occurs as interstitial pneumonia with poor physical data. The clinical picture is dominated by general toxic signs of infection - headache and muscle pain, fever, vomiting, sleep disturbances. Characterized by bradycardia, hypotension, dry tongue, flatulence, enlarged liver and spleen. The diagnosis is confirmed by an epidemiological history (contact with birds) and a skin allergy test.

Pneumonia due to respiratory viral infections develop under the influence of viral-bacterial associations. They are more often diagnosed during epidemics of viral infections. The main role of respiratory viruses is to damage the bronchial epithelium and suppress general and local immunity, which leads to the activation of opportunistic microorganisms and the penetration of infection (most often pneumococcus and Haemophilus influenzae) into the respiratory sections of the lungs. The diagnosis of viral-bacterial pneumonia is usually based on an assessment of the epidemiological conditions of the disease. Clinically, viral-bacterial pneumonia occurs as focal or focal-confluent with a noticeable reaction of the interstitial tissue of the lungs. With various viral infections, pneumonia has its own clinical characteristics. To detect and identify viruses, serological methods, enzyme-linked immunosorbent assay and polymerase chain reaction (PCR) are used.

Pneumonia due to influenza infection usually develop in the first three days from the onset of the disease and are characterized by severe intoxication and symptoms of hemorrhagic bronchitis. A two-wave fever is characteristic - the first wave reflects a viral infection, and the second - a bacterial infection.

Pneumonia due to adenovirus infection accompanied by symptoms typical of adenovirus infection - conjunctivitis, pharyngitis, enlarged peripheral lymph nodes.

Pneumonia due to respiratory syncytial virus infection is characterized by the development of bronchiolitis and obstructive bronchitis with intoxication and severe broncho-obstructive syndrome.

Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa in most cases are the causes of nosocomial pneumonia.

Staphylococcal pneumonia characterized by a severe course and rapid development of purulent destructive complications - lung abscesses, pleural empyema. Often develops after influenza with a decrease in general and local bronchopulmonary protective mechanisms. It begins acutely, with chills and high fever, cough with purulent sputum, shortness of breath, chest pain, which resembles lobar pneumonia. The severity of the condition does not always correspond to physical data. Characterized by a clear segmentation of the lesion involving several segments of the lungs and a tendency to rapid abscess formation with the formation of multiple thin-walled cavities. When abscesses open into the pleural cavity, pyopneumothorax occurs.

Friedlander's pneumonia Caused by Gram-negative endotoxin-producing Friedlander's bacillus or Klebsiella pneumoniae. It often affects people who abuse alcohol, the elderly, people with diabetes, and injection drug addicts. Men get sick 5-7 times more often. An acute onset with severe intoxication, an increase in body temperature to 38-39 o, the appearance of chest pain when breathing, and a painful cough resembles severe pneumococcal pneumonia. From the first day, profuse, viscous, bloody sputum appears with the smell of burnt meat. Due to the large amount of exudate clogging the lumen of the alveoli and bronchi, a small amount of wheezing is heard. The appearance of early multiple destruction of lung tissue (in the first two days) is convincing evidence in favor of pneumonia caused by Klebsiella. Frequent involvement of the upper lobe of the lung may cause an erroneous diagnosis of tuberculosis. Friedlander's pneumonia is characterized by a protracted course with the outcome in pneumofibrosis of the affected lobe.

Pneumonia caused by Pseudomonas aeruginosa stick usually develops in the postoperative period, in patients on mechanical ventilation (ventilator-associated pneumonia). It begins acutely with high fever with chills, severe intoxication, and respiratory failure. Physical examination reveals signs of focal lung damage. Pleural complications and abscess formation are typical. The disease is characterized by a particularly severe course and high mortality, reaching 50–70% in elderly weakened patients.

Laboratory and instrumental diagnosis of pneumonia:

General blood analysis reveals neutrophilic leukocytosis with a shift in the leukocyte formula to the left, an increase in ESR. The degree of these changes determines the prevalence and severity of the process: with lobar pneumonia, leukocytosis reaches 20-30 thousand with a shift of the leukocyte formula to the left to juvenile forms. Toxic granularity of neutrophils (++++), aneosinophilia are detected. With focal bacterial pneumonia, the changes are less pronounced - leukocytosis in the range of 10-12 thousand, a shift to the left up to 10% of stabs, toxic granularity of neutrophils (++). Viral pneumonia is characterized by leukopenia with a low ESR. With mycoplasma and psittacosis infections, a normal leukocyte count or leukopenia can be combined with a high ESR.

