ACUTE PNEUMONIA Acute pneumonia is a group of acute infectious inflammatory diseases of the lungs, different in etiology, pathogenesis and morphological characteristics, with a predominant lesion of the respiratory sections and the presence of intraalveolar exudate. Most often caused by bacteria, mycoplasmas and viruses. According to clinical and morphological features, croupous (lobar) pneumonia, bronchopneumonia (focal) and interstitial pneumonia are distinguished.

croupous pneumonia There are the following synonyms that reflect the morphological features of lung lesions: lobar, fibrinous, pleuropneumonia. Croupous pneumonia is an infectious-allergic disease. It is an independent nosological form. Pathogen - pneumococci of the 1st, 2nd and 3rd types, rarely - Klebsiella (Fridlander's diplobacillus). In pathogenesis, an immediate-type hypersensitivity reaction is of great importance. Characteristic is the defeat of the alveoli of the entire lobe at the same time while maintaining the bronchi intact. Always accompanied by fibrinous pleurisy (pleuropneumonia).

Stages of croupous pneumonia. 2. Stage of red hepatization. 2nd day. Microscopic picture: alveoli are filled with exudate consisting of fibrin and erythrocytes. Macroscopic picture: the affected proportion is enlarged, dense (hepatization), red in color, fibrinous overlays on the pleura (fibrinous pleurisy).

Stages of croupous pneumonia. 3. Stage of gray hepatization. 4-6th day. Microscopic picture: the capillaries become empty, in the alveolar exudate - fibrin, leukocytes, macrophages, fibrinous overlays on the pleura. Macroscopic picture: the affected part is enlarged, dense, granular on the cut, homogeneous appearance, gray.

COMPLICATIONS OF PNEUMONIA 1. Pulmonary. A. Carnification (organization of exudate in the lumen of the alveoli). b. Lung abscess. V. Gangrene (wet). 2. Extrapulmonary. They occur with lymphogenous or hematogenous spread of the infection. They include purulent mediastinitis, pericarditis, peritonitis, purulent arthritis, acute ulcerative endocarditis (usually of the tricuspid valve), purulent meningitis, brain abscess.

COMPLICATIONS OF PNEUMONIA Pathomorphosis. It is manifested by the loss of one or another stage and abortive forms, a decrease in the frequency of complications. Causes of death. Mortality is about 3%. Death occurs from acute cardiopulmonary failure or purulent complications.

COMPLICATIONS OF PNEUMONIA Lobar Friedlander's pneumonia. It often occurs as a nosocomial (nosocomial) infection. Old people, newborns and patients with alcoholism get sick. Characterized by necrosis of the alveolar septa with frequent formation of abscesses, foci of carnification and severe interstitial fibrosis.

BRONCHOPNEUMONIA (FOCAL PNEUMONIA) Makes up the bulk of acute pneumonia. Polyetiological. The most common pathogens are bacteria: pneumococci, staphylococci, streptococci, Pseudomonas aeruginosa, etc. It can occur as a nosocomial infection in debilitated patients, usually caused by gram-negative microorganisms (Klebsiella, Pseudomonas aeruginosa and E. coli) and Staphylococcus aureus.

BRONCHOPNEUMONIA More often occurs as an autoinfection. Depending on the characteristics of the pathogenesis, autoinfectious bronchopneumonia can be aspiration, hypostatic, postoperative, and also developing against the background of immunodeficiency. More often it is a complication of other diseases. Bronchopneumonia in newborns and the elderly, as well as some etiological variants of bronchopneumonia (for example, legionella) can be considered as independent nosological forms.

BRONCHOPNEUMONIA Morphological manifestations. The bronchi are initially affected. Inflammation spreads to the alveoli from the wall of the bronchus in a descending way with endobronchitis or peribronchially with panbronchitis or destructive bronchiolitis. Exudate can be serous, purulent, hemorrhagic, mixed. According to the prevalence of the process, acinous, lobular, confluent lobular, segmental, miliary pneumonia are distinguished.

Features of some common bacterial bronchopneumonias a. Pneumococcal pneumonia. It is more common in elderly and debilitated patients, especially with cardiopulmonary pathology (hypostatic pneumonia). Often complicated by pleural empyema.

Staphylococcal pneumonia Staphylococcal pneumonia (Staphylococcus aureus). Usually occurs as a complication of respiratory viral infections (flu, etc.). It often develops in drug addicts with intravenous infection, as well as in debilitated elderly patients with chronic pulmonary diseases. Characteristically abscessed, the development of pleural empyema, often serves as a source of septicopyemia.

Pneumonia caused by Pseudomonas aeruginosa. Pneumonia caused by Pseudomonas aeruginosa. One of the most common nosocomial infections. Characterized by abscess formation and pleurisy. With hematogenous infection in the lungs (usually from extensive festering wounds), coagulative necrosis and a hemorrhagic component are characteristic. The prognosis is bad.

INTERSTITIAL PNEUMONIA Inflammation develops predominantly in the alveolar septa with secondary accumulation of exudate in the lumen of the alveoli. Synonyms: alveolitis, pneumonitis. The process may be diffuse or limited. It is caused by certain pathogens: viruses, fungi, mycoplasmas, chlamydia (psittacosis), rickettsia (Q-fever-pneumorickettsiosis), pneumocysts.

VIRAL PNEUMONIA a. Viral pneumonia. Most common in childhood. More often caused by influenza viruses, parainfluenza, respiratory syncytial virus, adenovirus (see "Airborne infections"). Characterized by hyperplasia of the alveolar epithelium with the formation of giant cells that differ in their appearance in different diseases, squamous metaplasia of the bronchiolar epithelium is possible. Often complicated by a secondary bacterial infection.

VIRAL PNEUMONIA Cytomegalovirus pneumonia (opportunistic infection) is the most common viral pneumonia in immunodeficiency states. It is characterized by predominantly mononuclear infiltration of the alveolar septa, hyperplasia of the alveolar epithelium, the appearance of large cells with characteristic intranuclear inclusions, serous fluid in the lumen of the alveoli

Mycoplasma pneumonia. Also known as SARS. One of the most common forms of non-bacterial pneumonia. It usually occurs in children and adolescents. The onset is more inconspicuous, erased than with bacterial pneumonia. It is characterized by an inflammatory lymphoplasmacytic infiltrate of the alveolar septa, hyperplasia of the alveolar epithelium, the presence of intraalveolar hyaline membranes, exudate in the lumen of the alveoli may be absent, but is often combined with changes characteristic of bronchopneumonia: the appearance of leukocytes in the lumen of the bronchioles and alveoli.

Pneumocystis pneumonia. Opportunistic infection, most characteristic of patients with HIV infection. It also occurs in other forms of immunodeficiency. It is caused by P. carinii, an opportunistic pathogen belonging to the simplest (some refer to it as a fungus). In persons with impaired cellular immunity, it may develop due to the previous presence of pneumocysts in the pulmonary foci of a latent infection or as a result of fresh infection.

Pneumocystis pneumonia. Desquamation of cells of the alveolar epithelium and filling of the alveoli with a foamy liquid, which contains pneumocysts, as well as plethora and lymphohistiocytic infiltration of the alveolar septa with their possible destruction are characteristic. Increasing shortness of breath against the background of mild physical and radiological signs is characteristic. It can occur as a mixed infection with the addition of other flora (fungi, cytomegalovirus, cocci, mycobacteria, etc.).

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PNEUMONIA

STRUCTURE OF THE HUMAN RESPIRATORY SYSTEM

PNEUMONIA is an acute infectious disease in which the alveoli are damaged, accompanied by exudation and infiltration of the parenchyma by inflammatory cells as a response to the introduction and proliferation of microorganisms into the normally sterile parts of the respiratory tract.

AVL CORNELIUS CELUS (I century BC) - the first mention of inflammation in the respiratory sections of the respiratory tract; WILLIS (1684) - described in detail the symptoms of acute fever, cough and difficulty breathing; LAENNEK (1781-1826) - described the auscultatory picture of pneumonia. ROKITANSKY (1804-1878) - identified 2 morphological variants of pneumonia - lobar and bronchopneumonia. RENTGEN (1845-1923) - discovered X-rays and investigated their properties.

