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Acute pneumonia.

Acute pneumonia is a group concept used to refer to acute polyetiological infectious inflammatory lung diseases. Acute pneumonia refers to polyetiological diseases that have particular pathogenesis and a common clinical and morphological manifestations. The main morphological manifestation of acute pneumonia is the development of acute inflammation in the bronchopulmonary system involving the respiratory departments of the lungs.

In cases where acute inflammation extends mainly to the alveolar wall with secondary accumulation of exudate in the lumens of the alveoli, they speak of interstitial pneumonia and denote it by the term acute pneumonitis.

Epidemiology of acute pneumonia. Acute pneumonia is one of the most common diseases with a relatively high mortality rate among newborns and the elderly. In Russia, the incidence of acute pneumonia has changed little over the past 25 years, despite the use of antibiotic therapy.

With pneumonia, a relatively high mortality rate is observed, respectively, 1.2% and 0.7%. In the United States, acute pneumonia along with influenza is the third leading cause of death and is found in 3% of deaths.

Currently, all acute pneumonia is divided into contagious and nosocomial. The highest morbidity is registered among hospital patients (8.5% hospitalized), especially in intensive care units (13%) and tumor chemotherapy (30%).

Nosocomial, or nosocomial, acute pneumonia is defined as pneumonia that developed no earlier than 48 hours after hospitalization of the patient. They are divided into two groups: arising in the first 4 days of hospital stay, and also after more than 4 days. The development of nosocomial pneumonia can be associated mainly with two factors - problems in the ventilation system of the hospital, as well as with the particular etiology and altered reactivity of people suffering from other diseases and often receiving immunosuppressive and cytostatic therapy. In acute nosocomial pneumonia, as a rule, we are talking about activation of autoflora or gram-negative aerobic bacteria obtained by the patient through medical personnel. Often, mixed flora is found.

Etiology. The main etiological factor of pneumonia - Streptococcus Pneumoniae - is found in more than 90% of cases of diseases. All 82 serological types of pneumococcus can cause acute pneumonia. Among adult patients, 70% of cases of diseases are associated with types 1,3,4,5,7,8,12,14 and 19. In children, pneumococci of types 1,6,14,16 are more often found. Pneumococci of the 1,2,5,7,12,14th type are highly virulent and can affect completely healthy people. Types 4,6,10,18,19,22,23 are less virulent and penetrate, as a rule, into previously changed tissues, therefore they are more often detected in acute pneumonia in debilitated patients and can be considered opportunistic infections. Pneumonia caused by type 3 pneumococcus has a poor prognosis.

It should also be noted that pneumococci can cause both croupous and bronchopneumonia.

Other bacteria can also cause pneumonia (Klebsiella, Pseudomonas aeruginosa, Pfeiffer, Streptococcus, Staphylococcus, Escherichia coli, Proteus, Haemophilus influenzae), Mycoplasma, viruses, as well as mixed flora.

Among the risk factors for acute pneumonia are infections of the upper respiratory tract (primarily viral), obstruction of the bronchial tree, immunodeficiencies, alcohol, smoking, inhalation of toxic substances and dust, trauma, injuries, impaired pulmonary hemodynamics, postoperative period, massive infusion therapy, old age, malignant tumors, hypothermia, stress.

Pathogenesis. The mechanisms of pneumonia are different. There are 4 main routes of entry of microorganisms into the lungs: airborne droplets with inhaled air, aspiration from the nasopharynx and oropharynx, the hematogenous pathway from distant foci of infection, and the contagious pathway from a neighboring infected site. With the development of acute pneumonia, the most important are the airborne and aspiration routes of infection, which is combined with damage to the pulmonary defense barrier systems.

Viral particles, as a rule, are able to penetrate into the respiratory parts of the lung, damage first order pneumocytes and the alveolar wall, leading to the development of interstitial inflammation with characteristic mononuclear infiltrate and cellular immunity reactions. On the contrary, pyogenic bacteria, damaging the pulmonary parenchyma and having a chemotactic effect on leukocytes, lead to exudative inflammation with accumulation of exudate in the cavities of the alveoli, alveolar passages, bronchioles.