Blood chemistry reveals an increase in α 2 - globulins, sialic acids, seromucoids, and the appearance of C-reactive protein. In severe pneumonia, signs of blood hypercoagulation are revealed - the level of fibrinogen increases 2-3 times, the platelet count decreases. When the inflammatory process resolves, the fibrinolytic activity of the blood increases sharply.

Sputum analysis detects leukocytes, erythrocytes (with lobar, Friedlander, post-influenza pneumonia), elastic fibers (with abscess formation). During its bacteriological examination, the type of pathogen and its sensitivity to antibiotics are determined.

X-ray of the lungs is the most informative diagnostic method. With lobar pneumonia, an intense, uniform darkening is determined within a lobe or segment, which completely resolves under the influence of treatment within 2-3 weeks. Lobar lesions (usually the upper lobe) are characteristic of Friedlander pneumonia, and segmental lesions are characteristic of staphylococcal pneumonia. The last two variants of pneumonia are characterized by the rapid development of multiple destruction of lung tissue.

With focal pneumonia, foci of infiltration of various sizes and intensity are detected, most often in the lower parts of the lungs. With adequate treatment, pulmonary infiltrates resolve within 7-10 days. Viral, rickettsial and mycoplasma pneumonias are characterized by a severe pulmonary pattern due to the interstitial component of inflammation.

Spirography detects disturbances in the function of external respiration of a restrictive type, which is manifested by a decrease in minute volume of respiration (MVR), vital capacity (VC) and maximum pulmonary ventilation (MVL). In case of focal pneumonia that has developed against the background of chronic obstructive bronchitis, disturbances in the function of external respiration of the obstructive type are detected, as evidenced by a decrease in the forced expiratory volume in 1 second (FEV 1) and the Votchal-Tiffen test (FEV 1 / VC).

Serological blood tests help in the diagnosis of mycoplasma, rickettsial, legionellosis, ornithosis and viral pneumonia. The titer of antibodies to the pathogen is determined by the method of paired sera (an increase in titer of 4 times or more is reliable).

Sometimes, with severe or atypical pneumonia, it becomes necessary to use more complex examination methods, such as bronchoscopy with biopsy, computed tomography of the lungs, examination of pleural fluid, ultrasound of the heart and abdominal organs.

Summarizing the above data, we can determine “gold” diagnostic standard(A.G. Chuchalin, 2000) for early diagnosis of pneumonia already at the outpatient stage:

1. Acute onset of the disease with fever and intoxication.

2. The appearance of a dry cough or with phlegm, chest pain.

3. Dullness of percussion sound and the appearance of auscultatory phenomena of pneumonia (crepitus, fine moist rales).

4. Leukocytosis or, less commonly, leukopenia with a shift to the left.

5. Detection of infiltrate in the lung during x-ray examination.

By severity all pneumonias are conditionally divided into three groups:

1. Pneumonia with a light current, not requiring hospitalization. This group accounts for up to 80% of all pneumonias. Patients can be treated on an outpatient basis under the supervision of a doctor or in a day hospital at a clinic. Mortality in this group does not exceed 1-5%.

2. Moderate pneumonia, requiring hospitalization patients to the hospital. This group includes about 20% of all pneumonias, which usually occur against the background of chronic diseases of internal organs and have pronounced clinical symptoms. The mortality rate of hospitalized patients reaches 12%.

Direct indications for hospitalization for pneumonia are: age of patients over 70 years old, obstructive respiratory diseases, chronic diseases of internal organs and the nervous system, diabetes mellitus, pleural pain, disturbances of consciousness, tachycardia (more than 125 beats per minute), tachypnea (more than 30 breaths per minute), cyanosis, arterial hypotension (90/60 mm Hg and below), the inability to provide effective care on an outpatient basis or the lack of effect of treatment within three days, the appearance of complications of the disease, such as exudative pleurisy, abscess formation, infectious metastases.

3. Severe pneumonia, requiring hospitalization sick in intensive care and resuscitation departments. The mortality risk in this group is high - about 40 - 50%.