PREVALENCE 3-15 PER 1000 POPULATION MORTALITY from community-acquired pneumonia - 5%; from nosocomial pneumonia - 20%; in the elderly - 30% ERRORS IN DIAGNOSIS 20% PNEUMONIA DIAGNOSIS DURING THE FIRST 3 DAYS IS MADE IN 35% OF ILLNESSES

ETIOLOGY Mycoplasma pneumoniae Streptococcus pneumoniae Haemophilus influenza Chlamydia pneumoniae Legionella pneumoniae Staphilococcus aureus

Community-acquired PNEUMONIA Streptococcus pneumoniae (30-90%); Mycoplasma pneumoniae (up to 30% under 45 and up to 9% over 45); Haemophilus influenza (5-18%); Chlamydia pneumoniae (2-8%); Legionella pneumoniae (2-10%); Staphylococcus aureus (less than 5%); Gram-negative microorganisms (rarely); Influenza virus (during the epidemic); 20-30% of the etiology of pneumonia is not established ETIOLOGICAL CLASSIFICATION. 1

ETIOLOGY Pseudomonas aeruginosa Klebsiella pneumoniae Enterobacter spp. Staphylococcus aureus

HOSPITAL HOSPITAL PNEUMONIA Develops 48 or more hours after the patient's admission to the hospital Gram-negative aerobic microorganisms, especially: Pseudomonas aeruginosa; Klebsiella pneumoniae; Enterobacter spp. Gram-positive: Staphilococcus aureus ETIOLOGICAL CLASSIFICATION. 2

PNEUMONIA IN PERSONS WITH IMMUNODEFICIENCY Cytomegalovirus; pathogenic fungi; HIV-associated pneumonia: Pneumocystis carinii; Mycobacterium tuberculosis; Streptococcus pneumoniae; Haemophilus influenzae. ETIOLOGICAL CLASSIFICATION. 3

PATHOGENESIS Etiological factors Release of endo- and exotoxins Colonization of epithelial cells Clinical manifestations of the disease Inflammation of the alveoli and bronchioles Invasion and intracellular persistence of the pathogen Adhesion to epithelial cells Activation of opportunistic microflora Violation of the leg. blood circulation Decrease in general nonspec. protection Suppression of local protective mechanisms Facilitating and risk factors Formation of antibodies and immune complexes

CLASSIFICATION (International Consensus and Russian Therapeutic Protocol, Order of the Ministry of Health of the Russian Federation No. 300, 1998). HOSPITAL PNEUMONIA (HOSPITAL, NOSOCOMIAL). Community-acquired PNEUMONIA (PRIMARY, HOME). ASPIRATION PNEUMONIA. PNEUMONIA IN PERSONS WITH IMMUNODEFICIENCY (congenital or acquired).

CLINICAL CLASSIFICATION QI Focal pneumonia (bronchopneumonia) Croupous (lobar) pneumonia Interstitial pneumonia

STAGES OF DIAGNOSIS OF PNEUMONIA Establish the presence of pneumonia. Conduct differential diagnosis to exclude syndromic similar conditions. Approximately (empirically) determine the etiological option for choosing the optimal treatment program.

CLINICAL PICTURE GENERAL SYMPTOMS (EXTRA-PULMONARY): weakness, lethargy, adynamia, loss of appetite, fever, chills, sweating, headache, symptoms of damage to organs and systems in infectious-toxic manifestations x. LOCAL SYMPTOMS (PULMONARY): cough, presence of sputum, its character (mucous, purulent, mucopurulent, rusty, hemoptysis), chest pain, its connection with breathing, shortness of breath.

CLINICAL PICTURE of lobar pneumonia PHYSICAL DATA: EXAMINATION: pallor of the skin, blush on the affected side of the lungs, herpes, lagging of the affected side of the chest during breathing

Forced position of the patient Herpes nasalis, labialis Blush on the affected side of the lungs

CLINICAL PICTURE of lobar pneumonia PHYSICAL DATA: PALPATION: increased voice trembling, PERCUSSION: - dullness of percussion sound (in stages I and III), dull (femoral) percussion sound (in stage II), AUSCULTATION: - bronchovesicular (hard) breathing (in stages I and III), bronchial breathing (in stage II), crepitus (in stages I and III) ), pleural friction noise (stage II), increased bronchophony

CLINICAL PICTURE of focal pneumonia PHYSICAL DATA: PALPATION: increased voice trembling, PERCUSSION: dullness of percussion sound AUSCULATION: bronchovesicular (hard) breathing, ringing fine bubbling rales increased bronchophony

INSTRUMENTAL METHODS OF DIAGNOSTICS - RADIOGRAPHY OF THE ORGANS OF THE CHEST in 2 projections (it is also prescribed for an incomplete set of clinical symptoms)

INSTRUMENTAL DIAGNOSIS METHODS CLINICAL BLOOD ANALYSIS MICROBIOLOGICAL STUDY: - Gram stain; - culture of sputum to isolate the pathogen and determine its sensitivity to antibiotics Staphylococcus aureus in pus. Gram stain. Culture sensitive (left) and insensitive (right) to an antibiotic

DISEASES AND SYNDROMES FOR THE DIFFERENTIAL DIAGNOSIS OF PNEUMONIA Lung cancer Lung infarction Atelectasis Lung contusion Pulmonary tuberculosis SARS Bronchitis "Non-pneumonic" pleural effusion Pneumonitis (drug, toxic, radiation, with systemic vasculitis) Infectious diseases (typhoid)

ADDITIONAL OBJECTIVE CRITERIA FOR DIFFERENTIAL DIAGNOSIS OF PNEUMONIA - X-ray tomography, computed tomography (with lesions of the upper lobes, lymph nodes, mediastinum, decrease in the volume of the lobe, suspicion and abscess formation, with the ineffectiveness of adequate antibiotic therapy). - Microbiological examination of sputum, pleural fluid, urine, blood, including mycological examination with ongoing fever, suspected sepsis, tuberculosis, superinfection, AIDS. - Serological examination (determination of antibodies to fungi, mycoplasma, chlamydia, legionella, cytomegalovirus) for atypical pneumonia at risk in alcoholics, drug addicts, with immunodeficiency (including AIDS), in elderly people.

PNEUMOCOCCAL PNEUMONIA (30-95%) Most common in winter and early spring During an epidemic of acute respiratory viral infections and influenza In patients with chronic lung diseases The lower lobes and posterior segments of the upper lobe are most often affected Often the "classic" picture of croupous pneumonia UP TO 25% of such pneumonia occur with bacteremia and these cases are fatal.

STAPHYLOCOCCAL PNEUMONIA Often complicates viral infections Often nosocomial and develops in patients with severe background disease after recent surgery Development of multifocal broncho-pneumonia with peribronchial easily draining abscesses Often complicated by pleurisy and pyopneumo-thorax Hospital strains of staphylococcus are resistant to most antibiotics

MYCOPLASMA PNEUMONIA Develops more often in childhood, adolescence and young age Epidemic outbreaks in organized groups (schoolchildren, military personnel) At the onset of the disease, symptoms of ARVI Often extrapulmonary symptoms - chills, muscle and headaches, symptoms of ARVI Often cervical lymphadenopathy, polymorphic skin rash, hepatosplenomegaly Physicist palpable symptoms are scarce: often there is no change in percussion sound, locally - small - bubbling rales Rapid decompensation of concomitant diseases progression of pneumonia SARS 1

CHLAMYDIAL PNEUMONIA C. trachomona - isolated cases of pneumonia in newborns C . psittaci - lesion of the lungs as part of psittacosis (ornithosis) C . pneumoniae is one of the main causative agents of AP Onset of the disease with dry cough, sore throat, hoarseness of voice (pharyngitis, laryngitis), malaise Fever On X-ray examination, more often small-focal in size 2-3 cm, often multifocal infiltration Lobar infiltration, cavity formation and pleural effusion are atypical, mild, but protracted course ATYPICAL PNEUMONIA 3

LEGIONELLA ZKNING PNEUMONIA It is more often observed in large buildings (hotels, hospitals) People of middle and old age get sick more often The clinical debut is characterized by unmotivated general weakness, anorexia, lethargy, persistent headaches Hemoptysis and chest pain in every 3rd patient Febrile fever, shortness of breath Physical symptoms: dullness, bronchial breathing, crepitus, wet wheezing SARS 5

LEGIONELLA KNOWING PNEUMONIA Cases of sinusitis, paraproctitis, pancreatitis, brain abscess are described. X-ray at the beginning - focal infiltrates, later their consolidation. The infiltrates adjoining to a pleura can remind a lung infarction. Pleural effusion in 1/3 of patients Often bradycardia, hypotension May be urinary syndrome SARS 6

Common to all atypical pneumonias - Inability to detect the pathogen in sputum - Specific serological data (immune - enzyme analysis with the detection of specific IgG, IgM) - Ineffectiveness of ß-lactam antibiotics - Efficiency of macrolides, tetracyclines, fluoroquinolones

FORMULATION OF THE DIAGNOSIS 1 NOSOLOGICAL FORM: Focal pneumonia (bronchopneumonia) (the inflammatory process captures certain areas of the lung tissue - the alveoli and adjacent bronchi.) Croupous (lobar) pneumonia (characterized by the rapid involvement in the process of a lobe or part and the adjacent area of ​​the pleura.) Interstitial pneumonia (due to a predominant lesion of the connective (intermediate) tissue of the lungs) OUT OF HOSPITAL OR INTERNAL PAIN - INTERNAL

FORMULATION OF THE DIAGNOSIS 2 ETIOLOGICAL OPTION (indicative or verified) PREVALENCE GRAVITY COMPLICATIONS (pulmonary and extrapulmonary) PHASE OF THE DISEASE (height, resolution, protracted course)

TACTICS OF TREATMENT OF PATIENTS WITH ACUTE PNEUMONIA The choice of treatment site (outpatient or inpatient) is determined by the severity of the condition, including the presence of concomitant diseases and the degree of their compensation.