Classification of acute pneumonia. In Russian pulmonology, the classification of E.V. Gembitskaya (1983) is used, based on 7 basic principles: etiological, pathogenetic, clinical and morphological, nosological, prevalence of the process, severity and nature of the course.

Knowledge of the etiology of acute pneumonia is necessary to develop the right therapeutic tactics and prescribe effective antibacterial drugs. Therefore, the diagnosis of each case of acute pneumonia begins with establishing the cause.

According to the pathogenesis of pneumonia, they are divided into primary and secondary. Acute pneumonia is considered primary if a person does not have any pulmonary pathology and diseases of other organs and systems that can be complicated by pneumonia and contribute to its occurrence. Vivid examples of primary pneumonia are croupous pneumonia, mycoplasma pneumonia, and the disease of legionnaires.

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

Among secondary pneumonias, aspiration, hypostatic, and postoperative pneumonias occupy a large proportion. All of them develop due to the activation of autoinfection. With aspiration pneumonia in the first stage of development, damage to the pulmonary parenchyma with acid from the gastric contents is important. Hypostatic and postoperative pneumonia develops against the background of mucociliary clearance in the bronchial system and circulatory disorders. In accordance with the 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 (croupous), bronchopneumonia (focal) and acute interstitial (acute alveolitis). Lobar, croupous pneumonia is a nosological form, refers to contagious infectious and allergic diseases. In the vast majority of cases, bronchopneumonia develops as a complication of another disease.

However, there are special etiological variants of bronchopneumonia, which can be considered as independent diseases (for example, the disease of legionnaires), as well as bronchopneumonia of newborns and the elderly.

Acute interstitial pneumonia, or pneumonitis, occurs with certain pathogens - viruses, ornithosis, mycoplasma, rickettsia, chlamydia and pneumocystis. In the literature, such lung diseases are also denoted by the term "atypical pneumonia", which emphasizes that these acute infectious lung diseases differ from pneumonia not only in the clinic, but also require other treatment methods. They can be of a secondary nature (pneumocystic pneumonia) or be an independent nosological form.

In terms of prevalence, acute pneumonia can be one-and two-sided, and in the size of foci, comparable with those or other pulmonary structures, acinar, miliary (the size of a millet grain), segmental, polysegmental, focal-drain.
If the foci are found within the lobe, then they talk about focal pneumonia with damage to the lobe of the lung, and if the foci spread throughout the lung, then about total lobar pneumonia.

By the nature of the course of pneumonia can be: severe, moderate, light; and in duration - acute and protracted.

In the clinical literature of past years, the so-called atypical pneumonias, which are represented, in fact, by true interstitial pneumonias, were distinguished by the clinical course.

Lobar pneumonia (croupous pneumonia). Lobar, or croupous, pneumonia is an acute infectious and allergic inflammatory disease of the lungs. It has several synonyms: lobar (lobar), since one or more lung lobes is affected; pleuropneumonia, in connection with the involvement of the visceral pleura of the affected lobe and the development of pleurisy; fibrinous, croupous, which reflects the nature of exudative inflammation in the lungs.

It is caused by pneumococci of the 1st, 2nd, 3rd types, less often Klebsiella. The fact that this is a real infectious disease is confirmed by the facts of infection with lobar pneumonia described in the literature, which requires the use of all precautions at home and in the hospital to prevent its spread. The literature describes nosocomial outbreaks of croupous pneumonia.

Infection occurs, as a rule, from a patient or carrier. People aged about 30 and older than 50 years old who do not have immunity to these virulent strains of pneumococcus become sick. The route of infection is airborne. The spread of bacteria is favored by intoxication, cooling, anesthesia, inhalation of toxic poisons and dusts. Mortality is about 3%, despite antibiotic therapy.