The criteria for intensive care are: acute respiratory failure (hypoxemia, signs of respiratory muscle fatigue, need for artificial ventilation), unstable hemodynamics (shock, need for vasopressors for more than 4 hours, urine output less than 20 ml/hour), acute renal failure requiring hemodialysis, disseminated intravascular coagulation syndrome, meningitis, coma.

Differential diagnosis of pneumonia held:

With infarction pneumonia with thromboembolism of the pulmonary artery (PE) mainly of its small and medium branches. Characterized by a sudden, often paroxysmal appearance of shortness of breath and dry cough with sharp chest pain, and after 2-3 days - an increase in body temperature and the appearance of hemoptysis in the absence of severe intoxication. Physical data are scarce. Clinical and ECG signs of acute overload of the right heart are revealed (P-pulmonale, T wave inversion in the right precordial leads, right bundle branch block). An important role for diagnosis is played by the x-ray picture - bulging of the pulmonary cone and regional disappearance of the pulmonary pattern, and then the appearance of darkening of the lung tissue in the shape of a triangle, pear or rocket with the apex directed towards the root. A general blood test is nonspecific. The diagnosis is helped by identifying risk factors for pulmonary embolism: peripheral phlebothrombosis, prolonged immobilization, abdominal surgery, bone fractures, intravenous drug use, etc.

With peripheral and central lung cancer. The peripheral form of cancer is characterized by focal darkening of the lung tissue of a polydiagonal shape, and the central form is characterized by the development of atelectasis of the lung lobe due to obstruction of the lobar bronchus by a growing tumor. In areas of the lung tissue that are hypoventilated due to the neoplasm, secondary pneumonia often develops. In differential diagnosis, it is necessary to take into account the presence of risk factors for cancer in the patient (long-term smoking, family history, unfavorable environmental and professional conditions), the early appearance of a dry cough that worsens in a horizontal position, hemoptysis, chest pain, and weight loss. To clarify the diagnosis, fibrobronchoscopy with biopsy and computed tomography of the lungs are used.

With infiltrative tuberculosis lungs, which is characterized by a gradual onset, absence of severe fever and intoxication, paucity of physical data, lack of effect from conventional antibacterial therapy, and a certain social status of the patient. In the decay stage, hemoptysis appears, and sometimes pulmonary hemorrhage. A general blood test reveals neutrophilic leukocytosis with a shift to the left, lymphopenia, and monocytosis. X-ray reveals large-focal inhomogeneous infiltration of the lung tissue, usually in the poorly ventilated upper lobes, with a “path” to the root (due to lymphangitis) and foci of screening in the parts of the lung adjacent to the infiltrate. Calcifications are often detected in the affected area or roots of the lungs. VK can be detected in sputum. Caseous specific pneumonia clinically resembles lobar pneumonia, but the sputum quickly becomes greenish-purulent, hectic fever, and night sweats are noted. Early signs of decay of the lung tissue appear with the release of VK in the sputum. Positive tuberculin tests help diagnose tuberculosis.

With exudative pleurisy. In the lower parts of the affected side of the chest, weakened vocal tremor, percussion dullness with an oblique upper border along the Demoiseau line and the absence of respiratory sounds are detected. The mediastinal organs shift to the healthy side. X-ray examination reveals a homogeneous darkening with a characteristic oblique upper border. The results of pleural puncture are of decisive importance in diagnosis.

Complications of pneumonia (pulmonary and extrapulmonary):

1. Acute respiratory failure.

2. Acute respiratory distress syndrome– non-cardiogenic pulmonary edema associated with increased permeability of the alveolo-capillary membrane under the influence of toxins of infectious microorganisms and endogenous inflammatory mediators.

3.Parapneumonic pleural effusion and much less often–empyema of the pleura.

4. Lung abscess.

5 . Bronchospastic syndrome.

6. Infectious-toxic shock with symptoms of acute vascular, left ventricular and renal failure, ulceration of the mucous membrane of the digestive tract and bleeding, the development of disseminated intravascular coagulation.

7. Acute cor pulmonale with total pneumonia.

8. Infectious-allergic myocarditis.

9. Intoxication psychoses.

10.Toxic hepatitis.

It is also possible to develop infective endocarditis, pericarditis, meningitis, and sepsis against the background of pneumonia.

Treatment for patients with pneumonia should be early, rational and comprehensive, affecting the infection, various parts of pathogenesis and individual manifestations of the disease (etiotropic, pathogenetic and symptomatic).