ALGORITHM FOR THE TREATMENT OF A PATIENT WITH HOSPITAL PNEUMONIA, ACCORDING TO THE SERIOUSITY OF THE DISEASE CLINICAL AND RADIOLOGICAL SIGNS OF PNEUMONIA AND ASSESSMENT OF SERIOUSITY AND PROGNOSIS pulmonary PNEUMONIA Oral a/b therapy MACROLIDES, RESPIRATORY FLUOROQUINOLONS P SEVERE AND MODERATE NEUMONIA Parenteral a/b therapy CEPHALOSPORINS III + MACROLIDES

ANTIMICROBIALS 1 PENICILLINS: NATURAL - benzylpenicillin SEMI-SYNTHETIC - methicillin, oxacillin, cloxacillin, ampicillin, amoxicillin, carbenicillin, azlocillin, etc. Combined antibiotics (ampiox, amoxiclav, augmentin)

ANTIMICROBIAL DRUGS 2 CEPHALOSPORINS: CFS 1 - highly active in relation to gram (+), stable to the action of staphylococcal beta-lactamase, but hydrolyzed by beta-lactamase gram (-) bacteria (cefazolin) CFS II - highly active in relation to gram (-) (cefamandol, cefataxime - claforan, etc.) CFS III - and greater activity against Pseudomonas aeruginosa (ceftazidime - fortum) CFS IV - active against bacteroids and other anaerobes, stable to the action of beta-lactamase (moxalactam - moxam)

ANTIMICROBIAL DRUGS 3 CARBAPENEMS: Highly active against gram (-), including causative agents of nosocomial pneumonia (imipenem - celastin, meropenem) GLYCOPEPTIDES: Act on gram (+) - vancomycin, ristomycin AMINOGLYCOSIDES: wide spectrum of action, including gram (-). 1st generation (monomycin) 2nd generation (gentamicin) 3rd generation (amikacin)

ANTIMICROBIAL DRUGS 4 MACROLIDES: Accumulate inside the cell and used in atypical pneumonia (erythromycin, spiramycin, sumamed, rulid, etc.) TETRACYCLINES: Broad spectrum of action, including intracellular microorganisms (doxycycline, monocycline, etc.) Actal, etc.)

DURATION OF A / B THERAPY OF COMMUNITY-ACQUIRED PNEUMONIA Determined by the response to therapy, the severity of pneumonia, the presence of complications, the etiological variant In uncomplicated pneumonia caused by S. pneumoniae or H. influence the duration of a / b therapy 7-10 days In case of pneumonia caused by intracellular pathogens, in the presence of complications (abscess, etc.), the duration of treatment can reach 21 days

RADIOLOGICAL RESOLUTION OF PNEUMONIA AND NORMALIZATION OF ESR OCCUR LATER THAN THE SIGNS OF INTOXICATION AND PHYSICAL SYMPTOMS ARE DISAPPEARED

Consequences of frequent acute respiratory infections Development of bacterial complications Formation of respiratory allergosis Delay in psychomotor and physical development Formation of immunological incompetence Restriction of social activity of children (attendance of children's groups) High mortality from SARS and influenza remains The economic damage is an order of magnitude higher than the damage caused by all other infectious diseases

Development of bacterial complications Formation of respiratory allergy Delay of psychomotorical and physical development Formation of immunological insolvent Restriction of social activity of children (attendance of children’s collectives) There is a high mortality from ORVI and flu The economic damage on an order exceeds a damage put by all other infectious diseases

ETIOLOGY ARI viruses: influenza, parainfluenza, adenoviruses, reoviruses, coronaviruses, respiratory syncytial viruses, enteroviruses, etc. Each of the infections has its own face. pneumotropic bacteria: Streptococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, Klebsiella pneumoniae, Pseudomonas aeruginosa and other intracellular microbes: mycoplasma, chlamydia Fungi, protozoa

flu, paraflu, adenoviruses, reoviruses, koronaroviruses, respiratory-sencitial viruses, entero-viruses, etc. Each of infections has "the person" . pne u motrop e bacteria: Streptococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenza a, Klebsiella pneumoniae, Pseudomonas aeruginosa, etc. endocellular microbes: mycoplasma, c chlamidiya Mushrooms

Epidemiology of ARI: — — Similarity of the epidemiological process; ; - - Localization in the epithelium of the upper respiratory tract; ; - - The source of infection is a sick person (anthroponoses); ; — — Airborne transmission mechanism; ; - - Occur in the form of sporadic cases and epidemic outbreaks.

— Similarity of epidemiological process; - Localization in an epithelial cell of the upper respiratory ways; - An infection source - the sick person (antroponosis); — Airborne mechanism of transfer; — Meet in the form of sporadic cases and epidemic flashes.

GENERAL FEATURES OF PATHOGENESIS introduction and reproduction of pathogens in the affected epithelial cells of the respiratory tract: (primary localization) influenza - larynx-trachea parainfluenza - adeno larynx - nose, larynx, bronchi RSRS - bronchi rhinoviruses - nose viremia with the development of toxic and toxic-allergic reactions exodus

introduction and reproduction of activators in the epithelial cells of a respiratory path: (primary localization) flu – a throat trachea paraflu – the throat adeno-nose, throat, bronchial tubes

The target organ is the cells of the cylindrical epithelium of the nasal passages and trachea. Local factors of nonspecific protection: lysozyme, secretory Ig A and phagocytosis. Cytoplasmic and intranuclear destruction of epithelial cells. Violation of the functional activity and integrity of the cilia and mucociliary clearance. Dystrophic changes in the epithelium and the appearance of serous and serous-hemorrhagic exudate in the lumen of the respiratory tract

Target organ - cylindrical cell in an epithelial of nasal courses and trachea. Local factors of nonspecific protection: lysozyme, secretory Ig A and phagocytosis. Cytoplasmic and intra nuclear destruction of epithelial cells. Violation of functional activity and integrity of eyelashes and muco-ciliary clearance. Dystrophic changes on an epithelial and emergence of serous and hemorrhagic exudate in a gleam of respiratory ways.

Influenza There are three types of influenza virus - A, B and CC: A A causes major epidemics and pandemics, is characterized by rapid spread, high infectiousness (morbidity - mortality) and antigenic structure lability (mutations). BB has a constancy of antigenic structure: it is less prone to mutations. SS has a constancy of antigenic structure, is of little importance in human pathology. DRIFT - a gradual change of antigenic variants within the same serotype (H 22 NN 2 2 - - HH 33 NN 22).). SHIFT - abrupt changes and NN associated not with mutation, but with genetic recombination (H (H 11 NN 11 - H 22 NN 22) (hemagglutinin, neurominidase)

Distinguish three types of a virus of flu - A, B, C: A - causes large epidemics and pandemics, it is characterized by fast distribution, high infectivity (incidence - mortality) and lability of anti-gene structure (mutation). B - In possesses constancy of anti-gene structure: is less subject to mutations. C - possesses constancy of anti-gene structure, it is little significant in pathology of the person. DRIFT - gradual change of anti-gene options within one type (H 2 N 2 - H 3 N 2). Sh. IFT - sharp changes, connected not with a mutation, and with a genetic recombination (H 1 N 1 - H 2 N 2) (hemaglutinine and neuraminidase)