The pathogenesis of croupous pneumonia is explained by the development of an immediate type hypersensitivity reaction (type III hypersensitivity reaction with an immunocomplex mechanism) on the territory of the respiratory departments of the lung, including alveoli and alveolar passages. There are two points of view about the early stages of the pathogenesis of croupous pneumonia. According to the first, pneumococci enter the upper respiratory tract and cause sensitization of the macroorganism. Under the action of resolving factors (hypothermia, etc.), the pathogen is aspirated into the alveoli and a hyperergic reaction with the development of croupous pneumonia sets in. According to the second point of view, the pathogen from the nasopharynx penetrates into the pulmonary parenchyma, organs of the reticuloendothelial system, where immune reactions are tied, and then into the bloodstream. The stage of bacteremia comes. When pneumococci re-enter with blood in the lungs, they interact with antibodies, complement. Immunocomplex damage to the microvasculature occurs with a characteristic exudative tissue reaction.

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

The morphogenesis of croupous pneumonia in the classical version consists of four stages: flushing (inflammatory edema), red hepatitis, gray hepatization and resolution.

The stage of the tide lasts for a day from the onset of the disease and is characterized by a sharp plethora of alveolar capillaries, interstitial edema and the accumulation of fluid exudate, resembling edematous fluid, in the alveolar lumens. The exudate is formed extremely quickly and along the alveolar passages and pores of Kona spreads to the territory of a whole share. The exudate contains a large number of microbes that actively proliferate here, as well as single alveolar macrophages and polymorphonuclear leukocytes. The morphological picture resembles that of pulmonary edema. Therefore, methods to detect pneumococcus (crops, smears) can be of great help in diagnosing this stage of pneumonia. At the same time, edema and inflammatory changes in the pleura occur, which in the clinic is manifested by acute pains in the side on the side of the affected lung lobe.

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

The stage of red hepatization develops on the 2nd day of the disease, when a large number of red blood cells appears in the exudate, single polymorphonuclear leukocytes, macrophages, fibrin falls out. The macroscopically affected lobe is airless, dense, red, resembles liver tissue, which is the name of this stage of the disease. On the thickened pleura, fibrinous overlays are clearly visible.

Stage gray hepatization takes 4-6 days of illness. At this time, there was a decline in pulmonary capillaries, a concentration in the exudate of living and dead polymorphonuclear leukocytes, macrophages and fibrin. Granulocytes mainly carry out phagocytosis of opsonized pneumococci and fibrin lysis, and macrophages - necrotic detritus. Macroscopically affected proportion is increased in size, heavy, dense, airless, in section with a granular surface. The pleura is thickened, turbid with fibrinous overlays.

The resolution stage begins 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 by the lymphatic drainage of the lung and is separated with sputum. Fibrinous deposits on the pleura absorb. Morphological changes are usually somewhat delayed compared with the clinical manifestations of the disease and can be detected within a few weeks after clinical recovery.

Complications of croupous pneumonia are divided into pulmonary and extrapulmonary. Pulmonary complications include: lung carnification (from Latin - carno, meat) - the organization of exudate, which usually develops due to insufficiency of polymorphonuclear leukocyte and / or macrophage; the formation of an acute abscess or gangrene of the lung with excessive activity of a polymorphic nuclear leukocyte; empyema of pleura. Extrapulmonary complications are associated with the possibility of the spread of infection along the lymphogenous and circulatory pathways. It should be noted that bacteremia with croupous pneumonia is recorded in 30% of cases. With lymphogenous generalization, purulent mediastinitis and pericarditis occur, with hematogenous - metastatic abscesses in the brain, purulent meningitis, acute ulcerative and polypous-ulcerative endocarditis, more often tricuspid valve, purulent arthritis, peritonitis, etc.

Pathomorphism of croupous 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 croupous pneumonia occurs from acute pulmonary heart failure or purulent complications.

Lobar Friedlander’s pneumonia is relatively rare (0.5-0.4% of cases of pneumonia) and can be attributed to nosocomial infections, as in hospitals it makes up 8-9.8% of acute pneumonia. Infection occurs by aspiration of a microbe - Friedlander diplobacillus into the upper respiratory tract. Distributed among alcoholics and newborns. Men get sick 5-7 times more often than women, older - more often than young. It is localized, as a rule, in the upper right lobe, but it can also be multilobar. Unlike croupous pneumonia caused by pneumococcus, necrosis of the alveolar septa is characteristic with frequent formation of abscesses, foci of carnification and severe interstitial fibrosis in the outcome.

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