Therapeutic measures include a therapeutic regimen and a balanced diet rich in proteins and vitamins, drug therapy and physiotherapy.

Antibacterial therapy according to the Russian therapeutic protocol, it is prescribed taking into account the epidemiological characteristics of pneumonia. At the first stage of treatment, before the etiology of pneumonia is clarified, the choice of antibacterial drugs is based on an empirical approach, since a delay in antibacterial therapy for several hours leads to the development of complications and increased mortality.

I. For community-acquired pneumonia Taking into account the most likely etiology of the disease, the drugs of choice are aminopenicillins, including those “protected” by clavulonic acid, modern macrolides and cephalosporins of II–III generations. The method of administration and dose of drugs depend on the severity of pneumonia.

For mild pneumonia that do not require hospitalization are prescribed oral monotherapy amoxicillin 0.5–1.0 g 3 times a day or modern macrolides – clarithromycin 0.25 – 0.5 g 2 times a day, azithromycin 0.5–1 g 1 time per day for 3 days, roxithromycin 0.15 g 2 times a day. It should be noted that azithromycin ( sumamed) is the only oral antibiotic that is taken once a day for only three days for pneumonia. The average treatment time with other antibiotics is 7-10 days.

In outpatients with risk factors for the emergence of antibiotic-resistant strains of pneumococci, gram-negative bacteria and atypical microorganisms as pneumonia pathogens (age over 65 years, β-lactam therapy within the last three months, alcoholism, immunodeficiency states, therapy with systemic corticosteroids), combination oral therapy is prescribed. The following schemes are most effective:

1) amoxicillin/clavulonate ( amoxiclav, augmentin) 0.625 g 3 times a day in combination with macrolides or doxycycline ( vibramycin) 0.1 g 2 times a day;

2) second generation cephalosporin cefuroxime ( zinacef, ketocef) 0.5 g 2 times a day in combination with macrolides or doxycycline;

3) possible monotherapy with “respiratory” fluoroquinolones – levofloxacin (tavanik) 0.5 g 1 time per day or moxifloxacin (avelox) 0.4 g 1 time per day.

In some cases, if parenteral therapy is necessary, a third generation cephalosporin is prescribed ceftriaxone (lendacin), which has high activity against pneumococcus and a long half-life, due to which it is administered intramuscularly once a day, 1-2 g.

For pneumonia with atypical intracellular pathogens (mycoplasma, chlamydia, legionella), the drugs of choice are macrolides and doxycycline, which are used for 14-21 days.

Antibacterial therapy severe community-acquired pneumonia includes parenteral use of the following drugs:

1) III-IV generation cephalosporins ( cefotaxime 1–2 g 3 times a day or ceftriaxone 1–2g 1 time per day or cefepime 1 g 2 times a day) in combination with macrolides ( clarithromycin intravenously 0.5 g 1 time per day);

2) amoxicycline/clavunate 1.2 g intravenously 3 times a day in combination with macrolides;

3) monotherapy with modern fluoroquinolones – levofloxacin (tavanik) 0.5 g intravenously 1 time per day, moxifloxacin (avelox) 0.4 1 time per day) and less effective ciprofloxacin (tsiprolet, tsiprobay) 0.2 - 0.4 g intravenously 2 times a day.

The use of sulfamethoxazole/trimethoprim is not recommended ( biseptol) and other sulfonamide drugs due to the high resistance of pneumonia pathogens to it (up to 52%) and frequent allergic skin reactions. It is a mistake to prescribe aminoglycosides and lincomycin for community-acquired pneumonia, since they have very low activity against pneumococci, Haemophilus influenzae, intracellular pathogens and other most common etiological factors of community-acquired pneumonia. To cephalosporins of the first generation ( cefazolin), the spectrum of action of which differs little from benzylpenicillin, many strains of pneumonia pathogens are resistant, which determines the low activity of the drug.

Old antibacterial drugs - ampicillin and combination drug ampiox or oxapm(ampicillin + oxacillin) are slightly toxic and are sometimes used in clinical practice, but are inactive against many gram-positive and gram-negative microorganisms and inactive against intracellular pathogens. When using “protected” ampicillin ( ampicillin/sulbactam) the spectrum of action of the drug is expanding in relation to penicillin-resistant strains of microorganisms. ABOUT xacillin in the maximum permissible dose can be used in the treatment of staphylococcal pneumonia.