EPIDEMIOLOGY OF INFLUENZA Source - a sick person from the end of the incubation period to 4-7 days of illness, erased forms are dangerous Transmission mechanism - airborne transmission Ways of transmission - airborne dust airborne contact (household contact) Susceptibility - - everyone who does not have immunity is susceptible Seasonality - winter, spring Immunity - persistent, type- and strain-specific

Source – the sick person since the end of the incubatory period to 4 -7 days of an illness, the erased forms are dangerous The transfer mechanism – airborne Transfer ways – air and dust the airborne contact (contact and household) Susceptibility – everything which do not have immunity are susceptible Seasonality – winter, spring Immunity – resistant, type-specific

DIAGNOSIS OF INFLUENZA Epidemic situation Clinical symptoms: acute onset, fever toxicosis (neurotoxicosis) poor catarrhal manifestations of UAC: leukopenia, shift of the leukocyte formula to the left in the first days of the disease later replaced by lymphocytosis, normal ESR

Epidemic situation Clinical symptoms: sharp beginning fever, toxicosis (neurotoxicosis) poor catarrhal phenomena analysis of blood: the le u kopeni a , shift of a le u ko cyte formula to the left in the first days of an illness the late is replaced l y m ph o cy to sis , normal SO

Complications: bacterial and allergic on the part of the lungs: laryngitis, tracheitis bronchitis segmental pulmonary edema pneumonia (interstitial, hemorrhagic, focal viral-bacterial) SSCCSS myocardial dystrophy (lethargy, immobility, pallor, pulse lability, systolic murmur, decreased P and T waves) myocarditis (deafness of tones, expansion of boundaries, blood pressure) nervous system encephalitis itis, meningoencephalitis neuritis, neuralgia

Complications: bacterial and allergic from lungs: laryngitis, tracheitis bronchitis segmentary hypostasis of lungs pneumonia (inters titial , hemorrhagic, virus and bacterial) cardiovascular system (CVS) mio c ardiod y strofi c (slackness, low-mobility, pallor, lability of pulse, systolic sound, decrease in a teeth of R and T) myocarditis (dullness of tones, expansion of borders, arterial pressure - low) nervous system encephalitis, neuritis, neuralgia

Parainfluenza RNA-containing virus of the Paramyxoviridae family Rise in incidence every 3-5 years Source of infection - a sick person, carriage of 0.2-1.7% Way of transmission: aerosol Susceptible population: - children, especially young children Immunity: not persistent, type-specific "Visit card of infection" - acute stenosing laryngotracheitis

P araflu RNA - a containing virus of Paramyxoviridae family Incidence liftings each 3 -5 years Infection source - the sick person, a carrier - in 0.2 -1.7% Transfer way: the aerosol Susceptible contingent: - children, especially early age

FALSE CROUPS FORMS OF STENOSE OF THE LARYNX Pathogenetically stenosis of the larynx is caused by: Reflex spasm of the muscles of the larynx Edema and infiltration of the mucous membrane of the larynx and subglottic space Obturation of the respiratory tract with thick sputum, accumulation of collapsing cells Forms: edematous, infiltrative, obstructive

FALSE CROUP OF THE FORM OF THE STENOSIS OF THE THROAT Pathogen esis of stenosis of a throat is caused by: Reflex spasm of muscles of a throat edema and infiltrat ion mucous of throat and space below the vocal cords

DEGREES OF STENOSIS OF THE LARRINS The severity of stenosis of the larynx is determined by the degree of respiratory failure II degree (compensated stenosis) moderate retraction of the jugular fossa and compliant places of the chest with anxiety (breathing is free at rest) shortness of breath, no cyanosis, Ra. CO 22 , Ra. O 22, KOS - NN

DEGREES OF THE STENOSIS OF THE THROAT severity of stenosis of throat is defined by degree of respiratory insufficiency I degree (the compensated stenosis) moderate in drawing of a jugular pit and compliant places of a thorax at concern (in rest breath free) Breathing insufficiency, cyanosis absent

IIII degree (subcompensated stenosis) retraction of the sternum and compliant places of the chest at rest noisy breathing with difficulty breathing (inspiratory dyspnea) tachycardia, cyanosis with anxiety periodic anxiety of the child Ra. CO 22< 60 -70 мм. рт. ст. , КОС — появление метаболического ацидоза

II degree (the sub compensated stenosis) involving chest and compliant places of a thorax at rest noisy breathing with difficulty in inspiration (inspiratory short wind) tachycardia, cyanosis at concern periodic concern of the child CO 2 - 35 -49 mm Hg, PO 2 - 60 -70 mm Hg, - the emergence of metabolic acidosis

III degree (uncompensated stenosis) pronounced retraction of the sternum shallow breathing constant pallor of the skin, marbling, general cyanosis the skin is cold; cold, sticky sweat muffled heart tones, tachycardia gives way to bradycardia loss of a pulse wave on inhalation pronounced anxiety of the child, sleep disturbance, trembling may be convulsions of Ra. CO 22 >35 -49 mm. rt. Art. , Ra. About 22< 60 -70 мм. рт. ст. , КОС – метаболический и респираторный ацидоз

III degree (uncompensated stenosis) expressed involving chest superficial breathing constant pallor of integuments, marbleness, general cyanosis Cold integuments; cold sticky sweat the sub muted of heart sounds, tachycardia is replaced by bradycardia loss of a pulse wave on a breath the expressed concern of the child, sleep disturbance, wince there can be convulsions CO 2 - 35 -49 mm Hg, PO 2 - 60 -70 mm Hg, metabolic and respiratory acidosis

IV degree (asphyxia) - preagonal state of coma, arrhythmic breathing, no superficial retraction of compliant chest areas, sharp pallor, total cyanosis, bradycardia, arrhythmia, cardiac arrest Ra. CO 22 >> 100 mm. rt. Art. pronounced decompensated acidosis in combination with respiratory alkalosis

The IV degree (asphyxia) coma A rhythmic breathing , superficial there are no compliant places of a thorax sharp pallor, total cyanosis bradycardia, arrhythmia, cardiac arrest CO 2 - 100 mm Hg. the expressed de compensated acidosis in a combination with respiratory alkalosis

INDICATIONS TO THE INTUBATION Progressing cyanosis Loss pulse waves on a breathing Disturbance in breathing rhythm Sticky cold sweat

TREATMENT OF STENOSIS OF THE LARNOOSE Mandatory hospitalization, calm environment Warm alkaline drink Warm (30 ° C), moist air (relieves swelling and spasm, dilutes sputum, promotes the discharge of crusts) Steam aerosol inhalations, microwave on the larynx Distracting procedures Vasoconstrictive drops Fight against hyperthermia (lytic mixture) Desensitizing (tavegil 0, 1 ml/year i/m)

Obligatory hospitalization, quiet situation Warm alkaline drink Warm (30°C), damp air (removes edema and a spasm, dilutes the phlegm, promotes an expectorat ion of crusts) Steam aerosol inhalations Distracting procedures Vasoconstrictive drops Fight against a hyperthermia (lytic mix) Desensibili sation remedy (tavegil 0.1 ml/years in/m)

TREATMENT OF STENOSE OF THE LARNOOSE Fighting edema and inflammation - glucocorticoid hormones (inhalation, parenteral) Fighting bronchospasm (bronchodilators, hormones) Mucolytics (ambrohexal, bromhexine, ACC) With stenosis of the larynx for more than 3 days - antibiotics With edematous form - lasix 1 mg / kg Infusion therapy with caution, especially with walls oze IIIIII degree, edema may increase (20-30 ml / kg, do not abuse saline solutions)

Fight against hypostasis and inflammation - glucocorticoid hormones (it is inhalation, parenteral intake) Fight against a bronchospasm (bronchial spasmolytics, hormones) plify edema (20 -30 ml/kg not to abuse salt solutions)

ADENOVIRUS INFECTION DNA-containing virus of the Adenoviridae family ARI characterized by fever, damage to the lymphoid tissue, mucous membranes of the respiratory tract, often the conjunctiva of the eyes, intestines and moderate symptoms of intoxication Incubation period - - 1-14 days Source of infection: a sick person, virus carrier Route of transmission: airborne fecal-oral months to 5 years

DNA - a containing virus of Adenoviridae family ORZ being characterized fever, defeat of a lymphatic tissue, mucous membranes of respiratory ways, quite often conjunctivas of eyes, intestines and moderately expressed symptoms of intoxication The incubatory period - 1 -14 days Infection source: sick person, virus carrier Transfer way: the airborne the fecal and oral Susceptible contingent: more often children from 6 months to 5 years

ADENOVIRUS INFECTION The “visiting card” of the infection is conjunctivitis: catarrhal, follicular or membranous More often one eye is affected, the second after a few days, it will continue. 10 -14 days

Infection "card" - conjunctivitis: catarrhal, follicular or filmy one eye, the second in some days. second in a few days, will continue. 10 -14 days.