Against the background of adequate antibacterial therapy, after 2-3 days the body temperature decreases and intoxication decreases; if there is no effect, the drugs are replaced. The average duration of antibacterial treatment is 7-10 days.

The main criterion for discontinuing an antibiotic is regression of clinical symptoms with possible persistence of individual laboratory or radiological changes.

II. For nosocomial pneumonia Taking into account the most typical pathogens, parenteral antibacterial drugs with high activity against gram-negative microflora, staphylococcus and anaerobic bacteria are prescribed - amoxicillin / clavulanate, cephalosporins of III-IV generations, modern aminoglycosides, “respiratory” fluoroquinolones, carbapenems, metronidazole. Usually a combination of two, or less often three, antibacterial agents is used:

1) amoxicycline/clavunate ( amoxiclav 1.2 g intravenously 3 times a day) + aminoglycosides ( gentamicin intramuscularly 80 mg 3 times a day or amikacin 0.5 g 2 – 3 times a day);

2) cephalosporins of III-IV generations ( cefotaxime, ceftriaxone. klaforan, fortum)+ aminoglycosides;

3) “respiratory” fluoroquinolones + aminoglycosides;

4) “protected” antipseudomonas ureidopenicillins (azlocillin)+ aminoglycosides.

If there is no effect, monotherapy with carbapenems is indicated. Their combination with aminoglycosides is possible.

For possible anaerobic infection, a combination of cephalosporins with macrolides or metronidazole or “respiratory” fluoroquinolones with aminoglycosides is indicated.

In case of particularly severe Pseudomonas aeruginosa infection, the likelihood of which is high in pneumonia that has developed in patients on mechanical ventilation, antibiotics with high anti-Pseudomonas aeruginosa activity are prescribed - ceftazidime (fortum), azlocillin, carbapinems in combination with fluoroquinolones or aminoglycosides.

For staphylococcal pneumonia, treatment regimens include clindamycin and vancomycin.

It must be remembered that the wider the spectrum of action of an antibiotic, the more side effects it has. The prescription of broad-spectrum antibacterial drugs and reserve drugs must be strictly justified.

III. Pneumonia due to immunodeficiency conditions are treated with broad-spectrum antibiotics, antimycotic and antiviral drugs against the background of immunoreplacement or immunomodulatory therapy. The antifungal drug of choice is fluconazole (mycocyst mycoflucan) 0.1–0.2 g per day

III. Aspiration pneumonia, usually associated with anaerobic and gram-negative microflora, require the administration of III-IV generation cephalosporins and aminoglycosides in combination with metronidazole ( metrogil 0.5 g intravenously drip 2-3 times a day) or clindamycin ( dalacin 0.3 - 0.6 g intravenously 2 times a day). Carbapenems are highly active ( tienam intravenously or intramuscularly 0.5 - 1 g every 8 hours).

Pathogenetic therapy. In order to restore bronchial patency, bronchodilators are used ( aminophylline, teopec, broncholitin) and mucolytics ( bromhexine, ambroxol, ambrobene, mucaltin, acetylcysteine). For bronchospastic syndrome, β 2 - adrenergic agonists are prescribed ( Berotek), M-anticholinergic atrovent, combination drug berodual.

With the development of infectious-toxic shock or severe obstructive syndrome, corticosteroids are used (60 - 90 mg prednisone intravenously), refortan(HES 10%) and other plasma substitutes.

For the purpose of detoxification, saline solutions (up to 1–2 liters per day), 5% glucose solution (0.4–0.8 liters per day), rheopolyglucin (400 ml), 20% albumin (100 ml) are administered intravenously.

To improve microcirculation, heparin or low molecular weight heparins are prescribed ( fraxiparine, clexane), disaggregants ( chimes, trental, acetylsalicylic acid).

Weakened patients are given immunoreplacement therapy - donor immunoglobulin, normal intramuscularly 1.5 - 3.0 ml daily during the first 5-7 days of illness or immunovenin intravenously, for staphylococcal pneumonia - anti-staphylococcal immunoglobulin or hyperimmune plasma. In severe cases, intravenous infusions of native or fresh frozen plasma (150–200 ml) are possible. for immunoglobulin 5.0 ml.

For indolent pneumonia, immunomodulators are used ( Thymalin, bronchomunal, immunal). Stimulates leukopoiesis during leukopenia methyluracil.