ADENOVIRUS INFECTION According to the main syndrome, there are: Catarrh of the upper respiratory tract Rhinopharyngoconjunctival fever Conjunctivitis, keratoconjunctivitis Bronchitis, more often obstructive Tonsillopharyngitis Pneumonia Diarrhea

On the main syndrome: catarrh of the upper respiratory tract Rhin o-p haryng o-c onjunctiv al Conjunctivitis Bronchitis, is more often the obstructive T onsill o- pharyngitis Pneumonia Diarrhea

RESPIRATORY SYNCYTIAL INFECTION Pathogen: RNA-containing virus of the Paramyxoviridae family, genus Pneutovirus Source of infection: sick person, virus carrier (4%) Transmission route: airborne Susceptible population: more often children from birth to 2 years of age SARS characterized by mild intoxication and predominant damage to the lower respiratory tract, with a very frequent development of bronchitis, bronchiolitis , possible croup.

RC- INFECTION Activator: RNA - a containing virus of Paramyxoviridae family, the sort Pneutovirus Infection source: sick person, virus carrier (4 %) Transfer way: the airborne Susceptible contingent: more often children since the birth and to 2 years

RHOVIRUS INFECTION RNA-containing virus of the family Picornaviridae, genus Rhinovirus Source of infection - a sick person Transmission route - airborne contact Susceptible contingent - everyone is susceptible, children are more often sick preschool age"Business card" - severe rhinitis

Rhinovirus infection RNA - a containing virus of Picornaviridae family, the sort Rhinovirus Infection source - the sick person Transfer way - airborne the contact The susceptible contingent - are susceptible all, more often children of preschool age are ill "Card" - the expressed rhinitis

REOVIRUS INFECTION Pathogen: RNA-containing virus of the Reoviridia family Business card: damage to the upper respiratory tract and small intestine. Cough, loose stools, swollen lymph nodes, liver, spleen, skin rashes, herpetic sore throat.

Reoviruses infection Activator: RNA - a containing virus of Reoviridia family "Visit with ard": defeat of the top respiratory ways and small intestines. Cough, liquid stool, increase lymph nodes, a liver, a spleen, skin rash, herpetic angina

Laboratory diagnosis of KLA - leukopenia, lymphocytosis, ESR - NN. . Possible - leukocytosis with a shift to the left, >> ESR, at the stage of recovery - moderate monocytosis, less often - - eosinophilia. Virological methods - isolation of the virus from nasopharyngeal swabs (blood, feces of the patient). Serological - reactions of RSK and RTGA in paired sera (3-4 and after 8-10 days). . ((> > 3-4 times) Express method: immunofluorescent (smears-prints from the nasal mucosa + virus antibodies labeled with fluorescein isothiocyanate) (glow). The most promising method is enzyme immunoassay (ELISA).

Laboratory diagnostic: General analysis of blood - a le uc openia , lymphocytosis, SOE - N . It is possible - leukocytosis with shift to the left; SOE, at a recovery stage – moderated monocytosis, is more rare – an eosinophilia. Virologic methods - virus allocation from nasopharyngeal washouts (blood, excrements of the patient). The s erologic al methods – RSK and RTGA reactions in pair serums (3 -4 and in 8 -10 days) (increase in 3 -4 times) Express method: immunofluorescent (dabs prints with mucous a nose + antibodies of viruses marked fluores cent) (luminescence). The most perspective method is IFA.

PATHOGENETIC TREATMENT OF ARI Bed rest - only in the period of acute manifestations of the disease. The room temperature is not higher than 20°C and 3-4°C lower during sleep. Nutrition should not be different from the usual. While maintaining a full-fledged diet, the appointment of vitamins is unnecessary. Give the patient plenty of water: fruit drinks, juices, sweet tea are well absorbed.

Confinement to bed - only in the period of sharp manifestations of a disease. The temperature indoors not above 20°C and 3 -4°C lower during sleep. A food shouldn't differ from the usual. At preservation of a high-grade diet purpose of vitamins excessively. Give plenty of drink to the patient: berry juices, juice, sweet tea.

RULES FOR PRESCRIBING ANTYVERTISM IN ORIORI Previously healthy children: with a body temperature above 39.0 ° C and / or with muscle aches and / or headaches. Children with a history of febrile convulsions and with severe heart and lung diseases: with a body temperature above 38.0 -38.5 ° C. Children of the first 3 months life: at a body temperature above 38, 0 ° C. Antipyretic Paracetamol 10-15 mg / kg, daily-60 mg / kg, Ibuprofen (Nurofen) - 5-10 mg / kg If there is no effect, Analgin is administered intramuscularly. Aspirin is categorically contraindicated (due to the risk of developing Reye's syndrome).

To healthy earlier children: at body temperature above 39.0°C and/or muscular ache and/or at a headache To children of the first 3 months of life: at body temperature above 38.0°C. The contrafeveral drugs: Paracetamol of 10-15 mg/kg, daily-60 mg/kg, Ibuprofen (Nurofen) - 5-10 mg/kg In the absence of effect intramuscularly enter analgesics. Aspirin is categorically contraindicated (because of danger of development of a syndrome of Rey).

The main groups of drugs for the treatment of acute respiratory viral infections: Pathogenetic (antipyretic, antihistamine, Erespal) Etiotropic (inactivating the virus or preventing its production) Immunocorrective, immunomodulating and immunorehabilitating Antibacterial agents

The main groups of preparations for ORVI treatment: Pathogenetic (antipyeretics , anti histamine , Erespal) Etiotrop ical (inactivating a virus or interfering its production) Immunocorrect ion , immunomodelling and immunoreh abilit ation Antibacterial

ETIOTROPIC MEANS: Native leukocyte interferon, fluferon, viferon, interferon preparation; ; Ribamidil (ribaverin, virazole) - inhibit the synthesis of viral RNA and DNA; ; Arbidol, amixin, agri, anaferon, cycloferon - interferon inducers; ; Oxolinic ointment, lokferon, bonafton; ; Influenza-staphylococcal immunoglobulin for i/m

Etiological therapy Nativ e le uc o cytic interferon, viferon, interferon and others; Ribamidil (ribaverin, virazole) – arrest synthesis of virus RNA and DNA; Arbidol, Agra, anaferon, cycloferon - interferon inductors; Oksolin al ointment, lokferon, bonafton; Influenzal and staphylococcal antibody

Systemic antiviral drugs Cyclic amines - rimantadine Other antiviral drugs Isoprinosine, Oseltamivir-Tamiflu Homeopathic remedies Anaferon - antiviral drug Antigripin - symptomatic remedy

System antiviral preparations Cyclic amines – rimantadine Other antiviral preparations Izoprinozin, Ozeltamivir-Tamifl u Homeopathic remedies Anaferon – an antiviral preparation Antigrip– symptomatic means

IMMUNOREHABILITIVE DRUGS: IRS-19, broncho-munal P - a mixture of bacterial cell walls that most often cause respiratory inflammation (vaccinating effect). IRS-19 - 1 dose (in each nasal passage) 2-5 times a day (from 3 months of age). Course 2-4 weeks. Bronchomunal P - 1 capsule in the morning for 10-30 days. Course - 3 months.

IRS-19, broncho-munal P – a mix of cellular walls of the bacteria most often causing a respiratory inflammation (vaccinating action). IRS-19 - 1 dose (in each nasal course) 2-5 times per day (since 3 months of life). Course of 2-4 weeks. Bronchomunal P - 1 capsule in the morning of 10 -30 days. A course - 3 months.

Ribomunil - ribosomal immunomodulator - consists of ribosomes of the main pathogens of ENT infections. Membrane factors of the main ARI bacteria: Licopid 1 mg 1-3 times a day for 10 days (from 1 year), Biostim Immudon - lozenges, increase the content of secretory Ig. A, interferon, lysozyme, stimulate phagocytosis. Sodium nucleinate, thymogen, other thymus preparations - you can ...

Ribomunil – a ribosomal immunomodulator – consists of ribosomes of the main causative agents of infections of the ear nose throat organs. Membrane factors of the main bacteria ARI: Likopid on 1 mg 1 -3 times per day 10 days (since 1), Biostim Immudon - tablets for a resorption, raise the maintenance of secretor y Ig. A, interferon, lysozyme, stimulate phagocytosis. Nukleinat of sodium, other preparations of thymus – it is possible …

PNEUMONIA Pneumonia is an acute infectious disease of the lung parenchyma, diagnosed by the syndrome of respiratory disorders and / or physical data, as well as infiltrative changes on the radiograph. In the ICD-10 it is encoded under headings J 12 -J 18 depending. From etiology, as well as J 10 and J J 11 (influenza with pneumonia)

Pneumonia — the acute infectious disease of a pulmonary parenchyma diagnosed on a syndrome of respiratory disturbance and\or physical signs, and also infiltration changes on the X-ray. In MKB-10 it is coded in the headings J 12 - J 18 in we depended from an etiology, and also J 10 and J 11 (flu with pneumonia)

ETIOLOGY OF PNEUMONIA The etiological spectrum of pneumonia is determined by age and the place where the disease occurred - at home or in the hospital. In newborns - pneumonia is caused by chlamydia, fungi, protozoa; when infected in the maternity hospital - - staphylococci and gram-negative flora. In children 1 - 6 months. streptococci, more often pneumococcus, staphylococcus. From 6 months up to 6 years - viruses, streptococci, Haemophilus influenzae, mycoplasma, chlamydia In older children - Haemophilus influenzae and mycoplasma.

The etiologic range of pneumonia is defined by age and a place where there was a disease – houses or at hospital. At newborns - pneumonia is caused by chlamydia, mushrooms, the elementary; at infection in maternity hospital - staphylococci and gram negative flora. At children is 1 -6 month - streptococci, is more often a pneumococcus, staphylococci. From 6 months to 6 years - viruses, streptococci, a hemophilic stick, a mycoplasma, chlamydia At children of the senior age - a hemophilic stick and mycoplasma.

ETIOLOGY OF PNEUMONIA Hospital-acquired pneumonia is more often caused by Escherichia coli, Klebsiella pneumoniae, proteus, Pseudomonas aerugenosae. Ventilator-associated pneumonia (VAP) - in the 1st 72 hours of the patient's autoflora, from 4 days - Pseudomonas, serrations, Klebsiela. In immunocompromised patients - pneumocystis, CMV, fungi. With humoral immunodeficiencies - - pneumococci, staphylococci, enterobacteria.

Hospital pneumonia is more often caused by Escherichia coli, Klebsiella pneumoniae, proteus, Pseudomonas aerugenosae. The ventilator - the associated pneumonia (VAP) - at the 1 st 72 hrs autoflory the patient, since 4 days - pseudomonads, serratsiya, k lebsiella. At patients with an immunoscarce condition - p neumocystis, cytomegalovirus, mushrooms. At humoral immunodeficiencies - pneumococci, staphylococci, enterobacteria.

CLASSIFICATION - - Community-acquired, - nosocomial (hospital, nosocomial), developed after 72 hours of hospital stay or within 72 hours after discharge; - pneumonia in immunocompromised individuals; - associated with ventilation of the lungs (VAP) early (the first 72 hours of mechanical ventilation), late (4 and and > > days on mechanical ventilation); In newborns: - - intrauterine (congenital, which developed in the first 72 hours of life) and acquired (postnatal - out-of-hospital and hospital).

Extra sick-lists, - intrahospital (hospital, nozokomialny), the stay which have developed through 72 hours in a hospital or within 72 hours after an extract; - pneumonia in persons with an immunoscarce condition; - associated with ventilation of easy (VAP) early (the first 72 hours of IVL), late (4 days on IVL); At newborns: - pre-natal (congenital which developed at the 1 st 72 hrs of life) and acquired (the post-natal - extra hospital and hospital).

CLASSIFICATION According to clinical and radiological data, focal, focal-confluent, lobar (croupous), segmental, interstitial pneumonia are distinguished; By severity, non-severe and severe pneumonias are distinguished - not complicated and complicated (bulls, abscess, pneumothorax, pyopneumothorax and extrapulmonary complications - acute heart failure, convulsive syndrome, sepsis, infectious-toxic shock; Acute (no more than 4 weeks) and protracted (1, 5 - 6 months), recurrent.

According to clinic -radiological data, chamber-drain, lobar, segmentary, interstitial pneumonia; On severity- acute and chronic pneumonia - not complicated and complicated (bull ou s, abscess, p n eumothorax, pyro pneumothorax and out of pulmonary complications - sharp warm insufficiency, a convulsive syndrome, sepsis, infectious and toxic shock; On a current distinguish sharp (no more than 4 weeks) and long (1, 5 -6 months), recurrent.

PATHOGENESIS OF PNEUMONIA RESPIRATORY INSUFFICIENCY. . HYPOXEMIA: A) A) Violation of the ventilation-perfusion ratio - there is an undersaturation of blood with oxygen B) a violation of the diffusion of gases through the alveolar-capillary membrane due to edema and / or cell infiltration INFECTIOUS TOXICOSIS Violation of the regulation of the function of vital organs - blood circulation, digestion, cerebral cortex, etc.

RESPIRATORY INSUFFICIENCY. hypoxic: A) Violation ventilating ventilation-perfusion ratio - occurs a decreasing the saturation of blood oxygen B) violation of diffusion of gases through an alveolar and capillary membrane because of edema and/or a cellular infiltration INFECTIOUS TOXICOSIS Violation of regulation of function of vitals - blood circulations, digestion, a cerebral cortex, etc.

Algorithm for the clinical diagnosis of pneumonia (V. K. Tatochenko 2006) X-ray and / or start of treatment Start of examination: T o > 38 0 > 3 days and / or Shortness of breath and / or chest indrawing without obstruction Local symptoms: Shortening of percussion sound and / or Weakened or bronchial breathing and / or Local rales Asymmetry of moist rales Signs of toxicosis SARS no no no. YES YES

TREATMENT Possible at home. Children with a serious condition at the onset of the disease, with severe background conditions and according to epidemiological and social indications are subject to hospitalization. Mode - restriction of physical and emotional stress. Diet for infants: frequent metered feeding. For older children - easily digestible food according to appetite.

Treatment Probably in house conditions. Hospitalization of children with a serious condition in a disease debut, with serious background conditions and according to epidemiological and social indications are subject. Mode - restriction of physical and emotional activity. A diet for children of chest age: the frequent dosed-out feeding. For children of advanced age – easily food on appetite.

PATHOGENETIC THERAPY Oxygen therapy. . In young children, an oxygen tent or oxygen through a nasal tube. The fight against infectious toxicosis - - infusion therapy, correction of acid-base balance. SYMPTOMATIC THERAPY. . When coughing - antitussive drugs, bronchodilators, inhalations ... In heart failure - cardiotropic drugs, etc. ADDITIONAL THERAPY. . Physiotherapeutic procedures in the period of resolution of pneumonia, massage, breathing exercises.

Pathogenetic therapy Oxygen therapy. Small children have an oxygen tent or supply of oxygen through a nasal probe. Fight against infectious toxicosis – infu s ion therapy, correction of the acid and electrolyte balance. SYMPTOMATIC THERAPY. For cough – mycolytics preparations, bronchodilatat ion remedy, inhalations … At warm insufficiency – cor preparations etc. AUXILIARY THERAPY. Physiotherapeutic procedures in the period of permission of pneumonia, massage, respiratory exercises.

Not only antibacterial treatment, but also antiviral, antifungal, anti-parasitic Starting an antibiotic – a wide range of action + phlegm crops on sensitivity Course of antibacterial therapy of 7 -10 days. Control of laboratory indicators.

Broad-spectrum antibiotics semi-synthetic penicillins (ampicillin, amoxicillin, carbenicillin); cephalosporins, (III - cefotaxime, ceftazidime) and ((IV - cefpirome, cefepime) generations; carbapenems (imipenem, meronem, thienam); levomycetin; tetracyclines; aminoglycosides (gentamicin, tobramycin, amikacin); rifamycins (rifocin, rifamide, rifampicin).

semi-synthetic penicillin (ampicillin, amoxicillin, carbenicillin); cephalosporins, (III - cefotaxami, cefotazimi) and (IV-cefepimi) generations; carbapenems (imipen, meron em, tienam); chloramphenicol; tetracyclines; aminoglycosides (gentamycin, tobramycin, amikacin); rifamycins (rifocin, rifamide, rifampicin).

Pneumonia is an inflammation of the lungs of an infectious nature with the involvement of all structural elements lung tissue and obligatory lesion of lung tissue. Pneumonia is an inflammation of the lungs of an infectious nature with the involvement of all structural elements of the lung tissue and obligatory damage to the lung tissue.