Symptomatic therapy. For a non-productive dry cough, antitussives are prescribed in the first days of illness. (codelac, libexin, broncholitin), if there is difficulty in sputum discharge, expectorants (infusion of thermopsis herb, marshmallow root, licorice).

For fever and pain, antipyretics and analgesics are prescribed ( acetylsalicylic acid, paracetamol, diclofenac (ortofen, voltaren).

For elderly patients and for concomitant diseases of the cardiovascular system, injections of camphor or sulfocamphocaine are sometimes used, and for heart failure - cardiac glycosides (korglukon).

For hemoptysis, add to treatment ascorutin or dicynone. In case of respiratory failure, oxygen therapy is performed.

Physiotherapeutic treatment is prescribed when the temperature is less than 38 o, there is no hemoptysis, heart failure and severe intoxication. In the acute period of pneumonia, UHF therapy in a low-thermal dose is prescribed to improve microcirculation and reduce inflammatory exudation. The restoration of bronchial patency is facilitated by inhalation with alkalizing, mucolytic and bronchodilator agents or with an antibacterial drug - bioparox. Resorption of pneumonia is facilitated by inductothermy, microwave (deci- and centimeter-wave) therapy, electrophoresis with potassium iodide, calcium chloride, hydrocortisone, etc. Along with the effect on the source of inflammation, decimeter therapy of the adrenal glands is used to activate their glucocorticoid function. To hyposensitize the body, ultraviolet irradiation of the chest with separate fields is performed. Resolution of pneumonia is facilitated by chest massage and early physical therapy, primarily breathing exercises.

To accelerate the resorption of inflammatory changes, thermal procedures are also used: paraffin and ozokerite applications on the chest, irradiation with a Sollux lamp.

After recovery, patients with pneumonia move to the dispensary and polyclinic stage of rehabilitation, which should last at least 6 months. In case of residual clinical and radiological phenomena of the disease or persistent asthenia of the body, sanatorium-resort treatment is recommended both in local sanatoriums (Yumatovo, Green Grove) and in climatic resorts (Anapa, Gelendzhik, Kislovodsk, Southern Coast of Crimea, etc.).

Prevention. It consists of general sanitary and hygienic measures and personal preventive measures (hardening the body, physical education, sanitizing foci of infection, giving up bad habits, etc.). Prevention and timely treatment of acute respiratory diseases, including annual influenza vaccination, are of great importance.

– an acute inflammatory process in the parenchyma and interstitium of the lungs, in the etiology of which the infectious factor plays a decisive role. Acute pneumonia is accompanied by chills, persistent fever, cough with mucopurulent sputum, malaise, headache, shortness of breath and tachycardia. Pneumonia is diagnosed by clinical and radiological picture, auscultatory data, and laboratory test results. Therapy of acute pneumonia is aimed at all stages of etiopathogenesis and includes the prescription of antibiotics, mucolytics, bronchodilators, expectorants and antihistamines, infusion therapy, oxygen therapy, and physical treatment.

General information

Acute pneumonia can occur after exposure to the respiratory tract of light chemical and physical agents (concentrated acids and alkalis, temperature, ionizing radiation), usually in combination with secondary bacterial infection with autogenous microflora from the pharynx and upper respiratory tract. Due to the long-term use of antibiotics in the development of acute pneumonia, the role of opportunistic microflora has become more significant. There are cases of allergic (eosinophilic) acute pneumonia caused by helminthiases and medications. Acute pneumonia can occur uncomplicated and with complications; mild, moderate or severe; with the absence or development of functional disorders.

Various factors that reduce the resistance of the macroorganism predispose to the occurrence of acute pneumonia: prolonged intoxication (including alcohol and nicotine), hypothermia and high humidity, concomitant chronic infections, respiratory allergies, nervous shock, infancy and old age, prolonged bed rest. The penetration of infection into the lungs is facilitated by impaired patency and drainage function of the bronchi, inhibition of the cough reflex, insufficiency of mucociliary clearance, defects in pulmonary surfactant, decreased local immunity, including phagocytic activity, levels of lysozyme and interferon.