Classification. Classification. 1. By etiology: - bacterial (pneumococcus, influenza bacillus, staphylo-streptococcus, bacteria of the intestinal group, etc.); – bacterial (pneumococcus, influenza bacillus, staphylostreptococcus, bacteria of the intestinal group, etc.); – viral (influenza, parainfluenza, adenovirus, cytomegalovirus, etc.); – viral (influenza, parainfluenza, adenovirus, cytomegalovirus, etc.); – mycoplasma or rickettsial; – mycoplasma or rickettsial; - due to chemical or physical factors; - due to chemical or physical factors; – mixed etiology; – mixed etiology; unspecified etiology. unspecified etiology.

2. According to clinical and morphological variants: – croupous (lobar, fibrinous, pleuropneumonia); – croupous (lobar, fibrinous, pleuropneumonia); – focal (lobular, bronchopneumonia); – focal (lobular, bronchopneumonia); – interstitial. – interstitial. 3. Downstream: -acute; – acute; - lingering. - lingering.

4. By localization: – right, left lung; - right, left lung; - bilateral; - bilateral; – share, segment. – share, segment. 5. According to the functional state of the respiratory apparatus: - without functional disorders; – without functional disorders; – with functional disorders (3 degrees). – with functional disorders (3 degrees).

6. According to the presence of complications: – uncomplicated; – uncomplicated; -complicated (pleurisy, abscess, etc.). -complicated (pleurisy, abscess, etc.). 7. There are also community-acquired and hospital-acquired pneumonia. This division is important because these diseases are caused by different agents, the course of nosocomial pneumonia is more severe, they are refractory to therapy. Hospital pneumonia is considered to occur after 2 days or later from the moment the patient was admitted to the hospital for any other disease. The main microbial associations that cause nosocomial pneumonia are representatives of the gram-negative flora - staphylococci, anaerobes, Pseudomonas aeruginosa.

Morbidity. At 15-17 years old - 236 cases per year. Among the entire population - out-of-hospital 1200 per hospitalizations per year. Men are more often ill. Morbidity. At 15-17 years old - 236 cases per year. Among the entire population - out-of-hospital 1200 per hospitalizations per year. Men are more often ill. Mortality. In the 30s of the twentieth century - 24%. In the 40s - 12%. Currently, 1 to 5-6% in young people and 15-20% in the elderly. Mortality. In the 30s of the twentieth century - 24%. In the 40s - 12%. Currently, 1 to 5–6% in young adults and 15–20% in the elderly

Pneumonia is traditionally divided into focal and croupous. These differences can be seen in this figure. Pneumonia is traditionally divided into focal and croupous. These differences can be seen in this figure. Focal pneumonia often occurs against the background of previous bronchitis of various etiologies, as a result of which they are also called bronchopneumonia, emphasizing its connection with primary bronchitis. Focal pneumonia often occurs against the background of previous bronchitis of various etiologies, as a result of which they are also called bronchopneumonia, emphasizing its connection with primary bronchitis. In some cases, inflammation begins primarily in the lung tissue, without prior bronchitis. If this inflammation is stormy, hyperergic in nature, then it usually captures a large area of ​​the lung, often a whole lobe, and then they talk about lobar, or croupous, pneumonia (Fig.). At the same time, the pleura is often involved in the process, so this pneumonia is also called pleuropneumonia. In some cases, inflammation begins primarily in the lung tissue, without prior bronchitis. If this inflammation is stormy, hyperergic in nature, then it usually captures a large area of ​​the lung, often a whole lobe, and then they talk about lobar, or croupous, pneumonia (Fig.). At the same time, the pleura is often involved in the process, so this pneumonia is also called pleuropneumonia.

Such hyperergic development of pleuropneumonia indicates the participation of the immune system in their development. Such hyperergic development of pleuropneumonia indicates the participation of the immune system in their development. Indeed, with these pneumonias, a decrease in the number of T cells, the C3 component of the complement, an increase in the number of B cells and immunoglobulins, and circulating immune complexes are detected in the blood. These complexes, affecting the vessels of the lungs, contribute to the development and generalization of inflammation. Indeed, with these pneumonias, a decrease in the number of T cells, the C3 component of the complement, an increase in the number of B cells and immunoglobulins, and circulating immune complexes are detected in the blood. These complexes, affecting the vessels of the lungs, contribute to the development and generalization of inflammation. It has also been established that in these cases the activity of alveolar macrophages and neutrophils is reduced, and the amount of pro-inflammatory cytokines is increased. It has also been established that in these cases the activity of alveolar macrophages and neutrophils is reduced, and the amount of pro-inflammatory cytokines is increased.

Complaints. With lobar pneumonia, the main complaints are high fever, chills, cough with a moderate amount of sputum, chest pain, herpes on the face, and general malaise. Complaints. With lobar pneumonia, the main complaints are high fever, chills, cough with a moderate amount of sputum, chest pain, herpes on the face, and general malaise.

Anamnesis morbi. Here you should get answers to questions about when the patient fell ill, what the disease is associated with. If we are talking about a patient who is in the hospital, then for the differentiation of nosocomial and community-acquired pneumonia, the timing of the disease is specified - before admission or after. If treated, what was the treatment and the effectiveness of the treatment. Anamnesis morbi. Here you should get answers to questions about when the patient fell ill, what the disease is associated with. If we are talking about a patient who is in the hospital, then for the differentiation of nosocomial and community-acquired pneumonia, the timing of the disease is specified - before admission or after. If treated, what was the treatment and the effectiveness of the treatment.

Anamnesis vitae. The life history assessment should focus on identifying risk factors for the disease, including this case, pneumonia. Risk factors are factors that, although not direct etiological factors, nevertheless contribute to its development. With pneumonia, they can be: cooling, smoking, profession, chest injuries, surgical interventions, alcoholism, various serious illnesses, immunodeficiency states, hospitalization, etc. Seasonality is also a risk factor for pneumonia. A history of tuberculosis is important for differential diagnosis. Anamnesis vitae. The life history assessment should focus on identifying risk factors for disease, in this case pneumonia. Risk factors are factors that, although not direct etiological factors, nevertheless contribute to its development. With pneumonia, they can be: cooling, smoking, profession, chest injuries, surgical interventions, alcoholism, various serious illnesses, immunodeficiency states, hospitalization, etc. Seasonality is also a risk factor for pneumonia. A history of tuberculosis is important for differential diagnosis.

Data from an objective study. Data from an objective study. On the days: complaints of severe chills (internal feeling of cold, accompanied by trembling throughout the body), fever, headache, dry cough, chest pain, aggravated by coughing, deep breathing, poor general health. On the days: complaints of severe chills (internal feeling of cold, accompanied by trembling throughout the body), fever, headache, dry cough, chest pain, aggravated by coughing, deep breathing, poor general health. On examination - moderate cyanosis of the face, shortness of breath at rest with the participation of the wings of the nose in breathing; retardation of respiratory mobility of the side of the chest where there is pneumonia (sparing due to pain associated with concomitant pleurisy). On examination - moderate cyanosis of the face, shortness of breath at rest with the participation of the wings of the nose in breathing; retardation of respiratory mobility of the side of the chest where there is pneumonia (sparing due to pain associated with concomitant pleurisy). With percussion: on the first day, shortening of percussion sound A (the so-called dull-tympanic sound), which depends on the simultaneous presence of fluid and air in the alveoli; shortening of percussion sound. With percussion: on the first day, shortening of percussion sound A (the so-called dull-tympanic sound), which depends on the simultaneous presence of fluid and air in the alveoli; shortening of percussion sound. Auscultatory in the area of ​​shortening of percussion sound A - the so-called initial crepitus (crepitatio indux). There is tachycardia. Auscultatory in the area of ​​shortening of percussion sound A - the so-called initial crepitus (crepitatio indux). There is tachycardia.

Headache, weakness, cough persist for days, sputum appears, scanty, viscous, brown in color (“rusty”. Shortness of breath, pain in the side persists, may increase. Bubble rashes on the lips, wings of the nose (herpes labialis et nosalis). Percussion dullness corresponding to an entire lobe or lobes. New trembling and bronchophony are increased.Tachycardia persists, there is a tendency to fall in blood pressure, cyanosis persists or even increases.Temperature remains high.Headache, fatigue, cough persist for days, sputum appears, scanty, viscous, brown in color ("rusty". Shortness of breath, pain in the side persists, may increase. Bubble rashes on the lips, wings of the nose (herpes labialis et nosalis Percussion dullness corresponding to a whole lobe or shares. Auscultatory - in the same place breathing of a bronchial type. A pleural friction noise may appear. Voice trembling and bronchophony are increased. Tachycardia persists, there is a tendency to fall in blood pressure, cyanosis persists or even increases. The temperature remains high.