In acute pneumonia, inflammation affects the alveoli, interalveolar septa and vascular bed of the lungs. Moreover, in different parts of the affected lung, different phases can be simultaneously observed - flushing, red and gray “hepatization”, resolution. Morphological changes in acute pneumonia vary depending on the type of pathogen. Some microorganisms (staphylococcus, Pseudomonas aeruginosa, streptococcus) secrete exotoxins that cause deep damage to the lung tissue with the appearance of multiple small, sometimes merging foci of abscess pneumonia. In acute Friedlander pneumonia, extensive infarct-like necrosis occurs in the lungs. Interstitial inflammation dominates in pneumonia of pneumocystis and cytomegalovirus origin.

Classification

The classification of acute pneumonia is based on differences in etiology, pathogenesis, anatomical and clinical manifestations. Based on clinical and morphological properties, parenchymal and interstitial pneumonia are distinguished; lobar (lobar or pleuropneumonia) and focal (bronchopneumonia); according to the prevalence of inflammation - small-focal, focal (within the boundaries of several lobules), large-focal and confluent (covering most of the lobe).

Acute pneumonia occurs primarily or secondarily as complications of infectious diseases (ARVI, influenza, measles), chronic pathology of the respiratory system (bronchitis, tumors), cardiovascular system, kidneys, blood, systemic diseases, metabolic disorders. Taking into account epidemic criteria, community-acquired and hospital-acquired forms of acute pneumonia are distinguished.

According to the causative factor, infectious (bacterial, viral, mycoplasma, rickettsial, fungal, mixed), allergic, congestive, post-traumatic acute pneumonia, as well as pneumonia caused by chemical or physical irritants are distinguished. Aspiration pneumonia can develop when foreign bodies (food particles, vomit) are inhaled; heart attack-pneumonia - due to thromboembolism of the pulmonary vasculature.

Symptoms of acute pneumonia

The clinical picture of acute pneumonia may differ in the level of severity of general and bronchopulmonary manifestations, which is largely determined by the pathogen, the patient’s health status, and the course of concomitant pathology. Most forms of acute pneumonia are characterized by the constant presence of general disorders: chills, a sharp rise in temperature and persistent fever, general weakness, sweating, headache, tachycardia, agitation or weakness, sleep disturbance. Cough in acute pneumonia is of a different nature, accompanied by the release of mucopurulent sputum, rapid breathing (up to 25-30 per minute), pain in the chest or under the shoulder blade. Focal pneumonia (bronchopneumonia) in most cases begins against the background of bronchitis or acute catarrh of the upper respiratory tract. Febrile fever of the wrong type is typical; elderly and weakened individuals may have a normal or subfebrile temperature.

Influenza pneumonia usually develops acutely in the first to third days of influenza illness. As a rule, the course is milder than the bacterial one, but sometimes it can acquire a severe course with significant intoxication and high fever, persistent cough, and rapid development of pulmonary edema. Late pneumonia, which occurs during recovery from influenza, is caused by bacterial microflora.

Culture of sputum, blood, and urine makes it possible to establish the pathogen and its antibiotic sensitivity. Changes in respiratory function of the restrictive type (decrease in VC, MVL, increase in MOP) are characteristic of extensive confluent focal and lobar pneumonia. Bronchoscopy and bronchography are performed in cases of prolonged acute pneumonia, which makes it possible to detect the presence of bronchiectasis, decay cavities in the lung tissue. As part of the diagnosis, bronchitis, lung cancer, tuberculosis, pulmonary infarction, and atelectatic bronchiectasis are excluded.

Treatment of acute pneumonia

Patients with acute pneumonia require early treatment, usually in a hospital setting. During the febrile period, bed rest, drinking plenty of fluids, easily digestible high-calorie foods, and vitamins are recommended. In acute pneumonia, etiotropic therapy with antibacterial drugs prescribed based on clinical and radiological characteristics is effective. Semi-synthetic penicillins (ampicillin, amoxicillin), aminoglycosides (gentamicin), cephalosporins (ceftriaxone), macrolides (erythromycin, azithromycin), tetracyclines are used, with rifampicin and lincomycin as reserve drugs. In the acute phase and in severe cases, 2-3 antibiotics or a combination of an antibiotic with metronidazole or sulfonamides can be prescribed. The intensity of the course of antibiotic therapy depends on the severity and extent of lung damage.

Measures to prevent acute pneumonia include giving up bad habits, playing sports and hardening, good nutrition, sanitizing chronic foci of infection, vaccination against influenza, and preventing stress. Those who have recovered from acute pneumonia are monitored by a pulmonologist for six months.