By the end of the week, the temperature drops, the condition improves, shortness of breath, tachycardia decrease. Cough worries less, but the amount of sputum increases, which is easier to expectorate and loses its “rusty” color, brightens; herpetic eruptions begin to heal, form crusts, cyanosis is not pronounced, the affected side of the chest is well involved in the act of breathing, the patient does not notice pain during breathing. Auscultatory crepitation of the resolution (crepitatio redux) is heard again. Percussion dullness decreases; voice trembling and bronchophony become weaker. With a favorable course, gradually all pathological phenomena disappear. By the end of the week, the temperature drops, the condition improves, shortness of breath, tachycardia decrease. Cough worries less, but the amount of sputum increases, which is easier to expectorate and loses its “rusty” color, brightens; herpetic eruptions begin to heal, form crusts, cyanosis is not pronounced, the affected side of the chest is well involved in the act of breathing, the patient does not notice pain during breathing. Auscultatory crepitation of the resolution (crepitatio redux) is heard again. Percussion dullness decreases; voice trembling and bronchophony become weaker. With a favorable course, gradually all pathological phenomena disappear.

Additional examination data Additional examination data X-ray: at an early stage, an increase in the pulmonary pattern, at a later stage - intense pneumonic infiltration (darkening) corresponding to the affected lobe (or lobes). In the later stages, the darkening disappears, but often the strengthening of the pulmonary pattern, heaviness in the affected lobe often lasts for a long time. X-ray: at an early stage, an increase in the pulmonary pattern, at a later stage, intense pneumonic infiltration (darkening) corresponding to the affected lobe (or lobes). In the later stages, the darkening disappears, but often the strengthening of the pulmonary pattern, heaviness in the affected lobe often lasts for a long time.

Blood: already in the first days there is a high leukocytosis - 10-15 109 / l or more, predominantly neutrophilic, often with a shift to the left and toxigenic granularity. Leukocytosis lasts 8-10 days, then both the total number of leukocytes and the formula normalize. ESR is increased from the very first day and lasts for a long time, often not reaching the norm even by the time of discharge (the average length of a patient's stay in the hospital for lobar pneumonia is 18–20 days). Blood: already in the first days there is a high leukocytosis - 10-15 109 / l or more, predominantly neutrophilic, often with a shift to the left and toxigenic granularity. Leukocytosis lasts 8-10 days, then both the total number of leukocytes and the formula normalize. ESR is increased from the very first day and lasts for a long time, often not reaching the norm even by the time of discharge (the average length of a patient's stay in the hospital for lobar pneumonia is 18–20 days).

Sputum: in the early days a lot of erythrocytes, a moderate amount of leukocytes, alveolar epithelium. On the 5th–7th–9th day, the number of leukocytes increases, the sputum becomes mucopurulent, with a yellowish color. Subsequently, sputum brightens, the number of formed elements decreases. Sputum: in the early days a lot of erythrocytes, a moderate amount of leukocytes, alveolar epithelium. On the 5th–7th–9th day, the number of leukocytes increases, the sputum becomes mucopurulent, with a yellowish color. Subsequently, sputum brightens, the number of formed elements decreases. It is possible to conduct bacterioscopic and bacteriological studies of sputum, although they are of little practical importance (due to the inaccuracy of the bacterioscopic and the delayed response of the bacteriological study). It is possible to conduct bacterioscopic and bacteriological studies of sputum, although they are of little practical importance (due to the inaccuracy of the bacterioscopic and the delayed response of the bacteriological study).

When studying the function of external respiration, VC can be reduced (turning off a significant proportion of lung tissue from breathing, limiting deep breathing). Due to changes in bronchial reactivity and a tendency to obstruction, FVC may decrease, and the Tifno-Votchal test may be positive. Due to shortness of breath (rapid breathing), the MOD may be increased. When studying the function of external respiration, VC can be reduced (turning off a significant proportion of lung tissue from breathing, limiting deep breathing). Due to changes in bronchial reactivity and a tendency to obstruction, FVC may decrease, and the Tifno-Votchal test may be positive. Due to shortness of breath (rapid breathing), the MOD may be increased.

Pneumonia pathomorphosis: typical chills occur only in 25% of patients, shortness of breath is less pronounced; in most patients, it is not possible to identify typical lobar dullness of percussion sound - dullness is present, but it does not occupy a large area. Auscultatory bronchial breathing is rare. Often the temperature reaches high numbers, but falls already on the 3-4th day. The general condition of the patient also improves by this time. In general, general intoxication is much less pronounced; in most patients, leukocytosis is almost not observed, the increase in ESR is moderate. X-ray - limited segmental infiltration of the lungs. Rarely, concomitant pleurisy occurs. Pneumonia pathomorphosis: typical chills occur only in 25% of patients, shortness of breath is less pronounced; in most patients, it is not possible to identify typical lobar dullness of percussion sound - dullness is present, but it does not occupy a large area. Auscultatory bronchial breathing is rare. Often the temperature reaches high numbers, but falls already on the 3-4th day. The general condition of the patient also improves by this time. In general, general intoxication is much less pronounced; in most patients, leukocytosis is almost not observed, the increase in ESR is moderate. X-ray - limited segmental infiltration of the lungs. Rarely, concomitant pleurisy occurs.

Thus, at present, in many cases, CP proceeds as a focal one, and their differentiation is difficult. This phenomenon is explained by the influence of modern antibiotic treatment, as well as a change in the reactivity of the organism. Many scientists prefer to talk about acute pneumonia, without subdividing it into focal and croupous. This is true in cases that are difficult to differentiate. Thus, at present, in many cases, CP proceeds as a focal one, and their differentiation is difficult. This phenomenon is explained by the influence of modern antibiotic treatment, as well as a change in the reactivity of the organism. Many scientists prefer to talk about acute pneumonia, without subdividing it into focal and croupous. This is true in cases that are difficult to differentiate. If the picture is clear, a more accurate diagnosis of focal or lobar pneumonia should be made. If the picture is clear, a more accurate diagnosis of focal or lobar pneumonia should be made.

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Pneumonia (other Greek πνευμονία from πνεύμων) (pneumonia) - inflammation of the lung tissue, usually of infectious origin with a primary lesion of the alveoli

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The term "pneumonia" unites a large group of diseases, each of which has its own etiology, pathogenesis, clinical picture, radiological signs, characteristic laboratory data and features of therapy. It can occur as an independent disease or as a complication of other diseases.

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The main method of diagnosis is x-ray examination of the lungs.

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The main method of treatment is antibiotic therapy.

• Antibiotics are the cornerstone of pneumonia treatment. The choice of antibiotic is made depending on the microorganism that caused the pneumonia.
• Also used are drugs that dilate the bronchi and thin the sputum - orally or in the form of inhalation, corticosteroids, intravenous saline solutions, oxygen.
• Sometimes pleural puncture and bronchoscopy are performed.
• Physiotherapy is often used: UV, vibration massage, exercise therapy, paraffin, ozocerite

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• Late diagnosis and delay in starting antibiotic therapy (more than 8 hours) worsen the prognosis of the disease.
• Possible death.
• Serious complications of pneumonia can be: lung abscess and gangrene, pleurisy, pleural empyema, obstruction, acute respiratory failure, endocarditis, pericarditis, meningitis, pulmonary edema, sepsis

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healthy person's lungs

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X-ray of the lungs of a person with pneumonia

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Pneumonia may be

• focal - that is, occupy a small focus of the lung (bronchopneumonia - respiratory sections + bronchi);
• segmental - spread to one or more segments of the lung;
• lobar - to capture a lobe of the lung. A classic example of lobar pneumonia is lobar pneumonia - mainly the alveoli and the adjacent pleura;
• drain - the merger of small foci into larger ones;
• total - pneumonia is called if it spreads to the entire lung.

Also, pneumonia can be

Unilateral, if only one lung is affected

Bilateral, if both lungs are affected.

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• The incidence of pneumonia depends on many factors: standard of living, social and family status, working conditions, contact with animals, travel, availability bad habits contact with sick people, individual characteristics a person, the geographical distribution of a particular pathogen.
• Pneumonia remains one of the most common causes of death of children and the elderly in our time, especially in social institutions (orphanages, boarding schools, places of detention).
• The frequency of pneumonia increases sharply in elderly patients at a time when they are being treated in hospitals for another disease.

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